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Biomedical subjects

R Demling

Publications and source records attributed to R Demling.

At least 55 records · Page 3Linked to original sources
PubMed1981

Testing and treatment of arterial graft thrombosis.

The in vivo technique of Sauvage et al for determining prosthetic arterial graft thrombogenicity was employed in the sheep carotid model using 4 mm commercial expanded polytetrafluoroethylene (Gore-Tex) grafts. Expanded polytetrafluoroethylene was found to be thrombogenic at 4 hours of low flow in this model. At 24 hours all of these grafts were totally occluded at low flow rates. Intravenous use of ibuprofen (Motrin), a thromboxane inhibitor, in this model markedly reduced occlusion and thrombogenicity at 4 and 24 hours. All grafts were patent at 24 hours when ibuprofen was used.

Animals↗
PubMed1981

Pulmonary microvascular injury from lipoxygenase infusion: comparison with endotoxemia.

We compared the response of the pulmonary microcirculation to a 5-hr infusion of soybean lipoxygenase with that seen after endotoxin. We monitored microvascular integrity using lung lymph flow QL and lymph/plasma (L/P) protein ratio in unanesthetized sheep. We noted a twofold to threefold increase in QL and a slight decrease in L/P ratio beginning about 1 hr after onset of the lipoxygenase infusion. Leukocyte count decreased significantly and lymph lysosomal enzyme activity increased. Pulmonary artery pressure initially increased from 16 to 31 mm Hg, then decreased to 25 mm Hg during continued infusion. Platelet count remained constant. Parameters returned to baseline several hours after infusion. This pulmonary vascular pressure and lymph flow response was very similar to that seen in the increased permeability phase of endotoxin. A decrease on the L/P ratio and a constant rather than a decreased platelet count were findings different from those seen after endotoxin.

Animals↗
PubMed1978

Acute leukopenia during topical burn therapy with silver sulfadiazine.

Leukopenia, with a mean white blood cell count of 2,680/mm3, was observed in nine patients with thermal injury early in the course of topical treatment with silver sulfadiazine. All manifested absolute neutropenia with a concomitant increase in immature band forms in the peripheral blood smear. The leukocyte counts returned to within normal limits within 48 to 72 hours of discontinuation of silver sulfadiazine therapy in four patients, and also did so in five patients in whom silver sulfadiazine therapy was continued. Leukopenia secondary to silver sulfadiazine application is currently believed to be an innocuous, self-limited phenomenon.

Acute Disease↗
PubMed1976

Management of thyroid nodules in the elderly.

Eleven malignant thyroid tumors were found in 100 consecutive patients more than sixty years old having thyroid operations. Based on preoperative findings, these 100 patients could be separated into two groups according to high and low risk for malignancy. Clinical manifestations in the high risk group were presence of a discrete cold thyroid nodule, hoarseness, dysphagia, an enlarging mass, or palpable ipsilateral cervical adenopathy; and in the low risk group, asymptomatic multinodular goiter, diffusely enlarged glands with elevated antithyroid antibody titers, and a family history of goiter. All eleven patients with malignant thyroid tumors were found in the sixty-six patients considered at high risk, whereas no malignant lesions were found in the low risk patients. Six of the malignant thyroid tumors were undifferentiated and in three of these a thyroid nodule had been present for more than fifteen years. There were no operative deaths and only one significant complication, a recurrent laryngeal nerve injury. Thyroidectomy is indicated for elderly patients with thyroid nudules who have features of the high risk group, whereas patients in the low risk group can be safely followed.

Age Factors↗
PubMed1975

Unusual manifestations of pancreatic pseudocysts and their surgical management.

