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Diabetes in the Emergency Department:
Acute Care of Diabetes Patients
Candace D. McNaughton, MD, Wesley H. Self, MD, and Corey Slovis, MD
D
iabetes is a common condition, afflicting > 20% of
the American population
over the age of 60 years.1 Patients
with diabetes, particularly those
with lower socioeconomic status
or limited access to primary care,
frequently seek care in hospital
emergency departments.2–6 This
article will review the most common
and immediately life-threatening
diabetes-related complications seen
in emergency departments: diabetic
ketoacidosis (DKA), hyperglycemic hyperosmolar state (HHS), and
hypoglycemia. It will also address the
evaluation of patients with hyperglycemia and no previous diagnosis of
diabetes.
Hyperglycemic Crisis: DKA and HHS
DKA is responsible for > 110,000
hospitalizations annually in the
United States, with mortality ranging
from 2 to 10%.7–9 HHS is much less
common but confers a much greater
mortality.10 In both diseases, mortality is largely related to underlying
comorbidities such as sepsis.11
Clinical presentation
DKA and HHS are characterized by
absolute or relative insulin deficiency,
which prevents the body from metabolizing carbohydrates and results
in severe hyperglycemia. As blood
glucose levels rise, the renal glucose
threshold is overwhelmed, and urine
becomes more dilute, leading to polyuria, dehydration, and polydipsia.
Patients with DKA classically
present with the triad of uncon-
CLINICAL DIABETES • Volume 29, Number 2, 2011
trolled hyperglycemia, metabolic
acidosis, and increased total body
ketone concentration. On the other
hand, HHS is defined by altered
mental status caused by hyperosmolality, profound dehydration, and
severe hyperglycemia without significant ketoacidosis (Table 1).9,12
Initial evaluation
Patients with severe hyperglycemia
should immediately undergo assessment and stabilization of their airway
and hemodynamic status. Naloxone,
to reverse potential opiate overdose,
should be considered for all patients
with altered mentation. Thiamine,
for acute treatment of Wernicke’s
encephalopathy, should be considered
in all patients with signs of malnutrition. In cases requiring intubation,
the paralytic succinylcholine should
not be used if hyperkalemia is suspected; it may acutely further elevate
potassium.
Immediate assessment also
includes placing patients on a carIN BRIEF
This article reviews the most
common and immediately lifethreatening diabetes-related
conditions seen in hospital
emergency departments: diabetic
ketoacidosis, hyperglycemic
hyperosmolar state, and hypoglycemia. It also addresses the
evaluation of patients with
hyperglycemia and no previous
diagnosis of diabetes.
diac monitor and oxygen as well as
obtaining vital signs, a fingerstick
glucose, intravenous (IV) access, and
an electrocardiogram to evaluate for
arrhythmias and signs of hyper- and
hypokalemia.
The differential diagnosis for
hyperglycemic crisis includes the
“Five I’s”: infection, infarction,
infant (pregnancy), indiscretion
(including cocaine ingestion), and
insulin lack (nonadherence or
inappropriate dosing). In addition
to clinical history and physical
examination, diagnostic tests should
include a venous blood gas,13–15
complete blood count, basic metabolic panel, and urinalysis; a urine
pregnancy test must be sent for all
women with childbearing potential.
Critically ill patients should
undergo additional testing as clinically indicated, including a complete
metabolic panel, serum osmolality, phosphate, lactate, and cardiac
markers for older patients. A urine
drug screen, blood alcohol level, and
aspirin and acetaminophen levels
should be sent for any patient with
unexplained DKA and all patients
with HHS. Evaluation for infection
or injury should be guided by history and the physical examination.
Effective serum osmolality should
be calculated (Table 1). The corrected serum sodium is estimated by
decreasing measured serum sodium
by 1.6 mEq/L for every 100 mg/dl
increase in blood glucose over a
baseline of 100 mg/dl16,17; for every
100 mg/dl increment increase in
51
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Table 1. Diagnosis of HHS and DKA
Plasma
glucose
(mg/dl)
Venous or
arterial pH
Serum
bicarbonate
(mEq/L)
Urine or serum
ketones*
Effective
serum
osmolality**
(mOsm/kg)
Anion
gap***
Mental status
Mild
DKA
> 250
7.25–7.30
15–18
Positive
Variable
> 10
Alert
Moderate
DKA
> 250
7.00 to < 7.24
10–15
Positive
Variable
> 12
Alert/drowsy
Severe
DKA
> 250
< 7.00
< 10
Positive
Variable
> 12
Stupor/coma
HHS
> 600
> 7.3
> 18
Small
> 320
Variable
Stupor/coma
By nitroprusside reaction method.
