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Practical Internal Medicine Don’t Throw Your Hands Up! Keep It All Down Managing the Vomiting Companion Animal Wendy Blount, DVM Nacogdoches, TX Housekeeping • Handouts other than PowerPoint slides are already in your notebook • You will get copies of the PowerPoint slides after each section •Course materials are also downloadable at http://wendyblount.com •Click on “Presentation Notes” •Click on the link for this seminar Housekeeping • Proceedings – TOC, Abbreviations, Evaluation – Put each PowerPoint handout behind the colored tab for that section and in front of the first blue subdivider – Then you will find client handouts, diagnostic and treatment aids, lab submission forms, etc. • CE certificates in your notebook – I will sign at the end of the seminar – Please bring your completed evaluation Housekeeping • • • • Breakfast, coffee and registration 7:30-8am Morning Session 8am-12noon Afternoon session 1:30-5pm We’ll break the last 10 minutes of every hour • Lunch break 12-12:30pm • Dry Lab 12:30-1:30pm – Small groups for the dry lab – Dry lab group assignments and schedule are in your Proceedings • PLEASE PARTICIPATE!! • But take private conversations out in the hall Practical Medicine Philosophy • As referral medicine becomes more advanced, it by default becomes more expensive • Growing gap between general practice and specialty practices • These seminars help us fill those gaps • Everything we talk about this weekend can be done in a rural mixed animal practice Practical Medicine Philosophy • Some are already doing these things – Feeding tubes, managing DKA, liver aspirates • Some will be ready to begin • Some will need some hand holding, at least at first – TexasVets – Yahoogroups – Moderator Rosemary Lindsey [email protected] • Some will be happy to be better referring vets Agenda Saturday – 8am-12noon, 12:30-5pm • Vomiting • Regurgitation • Dry Lab – Liver Aspiration Cytologies, Abaxis equipment • Elevated Liver Ezymes • Liver Failure • (Sign CE Certificates) Agenda Sunday – 8am-12noon, 12:30-5pm • Diarrhea • Pancreatitis • Dry Lab Time if needed • Managing Feeding Tubes • The Acute Abdomen • Sign CE Certificates Causes of Vomiting • Vomiting is the most common sign of gastric disease • But not all vomiting dogs have gastric disease • Not all dogs with gastric disease vomit Causes of Vomiting – GI Disease Distal Esophagus Stomach Small Intestine Large intestine Pancreas Liver & Biliary Tract Causes of Vomiting – ExtraGI Abdominal Dz – Acute or Chronic Obstruction/Irritation from outside GI Tract Foreign Substance in GI Lumen Neurologic Disease Systemic Disease Toxicity Environmental/Behavioral Causes of Vomiting That’s about a jillion causes How do you find the cause in a particular patient? Acute or Chronic? 2 weeks Mild, Moderate or Severe? -Treat mild disease empirically -Diagnose and Treat Severe Dz ASAP -Proceed after discussion with Mild-Mod chronic & Mod acute vomiting Compartmentalize, then DAMNIT-V Compartmentalization Is the vomiting from GI disease or secondary to something else? Is the dog relatively well and vomiting, or very sick and also vomiting? Are there other symptoms not attributed to the GI tract? Systemic Diagnostics for Systemic Disease Minimum database, imaging diagnostic surgery GI diagnostics GI Lab Tests, endoscopy diagnostic surgery DAMNIT- V D – Degenerative A – Anomalous M – Metabolic N – Neoplastic, Nutritional I – Infectious, Inflammatory, Immune Mediated, Idiopathic T – Toxic, Traumatic V - Vascular Distal Esophageal Disease chronic vomiting and regurgitation DAMNIT-V A – hiatal hernia N – neoplasia – leiomyoma/leiomyosarcoma I – GERD and distal esophagitis, Spirocerca lupi GERD – GastroEsophageal Reflux Disease Gastric Disease DAMNIT-V D - Degenerative – chronic » gastric hypomotility » gastric dysrhythmia stomach motility seems normal when the stomach is empty, but is incoordinated in response to solid food » Dysautonomia A – Anomalous - chronic pyloric outflow obstruction (mucosal or muscular) Gastric Disease DAMNIT-V N – Nutrition - acute » Eating spoiled food » Abrupt dietary change, when diet is uniform » Gastric foreign body/material » Eating too rapidly Nutrition - chronic » Dietary intolerance Gluten in Irish Setters » Food allergy Gastric Disease DAMNIT-V N – Nutrition - acute » Eating spoiled food » Abrupt dietary change, when diet is uniform » Gastric foreign body/material » Eating too rapidly Nutrition - chronic » Dietary intolerance Gluten in Irish Setters » Food allergy Gastric Disease DAMNIT-V N – Nutrition - acute » Eating spoiled food » Abrupt dietary change, when diet is uniform » Gastric foreign body/material » Eating too rapidly Buster Maze Bowl Nutrition - chronic » Dietary intolerance Gluten in Irish Setters » Food allergy Gastric Disease DAMNIT-V N – Nutrition - acute » Eating spoiled food » Abrupt dietary change, when diet is uniform » Gastric foreign body/material » Eating too rapidly Buster Maze Bowl Nutrition - chronic » Dietary intolerance Gluten in Irish Setters » Food allergy Gastric Disease DAMNIT-V N – Nutrition - acute » Eating spoiled food » Abrupt dietary change, when diet is uniform » Gastric foreign body/material » Eating too rapidly Kyjen “Hills” Slo-Bowl Nutrition - chronic » Dietary intolerance Gluten in Irish Setters » Food allergy Gastric Disease DAMNIT-V N – Nutrition - acute » Eating spoiled food » Abrupt dietary change, when diet is uniform » Gastric foreign body/material » Eating too rapidly Kyjen “Coral” Slo-Bowl Nutrition - chronic » Dietary intolerance Gluten in Irish Setters » Food allergy Gastric Disease DAMNIT-V N – Nutrition - acute » Eating spoiled food » Abrupt dietary change, when diet is uniform » Gastric foreign body/material » Eating too rapidly Kyjen “Drop” Slo-Bowl Nutrition - chronic » Dietary intolerance Gluten in Irish Setters » Food allergy Gastric Disease DAMNIT-V N – Nutrition - acute » Eating spoiled food » Abrupt dietary change, when diet is uniform » Gastric foreign body/material » Eating too rapidly Kyjen “Flower” Slo-Bowl Nutrition - chronic » Dietary intolerance Gluten in Irish Setters » Food allergy Gastric Disease DAMNIT-V N – Nutrition - acute » Eating spoiled food » Abrupt dietary change, when diet is uniform » Gastric foreign body/material » Eating too rapidly Nutrition - chronic » Dietary intolerance Gluten in Irish Setters » Food allergy Gastric Disease DAMNIT-V N – Nutrition - acute » Eating spoiled food » Abrupt dietary change, when diet is uniform » Gastric foreign body/material » Eating too rapidly Buster-Cubes Nutrition chronic » Dietary intolerance Gluten in Irish Setters » Food allergy Gastric Disease DAMNIT-V Green Bowl N – Nutrition - acute » Eating spoiled food » Abrupt dietary change, when diet is uniform » Gastric foreign body/material » Eating too rapidly Nutrition - chronic » Dietary intolerance Gluten in Irish Setters » Food allergy Gastric Disease DAMNIT-V N – Neoplasia – usually chronic Lymphoma (LSA) » most common gastric neoplasia in the cat » 2nd most common gastric neoplasia in the dog adenocarcinoma » most common gastric neoplasia in the dog » Most commonly in the pylorus Leiomyoma - GIST » Most commonly in the cardia » Usually asymptomatic unless pyloric outflow obstruction Schirrhous adenocarcinoma, Fibroma/FSA SCC, plasma cell tumor, MCT Gastric Polyp – symptomatic if pyloric obstruction Gastric Disease DAMNIT-V I – Infectious, Inflammatory – acute or chronic • Bacterial - Helicobacter gastritis - chronic • Fungal – phycomycosis, Histoplasma - chronic • Parasitic » Ascarids – puppies » Physaloptera spp – acute » Ollulanus spp » Giardia spp – acute or chronic » Neorickettsia spp (salmon poisoning) - acute • Chronic Gastritis superficial, atrophic, hypertrophic • Gastric Ulcer – acute or chronic Gastric Disease DAMNIT-V I – Idiopathic – chronic • • Chronic gastric dilatation » Anaerobic bacteria » aerophagia » Hypomotility • Acquired mucosal hypertrophy • Acquired muscularis hypertrophy Duodenogastric reflux (bilious vomiting) Immune Mediated – chronic • Inflammatory bowel disease Gastric Disease DAMNIT-V T – Toxic, Traumatic • Drugs – acute or chronic Antibiotics, NSAIDs, immunosuppressives, cardiac glycosides, anticholinergics, emetics • Toxins » caustic substances – usually acute pot pourri oil, cleaning supplies, fertilizers petroleum distillates, organophosphates, toxic plants » Heavy metals - chronic lead, zinc » Ethylene glycol - acute • Trauma – GDV, Diaphragmatic Hernia usually acute, but can be chronic Gastric Disease Helicobacter Gastritis • Associated with chronic gastritis, gastric and duodenal ulcers, gastric carcinoma, gastric LSA • Infection is often asymptomatic • Treatment – triple therapy x 14 days 1. antibiotic 1 – metronidazole 2. Antibiotic 2 – amoxicillin or oxytetracycline 3. Antacids – bismuth or proton pump blocker BTM – bismuth, tetracycline, metronidazole OAM – omeprazole, amoxicillin, metronidazole Small Intestine Bile in vomit indicates duodenogastric reflux DDx similar to gastric vomiting DAMNIT-V N – Neoplasia – acute or chronic • Strangulation by a pedunculated tumor causing volvulus (lipoma) • Intussusception of tumor • Obstruction by tumor or fungal mass I – Infectious, Inflammatory • • Antibiotic responsive diarrhea – chronic Hemorrhagic gastroenteritis (HGE) - acute Small Intestine DAMNIT-V I – Infectious – viral • Parvovirus • Coronavirus Canine distemper virus • I – Idiopathic • Reverse intestinal peristalsis T – Traumatic - acute • Mesenteric volvulus • Intussusception most commonly secondary to severe diarrhea Large Intestine Acute or chronic DAMNIT-V M – Metabolic - chronic • Hypothryoidism can predispose to megacolon I – Inflammatory • • • HGE – acute or relapsing Colitis – acute or chronic IBS - irritable bowel syndrome T– Traumatic • Constipation – acute or chronic Pancreas Acute Pancreatitis Chronic Pancreatitis Liver & Biliary Tract Vomiting more common when there is cholestasis Most icteric dogs vomit Why do dogs with non-icteric liver disease vomit? » Decreased gastric mucus, due to abnormal protein synthesis. » Decreased gastric epithelial cell renewal due to abnormal protein synthesis. » Decreased gastric blood flow, due to altered vasoactive factors. Liver & Biliary Tract DAMNIT-V • M – Metabolic - chronic Biliary sludging and/or mucocoele • Gall stone obstruction N – Neoplasia - chronic • Hepatic carcinoma • Biliary carcinoma • LSA Liver & Biliary Tract DAMNIT-V • I – Infectious – acute or chronic Acute or chronic bacterial cholangiohepatitis • Viral hepatitis – chronic • Heterobilharzia spp – chronic • Fungal hepatitis I – Inflammatory, Immune mediated – acute or chronic • Acute hepatic necrosis • Chronic active hepatitis T - Trauma – acute • Biliary tract rupture Abdominal Disease Peritonitis (ascitic exudate) and resulting ileus Abdominal pain Impingement on the biliary and/or GI tracts by mass DDx Peritonitis • Septic – perforated bowel or abscess, or localized infection • Bile – ruptured biliary tract • Uroabdomen – ruptured urinary tract • chyloabdomen • Generalized enteritis • Pancreatitis • Viral - FIP Abdominal Disease DDx Abdominal pain – acute abdomen • • Passing a kidney stone • pancreatitis • Biliary obstruction • GI obstruction Rapidly growing mass in an encapsulated organ (kidney, liver, spleen) • Abdominal abscess • Pyelonephritis • Splenic