Urine toxicology screening in Austrian trauma patients: a prospective study.

INTRODUCTION: The question as to whether the patient consumed drugs prior to the trauma and which drugs were consumed, is of prime importance for the anesthesia required during surgery. However, many patients are unwilling or unable (including those with multiple trauma or impaired consciousness, or unconscious patients) to answer this question. The purpose of our prospective multicenter study was to collect data about drug consumption in Austria to determine whether drugs are identifiable in the urine of recently injured individuals and to establish the types of drugs consumed. MATERIALS AND METHODS: This prospective study included severely and moderately injured patients admitted to the Lorenz Boehler Trauma Hospital (Vienna, Austria), the Trauma Hospital Linz (Linz, Austria) and the Department of Trauma Surgery of the General Hospital Horn (Horn, Austria) during an 18-month period (October 2003-March 2005). All patients were suffering from injuries urgently requiring surgery. Urine samples were gained from all patients immediately after admission. Urinary samples were tested by Immuno-Assay (Triage 8 Immuno-Assay, Biosite, San Diego, USA). Urine samples were screened simultaneously for opiates, methadone, cocaine, barbiturates, amphetamines, cannabinoids, benzodiazepines and tricyclic antidepressants. RESULTS: Our prospective study included a total of 664 patients (320 from Vienna, 193 from the city of Linz, and 151 from Horn). Six hundred and forty-two patients were moderately injured (ISS < 16), suffering mostly from injuries to the extremities (504 patients) and 22 patients were severely injured (ISS > 16). Of the 664 patients, 178 (26.8%) tested positive for one or more drugs. The drugs most commonly detected were benzodiazepines (111 patients, 16.7%), cannabinoides (39 patients, 6%), tricyclic antidepressants (28, 4.2%) and opiates (26, 3.9%). CONCLUSION: Drug use is widespread in patients presenting to urban trauma centers in Austria. Physicians should maintain a high index of suspicion that their patients may be intoxicated and should perform drug testing routinely.

Tryptophan degradation in multiple trauma patients: survivors compared with non-survivors.

Immune dysfunction in trauma patients is associated with immune system activation and inflammation. The cytokine-inducible enzyme IDO (indoleamine 2,3-dioxygenase) initiates the degradation of the essential aromatic amino acid tryptophan via the kynurenine pathway and could contribute to deficient immune responsiveness. Activated IDO is indicated by an increased kyn/trp (kynurenine/tryptophan) ratio. The aim of the present study was to investigate whether tryptophan degradation is associated with outcome in patients post-trauma. Tryptophan and kynurenine concentrations were measured by HPLC in serum specimens of 15 patients post-trauma during 12-14 days of follow-up. Up to five samples within this observation period from each patient were included in this analysis, and a total a 69 samples were available. For further comparisons, concentrations of the immune activation marker neopterin were measured. Compared with healthy controls, the average kyn/trp ratio and kynurenine concentrations were increased in patients, whereas tryptophan concentrations were decreased. During follow-up, increased kyn/trp ratio and kynurenine concentrations (all P<0.001) were observed, whereas the changes in tryptophan concentrations were not significant. Non-survivors had higher kyn/trp ratios and kynurenine concentrations compared with survivors. The kyn/trp ratio correlated with neopterin concentrations (r(s)=0.590, P<0.001). In conclusion, these results imply that increased tryptophan degradation in patients is due to activated IDO, which most probably is a consequence of a host defence response. These findings support a possible role for IDO in the development of immunodeficiency and death in patients.

Cholecystitis after trauma.

