Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 911 - файл
.pdf
206
https://t.me/medicina_free
TABLE28.1 SIGNS AND SYMPTOMS OF
PHEOCHROMOCYTOMA
Signs Frequency
MANAGEMENT
a
Initial management of the patient is directed at rapid control of blood pressure and heart rate. e surgeons should
Hypertension ++++
Sustained
++
be alerted to the possibility of a catecholamine- secreting
tumor so they can delay further tissue manipulation
until hemodynamic control is obtained. e magnitude
Paroxysmal
Postural Hypotension ++
Tachycardia or reex bradycardia +++
++
of the blood pressure increase and heart rate change will
inuence the choice of treatment. Sodium nitroprusside (SNP) is rapid acting and has a short duration of
action, but has the risk of cyanide toxicity. Nicardipine
Pallor ++
Flushing (rare) +
Weight Loss +
is an eective arterial vasodilator with no direct cardiac eects. Selection of the initial treatment regimen
is largely dependent on the anesthesiologist’s experience
with vasoactive drugs (Tables 28.2, 28.3,). An intraopera-
Fasting Hyperglycemia ++
Decreased gastrointestinal motility +
Increased respiratory rate +
tive echocardiogram can provide important information
about cardiac function and should be considered at the
earliest possible time. Beta- adrenergic blockers should be
used very cautiously, if at all, during the early phases of a
Psychosis +
Symptoms Frequency
Headache ++++
Palpitations ++++
Excessive sweating ++++
Anxiety/ nervousness +++
Tremulousness ++
Pain in chest/ abdomen ++
Weakness/ fatigue ++
Nausea/ vomiting ++
Dizziness/ faintness +
Paresthesias +
Constipation (rarely diarrhea) +
Visual disturbances +
a
Highest (++++)to lowest (+)frequency.
Adapted from:Eisenhofer G, Rivers G, Rosas A, etal.:Adverse Drug Reactions in Patients
with Phaeochromocytoma. Drug Saf 2007;30:1031– 62.
a
catecholamine storm. Depression of cardiac contractility
with beta- adrenergic blockers during periods of uncontrolled hypertension may precipitate severe myocardial
failure. e depth of anesthesia can be increased with
inhaled anesthetics, but higher concentrations of these
drugs may further depress cardiac function as well. An
in- dwelling arterial catheter should be inserted for direct
measurement of blood pressure and frequent measurement of acid- base status. Surgery can resume aer hemodynamic control has been achieved. Communication
between the surgeon and the anesthesiologist with regard
to the eect of tumor manipulation is important. Aer
the tumor has been excised, blood pressure may decrease
precipitously, as the source of the catecholamines has been
removed.
Hypotension is best treated with direct- acting vasoconstrictors such as norepinephrine, phenylephrine, or
vasopressin (Table 28.4).4 Increased infusion of intravenous uids is necessary, as many patients with PCC and
PGL are chronically volume depleted. e transesophageal echo can provide invaluable information about cardiac lling and volume status.
should arouse the suspicion for a catecholamine- secreting
tumor. Although intraoperative hypertension can occur
with inadequate levels of anesthesia or as a manifestation of
poorly controlled chronic hypertension, the hemodynamic
variability in patients with PCC/ PGL is much more pronounced. When the tachycardia and hypertension occurs
with manipulation of an intra- abdominal mass, the presence of a catecholamine- secreting tumor is almost certain.
206 SECTION A. METABOLIC DISTURBANCES
CONSIDERATIONS FORANESTHESIA
e anesthesiologist is confronted with two dierent
clinical situations when managing patients with a pheochromocytoma or paraganglioma. e rst, as illustrated
by this patient, is the undiagnosed pheochromocytoma.
e second is preparation of the patient with a known
pheochromocytoma.
https://t.me/medicina_free
207
TABLE28.2 INTRAVENOUS DRUGS FORTHE TREATMENT
OFHYPERTENSION DURING PHEOCHROMOCYTOMA
TABLE28.4 INTRAVENOUS DRUGS FORTHE TREATMENT OF
HYPOTENSION AFTER PHEOCHROMOCYTOMA RESECTION
RESECTION
Drug Dose
Drug Dose
Sodium nitroprusside 0.5–5 mcg/ kg/ min
(Direct vasodilator)
Calcium channel antagonists
Nicardipine 1–10 mcg/ kg/ minute
Clevidipine 0.5–3.0 mcg/ kg/ minute
Magnesium sulfate 2–4 gram load
(Direct vasodilator) 1–2 grams/ hour (maintenance)
Norepinephrine (α- 1, α- 2, β- 1)
Phenylephrine (α- 1)
Epinephrine (α- 1, α- 2, β- 1, β- 2)
Dopamine (α- 1, β- 1, β- 2, DA- 1)
Vasopressin 0.04 IU/ min
All drugs need to be titrated to desired effect.
