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adequate for patients receiving chronic steroid therapy.
Patients undergoing extremely stressful surgery may,
however, require more corticosteroid.
micrograms/ dL) should be obtained. Immediately
aer the blood sample has been obtained, intravenous
hydrocortisone (1 mg/ kg) should be administered.
4. Should “stress dose” steroids have been administered
during the induction of anesthesia? If so, what steroid
preparation and how much should be given? e
corticosteroid should be administered at the time of
induction to minimize the risk of anesthetic induced
hypotension. Although there are several dierent
corticosteroid preparations, it seems logical that
hydrocortisone, the most physiologic form, would be
the best choice. Scientic evidence establishing the
superiority of hydrocortisone over other preparations,
however, is lacking.
5. What might the intraoperative presentation of
the patient with undiagnosed chronic AI be? e
most common clinical sign of acute intraoperative
AI is hypotension. Hypotension, unfortunately,
is nonspecic and can be caused by many things.
Other clues to AI include a history of nausea and
weight loss. Hyperpigmentation of the skin may
be evident, especially if the patient has no tan lines
and skin creases are hyperpigmented. Elevated levels
of ACTH stimulate skin melanocytes to increase
melanin production. If acute AI is suspected, a blood
sample for measurement of ACTH (normal=9–52
picograms/ mL) and cortisol (normal=6–23
REFERENCES
1. Charmandari E, Nicolaides NC, Chrousos GP. Adrenal insuciency. Lancet. 2014;383:2152– 67.
2. Allolio B. Adrenal crisis. European Journal of Endocrinology.
2015;172:R115– 24.
3. ∅ksnes M, Ross R, Lovas K. Optimal glucocorticoid replacement in adrenal insuciency. Best Practice & Research:Clinical
Endocrinology & Metabolism. 2015;29:3– 15.
4. uinkler M, Oelkers W, Remde H, Allolio B. Mineralocorticoid
substitution and monitoring in primary adrenal insuciency.
Best Practice & Research:Clinical Endocrinology & Metabolism.
2015;29:17– 24.
5. van den Heuvel I, Wurmb TE, Bottiger BW, Bernhard M. Pros and
cons of etomidate- more discussion than evidence? Current Opinion
in Anesthesiology. 2013;26:404– 8.
6. Coursin DB, Wood KE. Corticosteroid supplementation for adrenal insuciency. Journal of the American Medical Association.
2002;287:236– 40.
7. Puar THK, Stikkelbroeck NMML, Smans LCCJ, Zelissen PMJ,
Hermus ARMM. Adrenal crisis:still a deadly event in the 21st century. American Journal of Medicine. 2016;129:339.e1– 339.e9.
8. Jung C, Inder WJ. Management of adrenal insuciency during the
stress of medical illness and surgery. Medical Journal of Australia.
2008:188:409– 13.
9. Kelly KN, Domajnko B. Perioperative stress- dose steroids. Clinics in
Colon and Rectal Surgery. 2013;26:163– 67.
10. Husebye ES, Allolio B, Arlt W, etal. Consensus statement on the
diagnosis, treatment and follow- up of patients with adrenal insuciency. Journal of Internal Medicine. 2014;275:104– 15.
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30.
CUSHING’S DISEASE
Doris M. Hardacker
CLINICALCASE
A 43- year- old female was diagnosed with an ACTH secret-
BOX 30.1 CAUSES OFCUSHING’S SYNDROME
ACTH- Dependent(80%)
ing pituitary tumor. Her presenting signs and symptoms
were recent weight gain, menstrual irregularities, depression, and hypertension. She was admitted to the hospital
Pituitary adenoma
Pituitary hyperplasia
and scheduled for resection of the pituitary tumor. Vital
signs at admission were:weight 94kg, BMI 37; heart rate
124 beats per minute; blood pressure 196/ 102mmHg; and
EctopicACTH
Malignant endocrinetumors
respiratory rate 10 breaths per minute. Laboratory studies:serum glucose 194 mg/ dL, serum potassium 3.0mmol/
L, bicarbonate 39 mmol/ L, serum cortisol 244 micro-
Benign endocrinetumors
ACTH- Independent(20%)
grams/ dL (normal 10– 25 micrograms/ dL).