BACKGROUND: The goal of this project was to investigate incidence, risk factors, histologic findings, and mortality rate of posttraumatic cholecystitis requiring surgical treatment. METHODS: Retrospective analysis of all patients admitted to the intensive care unit of an urban trauma center between April 1998 and January 2005. Data from the hospital and intensive care documentation systems databases and patients' charts were reviewed. All patients with cholecystitis treated by cholecystectomy were selected for further study. Potential risk factors, diagnostic, and histologic findings were analyzed. RESULTS: Cholecystitis was a fairly frequent finding in critically ill trauma patients (67 of 2,625 patients, 2.6%). Almost 10% of the patients with severe multiple injuries developed cholecystitis. Histologic findings showed a wide variation; three main diagnoses were established: acute acalculous cholecystitis (n = 28), chronic acalculous cholecystitis (n = 25), and cholecystitis with cholecystolithiasis (n = 13). Patients with acute acalculous cholecystitis and chronic acalculous cholecystitis were significantly younger and had significantly higher injury severity scores than patients with either cholecystitis with cholecystolithiasis or without cholecystitis. Noninvasive diagnostic tools such as ultrasonographic signs and laboratory data did not correlate with histologic diagnosis. Well-timed cholecystectomy within 24 hours after clinical suspicion lead to a 4.4% mortality rate in this group of patients. CONCLUSION: Cholecystitis after trauma is not a uniform disease. Although trauma severity seems to play an important role in the development or exacerbation of acalculous cholecystitis or both, cholecystolithiasis may play a significant role in patients with moderate to minor trauma. Intensivists should be aware of this complication in critically ill trauma patients because it seems to occur more frequently than previously assumed. Diagnosis can only be made if clinical signs, laboratory data, and ultrasonographic findings are taken into consideration. If posttraumatic cholecystitis is treated in an early stage by cholecystectomy, mortality rate remains low.

Nonspecific increase of systemic neuron-specific enolase after trauma: clinical and experimental findings.

The aim of this clinical and experimental study was to determine whether systemic neuron-specific enolase (NSE) is a useful early marker of traumatic brain injury (TBI) and whether NSE is affected by ischemia/reperfusion damage of abdominal organs. Our study included patients with and without TBI (verified by computerized tomography) admitted within 6 h after trauma and male Sprague-Dawley rats with ischemia and reperfusion of the abdominal organs liver, gut, or kidney. Thirty-eight study patients included 13 with isolated TBI and 18 patients with multiple trauma and TBI. Seven patients had multiple trauma but no TBI. Fifteen rats were anaesthetized and subjected to isolated ischemia of the liver, gut, or kidney (n = 5 each) for 1 h, followed by reperfusion for 3 h. In patients, NSE increased over 2-fold versus the upper normal limit (10 microg/L) within 6 h after trauma, regardless of whether TBI had occurred or not. In rats, NSE increased over 3-fold versus laboratory controls during ischemia of the liver and kidney (both P < 0.0005), but not of the gut. NSE increased over 2-fold after onset of reperfusion of the liver and kidney (both P < 0.05), but not of the gut and increased over 3-fold after 3 h of reperfusion of the liver, gut (both P < 0.005), and kidney (P < 0.0005). Our data show that systemic NSE increases to similar degrees with and without TBI. Therefore, NSE is not a useful early marker of TBI in multiple trauma.

Anti-L-selectin antibody therapy does not worsen the postseptic course in a baboon model.

INTRODUCTION: Anti-adhesion molecule therapy prevents leukocytes from extravasating. During exaggerated inflammation, this effect is wanted; however, during infection, blocking diapedesis may be detrimental. In this study, therefore, the potential risks of anti-L-selectin antibody therapy were evaluated in a primate model of sepsis. METHODS: Sixteen baboons were anesthetized and randomized into two groups. The experimental group received 2 mg/kg of the anti-L-selectin antibody HuDREG-55 and the control group received Ringer's solution prior to the onset of a 2 h infusion of Escherichia coli (1-2 x 10(9) colony forming units (CFU)/kg body weight). Serial blood samples were drawn over a 72 h period for the measurement of tumour necrosis factor-alpha, IL-6 and polymorphonuclear elastase. In addition, blood gas analysis, hematology and routine clinical chemistry were determined to monitor cardiovascular status, tissue perfusion and organ function. RESULTS: The three-day mortality rate and the mean survival time after E. coli-induced sepsis were similar in the two groups. The bacterial blood CFU levels were significantly higher in the placebo group than in the anti-L-selectin group. Other parameters measured throughout the 72 h experimental period, including the cardiovascular, immunologic, and hematologic responses as well as indicators of organ function and tissue perfusion, were similar in the two groups, with the exception of serum creatinine and mean arterial pressure at 32 h after E. coli challenge. CONCLUSION: Anti-L-selectin therapy did not adversely affect survival, promote organ dysfunction or result in major side effects in the baboon sepsis model. Additionally, as anti-L-selectin therapy improved the bacterial clearance rate, it appears that this therapy is not detrimental during sepsis. This is in contrast to previous studies using the baboon model, in which antibody therapy used to block CD18 increased mortality.

