Acute GI Bleed Classification Upper (above ligament of Treitz) Lower (below ligament) History Prior bleeds, diverticular disease, prior GI or aortic surgery, trauma, coagulopathy, medications (ASA, NSAIDs, anticoagulants, steroids, antiplatelet medications), liver disease, alcohol abuse, renal insufficiency, poor cardiac output, hypertension, hypotension, recreational drugs (cocaine, amphetamines), rectal foreign objects (sexual activity or used to disimpact), history of STDs Etiology
Upper GI Bleeds (UGIB): Peptic ulcer disease (H. pylori or NSAIDs) Portal hypertensive gastropathy Varices Mallory-Weiss tear Erosive esophagitis (especially alcoholics) Vascular malformations Dieulafoy's lesion (an abnormally large submucosal artery located in the proximal stomach) Neoplasm Note that gastritis is not a cause of bleeding (possibly occult blood loss but not acute bleeding)
Rectal: Stool may appear bright red, maroon, black and tarry, or brown Look for evidence of hemorrhoids or fissures No guaiac necessary if concern of acute bleed. Guaiac should be used for colon cancer screening and workup of iron deficient anemia of unclear etiology not for acute hemoglobin drops. 1 cc of blood loss will result in a positive guaiac; 50 cc of blood loss results in melena. Therefore if recent bleeding you will find it without a guaiac. Labs CBC, chemistry panel, coags, type and cross, liver function tests Consider that the patient initially may have a normal Hgb value due to hemoconcentration BUN disproportionately elevated from Cr suggests an upper GI source Management
Access: 2 large bore IVs (14-18 gauge) Volume resuscitation with NS ICU management if orthostatic
NG tube placement and lavage: Note the volume of NS needed to clear the lavage fluid of bright red blood. If you are unable to clear the lavage fluid of bright red blood, this implies a 40% mortality without intervention! Clear nonbilious lavage = 15% chance of bleeding beyond pylorus. Clear bilious = 5% chance of active bleeding
Transfusion: keep Hgb > 9 (> 10 if cardiac disease) Serial Hgb q4hrs (anticipate a slight decline in values from hemodilution) Correct any coagulopathies (FFP if INR > 1.5; keep platelets > 50) Intubate patients at high risk for aspiration (i.e. active bleeding + AMS) especially cirrhotics Stop all anticoagulants and anti-platelet agents NPO except medications Do not give the patient sucralfate or antacids until after EGD, as they will interfere with the endoscopy
Acid suppression: IV PPI drip if suspect PUD x 72 hours (pantoprazole 80 mg IV x 1 then drip at 8 mg/hr x 72 hours) PPI IV/PO b.i.d. in other UGI bleeds (pantoprazole 40 mg IV/PO b.i.d.)
Octreotide: If strong suspicion for an ongoing variceal bleed/advanced liver disease Dose at 50 mg IV bolus followed by 50 mg/hr drip. GI consult urgently if there is evidence of active bleeding and hemodynamic instability. Reglan 10mg IV q6hrs until endoscopy in setting of UGI bleed
Colonoscopy prep: 1st choice for initial evaluation of LGIB For colon prep in setting of LGIB, GoLYTELY 800 cc/hour via NG tube. Start with 6 L but give as many liters until clear. Reglan 10mg IV 30min prior to and 2 hours after starting the prep. Do not do PO prep when trying to clear bleeding. Strict aspiration precautions.
