FLUID MANAGEMENT OF DEHYDRATIONPhase I: Treat hypovolemic shock: Normal saline: 20 mL/kg over 20 minRepeat if shock is not corrected: Normal saline: 20 mL/kg over 20 minPhase II:If dehydration is severe correct by: Rapid volume repletion: 20 mL/kg normal saline or Ringer Lactate (maximum = 1 L) over 2 hrPhase III:1. Calculate 24-hr fluid needs: maintenance + deficit volumea. Maintenance: 100 ml/kg (for 135 mEq/L) is associated with an increased risk of central pontine myelinolysis (CPM). The risk of CPM also increases with overly rapid correction of the serum sodium concentration, so it is best to avoid increasing the sodium by >12 mEq/L each 24 hr.2. Moderate hyponatremia:a. The magnitude of the sodium deficit may be calculated by the following formula:Na required= Na desired (135 mEq/L) Na oserved x 0.6x body weight b. Half of the deficit is replenished in the first 8 hours of therapy, and the remainder is given over the following 16 hours. Maintenance and replacement fluids should also be provided. The deficit plus maintenance calculations generally approximate 5% dextrose with 0.45% saline. c. The rise in serum [Na+] should not exceed 0.51.0 mEq/L/h or more than 12 mEq/L/24 h unless the patient demonstrates central nervous system (CNS) symptoms that warrant more rapid initial correction. d. The dangers of too rapid correction of hyponatremia include cerebral dehydration and injury due to fluid shifts from the ICF compartment.3. Severe Hyponatremia with convulsions:a. In general, 6 mL/ kg of 3% NaCl will raise the serum [Na+] by about 5 mEq/L. After convulsions cease, this may be followed by slow correction with glucose normal saline.

Hypernatremia Hypernatremia is a sodium concentration >145 mEq/L, although it is sometimes defined as >150 mEq/L 1. Causes:

WATER DEFICIT: Nephrogenic diabetes insipidus WATER AND SODIUM DEFICITS Gastrointestinal losses Diarrhea Emesis/nasogastric suction Osmotic cathartics (lactulose)Cutaneous losses Burns Excessive sweatingRenal losses Osmotic diuretics (mannitol) Diabetes mellitus Chronic kidney disease (dysplasia and obstructive uropathy) Polyuric phase of acute tubular necrosis

2. Clinical manifestations: a. Doughy feel of the skin, b. Woody consistency of the tongue, c. Alteration in sensorium, d. Patients are irritable, restless, weak, and lethargic. e. Some infants have a high-pitched cry and hyperpneaf. Seizures, and g. Intracranial bleeds: Patients may have subarachnoid, subdural, and parenchymal hemorrhage. 3. Treatment:a. Mild hypernatremia:i. Administration of ORS in conscious patients. ii. Free water or breast feeds should be offered to the child. b. Severe hypernatremia:i. Hypernatremic dehydration involves fluid therapy calculated over at least 48 hours. ii. The goal is to avoid dropping the sodium any faster than 2.5 mEq per four hours. iii. Calculate the water deficit.Replete water and electrolytes over 2 to 3 days. iv. Water deficit (in L) = [(current Na level in mEq/L 145 mEq/L) - 1] X 0.6 X weight (in kg)1. Eg. A child weighs 10 kg and has a plasma sodium concentration of 160 mEq/L.2. [(160 mEq/L 145 mEq/L) - 1] X 0.6 X 10 = 0.62 L.3. If the patient from the example calculation above has a TBW of 0.62, and if the replacement fluid contains 0.45% NaCl (Na concentration of 77 mEq/L), the replacement volume (in L) =0.62 L X [1 1 - (77 mEq/L 154 mEq/L)] = 1.25 L. This volume has to be replaced slowly over 48-72 hours. v. If the serum sodium concentration is more than 200 mEq/L, peritoneal dialysis should be performed using a high-glucose, low-sodium dialysate.

Hypokalemia:A. Causes1. Renal tubular defect (intrinsic or secondary to nephrotoxins)2. Starvation3. Chronic diarrhea or vomiting4. Diabetic ketoacidosis5. Hyperaldosteronism6. Chronic diuretic use7. Inadequate IV replacement8. Metabolic alkalosis9. Magnesium depletionB. Symptoms/Signs1. Muscle weakness, cramps2. Paralytic3. Hyporeflexia4. Lethargy, confusion5. EKG: prolonged QRS, U-Wave, low voltage T-wave; 6. Atrial & ventricular ectopy, increased sensitivity to digitalisC. Treatment (all orders must be in mEq/L)1. Oral replacement: Maintenance = 2 mEq/kg/day. 2. IV replacement if neede should be cautious: a. Maximum concentration through peripheral IV is 60 mEq/L.b. Maximum rate of KCl administration should be 0.3 mEq/kg/hr or 40 mEq(total)/hr, whichever is less.c. Any solution > 100 mEq/L: (1) two MD's must sign order; (2) cardiac monitoring must be performed at all times; (3) preferably patient should be in ICU; (4) serum K+ must be checked one hour after infusion is started, then every 2 hrs until stable and in normal range, then q4-12 hrs; when KCl drip is in use, K+ must be checked q2 hrs;

