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(R614C) in the human skeletal muscle calcium release channel cosegre-
ing its acute administration for an MH crisis. The half-life for
gates with malignant hyperthermia. Anesth. Analg. 1992; 75: 441“8.
dantrolene in breast milk was nine hours and the authors con-
19. Gillard, E. F., Otsu, K., Fujii, J. et al. A substitution of cysteine for arginine
cluded that it was safe for the newborn to breast feed two days 614 in the ryanodine receptor is potentially causative of human malignant
following discontinuation of intravenous dantrolene.53 hyperthermia. Genomics 1991; 11: 751“5.
20. Fagerlund, T. H., Islander, G., Twetman, E. R. et al. A search for the RYR1
gene mutation in 41 Swedish families with predisposition to malignant
Summary hyperthermia. Clin. Genet. 1995; 84: 12“16.
21. Hogan, K. Prospects for the noninvasive presymptomatic diagnosis of
Although episodes of MH have rarely been reported during preg- malignant hyperthermia susceptibility using molecular genetic techniques.
Anesthesiol. Clin. N. Am. 1994; 12: 571“97.
nancy, there is no evidence that pregnancy alters the response to
22. Larach, M. G. Should we use muscle biopsy to diagnose malignant
triggering agents. The increased use of regional anesthesia for
hyperthermia susceptibility? Anesthesiology 1993; 79: 1“4.
labor and delivery and C/S may partly explain the apparent 23. Sambuughin, N., Holley, H., Muldoon, S. et al. Screening of the entire
lower incidence from that in the overall population. The obstetric ryanodine receptor type 1 coding region for sequence variants associated
anesthesiologist must be prepared to diagnose and treat an unex- with malignant hyperthermia susceptibility in the North American popula-
tion. Anesthesiology 2005; 102: 515“21.
pected episode of MH and to manage a woman who is MHS who
24. Litman, R. S. & Rosenberg, H. Malignant hyperthermia. Update on suscept-
is admitted in labor. Management of an acute MH episode is
ibility testing. J.A.M.A. 2005; 293: 2918“24.
similar to that in the nonobstetric patient. With the advent of 25. Girard, T., J¨ hr, M., Schaefer, C. & Urwyler, A. Perinatal diagnosis of malignant
o
molecular genetic diagnosis it may be possible to diagnose MH hyperthermia susceptibility. Anesthesiology 2006; 104: 1353“4.
susceptibility in a newborn using umbilical cord blood. 26. Ording, H. Incidence of malignant hyperthermia in Denmark. Anesth.
Analg. 1985; 64: 700“4.
27. Hannallah, R. S. & Kaplan, R. F. Jaw relaxation after a halothane/succinyl-
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39. Habib, A. S., Millar, S., Deballi, P., 3rd & Muir, H. A. Anesthetic management
malignant hyperthermia susceptibility locus to human chromosome
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19q12“13.2. Nature 1990; 343: 562“4.
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14. Serfas, K. D., Bose, D., Patel, L. et al. Comparison of the segregation of the
40. Abel, D. E. & Grotegut, C. A. King syndrome in pregnancy. Obstet. Gynecol.
RYR1 C1840 T mutation with segregation of the caffeine/halothane con-
2003; 101: 1146“9.
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41. Larach, M. G., Localio, A. R., Allen, G. C. et al. A clinical grading scale to
Manitoba Mennonite family. Anesthesiology 1996; 84: 322“9.
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15. Wallace, A. J., Wooldridge, W., Kingston, H. M. et al. Malignant hyperther-
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mia “ a large kindred linked to the RYR1 gene. Anaesthesia 1996; 51: 16“23.
42. Nelson, T. E., Lin, M., Zapata-Sudo, G. & Sudo, R. T. Dantrolene sodium can
16. Healy, J. M. S., Heffron, J. J. A., Lehane, M. et al. Diagnosis of susceptibility to
increase or attenuate activity of skeletal muscle ryanodine receptor calcium
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1225“8.
43. Pessah, I. N. Complex pharmacology of malignant hyperthermia. (editorial)
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Anesthesiology 1996; 84: 1275“9.
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44. ˜rding, H., Hedengran, A. M. & Skovgaard, L. T. Evaluation of 119 anaes- 63. Abouleish, E., Abboud, T., Lechevalier, T. et al. Rocuronium (Org 9426) for
thetics received after investigation for susceptibility to malignant caesarean section. Br. J. Anaesth. 1994; 73: 336“41.
hyperthermia. Acta Anaesthesiol. Scand. 1991; 35: 711“16. 64. Mitchell, L. W. & Leighton, B. L. Warmed diluent speeds dantrolene recon-
45. Allen, G. C., Rosenberg, H. & Fletcher, J. E. Safety of general anesthesia in stitution. Can. J. Anesth. 2003; 50: 127“30.
patients previously tested negative for malignant hyperthermia suscept- 65. Iaizzo, P. A., Kehler, C. H., Zink, R. S. et al. Thermal response in
ibility. Anesthesiology 1990; 72: 619“22. acute porcine malignant hyperthermia. Anesth. Analg. 1996; 82: 782“9.
