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Background: Hypothermia, defined as a body core temperature below 35 °C, could be divided into an endogeneous, therapeutic and accidental hypothermia. At admission in the emergency room multiple trauma patients show a hypothermic core temperature in up to 66 %. A core temperature below 34 °C seems to be critical in these patients as this temperature limit has been demonstrated to be associated with an increased risk for post-traumatic complications and a decreased survival. In polytraumatised patients with a core temperature below 32 °C a mortality rate of 100 % has been described., Material and Methods: The main pathophysiological effects of hypothermia concern the haemo-dynamic, coagulatory and immune systems. Mild hypothermia (35-32 °C) leads to a vasoconstriction, tachycardia and increased cardiac output. After an increasing arrhythmia and bradycardia severe hypothermia (< 32 °C) finally results in a cardiac arrest. Hypothermia-induced coagulopathy comprises a dysfunction of the cellular and plasmatic coagulation with an increased blood loss. Due to the attenuation of the post-traumatic, pro-inflammatory immune response and enhancement of anti-inflammatory reactions, hypothermia counteracts an overwhelming systemic inflammation, concomitantly resulting in an increased susceptibility for infectious complications., Results: Because of the negative effects of the -accidental hypothermia, effective rewarming is essential for adequate bleeding control and successful resuscitation. As aggressive rewarming (> 0.5 °C / h) has been reported to be associated with an increased mortality during the further course, this procedure should only be applied in hypothermic multiple trauma patients with haemorrhagic shock., Conclusion: Accidental hypothermia represents a serious problem in multiple trauma patients due to its frequency and negative pathophysiological effects. Therefore, early and effective re-warm-ing is essential in the treatment of hypothermic trauma patients. Possible protective effects of a therapeutic hypothermia in the treatment of trauma patients after initial resuscitation and operative bleeding control have to be clarified in further experimental and clinical studies., (© Georg Thieme Verlag KG Stuttgart ˙ New York.)

Unlabelled: It was the objective of this investigation to describe the results after stabilisation of pelvic fractures with the pelvic clamp in polytraumatized patients with unstable pelvic ring fractures., Patients: Between 1999 and 2001 11 polytraumatized patients with an average age of 38 years with unstable fractures of the pelvic ring were treated with the "pelvic clamp" (PC)., Method: The patient's data were analysed retrospectively from the moment they were admitted to our department until 48 hours after the treatment with the pelvic clamp. The following data were observed: -- The time period until the pelvic clamp was placed. -- The mean blood pressure. -- The oxygenation level (PaO (2)/FiO (2) coefficient). -- The number of requested blood units. -- The time period until hemodynamic stabilisation took place., Results: 8 patients survived their injuries. 5 of them were admitted primarily to our department (ISS 39.8, PTS 35), the other 3 were secondarily admitted to our department (ISS 48.3, PTS 39). 3 of 11 patients (27 %) died averaged within the first 45 minutes after admittance. They also were treated in other units before admittance to our department. 8 surviving patients showed -- a hemodynamic stabilisation 6 hours after the treatment with the PC. -- an increase of the mean blood pressure about 25 % 20 minutes after the treatment with the PC. -- a stabilisation of the oxygenation level 6 hours after the treatment with the PC. -- a decrease of the number of requested blood units 6 hours after treatment with the PC., Conclusion: Even if the number of patients who were treated is small, the study shows a positive trend in terms of stabilisation of the vital parameters after stabilisation of the pelvic fracture with the pelvic clamp.

