Diabetic Ketoacidosis and

Hyperosmoler Hyperglicemic
State

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.

PATHOGENESIS
Glucose

Hyperglycemia
Glycosuria
Osmotic
Diuresis

Ketones

Ketoacidosis
is a state of
uncontrolled catabolism
associated with
insulin deficiency.
Fluid & Electrolyte
Depletion
Renal Hypoperfusion

Impaired Excretion of
Ketones & Hydrogen ions

Acidosis

Vomiting

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)DKA
Fruity odor to breath (due to acetone)
Dry mucus membranes
Confusion
Abdominal tenderness

Diagnostic Studies in DKA/HHS

Chemistry

Glucose
Bicarbonate
Anion gap = (Na+) (Cl- + HCO3-)
Frequently seen:

Serum acetones

BUN/creatinine (dehydration)
potassium
sodium
Pseudohyponatremia: to correct, add
1.6 mEq of sodium to every 100mg/dL
of glucose above normal

Positive in DKA; Possibly small in HNS

Urinalysis

Ketones (for DKA); leukocyte esterase,

WBC (for UTI)

CBC

Amylase/Lipase

Leukocytosis (possible
infection)
To evaluate for pancreatitis
BUT, DKA by itself can also
increase them!

EKG

Evaluate for possible MI

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

Treatment of DKA

HYDRATION!!!

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

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

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!!!

Find underlying cause and treat!

Insulin drip

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

Potassium replacement.

Potassium (1)

Despite total-body potassium depletion, mild to

moderate hyperkalemia is not uncommon in
pts with hyperglycemic crises. Insulin therapy,
correction of acidosis, and volume expansion
decrease serum potassium concentration.
To prevent hypokalemia, potassium
replacement is initiated after serum levels fall
below 5.5 mEq/l, assuming the presence of
adequate urine output.

Potassium (2)

Generally, 2030 mEq potassium (2/3 KCl and

1/3 KPO4) in each liter of infusion fluid is
sufficient to maintain a serum potassium
concentration within the normal range of 45
mEq/l.
Rarely, DKA pts may present with significant
hypokalemia. In such cases, potassium
replacement should begin with fluid therapy,
and insulin treatment should be delayed until
potassium concentration is restored to >3.3
mEq/l to avoid arrhythmias or cardiac arrest
and respiratory muscle weakness.

Bicarbonate (1)

Bicarbonate use in DKA remains controversial.

At a pH >7.0, reestablishing insulin activity
blocks lipolysis and resolves ketoacidosis
without any added bicarbonate. Prospective
randomized studies have failed to show either
beneficial or deleterious changes in morbidity
or mortality with bicarbonate therapy in DKA
with pH between 6.9 and 7.1.
No prospective randomized studies concerning
the use of bicarbonate in DKA with pH values
<6.9 have been reported.

Bicarbonate (2)

Given that severe acidosis may lead to a myriad

of adverse vascular effects, it seems prudent that
for adult pts with a pH <6.9, 100 mmol sodium
bicarbonate be added to 400 ml sterile water and
given at a rate of 200 ml/h.
In pts with a pH of 6.97.0, 50 mmol sodium
bicarbonate is diluted in 200 ml sterile water and
infused at a rate of 200 ml/h.
No bicarbonate is necessary if pH is >7.0.

Possible Complications of DKA

Hypophosphatemia

Cerebral edema

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