Journal of Research and Innovation in Anesthesia
Volume 4 | Issue 2 | Year 2019

Diabetic Ketoacidosis and Intensive Care

Gauri Raman Gangakhedkar

Department of Anesthesiology, Seth GS Medical College and KEM Hospital, Mumbai, Maharashtra, India

Corresponding Author: Gauri Raman Gangakhedkar, Department of Anesthesiology, Seth GS Medical College and KEM Hospital, Mumbai, Maharashtra, India, Phone: +91 9096266328, e-mail:

How to cite this article Gangakhedkar GR. Diabetic Ketoacidosis and Intensive Care. Res Inno in Anesth 2019;4(2):29–31.

Source of support: Nil

Conflict of interest: None


Diabetic ketoacidosis (DKA) is one of the most common hyperglycemic complications of diabetes mellitus (DM) that is encountered in clinical practice as anesthesiologists and intensivists. Various stressors can lead to DKA in a diabetic patient, but it also remains a common manifestation at the outset of the disease among young diabetics. Thorough knowledge of the disease pathophysiology and treatment modalities help to reduce both duration of ICU stay and the morbidity and mortality associated with DKA.

Keywords: Complication, Diabetes, Diabetic ketoacidosis, Intensive care.


Diabetic ketoacidosis (DKA), which is the most common hyperglycemic complication of type I diabetes mellitus (DM), is defined as an acute metabolic complication of diabetes which comprises a biochemical triad of hyperglycemia (plasma glucose >250 mg/dL), hyperketonemia (urine acetoacetate +), and metabolic acidosis (pH %3C; 7.3).1

Diabetic ketoacidosis has been found to the second most common presenting symptom of type I DM, with figures varying from 15% to 67%.2 This is particularly true in patients under the age of 6 years, where up to 44% of the children were found to present with DKA.3 However, there is an increase in the incidence of “ketone prone type 2 DM (T2DM) syndrome” also known as “Flatbush Diabetes”.4 Though this variant has been primarily found in obese, African-Americans, its incidence is gradually increasing across all ethnicities.


Diabetic ketoacidosis represents an absolute or relative insulin deficiency with the body having to resort to the use of amino acids and triglycerides as sources of energy. The relative insufficiency of insulin occurs when physiologic or pharmacologic stressors push the insulin balance such that the demand far exceeds the supply. Table 1 given below indicates the common stressors.1,46

Absolute deficiency is usually caused by slips of administration of insulin among diagnosed diabetics.

There is also an increase in insulin counter regulatory hormones, such as, glucagon, glucocorticoids, catecholamines, and growth hormones. The breakdown of triglycerides for energy leads to increased glycerol and fatty acids, while muscle break down leads to increased alanine levels. The glucagon stimulates hepatic gluconeogenesis using glycerol and alanine while fatty acids are now converted to ketones by mitochondria. The insulin deficiency causes unhindered ketosis which would normally have a negative regulatory effect. Additionally, there is impaired glucose utilization in the periphery. This acute metabolic imbalance results in the ketosis, acidosis, and hyperglycemia, which herald the DKA.1,5 Recent evidence suggests that DKA is a severe inflammatory state characterized by an elevation of proinflammatory cytokines (tumor necrosis factor-α and interleukin-β, -6, and -8), C-reactive protein, reactive oxygen species, and lipid peroxidation.7

Table 1: Common stressors
S. no.PhysiologicPharmacologic
1Acute infection*Corticosteroids
2Myocardial infarctionThiazide diuretics
4PancreatitisSodium glucose co-transporter 2 (SGLT-2) inhibitors
5TraumaMalfunction of subcutaneous insulin pumps

* Most commonly, lower respiratory tract infection, urinary tract infection

Hyperglycemia results in osmotic diuresis, with a loss of free water and electrolytes resulting in dehydration. Ketosis is due to strong organic acids, acetoacetic acid, and β-hydroxybutyric acid, which contribute to the acidosis.

