hyperglycemic emergencies dka/honc
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Hyperglycemic EmergenciesDKA/HONC
William Harper, MD, FRCPC
Endocrinology & Metabolism
Assistant Professor of Medicine, McMaster University
DKA
A collection of severe and potentially life-threatening metabolic disturbances:
• Hyperglycemia Osmotic diuresis» Urinary loss of fluids & electrolytes
» ECFv contraction
» Depletion of total body K+ stores
(even though may be hyperkalemic 2° to cell shift)
• Ketone production Metabolic acidosis» Compensatory Respiratory alkalosis (hopefully!)
• Uncontrolled lipolysis severe TG
DKA physiology: Insulin & Lipids
DKA: Pathophysiology
Glucose
Pyruvate
Acetyl-CoA
Ketoacids
Kreb’s
+ PFKInsulin
fat cellTG
FFA
HSL
Liver Cell
FattyAcyl-CoA
Insulin -
VLDL (TG)
GlucagonInsulin
+
+
DKA: Pathophysiology
Glucose
Pyruvate
Acetyl-CoA
Ketoacids
Kreb’s
+ PFKInsulin
fat cellTG
FFA
HSL
Liver Cell
FattyAcyl-CoA
Insulin -
VLDL (TG)
GlucagonInsulin
+
+
DKA risk factors
• T1DM• 1st presentation• Acute-illness• Insulin omission (inappropriate sick-day management,
noncompliance, Eating Disorders)
• T2DM• During stress• Ethnicity: African-American, Hispanic
• Extremes of age• Poor glycemic control• MDI with CSII
DKA: Precipitating Factors
Acute illness(MI, GIB, trauma,pancreatitis)
New-onset DM
Insulin omission
Infections
10-20%
5-39%
33%
20-38%
DKA: Diagnosis
• Symptoms & Signs:• Polyuria, polydipsia, weight-loss
• Fatigue
• N/V, abdominal pain ECFv, Kussmaul’s, Acetone breath, mild impairment in
cognition
• Laboratory:• pH < 7.3, serum HCO3 < 15 mEq/L, AG > 14 mM
• Raised serum ketones (and urine ketones)
• BS > 14 mM (occasionally normal or only mild BS)
DKA: Management
1. Monitoring
2. IV Fluid Resuscitation (3-9L deficit)
3. Potassium (“no pee no K”)• K+ deficit 3-5 mEq/Kg
4. IV insulin
5. Identify & Rx underlying cause• Noncompliance, infection, MI, etc.
DKA: Monitoring• Consider ICU:
• pH < 6.9, inadequate respiratory compensation• decreased LOC• Severe K+ disturbance (K+ < 3.0 or > 6.0 mEq/L)
• Stepdown/Telemetry: all others• Ward:
• Only very mild DKA!• pH > 7.2, serum HCO3 > 20, AG < 14• ECFv near normal• Not elderly, no hi-risk DKA precipitant (ex. MI)
DKA: Monitoring• CBG q1-2h on IV insulin gtt• q2h: Serum lytes, creatinine, glucose• q4-6h:
• pH > 7.2, HCO3 > 20, AG < 15• ECFv stable and IV fluids @ maintenance rates• normal K+
• Calcium profile:• Initially, then q12-24h unless abnormal• Phospate levels can be high at 1st but drop with Rx
of DKA
• Flowcharts to record biochemical parameters shown to be useful
DKA: Monitoring
• EKG, cardiac enzymes: r/o ACS (silent MI)
• Septic w/up: cultures, CXR, urinalysis, etc.
• Consider pulmonary embolism?
DKA: IV Fluids
• IV NS 0.5-1L/h x 1-2h or longer so no more tachycardia, hypotension, orthostatic changes, low JVP.
• Then change to 1/2 NS:• 200-500 cc/h over 12h in order to replace ½ estimated deficit• Then lower to 100-150 cc/h until deficit restored and
eating/drinking well
• If hypotension recalcitrant to fluids consider AI (Schmidt PGAS II) and send stat plasma cortisol and ACTH, then give solucortef 100 mg IV q8h.
DKA: Mortality
• Adults 2-4%• Hypokalemia
• MI, CVA, pneumonia, pulm. embolism, etc.
