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236
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infection (pneumonia, urosepsis). e patient should also
be evaluated for an underlying myocardial infarction or
cerebrovascular accident.
is patient was transferred to the intensive care unit
following surgery for repair of a perforated bladder and
peritonitis. Due to his preoperative obtundation, he was
kept intubated and maintained on mechanical ventilation.
irty- six hours aer surgery, his mental status improved
and his serum osmolarity and serum electrolytes were normal. He was extubated without diculty.
is patient recovered from his emergent surgery and
episode of HHS. He will, however, require close monitoring of his glycemic control. Mortality risk aer an episode
of a hyperglycemic, hyperosmolar crisis in elderly patients is
elevated for several years.
10
hour of rehydration, if the sodium level increases, the
intravenous uids can be changed to 0.45% saline.
3. Do patients with HHS require insulin? Patients with
HHS typically have enough insulin to suppress lipolysis
and prevent acidosis, unlike patients with DKA.
Hydration reduces plasma glucose levels by inhibiting
the release of counterregulatory hormones and increasing
glucose excretion by improving renal perfusion. Insulin
should be withheld until aer hydration is well underway.
If, aer adequate hydration, the plasma glucose level is
still signicantly elevated then a bolus dose of regular
insulin (0.1 unit/ kg) can be administered or an insulin
infusion started at 0.025 units/ kg/ hr. Glucose levels
should be measured frequently and insulin therapy
adjusted to avoid hypoglycemia. e target range for
plasma glucose is 250– 300mg/ dL.
CASE- BASED LEARNING DISCUSSION
4. What are the precipitating causes of HHS? Precipitants
of HHS in patients with diabetes mellitus include
1. How do patients with HHS dier from patients with
DKA? Patients with HHS are typically older, have
more comorbidities, and have severe dehydration.
Prominent laboratory ndings in patients with HHS
are a plasma glucose > 600 mg/ dL, serum osmolality
> 320, arterial pH > 7.30, and serum bicarbonate > 15
mEq/ L. In contrast, patients with DKA have a plasma
glucose of 250– 500 mg/ dL, a serum osmolality <
310, an arterial pH < 7.20, and a serum bicarbonate
< 10 mEq/ L. e dominant eect of HHS is severe
dehydration and stupor/ coma from hyperosmolality.
Water decits in patients with HHS exceed the water
decits of DKA patients by 50% to 100%. e central
feature of DKA is insulin deciency and acidosis from
lipolysis.
2. What intravenous uids should be administered to
patients with HHS? Fluid therapy for patients with
HHS must be controlled with close monitoring of
hemodynamics and metabolic parameters. Older
patients with HHS frequently have preexisting cardiac
and renal dysfunction, and rapid hydration can cause
pulmonary edema. Initial uid therapy should be with
0.9% saline at a rate of 15– 20 mL/ kg/ hr. At the end of
the rst hour, plasma glucose, sodium, potassium, and
osmolality should be measured. e patient’s initial
inadequate dosing of insulin, pneumonia, urinary tract
infection, pancreatitis, myocardial infarction, and
stroke. Drugs such as corticosteroids, thiazide diuretics,
and antipsychotics that aect carbohydrate metabolism
can cause hyperglycemia and HHS. irty percent of
patients over 65years of age with HHS, however, have
no history of diabetes. Elderly people have a diminished
sense of thirst, and any condition that further reduces
water intake (e.g., acute illness) will exacerbate
dehydration and could lead to HHS. e increased
mortality of HHS compared with DKA may reect the
older age of HHS patients.
5. Why do patients with HHS have signicant changes
in their mental status? e patient with severe
obtundation or coma presents a diagnostic challenge.
Since only 30% of patients with HHS present with
coma, the term “hyperglycemic, hyperosmolar coma”
has been replaced with the term “hyperglycemic
hyperosmolar state.” e degree of altered mental status
is directly related to the patient’s serum osmolality
and usually occurs when the osmolality exceeds 350.
Rapid correction of the hyperglycemia can cause
hyponatremia that progresses to osmotic demyelination
syndrome (ODS), which results in severe neurologic
dysfunction.
sodium level may be low because of hyperglycemia and
dilution of plasma from movement of intracellular
water into the vascular space. Rehydration and
correction of hyperglycemia will reestablish water
balance, and sodium levels may increase. Aer the rst
REFERENCES
1. Scott AR. Management of hyperosmolar hyperglycaemic state in
adults with diabetes. Diabetic Medicine. 2015;32:714– 24.
236 SECTION B. ENDOCRINE DISTURBANCES
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237
2. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crisis in adult patients with diabetes. Diabetes Care. 2009;32:1335– 43.