torsion • Cryptorchid testicular torsion Abdominal Disease DDx Impingement on the biliary and/or GI tracts by mass Neoplasia Cyst • Pancreatic cyst • Perirenal cyst • Choledochal cyst • Hepatic cyst Abscess Granuloma Abdominal Disease DDx Impingement on the biliary and/or GI tracts by mass DDx Granuloma I – Infectious - chronic • • L-form bacteria Ureaplasma, Mycoplasma spp • Mycobacterium spp • Bartonella spp • FIP • Many fungal infections Abdominal Disease DDx Impingement on the biliary and/or GI tracts by mass DDx Granuloma I – Inflammatory – necrosis or saponification of fat • • Pancreatitis • Pansteatitis Pancreatic adenocarcinoma • lymphangiectasia I - rarely immune mediated • • Idiopathic Post rabies vaccine steatitis Neurologic Limbic Epilepsy Seizure locus at the vomiting center Responds to anticonvulsants (don’t use bromide) Vestibular Disease Neoplasia Vomiting center or CRTZ Increased CSF pressure Many things that increase CSF Systemic Disease Why do dogs with systemic disease vomit? Chemical stimulation of the vomiting center & chemoreceptor trigger zone. Drugs that suppress this center work best Cerenia® Systemic Disease DAMNIT-V M- Metabolic (ileus) » Hypercalcemia » Acute hypocalcemia Eclampsia » Hypokalemia » hypomagnesemia » hypothyroidism » hypoadrenocorticism » Hyperadrenocorticism Systemic Disease DAMNIT-V M- Metabolic (toxic) » Uremia » Jaundice » Sepsis » Acidosis (lactate, ketones, necrosis, etc.) Metabolic (idiopathic) » Hyperthyroidism Metabolic (shock) Systemic Disease DAMNIT-V N – Neoplasia (paraneoplastic effects) • • High gastrin levels Gastrinoma MCT • Hypercalcemia Systemic inflammation I – Infectious (unknown mechanism) » Feline heartworm disease » Systemic fungal infection Systemic Disease DAMNIT-V T - Toxicity » Hypercalcemia Cholecalciferol rodenticide Eczema cream (calcipotriol – Dovonex®) toxicity » NSAIDs » corticosteroids » Acidosis – ethylene glycol Systemic Disease Why do dogs with renal failure vomit? Direct toxicity to the gastric mucosa my renal toxins Decreased renal metabolism of gastrin by the kidneys, leading to elevated gastrin levels, and increased HCl secretion in the stomach. Drugs that protect the GI tract and stop gastric acid secretion work best sucralfate Proton pump blockers >> H2 blockers Systemic Disease Why do dogs with NSAID toxicity vomit? Direct toxicity to the gastric mucosa Inhibition of gastroprotective prostaglandins » Piroxicam, ibuprofen and naproxen undergo more complete enterophepatic circulation, and thus have prolonged half life in the dog and cat. » COX2 selective are not as GI toxic as COX nonselective, but both can cause problems. Prostaglandin analogs work best misoprostol ( Cytotec® ) Systemic Disease Why do dogs with corticosteroid toxicity vomit? Decreased mucosal cell growth and mucus production Increased gastric acid secretion High doses required for acute toxicity Chronic toxicity when other risk factors present: NSAIDs, hypotension, bile acid reflux, spinal cord disease, liver disease, renal disease, Addison’s disease, mast cell tumor degranulation, gastrinoma. H2 blockers & sucralfate work best Environmental/Behavioral Motion sickness Heat Stroke Pain Fear Excitement Dozens of Causes of Vomiting Did that help us diagnose and treat our vomiting patients? Not a Lot! Dozens of Causes of Vomiting Did That Help? Not a Lot! Working Up the Vomiting Patient Empirical Treatment first if indicated Pattern Recognition Step Wise Work-Up Step 1 – Empirical Treatment 1. Cerenia PO SID x 1-4 days 2. Metronidazole 10-15 mg/kg PO BID x 7 days 250 mg tab – ¼ tab per 10 lbs 500 mg tab – ¼ tab per 20 lbs Max dose 500mg 3. Deworm pyrantel or Profender for cats fenbendazole for dogs Physaloptera spp. Always deworm vomiting animals Presentation: acute or chronic onset of profuse