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.
·Dysrhythmias, hypotension.
·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;
·Shock.
·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.
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