[Pathophysiology of multiple trauma (author's transl)].
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During an 11 year period, 10 cases of delayed traumatic intracranial haematomas, following the correction of shock, were discovered. The intracranial haematomas were not present on initial computerized tomography (CT) scans after stabilization of the vital signs. Skull fractures were found in six patients; five of them had epidural haematomas at the site of their skull fracture. Four patients developed intracranial haematomas during general anaesthesia for extracranial surgery. All the delayed intracranial haemorrhages (seven epidural haematomas and three delayed intracranial haematomas) occurred within 12 hours after initial resuscitation. Seven out of eight patients made a good recovery after surgical removal of their intracranial haematoma. The initial hypotension may have acted as a protective mechanism, obscuring the intracranial haemorrhage. Awareness of this possibility, and a high degree of suspicion in those patients who deteriorate following correction of their shock, is important. We suggest that, even with a negative initial CT scan the duration of extracranial surgery in the acute period should be as short as possible in patients with suspected head injury. If these patients fail to wake up as expected following anaesthesia or new neurologic deficits develop, an urgent follow up CT scan should be performed.
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Blood coagulation problems, either disseminated intravascular coagulation (DIC) or adult respiratory distress syndrome (ARDS) are frequent complications during the recovery of the polytraumatized surgical patient or accident victims. The key to their successful control lies in prompt recognition and aggressive treatment of the disease as soon as it appears. Unfortunately their onset is not usually well defined clinically and success in handling usually depends upon clinical expertise in recognising "high risk" situations coupled with measurements in the haematological laboratory of changes in plasma coagulation factors. It is suggested in this communication that a relatively simple examination of plasma complement profiles in the high risk, intensive care patient, may not only provide early warning of the onset of a coagulopathy but also distinguish the type. Simple tests are described, based on the assessment of plasma complement C5 levels, which have a high predictive value for the onset of ARDS, a disease with few early clinical manifestations and notably lacking in early changes in haematological parameters. In prospective trials complement tests correctly identified 18 patients who later developed ARDS but were no more effective than haematological tests in the identification of 24 patients who subsequently developed DIC.
During the last 3 years we have performed a detailed study in 50 patients using the Swan-Ganz catheter to provide prognostic haemodynamic and metabolic values at an early stage. There was a total of 320 severe injuries in these 50 patients with a statistical mean of six to seven. The severity of injuries is documented by the volume replacement necessary within the first 24 hr. On average more than 8 litres of whole blood, albumin and dextran were given intravenously. Out of 50 patients, 28 survived. During the first 2h there was a significant difference between survivor and non-survivor in systolic blood pressure and shock index. From the very beginning the surviving patients demonstrated a higher cardiac index than non-survivors. Pulmonary artery pressure and total pulmonary resistance were also elevated from the very beginning. The right ventricular stroke work index was increased; the left ventricular stroke work index was decreased in the group of non-survivors. The arteriovenous oxygen content difference as well as oxygen extraction ratio was elevated, and the oxygen availability was decreased in the group of the non-surviving patients. Of the metabolic parameters, an increase in the lactate/pyruvate ratio as well as in serum glucose and a decrease in base excess values permit an early prediction of a favourable outcome. There were significant differences in the enzymes SGOT, SGPT, LDH, CHE, as well as bilirubin concentrations between survivors and non-survivors from sixth day on.
Management of inflicted or self-inflicted trauma to accomplish homicide or suicide is no novelty in the practice of medicine. However, it takes an astute clinician to recognize serious poisoning in the midst of life-threatening injuries. We describe two cases where homicide and suicide attempts were accompanied with the ingestion of methanol. Both patients recovered with proper management of the injuries as well as early recognition and treatment of the methanol poisoning.
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This study investigated the alterations in circulating proinflammatory cytokines and cytokine production by peripheral blood mononuclear cells (PBMCs) in response to lipopolysaccharide (LPS) or phytohemagglutinin (PHA) after severe trauma. Plasma and PBMCs were collected from 17 severely injured trauma patients and 10 healthy subjects. Plasma was stored at -80 degrees C and analyzed for cytokines. Isolated PBMCs from each subject were stimulated with LPS or PHA and incubated at 5% CO2 for 24 hours. Supernatants were collected and analyzed for cytokines. There was no significant change in the plasma concentration of free TNF-alpha and IL-1beta between healthy subjects and trauma patients. Plasma IL-6, total TNF-alpha, and total IL-1beta were significantly increased in severely traumatized patients compared with healthy control subjects. PBMCs from trauma patients produced higher levels of TNF-alpha in response to LPS but it showed no significant change in IL-1beta and IL-6 production in response to PHA or LPS in comparison to PBMCs from control subjects. We conclude that severe trauma results in a significant increase in plasma proinflammatory cytokine IL-6. Free TNF-alpha and IL-1beta in plasma remain at levels comparable to those in uninjured controls, while plasma free IL-6 levels in trauma patients remain high. Serious injury is associated with an enhanced production of TNF-alpha by PBMCs stimulated with LPS.
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