EM@3AM: Diabetic Ketoacidosis
- Apr 14th, 2018
- Brit Long
Author: Brit Long, MD (@long_brit, EM Attending Physician, San Antonio, TX) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)
Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.
A 37-year-old female presents with dysuria, polyuria, polydipsia, and lightheadedness. She has a history of insulin-dependent diabetes. She has not checked her blood glucose at home within the last week, as she ran out of her testing strips. She denies vomiting, but has had significant nausea and suprapubic pain.
Initial VS include T 37.2C, HR 112, BP 110/61, RR 28, SpO2 97% RA.
Exam reveals dry oral mucosa and suprapubic tenderness. No CVA tenderness is elicited, and the rest of the exam is normal. ECG reveals sinus tachycardia, but POC glucose is 422 mg/dL.
What is the patient’s diagnosis? What’s the next step in your evaluation and treatment?
Answer: Diabetic Ketoacidosis (DKA)
- Definition: A state of hyperglycemia and acidemia due to insulin deficiency: glucose > 250 mg/dL, acidosis (pH < 7.3), ketosis.
- Hyperglycemia: Insulin deficiency leads to elevated serum glucose, which results in osmotic diuresis and electrolyte depletion (Na, Mg, Ca, Ph).
- Acidosis: Lipolysis and ketoacid accumulation results in metabolic acidemia (with elevated anion gap).
- Inability to metabolize glucose leads to fatty acid breakdown and ketone production, which includes acetoacetate and beta-hydroxybutyrate.
- Dehydration results in activation of renin angiotensin aldosterone system and further osmotic diuresis.
- Background: Incidence is approximately 10,000 cases per year in the U.S., with mortality approaching 5%. However, before insulin administration, mortality reached 100%.
- Causes: Acute insult to a chronic disease state results in insulin deficiency, or DKA can be the first sign of new onset diabetes.
- Triggers include infection, myocardial ischemia, medication non-compliance, steroid use, drug or EtOH abuse, pregnancy, hyperthyroidism, hemorrhage, stroke, pancreatitis, renal failure. See this great emDocs post on triggers for more.
- History: Polydipsia, polyuria, polyphagia, weakness, weight loss, abdominal pain, nausea/vomiting. Obtain information concerning recent triggers, medication compliance, and prior episodes of diabetic complications.
- Exam: Acetone odor on breath, Kussmaul’s respirations (tachypnea and hyperpnea), hypotension, tachycardia, confusion/altered mental status, abdominal tenderness (from ketone production or GI pathology). Closely evaluate for inciting etiology (infection).
- Testing: Vital to official diagnosis of DKA.
- Serum glucose (usually > 350 mg/dL). Euglycemic DKA can occur in up to 18% of patients.
- Blood Gas: Venous blood gas (VBG) may be used in place of arterial blood (gas). VBG will demonstrate anion gap metabolic acidemia. Difference in pH between VBG and ABG is +0.02 units.
- Electrolytes: Significant number of changes due to underlying pathophysiology.
- Potassium: DKA results in total body depletion of K with osmotic diuresis and vomiting (result in 100s of mEq depletion). Initial levels may be elevated due to acidemia (occurs in 5-10% of patients).
- Sodium: Depletion due to diuresis and GI losses, but dilutional hyponatremia can be caused by hyperglycemia and fluid shift. Correction factor of 1.6 mEq/L Na for every 100 mg/dL of glucose above normal. However, a more recent study suggests 2.4 mEq/L is more accurate. Do not use corrected sodium for anion gap calculation.
- BUN/Cr ratio is often elevated due to prerenal effects and intravascular fluid depletion.
- Urinalysis: May be falsely negative for ketones (does not measure beta-hydroxybutyrate). May have high urinary glucose or depict evidence of urinary tract infection (UTI).
- Electrocardiogram (ECG): Assess for cardiac dysfunction/ischemia.
- Chest X-ray: May obtain for concern of underlying pulmonary trigger (pneumonia).
- Ketones: Beta-hydroxybutyrate is elevated. Serum acetoacetate may not be positive.
