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Biomedical subjects

R H Demling

Publications and source records attributed to R H Demling.

At least 37 records · Page 2Linked to original sources
PubMed1993

Blunt chest trauma.

Chest trauma remains the major initiating cause of respiratory failure in the trauma patient. The degree of injury can be substantially modified with appropriate early preventive and treatment measures. The lung injury itself can be divided into early and late phases. The early phase is primarily the result of mechanical forces transmitted to the chest. Initial management should focus not just on the lung; there should also be a search for commonly present, associated, nonpulmonary injuries. Optimizing early restoration of perfusion is also crucial in the multiple trauma patient, instead of too "wet" or too "dry." The most complex phase is the late phase resulting from the host inflammatory response to injury, both local and systemic. Stress modification and control of inflammation are the keys to controlling this aspect of the disease process.

Biomechanical Phenomena↗
PubMed1993

Smoke inhalation injury.

Smoke inhalation injury is a complex of disease processes best understood and treated when defined in terms of the time period after injury. The early phase (0 to 36 hrs) is characterized by diagnosis and treatment of carbon monoxide and cyanide toxicity and by management of early airways edema, bronchorrhea, and bronchoconstriction with aggressive pulmonary toilet. Between 1 and 5 days, the major characteristic is airways mucosal slough, tracheobronchitis, and increasing lung water and impaired gas exchange. Pulmonary toilet and infection control, as well as close management of fluid shifts, is the major treatment. With onset of the inflammation-infection phase, the risk of nosocomial pneumonia increases markedly, as does the impairment in lung function as a result of marked increase in oxygen consumption and CO2 production. Nutrition, stress modification, avoidance of muscle fatigue, and control of infection are the key treatment modalities.

Carbon Monoxide Poisoning↗
PubMed1993

Aspiration lung injury.

Aspiration lung injury is caused by a failure of the normal protective mechanisms that prevent aspiration of gastric contents. Prevention measures are focused on preserving these protective mechanisms. There are three components to the lung injury. The first component is mechanical obstruction to airways from particles in the aspirate. Treatment is aggressive pulmonary toilet to restore airway patency. The second component, seen beginning in the first several hours, is a chemical injury to the airways, leading initially to bronchorrhea, airway constriction, and edema. Later, there is a marked increase in the risk of bacteria due to altered lung defenses. Treatment is supportive care. The third component is lung injury due to the inflammatory response. This process can evolve to an adult respiratory distress syndrome pattern. With modulation of lung inflammation (currently being developed), morbidity and mortality rates will decrease.

Causality↗
PubMed1993

Respiratory failure after cerebral injury.

Pulmonary dysfunction is a common complication of severe head injury. The degree of initial hypoxemia that develops appears to correspond with the location and magnitude of the head injury. If unrecognized and not aggressively treated, the hypoxic insult will magnify the cerebral insult. A severe postinjury hypermetabolic state also develops and, if unrecognized and not managed aggressively with nutritional support, can also lead to severe catabolism, increased infection, and further lung dysfunction. Although supportive care is the major treatment at present, pharmacologic manipulation of the increased catecholamine activity, which is considered to be causative, may be effective in controlling both the impaired gas exchange and the hypermetabolic state. A knowledge of the various lung dysfunction states that occur in the head-injured patient population is required to optimize recovery and minimize complications.

Craniocerebral Trauma↗
PubMed1992

The Surgical Infection Society's policy on human immunodeficiency virus and hepatitis B and C infection. The Ad Hoc Committee on Acquired Immunodeficiency Syndrome and Hepatitis.

The Ad Hoc Committee on Acquired Immunodeficiency Syndrome and Hepatitis of The Surgical Infection Society has outlined its policy regarding three deadly blood-borne viral infections. The risk of transmission of these microbes, the role of preoperative testing, the problem of the human immunodeficiency virus-infected surgeon, and conduct in the operating room are discussed.

General Surgery↗
PubMed1992

Oxygen consumption early postburn becomes oxygen delivery dependent with the addition of smoke inhalation injury.

We determined the relationship between oxygen delivery, DO2, and oxygen consumption, VO2, in sheep after a moderate smoke inhalation injury and 15% TBSA third-degree burn compared with burn alone and controls. Comparison was made beginning three hours after injury when carboxyhemoglobin levels were back to baseline values. We decreased DO2 between three and eight hours by 25% by either removing blood (controls) or decreasing the resuscitation fluid infusion rate. Lung oxidant, measured as tissue malondialdehyde (MDA) levels, and histologic changes were also assessed. Animals were killed at 24 hours. We found that in controls and animals with a burn alone, a 25% decrease in DO2 was compensated for by an increase in O2 extraction, maintaining VO2 constant. Correlation of DO2 to VO2 was r2 = 0.3, indicating independence of VO2 from DO2. With the combined injury, VO2 decreased in proportion to DO2, since O2 extraction did not increase. The correlation of DO2 to VO2 was r2 = 0.9, indicating delivery-dependent consumption, a pathologic process most likely caused by increased inflammatory mediators from the combined injury. Lung lipid peroxidation was markedly increased in the combined injury, 148 +/- 18 nmol MDA/gram of tissue compared with burn alone, 64 +/- 5 nmol/g, or controls, 45 +/- 4 nmol/g. However, no decrease in arterial O2 tension or increase in lung water was noted, i.e., the sheep did not have ARDS, which is known to impair O2 extraction. We conclude that a pathologic O2 delivery-dependent consumption develops with the combination of burn and inhalation injury, increasing the potential for tissue hypoxemia. This change corresponds with increased lung tissue oxidant change.