Neuron-specific-enolase is increased in plasma after hemorrhagic shock and after bilateral femur fracture without traumatic brain injury in the rat.

Neuron-specific enolase (NSE) is an acknowledged marker of traumatic brain injury. Several markers originally considered reliable in the setting of traumatic brain injury have been challenged after having been studied more extensively. The aim of our experimental study was to determine whether NSE is a reliable marker of traumatic brain injury early after trauma. Hemorrhagic shock was achieved by bleeding anesthetized rats to a mean arterial pressure (MAP) of 30-35 mmHg through a femoral catheter until incipient decompensation. MAP was maintained at 30-35 mmHg until 40% of shed blood had been administered as Ringer's solution and was then increased and maintained at 40-45 mmHg for 40 min by further administration of Ringer's solution, mimicking the phase of inadequate preclinical resuscitation. Blood samples were drawn at the end of the 40-min period of inadequate resuscitation. Femur fracture was achieved in anesthetized rats by bilateral application of forceps. Blood samples were drawn 30 and 60 min after fracture. Hemorrhagic shock caused NSE increase versus laboratory controls at the end of inadequate resuscitation (P < 0.01). Bilateral femur fracture caused NSE increase versus laboratory controls 30 min after fracture, which was significant 60 min after fracture (P < 0.01). During femur fracture, MAP remained at a level that is not associated with shock in rats. Our findings show for the first time that NSE increases after hemorrhagic shock as well as after femur fracture without hemorrhagic shock in rats. From a clinical point of view, these findings indicate that NSE cannot be considered a reliable marker of traumatic brain injury early after trauma in cases associated with hemorrhagic shock and/or femur fracture.

Hemorrhagic shock induces an S 100 B increase associated with shock severity.

S 100 B is a glial marker of cerebral Injury. In a previous clinical study, we found an S 100 B increase within the first 24 h in patients with multiple trauma and hemorrhagic shock but without cerebral trauma. The aim of our current experimental study was to determine whether this posttraumatic S 100 B increase is caused by extracerebral soft tissue injury or by hemorrhagic shock and whether it is associated with the severity of hemorrhagic shock. Hemorrhagic shock was achieved by bleeding anesthetized rats to a mean arterial pressure (MAP) of 30-35 mmHg through a femoral catheter and maintaining this MAP until incipient decompensation. At incipient decompensation, MAP was either increased immediately to 40-45 mmHg (moderate shock) or was maintained until 40% of shed blood had been returned (severe shock), and then increased to 40-45 mmHg. Resuscitation was provided after 40-45 mmHg MAP had been maintained for 40 min. Soft tissue injury was achieved by midline laparotomy performed at the onset of hemorrhagic shock or without shock and was maintained for 30 min. Hemorrhagic shock caused an early S 100 B increase at the onset of decompensation. S 100 B remained increased for 24 h and was significantly higher after severe than after moderate shock. In contrast, soft tissue injury without hemorrhagic shock caused no S 100 B increase. The data presented demonstrate for the first time that the S 100 B increase is induced by hemorrhagic shock and is associated with the severity of shock.

Serum S 100 B: a marker of brain damage in traumatic brain injury with and without multiple trauma.

