Pediatric CCRN

SIADH lab values DI lab values Osmolality formula Normal blood osmolality Normal urine osmolality ADH DKA expected lab values Risk factors for cerebral edema S/S of Hypernatremia What rate should the Na be increased in SIADH How fast should the glucose be lowered in DKA to prevent cerebral edema SIADH management Serum Na <130, serum osm <280, BUN <10, urine osm >600, USG >1.030 Serum osm >285, serum Na >145, urine osm <200, USG <1.010 (Na x 2) + glucose/18 + BUN/2.8 280 300 Stored in posterior pituitary Allows renal tubules to be more perme- able to water -> more concentrated urine Increased serum osm (hyper osmolality with osmotic diuresis) Ph < 7.3 HCO3 < 15 Increased K Increased Phos Increased Na Less than 5 yo Newly diagnosed Elevated BUN Received Bicarbonate Lethargy Irritability Seizures Dry mucous membranes Intense thirst 0.5-1 mEq/L/hr 50-100 mg/do/hr Restrict fluids Hypertonic saline Lasix (loop diuretics) Pediatric CCRN 2 / 2 DI management What does insulin stimulate Hypoglycemia S/S S/S of hyponatremia S/s hyperglycemia DKA triad S/S SIADH S/S DI Lab results with acute renal failure Replace fluid deficit and ongoing losses ADH replacement: synthetic vasopressin or DDVAP Glycogenesis (formation of glycogen) Protein synthesis Formation of adipose Anxiety, tachycardia, diaphoresis, hy- potonia, seizures, tremors, decreased LOC, hungry, dizzy, grumpy, headache Altered LOC abd cramping Diarrhea Hypoactive reflexes Extreme thirst, blurred vision, hunger, nausea, drowsiness, dry skin Hyperglycemia Ketosis Acidosis ^ADH, ^fluid retention, ^BP, decreased UOP, decreased NA, edema Low BP, ^Na, excessive UOP, low spec grav, thirty, hypovolemic Metabolic acidosis, ^anion gap, ^K, ^mag, ^phos