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Washington University Experience | VASCULAR | Vasculitis - Giant Cell Arteritis | 2A0 Case 2 History
Case 2 History ---- The patient was an 81 year old woman with a history of headaches of unknown etiology. In 8/91, the patient developed headaches which were treated with prednisone for presumed temporal arteritis. The severity of the patient's headaches decreased but the patient was bothered by the side effects of the prednisone. A subsequent neurologic evaluation resulted in a diagnosis of migraine headache. However, when her steroids were tapered; the patient's headaches returned and during the six months prior to her admission she experienced weight loss. The patient was admitted to BH in 6/92 for further evaluation. Her neurologic examination was unremarkable. Laboratory values obtained at admission showed a white blood count of 7200, hemoglobin 9.4, hematocrit 29.6%, platelets 489K, a reticulocyte count of 3, sedimentation rate of 111, an MCV of 76.B, an MCH of 24.5, iron 31, total iron binding capacity of 331. An ANA was negative. On 6/16 a temporal artery biopsy was performed. Pathologic examination showed lymphocytic infiltration of the temporal artery but no giant cells or necrosis. Nonetheless, the results were felt to be consistent with temporal arteritis. On 6/18, the patient was noted to be lethargic. A head CT showed an acute left occipital infarct, an old subcortical infarct in the medial right frontal lobe and an old infarct in the right gyrus rectus. A lumbar puncture showed an opening pressure of 14, a glucose of 80, and two cells per cubic mm. On 6/19, the patient was totally unarousable and her toes were upgoing. An angiogram was performed which showed a complete blockage of the left internal carotid artery above the ophthalmic artery and complete blockage of the right and left vertebral arteries at the base of the brain. Her neurologic status continued to decline. She expired on 6/20. ---- At autopsy the unfixed brain weighed 1,300g. The arteries at the base of the brain were normally distributed and showed moderate to severe atherosclerosis. Serial sections showed complete thrombotic occlusion of the left internal carotid artery and the basilar artery. The brainstem was soft and edematous. Coronal sections of the cerebral hemispheres show an old 2 x 2 x 2 cm cystic infarct in the left basal ganglia and diffuse acute infarction of the territory of the posterior cerebral artery which arose from the basilar artery. Transverse sections of the softened brainstem show cystic tissue loss, initially thought to represent old cystic lacunes; however, the clinical history was inconsistent with such remote large pontine infarcts and microscopic examination of the pons showed only acute infarction and likely loss of friable infarcted tissue. Sections of the basilar and left internal carotid artery showed giant cell arteritis with superimposed thrombosis. Sections of the occipital lobe and cerebellum show acute infarction. Emboli and small multifocal areas of acute ischemic damage were, however, present throughout the brain. Sections of the right and left basal ganglia show old infarcts. No evidence of vasculitis was seen in the kidneys or any other systemic vessels except for the cerebral arteries.
