Fluid and electrolytes: abnormalities
Assess the problem. Is the patient hypovolaemic or overloaded?
· Associations: hypovolaemia and low urine Na (<10mmol/L).
· Causes: inadequate Na intake, excessive Na losses.
· Treatment: restore circulation, replace water and salt deficits.
· Symptomatic therapy (<120mmol/L): if there are seizures, the serum Na level should be acutely raised by 5–10mmol/L in about 1hr. Use 3mmol NaCl/kg IV over 30–60min.
· Associations: normovolaemia (occasionally overload), paradoxically high urine Na (usually >300mmol/L), and sometimes cerebral oedema.
· Causes: impaired water excretion; excess water given.
· Treatment: correct the volume overloaded circulation with diuretics (furosemide 0.5–1.0mg/kg IV). Provide oxygen and inotropes if required. Restrict fluids to less than maintenance.
· SIADH: There are many causes of SIADH. The features are low urine volume and high urine osmolality in the absence of hypovolaemia, renal disease, and adrenal disease. Urine Na is paradoxically high (20–30mmol/L) in the presence of hyponatraemia secondary to volume overload.
Besides hypernatraemic dehydration and salt poisoning, you will see hypernatraemia in diabetes insipidus (DI), where there is excess renal water loss. The urine is 5–10 times usual volume, with low osmolality (50–100mOsm/L), in the absence of glycosuria. So, assess the underlying problem, and restore compromised circulation.
· Causes: severe asphyxia, and CNS trauma, surgery, or infection.
· Treatment: use two IV solutions—one at 30–40% maintenance for replacement of insensible losses; the other for replacing urine losses. Check urine Na/K and prepare IV replacement solution to match.
· Hormone replacement: DI is sometimes transient and so initial fluid therapy is reasonable. However, if this problem is established, hormonal replacement is needed: nasal deamino-8-d-arginine vasopressin (DDAVP) 1–40micrograms/day in 1 or 2 doses; parenteral (IV) DDAVP 2–4micrograms/day in 2 doses. You should see a response within 1hr.
·ECG changes: flattened, prolonged, or inverted T waves; prominent U waves; ST segment depression; atrioventricular block.
·Neuromuscular: weakness; hypotonia; hyporeflexia; paraesthesiae.
·GI: ileus; constipation.
·Urgent: ECG changes, children on digoxin, or serum <2.5mmol/L.
·Treatment. use 0.5mmol KCl/kg IV over 1hr via a central line. The bolus should not exceed 20mmol, and should not be more concentrated than 40mmol/L KCl/L. Monitor with continuous ECG and repeat serum K level after 1–2hr.
·ECG changes: peaked T waves; widened QRS; depressed ST segments progressing to increasingly aberrant ECG complexes;
·Dysrhythmias: bradycardia; VT; VF; cardiac arrest.
Treatment guided by the level, but first repeat a venous sample in case of haemolysis. Stop all potassium and monitor the ECG, while you wait for the result.
·Protect the myocardium: calcium gluconate 10% (100mg/kg/dose IV at maximum rate 100mg/min; 1.5–3.3mL/min, 50mg/mL) and monitor for bradycardia and hypotension.
·Increase intracellular K uptake: NaHCO3 (1–2mmol/kg IV over 5–10min); insulin with glucose (0.1unit/kg IV with dextrose 25% 0.5g/kg IV over 30min).
·Induce kaluresis: salbutamol nebulizer.
·Decrease total load of K: Kayexalate® (1g/kg/dose PR 2-hourly with 5mL 20% sorbitol).
Low ionized values of Ca can result in:
·ECG changes: prolonged QT, AV block;
·CNS effects: seizures, tetany, and weakness.
·Calcium gluconate 10% for seizures, tetany, hypotension, arrhythmias.
·Monitor HR and BP during treatment.
·Check magnesium level and serum albumin: if low, correct (25–50mg/kg. IV magnesium sulphate over 30min, 6-hourly for 3 doses).
· If these are normal, with raised phosphate, decrease phosphate intake and use phosphate binders. Check renal function.