Cases reported "Death, Sudden"

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1/13. Unexpected childhood death due to hemolytic uremic syndrome.

    Two cases of unexpected childhood death due to hemolytic uremic syndrome are reported. A 21-month-old girl who was discovered dead in bed following a short illness was found at autopsy to have overwhelming sepsis resulting from transmural colitis. escherichia coli serotype 0157A was isolated from the intestine, and renal changes of hemolytic uremic syndrome were found. A 4-year-old girl died suddenly in hospital from intracranial hemorrhage while being treated for hemolytic uremic syndrome-related renal failure. culture of urine and feces grew verocytotoxin producing E. coli. These cases demonstrate that hemolytic uremic syndrome may be a rare cause of unexpected childhood death and that the diagnosis may not be established prior to autopsy. Postmortem culture of tissues and fluids in cases of suspected sepsis in children may be essential in establishing this diagnosis, because histologic evaluation may be compromised by profound sepsis and tissue putrefaction. Accuracy in diagnosis may have significant public health and medicolegal consequences.
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2/13. Osler-Weber-Rendu syndrome--pathological manifestations and autopsy considerations.

    An 18-year-old university student with Osler-Weber-Rendu disease collapsed in the bathroom. Attempted resuscitation was unsuccessful. Her past history included recurrent epistaxes, mucosal telangiectasias, intracranial arteriovenous malformations with previous hemorrhage, a single pulmonary arteriovenous malformation, recent onset of grand mal seizures, and depression. There was a positive paternal family history. At autopsy the pulmonary arteriovenous malformation was confirmed. In addition, within the brain there were widespread areas of gliosis with hemosiderin deposition and small vascular malformations. No other significant abnormalities were detected and toxicological screening revealed only moderately elevated levels of carbemazepine. Death was attributed to epilepsy associated with glial scarring from previous microhemorrhages. The detection of vascular malformations in the lung or brain at autopsy should prompt careful examination of all tissues for similar lesions. Given the possibility of Osler-Weber-Rendu disease in such cases, fibroblast cultures should be undertaken to enable molecular studies to proceed. The heritable nature of this disorder necessitates accuracy of diagnosis at autopsy; once the diagnosis is confirmed family screening should be recommended.
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3/13. Unexpected childhood death due to a rare complication of ventriculoperitoneal shunting.

    A 10-year-old boy with arnold-chiari malformation, spina bifida, and a ventriculoperitoneal shunt for hydrocephalus died unexpectedly, having appeared to be only mildly unwell with fever on the night before death. At autopsy, the shunt was partially obstructed with an associated enterococcal meningitis. The tip of the shunt was located within the transverse colon, which was embedded in a mass of fibrous adhesions resulting from previous abdominal surgery. blood cultures were sterile. intestinal perforation is a rare complication of ventriculoperitoneal shunting that may be associated with the development of meningitis and unexpected death. The autopsy assessment of children with such indwelling devices requires examination of the functional state of the shunt, full septic workup, and determination of the precise location of the tip of the catheter within the peritoneal cavity.
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4/13. Pseudomembranous bronchitis (non-diphtherial) resulting in sudden death: an autopsy report.

    A 69-year-old woman was admitted because of dyspnea. Thereafter, she fell into a state of shock. Resuscitation was attempted but she did not respond to it and died on the second hospital day. According to the autopsy findings, a wide range of area from the larynx to the trachea was covered with pseudomembrane. In the culture of bacteria, alpha Streptococcus and corynebacterium genus (non-diphtherial) were all that was detected. These findings suggest that pseudomembranous lesion, an endogenous foreign matter of the air passage should be suspected when a patient presents with sudden dyspnea.
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5/13. Sudden death secondary to fulminant intracranial aspegillosis in a healthy teenager after posterior fossa surgery: the role of corticosteroids and prophylactic recommendations.

    postoperative complications from corticosteroids in neurosurgical patients are not uncommon. Too often the deleterious immunosuppressive effects of corticosteroids are overlooked in neurosurgery patients and can lead to serious and lethal infections. EXPERIMENTAL DESIGN: case report of a 16-year-old healthy male who presented for elective resection of a recurrent juvile pilocytic astrocytoma of the posterior fossa 4 years after initial resection. SETTING: major University institutional practice. INTERVENTION/RESULTS: a standard suboccipital craniotomy with gross total resection. Postoperatively, the patient suffered from posterior fossa syndrome and diminished gag reflex requiring nasogastric feeds with progressive improvement. While awaiting transfer to a rehabilitation center on postoperative day 12 he suffered a sudden temperature spike followed by neurological decline. A stat computed tomography scan of the brain revealed a diffuse miliary process with severe cerebral edema. sputum and cerebrospinal fluid cultures identified aspergillus. Despite immediate therapy to combat the malignant cerebral edema, the patient died within 24 hours of onset of the symptoms. Corticosteroids are used routinely in neurosurgery to combat cerebral edema without much consideration for the immunosuppressive effects. This case demonstrates how the immunosuppressive effects of corticosteroids can lead to a fulminant lethal fungal infection. Neurosurgeons should be aware of the anticatabolic medications now available to combat the deleterious side effects of corticosteroids.
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6/13. Sudden unexpected death in a child with varicella caused by necrotizing fasciitis and streptococcal toxic shock syndrome.

