110 Notes Notes GASTROENTEROLOGY Section Editor: Dr Winnie Wong Nausea and Vomiting DIFFERENTIAL DIAGNOSIS NEUROLOGIC ORGANIC infections, tumors, multiple sclerosis, vestibular nerve or brain stem lesions DRUGS chemotherapy, SSRI, opioids, antibiotics PSYCHIATRIC anorexia nervosa, bulimia nervosa, rumination GASTROINTESTINAL INFECTIONS acute gastroenteritis, food poison ing, pyelonephritis, pneumonia NEOPLASTIC gastric, ovarian, paraneoplastic, renal OBSTRUCTION stomach, small bowel, colon, functional, gastric volvulus POSTOP vagotomy, gastrectomy, fundoplication PEPTIC ULCER DISEASE esophagus, stomach, duodenum GASTROPARESIS ischemic, diabetic, amyloidosis, scleroderma, drugs OTHERS eosinophilic gastroenteritis, hepatobiliary disease, pancreatic disease, peritoneal irritation METABOLIC ENDOCRINE diabetes, adrenal insufficiency, hyper calcemia, hyperthyroidism, hyperemesis gravidarum OTHERS uremia, pregnancy IDIOPATHIC PATHOPHYSIOLOGY REFLEX PATHWAY AFFERENT (1) humoral drugs, toxins, neurotrans mitter, peptides ! area postrema in floor of 4th ventricle (chemoreceptor trigger zone) ! nucleus tractus solitarius (NTS) in medulla serves as central pattern generator for vomiting; (2) neuronal GI tract stimuli ! vagus nerve ! NTS; (3) nocicep tive stimuli ! sympathetic nervous system ! brain stem nuclei and the hypothalamus EFFERENT NTS ! paraventricular nuclei of the hypothalamus and the limbic and cortical regions ! gastric electromechanical events are perceived as normal sensations or nausea or discomfort ! vagus nerve ! gastric and lower esophageal sphincter relaxation, retrograde contraction in proximal small PATHOPHYSIOLOGY (CONT’D) bowel and antrum, abdominal muscle contraction and initial cricopharyngeus contraction followed by relaxation seconds before vomiting INVESTIGATIONS BASIC CBCD, lytes, urea, Cr, glucose, Ca, Mg, PO4, AM cortisol, urinalysis MICROBIOLOGY urine C&S IMAGING CXR, AXR SPECIAL LABS GASTROSCOPY CT HEAD MANAGEMENT SYMPTOM CONTROL H1 ANTAGONISTS dimenhydrinate 50 mg PO/PR q4h, diphenhydramine 25 50 mg PO/IV/IM q6h, cyclizine 50 mg PO/IM q4h or 100 mg PR q4h, meclizine 25 50 mg PO daily, promethazine 12.5 25 mg PO/IM q4h or 12.5 25 mg PR daily D2 ANTAGONISTS benzamides (metoclopramide 10 mg PO/IV/IM q4h), phenothiazine (pro chlorperazine 10 mg PO q6 8h, chlorpromazine 10 25 mg PO q4 6h), butyrophenones (droper idol 1.25 mg IM q4 h, haloperidol 0.5 mg IV/ PO q4h) 5HT3 ANTAGONISTS ondansetron mg PO/IV daily BID, granisetron mg PO or mg IV, dolase tron 100 mg PO/IV daily M1 ANTAGONISTS scopolamine 1.5 mg TD q72h STEROID dexamethasone mg BID TID PO/SC/IV TUBE FEED NJ tube, G tube TREAT UNDERLYING CAUSE Related Topics Chemotherapy Induced Nausea and Vomiting (p 229) Nausea and Vomiting in the Palliative Setting (p 395) D Hui, Approach to Internal Medicine, DOI 10.1007/978 4419 6505 5, ể Springer ScienceỵBusiness Media, LLC 2006, 2007, 2011 111 112 Dysphagia Dysphagia DIFFERENTIAL DIAGNOSIS OROPHARYNGEAL (upper esophagus and phar ynx, or upper esophageal sphincter dysfunction) NEUROLOGICAL stroke, multiple sclerosis, Parkinson’s, dementia, amyotrophic lateral sclerosis, Guillain Barre, myasthenia gravis, cer ebral palsy, Huntington’s, tardive dyskinesia, brain stem tumors, trauma MYOPATHIC myotonic dystrophy, dermatomyo sitis, connective tissue disease, sarcoidosis, paraneoplastic STRUCTURAL cricopharyngeal bar, Zenker’s