GASTROENTEROLOGY

 

GI Bleeding

1.       Upper GI bleed = originates above the ligament of Treitz

a.       Mnemonic: GUM BLEEDING = Gastritis; Ulcer; Mallory-Weiss; Biliary (hemobilia, secondary to trauma); Large varices (in portal hypertension); Esophageal ulcer or esophagitis; Enteroarotic fistula (in patients with aortic graft); Duodenitis; Inflammatory Bowel Disease (upper GI tract Crohn's disease); Neovasculization (AVM); Gastric cancer

2.       Lower GI bleed = originates below the ligament of Treitz

a.       Mnemonic: DRAIN = Diverticulosis; Radiation colitis; Angiodysplasia; Ischemia, inflammation, infection; Neoplasm

3.       Risk factors: previous GI bleed, ASA, NSAIDs, steroids, "blood thinners", EtOH, and smoking

4.       Physical exam

a.       Orthostatics – positive tilt if pulse increases > 20 and systolic BP decreases > 20 and/or diastolic BP decrease > 10 from lying to standing.

b.      Digital rectal exam – black stools may be seen if patients takes bismuth or Fe supplements.

c.       NG tube – if you suspect hematemesis, insert NG tube and aspirate.  A negative result does not rule out a bleed (bleed could be from duodenal bulb without reflux into the stomach).

5.       Tests

a.       Hgb/Hct

b.      Type and cross – with significant bleed, otherwise type and screen.

c.       FBP – BUN increases with bleed, in the absence of renal disease.

d.      PT/INR/PTT – rule out any bleeding disorders.

e.      Abdominal flat and upright – air under the right diaphragm indicates a perforation and requires immediate surgical intervention.

6.       Admission criteria to ICU with a GI bleed

a.       Mnemonic: VISA = Variceal bleeding (suspected or confirmed); Instability of vital signs; Serious cormorbid condition (e.g. CAD, COPD); Active GI bleeding

           

Acute Pancreatitis

1.       Etiology

a.       Most common causes: EtOH and gallstones.

b.      Other causes: drugs (list is extensive), iatrogenic (ERCP or surgery), hyperlipidemia, hypercalcemia, scorpion bite (extremely rare but sounds good when giving differential).

c.       Mnemonic: BAD HITS = Biliary Stones; Alcohol abuse; Drugs; Hyperlipidemia or hypercalcemia; Idiopathic or infectious; Trauma; Surgery (ERCP) or scorpion bite.

2.       Signs of hemorrhagic pancreatitis

a.       Cullen's sign – around the umbilicus.

b.      Grey Turner's – around the flank (think Turn = sides).

3.       Tests

a.       Amylase, lipase – elevated.

b.      LFTs – with EtOH hepatitis, AST/ALT > 2:1.

c.       Ultrasound – if gallstones are suspected.

4.       Ranson's Criteria – provides prognosis during first 24 hrs

a.       At admission, use the mnemonic GA LAW = Glucose > 200 mg/dL; Age > 55 yo; LDH > 350; AST > 250; WBC > 16,000.

b.      During the initial 48 hours, criteria include:

i.                     ― Hct > 10% with hydration or Hct £30%

ii.                   ­ BUN > 5 mg/dL

iii.                  Ca2+ < 8 mg/dL

iv.                 PaO2 < 60 mmHg

v.                   Fluid sequestration > 5000 mL

c.       Patient will have increased mortality with three or more signs.

5.       Treatment

a.       NPO, IVF, NG suction (if patient is vomiting or has ileus).

b.      Demerol for pain – demerol causes less spasm of the sphincter of Oddi than other narcotics.

c.       Correct electrolyte abnormalities.

d.      Consider DT prophylaxis in EtOH-induced pancreatitis with Ativan – DT usually occurs during first 12- 48 hrs after withdrawl from EtOH, most prominent around 24-36 hrs.  Signs include tremors, tachycardia, and agitation.

 

Inflammatory Bowel Disease

1.       Crohn's Disease – can be anywhere in the GI tract.  "Skip lesions."   Transmural involvement with lymphoid aggregates.  Non-caseating granulomas.  Can lead to strictures and fistulas.

2.       Ulcerative Colitis – extends continuously from the rectum in proximal fashion.  Only mucosal inflammation.  Increased risk of colon carcinoma.  Associated with sclerosing cholangitis.

3.       Extraintestinal manifestations – can be seen in both CD and UC, and includes migratory polyarthritis, sacroilitis, ankylosing spondylitis, uveitis, and erythema nodosum.