Radionuclide imaging: detects bleeding at 0.1 to 0.5 ml/min
Angiography: For faster bleeds 1.0 to 1.5 ml /min A positive angiogram is associated with high likelihood of requiring surgical intervention
Comments: First consideration is ABCs. Secure airway (intubate if necessary). Achieve hemodynamic stability. Resuscitation is the most important treatment Endoscopy/Colonoscopy after blood and fluid resuscitation, ICU stabilization, and correction of coagulopathy and administration of IV PPI or octreotide gtt if indicated. Admit patients with multiple comorbidities, orthostatic vitals that cannot be corrected quickly with IV fluids, and advanced age to ICU as they have a higher mortality rate. Approximately 70-80% of all GI bleeds stop spontaneously. Pepto-Bismol, iron, and spinach can turn stools black! Nasogastric Lavage Get NG tube, chucks, 30 cc cath tip syringe, cup of water, straw, Surgilube, tape strips and normal saline. Sit the patient up as straight as possible. Determine the length of tube that is needed. Measure from the patient's navel®ear®tip of nose. Lubricate distal end of the tube. Put the NG tube straight posteriorly into patient's nose. Ask the patient to swallow (sip the water) as you slowly push the NG tube. Gagging or vomiting suggests going down the esophagus. Coughing suggests going down the trachea®pull back. Push until you reach predetermined line. Push 30 cc of air from syringe through tube and listen to the area over the stomach with your stethoscope for gurgling. Tape the NG tube to the patient's nose. Try sucking back with the syringe. If there is no fluid returned or if there is a question about proper placement, consider CXR to verify proper placement. Lavage stomach with normal saline. Note the presence of blood or coffee grounds. If present, lavage until clear and take note how much fluid required to clear the blood. Note if bile-tinged fluid is detected (indicates you are sampling contents of early duodenum as well) If the coffee grounds clear or if the lavage was completely clear, the NG tube can usually be pulled out. NG tube should be left in place if any suspicion of LGI bleeding in order to prep the patient. If NG tube is to be left in place, check a CXR to confirm proper placement. Abdominal Pain Initial Considerations Rule out the presence of the surgical abdomen as this can kill the patient quickly. Make sure that the patient is hemodynamically stable. History
Timing: acute versus chronic, gradual versus sudden
Location: localized versus referred pain
Quality: sharp, dull, tearing, burning, boring; has the quality changed over time? Prior episodes of similar pain, relationship to menstrual cycles Associated symptoms such as nausea, vomiting, fever, diarrhea, etc. Previous intra-abdominal procedures (appendectomy, cholecystectomy, laparoscopies) Last bowel movement - time and quality (soft, hard) Exacerbating or relieving factors (such as food, BMs, deep breath, positional etc.) Presence fresh blood (hematochezia) vs old blood (melena)
Generalized: appendicitis, intestinal obstruction or infection, IBD, peritonitis, DKA, sickle cell crisis, acute intermittent porphyria, acute adrenocortical insufficiency. Physical Exam Focus on any signs of an MI as angina may present as epigastric pain Check for localized tenderness, rebound, guarding, bowel sounds Stool guaiac Any woman who complains of lower abdominal/pelvic pain should get a pelvic examination
Murphy sign: pain on palpation of the right subcostal area during inspiration®cholecystitis
Psoas or obturator sign: passive extension of the thigh with knees extended-->appendicitis Rectal exam (unless contraindicated by neutropenia)
Carnett test: used to distinguish intraabdominal pain from abdominal wall pain Press in the location of the pain and have patient do a sit-up. If the pain worsens with the sit-up®abdominal wall pain. Pain out of proportion to abdominal exam suggestive of mesenteric ischemia Immunosuppressed may have benign exam despite surgical abdomen Labs CBC, chemistry panel, liver function tests, amylase and lipase, lactate, coags Clot for type and cross (if surgical abdomen or blood in stool) Urinalysis and urine pregnancy test In a patient with ascites, a paracentesis must be done to rule out SBP Radiology
Abdominal series: rule out the presence of free air under the diaphragm, obstruction, volvulus, sentinel loop, toxic megacolon (> 7 cm in midtransverse colon diameter), pleural effusion (pleurisy, pancreatitis if effusion is left-sided), etc.
Ultrasound: to investigate hepatobiliary pathology if RUQ pain
CT abdomen/pelvis: to rule out diverticular disease, appendicitis, colitis Other studies will depend on the patient's specific situation Treatment If there is potential for a surgical abdomen, request a surgical consultation. Keep NPO. Consider IV hydration. Type and cross for PRBC. Watch for septic/hypovolemic shock. Hang appropriate antibiotics early if there's suspicion for ascending cholangitis, diverticulitis, sepsis, etc. Try a GI cocktail (30 cc of Mylanta or Maalox + 10 cc of viscous lidocaine +/- 10 cc of Donnatal) if dyspepsia is a possibility Acute Pancreatitis Goal Rest the pancreas and support as necessary. Etiologies Alcohol Gallstones Blunt trauma Hypertriglyceridemia Hypercalcemia
Infections: mumps, CMV, HIV, E. coli Scorpion sting
Mechanical: post-ERCP, sphincter of Oddi dysfunction, pancreatic divisum, malignancy, perforated peptic ulcer
Miscellaneous: cystic fibrosis, genetic mutations Clinical Signs and Symptoms Constant, epigastric tenderness +/- radiation to back, nausea/vomiting, relief with bending forward Physical Exam Hypovolemia, abdominal tenderness, guarding, decreased bowel sounds, signs of retroperitoneal hemorrhage (Cullen's and Turner's signs) Diagnosis
Labs: amylase, lipase, liver function tests, calcium, chemistry panel, C-reactive protein Amylase is a sensitive diagnostic method if patient presents within hours of the onset of pain. Returns to normal faster than lipase. Nonpancreatic sources of amylase include salivary glands, lung CA, ovaries, fallopian tubes. Amylase levels tend not to be as high in alcoholic pancreatitis as in nonalcoholic forms. Lipase is a more sensitive and specific test. It is made only in the pancreas and stomach. Nonpancreatic elevation may be seen if the bowels are inflamed and the lipase is reabsorbed after being properly secreted from the pancreas. Note that renal insufficiency and inflammation/perforation of small bowel can lead to elevated amylase/lipase levels without active pancreatitis. Increase in ALT to >= 3x the baseline points more to gallstone-induced pancreatitis. Degree of amylase and lipase elevation does not correlate with severity.
