Category Archive Gastrointestinal & Liver Disease

Autoimmune orchitis defined as the inflammation of the testicle unilaterally or bilaterally usually caused by viruses and bacteria inflammatory infiltrates in the testis (orchitis), epididymis (epididymitis), and vas deferens (vasitis) is a relevant cause of decreased fecundity in males, and it is defined as direct aggression to the testis with the concomitant presence of anti-sperm antibodies (ASA). The presence of these specific antibodies has been observed in approximately 5-12% of infertile male partners. Primary autoimmune orchitis is defined by isolated infertility with ASA but without evidence of systemic disease. Secondary causes of orchitis and/or testicular vasculitis are uniformly associated with autoimmune diseases, mainly in primary vasculitides such as polyarteritis nodosa, Behçet’s disease, and Henoch-Schönlein purpura.

Autoimmune orchitis is characterized by testis inflammation and the presence of specific anti-sperm antibodies (ASA). It is classified into two categories. Primary autoimmune orchitis is defined by infertility and asymptomatic orchitis associated with ASA (100%) directed to the basement membrane of seminiferous tubules in infertile men, without any systemic disease and usually asymptomatic. Secondary autoimmune orchitis is characterized by symptomatic orchitis and/or testicular vasculitis associated with a systemic autoimmune disease, particularly vasculitis. These patients typically demonstrate testicular pain, erythema, and/or swelling. ASA in secondary autoimmune orchitis has been reported in up to 50% of patients, especially in systemic lupus erythematosus patients.

Causes of Autoimmune Orchitis

Various bacteria and viruses cause orchitis.

• Orchitis in young patients is usually viral, with mumps and rubella being the most common causes. Reports exist of cases of orchitis have after the measles, mumps, and rubella (MMR) vaccine.[rx]
• Other viruses include coxsackievirus, varicella, echovirus, and cytomegalovirus.
• Bacterial infections of the prostate and urinary tract infection can cause orchitis. Common causes of bacterial orchitis include Escherichia coli, Klebsiella pneumonia, Pseudomonas aeruginosa, and Staphylococcus and Streptococcus species.
• Bacteria that can cause sexually transmitted infections can also cause orchitis in sexually active males. Common organisms are Neisseria gonorrhoeae, Chlamydia trachomatis, and Treponema pallidum
• Mycobacterium avium complex, Cryptococcus neoformans, Toxoplasma gondii, Haemophilus parainfluenzae, and Candida albicans have been reported to cause orchitis in immunocompromised patients.

There are also reports of orchitis caused by autoimmunity, which can classify as primary and secondary.[rx]

Symptoms of Autoimmune Orchitis

Orchitis signs and symptoms usually develop suddenly and can include:

• Swelling in one or both testicles
• Pain ranging from mild to severe
• Fever
• Nausea and vomiting
• General feeling of unwellness (malaise)

The terms “testicle pain” and “groin pain” are sometimes used interchangeably. But groin pain occurs in the fold of skin between the thigh and abdomen — not in the testicle. The causes of groin pain are different from the causes of testicle pain.

Diagnosis of Autoimmune Orchitis

The patient usually presents with acute onset of testicular pain, which may initially involve one testis, and then may spread to include the whole scrotum. The patient may also complain of fever accompanied by malaise, fatigue, and chills.

• Physical Examination findings – may include testicular enlargement, tenderness, and induration. Scrotal edema and erythema may also be present. Epididymis may also be enlarged if orchitis is accompanied with epididymitis. Cremasteric reflex is normal in affected individuals. Mumps orchitis may present with bilateral parotid enlargement and usually present 4 to 8 days after onset of parotitis.
• STI screen – If you have discharge from your urethra, a narrow swab is inserted into the end of your penis to obtain a sample of the discharge. The sample is checked in the laboratory for gonorrhea and chlamydia. Some STI screens are done with a urine test.
• Urine test – A sample of your urine is analyzed to see if anything’s abnormal.
• Ultrasound – This imaging test is the one most commonly used to assess testicular pain. Ultrasound with color Doppler can determine if the blood flow to your testicles is lower than normal — indicating torsion — or higher than normal, which helps confirm the diagnosis of orchitis.

Treatment of Autoimmune Orchitis

In an emergency, physicians must distinguish between torsion and inflammation of the testis. Antibiotics are not necessary for viral causes of the disease, supportive therapies such as bed rest, antipyretics, analgesics, scrotal support, and hot or cold packs for analgesia are advisable.

• Nonsteroidal anti-inflammatory drugs, such as ibuprofen (Advil, Motrin IB, others) or naproxen sodium (Aleve)
• Antibiotics should start empirically based on the likely pathogens according to age and sexual history.
• If there is suspicion of an enteric bacteria is suspected, then fluoroquinolones (ciprofloxacin, ofloxacin, levofloxacin) for 10 to 14 days are the preferred drugs. Trimethoprim-sulfamethoxazole is also an option for these pathogens.
• If there is suspicion of a sexually transmitted pathogen, then treatment should consist of ceftriaxone 250 mg single shot intramuscularly and doxycycline 100 mg twice daily for 10 to 14 days. An azithromycin is also an option in place of doxycycline.
• Most people with viral orchitis start to feel better in three to 10 days, although it can take several weeks for the scrotal tenderness to disappear.

Sexual partners of the patient with sexually transmitted pathogens should receive treatment.[rx] The inability to take oral antibiotics, signs of sepsis and failure of previous outpatient therapy should warrant inpatient therapy.

References

Autoimmune pancreatitis (AIP) is a distinct, infrequent, progressive inflammatory, gastrointestinal disorders that lead to irreversible destruction of exocrine and endocrine pancreatic parenchyma caused by atrophy and/ or replacement with fibrotic tissue with a form of pancreatitis in children with a poorly understood pathophysiology with a systemic autoimmune condition that involves not only the pancreas but also a variety of other organs such as the bile duct[rx], the retroperitoneum[rx], and lymph nodes[rx]. AIP is also known by other names including lymphoplasmacytic sclerosing pancreatitis with cholangitis, idiopathic duct destructive pancreatitis, primary inflammatory pancreatitis, non-alcoholic duct destructive chronic pancreatitis, tumefactive pancreatitis, and destructive pancreatitis depending on the specific tissue changes found on biopsy or the predominant and accompanying symptoms.

Autoimmune pancreatitis (AIP) is a chronic inflammation identified by a distributed abnormal contraction of the main pancreatic duct, distributed expansion of the pancreas, antibodies, raised levels of serum gamma globulin or IgG, pancreas fibrosis, and critical lymphoplasmacytic infiltration [rx–rx].

Types of Autoimmune Pancreatitis

• Type 1[lymphoplasmacytic sclerosing pancreatitis (LPSP)] and
• Type 2 [idiopathic duct-centric pancreatitis (IDCP) or AIP with a granulocytic epithelial lesion (GEL)].

Causes of Autoimmune Pancreatitis

Causes of chronic pancreatitis include alcohol abuse, ductal obstruction (malignancy, stones, trauma), genetics (cystic fibrosis, hereditary pancreatitis), chemotherapy, and autoimmune diseases such as systemic lupus erythematosus (SLE) or autoimmune pancreatitis. New studies are finding that deficiencies in certain vitamins and antioxidants may be linked to the disease.[rx][rx]

The most common cause is alcohol consumption. The alcohol increase secretion of proteins from acinar cells, causing the fluid to become viscous, leading to ductal obstruction, acinar fibrosis, and atrophy. Fortunately, less than 10% of alcoholics develop. In chronic pancreatitis, suggesting that other mechanisms play a role in the pathology.

Common etiologies of acute pancreatitis are listed below.[rx][rx][rx]

• Alcohol use
• Gallstones
• Hypertriglyceridemia
• Idiopathic
• Drug-induced pancreatitis
• Post-procedural (ERCP or abdominal surgery)
• Ampullary stenosis is formerly known as sphincter of Oddi dysfunction type I
• Autoimmune pancreatitis, type I (systemic IgG4 disease-related), and type II
• Viral infection (Coxsackie, Cytomegalovirus, Echovirus, Epstein-Barr virus, Hepatitis A/B/C, HIV, Mumps, Rubella, Varicella)
• Bacterial infection (Campylobacter jejuni, Legionella, Leptospirosis, Mycobacterium avium, Mycobacterium tuberculosis, Mycoplasma)
• Trauma
• Smoking
• Peptic ulcer disease
• Cholangitis
• Cholecystitis
• Bowel perforation
• Bowel obstruction
• Mesenteric ischemia
• Acute hepatitis
• Diabetic ketoacidosis
• Basilar pneumonia
• Myocardial infarction
• Renal colic
• Aortic dissection
• Congenital anomalies (annular pancreas)
• Genetic disorders (hereditary pancreatitis, cystic fibrosis, alpha 1-antitrypsin deficiency)
• Hypercalcemia
• Parasitic infections (Ascaris lumbricoides, Cryptosporidium, Clonorchis sinensis, Microsporidia)
• Renal disease (Hemodialysis)
• Toxins (Scorpion bites, organophosphate poisoning)
• Vasculitis (Polyarteritis nodosa, Systemic lupus erythematosus)
• Hypercalcemia
• Hyperlipidemia (usually types 1 and V)
• Nutrition
• Obstruction of the duct (either congenital or acquired)
• Medications

Symptoms of Autoimmune Pancreatitis

• Jaundice (>60%)
• Abdominal Pain (>30%)
• Dark urine
• Pale stools or stools that float in the toilet
• Yellow skin and eyes (jaundice)
• Pain in your upper abdomen or middle part of your back
• Nausea and vomiting
• Weakness or extreme tiredness
• Loss of appetite or feelings of fullness
• Weight loss for no known reason
• Prolonged abdominal pain with intermittent pain-free periods,
• Weight loss, and relief of abdominal pain when leaning forward.
• Nausea, vomiting, and steatorrhea or greasy, foul-smelling, difficult-to-flush stools can also occur.

AIP is characterized by the following features

• Scleral Icterus (yellow eyes), jaundice (yellow skin) which is usually painless, usually without acute attacks of pancreatitis.
• Relatively mild symptoms, such as minimal weight loss or nausea.
• Increased serum levels of gamma globulins, immunoglobulin G (IgG) or IgG4.
• The presence of serum autoantibodies such as anti-nuclear antibody (ANA), anti-lactoferrin antibody, anti-carbonic anhydrase II antibody, and rheumatoid factor (RF).
• Contrast-enhanced CT demonstrates a diffusely enlarged (sausage-shaped) pancreas.
• Diffuse irregular narrowing of the main pancreatic duct, and stenosis of the intrapancreatic bile duct on endoscopic retrograde cholangiopancreatography (ERCP).
• Rare pancreatic calcification or cyst formation.
• Marked responsiveness to treatment with corticosteroids.

Diagnosis of Autoimmune Pancreatitis

Basic lab studies for chronic pancreatitis can include a CBC, BMP, LFTs, lipase, amylase, lipid panel, and a fecal-elastase-1 value. Lipase and amylase levels can be elevated, but they are usually normal secondary to significant pancreatic scarring and fibrosis. Of note, amylase and lipase values should not be considered diagnostic nor prognostic.

In cases where chronic autoimmune pancreatitis is suspected, inflammatory markers including ESR, CRP as well as ANA, RF, antibodies, and immunoglobulins can be obtained. To workup steatorrhea, a 72-hour quantitative fecal fat is the gold standard (whereby values greater than 7 gm per day is confirmatory). As an alternative, a fecal elastase-1 level can be obtained from a single random stool sample to help evaluate pancreatic insufficiency. This is the most sensitive and specific alternative to the qualitative fecal fat test available.

The MRCP is the premier diagnostic imaging study because it can reveal calcifications (hallmark sign), pancreatic enlargement, ductal obstruction, or dilation. MRCP has higher sensitivity and specificity for chronic pancreatitis than does the transabdominal ultrasound or plain films (though both can reveal calcifications). Management could also include a CT scan of the abdomen as an alternative.

ERCP has been the traditional test of choice in diagnosing chronic pancreatitis. It is used when there is no steatorrhea or when plain films do not reveal calcifications. However, currently, many hospitals are trending towards using MRCPs instead and are relying on ERCP only when therapeutic intervention is needed. Endoscopic ultrasound is another imaging modality that can be used to diagnose the disease.[rx][rx][rx]

Specific tests may include

• Laboratory – work ordered on admission should include a complete metabolic panel, complete blood count, serum lipase, lactate, serum triglycerides, and C-reactive protein (CRP) levels. The best assessment of evolvement of acute pancreatitis can be made using a rising blood urea nitrogen (BUN) level or a rising hematocrit level. [rx]Systemic inflammatory response syndrome (SIRS) criteria can also be used to assess the clinical status of the patient.[rx]
• Imaging tests – Tests of your pancreas and other organs may include CT, MRI, endoscopic ultrasound (EUS) and endoscopic retrograde cholangiopancreatography (ERCP).
• Blood tests – You will be tested for elevated levels of an immunoglobulin called IgG4, produced by your immune system. People with type 1 AIP, but usually not with type 2 AIP, will have highly elevated blood levels of IgG4. However, a positive test doesn’t necessarily mean that you have the disease. A small number of people who don’t have autoimmune pancreatitis, including some with pancreatic cancer, also have high blood levels of IgG4.
• Endoscopic core biopsy – In this test, pathologists analyze a sample of pancreatic tissue in the laboratory. AIP has a distinctive appearance that can be easily recognized under a microscope by an expert pathologist. Doctors insert a small tube (endoscope) through the mouth into the stomach and, guided by ultrasound, remove some tissue from the pancreas using a special needle. The challenge is obtaining a sample of tissue large enough to analyze, rather than just a few cells. This procedure is not widely available, and the results may not be conclusive.
• Steroid trial – Autoimmune pancreatitis generally responds to steroids; doctors sometimes use a trial course of this drug to confirm a diagnosis. However, this strategy should ideally be under expert guidance, be used sparingly, and only be done when there is strong evidence to support a diagnosis of autoimmune pancreatitis. Response to corticosteroids is measured by CT and improvement in serum IgG4 levels.
• Tests to assess the pancreas – Tests to assess pancreatic function are sensitive but need to be done early. Duodenal aspirates can help determine the output of amylase, pancreatic bicarbonate, and lipase. The pancreatic duct can be cannulated during ERCP and the pancreatic juice can be assessed for the same parameters.
• Computed tomography (CT scan) – The introduction of CT scan realized a revolution in the prognostic evaluation of acute pancreatitis. Ranson and Balthazar described two scoring systems. The first one was based on the presence of extra-pancreatic collections and the second associated both extra-pancreatic collections and non-enhancement of the pancreas on angioscanner (rx).
• Ultrasonography – Ultrasonography gives less precise pieces of information on pancreatic and peri-pancreatic lesions than CT-scan but is necessary for the search of gallstones. It may be helpful to guide percutaneous fine-needle aspiration of collections or insert drains.
• Magnetic Resonance Imaging – MRI gives information equivalent to that of a CT scan but its prognostic value is not yet thoroughly evaluated in acute pancreatitis

Current Guidelines

• CT is the ideal test to image the abdomen and assess pancreas morphology
• CT scan can also help exclude other pathologies
• MRCP is indicated when the CT is normal
• Secretin stimulated MRCP can define subtle changes in the ducts, and also helps assessment of ductal compliance and exocrine function.
• Endoscopic ultrasound can be used to assess ductal and parenchymal changes early in the course of the disease.

In 2002, the Japanese Pancreas Society proposed the following diagnostic criteria for autoimmune pancreatitis

• I. Pancreatic imaging studies show diffuse narrowing of the main pancreatic duct with an irregular wall (more than 1/3 of the length of the entire pancreas).
• II. Laboratory data demonstrate abnormally elevated levels of serum gamma globulin and/or IgG or the presence of autoantibodies.
• III. Histopathologic examination of the pancreas shows fibrotic changes with lymphocyte and plasma cell infiltrate.

For diagnosis, criterion I (pancreatic imaging) must be present with criterion II (laboratory data) and/or III (histopathologic findings).^[dx]

Treatment of Autoimmune Pancreatitis

• Lactated Ringer’s solution – Management for acute pancreatitis remains early aggressive fluid resuscitation. Lactated Ringer’s solution is the recommended fluid with an initial bolus of 15 to 20 mL/kg and following rates of 3 mL/kg per hour (usually approximately 250 to 500 mL per hour) for the first 24 hours if no other contraindications are present. The fluid resuscitation is monitored with a combination of blood urea nitrogen, hematocrit, and urine output, monitoring every 4 to 6 hours in the first 24 hours of resuscitation to adjust the fluid rate. Continued non-response indicates a high likelihood of ensuing MODS and is grounds for upgrading the level of care.[rx][rx][rx]
• NSAIDs – In cases where pain relief is not achieved with enzyme replacement treatment and dietary modification, non-opioid regimens should be utilized (TCA, NSAIDs, pregabalin) initially before starting a trial of opioids. Studies regarding the benefit of antioxidants are unconfirmed. New studies show some benefits of using medium-chain triglycerides. Surgery should be considered in patients who fail medical therapy and continue to have pain.[rx][rx][rx]
• Prophylactic antibiotics – If the infection is suspected, empirical antibiotics are appropriate until culture results are back. Indication for antibiotics is limited to the presence of infected necrosis. The preferred antibiotic regimen includes a carbapenem alone, or a combination of quinolone, ceftazidime, or cefepime with metronidazole. Antibiotics are continued for 4 to 6 weeks.[rx]
• Corticosteroids – Prednisone is usually initiated at a dose of 0.4-0.6 mg/kg per day for a period of months. Although a detailed steroid schedule has not yet been fully defined, most patients are usually treated for a period of 2-3 mo, with a tapering schedule of 5 mg every 1-2 wk. Prednisone is relatively low, about 0.5–0.6 mg/kg/day. Others initiate the treatment with 40 mg prednisone/day. After 3–4 weeks with this treatment, the steroid dose is tapered, reducing it 5 mg/day every 2 weeks.
• Immunosuppressants and immunomodulators – steroid-sparing agent, azathioprine (1.0–1.5 mg/kg/day) or mycophenolate (2 to 3 g/day) for several years. If these treatments fail, rituximab has been shown effective in the treatment of the first episode of the disease and also in its recurrence include mycophenolate (CellCept), mercaptopurine (Purinethol, Puritan), azathioprine (Imuran, Azasan), and rituximab (Rituxan). In our experience, steroid treatment with or without steroid-sparing agents was effective in all but one case; we recently used rituximab 1000 mg repeated in 15 days, i.e., 2000 mg as total dose, in one exceptional patient, with a good initial result. The Mayo Clinic experience [rx] is in favor to repeat rituximab 1000 mg every 2–6 months and use it as maintenance treatment. [rx]
• Pancreatic enzymes – are usually taken with a meal and help lower the pain. However, the benefits of pancreatic enzymes still remain questionable.
• Monitoring of other organ involvement – Type 1 AIP often is associated with other organ involvement, including enlarged lymph nodes and salivary glands, scarring of the bile ducts, liver inflammation, and kidney disease. Although these signs may lessen or disappear completely with steroid therapy, your doctor will continue to monitor you

Surgery is required for

• Pancreatic abscess, fistula, or pseudocyst
• Pancreatic ascites
• Mechanical obstruction of the common bile duct
• Stenosis of the duodenum leading to gastric outlet obstruction
• Variceal bleeding due to splenic vein thrombosis

Surgery to resect the pancreas can produce good results in the hands of experienced surgeons, but the operative mortality can exceed 10% and the quality of life is impaired without a functioning pancreas.

