Small Animal Internal Medicine - Darcy H. Shaw - E-Book

Small Animal Internal Medicine E-Book

Darcy H. Shaw

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Beschreibung

Review in concise, outline format for veterinary students preparing for National Boards. Includes exam-style review questions.

Das E-Book Small Animal Internal Medicine wird angeboten von John Wiley & Sons und wurde mit folgenden Begriffen kategorisiert:
Veterinärmedizin, Veterinärmedizin / Innere Medizin, Veterinary Internal Medicine, Veterinary Medicine

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Veröffentlichungsjahr: 2013

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Contents

Preface

Acknowledgements

PART I Clinical Problems

Chapter 1 Halitosis

Chapter 2 Dysphagia and Regurgitation

Chapter 3 Vomiting

Chapter 4 Diarrhea

Chapter 5 Melena and Hematochezia

Chapter 6 Tenesmus and Dyschezia

Chapter 7 Constipation and Obstipation

Chapter 8 Acute Abdominal Distress

Chapter 9 jaundice

Chapter 10 Abdominal Distention and Ascites

Chapter 11 Weight Loss

Chapter 12 Weight Gain

Chapter 13 Anorexia

Chapter 14 Polyuria and Polydipsia

Chapter 15 Polyphagia

Chapter 16 Fever and Hyperthermia

Chapter 17 Peripheral Edema

Chapter 18 Weakness

Chapter 19 Syncope

Chapter 20 Trembling and Shivering

Chapter 21 Ataxia, Paresis, and Paralysis

Chapter 22 Altered Consciousness

Chapter 23 Blindness and Anisocoria

Chapter 24 Seizures

Chapter 25 Head Tilt

Chapter 26 Pain

Chapter 27 Coughing

Chapter 28 Dyspnea and Tachypnea

Chapter 29 Hemoptysis and Epistaxis

Chapter 30 Cyanosis

Chapter 31 Pallor and Shock

Chapter 32 Dysuria

Chapter 33 Discolored Urine

Chapter 34 Urinary Retention

Chapter 35 Pruritus

Chapter 36 Alopecia

Chapter 37 Dermatologic Manifestations of Systemic Disease

Chapter 38 Ocular Manifestations of Systemic Disease

PART II Diseases of Organ Systems

Chapter 39 Cardiovascular Diseases

STUDY QUESTIONS

ANSWERS AND EXPLANATIONS

Chapter 40 Respiratory Diseases

STUDY QUESTIONS

ANSWERS AND EXPLANATIONS

Chapter 41 Gastrointestinal Diseases

STUDY QUESTIONS

ANSWERS AND EXPLATIONATIONS

Chapter 42 Hepatobiliary and Exocrine Pancreatic Diseases

STUDY QUESTIONS

ANSWERS AND EXPLANATIONS

Chapter 43 Urinary Tract Diseases and Fluid and Electrolyte Disorders

STUDY QUESTIONS

ANSWERS AND EXPLANATIONS

Chapter 44 Endocrine Diseases

STUDY QUESTIONS

ANSWERS AND EXPLANATIONS

Chapter 45 Reproductive Diseases

STUDY QUESTIONS

ANSWERS AND EXPLANATIONS

Chapter 46 Joint Diseases

STUDY QUESTIONS

ANSWERS AND EXPLANATIONS

Chapter 47 Neuromuscular Diseases

STUDY QUESTIONS

ANSWERS AND EXPLANATIONS

Chapter 48 Hematologic and Immunologic Diseases

STUDY QUESTIONS

ANSWERS AND EXPLANATIONS

Chapter 49 Infectious Diseases

STUDY QUESTIONS

ANSWERS AND EXPLANATIONS

Chapter 50 Oncologic Diseases

STYDY QUESTIONS

ANSWER AND EXPLANATIONS

PART III Comprehensive Exam

QUESTIONS

ANSWERS AND EXPLANATIONS

Appendix

Index

©2006 Blackwell Publishing

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Authorization to photocopy items for internal or personal use, or the internal or personal use of specific clients, is granted by Blackwell Publishing, provided that the base fee is paid directly to the Copyright Clearance Center, 222 Rosewood Drive, Danvers, MA 01923. For those organizations that have been granted a photocopy license by CCC, a separate system of payments has been arranged. The fee codes for users of the Transactional Reporting Service are ISBN-13: 978-0-6830-7670-7/2006.

First edition, 1997

Library of Congress Cataloging-in-Publication Data

Shaw, Darcy H.

Small animal internal medicine / Darcy H. Shaw, Sherri L. Ihle. — 1st ed.

p. cm — (The national veterinary medical series for independent study)

Includes index.

ISBN-13: 978-0-6830-7670-7

ISBN-10: 0-6830-7670-1

1. Dogs—Diseases. 2. Cats—Diseases. 3. Veterinary internal medicine. I. Ihle, Sherri L. II. Title. III. Series.

SF991.S53 1997

636.7’0896—dc21                     97-3958

The last digit is the print number: 9

Dedication

To Tao, Ted, Wally, Henry, and Norm, truly wonderful cats who have enriched my life immensely with their antics, eccentricities, and unconditional affection.

To all of my canine and feline patients who through my mistakes and successes have taught me so much about medicine and life.

To my past students who have kept me honest and enthused.

To my wife, Shelly Burton, who is my best friend and who makes it all worthwhile.

