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M S Lewis

Publications and source records attributed to M S Lewis.

98 records · Page 6Linked to original sources
PubMed1967

Studies on the intracerebral toxicity of ammonia.

Interference with cerebral energy metabolism due to excess ammonia has been postulated as a cause of hepatic encephalopathy. Furthermore, consideration of the neurologic basis of such features of hepatic encephalopathy as asterixis, decerebrate rigidity, hyperpnea, and coma suggests a malfunction of structures in the base of the brain and their cortical connections. The three major sources of intracerebral energy, adenosine triphosphate (ATP), phosphocreatine, and glucose, as well as glycogen, were assayed in brain cortex and base of rats given ammonium acetate with resultant drowsiness at 5 minutes and subsequent coma lasting at least 30 minutes. Cortical ATP and phosphocreatine remained unaltered during induction of coma. By contrast, basilar ATP, initially 1.28 +/- 0.15 mumoles per g, was unchanged at 2.5 minutes but fell by 28.1, 27.3, and 26.6% (p < 0.001) at 5, 15, and 30 minutes after NH(4)Ac. At comparable times, basilar phosphocreatine fell more strikingly by 62.2, 96, 77.1, and 71.6% (p < 0.001) from a control level of 1.02 +/- 0.38 mumoles per g. These basilar changes could not be induced by anesthesia, psychomotor stimulation, or moderate hypoxia and were not due to increased accumulation of ammonia in the base. Glucose and glycogen concentrations in both cortex and base fell significantly but comparably during development of stupor, and prevention of the cerebral glucose decline by pretreatment with glucose did not obviate ammonia-induced coma or the basilar ATP fall. These findings represent the first direct evidence that toxic doses of ammonia in vivo acutely affect cerebral energy metabolism and that this effect is preferentially localized to the base of the brain.

Adenosine Triphosphate↗
PubMed1966

A scapular vest.

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Humans↗
PubMedDate not supplied

Treatment of toxic epidermal necrolysis by burn units: another market or another threat?

A survey of burn care facilities in the United States has provided information regarding the treatment of toxic epidermal necrolysis and related diseases in burn units. The survey suggests that a disproportionate share (12% to 15%) of the projected number of cases of toxic epidermal necrolysis that occur annually are being transferred to the 2% of United States hospitals that have burn units. Because of the potential for a complex hospital course and extended length of stay, treatment of these patients in a prospective payment system poses a significant fiscal threat to hospitals with burn units.

Burn Units↗
PubMedDate not supplied

Serum calcitonin may be a marker for inhalation injury in burns.

One of the principal causes of death from burns is inhalation injury. The pulmonary neuroendocrine cell contains and secretes immunoreactive calcitonin (iCT), and, under the influence of various irritative stimuli, can be induced to secrete iCT in excess. A prospective study of serum iCT levels in 41 patients with burns was undertaken. Mean serum iCT levels were four times normal values at the time of admission and reached 31 times normal values by 24 hours after injury. These levels did not correlate specifically with burn size. However, serum iCT had a very strong positive correlation with mortality, and in addition, was highest in patients who died early after injury compared with those who died late after injury. Patients who were clinically suspected to have pulmonary injury and who died had markedly higher levels of iCT than those who survived. In addition, serum iCT correlated positively with the need for mechanical ventilation and the amount of pulmonary shunting. Although other factors may also play a role in hypercalcitoninemia, serum iCT may be an important marker for the presence of inhalation injury, as well as a prognostic indicator.

Adult↗