The Role of Exudate Losses in the Protein and Electrolyte Imbalance of Burned Patients

metabolic Derangements Imperiling the Perforated Ulcer Patient

“…In 1944, Coller and his associates described a fall of the chloride level associated with chloride retention.5 A subsequent study of severe burns in this hospital afforded an opportunity to observe a similar lowering of the sodium level during a period of post-traumatic so¬ dium retention. 11 The paradoxical nature of these observations is mentioned by Coller and has been emphasized more recently by Moore,f who finds the paradox to be a characteristic postoperative phenomenon. To explain this extraordinary situation, Moore has suggested that sodium shifts into muscle cells or bone after trauma.f In these studies of patients with perforated peptic ulcers, we have found that the apparent paradox of falling sodium and chloride concentrations during sodium and chloride retention can be simply explained without invoking the con¬ cept of intracellular accumulation of these extracellular electrolytes.…”

Current problems in burn hypermetabolism

“…6,7 Francis D. Moore and others then furthered the understanding of burn hypermetabolism in the early 1940s by further quantifying the causes of hypermetabolism, including sources of nitrogen and exudative ion losses. 8,9 Subsequently, Dr. Moore began using patient weights to guide fluid resuscitation and feeding, noting that weight loss signified a dire situation in trauma and burn patients, in part reflecting severe electrolyte and nutritional deficiencies. 10 Based on their research, resuscitative protocols for severely burned individuals emerged.…”

Protein metabolism following injury.

“…Increased urinary nitrogen excretion also occurs in patients with injuries of similar severity (Flear and Clarke, 1955) and in patients with burns of up to one third of the body surface (Moore, Langohr, Ingebretsen, and Cope, 1950). Moderate injuries, such as an open compound fracture of the femur or burns involving more than one third of the body surface, and severe injuries arising from multiple fractures show a prolonged and greatly increased rate of catabolism of albumin and y G globulin (Birke, Liljedahl, Plantin, and Wetterfors, 1959/60;Bull, 1962 and and nitrogen excretion in urine (Moore et al, 1950;Moore and Ball, 1952). In these moderate and severe injuries prompt therapy of substantial haemorrhage by the transfusion of a volume of blood equal to that lost results in a less severe catabolic response than if the lost blood is only partly replaced (Flear and Clarke, 1955).…”

“…The operative repair of a fractured tibia by compression plating is a more severe injury and causes a transient twofold increase in the rate of albumin catabolism (Davies et al, 1970b). Increased urinary nitrogen excretion also occurs in patients with injuries of similar severity (Flear and Clarke, 1955) and in patients with burns of up to one third of the body surface (Moore, Langohr, Ingebretsen, and Cope, 1950). Moderate injuries, such as an open compound fracture of the femur or burns involving more than one third of the body surface, and severe injuries arising from multiple fractures show a prolonged and greatly increased rate of catabolism of albumin and y G globulin (Birke, Liljedahl, Plantin, and Wetterfors, 1959/60;Bull, 1962 and and nitrogen excretion in urine (Moore et al, 1950;Moore and Ball, 1952).…”