D. H. S.

Preface

The objectives of NVMS Small Animal Internal Medicine are to provide students with a concise, well-organized, and up-to-date overview of the discipline and to offer the opportunity to test comprehension of the material. In our effort to be concise and emphasize the key points regarding clinical signs, diagnosis, and treatment, information relating to pathophysiologic mechanisms and detailed treatment strategies is decidedly brief. Consequently, other text­books and scientific publications should be sought for this information.

The main audience for NVMS Small Animal Internal Medicine is third- and fourth-year veterinary students, but interns, residents, and private practitioners will also find the book useful. NVMS Small Animal Internal Medicine is organized into three general sections. The first section, Chapters 1 through 38, deals with clinical problems and their causes. The next section, Chapters 39 through 50, covers diseases associated with organ systems. A self-assess­ment section containing a 100-question multiple choice examination concludes the book.

We are confident that readers will find this a current, accurate, and complete overview of small animal internal medicine and will be challenged by the self-assessment activities. A companion volume, NVMS Small Animal Internal Medicine Case Management Test Booklet, is also available to readers who wish to practice working through cases similar to those encountered in clinical practice and on national board examinations.

Darcy H. Shaw

Sherri L. Ihle

Acknowledgments

The authors would like to thank Williams & Wilkins for providing us with the opportunity to write this book, and Melanie Cann, our development editor, for her patience, timely prod­ding, and editorial contributions. We would also like to thank Lisa Kiesel and Lynne Stockton for their editorial contributions.

PART I

CLINICAL PROBLEMS

Chapter 1

Halitosis

I. DEFINITION. Halitosis is offensive or foul-smelling breath.
II. CAUSES of halitosis are listed in Table 1-1.
A. In many cases, necrotic tissue, bacterial proliferation in retained food particles, or both are responsible for the odor.
B. Consumption of a foul-smelling substance can cause transient halitosis.
III. CLINICAL FINDINGS vary with the underlying disease.
A. Drooling may be seen with any of the oral or pharyngeal disorders listed in Table 1-1.
B. Oral pain may indicate periodontal disease, neoplasia, or inflammation.
C. Dysphagia in the presence of normal food prehension may indicate pharyngeal or esophageal disease.
IV. DIAGNOSTIC APPROACHES
A. History and physical examination, including a full oral examination, will usually narrow the list of differential diagnoses.
B. Viral serology or biopsy may be useful if oral ulceration or a mass is found.

TABLE 1-1. Causes of Halitosis

Oral disease
Dental tartar or periodontal disease
Neoplasia
Granuloma
Stomatitis or pharyngitis
Food retention
Esophageal disease
Neuromuscular disease with retention of food
Neoplasia
Granuloma
Miscellaneous causes
Gastritis (rare)
C. Complete blood count (CBC), serum biochemical profile, and urinalysis may help rule out systemic diseases that may cause oral lesions.
D. Observation of the animal eating, to assess food prehension and swallowing, may be helpful in the absence of dental tartar, oral ulceration, or oral masses (see Chapter 2).
V.TREATMENT is aimed at the primary disease.

Chapter 2

Dysphagia and Regurgitation

I. DEFINITION
A. Dysphagia is difficulty in prehending or swallowing food.
B. Regurgitation is the passive expulsion of undigested food from the esophagus.
II. CAUSES
A. Dysphagia. The causes of dysphagia are listed in Table 2-1.
B. Regurgitation. The causes of regurgitation are listed in Table 2-2.
III. CLINICAL FINDINGS
A. Dysphagia. A dysphagic animal may attempt to eat but is either unable to prehend the food, chew the food, or move the food to or beyond the pharyngeal region. The extent to which the animal is able to proceed with food consumption is determined by the site and type of disease. The clinical findings vary according to the underlying disorder.
1. Drooling may result from an inability or reluctance to swallow.
2. Pain
a. Oral pain may occur with oral or pharyngeal trauma or foreign bodies.
b. Oral pain accompanied by halitosis may occur with periodontitis, stomatitis or pharyngitis, neoplasia, or granuloma.
3. Neurologic abnormalities
a. A “dropped jaw” will be found with trigeminal nerve dysfunction.
b. Facial muscle pain or atrophy may occur with facial myositis.
c. The presence of other neurologic abnormalities (e.g., weakness, abnormal mentation, ataxia) suggests the presence of a central nervous system (CNS) disorder or a neuromuscular disease.
B. Regurgitation. Food prehension, mastication, tongue movement, and pharyngeal motility are usually normal, but esophageal structure or function is abnormal. The ejected material is often tubular in shape and alkaline.
IV. DIAGNOSTIC APPROACHES. If differentiation between dysphagia and regurgitation is not possible from the history, watching the animal eat and drink may be helpful.
A. Dysphagia (see Table 2-1). A thorough neurologic and oral examination should be performed on all dogs and cats with dysphagia.
1. If neurologic abnormalities are present, useful tests include a cerebrospinal fluid (CSF) tap, electrodiagnostic tests, and nerve or muscle biopsy.
2. If oral lesions are present, a biopsy or further dental evaluation may be needed.
3. If no abnormalities are found, then contrast radiographs with fluoroscopy may delineate a pharyngeal or upper esophageal sphincter problem.

