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Urine Culture – Indications, Procedure, Mechanism, Result

A urine culture is a test to find germs (such as bacteria) in the urine that can cause an infection. Bacteria can enter through the urethra and cause a urinary tract infection (UTI). A sample of urine is added to a substance that promotes the growth of germs. If no germs grow, the culture is negative.

A urine culture is a test that can detect bacteria in your urine. This test can find and identify the germs that cause a urinary tract infection (UTI). Bacteria, which typically cause UTIs, can enter the urinary tract through the urethra. In the environment of your urinary tract, these bacteria can grow rapidly and develop into an infection.

Specimen Collection

There are a variety of methods aimed at specimen collection to diagnose a UTI. Some of the factors that dictate the method used include patient comfort, the ability to void, and reducing the small risk of iatrogenic infection. Sterile collection methods can be employed, such as a suprapubic puncture or urethral catheterization, in an effort to reduce overdiagnosis and subsequent overtreatment.[rx] Even so, patients are instructed to collect their own samples from a variety of acceptable techniques.

Specimen Collection 

There are a variety of collection techniques for urine culture, including suprapubic aspiration, straight catheter technique, and mid-stream catch with or without cleansing. In pediatric patients who are not toilet trained, diaper collection, and sterile bag, urine collection methods are used. Suprapubic collection is the best method to avoid specimen contamination with bacteria, particularly in the distal urethra. Owing to patient discomfort, invasiveness, lack of indication (except in rare instances), and inappropriate resource use, this method is rarely deployed. Urine collection with a single catheter (straight catheter technique) is the next best option. Still, due to labor intensiveness as well as the possibility of introducing bacteria into the bladder, potentially causing a UTI, this technique is seldom used and only when indicated. The previously aforementioned methods of specimen collection are therefore reserved for those patients who are unable to self-collect. Hence, the most common method a urine sample is obtained for urine culture is via a clean-catch midstream technique, which is neither invasive nor uncomfortable. Colony counts from these samples correlate reasonably well compared to suprapubic aspiration and single catheter technique.[rx]

The current standards for self-collection include mid-stream clean-catch technique, mid-stream catch without prior cleansing, and random sampling delivered without instruction. There are no clinically significant differences seen between the various self-collection techniques.[rx] However, studies have shown that depending on the patient’s demographic, such as adult male, adult female, or infant/child, there may be preferred methods of sample collection over other methods. For females, contamination and diagnostic accuracy did not significantly change between midstream urine collection with or without prior cleansing; there is no recommendation without regard to cleansing prior to collection.[rx] In adult males, contamination was significantly decreased when mid-stream catch is utilized as the method of collection, becoming favorable over first-void specimen collection. Mid-stream collection was not significantly altered with prior cleansing. However, in children and infants, mid-stream collection with prior cleansing was favorable in reducing contamination over other methods, including mid-stream collection without cleansing, sterile bag urine collection, and diaper collection.[rx] Therefore, pre-collection cleansing procedures have been considered unnecessary in most adult populations as they do not decrease the risk of contamination from commensal bacteria.[rx][rx][rx] Even so, patients continue to follow the traditional directive of cleansing as the first step in urine specimen collection despite no change in diagnosis, course, or treatment.

Specimen Transportation

Owing to the probable increase risk of growth of colony-forming units (CFU) non-indicative of the patient’s true sample, urine specimens must be plated within two hours of collection, unless refrigerated or placed in a preservative.[rx] This measure decreases the risk of false-positive cultures, directly leading to a decrease in overtreatment while maintaining appropriate antibiotic stewardship.


Specimen Preservation and Processing

Preservation of the urine sample can be achieved with a boric acid solution or refrigeration for up to 24 hours. Both techniques yield adequate preservation of the sample. Samples that are left at room temperature for greater than 4 hours run the risk of bacterial overgrowth of causative and contamination organisms.[rx] However, based on a meta-analysis of preservation techniques, the statistical analysis of this data was rated as low.[rx] Nonetheless, common gram-negative organisms causing UTIs such as Escherichia coli and Klebsiella pneumoniae, have been noted to be inhibited when boric acid is used as a storage medium. Therefore, careful consideration of the storage medium should be practiced, and timely refrigeration must be prioritized.

Specimens are processed routinely using calibrated loops for plating. This method allows for CFU/mL findings as well as the isolation of colonies for identification and susceptibility testing. Some of the most utilized media are blood agar and MacConkey agar. The temperature of the plates should be kept between 35 to 37 degrees Celcius with a recommended incubation time of 24 to 48 hours. However, Oligella urolytica, a slow-growing, gram-negative, and rare UTI-causing organism, has been reported to have an incubation of over 48 hours.[rx] Specimens from outpatients do not need to be plated on selective media. However, in hospitalized patients, where enterococci are the second leading cause of UTI, laboratory technicians should consider inoculating urine specimens to a medium that is selective for these gram-positive cocci.[rx]


Routine bacterial urine cultures are not always necessary in the evaluation of outpatients with uncomplicated UTIs and simple lower UTIs, such as uncomplicated cystitis.[rx][rx] An important classification of uncomplicated UTI versus complicated UTI distinguishes the need for urine culture. Since UTIs are composed of lower UTIs (e.g., cystitis) and upper UTIs (e.g., pyelonephritis), clinically differentiating the two by symptomology is necessary as the first step in determining the need for urine culture. A patient experiencing cystitis could report dysuria (with or without frequency), urgency, hematuria, or suprapubic pain, while a patient suffering from pyelonephritis may or may not have the symptoms of cystitis, but will typically report fever, chills, flank pain with or without costovertebral tenderness.[rx][rx] Should these patients have a complicating factor, a urine culture is likely warranted. Some of the complicating factors include male sex, chronic obstruction, chronic renal insufficiency, nephrolithiasis, poorly controlled diabetes, pregnancy, indwelling urinary catheters, indwelling urinary stent or nephrostomy tube, and immunosuppression (chronic high-dose corticosteroid use, use of other immunosuppressive agents, neutropenia, etc.).[rx] Furthermore, outpatients with recurrent UTIs, treatment failure, complicated UTIs, and inpatient UTIs require urine culture to not only document infection, but to confirm the causative organism in order to prevent complications and for antimicrobial susceptibility resistance. These examples warrant further investigation beyond clinical diagnosis and urinalysis.

Additionally, new-onset or worsening sepsis without evidence of an alternate source is also another appropriate indication for urine culture. New-onset or worsening sepsis is a major cause of morbidity and mortality in hospitalized patients globally and should be swiftly recognized clinically for the purposes of swift urine culture collection.[rx] Fever or alteration of consciousness without evidence of a source may also warrant a urine culture. For patients in early pregnancy or prior to certain urology procedures, screening for asymptomatic bacteriuria is warranted. Additionally, preoperative evaluations may trigger the utilization of urine culture, especially when mucosal bleeding is expected. Finally, urine cultures are sometimes appropriate in cases of spinal cord injury, where the patient may experience an increase in spasticity, autonomic dysreflexia, and a sense of unease.[rx] These patients are at an increased risk of UTI due to autonomic dysregulation leading to stagnating urine, which becomes a nidus for infection.

Urine culture is not indicated and is therefore deemed inappropriate when the urine characteristics are odorous, cloudy, or discolored in the absence of other localizing signs or symptoms, reflex urine cultures based on results of urinalysis such as pyuria in the absence of other indications, and to document successful response to therapy.[rx][rx] Screening for asymptomatic bacteria in most groups is also unnecessary, as it does not alter the course of therapy. Patients with asymptomatic bacteriuria are typically not treated unless pregnant. Yet, some studies have shown that in pregnant women with pyelonephritis, the patient course dictates antibiotic treatment, not necessarily the culture and sensitivities themselves.[rx]

What is being tested?

Urine is the fluid produced by the kidneys that carry water and wastes through the urinary tract and then is eliminated from the body. The urine culture is a test that detects and identifies bacteria and yeast in the urine, which may be causing a urinary tract infection (UTI).

The kidneys, a pair of bean-shaped organs located at the bottom of the ribcage in the right and left sides of the back, filter wastes out of the blood and produce urine, the yellow fluid that carries wastes out of the body. Urine travels through tubes called ureters from the kidneys to the bladder, where it is stored temporarily, and then through the urethra as it is voided. Urine contains low levels of microbes, such as bacteria or, yeast which move from the skin into the urinary tract and grow and multiply, causing a urinary tract infection.

Most UTIs are considered uncomplicated and are easily treated. However, if they are not addressed, the infection may spread from the bladder and ureters into the kidneys. A kidney infection is more dangerous and can lead to permanent kidney damage. In some cases, an untreated urinary tract infection may spread to the bloodstream (septicemia) and cause sepsis, which can be life-threatening.

Women and girls get urinary tract infections more often than men and boys. Even preteen girls may have frequent UTIs. For men and boys with a UTI confirmed by a urine culture, further tests may be done to rule out the presence of a kidney stone or structural abnormality that could cause the infection.

People with kidney disease or with other conditions that affect the kidneys, such as diabetes or kidney stones, and people with weakened immune systems may be more prone to frequent, repeated, and/or complicated UTIs.

  • For a urine culture, a small sample of urine is placed on one or more agar plates (a thin layer of nutrient media) and incubated at body temperature. Any bacteria or yeast that are present in the urine sample grow over the next 24 to 48 hours.
  • A laboratory professional studies the colonies on the agar plate, counting the total number and determining how many types have grown. The size, shape, and color of these colonies help to identify which bacteria are present, and the number of colonies indicates the number of bacteria originally present in the urine sample. The quantity can differentiate between normal levels of bacteria versus infection.
  • Ideally, if a good clean catch sample was collected for the test, only bacteria causing a UTI are present. Typically, this will be a single type of bacteria that will be present in relatively large numbers.
  • Sometimes, more than one type of bacteria will be present. This may be due to an infection that involves more than one pathogen; however, it is more likely due to skin, vaginal, or fecal contamination picked up during the urine collection.
  • The laboratorian will take a colony from each type and perform other tests, such as a gram stain, to identify the type (species) of bacteria or another microbe (i.e., yeast). Susceptibility testing may be done to determine which antibiotics will likely cure the infection.

If there is no or little growth on the agar after 24 to 48 hours of incubation, the urine culture is considered negative and the culture is complete, suggesting infection is not present.

How is the sample collected for testing?

Although there are several types of urine samples, the mid-stream clean catch is the type most commonly submitted for culture.

  • It is important to first clean the genital area before collecting your urine because of the potential to contaminate the urine with bacteria and cells from the surrounding skin during collection (particularly in women).
  • Start first by washing your hands.
  • Women should then spread the labia of the vagina and clean it from front to back using a wipe provided by your healthcare practitioner or the laboratory. It is recommended to repeat with a second towel or wipe.
  • Men should wipe the tip of the penis.
  • Start to urinate, let some urine fall into the toilet, and then collect one to two ounces of urine directly into the sterile container provided, then void the rest into the toilet. Do not allow the inside of the container to come into contact with skin and do not scoop the urine from the toilet (or any other container).

For catheterized specimens, a urine sample is taken by inserting a thin flexible tube or catheter through the urethra into the bladder. This is performed by a trained healthcare practitioner. The urine is collected in a sterile container at the other end of the tube. Rarely, a needle and syringe may be used to collect by aspirating urine directly from the bladder. For infants, a collection bag may be placed on the genital area to collect any urine produced.

Is any test preparation needed to ensure the quality of the sample?

Generally, no preparation is needed, but depending on the type of culture, you may be given special instructions. For example, you may be asked not to urinate for at least one hour before the test and/or to drink a glass of water 15-20 minutes before sample collection. This will help to ensure that you can produce enough urine for the test. Sometimes you may be instructed to collect the first urine you void in the morning. Antibiotics taken prior to the test may affect your results. Tell your healthcare practitioner if you have taken antibiotics recently.

Potential Diagnosis

The positive findings of a urine culture can lead to the diagnosis of UTI (uncomplicated vs. complicated), asymptomatic bacteriuria (ASB), catheter-associated UTI (CA-UTI), and catheter-associated asymptomatic bacteriuria (CA-ASB). These diagnoses lead to the possible identification of the source of sepsis. Proper diagnosis lends itself to proper antibiotic stewardship and decreases in morbidity and mortality. As up to 25% of hospitalized patients in North America receive indwelling catheter placement, utilization of the urine culture is of utmost importance to determine potential diagnoses.[rx][rx] Consequently, differentiation between catheterized patients and non-catheterized patients is common, as is the differentiation between UTI and asymptomatic bacteriuria.

Normal and Critical Findings

Normal Findings

Urine is normally sterile. However, there is a possibility of contamination. Hence, samples from patients without UTI symptoms with low colony counts certainly below the threshold for bacteriuria, and no detection of organisms, are considered to be normal samples.

Critical Findings

  • UTI – UTI symptoms. Gold standard confirmation is the urine culture.[rx] Positive urine cultures are observed when there is significant microbial growth determined by standard microbiological criteria.[rx] Although not completely standardized, many laboratories set the cut-off at greater than or equal to 100,000 CFUs/ml for a UTI. However, this particular threshold may miss relevant infections. Consequently, other recommendations have noted a cut-off of greater than or equal to 1,000 CFUs/ml in order to capture other bacterial infections.[rx]
  • CA-UTI – According to the Infectious Diseases Society of America’s (IDSA) 2010 guideline for diagnosis of CA-UTI, it is defined as patients with an indwelling catheter with the presence of symptoms or signs compatible with UTI with no other identified source of infection. They must also have greater than or equal to 1000 CFU/ml with more than one bacterial species in a single catheter urine specimen or in a midstream voided urine specimen in patients whose urinary catheter (urethral, suprapubic or condom) has been removed within the past 48 hours. According to the United States Centers for Disease Control and Prevention (CDC), the patient must meet the following three criteria: 1) The patient must have an indwelling urinary catheter in place for more than 2 days on the date of the event, 2) The patient has a fever (of greater than or equal to 38 degrees Celsius, costovertebral angle (CVA) pain or tenderness, suprapubic tenderness, urgency, frequency or dysuria, and 3) The patient has a urine culture with no more than two species of organisms identified, at least one being a bacterium of greater than or equal to 1000 CFU/ml.[rx]
  • CA-ASB – Positive urine culture in the absence of UTI symptoms.[rx] Asymptomatic catheter-associated bacteriuria and candiduria exhibit a urine culture of at least 100,000,000 CFU/mL of an identified organism(s) in the absence of signs and symptoms of a UTI.[rx][rx] These cases do not require treatment and generally resolve upon the removal of catheters.[rx]
  • Bacteriuria – The most commonly used cut-off for significant bacteriuria is greater than or equal to 100,000 CFU/ml of urine.[rx] Asymptomatic bacteriuria is present when the patient does not have any signs of a UTI clinically coupled with 100,000 CFU/ml exceeded in two consecutive samples of midstream urine (from women). For men, a single detection of more than 100,000 CFU/ml is adequate for diagnosis.[rx] Although pyuria is non-diagnostic in itself, the detection of leukocytes could support the diagnosis of CA-ASB.

The most common cause of UTIs in both inpatient and outpatient settings is Escherichia coli, accounting for the overwhelming majority of cases. E. coli is followed by coagulase-negative staphylococci, Klebsiella species, Proteus species, and Enterobacter species.[rx] Each unique organism can be part of urine culture results. Owing to the differences in the microbiology of each organism, proper identification leads to increased antibiotic stewardship by selecting the proper antibiotic coverage, subsequently leading to decreases in antibiotic resistance.

  • Protein – in the urine (proteinuria) can usually be detected by dipstick when present in large amounts. Protein may appear constantly or only intermittently in the urine, depending on the cause. Proteinuria may occur normally after strenuous exercises, such as marathon running, but is usually a sign of a kidney disorder. Small amounts of protein in the urine may be an early sign of kidney damage due to diabetes. Such small amounts may not be detected by dipstick. In these cases, urine will need to be collected over a period of 12 or 24 hours and tested by a laboratory.
  • Glucose – in the urine (glucosuria) can be accurately detected by dipstick. The most common cause of glucose in the urine is diabetes mellitus, but the absence of glucose does not mean a person does not have diabetes or that the diabetes is well controlled. Also, the presence of glucose does not necessarily indicate diabetes or another problem.
  • Ketones – in the urine (ketonuria) can often be detected by dipstick. Ketones are formed when the body breaks down fat. Ketones can appear in the urine as a result of starvation or uncontrolled diabetes mellitus and occasionally after drinking significant amounts of alcohol.
  • Blood – in the urine (hematuria) is detectable by dipstick and confirmed by viewing the urine with a microscope and other tests. Sometimes the urine contains enough blood to be visible, making the urine appear red or brown.
  • Nitrites – in the urine (nitrituria) are also detectable by dipstick. High nitrate levels indicate a urinary tract infection.
  • Leukocyte esterase – (an enzyme found in certain white blood cells) in the urine can be detected by dipstick. Leukocyte esterase is a sign of inflammation, which is most commonly caused by a urinary tract infection.
  • The acidity (pH) of urine – is measured by a dipstick. Certain foods, chemical imbalances, and metabolic disorders may change the acidity of urine. Sometimes a change in acidity can predispose the person to kidney stones.
  • The concentration – of urine (also called the osmolality, roughly indicated by specific gravity) can vary widely depending on whether a person is dehydrated, how much fluid a person has drunk, and other factors. Urine concentration is also sometimes important in diagnosing abnormal kidney function. The kidneys lose their capacity to concentrate urine at an early stage of a disorder that leads to kidney failure. In one special test, a person drinks no water or other fluids for 12 to 14 hours. In another test, a person receives an injection of vasopressin (also called antidiuretic hormone). Afterward, urine concentration is measured. Normally, either test should make the urine highly concentrated. However, in certain kidney disorders (such as nephrogenic diabetes insipidus), the urine cannot be concentrated even though other kidney functions are normal.
  • Sediment – in urine can be examined under a microscope to provide information about a possible kidney or urinary tract disorder. Normally, urine contains a small number of cells and other debris shed from the inside of the urinary tract. A person who has a kidney or urinary tract disorder usually sheds more cells, which form sediment if urine is spun in a centrifuge (a laboratory instrument that uses centrifugal force to separate components of a liquid) or allowed to settle.

Interfering Factors

Urine culture results may be deemed faulty and inconclusive due to patient factors. Recent antibiotic use is a major culprit, as this therapy may mask the presence of UTI-causing organisms. Furthermore, the use of diuretics or the consumption of large amounts of fluids may also dilute the urine and invariably lead to a decrease in the number of bacteria present in the sample. Moreover, the large consumption of ascorbic acid has been long known to interfere with the results of urine dipstick results.[rx]

Culture results are invariably affected by faulty collection techniques, leading to the contamination of urine and invariably, by urogenital flora.[rx] Operator error in the handling of urine specimens may also lend to increasing CFUs, leading to false-positive results. Unless refrigerated or kept in a preservative, urine samples should be plated within two hours of collection.[rx] Urine samples where plating is delayed, especially over 24 hours, are deemed useless due to the possibility of a bacterial overgrowth that is not representative of the patient’s original sample. Consequently, laboratory delay is a significant issue interfering with the validity of the urine culture.


The various stages of urine collection, whether collection itself, storage, and preservation, have a tremendous impact on the results of a urine culture. Without adequate care, specimens can become contaminated with perineal, vaginal, or periurethral flora. The presence of the true pathogenic agent can be obscured due to the contamination, whether due to an overgrowth or an inhibition of the true pathogens. Even more than that, the medium in which the specimen is stored also plays a significant role in the true urinary pathogen. Inhibition of Escherichia coli and Klebsiella pneumoniae have been observed with the use of boric acid as the storage and preservation medium.[rx] Owing to these issues with contamination and obscuration of true UTI-causative organisms, misdiagnosis, and subsequent poor patient management and faulty antibiotic stewardship will result, with the most feared complication becoming a complicated UTI and possibly leading to urosepsis.[rx] Consequently, proper detection of UTI or asymptomatic bacteriuria is of paramount importance. For instance, swift detection of asymptomatic bacteriuria in pregnancy is necessary in order to prevent the feared complication of pyelonephritis with subsequent harm to the child.[rx] Ordering urine cultures when indicated and proper handling of the urine specimen provides for proper diagnosis and therefore preventing complications associated with poorly diagnosed and treated UTI.

Patient Safety and Education

Specimen collection by means of clean-catch midstream technique poses no risk to the patient. Despite the longstanding belief that pre-cleansing yields an uncontaminated specimen, several studies have shown that pre-cleansing has no significant effect on test results. Prevention of UTI is worthy of discussion and has been traditionally under-researched in the past. Patients should be educated on correct wiping methods, adequate hydration, frequent urination, avoiding feminine products, precoital bathing, and postcoital voiding, and avoid the use of a number of certain birth control products. With these increased measures aimed at improving hygiene, health behaviors, and sexual practices, UTI-related morbidity, and the use of antibiotics for these infections would invariably decrease.[rx][rx]

Common Questions

How is the test used?

  • The urine culture is used, along with results from a urinalysis, to diagnose a urinary tract infection (UTI) and to identify the bacteria or yeast causing the infection. If a urine culture is positive, susceptibility testing may be done to determine which antibiotics will inhibit the growth of the microbe causing the infection. The results will help a healthcare practitioner determine which drugs are likely to be most effective in treating your infection.
  • A urine culture is used, as recommended by several health organizations, to screen pregnant women for asymptomatic bacteriuria, a condition in which significant amounts of bacteria are in the urine but do not cause symptoms. About 2%-10% of pregnant women in the U.S. have this condition that can lead to more serious kidney infections as well as increased risk of preterm delivery and low birth weight.

When is it ordered?

  • A urine culture may be ordered when you have signs and symptoms of a urinary tract infection (UTI) and/or results of a urinalysis show that you may have a UTI.

Some signs and symptoms of a UTI include:

  • A strong, frequent urge to urinate, even when you have just gone and there is little urine voided
  • Pain and/or a burning sensation during urination
  • Cloudy, strong-smelling urine
  • Lower back pain
  • You may also have pressure in the lower abdomen and small amounts of blood in the urine. If the UTI is more severe and/or has spread into the kidneys, it may cause flank pain, high fever, shaking, chills, nausea or vomiting.
  • Sometimes, antibiotics may be prescribed without requiring a urine culture for young women with signs and symptoms of a UTI and who have an uncomplicated lower urinary tract infection. If there is suspicion of a complicated infection or symptoms do not respond to initial therapy, then a culture of the urine is recommended.
  • Pregnant women without any symptoms are recommended to be screened with a urine culture early in their pregnancy (e.g., during the second trimester) or during the first prenatal visit for bacteria in their urine.

What does the test result mean?

  • Results of a urine culture are often interpreted in conjunction with the results of a urinalysis and with regard to how the sample was collected and whether symptoms are present. Since some urine samples have the potential to be contaminated with bacteria normally found on the skin (normal flora), care must be taken with interpreting some culture results.

Positive urine culture: Typically, the presence of a single type of bacteria growing at high colony counts is considered a positive urine culture.

  • For clean catch samples that have been properly collected, cultures with greater than 100,000 colony forming units (CFU)/milliliter of one type of bacteria usually indicate infection.
  • In some cases, however, there may not be a significantly high number of bacteria even though an infection is present. Sometimes lower numbers (1,000 up to 100,000 CFU/mL) may indicate infection, especially if symptoms are present.
  • Likewise, for samples collected using a technique that minimizes contamination, such as a sample collected with a catheter, results of 1,000 to 100,000 CFU/mL may be considered significant.
  • Results from a urinalysis can be used to help interpret the results of a urine culture. For example, a positive leukocyte esterase (a marker of white blood cells) and nitrite (a marker for bacteria) help confirm a UTI.
  • If a culture is positive, susceptibility testing may be performed to guide treatment. (See the article on Antibiotic Susceptibility Testing for more details on results.)
  • Although a variety of bacteria can cause UTIs, most are due to Escherichia coli (E. coli), bacteria that are common in the digestive tract and routinely found in stool.

Other bacteria that commonly cause UTIs to include

  • Proteus
  • Klebsiella
  • Enterobacter
  • Staphylococcus
  • Acinetobacter

Occasionally, a UTI may be due to yeast, such as Candida albicans.

  • Negative urine culture: A culture that is reported as “no growth in 24 or 48 hours” usually indicates that there is no infection. If the symptoms persist, however, a urine culture may be repeated on another sample to look for the presence of bacteria at lower colony counts or other microorganisms that may cause these symptoms. The presence of white blood cells and low numbers of microorganisms in the urine of an asymptomatic person is a condition known as acute urethral syndrome.
  • Contamination: If a culture shows the growth of several different types of bacteria, then it is likely that the growth is due to contamination. This is especially true in voided urine samples if the organisms present include Lactobacillus and/or other common nonpathogenic vaginal bacteria in women. If the symptoms persist, the healthcare practitioner may request a repeat culture on a sample that is more carefully collected. However, if one type of bacteria is present in significantly higher colony counts than the others, for example, 100,000 CFUs/mL versus 1,000 CFUs/mL, then additional testing may be done to identify the predominant bacteria.

Can a urine culture be used to test for infections other than UTIs, such as sexually transmitted diseases (STDs)?

  • Yes. Urine cultures can detect some sexually transmitted diseases. However, a urine culture is not the test of choice for sexually transmitted diseases in adults. Some STDs such as chlamydia may be tested using a urine sample, but the testing method used detects chlamydia genetic material in the urine and is not a culture. Tell your healthcare practitioner if you think you have a sexually transmitted disease, so the practitioner can order the appropriate test. (For example, read the articles on Chlamydia Testing and Gonorrhea Testing.) Urine cultures may be used to test for STDs in children.
  • For another example, a urine culture may be used to help diagnose infections of the urinary tract and genital tract caused by mycobacteria. Typically, this test requires that the first urine voided in the morning be collected.

My healthcare practitioner’s office called to say they need a new urine sample, the first was contaminated. What happened?

  • If the skin and genital area were not cleaned well prior to collecting the sample, the urine culture may grow three or more different types of bacteria and is assumed to be contaminated. The culture will be discarded because it cannot be determined if the bacteria originated inside or outside the urinary tract. A contaminated specimen can be avoided by following the directions to carefully clean yourself and by collecting a midstream clean catch urine sample.

My healthcare practitioner said I had symptoms of a urinary tract infection and prescribed antibiotics without performing a urine culture. Why?

  • Bacteria are known as Escherichia coli (E. coli) cause the majority of lower urinary tract infections. This microbe is usually susceptible to a variety of antibiotics, such as trimethoprim-sulfamethoxazole, ciprofloxacin, and nitrofurantoin. In most people with an uncomplicated UTI, the infection will be cured after treatment with one of these antibiotics. Based on this information, your healthcare practitioner may prescribe one of them without performing a culture.

What happens if my infection goes untreated?

  • If your infection is not treated, it can move from the lower urinary tract to the upper urinary tract and infect the kidneys and possibly spread to the bloodstream, causing septicemia and sepsis, a serious and potentially life-threatening condition. Signs and symptoms of septicemia include fever, chills, elevated white blood cell count, and fatigue. If a healthcare practitioner suspects septicemia, the practitioner will typically order a blood culture as well as other tests and will prescribe antibiotics accordingly.

What puts me at risk for recurrent urinary tract infections?

  • There are a wide variety of factors that predispose a person to get a UTI. UTIs are more common in girls and women than in boys and men because of the differences in their genitals and urinary tracts. Some infants and young children have abnormalities of the urinary tract that they are born with (congenital) that increase their risk of UTIs. In adults, sexual intercourse, diabetes, pregnancy, poor bladder control, kidney stones, and tumors are examples of factors that increase the risk of UTIs. In a hospital, nursing home, or home care setting, urinary catheters are major risk factors for UTIs.

Is there anything else I should know?

  • If you have frequent and/or recurrent UTIs, culture and susceptibility testing may be performed with each infection. If you have frequent UTIs, careful selection of antibiotics and completing the full course of treatment can be important.



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Peritoneal Dialysis – Indications, Contraindications

Peritoneal dialysis is a way to remove waste products from your blood when your kidneys can’t adequately do the job any longer. This procedure filters the blood in a different way than does the more common blood-filtering procedure called hemodialysis.

