Gastroenterology
Xiushui (Mike) Ren, M.D.
Neil Stollman, M.D.
1. Goal: Rest the pancreas and to provide supportive care.
2. Factoids:
· Notice that amylase and lipase are not included in the Ranson criteria. They do not correlate well with disease severity, and while an elevated level may help confirm your clinical suspicion of pancreatitis, they do not need to be followed closely.
· Around 25% of patients with acute pancreatitis have a normal amylase.
· Lipase is more sensitive and specific than amylase. Lipase is also present longer after an episode of pancreatitis.
· Early enteral feeding is now a validated option in cases of mild-to-moderate acute pancreatitis.
· Alcohol
· Gallstones
· Trauma: both blunt and iatrogenic, with an incidence of 2%-5% after ERCP
· Other: hypertriglyceridemia (when greater than 1000 mg/dl); hypercalcemia; medications such as pentamidine, antiretrovirals, thiazides diuretics, and sulfa antibiotics; pancreatic divisum; infections such as mumps, CMV, HIV, and E. coli; and the dreaded scorpion sting.
· ADMIT: ICU vs. floor – use the Ranson criteria.
· NURSING: NG tube to suction, only for nausea/vomiting.
· DIET: Classically, NPO until pain-free and off narcotics. More recently, let the patient’s symptoms guide you: it is okay to initiate feeding when the patient tells you they’re hungry (trust their symptoms more than the labs).
· IV: Rehydrate. Be aware that fluid shifts and sequestration are common.
· MEDS: Morphine is commonly used for analgesia, although in theory it can cause spasm of the sphincter of Oddi. Meperidinemay cause seizures in large amounts, although it is the 'textbook' favorite.
· LAB: QD: CBC, lytes, BUN, creatinine, glucose, calcium, LDH, LFT. Check amylase and lipase QOD if necessary – they have minimal utility in daily patient management.
· STUDIES: ABG and CXR if any evidence of respiratory compromise. Abdominal CTs should include IV and oral contrast with a ‘rapid bolus’ or ‘dynamic’ or ‘pancreatic’ protocol (with thin cuts through the pancreas) to delineate necrosis from edema. Non-necrotizing disease generally has an excellent prognosis, whereas necrotizing pancreatitis markedly increases the risk of complications (see below).
· Dehydration: pour in the fluids.
· Electrolytes: follow K+, Mg++, and replete as necessary.
· In general, with clinical deterioration do the following: pan culture, CT the abdomen (pancreatic protocol), and cover for bowel flora. Use of empiric antibiotics should be limited to patients with severe, necrotizing disease, and even in this setting, is still controversial. Imipenim has the best pancreatic penetration and tissue levels. Look for pancreatic necrosis (that may be sterile or infected) and abscesses. To rule out infected necrosis, especially with continued fevers, consider a FNA for organisms on gram stain. If FNA is positive, this represents infected necrosis and is generally managed with surgical debridement/necrosectomy.
· Pulmonary: atelectasis, effusion, ARDS.
· Renal failure: from severe intravascular volume depletion.
· Sepsis/multisystem organ failure.
· The presence of a pseudocyst is a chronic complication, suggested by persistent pain and high amylase. The pseudocyst may resolve spontaneously after weeks of bowel rest with TPN or may need surgical intervention. Suspect this with clinical deterioration after initial improvement.
· Hungry, and tolerating PO’s.
· Decreasing amylase/lipase (poor marker).
Ranson's Criteria:s
9. evere acute pancreatitis if > 3 Ranson criteria or if any of the following:shock, renal insufficiency, or respiratory distress.
|
Admission |
48 hrs |
|
Non–gallstone pancreatitis |
|
|
Age > 55 |
Decrease in Hct > 10% |
|
WBC > 16K |
Increase in BUN > 5 mg/dl |
|
Glucose > 200 mg/dl |
Ca++ < 8 mg/dl |
|
LDH > 350 U/L |
pO2 < 60 mmHg |
|
AST > 250 u/L |
Base deficit > 4 mM |
|
|
Fluid deficit > 6 L |
|
Gallstone pancreatitis |
|
|
Age > 70 |
Decrease in Hct > 10% |
|
WBC > 18K |
Increase in BUN > 2 mg/dl |
|
Glucose > 220 mg/dl |
Ca++ < 8 mg/dl |
|
LDH >400 U/L |
Base deficit > 5 mM |
|
AST >250 u/L |
Fluid deficit > 4 L |
|
Risk factors |
Mortality |
|
1–2 |
< 1% |
|
3–4 |
15% |
|
6–7 |
100% |
Steinberg W, Tenner S. Acute pancreatitis. N Engl J Med. 1994 Apr 28;330(17):1198-210.
