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AACN Advanced Critical Care

Volume 24, Number 3, pp.314-324


© 2013 AACN

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 and thus lower plasma glucose concentra-
the following 3 potential complications is tions to an abnormally low level, which exposes
required: diabetic ketoacidosis, hyperosmolar the patient to potential harm. This article
hyperglycemic state, and iatrogenic hypogly- reviews the pathogenesis, precipitating or risk
cemia. The hyperglycemic crises diabetic factors, diagnosis or identification, and treat-
ketoacidosis and hyperosmolar hyperglycemic ment of these critical complications of diabetes.
state are the 2 most serious metabolic com- In addition, a case study on diabetic ketoaci-
plications of diabetes. Hypoglycemia, specifi- dosis is provided.
cally iatrogenic hypoglycemia, results from Keywords: diabetes, hyperglycemia, hypo-
treatments that raise circulating insulin levels glycemia, ketoacidosis

I n acute diabetes, management of the following


3 potential complications is required: diabetic
ketoacidosis (DKA), hyperosmolar hyperglyce-
severity, and it clinically presents with less
ketosis and greater hyperglycemia than DKA.1
Patients with moderate or severe DKA and HHS
mic state (HHS), and iatrogenic hypoglycemia. are usually admitted to the critical care unit.
Hyperglycemic crises (DKA and HHS) are the Among adults with diabetes, hyperglycemic
2 most serious metabolic complications of dia- crises accounted for 16.2 emergency depart-
betes. The triad of severe hyperglycemia, meta- ment visits per 1000 adults with diabetes in
bolic acidosis, and increased total body ketone 20092 and were similar between men and
concentration characterizes DKA. Severe hyper- women.3 Hospital discharges with DKA diag-
glycemia, hyperosmolality, and dehydration nosis increased by 57% from 1988 to 2009,4
with no significant ketoacidosis characterize and of these discharges, rates were higher
HHS. Both metabolic imbalances occur as a among people younger than 45 years.5 Fortu-
result of absolute and/or relative insulin defi- nately, hyperglycemic crisis as the underlying
ciency and an increase of counterregulatory hor- cause of death declined in all age groups from
mones (glucagon, catecholamines, cortisol, and 1980 to 2009 per 100 000 people with diabe-
growth hormone). Diabetic ketoacidosis is clas- tes, with the largest decrease occurring among
sified as mild, moderate, or severe on the basis
of the severity of metabolic acidosis (blood pH, Faith Pollock is Diabetes Clinical Nurse Specialist, Allina
bicarbonate, and ketones). Patients with type 1 Health, Abbott Northwestern Hospital, 800 E 28th St, Minne-
diabetes are more likely to have DKA, but apolis, MN 55407 (faith.pollock@allina.com).
patients with type 2 diabetes also can be at risk Donna C. Funk is Diabetes Clinical Nurse Specialist, Borgess
with the catabolic stress of acute illness, such as Medical Center, Kalamazoo, Michigan.
infections, surgery, or trauma. Hyperosmolar The authors declare no conflicts of interest.
hyperglycemic state is not classified by levels of DOI: 10.1097/NCI.0b013e31829b7d38

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those aged 75 years or older. The oldest age inpatients admitted to intensive care units, 102
group had the highest death rates from hyper- (1.9%) had at least 1 episode of severe hypo-
glycemic crises at the beginning of the study glycemia (blood glucose <40 mg/dL).10 The
period, but the rates steadily declined at the risk factors for hypoglycemia in hospitalized
study end to become lower than the rates of patients include older age, existing comorbidi-
the youngest age group.6 ties, diabetes, receiving more oral antidiabetic
Hypoglycemia, specifically iatrogenic hypo- agents, tight glycemic control, septic shock,
glycemia, results from treatments that raise cir- renal insufficiency, mechanical ventilation,
culating insulin levels and thus lower plasma and severity of illness.9,10 Severe hypoglycemia
glucose concentrations to an abnormally low (blood glucose ≤50 mg/dL) was found in
level, which exposes the patient to potential 7.7% of hospital admissions after a retrospec-
harm.7,8 Hypoglycemia in diabetes cannot be tive analysis of 4368 admissions involving
defined as a single threshold value for plasma 2582 patients with diabetes admitted to a gen-
glucose concentration, because symptoms asso- eral ward. Patients with hypoglycemia had an
ciated with hypoglycemia shift to lower plasma increased length of stay by 2.5 days for each
glucose concentrations after a recent hypoglyce- day with hypoglycemia. Inpatient mortality
mic event or to higher plasma glucose concentra- and mortality 1 year after hospital discharge
tions for patients with poorly controlled diabetes were greater for patients who had at least
who experience infrequent hypoglycemia.8 In 1 hypoglycemic episode than for those patients
2013, the American Diabetes Association with no episodes of hypoglycemia.11
Workgroup on Hypoglycemia suggested classi-
fying hypoglycemia in diabetes as (1) severe DKA and HHS
hypoglycemia, (2) documented symptomatic
hypoglycemia, (3) asymptomatic hypoglyce- Pathogenesis
mia, (4) probable symptomatic hypoglycemia, In DKA, hyperglycemia and ketosis develop
and (5) pseudohypoglycemia (see Table 1).8 as a result of insulin deficiency, absolute or
Among hospitalized patients with diabetes, relative, and increased concentrations of
the true incidence and prevalence of hypogly- counterregulatory hormones (catecholamines,
cemia are not known. In 2007, a retrospec- cortisol, glucagon, and growth hormone).
