Fatal nonmeningitic Listeria rhombencephalitis. Report of two cases.

Two cases of rapidly fatal Listeria rhombencephalitis with normal cerebrospinal fluid (CSF) findings occurred in previously healthy adults. The infection presented with nausea and headache followed by fever and signs of lower cranial nerve dysfunction, without associated meningismus, and progressed to death within four and six days of hospitalization. Because of normal CSF findings (including ventricular fluid in one patient) and negative culture results of both blood and CSF, the diagnosis was not suspected. Listeriosis should be considered early in any febrile patient presenting with signs of brain-stem dysfunction, even if CSF findings are normal.

Hemodynamic, gas exchange, and hormonal consequences of LBPP during PEEP ventilation.

Hemodynamic, gas exchange, and hormonal response induced by application of a 25- to 40-mmHg lower body positive pressure (LBPP), during positive end-expiratory pressure (PEEP; 14 +/- 2.5 cmH2O) were studied in nine patients with acute respiratory failure. Compared with PEEP alone, LBPP increased cardiac index (CI) from 3.57 to 4.76 l X min-1 X m-2 (P less than 0.001) in relation to changes in right atrial pressure (RAP) (11 to 16 mmHg; P less than 0.01). Cardiopulmonary blood volume (CPBV) measured in five patients increased during LBPP from 546 +/- 126 to 664 +/- 150 ml (P less than 0.01), with a positive linear relationship between changes in RAP and CPBV (r = 0.88; P less than 0.001). Venous admixture (Qva/QT) decreased with PEEP from 24 to 16% (P less than 0.001) but did not change with LBPP despite the large increase in CI, leading to a marked O2 availability increase (P less than 0.001). Although PEEP induced a significant rise in plasma norepinephrine level (NE) (from 838 +/- 97 to 1008 +/- 139 pg/ml; P less than 0.05), NE was significantly decreased by LBPP to control level (from 1,008 +/- 139 to 794 +/- 124 pg/ml; P less than 0.003). Plasma epinephrine levels were not influenced by PEEP or LBPP. Changes of plasma renin activity (PRA) paralleled those of NE. No change in plasma arginine vasopressin (AVP) was recorded. We concluded that LBPP increases venous return and CPBV and counteracts hemodynamic effects of PEEP ventilation, without significant change in Qva/QT. Mechanical ventilation with PEEP stimulates sympathetic activity and PRA apparently by a reflex neuronal mechanism, at least partially inhibited by the loading of cardiopulmonary low-pressure reflex and high-pressure baroreflex. Finally, AVP does not appear to be involved in the acute cardiovascular adaptation to PEEP.

Lower body positive pressure vs. dopamine during PEEP in humans.

The application of lower body positive pressure (LBPP) of approximately 40 Torr was used to increase cardiac index (CI) in eight patients with acute respiratory failure (ARF) during positive end-expiratory pressure (PEEP) ventilation. The effects of LBPP on hemodynamics and gas exchange were compared with those of dopamine at the same level of CI without blood volume expansion. LBPP increased CI via an increase in stroke index without associated tachycardia, whereas dopamine combined both effects. A positive linear relationship (r = 0.82) was evidenced between CI and right atrial pressure (Pra) during application of LBPP according to the Frank-Starling mechanism, whereas dopamine did not increase Pra. The increase in CI with dopamine was associated with a significant rise in venous admixture (r = 0.84, P less than 0.001), whereas no such effect was observed with LBPP (r = 0.088). Changes in venous admixture were directly related to changes in mixed venous O2 pressure (PVO2) in both situations (r = 0.733, P less than 0.01), but the increase in PVO2 was more pronounced with dopamine than with LBPP (P less than 0.04). We conclude that LBPP can effectively counterbalance peripheral venous blood pooling during PEEP ventilation in humans with ARF and that changes in PVO2 appear as a major determinant of venous admixture in this setting.

Recurrent high-permeability pulmonary edema associated with diabetic ketoacidosis.

Delayed-onset pulmonary edema complicating severe diabetic ketoacidosis was observed twice in one patient. Hemodynamic measurements during the second episode showed normal transmural pulmonary capillary wedge pressure, suggesting an alteration in alveolocapillary permeability. Hyperventilation and acidosis may underlie this alteration. Vigorous fluid therapy, while decreasing oncotic pressure, may also contribute to the pulmonary edema. The two episodes in one patient suggest that pulmonary microvascular diabetic angiopathy may predispose some diabetics with severe ketoacidosis to increased-permeability pulmonary edema.