and a 1- L bolus of lactated Ringer’s solution were used to
0.01–0.1 mcg/ kg/ min
0.15–0.75 mcg/ kg/ min
0.15–0.30 mcg/ kg/ min
2–10 mcg/ kg/ min
stabilize the blood pressure. Closure of the surgical incision
Fenoldopam 1.0–1.6 mcg/ kg/ minute
(Dopamine- 1 receptor agonist)
was uneventful. At the conclusion of surgery, the patient was
awakened and the trachea was extubated. Initial vital signs
in the recovery room (PACU) were: BP 126/51 mmHg,
Phentolamine 5–15 mg (initial)
(Non- selective α- adrenergic
blocker)
Urapidil 10–50 mg IV bolus
(Selective alpha- 1- adrenergic
blocker)
Esmolol 250–500 mcg/ kg load
(Selective beta- 1 adrenergic
blocker)
0.2–2.0 mg/ minute
(maintenance)
2 mg/ minute (maintenance)
50–300 mcg/ kg/ minute
(maintenance)
heart rate 102 beats per minute, and respiratory rate 19
breaths per minute, and SpO2 (room air) was98%.
Subsequent TreatmentSteps
Patients with PCC/ PGL should be managed in the intensive care unit (ICU) for at least 24 hours aer surgery.
Hemodynamic instability may continue, and close monitoring of the cardiovascular and metabolic systems is necessary. Glucose levels should be monitored, as the loss of
excessive catecholamines aer tumor resection can cause
Initial TreatmentSteps
hypoglycemia.
is patient was young, and his postoperative course
For this patient an SNP infusion was initiated but did not
provide acceptable blood pressure control. Phentolamine,
was uneventful. Older patients with comorbidities can have
a more complicated postoperative course.
a reversible nonselective alpha- adrenergic antagonist (two
1- mg doses) and intermittent doses of nicardipine were also
administered. Fieen minutes aer removal of the tumor,
the patient became hypotensive. Aphenylephrine infusion
Preparation ofthe Patient witha Known PCC/ PGL
e goals of preoperative pharmacologic preparation of the
patient with a known PCC/ PGL are:(1)control of blood
TABLE28.3 INTRAVENOUS DRUGS FOR THE TREATMENT OF
HYPOTENSION AFTER PHEOCHROMOCYTOMA RESECTION
pressure, (2)control of heart rate, (3)control of cardiac dysrhythmias, and (4)restoration of intravascular volume. e
target for blood pressure aer pharmacologic preparation
Drug Dose
Norepinephrine (α- 1, α- 2, β- 1)
0.01–0.1 mcg/ kg/ min
is a systolic blood pressure of less than 130mmHg when
seated but greater than 90mmHg when standing. e heart
rate target is 60 to 70 when seated and 70 to 80 beats per
Phenylephrine (α- 1)
Epinephrine (α- 1, α- 2, β- 1, β- 2)
Dopamine (α- 1, β- 1, β- 2, DA- 1)
Vasopressin 0.04 IU/ min
All drugs need to be titrated to desired effect.
0.15–0.75 mcg/ kg/ min
0.15–0.30 mcg/ kg/ min
2–10 mcg/ kg/ min
minute when standing.
ere are no randomized, controlled studies that compare dierent preparation regimens, and no consensus
exists as to the optimal approach or the duration of therapy (Box 28.1). Weingarten etal. compared the preoperative preparation protocols at two major tertiary medical
5
UNDIAGNOSED PHEOCHROMOCYTOMA 207
208
https://t.me/medicina_free
alpha- adrenoreceptors. e prolonged action of phenoxy-
BOX 28.1 DRUGS FORPREOPERATIVE PREPARATION
OFPATIENTS WITHPHEOCHROMOCYTOMA
alpha- Adrenergic Antagonists
benzamine can lead to postural hypotension, reex tachycardia, dizziness, syncope, and nasal congestion. e initial oral
dose of phenoxybenzamine is 10 mg twice daily and can be
increased until the target blood pressure is achieved.
Phenoxybenzamine (non- selective)
Phentolamine (non- selective)
Competitive and short- acting alpha- 1- adrenergic
antagonists used for preoperative preparation are prazosin,
terazosin, and doxazosin. e advantages of pretreatment
Prazosin (selectiveα- 1)
Doxazosin (selectiveα- 1)
with these selective antagonists include a shorter preparation time, fewer side eects, and less intraoperative hypotension.7 Treatment with a nonselective alpha- adrenergic
Terazosin (selectiveα- 1)
Urapidil (selectiveα- 1)
blocker, however, results in fewer episodes of intraoperative
hypertension, but more hypotension aer tumor removal.