1. Alcoholic liver disease includes three overlapping syndromes: fatty liver, alcoholic hepatitis, and micronodular cirrhosis. Mortality is 20-65% at 6 months with severe alcoholic hepatitis.
2. Symptoms: anorexia (87%), fever (50-75%), N/V (55%), weight loss (60%). Other symptoms include jaundice, ascites, edema, encephalopathy, and bilateral parotid enlargement. Differentiate alcoholic hepatitis from cholecystitis and cholelithiasis.
· Treat by stopping EtOH, supporting nutrition, and prophylaxis against DTs.
· Steroids may be indicated too. Calculate a discriminant function as follows: 4.6 x [PT – control time] + T.bili. If it is >32 or if patient has encephalopathy, there is a short-term improvement in mortality from taking 40 mg/day prednisolone or equivalent for 4 weeks. (A functioning liver is necessary to convert prednisone to prednisolone.) If the hepatitis is severe enough that you are considering using steroids, you should probably involve the GI service. Contraindications include bleeding, infection, and a creatinine greater than or equal to 2.3 mg/dl.
1. Avoid anything PO if patient is impacted or obstructed—eating will cause pain, and can cause perforation. Always do a rectal exam and a KUB to rule out fecal impaction and obstruction before starting medical therapy.
2. Do not give magnesium-containing products to patients with renal dysfunction (e.g. MOM).
3. All patients on chronic narcotics or who are bed-bound should be on a bowel regimen such as colace or senna.
4. Colace alone is often ineffectual.
· Afterload: dulcolax suppository, Fleets enema, mineral oil enema
· Preload: MOM 30 cc po QID prn
· Inotropy: senna 1-2 tabs po qd-bid, if unsuccessful, lactulose 30 cc q2h until stools, Mag citrate 1 bottle.
· Stool softeners: Colace 100-250 mg po bid
· If all else fails, consider PO naloxone in patients who have opiate-induced constipation (ask your local pharmacy for dosing. Because naloxone is minimally absorbed, there is no effect on pain control).
· Risk factors for the development of encephalopathy include the following: dietary indiscretion, infection, GI bleeding, and virtually any type of sedative (don’t give benzodiazepines to the cirrhotic with cloudy mentation).
· Treatment: lactulose—start at 15 cc TID and titrate to 3 to 5 loose stools per day.
2. Spontaneous bacterial peritonitis (SBP):
· Classically, SBP presents as a patient with pre-existing ascites who develops abdominal pain, fever, decreased bowel sounds, worsened hepatic encephalopathy, and hypotension. However, fever is present only 70% of the time, abdominal pain 60%, and encephalopathy only 50%. One in ten patients with SBP will have no symptoms at all. Therefore, have a low threshold for performing diagnostic paracentesis on cirrhotic patients with ascites.
· Risk factors include low-protein ascites, a bilirubin > 2.5 mg/dl, GIbleed (20% of GI bleeders will have SBP on admission), UTI, catheterization, and a prior episode (over 40% will have SBP again in 6 months). The 1-2 year mortality is 25%.
· Diagnostic test is based on paracentesis cell count and differential:
- PMN > 250/mm3: the sensitivity and specificity of this value is above 90%. Traumatic taps generate 1 WBC per 250 RBCs, and 1 lymph per 750 RBCs. WBC greater than 10,000 is suggestive of secondary peritonitis. (Pearl: hepatocongestion facilitates RBC diapedesis, so an elevated numbers of RBCs suggests cardiac ascites. However, most bloody taps are from the trauma of the procedure.)
- A positive Gram stain occurs 5-20% of the time, and is not only diagnostic, but can quickly rule-in bowel perforation when polymicrobial.
· A positive culture is diagnostic of SBP and will narrow therapy.
· Most common organisms are E. coli, Strep species, and pneumococci.
· Treat with third generation cephalosporin (e.g. cefotaxime, ceftriaxone).