Effective serum osmolality: 2[measured Na+(mEq/L)] + [glucose (mg/dl)]/18 + [blood urea nitrogen (mg/dl)/2.8].
***
Anion gap: [Na+(mEq/L) – [(Cl–mEq/L)+ HCO3(mEq/L)].
Adapted from refs. 11 and 13.
*
**
blood glucose > 400 mg/dl, measured
serum sodium is decreased by an
additional 4 mEq/L.18
Although DKA and HHS share
some similar features, they should
be treated as distinct clinical entities
with different etiologies and treatments. Patients with DKA require
insulin to reverse their ketoacidosis.
Patients with HHS require fluid
resuscitation first and foremost; they
may or may not require insulin, and
those who do rarely require a continuous infusion. An algorithm for
the initial evaluation and treatment
of patients with DKA can be found
in Figure 1.
Intravenous Fluid
Critically ill patients with severe
hyperglycemia resulting from DKA
or HHS should be treated immediately with a bolus of normal saline.11,19
The average fluid deficit for patients
with DKA is 3–5 liters; fluid resuscitation in young, otherwise healthy
patients should begin with a rapid
bolus of 1 liter of normal saline followed by an infusion of normal saline
at 500 ml/hour for several hours.11,19–21
52
Patients with HHS are often
severely dehydrated, with cumulative fluid deficits of 10 liters or
more. However, because they tend
to be older and sicker, they require
careful resuscitation. Expert opinion advocates for a rapid bolus of
250 ml of normal saline repeated
as needed until the patient is well
perfused.19,22,23 Fluid therapy is then
continued at a rate of 150–250 ml/
hour based on cardiopulmonary
status and serum osmolality.23–25
The choice and rate of IV fluid
for patients with DKA who are not
critically ill should be based on their
corrected serum sodium and overall
fluid status. While awaiting laboratory study results, most of these
patients may be given a bolus of 500
ml of normal saline.11,19 Patients with
mild to moderate DKA should be
given normal saline at 250 ml/hour;
those with an elevated corrected
serum sodium should be given halfnormal saline at 250 ml/hour.26
Insulin therapy
Critically ill patients with DKA
should be given a loading dose of
regular insulin at 0.1 units/kg body
weight to a maximum of 10 units
followed by an infusion of regular
insulin at 0.1 units/kg body weight/
hour, to a maximum of 10 units/
hour.11,19 Other doses and routes of
insulin administration have been
studied,27–29 but these have not been
evaluated outside of the research setting or in critically ill patients.11
Less seriously ill patients with
DKA should be given an infusion
of regular insulin at 0.1 units/kg
body weight/hour without a loading dose to minimize the risk of
hypoglycemia. Insulin should not be
started until hypovolemia has been
addressed and serum potassium has
been confirmed to be > 3.5 mEq/L.
Giving insulin to patients with a
serum potassium level < 3.5 mEq/L
may precipitate life-threatening
arrhythmias.
Expert opinion regarding the use
of insulin for patients with HHS is
mixed.11,19,22 Because some patients
with HHS achieve euglycemia with
fluid resuscitation alone,30 and given
the theoretical risks of precipitating oliguric renal failure or cerebral
edema in inadequately fluid-resuscitated patients,22 insulin should not
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Figure 1. Initial evaluation and treatment of DKA in the emergency department.
*Laboratory studies: complete blood count, basic metabolic panel, venous blood
gas, urinalysis, urine pregnancy test if female and childbearing age. If critically ill
or clinically indicated: complete metabolic panel, serum osmolality, phosphate, lactate, cardiac markers, urine drug screen, blood alcohol level, chest X-ray, or other
imaging studies. Calculate effective serum osmolality and corrected serum sodium.