4.       Treatment

a.       Sulfasalazine, Asacol, and Rowasa – effective in UC and in CD confined to colon.

b.      Steroids – retention enemas can be helpful in those patients with disease in the rectum accompanied by tenesmus.

c.       Immunosuppressants – azathioprine, cyclosporine, mercaptopurine are helpful in refractory cases.

 

Liver Diseases

1.       Hallmark of liver dieases - hepatomegaly, splenomegaly, gynecomastia, palmar erythema, spider angiomata (>3 in women, >1 in men), testicular atrophy, Dupuytren's contracture, caput medusae, jaundice, ecchymoses, ascites

2.       Etiology of cirrhosis: EtOH and hepatitis C are most common causes in Western world

a.       EtOH abuse

b.      Hepatitis B or C – look for risk factors such as IVDA, transfusion, prostitutes, tattoos

c.       Primary biliary cirrhosis – pruritus, xanthomas, and hyperlipoproteinemia in middle-aged or elderly women and is associated with Sjogren's, CREST, and scleroderma.  Patients have a high antimitochondrial antibody titer.

d.      Secondary biliary cirrhosis – obstruction of common bile duct (gallstones, pancreatic cancer, sclerosing cholangitis, stricture).

e.      Drugs – isoniazid, methotrexate, acetominophen.

f.         Hemochromatosis – "bronze diabetes" (hyperpigmentation, diabetes, arthritis, impotence).  Patients have elevated ferritin and transferrin saturation levels.

g.      Wilson's Disease – Kayser-Fleischer rings in the cornea.  Decreased ceruloplasmin.

h.       Alpha-1-antitrypsin deficiency – family history with lung and liver pathology.  Decreased alpha-1-globulin levels.

i.         Autoimmune hepatits – amenorrhea, rash, acne, vasculitis, Sjogren’s or thyroiditis in young women.  Patients have high ANA titer (>1:150), anti-smooth muscle antibody, and liver and kidney microsomal (LKM) antibody.

j.         Cryptogenic

3.       See above for discussion of liver function test evaluation.

4.       Complications of cirrhosis

a.       Portal hypertension – collaterals between the portal and systemic circulations leading to esophageal varices, caput medusae, and hemorrhoids.

b.      Child's classification of portal hypertension is often used.  It utilizes the serum bilirubin, albumin, ascites, encephalopathy, and nutrition to determine class A, B, and C.

i.                     Treatment

(1)     Surgical shunts and TIPS (transjugular intrahepatic portosystemic shunt) – does not decrease mortality and may lead to encephalopathy

(2)     Esophageal varices bleeding may be prevented through the use of non-selective beta-blockers. Propanolol is most commonly used.  Nadolol can also be used, and it has less CNS side effects than propanolol.  Beta-blockers should be titrated up to decrease the heart rate by 25%.

(3)     Vasopressin, octreotide, and somatostatin can be used to decrease portal flow and pressure in acute settings

c.       Hepatic encephalopathy – altered mental status due to impairment of liver function and subsequent accumulation of nitrogenous compounds and other toxins.  Encephalopathy is classified in grades I through IV.  Clinical signs include asterixis, myoclonus, and hyperreflexia.  Blood level of ammonia correlates poorly with degree of encephalopathy.

i.                     Treatment of hepatic encephalopathy

(1)     Decrease protein intake

(2)     Lactulose – converts ammonia (NH3) to ammonium (NH4) which can be excreted in the stool.  Lactulose should be titrated until patient has 2 to 4 stools daily

(3)     Neomycin – decreases urease-containing bacteria in the colon which produces NH3.

d.      Ascites – caused by increased hydrostatic pressure in the splanchnic capillaries and decreased oncotic pressure secondary to hypoalbuminemia.

i.                     Diagnostic paracentesis – send fluid for LDH, glucose, albumin, cell count, and differential.  If malignancy is suspected, consider CEA level and cytologic evaluation

ii.                   A transudate with protein < 3 and serum-ascites albumin gradient > 1.1 is likely to be secondary to cirrhosis.

iii.                  Treatment of ascites

(1)     Restrict sodium and fluid intake.

(2)     Spironolactone and Lasix

(3)     In patients with large ascites, a pleural effusion may be present.  Fluid accumulates in pleural space through small fenestrations in the diaphragm.

e.      Spontaneous bacterial peritonitis – patients present with fever, abdominal pain, and tenderness.  Ascitic fluid PMN count > 250.  Culture confirms diagnosis.  Patients with cirrhosis should be on prophylaxis with Cipro or Bactrim.

f.         Hepatocellular carcinoma – elevated AFP levels.