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BACKGROUND: Hemorrhagic shock produces a marked decrease in hepatic ATP, adenylate energy charge, and total adenosine nucleotides. This is followed by slow recovery to normal levels after resuscitation. Nucleotide metabolites are increased following shock and resuscitation. Previous experimental work has shown that supraphysiologic doses of insulin have salutary effects in animals with hemorrhagic shock and in cardiac patients. It appears that insulin causes increased availability of glucose and energy-producing substrates. This study examined whether resuscitation with glucose and insulin after hemorrhagic shock would alter the changes previously seen to occur in hepatic ATP levels, adenylate energy charge, or nucleotide metabolites. METHODS: Male Sprague-Dawley rats were bled to a mean arterial blood pressure of 40 mm Hg for 30 min. They were then resuscitated with the shed blood and one of three fluids: (1) lactated Ringer's, (2) lactated Ringer's with 10% glucose, (3) lactated Ringer's with 10% glucose + 6 units/kg regular insulin. Liver biopsies were obtained prior to shock (baseline), after 30 min of shock (shock), and 90 min after resuscitation (90 min). Tissue levels of ATP, ADP, AMP, adenosine, inosine, hypoxanthine, and xanthine were measured. Serum at 90 min was evaluated for potassium, glucose, and tumor necrosis factor alpha (TNF-alpha). RESULTS: The insulin-treated group had significantly increased hepatic ATP and energy charge following resuscitation compared with the other two groups. The insulin group also exhibited significant hypoglycemia. Total adenine nucleotides (ATP, ADP, and AMP) were significantly elevated 90 min postresuscitation in the insulin group. Mean blood pressures throughout the experiment were not significantly different among groups. TNF-alpha was highest in the insulin-treated group, but this was not significant. CONCLUSIONS: Resuscitation with insulin and dextrose significantly increased hepatic ATP and adenylate energy charge after hemorrhagic shock in rats. Total nucleotide pool levels were not different between groups, indicating that there was a shift of the equilibrium away from the metabolites toward ATP and ADP in the insulin-treated group. Insulin treatment had no significant effect on blood pressure or TNF-alpha. However, it caused significant hypoglycemia and hypokalemia.

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OBJECTIVE: This is a retrospective study designed to evaluate the pattern and severity of injuries that result from low falls, defined as falls from less than 20 ft, subsequent mortality, and requirements of hospital resources. Our hypothesis is that many of these injuries, even without cardiopulmonary instability, are worthy of trauma center care. METHODS: The records of all patients entered into the hospital trauma registry at an urban Level I trauma center during the years 1991 through 1997 who suffered low falls and who either died after admission or were hospitalized for at least 3 days were reviewed. Patients suffering isolated hip fractures were excluded. One hundred seventy-six patients constituted the study population. This group accounts for about 2% of all admissions for falls at our institution. Patterns of injury were examined. Age, mechanism of injury, Injury Severity Score (ISS), and cardiopulmonary or neurologic instability on admission were documented. Mortality, length of intensive care unit and hospital stays, as well as billed hospital charges, were reviewed. RESULTS: The majority of patients (62%) were younger than 50 years. Sixty patients had ISS >15 and 116 patients had ISS >9. Sixty patients had multisystem injuries requiring specialty care. Head injuries were found in 81 patients (35%), and vertebral fractures or spinal cord injuries were found in 49 patients (22%), including 9 quadriplegics and 5 paraplegics. There were seven patients with intra-abdominal injuries (five spleen and two bowel injuries). There was one patient with a rupture of the thoracic aorta. Seventeen patients had deteriorating neurologic or pulmonary function on arrival, but the majority (90%) were stable. Of the 159 "stable" patients, 48 suffered head injuries, 7 were quadriplegic, and 3 were paraplegic. All intra-abdominal injuries were in this group. Overall, 14 of 176 patients (8%) died. Seven deaths were in patients older than 60 years, and seven deaths were in younger patients (p = 0.04). The majority of deaths (9 of 14) were from head trauma. Care in the intensive care unit was required in 92 of 176 patients. Nine patients had billed charges exceeding $100,000. CONCLUSION: Low falls can cause significant injuries, most commonly to the head and spine. Based on mechanism of injury alone, patients injured in low falls might not be taken to trauma centers. We have found, however, that many of these patients sustain serious multisystem injuries, even though they are stable initially. Although these patients represent only a fraction of those who fall, our study would support adjustment of triage guidelines to recommend transport of such patients, particularly elderly patients, to trauma centers.

