Successful emergent thoracotomy for pericardial tamponade caused by late constrictive pericarditis after trauma.
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Biomedical subjects
Publications and source records attributed to K Waxman.
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Interleukin-6 (IL-6) has been identified as a marker of ischemia. However, its association with bowel obstruction has not been studied. Fifty-seven patients diagnosed with bowel obstruction were evaluated in a prospective blinded study and managed either medically (n = 29) or surgically (n = 28) per decision of attending surgeon. Serum IL-6 levels were obtained at the time of diagnosis and serially during hospitalization. Mean IL-6 levels at the time of diagnosis were significantly higher in patients who required operation compared with medically treated patients (63.9 vs 19.6 pg/mL respectively; P = 0.027). Levels returned to those seen in medically treated patients 3 days after operation. There was no difference in temperature, white blood cell count, or lactic acid levels. Five patients required resection for ischemic bowel. Patients with ischemic bowel had significantly higher initial mean IL-6 (146.6 vs 45.9 pg/mL; P = 0.034) and lactic acid (23.6 vs 11.8 mg/dL; P = 0.035) at time of diagnosis compared with surgically treated patients without bowel ischemia. No difference in white blood cell count was seen. IL-6 was a sensitive predictor of patients with bowel obstruction requiring operation and for presence of ischemic bowel. IL-6 screening may allow for earlier and more selective operation potentially decreasing morbidity and mortality.
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The common clinical practice of gradually tapering total parenteral nutrition (TPN) to prevent hypoglycemia may be unnecessary. This randomized prospective study assessed the blood glucose profiles of patients whose TPN was abruptly discontinued in comparison with those whose TPN was gradually tapered to determine whether abrupt cessation can be performed safely. Patients were randomized into the abrupt cessation or the tapered protocol. A symptomatic hypoglycemic questionnaire was administered at regular intervals. Fingerstick glucose sampling was performed at 30-minute intervals and compared prospectively. From October 1996 through July 1997, 21 patients receiving TPN consented to participate in this study. Inclusion criteria included 1) duration of TPN infusion >24 hours, 2) age >18 years, and 3) establishment of enteral feeding at the time of TPN discontinuation. Patients had a baseline blood glucose level followed by repeat glucose measurements at 30-minute intervals until 90 minutes after TPN was completely discontinued in the tapered group and 120 minutes after cessation in the abrupt group. The rate of TPN tapering was in 25 per cent increments over 90-minute intervals. Ten patients were randomized into the tapered group and 11 patients in the abrupt group. None of the patients developed symptomatic hypoglycemia. There was no difference between the lowest blood glucose in the abrupt group in comparison with that of the tapered group (108.6+/-11.5 vs 108.2+/-9.8 respectively; P = 0.98). No patient had a significant change in hypoglycemia questionnaire score. There was no significant difference in age, duration of TPN, steroid use, or enteral caloric intake between the two groups. We conclude that there was no symptomatic hypoglycemia, and glucose profiles returned to a similar baseline level in those whose TPN was abruptly stopped when compared with those in the tapered group. These data demonstrate that patients receiving TPN can have parenteral nutrition abruptly stopped without the development of significant hypoglycemia.
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PURPOSE: To determine the degree of neutrophil activation caused by hemorrhagic shock and resuscitation. METHODS: Awake swine underwent 15-minute 40% blood volume hemorrhage, and a 1-hour shock period, followed by resuscitation with: group I, lactated Ringer's solution (LR); group II, shed blood; and group III, 7.5% hypertonic saline (HTS). Group IV underwent sham hemorrhage and LR infusion. Neutrophil activation was measured in whole blood using flow cytometry to detect intracellular superoxide burst activity. RESULTS: Neutrophil activation increased significantly immediately after hemorrhage, but it was greatest after resuscitation with LR (group I, 273 vs. 102%; p < 0.05). Animals that received shed blood (group II) and HTS (group III) had neutrophil activity return to baseline state after resuscitation. Group IV animals had an increase in neutrophil activation (259 vs. 129%; p < 0.05). CONCLUSION: Neutrophil activation occurring after LR resuscitation and LR infusion without hemorrhage, but not after resuscitation with shed blood or HTS, suggests that the neutrophil activation may be caused by LR and not by reperfusion.
Associated factors related to outcome following blunt intestinal trauma requiring operative therapy were retrospectively reviewed in all trauma patients admitted to one Level I trauma center. Over 4.5 years, 7598 trauma patients were evaluated, with 62 patients having sustained 92 blunt intestinal injuries requiring operative intervention. Mean age was 34.5 years; mean Injury Severity Score was 22. Mechanism of injury was motor vehicle accident in 50 (81%), with 80 per cent being drivers. Associated intra-abdominal injuries occurred in 46 (74%) patients. Extra-abdominal injuries occurred in 56 patients (90%). Thirty-one patients suffered 82 complications or 2.6 complications per patient (comp/pt). Mortality from operative blunt trauma was associated with admission blood pressure < or = 90 mm Hg (57 vs 13%; P < 0.05), age > or = 24 years (26 vs 0%; P < 0.05), and Injury Severity Score > or = 35 (70 vs 8%; P < 0.05). Morbidity was associated with age > or = 24 years (1.5 vs 0.7 comp/pt; P < 0.05) and delay in operative therapy > or = 24 hours (3.3 vs 1.1 comp/pt; P < 0.05). Overall mortality was 18 per cent.
