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plasma glucose and electrolyte levels, and acid-base parameters (75%), but bilateral adrenal hyperplasia or adrenal carcinoma are
also possible.114 Approximately 5% of cases are caused by familial
prior to inducing any form of anesthesia. The greatest hazard
glucocorticoid-responsive hyperaldosteronism.115
during labor and delivery is severe hypertension. Thus, BP should
be monitored frequently and appropriate treatment initiated Antihypertensive therapy with methyldopa, ß-adrenergic
promptly. Control of BP with hydralazine or labetalol is recom- blockade, or calcium channel blockade is used to control hyper-
mended. Severe hypertension may be associated with cardiac tension. Some patients respond to glucocorticoid supplementa-
failure, which necessitates invasive monitoring. Polyuria and dia- tion. Spironolactone does not appear to be teratogenic, but does
betes mellitus are frequent complications of Cushing syndrome have feminizing effects. Enalapril is not recommended for use in
and should be treated appropriately. Other complications include pregnancy. Potassium therapy may be necessary to correct hypo-
fluid retention, hypokalemia, and alkalosis. kalemia. If medical therapy fails, then laparoscopic adrenalect-
If regional anesthesia is planned, it may be technically difficult omy in the second trimester is preferred.
due to central obesity, muscle wasting, osteoporosis with the
Anesthetic implications
potential for vertebral body collapse, and thinning and bruising
of the skin.112 Coagulation abnormalities or psychiatric distur- Epidural analgesia or GA may be used safely as long as attention
bances may preclude regional anesthesia. There may be an exag- is paid to hemodynamic stability, volume status, glucose levels,
gerated hemodynamic response to vasopressors, endogenous and electrolytes. Consider invasive cardiovascular monitoring if
catecholamines, or sympathectomy. Hypotension should be CHF is suspected or intravascular volume status is unclear.
avoided by careful positioning with left uterine tilt to avoid aorto- Hypokalemia may lead to dysrhythmias and may potentiate the
caval compression, adequate fluid administration, and incre- effects of neuromuscular blockade.
mental injection of local anesthetics.
Many of these women require operative delivery. Either regional
Congenital adrenal hyperplasia
anesthesia or GA is appropriate, with the recognition that hemo-
dynamic lability may be significant. Intraoperatively, invasive Congenital adrenal hyperplasia (CAH) includes a family of
hemodynamic monitoring can assist in the management of serious genetic disorders of steroidogenesis. The most common is



