Cases reported "Death, Sudden"

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1/13. Human herpesvirus-6 and sudden death in infancy: report of a case and review of the literature.

    Investigation of sudden death in infancy is a vital function of the medical examiner's office. Surveillance of these cases may lead to recognition of new diseases or new manifestations of previously described diseases. Human herpesvirus-6 (HHV-6) is a relatively newly described virus that has been recognized as a cause of acute febrile illness in early childhood. While most cases are apparently self-limited, seven fatal cases have been reported. We present a case of a seven-month-old Latin American male with recent otitis media and vomiting who was found dead in bed. autopsy revealed interstitial pneumonitis with an atypical polymorphous lymphocytic infiltrate in the liver, kidney, heart, spleen, lymph nodes, and bone marrow, associated with erythrophagocytosis. polymerase chain reaction (PCR) analysis of formalin-fixed paraffin-embedded tissue was positive for HHV-6 and negative for Epstein-Barr virus (EBV) and cytomegalovirus (CMV). HHV-6 was also detected in the atypical lymphoid infiltrate by in-situ hybridization.
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2/13. Sudden unexpected death associated with HHV-6 in an adolescent with tuberous sclerosis.

    A 14-year-old female with tuberous sclerosis and history of seizures was found dead in bed at home 3 days after she had been assessed as doing well at a routine neurology clinic appointment. She had been treated with an antiepileptic drug, felbamate, for 36 months and had been seizure-free except for one seizure episode 5 months before death. Postmortem examination revealed cerebral edema, with uncal and tonsillar herniation, and pulmonary edema, consistent with seizure-induced apnea. Multiple microglial nodules with mature perivascular lymphocytic cuffing and diffuse infiltrates were identified around subependymal tuberous sclerosis giant cell nodules. Immunostaining and electron microscopy revealed human herpesvirus-6-infected macrophages, astrocytes, lymphocytes, and endothelial cells in the subependymal tuberous sclerosis lesions and choroid plexus. Subacute human herpesvirus-6 encephalitis is postulated to have precipitated a seizure and thus sudden unexpected death in epilepsy in this otherwise stable adolescent patient.
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3/13. achondroplasia and cervicomedullary compression: prospective evaluation and surgical treatment.

    The association between sudden death and cervicomedullary compression in infants with achondroplasia has been well described. Prospective clinical and imaging evaluations have been recommended to identify those infants with achondroplasia who are at risk of dying suddenly from respiratory arrest secondary to unrecognized cervicomedullary compression. Since 1988, we have prospectively evaluated 11 infants (average age 13 weeks) with achondroplasia who were asymptomatic for cervicomedullary compression on initial clinical evaluation. Craniocervical magnetic resonance imaging (MRI) findings included narrowing of the foramen magnum, effacement of the subarachnoid spaces at the cervicomedullary junction, abnormal intrinsic cord signal intensity and mild to moderate ventriculomegaly. Two patients with severe cord compression underwent immediate decompression. Two patients developed opisthotonic posturing within 3 months of evaluation and underwent foramen magnum decompression, including suboccipital craniectomy and atlantal laminectomy. Surgery in all cases revealed forward extension of the squamous portion of the occipital bone, thickened posterior rim of the foramen magnum and a dense fibrotic epidural band. There were no complications from surgery. Seven patients did not require surgery and were followed closely. All 11 patients remain asymptomatic at follow-up (mean 4.6 years; range 16 months to 7.3 years), and no patient has required a diversionary shunt procedure. The results of this prospective study confirm that early clinical and MRI evaluations are necessary to determine whether infants with achondroplasia have cervicomedullary compression. With early recognition, an immediate decompression can be performed safely to avoid serious complications associated with cervicomedullary compression, including sudden death. copyright copyright 1999 S. Karger AG, Basel
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4/13. Sudden death from pelvic hemorrhage after bilateral central fracture dislocations of the hip due to an epileptic seizure.

