Diabetic Ketoacidosis (Dka)

Diabetic Ketoacidosis
dr.Bobi Ahmad S, S. Kep

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 ½ 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 patient’s 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
patient’s 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.

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Diabetic Ketoacidosis

dr.Bobi Ahmad S, S. Kep

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

Serum Ketones Positive Positive Positive Small

Serum Osmolality Variable Variable Variable > 320

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

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