Notes on Canine Internal Medicine E-Book

Victoria L. Black

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Serie: Notes On
• Sprache: Englisch

Seitenzahl: 955

Veröffentlichungsjahr: 2022

Beschreibung

Canine Internal Medicine A thorough yet concise guide to diagnosing and managing canine medical conditions The newly revised Fourth Edition of Notes on Canine Internal Medicine delivers a comprehensive guide to the diagnosis of common and uncommon medical conditions in dogs. Written to act as a practical and fast-access subject reference for veterinary practitioners and students, Notes on Canine Internal Medicine encourages physicians to take a logical and evidence-based approach to canine medicine. Divided into five sections, the first four are dedicated to clinical presentations, physical and laboratory abnormalities, and - new to this edition - imaging patterns. It concludes with a section on the organ systems of canines, providing a robust summary of how to diagnose and manage common specific conditions of each system. This new edition includes: * A thorough introduction to the clinical presentations of a variety of presenting complaints, with both common and uncommon causes of each complaint and a logical diagnostic approach * In-depth examinations of common and uncommon physical problems, with a complete diagnostic approach including lab results and key imaging findings that aid in diagnosis * Comprehensive explorations of laboratory abnormalities in haematology, serum biochemistry, and urinalysis * Practical discussions of diagnostic imaging patterns, including plain radiographic, ultrasonographic, contrast radiographic, and cross-sectional imaging Notes on Canine Internal Medicine Fourth Edition is designed to be a useful resource for all veterinary clinicians; as a handy point of reference for veterinary students, recently graduated veterinary surgeons and those returning to work after career breaks, but also for experienced veterinary surgeons dealing with particularly difficult or challenging cases.

Leseprobe

Table of Contents

Cover

Title Page

Copyright Page

Dedication

PREFACE

ACKNOWLEDGEMENTS

USING THIS BOOK

COMMONLY USED ABBREVIATIONS

SECTION 1: PRESENTING COMPLAINTS

1.1 ABORTION

1.2 ALOPECIA

1.3 ALTERED BEHAVIOUR

1.4 ALTERED CONSCIOUSNESS

1.5 ANOREXIA/HYPOREXIA/INAPPETENCE

1.6 ANOSMIA

1.7 ANURIA/OLIGURIA

1.8 ATAXIA

1.9 BLEEDING

1.10 BLINDNESS

1.11 CONSTIPATION

1.12 CORNEAL OPACITY

1.13 COUGHING

1.14 DEAFNESS

1.15 DIARRHOEA

1.16 DROOLING

1.17 DYSPHAGIA

1.18 DYSPNOEA/TACHYPNOEA

1.19 DYSURIA

1.20 DYSTOCIA

1.21 EPISTAXIS

1.22 EXERCISE INTOLERANCE

1.23 FAECAL INCONTINENCE

1.24 FLATULENCE/BORBORYGMI

1.25 HAEMATEMESIS

1.26 HAEMATOCHEZIA

1.27 HAEMATURIA AND DISCOLOURED URINE

1.28 HAEMOPTYSIS

1.29 HALITOSIS

1.30 HEAD TILT

1.31 MELAENA

1.32 NASAL DISCHARGE

1.33 NYSTAGMUS

1.34 PARESIS/PARALYSIS

1.35 PERINATAL DEATH

1.36 POLYPHAGIA

1.37 POLYURIA/POLYDIPSIA (PU/PD)

1.38 PREPUTIAL DISCHARGE

1.39 PRURITUS

1.40 RED EYE (AND PINK EYE)

1.41 REGURGITATION

1.42 SEIZURES

1.43 SNEEZING

1.44 STIFFNESS, JOINT SWELLING AND GENERALISED LAMENESS

1.45 STUNTING

1.46 TENESMUS AND DYSCHEZIA

1.47 TREMORS

1.48 URINARY INCONTINENCE

1.49 VOMITING

1.50 VULVAL DISCHARGE

1.51 WEAKNESS, COLLAPSE AND SYNCOPE

1.52 WEIGHT GAIN/OBESITY

1.53 WEIGHT LOSS

SECTION 2: PHYSICAL ABNORMALITIES

2.1 ABDOMINAL ENLARGEMENT

2.2 ABDOMINAL MASSES

2.3 ABNORMAL LUNG SOUNDS

2.4 ARRHYTHMIAS

2.5 ASCITES

2.6 CYANOSIS

2.7 EYE LESIONS

2.8 HEPATOMEGALY

2.9 HORNER’S SYNDROME

2.10 HYPERTENSION

2.11 HYPOTENSION

2.12 HYPOTHERMIA

2.13 ICTERUS/JAUNDICE

2.14 LYMPHADENOPATHY

2.15 MURMUR

2.16 ORAL MASSES

2.17 PAIN

2.18 PALLOR

2.19 PERINEAL LESIONS

2.20 PERIPHERAL OEDEMA

2.21 PLEURAL EFFUSION

2.22 PNEUMOTHORAX

2.23 PROSTATOMEGALY

2.24 PULSE ABNORMALITIES

2.25 PYREXIA AND HYPERTHERMIA

2.26 SKIN LESIONS

2.27 SKIN PIGMENTATION CHANGES

2.28 SPLENOMEGALY

2.29 STOMATITIS

2.30 STRIDOR AND STERTOR

SECTION 3: LABORATORY ABNORMALITIES

3A BIOCHEMICAL TESTS

3.1 ACID–BASE

3.2 AMMONIA

3.3 AMYLASE AND LIPASE

3.4 AZOTAEMIA

3.5 BILE ACIDS

3.6 BILIRUBIN

3.7 CALCIUM

3.8 CARDIAC BIOMARKERS

3.9 CHLORIDE

3.10 COBALAMIN

3.11 CORTISOL (BASAL)

3.12 CREATINE KINASE

3.13 CREATININE

3.14 C‐REACTIVE PROTEIN (CRP)

3.15 FOLATE

3.16 FRUCTOSAMINE

3.17 GLUCOSE

3.18 IRON PROFILE

3.19 LIPIDS

3.20 LIVER ENZYMES

3.21 PANCREATIC LIPASE (cPL)

3.22 PHOSPHATE

3.23 POTASSIUM

3.24 SODIUM

3.25 SYMMETRIC DIMETHYLARGININE (SDMA)

3.26 THYROID HORMONE

3.27 TOTAL PROTEIN (ALBUMIN AND GLOBULIN)

3.28 TRYPSIN‐LIKE IMMUNOREACTIVITY (TLI)

3.29 UREA

3B HAEMATOLOGY

3.30 RED BLOOD CELLS (RBCs)

3.31 PLATELETS

3.32 WHITE BLOOD CELLS (WBCs)

3.33 PANCYTOPENIA

3C URINALYSIS

3.34 BIOCHEMICAL ANALYSIS

3.35 SEDIMENT

3.36 URINE PROTEIN: CREATININE (UPC) RATIO

3.37 URINE SPECIFIC GRAVITY (USG)

SECTION 4: IMAGING PATTERNS

4.1 ABDOMEN

4.2 BONE

4.3 THORAX

SECTION 5: ORGAN SYSTEMS

5.1 ALIMENTARY SYSTEM

5.1.1 OROPHARYNX

5.1.1A CRANIOMANDIBULAR OSTEOPATHY

5.1.1B CRICOPHARYNEAL ACHALASIA

5.1.1C MASTICATORY MYOSITIS

5.1.1D ORAL NEOPLASIA

5.1.1E STOMATITIS

5.1.2 SALIVARY GLANDS

5.1.2A HYPERSIALOSIS/SALIVARY GLAND INFARCTION/SIALOADENITIS

5.1.3 OESOPHAGUS

5.1.3A FOREIGN BODY

5.1.3B MEGAOESOPHAGUS (MO)

5.1.3C OESOPHAGITIS

5.1.3D SLIDING HIATAL HERNIA

5.1.3E STRICTURE

5.1.4 STOMACH

5.1.4A ACUTE GASTRITIS

5.1.4B CHRONIC GASTRITIS

5.1.4C GASTRIC CARCINOMA

5.1.4D GASTRIC DILATATION‐VOLVULUS (GDV)

5.1.4E DELAYED GASTRIC EMPTYING

5.1.4F GASTRIC ULCER

5.1.5 SMALL INTESTINE

5.1.6 LARGE INTESTINE

5.1.6A ACUTE COLITIS

5.1.6B CHRONIC COLITIS

5.1.6C CONSTIPATION

5.1.6D GRANULOMATOUS (HISTIOCYTIC ULCERATIVE) COLITIS

5.1.6E LARGE INTESTINAL NEOPLASIA

5.1.7 PANCREAS

5.1.7A ACUTE PANCREATITIS

5.1.7B CHRONIC PANCREATITIS

5.1.7C EXOCRINE PANCREATIC INSUFFICIENCY (EPI)

5.2 CARDIOVASCULAR SYSTEM

5.2.1 ACQUIRED CARDIAC DISEASES

5.2.1A ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY (ARVC)

5.2.1B DILATED CARDIOMYOPATHY (DCM)

