USMLE GI V

• Most commonly occur following blunt abdominal trauma (BAT).
• More commonly seen in children due to a number of anatomic differences including thinner abdominal wall musculature, less abdominal adipose tissue. and more pliable ribs (which absorb less force than the stiffer ribs of adults).
• DH commonly occurs when a blunt force rapidly compresses the duodenum against the vertebral column.
• Following trauma, blood collects between the submucosal and muscular layers of the duodenum causing partial or complete obstruction.
• Patients with DH due to BAT may Initially have only symptoms of abdominal wall trauma, which may improve before subsequent clinical deterioration as the DH expands.
• Patients classically present 24-36 hours after the initial event with epigastric pain and vomiting due to failure to pass gastric contents beyond the obstructing hematoma.
• Diagnosis is confirmed with CT imaging of the abdomen.
• Most DHs will resolve In 1-2 weeks.
• Management involves decompression by nasogastric tube and, in many patients, parenteral nutrition.
• Surgery or percutaneous drainage may be considered to evacuate the hematoma if nonoperative management fails.

• is more frequently associated with penetrating abdominal trauma,
• It can also result from BAT due to damage to the mesenteric blood supply, subsequent Gl necrosis, and eventual perforation.
• Consequently, although injury due to penetrating trauma may present acutely, signs and symptoms of perforation due to BAT may take several days to present.
• Therefore, patients with any evidence of injury to the mesenteric vessels should be considered for longer periods of observation and monitoring.
• When perforation does occur, the jejunum is most frequently involved, whereas the stomach and colon are less frequently injured.

• 
• Patient who presents after a motor vehicle collision with diffuse abdominal tenderness concerning for blunt abdominal trauma (BAT), is at significant risk of intra-abdominal injury.
• A number of signs are suggestive of serious intra abdominal injury, including "seat belt sign" (ecchymosis over the abdomen in the pattern of a seat belt), hypotension, rebound tenderness, abdominal guarding/distension, and coexisting femur fracture.
• The first step after fluid resuscitation is to determine if a patient needs surgical management.
• Patients with BAT should be assessed for intraperitoneal free fluid or hemorrhage.
• The most commonly used approach is the Focused Assessment with Sonography for Trauma (FAST), which evaluates both the abdomen and pericardium for evidence of organ injury or hemorrhage; it should be the first step in alert and hemodynamically stable (eg, systolic blood pressure >90 mm Hg} patients.
• FAST can be performed rapidly at the bedside and has good sensitivity and specificity for detecting hemoperitoneum, pericardial effusion, and intraperitoneal fluid.
• If FAST is limited or equivocal, a diagnostic peritoneal lavage (DPL) can be done to evaluate for hemoperitoneum.
• Hemodynamically stable patients with positive findings may undergo subsequent testing with abdominal CT scan to determine the need for laparotomy.
• Hemodynamically unstable patients with a positive finding on either DPL or FAST should undergo exploratory laparotomy.

• Risk Factor: history of prior abdominal surgery Is an important risk factor due to adhesion development
• Clinical presentation
• • Colicky abdominal pain, vomiting
• • Inability to pass flatus or stool
• • Hyperactive to absent bowel sounds
• • Distended & tympanic abdomen, Diffuse Tenderness
• Diagnosis
• • Dilated loops of bowel with air-fluid levels
• • Partial: Air in colon
• • Complete: Transition point (abrupt cutoff), no air in colon
• Complications
• • Ischemia/necrosis (strangulation)
• • Bowel perforation
• Management
• • Bowel rest, nasogastric tube suction, intravenous fluids
• • Surgical exploration for signs of complications

• Most patients with SBO can be managed initially with conservative measures (eg, bowel rest, nasogastric tube suction, correction of metabolic derangements).
• Complicated SBO with increased risk of impending ischemia, strangulation, and necrosis, warranting emergency abdominal exploration. These findings include changes in the character of the pain, fever, hemodynamic instability (hypotension, tachycardia), guarding, leukocytosis, and significant metabolic acidosis (low bicarbonate).
• Delay in surgery may lead to perforation and significant risk of mortality.