During peritoneal dialysis, a cleansing fluid flows through a tube (catheter) into part of your abdomen. The lining of your abdomen (peritoneum) acts as a filter and removes waste products from your blood. After a set period of time, the fluid with the filtered waste products flows out of your abdomen and is discarded.

Peritoneal dialysis (PD) accounts for a small percentage (less than 7%) of the prevalent dialysis population in the United States compared to Canada (more than 50%). Better early survival on PD compared to hemodialysis (HD) has also been reported by several observational studies, including national registries from different parts of the world.  The cost of HD per patient per year remains significantly higher than for PD ($87,945 for HD versus $71,630 for PD in 2011). Patients have a choice when initiating dialysis to use HD or PD. Choice should be patient-centered and made after careful considerations of all factors that may alter outcomes. A large US cohort study of over 6000 matched pairs of dialysis patients beginning dialysis in 2003, showed that 1-year patient survival was significantly higher for PD when compared to HD (85.8% versus 80.7% (p < 0.01)). However, 80% of end-stage renal disease (ESRD) patients in the United States start hemodialysis (HD) with a tunneled hemodialysis catheter (TDC), and 60% continue to dialyze using an HDC for 91 days after dialysis initiation.  This initial catheter (modality) choice has had a major impact on the mortality of ESRD patients. Patient mortality in the first 90 days of HD as a result of catheter-associated bacteremia and sepsis from TDC use is higher when compared to patients initiating dialysis on PD.  A significant percentage of deaths in HD occurred within the first the 90 days on dialysis.

Alternative Names

Artificial kidneys – peritoneal dialysis; Renal replacement therapy – peritoneal dialysis; End-stage renal disease – peritoneal dialysis; Kidney failure – peritoneal dialysis; Renal failure – peritoneal dialysis; Chronic kidney disease – peritoneal dialysis


Medicine is moving to quality-driven models; every clinician needs to weigh the risk of early use TDC to start HD compared to the benefit of starting peritoneal dialysis using a peritoneal dialysis catheter (PDC).


PD is contraindicated in patients with:

  • Uncorrected abdominal wall hernia
  • Pleuroperitoneal shunt
  • Abdominal adhesions


PD Catheter Placement

Utilizing several different techniques, the success rate of PDC placement reported in the literature varied from 80% to 100%. Are there any differences in catheter outcomes based on the technique used to place PDC? The answer to this question is difficult, as there are wide variations in inpatient and operator factors that cannot be controlled across populations. Overall, open surgical placement was associated with the highest number of complications, including poor function, leaks, and catheter migrations; there was a trend toward higher catheter survival after laparoscopic insertion. (See Table 1) Randomized control trial comparing fluoroscopic versus laparoscopic PDC placement included 113 patients showed a complication-free catheter survival that was significantly higher at 42.5% (95% CI 29.3 – 55.0) in the percutaneous group compared with 18.1% (95% CI 8.9 – 29.8) in the laparoscopic group (p = 0.03). One-year patient and catheter survival in the 2 groups was no different.

Both surgical and percutaneous procedures have low complication rates when performed by experienced operators. Obese patients who have had previous abdominal surgery or with previous episodes of PD-related peritonitis can benefit from the advanced laparoscopic placement of the catheter. Surgical PD catheter implantation typically takes longer, including referral and consultation delays to a surgeon, operating room scheduling, and preoperative medical and anesthesia clearance. In contrast, nephrology-guided PD catheter placement can be performed relatively quickly, usually under procedure sedation analgesia in an outpatient setting. This is particularly useful in an acute emergent setting with a relatively short window of notice required before dialysis initiation.


Peritoneal Dialysis Benefit

Starting dialysis with a PDC is preferable to an HDC in terms of patient morbidity, mortality, and cost. It has also been shown in large observational retrospective studies that there is a survival advantage for PD over HD in the first 1 to 3 years of dialysis. The 2013 Annual Data Report from the United States Renal Data System also shows a significantly improved adjusted probability of 5-year survival with PD compared to HD. This early survival, for the most part, may be explained by selection bias because healthier patients may be more likely to choose PD as their modality. Patients with comorbid conditions tend to start HD after an acute illness and have high early mortality that is wrongly attributed to their HD modality.

Two recent studies from Canada tried to address the selection bias in PD outcomes. Quinn et al. studied 6573 patients who had at least 4 months of follow-up with nephrologists and had an elective outpatient start of dialysis. There was no difference in 2-year mortality between PD and HD, and in patients without diabetes, PD was associated with a survival benefit that extended beyond 2 years of follow-up. Similarly, Perl et al., comparing incident ESRD patients from a cohort of 40,000 patients in Canada, noted an 80% increased risk of death in patients starting HD using a central venous catheter (CVC) but no difference in mortality between PD and HD using AVF or arteriovenous graft (AVG) for dialysis.


Peritoneal dialysis is one of the modalities utilized for dialysis. There are several advantages of PD versus HD. Patients using PD will not need to leave home every other day to get dialysis, rather they perform their treatments at home using a very simple principle for removing toxins from their body.

Patients selected for PD will undergo PD catheter placement using one of the several techniques described above. Once the catheter has healed, they undergo technique training at a dialysis unit for 2 to 3 weeks, learning the proper aseptic technique to use the catheter for dialysis. The basis of toxin removal in PD is diffusion of uremic toxins out of the blood through the peritoneal membrane into the peritoneal fluid, that is then discarded after a specified amount of time in the peritoneal cavity.

The process of PD can be automated using a simple machine attached to peritoneal dialysis fluid bags. The machine is programmed to infuse the predetermined volume of fluid into the peritoneal cavity, dwell fluid in the peritoneal cavity for a specified time, and automatically drain the fluid. Cycles are repeated several times based on patients needs and peritoneal membrane diffusion characteristics. Manual exchanges require the installation and draining of fluid to be performed by the patient, repeating the process several times during the day to achieve the required clearance of toxins.

What you can expect

During peritoneal dialysis:

  • The dialysate flows into your abdomen and stays there for a prescribed period of time (dwell time) — usually four to six hours
  • Dextrose in the dialysate helps filter waste, chemicals and extra fluid in your blood from tiny blood vessels in the lining of your abdominal cavity
  • When the dwell time is over, the solution — along with waste products drawn from your blood — drains into a sterile collection bag

The process of filling and then draining your abdomen is called an exchange. Different methods of peritoneal dialysis have different schedules of exchange. The two main schedules are:

  • Continuous ambulatory peritoneal dialysis (CAPD)
  • Continuous cycling peritoneal dialysis (CCPD)

Continuous ambulatory peritoneal dialysis (CAPD)

You fill your abdomen with dialysate, let it remain there for a prescribed dwell time, then drain the fluid. Gravity moves the fluid through the catheter and into and out of your abdomen.

With CAPD:

  • You may need three to five exchanges during the day and one with a longer dwell time while you sleep
  • You can do the exchanges at home, work or any clean place
  • You’re free to go about your normal activities while the dialysate dwells in your abdomen

Continuous cycling peritoneal dialysis (CCPD)

Also known as automated peritoneal dialysis (APD), this method uses a machine (automated cycler) that performs multiple exchanges at night while you sleep. The cycler automatically fills your abdomen with dialysate, allows it to dwell there and then drains it to a sterile bag that you empty in the morning.

With CCPD:

  • You must remain attached to the machine for about 10 to 12 hours at night.
  • You aren’t connected to the machine during the day. But in the morning you begin one exchange with a dwell time that lasts the entire day.
  • You might have a lower risk of peritonitis because you connect and disconnect to the dialysis equipment less frequently than you do with CAPD.

To determine the method of exchange that’s best for you, your doctor will consider your medical condition, lifestyle and personal preferences. Your doctor might suggest certain modifications to individualize your program.


Many factors affect how well peritoneal dialysis works in removing wastes and extra fluid from your blood. These factors include:

  • Your size
  • How quickly your peritoneum filters waste
  • How much dialysis solution you use
  • The number of daily exchanges
  • Length of dwell times
  • The concentration of sugar in the dialysis solution

To check if your dialysis is removing enough waste products, your doctor is likely to recommend tests, such as:

  • Peritoneal equilibration test (PET). This test compares samples of your blood and your dialysis solution during an exchange. The results indicate whether waste toxins pass quickly or slowly from your blood into the dialysate. That information helps determine whether your dialysis would be improved if the solution stayed in your abdomen for a shorter or longer time.
  • Clearance test. A blood sample and a sample of used dialysis solution are analyzed to determine how much of a certain waste product (urea) is being removed from your blood during dialysis. If you still produce urine, your doctor may also take a urine sample to measure its urea concentration.

If the test results show that your dialysis schedule is not removing enough wastes, your doctor might change your dialysis routine to:

  • Increase the number of exchanges
  • Increase the amount of dialysate you use for each exchange
  • Use a dialysate with a higher concentration of dextrose

You can improve your dialysis results and your overall health by eating the right foods, including foods low in sodium and phosphorus. A dietitian can help you develop an individualized meal plan. Your diet will be based on your weight, your personal preferences, and your remaining kidney function and other medical conditions, such as diabetes or high blood pressure.

Taking your medications as prescribed also is important for getting the best possible results. While receiving peritoneal dialysis, you’ll likely need various medications to control your blood pressure, stimulate the production of red blood cells, control the levels of certain nutrients in your blood and prevent the buildup of phosphorus in your blood.

After the Procedure

Call your provider right away if you notice:

  • Signs of infection, such as redness, swelling, soreness, pain, warmth, or pus around the catheter
  • Fever
  • Nausea or vomiting
  • Unusual color or cloudiness in used dialysis solution
  • You are not able to pass gas or have a bowel movement

Also call your provider if you experience any of the following symptoms severely, or they last more than 2 days:

  • Itching
  • Trouble sleeping
  • Diarrhea or constipation
  • Drowsiness, confusion, or problems concentrating


Infection of the peritoneal cavity is the most important complication that will not only increase the risk of PD failure but also potentially be life-threatening to the patient. The rate of PD infections can be lowered by proper technique and constant patient education to emphasize proper aseptic technique while using the PDC. Most infections will present with abdominal pain and cloudy peritoneal fluid and are diagnosed by looking for white blood cells (WBCs) in the PD fluid. A cell count of more than 100 WBCs per mL of the fluid suggests infection and should be promptly addressed per guidelines.



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Spirometry – Indications, Contraindications, Procedure

Spirometry is a simple test used to help diagnose and monitor certain lung conditions by measuring how much air you can breathe out in one forced breath. It’s carried out using a device called a spirometer, which is a small machine attached by a cable to a mouthpiece.

Spirometry is one of the most commonly used approaches to test pulmonary function. It measures the volume of exhaled air vs. time. This activity highlights its role in the evaluation of pulmonary disease by the interprofessional team.

Spirometry is one of the most readily available and useful tests for pulmonary function. It measures the volume of air exhaled at specific time points during complete exhalation by force, which is preceded by a maximal inhalation.

The most important variables reported include total exhaled volume, known as the forced vital capacity (FVC), the volume exhaled in the first second, known as the forced expiratory volume in one second (FEV1), and their ratio (FEV1/FVC). These results are represented on a graph as volumes and combinations of these volumes termed capacities and can be used as a diagnostic tool, as a means to monitor patients with pulmonary diseases and to improve the rate of smoking cessation according to some reports.

Anatomy and Physiology

Lungs provide life-sustaining gas exchange by way of introducing oxygen for metabolism and eliminating the by-product carbon dioxide. Air-inspired will pass through the oropharynx to the trachea, which is a membranous tube covered by cartilage bifurcating at the carina as two bronchi at the level of C6. After passing the trachea, the air enters the right and left bronchi, which divide to give several million terminal bronchioles that end in alveoli. The alveoli and surrounding vessels provide a surface where the gas exchange takes place.


Apart from being a key diagnostic test for asthma and chronic obstructive pulmonary disease, spirometry in indicated in several other places, as listed below:

Diagnostic Indications

  • Evaluation of the signs and symptoms of a patient or their abnormal investigations and lab tests
  • Evaluation of the effect a certain disease has on pulmonary function
  • Screening and early detection of individuals who are at risk of pulmonary disease
  • Assessing surgical patients for preoperative risk
  • Assessing the severity and the prognosis of pulmonary disease

Monitoring Indications

  • Assessment of the efficiency of a therapeutic intervention such as bronchodilator therapy
  • Describing the course and progression of a disease that is affecting pulmonary function such as interstitial lung disease or obstructive lung disease
  • Monitoring pulmonary function in individuals with high-risk jobs
  • Sampling data that can be used for epidemiologic surveys

Spirometry is indicated for the following reasons

  • to diagnose or manage asthma[rx][rx][rx]
  • to detect respiratory disease in patients presenting with symptoms of breathlessness, and to distinguish respiratory from cardiac disease as the cause[rx]
  • to measure bronchial responsiveness in patients suspected of having asthma[rx]
  • to diagnose and differentiate between obstructive lung disease and restrictive lung disease[rx]
  • to follow the natural history of disease in respiratory conditions[rx]
  • to assess impairment from occupational asthma[rx]
  • to identify those at risk from pulmonary barotrauma while scuba diving[rx]
  • to conduct a pre-operative risk assessment before anesthesia or cardiothoracic surgery[rx]
  • to measure response to treatment of conditions which spirometry detects[5]
  • to diagnose the vocal cord dysfunction.


Spirometry has proved itself as an accessible utility to assess lung function. However, it may not be for every patient, and care must be taken in some cases, where it may be absolutely or relatively contraindicated.

Absolute Contraindications

  • Hemodynamic instability
  • Recent myocardial infarction or acute coronary syndrome
  • Respiratory infection, a recent pneumothorax or a pulmonary embolism
  • A growing or large (>6 cm) aneurysm of the thoracic, abdominal aorta
  • Hemoptysis of acute onset
  • Intracranial hypertension
  • Retinal detachment
  • Hemoptysis of unknown origin
  • Pneumothorax
  • Unstable cardiovascular status (angina, recent myocardial infarction, etc.)
  • Thoracic, abdominal, or cerebral aneurysms
  • Cataracts or recent eye surgery
  • Recent thoracic or abdominal surgery
  • Nausea, vomiting, or acute illness
  • Recent or current viral infection
  • Undiagnosed hypertension

Relative Contraindications

  • Patients who cannot be instructed to use the device properly and are at risk of using the device inappropriately such as children and patients with dementia
  • Conditions that make it difficult to hold the mouthpiece such as facial pain
  • Recent abdominal, thoracic, brain, eye, ear, nose or throat surgeries
  • Hypertensive crisis


The first requirement for spirometry is physical space in order for the patient to be positioned comfortably. The minimum space recommended is a 2.5* 3m room with 120 cm side doors.

Spirometers are classified into closed-circuit and open-circuit spirometers. Closed-circuit spirometers are further sub-classified into wet and dry spirometers, which consist of a piston or a bellow acting as an air collecting system and a supported recording system that moves at the desired rate.

Open-circuit spirometers, which are more commonly used at present, do not have an air collecting system and instead measure the airflow, integrate the results, and calculate the volume. The most commonly used open-circuit spirometer is the turbine flow meter, which records the rate at which turbines turn and derives the flow measurement based on proportionality. Pneumotachographs are another example, which measures the airflow by measuring the pressure difference generated as the laminar flow passes through a certain resistance. Hotwire spirometers, in which a hot metal wire is heated, and the air used to cool it is used to calculate the flow, are also an example of open-circuit spirometers. Ultrasound spirometers can be based on any of the aforementioned open-circuit spirometer principles.

The minimum specifications for a spirometer are the ability to measure a volume of 8L with an accuracy of ±3% or ±50ml with a flow measurement range of ±141 and a sensitivity of 200ml/s. It is recommended that the spirometer can record at 15 s of the expiration time for the forced maneuver.


The personnel performing the procedure must be familiar with respiratory symptoms and signs. They have to undergo training to understand the technical and physiological background of the tests in order to be competent in performing the techniques of the operation of the device, be able to apply the universal precautions, instruct the patients properly to avoid complications, and act accordingly if any of the complications arise. The personnel should be able to identify responses to therapy, the need for initiating therapy or discontinuing an inefficient one. Continuity of training and periodic retraining is a must for staff in charge of spirometry.


All patients must be informed that they must abstain from smoking, physical exercise in the hours before the procedure. Any bronchodilator therapy must also be stopped beforehand.

The procedure must be carefully explained to the patient focusing on the importance of the patient’s cooperation to provide the most accurate results. The patient’s weight and height must be recorded with the patient barefoot and wearing only light clothing. In the case of chest deformities such as kyphoscoliosis, the span should be measured from the tip of one middle finger to the tip of the other middle finger with the hands crossed, and the height can be estimated from the formula: height = span/1.06. The patient’s age must be recorded. The procedure should be performed with the patient sitting upright wearing light clothing and without crossing their legs. Children can perform the test sitting or standing, but the same procedure should be carried out for the same individual every time.

During the procedure, the back must be supported by a backrest and must not lead forward. Dentures have to be removed if they interfere with the procedure. Manual occlusion of the nares with the help of nose clips helps to prevent air leakage through the nasal passages, although it is not mandatory to occlude nasal passages. The calibration of the spirometer has to be confirmed on the day of the test.

Any contraindications or infectious diseases that require special measures will lead to a delay in the procedure.

Patient positioning

Correct measurement posture is as follows.

  • Sit upright: there should be no difference in the amount of air the patient can exhale from a sitting position compared to a standing position as long as they are sitting up straight and there are no restrictions.
  • Feet flat on the floor with legs uncrossed: no use of abdominal muscles for leg position.
  • Loosen tight-fitting clothing: if clothing is too tight, this can give restrictive pictures on spirometry (give lower volumes than are true).
  • Dentures normally left in: it is best to have some structure to the mouth area unless dentures are very loose.
  • Use a chair with arms: when exhaling maximally, patients can become light-headed and possibly sway or faint.

    Infection control

    Hands must be washed between patients. Bacterial–viral filters should be used for all patients and thrown away by the patient at the end of testing. If an infectious patient requires testing, this should be performed at the end of the session and the equipment should be stripped down and sterilized/parts replaced (depending on what is being used) before being used again.


    The patient must place the mouthpiece in their mouth, and the technician must ensure that there are no leaks, and the patient is not obstructing the mouthpiece. The procedure is carried out as follows:

    • The patient must breathe in as much air as they can with a pause lasting for less than 1s at the total lung capacity.
    • The mouthpiece is placed just inside the mouth between the teeth, soon after the deep inhalation. The lips should be sealed tightly around the mouthpiece to prevent air leakage. Exhalation should last at least 6 seconds, or as long as advised by the instructor. If only the forced expiratory volume is to be measured, the patient must insert the mouthpiece after performing step 1 and must not breathe from the tube.
    • If any of the maneuvers are incorrectly performed, the technician must stop the patient in order to avoid fatigue and re-explain the procedure to the patient.
    • The procedure is repeated in intervals separated by 1 minute until two matching, and acceptable results are acquired.


    The complications of spirometry are fairly limited and will render the procedure as inaccurate or ineffective once they occur. They include:

    • Respiratory alkalosis as a result of hyperventilation
    • Hypoxemia in a patient whose oxygen therapy has been interrupted
    • Chest pain
    • Fatigue
    • Paroxysmal coughing
    • Bronchospasm
    • Dizziness
    • Urinary incontinence
    • Increased intracranial pressure
    • Syncopal symptoms
    Flow-Volume loop showing successful FVC maneuver. Positive values represent expiration, negative values represent inspiration. At the start of the test both flow and volume are equal to zero (representing the volume in the spirometer rather than the lung). The trace moves clockwise for expiration followed by inspiration. After the starting point the curve rapidly mounts to a peak (the peak expiratory flow). (Note the FEV1 value is arbitrary in this graph and just shown for illustrative purposes; these values must be calculated as part of the procedure).
    MeSH D013147
    OPS-301 code 1-712
    Lungvolumes Updated.png
    TLC Total lung capacity: the volume in the lungs at maximal inflation, the sum of VC and RV.
    TV Tidal volume: that volume of air moved into or out of the lungs during quiet breathing (TV indicates a subdivision of the lung; when tidal volume is precisely measured, as in gas exchange calculation, the symbol TV or VT is used.)
    RV Residual volume: the volume of air remaining in the lungs after a maximal exhalation
    ERV Expiratory reserve volume: the maximal volume of air that can be exhaled from the end-expiratory position
    IRV Inspiratory reserve volume: the maximal volume that can be inhaled from the end-inspiratory level
    IC Inspiratory capacity: the sum of IRV and TV
    IVC Inspiratory vital capacity: the maximum volume of air inhaled from the point of maximum expiration
    VC Vital capacity: the volume of air breathed out after the deepest inhalation.
    VT Tidal volume: that volume of air moved into or out of the lungs during quiet breathing (VT indicates a subdivision of the lung; when tidal volume is precisely measured, as in gas exchange calculation, the symbol TV or VT is used.)
    FRC Functional residual capacity: the volume in the lungs at the end-expiratory position
    RV/TLC% Residual volume expressed as a percent of TLC
    VA Alveolar gas volume
    VL The actual volume of the lung including the volume of the conducting airway.
    FVC Forced vital capacity: the determination of the vital capacity from a maximally forced expiratory effort
    FEVt Forced expiratory volume (time): a generic term indicating the volume of air exhaled under forced conditions in the first t seconds
    FEV1 The volume that has been exhaled at the end of the first second of forced expiration
    FIFA Forced expiratory flow related to some portion of the FVC curve; modifiers refer to the amount of FVC already exhaled
    FEFmax The maximum instantaneous flow achieved during an FVC maneuver
    FIF Forced inspiratory flow: (Specific measurement of the forced inspiratory curve is denoted by nomenclature analogous to that for the forced expiratory curve. For example, maximum inspiratory flow is denoted FIFmax. Unless otherwise specified, volume qualifiers indicate the volume inspired from RV at the point of measurement.)
    PEF Peak expiratory flow: The highest forced expiratory flow measured with a peak flow meter
    MVV Maximal voluntary ventilation: volume of air expired in a specified period during repetitive maximal effort


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    Electrocardiogram – Indications, Contraindications

    The electrocardiogram (abbreviated as ECG or EKG) represents an electrical tracing of the heart and is recorded non-invasively from the surface of the body. The word ECG derives from the German language. In German, it is elektro-kardiographie. In 1902, the Dutch physician Einthovan invented ECG, and his tremendous input in the clinical studies for about ten years led to full recognition of the clinical potential of the technique. Many arrhythmias and EKG changes associated with angina and atherosclerosis were identified by 1910. William Einthoven was named the “father of electrocardiography” and was awarded Nobel Prize in Medicine in 1924 for his hard work that laid the foundation of the most fundamental technique of investigating heart disorders. ECG was soon recognized as a robust screening and a clinical diagnostic tool, and today it is used globally in almost every healthcare setting.

    ECG is a non-invasive diagnostic modality that has a substantial clinical impact on investigating the severity of cardiovascular diseases. ECG is increasingly being used for monitoring of patients on antiarrhythmics and other drugs, as an integral part of preoperative assessment of patients undergoing non-cardiac surgery, and for screening individuals in high-risk occupations and those who are participating in sports. Also, EKG serves as a research tool for surveillance and experimental trials of drugs with recognized cardiac effects. Cardiovascular disease, as the number one cause of death, puts a great emphasis on healthcare providers to develop skills and knowledge in interpreting ECGs to provide the best care promptly. Many healthcare providers find the advanced interpretation of ECG findings a complicated task. Errors in the analysis can lead to misdiagnosis resulting in delaying the appropriate treatment. This activity seeks to provide a general understanding of the ECG mechanisms, interpretation techniques, and commonly encountered ECG findings.

    Anatomy and Physiology

    A basic understanding of cardiac anatomy and coronary distribution is essential to understand the electrocardiographic findings.

    The heart is a vital organ of the body and occupies the space in the central chest between the lungs. Together with the blood vessels and blood, it constitutes the circulatory system of the body. The heart is a muscular organ comprised of four chambers that includes two atria (right and left) opening into right and left ventricles via tricuspid and mitral valves, respectively. A wall of muscle called the septum separates all four chambers. The heart receives deoxygenated blood from the whole body via superior and inferior vena cava, which first enters the right atrium. From here, it transits through the right ventricle and then passes into the lungs via the right and left pulmonary arteries, where it is oxygenated. The oxygenated blood from the lungs pours into the left atrium through the right and left pulmonary veins, and from here, it is pumped by the left ventricle into the aorta to the rest of the body. The heart derives its blood supply from the coronary arteries that branch off from the aorta. The right and left coronary arteries lie on the surface of the heart. With considerable heterogeneity among the general population, different regions of the heart receive vascular supply by the various branches of the coronary arteries. This anatomic distribution is significant because these cardiac regions are assessed by a 12-lead ECG to help localize and diagnose ischemic or infarcted areas. Written below are the following regions supplied by the different coronary arteries.

    • Inferior Wall – Right coronary artery
    • Anteroseptal – Left anterior descending artery
    • Anteroapical – Left anterior descending artery (Distal)
    • Anterolateral – Circumflex artery
    • Posterior Wall – Right coronary artery

    The heart is a mechanical pump whose activity is governed by the electrical conduction system. It is essential to have a good understanding of the physiology of the cardiac cells as this will help the reader appreciate how the heart works and the implications of findings on the ECG. The heart is made up of specialized cardiac muscle, which is striated and organized into sarcomeres. These muscle fibers contain a single central nucleus, numerous mitochondria, and myoglobin molecules. Extensive branching of the cardiac muscle fibers and their end-to-end connection with each other through intercalated discs make them contract in a wave-like fashion. This mechanical work of pumping blood to the whole body occurs in a synchronized manner and is under the control of the cardiac conduction system. It is comprised of two types of cells, pacemaker and non-pacemaker cells. Pacemaker cells are located primarily in the SA and AV node, and it is the SA node, which drives the rate and rhythm of the heart. The AV node gets suppressed by the more rapid pace of the SA node.  The specialized function associated with the pacemaker cells is their spontaneous depolarization with no true resting potential. When spontaneous depolarization reaches the threshold voltage, it triggers a rapid depolarization followed by repolarization. The non-pacemaker cells mainly comprise the atrial and ventricular cardiac muscle cells and Purkinje fibers of the conduction system. They consist of true resting membrane potential, and upon initiation of an action potential, rapid depolarization is triggered, followed by a plateau phase and subsequent repolarization. Action potentials are generated by ion conductance via the opening and closing of the ion channels. Knowing which ECG leads corresponds to specific arteries helps in localizing the obstruction in acute ST-elevation MI or an age-indeterminate Q-wave infarction by observing predictable patterns on the ECG.

    Indications of Electrocardiogram

    The evolution of EKG from a string galvanometer to the modern-day advanced computerized machine has led to its use as a diagnostic and screening tool, making it the gold standard for diagnosing various cardiac diseases.

    Owing to its widespread use in the field of medicine, the EKG has several indications listed below:

    • Symptoms are the foremost indication in use for the EKG which includes palpitation, dizziness, cyanosis, chest pain, syncope, seizure, and poisoning
    • Symptoms or signs associated with heart disease including tachycardia, bradycardia and clinical conditions including hypothermia, murmur, shock, hypotension, and hypertension
    • To detect myocardial injury, ischemia, and the presence of prior infarction as well
    • Rheumatic heart disease
    • EKG changes in cases like drowning and electrocution are very valuable in the determination of necessary interventions
    • Detecting pacemaker or defibrillator device malfunction, evaluate their programming and function, verify the analysis of arrhythmias and monitor for delivery of the appropriate electrical pacing in patients with defibrillators and pacemakers
    • Evaluation of metabolic disorders
    • Helpful for the assessment of blunt cardiac trauma
    • Cardiopulmonary resuscitation
    • Valuable aid in the study and differential diagnosis of congenital heart diseases
    • Electrolyte imbalance and rhythm disorders
    • To monitor the pharmacotherapeutic effects and adverse effects of drug therapy
    • Perioperative anesthesia monitoring including preoperative assessment and intraoperative and postoperative monitoring
    • Screening tool in a sports physical exam to rule out cardiomyopathy

    Contraindications of Electrocardiogram

    There are no absolute contraindications for EKG. The relative contraindications to its use include:

    • Patient refusal
    • Allergy to the adhesive used to affix the leads


    The American College of Cardiology (ACC), in conjunction with American Heart Association (AHA) and the Heart Rhythm Society (HRS), has formulated guidelines and also set technical standards for ECG equipment . With advancements, most of the EKG machines are digital and can autogenerate preliminary findings based on the morphology criteria.