5.2.1C HEARTWORM DISEASE/DIROFILARIASIS

5.2.1D MYXOMATOUS MITRAL VALVE DISEASE

5.2.2 CONGENITAL CARDIAC DISEASES

5.2.2A AORTIC STENOSIS

5.2.2B MITRAL VALVE DYSPLASIA

5.2.2C PATENT DUCTUS ARTERIOSUS

5.2.2D PULMONIC STENOSIS

5.2.2E TETRALOGY OF FALLOT

5.2.2 FTRICUSPID DYSPLASIA

5.2.2G VENTRICULAR SEPTAL DEFECT

5.2.3 CONGESTIVE HEART FAILURE (CHF)

5.2.3A LEFT‐SIDED CONGESTIVE HEART FAILURE

5.2.3B RIGHT‐SIDED CONGESTIVE HEART FAILURE

5.2.4 ARRHYTHMIAS

5.2.5 PERICARDIAL DISEASES

5.2.5A PERICARDIAL EFFUSION

5.2.5B PERITONEAL PERICARDIAL DIAPHRAGMATIC HERNIA (PPDH)

5.3 ENDOCRINE SYSTEM

5.3.1 DIABETES INSIPIDUS (DI)

5.3.2 DIABETES MELLITUS (DM)

5.3.3 GROWTH HORMONE DISORDERS

5.3.3A ACROMEGALY (HYPERSOMATOTROPISM)

5.3.3B PITUITARY DWARFISM

5.3.4 ADRENAL GLAND DISORDERS

5.3.4A HYPERADRENOCORTICISM (HAC)

5.3.4B HYPOADRENOCORTICISM (ADDISON’S DISEASE)

5.3.5 HYPOTHYROIDISM

5.3.6 INSULINOMA

5.3.7 PARATHYROID DISEASES

5.3.7A PRIMARY HYPERPARATHYROIDISM (PHPT)

5.3.7B HYPOPARATHYROIDISM

5.4 HAEMOPOIETIC SYSTEM

5.4.1 ANAEMIA OF CHRONIC KIDNEY DISEASE (CKD)

5.4.2 IMMUNE‐MEDIATED HAEMOLYTIC ANAEMIA (IMHA)

5.4.3 IRON‐DEFICIENCY ANAEMIA

5.4.4 LYMPHOID LEUKAEMIA

5.4.5 OTHER HAEMOPOIETIC NEOPLASMS

5.4.6 LEUKOPENIA

5.4.7 THROMBOSIS

5.5 HAEMOSTATIC SYSTEM

5.5.1 ANTICOAGULANT RODENTICIDE POISONING

5.5.2 DISSEMINATED INTRAVASCULAR COAGULATION (DIC)

5.5.3 FACTOR VIII DEFICIENCY (HAEMOPHILIA A)

5.5.4 HYPERFIBRINOLYSIS

5.5.5 IMMUNE‐MEDIATED THROMBOCYTOPENIA (IMTP)

5.5.6 VON WILLEBRAND DISEASE

5.5.7 VASCULITIS

5.6 HEPATOBILIARY SYSTEM

5.6.1 CHRONIC HEPATITIS (CH)/CIRRHOSIS

5.6.2 CHOLANGITIS/CHOLANGIOHEPATITIS

5.6.3 CHOLECYSTITIS

5.6.4 CONGENITAL PORTO‐SYSTEMIC SHUNT (PSS)

5.6.5 COPPER‐ASSOCIATED CHRONIC HEPATITIS

5.6.6 EXTRA‐HEPATIC BILE DUCT OBSTRUCTION (EHBDO)

5.6.7 GALL BLADDER MUCOCOELE

5.6.8 HEPATIC NEOPLASIA

5.6.9 INFECTIOUS CANINE HEPATITIS

5.6.10 NODULAR HYPERPLASIA

5.6.11 PORTAL VEIN HYPOPLASIA (PVH)

5.6.11A MICROVASCULAR DYSPLASIA (MVD)

5.6.11B NON‐CIRRHOTIC PORTAL HYPERTENSION/JUVENILE HEPATIC FIBROSIS

5.6.12 STEROID HEPATOPATHY

5.6.13 VACUOLAR/REACTIVE HEPATOPATHY

5.7 IMMUNE SYSTEM

5.7.1 (AUTO)IMMUNE‐MEDIATED DISORDERS

5.7.2 NEOPLASIA OF IMMUNE CELLS

5.8 NEUROLOGICAL SYSTEM

5.8.1 CEREBROVASCULAR DISEASE

5.8.2 CORTICOSTEROID‐RESPONSIVE TREMOR SYNDROME

5.8.3 HYDROCEPHALUS

5.8.4 IDIOPATHIC EPILEPSY

5.8.5 IDIOPATHIC HEAD TREMOR

5.8.6 IDIOPATHIC VESTIBULAR DISEASE

5.8.7 INFECTIOUS DISEASES AFFECTING THE NERVOUS SYSTEM

5.8.8 MOVEMENT DISORDERS

5.8.9 MENINGOENCEPHALITIS OF UNKNOWN ORIGIN (MUO)

5.8.10 MYASTHENIA GRAVIS (MG)

5.8.11 NEOPLASIA OF THE NEUROLOGICAL SYSTEM

5.8.12 POLYRADICULONEURITIS

5.8.13 STEROID‐RESPONSIVE MENINGITIS‐ARTERITIS (SRMA)

5.9 REPRODUCTIVE SYSTEM

5.9.1 MAMMARY GLAND DISEASE

5.9.1A MASTITIS

5.9.1B MAMMARY NEOPLASIA

5.9.2 OVARIAN REMNANT SYNDROME

5.9.3 PROSTATIC DISEASE

5.9.4 PSEUDOCYESIS (FALSE PREGNANCY)

5.9.5 PYOMETRA

5.9.6 TESTICULAR NEOPLASIA

5.9.7 VAGINITIS

5.10 RESPIRATORY SYSTEM

5.10.1 NASAL DISORDERS

5.10.1A CHRONIC IDIOPATHIC RHINITIS

5.10.1B SINONASAL ASPERGILLOSIS (FUNGAL RHINITIS)

5.10.2 UPPER‐AIRWAY DISORDERS

5.10.2A BRACHYCEPHALIC OBSTRUCTIVE AIRWAY SYNDROME (BOAS)

5.10.2B INFECTIOUS TRACHEOBRONCHITIS

5.10.2C LARYNGEAL PARALYSIS

5.10.2D TRACHEAL COLLAPSE

5.10.2E TRACHEOBRONCHIAL FOREIGN BODY

5.10.3 LOWER‐AIRWAY DISORDERS

5.10.3A CHRONIC BRONCHITIS

5.10.3B EOSINOPHILIC BRONCHOPNEUMOPATHY

5.10.3C LUNGWORM (

ANGIOSTRONGLYLUS VASORUM

)

5.10.4 PULMONARY PARENCHYMAL DISEASE

5.10.4A PNEUMONIA

5.10.4B NON‐CARDIOGENIC PULMONARY OEDEMA

5.10.4C PULMONARY FIBROSIS

5.10.4D PULMONARY NEOPLASIA

5.10.5 PLEURAL SPACE DISEASE

5.10.5A IDIOPATHIC CHYLOTHORAX

5.10.5B PNEUMOTHORAX

5.10.5C PYOTHORAX

5.11 SYSTEMIC INFECTIONS

5.11.1 ANAPLASMOSIS

5.11.2 BABESIOSIS

5.11.3 BORRELIOSIS (LYME DISEASE)

5.11.4 BRUCELLOSIS

5.11.5 DISTEMPER

5.11.6 EHRLICHIOSIS

5.11.7 HEPATOZOONOSIS

5.11.8 LEISHMANIOSIS

5.11.9 LEPTOSPIROSIS

5.11.10 NEOSPOROSIS

5.11.11 RABIES

5.11.12 TOXOPLASMOSIS

5.12 URINARY SYSTEM

5.12.1 KIDNEY DISEASES

5.12.1A ACUTE KIDNEY INJURY

5.12.1B CHRONIC KIDNEY DISEASE

5.12.1C GLOMERULAR DISORDERS

5.12.1D PYELONEPHRITIS

5.12.1E RENAL TUBULAR DISORDERS

5.12.2 LOWER URINARY TRACT DISEASES

5.12.2A FUNCTIONAL DISORDERS OF URINATION

5.12.2B NEOPLASIA OF THE URINARY SYSTEM

5.12.2C URETHRITIS

5.12.2D URINARY TRACT INFECTION (UTI)

5.12.2E UROLITHIASIS

ABBREVIATIONS

Index

End User License Agreement

List of Illustrations

Chapter 3

Figure 3.1

Regenerative anaemia.

Peripheral blood smear showing marked red b...

Chapter 4

Figure 4.1.1

Abdominal enlargement and masses

4.1.1a

HepatomegalyRight la...

Figure 4.1.2

Calcification

4.1.2a

Oesophageal foreign bodyAlthough not an...

Figure 4.1.3

Pneumoperitoneum

4.1.3a

Gastrointestinal perforationRight abdom...

Figure 4.1.4

Gas dilation of GI tract

4.1.4a

Gastric dilatation‐volvulus...

