OBJECTIVES: Very commonly febrile patients with bacteraemia develop a variety of acid-base and electrolyte disturbances which play a significant role in the morbidity and mortality of these patients. This study was undertaken to describe the pathogenetic mechanisms of these abnormalities in febrile patients with bacteraemia. METHODS: Fifteen febrile patients with bacteraemia, aged 24-62 years, were studied. In all patients blood cultures revealed Gram-negative rods. None of them had septic shock, diabetes mellitus, renal or liver failure and none was receiving drugs influencing acid-base balance and electrolyte levels or was a heavy alcohol consumer. RESULTS: Nine patients had respiratory alkalosis, which was possibly due to bacterial toxins, while the remaining 6 had a wide-gap metabolic (lactic) acidosis coexisting with respiratory alkalosis. Hypokalaemia was found in four patients and was mainly due to respiratory alkalosis. However, kaliuria due to hypomagnesaemia contributed to hypokalaemia in 2 patients. Hypomagnesaemia was detected in 3 patients and was attributed to respiratory alkalosis as well as to magnesiuria induced by metabolic acidosis or phosphate depletion. Hypophosphataemia was found in 5 patients who also had respiratory alkalosis and/or phosphaturia due to metabolic acidosis or hypomagnesaemia. Finally, one patient had multifactorial origin hypocalcaemia. CONCLUSION: Febrile patients with bacteraemia develop a number of acid-base and electrolyte disturbances attributed to various pathogenetic mechanisms.
OBJECTIVES: Very commonly febrile patients with bacteraemia develop a variety of acid-base and electrolyte disturbances which play a significant role in the morbidity and mortality of these patients. This study was undertaken to describe the pathogenetic mechanisms of these abnormalities in febrile patients with bacteraemia. METHODS: Fifteen febrile patients with bacteraemia, aged 24-62 years, were studied. In all patients blood cultures revealed Gram-negative rods. None of them had septic shock, diabetes mellitus, renal or liver failure and none was receiving drugs influencing acid-base balance and electrolyte levels or was a heavy alcohol consumer. RESULTS: Nine patients had respiratory alkalosis, which was possibly due to bacterial toxins, while the remaining 6 had a wide-gap metabolic (lactic) acidosis coexisting with respiratory alkalosis. Hypokalaemia was found in four patients and was mainly due to respiratory alkalosis. However, kaliuria due to hypomagnesaemia contributed to hypokalaemia in 2 patients. Hypomagnesaemia was detected in 3 patients and was attributed to respiratory alkalosis as well as to magnesiuria induced by metabolic acidosis or phosphate depletion. Hypophosphataemia was found in 5 patients who also had respiratory alkalosis and/or phosphaturia due to metabolic acidosis or hypomagnesaemia. Finally, one patient had multifactorial origin hypocalcaemia. CONCLUSION: Febrile patients with bacteraemia develop a number of acid-base and electrolyte disturbances attributed to various pathogenetic mechanisms.