gastrin secretion following burns

1
296 Burns,8,296-298 Printedin GreatBritain Abstracts CLINICAL STUDIES and there should be serial monitoring of pulmonary extravascular water volumes. Tracheostomv should be Gastrin secretion following burns avoided. Getzen L. C. and Pollak E. W. (198 1) Fatal respira- Basal serum gastrin concentrations and the serum tory distress in burned patients. Surg. Gynecol. Obstet. gastrin responses to a meal have been studied in 5 152,741. patients with burns covering between 14 and 58 per cent of the bodv surface. Comoared with the resoonses Chanaes in ventilation and oerfusion observed aher healing of the wound was complete the acute studies within days of injury showed the serum Multiple inert gas analyses have been used to differen- gastrin responses to a meal to be reduced by 38 per tiate the relative contributions of intrapulmonary cent (PC 0.025). In contrast there was no change in shunts and low ventilation perfusion changes in the basal concentrations of gastrin in serum between patients suffering from smoke inhalation injury. It was the early and late studies. These results do not support found that early alterations of ventilation and per- the suggestion that stress ulcers are related to fusion were due to high ventilation perfusion compart- hypergastrinaemia. ments and dead space ventilation. Later alterations Steen J., Muchardt O., Sorensen B, et al. (1981) included significantly increased perfusion of low Depressed gastrin secretion in burns. Burns 8, 19. ventilation perfusion compartments and the return of high ventilation perfusion compartments to baseline ventilation values. True intrapulmonary shunting was Stress ulcers and burn8 not found. These results may represent-early regional uulmonarv vasospasm followed bv reaional bronchial obstruction and gradual alveolar collapse secondary to bronchospasm, bronchial oedema or partial occlusion by cellular debris. Stress induced or Curling’s ulcers of the stomach and duodenum in very extensively burned patients are due to a defect in the mucosal barrier to secreted acid. The cause of this defect is related partly to mucosal ischaemia which is aggravated by hypotension, sepsis and hypoxia. Early prophylactic administration of antacids and cimetidine, singly or combined, has significantly reduced the incidence of these ulcers. Gastric resection and vagotomy appear to be the method of choice when preventive measures have failed or have not been used and massive bleeding or perforation has occurred. Robinson N. B., Hudson L. D., Robertson H. T. et al. (1981) Ventilation and perfusion alterations after smoke inhalation injury. Surgery90,352. Pruitt B. A. and Goodwin C. W. (I 98 I) Stress ulcer disease in the burned patient. World J. Surg. 5, 209. Causes of fatal respiratory distress Inhalation injury and lung water content Extravascular lung water volume was measured in burn patients with and without inhalation injury and found to be significantly elevated (10.12 f 3.43 ml/kg) in the patients with inhalation injury. The volume in patients without inhalation injury was 3.91 f I.49 ml/kg. Both accumulation of extravascular lune water volume and ventilation perfusion abnorm&ties occurred within hours of smoke inhalation but were not closely correlated with Ten of 167 patients with very extensive burns severity of inhalation injury. In this study, presence of developed fatal respiratory distress. It was caused by facial or oropharyngeal burns, carboxyhaemoglobin fluid overload in 5 patients with anuria within 48 levels, carbonaceous sputum or closed space injury did hours of admission. Later deaths were due to fluid not differentiate patients with only airway injury from overload and pulmonary sepsis. Three of the 4 patients those with parenchymal injury. Patients in both who had a tracheostomy died of pulmonary sepsis groups who died with sepsis had significant increases whereas all IO patients who had endotracheal in extavascular lung water content 24 to 48 hours after intubation survived. Preventable causes of fatal the clinical onset of sepsis. The normal hydrostatic respiratory dist:ess were found in all 10 patients. pressures in these septic patients suggested that the Colloid should be given during early fluid resuscitation increase in extravascular lung water content associated

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296 Burns,8,296-298 Printedin GreatBritain

Abstracts

CLINICAL STUDIES and there should be serial monitoring of pulmonary extravascular water volumes. Tracheostomv should be

Gastrin secretion following burns avoided.

Getzen L. C. and Pollak E. W. (198 1) Fatal respira- Basal serum gastrin concentrations and the serum tory distress in burned patients. Surg. Gynecol. Obstet. gastrin responses to a meal have been studied in 5 152,741. patients with burns covering between 14 and 58 per cent of the bodv surface. Comoared with the resoonses Chanaes in ventilation and oerfusion observed aher healing of the wound was complete the acute studies within days of injury showed the serum

Multiple inert gas analyses have been used to differen-

gastrin responses to a meal to be reduced by 38 per tiate the relative contributions of intrapulmonary

cent (PC 0.025). In contrast there was no change in shunts and low ventilation perfusion changes in

the basal concentrations of gastrin in serum between patients suffering from smoke inhalation injury. It was

the early and late studies. These results do not support found that early alterations of ventilation and per-

the suggestion that stress ulcers are related to fusion were due to high ventilation perfusion compart-

hypergastrinaemia. ments and dead space ventilation. Later alterations

Steen J., Muchardt O., Sorensen B, et al. (1981) included significantly increased perfusion of low

Depressed gastrin secretion in burns. Burns 8, 19. ventilation perfusion compartments and the return of high ventilation perfusion compartments to baseline ventilation values. True intrapulmonary shunting was

Stress ulcers and burn8 not found. These results may represent-early regional uulmonarv vasospasm followed bv reaional bronchial obstruction and gradual alveolar collapse secondary to bronchospasm, bronchial oedema or partial occlusion by cellular debris.

Stress induced or Curling’s ulcers of the stomach and duodenum in very extensively burned patients are due to a defect in the mucosal barrier to secreted acid. The cause of this defect is related partly to mucosal ischaemia which is aggravated by hypotension, sepsis and hypoxia. Early prophylactic administration of antacids and cimetidine, singly or combined, has significantly reduced the incidence of these ulcers. Gastric resection and vagotomy appear to be the method of choice when preventive measures have failed or have not been used and massive bleeding or perforation has occurred.

Robinson N. B., Hudson L. D., Robertson H. T. et al. (1981) Ventilation and perfusion alterations after smoke inhalation injury. Surgery90,352.

Pruitt B. A. and Goodwin C. W. (I 98 I) Stress ulcer disease in the burned patient. World J. Surg. 5, 209.

Causes of fatal respiratory distress

Inhalation injury and lung water content Extravascular lung water volume was measured in burn patients with and without inhalation injury and found to be significantly elevated (10.12 f 3.43 ml/kg) in the patients with inhalation injury. The volume in patients without inhalation injury was 3.91 f I.49 ml/kg. Both accumulation of extravascular lune water volume and ventilation perfusion abnorm&ties occurred within hours of smoke inhalation but were not closely correlated with

Ten of 167 patients with very extensive burns severity of inhalation injury. In this study, presence of developed fatal respiratory distress. It was caused by facial or oropharyngeal burns, carboxyhaemoglobin fluid overload in 5 patients with anuria within 48 levels, carbonaceous sputum or closed space injury did hours of admission. Later deaths were due to fluid not differentiate patients with only airway injury from overload and pulmonary sepsis. Three of the 4 patients those with parenchymal injury. Patients in both who had a tracheostomy died of pulmonary sepsis groups who died with sepsis had significant increases whereas all IO patients who had endotracheal in extavascular lung water content 24 to 48 hours after intubation survived. Preventable causes of fatal the clinical onset of sepsis. The normal hydrostatic respiratory dist:ess were found in all 10 patients. pressures in these septic patients suggested that the Colloid should be given during early fluid resuscitation increase in extravascular lung water content associated