Clinical presentation, diagnosis, treatment, and outcome in 8 dogs and 2 cats with global hypoxic-ischemic brain injury (2010-2022)

Abstract

Background: Global hypoxic-ischemic brain injury (GHIBI) results in variable degrees of neurological dysfunction. Limited data exists to guide prognostication on likelihood of functional recovery.

Hypothesis: Prolonged duration of hypoxic-ischemic insult and absence of neurological improvement in the first 72 hours are negative prognostic indicators.

Animals: Ten clinical cases with GHIBI.

Methods: Retrospective case series describing 8 dogs and 2 cats with GHIBI, including clinical signs, treatment, and outcome.

Results: Six dogs and 2 cats experienced cardiopulmonary arrest or anesthetic complication in a veterinary hospital and were promptly resuscitated. Seven showed progressive neurological improvement within 72 hours of the hypoxic-ischemic insult. Four fully recovered and 3 had residual neurological deficits. One dog presented comatose after resuscitation at the primary care practice. Magnetic resonance imaging confirmed diffuse cerebral cortical swelling and severe brainstem compression and the dog was euthanized. Two dogs suffered out-of-hospital cardiopulmonary arrest, secondary to a road traffic accident in 1 and laryngeal obstruction in the other. The first dog was euthanized after MRI that identified diffuse cerebral cortical swelling with severe brainstem compression. In the other dog, spontaneous circulation was recovered after 22 minutes of cardiopulmonary resuscitation. However, the dog remained blind, disorientated, and ambulatory tetraparetic with vestibular ataxia and was euthanized 58 days after presentation. Histopathological examination of the brain confirmed severe diffuse cerebral and cerebellar cortical necrosis.

Conclusions and clinical importance: Duration of hypoxic-ischemic insult, diffuse brainstem involvement, MRI features, and rate of neurological recovery could provide indications of the likelihood of functional recovery after GHIBI.

Keywords: canine; cerebral; feline; hypoxia; ischemic.

FIGURE 1

Magnetic resonance images of the head of a 1.5‐year‐old Maine Coon cat that presented for further investigation of cluster seizures after prolonged recovery from general anesthesia for a dental procedure. T2‐weighted (A and C) and T2‐weighted FLAIR (B and D) transverse images at the level of the interthalamic adhesion (A and B) and medial geniculate nuclei (C and D) show mild, ill‐defined areas of hyperintensity of the cerebral gray matter (arrows) of the parietal and occipital lobes secondary to presumed global HIBI. Hyperintensities are reported relative to normal gray matter.

FIGURE 2

Magnetic resonance images of the head of a 2.5‐year‐old intact male spaniel crossbreed dog that presented after cardiopulmonary arrest and successful resuscitation at the referring veterinary surgeon's hospital. T2‐weighted sagittal (A) and transverse images at the level of the head of the caudate nuclei (B) and rostral colliculi (C) show a diffusely swollen brain with almost complete obliteration of the cerebral sulci (arrowheads) and ventricular compression. There is diffuse bilateral subtle to moderate loss of gray and white matter differentiation. These changes are more severe dorsally within the parietal and occipital lobes. There is caudal transtentorial herniation (asterisk) with compression and caudal displacement of the rostral cerebellum. Additionally, the cerebellum is protruding into the foramen magnum (arrow) with severe compression of the underlying medulla oblongata. The cervical spinal cord is swollen with obliteration of the surrounding cerebrospinal fluid signal. The caudal aspect of the nasal cavity, nasopharynx, caudal aspect of the oral cavity and frontal sinuses contains T2W hyperintense material (likely compatible with regurgitation of gastric contents). Hyperintensities are reported relative to normal gray matter.

FIGURE 3

Gross pathology and histopathology of the brain of a 2.5‐year‐old intact male spaniel crossbreed dog that was euthanized after in‐hospital cardiopulmonary arrest. (A) Head and proximal cervical spinal cord with the caudodorsal calvarium and dorsal vertebral column removed. The cerebellum is positioned caudally within the skull (associated with in situ foramen magnum herniation) and the brainstem and proximal cervical spinal cord are reddened (arrow). (B) Cerebellum, Hematoxylin & eosin (H&E). Mild cerebellar edema in the granular cell layer (asterisk). Scale bar, 500 μm. (C) Proximal cervical spinal cord, H&E. Multifocal areas of acute hemorrhage expanding the gray and white matter (arrow). Scale bar, 250 μm.

FIGURE 4

A 6‐month‐old intact male Weimaraner that presented after an out‐of‐hospital cardiopulmonary arrest secondary to trauma. (A and B) CT reconstruction of the head showed no evidence of head trauma. (C and D) MRI of the head (T2W sagittal [C] and transverse image at the level of the rostral colliculi [D]) identified diffuse loss of differentiation between cerebral gray and white matter, diffuse cortical hyperintensity on T2W with swelling of the cortical gray matter (asterisk), loss of cerebral sulci, and severe foramen magnum (arrow) and caudal transtentorial herniation (arrowhead) with secondary brainstem compression. These changes were consistent with a global HIBI and euthanasia was elected given the severity of the clinical presentation and MRI findings. Necropsy was not performed. Hyperintensities are reported relative to normal gray matter.

FIGURE 5

Gross pathology and histopathology of the brain of a 7‐month‐old intact male Cocker Spaniel with asphyxiation secondary to laryngeal obstruction. (A) Cerebrum, formalin fixed serial sections. Severe thinning and discoloration of the parietal and temporal cerebral cortex (arrows). (B) Cerebrum, H&E sections corresponding to (A). Diffuse pallor of the cortical gray matter with areas of neuropil loss. Scale bars, 5 mm. (C) Occipital cortex, H&E. Severe cortical spongiosis and necrosis (asterisk) with neovascularization. Scale bar, 1 mm. (D) Hippocampus, CA1 region, H&E. Severe neuronal degeneration (arrow) and loss. Scale bar, 100 μm. (E) Cerebellar folia, H&E. Marked Purkinje cell loss. Scale bar, 250 μm.