Adrenal adenoma
PATHOPHYSIOLOGY
Cortisol has profound eects on normal physiologic func-
Adrenal carcinoma
Adrenal hyperplasia
tion. Overproduction or underproduction of cortisol
causes serious organ dysfunction. Circadian, metabolic,
and stress inputs to specialized hypothalamic cells release
corticotrophin- releasing hormone (CRH), which, in turn,
increases the release of adrenocorticotrophic hormone
(ACTH) from the anterior pituitary gland. e ACTH
stimulates the release of cortisol by the adrenal cortex.
Increased cortisol levels subsequently inhibit the release
of CRH and ACTH (see chapter “Perioperative Adrenal
Crisis”). Cortisol levels are highest between 6 and 9 AM
and are lowest between 11 PM and1AM.
1
Cushing’s syndrome is caused by any condition that causes
excess secretion of cortisol. Cushing’s disease is more precisely
dened as hypercortisolism caused by an ACTH- secreting
tumor of the pituitary. In adults, Cushing’s disease is responsible for 70% of the cases of Cushing’s syndrome (Box30.1).
Overproduction of glucocorticoids results in hyperglycemia, insulin resistance, dyslipidemia, hypertension, hypokalemia, metabolic alkalosis, obstructive sleep apnea, truncal
obesity, osteoporosis, proximal muscle wasting, bualo
hump, and purple skin striae. Cortisol can cause hypo- or
hypercoagulability. Neurocognitive disorders caused by
excessive cortisol include mood alteration, major depression, anxiety, mania, and brain atrophy (Table 30.1).
2
Endogenous origins of cortisol overproduction include
ACTH- producing anterior pituitary adenomas (70%),
primary adrenal cortical tumors (15%), and ectopic
ACTH- producing tumors (e.g., oat cell carcinoma) (15%).
Pituitary adenomas predominate in women (5 female:1
male). e increased use of abdominal imaging has resulted
in increased discovery of adrenal tumors (adrenal inciden-
MECHANISM
Cortisol, a glucocorticoid, has widespread systemic catabolic, cardiovascular, and anti- inammatory eects.
talomas) that are nonfunctioning in 70% of patients. irty
percent, however, have varying degrees of increased circulating cortisol levels that may be associated with an increased
risk of adverse cardiovascular events.
3
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RISK
Patients with Cushing’s syndrome are at increased risk for
cardiac dysfunction secondary to chronic hypertension,
metabolic syndrome, and premature coronary arteriosclerosis. Le ventricular dysfunction is caused by direct and indirect eects of cortisol excess. High levels of cortisol have
a mineralocorticoid eect that leads to sodium and water
retention. is eect produces le ventricular hypertrophy
e nonspecic nature of the signs and symptoms of
Cushing’s syndrome usually delays diagnosis by many years.
Laboratory testing can be complex, oen requiring several
hormone assays and suppression tests. e interpretation of
these tests should be le to experienced endocrinologists.
Advanced imaging techniques have provided a signicant
aid in earlier diagnosis and localization of ACTH- and
cortisol- producing tumors.
and diastolic dysfunction. Hypokalemia and alkalosis may
induce cardiac dysrhythmias. All told, adverse cardiac eects
ASSESSMENT OFTHE PATIENT
are responsible for a two- to fourfold increase in mortality
for patients with Cushing’s syndrome when compared with
the general age- and gender- matched population.
4
Systemic eects of excess cortisol are widespread. Protein
wasting causes proximal muscle weakness and atrophy, thin
skin, easy bruising, and slow healing. Muscle weakness and
obesity can lead to obstructive sleep apnea. Osteoporosis may
predispose to fractures. Impaired immune function is responsible for an increased incidence of infection and sepsis.
In some patients, severe hypercortisolism can cause
hypertensive crises, life- threatening sepsis, and respiratory
insuciency. Emergent resection of an ACTH- producing
adenoma or a cortisol- producing adrenal adenoma would
be indicated for such patients.