TABLE 2-1. Causes of and Diagnostic Tests for Dysphagia

CauseDiagnostic TestNeuromuscular disease    Oral       MyositisSerum creatine kinase, electromyography, biopsy      Trigeminal nerve dysfunctionPhysical examination, biopsy      Neuromuscular trauma. . .   Pharyngeal       Cricopharyngeal achalasiaContrast radiographs with fluoroscopy      Myasthenia gravisAcetylcholine receptor antibody titer      MyositisSerum creatine kinase, electromyography, biopsy      RabiesHistopathologic studies      Idiopathic. . .Obstructive disease    TumorBiopsy   GranulomaBiopsy   Foreign bodiesOral examination, radiography   SialocoeleOral examinationInfectious and inflammatory disease    PeriodontitisOral examination   Stomatitis or pharyngitisOral examination, biopsy   Abscess (tooth root, retrobulbar)Oral examination, radiography   OsteomyelitisRadiography, biopsy, cultureMiscellaneous causes    Trauma (e.g., fracture, laceration, hematoma)Oral examination, radiography   Temporomandibular joint problemsPhysical examination, radiography

TABLE 2-2. Causes of Regurgitation

Esophageal obstruction
Foreign body
Granuloma
Periesophageal mass or fibrosis
Persistent right aortic arch (PRAA) and other vascular ring anomalies
Stricture
Megaesophagus
Idiopathic megaesophagus
Congenital
Acquired
Secondary megaesophagus
Miscellaneous causes
Esophagitis
Esophageal diverticulum
Esophageal fistula
Hiatal hernia
B. Regurgitation must be differentiated from vomiting (see Chapter 3). Diagnostic approaches to esophageal disease are discussed in Chapter 41 II A 4.
V. TREATMENT
A. Dysphagia. Treatment is aimed at the primary disorder. Parenteral fluid administration may be necessary.
B. Regurgitation. Treatment is aimed at the primary disorder. Retention of ingesta in the esophagus should be minimized by elevating the food and water supply and feeding the animal multiple small meals, consisting of a food of optimal consistency (the optimal consistency varies with the individual).

Chapter 3

Vomiting

I. DEFINITION
A. Vomiting is a reflex act characterized by forceful expulsion of gastric or small intestinal contents from the stomach, coordinated by the vomiting center in the medulla.
1. The vomiting center can be stimulated directly by drugs and toxins (endogenous and exogenous).
2. It can be triggered by afferent nerves from the viscera (especially the abdominal viscera), the chemoreceptor trigger zone, the vestibular apparatus, or the cerebrum.
B. Hematemesis is the vomiting of blood.
II. CAUSES of vomiting are summarized in Tables 3-1 through 3-4.
A. Vomiting soon after eating is most commonly due to overeating, dietary indiscretion, or gastritis.
B. Vomiting more than 8 hours after eating is more suggestive of gastric outflow obstruction or a motility disorder.
III. CLINICAL FINDINGS
A. Vomiting is usually preceded by nausea (evidenced by hypersalivation, frequent swallowing, and restlessness) and anxiety and is accompanied by repeated contractions of the diaphragm and abdomen. The ejected material may be digested or undigested and often contains bile.
B. Clinical findings that may accompany vomiting vary according to the cause of the vomiting (see Tables 3-1 through 3-4).

TABLE 3-1. Causes of Acute Vomiting without Systemic Signs of Illness

Cause

Common Concurrent Clinical Findings

Change in diet

Diarrhea

Dietary intolerance

Diarrhea

Dietary indiscretion

Diarrhea

Gastric foreign body

Abdominal discomfort

Motion sickness

Usually none

Medication

Variable, depending on the medication

Parasitic infection

Diarrhea

Psychogenic

Usually none

Early stage of a more chronic or serious disorder

Variable

TABLE 3-2. Causes of Acute Vomiting with Systemic Signs of Illness

Cause

Possible Concurrent Clinical Findings

Extra-gastrointestinal disorders

 

   Central nervous system (CNS) disease

Abnormal mentation, neurologic deficits

   Diabetic ketoacidosis

Polyuria, polydipsia, anorexia, depression, dehydration, weight loss, polyphagia

   Hepatic disease

Anorexia, diarrhea, icterus, ascites, neurologic abnormalities

   Hypercalcemia

Weakness, anorexia, polyuria, polydipsia

   Hypoadrenocorticism

Anorexia, diarrhea, dehydration, weakness, bradycardia

   Hypocalcemia

Anorexia, muscle twitches, tetany

   Hypokalemia

Weakness, polyuria

   Pancreatitis

Anorexia, cranial abdominal discomfort, fever, dehydration, diarrhea, icterus

   Peritonitis

Anorexia, depression, dehydration, abdominal pain, shock

   Prostatitis

Anorexia, fever, hematuria, palpable prostatomegaly, prostatic pain

   Pyometra

Anorexia, polyuria, polydipsia, vaginal discharge, depression, fever

   Renal disease

Anorexia, depression, weight loss, polyuria or oliguria

   Sepsis

Anorexia, fever, depression, dehydration

   Urinary obstruction

Anorexia, abdominal discomfort

   Vestibular disease

Head tilt, nystagmus

Primary gastrointestinal disorders

 

   Gastric dilatation

Anorexia, cranial abdominal distention

   Gastric dilatation/volvulus (GDV)

Cranial abdominal distention, nonproductive retching, shock

   Gastritis or enteritis

Anorexia, diarrhea, dehydration

   Hemorrhagic gastroenteritis (HGE)

