1. What is diabetic ketoacidosis (DKA) ?
Ans. Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes characterized by hyperglycemia, ketoacidosis, and ketonuria. It occurs when absolute or relative insulin deficiency inhibits the ability of glucose to enter cells for utilization as metabolic fuel, the result being that the liver rapidly breaks down fat into ketones to employ as a fuel source. The overproduction of ketones ensues, causing them to accumulate in the blood and urine and turn the blood acidic. DKA occurs mainly in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. Laboratory studies for DKA include glucose blood tests, serum electrolyte determinations, blood urea nitrogen (BUN) evaluation, and arterial blood gas (ABG) measurements. Treatment includes correction of fluid loss with intravenous fluids; correction of hyperglycemia with insulin; correction of electrolyte disturbances, particularly potassium loss; correction of acid-base balance; and management of concurrent infection (if present).
2. How does pneumonia or stress precipitate DKA ?
Ans.
3. How does DKA cause renal failure ?
Ans. DKA is associated with hyperglycemic crises and featured by metabolic acidosis, the production of ketoacids, volume depletion, and electrolyte imbalance. Due to glucose-induced osmotic polyuria and even emesis, volume depletion is a major cause of acute kidney injury (AKI) in DKA patients
4. How does DKA cause NAFLD ?
Ans. It has been observed that the fatty liver, obesity and insulin resistance act as co-factors to cause liver damage. Fatty liver is the result of an intracellular accumulation of triglycerides because of increased uptake of free fatty acids and de novo liponeogenesis in the hepatocytes. At the same time, there is a reduction in the hepatic secretion of very low density lipoproteins. The liver damage consists of cellular necrosis and inflammation, and these disorders result from an increase in mitochondrial oxidative stress on triglycerides with the consequential generation of free radicals and peroxisomes. The mitochondrial oxidative stress is increased also by the action of adipokines (cytokines produced by the adipocytes) such as leptin and tumor necrosis factor-α (TNF-α), which are produced in excess. The reduction of adiponectin, which is a regulatory adipokine, favors the activity of inflammatory adipokines. These chemical mediators, derived from inflammation and cell necrosis, as well as the adipokines activate the liver stellate cells and induce them to increase production of collagen, connective tissue growth factor and accumulation of extracellular matrix, in turn favoring fibrosis.
5. What is a phantom tumor ?
Ans. A pulmonary pseudotumour is no more than 'something' which mimics a tumour.
Most frequently it is caused by a loculated pleural effusion (pleural pseudotumour) trapped in the pleural fissures. Other entities which have been described with the term pseudotumours.
6. How will you come to a diagnosis of DKA ?
Ans. Diabetic ketoacidosis is typically characterized by hyperglycemia over 250 mg/dL, a bicarbonate level less than 18 mEq/L, and a pH less than 7.30, with ketonemia and ketonuria.
In patients with DKA, arterial blood gases (ABGs) frequently show typical manifestations of metabolic acidosis, low bicarbonate, and low pH (less than 7.3).
Serum potassium levels initially are high or within the reference range in patients with DKA. This is due to the extracellular shift of potassium in exchange of hydrogen, which is accumulated in acidosis, in spite of severely depleted total body potassium.
Even in the absence of infection, the CBC shows an increased white blood cell (WBC) count in patients with diabetic ketoacidosis. High WBC counts (greater than 15 X 109/L) or marked left shift may suggest underlying infection.
Plasma osmolarity usually is increased (greater than 290 mOsm/L) in patients with diabetic ketoacidosis. If plasma osmolarity cannot be measured directly, it may be calculated with the following formula: plasma osmolarity = 2 (Na + K) + BUN/3 + glucose/18. Urine osmolarity also is increased in affected patients.
Patients with diabetic ketoacidosis who are in a coma typically have osmolalities greater than 330 mOsm/kg H2 O. If the osmolality is less than this in a patient who is comatose, search for another cause of obtundation.
In patients with DKA, serum ketones are present. Blood beta-hydroxybutyrate levels measured by a reagent strip (Ketostix, N-Multistix, and Labstix) and serum ketone levels assessed by the nitroprusside reaction are equally effective in diagnosing DKA in uncomplicated cases.
7. When should insulin be started in DKA ?
Ans. Insulin infusion can be discontinued 30 minutes later. If the patient is still nauseated and cannot eat, dextrose infusion should be continued and regular or ultra–short-acting insulin should be administered SC every 4 hours, according to blood glucose level, while trying to maintain blood glucose values at 100-180 mg/dL.
The 2011 JBDS guideline recommends the intravenous infusion of insulin at a weight-based fixed rate until ketosis has subsided. Should blood sugar fall below 14 mmol/L (250 mg/dL), 10% glucose should be added to allow for the continuation of fixed-rate insulin infusion.
8. How should the dehydration be managed ?
Ans. Intravenous solutions replace extravascular and intravascular fluids and electrolyte losses. They also dilute both the glucose level and the levels of circulating counterregulatory hormones.
Initial correction of fluid loss is either by isotonic sodium chloride solution or by lactated Ringer solution. The recommended schedule for restoring fluids is as follows:
Administer 1-3 L during the first hour.
Administer 1 L during the second hour.
Administer 1 L during the following 2 hours
Administer 1 L every 4 hours, depending on the degree of dehydration and central venous pressure readings
9. What should be the insulin dose ?
Ans. SC use of the fast-acting insulin analog (lispro) has been tried in pediatric DKA (0.15 U/kg q2h). The results were shown to be comparable to IV insulin, but ketosis took 6 additional hours to resolve. Such technically simplified methods may be cost-effective and may preclude admissions to intensive care units in patients with mild cases. Use of subcutaneous insulin analog (aspart) has been shown to be effective as well in adults.
The initial insulin dose is a continuous IV insulin infusion using an infusion pump, if available, at a rate of 0.1 U/kg/h. A mix of 24 units of regular insulin in 60 mL of isotonic sodium chloride solution usually is infused at a rate of 15 mL/h (6 U/h) until the blood glucose level drops to less than 180 mg/dL; the rate of infusion then decreases to 5-7.5 mL/h (2-3 U/h) until the ketoacidotic state abates.
LEARNING POINTS
I learnt about the pathophysiology of DKA and how pneumonia and stress can precipitate a case of DKA.
I also got to know how a DKA case can be diagnosed seeing ABG , serum electrolytes and other parameters.
The case helped me in knowing how much of insulin and fluid resuscitation has to be given to a patient of DKA.
I also learn about the complications of DKA which includes severe hypoglycemia and coma.
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