vomiting weight loss is usual Sometimes anorexic, sometimes not Diagnosis: Almost never see the eggs on fecal Deworming empirically prevents the need for diagnosis by endoscopy Physaloptera spp. Physaloptera spp. Physaloptera spp. Clues in the Signalment Deep chested breeds - GDV Poodles – hypoadrenocorticism Brachycephalic breeds - GERD, hiatal hernia, pyloric mucosal hypertrophy GSD – antibiotic responsive diarrhea Clues in the History If weight loss associated with increased appetite - diabetes, hyperthyroidism & IBD Most common clinic sign of gastric neoplasia – anorexia, then weight loss, then vomiting Step-Wise Plan for Diagnosing Vomiting 1. Minimum Database 2. Imaging, GI Lab, ACTH Stim – radiographs + contrast, US 3. Flexible Endoscopy 4. Surgery with biopsies 5. Fluoroscopy 6. Empirical Tx for limbic epilepsy & motility disorders Step-Wise Plan for Diagnosing Vomiting 1. Minimum Database • • • • • • • • CBC Profile Electrolytes/blood gases Urinalysis Fecal T4/free T4 for older cats HW Test for dogs Coagulation panel if hematemesis Clues in the MDB Polycythemia- HGE, neoplasia • Albumin normal with HGE, high with dehydration, globulins high with neoplasia Low albumin and globulin – protein losing enteropathy, GI blood loss • HCT normal with PLE, low with GI blood loss Low albumin, normal globulin – liver disease, protein losing nephropathy, vasculitis Clues in the MDB Azotemia • • High BUN with normal creat and phos - GI blood or high protein diet High BUN, high creat, high phos - Check urine specific gravity to confirm renal disease Liver Disease Pattern • • • • High liver enzymes High bili with normal PCV Low albumin, glucose Abnormal cholesterol, triglycerides Clues in the MDB Cat – icterus w/normal PCV and liver enzymes • • • Pancreatitis FIP Lymphoma Diagnostic Trifecta for FIP • • • • • • • Lymphopenia <1500/ul Titer 1:160 or greater Globulins >5.1 g/dl Positive predictive value 89% Negative predictive value 99% Histopath and fluid analysis supportive Fluid analysis chart – pancreatitis section Clues in the MDB Pancreatitis pattern • • • • • • • • • • • icterus hypocalcemia Acidosis Hyperglycemia Elevated fPL or cPL, TLI Elevated lipase lipemia Amylase not helpful if azotemic Abdominal pain Whacked out insulin response if diabetic Ketonuria if diabetic Clues in the MDB Ethylene glycol toxicity pattern • • • Period of ataxia at onset Increased anion gap Calcium oxalate crystals in the urine Neoplasia pattern • • • • • Really sick with pretty boring bloodwork Intermittent low grade fever Hypercalcemia Increased globulins Increased white count Clues in the MDB Addison’s Disease pattern • • • • • • • Signs wax and wane Hematemesis, hematochezia Azotemia with moderately concentrated urine (1.020’s) Hypoalbuminemia Hypercalcemia High potassium and/or low sodium Remember whipworms can cause hyperkalemia and hyponatremia, as can repeated abdominocentesis TAMU GI Lab Tests • • • • TLI/PLI – do you have significant pancreatic disease? B12/folate – do you have significant intestinal disease? Bile acids – do you have significant liver disease? Tritrichomonas PCR – chronic diarrhea in cats Gastrin • • • • Made by gastric mucosa, pancreas Eliminated by the kidneys Increased with MCT, CRF, chronic proton pump administration, gastrinoma Stimulates the gastric mucosa to make HCl Causes problems: • • • • GERD Distal esophagitis and regurgitation Ulcers in esophagus, stomach, duodenum Chronic gastritis, duodenitis When to do a barium study? • • • • • • • • NOT just prior to an abdominal US NOT just prior to a scope NOT if perforation is suspected If evidence of mural GI disease – to check for obstruction If you suspect a foreign body If you suspect a motility disorder Abdominal contents are malpositioned If you suspect a diaphragmatic hernia Barium study for vomiting Avoid drugs that inhibit GI motility • • • Opiates beta agonists (bronchodilators) Anticholintergics (atropine, aminopentamide) 1. Shoot scout films 2. Give barium – – 4-6 ml/lb small dogs and cats 2-4 ml/lb large dogs 3. Within 5 minutes for gastrogram 4. 