tive study of 31 970 patients admitted to Inadequate insulin triggers other physiologi-
general wards of an academic medical center cal functions that elevate glucose levels indi-
identified that 3349 patients (10.5%) had at rectly. As a result, hyperglycemia develops by
least 1 episode of hypoglycemia (blood glu- means of (1) increased gluconeogenesis (the
cose ≤70 g/dL).9 In another review of 5365 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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protein breakdown), (2) accelerated glycogen- decreased with improvement of technology and
olysis (glucose production from the liver), and patient education, but additional studies are
(3) impaired glucose uptake by the peripheral needed to document reduction of DKA inci-
tissues. Insulin resistance, as a result of hor- dence.1 Some causes of a patient receiving inad-
monal imbalance and elevated free fatty acids, equate insulin with insulin pump therapy may
increases the hyperglycemia even more. When include the following: (1) the infusion set in
glucose cannot enter the cells because of insu- subcutaneous insulin administration has not
lin deficiency, the body responds by breaking been replaced by the patient for more than 3 to
down adipose tissue (lipolysis), increasing 4 days, and the site has poor absorption; (2) the
free fatty acid concentrations and hepatic infusion set may have recently been replaced by
fatty acid oxidation in the liver. Ketone bodies the patient, but the flow of insulin is impaired
(β-hydroxybutyrate and acetoacetate) are as a result of a kinked cannula or tissue obstruc-
produced, resulting in ketonemia and meta- tion; (3) the pump ran out of insulin; or (4) the
bolic acidosis.1 In HHS, hyperglycemia devel- pump battery ran out of power supply.
ops as a result of insulin deficiency. However, Drugs that affect carbohydrate metabolism
endogenous insulin secretion (produced by can precipitate development of DKA and HHS.
the body) is greater, and these insulin levels These drugs include corticosteroids, thiazides,
are adequate to prevent lipolysis and subse- sympathomimetic agents, pentamidine, and
quent ketogenesis and metabolic acidosis. The excessive use of diuretics in the elderly. Other
degree of dehydration is greater than that in drugs that can precipitate HHS by causing a
DKA due to osmotic diuresis.1 reversible deficiency in insulin action or insulin
secretion include diuretics, β-adrenergic block-
Precipitating Factors ers, and phenytoin.12 Conventional and atypi-
Infection is a common precipitating factor in cal antipsychotic drugs also may cause
DKA and HHS, with the most common being hyperglycemia, leading to DKA and HHS.1
pneumonia and urinary tract infections. Other Underlying medical illnesses causing severe
precipitating factors include omission of dehydration can precipitate HHS. Dehydration
insulin or inadequate insulin therapy, pancrea- can ensue from the increased release of coun-
titis, myocardial infarction, stroke, and drugs. terregulatory hormones or if access to water is
Up to 20% of patients may come to the emer- compromised. Water intake may be restricted
gency department with either DKA or HHS as a result of a patient being bedridden and is
without a previous diagnosis of diabetes.1,12 exacerbated by the diminished thirst response
Omission of insulin therapy is related to in the elderly.1
psychological factors and poor compliance. In Diabetic ketoacidosis cases without a pre-
young patients with type 1 diabetes, psycho- cipitating cause have been reported in subjects
logical problems complicated by eating disor- with type 2 diabetes, mainly in blacks and His-
ders may be a contributing factor in 20% of panics. Aggressive management with insulin
recurrent cases of DKA. Other potential fac- improves insulin secretion, and insulin therapy
tors leading to insulin omission are (1) fear of is eventually discontinued. Glycemic control is
weight gain with improved metabolic control, maintained through diet and possibly oral
(2) fear of hypoglycemia, (3) reduction or elim- antihyperglycemic agents. Most recently, this
ination of insulin doses as a result of limited variant of diabetes has been referred to in the
