Diabetic Ketoacidosis : Risk Factors, Clinical Features

Diabetic ketoacidosis is a condition that is caused by the accumulation of ketoacids like acetoacetate and beta-hydroxybutyrate. It usually occurs in insulin-dependent Diabetes mellitus or in illnesses like an infection, pancreatitis, or gastroenteritis which increases the requirement of insulin temporarily or acutely. It is characterized by hyperglycemia, ketonemia, and high anion gap acidosis. The plasma glucose level may be normal or slightly elevated in the starvation ketoacidosis. If severe it is a dangerous situation therefore the patient requires regular monitoring.

Risk Factors of Diabetic Ketoacidosis 

• Stress Conditions- This leads to excess ketone production.
• The Counter- Regulatory hormones downgrade the ketolysis.
• Surgery- It is also a stress condition to the body that can trigger diabetic ketoacidosis.
• Cocaine use
• Insulin Pump Malfunction- If the patient skips the insulin doses or if the patient is poorly compliant with insulin that can lead to insulin pump malfunction.
• Infarction
• Infection

Clinical Features Of Diabetic Ketoacidosis 

• The patient will present with epigastric pain, nausea, and vomiting.
• The epigastric pain will be present with rebound tenderness and specifically amylase will be elevated. It is very important to diagnose it clearly because it is mostly misdiagnosed as acute abdomen.
• Encephalopathy
• Osmotic Diuresis- It is majorly manifested with polyuria. There will be a lot of free water loss.
• There will be an increase in blood osmolarity. This causes the shifting of fluid across the brain. The conditions will arise that will lead to sudden pH changes and hence worsen the condition.

Pathophysiology Of Diabetic Ketoacidosis

• Diabetic ketoacidosis mainly occurs in patients with type 1 diabetes mellitus. In these patients, there is an absolute insulin deficiency.
• The muscles are not able to update sugar and hence causing intracellular starvation.
• This subcutaneous fat oxidation occurs and that leads to weight loss.
• There will be the generation of free fatty acids. The default in metabolic pathways will lead to the generation of ketones.
• The production of ketones causes acidotic hyperventilation by acting on the respiratory system and this is called Kussmaul’s breathing.
• There will be a progressive decline in blood pH.
• The manifestations of all the above scenarios can lead to damage to the blood-brain barrier.
• This can lead to the occurrence of cerebral edema in the patient.
• The ketosis in diabetic ketoacidosis is mainly due to ketone bodies. These ketone bodies are acetone (fruity odor of breath), acetylacetone, and beta-hydroxybutyrate.
• The patient will also have lactic acidosis. The patient's plasma lactate levels will be high.

Diagnosis Of Diabetic Ketoacidosis

• The patient will present to the office with clinical signs of Diabetic Ketoacidosis.
  • The first important sign is a fruity odor in the breath.
  • Tachycardia
  • Low blood pressure
  • Increase in the respiratory rate (Kussmaul’s Breathing).
• Urine ketostix ( Urinalysis)
• Plasma beta-hydroxybutyrate levels.
• Random blood sugar levels- It will be between 250 to 600 mg/dl.
• Serum Electrolytes- As the patient comes to the clinic with a lot of vomiting therefore it will reduce total body potassium level. Insulin also worsens hypokalemia therefore potassium correction is done with providing KCL.
• Sodium- It is reduced due to more and more infusion of normal saline, also the high blood sugar levels draw in water and sodium along with water leading to hypertonic hyponatremia.
• Kidney Function Test- It will show an increase in BUN and creatinine.
• Arterial Blood Gases- pH, CO2, and HCO3 will be less. It indicates partially compensated metabolic acidosis.
• There will be a high anion gap due to less bicarbonate ions.
• High serum amylase and lipase levels.
• There will be an elevation in total leukocyte count.
• The patient should be admitted to ICU if the pH is less than 7, breathing is laboured, and there are impaired level of arousal or awareness of surroundings.

Treatment Of Diabetic Ketoacidosis

• If the patient comes to the hospital with symptoms of shock or reduced level of consciousness or coma then resuscitation methods should be started.
• If the patient presents with moderate or greater dehydration but not in shock or acidotic vomiting, then intravenous therapy with 0.9% saline 10-20 ml/kg over 20-30 min should be provided.
  • Calculate the fluid requirements and correct the deficit within 24 to 48 hours.
  • Add potassium 40mmol/L fluid.
  • Continue intravenous insulin infusion at 0.05-0.1 unit/kg/hr starting 1 hour after intravenous fluids are initiated.
  • It is very important to critically observe or monitor the early blood glucose, early fluid input, and output. The neurological status should be observed at least hourly.
• If the patient presents with minimal dehydration or the patient is tolerating the oral fluid then start with subcutaneous insulin therapy. The oral hydration should be continued. If the patient is not showing any improvement in subcutaneous insulin and oral hydration then it should be shifted to intravenous therapy.

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