MANAGEMENT of DkA

■ The management of children differs from adults because of

their increased risk of cerebral oedema; it is particularly
important to avoid too rapid fluid replacement and overload.
■ A management regimen for diabetic ketoacidosis Fluid Up to 10 L of
fluid may be needed in the first 24 h: 1 L over first h 3 L over the next
6 h 1 L every 6-8 h depending on fluid deficit Use isotonic (normal -
0.9%) saline 10% glucose (125 mL/h)should be administered once
the blood glucose falls below 14mmol/L (~250 mg/dL) alongside the
saline More fluid may be needed if the patient is hypotensive on
admission Potassium replacement On average, 40 mol/L (40 mEq/L)
KCI should be added to each litre of fluid depending on serum
potassium concentration. Saline with pre-added KCI reduces the
chance of user-error Plasma potassium Potassium added 5.5
mol/L(>5.5 mEg/L) ^ Fluid rate or 1⁄2 KCI concentration (senior advice
required) 40 mol/L /40 mEq/L) None Insulin Insulin should be given
by continuous infusion at a dose of 0.1 unit/kg/h Continue long-acting
basal insulin analogue Acidosis 50 mL 8.4% bicarbonate should only
be given if there is severe acidosis (pH < 7.0) despite adequate fluid
and insulin replacement (senior advice required)
■ Other measures Search for the precipitating cause Insert nasogatric
tube in those with impaired conscious level Consider central venous
pressure line, especially in the elderly or those with cardiac disease, to
help monitor circulatory status Insert urinary catheter if no urine
passed within 4 h to assess renal function accurately.

Dehvdration in DKA may cause pre-renal renal failure, making it

important to monitor urine outout otherwise potassium may
accumulate, leading to dangerous hyperkalaemla. There Is. debate
about the need for a urinary catheter. As patients are significantly
dehydrated on admission, it is unlikely that they will pass urine for
several hours after the initiation of fluid replacement. It therefore
seems reasonable to delay the insertion of a urinary catheter for
up to 4 h. A central venous cannula mav be required to monitor
luid balance in elderly patients and those with cardiac disease.
■ Once insulin treatment is initiated, blood glucose concentration will
fall and care is necessary to prevent hypoglycaemia, whichmight
precipitate cardiac arrhythmias, acute brain injury anddeath.
Furthermore, it would increase secretion of counter regulatory
hormones that may prolong the ketosis. In order to prevent this,
intravenous 10% glucose should be initiated alongside the saline once
the glucose concentration has fallen below 14 mmol/L(~250 mg/dl)
■ Sodium bicarbonate Fluid and insulin replacement will frequently
correct the acidosis and sodium bicarbonate should only be
considered, with supervision by a senior doctor, if there is persistent
acidosis (pH ≤ 7.0), as bicarbonate administration may worsen
intracellular acidosis. Sodium bicarbonate may also predispose to
cerebral edema, an important cause of death in DKA. Repeat venous
blood gas measurement can be used to monitor resolution of the
acidosis.

Transfer to subcutaneous insulin Unless there is good reason, the previous insulin
regimen should be re-started once the acute metabolic abnormality has been
correced and the patient is ready for a meal..
Bolus insulin is given with the meal () and the intravenous insulin infusion should
be continued until some form of basal insulin has been re-instituted.
For those who remained on their long-acting basal analogue insulin during the
episode of DKA, the insulin infusion and fluids can be discontinued 30 min after
the meal. If the long-acting insulin had been stopped, the intravenous insulin
infusion and fluids should
■ be continued until some form of background insulin has been. given
and for at least 10-60 min after the meal. For those.on«sil, the batal
pump rate should be re introduced prior to discontnuing the
intravenous insulin infusion. For those ontwice dally mied insulin, this
should only be re introduced before smaklast ar the evenion meal.
■ Cerebral oedema is relatively uncommon in adults with DKA, but is
more common in children). It is potentially fatal and accounts for 70
80% of all deaths in children with DKA. The oedema are unclear, but
one possibility is cerebralmechanisms responsible for the
development of cerebral hypoperfusion with subsequent reperfusion.
It is important to ensure that fluid replacement matches the patient's
losses as oedema. If cerebral oedema occurs, intravenous mannitol
and excessive fluid replacement may be a further cause of cerebral
mechanical ventilation may be used. A common cause of death in
patients with
■ A common cause of death in patients with DKA is aspiration of vomit.
A nasogastric tube should be inserted to empty stomach distress
syndrome occasionally occurs in DKA. Features include secretions if
the conscious level is impaired. Adult respiratory shortness of breath,
central cyanosis and hypoxemia. The chest pulmonary edema. The
management involves intermittentX-ray characteristically shows
bilateral infiltrates that resemble positive pressure ventilation and the
avoidance of fluid overload.Thromboembolism is a further potentially
fatal complication of DKA, which arises from dehydration, increased
blood viscosity and coagulability. The place of prophylactic
anticoagulation remains controversial and routine anticoagulation is
not recommended
■ A continuous Intravenous Insulin infusion should be initiated ata rate
of 0.1 units/kg/h as soon as possible after the fluid replacement has
been started. Where the patient's weight isnot known, this can be
estimated. An initial loading dose isnat needed unless there is
considerable delay in setting up theinfusion. Previously, the insulin
dose was titrated according ta the bloed glucose (the so called 'sliding
scale'). From a pragmatic perspective, the fixed rate is simpler than
the hourly dose adjustment and has been shown to be effective inthe
promotion of ketone clearance.