30 minutes, and every hour until barium is gone from stomach Barium study for vomiting Thumb Rules • • • Barium should be in duodenum within 20 minutes Stomach should be empty within 3-4 hours Barium coated food can remain in the stomach for 12-15 hours When to recommend endoscopy? • • • • • No evidence of systemic disease outside the GI tract Not suspecting lymphoma, which is more often in the muscularis Low albumin – poor surgical risk Abnormal B12/folate indicate significant intestinal disease Owner wants low morbidity procedure Preparation for endoscopy • Withhold water the morning of scope Upper GI: • Withhold food and barium for 24 hours • Withhold food for 48 hours for lower GI Lower GI: • Withhold food and barium for 48 hours • Biscodyl 5 mg PO 24 hours before • Enemas 24, 12 and 1-2 hours before • Or use GoLytely When do you suspect a Motility Disorder? • • Minimum database and imaging NSAF Prolonged GI transit on contrast study without obstruction Regurgitation without an identifiable cause Other signs of peripheral neuropathy • • – – – • • Laryngeal paralysis Spinal or cranial nerve deficits (LMN) constipation Other signs of dysautonomia Presence of hypothyroidism, Cushing’s Disease, Addison’s Disease, Myasthenia Gravis, spinal cord disease, uremia, hypercalcemia, hypocalcemia, etc. Treating Motility Disorders • • • Prokinetics work best Metoclopramide works only on the stomach Cisapride may also work on the esophagus and colon, at least somewhat Erythromycin and ranitidine have prokinetic characteristics • – • • Erythromycin lower dose 0.25-0.5 mg/kg PO TID Reduced dietary fiber and fat speed gastric emptying Worsened by aminopentamide (Centrine®), opiates, beta agonists DDx Hematemesis • Blood swallowed • Blood coming from the erosive disease in the stomach • Blood coming from erosive disease in the duodenum and refluxed into the stomach • Trauma • Coagulopathy DDx Hematemesis Blood swallowed and then vomited and/or produces melena – Trauma or coagulopathy can result in bleeding from any of these areas 1. Respiratory tract » Neoplasia » Pulmonary thromboembolism 2. Caudal nasopharynx (rostral nasal cavity bleeding usually results in epistaxis) » Neoplasia » Fungal infection 3. Oral cavity » Dental disease » Neoplasia DDx Hematemesis Bleeding from the duodenum, refluxed into the stomach. –Ulcerative/erosive duodenal disease – see differentials for gastric ulcerative/erosive disease. –Parasites – Coccidia, hookworms. –See also Melena in the Diarrhea Section. DDx Hematemesis Causes of erosive gastritis » » » » » » » » » » » Liver failure. Kidney failure. Hypoadrenocorticism. Gastric neoplasia – see chronic vomiting. Pancreatic neoplasia – gastrinoma. Toxicity – NSAIDs, glucocorticoids, lead Toxicity – caustic substances » cleaning supplies » pot pourri oil Trauma to the gut. Shock – anaphylaxis, hypovolemia, septic, HGE. Anesthesia (hypovolemia). Spinal trauma. DDx Hematemisis Coagulopathy 1. Factor deficiency » Liver failure » Anti-vitamin K rodenticide toxicity » congenital 2. Platelet problem » Thrombocytopenia » Platelet function defect 3. Blood vessel problem – vasculitis, hypertension, hyperviscosity 4. Combination - DIC DDx Hematemisis Recurring Hematemisis and Hematochezia are special indications for ACTH Stim Even if electrolytes are normal Tx Hematemisis • • Treat underlying cause Continue proton pump or H2 blockers for 14 days after hematemesis resolves H2 Blockers • Cimetidine (Tagamet®) 2.5-5 mg/lb PO IM IV TID-QID. – Inhibits hepatic microsomal