5
Preoperative assessment of the patient with Cushing’s syndrome must include careful evaluation of the many systemic eects of hypercortisolism. Hypertension is present
in 85% of the patients, and 60% have impaired glucose
tolerance. is patient exhibited many of the features of
Cushing’s syndrome such as hypertension, hyperglycemia,
and obesity. Apreoperative transthoracic echocardiogram
revealed le ventricular hypertrophy, asymmetric septal
hypertrophy, an ejection fraction of 50%, and grade 2 diastolic dysfunction. e hypokalemia and increased serum
bicarbonate levels were typical of the associated metabolic
alkalosis.
CONSIDERATIONS FORANESTHESIA
TABLE30.1 CLINICAL FEATURES OFCUSHING’S SYNDROME
System Clinical Feature
Appearance Moon face, truncal obesity, buffalo hump
Musculoskeletal Proximal myopathy, backache osteoporosis,
vertebral body collapse
Although there are no contraindications to specic anesthetic agents for patients with Cushing’s disease, there are
several concerns about administering anesthesia to patients
with Cushing’s syndrome. Eorts are instead directed
toward managing the many systemic eects of excess cortisol. Hypertension and le ventricular dysfunction may
Skin Purple striae on abdomen, and thighs, fragile skin,
ecchymoses, acne, hirsutism, female balding
predispose to exaggerated cardiovascular eects of inhaled,
halogenated anesthetics. Hypotension that may occur dur-
Endocrine Impaired glucose tolerance, diabetes mellitus
Cardiovascular Hyper tension, LVH, diastolic dysfunction, ECG
changes
Respiratory Sleep apnea
Gastrointestinal Gastroesophageal reux, abdominal pain
Metabolic Hypokalemic metabolic alkalosis, hypernatremia,
obesity
Respiratory masculinization
Genitourinary Renal stones, menstrual changes, decreased
libido, masculinization
Neuropsychiatric Headache, cognitive dysfunction, lethargy,
depression
Immunologic Recurrent infections
ing anesthesia can be treated with vasoactive drugs. Patients
with Cushing’s syndrome may, however, be more sensitive
to exogenous vasoactive medications. Hyperglycemia (glucose > 180 mg/ dL) can be treated with intravenous insulin. Close monitoring of plasma glucose levels is indicated
in order to avoid hypoglycemia. e anesthesiologist may
rarely be confronted with an emergent case of severe hypercortisolism in a patient with respiratory failure, malignant
hypertension, severe hypokalemia, metabolic alkalosis, and
sepsis. Etomidate can be eective in reducing serum cortisol levels in preparation for urgent surgery. Etomidate suppresses cortisol production by inhibiting three enzymes
in the steroid synthetic pathway: 17α- hydroxylase,
11 α- hydroxylase, and 11- deoxycortisol β- hydroxylase.
Administration of etomidate causes adrenal suppression
218 SECTION A. METABOLIC DISTURBANCES
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219
within 30 minutes. Low- dose infusions of etomidate
(2–3mg per hour) have been used to reduce cortisol levels
in emergent situations.
6,7
Although the muscle weakness present in patients with
Cushing’s syndrome can be signicant, there is no evidence
that such patients are more sensitive to depolarizing or
nondepolarizing muscle relaxants. Obesity and a history of
obstructive sleep apnea can certainly inuence postoperative ventilatory monitoring and management.
Concerns for anesthesia in patients undergoing pituitary surgery include the head- up position (venous air embolism, reduced cerebral blood ow), sensitivity to mucosal
injection of epinephrine (hypertension, tachycardia), and
potential for hemorrhage. Insertion of an arterial cannula
is strongly recommended for close monitoring of blood
normocarbia and prevent a greater degree of alkalosis.
e intraoperative course was uneventful. e patient was
extubated at the conclusion of surgery when she was fully
awake and responsive to verbal commands. e immediate postoperative course in the postanesthesia care unit
(PACU) was unremarkable. She was transferred to the
intensive care unit (ICU) for close monitoring of metabolic parameters for 48 hours. Her urine output the rst
24 hours aer surgery was 11 liters with a urine specic
gravity of 1.003. e serum sodium was 153mmol/ L. In
view of the excessive urine output and increasing serum
sodium, desmopressin (2 micrograms) was administered
intravenously. Urine output and serum sodium decreased
over the next 48 hours. e DI was transient, and urine
output and serum sodium normalized in 3days.
