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