Figure 4.1.5

Metal FB

Whilst metal fragments in the GI tract may be inciden...

Figure 4.1.6

Organ displacement

4.1.6a

MicrohepaticaRight lateral plain a...

Figure 4.1.7

Free fluid (splenic mass)

Ultrasound image showing a heterogen...

Figure 4.1.8

Mesenteric lymph node ultrasound

Ultrasound image of mesenteri...

Figure 4.2.1

Craniomandibular osteopathy

Radiograph of the mandibular area...

Figure 4.2.2

Lucencies and proliferative lesions

4.2.2a

OsteosarcomaMottl...

Figure 4.3.1

Alveolar pattern

4.3.1a

Alveolar – aspiration pneumoniaDorso...

Figure 4.3.2

Bronchial pattern

Lateral (4.3.2a) and ventro‐dorsal (4.3.2b) ...

Figure 4.3.3

Cardiac outline

4.3.3a

Left sideOutline of normal heart and ...

Figure 4.3.4

Changes in cardiac outline

‐‐‐‐‐‐ indicates displacement of out...

Figure 4.3.5

Congestive heart failure

Left lateral thoracic radiograph of ...

Figure 4.3.6

Interstitial pattern

4.3.6a

DiffuseLateral thoracic radiogra...

Chapter 5.1

Figure 5.1.1

Alimentary ultrasound

5.1.1a

Alimentary lymphomaTransverse i...

Figure 5.1.2

Megaoesophagus

. Right lateral thoracic radiograph of a dog with...

Chapter 5.2

Figure 5.2.1

Auscultation

5.2.1a

Left‐side auscultationOutline of normal he...

Figure 5.2.2

Normal ECG

5.2.2a

Sinus rhythmLead II ECG showing normal sinus...

Figure 5.2.3

ARVC.

Lead II ECG in a Boxer with arrhythmogenic right ventricu...

Figure 5.2.4

Dilated cardiomyopathy.

M‐mode echocardiogram of a dog with dil...

Figure 5.2.5

Atrioventricular block

5.2.5a

Second‐degree Mobitz type ILeads...

Figure 5.2.6

Sick sinus syndrome.

Leads I, II and III ECG from a dog with si...

Figure 5.2.7

Atrial fibrillation.

Leads I, II and III ECG showing atrial fib...

Figure 5.2.8

Ventricular arrhythmias

5.2.8a

Couplets and tripletsLeads I, I...

Figure 5.2.9

Pericardial effusion.

Echocardiographic image of a pericardial ...

Chapter 5.4

Figure 5.4.1

Spherocytosis

.Blood smear from a dog with IMHA demonstrating ...

Chapter 5.6

; Figure 5.6.1

Gall bladder mucocoele.

Ultrasound image of a GB mucocoele wit...

Guide

ABBREVIATIONS

Cover Page

Title Page

Copyright

Dedication

PREFACE

ACKNOWLEDGEMENTS

USING THIS BOOK

COMMONLY USED ABBREVIATIONS

Table of Contents

Begin Reading

Index

WILEY END USER LICENSE AGREEMENT

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NOTES ON CANINE INTERNAL MEDICINE

Fourth Edition

Victoria L. Black,

MA, VetMB, FHEA, DipECVIM‐CA, MRCVS

Senior Clinician in Small Animal Medicine

EBVS® European Specialist in Small Animal Internal Medicine

RCVS Specialist in Small Animal Medicine

Langford Vets, Bristol Veterinary School

Bristol, UK

Kathryn F. Murphy,

BVSc, DSAM, PGCertHE, DipECVIM‐CA, FRCVS

EBVS® European Specialist in Small Animal Internal Medicine,

RCVS Specialist in Small Animal Medicine

Rowe Referrals, Bristol

VetCT

UK

Jessie Rose Payne,

BVetMed, MVetMed, PhD, DipACVIM (Cardiology), MRCVS

Senior Clinician in Cardiology

ACVIM Specialist in Veterinary Cardiology

RCVS Specialist in Veterinary Cardiology

Langford Vets, Bristol Veterinary School

Bristol, UK

Edward J. Hall,

MA, VetMB, PhD, DipECVIM‐CA, FRCVS

Emeritus Professor of Small Animal Internal Medicine

EBVS® European Specialist in Small Animal Internal Medicine

RCVS Specialist in Small Animal Medicine (Gastroenterology)

University of Bristol

Bristol, UK

This edition first published 2022© 2022 John Wiley & Sons Ltd

Edition HistoryWright Imprint by IOP Publishing Limited (1e, 1983; 2e, 1986)Blackwell Science Ltd (3e, 2003)

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Library of Congress Cataloging‐in‐Publication Data

Names: Hall, E. J. (Ed J.) author. | Black, Victoria L., 1985‐ author. | Murphy, K. F. (Kate F.), author. | Payne, Jessie Rose, 1985‐ author.Title: Notes on canine internal medicine / Victoria L. Black, Kathryn F. Murphy, Jessie Rose Payne, Edward J. Hall.Other titles: Canine internal medicineDescription: Fourth edition. | Hoboken, NJ : Wiley‐Blackwell, 2022. |  Hall’s name appears first in third edition.Identifiers: LCCN 2022000939 (print) | LCCN 2022000940 (ebook) | ISBN  9781119744771 (paperback) | ISBN 9781119744788 (adobe pdf) | ISBN 9781119744795 (epub)Subjects: MESH: Dog Diseases | Handbook Classification: LCC SF991 (print) | LCC SF991 (ebook) | NLM SF 991 | DDC  636.7/0896–dc23/eng/20220209LC record available at https://lccn.loc.gov/2022000939LC ebook record available at https://lccn.loc.gov/2022000940

Cover Design: WileyCover Images: Courtesy of Edward J. Hall, Jessie Rose Payne, Kathryn F. Murphy, and Victoria L. Black

We all recognise the patience and support of our respective families during the production of this book. However, individually we wish to dedicate it specifically to:

All the vets and vet students I have met with a curious approach to our patients – your enthusiasm continues to inspire and motivate.

Victoria L. Black

Those who inspired me to know more as a student and resident (particularly Ed!) and my colleagues, clients and patients who continue to encourage me to learn more.

Kathryn F. Murphy

My patients, who make each day different from the last and continue to inspire me to learn every day.

Jessie Rose Payne

All the Medicine Residents and colleagues (particularly Kate and Vicki!) I have worked with, who have pushed me to learn more.

Edward J. Hall

PREFACE

“When you hear hoofbeats, look for horses — not zebras.”*

In 1983, in the first edition of Notes on Canine Internal Medicine, Peter Darke provided a revolutionary new and simplified diagnostic approach to internal medicine problem solving. It was not long before his book was to be found in the pocket of every veterinary undergraduate in the UK, as well as being an important first source of information for practitioners. The second and third editions built on this success. However, it is now nearly 20 years since the third and last edition and, in that time, our knowledge of canine internal medicine and our ability to investigate and treat cases has grown almost exponentially. Standard internal medicine texts now often fill two large volumes, detailing the underlying pathophysiology that is essential to understand diseases fully. However, there remains a need for a concise text to aid students and busy practitioners.

Whilst we acknowledge the importance of pathophysiology in internal medicine, in first opinion practice knowing the three most likely differential diagnoses for a problem is of more use than knowing ten obscure and unlikely ones despite potentially similar pathophysiological mechanisms. Thus, in this book, we have provided separate lists of the ‘common causes’ of medical problems, and the ‘uncommon causes’. Our personal experiences and geographical location inevitably bias our opinions on what are the most common causes of any specific problem but please note that these two lists are in alphabetical order and not order of prevalence. We are also not indicating the relative incidence of specific problems seen in first opinion practice, although practitioners will already know that dermatological and GI problems are most common. Our opinions on what are the best approaches to a specific problem are based on the scientific evidence, where it is available, and on our personal experience.

This edition follows a similar pattern to the third edition, with sections on presenting complaints, physical findings, and laboratory abnormalities. We have added a new section on imaging patterns, and again finish with a section covering diseases of the major organ systems. The authorship has been expanded to ensure we have the expertise to cover all areas of internal medicine, including Peter Darke’s own discipline of cardiology. We have also included information on behavioural, dermatological and ophthalmological problems focused on where these are manifestations of systemic disease. We do not believe in a totally algorithmic approach as used in some texts and have highlighted key clinical clues which, when using the results of history‐taking, physical examination, laboratory tests and imaging findings, should guide the clinician’s investigation in the right direction and avoid unnecessary testing.

As noted in the first edition, the recognition that not everything in internal medicine is black and white is part of its challenge; and not every patient ‘reads the textbook’. We still believe in the advice of the first edition that ‘basic, careful history‐taking and thorough and, if necessary, repeated clinical examination are fundamental procedures that may yield a diagnosis in a complicated or unresolved case’. One should always remember that there is always one more question to be asked, or one more investigation to be performed on problem cases, and one should never be afraid to go back to the beginning and start again.

