AACN Advanced Critical Care
Volume 24, Number 3, pp.314-324
Acute Diabetes Management
Adult Patients With Hyperglycemic Crises and
Hypoglycemia
Faith Pollock, RN, MSN, ACNS-BC, CDE
Donna C. Funk, RN, MAEd, NP, CDE, BC-ADM
ABSTRACT
In acute diabetes conditions, management of
the following 3 potential complications is
required: diabetic ketoacidosis, hyperosmolar
hyperglycemic state, and iatrogenic hypogly-
cemia. The hyperglycemic crises diabetic
ketoacidosis and hyperosmolar hyperglycemic
state are the 2 most serious metabolic com-
plications of diabetes. Hypoglycemia, specifi-
cally iatrogenic hypoglycemia, results from
treatments that raise circulating insulin levels
I n acute diabetes, management of the following
3 potential complications is required: diabetic
ketoacidosis (DKA), hyperosmolar hyperglyce-
mic state (HHS), and iatrogenic hypoglycemia.
Hyperglycemic crises (DKA and HHS) are the
2 most serious metabolic complications of dia-
betes. The triad of severe hyperglycemia, meta-
bolic acidosis, and increased total body ketone
concentration characterizes DKA. Severe hyper-
glycemia, hyperosmolality, and dehydration
with no significant ketoacidosis characterize
HHS. Both metabolic imbalances occur as a
result of absolute and/or relative insulin defi-
ciency and an increase of counterregulatory hor-
mones (glucagon, catecholamines, cortisol, and
growth hormone). Diabetic ketoacidosis is clas-
sified as mild, moderate, or severe on the basis
of the severity of metabolic acidosis (blood pH,
bicarbonate, and ketones). Patients with type 1
diabetes are more likely to have DKA, but
patients with type 2 diabetes also can be at risk
with the catabolic stress of acute illness, such as
infections, surgery, or trauma. Hyperosmolar
hyperglycemic state is not classified by levels of
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NCI200282.indd 314
© 2013 AACN
and thus lower plasma glucose concentra-
tions to an abnormally low level, which exposes
the patient to potential harm. This article
reviews the pathogenesis, precipitating or risk
factors, diagnosis or identification, and treat-
ment of these critical complications of diabetes.
In addition, a case study on diabetic ketoaci-
dosis is provided.
Keywords: diabetes, hyperglycemia, hypo-
glycemia, ketoacidosis
severity, and it clinically presents with less
ketosis and greater hyperglycemia than DKA.1
Patients with moderate or severe DKA and HHS
are usually admitted to the critical care unit.
Among adults with diabetes, hyperglycemic
crises accounted for 16.2 emergency depart-
ment visits per 1000 adults with diabetes in
20092 and were similar between men and
women.3 Hospital discharges with DKA diag-
nosis increased by 57% from 1988 to 2009,4
and of these discharges, rates were higher
among people younger than 45 years.5 Fortu-
nately, hyperglycemic crisis as the underlying
cause of death declined in all age groups from
1980 to 2009 per 100 000 people with diabe-
tes, with the largest decrease occurring among
Faith Pollock is Diabetes Clinical Nurse Specialist, Allina
Health, Abbott Northwestern Hospital, 800 E 28th St, Minne-
apolis, MN 55407 (faith.pollock@allina.com).
Donna C. Funk is Diabetes Clinical Nurse Specialist, Borgess
Medical Center, Kalamazoo, Michigan.
The authors declare no conflicts of interest.
DOI: 10.1097/NCI.0b013e31829b7d38
7/13/13 2:11 PM
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those aged 75 years or older. The oldest age
group had the highest death rates from hyper-
glycemic crises at the beginning of the study
period, but the rates steadily declined at the
study end to become lower than the rates of
the youngest age group.6
Hypoglycemia, specifically iatrogenic hypo-
glycemia, results from treatments that raise cir-
culating insulin levels and thus lower plasma
glucose concentrations to an abnormally low
level, which exposes the patient to potential
harm.7,8 Hypoglycemia in diabetes cannot be
defined as a single threshold value for plasma
glucose concentration, because symptoms asso-
ciated with hypoglycemia shift to lower plasma
glucose concentrations after a recent hypoglyce-
mic event or to higher plasma glucose concentra-
tions for patients with poorly controlled diabetes
who experience infrequent hypoglycemia.8 In
2013, the American Diabetes Association
Workgroup on Hypoglycemia suggested classi-
fying hypoglycemia in diabetes as (1) severe
hypoglycemia, (2) documented symptomatic
hypoglycemia, (3) asymptomatic hypoglyce-
mia, (4) probable symptomatic hypoglycemia,
and (5) pseudohypoglycemia (see Table 1).8
Among hospitalized patients with diabetes,
the true incidence and prevalence of hypogly-
cemia are not known. In 2007, a retrospec-
tive study of 31 970 patients admitted to
general wards of an academic medical center
identified that 3349 patients (10.5%) had at
least 1 episode of hypoglycemia (blood glu-
cose ≤70 g/dL).9 In another review of 5365
inpatients admitted to intensive care units, 102
(1.9%) had at least 1 episode of severe hypo-
glycemia (blood glucose <40 mg/dL).10 The
risk factors for hypoglycemia in hospitalized
patients include older age, existing comorbidi-
ties, diabetes, receiving more oral antidiabetic
agents, tight glycemic control, septic shock,
renal insufficiency, mechanical ventilation,
and severity of illness.9,10 Severe hypoglycemia
(blood glucose ≤50 mg/dL) was found in
7.7% of hospital admissions after a retrospec-
tive analysis of 4368 admissions involving
2582 patients with diabetes admitted to a gen-
eral ward. Patients with hypoglycemia had an
increased length of stay by 2.5 days for each
day with hypoglycemia. Inpatient mortality
and mortality 1 year after hospital discharge
were greater for patients who had at least
1 hypoglycemic episode than for those patients
with no episodes of hypoglycemia.11
DKA and HHS
Pathogenesis
In DKA, hyperglycemia and ketosis develop
as a result of insulin deficiency, absolute or
relative, and increased concentrations of
counterregulatory hormones (catecholamines,
cortisol, glucagon, and growth hormone).