    The conventional ECG machine consists of 12 leads, which divide into two groups, i.e., limb leads and precordial leads. Limb leads are further categorized as standard bipolar limb leads I, II, and III, and augmented unipolar leads aVL, aVF, and aVR. The precordial leads include V1 to V6. The limb leads view the heart in a vertical plane, and the precordial leads record the electrical activity of the heart in the horizontal plane. The ECG represents a graphic recording of the electrical cardiac activity tracing on the electrocardiograph paper. The fundamental principle behind the recording of an ECG is an electromagnetic force, current, or vector that has both magnitude and direction. When a current of depolarization travels towards the electrode, it gets recorded as a positive deflection, and when it moves away from the electrode, it appears as a negative deflection.

    • A current of repolarization traveling away from the positive electrode is seen as a positive deflection and towards a positive electrode as a negative deflection
    • When the current is perpendicular to the electrode, it touches the baseline and produces a biphasic wave.

    These concepts are easily applied to the heart while recording the ECG. There are several types of ECG monitoring equipment available, including continuous ECG monitoring, hardwire cardiac monitoring, telemetry, ambulatory electrocardiography, transtelephonic monitoring, and wireless mobile cardiac monitoring systems, etc. Furthermore, a duo of ECG and electronic stethoscopes have been designed into a portable, handheld device that can review ECG rhythms and intervals at the bedside for analysis. With the evolution of technology, there are electronic wristwatches that can also provide monitoring of the heart rate and rhythm and have proven to be of value in detecting atrial fibrillation. The accuracy of these devices, however, may be somewhat inferior when compared to a 12-lead ECG; and when prompted for abnormal findings, these require confirmation by standardized clinical testing available in the Cardiology office.

    The equipment for performing a conventional 12-lead ECG includes:

    • Electrodes (sensors)
    • Gauze and skin preparation (alcohol rub) solution
    • Razors or clippers or a roll of tape (for hair removal)
    • Skin adhesive and/or antiperspirant
    • ECG paper
    • Cardiac monitor or electrocardiography machine


    The medical personnel that can perform the ECG procedure includes a doctor, nurse, or a qualified technician. Usually, it is performed by the technicians either in the clinics or hospitals and then interpreted by physicians. Often, these findings are confirmed by a cardiologist in a hospital-based setting.


    ECG merely requires special preparation. Before the procedure, a brief history regarding drugs and allergy to adhesive gel is necessary. The temperature of the room must be kept optimal to avoid shivering. The patient should be in a gown, and electrode sites identified. For good contact between the body surface and electrodes, it is advised to shave the chest hair and then apply the electrocardiographic adhesive gel for electrodes. Any metallic object like jewelry or a watch requires removal, if possible. Limb and precordial leads should be accurately placed to avoid vector misinterpretation. The patient must lie down and relax before recording the standard 10-second strip.


    ECG machines are designed to record changes in electrical activity by drawing a trace on a moving electrocardiograph paper. The electrocardiograph moves at a speed of 25mm/sec. Time is plotted on the x-axis and voltage on the y-axis. In the x-axis, 1 second is divided into five large squares, each of which represents 0.2 sec. Each large square is further divided into five small squares of 0.04 sec each. The EKG machine is calibrated in such a way that an increase of voltage by one volt should move the stylus by 1 cm. The conventional 12-lead EKG consisting of six limbs and six precordial leads is organized into ten wires. The limb leads include I, II, III, aVL, aVR, and aVF and named as RA, LA, RL, and LL. The limb leads are color-coded to avoid misplacement (red- right arm, yellow- left arm, green- left leg, and black- right leg). The precordial leads V1 to V6 are attached to the surface of the chest.  For the correct location, the “Angle of Louis” method is an option, and the exact placement is as follows:

    • V1 is placed to the right of the sternal border, and V2 is situated at the left of the sternal edge.
    • V4 is placed at the level of the fifth intercostal space in the mid-clavicular line. V4 should be placed before V3. V3 is placed between V2 and V4.
    • V5 is placed directly between V4 and V6.
    • V6 is placed at the level of the fifth intercostal space in the mid-axillary line.
    • V4 through V6 should line up horizontally along with the fifth intercostal space.


    ECG is a safe, non-invasive, painless test with no major risks or complications. An allergic reaction or skin sensitivity to the adhesive gel can occur and usually resolves as soon as the electrode patches are removed, and in most cases, do not require any treatment. Artifacts and distortions pose serious diagnostic difficulties and may result in an inaccurate interpretation of the ECGs that may potentially result in an adverse therapeutic intervention.

    There can be a potential for misdiagnosis due to the inadvertent misplacement of ECG leads.

    Clinical Significance

    Evaluation of Arrhythmia

    In patients suspected of arrhythmias, an electrocardiogram (EKG) is the first step and will usually give the diagnosis. However, at times, the patient may suffer from paroxysmal arrhythmia. The following modalities can be used for diagnosing based on the frequency of the symptoms a patient has secondary to a suspected arrhythmia.

    • Ambulatory EKG monitoring for patients with frequent symptoms
    • The event recorder needs to be triggered by the patient to record and will not a viable choice for patients with syncope.
    • Loop event recorder records up to 2 minutes before the trigger. It is good for patients with syncope.
    • Implantable loop recorder for patients with less frequent symptoms.


    Tachyarrhythmia is defined as an abnormal rhythm with a ventricular heart rate of 100 beats per minute or more. It can be further classified based on the origin of the arrhythmia into:

    Supraventricular Tachycardia (SVT): Arrhythmia originating from above the AV node (from atrial origin or AV junction origin).

    • Atrial fibrillation (AFib)
    • Atrial flutter
    • Atrial tachycardia
    • Atrial premature complex (PAC)
    • Atrioventricular nodal reentrant tachycardia (AVNRT)
    • Atrioventricular reentrant tachycardia (AVRT)
    • AV junctional extrasystoles

    Ventricular Tachycardia (VT): The origin of the arrhythmia is below the AV node.

    • Ventricular fibrillation (V-fib)
    • Ventricular premature beats (PVC)
    • Ventricular tachycardia (sustained or non-sustained)

    Tachyarrhythmias can also be classified based on the QRS complex duration into

    Narrow QRS complex tachycardia when QRS is <120 milliseconds in duration:

    • Sinus tachycardia
    • Atrial tachycardia (AT)
    • Atrial flutter
    • Atrioventricular nodal reentrant tachycardia (AVNRT)
    • Atrioventricular reentrant tachycardia (AVRT)
    • Junctional ectopic tachycardia
    • Sinoatrial nodal reentrant tachycardia (SANRT)
    • Atrial fibrillation (irregular QRS complexes)

    Wide QRS complex tachycardia (QRS ≥120 milliseconds in duration) is classified as monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, or ventricular fibrillation.

    Supraventricular Tachycardia Syndromes

    • These are usually narrow complex tachycardias with QRS width being less than 3 mm or 120 milliseconds on the EKG strip. Supraventricular tachycardia is further classified into atrioventricular reciprocating tachycardia, atrioventricular nodal reentrant tachycardia, and atrial tachycardia based on the mechanism of tachycardia.

    I. Atrioventricular reciprocating tachycardia (AVRT)

    As found in Wolff-Parkinson-White syndrome (the presence of delta wave without arrhythmia doesn’t require investigation or treatment).

    • Mechanism: Accessory pathway present outside of the AV node-Bundle of Kent. It can be further categorized into:
      • Antidromic: Conduction down the accessory pathway and up to AV node leading to the formation of a delta wave.
      • Orthodromic: Conduction down the AV node into an accessory pathway with no delta wave.
    • Signs & Symptoms: Palpitation, shortness of breath, or syncope.
    • EKG Findings: Slurred upstroke of the QRS, delta wave, may give an impression of the wide QRS complex.
    • Management: Amiodarone or procainamide. If this fails, the next step is synchronized cardioversion.
    • Definitive Therapy: Ablation of the accessory pathway.

     II. Atrioventricular Nodal Reentrant Tachycardia (AVNRT)

    • Mechanism: Slow & fast fibers present in AV node & peri-nodal tissue leading to re-entry. Signs & Symptoms: Sudden tachycardia, palpitation, shortness of breath, chest tightness, or syncope. EKG Findings: Narrow complex tachycardia with P waves hidden in T waves. Heart rate is in the range of 150-160 bpm.


    • Step 1: Carotid massage/Valsalva maneuver
    • Step 2: Adenosine
    • Step 3: Cardioversion
    • Step 4: Ablation or chronic suppressive therapy with beta-blockers and calcium channel blockers such as diltiazem/verapamil.

     III. Atrial fibrillation

    It is the most common arrhythmia in the United States. It affects more than 20% of the general population at some time in their lives. There are five types based on their duration:

      • New-onset]
      • Paroxysmal: Self-terminating or intermittent
      • Persistent: Fails to self-terminate within 7 days and requires treatments (medical or electrical cardioversion)
      • Long-standing Persistent: Lasts for ≥ 1 year
      • Permanent: Persistent for ≥ 1 year despite treatment
    • Mechanism: Multiple reentrant wavelets due to atrial ectopy from muscle fibers near the proximal part of the pulmonary vein.
    • Signs & Symptoms: It can be asymptomatic or can cause symptoms like palpitation, shortness of breath, irregularly irregular pulse, or even hypotension.
    • EKG Findings: Irregularly irregular narrow complex tachycardia with no discernable P-waves.
    • Management: The management strategy for atrial fibrillation can be classified into rate control or rhythm control. The decision to use a rate control or a rhythm-control strategy depends on the hemodynamic stability, candidacy for ablation, and the presence of co-morbidities. Patients with atrial fibrillation are at increased risk of ischemic-embolic stroke, and anticoagulation recommendations are based on the CHA2DS2VaSc score.
    • CHA2DS2VaSc score is determined by the presence of the following factors: Congestive heart failure (CHF) with ejection fraction (EF) less than 40%, hypertension, age > 65 years, diabetes mellitus, history of stroke (non-hemorrhagic) or transient ischemic attack (TIA), vascular disease (peripheral vascular disease – PVD), age > 75 years, female sex. Each factor adds a point to the score, except for a history of stroke/TIA, which adds 2 points.
      • If the score is 0: No anticoagulation or aspirin based on individual assessment
      • If the score is 1: Aspirin or anticoagulation based on individual assessment.
      • If the score is 2 or more: Anticoagulation is recommended if not at high risk of bleeding.
    • Rate Control Strategy: The heart rate goal is < 110 bpm in patients with chronic atrial fibrillation. It can be achieved with either beta-blockers or calcium channel blockers. Digoxin is usually used as adjuvant therapy in a patient with difficulty controlling rate or in heart failure patients.
    • Cardioversion Strategy: Cardioversion is preferred in hemodynamically unstable patients or if rate control fails. It is also preferred in a young patient with no other co-morbidities. Cardioversion can be performed within 36 hrs of the onset of atrial fibrillation, but if the presentation is delayed or is of unknown duration, the absence of thrombi needs to be confirmed with a transesophageal echocardiogram (TEE). If a thrombus is present on an echocardiogram, the patient will need anticoagulation for at least three weeks before cardioversion can be performed. The patient needs to be on anticoagulation for at least four weeks post cardioversion. Various modalities are available for cardioversion therapy and include synchronized electric cardioversion or chemical cardioversion with medications including flecainide, propafenone, amiodarone, or dronedarone. Maze procedure is usually reserved for the patient undergoing other cardiac surgery.

    Atrial Flutter

    • Mechanism: Reentrant circuit usually around the tricuspid annulus in the right atrium.
    • Signs & Symptoms: Can be asymptomatic, or it can cause palpitation, shortness of breath, or hypotension.
    • EKG Findings: Regular tachycardia with Saw-tooth appearance of P wave with a variable degree of AV block.
    • Management: General goals include control of ventricular rate with AV blocking agents (beta-blockers or calcium channel blockers), but the restoration of sinus rhythm through cardioversion or ablation is preferred.

    Multifocal Atrial Tachycardia (MAT)

    • Mechanism: multiple automatic atrial foci due to increased sympathetic tone secondary to various causes, including hypoxemia (chronic obstructive pulmonary disease (COPD), or stimulant use.
    • Signs & Symptoms: Usually asymptomatic. Patients will have symptoms of the underlying illness, such as dyspnea.
    • EKG Findings: Three or more P wave morphologies with different PR intervals.
    • Management: Oxygen therapy if hypoxemic and treatment of the underlying cause.
    • Refractory cases: Rate Control with calcium channel blockers as the first choice in the setting of COPD followed by beta-blockers.

    Junctional tachycardia

    Arrhythmia originating from or near the AV node.
    • Mechanism: Rhythm arising from the AV node.
    • Risk Factors: Post cardiac surgery, myocardial ischemia (or during reperfusion), or digoxin toxicity.
    • Signs & Symptoms: Usually well-tolerated and asymptomatic.
    • EKG Findings: Inverted P Wave in the lead 2 with short PR or No P waves with a narrow complex.
    • Management: Treat the underlying cause.

     IV. Ventricular Tachycardia

    Origin is below the AV node. It is the major cause of sudden cardiac deaths in the United States.

    a) Non-Sustained Ventricular Tachycardia: When the rapid ventricular rhythm terminates on its own within 30 seconds.

    • Mechanism: Channelopathies secondary to structural abnormality, electrolyte disturbances, metabolic imbalance, and the effect of pro-arrhythmic drugs.
    • Risk Factors: Structural or ischemic heart disease.
    • Signs & Symptoms: Asymptomatic or palpitations.
    • EKG Findings: Monomorphic wide complex with more than three beats in a row but lasts less than three seconds.
    • Management: Implantable cardioverter-defibrillator (ICD) and/or medical therapy.

    b) Sustained Ventricular Tachycardia

    • Mechanism: Presence of damaged fibers in ischemic heart disease leading to re-entry of current. Some patients do not have structural heart disease. Approximately 10% of the cases are idiopathic.
    • Risk Factors: Structural heart disease and post-myocardial infarction.
    • Signs & Symptoms: Palpitation, hypotension, or syncope.
    • EKG Findings: Monomorphic wide complex tachycardia.
    • Management: Intravenous lidocaine, amiodarone, or procainamide. Catheter ablation is an option too.

    c) Ventricular Fibrillation

    • Mechanism: Presence of damaged fibers in ischemic heart disease leading to re-entry of current leading to disorganized high-frequency excitation. Patients with Cardiomyopathies can have Ventricular fibrillation due to an increase in end-diastolic pressure, wall tension, or the presence of abnormal channels in ventricular fibers.
    • Risk Factors: Structural heart disease and post-myocardial infarction.
    • Signs & Symptoms: Syncope and death if not treated immediately.
    • EKG Findings: Polymorphic fibrillatory waves.
    • Management: Unsynchronized cardioversion followed by amiodarone.

    d) Torsades De Pointes

    • Mechanism: It is usually precipitated by premature ventricular contraction leading to “R on T phenomenon.”
    • Risk Factors: Congenital long QTc with hypokalemia and hypomagnesemia.
    • Signs & Symptoms: Syncope and death if not treated immediately.
    • EKG Findings: Polymorphic wide-complex tachycardia with a heart rate > 300 bpm.
    • Management: Intravenous magnesium or Isoproterenol, which increases heart rate and decreases QT-duration. Avoid hypokalemia and hypomagnesemia. Chronic therapy with beta-blockers in patients with long QT syndrome.

    3. Bradyarrhythmias

    Bradyarrhythmia is defined as a heart rate below 60 beats per minute (bpm) and comprises several rhythm disorders, including atrioventricular (A-V) blocks and sinus node disorders.

    Sinus Bradycardia

    • Mechanism: Increased vagal tone. It can be physiological in athletes.
    • Signs & Symptoms: Usually asymptomatic. It can lead to orthostasis or dizziness if pathological.
    • EKG Findings: Sinus rhythm with an upright P wave in lead II and biphasic in V1.
    • Management: No treatment is required unless pathological with an inadequate heart rate increase with leg raise test. Treat with isoproterenol or pacemaker if no relief.

    Atrioventricular Blocks

    • Mechanism: Atrial impulses are conducted with a delay or not at all when an electrical impulse reaches a tissue that not excitable or is in a refractory period.

    a) First Degree AV Block: Caused by increased vagal tone or conduction impairment or due to medications.

    • Signs & Symptoms: Generally asymptomatic but can cause dizziness.
    • EKG Findings: PR interval is greater than 200 milliseconds.
    • Management: Usually, no need to treat.

     b) Second Degree AV Block: Further classified into Mobitz I block, where there is a progressive prolongation of the PR interval followed by a skipped beat, and Mobitz II block, where there is a randomly dropped QRS complex on an EKG.

    • Sign & Symptoms: Can be asymptomatic, dizziness, palpitations, weakness, syncope.
    • EKG Findings: Mobitz type I shows progressive prolongation of the PR interval followed by a dropped QRS complex or dropped beat. Mobitz type II has randomly dropped QRS complexes.
    • Management: Pacemaker is indicated in symptomatic Mobitz I and all of Mobitz II heart block.

    c) Third Degree or complete AV Block

    • Mechanism: Lack of conduction of atrial impulse to ventricle leading to independent contractions.
    • Sign & Symptoms: Profound bradycardia, hypotension, and can lead to asystole and cardiac arrest.
    • EKG Findings: Bradycardia, P waves occur independently of QRS and Wide QRS for ventricular rhythm.
    • Management: Pacemaker placement.

    Sinus Node Dysfunction

    • Mechanism: Senescence of the SA node, an ischemic event involving SA node leading to impulse generation at a slower rate.

    a) Sinus Pause: When the SA node has delayed impulse generation.

    b) Sinus Arrest: Failure of impulse generation.

    c) SA Nodal Exit Block: Failure of impulse transmission.

    • Sign & Symptoms: Bradycardia, dizziness, palpitation, or syncope.
    • EKG Findings: P wave not originating at a determined rate with regularity
    • Management: Symptomatic patients require pacemaker placement.

    The goal of the ECG interpretation is the ability to determine whether the ECG waves and intervals are normal or pathological. Electrical signal interpretation gives a good approximation of heart pathology. A standard 12 lead ECG is shown in. The best way to interpret an ECG is to read it systematically:

    • RATE: For calculation of rate, the number of either small or large squares between an R-R interval should be first calculated. The rate can be calculated by either dividing 300 by the number of big squares or 1500 by the number of small squares between two R-waves. For an irregular rhythm, count the number of beats in a 10-second strip and multiply it by 6. Normal HR is 60 to 99 beats per minute. If it is less than 60, it’s called bradycardia and if greater than 100/min, it’s called tachycardia
    • RHYTHM: The leads I, II, aVF, and V1 require inspection for an accurate interpretation of rhythm. It involves looking for five points: the presence or absence of regular P waves, duration of QRS complexes (narrow or wide), the correlation between P waves and QRS complexes, whether the rhythm is regular or irregular, and also importantly, the morphology of P-waves. A regular rhythm ECG has regular P waves, each preceding a QRS complex in a regular rhythm. Also, normal sinus rhythm demonstrates positive P-waves in leads I, II, and aVF, suggesting a downward propagation of atrial activation from the SA node. These features also help in identifying if the arrhythmia is originating in the atria or ventricles. Many disorders are related to rhythm abnormalities. For example, in atrial fibrillation, no real P waves can be seen due to the very fast atrial activity, and only a few impulses get delivered to ventricles making the rhythm irregularly irregular. The presence of ‘irregularly irregular’ narrow QRS complexes with no discrete P waves is the hallmark feature in the identification of atrial fibrillation.
    • CARDIAC AXIS: It refers to the general direction of the heart’s depolarization wavefront in the frontal plane. The cardiac axis is related to the area of significant muscle bulk within the healthy conducting system. A typical cardiac axis is between -30 to +90 degrees. A quick way to estimate the axis is by looking at leads I and aVF. It can be defined as a normal axis when the QRS complex is positive in both leads I and aVF. A left axis deviation (between 0 and -90 degrees) is defined by the presence of positive QRS in the lead I and negative in lead aVF and right axis deviation(+90 and 180 degrees) by the presence of QRS negative in the lead I and positive in lead aVF. If both QRS complexes are negative in leads I and aVF, it is termed as extreme right axis deviation or indeterminate axis (-90 to 180 degrees). Other methods used for the determination of the cardiac axis include three lead analysis, isoelectric lead analysis, etc. There are several disorders in which the cardiac axis deviates.  Examples include conditions like old inferior MI, left ventricular hypertrophy, left bundle branch block where left axis deviation occurs while noting right axis deviation in conditions including right ventricular hypertrophy, pulmonary hypertension, hyperkalemia, and wolf-Parkinson-White syndrome, etc. The specific criteria on ECG for atrial and ventricular hypertrophy are devised from examining various leads and wave morphologies: for atrial abnormality (enlargement/ hypertrophy), leads II and V1 are usually assessed. Right atrial hypertrophy shows an increase in the amplitude in the first half of the P waves by 2.5 mm in inferior leads and a possible right axis deviation. It is often termed as P pulmonale because of its frequent association with chronic obstructive lung disease. Left atrial hypertrophy shows an increase in the amplitude of the terminal component and duration of the P wave, and it must descend at least 1 mm below the isoelectric line in lead V1 and must be at least 0.04 seconds (40 ms) in width. As the left atrium is electrically dominant, it shows no axis deviation.For the diagnosis of ventricular hypertrophy, it requires looking at several leads on the ECG. The right ventricular hypertrophy characteristically shows by right axis deviation along with the presence of a more significant R wave than S wave in lead V1, whereas in lead V6, a more significant S wave than R wave. Left ventricular hypertrophy is characterized by voltage criteria either by calculating the voltage of  R wave in V5 or V6 plus the S wave in V1 or V2 exceeding 35mm or by the voltage of R wave exceeding 13 mm in lead aVL. Infrequently, there is also the presence of secondary repolarization abnormalities, including asymmetric T wave inversion and downsloping  ST-segment depression, commonly also referred to as the strain pattern; the left axis deviation often accompanies this.
    • P-WAVE: It represents atrial depolarization on the ECG. As atrial depolarization initiates by the SA node located in the right atrium, the right atrium gets depolarized first, followed by left atrial depolarization. So the first half of the P-wave represents right atrial depolarization and the second half left atrial depolarization. Its duration is three small squares wide and 2.5 small squares high. It is always positive in the lead I and II, and consistently negative in lead aVR in normal sinus rhythm. It is commonly biphasic in lead V1. An abnormal P-wave may indicate atrial enlargement.
    • PR INTERVAL: It represents the time from the beginning of atrial depolarization to the start of ventricular depolarization and includes the delay that occurs at the AV node. The average interval is 3 to 5 small squares (120 to 200ms). Variations in the PR interval can lead to various disorders. Long PR interval may indicate first-degree AV block, and short interval may be present in conditions with accelerated AV conduction such as the presence of bypass tract or Wolf-Parkinson-White syndrome and Lown-Ganong-Levine syndrome.
    • Heart Block: A conduction block can occur due to any obstruction in the normal pathway of the electrical conduction. Their anatomical location can be categorized as sinus node, atrioventricular node, or bundle branch blocks.
    • Sinus node or sinoatrial exit block – occurs due to failed propagation of the impulses beyond SA node resulting in dropped P waves on the ECG. Common causes include sick sinus syndrome, increased vagal tone, inferior wall MI, vagal stimulation, myocarditis, drugs including digoxin, beta-blockers, etc.
    • Atrioventricular or AV block – is a conduction block that can occur anywhere between the SA node and Purkinje fibers. There are three variants of AV blocks: first-degree, second-degree, and third-degree. Clinically significant points in diagnosing the AV blocks include careful measurement of the PR interval and examination of the relationship of the P waves to QRS complexes.
    • First-degree heart block – is defined as prolongation of the PR interval by more than 200 milliseconds only. A single P wave precedes every QRS complex. It may be a normal finding in some individuals, but it can be an early sign of degenerative disease of the conduction system or a transient manifestation of myocarditis or drug toxicity, hypokalemia, acute rheumatic fever, etc. It usually does not require any treatment.
    • Second-degree heart block – is of two types, i.e., Mobitz type I (also known as Wenkebach block) and Mobitz type II. In type I, the block across the AV node or bundle of His is variable and increases with each ensuing impulse, ultimately resulting in a drop of the impulse (usually every third or fourth impulse). On ECG, it shows as a progressive prolongation of the PR interval, and then suddenly, a P wave is not followed by the QRS complex. This sequence repeats itself in a regular manner. Most patients with Mobitz type I second-degree AV block are asymptomatic. Mobitz type I AV block may occur in the setting of acute myocardial ischemia or myocarditis and may also result in clinical deterioration if the resulting ventricular rate is inadequate to maintain cardiac output. Most patients with Mobitz type I second-degree AV block are asymptomatic and do not require any specific intervention. Rarely, patients with Mobitz type I block are symptomatic and demonstrate hemodynamic instability and may require treatment with either atropine (emergently) and eventually cardiac pacing. In type II  AV block, there is a dropped beat without the progressive lengthening of the PR interval. It follows the all-or-nothing phenomenon. It usually occurs below the AV node at the level of the bundle of His. It clinically signifies a severe underlying heart disease that can progress to third-degree heart block. When diagnosed, it usually requires prompt treatment with a permanent pacemaker.
    • Third-degree heart block – is characterized by a complete electrical dissociation between the atria and ventricles, resulting in atria and the ventricles beat at their intrinsic rates. Degenerative disease of the conduction system is the leading cause of third-degree heart block. A complete heart block may present in acute myocardial infarction. Complete heart block may be reversible with prompt revascularization, especially in inferior MI. Lyme disease may be associated with a complete heart block and is potentially reversible with antibiotic therapy. In the case of irreversible or permanent complete heart block, a permanent pacemaker remains the mainstay of the treatment.
    • Bundle branch block – results from the conduction block of either left or right bundle branches. It gets diagnosed by examining the width and configuration of the QRS complexes. The right bundle branch block is represented on the ECG by the presence of a widened QRS complex greater than 0.12 seconds along with an RSR pattern in V1 and V2. Also, there may be ST-segment depression and T wave inversions, and reciprocal changes in leads V5, V6, I, and aVL. Conduction system disorders can cause the right bundle branch block, but it may be present as a standard variant in specific individuals. The left bundle branch block is represented on the ECG by a widened QRS complex greater than 0.12 seconds, broad or notched R wave with prolonged upstroke in the leads V5, V6, I, and aVL, along with ST-segment depression and T wave inversion, and reciprocal changes in leads V1 and V2. Usually, a left axis deviation is also present. The left bundle branch usually signifies an underlying pathology, such as degenerative disease of the conduction system or ischemic heart disease.
    • QRS COMPLEX: It represents ventricular depolarization as current passes down the AV node. A standard QRS complex has a duration of less than three small squares (under 120 ms, usually 60 to 100 ms). A prolonged QRS may indicate hyperkalemia or bundle branch block. A premature ventricular contraction or a ventricular rhythm can be associated with a wide QRS.
    • SEPTAL Q-WAVE: Q-wave often appears as a tiny negative deflection in leads I, aVL, V5, and V6. It represents the depolarization of the interventricular septum. Its amplitude is not bigger than 0.1mV; that is why septal depolarization is not always visible on the EKG. Pathological Q-waves on EKG can signify an old infarct. A Q-wave duration of greater than 40 milliseconds (one small box), depth greater than 1 mm, or a size greater than 25% of the QRS complex amplitude is considered to be pathologic.
    • R-WAVE: It is the tallest wave of the QRS complex, and it represents the electrical stimulus as it passes down the ventricles during depolarization. The R-wave progressively increases in amplitude moving right to the left in the precordial leads and is called R-wave progression. Lead V1 has the smallest R-wave, and lead V5 has the largest. A reduced R-wave progression has several causes, including prior anteroseptal MI, left ventricular hypertrophy or inaccurate lead placement, etc.
    • S-WAVE: It represents the final depolarization of the Purkinje fibers. It is any downward deflection after R-wave. It may not be present in all ECG leads. S-wave is most significant in V1 and progressively becomes smaller to no S-wave in the lead V6.
    • T-WAVE: It represents ventricular repolarization. Its morphology is highly susceptible to cardiac and noncardiac influences like ( hormonal, neurological). In leads with tall R-waves, it is usually positive (upward deflection). The suggested criteria for the typical T wave include the size of one-eighth or less than two-thirds of the size of the R wave and a height less than 10 mm. Abnormalities in the T-wave morphology can include inverted, flat, biphasic, or tall tented T-waves. T waves can be helpful in a variety of pathologies, tall T waves in anterior chest lead III, aVR, and V1 with a negative QRS complex may suggest acute myocardial ischemia. Other causes of T wave abnormalities are caused by physiological factors (e.g. postprandial state), endocrine or electrolyte imbalance, myocarditis, pericarditis, cardiomyopathy, postcardiac surgery state, pulmonary embolism, fever, infection, anemia, acid-base disorders, drugs, endogenous catecholamines, metabolic changes, acute abdominal process, intracranial pathology, etc.
    • ST SEGMENT: It depicts the end of ventricular depolarization and the beginning of ventricular repolarization. The average duration of ST segment is less than 2 to 3 small squares (80-120ms). ST-segment is an isoelectric line and lies at the same level as PR-interval. Elevation or depression of the ST segment by 1mm or more, measured at J point, is considered abnormal. A J point is a region between the QRS complex and the ST segment. ST-elevation is highly specific if present in two or more contiguous leads in the setting of acute myocardial infarction. If the vertical distance on the ECG trace and the baseline at a point 0.04 seconds after the J-point is at least 1 mm in a limb lead or 2 mm in a precordial lead is clinically significant for the diagnosis of acute myocardial infarction. Correct ST segment interpretation is crucial as there is a type of ST-segment elevation present in healthy individuals that occurs due to early repolarization and is termed as J-point elevation. It is distinguished by the fact that the T wave does not merge with the ST segment and remains an independent wave. Several other disorders are also associated with ST-elevation, i.e., Prinzmetal angina, acute pericarditis, acute myocarditis, hyperkalemia, blunt trauma, pulmonary embolism, subarachnoid hemorrhage, Brugada syndrome, ventricular aneurysm, and left bundle branch block. ST-elevations are diffuse in acute pericarditis and associated with PR-depression in reference to TP-segments (except for leads V1 and aVR).. In myocardial infarction, the ST elevation tends to be localized (inferior, anterior, posterior, lateral), often, but not always with reciprocal ST depression. Second, the PR segment displacement, which is attributable to the subepicardial atrial injury. PR elevation can present in aVR, and PR depression is best seen in II, aVF, V4-V6. PR-depression and slight downsloping appearance of TP segments are often known as Spodick’s sign of pericarditis and help distinguish acute pericarditis from acute MI. ST depression greater than 1 mm is often a sign of myocardial ischemia or angina. It can appear as a downsloping, upsloping, or horizontal segment on the ECG. A horizontal or downsloping ST depression greater than 0.5 mm at the J-point in two or more contiguous leads indicates myocardial ischemia. An upsloping ST depression in the precordial leads with prominent De Winter T waves is highly indicative of MI caused by occlusion of the left anterior descending artery. ST depression can represent a reciprocal change with a morphology that resembles “upside-down” ST elevation and typically seen in leads electrically opposite to the site of infarction. For example, posterior wall MI manifests as horizontal ST depression in leads V1-3 and is associated with tall R waves and upright T waves. Likewise, inferior wall STEMI produces reciprocal ST depression in leads I and aVL, and there is often a reciprocal ST-depression in leads III and aVF in lateral wall MI. ST depressions are also associated with several non-ischemic causes, including digoxin toxicity, hypokalemia, hypothermia, and tachycardia.
    • QT INTERVAL: It represents all start of depolarization to the end of repolarization of ventricles. The normal QT interval duration is somewhat controversial, and various normal durations have been previously suggested. In general, the normal QT interval is less than 400 to 440 milliseconds (ms), or 0.4 to 0.44 seconds. Women usually have a slightly longer QT interval than men. A QT interval has an inverse relation to the heart rate. A prolonged QT interval presents an imminent risk for serious ventricular arrhythmias, including Torsades de Pointes, ventricular tachycardia, and ventricular fibrillation. A common cause of QT prolongation includes medications, electrolyte abnormalities such as hypocalcemia and hypomagnesemia and congenital long QT syndrome.A short QT interval ( less than 360 milliseconds) may be present associated with hypercalcemia, acidosis, hyperkalemia, hyperthermia, or short QT syndrome.
    • U WAVE:  It is a small wave that follows the T wave. It represents the delayed repolarization of the papillary muscles or Purkinje fibers. It is commonly associated with hypokalemia.
    • J WAVE: also known as Osborn wave, is an abnormal EKG finding in hypothermia. It appears as an extra deflection on ECG at the junction of the QRS complex and ST-segment.
    • EPSILON WAVE: It is a small positive deflection usually found buried at the end of the QRS complex as a characteristic finding in arrhythmogenic right ventricular dysplasia.