V.L.B, K.F.M., J.R.P. and E.J.H.2022

Note

*

Source uncertain;

https://quoteinvestigator.com/2017/11/26/zebras/

ACKNOWLEDGEMENTS

The initial inspiration for this book was Peter Darke’s and we are honoured to write this new edition. The book retains its original title to emphasise its aim to be easily accessible notes for the veterinary practitioner and student to assist their diagnostic investigations of medically ill dogs.

USING THIS BOOK

SECTION 1

Presenting complaints

In this section, the common presenting complaints are listed alphabetically according to a stylised format.

Each problem is defined, and the expected clinical signs listed although not every case will show every sign.

Causes for the problem are divided into ‘common’ and ‘uncommon’ to guide the reader, but are only the opinion of the authors, and may vary in different geographical locations.

For each problem a logical diagnostic approach is suggested; any numbering indicates a suggested order for the investigations:

Clinical clues in the history.

Potential findings in the clinical examination.

Laboratory findings that aid the diagnosis.

Key results from imaging.

Special tests that may confirm the diagnosis.

SECTION 2

Physical problems

In this section, significant findings from the physical examination are listed alphabetically.

Each problem is defined.

Common and uncommon causes, listed alphabetically, are suggested for each problem.

Related clinical signs are listed.

For each problem a logical diagnostic approach is suggested.

Key findings to look for in the history and physical examination are noted; not all will be present in every case.

Laboratory findings that aid the diagnosis are noted.

Key results of imaging are noted.

Special tests that may confirm the diagnosis are listed.

SECTION 3

Laboratory abnormalities

In this section laboratory abnormalities of haematology, serum biochemistry and urinalysis are listed alphabetically.

The abnormality is defined.

Causes are listed alphabetically, and the likely degree of severity is suggested.

The diagnostic interpretation for the abnormality is given.

Adjunctive tests that may help support or confirm the diagnosis are given.

SECTION 4

Imaging patterns

Differential diagnoses for specific plain radiographic and ultrasonographic patterns and appearances are listed. Relevant further imaging modalities (contrast radiography, cross‐sectional imaging, i.e. CT and MRI) are suggested.

SECTION 5

Organ systems

The relevant clinical presentations and physical, laboratory and imaging abnormalities (identified in Sections 1–4, respectively) are given for each major internal organ system. Then the diagnostic approach and the methods of investigation of each organ system are briefly explained. Finally, the more common diseases of each system are covered alphabetically. For each, its aetiology, predisposition, historical clues, clinical signs, laboratory test results, treatment and monitoring, sequelae and prognosis are given in note form.

COMMONLY USED ABBREVIATIONS

Commonly used scientific and medical abbreviations listed here are used throughout the book without further expansion.

All other abbreviations are spelled out in each section, and are listed at the end of the book with the Index.

ACTH

adrenocorticotrophic hormone

ALP (SAP)

(serum) alkaline phosphatase

ALT

alanine aminotransferase

BID

twice daily (q12h)

CBC

complete blood count

ECG

electrocardiogram

EDTA

ethylenediaminetetra‐acetic acid

ELISA

enzyme‐linked immunosorbent assay

HCT

haematocrit

IgA

immunoglobulin A

IM

intramuscular

IV

intravenous

NPO

nil per os

(nothing by mouth)

NSAID

non‐steroidal anti‐inflammatory drug

PCR

polymerase chain reaction

PCV

packed cell volume

PO

per os

QID

four times daily (q6h)

q.v

.

quod vide

(see related material)

RBC

red blood cell

SC

subcutaneous

SID

once daily (q24h)

T4

thyroxine

TID

three times daily (q8h)

WBC

white blood cell

SECTION 1PRESENTING COMPLAINTS

In this section, the common presenting complaints are listed alphabetically according to a stylised format.

Each problem is defined, and the expected clinical signs listed, although not every case will show every sign.

Causes for the problem are divided into ‘common’ and ‘uncommon’ to guide the reader, but are only the opinion of the authors, and may vary in different geographical locations.

For each problem a logical diagnostic approach is suggested; any numbering indicates a suggested order for the investigations:

Clinical clues in the history.

Potential findings in the clinical examination.

Laboratory findings that aid the diagnosis.

Key results from imaging.

Special tests that may confirm the diagnosis

1.1 Abortion

1.2 Alopecia

1.3 Altered behaviour

1.4 Altered consciousness

1.5 Anorexia/hyporexia/inappetence

1.6 Anosmia

1.7 Anuria/oliguria

1.8 Ataxia

1.9 Bleeding

1.10 Blindness

1.11 Constipation

1.12 Corneal opacity

1.13 Coughing

1.14 Deafness

1.15 Diarrhoea

1.15.1 Acute diarrhoea

1.15.2 Chronic diarrhoea

1.16 Drooling

1.17 Dysphagia

1.18 Dyspnoea/tachypnoea

1.19 Dysuria

1.20 Dystocia

1.21 Epistaxis

1.22 Exercise intolerance

1.23 Faecal incontinence

1.24 Flatulence/borborygmi

1.25 Haematemesis

1.26 Haematochezia

1.27 Haematuria and discoloured urine

1.28 Haemoptysis

1.29 Halitosis

1.30 Head tilt

1.31 Melaena

1.32 Nasal discharge

1.33 Nystagmus

1.34 Paresis/paralysis

1.35 Perinatal death

1.36 Polyphagia

1.37 Polyuria/polydipsia (PU/PD)

1.38 Preputial discharge

1.39 Pruritus

1.40 Red eye (and pink eye)

1.41 Regurgitation

1.42 Seizures

1.43 Sneezing

1.44 Stiffness, joint swelling and generalised lameness

1.45 Stunting

1.46 Tenesmus and dyschezia

1.47 Tremors

1.48 Urinary incontinence

1.49 Vomiting

1.50 Vulval discharge

1.51 Weakness, collapse and syncope

1.52 Weight gain/obesity

1.53 Weight loss

1.1 ABORTION

DEFINITION

The spontaneous expulsion of one or more fetuses before the end of full‐term pregnancy, i.e. when the fetus is incapable of independent life.

RELATED CLINICAL SIGNS

Abdominal pain

Abnormal vulval discharge

Fever

Lethargy/depression

Premature whelping is reported with live or dead pups or no live pups at term

COMMON CAUSES

Infectious

Bacterial

Brucella canis

in endemic countries; not endemic in UK

Streptococcus

infection

Viral: Canine herpesvirus‐1 (CHV‐1)

Non‐infectious

Congenital defects: various lethal defects

Genetic causes: various lethal defects

Maternal factors:

Illness

Diabetes mellitus (DM)

Eclampsia

Pregnancy toxaemia

Drugs

Corticosteroids

Griseofulvin

Itraconazole

Phenylephrine

Prolactin inhibitors

Prostaglandins

Progesterone‐receptor blockers

Toxins: insecticides, plant toxins

Trauma

Hypoluteinization (low progesterone)

Advanced age

Traumatic: dystocia

UNCOMMON CAUSES

Infectious

Bacterial

Escherichia coli

Campylobacter

Leptospira

Salmonella

Fungal

Protozoal

Leishmania

Neospora

Toxoplasma

Viral

Bluetongue virus

Canine adenovirus 1

Canine distemper virus

Canine parvovirus 1 (minute virus)

DIAGNOSTIC APPROACH

Clinical clues

Predisposition

Advanced age

Previous history of abortion

Assess for hypoluteinization by checking progesterone concentrations

History

Abnormal vulval discharge

Bitch whelps early with live or dead pups or no pups at term

Clinical examination

Visual inspection

Often unremarkable

Physical examination

Abdominal contractions and expulsion of fetus(es) in later pregnancy

Vulval discharge: purulent, haemorrhagic, green, black, malodorous

Laboratory findings

Haematology

May be normal

HCT often low in pregnancy due to decreased plasma volume, e.g. 30–35% compared to 45–55%

Mild mature neutrophilia common in pregnancy, may sometimes be more pronounced changes or bands

Serum biochemistry

May be normal

Urinalysis

May show evidence of inflammation with free catch or catheter samples

Imaging

Plain radiographs

May show evidence of dystocia

Ultrasound

May show evidence of fetal death

Special tests

Examination of fetus post mortem

Virus isolation/bacterial culture/PCR of fetus/placenta/vaginal secretions/milk

Tests of dam

Serology ± PCR of dam for CHV‐1,

B. canis

Serum progesterone to assess if sufficient to maintain pregnancy: should be > 2 ng/ml (6 nmol/l); if less than these values for > 48 hours suggests hypoluteinization but can be seen due to fetal death

Thyroid hormone analysis: total T4/thyroid‐stimulating hormone (TSH)

1.2 ALOPECIA

DEFINITION

Absence of hair from areas of skin that normally carry hairs, due either to a failure of production or to an increased loss of hair. Hypotrichosis refers to thinning of hair. Hair loss may be focal or diffuse, and symmetrical or non‐symmetrical.

RELATED CLINICAL SIGNS

Endocrinopathies are likely to cause concurrent systemic signs such as changes in drinking, eating, exercise tolerance and body weight

Loss or absence of hair

Self‐traumatic lesions if pruritic skin disease

COMMON CAUSES

Primary follicular disease

Inherited abnormalities of follicular structure, ranging from absence of follicles that normally produce hair of a particular colour to complete absence of follicles, are uncommon except in specific breeds.