Aer alpha- adrenergic blockade has been established,
Calcium Channel Antagonists
Nifedipine
beta- adrenergic blockers such as metoprolol or atenolol
may be administered for control of tachycardia or cardiac
dysrhythmias. An esmolol infusion may be used during sur-
Nicardipine
Amlodipine
gery for heart rate control.
Calcium- channel antagonists (nifedipine, nicardipine)
block NE- mediated release of calcium into vascular smooth
beta- Adrenergic Antagonists
Metoprolol
muscle, thereby relaxing arteriolar smooth muscle and
reducing blood pressure. ese drugs generally do not typically cause hypotension aer tumor removal. Nicardipine is
Atenolol
Propranolol
the most ecacious of the calcium- channel antagonists for
patients with PCC/ PGL.
Magnesium sulfate reduces blood pressure by directly
Tyrosine Hydroylase Inhibitor
Metyrosine
relaxing blood vessel walls and inhibiting catecholamine
release. Magnesium also has antidysrhythmic properties.8
e usual magnesium regimen is an intravenous loading
Therapy is initiated with alpha- adrenergic antagonists. After
adequate alpha- adrenergic blockade, a beta- adrenergic
antagonist can be added for heart rate control. Increased
uid intake is recommended throughout the preparation
period.
dose of 2 grams followed by an infusion of 1 gram per hour.
Angiotensin- converting enzyme (ACE) inhibitors and
angiotensin receptor blockers (ARBs) may be useful for
PCC patients with congestive heart failure or cardiomyopathy. Lisinopril, losartan, or valsartan can be administered
orally during the preparation phase. Dexmedetomidine has
shown promise as an adjunctive drug for management of
centers.6 Although there were dierences in the protocols
and dierences in intraoperative hemodynamics, there
were no clinically signicant dierences in outcome. e
main dierence between the two protocols was the type of
alpha- adrenergic antagonist. One protocol used a nonselective alpha- adrenergic antagonist (phenoxybenzamine) and
the other regimen employed a selective alpha- 1- adrenergic
antagonist (doxazosin, terazosin, or prazosin).
Traditional preparation protocols require a 14- to
21- day course of phenoxybenzamine. Phenoxybenzamine
is a nonselective alpha- adrenergic antagonist that produces noncompetitive, irreversible adrenoreceptor blockade. Its eects only diminish aer synthesis of new
hypertension and tachycardia during pheochromocytoma
resection. Dexmedetomidine reduces the amount of norepinephrine at sympathetic postganglionic neurons.
9
Patients with severe hypertension, hypertension
unresponsive to alpha- adrenergic blockade, or metastatic PCC may benet from treatment with metytyrosine. Metytyrosine is a competitive inhibitor of tyrosine
hydroxylase, the rate- limiting enzyme in catecholamine
synthesis. Metytyrosine is primarily employed to control
extremely wide uctuations in blood pressure. Undesirable
eects that limit the use of metytyrosine to extreme cases
include crystalluria, extrapyramidal symptoms, and psychic
disturbances.
208 SECTION A. METABOLIC DISTURBANCES
https://t.me/medicina_free
209
Vasodilation from alpha- adrenergic blockade will
increase the need for increased uid intake. Increased uid
intake during the preparation phase can be done orally with
a high sodium diet or intravenously with a balanced salt
associated with a risk of a PGL in another anatomic location. Intermittent measurement of urinary and plasma
metanephrines and MR imaging of the neck, chest, and
abdomen will need to be performed on a regular schedule.
solution.
A few case reports have advanced the concept of rapid
preparation regimens for noncompliant patients or emer-
CASE- BASED DISCUSSION
gent situations that require only 24 to 72 hours. ese
regimens have employed magnesium sulfate, labetalol,
and urapidil (a short- acting alpha- 1 adrenergic antagonist). e need for any preoperative preparation in
patients with normotensive PCC has been questioned.
is recommendation, however, certainly represents a
minority opinion.
Combined regional and general anesthesia has been
1. Should the possibility of a catecholamine- secreting
tumor have been considered even though diagnostic
imaging suggested otherwise? Paragangliomas (PGL)
can be found throughout the body. Many PGLs do
not secrete catecholamines; however, because of the
potential for severe intraoperative hemodynamic
stability, consideration of that possibility is warranted.
successfully used for patients with PCC/ PGL. e sympathectomy produced by epidural anesthesia may attenuate hemodynamic responses during tumor manipulation.