· Give albumin on day 0 (1.5 g/kg of 25% albumin) and day 3 (1.0 g/kg of 25% albumin).
· In high-risk patients (those with total protein in ascites < 1.0, previous SBP, or s/p recent GI bleed), initiate SBP prophylaxis. Consider septra DS one tab QD, or ciprofloxacin 750 mg qweek.
|
Points scored |
1 |
2 |
3 |
|
Encephalopathy grade |
None |
1–2 (mild confusion/lethargy) |
3–4 (marked confusion/coma) |
|
Bilirubin (mg/dl)* |
< 1.5 |
1.5–2.3 |
> 2.3 |
|
Ascites |
None |
Easily controlled |
Poorly controlled |
|
Albumin (mg/dl) |
> 3.5 |
2.8–3.5 |
< 2.8 |
|
PT (sec >control) |
< 4 |
4–6 |
> 6 |
* Does not apply to primary cholestatic liver disease (e.g. primary biliary cirrhosis)
|
Total points |
Classification |
1 & 2 year survival |
|
5–6 |
Class A |
100%, 85% |
|
7–9 |
Class B |
80%, 60% |
|
10–15 |
Class C |
45%, 35% |
Garcia-Tsao
G. Current management of the complications of cirrhosis and portal hypertension:
variceal hemorrhage, ascites, and spontaneous bacterial peritonitis.
Gastroenterology. 2001 Feb;120(3):726-48
1. Factoids:
· The symptoms and signs of SBP are insensitive: have a low threshold for diagnostic paracentesis (See Gastroenterology: Spontanous bacterial peritonitis).
· Increased hydrostatic pressure (i.e. portal hypertension): cardiac (right-sided heart failure, constrictive pericarditis) and noncardiac (Budd-Chiari, cirrhosis, etc.).
· Decreased oncotic pressure: low albumin due to the inability to either retain or synthesize the protein.
· Increased capillary permeability: TB and peritoneal carcinomatosis, which may also cause lymphatic obstruction.
· Miscellaneous: pancreatitis.
3. Calculate the SAAG, or serum ascites-albumin gradient, by subtracting the ascites albumin from the serum albumin. A high gradient (> 1.1) means there is portal hypertension.
|
High gradient (> 1.1 g/dl) |
Low gradient (< 1.1 g/dl) |
|
Cirrhosis Alcoholic hepatitis Cardiac failure Massive liver metastases Fulminant hepatic failure Budd–Chiari syndrome Portal vein thrombosis Veno–occlusive disease Fatty liver of pregnancy Myxedema “Mixed” ascites |
Peritoneal carcinomatosis Peritoneal TB Pancreatic ascites Biliary ascites Nephrotic syndrome Serositis Bowel obstruction/infarction |
· The total protein concentration of the ascites, a proxy for complement levels, predicts risk of SBP (< 1 g/dl is high risk). A high total protein (> 2.5 g/dl) with portal hypertension can be seen in congestive heart failure.
- 2g sodium restriction.
- Diuretics: use lasix and spironolactone in a 2:5 ratio. Start with Lasix 40 mg to maximum of 160 mg/d, and 100 mg spironolactone PO to maximum of 400mg/d. Increase as BP allows and only incrementally every 2-3 days. Add metolazone 5-10 mg/day if unable to achieve desired diuresis. Shoot for reversal of the urine Na and K ratio – that is, the urine contains more sodium than potassium: this indicates a therapeutic diuretic dose.
- Approach either (1) midline below the umbilicus (be sure to have the patient empty their bladder or place a Foley), or (2) about 3 centimeters medial to the anterior superior iliac spine. Midline is preferred due to lack of vascular structures.
- Do not tap near sites of previous abdominal surgery (to avoid adherent bowel), or overlying infection; always use “Z” track (see Procedures sections).
- Coagulopathy or thrombocytopenia are not contraindications except in presence of DIC or fibrinolysis, and one does not need to correct the INR before performing the paracentesis; however, if patient is coagulopathic, use a 16 gauge or smaller needle. For a diagnostic tap, a 20 gauge needle will suffice. Use the “Z-track” technique to help prevent post-tap leakage; for patients who do leak afterwards, apply a colostomy bag to the abdomen.
