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ipose tissue
solute insulin deficiency
Stress/infection/insufficient insulin intake
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226
Ab
Ad
↑ Lipolysis
↑ FFA
Liver
↑ Ketone
body
production
Hyperketonemia
Ketoacidosis
↑ Glucagon
↑ Catecholamines
↑ Cortisol
↑ Growth hormone
Gluconeogenesis
Glycogenolysis
Proteolysis
↓ Protein
synthesis
Amino acids
Relative insulin deficiency
Peripheral
tissues
↓ Glucose utilization
Hyperglycemia
Glycosuria
+ osmotic diuresis
Impaired renal function
Minimal
ketogenesis
Hyperosmolarity
Dehydration
HHSDKA
Figure31.1 Metabolic pathways leading to diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state(HHS).
AG Na Cl HCO[][]
+
=−+
−−
3
[]
=×
++
(
)
(
)
(
)
+
1.6mEq/L for each 100 mg/dLglucose 10
++
=
+>
(
)
(00mg/dL)
+
=××−()[( )]
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227
low levels of insulin are insucient to prevent hyperglycemia but are sucient to prevent lipolysis and acidosis.
BOX 31.1 CALCULATIONS
Both DKA and HHS cause glycosuria and osmotic diuresis. Large volumes of free water and electrolytes are lost in
1. Anion Gap (AG) [normal <12– 16]
the urine, causing a total body water decit and low body
levels of potassium, chloride, phosphate, magnesium, and
calcium.
2. Serum Osmolality [normal=275– 295 mOsmol/ L]
Glucose levels in patients with DKA are usually less than
800 mg/ dL compared with glucose levels in patients with
HHS that may exceed 1000 mg/ dL. Patients with DKA are
3. Corrected Serum Sodium (CorrNa)
Glucosemg/dL /18BUN mg/dL/2.8[]
likely to present early in their disease course with nausea/
emesis, dyspnea, and abdominal pain. Patients with HHS
present later in the course of the disease with dehydration
and fatigue secondary to hyperosmolarity. Young patients
4. Free Water Decit (FWD) (Liters)
with DKA have a higher glomerular ltration rate and a
greater ability to excrete glucose. Hyperglycemia causes a
striking osmotic diuresis with large losses of free water in
Dosing Factor=0.6 for males and 0.5 for females
DKA and HHS patients. Poor oral intake and emesis compound volume losses. Despite an initial redistribution of
body water to maintain intravascular volume, patients can
be profoundly dehydrated.
Anion gap acidosis is a hallmark of DKA and is caused
is decreased secondary to a gastrointestinal infection is a
common precipitant of DKA. Drugs associated with DKA
include cocaine, glucocorticoids, thiazide diuretics, dobu-
tamine, and atypical antipsychotics.
by high levels of beta- hydroxybutyric acid and acetoacetic acid. Ketoacids are also converted to D- lactic acid that
accumulates and increases the anion gap elevation.
High plasma osmolality is more characteristic of HHS
than DKA. e resultant osmotic diuresis of hyperosmolality
drives water out of the cells, reduces the serum sodium, causes
more diuresis, and further exacerbates the hyperosmolality.
e osmotic ux of free water from the intracellular space to
the extracellular space may result in a falsely low sodium level.
As the hyperglycemia is corrected, severe hypernatremia can
RISK
If untreated, DKA can lead to severe acid- base and electrolyte
disturbances that can aect vital organ function. Cardiac dysrhythmias, cerebral edema, and respiratory failure can cause
severe morbidity and mortality. Mortality is inuenced by age
and the presence of coexisting conditions. Mortality can be less
than 1% for otherwise healthy children and young adults, but
can exceed 20% in patients older than 65years.
develop. e serum sodium level should, therefore, be corrected at an “eective” sodium level (Box31.1).
A patient experiencing a hyperglycemic crisis invariably
has a signicant total body potassium decit (3– 5 mEq/ kg)
that is belied by the deceptively “normal” serum potassium
concentration. As potassium is lost in the urine due to
osmotic diuresis and excreted as potassium ketoacid anion
salts, potassium migrates into the bloodstream as a result of
insulin deciency and intracellular uid contraction.
Hyperglycemic crisis is generally caused by a precipitating event, oen related to stress response, increased
glucose production, and/ or inadequate insulin therapy.
Infection and antidiabetic medication noncompliance are
also frequent causes. Acute major illnesses such as myocardial infarction, cerebrovascular accident, sepsis, or
pancreatitis have all been associated with hyperglycemic
crisis. Dehydration in elderly patients can promote HHS,
while discontinuation of insulin therapy when oral intake
ASSESSMENT OFTHE PATIENT
e time course of DKA usually develops over 24 hours.
