Hyperbaric oxygen therapy: types of injury and number of sessions--a review of 1506 cases.

OBJECTIVE: The aim of this work was to identify clinical data indicative of the number of hyperbaric oxygen therapy HBO2 sessions that should be prescribed for adjuvant treatment of tissue injuries of differing severity. PATIENTS: A total of 1730 cases of patients treated with HBO2 using an open protocol (without a predetermined number of sessions) was examined in this study. METHOD: A retrospective study involving charts review was conducted. Severity had been previously determined for the treatment of acute (fasciitis, myositis, gangrene, contaminated/infected perineal or lower extremity traumatic injuries) or chronic (osteomyelitis, pressure sore, diabetic or ischemic ulcer) injuries. Only patients that met or exceeded the supposed effective minimal treatment doses (5 sessions for acute, 10 sessions for chronic injuries) were included in the present study. RESULTS: The data analysis included 1506 cases. These consisted of 1014 patients with acute injuries, who required 11 to 18 sessions (depending on injury severity), and 492 patients with chronic injuries, who required a greater (p < 0.001) number of sessions (approximately 30/patient, independent of injury severity). Global mortality was 79/1506 patients. CONCLUSION: These results seem to support the initial indication of 15 HBO2 sessions for the treatment acute injuries, and 30 for treatment of chronic injuries. Prospective studies may better determine the number of sessions for the treatment of different types of injuries.

Is aortic occlusion advisable in the management of massive hemorrhage? Experimental study in dogs.

Occlusion of the thoracic aorta is meant to improve cerebral and cardiac perfusion in the moribund, exsanguinating trauma patient. Yet clinical and experimental experience shows no evident benefit from this critical maneuver, and hind limb paralysis (HLP) is a feared complication. Our study is intended to verify whether aortic occlusion can decrease further blood loss and therefore be useful during treatment of hemorrhagic shock. Four groups of 10 dogs were submitted to hemorrhagic shock and treated with blood (40 mL/kg) and saline (35 mL/kg). Group I was then submitted to intermittent intra-aortic occlusion (IIAO), Groups II and III to IIAO and to a second bleeding (rebleeding), and Group IV to rebleeding only, without IIAO. All dogs received volume replacement during this rebleeding phase and were kept alive for 8 days. Five dogs died and seven had HLP in the three groups submitted to IIAO. Death and HLP occurred even in the dogs of Group I, which were not submitted to a second bleeding. IIAO reduced blood loss from 139 mL/kg to 48 mL/kg. There were no complications or deaths among the 10 dogs in Group IV. Although efficient in reducing blood loss, IIAO was associated with a 16% mortality and 23% of HLP, whereas volume replacement alone was tolerated without complications or death. We conclude that IIAO is dangerous while treating severe hemorrhagic shock even after volume replacement and hemodynamic stabilization.

Inadequate granulopoiesis after major torso trauma: a hematopoietic regulatory paradox.

Late postinjury sepsis is largely the result of defective host defense including failure to maintain an adequate number of functioning phagocytic cells. In this study we used stem cell culture techniques to measure colony-stimulating activity and have quantitated the number of circulating myeloid stem cells to see if defects in granulopoiesis occur after major torso trauma. Forty-two acutely injured patients (13 blunt and 29 penetrating injuries; mean age, 29.7 years) undergoing laparotomy with an abdominal trauma index of 15 to 40 were studied prospectively. Blood samples were obtained on days 1, 5, and 10. Patients were segregated by injury severity: abdominal trauma index less than 25 (n = 25) versus abdominal trauma index greater than or equal to 25 (n = 17). The more severely injured (abdominal trauma index greater than or equal to 25) patients had fewer circulating granulocytes and monocytes. Colony-stimulating activity was below normal control levels in all patients and was decreased further with increased injury severity. The more severely injured patients had a blunted bone marrow response (significantly fewer circulating myeloid stem cells) and suffered more major septic complications (24% vs 8%). In conclusion, major trauma to the torso causes a paradoxic depression in granulopoiesis that worsens with increased injury severity and may contribute to late septic morbidity. This colony-stimulating activity deficiency state is similar to that seen after major burns and may be amenable to future modulation.

Postinjury shock and early bacteremia. A lethal combination.

