122 multiple trauma patients staying in the ICU for 5 or more days and needing mechanical ventilation were investigated to determine the effect of selective decontamination of the digestive tract on prevention of infection. The (retrospectively studied) control group of 59 patients received no antibiotic prophylaxis. The infection rate during ICU-stay was 81%. Most infections were caused by potentially pathogenic microorganisms (PPM) from the oral cavity or the intestines (i.e. endogenous infections). The oropharynx and the intestines were rapidly colonised with ICU-associated gram-negative bacilli. After 2 weeks more than 80% of patients were found colonised. This secondary colonisation of the digestive tract is a very important stage in the pathogenesis of infections. Sixty-three patients were selectively decontaminated with nonabsorbable antibiotics, administered through the gastric tube even if peristalsis was absent. Emphasis was laid on the selective decontamination of the oral cavity, using topical application of an antibiotic paste. With this technique the oral cavity was free of PPM within 3 days in most patients. No secondary colonisation was found. Rectal colonisation decreased significantly after 5 days. Secondary colonisation occurred in 9 patients with PPM sensitive to the antibiotics used. The prophylactic regimen included systemic cefotaxim, directed against early endogenous infection. The suppression and after some time the absence of the endogenous source of PPM resulted in a significant reduction of colonisation and infection. The total infection rate decreased to 16%.

In mechanically ventilated patients with septic shock, changes in bolus TDCO are reflected by calibrated MCO over a range of cardiac output values. A single calibration of the model appears sufficient to monitor continuous cardiac output over a 2-day period with a bias of -0.1 +/- 0.8 l/min.

Continuous infusion of 0.4-0.8 mg/h of neostigmine promotes defecation in ICU patients with a colonic ileus without important adverse reactions.

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Convincing evidence exists that bacterial translocation can occur in humans during various disease processes. However, it remains to be determined whether a causal relationship between bacterial translocation and MOF exists. MOF is probably multifactorial and not uniform in origin; when evaluating translocation as a causative factor in the absence of an infective focus, the type of initiating event and the period of time after which MOF develops should be taken into account. The origin of early MOF is probably a non-bacterial, extensive, inflammatory response resulting in massive generalized endothelial cell activation. Late MOF may be caused primarily by bacterial translocation inducing an imbalance between proinflammatory and anti-inflammatory cytokines.

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