This prospective clinical study was conducted to determine whether S 100 B is a reliable serum marker for traumatic brain injury (TBI) with and without multiple trauma. Fifty-five trauma patients (Injury Severity Score [ISS] > or = 24 and Glasgow Coma Score [GCS] < or = 8) were classified by radiography, computer tomography, ultrasound, and neurology as TBI without multiple trauma (n = 23), TBI with multiple trauma (n = 23), or multiple trauma without TBI (n = 9). S 100 B was measured initially after trauma and daily for a maximum of 21 days. Both survivors and nonsurvivors had markedly increased S 100 B initially. All survivors returned to normal or moderately increased S 100 B levels within the first 48 h after trauma. In contrast, all nonsurvivors of isolated TBI had S 100 B values that either increased consistently or dropped and then increased again 48 h after the initial increase after trauma. There was no relationship between localization, extent, or severity of TBI and S 100 B. According to receiver operating characteristic curve analysis and calculation of the area under the curve (AUC), S 100 B is equally accurate for mortality prediction at 24, 48, and 72 h after trauma and is most accurate >84 h after trauma. Sensitivity/specificity for mortality prediction are more accurate in TBI without multiple trauma (AUC 0.802-0.971) than in TBI with multiple trauma (AUC 0.693-0.783). Thus, though S 100 B may be a reliable marker of brain damage in TBI without multiple trauma 24 h after trauma and thereafter, it appears to be less reliable in TBI with multiple trauma.

Release of S100B differs during ischemia and reperfusion of the liver, the gut, and the kidney in rats.

S100B, an acknowledged marker of brain damage, is increased post-traumatically in plasma. The aim of this study was to investigate the diagnostic value of S100B release in experimental local extracranial ischemia and reperfusion. Anesthetized rats underwent laparotomy and ligation of the afferent blood vessels to the liver, gut, or kidney to achieve local ischemia in each organ separately. After 60 min of ischemia, ligatures were removed and resuscitation was performed for 3 h. S100B was determined in plasma by immunoluminometric assay 55, 65, and 240 min after the onset of ischemia (5 min before reperfusion and 5 min and 3 h after the onset of reperfusion). During ischemia of the liver, S100B increased before ligature removal and reperfusion, reaching significance early after the onset of reperfusion and remaining almost unchanged throughout reperfusion. In contrast, S100B did not increase during ischemia of the gut or kidney before ligature removal or during early reperfusion but increased significantly to similar levels as during reperfusion of the liver 240 min after the onset of ischemia (after 3 h of reperfusion). Our findings show for the first time that S100B increases during local extracranial ischemia and reperfusion. These experimental findings support the concept that brain damage is not necessarily the cause of increased S100B. Although S100B has been an acknowledged marker of brain damage for years, our experimental clinically relevant data indicate that S100B is, in fact, not specific as a marker of brain damage in the setting of local ischemia and reperfusion of the liver, gut, and kidney because local ischemia and reperfusion of these organs cause an S100B increase per se.

GFAP versus S100B in serum after traumatic brain injury: relationship to brain damage and outcome.

Research indicates that glial fibrillary acidic protein (GFAP), part of the astroglial skeleton, could be a marker of traumatic brain injury (TBI). S100B, an astroglial protein, is an acknowledged marker of TBI. Our goal was to analyze the relationship of GFAP/S100B to brain damage and outcome, and to compare the accuracy of GFAP/S100B for prediction of mortality after TBI. Our prospective study included 92 patients admitted <12 h after TBI (median injury severity score 25, median Glasgow Coma Scale 6). TBI was verfied by computerized tomography. GFAP/S100B were measured immunoluminometrically at admission and daily in the intensive care unit (average 10 days, range 1-21 days). We compared GFAP/S100B in non-survivors versus survivors, accuracy for mortality prediction according to receiver operated characteristic curve analysis, correlation between GFAP and S100B, relationship of GFAP/S100B to computerized tomography, cerebral perfusion pressure (CPP), mean arterial pressure (MAP) and 3-month Glasgow Outcome Score (GOS). GFAP (p < 0.005) and S100B (p < 0.0005) were higher in non-survivors than survivors. Both GFAP and S100B were accurate for mortality prediction (area under curve 0.84 versus 0.78 at <12 h after TBI). GFAP and S100B release correlated better later than 36 h after TBI (r = 0.75) than earlier (r = 0.58). GFAP was lower in focal lesions of <25 mL than in shifts of >0.5 cm (p < 0.0005) and non-evacuated mass lesions of >25 mL (p < 0.005). S100B was lower in focal lesions of <25 mL than in non-evacuated mass lesions (p < 0.0005) and lower in swelling than in shifts of >0.5 cm (p < 0.005). GFAP and S100B were lower in ICP < 25 than ICP > or = 25 (p < 0.0005), in CPP > or = 60 than CPP < 60 (p < 0.0005), in MAP > 70 than MAP < or = 70 mm Hg, and in GOS 4-5 than GOS 1 (p < 0.0005). Both measurement of GFAP and S100B is a useful non-invasive means of identifying brain damage with some differences based on the pattern of TBI and accompanying multiple trauma and/or shock.