Garcia-Tsao G. Current management of the complications of cirrhosis and portal hypertension:variceal hemorrhage, ascites, and spontaneous bacterial peritonitis. Gastroenterology. 2001 Feb;120(3):726-48
Factoids:
1. Pepto-Bismol, iron, spinach, and charcoal cause “false positive” melena, i.e. dark stools.
· It is only suggested by the H&P: for example a brisk upper GI bleeding can cause BRBPR, and conversely a slow, right-sided colonic bleed can cause melena. However, the presumed location of bleed will help guide appropriate studies: EGD, colonoscopy, sigmoidoscopy, angiography, radionuclide scan, etc.
· Other relevant history includes prior bleeds, prior abdominal surgery, prior AAA surgery, trauma, coagulopathy, anticoagulant meds, NSAID use, caffeine, and current use of beta-blockers.
· Orthostatics are unreliable, and vital signs are confounded by the use of beta-blockers.
|
|
Risk factors |
Symptoms/signs |
|
Upper GI Bleed |
· NSAID use · Varices · Peptic ulcer disease · Esophagitis |
· Mallory-Weiss tear · Liver disease · EtOH abuse |
· Epigastric pain · Hematemasis · Melena
|
|
Lower GI Bleed |
· Diverticulosis · Angiodysplasia · Colon cancer |
· Ischemic bowel · Bowel surgery · Inflammatory bowel disease (IBD) |
· Hematochezia · BRBPR
|
3. Clinical risk stratification: (before endoscopy):
· Clinical judgment always comes first.
· The goal of risk-stratifying with these clinical criteria is to determine the timing and urgency of endoscopy, and to determine where the patient should go.
· First, stratify. Next, see below for appropriate ER management guidelines. Then, use the risk-level to determine the need for admission to floor vs. telemetry vs. ICU. Admit moderate risk patients to the floor or telemetry; admit high-risk patients to the ICU.
Low risk |
Moderate risk |
High risk |
|
Age <60 |
Age >60 |
Age > 60 |
|
Initial SBP >100; vital signs now normal |
SBP <100 on admission and/or mild ongoing tachycardia |
Current SBP <100 and/or severe ongoing tachycardia |
|
Transfusion <2 units |
Transfusion >2 units |
Transfusion >5 units |
|
No active major co-morbid disease* |
Stable major co-morbid disease* |
Unstable major co-morbid disease* |
|
No liver disease |
Liver disease without coagulopathy or encephalopathy |
Decompensated liver disease |
|
No moderate or high-risk clinical features |
No high-risk clinical features |
|
* Major co–morbid disease defined as CAD, CHF, acute renal failure, sepsis, disseminated malignancy, altered mental status, pneumonia, COPD, asthma
|
Low risk |
Moderate risk |
High risk |
|
· Vital signs q30 min · Single IV okay · T&C 2 units PRBC |
· Continuous ECG · Vital signs q15 min with BP and O2 sat · Two IVs with isotonic fluid · T&C 2-4 PRBC |
· Continuous ECG · Vital signs q15 min with BP and O2 sat · Two IVs with isotonic fluid · T&C 2-4 units PRBC · Foley catheter · Transfuse if no response to crystalloid · Consider airway protection if massive hematemasis or AMS · Surgical consult |
· Remember that most deaths occur from respiratory, cardiovascular, and renal complications associated with bleeding, not exsanguination.
5. Endoscopic risk stratification: here are EGD findings the GI consultant will use to further risk-stratify the patient.
|
Low risk |
Moderate risk |
High risk |
|
· Gastritis · Esophagitis · Malloy-Weiss tear · Clean-based ulcer |
· Ulcer with clot · Diulafoy’s ulcer |
· Varices · Actively bleeding ulcer · Ulcer with visible vessel |
· Serial CBC, electrolytes, PT/PTT, LFTs, and a CXR. Get a KUB for abdominal distention, pain, or peritoneal signs; get an ECG for history of coronary artery disease or age >45.
· It is okay to place NGT if patient is coagulopathic or has suspected varices. Remember, it is often helpful to use Hurricane spray or Lidocaine jelly before inserting NG's. NG aspirate with 50-100 cc NS or tap water. It is okay to lavage, but watch for aspiration. Leave the NGT in.