3. Akhtar S, Barash PG, Inzucchi SE. Scientic principles and clinical implications of perioperative glucose regulation and control.
Anesthesia & Analgesia. 2010;110:478– 97.
4. Lipscombe LL, Austin PC, Alessi- Severini S, et al. Atypical antipsychotics and hyperglycemic emergencies:multicenter, retrospective cohort study of administrative data. Schizophrenia Research.
2014;154:54– 60.
5. Corwell B, Knight B, Oliveri L, Willis GC. Current diagnosis and
treatment of hyperglycemic emergencies. Emergency Medicine
Clinics of North America. 2014;32:437– 52.
6. Adeva MM, Souto G, Donapetry C, Portals M, Rodriquez A, Lamas
D. Brain edema in diseases of dierent etiology. Neurochemistry
International. 2012;61:166– 74.
7. Steenkamp DW, Alexanian SM, McDonnell ME. Adult hyperglycemic crisis: a review and perspective. Current Diabetes Reports.
2013;13:130– 37.
8. Khavandi K, Khavandi A, Asghar O, etal. Diabetic cardiomyopathya distinct disease? Best Practice & Research Clinical Endocrinology
& Metabolism. 2009;23:347– 60.
9. Nyenwe EA, Kitabchi AE. Evidence- based management of hyperglycemic emergencies in diabetes mellitus. Diabetes Research and
Clinical Practice. 2011;94:340– 51.
10. Huang C- C, Weng S- F, Tsai K- T, et al. Long- term mortality risk
aer hyperglycemic crisis episodes in geriatric patients with diabetes: a national population- based cohort study. Diabetes Care.
2015;38:746– 51.
HYPERGLYCEMIC HYPEROSMOLARSTATE 237
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33.
HYPOGLYCEMIA
Doris M. Hardacker
CLINICALCASE
MECHANISM
A 58- year- old 85- kg male with long- standing type 2 diabetes mellitus and chronic obstructive pulmonary disease
(COPD) underwent an aortic valve replacement and
four- vessel coronary artery bypass graing. He remained
intubated and heavily sedated because of marginal oxygenation aer surgery. His initial plasma glucose level in
the intensive care unit (ICU) was 420 mg/ dL, and an
insulin infusion was initiated. Serial blood samples for
glucose measurement (point- of- care [POC] glucometer)
were obtained during the rst 24 hours aer surgery.
Plasma glucose levels measured from arterial line samples
ranged from 140 to 180 mg/ dL. irty hours aer surgery, mediastinal bleeding increased and he was transferred to the operating room for mediastinal exploration.
Upon arrival in the operating room, it was noticed that
the arterial line ush solution contained dextrose. e
plasma glucose level obtained from the central venous
line was 32mg/ dL.
Glucose is the primary metabolic substrate of the brain, and
normal cerebral function depends on a steady supply of glucose. Almost all other tissues can utilize alternative energy
substrates during severe hypoglycemia. Neurons may utilize glucose directly as an energy substrate or may use other
metabolic intermediates supplied by astrocytes from metabolism of glucose. Brain glycogen is stored in astrocytes.2
Glucose transport into brain cells ceases when plasma glucose decreases to less than 30 mg/ dL. Soon aer glucose
transport ceases intracellular ATP levels decrease very rapidly. e brain has a very limited capacity to use alternative
fuels such as ketone bodies for a short period of time.
e initial symptoms of hypoglycemia that are mediated by the sympathetic nervous system include hunger,
sweating, palpitations, tremor, and anxiety. Symptoms of
central nervous system dysfunction include confusion,
amnesia, blurred vision, diplopia, and dysarthria. Profound
hypoglycemia causes seizures, coma, and neuronal death.3
All of these signs and symptoms are signicantly blunted
or nonexistent when a patient is heavily sedated or anesthe-
PATHOPHYSIOLOGY
Although hyperglycemia during the perioperative period
has been recognized for many decades, it was felt that this
was a normal, adaptive response to surgical stress and may
in fact be desirable. Over the past 15 years, however, the
detrimental eects of hyperglycemia have been elucidated.
ese eects include increased risk of infection, increased
hospital stay, and increased mortality. Tighter perioperative
glycemic control was consequently advocated, and therapy
with insulin infusions was recommended. Tight glycemic
control, however, has resulted in a higher incidence of signicant hypoglycemia. is is of great concern in patients
who are anesthetized or heavily sedated, as the signs and
symptoms of hypoglycemia are markedly attenuated or
undetectable.
1
tized. e only reliable method of detecting hypoglycemia
during anesthesia is measurement of plasma glucose levels.
