A complication of diabetes mellitus (DM) caused by absolute or relative insulin deficiency
It is diagnosed based on:
Hyperglycaemia >11 mM or known diabetes
Ketonaemia >3 mM or ketonuria >2+
Acidosis pH <7.3 and/or bicarbonate <15 mM
Mostly occurs in patients with type 1 DM. However, it occur in patients with type 2 DM, although they are much more likely to suffer with the related condition hyperglycaemic hyperosmolar state (HHS)
Epidemiology of DKA
Annual incidence of 1-5% amongst patients with type 1 DM
More common in women than men
Causes of DKA
Lack of compliance with insulin therapy
Acute illness (e.g. infection, MI, trauma)
Pathophysiology of DKA
Insulin deficiency renders cells unable to take up and metabolise glucose
Glucose remains trapped in the blood from where it is filtered by the kidneys in concentrations that exceed renal reabsorption capacity
Glycosuria causes a profound osmotic diuresis leading to severe dehydration
Unable to rely on carbohydrate metabolism, cells switch to fat metabolism and oxidise fatty acids to release acetyl coenzyme A (CoA) in concentrations that saturate the Kreb’s cycle
Excess acetyl CoA is converted to the ketone bodies acetone, acetoacetate and beta-hydroxybutyrate, which are released into the blood causing a raised anion gap metabolic acidosis
DKA mostly occurs in type 1 DM and is rare in type 2 DM because there is usually adequate levels of insulin to prevent ketogenesis
History in DKA
Polyuria
Polydipsia
Light-headedness
Nausea and vomiting
Abdominal pain
Dyspnoea
Drowsiness
Loss of consciousness
Lack of compliance with insulin therapy
Symptoms of the precipitant
Examination in DKA
Airway
May be compromised by reduced conscious level
Breathing
Kussmaul’s breathing
Hyperventilation to compensate for metabolic acidosis manifesting as ‘air hunger’
Acetone-smelling breath
Circulation
Cold, pale peripheries
Prolonged capillary refill times (CRT >2 s)
Decreased skin turgor
Reduced jugular venous pressure (JVP)
Sunken eyes
Dry lips, mouth and tongue
Tachycardia
Postural hypotension
Absolute hypotension
Cardiac arrhythmias precipitated by electrolyte disturbances
Disability
Confusion
Reduced conscious level
Exposure
Signs of the precipitant
Differential diagnosis of DKA
Hyperglycaemic hyperosmolar state (HHS)
Any cause of an acute abdomen (including medical causes) if presenting with abdominal pain
Other cause of raised anion gap metabolic acidosis
There is no need for an ABG unless you are concerned about gas exchange; a VBG provides the relevant other values accurately (i.e. pH, bicarbonate, K+, lactate).
Bloods
Full blood count (FBC)
Urea & electrolytes (U&Es)
Blood cultures
Electrocardiogram (ECG)
Urinalysis
Chest radiograph (CXR)
Initial management of DKA
Assess the patient from an ABCDE perspective
Maintain a patent airway: use manoeuvres, adjuncts, supraglottic or definitive airways as indicated and suction any sputum or secretions
Deliver high flow oxygen 15L/min via reservoir mask and titrate to achieve oxygen saturations (SpO2) 94-98% or 88-92% if known to have COPD
Attach monitoring
Pulse oximetry
Non-invasive blood pressure
Three-lead cardiac monitoring
Request 12 lead ECG and portable CXR
Obtain intravenous (IV) access and take bloods
Fluid resuscitation
If systolic blood pressure (SBP) <90 mmHg, give 0.9% saline 500 ml IV stat and repeat as necessary until SBP >90 mmHg
If SBP >90 mmHg, give
0.9% saline 1 L IV over 1 hour
0.9% saline 1 L IV over 2 hours
0.9% saline 1 L IV over 2 hours
0.9% saline 1 L IV over 4 hours
0.9% saline 1 L IV over 4 hours
0.9% saline 1 L IV over 6 hours
Fixed rate insulin IV infusion
Ask the nursing staff to draw up 50 units of actrapid in 50 ml of 0.9% saline (1 unit/ml) and run at 0.1 unit/kg/hour eg 7 units/hour for a 70 kg individual
Ketone levels should fall by 0.5 mM/hour; if this is not the case, increase the infusion rate by 0.1 unit/hour increments until this target rate is achieved
Rates adequate to switch off ketogenesis will usually render individuals hypoglycaemic so commence glucose 10% IV at 125 ml/hour once glucose <14 mM
Continue any long-acting insulin therapy at the usual dose and timing
Potassium replacement
Although potassium levels may be high on arrival, they will fall rapidly once the fixed rate insulin IV infusion commences. The supplementation suggested below should be added to the resuscitation fluid.
Potassium >5.5 mM requires no supplementation
Potassium 3.5-5.5 mM requires supplementation of replacement fluid with potassium chloride (KCl) 40 mM
Potassium <3.5 mM requires supplementation of replacement fluid with KCl 60-80 mM and high dependency unit (HDU) care
Anticoagulation
DKA is a hypercoagulable state so consider enoxaparin 1.5 mg/kg subcutaneously (SC)
Monitoring
Blood glucose and ketones should be checked hourly
VBG should be repeated at 1 hour, and 2 hourly thereafter
Aim for a urine output of >0.5 ml/kg/hour; insert a urethral catheter if necessary
Further management of DKA
Identify and treat the underlying cause
Identify and treat any complications
Consider critical care referral for those with markers of severity
Clinical features
Hypoxia
Hypotension
Reduced conscious level
Age >65 years
Significant cardiac or renal co-morbidities
Biochemical features
pH <7.1
Bicarbonate <5 mM
Ketonaemia >6 mM
Serum osmolalaity >320 mOsm/L
Potassium < 3.5 mM on admission
Complications of DKA
Hyperkalaemia
Hypokalaemia
Hypoglycaemia from fixed rate insulin IV infusion without glucose supplementation