Six cases representing selected complications of pancreatic pseudocyst are reported and their surgical management is discussed. Patients with mediastinal extension of a pseudocyst frequently present with symptoms in the chest rather than in the abdomen. Chronic recurrent pleural effusion, rich in protein and amylase, often accompanies mediastinal extension of a pancreatic pseudocyst. It is important to recognize that such an effusion almost certainly represents disruption of the pancreatic duct with formation of a pancreatic pseudocyst or a pancreaticopleural fistula. Internal drainage from below the diaphragm is the treatment of choice for pancreatic pseudocysts extending into the mediastinum. To be certain that obstructive jaundice is due to a pancreatic pseudocyst, there must be operative demonstration of compression of the common bile duct by the pseudocyst, relief of the obstruction by surgical drainage of the cyst, and subsequent disappearance of jaundice. Cysts that cause jaundice are located in the head of the pancreas, and cystoduodenostomy is the treatment of choice. Intraperitoneal rupture has been associated with a high mortality, but with adequate fluid replacement, prompt evacuation of the cyst contents from the peritoneal cavity, and adequate drainage, mortality can be lowered. Pancreatic ascites is much more common than is generally supposed and may result from a leaking pancreatic pseudocyst. In contrast to cirrhotic ascites, pancreatic ascites produces elevation of both the serum amylase level and protein concentration. Massive hemorrhage from pancreatic pseudocysts is usually due to the development of a false aneurysm in a branch of the celiac axis in the wall of the pseudocyst, with subsequent rupture of the aneurysm into the gut or peritoneal cavity. Any patient with a pancreatic pseudocyst who shows signs of bleeding should have prompt arteriography for determination of the bleeding site and appropriate surgical control. Pancreaticobronchial fistula is a rare complication. Treatment should be directed toward adequate drainage of the pseudocyst in the abdomen.

Adult↗
PubMedDate not supplied

The role of mediators in the response to thermal injury.

Inflammatory mediators play a major role in both the local burn wound and the systemic response to burn injury. Oxidant and arachidonic acid metabolites are involved in the initial burn edema process. The mediators as well as the cytokines released from activated macrophages also result in an early generalized inflammatory response. The later postburn hyper-metabolism is initiated and perpetuated by these same mediators, especially the cytokines, tumor necrosis factor, interleukin-1, and interleukin-2. Circulating endotoxin from the wound or the gut also appears to be involved. The postburn septic response is now recognized to be the result of inflammation; infection is not necessary. Mediator induced priming of the inflammatory cells by the burn itself results in an exaggerated response to infection in the postburn period. Defining the specific mechanism of injury and mediators involved can result in a major improvement in burn care, especially since many mediator inhibitors are already available for clinical use. It is essential that the clinician understand this pharmacologic manipulation in order to be able to optimally utilize these future advances.

Animals↗
PubMedDate not supplied

Haloperidol complications in burn patients.

Neuropsychiatric complications are commonly seen in major burn patients. Haloperidol is frequently used to treat severe psychopathic behavior. We have noted severe muscle rigidity-an extrapyramidal side effect of the agent-in a number of burn patients. Haloperidol causes a relative imbalance of dopaminergic and cholinergic neuronal activity in the basal ganglia with a relative increase in cholinergic activity being responsible for EPS. The burn patient may be more prone to extrapyramidal symptoms because of increased sensitivity of skeletal muscle neuromuscular junctions to acetylcholine after thermal injury.

Adolescent↗
PubMedDate not supplied

Increased lipid peroxidation and decreased antioxidant activity correspond with death after smoke exposure in the rat.

Oxidants are released directly from smoke and also as a result of the airways inflammation that occurs after smoke injury. We determined the relation between the degree of tissue oxidant change with the use of malondialdehyde content to measure lipid peroxidation and the degree of lung and systemic organ damage and resulting damage mortality 24 hours after a controlled smoke exposure in a rat model. We also monitored changes in the key tissue antioxidant catalase. We found that the degree of lung lipid peroxidation and the decrease in catalase activity directly correlated with mortality caused by respiratory failure and with the degree of lung inflammation but that they did not correlate with the peak carboxyhemoglobin level, a marker of smoke gas phase exposure. The lung oxidant changes also directly correlated with increased systemic lipid peroxidation and decreased catalase in liver and kidney tissue. We conclude that the initial smoke insult causes lung and in turn systemic inflammation with resulting release of oxidants, which leads to tissue oxidant injury. The degree of lung oxidant change significantly correlates with the degree of lung tissue injury, respiratory failure, and mortality, and the major source of the oxidant changes is tissue inflammation rather than oxidants in the smoke itself.

Animals↗
PubMedDate not supplied

Antioxidants prevent the cellular deficit produced in response to burn injury.