Common presenting signs include nausea/ vomiting,
abdominal pain, and hyperventilation. When acidosis and
plasma osmolality rise above a critical point, alterations in
mental status and coma develop.5 Signs of signicant hypovolemia include dry mucosa, decreased skin turgor, tachycardia, and hypotension. Oen, DKA patients have the
fruity odor of exhaled acetone.
e initial evaluation of a patient with suspected DKA
should include measurement of serum glucose and electrolytes, plasma osmolality, blood urea nitrogen (BUN),
creatinine, complete blood count with dierential, urine
ketones (dipstick), plasma osmolality, and arterial blood
gases. Free water decit, anion gap, and corrected serum
sodium should be calculated, and typical laboratory values
DIABETIC KETOACIDOSIS 227
228
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of patients with DKA are shown in Table 31.1. Classically,
DKA is dened as a plasma glucose > 250 mg/ dL, plasma
bicarbonate < 15 mEq/ L, pH < 7.20, ketonemia, and an
elevation in the anion gap. Although DKA and HHS
are separate disorders, one- third of patients with a hyperglycemic crisis present with overlap between DKA and
HHS. e dierential diagnosis of a hyperglycemic crisis should include alcoholic or fasting ketoacidosis, high
anion gap acidosis of other causes, and toxic metabolic
encephalopathy.
Diagnostic tests to identify precipitant causes of DKA
should also be considered. ese tests include urine and
blood cultures, chest x- ray, and ECG. Patients with mitochondrial disorders have a high incidence of diabetes mellitus. e likelihood of respiratory failure in such patients
ishigh.
CONSIDERATIONS FORANESTHESIA
Elective and semiurgent surgery should be postponed
until treatment of DKA has been initiated and signicant
improvement of the patient has occurred. Consultation
with the patient’s intensivist and/ or endocrinologist prior
to surgery is strongly recommended. e goals for therapy of DKA and the possible inuence of anesthesia and
surgery must be factored into the perioperative care plan.
For patients requiring emergent surgery, the anesthesiologist should begin therapy and attempt to identify the precipitant cause. Insertion of an arterial catheter or central
venous catheter to provide for frequent blood sampling is
mandatory. Transesophageal echocardiography can provide
valuable information about cardiac function and should
be strongly considered in elderly patients with DKA.
Correction of acid- base and electrolyte abnormalities in the
operating room should be done carefully, as rapid treatment
may precipitate undesired complications such as hypoglycemia or cerebral edema. Aer surgery, the patient should
be transferred to an intensive care unit (ICU) for denitive
therapy. Postoperative tracheal intubation and controlled
mechanical ventilation are strongly recommended for
patients with preoperative alterations in mental status, neuromuscular weakness, and severe metabolic abnormalities.
Perioperative Glycemic Control
e incidence of diabetes mellitus has tripled over the past
10years and is expected to increase by a similar amount in
the coming years. Diabetic patients will, consequently, present for surgery with increasing frequency. Ten to 20% of
elective surgical patients may have undiagnosed diabetes or
impaired glucose control. ese patients may, in fact, have
a higher risk of perioperative complications than patients
with known diabetes.6 Perioperative glycemic control is of
considerable interest to all healthcare providers responsible
for perioperative care. A widely cited study published in
TABLE31.1 DIAGNOSTIC CRITERIA INDIABETIC
KETOACIDOSIS AND HYPERGLYCEMIC
HYPEROSMOLARSTATE
DKA HHS
Mild Moderate Severe
Plasma
glucose
(mg/ dL)
Arterial pH 7.25–7.30 7.00–7.24 <7.00 >7.30
Anion gap >10 >12 >12 Variable
<250 >250 >250 >600
2001 reported promising reductions in morbidity and mortality by maintaining blood glucose levels below 100 mg/
dL with intensive insulin therapy in critically ill patients
in the surgical ICU.7 Additional trials, however, failed to
corroborate this nding, and intensive insulin therapy was
found to increase the risk of signicant hypoglycemia in
critically ill patients. A large, international, randomized
trial found that maintaining a target glucose level of 180
mg/ dL resulted in a lower mortality than a target of 81 to
108 mg/ dL. ere is currently insucient evidence among
perioperative patients to support the practice of intensive
insulin therapy to achieve tight glycemic control (80– 110
Serum
bicarbonate
(mEq/ L)
15–18 10–14 <10 >18
mg/ dL). Amore rational recommendation is a blood glucose target of 140– 180 mg/ dL in the perioperative period.
8
Serum
osmolality
Serum
ketones
Mental
status
228 SECTION B. ENDOCRINE DISTURBANCES
Variable Variable Variable >320 mOsm/L
Present Present Present Variable (small)
Alert Alert/ drowsy Stupor/
coma
Stupor/ coma
TREATMENT
erapy is directed at correction of volume depletion and
correction of signicant electrolyte decits (Table 31.2,
Boxes 31.2, 31.3, 31.4). Volume resuscitation is the critical
initial therapy for DKA. If the patient is not in cardiogenic
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229
TABLE31.2 WATER AND ELECTROLYTE DEFICITS INDKA
ANDHHS
DKA HHS
Total H2O Deficit (L) 6 9
H2O Deficit (ml/ kg) 100 100–200
Na+ Deficit (mEq/ kg) 7–10 5–13
K+ Deficit (mEq/ kg) 3–5 4–6
Cl- Deficit (mEq/ kg) 3–5 5–15
PO4 Deficit (mmol/ kg) 5–7 3–7
shock, uid repletion should begin early to improve perfusion, reduce stress hormone levels, and lower plasma
osmolality. Traditionally, 0.9% sodium chloride (normal
BOX 31.3 INSULIN THERAPY FORDIABETIC
KETOACIDOSIS
1. Administer regular insulin 0.1 U/ kg as an IVbolus
2. Begin insulin infusion at 0.1 U/ kg/ hour
3. Monitor blood glucose levels hourly until stable at
<250mg/ dL
4. If serum glucose level does not drop by 50– 70 mg/ dL
in rst hour, double the infusionrate.