Today, interventional radiology can be used to manage most complications including drainage and stent placement.

Celiac ganglion blockade can be performed to decrease pain but this is an invasive procedure with a risk of paralysis due to transverse myelopathy. Endoscopic methods of celiac nerve blocks have not been beneficial. Endoscopy is often used to relieve obstruction in the pancreatic duct but only works in 60% of patients.

Complications

Complications of acute pancreatitis can be divided into local and systemic. Local complications include the following:

• Pancreatic pseudocyst
• Walled-off necrosis
• Peri-pancreatic fluid collection
• Acute necrotic collection

Peripancreatic fluid collections usually develop in less than 4 weeks after the initial presentation of pancreatitis whereas a pseudocyst and walled-off necrosis more than 4 weeks after the onset of acute pancreatitis.

Systemic complications include the following:

• Acute respiratory distress syndrome (ARDS)
• Compartment syndrome
• Acute kidney injury (AKI)
• Disseminated intravascular coagulation(DIC)

Chronic pancreatitis has several complications including

• Formation of pseudocysts
• Diabetes
• Pseudoaneurysms
• Splenic vein thrombosis
• Recurrent acute pancreatitis
• Risk of progression to pancreatic cancer

Reference

Acute pancreatitis is an acute inflammation of the pancreas resulting from an auto-digestion of the gland. In 75–80% of cases, acute pancreatitis is a self-limiting disease that subsides spontaneously, but 20–25% of acute pancreatitis are severe, characterized by the development of pancreatic or peri-pancreatic necrosis, resulting in general and local complications responsible for a mortality rate of 8 to 35% (rx, rx).

Autoimmune pancreatitis (AIP) is a distinct, infrequent, progressive inflammatory, gastrointestinal disorders that lead to irreversible destruction of exocrine and endocrine pancreatic parenchyma caused by atrophy and/ or replacement with fibrotic tissue with a form of pancreatitis in children with a poorly understood pathophysiology with a systemic autoimmune condition that involves not only the pancreas but also a variety of other organs such as the bile duct[rx], the retroperitoneum[rx], and lymph nodes[rx]. AIP is also known by other names including lymphoplasmacytic sclerosing pancreatitis with cholangitis, idiopathic duct destructive pancreatitis, primary inflammatory pancreatitis, non-alcoholic duct destructive chronic pancreatitis, tumefactive pancreatitis, and destructive pancreatitis depending on the specific tissue changes found on biopsy or the predominant and accompanying symptoms.

Autoimmune pancreatitis (AIP) is a chronic inflammation identified by a distributed abnormal contraction of the main pancreatic duct, distributed expansion of the pancreas, antibodies, raised levels of serum gamma globulin or IgG, pancreas fibrosis, and critical lymphoplasmacytic infiltration [rx–rx].

Types of Acute Pancreatitis

The Atlanta classification is the new, clinically based classification of acute pancreatitis (5).

Acute pancreatitis

• mild
• severe

Interstitial edematous pancreatitis

is characterized by interstitial edema associated infrequently with fat necrosis.

necrotizing pancreatitis

• sterile
• infected

The main feature is necrosis of the pancreas and/or peripancreatic tissues. Necrosis can be sterile or infected.

Fluid collections – are defined as collections occurring early in the course of pancreatitis with no defined wall. More than half of these fluid collections disappear spontaneously in the course of the disease.

Post-acute pseudocysts – are defined as a collection of pancreatic juice limited by a fibrotic wall.

Pancreatic abscess – is a circumscribed collection of pus with minimal or no necrotic debris, developed in the peripancreatic spaces.

Types of Autoimmune Pancreatitis

• Type 1[lymphoplasmacytic sclerosing pancreatitis (LPSP)] and
• Type 2 [idiopathic duct-centric pancreatitis (IDCP) or AIP with a granulocytic epithelial lesion (GEL)].

Causes of Acute Pancreatitis

Causes of chronic pancreatitis include alcohol abuse, ductal obstruction (malignancy, stones, trauma), genetics (cystic fibrosis, hereditary pancreatitis), chemotherapy, and autoimmune diseases such as systemic lupus erythematosus (SLE) or autoimmune pancreatitis. New studies are finding that deficiencies in certain vitamins and antioxidants may be linked to the disease.[rx][rx]

The most common cause is alcohol consumption. The alcohol increase secretion of proteins from acinar cells, causing the fluid to become viscous, leading to ductal obstruction, acinar fibrosis, and atrophy. Fortunately, less than 10% of alcoholics develop. In chronic pancreatitis, suggesting that other mechanisms play a role in the pathology.

Common etiologies of acute pancreatitis are listed below.[rx][rx][rx]

• Alcohol use
• Gallstones
• Hypertriglyceridemia
• Idiopathic
• Drug-induced pancreatitis
• Post-procedural (ERCP or abdominal surgery)
• Ampullary stenosis is formerly known as sphincter of Oddi dysfunction type I
• Autoimmune pancreatitis, type I (systemic IgG4 disease-related), and type II
• Viral infection (Coxsackie, Cytomegalovirus, Echovirus, Epstein-Barr virus, Hepatitis A/B/C, HIV, Mumps, Rubella, Varicella)
• Bacterial infection (Campylobacter jejuni, Legionella, Leptospirosis, Mycobacterium avium, Mycobacterium tuberculosis, Mycoplasma)
• Trauma
• Smoking
• Peptic ulcer disease
• Cholangitis
• Cholecystitis
• Bowel perforation
• Bowel obstruction
• Mesenteric ischemia
• Acute hepatitis
• Diabetic ketoacidosis
• Basilar pneumonia
• Myocardial infarction
• Renal colic
• Aortic dissection
• Congenital anomalies (annular pancreas)
• Genetic disorders (hereditary pancreatitis, cystic fibrosis, alpha 1-antitrypsin deficiency)
• Hypercalcemia
• Parasitic infections (Ascaris lumbricoides, Cryptosporidium, Clonorchis sinensis, Microsporidia)
• Renal disease (Hemodialysis)
• Toxins (Scorpion bites, organophosphate poisoning)
• Vasculitis (Polyarteritis nodosa, Systemic lupus erythematosus)
• Hypercalcemia
• Hyperlipidemia (usually types 1 and V)
• Nutrition
• Obstruction of the duct (either congenital or acquired)
• Medications

Symptoms of Acute Pancreatitis

• Jaundice (>60%)
• Abdominal Pain (>30%)
• Dark urine
• Pale stools or stools that float in the toilet
• Yellow skin and eyes (jaundice)
• Pain in your upper abdomen or middle part of your back
• Nausea and vomiting
• Weakness or extreme tiredness
• Loss of appetite or feelings of fullness
• Weight loss for no known reason
• Prolonged abdominal pain with intermittent pain-free periods,
• Weight loss, and relief of abdominal pain when leaning forward.
• Nausea, vomiting, and steatorrhea or greasy, foul-smelling, difficult-to-flush stools can also occur.

AIP is characterized by the following features

• Scleral Icterus (yellow eyes), jaundice (yellow skin) which is usually painless, usually without acute attacks of pancreatitis.
• Relatively mild symptoms, such as minimal weight loss or nausea.
• Increased serum levels of gamma globulins, immunoglobulin G (IgG) or IgG4.
• The presence of serum autoantibodies such as anti-nuclear antibody (ANA), anti-lactoferrin antibody, anti-carbonic anhydrase II antibody, and rheumatoid factor (RF).
• Contrast-enhanced CT demonstrates a diffusely enlarged (sausage-shaped) pancreas.
• Diffuse irregular narrowing of the main pancreatic duct, and stenosis of the intrapancreatic bile duct on endoscopic retrograde cholangiopancreatography (ERCP).
• Rare pancreatic calcification or cyst formation.
• Marked responsiveness to treatment with corticosteroids.

Diagnosis of Acute Pancreatitis

Basic lab studies for chronic pancreatitis can include a CBC, BMP, LFTs, lipase, amylase, lipid panel, and a fecal-elastase-1 value. Lipase and amylase levels can be elevated, but they are usually normal secondary to significant pancreatic scarring and fibrosis. Of note, amylase and lipase values should not be considered diagnostic nor prognostic.

In cases where chronic autoimmune pancreatitis is suspected, inflammatory markers including ESR, CRP as well as ANA, RF, antibodies, and immunoglobulins can be obtained. To workup steatorrhea, a 72-hour quantitative fecal fat is the gold standard (whereby values greater than 7 gm per day is confirmatory). As an alternative, a fecal elastase-1 level can be obtained from a single random stool sample to help evaluate pancreatic insufficiency. This is the most sensitive and specific alternative to the qualitative fecal fat test available.

The MRCP is the premier diagnostic imaging study because it can reveal calcifications (hallmark sign), pancreatic enlargement, ductal obstruction, or dilation. MRCP has higher sensitivity and specificity for chronic pancreatitis than does the transabdominal ultrasound or plain films (though both can reveal calcifications). Management could also include a CT scan of the abdomen as an alternative.

ERCP has been the traditional test of choice in diagnosing chronic pancreatitis. It is used when there is no steatorrhea or when plain films do not reveal calcifications. However, currently, many hospitals are trending towards using MRCPs instead and are relying on ERCP only when therapeutic intervention is needed. Endoscopic ultrasound is another imaging modality that can be used to diagnose the disease.[rx][rx][rx]

Specific tests may include

• Laboratory – work ordered on admission should include a complete metabolic panel, complete blood count, serum lipase, lactate, serum triglycerides, and C-reactive protein (CRP) levels. The best assessment of evolvement of acute pancreatitis can be made using a rising blood urea nitrogen (BUN) level or a rising hematocrit level. [rx]Systemic inflammatory response syndrome (SIRS) criteria can also be used to assess the clinical status of the patient.[rx]
• Imaging tests – Tests of your pancreas and other organs may include CT, MRI, endoscopic ultrasound (EUS) and endoscopic retrograde cholangiopancreatography (ERCP).
• Blood tests – You will be tested for elevated levels of an immunoglobulin called IgG4, produced by your immune system. People with type 1 AIP, but usually not with type 2 AIP, will have highly elevated blood levels of IgG4. However, a positive test doesn’t necessarily mean that you have the disease. A small number of people who don’t have autoimmune pancreatitis, including some with pancreatic cancer, also have high blood levels of IgG4.
• Endoscopic core biopsy – In this test, pathologists analyze a sample of pancreatic tissue in the laboratory. AIP has a distinctive appearance that can be easily recognized under a microscope by an expert pathologist. Doctors insert a small tube (endoscope) through the mouth into the stomach and, guided by ultrasound, remove some tissue from the pancreas using a special needle. The challenge is obtaining a sample of tissue large enough to analyze, rather than just a few cells. This procedure is not widely available, and the results may not be conclusive.
• Steroid trial – Autoimmune pancreatitis generally responds to steroids; doctors sometimes use a trial course of this drug to confirm a diagnosis. However, this strategy should ideally be under expert guidance, be used sparingly, and only be done when there is strong evidence to support a diagnosis of autoimmune pancreatitis. Response to corticosteroids is measured by CT and improvement in serum IgG4 levels.
• Tests to assess the pancreas – Tests to assess pancreatic function are sensitive but need to be done early. Duodenal aspirates can help determine the output of amylase, pancreatic bicarbonate, and lipase. The pancreatic duct can be cannulated during ERCP and the pancreatic juice can be assessed for the same parameters.
• Computed tomography (CT scan) – The introduction of CT scan realized a revolution in the prognostic evaluation of acute pancreatitis. Ranson and Balthazar described two scoring systems. The first one was based on the presence of extra-pancreatic collections and the second associated both extra-pancreatic collections and non-enhancement of the pancreas on angioscanner (rx).
• Ultrasonography – Ultrasonography gives less precise pieces of information on pancreatic and peri-pancreatic lesions than CT-scan but is necessary for the search of gallstones. It may be helpful to guide percutaneous fine-needle aspiration of collections or insert drains.
• Magnetic Resonance Imaging – MRI gives information equivalent to that of a CT scan but its prognostic value is not yet thoroughly evaluated in acute pancreatitis

Current Guidelines

• CT is the ideal test to image the abdomen and assess pancreas morphology
• CT scan can also help exclude other pathologies
• MRCP is indicated when the CT is normal
• Secretin stimulated MRCP can define subtle changes in the ducts, and also helps assessment of ductal compliance and exocrine function.
• Endoscopic ultrasound can be used to assess ductal and parenchymal changes early in the course of the disease.

In 2002, the Japanese Pancreas Society proposed the following diagnostic criteria for autoimmune pancreatitis

• I. Pancreatic imaging studies show diffuse narrowing of the main pancreatic duct with an irregular wall (more than 1/3 of the length of the entire pancreas).
• II. Laboratory data demonstrate abnormally elevated levels of serum gamma globulin and/or IgG or the presence of autoantibodies.
• III. Histopathologic examination of the pancreas shows fibrotic changes with lymphocyte and plasma cell infiltrate.

For diagnosis, criterion I (pancreatic imaging) must be present with criterion II (laboratory data) and/or III (histopathologic findings).^[dx]

Treatment of Acute Pancreatitis

• Lactated Ringer’s solution – Management for acute pancreatitis remains early aggressive fluid resuscitation. Lactated Ringer’s solution is the recommended fluid with an initial bolus of 15 to 20 mL/kg and following rates of 3 mL/kg per hour (usually approximately 250 to 500 mL per hour) for the first 24 hours if no other contraindications are present. The fluid resuscitation is monitored with a combination of blood urea nitrogen, hematocrit, and urine output, monitoring every 4 to 6 hours in the first 24 hours of resuscitation to adjust the fluid rate. Continued non-response indicates a high likelihood of ensuing MODS and is grounds for upgrading the level of care.[rx][rx][rx]
• NSAIDs – In cases where pain relief is not achieved with enzyme replacement treatment and dietary modification, non-opioid regimens should be utilized (TCA, NSAIDs, pregabalin) initially before starting a trial of opioids. Studies regarding the benefit of antioxidants are unconfirmed. New studies show some benefits of using medium-chain triglycerides. Surgery should be considered in patients who fail medical therapy and continue to have pain.[rx][rx][rx]
• Prophylactic antibiotics – If the infection is suspected, empirical antibiotics are appropriate until culture results are back. Indication for antibiotics is limited to the presence of infected necrosis. The preferred antibiotic regimen includes a carbapenem alone, or a combination of quinolone, ceftazidime, or cefepime with metronidazole. Antibiotics are continued for 4 to 6 weeks.[rx]
• Corticosteroids – Prednisone is usually initiated at a dose of 0.4-0.6 mg/kg per day for a period of months. Although a detailed steroid schedule has not yet been fully defined, most patients are usually treated for a period of 2-3 mo, with a tapering schedule of 5 mg every 1-2 wk. Prednisone is relatively low, about 0.5–0.6 mg/kg/day. Others initiate the treatment with 40 mg prednisone/day. After 3–4 weeks with this treatment, the steroid dose is tapered, reducing it 5 mg/day every 2 weeks.
• Immunosuppressants and immunomodulators – steroid-sparing agent, azathioprine (1.0–1.5 mg/kg/day) or mycophenolate (2 to 3 g/day) for several years. If these treatments fail, rituximab has been shown effective in the treatment of the first episode of the disease and also in its recurrence include mycophenolate (CellCept), mercaptopurine (Purinethol, Puritan), azathioprine (Imuran, Azasan), and rituximab (Rituxan). In our experience, steroid treatment with or without steroid-sparing agents was effective in all but one case; we recently used rituximab 1000 mg repeated in 15 days, i.e., 2000 mg as total dose, in one exceptional patient, with a good initial result. The Mayo Clinic experience [rx] is in favor to repeat rituximab 1000 mg every 2–6 months and use it as maintenance treatment. [rx]
• Pancreatic enzymes – are usually taken with a meal and help lower the pain. However, the benefits of pancreatic enzymes still remain questionable.
• Monitoring of other organ involvement – Type 1 AIP often is associated with other organ involvement, including enlarged lymph nodes and salivary glands, scarring of the bile ducts, liver inflammation, and kidney disease. Although these signs may lessen or disappear completely with steroid therapy, your doctor will continue to monitor you

Surgery is required for

• Pancreatic abscess, fistula, or pseudocyst
• Pancreatic ascites
• Mechanical obstruction of the common bile duct
• Stenosis of the duodenum leading to gastric outlet obstruction
• Variceal bleeding due to splenic vein thrombosis

Surgery to resect the pancreas can produce good results in the hands of experienced surgeons, but the operative mortality can exceed 10% and the quality of life is impaired without a functioning pancreas.

Today, interventional radiology can be used to manage most complications including drainage and stent placement.

Celiac ganglion blockade can be performed to decrease pain but this is an invasive procedure with a risk of paralysis due to transverse myelopathy. Endoscopic methods of celiac nerve blocks have not been beneficial. Endoscopy is often used to relieve obstruction in the pancreatic duct but only works in 60% of patients.

Complications

Complications of acute pancreatitis can be divided into local and systemic. Local complications include the following:

• Pancreatic pseudocyst
• Walled-off necrosis
• Peri-pancreatic fluid collection
• Acute necrotic collection

Peripancreatic fluid collections usually develop in less than 4 weeks after the initial presentation of pancreatitis whereas a pseudocyst and walled-off necrosis more than 4 weeks after the onset of acute pancreatitis.

Systemic complications include the following:

• Acute respiratory distress syndrome (ARDS)
• Compartment syndrome
• Acute kidney injury (AKI)
• Disseminated intravascular coagulation(DIC)

Chronic pancreatitis has several complications including

• Formation of pseudocysts
• Diabetes
• Pseudoaneurysms
• Splenic vein thrombosis
• Recurrent acute pancreatitis
• Risk of progression to pancreatic cancer

Reference

Pseudo-Obstruction of Intestine/Intestinal pseudo-obstruction is severe impairment in the ability of the intestines to push food through or a condition characterized by impairment of the muscle contractions that move food through the digestive tract. It can occur at any time of life, and its symptoms range from mild to severe. The condition may arise from abnormalities of the gastrointestinal muscles themselves (myogenic) or from problems with the nerves that control the muscle contractions (neurogenic)

Intestinal pseudo-obstruction is a rare condition with symptoms that resemble those caused by a blockage, or obstruction, of the intestines, also called the bowel. However, when a health care provider examines the intestines, no blockage exists. Instead, the symptoms are due to nerve or muscle problems that affect the movement of food, fluid, and air through the intestines.