Although most of the attention concerning the adverse
eects of hypoglycemia is centered on the central nervous
system, the cardiovascular and immune systems are also
aected. Hypoglycemia activates the sympathoadrenal
system and causes the release of epinephrine, C- reactive
protein, inammatory cytokines, and counterregulatory
hormones and activates platelets (Box 33.1). e physiologic eect of these responses is to increase blood glucose
levels by glycogenolysis and gluconeogenesis. ese mediators also increase cardiac output by increasing heart rate
and myocardial contractility. Myocardial oxygen demand
is subsequently increased and myocardial ischemia and
dysrhythmias can develop. e EKG changes associated
with hypoglycemia include P- R interval shortening, ST
segment depression, T wave attening, and Q- T interval
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technical concerns about the measurement of glucose that
BOX 33.1 METABOLIC RESPONSES TOHYPOGLYCEMIA
the anesthesiologist should recognize. Glucose levels measured with POC devices may not be as accurate as measure-
Sympathoadrenal Activation
Release of epinephrine
ments obtained by the central clinical laboratory. Anemia
and extremes of PaO2 may aect the accuracy of POC
devices. Arterial blood glucose levels are higher than venous
Release of norepinephrine
blood glucose levels. If there is any question as to the accuracy of the POC device, samples should be measured for
Counterregulatory Hormones
Decreased insulin secretion
glucose in the central lab.5 Contamination of the sampling
site with exogenous glucose solutions resulting in a falsely
elevated glucose level and subsequent insulin therapy can
Release of glucagon
Release of cortisol
Release of growth hormone
cause lethal results.
RISK
6
Blood glucose levels are normally tightly controlled
Cardiovascular Effects
Increased heartrate
between 70 and 140 mg/ dL. Severe hypoglycemia in an
adult is dened as a glucose level < 50 mg/ dL (Table 33.1).
e absolute lower limit of glucose before physiologic
Increased myocardial contractility
Increased myocardial oxygendemand
changes occur, however, can vary between patients, and
arbitrary hypoglycemic levels must be regarded with some
skepticism.
e primary risk of severe hypoglycemia is injury to
the brain. e dependence of the brain on glucose as its
prolongation (Box 33.2). Cardiac ischemia is detected more
frequently during hypoglycemia than either normoglycemia or hyperglycemia.
4
e development of easy- to- use and inexpensive devices
for measurement of glucose levels in the 1970s revolutionized diabetic care. Similar devices have also been rec-
main metabolic substrate is the mechanism for the brain’s
vulnerability. e cerebral cortex, hippocampus, and basal
ganglia are especially sensitive to hypoglycemia, while the
brainstem and cerebellum are more resistant to the adverse
eects of hypoglycemia. If hypoglycemia is prolonged, the
patient is likely to remain in a vegetativestate.
ommended for perioperative care. ere are, however,
ASSESSMENT OFTHE PATIENT
Since the patient is anesthetized, the usual signs and
BOX 33.2 CARDIAC EFFECTS OFHYPOGLYCEMIA
symptoms of hypoglycemia that occur in the conscious
patient are of no value for signs of impending hypogly-
ECG Changes
Shortened P- R interval
cemia. If the situation permits, the patient should be
allowed to emerge from anesthesia for neurologic evaluation. If the patient cannot be awakened or remains
Prolonged Q- T interval
ST segment depression
T wave attening
Functional Changes
Myocardial ischemia
Ventricular dysfunction
Dysrhythmias
HYPOGLYCEMIA 239
unconscious despite the correction of hypoglycemia, a
TABLE33.1 AGE- RELATED GLUCOSE LEVELS THAT DEFINE
HYPOGLYCEMIA
Age Glucose Level (mg/ dL)
Adult < 50
Neonate (1–2days) < 35
Infant (> 2days) <45
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cranial scan using magnetic resonance imaging (MRI)
may be useful. Diuse abnormalities in gray and white
matter as detected by MRI may be indicative of perma-
blood glucose level was 260 mg/ dL. Blood glucose levels measured every 30 minutes over the next 4 hours were
between 116 mg/ dL and 148mg/ dL.
nent neurologic injury.7 Since the pathology is related to
metabolism, the MRI lesions are diuse and do not follow an arterial distribution.
Localized hemorrhages usually seen in the cranial MRI
of patients with anoxic- encephalopathy are not seen in
patients with hypoglycemic encephalopathy.
