Transcript Diabetic Ketoacidosis

Diabetic Ketoacidosis
Michele Ritter, M.D.
Argy Resident – February, 2007
Diabetic Ketoacidosis (DKA)
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A state of absolute or relative insulin deficiency
aggravated by ensuing hyperglycemia, dehydration, and
acidosis-producing derangements in intermediary
metabolism, including production of serum acetone.
Can occur in both Type I Diabetes and Type II
Diabetes
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In type II diabetics with insulin deficiency/dependence
The presenting symptom for ~ 25% of Type I Diabetics.
Hyperosmolar Hyperglycemic State
(HHS)
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An acute metabolic complication of diabetes
mellitus characterized by impaired mental
status and elevated plasma osmolality in a
patient with hyperglycemia.
Occurs predominately in Type II Diabetics
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A few reports of cases in type I diabetics.
The presenting symptom for 30-40% of Type
II diabetics.
Diagnostic Criteria for DKA and HHS
Mild DKA
Moderate DKA
Severe DKA
HHS
> 250
> 250
> 250
> 600
7.25-7.30
7.00-7.24
< 7.00
> 7.30
Sodium Bicarbonate
(mEq/L)
15 – 18
10 - <15
< 10
> 15
Urine Ketones
Positive
Positive
Positive
Small
Serum Ketones
Positive
Positive
Positive
Small
Serum Osmolality
(mOsm/kg)
Variable
Variable
Variable
> 320
Anion Gap
> 10
> 12
> 12
variable
Mental Status
Alert
Alert/Drowsy
Stupor/Coma
Stupor/Coma
Plasma glucose
(mg/dL)
Arterial pH
Causes of DKA/HHS
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Stressful precipitating event that results in increased
catecholamines, cortisol, glucagon.
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Infection (pneumonia, UTI)
Alcohol, drugs
Stroke
Myocardial Infarction
Pancreatitis
Trauma
Medications (steroids, thiazide diuretics)
Non-compliance with insulin
Symptoms of DKA/HHS
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Polyuria
Polydypsia
Blurred vision
Nausea/Vomiting
Abdominal Pain
Fatigue
Confusion
Obtundation
Physical Examination in DKA/HHS
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Hypotension, tachycardia
Kussmaul breathing (deep, labored breaths)
Fruity odor to breath (due to acetone)
Dry mucus membranes
Confusion
Abdominal tenderness
Diagnostic Studies in DKA/HHS
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Chemistry
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 Glucose
 Bicarbonate
Anion gap = (Na+) – (Cl- + HCO3-)
Frequently seen:
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Positive in DKA; Possibly small in HNS
Urinalysis
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Ketones (for DKA); leukocyte esterase,
WBC (for UTI)
CBC
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 BUN/creatinine (dehydration)
 potassium
 sodium
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Pseudohyponatremia: to correct, add
1.6 mEq of sodium to every 100mg/dL
of glucose above normal
Serum acetones
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Leukocytosis (possible
infection)
Amylase/Lipase
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To evaluate for pancreatitis
BUT, DKA by itself can also
increase them!
EKG
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Evaluate for possible MI
Treatment of DKA
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HYDRATION!!!
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Insulin
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Insulin drip: Bolus: 0.15 units/kg, then infuse at 0.1 mg/kg/hr
Ideally should decrease glucose 50-100 mg/dL per hour
In DKA: Change to subcutaneous regimen once anion gap has closed and
patient is ready to eat.
Need to give long-acting insulin dose several hours prior to stopping insulin
drip.
Accuchecks
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Normal Saline – 500-1000 cc/hr for 4 hours, then 250 – 500 cc/hr for 4 hours,
then 125-250 cc/hr
Once glucose is < 200, should change fluids to D5 ½ NS until insulin drip is
stopped
Every 1 hour initially, then every 2 hours, and so on.
Serial Electrolytes
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Potassium repletion
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Should add potassium to IV fluids once potassium < 5
Treatment of HHS
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Hydration!!!
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Find underlying cause and treat!
Insulin drip
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Even more important than in DKA
Should be started only once aggressive hydration has
taken place.
Switch to subcutaneous regimen once glucose < 200
and patient eating.
Serial Electrolytes
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Potassium replacement.
Possible Complications of DKA
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Hypophosphatemia
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Cerebral edema
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Occurs after aggressive hydration/treatment
Monitor phosphorus and replete as needed to keep > 1
Rare, but life threatening
Usually in pediatric, adolescent patients
Symptoms: Headache, altered mental status
Treat with mannitol, hyperventilation
Myocardial infarction, DVT/PE, cardiac dysrhythmias
Case # 1
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A 72-year old female with a history of
diabetes mellitus, hypertension, GERD and
obstructive sleep apnea, presents to the
emergency room with nausea/vomiting and
lethargy. Patient states that she skipped “a
few” doses of her lantus, but has otherwise
been good about her insulin. She admits to
blurred vision, and some mild abdominal
discomfort.
Case # 1 (cont.)
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Physical Exam:
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38.1, 110/78, 110, 22, 99% on RA
Gen: Obese female, alert and oriented x 3; in NAD
HEENT: very dry mucus membranes
CV: RRR
Resp: LCTA bilaterally
Abd: soft, mildly tender diffusely, no rebound/guarding
Ext: no LE edema
Case # 1 (cont.)
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Labs:
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Sodium: 130
Potassium: 5.9
Chloride: 102
Bicarbonate: 18
BUN: 38
Cr: 1.9
Glucose: 602
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WBC: 14.3
Hgb: 13.9
Hct: 42
Platelets: 291
Urinalysis:
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Trace ketones
Trace blood
Leuk. Est: 4 +
WBC > 50
Case # 1
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What does this patient have?
How should you acutely treat this patient?
What other tests would you send?
What do you do when the patient’s glucose
falls below 200?
Question #2
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A 32-year old woman is admitted to the
hospital in a semi-comatose, volume-depleted
state, exhibiting marked air hunger. She has
had type 1 diabetes mellitus for 12 years and
ran out of insulin 3 days ago.
Labs:
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Glucose: 1075 mg/dL Serum bicarbonate: 4.5 mEq/L
Potassium: 3.8
ABG: pH 6.90, PCO2: 23 mm Hg
Question # 2(cont.)
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After 4 hours of treatment that includes
standard doses of insulin (10 units/h) fluids,
intravenous potassium chloride (10 mEq/L)
plus 150 meq/L of sodium bicarbonate, the
patient’s pH increases to 7.10. However, she
suddenly develops respiratory failure
followed by cardiac arrest.
Question # 2 (cont.)
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What is the most likely therapeutic misjudgement?
(A) She was given too much potassium chloride and had suppression of
all cardiac pacemaker activity.
(B) She was given too little potassium chloride and developed respiratory
muscle paralysis followed by ventricular fibrillation.
(C) She was given too little insulin in the face of an unusually high
plasma glucose concentration and developed cerebral edema.
(D) She was given too much bicarbonate, which led to cerebrospinal fluid
acidosis and suppression of the brain stem respiratory center.
(E) She should have been given her potassium as potassium phosphate in
order to prevent respiratory muscle paralysis from hypophosphatemia
caused by insulin administration.