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EM GI Bleed
EM GI Bleeding
| Question | Answer |
|---|---|
| What divides upper and lower GI bleed classification? | Ligament of Treitz |
| Most common cause of Upper GI bleeds | Peptic ulcer dz (duodenal ulcers 29% will rebleed in 10% of cases within 24-48h) |
| Causes of Upper GI bleed | Erosive gastritis, esophagitis, duodenitis some causes are ETOH, ASA, NSAID’s.Esophageal and gastric varices causes by portal hypertension. Mallory-Weiss Syndrome caused by repeated retching |
| Causes of Upper GI bleed causes contd | stress ulcers, arteriovenous malformation, malignancy, aortoenteric fistula |
| Causes of lower GI bleed | Hemorrhoids (most common cause), Diverticulosis (painless), Arteriovenous malformations (common and seen in pt with htn and aortic stenosis), CA/polyps, IBD, Infectious gastroenteritis, Meckel diverticulum |
| History to gather in a GI bleed | hematemesis, coffee-ground emesis, melena, hematochezia, weight loss, change in bowel habits, vomiting, hx of aortic graft, ASA, NSAIDs, Steroids, ETOH abuse, hx of iron or bismuth (melena), beets |
| PE in a bleed includes: vital signs may show hypotension, tachycardia, cool, clammy skin when in shock, spider angiomata, palmer erythema, jaundice, and gynecomastia. PLUS | Petechiae and purpura seen in coagulopathy, Careful ENT exam to r/o causes that can mimic upper GI bleeds, abdominal exam and rectal exam |
| ENT cause that can mimic GI bleeds | Epistaxis (swallowed) |
| Labs in GI bleeds | CBC (Hct, Hgb), Electrolytes, Glucose, BUN/Creatine (BUN elevated in upper GI bleeds), Coagulation studies, LFTs, Type and cross-match |
| Diagnostic tests in GI bleeds | ECG (induced ischemia infarct), Abdominal series (free air perforation), angiography (requires brisk bleed), bleeding scans (slower bleeding rates; more sensitive than angiography), Colonoscopy (most accurate) |
| Tx of GI Bleeds | Large bore IV lines with fluid replacement, I+II: Crystalloid, III +IV: crystalloid and blood, NG tube should be placed and can help determine upper from lower GI bleed (will not worsen varices). Foley catheter for hypotensive pts to monitor output |
| Class I hemorrhage | up to 15% loss of blood vol. Vital signs unchanged. Fluid resuscitation usually not necessary |
| Class II hemorrhage | 15-30% loss of total blood volume. Tachycardic, narrowing Pulse pressure, body compensates with peripheral vasoconstriction, skin pale and cool to touch, slight change in behavior, volume resuscitation with crystalloids. Blood transfusion not usually |
| Class III Hemorrhage | 30-40% loss of circulating blood volume. BP drops, HR increases, Shock, poor capillary refill, mental status changes. Fluid resuscitation with crystalloid and blood transfusion are generally necessary |
| Class IV Hemorrhage | involves loss of >40% of circulating blood volume. The limit of the body's compensation is reached and aggressive resuscitation is required to prevent death. |
| GI Bleed TX | Proton Pump Inhibitor, Endoscopy, Somatostatin, Octretide for varices, balloon tamponade, surgery, must get early consult with gastroenterologist and general surgeon for signif. GI bleeds |
| PUD Epidemiology | 10% of Americans at some time in life. AA 45% of H. pylori by age 25. |
| Stress ulcers | do not extend through the muscularis mucosa |
| Duodenal ulcers | occur in the first portion of the duodenum |
| Gastric ulcers | usually occur in the lesser curvature of the stomach |
| H. pylori is seen in 95% of patients with duodenal ulcers and 80% of gastric ulcers. Only 10-20% of pts who are infected with H. pylori will develop ulcers | 'Its production of urease, cytotoxins, proteases and other compounds disturb the gel and increase tissue exposure to acid and pepsin. |
| Causes of PUD | NSAIDs, Zollinger-Ellison syndrome, Cigarette smoking, bile salts, stress, type O blood, prolonged use of corticosteroids, caffeinated drinks. Diet & ETOH do not predispose |
| MOA of NSAIDs and PUD | inhibit prostaglandins which in turn increases tissue exposure to acid and pepsin. |
| MOA of Cigarette smoking and PUD | inhibits bicarbonate ion production and increases gastric emptying. |
| Zollinger-Ellison Syndrome | inhibits bicarbonate ion production and increases gastric emptying. |
| Clinical Features of PUD | Epigastric pain, pain shortly after eating, Duodenal ulcers usually awaken pts at night and are relieved by food. Epigastric tenderness |
| Diagnosing PUD | Invasive: endoscopy (may include a rapid urease test, histologic study or culture). NonInvasive: serologies, urea breath test and stool antigens can confirm cure |
| Definite diagnosis of PUD | only by visualization with an upper GI or endoscopy. Able to take biopsy which is required in gastric ulcers to r/o malignancy |
| Tx of PUD | Stop offending agents, bland diets with frequent feedings not shown to be effective,Antacids, H2 agonists, PPIs, Sulcralfate, Misoprostol, Bismuth |