· If content is clear, it only means no active bleed in stomach (pylorus likely closed and duodenal bleed cannot be assessed) If content is bilious, there is likely no active duodenal bleed but the visual assessment of the presence of bile is inaccurate. Remember: guaiac gastric content not helpful; NGT is used primarily to assess active upper GI bleed (UGIB).
· Volume resuscitate with IV NS to correct vital signs. Patient should have two large-bore IVs, and be typed and crossed.
· Transfuse hematocrit to >25% (>30% if CAD) and platelets >50K.
· Consider FFP, vitamin K if INR >1.5, DDAVP (0.3 mcg/kg IV q12h x 2) if uremic bleeding.
· Octreotide for patients with acute bleeding and evidence of advanced liver disease or portal HTN. Dosing: 100 mcg bolus then 50 mcg/hr x 2-5 days.
· NPO until after endoscopy
· Start empiric proton pump inhibitor (e.g. protonix 40 mg PO BID). Avoid NSAIDs, ASA, anticoagulants. If active UGIB, consider IV Protonix (recently shown to decrease rebleeding when administered after endoscopy in patients with high-risk endoscopic features such as visible vessels or active bleeding; there is no good evidence yet supporting the empiric use of IV PPIs on presentation in ‘all-comers’ with UGIB).
· After the acute bleed has resolved, in patients with portal hypertension, start prophylaxis against esophageal variceal bleeding by giving nonspecific beta-blockers, such as propranolol or nadolol. Titrate to a dose that lowers the baseline heart rate 25%.
· Ask GI when it is okay for the patient to eat. They are guided by endoscopic risk factors, the matter simply being that GI wants an empty stomach for a re-scope, if needed.
· Don't forget Helicobacter pylori! Check H. pylori serology and initiate empiric H. pylori treatment unless it is NSAID-associated.
· Generally if patients are admitted they are often observed for re-bleeding after endoscopy. Length of time depends on endoscopic and clinical risk criteria. Rapid post-endoscopy discharge is reasonable for some patients with low-risk endoscopic findings; others, with high-risk stigmata, will generally be observed for up to 72 hours.
Corley, DA, Stefan, AM, Wolf, M, et al. Early indicators of prognosis in upper gastrointestinal hemorrhage. Am J Gastroenterol 1998; 93:336.
Zuccaro, G. Management of the adult patient with acute lower gastrointestinal bleeding. Am J Gastroenterol 1998; 93:1202.
1. Differential diagnosis:
· Electrolytes: hypokalemia, hyponatremia, and hypocalcemia
· Esophagitis (chemical, infectious)
· Drugs: metoclopramide, sulfa, alcohol and benzodiazepines, steroids, barbiturates
· CNS disorder (metastases, encephalitis, multiple sclerosis, and stroke)
· Uremia
· Pleural or sub-diaphragmatic disease: PNA, peritonitis, gastric distention
· Phrenic or vagal nerve irritation
· Psychogenic
· Idiopathic
2. Treatment: empiric and paradoxical
· Chlorpromazine (Thorazine) or Haldol
· Metoclopramide (Reglan)
· Valsalva maneuvers
· Lorazepam (Ativan)
· Baclofen
1. First line:
· Prochlorperazine (Compazine) 10 mg PO/IM/IV q6h or 25 mg PR q12h PRN. Extrapyramidal symptoms are a possible side effect.
· Promethazine (Phenergan) 12.5-25 mg PO/IM/PR q4-6h.
· Lorazepam (Ativan) 0.5-2.0 mg PO/IV q4-6h prn.
· Metoclopramide (Reglan) 10 mg PO/IV q4-6h prn.
· Dexamethasone (Decadron) 10 mg PO/IV q6h prn.
2. Second line:
· Dronabinol (Marinol) 2.5-10 mg po q6h
· Granisetron (Kytril) and ondansetron (Zofran) are expensive antiemetics typically only for chemotherapy-induced nausea, or overdose with an anticholinergic medication that is associated with nausea/vomiting.
3. General tips:
· Beware neuroleptic malignant syndrome or dystonic reaction with excessive use of compazine or droperidol (treat with benadryl 50 mg IV/IM or Cogentin 10 mg IV)
· Compazine and Marinol are relatively contraindicated in patients with known seizure disorder.
· A common side-effect of many anti-emetics is drowsiness.
· As with other drug therapy, combinations of anti-emetics can sometimes succeed when single agents fail.