Stress ulcer disease in the burned patient.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to C W Goodwin.
Explore the source record for details and available documents.
To determine if visceral blood flow was altered by thermal injury, effective renal blood flow (ERBF) was measured by para-aminohippurate clearance in five control subjects and 13 nonbacteremic burn patients (mean burn size: 50% total body surface, range: 24.5-83.5) 6-25 days after burn injury. Splanchnic blood flow (SBF) and cardiac output were determined in a matched group of ten patients by indocyanine green clearance and dilution techniques, respectively. Renal and splanchnic oxygen consumptions (VO2) were calculated from regional arteriovenous O2 differences and blood flows. ERBF was not significantly elevated in these patients (780 +/- 68 ml/min x m2, mean +/- SE, versus 552 +/- 37 in controls). SBF, at 1463 +/- 96 ml/min x m2, was twice normal and 19% of the cardiac index (7764 +/- 393 ml/min x m2). Individual variations in ERBF and SBF were unrelated to burn size or the time after injury, but ERBF varied with 24-hour sodium excretion. Renal and splanchnic VO2 were twice normal levels at 33 +/- 6 and 66 +/- 4 ml/min, respectively. These results indicate that an increase in ERBF is not an obligatory response to burn injury, but is dependent on sodium load and/or vascular volume. Conversely, SBF is consistently increased by thermal injury and contributes to the rise in cardiac output after injury. While the increase of SBF is appropriate for the rise in local VO2, the cause of the apparent splanchnic vasodilation is unknown.
Hyperoncotic albumin proved ineffective as a plasma volume expander in the resuscitation of four acutely burned children. Hypovolemia and pulmonary edema were apparently intensified by an obligatory fluid shift following tissue extravasation of protein. We conclude that, when used, hyperoncotic albumin should be suspended in a sufficient volume of saline to produce a solution isotonic and iso-oncotic relative to plasma.
Ninety-seven of 763 patients admitted to a burn center during a 3-year period had histologically confirmed bacterial or fungal burn wound invasion. Nine of these 97 patients survived and 88 died. Burn wound infection was the principal cause of death in 57 patients and was diagnosed perimortem in an additional 31 patients but was not judged to be the primary cause of death. Pseudomonas aeruginosa continues as the most frequent offending organism. The variety of mycotic and bacterial organisms identified, however, suggests that the compromise of the host is the critical factor, and not any particular microorganism. A variety of combinations of treatments are described: the selection of treatment depends upon the type and extent of infection.
Renal blood flow was elevated in convalescent burn patients shortly before discharge (992 +/- 112 mL/min/sq m in burn patients vs 551 +/- 37 mL/min/sq m in normal subjects; mean +/- SE). Autopsy studies demonstrated that renal enlargement was a constant feature of patients after a prolonged hospital course; the kidneys of 28 patients who died after 60 days of hospitalization weighed 241 +/- 10 g vs 153 +/- 8 g in control subjects. The increase in renal weight was primarily related to cellular hypertrophy and hyperplasia. These physiological and morphological findings in thermally injured patients may be a form of renal work hypertrophy following increased protein catabolism accompanying severe injury.
In this prospective study of thyroid catecholamine interactions, 15 severely burned patients were divided into two groups. Nine patients receiving 200 micrograms/day of triiodothyronine constituted the T3-treated group. Eight additional patients constituted the untreated group. Mean serum concentrations of T3 were significantly lower in the untreated group than in the treated group. Mean serum thyroxine (T4) concentrations were significantly higher in the untreated group than in the treated group. The mean plasma norepinephrine concentration in the untreated group was significantly greater than that of the treated group. In the untreated group, log plasma norepinephrine correlated inversely with serum T3. Similarly, in the untreated group, log plasma epinephrine correlated inversely with serum T3. Metabolic rates were not different between groups. These data suggest that a reciprocal relationship exists between plasma concentration of T3 and both norepinephrine and epinephrine in untreated burn patients and that treatment with the metabolically active hormone, triiodothyronine, does not alter the level of hypermetabolism accompanying thermal injury.
