Download Pediatrics On Call (LANGE On Call) by Charles Pohl, Kathleen Bradford, Clara Callahan, J. Carlton PDF

By Charles Pohl, Kathleen Bradford, Clara Callahan, J. Carlton Gartner

I. On-Call ProblemsII. Laboratory TestsIII. Bedside ProceduresIV. Fluids and ElectrolytesV. dietary administration of the Pediatric sufferer VI. Blood part TherapyVII. Ventilator ManagementVIII. administration of Perioperative ComplicationsIX. standard MedicationsAppendix

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Extra info for Pediatrics On Call (LANGE On Call)

Sample text

ABGs. 44 and determine if primary disturbance is respiratory or metabolic (PCO2 or HCO3). 2. Electrolytes and calcium. Evaluate K+ and Cl− status; pattern may be suggestive of diagnosis (ie, hypochloremic, hypokalemic alkalosis seen with pyloric stenosis; hypokalemic 5. ALKALOSIS 25 alkalosis seen with Bartter syndrome). Low Ca2+ levels are noted in milk-alkali syndrome. 3. Spot urine electrolytes. Help to determine type of metabolic alkalosis and future management (ie, response to Cl− and fluid replacement).

Although emesis may ultimately require surgical intervention, hydration and electrolyte status are the primary concerns in initial management. Replacing fluid losses through adequate 24 I: ON CALL PROBLEMS hydration and correction of electrolyte alterations should be the first steps in resuscitation of this infant. If fluid status is not addressed, infant may progress to a state of hypovolemic shock or symptomatic hypokalemia. III. Differential Diagnosis. 44) and determine whether primary etiology is respiratory (decrease in PCO2) or metabolic (increase in HCO3).

Metabolic Acidosis. May be associated with a normal or an increased AG. This division greatly facilitates diagnosis. 1. Elevated AG acidosis. Causes include lactic acidosis (tissue hypoxia, shock, cardiac arrest, sepsis, hematologic emergencies), ketoacidosis (diabetes, alcohol induced, starvation), renal failure (uremic metabolic acidosis), and toxins (salicylates, methanol, ethylene glycol). 2. Normal AG metabolic acidosis. Usually the result of HCO3 loss from bowel or kidneys but can occur from treatment with exogenous acids (eg, HCl).

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