• Rehydration. Adequate rehydration is an important aspect of treatment that contributes directly to reductions in hypergly-caemia and counter-regulatory hormone levels. Considerable variation in fluid and electrolyte disturbances are observed between patients and the following recommendations represent only a guide to therapy.
o Rehydration is commenced with isotonic (0.9 per cent, containing 150 mmol each of Na+ and CP) saline containing appropriate potassium supplements (see below). Isotonic saline is used in preference to hypotonic saline - unless plasma osmolarity is significantly raised - in order to minimise the rapid movement of extracellular water into cells as blood glucose and osmolarity fall with treatment; such shifts have been implicated in the pathogenesis of the serious complication of cerebral oedema, discussed below. Rehydration of the patient must take account of continuing polyuria and approximately 6-10 L of fluid may be required during the first 24 h.
o In an average adult, 1 L of saline is infused every hour for the first two to three hours. The rate of infusion is then adjusted according to the clinical state of the patient. Care is required in elderly patients or those with cardiac disease; monitoring of central venous pressure or pulmonary wedge pressure is recommended in these circumstances.
o Occasionally, patients with relatively low admission plasma glucose concentrations may require a simultaneous infusion of dextrose to allow administration of sufficient insulin to suppress lipolysis and ketogenesis without inducing hypo-glycaemia.
o A rising serum sodium concentration (above 150 mmol/L) may necessitate the temporary substitution of hypotonic saline (75 mmol/L each of Na+ and Cl_) or even 5 per cent dextrose (with an appropriate increase in the dose of insulin if dextrose is used).
o When plasma glucose has fallen to <15 mmol/L, saline is discontinued and replaced immediately by 5 per cent dextrose, usually at a rate of around 250 mL/h. Undue delay in commencing dextrose infusion at this point may result in hypoglycaemia. Intravenous dextrose is given without interruption until the patient is eating again, since intravenous insulin must be continued (albeit usually at a lower dose - see below).
o Although the use of hypertonic (10 per cent) dextrose at this stage of treatment produces a slightly faster fall in total ketone bodies, this is not reflected in a more rapid resolution of the acidosis.
• Potassium replacement. Cardiac arrhythmias induced by iatrogenic hypokalaemia represent a major and avoidable cause of death. Hypokalaemia may also induce life-threatening weakness of respiratory muscles. Potassium is predominantly (98 per cent) an intracellular ion. Insulin treatment and rising pH stimulate the entry of extracellular potassium into cells.
o On average 20 mmol of potassium (administered as 1.5 g potassium chloride) will be required in each litre of fluid following the start of insulin therapy. Continuous electro-cardiographic monitoring may indicate signs of hyper- or hypokalaemia, but plasma potassium concentration should be checked regularly (2 hourly at first) and potassium supplements adjusted appropriately.
o Particular care must be exercised in patients with renal failure, anuria or oliguria (less than 40 mL/h).
o If hypokalaemia is present (plasma potassium < 3.5 mmol/L) potassium supplements should be doubled to 40 mmol/h; if hyperkalemia develops potassium should be temporarily halted, pending the result of further measurements.
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