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Diabetic Ketoacidosis, Emergency Medicine

Basics

Description

- Medication noncompliance (>50%) - New-onset diabetes (type I or II) - Underlying medical illness (increased counterregulatory hormones and insulin resistance): - Infectious process - MI - GI bleed - CNS event

- Venous blood gas: - Essential to assess patients pH - pH correlates well with arterial pH - Avoids need for repeated arterial sticks - ABG should be performed if oxygenation/ventilation needs assessment.

- Serum osmolarity: - May be measured in the lab and calculated - Calculated: 2(Na) + glucose/18 + BUN/2.8 (normal 285-300 mOsm/L) - Significant hyperosmolarity >320

- Other lab tests: - Amylase: Elevation is nonspecific in DKA - Lipase: Elevation specific for pancreatitis - Calcium, Mg, Phosphate: All usually decreased as is K+

- Cerebral edema: - Occurs in 1-2% of children with DKA - Causes 31% of deaths associated with DKA - Exact causes unclear - Suspect with coma, fluctuating mental status, bradycardia, HTN, severe headache, decreased urine output, or quickly falling corrected Na+ or osmolality to below normal levels - Mannitol: 0.25-1 g/kg IV over 30 min should be given immediately and can be repeated hourly. - Fluid rate should be decreased and other supportive measures instituted.

Insulin deficiency and excess of counterregulatory hormones (catecholamines, glucagon, growth hormone, and cortisol) resulting in:

  • Dehydration (osmotic, hyperglycemic, diuresis, and decreased oral intake)
  • Acidosis (anion gap metabolic acidosis)
  • Ketone formation (unrestrained lipolysis and ketogenesis)
  • Hyperglycemia (unrestrained glycogenolysis and gluconeogenesis)
  • Electrolyte disturbances (hypokalemia, hypo/hypernatremia, hypophosphatemia)

Etiology

  • Medication noncompliance (>50%)
  • New-onset diabetes (type I or II)
  • Underlying medical illness (increased counterregulatory hormones and insulin resistance):Infectious processMIGI bleedCNS event
  • Pregnancy (relative insulin deficiency and counterregulatory hormone excess)
  • Medications (protease inhibitors and atypical antipsychotics: Olanzapine, clozapine)
  • Alcohol abuse

Diagnosis

Signs and Symptoms

History

  • Medication noncompliance
  • Polyuria, polydipsia
  • Weakness
  • Abdominal pain, nausea, vomiting
  • Altered mental status
  • Chest pain
  • Febrile illness

Physical Exam

  • Tachycardia
  • Hypotension (dehydration, sepsis)
  • Tachypnea (hyperpnea)
  • Kussmaul respirations
  • Hyperthermia/hypothermia (coexisting infection)
  • Dehydration:Poor skin turgorDry mucous membranes
  • Odor of ketones on breath
  • Diffuse abdominal tenderness

Essential Workup

  • Diagnostic criteria:pH <7.3 with ketonemiaBicarbonate <15 mEq/LGlucose >250 mg/dL
  • Bedside glucose measurement
  • Venous blood gas
  • Urine dip for ketones
  • Serum electrolytes, glucose, BUN/creatinine
  • Search for precipitating cause