pressure and frequent monitoring of arterial blood gases,
electrolytes, and glucose. Postoperative concerns include
control of nausea and vomiting, pain (headache), and disorders of water balance (Box 30.2). Diabetes insipidus (DI) or
inappropriate secretion of antidiuretic hormone (SIADH)
has been reported in up to 25% of patients aer pituitary
resection. Diabetes insipidus typically develops 24 to 48
hours aer surgery and is generally transient. Treatment
with desmopressin is indicated if urine output is excessive
and serum sodium exceeds 145mmol/ L. Diagnostic features of SIADH include a serum sodium concentration
less than 135mmol/ L, a low serum uric acid level, and a
high urinary sodium level (> 40 mEq/ L). Close monitoring of serum electrolytes and water balance are indicated for
patients aer pituitary surgery.
7
TREATMENT
e primary treatment of Cushing’s syndrome is resection
of the ACTH- or cortisol- producing tumor. In this case,
the tumor was an ACTH- producing tumor in the anterior
pituitary, and transsphenoidal resection (TSS) of the pitu-
itary tumor was the treatment of choice. Hypopituitarism,
however, occurs in 13% to 81% of patients aerTSS.
Options for the patient that is a poor surgical risk or
one that refuses surgical therapy include pituitary irradiation and/ or medications that suppress cortisol production
(Table 30.2). ese drugs include pituitary antitumor
drugs such as pasireotide, cabergoline, and temozolomide;
steroidogenesis inhibitors such as etomidate, metyrapone,
Anesthesia was induced with etomidate (0.2 mg/
kg) and tracheal intubation was performed without difculty aer relaxation with cis- atracurium (0.8 mg/ kg).
Anesthesia was maintained with sevourane and fentanyl. Controlled ventilation was adjusted to maintain
TABLE30.2 DRUGS FORTHE TREATMENT
OFHYPERCORTISOLISM
Inhibit Steroid Synthesis Route of Administration
BOX 30.2 SIGNS AND SYMPTOMS OFDIABETES INSIPIDUS
Excessive thirst; craving for ice coldwater
Hypotonicurine
Specic gravity <1.005
Urine osmolality < 200 mOsm/ kg
Urine output high:4– 18 liters per 24hours
Serum hyperosmolality:> 300 mOsm/ kg
Serum hypernatremia:> 145mmol/ L
CUSHING’S DISEASE 219
Etomidate intravenous
Metypyrone oral
Mitotane oral
Ketoconozole oral
Glucocorticoid Receptor Antagonist
Mifepristone oral
Dopamine- 2 Receptor Agonist
Carbegoline oral
Somatostain Analog
Pasireotide subcutaneous injection
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mitotane, and ketoconazole; and glucocorticoid- receptor
antagonists such as mifepristone. Medical therapy for
Cushing’s syndrome has produced variable success and is
clearly secondary to surgery for ecacy.
FOLLOW- UP
8
e pituitary tumor was benign. Her DI recurred aer discharge, and she required chronic therapy with intranasal
desmopressin.9 Her course with respect to DI was a triphasic response, as she developed DI immediately aer surgery
that proved to be transient but was followed by chronic DI
that developed several weeks aer surgery.
Despite successful resection of the pituitary tumor, she
will require long- term monitoring of all pituitary functions.
Aer several weeks, her cortisol levels became low and she
required chronic glucocorticoid replacement. Other endocrine function (thyroid) remained normal. One year aer
surgery, her echocardiogram revealed decreased le ventricular wall thickness with improved systolic and diastolic
function.
e remission rate in patients aer surgical therapy
for Cushing’s syndrome is over 60%. Even aer successful resection of the ACTH- secreting adenoma, the risk
of adverse cardiovascular events persists for patients with
Cushing’s disease. Follow- up with an endocrinologist is,
consequently, indicated for the rest of the patient’slife.
increase in le ventricular mass and reduced systolic
and diastolic function. Most patients have an
improvement in cardiac function aer cortisol
levels decrease.