We studied the effect of water-soluble antioxidants on the cell energetics in multiple organs in rats in response to a 20% total body surface area third-degree burn injury. Liver, lung, and heart tissue were studied. Cell energetics were measured as tissue energy charge potential (ECP), adenosine triphosphate (ATP) content, and total adenine nucleotides. The enzymatic antioxidant catalase was used as a marker of endogenous cell antioxidant activity, especially to hydrogen peroxide. The water-soluble antioxidants glutathione, N-acetylcysteine, and vitamin C were given orally beginning at the time of burn injury and for the 6-day study period. All rats were fluid resuscitated according to the Parkland formula. The mortality rate was 0% for this size burn. The ECP in lung, liver, and heart, was normal on day 1 after the burn injury. However, the ECP was significantly decreased from the controls in the liver by day 3, with a peak decrease at day 6 as inflammation increased. A decrease in the heart ECP occurred between day 3 and day 6. Total adenine nucleotides did not decrease, indicating the decrease in ECP to be the result of a decrease in ATP. ECP remained normal in the lung. Catalase was also decreased in the liver and the heart and remained at normal levels in the lung. The decrease in the liver and heart ECP and ATP was eliminated with the oral antioxidant administration after the burn injury. We conclude that a modest burn injury decreases cellular energy charge in the heart and liver not immediately after burn but 3 to 6 days later. The decrease in antioxidant activity precedes the decrease in ECP. The lung appears to be protected. Water-soluble antioxidants, given after burn injury, prevent the altered cell energetics-strongly suggesting a cause-and-effect relationship between increased oxidant release with inflammation, decreased antioxidant activity, and altered cell energetics.

Analysis of Variance↗
PubMedDate not supplied

Plasma catalase and glutathione levels are decreased in response to inhalation injury.

We determined the effect of a severe smoke exposure on plasma oxidant and antioxidant activity. Adult sheep were given a smoke exposure while under anesthesia that produced a carboxyhemoglobin level of 45% +/- 3%. Twelve sheep were studied; six were given smoke alone and volume-resuscitated with sufficient lactated Ringer's solution to maintain baseline hemodynamics. This response was compared with six control sheep during a 6-hour period. The smoke inhalation injury produced a significant increase in plasma hydrogen peroxide and a significant decrease in plasma lipid peroxidation. Circulating lipid peroxidation did not correlate with tissue lipid peroxidation because lung and liver lipid peroxidation were significantly increased. The plasma antioxidants glutathione, catalase, and vitamin E were significantly reduced in response to the injury. Vitamin C remained unchanged from control. Circulatory failure is not a key element in this study, because lactate levels were controlled with volume resuscitation. The degree of smoke inhalation to the airway produced distant organ lipid peroxidation and a decrease in circulating antioxidants--without producing an increase in circulating lipid peroxidation. Maintaining circulating antioxidants may prevent distant organ lipid peroxidation and may be of clinical use in devising treatment strategies for smoke inhalation injury with the availability of antioxidants.

Animals↗
PubMedDate not supplied

Development of a burn rehabilitation unit: impact on burn center length of stay and functional outcome.

In 1995 we initiated the development of a specialized burn rehabilitation unit within an acute rehabilitation hospital, geographically separated from our burn center. The purpose was to allow an earlier initiation of an intensive rehabilitation program while still maintaining optimal burn wound care and nutritional support. The unit was directed by a burn center nurse coordinator who spent 50% of the time in the burn center and 50% in the rehabilitation unit training and supervising care. By 1996 the unit was able to manage open wounds, including skin substitutes of as much as 18% total body surface area, with 2- to 3-day returns to the center for wound coverage (2.5 +/- 0.5 procedures/patient). Our length of stay in 1996 for burns requiring inpatient rehabilitation (mean size 54% +/- 7% total body surface area) decreased by 21 +/- 5 days with respect to those in 1994 and 1995, with no increased morbidity. This length of stay was also significantly shorter (24%) than that predicted by the American Burn Association Registry formula. In addition, the rehabilitation unit length of stay required to restore the same degree of function according to a standardized measurement was significantly shorter (by 9 +/- 3 days) than for patients referred to other rehabilitation facilities in 1996. We conclude that the benefits of a burn rehabilitation unit include not only a decreased burn center length of stay but also a more rapid restoration of function.

Adult↗