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4 Metabolic disorders


21-hydroxylase deficiency, resulting in impaired cortisol produc-
Table 16.9 Presenting symptoms of hypercalcemia
tion. Mineralocorticoid production may be affected as well. In
response to impaired synthesis of cortisol, the hypothalamus Cardiovascular Hypertension
increases ACTH secretion and ACTH stimulates adrenal precur- Dysrhythmias
sors that lead to excess androgen production. Virilization of the Neuropsychiatric Depression
female fetus with CAH can be avoided by dexamethasone admin- Psychosis
istration to the mother. Therapy is begun before week nine of Seizures
gestation in a high-risk woman. Genetic testing with amnio- Obtundation
centesis or chorionic villus sampling is completed to determine Coma
the fetal sex and the presence or absence of the genetic mutation. Gastrointestinal Peptic ulcer disease
Steroid therapy is continued only for women carrying an affected Hyperemesis gravidarum
female fetus.116 Constipation
Women with CAH often have amenorrhea, but may become Anorexia
pregnant with adequate steroid therapy and pharmacologic Nausea/vomiting
induction of ovulation.117 Steroid therapy should be continued Pancreatitis
throughout pregnancy for women carrying a female fetus, Urinary Nephrolithiasis
because androgens, if allowed to develop, may cross the placenta Nephrocalcinosis
and virilize the fetus. On the other hand, excess exogenous steroid Polyuria
also may cross the placenta and suppress the fetal adrenals, Neuromuscular Weakness
leading to transient adrenocortical insufficiency in the neonate. Skeletal Osteoporosis
Cesarean section rates may be as high as 50% in women with CAH Pathologic fracture
because of abnormal maternal external genitalia or a small bony Miscellaneous Thirst
pelvis.118 Women on dexamethasone therapy will need steroid Pruritus
supplementation during labor and delivery.
Adapted from Nader, S. Other endocrine disorders of pregnancy. In
Creasy, R. K., Resnik, R., Iams, J. D. (eds.), Maternal“Fetal Medicine:
Parathyroid glands Principles and Practice, 5th edn. Philadelphia: Saunders, 2004:
pp. 1083“107.
The four parathyroid glands produce parathyroid hormone (PTH).
Along with vitamin D and calcitonin, PTH regulates Ca2þ homeo-
stasis. During pregnancy, PTH-related peptide (PTHrP) is
released by the fetus and placenta. This hormone shares a com- placenta and through the kidneys. Thirdly, up to 80% of women
mon receptor with PTH, and regulates active transport of Ca2þ with hyperparathyroidism are asymptomatic or experience vague
across the placenta, creating a relative fetal hypercalcemia. It is symptoms attributed to normal changes of pregnancy.
found also in uterine smooth muscle where it is thought to regulate The majority of cases are caused by a single parathyroid ade-
myometrial tone and blood flow. High levels of PTHrP may over- noma (80%). Less common etiologies include parathyroid gland
load local hormone metabolism, lead to systemic maternal hyper- hyperplasia, multiple adenomas, and carcinoma, and secondary
parathyroid activity, and suppress maternal PTH release. hyperparathyroidism. Women who rely on calcium carbonate
Up to 30 g of Ca2þ are delivered across the placenta to the fetus antacids to control gastroesophageal reflux symptoms may pre-
during a normal pregnancy. Nevertheless, maternal ionized Ca2þ sent with exogenous hypercalcemia with normal or decreased
PTH levels.119,120
levels are normally homeostatically regulated and stable through
pregnancy at 1.5“2.5 mEq/dl. This active, ionized form represents Women with hyperparathyroidism present with a variety of
only 40% of total blood Ca2þ. On the other hand, close to 50% of symptoms (see Table 16.9), and the maternal complication rate
circulating Ca2þ is bound to albumin, and total blood Ca2þ levels may be as high as 67%.121 Nephrolithiasis appears to be the
fall because plasma albumin falls. The remaining 10% of circulat- most common complication seen in 20“36%, and is associated
ing Ca2þ is chelated and physiologically inactive. with an increased risk of urinary tract infections (10“20%).122
Radiographically demonstrated bone disease is apparent in
13“19%. In 10% of cases, calcification blocks the pancreatic
Hyperparathyroidism
ducts and lead to pancreatitis.123 Hypercalcemic crisis is rare
but serious, and is seen in patients with serum Ca2þ levels greater
The overall incidence of hyperparathyroidism is 0.15%, but is
rarely reported in pregnant women. Hyperparathyroidism in than 13 g/dl. Patients experience vomiting, hypertension, gener-
pregnancy may be underreported; the true incidence may alized weakness, dehydration, or mental status changes. The syn-
approach that of the nonpregnant population. This contradiction drome may be mistaken for hyperemesis gravidarum or
is explained by three considerations. Firstly, hyperparathyroid- preeclampsia. The greatest risk may be in the postnatal period,
after transplacental shunting of Ca2þ to the fetus has stopped.
ism is associated with an increased rate of early pregnancy loss.
Secondly, the physiology of Ca2þ metabolism in pregnancy In asymptomatic women, the first sign of maternal hyperpara-
tends to be protective, with increased Ca2þ excretion across the thyroidism may be neonatal hypocalcemia and tetany within 48