• Categorized by anatomic location (ie, proximal versus mid/distal) or simple versus strangulated.
• Complete proximal obstructions: are characterized by early vomiting, abdominal discomfort, and abnormal contrast filling on x-ray.
• Mid or distal obstructions: typically present as colicky abdominal pain, delayed vomiting, prominent abdominal distension, constipation-obstipation. hyperactive bowel sounds, and dilated loops of bowel on abdominal x-ray.
• Simple obstruction: refers to luminal occlusion; Strangulation: refers to loss of blood supply to the bowel wall.
• Patients with strangulated obstructions may have peritoneal signs (eg, rigidity, rebound) and signs of shock; fever, tachycardia, and leukocytosis are late findings.

• Often seen in elderly patients who are institutionalized (eg, nursing home) and have an underlying neurologic disorder (eg, dementia).
• Colonic dysmotllity and redundant sigmoid colon, likely from chronic constipation,increase the risk of torsion of the sigmoid colon around its mesentery.
• This can lead to mechanical obstruction and ischemia of the intestines, predisposing the colon to dilation, necrosis, and perforation.
• Clinical presentation: variable.
• Elderly are at risk for a delayed presentation due to milder initial symptoms, but necrosis and bowel perforation can result in a more acute presentation.
• Most patients have progressive abdominal pain, obstipation, abdominal distension, and subsequent nausea and vomiting.
• High-pitched bowel sounds imply active intestinal motility with severe narrowing or obstruction.
• Discomfort during rectal examination and no stool in the rectal vault may be present.
• On radiograph, the dilated colon (no haustra) appears as an Inverted U shape; a transition point at the site of torsion leads to no air in the rectum.

• Risk Factors: Seen in severely ill patients in the intensive care unit with multiorgan failure, severe trauma, surgery, burns, sepsis , or prolonged parenteral nutrition.
• Pathogenesis:
• Acalculous cholecystitis is likely due to cholestasis and gallbladder ischemia leading to secondary infection by enteric organisms and resultant edema and necrosis of the gallbladder.
• Most patients affected by this condition have no prior history of gallbladder disease.
• Acalculous cholecystitis is a serious condition that can lead to sepsis and death if undetected.
• The clinical signs of disease: (eg, fever, leukocytosis) are vague
• The best way to make the diagnosis is a high degree of clinical suspicion and confirmation with imaging studies.
• Radiologic signs: include gallbladder wall thickening and distension and the presence of pericholecystlc fluid.
• Immediate treatment: in critically ill patients includes antibiotics followed by percutaneous cholecystostomy under radiologic guidance.
• Cholecystectomy with drainage of any associated abscesses is the definitive therapy once the patient's medical condition improves.

• Risk factors:
• • Diabetes mellitus, Gallstones
• • Vascular compromise(obstruction or stenosis of the cystic artery)
• • Immunosuppression
• Clinical presentation:
• • Fever, right upper quadrant pain, nausea/vomiting
• • Crepitus in abdominal wall adjacent to gallbladder
• Diagnosis:
• • Air fluid levels in gallbladder, gas in gallbladder wall
• • Cultures with gas-forming Clostridium, Escherichia coli
• • Unconjugated hyperbilirubinemia (eg, from Clostridium-induced hemolysis), mildly elevated aminotransferases
• Treatment:
• • Emergent cholecystectomy
• • Broad-spectrum antibiotics with Clostridium coverage (eg, amptcillin-sulbactam)
• Complications: include gangrene and perforation

• Gallstone Ileus occurs when a gallstone passes through a biliary-enteric fistula into the small bowel.
• As the stone advances it may cause Intermittent ''tumbling" obstruction with diffuse abdominal pain and vomiting until finally lodging in the ileum, the narrowest section of the bowels, several days later.
• In addition to experiencing colicky pain and vomiting, patients may report distension and inability to pass flatus or stool and show signs of hypovolemia (eg, hypotension, tachycardia).
• Stones can occasionally also lodge in the stomach, jejunum, or colon.
• Cholecystitis, which predisposes to biliary-enteric adhesions, is the most important risk factor, and patients are more commonly elderly women, which reflects their higher prevalence of gallstone disease.
• Diagnosis: can be confirmed by abdominal CT scan, which may reveal gallbladder wall thickening, pneumobllla, and an obstructing stone.
• Treatment: is surgical and involves removal of the stone and either simultaneous or delayed holecystectomy.