Signs of critical illness include 1) altered mental status: 2) signs of hypoperfusion;
3) significant derangement in heart rate, blood pressure, respiratory rate, temperature, or oxygen saturation; or 4) signs of severe acidosis such as marked Kussmaul
respirations. BMP, basic metabolic panel; BP, blood pressure; ECG, electrocardiogram; HR, heart rate; hyperK, hyperkalemia; IVF, IV fluids; IVP, IV push; NS,
normal saline; O2, oxygen; O2 sat, oxygen saturation; pt, patient; RR, respiratory
rate; SC, subcutaneous; temp, temperature; VBG, venous blood glucose.
be given as part of initial therapy.31–33
However, if the patient’s serum glucose does not decrease by 50–70 mg/
dl per hour despite appropriate fluid
management, a bolus of IV regular
insulin at 0.1 units/kg body weight to
a maximum of 10 units may be given.
Electrolyte replacement
Patients with DKA or HHS experience rapid shifts in potassium during
CLINICAL DIABETES • Volume 29, Number 2, 2011
resuscitation that may trigger lifethreatening arrhythmias. Death
during initial resuscitation of patients
with DKA is usually caused by
hyperkalemia, whereas hypokalemia
is the most common cause of death
after treatment has been initiated.
Therefore, serum potassium should
be checked every 2 hours until it has
stabilized in all patients with hyper-
glycemic crisis, and these patients
should remain on a cardiac monitor.
Guidelines for the treatment of hyperkalemia and hypokalemia in patients
with hyperglycemic crisis based on
expert opinion and our clinical experience are found in Table 2.
Many critically ill patients with
DKA manifest hypophosphatemia during resuscitation. To avoid
potential cardiac and skeletal muscle
weakness and respiratory depression from hypophosphatemia, a
serum phosphate of < 1.5 mg/dl
should be repleted with K2PO4 at 0.5
ml/hour.34 No studies have evaluated
replacement of phosphate in HHS,
but critically ill patients with HHS
should have their phosphate monitored and replaced appropriately.
Bicarbonate should not be used
routinely in the treatment of DKA or
HSS.19 Expert opinion suggests that
it may be used in patients with DKA
and severe acidosis (pH < 6.9) or in
patients with severe hyperglycemia
who present with a wide-complex
or disorganized cardiac rhythm
thought to be caused by hyperkalemia. Several small studies have
shown no improvement in mortality
when bicarbonate is used in patients
with a pH > 6.9.35 Additionally,
bicarbonate may prolong hypokalemia,36 has been associated with
longer hospitalizations,37 and is
thought to cause paradoxical acidosis of the cerebral spinal fluid and
decrease oxygen tissue delivery.22
In children, its use has been associated with increased risk of cerebral
edema.38
Continued evaluation and treatment
All patients with hyperglycemic
crisis require fingerstick glucose
measurements hourly until they have
stabilized. In patients with DKA, an
additional bolus of regular insulin
at 0.14 units/kg body weight by IV
administration should be given if the
blood glucose level does not decrease
53
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Table 2. Replacement Thresholds for Potassium in Hyperglycemic Crisis
Serum potassium (mEq/L)
Action
> 5.3
No additional potassium; recheck in 1 hour
4.0–5.3
Add KCl 10 mEq/L/hour to IV fluids
3.5 to < 4.0
Add KCl 20 mEq/L/hour
< 3.5
Hold insulin
Add KCl 20–60 mEq/L/hour
Continuous cardiac monitoring
by 10% in the first hour; the continuous infusion of regular insulin should
then resume at the original dose.
For patients with DKA, dextrose
should be added to the continuous
IV fluids once blood glucose has
decreased to < 250 mg/dl. Patients
with HHS whose blood glucose level
decreases to < 300 mg/dl should be
observed closely for signs of oliguric renal failure and cardiovascular
collapse; these patients may require
the addition of dextrose to IV fluids,
even without administration of
insulin.
In the treatment of DKA, expert
opinion recommends continuing an
insulin infusion until acidosis has
resolved and an anion gap is no longer present, but there are no formally
endorsed criteria for discontinuing
insulin. When converting to subcutaneous insulin, a subcutaneous
dose should be given 1 hour before
stopping the IV infusion to prevent
rebound hyperglycemia.11,19 Each
institution should devise a standard
protocol to provide consistent care
for its patients.39
Patients with DKA or HHS rarely
meet criteria to be safely discharged
from emergency departments.1 These
patients typically require admission
to the hospital with hourly blood
glucose and neurological checks
until they have stabilized.