financial resources, (4) reduction or omission literature as ketosis-prone diabetes.1
of insulin doses when ill, (5) rebellion against
authority, and (6) stress of chronic disease.1,13 Diagnosis
When appropriate, the patient and/or family
need to be asked whether any of these factors Patient History
are cause for the patient to omit insulin doses. Patient history usually includes polyuria, poly-
Resources, such as education, social work, dipsia, weight loss (if insulin deficiency is pre-
psychiatric care, and/or counseling, may need sent long enough), blurred vision, vomiting,
to be provided. dehydration, weakness, abdominal pain, and
Patients’ use of continuous subcutaneous mental status changes. Patients often report
insulin infusion devices (insulin pumps) had drinking a significant amount of fluids, trying
been associated with an increased incidence of to quench their thirst. Urgency of urination
DKA before 1993. The frequency of DKA has can even lead to incontinence. Some patients

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confuse the vomiting and overall ill-feeling as side reaction, but more accurately with serum
having the flu.1,13 β-hydroxybutyrate, as it is the main metabolic
product in ketoacidosis. As ketoacids accumu-
Physical Findings late, an increase is found in the anion gap.1
Physical assessment may reveal poor skin turgor, The plasma anion gap is calculated by sub-
Kussmaul respirations (in DKA), tachycardia, tracting chloride and bicarbonate (anions)
and hypotension. Mental status can range from from sodium (cation). An anion gap larger
profound lethargy (more frequent with HHS) to than 10 to 12 mEq/L indicates metabolic aci-
full alertness. Focal neurological findings and dosis (normal gap = 7-9 mEq/L).12
seizures may be found with HHS. Temperature Hyperglycemia is present in DKA at serum
may be normal or hypothermic. Patients with glucose levels greater than 250 mg/dL, but the
DKA frequently have nausea, vomiting, “fruity” levels can vary widely on presentation. Arterial
or acetone breath, and abdominal pain marked pH is less than 7.3, and serum bicarbonate
by tenderness to palpation, diminished bowel level is less than 15 mEq/L. Patients with severe
sounds, and some muscle guarding.1,13 DKA typically have a bicarbonate level less
than 10 mEq/L and/or a pH less than 7.0 and
Laboratory Values and Tests altered mental status.12
Initial laboratory values to be obtained should Serum potassium levels can vary from low
include plasma glucose, blood urea nitrogen, to high. Elevated potassium indicates an extra-
creatinine, electrolytes (with calculated anion cellular shift of potassium caused by insulin
gap), serum osmolality, serum ketones or serum deficiency, hypertonicity, and acidemia. Low
β-hydroxybutyrate (if available), calcium and normal or low potassium level indicates that
phosphorus concentrations, arterial blood gases, the patient has severe total-body potassium
complete blood cell count with differential, and deficiency and requires vigorous potassium
urinalysis. In addition, an electrocardiogram, replacement with cardiac monitoring. Treat-
chest radiograph, and urine, sputum, or blood ment lowers potassium even further, which can
cultures should be obtained.1,13 The diagnostic provoke cardiac arrhythmias. Serum sodium
criteria for DKA and HHS are given in Table 2. level is usually low as a result of osmotic flux
Diabetic ketoacidosis is diagnosed by the of water from the intracellular to extracellular
elevation of blood ketones using the nitroprus- 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 the precipitating event(s). Protocols are often
of phosphate out of the cells, with the intracel- used for the management of patients with
lular to extracellular space shift. Leukocytosis DKA and HHS. These protocols are complex
of 10 000 to 15 000 mm3 cell count is common because of frequent laboratory tests, intrave-
in DKA and may not indicate an infectious nous fluid changes, electrolyte replacement,
process. The stress of ketoacidosis causes leu- and insulin infusion changes that require
kocytosis. Serum lipase level may be elevated frequent monitoring of patients,1 but the use of
with ketoacidosis but may be beneficial in the a protocol improves the outcomes of patients.
