Objective—To determine the minimal ultrasonic aspirator
pressure necessary to damage the cerebral cortex
of healthy dogs.
Animals—9 mixed-breed dogs.
Procedure—The study comprised 2 parts. In part A,
6 dogs were euthanatized immediately prior to the
experiment. In part B, 3 dogs were anesthetized for
recording of physiologic variables. In both parts,
craniectomy and durotomy were performed to bilaterally
expose the lateral aspect of the cerebral cortex.
An ultrasonic aspirator was placed in contact with various
areas of the cerebral cortex, and aspirator power
was altered (10, 20, 30, and 40%). Duration of contact
at each power was 5 and 10 seconds.
Subsequently, gross morphologic and histologic damage
was assessed in the cortex.
Results—Gross observations for all dogs were similar.
At 10% power, visible or histologic damage was
not evident in the cortex. At 20% power, the cortex
was slightly indented from contact with the hand
piece; however, cortical disruption was not evident.
Cortical disruption was initially detectable at 30%
power in some dogs and was consistently evident at
40% power in both sets of dogs.
Conclusions and Clinical Relevance—Ultrasonic
aspirator power of < 20% created minimal acute morphologic
damage to the cortex. Power settings
between 20 and 30% may superficially damage the
cerebral cortex in healthy dogs, whereas 40% power
consistently damages the cerebral cortex. Knowledge
of the degree of damage to cerebral cortex caused by
various amounts of power for ultrasonic aspirators
will allow surgeons to avoid damaging normal brain
tissues during surgery. (Am J Vet Res 2001;62:
To compare serum cardiac troponin I (cTnI) concentrations between sea otters with and without cardiomyopathy and describe 2 cases of cardiomyopathy with different etiologies.
25 free-ranging southern sea otters (Enhydra lutris nereis) with (n = 14; cases) and without (11; controls) cardiomyopathy and 17 healthy managed southern sea otters from aquariums or rehabilitation centers (controls).
Serum cTnI concentration was measured in live sea otters. Histopathologic and gross necropsy findings were used to classify cardiomyopathy status in free-ranging otters; physical examination and echocardiography were used to assess health status of managed otters. Two otters received extensive medical evaluations under managed care, including diagnostic imaging, serial cTnI concentration measurement, and necropsy.
A significant difference in cTnI concentrations was observed between cases and both control groups, with median values of 0.279 ng/mL for cases and < 0.006 ng/mL for free-ranging and managed controls. A cutoff value of ≥ 0.037 ng/mL yielded respective sensitivity and specificity estimates for detection of cardiomyopathy of 64.3% and 90.9% for free-ranging cases versus free-ranging controls and 64.3% and 94.1% for free-ranging cases versus managed controls.
CONCLUSIONS AND CLINICAL RELEVANCE
Cardiomyopathy is a common cause of sea otter death that has been associated with domoic acid exposure and protozoal infection. Antemortem diagnostic tests are needed to identify cardiac damage. Results suggested that serum cTnI concentration has promise as a biomarker for detection of cardiomyopathy in sea otters. Serial cTnI concentration measurements and diagnostic imaging are recommended to improve heart disease diagnosis in managed care settings.