3. What is the medical treatment for acute, severe
Cushing’s syndrome? If the patient is not a surgical
candidate for resection of the ACTH- or cortisolproducing tumors, there are several drugs that may
be eective. Etomidate (0.03 and 0.3 mg/ kg/ hour)
inhibits cortisol production and has a rapid onset of
action. Metypyrone and ketoconazole inhibit steroid
synthesis, and mifepristone is a glucocorticoid- receptor
antagonist. Etomidate is the only drug that can be
given intravenously and is eective for patients with
severe manifestations of hypercortisolism:uncontrolled
hypertension, psychosis, and infection.
4. How can intraoperative DI be diagnosed? Any pituitary
surgery can result in DI. Ahigh index of suspicion for
the potential risk of DI is warranted during resection
of a pituitary tumor or a craniopharyngioma. Frequent
measurement of plasma electrolytes and urinary output
should be done during these types of surgery. Evidence
of DI includes excessive urine output (> 4 mL/ kg/ hr), a
plasma sodium of greater than 145mmol/ L, and a urine
specic gravity of <1.005.
5. What is the treatment for perioperative DI? e
incidence of postoperative DI aer pituitary surgery
CASE- BASED LEARNING DISCUSSION
1. How do Cushing’s syndrome and Cushing’s disease
dier? Cushing’s syndrome is dened as any cause of
hypercortisolism. Cushing’s disease is caused by an
ACTH- secreting pituitary tumors and accounts for
the majority of the cases of Cushing’s syndrome. ere
are other sources of excess secretion of cortisol such as
adrenal and extra- adrenal tumors.
2. What are the cardiovascular eects of excessive
cortisol production? Hypertension is the
is around 20%. Diabetes insipidus is characterized by
polyuria, dilute urine, and hypernatremia. Perioperative
polyuria can also be caused by hyperglycemia and
intraoperative administration of mannitol. If the
patient is conscious, increased uid intake may be
mediated by an increased thirst sensation. If oral intake
is not possible, uid resuscitation with normal saline
and administration of desmopressin can be initiated.
Careful monitoring of plasma sodium and urine output
are required to avoid overshoot and hyponatremia.
Carbamazepine, chlorpropamide, or clobrate may be
eective for treatment of mildDI.
predominant eect of hypercortisolism and is
characteristic of an ACTH- induced increase of
cortisol production by the adrenal gland. It is
REFERENCES
also possible that increased cortisol production
contributes to the development of essential
hypertension in patients without Cushing’s
syndrome. Cortisol- induced obesity, hyperglycemia,
and dyslipidemia increase the risk of coronary
arteriosclerosis. Cardiac ndings include an
1. Ra H, Carroll T. Cushing’s syndrome: from physiological
principles to diagnosis and clinical care. Journal of Physiology.
2015;593:493– 506.
2. Pivonello R, Simeoli C, DeMartino MC, etal:Neuropsychiatric disorders in Cushing’s syndrome. Frontiers in Neuroscience. 2015;9:129.
3. Di Dalmazi G, Vicennati V, Garelli S, Casadio E, Rinaldi E,
Gioampalma E, Goleri R, et al. Cardiovascular events and
220 SECTION A. METABOLIC DISTURBANCES
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221
mortality in patients with adrenal incidentalomas that are either
non- secreting or associated with intermediate phenotype or subclinical Cushing’s syndrome: 1 15- year retrospective study. Lancet
Diabetes & Endocrinology. 2014;2:396– 405.
4. Sharma ST, Nieman LK, Feelders RA. Comorbidities in Cushing’s
disease. Pituitary. 2015;18:188– 94.
5. Lutgers HL, Vergragt J, Dong P- V, etal. Severe hypercortisolism:a
medical emergency requiring urgent intervention. Critical Care
Medicine. 2010;38:1598– 1601.
6. Heyn J, Geiger C, Hinske CL, Briegel J, Weis F. Medical suppression
of hypercortisolemia in Cushing’s syndrome with particular consideration of etomidate. Pituitary. 2012;15:117– 25.
7. Nemergut EC, Dumont AS, Barry UT, Laws ER. Perioperative
management of patients undergoing transsphenoidal pituitary surgery. Anesthesia & Analgesia. 2005;101:1170– 81.
8. Dabbagh A, Sa’adat N, Heidari Z. Etomidate infusion in the critical
care setting for suppressing the acute phase of Cushing’s syndrome.
Anesthesia & Analgesia. 2009;108:238– 9.