Gut bacteria translocation has been invoked as a prime cause of early postinjury death. To examine this hypothesis, we obtained emergency department blood cultures in 132 acutely injured patients requiring urgent laparotomy for trauma. In the latter half of these patients, mesenteric lymph node and liver biopsy cultures were also performed. The incidence of early bacteremia was 11% (10/94) in the patients without shock compared with 32% (12/38) in the group with shock. The majority (73%) were gram-positive bacteremias. Most notably, Staphylococcus was isolated in 13% (5/38) of the patients with shock, but these isolates were of no apparent clinical significance. In contrast, 18% (7/38) of the patients with shock had enteric bacteremias, and all of these patients died. Cultures were positive in 11% of the liver samples and 15% of the mesenteric lymph nodes. With the exception of two patients with concurrent enteric bacteremias, these hepatic and mesenteric lymph node bacteria were of no clinical significance. In conclusion, bacterial translocation occurs infrequently, and virtually all enteric bacteria were found in dying patients; the cause or effect remains to be defined.

Liver injury is a reversible neutrophil-mediated event following gut ischemia.

The purposes of this study were to characterize the temporal relationship of distant organ dysfunction after mesenteric ischemia/reperfusion (I/R), and to ascertain if the neutrophil is critical to this process. Normal and neutrophil-depleted rats (vinblastine sulfate, 0.75 mg/kg intravenously) underwent 45 minutes of superior mesenteric artery occlusion and after 0, 6, and 18 hours of reperfusion, blood was sampled and liver and lungs were harvested. Iodine 125 albumin leak was used as a marker for pulmonary and liver injury, and serum acetoacetate/3-hydroxybutyrate (AcAc/3-OHB) was used as an index of hepatic mitochondrial redox state. Gut I/R at 6 hours increased 125I-albumin lung/blood ratio (gut I/R, 0.077 +/- 0.006; control, 0.045 +/- 0.004) and 125I-albumin liver/blood ratio (gut I/R, 0.120 +/- 0.007; control, 0.077 +/- 0.003), while AcAc/3-OHB decreased significantly (gut I/R, 0.420 +/- 0.040; control, 0.880 +/- 0.120). Neutrophil depletion eliminated these changes at 6 hours (blood AcAc/3-OHB, 0.720 +/- 0.100; 125I liver/blood, 0.068 +/- 0.006; 125I lung/blood, 0.046 +/- 0.007). We conclude the following: (1) intestinal I/R produces simultaneous liver and lung injury; (2) injury was present at 6 hours but is reversed at 18 hours; and (3) the I/R-induced liver and lung injuries were neutrophil mediated.

Laparoscopic pneumoperitoneum in acute peritonitis does not increase bacteremia or aggravate metabolic or hemodynamic disturbances.

The use of laparoscopy in generalized peritonitis has become increasingly frequent in recent years. However, CO2 pneumoperitoneum in association with increased intraperitoneal pressure may have deleterious effects in patients with hemodynamic or metabolic disturbances caused by bacterial peritonitis. The purpose of this study was to investigate the effect of CO2 pneumoperitoneum on bacteremia, mean arterial pressure, and blood gas disturbances in an animal model of bacterial peritonitis. Dogs were anesthetized, orally intubated, and subjected to experimental peritonitis by intraperitoneal inoculation of a suspension containing Escherichia coli and sterile dog feces. The animals were randomly assigned to two groups: control animals were maintained under anesthesia, and the insufflated animals were subjected to intraperitoneal CO2 insufflation. Bacterial peritonitis provoked the appearance of bacteremia and a significant decrease in mean arterial pressure, pH, bicarbonate, and base deficit. The induction of bacterial peritonitis did not significantly influence pH in the control group and partial pressure of arterial CO2 in either group. Thirty minutes of CO2 pneumoperitoneum did not influence the effect of bacterial peritonitis on the analyzed variables. These results suggest that laparoscopic CO2 pneumoperitoneum does not aggravate bacteremia or metabolic and hemodynamic disturbances induced by bacterial peritonitis.

Cardiac herniation mimics cardiac tamponade in blunt trauma. Must early resuscitative thoracotomy be done?

Blunt rupture of the pericardium is a rare injury. Strangulated cardiac hernia following blunt trauma is one cause of reversible cardiac arrest. Traumatic pericardial tears usually have delayed diagnoses and carry high mortality rates (64%). Clinical signs mimic cardiac tamponade during the primary survey. We report here two cases of blunt trauma. Both patients arrived alive in the emergency room and presented signs of cardiac tamponade caused by pericardial rupture.