Background: In trauma patients hypothermia is a frequent event. According to the literature the majority of trauma patients are presenting a core temperature of less than 34 degrees C at admission. In contrast to the benefit of hypothermia in elective surgery, clinical experience with hypothermia in trauma patients has identified hypothermia to be one major cause of severe posttraumatic complications. It was hypothetized that this diverse effect of hypothermia is related to depletion of high energy phosphates like adenosine-tri-phosphate (ATP) in trauma patients. To verify this hypothesis the relation of ATP plasma levels and hypothermia was examined in a clinical study., Methods: Three different groups of patients were under study. The first group (group A, normothermic control group) included patients (n = 15) undergoing elective surgery of the lower limb with a mean operation time of 113 minutes. The second study group, hypothermic control (group B), comprised patients (n = 15) that were subjected to elective coronary artery bypass operation under hypothermia (31 degrees C for 48 minutes, mean total operation time being 205 minutes). The third study group (group C) included trauma patients (n = 23, mean ISS of 24.7). At the time of admission 10 patients presented a core temperature > or = 34 degrees C (group C1, mean ISS 25.2, mean TA 34.5 degrees C), 13 patients presented a TA < 34 degrees C (group C2, mean ISS 26.0, mean TA 32.9 degrees C). In both groups of surgical patients the ATP plasma level was measured preoperatively, at 2 hr, 4 hr and 24 hr postoperatively. In trauma patients this measurement was performed at admission and 24 hours later. Within the same schedule body core temperature was recorded and the clinical course was documented as well., Results: Elective limb surgery in normothermic patients resulted only in a transient decrease in ATP plasma levels (preoperative: 87.8 mumol/dl, 4 hr postoperative: 52.0 mumol/dl). At 24 hours the ATP plasma level (62.6 +/- 10.0 mumol/dl) has increased towards baseline level. Elective hypothermia in patients subjected to coronary bypass also resulted only in a transient decrease in ATP plasma levels. During the operation period, including hypothermia, the ATP plasma level was comparable (50.4 mumol/dl) to group A and also returned back towards normal values at 24 hours (58.2 mumol/dl). All trauma patients revealed a significant low ATP plasma level at admission as compared to both control groups. Looking at subdivided groups the most significant drop in ATP plasma level (28.5 mumol/dl) was noted in patients presenting an initial core temperature < 34 degrees C and ISS > 30. Even 24 hours later the ATP level of this subgroup was significantly diminished despite a rise up to 44.4 mumol/dl. In contrast an only moderate drop in ATP plasma concentration (59.2 mmol/dl) was noted in the group of TA > or = 34 degrees C and ISS < 20. This group revealed almost normal values (68.3 mmol/dl) 24 hours after trauma. Beside hypothermia the metabolic state, reflected by the plasma lactate levels, significantly influenced the ATP plasma levels, as high lactate levels were paralleled by low ATP levels. Also the over all outcome was related to injury severity and hypothermia., Conclusion: Hypothermia in elective surgery, established by active cooling, preserves the ATP storage and maintains an aerobic metabolism, which both contribute to the beneficial effect of hypothermia in ischemia/reperfusion in cardiovascular surgery. However, in trauma patients hypothermia is caused by insufficient heat production due to utilization of ATP under anaerobic metabolic conditions. Low ATP plasma levels combined with hypothermia seem to be a predisposition for posttraumatic complications like organ failure.

Multiple organ failure is with an incidence of 10-25% and a mortality of 50-70% the most severe complication after severe trauma. Intestinal ischemia and a corresponding impaired gut barrier function is thought to have a high impact on the development of multiple organ failure after severe trauma. Under normal conditions the intestinal wall is a sufficient barrier against bacteria and their products. Gut ischemia is followed by mucosal lesions, the intestinal permeability is increased. Translocating bacteria and bacterial products (endotoxin, peptidoglykan) can lead to a local and/or systemic immun-inflammatory response, which is made responsible for the development of multiple organ failure. Tonometry as a possibility of monitoring intestinal ischemia as well as a tool to estimate the prognosis of multiple trauma patients is still discussed controversially. Dopexamin, which directly influences intestinal ischemia (goal directed therapy) might be a successful treatment option, however until now no clinical study about beneficial effects of dopexamine in severely injured patients is available. Selective gut decontamination showed no clinical benefits in multiple trauma patients. Early enteral nutrition especially with immunomodulating ingredients ("immunonutrition") decreases posttraumatic complications as well as the incidence of MOF. However a reduction of mortality could not be described in severely injured patients so far.

