Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032290 (aspiration pneumonia)
 2,291 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An assessment of morbidity in near-drowning was made from a review of emergency room and hospital records of 72 patients, ages 9 months to 20 years, who suffered near-drowning during the period January 1972 through June 1974. Fifteen patients (21% evidenced severe anoxic encephalopathy; the remainder had no detectable neurologic deficits. Hypoxemia was demonstrated in 56 patients. Severe acidosis was not present unless respiratory failure occurred. Neither electrolytes, red blood cell hemolysis, nor cardiac arrhythmias presented a problem. Respiratory complications included pulmonary edema, aspiration pneumonia, atelectasis, shock lung, pneumothorax, and pneumomediastinum. All children requiring cardiopulmonary resuscitation in the emergency room suffered anoxic encephalopathy. The occurrence of seizures, fixed and dilated pupils, flaccid extremities, and lack of response to deep pain in the emergency room had almost universal correlation with resultant severe anoxic encephalopathy, as did a submersion period of six or more minutes. The morbidity of near-drowning is significant with regard to the number of children affected and the severity of the central nervous system insult received. The statement by the American Heart Association that resuscitative efforts in children should be continued for periods longer than ten minutes needs reevaluation, since neurologic recovery did not occur in any child requiring cardiopulmonary resuscitation (CPR) in the emergency room. More importantly, new methods of cerebral resuscitation need to be developed and established. In short, medical personnel need to think in terms of cardiopulmonary cerebral resuscitation (CPCR) rather than in terms of CPR.
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PMID:Morbidity of childhood near-drowning. 84 May 54

A case of autoptically verified progressive subcortical gliosis (PSG) is reported. The 79 year old woman developed subacutely a right sided hemisyndrome and a cerebellar syndrome. Generalized action myoclonus of the left leg evolved into left sided Epilepsia partialis continua and dementia appeared. After a 6 month course the patient died of aspiration pneumonia. There was no indication of alcoholism or HIV-dementia neither clinically nor at autopsy. Morphologically the brain showed a diffuse proliferation of astrocytes in the subcortical white matter, thalamus, basal ganglia, brain stem and cerebellum. A severe neuronal dropout was found in medial thalamic neurons but Wernickes encephalopathy was ruled out. 21 cases of PSG confirmed by autopsy were found in the literature. Clinics, neuropathology and classification of PSG is discussed.
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PMID:[Progressive subcortical gliosis]. 193 41

A 25 year old man with a five year history of petrol sniffing developed an acute encephalopathy with abnormal body movements and died of aspiration pneumonia. Neuropathological findings included chromatolysis of neurons in the reticular formation and cerebral cortex and loss of neurons in the h3-5 sector of Ammon's horn and the cerebellum. Toxicological studies suggest that the encephalopathy is caused by the tetraethyl-lead additive in the petrol. These data support previous human and experimental studies.
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PMID:Acute encephalopathy and death due to petrol sniffing: neuropathological findings. 347 Nov 99

An 11-year-old girl developed a severe brainstem encephalopathy thought to be due to multiple sclerosis. She has been left with a severe long-standing bulbar palsy and a permanent tracheostomy. A new operation of laryngeal closure is described which gave relief from recurrent aspiration pneumonia and cardiorespiratory failure.
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PMID:Laryngeal closure in the management of severe long-standing bulbar palsy in a child. 731 4

A 61-year-old woman was treated with cisplatin and etoposide for ovarian carcinoma. After the second course of chemotherapy she developed acute encephalopathy which manifested itself as headache, fever, a partial seizure, confusion, and mild right hemiparesis, although no evidence of a central nervous system infection was found. Ten days after the onset of neurological symptoms, she experienced a sudden loss of vision in both eyes. Neurological findings were compatible with cortical blindness. Neurological symptoms subsided and visual acuity completely returned over the next months. The total cumulative dose of cisplatin was 325 mg/m2. She died of aspiration pneumonia on the 43rd day. Postmortem examination revealed severe nerve cell loss, gliosis and spongy changes in the bilateral occipital cortex including visual field, and slight to moderate demyelination in the subcortical white matter of the occipital cortex, Goll's tract, and dorsal root ganglia. As far as we know this encephalopathy is the second report in which the neuropathological changes associated with cisplatin therapy have been demonstrated by autopsy findings. The first was a case report of leukoencephalopathy, which differed significantly from our case in the primary lesions of the brain. We measured the platinum level in several parts of the cerebrum and cerebellum, optic nerve, spinal cord, and cauda equina by using an atomic absorption spectrophotometric technique. Platinum was detected in the bilateral occipital cortex, spinal cord, and cauda equina. These results were consistent with the distribution of pathological lesions. The mechanism of cisplatin-induced focal encephalopathy remains speculative.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinicopathological report of cisplatin encephalopathy]. 778 Dec 18

A 15-year-old girl with a former clinical diagnosis of cerebral palsy was found to have isolated deficiency of 3-methylcrotonyl-CoA carboxylase (MCC) on gas chromatography-mass spectrometry (GC/MS) analysis and enzyme determination. Her symptoms included marked growth retardation from birth, profound mental retardation, tonic seizures, rigospastic quadriplegia with opisthotonic dystonia, gastroesophageal reflux with poor esophageal peristalsis, and recurrent episodes of aspiration pneumonia. Brain MRI revealed marked brain atrophy, involving both the gray and white matter. Although she did not exhibit acute metabolic decompensation or acute encephalopathy, her neurological symptoms continuously worsened. This patient is the oldest among reported cases of MCC deficiency who had symptoms at birth, and this case may have the severest sequelae of the longest known natural course of this inborn error of metabolism.
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PMID:Isolated 3-methylcrotonyl-CoA carboxylase deficiency in a 15-year-old girl. 918 84