Hypoglycemia Emergencies
A definitive diagnosis of hypoglycemia requires Whipple’s triad:
54
symptoms consistent with hypoglycemia, low blood glucose, and
resolution of symptoms once blood
glucose levels normalize.40 In practice,
hypoglycemia is generally defined as
a blood glucose level < 60 mg/dl.31,41
Severe hypoglycemia, requiring the
assistance of another person to regain
euglycemia, can cause significant
morbidity, particularly in the chronically ill or elderly; it is the cause of
death in ~ 3% of insulin-dependent
diabetic patients.42
Iatrogenic hypoglycemia is
often the limiting factor in glycemic management of diabetes.43–46
In the landmark Diabetes Control
and Complications Trial,42 27% of
patients with type 1 diabetes on
intensive insulin regimens developed
severe hypoglycemia annually.
Hypoglycemia is one of the
most frequent diabetes-related
chief complaints seen in emergency departments.47 Because of
the high frequency of hypoglycemia as a cause of altered mental
status, all patients who present to
an emergency department with
altered mentation should undergo
immediate bedside blood glucose
measurement.
Oral hypoglycemic agents and insulin
as a cause of hypoglycemia
Although the differential diagnosis
for hypoglycemia includes liver
failure, severe sepsis, and renal
disease, this article will focus on the
most common cause of hypoglycemia
in patients with diabetes: the use of
insulin and oral antidiabetes medications for glycemic control.
The type and dose of medication used for glycemic control is
crucially important in determining
the risk for recurrent hypoglycemia. Biguanides such as metformin
decrease hepatic production and
intestinal absorption of glucose
and decrease the oxidation of fatty
acids. Alpha-glucosidase inhibitors
decrease postprandial absorption of
carbohydrates, and thiazolidinediones enhance the effects of insulin
without increasing its secretion.
These anti-hyperglycemic medications do not cause hypoglycemia
when used in isolation.
In contrast, sulfonylureas and
meglitinides increase insulin secretion and activity and therefore can
cause hypoglycemia.48 The half-life
for most sulfonylurea medications is
14–16 hours; they can cause severe,
prolonged hypoglycemia. Although
meglitinides have a shorter half-life,
the risk of recurrent hypoglycemia
from these medications is unknown;
experts urge caution and recommend assuming that these patients
have a high risk of recurrent
hypoglycemia.49
Treatment of hypoglycemia
As with patients who present in
hyperglycemic crisis, the initial
evaluation of patients with suspected
hypoglycemia includes securing the
airway and assessing hemodynamic
status. Altered mentation and signs of
malnutrition should prompt administration of naloxone and thiamine,
respectively. Naloxone and dextrose
may completely reverse coma and
eliminate the need for intubation;
whenever possible, they should be
given before proceeding to intubation.
Once bedside glucose measurement confirms hypoglycemia,
treatment should be accomplished
immediately with either oral intake
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Figure 2. Treatment of hypoglycemia.BG, blood glucose, IM, intramuscular; SC,
subcutaneous.
of food, IV dextrose, or intramusDextrose is the treatment of
cular glucagon. When decreased
choice for hypoglycemia. Glucagon,
mentation precludes oral intake
1 mg, may be administered subcuof food, IV dextrose is the firsttaneously or intramuscularly if IV
line therapy. One amp of dextrose
access is not available, but it requires
provides ~ 100 calories, raising
15 minutes or more for onset of
blood glucose levels for 30–60 minaction and is associated with
utes (Figure 2). The treatment for
vomiting.
hypoglycemia may have a shorter
Blood glucose levels should
duration of action than many of the
be checked hourly at a minimum.
precipitating drugs, and patients
Patients who develop recurrent
who are successfully treated initially
hypoglycemia or whose blood
may require repeat doses of glucose.
glucose levels decrease despite
Additionally, depending on the
administration of dextrose should be
cause of hypoglycemia (e.g., sulfostarted on continuous IV dextrose.
nylurea ingestion), administration
These patients require more frequent
of dextrose may precipitate rebound
hypoglycemia.
blood glucose checks—as often as
CLINICAL DIABETES • Volume 29, Number 2, 2011
every 15 minutes—and admission to
the hospital’s intensive care unit.
