Should general surgeons provide critical care?
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Biomedical subjects
Publications and source records attributed to F A Moore.
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Despite intensive investigation, the pathogenesis of postinjury multiple organ failure (MOF) remains elusive. Laboratory and clinical research strongly implicate that the gastrointestinal tract plays a pivotal role. Shock with resulting gut hypoperfusion appears to be one important inciting event. While early studies persuasively focused attention on bacterial translocation as a unifying mechanism to explain early and late sepsis syndromes that characterize postinjury MOF, subsequent studies suggest that other gut-specific mechanisms are operational. Based on our Trauma Research Center observations and those of others, we conclude that: 1) bacterial translocation may contribute to early refractory shock; 2) for patients who survive shock, the reperfused gut appears to be a source of proinflammatory mediators that may amplify the early systemic inflammatory response syndrome; and 3) early gut hypoperfusion sets the stage for progressive gut dysfunction such that the gut becomes a reservoir for pathogens and toxins that contribute to late MOF.
BACKGROUND: Soluble tumor necrosis factor receptor (sTNFr) and interleukin-1 receptor antagonist (IL-1ra) have been identified as endogenous inhibitors of TNF-alpha and IL-1beta. While TNF-alpha and IL-1beta levels are not systematically elevated in postinjury patients who developed multiorgan failure (MOF), their involvement at the tissue level has been suggested. Our study hypothesis was that levels of sTNFr-I and IL-1ra would discriminate patients at risk for postinjury MOF. METHODS: Serial plasma levels of sTNFr and IL-1ra were measured in 29 trauma patients at high risk for postinjury MOF. RESULTS: sTNFr-I levels were higher in MOF compared with non-MOF patients at 12, 84, and 132 hours postinjury. MOF patients also had higher IL-1ra values 36, 60, 84, and 132 hours postinjury. CONCLUSIONS: Anti-inflammatory mechanisms are activated after trauma. Since increased levels of sTNFr and IL-1ra correlate with postinjury MOF, they may contribute to our understanding of the pathogenesis as well as prediction of outcome. High levels of antagonists to TNF-alpha and IL-1beta suggest tissue level involvement of these cytokines in postinjury hyperinflammation.
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BACKGROUND: Subclavian artery (SCA) injuries are rare vascular injuries and may be difficult to manage. The majority of SCA injuries are secondary to penetrating trauma. The purpose of this report is to examine the injury patterns, diagnostic and therapeutic approaches, and outcome of patients with blunt and penetrating SCA injuries. METHODS: Retrospective review RESULTS: Fifty-six patients sustained SCA injuries (25 blunt, 31 penetrating). SCA injury location was evenly distributed between the proximal, middle, and distal SCA after penetrating trauma; proximal injuries were rare (2 of 25) with blunt mechanisms. A radial arterial pulse deficit was present in only 3 of 25 blunt injuries and 9 of 31 penetrating injuries. Complications occurred more commonly in both groups of patients with initial systolic blood pressures less than 90 mm Hg. Survival was 76% in blunt and 81% in penetrating groups; limb salvage was similar (92% in blunt and 97% in penetrating groups). Complete brachial plexus injuries were more common with blunt injuries. CONCLUSION: SCA injuries are rare vascular injuries with an associated high morbidity and mortality, regardless of mechanism. Blunt mechanisms result in more middle and distal injuries and more frequent complete brachial plexus injuries. Complications are related to the hemodynamic status of the patient upon presentation, and not to mechanism of injury.
