Significance of lung contusion in mortality following polytrauma. Possibilities for therapeutic influence

Multiple trauma is often associated with blunt thoracic injuries. Especially lung contusion can result in respiratory insufficiency and therefore a higher mortality rate. In our prospective study comparing 8 multiple trauma patients with and without associated lung contusion, we found that respiratory function was already significantly disturbed (decrease of paO2/FiO2 and increase of AaDO2, a rise in extravascular lung water (EVLW) both early after trauma and also with a second peak following the 4th day. This group (LK) developed significantly more cases of respiratory distress (ARDS). The disturbance of respiratory function seen initially was interpreted as a consequence of the direct mechanical impact, leading to the formation of interstitial fluid and hematoma. The frequent development of ARDS in the LK-group probably results from a pronounced activation of cellular and humoral mechanisms and therefore an enforced injury of the pulmonary capillary bed. A significant increase of pulmonary infections or the development of sepsis was not seen in the LK-group and is probably not responsible for the higher ARDS-rate in this group.     

Regulation of guinea pig ileal electrolyte transport by M3-muscarinic acetylcholine receptors in vitro

To determine the muscarinic receptor subtype mediating guinea pig ileal mucosal electrolyte secretion, we compared the potencies (Kb) of selective M1 (pirenzepine) (PZ), M2 (AF-DX 116, methoctramine), and M3 [4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP), hexahydrosiladifenidol (HHSiD)] antagonists as inhibitors of carbachol-induced reductions in guinea pig atrial heart rate and ileal longitudinal muscle contractions, responses mediated by M2 and M3 receptors, respectively. Pretreatment with all five muscarinic antagonists shifted the carbachol concentration-response curve to the right, in a manner suggesting competitive antagonism. The following affinity profiles (Kb, nM) were obtained for: 1) ileal mucosa: 4-DAMP (2.7) greater than HHSiD (23.0) greater than PZ (110) greater than or equal to methoctramine (395) greater than AF-DX 116 (784); 2) atrial heart rate: 4-DAMP (9.5) congruent to methoctramine (11) greater than AF-DX 116 (63) greater than HHSiD (222) greater than PZ (256); and 3) ileal longitudinal muscle: 4-DAMP (3.1) greater than HHSiD (21) greater than PZ (143) greater than methoctramine (388) greater than or equal to AF-DX 116 (482). The selectivity profiles of these antagonists suggest that muscarinic receptors in the ileal mucosa more closely resemble those in the ileal muscle (M3) than those in atrial muscle (M2). Moreover, M1-muscarinic receptors appear to be relatively unimportant in mediating the effects of carbachol on short circuit current (ISC). Carbachol-induced increases in ISC were also unaffected by pretreatment with 0.5 microM tetrodotoxin, suggesting that electrolyte transport in the guinea pig ileal mucosa may be mediated, in part, by postsynaptic M3-muscarinic receptors on the enterocytes.     

Intensivmedizin aus Sicht des Unfallchirurgen

Severe injuries in patients of all ages and injuries in elderly multi-morbid subjects are a relevant medical and economic challenge. Optimal care of the polytraumatized patient can be best delivered by physicians specializing both in causal treatment of the injury or underlying disease and in intensive care. For care of critically ill injured patients, trauma surgeons with a certified specialty in intensive care medicine appear best suited. Of course, directing a surgical or trauma intensive care unit has to be full-time. Specialization of trauma surgeons (e.g., in the USA) has resulted in a considerable improvement in outcomes at least partly related to specialized trauma intensive care. Further improvement of trauma care relies on competent and innovative research not only in the fields of general intensive care, e.g., ventilation, but particularly in the complex aspects of the causality of the traumatic disease. An integrative view of the pathobiochemical, pathophysiological, and immunopathological sequelae of severe trauma under consideration of the various surgical and therapeutic strategies is the actual focus of research in surgical critical care medicine. Organ dysfunctions have to be modulated as they develop. Surgeons and trauma surgeons lead worldwide in this field of research. Obviously, competent research in polytrauma care requires competence in polytrauma intensive care.     

The AIDS problem in accident surgery

In trauma surgery there is a particularly high proportion of patients in the age group most at risk of infection with AIDS. The result of an epidemiological study in our patients (HIV screening of all patients scheduled for surgery at a trauma center over 18 months) showed a prevalence of 0.1%. Specific therapeutic strategies must be developed to deal with the weakened immunity of HIV-infected patients. Fracture treatment in HIV-infected hemophiliacs is a special problem. Homogenous bone transplantation is described with reference to HIV. The particular danger of injury in trauma surgery is also investigated. The chain of infection is illustrated and used to demonstrate the precautions that can be taken against nosocomial HIV infections. Following infection with fluids containing HIV, specific measures must be taken. The legal aspects of HIV-antibody testing in the Federal Republic of Germany are elucidated. Finally, the problems of general preoperative HIV-antibody testing are discussed.     

PLASMA PHOSPHOLIPASE A2 ACTIVITY IN CLINICAL ACUTE MYOCARDIAL INFARCTION

1. Phospholipase A2 (PLA2) cleaves phospholipids to produce a lyso-phospholipid and free fatty acid and, in view of the biological activity of the products, PLA2 may play a role in many disease states. Lyso-phospholipids and free arachidonic acid increase in ischaemic myocardium, indicating that ischaemia activates the enzyme. 2. Plasma PLA2 activity was measured in patients with acute myocardial infarction, based on the release of labelled arachidonic acid from Escherichia coli cell membrane. Fourteen males (peak serum creatine phosphokinase (CK) above twice upper normal) were studied on day 1 (within 6 h of chest pain onset), days 2-4, and days 6-9. Normal age matched males (n = 13) were also studied. 3. Plasma PLA2 in patients with uncomplicated myocardial infarction (n = 12) was, initially, 1.14 +/- 0.10 (s.e.m.) nmol/min per mL plasma, similar to that in the normal group (1.52 +/- 0.14). On days 2-4, PLA2 activity increased to 1.94 +/- 0.18 (P less than 0.001) and this activity was correlated with the earlier peak CK level (P less than 0.02). On days 6-9, PLA2 activity was 1.49 +/- 0.13 while in two patients who developed complications and underwent open-heart surgery between the last two measurements, there were further increases to 4.22 and 4.04 nmol/min per mL. 4. The increase in plasma PLA2 in uncomplicated myocardial infarction is likely to be due to release from the damaged myocardium; whether it contributes to pathophysiology is uncertain.