Patients present with symptoms, which include, but are not restricted to, a rapidly evolving, polyuria, polydipsia, weight loss, nausea, vomiting, and abdominal pain.1,2,8 Mental obtundation, though more common with HHS, can also be found with DKA, on account of severe systemic acidosis and hyperosmolarity.9 Cerebral edema is a rare complication of DKA, in young children, with an incidence of 6.8 per 1000 episodes and a mortality of 24%.10


The American Diabetes Association (ADA) classifies DKA into mild, moderate, and severe as shown below (Table 2).1

Table 2: American Diabetic Association classification of DKA
Mild (plasma glucose %3E;250 mg/dL)Moderate (plasma glucose >250 mg/dL)Severe (plasma glucose >250 mg/dL)
Arterial pH7.25–7.307.00 to <7.24<7.00
Serum bicarbonate (mEq/L)15–1810 to <15<10
Urine ketonePositivePositivePositive
Serum ketonePositivePositivePositive
Effective serum osmolalityVariableVariableVariable
Anion gap>10>12>12
Mental statusAlertAlert/drowsyStupor/coma


The treatment of DKA is targeted to correct the dehydration, acidosis, hyperglycemia, and reverse the process of ketosis. At the same time, monitoring for dyselectrolytemia and other complications of DKA is vital.

The role of glargine insulin and intravenous thiamine in the management of DKA is being investigated.1 Hourly clinical and biochemical monitoring of serum electrolytes and blood gas analysis is recommended to track the therapeutic progress. The presence of indicators, such as, arterial pH %3C; 7.1, blood ketones < 6.0 mmol/L, serum bicarbonate < 5 mmol/L, serum potassium < 3.5 mmol/L, impaired consciousness, saturation < 92%, and hemodynamic compromise, demands the need for critical care.11

Regular, consistent monitoring is necessary till evidence of resolution can be obtained. Markers of resolution include11,12

Urine ketostix forms an essential part of diagnosing DKA but is not recommended for monitoring since they only detect the acetoacetate in the urine. β-hydroxybutyrate is predominantly present in the blood and gets converted to acetoacetate. This could lead to a false impression of nonresolution of DKA.11

Transition to multiple doses of subcutaneous insulin is usually done when the DKA has resolved and the patient has started eating. The ADA recommends the switch when at least two of the following criteria are met: anion gap <12 mEq/L, serum bicarbonate >15 mEq/L, and pH >7.3.11 Intravenous insulin is continued for two hours after initiation of subcutaneous therapy to prevent rebound hyperglycemia. Patients who were already on insulin before the episode can go back to their previous regimens. Insulin naïve patients are usually started with a weight-based subcutaneous regimen, using a total dose of 0.5–0.7 U/kg/day, giving 50% of the total dose as once daily basal insulin and dividing the other 50% equally between prebreakfast, prelunch, and presupper doses of rapid acting insulin.1,11,12 Till the patients are able to start oral feeds, intravenous infusions are the best therapeutic regimen.


The incidence of DKA is increasing and it accounted for over 1,60,000 hospital admissions in 2017, in the USA alone.1 The annual burden in the USA due to DKA is estimated at a staggering $2.4 bn.16 However, with the advent of point-of-care monitoring and availability of prompt medical attention, the mortality with DKA has reduced to <1% in most populations except those with major systemic illness and those with advanced ages.17 The average length of hospital stay has reduced from 5.7 to 3.4 days with shorter durations of stay required in those admitted due to lapses in insulin administration.18 The in-hospital mortality has been found to be significantly higher in patients who were not on insulin therapy.19 While the statistical evidence points to improved outcomes after intensive care unit admissions, the 5-year readmission and mortality remain at 46.4% and 35%, respectively, thus proving that early targeted interventions may be the only way to reduce the morbidity and burden caused by this illness.20


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