5. When serum glucose reaches 200 mg/ dL, lower
insulin infusion rate to 0.02– 0.05 U/ kg/ hour
6. Keep serum glucose between 150– 200 mg/ dL until
DKA resolves. Continue IV insulin infusion for 1– 2
hours after initiating SC insulin.
saline) was the recommended uid. Several recent studies, however, showed that patients who received plasmalyte
had a faster resolution of metabolic acidosis compared with
patients who received normal saline.9 One randomized,
controlled study comparing lactated Ringer’s (LR) solution
to normal saline for resuscitation from DKA found no benet to LR. Blood glucose levels, in fact, required a longer
time to normalize with LR compared to NS.10 ere is no
evidence that resuscitation with colloid solutions provides
any benet. Fluids should be administered at a rate of 15–
20 mL/ kg lean body weight for the rst 1 to 2 hours. Aer
this initial uid bolus, the corrected sodium level can be
approximated by adding 2 mEq/ L to the measured plasma
sodium concentration for each 5.5 mmol/ L increase above
normal in glucose concentration. If the corrected sodium
concentration is less than 135 mEq/ L, volume repletion
should continue at a rate of 250– 500 mL/ hour. If the corrected sodium concentration is normal or high, the uid
can be changed to a hypotonic solution such as 0.45%
sodium chloride at 250– 500 mL/ hour.
Aer the initiation of volume repletion, correction of
the potassium decit should proceed. If the serum potassium upon admission is < 5.3 mEq/ L, potassium chloride
should be administered. If the serum potassium level is <
3.3 mEq/ L, aggressive repletion should be initiated at the
BOX 31.2 FLUID THERAPY FORDIABETIC KETOACIDOSIS
Fluid Management
DETERMINE VOLUMESTATUS
1. If volume overloaded or concern for cardiac shock,
consider hemodynamic monitoring and/ or pressors.
2. If severe hypovolemia, resuscitate with balanced salt
solution (BSS) at 1 L perhour.
3. If mild hypovolemia, assess corrected Na+level
a. If Na+ is high or normal, dilute solution such as
0.45% NaCl at 250– 500 mL/ hour
b. If Na+ is low, BSS at 250– 500 mL/ hour
4. When serum glucose is 200 mg/ dL or lower, switch to
D5 0.45% NaCl at 150– 250 mL/ hour
DIABETIC KETOACIDOSIS 229
BOX 31.4 POTASSIUM REPLETION FORDIABETIC
KETOACIDOSIS
1. Establish normal renal function urine output
~ 50 mL/ hour
2. If serum K+ is < 3.3 mEq/ L, hold insulin and give
40mEq K+ per hour until K+ >3.3mEq/ L.
3. If K+ > 5.3 mEq/ L, do not replete K+, but check level
every 2hours.
4. If K+ is between 3.3 and 5.3 mEq/ L, administer
20– 30 mEq/ L K+ per hour to keep serum K+ level
between 4 and 5mEq/ L.
5. IV K+ repletion is preferred to oral route until DKA has
resolved and oral intake resumes.
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rate of 40 mEq per hour and insulin therapy held until the
serum potassium level reaches 3.3 mEq/ L. For initial potassium levels between 3.3 and 5.3 mEq/ L, 20 to 30 mEq of
potassium chloride should be added to each liter of intravenous replacement uid. Potassium replacement should
continue until the serum potassium target level of 4 to 5
mEq/ L is reached. It should be remembered that potassium
is as osmotically active as sodium. erefore, if potassium is
administered concurrently with volume expansion, a hypotonic intravenous uid may be preferred.
Insulin therapy is initiated aer volume expansion and
potassium replacement are underway. Regular insulin (0.1
unit/ kg) should be administered as an intravenous bolus.
is bolus is then followed by a continuous regular insulin
infusion at 0.1 unit/ kg/ hour. If the serum glucose level has
not decreased by 50 to 70 mg/ dL in one hour, the insulin
infusion rate should be doubled. Measurement of glucose
levels during the early phases of therapy should be done in
the central laboratory, as POC glucose devices are unreliable
at high glucose levels. Glucose levels should be measured
each hour until the glucose level stabilizes at < 250 mg/ dL.
Compared with regular insulin, rapid- acting insulin analogs are eective for treatment of hyperglycemia and DKA.