Bystander trauma care--effect of the level of training.

BACKGROUND: The bystander is often the first person present at the scene of an accident. Our aim was to determine how often and how well bystanders perform trauma care and whether trauma care is affected by the bystander's level of training, relationship to the patient and numbers of bystanders present. PATIENTS AND METHODS: In a prospective 1-year study, the emergency medical service in two European cities collected data on trauma calls. Questionnaires were used to document the bystanders' level of training (none, basic, advanced, professional), the bystander's relationship to the patient, and the number of bystanders present, and to assess whether five separate measures of trauma care (ensuring scene safety, extrication of the patient, positioning, control of haemorrhage, prevention of hypothermia) were performed correctly, incorrectly, or not at all. RESULTS: Two thousand nine hundred and thirty-two trauma calls were documented and bystanders were present in 1720 (58.7%). All measures except ensuring scene safety and prevention of hypothermia were affected by the bystander's level of training. Correct extrication, positioning, and control of haemorrhage increased with the level of bystander training while the number of patients who were not attended decreased (P < 0.05, P < 0.005, P < 0.005), respectively. The relationship to the patient did not affect whether, or how well, any measure was performed. The number of bystanders present only affected prevention of hypothermia, which was performed most often when only one bystander was present. CONCLUSION: Improved, more widespread training could increase the frequency and quality of bystander trauma care further.

[First aid measures by bystanders at the place of accident. A prospective, epidemiologic study in the Vienna area]. / Massnahmen durch Ersthelfer am Unfallort. Eine prospektive, epidemiologische Studie im Raum Wien.

The object of this prospective, epidemiological study was to determine whether bystanders provided necessary first aid measures in the prehospital trauma setting, whether they performed these measures correctly, and whether the level of first aid training affected the quality of first aid measures performed. Data were collected by means of a questionnaire, which was filled out between March and July 2000 for all cases attended to by the Vienna Ambulance Service. A total of 2812 cases were documented. The most frequent causes of trauma were falls from heights less than 1 meter (50%) and traffic accidents (17%). The most frequent injuries were injuries to the extremities (59%) and head and traumatic brain injuries (42%). Most patients were "moderately" or "severely" injured (69% and 29%, respectively), but life-threatening injuries were rare (2%). Bystanders were present in 57% of the cases. The most frequently required first aid measures were "application of a dressing" and "positioning" of the patient. "Control of haemorrhage", "ensuring accident site safety" and "extrication" of the patient were less frequently required. "Clearing of the airway", "precautions against hypothermia" and cardio-pulmonary resuscitation were very rarely required. Bystanders were most frequently policemen, relatives or friends of the patient, and strangers. The vast majority of bystanders had no training in first aid or had only attended the first aid course required to attain a driving license. We found a clear relationship between the level of first aid training and the quality of first aid measures provided. It would be advisable to offer an increased amount of refresher courses in first aid to improve bystander trauma care.

Accelerated tryptophan degradation predicts poor survival in trauma and sepsis patients.