Many of the studies, however, demonstrating the advantages of epidural anesthesia were performed prior to the
introduction of many new vasoactivedrugs.
Preoperative preparation must be individualized.
Goals are dependent on many factors, and the patient’s
comorbidities must be considered. e elderly patient
with arteriosclerotic heart and cerebral disease has a much
higher risk of serious perioperative complications with
inadequate preparation than the young adult with minimal
comorbidities.
e planned surgical approach is dependent on the size
of the tumor and the body habitus of the patients. Tumors
less than 6cm in size are usually amenable to laparoscopic
resection. Malignant tumors or syndromes associated with
bilateral tumors may require an open approach.
Despite thorough pharmacologic preparation of
patients with PCC/ PGL and minimally invasive surgical
approaches, the anesthesiologist should be prepared with a
full complement of vasoactive drugs.10 e availability of a
variety of such drugs oers many dierent options for the
management of intraoperative uctuations in heart rate and
blood pressure.
2. When the tachycardia and hypertension occurred, was
the selection of sodium nitroprusside (SNP) as the
initial vasodilator the best choice? Why? Nicardipine
and dexmedetomidine are more readily available in
this operating room. Would there have been better
choices? Aer the tumor was removed and hypotension
developed, was phenylephrine a good choice as an
initial vasoconstrictor? Why? What about using
norepinephrine or vasopressin?
3. What additional monitors would be helpful aer
the hypertension and tachycardia developed? Which
would you choose? Atransesophageal echo (TEE)
should be immediately considered, as it provides
rapid assessment of cardiac function and cardiac
lling. Should a pulmonary artery catheter have been
considered instead? What are the dierent types of
information that can be learned fromeach?
4. If the diagnosis of PCC/ PGL had been made prior to
surgery, how should the patient be prepared? Although
there is no consensus on pharmacologic preparation
of patients with pheochromocytoma, which regimen
would you consider? Would your choice be dierent
in an elderly patient with coexisting cardiac and/ or
cerebrovascular disease?Why?
FOLLOW- UP
During the rst 12 hours aer surgery, this patient had
several episodes of moderate hypotension that responded
to intravenous boluses of lactated Ringer’s solution.
Although a phenylephrine infusion was readily available, it
was not required. Several weeks aer surgery, genetic testing revealed that the patient had a heterozygous mutation
UNDIAGNOSED PHEOCHROMOCYTOMA 209
5. Does regional anesthesia have a role in the perioperative
management of a patient with a known PCC/
PGL? Although epidural anesthesia may reduce the
likelihood of large increases in blood pressure during
tumor resection, what implications will that have on
the remainder of the hospital course for this patient?
Would you consider adding low- dose epinephrine to
the epidural solution?
210
https://t.me/medicina_free
REFERENCES
6. Weingarten TN, Cata JP, O’Hara JF, etal. Comparison of two preoperative medical management strategies for laparoscopic resection
1. Prejbisz A, Lenders LWM, Eisenhofer G, et al. Cardiovascular
manifestations of phaeochromocytoma. Journal of Hypertension.
2011;29:2049– 60.
2. Lenders JWM, Duh QY, Eisenhofer G, etal. Pheochromocytoma
and paraganglioma:an Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology & Metabolism. 2014;
99:1915– 42.
3. Fishbein L. Pheochromocytoma and paraganglioma. Hematology/
Oncology Clinics of North America. 2016;30:135– 50.
4. Ferguson- Myrthil N. Vasopressor use in adult patients. Cardiology
in Review. 2012;20:153– 58.
5. Kiernan CM, Solorzano CC. Pheochromocytoma and paraganglioma. Surgical Oncology Clinics of North America. 2016;
25:119– 38.
of pheochromocytoma. Urology. 2010;76:508.e6– e11.
7. Van der Zee PA, de Boer A. Pheochromocytoma: a review on
preoperative treatment with phenoxybenzamine or doxazosin.
Netherlands Journal of Medicine. 2014;72:190– 201.
8. James MF, Cronje L. Pheochromocytoma crisis:use of magnesium
sulfate. Anesthesia & Analgesia. 2004;99:680– 86.
9. Bryskin R, Weldon BC. Dexmedetomidine and magnesium sulfate
in the perioperative management of a child undergoing laparoscopic
resection of bilateral pheochromocytomas. Journal of Clinical
Anesthesia. 2010;22:126– 29.
10. Lord MS, Augoustides JGT. Perioperative management of pheochromocytoma: focus on magnesium, clevidipine, and vasopressin. Journal of Cardiothoracic and Vascular Anesthesia. 2012;
26:526– 31.