enzymes. – May increase half life of drugs that are metabolized in the liver – theophylline, warfarin, phenobarbital. – Can cause mental depression. • Ranitidine (Zantac®) 1 mg/lb PO SQ IM IV BIDTID – 5x as potent as cimetidine. – Also a prokinetic, by inhibiting acetylcholinesterase. – Inhibits hepatic microsomal enzymes as cimetidine, but to a lesser extent. H2 Blockers • Famotidine (Pepcid®) 0.25-0.5 mg/lb PO IV SIDBID. – Inhibits hepatic microsomal enzymes as cimetidine, but to a lesser extent. – 20x as potent as cimetidine. • Nizatidine (Axid®) 1.25-2.5 mg/lb PO SID. – 5x as potent as cimetidine. – Also a prokinetic. Proton Pump Blockers – More effective than H2 blockers for mast cell degranulation. – Stronger suppressors of gastric acid secretion than H2 blockers. – Diminishes proteolytic effect of pepsin. – Maximum effect at the 5th dose (may need to use with H2 blockers for the first 3-4 days). – Prolonged use (greater than 4 weeks) can cause reversible gastric mucosal hypertrophy. – Rebound hypersecretion of HCl can occur if stopped abruptly (high gastrin levels due to lack of feedback). Proton Pump Blockers – Omeprazole (Prilosec®) » 5 mg (1/2 capsule) PO SID, for dogs <11 lbs. » 10 mg PO SID, for dogs 11-45 lbs. » 20 mg PO SID, for dogs greater than 45 lbs. – Lansoprazole (Prevacid®) » 15 mg PO SID for small dogs » 30 mg PO SID for large dogs. – Esomeprazole (Nexium®) » 0.7 mg/kg PO SID for dogs. » Granules in capsule inactivated if sprinkled on food. – Pantoprazole (Protonix®) – 10-40 mg PO SID; 1 mg/kg IV SID. – Rabeprazole (Aciphex®) – 5-20 mg PO SID. Antiemetics Central Antiemetics • Phenothiazines - Act at both the CRTZ and the vomiting center. – Use only in well hydrated patients, without low blood pressure, as they are hypotensives. – Prochlorperazine (Compazine®) 0.25 mg/lb SQ IM TID – Chlorpromazine (Thorazine®) 0.15-0.25 mg/lb SQ TID. • Antihistamines - Act at the CRTZ – Diphenhydramine (Benadryl®) 05-2 mg/lb PO IM or SLOWLY IV. – Dimenhydrinate (Dramamine®) 2-4 mg/lb PO TID. – Meclizine (Antivert®) 12.5 mg PO SID for small dogs and cats; 25 mg PO SID for medium to large dogs. Antiemetics Central Antiemetics • Central Anticholinergics – Scopolamine (Hyoscine®) 0.02 mg/lb SQ IM QID. – Acts at vestibular center and CRTZ. – Side effects ileus, dry mouth, sedation. • Yohimbine (Yobine®) – Acts at the CRTZ and the vomiting center. – 0.15-0.25 mg/lb SQ IM BID. Antiemetics Peripheral Antiemetics • Cisapride (Propulsid®) – Antiemetic and prokinetic. – Acts peripherally on the GI tissue – does not cross the blood brain barrier, so no associated extrapyramidal side effects. – 0.05-0.25 mg/lb PO TID. • Anticholinergics – Aminopentamide (Centrine®) 0.1-0.4 mg IM SQ BIDTID. – Side effect – ileus (undesirable when there is ileus or motility disorder). Antiemetics Peripheral and Central Antiemetics*** • Metoclopramide (Reglan®) - Antidopaminergic and antihistaminic, acts at the CRTZ – – – – – Antiemetic as well as prokinetic 0.2-0.4 mg/kg PO, SQ, IV TID-QID. CRI – 0.5-1 mg/lb/day IV. Reduce dose by 50% in pets with renal failure Side effects hyperactivity and constipation (extrapyramidal signs) - more common in the cat – For severe metoclopramide side effects, give Benadryl. – Because serotonin receptors dominate in the feline CRTZ rather than dopamine, metoclopramide may not work as well as an antiemetic in cats, when compared to dogs. Antiemetics Peripheral and Central Antiemetics*** Block vagal afferent neurons, and act at the CRTZ NK antagonists – inhibit substance P – Maropitant (Cerenia®) 1 mg/kg SC SID, 2 mg/kg PO SID for acute vomiting, no more than 5 days in a row (skip 1-2 days) – 8 mg/kg PO 2 hours prior to travel for motion sickness, for no more than 2 days in a row (skip 3 days) 5HT antagonists – Ondansetron (Zofran®) 