The intestines are part of the gastrointestinal (GI) tract and include the small intestine and the large intestine. The small intestine is the organ where most digestion occurs. The small intestine measures about 20 feet and includes the

• duodenum, the first part of the small intestine
• jejunum, the middle section of the small intestine
• ileum, the lower end of the small intestine

The large intestine absorbs water from stool and changes it from a liquid to a solid form, which passes out of the body during a bowel movement. The large intestine measures about 5 feet and includes the

• the cecum, the first part of the large intestine, which is connected to the ileum
• colon, the part of the large intestine extending from the cecum to the rectum
• rectum, the lower end of the large intestine leading to the anus

Who is more likely to have intestinal pseudo-obstruction?

This condition can occur in people of any age. Some infants are born with congenital intestinal pseudo-obstruction, and some people develop this condition as adults. Intestinal pseudo-obstruction may be acute, occurring suddenly and lasting a short time, or it may be chronic, or long-lasting.

Acute colonic pseudo-obstruction, also called Ogilvie syndrome or acute colonic ileus, mostly affects older adults. In this condition, the colon becomes distended, or enlarged, after

• surgery, such as operations to open the abdomen or replace a hip or knee
• injury, such as a hip fracture
• illness, such as a serious infection

Acute colonic pseudo-obstruction can lead to serious complications. However, people with the condition usually get better with treatment.

What causes intestinal pseudo-obstruction?

The protein produced from the FLNA gene, filamin A, attaches (binds) to proteins called actins and helps them form the branching network of filaments that make up the cytoskeleton, which gives structure to cells and allows them to change shape and move. FLNA gene mutations that cause intestinal pseudo-obstruction are thought to reduce levels of the filamin A protein or impair its function. Research suggests that decreased filamin A function may affect the shape of cells in the smooth muscles of the gastrointestinal tract during development before birth, causing abnormalities in the layering of these muscles. Smooth muscles line the internal organs; they contract and relax without being consciously controlled. In the gastrointestinal tract, abnormal layering of these muscles interferes with the ability to produce the coordinated waves of contractions (peristalsis) that move food along during digestion.

Deletions or duplications of genetic material can affect all or part of the FLNA gene, and may also include adjacent genes on the X chromosome. Changes in adjacent genes may account for some of the other signs and symptoms that can occur with intestinal pseudo-obstruction.

The ACTG2 gene provides instructions for making a member of the actin family called gamma (γ)-2 actin. The γ-2 actin protein is found in smooth muscle cells of the intestinal and urinary tracts. It is necessary for the contraction of the smooth muscles in the intestines and bladder. These contractions move food through the intestines as part of the digestive process and empty urine from the bladder. ACTG2 gene mutations hinder the formation of actin filaments in the cytoskeleton and reduce the ability of smooth muscles in the intestines and bladder to contract, leading to the signs and symptoms of intestinal pseudo-obstruction.

Secondary intestinal pseudo-obstruction occurs as a complication of other disorders that damage muscles or nerves in the intestinal tract, such as Parkinson’s disease, type 2 diabetes, various types of muscular dystrophy, or Kawasaki disease. Additionally, the condition is a characteristic feature of certain inherited syndromes such as megacystis-microcolon-intestinal hypoperistalsis syndrome (MMIHS) or mitochondrial neurogastrointestinal encephalopathy disease (MNGIE disease). Infections, surgery, or certain drugs can also cause secondary intestinal pseudo-obstruction.

Mutations in other genes involved in smooth muscle contraction can also cause intestinal pseudo-obstruction. Studies suggest that mutations in additional genes that have not been identified can also result in this condition. In some affected individuals, the cause of intestinal pseudo-obstruction is unknown.

Problems with nerves, muscles, or interstitial cells of Cajal cause intestinal pseudo-obstruction. The interstitial cells of Cajal are called “pacemaker” cells because they set the pace of intestinal contractions. These cells convey messages from nerves to muscles.

Problems with nerves, muscles, or interstitial cells of the Cajal prevent normal contractions of the intestines and cause problems with the movement of food, fluid, and air through the intestines.

Primary or idiopathic intestinal pseudo-obstruction is intestinal pseudo-obstruction that occurs by itself. In some people with primary intestinal pseudo-obstruction, mutations, or changes, in genes—traits passed from parent to child—cause the condition. However, health care providers do not typically order genetic testing for an intestinal pseudo-obstruction, as they don’t commonly recognize gene mutations as a cause.

Some people have duplications or deletions of genetic material in the FLNA gene. Researchers believe that these genetic changes may impair the function of a protein, causing problems with the nerve cells in the intestines.¹ As a result, the nerves cannot work with the intestinal muscles to produce normal contractions that move food, fluid, and air through the digestive tract. Also, these genetic changes may account for some of the other signs and symptoms that can occur with intestinal pseudo-obstruction, such as bladder symptoms and muscle weakness.

A condition called mitochondrial neurogastrointestinal encephalopathy may also cause primary intestinal pseudo-obstruction. In people with this condition, mitochondria—structures in cells that produce energy—do not function normally. Mitochondrial neurogastrointestinal encephalopathy can also cause other symptoms, such as problems with nerves in the limbs and changes in the brain.

Secondary intestinal pseudo-obstruction develops as a complication of another medical condition. Causes of secondary intestinal pseudo-obstruction include

• abdominal or pelvic surgery
• diseases that affect muscles and nerves, such as lupus erythematosus, scleroderma, and Parkinson’s disease
• infections
• medications, such as opiates and antidepressants, that affect muscles and nerves
• radiation to the abdomen
• certain cancers, including lung cancer

What are the symptoms of intestinal pseudo-obstruction?

Symptoms of pseudo-obstruction vary in presentation and severity. The most common symptoms of pseudo-obstruction in children are nausea, vomiting, abdominal distention and pain, and constipation. Diarrhea, early satiety (fullness), food aversion, and weight loss may also be present. Over time, pseudo-obstruction can cause bacterial infections, malnutrition, and muscle problems in other parts of the body. Many children with congenital pseudo-obstruction also have bladder disease.

Intestinal pseudo-obstruction symptoms may include

• abdominal swelling or bloating also called distension
• abdominal pain
• nausea
• vomiting
• constipation
• diarrhea

Over time, the condition can cause malnutrition, bacterial overgrowth in the intestines, and weight loss. Malnutrition is a condition that develops when the body does not get the right amount of the vitamins, minerals, and other nutrients it needs to maintain healthy tissues and organ function.

• Symptoms may include cramps, abdominal pain, nausea, vomiting, bloating, constipation, and occasionally diarrhea.

Some people develop problems with their esophagus, stomach, or bladder.

How is intestinal pseudo-obstruction diagnosed?

To diagnose intestinal pseudo-obstruction, a health care provider may suggest the person consult a gastroenterologist—a doctor who specializes in digestive diseases. A health care provider will perform a physical exam; take a complete medical history, imaging studies, and a biopsy; and perform blood tests. A health care provider may order other tests to confirm the diagnosis. The health care provider also will look for the cause of the condition, such as an underlying illness.

Intestinal pseudo-obstruction can be difficult to diagnose, especially primary intestinal pseudo-obstruction. As a result, a correct diagnosis may take a long time.

Physical Exam

A physical exam is one of the first things a health care provider may do to help diagnose intestinal pseudo-obstruction. During a physical exam, a health care provider usually

• examines a person’s body
• uses a stethoscope to listen to bodily sounds
• taps on specific areas of the person’s body

Medical History

The health care provider will ask a person to provide a medical and family history to help diagnose intestinal pseudo-obstruction.

Imaging Studies

A health care provider may order the following imaging studies:

• Abdominal x-ray – An x-ray is a picture recorded on film or a computer that a technician takes using low-level radiation. The amount of radiation used is small. An x-ray technician takes the x-ray at a hospital or an outpatient center, and a radiologist—a doctor who specializes in medical imaging—interprets the images. A person does not need anesthesia. The person will lie on a table or stand during the x-ray. The technician positions the x-ray machine over the abdominal area. The person will hold his or her breath as the technician takes the picture so that the picture will not be blurry. The technician may ask the person to change position for additional pictures. An x-ray of the abdominal area will show whether symptoms are due to an intestinal blockage.
• Upper GI series – A health care provider may order an upper GI series to look at the small intestine. An x-ray technician performs the test at a hospital or an outpatient center, and a radiologist interprets the images; the health care provider may give infants and children anesthesia. A person should not eat or drink for 8 hours before the procedure, if possible. During the procedure, the person will stand or sit in front of an x-ray machine and drink barium, a chalky liquid. Infants lie on a table and the technician will give them barium through a tiny tube placed in the nose that runs into the stomach. Barium coats the lining of the small intestine, making signs of obstruction show up more clearly on x-rays. A person may experience bloating and nausea for a short time after the test. Barium liquid in the GI tract causes stools to be white or light-colored for several days or longer in people with intestinal pseudo-obstruction. A health care provider will give the person-specific instructions about eating and drinking after the test.
• Lower GI series – A health care provider may order a lower GI series, an x-ray exam to look at the large intestine. An x-ray technician performs the test at a hospital or an outpatient center, and a radiologist interprets the images. A person does not need anesthesia. The health care provider may provide written bowel prep instructions to follow at home before the test. The health care provider may ask the person to follow a clear liquid diet for 1 to 3 days before the procedure. A person may need to use a laxative or an enema before the test. A laxative is a medication that loosens stool and increases bowel movements. An enema involves flushing water or laxative into the anus using a special squirt bottle.
• For the test – the person will lie on a table while the health care provider inserts a flexible tube into the person’s anus. The health care provider will fill the large intestine with barium, making signs of underlying problems show up more clearly on x-rays. The test can show problems with the large intestine that are causing the person’s symptoms.
• Barium liquid in the GI tract – causes stools to be white or light-colored for several days or longer in people with intestinal pseudo-obstruction. Enemas and repeated bowel movements may cause anal soreness. A health care provider will provide specific instructions about eating and drinking after the test.
• Computerized tomography (CT) scan –  CT scans use a combination of x-rays and computer technology to create images. An x-ray technician performs the test at a hospital or an outpatient center, and a radiologist interprets the images. For a CT scan, a health care provider may give the person a solution to drink and an injection of a special dye, called contrast medium. CT scans require the person to lie on a table that slides into a tunnel-shaped device where the technician takes the x-rays. CT scans can show both the internal and external intestinal wall. The health care provider may give children a sedative to help them fall asleep for the test.
• Upper GI endoscopy – This procedure involves using an endoscope—a small, flexible tube with a light—to see the upper GI tract, which includes the esophagus, stomach, and duodenum. A gastroenterologist performs the test at a hospital or an outpatient center. The gastroenterologist carefully feeds the endoscope down the esophagus and into the stomach and duodenum. A small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the intestinal lining. A health care provider may give a person a liquid anesthetic to gargle or may spray anesthetic on the back of the person’s throat. A health care provider will place an intravenous (IV) needle in a vein in the arm to administer sedation. Sedatives help patients stay relaxed and comfortable. This test can show blockages or other conditions in the upper small intestine. A gastroenterologist may obtain a biopsy of the lining of the small intestine during an upper GI endoscopy.
• Biopsy – A gastroenterologist can obtain a biopsy of the intestinal wall during endoscopy or during surgery if the person has surgery for intestinal pseudo-obstruction and the cause is unknown. If the health care provider needs to examine the nerves in the intestinal wall, a deeper biopsy, which a gastroenterologist can typically obtain only during surgery, is necessary. A biopsy is a procedure that involves taking a piece of the intestinal wall tissue for examination with a microscope. A health care provider performs the biopsy in a hospital and uses light sedation and local anesthetic; the health care provider uses general anesthesia if performing the biopsy during surgery. A pathologist—a doctor who specializes in diagnosing diseases—examines the intestinal tissue in a lab. Diagnosing problems in the nerve pathways of the intestinal tissue requires special techniques that are not widely available
• Blood Tests – A blood test involves drawing blood at a health care provider’s office or a commercial facility and sending the sample to a lab for analysis. The blood test can show the presence of other diseases or conditions that may be causing a person’s symptoms. The blood test also can show levels of essential vitamins and minerals to help detect malnutrition.
• Manometry – Manometry is a test that measures muscle pressure and movements in the GI tract, such as how well the smooth muscles of the stomach and small intestine contract and relax. A gastroenterologist performs the test at a hospital or an outpatient center. While the person is under sedation, a health care provider places a thin tube, or manometry tube, into the stomach and moves it down into the small intestine. A gastroenterologist may use an endoscope to place this tube. A health care provider will move the person to a manometry room and connect the manometry tube to a computer. When the person wakes up from sedation, the computer records the pressure inside the intestine while the person is fasting and after the person has eaten a meal. Manometry can confirm the diagnosis of intestinal pseudo-obstruction and show the extent of the condition.
• Gastric Emptying Tests – Gastric emptying tests can show if a disorder called gastroparesis is causing a person’s symptoms. People with gastroparesis, which literally refers to a paralyzed stomach, have severely delayed gastric emptying, or the delayed movement of food from the stomach to the small intestine. Some patients with intestinal pseudo-obstruction also have gastroparesis.

Types of gastric emptying tests include the following

• Gastric emptying scintigraphy – This test involves eating a bland meal—such as eggs or an egg substitute—that contains a small amount of radioactive material. A specially trained technician performs the test in a radiology center or hospital, and a radiologist interprets the results; the person does not need anesthesia. An external camera scans the abdomen to show where the radioactive material is located. The radiologist is then able to measure the rate of gastric emptying at 1, 2, 3, and 4 hours after the meal. Normal values depend on the composition of the meal. With some meals, if more than 10 percent of the meal is still in the stomach at 4 hours, a health care provider confirms the diagnosis of gastroparesis. Obtaining scans for 4 hours after the meal is essential. When the technician only obtains scans 1 to 2 hours after the meal, the results are often unreliable.
• Breath test – With this test, the person eats a meal containing a small amount of nonradioactive material. Then, the health care provider takes breath samples over a period of several hours to measure the amount of nonradioactive material in the exhaled breath. The results allow the health care provider to calculate how fast the stomach is emptying.
• SmartPill – The SmartPill is a small electronic device in capsule form. The SmartPill test is available at specialized outpatient centers. The person swallows the device so that it can move through the entire digestive tract and send information to a cell-phone-sized receiver worn around the person’s waist or neck. The recorded information provides details about how quickly food travels through each part of the digestive tract.

How is intestinal pseudo-obstruction treated?

A health care provider will treat intestinal pseudo-obstruction with nutritional support, medications, and, in some cases, decompression. Rarely, a person will need surgery. If an illness, a medication, or both cause intestinal pseudo-obstruction, a health care provider will treat the underlying illness, stop the medication, or do both.

Nutritional Support

People with intestinal pseudo-obstruction often need nutritional support to prevent malnutrition and weight loss. Enteral nutrition provides liquid food through a feeding tube inserted through the nose into the stomach or placed directly into the stomach or small intestine. A health care provider inserts the feeding tube, sometimes using an x-ray or endoscopy for guidance, and teaches the person how to care for the tube after returning home. Enteral nutrition is sufficient for most people with intestinal pseudo-obstruction. In a severe case, a person may need IV feeding, also called parenteral nutrition, which provides liquid food through a tube placed in a vein.

Enteral nutrition is possible because the intestinal lining is normal in most people with intestinal pseudo-obstruction. Enteral nutrition is preferred over parenteral nutrition because it has a much lower risk of complications.

Decompression

A person with acute colonic pseudo-obstruction and a greatly enlarged colon who does not respond to medications may need a procedure, called decompression, to remove gas from the colon. A gastroenterologist can perform the procedure in a hospital or an outpatient center. The gastroenterologist may choose to decompress the colon by using colonoscopy. During a colonoscopy, the gastroenterologist inserts a flexible tube into the colon through the anus. A health care provider gives the person a light sedative, and possibly pain medication, to relax. If the person requires long-term decompression, the gastroenterologist also can decompress the colon through a surgical opening in the cecum. In this case, the health care provider gives the person local anesthesia.

Surgery

In severe cases of intestinal pseudo-obstruction, a person may need surgery to remove part of the intestine. However, surgery should be performed rarely, if at all, because intestinal pseudo-obstruction is a generalized disorder that typically affects the entire intestine. Removing part of the intestine cannot cure the disease.

A surgeon—a doctor who specializes in surgery—will perform the surgery at a hospital; a person will need general anesthesia. A few highly specialized treatment centers offer small intestine transplantation. A health care provider may recommend small intestine transplantation when all other treatments have failed.

References

Paralytic ileus/Intestinal pseudo-obstruction is severe impairment in the ability of the intestines to push food through or a condition characterized by impairment of the muscle contractions that move food through the digestive tract. It can occur at any time of life, and its symptoms range from mild to severe. The condition may arise from abnormalities of the gastrointestinal muscles themselves (myogenic) or from problems with the nerves that control the muscle contractions (neurogenic)

Intestinal pseudo-obstruction is a rare condition with symptoms that resemble those caused by a blockage, or obstruction, of the intestines, also called the bowel. However, when a health care provider examines the intestines, no blockage exists. Instead, the symptoms are due to nerve or muscle problems that affect the movement of food, fluid, and air through the intestines.

The intestines are part of the gastrointestinal (GI) tract and include the small intestine and the large intestine. The small intestine is the organ where most digestion occurs. The small intestine measures about 20 feet and includes the

• duodenum, the first part of the small intestine
• jejunum, the middle section of the small intestine
• ileum, the lower end of the small intestine

The large intestine absorbs water from stool and changes it from a liquid to a solid form, which passes out of the body during a bowel movement. The large intestine measures about 5 feet and includes the

• the cecum, the first part of the large intestine, which is connected to the ileum
• colon, the part of the large intestine extending from the cecum to the rectum
• rectum, the lower end of the large intestine leading to the anus

Who is more likely to have intestinal pseudo-obstruction?

This condition can occur in people of any age. Some infants are born with congenital intestinal pseudo-obstruction, and some people develop this condition as adults. Intestinal pseudo-obstruction may be acute, occurring suddenly and lasting a short time, or it may be chronic, or long-lasting.

Acute colonic pseudo-obstruction, also called Ogilvie syndrome or acute colonic ileus, mostly affects older adults. In this condition, the colon becomes distended, or enlarged, after

• surgery, such as operations to open the abdomen or replace a hip or knee
• injury, such as a hip fracture
• illness, such as a serious infection

Acute colonic pseudo-obstruction can lead to serious complications. However, people with the condition usually get better with treatment.

What causes intestinal pseudo-obstruction?