differential diagnosis of pancreatitis.1 A protocol for management of adult patients
Serum osmolality, if 320 mOsm/kg or with DKA or HHS is shown in Figure 1.
greater, is indicative of HHS in combination
with altered mental status, which is a result of Goal 1: Rehydrate
the patient’s severe dehydration. Plasma glucose Initial fluid therapy focuses on restoring the
level will be significantly elevated (>600 g/dL), patient’s intravascular, interstitial, and intracel-
and blood ketones will be small.1 lular volume and restoration of renal perfu-
sion. Fluid replacement should correct deficits
Treatment in 24 hours. Isotonic saline (0.9% NaCl) is
The treatment goals of DKA and HHS are to infused at a rate of 1 to 1.5 L in the first hour
(1) rehydrate, (2) restore and maintain normal (if no risk of cardiac compromise). If the cor-
glucose metabolism, (3) correct electrolyte def- rected sodium level is normal or elevated,
icits and acidosis, (4) provide glucose when 0.45% NaCl is infused at 200 to 500 mL/hour.
needed, and (5) prevent complications. With Monitoring consists of hemodynamic monitor-
these goals is the need to identify and correct 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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output, frequent laboratory values (such as the potassium level between 4.0 and 5.0 mEq/L.
glucose, potassium, sodium, chloride, bicarbo- Potassium is generally replaced via each liter of
nate, anion gap, osmolality), and clinical intravenous fluids at a concentration of 20 to
examination. In patients with renal and car- 30 mEq. If a patient presents with hypoka-
diac compromise, monitoring of serum osmo- lemia, insulin treatment should be delayed until
lality and assessment of cardiac, renal, and the serum potassium level is greater than
mental status are important to prevent iatro- 3.3 mEq/L to avoid life-threatening arrhyth-
genic fluid overload.1 mias and respiratory weakness.1
Replacement of bicarbonate is recommended
Goal 2: Restore and Maintain in DKA, only if the patient has a pH of less
Normal Glucose Metabolism than 6.9 to prevent impaired myocardial con-
All patients need insulin. Insulin therapy usu- tractility, cerebral vasodilation and coma, and
ally involves regular insulin via a continuous gastrointestinal complications. Patients should
intravenous administration. Mild DKA may be receive 100 mmol of sodium bicarbonate in
treated with frequent subcutaneous rapid 400 mL of sterile water (an isotonic solution)
insulin injections in a non–critical care unit. with 20 mEq potassium chloride administered
For patients with moderate to severe DKA, at a rate of 200 mL/hour for 2 hours until the
placement in a critical care unit is optimal venous pH is greater than 7.0.1
because of frequent monitoring and titration Serum phosphate level is often normal at
of the continuous insulin infusion. Treatment presentation and decreases with insulin ther-
algorithms may or may not include an initial apy. No benefit has been shown to replace
intravenous bolus of regular insulin. Algo- phosphate, and aggressive phosphate therapy
rithms with an initial intravenous bolus are can cause severe hypocalcemia. Phosphate
typically dosed at 0.1 units/kg followed by the replacement may be necessary in patients with
infusion at 0.1 units/kg per hour. Algorithms cardiac dysfunction, anemia, or respiratory
without an initial bolus initiate the insulin depression if their serum phosphate level is
infusion at a rate of 0.14 units/kg per hour. less than 1.0 mg/dL. Replacement consists of
The goal of the insulin infusion is to decrease 20 to 30 mEq/L potassium phosphate in intra-
the plasma glucose concentration at a rate of venous fluids.1
50 to 75 mg/hour. The infusion rate is to be
increased every hour for a steady state of Goal 4: Provide Glucose When
glucose decline. When the plasma glucose level Needed
reaches 200 mg/dL for DKA and 300 mg/dL Dextrose (5%) is to be added to the replacement
for HHS, the insulin infusion rate may be fluids when the plasma glucose reaches approxi-
decreased to 0.01 to 0.05 units/kg per hour, mately 200 mg/dL. In DKA, hyperglycemia is
and dextrose is added to the intravenous fluids corrected faster than acidosis. The addition of