9. Loh JA, Verbalis JG. Diabetes insipidus as a complication aer pituitary surgery. Nature Clinical Practice Endocrinology & Metabolism.
2007;489– 94.
CUSHING’S DISEASE 221
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SECTIONB
ENDOCRINE DISTURBANCES
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31.
DIABETIC KETOACIDOSIS
Anne Newcomer and Michael Gropper
CLINICALCASE
e Centers for Disease Control (CDC) estimates that
there were 140,000 hospital discharges for DKA in 2009.
A 42- year- old, 70- kg woman with type 1 diabetes and a history of acute pyelonephritis is scheduled for a ureteral stent
exchange. Upon admission, the laboratory studies are notable: serum glucose 500 mg/ dL; serum sodium 139 mEq/
L; serum chloride 112 mEq/ L; serum bicarbonate 14 mEq/
L; serum potassium 5.1 mEq/ L; positive urine and serum
beta- hydroxybutyrate. An arterial blood gas showed: pH
7.13; PaCO2 12mmHg; PaO2 100mmHg. Her physical
examination is signicant for signs of dehydration, tachyp-
is represented an increase of 80,000 since 1988. Similar
data for HHS is lacking, but hospital admission rates are
lower for HHS. Although the mortality from HHS (5%–
40%) is higher than the mortality for DKA (1%– 5%), the
overall mortality rate for hyperglycemic crises decreased
between 1980 and 2009.4 In most cases, underlying ill-
nesses cause mortality in patients with hyperglycemic crisis.
Extremes of age, the presence of hypotension, or coma her-
ald a markedly worse prognosis.
nea, and lethargy.
PATHOPHYSIOLOGY
Hyperglycemic crisis is a serious condition with important
implications for perioperative clinical care. Diabetic patients
may develop diabetic ketoacidosis (DKA) and/ or hyperglycemic hyperosmolar state (HHS) in the setting of infection
or trauma that requires urgent surgery.1 Preoperative stabilization to correct life- threatening intravascular volume
and electrolyte imbalances is necessary for the prevention
of intraoperative cardiac dysrhythmias and hemodynamic
instability. Alternatively, patients may develop hyperglycemic crisis during or aer surgery as a direct result of the
stress response to surgery. Perioperative glycemic control is
important, since hyperglycemia can have adverse eects on
wound healing immune and inammatory responses, and
may impair postoperative recovery.
2
Diabetic ketoacidosis is classically associated with type
1 diabetes, but may develop in type 2 diabetics under highstress conditions such as trauma, surgery, sepsis, myocardial
infarction, or cerebrovascular accident.3 Diabetic ketoacidosis is more common in individuals under 65years of age,
while HHS is more common in patients older than 65years
of age with comorbid conditions. As the incidence of type
2 diabetes increases in teenagers and young adults, the incidence of HHS in younger patients may also increase.
MECHANISM
e mechanism of DKA is better delineated than the mechanism for HHS. However both arise from a net reduced
eect of circulating insulin with a concomitant increased
secretion of counterregulatory hormones such as glucagon,
catecholamines, cortisol, and growth hormone. Both DKA
and HHS may be regarded as related disorders on a disease
continuum (Figure 31.1). Pure DKA represents hyperglycemia in the absence of circulating insulin without signicant hyperosmolarity. Patients with HHS, however, have a
relative resistance to insulin. Sucient insulin is present to
suppress ketone production, but not enough to normalize
glucose levels. Over several days, this process culminates in
more severe hyperglycemia and hyperosmolarity.
In clinical practice, a mixed presentation of DKA and
HHS is likely to occur depending on the precipitant, coexisting diseases, and length of illness. In both DKA and
HHS, hepatic gluconeogenesis and glycogenolysis increase
and peripheral glucose utilization decreases, leading to
severe hyperglycemia. In DKA, the accompanying increase
in counterregulatory hormones (glucagon, catecholamines,
cortisol, growth hormone) leads to unchecked lipolysis in
adipose tissue. e liver oxidizes these lipolytic substrates
to ketone bodies (beta- hydroxybutyrate and acetoacetate).
Beta- hyroxybutyrate (β- OHB) and acetoacetate accumu-
late and cause a marked metabolic acidosis. In HHS, the
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