To prevent and treat undiagnosed Wernicke’s encephalopathy,
thiamine at 100 mg IV should be
administered to all patients who
present with altered mentation
and any signs of malnutrition.50
Despite traditional teaching to the
contrary, there is no evidence that
a dextrose load to reverse hypoglycemia without thiamine replacement
acutely precipitates Wernicke’s
encephalopathy. Therefore, when
treating a patient with altered
mental status and confirmed hypoglycemia, or possible hypoglycemia
without access to a bedside glucose
meter, dextrose should be given
immediately; thiamine should be
administered as soon thereafter as
possible. Treatment with dextrose
should not be delayed if thiamine is
not immediately available.51
Patients without seizure should
return to their baseline mental status
immediately once euglycemia is
achieved. In the case of a seizure
caused by hypoglycemia, phenytoin
is should not be considered first-line
therapy because it is known to affect
insulin secretion and action.52–54
Instead, benzodiazepines, phenobarbital, or levetiracetam may be used.55
Altered mental status that lasts > 15
minutes despite return to euglycemia
should prompt reassessment of the
patient and broadening of the differential diagnosis to include traumatic
or anoxic brain injury, stroke,
alcohol intoxication or withdrawal,
opioid ingestion, central nervous
system infection, liver failure,56 and
renal failure. If lumbar puncture
is performed, clinicians should be
aware that glucose levels in cerebral
spinal fluid remain low for several
hours after the serum blood glucose
level has been corrected.56
55
F E A T U R E
Disposition of patients
Patients who meet all of the following criteria may be considered
for discharge from the emergency
department after an episode of
hypoglycemia.31
The episode of hypoglycemia was:
• Isolated (a single episode of hypoglycemia without recurrence)
• Completely and rapidly reversed
without the need for a continuous
dextrose infusion
• The result of an identified cause
that is unlikely to cause recurrence
• Accidental
• Not caused by an oral hypoglycemic medication or long-acting
insulin
And the patient:
• Completed an uneventful 4-hour
observation period with serial
blood glucose measurements in
the normal range and not trending
downward
• Ate a full meal during the observation period
• Has no comorbidities that would
interfere with proper administration of medications and intake of
food
• Understands how to prevent future
episodes of hypoglycemia
• Can accurately monitor blood
glucose at home
• Will be with a responsible adult
who will monitor the patient
• Has close, reliable follow-up with a
primary care provider
Patients who meet these criteria
and are discharged from the emergency department should reduce
their insulin dose by 25% for at least
the next 24 hours to reduce the risk
of recurrent hypoglycemia.
Many states require that patients
with symptomatic hypoglycemia
refrain from driving for 6–12 months
and obtain clearance from a physician before resuming driving.
56
A R T I C L E
Research has shown that this issue
is rarely addressed in the emergency
department;57 for public health and
the safety of patients, it must be
included in discharge instructions.
Patients who do not meet all of
the above discharge criteria warrant
hospital admission. Oral hypoglycemic agents and intermediate- or
long-acting forms of insulin (lente,
NPH, glargine, and ultralente) are
likely to cause recurrent hypoglycemia, and patients taking these
medications generally should be
admitted.
Patients with hypoglycemia that
cannot be completely reversed, was
caused by massive ingestion or overdose, or is associated with sepsis,
starvation, liver failure, or adrenal
insufficiency should be admitted to
the hospital’s intensive care unit.
Suicide attempts, factious disorder,
or other psychiatric illnesses should
be addressed with a psychiatric
consultation.
Patients With Undiagnosed
Prediabetes or Diabetes
Of the 23.6 million Americans
with diabetes in 2007, 5.7 million
were unaware they had the disease.
Additionally, 54 million Americans
had prediabetes (impaired fasting
glucose and impaired glucose tolerance).1 Patients who present to the
emergency department are at high
risk for undiagnosed diabetes;58 in one
study, nearly four out of five patients
in an urban emergency department
met American Diabetes Association
(ADA) criteria for diabetes
screening.59
Currently, the diagnosis of
diabetes requires testing performed
on two separate occasions unless
“unequivocal hyperglycemia” is
present.60–62 Patients with unequivocal signs of hyperglycemia such as
polyuria, polydipsia, nocturia, or
acidosis are likely to need hospital
admission, where further testing
may be performed. Using an insulin
protocol, treatment of hyperglycemia should ideally begin before
admission and should not be delayed
by confirmatory testing.63
Although hospital emergency
departments cannot offer confirmatory testing, patients who are at
high risk for prediabetes or diabetes
can be identified, and these patients
should be counseled regarding their
likely diagnosis and lifestyle interventions. A prospective cohort study
conducted in an urban emergency
department found that all patients
with risk factors for diabetes (age
> 45 years, polyuria, and polydipsia) and a random blood glucose
> 155 mg/dl were later diagnosed
with prediabetes or diabetes.63
The use of A1C as a screening
tool in emergency departments is
being studied59 but is not currently
recommended.60
Because most lifestyle interventions are initially unsuccessful,64
certain patients with extremely
high risk for undiagnosed diabetes
may be considered candidates for
initiating the anti-hyperglycemic
medication metformin in the emergency department. These patients
include those with obesity, family
history of diabetes, and polyuria
who also have a blood glucose level
> 200 mg/dl with no other obvious
cause such as trauma or infection.