| Antacid notes | good for acute pain relief and healing ulcers, poor compliance due to frequent doses, inhibits absorption of warfarin, digoxin and some abx and anticonvulsants, aluminum and magnesium |
| Who should aluminum not be given to? | aluminum causes constipation and should not be given with renal failure patients due to accumulation which can cause osteoporosis and encephalopathy. |
| _____ is only indicated for prevention of NSAID-induced gastric ulcers in high risk pts | Misoprostol. CI in pregnant women. |
| Tx of H.pylori | Usually done with a triple or quadruple tx regimen including abx. Ex: metronidazole, tetracycline, amoxicillin, clarithromycin |
| Complications of PUD | Perforations, Gastric outlet obstruction, |
| Tx of complications of PUD | IV fluids, electrolyte corrections, NG tube, broad spectrum antibiotics and surgery. |
| Most common cause of lower GI bleed | Hemorrhoids |
| Colonoscopy is diagnostic and therapeutic and is more accurate than bleeding scans and angiography for GI bleeds. | True |
| Subjective sensation that suggest the presence of an organic abnormality in the passage of liquids or solids from the oral cavity to the stomach | Dysphagia |
| Dysphagia can be classified as either | oropharyngeal or esophageal |
| Oropharyngeal dysphagia | arises from disorders that affect the function of the oropharynx, larynx,and upper esophageal sphincter. |
| Esophageal Dysphagia | arises within the body of the esophagus, the lower esophageal sphincter or cardia , and is most commonly due to a mechanical causes or a motility disturbance |
| Cornerstone of diagnosing cause of dysphagia | careful history |
| Diagnostic tests for Dysphagia | Barium swallow (not if you suspect obstruction), endoscopy, esophageal manometry, Biopsy |
| Sx of GERD | chronic heartburn, regurgitations, nausea, epigastric pain |
| Causes of GERD | High fat food, nicotine, ETOH, Caffeine, Medications (nitrates, CA channel blockers, anticholinergics, progesterone), Pregnancy |
| Tx of Mild GERD | Lifestyle and dietary cchanges. Antacids and nonprescription histamine (zantac) 2(H2) receptor antagonist are usually sufficient |
| Tx of severe GERD | PPI, sleep with bed at 30 degrees, avoid eating 3 hours before sleep, surgery (Touplet fundoplication, HIll repair and Belsey Mark IV) |
| Cause of Esophageal Perforation | most iatrogenic, perforation. Spontaneous rupture (Boerhaven syndrome) occurs secondary to sudden incresae in intraluminal pressure (usually due to violent vomiting and often preceded by heavy eating or ETOH) |
| Esophageal Perforation Causes | Trauma, FB, Infection, Tumor, Aortic Pathology, Barrett esophagus, Zollinger-Ellison Syndrome |
| Classic Presentation of Esophageal Perforation | Subcutaneous emphysema neck/chest, tachycardia/tachypnea, Mackler triad (vomiting, chest pain, subqemphysema), delayed presentation pts may have signif. hypotension and illness |
| Esophageal bleeding | Esophgeal varices, mallory weiss syndrome, esophgeal neoplastic process, trauma, Barrett's esophagus |
| Tx of Esophageal bleeding | Broad spectrum abx, NPO, NG tube, Emergent airway if indicated, small tear (conservative approach), Larger tears (surgery, stenting, resection, drain placement) |
| Dx of Esophageal bleeding | Endoscopy, Endoscopic US helpful to distinguish between varices and folds, Portal vein angio, barium studies, Capsule endoscopy of the esophagus |
| Which test can help determine between varices and folds in esophageal bleeding? | Endoscopic US |
| ___ % of variceal bleeding resolves with supportive care alone | 60%. |
| Most common cause of vomiting and diarrhea | gastroenteritis. Viral: norovirus (90% in adults), Rota virs in infants and children. Usually self-limiting. Dehydration danger seen in very young and very old. Bacterial gastroenteritis: often food borne (Shigella, Salmonella, E.coli, CampylobacterJ) |
| High fever and vomiting | most likely infectious, not viral. |
| Chest pain and vomiting suggests | Acute coronary syndrome |
| Main complaint of PUD | Epigastric pain (gnawing, aching, burning) |
| Gastric ulcers vs. Duodenal ulcers | Gastric ulcers usually develop pain shortly after eating; Duodenal ulcers usually develop pain 2-3 hours post prandial and awaken patients at night. Relieved by food. |
| AE of many tx for PUD | diarrhea and cramping |
| Most common cause of upper GI bleeding | PUD |
| Perforation notes: | anterior perf: shows free air in 60-70%, posterior perf: no free air. No free air on X-rays cannot r/o perforation. |
| PUD with abdominal x-ray dilation and air/fluid level may be | gastric outlet obstruction. Scaring from healed ulcers or edema from active ulcer with development of obstruction. |
| Boerhaven syndrome | spontaneous esophageal rupture occurs secondary to sudden increase in intraluminal pressure-- usually due to violent retching. Often preceded by heaving eating of ETOH |
| Mackler Triad | Seen in Esophageal perforation: Vomiting, Chest pain, subacute emphysema |
| Acute diarrhea | <2 weeks. Chronic >2 weeks |
Created by:
ltm12