(see goal 4). From then on, the goal is to main- dextrose to the fluids allows continued insulin
tain glucose values between 150 and administration until the ketonemia is cleared,
200 mg/dL in DKA or 250 to 300 mg/dL in while preventing hypoglycemia.1
HHS until the crisis is resolved. To keep the
glucose within the target range, the rate of the Goal 5: Prevent Complications
insulin infusion or the concentration of dex- Hypoglycemia and hypokalemia are the pri-
trose in the intravenous administration of solu- mary treatment complications. Hypoglycemia
tions may need to be adjusted.1 is a result of overzealous treatment with insu-
lin. To identify hypoglycemia, clinicians must
Goal 3: Correct Electrolyte Deficits frequently monitor blood glucose levels (every
and Acidosis 1-2 hours), because many patients with DKA
Mild to moderate hyperkalemia occurs with do not experience adrenergic manifestations of
hyperglycemic crises, despite total body potas- sweating, nervousness, fatigue, hunger, and
sium depletion. With insulin therapy, volume tachycardia.1 Hypokalemia is a result of inade-
expansion, and correction of acidosis, potas- quate potassium replacement or bicarbonate
sium levels decrease. Potassium replacement is use. Hyperglycemia may result when inade-
initiated when serum levels fall below 5.0 to quate insulin is provided during the transition
5.2 mEq/L, the upper end of normal, to prevent from intravenous insulin administration to sub-
hypokalemia. The goal of treatment is to keep cutaneous treatment when the hyperglycemic

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crisis has resolved (see “Resolution of Hyper- dehydration, hyperglycemia, and electrolyte
glycemic Crises” section below).1,13 imbalances. Frequent monitoring of the patient
Cerebral edema is a rare complication in is required, in addition to following a com-
the treatment of DKA in adults; however, plex protocol. Resolution of DKA occurs
when it occurs, it is associated with a mortal- when the patient’s blood glucose level is lower
ity rate of 20% to 40%. The symptoms of cer- than 200 mg/dL, and 2 of the following
ebral edema can include onset of headache, criteria are met: a serum bicarbonate level of
gradual deterioration in level of conscious- 15 mEq/L or greater, a venous pH of greater
ness, seizures, sphincter incontinence, pupil- than 7.3, and an anion gap of 12 mEq/L or
lary changes, papilledema, and respiratory less. Hyperosmolar hyperglycemic state is
arrest. Prevention includes avoidance of exces- resolved when osmolality and mental status
sive hydration and rapid reduction of plasma are normal. With the hyperglycemic crisis
osmolarity, gradual decrease of serum glucose, resolved, the patient can be transitioned to
and maintenance of serum glucose level subcutaneous insulin.
between 250 and 300 mg/dL until osmolality
is normal and mental status is improved.1 Case Study
A.S. is a 48-year-old white man with a history
Resolution of Hyperglycemic Crises of type 2 diabetes of 10 years’ duration. He
Resolution of DKA is considered to have has required insulin for 6 years. A.S. is
occurred when the blood glucose level is less employed as a truck driver. His employer dis-
than 200 mg/dL, and 2 of the following covered him unresponsive in the back of the
criteria are met: a serum bicarbonate level of truck. The nearest hospital was 2 hours away.
15 mEq/L or greater, a venous pH of greater His employer drove him to the nearest hospi-
than 7.3, and/or an anion gap of 12 mEq/L or tal emergency department.
less. Resolution of HHS has occurred when Medical history is significant for hypothy-
osmolality is normal and the patient’s mental roidism, treated with levothyroxine 75 mcg
status is back to baseline. Until this point, the daily, with no history of recreational drug
patient has taken nothing by mouth (NPO) or use, alcohol other than socially, or smoking.
has just started clear liquids. At this time, the His type 2 diabetes regimen is with glargine
patient can be transitioned to subcutaneous 30 units at bedtime and aspart 9 to 14 units
insulin. To prevent recurrence of hyperglyce- prior to each meal. According to his wife, this
mia and ketoacidosis, clinicians must admin- incidence of loss of consciousness was his first.