    A 4-year-old child with chickenpox infection for 5 days prior to death complained of swelling and pain in his right leg that required medical assistance in the emergency department. Radiologic study was normal, and analgesic and bandage of the leg were prescribed. Some hours later, he presented cyanosis, dizziness, and vomiting and collapsed. A complete forensic autopsy was performed 12 hours after death. External examination of the body showed numerous crusty varicella skin lesions, especially over the trunk, and swelling and reddening of his right leg. The brain was swollen, with cerebellar herniation, and both adrenal glands were hemorrhagic.Microscopically, neutrophilic infiltration and muscle fiber necrosis were observed in soft tissues of his right leg, and fibrin microthrombus were numerous in capillaries of the plexus choroideus, larynx, lungs, and adrenals. Bacterial emboli were present in most of the tissues. Microbiologic cultures of blood and cerebrospinal fluid showed group A beta-hemolytic streptococcus (streptococcus pyogenes). Death was attributed to fulminant streptococcal toxic shock syndrome, with necrotizing fasciitis as a complication of varicella.
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7/13. Postmortem computed tomography for detecting causes of sudden death in infants and children: retrospective review of cases.

    PURPOSE: The aim of this study was to investigate the usefulness of postmortem computed tomography (PMCT) in detecting causes of sudden death in infants and children. MATERIALS AND methods: Our subjects were 15 nontraumatically deceased patients (nine boys and six girls, ranging in age from 20 days after birth to 12 years old, mean age 1.6 years), who had been in a state of cardiopulmonary arrest on arrival at our hospital. PMCT was performed within 2 h after certification of death: head (15 cases), chest (11 cases), and abdomen (12 cases). blood was collected from 11 of the patients at the time of cardiopulmonary resuscitation. An autopsy was conducted on two. RESULTS: PMCT did not show any traumatic changes indicating child abuse. It was difficult to presume the cause of death with PMCT alone, but the cause of death in 14 of 15 cases could be presumed by combining information from their medical history, clinical course before death, PMCT findings, laboratory data, and bacterial culture. The remaining subject was classified as cause unknown. CONCLUSION: The causes of sudden death in infants and children were detected at a high rate when we comprehensively investigated the PMCT and other examination findings.
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8/13. Sudden death due to streptococcal infection.

    Sudden unexpected deaths form a large population of medical examiner caseloads. Presented are the clinical, pathologic, and virulence features of sudden death due to Group A beta-hemolytic streptococcus. Emphasis is placed on the importance of post-mortem cultures. Case histories are included to illustrate the sometimes unusual presentation of this disease. Recent publicity has led to a heightened public awareness of this unusually virulent entity.
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9/13. 3-Hydroxydicarboxylic aciduria due to long-chain 3-hydroxyacyl-coenzyme a dehydrogenase deficiency associated with sudden neonatal death: protective effect of medium-chain triglyceride treatment.

    Two siblings were found to be affected by long-chain 3-hydroxyacyl-coa dehydrogenase deficiency, one of which died suddenly and unexpectedly on the 3rd day of life suffering from extreme hypoketotic hypoglycaemia. The younger sibling started to have feeding problems, lowered consciousness, and liver dysfunction at the age of 5 months. Her urine contained large amounts of C6-C14 3-hydroxydicarboxylic acids and conjugated 3-hydroxyoctanoic acid, as verified by gas chromatography/mass spectrometry. plasma long-chain acylcarnitine was increased. A clue to the diagnosis was given by the results of a phenylpropionic acid loading test. This revealed small, but significant amounts of conjugated 3-hydroxyphenylpropionic acid (phenylhydracrylic acid) in the patient's urine. Subsequently, the activity of long-chain 3-hydroxyacyl-coa dehydrogenase was found to be deficient in cultured skin fibroblasts. Based on the findings obtained by a medium-chain triglyceride load, a diet enriched in this type of fat was prescribed. On this regimen the patient started to thrive, signs of cardiomyopathy disappeared, and her liver function normalized.
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10/13. Unexpected death as a result of infective endocarditis.

    Thirteen cases of infective endocarditis (IE) diagnosed for the first time at autopsy or, in those patients with a previous diagnosis of IE, not thought to be active at the time of death, are presented. Of the six patients who died within 24 h of the onset of symptoms, two died of obstruction of a valve orifice, two died of sepsis, one died of sepsis and alcoholic cardiomyopathy, and one died of a coronary artery embolus. Of the five patients with symptoms lasting more than 24 h, three died of sepsis and congestive heart failure. One died from sepsis alone and one died from congestive heart failure (CHF). In two patients whose duration of symptoms is unknown, one died of sepsis and CHF, and in the other the mechanism of death is unknown. Predisposing factors present in 11 of 13 patients included alcoholism (three), intravenous (IV) drug abuse (three), prosthetic valves (three), aortic stenosis (two), past rheumatic fever (one), and nonstenotic congenitally bicuspid valves (two). The reasons for no antemortem diagnosis were a missed or incorrect clinical diagnosis in three patients seen by a physician shortly before death, no signs or symptoms or found dead (four), non-specific signs and symptoms (three), refusal of medical treatment (one), and a solitary lifestyle (one); there was insufficient information about one patient. Individuals with needle tracks, generalized petechiae. Osler's nodes, splinter hemorrhages, intravenous catheters, pacemaker wires, and infected aortic-valve (A-V) shunts are at risk of IE. blood and the vegetations should be cultured. The attending physician should be notified of the diagnosis in such cases.
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