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Urinary System – Anatomy, Structure, Functions

The urinary system’s function is to filter blood and create urine as a waste by-product. The organs of the urinary system include the kidneys, renal pelvis, ureters, bladder and urethra. The body takes nutrients from food and converts them to energy.

The urinary system is the kidneys of our body’s sewage treatment plant. They filter toxins out of the body, as well as other substances that we no longer need. These waste products leave your body in the urine produced in your kidneys. This is how water and substances like urea, uric acid, salts, and amino acids are removed from the blood. Every day, all of the blood in your body (between five and six liters) passes through the kidneys about 300 times. So your kidneys filter about 1,700 liters of blood per day in total. This leads to the daily production of about 170 liters of primary urine (glomerular filtrate) – which later becomes urine.

Inside the kidney, there is a renal medulla, which has small tubules and larger collecting tubes running through it. As the primary urine flows through this system of tubes, the kidney cells re-absorb about 99 percent of the fluid in it, as well as many substances that can still be used, and at the same time release other substances. About 1.7 liters of urine are produced like this each day. The urine passes from the kidneys through the ureter into the urinary bladder, where it is stored.

Overview of the Urinary System

The urinary system works with the lungs, skin, and intestines to maintain the balance of chemicals and water in the body. Adults eliminate about 27 to 68 fluid ounces (800 to 2,000 milliliters) per day based on typical daily fluid intake of 68 ounces (2 liters), National Institutes of Health (NIH). Other factors in urinary system function include fluid lost through perspiring and breathing. In addition, certain types of medications, such as diuretics that are sometimes used to treat high blood pressure, can also affect the amount of urine a person produces and eliminates. Some beverages, such as coffee and alcohol, can also cause increased urination in some people.

The primary organs of the urinary system are the kidneys, which are bean-shaped organs that are located just below the rib cage in the middle of the back. The kidneys remove urea — a waste product formed by the breakdown of proteins — from the blood through small filtering units called nephrons. Each nephron consists of a ball formed of small blood capillaries, called a glomerulus, and a small tube called a renal tubule. Urea, together with water and other waste substances, forms the urine as it passes through the nephrons and down the renal tubules of the kidney.

Muscles in the ureter walls continually tighten and relax to force urine away from the kidneys, according to the NIH. A backup of urine can cause a kidney infection. Small amounts of urine are emptied into the bladder from the ureters about every 10 to 15 seconds.

The bladder is a hollow, balloon-shaped organ that is located in the pelvis. It is held in place by ligaments attached to other organs and the pelvic bones, according to the Kidney & Urology Foundation of America. The bladder stores urine until the brain signals the bladder that the person is ready to empty it. A normal, healthy bladder can hold up to 16 ounces (almost half a liter) of urine comfortably for two to five hours.

To prevent leakage, circular muscles called sphincters close tightly around the opening of the bladder into the urethra, the tube that allows urine to pass outside the body. The only difference between the female and male urinary system is the length of the urethra, according to Merck Manuals. In females, the urethra is about 1.5 to 2 inches long (3.8 to 5.1 cm) and sits between the clitoris and the vagina. In males, it is about 8 inches (20 cm) long, runs the length of the penis and opens at the end of the penis. The male urethra is used to eliminate urine as well as semen during ejaculation.

The urinary system maintains blood homeostasis by filtering out excess fluid and other substances from the bloodstream and secreting waste.

Structure

The urinary system refers to the structures that produce and transport urine to the point of excretion. In the human urinary system, there are two kidneys that are located between the dorsal body wall and parietal peritoneum on both the left and right sides.

The formation of urine begins within the functional unit of the kidney, the nephrons. Urine then flows through the nephrons, through a system of converging tubules called collecting ducts. These collecting ducts then join together to form the minor calyces, followed by the major calyces that ultimately join the renal pelvis. From here, urine continues its flow from the renal pelvis into the ureter, transporting urine into the urinary bladder. The anatomy of the human urinary system differs between males and females at the level of the urinary bladder. In males, the urethra begins at the internal urethral orifice in the trigone of the bladder, continues through the external urethral orifice, and then becomes the prostatic, membranous, bulbar, and penile urethra. Urine exits through the external urethral meatus. The female urethra is much shorter, beginning at the bladder neck and terminating in the vaginal vestibule.

Key Points

The renal system eliminates wastes from the body, controls levels of electrolytes and metabolites, controls the osmoregulation of blood volume and pressure and regulates blood pH.

The renal system organs include the kidneys, ureter, bladder, and urethra. Nephrons are the main functional component of the kidneys.

The respiratory and cardiovascular systems have certain functions that overlap with renal system functions.

Metabolic wastes and excess ions are filtered out of the blood, combined with water, and leave the body in the form of urine.

A complex network of hormones controls the renal system to maintain homeostasis.

Key Terms

  • ureter: These are two long, narrow ducts that carry urine from the kidneys to the urinary bladder.
  • osmoregulation: The most important function of the renal system, in which blood volume, blood pressure, and blood osmolarity (ion concentration) is maintained in homeostasis.

The Renal System

The renal system, which is also called the urinary system, is a group of organs in the body that filters out excess fluid and other substances from the bloodstream. The purpose of the renal system is to eliminate wastes from the body, regulate blood volume and pressure, control levels of electrolytes and metabolites, and regulate blood pH.

The renal system organs include the kidneys, ureters, bladder, and urethra. Metabolic wastes and excess ions are filtered out of the blood, along with water, and leave the body in the form of urine.

This is an illustration of the major organs of the renal system. In this schematic view of the urinary system, shown in descending order, we see the kidney, ureter, bladder, and urethra. 

Components of the renal system: Here are the major organs of the renal system.

Renal System Functions

The renal system has many functions. Many of these functions are interrelated with the physiological mechanisms in the cardiovascular and respiratory systems.

  • Removal of metabolic waste products from the body (mainly urea and uric acid).
  • Regulation of electrolyte balance (e.g., sodium, potassium, and calcium).
  • Osmoregulation controls the blood volume and body water contents.
  • Blood pressure homeostasis: The renal system alters water retention and thirst to slowly change blood volume and keep blood pressure in a normal range.
  • Regulation of acid-base homeostasis and blood pH, a function shared with the respiratory system.

Many of these functions are related to one another as well. For example, water follows ions via an osmotic gradient, so mechanisms that alter sodium levels or sodium retention in the renal system will alter water retention levels as well.

Organs of the Renal System

Kidneys and Nephrons

Kidneys are the most complex and critical part of the urinary system. The primary function of the kidneys is to maintain a stable internal environment (homeostasis) for optimal cell and tissue metabolism. The kidneys have an extensive blood supply from the renal arteries that leave the kidneys via the renal vein.

Nephrons are the main functional component inside the parenchyma of the kidneys, which filter blood to remove urea, a waste product formed by the oxidation of proteins, as well as ions like potassium and sodium. The nephrons are made up of capsule capillaries (the glomerulus) and a small renal tube.

The renal tube of the nephron consists of a network of tubules and loops that are selectively permeable to water and ions. Many hormones involved in homeostasis will alter the permeability of these tubules to change the amount of water that is retained by the body.

Kidney and urinary system parts and their functions

  • Two kidneys. This pair of purplish-brown organs is located below the ribs toward the middle of the back. Their function is to:
    • Remove waste products and drugs from the body
    • Balance the body’s fluids
    • Release hormones to regulate blood pressure
    • Control production of red blood cells

The kidneys remove urea from the blood through tiny filtering units called nephrons. Each nephron consists of a ball formed of small blood capillaries, called a glomerulus, and a small tube called a renal tubule. Urea, together with water and other waste substances, forms the urine as it passes through the nephrons and down the renal tubules of the kidney.

  • Two ureters. These narrow tubes carry urine from the kidneys to the bladder. Muscles in the ureter walls continually tighten and relax forcing urine downward, away from the kidneys. If urine backs up, or is allowed to stand still, a kidney infection can develop. About every 10 to 15 seconds, small amounts of urine are emptied into the bladder from the ureters.
  • Bladder. This triangle-shaped, hollow organ is located in the lower abdomen. It is held in place by ligaments that are attached to other organs and the pelvic bones. The bladder’s walls relax and expand to store urine, and contract and flatten to empty urine through the urethra. The typical healthy adult bladder can store up to two cups of urine for two to five hours.

Upon examination, specific “landmarks” are used to describe the location of any irregularities in the bladder. These are:

  • Trigone: a triangle-shaped region near the junction of the urethra and the bladder
  • Right and left lateral walls: walls on either side of the trigone
  • Posterior wall: back wall
  • Dome: roof of the bladder
  • Two sphincter muscles. These circular muscles help keep urine from leaking by closing tightly like a rubber band around the opening of the bladder.
  • Nerves in the bladder. The nerves alert a person when it is time to urinate or empty the bladder.
  • Urethra. This tube allows urine to pass outside the body. The brain signals the bladder muscles to tighten, which squeezes urine out of the bladder. At the same time, the brain signals the sphincter muscles to relax to let urine exit the bladder through the urethra. When all the signals occur in the correct order, normal urination occurs.

Human Osmoregulation

The kidneys play a very large role in human osmoregulation by regulating the amount of water reabsorbed from the glomerular filtrate in kidney tubules, which is controlled by hormones such as antidiuretic hormone (ADH), renin, aldosterone, and angiotensin I and II.

A basic example is that a decrease in water concentration of blood is detected by osmoreceptors in the hypothalamus, which stimulates ADH release from the pituitary gland to increase the permeability of the wall of the collecting ducts and tubules in the nephrons. Therefore, a large proportion of water is reabsorbed from fluid to prevent a fair proportion of water from being excreted.

The extent of blood volume and blood pressure regulation facilitated by the kidneys is a complex process. Besides ADH secretion, the renin-angiotensin feedback system is critically important to maintain blood volume and blood pressure homeostasis.

Function

The main functions of the urinary system and its components are to:

  • Regulate blood volume and composition (e.g. sodium, potassium and calcium)
  • Regulate blood pressure.
  • Regulate pH homeostasis of the blood.
  • Contributes to the production of red blood cells by the kidney.
  • Help synthesize calcitriol (the active form of Vitamin D).
  • Stores waste products (mainly urea and uric acid) before it and other products are removed from the body.

References

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Chronic Inflammation – All About You Need To Know

Chronic inflammation is also referred to as slow, long-term inflammation lasting several months to years. Generally, the extent and effects of chronic inflammation vary with the cause of the injury and the ability of the body to repair and overcome the damage. This activity reviews the pathophysiology of chronic inflammation and highlights the role of the interprofessional team in taking steps to control the pathology.

Inflammation is part of the body’s defense mechanism. It is the process by which the immune system recognizes and removes harmful and foreign stimuli and begins the healing process. Inflammation can be either acute or chronic.

Types of Chronic Inflammation

  • Acute Inflammation – Tissue damage due to trauma, microbial invasion, or noxious compounds can induce acute inflammation. It starts rapidly, becomes severe in a short time and symptoms may last for a few days for example cellulitis or acute pneumonia. Subacute inflammation is the period between acute and chronic inflammation and may last 2 to 6 weeks.
  • Chronic Inflammation – Chronic inflammation is also referred to as slow, long-term inflammation lasting for prolonged periods of several months to years. Generally, the extent and effects of chronic inflammation vary with the cause of the injury and the ability of the body to repair and overcome the damage. This article reviews chronic inflammation.

Types of Chronic Inflammation

  • Nonspecific proliferative: Characterized by the presence of non-specific granulation tissue formed by infiltration of mononuclear cells (lymphocytes, macrophages, plasma cells) and proliferation of fibroblasts, connective tissue, vessels, and epithelial cells, for example, an inflammatory polyp-like nasal or cervical polyp and lung abscess.
  • Granulomatous inflammation: A specific type of chronic inflammation characterized by the presence of distinct nodular lesions or granulomas formed with an aggregation of activated macrophages or its derived cell called epithelioid cells usually surrounded by lymphocytes. The macrophages or epithelioid cells inside the granulomas often coalesce to form Langhans or giant cells such as foreign body, Aschoff, Reed-Sternberg, and Tumor giant cells. There are two types:
  • Granuloma formed due to foreign body or T-cell mediated immune response is termed as foreign body granuloma, for example, silicosis.
  • Granuloma formed due to chronic infection is termed as infectious granuloma, for example, tuberculosis and leprosy.

Causes of Chronic Inflammation

Chronic inflammation can result from the following:

  • Failure of eliminating the agent causing an acute inflammation such as infectious organisms including Mycobacterium tuberculosis, protozoa, fungi, and other parasites that can resist host defenses and remain in the tissue for an extended period.
  • Exposure to a low level of a particular irritant or foreign material that cannot be eliminated by enzymatic breakdown or phagocytosis in the body including substances or industrial chemicals that can be inhaled over a long period, for example, silica dust.
  • An autoimmune disorder in which the immune system recognizes the normal component of the body as a foreign antigen, and attacks healthy tissue giving rise to diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE).
  • A defect in the cells responsible for mediating inflammation leading to persistent or recurrent inflammation, such as auto-inflammatory disorders (Familial Mediterranean Fever).
  • Recurrent episodes of acute inflammation. However, in some cases, chronic inflammation is an independent response and not a sequel to acute inflammation for example diseases such as tuberculosis and rheumatoid arthritis.
  • Inflammatory and biochemical inducers are causing oxidative stress and mitochondrial dysfunction such as increased production of free radical molecules, advanced glycation end products (AGEs), uric acid (urate) crystals, oxidized lipoproteins, homocysteine, and others.

Epidemiology

Chronic inflammatory diseases are the most significant cause of death in the world. The World Health Organization (WHO) ranks chronic diseases as the greatest threat to human health. The prevalence of diseases associated with chronic inflammation is anticipated to increase persistently for the next 30 years in United States. in 2000, nearly 125 million Americans were living with chronic conditions and 61 million (21%) had more than one. In recent estimates by Rand Corporation, in 2014 nearly 60% of Americans had at least one chronic condition, 42% had more than one, and 12% of adults had 5 or more chronic conditions. Worldwide, 3 of 5 people die due to chronic inflammatory diseases like stroke, chronic respiratory diseases, heart disorders, cancer, obesity, and diabetes. The prevalence of some specific chronic inflammation-mediated diseases are as follows:

  • DiabetesAccording to the American Diabetes Association, 30.3 million people or 9.4% of the American population, had diabetes in 2015 and it was the 7th leading cause of death in the United States.
  • Cardiovascular diseases: In line with 2017 updated report from the American Heart Association, cardiovascular diseases (CVDs) accounts for 1 out of every three deaths or approximately 800,000 deaths in the United States. Globally, CVD accounts for 31% of all deaths, and coronary heart disease (CHD) accounts for most deaths due to CVD, followed by stroke (1 of 20 deaths in the United States) and heart failure.
  • Arthritis and Joint Diseases: These affect approximately 350 million people worldwide and nearly 43 million people in the United States or almost 20% of the population. This number is expected to exceed 60 million by 2020. Nearly, 2.1 million Americans suffer from rheumatoid arthritis.
  • Allergies: These rank among the sixth leading cause of chronic human diseases in the United States and affect more than 50 million Americans each year. Asthma affects more than 24 million people in the United States including more than 6 million children. In 2015, 8.2% of adults and 8.4% of children were diagnosed with hay fever.
  • Chronic Obstructive Pulmonary Disease (COPD): The third most common cause of death in the United States in 2014, and nearly 15.7 million Americans (6.4%) were reported to have been diagnosed with COPD.

Pathophysiology

Most of the features of acute inflammation continue as the inflammation becomes chronic, including the expansion of blood vessels (vasodilation), increase in blood flow, capillary permeability and migration of neutrophils into the infected tissue through the capillary wall (diapedesis). However, the composition of the white blood cells changes soon and the macrophages and lymphocytes begin to replace short-lived neutrophils. Thus the hallmarks of chronic inflammation are the infiltration of the primary inflammatory cells such as macrophages, lymphocytes, and plasma cells in the tissue site, producing inflammatory cytokines, growth factors, enzymes and hence contributing to the progression of tissue damage and secondary repair including fibrosis and granuloma formation, etc.

In response to foreign or self-antigens, the tissue immune cells such as macrophages and dendritic cells release cytokines such as IL-1 and TNF-α. These cytokines induce the injury-site-endothelial cells to release Selectins and Integrins which stimulate chemotaxis and diapedesis of the circulating leukocytes. In addition to the recruitment of leukocytes, the tissue macrophages, and dendritic cells also play a role in the clearing of the antigen by phagocytosis, the release of cytokines and serving as antigen-presenting cells to lymphocytes. Once the circulating leukocytes enter the local injury site, they are activated by various cytokines and chemokines secreted by the macrophages and dendritic cells. On activation, the leukocytes further release cytokines and mediators of inflammation. Neutrophils are the initial cells and most predominant in the acute phase of inflammation. Neutrophils contain granules rich with lysozyme, matrix metalloproteinases, myeloperoxidase which are released on the foreign or self-antigen leading to its destruction. Neutrophils also destroy the antigen by phagocytosis, the release of reactive oxygen species and cytokines such as IL-1, IL-6, and TNF-α. Lymphocytes including T-lymphocytes and B-lymphocytes are the next line of defense, and they play a crucial role in mediating inflammation by several complex mechanisms including secreting of cytokines, costimulation of lymphocytes, and production of antibodies and immune complexes. Circulating platelets can also play a role in inflammation by platelet aggregation, thrombus formation and degranulation releasing chemokines and inflammatory mediators.

Diagnosis of Chronic Inflammation

Risk Factors Associated with Chronic Inflammation

Several risk factors promote a low-level inflammatory response. These include:

  • Age: Increasing age is positively correlated with elevated levels of several inflammatory molecules. The age-associated increase in inflammatory molecules may be due to mitochondrial dysfunction or free radical accumulation over time and other age-related factors like an increase in visceral body fat.
  • Obesity: Many studies have reported that fat tissue is an endocrine organ, secreting multiple adipokines and other inflammatory mediators. Some reports show that the body mass index of an individual is proportional to the amount of pro-inflammatory cytokines secreted. Metabolic syndrome typifies this well.
  • Diet: Diet rich in saturated fat, trans-fats, or refined sugar is associated with higher production of pro-inflammatory molecules, especially in individuals with diabetes or overweight individuals.
  • Smoking: Cigarette smoking is associated with lowering the production of anti-inflammatory molecules and inducing inflammation.
  • Low Sex Hormones: Studies show that sex hormones like testosterone and estrogen can suppress the production and secretion of several pro-inflammatory markers and it has been observed that maintaining sex hormone levels reduces the risk of several inflammatory diseases.
  • Stress and Sleep Disorders: Both physical and emotional stress is associated with inflammatory cytokine release. Stress can also cause sleep disorders. Since individuals with irregular sleep schedules are more likely to have chronic inflammation than consistent sleepers, sleep disorders are also considered as one of the independent risk factors for chronic inflammation.

Symptoms of Chronic Inflammation

Some of the common signs and symptoms that develop during chronic inflammation are listed below.

  • Body pain, arthralgia, myalgia
  • Chronic fatigue and insomnia
  • Depression, anxiety and mood disorders
  • Gastrointestinal complications like constipation, diarrhea, and acid reflux
  • Weight gain or weight loss
  • Frequent infections

Evaluation

Tests for Chronic Inflammation

Unfortunately, there are no highly effective laboratory measures to assess patients for chronic inflammation, and diagnoses are only undertaken when the inflammation occurs in association with another medical condition.

  • Serum protein electrophoresis (SPE) can show concomitant hypoalbuminemia and polyclonal increase in all gamma globulins (polyclonal gammopathy).
  • The two blood tests that are inexpensive and good markers of systemic inflammation include high-sensitivity C-reactive protein (hsCRP) and fibrinogen. High levels of hs-CRP indicate inflammation, but it is not a specific marker for chronic inflammation since it is also elevated in acute inflammation resulting from a recent injury or sickness. The normal serum levels for hsCRP are less than 0.55 mg/L in men and less than 1.0 mg/L in women. The normal levels of fibrinogen are 200 to 300 mg/dl. SAA (Serum Amyloid A) can also mark inflammation but is not a standardized test.
  • Detecting pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1beta), interleukin-6 (IL-6), and interleukin-8 (IL-8) is an expensive method but may identify specific factors causing chronic inflammation. Again, the assays are not standardized like hs-CRP, fibrinogen, and SPE.

Treatment of Chronic Inflammation

Many dietary and lifestyle changes may be helpful in removing inflammation triggers and reducing chronic inflammation as listed below. The most effective is weight loss. For example, in patients with psoriatic arthritis which is chronic inflammatory arthritis, weight loss alone has been shown to be independently associated with clinically significant improvement in disease activity and inflammation.

  • Low-glycemic diet: Diet with a high glycemic index is related to a high risk of stroke, coronary heart disease, and type 2 diabetes mellitus. It is beneficial to limit the consumption of inflammation-promoting foods like sodas, refined carbohydrates, fructose corn syrup in a diet.
  • Reduce intake of total, saturated fat, and trans fats: Some dietary saturated and synthetic trans-fats aggravate inflammation, while omega-3 polyunsaturated fats appear to be anti-inflammatory. Processed and packaged foods that contain trans fats such as processed seed and vegetable oils, baked goods (like soybean and corn oil) should be reduced from the diet.
  • Fruits and vegetables: Blueberries, apples, Brussels sprouts, cabbage, broccoli, and cauliflower, which are high in natural antioxidants and polyphenols, and other anti-inflammatory compounds, may protect against inflammation. Cherries and cherry juice consumption has been shown to be uricosuric and inhibitory for IL-1 in patients with gout.
  • FiberHigh intake of dietary soluble and insoluble fiber is associated with lowering levels of IL-6 and TNF-alpha.
  • Nuts: such as almonds are associated with lowering the risk of cardiovascular disease and diabetes.
  • Green and black tea polyphenols: Tea polyphenols are associated with a reduction in CRP in human clinical studies.
  • Curcumin: a constituent of turmeric has been shown to be associated with significant improvement in several inflammatory diseases in animal models.
  • Fish Oil: The richest source of omega-3 fatty acids. Higher intake of omega-3 fatty acids is associated with lowering levels of TNF-alpha, CRP, and IL-6.
  • Mung bean: Rich in flavonoids (particularly vitexin and isovitexin). It is a traditional food and herbal medicine known for its anti-inflammatory effects.
  • Micronutrients: Magnesium, vitamin D, vitamin E, zinc, and selenium). Magnesium is listed as one of the most anti-inflammatory dietary factors, and its intake is associated with the lowering of hsCRP, IL-6, and TNF-alpha activity. Vitamin D exerts its anti-inflammatory activity by suppressing inflammatory mediators such as prostaglandins and nuclear factor kappa-light-chain-enhancer of activated B cells. Vitamin E, zinc, and selenium act as antioxidants in the body.
  • Sesame Lignans: Sesame oil consumption reduces the synthesis of prostaglandin, leukotrienes, and thromboxanes and is known for its potential hypotensive activity.

Physical Exercise

In human clinical trials, it is shown that energy expenditure through exercise lowers multiple pro-inflammatory molecules and cytokines independently of weight loss.

Conventional Drugs that Combat Chronic Inflammation

  • Metformin is commonly used in the treatment of type II diabetic patients with dyslipidemia and low-grade inflammation. The anti-inflammatory activity of metformin is evident by reductions in circulating TNF-alpha, IL-1beta, CRP, and fibrinogen in these patients.
  • Statins are anti-inflammatory as they reduce multiple circulating and cellular mediators of inflammation. This pleiotropic effect appears to contribute in part to the reduction in cardiovascular events.
  • Non-steroidal anti-inflammatory drugs (NSAIDs) like naproxen, ibuprofen, and aspirin acts by inhibiting an enzyme cyclooxygenase (COX) that contributes to inflammation and are mostly used to alleviate the pain caused by inflammation in patients with arthritis.
  • Corticosteroids also prevent several mechanisms involved in inflammation. Glucocorticoids are prescribed for several inflammatory conditions including inflammatory arthritis, systemic lupus, sarcoidosis, and asthma.
  • Herbal supplements like ginger, turmeric, cannabis, hyssop, and Harpagophytum procumbens are shown to have anti-inflammatory properties however one should always consult with a doctor before their use and caution should be taken for using some herbs like hyssop and cannabis.

Complications

Although chronic inflammation progresses silently, it is the cause of most chronic diseases and presents a major threat to the health and longevity of individuals. Inflammation is considered a major contributor to several diseases.

  • Cardiovascular diseases: Many clinical studies have shown strong and consistent relationships between markers of inflammation such as hsCRP and cardiovascular disease prediction. Furthermore, Atherosclerosis is a pro-inflammatory state with all the features of chronic low-grade inflammation and leads to increase cardiovascular events such as myocardial infarction, stroke, among others.
  • Cancer: Chronic low-level inflammation also appears to participate in many types of cancer such as kidney, prostate, ovarian, hepatocellular, pancreatic, colorectal, lung, and mesothelioma.
  • Diabetes: Immune cells like macrophages infiltrate pancreatic tissues releasing pro-inflammatory molecules in diabetic individuals. Both circulating and cellular biomarkers underscore that diabetes is a chronic inflammatory disease. Chronic complications linked to diabetes include both microvascular and macrovascular complications. Diabetes not only increases the risk of macrovascular complications like strokes and heart attacks but also microvascular complications like diabetic retinopathy, neuropathy, and nephropathy.
  • Rheumatoid arthritis: In a genetically susceptible host, chronic inflammation induced by several environmental factors such as smoking and infections leads to a systemic autoimmune response that causes a local inflammatory response in joints, infiltration of immune cells, and release of cytokines. The persistence of chronic inflammation in the synovium in inadequately treated RA has been associated with a worse prognosis and radiographic progression of the disease.
  • Allergic asthma: A complex, chronic inflammatory disorder associated with inappropriate immune response and inflammation in conducting airways involving a decline in airway function and tissue remodeling.
  • Chronic obstructive pulmonary disease (COPD): An obstructive lung disease, develops as a chronic inflammatory response to inspired irritants and characterized by long-term breathing problems.
  • Alzheimer’s disease: In older adults, chronic low-level inflammation is linked to cognitive decline and dementia.
  • Chronic kidney disease (CKD): Low-grade inflammation is a common feature of chronic kidney disease. It can lead to the retention of several pro-inflammatory molecules in the blood and contributes to the progression of CKD and mortality. Amyloidosis can be a result of underlying chronic inflammation that can lead to severe renal complications.
  • Inflammatory Bowel Disease (IBD) is a group of chronic inflammatory disorders of the digestive tract. It can develop as ulcerative colitis causing long-lasting inflammation and ulcers in the lining of the large intestine and rectum or Crohn’s disease characterized by inflammation of the lining of the digestive tract dispersing into affected tissues such as mouth, esophagus, stomach, and anus.

Deterrence and Patient Education

Chronic inflammation can have a deleterious effect on the body and is a key factor causing almost all chronic degenerative diseases. The following are some of the most effective ways to prevent chronic inflammation.

  • Increase uptake of anti-inflammatory foods: It is important to avoid eating simple sugars, refined carbohydrates, high-glycemic foods, trans fats, and hydrogenated oils. Consuming whole grains, natural foods, plenty of vegetables and fruits such as avocados, cherries, kale, and fatty fish like salmon is helpful in defeating inflammation.
  • Minimize intake of antibiotics and NSAIDs: The use of antibiotics, antacids, and NSAIDs should be avoided as it could harm the microbiome in the gut causing inflammation in intestinal walls known as leaky gut which in turn releases toxins and triggers chronic, body-wide inflammation.
  • Exercise regularly to maintain an optimum weight: It is largely known that adipose tissue in obese or overweight individuals induces low-grade systemic inflammation. Regular exercise is helpful not only in controlling weight but also in decreasing the risk of cardiovascular diseases and strengthening the heart, muscles, and bones.
  • Sleep longer: Overnight sleep (ideally at least 7 to 8 hours) helps stimulating human growth hormones and testosterone in the body to rebuild itself.
  • Stress Less: Chronic psychological stress is linked to a greater risk for depression, heart disease, and the body losing its ability to regulate the inflammatory response and normal defense. Yoga and meditation are helpful in alleviating stress-induced inflammation and its harmful effects on the body.

References

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HMSN – Causes, Symptoms, Diagnosis, Treatment

HMSN/Hereditary Motor and Sensory Neuropathy/Charcot-Marie-Tooth disease (CMT) is slowly progressive neurodegenerative hereditary chronic motor and sensory neuropathy disease and one of a group of disorders that cause damage to the peripheral nerves, the nerves that transmit information and signals from the brain and spinal cord to and from the rest of the body, as well as sensory information such as touch back to the spinal cord and brain.  CMT can also directly affect the nerves that control the muscles.  Progressive muscle weakness typically becomes noticeable in adolescence or early adulthood, but the onset of disease can occur at any age.  Because longer nerves are affected first, symptoms usually begin in the feet and lower legs and then can affect the fingers, hands, and arms.  Most individuals with CMT have some amount of physical disability, although some people may never know they have the disease.

CMT, also known as hereditary motor and sensory neuropathy, slowly progressive inherited neurological disorders distal motor neuropathy of the arms and legs usually beginning in the first to third decade and resulting in weakness and atrophy of the muscles in the feet and/or hands is one of the most common neuropathy affecting an estimated. It is possible to have two or more types of CMT, which happens when the person has mutations in two or more genes, each of which causes a form of the disease.  CMT is a heterogeneous genetic disease, meaning mutations in different genes can produce similar clinical symptoms.

Charcot-Marie-Tooth (CMT) disease is a heterogeneous group of genetic disorders presenting with the phenotype of a chronic progressive neuropathy affecting both the motor and sensory nerves. During the last decade over two dozen genes have been identified in which mutations cause CMT. The disease illustrates a multitude of genetic principles, including diverse mutational mechanisms from point mutations to copy number variation (CNV), allelic heterogeneity, age-dependent penetrance and variable expressivity.

Other Names for This Condition

  • Charcot-Marie-Tooth hereditary neuropathy
  • Charcot-Marie-Tooth syndrome
  • CMT
  • Hereditary motor and sensory neuropathy
  • HMSN
  • Peroneal muscular atrophy
  • PMA

Types of Charcot-Marie-Tooth Disease

There are many different types of CMT disease, which may share some symptoms but vary by pattern of inheritance, age of onset, and whether the axon or myelin sheath is involved.

In general the three autosomal dominant neuropathy types based on NCV (normal >40-45 meters/second) were the following []:

  • Demyelinating (CMT1) defined as NCV <35 m/s. The clinical findings of distal muscle weakness and atrophy and sensory loss were usually slowly progressive and often associated with pes cavus foot deformity and bilateral foot drop. Affected individuals usually became symptomatic between ages five and 25 years. Fewer than 5% of individuals became wheelchair dependent. Life span was not shortened.
  • Axonal (non-demyelinating) (CMT 2) defined as NCV >45m/s. The clinical findings were distal muscle weakness and atrophy. Although axonal peripheral neuropathy shows extensive clinical overlap with demyelinating peripheral neuropathy, in general individuals with axonal neuropathy tended to be less disabled and have less sensory loss than individuals with demyelinating neuropathy.
  • Dominant intermediate CMT (DI-CMT) defined as NCV 35-45 m/s. The clinical findings are a relatively typical CMT phenotype. NCVs are so variable that within a family some  individuals fall in the demyelinating neuropathy range, whereas others fall in the axonal neuropathy range.

CMT1 – is caused by abnormalities in the myelin sheath.  The autosomal dominant disorder has six main subtypes.

  • CMT1A – results from a duplication of the gene on chromosome 17 that carries the instructions for producing the peripheral myelin protein-22 (PMP22).  The PMP22 protein is a critical component of the myelin sheath.  Overexpression of this gene causes the abnormal structure and function of the myelin sheath.  CMT1A is usually slowly progressive.  Individuals experience weakness and atrophy of the muscles of the lower legs beginning in childhood; later they experience hand weakness, sensory loss, and foot and leg problems.  A different neuropathy distinct from CMT1A called hereditary neuropathy with predisposition to pressure palsy (HNPP) is caused by a deletion of one of the PMP22 genes.  In this case, abnormally low levels of the PMP22 gene result in episodic, recurrent demyelinating neuropathy.
  • CMT1B – is caused by mutations in the gene that carries the instructions for manufacturing the myelin protein zero (MPZ, also called P0), which is another critical component of the myelin sheath.  Most of these mutations are point mutations, meaning a mistake occurs in only one letter of the DNA genetic code.  To date, scientists have identified more than 120 different point mutations in the P0 gene.  CMT1B produces symptoms similar to those found in CMT1A.
  • Other less common causes of CMT1 result from mutations within the SIMPLE (also called LITAF), EGR2, PMP22, and NEFL genes, respectively.

CMT2

  • Results from abnormalities in the axon of the peripheral nerve cell, rather than the myelin sheath, and is less common than CMT1.  This autosomal dominant disorder has more than a dozen subtypes (some of which have their own variants), with each subtype being associated with mutations in a specific gene.  Symptoms are similar to those seen in CMT1, but people with CMT2 often have less disability and sensory loss than individuals with CMT1.  The onset of CMT2 is usually in childhood or adolescence.  Some types of CMT2 may have vocal cord or phrenic nerve involvement, causing speech or breathing problems.

CMT3, or Dejerine-Sottas disease

  • It is a particularly severe demyelinating neuropathy that begins in infancy.  Infants have severe muscle atrophy, weakness, delayed motor skills development, and sensory problems.  Symptoms may progress to severe disability, loss of sensation, and curvature of the spine.  This rare disorder can be caused by mutations in multiple genes, including PMP22, MPZ, and EGR2, and can be inherited either dominantly or recessively.

CMT4

  • It comprises several different subtypes of demyelinating and axonal and motor neuropathies that are inherited autosomal recessively.   Each neuropathy subtype is caused by a mutation in a different gene (several genes have been identified in CMT4).  The mutations may affect a particular ethnic population and produce distinct physiologic or clinical characteristics.  People with CMT4 generally develop symptoms of leg weakness in childhood and by adolescence they may not be able to walk.  CMT4 is rare in the United States.