Inadequate insulin triggers other physiologi-
cal functions that elevate glucose levels indi-
rectly. As a result, hyperglycemia develops by
means of (1) increased gluconeogenesis (the
production of glucose from amino acids with

Table 1: Differentiation Among Hypoglycemia Classificationsa

Hypoglycemia Presence or Absence of Typical
Classification Hypoglycemia Symptoms Glucose Levels
Severe hypoglycemia Severe neurological impairment May or may not be measured;
to the extent that assistance of typically defined as <40 mg/dL
another person is required to
actively administer carbohydrates,
glucagon, or other intervention to
return plasma glucose to normal for
neurological recovery
Documented symptomatic Present ≤70 mg/dL (≤3.9 mmol/L)
hypoglycemia
Asymptomatic hypoglycemia Not present ≤70 mg/dL (≤3.9 mmol/L)
Probable symptomatic Present Not available, but presumed to be
hypoglycemia ≤70 mg/dL (≤3.9 mmol/L)
Pseudohypoglycemia Present >70 mg/dL (>3.9 mmol/L)
a
Derived from Seaquist et al.8

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 P O LLOC K A N D F UNK
protein breakdown), (2) accelerated glycogen-
olysis (glucose production from the liver), and
(3) impaired glucose uptake by the peripheral
tissues. Insulin resistance, as a result of hor-
monal imbalance and elevated free fatty acids,
increases the hyperglycemia even more. When
glucose cannot enter the cells because of insu-
lin deficiency, the body responds by breaking
down adipose tissue (lipolysis), increasing
free fatty acid concentrations and hepatic
fatty acid oxidation in the liver. Ketone bodies
(β-hydroxybutyrate and acetoacetate) are
produced, resulting in ketonemia and meta-
bolic acidosis.1 In HHS, hyperglycemia devel-
ops as a result of insulin deficiency. However,
endogenous insulin secretion (produced by
the body) is greater, and these insulin levels
are adequate to prevent lipolysis and subse-
quent ketogenesis and metabolic acidosis. The
degree of dehydration is greater than that in
DKA due to osmotic diuresis.1
Precipitating Factors
Infection is a common precipitating factor in
DKA and HHS, with the most common being
pneumonia and urinary tract infections. Other
precipitating factors include omission of
insulin or inadequate insulin therapy, pancrea-
titis, myocardial infarction, stroke, and drugs.
Up to 20% of patients may come to the emer-
gency department with either DKA or HHS
without a previous diagnosis of diabetes.1,12
Omission of insulin therapy is related to
psychological factors and poor compliance. In
young patients with type 1 diabetes, psycho-
logical problems complicated by eating disor-
ders may be a contributing factor in 20% of
recurrent cases of DKA. Other potential fac-
tors leading to insulin omission are (1) fear of
weight gain with improved metabolic control,
(2) fear of hypoglycemia, (3) reduction or elim-
ination of insulin doses as a result of limited
financial resources, (4) reduction or omission
of insulin doses when ill, (5) rebellion against
authority, and (6) stress of chronic disease.1,13
When appropriate, the patient and/or family
need to be asked whether any of these factors
are cause for the patient to omit insulin doses.
Resources, such as education, social work,
psychiatric care, and/or counseling, may need
to be provided.
Patients’ use of continuous subcutaneous
insulin infusion devices (insulin pumps) had
been associated with an increased incidence of
DKA before 1993. The frequency of DKA has
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decreased with improvement of technology and
patient education, but additional studies are
needed to document reduction of DKA inci-
dence.1 Some causes of a patient receiving inad-
equate insulin with insulin pump therapy may
include the following: (1) the infusion set in
subcutaneous insulin administration has not
been replaced by the patient for more than 3 to
4 days, and the site has poor absorption; (2) the
infusion set may have recently been replaced by
the patient, but the flow of insulin is impaired
as a result of a kinked cannula or tissue obstruc-
tion; (3) the pump ran out of insulin; or (4) the
pump battery ran out of power supply.
Drugs that affect carbohydrate metabolism
can precipitate development of DKA and HHS.