FOLLOW- UP
At the conclusion of the mediastinal exploration, neuromuscular blockade was reversed with neostigmine and
glycopyrrolate and all anesthetics and sedatives were discontinued. e patient, however, did not regain conscious-
MANAGEMENT
e obvious treatment of this patient is discontinuation of
the insulin infusion and the intravenous administration of
50% dextrose (0.2 to 0.5 grams/ kg). Frequent measurement
of blood glucose levels must be performed until the glucose
level has stabilized.
ness. An EEG performed 24 hours aer surgery showed
diuse low- amplitude, low- frequency activity. A repeat
cranial MRI demonstrated diuse gray and white matter
injury. Four days aer surgery, a tracheostomy and percutaneous insertion of a gastrostomy tube were performed. e
patient was subsequently transferred to a long- term care
facility. Although severe hypoglycemia can cause irreversible damage, complete recovery can occur in some patients
with severe hypoglycemia. is patient, however, did not
CONSIDERATIONS FORANESTHESIA
recover.
e recognition that perioperative hyperglycemia can lead
to adverse outcomes created the demand for tighter glyce-
CASE- BASED LEARNING DISCUSSION
mic control. Detrimental eects of hyperglycemia include
cardiac dysfunction, increased risk of surgical wound
infection, and compromised immune function. e cause
and eect relationships between hyperglycemia and these
reported complications are complex and controversial.8
ere is, however, consistent evidence that the primary
complication of tight glycemic control is signicant hypoglycemia and increased mortality.
9,10
Preoperative consultation with the patient’s endocrinologist and/ or intensivist may help the anesthesiologist
develop an individualized plan for intraoperative glucose
control. It should be anticipated that intraoperative glucose levels will increase as halogenated, inhaled anesthetics
suppress insulin release and the stress response to surgical
trauma will both increase glucose levels. Coexisting renal
disease, very common in diabetic patients, will prolong
insulin clearance and may be a factor that inuences glucose
levels. Since it is dicult to predict these inuences and the
eects of exogenously administered insulin, frequent measurement of blood glucose levels is mandatory.
1. Why has tight glycemic control been recommended for
surgical and critically ill patients? e normal response
to surgical trauma is an increase in glucose that is
secondary to initiation of the stress response. Glucose
may increase further as halogenated, inhaled anesthetics
suppress insulin secretion. In the 1990s, studies
showed an association between adverse perioperative
outcomes and hyperglycemia (>180 mg/ dL). Adverse
outcomes included an increased rate of postoperative
infection, higher mortality, and increased length of
hospitalization. Aer these reports, recommendations
were made for tight glycemic control (80– 110 mg/ dL)
with continuous infusions of insulin. It subsequently
became evident that in an attempt to achieve this goal,
there was a signicant incidence of hypoglycemia. e
most recent guidelines recommend maintenance of
glucose between 140 and 180 mg/ dL. is therapeutic
target reduces the incidence of hyperglycemia while
decreasing the likelihood of hypoglycemia.
TREATMENT
As soon as the glucose level of 36 mg/ dL was reported to
the anesthesiologist, the patient received 50 mL of 50% dextrose intravenously and the insulin infusion was stopped.
Fieen minutes aer the administration of dextrose, the
240 SECTION B. ENDOCRINE DISTURBANCES
2. What blood glucose level denes severe hypoglycemia
in adults? e precise glucose level that denes severe
hypoglycemia is not well dened. Although many
medical textbooks dene hypoglycemia as < than 50 mg/
dL, the body initiates countermeasures when the glucose
level decreases by 10– 15 mg/ dL. e countermeasures
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241
accelerate when the glucose level decreases to 65 mg/ dL.
In order to avoid signicant hypoglycemia by initiating
prompt therapy, it may be wise to dene hypoglycemia at
a level of 75 mg/ dL. e adverse eects of hypoglycemia
should not be underestimated, as frequent episodes
of hypoglycemia may increase the risk of neurologic
dysfunction and dementia.
3. Why is the brain so vulnerable to the adverse eects of
severe hypoglycemia? Glucose is the primary metabolic
substrate for the brain, and glucose oxidation provides
90% of the brain’s energy. Neurons cannot synthesize
glucose and cannot use alternative energy sources. e
brain is subsequently dependent on a continuous supply
of glucose. Glucose transport stops when the plasma
glucose level decreases to 30 mg/ dL and residual stores
of glucose in the astrocytes are quickly depleted. Once
these glucose reserves are exhausted, central nervous
system dysfunction occurs and neuronal death ensues.
laboratory? Point- of- care devices that allow the rapid
measurement of blood glucose levels allow patients with
diabetes mellitus to frequently measure their glucose
levels and adjust their therapy. When the interest in
tighter perioperative glycemic control surged, it was
only logical that these POC devices were introduced
into the operating room. Are these devices reliable
and accurate? e FDA only requires glucometers
to be within 20% of the reference value at 75.68 mg/
dL. ere are also physiologic changes such as anemia
and low or high oxygen concentrations that may aect
glucose measurement. Testing of dierent devices has
uncovered potential errors that may aect clinical
management; consequently, glucose measurements that
would warrant a signicant change in therapy should
be conrmed by samples sent to the central laboratory.
