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
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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 ).
Lesen Sie weiter in der vollständigen Ausgabe!
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