Hematemesis, hemorrhagic diarrhea, dehydration

   Intestinal volvulus

Abdominal pain, shock

   Neoplasia

Variable, depending on the type and site of neoplasia

   Obstipation

Anorexia; dehydration; palpable, distended, firm colon

   Obstruction (gastric or intestinal)

Diarrhea, abdominal discomfort, dehydration, shock

   Parasitic infection

Diarrhea

   Ulcers

Hematemesis, melena, abdominal discomfort, pale mucous membranes

   Viral infection

Diarrhea, fever

   Early stage of a more chronic disorder

Variable

Miscellaneous causes

 

   Diaphragmatic hernia

Anorexia, respiratory distress, history of trauma

   Hyperthermia

Hyperthermia, depression, shock

   Medications

Variable, depending on the medication

   Toxins

Variable, depending on the toxin

TABLE 3-3. Causes of Chronic or Intermittent Vomiting

Cause

Possible Concurrent Clinical Findings

Extra-gastrointestinal disorders

 

   Diabetes mellitus

Polyuria, polydipsia, weight loss, polyphagia

   Heartworm disease (cats)

Anorexia, coughing, dyspnea

   Hepatic disease

Anorexia, diarrhea, icterus, ascites

   Hyperthyroidism (cats)

Polyuria, polydipsia, polyphagia, weight loss, diarrhea, hyperactivity, palpable cervical mass

   Hypoadrenocorticism

Anorexia, diarrhea, weight loss, weakness, bradycardia

   Hypocalcemia

Anorexia, muscle twitching, tetany

   Pancreatitis

Anorexia, cranial abdominal discomfort, fever, diarrhea

   Renal disease

Anorexia, depression, polyuria and polydipsia or oliguria, weight loss

Primary gastrointestinal disorders

 

   Colitis

Large bowel diarrhea

   Chronic inflammatory gastritis

Anorexia, weight loss, diarrhea

   Enterogastric reflux (bilious vomiting syndrome)

Usually none

   Fungal infection

Anorexia, fever, diarrhea, lymphadenopathy, other organ involvement

   Idiopathic gastric hypomotility

Anorexia

   Inflammatory bowel disease

Anorexia, diarrhea, weight loss

   Irritable bowel syndrome

Diarrhea

   Neoplasia

Variable, depending on the type and site of neoplasia

   Obstruction

 

      Gastric antral mucosal hypertrophy

Usually none

      Pyloric stenosis

Usually none

      Upper intestinal (partial)

Diarrhea, anorexia, weight loss

   Parasitic infection

Diarrhea

   Ulcers (usually secondary to another disorder)

Anorexia, hematemesis, melena, abdominal discomfort, pale mucous membranes, other signs specific to the underlying disease

Miscellaneous causes

 

   Diaphragmatic hernia

Anorexia, history of trauma

   Abdominal neoplasia

Variable, depending on the type and site of neoplasia

TABLE 3-4. Causes of Hematemesis

Cause

Possible Concurrent Clinical Findings

Gastrointestinal disorders

 

   Gastritis or enteritis

Anorexia, diarrhea, dehydration

   Hemorrhagic gastroenteritis (HGE)

Depression, hemorrhagic diarrhea, dehydration

   Neoplasia

Variable, depending on the type and site of neoplasia

   Ulcers (usually secondary to another disorder)

Anorexia, melena, abdominal discomfort, pale mucous membranes, other signs specific to the underlying disorder

Other causes

 