210 SECTION A. METABOLIC DISTURBANCES
https://t.me/medicina_free
211
29.
PERIOPERATIVE ADRENALCRISIS
Jing Tao and Jeffrey J. Schwartz
CLINICALCASE
A 62- year- old woman underwent an exploratory laparot-
TABLE29.1 CORTISOL:ACTION AND DEFICIENCY
Action Signs/ Symptoms
of Deciency
omy for a ruptured colonic diverticulum. She had a history
of rheumatoid arthritis for which she takes prednisone
20 mg daily. In the postanesthesia care unit (PACU), her
blood pressure is 80/ 40mmHg. Her blood pressure does
not increase despite a 2000- mL bolus of lactated Ringer’s
solution and the initiation of a norepinephrine infusion.
Other vital signs are:heart rate 90 beats per minute; respiratory rate 12 breaths per minute; oral temperature 101
degrees F. Laboratory results: hematocrit 34%; sodium
135 mmol/ L, potassium 4.1 mmol/ L; ionized calcium
Endocrine Stimulates gluconeogenesis,
glycogenesis, proteolysis,
lipolysis
Increases insulin resistance
Immunologic Inhibits IL- 2, IL- gamma, TNF- alpha,
T- helper cells
Stimulates IL- 4, IL- 10,IL- 14
Suppresses overstimulation of
immunologic response
Neurologic Stimulates cognitive function
Increases mood, REM sleep
Hypoglycemia
Depression
Fatigue/ lethargy
1.3mmol/ L.
Renal Diuresis
Increases renal blood ow, GFR,
PATHOPHYSIOLOGY
Cardiovascular Indirectly increases cardiac
Adrenal insuciency (AI) typically occurs when there is an
absolute or relative lack of adrenal glucocorticoid production, although mineralocorticoid deciency can contribute
to some types of AI. e adrenal cortex secretes several classes
Musculoskeletal Maintains muscle tone Weakness
Gastrointestinal Nausea/vomiting
sodium retention, potassium
excretion
output, arteriolar tone
Increases epinephrine synthesis
of hormones. e two most important are the glucocor ticoids
Hypovolemia
Hyponatremia
Hypotension
Abdominal pain
and the mineralocorticoids. Both play a vital role in homeostasis and the body’s response to stress. Cortisol, the primary
glucocorticoid secreted, is responsible for maintaining circulatory tone, enhancing immune function, increasing glucose levels, and heightening mental awareness (Table 29.1).
Cortisol is regulated by the hypothalamic- pituitary- adrenal
axis (HPA axis) (Figure 29.1). Aldosterone, the main mineralocorticoid secreted, governs sodium, potassium, and water
balance and is regulated by the renin- angiotensin system
(Table 29.2).
1
e HPA axis begins with secretion of corticotropinreleasing hormone (CRH) by the hypothalamus. e
CRH signals the anterior pituitary to produce adrenocorticotropic hormone (ACTH), which signals the adrenal
gland to produce cortisol. Cortisol then acts as a negative
feedback stimulant to both the pituitary gland and the
hypothalamus to decrease ACTH production. Cortisol is
normally produced in a diurnal pattern, with the highest
production in the morning, decreasing throughout the day.
e average daily cortisol production is 15 mg; however,
under stress conditions, production can increase to 300 mg
in a 24- hour period.
Adrenal insuciency occurs when there is an inadequate response by the adrenal cortex to a stressed state or
there are insucient adrenal hormones in an unstressed
state. Adrenal insuciency can be primary or secondary. Primary AI (Addison disease) is a rare condition that
results from destruction of the adrenal cortex leading to low
211
212
(–)
https://t.me/medicina_free
Stress:
Surgery
Infection
Pain
Anxiety
(+)
Hypothalamus
CRH
cortisol and acute AI. Cortisol requirements are increased
during a critical illness. Trauma, surgery, sepsis, and myocardial infarction are common precipitants of acute AI.
Paradoxically, patients with secondary AI may have signs
of glucocorticoid excess (moon facies, truncal obesity,
abdominal striae) from their exogenous glucocorticoids
while manifesting signs of acute glucocorticoid deciency
Anterior
Pituitary
(hypotension).
Acute AI is oen called an “Addisonian crisis.” Such
terminology can be misleading, as Addison disease speci-
ACTH
cally refers to primary adrenal gland failure, while acute AI
can be primary or secondary. Chronic AI is characterized by
malaise, fatigue, weight loss, and hyperpigmentation of the
Adrenal Cortex
skin. Untreated or poorly treated chronic AI can become
acute during periods of physiologic stress or critical illness.
Cortisol
Figure 29.1 The hypothalamic-pituitary-adrenal axis.
