Diabetic ketoacidosis (DKA) is a potentially life threatening condition that can occur to people with diabetes. It is observed primarily in people with type 1 diabetes (insulin dependent), but it can occur in type 2 diabetes (non-insulin dependent) under certain circumstances. The reason for why it is not often seen in people with type 2 diabetes is because their body is still able to produce insulin, so the pathophysiology explained in the flowchart below is not as dramatic as compared to people with type 1 diabetes who do not make any insulin at all.
There are various symptoms associated with DKA including:
- Polyphagia (increased appetite and hunger)
- Polydipsia (increased thirst)
- Polyuria (increased urination)
- Glycosuria (glucose in the urine)
- Ketonuria (ketones in urine)
- Ketones in blood
- Sweet, fruity breath
- Tachypnoea leading to Kussmaul breathing (deep and laboured breathing pattern)
- The body tries to compensate for the ketone bodies (acid) by eliminating carbon dioxide (also an acid) thereby attempting to make the body more alkalotic to normalise the pH
- The compensation between the metabolic and respiratory system can be read about in this article
- Decreased bicarbonate
- The body tries to use the available bicarbonate (base) to buffer the ketone bodies (acid) in order to improve the metabolic ketoacidosis
- This actually worsens the situation the lower the bicarbonate becomes with a continual production of ketones
- Increased drowsiness/decreased level of consciousness
- As the pH decreases and becomes more acidotic, it has a direct effect on decreasing the level of consciousness in a person
- Increased urea
- Electrolyte disturbances
- Tachycardia and other cardiac arrhythmias
- Tachycardia is often a compensatory mechanism for the hypotension
- Cardiac arrhythmias are often attributed to the electrolyte disturbances, specifically potassium, that occur due to the osmotic diuresis
There is no need to memorise all of the symptoms listed above. If you understand the pathophysiological process of hyperglycaemia, you will understand the symptoms that arise as a result of these pathological processes. The flowchart below depicts the pathological process observed in DKA.
It is important to note that in DKA, there is more than enough glucose available in the body. The problem is that glucose requires insulin to move from the blood into the cells. In DKA, there is insufficient insulin to facilitate the uptake of glucose from the blood into the cells. As the cells are not receiving any glucose, the body thinks that there is insufficient glucose (even though there is plenty, it is just in the wrong spot). As a result, the body tries to increase the amount of glucose in the body to meet the functional demands of the cells by breaking down the lipids and proteins within the body. By doing so, the glucose continues to rise in the blood as it still cannot get into the cells and the byproducts of the lipids and proteins start to accumulate within the body.
The increase in glucose within the blood also increases the osmolality of the blood. In an attempt to reduce the osmolality of the blood, there is a fluid shift within the body. Fluid is dragged from the intracellular and interstitial spaces in the body, into the intravascular space in an attempt to dilute the high glucose levels. However, the increased amount of fluid in the intravascular space is excreted via the kidneys in a process known as an osmotic diuresis. As the fluid is excreted, so are the electrolytes that are dragged along with the excreted fluid. Over time, the patient becomes fluid and electrolyte depleted in the intracellular, interstitial and intravascular spaces. This leads to electrolyte derangements, dehydration, hypovolemia, hypotension and eventually shock.
The further down the flowchart the patient gets, the more serious their symptoms become. For this reason, there are varying degrees of severity with DKA:
- Mild: pH 7.25 – 7.30, bicarbonate decreased to 15–18 mmol/L, the person is alert
- Moderate: pH 7.00 –7.25, bicarbonate 10–15 mmol/L, drowsiness may be present
- Severe: pH below 7.00, bicarbonate below 10 mmol/L, stupor or coma may occur
A patient with moderate to severe DKA usually requires management in a critical care setting. From my experience, a severe DKA patient can be one of the busiest shifts you can have! To manage a patient with DKA, remember the following mnemonic: ACTRAPID!
Airway, Breathing, Circulation as per any emergency
DKA patients needs to have their airway, breathing and circulation assessed immediately. A patient that is in severe DKA may be unconscious with an unprotected airway and compromised breathing. They are also at risk of circulatory collapse from severe dehydration, with a loss of 6 – 10 litres of fluid volume on presentation to the hospital not being uncommon. Due to the extremely acidotic environment and electrolyte derangements, these patients are also at high risk of experiencing a cardiac arrest.
Commence fluid resuscitation
Due to the increased blood glucose levels and increased ketones, there is an increase in intravascular osmolality. This leads to a large fluid depletion due to the osmotic diuresis which fluid resuscitation rectifies. Fluid resuscitation also independently decreases blood glucose levels, increases renal perfusion thereby increasing the removal of glucose via the urine and increases tissue perfusion thereby aiding in insulin mobilisation. Half of the fluid resuscitation should be given over the first 8 hours, with the remainder over the next 16 hours. The amount of fluid resuscitation required in severe DKA is usually 6 – 10 litres.
Due to the increased level of ketones in the body, there is an increased level of extracellular hydrogen ions (acid) which are exchanged for intracellular potassium (buffered) in an attempt to help the metabolic acidosis improve. This initially results in a high potassium level within the intravascular space that may require insulin to help push the potassium back into the intracellular space. However, due to the osmotic diuresis observed in DKA, potassium will be excreted via the urine leading to an eventual overall depletion of potassium in both the intravascular and intracellular space. Therefore, potassium needs to be closely monitored and replaced as required (usually with an intravenous potassium infusion).
The replacement of insulin is the cornerstone of rectifying DKA. When insulin therapy begins, glucose must not be decreased by more than 3 mmol/L each hour. This is because a rapid change in glucose will result in a rapid change in osmolality that can result in cerebral oedema, one of the biggest complications of DKA management. For this reason, osmolality is also monitored to ensure that it does not decrease by more than 3 mOms/L each hour.
Osmolality = 2 (sodium + potassium) +urea +glucose
Due to the effect of insulin pushing potassium back into the intracellular space, insulin should not be replaced until the potassium is at least 3.5 mmol/L.
Acidosis is only actively managed with replacing bicarbonate if pH < 7.0, although there is no evidence showing a benefit in clinical outcomes or mortality rate for patients in DKA. As the ketone levels deplete via fluid resuscitation and insulin therapy, the acidosis will improve on its own. Blood glucose levels will usually return to a normal range prior to the ketoacidosis resolving; ensure that insulin therapy is continued at a low dose with a concurrent 5% dextrose infusion to avoid hypoglycemia. This ensures that sufficient time is given for the ketoacidosis to resolve.
Complications usually result from the pathological process of DKA or too fast a reversal of the hyperglycaemia/osmolality. Complications can include dehydration, hypovolemia, hypotension, electrolyte abnormalities, cardiac arrhythmias, cardiac arrest and cerebral oedema.
Information for patients
Patients need to be educated on the risks of avoiding their insulin in order to prevent re-admission with DKA. It is beneficial to review the reason for why the insulin may not have been taken and organise social support to rectify the issue in the future.
The aim is to discharge the patient with sufficient education to prevent re-admission with DKA in the future.
Emmett, M., Hirsch, I. B., & Kitabchi, A. E. (2015). Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment. Retrieved from: http://www.uptodate.com/contents/diabetic-ketoacidosis-and-hyperosmolar-hyperglycemic-state-in-adults-treatment
Simon Plapp – ICU Education Consultant, Western Private
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