   Coagulopathy

Petechiae, ecchymoses, other types of hemorrhage

   Swallowed blood from hemoptysis

Cough, hemoptysis, tachypnea

   Swallowed blood from Oral hemorrhage

Oral lesions

IV. DIAGNOSTIC APPROACHES
A. Acute vomiting without systemic signs of illness
1. The diagnosis is often one of exclusion based on the history and the physical examination. A lack of response to conservative medical therapy indicates a need for additional testing.
2. Ascariasis is detected by fecal examination or response to treatment with pyrantel pamoate.
B. Acute vomiting with systemic signs of illness or chronic intermittent vomiting
1. Complete blood count (CBC)
a. Leukocytosis may be seen with pancreatitis, peritonitis, pyometra, sepsis, or severe gastrointestinal (GI) inflammation.
b. An increased hematocrit but normal serum protein concentration in a dog with hematemesis and bloody diarrhea is highly suggestive of hemorrhagic gastroenteritis (HGE).
c. Nonregenerative anemia may be seen with chronic disease, peracute or chronic blood loss, or malnutrition.
d. Regenerative anemia may be seen with subacute gastric hemorrhage.
e. Eosinophilia may be seen with some parasitic infections, eosinophilic gastroenteritis, or hypoadrenocorticism.
2. Serum biochemical profile
a. Hypochloremic metabolic alkalosis suggests loss of gastric acid because of gastric or upper duodenal vomiting.
b. Hyper- or hypocalcemia may be the cause of the vomiting.
c. Hypoproteinemia may result from blood loss, severe inflammation, or hepatic failure (hypoalbuminemia).
d. Hyperglycemia is consistent with diabetes mellitus if concurrent glucosuria is present.
e. Increased serum hepatic enzyme concentrations may be seen with hepatic disease.
f. Hypoalbuminemia may be seen with hepatic failure, severe inflammatory disease, or severe GI hemorrhage.
g. Hypoglycemia may be seen with hypoadrenocorticism, pancreatitis, hepatic failure, and sepsis.
h. Hyperkalemia, hyponatremia, and hypochloremia may be seen with hypoadrenocorticism.
i. Increased serum amylase and lipase concentrations are suggestive of pancreatitis.
j. Azotemia with concurrent isosthenuria is most consistent with renal failure but can also be seen with acute hypoadrenocorticism.
k. Hyperbilirubinemia may be seen with hepatic disease or biliary obstruction caused by pancreatitis.
3. Urinalysis
a. Glucosuria is consistent with diabetes mellitus if hyperglycemia is also present. Concurrent ketonuria suggests diabetic ketoacidosis.
b. Isosthenuria may be seen with diabetes mellitus, hepatic failure, hypercalcemia, hypoadrenocorticism, hypokalemia, pyometra, and renal failure.
4. Fecal flotation may reveal parasitic infection.
5. Radiology
a. Survey radiographs
(1) Hepatomegaly or microhepatica may be seen with hepatic disease.
(2) Loss of cranial abdominal detail may be seen with pancreatitis.
(3) A generalized loss of abdominal detail may be seen with ascites (e.g., hepatic failure) or peritonitis.
(4) A large, fluid-filled tubular structure (i.e., an enlarged uterus) may be seen in the caudal abdomen with pyometra.
(5) Renomegaly or small kidneys may be seen with renal disease.
(6) Radiographic findings suggestive of gastric disease are discussed in Chapter 41 III A 5 a (1).
(7) A mass, lymphadenopathy, or other organomegaly may also be diagnostic.
b. Contrast radiographs (with fluoroscopy if possible) may be helpful [see Chapter 41 III A 5 a (2)].
6. An adrenocorticotrophic hormone (ACTH) stimulation test is indicated if the history, clinical findings, or laboratory results suggest hyperadrenocorticism.
7. Serum bile acid concentrations should be assessed if the history, clinical findings, or laboratory results suggest hepatic failure.
8. Ultrasound
a. A gastric foreign body, mass lesion, or gastric wall thickening may be visible.
b. Ultrasound can better assess any mass or change in organ size seen on survey radiographs.
9. Endoscopic evaluation (see Chapter 41 III A 5 c) may help with the diagnosis.
10. Exploratory laparotomy
a. Full-thickness gastrointestinal biopsies and biopsies of multiple organs can be obtained.
b. Surgery may be diagnostic as well as therapeutic in some situations (e.g., foreign bodies, neoplasms, obstructive lesions, peritonitis).
C. Hematemesis is usually an indication for a diagnostic evaluation.
1. History. The owner should be questioned about any current medications or the presence of a cough.
2. Physical examination
a. The mouth and nose should be examined for hemorrhage.
b. The skin should be evaluated for any masses (i.e., possible mast cell tumors).
3. Laboratory tests can be assessed to rule out extra-GI causes of GI ulceration or hemorrhage (see Chapter 41 III B 4) if no abnormalities are found on physical examination. Useful tests include the following:
a. CBC
b. Serum biochemical profile
c. Urinalysis
d. Clotting tests [i.e., activated clotting time or prothrombin time (PT) and partial thromboplastin time (PTT)]
4. Upper GI endoscopy should be performed if laboratory test results are within normal limits. Endoscopy may be used to look for erosions or ulcers and to obtain biopsies for histopathology.
V. TREATMENT
A. Acute vomiting without systemic signs of illness. Food and water should be withheld for at least 12 hours to rest the GI tract, progressing to small amounts of water for 12–24 hours and later small meals of a bland, low-fat diet (e.g., cottage cheese or boiled meat mixed with rice or potatoes).
B. Acute vomiting with systemic signs of illness
1. The primary disorder should be treated.
2. Food and water should be withheld for at least 12–24 hours to rest the GI tract. Parenteral fluids are often needed during this time to correct or prevent dehydration and to correct electrolyte imbalances.
3. Antiemetics (e.g., chlorpromazine, prochlorperazine, metoclopramide) can be considered if vomiting is excessive; however, it should be remembered that these agents do not resolve the main problem. Metoclopramide is contraindicated in the presence of an obstruction. Phenothiazines are contraindicated in animals with severe seizure disorders.
C. Chronic intermittent vomiting
1. The primary disorder should be treated.
2. Parenteral fluid administration is not often needed but should be instituted if dehydration or electrolyte imbalances are present.
D. Hematemesis
1. Food and water should be withheld and parenteral fluid administered to correct and maintain hydration and to correct any electrolyte imbalances.
2. A transfusion may also be needed if the hemorrhage is severe.
3. Because gastrointestinal ulceration is the most common cause of hematemesis, treatment with sucralfate and a histamine-2 (H2) antagonist may be instituted while awaiting the results of diagnostic tests.