• Kids 0.2-0.4%• Cerebral edema
DKA: Potassium• K+ defecit: 3-5 mEq/Kg (350 mEq for 70Kg)• Normal to high serum K+
K+ K+
H+ H+
Ketoacidosis
Insulin
DKA: Potassium• K+ deficit 3-5 mEq/kg (350 mEq 70kg)
• Need K with initial IV fluid & insulin Rx unless:
• Anuric
• K > 5.5 mEq/L or hyperkalemic ECG changes
Initial [K] Replacement
> 5.5 mEq/L nil (initially)
5.2-5.5 mEq/L 10 mEq/h
4-5.2 mEq/L 20 mEq/h
3-4 mEq/L 30 mEq/h
< 3 mEq/L 40 mEq/h
> 20 mEq/h:Cardiac monitor
> 60 mEq/L:Central line
DKA: IV Insulin
• Might delay starting IV insulin for a few hours if K+ severely low (< 3.0 mEq/L) and metabolic acidosis not severe (pH > 7.0)
• Humulin R or Novolin Toronto• Bolus 0.1-0.2 U/kg IV• Then IV gtt @ 0.1-0.2 U/kg/h (50 U of regular insulin in 500cc D5W; 1U/10cc)• Aim is to demonstrate correction of Anion Gap (AG) and
decrease in BS 4.4 mM/L/h• Monitoring serial serum ketones NOT useful as most assays
measure Acetoacetate only:ßHß (not detected) DKA Rx Acetoacetate (detected)
DKA: IV Insulin
• Using insulin to treat 2 different and separate metabolic disturbances in DKA:
1. Ketoacidosis
2. Hyperglycemia
DKA: IV Insulin
• If AG not correcting and/or BS not decreasing then increase IV gtt rate 1.5-2X
• If BS < 13 but AG still not corrected do NOT decrease insulin IV gtt.
• Instead start IV glucose gtt:• D5W-D10W @ 100-200 cc/h
• Once AG corrected than titrate IV insulin to BS
• When BS < 13 and AG normal: reduce IV insulin gtt to 1-2 U/h and add IV glucose if not already done.
DKA: Switch to S.C. insulin
• Can consider switch to SC insulin when:• AG normalized
• BS < 15 mM
• Insulin IV gtt requirements < 2U/h
• Patient able to eat
• Overlap insulin IV gtt with 1st SC insulin by 2-4h to avoid recurrent ketosis
• T2DM patients with DKA:• Don’t necessarily have to be d/c on insulin SC (I often do!)
• Once acute stress resolved, many do well on OHA
DKA: Other Rx
• Bicarbonate• May exacerbate hypokalemia• Only give if pH < 6.9 AND evidence of cardiovascular
instability (arrythmia, CHF, hypotension)• 1-2 amps bicarb in 1L D5W IV with 10-20 mEq of added KCl
given over 2h or until pH > 7.1
• Phosphate• Routine IV not recommended• Rx symptomatic hypophosphatemia (rhabdo, unexplained
CHF or respiratory failure, severe confusion)• 10cc K Phos soln (3.0mEq Pi and 4.4 mEq K/cc) in 1L NS IV
over 8-12h
DKA: Other Rx
• Cerebral Edema• Usually only kids
• Persistent decreased LOC despite standard Rx of DKA
• CT scan to confirm diagnosis
• Decadron 10 mg IV
• Mannitol 25 mg IV
DKA: Management
1. Monitoring• ICU: pH < 6.9, severe K (< 3, > 6), decr LOC
2. IV Fluid Resuscitation (3-9L deficit)
3. Potassium (“no pee no K”)
4. IV insulin
5. Identify & Rx underlying cause• Noncompliance, infection, MI, etc.
DKA Rx: EBM
• In patients not in shock, recovery is more rapid with slower rates of IV fluids (500 mL/h x 4h, then 250 mL/h)
• RCT: Adrogue et al, 1989, JAMA: 262:2108-13
• Low-dose insulin (0.1-0.2 U/Kg bolus, then rate of 0.1-0.2 U/Kg/h) has similar rate of recovery and less hypokalemia than high-dose insulin (50-150 U/h)
• RCT: Kitabchi et al, 1976, Ann Intern Med: 84:633-8
• RCT: Heber et al, 1977, Arch Intern Med: 137:1377-80
• No clinical benefit to giving IV HCO3• RCT: Gamba et al, 1991, Rev Invest Clin: 43:234-48
• No benefit to giving IV phosphate• RCT: Fischer et al, 1983, JCEM:57:177-80
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