Extrahepatic bile ducts injury: a report on 14 cases.

Traumatic injuries of the extrahepatic biliary tract are infrequent, occurring in approximately 0.5% of all patients with blunt and penetrating abdominal trauma. The incidence of this injury due to blunt abdominal trauma is rare. This study reviewed patients with injuries of the extrahepatic biliary tract due to abdominal trauma over a 6-year period to determine the incidence, trauma scores, associated injuries, surgical treatment performed, complications and mortality rate. We report our experience with 14 patients with extrahepatic biliary tract trauma. A review of the literature and the discussion about the management are presented.

Gallstone ileus as a cause of upper intestinal obstruction.

Gallstone ileus, a mechanical intestinal obstruction caused by the passage of a gallstone into the intestinal lumen through a fistula, although not common, deserves to more carefully studied due to its morbidity and mortality. Its incidence among older-age groups explains its association with chronic and degenerative diseases, which increase the complexity of the treatment choice. The need and appropriateness of a surgical approach to a cholecystenteric fistula to solve the obstructive emergency, in a one or two stage procedure, has been discussed in the literature. It has also been reported that gallstone ileus is an uncommon cause of upper intestinal obstruction. Intestinal obstruction is seen more frequently after a gallstone impacts at the ileocecal valve. The authors report a case of gallstone ileus as a cause of upper intestinal obstruction and discuss its diagnosis and treatment.

Gallstone ileus resulting in strong intestinal obstruction.

Mechanic intestinal obstruction, caused by the passage of biliary calculus from vesicle to intestine, through fistulization, although not frequent, deserve study due to the morbi-mortality rates. Incidence in elder people explains the association with chronic degenerative diseases, increasing complexity in terms of therapy decision. Literature discusses the need and opportunity for the one or two-phase surgical attack of the cholecyst-enteric fistule, in front of the resolution on the obstructive urgency and makes reference to Gallstone Ileus as an exception for strong intestinal obstruction. The more frequent intestinal obstruction observed is when it occurs a Gallstone Ileus impacting in terms of ileocecal valve. The authors submit a Gallstone Ileus manifestation as causing strong intestinal obstruction, discussing aspects regarding diagnostic and treatment.

[Abdominal surgical emergencies in patients with acquired immunodeficiency syndrome]. / Urgências cirúrgicas abdominais em pacientes com síndrome da imunodeficiência adquirida.

UNLABELLED: Patients with Acquired Immunodeficiency Syndrome (AIDS) may present acute abdomen with modified clinical manifestations which may lead to errors and delays in preoperative diagnosis, with frequent delays in treatment. PURPOSE: To study clinical signs, diagnostic criteria, etiology, surgical management and mortality in patients with AIDS submitted to exploratory laparotomy. METHODS: We reviewed the records of thirty-one AIDS patients admitted in the period 1986-1993 at the Emergency Surgical Service--Hospital das Clínicas, University of São Paulo submitted to exploratory celiotomy due to acute abdome. RESULTS: Abdominal pain was the most frequent symptom and the diagnosis of acute abdome was made based upon physical examination, laboratory tests and imaging techniques. Gastrointestinal tract perforation was the most frequent cause of acute abdome, mainly due to Cytomegalovírus infection. All patients presented postoperative complication, specially wound infection. Mortality rate was 42% due to sepsis and multiple organ failure. CONCLUSION: Based upon these data we conclude that: AIDS patients usually present masked clinical signs of acute abdomen; stomas should be formally indicated. Mortality is extremely high due to immunocompromised state, delayed diagnosis and treatment and non therapeutic celiotomies.

[Traumatic injuries of the gallbladder and of the extrahepatic biliary tract: analysis of 45 cases]. / Lesões traumáticas da vesícula e trato biliar extra-hepático: análise de 45 casos.