CMTX1 (also called CMT X, Type 1)

  • It is the second most common form of CMT.  This X-linked disease is caused by mutations in a gene that provides instructions for making the protein connexin-32.  The connexin-32 protein is found in myelinating Schwann cells—cells that wrap around nerve axons and make up the myelin sheath.  Males who inherit the mutated gene show moderate to severe symptoms of the disease beginning in late childhood or adolescence.  Females who inherit a mutated gene often develop milder symptoms than males or do not show symptoms.

Disease phenotypes

  • Charcot–Marie–Tooth Disease  – As CMT1 and CMT2 present with similar clinical features, distinction on the basis of the neurological exam is often impossible. The onset of clinical symptoms is in the first or second decade of life. Weakness starts distally in the feet and progresses proximally in an ascending pattern. Neuropathic bony deformities develop including pes cavus (high-arched feet) and hammer toes. With further progression the hands become weak. Muscle stretch reflexes disappear early in the ankles and later in the patella and upper limbs. Mild sensory loss to pain, temperature or vibration sensation in the legs is consistent with the phenotype. Patients also complain of numbness and tingling in their feet and hands, but paresthesias are not as common as in acquired neuropathies. Restless leg syndrome occurs in nearly 40% of patients with the axonal form.
  • Hereditary neuropathy with liability to pressure palsies (MIM 162500) – The clinical phenotype is characterized by recurrent nerve dysfunction at compression sites. Asymmetric palsies occur after relatively minor compression or trauma. Repeated attacks result in the inability of full reversal. Thus with ageing the patients with hereditary neuropathy with liability to pressure palsies (HNPP) can have significant clinical overlap with CMT1. Electrophysiological findings include mildly slowed NCV, increased distal motor latencies and conduction blocks. The neuropathological hallmark is sausage-like thickening of myelin sheaths (tomacula).
  • Dejerine–Sottas neuropathy (MIM 145900) – Dejerine–Sottas neuropathy (DSN) is a clinically distinct entity defined by delayed motor milestones. Signs of lower motor neuron-type lesion accompany the delayed motor milestones. Neurophysiological studies reveal severe slowing of NCV (<10 m/s). Neuropathology reveals pronounced demyelination, and a greater number of onion bulbs are present compared to CMT. Cerebrospinal fluid proteins may be elevated. Most patients have significant disability.
  • Congentital hypomyelinating neuropathy (MIM 605253) – Congentital hypomyelinating neuropathy (CHN) is usually present at birth, although frequently the delayed motor development draws the first attention to the peripheral neuropathy. The distinction between DSN and CHN is often difficult by clinical examination as they both may present as a hypotonic infant. The differentiation of CHN and DSN is based on pathology: the presence of onion bulbs suggest DSN whereas their absence indicate CHN. CHN may present as arthrogryposis multiplex congenita.
  • Roussy–Levy syndrome (MIM 180800) – Roussy–Levy syndrome (RLS) was originally described as demyelinating CMT associated with sensory ataxia and tremor. As molecular data became available, it was shown that these patients have the same molecular abnormalities as observed in patients clinically classified as demyelinating CMT. RLS represents the spectrum of CMT.
Genetic classification of Charcot–Marie–Tooth disease and related peripheral neuropathies
CMT Locus Gene Product OMIM
CMT1A 17p11.2 PMP22 Peripheral myelin protein 22 118220
CMT1B 1q22 MPZ Myelin protein zero 118200
CMT1C 16p13.1–p12.3 SIMPLE/LITAF SIMPLE 601098
CMT1D 10q21.1–q22.1 EGR2 Early growth response protein 2 607678
CMT1E 17p11.2 PMP22 Peripheral myelin protein 22 118220
CMT1F 8p21 NEFL Neurofilament triplet L protein 607684
CMT2A 1p36 MFN2 Mitofusin 2 118210
CMT2B 3q21 RAB7 Ras-related protein Rab-7 600882
CMT2B1 1q21.2 LMNA Lamin A/C 605588
CMT2B2 19q13.3 Unknown Unknown 605589
CMT2C 12q23–q24 Unknown Unknown 606071
CMT2D 7p15 GARS Glycyl-tRNA synthetase 601472
CMT2E/F1 8p21 NEFL Neurofilament triplet L protein 607684
CMT2F 7q11–q21 HSPB1 Heat-shock protein B1 606595
CMT2G 12q12–q13 Unknown Unknown 608591
CMT2H 8q21.3 Unknown Unknown 607731
CMT2I 1q22 MPZ Myelin protein zero 118200
CMT2J 1q22 MPZ Myelin protein zero 118200
CMT2K 8q13–q21.1 GDAP1 Ganglioside-induced differentiation protein 1 214400
CMT2L 12q24 HSPB8 Heat shock protein B8 608673
CMT4A 8q13–q21.1 GDAP1 Ganglioside-induced differentiation protein 1 214400
CMT4B1 11q22 MTMR2 Myotubularin-related protein 2 601382
CMT4B2 11p15 SBF2/MTMR13 SET binding factor 2 604563
CMT4C 5q32 SH3TC2 SH3TC2 601596
CMT4D 8q24.3 NDRG1 NDRG1 protein 601455
CMT4E 10q21.1–q22.1 EGR2 Early growth response protein 2 607678
CMT4F 19q13.1–q13.2 PRX Periaxin 145900
CMT4G 10q23.3 Unknown Unknown 605285
CMT4H 12p11.21–q13.11 FGD4 FRABIN 609311
CMT4J 6q21 FIG4 FIG4 611228
DI-CMTA 10q24.1–q25.1 Unknown Unknown 606483
DI-CMTB 19p12–13.2 DNM2 Dynamin 2 606482
DI-CMTC 1p35 YARS Tyrosyl-tRNA synthetase 608323
DI-CMTD 1q22 MPZ Myelin protein zero 607791
CMTX Xq13.1 GJB1 Gap junction β-1 protein, connexin 32 302800

Causes Charcot-Marie-Tooth Disease

A nerve cell communicates information to distant targets by sending electrical signals down a long, thin part of the cell called the axon.  The axon is surrounded by myelin, a covering that acts like the insulation on an electrical wire and aids the high-speed transmission of electrical signals.  Without an intact axon and myelin sheath, signals that run along the nerve and axon are either slow or have a weak signal, meaning that the peripheral nerve cells become unable to activate muscles or relay sensory information from the limbs back to the spinal cord and the brain.

CMT is caused by mutations in genes that support or produce proteins involved in the structure and function of either the peripheral nerve axon or the myelin sheath. More than 40 genes have been identified in CMT, with each gene linked to one or more types of the disease.  In addition, multiple genes can be linked to one type of CMT.  More than half of all cases of CMT are caused by a duplication of the PMP22 gene on chromosome 17.

Although different proteins are abnormal in different forms of CMT disease, all of the mutations mainly affect the normal function of the peripheral nerves.  Gene defects in myelin cause dysfunction of the coating, which distorts or blocks nerve signals, while other mutations limit axon function and cause axonal loss.

CMTs may occur due to any one of the following molecular and cellular mechanisms

  • Myelin assembly – genes involved in myelin compaction (MPZ), gap junctions formation (GJB1), the interaction of Schwann cells with the extracellular matrix as well as in regulating cell spreading, cell migration and apoptosis (PMP22)
  • Cytoskeletal structure – genes involved in actin polymerization (INF2), membrane-protein interactions to stabilize the myelin sheath (PRX), intermediate filaments (NEFL), cell signaling (FGD4), axonal transport (DYNC1H1)
  • Endosomal sorting and cell signaling – genes regulating vesicular transport, membrane trafficking, transport of intracellular organelles and cell signaling (LITAFMTMR2SBF1SBF2SH3TC2NDRG1FIG4RAB7ATFGDNM2SIMPLE)
  • Proteasome and protein aggregation – genes regulating microtubules (HSPB1HSPB8), cell adhesion (LRSAM1), ubiquitin ligase (TRIM2)
  • Mitochondria – genes regulating mitochondrial dynamics, structure, and the function of the respiratory chain (MFN2GDAP1MT-ATP6PDK3)
  • Others – genes regulating cell fusion-fission apparatus (DNM2), calcium homeostasis (TRPV4) glucose metabolism (HK1), transcription (EGR2HINT1PRPS1AARSGARSMARSKARSYARS)

Because of the close functional interaction, demyelinating neuropathies eventually lead to functional axonopathies and clinically manifest secondary axonal degeneration. Thus common secondary phenomena in CMTs include axonal loss, secondary Schwann cell proliferation, and acceleration of pathology due to immune-mediated mechanisms.

Symptoms of Charcot-Marie-Tooth Disease

CMT affects both sensory and motor nerves (nerves that trigger an impulse for a muscle to contract) in the arms, hands, legs, and feet.  The affected nerves slowly degenerate and lose the ability to communicate with their distant targets.  Motor nerve degeneration results in muscle weakness and a decrease in muscle bulk (atrophy) in the arms, legs, hands, or feet.

Typical early features include weakness or paralysis of the foot and lower leg muscles, which can cause difficulty lifting the foot (foot drop) and a high-stepped gait with frequent tripping or falling.  Individuals also may notice balance problems.  Foot deformities, such as high arches and curled toes (hammertoes), are also common in CMT.  The lower legs may take on an “inverted champagne bottle” shape due to the loss of muscle bulk.  As the disease progresses, weakness and atrophy may occur in the hands, causing difficulty with fine motor skills.  Degeneration of sensory nerve axons may result in a reduced ability to feel heat, cold, and touch.  The senses of vibration and position (proprioception) are often decreased in individuals with CMT.  The disease also can cause curvature of the spine (scoliosis) and hip displacement.  Many people with CMT develop contractures—chronic shortening of muscles or tendons around joints, which prevents the joints from moving freely.  Muscle cramping is common.  Nerve pain can range from mild to severe, and some individuals may need to rely on foot or leg braces or other orthopedic devices to maintain mobility. Some people with CMT experience tremors and vision and hearing can also be affected. In rare cases, breathing difficulties may occur if the nerves that control the muscles of the diaphragm are affected.

The severity of symptoms can vary greatly among individuals and even among family members with the disease and gene mutation.  Progression of symptoms is gradual.

Signs and symptoms of Charcot-Marie-Tooth disease may include

  • Weakness in your legs, ankles and feet
  • Loss of muscle bulk in your legs and feet
  • High foot arches
  • Curled toes (hammertoes)
  • Decreased ability to run
  • Difficulty lifting your foot at the ankle (footdrop)
  • Awkward or higher than normal step (gait)
  • Frequent tripping or falling
  • Decreased sensation or a loss of feeling in your legs and feet

Early symptoms of CMT

CMT is a progressive condition, which means the symptoms gradually get worse over time.

This means it may be difficult to spot symptoms in young children who have CMT.

Signs that a young child may have CMT include:

  • appearing unusually clumsy and accident-prone for their age
  • difficulty walking because they may have problems lifting their feet from the ground
  • their toes dropping forward as they lift their feet (foot drop)

Main symptoms of CMT

The main symptoms of CMT usually appear between the ages of 5 and 15, although they sometimes do not develop until well into middle age or later.

Some of the main symptoms of CMT include:

  • muscle weakness in the feet, ankles and legs at first
  • feet that are very highly arched, which can make the ankle unstable, or having very flat feet
  • curled toes (hammer toes)
  • an awkward or high step and difficulty using the ankle muscles to lift the foot, which makes walking more difficult
  • a lack of sensation in the arms and feet
  • cold hands and feet caused by poor circulation
  • wasting of the muscles in the lower legs, causing legs to have a distinctive “upside-down champagne bottle” shape
  • feeling tired a lot of the time as a result of the extra effort it takes to move around
  • uncontrollable shaking (tremor)
  • abnormal curvature of the spine (scoliosis)
  • problems speaking, breathing or swallowing (dysphagia) – these symptoms are rare in CMT

Later symptoms of CMT

As CMT progresses, the muscle weakness and lack of sensation gets worse and starts to affect your hands and arms more.

This can lead to problems with both manual dexterity and hand strength, making tasks like doing up the buttons of a shirt very difficult.

Persistent problems with walking and posture can put excessive strain on your body, which often leads to muscle and joint pain.

Less commonly, damaged nerves may also cause pain, known as neuropathic pain.

Problems with mobility and walking tend to get worse with age. It’s uncommon to lose the ability to walk completely, but older people with CMT often need a walking aid to get around.

As Charcot-Marie-Tooth disease progresses, symptoms may spread from the feet and legs to the hands and arms. The severity of symptoms can vary greatly from person to person, even among family members.

Diagnosis of Charcot-Marie-Tooth disease

Diagnosis of CMT begins with a detailed medical history, family history, and neurological examination.

Family History

  • A three-generation family history with attention to other relatives with neurologic signs and symptoms should be obtained. Documentation of relevant findings in relatives can be accomplished either through direct examination of those individuals or review of their medical records, including the results of molecular genetic testing and EMG and NCV studies.

Physical Exam

  • A physician will look for evidence of muscle weakness in the arms, legs, hands, and feet, decreased muscle bulk, reduced tendon reflexes, and sensory loss.  The physician will also look for evidence of foot deformities and other orthopedic problems, such as mild scoliosis or an abnormal formation of the hip joint.  A specific sign that may be found in individuals with CMT1 is nerve enlargement that may be felt or even seen through the skin, especially at the elbow.  These enlarged nerves, called hypertrophic nerves, are caused by abnormally thickened myelin sheaths.

Peripheral neuropathy

  • Motor nerve conduction velocities (NCVs) of affected males reveal delayed distal latencies and decreased amplitudes with relatively normal velocities (median motor NCV ≥38 m/s), consistent with axonal neuropathy.
  • Compound motor/sensory action potentials are not induced.
  • Needle electromyography (EMG) reveals polyphasic potentials with prolonged duration and reduced recruitment pattern.

Early-onset sensorineural hearing loss

  • Pure tone audiograms demonstrate bilateral profound sensorineural hearing loss.
  • Auditory brain stem response waveforms may not be obtained.
  • Temporal bone computed tomography reveals no abnormal findings.

Optic neuropathy

  • Fundoscopic examination shows bilateral optic disc pallor, indicating optic atrophy.
  • Visual evoked potentials demonstrate delayed latency and decreased amplitudes of P100.
  • Electroretinogram is normal.

Lab Testing

  • Phosphoribosylpyrophosphate synthetase (PRS) – enzyme activity can be analyzed in fibroblasts, lymphoblasts, and erythrocytes []. PRS enzyme activity in three individuals with CMTX5 was decreased compared to controls []. Note: Because it is difficult to assay PRS1 enzyme activity separately from that of the other two isoforms (PRS2 and PRS3), a decrease in PRS enzyme activity is assumed to reflect the decreased activity of PRS1, not PRS2 or PRS3.
  • Serum uric acid concentrations – measured in three individuals with CMTX5 of Korean descent and two of European descent (originally reported as having Rosenberg-Chutorian syndrome) were within the normal range [].
  • Molecular Genetic Testing GenePRPS1 encoding phosphoribosyl pyrophosphate synthetase I, is the only  in which pathogenic variants are known to cause CMTX5. Health care providers ordering genetic testing should be familiar with the genetics of CMT. Given the complexity of interpreting genetic test results and their implications for genetic counseling, health care providers should consider referral to a neurogenetics center or a genetic counselor specializing in neurogenetics
  • Molecular genetic testing approaches – can include gene-targeted testing (single-gene testing and multigene panel) and comprehensive genomic testing (exome sequencing, exome array). Gene-targeted testing requires the clinician to hypothesize which gene(s) are likely involved, whereas genomic testing does not.
  • A nerve biopsy – involves removing and analyzing a small piece of peripheral nerve under the microscope, usually taken from the calf of the leg through an incision in the skin.  People with CMT1 typically show signs of abnormal myelination.  Specifically, formations that look like onion bulbs may be seen which represent axons surrounded by layers of remyelinating Schwann cells.  People with CMT2 usually show signs of axon degeneration without evidence of demyelination.
  • Nerve Conduction Studies – The physician may order nerve conduction studies and electromyography (EMG).  During nerve conduction studies, electrodes are placed on the skin over a muscle or nerve.  These electrodes produce a small electric impulse that stimulates nerves and provides quantifiable information by capturing electrical activity from a distal muscle or nerve (those in the hands, lower arms, lower legs, and feet) that can help the doctor to arrive at a diagnosis.  EMG involves inserting a needle electrode through the skin to the muscle and measuring the bioelectrical activity of muscles.  Specific abnormalities in the readings signify axon loss.  EMG may be useful in further characterizing the distribution, activity, and severity of peripheral nerve involvement.
  • Ancillary diagnostic tests – include electrophysiological studies and sural nerve biopsy. Recently, peripheral nerve MRI and skin biopsy have emerged as potential diagnostic aids in certain types of hereditary neuropathies, though further research studies are needed. EMG and nerve conduction studies (NCS) are extremely helpful in the clinical classification of hereditary peripheral neuropathies and in guiding genetic testing. Electrophysiological studies distinguish two major types – the demyelinating form, which is characterized by symmetrically slowed nerve conduction velocity (NCV; usually <38 m/s), and the axonal form, which is associated with normal or subnormal NCV and reduced compound muscle action potential. The term intermediate CMT is used without consensus in the literature. It identifies the group of patients who cannot be classified readily as either CMT1 or CMT2, as they tend to have features of both demyelination and axonopathy. The NCV falls in the 30–45 m range, with overlap with both the demyelinating and the axonal form. If this pattern is recognized, certain genes are more likely to be involved than others (eg, GJB1 and MPZ).
  • Sural nerve biopsies – from patients with the demyelinating type reveal segmental demyelination and onion bulb formation, whereas the nerve biopsies from patients with the axonal form show axonal loss, absent or few onion bulbs and no evidence of demyelination. With the advent of genetic testing, invasive diagnostic tests such as nerve biopsy are reserved for patients in whom genetic testing does not yield to a molecular diagnosis, patients with atypical presentation or patients in whom inflammatory neuropathy is suspected.
  • Nerve ultrasound and Magnetic Resonance Neurography – are increasingly used in the evaluation of neuropathies. In CMTs, there is diffuse enlargement, including roots, plexuses, and peripheral nerves, without any variation between entrapment and non-entrapment sites. Enlarged cranial nerves have also been described. The enlargement is more pronounced in upper limbs and CMT1A as compared to other CMTs. In CMT2, there is no significant increase in the cross-sectional area (CSA) of peripheral nerves. An increase in CSA correlates with disability and disease progression. Post-contrast enhancement, vascularity, altered signal characteristics within the nerve, and fascicular architecture differentiates CMTs from other differential diagnoses such as chronic inflammatory demyelinating polyneuropathy (CIDP) and leprosy, among others. Besides, muscle volume and intramuscular fat accumulation (IMFA) in legs also correlate with disability.

Being diagnosed with CMT

Everyone reacts differently when told they have CMT.

You may experience feelings of shock, denial, confusion or fear. Some people are relieved that there’s finally an explanation for their symptoms.

If you have recently been diagnosed with CMT, you may find it useful to:

  • take all the time you need – do not rush into making important decisions about your health
  • find the support you need – talk to your family and friends when you feel ready; you may also find it helpful to contact other people with CMT through the charity Charcot-Marie-Tooth UK
  • find out what you can about CMT – both from your healthcare team and reliable online resources, such as Charcot-Marie-Tooth UK
  • get involved in your care – work closely with your healthcare team to come up with a treatment plan that best suits you

Tests before and during pregnancy

Couples with a family history of CMT who are thinking of having a baby can be referred to a genetics specialist for advice.

A genetic counsellor can help you work through the decision-making process and explain possible tests that can be carried out and any alternatives you may want to consider, such as adoption.

The main tests that can be carried out during pregnancy to check if a baby will develop certain types of CMT are:

  • chorionic villus sampling (CVS) – where a small sample of placenta is removed from the womb and tested for known CMT genes, usually during weeks 11 to 14 of pregnancy
  • amniocentesis – where a sample of amniotic fluid is taken for testing, usually during weeks 15 to 20 of pregnancy

If these tests show that your child is likely to have CMT, you can discuss with your genetic counsellor whether you want to continue the pregnancy or have a termination (abortion). It’s important to be aware that the results of these tests will not indicate how serious your child’s CMT will be. This is because the symptoms and progression of the condition can vary widely, even among family members with the same type of CMT.

It’s also important to bear in mind that both tests can slightly increase your chances of having a miscarriage.

Pre-implantation genetic diagnosis

For some couples at risk of having a child with CMT, pre-implantation genetic diagnosis (PGD) may be an option.

PGD involves using in vitro fertilisation (IVF), where eggs are removed from a woman’s ovaries before being fertilised with sperm in a laboratory. After a few days, the resulting embryos can be tested for certain types of CMT and a maximum of 2 unaffected embryos transferred into the womb.

Funding for PGD is decided on an individual basis.

For example, you may be considered ineligible for PGD on the NHS if you already have unaffected children or if the chances of having a successful pregnancy are thought to be low.

Treatment of Charcot-Marie-Tooth

Non Pharmacological

There is no cure for CMT, but physical and occupational therapies, braces and other orthopedic devices, and orthopedic surgery can help people cope with the disabling symptoms of the disease.  In addition, pain-relief drugs can be prescribed for individuals who have severe nerve pain.

  • Maintaining mobility, flexibility, and muscle strength – Beginning a treatment program early may delay or reduce nerve degeneration and muscle weakness before it progresses to the point of disability.  Physical therapy includes muscle strength training, muscle and ligament stretching, and moderate aerobic exercise.  A specialized exercise program approved by the person’s physician can help build stamina, increase endurance, and maintain overall health.
  • Braces – Many individuals with CMT require ankle braces and other orthopedic devices to maintain everyday mobility and prevent injury.  Braces can help prevent ankle sprains by providing support and stability during activities such as walking or climbing stairs.  High-top shoes or boots also can give the person support for weak ankles.  Thumb splints can help with hand weakness and loss of fine motor skills.  Assistive devices should be used before disability sets in because the devices may prevent muscle strain and reduce muscle weakening. Some people with CMT may decide to have orthopedic surgery to treat severe foot and joint deformities, improve the ability to walk, and lessen pain.
  • Occupational therapy –  involves learning new ways to cope with the activities of daily living.  For example, individuals with weakness in their arms and hands may learn to use Velcro closures or clasps instead of buttons on their clothes, or new ways of feeding themselves using assistive technology.
  • Genetic counseling – Because CMT follows the principles of Mendelian inheritance, genetic counseling for recurrence of CMT1 and CMT2 is relatively straightforward if the family history for an affected individual is defined. Because of intrafamilial variability in disease expression, definition of parental disease status requires either testing for a mutation defined in the propositus or, if the mutation is not identifiable, a thorough neurological exam with objective NCS.

Medications

Symptomatic treatment may have a substantial impact on the quality of life.

  • NSAIDs – Nonsteroidal anti-inflammatory drugs may help to relieve lower back or leg pain.
  • Antiepileptic drugs – Neuropathic pain can be treated with antiepileptic drugs (gabapentin, pregabalin, topiramate) or tricyclic antidepressants (amitriptyline).,
  • Beta-blockers – The tremor may respond to β-blockers or primidone. Caffeine and nicotine can aggravate the fine intentional tremor, thus avoidance of these substances is recommended.
  • Neurotoxic drugs – excessive alcohol should be avoided. A small dose of vincristine can produce a devastating effect in patients with CMT, thus early detection of HMSN can avoid life-threatening vincristine neurotoxicity.
  • Vitamin C – Potential therapeutic approaches aiming at normalizing dosage by small molecules in the CMT1A duplication models include vitamin C and onapristone, a progesterone antagonist., ,  An alternate molecular mechanism, point mutations in Pmp22 in the Trembler and Trembler J mouse models cause peripheral neuropathy; the disease was modified by the administration of curcumin likely by alleviating the unfolded protein response.
  • Systemic biology-based modeling – anti-sense oligonucleotides, adenoviral vector-based drug delivery, and RNA interference technology. In CMT1A, agents target PMP22 overexpression such as ascorbic acid, onapristone, geldanamycin, and rapamycin have been beneficial in animal models and cell lines with improved muscle mass and weakness. However, these agents were not useful in human clinical trials. PXT3003 (a combination of baclofen, naltrexone, and d-sorbitol) has shown a reduction in the toxic effects of PMP22 over-expression in mice and humans. A significant number of subjects who received PXT3003 showed non-deterioration or improvement in CMT Neuropathy score(CMTNS), Overall Neuropathy Limitations Scale (ONLS), 10-meter walk test, and conduction velocities as compared to placebo. PXT3003 was well tolerated and safe. Curcumin reduces endoplasmic reticulum stress and improves MPZ associated neuropathy in mice.

Lifestyle and home remedies

Some habits may prevent complications caused by Charcot-Marie-Tooth disease and help you manage its effects.

Started early and followed regularly, at-home activities can provide protection and relief:

  • Stretch regularly – Stretching can help improve or maintain the range of motion of your joints and reduce the risk of injury. It’s also helpful in improving your flexibility, balance and coordination. If you have Charcot-Marie-Tooth disease, regular stretching can prevent or reduce joint deformities that may result from uneven pulling of muscle on your bones.
  • Exercise daily – Regular exercise keeps your bones and muscles strong. Low-impact exercises, such as biking and swimming, are less stressful on fragile muscles and joints. By strengthening your muscles and bones, you can improve your balance and coordination, reducing your risk of falls.
  • Improve your stability – Muscle weakness associated with Charcot-Marie-Tooth disease may cause you to be unsteady on your feet, resulting in falls and serious injury. Walking with a cane or a walker can increase your stability. Good lighting at night can help you avoid stumbling and falling.

Here are some important points of which to take note

  • CMTs are common inherited neuromuscular disorders characterized by progressive weakness, wasting, and skeletal deformities.
  • Electrophysiological tests are useful to confirm the diagnosis of neuropathy and exclude alternative conditions that present with foot drop and/or foot deformities such as distal myopathies, muscular dystrophies, and idiopathic pes cavus, among others.
  • Electrophysiological tests are useful to screen other family members for asymptomatic neuropathy.
  • Patients of demyelinating CMTs have slowed conduction velocities within the first few years of life. Clinical manifestations of weakness, wasting, and deformities arise from axonal loss over the years.
  • There is striking phenotypic variability suggesting the potential role for modifier genes and epigenetic factors.
  • A detailed pedigree chart covering three or four generations is essential to find the pattern of inheritance. This is necessary before carrying out genetic studies.
  • All patients should have genetic counseling before genetic testing.
  • In the case of demyelinating neuropathies, the patient should first undergo testing for PMP22 duplication since it is the commonest genetic abnormality. After excluding copy number variations in PMP22, they need targeted gene sequencing or whole-exome sequencing.
  • In the case of axonal neuropathies, the patient is first tested for mutations in MFN2. Alternately, the patient can directly undergo target gene sequencing or whole-exome sequencing.
  • Establishing the genetic diagnosis is crucial for genetic counseling, reproductive planning, and considering the patient for potential upcoming therapies.
  • Patients need to undergo specific tests to detect subclinical involvement of other organs/ systems to recommend timely prophylactic measures.
  • Patients should avoid using drugs that worsen neuropathy.
  • Patient education and counseling, regular follow-up, emphasis on rehabilitation measures, and consideration for therapeutic trials by a multi-disciplinary team are very important.

What research is being done?

The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease.  The NINDS is a component of the National Institutes of Health (NIH), the leading supporter of biomedical research in the world.

Ongoing research on CMT includes efforts to identify more of the mutant genes and proteins that cause the various disease subtypes, discover the mechanisms of nerve degeneration and muscle atrophy with the goal of developing interventions to stop or slow down these debilitating processes, and develop therapies to reverse nerve degeneration and muscle atrophy.

The NINDS supports the NIH’s Rare Diseases Clinical Research Network, which is made up of different research consortia aimed at improving the availability of rare diseases information, clinical studies, and clinical research information.  The Network’s Inherited Neuropathies Consortium conducts studies that include a natural history analysis of CMT, the search for new genes and those that modify an individual’s symptoms, therapy development, and training programs to educate future investigators for the inherited neuropathies.  For more information on the Rare Diseases Clinical Research Network and its consortia, see Rare Diseases Info.

Scientists are studying PMP22 gene regulation to design and validate assays that measure the presence, amount, or activity of a target object.  Other studies examine the effects of small molecules on the biological system in order to develop novel treatments.  High-throughput screens (a way to quickly assess the biological activity of large numbers of compounds) may identify candidate medications that reduce PMP22 levels. Additional research focuses on how the mitochondria, the cell’s power plant, may play a role in the axonal degeneration seen in CMT, as well as other diseases.

An NIH longitudinal collaborative study hopes to determine the natural history of CMT and how the presence of a certain gene mutation may result in disease types and symptoms.  Also, a two-part study is looking for new genes that cause the disease as well as genes that do not cause the disease but may modify a person’s symptoms.  Other NIH-funded scientists are using next-generation sequencing (which can quickly identify the structure of millions of small fragments of DNA at the same time) to identify novel CMT genes.

Gene therapy is another promising area of research.  Experiments involving cell cultures and animal models of the disease have shown that it is possible to deliver genes to Schwann cells and muscles.  Other studies show trophic factors or nerve growth factors, such as the hormone androgen that prevent nerve degeneration.

References

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Bankart Lesion – Causes, Symptoms, Diagnosis, Treatment

Bankart lesion is an injury of the anterior (inferior) glenoid labrum of the shoulder due to anterior shoulder dislocation. It is characterized as a detachment of the anteroinferior capsulolabral glenoid complex, resulting in loss of labral height and elongation of the anterior band of the inferior glenohumeral ligament. This anatomical defect was described by Bankart as the “essential lesion,” responsible for the perpetuation of shoulder instability. When this happens, a pocket at the front of the glenoid forms that allow the humeral head to dislocate into it. It is an indication for surgery and often accompanied by a Hill-Sachs lesion, damage to the posterior humeral head.[rx]

A Bankart lesion is the avulsion of the anteroinferior capsule and labrum from the glenoid rim and is usually associated with a traumatic anterior glenohumeral dislocation in a young population.[rx,rx] A traumatic anterior glenohumeral dislocation may also be associated with an avulsion fracture of the anterior glenoid rim. This is known as a bony Bankart lesion and the amount of bone loss is an important factor in recurrent glenohumeral instability.[rxrx] The Bankart lesion is named after English orthopedic surgeon Arthur Sydney Blundell Bankart (1879–1951).[rx] bony Bankart is a Bankart lesion that includes a fracture of the anterior-inferior glenoid cavity of the scapula bone.[rx]

Types of Bankart Lesion

Bankart lesion is often associated with the Hill-Sachs lesion due to their common mechanism of injury. Bankart Lesion may involve the labrum only (“soft Bankart“), or involve the glenoid bone itself (“bony Bankart”).

  • The soft tissue Bankart lesion involves injury to the anterior or anteroinferior glenoid labrum, the fibrocartilagenous structure that surrounds and deepens the bony glenoid.
  • An osseous or bony Bankart lesion – (a, b) is a fracture of the anterior-inferior glenoid cortical rim on which the labrum rests
  • Like the Hill-Sachs lesion – a Bankart lesion may result in anterior shoulder joint instability and recurrent dislocations.
  • Perthes lesion – Perthes lesion is a variant of Bankart lesion in where there is a tear of the glenoid labrum, with an intact scapular periosteum. There is only minimal displacement of the torn anterior labrum in this case, and hence the lesions are difficult to understand and diagnose on routine MRI or MRA. MRA with the arm in ABER stretches the anteroinferior joint capsule, IGHL, and helps in better delineation of the lesion.[rx,rx] It is important to detect this on MRA as it can be missed on arthroscopy because of the minimal displacement it occurs.
  • Anterior labroligamentous periosteal sleeve avulsion (ALPSA) – ALPSA lesion was first defined by Neviaser et al.[rx] as avulsion and medial rolling of the inferior labor-ligamentous complex structure along the scapular neck. This is an important diagnosis to make as the lesion can be easily missed on arthroscopy.[rx] An ALPSA lesion, during an operative procedure, needs to be converted to a Bankart lesion (reapposition of the medially rolled labrum to the glenoid rim) followed by a Bankart repair. The procedure needs relatively more expertise and more operating time. Preoperative proper knowledge of the severity of the lesion is useful for the operating surgeon and their team.
  • Glenolabral articular disruption (GLAD) – As described by Neviaser[rx] a GLAD lesion consists of a superficial anterior-inferior labral tear associated with an anterior-inferior articular cartilage injury. The use of intra-articular contrast in the MRA helps to visualize small tears at the level of the anterior-inferior glenoid rim. GLAD lesions are usually not a cause of instability unless associated with other labral pathologies. They can present with clicking during shoulder joint movement.
  • Superior labral anterior-posterior (SLAP) type 5 lesion – The SLAP lesion, described by Snyder et al,[rx] is an injury involving the superior aspect of the glenoid labrum, which includes the biceps tendon anchor. SLAP tears were initially classified into four distinct but related types of lesions. Maffet et al.[16] added three more types. Currently, ten types or patterns are recognized.[rx,rx] A sagittal MRI or MRA can demonstrate the complete extent of the labral tear.
  • Humeral avulsion of glenohumeral ligament (HAGL) lesion – HAGL lesions are much less common than Bankart lesions as a cause of anteroinferior instability.[rx] On MRA, or in the presence of joint effusion, the normal distended axillary pouch is a U-shaped structure, which changes into a J-shape as the anterior band of the inferior glenohumeral ligament (IGHL) droops inferiorly.
  • Bony humeral avulsion of the glenohumeral ligaments (BHAGL) lesion – In the BHAGL lesion, there is a small avulsed osseous fragment attached to the torn end of the humeral attachment of the IGHL.[rx]
  • Glenoid avulsion of the glenohumeral ligaments (GAGL) lesion – Glenoid avulsion of the glenohumeral ligaments (GAGL) implies an avulsion of the IGHL from the inferior pole of the glenoid, without an associated inferior labral disruption[rx].
  • Inferior ALPSA or cul-de-sac lesion – In this case, there is the medial displacement of both the anterior-inferior labrum and the IGHL under the inferior neck of the glenoid. On coronal MRI images, there is the characteristic greater medial displacement of the capsule (and IGHL) relative to the anteroinferior labrum[rx].
  • Hill-Sachs lesion – Hill-Sachs lesion consists of a bony injury to the posterosuperior humeral head as a result of inferior displacement. In Hill-Sachs and reverse Hill-Sachs lesions, preoperative determination of the extent of bone loss is surgically important as greater than 30% loss increases the chance of repeated dislocations and necessitates bone grafting.
  • Findings in posterior instability – Less common than anteroinferior instability, posterior instability represents only instability cases.[rx] It can occur as a component of multidirectional instability (MDI) as well as after trauma. The prevalence of posterior labral tears in patients with posterior instability is less and more variable. Ligamentous abnormality involving the posterior band of the inferior glenohumeral ligament may be seen in isolation or in posterior or anteroinferior instability.[rx]
  • Reverse Hill-Sachs lesion – This consists of an anteromedial superior humeral head impaction fracture that is often associated with a reverse Bankart lesion (posterior glenoid labrum disruption).
  • Reverse HAGL lesion – In posterior instability there is sometimes complete avulsion of the posterior attachment of the shoulder capsule and the glenohumeral ligament from the posterior humeral neck[rx] .
  • Posterior GLAD lesion (focal posterior cartilage deficiency) – This lesion has been described recently and can be associated with posterior instability.[rxrx]
    Posterior glenoid rim deficiency – In recurrent posterior instability, two shapes of the posterior-inferior glenoid – the “lazy J” and the “delta” shapes – are reported to be more often found than in normal subjects.[rx]
  • Bennett lesion – It is an extra-articular crescentic posterior ossification associated with posterior labral injury and capsular avulsion. It is best visualized on CT; it may be missed on arthroscopy as it is extra-articular.[rx,rx]
  • Rotator cuff interval tear – RCI tears typically do not appear as complete disruption of the fibers of its components but as thinning irregularity, or focal discontinuity of the rotator interval capsule[rx].