Secondary follicular disease

Bacterial folliculitis/superficial pyoderma

Demodectic mange

Hyperadrenocorticism (HAC)

Iatrogenic

Pituitary‐ or adrenal‐dependent

Hypothyroidism

Interdigital pyoderma

Malassezia

infection

Seasonal flank alopecia (cyclic follicular dysplasia)

Self‐trauma when pruritic

Atopy

Fleas and flea‐allergic dermatitis

Pyotraumatic dermatitis (‘hot spot’)

Sarcoptic mange

Secondary bacterial pyoderma

UNCOMMON CAUSES

Primary follicular disease

Alopecia areata

Alopecia mucinosa/follicular mucinosis: Shar pei

(Auto)immune skin disease

Dermatomyositis

Erythema multiforme

Exfoliative cutaneous lupus erythematosus (ECLE)

Systemic lupus erythematosus

Pemphigus foliaceous

Sebaceous adenitis

Catagen arrest: Weimaraners

Colour mutant/dilution

Congenital hypotrichosis/alopecia

Follicular dysplasia

Black hair follicular dysplasia

Breed‐specific follicular dysplasia

Loss of primary but retention of secondary hairs changing coat to reddish‐brown: Siberian Husky and Alaskan Malamute

Flank and saddle region involved initially in red or black dogs: Dobermann

Flank and saddle hair loss: Airedale terrier, Boxer, English bulldog, Staffordshire terrier

Hair loss around face and over dorsum; cyclic initially but eventually permanent: Curly‐coated Retriever, Irish Water spaniel, Portuguese Water dog

Medullary trichomalacia: German shepherd

Pili torti

Trichorrhexis nodosa

Follicular lipidosis: Rottweiler

Hairless breeds

Pattern baldness

Caudal thigh: Greyhounds

Neck, trunk and thighs: Portuguese Water dog, American Water spaniel

Pinnal: Dachshund

Ventral and caudal: Boston Terrier, Chihuahua, Dachshund, Manchester Terrier, Whippet

Pressure/traction alopecia: focal hair loss over bony prominences and sites of friction by collars, harnesses and coats

Pseudopelade

Subcorneal pustular dermatosis

Trichoptilosis: Golden retriever

Secondary follicular disease

Adrenal sex hormone imbalance/adrenal hyperplasia syndrome (alopecia X)

Anagen defluvium

Cancer chemotherapy – greatest risk with curly‐ or wire‐haired coats

Endocrinopathies

Infection

Cicatricial (scar‐related)

Cold agglutinin disease

Contact dermatitis

Cutaneous vasculitis

Dermatomyositis

Dermatophytosis

Epitheliotropic lymphoma including mycosis fungoides

Follicular arrest

Post‐clipping

Protein/calorie malnutrition

Hepatocutaneous sydrome: more typically causes painful footpad hyperkeratosis

Hyperoestrogenism

Adrenal gland disease

Excessive oestrogen administration (for urinary incontinence)

Excessive phytoestrogen ingestion (e.g. flaxseed)

Inadvertent exposure to human transdermal hormone replacement product

Ovarian remnant follicular cyst formation or malignant transformation

Testicular Sertoli cell tumour

Hypo‐oestrogenism

Hyposomatotropism (pituitary dwarf)

Hypotestosteronism

Leishmaniosis

Nutritional

Biotin deficiency

Vitamin A or E deficiency

Radiation therapy

Systemic lupus erythematosus (SLE)

Telogen effluvium

Injection reaction

Epidural

Post‐vaccinal

Post‐partum

Pregnancy

“Stress”

Thallium poisoning

Vitamin A deficiency

Zinc‐responsive dermatosis

Self‐mutilation

Acral lick/flank sucking/neurodermatitis

Cheyletiella

Food allergy

Lice

Trombicula

(Harvest mite)

DIAGNOSTIC APPROACH

Identification of infectious agents by sellotape strips, skin scrapes, hair plucks, bacterial and fungal cultures, and empirical treatment trials.

The presence or absence of pruritus narrows the differential diagnosis.

If pruritic:

After ruling out infectious causes, trial therapy for bacterial pyoderma, fleas and possibly also for

Sarcoptes

, is acceptable

Intradermal skin testing is performed to identify atopic reactions

If all negative, an exclusion food trial is indicated

If non‐pruritic:

Consider endocrinopathy or breed‐related problem

Skin biopsy is indicated if no cause is obvious

Clinical clues

Pattern of hair loss and sites of self‐mutilation can be informative

q.v. Clinical examination

Broken hairs on trichogram and ulcerated skin suggest self‐trauma due to pruritus

Concurrent systemic signs of polyuria/polydipsia (PU/PD), exercise intolerance, polyphagia or weight gain are suggestive of an endocrinopathy

Non‐symmetrical alopecia is suggestive of self‐trauma or infection

Presence of fleas or ‘flea dirt’ is diagnostic

Repeated scratching and rubbing indicate pruritic causes

Seasonality is suggestive of atopy, ectoparasites or seasonal flank alopecia

Symmetrical alopecia is suggestive of an endocrinopathy

Bilaterally symmetrical alopecia starting on the trunk is considered the hallmark of an endocrinopathy, but pruritic skin disease can also appear symmetrical.

Evidence of pruritus:

Positive scratch reflex

Broken hairs, not hair loss

Predisposition

Breed predisposition may suggest primary follicular diseases:

Canine hairless breeds: American Hairless Terrier, Argentine Pila, Chinese Crested, Mexican Hairless (Xoloitzcuintli), Peruvian Inca Orchid

Colour‐mutant alopecia: blue/fawn/red Dobermann, blue Chow Chow, blue Dachshund, blue Great Dane, blue Whippet, fawn Irish setter

Follicular dysplasia: Curly‐coated Retriever, Irish Water Spaniel, Portuguese Water dog

Dermatomyositis: Collies

History

Colour‐mutant alopecia develops in young adults

Congenital or hereditary hypotrichosis is usually evident from an early age

Slow onset and bilateral truncal alopecia is suggestive of endocrinopathy

Testicular mass, pendulous prepuce and attractiveness to other male dogs is suggestive of functional Sertoli cell tumour

Other clinical signs (e.g. PU/PD, weight change) suggest a possible endocrinopathy

Clinical examination

Visual inspection

Broken hairs if pruritic, otherwise hairs are absent

Lesions secondary to self‐trauma:

erythema, excoriation, lichenification, hyperpigmentation

Presence of fleas or ‘flea dirt’

Pustules, erythema, scaling in pyoderma

Physical examination

Thickened skin in hypothyroidism

Thinned skin in HAC

Distribution of self‐mutilation

Dorso‐lumbar with flea‐allergic dermatitis

Ear margins and elbows with sarcoptic mange

Face, feet and ventrum with atopy

Feet and ventrum with contact allergy

Face, ears and feet with food allergy

Face, ears, feet or multifocal with demodecosis

Face, feet, mucocutaneous junctions with autoimmune skin disease

Distribution of hair loss

Focal

Alopecia areata

Cicatricial

Demodecosis

Dermatophytosis

Injection reaction

Pattern baldness

Superficial pyoderma/bacterial folliculitis

Multifocal or diffuse but patchy

Colour dilution

Demodecosis

Dermatomyositis

Dermatophytosis

Epitheliotropic lymphosarcoma

Follicular dysplasia

Superficial pyoderma/bacterial folliculitis

Symmetrical, generalised, diffuse

Demodecosis

Dermatophytosis

Endocrinopathies

Superficial pyoderma/bacterial folliculitis

Telogen effluvium

Hair loss from the caudal trunk and thighs

Flea allergic dermatosis

Follicular dysplasia

Hyperoestrogenism

Pattern baldness of Greyhounds

Hair loss from the pinnae

Atopy

Cold agglutinin disease

Dermatophytosis

Demodectic mange

Otitis externa

Pemphigus erythematosus

Pemphigus foliaceous

Pinnal pattern baldness

Sarcoptic mange

Subcorneal pustular dermatosis

Hair loss from the feet

Atopy

Contact dermatitis

Demodectic mange

Pemphigus diseases

Interdigital pyoderma

Thallium poisoning

Laboratory findings

Haematology and serum biochemistry

Unremarkable unless underlying endocrinopathy, e.g. hypercholesterolaemia in hypothyroidism, increased ALP activity in HAC

Dermatological investigations

Bacterial and fungal cultures

Hair plucks –

Demodex

, ringworm

Hypercholesterolaemia and increased ALP in HAC

Sellotape strips cytology:

Malassezia

Skin scrapes:

Sarcoptes

,

Demodex

Imaging

Usually unnecessary and unremarkable unless systemic signs (e.g. endocrinopathy)

Special tests

Dynamic cortisol testing for HAC

Exclusion diet trial

Intradermal skin tests

Sarcoptic mange antibody

Therapeutic trial for sarcoptic mange

Skin biopsy

Thyroid function tests

1.3 ALTERED BEHAVIOUR

DEFINITION

A change in response to or interaction with the environment. Abnormal behaviour can be observed as a spectrum of consciousness (q.v. section 1.4) ranging from reduced response to even noxious stimuli to manic behaviour and hyperactivity. Animals may also demonstrate changes in sleep‐wake cycles, social relationships, repetitive activities, or spatial disorientation.

