Hugo A. Linares

Increased mortality with intravenous supplemental feeding in severely burned patients

Patients with large cutaneous burns are characterized by an elevated metabolic rate and lose up to 25% of their body weight within 3 weeks. A previous study suggested that intravenous supplementation to attain nutritional requirements was of no benefit in patients with cutaneous burns covering greater than 50% of their total body surface area. In this study 39 patients with burns greater than 50% of their total body surface area were randomly assigned to receive intravenous supplementation of enteral calories (n = 16) or enteral calories alone (n = 23). Intravenous supplementation decreased the amount of enteral calories that patients with burns could tolerate. The mortality rate was significantly higher (p less than 0.05) in the intravenously supplemented group at 63% as compared with 26% in the group receiving enteral calories alone. Both groups showed significant decrease in natural killer cell activity when compared with controls at both 0 to 7 and 7 to 14 days after injury. T cell helper/suppressor ratios were depressed in both groups when compared with controls; however, the intravenously supplemented group was significantly depressed at 7 to 14 days after burn. Both groups demonstrated hepatomegaly, moderate fatty infiltration, and cholestasis. It is suggested that intravenous supplementation should be carefully evaluated and used only in patients with total enteral failure.

The pathophysiology of smoke inhalation injury in a sheep model

This study describes an experimental model of smoke inhalation injury in sheep, in which the same pathophysiologic alterations occur as with clinical inhalation in man. Both the patients and the experimental sheep develop diffuse pulmonary mucosal sloughing, pulmonary edema, and a decrease in systemic oxygen tension. The results of this study indicate that the pulmonary edema is the result of an increase in microvascular permeability, characterized by increases in lung lymph flow (Qlym), lymph-to-plasma protein concentration ratio (L/P), and transvascular protein flux (Qlym X lung lymph protein concentration), while pulmonary vascular pressures remain constant. Neutrophil degranulation may contribute to the increased microvascular permeability.

Endotoxin (LPS) increases mesenteric vascular resistance (MVR) and bacterial translocation (BT).

Endotoxemia is responsible for many of the pathophysiologic alterations that occur with Gram-negative sepsis. We utilized a chronic ovine model to determine the hemodynamic disturbances in the gastrointestinal tract during endotoxemia. Sheep with indwelling arterial, venous, and pulmonary arterial catheters were used. An ultrasonic flow probe was placed on the cephalic mesenteric artery. The animals were subjected to: 1) Ringers lactate infusion (sham n = 6); or 2) 1.5 mcg/kg E. coli endotoxin (n = 6) over over a period of one half hour and were monitored for 48 hours. They were then sacrificed and specimens of mesenteric lymph node, liver, spleen, kidney, and lung obtained for bacteriologic cultures and histologic analysis. Sheep receiving endotoxin showed more than 50% reduction in the mesenteric blood flow. Mesenteric vascular resistance increased while non-mesenteric systemic vascular resistance decreased. The increase in the total systemic vascular resistance, noted during endotoxemia, was thus likely due to the increase in the mesenteric vascular resistance. At autopsy there were positive cultures for microorganism in the mesenteric lymph nodes in six out of six sheep with endotoxemia as compared to one out of six of control. Thus the vasoconstriction in the mesenteric areas may have resulted in bacterial translocation from the GI tract.

Inhalation injury in burned patients: effects and treatment.

Pulmonary pathology in major thermal injury is found in 30-80 per cent of burn fatalities. The incidence and mortality from inhalation injury increases both with age and increasing burn size. Toxic smoke inhalation injury, characterized by increased lung microvascular permeability, is attenuated by increasing cardiac output to normal levels, indicating that fluid restriction after inhalation injury may lead to excessive lung fluid formation and hypoxia. Fluid administration of approximately 2 ml/kg/% area burned above the calculated resuscitation volume is required following an inhalation injury to provide adequate support for the systemic circulation and maintain cardiac output at normal levels. This additional volume does not contribute to the development of pulmonary oedema, but may decrease its formation by increasing shear forces thus reducing polymorphonuclear leucocyte deposition in the pulmonary microcirculation. Nasotracheal intubation is preferred when airway integrity is compromised by inhalation injury. The advantages are non-operative placement, ease of discontinuation, minimal bacterial contamination and leaving neck burns undisturbed. The administration of the appropriate antibiotics for documented infection is recommended, while steroids have been shown to be of no benefit.

Failure of TPN supplementation to improve liver function, immunity, and mortality in thermally injured patients.

