Blackwell's Five-Minute Veterinary Consult: Reptile and Amphibian. Javier G. Nevarez
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Author Christopher S. Hanley, DVM, DACZM
Cardiac Disease
BASICS
DEFINITION/OVERVIEW
Cardiovascular disease encompasses a group of disorders of the heart and blood vessels including:
Cardiomyopathy
Septic endocarditis
Valvular insufficiency (with no current evidence of primary degenerative endocardiosis)
Myocarditis
Pericardial effusion
Infarct
Atherosclerosis
Aneurysm (rupture of aortic or carotid aneurysm)
Gout
Arterial calcification
Thrombus
Parasitic infestations
Congenital heart defects
Tumors
ETIOLOGY/PATHOPHYSIOLOGY
Infectious
Often secondary to systemic infections in captive reptiles.
Bacterial: aerobic Gram‐negative bacteria: Salmonella spp., Corynebacterium spp., Pseudomonas spp. (endocarditis). Flavobacterium spp. and Vibrio spp. in a Barber’s map turtle (Graptemys barbouri) (myocarditis).
Parasitic: Trematodes (spirorchid flukes: Spirorchis spp., Learedius spp.) have been reported in the heart chambers and major vessels of sea and freshwater turtles (Chelonia mydas, Trachemys scripta elegans, Chrysemys picta), causing arteritis, endocarditis, granulomatous myocarditis, thrombosis and aneurysm.
Non‐Infectious
Neoplastic (primary neoplasia is uncommon in reptiles): hemangioma, hemangiosarcoma, cardiac rhabdomyosarcoma, fibrosarcoma; disseminated coelomic papillomas affecting various organs, including the heart, are frequently found in sea turtles with fibropapillomatosis.
Metastasis to the heart: metastatic chondrosarcoma, metastasis of oviductal adenocarcinoma, disseminated mast cell tumor, multicentric lymphoblastic lymphoma and lymphoblastic malignant lymphoma.
Metabolic: visceral gout can cause urate crystals deposition in the pericardium.
Cardiomyopathy is of undetermined origin in reptiles. Myocardial degeneration can be the consequence of gout (of metabolic, nutritional or iatrogenic origin) and/or vitamin E and selenium deficiencies. The myocardium and the major arteries may also be subject to mineralization (calcification) with a diet of excessive levels of calcium and vitamin D3.
Pericardial effusion is reported in many species but a small amount of fluid within the pericardial sac may also be normal. The etiology of pathologic pericardial effusion is unknown.
SIGNALMENT/HISTORY
There are no known species, sex, or age predilections.
Weakness and dyspnea
Swelling in the area of the neck and/or peripheral edema.
CLINICAL PRESENTATION
Presentation is similar to that seen in mammals.
Some differences exist due to differing cardiovascular physiology and anatomy.
Non‐specific clinical signs such as lethargy, depression, anorexia, weight loss, weakness, dyspnea, bilateral exophthalmia, and sudden death.
Cyanosis
Peripheral edema (e.g., in gular region)
Pulmonary edema, ascites
Neurological signs such as ataxia and head tilt in case of brain anoxia.
Peripheral thrombosis and necrosis in case of filarial infestation of the cardiovascular system.
Coughing is not a feature of congestive heart failure as observed in mammals.
RISK FACTORS
Husbandry
Inadequate husbandry, resulting in chronic stress, immune suppression and malnutrition, is the most likely common predisposing factor for the development of cardiovascular conditions in captive reptiles.
Others
Atherosclerosis and viral diseases can also be predisposing factors.
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
All other diseases that induce lethargy and/ or respiratory distress.
DIAGNOSTICS
Ambient temperature can influence cardiopulmonary parameters in reptiles so must be considered during examination.