diverticulum, cervical webs, oropharyngeal tumors, osteophytes and skeletal abnormality, congenital abnormality INFECTIOUS syphilis, Lyme disease, botulism, mucositis METABOLIC Cushing’s, thyrotoxicosis, Wilson’s, amyloidosis IATROGENIC chemotherapy, neuroleptics, post surgical, radiation ESOPHAGEAL (body of esophagus, lower esopha geal sphincter, cardia) STRUCTURAL tumors (benign, malignant), eso phagitis/stricture (reflux, caustic/erosive, infec tious, eosinophilic, pill, radiation), tylosis, diver ticula, iatrogenic (post surgery, radiation), esophageal ring/web, extrinsic compression (enlarged aorta, left atrium, mediastinal mass, osteophytes, subclavian artery) MOTILITY achalasia, scleroderma, Chagas dis ease, diffuse esophageal spasm, hypertensive lower esophageal sphincter, nutcracker esopha gus, non specific esophageal motility disorders FUNCTIONAL CLINICAL FEATURES (CONT’D) Difficulty swallowing both solids and liquids? If yes, consider motility disorders and proceed to step If progressing from solids to liquids, sider structural disorders and proceed to step For motility disorders, is the dysphagia pro gressive? If yes, consider achalasia or sclero derma If intermittent, consider diffuse esopha geal spasm or non specific esophageal motility disorder For structural disorders, is the dysphagia progres sive? If yes, consider tumors and peptic stricture If intermittent, consider esophageal ring Any caustic ingestion history? Solids Persistent Progressive Heartburn No heartburn Peptic stricture Cancer Intermittent Intermittent +/– heartburn Schatzki Ring Eosinophlic Esophagitis Solids + Liquids Persistent Progressive Heartburn No heartburn Scleroderma Achalasia Intermittent Diffuse esophageal spasm CLINICAL FEATURES DIAGNOSTIC CLUES history of heartburn may sug gest GERD leading to erosive esophagitis, peptic stricture, or esophageal adenocarcinoma History of atopic diseases especially in a young adult with recur rent dysphagia may suggest eosinophilic esophagitis Also check for odynophagia, regurgitation, hematem esis, coffee ground emesis, respiratory symptoms, and weight loss PRACTICAL APPROACH TO DYSPHAGIA Features of oropharyngeal dysphagia (problems initiating swallowing, extending neck/arms when swallowing, changes in speech, coughing, chok ing, or nasal regurgitation)? Consider workup for oropharyngeal dysphagia Otherwise, proceed to step INVESTIGATIONS BASIC barium swallow (esophageal), video fluoroscopy (oropharyngeal) SWALLOWING ASSESSMENT occupational therapy or speech pathology SPECIAL GASTROSCOPY for esophageal lesions and biopsy for eosinophilic esophagitis ESOPHAGEAL MANOMETRY definitive for achala sia, useful for diffuse esophageal spasm IMAGING 113 Dyspepsia SPECIFIC ENTITIES (CONT’D) INVESTIGATIONS (CONT’D) PH MONITORING for GERD, especially if gastro scopy normal FIBEROPTIC NASOPHARYNGEAL LARYNGOSCOPY for oropharyngeal dysphagia MANAGEMENT SYMPTOM CONTROL postural/nutritional/beha vioral modifications, swallowing rehabilitation, eso phageal dilation TREAT UNDERLYING CAUSE SPECIFIC ENTITIES ACHALASIA a motor disorder with lack of peristalsis in the body of the esophagus and incomplete relaxation of the lower esophageal sphincter on manometry DIAGNOSIS endoscopy is essential for ruling out malignancy Barium swallow (beak like narrow ing), esophageal manometry (definitive) PATHOPHYSIOLOGY endoscopic intrasphincteric injec