Medical School Lesson Plan – Diabetic Ketoacidosis

The VBG shows a metabolic acidaemia with a compensatory respiratory alkalosis.

There is a raised lactate with normal strong ion difference. It also shows hyperkalaemia and hyperglycaemia, with a significant base deficit and low bicarbonate level.

The UK diagnostic criteria for DKA^​1​ are:

• Ketonaemia >3.0mmol/l or urine ketones >2
• Blood glucose >11mmol/l or known diabetes
• Bicaronate >15 and/or venous pH <7.3

Common underlying causes include:

• Insulin non-adherence, inadequate dosing or insulin pump failure
• Infection
• Pancreatitis
• Pregnancy
• Trauma/surgery
• Substance misuse/alcohol
• Medications ( steroids, atypical antipsychotics, sympathomimetics, anti retroviral, SGLT-2 inhibitors)

DKA treatment will likely cause potassium to drop significantly.

The initial hyperkalaemia will resolve rapidly and should not require any additional treatment, beyond the usual management (insulin pushes potassium back into cells).

It is likely that you will be replacing potassium later during treatment, despite the initial hyperkalaemia.

A dose of calcium chloride/gluconate can be considered if there are ECG changes or if there is expected to be a delay in starting insulin therapy.

High risk groups include:

• Elderly
• Younger (18-25)
• Pregnant
• Heart or renal failure

High risk features include:

• Oxygen sats <92%
• Systolic BP <90
• Pulse >100
• GCS <12
• Blood ketones >6
• Bicarbonate <5mmol/l
• pH <7
• Potassium <3.5mmol/l
• Serum osmolarity >320

This patient has a pH of 6.82 despite a blood ketone level of only 3.8mmol/l. She also has a respiratory rate of 38, resulting in a respiratory alkalosis with a venous pCO2 of 1.75. Her lactate is normal at 1.9mmol/l.

Looking at her electrolyte levels, she has a reduced strong ion difference of 20, with a raised chloride resulting in a hyperchloremic acidosis. This will have a significant contribution towards her overall metabolic derangement.

UK guidelines recommend 0.9% sodium chloride as the initial fluid of choice for DKA. This is predominantly due to an absence of evidence that alternative fluids are superior, combined with a greater familiarity and availability of ‘normal saline’.

In this case, the patient already has a raised chloride level, and 0.9% sodium chloride may not be the best choice, containing 154mmol/l of chloride. This may initially worsen the hyperchloremia and lower the pH in the early phases of resuscitation^​2​.

Alternative fluids include Hartmanns and Plasmalyte^TM, both of which have a lower chloride content, but are also relatively hypotonic when compared to 0.9% sodium chloride. Remember to be guided by local guidelines and policies.

The mainstay of treatment of DKA is a fixed rate insulin infusion of 0.1units/kg/hr.

Long acting sub-cutaneous insulin should be continued, and fluid resuscitation should be guided by the haemodynamic status of the patient.

DKA will often result in significant fluid depletion and careful attention should be put towards managing fluid balance.

DKA is a hypercoagulable state, and prophylactic low-molecular weight heparin should be given unless contraindicated.

Treatment progress should be monitored with hourly blood glucose and ketone levels, and 2 hourly VBG in the early stages of treatment.

The goals of treatment should be a reduction in blood ketone levels of 0.5mmol/hr with a maintenance of potassium of 4 – 5.5mmol/l. In the absence of a blood ketone meter, an increase in venous bicarbonate of 3mmol/l/h can be used as a surrogate.

When the blood glucose level drops below 14, an infusion of 10% glucose should be started to allow the insulin infusion to continue.

The most serious complication of DKA is cerebral oedema. This is more common in children and young adults^​3​ and may be caused by rapid changes in serum osmolarity, although the exact pathophysiology in unclear.

Suspect cerebral oedema in any patient being managed for DKA who has a drop in their level of consciousness or signs of raised ICP such as worsening headache or vomiting.

Management involves the use of osmotically active agents such as mannitol and hypertonic saline, and urgent referral to critical care for neuroprotection.