46. Islander, G. & Ranklev-Twetman, E. Evaluation of anaesthesia in malignant 66. Beebe, J. J. & Sessler, D. I. Preparation of anesthesia machines for patients
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47. Strazis, K. P. & Fox, A. W. Malignant hyperthermia: a review of published 67. McGraw, T. T. & Keon, T. P. Malignant hyperthermia and the clean
cases. Anesth. Analg. 1993; 77: 297“304. machine. Can. J. Anaesth. 1989; 36: 530“2.
48. Liebenschutz, F., Mai, C. & Pickerodt, V. W. A. Increased carbon dioxide 68. Hankins, G. D. V., Berryman, G. K., Scott, R. T. et al. Maternal arterial desa-
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49. Lips, F. J., Newland, M. & Dutton, G. Malignant hyperthermia triggered by 69. Phelan, J. P., Meguiar, R. V., Matey, D. & Newman, C. Dramatic pyrexic and
cyclopropane during cesarean section. Anesthesiology 1982; 56: 144“6. cardiovascular response to intravaginal prostaglandin E2. Am. J. Obstet.
50. Douglas, M. J., O™Connor, G. A. & Allanson, J. E. Malignant hyperthermia in Gynecol. 1978; 132: 28“32.
British Columbia. British Columbia Medical Journal 1983; 25: 299“300. 70. Hughes, W. A. & Hughes, S. C. Hemodynamic effects of prostaglandin E2.
51. Cupryn, J. P., Kennedy, A. & Byrick, R. J. Malignant hyperthermia in preg- Anesthesiology 1989; 70: 713“16.
nancy. Am. J. Obstet. Gynecol. 1984; 150: 327“8. 71. Sim, A. T. R., White, M. D. & Denborough, M. A. The effect of oxytocin on
52. Tettambel, M. Malignant hyperthermia in an obstetric patient. J. Amer. porcine malignant hyperpyrexia susceptible skeletal muscle. Clin. Exper.
Osteopathic. Assoc. 1980; 79: 773“5. Pharmacol. Physiol. 1987; 14: 605“10.
53. Fricker, R. M., Hoerauf, K. H., Drewe, J. & Kress, H. G. Secretion of dantro- 72. Nanson, J. K. & Sheikh, A. Anaesthesia for emergency caesarean section in a
lene into breast milk after acute therapy of a suspected malignant parturient with bleeding placenta praevia and a potentially malignant
hyperthermia crisis during cesarean section. Anesthesiology 1998; 89: hyperthermia-susceptible fetus. Int. J. Obstet. Anesth. 2000; 9: 276“8.
1023“5. 73. Pollock, N. A. & Langton, E. E. Management of malignant hyperthermia
54. Wadhwa, R. K. Obstetric anesthesia for a patient with malignant hyperther- susceptible parturients. Anaesth. Intensive Care 1997; 25: 398“407.
mia susceptibility. Anesthesiology 1977; 46: 63“4. 74. Sewall, K., Flowerdew, R. M. M. & Bromberger, P. Severe muscular rigidity at
55. Khalil, S. N., Williams, J. P. & Bourke, D. L. Management of a malignant birth: malignant hyperthermia syndrome? Can. Anaesth. Soc. J. 1980; 27: 279“82.
hyperthermia susceptible patient in labor with 2-chloroprocaine epidural 75. Craft, J. B., Goldberg, N. H., Lim, M. et al. Cardiovascular effects and pla-
anesthesia. Anesth. Analg. 1983; 62: 119“21. cental passage of dantrolene in the maternal“fetal sheep model.
56. Sorosky, J. I., Ingardia, C. J. & Botti, J. J. Diagnosis and management of Anesthesiology 1988; 68: 68“72.
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57. Douglas, M. J. & McMorland, G. H. The anaesthetic management of the 77. Shime, J., Gare, D., Andrews, J. & Britt, B. Dantrolene in pregnancy: lack of
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58. Willatts, S. M. Malignant hyperthermia susceptibility: management during 78. Weingarten, A. E., Korsh, J. I., Neumann, G. G. et al. Postpartum uterine atony
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59. Lucy, S. J. Anaesthesia for caesarean delivery of a malignant hyperthermia 79. Shin, Y. K., Kim, Y. D., Collea, J. V. et al. Effect of dantrolene sodium on
susceptible parturient. Can. J. Anaesth. 1994; 41: 1220“6. contractility of isolated human uterine muscle. Int. J. Obstet. Anesth. 1995;
