1.2 Canine Common Clinical Diseases & Medicine

1.2 Canine Common Clinical Diseases & Medicine

Understanding the pathophysiology, clinical presentation, diagnostic approach, and management of common canine diseases is a cornerstone of the NAVLE.

1. Canine Parvovirus Enteritis

Canine Parvovirus (CPV-2) is a highly contagious, stable virus that targets rapidly dividing cells, specifically the crypt cells of the small intestinal mucosa and hematopoietic progenitor cells in the bone marrow.

• Pathophysiology: Destruction of intestinal crypt cells leads to villous atrophy, severe malabsorption, and mucosal barrier breakdown, predisposing the dog to bacterial translocation. Concurrently, bone marrow destruction leads to severe leukopenia and neutropenia, leaving the patient vulnerable to sepsis.
• Clinical Signs: Acute onset of severe, hemorrhagic diarrhea, projectile vomiting, anorexia, lethargy, fever, and hypovolemic shock.
• Diagnostics: Fecal ELISA antigen test is the standard diagnostic tool. False negatives can occur if tested very early in the disease course or after the shedding window has passed. False positives may occur 4–10 days following vaccination with a modified live virus vaccine.
• Therapeutic Management: Intensive supportive care is critical. This includes aggressive intravenous fluid therapy (isotonic crystalloids, supplemented with potassium chloride and dextrose as needed, plus colloids if hypoalbuminemic), antiemetics (e.g., maropitant and metoclopramide), and broad-spectrum intravenous antibiotics (e.g., ampicillin and enrofloxacin) to prevent sepsis. Early enteral nutrition via a nasoesophageal or nasogastric tube is associated with faster mucosal healing and improved survival.

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2. Immune-Mediated Hemolytic Anemia (IMHA)

IMHA is a type II hypersensitivity reaction where antibodies (typically IgG or IgM) target erythrocyte membrane antigens, leading to premature destruction of red blood cells.

• Pathophysiology: RBCs are destroyed intravascularly (complement-mediated lysis) or, more commonly, extravascularly by splenic and hepatic macrophages. Macrophages may partially phagocytize the erythrocyte membrane, resulting in spherocytes—small, dense RBCs that lack central pallor.
• Clinical Signs: Pale mucous membranes, icterus, lethargy, tachypnea, tachycardia, splenomegaly, and pigmenturia (hemoglobinuria/bilirubinuria).
• Diagnostics: Hallmark findings include a regenerative anemia (in acute cases, it may initially be non-regenerative for 3–5 days), marked spherocytosis, a positive saline agglutination test (visualized as macro- or microscopic clumping that persists after adding normal saline, which differentiates it from rouleaux), and a positive Coombs' test.
• Therapeutic Management: Immunosuppression is the primary treatment, initiated with prednisone (2.0–4.0 mg/kg/day) or dexamethasone, often combined with secondary agents like cyclosporine or mycophenolate mofetil. To address the hypercoagulable state and prevent pulmonary thromboembolism (PTE)—the leading cause of death in IMHA patients—antithrombotic therapy using clopidogrel, low-dose aspirin, or heparin must be initiated immediately.

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3. Dilated Cardiomyopathy (DCM)

DCM is a primary myocardial disease characterized by decreased myocardial contractility (systolic dysfunction), which leads to eccentric hypertrophy and dilation of the cardiac chambers, primarily the left ventricle and atrium.

• Clinical Signs & Breeds: Primarily affects large and giant breeds (Doberman Pinscher, Great Dane, Irish Wolfhound, Boxer). Signs include exercise intolerance, cough, dyspnea, syncope, weak femoral pulses, and ascites due to congestive heart failure (CHF). Boxers can present with a specific phenotype characterized by ventricular arrhythmias, often called Boxer cardiomyopathy (ARVC).
• Diagnostics: Thoracic radiographs show generalized cardiomegaly and pulmonary venous congestion. Electrocardiography (ECG) may show ventricular premature contractions (VPCs), ventricular tachycardia, or atrial fibrillation. Echocardiography is the diagnostic standard, showing left ventricular dilation and reduced fractional shortening (FS).
• Therapeutic Management: Medical management for dogs in CHF consists of the "quadruple therapy": diuretics (furosemide), positive inotropes (pimobendan), ACE inhibitors (enalapril or benazepril), and aldosterone antagonists (spironolactone). Ventricular tachyarrhythmias are managed with sotalol or mexiletine.

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4. Hypoadrenocorticism (Addison's Disease)

Addison's disease is caused by immune-mediated destruction of the adrenal cortex, leading to a deficiency in both glucocorticoids (cortisol) and mineralocorticoids (aldosterone).

• Pathophysiology: Aldosterone deficiency impairs sodium retention and potassium excretion by the distal renal tubules, resulting in hyponatremia, hyperkalemia, and severe hypovolemia. Cortisol deficiency causes gastrointestinal signs and hypoglycemia, and prevents the body from handling stress.
• Clinical Signs: Often called "The Great Imitator" because signs are waxy and waning. Signs include vomiting, diarrhea, lethargy, anorexia, weight loss, and bradycardia in the face of hypovolemic shock.
• Diagnostics: Classic blood work reveals a sodium-to-potassium ratio < 27:1 (often < 23:1), mild to moderate azotemia, and the absence of a stress leukogram (i.e., lymphocytosis or eosinophilia in a critically ill patient). The definitive test is the ACTH stimulation test, which shows a flatline cortisol concentration (< 2.0 µg/dL post-ACTH).
• Therapeutic Management: Acute Addisonian crisis is a life-threatening emergency treated with aggressive fluid therapy (0.9% NaCl is preferred), dexamethasone (which does not cross-react with the cortisol assay), and treatment for hyperkalemia if severe (calcium gluconate to protect the myocardium, dextrose, and insulin). Long-term maintenance requires mineralocorticoid replacement with desoxycorticosterone pivalate (DOCP) injections every 25–30 days and daily oral prednisone.