• The sphincter of Oddi is a muscular valve controlling the flow of bile and pancreatic juice into the duodenum.
• SOD, which can develop follow any Inflammatory process (eg, surgery, pancreatitis), encompasses 2 separate physiologic entities: dyskinesia and stenosis of the sphincter of Oddi.
• Obstruction of flow through the sphincter may result in retention of bile, causing a functional biliary disorder that mimics a structural lesion.
• Recurrent, episodic pain in the right upper quadrant or epigastric region, with corresponding aminotransferase and alkaline phosphatase elevations is common;
• Visualization of a dilated common bile duct in the absence of stones increases the likelihood of SOD.
• Opioid analgesics (eg, morphine) may cause sphincter contraction and precipitate symptoms of SOD
• Sphincter of Oddi manometry: Is the gold standard for the diagnosis of SOD
• Sphincterotomy: Is the treatment of choice in most cases.

• Diverticulitis can be classified as uncomplicated (75%) or complicated (25%).
• Uncomplicated diverticulitis: in stable patients can be managed in the outpatient setting with bowel rest, oral antibiotics, and observation.
• However, hospitalization and Intravenous antibiotics are recommended for patients who are elderly, Immunosuppressed, have high fever or significant leukocytosis, or have significant comorbidities.
• Complicated diverticulitis: refers to diverticulitis associated with an abscess , perforation, obstruction, or fistula formation.
• Fluid collection less than 3 cm can be treated with intravenous antibiotics and observation, with surgery reserved for patients with worsening symptoms.
• However, a fluid collection more than 3 cm should have CT guided percutaneous drainage
• If the symptoms are not controlled by the fifth day, surgical drainage and debridement are recommended.
• Sigmoid resection: is generally reserved for patients with fistulas, perforation with peritonitis, obstruction, or recurrent attacks of diverticulitis.

• Risk factors:
• • Age >60
• • Chronic renal disease/hemodialysis
• • Atherosclerotic vascular disease & procedures (AAA Repair)
• • Myocardial infarction
• Involved segments of the colon: include the splenic flexure at the "watershed" line between the territory of the superior and inferior mesenteric arteries and the rectosigmoid junction at the watershed between the sigmoid artery and superior rectal artery.
• Clinical features:
• • Mild pain & tenderness
• • Hematochezia, diarrhea
• • Metabolic (lactic) acidosis
• Diagnosis:
• • CT scan: Thickened bowel wall, double halo sign, pneumatosis coli
• • Colonoscopy: Mucosal pallor or cyanosis, petechia, hemorrhagic ulcerations with a sharp transition from affected to unaffected mucosa
• Management:
• • Supportive care: Intravenous fluids, bowel rest
• • Intravenous antibiotics
• • Colon resection (bowel infarct or clinical deterioration)

• Is most commonly due to abdominal surgery but can also be seen in other conditions such as retroperitoneal/abdominal hemorrhage or inflammation, intestinal ischemia, and electrolyte abnormalities.
• Pathophysiology of ileus: include increased splanchnic nerve sympathetic tone following irritation of the peritoneum, local release of inflammatory mediators, and opioid analgesic use.
• Signs and symptoms of Ileus: nausea, vomiting, abdominal distension, failure to pass flatus or stool (obstipation) and hypoactive or absent bowel sounds.
• Persistence of the signs and symptoms (more than 3-5 days postoperatively) is termed prolonged (or " pathologic") postoperative ileus (PPI).
• Abdominal x-rays: (classically revealing dilated gas filled loops of bowel with no transition point) can be helpful in confirmation.
• Management: is conservative and includes bowel rest, supportive care, and treatment of secondary causes.
• Techniques to prevent Post Operative ileus: include epidural anesthesia, minimally invasive surgery, and judicious perioperative use of intravenous fluids (to minimize gastrointestinal edema)

