[Volume replacement in intensive care medicine]. / Volumentherapie in der Intensivmedizin.

Volume substitution represents an essential component of intensive care medicine. The amount of fluid administered, the composition and the timing of volume replacement seem to affect the morbidity and mortality of critically ill patients. Although restrictive volume strategies bear the risk of tissue hypoperfusion and tissue hypoxia in hemodynamically unstable patients liberal strategies favour the development of avoidable hypervolemia with edema and resultant organ dysfunction. However, neither strategy has shown a consistent benefit. In order to account for the heavily varying oxygen demand of critically ill patients, a goal-directed, demand-adapted volume strategy is proposed. Using this strategy, volume replacement should be aligned to the need to restore tissue perfusion and the evidence of volume responsiveness. As the efficiency of volume resuscitation for correction of tissue hypoxia is time-dependent, preload optimization should be completed in the very first hours. Whether colloids or crystalloids are more suitable for this purpose is still controversially discussed. Nevertheless, a temporally limited use of colloids during the initial stage of tissue hypoperfusion appears to represent a strategy which uses the greater volume effect during hypovolemia while minimizing the risks for adverse reactions.

Thrombelastometry-guided thrombolytic therapy in massive pulmonary artery embolism.

We report a case of a patient who suffered a massive pulmonary embolism with cardiac arrest on post-operative day 4 after a Whipple operation. Despite thrombolytic therapy with the recommended maximal bolus of 50 mg recombinant tissue type plasminogen activator (rt-PA), thrombelastometry showed no signs of fibrinolysis and cardiogenic shock persisted, after only a transient hemodynamic improvement. Not until a repeat bolus of 25 mg rt-PA and an infusion of 50 mg/h did thrombelastometry demonstrate complete fibrinolysis. Although only residual emboli were seen on computed tomography, the patient died secondary to refractory right heart failure. This demonstrates that the standard dosing of thrombolytics may fail in a subgroup of patients, and suggests that thrombelastometry may be useful for early dose adjustment when standard dosing regimens fail.

Monocyte phagocytosis of viable Staphylococcus aureus is impaired by barbiturates, but not by propofol.

BACKGROUND: Barbiturates and propofol are used for deep sedation of patients with elevated intracranial pressure refractory to standard therapeutic regimens. Such patients often suffer from bacterial infections, which are most commonly caused by Staphylococcus aureus. Various interactions of anesthetics with components of the host defense have been documented, but very little is known about the influence on monocytes, which are a first-line defense against bacterial invasion. Therefore, we studied the effects of thiopental, methohexital, and propofol on monocyte phagocytosis using an in vitro whole blood model of viable S. aureus. MATERIALS AND METHODS: Whole blood samples were preincubated with different concentrations of thiopental, methohexital, and propofol. Phagocytosis was stopped at different time points after addition of viable S. aureus. Monocytes then were stained with monoclonal antibodies for flow cytometric analysis of monocyte recruitment (ratio of ingesting monocytes). Furthermore, the fluorescence intensity of ingested bacteria served as semiquantitative measurement of phagocytosis activity. RESULTS: Both barbiturates inhibited monocyte recruitment and phagocytosis activity concentration-dependently, whereas propofol did not affect any of the investigated parameters. At concentrations of 7.6 x10(-3) M thiopental or 1.1 x 10(-3) M methohexital and greater, monocyte recruitment and phagocytosis activity were significantly inhibited. The calculated half-maximum inhibitory concentration (IC50) of thiopental was 8.4 x 10(-3) M for monocyte recruitment and 8.6 x 10(-3) M for phagocytosis activity. The corresponding values for methohexital were 4.1 x 10(-3) M and 1.1 x 10(-3) M, respectively. CONCLUSION: The two barbiturates induce concentration-dependent inhibition of monocyte phagocytosis, whereas propofol is without effect. In combination with previously described effects on granulocyte function, these findings suggest that defense against bacterial infection might be reduced by barbiturates.

[Aortocaval compression syndrome]. / Aortokavales Kompressionssyndrom.

Aortocaval compression syndrome (supine hypotensive syndrome) represents a common complication mainly of late pregnancy, although the syndrome has been described to occur as early as 16 weeks of gestation. The nature and severity of symptoms range from unspecific complaints to severe maternal hypotension, loss of consciousness, cardiovascular collapse, and consecutive fetal depression. Predominantly, the syndrome is provoked by placing the parturient supine. Since supine positioning is required for diverse diagnostic and therapeutic procedures in obstetrics, these involve increased risk of aortocaval compression. For the anesthetist, cesarean section is most relevant, because of the coincidence of several risk factors. The following article begins by reviewing the pathophysiology of the syndrome, known risk factors and anesthesiological procedures that predispose to the syndrome. The second part is concerned with prophylactic measures and therapeutic options, together with the discussion of a clinically practicable algorithm.