Most institutions, however, prefer the use of regular insulin
because of clinical experience and cost considerations.
e administration of sodium bicarbonate to patients
with DKA may be useful when the pH is less than 6.9. Data
on the ecacy of bicarbonate therapy, however, is lacking.
Sodium bicarbonate is not recommended for patients at
risk for developing acute renal injury. Although total body
phosphate depletion oen occurs with DKA, routine phosphate replacement is not recommended.
Resolution of a hyperglycemic crisis is dened as:(1)resolution of ketoacidosis and normalization of the anion gap
10 to 12 hours, it was the urologist’s opinion that a delay of
that length would jeopardize her renal function and increase
the likelihood of urosepsis. e anesthesiologist felt that
DKA therapy could be immediately initiated and continued
during surgery. Since the surgical procedure was going to be
of relatively short duration, it was decided to delay surgery
for 2 hours in order to hydrate the patient and begin insulin
therapy. Atransthoracic echocardiogram was performed as
volume repletion was initiated and a le radial arterial line
was inserted. e echo showed good le ventricular (LV)
function with severe hypovolemia. e LV ejection fraction
measured by Simpson’s method was 80%, and LV end- systolic
volume was zero. Over the next hour she received 1.5 liters
of intravenous normal saline with a total of 30 mEq potassium chloride. Aer the initial uid bolus, 7 units of regular
insulin were administered and an insulin infusion at the rate
of 7 units per hour was started. e plasma glucose level 30
minutes aer the insulin bolus had decreased from 500 mg/
dL to 320 mg/ dL and the serum potassium had declined to
4.6 mEq/ L. e plasma glucose level measured 1 hour aer
the start of the insulin infusion was 260 mg/ dL. Although
her mental status was improving, she was still quite lethargic
immediately prior to the induction of anesthesia. Anesthesia
was slowly induced with propofol (2 mg/ kg), fentanyl (1
microgram/ kg) and cis- atracurium (0.1 mg/ kg). Her trachea
was intubated, and anesthesia was maintained with a mixture
of inhaled oxygen, air, and sevourane. e ureteral stent was
placed within 60 minutes. Since her mental status was still
uncertain, she was transferred to the ICU directly from the
operating room and remained intubated. Intravenous and
insulin therapy was continued for the next 12 hours. During
that period her glucose and electrolyte levels stabilized and
her mental status returned to baseline. She was extubated 10
hours aer surgery.
to less than 12 mEq/ L, (2)return to baseline mental status and a plasma osmolality less than 315 mOsmol/ L, and
(3)the ability of the patient to ingest oral nutrition. Once
CASE- BASED LEARNING DISCUSSION
the blood glucose levels have stabilized at less than 200 mg/
dL, the insulin infusion can be replaced with subcutaneous
insulin. e insulin infusion, however, should be continued
for 1 to 2 hours aer initiation of subcutaneous insulin.
is overlap in insulin therapy should prevent recurrent
hyperglycemia.
1. How does the patient’s DKA aect the plan for anesthesia?
Although it would be desirable to delay the anesthetic
until the DKA is controlled, delaying the ureteral stent
insertion may result in deterioration of renal function that
would adversely aect control of the patient’s diabetes. e
acidosis and electrolyte disturbances produced by DKA
FOLLOW- UP
e urologist, intensivist, and anesthesiologist discussed the
need for emergent cystoscopy for relief of ureteral obstruction
and necessity for emergent treatment of the patient’s DKA.
Although her intensivist suggested that surgery be delayed for
may accentuate the cardiovascular and neurologic eects
of anesthetic drugs. Fortunately, the procedure is not
invasive and can be done quickly. An arterial line should
be inserted prior to induction for measurement of glucose
and electrolytes, and to help guide volume resuscitation.
Airway management with a laryngeal mask airway can
230 SECTION B. ENDOCRINE DISTURBANCES
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231
be done for most patients undergoing this procedure;
however the tenuous metabolic condition of this patient
warrants tracheal intubation. Potential postoperative
hemodynamic instability and mental obtundation may
preclude tracheal extubation at the end of the procedure.
2. Can LR solution be used for volume resuscitation
of a patient with DKA? Normal saline (0.9% NaCl)
has been the traditionally recommended uid for
intravenous volume resuscitation for DKA. ere
are very few studies, however, that compare normal
saline to LR solution or plasmalyte. e pH of
normal saline is 5.5 and the chloride content relative
to plasma is high, and infusion of large volumes of
infused normal saline can produce a hyperchloremic
metabolic acidosis. Ringer’s lactate and plasmalyte
contain more physiologic amounts of chloride and
contain the alkalinizing agents lactate (LR) and
glycemic control. Insulin analogs are more expensive
than naturally derived insulin products, and there is
some concern about potential carcinogenicity of longterm analog use. For the treatment of DKA, however,
regular insulin is administered intravenously and the
short- acting analogs do not oer any clear advantages.