Devices that give falsely elevated glucose levels and
result in increased insulin therapy could be especially
dangerous.
4. What are the cardiac eects of hypoglycemia? e
mechanisms for glucose control are complex and
involve regulation of insulin secretion and release of
REFERENCES
counterregulatory hormones. Adecrease in plasma
glucose of 10– 15 mg/ dL suppresses insulin release in an
attempt to prevent further decline. Counterregulatory
hormones are released when the plasma glucose level
drops to 65 mg/ dL. Glucose sensors in the brain
respond to hypoglycemia by causing the release of
growth hormone and adrenocorticotropic hormone.
Neural stimulation of the adrenal medulla also occurs,
thus increasing the release of cortisol, epinephrine, and
glucagon in order to release glucose from other tissues.
e cardiovascular responses to hypoglycemia include
tachycardia and an increase in myocardial contractility.
Whether these cardiac responses are a direct result
of hypoglycemia or secondary to stimulation by
counterregulatory hormones is unclear. If the patient
has limited cardiac reserve from preexisting heart
disease, the increased demand may trigger ischemia and
dysrhythmias.
5. Are POC glucose- measuring devices as accurate as
glucose measuring techniques used in the central
1. Evans CH, Lee J, Ruhlman MK. Optimal glucose management
in the perioperative period. Surgical Clinics of North America.
2015;95:337– 54.
2. Suh SW, Hamby AM, Swanson RA. Hypoglycemia, brain energetics, and hypoglycemic neuronal death. Glia. 2007;55:1280– 86.
3. Martens P, Tits J. Approach to the patient with spontaneous hypoglycemia. European Journal of Internal Medicine. 2014;25:415– 21.
4. Sanon VP, Sanon S, Kanakia R, etal. Hypoglycemia from a cardiologist’s perspective. Clinical Cardiology. 2014;37:499– 504.
5. Rice MJ, Pitkin AD, Coursin DB. Glucose measurement in the
operating room: more complicated than it seems. Anesthesia &
Analgesia. 2010;110:1056– 65.
6. Brennan KA, Eapen G, Turnbull D. Reducing the risk of fatal and
disabling hypoglycemia: a comparison of arterial blood sampling
systems. British Journal of Anaesthesia. 2010;104:446– 51.
7. Ma J- H, Kim Y- J, Yoo W- J, etal. MR imaging of hypoglycemic
encephalopathy: lesion distribution and prognosis prediction by
diusion- weighted imaging. Neuroradiology. 2009:51:641– 49.
8. Akhtar S, Barash PG, Inzucchi SE. Scientic principles and clinical implications of perioperative glucose regulation and control.
Anesthesia & Analgesia. 2010;110:478– 97.
9. Inzucchi SE, Siegel MD. Glucose control in the ICU— how tight is
too tight? New England Journal of Medicine. 2009;360:1346– 49.
10. Krinsley JS, Grover A. Severe hypoglycemia in critically ill
patients: risk factors and outcomes. Critical Care Medicine.
2007;35:2262– 67.
HYPOGLYCEMIA 241
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34.
THYROTOXICOSIS
Nicole D.Horn
CLINICALCASE
controlled by a negative feedback system involving the
hypothalamus, pituitary, and the thyroid gland. e
A 42- year- old man presented to the emergency department (ED) with severe right- sided abdominal pain, nausea, vomiting, and fever. Aer obtaining a computed
tomography scan of the abdomen with contrast, a diagnosis of acute appendicitis was conrmed and he was
taken to the operating room for an emergent laparoscopic
appendectomy. His past medical history was signicant
for chronic hypertension and the recent onset of weight
loss, dysphagia, heat intolerance, palpitations, diarrhea,
and dyspnea upon exertion. He had received several anesthetics for orthopedic procedures in the past without
complications.