ister subcutaneous insulin 2 hours before On arrival at the emergency department, the
discontinuation of the insulin infusion. Basal- patient was obtunded, with limited ability to
bolus subcutaneous insulin regimens are opti- provide history. Physical findings included tach-
mal, as they more closely approximate normal ycardia, blood pressure within normal limits,
physiology, especially for patients with type 1 oxygen saturation of 88% on room air, oral
diabetes. This regimen will provide the patient mucosa dry, right-sided rhonchi, abdomen soft
prandial insulin needed for oral nutrition. and nontender, arousable but disoriented, and
Patients with known diabetes can resume 5/5 muscle strength. The chest radiograph
their home insulin regimen if their glucose revealed a right lower lobe infiltrate consistent
levels were under control prior to the crisis. with pneumonia. The electrocardiogram showed
For patients with newly diagnosed diabetes, sinus tachycardia, rate 140, right axis devia-
the basal-bolus regimen should be started at tion, and non–specific ST-T–wave changes with
0.5 to 0.8 units/kg per day.1 no acute elevation or depression. See Table 3
for the patient’s emergency department labora-
DKA and HHS Summary tory value results.
Diabetic ketoacidosis and HHS are the 2 most A.S. was transferred to the critical care unit.
serious acute metabolic complications of dia- By this time, he had received intravenous
betes. The hallmark of DKA is acidosis with hydration of 2 L of sodium chloride at 1000
hyperglycemia and dehydration. Hyperosmo- mL/hour. After his serum potassium level was
lar hyperglycemic state is characterized by determined to be greater than 3.3 mEq/L (see
hyperosmolality with hyperglycemia and severe Table 3), regular insulin via an intravenous
dehydration in the absence of acidosis. Treat- insulin administration was initiated at 10 units
ment of both conditions includes correction of 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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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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“…is most often caused by recent antecedent meals, reduction of the rate of intravenous
iatrogenic hypoglycemia and is at least dextrose, and unexpected interruption of
partly reversible by scrupulous avoidance of enteral feedings or parenteral nutrition.15 Being
hypoglycemia.”8(p4) The increased risk of severe cognizant of these risk factors, along with clin-
hypoglycemia during intensive insulin treat- ical judgment, is important in being proactive
ment is 25-fold with HAAF.8 in the prevention of hypoglycemia.
Insulin is the preferred treatment for
Identification patients with hyperglycemia. In critical care,
Hypoglycemia can be severe, defined by the intravenous administration of insulin is recom-
American Diabetes Association as a glucose mended for most patients. Oral antihypergly-
level lower than 40 mg/dL.15 Severe hypoglyce- cemic agents and injectable noninsulin
mia is also classified as an event that requires therapies (GLP1 analogs and pramlintide) have
assistance of another person to actively admin- a limited role in the management of hypergly-
ister carbohydrates or glucagon or take other cemia in conjunction with acute illness and
corrective action to return plasma glucose to should be discontinued in favor of insulin
normal for neurological recovery. A plasma while patients are hospitalized. Oral agents are
glucose concentration of less than 70 mg/dL is difficult to titrate with acute changes in patient
the alert value identifying the patient with status, such as NPO or poor nutritional intake,
hypoglycemia. However, a patient may report putting the patient at risk for hypoglycemia.15
typical symptoms of hypoglycemia with a Older adults are especially vulnerable to
measured plasma glucose concentration of hypoglycemia. Decline in renal function and
greater than 70 mg/dL.8 hepatic enzyme activity may interfere with
In any case, patients at risk for hypoglyce- metabolism of insulin and sulfonylureas.