Injury of the extra-hepatic biliary tract is infrequent, occurring in approximately 3.5% of all patients with blunt and penetrating abdominal trauma. The incidence of this injury caused by blunt abdominal trauma is rare. PURPOSE--Retrospective analysis of 5069 patients with abdominal trauma treated at the Department of Surgery University of São Paulo School of Medicine over a six-year period from 1986 through 1991. METHODS--Forty five patients with gallbladder and extra-hepatic ducts injury were identified (0.89%) and divided in two groups according to the nature of trauma: 12 caused by non-penetrating injuries and 33 to penetrating injuries. Records, including operative and pathology reports, were reviewed to study the site of injury, associated intra-abdominal injuries, incidence, trauma scores, treatment, morbidity, mortality rates and correlated with the nature of the trauma. RESULTS--Overall mortality was 24.4%. The incidence was greater in patients sustaining penetrating abdominal trauma (p < 0.05). Forty of the 45 patients (88.9%) had liver lacerations, the most commonly seen injuries. The patients with blunt abdominal trauma had significant different trauma scores (p < 0.05) than those with penetrating trauma, indicating greater severity in this group of patients. CONCLUSION--There is a relation between severity of trauma and incidence of extra-hepatic biliary tract injury. However, in the penetrating trauma, the incidence of trauma is correlated with the direction of the wound and there is no relation with the severity of trauma. The greater mortality seen in the patients sustaining non-penetrating injury (p < 0.05) supports this observation.

[The role of the polymorphonuclear neutrophil in the failure of multiple organs and systems]. / Papel do pmn na falência de múltiplos órgãos e sistemas.

The role of the polymorphonuclear neutrophil (PMN) on MOF is analyzed either as PMN activation for superoxide and enzyme release, or as PMN function depression after trauma and surgery. The authors stress: 1) the signal transduction pathway from the PMN membrane receptors to the effector response; 2) the PMN-NADPH system structure and function; 3) the functional states of the PMN (quiescente, primed, activated, non-responsive) in terms of the NADPH system activation; 4) the mechanism of tissue injuiry by the PMN. Clinical investigations on the PMN activation state, and therapeutical goals based on recent clinical investigations are also discussed.

[Mechanisms and evaluation of multiple organ and system failure after trauma]. / Mecanismos e mediadores da falencia de múltiplos órgäos e sistemas após trauma, aspectos atuais.

Multiple organ failure (MOF) is a major cause of death of ICU trauma patients. Despite intensive clinical and experimental investigation, the exact physiopathology of this syndrome is unclear. Although diverse cellular and humoral mediators have been identified, their mechanistic role is still debated. In this article the authors discuss recent results of this investigation. They present recently published criteria for MOF quantification, and focus on the mechanisms and mediators of MOF syndrome, emphasizing the role of sepsis, the intestinal ischemia/reperfusion MOF model, the role of polymorphonuclear neutrophil, and the relationship between adult respiratory distress syndrome (ARDS) and the development of MOF syndrome.

Simultaneous liver and lung injury following gut ischemia is mediated by xanthine oxidase.

We have previously shown that gut ischemia/reperfusion (I/R) causes simultaneous liver and lung dysfunction and that neutrophils play a critical role in this process. The purpose of this study was to ascertain whether xanthine oxidase (XO) was likewise operational. Normal and XO-inactivated rats (given a tungsten-enriched, molybdenum-depleted diet for 3 weeks) underwent 45 minutes of occlusion of the superior mesenteric artery, and control rats were subjected to a sham laparotomy. After zero and six hours of reperfusion, blood was sampled and livers and lungs harvested. Iodine-125-labeled albumin leak was used as a marker for pulmonary and liver capillary permeability barrier function, and serum acetoacetate/3-hydroxybutyrate (AcAc/3-OHB) levels as an index of hepatic mitochondrial redox state. Gut ischemia/six hours of reperfusion (I/R) increased the 125I albumin lung/blood ratio and the 125I albumin liver/blood ratio; AcAc/3-OHB levels decreased significantly. Xanthine oxidase activation eliminated the observed lung and liver capillary leak as well as the hepatic metabolic derangement induced by gut I/R. In conclusion, the simultaneous lung and liver dysfunction produced by gut I/R is mediated by XO.

Gut ischemia/reperfusion-induced liver dysfunction occurs despite sustained oxygen consumption.

