Intensive care medicine
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Intensive care medicine · Jun 1998
Case ReportsCombined lung injury, meningitis and cerebral edema: how permissive can hypercapnia be?
We describe a patient with combined meningococcal septicemia and meningitis, cerebral edema and acute respiratory distress syndrome, in whom we balanced the conflicting carbon dioxide strategies for optimal pulmonary and neurological management using jugular oxygen saturation (SjvO2) monitoring to identify the upper limit of "tolerable" hypercapnia. Our observations suggest that significant acidosis was not well tolerated; however, cautious induction of pH down to 7.32 and an arterial carbon dioxide tension (PaCO2) < 5.9 kPa was tolerated acutely without significant cerebral hyperemia. ⋯ In similar cerebro-pulmonary circumstances we suggest that these findings warrant consideration. Alternatively, invasive monitoring of SjvO2 could be undertaken so that patient-specific criteria for permissive hypercapnia can be determined.
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To investigate any relationship between the pathological features of amiodarone-induced pulmonary toxicity (APT) and clinical use of amiodarone in patients dying from acute respiratory distress syndrome (ARDS). ⋯ Acute amiodarone pulmonary toxicity is a definite pathological entity in ICU patients. High oxygen concentrations may be a risk factor, while pre-existing pathology, e. g. ARDS, may mask its development. Amiodarone should be used with caution in this group of patients.
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Intensive care medicine · Jun 1998
Reduction of NO-induced methemoglobinemia requires extremely high doses of ascorbic acid in vitro.
The objective of the present study was to investigate the treatment of nitric oxide (NO)-induced methemoglobinemia by ascorbate and its consequences on red blood cell (RBC) glutathione in vitro. RBC were obtained from five healthy volunteers. The following experiments were carried out: (1) After methemoglobin generation by NO, ascorbate was added (2) RBC were simultaneously exposed to NO and ascorbate (3) Methemoglobin was generated by NO, ascorbate was added and incubation with NO continued. (1) After discontinuation of NO, the mean half life for methemoglobin was reduced from 195 min (controls) to 60 min (10 mM ascorbate) in a dose-dependent manner. (2) Methemoglobin formation after 3 h of NO exposure was 2.7 +/- 0.3% in controls and 1.8 +/- 0.1% with 10 mM ascorbate (p < 0.01). (3) Further methemoglobin formation was inhibited only by 10 mM ascorbate (p < 0.001). ⋯ Treatment with 10 mM ascorbate significantly decreased glutathione (p < 0.002). In vitro, NO-induced methemoglobin formation is significantly decreased only by a high (10 mM) ascorbate concentration. Glutathione, critical for ascorbate activity, is not influenced by NO.
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Intensive care medicine · Jun 1998
Circulating cardiac troponin I in trauma patients without cardiac contusion.
To describe the evolution and the diagnostic value of cardiac troponin I (cTnI) and to relate its concentrations with the indicators of injury in trauma patients. ⋯ Taking into account the high reported sensitivity and specificity of cTnI dosage, the present results suggest cTnI can play a role in the evaluation of indirect myocardial injury following traumatic shock.