60. Hinkle, A. J. & Dorsch, J. A. Maternal masseter muscle rigidity/neonatal 4: 197“200.
fasciculations after induction for emergency cesarean section. 80. Karan, S. M., Lojeski, E. W., Haynes, D. H. et al. Intravenous lecithin-coated
Anesthesiology 1993; 79: 175“7. microcrystals of dantrolene are effective in the treatment of malignant
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62. Gronert, G. A. & Milde, J. H. Variations in onset of porcine malignant Dantrolene “ a review of its pharmacology, therapeutic use and new
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273
RARE ENDOCRINE DISORDERS
16
J. M. Mhyre and L. S. Polley




Introduction Because the consequences of thyroid storm are life threatening,
management should commence once the diagnosis is suspected.
Endocrinopathies can complicate pregnancy with adverse mater-
Laboratory tests of thyroid function typically require at least eight
nal and fetal effects. Pregnancy can mask or mimic signs and
hours of analytic time, and are of little value in distinguishing
symptoms of endocrine disease making diagnosis difficult.
thyroid storm from untreated hyperthyroidism. Leukocytosis
may be present, but may also signal an underlying infection that
Thyroid disease precipitated the metabolic derangement.
The differential diagnosis includes malignant hyperthermia
Hyperthyroidism
(MH), pheochromocytoma, neuroleptic malignant syndrome,
Hyperthyroidism is relatively common in the general population and sepsis.
and occurs in 2 of 1000 pregnancies.1 Graves disease causes
Fetal effects
80“95% of cases of hyperthyroidism in pregnancy. Other causes
include thyroiditis, toxic adenoma, multinodular goiter, viral Thyroid storm may result in preterm labor, premature birth, pre-
thyroiditis, and tumors of the pituitary or ovary. Human chorio- eclampsia, and intrauterine fetal demise. If the fetus is alive when
nic gonadotropin (hCG), which peaks between 8 and 14 weeks, the mother presents with thyroid crisis, then fetal heart rate (FHR)
weakly stimulates thyroid stimulating hormone (TSH) receptors, tracing may show tachycardia, decreased or absent beat-to-beat
and in some cases leads to transient hyperthyroidism associated variability, and late decelerations. These abnormal FHR patterns
with hyperemesis gravidarum.2 High levels of hCG with clinical generally improve with correction of the maternal metabolic
hyperthyroidism may also be seen with gestational trophoblastic derangement.
disease and multiple pregnancies.
Management and anesthetic implications
Subclinical hyperthyroidism occurs in pregnancy (1.7% of all
screened women), and, in the general population, has long-term Pregnant women with thyroid storm should be admitted for inva-
sequelae such as osteoporosis, cardiovascular morbidity, and sive central monitoring because they are often dehydrated and
progression to overt thyrotoxicosis.3 These women have sup- require vigorous hydration with crystalloids in the face of poten-
pressed TSH but normal free thyroxine (T4) levels. African- tial cardiac dysfunction. Glucose and electrolyte abnormalities
American and parous women are more likely to be affected, but must be corrected and fever treated with cool intravenous (i.v.)
there are no adverse pregnancy outcomes. Identification of sub- fluids, a cooling blanket, and acetaminophen. Aspirin should be
clinical hyperthyroidism and treatment during pregnancy is avoided because it may increase circulating active T3 and T4 by
unwarranted.3 reducing protein binding.
Propylthiouracil (PTU) inhibits the iodination of thyroglobulin
in the thyroid, and blocks the peripheral conversion of T4 to T3.
Thyrotoxic crisis (thyroid storm)
Potassium iodide and sodium iodide block the release of thyroid
Thyroid storm is the most serious complication of hyperthyroid- hormone from the thyroid gland. Propranolol inhibits the adre-
ism. This exaggerated hypermetabolic state occurs in 2% of preg- nergic effects of thyroid hormone and blocks the peripheral con-
nancies complicated by hyperthyroidism with a reported version of T4 to T3. In cases with significant cardiac dysfunction
maternal mortality rate of 15% and a 24% rate of stillbirth. or bronchospastic airway disease, a titratable esmolol infusion or
Thyroid storm is often precipitated in women with Graves thyro- diltiazem may be preferred. Dexamethasone also decreases thy-
toxicosis by common obstetric complications such as hemor- roid hormone release and blocks the peripheral conversion of T4
rhage, severe preeclampsia, and sepsis.4 to T3. A treatment protocol is summarized in Table 16.1.
