Passive leg raising: Simple and reliable technique to prevent fluid overload in critically ill patients

Background: Dynamic measures, the response to stroke volume (SV) to fluid loading, have been used successfully to guide fluid management decisions in critically ill patients. However, application of dynamic measures is often inaccurate to predict fluid responsiveness in patients with arrhythmias, ventricular dysfunction or spontaneously breathing critically ill patients. Passive leg raising (PLR) is a simple bedside maneuver that may provide an accurate alternative to guide fluid resuscitation in hypovolemic critically ill patients. Methods: Pertinent medical literature for fluid responsiveness in the critically ill patient published in English was searched over the past three decades, and then the search was extended as linked citations indicated. Results: Thirty-three studies including observational studies, randomized control trials, systemic review, and meta-analysis studies evaluating fluid responsiveness in the critically ill patient met selection criteria. Conclusions: PLR coupled with real-time SV monitors is considered a simple, noninvasive, and accurate method to determine fluid responsiveness in critically ill patients with high sensitivity and specificity for a 10% increase in SV. The adverse effect of albumin on the mortality of head trauma patients and chloride-rich crystalloids on mortality and kidney function needs to be considered when choosing the type of fluid for resuscitation

A Teenager Presents With Hypokalemia and Metabolic Alkalosis: Hypokalemia

Hypokalemia is one of the most common electrolyte disorders in hospitalized patient. Causes of hypokalemia include impaired renal potassium (K+) excretion, gastrointestinal losses or transcelluar shifts. Assessments of urinary K+excretion, acid-base status, and blood pressure are three major components to the causes ofhypokalemia.A random urine K+-to-creatinine (K+/Cr) less than 13 mEq/g Cr (<1.5 mEq/mmol) in a patient with hypokalemic metabolic alkalosis suggests poor intake, surreptitious vomiting, congenital pyloric stenosis, a shift of K+from extracellular fluid into the cells, laxative abuse, familial or sporadic periodic paralysis. In the setting of hypertension, urine K/Cr >1.5 mEq/mmol indicates primary and secondary hyperaldosteronism, Liddle syndrome, or apparent mineralocorticoid excess. By contrast, in the absence of hypertension, a urine K+ /Cr>1.5, is usually suggestive of surreptitious use of diuretic, Bartter syndrome or Gitelman syndrome. Measurements of the plasma renin activity and plasma aldosterone concentration are necessary to differentiate these conditionsfrom one another.Severe or symptomatic hypokalemia, if not recognized early or treated appropriately can lead to significant mortality and morbidity. In this article the basic principles of normal K+homeostasis and the pathophysiology that can disturb this balance are discussed. A selected case report focusing on the essential aspect of patient’s presentation, signs and laboratory data followed by series of questions with particular attention to the diagnosis and management of hypokalemia needed to assist in the differential diagnosis and treatmentare also discussed.Each question is followed by detailed discussion and reviews the recent publications that are useful at thebedside. Keywords:Hypokalemia; Metaboloc alkalosis; Causes; Diagnoses; Treatment

Effects of Prenatal Alcohol Exposure on the Developing Kidneys

Objective: Clinical and experimental studies strongly suggest that prenatal alcohol exposure is associated with zinc deficiency and impaired renal tubular function. Whether maternal alcohol consumption during pregnancy causes renal tubular cell injury is unknown. Material & Methods: Renal function was studied in 8 infants with fetal alcohol syndrome (FAS) and 8 healthy age-matched infants. Renal function and structure were also examined in 11 offspring of rats exposed to alcohol during gestation. Findings: Infants with FAS had limited ability to concentrate urine after water restriction (P<0.001) and impaired acidification after acute acid loading (P<0.001) compared to control group. Plasma zinc levels were lower (P<0.001) and urinary zinc excretion was higher (P<0.001) in infants with FAS compared to control infants. Scanning electron microscopic studiesrevealed cytoplasmic mitochondrial hypertrophy and vacuolar structures of the epithelial cells of thecortical collectingducts in the rat kidney following fetal exposure to alcohol. Conclusion: These findings suggest that offspring of rats exposed to alcohol during fetal life have renal functional and structural abnormalities that may be responsible in the genesis of renal functional abnormalities as described in infants with FAS

Are Cytomegalovirus-Naive Kidney Transplant Recipients at Increased Risk of Vascular Thrombosis? CMV infection and kidney transplant

Not applicabl