• A perianal abscess is due to occlusion of an anal crypt gland, which allows for bacterial Infection.
• Abscesses can form relatively acutely following gland obstruction due to the high levels of bacteria in the area.
• Risk factors for abscess development: Include anoreceptive intercourse and constipation
• C/F: Initially, a perianal abscess may cause pain only with defecation and mild pruritus, but as the infection progresses, the pain becomes constant and can be associated with systemic manifestations such as fever.
• Drainage may not be apparent unless a fistula forms.
• Complication: Untreated perianal abscesses often progress to form anorectal fistulae, communications between the abscess and perirectal skin or nearby organs.
• Mgmt: Early recognition followed by incision and drainage is essential to avoid such progression.

• Risk Factors: PD most frequently affects individuals age 15-30, particularly young males, obese individuals, those with sedentary lifestyles or occupations, and those with deep gluteal clefts.
• C/F: Common presenting manifestations include a painful, fluctuant mass 4-5 cm cephalad to the anus in the intergluteal region with associated mucoid, purulent, or bloody drainage.
• Pain is frequently worsened by activities that stretch the overlying skin (eg, bending down).
• Pathogenesis: PD develops when an edematous, infected hair follicle in the intergluteal region becomes occluded.
• The infection spreads subcutaneously and forms an abscess, which can rupture and create a pilonidal sinus tract.
• As the patient sits or stands, hair and debris are forced into the sinus tract, resulting in recurrent infections and foreign-body reactions.
• Treatment: Drainage of abscesses and collected debris followed by excision of sinus tracts. Despite longer healing times, open closure is preferred due to decreased recurrence rates.

• Pathogenesis: PA occurs from either hematologic seeding from a distant Infection or from direct extension of an lntraabdomlnal infection (eg, diverticulitis, vertebral osteomyelitis).
• Risk factors: include HIV, Intravenous drug use, diabetes, and Crohn disease.
• Clinical presentation:
• • Subacute fever, abdominal/flank pain radiating to groin
• • Anorexia, weight loss
• • Abdominal pain with hip extension (psoas sign)
• Diagnosis:
• • CT scan of the abdomen & pelvis: Required to confirm the diagnosis
• • Leukocytosis, Thrombocytosis, elevated inflammatory markers
• • Blood & abscess cultures
• Treatment:
• • Drainage
• • Broad-spectrum antibiotics

• BGT is rarely life-threatening unless the kidneys or renal vasculature are involved.
• However, due to their retroperitoneal location and the protection afforded by the ribs, these structures are infrequently injured in BGT.
• When injury does occur, the most common renal lesions are contusions, lacerations, and renovascular injuries (eg, pedicle avulsion, renal artery dissection).
• All patients should undergo urinalysis, and hemodynamically stable patients with evidence of hematuria should undergo further imaging with a contrast-enhanced CT scan of the abdomen and pelvis.
• Hemodynamically unstable patients with evidence of renal trauma should undergo intravenous pyelography prior to surgical evaluation.
• Other studies that should be considered in patients with BGT include plain radiographs to evaluate for fractures, ultrasound to evaluate for testicular injuries, and retrograde cystourethrograms to evaluate for urethral injury and bladder rupture.
• However, patients requiring retrograde cystourethrograms typically have gross hematuria, difficulty urinating, and blood at the meatus (urethral injury) or suprapubic pain (bladder rupture)

• is due to an incomplete closure of the abdominal muscles around the umbilical ring at birth.
• It is most commonly associated with African American race, premature birth, Ehlers-Danios syndrome, Beckwith-Wiedemann syndrome. and hypothyroidism.
• Physical examination: shows a soft, non-tender bulge covered by skin that protrudes during crying, coughing, or straining.
• The hernia may contain omentum or portions of the small Intestine.
• Most umbilical hernias are reduced easily through the umbilical ring with very low risk of incarceration and strangulation. Small umbilical hernias typically close spontaneously by concentric fibrosis and scar tissue formation.
• Spontaneous closure is less likely with large (>1 .5 cm diameter) hernias or in patients with underlying medical problems.
• Surgery is recommended around age 5 for persistent hernias, or sooner if it is bothersome or causing complications.