HyperkalemiaA. Causes1. Renal failure2. Hemolysis3. Tissue necrosis4. Hypoaldosteronism (e.g., Addison's disease and pseudohypoaldosteronism)5. Congenital adrenal hyperplasia6. Potassium-sparing diuretics (e.g., spironolactone, amiloride)7. Overdose of potassium supplements (PO, IV)B. Symptoms1. Primarily cardiac2. EKG changes:a. Peaked T-Waveb. Increased P-R intervalc. Widened QRSd. Depressed ST segmente. AV or intraventricular heart blockf. Ventricular flutter, fibrillation3. Other: tingling, paresthesias, weakness, paralysisC. Treatment1. Obtain EKG and initiate cardiac monitoring2. D/C all sources of potassium3. If mild (K < 7.0 and EKG normal):a. begin Kayexalate - 1 gm/kg/dose PO/PR. 1 gm/kg in 20% sorbitol PO or in 70% sorbitol per rectum (must be retained for 20-30 min. minimum in colon). May be repeated every 4- 6 hrs. 1 gm/kg will decrease serum K+ by 1 mEq/L; use with care in patients with oliguric renal failure or cardiac disease as Kayexalate imposes a Na+ load.4. If severe (K > 7.0 and/or EKG abnormal):1. Begin Kayexalate;2. Calcium gluconate - 100 mg/kg IV over 5-10 min. (generally used in face of arrhythmias); effect begins within min, but is short-lived and can be repeated after 5 min if EKG changes persist or recur. Ca2+ should be used only when absolutely necessary in patients with elevated serum phosphorous levels given the risk of CaPO4 precipitation and in patients taking digoxin because hypercalcemia can precipitate digoxin toxicity.3. Sodium bicarbonate 1-2 mEq/kg IV over 5-10 min; check Ca2+ before infusing bicarbonate as raising pH decreases Ca2+, aggravating membrane instability. May be repeated within 15-30 min.4. Glucose/insulin1. Nondiabetics administer 0.5-1 gm/kg glucose IV over 1-2 hrs which will enhance endogenous insulin secretion. This usually lowers plasma K+ 1-2 mEq/L within 1 hr.2. Diabetics or patients with insulin resistance with hyperglycemia -insulin alone may be sufficient.5. Prepare for dialysis (used in face of life-threatening arrhythmias).

Calcium:Calcium in serum: Ionized - 45%, Bound to proteins (mostly albumin) - 45%, Complexed (with bicarbonate, phosphate, citrate) - 10%Normal serum concentration: Total: 8.8-10.5 mg/dl (decreased when serum protein is low). Ionized: 4.0-5.6 mg/dl (decreased in alkalosis; increased in acidosis).

Hypocalcemia:Causes:1. Neonatal (early, late). Low calcium intake in premature infants.2. PTH System abnormalities:a. Hypoparathyroidism (cong., acquired)b. Polyglandular autoimmune diseasec. Post surgeryd. Hypomagnesemiae. Pseudohypoparathyroidism (type I, II)3. Vit. D. System abnormalities:a. Reduced intake, sunlight exposure or absorptionb. Hepatic diseasec. Anticonvulsantsd. Chronic renal failuree. Vit. D. dependent rickets (type I, II)4. Other: Acute renal failure, acute pancreatitisClinical Manifestations:Neuromuscular: Irritability (positive Trausseau or Chvostak sign), tetanyCNS: SeizuresCardiac: Prolonged Q-T interval, arrhythmia, cardiac arrest; RISK FACTOR: ALKALOSIS!Chronic: Rickets, lethargy and poor feeding (newborn), cataracts, ectopic calcifications(pseudohypoparathyroidism).Treatment:Parenteral:Calcium gluconate 10% = 100 mg/ml Ca Gluconate (9 mg elemental calcium/100 mgcalcium gluconate)Cardiac arrest: 100 mg/kg/dose repeated q 10 minMaintenance: 100 mg/kg/dose q 4 hrs as indicatedCalcium chloride 10% = 100 mg/ml CaCl2 (27 mg elemental calcium/100 mg calciumchloride)Cardiac arrest: 20 mg/kg/dose over 5 min q 10 minMaintenance: 20 mg/kg q 4 hrs as indicatedShould only be given in a central vein.Administer IV calcium under ECG monitoring. Watch for bradycardia, hypotension,extravasation.Oral:Combined treatment with calcium supplements and vitamin D.Dose of oral calcium: 1-5 mMol (40 mg - 200 mg elemental calcium)/ kg/day.

HypomagnesemiaCauses:GASTROINTESTINAL DISORDERS

Diarrhea

Nasogastric suction or emesis

Inflammatory bowel disease

Celiac disease

Cystic fibrosis

Pancreatitis

Protein-calorie malnutrition

Hypomagnesemia with secondary hypocalcemia

RENAL DISORDERS

Loop diuretics

Mannitol

Aminoglycosides

Thiazide diuretics

Diabetes

MISCELLANEOUS CAUSES

Insulin administration

Pancreatitis

Intrauterine growth retardation

Infants of diabetic mothers

Exchange transfusion

Clinical Manifestations 1. Hypomagnesemia causes secondary hypocalcemia by impairing the release of PTH by the parathyroid gland and through blunting of the tissue response to PTH. Thus, hypomagnesemia is part of the differential diagnosis of hypocalcemia. It usually occurs only at magnesium levels