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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary edema is reported in central nervous system disorders, especially trauma. With head injury, a common associated factor is said to be raised intracranial pressure. Among more than 2,100 patients with serious head injuries and 132 serious cervical spinal cord and/or cervical spinal column injuries, only two clear examples of pulmonary edema that might be considered related solely to such injury were found. Another group of patients with non-traumatic central nervous system disorders in whom pulmonary edema developed was also analyzed. In any case, conclusive pathophysiologic explanations for its production are difficult to find. We believe pulmonary edema occurs only rarely in patients with lesions of the central nervous system whether of traumatic or non-traumatic nature and that the mechanism of its production is not clear.
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PMID:Pulmonary edema and the central nervous system: a clinico-pathological study. 117 48

To examine the role of central nervous system injury in the pathogenesis of pulmonary edema, we injected Escherichia coli endotoxin (5 mg/kg) into the cisterna magna of six dogs (group E) and compared, over 4 h, both the pulmonary edema and cerebrospinal fluid (CSF) abnormalities with those in six control dogs (group C). In group E, intracisternal endotoxin raised intracranial pressure from 21 +/- 6 to 38 +/- 8 cmH2O (P less than 0.001), CSF total protein from 18 +/- 6 to 54 +/- 19 mg/dl (P less than 0.001), and CSF malondialdehyde from 0.12 +/- 0.11 to 0.61 +/- 0.35 nmol/ml (P less than 0.05); all were unchanged in group C. When the pulmonary wedge pressure was maintained at 10 mmHg by fluid infusion, extravascular thermal volume in group E increased from 7.2 +/- 1.2 to 12.0 +/- 2.7 ml/kg (P less than 0.005) at 4 h when the excised lungs weighed 13.6 +/- 1.5 g/kg; in group C, extravascular thermal volume did not increase, and the excised lungs weighed less (10.8 +/- 1.3 g/kg, P less than 0.05) than those in group E. The dry weights of the lungs were not different between groups, and the alveolar lining fluid-to-plasma albumin ratio in both groups remained low, 0.1-0.2. Fluid infusion in group E (9.2 +/- 2.9 liters) caused colloid oncotic pressure to decrease 4.5 +/- 2.8 mmHg; colloid oncotic pressure fell less (0.8 +/- 1.9 mmHg, P less than 0.001) in group C as less fluid (2.2 +/- 1.5 liters, P less than 0.001) was required to maintain pulmonary wedge pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathogenesis of pulmonary edema associated with intracisternal endotoxin in dogs. 218 63

Increased intracranial pressure may result in the Cushing response. We applied a short pulse of pressure to the cranial cavity of anesthetized cats which were intubated, curarized, ventilated, and the cranium exposed to an 80- to 100-msec pulse of pressure at 5.3 atm. The following significant increases developed: Intracranial pressure rose from 7.4 +/- 1.5 to 150.6 +/- 19.4 mm Hg, systolic arterial peak pressure from 130.7 +/- 8.1 to 299.0 +/- 11.4, pulmonary peak pressure from 18.9 +/- 1.9 to 42.9 +/- 4.9. Alveolar lavage protein in controls was 6.7 +/- 0.4 mg/g lung compared to 11.9 +/- 2.0 in the experimental group. Extravascular lung water/dry weight ratios increased from 3.36 +/- 0.04 in controls to 3.51 +/- 0.09 but varied inversely with pulmonary systolic peak pressure (r = 0.59). These results showed that a pulse of pressure applied to the cranium of cats produced lung edema which was inversely related to pulmonary artery pressures.
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PMID:Cardiopulmonary response to an induced pulse in intracranial pressure. 396 Aug 55

Two young patients with head injuries subsequently developed neurogenic pulmonary oedema. The origin and pathways of the reflex response to cerebral trauma are discussed, with emphasis on the role of raised intracranial pressure and the sympathetic division of the autonomic nervous system in precipitating movement of systemic circulatory volume into the pulmonary circulation. Therapeutic measures are discussed which correct the progression of this condition by reducing intracranial pressure and blocking the systemic effects of autonomic reflex activity. This leads to the basis of a simple regime to treat future cases.
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PMID:Neurogenic pulmonary oedema. 674 84

Plasmodium falciparum is the most common cause of severe and life-threatening malaria. Falciparum malaria causes over one million deaths every year. In Africa, a vast majority of these deaths occur in children under five years of age. The presentation of severe malaria varies with age and geographical distribution. The mortality rate is higher in adults than in children but African children develop neuro-cognitive sequelae following severe malaria more frequently. The management of severe malaria includes prompt administration of appropriate parenteral anti-malarial agents and early recognition and treatment of the complications. In children, the complications include metabolic acidosis (often caused by hypovolaemia), hypoglycaemia, hyperlacticacidaemia, severe anaemia, seizures and raised intracranial pressure. In adults, renal failure and pulmonary oedema are more common causes of death. In contrast, concomitant bacterial infections occur more frequently in children and are associated with mortality in children. Admission to critical or intensive care units may help reduce the mortality, and the frequency and severity of sequelae related to severe malaria.
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PMID:Management of severe falciparum malaria. 1504 99

High-altitude retinopathy is one of altitude-related illnesses. Its signs include high-altitude retinal hemorrhages, dilated vessels and peripapillary hyperemia. Increased intracranial pressure seems to be the main cause of all high-altitude diseases including high-altitude retinopathy, cerebral oedema and high-altitude pulmonary oedema. We present the case of high-altitude retinopathy in a 35-year-old woman who reported decreased vision in her right eye, scotomas and high-altitude retinopathy after ascending to more than 7000 meters above sea level. The associated optical coherence tomography findings, fundus photography and literature review are presented. High-altitude retinopathy is an important multifactorial condition of unknown mechanism and etiology, which significantly impacts human vision. Climbing high mountains can cause retinopathy in otherwise healthy people and may lead to permanent sequelae such as retinal nerve fiber layer and optic nerve defects. These symptoms, however, may resolve without causing any permanent damage to the retina. Conservative treatment may help to relieve them. With increasing popularity of mountaineering, ophthalmologists should be prepared to diagnose and treat high-altitude retinopathy.
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PMID:High-altitude retinopathy--case report. 2579 81

The infrequency of deaths from work-related heat stress may be due to self-pacing, whereby workers adjust their work rate in response to thermal discomfort. Thirteen cases attributed after coronial investigation to work-related heat stress were studied to evaluate the causal contribution of environmental and personal risk factors. Meteorological records and coronial records were examined to estimate environmental and metabolic heat loads and to identify any personal risk factors likely to have contributed to death. Seven deaths occurred in workers within one week of hiring, demonstrating not only the importance of acclimatisation but also the likelihood of compromised self-pacing in recently-hired workers. Personal risk factors identified included intercurrent illness, cardiovascular disease and obesity. Four deaths occurred following indoor work, where the probable critical risk parameter was low air velocity. Cerebral and pulmonary oedema were reported in some autopsy reports, and uncal herniation was found in one case. Modified work rates and close supervision are essential in recently-hired workers. The risk of death from raised intracranial pressure suggests the need for specific remediation of cerebral oedema in hyperthermic individuals.
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PMID:Deaths in Australia from Work-Related Heat Stress, 2000-2015. 3156 63