5. Can dexamethasone be administered intraoperatively
as prophylaxis against nausea to patients with stable
diabetes mellitus? Glucocorticoids increase hepatic
glucose production and increase insulin resistance
by inhibiting transport of glucose into muscle cells.
e overall eect is an increase in plasma glucose
levels. Chronic corticosteroid administration can
lead to chronic elevation of plasma glucose. However
several studies have demonstrated that a single dose of
intraoperative dexamethasone does not increase plasma
glucose in diabetics or nondiabetics.
acetate (plasmalyte). Small clinical studies have,
in fact, suggested that LR and plasmalyte may be
better uids than normal saline for the treatment of
DKA. Irrespective of the intravenous uid that is
administered, volume resuscitation must be guided by
frequent measurement of plasma glucose, electrolytes,
and acid- base status. Such measurements will permit
logical adjustments in uid therapy.
3. Is insulin therapy for DKA dierent from insulin
therapy for HHS? Volume resuscitation of patients
with HHS may signicantly lower plasma glucose
levels, and some patients may not require insulin
therapy. Volume resuscitation of patients with DKA
may lower glucose levels slightly, but insulin is almost
always required and should be administered early.
e rate of administration of insulin for patients with
DKA is, however, similar to insulin recommendations
for HHS patients, who require insulin for further
lowering of glucose levels aer volume resuscitation.
4. Can rapid- acting insulin analogs be used for treatment
of DKA? Insulin analogs are genetically modied
derivatives of human insulin. ese modications were
designed to improve insulin absorption, and achieve
more consistent insulin blood levels, with better
REFERENCES
1. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic
crises in adult patients with diabetes. Diabetes Care.
2009;32:1335– 43.
2. Coursin DB, Connery LE, Ketzler JT. Perioperative diabetic
and hyperglycemic management issues. Critical Care Medicine.
2004;32:S116– 125.
3. Kitabchi AE, Nyenwe EA. Hyperglycemic crises in diabetes mellitus. Endocrinology and Metabolism Clinics of North America.
2006;35:725– 51.
4. Wang J, Willimas DE, Narayan KM, Geiss LS. Declining death
rates from hyperglycemic crisis among adults with diabetes, U.S.,
1985–2002. Diabetes Care. 2006; 29:2018– 22.
5. Nyenwe EA, Razavi LN, Kitabchi AE, Khan AN, Wan AY.
Acidosis:the prime determinant of depressed sensorium in diabetic
ketoacidosis. Diabetes Care. 2010;33:1837– 39.
6. Sebranek JJ, Lugli AK, Coursin DB. Glycaemic control in the perioperative period. British Journal of Anaesthesia. 2013;111:i18– i34.
7. van den Berghe G, Wouters P, Weekers F, Verwaest C, Bruyninckx
F, Schetz M. Intensive insulin therapy in critically ill patients New
England Journal of Medicine. 2001;345:1359– 67.
8. Lipshutz AK, Gropper MA. Perioperative glycemic control: an
evidence- based review. Anesthesiology. 2009;110:408– 21.
9. Mahler SA, Conrad SA, Wang H, Arnold TC. Resuscitation with
balanced electrolyte solution prevents hyperchloremic metabolic
acidosis in patients with diabetic ketoacidosis. American Journal of
Emergency Medicine. 2011;29:670– 74.
10. Van Zyl DG, Rheeder P, Delport E. Fluid management in diabetic
acidosis— Ringer’s lactate versus normal saline: a randomized controlled study. uarterly Journal of Medicine. 2012;105:337– 43.
DIABETIC KETOACIDOSIS 231
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32.
HYPERGLYCEMIC HYPEROSMOLARSTATE
ShamsuddinAkhtar
CLINICALCASE
factor and inuences substrate metabolism, energy storage,
and protein synthesis. Activation of receptors by insulin
A 73- year- old man presented to the Emergency Department
(ED) with recent mental status changes. He lives in a retirement community home and was found obtunded in his room.
Ten days prior to this admission, he had undergone routine
cystoscopy for evaluation of recurrent bladder cancer. He had
complained of not feeling well to his caregivers for 7 days.
Medical history includes diabetes mellitus (treated with
oral hypoglycemics), hypertension, and chronic obstructive
pulmonary disease. Initial vital signs in the ED were:blood
stimulates downstream pathways that translocate specic
glucose transporters (GLUT) to the cell membrane and
allows glucose to enter the cell. Not all tissues require insu-
lin for glucose transport. Muscle and fat, however, require
insulin for glucose transport. Deciency or ineective-
ness of insulin (insulin resistance) causes hyperglycemia.3
Inammatory mediators can increase resistance to insulin.
Hyperglycemic crises increase oxidative stress and increase
levels of proinammatory cytokines.
pressure 85/ 40mmHg; heart rate 110 beats per minute; respiratory rate 20 breaths per minute; SpO2 94% on room air;
temperature 37.6 degrees Celsius. e nger stick glucose
level was out- of- range of the point- of- care device. Laboratory
studies measured at the central lab were: blood glucose of
900 mg/ dL; BUN 79; serum sodium 131mmol/ L, pH 7.31,
bicarbonate 18 mEq/ L, and the anion gap was calculated to
be 14. His abdomen was tender to palpation with positive
peritoneal signs. He is scheduled to undergo emergent exploratory laparotomy for a suspected perforated viscus.