Vital signs in the ED were:heart rate of 127 beats per
minute; blood pressure of 156/ 94mmHg; and temperature
of 38.6 degrees Celsius. Anesthesia was induced with fentanyl (1 mcg/ kg ) and propofol (2.5 mg/ kg ). Rocuronium
(0.6 mg/ kg) was administered to provide muscle relaxation for tracheal intubation. Immediately aer intubation,
his heart rate increased to 174 beats per minute and blood
pressure increased to 194/ 112. e EKG showed ST- T
hypothalamus produces thyrotropin- releasing hormone
(TRH), which stimulates the pituitary to secrete thyroidstimulating hormone (TSH), which, in turn, causes the
thyroid to release T4 and T3. Increasing levels of T4 and
T3 inhibit the release of TRH and TSH in order to prevent overproduction. Disruption of this control system
leads to high levels of thyroid hormone and accelerated
metabolism. Signs and symptoms of thyrotoxicosis are
secondary to increased metabolism and include tachycardia, hypertension, palpitations, nervousness, fatigue,
weight loss, heat intolerance, increased sweating, and
diarrhea (Box 34.1). yrotoxicosis can cause severe
complications such as congestive heart failure, thromboembolism, altered mental status, cardiovascular collapse,
and death.
1
e presence of excess thyroid hormone is most oen
caused by Grave’s disease, but may also be a result of thyroiditis, toxic multinodular goiter, thyroid adenomas,
iodine ingestion, TSH- secreting pituitary tumors, or an
overdose of thyroid replacement hormone.
depression.
PATHOPHYSIOLOGY
yroid disorders are oen insidious in onset. Patients and
medical providers frequently do not recognize the early
stages of thyroid dysfunction. e diagnosis is consequently
delayed, and the severity of the problem only manifests
when an intercurrent medical problem develops.
Grave’s Disease
Grave’s disease is the most common cause of hyperthyroidism in developed countries and accounts for 75% of
cases of hyperthyroidism.2 It is an autoimmune disease
mediated by antibodies that stimulate the TSH receptor,
leading to excess secretion of thyroid hormone and hyperplasia of thyroid follicular cells. In addition to the traditional signs and symptoms of hyperthyroidism, patients
with Grave’s disease develop a diuse goiter, ophthal-
MECHANISM
yrotoxicosis is caused by excess circulation of thyroxine (T4) and/ or triiodthyronine (T3). e regulation
of thyroid hormone production and release is normally
mopathy, pretibial myxedema, and acropachy. e onset
of symptoms is gradual over a period of weeks to months.
Mild symptoms can exist for years before an accurate diagnosis is made. On occasion, the onset of signs and symptoms can be abrupt.
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243
neck pain, fever, and swelling. Inammation of thyroid tissue
BOX 34.1 SIGNS AND SYMPTOMS OFTHYROTOXICOSIS
causes thyroid hormone to leak into the circulation leading
to thyrotoxicosis. Subacute thyroiditis is usually self- limiting,
Symptoms
Anxiety/ Confusion
Emotional lability
Diarrhea
Goiter
Palpitations
Dyspnea
Doublevision
but may include a transient period of hypothyroidism.
Iodine- Induced Hyperthyroidism
Administration of iodine, classically iodinated contrast, can
cause areas of the thyroid to autonomously function and
increase release of thyroid hormone. In normal individuals,
excess iodine triggers the Wol- Chaiko eect that inhibits
the oxidation of iodine and synthesis of thyroid hormone.4
Patients with underlying thyroid disease, however, may fail
to adapt to excess iodine and become hyperthyroid.
Menorrhea
Signs
Hyperreexia
Tremor
Sinus tachycardia
Atrial brillation
Heart failure
Pretibial myxedema
Exophthalmos
Toxic MultinodularGoiter
Toxic multinodular goiter is common in third world countries due to iodine- decient diets and in elderly people secondary to poor dietary choices. yrotoxicosis is caused by
uncontrolled release of thyroid hormones from multiple,
separate functioning nodules in the thyroid gland. is
condition is indolent and symptoms are typically mild
with only slight increases in circulating thyroid hormone.
Antithyroid drugs are not very eective for long- term management of patients with toxic multinodular goiter. erapy
with radioactive iodine or surgery is required.
3
RISK
e prevalence of thyrotoxicosis in the United States is
estimated at 1.2%; 0.5% are symptomatic, and 0.7% are
subclinical. Patients at increased risk for thyrotoxicosis
include those with type 1 diabetes mellitus, nodular goiter,
autoimmune diseases, and a family history of hyperthyroidism or hypothyroidism. Medications that increase the risk
of thyrotoxicosis include amiodarone, alpha- interferon,
interleukin- 2, lithium, and iodine. Iodinated contrast agents
(radiographic imaging) increase the risk of thyrotoxicosis
in patients with preexisting autoimmune disease or nodular
thyroid disease. Herbal medicines and dietary supplements
containing kelp may be sources of large amounts of iodine.
ASSESSMENT OFTHE PATIENT
is patient responded to the sympathetic stimulation of
laryngoscopy and tracheal intubation with an exaggerated increase in heart rate and blood pressure. Additional
fentanyl and an increase in the inhaled concentration of
sevourane reduced the heart rate and blood pressure.