The protein produced from the FLNA gene, filamin A, attaches (binds) to proteins called actins and helps them form the branching network of filaments that make up the cytoskeleton, which gives structure to cells and allows them to change shape and move. FLNA gene mutations that cause intestinal pseudo-obstruction are thought to reduce levels of the filamin A protein or impair its function. Research suggests that decreased filamin A function may affect the shape of cells in the smooth muscles of the gastrointestinal tract during development before birth, causing abnormalities in the layering of these muscles. Smooth muscles line the internal organs; they contract and relax without being consciously controlled. In the gastrointestinal tract, abnormal layering of these muscles interferes with the ability to produce the coordinated waves of contractions (peristalsis) that move food along during digestion.

Deletions or duplications of genetic material can affect all or part of the FLNA gene, and may also include adjacent genes on the X chromosome. Changes in adjacent genes may account for some of the other signs and symptoms that can occur with intestinal pseudo-obstruction.

The ACTG2 gene provides instructions for making a member of the actin family called gamma (γ)-2 actin. The γ-2 actin protein is found in smooth muscle cells of the intestinal and urinary tracts. It is necessary for the contraction of the smooth muscles in the intestines and bladder. These contractions move food through the intestines as part of the digestive process and empty urine from the bladder. ACTG2 gene mutations hinder the formation of actin filaments in the cytoskeleton and reduce the ability of smooth muscles in the intestines and bladder to contract, leading to the signs and symptoms of intestinal pseudo-obstruction.

Secondary intestinal pseudo-obstruction occurs as a complication of other disorders that damage muscles or nerves in the intestinal tract, such as Parkinson’s disease, type 2 diabetes, various types of muscular dystrophy, or Kawasaki disease. Additionally, the condition is a characteristic feature of certain inherited syndromes such as megacystis-microcolon-intestinal hypoperistalsis syndrome (MMIHS) or mitochondrial neurogastrointestinal encephalopathy disease (MNGIE disease). Infections, surgery, or certain drugs can also cause secondary intestinal pseudo-obstruction.

Mutations in other genes involved in smooth muscle contraction can also cause intestinal pseudo-obstruction. Studies suggest that mutations in additional genes that have not been identified can also result in this condition. In some affected individuals, the cause of intestinal pseudo-obstruction is unknown.

Problems with nerves, muscles, or interstitial cells of Cajal cause intestinal pseudo-obstruction. The interstitial cells of Cajal are called “pacemaker” cells because they set the pace of intestinal contractions. These cells convey messages from nerves to muscles.

Problems with nerves, muscles, or interstitial cells of the Cajal prevent normal contractions of the intestines and cause problems with the movement of food, fluid, and air through the intestines.

Primary or idiopathic intestinal pseudo-obstruction is intestinal pseudo-obstruction that occurs by itself. In some people with primary intestinal pseudo-obstruction, mutations, or changes, in genes—traits passed from parent to child—cause the condition. However, health care providers do not typically order genetic testing for an intestinal pseudo-obstruction, as they don’t commonly recognize gene mutations as a cause.

Some people have duplications or deletions of genetic material in the FLNA gene. Researchers believe that these genetic changes may impair the function of a protein, causing problems with the nerve cells in the intestines.¹ As a result, the nerves cannot work with the intestinal muscles to produce normal contractions that move food, fluid, and air through the digestive tract. Also, these genetic changes may account for some of the other signs and symptoms that can occur with intestinal pseudo-obstruction, such as bladder symptoms and muscle weakness.

A condition called mitochondrial neurogastrointestinal encephalopathy may also cause primary intestinal pseudo-obstruction. In people with this condition, mitochondria—structures in cells that produce energy—do not function normally. Mitochondrial neurogastrointestinal encephalopathy can also cause other symptoms, such as problems with nerves in the limbs and changes in the brain.

Secondary intestinal pseudo-obstruction develops as a complication of another medical condition. Causes of secondary intestinal pseudo-obstruction include

• abdominal or pelvic surgery
• diseases that affect muscles and nerves, such as lupus erythematosus, scleroderma, and Parkinson’s disease
• infections
• medications, such as opiates and antidepressants, that affect muscles and nerves
• radiation to the abdomen
• certain cancers, including lung cancer

What are the symptoms of intestinal pseudo-obstruction?

Symptoms of pseudo-obstruction vary in presentation and severity. The most common symptoms of pseudo-obstruction in children are nausea, vomiting, abdominal distention and pain, and constipation. Diarrhea, early satiety (fullness), food aversion, and weight loss may also be present. Over time, pseudo-obstruction can cause bacterial infections, malnutrition, and muscle problems in other parts of the body. Many children with congenital pseudo-obstruction also have bladder disease.

Intestinal pseudo-obstruction symptoms may include

• abdominal swelling or bloating also called distension
• abdominal pain
• nausea
• vomiting
• constipation
• diarrhea

Over time, the condition can cause malnutrition, bacterial overgrowth in the intestines, and weight loss. Malnutrition is a condition that develops when the body does not get the right amount of the vitamins, minerals, and other nutrients it needs to maintain healthy tissues and organ function.

• Symptoms may include cramps, abdominal pain, nausea, vomiting, bloating, constipation, and occasionally diarrhea.

Some people develop problems with their esophagus, stomach, or bladder.

How is intestinal pseudo-obstruction diagnosed?

To diagnose intestinal pseudo-obstruction, a health care provider may suggest the person consult a gastroenterologist—a doctor who specializes in digestive diseases. A health care provider will perform a physical exam; take a complete medical history, imaging studies, and a biopsy; and perform blood tests. A health care provider may order other tests to confirm the diagnosis. The health care provider also will look for the cause of the condition, such as an underlying illness.

Intestinal pseudo-obstruction can be difficult to diagnose, especially primary intestinal pseudo-obstruction. As a result, a correct diagnosis may take a long time.

Physical Exam

A physical exam is one of the first things a health care provider may do to help diagnose intestinal pseudo-obstruction. During a physical exam, a health care provider usually

• examines a person’s body
• uses a stethoscope to listen to bodily sounds
• taps on specific areas of the person’s body

Medical History

The health care provider will ask a person to provide a medical and family history to help diagnose intestinal pseudo-obstruction.

Imaging Studies

A health care provider may order the following imaging studies:

• Abdominal x-ray – An x-ray is a picture recorded on film or a computer that a technician takes using low-level radiation. The amount of radiation used is small. An x-ray technician takes the x-ray at a hospital or an outpatient center, and a radiologist—a doctor who specializes in medical imaging—interprets the images. A person does not need anesthesia. The person will lie on a table or stand during the x-ray. The technician positions the x-ray machine over the abdominal area. The person will hold his or her breath as the technician takes the picture so that the picture will not be blurry. The technician may ask the person to change position for additional pictures. An x-ray of the abdominal area will show whether symptoms are due to an intestinal blockage.
• Upper GI series – A health care provider may order an upper GI series to look at the small intestine. An x-ray technician performs the test at a hospital or an outpatient center, and a radiologist interprets the images; the health care provider may give infants and children anesthesia. A person should not eat or drink for 8 hours before the procedure, if possible. During the procedure, the person will stand or sit in front of an x-ray machine and drink barium, a chalky liquid. Infants lie on a table and the technician will give them barium through a tiny tube placed in the nose that runs into the stomach. Barium coats the lining of the small intestine, making signs of obstruction show up more clearly on x-rays. A person may experience bloating and nausea for a short time after the test. Barium liquid in the GI tract causes stools to be white or light-colored for several days or longer in people with intestinal pseudo-obstruction. A health care provider will give the person-specific instructions about eating and drinking after the test.
• Lower GI series – A health care provider may order a lower GI series, an x-ray exam to look at the large intestine. An x-ray technician performs the test at a hospital or an outpatient center, and a radiologist interprets the images. A person does not need anesthesia. The health care provider may provide written bowel prep instructions to follow at home before the test. The health care provider may ask the person to follow a clear liquid diet for 1 to 3 days before the procedure. A person may need to use a laxative or an enema before the test. A laxative is a medication that loosens stool and increases bowel movements. An enema involves flushing water or laxative into the anus using a special squirt bottle.
• For the test – the person will lie on a table while the health care provider inserts a flexible tube into the person’s anus. The health care provider will fill the large intestine with barium, making signs of underlying problems show up more clearly on x-rays. The test can show problems with the large intestine that are causing the person’s symptoms.
• Barium liquid in the GI tract – causes stools to be white or light-colored for several days or longer in people with intestinal pseudo-obstruction. Enemas and repeated bowel movements may cause anal soreness. A health care provider will provide specific instructions about eating and drinking after the test.
• Computerized tomography (CT) scan –  CT scans use a combination of x-rays and computer technology to create images. An x-ray technician performs the test at a hospital or an outpatient center, and a radiologist interprets the images. For a CT scan, a health care provider may give the person a solution to drink and an injection of a special dye, called contrast medium. CT scans require the person to lie on a table that slides into a tunnel-shaped device where the technician takes the x-rays. CT scans can show both the internal and external intestinal wall. The health care provider may give children a sedative to help them fall asleep for the test.
• Upper GI endoscopy – This procedure involves using an endoscope—a small, flexible tube with a light—to see the upper GI tract, which includes the esophagus, stomach, and duodenum. A gastroenterologist performs the test at a hospital or an outpatient center. The gastroenterologist carefully feeds the endoscope down the esophagus and into the stomach and duodenum. A small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the intestinal lining. A health care provider may give a person a liquid anesthetic to gargle or may spray anesthetic on the back of the person’s throat. A health care provider will place an intravenous (IV) needle in a vein in the arm to administer sedation. Sedatives help patients stay relaxed and comfortable. This test can show blockages or other conditions in the upper small intestine. A gastroenterologist may obtain a biopsy of the lining of the small intestine during an upper GI endoscopy.
• Biopsy – A gastroenterologist can obtain a biopsy of the intestinal wall during endoscopy or during surgery if the person has surgery for intestinal pseudo-obstruction and the cause is unknown. If the health care provider needs to examine the nerves in the intestinal wall, a deeper biopsy, which a gastroenterologist can typically obtain only during surgery, is necessary. A biopsy is a procedure that involves taking a piece of the intestinal wall tissue for examination with a microscope. A health care provider performs the biopsy in a hospital and uses light sedation and local anesthetic; the health care provider uses general anesthesia if performing the biopsy during surgery. A pathologist—a doctor who specializes in diagnosing diseases—examines the intestinal tissue in a lab. Diagnosing problems in the nerve pathways of the intestinal tissue requires special techniques that are not widely available
• Blood Tests – A blood test involves drawing blood at a health care provider’s office or a commercial facility and sending the sample to a lab for analysis. The blood test can show the presence of other diseases or conditions that may be causing a person’s symptoms. The blood test also can show levels of essential vitamins and minerals to help detect malnutrition.
• Manometry – Manometry is a test that measures muscle pressure and movements in the GI tract, such as how well the smooth muscles of the stomach and small intestine contract and relax. A gastroenterologist performs the test at a hospital or an outpatient center. While the person is under sedation, a health care provider places a thin tube, or manometry tube, into the stomach and moves it down into the small intestine. A gastroenterologist may use an endoscope to place this tube. A health care provider will move the person to a manometry room and connect the manometry tube to a computer. When the person wakes up from sedation, the computer records the pressure inside the intestine while the person is fasting and after the person has eaten a meal. Manometry can confirm the diagnosis of intestinal pseudo-obstruction and show the extent of the condition.
• Gastric Emptying Tests – Gastric emptying tests can show if a disorder called gastroparesis is causing a person’s symptoms. People with gastroparesis, which literally refers to a paralyzed stomach, have severely delayed gastric emptying, or the delayed movement of food from the stomach to the small intestine. Some patients with intestinal pseudo-obstruction also have gastroparesis.

Types of gastric emptying tests include the following

• Gastric emptying scintigraphy – This test involves eating a bland meal—such as eggs or an egg substitute—that contains a small amount of radioactive material. A specially trained technician performs the test in a radiology center or hospital, and a radiologist interprets the results; the person does not need anesthesia. An external camera scans the abdomen to show where the radioactive material is located. The radiologist is then able to measure the rate of gastric emptying at 1, 2, 3, and 4 hours after the meal. Normal values depend on the composition of the meal. With some meals, if more than 10 percent of the meal is still in the stomach at 4 hours, a health care provider confirms the diagnosis of gastroparesis. Obtaining scans for 4 hours after the meal is essential. When the technician only obtains scans 1 to 2 hours after the meal, the results are often unreliable.
• Breath test – With this test, the person eats a meal containing a small amount of nonradioactive material. Then, the health care provider takes breath samples over a period of several hours to measure the amount of nonradioactive material in the exhaled breath. The results allow the health care provider to calculate how fast the stomach is emptying.
• SmartPill – The SmartPill is a small electronic device in capsule form. The SmartPill test is available at specialized outpatient centers. The person swallows the device so that it can move through the entire digestive tract and send information to a cell-phone-sized receiver worn around the person’s waist or neck. The recorded information provides details about how quickly food travels through each part of the digestive tract.

How is intestinal pseudo-obstruction treated?

A health care provider will treat intestinal pseudo-obstruction with nutritional support, medications, and, in some cases, decompression. Rarely, a person will need surgery. If an illness, a medication, or both cause intestinal pseudo-obstruction, a health care provider will treat the underlying illness, stop the medication, or do both.

Nutritional Support

People with intestinal pseudo-obstruction often need nutritional support to prevent malnutrition and weight loss. Enteral nutrition provides liquid food through a feeding tube inserted through the nose into the stomach or placed directly into the stomach or small intestine. A health care provider inserts the feeding tube, sometimes using an x-ray or endoscopy for guidance, and teaches the person how to care for the tube after returning home. Enteral nutrition is sufficient for most people with intestinal pseudo-obstruction. In a severe case, a person may need IV feeding, also called parenteral nutrition, which provides liquid food through a tube placed in a vein.

Enteral nutrition is possible because the intestinal lining is normal in most people with intestinal pseudo-obstruction. Enteral nutrition is preferred over parenteral nutrition because it has a much lower risk of complications.

Decompression

A person with acute colonic pseudo-obstruction and a greatly enlarged colon who does not respond to medications may need a procedure, called decompression, to remove gas from the colon. A gastroenterologist can perform the procedure in a hospital or an outpatient center. The gastroenterologist may choose to decompress the colon by using colonoscopy. During a colonoscopy, the gastroenterologist inserts a flexible tube into the colon through the anus. A health care provider gives the person a light sedative, and possibly pain medication, to relax. If the person requires long-term decompression, the gastroenterologist also can decompress the colon through a surgical opening in the cecum. In this case, the health care provider gives the person local anesthesia.

Surgery

In severe cases of intestinal pseudo-obstruction, a person may need surgery to remove part of the intestine. However, surgery should be performed rarely, if at all, because intestinal pseudo-obstruction is a generalized disorder that typically affects the entire intestine. Removing part of the intestine cannot cure the disease.

A surgeon—a doctor who specializes in surgery—will perform the surgery at a hospital; a person will need general anesthesia. A few highly specialized treatment centers offer small intestine transplantation. A health care provider may recommend small intestine transplantation when all other treatments have failed.

References

Narrowing of The Arteries/Coronary Artery Disease (CAD), also called coronary heart disease (CHD), ischemic heart disease (IHD), or simply heart disease, is a chronic and gradual reduction of blood flow to the heart muscle specially myocardium due to the build-up of accessive plaque (atherosclerosis) in the arteries inner sidewall of the heart and myocardial wall and systolic thickening. It is almost always due to subintimal atheroma deposition, leading to arterial luminal stenosis or occlusion and wall thickening. It is the most common of cardiovascular diseases.^[rx] Types include stable angina, unstable angina, myocardial infarction, and sudden cardiac death.^[rx] A common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw.^[rx]

The condition is usually caused by cholesterol-containing deposits called plaque. It is a waxy substance with a combination of cholesterol, fat, and other substances which stick to the walls lining the blood vessels. Over time they make arteries become harder and narrower and may cause a condition called atherosclerosis. Plaque buildup narrows coronary arteries, thereby decreasing the blood flow to the heart which eventually causes chest pain, shortness of breath, or other signs and symptoms of coronary artery disease. Uncontrolled coronary artery disease or a complete blockage of arteries can cause a heart attack.

Another name

Also known as 

• Coronary Artery Disease, 
• Coronary Microvascular Disease, 
• Coronary Syndrome X, 
• Ischemic Heart Disease, 
• Nonobstructive Coronary Artery Disease, 
• Obstructive Coronary Artery Disease
• Hardening of the arteries
• Narrowing of the arteries

Causes of Obstructive Coronary Artery Disease

Non-Modifiable

• Age
• Gender
• Race
• Family history

Modifiable

• Type 2 diabetes mellitus
• Hypertension
• Smoking
• Dyslipidemia
• Chronic kidney disease
• Obesity and metabolic syndrome
• Acute pericarditis
• Anxiety disorders
• Aortic stenosis
• Asthma
• Dilated cardiomyopathy
• Emergent treatment of gastroenteritis
• Esophagitis
• Hypertensive emergencies in emergency medicine
• Myocardial infarction
• Myocarditis

Enhancing factors

• Abdominal obesity (waist/hip ratio) (greater than 0.90 for males and greater than 0.85 for females)
• Psychosocial factors such as depression, loss of the locus of control, global stress, financial stress, and life events including marital separation, job loss, and family conflicts
• Lack of daily consumption of fruits or vegetables
• Lack of physical activity
• Premature menopause
• Preeclampsia
• Chronic inflammatory conditions (for example rheumatoid arthritis, HIV, psoriasis)
• Persistently elevated triglycerides

Structural

• Ischemic cardiomyopathy (most common structural cardiac etiology of syncope)
• Valvular abnormalities (second most common structural etiology, most commonly aortic stenosis)
• Nonischemic/Dilated cardiomyopathy (third most common structural etiology)
• Hypertrophic obstructive cardiomyopathy
• Aortic dissection
• Cardiac tamponade
• Obstructive cardiac tumors
• Pericardial disease
• Pulmonary hypertension
• Pulmonary emboli
• Arrhythmogenic right ventricular cardiomyopathy[rx][rx]

Electrical

• Drug-Induced
  • (bradycardias, tachycardias, QT interval prolongation, cardiotoxins, etc.).[rx]

Symptoms of Obstructive Coronary Artery Disease

• Chest pain (angina) – You may feel pressure or tightness in your chest as if someone were standing on your chest. This pain, called angina, usually occurs on the middle or left side of the chest. Angina is generally triggered by physical or emotional stress. The pain usually goes away within minutes after stopping the stressful activity. In some people, especially women, the pain may be brief or sharp and felt in the neck, arm, or back.
• Shortness of breath – If your heart can’t pump enough blood to meet your body’s needs, you may develop shortness of breath or extreme fatigue with activity.
• Heart attack – A completely blocked coronary artery will cause a heart attack. The classic signs and symptoms of a heart attack include crushing pressure in your chest and pain in your shoulder or arm, sometimes with shortness of breath and sweating.
• Fatigue – A significant change in energy level, something out of the norm that lasts more than a few days. At 70%, unusual fatigue is the single most common long-term symptom for women.
• Sleep difficulties – Trouble falling asleep, or waking up in the night more than usual, often because of an ache or pain that won’t let you sleep.
• Shortness of breath – Becoming winded doing the most basic activities, but especially during exercise.
• Indigestion – Feeling uncomfortably full soon after eating, sometimes with pain or burning in the upper abdomen.
• Chest discomfort – It may be mild discomfort, it may seem like indigestion.
• Anxiety – Feeling nervous or apprehensive for no apparent reason, or more than usual.
• Chest pain or discomfort (angina)
• Weakness, light-headedness, nausea (feeling sick to your stomach), or a cold sweat
• Pain or discomfort in the arms or shoulder

An acute coronary event, such as a heart attack, may cause the following symptoms

• Angina, which can feel like pressure, squeezing, burning, or tightness during physical activity. The pain or discomfort usually starts behind the breastbone, but it can also occur in the arms, shoulders, jaw, throat, or back. The pain may feel like indigestion.
• Cold sweats
• Dizziness
• Light-headedness
• Nausea or a feeling of indigestion
• Neck pain
• Shortness of breath, especially with activity
• Sleep disturbances
• Weakness

Women are somewhat less likely than men to experience chest pain. Instead, they are more likely to experience

• Chest pain – While men having a heart attack often report a crushing or stabbing pain in their chest, many women say they felt pressure, tightness, or aching in their chest or back.
• Fatigue – More than feeling tired, this overwhelming fatigue makes it hard to do anything.
• Breathing difficulties – It’s suddenly a struggle to take a full breath.
• Radiating pain – Pain spreads across the jaw, arm, shoulder or radiating across the back
• Dizziness
• Fatigue
• Nausea
• Pressure or tightness in the chest
• Stomach pain
• Women are also more likely than men to have no symptoms of coronary heart disease.

