Diabetic ketoacidosis is a potentially life-threatening complication of diabetes mellitus. It is most commonly associated with type 1 DM, but has some occurrence in type 2, which may also be drug related. This video from the Osmosis team provides an introduction: https://www.youtube.com/watch?v=-B-RVybvffU
There is usually an absolute insulin deficiency (hence being primarily a feature of type 1). This leads to inadequate intracellular utilisation of glucose. This leads to a number of physiological responses:
The hyperglycaemia results in a significant osmotic diuresis, with dehydration and electrolyte disturbances, including due to osmotic loss in the urine. The high level of ketone production leads to an acidosis as the buffering capacity is outstripped, also contributing to the electrolyte disturbance.
This may be additionally contributed to by the vomiting and reduced oral intake that may arise from the condition
This all results in the triad of DKA
DKA may be the first presentation of DM in a child or young adult, or may be triggered by an event. Some key triggers include:
Non compliance with medications
New medications e.g. steroids
Trauma, inc. surgery
The presentation can be related to the presenting illness as well as the effects of the pathophysiology i.e. of notable dehydration and acidosis.
Abdominal upset - vomiting, pain
Altered conscious level
Acetone breath (like pear drops)
Features of respiratory tract infection
Dry mucous membranes
Altered mental state e.g. confusion
Decreased conscious level
Temperature - low or high
These are to assess for the complications of the DKA, as well as investigate for potential triggers. Bloods
FBC - raised WBC
U&E - electrolyte disturbances, AKI
Blood gas - profound metabolic acidosis with incomplete resp compensation
Ketones - near patient testing of blood ketones should be available
Pregnancy test - potential trigger
CXR - assessing for consolidation
CT head may be needed in cases of altered consciousness
Venous blood gases are recommended for assessment as there are minimal differences in the values, with venous usually being more easily obtained. . This can also provide electrolyte values, with intermittent laboratory testing.
Plasma osmolality can be calculated: [2Na]+[k]+[Urea]+[Glucose]
The diagnostic criteria are based on the components of the triad.
Hyperglycaemia - blood glucose >11mol/l or known diabetic
Ketosis - ketonaemia >3mmol/l or significant ketonuria (>2+ on dip)
Patients should be monitored and cared for in an appropriate care environment, which is likely to be a critical care area in cases of more severe disease.
Correction of the fluid deficit is a priority of treatment. These patients are usually profoundly dehydrated - on average 10% of total. Crystalloid resuscitation is therefore the first step in their management, after securing large bore IV access. 0.9% NaCl is commonly used, but other balanced crystalloids are acceptable. 0.9% is generally more available with supplementary potassium, as is needed.
In the shocked patient, this may need to be done aggressively to support the circulation. In CVS stable patients, this is still rapid, but with slight more caution because of the risk of cerebral oedema. Guidelines exist which are quite prescriptive on the amount and rates, especially in children.
Monitoring fluid balance is important here. Catheterisation may be indicated in severe cases.
Correcting Electrolyte Disturbance
The patient may have normal potassium measurements but is likely to have significant total body deficit due to the osmotic diuresis. With the subsequent initiation of insulin, this will drop further as the K+ is driven intracellularly. As such, potassium replacement in fluids is essential, being commenced when the value is below 5.5 mmol/L.
There are also usually notable deficits of sodium and chloride, hence the common use of 0.9% NaCl as the crystalloid.
The metabolic acidosis is often profound, with partial respiratory compensation. This will respond to correction of the other metabolic components (rehydration, switching off ketogenesis) and specific correction is not recommended. It is important to be mindful of how important the respiratory compensation is, which may be compromised during transition to mechanical ventilation, and hard to maintain with a ventilator. Bicarbonate administration is not recommended except in cases of profound hypokalemia or acidosis leading to CVS dysfunction.
There can be significant phosphate depletion in these patients, although replacement is not advocated unless there are significant symptoms e.g. muscle weakness.
Switching Off Ketogenesis
This goal involves both reducing ketosis and hyperglycaemia by providing the insulin needed for the body to effectively utilise glucose again.
Reduce ketones by 0.5 mmol/l/hr
Raise venous bicarb by 3 mmol/l/hr
Reduce glucose by 3mmol/l/hr
Avoid hypoglycemia - commence glucose
Treatment is with a fixed rate insulin infusion (FRII). This has been shown to have better correction of ketosis than a variable one. A rate of 0.1 unit/kg/hr is used in adults, with a lower starting rate also possible in children. An initial bolus is not recommended. There is some evidence that excessively early administration (within the first hour) is a risk factor for cerebral oedema, so paediatric guidance recommends waiting until 1 hour after presentation to allow fluid repletion to commence. It is recommended that any long acting insulin that the patient is normally on is continued.
Hypoglycemia should be avoided, and may occur with insulin treatment despite ongoing ketosis. As such, glucose administration is recommended once the glucose drops below 14 mmol/L. This 10% glucose, in addition to crystalloid fluid resuscitation.
Resolution of DKA is identified as:
pH > 7.3
Bicarb > 15 mmol/L
Ketones < 0.6 mmol/L
Cerebral oedema remains the main cause of mortality, especially in children. This is less of a risk in adults. The pathophysiology is unclear, but may involved:
Changes in osmolality
Relative hyperperfusion of brain after pretreatment hypoperfusion