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Certain tissues are known to be susceptible to shock-induced damage: liver, small bowel mucosa, and small bowel wall. This study was done to assess the changes in adenine nucleotides induced by hemorrhagic shock. Male Sprague-Dawley rats (n = 21; 300-350 g) were anesthetized with sodium pentobarbital (50 mg/kg, ip) and mechanically ventilated. The external jugular vein and common carotid artery were cannulated. Laparotomy was done. Hemorrhagic shock was induced by withdrawing blood into a heparinized syringe until a mean arterial blood pressure of 40 mm Hg was obtained and was maintained for 30 min by continued withdrawals. Shed blood was then reinfused through the venous catheter. No additional fluid was administered. The animals were observed for another 60 min. Throughout the procedure, biopsies were taken of liver and small bowel. The small bowel biopsies were separated into mucosal and wall fractions. Nucleotides were extracted. ATP, ADP, AMP, adenosine, inosine, xanthine, and hypoxanthine were measured with gradient HPLC. Cellular ATP concentrations decreased significantly during shock (P < 0.05). Liver ATP dropped from 8.93 +/- 0.55 to 2.91 +/- 0.16 micromol/g dry tissue (mean +/- SEM) (33%), small bowel mucosal ATP from 9.40 +/- 1.04 to 3.26 +/- 0.21 (35%), and small bowel wall ATP from 5.47 +/- 0.36 to 2.74 +/- 0.18 (50%). The nucleotide response to shock in small bowel mucosa was closer to that of liver than to that of small bowel wall. After reperfusion, ATP levels were partially restored in liver, small bowel mucosa, and small bowel wall, but not to preshock values. All of the metabolites (adenosine, inosine, hypoxanthine, and xanthine) increased during shock (P < 0.05), and did not return to preshock levels after reperfusion. The abnormalities in ATP and its metabolites, and their persistence after reperfusion, suggest a possible mechanism for the production of postshock damage.

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Salvage of the injured spleen is important in the trauma patient. Loss of the spleen can result in both early and late infectious complications due to immunologic and phagocytic deficits. Splenic salvage techniques include the use of polyglycolic acid (PGA) mesh to wrap and tamponade the damaged and bleeding spleen. However, the use of mesh may increase the incidence of infection in the presence of intraperitoneal contamination. We examined whether mesh in the contaminated field increases the infection rate compared to splenectomy in a murine model. Sixty male Sprague-Dawley rats were divided into three groups of 20 each: splenectomy, splenic wrap with PGA, and control (with splenic mobilization). All rats were subjected to a standard inoculum of enteric bacteria at the time of celiotomy. Sixteen (80%) of the splenectomy rats, 10 (50%) of the PGA mesh wrapped rats, and four (20%) of the control rats expired (P < 0.5). In surviving rats, necropsy at 7 days demonstrated abscess formation in all four (100%) of splenectomy, four of 10 (40%) in PGA mesh wrapped, and two of 16 (13%) of control rats. All of the abscesses in the wrap group involved the mesh. Overall infection rates (including fatal peritonitis, abscess formation, and empyema) were 100% for splenectomy, 75% for PGA mesh wrapped, and 30% for control rats (P < 0.05). We conclude in this experimental model that the use of PGA mesh wrap does increase susceptibility to infection, but much less so than splenectomy in the presence of intraperitoneal contamination.

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This study compares nerve repair following tissue expansion with nerve repair using an interposed graft in the rat. Group I had expansion conducted over 2 weeks at 40 mmHg. A 4 mm segment was excised from the lengthened nerve and repaired primarily. Group II had a 4 mm segment of nerve excised and then replaced as an interposition graft. Group III was sham-operated controls. Thirteen weeks postoperatively, all animals were evaluated using walking track analysis. Thirty-five rats finished the study: Eleven in group I, 10 in group II, and 14 in group III. The Sciatic Functional Index (SFI) was calculated for each group as follows: group I, -57 +/- 11 (mean +/- standard deviation); group II, -59 +/- 25; group III, -13 +/- 6.5. The control group was significantly better than either experimental group (P < 0.01). The two experimental groups were not statistically different. Nerve repair following expansion allowed only one coaptation to be used. Functional results were the same as with interposition grafting. Repair by the expansion technique would eliminate the need to harvest a nerve graft, and the subsequent donor defect.

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Argon-enhanced coagulation (AEC) is a method for operative coagulation of tissues that utilizes a jet of argon gas encompassing an electrofulguration arc. Concern has been raised that the argon jet may produce harmful venous gas embolization. Two questions were addressed by this study. First, does AEC result in generation of venous gas emboli, and if so, what is the influence of gas flow rate and coagulation power on the amount of gas emboli generated? Second, does the amount of venous gas emboli generated by AEC produce harmful hemodynamic effects? Two AEC units were evaluated during coagulation of cut sections of the liver in pigs. The number of gas emboli generated was measured by an ultrasonic Doppler flow cuff placed around the caudal vena cava. Hemodynamic variables measured following AEC included systemic and pulmonary arterial pressure, pulmonary wedge pressure, and cardiac output by thermodilution. Venous gas emboli were produced during AEC of the liver. The number of gas emboli generated increased with increasing gas flow rates, but was not affected by coagulation power. No change in any of the measured hemodynamic variables was observed following AEC of the liver. The following recommendations were made: (1) Surgeons using AEC should select an argon flow rate as low as feasible to clear a bleeding tissue surface of blood and debris. (2) Although AEC seems to be associated with tolerable amounts of venous gas embolism, surgeons and anesthesiologists should be aware that the potential for harmful venous gas embolism exists. (3) In patients where extensive use of AEC is planned, appropriate monitoring and precautions for gas embolism should be undertaken.