Imaging: Ultrasound is the most sensitive way of evaluating the biliary tract in acute pancreatitis Contrast-enhanced CT (p.o. and IV) with pancreatic protocol is used to diagnose as well as to determine potential complications. Indicated for those patients who are clinically deteriorating or have severe pancreatitis (necrosis may not be apparent for first 2-3 days) MRCP can also be used to exclude choledocholithiasis Management IV hydration NPO until symptomatically improved (pain-free, hungry) Repletion of electrolytes NGT to suction only if protracted nausea and vomiting to prevent aspiration not to help pancreas as previously believed Treat infections if clinically suspected
Pain control: meperidine (morphine in theory causes spasm of sphincter of Oddi; no evidence in humans and most feel clinically safe) Patients with gallstone-induced pancreatitis who develop cholangitis require urgent ERCP Complications Acute fluid collection, pseudocyst, necrosis, Infection, abscesses, ARDS, renal failure, sepsis Prognosis Outcomes depend on whether disease is interstitial versus necrotizing Interstitial mortality rate < 1% Necrotizing (defined as necrosis of 30% of the gland seen on CT) mortality rate 10-30% mortality risk with a 70% complication risk
Scoring systems: Ranson, Glasgow, Apache II (none are completely accurate)
Ranson's Criteria for Acute Pancreatitis
Non-gallstone
Gallstone
On Admission
Age > 55 years
Age > 70 years
WBC > 16,000/mm3
WBC > 18,000/mm3
Glucose > 200 mg/dl
Glucose > 220 mg/dl
LDH > 350 IU/L
LDH > 400 IU/L
AST > 250 IU/L
AST > 250 IU/L
Within 48 Hours
dec Hematocrit > 10%
dec Hematocrit > 10%
inc BUN > 5 mg/dl
inc BUN > 2 mg/dl
Serum calcium < 8 mg/dl
Serum calcium < 8 mg/dl
Base deficit > 4 mEq/L
Base deficit > 5 mEq/L
Fluid deficit > 6 L
Fluid deficit > 4 L
PO2 < 60 mmHg
Mortality Risk
< 3 risk factors
1% mortality
4 risk factors
15% mortality
5-6 risk factors
40% mortality
>7 risk factors
100% mortality
Small Bowel Obstruction Consider the possibility that the patient is having strangulation of the bowels vs a simple mechanical obstruction. History
Symptoms: crampy abdominal pain, decreased or absent flatus and stool, nausea and vomiting. Prior episodes, intra-abdominal surgeries, adhesions and hernias History of Crohn's disease? If positive, ask about recent meals. Impaction of undigested foods can often cause obstruction in a strictured area. Previous radiation exposure? History of ovarian cancer Physical Evidence of hypovolemia? Abdominal distention: the lower the obstruction, the greater the degree of distention. High pitched tinkling bowel sound Hernias and surgical scars? Labs CBC and a chemistry panel. The presence of marked leukocytosis suggests strangulation or ischemia. Radiology Abdominal series to rule out the presence of free air under the diaphragm, air-fluid levels, and possible volvulus. Consider getting a CT scan with contrast to attempt to localize the site of transition. Look for evidence of strangulation! Treatment Correct the hypovolemia and electrolyte abnormalities Make the patient NPO Insert an NG tube and place on intermittent suction for decompression and symptom relief Surgery consult Acute Nausea General Medications (see table of Antiemetic Agents for Chemotherapy Patients in Hem/Onc section)
Prochlorperazine (Compazine) 5-10 mg PO/IV/IM t.i.d. Selectively antagonizes dopamine D2 receptors Side effects include urinary retention, hypotension, spastic torticollis, dystonia (treat with Benadryl), cytopenias, and QT prolongation
Metoclopramide (Reglan) 10 mg PO/IV q6hrs Antagonizes central and peripheral dopamine receptors Side effects include extrapyramidal symptoms, urinary frequency, cytopenias, SVT, HTN, sedation.