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    How to Examine Knee Joint – All About You Need To Known

    How to Examine Knee Joint /The knee examination, in medicine and physiotherapy, is performed as part of a physical examination, or when a patient presents with knee pain or a history that suggests a pathology of the knee joint.

    The knee examination, in medicine and physiotherapy, is performed as part of a physical examination, or when a patient presents with knee pain or a history that suggests a pathology of the knee joint. The exam includes several parts: position lighting draping. inspection.

    It is important to have a systemic plan for the examination of the knee to arrive at the correct diagnosis, to identify its impact on the patient, to understand the patients’ needs and concerns and then to formulate a treatment plan that is individualized for the particular patient. Thorough knowledge of the normal anatomy, biomechanics of the knee and the pathology of various knee disorders is a must for proper examination of the knee and for the interpretation of physical findings.

    First, listen to the patient carefully to understand his concerns and needs and also to gain his confidence.
    The involved and the normal knee should be adequately exposed to examine the knee. Always examine the spine and the hip to rule out conditions that lead to referred pain in the knee and any associated hip and spine disorders.
    Always compare with the uninvolved side as a wide range of anatomic and functional variations exist.
    The examination should be gentle and as painless as possible to avoid worsening of injury and to ensure a cooperative patient. The function of the knee is assessed by the patient’s ability to weight bear, walk, ability to squat, sit cross-legged, run, stair climb and the level of restriction of activities of daily living and occupational and recreational activities.


    Presenting complaints – Give the presenting complaints in chronological order.


    • Duration – How long the pain is present?
    • Onset – How it started? Symptoms may begin after a traumatic event, after unaccustomed activity. It may start suddenly or gradually. Acute onset of symptoms is seen with trauma, infections and crystal deposition disorders.
    • Progress – What has happened to the pain after it started? Has it increased, decreased or remain in the same intensity. Is it constant or intermittent? What is its present status?
    • Site – Ask the patient to pinpoint the site of pain with a single finger. Note down whether in the joint line medially or laterally, around the patella or popliteal fossa. Don’t use vague terms like pain in the hip. Remember that a patient with the hip disease may present with knee pain.
    • Severity – How disabling is the pain? What is its effect on routine activities, self-care, locomotion, occupation and recreational activities?
    • Character – What is the nature of pain? The throbbing pain is due to inflammatory causes, burning pain is due to neuropathic causes.
    • Radiation – Pain of the hip may radiate to the knee or thigh. Pain radiating below the knee is due to sciatica.
    • Aggravating and relieving factors- Mechanical pain due to osteoarthritis or impingement is aggravated by activity and relieved by rest. Pain due to inflammatory arthritis is aggravated by rest and partially relieved by activity.
    • Diurnal variation – Pain of osteoarthritis is more towards the evening and less when a patient gets up in the morning. The pain of inflammatory arthritis is more in the morning and less in the evening. Nocturnal pain that interferes with sleep is an ominous sign of malignancy or infection.


    • How long the deformity is present?
    • How did it start?
    • How is it progressing?
    • Any associated symptoms such as giving way, locking, popping, catching, grinding?
    • Is there any history of trauma or infection?
    • Is there any history of patellar instability?

    Limb length discrepancy

    • How long it is present?
    • Is it static or progressive?
    • Associated symptoms?
    • Any history of infection or trauma?

    History to assess function

    • Walking ability
    • Normal or altered
    • Restricted or unrestricted
    • Aided or unaided
    • If aided; which aid is used
    • Ability to stand, squat and kneel
    • Ability to sit cross-legged
    • Ability to jog, sprint, go up or down the hill, go up or down the stairs
    • Pivoting and cutting ability
    • Ability to stand, squat and kneel


    • Whether associated with chills and rigour, severity continued or intermittent and the treatment is taken.

    History of trauma

    • What was the mechanism of injury? Direct trauma
    • Whether the foot was grounded or not?
    • Any twisting or hyperextension of the knee?
    • What were the symptoms immediately after trauma?
    • Was the patient’s knee deformed?
    • Was there a loud pop?
    • Was he able to walk or use the limb?
    • Was there knee swelling? If yes when it appeared? Effusion of meniscus injury develops late.
    • What was the emergency treatment given?
    • How long the patient was immobilised or advised rest at that time?
    • Did the joint return to pre-injury status after initial treatment?
    • What are the present symptoms? Instability? Locking? Abnormal sounds? Pain? Deformity?
    • What brings the patient now? What does he want?

    Past history

    • History of similar episodes in the past
    • Past injuries and their treatment
    • Hypertension
    • Diabetes mellitus
    • Inflammatory arthropathy
    • Septic arthritis
    • Tuberculosis
    • Umbilical sepsis
    • H/o prolonged IV infusion in childhood
    • Blood Dyscrasias
    • Frequent episodes of bleeding
    • Frequent episodes of infection
    • H/o Childhood limping
    • Previous hospital admission
    • Previous surgery
    • Previous trauma

    Personal history

    • Prolonged drug intake
    • Alcohol abuse
    • Smoking
    • Diet
    • Menstrual history
    • Occupational history
    • Recreational activities
    • Treatment History
    • Family history
    • Any family history of dwarfism
    • Any family history of angular deformities
    • Metabolic disorders
    • Similar illness
    • Tuberculosis


    Head to foot examination

    • Eyes- Blue sclera, iritis, uveitis, squint, microphthalmos, cornea, pigmentation of the sclera.
    • Pinna- Low set, blackish discolouration.
    • Cheeks- Malar rash.
    • Mouth – Normal dental hygiene, arch of the palate.
    • Hair Line- Normal or low
    • Neck – Webbing, thyroid swelling.
    • Nipples- Normal level or not.
    • The shape of the chest wall- Pectus carinatum/ excavatum.
    • Abdomen- Protuberant , undescended testis , hernias.
    • Nails- Pitting.
    • Palms and soles- Hyperkeratosis.
    • Thickening of lower end radius, malleoli and costochondral junctions.
    • Ligamentous laxity (Wynne-Davis Criteria- 3 out of 5 needed for diagnosing generalized laxity)
    • Apposition of thumb to flexor aspect of the forearm?
    • Passive extension of fingers so that they lie parallel to the forearm.
    • Hyperextension of elbow at least 10 degrees
    • Hyperextension of knee at least 10 degrees
    • Excessive passive dorsiflexion of ankle (45 degrees) with eversion of the foot.
    • Neurocutaneous markers


    • Watch how the patient walks into the examination room. Is the gait normal? Is it painful? Is any deformity or shortening? Is there any incoming?
    • Make the patient stand with his feet and knee together. Look for any varus or valgus deformity by observing the patient from the front. Observe from the side to identify any flexion deformity or hyperextension deformity. Look at the popliteal fossa from behind. Observe muscle bulk and symmetry especially of the quadriceps.
    • Make the patient sit on a chair with the knee bend to 90 degrees. Observe the position of the patella. In the normal, the anterior surface of the patella will be at an angle of 45 degrees to the floor and it will be placed centrally within the femoral trochlea. In patella Alta, it will be more horizontal and in patella infra, it will be more vertical.
    • Make the patient lie supine on a couch. Look suprapatellar and parapatellar fullness. Observe the position of the tibial tuberosity.
    • Look at the shape of the bones of the knee and the soft tissues to detect any swelling or muscle wasting.
    • Observe the medial and lateral surfaces of the knee from either side.
    • Make the patient prone and observe the back of the thigh, popliteal fossa and the calf.


    • First feel for elevated temperature with the dorsum of examiners fingers at the joint line, patella, suprapatellar pouch, femoral and tibial condyles, popliteal fossa and the calf. Many times it helps to pinpoint the area of pathology.
    • When palpating anatomic structures, feel for tenderness, break in continuity, swelling, thickening and their position in relation to normal location.
    • First, flex the knee to 90 degrees to locate the joint line. Palpate the joint line on the medial and lateral side, palpate the medial and lateral femoral condyles, then palpate the tibial condyles and the tibial tuberosity. From the tibial tuberosity palpate up the patellar tendon to the inferior pole of the patella. Extend the knee, displace the patella laterally and medially and then insinuate the examiner’s fingers to feel the undersurface of patella.
    • Palpate the superior border of patella and then roll the fingers superolaterally and superomedially to detect synovial thickening. Palpate the suprapatellar pouch for any synovial thickening and loose bodies. Milk the suprapatellar pouch down to evacuate the fluid to the area beneath the patella and do the Patellar tap test
    • Palpate down towards the tibia. Palpate the fibular head and the common peroneal nerve winding around it. Place the knee into the figure 4 position and feel the cord like fibular collateral ligament from the fibular head to the lateral epicondyle.
    • Make the patient prone, palpate the back of thigh, popliteal fossa and the calf. Palpate the hamstrings and feel for the popliteal pulse.


    • Movements of the knee occur in the sagittal plane. Normal range of movements of the knee is from 5-10 degrees of hyperextension to 135 degree flexion. Movements should be assessed actively and passively and should be measured with a goniometer. During passive movements the amount of joint play and the quality of end point should be assessed. The end point may be of six types; tissue approximation, capsular feel spasm, springy block, empty feel or bone to bone.
    • If movement is painful then the relationship between the appearance of pain and the resistance to the movement should be noted. In acute conditions, the pain appears before resistance to movement. The appearance of pain and resistance to movement appear together in subacute conditions. Resistance to movement occurs before the appearance of pain in chronic conditions.


    Q Angle

    • It is the angle between the axis of the pull of the quadriceps and the axis of the patellar tendon. Normally is 10-200. It should be measured in full extension, 300 flexions and in the sitting position with knee flexed to 900 (tubercle-sulcus angle). Mark the centres of the patella, tibial tuberosity and the anterior superior iliac spine (ASIS). Draw a line from the centre of ASIS through the centre of the patella and beyond. Draw another line from the centre of tibial tuberosity to the centre of the patella and beyond. Measure the angle between the lines.


    Measure the circumference at the following levels.

    • At the joint line
    • 2- 5 cm above the joint line to assess effusion or vastus medialis obliquus wasting=
    • 3- 15 cm above the joint line to assess quadriceps bulk
    • 4- 15 cm below the joint line to assess the calf muscle bulk


    Special tests are done to detect specific disorders or to detect injury to specific anatomic structures. Four sets of tests are usually done; one set each for evaluation of knee joint effusion, patellofemoral disorders, meniscus or articular cartilage lesions and ligamentous instability.

    Special tests to detect knee effusion

    Patellar tap test

    • Patient position – Supine.
    • Joint position – Knee maximally extended. Quadriceps relaxed.
    • Procedure – Milk the suprapatellar pouch to displace the fluid collected there into the retropatellar area. Sharply tap the patella posteriorly towards the femoral trochlea.
    • Interpretation – If there is moderate effusion the patella will be floating with no contact with the femur. When tapped it will move posteriorly till it contacts the femur and bounces back. It needs about 50 ml of fluid within the joint to make the patellar tap test positive.

    Fluctuation test

    • Patient position- Supine.
    • Joint position- Knee maximally extended. Quadriceps relaxed.
    • Procedure- Milk the suprapatellar fossa to displace the maximal amount of fluid into the rest of the joint cavity. Place index finger and thumb of one hand on either side of patella superiorly. Place the index finger and thumb of another hand on either side of the patella inferiorly. Alternatively, press the fingers of either hand to elicit fluctuation.
    • Interpretation- In presence of effusion, fluctuation can be elicited between the fingers.

    Stroke test

    • Patient position- Standing.
    • Joint position- Knee fully extended. Quadriceps relaxed.
    • Procedure- Gently stroke the lateral aspect of the knee from the superolateral aspect of the patella to the lateral joint line. Observe the medial side for a wave-like displacement of fluid. Repeat the same on the medial side.
    • Interpretation- Will be positive in presence of effusion. Effusion is graded as follows.
    • Zero – No wave produced on downstroke
    • Trace – Small wave on the medial side with a downstroke
    • 1+ – Larger bulge on the medial side with dowstroke\2+ – Effusion spontaneously returns to the medial side after upstroke (no downstroke necessary)\3+ – So much fluid that it is not possible to move the effusion out of the medial aspect of the knee

    Special tests for patellofemoral disorders

    Fairbank Apprehension Test

    • Patient position- Supine on the examination couch.
    • Joint position- Knee extended. Quadriceps relaxed.
    • Procedure- Hold the patella by placing the examiner’s fingers on the medial and lateral border of the patella. Try to displace the patella. Note the response of the patient.\
    • Interpretation- Discomfort or apprehension during the test indicates patellar instability.

    Patellar glide test

    • Patient position – Supine on the examination couch
    • Joint position – Knee flexed to 300. Quadriceps relaxed.
    • Procedure – Hold the patella by placing the examiner’s fingers on the medial and lateral border of the patella. Try to displace the patella medially and laterally. Note the amount of displacement possible as the percentage patellar width or in millimetres.
    • Interpretation – If the medial glide is less than 25% or <5mm, then there is tightness of the lateral patellar retinaculum. If the medial or lateral glide is more than 75%, then there is a laxity of the parapatellar retinaculum. Discomfort or apprehension during the test indicates patellar instability.

    Patellar tilt test

    • Patient position- Supine on the examination couch
    • Joint position- Knee kept in extension. Quadriceps relaxed.
    • Procedure- Hold the patella by placing the examiner’s fingers on the medial and lateral border of the patella. Try to lift the medial border of the patella off the femur while depressing the lateral border and vice versa. Note the amount of tilt possible.
    • Interpretation- Normally lateral border can be tilted slightly beyond the horizontal. If the lateral border can be tilted less than normal then there is tightness of the lateral patellar retinaculum. If the medial border can be tilted more if there is laxity of the medial patella retinaculum.

    Clarke’s patellar grind test

    • Patient position- Supine on the examination couch
    • Joint position- Knee extended. Quadriceps relaxed.
    • Procedure- Examiner places his hand on the patella and compresses the patella against the femur. Ask the patient to contract his quadriceps muscle actively.
    • Interpretation- Pain indicates disease of the articular cartilage of the patella.

    McConnell’s test

    • Patient position- Seated on the couch with legs hanging down the edge of the table.
    • Joint position- Knee bend to 90 degrees.
    • Procedure- Ask the patient to externally rotate the limb while performing resisted isometric contractions of the quadriceps at 0, 30, 600, 90 and 120 degrees. During these resisted isometric quadriceps contractions, apply a medially directed pressure and laterally directed pressure on the patella.
    • Interpretation- Pain or discomfort during isometric contractions when applying laterally directed pressure indicates symptoms due to patellar maltracking.

    Patellar tracking

    • Patient position- Seated with the knee flexed and limb hanging freely
    • Procedure- Ask the patient to move the knee joint actively through the entire arc of flexion extension several times. Observe the movement of the patella.
    • Interpretation- Normally the patella progressively becomes engaged in the trochlea with increasing degrees of knee flexion. Patella is pulled axially by the rectus femoris and the vastus intermedius and obliquely by the vastus lateralis and the vastus medialis. Static stabilization is provided by the medial and lateral parapatellar retinaculum. The shape of the trochlea and the position of the patella and the location of tibial tuberosity also influence patellar tracking. J sign is seen if the patella was laterally subluxated in full extension and suddenly moves medially and engages the trochlea during flexion.

    Special tests for meniscus pathology

    McMurray’s test

    • Patient position- supine on the examination couch.
    • Joint position- Knee flexed fully. Quadriceps relaxed. Procedure- Hold the foot of the patient with one hand. On the other hand, stabilize the knee and keep one finger on the joint line. To test for medial meniscus, apply valgus and external rotation stress on the knee. Gradually extend the knee fully. To test lateral meniscus, apply a varus and internal rotation stress.
    • Interpretation- If clicks or thud from the joint, or if the patient complains of pain then the test is positive for the meniscus injury.

    Bragard’s test

    • Patient position – supine on the examination couch
    • Joint position – Knee flexed to 90 degrees.
    • Procedure – Palpate the medial joint line for tenderness in neutral rotation. Extend the knee and externally rotate the knee and palpate for medial joint line tenderness. Interpretation- If there is no tenderness in flexion and neutral rotation and if there is tenderness in the medial joint line on extension and external rotation, the test is positive for the medial meniscus injury. The reason is that the medial meniscus becomes more anterior in extension and external rotation.

    Steinman’s first test

    • Patient position – Supine
    • Joint position – Hip flexed. Knee flexed to 90.
    • Procedure – Rotate the tibia externally and internally. Interpretation- Pain on external rotation indicate medial meniscus injury and pain on external rotation indicate lateral meniscus injury.

    Bounce home test

    • Patient position – Supine.
    • Joint position – Knee fully flexed.
    • Procedure – Keep the heel of the patient’s foot in the palm and allow the knee to extend.
    • Interpretation – Normally the knee will extend fully. Limitation of full extension with a rubbery end feel is suggestive of a locked knee due to bucket handle tear of the meniscus.

    Steinman’s second test

    • Patient position – supine on the examination couch.
    • Joint position – Knee flexed fully.
    • Procedure – Palpate the joint line for tenderness with the knee in flexion and in extension.
    • Interpretation – If the area of tenderness moves posteriorly with knee flexion and anteriorly with knee extension then the test is positive for the meniscus Injury.

    Apley’s grinding test

    • Patient position – Prone
    • Joint position – Knee flexed to 90 degrees.
    • Procedure – Fix the limb by placing the knee of the examiner on the patient’s thigh. Hold the foot of the patient. Distract the knee and rotate internally and externally. Give axial compression and rotate internally and externally. Note any restriction or excessive rotation and pain during these manoeuvres.
    • Interpretation – More pain during compression indicate meniscus injury and more pain during distraction indicate ligamentous injury.

    Bohler’s test

    • Patient position – supine on the examination couch.
    • Joint position – Knee extended.
    • Procedure – Apply valgus stress and varus stress.
    • Interpretation – Pain felt at the medial joint line on varus stress indicate medial meniscus injury and pain felt at the lateral joint line on valgus stress indicate lateral meniscus injury.

    Thessaly test

    • Patient position – Standing on the affected limb. Another limb is off the ground. The examiner supports the patient by holding extended hands.
    • Joint position – Knee flexed to 5 degrees and then to 20 degrees.
    • Procedure – Ask the patient to twist the body to the left and the right side to rotate the weight-bearing knee internally and externally.
    • Interpretation – Pain felt at the joint line indicate meniscus or chondral lesion.
    • Reliability of Thessaly test – Sensitivity of 90.3%, specificity of 97.7%, the positive predictive value of 98.5%, the negative predictive value of 86.0%, the likelihood ratio for a positive test of 39.3, likelihood ratio for a negative test of 0.09, and diagnostic accuracy of 88.8%.
    • Harrison BK, Abell BE, Gibson TW – The Thessaly test for detection of meniscal tears: validation of a new physical examination technique for primary care medicine. Clin J Sports Med.  2009 Jan;19(1):9-12. doi: 10.1097/JSM.0b013e31818f1689.

    Squat test (Ege’s test)

    • Patient position – Standing on both lower limbs.
    • Joint position – Hip and knee extended.
    • Procedure – Ask the patient to squat first with the foot turned in internal rotation and then in external rotation.
    • Interpretation – Pain on squatting with the foot externally rotated indicate medial meniscus lesion and pain with a foot in internal rotation indicate lateral meniscus lesion.

    Duck walking test (Childress test)

    • Patient position – Sitting in the deep squatting position.
    • Joint position – Hip and knee in maximum flexion.
    • Procedure – Ask the patient to duck walk in deep knee flexion.
    • Interpretation – Pain felt at the joint line suggestive of meniscus lesion.

    Merkel’s test

    • Patient position – Standing on the affected lower limb with the other limb off the ground.
    • Joint position – Knee in extension.
    • Procedure – Ask the patient to slightly bend the knee and then rotate the body to the left and right.
    • Interpretation – Pain felt at the joint line indicate meniscus pathology.

    Peyer’s test

    • Patient position – Sitting in the cross-legged sitting position (Turkish or Indian sitting position)
    • Joint position – Hip in flexion and external rotation. Knee fully flexed.
    • Procedure – Ask the patient to sit in the Turkish sitting position.
    • Interpretation – Pain on the medial aspect of the knee indicate medial meniscus lesion.

    Helfet’s test

    • Patient position – Seated on the couch with a limb hanging over the edge of the couch.
    • Joint position – Knee flexed to 90 degrees.
    • Procedure – Ask the patient to extend the knee. Note the position of the tibial tuberosity in relation to the midline of the patella.
    • Interpretation – During extension, the tibia externally rotates during the final degrees of knee extension as the medial femoral condylar articular surface is longer than the lateral femoral condyle. Hence the tibial tuberosity becomes more laterally placed in full extension. If the normal external rotation is absent it indicates injury to the medial meniscus.

    Tests for ligamentous instability

    Valgus stress test

    • Purpose – To assess the structural integrity of the medial collateral ligament.
    • Patient position – supine on the examination couch.
    • Joint position – Initially the knee is flexed to 30 degrees. Then the knee is kept in 0-degree extension.
    • Procedure – Hold the leg with one hand at the ankle. With the other hand hold the knee in such a way that the thumb is over the medial joint line to detect the amount of opening of the joint and the other fingers are on the lateral side to act as the fulcrum for the application of valgus stress. Bend the knee to 30 degrees and apply valgus stress. Note the amount of widening of the medial joint line. Repeat the test at 0-degree extension. Do the test on the other limb and compare the amount of widening.
    • Interpretation – If there is widening of the medial joint space in excess to the normal side in 30-degree flexion of the knee there is an injury to the medial collateral ligament. If there is excessive opening up of medial joint space in 0 extensions as well as in 30-degree flexion, then there is an injury to the MCL and the cruciate ligaments. The laxity is graded as follows. 0-5mm opening in comparison to the opposite side. 5-10mm opening >10mm opening

    Varus stress test

    • Purpose – To assess the structural integrity of the fibular collateral ligament.
    • Patient position – supine on the examination couch.
    • Joint position – Initially the knee is flexed to 30flexion. Then the knee is kept in 0-degree extension.
    • Procedure – Bring the lower limb of the patient beyond the edge of the table. Hold the leg with one hand at the ankle. With the other hand hold the knee in such a way that the thumb is over the lateral joint line to detect the amount of opening of the joint and the other fingers are on the medial side to act as the fulcrum for the application of varus stress. Bend the knee to 30 degrees and apply varus stress. Note the amount of widening of the lateral joint line. Repeat the test at 0-degree extension. Do the test on the other limb and compare the amount of widening.
    • Interpretation – If there is widening of the lateral joint space in excess to the normal side in 30-degree flexion of the knee there is an injury to the lateral collateral ligament. If there is the excessive opening up of lateral joint space in 0-degree extension then there is an injury to the LCL and the cruciate ligaments. The laxity is graded as follows.
    • 0-5mm opening in comparison to the opposite side.
    • 5-10mm opening
    • >10mm opening

    Cabot manoeuvre

    • Patient position – Supine.
    • Joint position – Knee kept in figure of 4 position.
    • Procedure – Feel the lateral collateral ligament as a cord-like structure between the lateral epicondyle and fibular head.
    • Interpretation – Inability to feel the lateral collateral ligament as a cord-like structure indicate injury.