Causes of Bankart Lesion

Bankart lesions are frequently the result of high-energy trauma and sports injuries (either acute injuries or overuse injuries from repetitive arm motions). Though anyone can sustain this injury, young people in their twenties are most susceptible.

Possible causes of shoulder dislocations and lesions:

  • Car accidents – A sudden blow to the shoulder can knock the ball from its socket, tearing the labrum.
  • Sports collisions – Crashing into another person with speed and force — for example, during a football or hockey tackle  — can shove the shoulder out of alignment or drag the arm forward or backward, leading to dislocations.
  • It Falls from sports – Falling and landing on one’s shoulder can lead to shoulder dislocations in athletes, especially in sports where falling with height or speed is common, like gymnastics, skating, rollerblading, or skiing. Sliding into bases during softball or baseball can also harm the shoulder.
  • Falls not from sports – Falling off a ladder or tripping on a crack in the sidewalk can deliver enough force to dislocate the shoulder.
  • Overuse injuries – In some athletes, overuse of the shoulder can lead to loose ligaments and instability. Swimmers, tennis players, volleyball players, baseball pitchers, gymnasts, and weight lifters are prone to this problem. In addition, non-athletes may develop instability from repeated overhead motions of the arm (for example, swinging a hammer).
  • Loose ligaments  – Some people have a genetic predisposition to loose ligaments throughout the body (e.g., double-jointed individuals). They may find that their shoulders pop out of alignment easily. Treatment for these patients is often more complex.
  • The acromioclavicular joint injury that also causes shoulder dislocation
  • Bicipital tendonitis problem
  • Clavicle fractures in acute or chronic injury
  • Rotator cuff muscle injury may also cause a shoulder dislocation
  • Shoulder subluxation also causes shoulder dislocation
  • Swimmer’s shoulder joints injury most often causes shoulder dislocation
  • Traumatic injury, unilateral or by lateral, bankart lesion in most commonly, surgical abnormal.
  • Atraumatic injury, multidirectional movement injury, bilateral disorder,
  • Proper or lake of rehabilitation timely also causes shoulder dislocation,
  • Inferior capsular shift injury also causes shoulder dislocation
  • Unilateral- or multi-directional instability injury
  • Atraumatic injury cases are often multidirectional with the associated hyperlaxity problems.
  • Traumatic injury in most cases is often unidirectional injury with an associated capsulolabral injury.
  • Lake of presence or absence of accompanying soft-tissue hyperlaxity problem may also cause a shoulder dislocation
  • In most cases of soft tissue hyperlaxity, including patulous capsular laxity injury,

Symptoms of Bankart Lesion

This type of labrum tear shares many symptoms with other shoulder injuries. A thorough doctor’s exam is necessary to properly diagnose symptoms.

Symptoms of a Bankart lesion can include

  • Pain – When reaching overhead, at night, or with daily activities. Pain that does not improve with rest, change in activity, OTC medications, or ice, warrants consultation with your healthcare provider.
  • Instability and weakness – The shoulder may feel ‘loose’. Patients may report apprehension about moving the shoulder into certain positions away from the body. Patients may also report recurrent instability, subluxation, or dislocation with low energy movements, like rolling over in bed or putting on a seat belt.
  • Limited range of motion  
  • Mechanical symptoms – Grinding, catching (not moving fluidly), locking in place, or popping can all be symptoms of torn tissue getting caught in the joint.
  • A feeling of pain and tightness in the whole shoulder area causes pain for shoulder dislocation
  • A feeling of tightness especially when you are throwing a ball overarm in cricket-playing, golf
  • Decrease range of motion is lost in the following direction such as external rotation, abduction, internal rotation, forward flexion.
  • Pain on the back and decrease the range of motion.
  • Dull, aching pain with paresthesia, itching, numbness
  • The referred pain and may felt in whole shoulder joints to the arms, forearms
  • The sleep disturbance and the problem with deprivation
  • Severe sharp pain and with rapid movement (eg. trying to catch mobile phone)
  • The difficulty with activities of daily living such as dressing, driving, and personal care.
  • Lack of movement in all directions of your hand
  • Symptoms will worsen at night and morning stiffness may be felt.
  • Muscle contraction of the coracohumeral ligament limits external rotation of the arm and forearms
  • Muscle contracture and tendinopathy and capsulitis may be felt.
  • Dull or deep-seated pain in the rotator cuff muscle and spread into the biceps muscles.

Helpful Clues for Common Diagnoses

  • It May be either “cartilaginous” (labrum) or “bony” (glenoid fracture with labrum attached)
  • Most common labral injury in 1st-time dislocators
  • Labroligamentous structures are completely avulsed from glenoid with periosteal sleeve tear; ± fracture
  • Acute cartilaginous: Discrete or fragmented tear across the labral base
  • Chronic cartilaginous: “Fibrotic” medial mass
  • Bony: Describe the size of fracture fragment (> 25% of the glenoid face will likely require open surgical procedure)
  • It May be either “cartilaginous” (labrum) or “bony” (glenoid fracture with labrum attached
  • Glenoid labrum articular disruption
  • Labral tear and adjacent articular cartilage damage
  • Assess for displaced articular cartilage fragment

Diagnosis of Bankart Lesion

  • Labral height – This parameter was assessed in two moments: prior to the Bankart lesion and after the knotting. A depth digital caliper (0–150 mm/6″; resolution 0.01 mm/0.005″; Digimess) was used for measurement. The measurement was performed three times, and the arithmetic mean of the measurements was used.
  • Biomechanical traction test – For biomechanical evaluation, the specimens were submitted to the traction test using the universal Emic DL500-MF test machine with a 500 N load cell. The scapula was attached to the lower surface with the aid of a pressure clamp, and the capsule was attached to the upper clamp with an Ethibond No. 5.0 suture. The test was performed by applying traction to the capsule perpendicularly to the articular surface. Initially, traction of 55 N was applied for two minutes to calibrate the system; subsequently, the capsular thickness was measured with an external micrometer with SPC output (Mitutoyo, graduation 0.001 ± 0.002 mm) at three equidistant points.
  • Biomechanical traction test – The tests were interrupted after glenoid anchor avulsion occurred in 30% of the cases; in another 30%, after a tear at the knot-capsule interface, and in the remaining 40%, after an intrasubstance capsular tear. The required strength at the end of the test was greater in the shoulders with simple sutures than in those with Mason-Allen sutures. However, there was no statistically significant difference between the groups with simple sutures and Mason-Allen sutures.
  • Western Ontario Shoulder Instability Index Western Ontario Shoulder Instability Index (WSI), which is a subjective quality of life measurement tool specific to shoulder instability. Walch-Duplay score, which is the gold standard score used in Europe.
    The WOSI consists of four subscales: physical symptoms and pain; sport, recreation, and work function; lifestyle and social functioning; and emotional well-being. Twenty-one items are scored using a Visual Analogue Scale measuring 100 mm horizontally placed under each question. This questionnaire requires a minimum of explanations to the patient for the filling of scales. The best possible score indicating the highest possible shoulder-related quality of life is 0 and the worst possible score indicating the poorest quality of life is 2100. [rx]
  • Walch DuplayThe European Society of Shoulder and Elbow Surgery recommended using the Walch-Duplay score which was inspired by the Rowe rating scale and takes into account both subjective and objective data (stability, pain, sport level recovery, mobility) to assess clinical outcome. The Walch-Duplay Score is the most currently used score in Europe for the assessment of the patient undergoing shoulder stabilization surgery. However, it is not a self-administrated questionnaire.
    The Walch-Duplay score (0 to 100 points) and the WOSI (0 to 2100 points) were recorded at the last follow-up. The Walch-Duplay score is composed of four items: activity, stability, pain, and mobility. According to the Walch-Duplay score, results were classified as excellent (91 and 100 points), good (76 and 90 points), fair (51–75 points) or poor (under 50).
    The correlation between the Walch-Duplay score and the WOSI is strong. The better the Walch-Duplay score is, the lower the WOSI is.[rx]
  • The instability shoulder index scoreThe Instability Shoulder Index Score (ISIS) was developed to predict the success of arthroscopic Bankart repair. Scores range from 0 to 10, with higher scores predicting a higher risk of recurrence after stabilization. The Instability Shoulder Index Score (ISIS) to predict the success of isolated arthroscopic Bankart repairs for recurrent anterior shoulder instability.
    Patients who underwent more complex arthroscopic procedures such as Hill-Sachs remplissage or open Latarjet had higher preoperative ISIS outcomes. A 10-point score was created and applied retrospectively. A score above 6 was associated with a 70% risk of recurrence, and the authors proposed using supplemental surgical procedures (such as an open Latarjet) to address this high risk. ISIS has been used in several clinical studies. The studies have shown that you can use ISIS to investigating several pathologies.
    It also correlates with the number of prior dislocations but not with patients’ perceptions of instability as reported by quality-of-life questionnaires. In the 5 academic centers involved, a higher ISIS was predictive of patients undergoing more complex surgery (Hill- Sachs remplissage or open Latarjet. [rx]
  • Hawkins’ Test – Firstly, the examinator has to hold the arms in 90 degrees anteflexion. Then he has to do passive information of the arm by use of his other arm. If the test is positive, it causes pain in the region of the deltoideus. During this maneuver, the tuberculum majus drives under the coracoacromial ligament. This is the cause of the pain. The test was positive for 31% of Bankart lesions. [rx]

Lab Tests

  • Laboratory tests – Leukocytosis is one of the most important tests for shoulder dislocation that supports the possibility of infection and bone-related disease.
  • Serological test – Blood cultures, urine examination, stool examination, or other possible primary symptoms of shoulder dislocation, a bone infection that obligatory when a septic infectious shoulder dislocation is being considered for examination. The and elevated inflammatory condition markers like ESR or CRP include suggesting an infectious or inflammatory disease condition of the shoulder dislocation
  • A serum uric acid level – It is often considered by clinicians and doctors when got shoulder dislocation, tendonitis is suspected, but it is not a reliable and dangerous condition as it may be spuriously elevated or high in acute inflammatory conditions or acutely during a or not.
  • Random blood glucose –  The reference values for a normal random glucose test in an average adult are 80–140mg/dl (4.4–7.8 mmol/l), between 140-200mg/dl (7.8–11.1 mmol/l) is considered pre-diabetes, and ≥ 200 mg/dl is considered diabetes according to ADA guidelines you should visit your doctor or a clinic for additional tests to over sure.
  • Ultrasound – It is basically done to investigate the thickness of the fascia, ligament injury with a shoulder dislocation are likely to have a thickened tendon with the associated fluid collection and that thickness values >4.0 mm that are the diagnostic of in shoulder dislocation []
  • Musculoskeletal ultrasound – It can further visualize the tendon and bony attachment of the thigh sites, muscles, ligaments, and nerves. Ultrasound can also be used to identify the area and extent, nature of the injury shoulder dislocation and used to evaluate periodically during the recovery phase. The most common findings on ultrasound are focal, fluid, tenosynovitis changes in the common flexor tendon position, how much thickening of the tendon sheath, partial or full-thickness tears, and tear of the tendon. Ultrasound did for dynamic imaging studies, which can provide the additional benefit in regards to evaluation for shoulder dislocation
  • Muscle Biopsy – Muscle biopsy is basically done to investigate abnormal congenital problems such as dutchmen muscular dystrophy, myasthenia graves, hemophilia, etc. A small part of the cell or tissue is collected from the thigh and send to investigate other abnormalities in shoulder dislocation.

Imaging

  • X-Ray – Conventional x-ray and radiography is the most widely used imaging modality and allows for the detection of bone fractures, osteoporosis, and abnormal pathologies condition like fracture, osteoporosis, erosions, osteonecrosis, osteoarthritis, or a juxta-articular bone tumor, neoplasm, and shoulder dislocation. Characteristic features of shoulder dislocation include marginal osteophytes formation in shoulder joint space gradually narrowing, subchondral sclerosis formation in the shoulder dislocation.
  • CT Scan – High contrast CT scan is more effective to diagnose procedures to investigate the shoulder dislocation. Abnormal tendon, ligament, cartilage, muscle and osteophyte, synovial fluid. It also helps to identify the bone tumor, necrosis, abnormal joint condition, etc.
  • MRI – It is called magnetic radical imaging is also helpful to find the bone conditions, abnormal tendon, ligament, cartilage, muscle and osteophyte, synovial fluid. It also helps to identify the bone tumor, necrosis, abnormal joint condition, shoulder dislocation. It is the final stage test to confirm that all shoulder dislocation or any other abnormality suspected others condition forearms pain, such as shoulder pigmentation, soft tissue injury and bone tumors, osteonecrosis, osteomyelitis, arthritis, and stress fracture.[,]
  • Bone scintigraphy – It is the most important test to diagnose bone cancer, neoplasm, fractures, necrosis of bone, and joints. It also helps to identify the tendon, sprained ligament, cartilage, muscle spasm, sprain, and strain with a shoulder dislocation. In where the latter may be projectional radiography (in cases of bony Bankart) and/or MRI of the shoulder. The presence of intra-articular contrast allows for better evaluation of the glenoid labrum.[rx] Type V SLAP tears extend into the Bankart defect.[rx]
  • Nerve Conduction velocity test – It a special test for leg pain or thigh pain. It is the procedure where test the sensation of the peripheral nerve stimuli to send the central nervous system means brain. It helps to identify the sensory and motor nervous system problem from the central to the peripheral cell.

Treatment of Bankart Lesion

Arthroscopic repair of Bankart injuries has good success rates, though nearly one-third of patients require further surgery for continued instability after the initial procedure in a study of young adults, with higher re-operation rates in those less than 20 years of age.[rx] Options for repair include an arthroscopic technique or a more invasive open Latarjet procedure,[rx] with the open technique tending to have a lower incidence of recurrent dislocation, but also a reduced range of motion following surgery.[rx]

Non-pharmacological treatment

  • Physiotherapy – It is one of the most common and effective non-pharmacological treatments in the world. It has a variety of treatment modules to erase acute and chronic pain. It is especially helpful in muscle spasticity, spasms related to tennis elbow or lateral epicondylitis, and elbows upper side pain front side and backside pain, and shoulder dislocation. Inflammatory and noninflammatory pain is treated by ultrasound therapy, MRI, Shortwave, microwave, wax therapy, IRR, laser therapy, interferential current therapy, iontophoresis, short-wave diathermy (SWD), and pulsed short-wave diathermy (PSWD)search faradic current, galvanic current therapy, and wax therapy. Some studies have reported good outcomes with physiotherapy regimes of stretching and strengthening, with more favorable results than rest and reduced activity at short-term follow-up.
  • Deep transverse friction massage – AIt is a special type of massage technique called transverse friction massage is often used in shoulder dislocation patients. It is applied to the tendons and the muscles, using the tips of one or two fingers to heal shoulder dislocation.
  • Transcutaneous electrical nerve stimulation (TENS) – It is called  TENS devices that help to transfer electrical impulses that are helpful for the treatment of shoulder dislocation. These are supposed to keep the pain signals from reaching the brain by blocking pain message signals and increase the secretion of endorphins that are the body’s natural pain killer.
  • Extracorporeal shockwave therapy (ESWT) – It is a physiotherapy device that generates shock or pressure waves that are transferred to the tissue through the skin for healing shoulder dislocation. This is case assumed that to improve the circulation of blood in the tissue and speed up the healing process of shoulder dislocation
  • Eccentric exercises – It is partial help to healing tendons that are the mainstays of physiotherapy regimes. A stable shoulder and scapula function and strength are necessary for correct shoulder functioning; strengthening exercises of the scapular stabilizers that are including the lower trapezius, serratus anterior, and rotator cuff muscles.
  • Percutaneous radiofrequency thermal treatment – A radiofrequency electrode pad is attached percutaneously under an ultrasound guideline which produces a thermal effect in the injured shoulder dislocation when activated, inducing visual microanatomy and removing all pathological injured tissue. Good outcomes have been reported, and no reduction in tendon size has been observed in this case.
  • Acupuncture – It is the China-oriented acute and chronic treatment system where are needle is used to stimulate the pain receptor to reduce pain. It is also helpful in some spasticity formation pain, stroke, hemiplegia, and chronic rheumatoid arthritis pain in the hand, and shoulder dislocation.
  • Extracorporeal shock-wave therapy (ECSW) – It has been proposed as an alternative to non-operative management for shoulder dislocation. It worked by the generator of specific frequency sound waves that are applied directly onto the overlying skin of the shoulder dislocation tendon.
  • The use of low-level laser therapy – It has been proposed due to the stimulating effect of laser on collagen or types 2 collagen production in tendons to increase the healing of shoulder dislocation. Although laser was not initially viewed as particularly useful among frozen shoulder or adhesive capsulitis therapies and shoulder dislocation, a recent study has to indicate some short-term benefits when using an adequate dose and wavelength.
  • Armpit stretch – It is done with the support of your healthy arm, lift the arm with the frozen shoulder upper direction shoulder dislocation, and rest arms on a surface at about chest level. In this position, gradually or slowly bend your knee joints so that your armpit opens up and you can feel it stretching. Then stand up straight again.
  • External rotation stretch – It is a manual test perform by standing in a doorframe with the affected arm placed out to the side of your body, and the elbow joints bent at a 90-degree angle so that your forearm places is parallel to the floor. Keep the upper arm at your side. Then place the palm of your hand on the doorframe to stop the arm from moving. Now turn your upper body away from the arm to stretch the shoulder. It can be done with the supervision of a physiotherapist
  • Internal rotation stretch – In this case, patients stand with their back to the doorframe. Place the back of your hand on the affected side against your bottom so that your arm is at a slight angle. Now lean the back of that elbow against the doorframe gently “trapping” your elbow to keep it in place and turn your upper body slightly inward towards the arm.
  • Manipulation under anesthesia (MUA) – In this treatment in which the shoulder is freed by rotation while the patient is under short general or local anesthesia. This is usually a day procedure treatment system and generally lasts a maximum of 15 minutes including anesthetic time. There is an increased chance of the risk of homers fractures.
  • Whole-body cryotherapy (WBC) -It involves the exposure of extreme cold to the unclothed body in a chamber that circulates very cold air that is maintained between –110 ℃ to –140 ℃ for 2 minutes to 3 minutes. WBC is assumed to provide anti-inflammatory and analgesic effects to the body.[rx]
  • Diet – Diet may be normal or according to the doctor mentions food you can take for you, such as papaya, banana, potato, nut cereal, seasonal fruits, and drink of water. In your daily routine meal must have magnesium, calcium, iron, zinc, folate, vitamin B complex, Vitamin A, Vitamin C, etc.

Medications

  • Non-steroidal anti-inflammatory drugs (NSAIDs) – It is considered to be the fast-acting nonsteroidal anti-inflammatory drugs (NSAIDs) as including acetylsalicylate, aspirin, naproxen, ibuprofen, indomethacin, and etodolac, ketorolac in pain is acute. NSAIDs drugs work by inhibiting cyclo-oxygenase enzyme to prevent the synthesis of prostaglandins, prostacyclin, and thromboxanes. It has also some side effects of aspirin at high doses when used are including tinnitus, hearing loss, and gastric intolerance.[rx]
  • Nerve relaxant –  It is basically used to reduce neuropathic pain, inflammation, nerve root entrapment, myalgia, neuralgia, and fibromyalgia, and frozen shoulder or adhesive capsulitis and shoulder dislocation. Your doctor may prescribe gabapentin, pregabalin, vitamin B1, B6, B12, etc. Major side effects are abdominal pain, nausea- vomiting.
  • Vitamin B1, B6, and B12 – It is essential for neuropathic pain management, pernicious anemia, tennis elbow, with vitamin b complex deficiency pain, paresthesia, numbness, itching with diabetic neuropathy pain, myalgia, shoulder dislocation, etc. A side effect may be nausea- vomiting, abdominal pain, cramping [rx]
  • Topical diclofenac, camphor, menthol, and nitroglycerin – or glyceryl trinitrate has shown short-term benefits in the frozen shoulder or adhesive capsulitis but overall results for treatment for tendinopathy or shoulder dislocation have been mixed depending on the site of application.
  • Oral corticosteroids – These provide short-term pain relief for improved range of motion and function. The benefits often do not last longer than a few weeks, and the result is excellent for the treatment of shoulder dislocation. Oral medications such as non-steroidal anti-inflammatory drugs (NSAIDs) and oral steroids can be used at the same time. Although the use of oral steroids has some limitations and is described in the literature they are not a commonly used interventional treatment in the UK. Major side effects are increase metabolism, muscle cramp, abdominal pain, electrolyte imbalance, etc.[rx]
  • Intra-articular steroid injections – In shoulder dislocation treatment the intraarticular steroid such as methylprednisolone, and triamcinolone injections have been shown to improve function more quickly, decrease pain, and increase range of motion. Often patients who receiving injections early in the shoulder dislocation course are more likely to obtain a benefit. Multiple injections can be given to provide symptomatic relief permanently.[rx] Major side effects are increase metabolism, muscle cramp, abdominal pain, electrolyte imbalance, etc.[]
  • Hydrosilation or Arthrographic distension – In this treatment modality, the joint is injected with saline and steroid to dilate the glenohumeral capsule, tendons, ligament, or in which increased and dilatated of the joint capsule with sterile saline or other solution such as local anesthetic or steroid are used at the same time in supervision or guided by radiological imaging such as arthrography. This has been shown to reduce pain and improve range of motion and function in the short term. [rx]
  • Suprascapular nerve blocks – It is another treatment procedure that may be beneficial in terms of pain relief but not a movement or increase range of motion of shoulder joints, and repeated joint distension may improve movement.rx]
  • Sodium hyaluronate injection – A small number of diverse studies have found that sodium hyaluronate injection in the shoulder dislocation is very effective that helps to control pain and increase range of motion. It may have a high risk of bias, provide insufficient evidence to make conclusions about the effectiveness of sodium hyaluronate in the treatment of shoulder dislocation.]

Surgery

If your shoulder continues to dislocate or feel unstable, see a doctor for further evaluation. Your doctor may use  X-rays, an MRI, and/or a thorough physical exam to help make a diagnosis.

Depending on the cause and severity of your shoulder instability, you may be prescribed an exercise program and/or surgery to stabilize the shoulder joint.

  • Shoulder arthroscopy – Most often, minimally invasive procedures can be used to repair the labrum. Your doctor can use a scope and small surgical tools to locate and examine the tear, remove damaged fragments, and repair them. Your doctor will place anchors in the bone near your tear. Sutures attached to these anchors are pulled tight, reattaching the torn piece of the labrum to the bone.
  • Open surgery – In some cases, orthopedists may prefer to use open surgery for this procedure. Which method your doctor chooses depends on variables like the type and location of your injury, the condition of your tissue, and how much additional damage you may have sustained.

If you are healthy, the outlook for shoulder surgery of this kind is generally good, with most patients resuming gentle movement and non-contact sports within 6-12 weeks. Most patients will need to avoid heavy lifting and contact sports for at least three months while they undergo physical therapy to regain strength and range of motion in the shoulder.

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The Pain – Causes, Symptoms, Diagnosis, Treatment

The Pain is an unpleasant sensation that can range from mild, localized discomfort to agony. Pain has both physical and emotional components. The physical part of pain results from nerve stimulation. Pain may be contained to a discrete area, as in an injury, or it can be more diffuse, as in disorders like fibromyalgia. Pain is mediated by specific nerve fibers that carry the pain impulses to the brain where their conscious appreciation may be modified by many factors.

Types of Pain

According to the  pattern of pain there are three classes of pain

  • Nociceptive pain,
  • Inflammatory pain which is associated with tissue damage and the infiltration of immune cells, and
  • Pathological pain is a disease state caused by damage to the nervous system or by its abnormal function (e.g. fibromyalgia, peripheral neuropathy, tension-type headache, etc.)

According to the severity three main categories of pain

  • Acute pain – lasts for a short time and occurs following surgery or trauma or other condition. It acts as a warning to the body to seek help. Although it usually improves as the body heals, in some cases, it may not.
  • Chronic pain – lasts beyond the time expected for healing following surgery, trauma or other condition. It can also exist without a clear reason at all. Although chronic pain can be a symptom of another disease, it can also be a disease in its own right, characterized by changes within the central nervous system.

A brief explanation of classes of pain is thus useful clinically to assist in the management of pain as a symptom and possible diagnosis of the underlying condition.

  • Acute pain – At the site of local tissue injury, the activation of nociceptive transducers contributes to this form of pain. The local injury environment may further alter the characteristics of nociceptors, central connections, and the autonomic nervous system.
  • Chronic pain – Persistent pain is frequently related to conditions (e.g., diabetes mellitus, arthritis, and tumor growth) which potentiates chronic tissue inflammation or alteration of the properties of peripheral nerves (neuropathic). Given the unrelenting nature of chronic pain, expectations are that external factors such as stress, emotions, and the environment may produce a summative effect with the damaged tissue to enhance the intensity and persistence of the pain. [1-4]
  • Somatic pain – This form of pain may be acute or chronic and is pain activated by the nociceptors in the cutaneous or deep tissues. In the case of cutaneous somatic pain, for instance, in the case of a skin cut, it is described as sharp or burning and is well localized. In the case of somatic pain arising from the deep tissues, such as in the joints, tendons, and bones, it is described as more throbbing or aching and is less localized.
  • Visceral pain – This pain arises mainly from the viscera and deep somatic structures (e.g., pain from the gastrointestinal tract). Visceral pain that is not distinctly localized is carried by the C fibers from the deep structures to the spinal cord.
  • Neuropathic – This persistent pain is often a consequence of damage to these nerve fibers, leading to increased spontaneous firing or alterations in their conduction or neurotransmitter properties.
  • Allodynia – Pain resulting from a typically harmless stimulus is referred to as allodynia. Though the mechanism is not fully understood, it is thought to potentially arise from 1) sensitization of the skin, leading to a decreased threshold of silent nociceptors or 2) damage to peripheral neurons inducing structural changes leading touch-sensitive fibers to reroute and form synapses in areas of the spinal cord that normally receive pain input.
  • Hyperalgesia – Occurs when noxious stimuli generate an exaggerated pain response. Similar mechanisms as proposed in the case of allodynia, with patients demonstrating amplification of pain or hyperalgesia, as well as a lengthened persistence of the pain.
  • Referred pain – When there is pain perception at a location other than the site of the painful stimulus, it is known as referred pain. The classical example of referred pain involves pain brought down the neck, shoulders, and back following myocardial infarction. There is no current consensus regarding the true mechanisms behind referred pain, and there are several theories.  Referred pain may be visceral or somatic, with the former describing pain from an organ and the latter describing pain from the deep tissues such as muscles or joints.

Acute pain can last a moment; rarely does it become chronic pain. Chronic pain persists for long periods.

According to the treatment pattern, pain is following

  • Chronic Pain – Learn about how chronic pain occurs, and why chronic pain sometimes lingers.
  • Nerve Pain – When nerve fibers get damaged, the result can be chronic pain. Read about the very common causes of neuropathic pain, like diabetes.
  • Psychogenic Pain – Depression, anxiety, and other emotional problems can cause pain — or make existing pain worse.
  • Musculoskeletal Pain – Musculoskeletal pain is pain that affects the muscles, ligaments and tendons, and bones. Learn about the causes, symptoms, and treatments.
  • Chronic Muscle Pain – Use your muscles incorrectly, too much, too little — and you’ve got muscle pain. Learn the subtle differences of muscle injuries and pain.
  • Abdominal Pain – Learn common causes of abdominal pain and when to contact your doctor.
  • Joint Pain – See the causes of joint pain and how to treat it with both home remedies and prescribed medication.
  • Central Pain Syndrome – A stroke, multiple sclerosis, or spinal cord injuries can result in chronic pain and burning syndromes from damage to brain regions. Read this brief overview.
  • Complex Regional Pain Syndrome – It’s a baffling, intensely painful disorder that can develop from a seemingly minor injury, yet is believed to result from high levels of nerve impulses being sent to the affected disorder. Learn more about this disorder.
  • Diabetes-Related Nerve Pain (Neuropathy) – If you have diabetes, nerve damage can be a serious complication. This nerve complication can cause severe burning pain especially at night. Learn more about diabetic neuropathy.
  • Shingles Pain (Postherpetic Neuralgia) – Shingle is a painful condition that arises from varicella-zoster, the same virus that causes chickenpox. Learn more about the symptoms and risk factors.
  • Trigeminal Neuralgia – It’s considered one of the most painful conditions in medicine. The face pain it causes can be treated. Learn more about what causes trigeminal neuralgia and treatments for face pain caused by it.
  •  Phantom pain – Phantom pain is pain felt in a part of the body that has been amputated, or from which the brain no longer receives signals. It is a type of neuropathic pain. The prevalence of phantom pain in upper limb amputees is nearly 82%, and in lower limb amputees is 54%. One study found that eight days after amputation, 72% of patients had phantom limb pain, and six months later, 67% reported it. Some amputees experience continuous pain that varies in intensity or quality; others experience several bouts of pain per day, or it may reoccur less often.
  • Nociceptive – Nociceptive pain is caused by stimulation of sensory nerve fibers that respond to stimuli approaching or exceeding harmful intensity (nociceptors), and maybe classified according to the mode of noxious stimulation. The most common categories are “thermal” (e.g. heat or cold), “mechanical” (e.g. crushing, tearing, shearing, etc.), and “chemical” (e.g. iodine in a cut or chemicals released during inflammation). Some nociceptors respond to more than one of these modalities and are consequently designated polymodal.
  • Breakthrough  –  Breakthrough pain is transitory acute pain that comes on suddenly and is not alleviated by the patient’s regular pain management. It is common in cancer patients who often have background pain that is generally well-controlled by medications, but who also sometimes experience bouts of severe pain that from time to time “breaks through” the medication. The characteristics of breakthrough cancer pain vary from person to person and according to the cause.
  • Neuropathic -Neuropathic pain is caused by damage or disease affecting any part of the nervous system involved in bodily feelings (the somatosensory system). Peripheral neuropathic pain is often described as “burning”, “tingling”, “electrical”, “stabbing”, or “pins and needles”.Bumping the “funny bone” elicits acute peripheral neuropathic pain.
  • Allodynia – Allodynia is pain experienced in response to a normally painless stimulus. It has no biological function and is classified by stimuli into dynamic mechanical, punctate and static. In osteoarthritis, NGF has been identified as being involved in allodynia. The extent and intensity of sensation can be assessed through locating trigger points and the region of sensation, as well as utilizing phantom maps.

The suggested ICD-11 chronic pain classification suggests 7 categories for chronic pain

  • Chronic primary pain: defined by 3 months of persistent pain in one or more anatomical regions that is unexplainable by another pain condition.
  • Chronic cancer pain: defined as cancer or treatment-related visceral, musculoskeletal, or bony pain.
  • Chronic posttraumatic pain: pain lasting 3 months post-trauma or surgery, excluding infectious or preexisting conditions.
  • Chronic neuropathic pain: pain caused by damage to the somatosensory nervous system damage.
  • Chronic headache and orofacial pain: pain that originates in the head or face, and occurs for 50% or more days over a 3 months period.
  • Chronic visceral pain: pain originating in an internal organ.
  • Chronic musculoskeletal pain: pain originating in the bones, muscles, joints, or connective tissue.
Common types of pain and typical drug management
Pain type typical initial drug treatment comments
headache paracetamol /acetaminophen, NSAIDs doctor consultation is appropriate if headaches are severe, persistent, accompanied by fever, vomiting, or speech or balance problems; self-medication should be limited to two weeks
migraine paracetamol, NSAIDs triptans are used when the others do not work, or when migraines are frequent or severe
menstrual cramps NSAIDs some NSAIDs are marketed for cramps, but any NSAID would work
minor trauma, such as a bruise, abrasions, sprain paracetamol, NSAIDs opioids not recommended
severe trauma, such as a wound, burn, bone fracture, or severe sprain opioids more than two weeks of pain requiring opioid treatment is unusual
strain or pulled muscle NSAIDs, muscle relaxants if inflammation is involved, NSAIDs may work better; short-term use only
minor pain after surgery paracetamol, NSAIDs opioids rarely needed
severe pain after surgery opioids combinations of opioids may be prescribed if the pain is severe
muscle ache paracetamol, NSAIDs if inflammation involved, NSAIDs may work better.
toothache or pain from dental procedures paracetamol, NSAIDs this should be short term use; opioids may be necessary for severe pain
kidney stone pain paracetamol, NSAIDs, opioids opioids usually needed if the pain is severe.
pain due to heartburn or gastroesophageal reflux disease antacid, H2 antagonist, proton-pump inhibitor heartburn lasting more than a week requires medical attention; aspirin and NSAIDs should be avoided[32]
chronic back pain paracetamol, NSAIDs opioids may be necessary if other drugs do not control pain and pain is persistent
osteoarthritis pain paracetamol, NSAIDs medical attention is recommended if pain persists.
fibromyalgia antidepressant, anticonvulsant evidence suggests that opioids are not effective in treating fibromyalgia

Causes of Pain

Common causes of musculoskeletal pain include:

  • Chronic exertional compartment syndrome
  • Chronic fatigue syndrome
  • Claudication
  • Dermatomyositis
  • Dystonia
  • Fibromyalgia
  • Hypothyroidism (underactive thyroid)
  • Influenza (flu) and other viral illness (influenza-like illness)
  • Lyme disease
  • Medications, especially the cholesterol medications known as statins
  • Muscle cramp
  • Myofascial pain syndrome
  • Polymyalgia rheumatica
  • Polymyositis (an inflammatory disease that causes muscle weakness)
  • Repetitive strain injuries
  • Rheumatoid arthritis (inflammatory joint disease)
  • Rocky Mountain spotted fever
  • Sprains and strains
  • Years of poor posture
  • Improper lifting and carrying of heavy objects
  • Being overweight, which puts excess strain on the back and knees
  • A congenital condition such as curvature of the spine
  • Traumatic injury
  • Wearing high heels
  • Sleeping on a poor mattress
  • No obvious physical cause
  • Ordinary aging of the spine (degenerative changes)
  • Cervical sprain and strain
  • Cervical myofascial pain
  • Cervical disc disease
  • Cervical fracture
  • Chronic pain syndrome
  • Fibromyalgia
  • Adhesive capsulitis
  • Brachial plexopathy
  • Thoracic outlet syndrome
  • Carpal tunnel syndrome
  • Cubital tunnel syndrome
  • Parsonage-Turner syndrome
  • Multiple sclerosis
  • Vitamin B12 deficiency
  • Amyotrophic lateral sclerosis
  • Guillain-Barre syndrome
  • Vertebral metastasis
  • Discitis/osteomyelitis

Diagnosis of Pain

History

Like all workups, chest pain evaluation starts with taking a complete history. Start by getting a good understanding of their complaint.

