Sugar is a main source of energy for the cells that make up your muscles and other tissues. Normally, insulin helps sugar enter your cells.

Without enough insulin, your body can’t use sugar properly for energy. This prompts the release of hormones that break down fat as fuel, which produces acids known as ketones. Excess ketones build up in the blood and eventually “spill over” into the urine.


  • An illness. An infection or other illness can cause your body to produce higher levels of certain hormones, such as adrenaline or cortisol. Unfortunately, these hormones counter the effect of insulin — sometimes triggering an episode of diabetic ketoacidosis. Pneumonia and urinary tract infections are common culprits.
  • A problem with insulin therapy. Missed insulin treatments or inadequate insulin therapy or a malfunctioning insulin pump can leave you with too little insulin in your system, triggering diabetic ketoacidosis.
  • Physical or emotional trauma
  • Heart attack or stroke
  • Pancreatitis
  • Pregnancy
  • Alcohol or drug abuse, particularly cocaine
  • Certain medications, such as corticosteroids and some diuretics
  • Have type 1 diabetes

Clinical Features

  • Nausea/vomiting
  • Thirst/polyuria
  • Abdominal pain
  • Shortness of breath
  • Tachycardia
  • Dehydration
  • Hypotension can occur because of volume depletion in combination with peripheral vasodilatation.  Tachypnea / respiratory distress
  • Kussmaul respirations and a fruity odor on the patient’s breath (secondary to metabolic acidosis and increased acetone) are classic signs of the disorder
  • Abdominal tenderness (may resemble acute pancreatitis or surgical abdomen)
  • Lethargy/obtundation/cerebral edema/possibly coma


Commit to managing your diabetes. Make healthy eating and physical activity part of your daily routine. Take oral diabetes medications.

Monitor your blood sugar level.

Check your ketone level. When you’re ill or stressed, test your urine for excess ketones


DKA results from relative or absolute insulin deficiency combined with counterregulatory hormone excess (glucagon, catecholamines, cortisol, and growth hormone). Both insulin deficiency and glucagon excess, in particular, are necessary for DKA to develop. The decreased ratio of insulin to glucagon promotes gluconeogenesis, glycogenolysis, and ketone body formation in the liver, as well as increases in substrate delivery from fat and muscle (free fatty acids, amino acids) to the liver. Markers of inflammation (cytokines, C-reactive protein) are elevated in DKA.

The increased levels of glucagon and catecholamines in the face of low insulin levels promote glycogenolysis.

Ketosis results from a marked increase in free fatty acid release from adipocytes, with a resulting shift toward ketone body synthesis in the liver. Reduced insulin levels, in combination with elevations in catecholamines and growth hormone, increase lipolysis and the release of free fatty acids. Normally, these free fatty acids are converted to very low-density lipoprotein (VLDL) in the liver. However, in DKA, hyperglucagonemia alters hepatic metabolism to favor ketone body formation.


Blood CBC,Urea Creatinine ,Blood sugar level.

Anionic Gap

Ketone level.

Blood electrolyte tests


Chest X-ray





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