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DKA Algorithm

Diabetic Ketoacidosis (DKA) is characterized by hyperglycemia, acidosis, and ketosis, with common symptoms including polyuria, polydipsia, and abdominal pain. Diagnosis requires specific criteria, and treatment involves fluid resuscitation, insulin therapy, and careful monitoring of electrolytes, particularly potassium. Complications can include hypoglycemia, hyperkalemia, and cerebral edema, which requires immediate intervention.

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4 views6 pages

DKA Algorithm

Diabetic Ketoacidosis (DKA) is characterized by hyperglycemia, acidosis, and ketosis, with common symptoms including polyuria, polydipsia, and abdominal pain. Diagnosis requires specific criteria, and treatment involves fluid resuscitation, insulin therapy, and careful monitoring of electrolytes, particularly potassium. Complications can include hypoglycemia, hyperkalemia, and cerebral edema, which requires immediate intervention.

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555g8k7rn6
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd

Diabetic Ketoacidosis (DKA)

Algorithm

Source: Manual of Medicine — [Link]

Presentation

Classic 3Ps: - Polyuria - Polydipsia - Polyphagia

Non-specific symptoms: - Weakness - Vomiting - Abdominal


pain - Blurry vision

Physical Examination findings: - Acetone (fruity) smell on


breath - Dehydration / tachycardia / hypotension / shock -
Kussmaul's respiration — deep, labored breathing secondary to
metabolic acidosis

Diagnosis

DKA is diagnosed when all three of the following criteria are


met:

Criterion Threshold

Hyperglycemia Serum glucose > 250 mg/dL

Arterial pH < 7.3, Anion gap > 10, Serum


Acidosis
bicarbonate < 18 mEq/L

Ketosis Ketonuria or ketonemia

Note: Serum beta-OH-butyrate is the preferred method for


measuring ketonemia.
Causes (The "8 I's")

Cause Details

UTI, pneumonia, gastroenteritis, pancreatitis —


Infection
accounts for 40–50% of cases

Acute Coronary Syndrome (ACS), Myocardial


Infarction
Infarction (MI)

Infraction Patient noncompliance with insulin therapy

Infant Pregnancy

Ischemic Cerebrovascular accident (CVA)

Illegal Alcohol, drug abuse / cocaine abuse

Iatrogenic Prescription drug interactions (e.g., corticosteroids)

Idiopathic New onset Type 1 diabetes or unknown cause

Treatment

Initial Resuscitation

• Altered sensorium is based on a combination of


hyperosmolarity and acidosis [cite:1]
• Start with 2L IV Normal Saline bolus empirically
before labs
• Fluid deficit is approximately 100 ml/kg (7–8 L deficit)
secondary to glucose osmotic diuresis
• IV fluids alone can decrease glucose by up to 300 mg/dL

Sodium Management

• Serum sodium is falsely lowered (pseudohyponatremia)


secondary to hyperglycemia
• Correction formula: Add 1.6 to Na for every 100 over
100 in glucose level
• Sodium corrects with IV fluid administration
• Switch to 1/2 Normal Saline when sodium normalizes
Insulin

Mechanism of Action: Stops ketogenesis and breakdown of


fatty acids

Key Cautions

• ⚠ Hypokalemia risk — Prevalence of hypokalemia in


DKA patients is ~5.6% (3 out of 54 patients) [cite:3]
• Do NOT start insulin until potassium is checked
• If patient is hypokalemic, insulin can drop K+ even
further → risk of arrhythmia
• Hold insulin until K⁺ > 3.3 mEq/L

Insulin Dosing

• Standard dose: 0.1 U/kg/h continuous IV infusion (no


bolus needed)
• Insulin bolus is NOT associated with additional benefit
[cite:4]
• A priming dose is unnecessary if dosing adequately
[cite:5]
• Optional bolus dosing: Bolus 0.1 U/kg, then gtt 0.1 U/
kg/h

Monitoring and Titration

• If glucose does NOT decrease by ≥50 mg/dL in the first


hour → double the infusion rate or give SQ insulin
bolus
• If glucose > 1000 mg/dL, rapid correction puts the
patient at risk for cerebral edema