Behavioural disorders and medical disorders causing behaviour change present a significant challenge due to the considerable overlap in presentations. Behavioural disorders can be considered after medical disorders have been excluded and are more common in younger animals presenting with increased reactivity or vigilance.

RELATED CLINICAL SIGNS

Aggression

Dullness and reduced responsiveness,

q.v

.

section 1.4

Excessive grooming

Hyperactivity (excessive pacing, circling, altered sleep patterns)

Inappropriate elimination

Repetitive behaviours (fly catching, over‐grooming, tail chasing, flank sucking)

COMMON CAUSES

Pain

Ear disease

Neuropathic

Orthopaedic

Intracranial disorders

Cognitive dysfunction

Hydrocephalus

Idiopathic epilepsy

Inflammatory (meningoencephalitis of unknown origin)

Neoplasia

Metabolic disorders

Hepatic encephalopathy (portosystemic shunts, chronic hepatitis, acute hepatic failure)

Hyperadrenocorticism

Hypertension

Hypothyroidism

Toxins

Intestinal disorders

Idiopathic chronic inflammatory enteropathy (CIE)/inflammatory bowel disease (IBD)

Neoplasia

Urinary tract disorders

Atopy

Dermatological disorders

Ectopic ureters

Parasitic infection

Urinary tract infection

Urolithiasis

UNCOMMON CAUSES

Metabolic disorders

Hyperthyroidism

Phaeochromocytoma

Intracranial disorders

Infectious disease, e.g.

Cryptococcus

, distemper,

Toxoplasma

,

Neospora

Storage disease

Dermatological disorders

Bacterial hypersensitivity

Ocular disorders causing pain or impairing vision

Cataracts

Progressive retinal atrophy

Uveitis

DIAGNOSTIC APPROACH

Thorough screening for medical disorders should be considered in young animals, or in patients with acute onset change. Environment, social interactions, exercise routine, and training history may influence likelihood of behavioural disorders.

Clinical clues

Predisposition

Cognitive dysfunction and orthopaedic pain: older dogs

Portosystemic shunt (PSS): young dogs and some breeds are predisposed (e.g. Yorkshire terriers, Miniature schnauzers, Pugs, Irish Wolfhounds)

Some repetitive behaviours have breed associations:

Flank sucking: Dobermanns

Fly catching: CKCS

Hind‐end checking: Miniature Schnauzers

Self‐mutilation: Springer spaniels

Tail chasing: German shepherds

Neuropathies can be heritable disorders, e.g. sensory neuropathy in Border collies

History

Assess for risk of toxin exposure if acute onset change

Circumstance of occurrence may increase suspicion of

pain disorders after rest or after exercise

metabolic disease, e.g. after eating may increase suspicion of a PSS

Clinical examination

Visual inspection

Behaviour during consultation, or during circumstance of typical occurrence: video recordings of abnormal behaviour are encouraged

Haircoat changes are suggestive of endocrine disorders

In young dogs, examine for

disproportionate stunting, e.g. congenital hypothyroidism

domed cranium ± open fontanelle in hydrocephalus

stature, e.g. small size in EPI, PSS

Physical examination

Thorough examination for source of pain, with specific attention to musculoskeletal system

Neurological and ophthalmic examination

Rectal examination in cases of inappropriate elimination to assess for rectal, urethral, and prostatic disorders

Laboratory findings

Haematology

May reveal microcytosis ± hypochromasia in PSS

Mild, normocytic, normochromic, poorly‐regenerative anaemia in hypothyroidism

Serum biochemistry

Evidence of hepatic dysfunction (e.g. decreased albumin, cholesterol, urea, glucose, increased ammonia), including increased bile acids; increased liver enzyme activities not typical in PSS but detected in other hepatopathies

Enteropathy may present with panhypoproteinaemia (hypoalbuminaemia and hypoglobulinaemia) ± low serum cholesterol

Hypercholesterolaemia in hypothyroidism

Imaging

Plain radiographs

In cases with excessive grooming may detect underlying musculoskeletal disease including degenerative joint disease or neoplasia

Ultrasound

Abnormal vessel ± renomegaly may be observed in PSS

Adrenal gland size in cases suspicious for hyperadrenocorticism

Intestinal wall layering for enteropathy

Liver size and echotexture when suspicious of hepatic dysfunction

Special tests

Cobalamin and folate in cases with a suspicion of enteropathy, particularly relevant to cases of fly catching, inappropriate elimination, or pica

Computed tomography (CT) angiogram to assess for PSS if not detected on ultrasound examination

Low‐dose dexamethasone suppression LDDS test (± ACTH stimulation test) to assess for hyperadrenocorticism

Liver biopsy for hepatopathy

Total thyroxine and TSH to assess for hypothyroidism

Treatment trials

Non‐steroidal anti‐inflammatory drug (NSAID) or other analgesic trial for suspected pain

Antiepileptic therapy where partial seizures are a consideration

Exclusion diet trial where atopy or enteropathy is suspected

1.4 ALTERED CONSCIOUSNESS

DEFINITION

Consciousness is the state of arousal and ability to respond to the external environment. Diminished consciousness can be graded based upon lack of responsiveness to increasingly stimulatory external events. State of consciousness is an important component of the modified Glasgow Coma Scale (MGCS), useful prognostically and for monitoring purposes.

Consciousness is primarily determined by the ascending reticular activating system, an important set of neurons found within the brainstem. Disorders of the brainstem can result in dysfunction of these neurons, with a consequent reduced state of arousal of the individual. Diffuse forebrain dysfunction (cerebral disorders) may also result in diminished consciousness in some circumstances (q.v. modified Glasgow Coma Scale in section 5.8).

RELATED CLINICAL SIGNS

Grades of dysfunction

Depressed or obtunded

Reduced responsiveness to external visual or auditory stimuli

Associated with brainstem, diffuse forebrain disorders, or systemic disease

Can have intermittent periods of more normal mentation

Stuporous

Semi‐comatose, responsive only to repeated noxious stimuli

Typically associated with brainstem disorders, including brain herniation

Comatose

Unresponsive to repeated noxious stimuli

Typically associated with brainstem disorders, including brain herniation

Delirious

Hyperactive with excessive or abnormal responses to external stimuli

Typically associated with forebrain disease

COMMON CAUSES

Congenital

Hydrocephalus

PSS

Inflammatory

Meningoencephalitis of unknown origin (MUO)

Infectious

Bacterial empyema, e.g. extension of otitis media

Lungworm (

Angiostrongylus vasorum

)

Iatrogenic

Head trauma

Toxins or drugs, e.g. sedation or anaesthesia, hallucinogens

Metabolic

Electrolyte disturbances, especially changes in osmolarity due to too‐rapid correction of sodium disturbances

Hepatic encephalopathy

Hypoglycaemia

Severe systemic disease, e.g. sepsis, congestive heart failure, etc.

Neoplastic

Primary central nervous system (CNS) tumours:

meningioma, glioma, lymphoma

Vascular

Thromboembolic or haemorrhagic stroke

UNCOMMON CAUSES

Congenital

Storage disease: signs may develop as dog ages

Infectious

Distemper

Protozoal:

Toxoplasma

,

Neospora

Rabies

Iatrogenic

Complication of cerebrospinal fluid (CSF) sampling in dogs with increased intracranial pressure

Vascular

Hyperviscosity, e.g. hyperglobulinaemia, hyperlipidaemia, primary erythrocytosis

DIAGNOSTIC APPROACH

Clinical clues

Predisposition

Congenital disorders maybe suspected in young dogs, especially those with conformational changes

Disproportionate stunting, e.g. congenital hypothyroidism (

q.v

.

section 1.45

)

Domed cranium ± open fontanelle in hydrocephalus

Small stature in PSS

Small purebred middle‐aged dogs are predisposed to meningoencephalitis of unknown origin (e.g. Maltese terrier, Pug, West Highland White terrier [WHWT])

History

Anti‐parasitic prophylaxis may indicate lesser risk of

Angiostrongylus

infection

Lifestyle may increase index of suspicion for infectious disease, e.g. raw‐fed may increase suspicion of toxoplasmosis or exposure to toxins or risk of trauma

Clinical examination

Visual inspection

Interaction with the environment, increasing external stimuli (to include visual and auditory tests)

Physical examination

Assess for signs of systemic disease in cases of obtundation; mentation changes may be secondary to this, or, in multisystemic disease, may detect abnormalities on examination

Heart rate and blood pressure (BP): a patient with bradycardia (pulse rate < 60 beats/minute) and hypertension (systolic BP > 160 mmHg) is at risk of increased intracranial pressure (Cushing’s reflex)

Neurological examination

Cranial nerve assessment is particularly important in stuporous and comatose animals given the high suspicion of a brainstem disorder

Focus on assessment of forebrain (mentation, proprioception, menace response and response to nasal stimulation) and brainstem (proprioception and cranial nerves) functions

MUO typically presents with a multifocal lesion localisation, whereas metabolic disease typically results in symmetrical deficits localising to the forebrain

Ophthalmic examination

Papilloedema (optic disc swelling) is suggestive of increased intracranial pressure

Laboratory findings

Haematology

Assess for signs of severe systemic disease (e.g. marked leukocyte changes supportive of an inflammatory focus)

Increased PCV in primary erythrocytosis (typically > 68%)

May reveal microcytosis ± hypochromasia in PSS

Serum biochemistry

Evidence of hepatic dysfunction (low albumin, cholesterol, urea, glucose, increased ammonia) and increased bile acids

Increased liver enzyme activities are not typical in PSS but are detected in other hepatopathies

Hypoglycaemia

Sodium concentrations: review previous results in hospitalised animals to assess for changes in sodium indicating too‐rapid correction of marked hypernatraemia

Imaging

NB: Cross‐sectional imaging (MRI) is often indicated for primary CNS diseases

Plain radiographs

Screening in cases with a high suspicion of multisystemic disorders (e.g. assessing for neoplasia)

Skull radiographs may be useful in cases of head trauma, but rarely in hydrocephalus

Ultrasound

Assess for liver size and echotexture when suspicious of hepatic dysfunction. Renomegaly may also be observed in PSS.

