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Biomedical subjects

C S Houston

Publications and source records attributed to C S Houston.

At least 145 records · Page 8Linked to original sources

Nitrogen washout studies in acute mountain sickness.

We assessed the severity of Acute Mountain Sickness (A.M.S.), indices of pulmonary gas exchange and nitrogen washout curves in healthy volunteers acutely exposed to high altitude. Symptoms of A.M.S. ranged from malaise to vomiting with intractable headache. The slope of phase III of the nitrogen washout curve increased most in those subjects with the most severe A.M.S. and who were most hypoxemic. The sickest subject also had the greatest increase in (A-a)DO2 and the largest increase in the slope of phase III. These abnormalities in gas exchange and nitrogen washout curves in the subjects with the most marked A.M.S. suggest that the manifestations of cerebral and pulmonary dysfunction at altitude develop simultaneously, although not necessarily by identical mechanisms.

Adolescent↗

Pulmonary gas exchange in acute mountain sickness.

The severity of acute mountain sickness (AMS) was investigated in healthy volunteers, airlifted to high altitude (5,360 m). Blood gases were measured at 2,990 m and 5,360 m. Symptoms of AMS were found in all subjects, but ranged from malaise to vomiting with intractable headache. The clinical severity of AMS was directly related to the arterial PCO2 and inversely to pH, but unrelated to the PO2 on arrival at high altitude. However, PO2 fell and was lowest 48 h after arrival at high altitude in those subjects with the most severe AMS. These were the only subjects to show an increase in the alveolar-arterial PO2 difference and in the venous admixture ratio during the first 48 h. These abnormalities in gas exchange, which developed in the subjects with the most marked cerebral symptoms, suggest that the manifestations of cerebral and pulmonary dysfunction at altitude develop simultaneously, a finding that suggests coexisting cerebral and pulmonary edema.

Acute Disease↗

Cerebral form of high-altitude illness.

Twelve cases of severe altitude illness are reported in which the neurological signs and symptoms dominated the clinical picture. Pulmonary oedema, retinal haemorrhage, thrombophlebitis and pulmonary embolism, bronchopneumonia, and coronary-artery disease were also present in several of the patients but the primary problem seems to have been cerebral oedema. Other published cases support this impression. Patients who were returned to low altitude early in the disease fared well; two patients died, and in both cases evacuation had been delayed. The most effective prevention lies in slow ascent, though in one case reported here the rate of climb was well within the recommended limit. Recommended management is rapid descent to low altitude at earliest indication of cerebral or pulmonary oedema, intravenous dexamethasone or betamethasone in large doses, hydration, diuresis (frusemide has been most used), and perhaps other intravenous therapy with hyperosmolar materials such as mannitol, urea, 50% saline, or 50% sucrose. Prognosis is good if descent and treatment are started early, but permanent damage may be anticipated if the patient is unconscious for any prolonged period before descent.

Adult↗

Hormonal and electrolyte response to exposure to 17,500 ft.

Hormone, electrolyte, and body fluid compartment changes were studied in subjects who either spent time at 10,000 ft before flying to 17,500 ft or were premedicated with acetazolamide and flown directly to 17,500 ft. In the former group, at 10,000 ft, renin and aldosterone were not different from control. Cortisol increased significantly from 9.8 to 19.5 mug/100 ml on the third day. At 17,500 ft, renin, aldosterone and cortisol were significantly elevated on day 3 but had returned to control levels by day 5. Sodium and potassium excretion was significantly reduced at both altitudes. Total body water, extracellular and plasma volume were reduced (P less than 0.05) at 17,500 ft. Subjects pretreated with acetazolamide and flown directly to 17,500 ft had significant increases (P less than 0.001) in plasma renin, aldosterone, and cortisol levels during the first 4 days at altitude. On day 1 there was a decrease of 45% in sodium and 38% in potassium excretion. On day 4 there was a decrease of 63% and 51%, respectively. These changes are not associated with the premedication. The initial changes may reflect the immediate response to stress and alkalosis followed by a return to control levels as the body adapts to altitude.

Acetazolamide↗

Effect of altitude exposure on platelets.

Since decompression from depth is known to produce a fall in platelet count, the effect of altitude decompression and high-altitude exposure on platelets was investigated. Sixteen subjects decompressed without hypoxia to 20,000 ft simulated altitude for two hours showed a significant (P less than 0.01) drop in circulating platelet count of approximately 10% for three days following decompression. Four of five subjects similarly exposed had a shortened autologous platelet survival compared to that prior to exposure. Subjects exposed to 9,800 ft and then 17,600 ft in a mountain environment showed a significant mean decrease in platelet count on day 2 of 7% and 25% respectively, which had returned to control by day 5. Nonhypoxic and hypoxic decompressed rabbits which received homologous chromium-51-labeled platelets had an increase in lung radioactivity compared with sea-level controls. It is postulated that altitude decompression produces platelet reductions similar to these seen after decompression from depth, and that platelets sequester in the pulmonary vascular bed.

Altitude↗

Recurrent urinary infections in girls: relation to enuresis.

Maximum bladder capacities (MBC) have been studied in 89 girls receiving treatment for urinary infections at a time when the infection had been controlled. Fifty-six of the girls had been enuretic when first seen, 40 remained enuretic even when the infection had been cured. The MBC's of the enuretic children were significantly smaller than those who were not or had not been enuretic. The enuresis and small bladder capacities were therefore not usually due to the urinary infection. It is concluded that in girls either enuresis predisposes towards the development of urinary infections, or that a common underlying pathology predisposes to both entities.

Adolescent↗

Hypophosphatasia.

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Alkaline Phosphatase↗