mia should be asked whether they have symp- Impairment of counterregulatory (glucagon and
tomatic and asymptomatic hypoglycemia. If growth hormone) hormone responses to lower-
possible, have the patient provide a glucose ing plasma glucose has been identified in older
value for which he or she becomes sympto- adults. Clinical complications and comorbidi-
matic and describe his or her symptoms. If a ties, which exist at disproportionate levels in
patient has hypoglycemia unawareness or older adults, can be exacerbated by or contrib-
HAAF, tight glucose control is not safe. ute to hypoglycemic events.8
Patients with low and/or declining cognition
need increased vigilance for hypoglycemia. Treatment
Raising glycemic targets for these patients is The preferred oral treatment of hypoglycemia
recommended to prevent an unidentified hypo- requires ingestion of 15 to 20 g of glucose (eg,
glycemic event.15 glucose tablets, gel, liquid, or powder). How-
ever, any form of carbohydrate foods that
Risk Factors contains glucose will raise blood glucose. Fat-
In the hospital, multiple risk factors exist for containing foods will retard glucose absorp-
iatrogenic hypoglycemia. Patients may experi- tion and recovery from the hypoglycemic
ence hypoglycemia associated with altered event. Ongoing action of insulin, sulfonylu-
nutritional state, heart failure, renal disease, reas, or glinides may lead to recurrence of
liver disease, malignancy, infection, or sepsis.15 hypoglycemia, so glucose monitoring every
In critically ill patients, intensive glycemic 15 minutes with additional treatment as
control can increase the risk of severe hypogly- needed until glucose level is greater than
cemia and may be associated with increased 70 mg is essential. A carbohydrate snack
mortality rate. Therefore, tight glycemic goal containing 15 g of carbohydrate, with a pro-
ranges, such as 81 to 108 mg/dL, are not tein, is recommended if the patient is not able
recommended in critically ill patients.16 to eat a meal within the hour.15
Additional events that can lead to hypogly- Patients who are NPO or are experiencing
cemia in critically ill patients include sudden severe hypoglycemia with confusion or uncon-
reduction of corticosteroid doses, altered abil- sciousness that cannot be treated with oral
ity of the patient to report hypoglycemic symp- glucose should be treated with intravenous
toms, reduction of oral nutritional intake, glucose (if intravenous access is available) or
emesis, new NPO status, inappropriate timing glucagon injection. Note that glucagon should
of short or rapid-acting insulin in relation to be repeated only once. Hospitals should

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have a hypoglycemic treatment protocol that 2. Centers for Disease Control and Prevention. Emer-
gency department visit rates for hyperglycemic crisis as
registered nurses can implement, without a first-listed diagnosis per 1,000 diabetic adults aged
physician order, to avoid the delay of patient 18 years or older, by age, United States, 2006–2009.
treatment and prevent harm.15 CDC Diabetes Data & Trends Web site. http://www.cdc
.gov/diabetes/statistics/hyperglycemia/fig5byage.htm.
In all cases of hypoglycemia, the patient Published 2012. Updated 2012. Accessed May 4, 2013.
must not be left alone because of risk of fall 3. Centers for Disease Control and Prevention. Age-
adjusted emergency department visit rates for hypergly-
or other injury.15 Prevention of another epi- cemic crisis as first-listed diagnosis per 1,000 diabetic
sode of hypoglycemia is warranted. The pro- adults aged 18 years or older, by sex, United States,
vider responsible for glucose management 2006–2009. DC Diabetes Data & Trends Web site.
http://www.cdc.gov/diabetes/statistics/hyperglycemia/
should be notified as soon as possible or cer- fig5bysex.htm. Published 2012. Updated 2012. Accessed
tainly before administering the next insulin or May 4, 2013.
oral diabetes agent dose for medication and 4. Centers for Disease Control and Prevention. Number (in
thousands) of hospital discharges with diabetic ketoaci-
glucose-monitoring orders. dosis as first-listed diagnosis, United States, 1988–2009.
CDC Diabetes Data & Trends Web site. http://www
.cdc.gov/diabetes/statistics/dkafirst/fig1.htm. Published
Hypoglycemia Summary 2012. Updated 2012. Accessed May 4, 2013.
Iatrogenic hypoglycemia in hospitalized 5. Centers for Disease Control and Prevention. Hospital
patients is the interplay of relative or absolute discharge rates for diabetic ketoacidosis as first-listed
diagnosis per 1,000 diabetic population, by age, United
therapeutic insulin excess and compromised States 1988–2009. CDC Diabetes Data & Trends Web site.
patient defenses against falling plasma glucose http://www.cdc.gov/diabetes/statistics/dkafirst/fig4.htm.
concentrations. These compromised defenses Published 2012. Updated 2012. Accessed May 4, 2013.
6. Centers for Disease Control and Prevention. Death
include decrease in insulin secretion, increase rates for hyperglycemic crises as underlying cause per
in glucagon secretion, and increase in epineph- 100,000 diabetic population, by age, United States,
1980–2009. CDC Diabetes Data & Trends Web site.
rine secretion, and often exist in patients with http://www.cdc.gov/diabetes/statistics/mortalitydka/
type 1 diabetes or long-standing type 2 diabe- fRateDKADiabByAge.htm. Published 2012. Updated
tes. Hypoglycemia unawareness and HAAF 2012. Accessed May 4, 2013.
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