OBJECTIVE: To determine the incidence and type of delayed complications from nonoperative management of adult splenic injury. DESIGN: Retrospective medical record review. SETTING: University teaching hospital, level I trauma center. PATIENTS: Two hundred eighty patients were admitted to the adult trauma service with blunt splenic injury during a 4-year period. Men constituted 66% of the population. The mean (+/-SEM) age was 32.2+/-1.0 years and the mean (+/-SEM) Injury Severity Score was 22.8+/-0.9. Fifty-nine patients (21%) died of multiple injuries within 48 hours and were eliminated from the study. One hundred thirty-four patients (48%) were treated operatively within the first 48 hours after injury and 87 patients (31%) were managed nonoperatively. MAIN OUTCOME MEASURES: We reviewed the number of units of blood transfused, intensive care unit length of stay, overall length of stay, outcome, and complications occurring more than 48 hours after injury directly attributable to the splenic injury. RESULTS: Patients managed nonoperatively had a significantly lower Injury Severity Score (P<.05) than patients treated operatively. Length of stay was significantly decreased in both the number of intensive care unit days as well as total length of stay (P<.05). The number of units of blood transfused was also significantly decreased in patients managed nonoperatively (P<.05). Seven patients (8%) managed nonoperatively developed delayed complications requiring intervention. Five patients had overt bleeding that occurred at 4 days (3 patients), 6 days (1 patient), and 8 days (1 patient) after injury. Three patients underwent splenectomy, 1 had a splenic artery pseudoaneurysm embolization, and 1 had 2 areas of bleeding embolization. Two patients developed splenic abscesses at approximately 1 month after injury; both were treated by splenectomy. CONCLUSION: Significant numbers of delayed splenic complications do occur with nonoperative management of splenic injuries and are potentially life-threatening.
BACKGROUND/PURPOSE: Pediatric truncal vascular injuries are rare, but the reported mortality rate is high (35% to 55%), and similar to that in adults (50% to 65%). This report examines the demographics, mechanisms of injury, associated trauma, and results of treatment of pediatric patients with noniatrogenic truncal vascular injuries. METHODS: A retrospective review (1986 to 1996) of a pediatric (< or = 17 years old) trauma registry database was undertaken. Truncal vascular injuries included thoracic, abdominal, and neck wounds. RESULTS: Fifty-four truncal vascular injuries (28 abdominal, 15 thoracic, and 11 neck injuries) occurred in 37 patients (mean age, 14+/-3 years; range, 5 to 17 years); injury mechanism was penetrating in 65%. Concomitant injuries occurred with 100% of abdominal vascular injuries and multiple vascular injuries occurred in 47%. Except for aortic and one SMA injury requiring interposition grafts, these wounds were repaired primarily or by lateral venorrhaphy. Nonvascular complications occurred more frequently in patients with abdominal injuries who were hemodynamically unstable (systolic blood pressure [BPS] <90) on presentation (19 major complications in 11 patients versus one major complication in five patients). Thoracic injuries were primarily blunt rupture or penetrating injury to the thoracic aorta (nine patients). Thoracic aortic injuries were treated without bypass, using interposition grafts. In patients with thoracic aortic injuries, there were no instances of paraplegia related to spinal ischemia (clamp times, 24+/-4 min); paraplegia occurred in two patients with direct cord and aortic injuries. Concomitant injuries occurred with 83% of thoracic injuries and multiple vascular injuries occurred in 25%. All patients with thoracic vascular injuries presenting with BPS of less than 90 died (four patients), and all with BPS 90 or over survived (eight patients). There were 11 neck wounds in 9 patients requiring intervention, and 8 were penetrating. Overall survival was 81%; survival from abdominal vascular injuries was 94%, thoracic injuries 66%, and neck injuries 78%. CONCLUSIONS: Survival and subsequent complications are related primarily to hemodynamic status at the time of presentation, and not to body cavity or vessel injured. Primary anastomosis or repair is applicable to most nonaortic wounds. The mortality rate in pediatric abdominal vascular injuries may be lower than previously reported.