Animals↗
PubMed1992

Effect of dobutamine infusion on endotoxin-induced lipid peroxidation in awake sheep.

beta-agonists are known to not only increase oxygen delivery, but also attenuate the inflammatory response. We studied the effect of infusing the beta-agonist, dobutamine, on the oxidant-induced lung and liver tissue lipid peroxidation seen after endotoxemia. Twelve unanesthetized adult sheep with lung and soft tissue (prefemoral) lymph fistulae were given 5 micrograms/kg of Escherichia coli endotoxin intravenously. In six sheep, dobutamine 10 to 15 micrograms/kg/min was infused beginning 3 hours after endotoxin to increase oxygen delivery by 75% above baseline. Animals were killed at 6 hours, and lung and liver lipid peroxidation, measured as malondialdehyde, was obtained. Data were compared to six control sheep. Endotoxin alone produced increased lung and soft tissue vascular permeability as evidenced by a twofold increase in protein-rich lymph flow. Lung and liver malondialdehyde increased to 116 +/- 40 nmol/gm and 202 +/- 64 nmol/gm, respectively, compared to control values of 42 +/- 7 nmol/gm and 110 +/- 20 nmol/gm, respectively. Dobutamine infusion after endotoxin increased oxygen delivery by 75%, although changes in total oxygen consumption were not different from those seen with endotoxin alone. Lung and soft tissue lymph flow did not change with dobutamine. However, lung malondialdehyde was 41 +/- 17 nmol/gm, not different from controls. Liver malondialdehyde remained elevated at 164 +/- 26 nmol/gm. We conclude that dobutamine infusion prevents further oxidant-induced lung tissue lipid peroxidation but does not reverse the increased permeability already present. Liver lipid peroxidation was not decreased, suggesting the liver oxidant process may not be caused by the same mechanism as the lung lipid peroxidation.

Animals↗
PubMed1991

Effect of sequential early burn wound excision and closure on postburn oxygen consumption.

OBJECTIVE: To determine the effect of early excision and closure of burns on postburn hypermetabolism, measured as oxygen consumption (VO2). METHODS: Twelve patients with deep burns of 30% to 50% of total body surface underwent sequential excisions and wound coverage, beginning 1 to 3 days after burn. The majority of the deep burn was removed by day 7, but with the addition of a donor site area of 20% to 25% of total body surface. RESULTS: No decrease in VO2 was noted in relation to the percent removal of burn tissue. In addition, a transient further increase in VO2 was noted early after excision, especially with surgical procedures performed after 5 days. This response could not be attributed to wound manipulation-induced bacteremias. CONCLUSION: We conclude that early surgical excision and closure of burns in excess of 30% to 50% of total body surface do not decrease postburn hypermetabolism in proportion to the area closed. It is possible that remaining open wounds in the form of donor sites and nonexcised burn are sufficient to perpetuate the hypermetabolic process, once established.

Adult↗
PubMed1991

Relationship between the lung and systemic response to endotoxin: comparison of physiologic change and the degree of lipid peroxidation.

The lung and systemic response to Escherichia coli endotoxin either 2 or 5 micrograms/kg was measured in 16 sheep with chronic lung and soft tissue lymph fistulae. Oxidant-induced lung and liver lipid peroxidation was measured as tissue malondialdehyde (MDA). Conjugated dienes were also monitored. Both doses produced a comparable pulmonary hypertension and hypoxia as well as a comparable increase in protein-rich lymph flow, QL. However, lung MDA was significantly greater with the 5 micrograms/kg than with the 2 micrograms/kg dose, both being more than twofold greater than controls. The systemic physiologic responses between the two doses were quite different. The 5 microgram/kg dose resulted in a significant increase in oxygen delivery (DO2), oxygen consumption (VO2), and decrease in arterial O2 extraction in the 3-5 hr postendotoxin period compared with the 2 microgram/kg dose. A twofold increase in protein-rich soft tissue QL was also seen after the 5 micrograms/kg dose, whereas QL was not changed after 2 micrograms/kg. Liver MDA was only increased by 30% over controls with both doses. We conclude that the relationship between oxidant change and physiologic response varies considerably between lung and systemic tissues after endotoxemia with the degree of lung lipid peroxidation corresponding with the degree of impairment in systemic tissue O2 extraction and the onset of delivery-dependent O2 consumption.

Animals↗
PubMed1991

Topical flurbiprofen decreases burn wound-induced hypermetabolism and systemic lipid peroxidation.