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Elongation of peripheral nerves would facilitate the repair of peripheral nerve injuries. The purpose of this study was to determine the efficacy of nerve expansion and the effect of different levels of intraluminal expander pressure upon nerve conduction. A 2-mL Silastic expander was placed under one sciatic nerve of adult male rats. The other nerve served as a control. Electroneuromyography (ENMG) was done at the time of initial expansion in seven animals. At 40 mm Hg expansion pressure a significant change in latency was found with an increase of 17% +/- 5%. Expansion was carried out for 14 days in two groups of seven rats, group I at 20 mm Hg and group II at 40 mm Hg. Length gain on the expanded side was 30% in group I and 40% in group II. No significant changes in latency or velocity were found after expansion. We conclude that nerves can be expanded at low pressures with no significant conduction changes but long-term recovery of histologic changes needs to be evaluated.

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The Harris-Benedict equation, as cited in a selection of textbooks of medicine, surgery, and nutrition, was compared with the original monograph published by the Carnegie Foundation. A significant amount of variation was found in published versions of this equation. Of 24 published versions, eight were sufficiently variant to produce errors of 7% to 55% in calculations of nutrition requirements. The error is usually in the constant term for one of the two Harris-Benedict equations. Either the constant term for men is increased to a value approximately the same as for women, or the constant term for women is reduced to be approximately equal to that for men. The primary reason appears to be the lack of availability in medical libraries of the original Carnegie Foundation publication by Harris and Benedict.

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Measurement of energy expenditure with indirect calorimetry allows determination of caloric balance. The present study was done to determine the predictive value of caloric and nitrogen balances for nutritional outcome. Energy expenditure was obtained weekly and interpolated between measurements for daily caloric balance. Nitrogen balance was obtained weekly. Because nitrogen output fluctuated, interpolation of daily values was not possible. Nutritional outcome was defined by whether body weight was lost or maintained and by levels of visceral proteins (albumin, prealbumin, and transferrin). The study group included 12 patients with 7% to 82.5% total body surface area burns. Eleven patients survived their burn injuries, and one died of congestive heart failure at 38 days, after her burn wounds had healed. Nine patients had good nutritional outcomes (group 1) and three had poor nutritional outcomes (group 2) (including the one who died). Nitrogen balance was 1.3 +/- 1.0 gm/day in group 1 and 4.5 +/- 1.7 gm/day in group 2 (mean +/- SEM; p > 0.10). Caloric balance was 515 +/- 130 kcal/day in group 1 and -667 +/- 140 in group 2 (p < 0.001). Caloric balance was significantly different between the two groups, whereas nitrogen balance was not. Caloric intake correlated positively with nitrogen intake (r = 0.92). Nitrogen intake was 16% of total caloric intake. Nitrogen intake from blood products was appreciable and averaged 15% of total nitrogen intake (range, 0% to 47%); 11.3 +/- 1.6 gm/day in group 1 and 14.8 +/- 3 gm/day in group 2 (p > 0.10).(ABSTRACT TRUNCATED AT 250 WORDS)

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Carbon dioxide laser incisions are reported to be less painful, less bloody, and less prone to seroma formation and to heal better than scalpel or electrosurgical incisions. We compared all three modalities in a prospective randomized study of cholecystectomy incisions. Time required for the incision and incisional blood loss was less with electrosurgery than with the carbon dioxide laser or scalpel. Postoperative pain and wound healing, however, were the same for all three techniques. The carbon dioxide laser appears to offer no advantage over conventional means of making a standard incision.

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After injury, the stress reaction causes hypermetabolism and consequent depletion of the body's tissues. Nutritional support should be begun early and should be given by the enteral route if possible. New developments may allow the modulation of the stress and immune responses by nutrient therapy.

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Intrathoracic and intravascular migratory foreign bodies are a small but distinctive subgroup of missile injuries. The intravascular bullet embolus can be treated like arterial or venous emboli of any other sort and removed as indicated. Wandering bullets in body cavities should be removed when they need to be, just like bullets imbedded in the body in a fixed position. And, contrary to the popular belief, very few bullets wander.

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Technologic aid is available for the three central problems of hemorrhage, lung damage, and cardiac damage. Autotransfusion, new modes of ventilator support, extracorporeal oxygenation, balloon pumping, and left ventricular assist are available for the trauma patient. The author explains these new devices and their role in thoracic trauma cases.

