NEW YORK-Betty Shabazz’s burns made her whole body weep.   The fire that destroyed 90% of her skin set off microvascular leaks that affected every organ and led to extreme edema. At the same time, histamine, bradykinins, and oxygen free radicals released by burns increased vascular permeability.   In the kind of burn that the widow of Malcolm X suffered, all body processes accelerate. Metabolism, core temperature, protein breakdown, lipolysis, and stress hormones increase. Patients lose muscle and become more susceptible to infection. Pain activates the limbic system.   Because of massive edema, patients are hugely swollen, occasionally doubling their original weight. But if they aren’t adequately nourished their muscle mass can waste away. “You’re as sick as you can get,” says Dr. David Heimbach of the University of Washington’s burn center.   While better nutrition, early debridement, improved grafts, and artificial skin have boosted survival rates, new layers of complexity in burn wounds are emerging, according to interviews and to reports at the American Burn Association meeting here. Cytokines, especially interleukins 1 and 6 and tumor necrosis factor, may be key to many of the local and systemic effects. They’re called the new frontier of burn therapy.   IL-1 receptor antagonist has been tried as adjunctive therapy for postburn sepsis. But its efficacy is dose-dependent in a narrow window, and it may require individual dosing based on IL-1 levels, says a Cincinnati Shriners Burns Institute report.   Researchers there think that IL-1 and tumor necrosis factor promote muscle catabolism after burn injury by blocking the anabolic effect of insulin-like growth factor. But their studies indicate that IL-1 and TNF don’t induce muscle proteolysis by a direct effect or by inhibiting IGF-1.   IL-4 and IL-6, which down-regulate the inflammatory response, were studied in 14 burn patients by Dr. John Cone’s University of Arkansas team. Serum levels of IL-4 and IL-6 weren’t markedly elevated after serious burns, but IL-4 levels were much higher in the nine who survived.   Fluid resuscitation is the first step in therapy. Patients may get 20 to 30 liters the first day and need almost as much the second, says Dr. Bruce Greenstein, head of the Jacobi Hospital unit here that treated Shabazz. Some compare it to filling a sieve. At Cincinnati Shriners, a duodenal tube is inserted on admission for enteral feeding, based on the burn size, patient’s age, and status. Dr. Michele Gottschlich says the tube-feeding menu-25% protein, folic acid, vitamins A and C, multivitamins, and zinc-almost doubles the patient’s preburn caloric intake.   Dr. Gottschlich says if food does not get into the gut, its microvilli atrophy and GI infections are more likely. But despite careful nutrition, burned children lose lean body mass, becoming peripherally skinny and centrally fat. Growth hormone can reduce their weight loss and stimulate protein synthesis, says Dr. David Herndon’s team at the Galveston Shriners Burns Institute.   Cerebral symptoms in burns are more prevalent than realized, says Dr. Hugo Linares, a Galveston Shriners pathology researcher. He says about 90% of autopsies of burn patients’ brains showed generalized edema and focal or diffuse neuron loss.   Heart output falls precipitously after a burn, and cardiovascular function mediators such as epinephrine, norepinephrine, vasopressin, and angiotensin II increase. Even moderate thermal injury can cause myocardial dysfunction, and Dr. Joseph Murphy of UT Southwestern in Dallas suggests using troponin I as a more specific marker than CPK or its MB isoenzyme. In a study of 21 patients he found troponin I increased a mean 4.5 hours after injury.   To decrease cardiac work, prolonged use of propranolol is safe, says Dr. Herndon’s team. It found the average heart rate fell 10% to 13% in 23 youngsters who were given 0.5 to 1.0 mg/kg of oral or IV propranolol every eight hours for 10 days.   Hematopoiesis is changed by burns. Platelets and red and white cells fall, and bacterial proliferation in the eschar attracts neutrophils that release large amounts of proteolytic enzymes and inflammatory mediators.   Thromboembolic complications may be underestimated. A U.S. Army team at Fort Sam Houston found 1.77% of 1,300 burn patients had DVT or pulmonary embolism. The sum of a patient’s age and area burned can show the risk, it says.   The liver may increase to twice its normal size and cause breathing problems by restricting the diaphragm.   Acute renal failure is relatively rare in burn patients but often fatal. Most frequently the result of fulminant sepsis or multiple system organ failure, it may respond to continuous veno-venous hemodialysis, says Dr. Donald Parks’ Houston team. But 5% of 406 patients developed renal failure at Detroit Receiving Hospital’s burn center, Dr. Jai Prasad’s team reported, particularly those dehydrated from drinking alcohol.   Osteoporosis, new bone formation, and pericapsular calcification are fairly common after burns because of immobilization, hyperemia, and adrenocortical hyperactivity, says Dr. E. Burke Evans of the Galveston Shriners.   Cornell physiotherapist Robin Silverberg says heterotopic bone forms most often around the elbow, and she has treated many burn patients for frozen shoulders, joint capsular tightness, and peripheral neuropathy. She finds rehabilitative therapy more complicated after burns than after spinal-cord injuries. -Elsie Rosner