These drugs include corticosteroids, thiazides,
sympathomimetic agents, pentamidine, and
excessive use of diuretics in the elderly. Other
drugs that can precipitate HHS by causing a
reversible deficiency in insulin action or insulin
secretion include diuretics, β-adrenergic block-
ers, and phenytoin.12 Conventional and atypi-
cal antipsychotic drugs also may cause
hyperglycemia, leading to DKA and HHS.1
Underlying medical illnesses causing severe
dehydration can precipitate HHS. Dehydration
can ensue from the increased release of coun-
terregulatory hormones or if access to water is
compromised. Water intake may be restricted
as a result of a patient being bedridden and is
exacerbated by the diminished thirst response
in the elderly.1
Diabetic ketoacidosis cases without a pre-
cipitating cause have been reported in subjects
with type 2 diabetes, mainly in blacks and His-
panics. Aggressive management with insulin
improves insulin secretion, and insulin therapy
is eventually discontinued. Glycemic control is
maintained through diet and possibly oral
antihyperglycemic agents. Most recently, this
variant of diabetes has been referred to in the
literature as ketosis-prone diabetes.1
Diagnosis
Patient History
Patient history usually includes polyuria, poly-
dipsia, weight loss (if insulin deficiency is pre-
sent long enough), blurred vision, vomiting,
dehydration, weakness, abdominal pain, and
mental status changes. Patients often report
drinking a significant amount of fluids, trying
to quench their thirst. Urgency of urination
can even lead to incontinence. Some patients
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confuse the vomiting and overall ill-feeling as
having the flu.1,13
Physical Findings
Physical assessment may reveal poor skin turgor,
Kussmaul respirations (in DKA), tachycardia,
and hypotension. Mental status can range from
profound lethargy (more frequent with HHS) to
full alertness. Focal neurological findings and
seizures may be found with HHS. Temperature
may be normal or hypothermic. Patients with
DKA frequently have nausea, vomiting, “fruity”
or acetone breath, and abdominal pain marked
by tenderness to palpation, diminished bowel
sounds, and some muscle guarding.1,13
Laboratory Values and Tests
Initial laboratory values to be obtained should
include plasma glucose, blood urea nitrogen,
creatinine, electrolytes (with calculated anion
gap), serum osmolality, serum ketones or serum
β-hydroxybutyrate (if available), calcium and
phosphorus concentrations, arterial blood gases,
complete blood cell count with differential, and
urinalysis. In addition, an electrocardiogram,
chest radiograph, and urine, sputum, or blood
cultures should be obtained.1,13 The diagnostic
criteria for DKA and HHS are given in Table 2.
Diabetic ketoacidosis is diagnosed by the
elevation of blood ketones using the nitroprus-
side reaction, but more accurately with serum
β-hydroxybutyrate, as it is the main metabolic
product in ketoacidosis. As ketoacids accumu-
late, an increase is found in the anion gap.1
The plasma anion gap is calculated by sub-
tracting chloride and bicarbonate (anions)
from sodium (cation). An anion gap larger
than 10 to 12 mEq/L indicates metabolic aci-
dosis (normal gap = 7-9 mEq/L).12
Hyperglycemia is present in DKA at serum
glucose levels greater than 250 mg/dL, but the
levels can vary widely on presentation. Arterial
pH is less than 7.3, and serum bicarbonate
level is less than 15 mEq/L. Patients with severe
DKA typically have a bicarbonate level less
than 10 mEq/L and/or a pH less than 7.0 and
altered mental status.12
Serum potassium levels can vary from low
to high. Elevated potassium indicates an extra-
cellular shift of potassium caused by insulin
deficiency, hypertonicity, and acidemia. Low
normal or low potassium level indicates that
the patient has severe total-body potassium
deficiency and requires vigorous potassium
replacement with cardiac monitoring. Treat-
ment lowers potassium even further, which can
provoke cardiac arrhythmias. Serum sodium
level is usually low as a result of osmotic flux
of water from the intracellular to extracellular
space with hyperglycemia. Serum phosphate

Table 2: Diagnostic Criteria for Diabetic Ketoacidosis and Hyperosmolar

Hyperglycemic Statea
DKA HHS
Mild Moderate Severe
(Plasma Glucose (Plasma Glucose (Plasma Glucose Plasma Glucose
>250 mg/dL) >250 mg/dL) >250 mg/dL) >600 mg/dL
Arterial pH 7.25–7.30 7.00 to 7.24 <7.00 >7.30
Serum bicarbonate, 15–18 10 to 14 <10 >18
mEq/L
Urine ketoneb Positive Positive Positive Small
Serum ketoneb Positive Positive Positive Small
Effective serum Variable Variable Variable >320 mOsm/kg
osmolalityc
Anion gapd >10 >12 >12 Variable
Mental status Alert Alert/drowsy Stupor/coma Stupor/coma
Abbreviations: DKA, diabetic ketoacidosis; HHS, hyperosmolar hyperglycemic state.
a
From Kitabchi et al.1 Used with permission from American Diabetes Association.
b
Nitroprusside reaction method.
c
Effective serum osmolality: 2[measured Na+ (mEq/L)] + glucose (mg/dL)/18.
d
Anion gap: (Na+) − [(Cl−+ HCO3− (mEq/L)].