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Because clinical assessment of bowel viability is unreliable, other methods of determining intestinal perfusion have been recommended. Since none of these quantifies intestinal blood flow, we measured flow at the detection thresholds of Doppler ultrasound, photoplethysmography, and intravenously administered fluorescein, perfused the intestines at these threshold levels, and assessed histologic evidence of ischemic damage. The intestines of five anesthetized dogs were perfused for 4 hours via an in-line pulsatile extra-corporeal circuit assembled between the iliac and superior mesenteric arteries at either relatively physiologic (approximately 20 ml/min/kg body weight) levels or reduced levels representing the flow detection thresholds of Doppler ultrasound or photoplethysmographic probes (approximately 4 ml/min/kg). Intravenously administered fluorescein was detected at even lower perfusion levels (approximately 2.1 ml/min/kg). Clear-cut ischemic changes were documented histologically in all subjects perfused at Doppler/PPG flow detection thresholds but in none of those perfused at normal levels. We conclude that threshold blood flow detection by any one of these methods, especially fluorescein, occurs at levels inadequate to guarantee tissue viability.

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Gastric suction has traditionally been available in three modes: continuous, sump, and intermittent. An intermittent air injection suction system (IAIS) has been developed in which small (20 to 30 mm) amounts of air are injected two to three times a minute. Very low (20 mm Hg) suction levels are applied. The hypothesis of the present study is that such a device will prevent suction-induced gastric mucosal damage, probably produced by suctioning of mucosa into the holes of the NG tube. IAIS should prevent this by physically expelling the mucosa out of the holes and allowing use of much lower suction levels. In 25 animals, gastric suction for 24 h in anesthetized dogs routinely produced ulcers. However, IAIS produced significantly fewer ulcers and in fewer animals. In 37 animals, the effectiveness of suction, measured by recovery of fluid instilled in the stomach, and the tendency of the tube to block were studied. Effectiveness was the same for all modes studied. Blockage was significantly less with IAIS.

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Cardiac dysrhythmias are easy. Unlike the lung (which has formidable neuroendocrine, metabolic, and respiratory responsibilities), the heart is simple. It is an innervated muscular pump. A resting Purkinje or ventricular muscle cell membrane maintains a charge of about 90 millivolts. The five phases of a cardiac action potential are similar to the action potential in skeletal muscle, however, the cardiac action potential lasts a hundred times longer. When sodium specific "fast" channels and calcium specific "slow" channels open, positive ions rush into the myocardial cell, thus causing rapid membrane depolarization. In order to produce an action potential, some stimulus must decrease the membrane potential from -90 millivolts to "threshold" or -60 millivolts. Purkinje fibers do not have a stable phase for diastolic potential. These fibers continuously depolarize during diastole. Hypoxemia or hypokalemia may exacerbate this diastolic depolarization, thus promoting "hyperexcitability" or "automatic" ectopy. When myocardium is damaged, characteristically with myocardial ischemia, rapid conduction of cardiac impulses may be slowed dramatically. Very slow impulses may course through muscle such that by the time the activation wave front returns to the initiating site, this origin has had a chance to repolarize. This is the basis for re-entrant dysrhythmias. All cardiac dysrhythmias are automatic, re-entrant or both.

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The two primary goals in dysrhythmia therapy are: to control the ventricular rate (between 70 and 100 beats per minute) and to maintain sinus rhythm. Maintenance of sinus rhythm is definitely secondary. If a patient is hemodynamically unstable, but has a ventricular rate between 60 and 100 beats per minute, the trouble is almost certainly not due to the cardiac rhythm. Normal conduction velocity is fast. An impulse is transmitted by healthy Purkinje fibers at 2 to 3 meters per second. This means that the entire ventricle, when activated by the Purkinje system, is activated in 80 milliseconds. When a superventricular impulse is transmitted to the ventricles via the A-V node, the ventricle should be activated (depolarized) in less than 80 milliseconds. Conversely, if an impulse is generated at an ectopic ventricular site, it does not access the high velocity Purkinje system as rapidly. A ventricular origin beat (PVC) thus, takes longer to activate the entire ventricle. The QRS is, therefore, longer (or wider). A wide QRS signifies aberrant ventricular conduction. When a dysrhythmia originates above the A-V node, the therapy is pharmacologic A-V nodal blockade (verapamil). When a dysrhythmia originates below the A-V node, therapy is pharmacologic (Lidocaine) or electrical (cardioversion). If uncertain or a patient is unstable, cardioversion is always acceptable. Thus; with an unstable patient, proceed immediately to cardioversion; with a narrow complex tachycardia (superventricular) proceed to verapamil; and with a wide complex (ventricular) tachycardia give Lidocaine and proceed to cardioversion.

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