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[Incidence and forensic value of liver cell hydrops in external asphyxia and sudden infant death].
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A histological examination was carried out in 108 cases of asphyxia, 28 cases of SIDS, and 33 cases with other causes of death to assess the occurrence of liver-cell hydrops. In almost all cases of violent suffocation of newborns and children up to 10 years of age hydrops of the hepatocytes were
Postobstructive pulmonary edema in a 40-year-old man after suffocation by a swimming pool cover.
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BACKGROUND
Postobstructive pulmonary edema (POPE) is a form of sudden onset, noncardiogenic pulmonary edema that can occur after the relief of an upper airway obstruction.
OBJECTIVE
Since POPE is an uncommon diagnosis made in the emergency department (ED), this case is presented to increase
Cerebral edema caused by perinatal asphyxia. Detection and follow-up.
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Cerebral edema due to perinatal asphyxia in 2 full-term newborns was detected and monitored with a combination of real time ultrasound, computed tomography, and serial pulsatility-index determinations of the cerebral arteries using Doppler ultrasound. In both babies, real time ultrasound showed
Can perinatal asphyxia cause cerebral edema and affect cerebral blood flow velocity?
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Cerebral blood flow velocity (C.B.F.V.) was estimated in 49 newborn babies by calculating the pulsatility-index (P.I.) of the anterior cerebral arteries (A.C.A.) using Doppler ultrasound. We studied the changes in P.I. of the A.C.A. in relation to the clinical condition in three full-term babies
Suffocation due to Acute Airway Edema in a Patient with Hereditary Angioedema Highlighted the Need for Urgent Improvements in Treatment Availability in Japan.
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A 42-year-old Japanese man with hereditary angioedema suffered accidental trauma to his jaw in Shizuoka Prefecture, Japan, which gradually caused facial edema. Since plasma-derived human C1 inhibitor (pdh C1-INH) was unavailable, he had to be transferred to Juntendo University Hospital in Tokyo. Due
Nonimmune hydrops fetalis and activation of the renin-angiotensin system after asphyxia in preterm fetal sheep.
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This study examined the hypothesis that the development of hydrops fetalis after asphyxia in the 0.6 gestation sheep fetus would be associated with activation of the fetal renin-angiotensin system (RAS). Fetuses were randomly assigned to either sham occlusion (n = 7) or to 30 min of asphyxia induced
Cerebrovascular mechanisms in perinatal asphyxia: the role of vasogenic brain edema.
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Previous studies from our laboratory have demonstrated penetration of Evan's blue dye into the brain in profound fetal asphyxia, suggesting that vasogenic brain edema (BE) might be an immediate contributing factor in asphyxial brain injury. We modified the 125I-labeled albumin method of Pappius and
Glycocalyx degradation leads to blood-brain barrier dysfunction and brain edema after asphyxia cardiac arrest in rats.
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The role of glycocalyx in blood-brain barrier (BBB) integrity and brain damage is poorly understood. Our study aimed to investigate the impacts of endothelial glycocalyx on BBB function in a rat model of cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). Male Sprague-Dawley rats subjected
Asphyxiation by laryngeal edema in patients with hereditary angioedema.
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OBJECTIVE
To describe the occurrence of fatal laryngeal edema in patients with hereditary angioedema due to C1 esterase inhibitor deficiency.
METHODS
We describe 6 patients from various regions of Germany who died from laryngeal edema within the last 10 years. Furthermore, we conducted a
Laryngeal edema and death from asphyxiation after tooth extraction in four patients with hereditary angioedema.
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BACKGROUND
Recurrent angioedema is the hallmark of various inherited or acquired angioedema diseases. Hereditary angioedema, or HAE, due to C1 inhibitor, or C1NH, deficiency has considerable implications for dental health care providers because dental surgery may trigger distressing and even
[Clinical and computed tomographic observations on newborn infants with generalized brain edema due to perinatal asphyxia].
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We observed a sudden respiratory arrest in four term newborn infants after a clinically symptom-free period. There were no cardiac, pulmonary or metabolic changes responsible for these events. Signs of cerebral dysfunction existed (muscular hypotonia, jitterness, seizures). Cranial computerized
[Role of brain edema in the restoration of neurologic function in resuscitation following mechanical asphyxia].
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[Attempted therapy of dyspnea and asphyxia following acute edema of the larynx].
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Cerebral edema in developing brain. II. Asphyxia in the five-day-old rat.
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[Case report; a case of hereditary angioedema with laryngeal edema leading to suffocation].
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