Sequential organ failure after multiple trauma emerges from a whole-body inflammatory process which develops as a complex host defense response to hypovolemic shock/resuscitation and traumatic tissue injury. Successful prevention and treatment involves exact assessment of inflicted damage and profound knowledge of the different stages of posttraumatic immune alterations. Local release of potent inflammatory mediators (cytokines, complement, arachidonic acid derivatives, reactive oxygen metabolites) primarily induces a repair process. However, massive soft tissue and bone injury, follow-up surgery, infections and blood transfusions trigger a systemic spill over of these mediators orchestrating a generalized inflammatory response (Systemic Inflammatory Response Syndrome, SIRS). Diffuse capillary leakage and microcirculatory disorder prepare cellular dysfunction. Secondary severe immune defects support septic complications which maintain an autodestructive process. Therapeutical advances depend on the analysis of local and time-dependent expression of relevant inflammatory mediators and cellular signalling systems.

Adequate prehospital care of the severely traumatised patient is important to prevent or attenuate early as well as late life threatening complications, such as tissue hypoxia, ischemia/reperfusion injury and finally multiple organ failure. A mismatch of oxygen supply and oxygen demand is a hallmark in the pathophysiology of multiple trauma. Oxygen supply may be diminished by the following factors: shock-related decrease of cardiac output, anemia and hypoxia. On the other hand, oxygen demand may be increased by pain, panic, and agitation. Hence, it is a central point in prehospital care to reduce this supply-demand imbalance by identification and prompt reversal of the underlying causes. Most often, shock is caused by hypovolaemia and tissue injury ("traumatic-hemorrhagic shock"). However, shock may also be a result of central nervous system injury (neurogenic shock as a special form of distributive shock) or circulatory obstruction, e.g tension pneumothorax or cardiac tamponade (obstructive shock). Volume resuscitation by means of crystalloid or colloid solutions is an essential part in the therapy of the traumatic-haemorrhagic shock. In addition, catecholamines may be necessary in order to achieve an adequate arterial pressure. However, if bleeding cannot be controlled in the prehospital setting, only moderate volume support and permissive hypotension as well as rapid transportation into the next hospital may be preferable. This may be the case in penetrating thoracic or abdominal injuries as well as in traumatic amputations of the proximal limb. On the contrary, in patients with severe head injury, hypotension must be avoided by all means. Obstructive shock has to be treated urgently by insertion of a chest drain or drainage of the pericardium, respectively. Under all circumstances, it is an essential part of prehospital therapy to provide sufficient analgesia as soon as possible. Prehospital anesthesia, combined with artificial ventilation may be necessary for optimal patient management. Furthermore, ventilatory support is indicated when respiratory failure, loss of consciousness, or severe shock are present. Additional oxygen should be given whenever possible, even in the absence of an overt hypoxic state. Important additional measures are cervical spine immobilisation and reposition as well as splinting of long bone fractures or luxations, in order to avoid secondary injury of the spinal cord or ongoing tissue and vascular damage.

Multiple trauma often leads to systemic inflammatory reaction and multiple organ dysfunction. Modulation of this response may be promising. Several pharmacologic approaches, such as antioxidants (e.g. superoxidedismutase), calcium channel blockers (e.g. diltiazem), cytokines (e.g. interferone gamma), and modulators of intracellular signal transduction pathways (e.g. pentoxiphylline) have been shown to improve outcome in experimental models and/or in clinical pilot studies. However, up to now no definitive evidence has been provided in prospective, randomized, and blinded "intention to treat" trials that these agents are able to reduce mortality and morbidity of the traumatized patient. Hence, supportive care of failing organs, treatment of hypoxemia and maintenance of an appropriate systemic blood pressure remain the mainstay of critical care therapy. Widely accepted therapeutic measures are (i) immediate treatment of hypoxia by administration of oxygen and ventilatory support, if needed, to maintain an oxygen tension of 60 mmHg or higher (ii) maintenance of adequate oxygen content by transfusion of red packed cells in order to restore a hematocrit of 23-30% (iii) treatment of hypovolemia by infusion of crystalloids, colloids and blood products (iv) normoventilation and restoration of a normal or elevated blood pressure in patients with severe head injury (v) immobilisation and early administration of methylprednisolone in patients with spinal cord injury (vi) analgesia by administration of opioids, non-steroidal antiinflammatory drugs, or ketamine (vii) sedation with benzodiazepines, gamma-hydroxbutyrate or propofol (viii) early enteral nutrition (ix); antibiotic therapy of infections (x) pressure controlled ventilation in patients with acute lung injury (xi) continuous veno-venous hemofiltration in patients developing acute renal failure and (xii) early surgical interventions to control bleeding and/or to evacuate intracerebral hematomas.