Chronic (long-term) coronary heart disease can cause symptoms such as the following:

• Angina
• Shortness of breath with physical activity
• Fatigue
• Neck pain

Diagnosis of Obstructive Coronary Artery Disease

On physical exam, the most common signs encountered are:

• Rales on lung auscultation indicative of pulmonary edema
• Decreased breath sounds on lung auscultation suggestive of pleural effusion
• S3 gallop on heart auscultation indicative of elevated left ventricular end-diastolic pressure
• Point of maximal impulse displaced laterally on palpation characteristic of increased heart size
• Jugular venous distention (jugular venous pressure over 8 cm of water) indicative of elevated right atrial pressure
• Positive hepatojugular reflux (exerting manual pressure on the congested liver causing increased jugular venous pressures)
• Increased abdominal girth due to ascites
• Swelling of the scrotum
• Low blood pressure and rapid heart rate can occur in severely decompensated failure due to decreased cardiac output

The three components in the evaluation of MI are clinical features, ECG findings, and cardiac biomarkers.

Laboratory tests

• Cardiac troponins should be the only marker ordered
• CBC
• Lipid profile
• Renal function
• Metabolic panel
• B-type natriuretic peptide (BNP) – should not be ordered as a marker for MI, but it is better used to stratify risk, especially in patients with MI who develop heart failure.
• Brain natriuretic peptide (BNP) or NT-proBNP – may be the most helpful as it can differentiate acute heart failure from other causes of shortness of breath. However, this test lacks specificity, and a high level of this hormone is not diagnostic of acute heart failure.[rx][rx]
• Troponin T – (to detect myocardial infarction, although the levels may be high due to heart failure itself), complete blood count, basic metabolic panel (low sodium, in particular, indicates advanced disease) and liver function tests (to detect liver injury due to volume overload).

Imaging Test

• 2D echocardiography – is useful to evaluate right and left ventricular size, mean pulmonary artery pressure in left to right shunt, and evaluation of regional or global left ventricular systolic function.[rx]
• Heart angiography – remains the primary diagnostic and therapeutic modality in the assessment of the fistula and embolization with coils and devices.[rx] Heart Angiogram is the most promising test to identify blocked arteries. In an angiogram for the heart, your doctor will inject a special dye into the coronary arteries through a long, thin, flexible tube called a catheter. It is threaded through an artery, usually in the leg to the arteries in the heart. The dye outlines narrow spots and artery blockages.
• Holter monitoring – is a type of ECG where the individual wears a portable monitor for 24 hours while going through regular activities. The device captures any abnormalities and can also suggest inadequate blood flow to the heart.
• Coronary Angiography – Coronary angiography also called cardiac catheterization, is a minimally invasive study that is considered the gold standard for diagnosing coronary artery disease. This test is performed under local anesthesia and involves injecting X-ray dye or contrast medium into the coronary arteries via tubes called catheters. An X-ray camera films the blood flow to show the location and severity of artery narrowing. This test can show if the blood vessels in your heart have narrowed, your heart is pumping normally and blood is flowing correctly and your heart valves are functioning properly. It also can identify any heart abnormalities you may have been born with or congenital abnormalities.
• Multidetector computed tomography – is useful for the 3-dimensional anatomic evaluation for origin, patency, and termination of the CAVF.[rx]
• Exercise stress test – If your signs and symptoms occur most often during exercise, your doctor may ask you to walk on a treadmill or ride a stationary bike during an ECG. Sometimes, an echocardiogram is also done while you do these exercises. This is called a stress echo. In some cases, medication to stimulate your heart may be used instead of exercise.
• Stress Thallium Test – Stress thallium tests have two components — a treadmill stress test and heart scan after injection of a radionuclide material, such as thallium, which allows doctors to see the coronary arteries and the shape and function of the heart. It has been used in this manner safely for many years to demonstrate the amount of blood the heart is getting under various conditions — rest and stress.
• Nuclear stress test – This test is similar to an exercise stress test but adds images to the ECG recordings. It measures blood flow to your heart muscle at rest and during stress. A tracer is injected into your bloodstream, and special cameras can detect areas in your heart that receive less blood flow.
• Cardiac catheterization and angiogram – During cardiac catheterization, a doctor gently inserts a catheter into an artery or vein in your groin, neck, or arm and up to your heart. X-rays are used to guide the catheter to the correct position. Sometimes, dye is injected through the catheter. The dye helps blood vessels show up better on the images and outlines any blockages.
• Cardiac catheterization (left heart catheterization) – During this procedure, your doctor injects a special dye into your coronary arteries through a catheter inserted through an artery in your groin or forearm. The dye helps enhance the radiographic image of your coronary arteries to identify any blockages.
• Cardiac CT scan – A CT scan of the heart can help your doctor see calcium deposits in your arteries that can narrow the arteries. If a substantial amount of calcium is discovered, coronary artery disease may be likely.
• Treadmill testing – to measure how well the heart functions when challenged to work harder than normal (during exercise)
• Nuclear perfusion imaging – to identify areas of the heart that are receiving less blood
• Nuclear ventriculography – This uses tracers, or radioactive materials, to create an image of the heart chambers. A doctor will inject the tracers into the vein. The tracers then attach to red blood cells and pass through the heart. Special cameras or scanners trace the movement of the tracers.
• Coronary calcium scan – to measure the amount of calcium in the walls of your coronary arteries. The buildup of calcium can be a sign of atherosclerosis, coronary artery disease, or coronary microvascular disease. This test is a type of cardiac CT scan. Coronary calcium scans can also help assess coronary heart disease risk for people who smoke or for people who do not have heart symptoms.
• Cardiac MRI (magnetic resonance imaging) – to detect tissue damage or problems with blood flow in the heart or coronary arteries. It can help your doctor diagnose a coronary microvascular disease or nonobstructive or obstructive coronary artery disease. Cardiac MRI can help explain results from other imaging tests such as chest X-rays and CT scans.
• Cardiac positron emission tomography (PET) scanning – to assess blood flow through the small coronary blood vessels and into the heart tissues. This is a type of nuclear heart scan that can diagnose coronary microvascular disease.
• Coronary angiography – to show the insides of your coronary arteries. To get the dye into your coronary arteries, your doctor will use a procedure called cardiac catheterization. This procedure is often used if other tests show that you are likely to have coronary artery disease. To diagnose coronary microvascular disease, your doctor will use coronary angiography with guidewire technology. A guidewire with sensors is inserted into the heart’s arteries. The sensors measure how easily blood flows through the small vessels. Usually, measurements are done before and after giving you medicine to enhance blood flow in your heart.
• Coronary computed tomographic angiography – to show the insides of your coronary arteries rather than an invasive cardiac catheterization. It is a noninvasive imaging test using CT scanning.
• ECG – The resting 12 lead ECG is the first-line diagnostic tool for the diagnosis of the acute coronary syndrome (ACS). It should be obtained within 10 minutes of the patient’s arrival in the emergency department.[rx] Acute MI is often associated with dynamic changes in the ECG waveform. Serial ECG monitoring can provide important clues to the diagnosis if the initial EKG is non-diagnostic at the initial presentation.[rx] Serial or continuous ECG recordings may help determine reperfusion or re-occlusion status. A large and prompt reduction in ST-segment elevation is usually seen in reperfusion.[rx]

ECG findings suggestive of ongoing coronary artery occlusion (in the absence of left ventricular hypertrophy and bundle branch block):[rx]

ST-segment elevation in two contiguous lead (measured at J-point) of

• Greater than 5 mm in men younger than 40 years, greater than 2 mm in men older than 40 years, or greater than 1.5 mm in women in leads V2-V3 and/or
• Greater than 1 mm in all other leads

ST-segment depression and T-wave changes

• New horizontal or down-sloping ST-segment – depression greater than 5 mm in 2 contiguous leads and/or T inversion greater than 1 mm in two contiguous leads with prominent R waves or R/S ratio of greater than 1
• The hyperacute T-wave amplitude – with prominent symmetrical T waves in two contiguous leads, may be an early sign of acute MI that may precede the ST-segment elevation. Other ECG findings associated with myocardial ischemia include cardiac arrhythmias, intraventricular blocks, atrioventricular conduction delays, and loss of precordial R-wave amplitude (less specific finding).[rx]
• ECG findings alone are not sufficient to diagnose acute myocardial ischemia or acute MI as other conditions such as acute pericarditis, left ventricular hypertrophy (LVH), left bundle branch block (LBBB), Brugada syndrome, Takatsubo syndrome (TTS), and early repolarization patterns also present with ST deviation.

ECG changes associated with prior MI (in the absence of left ventricular hypertrophy and left bundle branch block):

• Any Q wave in lead V2-V3 greater than 0.02 s or QS complex in leads V2-V3
• Q wave > 03 s and greater than 1 mm deep or QS complex in leads I, II, aVL, aVF or V4-V6 in any two leads of contiguous lead grouping (I, aVL; V1-V6; II, III, aVF)
• R wave > 0.04 s in V1-V2 and R/S greater than 1 with a concordant positive T wave in the absence of conduction defect.

Electrocardiogram (EKG) 

EKG is a very basic yet enormously helpful test in the evaluation of coronary artery disease. It measures electrical activity in the cardiac conduction system and is measured by 10 leads attached to the skin at standardized locations. It provides information about both the physiology and anatomy of the heart. It typically has 12 leads on the paper that is printed once the test is performed and each lead correlates with the specific location of the heart. Important information to notice on an EKG is a heart’s rate, rhythm, and axis. After that, information regarding acute and chronic pathologic processes can be obtained. In acute coronary syndrome, one can see ST-segment changes and T wave changes. If an ACS has degenerated into arrhythmias, that can also be seen. In chronic settings, EKG can show information like axis deviation, bundle branch blocks, and ventricular hypertrophy. EKG is also a cost-effective and readily available testing modality that is not user-dependent.

Echocardiography

Echocardiography is an ultrasound of the heart. It is a useful and non-invasive mode of testing that is performed in both acute and chronic and inpatient and outpatient settings. In acute settings, it could tell about wall motion, valvular regurgitation and stenosis, infective or autoimmune lesions, and chamber sizes. It also is useful in the diagnosis of acute pulmonary pathologies like pulmonary embolism. It also evaluates the pericardial cavity. In chronic settings, it can be done to see the same information mentioned above and also a response to the therapy. It also is used in an outpatient setting as part of stress testing. In addition to diagnostics, it also has a role in therapeutics for example, pericardiocentesis could be performed with the needle-guided by echocardiography. This test is user-dependent and could be costly compared to EKG.[rx]

Stress Test

The stress test is a relatively non-invasive test to evaluate for coronary artery disease. It is used in the setting of suspected angina or angina equivalent and is helpful in ruling in or out coronary pathology when interpreted in an appropriate setting. During the test, the heart is artificially exposed to stress and if the patient gets certain abnormal EKG changes in ST segments or gets symptoms of angina, the test is aborted at that point and coronary artery disease is diagnosed. EKGs are obtained before, during, and after the procedure, and the patient is continuously monitored for any symptoms. There are mainly two types of stress tests; exercise stress test and pharmacologic stress test. In exercise stress tests, the patient has to run on a treadmill until he achieves 85% of the age-predicted maximal heart rate. If a patient develops exertional hypotension, hypertension (>200/110 mmHg), ST-segment elevations or depression, or ventricular or supraventricular arrhythmias.[rx]

Chest X-ray

Chest X-ray is an important component of the initial evaluation of cardiac disease. The standard imaging films include standing posteroanterior (PA) and left lateral decubitus. Sometimes, anteroposterior (AP) projection is obtained especially in inpatient settings with the patient lying down, however, this interpretation of AP films is significantly limited. Proper analysis of PA and AP views provides useful and cost-effective information about the heart, lungs, and vasculature. Interpretation should be done in a stepwise pattern so that important information is not overlooked.

Blood Work

Blood work aids in establishing the diagnosis and assessing therapeutic responses. In acute settings, cardiac enzymes and B-type natriuretic peptides are often done along with complete blood counts and metabolic panels. BNP provides information about volume overload of cardiogenic origin however it has its limitations. It can be falsely elevated in kidney diseases and falsely low in obesity. Cardiac enzymes like CK and troponin provide information about an acute ischemic event. In chronic settings, lipid panel provides important prognostic information. C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) aid in assessing disease like acute pericarditis. Liver function tests (LFT) can be done to evaluate for an infiltrative process that can affect the liver and heart simultaneously like hemochromatosis. Liver tests are also done to assess increased right heart pressures, especially in chronic settings.

Cardiac Catheterization

Cardiac catheterization is the gold standard and most accurate modality to evaluate ischemic coronary heart disease. It is however an invasive procedure with associated complications. Not everyone is a candidate for the procedure. In non ACS settings, patients with intermediate pretest probability for CAD are usually the right candidates for it. In the ACS setting, all STEMI patients and selected NSTEMI patients get an emergent cardiac catheterization. This procedure is done in a cardiac catheterization lab, is expertise dependent, and is done under moderate sedation. There is contrast exposure in the procedure which could cause serious allergic reactions and kidney injury.

Treatment of Obstructive Coronary Artery Disease

Nonpharmacological

Your doctor may recommend that you adopt lifelong heart-healthy lifestyle changes, including:

• Fish and fish oil – Fish and fish oil are the most effective sources of omega-3 fatty acids. Fatty fish — such as salmon, herring, and light canned tuna — contain the most omega-3 fatty acids and, therefore, the most benefit. Fish oil supplements may offer benefits, but the evidence is strongest for eating fish.
• Flax and flaxseed oil – Flax and flaxseed oil also contain beneficial omega-3 fatty acids, though studies have not found these sources to be as effective as fish. The shells on raw flaxseeds also contain soluble fiber, which can help with constipation. More research is needed to determine if flaxseed can help lower blood cholesterol.
• Other dietary sources of omega-3 fatty acids – Other dietary sources of omega-3 fatty acids include canola oil, soybeans, and soybean oil. These foods contain smaller amounts of omega-3 fatty acids than do fish and fish oil, and evidence for their benefit to heart health isn’t as strong.
• Aiming for a healthy weight – Losing just 3% to 5% of your current weight can help you manage some coronary heart disease risk factors, such as high blood cholesterol and diabetes. Greater amounts of weight loss can also improve blood pressure readings.
• Being physically active – Routine physical activity can help manage coronary heart disease risk factors such as high blood cholesterol, high blood pressure, or overweight and obesity. Before starting any exercise program, ask your doctor what level of physical activity is right for you.
• Heart-healthy eating – such as the DASH (Dietary Approaches to Stop Hypertension) eating plan. A heart-healthy eating plan includes fruits, vegetables, and whole grains and limits saturated fats, trans fats, sodium (salt), added sugars, and alcohol.
• Managing stress – Learning how to manage stress, relax, and cope with problems can improve your emotional and physical health.
• Quitting smoking – Although these resources focus on heart health, they include basic information about how to quit smoking. For free help and support to quit smoking, you can call the National Cancer Institute’s Smoking Quitline at 1-877-44U-QUIT (1-877-448-7848). Talk to your doctor if you vape. There is scientific evidence that nicotine and flavorings found in vaping products may damage your heart and lungs.
• Get enough good-quality sleep – The recommended amount for adults is 7 to 9 hours of sleep a day.
• Become more active, and stay active, all through life – A good goal is at least 150 minutes (2.5 hours) of moderate exercise each week, or 75 minutes (1.25 hours) of vigorous aerobic exercise each week. Or aim to be active for 30 minutes a day, most days of the week. Check with your doctor before you launch a new workout program if you’ve never worked out before.
• Keep your weight within the normal range on a Body Mass Index (BMI) chart – If you’re overweight, losing just 5 percent to 10 percent of your current weight will lower your risk of developing coronary artery disease.
• Find healthy outlets for your stress – Some stress is unavoidable in life. But it tends to push us toward not-so-great habits (overeating, drinking, sitting too much). You’ll be more heart-healthy if you can offload stress in ways you enjoy and that are good for you, such as exercise, meditation, and relaxing with friends, says McEvoy. A stress-management program can help.
• Manage blood pressure – Blood pressure should be checked regularly, especially in those who have blood pressure higher than normal or have a history of heart disease. Follow the doctor’s advice in managing blood pressure with drugs and diet.
• Manage cholesterol – You have to manage blood cholesterol levels regularly to keep a check. It includes observing the levels of LDL, HDL, and TG. Know more about good cholesterol and bad cholesterol and the foods that help in managing them.
• Manage blood sugar levels – In patients who are diabetic, tight blood sugar management can help manage coronary artery disease.
• Following a healthy diet – Eat healthy food that includes plant-based foods, such as fruits, vegetables, whole grains, legumes, and nuts, and also food that is low in saturated fat, cholesterol, and sodium. This can help you control your weight, blood pressure, and cholesterol. Avoid saturated fat and trans fat, excess salt, and excess sugar.