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level is usually elevated as a result of movement
of phosphate out of the cells, with the intracel-
lular to extracellular space shift. Leukocytosis
of 10 000 to 15 000 mm3 cell count is common
in DKA and may not indicate an infectious
process. The stress of ketoacidosis causes leu-
kocytosis. Serum lipase level may be elevated
with ketoacidosis but may be beneficial in the
differential diagnosis of pancreatitis.1
Serum osmolality, if 320 mOsm/kg or
greater, is indicative of HHS in combination
with altered mental status, which is a result of
the patient’s severe dehydration. Plasma glucose
level will be significantly elevated (>600 g/dL),
and blood ketones will be small.1
Treatment
The treatment goals of DKA and HHS are to
(1) rehydrate, (2) restore and maintain normal
glucose metabolism, (3) correct electrolyte def-
icits and acidosis, (4) provide glucose when
needed, and (5) prevent complications. With
these goals is the need to identify and correct
the precipitating event(s). Protocols are often
used for the management of patients with
DKA and HHS. These protocols are complex
because of frequent laboratory tests, intrave-
nous fluid changes, electrolyte replacement,
and insulin infusion changes that require
frequent monitoring of patients,1 but the use of
a protocol improves the outcomes of patients.
A protocol for management of adult patients
with DKA or HHS is shown in Figure 1.
Goal 1: Rehydrate
Initial fluid therapy focuses on restoring the
patient’s intravascular, interstitial, and intracel-
lular volume and restoration of renal perfu-
sion. Fluid replacement should correct deficits
in 24 hours. Isotonic saline (0.9% NaCl) is
infused at a rate of 1 to 1.5 L in the first hour
(if no risk of cardiac compromise). If the cor-
rected sodium level is normal or elevated,
0.45% NaCl is infused at 200 to 500 mL/hour.
Monitoring consists of hemodynamic monitor-
ing (blood pressure and heart rate), intake and

Figure 1: Protocol for management of adult patients with DKA or HHS. DKA diagnostic criteria: blood
glucose, 250 mg/dL; arterial pH, 7.3; bicarbonate, 15 mEq/L; and moderate ketonuria or ketonemia.
HHS diagnostic criteria: serum glucose, >600 mg/dL; arterial pH, >7.3; serum bicarbonate, >15 mEq/L;
and minimal ketonuria and ketonemia. a15-20 mL/kg per hour. bSerum sodium should be corrected for
hyperglycemia (for each 100 mg/dL glucose, add 1.6 mEq to sodium value for corrected serum value).
Abbreviations: Bwt, body weight; BUN, blood urea nitrogen; DKA, diabetic ketoacidosis; HHS, hyperosmolar
hyperglycemic state; IV, intravenous; SC, subcutaneous. Used with permission from American Diabetes
Association. Diabetes Care. 2009:32(7).

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 VOL UME 2 4 • N U MBER 3 • JULY–SEPTEM BER 2013
output, frequent laboratory values (such as
glucose, potassium, sodium, chloride, bicarbo-
nate, anion gap, osmolality), and clinical
examination. In patients with renal and car-
diac compromise, monitoring of serum osmo-
lality and assessment of cardiac, renal, and
mental status are important to prevent iatro-
genic fluid overload.1
Goal 2: Restore and Maintain
Normal Glucose Metabolism
All patients need insulin. Insulin therapy usu-
ally involves regular insulin via a continuous
intravenous administration. Mild DKA may be
treated with frequent subcutaneous rapid
insulin injections in a non–critical care unit.
For patients with moderate to severe DKA,
placement in a critical care unit is optimal
because of frequent monitoring and titration
of the continuous insulin infusion. Treatment
algorithms may or may not include an initial
intravenous bolus of regular insulin. Algo-
rithms with an initial intravenous bolus are
typically dosed at 0.1 units/kg followed by the
infusion at 0.1 units/kg per hour. Algorithms
without an initial bolus initiate the insulin
infusion at a rate of 0.14 units/kg per hour.
The goal of the insulin infusion is to decrease
the plasma glucose concentration at a rate of
50 to 75 mg/hour. The infusion rate is to be
increased every hour for a steady state of
glucose decline. When the plasma glucose level
reaches 200 mg/dL for DKA and 300 mg/dL
for HHS, the insulin infusion rate may be
decreased to 0.01 to 0.05 units/kg per hour,
and dextrose is added to the intravenous fluids
(see goal 4). From then on, the goal is to main-
tain glucose values between 150 and
200 mg/dL in DKA or 250 to 300 mg/dL in
HHS until the crisis is resolved. To keep the
glucose within the target range, the rate of the
insulin infusion or the concentration of dex-
trose in the intravenous administration of solu-
tions may need to be adjusted.1
Goal 3: Correct Electrolyte Deficits
and Acidosis
Mild to moderate hyperkalemia occurs with
hyperglycemic crises, despite total body potas-
sium depletion. With insulin therapy, volume
expansion, and correction of acidosis, potas-
sium levels decrease. Potassium replacement is
initiated when serum levels fall below 5.0 to
5.2 mEq/L, the upper end of normal, to prevent
hypokalemia. The goal of treatment is to keep
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the potassium level between 4.0 and 5.0 mEq/L.
