Acetazolamide Therapy for Metabolic Alkalosis in Pediatric Intensive Care Patients. (Dodd)

López C, et al. Acetazolamide Therapy for Metabolic Alkalosis in Pediatric Intensive Care Patients. Pediatr Crit Care Med. 2016 Dec; 17(12):e551-e558.

OBJECTIVE: Patients in PICUs frequently present hypochloremic metabolic alkalosis secondary to loop diuretic treatment, especially those undergoing cardiac surgery. This study evaluates the effectiveness of acetazolamide therapy for metabolic alkalosis in PICU patients.

DESIGN: Retrospective, observational study.

SETTING: A tertiary care children’s hospital PICU.

PATIENTS: Children receiving at least a 2-day course of enteral acetazolamide.


MEASUREMENTS AND MAIN RESULTS: Demographic variables, diuretic treatment and doses of acetazolamide, urine output, serum electrolytes, urea and creatinine, acid-base excess, pH, and use of mechanical ventilation during treatment were collected. Patients were studied according to their pathology (postoperative cardiac surgery, decompensated heart failure, or respiratory disease). A total of 78 episodes in 58 patients were identified: 48 were carried out in cardiac postoperative patients, 22 in decompensated heart failure, and eight in respiratory patients. All patients received loop diuretics. A decrease in pH and PCO2 in the first 72 hours, a decrease in serum HCO3 (mean, 4.65 ± 4.83; p < 0.001), and an increase in anion gap values were observed. Urine output increased in cardiac postoperative patients (4.5 ± 2.2 vs 5.1 ± 2.0; p = 0.020), whereas diuretic treatment was reduced in cardiac patients. There was no significant difference in serum electrolytes, blood urea, creatinine, nor chloride after the administration of acetazolamide from baseline. Acetazolamide treatment was well tolerated in all patients.

CONCLUSIONS: Acetazolamide decreases serum HCO3 and PCO2 in PICU cardiac patients with metabolic alkalosis secondary to diuretic therapy. Cardiac postoperative patients present a significant increase in urine output after acetazolamide treatment.

Mechanisms of cardiac and renal dysfunction in patients dying of sepsis. (Fortenberry)

Am J Respir Crit Care Med. 2013 Mar 1;187(5):509-17. PMID: 23348975

RATIONALE: The mechanistic basis for cardiac and renal dysfunction in sepsis is unknown. In particular, the degree and type of cell death is undefined.

OBJECTIVES: To evaluate the degree of sepsis-induced cardiomyocyte and renal tubular cell injury and death.

METHODS: Light and electron microscopy and immunohistochemical staining for markers of cellular injury and stress, including connexin-43 and kidney-injury-molecule-1 (Kim-1), were used in this study.

MEASUREMENTS AND MAIN RESULTS: Rapid postmortem cardiac and renal harvest was performed in 44 septic patients. Control hearts were obtained from 12 transplant and 13 brain-dead patients. Control kidneys were obtained from 20 trauma patients and eight patients with cancer. Immunohistochemistry demonstrated low levels of apoptotic cardiomyocytes (<1-2 cells per thousand) in septic and control subjects and revealed redistribution of connexin-43 to lateral membranes in sepsis (P < 0.020). Electron microscopy showed hydropic mitochondria only in septic specimens, whereas mitochondrial membrane injury and autophagolysosomes were present equally in control and septic specimens. Control kidneys appeared relatively normal by light microscopy; 3 of 20 specimens showed focal injury in approximately 1% of renal cortical tubules. Conversely, focal acute tubular injury was present in 78% of septic kidneys, occurring in 10.3 ± 9.5% and 32.3 ± 17.8% of corticomedullary-junction tubules by conventional light microscopy and Kim-1 immunostains, respectively (P < 0.01). Electron microscopy revealed increased tubular injury in sepsis, including hydropic mitochondria and increased autophagosomes.

CONCLUSIONS: Cell death is rare in sepsis-induced cardiac dysfunction, but cardiomyocyte injury occurs. Renal tubular injury is common in sepsis but presents focally; most renal tubular cells appear normal. The degree of cell injury and death does not account for severity of sepsis-induced organ dysfunction.

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