When Glucose Reaches 200 mg/dL

• Option i: Reduce insulin gtt to 0.02–0.05 U/kg/hr, OR


• Option ii: Rapid-acting insulin 0.1 U/kg SC every 2
hours
When Anion Gap Closes (Goal = Resolution of Acidosis/
Ketosis, NOT euglycemia)

• Transition to SQ insulin (5 units per 50 mg/dL over 150


mg/dL — max 20 units)
• Discontinue insulin gtt one hour AFTER first SQ dose
is given

Dextrose

• When glucose falls below 200 mg/dL, add D5 to


replacement fluids
• This allows continued insulin administration to close the
anion gap while preventing hypoglycemia

Potassium

• Total body potassium deficit: average 3–5 mEq/kg


• May see relative hyperkalemia due to acidosis
(intracellular K⁺ shifts extracellularly)
• Repletion: PO (if tolerated) AND IV
• Do NOT start insulin until K⁺ > 3.3 mEq/L

Bicarbonate (HCO₃⁻)

• Use is controversial; ADA recommends consideration


only for pH < 7.0
• Retrospective studies show no improvement in
outcomes [cite:6]
• No prospective randomized controlled trials on
bicarbonate use in DKA with pH < 6.9 have been
published [cite:7]

Other Electrolytes

• Magnesium: Depleted secondary to osmotic diuresis —


replete as needed
• Phosphorus: May drop precipitously during DKA
treatment — must replete
Monitoring

Parameter Frequency

Blood glucose Every 1 hour

pH and
Every 2–4 hours
electrolytes

VBG is adequate; ABG not routinely required


Blood gas
[cite:8]

Complications

Complication Notes

Hypoglycemia From overzealous DKA treatment

Hyperglycemia From undertreatment

Caused by insulin therapy, correction of


Hypokalemia
acidosis, and volume expansion

Must bridge with SQ insulin before stopping


Return of DKA
insulin gtt

Hyperchloremia From large-volume Normal Saline resuscitation

Cerebral Edema Most dangerous complication; see below

Cerebral Edema

• Prognosis: Mortality 20–50%; 1/3 of survivors may be in


a vegetative state
• Risk factors: Age < 5 years, new-onset diabetes mellitus
• Symptoms: Depressed level of consciousness / Altered
Mental Status (AMS), pupillary changes, seizures
• Treatment:
• Mannitol 1–2 g/kg IV
• Consider: Intubation, Dexamethasone, Hypertonic saline
(5–10 mL/kg)
References

1. Kitabchi AE, et al. Hyperglycemic crises in adult patients


with diabetes. Diabetes Care. 2009;32(7):1335-43.
[Link]
2. Nyenwe EA, et al. Acidosis: the prime determinant of
depressed sensorium in diabetic ketoacidosis. Diabetes
Care. 2010;33(8):1837-9. https://
[Link]/20484127/
3. Arora S, et al. Prevalence of hypokalemia in ED patients
with diabetic ketoacidosis. Am J Emerg Med.
2012;30(3):481-4. [Link]
21316179/
4. Goyal N, et al. Utility of initial bolus insulin in the
treatment of diabetic ketoacidosis. J Emerg Med.
2010;38(4):422-7. [Link]
18514472/
5. Kitabchi AE, et al. Is a priming dose of insulin necessary
in a low-dose insulin protocol for the treatment of
diabetic ketoacidosis? Diabetes Care.
2008;31(11):2081-5. [Link]
18694978/
6. Viallon A, et al. Does bicarbonate therapy improve the
management of severe diabetic ketoacidosis? Crit Care
Med. 1999;27(12):2690-3. https://
[Link]/10628611/
7. Latif KA, et al. The use of alkali therapy in severe diabetic
ketoacidosis. Diabetes Care. 2002;25(11):2113-4. https://
[Link]/12401775/
8. Middleton P, et al. Agreement between arterial and
central venous values for pH, bicarbonate, base excess,
and lactate. Emerg Med J. 2006;23(8):622-4. https://
[Link]/16858095/

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