    Lachmann- Tillat test

    • Patient position – Supine
    • Joint position – Knee flexed to 15 degrees. Slight external rotation of the hip helps in relaxing the quadriceps muscle.
    • Procedure – Stabilize the distal femur with one hand and stabilize the proximal tibia with the other hand. If the patient’s thigh is of large size, then the examiner places his bend knee under the patient’s thigh and one hand over the distal femur to stabilize the knee. Apply anteriorly directed and then posteriorly directed force on the proximal tibia.
    • Interpretation – Excessive anterior translation of tibia when compared to the opposite side with a soft endpoint is suggestive of anterior cruciate ligament injury. Excessive posterior translation of tibia, when compared to the opposite side with a soft endpoint, is suggestive of posterior cruciate ligament injury.
    • Validity – Sensitivity ranges from 80-99%. Specificity under anaesthesia is 95%.

    Anterior drawer test

    • Patient position – Supine.
    • Joint position – Hip flexed to 45° and knee flexed to 90°.
    • Procedure – Sit on the patient’s foot in neutral rotation to stabilize it. Palpate the hamstring tendons to ensure that they are relaxed. Observe from the side to rule out any posterior sagging of tibia suggestive of posterior cruciate ligament tear. Place the hands behind the proximal tibia and thumbs on either side of the patellar tendon with the tip of the thumb over the femoral condyles. Apply an anteriorly directed force to the proximal tibia. Should be done in neutral rotation, 30-degree internal rotation and 30-degree external rotation.
    • Interpretation – Increased anterior displacement of tibia when compared with the opposite side is indicative of an anterior cruciate ligament tear. It may be falsely negative in patients with bucket handle meniscus tear with locking. External rotation tightens the PCL and the posterolateral corner and if they are intact the test is negative in external rotation.
    • Validity – Sensitivity increases when performed under anaesthesia. Sensitivity is less in acute injuries. The sensitivity of the test is between 20-40% in acute cases and between 40-70% in chronic cases. The sensitivity of the test is between 60-95% when examined under anaesthesia.

    Posterior drawer test

    • Patient position – Supine.
    • Joint position – Hip flexed to 45° and knee flexed to 90°.
    • Procedure – Examiner sits on the subject’s foot in neutral rotation to stabilize it. Palpate the hamstring tendons to ensure that they are relaxed. Place the hands around the proximal tibia and thumbs on the tibial tuberosity. Apply a posteriorly directed force to the proximal tibia.
    • Interpretation – Increased posterior tibial displacement compared with the opposite side is indicative of posterior cruciate ligament tear.
    • Validity-

    External rotation recurvatum test

    Sag test

    • Patient position – Supine.
    • Joint position – Hip flexed to 45° and knee flexed to 90°. Stabilise the foot in neutral rotation.
    • Procedure – Observe the position of the tibia in relation to the femoral condyles. Normally the tibial tuberosity lies one centimetre anterior to the femoral condyles resulting in a step-off.
    • Interpretation – When the posterior cruciate ligament is torn, the tibia is subluxated posteriorly due to the effect of gravity.
    • Validity-

    Godfrey’s test

    • Patient position – Supine.
    • Joint position – Hip flexed to 90° and knee flexed to 90°. Stabilise the foot in neutral rotation. Ask the patient to extend the knee.
    • Procedure – Observe the position of the tibia in relation to the femoral condyles. Normally the tibial tuberosity lies one centimetre anterior to the femoral condyles resulting in a step-off.
    • Interpretation – When the posterior cruciate ligament is torn, the tibia is subluxated posteriorly due to the effect of gravity. The active contraction of the quadriceps leads to the reduction of gravity-induced posterior subluxation of tibial condyles.

    Quadriceps active test

    • Knee flexed to 150 ask the patient to contract the quadriceps keeping the knee in flexion.

    Actively resisted extension test

    • Keep the knee in 150 flexions. Ask the patient to extend the knee against resistance.

    Patellar reflex reduction test

    • Keep the knee in 300 flexions. Elicit patellar tendon reflex. Active quadriceps contraction leads to correction of posterior sag.

    McIntosh’s Pivot shift test

    • Patient position – Supine
    • Joint position – Knee extended.
    • Procedure – Examiner lifts up the patient’s leg with the knee in extension by holding at the ankle with one hand. Apply an internal rotation force. On the other hand, support the limb with the palm over the posterolateral aspect of the knee close to the fibular head. Apply a strong valgus force and flex the knee.
    • Interpretation – Pivot shift is anterior subluxation of lateral tibial condyle when the knee is extended and the reduction of subluxation when the knee is flexed. Internal rotation exaggerates the subluxation and the valgus force prevents easy reduction of subluxation. When the knee is flexed with valgus force initially the lateral tibial condyle remains subdued and suddenly gets reduced beyond 30-degree flexion with a demonstrable thud. When the knee is flexed the iliotibial band passes posterior to the centre of rotation of the knee exerting a posterior pull reducing the anterior subluxation of the lateral tibial condyle.

    Noye’s flexion rotation drawer test

    Noyes glide pivot shift test

    • Pivot shift test is done with axial compression and without internal rotation.

    Hughston’s jerk test

    • Pivot shift demonstrated from flexion to extension. It demonstrates the subluxation of the lateral tibial condyle anteriorly during extension. It is done with valgus stress and internal rotation while the knee is moved from flexion to extension.

    Losee’s test

    Slocum’s Anterolateral Rotary Instability (ALRI) Test /Larson’s test

    • Patient position – patient lies in the lateral position with the affected limb up. The pelvis is tilted slightly posteriorly. The affected limb rests with only the heel in contact with the examination couch with the knee in extension. This will exert internal rotation stress on the knee leading to anterior subluxation of the lateral condyle of the tibia.
    • Joint position – Knee in extension.\
    • Procedure – Lift up the limb by holding the ankle with one hand to apply valgus stress on the knee. Keep the other hand on the joint line. Flex the knee.
    • Interpretation – If there is rotatory instability due to ACL deficiency, the knee can be felt to reduce at about 400 of flexion.

    Reverse pivot shift test

    • Patient position – Supine
    • Joint position – Knee flexed.
    • Procedure – Examiner lifts up the patient’s leg with the knee in flexion by holding at the ankle with one hand. Apply an external rotation force. On the other hand, support the limb with the palm over the lateral aspect of the knee. Apply a strong valgus force and extend the knee.
    • Interpretation – Reverse pivot shift is posterior subluxation of lateral tibial condyle when the knee is flexed and the reduction of subluxation when the knee is extended. External rotation exaggerates the subluxation and the valgus force prevents easy reduction of subluxation. When the knee is extended with valgus force, initially the lateral tibial condyle remains subdued and then suddenly gets reduced with extension with a demonstrable thud.

    Tests for posterolateral corner injuries

    Tibial external rotation test (Dial test)

    • Patient position- Prone.
    • Knee tested in 30-degree flexion and 90-degree flexion
    • Procedure- Hold the foot and externally rotate the knee on both sides. Compare the amount of external rotation present on both sides.
    • Interpretation- If the amount of external rotation on the affected side exceeds the other side by more than 10 degrees then there is PLC injury.

    External rotation recurvatum test

    • Patient position – Supine.
    • Joint position – Knee in full extension
    • Procedure – Examiner stands at the foot end of the examination couch. The limb is lifted up by holding the big toe which hill exert varus-external rotation-extension stress on the knee. Assess the amount of hyperextension, external rotation and varus that is present on both limbs.
    • Interpretation – In patients with PLC injury, the affected knee goes into excessive varus hyperextension and external rotation in comparison to the opposite side.

    Posterolateral external rotation drawer test

    • Patient position – Supine.
    • The hip flexed to 45 degrees and the knee is flexed to 90 degrees.
    • Externally rotate the foot and fix it by sitting over it while the hip flexed to 45 degrees and the knee is flexed to 90 degrees. Do a posterior drawer test. Repeat at 30-degree flexion of the knee. Look for posterior subluxation of lateral tibial condyle.\Interpretation- If there is posterior subluxation of lateral tibial condyle when the test was done at 300 knee flexion and is absent at 900 flexions, then there is isolated PLC injury.

    Posteromedial rotational instability test


    Assessment of effusion

    The absence of normal grooves around the patella may indicate a patellar intra-articular effusion. There are two ways to confirm the effusion. The knee is extended fully before the examination begins. This first way is the patellar tap. It is to squeeze the fluid between the patella and the femur by pressing at the medial patella using a non-dominant hand. Then, using the dominant hand to press on the patella vertically. If the patella is ballotable, then patellar intra-articular effusion is present. Another way is the milking of the patella. First, the effusion is milked at the medial border of the patella from the inferior to superior aspect. Then, using another hand, the effusion is milked at the lateral border of the patella from superior to inferior aspect. If the effusion is present, a bulge will be appearing at the medial border of the patella because the effusion is milked back to the medial patella.[rx]

    Assessment of range of motion

    Both the active and passive range of motion should be assessed. The normal knee extension is between 0 to 10 degrees. The normal knee flexion is between 130 to 150 degrees. Any pain, abnormal movement, or crepitus of the patella should be noted. If there is pain or crepitus during active extension of the knee, while the patella is being compressed against the patellofemoral groove, patellofemoral pain syndrome or chondromalacia patellae should be suspected. Pain with active range of motion but no pain during passive range of motion is suggestive of inflammation of the tendon. Pain during active and passive range of motion is suggestive of pathology in the knee joint.[rx]

    Assessment of collateral ligaments

    Valgus stress test can be performed with the examined knee in 25 degrees flexion to determine the integrity of the medial collateral ligament. Similarly, varus stress test can be performed to access the integrity of the lateral collateral ligament. The degree of collateral ligament sprain can also be assessed during the valgus and varus tests. In a first degree tear, the ligament has less than 5 mm laxity with a definite resistance when the knee is pulled. In a second degree sprain, there is laxity when the knee is tested at 25 degrees of flexion, but no laxity at extension with a definite resistance when the knee is pulled. In a third-degree tear, there will be 10 mm laxity with no definite resistance either with knee with full extension or flexion.[rx]

    Assessment of anterior cruciate ligament

    The anterior drawer and Lachman tests can be used to access the integrity of the anterior cruciate ligament. In the anterior drawer test, the person being examined should lie down on their back (supine position) with the knee in 90 degrees flexion. The foot is secured on the bed with the examiner sitting on the foot. The tibia is then pulled forward by using both hands. If the anterior movement of the affected knee is greater than the unaffected knee, then the anterior drawer test is positive. The Lachman test is more sensitive than the anterior drawer test. For the Lachman test, the person lies down in a supine position with the knee flexed at 20 degrees and the heel touching the bed. The tibia is then pulled forward. If there are 6 to 8 millimetres of laxity, with no definitive resistance when the knee is pulled, then the test is positive thus raising concern for a torn anterior cruciate ligament. A large collection of blood in the knee can be associated with bony fractures and cruciate ligament tear.[rx]

    Assessment of posterior cruciate ligament

    Posterior drawer test and tibial sag tests can determine the integrity of the posterior cruciate ligament. Similar to the anterior drawer test, the knee should be flexed 90 degrees and the tibia is pushed backwards. If the tibia can be pushed posteriorly, then the posterior drawer test is positive. In the tibial sag test, both knees are flexed at 90 degrees with the person in the supine position and bilateral feet touching the bed. Bilateral knees are then watched for the posterior displacement of the tibia. If the affected tibia slowly displaced posteriorly, the posterior cruciate ligament is affected.[rx]

    Assessment of meniscus

    Those with meniscal injuries may report symptoms such as clicking, catching, or locking of knees. Apart from joint line tenderness, there are three other methods of accessing meniscus tear: the McMurray test, the Thessaly test, and the Apley grind test. In the McMurray test, the person should lie down in a supine position with the knee should in 90 degrees flexion. the examiner put one hand with the thumb and the index finger on the medial and lateral joint lines respectively. Another hand is used to control the heel. To test the medial meniscus, the hand at the heel applies a valgus force and externally rotate the leg while extending the knee. To test for the lateral meniscus, the varus force, internal rotation are applied to the leg while extending the knee. Any clicking, popping, or catching at the respective joint line indicates the corresponding meniscal tear.[rx]

    In the Apley compression test, the person lie down in a prone position with the knee flexed at 90 degrees. One hand is used to stabilise the hip and another hand grasp the foot and apply a downward compression force while external and internal rotates the leg. Pain during compression indicates meniscal tear. Examination for anterior cruciate ligament tear should be done for those with meniscal tear because these two conditions often occur together.[rx]



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    Clinical Examination of Lower Limb Deformity

    Clinical Examination of Lower Limb Deformity/When a child is born, it has 10-15 degrees of physiological genu varum, 5-degree internal tibial torsion and external rotation contracture of the hip. It reaches the maximum by about 9-12 months. This usually gets corrected to neutral by the age of 18-24 months then the limb develops a valgus angulation, which reaches the maximum of about 12 degrees by the age of 3-4 years. This physiologic valgus usually gets corrected to the adult value of 7 degrees of valgus by the age of 8 years. Physiologic valgus is bilateral and symmetrical; less than 15 degrees and the inter-malleolar distance doesn’t exceed 8 centimetres.

    Tibial torsion is the angle between the transverse axis of the knee and the transmalleolar axis. The tibia is internally rotated at birth. Internal tibial torsion is 5 degrees at birth and gets corrected to neutral by 4-5 years of age. The tibia then gradually becomes externally rotated and reach the adult value of 20-25 degrees of external rotation by the age of 8 years.

    Femoral anteversion is the angle between the transcondylar axis and the longitudinal axis of the femoral neck in the horizontal plane. Femoral anteversion is 40 degrees at birth and reaches the adult value of fewer than 15 degrees by the age of 8 years. It produces intoeing gait which gradually increases during the first five years of life due to the summation of deformities. It gets corrected by 8 years of age.

    The deformity is defined as a deviation from normal structure or function which may be symptomatic or has the potential to produce symptoms.

    Goals of deformity assessment

    The goal of the deformity assessment is to answer the following questions.

    1. Is there a deformity?

    • One should be able to differentiate between physiological and pathologic malalignment.

    2. What is the deformity?

    • Identify the name of the deformity.

    3. Where is the deformity?

    • Identify the site of deformity whether it is at the joint level or in the bone. If in the bone, then it is in the epiphysis, metaphysis or diaphysis. Deformities due to tilting of the joint line becomes less when the joint is flexed. This is because the area of contact between the articular surfaces is altered during flexion.

    4. Which is the plane of deformity?

    • Identify the alteration produced by the deformity in all three planes and any associated limb length discrepancy as well. Thus a deformity may have a component of flexion or extension in the sagittal plane, varus or valgus in the coronal plane, internal or external rotation in the axial plane; in addition, there may be shortening or lengthening as well.

    5. How severe is the deformity?

    • Identify the severity of deformity in each plane and also the severity of limb length discrepancy. Assess how much of passive correction of the deformity is possible.

    6. Why there is a deformity?

    • Identify the cause of the deformity. Identify whether it is a localised problem or part of systemic disease. Try to detect whether it is due to soft tissue contracture, muscle paralysis or spasm or rupture, joint dislocation or subluxation or malformation and lastly bony malunion or nonunion or deformation.

    7. Are there any consequences of the deformity?

    • Identify whether there are any compensatory malposition of neighbouring joints and secondary effects such as osteoarthritis on the concave side or laxity of ligaments on the convex side. Assess whether it is associated with any secondary joint instability such as patellofemoral instability in genu valgum. Identify how it is affecting the gait or joint function.

    8. When does the deformity occur?

    • Identify whether it is a static or dynamic deformity.


    From the history try to understand the relevant details about the deformity, look hints that help identify the cause and understand the secondary effects of the deformity and its impact on function. History should start with the following questions.

    • How long the deformity is present?
    • How did it start?
    • How is it progressing?
    • Any associated symptoms?
    • Is there any history of trauma or infection?

    In children get perinatal history

    • Did the mother take any drugs during pregnancy especially in the first trimester?
    • Did the mother have any infections especially in the first trimester?
    • Did the mother have any history of substance abuse?
    • Is there any maternal health problems?
    • Did prenatal ultrasounds show any abnormality?
    • Was there any abnormality in previous pregnancies?

    Get a natal history in an appropriate case.

    • Was it a full-term delivery?
    • What was the type of delivery?
    • What was the type of presentation at birth?
    • What was the birth weight?
    • Was there any delay in first cry?
    • Were there any complications during delivery?

    Get details of nutrition to assess the chance of nutritional deficiencies like rickets.

    • Vegetarian or non-vegetarian
    • Calorie intake
    • Food fads
    • Exposure to sunlight
    • Whether the diet is balanced or not

    Family history

    • H/o similar or other deformities

    Developmental history

    • When did a social smile appear?
    • When did the child achieve
    • Neck steadiness
    • Sitting
    • Standing
    • Crawling
    • Walking
    • Stair climbing and descending
    • Hand to hand transfer

    General Examination

    • In general examination look for features of generalised ligamentous laxity, general manifestations of rickets or known dysplasias.


    Inspect the patient in standing, sitting, walking and in the supine position. Inspect from the front, back and both sides. Look for any asymmetry in size, shape and function.

    • Look at
    • Head tilt and rotation
    •  Level of shoulders, scapula and iliac crest
    • Look for spinal deformities such as scoliosis or kyphosis
    • Look for lumbar lordosis suggestive of flexion deformity of the hip when the patient is supine on a hard surface
    • Look for knee deformity in all three planes
    • Look for ankle equinus or calcaneus deformity from the side
    • Look for any hindfoot varus or valgus from the back
    • Look for any forefoot or toe deformity


    • Palpate the bone, soft tissues and joints. Look for a change in temperature; the limb with post-polio residual contracture is cold. Look for any tenderness and note the site of tenderness. When palpating bony and soft tissues; look for any asymmetry, thickening, swelling or defect.


    • Assess the active and passive movements of the spine, hip, knee and foot and ankle. Record the range of movement. Look for restriction of range of movement, pain during joint movement, ligamentous laxity, joint instability and any abnormal sounds during joint movement. While moving the joint passively, watch out for muscle spasm. Movement should be assessed in all three planes depending on the normal movement for that particular joint.


    • Measurement is done to detect any limb length discrepancy, to assess the degree of muscle wasting. Limb length discrepancy may be true or functional. True LLD is due to real shortening or lengthening. Functional LLD is due to abnormal joint positioning such as adduction contracture of the hip. The girth of the thigh is measured 15 cm above the knee joint line and the girth of the calf is measured at the bulkiest area.
    • In addition, measure the intercondylar distance between medial femoral condyles in the standing position for genu varum. In cases of genu valgum measure the intermalleolar distance in the standing position.

    Torsional profile of the lower limb

    • Torsional abnormalities may be in the femur, tibia or foot. Torsional abnormalities lead to either in-toeing or out-toeing. Intoeing is more common. The commonest cause of in-toeing in children below one year is metatarsus adductus, commonest cause from 1-3 years is internal tibial torsion, and after 3 years of age excessive femoral anteversion is the commonest cause. It is identified by assessment of foot progression angle. Foot progression angle is the angular difference between the direction of walking and the long axis of the foot. If the foot is externally rotated then the angle is positive and if internally rotated then the angle is negative. The normal value for children and adolescents is 10 degrees.

    Femoral anteversion is assessed by doing Craig’s test. It is done in the following method.

    • Patient position – Prone
    • Joint position – Knee flexed to 90 degrees.
    • Procedure- One hand of the examiner is placed flat on the greater trochanter. Hold the leg and gently rotate the hip in both directions till the greater trochanter is maximally prominent. The amount of internal rotation needed to make the greater trochanter maximally prominent is the degree of anteversion.
    • In addition, the range of rotational movement of the hip is also recorded. The patient is made prone and the pelvis is made level. Then rotate the hip internally and externally to the maximum point to which it is maintained by gravity alone. In patients with excessive femoral anteversion, the range of internal rotation is increased and external rotation is diminished. In femoral retroversion, the external rotation is increased and internal rotation diminished.
    • Tibial torsion is assessed by the thigh foot angle or angle of the transmalleolar axis.

    Thigh foot angle is assessed by the following method.

    • Patient position – Prone
    • Joint position – Knee flexed to 90 degrees, ankle in neutral position.
    • Procedure – Measure the angle between the thigh axis and the foot axis. Angle is negative if internally rotated and positive if externally rotated. Normally the angle is 10 degrees in adults. In the newborn, there is 5 degrees internal tibial torsion normally.
    • If the foot is not normal, then measure the angle of the transmalleolar axis.
    • Patient position – The patient is asked to lie prone on a couch with the knee flexed to 90 degrees.
    • Procedure – The centre of each malleolus are marked. Connect these points by a line across the plantar surface of the sole. Draw a line perpendicular to it.
    • Interpretation – The angle between the thigh axis and a line perpendicular to the transmalleolar axis is measured, which is equal to the tibial torsion.
    • Torsional deformity of the foot is assessed by the heel bisector line. The heel bisector line divides the heel into two equal halves in the longitudinal axis. In the normal foot, it passes through the second toe. If it passes medial to the second toe, the forefoot is abducted and if it passes lateral to the second toe, the forefoot is adducted. If it passes through the third metatarsal, adduction deformity is mild, through the fourth metatarsal is considered moderate and through the fifth metatarsal is considered to be severe metatarsus adductus.
    • In newborn feet, V- finger test is done to assess the forefoot adduction. The heel of the child is placed in the second interdigital cleft of the examiner. Normally the lateral border of the foot is straight and will be in contact with the examiner’s finger. If the lateral border of the foot beyond the fifth metatarsal base is not in contact with the examiner’s finger due to medial deviation, then there is metatarsus adductus deformity.

    Angular profile of the lower limb

    • Angular deformities may be physiological or pathological. It is more likely to be pathological if it is unilateral; asymmetrical; painful or if progressive.
    • Ask the patient to stand with his feet and knee touching each other while the patella is facing forwards. When inspected from the front, there will be a gap between the knees in patients with genu varum. In patients with genu valgum, the ankles will be kept apart. Inspect from the side, specifically looking for equinus or calcaneus deformity of the ankle, flexion deformity or hyperextension deformity of the knee.
    • Ask the patient to lie supine on a hard couch and look for any lumbar lordosis suggestive of fixed flexion contracture of the hip. If present does the Thomas test to assess the severity of flexion deformity.

    Thomas well leg raising test

    • Patient position- Supine
    • Examiner position – Stand on the right side of the patient with one hand under the lumbar spine of the patient. With the other hand hold the unaffected side.
    • Procedure- Flex the unaffected knee fully, then flex the unaffected hip till the excessive lumbar lordosis disappears. Measure the angle between the thigh of the affected side and the couch to assess the angle of fixed flexion deformity of the hip.
    • Intercondylar distance is measured to assess the severity of genu varum deformity. Ask the patient to stand with his medial malleoli touching each other and then measure the distance between the medial femoral condyles. Intermalleolar distance is measured in patients with genu valgum deformity. Ask the patient to stand with his medial femoral condyles touching each other and the foot should be in neutral rotation, measure the distance between the medial malleoli. Both these measurements have the disadvantage of being influenced by the size of the patient. In this situation, measurement of the tibiofemoral angle using a goniometer is essential. This is measured in the standing position. Lateral thigh leg angle is measured by keeping the arms of the goniometer on the lateral surface of the thigh and leg and the hinge of the goniometer at the level of the knee. Another method is by keeping the arms of the goniometer on the anterior surface of the thigh and leg and the hinge of the goniometer over the centre of the patella.

    In patients with genu valgum, one should do the Ober’s test to rule out ITB contracture and assess the patient for patellofemoral instability. Measure the standing height, sitting height and arm span of the patient.

    Assessment of lower limb length discrepancy

    • Limb length discrepancy(LLD) may be true or functional. True limb length discrepancy is due to shortening or lengthening of bone or joint dislocation. Functional LLD is due to abnormal joint positioning such as pelvic obliquity due to adduction contracture or flexion deformity of the knee.
    • LLD may be due to abnormal pelvic height, femoral length, tibial length or foot height. LLD may lead to abnormal gait, cosmetic problem, osteoarthritis due to abnormal weight transmission or a low backache. LLD up to 2 cm at skeletal maturity is considered physiological as only about 25-30% of normal population have equal limb length. The left lower limb is longer than the right in a ratio of 3.5:1.
    • When the patient is standing; assess whether the shoulder, iliac crest and the popliteal and the gluteal creases are at the same level. Look for compensatory scoliosis, which will disappear if the patient is made to sit. LLD may be masked by flexion of the opposite knee and plantar flexion of the ankle.
    • LLD is best measured using blocks of known height under the foot of the affected side; till the pelvis is level and the compensatory lordosis disappears. Lower limb length measurement includes measurement of the whole lower limb and measurement of the length of individual limb segments. Whole length measurement is done either by placing blocks of known thickness under the shorter limb till the pelvis is level or by measuring using a measuring tape.

    With measuring tape; measure both the true length and apparent length. Apparent length is measured from the xiphisternum or umbilicus to the inferior tip of the medial malleolus when the limbs are kept parallel. To measure the true length, both the limbs should be kept in an identical position. Hence if there is a fixed adduction deformity of the hip; first make the pelvis level by adducting the affected hip till both the anterior superior iliac spines (ASIS) are at the same level. Measure the true length if the affected limb from the inferior edge of ASIS to the inferior edge of the medial malleolus. Now keep the opposite hip also in an identical degree of adduction and then measure the other side as well.

    The lower limb has 4 segments; subtrochanteric (pelvic), intertrochanteric (femur), tibial and foot segments. The intertrochanteric segment is measured from the tip of the greater trochanter to the lateral joint line of the knee. The tibial segment is measured from the medial joint line of the knee to the tip of the medial malleolus.

    Supratrochanteric segment is measured by drawing Bryant’s triangle, Nelaton’s line or Shoemaker’s line. Bryant’s triangle is drawn by drawing three lines in the supine position. First-line from the inferior edge ASIS vertically down towards the examination table. Second-line is drawn from the ASIS to the tip of the greater trochanter. The third line is from the tip of the trochanter to the first line. Measure each sides of the triangle and compare it with the other lower limb. The difference in the length of the third line suggests subtrochanteric shortening. Supratrochanteric shortening may be due to hip arthritis, hip dislocation, fracture neck of the femur or coxa vara.

    Galeazzi test or Allis test

    The patient is supine on the table. Flex both the hip and knees and place both the feet together. Note the level of the knee. In the case of LLD, the levels will be different. Now look from the side. If the shortening is in the femoral segment; the level of the knee will be proximal to the other knee and if shortening is in the tibial segment, the knee will be distal to another knee.

    Cover-up test

    Done between the ages of 1-3 years. The child is either standing or lying supine. The part of the tibia distal to the proximal third is covered by a hand and observe the angular relationship between the thigh and proximal tibia. If in neutral or valgus, no need to observe for tibia vara. If in varus then observe to rule out tibia vara.



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    Lower Limb Examination – Technique, Procedure, Result

    The lower limb examination is a skill to elicit neurological signs, such as nerve problems that supply the legs and feet. Patients may present with a number of complaints including altered sensation, for example, pins and needles or numbness or loss of power of a limb. It may be intermittent such as multiple sclerosis or permanent such as motor neuron disease.

    Neuropathies can also occur and can be mono such as foot drop or poly such as “glove and stocking” which can occur in diabetes mellitus.

    A full neurological examination, therefore, includes an assessment of both the motor and sensory systems of the legs. In exams, you may be asked to focus on one part, such as the sensory or the motor. For reference, this guide will include both.

    Procedure Steps

    Step 01

    As with all examinations, the best method is your own – one with which you are comfortable and familiar. The one explained here takes the following format:

    • Tone.
    • Power.
    • Reflexes.
    • Function.
    • Sensation.

    Step 02

    Wash your hands, introduce yourself to the patient and clarify their identity. Explain the procedure you about to perform and obtain consent.

    Step 03

    Ideally, the patient should have their lower body exposed, although for the purpose of the exam the patient will likely be in shorts. Begin by observing the patient’s legs, looking for any muscle wasting, fasciculations, or asymmetry.

    Step 04 – Tone

    Roll the leg on the bed to see if it moves easily, then pulls up on the knee to check its tone. Check for ankle clonus by placing the patient’s leg turned outwards on the bed, moving the ankle joint a few times to relax it, and then sharply dorsiflexing it. Any further movement of the joint may suggest clonus.

    Assess leg tone
    Assess leg tone
    Assess knee tone
    Assess knee tone
    Check for ankle clonus
    Check for ankle clonus

    Step 05 – Power

    Start at the hip asking the patient to abduct, adduct, flex, and extend against your hand so you can assess how much force they can overcome. Do the same for flexion and extension at the knee and ankle as well as the toes.