288
Chapter 16


hours postpartum.124 Historically, the perinatal complication rate The clinical presentation of acute hypocalcemia includes
has been as high as 80%. However, with appropriate therapy and inspiratory stridor, skeletal muscle irritability, laryngospasm, par-
perinatal surveillance, the complication rate may be reduced by esthesia, and seizures. Chronic hypocalcemia may lead to symp-
a factor of four.125 Complications include IUGR, low birth weight, toms of fatigue, skeletal muscle cramping and weakness, lethargy,
fetal loss, preterm delivery, and neonatal hypocalcemia with or and personality changes. Signs of hypocalcemia include Chvostek
without tetany or seizures. For the fetus exposed to maternal sign (facial muscle spasm when the facial nerve is tapped) and
hypercalcemia, fetal parathyroid development may be impaired, Trousseau sign (carpopedal spasm when a BP cuff is inflated for
leading to either temporary or permanent neonatal hypo- three minutes). Cardiovascular consequences of hypocalcemia
parathyroidism. include hypotension, elevated LV pressure, myocardial dysfunc-
tion, cardiac dysrhythmia with prolongation of the QT interval,
Management and CHF. Fetal consequences include prematurity, fetal loss,
Asymptomatic patients and those with mild symptoms may be intracranial bleeding, fetal and neonatal hyperparathyroidism,
managed conservatively with oral hydration, oral phosphates, fetal bone demineralization with fractures, neonatal respiratory
limitation of Ca2þ intake, and electrolyte and fetal surveil- distress syndrome, and IUGR.129 Fetal death from complications
lance.126 Patients with life-threatening complications such as of fractures may occur.
pancreatitis, mental status changes, dysrhythmias, or hyper-
Management
calcemic crisis should be hospitalized and treated more aggres-
sively. Therapy includes fetal surveillance, i.v. fluid resuscitation Women with hypoparathyroidism should have regular electrolyte
monitoring, including Ca2þ, magnesium, and phosphate levels. For
followed by i.v. furosemide, electrolyte and cardiac monitoring,
and surgical consultation. Calcitonin (pregnancy category B), patients with mild or asymptomatic hypocalcemia, a diet high in
Ca2þ and low in phosphate may be combined with Ca2þ and vita-
oral phosphates (pregnancy category C), and bisphosphonates
(pregnancy category C) may be considered. If symptoms persist, min D supplementation. Calcitrol, the physiologically active form of
parathyroidectomy has a 95% success rate, and is most safely vitamin D, is used most often, and is titrated to maintain ionized
serum Ca2þ concentrations between 2.0 and 2.2 mmEq/l.129 Doses
completed during the second trimester for patients with a single
adenoma.127 typically increase throughout pregnancy, and then fall rapidly
postpartum, particularly in lactating women.130 Thiazide diure-
tics and Naþ restriction may be helpful. Symptomatic or severe
Anesthetic implications
Women with hyperparathyroidism may receive usual anesthetic hypocalcemia (< 3.5 mg/dl) should be corrected with calcium
care with either regional anesthesia or GA depending on the gluconate (5“10 ml of a 10% solution) until signs of neuro-
clinical circumstances. However, it is important to first measure muscular irritability or cardiovascular dysfunction subside.
both total and ionized serum Ca2þ levels and to assess volume
Anesthetic implications
status. In the presence of significant hypercalcemia, hydration
Anesthetic management should be directed at maintaining Ca2þ
with normal saline should be titrated to ensure adequate urinary
output and to reduce the total Ca2þ level below 14 mg/dl. levels and minimizing the consequences of hypocalcemia.
Hypovolemia and hypercalcemia may lead to hemodynamic Calcium, phosphate and magnesium levels should be checked
instability and cardiac dysrhythmias. Perioperative monitoring before any anesthetic procedure. Maternal hyperventilation and
of the EKG for prolonged PR interval, wide QRS complex, or a respiratory alkalosis will acutely exacerbate hypocalcemia, so
shortened QT interval may help identify physiologically signifi- regional anesthesia for labor and delivery may help to minimize
shifts in Ca2þ concentrations. Either regional anesthesia or GA may
cant hypercalcemia. Somnolence and muscle weakness increase
the risk of aspiration and may decrease anesthetic dose require- be used for C/S. The EKG should be monitored for prolongation of
ments. Muscle weakness and electrolyte imbalance may also lead the QT interval or cardiac dysrhythmias including 2:1 heart block.
to unpredictable responses to succinylcholine, nondepolarizing Calcium monitoring is particularly important if rapid transfusion
muscle relaxants, and neuromuscular blockade reversal agents. of citrated blood becomes necessary. Hypocalcemia also may
Careful positioning is important, particularly in patients with impair coagulation, and a review of coagulation parameters prior
osteoporosis at risk for pathologic fracture.128 to regional anesthesia is prudent. Finally, extubation may be com-
plicated by laryngospasm in patients with acute hypocalcemia.

Hypoparathyroidism
Conclusions
Hypoparathyroidism is rare during pregnancy. It is most com-
monly iatrogenic following thyroidectomy or parathyroidectomy. Rare endocrine disorders are often a manifestation of a multi-
Other etiologies include genetic, hypomagnesemia, chronic renal system disorder, and may result from altered regulation of circu-
failure, or autoimmune related dysfunction. Significant hypocal- lating hormone levels. Crises and emergencies typify the
cemia is present when the total serum Ca2þ level is < 4.5 mg/dl or problems in diagnosis and management of rare and complex
the ionized Ca2þ concentration is < 2.0 mEq/l. The differential endocrine disorders. We recommend a coordinated team
diagnosis of hypocalcemia includes vitamin D deficiency, chela- approach, with early consultation of the anesthesiologist, to facil-
tion following rapid blood transfusion, pancreatitis, and sepsis. itate medical management.



289
4 Metabolic disorders


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