Immune system activation and inflammation accompanies immune dysfunction in trauma and sepsis patients. Immunodeficiency may develop in such patients as one consequence of an activated chronic pro-inflammatory response. According to recent data, degradation of L-tryptophan (TRP) via the kynurenine (KYN) pathway by the cytokine-inducible enzyme indoleamine 2,3-dioxygenase (IDO) could represent an important contributor to the deficient responsiveness of immunocompetent cells. Compared to healthy controls, patients post trauma or with sepsis had increasing KYN concentrations and KYN to TRP ratios (KYN/TRP) whereas TRP concentrations decreased. Likewise, concentrations of cytokines tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) and of immune activation marker neopterin increased in patients (all p < 0.001). Furthermore in patients KYN/TRP, KYN and neopterin concentrations were further increasing (all p < 0.001), whereas the changes of TRP, TNF-α and IL-6 concentrations were not significant. Compared to the survivors, the non-survivors had a higher concentration of KYN, neopterin, TNF-α and IL-6 as well as a higher KYN/TRP ratio. KYN/TRP correlated with neopterin (p < 0.001) and also with TNF-α (p < 0.01) and IL-6 concentrations (p < 0.05) and inversely with the in vitro response of stimulated monocytes. We conclude that increased TRP degradation in patients post trauma is closely associated with immune activation. Cytokines released during the pro-inflammatory response may induce the activity of IDO and thus accelerate TRP degradation. Thus, increased IDO activity most likely represents a result of host response to pro-inflammation in patients. Data support a possible role of inflammation-induced IDO in the diminished immunoresponsiveness in patients.

Assessment of bone union/nonunion in an experimental model using microcomputed technology.

BACKGROUND: High-resolution microcomputed tomography (microCT) is one of the most recent technical developments to visualize and quantify primarily cancellous bone. Regarding bone formation, microCT is becoming increasingly important, although its reliability has not yet been evaluated. Our study had two goals: to develop a reproducible nonunion model and to determine the efficacy of microCT for the assessment of bone healing in this model. METHODS: The designed fracture model in the rat simulates secondary fracture healing. After plate fixation to the femur, diaphysis transverse middiaphyseal osteotomy was performed with a reciprocating saw, resulting in a 0.38-mm gap with a defect of bone and periosteum corresponding to the thickness of the blade. Proximally and distally to this gap, the periosteum was preserved. Thus, three separate zones were defined: proximal femur diaphysis with periosteum, gap, and distal femur diaphysis with periosteum. In the nonunion group (NM group), a model of impaired bone healing (nonunion), silicone foil was wrapped around the femur diaphysis to block any influence from surrounding tissue. Coverage of the bone repair site by thigh muscles was designed for a model of bone union (M group). Four weeks postoperatively, callus formation was determined by conventional anterior-posterior and lateral plain radiographs. Ten weeks later, a second x-ray series was done as the clinical standard evaluation method. Afterward, specimens were harvested for microCT examination (two-dimensional and three-dimensional [3D]). Biomechanical testing was carried out to determine fracture healing. RESULTS: Our model is highly reproducible and results in bone nonunion in five out of six cases (83.3%). In determining fracture site, plain radiographs the least reliable method in comparison to the biomechanical testing which is the most accurate reference method. In contrast, microCT (the 3D reconstruction) showed significant correlation (r = 1) to the results assessed by biomechanical testing, whereas microCT was correct in 100%. We found bone healing in five out of six animals in the M group verified by microCT (in accordance to biomechanical data). In the M group, significantly enhanced bone formation (50%) (p = 0.008) was observed within the osteotomy site (i.e. within the gap), but there was no difference in periosteal bone formation between the groups proximally and distally to the gap. Interestingly, we did not find statistically significant differences in mineralization. CONCLUSION: We conclude that microCT with 3D reconstruction is the optimal method diagnostic tool in fracture healing, especially in nonunion. Furthermore, direct coverage of the fracture site by muscle flaps results in a mineralized enhanced bone formation within the osteotomy site (i.e. within the gap). Skeletal muscle coverage hypothetically might have osteogenic augmentation potential, thus being able to prevent pseudoarthrosis.