  • Onset – In addition to when the pain started, ask what the patient was doing when the pain started. Was the pain brought on by exertion or were they at rest?
  • Location – Can the patient localize the pain with one or is it diffuse?
  • Duration – How long did the pain last?
  • Character – Let the patient describe the pain in his or her own words.
  • Aggravation/alleviating factors – It is very important to find out what makes the pain worse.
    • Is there an exertional component, is it associated with eating or breathing?
    • Is there a positional component?
    • Don’t forget to ask about new workout routines, sports, and lifting.
    • Ask what medications they have tried.
  • Radiation – This may clue you into pain.
  • Timing – How many times do they experience this pain? For how long does it let up?

The physical exam should include

  • Full set of vitals including blood pressure (BP) measurements in both arms
  • General appearance, noting diaphoresis and distress
  • Skin exam for the presence of lesions (shingles)
  • Neck exam for jugular venous distension (JVD), especially with inspiration (Kussmaul sign)
  • Chest, palpate for reproducible pain and crepitus
  • Heart exam
  • Lung exam
  • Abdominal exam
  • Extremities for unilateral swelling, calf pain, edema, and symmetric, equal pulses

Lab Tests

  • Laboratory tests – Leukocytosis is one of the most important tests for neck osteoarthritis and rheumatoid arthritis that supports the possibility of infection and bone-related disease. Blood cultures, urine examination, or other possible primary sites of bone infection that obligatory, when a septic infectious joint in the neck is being considered for examination. The CRP and ESR are elevated inflammatory condition markers like ESR or CRP include suggesting an infectious or inflammatory disease condition, tuberculosis of the spine.
  • Rheumatoid factor and anti-CCP – cyclic citrullinated peptide antibodies test should be increased if there is clinical abnormality for ankle osteoarthritis and rheumatoid arthritis in right and left side neck pain are found.
  • A serum uric acid level – It is often considered by clinicians and doctors when gout, pseudogout is suspected, but it is not a reliable and dangerous condition as it may be spuriously elevated or high in acute inflammatory conditions or acutely during a true gout attack or not.
  • Synovial fluid analysis – A joint arthrocentesis or the system of aspiration of synovial fluid with blood and synovial fluid analysis that are mandatory if an infection is suspected or dangerous. Such as the patients should also be started properly treatment by using empiric antibiotic therapy as soon as possible if the synovial fluid sample is obtained from the cervical joint. The fluid analysis or any kinds of abnormalities is also helpful in diagnosing crystal formation with osteophyte and steroid-induced arthritis. The degree of the high elevation of synovial fluid are founded by WBC count can be useful in differentiating inflammatory abnormality or from non-inflammatory causes of right and left side neck pain.

Imaging

  • Radiographs of the joint – Conventional x-ray and radiography is the most widely used imaging modality and allows for the detection of bone fractures, osteoporosis, and abnormal pathologies condition like fracture, osteoporosis, erosions, osteonecrosis, osteoarthritis, or a juxta-articular bone tumor, neoplasm. Characteristic features of neck rheumatoid arthritis, osteoarthritis include marginal osteophytes formation, joint space gradually narrowing, subchondral sclerosis formation, and cysts.
  • CT Scan – High contrast CT scan is more effective to diagnose the spinal cord, surrounding muscle, rheumatoid arthritis. Abnormal tendon, ligament, cartilage, muscle and osteophyte, synovial fluid are also found in this test. It also helps to identify the bone tumor, necrosis, spinal stenosis,  abnormal vertebrae condition, etc.
  • MRI – It is called magnetic radical imaging is also helpful to find the bone conditions, abnormal tendon, ligament, cartilage, muscle and osteophyte, synovial fluid. It also helps to identify the bone tumor, necrosis, abnormal joint condition, soft tissue, etc. It is the final stage test to confirm that all joint abnormality.
  • Bone scintigraphy – It is the most important test to diagnose bone cancer, neoplasm, fractures, necrosis of bone, and joints. It also helps to identify the tendon, sprained ligament, cartilage, muscle spasm.

Treatment of Pain

The list of nonpharmacological therapies for chronic pain is extensive. Nonpharmacological options include

  • heat and cold therapy,
  • cognitive behavioral therapy,
  • relaxation therapy,
  • biofeedback,
  • group counseling,
  • ultrasound stimulation,
  • acupuncture,
  • aerobic exercise,
  • chiropractic,
  • physical therapy,
  • osteopathic manipulative medicine,
  • occupational therapy, and TENS units.
  • Spinal cord stimulation, epidural steroid injections,
  • radiofrequency nerve ablations,
  • nerve blocks,
  • trigger point injections and intrathecal pain pumps are some of the procedures and techniques commonly used to combat chronic pain. The efficacy of TENS units has been variable, and the results of TENS units for chronic pain management are inconclusive. Deep brain stimulation is for post-stroke and facial pain as well as severe, intractable pain where other treatments have failed.

Medications

Several types of medications are available that can help treat chronic pain. Here are a few examples:

  • NSAIDs –  over-the-counter pain relievers, including acetaminophen (Tylenol) or nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin (Bufferin) or ibuprofen (Advil). opioid pain relievers, including morphine (MS Contin), codeine, and hydrocodone(Tussigon) adjuvant analgesics, such as antidepressants and anticonvulsants. Acute pain is usually managed with medications such as analgesics and anesthetics. Caffeine when added to pain medications such as ibuprofen, may provide some additional benefit. Ketamine can be used instead of opioids for short-term pain. Management of chronic pain, however, is more difficult and may require the coordinated efforts of a pain management team, which typically includes medical practitioners, clinical pharmacists, clinical psychologists, physiotherapists, occupational therapists, physician assistants, and nurse practitioners.
  • The initial treatment of neuropathic – is often with gabapentin or pregabalin. These are calcium channel alpha 2-delta ligands. They are indicated for postherpetic neuralgia, diabetic neuropathy, and mixed neuropathy. There is limited evidence in the use of other antiepileptic medications to treat chronic pain, where many of these, such as lamotrigine, have a more significant side effect profile. The exception is carbamazepine in the treatment of trigeminal neuralgia and other types of chronic neuropathic pain.
  • Antidepressants – such as dual reuptake inhibitors of serotonin and norepinephrine (SNRI) or tricyclic antidepressants (TCA) can is an option. Antidepressants are beneficial in the treatment of neuropathic pain, central pain syndromes, and chronic musculoskeletal pain. For neuropathic pain, antidepressants have demonstrated a 50 percent reduction of pain relief. Fifty percent is a significant reduction, considering the average decrease in pain from various pain treatments is 30%.
  • The serotonin-norepinephrine reuptake inhibitor (SNRI) – duloxetine is useful in treating chronic pain, osteoarthritis, and the treatment of fibromyalgia. Furthermore, the efficacy of duloxetine in the treatment of comorbid depression is comparable to other antidepressants. Venlafaxine is an effective treatment for neuropathic pain, as well. A TCA can also be utilized, such as nortriptyline. TCA medications may require six to eight weeks to achieve its desired effect.
  • Topical NSAIDs – Adjunctive topical agents such as topical lidocaine are a useful treatment for neuropathic pain and allodynia as in postherpetic neuralgia. Topical NSAIDs have been shown to improve acute musculoskeletal pain, such as a strain, but are less effective in chronic pain. Yet, topical NSAIDs are more effective than controls in the treatment of pain related to knee osteoarthritis. Separately, topical capsaicin cream is an option for chronic neuropathic or musculoskeletal pain unresponsive to other treatments. Botulinum toxin has also demonstrated effectiveness in the treatment of postherpetic neuralgia. The use of cannabis is also an area of interest in pain research. There is some evidence that medical marijuana can be an effective treatment of neuropathic pain, while the evidence is currently limited in treating other types of chronic pain.
  • Sugar (sucrose) – when taken by mouth reduces pain in newborn babies undergoing some medical procedures (lancing of the heel, venipuncture, and intramuscular injections). Sugar does not remove pain from circumcision, and it is unknown if sugar reduces pain for other procedures. Sugar did not affect pain-related electrical activity in the brains of newborns one second after the heel lance procedure. Sweet liquid by mouth moderately reduces the rate and duration of crying caused by immunization injection in children between one and twelve months of age.
  • Psychological – Individuals with more social support experience less cancer pain, take less pain medication, report less labor pain, and are less likely to use epidural anesthesia during childbirth, or suffer from chest pain after coronary artery bypass surgery.
  • Cognitive-behavioral therapy (CBT) – has been shown effective for improving quality of life in those with chronic pain but the reduction in suffering is modest, and the CBT method was not shown to have any effect on the outcome. Acceptance and Commitment Therapy(ACT) may also effective in the treatment of chronic pain.

Medical procedures for pain

Certain medical procedures can also provide relief from chronic pain. An example of a few are:

  • electrical stimulation, which reduces pain by sending mild electric shocks into your muscles
  • nerve block, which is an injection that prevents nerves from sending pain signals to your brain
  • acupuncture, which involves lightly pricking your skin with needles to alleviate pain
  • surgery, which corrects injuries that may have healed improperly and that may be contributing to the pain

Additionally, various lifestyle remedies are available to help ease chronic pain. Examples include:

References

Pain

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Jersey Finger – Causes, Symptoms, Treatment

Jersey Finger (also known as rugby finger) is an avulsion of the flexor digitorium profundus tendon (FDP) from its distal insertion on the distal phalanx (zone I). The mechanism of injury is typically a forced extension of a flexed digit, such as trying to grab the jersey of an opponent during a high-speed sporting event. On exam, the affected digit remains in slight extension compared to the other digits. No active flexion of the distal interphalangeal joint (DIP) is possible. Treatment is surgical with the treatment plan dictated by the acuity of injury, the zone of injury, and any associated fracture.

Causes of Jersey Finger

The distal phalanx suffers exposure to substantial forces during pull-away mechanisms. Flexor digitorium distal avulsion commonly presents in young athletes, especially in contact sports. The mechanism of injury typically results from forceful extension of a flexed digit. A common example is grabbing the jersey of an opposing player to make a tackle during American football or rugby, resulting in a forced extension of the flexor digitorium profundus tendon during maximum contraction of the muscle belly.

DIP joint hyperextension during maximal FDP muscle belly contraction (clenched fist) leads to failure. The injury occurs to the distal tendon insertion at the base of the phalanx as this area represents its weakest point.

Diagnosis of Jersey Finger

History and Physical

It is crucial to have a high level of suspicion for a jersey finger in athletes with finger pain and to associate these injuries to sport-related trauma. Pain and tenderness of the volar aspect of the injured finger are the common presentations. In a resting position, the injured finger will usually remain in extension compared to the other digits. Sometimes, the retracted tendon can be palpated proximally to the avulsion. Flexion of the DIP joint is absent. Grip and flexion against resistance will usually cause pain.

Evaluation

Although physical examination should be enough to reach the diagnosis of jersey finger, X-rays and ultrasound may play an important role. Plain radiographs are mandatory to rule out fractures. Antero-posterior and lateral views may reveal a bony fragment, if present. Ultrasound may be useful to asses tendon anatomy in cases without fracture. In chronic injuries, ultrasound becomes crucial to evaluate tendon retraction and guide further treatment.

MRI is rarely performed but can be used to determine the increased tendon-bone distance more accurately.

Treatment of Jersey Finger

Typical treatment for ersey finger injuries is surgery. Early treatment is essential to restore blood supply and function. Flexor tendons nourish themselves from blood vessels located inside the mesotendon (long and short vincula). Conservative treatment has been minimal reporting in cases of high-risk surgical patients.

Surgical management:
  • Acute: within 3 weeks after injury.

    • Without fracture: direct tendon repair or tendon reinsertion (mini-suture anchor).
    • Fracture fragment: calls for open reduction and internal fixation (mini-screws, wires). Currently, suture anchors are being used in cases of bony avulsions as well.

There are multiple, described proven treatment techniques for acute injuries. None of these seem to be significantly superior to the others.

  • Chronic: over 3 months after injury.

    • Two-stage tendon grafting (if the full range of motion is present).
    • DIP joint arthrodesis (if chronic stiffness is present). Joint arthrodesis requires careful discussion with each patient. The distal interphalangeal joint motion may be essential for some patients (occupation and hobbies), and tendon reconstruction may become a valid alternative. Unfortunately, tendon reconstruction requires a significant time commitment from the patient to achieve a successful long-term rehabilitation outcome.

Treatment Planning

The surgical approach in the presence of a bony avulsion is challenging. Preoperative planning should consider fragment size, fragment displacement, and soft tissue repair.

Treatment of a jersey finger should take into account each patient’s goals and expectations. Treatment in sport-related injuries may be influenced by the athlete’s playing position and the level of competition.

Staging

Jersey finger injury classification:

  • Type 1: Severe avulsion. The tendon retracts into the palm. Blood supply is severely compromised.
  • Type 2: The tendon retracts but remains at the A3 pulley (proximal interphalangeal joint).
  • Type 3: The avulsion includes a bony fragment. Both tendon and fracture fragment remain at the A4 pulley.
  • Type 4: Rare injury, defined by the presence of both a fracture and a tendon avulsion from the bony fragment. The tendon can retract into the palm.

Prognosis

Early diagnosis leads to expedited treatment with excellent functional outcomes. Surgery within 10 days after the injury correlates with excellent patient-reported outcomes.

Patients may return to sports with both full active functional range of motion and the absence of pain (approximately 8 to 12 weeks).

Functional consequences of impaired DIP joint motion includes loss of dexterity and loss of pinch strength.

Postoperative functional and aesthetic results depend on accurate reduction, repair quality, and an adequate rehabilitation protocol. Prevention of scar contracture formation is crucial to maintain finger function.

Complications

A tendon advancement of over 1 cm carries the risk of quadriga. The term quadriga refers to an inability to flex the digits adjacent to the involved digit from increased tension over the repaired tendon.

Other surgical complications include infection, skin necrosis, tendon repair rupture, nail matrix injury, and adhesions.

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Wrist Arthroscopy – Anatomy, Indications, Contraindication

Wrist arthroscopy has steadily gained prominence as a diagnostic and therapeutic procedure for several wrist and carpal pathologies. Advances in wrist arthroscopy have widened its indications since it was first described in the late 1970s.

Aatomy and Physiology

The anatomy involved with wrist arthroscopy consists of the radiocarpal joint and the ulnocarpal joint. The carpus of the hand is made of 8 bones arranged in 2 rows, proximal and distal. The proximal row is the most involved in wrist arthroscopy and is made of the scaphoid, lunate, triquetrum, and pisiform, in a radial to ulnar direction, respectively. The ulnocarpal joint consists predominantly of the triangular fibrocartilage complex (TFCC). This TFCC consists of ligamentous and fibrocartilaginous structures that aid in the stabilization of the wrist joint.

The standard dorsal radiocarpal portals used in wrist arthroscopy are named and placed in relationship to the dorsal extensor compartments. There are 6 dorsal extensor compartments of the wrist. The first compartment is the most radial and contains extensor pollicis brevis (EPB) tendon and abductor pollicis longus (APL) tendon. The second dorsal compartment contains the extensor carpi radialis brevis (ECRB) tendon and extensor carpi radialis longus (ECRL) tendon. The third compartment courses around Lister’s tubercle on its ulnar side and contains the extensor pollicis longus (EPL) tendon. The fourth extensor compartment contains multiple slips of the extensor digitorum communis (EDC) tendons and the extensor indicis proprius (EIP) tendon. The fifth extensor compartment contains the extensor digiti minimi (EDM) tendon. Finally, the sixth extensor compart is the most ulnar compartment, containing the extensor carpi ulnaris (ECU) tendon.

Indications of Wrist Arthroscopy

Wrist arthroscopy may be implemented for multiple pathologies of the wrist, including diagnostic evaluation of the joint surfaces and ligaments, loose body removal, TFCC pathology, carpal instability, direct visualization of the distal radius, or scaphoid intraarticular fracture reduction, capsulectomy, ganglion excision, and radial styloidectomy. With advances in wrist arthroscopy, indications continue to grows

Contraindications of Wrist Arthroscopy

Absolute contraindications include active wrist infection for an elective procedure using intraarticular implants such as suture anchors or suture materials and capsular tears that could lead to excessive fluid extravasation. Relative contraindications include bleeding disorders.

Equipment

For wrist arthroscopy, smaller arthroscopic equipment is needed. A 30° arthroscope measuring 2.7 mm or less should be used for visualization. A 70° arthroscope may also be used. Wrist joint distraction is performed using a commercial traction device which is commonly available. It is recommended to use small joint graspers and shavers measuring 3.5 mm or less. An arthroscopic video monitor, effective light source, and recording equipment are needed.

Personnel

Wrist arthroscopy is to be performed in the operating room suite. As such, it is recommended that general operating room staff should be present, including but not limited to: A single surgeon trained in the procedure, a surgical technician, surgical assistant, circulating nurse, and anesthetist

Preparation

A complete physical exam of the upper extremity is a necessity for appropriate patient selection. Preoperative planning should take place, including preoperative wrist and hand radiographs. Advanced imaging in the form of magnetic resonance imaging (MRI) of the wrist and/or hand, may be useful for the diagnosis of soft tissue injuries treated using wrist arthroscopy.

Appropriate patient selection and screening are necessary. Patients should undergo standardized preoperative testing to ensure it is safe for them to undergo this surgical procedure and be optimized preoperatively.

Technique

Prior to transport to the operative suite, the anesthesia team may elect to perform a regional nerve block for perioperative pain control. General anesthesia is recommended for this type of procedure but can be performed under monitored anesthesia care (MAC).

Once the patient is transported to the operating room, they should be positioned supine with operative extremity on an arm table. For hemostasis, a tourniquet can be used and should be placed as proximal on the operative extremity as possible. The entire upper extremity is prepped and draped in a routine sterile fashion. The traction device with sterilized components can be attached to the operative extremity using finger traps. It is recommended that no more than 10 lbs. of traction used during the procedure.

To gain access to the wrist joint using dorsal portals, the surgeon should be facing the dorsum of the hand and seated at the patient’s head. For volar portals, the converse is true, and the surgeon should be seated in the axilla facing the volar wrist. The dorsal 3-4 portal is the standard viewing portal and is established first. This portal is between extensor compartments 3 and 4 and is found by palpating the concavity just distal to Lister’s tubercle. A 22-gauge needle is then inserted into this space between EPL and EPC. Using the needle ensures that it is in an intraarticular position. Distend the joint with 5 to 10 ml of normal saline. The needle is then pulled, and using an 11 blade scalpel, and a skin incision is made. Blunt dissection is achieved using a hemostat to avoid iatrogenic injury to sensory nerves and/or extensor tendons. An arthroscopic cannula with trocar is then bluntly punctured through the joint capsule at a 10-degree dorsal-distal to proximal-palmar angle, which accounts for the volar tilt of the distal radius. The blunt trocar is removed, and a 30° 2.7 mm arthroscope is then inserted into the cannula. These steps are repeated to establish the remaining portals.

Following the 3-4 portal, the surgeon may choose to establish an inflow/outflow fluid portal, which is most commonly the 6-U portal. The 6-U denotes placement on the ulnar side of the 6th extensor compartment containing the ECU. This can be done under direct intra-articular visualization with the arthroscope in the 3-4 portal and using an 18 gauge needle inserted just ulnar to the ECU at the level of the joint line.

The 4-5 portal is the next to be established and is generally used as the working portal, located between the 4th and 5th extensor compartment (EDC and EDM). This portal is made by palpating the EDC and rolling your finger to the ulnar border of the compartment. A 22 gauge needle is inserted into the joint under direct visualization in the same manner as the 3-4 portal. The 4-5 portal is approximately 1 cm more proximal than the 3-4 portal due to the decrease in radial height on the ulnar side of the wrist. This portal serves mainly as the working portal and allows visualization of the TFCC.

Establishing the 6-R portal is achieved by palpating the radial edge of the ECU tendon and inserting a 22 gauge needle intra-articularly. Care should be taken when making this portal as not to injure the dorsal sensory branch of the ulnar nerve, which is in close proximity to the 6-R and 6-U portals.

The 1-2 portal can be made by palpating the dorsum of the anatomic snuffbox and radial to the EPL tendon. It is recommended to place this portal no more than 4.5 mm dorsal to the APL and EPB to reduce the risk of injury to the superficial radial nerve and the radial artery.

The volar radial sided portal can be made using an inside out technique by placing a blunt trocar or switching stick through the 3-4 portal. The trocar is then gently passed through space between the volar radioscaphocapitate and long radiolunate ligaments until tenting of the skin occurs. A skin incision is made over the tip of the trocar. This portal can be safely made without damaging the nearby radial artery and the superficial sensory branch of the radial nerve.

The volar ulnar portal is located ulnar to the flexor tendons of the digits . A 2 cm longitudinal incision is made at the level of the proximal wrist crease. Flexor tendons are retracted radially, and the flexor carpi ulnaris (FCU) and neurovascular bundle are retracted ulnarly. The radiocarpal joint is identified, and a 22 gauge needle is inserted through the capsule, ensuring appropriate placement.

Once relevant portals are established, the surgeon is then able to perform a various amount of procedures, including extensive debridement, ligament repair, and osseous procedures.

Complications

Wrist arthroscopy rarely results in complications. Thorough knowledge of wrist anatomy is necessary during the portal placement so as not to cause iatrogenic injury to local neurovascular and tendinous structures. Ahsan and colleagues performed a meta-analysis to quantify the overall complication rate of wrist arthroscopy and found it to be 4.8%. Some of the complications seen were those related to traction and arm position and injury to cutaneous nerves, vascular structures, flexor and extensor tendons, ligaments, and articular cartilage.

References

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Medial Meniscus Torn – Causes, Symptoms, Treatment

Medial Meniscus Torn /Medial Meniscus Injury is a crescent-shaped, cartilaginous band found between the medial tibia and medial femur. The primary function is to decrease the amount of stress on the knee joint. The medial meniscus receives vascular supply via a capillary network formed by the medial, lateral and middle geniculate arteries and receives its innervation from the posterior tibial, obturator, and femoral nerves.

The medial meniscus is a fibrocartilage semicircular band that spans the knee joint medially, located between the medial condyle of the femur and the medial condyle of the tibia. It is also referred to as the internal semilunar fibrocartilage. The medial meniscus has more of a crescent shape while the lateral meniscus is more circular. The anterior aspects of both menisci are connected by the transverse ligament. It is a common site of injury, especially if the knee is twisted.

A tear to the meniscus (also known as a cartilage tear) is a common injury that can cause pain and problems with sports and daily activities. The meniscus is a vital component of the knee that acts like a cushion between the femur (thigh) and tibia (shin) bones, providing shock absorption and stability.

Anatomy and Physiology

The meniscus is a C-shaped cartilage that serves as a cushion between the proximal tibia and the distal femur, comprising the knee joint.  The average width is 10 mm to 12 mm, and the average thickness is 4 mm to 5 mm. The meniscus is made of fibroelastic cartilage. It is an interlacing network of collagen, glycoproteins, proteoglycan, and cellular elements, and is about 70% water. Three ligaments attach to the meniscus. The coronary ligaments connect the meniscus peripherally. The transverse (inter-meniscal) ligament is anterior and serves as a connection between the medial and lateral meniscus. The meniscofemoral ligament joins the meniscus to the posterior cruciate ligament (PCL) and has two components: the Humphrey ligament anteriorly, and the ligament of Wrisberg posteriorly. The meniscofemoral ligament originates from the posterior horn of the lateral meniscus. The meniscus is supplied blood from the medial inferior genicular artery and the lateral inferior genicular artery. The meniscus is known to have a very poor blood supply, especially the central portion, which gets most of its nutrition via diffusion. The cartilage structure of the meniscus serves as a shock absorber and cushion or for the knee joint. There are several types of possible tears of the meniscus. These include flap tear, radial tear, horizontal cleavage, bucket handle tear, longitudinal tear, and degenerative tear.

Types of Medial Meniscus Torn

There are two categories of meniscal injuries – acute tears and degenerative tears.

  • An acute tear – usually occurs when the knee is bent and forcefully twisted, while the leg is in a weight bearing position. Statistics show that about 61 of 100,000 people experience an acute tear of the meniscus.
  • Degenerative tears – of the meniscus are more common in older people. Sixty percent of the population over the age of 65 probably has some sort of degenerative tear of the meniscus. As the meniscus ages, it weakens and becomes less elastic. Degenerative tears may result from minor events and there may or may not be any symptoms present.

A meniscal tear can be classified in various ways, such as by anatomic location or by proximity to blood supply. Various tear patterns and configurations have been described.[rx] These include

  • Radial tears
  • Flap or parrot-beak tears
  • Peripheral, longitudinal tears
  • Bucket-handle tears
  • Horizontal cleavage tears
  • Complex, degenerative tears

These tears can then be further classified by their proximity to the meniscus blood supply, namely whether they are located in the “red-red,” “red-white,” or “white-white” zones.

The functional importance of these classifications, however, is to ultimately determine whether a meniscus is repairable. The repairability of a meniscus depends on a number of factors. These include:

  • Age/strength
  • Activity level
  • Tear pattern
  • Chronicity of the tear
  • Associated injuries (anterior cruciate ligament injury)
  • Healing potential

or

There are different types of meniscal tears, describing the morphology of the injury. Identifying and accurately describing the type of meniscal tear can help the surgeon in patient education and planning of the surgical procedure. Meniscal tear types include

Basic tears

  • longitudinally oriented tears
      • horizontal tear (cleavage tear)
        • parallel to the tibial plateau involving one of the articular surfaces or free edge
        • divides the meniscus into superior and inferior parts
      • longitudinal tear (vertical tear)
        • perpendicular to the tibial plateau and parallel to the long axis of the meniscus
        • divides the meniscus into medial and lateral parts
        • Wrisberg rip – is a specific subtype
        • ramp lesion – is a specific subtype
  • radial tear – perpendicular to both the tibial plateau and the long axis of the meniscus
  • root tear – typically radial-type tear located at the meniscal root
  • complex tear – a combination of all or some of horizontal, longitudinal and radial-type tears
  • displaced tear – tear involving a component that is displaced, either still attached to the parent meniscus or detached:
    • flap tear: displaced horizontal or longitudinal tears
    • bucket-handle tear: displaced longitudinal tear
    • parrot beak tear: oblique radial tear

Medial Meniscus Injury

Causes of Medial Meniscus Torn

  • Inward (valgus) force – Usually, the medial collateral ligament, followed by the anterior cruciate ligament, then the medial meniscus (this mechanism is the most common and is usually accompanied by some external rotation and flexion, as when being tackled in football)
  • Outward (varus) force –  Often, the lateral collateral ligament, anterior cruciate ligament, or both (this mechanism is the 2nd most common)
  • Anterior or posterior forces and hyperextension –  Typically, the cruciate ligaments
  • Weight bearing and rotation at the time of injury – Usually, menisci
  • Motor vehicle accidents – A “dashboard injury” occurs when the driver’s or passenger’s bent knee slams against the dashboard, pushing in the shinbone just below the knee and causing the posterior meniscus tear.
  • Contact sports – Athletes in sports such as football and soccer can tear their posterior meniscus ligament when they fall on a bent knee with their foot pointed down. The shinbone hits the ground first and it moves backward. Being tackled when your knee is bent also can cause this injury.
  • The knee is hit directly – especially during sports like soccer, rugby, and football
  • A person lands on a bent knee – such as during a fall or misstep
  • Landing directly on the front of the shinbone – such as when a dancer comes down from a leap and falls
  • A person makes cutting or pivoting maneuvers – such as when an athlete plants a foot and shifts directions
  • A person lands on one leg – which can happen after a jump in basketball or volleyball
  • A direct blow to the bent knee in an automobile injury
  • A sports-related injury in which the knee bends
  • Pulling on the ligament in a twisting injury or hyperextension
  • A misstep on uneven terrain

Symptoms of Medial Meniscus Torn

If you’ve torn your meniscus, you might have the following signs and symptoms in your knee:

  • Localized pain near the area of the tear – In tears of the lateral meniscus, this discomfort will be present along the outside edge of the knee. Pain will manifest on the inside edge of the injured knee for tears of the medial meniscus.
  • Immediate pain after the injury – A torn meniscus will often be obvious from the moment that the injury occurs. In these instances, the tearing of the meniscus is typically accompanied by the feeling of a pop or snap within the leg during an overexerting twisting or stretching motion.
  • Slow onset of symptoms – Conversely, for some, the meniscus can tear without much of a sign or initial pain. This slow onset of symptoms is more common in older individuals and those with damaged knee cartilage from osteoarthritis.
  • Pain with movement – The pain will reflect the location of the tear but extend throughout the knee with movement. In the event that the knee has locked, bending it will cause searing pain to worsen.
  • Pain after resting – Pain will likely diminish somewhat with rest; however, it will return with movement in most cases. Movement may also exacerbate swelling.
  • Fluid accumulation within the knee joint – This accumulated fluid will cause the entire area to swell up and reduce mobility. This symptom, which may occur as a result of a number of knee injuries, is known as “water on the knee.”
  • Knee locking – If a piece of the meniscus breaks free of the disc structure due to a tear, it may lodge within the joint of the knee itself. This lodging can cause knee locking, in which a person loses the ability to fully straighten the leg when sitting or standing.
  • A popping sensation
  • Swelling or stiffness
  • Pain, especially when twisting or rotating your knee
  • Difficulty straightening your knee fully
  • Feeling as though your knee is locked in place when you try to move it
  • difficulty moving your knee or inability to move it in a full range of motion
  • the feeling of your knee locking or catching
  • the feeling that your knee is giving way or unable to support you
  • Feeling of your knee giving way
  • Pain in the knee
  • A popping sensation during the injury
  • Difficulty bending and straightening the leg
  • A tendency for your knee to get “stuck” or lock up

What are the signs?

You might feel a ‘pop’ if you tear your meniscus. Many people find they can still walk on their injured knee. However, it might become gradually stiffer and more swollen over the next day or so. Common symptoms include the following.

  • Pain in your knee, although this can vary. Some people only have mild pain, and for others, the pain may come and go.
  • Swelling, usually several hours after the injury.
  • Feeling as though your knee is catching or locking, usually when your knee is bent. You may notice it making clicking or popping sounds too.
  • Your knee feeling ‘loose’, as though it’s going to give way.
  • Being unable to bend and extend your knee fully.

Symptoms of severe meniscus tears

  • Popping, locking or catching
  • Inability to straighten the knee
  • Knee that gives way
  • Stiffness and swelling right after the incident

Diagnosis of Medial Meniscus Torn

Medical History

During your doctor’s appointment, he will ask you several questions about your knee pain. Examples of such questions include:

  • Where exactly is your knee pain located?
  • Did your knee swelling come on suddenly or did it gradually develop over days?
  • Are you experiencing any other symptoms besides pain and swelling, like your knee giving out or an inability to bend or extend your knee?
  • Have you experienced any trauma or injury to the knee?
  • Do you have a known history of knee osteoarthritis?

Physical examination

After noting symptoms, a physician can perform clinical tests to determine if the pain is caused by compression and impingement of a torn meniscus. The knee is examined for swelling. In meniscal tears, pressing on the joint line on the affected side typically produces tenderness.

  • Stress testing – Stress testing to evaluate ligament integrity helps distinguish partial from complete tears. However, if patients have significant pain and swelling or muscle spasm, testing is typically delayed until x-rays exclude fractures. Also, significant swelling and spasm may make joint stability difficult to evaluate. Such patients should be examined 2 to 3 days later (after swelling and spasm have subsided). A delayed physical examination of the knee is more sensitive than MRI of the knee (86% vs 76% [rx]) for diagnosis of meniscal and anterior cruciate ligament injuries.
  • Steinmann test – Steinman test is done to diagnose meniscal pathology at the knee joint.The test is divided into 2 parts i.e Steinman part 1 and Steinman part 2 or Steinman’s tenderness displacement test. This test is useful to distinguish meniscal pathology from injury to the ligament or osteophytes.
  • The McMurray test – involves pressing on the joint line while stressing the meniscus (using flexion–extension movements and varus or valgus stress). The test is often used to indicate cartilage injuries. With the patient laying on their back the therapist holds the knee with the upper hand and the heel with the lower hand. The therapist then applies a valgus (inward) stress to the knee whilst the other hand rotates the leg externally (outwards) and extends the knee. Pain and/or an audible click while performing this maneuver can indicate a torn medial meniscus.
  • Apley’s grind test – (a grinding maneuver while the person lies prone and the knee is bent 90°) and the Thessaly test (flexing the affected knee to 20 degrees, pivoting on the knee to see. Apley’s test is also used in cases of suspected meniscal tears. The patient is positioned on their front with the knee bent. The therapist grasps the heel and ankle and applies a compressive force through the lower leg. At the same time, they rotate the lower leg. Any reproduction of symptoms, pain or clicking is a positive response, suggesting a torn meniscus.
  • The Lachman test – is the most sensitive physical test for acute anterior cruciate ligament tears (rx). With the patient supine, the examiner supports the patient’s thigh and calf, and the patient’s knee is flexed 20°.The lower leg is moved anteriorly. Excessive passive anterior motion of the lower leg from the femur suggests a significant tear.