Chapter 4

Diarrhea

I. DEFINITIONS
A. Diarrhea is excess water in the feces.
1. Secretory diarrhea results from increased intestinal secretion of fluid.
2. Osmotic diarrhea results from increased luminal osmotic pressure and subsequent water retention.
3. Exudative diarrhea results from exudation of fluid and cells because of increased permeability.
B. Steatorrhea is excess fat in the feces.
II. CLINICAL SYNDROMES THAT MAY BE ASSOCIATED WITH DIARRHEA
A. Malassimilation is a syndrome, not a disease, that can result from maldigestion, malabsorption, or a combination of these two.
1. Maldigestion can result from digestive enzyme deficiency, bile acid deficiency, conditions that alter the activity of enzymes or bile acids, primary small intestinal disorders, bacterial overgrowth, and pancreatic duct obstruction. Exocrine pancreatic insufficiency (EPI), discussed in Chapter 42 II B 4, is the most common cause of maldigestion in dogs; bile acid deficiency is very rare. Diarrhea, weight loss, and sometimes steatorrhea are seen.
2. Malabsorption involves loss of mucosal cells (e.g., villous atrophy), problems with movement of absorbed nutrients from mucosal cells to capillaries and lymphatics (e.g., lymphocytic–plasmacytic enteritis) or problems with intestinal circulation because of venous or lymphatic obstruction (e.g., lymphangiectasia). Fat malabsorption may occur first because multiple steps are involved in fat digestion and a large portion of the intestine is needed for normal absorption. Protein and carbohydrate malabsorption occur with more severe generalized small intestinal disease. Diarrhea and weight loss are common.
B. Protein-losing enteropathy (PLE) is a syndrome, not a specific disease, caused by obstruction, infection, toxins, inflammation, and neoplasia. Inflammatory bowel disease, lymphosarcoma, and lymphangiectasia are the most common causes. Both albumin and globulins are lost (panhypoproteinemia), in contrast to the solitary hypoalbuminemia seen with protein-losing nephropathy and hepatic failure.
III. CAUSES of diarrhea are summarized in Tables 4-1 through 4-4.
IV. CLINICAL FINDINGS vary with the underlying disorder (see Tables 4-1 through 4-4). The typical clinical findings associated with small bowel diarrhea are differentiated from those of large bowel diarrhea in Table 4-5.

TABLE 4-1. Causes of Acute Diarrhea without Systemic Signs of Illness

Cause

Possible Concurrent Clinical Findings

Change in diet

Vomiting

Dietary intolerance

Vomiting

Dietary indiscretion

Vomiting

Parasitic infection

Vomiting

Early stage of a more chronic or serious disorder

Variable

TABLE 4-2. Causes of Acute Small Bowel Diarrhea with Systemic Signs of Illness

Cause

Possible Concurrent Clinical Findings

Extra-gastrointestinal disorders

 

   Hepatic disease

Anorexia, vomiting, icterus, ascites

   Hyperthyroidism (primarily cats)

Polyphagia, polyuria, polydipsia, weight loss, tachycardia, palpable cervical mass

   Hypoadrenocorticism

Anorexia, vomiting, weakness, bradycardia

   Pancreatitis

Anorexia, vomiting, fever, cranial abdominal discomfort

   Renal disease

Anorexia, vomiting, polyuria or oliguria, weight loss

   Right-sided heart failure

Anorexia, vomiting, ascites, pleural effusion

Primary gastrointestinal disorders

 

   Dietary indiscretion

Vomiting

   Hemorrhagic gastroenteritis (HGE)

Anorexia, hematemesis, depression, shock

   Infection

 

      Bacterial

Anorexia, vomiting, fever, depression

      Fungal

Anorexia, vomiting, fever, depression, lymphadenopathy, other organ involvement

      Rickettsial

Anorexia, vomiting, diarrhea, fever, lymphadenopathy, petechiae, lameness

      Viral

Anorexia, vomiting, depression

   Inflammatory bowel disease

Anorexia, vomiting, weight loss

   Irritable bowel syndrome

Vomiting

   Neoplasia

Variable, depending on the type and site of neoplasia

   Obstruction

 

      Foreign body

Anorexia, vomiting, intestinal "mass," or bunched intestines, abdominal pain, shock

      Intussusception

Anorexia, vomiting, tubular abdominal "mass," abdominal pain, shock

   Parasitic infection

Vomiting, weight loss

   Ulcers (duodenal)

Anorexia, vomiting, abdominal discomfort, other signs specific to the underlying cause

Other causes

 

   Toxins

Variable, depending on the toxin

TABLE 4-3. Causes of Chronic or Intermittent Small Bowel Diarrhea

Cause

Possible Concurrent Clinical Findings

Extra-gastrointestinal disorders

 

   Exocrine pancreatic insufficiency (EPI)

Weight loss, steatorrhea, polyphagia

   Hepatic disease

Anorexia, vomiting, icterus (less common), ascites

   Hyperthyroidism (primarily cats)

Polyphagia, polyuria, polydipsia, weight loss, tachycardia, palpable cervical mass

   Hypoadrenocorticism

Anorexia, vomiting, weakness, bradycardia

   Pancreatitis (chronic)

Anorexia, vomiting, cranial abdominal discomfort

   Renal disease

Anorexia, vomiting, weight loss, polyuria, polydipsia

Primary gastrointestinal disorders

 

   Dietary intolerance

Vomiting

   Infection

 

      Bacterial

Anorexia, fever

      Fungal

Anorexia, fever, lymphadenopathy, other organ involvement

      Viral (cats)

Anorexia, fever, pale mucous membranes, depression, weight loss

   Inflammatory bowel disease

Anorexia, vomiting, weight loss

   Irritable bowel syndrome

Vomiting

   Lymphangiectasia

Anorexia, vomiting, weight loss, abdominal fluid

   Neoplasia

Variable, depending on the type and site of neoplasia

   Obstruction

 