• The first step In the evaluation of his condition should be a careful screening for all hepatitis risk factors, including drug and alcohol intake, travel outside the United States, blood transfusions. or high-risk sexual practices.
• This aspect of the patient's history will provide insight as to whether the transaminase elevation could be caused by alcohol, medications (eg. NSAIDs, antibiotics, HMG-CoA reductase inhibitors, antiepileptic drugs, antituberculous drugs, herbal preparations)or viral agents.
• After thoroughly questioning the patient about his history and having him discontinue all alcohol and drug use, the next step in the evaluation process would be to repeat the liver function tests.
• If the transaminases persist in being elevated over a six-month period, they are categorized as chronic.
• Testing for viral hepatitis B and C, hemochromatosis. and fatty liver should then be undertaken to further evaluate chronically elevated transaminases.
• If these tests prove unremarkable, a search for muscle disorders (eg, polymyositis) and thyroid disease should be made.

• Pseudoachalasia,
• which Is due to narrowing of the distal esophagus secondary to causes other than denervatlon (eg, esophageal cancer), can closely mimic achalasia.
• Clues pointing to pseudoachalasla include significant weight loss, rapid symptom onset, and presentation at age >60.
• Consequently, endoscopy is recommended to exclude malignancy in all patients with suspected achalasia.

• Clinical Features: Chronic dysphagia to both solids and liquids, regurgitation, difficulty belching, and mild weight loss are all common manifestations of achalasia.
• Other symptoms include : chest pain and heartburn; therefore, many patients are initially diagnosed with gastroesophageal reflux.
• On average, patients have symptoms for approximately 5 years before receiving a diagnosis of achalasia.
• Pathogenesis : Achalasia is due to Impaired peristalsis of the distal esophagus and impaired relaxation of the lower esophageal sphincter (LES). This prevents food or liquid from passing through the LES until the hydrostatic pressure in the esophageal column is greater than the closing pressure of the sphincter. Being in the upright position increases the pressure in the esophagus and results in more effective swallowing.
• Manometry : is the most sensitive test and key to diagnosis.
• Barium esophagram : which may show a smooth "bird-beak" narrowing near the LES, can be helpful in patients with nondiagnostic manometry.

• Etiology :
• • VIral hepatitis (eg, HSV; CMV; hepatitis A, B, D & E)
• • Drug toxicity (eg, acetaminophen overdose, idiosyncrallc)
• • Ischemia (eg, shock liver, Budd-Chiari syndrome)
• • Autoimmune hepatitis
• • Wilson disease
• • Malignant infiltration
• Clinical presentation :
• • Generalized symptoms (eg, fatigue, lethargy, anorexia, nausea)
• • Right upper quadrant abdominal pain
• • Pruritus & jaundice due to hyperbilirubinemia
• • Renal insufficiency
• • Thrombocytopenia
• • Hypoglycemia
• Diagnostic requirements :
• • Severe acute liver injury (AL T & AST often >·1000 U/L)
• • Signs of hepatic encephalopathy (eg, confusion, asterixis)
• • Synthetic liver dysfunction (INR >1.5)
• • Cirrhosis or underlying liver disease should not be present.

• Is the most common cause of ALF in many developed countries and can be seen In Intentional overdose (suicide attempt) or accidental overdose in patients taking multiple sources of acetaminophen.
• Toxicity results from overproduction of the toxic metabolite N acetyl-p-benzoquinone imine (NAPQI), which leads to hepatic necrosis.
• NAPQI is normally safely detoxified through glucuronidation in the liver, but this pathway becomes overwhelmed in overdose.
• Chronic alcohol use is thought to potentiate acetaminophen hepatotoxicity by depleting glutathione levels and impairing the glucuronidation process.
• On the other hand, N-acetylcystelne increases glutathione levels and binds to NAPQI, so it is an effective antidote for acetaminophen overdose when given early.
• acetaminophen hepatotoxicity is characterized by relatively low serum bilirubin compared with that in other etiologies of ALF.

typically causes mild to moderate aminotransferase elevation (<500 UIL} in patients who drink heavily (>100 g/day). The AST/ALT ratio is usually >2:1.