    Assess hip flexion
    Assess hip flexion
    Assess hip extension
    Assess hip extension
    Assess knee flexion
    Assess knee flexion
    Assess knee extension
    Assess knee extension
    Toe dorsiflexion
    Toe dorsiflexion
    Toe plantarflexion
    Toe plantarflexion

    Step 06 – Reflexes

    There are three reflexes in the lower limb:

    • Patellar reflex
    • Ankle jerk reflex
    • Plantar reflex (elicited by stroking up the lateral aspect of the plantar surface)

    Patellar Reflex

    The patellar reflex is tested by placing the patient’s leg flexed at roughly 60 degrees, taking the entire weight of their leg with your arm, and hitting the patellar tendon with the tendon hammer. It is vital to get your patient to relax as much as possible and for you to take the entire weight of their leg.

    The patellar reflex test
    The patellar reflex test

    Ankle Jerk

    The ankle jerk is elicited by resting the patient’s leg on the bed with their hip laterally rotated. Pull the foot into dorsiflexion and hit the calcaneal tendon.

    The ankle jerk test
    The ankle jerk test

    Plantar Reflex

    Finally, with their leg out straight and resting on the bed, run the end of the handle of the tendon hammer along the outside of the foot. This gives the plantar reflex. An abnormal reflex would see the great toe extending.

    If you struggle with any of these reflexes, asking the patient to clench their teeth should exaggerate the reflex.

    Step 08 – Function

    For the lower limb you should assess the patient’s walking. Observe their gait and check for any abnormalities. Whilst they are standing you should perform Romberg’s test. Ask the patient to stand with their feet apart and then close their eyes. Any swaying may be suggestive of a posterior column pathology.

    Assess patient walking
    Assess patient walking
    Romberg's test
    Romberg’s test

    Step 09 – Sensation

    You should test light touch, pinprick, vibration, and joint position sense, or proprioception.

    Light Touch

    Ask the patient to place their legs out straight on the bed. Lightly touch the patient’s sternum with a piece of cotton wool so that they know how it feels.

    With the patient’s eyes shut, lightly touch their leg with the cotton wool. The places to touch the patient should test each of the dermatomes – make sure you know these! Tell the patient to say yes every time they feel the cotton wool as it felt before.

    Sensation test with cotton wool
    Sensation test with cotton wool

    Pin Prick

    Repeat the last step using a slight pinprick.

    Sensation test with a pin prick
    Sensation test with a pin prick


    To assess vibration you should use a sounding tuning fork. Place the fork on the patient’s sternum to show them how it should feel.

    Now place the tuning fork on their great toe and ask them if it feels the same. If it does, there is no need to check any higher. If it feels different you should move to the tibial epicondyle and then to the greater trochanter until it feels normal.

    Vibration test
    Vibration test


    Finally, assess proprioception. Hold the distal phalanx of the great toe on either side so that you can flex the interphalangeal joint.

    Show the patient that when you hold the joint extended, that represents Up whereas when you hold it flexed that represents Down. Ask the patient to close their eyes and, having moved the joint a few times hold it in one position – up or down. Ask the patient which position the joint is in.

    Flex the interphalangeal joint up
    Flex the interphalangeal joint up
    Flex the interphalangeal joint down
    Flex the interphalangeal joint down


    Allow the patient to dress and thank them.

    Wash your hands and report your findings to the examiner.



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    Plasmapheresis – Indications, Contraindications

    Plasmapheresis is a therapeutic intervention that involves extracorporeal removal, return, or exchange of blood plasma or components. The underlying mechanism of this procedure is accomplished by either centrifugation or filtration using semipermeable membranes. This activity reviews plasmapheresis as a therapeutic intervention that involves extracorporeal removal, return, or exchange of blood plasma or components. This intervention results in a filtered plasma product that can be used for the treatment of numerous diseases. It also highlights the interprofessional team strategies for improving care coordination and communication to advance plasmapheresis and improve outcomes.

    Plasmapheresis is a therapeutic intervention that involves extracorporeal removal, return, or exchange of blood plasma or components. The underlying mechanism of this procedure is accomplished by either centrifugation or filtration using semipermeable membranes. While centrifugation is based on the principle of separation using different specific gravities of various blood components, membrane plasma separation filters blood components based on their particle size.

    The preferred method of plasmapheresis in most centers worldwide is by automated centrifuge-based technology. However, in certain hospitals and patients on hemodialysis, plasmapheresis is done using membrane plasma separation. In plasmapheresis using centrifugation, filtered plasma is discarded, and RBCs and replacement fluid (donor plasma or colloids) are returned. Membrane plasma separation allows selective removal of undesired macromolecules; hence, filtered, processed plasma is returned to the patient, eliminating the need for replacement fluids.

    Indications 0f Plasmapheresis

    Therapeutic plasmapheresis is used for numerous diseases. The conditions involve the presence of a toxic substance in plasma (e.g., immunoglobulin), which can be filtered. The disorders where therapeutic plasmapheresis can be done are grouped into four categories by the Apheresis Applications Committee of the American Society for Apheresis (ASFA). Category 1 includes disorders where plasmapheresis can be done as a first-line treatment, category 2 includes disorders where plasmapheresis can be done as a second-line treatment in addition to the existing standard of care, category 3 includes disorders in which the evidence of the benefit of plasmapheresis is minimal, and therapy must be individualized, and category 4 includes disorders in which the evidence suggests that plasmapheresis is either ineffective or harmful, however, may be considered after approval from the institute ethics committee.

    The alphabetical list of various indications for plasmapheresis, along with their ASFA category, is as follows.

    Category 1

    • Acute inflammatory demyelinating polyradiculoneuropathy/Guillain-Barre syndrome
    • ANCA-associated rapidly progressive glomerulonephritis (dialysis-dependent or associated with diffuse alveolar hemorrhage)
    • Anti-glomerular basement membrane disease-Goodpasture syndrome (dialysis independent or associated with diffuse alveolar hemorrhage)
    • Chronic inflammatory demyelinating polyradiculoneuropathy
    • Focal segmental glomerulosclerosis (recurrent in the transplanted kidney)
    • Hyperviscosity in monoclonal gammopathies
    • Liver transplantation: Desensitization
    • Myasthenia gravis
    • N-methyl D-aspartate receptor antibody encephalitis
    • Paraproteinemic demyelinating neuropathies/chronic acquired demyelinating polyneuropathies (IgA/IgG/IgM mediated)
    • Progressive multifocal leukoencephalopathy associated with natalizumab
    • Renal transplantation: Desensitization and antibody-mediated rejection
    • Thrombotic microangiopathy (Factor H autoantibodies and ticlopidine)
    • Thrombotic thrombocytopenic purpura
    • Wilson disease (fulminant)

    Category 2

    • Acute disseminated encephalomyelitis
    • Cardiac transplantation: Desensitization
    • Catastrophic antiphospholipid syndrome
    • Cryoglobulinemia; symptomatic/severe
    • Dilated cardiomyopathy, idiopathic (NYHA 2-4)
    • Hashimoto encephalopathy: Corticosteroid responsive encephalopathy associated with autoimmune thyroiditis
    • Hematopoietic stem cell transplantation, ABO-incompatible
    • Lambert-Eaton myasthenic syndrome
    • Multiple sclerosis
    • Myeloma cast nephropathy
    • Neuromyelitis Optica spectrum disorders
    • Overdose, envenomation, and poisoning, such as mushroom
    • Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS)
    • Phytanic acid storage disease (Refsum disease)
    • Systemic lupus erythematosus (severe)

    Category 3

    • Acute liver failure
    • ANCA-associated rapidly progressive glomerulonephritis (dialysis independent)
    • Anti-glomerular basement membrane disease, Goodpasture syndrome (dialysis-dependent, no DAH)
    • Aplastic anemia, pure red cell aplasia
    • Autoimmune hemolytic anemia
    • Burn shock resuscitation
    • Cardiac neonatal lupus
    • Cardiac transplantation: Antibody-mediated rejection
    • Chronic focal encephalitis (Rasmussen encephalitis)
    • Complex regional pain syndrome; chronic
    • Erythropoietic porphyria, liver disease
    • Hemolysis liver enzymes low platelet (HELLP) syndrome (postpartum)
    • Hematopoietic stem cell transplantation, HLA desensitization
    • Hemophagocytic lymphohistiocytosis; hemophagocytic syndrome; macrophage activating syndrome
    • Henoch-Schonlein purpura
    • Heparin-induced thrombocytopenia and thrombosis
    • Hypertriglyceridemic pancreatitis
    • Immune thrombocytopenia; refractory
    • IgA nephropathy; crescentic
    • Lung transplantation: Desensitization and antibody-mediated rejection
    • Paraneoplastic neurological syndromes
    • Pemphigus Vulgaris; severe
    • Pruritus due to hepatobiliary diseases
    • Scleroderma (systemic sclerosis)
    • Sepsis with multiorgan failure
    • Stiff-person syndrome
    • Thrombotic microangiopathy (complement factor gene mutations, MCP mutations, clopidogrel, and calcineurin inhibitors)
    • Thyroid storm
    • Toxic epidermal necrolysis (refractory)
    • Vasculitis
    • Voltage-gated potassium channel antibodies

    Category 4

    • Amyloidosis, systemic
    • Dermatomyositis/polymyositis
    • HELLP syndrome (antepartum)
    • Lupus nephritis
    • Thrombotic microangiopathy (gemcitabine and quinine)

    Contraindications of Plasmapheresis

    The contraindications for therapeutic plasmapheresis are as follows:

    • Non-availability of central line access or large bore peripheral lines
    • Hemodynamic instability or septicemia
    • Known allergy to fresh frozen plasma or replacement colloid/albumin
    • Known allergy to heparin
    • Hypocalcemia (restricts the use of citrate as an anticoagulant during the procedure); relative contraindication
    • Angiotensin-converting enzyme (ACE) inhibitor used in last 24 hours; relative contraindication


    Venous access for this procedure is either by a central venous catheter or large bore peripheral lines. There are multiple manufacturers of centrifuge-based plasmapheresis machines.

    Another technique of performing plasmapheresis is by using semipermeable membrane filters with a standard hemodialysis machine. However, for this technique, central venous access is mandatory due to the need for higher blood flow rates of 100 mL/min to 150 mL/min. There are two membrane-based technologies that are currently available; hollow fiber and parallel plate. Hollow fiber dialyzers are cylindrical shell-like structures, consisting of multiple polysulfone capillary fibers.

    Parallel plate dialyzers consist of layered membranes, with ridges and grooves which facilitate filtration. Both these dialyzers allow plasma filtration based on particle size and pressure gradients. Hollow fiber dialyzers are more gentle as opposed to parallel plate dialyzers and are preferred for pediatric patients, whereas hollow fiber dialyzers use less blood volume, and hence require a reduced dose of citrate or heparin for anticoagulation.

    The major advantage of membrane-based plasmapheresis over centrifuge-based technology is that the removed processed plasma by ultrafiltration can be returned to the patient eliminating the need for replacement fluids or colloids.


    Plasmapheresis was traditionally performed in blood banks by centrifuge-based techniques. However, therapeutic plasmapheresis procedures are routinely performed by critical care specialists in the intensive care unit, nephrologists, and dialysis-technicians after specialized skill-based training.


    No specific patient preparation is needed for this procedure. However, while inserting a central line, a local anesthetic may be needed. For this purpose, 2% lidocaine injection is used routinely. In pediatric patients, sedation with opioids and benzodiazepines may be considered for pain and anxiety control.

    The patient is positioned supine for plasmapheresis; however, the position, especially of the neck, maybe altered according to the location of central venous access to maintain adequate blood flow throughout the procedure.

    A close watch on patient vitals is recommended throughout the procedure to assess for volume depletion, hypocalcemia, and complications of fresh frozen plasma transfusion.


    The steps for performing plasmapheresis using centrifuge-based equipment are as follows:

    • Initially, a waste of around 3-5 mL of blood from the central venous catheter is discarded.
    • After drawing baseline samples for complete hemogram, calcium, and fibrinogen, it is flushed with 5-10 mL of heparinized saline.
    • The double lumen catheter is now connected to the machine tubing to start the priming procedure.
    • The machine calculates the total body volume (TVB), and the effective plasma volume (which equals TVB × (1 – hematocrit)) of the patient based on the operator’s entered height and weight.
    • The replacement product to be used and its desired volume (40 – 60 mL/kg) is decided by the clinician, and entered into the machine, based on which it calculates the centrifuge speed.
    • The separated plasma is discarded by the machine, and the RBCs are returned back to the patient along with the replacement fluid.
    • Finally, post-procedure, tubings are connected to heparinized saline, and reinfusion is initiated.
    • Post-plasmapheresis blood for fibrinogen and calcium is sent again, and lumens of central venous catheters are flushed.


    There are multiple complications of blood transfusions, including infections, hemolytic reactions, allergic reactions, transfusion-related lung injury (TRALI), transfusion-associated circulatory overload, and electrolyte imbalance.

    According to the American Association of Blood Banks (AABB), febrile reactions are the most common, followed by transfusion-associated circulatory overload, allergic reaction, TRALI, hepatitis C viral infection, hepatitis B viral infection, human immunodeficiency virus (HIV) infection, and fatal hemolysis which is extremely rare, only occurring almost 1 in 2 million transfused units of RBC.

    Adverse Event And Approximate Risk Per Unit Transfusion Of RBC

    • Febrile reaction: 1:60
    • Transfusion-associated circulatory overload: 1:100
    • Allergic reaction: 1:250
    • TRALI: 1:12,000
    • Hepatitis C infection: 1:1,149,000
    • Human immunodeficiency virus infection: 1:1,467,000
    • Fatal hemolysis: 1:1,972,000

    Febrile reactions are the most common transfusion adverse event. Transfusing with leukocyte-reduced blood products, which most blood products in the United States are, may help reduce febrile reactions. If this occurs, the transfusion should be halted, and the patient evaluated, as a hemolytic reaction can initially appear similar and consider performing a hemolytic or infectious workup. The treatment is with acetaminophen and, if needed, diphenhydramine for symptomatic control. After treatment and exclusion of other causes, the transfusion can be resumed at a slower rate.

    Transfusion-associated circulatory overload is characterized by respiratory distress secondary to cardiogenic pulmonary edema. This reaction is most common in patients who are already in a fluid overloaded state, such as congestive heart failure or acute renal failure. Diagnosis is based on symptom onset within 6 to 12 hours of receiving a transfusion, clinical evidence of fluid overload, pulmonary edema, elevated brain natriuretic peptide, and response to diuretics.

    Preventive efforts, as well as treatment, including limiting the number of transfusions to the lowest amount necessary, transfusing over the slowest possible time, and administering diuretics before or between transfusions.

    Allergic reaction, often manifested as urticaria and pruritis, occurs in less than 1% of transfusions. More severe symptoms, such as bronchospasm, wheezing, and anaphylaxis are rare. Allergic reactions may be seen in patients who are IgA deficient as exposure to IgA in donor products can cause a severe anaphylactoid reaction. This can be avoided by washing the plasma from the cells prior to transfusion. Mild symptoms, such as pruritis and urticaria can be treated with antihistamines. More severe symptoms can be treated with bronchodilators, steroids, and epinephrine.

    Transfusion-related lung injury (TRALI) is uncommon, occurring in about 1:12,000 transfusion. Patients will develop symptoms within 2 to 4 hours after receiving a transfusion. Patients will develop acute hypoxemic respiratory distress, similar to acute respiratory distress syndrome (ARDS). Patients will have pulmonary edema without evidence of left heart failure, normal CVP. Diagnosis is made based on a history of recent transfusion, chest x-ray with diffuse patchy infiltrates, and the exclusion of other etiologies. While there is a 10% mortality, the remaining 90% will resolve within 96 hours with supportive care only.

    Infections are a potential complication. The risk of infections has been decreased due to the screening of potential donors so that hepatitis C and human immunodeficiency virus risk are less than 1 in a million. Bacterial infection can also occur, but does so rarely, about once in every 250,000 units of red cells transfused.

    Fatal hemolysis is extremely rare, occurring only in 1 out of nearly 2 million transfusions. It is the result of ABO incompatibility, and the recipient’s antibodies recognize and induce hemolysis in the donor’s transfused cells. Patients will develop an acute onset of fevers and chills, low back pain, flushing, dyspnea as well as becoming tachycardic and going into shock. Treatment is to stop the transfusion, leave the IV in place, intravenous fluids with normal saline, keeping urine output greater than 100 mL/hour, diuretics may also be needed, and cardiorespiratory support as appropriate. A hemolytic workup should also be performed which includes sending the donor blood and tubing as well as post-transfusion labs (see below for list) from the recipient to the blood bank.

    • Retype and crossmatch
    • Direct and indirect Coombs tests
    • Complete blood count (CBC), creatinine, PT, and PTT (draw from the other arm)
    • Peripheral smear
    • Haptoglobin, indirect bilirubin, LDH, plasma free hemoglobin
    • Urinalysis for hemoglobin

    Electrolyte abnormalities can also occur, although these are rare, and more likely associated with large volume transfusion.

    • Hypocalcemia can result as citrate, an anticoagulant in blood products binds with calcium.
    • Hyperkalemia can occur from the release of potassium from cells during storage. Higher risk in neonates and patients with renal insufficiency.
    • Hypokalemia can result as a result of alkalinization of the blood as citrate is converted to bicarbonate by the liver in patients with normal hepatic function.

    Transfusion Reactions

    Transfusion reactions that can occur with the transfusion of blood range from life-threatening reactions to circumstances in which transfusion can continue, once the cause of the reaction is determined (e.g. simple allergic reaction).  The most common reactions include the following:

    • Transfusion-associated circulatory overload (TACO)
    • Transfusion-related acute lung injury (TRALI)
    • Transfusion-associated dyspnea (TAD)
    • Simple allergic reaction
    • Anaphylactic reaction
    • Hypotensive transfusion reaction
    • Febrile non-hemolytic transfusion reaction (FNHTR)
    • Acute hemolytic transfusion reaction (AHTR)
    • Delayed hemolytic transfusion reaction (DHTR)
    • Delayed serologic transfusion reaction (DSTR)
    • Transfusion-associated graft vs. host disease (GVHD)
    • Post-transfusion purpura (PTP)
    • Transfusion-transmitted infection (TTI)



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    Blood Transfusions – Indications, Contraindications

    Blood transfusions are a relatively common medical procedure and while typically safe, there are multiple complications that practitioners need to be able to recognize and treat. This activity reviews the indications for blood transfusion, including for special patient populations, the pre-transfusion preparation and the potential complications of blood transfusions. This activity highlights the role of the interprofessional team in caring for patients undergoing blood transfusions.

    Indications of Blood Transfusions

    While standard hemoglobin values some by gender and race and normal value for hemoglobin and hematocrit vary slightly by the laboratory, anemia is usually defined as a hemoglobin level less than 13 g/dL in males and less than 12 g/dL in females. While currently, a more restrictive threshold is used to determine the indication for transfusion, previously a liberal strategy, typically using a cutoff of hemoglobin less than 10 g/dL was used, regardless of symptoms. Currently, guidelines for transfusion of red blood cells (RBC), generally follow a restrictive threshold. While there is some variation in the number for the threshold, 7 g/dL is an agreed-upon value for asymptomatic healthy patients. Multiple studies have shown that this is an acceptable threshold in other patients populations as well, including in those with gastrointestinal (GI) bleeding as well as in critically ill patients. The guidelines recommend a value of 8 g/dL as the threshold in patients with coronary artery disease or those undergoing orthopedic surgeries, but this may be secondary to the lack of literature on using a threshold of 7 g/dL in the evaluation studies of these patient populations. The guidelines and clinical trials (TRICC) also recommend a value of 7 g/dl as the threshold for patients who are critically ill. 

    Transfusion may also be indicated in patients with active or acute bleeding as well as in patients with symptoms related to anemia (for example, tachycardia, weakness, dyspnea on exertion) and hemoglobin less than 8 g/dL.

    Unless the patient is actively bleeding, it is recommended to transfuse 1 unit of packed red cells at a time, which will typically increase the hemoglobin value by 1 g/dL and hematocrit by 3%. Follow up by checking post-transfusion hemoglobin.

    Whole blood is often divided into component parts for ease of storage and administration.  These typically include Red Blood Cells (RBC), Platelets (thrombocytes), and Plasma.  Plasma can be further fractionated into Cryoprecipitate (i.e. cryoprecipitate antihemophilic factor) and many other clotting factor concentrates of variable purity.

    The indications for whole blood and blood component transfusion consist of increasing hemoglobin and oxygenation of tissues, maintaining adequate blood volume to avoid ischemia and hypovolemic shock, and reconstituting platelets, coagulation factors, and other plasma proteins to a functional status.  Hemoglobin and hematocrit along with clinical symptoms of anemia have been the traditional markers used to determine the threshold for transfusion of red blood cells. Hemoglobin of less than 10 g/dL or a hematocrit of less than 30% has traditionally been the benchmark as the laboratory indication for transfusion in the right clinical context.  Recently, there has been increasing evidence that a lower threshold is associated with better outcomes and conservation of precious blood resources, even in critically ill populations.  There is some evidence that the transfusion “trigger” level may be slightly higher in certain conditions such as sepsis with inadequate oxygen delivery, acute coronary syndrome with ischemia, and surgical hemorrhage or in specific populations such as the elderly.  However, due controlled trials and meta-analysis data there has been a decrease in the use of liberal transfusion protocols. Restrictive transfusion, even in patients with cardiovascular disease, acute illness, and traumatic brain injury using a threshold of hemoglobin of 7 to 8 g/dL has shown no increased risk of morbidity and mortality.  There is still variability globally in transfusion thresholds for particular patient populations.  Refer to specific articles on Indications for Red Blood Cell Transfusion for more information.

    Platelets are typically given when patients have a low platelet count (thrombocytopenia) or have platelets that are dysfunctional, due to medications or other acquired or inherited lesions.  Refer to specific articles on Indications for Platelet Transfusion for more information.

    Plasma can be used to replace coagulation factors in specific coagulopathies (such as in liver disease when bleeding is present), reversal of warfarin effect (when coagulation concentrates are not available) and for treatment of diseases such as thrombotic thrombocytopenic purpura.  It is sometimes used as a replacement fluid in plasmapheresis and can be used for coagulation factor deficiencies where specific concentrates are not available.  Refer to articles on Indications for Plasma Transfusion for more information.

    Cryoprecipitate is a blood product derived from plasma.  It can be used in emergencies as an alternative for supplying coagulation factors in inherited deficiencies such as von Willebrand disease, and hemophilia A (but only when specific concentrates are unavailable). It can also be used to replenish fibrinogen in acquired coagulopathies such as disseminated intravascular coagulation (DIC) and during trauma or childbirth.

    Contraindications of Blood Transfusions

    Articles on Patient Blood Management outline the decision-making process required before transfusing a patient.  Significant contraindications that merit consideration include the risk of transfusion in a patient who is volume overloaded or who has previously had a reaction to blood.   Another important consideration is to avoid transfusion of blood without prior compatibility testing and antibody screening unless it is an emergency.


    Per the American Association of Blood Banks, all blood bags and needles are sterile, used only once, and then discarded to avoid contamination from donor to donor that could later affect multiple recipients of transfusion. The equipment used for blood donation collection such as blood pressure monitors, scales, blood collection monitors/mixers, blood bag tube sealers, transportation boxes, and refrigerators are calibrated, cleaned, and serviced routinely. The chairs and couches used in the area of blood donation are to be of cleanable surfaces such as vinyl. Transport supplies and containers are also cleanable according to the World Health Organization guidelines. All blood bags should undergo routine inspection for sterility, expiration date, appearance, and any evidence of leakage or defects at the time of donation collection.


    Phlebotomy and collection should be via qualified personnel trained in blood donation. Donation monitoring is under the overall responsibility of a medical practitioner or authorized personnel who can manage blood donor adverse reactions.  Blood transfusion into patients is also performed with adequate oversight and under the purview of a medical practitioner or other qualified health care professional.  Real-time monitoring of patients during transfusion ensures that accurate information is available for the detection and work-up of suspected transfusion reactions. Laboratory technologists are trained and educated on the importance of appropriate testing for possible infectious agents before transfusion, blood group and compatibility, potential antibodies, and post-transfusion evaluations for hemolysis. Transfusion service personnel who are committed to following accepted guidelines and to determining and auditing thresholds for transfusion have significantly influenced blood product safety.


    To assure blood product safety, several measures require implementation during product collection, manufacturing, and storage. The World Health Organization has supported a global initiative to improve access to safe and sufficient blood supply. Once collected, the blood is tested for donor blood type and screened for any clinically significant donor antibodies. The collecting facility typically holds the blood until the appropriate preparation and routine screening for potential transfusion-transmitted infections is complete.  When all legal and industry standards have been met and the product is ready for transfusion, then it is “labeled” (i.e. identified as ready for use).

    Widespread prioritization of testing for transfusion-transmitted infections has improved blood product safety worldwide. There is a summary of information on countries that responded to questionnaires about their particular policies and guidelines surrounding the testing of donor blood in Figure 2 according to the World Health Organization 2016 Global Status Report on Blood Safety and Availability report. The survey found that the majority of responding countries had policies for testing the most common and clinically relevant transfusion-transmitted infections including HIV, hepatitis C, hepatitis B, and syphilis. Eighteen nations in Latin America reported having a policy for testing all blood donations for Trypanosoma cruzi along with twelve countries implementing selective testing for T cruzi in donors who have traveled to high-risk areas or have defined risk factors. Thirty-seven nations reported having a policy of testing all blood donations for antibody to human T-lymphotropic virus (HTLV-I/II) along with seven countries reporting selective additional testing for new donors.

    Following the collection of a blood donation, several procedures can take place during the preparation of blood for transfusion. Leukodepletion is a procedure to reduce the number of white blood cells in a blood product to reduce the risk of febrile reactions, HLA sensitization, and CMV transmission. Bacterial contamination testing of platelets can be performed prior to transfusion to avoid septic transfusion reactions. Plasma fractionation provides the opportunity to derive specific factors concentrates and intravenous immune globulin.  Gamma irradiation of blood products can be performed to reduce the risk of transfusion-associated graft-versus-host disease, which is nearly always fatal. Plasma reduction or washing of blood products limits the amount of plasma within a cellular blood product, which reduces the risk of allergic transfusion reactions or the effects of incompatible ABO antibodies.  Volume reduction can also be used to reduce excess potassium and cytokines which can cause electrolyte imbalance and febrile non-hemolytic transfusion reactions, respectively. Blood typing and screening for donor and recipient alloantibodies as well as compatibility testing are also important aspects of preparation for transfusion.  Screening the donated blood for alloantibodies is essential in the prevention of hemolytic transfusion reactions in recipients.

    The new frontier in blood product safety is pathogen reduction (pathogen inactivation) which is a broad term for various methodologies applied to blood products post-collection to reduce the risk of transmission of infectious agents. Many of these technologies confer protection across different classes of infectious agents including viruses, bacteria, and parasites. Another potential benefit is that some of these technologies also inactivate donor white blood cells, which has allowed some to gain approval for the prevention of transfusion-associated graft-versus-host disease (as an alternative to irradiation). Pathogen reduction procedures are currently approved in some countries for platelets and plasma. These novel technologies can increase the shelf life of platelets and decrease the incidence of adverse transfusion reactions and bacterial contamination. These approaches are increasingly common in practice and should help improve blood product safety profiles.


    An important aspect of the donation process is the donor screening questionnaire. Donor recruitment represents an essential front-line mechanism for ensuring blood safety. The highest rates of transfusion-transmitted infections are present among donors receiving monetary compensation, and conversely, the lowest rates of infection are among unpaid volunteer donors.   “Replacement” and “family” donors are relied on in some countries, but these are not considered as safe as true altruistic unpaid volunteers.  A great reduction in the risk of transfusion-transmitted HIV, HCV, HBV, and syphilis infections have transpired with the initial donor screening questions and improved testing, including serology and nucleic acid amplification testing. According to the United States, Food and Drug Administration, highly sensitive donor screening questionnaires designed to defer high-risk donors for infection transmission exclude an estimated 90% of potentially infectious donors from blood donation.  Donors that have incentives to donate (such as monetary gain or wanting to help a friend) may not be completely truthful during screening.