Acute Management

Reperfusion therapy is indicated in all patients with symptoms of ischemia of less than 12-hours duration and persistent ST-segment elevation. Primary percutaneous coronary intervention (PCI) is preferred to fibrinolysis if the procedure can be performed <120 minutes of ECG diagnosis. If there is no immediate option of PCI (>120 minutes), fibrinolysis should be started within 10 minutes of STEMI after ruling out contraindications. If transfer to a PCI center is possible in 60 to 90 minutes after a bolus of the fibrinolytic agent and the patient meets reperfusion criteria, a routine PCI can be done, or a rescue PCI can be planned.[rx][rx] If fibrinolysis is planned, it should be carried out with fibrin-specific agents such as tenecteplase, alteplase, or reteplase (class I).[rx]

• Aspirin – Aspirin is anti-thrombotic and reduces the risk of cardiovascular disease by irreversibly binding with the platelets. However, the use of low-dose aspirin (75 to 100 mg orally) for primary prevention is getting more controversial recently. Previous U.S. guidelines recommended aspirin for primary prevention in the settings of significant ASCVD risk factors. However, according to the recent ACC/AHA 2019 guidelines, the use of aspirin may be considered in patients (40 to 70 years old) with significant risk factors for cardiovascular disease and no risk of bleeding. The strength of recommendation is comparatively weaker, and a thorough evaluation with risk versus benefit assessment is necessary. These guidelines for primary preventions should undergo evaluation based on the individual patient basis, and risk versus analysis should always be based on the physician’s best clinical judgments.[rx]
• Relief of pain, breathlessness, and anxiety – The chest pain due to myocardial infarction is associated with sympathetic arousal, which causes vasoconstriction and increased workload for the ischemic heart. Intravenous opioids (e.g., morphine) are the analgesics most commonly used for pain relief (Class IIa).[rx] The results from the CRUSADE quality improvement initiative have shown that the use of morphine may be associated with a higher risk of death and adverse clinical outcomes.[rx] The study was done from the CIRCUS (Does Cyclosporine Improve outcome in STEMI patients) database, which showed no significant adverse events associated with morphine use in a case of anterior ST-segment elevation MI.[rx] A mild anxiolytic (usually a benzodiazepine) may be considered in very anxious patients (class IIa). Supplemental oxygen is indicated in patients with hypoxemia (SaO2 <90% or PaO2 <60mm Hg) (Class I).[rx]
• Intravenous Nitrates – Intravenous nitrates are more effective than sublingual nitrates with regard to symptom relief and regression of ST depression (NSTEMI). The dose is titrated upward until symptoms are relieved, blood pressure is normalized in hypertensive patients, or side effects such as a headache and hypotension are noted.[rx]
• Beta-blockers –  This group of drugs reduces myocardial oxygen consumption by lowering heart rate, blood pressure, and myocardial contractility. They block beta receptors in the body, including the heart, and reduce the effects of circulating catecholamines. Beta-blockers should not be used in suspected coronary vasospasm.
• Platelet inhibition – Aspirin is recommended in both STEMI and NSTEMI in an oral loading dose of 150 to 300 mg (non-enteric coated formulation) and a maintenance dose of 75 to 100 mg per day long-term regardless of treatment strategy (class I).[rx] Aspirin inhibits thromboxane A2 production throughout the lifespan of the platelet.[rx]
• Selective Beta-blockers. These drugs slow your heart rate and decrease your blood pressure, which decreases your heart’s demand for oxygen. If you’ve had a heart attack, beta-blockers reduce the risk of future attacks.
• Calcium channel blockers – These drugs may be used with beta-blockers if beta-blockers alone aren’t effective or instead of beta-blockers if you’re not able to take them. Calcium channel blockers to lower blood pressure by allowing blood vessels to relax. These drugs can help improve symptoms of chest pain.
• Ranolazine – This medication may help people with chest pain (angina)to treat coronary microvascular disease and the chest pain it may cause. It may be prescribed with a beta-blocker or instead of a beta-blocker if you can’t take it.
• Nitroglycerin – Nitroglycerin tablets, sprays, and patches can control chest pain by temporarily dilating your coronary arteries and reducing your heart’s demand for blood.
• Diuretics – Sometimes known as water pills, diuretics work by flushing excess water and salt from the body through urine.
• Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) – These similar drugs decrease blood pressure and may help prevent the progression of coronary artery disease. Angiotensin-2 receptor blockers (ARBs) work in a similar way to ACE inhibitors. They’re used to lower your blood pressure by blocking angiotensin-2. Mild dizziness is usually the only side effect. They’re often prescribed as an alternative to ACE inhibitors, as they do not cause a dry cough.
• Medication to manage blood cholesterol – Blood cholesterol is the main reason behind the plaque formation that clogs the arteries. Your doctor may recommend drugs to manage bad cholesterol (LDL) or improve good cholesterol (HDL). He may also recommend medication to manage triglycerides (TGs). Your doctor may choose from a range of cholesterol-lowering medications including statins, niacin, fibrates, and bile acid sequestrants.
• Medicines to control blood sugar – such as empagliflozin, canagliflozin, and liraglutide, help lower your risk for complications if you have coronary heart disease and diabetes.
• Most P2Y12 inhibitors – are inactive prodrugs (except for ticagrelor, which is an orally active drug that does not require activation) that require oxidation by the hepatic cytochrome P450 system to generate an active metabolite that selectively inhibits P2Y12 receptors irreversibly. Inhibition of P2Y12 receptors leads to inhibition of ATP-induced platelet aggregation. The commonly used P2Y12 inhibitors are clopidogrel, prasugrel, and ticagrelor.
• The loading dose for clopidogrel – is 300 to 600 mg loading dose followed by 75 mg per day.
• Prasugrel – 60 mg loading dose, and 10 mg per day of a maintenance dose have a faster onset when compared to clopidogrel.[rx] Patients undergoing PCI should be treated with dual antiplatelet therapy (DAPT) with aspirin + P2Y12 inhibitor and a parenteral anticoagulant. In PCI, the use of prasugrel or ticagrelor is found to be superior to clopidogrel. Aspirin and clopidogrel are also found to decrease the number of ischemic events in NSTEMI and UA.[rx]
• Heparin, enoxaparin, and bivalirudin – The anticoagulants used during PCI are unfractionated heparin, enoxaparin, and bivalirudin. The bivalirudin is recommended during primary PCI if the patient has heparin-induced thrombocytopenia.[rx]
• Lipid-lowering treatment – It is recommended to start high-intensity statins that reduce low-density lipoproteins (LDLs) and stabilize atherosclerotic plaques. High-density lipoproteins are found to be protective.[rx]
• Antithrombotic therapy – Aspirin is recommended lifelong, and the addition of another agent depends on the therapeutic procedure done, such as PCI with stent placement.
• ACE inhibitors – are recommended in patients with systolic left ventricular dysfunction, or heart failure, hypertension, or diabetes. Beta-blockers are recommended in patients with LVEF less than 40% if no other contraindications are present. Antihypertensive therapy can maintain a blood pressure goal of less than 140/90 mm Hg.
• Mineralocorticoid receptor antagonist therapy – is recommended in a patient with left ventricular dysfunction (LVEF less than 40%).
• Glucose lowering therapy – in people with diabetes to achieve current blood sugar goals. [rx]

Surgery

The following surgical procedures can open or replace blocked arteries if they have become very narrow, or if symptoms are not responding to medications:

• Laser surgery – This involves making several very small holes in the heart muscle. These encourage the formation of new blood vessels.
• Coronary bypass surgery – A surgeon will use a blood vessel from another part of the body to create a graft that bypasses the blocked artery. The graft may come from the leg, for example, or an inner chest-wall artery.
• Angioplasty and stent placement – A surgeon will insert a catheter into the narrowed part of the artery and pass a deflated balloon through the catheter to the affected area. When they inflate the balloon, it compresses the fatty deposits against the artery walls. They may leave a stent, or mesh tube, in the artery to help keep it open.
• Percutaneous coronary intervention (PCI) – to open coronary arteries that are narrowed or blocked by the buildup of atherosclerotic plaque. A small mesh tube called a stent is usually implanted after PCI to prevent the artery from narrowing again.
• Coronary artery bypass grafting (CABG) – to improves blood flow to the heart by using normal arteries from the chest wall and veins from the legs to bypass the blocked arteries. Surgeons typically use CABG to treat people who have severe obstructive coronary artery disease in multiple coronary arteries.
• Transmyocardial laser revascularization or coronary endarterectomy – to treat severe angina associated with coronary heart disease when other treatments are too risky or did not work.
• Heart transplant – Occasionally, when the heart is severely damaged and medicine is not effective, or when the heart becomes unable to adequately pump blood around the body (heart failure), a heart transplant may be needed.

Lifestyle and home remedies

Lifestyle changes can help you prevent or slow the progression of coronary artery disease.

• Stop smoking – Smoking is a major risk factor for coronary artery disease. Nicotine constricts blood vessels and forces your heart to work harder, and carbon monoxide reduces oxygen in your blood and damages the lining of your blood vessels. If you smoke, quitting is one of the best ways to reduce your risk of a heart attack.
• Smoking cessation – is the most cost-effective secondary measure to prevent MI. Smoking has a pro-thrombotic effect, which has a strong association with atherosclerosis and myocardial infarction.[rx]
• Diet, alcohol, and weight control – A diet low in saturated fat with a focus on whole grain products, vegetables, fruits, and fish is considered cardioprotective. The target level for bodyweight is body mass index of 20 to 25 kg/m2  and waist circumference of <94 cm for the men and <80 cm for the female.[rx]
• Control your blood pressure – Ask your doctor for a blood pressure measurement at least every two years. He or she may recommend more frequent measurements if your blood pressure is higher than normal or you have a history of heart disease. Optimal blood pressure is less than 120 systolic and 80 diastolic, as measured in millimeters of mercury (mm Hg).
• Check your cholesterol – Adults should get a baseline cholesterol test when in their 20s and at least every five years after. Ask your doctor what your cholesterol levels should be. Most people should aim for an LDL cholesterol level below 130 milligrams per deciliter (mg/dL), or 3.4 millimoles per liter (mmol/L). If you have other risk factors for heart disease, your target LDL cholesterol may be below 100 mg/dL (2.6 mmol/L). Ask your doctor what level LDL is best for you. If your test results aren’t meeting your targeted levels, you may need more frequent cholesterol tests.
• Keep diabetes under control – If you have diabetes, tight blood sugar management can help reduce the risk of heart disease.
• Eat heart-healthy foods – Eat plenty of fruits, vegetables, whole grains, legumes, and nuts. Avoid saturated fats and trans fats and reduce salt and sugar. Eating one or two servings of fish a week also may help keep your heart healthy.
• Avoid or limit alcohol – If you choose to drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women and up to two drinks a day for men.
• Get moving – Exercise helps manage weight and control diabetes, high cholesterol, and high blood pressure — all risk factors for coronary artery disease. Get at least 150 minutes of moderate aerobic activity or 75 minutes of vigorous aerobic activity a week, or a combination of moderate and vigorous activity.
• Maintain a healthy weight – Being overweight increases your risk of coronary artery disease. Losing even just a small amount of weight can help reduce risk factors for coronary artery disease.
• Participate in cardiac rehabilitation – If you’ve had surgery, your doctor may suggest you participate in cardiac rehabilitation — a program of education, counseling, and exercise training that’s designed to help improve your health.
• Manage stress – Reduce stress as much as possible. Practice healthy techniques for managing stress, such as muscle relaxation and deep breathing.
• Get your flu shot – Get your flu (influenza) vaccine each year to reduce your risk of having influenza.

Regular medical checkups are also important. Some of the main risk factors for coronary artery disease — high cholesterol, high blood pressure, and diabetes — have no symptoms in the early stages. Early detection and treatment can help you maintain better heart health.

Alternative medicine

Other supplements may help reduce your blood pressure or cholesterol level, two contributing factors to coronary artery disease. These include:

• Alpha-linolenic acid
• Barley
• Cocoa
• Coenzyme Q10
• Fiber, including blond psyllium and oat bran (found in oatmeal and whole oats)
• Garlic
• Plant stanols and sterols (found in supplements and some margarine, such as Promise, Smart Balance, and Benecol)

Always talk to your doctor before adding a new over-the-counter medication or supplement to your treatment plan. Some drugs and supplements can interfere with other medications and cause side effects or make them less effective.

Risk factors

Risk factors for coronary artery disease include:

• Age – Getting older increases your risk of damaged and narrowed arteries.
• Sex – Men are generally at greater risk of coronary artery disease. However, the risk for women increases after menopause.
• Family history – A family history of heart disease is associated with a higher risk of coronary artery disease, especially if a close relative developed heart disease at an early age. Your risk is highest if your father or a brother was diagnosed with heart disease before age 55 or if your mother or a sister developed it before age 65.
• Smoking – People who smoke have a significantly increased risk of heart disease. Breathing in secondhand smoke also increases a person’s risk of coronary artery disease.
• High blood pressure – Uncontrolled high blood pressure can result in hardening and thickening of your arteries, narrowing the channel through which blood can flow.
• High blood cholesterol levels – High levels of cholesterol in your blood can increase the risk of the formation of plaque and atherosclerosis. High cholesterol can be caused by a high level of low-density lipoprotein (LDL) cholesterol, known as the “bad” cholesterol. A low level of high-density lipoprotein (HDL) cholesterol, known as the “good” cholesterol, can also contribute to the development of atherosclerosis.
• Diabetes – Diabetes is associated with an increased risk of coronary artery disease. Type 2 diabetes and coronary artery disease share similar risk factors, such as obesity and high blood pressure.
• Overweight or obesity – Excess weight typically worsens other risk factors.
• Physical inactivity – Lack of exercise also is associated with coronary artery disease and some of its risk factors, as well.
• High stress – Unrelieved stress in your life may damage your arteries as well as worsen other risk factors for coronary artery disease.
• Unhealthy diet – Eating too much food that has high amounts of saturated fat, trans fat, salt, and sugar can increase your risk of coronary artery disease.
• Sleep apnea – This disorder causes you to repeatedly stop and start breathing while you’re sleeping. Sudden drops in blood oxygen levels that occur during sleep apnea increase blood pressure and strain the cardiovascular system, possibly leading to coronary artery disease.
• High-sensitivity C-reactive protein (hs-CRP) – This protein appears in higher-than-normal amounts when there’s inflammation somewhere in your body. High hs-CRP levels may be a risk factor for heart disease. It’s thought that as coronary arteries narrow, you’ll have more hs-CRP in your blood.
• High triglycerides – This is a type of fat (lipid) in your blood. High levels may raise the risk of coronary artery disease, especially for women.
• Homocysteine – Homocysteine is an amino acid your body uses to make protein and to build and maintain tissue. But high levels of homocysteine may increase your risk of coronary artery disease.
• Preeclampsia – This condition that can develop in women during pregnancy causes high blood pressure and a higher amount of protein in the urine. It can lead to a higher risk of heart disease later in life.
• Alcohol use – Heavy alcohol use can lead to heart muscle damage. It can also worsen other risk factors of coronary artery disease.
• Autoimmune diseases – People who have conditions such as rheumatoid arthritis and lupus (and other inflammatory conditions) have an increased risk of atherosclerosis.

Prevention

References

Digestive Tract/Gastrointestinal Tract /The digestive system is made up of the gastrointestinal tract also called the GI tract or digestive tract—and the liver, pancreas, and gallbladder. The GI tract is a series of hollow organs joined in a long, twisting tube from the mouth to the anus. The hollow organs that make up the GI tract are the mouth, esophagus, stomach, small intestine, large intestine, and anus. The liver, pancreas, and gallbladder are the solid organs of the digestive system.

The small intestine has three parts. The first part is called the duodenum. The jejunum is in the middle and the ileum is at the end. The large intestine includes the appendix, cecum, colon, and rectum. The appendix is a finger-shaped pouch attached to the cecum. The cecum is the first part of the large intestine. The colon is next. The rectum is the end of the large intestine.

Bacteria in your GI tract, also called gut flora or microbiome, help with digestion. Parts of your nervous and circulatory systems also help. Working together, nerves, hormones, bacteria, blood, and the organs of your digestive system digest the foods and liquids you eat or drink each day.

Why is digestion important?

Digestion is important because your body needs nutrients from food and drink to work properly and stay healthy. Proteins, fats, carbohydrates, vitamins, minerals, and water are nutrients. Your digestive system breaks nutrients into parts small enough for your body to absorb and use for energy, growth, and cell repair.

• Proteins break into amino acids
• Fats break into fatty acids and glycerol
• Carbohydrates break into simple sugars

How does my digestive system work?

Each part of your digestive system helps to move food and liquid through your GI tract, break food and liquid into smaller parts, or both. Once foods are broken into small enough parts, your body can absorb and move the nutrients to where they are needed. Your large intestine absorbs water, and the waste products of digestion become stool. Nerves and hormones help control the digestive process.

The digestive process

How does food move through my GI tract?

Food moves through your GI tract by a process called peristalsis. The large, hollow organs of your GI tract contain a layer of muscle that enables their walls to move. The movement pushes food and liquid through your GI tract and mixes the contents within each organ. The muscle behind the food contracts and squeezes the food forward, while the muscle in front of the food relaxes to allow the food to move.

• Mouth – Food starts to move through your GI tract when you eat. When you swallow, your tongue pushes the food into your throat. A small flap of tissue, called the epiglottis, folds over your windpipe to prevent choking and the food passes into your esophagus.
• Esophagus – Once you begin swallowing, the process becomes automatic. Your brain signals the muscles of the esophagus and peristalsis begins.
• Lower esophageal sphincter – When food reaches the end of your esophagus, a ringlike muscle—called the lower esophageal sphincter —relaxes and lets food pass into your stomach. This sphincter usually stays closed to keep what’s in your stomach from flowing back into your esophagus.
• Stomach – After food enters your stomach, the stomach muscles mix the food and liquid with digestive juices. The stomach slowly empties its contents, called chyme, into your small intestine.
• Small intestine – The muscles of the small intestine mix food with digestive juices from the pancreas, liver, and intestine, and push the mixture forward for further digestion. The walls of the small intestine absorb water and the digested nutrients into your bloodstream. As peristalsis continues, the waste products of the digestive process move into the large intestine.
• Large intestine – Waste products from the digestive process include undigested parts of food, fluid, and older cells from the lining of your GI tract. The large intestine absorbs water and changes the waste from a liquid into the stool. Peristalsis helps move the stool into your rectum.
• Rectum – The lower end of your large intestine, the rectum, stores stool until it pushes stool out of your anus during a bowel movement.

How does my digestive system break food into small parts my body can use?