Potassium is generally replaced via each liter of
intravenous fluids at a concentration of 20 to
30 mEq. If a patient presents with hypoka-
lemia, insulin treatment should be delayed until
the serum potassium level is greater than
3.3 mEq/L to avoid life-threatening arrhyth-
mias and respiratory weakness.1
Replacement of bicarbonate is recommended
in DKA, only if the patient has a pH of less
than 6.9 to prevent impaired myocardial con-
tractility, cerebral vasodilation and coma, and
gastrointestinal complications. Patients should
receive 100 mmol of sodium bicarbonate in
400 mL of sterile water (an isotonic solution)
with 20 mEq potassium chloride administered
at a rate of 200 mL/hour for 2 hours until the
venous pH is greater than 7.0.1
Serum phosphate level is often normal at
presentation and decreases with insulin ther-
apy. No benefit has been shown to replace
phosphate, and aggressive phosphate therapy
can cause severe hypocalcemia. Phosphate
replacement may be necessary in patients with
cardiac dysfunction, anemia, or respiratory
depression if their serum phosphate level is
less than 1.0 mg/dL. Replacement consists of
20 to 30 mEq/L potassium phosphate in intra-
venous fluids.1
Goal 4: Provide Glucose When
Needed
Dextrose (5%) is to be added to the replacement
fluids when the plasma glucose reaches approxi-
mately 200 mg/dL. In DKA, hyperglycemia is
corrected faster than acidosis. The addition of
dextrose to the fluids allows continued insulin
administration until the ketonemia is cleared,
while preventing hypoglycemia.1
Goal 5: Prevent Complications
Hypoglycemia and hypokalemia are the pri-
mary treatment complications. Hypoglycemia
is a result of overzealous treatment with insu-
lin. To identify hypoglycemia, clinicians must
frequently monitor blood glucose levels (every
1-2 hours), because many patients with DKA
do not experience adrenergic manifestations of
sweating, nervousness, fatigue, hunger, and
tachycardia.1 Hypokalemia is a result of inade-
quate potassium replacement or bicarbonate
use. Hyperglycemia may result when inade-
quate insulin is provided during the transition
from intravenous insulin administration to sub-
cutaneous treatment when the hyperglycemic
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 P O LLOC K A N D F UNK
crisis has resolved (see “Resolution of Hyper-
glycemic Crises” section below).1,13
Cerebral edema is a rare complication in
the treatment of DKA in adults; however,
when it occurs, it is associated with a mortal-
ity rate of 20% to 40%. The symptoms of cer-
ebral edema can include onset of headache,
gradual deterioration in level of conscious-
ness, seizures, sphincter incontinence, pupil-
lary changes, papilledema, and respiratory
arrest. Prevention includes avoidance of exces-
sive hydration and rapid reduction of plasma
osmolarity, gradual decrease of serum glucose,
and maintenance of serum glucose level
between 250 and 300 mg/dL until osmolality
is normal and mental status is improved.1
Resolution of Hyperglycemic Crises
Resolution of DKA is considered to have
occurred when the blood glucose level is less
than 200 mg/dL, and 2 of the following
criteria are met: a serum bicarbonate level of
15 mEq/L or greater, a venous pH of greater
than 7.3, and/or an anion gap of 12 mEq/L or
less. Resolution of HHS has occurred when
osmolality is normal and the patient’s mental
status is back to baseline. Until this point, the
patient has taken nothing by mouth (NPO) or
has just started clear liquids. At this time, the
patient can be transitioned to subcutaneous
insulin. To prevent recurrence of hyperglyce-
mia and ketoacidosis, clinicians must admin-
ister subcutaneous insulin 2 hours before
discontinuation of the insulin infusion. Basal-
bolus subcutaneous insulin regimens are opti-
mal, as they more closely approximate normal
physiology, especially for patients with type 1
diabetes. This regimen will provide the patient
prandial insulin needed for oral nutrition.
Patients with known diabetes can resume
their home insulin regimen if their glucose
levels were under control prior to the crisis.
For patients with newly diagnosed diabetes,
the basal-bolus regimen should be started at
0.5 to 0.8 units/kg per day.1
DKA and HHS Summary
Diabetic ketoacidosis and HHS are the 2 most
serious acute metabolic complications of dia-
betes. The hallmark of DKA is acidosis with
hyperglycemia and dehydration. Hyperosmo-
lar hyperglycemic state is characterized by
hyperosmolality with hyperglycemia and severe
dehydration in the absence of acidosis. Treat-
ment of both conditions includes correction of
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dehydration, hyperglycemia, and electrolyte
imbalances. Frequent monitoring of the patient
is required, in addition to following a com-
plex protocol. Resolution of DKA occurs
when the patient’s blood glucose level is lower
than 200 mg/dL, and 2 of the following
criteria are met: a serum bicarbonate level of
15 mEq/L or greater, a venous pH of greater
than 7.3, and an anion gap of 12 mEq/L or
less. Hyperosmolar hyperglycemic state is
resolved when osmolality and mental status
are normal. With the hyperglycemic crisis
resolved, the patient can be transitioned to
subcutaneous insulin.
Case Study
A.S. is a 48-year-old white man with a history
of type 2 diabetes of 10 years’ duration. He
has required insulin for 6 years. A.S. is
employed as a truck driver. His employer dis-
covered him unresponsive in the back of the
truck. The nearest hospital was 2 hours away.
His employer drove him to the nearest hospi-
tal emergency department.
Medical history is significant for hypothy-
roidism, treated with levothyroxine 75 mcg
daily, with no history of recreational drug
use, alcohol other than socially, or smoking.