BACKGROUND: There is controversy about the impact on morbidity from delayed diagnoses of blunt hollow viscus injuries. A recent study suggested that the increased morbidity was primarily from delayed diagnosis of blunt duodenal injury (BDI). STUDY DESIGN: We studied the medical records from a 10-year period from June 1987 to June 1997 examining the data on 22,163 cases of blunt trauma. We assessed the incidence and consequences of delayed diagnoses of BDI, and identified preoperative factors associated with these delayed diagnoses. RESULTS: Thirty-five patients (0.2%) were identified in the retrospective study of the records from 22,163 blunt trauma patients to have sustained BDI. Of these, 25 patients (71%) were male. Ages ranged from 1 to 58 years (mean 18.8 years), and the predominant mechanism was motor vehicle accident in 18 patients (51%). Seven patients (20%) (group I) had a diagnostic delay of > 6 hours; 28 patients (80%) (group II) were diagnosed in < 6 hours. Six of the seven group I patients (86%) were evaluated initially with CT scans, and five (83%) showed findings suggestive of BDI. Among the 28 group II patients, 14 (50%) underwent initial diagnostic peritoneal lavage (DPL), and 14 (50%) had a CT scan. In seven of the group II patients (50%) who were initially evaluated by CT scan, there were findings suggestive of BDI. Diagnostic peritoneal lavage was initially equivocal (red blood cell count=5,000 to 100,000) in the remaining one group I patient compared with three of the group II patients who had DPL. Deterioration found on physical examinations prompted followup CT scans in 6 group I patients (86%), and the scans were diagnostic for BDI in all cases. CONCLUSIONS: Blunt duodenal injury is an uncommon entity. Despite the presence of suggestive CT and DPL findings, the diagnosis was delayed in 20% of the 35 patients whose records were examined in the study; this delayed diagnosis was associated with increased abdominal complications. Patients with persistent abdominal complaints and equivocal CT or DPL findings should undergo laparotomy or repeat CT scan evaluations.
BACKGROUND: The incidence of hollow viscus injury (HVI) after blunt trauma (BT) is variable, and differences between children and adults have not been well described. The purpose of this study is to determine the age-group-related incidence and characteristics of BT-associated HVI as well as the clinical markers and consequences of delayed diagnosis. METHODS: A 9-year trauma registry review of all patients with HVI. RESULTS: A large sample of patients (19,621) with BT were evaluated (2,550 < or = 14 years old; 17,070 > 14 years old). One hundred thirty-nine of 17,070 (0.8%) adults had HVI compared with 27 of 2,550 (1%) children. HVI occurred more frequently in the duodenum in children (11 of 27) compared with adults (17 of 139) (p < 0.05). Among patients with abdominal wall ecchymosis, 13.5% of children had HVI compared with 10.6% of adults. Delays in diagnosis of HVI occurred in 9 of 27 children compared with 10 of 139 adults (p < 0.0 5). Delayed diagnosis was associated with increased abdominal septic complications in both children (4 of 9) and adults (2 of 10) compared with diagnosis at presentation (p < 0.05). CONCLUSION: HVI occurs with a similar low frequency in both children and adults. Duodenal injuries are more common in pediatric BT patients. Abdominal wall ecchymosis is associated with increased HVI but is less predictive of HVI than previously described. Contrary to previous reports, delays in diagnosis are associated with increased morbidity.
BACKGROUND: The failure of therapies aimed at modulating systemic inflammatory response syndrome and decreasing multiple organ failure (MOF) has been attributed in part to the inability to identify early the population at risk. Our objective, therefore, was to develop predictive models for MOF at admission and at 12, 24 and 48 hours after injury. METHODS: Logistic regression models were derived in a data set with 411 adult trauma patients using indicators of tissue injury, shock, host factors, and the Acute Physiology Score-Acute Physiology and Chronic Health Evaluation III (APS-APACHE III). RESULTS: MOF was diagnosed in 78 patients (19%). Injury Severity Score, platelet count, and age emerged as predictors in all models. Transfused blood, inotropes, and lactate were significant predictors at 12, 24, and 48 hours, but not at admission. The APS-APACHE III emerged only in the 0- to 48-hour model and offered minimal improvement in predictive power. Good predictive power was achieved at 12 hours after injury. CONCLUSION: Postinjury MOF can be predicted as early as 12 hours after injury. The APS-APACHE III added little to the predictive power of tissue injury, shock and host factors.