Diagnosis Tests & Interpretation

Lab

  • Serum glucose measurement:
  • Electrolyte measurement:Increased anion gap metabolic acidosis: [Na - (Cl + HCO3)] >12Sodium:Pseudohyponatremia (from hyperglycemia) correction factor; add 1.6 mEq/L to the measured sodium for every 100 mg/dL of blood glucose >100 mg/dL.Potassium:Initial serum level may be normal to high owing to extracellular shift as compensation for acidosis.Total body deficit usually 3-5 mEq/kgAs acidosis improves, for every 0.1 increase in the pH, serum potassium decreases 0.5 mEq/L.Can drop precipitously with insulin and fluidsBicarbonate:Usually <15 mEq/LMay be higher owing to coexisting volume contraction alkalosis
  • BUN/creatinine:Usually shows prerenal azotemia owing to dehydration
  • Serum ketones:Must be present to make diagnosis of DKA.β-Hydroxybutyrate is the predominant ketoacid, but acetoacetate and acetone are also present:β-Hydroxybutyrate is not measured by most hospital serum and urine ketone tests (nitroprusside reaction measures only acetoacetate and acetone), thus there is a theoretical risk of missing the presence of ketones using these tests.Urine ketone dip test (UKDT) is 97% sensitive for presence of serum ketones and a negative UKDT has a negative predictive value of 100% in ruling out the presence of DKA.Point-of-care capillary testing for β-hydroxybutyrate is 98% sensitive for serum ketones:May be used with capillary glucose testing in triage to detect DKA early in the ED course.
  • Urinalysis:Ketonuria, glucosuriaPregnancy (UhCG)
  • Venous blood gas:Essential to assess patients pHpH correlates well with arterial pHAvoids need for repeated arterial sticksABG should be performed if oxygenation/ventilation needs assessment.
  • Serum osmolarity:May be measured in the lab and calculatedCalculated: 2(Na) + glucose/18 + BUN/2.8 (normal 285-300 mOsm/L)Significant hyperosmolarity >320
  • CBC:Leukocytosis may be present without infection.If left shift in differential, suspect infection.
  • Other lab tests:Amylase: Elevation is nonspecific in DKALipase: Elevation specific for pancreatitisCalcium, Mg, Phosphate: All usually decreased as is K+

Imaging

  • CT head to rule out other causes of altered mental status.
  • CXR if pneumonia suspected as precipitant or hypoxia present
  • EKG to rule out ischemia as a precipitant and look for signs of hyper/hypo K+

Differential Diagnosis

  • Other causes of anion gap acidosis
  • Use ACAT MUD PILES mnemonic:Alcoholic ketoacidosisCarbon monoxide/cyanideAspirinTolueneMethanolUremiaDiabetic ketoacidosisParaldehydeIron/isoniazidLactic acidosisEthylene glycolStarvation/sepsis
  • Hyperglycemic hyperosmolar nonketotic syndrome

Treatment

Pre-Hospital

  • Fluid bolus often initiated in field
  • Quantify amount given by paramedics to guide further ED fluids.

Initial Stabilization/Therapy

  • ABCs for patients with altered mental status
  • Coma cocktail for AMS: Naloxone, thiamine, blood sugar
  • 0.9% NS bolus for hypotension/tachycardia

Ed Treatment/Procedures

  • Cardiac monitor and pulse oximetry for patients with abnormal vitals
  • Fluids:Average adult water deficit is 100 mL/kg (5-10 L).Initial 1-2 L bolus of 0.9% NS to restore intravascular volume over 1st hr.If corrected serum sodium is low, continue with 0.9% NS, giving 1-2 more liters over the next 2-4 hr.If corrected serum sodium is normal or elevated, use 0.45% NS giving 1-2 more liters over next 2-4 hr.Be careful to avoid fluid overload in patients with cardiac disease.Avoid precipitous falls in serum sodium/osmolality, as this may contribute to cerebral edema.Total fluid replacement should take 24-36 hr.
  • Insulin:Reverses ketogenic state and down-regulates counterregulatory hormonesAdministered as continuous IV infusion of regular insulin at 0.1 U/kg/h:Adjust infusion in response to changes in glucose and anion gapContinue until pH >7.3 and resolution of anion gapSerum glucose will fall sooner than resolution of acidosis and should be kept >250 mg/dL with glucose-containing fluids such as D5 45% NS.
  • Potassium:Administration is essential.Total body deficit of 3-5 mEq/kgWill drop precipitously with administration of fluid and insulinAdminister KCl, 10 mEq/h IV once renal function is established and K+ is known to be <5.5 mEq/L.May need to give up to 20-40 mEq/h IV in cases where initial K+ is <3.5 mEq/LIn hypokalemic patients, insulin therapy should be delayed until K+ is >3.5 mEq/L.Should measure q1-2h during 1st 4-6 hr of therapy
  • Bicarbonate:No studies have shown clinical benefit in DKA, and its routine use is not advocated.Complications include hypokalemia, alkalosis, cerebral acidosis, and edema.Some advocate its use for pH <6.9 with cardiac instability.
  • Phosphate:Not routinely replaced during initial ED therapyMay supplement if <1 mg/dL and symptomatic muscle weakness.Administer as potassium phosphate.
  • Magnesium:May supplement if <1.2 mg/dLAdminister 2 g MgSO4 IV over 1 hr.
  • Identify and treat precipitating cause.
  • Fluids:Average fluid deficit is 100 mL/kg.Initial 10-20 mL/kg bolus of 0.9% NS to restore intravascular volumeMay repeat once in severely dehydrated childrenShould not exceed 40-50 mL/kg of fluid in 1st 4 hr of therapyReplace remainder of deficit at 1.5-2 times maintenance over 24-36 hr.Overzealous fluid administration is thought to contribute to cerebral edema.
  • Cerebral edema:Occurs in 1-2% of children with DKACauses 31% of deaths associated with DKAExact causes unclearSuspect with coma, fluctuating mental status, bradycardia, HTN, severe headache, decreased urine output, or quickly falling corrected Na+ or osmolality to below normal levelsMannitol: 0.25-1 g/kg IV over 30 min should be given immediately and can be repeated hourly.Fluid rate should be decreased and other supportive measures instituted.