- End Tidal CO2: ETCO2 > 35 mm Hg can rule out DKA (100% sensitivity). Levels < 21 mm Hg can rule in DKA (100% specificity).
- Management: Start with ABCs, bilateral IVs (often require multiple medications), monitor, ECG.
- Search for the underlying etiology/inciting event (infection).
- IV fluids should be provided to replete intravascular volume and improve GFR. Patients are often > 6 L down.
- Start with 10-20cc/kg in fluid depleted patients. May need to repeat fluid boluses for hydration. Once fluid boluses are given, consider providing 200 mL/hr of IV fluid.
- Options include normal saline, plasma-lyte, lactated ringers.
- NS is the typical fluid, but large volumes may result in hyperchloremic metabolic acidemia. If patients have significant acidemia or fluid depletion, consider a different option.
- LR is closer to physiologic parameters and will not worsen acidemia. Plasma-lyte is another great option.
- Electrolytes are key in management.
- Sodium is often low, due to dilution. This typically corrects with hyperglycemia treatment. If hyponatremic after correction, use NS for fluid repletion.
- Potassium is the most important electrolyte, and active repletion is needed. Insulin infusion shifts potassium intracellularly, resulting in K decrease.
- If K > 5.2 mEq/L, no repletement is necessary, and insulin can be started.
- If K is 3.3-5.2 mEq/L, provide PO K (20 mEq) and peripheral IV at 10 mEq/hr while starting insulin.
- If K < 3.3 mEq/L, hold insulin until > 3.3. Start PO and IV potassium.
- Though specific levels differ for potassium repletion, the key is checking potassium and providing repletion.
- Magnesium is often low due to hypokalemia. If the patient is hypokalemic (and thus likely hypomagnesemic, provide 1-2 g MgSO4 IV.
- Phosphorus < 1 requires repletement.
- Insulin: Patients require insulin to halt ketosis and correct acidemia. However, insulin should NOT be administered until serum K is known.
- Bolus is unnecessary and may increase risk of hypoglycemia and length of stay.
- Insulin infusion at 0.1-0.14 units/kg IV per hour is recommended.
- Leave the insulin drip rate the same until serum bicarbonate and anion gap are improving.
- If serum glucose is dropping (or once it drops to < 250-300 mg/dL), begin dextrose 5% 50-200 mL/hr.
- Continue IV insulin infusion for 2 hours after subcutaneous insulin is started.
- May provide long acting insulin if patient has been non-compliant.
- Subcutaneous insulin may be given if the patient is not critically ill (0.3 units/kg body weight of aspart, then 0.1 units/kg every hour).
- Remove insulin pump if present.
- Bicarbonate: Controversial, as the ADA recommends bicarbonate for patients with pH < 6.9. However, literature does not support this. To increase serum pH, the body has to blow off CO2, and in DKA, patients have maximized their ability to blow off CO2.
- Bicarbonate will lower serum K and result in intracellular acidosis, inhibit RBC oxygen release, and delay ketosis correction.
- Provide bicarbonate in patients in cardiac arrest and DKA, hyperkalemia with life-threatening dysrhythmia, and if in severe hemodynamic collapse.
- Intubation: Avoid intubation if possible unless the patient is in respiratory failure and cannot compensate due to severe fatigue.
- Risks: Rise in CO2 during sedation/paralysis and worsening acidemia, aspiration due to gastroparesis, and hemodynamic collapse.
- If intubation is needed, avoid succinylcholine. Try to decrease apnea time and use SIMV with NIPPV mask while waiting for sedative and paralytic to kick in. Once intubated, set rate to > 30. Check for auto-PEEP and plateau pressures.
- Continued Monitoring
- Evaluate vital signs, urine, and serum glucose/electrolytes regularly (every 1-2 hours).
- Closely evaluation for complications: cerebral edema, hypokalemia, hypoglycemia, other electrolyte abnormalities.
- Most patients will require admission. Patients with critical illness require the ICU.