• In ALF due to acetaminophen toxicity, LT is firmly indicated in patients with grade III or IV HE, PT >100 seconds, and serum creatinine >3.4 mg/dl (such as this patient).
• Oneyear survival following L T for ALF Is approximately 80%.

• Etiology
• • Chronic alcohol use (- 40%)
• • Gallstones (- 40%)
• • Hypertriglyceridemia (type I, IV , V)
• • Drugs (eg, azathioprine, valproic acid, Didanosine thiazides)
• • Infections (eg, CMV, Legionella, Aspergillus)
• • Trauma
• • Iatrogenic (post·ERCP, ischemic/atheroembolic)
• Diagnosis (requires 2 of the following)
• • Acute epigastric pain radiating to the back
• • Increase Amylase or lipase >3 times normal limit
• • Abdominal imaging showing focal or diffuse pancreatic enlargement with heterogeneous enhancement with intravenous contrast (CT) or diffusely enlarged & hypoechoic pancreas (ultrasound)
• Other findings :
• • Nausea, vomiting, leukocytosis
• • ALT level >150 U/L suggests biliary pancreatitis
• • Severe disease: Abdominal Tenderness, Fever, tachypnea, hypoxemia, hypotension
• Complications
• • Pleural effusion
• • Ileus
• • Pancreatic pseudocysUabscess/necrosis
• • Acute respiratory distress syndrome

• Early in pancreatitis, the pancreas synthesizes digestiVe enzymes but cannot secrete them.
• These enzymes leak out of the acinar cells into the systemic circulation.
• Amylase rises within 6-12 hours of symptom onset and may remain elevated for 3-5 days.
• Lipase rises within 4-8 hours of symptom onset but remains elevated longer than amylase (8-14 days). As a result.
• lipase is more useful and sensitive than amylase for diagnosis (especially in alcoholics and patients presenting later in the disease course).

• Gall Stone Pancreatitis
• High BMI, alanine aminotransferase >150 U/L, and elevated alkaline phosphatase suggest gallstone pancreatitis.
• A right upper-quadrant ultrasound is advised for all patients with suspected gallstone pancreatitis as it provides the most accurate information regarding the presence of gallstones.
• If the ultrasound is nondiagnostic and there is high clinical suspicion for common bile duct disease, endoscopic retrograde cholangiopancreatography (ERCP) may be performed to better visualize the biliary tree.

• The serum triglyceride level generally must be >1,000 m g/dL to be considered a potential cause of pancreatitis.
• The yellow-red papules on this patient's arms and shoulders suggest eruptive xanthomas, which are due to subcutaneous fat deposition.
• Eruptive xanthomas are usually associated with marked hypertriglyceridemia (> 1,000 mg/dl), typically due to familial hypertriglyceridemia (look for history of MI in family).
• A fasting serum lipid profile can determine if hypertriglyceridemia is the underlying cause of this patient's xanthomas and pancreatitis.

• Patients with risk factors for aortic atherosclerosis (eg, hypercholesterolemia, diabetes, peripheral vascular disease) who undergo cardiac catheterization or a vascular procedure are at Increased risk for cholesterol emboli as a result of vascular manipulation. These emboli can occlude blood vessels and cause the following:
• • Skin manifestations: Livedo reticularis (reticulated, mottled, discolored skin), blue toe syndrome
• • Kidney manifestations: Acute kidney injury
• • Gastrointestinal manifestations: Pancreatitis, mesenteric ischemia
• Supportive care (eg, pain control, Intravenous fluids, bowel rest) is recommended for uncorrectable causes of acute pancreatitis (eg, hypotension, ischemia, viruses, atheroembollsm).
• Most acute pancreatitis attacks are self-limiting and improve in 4-7 days with conservative management.
• This patient should receive nothing by mouth except essential medications (le, antiplatelet therapy to prevent stent thrombosis).