    Fracture and dislocation of major joints may be caused by the forceful tonic muscular contractions of seizure activity. A 77-year-old man who was found dead in bed with no sign of external trauma had bilateral central fracture dislocations of the femoral head through the acetabular floor with fatal pelvic hemorrhage and extensive pulmonary fat and bone marrow embolism. He had epilepsy, but the last seizure was 6 years earlier, and he had long discontinued medication. The fractures were attributed to a new unwitnessed seizure. This is the twentieth case of central fracture dislocation of the hip since 1970, when better anesthesia eliminated convulsive therapy-induced fractures. The authors review these 20 cases. seizures followed inflammation, infarction or neoplasia of the brain, eclampsia, metabolic or iatrogenic causes, or epilepsy (6 cases, 2 of which had no prior seizures for 5 years). There were 11 men (mean age, 64 years) and 9 women (mean age, 47 years). Fractures were unilateral in 13 and bilateral in 7. Additional fractures (in vertebrae, shoulders, or femur) were present in eight. Only eight had prior bone disease. Local symptoms led to diagnosis in most, but two were identified incidentally on imaging. The current patient was the only one to die suddenly, but six other patients presented with shock and three died (one of whom had injuries that led to a suspicion of manslaughter). Central fracture-dislocation of the hip is a rare and little known consequence of seizures, with strong potential for misdiagnosis and lethal complications.
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5/13. Fatal parvovirus B19 myocarditis in an 8-year-old boy.

    A report is given on an 8-year-old boy who suddenly and unexpected died. autopsy findings point to acute heart failure. Microscopic examination of the heart showed increased interstitial and perivasal fibrosis and myocarditis with macrophage infiltration. polymerase chain reaction (PCR) analysis for parvovirus B19 was positive in heart samples and in the spleen. Immunostaining for parvoviral surface antigens was negative. Although the virus does not appear to have infected the cardiomyocytes, we speculate that myocarditis arose from immunological cross-reaction to epitopes shared between the virus and the myocardium.
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6/13. An autopsy case of sudden death in a patient with giant cell myocarditis.

    We present a case of a 28-year-old male weight lifter who died suddenly while driving a bicycle. Forensic autopsy and histopathological examinations revealed granulomatous lesions in the myocardium and hilar lymph nodes. The latter had massive caseation necrosis, epithelioid granulomas and Langhans' giant cells suggestive of tuberculosis. However, the myocardium showed predominantly multinucleated foreign body and myogenic giant cells, lymphocytes, plasma cells, macrophages, eosinophils. Staining for acid-fast bacilli was negative. The present case highlights the difficulty in establishing whether the granulomatous lesions in the hilar lymph nodes and the myocardium are incidental findings or whether they are related by the same pathogenetic mechanisms.
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keywords = macrophage
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7/13. Sudden death from secondary massive pulmonary embolism derived from marrow emboli trapped by Chiari's network.

    We report a case of fatal massive pulmonary embolism in an 86-year-old woman. The embolus occurred as a result of embolic bone marrow particles from a fractured femur becoming trapped by a Chiari's network which then acted as a source for propagation of a large thrombus which detached and caused sudden death from massive pulmonary embolism. To our knowledge this is the first report of such a case.
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8/13. neuritis cordis due to the acute polyneuritis of the guillain-barre syndrome.

    Three patients with the guillain-barre syndrome which followed the course of Landry's acute ascending paralysis died a sudden cardiac death. Autonomic dysfunction had appeared clinically, consisting of sphincter disturbances in one patient and fluctuating blood pressure and bradycardia in the other. In a twenty-three year old female patient cardiac function had been inconspicuous, apart from tachycardia, but the ECG showed S-T segment depression and flat T waves. Postmortem examination revealed acute inflammatory demyelinating polyradiculoneuritis involving the peripheral autonomic nervous system and especially the nerves of the heart. Immunohistochemically, the inflammatory cell infiltrations of this neuritis cordis consisted of macrophages (MAC 387 positive) and T lymphocytes (UCHL1 positive). No indication of a direct viral infection of the inflamed cardiac nerves was detectable by immunohistochemistry (HSV, CMV, influenza virus) nor by electron microscopy. The neuritis cordis was classified as an inflammatory cardio-neuropathy secondary to a patchy acute polyneuritis of the guillain-barre syndrome, involving the autonomic nervous system. myocarditis could be discounted, and the neuritis cordis was thought to be responsible for the sudden cardiac death.
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keywords = macrophage
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9/13. Sudden death resulting from chicken bone perforation of the esophagus.

    Sudden death caused by foreign-body perforation of the esophagus is distinctly uncommon. We report the death of an elderly patient in a nursing home who exsanguinated after she swallowed a chicken bone that perforated her esophagus and right common carotid artery.
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10/13. Sudden unexpected death associated with atlanto-occipital fusion.

    A case of sudden, unexplained death in a 24-year-old male is presented. There were two previous spells of loss of consciousness. There was remarkable narrowing of the foramen magnum with indentation of the medulla. The atlas was partly fused with the occipital bone and a portion of abnormal bone compromised the foramen magnum from anterior reducing its anteroposterior dimensions to 16 mm (n 25-35 mm). Close clinical examination of this area in patients with acute intermittent symptomatology, or at the time of autopsy in cases of sudden unexpected death is stressed.
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