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When motoneuron axons in peripheral nerves are injured, the expression of the p75 low-affinity neurotrophin receptor (p75) increases in their cell bodies and axons, as well as in the Schwann cells undergoing Wallerian degeneration in the distal excised nerve segment. To understand the role of p75 in the events following nerve injury, we have examined the survival and regeneration of motoneurons in mice lacking the p75 receptor. In adult p75 (-/-) mice, functional recovery of whiskers movement following a facial nerve crush occurred slightly earlier than in p75 (+/+) mice, and some recovery of function over a 25-day interval following a nerve cut occurred more frequently in p75 (-/-) mice. Motoneuron profile numbers were slightly reduced in p75 (-/-) mice, and there were correspondingly fewer axons in the facial nerve. At 25 days following axotomy, profile survival in the adult p75 (-/-) mice was significantly improved compared to p75 (+/+) mice (mean 85%+/-standard error of the mean 3%, n = 11 vs. 67+/-5%, n = 11 in CD-1 mice and 68.0+/-4%, n = 6 in balb/c mice), and significantly more regenerating axons were present in the distal facial nerve. After axotomy on postnatal day 1, there was almost total loss of motoneuron profiles in the lateral facial nucleus in p75 (+/+) mice (1.7+/-0.3% remained, n = 5), while significantly more survived in p75 (-/-) mice (17 +/-2.5 %, n = 6). We conclude that expression of p75 in motoneurons or Schwann cells following facial nerve injury is not necessary for motoneuron survival or prompt regeneration of their axons; rather, p75 may increase their risk of dying.
OBJECTIVE: To determine whether expression of neutrophil integrin receptors is related to the degree of post-traumatic shock. DESIGN: Data were collected prospectively on patients with major trauma admitted to the surgical intensive care unit. SETTING: Denver General Hospital, Colorado. PATIENTS AND PARTICIPANTS: 17 severely injured adults. MEASUREMENTS AND RESULTS: The mean fluorescence intensity and per cent positive of neutrophil integrin receptors CD11 b, CD18 and CD11 a, and systolic blood pressure, blood transfusion, lactate and base deficit as indices of shock. CD11 b expression on circulating neutrophils was increased 6 and 12 h after trauma. After correcting for the other shock indices, base deficit predicted CD11 b expression at 12 h. CD11 b expression was negatively correlated with the circulating neutrophil count. CONCLUSIONS: The degree of metabolic acidosis after trauma correlates directly with CD11 b receptor expression on circulating neutrophils. This relation may be the mechanism whereby post-traumatic shock results in neutrophil sequestration and neutrophil-mediated organ injury and failure.
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BACKGROUND: The abdominal compartment syndrome (ACS) is now recognized as a frequent confounder of surgical critical care following major trauma; however, few prospective data exist concerning its characterization, evolution, and response to decompression. METHODS: Acutely injured patients with an injury severity scale (ISS) score >15 requiring emergent laparotomy and intensive care unit (ICU) admission were prospectively evaluated for the development of ACS. The syndrome was defined as an intra-abdominal pressure (IAP) >20 mm Hg complicated by one of the following: peak airway pressure (PAP) >40 cm H2O, oxygen delivery index (DO2I) <600 mL O2/min/m2, or urine output (UO) <0.5 mL/kg/hr. Physiologic response to decompression was similarly documented prospectively. RESULTS: Over a 14-month period ending December 1995, 21 (14%) of 145 patients (ISS >15) requiring laparotomy and admitted to our surgical ICU developed ACS; mean age was 39 +/- 9 years; injury mechanism was blunt in 60%; ISS 26 +/- 6. At initial laparotomy, 67% underwent abdominal packing (57% for major liver injuries). Mean IAP was 27 +/- 2.3 mm Hg, and time from laparotomy to decompression was 27 +/- 4 hours; 24% were planned whereas the remaining were prompted by deteriorating organ function as defined above (cardiopulmonary in 43%; renal in 19%; both renal and cardiopulmonary in 14%). Following decompression, there was an increase in cardiac index, oxygen delivery, urine output, and static compliance while there was a decrease in pulmonary capillary wedge pressure, systemic vascular resistance, and peak airway pressure. CONCLUSIONS: The abdominal compartment syndrome occurs in a significant number of severely injured patients, and it develops quickly (27 +/- 4 hours). Cardiopulmonary deterioration is the most frequent reason prompting decompression. Timely decompression of the ACS results in improvements in cardiopulmonary and renal function. These data support the use of the proposed ACS grading system for selective management of the syndrome.