Imaging tests

  • Imaging tests may be ordered to confirm a tear of the meniscus. These include:

Knee X-ray

  • This test won’t show a meniscus tear. However, it can be helpful to determine if there are any other causes of your knee pain, like osteoarthritis.

MRI

  • An MRI uses a magnetic field to take multiple images of your knee. An MRI will be able to take pictures of cartilage and ligaments to determine if there’s a meniscus tear.
  • While MRIs can help your doctor make a diagnosis, they aren’t considered 100 percent reliable. According to a study from 2008 published in the Journal of Trauma Management & OutcomesTrusted Source, the MRI’s accuracy for diagnosing lateral meniscus tears is 77 percent.
  • Sometimes, meniscus tears may not show up on an MRI because they can closely resemble degenerative or age-related changes. Additionally, a doctor may make an incorrect diagnosis that a person has a torn meniscus. This is because some structures around the knee can closely resemble a meniscus tear.

Ultrasound

  • An ultrasound uses sound waves to take images inside the body. This will determine if you have any loose cartilage that may be getting caught in your knee.

Arthroscopy

  • If your doctor is unable to determine the cause of your knee pain from these techniques, they may suggest arthroscopy to study your knee. If you require surgery, your doctor will also most likely use an arthroscope.
  • With arthroscopy, a small incision or cut is made near the knee. The arthroscope is a thin and flexible fiber-optic device that can be inserted through the incision. It has a small light and camera. Surgical instruments can be moved through the arthroscope or through additional incisions in your knee.
  • After an arthroscopy, either for surgery or examination, people can often go home the same day.

Treatment of Medial Meniscus Torn

Non Surgical Injury

  • Protection  – the joint from further injury by taping/strapping the knee joint, or wearing a knee support which has additional support at the sides.
  • Rest – Avoid activities that aggravate your knee pain, especially any activity that causes you to twist, rotate or pivot your knee. If your pain is severe, using crutches can take pressure off your knee and promote healing.
  • Ice – Ice can reduce knee pain and swelling. Use a cold pack, a bag of frozen vegetables or a towel filled with ice cubes for about 15 minutes at a time, keeping your knee elevated. Do this every four to six hours the first day or two, and then as often as needed. Ice your knee to reduce pain and swelling. Do it for 15-20 minutes every 3-4 hours for 2-3 days or until the pain and swelling is gone.
  • Elevate your knee – with a pillow under your heel when you’re sitting or lying down.
  • A stabilized knee brace –  has flexible springs in the sides for additional support or for more severe injuries a hinged knee brace with solid metal supports linked by a hinge will help protect the joint from sideways or lateral movement. Compression will also help reduce swelling.
  • Rest the knee –  Limit activities to include walking if the knee painful. Use crutches to help relieve pain.
  • Compress your knee. Use an elastic bandage or a neoprene type sleeve on your knee to control swelling.
  • Use stretching and strengthening exercises to help reduce stress to your knee – Ask your doctor to recommend a physical therapist for guidance.
  • Avoid impact activities such as running and jumping 
  • Full weight bearing is not permitted for 1 – 6 weeks – after surgery, depending on the type of injury and repair. Crutches will be used initially following surgery. Many surgeons brace the knee and restrict motion for 6 weeks, to prevent excessive flexion and extension.
  • Range of motion exercises – begin anywhere from 0 – 6 weeks after surgery, depending on the type of repair.
  • Strengthening exercises – begin once full range of motion has returned.
  • Return to vigorous activities – such as sports, may begin 3 – 4 months after repair.

Physiotherapy

  • A professional therapist will undertake a thorough assessment and make an accurate diagnosis to confirm cartilage meniscus injury and they may undertake an MRI scan to determine the extent of the injury.
  • A physical therapist will focus on improving mobility, strength, flexibility, and balance, which can help speed up recovery time and improve performance once the injury has healed.
  • Walking (weight-bearing) is initiated as soon as possible.
  • Knee straightening (extension) and bending (flexion) are encouraged. Pool therapy is helpful.
  • Stationary cycling is initiated as soon as adequate motion is achieved.
  • Quadriceps strengthening exercises are started, such as standing squats with toe raises and leg press.
  • Hamstring exercise may be modified for 6 months.
  • Surgery is avoided in most cases unless other major ligaments are disrupted.

Medication

  • Take anti-inflammatory medications. Non-steroidal anti-inflammatory drugs (NSAIDs), like will help with pain and swelling. However, these drugs can have side effects, such as an increased risk of bleeding and ulcers. They should be only used occasionally, unless your doctor specifically says otherwise.
  • Antibiotic – Cefuroxime or Azithromycin, or  Flucloxacillin or any others cephalosporin/quinolone antibiotic must be used to prevent infection or clotted blood remove to prevent furthers swelling and edema.
  • NSAIDs – Prescription-strength drugs that reduce both pain and inflammation. Pain medicines and anti-inflammatory drugs help to relieve pain and stiffness, allowing for increased mobility and exercise. There are many common over-the-counter medicines called non-steroidal anti-inflammatory drugs (NSAIDs). They include and KetorolacAceclofenacNaproxen, Etoricoxib.
  • Corticosteroids – Also known as oral steroids, these medications reduce inflammation.
  • Muscle Relaxants –  These medications provide relief from associated muscle spasms.
  • Neuropathic Agents – Drugs(pregabalin & gabapentin) that address neuropathic—or nerve-related—pain. This includes burning, numbness, and tingling.
  • Opioids – Also known as narcotics, these medications are intense pain relievers that should only be used under a doctor’s careful supervision.
  • Topical Medications – These prescription-strength creams, gels, ointments, patches, and sprays help relieve pain and inflammation through the skin.
  • Calcium & vitamin D3 – to improve bone health and healing fracture. As a general rule, men and women age 50 and older should consume 1,200 milligrams of calcium a day, and 600 international units of vitamin D a day.
  • Antidepressants – A drug that blocks pain messages from your brain and boosts the effects of endorphins (your body’s natural painkillers).
  • Glucosamine & DiacereinChondroitin sulfate – can be used to tightening the loose tension, cartilage, ligament, and cartilage, ligament regenerates cartilage or inhabits the further degeneration of cartilage, ligament. They are structural components of articular cartilage, and the thought is that a supplement will aid in the health of articular cartilage.
  • Intra-articular corticosteroid injections – may be useful for symptomatic menicus injury especially where there is a considerable inflammatory component. The delivery of the corticosteroid directly into the knee may reduce local inflammation associated with meniscus injury and minimize the systemic effects of the steroid.
  • Intra-articular hyaluronic acid injections (HA) – injections are another injectable option for knee meniscus injury. HA is a glycosaminoglycan that is found throughout the human body and is an important component of synovial fluid and articular cartilage. HA breaks down during the process of meniscus injury and contributes to the loss of articular cartilage as well as stiffness and pain. Local delivery of HA into the joint acts as a lubricant and may help increase the natural production of HA in the joint.

Surgery

Grade 3 meniscus tears usually require surgery, which may include:

  • Arthroscopic repair — An arthroscope is inserted into the knee to see the tear. One or two other small incisions are made for inserting instruments. Many tears are repaired with dartlike devices that are inserted and placed across the tear to hold it together. The body usually absorbs these over time. Arthroscopic meniscus repairs typically takes about 40 minutes. Usually you will be able to leave the hospital the same day.
  • Arthroscopic partial meniscectomy – The goal of this surgery is to remove a small piece of the torn meniscus in order to get the knee functioning normally.
  • Arthroscopic total meniscectomy – Occasionally, a large tear of the outer meniscus can best be treated by arthroscopic total meniscectomy, a procedure in which the entire meniscus is removed.

Trephination/ Abrasion Technique

  • This procedure is used for stable tears located on the periphery near the meniscus and joint capsule junction, where there’s a good blood supply. Multiple holes or shavings are made in the torn part of the meniscus to promote bleeding, which enhances the healing process.

Partial Resection

  • This surgical procedure is used for tears located in the inner 2/3 of the meniscus where there is no blood supply. The goal is to stabilize the rim of the meniscus by removing as little of the inner meniscus as possible. Only the torn part of the meniscus is removed. If the meniscus remains mostly intact with only the inner portion removed, the patient usually does well and does not develop early arthritis.

Complete Resection

  • This procedure involves the complete removal of the damaged meniscus. This technique is only performed if absolutely necessary. Removal of the entire meniscus frequently leads to the development of arthritis.

Meniscal Repair

  • Repairs are performed on tears near the outer 1/3 of the meniscus where a good blood supply exists, or on large tears that would require a near-total resection. The torn portion of the meniscus is repaired by using either sutures or absorbable fixation devices. These devices include arrows, barbs, staples, or tacks that join the torn edges of the meniscus so they can heal.

Meniscal Replacement

  • Experimental attempts to replace damaged meniscus are seen as important recent advances in orthopaedic medicine. The new technology mentioned here has been performed at a few surgical centers across the country on a small number of patients

Collagen meniscus implant

  • This is a scaffold of collagen inserted into the patient’s knee. Over time, a new meniscus may grow within the joint. This procedure is currently in FDA trials in the United States and has just been approved as an accepted surgical procedure in Europe.

Meniscal transplant

  • This procedure involves transplanting a meniscus from a donor into the injured knee. Only a limited number of surgeons perform this procedure on a routine basis. The long-term outcomes are still being evaluated.

Meniscus transplants

Meniscus transplants are accomplished successfully regularly, although it is still somewhat of a rare procedure and many questions surrounding its use remain. Side effects of meniscectomy include:

  • The knee loses its ability to transmit and distribute load and absorb mechanical shock.
  • Persistent and significant swelling and stiffness in the knee.
  • The knee may be not be fully mobile; there may be the sensation of knee locking or buckling in the knee.
  • The full knee may be in full motion after tear of meniscus.
  • Increases progression of arthritis and time to knee replacement.

Post-Surgical Rehabilitation

Typical locations of arthroscopic surgery incisions in a knee joint following surgery for a tear in the meniscus

After a successful surgery for treating the destroyed part of the meniscus, patients must follow a rehabilitation program to have the best result. The rehabilitation following a meniscus surgery depends on whether the entire meniscus was removed or repaired.

If the destroyed part of the meniscus was removed, patients can usually start walking using a crutch a day or two after surgery. Although each case is different, patients return to their normal activities on average after a few weeks (2 or 3). Still, a completely normal walk will resume gradually, and it’s not unusual to take 2–3 months for the recovery to reach a level where a patient will walk totally smoothly. Many meniscectomy patients don’t ever feel a 100% functional recovery, but even years after the procedure they sometimes feel tugging or tension in a part of their knee. There is little medical follow-up after meniscectomy and official medical documentation tends to ignore the imperfections and side-effects of this procedure.

If the meniscus was repaired, the rehabilitation program that follows is a lot more intensive. After the surgery a hinged knee brace is sometimes placed on the patient. This brace allows controlled movement of the knee. The patient is encouraged to walk using crutches from the first day, and most of the times can put partial weight on the knee.

Phase I

There are three phases that follow meniscal surgery. Each phase consists of rehabilitation goals, exercises, and criteria to move on to the next phase. Phase I starts immediately following surgery to 4–6 weeks or until the patient is able meet progression criteria. The goals are to restore normal knee extension, reduce and eliminate swelling, regain leg control, and protect the knee (Fowler, PJ and D. Pompan, 1993). During the first 5 days following the surgery, a passive continuous motion machine is used to prevent a prolonged period of immobilization which leads to muscular atrophy and delays functional recovery.[rx] During the 4–6 weeks post-surgical, active and passive non-weight bearing motions which flex the knee up to 90° are recommended. For patients with meniscal transplantation, further knee flexion can damage the allograft because of the increased shear forces and stresses.

Phase II

This phase of the rehabilitation program is 6 to 14 weeks after the surgery. The goals for Phase II include being able to restore full ROM, normalized gait, and performing functional movements with control and no pain (Fowler, PJ and D. Pompan, 1993). Also, muscular strengthening and neuromuscular training are emphasized using progressive weight bearing and balance exercises. Exercises in this phase can increase knee flexion for more than 90°.[rx] Advised exercises include stationary bicycle, standing on foam surface with two and one leg, abdominal and back strengthening, and quadriceps strengthening. The proposed criteria include normal gait on all surfaces and single leg balance longer than 15 seconds (Ulrich G.S., and S Aroncyzk, 1993).

Balance exercises on a foam surface in phase 2. The patient tries to maintain balance first with both legs, then with only the affected leg.

Phase III

Patients begin exercises in phase III 14 to 22 weeks after surgery. Phase III’s goal and final criteria is to perform sport/work specific movements with no pain or swelling (Fowler, PJ and D. Pompan, 1993). Drills for maximal muscle control, strength, flexibility,[rx] movements specific to patient’s work/sport, low to high rate exercises, and abdominal and back strengthening exercises are all recommended exercises (Ulrich G.S., and S Aroncyzk, 1993). Exercises to increase cardiovascular fitness are also applied to fully prepare the patients to return to their desired activities.

Next steps

Tips to help you get the most from a visit to your healthcare provider:

  • Know the reason for your visit and what you want to happen.
  • Before your visit, write down questions you want answered.
  • Bring someone with you to help you ask questions and remember what your provider tells you.
  • At the visit, write down the name of a new diagnosis, and any new medicines, treatments, or tests. Also write down any new instructions your provider gives you.
  • Know why a new medicine or treatment is prescribed, and how it will help you. Also know what the side effects are.
  • Ask if your condition can be treated in other ways.
  • Know why a test or procedure is recommended and what the results could mean.
  • Know what to expect if you do not take the medicine or have the test or procedure.
  • If you have a follow-up appointment, write down the date, time, and purpose for that visit.
  • Know how you can contact your provider if you have questions.

Prevention

Although it’s hard to prevent accidental knee injuries, you may be able to reduce your risks by:

  • Warming up and stretching before participating in athletic activities
  • Exercising to strengthen the muscles around your knee
  • Avoiding sudden increases in the intensity of your training program
  • Wearing comfortable, supportive shoes that fit your feet and your sport
  • Wearing appropriate protective gear during activities, including athletic activities, in which knee injuries are common (especially if you’ve had knee injuries before).

References

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Medial Meniscus Tear – Causes, Symptoms, Treatment

Medial Meniscus Tear/Medial Meniscus Injury is a crescent-shaped, cartilaginous band found between the medial tibia and medial femur. The primary function is to decrease the amount of stress on the knee joint. The medial meniscus receives vascular supply via a capillary network formed by the medial, lateral and middle geniculate arteries and receives its innervation from the posterior tibial, obturator, and femoral nerves.

The medial meniscus is a fibrocartilage semicircular band that spans the knee joint medially, located between the medial condyle of the femur and the medial condyle of the tibia. It is also referred to as the internal semilunar fibrocartilage. The medial meniscus has more of a crescent shape while the lateral meniscus is more circular. The anterior aspects of both menisci are connected by the transverse ligament. It is a common site of injury, especially if the knee is twisted.

A tear to the meniscus (also known as a cartilage tear) is a common injury that can cause pain and problems with sports and daily activities. The meniscus is a vital component of the knee that acts like a cushion between the femur (thigh) and tibia (shin) bones, providing shock absorption and stability.

Anatomy and Physiology

The meniscus is a C-shaped cartilage that serves as a cushion between the proximal tibia and the distal femur, comprising the knee joint.  The average width is 10 mm to 12 mm, and the average thickness is 4 mm to 5 mm. The meniscus is made of fibroelastic cartilage. It is an interlacing network of collagen, glycoproteins, proteoglycan, and cellular elements, and is about 70% water. Three ligaments attach to the meniscus. The coronary ligaments connect the meniscus peripherally. The transverse (inter-meniscal) ligament is anterior and serves as a connection between the medial and lateral meniscus. The meniscofemoral ligament joins the meniscus to the posterior cruciate ligament (PCL) and has two components: the Humphrey ligament anteriorly, and the ligament of Wrisberg posteriorly. The meniscofemoral ligament originates from the posterior horn of the lateral meniscus. The meniscus is supplied blood from the medial inferior genicular artery and the lateral inferior genicular artery. The meniscus is known to have a very poor blood supply, especially the central portion, which gets most of its nutrition via diffusion. The cartilage structure of the meniscus serves as a shock absorber and cushion or for the knee joint. There are several types of possible tears of the meniscus. These include flap tear, radial tear, horizontal cleavage, bucket handle tear, longitudinal tear, and degenerative tear.

Types of Medial Meniscus Tear

There are two categories of meniscal injuries – acute tears and degenerative tears.

  • An acute tear – usually occurs when the knee is bent and forcefully twisted, while the leg is in a weight bearing position. Statistics show that about 61 of 100,000 people experience an acute tear of the meniscus.
  • Degenerative tears – of the meniscus are more common in older people. Sixty percent of the population over the age of 65 probably has some sort of degenerative tear of the meniscus. As the meniscus ages, it weakens and becomes less elastic. Degenerative tears may result from minor events and there may or may not be any symptoms present.

A meniscal tear can be classified in various ways, such as by anatomic location or by proximity to blood supply. Various tear patterns and configurations have been described.[rx] These include

  • Radial tears
  • Flap or parrot-beak tears
  • Peripheral, longitudinal tears
  • Bucket-handle tears
  • Horizontal cleavage tears
  • Complex, degenerative tears

These tears can then be further classified by their proximity to the meniscus blood supply, namely whether they are located in the “red-red,” “red-white,” or “white-white” zones.

The functional importance of these classifications, however, is to ultimately determine whether a meniscus is repairable. The repairability of a meniscus depends on a number of factors. These include:

  • Age/strength
  • Activity level
  • Tear pattern
  • Chronicity of the tear
  • Associated injuries (anterior cruciate ligament injury)
  • Healing potential

or

There are different types of meniscal tears, describing the morphology of the injury. Identifying and accurately describing the type of meniscal tear can help the surgeon in patient education and planning of the surgical procedure. Meniscal tear types include

Basic tears

  • longitudinally oriented tears
      • horizontal tear (cleavage tear)
        • parallel to the tibial plateau involving one of the articular surfaces or free edge
        • divides the meniscus into superior and inferior parts
      • longitudinal tear (vertical tear)
        • perpendicular to the tibial plateau and parallel to the long axis of the meniscus
        • divides the meniscus into medial and lateral parts
        • Wrisberg rip – is a specific subtype
        • ramp lesion – is a specific subtype
  • radial tear – perpendicular to both the tibial plateau and the long axis of the meniscus
  • root tear – typically radial-type tear located at the meniscal root
  • complex tear – a combination of all or some of horizontal, longitudinal and radial-type tears
  • displaced tear – tear involving a component that is displaced, either still attached to the parent meniscus or detached:
    • flap tear: displaced horizontal or longitudinal tears
    • bucket-handle tear: displaced longitudinal tear
    • parrot beak tear: oblique radial tear

Medial Meniscus Injury

Causes of Medial Meniscus Tear

  • Inward (valgus) force – Usually, the medial collateral ligament, followed by the anterior cruciate ligament, then the medial meniscus (this mechanism is the most common and is usually accompanied by some external rotation and flexion, as when being tackled in football)
  • Outward (varus) force –  Often, the lateral collateral ligament, anterior cruciate ligament, or both (this mechanism is the 2nd most common)
  • Anterior or posterior forces and hyperextension –  Typically, the cruciate ligaments
  • Weight bearing and rotation at the time of injury – Usually, menisci
  • Motor vehicle accidents – A “dashboard injury” occurs when the driver’s or passenger’s bent knee slams against the dashboard, pushing in the shinbone just below the knee and causing the posterior meniscus tear.
  • Contact sports – Athletes in sports such as football and soccer can tear their posterior meniscus ligament when they fall on a bent knee with their foot pointed down. The shinbone hits the ground first and it moves backward. Being tackled when your knee is bent also can cause this injury.
  • The knee is hit directly – especially during sports like soccer, rugby, and football
  • A person lands on a bent knee – such as during a fall or misstep
  • Landing directly on the front of the shinbone – such as when a dancer comes down from a leap and falls
  • A person makes cutting or pivoting maneuvers – such as when an athlete plants a foot and shifts directions
  • A person lands on one leg – which can happen after a jump in basketball or volleyball
  • A direct blow to the bent knee in an automobile injury
  • A sports-related injury in which the knee bends
  • Pulling on the ligament in a twisting injury or hyperextension
  • A misstep on uneven terrain

Symptoms of Medial Meniscus Tear

If you’ve torn your meniscus, you might have the following signs and symptoms in your knee:

  • Localized pain near the area of the tear – In tears of the lateral meniscus, this discomfort will be present along the outside edge of the knee. Pain will manifest on the inside edge of the injured knee for tears of the medial meniscus.
  • Immediate pain after the injury – A torn meniscus will often be obvious from the moment that the injury occurs. In these instances, the tearing of the meniscus is typically accompanied by the feeling of a pop or snap within the leg during an overexerting twisting or stretching motion.
  • Slow onset of symptoms – Conversely, for some, the meniscus can tear without much of a sign or initial pain. This slow onset of symptoms is more common in older individuals and those with damaged knee cartilage from osteoarthritis.
  • Pain with movement – The pain will reflect the location of the tear but extend throughout the knee with movement. In the event that the knee has locked, bending it will cause searing pain to worsen.
  • Pain after resting – Pain will likely diminish somewhat with rest; however, it will return with movement in most cases. Movement may also exacerbate swelling.
  • Fluid accumulation within the knee joint – This accumulated fluid will cause the entire area to swell up and reduce mobility. This symptom, which may occur as a result of a number of knee injuries, is known as “water on the knee.”
  • Knee locking – If a piece of the meniscus breaks free of the disc structure due to a tear, it may lodge within the joint of the knee itself. This lodging can cause knee locking, in which a person loses the ability to fully straighten the leg when sitting or standing.
  • A popping sensation
  • Swelling or stiffness
  • Pain, especially when twisting or rotating your knee
  • Difficulty straightening your knee fully
  • Feeling as though your knee is locked in place when you try to move it
  • difficulty moving your knee or inability to move it in a full range of motion
  • the feeling of your knee locking or catching
  • the feeling that your knee is giving way or unable to support you
  • Feeling of your knee giving way
  • Pain in the knee
  • A popping sensation during the injury
  • Difficulty bending and straightening the leg
  • A tendency for your knee to get “stuck” or lock up

What are the signs?

You might feel a ‘pop’ if you tear your meniscus. Many people find they can still walk on their injured knee. However, it might become gradually stiffer and more swollen over the next day or so. Common symptoms include the following.

  • Pain in your knee, although this can vary. Some people only have mild pain, and for others, the pain may come and go.
  • Swelling, usually several hours after the injury.
  • Feeling as though your knee is catching or locking, usually when your knee is bent. You may notice it making clicking or popping sounds too.
  • Your knee feeling ‘loose’, as though it’s going to give way.
  • Being unable to bend and extend your knee fully.

Symptoms of severe meniscus tears

  • Popping, locking or catching
  • Inability to straighten the knee
  • Knee that gives way
  • Stiffness and swelling right after the incident

Diagnosis of Medial Meniscus Tear

Medical History

During your doctor’s appointment, he will ask you several questions about your knee pain. Examples of such questions include:

  • Where exactly is your knee pain located?
  • Did your knee swelling come on suddenly or did it gradually develop over days?
  • Are you experiencing any other symptoms besides pain and swelling, like your knee giving out or an inability to bend or extend your knee?
  • Have you experienced any trauma or injury to the knee?
  • Do you have a known history of knee osteoarthritis?

Physical examination

After noting symptoms, a physician can perform clinical tests to determine if the pain is caused by compression and impingement of a torn meniscus. The knee is examined for swelling. In meniscal tears, pressing on the joint line on the affected side typically produces tenderness.

  • Stress testing – Stress testing to evaluate ligament integrity helps distinguish partial from complete tears. However, if patients have significant pain and swelling or muscle spasm, testing is typically delayed until x-rays exclude fractures. Also, significant swelling and spasm may make joint stability difficult to evaluate. Such patients should be examined 2 to 3 days later (after swelling and spasm have subsided). A delayed physical examination of the knee is more sensitive than MRI of the knee (86% vs 76% [rx]) for diagnosis of meniscal and anterior cruciate ligament injuries.
  • Steinmann test – Steinman test is done to diagnose meniscal pathology at the knee joint.The test is divided into 2 parts i.e Steinman part 1 and Steinman part 2 or Steinman’s tenderness displacement test. This test is useful to distinguish meniscal pathology from injury to the ligament or osteophytes.
  • The McMurray test – involves pressing on the joint line while stressing the meniscus (using flexion–extension movements and varus or valgus stress). The test is often used to indicate cartilage injuries. With the patient laying on their back the therapist holds the knee with the upper hand and the heel with the lower hand. The therapist then applies a valgus (inward) stress to the knee whilst the other hand rotates the leg externally (outwards) and extends the knee. Pain and/or an audible click while performing this maneuver can indicate a torn medial meniscus.
  • Apley’s grind test – (a grinding maneuver while the person lies prone and the knee is bent 90°) and the Thessaly test (flexing the affected knee to 20 degrees, pivoting on the knee to see. Apley’s test is also used in cases of suspected meniscal tears. The patient is positioned on their front with the knee bent. The therapist grasps the heel and ankle and applies a compressive force through the lower leg. At the same time, they rotate the lower leg. Any reproduction of symptoms, pain or clicking is a positive response, suggesting a torn meniscus.
  • The Lachman test – is the most sensitive physical test for acute anterior cruciate ligament tears (rx). With the patient supine, the examiner supports the patient’s thigh and calf, and the patient’s knee is flexed 20°.The lower leg is moved anteriorly. Excessive passive anterior motion of the lower leg from the femur suggests a significant tear.

Imaging tests

  • Imaging tests may be ordered to confirm a tear of the meniscus. These include:

Knee X-ray

  • This test won’t show a meniscus tear. However, it can be helpful to determine if there are any other causes of your knee pain, like osteoarthritis.

MRI

  • An MRI uses a magnetic field to take multiple images of your knee. An MRI will be able to take pictures of cartilage and ligaments to determine if there’s a meniscus tear.
  • While MRIs can help your doctor make a diagnosis, they aren’t considered 100 percent reliable. According to a study from 2008 published in the Journal of Trauma Management & OutcomesTrusted Source, the MRI’s accuracy for diagnosing lateral meniscus tears is 77 percent.
  • Sometimes, meniscus tears may not show up on an MRI because they can closely resemble degenerative or age-related changes. Additionally, a doctor may make an incorrect diagnosis that a person has a torn meniscus. This is because some structures around the knee can closely resemble a meniscus tear.

Ultrasound

  • An ultrasound uses sound waves to take images inside the body. This will determine if you have any loose cartilage that may be getting caught in your knee.

Arthroscopy

  • If your doctor is unable to determine the cause of your knee pain from these techniques, they may suggest arthroscopy to study your knee. If you require surgery, your doctor will also most likely use an arthroscope.
  • With arthroscopy, a small incision or cut is made near the knee. The arthroscope is a thin and flexible fiber-optic device that can be inserted through the incision. It has a small light and camera. Surgical instruments can be moved through the arthroscope or through additional incisions in your knee.
  • After an arthroscopy, either for surgery or examination, people can often go home the same day.

Treatment of Medial Meniscus Tear

Non Surgical Injury

  • Protection  – the joint from further injury by taping/strapping the knee joint, or wearing a knee support which has additional support at the sides.
  • Rest – Avoid activities that aggravate your knee pain, especially any activity that causes you to twist, rotate or pivot your knee. If your pain is severe, using crutches can take pressure off your knee and promote healing.
  • Ice – Ice can reduce knee pain and swelling. Use a cold pack, a bag of frozen vegetables or a towel filled with ice cubes for about 15 minutes at a time, keeping your knee elevated. Do this every four to six hours the first day or two, and then as often as needed. Ice your knee to reduce pain and swelling. Do it for 15-20 minutes every 3-4 hours for 2-3 days or until the pain and swelling is gone.
  • Elevate your knee – with a pillow under your heel when you’re sitting or lying down.
  • A stabilized knee brace –  has flexible springs in the sides for additional support or for more severe injuries a hinged knee brace with solid metal supports linked by a hinge will help protect the joint from sideways or lateral movement. Compression will also help reduce swelling.
  • Rest the knee –  Limit activities to include walking if the knee painful. Use crutches to help relieve pain.
  • Compress your knee. Use an elastic bandage or a neoprene type sleeve on your knee to control swelling.
  • Use stretching and strengthening exercises to help reduce stress to your knee – Ask your doctor to recommend a physical therapist for guidance.
  • Avoid impact activities such as running and jumping 
  • Full weight bearing is not permitted for 1 – 6 weeks – after surgery, depending on the type of injury and repair. Crutches will be used initially following surgery. Many surgeons brace the knee and restrict motion for 6 weeks, to prevent excessive flexion and extension.
  • Range of motion exercises – begin anywhere from 0 – 6 weeks after surgery, depending on the type of repair.
  • Strengthening exercises – begin once full range of motion has returned.
  • Return to vigorous activities – such as sports, may begin 3 – 4 months after repair.

Physiotherapy

  • A professional therapist will undertake a thorough assessment and make an accurate diagnosis to confirm cartilage meniscus injury and they may undertake an MRI scan to determine the extent of the injury.
  • A physical therapist will focus on improving mobility, strength, flexibility, and balance, which can help speed up recovery time and improve performance once the injury has healed.
  • Walking (weight-bearing) is initiated as soon as possible.
  • Knee straightening (extension) and bending (flexion) are encouraged. Pool therapy is helpful.
  • Stationary cycling is initiated as soon as adequate motion is achieved.
  • Quadriceps strengthening exercises are started, such as standing squats with toe raises and leg press.
  • Hamstring exercise may be modified for 6 months.
  • Surgery is avoided in most cases unless other major ligaments are disrupted.

Medication

  • Take anti-inflammatory medications. Non-steroidal anti-inflammatory drugs (NSAIDs), like will help with pain and swelling. However, these drugs can have side effects, such as an increased risk of bleeding and ulcers. They should be only used occasionally, unless your doctor specifically says otherwise.
  • Antibiotic – Cefuroxime or Azithromycin, or  Flucloxacillin or any others cephalosporin/quinolone antibiotic must be used to prevent infection or clotted blood remove to prevent furthers swelling and edema.
  • NSAIDs – Prescription-strength drugs that reduce both pain and inflammation. Pain medicines and anti-inflammatory drugs help to relieve pain and stiffness, allowing for increased mobility and exercise. There are many common over-the-counter medicines called non-steroidal anti-inflammatory drugs (NSAIDs). They include and KetorolacAceclofenacNaproxen, Etoricoxib.
  • Corticosteroids – Also known as oral steroids, these medications reduce inflammation.
  • Muscle Relaxants –  These medications provide relief from associated muscle spasms.
  • Neuropathic Agents – Drugs(pregabalin & gabapentin) that address neuropathic—or nerve-related—pain. This includes burning, numbness, and tingling.
  • Opioids – Also known as narcotics, these medications are intense pain relievers that should only be used under a doctor’s careful supervision.
  • Topical Medications – These prescription-strength creams, gels, ointments, patches, and sprays help relieve pain and inflammation through the skin.
  • Calcium & vitamin D3 – to improve bone health and healing fracture. As a general rule, men and women age 50 and older should consume 1,200 milligrams of calcium a day, and 600 international units of vitamin D a day.
  • Antidepressants – A drug that blocks pain messages from your brain and boosts the effects of endorphins (your body’s natural painkillers).
  • Glucosamine & DiacereinChondroitin sulfate – can be used to tightening the loose tension, cartilage, ligament, and cartilage, ligament regenerates cartilage or inhabits the further degeneration of cartilage, ligament. They are structural components of articular cartilage, and the thought is that a supplement will aid in the health of articular cartilage.
  • Intra-articular corticosteroid injections – may be useful for symptomatic menicus injury especially where there is a considerable inflammatory component. The delivery of the corticosteroid directly into the knee may reduce local inflammation associated with meniscus injury and minimize the systemic effects of the steroid.
  • Intra-articular hyaluronic acid injections (HA) – injections are another injectable option for knee meniscus injury. HA is a glycosaminoglycan that is found throughout the human body and is an important component of synovial fluid and articular cartilage. HA breaks down during the process of meniscus injury and contributes to the loss of articular cartilage as well as stiffness and pain. Local delivery of HA into the joint acts as a lubricant and may help increase the natural production of HA in the joint.

Surgery

Grade 3 meniscus tears usually require surgery, which may include:

  • Arthroscopic repair — An arthroscope is inserted into the knee to see the tear. One or two other small incisions are made for inserting instruments. Many tears are repaired with dartlike devices that are inserted and placed across the tear to hold it together. The body usually absorbs these over time. Arthroscopic meniscus repairs typically takes about 40 minutes. Usually you will be able to leave the hospital the same day.
  • Arthroscopic partial meniscectomy – The goal of this surgery is to remove a small piece of the torn meniscus in order to get the knee functioning normally.
  • Arthroscopic total meniscectomy – Occasionally, a large tear of the outer meniscus can best be treated by arthroscopic total meniscectomy, a procedure in which the entire meniscus is removed.

Trephination/ Abrasion Technique

  • This procedure is used for stable tears located on the periphery near the meniscus and joint capsule junction, where there’s a good blood supply. Multiple holes or shavings are made in the torn part of the meniscus to promote bleeding, which enhances the healing process.

Partial Resection

  • This surgical procedure is used for tears located in the inner 2/3 of the meniscus where there is no blood supply. The goal is to stabilize the rim of the meniscus by removing as little of the inner meniscus as possible. Only the torn part of the meniscus is removed. If the meniscus remains mostly intact with only the inner portion removed, the patient usually does well and does not develop early arthritis.

