Medico

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Diabetic Ketoacidosis
DAVID E. TRACHTENBARG, M.D., University of Illinois College of Medicine, Peoria, Illinois

Patient information:
A handout on diabetic
ketoacidosis is provided
on page 1721.

M



any patients with diabetes
die from diabetic ketoacidosis (DKA) every year. DKA is
caused by reduced insulin levSee editorial on page
els, decreased glucose use, and increased
1659.gluconeogenesis from elevated counter reguSee related article on
latory hormones, including catecholamines,
page 1723.
glucagon, and cortisol. DKA primarily affects
See page 1635 for
patients with type 1 diabetes, but also may
strength-of-recommenoccur in patients with type 2 diabetes, and
dation labels.
is most often caused by omission of treatment, infection, or alcohol abuse.1 Use ofa
standard protocol provides consistent results
in treating DKA.2 An evidence-based guideline for the management of DKA from the
American Diabetes Association
(ADA) is the basis for much of
Patients with diabetic keto this article.3
acidosis usually present




with polyuria, polydipsia,
polyphagia, weakness, and
Kussmaul’s respirations;
nausea and vomiting are
present in 50 to 80percent
of patients.

Initial Evaluation
Initial evaluation of patients with
DKA includes diagnosis and
treatment of precipitating factors
(Table 14-18). The most common
precipitating factor is infection,
followed by noncompliance with
insulin therapy.3 While insulin pump therapy
has been implicated as a risk factor for DKA
in the past, most recent studies show that with

May 1,2005



Volume 71, Number 9

w ww.aafp.org/afp

ILLUSTRATION BY MICHAEL KRESS-RUSSICK

A diagnosis of diabetic ketoacidosis requires the patient’s plasma
glucose concentration to be above 250 mg per dL (although it usually
is much higher), the pH level to be less than 7.30, and the bicarbonate level to be 18 mEq per L or less. Beta-hydroxybutyrate is a better
measurement of the degreeof ketosis than serum ketones. Intravenous
insulin and fluid replacement are the mainstays of therapy, with careful monitoring of potassium levels. Phosphorous and magnesium also
may need to be replaced. Bicarbonate therapy rarely is needed. Infection, insulin omission, and other problems that may have precipitated
ketoacidosis should be treated. Myocardial infarction is a precipitating
causeof diabetic ketoacidosis that is especially important to look for in
older patients with diabetes. Cerebral edema is a major complication
that occurs primarily in children. Education to prevent recurrence
should be offered to all patients, including how to manage sick days
and when to call a physician. (Am Fam Physician 2005;71:1705-14,
1721-2. Copyright© 2005 American Academy of FamilyPhysicians.)
proper education and practice using the pump,
the frequency of DKA is the same for patients
on pump and injection therapy.19
DIFFERENTIAL DIAGNOSIS

Three key features of diabetic acidosis are
hyperglycemia, ketosis, and acidosis. The
conditions that cause these metabolic abnormalities overlap. The primary differential
diagnosis for hyperglycemia is hyperosmolar
hyperglycemicstate (Table 2 3,20), which is
discussed in the Stoner article21 on page 1723
of this issue. Common problems that produce
ketosis include alcoholism and starvation.
Metabolic states in which acidosis is predominant include lactic acidosis and ingestion of
drugs such as salicylates and methanol.
Abdominal pain may be a symptom of
ketoacidosis or part of the inciting cause of
DKA, such asappendicitis or cholecystitis. If
surgery is necessary, the timing needs to be
individualized for each patient with input
from a surgical consultant.
SIGNS AND SYMPTOMS

DKA can develop in less than 24 hours.3
Metabolic changes occur one and one half to
two hours earlier in patients who are managed only with a short-acting insulin such as
American Family Physician 1705

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