Myocardial Failure in a Two-Toed Sloth (Choloepus didactulus)
IAAAM 2000
Stuart Ray Rosenburg1, DVM; Patti S. Snyder2, DVM, MS, DACVIM
1Silver Springs Attraction, Silver Springs, FL, USA; 2Department of Small Animal Medicine, College of Veterinary Medicine, University of Florida, Gainesville, FL, USA

Abstract

A greater than 20-yr-old two-toed sloth (Choloepus didactulus) presented for weakness and falling off his perch for a 2-day duration. Radiographs, abdominocentesis, and ultrasound revealed myocardial failure. He was successfully treated with oral furosemide, enalapril, digoxin and taurine.

Case Report

On 26 May 1999, a greater than 20-yr-old two-toed sloth presented for weakness, ataxia, and falling off his perch for a 2-day duration. The physical examination required only minimal manual restraint and revealed pale mucous membranes, a capillary refill time of approximately 2 sec, severe generalized pitting edema, a distended abdomen, a core body temperature of 30°C (normal = 24-33°C), a respiratory rate of 40 bpm, and a body weight of 8.5 kg (normal for this animal: 5.5-6.2 kg). The pitting edema interfered with palpation and auscultation of the heart, and the cause of the distended abdomen could not be determined at presentation.

Differential diagnoses for generalized edema were decreased plasma oncotic pressure from hypoproteinemia (hepatic failure, protein losing nephropathy or enteropathy, malabsorption, severe malnutrition, endoparasitism) increased plasma hydrostatic pressure (congestive heart failure), generalized vascular disease allowing exudation of fluid into the subcutaneous tissues (vasculitis) or neoplasia.

Because of the severe edema, acquisition of blood samples was not possible. Thoracic radiography revealed enlargement of the cardiac silhouette and an interstitial pattern in the caudal dorsal lung fields. Abdominal radiographs showed a large cecum and loss of detail in the peritoneal cavity. Abdominocentesis was performed, and a clear colorless fluid was easily obtained. Limited in- house analysis of the fluid showed a total protein of 2.4 g/dl; the sediment showed low numbers of red blood cells and occasional white blood cells. These findings were consistent with that of a modified transudate. A direct fecal examination and fecal floatation were negative for parasites and no external parasites were observed. A free-catch urine sample, obtained 3 hr after the administration of furosemide (3 mg/kg i.m., Lasix®, Hoecht Roussel Vet, Sommerville, NJ 08876 USA), was isosthenuric. The remainder of the urinalysis was unremarkable by dipstick (Multistix®, Bayer Corporation, Elkhart, IN 46515 USA) and microscopic evaluation. The most likely differential diagnoses for the enlarged cardiac silhouette were cardiomegaly (from myocardial disease such as dilated or hypertrophic cardiomyopathy; valvular heart disease such as endocarditis, or heartworm disease) or pericardial effusion. Protein-losing nephropathy was unlikely to be a cause for the peripheral edema because of the lack of proteinuria. Protein-losing enteropathy was an unlikely cause since the feces were normal; however, measurement of a normal serum protein would be necessary to exclude it from the differential diagnosis list. Until blood was obtained to evaluate the complete blood count and serum biochemistry panel, hepatic disease was also a consideration. Systemic infection and neoplasia were considered less likely but additional diagnostics would be necessary to exclude these differentials. Furosemide was initiated (3 mg/kg i.m. q 12 hr) pending the abdominal fluid analysis results. The animal was admitted to the hospital and given lactated Ringer's solution (350 ml s.c., Abott Laboratories, North Chicago, IL 60064 USA and thiamine (50 mg s.c., Vitamin B Complex, Phoenix Scientific, Inc., St. Joseph, MO 64508 USA) to help keep him hydrated and to act as an appetite stimulant, respectively.

The following day the sloth was more responsive and he did eat his normal diet of primate chow and mixed vegetables overnight. Abdominocentesis was performed again to remove 350 ml of clear colorless fluid. Furosemide was continued. Cytologic evaluation (Antech Diagnostics®, Farmingdale, NY 11735 USA) supported the finding of a modified transudate in the abdomen and the suspicion of primary heart cardiac disease in conjunction with radiographic evidence of an enlarged cardiac silhouette.

Ultrasound examination 7 days after presentation showed generalized cardiac enlargement and suspect heartworms in the right atrium. The edema was resolving slowly, and blood from the femoral vein was obtained with ultrasound guidance. Multiple serologic heartworm tests were run to investigate the suspicion of heartworm infection as the cause of right heart failure; antigen tests (Dirochek® Synbiotics, San Diego, CA 92127 USA and Snap® Idexx, Westbrook, ME 04092 USA), a modified Knott test, and direct blood smear examination were all negative for heartworm infection. Heartworm antibody tests were not performed, as they are host species dependent tests. A complete blood count was within normal limits. The chemistry panel showed azotemia with an increase in BUN (160 mg/dl; normal 7-100 mg/dl). All other values were within acceptable limits. Although the ascites could be explained by right heart failure secondary to heartworms, the generalized edema could not.