      Partial mechanical obstruction

Anorexia, vomiting, weight loss

      Physiologic obstruction

Variable, depending on the underlying cause

   Parasitic infection

Vomiting, weight loss

   Small intestinal bacterial overgrowth

Anorexia, vomiting, weight loss

   Villous atrophy

Anorexia or polyphagia, weight loss

TABLE 4-4. Causes of Chronic or Intermittent Large Bowel Diarrhea

Dietary intolerance
Infection
Algal
Bacterial
Fungal
Parasitic
Viral (cats)
Inflammatory colitis
Neoplasia
Obstruction
Cecocolic intussusception or cecal inversion
Foreign body
Stricture
Stress colitis or irritable colon

TABLE 4-5. Comparison of Clinical Findings in Small Bowel Diarrhea and Large Bowel Diarrhea

Small Bowel

Large Bowel

Volume

Usually increased

Usually decreased because of increased frequency

Frequency of defecation

Normal or slightly increased

Increased

Steatorrhea

May be present

Absent

Mucus

Rare

Usually present

Melena

May be present

Absent

Frank blood

Rare

May be present

Tenesmus

Absent

Usually present

Weight loss

May be present

Rare

Vomiting

May be present

May be present

Appetite

Usually normal or decreased

Usually normal

Borborygmus

May be present

Absent

V. DIAGNOSTIC APPROACHES. The diagnostic approach varies depending on the severity and chronicity of the problem and whether the diarrhea is large bowel or small bowel in origin.
A.Acute diarrhea without systemic signs of illness
1. The diagnosis is often a diagnosis of exclusion based on the history and physical examination. Lack of response to conservative medical therapy indicates a need for additional testing.
2. Parasitic infection may be diagnosed by a fecal flotation, direct fecal examination, or by response to treatment with fenbendazole.
B.Acute small bowel diarrhea with systemic signs of illness or chronic or intermittent small bowel diarrhea
1. Complete blood count (CBC)
a. An increased hematocrit with normal serum total solids will occur with hemorrhagic gastroenteritis (HGE).
b. Lymphopenia may occur with stress or lymphangiectasia.
c. Leukopenia may be seen with parvoviral infection or sepsis.
d. Leukocytosis may be seen with severe intestinal inflammation or perforation.
e. Nonregenerative anemia can be seen with peracute or chronic hemorrhagic diarrhea, chronic disease, or malnutrition.
f. Regenerative anemia can be seen with subacute intestinal hemorrhage caused by ulceration, inflammation, or neoplasia.
g. Eosinophilia can be seen with some parasitic and fungal infections and eosinophilic enteritis.
2. Serum biochemical profile
a. Electrolyte abnormalities, especially hypokalemia, hyponatremia, and hypochloremia, may be seen with many disorders involving diarrhea.
b. Hyperkalemia with concurrent hyponatremia and hypochloremia is suggestive of hypoadrenocorticism but can also occur with renal disease and primary gastrointestinal disorders.
c. Panhypoproteinemia is typically seen in patients with PLE or severe blood loss, although globulin concentrations may be normal or increased if concurrent inflammation is seen.
d. Hypoalbuminemia alone may be seen with hepatic failure.
e. Increased serum hepatic enzyme concentrations may be seen with hepatic disease or hepatic congestion secondary to right-sided heart failure.
f. Increased serum amylase and lipase concentrations are suggestive of pancreatitis.
g. Azotemia with concurrent isosthenuria is most consistent with renal failure but can also be seen with acute hypoadrenocorticism.
h. Hypercalcemia is commonly associated with lymphosarcoma.
i. Hypoglycemia may occur with hypoadrenocorticism, pancreatitis, sepsis, hepatic failure, or as a result of inadequate food intake or malassimilation in young animals.
j. Hyperbilirubinemia may be seen with hepatic disease or biliary obstruction due to pancreatitis.
3. Urinalysis is needed to rule out proteinuria as a cause of hypoproteinemia or hypoalbuminemia. Isosthenuria may be seen with renal disease, hepatic failure, hypoadrenocorticism, and hyperthyroidism.
4. Fecal examination [see Chapter 41 IV A 5 a (4)] may be of value.
5. Radiology
a. Survey radiographs
(1) Hepatomegaly or microhepatica may be seen with hepatic disease.
(2) Loss of cranial abdominal detail may be seen with pancreatitis.
(3) A generalized loss of abdominal detail may be seen with ascites (e.g., as a result of hepatic failure or severe hypoproteinemia), peritonitis, or cachexia.
(4) Renomegaly or small kidneys may be seen with renal disease.
(5) Cardiomegaly or pleural effusion may be seen with right-sided heart failure.
(6) Radiographic findings suggestive of small intestinal disease are discussed in Chapter 41 IV A 5 b (1).
(7) Finding a mass, lymphadenopathy, or other type of organomegaly may also help lead to the diagnosis.
b. Contrast radiographs may be helpful [see Chapter 41 IV A 5 b (2)].
6. An adrenocorticotropic (ACTH) stimulation test should be run if the history, clinical findings, or laboratory results suggest hyperadrenocorticism.
7. Serum bile concentrations should be assessed if hepatic failure is suspected.
8. Serum thyroxine concentration should be assessed for all middle-aged to older cats with small bowel diarrhea and systemic signs of illness.
9. Serologies for feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) should be considered in cats with chronic diarrhea.
10. Tests for malassimilation are discussed in Chapter 41 IV A 5 a (5).