Hypermetabolism with negative nitrogen balance and immune deficiencies characterize the systemic response to major thermal injury. Patients with burns greater than 50% of the total body surface area (TBSA) initially have poor gastrointestinal function, making it difficult to deliver sufficient enteral calories to meet nutritional requirements. Controversy has developed over whether to supplement oral alimentation with total parenteral nutrition (TPN) early in their treatment. This study randomly assigned 28 patients with burns greater than 50% TBSA to receive TPN supplementation or no TPN supplementation in the first 10 days postburn. Patients receiving TPN supplementation had significantly lower T-cell helper-to-suppressor cell ratios than the unsupplemented group. However, there was no difference in mortality between the groups (eight in each). All patients who died developed hepatomegaly associated with fatty infiltration cholestasis and antemortem liver function abnormalities, indicating that this syndrome is the result of burn injury itself, not TPN.

In vitro toxicity of topical antimicrobial agents to human fibroblasts

Topical antimicrobial agents are essential to optimal burn care. However, exposure of WI-38 human diploid fibroblasts (ATCC CCL 75) and fresh donor human dermal fibroblasts to silver sulfadiazine and mafenide acetate results in a significant reduction in cell proliferation, as determined by hemocytometer cell counts and total matrix protein assays, within 48 hr of exposure. Changes in cellular morphology and progressive deterioration of cytoplasmic organelles and the nucleus are seen with phase-contrast microscopy and transmission electron microscopy. These findings may explain the clinical observation of delayed wound healing after the use of topical antimicrobial agents.

The Quality of Life after Major Thermal Injury in Children: An Analysis of 12 Survivors with 80% Total Body, 70% Third-degree Burns

Twenty-one children admitted between December 1981 and May 1985, with greater than 80% total body surface area burn (TBSAB), underwent total excision and grafting of all of their wounds within 72 hours of injury. Twelve survivors (with an average TBSAB of 89%, 82% third degree) were studied in detai

Pulmonary Injury in Burned Patients

Inhalation injury has emerged as the number one cause of fatality in the burn patient. Fiberoptic bronchoscopy and 133Xe scanning complement traditional clinical signs of inhalation injury and have led to discovery of a higher incidence of these injuries among patients with burns. Patients with inhalation injury typically demonstrate three stages: acute pulmonary insufficiency, pulmonary edema, and bronchopneumonia, all of which carry at least 50 per cent mortality rates. The major early pathophysiologic changes in the lungs of burned patients are related to upper-airway obstruction and lower-airway permeability edema. Treatment consists of intubation for signs of respiratory distress, pulmonary toilet, humidification of inspired air, and antibiotics for documented infection.

The pathophysiology of inhalation injury - a review

The inhalation of smoke results in a series of pathophysiological events involving the respiratory and circulatory systems. Upper airway injury is mainly the result of heat damage. The lesions of the tracheobronchial and parenchymal areas are more related to the chemicals present in the smoke. The initial damage of the tracheobronchial mucosa results in chemotaxis of leucocytes into the airway tissues, with release of inflammatory mediators and formation of exudative materials. Bronchial oedema, bronchoconstriction, and bronchial obstruction by cast materials develop. The pulmonary microvasculature shows a permeability type of lesion, which is the result of mediator release from entrapped polymorphonuclear cells. This parenchymal lesion may relate to the tracheobronchial damage and be the result of a reperfusion injury. The systemic changes which have been identified relate to an increase in microvascular permeability and a reduction of myocardial contractility secondary to the inhalation of the toxic products of smoke. These latter findings may help to explain the difficulty encountered in resuscitating some of the burn victims who have concomitant inhalation injury.

A report of 115 consecutive autopsies in burned children: 1966–1980

The overall mortality rate at the Shriners Burns Institute, Galveston Unit, decreased from 14 per cent in 1966, to 2.8 per cent in 1980. In all, 74.8 per cent of the deaths were associated with sepsis, and pulmonary lesions were the most frequent fatal complications (75.6 per cent). The burn wound was the major source of sepsis (62.7 per cent). Pseudomonas, E. coli, Klebsiella, Candida spp. and Staphylococcus aureus were the most common cultured bacteria. After a new standard fluid resuscitation programme, tangential excision and surgical management of the burn wound sepsis were adopted, the fatalities decreased from an average annual mortality rate of 11.5 per cent in the years 1966-75, to an average annual mortality rate of 2.8 per cent in the period 1976-80. After the routine antacid and milk diet were adopted (1970), the percentage of stomach and duodenal ulcers found at autopsy decreased from 2.0 per cent to 0.8 per cent, and from 3.5 per cent to 0.5 per cent respectively. The morphological alterations in the lymphoid tissue, reflecting a defect in T-cell function and stimulation of B-cell function, were present up to 114 days post burn.