70 year old patient critically unwell, with life threatening hyperkalaemia requiring non invasive cardiac monitoring in resuscitation bay and urgent reduction of potassium.
1. Severe life threatening hyperkalaemia
high anion gap metabolic acidosis with additional respiratory acidosis (expected CO2 33)
acute renal failure
osmolality 313 with glucose 40 – indicates likely HHS (using uncorrected sodium)
pseudohyponatraemia (corrected 134)
Very high lactate – critically unwell with poor end organ perfusion and shock
2. HHS – precipitants include infection (UTI, pneumonia, cellulitis, septic knee, sepsis), medications(digoxin, diuretics, other), non compliance, underlying disease (MI, CVA, PE, mesenteric thrombosis), alcohol abuse
HAGMA – Acute renal failure, sepsis, shock (consider cardiogenic shock – bradycardia, hypotension), consider toxins
ARF – fluid depletion (large pre renal component – severe fluid depletion >10 litres deficit in HHS), ATN (fluid loss, direct insult, hypoxic injury), consider obstructive cause
Hyperkalaemia – ARF, digoxin related, diuretic use (thiazides)
Respiratory acidosis – aspiration, pneumonia, PE, altered GCS
3. First priority – ECG, confirm hyperkalaemia and treat (Insulin, Ca gluconate, Ca resonium, Salbutamol nebs, ??dialysis), check for digoxin (toxicity) prior to Calcium administration.
a. fluid resuscitation (2-3 litres in the first 2-3 hours, will require up to 10 litres over 1-2 days – choice of fluid??), followed by inotropes and invasive monitoring
b. Electrolytes – monitor potassium, check Ca, Mg, PO4, consider choice of fluid according to corrected Na after initial resuscitation
c. Insulin therapy – 0.1 U/kg/hr with aim to reduce glucose by 2-3 mmol/hr. Will require insulin bolus initially to reduce potassium
d. Seek and treat underlying cause
These patients usually require VTE prophylaxis, consider arterial / venous thrombosis in this setting.
Usually result from inadequate treatment and include mesenteric artery occlusion, AMI, VTE, DIC, rhabdomyolysis
Too much fluid can cause cerebral oedema and ARDS