    Individual blood service organizations may have subtle variations in collection procedures, but the World Health Organization provides guidelines on the proper technique for venipuncture for blood donation.  These standardize the process and are in place to prevent transfusion-transmitted infections. A safe collection is paramount to ensure that blood products remain safe through the collection, storage, and transfusion.

    Bacterial contaminants typically come from normal skin flora; therefore, proper antiseptic technique before the collection is required. The recommended procedure by the World Health Organization includes the application of a combination 2% chlorhexidine gluconate and 70% isopropyl alcohol for 30 seconds followed by 30 seconds drying time.  A closed collection system (not open to the air) is used to ensure sterility.   This procedure means that the anticoagulant-containing collection bag has an intrinsically attached tube and needle. The first 15 to 20 mL of blood is collected in a diversion bag so that, in the case of possible skin contamination, the initial blood collected is used for laboratory testing and not transfused. This diverted blood is the most likely to be contaminated by skin flora and the skin plug (created by the needle), therefore removing this from the transfusion reduces contamination risk.  Blood volumes collected vary by the technique used. According to the World Health Organization, generally for whole blood transfusion, 350 milliliters of blood is collected, and for double or triple bags to make packed red cells, fresh frozen plasma, and platelet concentrations, a volume of 450 milliliters is necessary. The volume is selected to prevent donor transfusion-associated anemia and other adverse events.

    Blood donations can be separated into four main components (red blood cells, platelets, plasma, and cryoprecipitate) or left as whole blood. Once the blood has undergone processing, it is stored at appropriate temperatures (often +2 C to +6 C).  Platelets and fresh frozen plasma (FFP) require preparation within 8 hours of collection. Platelets are stored at room temperature and with agitation typically for five days unless additional shelf life-extending mechanisms are employed.  Depending on the national regulations, fresh frozen plasma can remain stored at −18 C for one year, −25 C for 36 months, or at −65 C for seven years.   Many countries are moving toward making “plasma” instead of FFP, which gives them up to 24 hours after collection before processing and freezing are required.  The temperature and duration of storage depend on blood service guidelines and storage capabilities of individual institutions. Sterility is maintained during processing and storage steps to avoid contamination. Blood units are unavailable for transfusion until undergoing appropriate testing, including ABO and Rh blood group typing and antibody screening, as well as serologic testing for transfusion-transmitted infections.


    Red Blood Cells

    The literature strongly supports adhering to a restrictive transfusion strategy (7 g/dL) in hospitalized adult and pediatric intensive care patients who are hemodynamically stable. The evidence is not as compelling for patients with cardiovascular disease, but recommendations are to adhere to a restrictive strategy (hemoglobin 8 gm/dL) for patients with preexisting cardiovascular disease. There is insufficient evidence to make recommendations for patients with the acute coronary syndrome.

    RBC transfusion is indicated in actively bleeding patients. The amount should be based on clinical assessment and, if possible, by laboratory tests to guide targeted therapy. However, in patients with upper gastrointestinal bleeding, patients with a restrictive transfusion strategy may have better outcomes.


    There is minimal guidance for plasma transfusion. However, plasma is a frequently prescribed intervention, often for mild to moderate elevations in prothrombin time or an international normalized ratio (INR). This continues to occur despite numerous studies that failed to show a relationship between these elevations and the risk of bleeding or that INR has any ability to predict bleeding.

    The Cochrane Reviews found no evidence to support plasma transfusions in patients who were not coagulopathic undergoing elective cardiac surgery or critically ill patients.

    The British Society of Haematology (BSH) published recommendations in 2018 for various patient groups in the absence of major bleeding.

    • There is no evidence to support the prophylactic use of plasma in non-bleeding patients with abnormal standard coagulation tests pre-procedure
    • The impact of commonly used doses to correct clotting results or to reduce the bleeding risk is very limited, especially when the PT ratio or INR is between 1.5 to 1.9.
    • Vitamin K should be administered in patients with prolonged PT that is likely to be due to acquired vitamin K deficiency.

    In patients with liver disease, plasma is often transfused to correct a prolonged INR. British Society of Haematology recommends these guidelines:

    • PT and APTT do not reflect the true hemostatic status of patients with advanced liver disease.
    • There is no good evidence to endorse the use of prophylactic plasma for correction of abnormal clotting tests in non-bleeding patients prior to interventions such as elective variceal bleeding.
    • There is no good evidence to support a role for prophylactic plasma to reduce the risk of bleeding from a percutaneous liver biopsy.
    • Prophylactic transfusion of plasma should not be given in low bleeding risk procedures.
    • Do not use plasma for volume replacement.

    And for sites that have 4-Factor Prothrombin Concentrates such as K-Centra and Bebulin, this should always be the first therapeutic of choice to reverse warfarin emergently.


    There are little data on the use of cryoprecipitate in non-bleeding patients, and it is often used prophylactically but not based on good quality evidence.

    The British Society of Haematology recommends:

    • There is insufficient evidence on which to base a recommendation about the threshold of fibrinogen to transfuse cryoprecipitate, or the optimal dose, in patients with hypofibrinogenemia undergoing procedures.
    • If fibrinogen is <1.0g/L (100 mg/dL) and other factors (i.e., personal/family bleeding history, drug history, bleeding risk associated with planned procedure) indicate a significant bleeding risk before a procedure, a starting dose of two five donor pools of cryoprecipitate [10 individual units] can be considered (but there is no evidence to support this).

    Many US sites consider fibrinogen <2.0 g/L (<200 mg/dL) in a bleeding obstetric patient as an indication to transfuse cryoprecipitate.


    Common guidelines for platelet transfusions include:

    • Prophylaxis against bleeding—PLT count <10,000 mg/dL
    • Neonate—PLT count <50,000 mg/dL
    • Bedside procedure—PLT count <50,000 mg/dL
    • Kidney or liver biopsy—PLT count <50,000 mg/dL
    • Bronchoscopy without biopsy—PLT count <50,000 mg/dL
    • Bronchoscopy with biopsy—PLT count <75,000 mg/dL
    • Intra-/postoperative bleeding—PLT count <50,000 mg/dL
    Clinical bleeding with dysfunctional PLTs
    • PLT count <50,000 mg/dL (medical)
    • PLT count <100,000 mg/dL (surgical
    • Neurosurgery—PLT count <100,000 mg/dL

    Cell Salvage

    The Association of Anaesthetists guidelines make the following transfusion recommendations: Use cell salvage when it can be expected to reduce the likelihood of allogeneic (donor) red cell transfusion and/or severe postoperative anemia. Collection of blood for potential cell salvage (‘collect only’ mode) should be considered for surgical procedures where blood loss may exceed 500 ml (or > 10% of calculated total blood volume) in adult patients or > 8 mL/kg (> 10% of calculated total blood volume) in children weighing > 10 kg.

    Whole Blood

    There has been increasing interest in using low titer group O whole blood (LTOWB) in military and civilian trauma, and there is evidence to show that it saves lives.  It has also been used in non-trauma massive hemorrhage cases. LTOWB provides all of the components of blood (RBCs, platelets, and plasma with fibrinogen) and provides a balanced resuscitation addressing oxygen needs and coagulopathy in a single bag of blood. The whole blood has a critical titer of anti-A and anti-B of less than 50 to 200). The transfusion of up to 4 units of whole blood has been shown to be safe.


    There are multiple complications of blood transfusions, including infections, hemolytic reactions, allergic reactions, transfusion-related lung injury (TRALI), transfusion-associated circulatory overload, and electrolyte imbalance.

    According to the American Association of Blood Banks (AABB), febrile reactions are the most common, followed by transfusion-associated circulatory overload, allergic reaction, TRALI, hepatitis C viral infection, hepatitis B viral infection, human immunodeficiency virus (HIV) infection, and fatal hemolysis which is extremely rare, only occurring almost 1 in 2 million transfused units of RBC.

    Adverse Event and Approximate Risk Per Unit Transfusion of RBC

    • Febrile reaction: 1:60
    • Transfusion-associated circulatory overload: 1:100
    • Allergic reaction: 1:250
    • TRALI: 1:12,000
    • Hepatitis C infection: 1:1,149,000
    • Human immunodeficiency virus infection: 1:1,467,000
    • Fatal hemolysis: 1:1,972,000

    Febrile reactions are the most common transfusion adverse event. Transfusing with leukocyte-reduced blood products, which most blood products in the United States are, may help reduce febrile reactions. If this occurs, the transfusion should be halted, and the patient evaluated, as a hemolytic reaction can initially appear similar and consider performing a hemolytic or infectious workup. The treatment is with acetaminophen and, if needed, diphenhydramine for symptomatic control. After treatment and exclusion of other causes, the transfusion can be resumed at a slower rate.

    Transfusion-associated circulatory overload is characterized by respiratory distress secondary to cardiogenic pulmonary edema. This reaction is most common in patients who are already in a fluid overloaded state, such as congestive heart failure or acute renal failure. Diagnosis is based on symptom onset within 6 to 12 hours of receiving a transfusion, clinical evidence of fluid overload, pulmonary edema, elevated brain natriuretic peptide, and response to diuretics.

    Preventive efforts, as well as treatment, including limiting the number of transfusions to the lowest amount necessary, transfusing over the slowest possible time, and administering diuretics before or between transfusions.

    Allergic reaction, often manifested as urticaria and pruritis, occurs in less than 1% of transfusions. More severe symptoms, such as bronchospasm, wheezing, and anaphylaxis are rare. Allergic reactions may be seen in patients who are IgA deficient as exposure to IgA in donor products can cause a severe anaphylactoid reaction. This can be avoided by washing the plasma from the cells prior to transfusion. Mild symptoms, such as pruritis and urticaria can be treated with antihistamines. More severe symptoms can be treated with bronchodilators, steroids, and epinephrine.

    Transfusion-related lung injury (TRALI) is uncommon, occurring in about 1:12,000 transfusion. Patients will develop symptoms within 2 to 4 hours after receiving a transfusion. Patients will develop acute hypoxemic respiratory distress, similar to acute respiratory distress syndrome (ARDS). Patients will have pulmonary edema without evidence of left heart failure, normal CVP. Diagnosis is made based on a history of recent transfusion, chest x-ray with diffuse patchy infiltrates, and the exclusion of other etiologies. While there is a 10% mortality, the remaining 90% will resolve within 96 hours with supportive care only.

    Infections are a potential complication. The risk of infections has been decreased due to the screening of potential donors so that hepatitis C and human immunodeficiency virus risk are less than 1 in a million. Bacterial infection can also occur, but does so rarely, about once in every 250,000 units of red cells transfused.

    Fatal hemolysis is extremely rare, occurring only in 1 out of nearly 2 million transfusions. It is the result of ABO incompatibility, and the recipient’s antibodies recognize and induce hemolysis in the donor’s transfused cells. Patients will develop an acute onset of fevers and chills, low back pain, flushing, dyspnea as well as becoming tachycardic and going into shock. Treatment is to stop the transfusion, leave the IV in place, intravenous fluids with normal saline, keeping urine output greater than 100 mL/hour, diuretics may also be needed, and cardiorespiratory support as appropriate. A hemolytic workup should also be performed which includes sending the donor blood and tubing as well as post-transfusion labs (see below for list) from the recipient to the blood bank.

    • Retype and crossmatch
    • Direct and indirect Coombs tests
    • Complete blood count (CBC), creatinine, PT, and PTT (draw from the other arm)
    • Peripheral smear
    • Haptoglobin, indirect bilirubin, LDH, plasma free hemoglobin
    • Urinalysis for hemoglobin

    Electrolyte abnormalities can also occur, although these are rare, and more likely associated with large volume transfusion.

    • Hypocalcemia can result as citrate, an anticoagulant in blood products binds with calcium.
    • Hyperkalemia can occur from the release of potassium from cells during storage. Higher risk in neonates and patients with renal insufficiency.
    • Hypokalemia can result as a result of alkalinization of the blood as citrate is converted to bicarbonate by the liver in patients with normal hepatic function.

    Transfusion reactions

    Transfusion reactions that can occur with the transfusion of blood range from life-threatening reactions to circumstances in which transfusion can continue, once the cause of the reaction is determined (e.g. simple allergic reaction).  The most common reactions include the following:

    • Transfusion-associated circulatory overload (TACO)
    • Transfusion-related acute lung injury (TRALI)
    • Transfusion-associated dyspnea (TAD)
    • Simple allergic reaction
    • Anaphylactic reaction
    • Hypotensive transfusion reaction
    • Febrile non-hemolytic transfusion reaction (FNHTR)
    • Acute hemolytic transfusion reaction (AHTR)
    • Delayed hemolytic transfusion reaction (DHTR)
    • Delayed serologic transfusion reaction (DSTR)
    • Transfusion-associated graft vs. host disease (GVHD)
    • Post-transfusion purpura (PTP)
    • Transfusion-transmitted infection (TTI)



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    Bleeding Time – Indications, Contraindications

    Bleeding time is a clinical laboratory test performed to evaluate platelet function. It involves the creation of a standardized incision and timing the cessation of bleeding. The historical indications were the pre-operative assessment of patients taking aspirin or NSAIDs and screening for von-Willebrand disease. Unfortunately, it is insensitive and lacks reproducibility. Platelet function assay (i.e PFA 100) has largely replaced bleeding time. Despite the standardization of methods, the sensitivity and specificity of the bleeding time for platelet-mediated coagulopathy is low.

    Many hospitals and health systems have removed the test without any demonstrated harm. In most cases, a thorough history and physical is the only workup needed for the pre-operative assessment of bleeding risk. When the clinical effectiveness of platelet aggregation is desired, a modern platelet function assay can provide the necessary information. This is being increasingly utilized in intracranial hemorrhage on various antiplatelet agents prior to pooled platelet transfusion.

    Specimen Collection

    While measuring the bleeding time requires trained personnel, no gross specimen collection is necessary. Modern alternative platelet function analyzers require a small aliquot of peripheral blood. Technicians utilize standardized instruments to perform and interpret the test.


    This test is performed via two primary methods based on the length and location of the incision.

    The IVY method is the most common. The patient’s arm is positioned at the level of the heart, and a blood pressure cuff inflated to 40 mmHg. After cleansing with alcohol, a standardized device is utilized to make a 10mm long and 1mm deep incision on the volar forearm. Using a timer the blood is blotted twice a minute. The time stops when there is no further bleeding after blotting.

    The Duke method involves a stab incision in the patient’s cleaned finger or earlobe with a lancet. Otherwise, the methodology is the same.

    The IVY method is more accurate but has an increased scarring risk. The Duke method is less accurate and carries a higher hematoma rate.

    Either method carries the risks of infection and bleeding. In addition, the discomfort is not insignificant. Different normal ranges exist for each method further confounding the interpretation of results by lay clinicians.


    The measurement of bleeding time is mostly of historical value in the screening of qualitative platelet abnormalities. It was used to screen for bleeding disorders and quantify platelet function in patients taking aspirin or non-steroidal anti-inflammatory medications. The American College of Clinical Pathologists position statement identifies a carefully conducted clinical history that includes family and previous dental, obstetric, surgical, traumatic injury, transfusion, and drug histories as the best predictor of bleeding risk. As most hospitals and laboratories have removed this exam from their offerings, it has fallen out of regular use. Most current uses are likely grounded in physician preference rather than clinical research.

    Potential Diagnosis

    • Thrombocytopenia

      • Decreased platelet count impairs primary hemostasis. Sepsis, drug reactions, hematologic malignancies, autoimmune conditions, and vitamin deficiencies are among the non-inherited causes. Spontaneous bleeding is not generally a problem seen until counts fall beneath 30,000.
    • Von Willebrand Disease (vWD)

      • Von Willebrand disease is an inherited deficiency in the quantity or function of the platelet aggregation protein Von Willebrand factor. Rather than bleeding time,  modern workup includes complete blood count, factor VIII levels, ristocetin cofactor activity, and GP-Ib binding assay.
    • Disseminated Intravascular Coagulation (DIC)

      • DIC is a symptom of other severe disease processes like sepsis, burns, trauma, pregnancy, and malignancy. The coagulopathy is consumptive from the formation of blood clots throughout the peripheral vasculature. Thrombocytopenia with low fibrinogen and a high INR are the classic laboratory abnormalities.
    • Glanzmann’s

      • Glanzmann’s thrombasthenia is an autosomal recessive inherited defect in the fibrinogen binding receptor glycoprotein IIb/IIIa.
    • Bernard-Soulier Disease

      • Bernard-Soulier Syndrome is a rare autosomal recessive genetic defect in glycoprotein Ib causing giant platelets with perceived thrombocytopenia. Platelet transfusion is the treatment of choice.
    • Platelet Function Inhibiting Medications (aspirin, clopidogrel, ticagrelor, etc.)

      • Aspirin and other novel antiplatelet agents inhibit platelet aggregation and secretion overall inhibiting their function.

    Normal and Critical Findings

    Normal bleeding time:

    • Duke – Less than 3 minutes
    • IVY – Less than 8 minutes

    Times greater than 5 minutes in the Duke method and 10 minutes in the IVY method are concerning for coagulopathy. Abnormalities would require further evaluation with a focus on the coagulation pathway of interest.



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    Platelet Transfusion – Indications, Contraindications

    Platelet transfusion is a lifesaving procedure that is carried out to prevent bleeding or stop ongoing bleeding in patients with low platelet count or functional platelet disorders. There are minimum thresholds at which platelets are transfused in these patients, as not all low levels of platelet warrants a transfusion. Platelet is a scarce resource as processing, preparing, and transfusing it requires a great deal of precision and effort to maintain a certain quality. This activity highlights the use of platelet transfusion by the interprofessional team.

    Since the first attempted blood transfusion in the 17th century, blood transfusion has evolved from transfusing whole blood to utilizing only its components for select indications such as packed red blood cells (RBC), platelets, rarely white blood cells (WBC), frozen plasma and plasma-derived products. Platelets play an integral role in hemostasis by its response to vascular injury. The relevance of platelet component therapy was better understood in the 1950s and 1960s when severe and fatal hemorrhagic complications of chemotherapy in leukemia were studied.

    In the middle of the last century, blood was collected in glass bottles, which depleted platelets on storage. Around the same time introduction of plastic bags revolutionized blood storage. It was also found to be gas permeable, which is essential for storing functional platelet. Over time, with the development of efficient separation techniques, platelet component with high platelet yield has been achieved with apheresis, changes in safety protocol reduced adverse outcomes of transfusions. A great deal has been done to minimize adverse outcomes, and further safety protocols are being explored.

    Platelet concentrates (PC) are widely used to support patients with severe thrombocytopenia. These could be patients with hematologic malignancy, bone marrow failure, or other immune and non-immune causes of platelet destruction, though rare cases could warrant transfusion with normal platelet counts. Platelet is a scarce resource, partly because of its short shelf life of 5 days; it is classified in the World Health Organization’s (WHO) list of “Essential Medicine.”

    Anatomy and Physiology

    Platelets are anucleated discoid cells, size averaging between 2.0 to 5.0 micrometers in diameter, 0.5 micrometers in thickness with a mean cell volume of 6 to 10 femtoliters. Platelets are produced in the bone marrow through megakaryopoiesis from a hematopoietic stem cell (HSC) under the influence of thrombopoietin and appropriate growth factors, and an estimated ten thousand platelets are pumped into the circulation every single day. It has a life span of 8 to 10 days, after which structural changes on its surface are recognized by the liver where these senescent platelets are cleared from the circulation.

    Platelets are primarily involved in the hemostasis by adhesion to the disrupted endothelium, secretion of mediators from its granules which promote aggregation, coagulation (by providing a surface to a host of proteins) and finally the clot retraction by the action of contractile proteins in the platelet together with its secretions and entrapped mesh of fibrin. Other roles played by platelet in the body include participation in inflammation, mitogenesis, wound healing, and antimicrobial host deficiencies.

    Structurally a platelet is divided into three zones:

    • Peripheral zone – this zone is primarily involved in adhesion and aggregation function

      1. Glycocalyx – This is the thick carbohydrate-rich structure found on the exterior surface of platelets and serves as the site of the first contact during the hemostatic response by platelets, and it is made up of major and minor glycoproteins. GP-Ib-IX-V complex involved in adhesion at site of vascular injury. GPIIb-IIIa is involved in aggregation by attachment through fibrinogen to other platelets.
      2. Unit membrane – It is made of a lipid bilayer and open canalicular system, which serves a vital role in the acceleration of coagulation through the anionic phospholipid, phosphatidylserine, provided by the surface of activated platelets when clotting is initiated which converts prothrombin to thrombin.
      3. The submembrane area – It plays a vital role in transmitting signals from the surface to organelles in the cytoplasm regulating signal processes of platelet activation.
    • Sol-gel zone – This is the matrix that is made of microtubules and microfilament, which plays a vital role in platelet structure and its support. This zone is responsible for various shape changes on activation during hemostasis and during ex vivo storage. Organelles are embedded within this matrix.
    • Organelle zone

      • Alpha-granules which stores fibrinogen fibronectin FV vWF, PDGF cytokines, chemokines, TG-beta-1 and VEGF
      • Dense- granules stores calcium ATP, ADP, serotonin, and pyrophosphate
      • Mitochondria- Are the powerhouse of platelets
      • Glycogen
      • Lysosome and peroxisome

    When a platelet is activated, secretions from the α and dense granules are involved in further platelet activation and aggregation. Secretions also have immune-mediated effects.


    Normal platelet count in humans ranges from 150,000 to 450,000 cells/microliter. Platelet transfusion is mainly indicated to treat or prevent bleeding in patients with thrombocytopenia or platelet function disorder.

    Platelet transfusion Threshold in Bleeding Patients

    • <50,000 cells/microliter in severe bleeding including disseminated intravascular coagulation (DIC)
    • <30,000 cells/microliter when bleeding, not life-threatening or considered not severe
    • <100,000 cells/microliter for bleeding in multiple trauma patients or patients with intracranial bleed.

    Prophylactic Transfusion Threshold

    Prophylactic platelet transfusion is indicated below a specific threshold and is indicated before specific procedures or to prevent spontaneous bleeding. These include the following:

    • To prevent spontaneous bleeding – transfuse at <10,000 cells/microliter, some recommend <5,000 cells/microliter
    • Before neurosurgery or ocular surgery – <100,000 cells/microliter
    • Before major surgery – <50,000 cells/microliter
    • In DIC – <50,000 cells/microliter
    • Before central line placement – <20,000 cells/microliter
    • Before epidural anesthesia – <80,000 cells/microliter
    • Before bronchoalveolar lavage (BAL) – 20,000 to 30,000 cells/microliter
    • Before endoscopic procedures – <50,000 cells/microliter for therapeutic procedures; <20,000 cells/microliter for low-risk diagnostic procedures
    • Vaginal delivery platelet transfusion is considered at <30,000 cells/microliter, and when traumatic delivery then <50,000 cells/microliter.
    • Before lumbar puncture – <20,000 cells/microliter in patients with hematologic malignancies and 40,000 to 50,000 cells/microliter in patients without hematologic malignancies
    • Platelet transfusion is not routinely indicated prior to bone marrow biopsy, peripheral, central catheter insertion, traction removal of tunneled central venous catheters, and cataract removal.

    Platelet Transfusion in Specific Settings

    • Idiopathic thrombocytopenic purpura (ITP) – transfusion is avoided unless severe bleeding is present.
    • Malignancy and chemotherapy – In most cancers, platelet transfusion thresholds are as indicated above except in acute promyelocytic leukemia in which there is increased bleeding risk. Hence transfusion is indicated at counts <30,000 cells/microliter. chemotherapy is carried out at counts >20,000 cells/microliter.
    • Cardiac surgery – Patients undergoing cardiac surgery get exposed to a blood-pumping circuit, which activates platelets that get destroyed once back in circulation; hence even at normal counts, platelet transfusion is indicated during cardiac surgery.
    • Inherited and acquired platelet disorders like Glanzmann thrombasthenia, Bernard-Soulier syndrome, and other congenital platelet defects, acquired platelet disorders like patients with uremia or drug-induced platelet dysfunction. In these situations, platelet transfusion is indicated only when bleeding Is present.
    • For pediatric patients, transfusion indications are otherwise similar in older infants and children compared to adults, as demonstrated by the PLADO study except in the following situation. We transfuse platelets when the platelet count is:

      • <30,000 cells/microliter in neonates without any bleeding or symptom and failure to produce platelet.
      • <50,000 cells/microliter in an infant with active bleed or undergoing an invasive procedure. For the same situation in a premature infant, we transfuse at <100,000 cells/microliter.
      • Patient undergoing extracorporeal membrane oxygenation (ECMO) and platelets <100,000 cells/microliter


    The only agreed upon contraindication to platelet transfusion is thrombotic thrombocytopenic purpura (TTP) due to increased risk of thrombosis, although studies on outcomes and mortality have shown mixed results. Platelet transfusion is reserved for life-threatening bleeding only.

    Heparin-induced thrombocytopenia (HIT) is another condition where platelet transfusion may increase the risk of thrombosis, but recent studies have shown no risk association. In HIT, transfusion is reserved only for pre-procedure or surgery, and in severe bleeding, prophylactic transfusion, however, is not indicated.


    Platelets are transfused at the bedside through intravenous tubing with an in-line filter (screen filter of 170-260 micrometer pore size) to remove fibrin clots and large debris. The tubing can be primed with normal saline or blood product itself.

    Emergency equipment as 0.9% normal saline, oxygen source, and emergency medication to treat anaphylaxis should be available at hand in case of transfusion reaction.


    This involves multidisciplinary departments from clinicians to ancillary medical services. Platelet to be transfused is to be ordered by the physician and administered by the transfusions, which can be a nurse, who verifies the identity of the patient and match the unit before transfusing.


    Preparation for platelet transfusion starts from the production of quality approved platelet concentrates (PC) in the blood banks. PC can be prepared from whole blood or by apheresis. 6 whole blood unit derived platelets equal one apheresis platelet which contains 3X10 platelets per unit, the shelf life of PC is five days within which it must be used. The normal dose of platelet transfused is calculated as 10 to 15 ml/kg of the patient.

    The blood bank receives a request for transfusion from the physician with a pretransfusion sample, which is verified by the staff at both ends, following which ABO and Rh blood grouping is confirmed. PC is issued as and when required, which is mentioned on the blood request form. Group-specific PC is recommended, although out of the group can also be issued. When an emergency request for platelet transfusion is made, such as in traumatic bleeding patients, the patient blood group may not be available. In such cases, “AB” group platelets are given if available or else across the group transfusion is considered. Serologic crossmatch is not required except in rare cases where PC have high RBC content.

    Consent from the patient must be obtained before sending a request to the blood bank, and the intravenous line must be set before the PC is issued from the blood bank. Staff at the issue counter does the final checks for details such as patient ID, unit no, blood group, and abnormal appearance or clumps suggestive of infection in the PC bag before issuing the unit.

    Special requirements such as leukoreduction to reduce HLA alloimmunization or to minimize CMV transmission, irradiation to prevent transfusion-associated graft vs. host disease (TAGvHD) might be needed in specific patient groups. This special request is mentioned on the blood request forms.


    The patient should have an appropriate IV cannula whose size ranges from 14G to 26G. In an adult, we normally use size 18G to 22G, while in the pediatric age group, it ranges from 25G to 26G. In rare cases where IV access is not available intraosseous route can also be used for transfusion.

    Pretransfusion medication has been used in certain situations such as antihistamines in patients with a previous history of an allergic reaction during transfusion, occasionally meperidine or corticosteroid are occasionally ordered in patients with a history of severe rigors during transfusion.

    The patient’s pretransfusion vitals are recorded by the transfusions, thereafter connecting the PC bag by aseptically spiking the blood transfusion set to the IV line. A standard blood transfusion set with an inline filter of 170 to 260 micron is used. A transfusion rate of 2 to 5 ml/min is used, thereby completing the transfusion in 1 to 2 hours. Slower flow rates are used in patients at risk of fluid overload. The patient is closely monitored during the transfusion with the vitals recorded every 15 minutes if a transfusion reaction is suspected at any point, the transfusion is stopped immediately with management protocol followed.


    Platelet transfusion can be associated with complications. These complications can be immune-mediated such as febrile non-hemolytic transfusion reaction (FNHTR), allergic/anaphylaxis, TAGvHD, transfusion-related acute lung injury (TRALI), post-transfusion purpura, transfusion-related immunomodulation (TRIM), platelet refractoriness or non-immune mediated such as transfusion-associated circulatory overload (TACO), physical injury, sepsis, viral infection transmission, hypotensive reaction.