His type 2 diabetes regimen is with glargine
30 units at bedtime and aspart 9 to 14 units
prior to each meal. According to his wife, this
incidence of loss of consciousness was his first.
On arrival at the emergency department, the
patient was obtunded, with limited ability to
provide history. Physical findings included tach-
ycardia, blood pressure within normal limits,
oxygen saturation of 88% on room air, oral
mucosa dry, right-sided rhonchi, abdomen soft
and nontender, arousable but disoriented, and
5/5 muscle strength. The chest radiograph
revealed a right lower lobe infiltrate consistent
with pneumonia. The electrocardiogram showed
sinus tachycardia, rate 140, right axis devia-
tion, and non–specific ST-T–wave changes with
no acute elevation or depression. See Table 3
for the patient’s emergency department labora-
tory value results.
A.S. was transferred to the critical care unit.
By this time, he had received intravenous
hydration of 2 L of sodium chloride at 1000
mL/hour. After his serum potassium level was
determined to be greater than 3.3 mEq/L (see
Table 3), regular insulin via an intravenous
insulin administration was initiated at 10 units
per hour in the emergency department and
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Table 3: A.S.’s Laboratory Results From moving all extremities spontaneously but was
the Emergency Department not following commands. His mental status
was fluctuating.
Laboratory Test Result (Normal Range)
The initial diagnoses were as follows: (1)
Sodium, mEq/L 138 (133–144) DKA, (2) aspiration pneumonia with right
Potassium, mEq/L 5.2 (3.4–5.3) middle and basal infiltrates, (3) altered mental
Chloride, mEq/L 110 (94–109)
status with standby for intubation if necessary,
(4) acute kidney failure, (5) lactic acidosis sec-
CO2, mEq/L 8 (20–32) ondary to shock, (6) severe dehydration, and
Anion gap, mEq/L 26 (6–17) (7) hypothyroidism. The treatment plan
Glucose, mg/dL >600 (60–99)
included fluid resuscitation, intravenous insu-
lin administration, electrolyte replacement,
Blood urea nitrogen, 28 (7–30) intravenous antibiotic drugs for infection, and
mg/dL
warfarin and pantoprazole prophylactically.
Creatinine, mg/dL 2.1 (0.52–1.04) Cultures were obtained for Streptococcus,
Calcium, mg/dL 5 (5–10.4) Mycoplasma pneumoniae, and Legionella. A
Lactic acid, mmol/L 6.6 (0.7–2.1)
nasal swab was done to test for influenza.
The focus of nursing management for A.S.
β-Hydroxybutyrate, 11.6 (0.4–0.5) included addressing and monitoring hydration,
mmol/L glucose and laboratory abnormalities, and res-
Glycosylated 14% (4.3–5.6) piratory status. Monitoring urine output is
hemoglobin crucial to assessing adequate hydration; there-
Arterial pH 7.11 (7.35–7.45) fore, an indwelling urinary catheter was
inserted. A.S. received an additional 2 L of
Arterial CO2, mm Hg 4 (35–45)
0.9% NaCl solution at 1000 mL/hour after
White blood cell 8.6 (5–10) arrival in critical care, and then it was
count, 109/L decreased to 200 mL/hour. Hyperchloremic
acidosis developed, with a sodium level of 149
mEq/L and a chloride level of 121 mEq/L. The
continued in the intensive care unit. A stat basic corrected sodium level was already 149 mEq/L
metabolic profile was drawn on arrival to the after the first 4 hours of treatment.
unit. Laboratory values were as follows: serum Subsequent to DKA, A.S. had worsening
potassium = 4.9 mEq/L, blood glucose = respiratory status, experienced a respiratory
577 mg/dL, bicarbonate = 8 mEq/L, and arrest, and was intubated. Sputum cultures
anion gap = 31. The insulin infusion rate came back positive for influenza and Strepto-
was increased. Piperacillin/tazobactam (Zosyn) coccus, and he developed methicillin-suscepti-
4.5 g was administered intravenously to address ble Staphylococcus aureus necrotizing
the pneumonia. pneumonia. A.S. experienced bilateral pneu-
The critical care admission physical exami- mothoraces, requiring extensive and repeated
nation demonstrated that the patient was chest tube insertions as well as antibiotic ther-
drowsy and disoriented. Vital signs were as fol- apy. To avoid risk of aspiration, clinicians ele-
lows: temperature = 36°C, pulse = 137 beats vated the head of the bed and inserted a
per minute, respirations = 30/min, and blood nasogastric tube placed to suction.
pressure = 137/74 mm Hg. Oxygen saturation Over the course of the first 8 hours, A.S.’s
at admission was 99% with a Ventimask. potassium level went from 5.2 mEq/L initially,
Pupils were equal and reactive, and the oral to 4.9 mEq/L 2.5 hours later, to 4.1 mEq/L in
mucosa was dry. No jugular venous distention another 90 minutes, and then to 3.5 mEq/L
or carotid bruit was present, and S1 and S2 were 4 hours later (approximately 8 hours total time).