OBJECTIVE: To determine whether early supply independent mitochondrial oxidative dysfunction occurs in trauma patients who develop multiple organ failure (MOF). DESIGN: Prospective focused observational trial. METHODS: High-risk patients were aggressively resuscitated while being continuously monitored by near infrared spectroscopy. Near infrared spectroscopy monitoring strips allow for a direct comparison of changes in tissue oxyhemoglobin levels (HbO2), which reflect local oxygen supply, and cytochrome a,a3 redox, which reflects mitochondrial oxygen consumption. Under normal conditions, HbO2 and a,a3 redox are tightly coupled. On the other hand, decoupled HbO2 and a,a3 redox is a sign of mitochondrial oxidative dysfunction. Outcomes included MOF, oxygen delivery, oxygen consumption, lactate, and the presence of decoupled HbO2 and a,a3 redox. RESULTS: Twenty-four high-risk patients were studied; nine (38%) developed MOF. At 12 hours of resuscitation, MOF and non-MOF patients did not have statistically different oxygen delivery and oxygen consumption, but lactate levels were significantly higher in MOF patients. Additionally, HBO2 and a,a3 redox were decoupled in eight (89%) MOF patients compared with two (13%) non-MOF patients (p < 0.05). CONCLUSION: Severely injured trauma patients who develop MOF preferentially display evidence of mitochondrial oxidative dysfunction early in the course of their resuscitation despite early goal-oriented maximization of oxygen delivery.
BACKGROUND: The pathogenesis of multiple organ failure after injury is believed to involve priming and activation of the inflammatory cascade, and the polymorphonuclear neutrophil (PMN) appears to be an integral effector. Characterization of the primed PMN is evolving. Because much research has focused on the respiratory burst, the synergistic role of cytotoxic proteases, especially elastase, has been largely ignored. In addition, CD11b has been identified as pivotal in PMN-mediated tissue injury. Our hypothesis is that the well-recognized postinjury mediators platelet-activating factor (PAF) and leukotriene B4 (LTB4) prime PMNs for the concordant release of elastase and superoxide (O2-) as well as for CD11b up-regulation. METHODS: Human PMNs were isolated and then incubated with PAF or LTB4 before N-formyl-methionyl-leucyl-phenylalanine activation. O2- generation was measured by reduction of cytochrome c. Elastase was measured by cleavage of Ala-Ala-Pro-Val p-nitroanilide. CD11b expression was quantified by incubation with R-phycoerythrin-labeled monoclonal antibodies followed by flow cytometry. RESULTS: PAF and LTB4 primed PMNs maximally within 5 minutes for the production of O2-, elastase release, and simultaneous up-regulation of CD11b expression on the PMN surface. CONCLUSION: PAF and LTB4 prime human PMNs for the concordant release of elastase, generation of O2-, and CD11b up-regulation. Understanding the physiologic characteristics of PMN priming may offer new therapeutic targets to avoid the development of multiple organ failure after injury.
We have previously documented the safety of 1 unit (50 gram) of human polymerized hemoglobin (Poly SFH-P) in healthy volunteers. This report describes the first patient trial to assess the therapeutic benefit of Poly SFH-P in acute blood loss. Thirty-nine patients received 1 (n = 14), 2 (n = 2), 3 (n = 15), or 6 (n = 8) units of Poly SFH-P instead of red cells as part of their blood replacement after trauma and urgent surgery. There were no safety issues related to the infusion of Poly SFH-P. The plasma hemoglobin concentration ([Hb]) after the infusion of 6 units (300 gram) of Poly SFH-P was 4.8 +/- 0.8 g/dL (mean +/- SD). Although the red cell [Hb] fell to 2.9 +/- 1.2 g/dL, the total [Hb] was maintained at 7.5 +/- 1.2 g/dL. Poly SFH-P maintained total [Hb], despite the marked fall in red cell [Hb] due to blood loss. The utilization of O2 (extraction ratio) was 27 +/- 16% from the red cells and 37 +/- 13% from the Poly SFH-P. Twenty-three patients (59%) avoided allogeneic transfusions during the first 24 hours after blood loss. Poly SFH-P effectively loads and unloads O2 and maintains total hemoglobin in lieu of red cells after acute blood loss, thereby reducing allogeneic transfusions. Poly SFH-P seems to be a clinically useful blood substitute.