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Washington University Experience | VASCULAR | Cardiac Arrest Encephalopathy | 6A0 Case 6 History
Case 6 History ---- The patient was 3170 gram full-term product of an uncomplicated pregnancy born to a 27 year old gravida 2, para 1, Ab O mother. The labor and delivery were complicated by fetal heart rate decelerations (with heart rate fall to 60) within 1 hour prior to delivery. At the time of delivery, the patient was heavily meconium stained. The Apgars were 1 and 1 at 1 and 5 minutes. The patient received cardiopulmonary resuscitation in the delivery room, receiving multiple doses of sodium bicarbonate. The initial capillary blood gas on 100% 02: pH 6.76, p02 143, pC02 47. Within the first few hours of life the infant developed jittery movements of the left upper extremity and fixed 3 mm. pupils. He was transferred to SLCH for further care. Admission examination was remarkable for a comatose infant, intubated, lying still with occasional jittery movements of the left upper extremity. On neurologic examination, the pupils were 3/3, non-reactive to light. Extra-ocular movements were intact to oculocephalic maneuvers. The corneal reflexes were absent bilaterally, the facies were symmetrical and no gag could be elicited. The infant had no response to pain in the upper or lower extremities. The tone was mildly decreased in all extremities, tendon reflexes could not be elicited. Over the next day, the infant deteriorated. Spontaneous respiratory efforts ceased, he became unresponsive to light and pinch, pupils were 5/5, non-reactive to light, the extra-ocular movements were restricted medially and full laterally to OCMs. The corneal reflexes were present bilaterally. Anterior fontanelle pressure (measured with Ladd monitor) was 165 mm. of water. In addition, the patient developed renal failure. On 3/2 the infant continued to deteriorate. The pupils were 5 mm, non-reactive to light, extra-ocular movements were absent, the corneal reflexes were present bilaterally, but the grimace and gag reflexes were not elicitable. No spontaneous movements were noted. The tone was diffusely increased, more so in the lower hand in the upper extremities. On 3/3 the infant had no corneal reflexes. All extremities were flaccid. Response to pain was present in the right upper extremities; all other extremities had a stereotyped extensor posturing to pain. Tendon reflexes were absent. It was felt that the infant had no evidence of cortical or brainstem function at that time. Ultrasound of the head on 3/1 showed unusual density in the thalami and the parenchyma just lateral to the internal capsule, as well as slit-like ventricles. This was felt to be compatible with either infarction or hemorrhage. LP Performed on 2/28 showed a CSF protein of 182, glucose 77, cells: without acid 5000, with acid 6. .EEG done on 3/1 was severely abnormal due to marked suppression of any activity. The clinical diagnoses were severe birth asphyxia with meconium aspiration with hypoxic ischemic encephalopathy, perithalamic/thalamic infarct vs. hemorrhage, and renal failure. ---- At autopsy coronal sections through the cerebral hemispheres demonstrate focal cortical discoloration with punctate hemorrhage involving the cerebral watershed distribution of the ACA/MCA arteries in the frontal and parietal lobes. In addition, there is evidence of bilateral, roughly symmetrical hemorrhagic necrosis involving the caudate, putamen, and globus pallidus as well as the anterior and mid thalamus. Sections of the uncus show cortical discoloration similar to the ACA-MCA watershed of the frontal lobes without punctate hemorrhages. Coronal sections through the brainstem show discoloration in the reticular formation/tegmentum of the midbrain and ventral medulla.
Examination of the cerebral neocortices in all regions demonstrated diffuse eosinophilic neuronal necrosis with scattered karyorrhexis, microglial proliferation with occasional nodule formation, petechial hemorrhages, endothelial prominence, and edema. The hippocampal formation was similarly affected, with the most severe changes involving the CA1 and CA4. The grossly demonstrated hemorrhagic infarcts within the basal ganglia and thalamus consisted of extensive areas of eosinophilic neuronal necrosis, necrosis of the neuropil, anastomosing lakes of intraparenchymal hemorrhage, a slight perivascular infiltrate of polymorphonuclear leukocytes, microglial proliferation, and edema. Within the white matter adjacent to the right lateral angle was an area of periventricular infarction. No viral inclusions or toxoplasma organisms were demonstrated.
Examination of the brainstem showed diffuse scattered eosinophilic neuronal necrosis as well as foci of necrosis involving neurons and adjacent neuropil, in some areas accompanied by clusters of microglia, endothelial prominence, edema, and axonal spheroids. These focal lesions were demonstrated within the tectum and substantia nigra of the midbrain, pontine tegmentum, dorsal and ventral medulla, and dorsal portion of the rostral spinal cord. Lesions ranged from areas of predominant neuronal necrosis to areas of confluent hemorrhagic infarction. Scattered fibrillary astrocytes were observed in the pontine nuclei. Sections of the cerebellum showed diffuse Purkinje cell eosinophilic necrosis, and apparent Purkinje cell loss. Sections of the cerebellar dentate nucleus showed subtotal neuron loss with marked proliferation of astrocytes and microglia. I have included this case (published many years ago Kreusser et al., PMID: 6486741) in this section even though there was no documented cardiac arrest.