The emergency room functions as a junction between preclinical and early clinical treatment of patients with multiple trauma and should have defined technical and room possibilities. The personal staff should continue resuscitation measures and perform clinical and technical diagnostic procedures according to trained algorithms. The recognition of life-threatening injuries, the set up of correct priorities and application of respective surgical procedures characterize a good emergency room management.

Despite a high standard of preclinical, clinical and rehabilitative trauma care, the number and degree of injuries will remain a social and medical challenge. Improvements of trauma care in the future may be possible in respect to social, economic, organisational, clinical and research issues. Prevention of trauma will be of major impact and improvements may be possible by preventive legislation and technical developments. Organisation of trauma care should integrate high level trauma centres early-on including a national, regional and local quality control system. The future preclinical and clinical individual care of multiple trauma patients should consider the complex pathophysiological mechanisms at all levels, while the understanding of these mechanisms is increasing continuously.

Operative procedures in multiple injured patients consist in the first stage in life-saving operations such as control of bleeding and cerebral decompression. Operative measures during the urgent second operative phase have to be undertaken under consideration of the development of a multiple organ failure syndrome. Early stabilization of relevant extremity fractures and thorough care of soft-tissue are of particular importance (day-1-surgery). Only second look procedures to optimize soft-tissue injuries and prevent infections may be allowed during this early intensive care period. Delayed operative procedures should only be performed after stabilization of the overall patient situation to prevent enhancement of the systemic inflammatory response. The required operative procedures of the multiple injuries have to be attributed to the respective operative phases.

The multiple organ dysfunction syndrome (MODS) with a mortality of 50% to 70% represents the number 1 cause of death in surgical intensive care units. It is divided in a primary and a secondary MODS based on time of manifestation and pathophysiological events which attribute to it. The therapy of the primary MODS includes sufficient and quick resuscitation, adequate oxygen delivery and early enteral nutrition to reduce or avoid the incidence of bacterial translocation. In addition, a reduction of the antigenic load by control of hemorrhage, radical wound debridement, decompression, and fixation of long bone fractures appears to be effective in reducing the occurrence of MODS. The treatment of the secondary MODS remains supportive and its prevention is essential. Further studies have to be carried out to evaluate the clinical significance of new therapeutical agents such as monoclonal antibodies or cytokine receptor antagonists.

The i.v. bolus infusion of 4 ml/kg b.w. of hypertonic (7.2-7.5%) saline solution represents a new concept for primary resuscitation from traumatic-hemorrhagic shock; it is called "small-volume resuscitation". Experimental studies have demonstrated that for the case of a 50% blood loss the infusion of 7.2-7.5% NaCl in a dose equivalent to 1/10 of the blood loss effectively restores cardiac filling pressures and cardiac output and significantly increases systemic pressure. Simultaneous application of a colloid (6-10% Dextran 60/70; 6-10% HAES 200,000/0.5) prolongs the circulatory effect of the hypertonic solution. Moreover, "small-volume resuscitation" by means of 7.2 NaCl/10% Dextran 60 was shown to completely restore nutritional organ blood flow already within only 5 minutes. The superiority of "small-volume resuscitation" using hypertonic-hyperoncotic solution as compared to conventional volume therapy consists of its effects on the microcirculation. Recent clinical trials have revealed the efficacy, practicability and safety of this new therapeutic concept for primary resuscitation from trauma and shock.

Disruption of the ulnar styloid process is a frequent injury in concomitance with fractures of the distal end of the radius. Healing occurs in many cases in the form of pseudoarthritis. Evaluation of 222 cases of distal radius fracture showed involvement of the ulnar styloid process to have no impact upon long-term wrist function.