11. Ultrasound. Ultrasonographic findings suggestive of small intestinal disease are discussed in Chapter 41 IV A 5 c. In addition, ultrasound can better assess any mass or change in organ size (e.g., liver or kidneys) seen on survey radiographs. Ultrasound may also be useful if abdominal fluid obscures radiographic detail. Other relevant findings include:
a. Pancreatic enlargement or a small amount of cranial abdominal fluid, which may indicate pancreatitis
b. Pericardial fluid or right-sided heart enlargement, which may suggest heart failure
12. Endoscopic evaluation (see Chapter 41 IV A 5 d) may help with the diagnosis.
13. Exploratory laparotomy
a. Full-thickness gastrointestinal biopsies and biopsies of multiple organs can be obtained.
b. Surgery may be diagnostic as well as therapeutic if the diarrhea is caused by foreign bodies, neoplasms, obstructive lesions, or peritonitis.
C. Chronic or intermittent large bowel diarrhea
1. CBC
a. Leukocytosis may be seen with inflammation or infection.
b. Nonregenerative anemia can be seen with chronic hemorrhage or chronic disease.
c. Eosinophilia can be seen with some parasitic and fungal infections and with eosinophilic colitis.
2. Multiple fecal examinations for parasites should be performed. Deworming with fenbendazole should also be considered before pursuing more costly or invasive diagnostic tests.
3. A rectal scraping for cytologic evaluation may reveal inflammatory cells, bacterial pathogens, or Histoplasma organisms.
4. A serum biochemical profile and urinalysis are usually unremarkable in dogs or cats with large bowel diarrhea.
5. Radiology
a. Survey radiographs are usually unremarkable in dogs or cats with large bowel diarrhea but may reveal a radiodense foreign body or regional lymphadenopathy.
b. Contrast radiographs. A barium enema may be considered if flexible colonoscopy is not feasible. A barium enema study can localize lesions of the transverse or ascending colon but does not allow definitive diagnosis; a biopsy is still required.
6. Proctoscopy may allow visualization of intraluminal masses (i.e., neoplasia or granuloma), erosions or ulcers (i.e., inflammation or neoplasia), hyperemia or an irregular mucosa (i.e., inflammation or neoplasia), a foreign body, parasites, stricture, or polyps of the descending colon. In some inflammatory conditions and submucosal diseases, the mucosa may appear grossly normal; therefore, multiple biopsies should be taken even if the mucosa is grossly normal.
7. Flexible colonoscopy allows visualization of the entire colon and should be considered if previous diagnostic tests do not yield a diagnosis.
VI. TREATMENT
A. Acute diarrhea without systemic signs of illness
1. Food should be withheld for at least 12–48 hours to rest the gastrointestinal (Gl) tract. Water can be given ad libitum if there is not concurrent vomiting. If the diarrhea lessens or resolves, then small meals of a bland, low-fat diet (e.g., cottage cheese, boiled meat mixed with rice or potatoes) can be fed.
2. Deworming with pyrantel pamoate (small bowel diarrhea) or fenbendazole (large bowel diarrhea) should be strongly considered, especially in young animals.
3. Antidiarrheals (e.g., bismuth subsalicylate, diphenoxylate, loperamide) are usually not needed and do not resolve the main problem. Bismuth subsalicylate may be effective for symptomatic control of mild to moderate diarrhea, but one of the opiates may be needed for severe cases. These agents should be used with caution in cats.
B. Acute small bowel diarrhea with systemic signs of illness. The primary disorder should be treated. Food should be withheld for at least 12–48 hours to rest the Gl tract. Antibiotics are indicated if the animal is febrile, neutropenic, or septic. Parenteral fluids should be administered if the animal is dehydrated or vomiting, is systemically ill, or to correct electrolyte imbalances. Electrolytes may be given orally if there is not vomiting and the clinical signs are not severe. Dextrose supplementation may be necessary for young, anorexic animals that have inadequate hepatic glucose reserves, or for animals with sepsis.
C. Chronic or intermittent small bowel diarrhea may respond to treatment of the primary disorder with no additional treatment. Parenteral fluids may be needed if concurrent anorexia, dehydration, or electrolyte imbalances are present.
D. Chronic large bowel diarrhea. The primary disorder should be treated. Supportive treatment for acute diarrhea without systemic signs (see VI A) may be helpful.

Chapter 5

Melena and Hematochezia

I. DEFINITIONS
A. Melena is black, tarry feces resulting from the presence of digested blood. If blood is swallowed or if upper gastrointestinal (Gl) hemorrhage occurs, the hemoglobin from the blood is oxidized and degraded as it passes through the intestinal tract. Thus, melena usually is an indication of upper Gl hemorrhage. Melena is rare in cats.
B. Hematochezia denotes fresh blood on the feces. Hematochezia is usually an indicator of large bowel or perianal disease. It can occasionally be seen with upper Gl hemorrhage if the hemorrhage is rapid, massive, or intestinal transit time is decreased.
II. CAUSES of melena and hematochezia are listed in Tables 5-1 and 5-2, respectively.
III. CLINICAL FINDINGS. Pale mucous membranes may result from anemia, and weakness or collapse may result from severe hemorrhage. Other associated clinical findings vary according to the underlying disorder (see and ).

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