Complete Resection

  • This procedure involves the complete removal of the damaged meniscus. This technique is only performed if absolutely necessary. Removal of the entire meniscus frequently leads to the development of arthritis.

Meniscal Repair

  • Repairs are performed on tears near the outer 1/3 of the meniscus where a good blood supply exists, or on large tears that would require a near-total resection. The torn portion of the meniscus is repaired by using either sutures or absorbable fixation devices. These devices include arrows, barbs, staples, or tacks that join the torn edges of the meniscus so they can heal.

Meniscal Replacement

  • Experimental attempts to replace damaged meniscus are seen as important recent advances in orthopaedic medicine. The new technology mentioned here has been performed at a few surgical centers across the country on a small number of patients

Collagen meniscus implant

  • This is a scaffold of collagen inserted into the patient’s knee. Over time, a new meniscus may grow within the joint. This procedure is currently in FDA trials in the United States and has just been approved as an accepted surgical procedure in Europe.

Meniscal transplant

  • This procedure involves transplanting a meniscus from a donor into the injured knee. Only a limited number of surgeons perform this procedure on a routine basis. The long-term outcomes are still being evaluated.

Meniscus transplants

Meniscus transplants are accomplished successfully regularly, although it is still somewhat of a rare procedure and many questions surrounding its use remain. Side effects of meniscectomy include:

  • The knee loses its ability to transmit and distribute load and absorb mechanical shock.
  • Persistent and significant swelling and stiffness in the knee.
  • The knee may be not be fully mobile; there may be the sensation of knee locking or buckling in the knee.
  • The full knee may be in full motion after tear of meniscus.
  • Increases progression of arthritis and time to knee replacement.

Post-Surgical Rehabilitation

Typical locations of arthroscopic surgery incisions in a knee joint following surgery for a tear in the meniscus

After a successful surgery for treating the destroyed part of the meniscus, patients must follow a rehabilitation program to have the best result. The rehabilitation following a meniscus surgery depends on whether the entire meniscus was removed or repaired.

If the destroyed part of the meniscus was removed, patients can usually start walking using a crutch a day or two after surgery. Although each case is different, patients return to their normal activities on average after a few weeks (2 or 3). Still, a completely normal walk will resume gradually, and it’s not unusual to take 2–3 months for the recovery to reach a level where a patient will walk totally smoothly. Many meniscectomy patients don’t ever feel a 100% functional recovery, but even years after the procedure they sometimes feel tugging or tension in a part of their knee. There is little medical follow-up after meniscectomy and official medical documentation tends to ignore the imperfections and side-effects of this procedure.

If the meniscus was repaired, the rehabilitation program that follows is a lot more intensive. After the surgery a hinged knee brace is sometimes placed on the patient. This brace allows controlled movement of the knee. The patient is encouraged to walk using crutches from the first day, and most of the times can put partial weight on the knee.

Phase I

There are three phases that follow meniscal surgery. Each phase consists of rehabilitation goals, exercises, and criteria to move on to the next phase. Phase I starts immediately following surgery to 4–6 weeks or until the patient is able meet progression criteria. The goals are to restore normal knee extension, reduce and eliminate swelling, regain leg control, and protect the knee (Fowler, PJ and D. Pompan, 1993). During the first 5 days following the surgery, a passive continuous motion machine is used to prevent a prolonged period of immobilization which leads to muscular atrophy and delays functional recovery.[rx] During the 4–6 weeks post-surgical, active and passive non-weight bearing motions which flex the knee up to 90° are recommended. For patients with meniscal transplantation, further knee flexion can damage the allograft because of the increased shear forces and stresses.

Phase II

This phase of the rehabilitation program is 6 to 14 weeks after the surgery. The goals for Phase II include being able to restore full ROM, normalized gait, and performing functional movements with control and no pain (Fowler, PJ and D. Pompan, 1993). Also, muscular strengthening and neuromuscular training are emphasized using progressive weight bearing and balance exercises. Exercises in this phase can increase knee flexion for more than 90°.[rx] Advised exercises include stationary bicycle, standing on foam surface with two and one leg, abdominal and back strengthening, and quadriceps strengthening. The proposed criteria include normal gait on all surfaces and single leg balance longer than 15 seconds (Ulrich G.S., and S Aroncyzk, 1993).

Balance exercises on a foam surface in phase 2. The patient tries to maintain balance first with both legs, then with only the affected leg.

Phase III

Patients begin exercises in phase III 14 to 22 weeks after surgery. Phase III’s goal and final criteria is to perform sport/work specific movements with no pain or swelling (Fowler, PJ and D. Pompan, 1993). Drills for maximal muscle control, strength, flexibility,[rx] movements specific to patient’s work/sport, low to high rate exercises, and abdominal and back strengthening exercises are all recommended exercises (Ulrich G.S., and S Aroncyzk, 1993). Exercises to increase cardiovascular fitness are also applied to fully prepare the patients to return to their desired activities.

Next steps

Tips to help you get the most from a visit to your healthcare provider:

  • Know the reason for your visit and what you want to happen.
  • Before your visit, write down questions you want answered.
  • Bring someone with you to help you ask questions and remember what your provider tells you.
  • At the visit, write down the name of a new diagnosis, and any new medicines, treatments, or tests. Also write down any new instructions your provider gives you.
  • Know why a new medicine or treatment is prescribed, and how it will help you. Also know what the side effects are.
  • Ask if your condition can be treated in other ways.
  • Know why a test or procedure is recommended and what the results could mean.
  • Know what to expect if you do not take the medicine or have the test or procedure.
  • If you have a follow-up appointment, write down the date, time, and purpose for that visit.
  • Know how you can contact your provider if you have questions.

Prevention

Although it’s hard to prevent accidental knee injuries, you may be able to reduce your risks by:

  • Warming up and stretching before participating in athletic activities
  • Exercising to strengthen the muscles around your knee
  • Avoiding sudden increases in the intensity of your training program
  • Wearing comfortable, supportive shoes that fit your feet and your sport
  • Wearing appropriate protective gear during activities, including athletic activities, in which knee injuries are common (especially if you’ve had knee injuries before).

References

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ACL Injury – Causes, Symptoms, Diagnosis, Treatment

ACL Injury/Anterior Cruciate Ligament Injury (ACL) is one of 2 cruciate ligaments which aids in stabilization of the knee joint. It is a strong band made of connective tissue and collagenous fibers that originate from the anteromedial aspect of the intercondylar region of the tibial plateau and extends posteromedially to attach to the lateral femoral condyle. The anteromedial bundle and posterolateral bundle form the 2 components of the ACL.   The ACL and the posterior cruciate ligament (PCL) together form a cross (or an “x”) within the knee and prevents excessive forward or backward motion of the tibia in relation to the femur during flexion and extension.

Anterior cruciate ligament injury is when the anterior cruciate ligament (ACL) is either stretched, partially torn, or completely torn. The most common injury is a complete tear. Symptoms include pain, a popping sound during injury, instability of the knee, and joint swelling. Swelling generally appears within a couple of hours.[rx] In approximately 50% of cases, other structures of the knee such as surrounding ligaments, cartilage, or meniscus are damaged.[rx]

Anterior Cruciate Ligament

Causes of Anterior Cruciate Ligament Injury

  • A sudden stop, twist, pivot or change in direction at the knee joint  – These knee movements are a routine part of football, basketball, soccer, rugby, gymnastics and skiing. For this reason, athletes who participate in these sports have an especially high risk of ACL tears.
  • Extreme hyperextension of the knee – Sometimes, during athletic jumps and landings, the knee straightens out more than it should and extends beyond its normal range of motion, causing an ACL tear. This type of ACL injury often occurs because of a missed dismount in gymnastics or an awkward landing in basketball.
  • Direct contact – The ACL may be injured during contact sports, usually during direct impact to the outside of the knee or lower leg. Examples are a sideways football tackle, a misdirected soccer kick that strikes the knee or a sliding tackle in soccer.

ACL tear Causes may include

  • Changing direction rapidly (also known as “cutting”)
  • Landing from a jump awkwardly
  • Coming to a sudden stop when running
  • Direct contact or collision to the knee (e.g. during a football tackle or a motor vehicle collision)
  • landing awkwardly from a jump
  • twisting movements, particularly when your foot is on the ground
  • quickly changing direction when running or walking
  • slowing down or stopping suddenly when running

These movements cause the tibia to shift away from the femur rapidly, placing strain on the knee joint and potentially leading to the rupture of the ACL. About 80% of ACL injuries occur without direct trauma. Risk factors include female anatomy, specific sports, poor conditioning, fatigue, and playing on a turf field.[rx]

Female predominance

Female athletes are two to eight times more likely to strain their ACL in sports that involve cutting and jumping as compared to men who play the same particular sports.[rx] NCAA data has found relative rates of injury per 1000 athlete exposures as follows:

  • Men’s basketball 0.07, women’s basketball 0.23
  • Men’s lacrosse 0.12, women’s lacrosse 0.17
  • Men’s football 0.09, women’s football 0.28

The highest rate of ACL injury in women occurred in gymnastics, with a rate of injury per 1000 athlete exposures of 0.33. Of the four sports with the highest ACL injury rates, three were women’s – gymnastics, basketball, and soccer.[rx]

Differences between males and females identified as potential causes are the active muscular protection of the knee joint, differences in leg/pelvis alignment, and relative ligament laxity caused by differences in hormonal activity from estrogen and relaxin.[rx][rx] Birth control pills appear to decrease the risk.[rx]

Dominance theories

Femur with Q angle – the angle formed by a line drawn from the anterior superior iliac spine through the center of the patella and a line drawn from the center of the patella to the center of the tibial tubercle

Some studies have suggested that there are four neuromuscular imbalances that predispose women to a higher incidence of ACL injury. Female athletes are more likely to jump and land with their knees relatively straight and collapsing in towards each other, while most of their body weight falls on a single foot and their upper body tilts to one side.[rx] Several theories have been described to further explain these imbalances. These include ligament dominance, quadriceps dominance, leg dominance, and trunk dominance theories.

Symptoms of Anterior Cruciate Ligament Injury

When an individual has an ACL injury, they are likely to hear a “pop” in their knee followed by pain and swelling. They may also experience instability in the knee once they resume walking and other activities, as the ligament can no longer stabilize the knee joint and keep the tibia from sliding forward.[rx].[rx]

  • Feeling a “pop” inside your knee when the ACL tears
  • Significant knee swelling and deformity within a few hours after injury
  • Severe knee pain that prevents you from continuing to participate in your sport (most common in partial tears of the ACL)
  • No knee pain, especially if the ACL has been completely torn and there is no tension across the injured ligament
  • A black and blue discoloration around the knee, due to bleeding from inside the knee joint
  • A feeling that your injured knee will buckle, “give out” or “give way” if you try to stand

Diagnosis of Anterior Cruciate Ligament Injury

Physical examination

Physical examination of the knee usually follows a relatively standard pattern.

  • The knee is examined for obvious swelling, bruising, and deformity.
  • Areas of tenderness and subtle evidence of knee joint fluid (effusion) are noted.
  • Most importantly, with knee injury ligamentous, stability is assessed. Since there are four ligaments at risk for injury, the examiner may try to test each to determine which one(s) is (are) potentially damaged. It is important to remember that a knee ligament injury might be an isolated structure damaged or there may be more than one ligament and other structures in the knee that are hurt.
  • In the acute situation, with a painful, swollen joint, the initial examination may be difficult because both the pain and the fluid limit the patient’s ability to cooperate and relax the leg. Spasm of the quadriceps and hamstring muscles often can make it difficult to assess ACL stability.
  • A variety of maneuvers can be used to test the stability and strength of the ACL. These include the Lachman test, the pivot-shift test, and the anterior drawer test. Guidelines from the American Academy of Pediatrics suggest the Lachman test is best for assessing ACL tears.
  • The Lachman test is performed as follows:
    • The damaged knee is flexed to 20-30 degrees.
    • The examiner grasps tibia and puts their thumb on the tibial tubercle (the bump of bone just below the knee where the patellar tendon attaches.
    • The examiners other hand grasps the thigh just above the knee.
    • The tibia is pulled forward and normally, there should be a firm stop if the ACL is intact. If the ligament is torn, the tibia will move forward and there will be no endpoint and it feels mushy.
  • The unaffected knee may be examined to be used as a comparison.

It may be difficult to examine some patients when muscle strength or spasm can hide an injured ACL because of the knee stabilization that they can provide.

Multiple maneuvers are employed to test the ACL and include the anterior drawer, the pivot shift, and the Lachman tests. These tests should be performed whenever there is suspicion for injury to the anterior cruciate ligament.

  • The anterior drawer test – is performed with the patient lying supine with their affected knee flexed to 90 degrees and the foot in a planted position (Sometimes it is easiest for the clinician to stabilize the patient’s foot by sitting on it). The clinician will grip the proximal tibia with both hands and pull with an anterior motion. If there is excessive anterior motion and instability, then the test is positive. It may also be useful to compare to the unaffected knee as patients may have increased laxity of the ACL that is not pathologic. This test has a sensitivity of 92% and specificity of 91% in chronic injuries, but not acute injuries.
  • The pivot shift test – is performed with the patient in the supine position. The clinician should hold the patient’s lower leg and begin with the knee in extension and flexion of the hip to 20 to 30 degrees. Next, the clinician will bring the tibia into the internal rotation with one hand and begin placing valgus stress on the knee using the other hand. While holding this position, the knee should now be flexed. This causes stress, instability, and ultimately subluxation of the ACL of the affected knee. With flexion of the knee, if the tibia subluxes posteriorly and one may feel a “clunk”; this would indicate a positive test. This test can be difficult to perform in patients who are guarding, and some may not allow the clinician to perform the test. This is a highly specific test (98%) when positive, but is insensitive (24%) due to the difficulty in evaluation secondary to patient pain and cooperation.
  • The Lachman test – is performed with the patient in the supine position with the knee flexed to about 30 degrees. The clinician should stabilize the distal femur with one hand and with the other hand pull the tibia toward themselves. If there is increased anterior translation, then this is a positive test. Again, comparing to the unaffected side may be helpful. This test has a sensitivity of 95% and specificity of 94% for ACL rupture.

Radiography

  • Tests – Your doctor may ask you to lie on your back and bend your hips and/or your knees at certain angles. He’ll then place his hands on different parts of your leg and gently shift you around. If any of your bones move in a way that isn’t normal, that could be a sign that your ACL is damaged.
  • X-ray – Soft tissues like the ACL don’t appear on X-rays, but your doctor may want to rule out broken bones.
  • MRI or ultrasound – These exams can show both soft tissue and bone. If you have a damaged ACL, it should appear on the images.
  • Arthroscopy – This literally means to “look within the joint.” During the exam, an orthopedic surgeon makes a small cut in your skin. He inserts a pencil-sized tool that contains a lighting system and lens (arthroscope) into the joint. The camera projects an image of the joint onto a TV screen. Your doctor can see what type of injury you have and repair or correct it, if needed.

Stage  of Anterior Cruciate Ligament

An ACL injury can further classify as a grade I, II, or III sprains.

  • Grade I – The ligamental fibers are stretched, with a tear that is less than one-third of the ligament. Mild tenderness and swelling are present. The knee joint feels stable with a knee laxity < 5 mm.
  • Grade II – A partial tear (between one-third to two-thirds of the ligamental fibers) is present. Mild tenderness and swelling with some loss of function are present. The joint may feel unstable with increased anterior translation (a knee laxity of 5 to 10 mm). The patient feels pain, and the pain may become exacerbated with Lachman’s and anterior drawer stress tests.
  • Grade III – The fibers have completely torn. Tenderness and limited pain (relative to the seriousness of the injury) are features. The degree of swelling may be variable. The knee feels unstable, with rotational instability (positive pivot shift test). A knee laxity is greater than 10  mm. Haemarthrosis (bleeding into the knee joints) is observable within 1 to 2 hours.

An acute ACL rupture commonly occurs among sports players, especially those aged 14 to 19 years. The incidence of ACL injury is higher among female athletes due to the following reasons:

  • Smaller ACL and narrower intercondylar notch – Females who are non-athletes and aged 41 to 65 are predisposed to ACL injuries if they have narrow intercondylar notches.
  • Wider pelvis and greater Q angle – A wider pelvis increases the angle of the femur toward the central patella. The greater the Q angle, the greater pressure is applied to the medial aspect of the knee, which can lead to an ACL tear.
  • Lax ligaments – Female ligaments with more elastic muscle fibers tend to be laxer than male ligaments. Excessive joint movements with increased flexibility may contribute to the higher incidence of ACL injury among females.
  • Greater quadriceps to hamstring strength ratio – Females tend to have poor hamstring strength compared to men. The imbalance of strength between the hamstring and quadriceps muscles may increase the risk of ACL injury.

Treatment of Anterior Cruciate Ligament Injury

Non-Surgical Treatment Options

  • Patient education
  • Activity modification
  • Physical therapy
  • Weight loss
  • Knee bracing
  • Acetaminophen
  • Nonsteroidal anti-inflammatory drugs (NSAIDs)
  • COX-2 inhibitors
  • Glucosamine and chondroitin sulfate
  • Corticosteroid injections
  • Hyaluronic acid (HA)

The American Academy Of Orthopedic Surgeons (AAOS) Recommends This Treatment.

  • Weight loss – is valuable in all stages of ACL injury. It is indicated in patients with symptomatic ACL injury with a body mass index greater than 25. The best recommendation to achieve weight loss is with diet control and low-impact aerobic exercise.
  • Knee bracing – in the setting of ACL injury includes unloader-type braces that shift the load away from the involved knee compartment. This may be useful in the setting where either the lateral or medial compartment of the knee is involved such as in a valgus or varus deformity.
  • Immobilization – Your doctor may recommend that you wear a brace for 3 to 4 weeks. This stabilizes the knee while it heals.
  • Weightbearing –  Because putting weight on the knee may cause pain and slow the healing process, your doctor may recommend using crutches for the first week or two after the injury.
  • Physical therapy – Once the knee has started to heal, your doctor will recommend physical therapy to help your child regain normal motion. Specific exercises will strengthen the thigh muscles holding the knee joint in place. Your commitment to the exercise program is important for a successful recovery. Typically return to activity 3 to 6 weeks after the injury.
  • Emergent closed reduction followed by vascular assessment/consult – If indications to considered an orthopedic emergency, vascular consult indicated if pulses are absent or diminished following reduction if arterial injury confirmed by arterial duplex ultrasound or CT angiography
  • Immobilization as definitive management – successful closed reduction without vascular compromise, most cases require some form of surgical stabilization following reduction, outcomes of worse outcomes are seen with nonoperative management/prolonged immobilization will lead to loss of ROM with persistent instability.
  • Rest Your Leg – Once you’re discharged from the hospital in a legislating, your top priority is to rest your and not further inflame the injury. Of course, the arm sling not only provides support, but it also restricts movement, which is why you should keep it on even during sleep. Avoiding the temptation to move your will help the bone mend quicker and the pain fades away sooner.
    • Depending on what you do for a living and if the injury is to your dominant side, you may need to take a couple of weeks off work to recuperate.
    • Healing takes between four to six weeks in younger people and up to 12 weeks in the elderly, but it depends on the severity of the radial head fractures.
    • Athletes in good health are typically able to resume their sporting activities within two months of breaking they’re ulnar styloid depending on the severity of the break and the specific sport.
    • Sleeping on your back (with the sling on) is necessary to keep the pressure off your shoulder and prevent stressing the hip injury.

Eat Nutritiously During Your Recovery

  • All bones and tissues in the body need certain nutrients in order to heal properly and in a timely manner. Eating a nutritious and balanced diet that includes lots of minerals and vitamins are proven to help heal ACL injury of all types. Therefore focus on eating lots of fresh produce (fruits and veggies), whole grains, lean meats, and fish to give your body the building blocks needed to properly repair your. In addition, drink plenty of purified water, milk, and other dairy-based beverages to augment what you eat.
  • ACL injury need ample minerals (calcium, phosphorus, magnesium, boron) and protein to become strong and healthy again.
  • Excellent sources of minerals/protein include dairy products, tofu, beans, broccoli, nuts and seeds, sardines, and salmon.
  • Important vitamins that are needed for bone healing include vitamin C (needed to make collagen), vitamin D (crucial for mineral absorption), and vitamin K (binds calcium to bones and triggers collagen formation).
  • Conversely, don’t consume food or drink that is known to impair bone/tissue healing, such as alcoholic beverages, sodas, most fast food items and foods made with lots of refined sugars and preservatives.

Medication

  • Antibiotic – Cefuroxime or Azithromycin, or  Flucloxacillin or any others cephalosporin/quinolone antibiotic must be used to prevent infection or clotted blood remove to prevent furthers swelling and edema.
  • NSAIDs – Prescription-strength drugs that reduce both pain and inflammation. Pain medicines and anti-inflammatory drugs help to relieve pain and stiffness, allowing for increased mobility and exercise. There are many common over-the-counter medicines called non-steroidal anti-inflammatory drugs (NSAIDs). They include and KetorolacAceclofenacNaproxen, Etoricoxib.
  • Corticosteroids – Also known as oral steroids, these medications reduce inflammation.
  • Muscle Relaxants –  These medications provide relief from associated muscle spasms.
  • Neuropathic Agents – Drugs(pregabalin & gabapentin) that address neuropathic—or nerve-related—pain. This includes burning, numbness, and tingling.
  • Opioids – Also known as narcotics, these medications are intense pain relievers that should only be used under a doctor’s careful supervision.
  • Topical Medications – These prescription-strength creams, gels, ointments, patches, and sprays help relieve pain and inflammation through the skin.
  • Calcium & vitamin D3 – to improve bone health and healing fracture. As a general rule, men and women age 50 and older should consume 1,200 milligrams of calcium a day, and 600 international units of vitamin D a day.
  • Antidepressants – A drug that blocks pain messages from your brain and boosts the effects of endorphins (your body’s natural painkillers).
  • Glucosamine & DiacereinChondroitin sulfate – can be used to tightening the loose tension, cartilage, ligament, and cartilage, ligament regenerates cartilage or inhabits the further degeneration of cartilage, ligament. They are structural components of articular cartilage, and the thought is that a supplement will aid in the health of articular cartilage.
  • Intra-articular corticosteroid injections – may be useful for symptomatic ACL injury especially where there is a considerable inflammatory component. The delivery of the corticosteroid directly into the knee may reduce local inflammation associated with osteoarthritis and minimize the systemic effects of the steroid.
  • Intra-articular hyaluronic acid injections (HA) – injections are another injectable option for knee ACL injury. HA is a glycosaminoglycan that is found throughout the human body and is an important component of synovial fluid and articular cartilage. HA breaks down during the process of  ACL injury and contributes to the loss of articular cartilage as well as stiffness and pain. Local delivery of HA into the joint acts as a lubricant and may help increase the natural production of HA in the joint.

Surgical Treatment

ACL tears are not usually repaired using suture to sew it back together, because repaired ACLs have generally been shown to fail over time. Therefore, the torn ACL is generally replaced by a substitute graft made of tendon.

  • Patellar tendon autograft (autograft comes from the patient)
  • Hamstring tendon autograft
  • Quadriceps tendon autograft
  • Allograft (taken from a cadaver) patellar tendon, Achilles tendon, semitendinosus, gracilis, or posterior tibialis tendon

Patient Considerations

Active adult patients involved in sports or jobs that require pivoting, turning or hard-cutting as well as heavy manual work are encouraged to consider surgical treatment. This includes older patients who have previously been excluded from consideration for ACL surgery. Activity, not age, should determine if surgical intervention should be considered.

In young children or adolescents with ACL tears, early ACL reconstruction creates a possible risk of growth plate injury, leading to bone growth problems. The surgeon can delay ACL surgery until the child is closer to skeletal maturity or the surgeon may modify the ACL surgery technique to decrease the risk of growth plate injury.

A patient with a torn ACL and significant functional instability has a high risk of developing secondary knee damage and should therefore consider ACL reconstruction.

It is common to see ACL injuries combined with damage to the menisci, articular cartilage, collateral ligaments, joint capsule, or a combination of the above. The “unhappy triad,” frequently seen in football players and skiers, consists of injuries to the ACL, the MCL, and the medial meniscus.

In cases of combined injuries, surgical treatment may be warranted and generally produces better outcomes. As many as half of meniscus tears may be repairable and may heal better if the repair is done in combination with the ACL reconstruction.

Surgical Choices

There are 4 types of grafts

  • Autografts – are taken from the patient’s own body and include portions of the extensor mechanism patellar tendon, iliotibial tract semitendinosus tendon, gracilis tendon and menisci.
  • Allografts – grafts taken from cadavers.
  • Xenografts – grafts taken from animals. Bovine xenografts in particular have been associated with high complication rates.
  • Synthetics – These can be further classified into 3 categories, biodegradable (carbon fibers), permanent prostheses (Gore-Tex and Dacron), and ligament augmentation devices.

Patellar tendon autograft –  The middle third of the patellar tendon of the patient, along with a bone plug from the shin and the kneecap is used in the patellar tendon autograft. Occasionally referred to by some surgeons as the “gold standard” for ACL reconstruction, it is often recommended for high-demand athletes and patients whose jobs do not require a significant amount of kneeling.

The pitfalls of the patellar tendon autograft are

  • Postoperative pain behind the kneecap
  • Pain with kneeling
  • Slightly increased risk of postoperative stiffness
  • Low risk of patella fracture

Hamstring tendon autograft – The semitendinosus hamstring tendon on the inner side of the knee is used in creating the hamstring tendon autograft for ACL reconstruction. Some surgeons use an additional tendon, the gracilis, which is attached below the knee in the same area. This creates a two- or four-strand tendon graft. Hamstring graft proponents claim there are fewer problems associated with harvesting of the graft compared to the patellar tendon autograft including:

  • Fewer problems with anterior knee pain or kneecap pain after surgery
  • Less postoperative stiffness problems
  • Smaller incision
  • Faster recovery

Hamstring tendon autograft prepared for ACL reconstruction

The graft function may be limited by the strength and type of fixation in the bone tunnels, as the graft does not have bone plugs. There have been conflicting results in research studies as to whether hamstring grafts are slightly more susceptible to graft elongation (stretching), which may lead to increased laxity during objective testing. Recently, some studies have demonstrated decreased hamstring strength in patients after surgery.

There are some indications that patients who have intrinsic ligamentous laxity and knee hyperextension of 10 degrees or more may have increased risk of postoperative hamstring graft laxity on clinical exam. Therefore, some clinicians recommend the use of patellar tendon autografts in these hypermobile patients.

Additionally, since the medial hamstrings often provide dynamic support against valgus stress and instability, some surgeons feel that chronic or residual medial collateral ligament laxity (grade 2 or more) at the time of ACL reconstruction may be a contraindication for use of the patient’s own semitendinosus and gracilis tendons as an ACL graft.

Quadriceps tendon autograft

The quadriceps tendon autograft is often used for patients who have already failed ACL reconstruction. The middle third of the patient’s quadriceps tendon and a bone plug from the upper end of the knee cap are used. This yields a larger graft for taller and heavier patients. Because there is a bone plug on one side only, the fixation is not as solid as for the patellar tendon graft. There is a high association with postoperative anterior knee pain and a low risk of patella fracture. Patients may find the incision is not cosmetically appealing.

Allografts

Allografts are grafts taken from cadavers and are becoming increasingly popular. These grafts are also used for patients who have failed ACL reconstruction before and in surgery to repair or reconstruct more than one knee ligament. The advantages of using allograft tissue include the elimination of pain caused by obtaining the graft from the patient, decreased surgery time and smaller incisions. The patellar tendon allograft allows for strong bony fixation in the tibial and femoral bone tunnels with screws.

However, allografts are associated with a risk of infection, including viral transmission (HIV and Hepatitis C), despite careful screening and processing. Several deaths linked to bacterial infection from allograft tissue (due to improper procurement and sterilization techniques) have led to improvements in allograft tissue testing and processing techniques. There have also been conflicting results in research studies as to whether allografts are slightly more susceptible to graft elongation (stretching), which may lead to increased laxity during testing.

Some published literature may point to a higher failure rate with the use of allografts for ACL reconstruction. Higher failure rates for allografts have been reported in young, active patients returning to high-demand sporting activities after ACL reconstruction, compared with autografts.

The reason for this higher failure rate is unclear. It could be due to graft material properties (sterilization processes used, graft donor age, storage of the graft). It could possibly be due to an ill-advised earlier return to sport by the athlete because of a faster perceived physiologic recovery, when the graft is not biologically ready to be loaded and stressed during sporting activities. Further research in this area is indicated and is ongoing.

Surgical Procedure

Before any surgical treatment, the patient is usually sent to physical therapy. Patients who have a stiff, swollen knee lacking full range of motion at the time of ACL surgery may have significant problems regaining motion after surgery. It usually takes three or more weeks from the time of injury to achieve full range of motion. It is also recommended that some ligament injuries be braced and allowed to heal prior to ACL surgery.

The patient, the surgeon, and the anesthesiologist select the anesthesia used for surgery. Patients may benefit from an anesthetic block of the nerves of the leg to decrease postoperative pain.

The surgery usually begins with an examination of the patient’s knee while the patient is relaxed due the effects of anesthesia. This final examination is used to verify that the ACL is torn and also to check for looseness of other knee ligaments that may need to be repaired during surgery or addressed postoperatively.

If the physical exam strongly suggests the ACL is torn, the selected tendon is harvested (for an autograft) or thawed (for an allograft) and the graft is prepared to the correct size for the patient.

After the graft has been prepared, the surgeon places an arthroscope into the joint. Small (one-centimeter) incisions called portals are made in the front of the knee to insert the arthroscope and instruments and the surgeon examines the condition of the knee. Meniscus and cartilage injuries are trimmed or repaired and the torn ACL stump is then removed.

Post-operative X-ray after ACL patellar tendon reconstruction (with picture of graft superimposed) shows graft position and bone plugs fixation with metal interference screws.

In the most common ACL reconstruction technique, bone tunnels are drilled into the tibia and the femur to place the ACL graft in almost the same position as the torn ACL. A long needle is then passed through the tunnel of the tibia, up through the femoral tunnel, and then out through the skin of the thigh. The sutures of the graft are placed through the eye of the needle and the graft is pulled into position up through the tibial tunnel and then up into the femoral tunnel. The graft is held under tension as it is fixed in place using interference screws, spiked washers, posts, or staples. The devices used to hold the graft in place are generally not removed.

Variations on this surgical technique include the “two-incision,” “over-the-top,” and “double-bundle” types of ACL reconstructions, which may be used because of the preference of the surgeon or special circumstances (revision ACL reconstruction, open growth plates).

Before the surgery is complete, the surgeon will probe the graft to make sure it has good tension, verify that the knee has full range of motion and perform tests such as the Lachman’s test to assess graft stability. The skin is closed and dressings (and perhaps a postoperative brace and cold therapy device, depending on surgeon preference) are applied. The patient will usually go home on the same day of the surgery.

Techniques for ACL reconstruction

Extra-articular reconstruction

Intra-articular reconstruction became the preferred choice but it does not fully restore knee kinematics by creating a static restraint and was usually accompanied by connecting the lateral femoral epicondyle to Gerdy’s tubercle with the collagenous restraint lying parallel to the intra-articular course of ACL. This also avoids the problem of lack of blood supply to the intra-articular reconstructions. Most of these procedures use the iliotibial band or tract connecting the lateral femoral epicondyle to the greedy tubercle, The optimal attachment point for the extra-articular reconstructions for anterolateral rotatory instability is found to be the Gerdy tubercle. This procedure is also used primarily in conjunction with an intra-articular reconstruction when severe anterior instability is due to injury or late stretching of the secondary stabilizing capsular structures or the lateral side of the knee.

Procedures

  • Macintosh method (iliotibial band tenodesis)
  • Macintosh, modified by Loseen method
  • Andrews method

Disadvantages

  • Diminish the anterolateral rotatory subluxation, but do not recreate the normal anatomy and function of the ACL.
  • When used alone has a high rate of failure.

Intra-articular Procedure

The advances made in the arthroscopy procedures have produced better results in ACL injury rehabilitation. This procedure may involve a small arthrotomy incision which preserves the vastus medialis oblique muscle to the patella. This procedure can be performed with both endoscopic technique or double incision arthroscopic technique.

Various tissues/grafts have been used to anatomically reconstruct the torn ACL which include portions of the extensor mechanism, patellar tendon, iliotibial tract, semitendinosus tendon, gracilis tendon, and menisci. These can all used in autografts i.e grafts taken from the person undergoing surgery. Other methods include the use of allografts and synthetic ligaments. This procedure has the following steps:

  • Graft selection – The graft to be used depends on the length of surgery. The most commonly used autograft is patellar bone graft and hamstring tendon graft (semitendinosus and gracilis).
  • Diagnostic arthroscopy – performed along with any necessary meniscal debridement or repair. Attention is given to partial-thickness tears, displaced bucket-handle tears, and the status of the articular surfaces, including the patellofemoral joint.
  • Graft Harvest – Mini incision extending from the distal pole of the patella to 2.5cm below the tibial tubercle is made to procure the graft. After retracting the other structures the graft to be taken is sharply outlined and a micro oscillating saw blade is used to harvest the graft/bone plug. A triangle bone plug profile is usually obtained.
  • Graft preparation – Graft is shaped into a 10mm tube shape for the femoral drill hole and an 11mm tube for the tibial tunnel.
  • Intercondylar notch preparation and notchplasty – Notchplasty is performed with 5.5mm burr from the anterior aspect of the intercondylar notch posteriorly and from distal to proximal and any residual tissue is also peeled off. The tissue is aggressively debrided with an arthroscopic shaver. If in the small intercondylar or notch area then further modifications are done.
  • Tibial tunnel placement – Tibial tunnel should be placed so that the graft is not impinged by the roof of the intercondylar notch and should reside within the middle third of the former ACL insertion site.
  • Femoral Tunnel placement – following a tibial tunnel placement, a femoral tunnel placement is completed so as to make a normal ACL like graft placement.
  • Graft placement – The graft after the tunnel placement is slid along with arthroscopic grasper through the tunnel. The graft may be rotated before tibial fixation.
  • Graft fixation – A Nitinol pin is then used to fix the graft with the bone and tunnel. The graft may be rotated before tibial fixation as an ACL has been shown to have external rotation within its fibers of approximately 90 degrees. The amount of graft tension created during fixation has a direct effect on ACL rehabilitation
  • Wound closure – Before closing, the graft harvest site is copiously injected with 0.25% Marcaine and it is also injected intra-articularly. The wound is closed with absorbable sutures with the knee in flexion. ACL reconstruction is one of the most common orthopedic surgeries, and commonly there is articular cartilage degeneration.
  • A total collateral ligament rupture and a full-thickness cartilage lesion would be seen on an MRI.
  • Patella tendon procedure: involves the central third of the ipsilateral patellar tendon. Fixation of the bone blocks within the tibia and femur.
  • Hamstring tendon procedure: four-layer, fold up of gracilis, and the semitendinosus tendons.