UNLABELLED: The purpose of this study was to evaluate the importance of nitric oxide (NO) upon outcome following hemorrhagic shock. L-Arginine, an NO precursor, and L-NMMA, an inhibitor of NO synthesis, were added to resuscitation in a prospective, randomized, and double-blinded experimental model, and the effects upon blood pressure and survival were measured. METHODS: 60 Sprague-Dawley rats were anesthetized and subjected to phlebotomy to induce hemmorrhagic shock. After a 45 min shock period, animals were resuscitated with either lactated Ringer's alone (control), L-NMMA in lactated Ringer's or L-arginine in lactated Ringer's. Blood pressure was monitored, and animals were observed for survival. As an additional control experiment, 15 additional animals underwent the same protocol, but underwent sham shock, i.e. were not haemorrhaged. RESULTS: L-NMMA increased blood pressure transiently following sham shock, but increased blood pressure to a greater extent and for a longer duration following hemorrhage. However, L-NMMA had no effect upon survival. L-Arginine had no measurable effect upon blood pressure, but significantly increased survival. CONCLUSION: NO may play an important role following hemorrhage. The effectiveness of L-NMMA as a pressor suggests that NO contributes to hypotension following hemorrhage. However, reversing hypotension with L-NMMA did not improve survival in this model. In contrast, L-arginine did not further lower blood pressure, but had significant survival benefit. This suggests a possible protective effect of NO after hemorrhage, perhaps by improving the distribution of capillary blood flow and/or by decreasing platelet aggregation and leukocyte adhesion within the microcirculation.
A high incidence of severe inhalation injuries can be expected in the combined injury patient. The initial management remains attention to the ATLS priorities of airway, breathing, and circulation, with prompt and safe transfer to a regional center of excellence. The treatment of either the burn or the associated injuries may be compromised by their combined presence, and a team approach is essential to their optimal management. Circulatory management goals based on oxygen consumption and delivery allow greater understanding and control of the physiologic demands placed on the patient by the disease process. The management of inhalation injury and ARDS is at an exciting turning point in history, and we now have in hand and use many techniques that allow salvage of these mortal conditions. Pain management is essential to humane care and requires frequent assessment and patient control to be effective. Rehabilitation of the burn and trauma patient starts on the day of injury and requires team dedication to the areas of greatest morbidity early in the planning of surgical priorities and physical therapy.
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OBJECTIVE: Lisofylline is an enantiomer-specific, alkyl-substituted methylxanthine, which has specific and potent activity in down-regulating leukocyte activation. This study was designed to test the efficacy of lisofylline in the resuscitation of rats subjected to experimental hemorrhagic shock. DESIGN: Prospective, randomized, and blinded survival studies were performed with two lisofylline dosing regimens added to fluid resuscitation in a shock model. In addition, white cell adhesiveness was measured to assess the effects of lisofylline. SETTING: Animal laboratory. SUBJECTS: Sixty Sprague-Dawley rats. INTERVENTIONS: Lisofylline or placebo was added to the resuscitation regimen, either as a single dose or over 24 hrs. MEASUREMENTS AND MAIN RESULTS: The 72-hr survival rate, white blood cell count, and platelet adhesiveness were determined. When a single 1-hr infusion of lisofylline was added to the initial resuscitation regimen, the 72-hr survival rate increased from 20% in controls to 50% (p < .009). When repeated doses of lisofylline were given over 24 hrs, the 72-hr survival rate increased from 40% in controls to 70% (p < .02). Control animals significantly increased leukocyte adhesiveness after shock and resuscitation. This increased adhesiveness was completely eliminated by lisofylline infusion. Platelet adhesiveness was not affected by lisofylline. CONCLUSIONS: Lisofylline improves survival in this model of hemorrhagic shock. Its beneficial effect may be related to down-regulation of leukocyte adhesiveness.
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The pathophysiology of shock after trauma and hemorrhage has traditionally been viewed as a result of ischemic cellular damage. However, it is now clear that ischemia alone does not result in all cellular damage after shock. Rather, much of the cellular injury follows reperfusion and subsequent inflammation. Sublethal ischemia alters (primes) cells. This priming is mediated by second messengers, such as intracellular calcium, cyclic adenosine monophosphate, phosphatidic acids, and reactive oxygen species (ROS). Cells so primed by ischemia are both more susceptible to injury by subsequent reperfusion and inflammation, and may be primed to participate as effectors in the subsequent inflammatory response. Reperfusion of ischemic cells results in an oxygen radical burst. The resulting ROS are both directly cytotoxic and activate transcription factors for new protein synthesis. This activation of transcription factors results in activation of leukocytes, macrophages, and endothelial cells, initiating an inflammatory state which may result in organ failure and death. Monitoring to detect evidence of reperfusion and inflammation will be of value as new therapeutic approaches are developed. Antioxidant therapy has the potential to limit cellular and organ damage from reperfusion and inflammation after shock.
Anti-oxidant therapy has been effective for treatment of experimental shock. In this study, the efficacy of Trolox (Aldrich Chemical Co., Milwaukee, WI), a water-soluble vitamin E analogue, and ascorbic acid (vitamin C) was evaluated in a rat model of hemorrhagic shock and resuscitation. In two prospective trials, rats were phlebotomized (27 mL/kg) and left in shock for 45 minutes. Resuscitation was then instituted by continuous IV infusion with lactated Ringer's (LR) (54 mL/kg) over 60 min. In Trial 1, rats were randomized to receive either placebo (LR) or Trolox (50 mg/kg) in LR. In Trial 2, rats were randomized to LR alone or ascorbic acid (50 mg/kg) in LR. Survival for ascorbic acid-treated rats (35 per cent) was not different than for control rats (35 per cent). However, the addition of Trolox to infusion significantly improved 72 hour survival, 75 per cent versus 40 per cent respectively, for Trolox-treated and control animals. These data demonstrate that Trolox is of survival benefit when added to resuscitation in this model. This benefit does not appear to be related to blood pressure or white cell adhesion. Trolox is more effective than ascorbic acid in this model.