MECHANISM
e underlying defect in HHS is ineective action of insulin
that leads to elevated levels of counterregulatory hormones
(catecholamines, glucagon, cortisol, growth hormone). e
counterregulatory hormones increase hepatic glucose pro-
duction and impair glucose utilization in peripheral tissues.
Plasma glucose levels that exceed the renal threshold (>180
mg/ dL) cause glycosuria, osmotic diuresis, and renal dysfunc-
tion that leads to dehydration and electrolyte abnormalities.
PATHOPHYSIOLOGY
e term “hyperglycemic hyperosmolar non- ketotic coma”
has been replaced with the term “hyperglycemic hyperosmolar state” (HHS). is term better describes the clinical
presentation, as many patients with HHS present without
coma and have detectable ketones. Hyperglycemic hyperosmolar state and diabetic ketoacidosis (DKA) represent
e near absolute insulinopenia of DKA decreases glycolysis
and increases gluconeogenesis, lipolysis, and fatty acid metab-
olism, which increases the level of circulating ketones. In
HHS, however, there is a sucient amount of insulin to pre-
vent lipolysis and ketogenesis. It takes only one- tenth as much
insulin to suppress lipolysis as it does to stimulate glucose uti-
lization. is results in lower levels of counterregulatory hor-
mones with HHS as compared with patients with DKA. e
severe hyperosmolar state of HHS may also inhibit lipolysis.
two extremes in the spectrum of decompensated diabetes mellitus. Diabetic ketoacidosis is more common than
HHS, but the mortality rate for HHS (10%– 20%) is
signicantly greater than the mortality for DKA (1%).
1,2
Hyperglycemic hyperosmolar state is characterized by
insulinopenia and diers from DKA only in the severity of
dehydration, ketosis, and metabolic acidosis. Insulin is critical for metabolic homeostasis. Insulin serves as a growth
Precipitating Factors forHyperglycemic
HyperosmolarState
Although HHS occurs more commonly in older patients
with type 2 diabetes, it has been reported in younger
patients and in patients with type 1 diabetes. irty per-
cent of patients admitted with HHS do not have a history
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233
of diabetes mellitus. While HHS is typically precipitated
by infection and/ or inadequate insulin therapy, therapeutic
noncompliance, dose reduction, or recent discontinuation
of diabetic medications does oen precede the development
of HHS. Mechanical malfunction of insulin pumps can also
causeHHS.
Drugs implicated as causes of HHS include corticosteroids, thiazide diuretics, sympathomimetic agents
(dobutamine, terbutaline), phenytoin, and antipsychotics (clozapine, olanzapine, risperidone, ziprasidone, quetiapine, perphenazine, and haloperidol). Hyperglycemic
emergencies secondary to antipsychotic medications are
rare in nondiabetic patients (1– 2 events per 1,000 person years of exposure), but are more common in patients
RISK
e mortality from HHS approaches 20% and is nearly
four times greater than the mortality from DKA. e
high mortality may be secondary to the older age of
patients with HHS that may have signicant coexisting
systemic diseases. Sepsis, cerebrovascular accidents, and
myocardial infarction are common causes of mortality
in patients with HHS. Stroke, myocardial infarction,
and peripheral arterial thrombosis may be secondary to
hypercoagulability.
Rapid correction of hyperglycemia and hyperosmolality may also contribute to morbidity and mortality. Major
complications that may occur while treating patients with
HHS are listedhere:
5
with preexisting diabetes (12 events per 1,000 person
4
years).
Less common precipitating factors for HHS include
myocardial infarction, cerebrovascular accident, pulmonary embolism, pancreatitis, and alcohol and drug abuse.
ere are reports of patients with pheochromocytoma presenting with HHS (Box32.1).
Hypoglycemia and hypokalemia— Aggressive
treatment of hyperglycemia with insulin can cause
rapid decreases in glucose and potassium levels. Recent
recommendations for a more gradual correction of
hyperglycemia have markedly reduced the likelihood of
hypoglycemia and hypokalemia.
BOX 32.1 PRECIPITATING FACTORS FORHYPERGLYCEMIC
HYPEROSMOLARSTATE
Decreased intake of insulin or oral hypoglycemicdrugs
Infection
Pneumonia
Urosepsis
Appendicitis
Pancreatitis
Peritonitis
Drug induced
Atypical antipsychotics
Cocaine
Corticosteroids
Sympathomimetics
Alcoholabuse
Pheochromocytoma
Myocardial Infarction
Stroke
Pulmonary embolism
Cerebral edema— Changes in white matter, as
demonstrated with MRI, may occur in patients with
HHS prior to the development of cerebral edema.