    Febrile Non-Hemolytic Transfusion Reaction (FNHTR)

    FNHTR is a relatively common complication with a frequency of 4% to 30%. It is characterized by the temperature rise of ≥1°C within the first 4hr of transfusion, which resolves within 48 hours, there can be associated with nausea, vomiting, dyspnoea, and hypotension.  Antibodies against HLA or leukocyte antigen in donor plasma are most commonly implicated. Antigen present on donor white cells binds to the antibody in the recipient, which leads to pyrogen and cytokine release such as TNF-alpha, IL1, and IL6. FNHTR can also occur due to biologic response modifiers (BRM) released during platelet storage, which is increased with storage. Platelet has maximum storage allowed for five days during which the release of substances such as CD40L, IL6, and IL8 can occur. FNHTR is diagnosed with the above-mentioned features and the possibility of chills, hemolytic causes are ruled out by further immunohematology workup and lab findings. FNHTR can be minimized by leukoreduction and by platelet additive solution (PAS), which replaces maximum plasma in stored platelets.

    Allergic and Anaphylaxis

    An allergic reaction is similar to FNHTR, and its frequency is between 0.09% and 21%. It manifests as pruritus, urticaria, or systematically as bronchoconstriction and seldom associated with fever. Pathogenesis is heterogeneous in origin ranging from proteins, antibodies, cytokines to BRM released during storage.

    Anaphylaxis can occur when the patient is IgA deficient and has antibodies against it and receives IgA-containing platelets, and this occurs 1 in 50,000 transfusions. Diagnosis is made clinically, and it is an can be prevented by giving washed platelets or platelets obtained from IgA deficient donors.

    Allergic reactions can be minimized by depleting plasma in platelets.

    Transfusion-associated Graft vs. Host Disease

    This a rare but fatal complication characterized by fever and multiple systemic manifestations such as skin, gastrointestinal tract, liver, and others. It is caused by the transfusion of viable lymphocytes that get a favorable environment in the recipient, where they engraft and proliferate subsequently attacking the host tissues. It can occur between 1 to 6 weeks from transfusion and occurs in an immunocompromised host, those with congenital T-cell defects, a population with low genetic diversity (homozygous HLA), or first-degree patient relatives. Symptoms involve multiple organs as skin, the intestine, liver, and the suppression of bone marrow. Diagnosis is that of exclusion and requires molecular methods of testing apart from microscopic features seen. This can be prevented by the irradiation of platelets.


    TRALI is another rare complication associated with the development of respiratory failure after ruling out other possible causes. Mainly caused by transfusion of antibodies in the plasma from the donor against HLA or human neutrophil antigens, an example is a platelet donated by a multiparous woman. TRALI occurs within 6 hours of transfusion. These patient develop acute worsening respiratory symptoms with characteristic features as hypoxemia: PaO/FIO ≤ 300 mm Hg with oxygen saturation <90%, all other causes of acute lung injury are ruled out before considering TRALI, it can be minimized by reducing plasma in platelets transfused such as the use of PAS.

    Post Transfusion Purpura

    A rare syndrome with a sudden drop in platelet count within 1 to 21 days of platelet transfusion, it is a self-limiting condition associated with wet purpura. Believed to be caused by autoantibody formation as a complication to platelet transfusion.

    Transfusion-related Immunomodulation

    The presence of leukocytes and biologic response modifiers released during storage have been implicated in immunomodulation. TRIM leads to a modified response of TH1/Th2 T-cells, which predisposed the patient to infection and delayed recovery from surgery. This can also be prevented by prestorage leukoreduction and depleting plasma from platelets. 

    Platelet Refractoriness

    This occurs when post-transfusion platelet recovery is not as expected. Though multiple causes can be there ranging from immune to non-immune, a multi transfused patient can develop antibodies against specific HPA(human platelet antigens) or HLA antigens. These antibodies are implicated in platelet refractoriness.  the antibodies cause platelet destruction by the immune system; in such patients, platelet crossmatching can reduce the incidence. HLA matched platelets, or if anti-human platelet antigen(HPA) antibody is involved matching HPA antigen is indicated.

    Transfusion Associated Circulatory Overload

    This adverse reaction is more likely in the pediatric group and patients with cardiac insufficiency. Slow transfusion with close monitoring in risk group is recommended

    Physical Injury

    This is possible at the site of intravenous access, which can cause complications like hematoma or nerve injury.

    Sepsis and Bacterial Infection

    Platelet concentrates are stored up to 5 days at temperatures 22 to 24 degrees C. This temperature is favorable for the growth of bacteria like Staphylococcus aureus and gram-negative bacteria. Possible sources of infections can be improper cleansing of donor phlebotomy site or if a donor has asymptomatic bacteremia. The risk of infection to the patient ranges from 0.14% to 1.41% with platelet transfusion. Pathogen reduction technology has been used to minimize infections in plasma and platelets.

    Transmission of Viral Infection

    All blood donations are screened for HIV, HCV, and HBV with other virus screening depending on the region. There remains a residual risk of transmission, as not all donors in the window period are detected. There is a possibility of transmission of infection by other viruses that are not routinely screened in the blood bank, more so of emerging infections. Pathogen reduction technology has been used to reduce this risk, but it’s not effective against all types of viruses.

    Hypotensive Reaction

    Patient on ACE inhibitors who receive bedside leukoreduction is at risk of hypotension. Exposure of the blood component to the negatively charged surface of the filter produces vasoactive bradykinin-related peptides, and this occurs within 5 minutes of transfusion. With ACE inhibitors present in the patient, these peptides are not metabolized, leading to hypotension. A proper history of medications before transfusion is important.



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    Ileostomy – Indications, Contraindications

    An ileostomy is a surgery that makes a temporary or permanent opening called a stoma. A stoma is a pathway from the lowest part of the small intestine, called the ileum, to the outside of your abdomen. This helps solid waste and gas exit the body without passing through the colon or the rectum.

    An ileostomy is a procedure in which the lumen of the ileum, part of the small bowel, is brought through the abdominal wall via a surgically-created opening called a stoma. The purpose of an ileostomy is to evacuate stool from the body via the ileum instead of the usual route via the anus. This activity reviews the indications, contraindications, and potential benefits of the ileostomy and highlights the role of the interprofessional team in the management of patients with a stoma.

    An ileostomy is when the lumen of the ileum (small bowel) is brought through the abdominal wall via a surgical opening (created by an operation). This can either be temporary or permanent, an end or a loop. The purpose of an ileostomy is to evacuate stool from the body via the ileum rather than the usual route of the anus. The output from an ileostomy consists of loose or porridge-like stool consistent with that expected to pass through the small bowel (as it is the large bowel that is responsible for making the stool more solid dependent upon water absorption). The output from an ileostomy can vary but typically ranges from 200 to 700 ml per day, and an Ileostomy is typically formed on the right side of the abdomen.

    Anatomy and Physiology

    An ileostomy is formed from a section of the ileum which is part of the small intestine. The small intestine begins at the pylorus of the stomach and is composed of three adjoining sections: the duodenum proximally, jejunum, and the ileum distally. The jejunum and ileum are intraperitoneal structures whereas the duodenum has a retroperitoneal component to it. The jejunum and duodenum are attached to the small bowel mesentery which are peritoneal folds containing blood vessels, lymphatics, and nerves. The small intestine is approximately 6 to 7 meters in length with a varying luminal diameter between 3 and 5 cm. It has multiple functions including food digestion, secretion of enzymes and proteins, and nutrient absorption . The wall of the intestine consists of the mucosa, the submucosa, muscularis propria (the muscular layer), the subserosa, and finally the serosa . The ileum terminates at the ileocaecal junction in a valve at the superior aspect of the caecum before it goes on to form the ascending colon. The caecum can be identified at this point of the bowel where the tinea converge.

    The anatomy of the anterior abdominal wall is important to be aware of when forming the trephine incision for the ileostomy. The layers encountered are the skin, subcutaneous fat, Scarpa’s and Camper’s fascia, anterior rectus sheath, muscle, posterior rectus sheath (if above the arcuate line), and the peritoneum. The muscles include the external and internal obliques, the transverse abdominis, and the rectus abdominis. The obliques and transverse abdominis attach at varying levels to the lower ribs and the iliac crests, whereas the rectus abdominis arises from the costal margin and xiphoid process before extending down to the symphysis pubis. The abdominal muscles are wrapped in fascia but also have dense tendons called aponeuroses that converge at the midline to form the linea alba.

    An ileostomy should be brought through the rectus muscle and sheath to reduce the risk of laterparastomal hernia formation, which occurs when the abdominal content pushes through the weakness created by the incision.


    There are different indications for forming an ileostomy but essentially arrive at the same result of diverting stool out of the body without it ever entering the colon.

    A loop ileostomy is when a distal loop of the ileum is brought out to the skin with 2 lumens draining into the stoma bag and is commonly used as a temporary diversion of stool usually to protect a distal anastomosis such as a colonic anastomosis in segmental colonic resections. The reason to protect such distal anastomoses is to reduce the risk of an anastomotic leak from when stool passes through the joint of the two ends of the bowel . Once the distal anastomosis has healed, both limbs of the loop ileostomy can be joined back together thereby restoring continuity to the gastrointestinal tract, which allows stool to pass through into the colon. With loop ileostomies, the proximal limb is the one that passes out the stool, and the distal limb usually acts as a mucous fistula, draining out the secretions produced within the mucosal lining from the lumen to the caecum. However, the distal limb does not drain out colonic secretions if the ileocaecal valve is competent, and therefore, does not decompress the colon. This is important to note if there is a colonic obstruction as then the patient would be at risk of perforation from a large bowel obstruction. This is because the colon is unable to decompress either proximally or distally to the obstructing source, causing secretions and flatus to build up under tension in an essentially closed loop of the bowel. At a later date, usually between three and six months, this temporary ileostomy can be “reversed” or re-joined back together to re-establish continuity of the bowel.

    An end ileostomy is when there is nothing distal to the proximal emptying limb, in other words, there is no bowel to be re-attached to this “end” at a later stage. The formation of an end ileostomy is usually considered following permanent removal of the entire colon, and therefore the patient manages their stoma for the rest of their life.

    In brief, the indications for forming an ileostomy include:

    • To defunction the rest of the bowel in order to protect a distal anastomosis
    • To evacuate stool from the body if the entire colon has been removed such as in colorectal cancer, Crohn’s disease, ulcerative colitis, and familial adenomatous polyposis
    • Relieve bowel obstruction


    There are no absolute contraindications to ileostomy formation, but the relative ones include:

    • Short mesentery disables the ileum from being exteriorized through the abdominal wall to the skin without tension. This, unfortunately, is more common in obese patients.
    • Carcinomatosis that prevents full mobilization of the ileum

    The ileostomy should be formed as distal as possible to allow enough bowel length for absorption of nutrients.

    A high output ileostomy can lead to electrolyte disturbances (particularly important to monitor for and treat in patients with renal impairment), as well as malabsorption leading to malnutrition.

    During ileostomy formation, it is important to spout the stump to get the effluent away from contact with the skin.

    An ileostomy should be sited away from scars, skin creases, and bony prominences to allow placement of the stoma appliance and avoid leakage.


    The equipment required can be split into the operative stage and the maintenance stage. In the operative stage, the formation of the trephine ileostomy involves the utilization of many instruments that are discussed below in the technique section. The maintenance stage is based on stoma education and how the patient manages their ileostomy. This includes the use of stoma bags, perhaps extra adhesive fixings such as spray, powder, paste, and rings, as well as belts, adhesive removal spray, wet wipes, and waste disposal bags.


    This includes both physical and psychological elements of preparation; the stoma nurses are again invaluable here to help support the patient through this process. Physical preparation varies somewhat on the nature of the operation involved and whether it is an emergency procedure or a planned elective operation.

    Points to consider include

    • Shaving of hair on the abdominal wall
    • Body mass index (BMI) of patients having a planned ileostomy in an elective setting: They may be asked to lose weight prior to the operation to not only improve their anesthetic suitability but also reduce the distance the small bowel mesentery has to traverse to be bought to the skin without being under tension.
    • Previous operative scars/deformities of the abdominal wall. A previous operation increases the extent of adhesions
    • The presence of herniae
    • Also in a planned setting, one would consider the effect of smoking and diabetic control on wound healing
    • Most importantly would be the positioning of the stoma site, which is usually on the right side of the abdomen at the lateral edge of the rectus muscle, at a level where the patient can see it, access it easily, and not have it interfering with belts or skin folds. It should also ideally avoid the coastal margin and umbilicus.
    • A nasogastric tube in cases of obstruction/perforation or if anticipating a postoperative ileus
    • Adequate fluid and electrolyte resuscitation.


    Ideally, the site would be marked pre-operatively with indelible ink or an “X” scored into the skin. This is so that the site can still be seen at the end of a long operation when the antiseptic prep or blood may have distorted the skin. If a laparotomy has been formed then the linea alba, which is the cut edge of the abdominal wall, is grasped with Kocher clamps or Littlewood clamps and retracted toward the midline to approximate the two wound edges together. As this will be the anatomically correct position of closure of the abdominal wall, it will also help identify where the ileostomy will be sited once the wound is closed. If a loop ileostomy is being made laparoscopically, then under vision the ileum can be grasped with a pair of Johan atraumatic graspers and bought towards the anterior abdominal wall to sit in a position where it is not under tension.

    A 2.5 to 3 cm circle or ellipse of skin is excised using monopolar diathermy (it may be helpful to lift the skin upward using an Alice clamp or Littlewood clamp). The tissue is then dissected down through the subcutaneous fat to the anterior fascial sheath of the rectus muscle, which is then opened through a cruciate incision. The rectus muscle is spread or retracted medially; however, caution must be taken to avoid injuring the epigastric vessels that run deeply in the center of this muscle. Once the muscle is retracted, the posterior sheath is seen underlying this which is usually closed attached to the peritoneum on its under-surface. Another cruciate incision is made to the posterior sheath, and then two Kelly clips are used to grasp the peritoneum and lift it up. Using dissection scissors, a cut is made in the peritoneum between the two clips which will gain access into the peritoneal cavity. The surgical defect is stretched to allow two fingers to traverse through it thus ensuring enough room for the small bowel to be bought up to form the ileostomy. The next step is to gently pass the selected segment of terminal ileum (which has been checked to have enough length, mobilization, and is tension-free) through the trephine that you just formed. If a loop ileostomy is being formed, it is the loop of ileum that is bought up through the abdominal wall defect to the skin. If an end ileostomy is being formed, then it is simply the stapled off the end of ileum that is bought up. The ileum should be positioned such that the proximal limb is cephalad and is at 12 o’clock. It should also protrude approximately 5 cm above the skin before a seromuscular absorbable stay suture (e.g., 3.0 monocryl or vicryl rapide) is placed on the skin to prevent the ileum from slipping back inside. This then allows you to perform your final checks (checking orientation, controlling hemostasis, washout, rectus sheath catheters, drains) prior to closing up the abdomen and protecting the wounds with dressings before focussing on the ileostomy formation. It is considered common practice to close any abdominal wounds prior to the formation of the ileostomy so as to prevent fecal contamination of the wound with stool from the ileum.

    Loop Ileostomy Formation

    The distal limb is opened transversely for two-thirds of its diameter in a position about halfway up from the skin level. Submucosal bleeding can be controlled with bipolar cautery. Interrupted absorbable sutures are placed at the 3, 9, and 12 o’clock position taking seromuscular bites at the lumen of the proximal limb as well as approximately 4 cm down the loop before taking a subcuticular bite of the skin at the trephine skin edge. The positions here are away from the supplying mesentery. A Langenbeck retractor can then be used to help evert the lumen so that the limb is now spouting. The interrupted sutures are then tied in place using square knots. The distal limb is also everted similarly, however, will be less spouted as there is less protrusion of the distal limb above skin level. Interrupted absorbable sutures are applied circumferentially around both limbs, taking care not to compromise the vascular supply of the mesentery.

    End Ileostomy

    The formation of the trephine is the same here as mentioned above. Once you pull the stapled end of the ileum through the abdominal wall defect and apply the stay suture, you still proceed to carry out the usual checks and close the wounds as previously mentioned. Then taking the monopolar diathermy, you excise the staple line from the ileal end and discard it. Some surgeons may choose to cut the staple line off using dissecting scissors. However, this increases the risk of bleeding from the cut edges of the bowel which can be troublesome at times to control. Once the staple line has been excised, open up the lumen and then apply the 3 interrupted absorbable sutures at the 3, 9, and 12 o’clock position taking seromuscular bites. Again using a Langenbeck retractor, evert the mucosa of the lumen so that the limb is now spouting. The interrupted sutures are then tied in place using square knots.

    Before the Procedure

    Always tell your provider what medicines you are taking, even medicines, supplements, or herbs you bought without a prescription.

    Before your surgery, talk with your provider about the following things:

    • Intimacy and sexuality
    • Pregnancy
    • Sports
    • Work

    The 2 weeks before your surgery

    • Two weeks before surgery, you may be asked to stop taking drugs that make it harder for your blood to clot. These include aspirin, ibuprofen (Advil, Motrin), Naprosyn (Aleve, Naproxen), and others.
    • Ask your provider which drugs you should still take on the day of your surgery.
    • If you smoke, try to stop. Ask your provider for help.
    • Always let your provider know about any cold, flu, fever, herpes breakout, or other illness you may have before your surgery.

    The day before your surgery

    • You may be asked to drink only clear liquids such as broth, clear juice, and water after some point.
    • Your provider will tell you when to stop eating and drinking.
    • Your provider may ask you to use enemas or laxatives to clear out your intestines.

    On the day of your surgery

    • Take the drugs you were told to take with a small sip of water.
    • You will be told when to arrive at the hospital.

    After the Procedure

    You will be in the hospital for 3 to 7 days. You may have to stay longer if your ileostomy was an emergency operation.

    You may be able to suck on ice chips on the same day as your surgery to ease your thirst. By the next day, you will probably be allowed to drink clear liquids. You will slowly add thicker fluids and then soft foods to your diet as your bowels begin to work again. You may be eating again 2 days after your surgery.

    What should I expect during surgery?

    You will receive general anesthesia before the surgery. The procedure may be done with:

    • A surgical incision, which is a large cut in the abdomen
    • Laparoscopic surgery, which involves less invasive small incisions. This method reduces pain and recovery time.
    • Bleeding inside the small intestine or from the stoma
    • Damage to nearby organs
    • Infection
    • Not being able to absorb enough nutrients from food
    • Intestinal blockage caused by scar tissue

    How long will it take to recover from surgery?

    Most patients stay in the hospital for up to 1 week after the procedure. Complete recovery from an ileostomy may take up to 2 months. During this time, you will have limits on what you can eat while the small intestine heals.

    If the ileostomy is temporary, you may need a reversal, or closure, surgery after the small intestine has healed. This surgery usually takes place about 12 weeks later.

    Ileostomy care

    Emptying your ileostomy bag – Once you have recovered from surgery, you will need to empty the ileostomy bag several times per day. You will not be able to control when stool and gas move into the pouch. It is best to empty it when the bag is less than half full.

    Ileostomy pouches come in many sizes and shapes, but there are 2 main types:

    • One-piece pouches attach directly to the skin barrier.
    • Two-piece pouches include a skin barrier and a pouch that can detach from the body.

    Most pouches are drained through an opening in the bottom. Ask your health care team about which type of ileostomy pouch you will receive and instructions on how to empty it.

    Draining waste with a catheter – If you have a continent ileostomy, the surgeon will leave a tube in the pouch so the waste can drain continuously, called an indwelling catheter. This will last for about 3 to 4 weeks. Once the indwelling catheter is removed, you will need to drain the pouch several times a day. This frequency will decrease over time.

    Caring for your skin – The skin surrounding the stoma is called peristomal skin. It will always look red and may bleed occasionally, which is normal. However, bleeding should not continue for long.

    It is important to make sure your pouch is correctly connected to your stoma. A pouch that fits poorly can irritate your skin. You should also keep this area clean and dry. If this skin appears wet, weepy, bumpy, itchy, or painful, it may be infected. Contact your healthcare team.

    Ileostomy concerns

    High stool output – During the first few days after surgery, you may have a larger than normal stool output. As your body gets used to the stoma and ileostomy, this amount will decrease. If it does not decrease after a few days, call your health care team. Passing large amounts of stool means you may be losing too many fluids. This could lead to an imbalance in your electrolyte levels. Electrolytes are minerals that help regulate the body.

    Managing gas – Just like with stool, you will also need to release gas from your ileostomy pouch. The way you do this depends on the type of pouch. Some pouches have a filter that deodorizes and vents gas. This prevents the bag from becoming too stretched, coming off of the abdomen, or bursting.

    Amounts of gas deposited into the pouch will vary based on the type of ileostomy and your diet. Foods and drinks such as beans, onions, milk, and alcohol can cause excess gas. Swallowing air can also increase the amount of gas in your small intestine. This happens when you chew gum or drink through a straw. You may have a lot of gas right after surgery. But this should decrease as your body heals. Your health care team can provide information on food and lifestyle choices to help reduce gas.

    Whole pills or capsules in the stool – Coated pills and extended-release capsules may come out intact in your pouch. This can mean that the medication was not fully absorbed in your body. Tell your health care team if this happens. They may be able to prescribe liquid or gel medications for you to take instead.

    Stoma obstruction – Sometimes your stoma may become blocked by a piece of undigested food and scar tissue. This means that stool and gas cannot pass through into the pouch. An obstruction may cause abdominal pain or swelling or nausea or vomiting.

    You may be able to remove the blockage at home. This can be done by avoiding solid foods and drinking more fluids, including warm drinks like tea. You can also try massaging your abdomen around the stoma or drawing your knees to your chest and rocking side to side. If these tips do not work, call your health care team right away.


    These can be classified as immediate, early, or late or as procedure-specific and general complications. It is important to note that complications following the creation of an intestinal stoma are experienced by 20% of the patients. General complications vary depending on the type of operation being undertaken for an ileostomy to be necessary. Procedure-specific complications include the following :

    • Stenosis
    • Ischemia/Necrosis
    • Hemorrhage
    • Infection/Abscess
    • A parastomal hernia
    • Retraction/Prolapse
    • Electrolyte imbalance due to the high output of the effluent from the ileostomy
    • Dehydration
    • Renal impairment
    • Hematoma/Seroma
    • Obstruction
    • Fistula formation
    • Skin irritation
    As with any surgery, complications can develop during or soon after an ileostomy operation. Discuss the risks with your surgeon before the procedure.

    Some of the main problems that can occur after an ileostomy or ileo-anal pouch procedure are described below.


    Sometimes the ileostomy does not function for short periods of time after surgery.

    This is not usually a problem, but if your stoma is not active for more than 6 hours and you experience cramps or nausea, you may have an obstruction.

    If you think you may have an obstruction, contact your GP or stoma nurse for advice.

    They may recommend:

    • avoiding solid foods for the time being
    • drinking plenty of fluids
    • massaging your tummy and the area around your stoma
    • lying on your back, pulling your knees up to your chest and rolling from side to side for a few minutes
    • taking a hot bath for 15 to 20 minutes to help relax the muscles in your tummy

    In persistent or severe cases, you may be advised to go to your nearest accident and emergency (A&E) department as there’s a risk your bowel could burst (rupture).


    You’re at an increased risk of becoming dehydrated if you have an ileostomy because the large intestine, which is either removed or unused if you have an ileostomy, plays an important role in helping absorb water from food waste.

    This makes it important to make sure you drink enough fluids to keep your urine a pale yellow colour to prevent complications of dehydration, such as kidney stones and even kidney failure.

    Rectal discharge

    People who have an ileostomy but have an intact large intestine often experience a discharge of mucus from their rectum.

    Mucus is a liquid produced by the lining of the bowel that acts as a lubricant, helping the passage of stools. It’s still produced even though it no longer serves any purpose.

    The mucus can vary from a clear “egg white” to a sticky, glue-like consistency.

    If there’s blood or pus in the discharge, contact your GP as it may be a sign of infection or tissue damage.

    Many people find the most effective method of managing rectal discharge is to sit on the toilet each day and push down as if passing a stool.

    This should help remove any mucus located in the rectum and prevent it building up.

    Contact your GP if you find this hard to do or it’s not helping, as you may need further treatment.

    Vitamin B12 deficiency

    Some people who have had an ileostomy will experience a gradual decrease in their levels of vitamin B12.

    Vitamin B12 plays an important role in keeping the brain and nervous system healthy.

    This decrease is thought to occur because the part of the intestine removed during the procedure is responsible for absorbing some vitamin B12 from the food you eat.

    In some people, the fall in vitamin B12 levels can cause a condition called vitamin B12 anaemia, which is also sometimes known as pernicious anaemia.

    Symptoms of vitamin B12 anemia include:

    • unexplained fatigue (extreme tiredness) and lethargy (lack of energy)
    • breathlessness
    • feeling faint
    • irregular heartbeats (palpitations)
    • headache
    • hearing sounds coming from inside the body rather than from an outside source (tinnitus)
    • loss of appetite

    If you have had an ileostomy and experience any of these symptoms, contact your GP. They’ll be able to arrange a blood test to check your vitamin B12 levels.

    It’s important not to ignore these types of symptoms. If vitamin B12 deficiency is left untreated, it can cause more serious problems with your nervous system, such as memory loss and damage to the spinal cord.

    If a diagnosis of vitamin B12 deficiency or anemia is confirmed, treating the condition is relatively straightforward and involves taking regular vitamin B12 supplements in the form of injections or tablets.

    Stoma problems

    Some people with an ileostomy experience problems related to their stoma, such as:

    • irritation and inflammation of the skin around the stoma
    • narrowing of the stoma (stoma stricture)
    • a section of the bowel pushing through the opening in the skin (stoma prolapse)
    • an internal part of the body, such as an organ, pushing through a weakness in the muscle or surrounding tissue wall (parastomal hernia)
    • the stoma sinking below the level of the skin after the initial swelling goes down (stoma retraction)
    • the stoma may get longer with time as more of the bowel pushes itself out of the abdomen (prolapse)

    If you think you may have a problem with your stoma, contact your GP or stoma nurse for advice.

    Skin irritation can usually be treated with topical treatments, such as a spray, but you may need to have further surgery to correct physical problems related to your stoma.

    Phantom rectum

    The phantom rectum is a complication that can affect people with ileostomies.

    The condition is similar to a phantom limb, where people who have had a limb amputated feel it’s still there.

    People with phantom rectum feel like they need to go to the toilet, even though they do not have a working rectum. This feeling can continue many years after surgery.

    Some people have found sitting on a toilet can help relieve this feeling.


    Pouchitis is when an internal pouch becomes inflamed. It’s a common complication in people with an ileo-anal pouch.

    Symptoms of pouchitis include:

    • diarrhea, which is often bloody
    • abdominal pains
    • stomach cramps
    • a high temperature (fever)

    Speak to your GP if you have symptoms of pouchitis.

    The condition can usually be successfully treated with a course of antibiotics.


    • Work – With the possible exception of jobs requiring very heavy lifting, an ileostomy should not interfere with work. People with ileostomies are successful business people, teachers, carpenters, welders, etc.
    • Sex and Social Life – Physically, the creation of an ileostomy usually does not affect sexual function. If there is a problem, it is almost always related to the removal of the rectum. The ileostomy itself should not interfere with normal sexual activity or pregnancy. It should not prevent one from dating and continuing relationships and friendships. UOAA Affiliated Support Groups are available for emotional support to couples.
    • Clothing – Depending on stoma location usually one is able to wear similar clothing as before surgery, including swimwear.
    • Sports and activities – With a securely attached pouch one can swim and participate in practically all types of sports. Caution is advised in heavy body contact sports and a guard or belt can be worn for protection. Travel is not restricted in any way. Bathing and showering may be done with or without the pouch in place.
    • Diet – For guidance, follow your nurse or doctor’s orders at each stage of your post-op adjustment. Individual sensitivity to certain foods varies greatly. You must determine, by trial, what is best for you. See our guide for special considerations for those with an ileostomy including absorption and blockages. A good practice for all is to chew your food thoroughly and always hydrate properly.



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