Screening in cases with a high suspicion of multisystemic disorders (e.g. assessing for neoplasia)

Special tests

Assessment of haemostasis (platelet count, buccal mucosal bleeding time, prothrombin time [PT] and activated partial thromboplastin time [aPTT], thromboelastography) to assess for risk of hypo‐ or hypercoagulability where vascular disorder is suspected

Baermann’s technique, AngioDetect

®

or faecal smear to identify

Angiostrongylus

infection

CSF analysis – cytology and biochemistry, PCR for

Toxoplasma

and

Neospora

EEG (electroencephalography) or BAER (brainstem auditory evoked response)

MRI

Response to mannitol or hypertonic saline in patients with suspected increased intracranial pressure

1.5 ANOREXIA/HYPOREXIA/INAPPETENCE

DEFINITION

A decline in food intake through loss of appetite whilst still physically able to eat

Anorexia indicates a complete lack of food intake

Dysorexia is a diminished, disordered or unnatural appetite (

q.v

.

section 1.36

)

Hyporexia is a significant reduction in food intake

Inappetence implies a decline in food intake through either a loss of appetite or a selective appetite

Pseudo‐anorexia is a condition where a dog wants to eat but is unwilling or physically unable to do so because of orthopaedic or neuromuscular dysfunction or pain associated with eating

RELATED CLINICAL SIGNS

Pseudo‐anorexia: the dog may try to eat but stop quickly because of pain or difficulty swallowing

True anorexia: the dog will not attempt to eat, or may turn away as if nauseated

COMMON CAUSES

Anorexia/inappetence

Diabetic ketoacidosis

Drugs: many

Fever

Gastrointestinal (GI) disease

Hepatic disease

Hypercalcaemia

Infectious/inflammatory diseases

Neoplasia

Pain

Pancreatitis

Uraemia

Pseudoanorexia

Dental disease

Abscessed tooth root

Fractured tooth

Oesophagitis

Retrobulbar abscess/periorbital cellulitis

Unpalatable diet

UNCOMMON CAUSES

True anorexia

Anosmia,

q.v

.

section 1.6

Cardiac failure

Drugs

Hypoadrenocorticism

Sialoadenitis

Severe respiratory disease

Advanced neoplasia (primary or metastatic)

Diaphragmatic rupture

Pneumonia

Pleural effusion

Neurological disease

Cerebral oedema

Hydrocephalus

Hypothalamic disease

Congenital cystic lesions

Infection/inflammation

Neoplasia

Trauma

Psychological (food aversion)

Anxiety

Hospitalisation

Loss of companion

Social stress

Pseudo‐anorexia

Blindness

Cranial nerve deficits

Craniomandibular osteopathy

Jaw fracture

Oropharyngeal inflammation/ulceration

Oropharyngeal neoplasia

Osteomyelitis of jaw

Temporal myositis

Temporomandibular joint (TMJ) disease

Jaw locking

TMJ dysplasia or dislocation

Tetanus

Trigeminal neuritis/neuropraxia

DIAGNOSTIC APPROACH

Anorexia/hyporexia are common, non‐specific findings with many potential causes.

Rule out dietary causes, drug administration, stressors.

Determine from history and direct observation whether the dog wants to eat or not and whether it is physically able to.

Pseudo‐anorexia will be caused by a cranial nerve deficit or a lesion in the mouth, pharynx or oesophagus.

Examination of the mouth may require sedation or anaesthesia, and imaging of the skull.

Complete physical examination and relevant lab tests and imaging for causes of true anorexia.

Clinical clues

Predisposition

Craniomandibular osteopathy in WHWT

History

Coughing or other respiratory signs

Does dog attempt to eat and then drop or regurgitate food, or does it avoid food?

Nausea (e.g. signs of lip‐smacking, retching, etc.) in metabolic or GI disease

PU/PD in liver and renal disease

Seizures if intracranial disease

Stressful event leading to food aversion

Traumatic event if jaw fracture

Vomiting and/or diarrhoea with GI disease and hypoadrenocorticism

Weight loss in excess of what is expected from not eating suggests increased energy usage, e.g. metabolic disease, neoplasia, etc.

Clinical examination

Visual inspection

Depression

Drooling saliva

Dyspnoea if cardiac failure

Open mouth if trigeminal neuropraxia or jaw locking

Unilateral exophthalmos if retrobulbar abscess

Physical examination

Abdominal masses palpable

Abnormal lung and heart sounds

Halitosis if oral disease

Pain or resistance on opening mouth if myositis, foreign body (FB) or retrobulbar abscess

Risus sardonicus

, erect ears, muscle stiffness and spasms in tetanus

Temporal muscle atrophy with myositis

Trismus with myositis or TMJ disorder

Laboratory findings

Variable, often within normal limits (WNL)

Haematology

Inflammatory leukogram with infection or inflammatory diseases

Biochemistry

Azotaemia

Plus isosthenuria in renal failure

Pre‐renal (hypersthenuria) in dehydration due to hypodipsia

Hypercalcaemia most frequently associated with malignancy, especially lymphosarcoma and anal sac adenocarcinoma; primary hyperparathyroidism is rare

Hyponatraemia / hyperkalaemia in hypoadrenocorticism

Increased liver enzyme activities, bile acids ± bilirubin in hepatic diseases

Special tests

Complete neurological examination

Multiple depending on suspected condition

1.6 ANOSMIA

DEFINITION

The loss of the sense of smell. The most common reason for presentation is when an owner of a hunting dog perceives their dog has lost the ability to find game, or a detection dog is unable to find the substance it has been trained to seek. Even then, other signs of nasal disease are more likely to prompt presentation.

RELATED CLINICAL SIGNS

Epistaxis, nasal discharge, sneezing

Facial deformity

Temporal muscle atrophy

Xerostomia

COMMON CAUSES

Diseases of the nasal cavity

Lymphoplasmacytic rhinitis

Neoplasia

Sino‐nasal aspergillosis

UNCOMMON CAUSES

Distemper

Forebrain disease

Sensory decline with age

Sensory overload (temporary)

Skull fracture(s)

Trigeminal neuritis

Traumatic/destructive lesions of the cribriform plate

Fungal infection

Neoplasia

DIAGNOSTIC APPROACH

It is difficult to assess olfaction but cranial nerve assessment, in particular nasal sensation, should be undertaken unless there is obvious nasal disease.

Clinical clues

Predisposition

Sino‐nasal aspergillosis in dolichocephalic dogs

History

Sneezing, nasal discharge and epistaxis all indicate nasal disease

Known traumatic event

Neurological signs: depression, obtundation, seizures, visual deficits

Clinical examination

Visual inspection

Epistaxis

Facial deformity

Nasal discharge

Physical examination

Deformity of nasal bones

Lack of air movement through nostrils

Neurological deficits

Laboratory findings

Haematology

Typically unremarkable unless significant blood loss due to epistaxis causing regenerative anaemia

Serum biochemistry

Usually unremarkable unless significant blood loss due to epistaxis causing hypoproteinaemia

Urinalysis

Unremarkable

Imaging

Skull radiographs to look for fractures, turbinate destruction or expansile lesions

CT is preferred as cribriform plate integrity can be assessed

Special tests

Aspergillus

serology not very sensitive but specific

Rhinoscopy with nasal biopsy

1.7 ANURIA/OLIGURIA

DEFINITION

Anuria is defined as a failure of the kidneys to produce urine; oliguria refers to cases with inadequate urine production. IRIS guidelines for acute kidney injury (AKI) define this in the context of fluid volume responsiveness over a 6‐hour period; with anuria defined as no urine produced and oliguria < 1 ml/kg/hour after intravenous fluid therapy to correct dehydration and hypovolaemia. These definitions are useful as part of decision making on whether renal replacement therapy is required.

Failure to produce normal volumes of urine may also occur due to pre‐renal causes (e.g. severe dehydration) and post‐renal causes (e.g. bilateral ureteric obstruction, urethral obstruction, ruptured bladder). These are important exclusions before determining a renal cause for lack of urine production.