Promethazine (Phenergan) 12.5-25 mg PO/IM/PR q6hrs (antihistamine®will also produce sedation) Antagonizes central and peripheral H1 receptors (non-selective antihistamine) Side effects include sedation, cytopenias, urinary retention.
Lorazepam (Ativan) 0.5-2 mg IV/PO q4-6hrs Benzodiazepine Side effects include delirium in the elderly, sedation, hypotension.
Droperidol (Inapsine) 0.625-2.5 mg IV/SQ Antagonizes dopamine and a-adrenergic receptors Side effects include sedation, delirium in the elderly, and prolonged QT interval
Chemotherapy-induced: consider using serotonin antagonists, such as ondansetron or granisetron (will need Heme/Onc consult approval). Fluid hydration If the patient cannot tolerate orals, consider making patient NPO and starting IV hydration. Radiology If an obstruction is a possible etiology, order an abdominal series x-ray. If there is evidence of an obstruction or ileus, place an NG Tube to help decompress the abdomen. Resolution As the symptoms resolve, slowly advance the diet from clears to pureed to soft mechanical to regular. Always ensure that the patient is adequately hydrated and that electrolytes are repleted. Constipation General Concepts Make sure there is no impaction or obstruction Do rectal exam and KUB before starting medical therapy
Do not give agents with magnesium to renal failure patients Make sure to start bowel regimen for patients on narcotics or who are bed-bound
ALWAYS MOVE FROM BELOW FIRST! Treatment
Diet: increase both total fiber and water intake. Psyllium 1 tsp daily-t.i.d. is a common 1st choice. If the patient is bed-bound and/or not drinking sufficient water, fiber can make the constipation worse.
Laxatives: separated into 4 groups according to their mechanism of action Emollients (stool softeners): mineral oil and docusate salts (Colace). Note: Mineral oil causes lipoid pneumonia if aspirated and decreases the absorption of fat-soluble vitamins if given with meals. Hyperosmolar agents: polyethylene glycol (MiraLax), lactulose, sorbitol, and glycerol. Both lactulose and sorbitol are very effective and are highly recommended for use in chronic constipation if fiber and fluid supplementation do not work alone. Saline Laxatives: Magnesium sulfate, phosphate, and citrate Should not be used in patients with renal insufficiency because of magnesium toxicity.
This is usually not a good long-term option in the elderly Stimulant Laxatives: castor oil, senna (Senokot), bisacodyl (Dulcolax)
Not recommended for long-term use. Dulcolax is a gastric irritant. Tablets are enteric coated and should not be broken or chewed.
Prokinetic: misoprostol increases gut motility (sometimes used in patients on opiates)
Enemas: can be used episodically for "salvage" therapy if an alternative bowel program has not produced a BM. Don't use Fleet's enemas in patients with renal insufficiency because of retention of phosphate®use tap water enemas instead.
Suppositories: Both glycerin and bisacodyl (Dulcolax) can be used. However, they can be associated with cramping. They can also be used for "salvage" therapy. Acute Diarrhea History Acute diarrhea usually has an infectious etiology (viral, bacterial, parasitic), but the pace of certain infections tends to vary among the different organisms.
Food exposure: diarrhea may occur between 12 hours and 10 days after ingestion of the offending meal.
Appearance of the stool: blood (inflammatory or invasive ulceration), mucus (IBS), or oil (malabsorption).
Volume: small (left colon or rectum), large (small bowel or proximal colon).
Urgency and tenesmus: inflammation of the colon.
Nocturnal diarrhea: suggests infectious or inflammatory etiology, not IBS.
Diet: caffeine intake, dietary foods with poorly absorbed sugars (sorbitol or mannitol), fiber, dairy products, gluten
Social history: travel, sexual preference, occupation, living situation History of gastrectomy, vagotomy, intestinal resection (short gut syndrome).
Risk factors for intestinal ischemia: hypertension, DM, chronic a-fib related emboli, hypercholesterolemia, etc. Post-obstructive diarrhea.
Immunocompromised hosts: in addition to more common pathogens, consider CMV, MAI, Cryptosporidium, Cyclospora, Isospora, Entamoeba histolytica, etc. Physical Exam Check for fever, hypovolemia, surgical abdomen. Evaluation Most episodes are self-resolving with OTC medications and dietary modifications.
