Diabetic ketoacidosis or DKA:
DKA is medically abbreviated as Diabetic ketoacidosis. It is a potentially life-threatening and acute complications of diabetes mellitus. So, it is characterized by high blood sugar levels in the blood and the production of ketones leading to metabolic acidosis.
DKA is commonly associated with type 1 diabetes but type 2 diabetics are also susceptible. In 25 patients, DKA presents a diagnosis of type 1 diabetes due to acute insulin deficiency.
Also if patients miss their injections or forget to take their insulin injections they can present with DKA. Whenever diabetics undergo physiological stress such as due to some infections or some medical conditions like myocardial infarction, post-surgery or even emotional stress can cause Diabetic ketoacidosis or DKA.
Pathophysiology of Diabetic ketoacidosis or DKA:
Glucose is the major source of energy in the body it comes from the digestion of carbohydrates and is carried by the bloodstream to various organs of the body. However, Insulin is a hormone produced by beta cells of the pancreas and it is responsible for driving glucose into the cells. Moreover, Insulin attaches to the insulin receptors that are present on the cell membrane. This allows the glucose to enter the cell through glucose transporters. So insulin acts as a key to opening the body cells to glucose.
When insulin is deficient as in type 1 diabetes the glucose cannot enter the cells. So it stays in the blood causing high blood sugar levels. Now that the cells of the body are starving because there is no glucose the body increases the levels of counter-regulatory hormones in response to starvation. These hormones have two major effects that are responsible for clinical presentation:
- Gluconeogenesis
- Ketogenesis
1. Gluconeogenesis:
First is gluconeogenesis which means that they produce more glucose in an attempt to supply energy to the cells. This is done by breaking down glycogen in the liver a process called glycogenolysis and by synthesizing glucose from non-carbohydrate substrates such as by breaking down proteins into amino acids and lipids into free fatty acids. All of these contribute to producing more glucose via gluconeogenesis in the liver. However, as the cells cannot use this glucose because there is no insulin. This process only results in more sugar in the blood.
2. Ketogenesis:
The second process is ketogenesis. In the liver, the free fatty acid metabolism produces ketone bodies as an alternate energy source. There are three types of ketones:
- Acetone
- Beta-hydroxybutyrate
- Acetoacetate
Lipolysis also produces some inflammatory cytokines.
Symptoms and signs of diabetic ketoacidosis or DKA:
Patients with DKA present with :
1. Abdominal pain, nausea, and vomiting:
That’s because the inflammatory cytokines that were produce during the process of lipolysis irritate the gastrointestinal tract.
2. Polyurea, polydipsia, and dehydration (osmotic dieresis):
As the blood sugar levels exceed the kidney's ability to reabsorb it. The glucose overflows into the urine taking water and electrolytes along with it in a process called osmotic dieresis. This causes a large volume of urine, excessive thirst, and dehydration. ketone bodies, unlike fatty acids, can cross the blood-brain barrier and they serve as fuel for the brain during glucose starvation.
3. Altered mental status:
They’re however very acidic and when produced in larger amounts they overwhelm the buffering capacity of blood plasma resulting in metabolic acidosis. Which can cause confusion and even comma in patients with DKA.
4.Kussmaul respiration (deep hyperventilation):
Patients with DKA may present with deep and labored breathing this is because the lungs are trying to reduce blood acidity by exhaling more carbon dioxide. This is called Kussmaul breathing or Kussmaul respiration.
5. Acetone-smelling breath (pear drop smell):
Acetone gives DKA patient's breath a characteristic sweet smell.
6. Hyperglycemia:
DKA patients will show high glucose levels in the blood.
7.Metabolic acidosis:
Arterial blood gases will indicate low ph and low bicarbonate levels.
8. Ketouria:
The urine dipstick will show ketones in the urine.
9.Hypokalemia:
Another mechanism for high acidity moves hydrogen ions into the cells in exchange for potassium. This leads to increased potassium in the blood but once insulin treatment starts potassium moves back into the cells and hypokalemia may result. Instead for this reason, the blood potassium level is monitor throughout treatment, and potassium replacement is usually require.
10. Dry or flushed skin, headache and blurred vision
Diabetic ketoacidosis or DKA diagnosis:
There are two different criteria to diagnose DKA first is by the American diabetes association (2009) and the second is by the joint British diabetes Society (2013). They’re almost the same they use the same factors that is glucose, ph, serum bicarbonate level, and the presence of ketones in the blood and urine to diagnose DKA. There are slight differences in the level of glucose and serum bicarbonate between the two diagnostic criteria.
1. American diabetes association (2009):
Glucose ˃13.8mmol/l Ph˂7.30 Serum bicarbonate˂ 18mmol/l Anion gap ˃ 10 Ketonemia
2. Joint British diabetes societies (2013):
Glucose ˃11mmol/l or known diabetes mellitus Ph˂7.30 Serum bicarbonate˂ 15mmol/l Ketones > 3 mmol/l or urine ketones ++ on dipstick
Diabetic ketoacidosis or DKA treatment:
1. Fluid replacement:
Patients with DKA are severely dehydrated so it is very important to start IV fluids as soon as possible.
2. Insulin:
An intravenous infusion of insulin should be starting at 0.1 unit per kg per hour . once the blood glucose is less than 15 millimoles per liter an infusion of 5 dextroses should be started to avoid hypoglycemia.
3. Correction of hypokalaemia:
As mentioned earlier that once the insulin treatment starts then the patient can go into hypokalemia, therefore, it is very important to replace potassium as required.