To characterize the role of the liver and kidney in the metabolic response to injury and infection, selective catheterization of the hepatic (42 veins) and renal veins (21 veins) was performed in 31 burn patients (mean burn size: 51% TBS), studied 4-129 days postinjury. Blood flow was determined by standard clearance techniques (ICG and PAH), and simultaneous arterial and hepatic and/or renal vein blood was obtained for oxygen, glucose, lactate, pyruvate, and amino acids. Patients studied in the first to third weeks postinjury were classified as noninfected (8 studies), bacteremic (8 studies), or bacteremic with complications (5 studies). There was no difference in age, weight, mean burn size, pulse rate, blood pressure, rectal temperature, total body oxygen consumption, or cardiac index among these groups. Estimated hepatic blood flow (EHBF) and hepatic substrate balance of these patients were compared with postabsorptive normal subjects in the literature (mean +/- SEM or range). :Formula: (See Text) Thermal injury alone resulted in marked increases in EHBF, hepatic oxygen uptake, and glucogenesis. The added insult of bacteremia significantly increased hepatic glucose output; as clinical sepsis progressed, glucose output decreased sharply. The kidney consistently demonstrated a net uptake of glucose in all studies. The changes in hepatic glucose output in bacteremic patients occurred without significant differences in EHBF, oxygen utilization or lactate uptake, but were associated with marked alterations in amino acid uptake.
A prospective study of thyroid function was performed in 25 thermally injured patients. These patients are divided into two groups. The first group contains five patients with greater than 50% burn size studied longitudinally during the first 15 days following thermal injury. Significant suppression of serum concentrations of 3,5,3'-triiodothyronine (T3) and elevation of serum concentrations of 3,3',5'-triiodothyronine (rT3) were seen. The free thyroxine index and serum TSH concentrations remained within the normal range. To assess the clinical significance of these alterations in peripheral thyroid hormone concentrations, a second group of 20 patients was studied. We measured the free serum levels of T4 (FT4) and T3 (FT3) in ten patients, mean age 34 years, mean burn size 56%, studied during a period of clinical deterioration, and in ten patients of comparable age and burn size who were clinically stable. Both FT4 and T3 values were significantly lower in the unstable patients (p < 0.01). All FT3 values for the unstable patients (M +/- SE), 193 +/- 14 pg/dl, were below the normal range for FT3 of 230 to 669 pg/dl, and significantly lower than those observed in the stable patients (M +/- SE), 430 +/- 59 pg/dl (p < 0.001). This correlation of biochemical hypothyrodisim with clinical deterioration may have functional significance for the critically ill trauma patient.
Explore the source record for details and available documents.
Interdigestive gastirc acid output and acid secretory response to histamine, insulin and pentagastrin were studied in five dogs before and after creation of a right to left extracardiac vascular shunt. The arterial PO2 decreased from 81.5 +/- 5.5 mm Hg to 39.8 +/- 6.0 mm Hg postoperatively with no change in arterial pH or PaCO2. Basal (interdigestive) acid output increased from 1.19 +/- 0.26 mEq/hr to 4.97 +/- 0.81 mEq/hr postoperatively. Acid secretory response to insulin was increased after the induction of chronic hypoxia. Increased sensitivity to pentagastric was also observed although parietal cell mass (maximum histamine-stimulated output) was unchanged postoperatively. Changes in acid secretory response and PaO2 were present at one week and were sustained through twelve weeks after shunting. Chronic hypoxia resulted in gastric acid hypersecretion secondary to enhanced sensitivity of the parietal cell to a combination of neural and humoral stimuli.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Newborn and adult dog heart mitochondria were prepared from animals chronically adjusted to varying arterial oxygen tensions. Similarly, rat liver and heart mitochondria were isolated from animals acutely exposed to lowered inspired oxygen. After isolation, all mitochondrial samples were assayed under normoxic conditions. These experiments illustrated the following effects of oxygen on mitochondrial function: 1) respiratory activity in State 3 or in the uncoupled state increased after hypoxia and decreased after increased in vivo oxygenation; 2) similarly, the turnover of cytochrome oxidase increased in hypoxia and decreased after increased oxygenation; 3) after chronic hypoxia cytochrome oxidase, cytochrome c and b concentrations decreased per miligram of mitochondrial protein; 4) all mitochondrial preparations were well coupled and exhibited normal capabilities to perform oxidative phosphorylation. The data are interpreted to indicate sensitive control of mitochondrial respiratory capacities by oxygen in vivo.
Recent studies have demonstrated that fracture healing normally takes place under hypoxic conditions. The present study evaluated the effect of a state of chronic systemic hypoxia on fracture healing in dogs. A significant delay in fracture healing was demonstrated in the hypoxic animals roentgenographically, histologically, and by strength-testing criteria. A further reduction in the available oxygen supply below that present during normal repair had an adverse effect on fracture healing.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.