Journal of Intensive Care Medicine

Lactic acidosis is frequently encountered in the intensive care unit. It occurs when there is an imbalance between production and clearance of lactate. Although lactic acidosis is often associated with a high anion gap and is generally defined as a lactate level >5 mmol/L and a serum pH <7.35, the presence of hypoalbuminemia may mask the anion gap and concomitant alkalosis may raise the pH. The causes of lactic acidosis are traditionally divided into impaired tissue oxygenation (Type A) and disorders in which tissue oxygenation is maintained (Type B). Lactate level is often used as a prognostic indicator and may be predictive of a favorable outcome if it normalizes within 48 hours. The routine measurement of serum lactate, however, should not determine therapeutic interventions. Unfortunately, treatment options remain limited and should be aimed at discontinuation of any offending drugs, treatment of the underlying pathology, and maintenance of organ perfusion. The mainstay of therapy of lactic acidosis remains prevention.

Potassium is the principal intracellular cation, and maintenance of the distribution of potassium between the intracellular and the extracellular compartments relies on several homeostatic mechanisms. When these mechanisms are perturbed, hypokalemia or hyperkalemia may occur. This review covers hyperkalemia, that is, a serum potassium concentration exceeding 5 mmol/L. The review includes a discussion of potassium homeostasis and the etiologies of hyperkalemia and focuses on the prompt recognition and treatment of hyperkalemia. This disorder should be of major concern to clinicians because of its propensity to cause fatal arrhythmias. Hyperkalemia is easily diagnosed, and rapid and effective treatments are readily available. Unfortunately, treatment of this life-threatening condition is often delayed or insufficiently attentive or aggressive.

End-tidal CO ₂ (ET ^CO ₂ ) monitoring and transcutaneous (TC) CO ₂ monitoring were prospectively compared in 53 patients, 1 month to 16 years of age, with congenital heart disease (CHD). There were 32 patients with cyanotic CHD and 21 with acyanotic CHD. The TC-Pa CO ₂ difference was 2 ± 1 mm Hg and the ET-Pa CO ₂ difference was 5 ± 3 mm Hg ( P < .0001). The TC-Pa CO ₂ difference was≤2 mm Hg in 30 of 53 patients and≤5 mm Hg in 53 of 53 patients. The ETPa CO ₂ difference was≤2 mm Hg in 9 of 53 patients and≤5 mm Hg in 30 of 53 patients ( P < .001). No variation in the TC-Pa CO ₂ difference was noted based on the type of CHD (acyanotic vs cyanotic) or age. The ET-Pa CO ₂ difference was greater in patients with cyanotic versus acyanotic CHD (7 ± 3 mm Hg vs 4 ± 2 mm Hg, P < .0001) and in patients≤1 year of age versus patients ≥1 year of age (6 ± 3 mm Hg vs 4 ± 2, P = .008). In infants and children with CHD, TC monitoring provides a more accurate estimation of Pa CO ₂ than ET monitoring.

The objective of this retrospective study was to determine the optimal initial antibiotic regimen for hospital-acquired pneumonia using the frequency and sensitivity of Gram negative microorganisms found in sputum cultures. An antibiogram was constructed and compared with the hospital intensive care unit (ICU) antibiogram. The results yielded 191 microorganisms. The study-generated antibiogram showed that the highest percent susceptible antibiotics for all Gram-negative microorganisms were imipenem (75%) and amikacin (84%). Considering only Pseudomonas aeruginosa , the study-generated antibiogram and the hospital ICU antibiogram showed similar results, piperacillin and amikacin (86% and 82%, respectively, vs 91% and 85%, P = nonsignificant for both). The optimal empiric antibiotic regimen in the surgical ICU is different if directed against all possible microorganisms as opposed to the most prevalent microorganism P aeruginosa . Determining initial empiric antibiotic therapy using an ICU and culture-type specific antibiogram would result in a g reater likelihood that more patients would receive adequate initial antibiotic therapy.

Adult respiratory distress syndrome attributable to viral pneumonia is described mainly in immunodeficient persons. Adult respiratory distress syndrome caused by human herpes virus 6 is extremely rare, with only 1 case reported in the literature. The following is the case of a young woman who developed fatal pulmonary failure most probably attributable to human herpes virus 6 pneumonia.