25 year old male presents with altered level of consciousnessRespiratory Acidosis – pH7.31 pCO2 53mmHg
Compensation – Expected HCO3 = 24+(Measured pCO2-40/10) =25.3
Corrected Na = Na + (glucose-5/3) =183
Calculated Osmolality = 2XNa +urea +glucose +ethanol =421
The patient has a respiratory acidosis which is adequately compensated for. There is a markedly raised BSL and sodium, with the corrected sodium of 183mmol/l. The patient also has evidence of AI with a raised urea and creatinine. There is a moderately raised lactate and chloride and a markedly raised calculated osmolality. The measured osmolality is not available to calculate the osmolar gap.
This is the patients first presentation of diabetes mellitus, and has presented in a hyperglycaemic hyperosmolar state with a pH>7.1, serum HCO3 >18mmol/l, BSL. 33mmol/l, osmolality >320mOsmol/l, altered LOC and profound dehydration. The patients ketones are not available but should be low or absent in an HHS state. The recent surgery could have been a precipitant for the presentation, however other causes need to be excluded eg infection. The HHS has been complicated by AKI, hypernatraemia and lactic acidosis. The profound hypernatraemia is likely secondary to osmotic diuresis, confounded by the fact that the patient has an altered LOC and quadriplegic and therefore unable to obtain water himself leading to decreased oral intake. In this clinical context the respiratory acidosis is likely secondary to altered level of consciousness, made worse by underlying quadriplegia.
Causes of hypernatraemia
- Hypovolaemia – low total body sodium with high water loss
- renal water losses -post obstructive, osmotic – DKA/HHS, therapeutic
-extrarenal -excess sweating, vomiting,diarrhoea, GI drainage tubes
- Euvolaemic – normal total body sodium
-renal water losses – nephrogenic or central DI
-extrarenal water loss – respiratory and dermal – insensible losses, hypodipsia secondary to restricted access to water or deficit in thirst sensation
- Hypervolaemic – increased total body Na
-ARF, hypetonic dialysis, hypertonic sodium HCO3,sea water ingestion, hyperaldosteronism
Initial management needs to be resuscitation of the patient -normal saline or Hartman boluses until tissue perfusion is restored and increase in blood pressure to replace volume depletion
On going correction of sodium needs to be done at a rate of 0.5mmol/l/hr. This is done by calculating the water deficit
= Total Body water (0.6xweight) X (1-Desired Na/Actual Na)
Use 0.45% saline or 5% dextrose or oral water.
Too rapid correction can result in cerebral oedema
Need to treat HHS and underlying precipitants