normal with no murmurs, gallops, or rubs. No potassium was given until potassium phos-
Despite the chest radiography, breath sounds phate was ordered about 1 hour later. A.S.’s
were noted as clear bilaterally without rales or phosphorus level was checked initially about
rhonchi. The abdomen was soft and tender 4 hours after arrival. It fell from 2.3 mmol/L to
with bowel sounds present. No pedal edema 1.3 mmol/L over the next 4 hours. Although the
was noted, and extremities were warm with protocol suggests that phosphorus need not be
pedal pulses present. Neurologically, A.S. was replaced unless less than 1 mmol/L, 20 mEq of

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 P O LLOC K A N D F UNK W W W.A ACNA DVA NCE D CRIT ICA LCA RE .COM

sodium phosphorus was given intravenously. 4. What was 1 complication that occurred
Potassium phosphate tablets were ordered later with the treatment of A.S.’s DKA?
via the nasogastric tube. During this time, A.S.’s 5. At what time frame was the glucose rate of
sodium level rose to 149 mEq/L, and his cal- fall more than 50 to 75 mg/dL per hour?
cium level dropped to 8.1 mmol/L.
As noted previously, regular insulin infu-
sion was initiated at a rate of 10 units per Hypoglycemia
hour. See Table 4 for sequential blood glucose
levels and corresponding titration of the Pathophysiology in Diabetes
insulin infusion. When the blood glucose level Iatrogenic hypoglycemia in people with diabe-
reached 165 mg/dL, no adjustment to drip tes results from “…interplay of relative or
rate was made, but 5% dextrose was added absolute therapeutic insulin excess and com-
to the intravenous fluids. At the laboratory promised defenses against falling plasma glu-
measurement taken at 4:12 am, 8 hours into cose concentrations.”7(p53) Patients treated with
this stay, the anion gap had returned to medications that decrease plasma glucose,
14 mEq/L, and other laboratory values were including insulin, sulfonylureas (eg, glyburide,
moving back toward normal levels. A.S.’s glipizide, or glimepiride), and glinides (eg, nat-
DKA had resolved. eglinide and repaglinide), are at risk of iatro-
A.S. was ultimately discharged after a genic hypoglycemia.7
60-day length of stay. After multiple visits to When the plasma glucose level falls, the
the ambulatory diabetes center, his hemoglobin body has the following 3 critical physiological
A1C was 7.9% three months postadmission. defenses: (1) decrease in insulin secretion, (2)
Analysis of A.S.’s case: increase in glucagon secretion, and in the
absence of the latter, (3) increase in epinephrine
1. What type of diabetes did A.S. have? Is it secretion. The behavioral defense to falling
the typical type of diabetes for DKA? plasma glucose is ingestion of carbohydrates.
2. What were the precipitating factors for The recognition of the need for carbohydrates
DKA to develop? is prompted by the symptoms of hypoglycemia,
3. With a corrected sodium level of 149 mEq/L, largely the neurogenic symptoms facilitated by
what intravenous fluid should have been sympathetic neural activation.14
used? In type 1 diabetes and long-standing type 2
diabetes, all the defenses just described are
compromised. In patients with fully devel-
oped type 1 diabetes, circulating insulin levels
Table 4: Blood Glucose Values and
do not decrease as plasma glucose levels
Corresponding Insulin Infusion Rates
decline, and the α-cell glucagon response
Serum Point-of- Insulin is lost as a result of the absence of a β-cell sig-
Glucose, Care Rate, nal. Of note, glucagon stimulates releases of
Time mg/dL Glucose units/hour glucose from the liver. In the absence of these
8:01 PM >500 10 2 defenses, these patients depend on the third
defense, epinephrine secretion. However, the
9:31 PM >500 10
epinephrine response is often diminished,
10:32 PM >500 10 which causes defective glucose counterregula-
10:41 PM 577 12
tion and increases the risk of severe hypogly-
cemia. Add a reduced sympathetic neural
00:07 AM 456 12 response to this situation and hypoglycemia
01:09 AM 429 15 unawareness ensues, which is the impairment
01:59 AM 389 15 or loss of the warning signs of hypoglycemia.
Now the patient has lost the behavioral
03:10 AM 400 15
defense to ingest carbohydrates with a falling
04:02 AM 209 15 plasma glucose level.14
04:12 AM 165 15 Defective glucose counterregulation and
05:14 AM 169 15 hypoglycemia unawareness are components of
hypoglycemia-associated autonomic failure
05:44 AM 203 15
(HAAF) in patients with diabetes.8 HAAF

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 VOL UME 2 4 • N U MBER 3 • JULY–SEPTEM BER 2013
“…is most often caused by recent antecedent
iatrogenic hypoglycemia and is at least
partly reversible by scrupulous avoidance of
hypoglycemia.”8(p4) The increased risk of severe
hypoglycemia during intensive insulin treat-
ment is 25-fold with HAAF.8
Identification
Hypoglycemia can be severe, defined by the
American Diabetes Association as a glucose
level lower than 40 mg/dL.15 Severe hypoglyce-
mia is also classified as an event that requires
assistance of another person to actively admin-
ister carbohydrates or glucagon or take other
corrective action to return plasma glucose to
normal for neurological recovery. A plasma
glucose concentration of less than 70 mg/dL is
the alert value identifying the patient with
hypoglycemia. However, a patient may report
typical symptoms of hypoglycemia with a
measured plasma glucose concentration of
greater than 70 mg/dL.8
In any case, patients at risk for hypoglyce-
mia should be asked whether they have symp-
tomatic and asymptomatic hypoglycemia. If
possible, have the patient provide a glucose
value for which he or she becomes sympto-
matic and describe his or her symptoms. If a
patient has hypoglycemia unawareness or
HAAF, tight glucose control is not safe.