• Drug Induced Pancreatitis
• Other common drugs associated with pancreatitis include:
• 1. Diuretics (furosemide, thiazides)
• 2. Drugs for Inflammatory bowel disease (sulfasalazine, 5-ASA)
• 3. Immunosuppressive agents (azathioprine)
• 4. HIV-related medications (didanosine, pentamidine)
• 5. Antibiotics (metronidazole, tetracycline)

• Clinical Presentation:
• • Fever, tachycardia, hypotension
• • Dyspnea, tachypnea &/or basilar crackles
• • Abdomlnaltendemess &/or distension
• • Cullen sign. Penumbilical bluish coloration indicating hemoperitoneum
• • Grey-Turner sign: Reddish-brown coloration around flanks indicating retropentoneai bleed
• Associated with increased risk of severe pancreatitis:
• • Age >75
• • ObeSity
• • Alcoholism
• • C-reaclive protein >150 mg/dl at 48 hours after presentaion
• • Rising blood urea nitrogen & creatinine in the first 46 hours
• • Chest x-ray with pulmonary infiltrates or pleural effusion
• • Computed tomography scan/magnetic resonance cholangiopancreatography with pancreatic necrosis & extra pancreatic inflammation
• Complications:
• • Pseudocyst
• • Peripancreatic fluid collection
• • Necrotizing pancreatitis
• • Acute respiratory distress syndrome
• • Acute renal failure
• • Gastrointestinal bleeding

include Barrett's esophagus, obesity, high dietary calorie and fat intake, smoking, medications that promote GERD, etc.

smoking, alcohol, dietary deficiency of beta-carotene, vitamin B-1 , zinc, selenium, environmental viral infections, toxin producing fungi, hot food and beverages, pickled vegetables and food rich in N nitroso compounds, etc.

• Clinical Presentation:
• • Jaundice, anorexia, fever
• • Right upper quadrant &or epigastric pain
• • Abdommal distension due to ascites
• • Proximal muscle weakness from muscle wasting (if malnourished)
• • Possible hepatic encephalopathy
• Laboratory &/or Imaging studies:
• • Elevated AST & ALT, usually <300 U/L
• • AST:ALT ratio ≥2
• • Elevated gamma-glutamyltransferase, bilirubin, international normalized ratio
• • Leukocytosis, predominantly neutrophils
• • Decreased albumin if malnourished
• • Abdominal imaging may show fatty liver
• • Macrocytic anemia (mean corpuscular volume [MCV) >100/IJm,), thrombocytopenia

• Extraperitoneal causes
• • Cirrhosis
• • Acute liver failure
• • Alcoholic hepatitis
• • Budd-Chiari syndrome
• • Heart failure
• • Hypoalbuminemia
• • Malnutrition
• • Nephrotic syndrome
• Peritoneal causes
• • Malignancy (ovarian, pancreatic)
• • Infection (tuberculosis, fungal)

• Color:
• • Bloody: Trauma, malignancy, TB(rarely)
• • Milky: Chylous, pancreatic
• • Turbid: Possible infection
• • Straw color: Likely more benign causes
• Neutrophils :
• • Less than 250/mm3: No peritonitis
• • ≥250/mm3: Peritonitis (secondary or spontaneous bacterial)

• • ≥2.5 g/dl (high-protein ascites):
• CHF, constrictive pericarditis, peritoneal carcinomatosis, TB, Budd-Chiari syndrome, fungal (eg, coccidioidomycosis)
• • less than 2.5 g/dl (low-protein ascites):
• Cirrhosis, nephrotic syndrome

• ≥1.1 g/dl (indicates portal hypertension) :
• o Cardiac ascites, cirrhosis, Budd-Chiari syndrome
• <1.1 g/dl (absence of portal hypertension):
• o TB, peritoneal carcinomatosis. pancreatic ascites, nephrotic syndrome

In evaluating ascites, a serum-to-ascites albumin gradient (SAAG) more than or equal to 1.1 g/dl indicates portal hypertensive etiologies (eg, cardiac ascites, cirrhosis) while a SAAG <1.1 suggests non-portal hypertensive etiologies (eg, malignancy, pancreatitis, nephrotic syndrome, tuberculosis).