tion of botulinum toxin, pneumatic dilation, and surgical myotomy INFECTIOUS ESOPHAGITIS PATHOPHYSIOLOGY common organisms include Candida albicans, CMV, and HSV Happens more likely in immunocompromised host DIAGNOSIS gastroscopy and biopsy/viral cultures EOSINOPHILIC ESOPHAGITIS PATHOPHYSIOLOGY food allergens and genetic factors leading to eosinophilic infiltration and stricture DIAGNOSIS gastroscopy and biopsy TREATMENTS dilatation, dietary modification, swallowed inhaled steroids, and oral steroids TREATMENTS Related Topics Esophageal Cancer (p 195) Stroke (p 299) Dyspepsia DIFFERENTIAL DIAGNOSIS NON GASTRIC CAUSES cardiac (myocardial infarc tion), pulmonary (pneumonia), hepatobiliary (biliary colic), pancreatic (pancreatitis), colonic (irritable bowel disease), musculoskeletal, dietary indiscretion PEPTIC ULCER DISEASE (PUD, 10 20%) H pylori, ASA, NSAIDs (COX inhibitors slightly decreased risk), cancer, Zollinger Ellison, smoking MEDICATION SIDE EFFECTS NSAIDs, ASA, theo phylline, calcium channel blockers, erythromycin, metronidazole, bisphosphonates, orlistat, acarbose, iron, potassium supplements GASTROESOPHAGEAL REFLUX DISEASE (GERD, 20%) HACIDSH Acid hypersecretion Zollinger Ellison disease Alcohol abuse Connective tissue disease scleroderma Infections of esophagus CMV, HSV, candidiasis Diabetic gastroparesis Drug therapy Smoking NON ULCER DYSPEPSIA (50%) cause unclear Diagnosis of exclusion (rule out organic cause and irritable bowel disease) PATHOPHYSIOLOGY COMPLICATIONS OF PUD perforation, hemor rhage, gastric outlet obstruction, pancreatitis PATHOPHYSIOLOGY (CONT’D) COMPLICATIONS OF GERD esophageal complica tions include esophagitis, esophageal ulcer, esopha geal stricture, and Barrett’s syndrome Extra esopha geal complications include asthma, aspiration, chronic cough, hoarseness, chronic laryngitis, and dental erosions CLINICAL FEATURES SYMPTOM DEFINITIONS DYSPEPSIA chronic or recurrent epigastric pain, often with regurgitation, heartburn, bloating, nau sea, and post prandial fullness (indigestion) HEARTBURN retrosternal burning sensation sec ondary to lower esophageal sphincter relaxation = more specific for GERD RATIONAL CLINICAL EXAMINATION SERIES: CAN THE CLINICAL HISTORY DISTINGUISH BETWEEN ORGANIC AND FUNCTIONAL DYSPEPSIA? Organic dyspepsia Diagnosis reached by the clinician or computer model Peptic ulcer disease Diagnosis reached by the clinician or computer model LR+ LR 1.6 0.46 2.2 0.45 114 Dyspepsia CLINICAL FEATURES (CONT’D) MANAGEMENT LR+ LR Esophagitis Diagnosis reached by the clinician 2.4 0.5 or computer model APPROACH ‘‘functional dyspepsia is defined as pain or discomfort centered in the epigas trium with a normal endoscopy Neither clinical impression nor computer models that incorpo rated patient demographics, risk factors, history items and symptoms adequately distinguished between organic and functional disease in patients referred for endoscopic evaluation of dyspepsia’’ JAMA 2006 295:13 PRACTICAL APPROACH TO DYSPEPSIA Consider non gastric causes of dyspepsia (car diac, pulmonary, hepatobiliary, colonic, musculos keletal, medications, and dietary indiscretion) and investigate those causes if likely Otherwise pro ceed to step 2 If age >50 or alarm symptoms HVery BADH (Vomiting, Bleed/anemia, Abdominal mass/ weight loss, Dysphagia), refer for gastroscopy to check for gastric cancer Otherwise proceed to step 3 