As food moves through your GI tract, your digestive organs break the food into smaller parts using:

• motion, such as chewing, squeezing, and mixing
• digestive juices, such as stomach acid, bile, and enzymes
• Mouth – The digestive process starts in your mouth when you chew. Your salivary glands make saliva, a digestive juice, which moistens food so it moves more easily through your esophagus into your stomach. Saliva also has an enzyme that begins to break down starches in your food.
• Esophagus  After you swallow, peristalsis pushes the food down your esophagus into your stomach.
• Stomach – Glands in your stomach lining make stomach acid and enzymes that break down food. Muscles of your stomach mix the food with these digestive juices.
• Pancreas – Your pancreas makes a digestive juice that has enzymes that break down carbohydrates, fats, and proteins. The pancreas delivers the digestive juice to the small intestine through small tubes called ducts.
• Liver – Your liver makes a digestive juice called bile that helps digest fats and some vitamins. Bile ducts carry bile from your liver to your gallbladder for storage, or to the small intestine for use.
• Gallbladder – Your gallbladder stores bile between meals. When you eat, your gallbladder squeezes bile through the bile ducts into your small intestine.
• Small intestine – Your small intestine makes digestive juice, which mixes with bile and pancreatic juice to complete the breakdown of proteins, carbohydrates, and fats. Bacteria in your small intestine make some of the enzymes you need to digest carbohydrates. Your small intestine moves water from your bloodstream into your GI tract to help break down food. Your small intestine also absorbs water with other nutrients.
• Large intestine – In your large intestine, more water moves from your GI tract into your bloodstream. Bacteria in your large intestine help break down remaining nutrients and make vitamin K. Waste products of digestion, including parts of food that are still too large, become stool.

What happens to the digested food?

The small intestine absorbs most of the nutrients in your food, and your circulatory system passes them on to other parts of your body to store or use. Special cells help absorbed nutrients cross the intestinal lining into your bloodstream. Your blood carries simple sugars, amino acids, glycerol, and some vitamins and salts to the liver. Your liver stores, processes, and delivers nutrients to the rest of your body when needed.

The lymph system, a network of vessels that carry white blood cells and a fluid called lymph throughout your body to fight infection, absorbs fatty acids and vitamins.

Your body uses sugars, amino acids, fatty acids, and glycerol to build substances you need for energy, growth, and cell repair.

How does my body control the digestive process?

Your hormones and nerves work together to help control the digestive process. Signals flow within your GI tract and back and forth from your GI tract to your brain.

Hormones

Cells lining your stomach and small intestine make and release hormones that control how your digestive system works. These hormones tell your body when to make digestive juices and send signals to your brain that you are hungry or full. Your pancreas also makes hormones that are important to digestion.

Nerves

You have nerves that connect your central nervous system—your brain and spinal cord—to your digestive system and control some digestive functions. For example, when you see or smell food, your brain sends a signal that causes your salivary glands to “make your mouth water” to prepare you to eat.

You also have an enteric nervous system (ENS)—nerves within the walls of your GI tract. When food stretches the walls of your GI tract, the nerves of your ENS release many different substances that speed up or delay the movement of food and the production of digestive juices. The nerves send signals to control the actions of your gut muscles to contract and relax to push food through your intestines.

References

GI Tract /Gastrointestinal Tract /The digestive system is made up of the gastrointestinal tract also called the GI tract or digestive tract—and the liver, pancreas, and gallbladder. The GI tract is a series of hollow organs joined in a long, twisting tube from the mouth to the anus. The hollow organs that make up the GI tract are the mouth, esophagus, stomach, small intestine, large intestine, and anus. The liver, pancreas, and gallbladder are the solid organs of the digestive system.

The small intestine has three parts. The first part is called the duodenum. The jejunum is in the middle and the ileum is at the end. The large intestine includes the appendix, cecum, colon, and rectum. The appendix is a finger-shaped pouch attached to the cecum. The cecum is the first part of the large intestine. The colon is next. The rectum is the end of the large intestine.

Bacteria in your GI tract, also called gut flora or microbiome, help with digestion. Parts of your nervous and circulatory systems also help. Working together, nerves, hormones, bacteria, blood, and the organs of your digestive system digest the foods and liquids you eat or drink each day.

Why is digestion important?

Digestion is important because your body needs nutrients from food and drink to work properly and stay healthy. Proteins, fats, carbohydrates, vitamins, minerals, and water are nutrients. Your digestive system breaks nutrients into parts small enough for your body to absorb and use for energy, growth, and cell repair.

• Proteins break into amino acids
• Fats break into fatty acids and glycerol
• Carbohydrates break into simple sugars

How does my digestive system work?

Each part of your digestive system helps to move food and liquid through your GI tract, break food and liquid into smaller parts, or both. Once foods are broken into small enough parts, your body can absorb and move the nutrients to where they are needed. Your large intestine absorbs water, and the waste products of digestion become stool. Nerves and hormones help control the digestive process.

The digestive process

How does food move through my GI tract?

Food moves through your GI tract by a process called peristalsis. The large, hollow organs of your GI tract contain a layer of muscle that enables their walls to move. The movement pushes food and liquid through your GI tract and mixes the contents within each organ. The muscle behind the food contracts and squeezes the food forward, while the muscle in front of the food relaxes to allow the food to move.

• Mouth – Food starts to move through your GI tract when you eat. When you swallow, your tongue pushes the food into your throat. A small flap of tissue, called the epiglottis, folds over your windpipe to prevent choking and the food passes into your esophagus.
• Esophagus – Once you begin swallowing, the process becomes automatic. Your brain signals the muscles of the esophagus and peristalsis begins.
• Lower esophageal sphincter – When food reaches the end of your esophagus, a ringlike muscle—called the lower esophageal sphincter —relaxes and lets food pass into your stomach. This sphincter usually stays closed to keep what’s in your stomach from flowing back into your esophagus.
• Stomach – After food enters your stomach, the stomach muscles mix the food and liquid with digestive juices. The stomach slowly empties its contents, called chyme, into your small intestine.
• Small intestine – The muscles of the small intestine mix food with digestive juices from the pancreas, liver, and intestine, and push the mixture forward for further digestion. The walls of the small intestine absorb water and the digested nutrients into your bloodstream. As peristalsis continues, the waste products of the digestive process move into the large intestine.
• Large intestine – Waste products from the digestive process include undigested parts of food, fluid, and older cells from the lining of your GI tract. The large intestine absorbs water and changes the waste from a liquid into the stool. Peristalsis helps move the stool into your rectum.
• Rectum – The lower end of your large intestine, the rectum, stores stool until it pushes stool out of your anus during a bowel movement.

How does my digestive system break food into small parts my body can use?

As food moves through your GI tract, your digestive organs break the food into smaller parts using:

• motion, such as chewing, squeezing, and mixing
• digestive juices, such as stomach acid, bile, and enzymes
• Mouth – The digestive process starts in your mouth when you chew. Your salivary glands make saliva, a digestive juice, which moistens food so it moves more easily through your esophagus into your stomach. Saliva also has an enzyme that begins to break down starches in your food.
• Esophagus  After you swallow, peristalsis pushes the food down your esophagus into your stomach.
• Stomach – Glands in your stomach lining make stomach acid and enzymes that break down food. Muscles of your stomach mix the food with these digestive juices.
• Pancreas – Your pancreas makes a digestive juice that has enzymes that break down carbohydrates, fats, and proteins. The pancreas delivers the digestive juice to the small intestine through small tubes called ducts.
• Liver – Your liver makes a digestive juice called bile that helps digest fats and some vitamins. Bile ducts carry bile from your liver to your gallbladder for storage, or to the small intestine for use.
• Gallbladder – Your gallbladder stores bile between meals. When you eat, your gallbladder squeezes bile through the bile ducts into your small intestine.
• Small intestine – Your small intestine makes digestive juice, which mixes with bile and pancreatic juice to complete the breakdown of proteins, carbohydrates, and fats. Bacteria in your small intestine make some of the enzymes you need to digest carbohydrates. Your small intestine moves water from your bloodstream into your GI tract to help break down food. Your small intestine also absorbs water with other nutrients.
• Large intestine – In your large intestine, more water moves from your GI tract into your bloodstream. Bacteria in your large intestine help break down remaining nutrients and make vitamin K. Waste products of digestion, including parts of food that are still too large, become stool.

What happens to the digested food?

The small intestine absorbs most of the nutrients in your food, and your circulatory system passes them on to other parts of your body to store or use. Special cells help absorbed nutrients cross the intestinal lining into your bloodstream. Your blood carries simple sugars, amino acids, glycerol, and some vitamins and salts to the liver. Your liver stores, processes, and delivers nutrients to the rest of your body when needed.

The lymph system, a network of vessels that carry white blood cells and a fluid called lymph throughout your body to fight infection, absorbs fatty acids and vitamins.

Your body uses sugars, amino acids, fatty acids, and glycerol to build substances you need for energy, growth, and cell repair.

How does my body control the digestive process?

Your hormones and nerves work together to help control the digestive process. Signals flow within your GI tract and back and forth from your GI tract to your brain.

Hormones

Cells lining your stomach and small intestine make and release hormones that control how your digestive system works. These hormones tell your body when to make digestive juices and send signals to your brain that you are hungry or full. Your pancreas also makes hormones that are important to digestion.

Nerves

You have nerves that connect your central nervous system—your brain and spinal cord—to your digestive system and control some digestive functions. For example, when you see or smell food, your brain sends a signal that causes your salivary glands to “make your mouth water” to prepare you to eat.

You also have an enteric nervous system (ENS)—nerves within the walls of your GI tract. When food stretches the walls of your GI tract, the nerves of your ENS release many different substances that speed up or delay the movement of food and the production of digestive juices. The nerves send signals to control the actions of your gut muscles to contract and relax to push food through your intestines.

References

Gastrointestinal Tract /The digestive system is made up of the gastrointestinal tract also called the GI tract or digestive tract—and the liver, pancreas, and gallbladder. The GI tract is a series of hollow organs joined in a long, twisting tube from the mouth to the anus. The hollow organs that make up the GI tract are the mouth, esophagus, stomach, small intestine, large intestine, and anus. The liver, pancreas, and gallbladder are the solid organs of the digestive system.

The small intestine has three parts. The first part is called the duodenum. The jejunum is in the middle and the ileum is at the end. The large intestine includes the appendix, cecum, colon, and rectum. The appendix is a finger-shaped pouch attached to the cecum. The cecum is the first part of the large intestine. The colon is next. The rectum is the end of the large intestine.

Bacteria in your GI tract, also called gut flora or microbiome, help with digestion. Parts of your nervous and circulatory systems also help. Working together, nerves, hormones, bacteria, blood, and the organs of your digestive system digest the foods and liquids you eat or drink each day.

Why is digestion important?

Digestion is important because your body needs nutrients from food and drink to work properly and stay healthy. Proteins, fats, carbohydrates, vitamins, minerals, and water are nutrients. Your digestive system breaks nutrients into parts small enough for your body to absorb and use for energy, growth, and cell repair.

• Proteins break into amino acids
• Fats break into fatty acids and glycerol
• Carbohydrates break into simple sugars

How does my digestive system work?

Each part of your digestive system helps to move food and liquid through your GI tract, break food and liquid into smaller parts, or both. Once foods are broken into small enough parts, your body can absorb and move the nutrients to where they are needed. Your large intestine absorbs water, and the waste products of digestion become stool. Nerves and hormones help control the digestive process.

The digestive process

How does food move through my GI tract?

Food moves through your GI tract by a process called peristalsis. The large, hollow organs of your GI tract contain a layer of muscle that enables their walls to move. The movement pushes food and liquid through your GI tract and mixes the contents within each organ. The muscle behind the food contracts and squeezes the food forward, while the muscle in front of the food relaxes to allow the food to move.

• Mouth – Food starts to move through your GI tract when you eat. When you swallow, your tongue pushes the food into your throat. A small flap of tissue, called the epiglottis, folds over your windpipe to prevent choking and the food passes into your esophagus.
• Esophagus – Once you begin swallowing, the process becomes automatic. Your brain signals the muscles of the esophagus and peristalsis begins.
• Lower esophageal sphincter – When food reaches the end of your esophagus, a ringlike muscle—called the lower esophageal sphincter —relaxes and lets food pass into your stomach. This sphincter usually stays closed to keep what’s in your stomach from flowing back into your esophagus.
• Stomach – After food enters your stomach, the stomach muscles mix the food and liquid with digestive juices. The stomach slowly empties its contents, called chyme, into your small intestine.
• Small intestine – The muscles of the small intestine mix food with digestive juices from the pancreas, liver, and intestine, and push the mixture forward for further digestion. The walls of the small intestine absorb water and the digested nutrients into your bloodstream. As peristalsis continues, the waste products of the digestive process move into the large intestine.
• Large intestine – Waste products from the digestive process include undigested parts of food, fluid, and older cells from the lining of your GI tract. The large intestine absorbs water and changes the waste from a liquid into the stool. Peristalsis helps move the stool into your rectum.
• Rectum – The lower end of your large intestine, the rectum, stores stool until it pushes stool out of your anus during a bowel movement.

How does my digestive system break food into small parts my body can use?

As food moves through your GI tract, your digestive organs break the food into smaller parts using:

• motion, such as chewing, squeezing, and mixing
• digestive juices, such as stomach acid, bile, and enzymes
• Mouth – The digestive process starts in your mouth when you chew. Your salivary glands make saliva, a digestive juice, which moistens food so it moves more easily through your esophagus into your stomach. Saliva also has an enzyme that begins to break down starches in your food.
• Esophagus  After you swallow, peristalsis pushes the food down your esophagus into your stomach.
• Stomach – Glands in your stomach lining make stomach acid and enzymes that break down food. Muscles of your stomach mix the food with these digestive juices.
• Pancreas – Your pancreas makes a digestive juice that has enzymes that break down carbohydrates, fats, and proteins. The pancreas delivers the digestive juice to the small intestine through small tubes called ducts.
• Liver – Your liver makes a digestive juice called bile that helps digest fats and some vitamins. Bile ducts carry bile from your liver to your gallbladder for storage, or to the small intestine for use.
• Gallbladder – Your gallbladder stores bile between meals. When you eat, your gallbladder squeezes bile through the bile ducts into your small intestine.
• Small intestine – Your small intestine makes digestive juice, which mixes with bile and pancreatic juice to complete the breakdown of proteins, carbohydrates, and fats. Bacteria in your small intestine make some of the enzymes you need to digest carbohydrates. Your small intestine moves water from your bloodstream into your GI tract to help break down food. Your small intestine also absorbs water with other nutrients.
• Large intestine – In your large intestine, more water moves from your GI tract into your bloodstream. Bacteria in your large intestine help break down remaining nutrients and make vitamin K. Waste products of digestion, including parts of food that are still too large, become stool.

What happens to the digested food?

The small intestine absorbs most of the nutrients in your food, and your circulatory system passes them on to other parts of your body to store or use. Special cells help absorbed nutrients cross the intestinal lining into your bloodstream. Your blood carries simple sugars, amino acids, glycerol, and some vitamins and salts to the liver. Your liver stores, processes, and delivers nutrients to the rest of your body when needed.

The lymph system, a network of vessels that carry white blood cells and a fluid called lymph throughout your body to fight infection, absorbs fatty acids and vitamins.

Your body uses sugars, amino acids, fatty acids, and glycerol to build substances you need for energy, growth, and cell repair.

How does my body control the digestive process?

Your hormones and nerves work together to help control the digestive process. Signals flow within your GI tract and back and forth from your GI tract to your brain.

Hormones

Cells lining your stomach and small intestine make and release hormones that control how your digestive system works. These hormones tell your body when to make digestive juices and send signals to your brain that you are hungry or full. Your pancreas also makes hormones that are important to digestion.

Nerves

You have nerves that connect your central nervous system—your brain and spinal cord—to your digestive system and control some digestive functions. For example, when you see or smell food, your brain sends a signal that causes your salivary glands to “make your mouth water” to prepare you to eat.

You also have an enteric nervous system (ENS)—nerves within the walls of your GI tract. When food stretches the walls of your GI tract, the nerves of your ENS release many different substances that speed up or delay the movement of food and the production of digestive juices. The nerves send signals to control the actions of your gut muscles to contract and relax to push food through your intestines.

References

References

Bowel Diversion/Ostomy surgery of the bowel, also known as bowel diversion, refers to surgical procedures that reroute the normal movement of intestinal contents out of the body when part of the bowel is diseased or removed. Creating an ostomy means bringing part of the intestine through the abdominal wall so that waste exits through the abdominal wall instead of passing through the anus.

Ostomy surgery of the bowel may be temporary or permanent, depending on the reason for the surgery. A surgeon specially trained in intestinal surgery performs the procedure in a hospital. During the surgery, the person receives general anesthesia.

Ostomy surgeries of the bowel include

• ileostomy
• colostomy
• ileoanal reservoir
• continent ileostomy

What is the bowel?

The bowel is another word for the small and large intestines. The bowel forms the largest part of the gastrointestinal (GI) tract—a series of hollow organs joined in a long, twisting tube from the mouth to the anus. The anus is a 1-inch-long opening through which stool leaves the body. Organs that make up the GI tract include the mouth, esophagus, stomach, small intestine, large intestine, and anus. The small intestine measures about 20 feet long in adults and includes

• the duodenum—the first part of the small intestine nearest the stomach
• the jejunum—the middle section of the small intestine between the duodenum and ileum
• the ileum—the lower end of the small intestine

Peristalsis—a wavelike movement of muscles in the GI tract—moves food and liquid through the GI tract. Peristalsis, along with the release of hormones and enzymes, helps food digest. The small intestine absorbs nutrients from foods and liquids passed from the stomach. Most food digestion and nutrient absorption take place in the small intestine.

The large intestine consists of the cecum, colon, and rectum. The cecum connects to the last part of the ileum and contains the appendix. The large intestine measures about 5 feet in adults and absorbs water and any remaining nutrients from partially digested food passed from the small intestine. The large intestine then changes waste from liquid to semisolid or solid feces, or stool. Stool passes from the colon to the rectum. The rectum measures 6 to 8 inches in adults and is located between the last part of the colon and the anus. The rectum stores stool prior to a bowel movement. During a bowel movement, stool moves from the rectum, through the anus, and out of the body.

Why does a person need ostomy surgery of the bowel?

A person may need ostomy surgery of the bowel if he or she has

• cancer of the colon or rectum
• an injury to the small or large intestine
• inflammatory bowel disease—longlasting disorders, such as Crohn’s disease and ulcerative colitis, that cause irritation or sores in the GI tract
• obstruction—a blockage in the bowel that prevents the flow of fluids or solids
• diverticulitis—a condition that occurs when small pouches in the colon called diverticula become inflamed, or irritated and swollen, and infected

What is a stoma?