RELATED CLINICAL SIGNS

Anuria is normally not the primary concern on presentation in patients; typically systemic causes of lack of glomerular filtration are the primary signs, including vomiting, anorexia, lethargy, or collapse related to potassium or central nervous system disturbances.

Failure to produce urine due to post‐renal causes is most commonly accompanied by stranguria and dysuria (

q.v

.

section 1.19

) except for ureteric causes, where abdominal pain and signs related to anuria may be the primary sign.

COMMON CAUSES

Infectious causes

Leptospirosis

Pyelonephritis

Toxins

Ethylene glycol

Grapes and raisins

Drugs

NSAIDs

Vascular

Severe hypotension or renal ischaemia, e.g. sepsis, multiple organ dysfunction, severe cardiac failure

Miscellaneous

Cutaneous and renal glomerulovasculopathy (CRGV, ‘Alabama rot’)

Hypercalcaemia

UNCOMMON CAUSES

Infectious

Babesia

Leishmania

Vascular

Renal infarction

Miscellaneous

Hyperviscosity, e.g. primary erythrocytosis, hyperglobulinaemia

Myoglobinuria or haemoglobinuria

Drugs

Radiographic contrast agents

ACE inhibitors

Neoplasia

Renal lymphoma likely bilateral if causing reduced glomerular filtration rate

DIAGNOSTIC APPROACH

Anuria or oliguria is usually detected in patients following identification of azotaemia on blood tests, or in systemically unwell patients where urine output is being monitored.

Exclude pre‐renal causes by assessing hydration status, urinary specific gravity (if urine is available), and measuring urinary bladder size and body weight.

Response to intravenous fluid therapy (aim to correct hydration over a 12‐hour period) can be monitored. Even with severe dehydration anuria is not anticipated.

Assess for post‐renal causes by establishing history, passing a urinary catheter and renal imaging to assess bilateral ureteric obstruction (uncommon in dogs). Placement of a urinary catheter is also useful to enable ongoing urinary output monitoring.

Response to furosemide (furosemide stress test) following rehydration can be utilised to determine if functional renal tissue is intact. If the patient does not produce urine in spite of furosemide administration, prognosis for renal recovery without renal replacement therapy is considered guarded.

Clinical clues

Predisposition

Patients that are severely systemically unwell for any reason (e.g. sepsis, pancreatitis) may be vulnerable to anuric AKI

Renal amyloidosis: Shar pei

History

Assess drinking patterns prior to presentation (polyuria and polydipsia may be present in patients with hypercalcaemia‐induced renal injury, or acute on chronic kidney disease)

Exposure to toxins or drugs (especially NSAIDs) inducing renal injury

Risk factors for AKI

CRGV: woodland environment, seasonality

Infectious disease: vaccination status, seasonality, wet environment, and lifestyle for risk of leptospirosis

Clinical examination

Visual inspection

Assess for hydration status (eye position)

Assess for evidence of concurrent systemic disease (e.g. jaundice in leptospirosis or pancreatitis)

Physical examination

Abdominal pain or pyrexia: may increase suspicion of pyelonephritis

Hydration (skin tent, mucous membrane moisture, body weight if recent measurements are available) and volume status (heart rate, mucous membrane colour)

Skin wounds in patients with suspicion of CGRV

Laboratory findings

Haematology

Leukocytosis with neutrophilia and monocytosis and left shift (band neutrophils and toxic change) may increase suspicion of infectious causes

Moderate‐marked poorly regenerative anaemia implies a more chronic process (acute on chronic disease) in the absence of comorbidities

Serum biochemistry

Azotaemia is detected in most oligo/anuric patients, so the degree of azotaemia is not prognostic in AKI. However, failure to produce urine in response to fluid therapy is

Potassium should be monitored closely in anuric patients (q2 hours); intervention may be indicated

Urinalysis is important in discriminating between pre‐renal and renal azotaemia; sediment analysis may detect calcium oxalate monohydrate (ethylene glycol), and may detect evidence of tubular injury (glucosuria esp. in leptospirosis, proteinuria) or increase the suspicion of pyelonephritis (active sediment examination)

Urine cytology submitted in an EDTA tube may be useful in cases with a high suspicion of pyelonephritis

Venous blood gas in ethylene glycol toxicity will display metabolic acidosis with a high anion gap and hypocalcaemia

Imaging

Plain radiographs

Excluding radio‐opaque uroliths as a cause of bilateral ureteric obstruction (uncommon in dogs cf. cats)

In patients with hypercalcaemia to screen for neoplastic causes

Ultrasound

Assess renal perfusion and architecture (small and irregular associated with more chronic disease, pyelonephritis may be detected by renal architectural change and renal pelvis dilation (although not 100% sensitive)), AKI cases may display hyperechoic renal cortices and perirenal retroperitoneal fluid

In patients with hypercalcaemia to screen for neoplastic causes

Special tests

Infectious disease testing, e.g. microscopic agglutination test (MAT) and blood or urine PCR for leptospirosis

Pyelocentesis for cytology and culture in cases with a high suspicion of pyelonephritis

Skin biopsy for histology may increase suspicion of CRGV

Toxin screen including ethylene glycol on urine or blood

1.8 ATAXIA

DEFINITION

Ataxia is defined as uncoordinated voluntary movement. This occurs when there is a dysfunction of the elements of the nervous system that are responsible for coordination. Disorders that can present with ataxia include cerebellar dysfunction, vestibular system dysfunction, and loss of proprioception (sensory).

RELATED CLINICAL SIGNS

Cerebellar ataxia

Can also present with vestibular dysfunction as this involves the cerebellum (flocculonodular lobe)

Hypermetria

Intention tremor

Wide‐based stance

Vestibular ataxia

Bilateral vestibular ataxia presents without a head tilt and falling to both sides, wide excursions of the head, and an uncoordinated gait

Falling/leaning to one side

Head tilt

Nystagmus

Proprioceptive (sensory) ataxia

Abnormal placement of limbs, e.g. crossing over legs when walking, or pacing (forelimb and hindlimb strides at the same time), knuckling

May stumble, e.g. stepping over objects

COMMON CAUSES

Cerebellar ataxia

Infectious – protozoal (

Toxoplasma

,

Neospora

),

Angiostrongylus vasorum

Inflammatory – meningoencephalitis of unknown origin

Neoplasia

Vascular – haemorrhagic or thromboembolic stroke

Vestibular ataxia

Peripheral vestibular

Cranial polyneuropathy (possible link with hypothyroidism)

Idiopathic (old dog vestibular)

Neoplasia

Otitis media

Central vestibular (brainstem or cerebellar)

Cerebellar disorders as above

Inflammatory – meningoencephalitis of unknown origin

Neoplasia

Trauma

Proprioceptive (sensory) ataxia

Degenerative disease, e.g. canine degenerative myelopathy (CDM)

Drug‐induced

Fibrocartilaginous embolism (FCE)

Intervertebral disc disease

Neoplasia

UNCOMMON CAUSES

Cerebellar ataxia

Cerebellar abiotrophy

Storage disease

Trauma

Vestibular ataxia

Central vestibular (brainstem or cerebellar)

Cerebellar disorders as above

Drug‐induced, e.g. metronidazole toxicity

Hyperviscosity: erythrocytosis, hyperglobulinaemia including multiple myeloma

Peripheral vestibular

Storage disease

Trauma

Proprioceptive (sensory) ataxia

Inflammatory – meningomyelitis

DIAGNOSTIC APPROACH

Clinical clues

Predisposition

Canine degenerative myelopathy is present in numerous breeds; German shepherd dogs (GSDs) are predisposed

Cerebellar abiotrophy has been described in more than 40 breeds of dog; there are neonatal (e.g. beagles), juvenile (e.g. Airedale terrier) and adult onset (Bernese mountain dog) disorders

Greyhounds are predisposed to thromboembolic cerebellar events (ischaemic stroke)

History

Duration and progression of signs may aid in index of suspicion (acute onset improving increases suspicion of vascular or drug‐induced, gradual onset progression may increase suspicion of degenerative or neoplastic disease, acute onset rapid progression may increase suspicion of inflammatory or infectious disease)

Clinical examination

Visual inspection

Mentation (

q.v

.

sections 1.3

,

1.4

) is expected to be impaired with central brainstem vestibular disorders

Physical examination

Thorough examination to assess for multisystemic disease

Neurological examination

Cerebellar: ipsilateral loss of proprioception and menace response, contralateral head tilt and direction of fast phase of nystagmus (paradoxical vestibular)

Proprioceptive ataxia: abnormal conscious and unconscious proprioception

Vestibular: head tilt and nystagmus

In brainstem disorders consciousness may be reduced and other cranial nerves may be affected, e.g facial nerve (blink reflex) and glossopharyngeal and vagal nerves (gag reflex)

Peripheral disorders may detect concurrent facial nerve abnormalities and Horner’s syndrome

Ophthalmic examination

May be useful to assess for infiltrative central nervous system disease, e.g. may detect papilloedema

Laboratory findings

Haematology