Insuation of the abdomen with CO2, however, resulted
in hyperthermia, hypotension, and the development of
atrial brillation. Initial treatment included infusion of a 1L intravenous bolus of normal saline, external cooling, and
5 mg of propranolol. Laboratory studies performed during
this crisis included a free T4 of 29 ng/ dL (normal:0.7– 1.9
Subacute Thyroiditis
yroiditis is an inammation of the thyroid gland following
a viral infection that causes additional release of preformed
thyroid hormone. Clinical manifestations include fatigue,
sore throat, and upper respiratory symptoms followed by
ng/ dL), a serum T3 of 410 ng/ dL (normal: 80– 180 ng/
dL), and an undetectable level of TSH.5 yroid storm in
patients with hyperthyroidism can be triggered by infection, illness, or surgery (Box 34.2). yrotoxicosis with
thyroid storm should be considered in the dierential diagnosis of new- onset atrial brillation.
THYROTOXICOSIS 243
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TABLE34.1 THYROID FUNCTION STUDIES (SERUM)
BOX 34.2 PRECIPITANTS OFTHYROIDSTORM
Withdrawal of antithyroidagents
Infection/ sepsis
Diabetic ketoacidosis
TSH Free T4
Normal
Hyperthyroidism Low High High
T3 Toxicosis Low Normal High
0.5–5 μU/ ml
0.9–2.4 ng/ dL 70–195 ng/ dL
Total T3
Myocardial infarction
Cerebrovascular accident
Cardiac failure
Euthyroid Normal Normal High
(On thyroid)
per minute and should not increase more than 50% with exer-
Surgery
Parturition
Trauma
Radioiodine
cise.8 If these cardiac criteria are not achieved, a beta- adrenergic
blocker can be added to the preoperative medication regimen.
TREATMENT
Treatment of thyroid storm requires aggressive volume
Iodinated contrast
Adverse drug reaction
resuscitation, administration of antithyroid drugs, and
administration of beta- adrenergic blockers to ameliorate
the eects of thyroid hormone on the heart (Table 34.2).9
Beta- adrenergic blockers also inhibit the conversion of T4
CONSIDERATIONS FORANESTHESIA
ere are two primary concerns for the anesthesiologist.
to T3. Intravenous propranolol (1 to 2 mg every 15 minutes) can be administered until cardiovascular stabilization
is achieved. Treatment is then directed toward suppression
of thyroid hormone production and excretion, inhibition of
e rst is the immediate recognition and treatment of lifethreatening thyroid storm, and the second is diagnosis of
the underling disorder that is causing thyrotoxicosis.
e cardiovascular eects of thyrotoxicosis include
sinus tachycardia, reduced systemic vascular resistance, and
increased myocardial oxygen consumption. e chronic
tachycardia may produce a cardiomyopathy. Some patients
with thyrotoxicosis develop pulmonary hypertension from
the direct inuence of thyroid hormone on the pulmonary
vasculature. e chronic hyperdynamic state results in a
decreased cardiac reserve that may be further compromised
by perioperative stress.6 yrotoxic patients are at increased
risk for perioperative complications such as cardiac dysrhythmias, tachycardia, congestive heart failure, and intraoperative bleeding during thyroidectomy.7 Aswollen and
hyperplastic thyroid can bleed excessively during thyroidectomy, but the eect of hyperthyroidism on the coagulation system promotes hypercoagulability and predisposes
to thromboembolism.
TABLE34.2 DRUGS FORTREATMENT OFTHYROTOXICOSIS/
THYROIDSTORM
Drug Dose
Thionamides
Propylthiouracil (PTU)
Methimazole
Beta- Adrenergic blockers
Propranolol
Esmolol 50–100 μg/ kg/ min IV
Metoprolol
Atenolol
Potassium iodide 5 drops (38 mg/ drop) PO q6 hours
600 mg PO load dose then 200 mg q6
hours
20 PO mg q6 hours
1–2 mg IV until heart rate declines
1–2 mg IV until heart rate declines
5 mg IV over 5 minutes until heart rate
declines
Elective surgery should be avoided in patients with thyrotoxicosis until they are rendered euthyroid. yroid function
tests should be measured 7 to 10days prior to elective surgery
to ensure that the patient is appropriately euthyroid (Table
34.1). e resting heart rate should be no greater than 90 beats
Corticosteroids
Hydrocor tisone
Dexamethasone
100 mg IV q8 hours
2 mg IV q6 hours
244 SECTION B. ENDOCRINE DISTURBANCES
https://t.me/medicina_free
245
the peripheral eects of thyroid hormone, and treatment of
underlying disorders. e most common antithyroid drugs
are the thionamides: propylthiouracil (PTU), methimazole, and carbimazole (United Kingdom). e thionamides
inhibit iodination and coupling steps in the synthesis of
thyroid hormone. Propylthiouracil is unique among the
thionamides in that it also inhibits the peripheral conversion of T4 to T3. ionamides exert immunosuppressive
eects by causing apoptosis of intrathyroidal lymphocytes.