The surgery takes place at 10 weeks post-injury

Double-bundle reconstructionSemitendinosus is used with the autograft through 2 tunnels in both the tibia and femur. The autograft method is bone to bone with hamstrings/semitendinosus grafts. 3 tunnels may also be used, 2 tunnels through the tibia, and 1 tunnel through the femur.

The most common procedures for this reconstruction

  • The autologous bone to patella and tendon to bone graft
  • The autologous four-strand hamstrings graft

For the bone to patella and tendon to bone graft, a couple of bone blocks from the patella and the tibial tubercle are taken. This procedure causes more anterior knee pain than the semitendinosus graft. In the second procedure, the graft is obtained from the distal end of the semitendinosus and the gracilis tendon.

Other procedures are the LARS artificial ligament,(Ligament Advanced Reinforcement System) iliotibial tract allografts, cadaveric allografts, synthetic materials and grafts from living related donor people, but all materials have their drawbacks. There is the potential for cross infections, breakage, immunological responses, chronic effusions and recurrent instability

Single bundle vs Double bundle ACL reconstruction

A kinematics study showed that the standard single-bundle ACL reconstruction does not create the same kinematics as the intact ACL in normal activities. Only anteroposterior stability seems to be reconstructed. When the leg turns, there is an abnormal tibial rotation in the knee. Single-bundle ACL reconstruction does not recreate normal rotation in the knee.

On the contrary, anterior translation after double-bundle reconstruction was comparable with the intact ACL at 0° flexion, but the most stable position of the knee is at 15° and 75° flexion.

Watch this video to learn more about ACL Reconstruction using patellar tendon

Rehabilitation

Physical therapy is a crucial part of successful ACL surgery, with exercises beginning immediately after the surgery. Much of the success of ACL reconstructive surgery depends on the patient’s dedication to rigorous physical therapy. With new surgical techniques and stronger graft fixation, current physical therapy uses an accelerated course of rehabilitation.

Postoperative Course

  • In the first 10 to 14 days after surgery, the wound is kept clean and dry, and the early emphasis is placed on regaining the ability to fully straighten the knee and restore quadriceps control.
  • The knee is iced regularly to reduce swelling and pain. The surgeon may dictate the use of a postoperative brace and the use of a machine to move the knee through its range of motion. Weight-bearing status (use of crutches to keep some or all of the patient’s weight off of the surgical leg) is also determined by physician preference, as well as other injuries addressed at the time of surgery.

Rehabilitation

  • The goals for the rehabilitation of ACL reconstruction include reducing knee swelling, maintaining mobility of the kneecap to prevent anterior knee pain problems, regaining full range of motion of the knee, as well as strengthening the quadriceps and hamstring muscles.
  • The patient may return to sports when there is no longer pain or swelling, when full knee range of motion has been achieved, and when muscle strength, endurance, and functional use of the leg have been fully restored.
  • The patient’s sense of balance and control of the leg must also be restored through exercises designed to improve neuromuscular control. This usually takes 4 to 6 months. The use of a functional brace when returning to sports is ideally not needed after a successful ACL reconstruction, but some patients may feel a greater sense of security by wearing one.

Complications

  • Infection – The incidence of infection after arthroscopic ACL reconstruction is very low.  There have also been reported deaths linked to bacterial infection from allograft tissue due to improper procurement and sterilization techniques.
  • Viral transmission – Allografts specifically are associated with the risk of viral transmission, including HIV and Hepatitis C, despite careful screening and processing. The chance of obtaining a bone allograft from an HIV-infected donor is calculated to be less than 1 in a million.
  • Bleeding, numbness – Rare risks include bleeding from acute injury to the popliteal artery and weakness or paralysis of the leg or foot. It is not uncommon to have numbness of the outer part of the upper leg next to the incision, which may be temporary or permanent.
  • Blood clot – Although rare, blood clot in the veins of the calf or thigh is a potentially life-threatening complication. A blood clot may break off in the bloodstream and travel to the lungs, causing pulmonary embolism or to the brain, causing a stroke.
  • Instability – Recurrent instability due to rupture or stretching of the reconstructed ligament or poor surgical technique is possible.
  • Stiffness – Knee stiffness or loss of motion has been reported by some patients after surgery.
  • Extensor mechanism failure – Rupture of the patellar tendon (patellar tendon autograft) or patella fracture (patellar tendon or quadriceps tendon autografts) may occur due to weakening at the site of graft harvest.
  • Growth plate injury – In young children or adolescents with ACL tears, early ACL reconstruction creates a possible risk of growth plate injury, leading to bone growth problems. The ACL surgery can be delayed until the child is closer to reaching skeletal maturity. Alternatively, the surgeon may be able to modify the technique of ACL reconstruction to decrease the risk of growth plate injury.
  • Kneecap pain – Postoperative anterior knee pain is especially common after patellar tendon autograft ACL reconstruction. The incidence of pain behind the kneecap varies greatly in studies, whereas the incidence of kneeling pain is often higher after patellar tendon autograft ACL reconstruction.

Complications associated with non-surgical treatment are largely associated with NSAID use.

Common Adverse Effects of NSAID Use

  • Stomach pain and heartburn
  • Stomach ulcers
  • A tendency to bleed, especially while taking aspirin
  • Kidney problems

Common Adverse Effects of Intra-Articular Corticosteroid Injection

  • Pain and swelling (cortisone flare)
  • Skin discoloration at the site of injection
  • Elevated blood sugar
  • Infection
  • Allergic reaction

Common Adverse Effects of Intra-Articular HA Injection

  • Injection site pain
  • Muscle pain
  • Trouble walking
  • Fever
  • Chills
  • Headache

Complications Associated with HTO

  • Recurrence of deformity
  • Loss of posterior tibial slope
  • Patella baja
  • Compartment syndrome
  • Peroneal nerve palsy
  • Malunion or nonunion
  • Infection
  • Persistent pain
  • Blood clot

Complications Associated with UKA

  • Stress fracture of the tibia
  • Tibial component collapse
  • Infection
  • Osteolysis
  • Persistent pain
  • Neurovascular injury
  • Blood clot
  • Infection
  • Instability
  • Osteolysis
  • Neurovascular injury
  • Fracture
  • Extensor mechanism rupture
  • Patellar maltracking
  • Patellar clunk syndrome
  • Stiffness
  • Peroneal nerve palsy
  • Wound complications
  • Heterotopic ossification
  • Blood clot

Prevention

Given the importance of neuromuscular factors and the etiology of ACL injuries, numerous programs have aimed to improve neuromuscular control during standing, cutting, jumping, and landing. [rx] The components of neuromuscular training are:

  • Balance training: balance exercises
  • Jump training – plyometrics: landing with increased flexion at the knee and hip
  • Strengthening that emphasizes proximal hip control mediated through gluteus and proximal hamstring activation in a close kinetic chain
  • Stretching
  • Skill training: Controlling body motions, especially in deceleration and pivoting maneuvers
  • Movement education and some form of feedback to the athlete during the training of these activities
  • Agility training: agility exercises

Examples of more recent neuromuscular training programs include: Sportsmetrics and Prevent Injury and Enhance Performance program. Both programs have a positive influence on injury reduction and improve athletic performance tests. [rx] The PEP plan includes: Warm Up, stretching, strengthening, plyometrics, and agility exercises. [rx]

References

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PCL Injury – Causes, Symptoms, Diagnosis, Treatment

PCL Injury/Posterior Cruciate Ligament Injury (PCL) is one of the four major ligaments of the knee joint that functions to stabilize the tibia on the femur. It originates from the anterolateral aspect of the medial femoral condyle in the area of the intercondylar notch and inserts onto the posterior aspect of the tibial plateau. It functions to prevent posterior translation of the tibia on the femur. To a lesser extent, the PCL functions to resist varus, valgus, and external rotation forces. It is approximately 1.3 to 2 times as thick and about twice as strong as the anterior cruciate ligament (ACL) and, consequently, less commonly subject to injury.

The posterior cruciate ligament (PCL) is the largest and strongest ligament in the human knee, and the primary posterior stabilizer. Recent anatomy and biomechanical studies have provided an improved understanding of PCL function. PCL injuries are typically combined with other ligamentous, meniscal and chondral injuries. Stress radiography has become an important and validated objective measure in surgical decision making and post-operative assessment. Isolated grade I or II PCL injuries can usually be treated non-operatively. However, when acute grade III PCL ruptures occur together with other ligamentous injury and/or repairable meniscal body/root tears, surgery is indicated. Anatomic single-bundle PCL reconstruction (SB-PCLR) typically restores the larger anterolateral bundle (ALB) and represents the most commonly performed procedure.

Anatomy of PCL Injury

The PCL is the largest and strongest intraarticular ligament of the knee joint, comprising of 2 functional bundles: the larger anterolateral bundle (ALB) and the smaller posteromedial bundle (PMB) (). The size of the femoral attachment of the ALB is nearly twice the size of its tibial attachment and has been reported to range from 112 to 118 mm2 (). The center of the femoral ALB footprint is located 7.4 mm from the trochlear point, 11.0 mm from the medial arch point, and 7.9 mm from the distal articular cartilage. Furthermore, ALB tibial attachment center is located 6.1 mm posterior to the shiny white fibers of the posterior medial meniscus root, 4.9 mm from the bundle ridge (which separates both bundles), and 10.7 mm from the champagne glass drop-off of the posterior tibia ().

The area of the PMB femoral attachment is between 60 mm2 and 90 mm2 in size and is located between the anterior and posterior meniscofemoral ligaments. The femoral PMB center is located 11.1 mm from the medial arch point and 10.8 mm from the posterior point of the articular cartilage margin. Meanwhile, the PMB tibial attachment center is located 4.4 mm anterior to the champagne glass drop-off of the posterior tibia and 3.1 mm lateral from the medial groove of the medial tibial plateau articular surface (). These measures have biomechanical and surgical implications, because an anatomic reconstruction of the ALB and PMB better restores native knee kinematics and has been reported to improve clinical outcomes

Posterior Cruciate Ligament

  • Origin the posterior intercondylar region of the tibia
  • Insertion  the anterolateral margin of the medial condyle of the femur
  • Function prevention of posterior translation of the tibia relative to the femur; generalized knee stability
  • Blood Supplymiddle geniculate artery
  • Sensory Innervation posterior articular nerve

The PCL is composed of two bundles: the anterolateral bundle and the posteromedial bundle

Anterolateral Bundle of the PCL

  • Taut in knee flexion
  • Lax in knee extension

Posteromedial bundle of the PCL

  • Taut in knee extension
  • Lax in knee flexion

Types of Posterior Cruciate Ligament Injury

Acute PCL injury

  • Isolated injury – Symptoms are often vague and minimal, with patients often not even feeling or noticing the injury. Minimal pain, swelling, instability and full range of motion is present, as well as a near-normal gait pattern.
  • Combination with other ligamentous injuries – Symptoms differ according to the extent of the knee injury. This includes swelling, pain, a feeling of instability, limited range of motion and difficulty with mobilisation. Bruising may also be present.

Chronic PCL injury

Patients with a chronic PCL injury are not always able to recall a mechanism of injury. Common complaints are discomfort with weight-bearing in a semi flexed position (e.g. climbing stairs or squatting) and aching in the knee when walking long distances. Complaints of instability are also often present, mostly when walking on an uneven surface. Retropatellar pain and pain in the medial compartment of the knee may also be present. Potential swelling and stiffness depend on the degree of associated chondral damage.

Ligaments

  • anterior cruciate ligament tear
      • anterior tibial translocation sign
      • deep lateral sulcus sign
      • positive PCL line sign
      • reconstruction
        • radiographic evaluation
        • complications
          • cyclops lesion
          • tibial tunnel cyst
  • anterior cruciate ligament ganglion cyst
  • anterior cruciate ligament mucoid degeneration
  • posterior cruciate ligament tear
  • medial collateral ligament tear
  • lateral collateral ligament tear
  • medial patellofemoral ligament tear
  • posterolateral corner injury
  • posteromedial corner injury

Tendons

  • patellar tendon rupture
  • quadriceps tendon rupture

Meniscal lesions

  • meniscal tear
      • longitudinal tear
        • horizontal tear
        • longitudinal tear
          • Wrisberg rip
      • radial tear
        • ghost meniscus
      • root tear
      • displaced tear
        • flap tear
        • bucket-handle tear
        • parrot beak tear
      • signs
        • absent bow tie sign
        • double PCL sign
        • Jack and Jill lesion
        • two-slice-touch rule
      • MRI grading system for meniscal signal intensity
  • meniscal contusion
  • meniscal extrusion
  • meniscal/parameniscal cyst
  • meniscal flounce
  • meniscal fraying
  • meniscal maceration
  • meniscocapsular separation
    • ramp lesion
    • floating meniscus
  • bursosynovial lesions
    • infrapatellar bursitis
    • pes anserinus bursitis
    • prepatellar bursitis
    • medial patellar plica syndrome
Posterior Cruciate Ligament Injury

Knee Joint Ligaments Anatomy Knee And Ankle Anatomy Musculoskeletal With Seegmiller At – Human Anatomy Library

Causes of Posterior Cruciate Ligament Injury

PCL tears are commonly seen in contact sports and non-contact sports. They often occur when:

  • Motor vehicle accidents – A “dashboard injury” occurs when the driver’s or passenger’s bent knee slams against the dashboard, pushing in the shinbone just below the knee and causing the posterior cruciate ligament to tear.
  • Contact sports – Athletes in sports such as football and soccer can tear their posterior cruciate ligament when they fall on a bent knee with their foot pointed down. The shinbone hits the ground first and it moves backward. Being tackled when your knee is bent also can cause this injury.
  • The knee is hit directly – especially during sports like soccer, rugby, and football
  • A person lands on a bent knee – such as during a fall or misstep
  • Landing directly on the front of the shinbone – such as when a dancer comes down from a leap and falls
  • A person makes cutting or pivoting maneuvers – such as when an athlete plants a foot and shifts directions
  • A person lands on one leg – which can happen after a jump in basketball or volleyball
  • A direct blow to the bent knee in an automobile injury
  • A sports-related injury in which the knee bends
  • Pulling on the ligament in a twisting injury or hyperextension
  • A misstep on uneven terrain

Symptoms of Posterior Cruciate Ligament Injury

The typical symptoms of a posterior cruciate ligament injury are:

  • Sharp or dull pain around the back of the knee – This can occur immediately or develop in the hours or days after the injury.
  • Swelling – Bleeding around the torn ligament may result in swelling. Swelling typically occurs within 2 to 3 hours of the injury.
  • Stiffness – Swelling may cause the knee to become stiff. A person may have trouble bending the knee, resulting in a limp or difficulty going up or down stairs.
  • Difficulty bearing weight – The injured knee may be difficult or painful to stand or walk on, especially for long periods of time.
  • Knee instability – Mild or moderate sprains may cause very little or no knee instability, while more severe sprains may cause a person to feel as if the knee is about to buckle or give out. In some cases, knee instability is a sign of an undiagnosed PCL tear that occurred months or even years earlier.
  • The back of the knee may be warm to the touch – This is due to bleeding within the knee joint caused by the injury.
  • Tenderness around the knee joint – The knee joint, particularly the back of the knee, may be tender or sensitive to touch.
  • Knee tingling or numbness – In more severe PCL injuries, people may report the feeling of tingling or numbness around the knee joint
  • The back of the knee may be warm to the touch – This is due to bleeding within the knee joint caused by the injury.
  • Tenderness around the knee joint – The knee joint, particularly the back of the knee, may be tender or sensitive to touch.
  • Knee tingling or numbness – In more severe PCL injuries, people may report the feeling of tingling or numbness around the knee joint.
  • Mild knee swelling, with or without the knee giving out when you walk or stand, and with or without limitation of motion
  • Mild pain at the back of the knee that feels worse when you kneel
  • Pain in the front of the knee when you run or try to slow down — This symptom may begin one to two weeks after the injury or even later.
  • Pain with swelling that occurs steadily and quickly after the injury
  • Swelling that makes the knee stiff and may cause a limp
  • Difficulty walking
  • The knee feels unstable, like it may “give out”

Diagnosis of Posterior Cruciate Ligament Injury

History and Physical

Patients often will present with complaints of acute onset of posterior knee pain, swelling, and instability.  A thorough history includes the mechanism of injury, such as trauma from falling onto a flexed knee or recent motor vehicle accident.  There may or may not be a complaint of a “pop” with PCL tears like those frequently reported with ACL tears.

A thorough knee exam should be performed, including gait assessment. The neurovascular integrity of the lower extremity distal to the injury should also be assessed.

  • Inspection – Affected knee will often present with mild to moderate joint effusion. Swelling is usually less than an ACL tear. Patients may present with antalgic gait on examination with obvious favoring of affected knee. They may have difficulty walking up or down stairs or at an incline. There may be a positive sag test; The sag test is performed with the patient supine, hip flexed to 45 degrees, and knee flexed to 90 degrees.  The tibia will be noted to sag distally relative to the femur as compared to the opposite knee.
  • Palpation – There may be an effusion on physical exam.
  • Muscle strength testing – Strength should be normal, but there may be weakness with knee extension and flexion secondary to guarding.
  • ROM – The passive range of motion may be limited 10 to 20 degrees with flexion. It may be further decreased with other concomitant injuries such as meniscal, muscular, or ligamentous etiology.
  • Special Testing – The posterior drawer test is the most accurate test for assessing PCL integrity.  It is performed with the patient in the supine position with the hip flexed to 45 degrees and knee flexed to 90 degrees. A posterior force is applied to the proximal tibia with one hand with stabilization of the femur with the other. Ligamentous and meniscal testing should be performed to assess the integrity of other structure of the knee. The Dial test can be performed to distinguish isolated PCL injuries with an associated posterolateral joint capsule, popliteus, medial collateral ligament, and posterior oblique ligament injuries.
  • The posterolateral drawer test – external rotation recurvatum test, and reverse pivot shift test can also be used to assess injuries to the posterolateral structures. However, a positive external rotation recurvatum test is more indicative of an ACL injury than a PCL injury and the reverse pivot shift test should be used with care because the test may yield positive results in about 30% of normal knees.

Posterior drawer test

  • The test is performed with the person lying on his or her back.
  • The examiner will ask the person to bend their hip to 45º with foot flat) and knee to 90º.
  • He or she will lean lightly on the person’s foot to stabilize the leg.
  • The examiner will wrap both hands around the joint line of the knee and attempt to move the tibia (shin bone) backwards.
  • This movement may be done several times to confirm the diagnosis.

By putting pressure on the shin bone, the doctor will be able to gauge resistance from the PCL; an injured PCL will have less resistance than an uninjured ligament, causing the tibia to move backwards.

Posterior sag sign test

posterior sag test, where, in contrast to the drawer test, no active force is applied. Rather, the person lies supine with the leg held by another person so that the hip is flexed to 90 degrees and the knee 90 degrees.[rx] The main parameter in this test is step-off, which is the shortest distance from the femur to a hypothetical line that tangents the surface of the tibia from the tibial tuberosity and upwards. Normally, the step-off is approximately 1 cm, but is decreased (Grade I) or even absent (Grade II) or inverse (Grade III) in injuries to the posterior cruciate ligament.[rx]

  • This test is performed with the person laying on his or her back.
  • The doctor will bend the affected knee so that it and the hip are each at a 90º angle, with the foot in the air, and hold the heel for support.
  • If there is an increased posterior sag in the affected knee (due to gravity), a PCL tear is likely present.

A doctor may also perform physical tests to determine if any other structures in the knee have been damaged. In addition to a physical exam, the doctor may order an x-ray or other medical imaging.

In some cases, your doctor may suggest one or more of the following imaging tests:

  • X-ray – While an X-ray can’t detect ligament damage, it can reveal bone fractures. People with posterior cruciate ligament injuries sometimes have breaks in which a small chunk of bone, attached to the ligament, pulls away from the main bone (avulsion fracture).
  • MRI scan – This painless procedure uses radio waves and a strong magnetic field to create computer images of the soft tissues of your body. An MRI scan can clearly show a posterior cruciate ligament tear and determine if other knee ligaments or cartilage also are injured.
  • Arthroscopy – If it’s unclear how extensive your knee injury is, your doctor might use a surgical technique called arthroscopy to look inside your knee joint. A tiny video camera is inserted into your knee joint through a small incision. The doctor views images of the inside of the joint on a computer monitor or TV screen.

Stage

Injuries to ligaments are referred to as “sprains.” These sprains are graded according to the severity of the injury.

  • Grade 1 sprains are injuries to the ligament where only mild damage has occurred. The ligament has been stretched slightly, but is still capable of providing stability to the knee joint.
  • Grade 2 sprains occur when the ligament is stretched to the point of permanent laxity and some tearing of the ligament has occurred. This type of sprain is often referred to as a partial tear.
  • Grade 3 sprains are complete tears of the ligament. In a grade 3 sprain, the ligament has been split into two pieces, making the knee unstable.

PCL Injuries are commonly seen in conjunction with injuries to other structures of the knee. The most commonly missed associated injury is an injury to the posterolateral corner of the knee.

Treatment of Posterior Cruciate Ligament Injury

Nonsurgical Treatment Options for PCL Injuries

Less severe posterior cruciate ligament (PCL) tears of the knee generally heal well without surgery. Immediately after the injury, management consists of the RICE method:

  • Rest – Any activities that causes knee pain, such as running or walking, should be avoided until symptoms are relieved.
  • Ice – A person may be advised to apply ice to the area to help reduce pain and swelling. Ice can be applied several times throughout the day for about 10 to 20 minutes at a time.
  • Compression – Swelling can be managed by wearing an elastic bandage around the affected knee.
  • Elevation – Keeping the knee supported above the waist can help with swelling.
  • Wear a knee brace – A knee brace provides stability and restricts side-to-side movement. Some people may choose to wear a functional knee brace, which allows for more movement, when they return to activity.
  • Use crutches – Crutches may be recommended to keep weight off the injured knee.

Physical therapist

  • A physical therapist will focus on improving mobility, strength, flexibility, and balance, which can help speed up recovery time and improve performance once the injury has healed.
  • Walking (weight-bearing) is initiated as soon as possible.
  • Knee straightening (extension) and bending (flexion) are encouraged. Pool therapy is helpful.
  • Stationary cycling is initiated as soon as adequate motion is achieved.
  • Quadriceps strengthening exercises are started, such as standing squats with toe raises and leg press.
  • Hamstring exercise may be modified for 6 months.
  • Surgery is avoided in most cases unless other major ligaments are disrupted.

Medication

  • Antibiotic – Cefuroxime or Azithromycin, or  Flucloxacillin or any others cephalosporin/quinolone antibiotic must be used to prevent infection or clotted blood remove to prevent furthers swelling and edema.
  • NSAIDs – Prescription-strength drugs that reduce both pain and inflammation. Pain medicines and anti-inflammatory drugs help to relieve pain and stiffness, allowing for increased mobility and exercise. There are many common over-the-counter medicines called non-steroidal anti-inflammatory drugs (NSAIDs). They include and KetorolacAceclofenacNaproxen, Etoricoxib.
  • Corticosteroids – Also known as oral steroids, these medications reduce inflammation.
  • Muscle Relaxants –  These medications provide relief from associated muscle spasms.
  • Neuropathic Agents – Drugs(pregabalin & gabapentin) that address neuropathic—or nerve-related—pain. This includes burning, numbness, and tingling.
  • Opioids – Also known as narcotics, these medications are intense pain relievers that should only be used under a doctor’s careful supervision.
  • Topical Medications – These prescription-strength creams, gels, ointments, patches, and sprays help relieve pain and inflammation through the skin.
  • Calcium & vitamin D3 – to improve bone health and healing fracture. As a general rule, men and women age 50 and older should consume 1,200 milligrams of calcium a day, and 600 international units of vitamin D a day.
  • Antidepressants – A drug that blocks pain messages from your brain and boosts the effects of endorphins (your body’s natural painkillers).
  • Glucosamine & DiacereinChondroitin sulfate – can be used to tightening the loose tension, cartilage, ligament, and cartilage, ligament regenerates cartilage or inhabits the further degeneration of cartilage, ligament. They are structural components of articular cartilage, and the thought is that a supplement will aid in the health of articular cartilage.
  • Intra-articular corticosteroid injections – may be useful for symptomatic PCL injury especially where there is a considerable inflammatory component. The delivery of the corticosteroid directly into the knee may reduce local inflammation associated with osteoarthritis and minimize the systemic effects of the steroid.
  • Intra-articular hyaluronic acid injections (HA) – injections are another injectable option for knee PCL injury. HA is a glycosaminoglycan that is found throughout the human body and is an important component of synovial fluid and articular cartilage. HA breaks down during the process of  PCL injury and contributes to the loss of articular cartilage as well as stiffness and pain. Local delivery of HA into the joint acts as a lubricant and may help increase the natural production of HA in the joint.

Surgery

Arthroscopic transtibial technique

  • standard arthroscopic portals with an accessory posteromedial portal posteromedial portal is placed 1 cm proximal to the joint line posterior to the MCL avoid injury to branches of the saphenous nerve during placement.
  • posteromedial corner of the knee is best visualized with a 70° arthroscope either through the notch (modified Gillquist view) or using a posteromedial portal transtibial drilling anterior to posterior
  • fix graft in 90° flexion with an anterior drawer results in knee biomechanics similar to native knee risk to popliteal vessels

Open (tibial inlay)

  • uses a posteromedial incision between medial head of gastrocnemius and semimembranosus used for ORIF of bony avulsion biomechanical advantage with a decrease in the “killer turn” with less graft attenuation and failure  screw fixation of the graft bone block is within 20 mm of the popliteal artery.

Single-bundle technique

  • arthroscopic or open reconstruct the anterolateral bundle tension at 90° of flexion

Double-bundle technique

  • arthroscopic or open techniques may be utilized anterolateral bundle tensioned in 90° of flexion posteromedial bundle tensioned in extension biomechanical advantage with knee function in flexion and extension clinical advantage has yet to be determined may be advantageous to perform with combined PCL/PLC injuries for better rotational control as PLC reconstructions typically loosen over time.

Rehabilitation of Posterior Cruciate Ligament Injury

Conservative management with Physiotherapy management

Grade 1 & II injuries

Two weeks of relative immobilisation of the knee (in a locked range of motion brace) is recommended by orthopaedic surgeons. Physiotherapy in this time period includes

  • Partial to full weight-bearing mobilisation
  • Reduce pain and inflammation
  • Reducing knee joint effusion
  • Restore knee range of motion
  • Knee strengthening (especially protective quadriceps rehabilitation)
    • Strengthening the quadriceps is a key factor in a successful recovery, as the quadriceps can take the place of the PCL to a certain extent to prevent the femur from moving too far forward over the tibia.
    • Hamstring strengthening can be included
    • Important to incorporate eccentric strengthening of the lower limb muscles
    • Closed chain exercises
  • Activity modification until pain and swelling subsides

After 2 weeks (on the orthopaedic surgeon’s recommendation)

  • Progress to full weight-bearing mobilisation
  • Weaning of range of motion brace
  • Proprioception, balance and coordination
  • Agility programme when strength and endurance has been regained and the neuromuscular control increased
  • Return to play between 2 and 4 weeks of injury

Grade III injuries

The knee is immobilised in range of motion brace, locked in extension, for 2-4 weeks. Physiotherapy management in this time includes:

  • Activity modification
  • Quadriceps rehabilitation
    • Initially isometric quadriceps exercises and straight-leg raises (SLR)

After 2-4 weeks

  • Avoid isolated hamstring strengthening
  • Active-assisted knee flexion <70°
  • Progress weight-bearing within pain limits
  • Quadriceps rehabilitation: Promote dynamic stabilisation and counteract posterior tibial subluxation
    • Closed chain exercises
    • Open kinetic chain eccentric exercises and eventually
    • Progress to functional exercises such as stationary cycling, leg press, elliptical exercises and stair climbing

Return to play is sport specific, and only after 3 months.

Chronic injuries

  • Chronic PCL injuries can be adequately treated with physiotherapy. A range of motion brace is used, initially set to prevent the terminal 15° of extension. After a while the brace is opened to full extension.

Post-operative rehabilitation

Post-operative rehabilitation typically lasts 6 to 9 months. The duration of each of the five phases and the total duration of the rehabilitation depends on the age and physical level of the patient, as well as the success of the operation. Also see page on PCL reconstruction.

General Guidelines for the post-operative PCL rehabilitation

  • Mobility should be restricted from 0-90 degrees in the first two weeks then facilitated gradually to full ROM.
  • Involved leg should be in non-weight bearing for the first 6 weeks then placed in mobilizer brace and progressed to rebound PCL brace for 6 months.
  • Avoid isolated hamstrings contraction for 4 months due to the hamstrings force in drawing tibia posteriorly which can apply an elongation force on the PCL graft causing instability
  • Avoid unsupported knee flexion for 4 months to prevent any posterior drawing forces on tibia.

Phase I: Early Post-operative phase

Early mobilisation and placing sub-maximal strain on graft lead to better outcomes.

Objectives of maximal protection and early rehabilitation:

  • Restore joint homeostasis
  • Scar tissue management
  • Restore joint ROM
  • Re-train quadriceps
  • Create an effective plan for your patient

Strategies of rehabilitation:

  • Perform ROM exercises from prone position to avoid posterior tibial sag and graft elongation
  • Teach patient to perform Quadriceps contraction/sets from day 1 post surgery if the patient is not on strong pain medications.
  • Patellofemoral mobilisation is important to prevent scarring and preserve joint volume for full range of flexion and extension
  • Ice and elevation for swelling and inflammation management
  • Progressing by applying strategies for increasing ROM and terminal knee extension

One of the huge advancement of PCL management is the utilisation of Dynamic PCL braces. This option may not always be available but if found make sure to utilise it. It’s a spring loaded brace aiming to place an anterior force on the tibia preventing posterior tibial sag and graft elongation by placing the graft in a shortened position. Immediately after surgery, it is recommended to place the leg in a mobiliser braces then progress to a dynamic brace once swelling is subsided. It should be used all the time and only taken off to perform exercises for 6 months. Then move into more functional bracing, worn all the time for 12 months.

Building weight bearing tolerance after 6 weeks of non weight bearing (NWB) should take place gradually and progressively between week 7-8 .

Phase II: Later Post-operative Rehabilitation

Begins 8 weeks after surgery. The aim is to create a plan for the patient to prepare them for returning to pre-operative functional capacity by addressing all MSK deficits.

Areas to address in late post-operative rehabilitation and suggested time-frames:

  • Muscular endurance (weeks:9-16)
  • Strength (weeks 17-22)
  • Power (weeks 23-28) with running progression if it needed (weeks 25-28)
  • Speed and agility (weeks 29-32 )
  • Return to training (week 33).
  • Return to sport : It varies from a sport to another but on average takes about with 3-4 weeks of training. Return to play around 36th week.

How can you care for yourself at home?

  • Put ice or a cold pack on your knee for 10 to 20 minutes at a time. Try to do this every 1 to 2 hours (when you’re awake) for the first 3 days after your injury or until the swelling goes down. Put a thin cloth between the ice and your skin.
  • Prop up your leg on a pillow when you ice it or anytime you sit or lie down. Do this for about 3 days after your injury. Try to keep your knee above the level of your heart. This will help reduce swelling.
  • Take anti-inflammatory medicines to reduce pain and swelling. These include ibuprofen (Advil, Motrin) and naproxen (Aleve). Be safe with medicines. Read and follow all instructions on the label.
  • Follow instructions about how much weight you can put on your leg and how to walk with crutches, if your doctor recommends them.
  • Wear a brace, if your doctor recommends it, to protect and support your knee while it heals. Wear it as directed.
  • Do stretches or strength exercises as your doctor suggests.

References

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Anterior Cruciate Ligament Injury – Symptoms, Treatment

Anterior Cruciate Ligament Injury (ACL) is one of 2 cruciate ligaments which aids in stabilization of the knee joint. It is a strong band made of connective tissue and collagenous fibers that originate from the anteromedial aspect of the intercondylar region of the tibial plateau and extends posteromedially to attach to the lateral femoral condyle. The anteromedial bundle and posterolateral bundle form the 2 components of the ACL.   The ACL and the posterior cruciate ligament (PCL) together form a cross (or an “x”) within the knee and prevents excessive forward or backward motion of the tibia in relation to the femur during flexion and extension.

Anterior cruciate ligament injury is when the anterior cruciate ligament (ACL) is either stretched, partially torn, or completely torn. The most common injury is a complete tear. Symptoms include pain, a popping sound during injury, instability of the knee, and joint swelling. Swelling generally appears within a couple of hours.[rx] In approximately 50% of cases, other structures of the knee such as surrounding ligaments, cartilage, or meniscus are damaged.[rx]

Anterior Cruciate Ligament

Causes of Anterior Cruciate Ligament Injury

  • A sudden stop, twist, pivot or change in direction at the knee joint  – These knee movements are a routine part of football, basketball, soccer, rugby, gymnastics and skiing. For this reason, athletes who participate in these sports have an especially high risk of ACL tears.
  • Extreme hyperextension of the knee – Sometimes, during athletic jumps and landings, the knee straightens out more than it should and extends beyond its normal range of motion, causing an ACL tear. This type of ACL injury often occurs because of a missed dismount in gymnastics or an awkward landing in basketball.
  • Direct contact – The ACL may be injured during contact sports, usually during direct impact to the outside of the knee or lower leg. Examples are a sideways football tackle, a misdirected soccer kick that strikes the knee or a sliding tackle in soccer.

