Biomedical subjects
Publications and source records attributed to W L Garner.
This article discusses the pathogenesis and reconstruction of hypertrophic scarring of the burned trunk. General reconstruction schemata are provided. Reconstruction of specific problems of the chest, abdominal wall, breasts, and perineum are also discussed.
Clinical tissue expansion has been quite successful but takes 2 to 3 months. This study compares the effects of a conventional tissue expansion regimen of 6 weeks with an accelerated regimen of 2 weeks in the dog model, which is biomechanically similar to the human. In 22 dogs, the skin expanded 34.4 percent in the 2-week and 35.8 percent in the 6-week protocol, excluding stretch and recruitment. There was thinning of the panniculus carnosus in the 6-week group and otherwise no significant decrease in dermal thickness in either group. The biomechanical properties of elasticity and creep did not differ in expanded skin from both groups, while stress/relaxation mildly decreased from a control value of 53.5 percent to 48.8 percent in the 6-week group (p less than 0.05). Collagen activity was increased in both the 6-week and the 2-week groups (p less than 0.001) over nonexpanded skin, and immunohistochemical staining with a monoclonal procollagen antibody demonstrated collagen synthesis by dermal fibroblasts in both groups. We conclude that rapid tissue expansion did not demonstrate any deleterious effects when compared with a conventional regimen.
A monoclonal antibody to procollagen type I (anti-pC) which specifically stains cells synthesizing collagen was used to study the healing of chicken flexor tendons in vivo. Healing was assessed using routine hematoxylin and eosin histology and immunoperoxidase staining with anti-pC. Studies showed that epitenon cells proliferate 3 days after injury and are producing collagen by 7 days after injury. Tenocytes do not begin producing collagen until 14 to 21 days after injury. From 3 to 5 weeks, the entire substance of the tendon becomes filled with collagen-synthesizing cells. These cells may have originated from the tendon sheath, the epitenon, or the endotenon; however, the evidence presented in this study suggests that the epitenon is a major source of these cells.
Although adequate tissue oxygenation is essential to maintain cellular metabolism, the use of hyperoxia to improve oxygen delivery or to improve metabolic performance is controversial. For example, supplemental inspired oxygen is reportedly beneficial in the treatment of some experimental infections; however, oxygen therapy also has well-documented adverse side effects. To evaluate the effect of increased inspired oxygen concentration (FIO2) in animals with fulminant sepsis, 117 Sprague-Dawley rats underwent cecal ligation and puncture. Animals were then exposed to an FIO2 of either 0.21, 0.4, or 0.8. Twenty sham-operated controls had no mortality with any FIO2. Increasing the FIO2 increased mortality from 70% to 85% in animals receiving 40% O2, and to 100% in those receiving 80% O2. Autopsies revealed mild pulmonary oxygen toxicity with 80% O2 exposure in both control and septic animals, but normal lung histologic appearance in animals receiving lower levels of oxygen. Arterial blood gases documented maintenance of oxygenation and ventilation. Thus, pulmonary oxygen toxicity does not appear to be the mechanism for increased mortality. Supplemental oxygen may worsen, rather than improve, survival after fulminant infection.
We designed a ventilation-perfusion index (VQI) to estimate venous admixture (Qsp/Qt) in a real-time fashion by simultaneous pulse and pulmonary artery oximetry in 17 patients with acute respiratory failure. Changes in Qsp/Qt were produced by altering the level of continuous positive airway pressure. VQI correlated well with Qsp/Qt (r = 0.78). This contrasts with the poor correlation found between Qsp/Qt and the commonly used oxygen tension based indices such as PaO2/FIO2 (r = -0.51), PaO2/PAO2 (r = 0.47), and PAO2-PaO2 (r = 0.23). The use of dual oximetry to derive a VQI appears to be a reliable and accurate method for real-time assessment of pulmonary gas exchange in patients with acute respiratory failure.
Critical review of cholescintigraphy in critically ill patients suggests the examination will not conclusively prove or disprove the diagnosis of acute cholecystitis. Of 17 scans performed in critically ill patients with clinical evidence of acute cholecystitis, 7 were true-negative, 1 was false-negative, 6 were false-positive, and 3 were nondiagnostic. Cholestasis and hepatocyte dysfunction, common in the critically ill, result in abnormal clearance of hepatobiliary radionuclide imaging agents, decreasing the usefulness of cholescintigraphy in this patient population. Diagnosing acute cholecystitis in a critically ill patient remains difficult.
A monoclonal antibody to procollagen type I, which specifically stains cells actively secreting collagen, was used to study the healing of chicken flexor tendons in vitro. Healing was assessed with histology, immunohistologic staining, and autoradiography. Studies showed that epitenon cells proliferate 2 days after injury and are producing collagen 4 days after injury. Endotenocytes remain dormant during this time period. Tendons in vitro demonstrate active collagen synthesis and thus the capacity for autonomous repair.
The clearance of amikacin during hemodialysis (HD) was determined in eight critically ill patients. The dialysis period averaged 3.4 h with a blood flow of 200 ml/min. The average amikacin clearance between dialysis was 7.30 +/- 4.78 (SD) ml/min which increased to 37.5 +/- 8.01 ml/min during dialysis. The average serum amikacin concentration before dialysis fell 27% after dialysis. The fraction of drug in the body removed only from dialysis averaged 21%. Although amikacin was cleared more effectively during HD compared to the interdialysis period, the small amount of drug removed suggests that routine supplemental dosing of amikacin after HD may not be necessary.
Prodigious quantities of blood are withdrawn from critically ill patients in intensive care units, adding to the cost of their care and, more important, to their morbidity. We undertook a simple study to record the volumes of blood drawn in two intensive care units. In one, specimens were ordered by the physicians, and in the other, blood was drawn in accordance with a protocol. Volumes of blood discarded to clear indwelling lines were also measured. After the staff had been informed of the results and the use of smaller collecting tubes had been instituted, a repeat study showed that the mean volume of blood drawn was reduced by nearly half. We suggest that only pertinent laboratory tests be ordered, that procedures to avoid discarding part of the sample be adopted, and that smaller collection tubes be used when appropriate.
The hypersplenism associated with portal hypertension usually resolves with a successful shunting procedure. Recurrent hypersplenism has been associated with shunt thrombosis. We describe a patient with pancytopenia, jaundice, and diffuse edema after a distal splenorenal shunt. His shunt was angiographically proved patent. Extensive evaluation revealed severe alcoholic cardiomyopathy with passive splenic congestion. He died of cardiac failure. Alcohol is a systemic toxin that affects other organs, as well as the liver.
The isolation of adenovirus from the liver of an infant with Reye's syndrome prompted a retrospective review to determine the role of this group of viruses in the cause of Reye's syndrome. A total of 34 patients with Reye's syndrome who were admitted to Vanderbilt University, Nashville, Tenn, during a ten-year period were identified. Six of the patients were younger than 1 year, and positive adenoviral cultures and increased serological responses were obtained in three of these children. The clinical and pathologic data from these three children suggest that adenovirus may be an important agent in initiating Reye's syndrome in the very young child. Further, the mitochondrial abnormalities present in the livers of the patients with adenovirus-associated disease tended to be mild in spite of severe clinical disease.
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