Why patients choose regional anesthesia for orthopedic and trauma surgery.

BACKGROUND: While both surgeons' and anesthesiologists' preference of regional over general anesthesia is increasing, the patients' preference remains limited. Little is known about why patients choose regional anesthesia. The aim of our study was to answer this question with regard to orthopedic and trauma surgery. METHODS: The study was carried out prospectively from 1999 to 2001 and included 238 patients scheduled for arthroscopy of the lower limb or other orthopedic or trauma surgery. All patients were informed about regional and general anesthesia in a pre-anesthesia interview and subsequently chose the method they preferred. RESULTS: Curiosity was the main reason why patients chose regional anesthesia for arthroscopy ( n=155, p<0.0001). For all other types of orthopedic or trauma surgery ( n=83), patients chose regional anesthesia to avoid postoperative pain ( p<0.01) and/or the side-effects of general anesthesia ( p<0.0001). Younger ( n=128) and low-risk ( n=184) patients chose regional anesthesia because they were curious ( p<0.01 and p<0.001, respectively), while older ( n=110) and unhealthier patients ( n=56) did so for safety ( p<0.01 and p<0.001, respectively). CONCLUSIONS: Patients choose different types of regional anesthesia for different reasons. While spinal anesthesia and femoral and sciatic block were chosen for curiosity reasons, brachial plexus block was chosen to avoid the side effects of general anesthesia. The patients' choice of regional anesthesia for orthopedic and trauma surgery is significantly influenced by the type of surgery, age, and health.

Acute acalculous cholecystitis after trauma: a prospective study.

OBJECTIVE: The purpose of this study was to identify risk factors for the development of acute acalculous cholecystitis (AAC) and useful criteria to facilitate the decision to perform cholecystectomy. METHODS: This was a prospective study of patients with an Injury Severity Score (ISS) > or = 12 requiring intensive care for > 4 days (n = 255), divided into three groups by ultrasound: AAC (n = 27), hydropic gallbladder (n = 37), and normal gallbladder (n = 191). Multivariate analysis was conducted for trauma scores and laboratory and intensive care unit (ICU) data and complemented by logistic regression analysis. RESULTS: Three factors sufficiently define the risk for AAC: ISS, heart rate, and units of packed red blood cells required at ICU admission. All patients who underwent cholecystectomy (n = 21) had both highly pathologic ultrasound and major clinical symptoms, and all had histologically verified AAC. There was no significant difference in daily laboratory data between patients with and without AAC. CONCLUSION: Patients with a high ISS who are tachycardic and have required several units of packed red blood cells at ICU admission should be monitored early by ultrasound. When ultrasound is highly pathologic together with major clinical symptoms, cholecystectomy should be performed. Daily laboratory data are of no additional value regarding the decision to perform cholecystectomy.

Bilateral lower leg replantation versus prosthetic replacement: long-term outcome of amputation after an occupational railroad accident.

BACKGROUND: This retrospective study investigated three very similar cases of bilateral lower leg amputation. The aim was to determine which of two therapeutical procedures is associated with better long-term outcome: replantation or primary treatment of the stumps and subsequent prosthetic replacement. METHODS: Evaluation included clinical examination, gait analysis, and a workup of the psychosocial background. Health problems were documented using the Nottingham Health Profile. Follow-up assessments were performed 6, 7, and 18 years after the trauma. RESULTS: One patient underwent successful bilateral lower leg replantation and continued to work for the same employer. Two patients underwent prosthetic replacement. One became a social outcast confined to a wheelchair. The other patient had a good psychosocial background, similar to that of the patient who underwent replantation. He showed a better gait analysis on even ground than the replantation patient, but the findings were vice versa for uneven ground. CONCLUSIONS: The decision between replantation and prosthetic replacement after bilateral lower leg amputation is case related and cannot be generalized. Patients who have undergone these procedures require long-term psychological and physiotherapeutic care to achieve a good long-term surgical outcome.