ACL tear Causes may include

  • Changing direction rapidly (also known as “cutting”)
  • Landing from a jump awkwardly
  • Coming to a sudden stop when running
  • Direct contact or collision to the knee (e.g. during a football tackle or a motor vehicle collision)
  • landing awkwardly from a jump
  • twisting movements, particularly when your foot is on the ground
  • quickly changing direction when running or walking
  • slowing down or stopping suddenly when running

These movements cause the tibia to shift away from the femur rapidly, placing strain on the knee joint and potentially leading to the rupture of the ACL. About 80% of ACL injuries occur without direct trauma. Risk factors include female anatomy, specific sports, poor conditioning, fatigue, and playing on a turf field.[rx]

Female predominance

Female athletes are two to eight times more likely to strain their ACL in sports that involve cutting and jumping as compared to men who play the same particular sports.[rx] NCAA data has found relative rates of injury per 1000 athlete exposures as follows:

  • Men’s basketball 0.07, women’s basketball 0.23
  • Men’s lacrosse 0.12, women’s lacrosse 0.17
  • Men’s football 0.09, women’s football 0.28

The highest rate of ACL injury in women occurred in gymnastics, with a rate of injury per 1000 athlete exposures of 0.33. Of the four sports with the highest ACL injury rates, three were women’s – gymnastics, basketball, and soccer.[rx]

Differences between males and females identified as potential causes are the active muscular protection of the knee joint, differences in leg/pelvis alignment, and relative ligament laxity caused by differences in hormonal activity from estrogen and relaxin.[rx][rx] Birth control pills appear to decrease the risk.[rx]

Dominance theories

Femur with Q angle – the angle formed by a line drawn from the anterior superior iliac spine through the center of the patella and a line drawn from the center of the patella to the center of the tibial tubercle

Some studies have suggested that there are four neuromuscular imbalances that predispose women to a higher incidence of ACL injury. Female athletes are more likely to jump and land with their knees relatively straight and collapsing in towards each other, while most of their body weight falls on a single foot and their upper body tilts to one side.[rx] Several theories have been described to further explain these imbalances. These include ligament dominance, quadriceps dominance, leg dominance, and trunk dominance theories.

Symptoms of Anterior Cruciate Ligament Injury

When an individual has an ACL injury, they are likely to hear a “pop” in their knee followed by pain and swelling. They may also experience instability in the knee once they resume walking and other activities, as the ligament can no longer stabilize the knee joint and keep the tibia from sliding forward.[rx].[rx]

  • Feeling a “pop” inside your knee when the ACL tears
  • Significant knee swelling and deformity within a few hours after injury
  • Severe knee pain that prevents you from continuing to participate in your sport (most common in partial tears of the ACL)
  • No knee pain, especially if the ACL has been completely torn and there is no tension across the injured ligament
  • A black and blue discoloration around the knee, due to bleeding from inside the knee joint
  • A feeling that your injured knee will buckle, “give out” or “give way” if you try to stand

Diagnosis of Anterior Cruciate Ligament Injury

Physical examination

Physical examination of the knee usually follows a relatively standard pattern.

  • The knee is examined for obvious swelling, bruising, and deformity.
  • Areas of tenderness and subtle evidence of knee joint fluid (effusion) are noted.
  • Most importantly, with knee injury ligamentous, stability is assessed. Since there are four ligaments at risk for injury, the examiner may try to test each to determine which one(s) is (are) potentially damaged. It is important to remember that a knee ligament injury might be an isolated structure damaged or there may be more than one ligament and other structures in the knee that are hurt.
  • In the acute situation, with a painful, swollen joint, the initial examination may be difficult because both the pain and the fluid limit the patient’s ability to cooperate and relax the leg. Spasm of the quadriceps and hamstring muscles often can make it difficult to assess ACL stability.
  • A variety of maneuvers can be used to test the stability and strength of the ACL. These include the Lachman test, the pivot-shift test, and the anterior drawer test. Guidelines from the American Academy of Pediatrics suggest the Lachman test is best for assessing ACL tears.
  • The Lachman test is performed as follows:
    • The damaged knee is flexed to 20-30 degrees.
    • The examiner grasps tibia and puts their thumb on the tibial tubercle (the bump of bone just below the knee where the patellar tendon attaches.
    • The examiners other hand grasps the thigh just above the knee.
    • The tibia is pulled forward and normally, there should be a firm stop if the ACL is intact. If the ligament is torn, the tibia will move forward and there will be no endpoint and it feels mushy.
  • The unaffected knee may be examined to be used as a comparison.

It may be difficult to examine some patients when muscle strength or spasm can hide an injured ACL because of the knee stabilization that they can provide.

Multiple maneuvers are employed to test the ACL and include the anterior drawer, the pivot shift, and the Lachman tests. These tests should be performed whenever there is suspicion for injury to the anterior cruciate ligament.

  • The anterior drawer test – is performed with the patient lying supine with their affected knee flexed to 90 degrees and the foot in a planted position (Sometimes it is easiest for the clinician to stabilize the patient’s foot by sitting on it). The clinician will grip the proximal tibia with both hands and pull with an anterior motion. If there is excessive anterior motion and instability, then the test is positive. It may also be useful to compare to the unaffected knee as patients may have increased laxity of the ACL that is not pathologic. This test has a sensitivity of 92% and specificity of 91% in chronic injuries, but not acute injuries.
  • The pivot shift test – is performed with the patient in the supine position. The clinician should hold the patient’s lower leg and begin with the knee in extension and flexion of the hip to 20 to 30 degrees. Next, the clinician will bring the tibia into the internal rotation with one hand and begin placing valgus stress on the knee using the other hand. While holding this position, the knee should now be flexed. This causes stress, instability, and ultimately subluxation of the ACL of the affected knee. With flexion of the knee, if the tibia subluxes posteriorly and one may feel a “clunk”; this would indicate a positive test. This test can be difficult to perform in patients who are guarding, and some may not allow the clinician to perform the test. This is a highly specific test (98%) when positive, but is insensitive (24%) due to the difficulty in evaluation secondary to patient pain and cooperation.
  • The Lachman test – is performed with the patient in the supine position with the knee flexed to about 30 degrees. The clinician should stabilize the distal femur with one hand and with the other hand pull the tibia toward themselves. If there is increased anterior translation, then this is a positive test. Again, comparing to the unaffected side may be helpful. This test has a sensitivity of 95% and specificity of 94% for ACL rupture.

Radiography

  • Tests – Your doctor may ask you to lie on your back and bend your hips and/or your knees at certain angles. He’ll then place his hands on different parts of your leg and gently shift you around. If any of your bones move in a way that isn’t normal, that could be a sign that your ACL is damaged.
  • X-ray – Soft tissues like the ACL don’t appear on X-rays, but your doctor may want to rule out broken bones.
  • MRI or ultrasound – These exams can show both soft tissue and bone. If you have a damaged ACL, it should appear on the images.
  • Arthroscopy – This literally means to “look within the joint.” During the exam, an orthopedic surgeon makes a small cut in your skin. He inserts a pencil-sized tool that contains a lighting system and lens (arthroscope) into the joint. The camera projects an image of the joint onto a TV screen. Your doctor can see what type of injury you have and repair or correct it, if needed.

Stage  of Anterior Cruciate Ligament

An ACL injury can further classify as a grade I, II, or III sprains.

  • Grade I – The ligamental fibers are stretched, with a tear that is less than one-third of the ligament. Mild tenderness and swelling are present. The knee joint feels stable with a knee laxity < 5 mm.
  • Grade II – A partial tear (between one-third to two-thirds of the ligamental fibers) is present. Mild tenderness and swelling with some loss of function are present. The joint may feel unstable with increased anterior translation (a knee laxity of 5 to 10 mm). The patient feels pain, and the pain may become exacerbated with Lachman’s and anterior drawer stress tests.
  • Grade III – The fibers have completely torn. Tenderness and limited pain (relative to the seriousness of the injury) are features. The degree of swelling may be variable. The knee feels unstable, with rotational instability (positive pivot shift test). A knee laxity is greater than 10  mm. Haemarthrosis (bleeding into the knee joints) is observable within 1 to 2 hours.

An acute ACL rupture commonly occurs among sports players, especially those aged 14 to 19 years. The incidence of ACL injury is higher among female athletes due to the following reasons:

  • Smaller ACL and narrower intercondylar notch – Females who are non-athletes and aged 41 to 65 are predisposed to ACL injuries if they have narrow intercondylar notches.
  • Wider pelvis and greater Q angle – A wider pelvis increases the angle of the femur toward the central patella. The greater the Q angle, the greater pressure is applied to the medial aspect of the knee, which can lead to an ACL tear.
  • Lax ligaments – Female ligaments with more elastic muscle fibers tend to be laxer than male ligaments. Excessive joint movements with increased flexibility may contribute to the higher incidence of ACL injury among females.
  • Greater quadriceps to hamstring strength ratio – Females tend to have poor hamstring strength compared to men. The imbalance of strength between the hamstring and quadriceps muscles may increase the risk of ACL injury.

Treatment of Anterior Cruciate Ligament Injury

Non-Surgical Treatment Options

  • Patient education
  • Activity modification
  • Physical therapy
  • Weight loss
  • Knee bracing
  • Acetaminophen
  • Nonsteroidal anti-inflammatory drugs (NSAIDs)
  • COX-2 inhibitors
  • Glucosamine and chondroitin sulfate
  • Corticosteroid injections
  • Hyaluronic acid (HA)

The American Academy Of Orthopedic Surgeons (AAOS) Recommends This Treatment.

  • Weight loss – is valuable in all stages of ACL injury. It is indicated in patients with symptomatic ACL injury with a body mass index greater than 25. The best recommendation to achieve weight loss is with diet control and low-impact aerobic exercise.
  • Knee bracing – in the setting of ACL injury includes unloader-type braces that shift the load away from the involved knee compartment. This may be useful in the setting where either the lateral or medial compartment of the knee is involved such as in a valgus or varus deformity.
  • Immobilization – Your doctor may recommend that you wear a brace for 3 to 4 weeks. This stabilizes the knee while it heals.
  • Weightbearing –  Because putting weight on the knee may cause pain and slow the healing process, your doctor may recommend using crutches for the first week or two after the injury.
  • Physical therapy – Once the knee has started to heal, your doctor will recommend physical therapy to help your child regain normal motion. Specific exercises will strengthen the thigh muscles holding the knee joint in place. Your commitment to the exercise program is important for a successful recovery. Typically return to activity 3 to 6 weeks after the injury.
  • Emergent closed reduction followed by vascular assessment/consult – If indications to considered an orthopedic emergency, vascular consult indicated if pulses are absent or diminished following reduction if arterial injury confirmed by arterial duplex ultrasound or CT angiography
  • Immobilization as definitive management – successful closed reduction without vascular compromise, most cases require some form of surgical stabilization following reduction, outcomes of worse outcomes are seen with nonoperative management/prolonged immobilization will lead to loss of ROM with persistent instability.
  • Rest Your Leg – Once you’re discharged from the hospital in a legislating, your top priority is to rest your and not further inflame the injury. Of course, the arm sling not only provides support, but it also restricts movement, which is why you should keep it on even during sleep. Avoiding the temptation to move your will help the bone mend quicker and the pain fades away sooner.
    • Depending on what you do for a living and if the injury is to your dominant side, you may need to take a couple of weeks off work to recuperate.
    • Healing takes between four to six weeks in younger people and up to 12 weeks in the elderly, but it depends on the severity of the radial head fractures.
    • Athletes in good health are typically able to resume their sporting activities within two months of breaking they’re ulnar styloid depending on the severity of the break and the specific sport.
    • Sleeping on your back (with the sling on) is necessary to keep the pressure off your shoulder and prevent stressing the hip injury.

Eat Nutritiously During Your Recovery

  • All bones and tissues in the body need certain nutrients in order to heal properly and in a timely manner. Eating a nutritious and balanced diet that includes lots of minerals and vitamins are proven to help heal ACL injury of all types. Therefore focus on eating lots of fresh produce (fruits and veggies), whole grains, lean meats, and fish to give your body the building blocks needed to properly repair your. In addition, drink plenty of purified water, milk, and other dairy-based beverages to augment what you eat.
  • ACL injury need ample minerals (calcium, phosphorus, magnesium, boron) and protein to become strong and healthy again.
  • Excellent sources of minerals/protein include dairy products, tofu, beans, broccoli, nuts and seeds, sardines, and salmon.
  • Important vitamins that are needed for bone healing include vitamin C (needed to make collagen), vitamin D (crucial for mineral absorption), and vitamin K (binds calcium to bones and triggers collagen formation).
  • Conversely, don’t consume food or drink that is known to impair bone/tissue healing, such as alcoholic beverages, sodas, most fast food items and foods made with lots of refined sugars and preservatives.

Medication

  • Antibiotic – Cefuroxime or Azithromycin, or  Flucloxacillin or any others cephalosporin/quinolone antibiotic must be used to prevent infection or clotted blood remove to prevent furthers swelling and edema.
  • NSAIDs – Prescription-strength drugs that reduce both pain and inflammation. Pain medicines and anti-inflammatory drugs help to relieve pain and stiffness, allowing for increased mobility and exercise. There are many common over-the-counter medicines called non-steroidal anti-inflammatory drugs (NSAIDs). They include and KetorolacAceclofenacNaproxen, Etoricoxib.
  • Corticosteroids – Also known as oral steroids, these medications reduce inflammation.
  • Muscle Relaxants –  These medications provide relief from associated muscle spasms.
  • Neuropathic Agents – Drugs(pregabalin & gabapentin) that address neuropathic—or nerve-related—pain. This includes burning, numbness, and tingling.
  • Opioids – Also known as narcotics, these medications are intense pain relievers that should only be used under a doctor’s careful supervision.
  • Topical Medications – These prescription-strength creams, gels, ointments, patches, and sprays help relieve pain and inflammation through the skin.
  • Calcium & vitamin D3 – to improve bone health and healing fracture. As a general rule, men and women age 50 and older should consume 1,200 milligrams of calcium a day, and 600 international units of vitamin D a day.
  • Antidepressants – A drug that blocks pain messages from your brain and boosts the effects of endorphins (your body’s natural painkillers).
  • Glucosamine & DiacereinChondroitin sulfate – can be used to tightening the loose tension, cartilage, ligament, and cartilage, ligament regenerates cartilage or inhabits the further degeneration of cartilage, ligament. They are structural components of articular cartilage, and the thought is that a supplement will aid in the health of articular cartilage.
  • Intra-articular corticosteroid injections – may be useful for symptomatic ACL injury especially where there is a considerable inflammatory component. The delivery of the corticosteroid directly into the knee may reduce local inflammation associated with osteoarthritis and minimize the systemic effects of the steroid.
  • Intra-articular hyaluronic acid injections (HA) – injections are another injectable option for knee ACL injury. HA is a glycosaminoglycan that is found throughout the human body and is an important component of synovial fluid and articular cartilage. HA breaks down during the process of  ACL injury and contributes to the loss of articular cartilage as well as stiffness and pain. Local delivery of HA into the joint acts as a lubricant and may help increase the natural production of HA in the joint.

Surgical Treatment

ACL tears are not usually repaired using suture to sew it back together, because repaired ACLs have generally been shown to fail over time. Therefore, the torn ACL is generally replaced by a substitute graft made of tendon.

  • Patellar tendon autograft (autograft comes from the patient)
  • Hamstring tendon autograft
  • Quadriceps tendon autograft
  • Allograft (taken from a cadaver) patellar tendon, Achilles tendon, semitendinosus, gracilis, or posterior tibialis tendon

Patient Considerations

Active adult patients involved in sports or jobs that require pivoting, turning or hard-cutting as well as heavy manual work are encouraged to consider surgical treatment. This includes older patients who have previously been excluded from consideration for ACL surgery. Activity, not age, should determine if surgical intervention should be considered.

In young children or adolescents with ACL tears, early ACL reconstruction creates a possible risk of growth plate injury, leading to bone growth problems. The surgeon can delay ACL surgery until the child is closer to skeletal maturity or the surgeon may modify the ACL surgery technique to decrease the risk of growth plate injury.

A patient with a torn ACL and significant functional instability has a high risk of developing secondary knee damage and should therefore consider ACL reconstruction.

It is common to see ACL injuries combined with damage to the menisci, articular cartilage, collateral ligaments, joint capsule, or a combination of the above. The “unhappy triad,” frequently seen in football players and skiers, consists of injuries to the ACL, the MCL, and the medial meniscus.

In cases of combined injuries, surgical treatment may be warranted and generally produces better outcomes. As many as half of meniscus tears may be repairable and may heal better if the repair is done in combination with the ACL reconstruction.

Surgical Choices

There are 4 types of grafts

  • Autografts – are taken from the patient’s own body and include portions of the extensor mechanism patellar tendon, iliotibial tract semitendinosus tendon, gracilis tendon and menisci.
  • Allografts – grafts taken from cadavers.
  • Xenografts – grafts taken from animals. Bovine xenografts in particular have been associated with high complication rates.
  • Synthetics – These can be further classified into 3 categories, biodegradable (carbon fibers), permanent prostheses (Gore-Tex and Dacron), and ligament augmentation devices.

Patellar tendon autograft –  The middle third of the patellar tendon of the patient, along with a bone plug from the shin and the kneecap is used in the patellar tendon autograft. Occasionally referred to by some surgeons as the “gold standard” for ACL reconstruction, it is often recommended for high-demand athletes and patients whose jobs do not require a significant amount of kneeling.

The pitfalls of the patellar tendon autograft are

  • Postoperative pain behind the kneecap
  • Pain with kneeling
  • Slightly increased risk of postoperative stiffness
  • Low risk of patella fracture

Hamstring tendon autograft – The semitendinosus hamstring tendon on the inner side of the knee is used in creating the hamstring tendon autograft for ACL reconstruction. Some surgeons use an additional tendon, the gracilis, which is attached below the knee in the same area. This creates a two- or four-strand tendon graft. Hamstring graft proponents claim there are fewer problems associated with harvesting of the graft compared to the patellar tendon autograft including:

  • Fewer problems with anterior knee pain or kneecap pain after surgery
  • Less postoperative stiffness problems
  • Smaller incision
  • Faster recovery

Hamstring tendon autograft prepared for ACL reconstruction

The graft function may be limited by the strength and type of fixation in the bone tunnels, as the graft does not have bone plugs. There have been conflicting results in research studies as to whether hamstring grafts are slightly more susceptible to graft elongation (stretching), which may lead to increased laxity during objective testing. Recently, some studies have demonstrated decreased hamstring strength in patients after surgery.

There are some indications that patients who have intrinsic ligamentous laxity and knee hyperextension of 10 degrees or more may have increased risk of postoperative hamstring graft laxity on clinical exam. Therefore, some clinicians recommend the use of patellar tendon autografts in these hypermobile patients.

Additionally, since the medial hamstrings often provide dynamic support against valgus stress and instability, some surgeons feel that chronic or residual medial collateral ligament laxity (grade 2 or more) at the time of ACL reconstruction may be a contraindication for use of the patient’s own semitendinosus and gracilis tendons as an ACL graft.

Quadriceps tendon autograft

The quadriceps tendon autograft is often used for patients who have already failed ACL reconstruction. The middle third of the patient’s quadriceps tendon and a bone plug from the upper end of the knee cap are used. This yields a larger graft for taller and heavier patients. Because there is a bone plug on one side only, the fixation is not as solid as for the patellar tendon graft. There is a high association with postoperative anterior knee pain and a low risk of patella fracture. Patients may find the incision is not cosmetically appealing.

Allografts

Allografts are grafts taken from cadavers and are becoming increasingly popular. These grafts are also used for patients who have failed ACL reconstruction before and in surgery to repair or reconstruct more than one knee ligament. The advantages of using allograft tissue include the elimination of pain caused by obtaining the graft from the patient, decreased surgery time and smaller incisions. The patellar tendon allograft allows for strong bony fixation in the tibial and femoral bone tunnels with screws.

However, allografts are associated with a risk of infection, including viral transmission (HIV and Hepatitis C), despite careful screening and processing. Several deaths linked to bacterial infection from allograft tissue (due to improper procurement and sterilization techniques) have led to improvements in allograft tissue testing and processing techniques. There have also been conflicting results in research studies as to whether allografts are slightly more susceptible to graft elongation (stretching), which may lead to increased laxity during testing.

Some published literature may point to a higher failure rate with the use of allografts for ACL reconstruction. Higher failure rates for allografts have been reported in young, active patients returning to high-demand sporting activities after ACL reconstruction, compared with autografts.

The reason for this higher failure rate is unclear. It could be due to graft material properties (sterilization processes used, graft donor age, storage of the graft). It could possibly be due to an ill-advised earlier return to sport by the athlete because of a faster perceived physiologic recovery, when the graft is not biologically ready to be loaded and stressed during sporting activities. Further research in this area is indicated and is ongoing.

Surgical Procedure

Before any surgical treatment, the patient is usually sent to physical therapy. Patients who have a stiff, swollen knee lacking full range of motion at the time of ACL surgery may have significant problems regaining motion after surgery. It usually takes three or more weeks from the time of injury to achieve full range of motion. It is also recommended that some ligament injuries be braced and allowed to heal prior to ACL surgery.

The patient, the surgeon, and the anesthesiologist select the anesthesia used for surgery. Patients may benefit from an anesthetic block of the nerves of the leg to decrease postoperative pain.

The surgery usually begins with an examination of the patient’s knee while the patient is relaxed due the effects of anesthesia. This final examination is used to verify that the ACL is torn and also to check for looseness of other knee ligaments that may need to be repaired during surgery or addressed postoperatively.

If the physical exam strongly suggests the ACL is torn, the selected tendon is harvested (for an autograft) or thawed (for an allograft) and the graft is prepared to the correct size for the patient.

After the graft has been prepared, the surgeon places an arthroscope into the joint. Small (one-centimeter) incisions called portals are made in the front of the knee to insert the arthroscope and instruments and the surgeon examines the condition of the knee. Meniscus and cartilage injuries are trimmed or repaired and the torn ACL stump is then removed.

Post-operative X-ray after ACL patellar tendon reconstruction (with picture of graft superimposed) shows graft position and bone plugs fixation with metal interference screws.

In the most common ACL reconstruction technique, bone tunnels are drilled into the tibia and the femur to place the ACL graft in almost the same position as the torn ACL. A long needle is then passed through the tunnel of the tibia, up through the femoral tunnel, and then out through the skin of the thigh. The sutures of the graft are placed through the eye of the needle and the graft is pulled into position up through the tibial tunnel and then up into the femoral tunnel. The graft is held under tension as it is fixed in place using interference screws, spiked washers, posts, or staples. The devices used to hold the graft in place are generally not removed.

Variations on this surgical technique include the “two-incision,” “over-the-top,” and “double-bundle” types of ACL reconstructions, which may be used because of the preference of the surgeon or special circumstances (revision ACL reconstruction, open growth plates).

Before the surgery is complete, the surgeon will probe the graft to make sure it has good tension, verify that the knee has full range of motion and perform tests such as the Lachman’s test to assess graft stability. The skin is closed and dressings (and perhaps a postoperative brace and cold therapy device, depending on surgeon preference) are applied. The patient will usually go home on the same day of the surgery.

Techniques for ACL reconstruction

Extra-articular reconstruction

Intra-articular reconstruction became the preferred choice but it does not fully restore knee kinematics by creating a static restraint and was usually accompanied by connecting the lateral femoral epicondyle to Gerdy’s tubercle with the collagenous restraint lying parallel to the intra-articular course of ACL. This also avoids the problem of lack of blood supply to the intra-articular reconstructions. Most of these procedures use the iliotibial band or tract connecting the lateral femoral epicondyle to the greedy tubercle, The optimal attachment point for the extra-articular reconstructions for anterolateral rotatory instability is found to be the Gerdy tubercle. This procedure is also used primarily in conjunction with an intra-articular reconstruction when severe anterior instability is due to injury or late stretching of the secondary stabilizing capsular structures or the lateral side of the knee.

Procedures

  • Macintosh method (iliotibial band tenodesis)
  • Macintosh, modified by Loseen method
  • Andrews method

Disadvantages

  • Diminish the anterolateral rotatory subluxation, but do not recreate the normal anatomy and function of the ACL.
  • When used alone has a high rate of failure.

Intra-articular Procedure

The advances made in the arthroscopy procedures have produced better results in ACL injury rehabilitation. This procedure may involve a small arthrotomy incision which preserves the vastus medialis oblique muscle to the patella. This procedure can be performed with both endoscopic technique or double incision arthroscopic technique.

Various tissues/grafts have been used to anatomically reconstruct the torn ACL which include portions of the extensor mechanism, patellar tendon, iliotibial tract, semitendinosus tendon, gracilis tendon, and menisci. These can all used in autografts i.e grafts taken from the person undergoing surgery. Other methods include the use of allografts and synthetic ligaments. This procedure has the following steps:

  • Graft selection – The graft to be used depends on the length of surgery. The most commonly used autograft is patellar bone graft and hamstring tendon graft (semitendinosus and gracilis).
  • Diagnostic arthroscopy – performed along with any necessary meniscal debridement or repair. Attention is given to partial-thickness tears, displaced bucket-handle tears, and the status of the articular surfaces, including the patellofemoral joint.
  • Graft Harvest – Mini incision extending from the distal pole of the patella to 2.5cm below the tibial tubercle is made to procure the graft. After retracting the other structures the graft to be taken is sharply outlined and a micro oscillating saw blade is used to harvest the graft/bone plug. A triangle bone plug profile is usually obtained.
  • Graft preparation – Graft is shaped into a 10mm tube shape for the femoral drill hole and an 11mm tube for the tibial tunnel.
  • Intercondylar notch preparation and notchplasty – Notchplasty is performed with 5.5mm burr from the anterior aspect of the intercondylar notch posteriorly and from distal to proximal and any residual tissue is also peeled off. The tissue is aggressively debrided with an arthroscopic shaver. If in the small intercondylar or notch area then further modifications are done.
  • Tibial tunnel placement – Tibial tunnel should be placed so that the graft is not impinged by the roof of the intercondylar notch and should reside within the middle third of the former ACL insertion site.
  • Femoral Tunnel placement – following a tibial tunnel placement, a femoral tunnel placement is completed so as to make a normal ACL like graft placement.
  • Graft placement – The graft after the tunnel placement is slid along with arthroscopic grasper through the tunnel. The graft may be rotated before tibial fixation.
  • Graft fixation – A Nitinol pin is then used to fix the graft with the bone and tunnel. The graft may be rotated before tibial fixation as an ACL has been shown to have external rotation within its fibers of approximately 90 degrees. The amount of graft tension created during fixation has a direct effect on ACL rehabilitation
  • Wound closure – Before closing, the graft harvest site is copiously injected with 0.25% Marcaine and it is also injected intra-articularly. The wound is closed with absorbable sutures with the knee in flexion. ACL reconstruction is one of the most common orthopedic surgeries, and commonly there is articular cartilage degeneration.
  • A total collateral ligament rupture and a full-thickness cartilage lesion would be seen on an MRI.
  • Patella tendon procedure: involves the central third of the ipsilateral patellar tendon. Fixation of the bone blocks within the tibia and femur.
  • Hamstring tendon procedure: four-layer, fold up of gracilis, and the semitendinosus tendons.

The surgery takes place at 10 weeks post-injury

Double-bundle reconstructionSemitendinosus is used with the autograft through 2 tunnels in both the tibia and femur. The autograft method is bone to bone with hamstrings/semitendinosus grafts. 3 tunnels may also be used, 2 tunnels through the tibia, and 1 tunnel through the femur.

The most common procedures for this reconstruction

  • The autologous bone to patella and tendon to bone graft
  • The autologous four-strand hamstrings graft

For the bone to patella and tendon to bone graft, a couple of bone blocks from the patella and the tibial tubercle are taken. This procedure causes more anterior knee pain than the semitendinosus graft. In the second procedure, the graft is obtained from the distal end of the semitendinosus and the gracilis tendon.

Other procedures are the LARS artificial ligament,(Ligament Advanced Reinforcement System) iliotibial tract allografts, cadaveric allografts, synthetic materials and grafts from living related donor people, but all materials have their drawbacks. There is the potential for cross infections, breakage, immunological responses, chronic effusions and recurrent instability

Single bundle vs Double bundle ACL reconstruction

A kinematics study showed that the standard single-bundle ACL reconstruction does not create the same kinematics as the intact ACL in normal activities. Only anteroposterior stability seems to be reconstructed. When the leg turns, there is an abnormal tibial rotation in the knee. Single-bundle ACL reconstruction does not recreate normal rotation in the knee.

On the contrary, anterior translation after double-bundle reconstruction was comparable with the intact ACL at 0° flexion, but the most stable position of the knee is at 15° and 75° flexion.

Watch this video to learn more about ACL Reconstruction using patellar tendon

Rehabilitation

Physical therapy is a crucial part of successful ACL surgery, with exercises beginning immediately after the surgery. Much of the success of ACL reconstructive surgery depends on the patient’s dedication to rigorous physical therapy. With new surgical techniques and stronger graft fixation, current physical therapy uses an accelerated course of rehabilitation.

Postoperative Course

  • In the first 10 to 14 days after surgery, the wound is kept clean and dry, and the early emphasis is placed on regaining the ability to fully straighten the knee and restore quadriceps control.
  • The knee is iced regularly to reduce swelling and pain. The surgeon may dictate the use of a postoperative brace and the use of a machine to move the knee through its range of motion. Weight-bearing status (use of crutches to keep some or all of the patient’s weight off of the surgical leg) is also determined by physician preference, as well as other injuries addressed at the time of surgery.

Rehabilitation

  • The goals for the rehabilitation of ACL reconstruction include reducing knee swelling, maintaining mobility of the kneecap to prevent anterior knee pain problems, regaining full range of motion of the knee, as well as strengthening the quadriceps and hamstring muscles.
  • The patient may return to sports when there is no longer pain or swelling, when full knee range of motion has been achieved, and when muscle strength, endurance, and functional use of the leg have been fully restored.
  • The patient’s sense of balance and control of the leg must also be restored through exercises designed to improve neuromuscular control. This usually takes 4 to 6 months. The use of a functional brace when returning to sports is ideally not needed after a successful ACL reconstruction, but some patients may feel a greater sense of security by wearing one.

Complications

  • Infection – The incidence of infection after arthroscopic ACL reconstruction is very low.  There have also been reported deaths linked to bacterial infection from allograft tissue due to improper procurement and sterilization techniques.
  • Viral transmission – Allografts specifically are associated with the risk of viral transmission, including HIV and Hepatitis C, despite careful screening and processing. The chance of obtaining a bone allograft from an HIV-infected donor is calculated to be less than 1 in a million.
  • Bleeding, numbness – Rare risks include bleeding from acute injury to the popliteal artery and weakness or paralysis of the leg or foot. It is not uncommon to have numbness of the outer part of the upper leg next to the incision, which may be temporary or permanent.
  • Blood clot – Although rare, blood clot in the veins of the calf or thigh is a potentially life-threatening complication. A blood clot may break off in the bloodstream and travel to the lungs, causing pulmonary embolism or to the brain, causing a stroke.
  • Instability – Recurrent instability due to rupture or stretching of the reconstructed ligament or poor surgical technique is possible.
  • Stiffness – Knee stiffness or loss of motion has been reported by some patients after surgery.
  • Extensor mechanism failure – Rupture of the patellar tendon (patellar tendon autograft) or patella fracture (patellar tendon or quadriceps tendon autografts) may occur due to weakening at the site of graft harvest.
  • Growth plate injury – In young children or adolescents with ACL tears, early ACL reconstruction creates a possible risk of growth plate injury, leading to bone growth problems. The ACL surgery can be delayed until the child is closer to reaching skeletal maturity. Alternatively, the surgeon may be able to modify the technique of ACL reconstruction to decrease the risk of growth plate injury.
  • Kneecap pain – Postoperative anterior knee pain is especially common after patellar tendon autograft ACL reconstruction. The incidence of pain behind the kneecap varies greatly in studies, whereas the incidence of kneeling pain is often higher after patellar tendon autograft ACL reconstruction.

Complications associated with non-surgical treatment are largely associated with NSAID use.

Common Adverse Effects of NSAID Use

  • Stomach pain and heartburn
  • Stomach ulcers
  • A tendency to bleed, especially while taking aspirin
  • Kidney problems

Common Adverse Effects of Intra-Articular Corticosteroid Injection

  • Pain and swelling (cortisone flare)
  • Skin discoloration at the site of injection
  • Elevated blood sugar
  • Infection
  • Allergic reaction

Common Adverse Effects of Intra-Articular HA Injection

  • Injection site pain
  • Muscle pain
  • Trouble walking
  • Fever
  • Chills
  • Headache

Complications Associated with HTO

  • Recurrence of deformity
  • Loss of posterior tibial slope
  • Patella baja
  • Compartment syndrome
  • Peroneal nerve palsy
  • Malunion or nonunion
  • Infection
  • Persistent pain
  • Blood clot

Complications Associated with UKA

  • Stress fracture of the tibia
  • Tibial component collapse
  • Infection
  • Osteolysis
  • Persistent pain
  • Neurovascular injury
  • Blood clot
  • Infection
  • Instability
  • Osteolysis
  • Neurovascular injury
  • Fracture
  • Extensor mechanism rupture
  • Patellar maltracking
  • Patellar clunk syndrome
  • Stiffness
  • Peroneal nerve palsy
  • Wound complications
  • Heterotopic ossification
  • Blood clot

Prevention

Given the importance of neuromuscular factors and the etiology of ACL injuries, numerous programs have aimed to improve neuromuscular control during standing, cutting, jumping, and landing. [rx] The components of neuromuscular training are:

  • Balance training: balance exercises
  • Jump training – plyometrics: landing with increased flexion at the knee and hip
  • Strengthening that emphasizes proximal hip control mediated through gluteus and proximal hamstring activation in a close kinetic chain
  • Stretching
  • Skill training: Controlling body motions, especially in deceleration and pivoting maneuvers
  • Movement education and some form of feedback to the athlete during the training of these activities
  • Agility training: agility exercises

Examples of more recent neuromuscular training programs include: Sportsmetrics and Prevent Injury and Enhance Performance program. Both programs have a positive influence on injury reduction and improve athletic performance tests. [rx] The PEP plan includes: Warm Up, stretching, strengthening, plyometrics, and agility exercises. [rx]

References

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