Cerebral edema may be secondary to hypovolemia and
inadequate cerebral perfusion.6 Pre- existing cerebral
edema may be aggravated by rapid correction of
hyperosmolarity. is is secondary to a rapid shi of
water into brain cells and/ or dysregulation of cerebral
perfusion.
Pulmonary edema— Resuscitation of patients with
HHS oen requires a large volume of intravenous
uids. Rapid infusion, especially in elderly patients
with compromised cardiac function (systolic and/ or
diastolic dysfunction), can lead to pulmonaryedema.
ASSESSMENT OFTHE PATIENT
Unlike DKA, HHS is insidious in onset and develops
over days to weeks. e most common presenting feature
is neurologic dysfunction. Subtle mental status changes
can progress to obtundation and coma. Patients obtunded
from HHS usually have a serum osmolality greater than
320 mOsm/ L. If the patient is obtunded and the serum
osmolality is less than 320 mOsm/ L, other causes for neurologic dysfunction should be considered. Patients may also
present with seizures or focal neurologic signs suggestive of
a stroke or brain tumor. Signs of dehydration such as dry
HYPERGLYCEMIC HYPEROSMOLARSTATE 233
234
Effectiveserumosmolality
()
18
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buccal mucosa, sunken eyes, tachycardia, and hypotension
are common. Abdominal pain is a frequent complaint of
patients with DKA, but is unusual in patients withHHS.
there is a total body potassium deciency. Potassium will
need to be replaced as hyperglycemia is corrected and volume
is replenished. Phosphate levels may also be low, although
replacement is rarely indicated. Awhite blood count greater
Laboratory Diagnosis
Patients with HHS typically have a blood glucose level
greater than 600 mg/ dL, a blood pH greater than 7.30, a
bicarbonate level greater than 20 mEq/ L, a urine that tests
negative or for a small amount of ketones, and a serum osmolality greater than 320 mOsm/ L (Table 32.1). e eective
serum osmolality can be calculated with the formula:
than 25,000 suggests a coexisting infection.
CONSIDERATIONS FOR ANESTHESIA
Management of the patient with a diabetic emergency in
the perioperative period is challenging. e anesthesiologist
must manage the diabetic emergency and any physiologic
aberrations caused by the surgical problem. e patient
should only undergo anesthesia and surgery if the situation
2serum sodiummEq/L
=× +()
serumglucose
(
mg/dL
is emergent. Patients with HHS are complex to treat and
usually have signicant comorbidities.7 Intensive monitoring is required during surgery and the immediate postop-
e central laboratory should measure glucose levels during the early phases of treatment, as point- of- care monitors
exhibit signicant variability at high glucose levels. Blood urea
nitrogen (BUN), creatinine, electrolytes, and ketones should
also be measured from blood samples. e urine should be
sampled for ketones, and the acid- base status determined from
arterial blood gas samples. Although these tests will help differentiate DKA from HHS, 30% of patients will have features
of both DKA and HHS. Fiy percent of patients with HHS
have an increased anion gap acidosis as a result of a concomitant ketoacidosis and/ or an increase in serum lactate levels.
Sodium can be normal or low despite osmotic diuresis. e
plasma sodium should be corrected by adding 2.4mmol/ L to
the measured serum sodium for every 100 mg/ dL. For example, if the serum glucose is 800 mg/ dL and the serum sodium
is 130mmol/ L, the corrected sodium level is 149mmol/ L.
Although the serum potassium level may be elevated secondary to dehydration, renal dysfunction, and insulin deciency,
erative period. e goal during surgery should not be rapid
correction of the metabolic abnormalities, but initiation of
therapy. e metabolic eects of surgery and the patient’s
ongoing primary issue, sepsis, will aect glucose levels. An
in- dwelling arterial catheter permits frequent measurement
of glucose and electrolyte levels. Transesophageal echocardiography can provide valuable information concerning
myocardial function and intravascular volume. Diabetic cardiomyopathy is characterized by an early subclinical phase
with diastolic dysfunction and le ventricular hypertrophy.
As the disease progresses, systolic dysfunction occurs.
8
Admission to an intensive care unit aer surgery is
almost always indicated, and postoperative mechanical
ventilation is frequently required. Indicators of severe HHS
include serum osmolality > 350 mOsm/ L; sodium level >
160mmol/ L; arterial blood pH < 7.1; serum potassium <
3.5mmol/ L or > 6.0mmol/ L; Glasgow Coma Scale < 12;
systolic blood pressure < 90mmHg, pulse rate > 100 or <
60; urine output < 0.5 mL/ kg/ hr. Other signicant comorbidities may include myocardial infarction and/ or stroke.
TABLE32.1 BIOCHEMICAL DIFFERENTIATION OFDIABETIC
KETOACIDOSIS (DKA) AND HYPERGLYCEMIC
HYPEROSMOLAR STATE(HHS)
DKA HHS
Plasma glucose (mg/ dL) >250 >600
TREATMENT
erapeutic goals for patients with HHS include (1) euvolemia
with eective tissue perfusion and adequate urine output;
(2) gradual reduction of serum glucose; (3) correction of
accompanying electrolyte abnormalities; and (4) identication
Arterial pH <7.0 >7.3
Bicarbonate (mEq/ L) <10 >18
Ketones (urine or blood) ++++ + or–
and management of precipitating causes (Box 32.2).
