practical internal medicine don’t throw your hands up! keep it all down managing the vomiting...

Practical Internal Medicine

Don’t Throw Your Hands Up!

Keep It All DownManaging 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

rosemarylindsey@sbcglobal.net • Some will be happy to be better

referring vets

AgendaSaturday – 8am-12noon, 12:30-5pm• Vomiting• Regurgitation

• Dry Lab – Liver Aspiration Cytologies, Abaxis equipment

• Elevated Liver Ezymes• Liver Failure• (Sign CE Certificates)

AgendaSunday – 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 ChronicObstruction/Irritation from outside GI Tract

Foreign Substance in GI Lumen

Neurologic Disease

Systemic Disease

Toxicity

Environmental/Behavioral

Causes of VomitingThat’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

CompartmentalizationIs 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- VD – Degenerative

A – Anomalous

M – Metabolic

N – Neoplastic, Nutritional

I – Infectious, Inflammatory,

Immune Mediated, Idiopathic

T – Toxic, Traumatic

V - Vascular

Distal Esophageal Diseasechronic 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

Nutrition - chronic» Dietary intolerance

Gluten in Irish Setters» Food allergy

Buster Maze Bowl

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

Buster Maze Bowl

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

Kyjen “Hills” Slo-Bowl

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

Kyjen “Coral” Slo-Bowl

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

Kyjen “Drop” Slo-Bowl

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

Kyjen “Flower” Slo-Bowl

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

Buster Cubes

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

Green Bowl

Gastric DiseaseDAMNIT-V

N – Neoplasia – usually chronicLymphoma (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 DiseaseDAMNIT-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 DiseaseDAMNIT-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 DiseaseDAMNIT-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 DiseaseHelicobacter 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 IntestineBile 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 IntestineDAMNIT-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 IntestineAcute 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 TractVomiting 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 TractDAMNIT-V

M – Metabolic - chronic

• Biliary sludging and/or mucocoele• Gall stone obstruction

N – Neoplasia - chronic

• Hepatic carcinoma• Biliary carcinoma

• LSA

Liver & Biliary TractDAMNIT-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 DiseasePeritonitis (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 DiseaseDDx 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 DiseaseDDx Impingement on the biliary and/or GI tracts by mass

Neoplasia

Cyst• Pancreatic cyst• Perirenal cyst

• Choledochal cyst• Hepatic cyst

Abscess

Granuloma

Abdominal DiseaseDDx 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 DiseaseDDx 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

NeurologicLimbic 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 DiseaseDAMNIT-V

M- Metabolic (ileus)» Hypercalcemia

» Acute hypocalcemia

Eclampsia» Hypokalemia

» hypomagnesemia» hypothyroidism

» hypoadrenocorticism» Hyperadrenocorticism

Systemic Disease

DAMNIT-VM- Metabolic (toxic)

» Uremia» Jaundice» Sepsis

» Acidosis (lactate, ketones, necrosis, etc.)

Metabolic (idiopathic)» Hyperthyroidism

Metabolic (shock)

Systemic DiseaseDAMNIT-V

N – Neoplasia (paraneoplastic effects)• High gastrin levels

Gastrinoma

MCT• Hypercalcemia

• Systemic inflammation

I – Infectious (unknown mechanism)» Feline heartworm disease» Systemic fungal infection

Systemic DiseaseDAMNIT-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 non-selective, 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 days250 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 MDBPolycythemia- 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 MDBAzotemia• 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 MDBCat – 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 MDBPancreatitis 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 MDBEthylene 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 MDBAddison’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 vomitingAvoid drugs that inhibit GI motility• Opiates• beta agonists (bronchodilators)• Anticholintergics (atropine, aminopentamide)

1. Shoot scout films2. Give barium

– 4-6 ml/lb small dogs and cats– 2-4 ml/lb large dogs

3. Within 5 minutes for gastrogram4. 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 HematemesisBlood 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 HematemesisBleeding 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 HematemesisCauses 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

Coagulopathy1. 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 BID-TID

– 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 SID-

BID.– 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.

AntiemeticsCentral 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.

AntiemeticsCentral 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.

AntiemeticsPeripheral 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 BID-

TID.– Side effect – ileus (undesirable when there is ileus or

motility disorder).

AntiemeticsPeripheral 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.

AntiemeticsPeripheral 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.

DysautonomiaFirst 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

DysautonomiaExam:

• 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

DysautonomiaDiagnosis:

• 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

DysautonomiaDiagnosis:

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

DysautonomiaTreatment:

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

DysautonomiaPrognosis:

Grave

Mortality 70-90%

Those who survive have significant disability and progressively debilitate

DysautonomiaPathology:

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

– Amoxicillin– Oral antacids– Bethanechol

– Bisacodyl– Bismuth subsalicylate– Cimetidine– Cisapride– Erythromycin– Famotidine

– Fenbendazole– Maropitant– Metoclopramide– Metronidazole– Omeprazole

– Praziquantel– Pyrantel pamoate– Ranitidine– Sucralfate

Handouts• Client Handouts

– Diaphragmatic hernia– Endoscopy– Hemorrhagic gastroenteritis