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5. Hyperadrenocorticism (Cushing's Disease)

Cushing's disease is characterized by chronic overproduction of cortisol. It is classified as pituitary-dependent hyperadrenocorticism (PDH) (80–85% of cases, caused by a pituitary adenoma) or adrenal-dependent hyperadrenocorticism (ADH) (15–20% of cases, caused by a functional adrenal tumor).

• Clinical Signs: Polyuria, polydipsia, polyphagia, abdominal distension ("pot-bellied" appearance due to muscle wasting and hepatomegaly), bilateral symmetrical alopecia, thin skin, and calcinosis cutis.
• Diagnostics: Common screening tests include the Low-Dose Dexamethasone Suppression Test (LDDST), where a lack of cortisol suppression at 8 hours is diagnostic, and the ACTH stimulation test. Differentiation between PDH and ADH is achieved via a High-Dose Dexamethasone Suppression Test (HDDST), endogenous ACTH levels, or abdominal ultrasound (which shows bilateral symmetrical adrenal enlargement in PDH, and a unilateral mass with contralateral atrophy in ADH).
• Therapeutic Management: Pituitary-dependent cases are medically managed using trilostane (a reversible inhibitor of 3-beta-hydroxysteroid dehydrogenase) or mitotane (an adrenolytic agent). Adrenal tumors are best treated via surgical adrenalectomy.

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6. Chronic Kidney Disease (CKD) & IRIS Staging

CKD is defined as structural or functional kidney damage persisting for at least 3 months. Staging is based on stable blood creatinine and symmetric dimethylarginine (SDMA) concentrations, measured on at least two occasions in a hydrated patient.

International Renal Interest Society (IRIS) Stages

• Stage 1: Creatinine < 1.4 mg/dL (SDMA < 18 µg/dL). No azotemia, but renal abnormalities (e.g., proteinuria, abnormal imaging) are present.
• Stage 2: Creatinine 1.4–2.8 mg/dL (SDMA 18–35 µg/dL). Mild renal azotemia; clinical signs are typically absent or mild.
• Stage 3: Creatinine 2.9–5.0 mg/dL (SDMA 36–54 µg/dL). Moderate renal azotemia; systemic signs (e.g., polyuria, polydipsia, anemia, uremic ulcers) are common.
• Stage 4: Creatinine > 5.0 mg/dL (SDMA > 54 µg/dL). Severe renal azotemia; patient is at high risk for systemic crisis and uremic encephalopathy.

Substaging Criteria

Substaging is based on:

1. Proteinuria: Assessed by the Urine Protein-to-Creatinine (UPC) ratio. For dogs, a UPC < 0.2 is non-proteinuric, 0.2–0.5 is borderline proteinuric, and > 0.5 is proteinuric.
2. Blood Pressure: Based on systolic blood pressure (BP):
   • Normotensive: < 140 mmHg (minimal risk of target organ damage)
   • Borderline hypertensive: 140–159 mmHg (low risk)
   • Hypertensive: 160–179 mmHg (moderate risk)
   • Severely hypertensive: >= 180 mmHg (high risk)

• Therapeutic Management: Consists of therapeutic renal diets (restricted phosphorus, moderate high-quality protein), intestinal phosphate binders (aluminum hydroxide) if target phosphorus levels are not met, subcutaneous fluids, ACE inhibitors (e.g., enalapril) or angiotensin receptor blockers (e.g., telmisartan) for proteinuria, and amlodipine for hypertension.

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7. Diabetes Mellitus (DM)

Diabetes mellitus in dogs is almost exclusively insulin-dependent (Type 1-like), resulting from immune-mediated destruction of pancreatic beta cells.

• Clinical Signs: Classic tetrad of polyuria, polydipsia, polyphagia, and progressive weight loss. Bilateral cataract formation due to sorbitol accumulation in the lens is a common, rapid complication.
• Diagnostics: Persistent fasting hyperglycemia (> 200 mg/dL) and concurrent glucosuria. If diabetes is complicated, it can progress to diabetic ketoacidosis (DKA), marked by ketonuria, metabolic acidosis, vomiting, dehydration, and depression.
• Therapeutic Management: Requires life-long twice-daily insulin therapy (e.g., NPH or Lente [Vetsulin]) combined with a high-fiber, low-simple-carbohydrate diet fed in equal portions concurrent with insulin administration. Consistent exercise is important to maintain stable glycemic control.

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8. Pancreatitis

Pancreatitis is caused by premature activation of digestive zymogens (specifically trypsinogen) within the pancreatic acinar cells, leading to local autodigestion, inflammation, and potential systemic inflammatory response syndrome (SIRS).

• Clinical Signs & Risk Factors: Often precipitated by ingestion of a high-fat meal. Predisposing factors include obesity and hyperlipidemia (particularly in Miniature Schnauzers). Signs include acute vomiting, anorexia, depression, and severe cranial abdominal pain (dogs may assume a "praying position").
• Diagnostics: Spec cPL (canine pancreatic lipase immunoreactivity) is the most sensitive and specific blood test. Abdominal ultrasound shows a hypoechoic pancreas surrounded by hyperechoic, inflamed mesentery (fat necrosis).
• Therapeutic Management: Treatment is supportive. Aggressive intravenous fluid therapy is vital to maintain pancreatic microperfusion. Pain management is paramount, using pure mu-agonist opioids (e.g., methadone, fentanyl). Antiemetics (maropitant) must be administered. Early enteral nutrition should be instituted as soon as vomiting is controlled.