RISK
Patients with chronic AI, whether treated or not, are at risk
for acute AI during stress if additional glucocorticoids are
not administered. Patients at risk for acute AI from HPA
suppression are dicult to predict. Although there is no
production of cortisol and aldosterone. e most common
cause of primary AI in the United States is autoimmune
disease, while throughout the rest of the world tuberculosis
is the most common cause of primary AI.2 Primary AI can
also be caused by other infections, trauma, cancer, medications, heparin- induced thrombocytopenia, and adrenal
infarction and hemorrhage.
Secondary AI is caused by disruption of the HPA
axis. Any pathologic process in the pituitary can disrupt
the HPA axis and decrease cortisol production, however,
the most common cause of secondary AI is due to exogenous steroid administration. Suppression of ACTH
secretion by exogenous steroids causes the adrenal glands
specic dose, duration of steroid use, or length of discontinuation that has been shown to predict the need for glucocorticoid supplementation, some guidelines have evolved
based on clinical practice (Table 29.3). ere is, however,
little rm scientic evidence on which to base these recommendations. e level of HPA axis suppression by exogenous glucocorticoids is highly variable among patients.
ere is general consensus that patients receiving 5 mg or
less of prednisone per day are not likely to have HPA axis
suppression and should not require perioperative glucocorticoid supplementation. On the other hand, patients
receiving 20 mg or more of prednisone per day and within
the 3months prior to surgery should receive glucocorticoid
to atrophy. Sudden withdrawal of steroids or a higher steroid requirement can then lead to inadequate circulating
TABLE29.3 STEROID SUPPLEMENTATION ACCORDING
TOHOME STEROIDUSE
TABLE29.2 ALDOSTERONE:ACTION AND DEFICIENCY
Action Signs/ Symptoms
of Deciency
Renal Increases sodium
reabsorption, potassium
and hydrogen excretion
Cardiovascular Increased ar teriolar tone Hypotension
Musculoskeletal Maintains muscle tone Weakness
Gastrointestinal Nausea/ vomiting
Severe Hypovolemia
Hyponatremia
Hyperkalemia
Abdominal pain
Home Steroid Use Steroid Requirement
Last steroid dose <3months
OR
Currently on steroids > 10mg
Last steroid dose > 3months
OR
Currently on steroids < 10mg
On high dose immunosuppression Given usual dose of
Stress dose steroids required
No stress does steroids required
immunosuppression only.
No additional stress dose steroids
required
212 SECTION A. METABOLIC DISTURBANCES
https://t.me/medicina_free
213
supplementation. e data suggest that if patients take their
usual dose of steroid on the day of surgery, the risk of acute
AI is very small. Some authorities have recommended preoperative testing for AI with an ACTH stimulation test,
but the time and expense of such testing is excessive com-
is patient had moderate hypotension refractory to
uids and vasopressors but normal sodium and potassium levels. e history of rheumatoid arthritis and glucocorticoid therapy should certainly raise the suspicion of
secondaryAI.
pared to the small risk of corticosteroid supplementation.
It must be noted, however, that even brief corticosteroid
supplementation can cause hypertension and uid retention and may have adverse eects on wound healing, infection, and glycemic control.
CONSIDERATIONS FORANESTHESIA
Despite eective modes of therapy for adrenal crisis, the
best course for perioperative management of patients with
ASSESSMENT OFTHE PATIENT
e most characteristic sign of acute AI is hypotension that
is refractory to uid and vasopressor therapy. Other ndings may include hypoglycemia, fever, and abdominal pain.
e diagnosis of AI in the surgical patient is complicated
chronic AI is prevention. At risk patients, such as those
receiving exogenous steroids or patients already diagnosed
with chronic AI need to be identied preoperatively. For
patients who require perioperative supplemental steroids,
dosing should be based on the degree of surgical stress
(Table 29.4). One suggested regimenis:
by the fact that the dierential diagnosis for hypotension
is broad and includes hypovolemia, septic shock, and myocardial dysfunction. e key to timely diagnosis is early
considerationofAI.
Patients with secondary AI will only have signs of cortisol deciency because dysfunction of the HPA axis does not
aect mineralocorticoid production. e clinical picture of
the patient with secondary AI is moderate hypotension and
normal sodium and potassium levels.
Patients with primary AI will have signs of both glucocorticoid and mineralocorticoid deciency because there is
complete or near complete destruction of the adrenal gland.
1. Minor surgery:25 mg of hydrocortisone IV during
induction of anesthesia. ese patients should resume
their home steroid regimen immediately aer surgery.