During ostomy surgery of the bowel, a surgeon creates a stoma by bringing the end of the intestine through an opening in the abdomen and attaching it to the skin to create an opening outside the body. A stoma may be three-fourths of an inch to a little less than 2 inches wide. The stoma is usually located in the lower part of the abdomen, just below the beltline. However, sometimes the soma is located in the upper abdomen. The surgeon and a wound, ostomy, and continence (WOC) nurse or an enterostomal therapist will work together to select the best location for the stoma. A removable external collection pouch, called an ostomy pouch or ostomy appliance, is attached to the stoma and worn outside the body to collect intestinal contents or stool. Intestinal contents or stool passes through the stoma instead of passing through the anus. The stoma has no muscle, so it cannot control the flow of stool, and the flow occurs whenever other digestive muscles contract. Ileostomy and colostomy are the two main types of ostomy surgery of the bowel during which a surgeon creates a stoma.

What is an ileostomy?

An ileostomy is a stoma created from a part of the ileum. For this surgery, the surgeon brings the ileum through the abdominal wall to make a stoma. An ileostomy may be permanent or temporary. An ileostomy is permanent when the surgeon removes or bypasses the entire colon, rectum, and anus. A surgeon may perform a temporary ileostomy for a damaged or an inflamed colon or rectum that only needs time to rest or heal from injury or surgery. After the colon or rectum heals, the surgeon repairs the opening in the abdominal wall and reconnects the ileum so stool will pass into the colon normally. An ileostomy is the most common temporary bowel diversion. A surgeon performs an ileostomy most often to treat inflammatory bowel disease or rectal cancer.

What is a colostomy?

A colostomy is a stoma created from a part of the colon. For this surgery, the surgeon brings the colon through the abdominal wall and makes a stoma. A colostomy may be temporary or permanent. The colostomy is permanent when the surgeon removes or bypasses the lower end of the colon or rectum. A surgeon may perform a temporary colostomy for a damaged or an inflamed lower part of the colon or rectum that only needs time to rest or heal from injury or surgery. Once the colon or rectum heals, the surgeon repairs the opening in the abdominal wall and reconnects the colon so stool will pass normally. A surgeon performs a colostomy most often to treat rectal cancer, diverticulitis, or fecal incontinence–the accidental loss of stool.

What is an ileoanal reservoir?

An ileoanal reservoir is an internal pouch made from the ileum. This surgery is a common alternative to an ileostomy and does not have a permanent stoma. Also known as a J-pouch or pelvic pouch, the ileoanal reservoir connects to the anus after a surgeon removes the colon and rectum. Stool collects in the ileoanal reservoir and then exits the body through the anus during a bowel movement. An ileoanal reservoir is an option after removal of the entire large intestine when the anus remains intat and disease-free. The surgeon often makes a temporary ileostomy before or at the time of making an ileoanal reservoir. Once the ileoanal reservoir heals from surgery, the surgeon reconnects the ileum to the ileoanal pouch and closes the temporary ileostomy. A person does not need a permanent external ostomy pouch for an an ileoanal reservoir.

A surgeon creates an ileoanal reservoir most often to treat ulcerative colitis or familial adenomatous polyposis. Familial adenomatous polyposis is an inherited disease characterized by the presence of 100 or more polyps in the colon. The polyps may lead to colorectal cancer if not treated. People with Crohn’s disease usually are not candidates for this procedure.

What is a continent ileostomy?

A continent ileostomy is an internal pouch, sometimes called a Kock pouch, fashioned from the end of the ileum just before it exits the abdominal wall as an ileostomy. The surgeon makes a valve inside the pouch so that intestinal contents do not flow out. The person drains the pouch each day by inserting a thin, flexible tube, called a catheter, through the stoma. The person covers the stoma with a simple patch or dressing. A continent ileostomy is an option for people who are not good candidates for an ileoanal reservoir because of damage to the rectum or anus and who do not want to wear an ostomy pouch.

Creating the Kock pouch is a delicate surgical procedure that requires a healthy bowel for proper healing. Therefore, a surgeon usually does not perform Kock pouch surgery during an acute attack of bowel disease. A continent ileostomy is now uncommon, and most hospitals do not have a specialist who knows how to perform this type of surgery. As with ileoanal reservoir surgery, the surgeon usually removes the colon and rectum to treat the original bowel disease, such as ulcerative colitis or familial adenomatous polyposis. People with Crohn’s disease are not usually candidates for this procedure.

What are the complications of ostomy surgery of the bowel?

Complications of ostomy surgery of the bowel may include

• skin irritation
• stoma problems
• blockage
• diarrhea
• bleeding
• electrolyte imbalance
• infection
• irritation of the internal pouch, or pouchitis
• vitamin B12 deficiency
• phantom rectum
• short bowel syndrome
• rectal discharge

Skin Irritation

Skin irritation is the most common complication for people with an ostomy. If the external ostomy pouch does not fit properly, stool or stool contents can leak out around the stoma and under the pouch. When irritated, a person’s skin will become itchy, red, and uncomfortable. When changing the pouch, a person can use an ostomy powder on the skin around the stoma to treat skin irritation. If the skin irritation does not improve, the person should talk with a WOC nurse or an enterostomal therapist—who is specially trained in ostomy care and rehabilitation—or another health care provider about the symptoms. Skin irritation may occur around the stoma for people who have an ileostomy or a colostomy. People who have ileoanal reservoir surgery may have skin irritation around the anus. Sometimes, using a barrier ointment to protect the skin around the anus can help treat and prevent irritation.

Stoma Problems

Stoma problems include the following:

• Hernia. A stoma hernia, seen as a bulge in the skin around the stoma, is a weakening of the abdominal wall around the stoma site. As with all hernias, a stoma hernia continues to increase in size and may eventually need surgical repair when it becomes too large. Rarely, the intestine gets trapped or kinked within the hernia and becomes blocked. A blocked intestine that loses its blood supply requires emergency surgery.
• Prolapse. A stoma prolapse occurs when the bowel pushes itself through the stoma. A person may be able to push the bowel back through the stoma and keep it in place with a stoma shield. If not, the stoma prolapse may require special care and a larger ostomy pouch. A stoma prolapse that becomes blocked or loses its blood supply requires surgical repair.
• Narrowing of the stoma. Narrowing of the stoma makes it difficult for stool to pass through the stoma. A narrowed stoma may need surgical repair.

Blockage

Occasionally, an ileostomy or a colostomy does not function for a short time. If the stoma has not passed intestinal content or stool for 4 to 6 hours and the person is experiencing cramping or nausea, the ileum or colon may be blocked. Blockage may occur when foods that are hard to digest get stuck in the ileum or colon.

Abdominal adhesions in the ileum or colon may cause a blockage as well. Abdominal adhesions are bands of fibrous tissue that form between abdominal tissues and organs, causing them to kink or narrow. Most blockages get better without additional surgery by not eating food and drinking only clear liquids to rest the bowel for a short time.

Diarrhea

Diarrhea is loose, watery stools. A person has diarrhea if he or she passes loose stools three or more times a day. Diarrhea occurs when intestinal contents pass through the small intestine too quickly for fluid and mineral absorption. When fluids and minerals such as sodium and potassium are not absorbed, they leave the body. Diarrhea can lead to dehydration, malnutrition, and weight loss. Diarrhea is common, even normal, with an ileostomy or ileoanal reservoir. In most cases of diarrhea, the only treatment necessary is replacing lost fluids and electrolytes to prevent dehydration. Electrolytes are minerals in body fluids that are part of salts, including sodium, potassium, magnesium, and chloride. People should maintain good daily hydration by drinking plenty of water and liquids, such as fruit juices, sports drinks, caffeine-free soft drinks, and broths. In some cases of diarrhea, a health care provider may recommend changes in diet and may prescribe medications to treat diarrhea.

Bleeding

As with any major surgery, ostomy surgery may cause internal bleeding. If too much blood is lost, the person may require a blood transfusion. Bleeding may also occur through the stoma or through the anus after surgery.

Electrolyte Imbalance

The main function of the large intestine is to absorb water, nutrients, and electrolytes from partially digested food that enters from the ileum. When a surgeon removes the large intestine, absorption of electrolytes does not occur to the same extent, making electrolyte imbalance more likely. Diarrhea, excessive sweating, and vomiting can increase the chance of developing electrolyte imbalance. Symptoms of electrolyte imbalance may include

• fatigue, or feeling tired
• weakness
• nausea
• muscle problems such as spasms, weakness, uncontrolled twitching, and cramps
• dizziness and confusion

People with these symptoms require medical care and should contact a health care provider.

People who have had their large intestine removed should talk with a health care provider or dietitian about diets that help maintain electrolyte balance.

Infection

The GI tract is filled with bacteria that can leak out during ostomy surgery and infect areas inside the abdomen. Bacteria entering the body through the stoma or anus can also cause an infection. The person’s skin around the stoma may also become infected with bacteria or skin fungus. Health care providers treat infections with antibiotics. Symptoms of infection may include

• fever
• back pain
• poor appetite
• nausea and vomiting

Irritation of the Internal Pouch, or Pouchitis

Pouchitis is an irritation or inflammation of the lining of an ileoanal reservoir or a continent ileostomy pouch. A health care provider treats pouchitis with antibiotics. For severe or chronic pouchitis, a health care provider may prescribe immunosuppressive medications, such as corticosteroids. Symptoms of pouchitis include

• frequent bowel movements with diarrhea
• an urgent need to have a bowel movement
• a feeling of pressure in the pouch
• abdominal pain
• cramping or bleeding
• dehydration
• low-grade fever
• a general unwell feeling

Vitamin B12 Deficiency

Ostomy surgery of the bowel may affect vitamin B12 absorption from food and result in a gradual drop in vitamin B12 levels in the body. Low levels of vitamin B12 can affect the body’s ability to use nutrients and may cause anemia. Anemia is a condition in which red blood cells are fewer or smaller than normal, which prevents the body’s cells from getting enough oxygen. Health care providers treat vitamin B12 deficiency with vitamin B12 supplements.

Phantom Rectum

The phantom rectum is the feeling of needing to have a bowel movement even though the rectum is not present. The phantom rectum is relatively common. Symptoms are usually mild and often go away without treatment. However, for some people, the phantom rectum may occur for years after a surgeon removes the rectum. Some people with phantom rectum may feel pain. Health care providers treat rectal pain with medications such as pain relievers and sometimes antidepressants. To help control phantom rectum, a health care provider may recommend complementary therapies such as guided imagery and other relaxation techniques.

Short Bowel Syndrome

A short bowel syndrome is a group of problems related to inadequate absorption of nutrients after removal of part of the small intestine. People with short bowel syndrome cannot absorb enough water, vitamins, and other nutrients from food to sustain life. Diarrhea is the main symptom of short bowel syndrome. Other symptoms may include

• cramping
• bloating
• heartburn
• weakness and fatigue
• vomiting
• excessive gas
• foul-smelling stool

Short bowel syndrome is uncommon and can occur with Crohn’s disease, trauma, or other conditions that lead to the removal of a large amount of the small intestine.

A health care provider will recommend a treatment for short bowel syndrome based on a person’s nutritional needs. Treatment may include nutritional support, medications, and surgery.

Rectal Discharge

People with an ileostomy or a colostomy whose lower colon, rectum, and anus are still present may experience a discharge of mucus from their rectum. Mucus is a clear fluid made by the GI tract that coats and protects the lining of the bowel. Mucus within the bypassed part of the colon may leak out of the rectum from time to time or gradually build up, forming a small, stool-like ball that passes out of the rectum. A person cannot control mucus production and rectal discharge. However, people who have rectal discharge can learn how to manage and cope with this problem.

Living with an Ostomy

At first, living with an ostomy can be overwhelming and scary for some people. However, most people adjust and lead active and productive lives. A WOC nurse or an enterostomal therapist will provide education, support, and medical advice on topics that include the following:

• what to expect after ostomy surgery
• caring for an ostomy
• resuming normal activities after ostomy surgery
• maintaining personal relationships after ostomy surgery
• coping with practical, social, and emotional issues

What to Expect after Ostomy Surgery

Once the person is home from the hospital, the first week or two are considered an extension of the hospital stay. Most people will tire quite easily when they first come home. Getting enough rest is important. Gradually, stamina and strength will improve. Most people can return to work about 6 to 8 weeks after surgery. People may have certain GI issues—such as gas, diarrhea, and constipation—as the bowel heals, depending on the type of bowel diversion.

Ileostomy and colostomy. During the early weeks and months after surgery, people with an ileostomy or a colostomy may have excessive gas. This extra gas will decrease once the bowel has had time to heal and the person resumes a regular diet.

Ileoanal reservoir. People with an ileoanal reservoir initially have about six to 10 bowel movements a day. The newly formed ileoanal reservoir takes several months to stretch and adjust to its new function. After the adjustment period, bowel movements decrease to as few as four to six a day. People with an ileoanal reservoir may have mild fecal incontinence and may have to get up during periods of sleep to pass stool.

Continent ileostomy. Similar to people with an ileostomy or a colostomy, people with a continent ileostomy may have excessive gas during the early weeks and months after surgery.

Caring for an Ostomy

During the recovery in the hospital and at home, a person will learn to care for the ostomy. The type of care required depends on the type of ostomy surgery. A WOC nurse or an enterostomal therapist will teach a person about special care after ostomy surgery.

Ileostomy and colostomy. People with an ileostomy or a colostomy will to learn how to attach, drain, and change their ostomy pouch and care for the stoma and the surrounding skin. Ostomy pouches, or pouching systems, may be one piece or two pieces. They include a barrier, also called a wafer or flange, and a disposable plastic pouch. In a two-piece system, the pouch can be detached or replaced without removing the barrier. For both systems, the barrier attaches to the skin around the stoma and protects it from stool. The length of time the barrier stays sealed to the skin depends on many things, such as

• how well the barrier fits
• the condition of the skin around the stoma
• the person’s level of physical activity
• the shape of the body around the stoma

Most people can leave the barrier on for 3 to 7 days. However, a person should change the barrier as soon as stool starts to go underneath it and onto the skin.

Most ostomy pouches empty through an opening in the bottom. Emptying the pouch several times a day reduces the chance of leakage and bulges underneath the person’s clothing. A person should empty the pouch when it is about one-third full. He or she should rinse the pouch in a two-piece system before reattaching it to the skin barrier.

How often a person needs to change his or her pouching system depends on the type of system. Many pouching systems may be worn for 3 to 7 days. Some pouching systems are made to be changed every day. When changing a pouch system, the person should

• wipe away any mucus on the stoma
• clean the skin around the stoma with warm water and a washcloth
• rinse the skin thoroughly
• dry the skin completely

People may use mild soap to clean the skin. However, the soap should not have oils, perfumes, or deodorants, which may cause skin problems or keep the skin barrier from sticking. A WOC nurse or an enterostomal therapist can give advice if a person has problems attaching the skin barrier or keeping it attached.

When changing the pouching system, people should inspect the stoma and contact a health care provider about any dramatic changes in stoma size, shape, or color. People should look for blood and signs of skin irritation around the stoma. Sensitivities or allergies to ostomy products such as adhesives, skin barriers, pastes, tape, or pouch materials can cause skin irritation. People with pouching systems can test different products to see if their skin reacts to them. People should use only ostomy products recommended by their health care provider.

Ileoanal reservoir. People with an ileoanal reservoir will learn how to care for irritated skin around the anus resulting from frequent stools or fecal incontinence. A WOC nurse or an enterostomal therapist may recommend pelvic floor exercises to help strengthen the muscles around the anus.

Continent ileostomy. People with a continent ileostomy will learn how to insert a catheter through the stoma to drain the internal pouch. They can drain the pouch by standing in front of the toilet or by sitting on the toilet and then emptying the catheter. During the first few weeks after a continent ileostomy, the person needs to drain the internal pouch about every 2 hours. After a few weeks, the person is able to go 4 to 6 hours between pouch drainings. The person should wash his or her hands with soap and water after using a catheter. The person should clean the skin around the stoma with warm water and a washcloth and let the skin dry completely.

Resuming Normal Activities after Ostomy Surgery

After ostomy surgery, people should be able to resume their normal activities after healing completes and their strength returns. However, they may need to restrict activities, including driving and heavy lifting, during the first 2 to 3 weeks after surgery. Strenuous activities, such as heavy lifting, increase the chance of a stoma hernia. A person who has recovered from the ostomy surgery should be able to do most of the activities he or she enjoyed before the ostomy surgery, even swimming and other water sports. The only exceptions may be contact sports such as football or karate. People whose jobs include strenuous physical activities should talk with their health care provider and employer about making adjustments to job responsibilities.

People should avoid extreme physical exercise and sports activities for the first 3 months. Walking, biking, and swimming are fine and should be encouraged as long as they are not overly strenuous.

People with an ostomy should talk with their health care provider about when they can resume normal activities.

Maintaining Personal Relationships after Ostomy Surgery

People with an ostomy should be able to maintain personal relationships just as before their surgery. Some people may worry that friends and relatives will have negative reactions to their ostomy and stoma. Only a spouse, sexual partner, or primary caretaker needs to know the details of the ostomy surgery. People can choose how much they share with others about their health condition, including the ostomy.

People can still maintain a satisfying sexual relationship after ostomy surgery and may resume sexual activity as soon as the health care provider says it is safe to do so. People should talk with their health care provider about any concerns they have with maintaining sexual relations. For people with ostomies, the health care provider can also give information about ways to protect the stoma during sexual activity. People with ostomies may want to ask about specially designed apparel to enhance intimacy. Communicating with a sexual partner is essential. People should share their concerns and wishes and listen carefully to their partner’s concerns.

Coping with Practical, Social, and Emotional Issues

Although ostomy surgery can bring great relief, many people have problems coping with the practical, social, and emotional issues related to having this type of surgery. Every person reacts differently. A person’s emotions may change frequently during recovery. People with an ostomy adjust faster and experience fewer problems when they have help from their family members, partners, and health care providers. Community and online resources for support and education are available to help people with an ostomy cope with practical, social, and emotional issues. A WOC nurse and an enterostomal therapist can provide a list of resources and support groups.

Eating, Diet, and Nutrition

For the first 6 to 8 weeks after ostomy surgery, the health care provider may recommend a low-fiber diet to give the bowel time to heal. The health care provider will tell a person when to add high-fiber foods to the diet. People should introduce fiber into the diet gradually, as high-fiber foods may cause blockage.

Most people are eventually able to resume their regular diet and eat what they like. However, various foods may affect the GI tract differently. Just as before ostomy surgery, certain foods are more likely to cause gas, diarrhea, constipation, or incomplete digestion. Foods such as cucumbers, cabbage, broccoli, onions, fish, eggs, and beans may cause more gas and odor than others. People should consume carbonated drinks and chew gum with moderation, as they may also cause gas. Constipation is often the result of an unbalanced diet or eating and drinking too little. After ostomy surgery, people should

• avoid large amounts of liquids with meals
• drink plenty of liquids between meals
• eat regularly
• avoid high-fiber foods on an empty stomach
• introduce new foods gradually
• chew foods thoroughly

People should talk with their health care provider or dietitian about what diet is right for them.

References