Patients with low and/or declining cognition
need increased vigilance for hypoglycemia.
Raising glycemic targets for these patients is
recommended to prevent an unidentified hypo-
glycemic event.15
Risk Factors
In the hospital, multiple risk factors exist for
iatrogenic hypoglycemia. Patients may experi-
ence hypoglycemia associated with altered
nutritional state, heart failure, renal disease,
liver disease, malignancy, infection, or sepsis.15
In critically ill patients, intensive glycemic
control can increase the risk of severe hypogly-
cemia and may be associated with increased
mortality rate. Therefore, tight glycemic goal
ranges, such as 81 to 108 mg/dL, are not
recommended in critically ill patients.16
Additional events that can lead to hypogly-
cemia in critically ill patients include sudden
reduction of corticosteroid doses, altered abil-
ity of the patient to report hypoglycemic symp-
toms, reduction of oral nutritional intake,
emesis, new NPO status, inappropriate timing
of short or rapid-acting insulin in relation to
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NCI200282.indd 323
ACUT E D IA BE T E S M A NAGE M E NT
meals, reduction of the rate of intravenous
dextrose, and unexpected interruption of
enteral feedings or parenteral nutrition.15 Being
cognizant of these risk factors, along with clin-
ical judgment, is important in being proactive
in the prevention of hypoglycemia.
Insulin is the preferred treatment for
patients with hyperglycemia. In critical care,
intravenous administration of insulin is recom-
mended for most patients. Oral antihypergly-
cemic agents and injectable noninsulin
therapies (GLP1 analogs and pramlintide) have
a limited role in the management of hypergly-
cemia in conjunction with acute illness and
should be discontinued in favor of insulin
while patients are hospitalized. Oral agents are
difficult to titrate with acute changes in patient
status, such as NPO or poor nutritional intake,
putting the patient at risk for hypoglycemia.15
Older adults are especially vulnerable to
hypoglycemia. Decline in renal function and
hepatic enzyme activity may interfere with
metabolism of insulin and sulfonylureas.
Impairment of counterregulatory (glucagon and
growth hormone) hormone responses to lower-
ing plasma glucose has been identified in older
adults. Clinical complications and comorbidi-
ties, which exist at disproportionate levels in
older adults, can be exacerbated by or contrib-
ute to hypoglycemic events.8
Treatment
The preferred oral treatment of hypoglycemia
requires ingestion of 15 to 20 g of glucose (eg,
glucose tablets, gel, liquid, or powder). How-
ever, any form of carbohydrate foods that
contains glucose will raise blood glucose. Fat-
containing foods will retard glucose absorp-
tion and recovery from the hypoglycemic
event. Ongoing action of insulin, sulfonylu-
reas, or glinides may lead to recurrence of
hypoglycemia, so glucose monitoring every
15 minutes with additional treatment as
needed until glucose level is greater than
70 mg is essential. A carbohydrate snack
containing 15 g of carbohydrate, with a pro-
tein, is recommended if the patient is not able
to eat a meal within the hour.15
Patients who are NPO or are experiencing
severe hypoglycemia with confusion or uncon-
sciousness that cannot be treated with oral
glucose should be treated with intravenous
glucose (if intravenous access is available) or
glucagon injection. Note that glucagon should
be repeated only once. Hospitals should
7/13/13 2:11 PM
 P O LLOC K A N D F UNK
have a hypoglycemic treatment protocol that
registered nurses can implement, without a
physician order, to avoid the delay of patient
treatment and prevent harm.15
In all cases of hypoglycemia, the patient
must not be left alone because of risk of fall
or other injury.15 Prevention of another epi-
sode of hypoglycemia is warranted. The pro-
vider responsible for glucose management
should be notified as soon as possible or cer-
tainly before administering the next insulin or
oral diabetes agent dose for medication and
glucose-monitoring orders.
Hypoglycemia Summary
Iatrogenic hypoglycemia in hospitalized
patients is the interplay of relative or absolute
therapeutic insulin excess and compromised
patient defenses against falling plasma glucose
concentrations. These compromised defenses
include decrease in insulin secretion, increase
in glucagon secretion, and increase in epineph-
rine secretion, and often exist in patients with
type 1 diabetes or long-standing type 2 diabe-
tes. Hypoglycemia unawareness and HAAF
may develop in these patients, putting them at
risk for severe hypoglycemia.
In critically ill patients, several risk factors
exist that can lead to hypoglycemia. Therefore,
intensive glycemic control is not recommended.
Awareness of these risk factors, along with
clinical judgment, is important in preventing
hypoglycemia. In the event of hypoglycemia,
access to a nurse-implemented hypoglycemic
treatment protocol is recommended to prevent
patient harm.
Conclusion
The acute diabetes management of DKA, HHS,
and iatrogenic hypoglycemia is multifaceted.
The role of critical care nurses is essential in
implementing complex protocols that require
frequent monitoring and communication with
physicians. Observance of the protocols is time
consuming and may need clarification by a
physician (for DKA and HHS in particular).
Vigilant care of the patient is important to
resolve these crises with optimal outcomes.
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