- Some patients may be appropriate for discharge if non-compliant with no suspicion of a dangerous etiology. Other criteria required if considering discharge: anion gap that normalizes, glucose < 250, bicarbonate > 20, stable vital signs, euvolemic state, access to follow up and insulin.
A 28-year-old man presents to the emergency department with lethargy and vomiting. He has a history of type I diabetes mellitus. Vital signs include heart rate 112 bpm and blood pressure 110/80 mm Hg. Laboratory analysis reveals sodium 135 mEq/L, potassium 4.0 mEq/L, chloride 100 mEq/L, bicarbonate 10 mEq/L, creatinine 1.4 mg/dL, glucose 558 mg/dL, pH 7.2. Normal saline and insulin have been ordered. Which of the following should be administered next?
A. 5% dextrose with 0.45% saline
C. Potassium chloride
D. Sodium bicarbonate
The diagnosis of diabetic ketoacidosis can be established with the presence of hyperglycemia, ketosis and acidemia. The goals of treatment are aimed at insulin therapy, fluid resuscitation and electrolyte replacement. The exact amount of insulin administered varies, however many start with a bolus of 0.1 U/kg or 10 U of regular insulin IV followed by a maintenance of 0.1 U/kg/hr regular insulin IV. Fluid resuscitation should start with a one to two liter bolus of normal saline in adults or a 20 mL/kg bolus in a child. Potassium levels are often initially high or normal due to severe acidemia. The potassium levels often decrease significantly as the acidemia is corrected along with the administration of insulin. Potassium should be administered with intravenous fluids when the potassium is less than or equal to 5.0 mEq/mL. In patients where the initial potassium is low (< 3.3 mEq/L), levels could become life-threatening following the administration of insulin, therefore potassium should be vigorously repleted in concentrations of 20 to 40 mEq/L prior to initiating insulin therapy.
Five percent dextrose with 0.45% saline (A) should be used once glucose decreases to below 200 mg/dL to avoid hypoglycemia. Magnesium (B) deficiency may induce vomiting, promote hypokalemia and hypocalcemia, or induce cardiac dysrhythmias. The average person requires 0.3 to 0.35 mEq/kg/day, thus it is reasonable to include 0.35 mEq/kg of magnesium in fluids in the first three to four hours. It would not, however, be the next best step in the above scenario. Sodium bicarbonate (D) may be indicated in patients with a pH less than 7.0.
This post is sponsored by www.ERdocFinder.com, a supporter of FOAM and medical education, who with their sponsorship are making FOAM material more accessible to emergency physicians around the world.
EMDocs.net: Myths in DKA Management
Diabetic Ketoacidosis (DKA) Myths
- Van Ness-Otunnu R, Hack JB. Hyperglycemic Crisis. Journal of Emergency Medicine. 2013;45(5): 797-805.
- Lebovitz HE. Diabetic ketoacidosis. Lancet 1995; 345: 767-772.
- Savage MW et al. Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabet Med. 2011; 28(5):508-15.
- Aurora S et al. Prevalence of hypokalemia in ED patients with diabetic ketoacidosis. Am J Emerg Med 2012; 30: 481-4.
- Boyd JC et al. Relationship of potassium and magnesium concentrations in serum to cardiac arrhythmias. Clin Chem 1984; 30(5): 754-7.
- 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.
- Goyal N et al. Utility of Initial Bolus insulin in the treatment of diabetic ketoacidosis. J Emerg Med 2010; 38(4): 422-7.
- Duhon B et al. Intravenous sodium bicarbonate therapy in severely acidotic diabetic ketoacidosis. Ann Pharmacother 2013; 47: 970-5.
- Green SM et al. Failure of adjunctive bicarbonate to improve outcome in severe pediatric diabetic ketoacidosis. Ann Emergency Medicine 1998; 31: 41-48.
- Villon A et al. Does bicarbonate therapy improve management of severe diabetic ketoacidosis? Crit Care Med 1999; 27: 2690-2693.
- Okuda Y et al. Counterproductive effects of sodium bicarbonate in diabetic ketoacidosis. J Clinical Endocrinology Metabolism 1996; 81: 314-320.
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