0.05-0.15 mg/lb PO or slowly IV SID-TID. – Dolasetron (Anzemet®) 0.4-0.6 mg IV SID-BID. – Side effects sedation and head shaking. Prokinetics – Reduce gastroesophageal reflux. – Help control vomiting by accelerating gastric emptying. – Improve coordination of antrum, pylorus and duodenum. – Increases propagation distance of peristaltic waves. – Contraindicated in cases with obstruction (can precipitate perforation). – Can usually wean prokinetics to the lowest effective dose. Cytoprotective Agents • Bind to the ulcer/erosion to create a physical protective barrier. • Inactivate pepsin. • Adsorb bile acids, which can be inflammatory. • Sucralfate (Carafate®) 0.5 g/15 lb PO BID-QID. • Barium sulfate 2-6 ml/lb PO (same as for upper GI series). • Side effect constipation. Mucosal Protective Agents • Increase mucosal mucus and bicarbonate production. • Decrease mucosal acid production. • Promote mucosal blood flow. • Indicated for NSAID gastritis. • Misoprostyl (Cytotec®) 1-2.5 ug/lb PO TID. • Side effects include: – Abdominal cramping. – Vomiting, diarrhea. – Abortion. Dysautonomia First cases in Scottish horses in the 19 century First reported in the cat in 1982, first dog in 1983 Degeneration of autonomic ganglia and failure of autonomic function History: • • Vomiting, regurgitation, diarrhea Anorexia weight loss, lethargy • Dyspnea, coughing • Photophobia • Dysphagia, dysphonia • dysuria • Onset over 1-2 weeks Dysautonomia Exam: • • Decreased anal tone • Absent PLR, moderate mydriasis • Third eyelid prolapse • Dry mucous membranes and eyes • Crusty nose, nasal discharge • Dyspnea, pulmonary crackles, fever • Cachexia, weakness Global LMN weakness and CP deficits on neuro exam • Large urinary bladder that is easy to express • Heart rate and blood pressure relatively low Dysautonomia Diagnosis: • Thoracic rads may show megaesophagus and/or aspiration pneumonia • Other neurologic deficits are absent • Ileus, bladder distension on abdominal imaging • Schirmer Tear Test less than 10mm OU • CBC, panel, CSF tap may be normal if no systemic complications Dysautonomia Diagnosis: Pilocarpine test • Place 1-2 drops 0.05% pilocarpine in one eye • Check PLR every 15 minutes for one hour • Normal dogs show minimal response If dysautonomia, miosis due to denervation hypersensitivity • Can be false negatives • • • Chronic OP toxicity can produce similar results Adding atropine will reverse the miosis in OP toxicity but not dysautonomia No tachycardia in response to atropine injection Dysautonomia Treatment: • Bethanechol 1.25-5 mg PO BID or 0.05 mg/kg SC BID • SC seems to work better • Can help with urination and secretion • Can gradually increase to effect Side effect – can increase vomiting and aspiration pneumonia • Pilocarpine eye drops Can assist tear production and photophobia Artificial tears OU PRN, Genteel, Soothe XP Elevated feedings, prokinetics, permanent Gtube Dysautonomia Prognosis: Grave Mortality 70-90% Those who survive have significant disability and progressively debilitate Dysautonomia Pathology: 50% have megaesophagus 20% have aspiration pneumonia Can diagnose with histopath on necropsy Widespread degeneration of the autonomic nerves and ganglia More than 50% are rural, outdoor dogs Exposure to Clostridium toxins and/or paraneoplastic disease may play a role in pathogenesis Handouts • • • .pdf of this PowerPoint – behind the red tab TAMU GI Lab Submission Form Client Drug Handouts – Fenbendazole – – – – Maropitant – Metoclopramide – Metronidazole Bisacodyl – Omeprazole Bismuth subsalicylate – Praziquantel Cimetidine – Pyrantel pamoate Cisapride – Ranitidine Erythromycin – Sucralfate Famotidine Amoxicillin Oral antacids Bethanechol – – – – – – Handouts • Client Handouts – – – Diaphragmatic hernia Endoscopy Hemorrhagic gastroenteritis