We studied the effect of the topical application of the nonsteroidal anti-inflammatory agent, flurbiprofen, on postburn hypermetabolism and systemic lipid peroxidation. Twelve sheep with a 15% total body surface third-degree burn were monitored over a 4-day postburn period. In six sheep, a single application of a 5% flurbiprofen cream was placed on the burn wound on day 3. Data were compared to both burned and nonburned controls (n = 6). All animals were killed on day 4. Oxygen consumption was increased at day 3 by 28% +/- 10% over the preburn value in all animals. Flurbiprofen significantly attenuated the increase in oxygen consumption, returning the value essentially to baseline by 12 hours after application. Lung and liver peroxidation, as measured by malondialdehyde, was significantly increased in the burned, nontreated sheep at day 4 from a control value of 45 +/- 9 and 110 +/- 12 to 60 +/- 6 and 310 +/- 71 nmol/gm tissue, respectively. In flurbiprofen-treated animals, values were 42 +/- 8 and 160 +/- 18 nmol/gm at day 4, significantly attenuated from burn alone. Protein-rich burn lymph flow remained fourfold increased in both groups, indicating a persistent increase in burn tissue vascular permeability, not modified by flurbiprofen. Burn wound biopsies revealed bacterial contents of less than 10(4) organisms/gram tissue in all animals. We conclude that topical flurbiprofen significantly decreases burn wound-induced systemic hypermetabolism and oxidant-induced lipid peroxidation seen at 3 days after burn injury, but does not attenuate the remaining local burn-wound vascular permeability.

Administration, Cutaneous↗
PubMed1990

Systemic lipid peroxidation and inflammation induced by thermal injury persists into the post-resuscitation period.

We determined the time course of the oxidant-induced systemic lipid peroxidation seen after burn injury. Twelve sheep were given a 15% of total body surface third-degree burn and monitored for 3 or 5 days. Circulating lipid peroxides were monitored by both malondialdehyde (MDA) and conjugated dienes (CD). Lung and liver tissue MDA was also measured and compared to controls. A significant but transient increase in circulating MDA and CD was noted several hours after burn. Venous plasma levels increased again 3-5 days postburn with onset of wound inflammation. Oxygen consumption, VO2, also increased by 35 +/- 12% at this time. Lung MDA, which increased to 64 +/- 5 from a control of 45 +/- 4 nMol/gm, at 12 hours after burn was still increased 3 days after injury. Marked lung inflammation was present early after injury and persisted for the 5-day study period. Liver MDA also increased from control value of 110 +/- 20 to 252 +/- 25 at 12 hours and remained increased over the 5-day period. Serum alkaline phosphatase was also increased. Burn biopsies revealed no infection to explain the ongoing lipid peroxidation process, i.e., bacterial content was less than 10(5) organisms/gram burn tissue. We conclude that an initial system lipid peroxidation occurs immediately after burn injury, and that this process continues well into the post-resuscitation period, corresponding in time with increased VO2, lung inflammation, and evidence of liver dysfunction. The ongoing oxidant changes with the presence of a burn may explain the accentuated organ dysfunction seen with an additional septic insult in burned patients.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Effect of endotoxin and a burn injury on lung and liver lipid peroxidation and catalase activity.

Both endotoxin and a burn alone produce oxidant-induced tissue lipid peroxidation. The endotoxin response is due in large part to hydrogen peroxide. The combination of endotoxin after a burn results in an increased liver, but not lung, oxidant injury. Our purpose was to determine whether the burn oxidant injury inactivated endogenous liver tissue catalase, thereby amplifying a subsequent H2O2 insult. Twenty-six adult sheep were studied. Twelve sheep had a 15% TBS burn. Tissue catalase activity, measured in lung and liver 3 days postburn, was significantly decreased from a control of 3.58 +/- 1.8 and 193 +/- 63, respectively, to 1.72 +/- 0.63 and 148 +/- 33 k(sec-1)/0.5 gram tissue. The addition of endotoxin 3 days postburn resulted in an increase in liver malondialdehyde, MDA, a measure of lipid peroxidation, from a control of 110 +/- 80 to 450 +/- 54 nmol/gram tissue. This value was significantly greater than the 210 +/- 80 nmol/gram tissue seen after endotoxin alone. Lung tissue MDA with burn and endotoxin was 65 +/- 8 compared to 42 +/- 7 for control and 80 +/- 6 nmol/gram for endotoxin alone. We conclude that a decrease in liver catalase activity occurs after a burn. The decrease corresponds to an accentuated oxidant-induced lipid peroxidation after an added endotoxin insult where H2O2 is known to be an etiologic agent. The catalase activity also decreases in postburn lung, but accentuated lung damage was not seen, indicating a variable tissue response from the burn-induced decrease in antioxidant activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Current concepts on the adult respiratory distress syndrome.

The shock- and trauma-induced process known as ARDS remains a major cause of mortality and morbidity. The time course of the clinical disease has changed dramatically as support systems have improved. In addition, it is becoming increasingly clear that ARDS is part of an inflammation-induced systemic disease state which can evolve to multi-system organ failure. It is MSOF which is now the leading cause of death in the post-trauma patient in the ICU. ARDS from shock and trauma must now be studied not solely as a primary pulmonary process but as a critical component of a generalized inflammatory reaction to distant tissue trauma.

Humans↗