Diabetic Ketoacidosis

Michele Ritter, M.D.

Argy Resident February, 2007
 Diabetic Ketoacidosis (DKA)
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
In type II diabetics with insulin deficiency/dependence
The presenting symptom for ~ 25% of Type I Diabetics.
Hyperosmolar Hyperglycemic State
(HHS)
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
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

Plasma glucose > 250 > 250 > 250 > 600
(mg/dL)
Arterial pH 7.25-7.30 7.00-7.24 < 7.00 > 7.30

Sodium Bicarbonate 15 18 10 - <15 < 10 > 15

(mEq/L)
Urine Ketones Positive Positive Positive Small

Serum Ketones Positive Positive Positive Small

Serum Osmolality Variable Variable Variable > 320

(mOsm/kg)
Anion Gap > 10 > 12 > 12 variable

Mental Status Alert Alert/Drowsy Stupor/Coma Stupor/Coma

Causes of DKA/HHS
Stressful precipitating event that results in increased
catecholamines, cortisol, glucagon.
Infection (pneumonia, UTI)
Alcohol, drugs
Stroke
Myocardial Infarction
Pancreatitis
Trauma
Medications (steroids, thiazide diuretics)
Non-compliance with insulin
Symptoms of DKA/HHS
Polyuria
Polydypsia
Blurred vision
Nausea/Vomiting
Abdominal Pain
Fatigue
Confusion
Obtundation
Physical Examination in DKA/HHS
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
Chemistry CBC
Glucose Leukocytosis (possible
Bicarbonate infection)
Anion gap = (Na+) (Cl- + HCO3-) Amylase/Lipase
Frequently seen: To evaluate for pancreatitis
BUN/creatinine (dehydration) BUT, DKA by itself can also
potassium increase them!
sodium EKG
Pseudohyponatremia: to correct, add
1.6 mEq of sodium to every 100mg/dL
Evaluate for possible MI
of glucose above normal
Serum acetones
Positive in DKA; Possibly small in HNS
Urinalysis
Ketones (for DKA); leukocyte esterase,
WBC (for UTI)
Treatment of DKA
HYDRATION!!!
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 NS until insulin drip is
stopped
Insulin
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
Every 1 hour initially, then every 2 hours, and so on.
Serial Electrolytes
Potassium repletion
Should add potassium to IV fluids once potassium < 5
Treatment of HHS
Hydration!!!
Even more important than in DKA
Find underlying cause and treat!
Insulin drip
Should be started only once aggressive hydration has
taken place.
Switch to subcutaneous regimen once glucose < 200
and patient eating.
Serial Electrolytes
Potassium replacement.
Possible Complications of DKA
Hypophosphatemia
Occurs after aggressive hydration/treatment
Monitor phosphorus and replete as needed to keep > 1
Cerebral edema
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
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.)
Physical Exam:
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.)
Labs: WBC: 14.3
Sodium: 130 Hgb: 13.9
Potassium: 5.9 Hct: 42
Chloride: 102 Platelets: 291
Bicarbonate: 18 Urinalysis:
BUN: 38
Trace ketones
Trace blood
Cr: 1.9 Leuk. Est: 4 +
Glucose: 602 WBC > 50
Case # 1
What does this patient have?
How should you acutely treat this patient?
What other tests would you send?
What do you do when the patients glucose
falls below 200?
Question #2
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:
Glucose: 1075 mg/dL Serum bicarbonate: 4.5 mEq/L
Potassium: 3.8
ABG: pH 6.90, PCO2: 23 mm Hg
Question # 2(cont.)
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
patients pH increases to 7.10. However, she
suddenly develops respiratory failure
followed by cardiac arrest.
Question # 2 (cont.)
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.