Lacking a parenteral preparation, thionamides are administered orally or via nasogastric tube. An initial dose of
600 mg of propylthiouracil can be followed by 200– 300
mg every 6 hours. Methimazole (20 mg) can be administered every 6 hours. Side eects of the thionamides include
hepatic toxicity and agranulocytosis. Since the thionamides
require time to exert their eect, they are most useful for
preparation of thyrotoxic patients for elective surgery. One
hour aer the oral administration of PTU or methimazole
ve drops of potassium iodide solution (38 mg per drop)
should be administered orally. Potassium iodide blocks thyroid hormone release and decreases the size and vascularity
of the thyroidgland.
A glucocorticoid (dexamethasone 2 mg IV every 6hours
or hydrocortisone 100 mg IV every 8 hours) should be
given to reduce the peripheral conversion of T4 to T3, treat
adrenal insuciency, and promote vasomotor stability.
If medical therapy is inadequate for the treatment of
thyroid storm, plasmapharesis and plasma exchange can be
used. ese therapies use plasma and albumin, which provide new binding sites for circulating thyroid hormones.
e eects of plasmapharesis, however, are only transient.
Peritoneal dialysis and cholestyramine can also provide
additional binding of thyroid hormones.
10
of thyroid hormone, and “thyroid storm” is a lifethreatening form of thyrotoxicosis. ese terms are
certainly not precise, and there is no objective test
that denes each entity. e terms “thyrotoxicosis”
and “thyroid storm” are oen used interchangeably.
Progression from thyrotoxicosis to thyroid storm
may be determined by the patient’s comorbidities.
Ayoung, healthy adult may tolerate a higher circulating
concentration of thyroid hormone than an elderly
patient with coronary artery disease. However if a
patient has thyrotoxicosis, prompt therapy must be
initiated before it becomes thyroidstorm.
2. How can thyroid storm be dierentiated from
malignant hyperthermia? e physiologic changes that
occur in the early stages of malignant hyperthermia
are very similar those that are caused by thyroid
storm. Muscle rigidity is more typical of malignant
hyperthermia, and the magnitude of metabolic acidosis
is far greater with malignant hyperthermia. An arterial
blood gas should be obtained in the early stages of
either disorder. Dantrolene will be very eective for
malignant hyperthermia and will have very little eect
for thyroid storm. e tachycardia that occurs with
thyroid storm usually responds to administration
of beta- adrenergic blockade, while beta- adrenergic
blockers will have little eect on the tachycardia caused
by malignant hyperthermia. If there is any doubt
about the diagnosis, it would be prudent to administer
dantrolenerst.
3. How should intraoperative thyrotoxicosis be treated?
erapy is directed at reducing thyroid hormone
production and blocking the peripheral metabolic
eects of thyroid hormone. Propylthiouracil and
FOLLOW- UP
is patient rapidly improved with treatment with propylthiouracil and propranolol. He was referred to an endocrinologist for chronic maintenance therapy and counseling
on factors that can precipitate thyroid storm. Other modalities of therapy for hyperthyroidism include thyroid ablation with radioactive iodine and surgical thyroidectomy.
methimazole (thionamides) inhibit thyroid hormone
synthesis within the thyroid gland. Since there are no
commercially available intravenous preparations for
either drug, they must be given orally, via nasogastric
tube, or rectally. Potassium iodide inhibits thyroid
hormone release and can be given aer a thionamide.
Potassium iodide by itself will stimulate thyroid
hormone synthesis; therefore it should only be
administered 60 minutes aer the thionamide. e
CASE- BASED LEARNING DISCUSSION
type of medication most readily available in the
operating room for the treatment of thyroid storm is
a beta- adrenergic blocker. Propranolol has been the
1. How do hyperthyroidism, thyrotoxicosis, and thyroid
storm dier? e term “hyperthyroidism” describes
an eect that results from overproduction of thyroid
hormone. “yrotoxicosis” is an excessive concentration
most frequently used beta- adrenergic blocker for the
treatment of thyrotoxicosis, but is less selective than
metoprolol or atenolol. One of these cardioselective
beta- adrenergic blockers may be preferable to
THYROTOXICOSIS 245
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