After internal medicine consultation the presumed pulmonary hypertension and right heart failure secondary to heartworm infection, amlodipine (Norvasc®, Pfizer, New York, NY 10017 USA), a pure arteriodilator, was initiated at the accepted feline dose (0.18 mg/kg p.o. q 24 hr).1 Amlodipine has shown promise in managing pulmonary hypertension in humans.3 Prednisone (1 mg/kg p.o. q 24 hr for 10 days and then q 48 hr) was administered since the interstitial lung pattern could also be consistent with pneumonitis. The furosemide dosage was decreased to 3 mg/kg p.o. q 24 hr. Oral medications were compounded at Frank's Pharmacy, Ocala, FL 34474 USA to increase patient compliance. Follow up radiographs of the thorax after the change in medications showed a marked decrease in the cardiac silhouette and interstitial pattern in the lung fields, as well as, an overall decrease in the subcutaneous edema. The furosemide dose was reduced further to 2 mg/kg p.o. q 24 hr. Milbemycin (5.75 mg monthly, Interceptor®, Novartis, Greensboro, NC 27404 USA) was added to protect the sloth from future heartworm infection.

Eight weeks after the initial presentation, the sloth was transported to the University of Florida Veterinary Medical Teaching Hospital (UFVMTH) for echocardiography and abdominal ultrasonography. Heartworms were not visualized using two dimensional echocardiography in any of the heart chambers including the pulmonary artery. Left ventricular contractility appeared reduced and the left atrium appeared enlarged (Table 1). Abdominal ultrasound showed no obvious abnormalities and an absence of abdominal fluid. Because no evidence of heartworms were seen during the echocardiographic study and the belief that myocardial failure was present, the prednisone was discontinued.

It was recommended that a normal sloth be examined for comparison since the sloth is an unusual animal, and there are no established normal echocardiographic values. Because the only other two-toed sloth available for examination was the pregnant mate, this comparison study was delayed until after parturition and the early neonatal period. An examination of the female sloth was performed at UFVMTH on 8/10/99. After confirmation that the echocardiographic values of the male sloth were substantially different from the normal female values (Table 1), a diagnosis of myocardial failure was made for the male sloth. Medication was adjusted as follows: amlodipine was discontinued; enalapril (0.5 mg/kg p.o. q 24 hr, compounded at Frank's Pharmacy, Ocala, FL 34474 USA) and digoxin (0.007 mg/kg p.o. q 48 hr, Cardoxin® Evsco Pharmaceuticals, Buena, NJ 08310 USA) were initiated. The sloth was closely monitored for any change in appetite or behavior. Ten days after starting the digoxin, a 7 hr post medicating level was low (0.2 ng/ml, normal 0.8-2 ng/ml). The digoxin dose was subsequently increased (0.01 mg/kg p.o. q 48 hr) and taurine (45 mg/kg p.o. s.i.d., Pet Ag, Hampshire, IL 60140 USA) was added. A plasma taurine concentration was not obtained prior to supplementation.

The sloth continued to improve and a desire to replace the sloth in his exhibit prompted a follow-up examination at the UFVMTH 6 mo after presentation (Table 1). The current medications were furosemide (1 mg/kg p.o. q 24 hr), enalapril (0.5 mg/kg p.o. q 24 hr), taurine (45 mg/kg p.o. q 24 hr), and digoxin (0.01 mg/kg p.o. q 48 hr). Periodic reevaluations of the CBC, plasma biochemistries, and digoxin level were scheduled, and necessary adjustments in medications would be dictated by the serum digoxin concentrations and the results of the biochemistry panel.

He was released to the care of the zoo staff for his medications and reintroduced to his mate and offspring. Shortly after his return to the home exhibit, breeding behavior was observed. Unfortunately, the animal died of non-heart related complications in January 2000.

Table 1. Significant echocardiographic findings.

Measurement

Normal female sloth
10 August 1999

Affected male sloth
22 July 1999

Affected male sloth
16 November 1999

LVIDD (cm)

1.3

1.8-2.1

1.4-1.9

   

mean = 1.9

mean = 1.6

LVIDS (cm)

0.6

1.4-1.5

0.9-1.3

     

mean = 1.2

LAA (cm)

1.4

1.9

1.7

LAA:Ao (cm)

1.75

1.9

1.3

LVIDD = left ventricular diameter during diastole; LVIDS = left ventricular diameter during systole; LAA = left atrial appendage; Ao= aortic root diameter

References

1.  Snyder PS. 1998. Amlodipine: A randomized blinded clinical trial in cats with systemic hypertension. J. Vet. Int. Med. 12: 157-162.

2.  Woodmansey PA, F Zhang, KS Channer, et al. 1993. Vasodilatory action of the calcium antagonist amlodipine on large and resident pulmonary arteries from normoxic and chronically hypoxic rats. Clin. Sci. 85: 361-366.

3.  Sajkov D, T Wang, PA Frith, et al. 1997. A comparison of two long acting vasoselective calcium antagonists in pulmonary hypertension secondary to COPD. Chest 111: 1622-1630.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Patti S. Snyder, DVM, MS, DACVIM

Stuart Ray Rosenburg, DVM


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