Medication

  • D50: 1 amp (25 g) of 50% dextrose IVP (peds: 2-4 mL/kg D25)
  • Insulin (100 U regular insulin in 100 mL NS) run at 0.1 U/kg/h
  • MgSO4: 2 g of 20% solution

Follow-Up

Disposition

Admission Criteria

  • ICU admission for pH <7, altered mental status, serious comorbid illness, and extremes of age (<2 yr or >60 yr)
  • Monitored unit for moderate DKA (pH 7.01-7.24) with CHF or cardiac history
  • General floor (nurses skilled with insulin infusions) for moderate DKA without comorbidities
  • Observation unit (<23 hr admission) for mild DKA (pH 7.25-7.30) without precipitating illness

Discharge Criteria

  • Resolution of anion gap acidosis
  • Tolerating PO fluids
  • No evidence of precipitating event
  • Clear instructions on home insulin regimen
  • Close primary care follow-up arranged

Pearls and Pitfalls

  • Decreasing or discontinuing insulin drip when glucose normalizes is a pitfall. Insulin should only be stopped when pH improves and anion gap normalizes.
  • Failure to replete potassium is a pitfall.

Additional Reading

  • Goyal N, Miller JB, Sankey SS, et al. Utility of initial bolus insulin in the treatment of diabetic ketoacidosis. J Emerg Med. 2010;38(4):422-427.
  • Kitabchi AE, Umpierrez GE, Murphy MB, et al.; American Diabetes Association. Hyperglycemic crises in diabetes. Diabetes Care. 2004;27(suppl 1):S94-S102.
  • Nyenwe EA, Kitabchi AE. Evidence-based management of hyperglycemic emergencies in diabetes mellitus. Diabetes Res Clin Pract. 2011;94(3):340-351.

See Also (Topic, Algorithm, Electronic Media Element)

Hyperosmolar Syndrome

Codes

ICD9

  • 250.10 type II diabetes mellitus [non-insulin dependent type] [NIDDM type] [adult-onset type] or unspecified type, not stated as uncontrolled, with ketoacidosis
  • 250.11 type I diabetes mellitus [insulin dependent type] [IDDM] [juvenile type], not stated as uncontrolled, with ketoacidosis
  • 250.12 Diabetes with ketoacidosis, type II or unspecified type, uncontrolled
  • 250.13 Diabetes with ketoacidosis, type I [juvenile type], uncontrolled
  • 250.1 Diabetes with ketoacidosis

ICD10

  • E10.10 Type 1 diabetes mellitus with ketoacidosis without coma
  • E10.11 Type 1 diabetes mellitus with ketoacidosis with coma
  • E13.10 Oth diabetes mellitus with ketoacidosis without coma
  • E13.11 Oth diabetes mellitus with ketoacidosis with coma
  • E10.1 Type 1 diabetes mellitus with ketoacidosis
  • E13.1 Other specified diabetes mellitus with ketoacidosis

SNOMED

  • 420422005 ketoacidosis in diabetes mellitus (disorder)
  • 420270002 Ketoacidosis in type I diabetes mellitus (disorder)
  • 421750000 Ketoacidosis in type II diabetes mellitus (disorder)
  • 111556005 Diabetic ketoacidosis without coma