Patients started on metformin in the
emergency department should be
otherwise healthy, with normal renal
function, and should have reliable,
close follow-up with a primary care
physician.
Recommendations from ADA and
the European Association for the
Study of Diabetes for initiating
therapy in patients with newly diagnosed diabetes are as follows:65
1.Begin low-dose metformin (500 mg)
once or twice daily with meals
(breakfast and/or dinner).
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2.After 5–7 days, if gastrointestinal
side effects have not occurred,
advance the dose to 850–1,000 mg
before breakfast and dinner.
3.If gastrointestinal side effects
appear as doses advance, decrease
dose to the previous lower dose and
try to advance at a later time.
4.The typical therapeutic dose is 850
mg twice daily. Higher doses, up
to 2,550 mg daily, can be used but
tend to be associated with more
significant side effects and are not
recommended as starting doses.
The most common side effects
of metformin are gastrointestinal,
including nausea, vomiting, diarrhea, and abdominal pain. Lactic
acidosis occurs in 3 per 100,000
patient-years, which is no higher
than in the general diabetic patient
population.64
Data from a before-after pilot
study66 conducted in an urban
emergency department suggest that
starting metformin in the emergency department may be safe and
effective. In this study, emergency
physicians treating patients with
hyperglycemia but no prior diagnosis of diabetes used an algorithm
that provided guidelines for starting and titrating metformin and/or
insulin. The majority of the patients
with severe hyperglycemia experienced rapid and safe decreases in
their blood glucose and A1C levels.
Emergency department visits for
patients in the intervention group
also decreased by 78% from baseline.
At a minimum, it is imperative
that patients with suspected prediabetes or diabetes be made aware
of their abnormal test results and
the need for urgent follow-up with a
primary care provider. They should
be counseled about lifestyle changes.
For select patients, starting metformin in the emergency department
may be a safe and effective initial
medical therapy. However, this
CLINICAL DIABETES • Volume 29, Number 2, 2011
A R T I C L E
area of diabetes care needs further
research and should only be considered as part of a multidisciplinary
approach that includes a protocol for
initiating diabetes medications that
was developed in conjunction with a
diabetologist.
Summary
Hypo- and hyperglycemia caused
by diabetes are commonly treated
in hospital emergency departments.
Physicians must be skilled in diagnosing and stabilizing patients with these
conditions.
Hypoglycemia related to oral
hypoglycemic medications or intermediate- and long-acting insulin
requires admission to the hospital.
DKA and HHS are best treated with
standardized protocols that specifically address electrolyte repletion,
insulin dosing, and fluid management. Mortality in both DKA and
HHS is often related to underlying
comorbidities and the precipitating
insult.
Patients with prediabetes and diabetes are frequently encountered in
emergency departments. A random
blood glucose level > 155 mg/dl in the
setting of risk factors for diabetes
should prompt a referral for a formal
evaluation for diabetes.
ACKNOWLEDGMENTS
This work was supported by the
Office of Academic Affiliations,
Department of Veterans Affairs, VA
National Quality Scholars Program,
with resources and the use of
facilities at the VA Tennessee Valley
Healthcare System in Nashville, Tenn.
(McNaughton and Self).
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Volume 29, Number 2, 2011 • CLINICAL DIABETES
F E A T U R E
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CLINICAL DIABETES • Volume 29, Number 2, 2011
A R T I C L E
Candace D. McNaughton, MD, is
a clinical instructor in Emergency
Medicine; Wesley H. Self, MD, is
an assistant professor in Emergency
Medicine; and Corey Slovis, MD,
is a professor and chairman of the
Department of Emergency Medicine
at Vanderbilt University in Nashville,
Tenn.
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