2. Moderate surgery:25 mg hydrocortisone IV with
induction of anesthesia and 75 to 100 mg in divided
doses over 24hours.
3. Major surgery:150 to 300 mg of hydrocortisone in
divided doses over 24 hours. e rst dose should be
given with induction of anesthesia. Steroids can be
tapered over 2 to5days
Acutely, these patients will also have refractory hypotension
with severe hypovolemia, hyponatremia, and hyperkalemia.
e hyperkalemia can be severe enough to cause ventricular
dysrhythmias.
3,4
Patients with primary AI will also need mineralocorticoid
replacement with udrocortisone (0.1 to 0.2 mg per day) to
maintain uid, sodium, and potassium balance.
TABLE29.4 STEROID SUPPLEMENTATION ACCORDING TOSURGICALSTRESS
Surgical Stress Type of Surgery Steroid Dosing
Minor Minor laparoscopic procedures
Moderate Hysterectomy
Severe Major orthopaedic spine reconstruction
PERIOPERATIVE ADRENALCRISIS 213
Hysteroscopy, dilation and curettage
Cystoscopy
Inguinal herniarepair
Removal of minor skin and subcutaneous lesions
Open cholecystectomy
Hip, knee replacement
Major laparoscopic procedures
Laminectomy
Major cardiothoracic, intracranial, oropharyngeal surger y
Major intra- abdominal resection/ reconstruction
Major vascularrepair
Emergency Surgery
Home steroid dose OR
Hydrocortisone 25 mg IV at induction
No further dosing required afterward
Patients may resume home steroids after surgery
Home steroid dose +
Hydrocortisone 25 mg IV at induction+
Hydrocortisone 75–100 mg/ 24hrsIV
Taper over 1–2days then resume home steroids
afterward
Home steroid dose +
Hydrocortisone 25 mg IV at induction+
Hydrocortisone 100–150 mg/ 24hrs IV for 48hours
Taper over 1–2days then resume home steroids
afterward
214
https://t.me/medicina_free
A single dose of etomidate may suppress cortisol production for as much as 72 hours. Etomidate reduces conversion
of cholesterol to cortisol by blockade of 11β- hydroxylase
and 17α- hydroxylase.5 Although the clinical signicance of
this suppression from a one dose of etomidate is unknown,
it would be prudent to avoid its use in patients with the
potential for AI. Etomidate derivatives with a second
ester linkage, such as methoxycarbonyl- etomidate, do not
adversely aect cortisol production.
hydrocortisone 100 mg every 6 hours for 24 to 48 hours
until the patient is stabilized. If an ACTH stimulation test
is contemplated, a one- time dose of 4 mg of dexamethasone
is a suitable alternative to hydrocortisone. Dexamethasone
has a potent glucocorticoid eect but does not interfere
with cortisol secretion.
Other goals of therapy include hydration, correction
of electrolyte abnormalities, and treatment of the inciting
cause. Aggressive volume replacement with isotonic uid
should be employed for the initial treatment of hypoten-
TREATMENT
Adrenal crisis is a life- threatening condition. Treatment
sion; however, vasopressors may be required. Hypoglycemia
is common, since cortisol plays a large role in glucose
homeostasis via gluconeogenesis, mobilization of glucose
must be started once the diagnosis is conrmed or suspected (Figure 29.2).
Initial Treatment
e mainstay of treatment for acute AI is high dose or
6– 9
TABLE29.5 RELATIVE ANTI- INFLAMMATORY POTENCIES OF
GLUCOCORTICOID PREPARATIONS
Preparation Dose Potency Plasma Half- Life
(mg)
(Minutes)
“stress dose” corticosteroid replacement. e term “stress
dose” refers to a dose that mirrors the maximal output of
the adrenal gland under conditions of severe physiologic
Hydrocortisone 20 1 90
Prednisone 5 4 60
stress. Steroids should be administered as soon as possible to supplement the lack of intrinsic control for circulatory support. ere are several dierent preparations of
steroids; however, hydrocortisone is the most physiologic
Prednisolone 5 4 200
Methylprednisolone 4 5 180
Dexamethasone 0.75 30 200
and is preferred (Table 29.5). e initial dose is 100 mg
of intravenously administered hydrocortisone followed by
• Volume resuscitation with crystalloid
• Vasopressors
HD
Support
• Large bore peripheral access
Obtain
Access
Invasive
Monitoring
Obtain
Medication
Postop
Destination
214 SECTION A. METABOLIC DISTURBANCES
• Central access if necessary
• Arterial line for continuous BP monitoring
• CVP if have central access
• Correct potassium, sodium, and glucose derangement
• Cortisol level at 0, 30, 90 minutes (ACTH stimulation test)
Labs
• Hydrocortisone 100 mg IV or dexamethasone 4 mg IV x1 then
• Hydrocortisone 100 mg IV Q8H for 24–48 hours
• ICU
Figure29.2 Treatment for Addisonian
Crisis
https://t.me/medicina_free
215
stores, and metabolism of proteins, carbohydrates, and fats.
erefore, supplemental dextrose in the resuscitation uids
is generally indicated.