Fluid Therapy
9
Osmolality (mOsm/ L) variable >320
Anion gap >12 variable
234 SECTION B. ENDOCRINE DISTURBANCES
Patients with HHS are volume depleted and uid losses
average 20% to 25% of body weight, or 100 to 220 mL/ kg.
e total body water decit can be as great as 9 to 12 liters.
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235
Insulin Therapy
BOX 32.2 INITIAL TREATMENT OFHYPERGLYCEMIC
HYPEROSMOLARSTATE
Hydration
1. Infusion of 0.9% NaCl 15– 20 mL/ kg during the rst
hour. Continue hydration until blood pressure and urine
output increases. Close monitoring of cardiac function is
required.
2. When plasma glucose decreases to 300 mg/ dL with
adequate hydration, change uid to 5% dextrose in
0.45%NaCl.
Although hydration alone will produce a modest decline
in glucose levels, supplemental insulin is usually required.
An initial bolus of regular insulin (0.1 unit/ kg) should
be followed by an infusion at 0.1 unit/ kg/ hr. An ideal
rate of glucose level decline is 50 to 70 mg/ dL per hour.
Once the blood glucose level has reached 300 mg/ dL,
the insulin infusion should be reduced to 0.05 units/ kg/
hr and the intravenous uid changed to 5% dextrose in
0.45%NaCl.
Electrolyte and Acid- Base Therapy
Insulin Therapy
Bicarbonate levels in HHS are typically > 15 mEq/ L.
Signicant acidosis and a low bicarbonate level are more
1. Regular insulin bolus of 0.1 units/ kg
2. Insulin infusion at 0.1 units/ kg/ hour
common in patients with DKA. Perturbations in potassium levels are common in both DKA and HHS. e initial
potassium level is oen normal or high despite an overall
3. Decrease insulin infusion to 0.05 units/ kg/ hour when
plasma glucose decreases to < 300mg/ dL
4. Goal for serum potassium is 3.3mEq/ L
potassium decit. is apparent paradox is due to hyperosmolarity, insulin deciency, and the intracellular exchange of
potassium for hydrogen ions. Potassium deciency is greater
in patients with HHS than patients with DKA. e average
Biochemical Monitoring
potassium deciency in DKA is 3 to 5 mEq/ kg and 4 to 6
mEq/ kg in patients with HHS. Hypokalemia oninitial lab-
1. Frequent monitoring of glucose and electrolyte levels
(q onehour)
2. Measure calcium, magnesium, and phosphatelevels
oratory testing in patients with DKA and HHS represents
a severe potassium deciency. Because there is little or no
underlying acidosis in patients with HHS, treatment with
insulin and uids can produce an accelerated shi of potassium from the intravascular space to the cells. Patients with
e initial goal is to replace half the water decit in the rst
12 to 24 hours. e usual resuscitation uid is 0.9% saline
(normal saline) and is administered at the rate of 15 to 30
mL/ kg during the rst hour. If the patient is hypernatremic,
0.45% saline is indicated. When the blood glucose level
reaches 300 mg/ dL, the intravenous uid can be changed to
5% dextrose on 0.45% NaCl. Hydration reduces the levels
of counterregulatory hormones, glucose, BUN, and potassium without aecting pH or bicarbonate levels. Frequent
measurement of electrolytes and glucose is clearly indicated
during the early phases of resuscitation. Blood glucose levels should not be corrected rapidly, as cerebral edema may
ensue, especially in children and elderly patients.
Volume therapy should always precede insulin therapy.
HHS may need as much as 20 to 30 mEq/hr for adequate
potassium replacement. Serum potassium levels should be
maintained above 3.3 mEq/ L. erapy with bicarbonate is
rarely required for patients with HHS. Phosphate replacement should be considered if the serum phosphate is less
than 2 mEq/ L or there is evidence of phosphate depletion
syndrome with rhabdomyolysis. Magnesium and calcium
levels should also be monitored. Frequent measurements of
blood chemistries (every hour) are clearly indicated.
Hyperglycemic hyperosmolar state is considered to be
resolved when the serum osmolarity is < 320 mOsm/ L and
the patient’s mental status improves. Clinical improvement
in mental status, however, may require twice the time for
biochemical recovery.
Insulin does not need to be administered at the time of diagnosis and should not be started until electrolyte measurements are available. Administering insulin before adequate
uid replacement can result in cardiovascular collapse.
Insulin- mediated glucose uptake moves water out of the
intravascular space and into cells causing severe hypovolemia.
FOLLOW- UP
Aer the patient recovers from the acute episode of HHS, a
careful search for precipitating causes should be undertaken.
Fiy percent of patients with HHS have an underlying
HYPERGLYCEMIC HYPEROSMOLARSTATE 235
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