If ASA or NSAIDs use, stop medications if possible If not, consider proton pump inhibitor/H2 blocker trial and proceed to step 4 If GERD predominant symptoms (heartburn, regurgitation), treat as GERD Otherwise, proceed to step 5 If H pylori urea breath test positive, treat with triple therapy Otherwise, proceed to step 6 If none of the above, diagnosis of non ulcer dyspepsia Canadian Dyspepsia Working Group Can J Gastroenterol 2005 19:5 INVESTIGATIONS BASIC CBCD, lytes, glucose, AST, ALT, ALP, bilirubin, lipase, Ca, albumin, fecal occult blood IMAGING upper GI series, U/S abd, CT abd SPECIAL LABS UREA BREATH TEST H PYLORI SEROLOGY 24-H ESOPHAGEAL PH MONITORING ENDOSCOPY WITH BIOPSY urease test, C&S for H pylori PROTON PUMP INHIBITOR TEST sens 78% for GERD PEPTIC ULCER DISEASE avoid NSAID use Anti secretory treatment (ranitidine 150 300 mg PO BID, omeprazole 20 40 mg PO daily, lansoprazole 15 30 mg PO daily, pantoprazole 40 mg PO BID) H pylori eradication (HCAOH: clarithromycin 500 mg PO BID, amoxicillin g PO BID, omeprazole 40 mg PO daily Â10 days; HCMOH (if penicillin allergy): clari thromycin 500 mg PO BID, metronidazole 250 mg PO QID, omeprazole 40 mg PO daily Â10 days; HBMTH (if macrolide allergy or failed first line): bismuth 30 mL PO QID, metronidazole 250 mg PO QID, tetracycline 500 mg PO QID Â2 weeks) GERD lifestyle changes (avoid coffee, alcohol, chocolate, high fat meals, acidic or spicy foods More frequent, smaller portions, weight loss, smoking cessation, elevate bed, loose garments) Antisecre tory treatment (proton pump inhibitors more effec tive than H2 blockers for esophagitis Use antacids as breakthrough) Nissen fundoplication NON ULCER DYSPEPSIA lifestyle changes (avoid alcohol, caffeine, tobacco) Antisecretory treatment (see above) H pylori eradication (may or may not relieve symptoms) Promotility agent (domperidone) Related Topics Esophageal Cancer (p 195) Gastric Cancer (p 197) Gastric Lymphoma (p 173) SPECIFIC ENTITIES GERD obesity, lower esophageal sphincter pres sure, decreased esophageal peristalsis, gastric acid hypersecretion, delayed gastric emptying, and overeating PATHOPHYSIOLOGY reflux of stomach contents, lead ing to a multitude of symptoms including heartburn, regurgitation, dysphagia, chest pain, complicated by esophagitis, esophageal stricture, Barrett’s esopha gus, and esophageal adenocarcinoma CLINICAL FEATURES esophageal (heartburn, regur gitation), extra esophageal (wheeze, cough, pneu monia, waterbrash, hoarseness, sore throat, glo bus, dental erosions) DIAGNOSIS clinical based on symptoms (!2/week) Endoscopy to look for complications and rule out other potential diagnoses NEJM 2008 359:16 NSAIDS INDUCED GASTROPATHY PATHOPHYSIOLOGY NSAIDs inhibit COX (nor mally protective effect through mucus secretion, CAUSES ... paraneoplastic, renal OBSTRUCTION stomach, small bowel, colon, functional, gastric volvulus POSTOP vagotomy, gastrectomy, fundoplication PEPTIC ULCER DISEASE esophagus, stomach, duodenum GASTROPARESIS... TREAT UNDERLYING CAUSE Related Topics Chemotherapy Induced Nausea and Vomiting (p 229) Nausea and Vomiting in the Palliative Setting (p 395) D Hui, Approach to Internal Medicine, DOI 10.1007/978 4419... step 3 If ASA or NSAIDs use, stop medications if possible If not, consider proton pump inhibitor/H2 blocker trial and proceed to step 4 If GERD predominant symptoms (heartburn, regurgitation),