A prematurely born 5-year-old boy with chronic lung disease, hypoxic-ischemic encephalopathy, cerebral palsy, repeated aspiration pneumonia, and stroke underwent percutaneous endoscopic jejunostomy (PEJ) to alleviate repeated aspiration pneumonia. Studies, including 24-hour esophageal pH monitoring, 99mTc gastric emptying time, upper gastroesophageal barium radiography, and endoscopic examinations showed severe gastroesophageal reflux and prolonged gastric emptying. Percutaneous endoscopic gastrostomy (PEG) was performed first, followed by placement of a polyurethane J-tube (9 French) through the preexisting gastrostomy site. We passed the style-guided J-tube through the pyloric ring endoscopically and advanced it to the jejunum. The position of the J-tube was confirmed by radiologic study. Feeding with an elemental formula, 20 mL/hour, commenced immediately after the procedure, and the rate was gradually increased to 50 mL/hour. No further episodes of aspiration pneumonia have occurred since J-tube placement. Our initial experience with jejunal feeding through a PEJ is encouraging.
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PMID:Pediatric percutaneous endoscopic jejunostomy by J-tube extension through a preexisting gastrostomy site: a preliminary report. 988 93

Bilateral hypoxic-ischaemic thalamic lesions are a rare type of neonatal encephalopathy with characteristic but often misinterpreted clinical features. This article describes history, clinical and diagnostic findings in a preterm and a term infant with hypoxic-ischaemic thalamic lesions after severe and abrupt intrauterine hypoxia. Both neonates presented with absent suckling and swallowing whereas other cranial nerves were unaffected. Characteristic findings in both newborns were profound muscular hypotonia and weak facial expressions together with feeding difficulties and frequent episodes of aspiration pneumonias. The term infant died at the age of 14 weeks following presumed aspiration pneumonia, the preterm infant, however, has developed severe extrapyramidal cerebral palsy. Absent suckling and swallowing with otherwise normal cranial nerve function appears to be characteristic of a bilateral hypoxic-ischaemic lesion of the thalamus. Animal experiments suggest that these lesions originate from a short but total ischaemia as it can be observed in cord prolapse or total placental abruption. Specific findings may initially be absent on ultrasound examination. Hence, magnetic resonance imaging of the brain should be performed on all patients with characteristic clinical symptoms even if the ultrasound scan is unremarkable. Evidence of bilateral ischaemic lesions of the thalamus usually indicates a poor prognosis.
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PMID:[Bilateral hypoxic-ischaemic thalamic lesions in newborns]. 1247 99

Activating mutations in the Kir6.2 subunit of the adenosine triphosphate-sensitive potassium (KATP) channel is a cause of neonatal diabetes associated with various neurological disorders that include developmental delay, epilepsy, and neonatal diabetes (known together as DEND syndrome). This article reports a girl who developed infantile spasms and early onset diabetes mellitus at the age of 3 months and revealed DEND syndrome with a heterozygous activating mutation in Kir6.2. Infantile spasms with hypsarrhythmia on the electroencephalogram were severe and refractory to steroids. Steroids combined with oral sulfonylurea, a drug that closes the ATP-sensitive potassium channel by an independent mechanism, allowed partial and transitory control of the epilepsy. However, the child still exhibited severe encephalopathy and died of aspiration pneumonia. The role of oral sulfonylurea as an anticonvulsant in DEND syndrome associated with Kir6.2 mutation is discussed.
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PMID:Infantile spasms as an epileptic feature of DEND syndrome associated with an activating mutation in the potassium adenosine triphosphate (ATP) channel, Kir6.2. 1789 Apr 19

Arnold-Chiari malformation is an occipitocervical malformation where the cerebellar amygdales descend below the occipital foramen. Acute respiratory failure is an exceptional inaugural sign. We report two cases disclosed by alveolar hypoventilation associated with type I Arnold-Chiari malformation. The two patients age 51 and 52 years had an uneventful past history and presented with hypercapnic encephalopathy with acute respiratory failure requiring ventilatory assistance. Respiratory function tests, helicoidal thoracic computed tomographic angiography, electromyogram, cardiac echography, and thyroid and immunological tests were normal. Blood gases and polysomnography were in favor of central hypoventilation without sleep apnea. Magnetic resonance imaging demonstrated type I Arnold-Chiari malformation. The course was complicated by recurrent respiratory failure in both patients. Surgical decompression performed for the first patient provided no improvement. This patient died two months after surgery subsequent to aspiration pneumonia. The second patient was treated with continuous positive pressure noninvasive ventilatory assistance and had a good outcome at 25 months. These two cases illustrate the absence of any neurological sign, acute respiratory failure being the only sign of Arnold-Chiari malformation.
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PMID:[Acute respiratory failure as the sol inaugural sign of Arnold-Chiari malformation. Two cases]. 1816 35


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