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Washington University Experience | VASCULAR | Herniation, tonsillar | 1A0 Case 1 History
Case 1 History ---- The patient was a 26 year old woman admitted to an OSH on 7/21 because of a 3 day history nausea and vomiting. Each episode was followed by diarrhea and accompanied by a severe frontal headache. The episodes started about 1.5 months prior. Her blood pressure in the ER was 258/140 mmHg. Her past medical history reveals diabetes mellitus for 10 years with episodes of ketoacidosis, hypertension for 2 years, history of retinopathy and photocoagulation, peripheral vascular disease, genital herpes and chronic renal failure treated with dialysis. Her family history is positive for diabetes and coronary artery disease. The patient was a smoker with 10 pack-years and drank no alcohol. Her medications consisted of: Valsartan (AT-2-inhibitor), Catapressan (alpha 2 agonist), Felodipine (Ca-channel blocker), metoprolol (beta-blocker), Acyclovir (DNA-Polymerase inhibitor), pantoprazole (Gastrointestinal: proton-pump inhibitor), sertraline (selective serotonin reuptake inhibitor), alprazolam (GABA/BZD-receptor agonist), tramadol (opioid agonist) and acetaminophen (non-opioid analgesic). On 7/24, she complained of headache and appeared somewhat hypersomnolent. In the evening, the patient was transferred to BJH with mental status alterations. A CT was performed and showed subarachnoid hemorrhage. The hemorrhage [Fischer Grade II (>1mm)] filled the basal cisterns as well as the sylvian fissure bilaterally. Shortly after the CT-scan, she had a bradycardic and hypotensive event followed the next day by non-reactive pupils, absent corneal reflexes, absence of oculocephalic reflex, no gag/cough reflex and did not respond to noxious stimuli. An apnea test was performed and she was pronounced brain dead on July, 25th. ---- Gross and microscopic examination of the brain, which weighed 1410 grams, confirmed global hypoxic/ischemic damage with uncal herniation and PCA compression, absence of aneurysms, evidence of cerebellar hemorrhage with subarachnoid extension and bilateral hemorrhagic cerebellar infarcts. Given the clinical history, this unfortunate event is likely accounted for by the patient's hypertension beginning with a cerebellar hemorrhage. Although multifocal hemorrhagic infarcts are also seen in areas including bilateral occipital lobes, thalami, lateral geniculate bodies, midbrain and brain stem, these finding can be explained by the adverse effect of uncal and tonsillar herniation in combination with brain edema.
