Rosen & Barkin's 5-Minute Emergency Medicine Consult (206 page)

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Authors: Jeffrey J. Schaider,Adam Z. Barkin,Roger M. Barkin,Philip Shayne,Richard E. Wolfe,Stephen R. Hayden,Peter Rosen

Tags: #Medical, #Emergency Medicine

BOOK: Rosen & Barkin's 5-Minute Emergency Medicine Consult
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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 turgor
    • Dry mucous membranes
  • Odor of ketones on breath
  • Diffuse abdominal tenderness
ESSENTIAL WORKUP
  • Diagnostic criteria:
    • pH <7.3 with ketonemia
    • Bicarbonate <15 mEq/L
    • Glucose >250 mg/dL
  • Bedside glucose measurement
  • Venous blood gas
  • Urine dip for ketones
  • Serum electrolytes, glucose, BUN/creatinine
  • Search for precipitating cause
DIAGNOSIS TESTS & NTERPRETATION
Lab
  • Serum glucose measurement:
    • Confirm bedside test.
  • Electrolyte measurement:
    • Increased anion gap metabolic acidosis: [Na – (Cl + HCO
      3
      )] >12
    • Sodium:
      • 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/kg
      • As acidosis improves, for every 0.1 increase in the pH, serum potassium decreases 0.5 mEq/L.
      • Can drop precipitously with insulin and fluids
    • Bicarbonate:
      • Usually <15 mEq/L
      • May 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, glucosuria
    • Pregnancy (UhCG)
  • Venous blood gas:
    • Essential to assess patient’s 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
  • CBC:
    • Leukocytosis may be present without infection.
    • If left shift in differential, suspect infection.
  • Other lab tests:
    • Amylase: Elevation is nonspecific in DKA
    • Lipase: Elevation specific for pancreatitis
    • Calcium, 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:
    • A
      lcoholic ketoacidosis
    • C
      arbon monoxide/cyanide
    • A
      spirin
    • T
      oluene
    • M
      ethanol
    • U
      remia
    • D
      iabetic ketoacidosis
    • P
      araldehyde
    • I
      ron/isoniazid
    • L
      actic acidosis
    • E
      thylene glycol
    • S
      tarvation/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 hormones
    • Administered as continuous IV infusion of regular insulin at 0.1 U/kg/h:
      • Adjust infusion in response to changes in glucose and anion gap
    • Continue until pH >7.3 and resolution of anion gap
    • Serum glucose will fall sooner than resolution of acidosis and should be kept >250 mg/dL with glucose-containing fluids such as D
      5
      45% NS.
  • Potassium:
    • Administration is essential.
    • Total body deficit of 3–5 mEq/kg
    • Will drop precipitously with administration of fluid and insulin
    • Administer 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/L
    • In 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 therapy
    • May supplement if <1 mg/dL and symptomatic muscle weakness.
    • Administer as potassium phosphate.
  • Magnesium:
    • May supplement if <1.2 mg/dL
    • Administer 2 g MgSO
      4
      IV over 1 hr.
  • Identify and treat precipitating cause.
Pediatric Considerations
  • Fluids:
    • Average fluid deficit is 100 mL/kg.
    • Initial 10–20 mL/kg bolus of 0.9% NS to restore intravascular volume
    • May repeat once in severely dehydrated children
    • Should not exceed 40–50 mL/kg of fluid in 1st 4 hr of therapy
    • Replace 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 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.
MEDICATION
  • D
    50
    : 1 amp (25 g) of 50% dextrose IVP (peds: 2–4 mL/kg D
    25
    )
  • Insulin (100 U regular insulin in 100 mL NS) run at 0.1 U/kg/h
  • MgSO
    4
    : 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.

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