Medical attention and treatment is indicated only for patients with moderate or severe illness: Severe diarrhea with dehydration Dysentery (passage of bloody or mucoid stools) Temperature > 38.5°C Passage of > 6 unformed stools per day. Duration of diarrhea of 48 hours or longer. Diarrhea with severe abdominal pain in a patient > 50 years old (consider mesenteric ischemia and intra-abdominal abscess)
In patients with the red flag symptoms, consider sending: Stools for markers of inflammation (leukocytes, guaiac) Bacterial cultures Assays for E. coli O157:H7 (in patients with hemolysis, uremia, or exposure to undercooked meat or raw vegetables) Ovocytes and Parasites (O&P) (in patients who have traveled recently) C. difficile toxin (in patients with recent institutionalization and/or antibiotic or chemotherapy exposure) Note that every lab is different in the panel they run when you ask for stool culture. Depending on the history, you may want to specify organisms like Campylobacter, microsporidia, Isospora, and cryptosporidia. Also consider Giardia antigen. Send 3 fresh samples for the cultures and toxin assays. Management Treat hypovolemia and electrolyte abnormalities. IV therapy can be used for severe illness, but oral rehydration fluids that contain K, Na, and glucose can be used for milder cases. Withhold milk and other dairy products for 24-48 hours and initiate refeeding with cereals, starches, soups, and broth. Don't treat potentially infectious causes of diarrhea with antimotility agents (i.e. opioids, Imodium, Lomotil), until stool studies come back negative. Consider stopping any new medications. Treat non-specifically with bulking agents such as Kaopectate, but do not stop bowel motility. Once the specific diagnosis is made for the cause of the diarrhea, treat with the appropriate medication. If an infectious etiology is ruled out, consider using Imodium or Lomotil. Consider using cholestyramine in post-cholecystectomy patients. Many physicians advise avoidance of lactose-containing foods during and immediately following a diarrheal illness. Consider octreotide in patients with dumping syndrome and chemotherapy-induced diarrhea if other treatments have failed. The initial dose is 50-100 mg SC q8hrs. The dose should be escalated gradually every 48 hours until symptoms are under control or a maximum dose of 500 mg q8hrs has been reached. Helicobacter Pylori Diagnosis
Recommendations for testing: Presence of active peptic ulcer disease or a history of a documented peptic ulcer or gastric MALT lymphoma Non-endoscopic studies are preferred for initial diagnosis
Commonly used tests: H. pylori antibody titer by ELISA is 90% sensitive, but cannot distinguish current from past infection. The antibody test can remain positive after eradication, so don't order to confirm successful treatment! Urea breath test (discontinue PPI, antibiotics, and bismuth at least 1 week prior to the test) Sensitivity 88-95% Specificity 95-100% H. pylori stool antigen Sensitivity 94% Specificity 86-92% Invasive test options: histology (from biopsy), culture. Treatment Controversial but most recent consensus recommends treatment for those patients with documented PUD irrespective of symptom severity, confounding factors, whether the episode is the initial or recurrent or whether ulcer is active or in remission.
Combination regimen: PPI + clarithromycin + amoxicillin x 1-2 weeks May substitute amoxicillin with metronidazole if penicillin allergic (500 mg p.o. b.i.d.) Perform post-treatment confirmation test (urea breath test) only if patient has severe symptomatic ulcer, complicated ulcer (bleeding, perforation), or recurrent symptoms. Wait at least 4 weeks post-treatment before repeating the test. Patients with ongoing symptoms or active ulcer should stay on PPI for 2-4 weeks after triple therapy has completed.
Systematically look at the different parts: Bones Bowel Gas Pattern Soft tissues: psoas, liver edge, occasionally the spleen, may see the kidneys check for extraluminal gas (i.e. free air under the diaphragm). other soft tissue masses
Significant findings/possible diagnoses: SBO: see multiple air-fluid levels Gallstone ileus: see air in the biliary tree Hernia: see bowel extending beyond inguinal line String of pearls: bowels filled with fluid; high degree of obstruction; very little air Gasless abdomen: either esophageal obstruction and nothing going through or marked obstruction because the loops are filled with fluid. Colitis: often do not see haustra. In long-standing UC, see a "lead pipe" (no haustra) image of the sigmoid/descending colon. Obstruction versus ileus: clues suggestive of obstruction include asymmetric dilation of bowel, no air in the cecum/rectum, a definite point of transition, alternating levels of air-fluid. RUQ Ultrasound In general, this test is the most sensitive in investigating hepatobiliary pathology. Abdominal CT Order this test when you are looking for masses.