Hyperkalemia and hyponatremia are also common during an adrenal crisis and should be treated with saline hydration, calcium, and bicarbonate for correction of acidosis.
Hyperkalemia- induced ventricular dysrhythmias can develop.
As the precipitating event resolves and the need for supplemental corticosteroids decreases, the corticosteroids can
be weaned. Surgical patients can generally be weaned to
their maintenance dose of corticosteroids over the course of
2 to 3days. If the adrenal crisis was the rst manifestation
of chronic AI, maintenance doses of a glucocorticoid and a
mineralocorticoid will need to be determined.
is patient required 4days of supplemental hydro-
Laboratory Testing
Although treatment should not be delayed for conrmatory
testing, a cortisol level can be obtained immediately prior
to treatment. Acortisol level less than 15 micrograms/ dL
(414nmol/ L) is presumptive evidence of acute AI. Alevel
greater than 15 micrograms/ dL does not, however, elimi-
cortisone due to a ruptured diverticulum and secondary peritonitis. Aer she recovered from surgery and
the peritonitis, her endocrinologist determined that her
maintenance dose of 20 mg prednisone was adequate
for baseline therapy. She did, however, recommend that
the patient receive supplemental corticosteroids for any
future surgery.
nate the possibility of acute AI. ere are a number of tests
that can be performed when the patient is under stable conditions. e most commonly performed test is the ACTH
CASE- BASED LEARNING DISCUSSION
stimulation test. For this test, 250 micrograms of cosyntropin (an ACTH analog) is injected and cortisol levels
are measured at 0, 30, and 60 minutes aer injection. e
diagnosis of AI is conrmed if the peak cortisol level does
not exceed 20 micrograms/ dL (550nmol/ L) or the cortisol level does not increase by more than 9 micrograms/ dL
(248nmol/ L). More recently, a low- dose ACTH stimulation test using 1 microgram has been introduced in order to
more closely mimic physiologic levels of ACTH produced
during stress. e low- dose stimulation test appears to have
increased sensitivity and specicity when compared with
the high- dose test. Athird test measures cortisol levels at
specic times of the day or when the patient is under maximum stress. Maximal cortisol is normally produced early in
the morning, and a cortisol level less than 10 micrograms/
dL is considered insucient. Acortisol level less than 18
micrograms/ dL during stress is also insucient. Despite
the simplicity of the third test, the results can be dicult to
interpret, especially in hypoalbuminemic patients. Cortisol
is 90% bound to albumin. If the patient’s albumin is less
than 2.5 grams/ L, the total cortisol level will be low even
though the level of active free cortisol is normal.
1. What is the dierential diagnosis of hypotension for
this patient? Perioperative hypotension is nonspecic
and can have many causes. Postoperative hemorrhage
would be a rst consideration and could most likely
be eliminated by the physical examination and a
hematocrit. Auid bolus would be the next logical
step to overcome an intraoperative uid decit. In her
case, the uid bolus was not eective. Although there
was no history of preexisting cardiac disease, cardiac
dysfunction should also be considered. Atransthoracic
echo performed in the recovery room could provide
a rapid assessment of cardiac function. e history
of rheumatoid arthritis and treatment with steroids
are important clues that adrenal insuciency may
be the cause of hypotension. An intravenous dose of
hydrocortisone could conrm the diagnosis and be
eective treatment.
2. If the surgery had been elective, should preoperative
testing for AI be performed? Testing for AI
secondary to suppression of the HPA axis can be
done, but the testing requires careful evaluation by
an endocrinologist, time, and expense. For this type
FOLLOW- UP
Patients in adrenal crisis typically have signicant hemodynamic and electrolyte instability and should be admitted to
an intensive care unit for monitoring and treatment. Aconsulting endocrinologist can help with diagnosis, guiding
therapy, and planning for long- term management.
10
of patient, the time and expense for testing is not
cost- eective. e short- term administration of stress
steroids has minimalrisk.
3. If the patient had taken her daily dose of 20 mg of
prednisone on the day of surgery, would she still require
“stress dose” steroids? Most clinical evidence suggests
that 20 mg of preoperative prednisone should be
PERIOPERATIVE ADRENALCRISIS 215
Соседние файлы в папке @xirurgi_2025