We have previously shown that gut ischemia/reperfusion (I/R) causes liver dysfunction in vivo (increased [I125]albumin leak, decreased mitochondrial redox potential). Our purpose was to investigate liver dysfunction due to gut I/R in an ex vivo model where oxygen delivery (DO2) could be controlled. Rats underwent laparotomy (sham) or 45 min of superior mesenteric artery (SMA) occlusion (I/R) and 6 hr later the gut and liver were isolated in situ. Pressures were monitored while recirculating blood was perfused via the hepatic artery (2.5 ml/min) for 90 min and the SMA (7.5 ml/min) for the first 30 min, then the portal vein (7.5 ml/min) for 60 min. Both gut and liver DO2 and VO2 (Fick method) were maintained throughout the study period in the gut I/R as well as sham groups. Despite maintenance of liver VO2, however, gut I/R resulted in a marked and persistent reduction in bile flow. In conclusion, dysfunctional bile production after gut I/R is not due to impaired VO2, but rather gut-liver signaling yet to be defined.

Autotransfusion with laparoscopically salvaged blood in trauma: report on 21 cases.

Autotransfusion is being increasingly used to avoid the complications of homologous blood transfusion. In abdominal trauma, however, the collected blood may be contaminated by intestinal contents when digestive or urinary lesions are present. In such situations, the reinfusion of blood is contraindicated. We present our experience with autotransfusion of blood collected by laparoscopy from the abdominal cavity of 21 trauma patients. Laparoscopy allowed the aspiration of blood and, at the same time, permitted diagnosis of visceral lesions, avoiding reinfusion of contaminated blood. No complications occurred, and hematocrit values were significantly elevated. This procedure may represent the only possible method of blood transfusion in Jehovah's Witnesses, as with one patient in our series.

Gut ischemia/reperfusion activates lung macrophages for tumor necrosis factor and hydrogen peroxide production.

BACKGROUND: Gut ischemia followed by reperfusion (I/R) is implicated as a prime initiating event in the mechanism of multiple organ failure after trauma and hemorrhagic shock. Several lines of evidence indicate that macrophages are involved in this prime event. Our purpose was to evaluate hydrogen peroxide (H2O2) and tumor necrosis factor (TNF) production and phagocytosis by lung macrophages in a gut I/R model of multiple organ failure in rats. METHODS: In the experimental group (I/R), Wistar rats (n = 35) were anesthetized and subjected to a median laparotomy, and the superior mesenteric artery was clamped for 45 minutes followed by 60 minutes of reperfusion. In the control group (LAP) (n = 37), animals underwent sham laparotomy. After the period of reperfusion, bronchoalveolar lavage (BAL) was performed and the resulting BAL cells were assayed for H2O2 production using the horseradish peroxidase-mediated red phenol oxidation method. TNF release was determined using the L929 cells bioassay. Zymosan phagocytosis by BAL macrophages was quantitated using phase microscopy. RESULTS: H2O2 release in BAL cells of I/R rats (19.90 +/- 7.98 nmol/L/2 x 10(5) cells) is statistically higher than in the LAP group (10.92 +/- 5.01 nmol/L per 2 x 10(5) cells) (p = 0.0155), and the TNF production by BAL cells of the I/R group (38.09 +/- 20.79 units per 10(6) cells) was significantly higher than that of LAP rats (17.16 +/- 13.35 units per 10(6) cells) (p = 0.0281). Phagocytic activity of BAL mac. Macrophages of I/R rats was not statistically different from LAP animals. CONCLUSION: These results suggest that BAL macrophage play a role in the mechanism of acute lung injury after trauma and hemorrhagic shock.

[Gallbladder injury in abdominal trauma: analysis of 32 cases]. / Lesão de vesícula biliar em trauma abdominal: análise de 32 casos.

Gallbladder lesion is infrequent, occurring in approximately 0.5 to 8.5% of all patients with blunt and penetrating abdominal trauma. The incidence of gallbladder injury in such cases is low. This study reviewed 32 patients with gallbladder injury due to abdominal trauma over a 6-year period to determine the complications, associated injuries, and mortality rate.

Bilateral diaphragmatic injury diagnosed by laparoscopy.

Rupture of the diaphragm from blunt trauma is uncommon, but greatly improved prehospital care and transportation of victims has increased the frequency at which patients who sustain this injury arrive at the emergency room alive. We report a case of bilateral diaphragmatic rupture from blunt abdominal trauma in a 33-year old man. Diagnosis was established by laparoscopy after suggestive chest X-rays, liver scintigraphy, CT scan and magnetic resonance imaging. The methods used to diagnose this condition are analyzed.