Surgical procedures should be postponed until the metabolic
Clinical features derangements of thyroid storm are controlled. If the mother™s
Pregnant women with thyroid storm demonstrate high fever, condition is unstable, emergent cesarean section (C/S) for fetal
dehydration, nausea, vomiting, and diarrhea. The cardiovascular indications may jeopardize the lives of both mother and fetus. As
system is hyperdynamic with tachycardia, dysrhythmia, and previously mentioned, the fetal condition generally improves
high-output congestive heart failure (CHF). Neurologic symp- with correction of the maternal metabolic derangement.
toms include skeletal muscle weakness, altered mental status, Following the diagnosis and institution of therapy, a search
and seizures, which may progress to coma and death. should be made for underlying precipitating conditions,


Obstetric Anesthesia and Uncommon Disorders, eds. David R. Gambling, M. Joanne Douglas and Robert S. F. McKay. Published by Cambridge University Press.
# Cambridge University Press 2008.
4 Metabolic disorders


sympathetic stimulation, but should be used with caution in the
Table 16.1 Management protocol for pregnant women with presence of CHF or asthma.
thyroid crisis With careful management, either general or regional anesthesia
is acceptable for C/S that is performed when the maternal con-
 Hospitalization and intensive nursing care
dition has been stabilized. Regional anesthesia can be adminis-
 Invasive hemodynamic monitoring with evaluation for heart
tered safely if there are no signs of high-output cardiac failure,7
failure and dysrhythmia
and may be therapeutic for thyroid storm. Continuous epidural
 Fetal monitoring: ultrasound, biophysical profile, or nonstress test
anesthesia has the advantage of slower onset of sympathetic
 Hydration and correction of glucose and electrolyte abnormalities
blockade, with time to position the patient and to administer
 Adrenergic blockade titrated to a 25% reduction in heart rate:
fluid boluses and small doses of phenylephrine (20“40 mg) to pre-
propranolol 1 mg/min i.v. up to 10 mg, may repeat q 4“6 h
vent hypotension. High levels of circulating thyroid hormones
or esmolol 500 mg/kg/min i.v. load over 1 min, then 25“200 mg/kg/min
increase beta-adrenergic receptors,8 and thus epinephrine should
or diltiazem 0.25 mg/kg load over 2 min, then 5“15 mg/h
not be added to local anesthetic solutions because of the risk of
 PTU 1000 mg po, then 200 mg q 6 h
an exaggerated circulatory response.
 Iodide solution starting 1 hour after giving PTU:
A diagnosis of thyroid storm during general anesthesia (GA) is
supersaturated potassium iodide (SSKI) 30 gtt po, then 5“10 gtt q 6 h
made on the basis of the history and intraoperative vital signs, which
or sodium iodide 0.5 g i.v. in 1 l of NS over 12 h
demonstrate a hypercatabolic state. In such cases, the differential
or lithium carbonate 300 mg po q 6 h if hypersensitive to SSKI
diagnosis should include MH,9 sepsis, and pheochromocytoma.
 Dexamethasone 2 mg i.v. q 6 h up to 8 mg
Regardless of anesthetic technique, postoperative monitoring is
 Consider
essential because a crisis can occur postpartum in the recovery unit.10
dantrolene
plasma exchange
spinal anesthesia to the fourth dermatomal level
Hypothyroidism
L-carnitine
Overt hypothyroidism complicates up to 3 of 1000 pregnan-
 Evaluate for precipitating causes
cies.1,11 Most women affected by hypothyroidism experience
Adapted from Wissler, R. N. Endocrine disorders. In Chestnut, D. H. chronic anovulation and increased rates of fetal loss, so the true
(ed.), Obstetric Anesthesia: Principles and Practice, 3rd edn. prevalence of hypothyroidism in pregnancy is difficult to assess.
Philadelphia: Elsevier Mosby, 2004; p. 747. Myxedema, the most severe complication of hypothyroidism, is
rare and, if untreated, can lead to myxedema coma.
The etiology of hypothyroidism includes autoimmune thyroid-
itis (Hashimoto disease), subtotal thyroidectomy, radioiodine
including infection (e.g. pyelonephritis, chorioamnionitis),
therapy, and primary hypothyroidism. Worldwide, the leading
thromboembolic disease, stroke, diabetic ketoacidosis, or hypo-
cause of hypothyroidism is iodine deficiency. Hypothyroidism
glycemia. Normal labor, hemorrhage, and preeclampsia may also
occurs in 10% of all type I diabetics.
precipitate thyroid storm.
Anesthetic management includes careful evaluation of the
Clinical features
airway, recognizing that significant enlargement of the thyroid
Clinical features in women of childbearing age consist of abnor-
gland can obstruct the trachea or a bronchus. Retrosternal goiter
mal menses, conception, and fertility. Also seen are diminished
may not be apparent on physical examination, and may require
deep tendon reflexes, fatigue, hair loss, dry skin, and brawny
computerized tomography (CT) to make the diagnosis. If the
edema. Diagnosis is confirmed by a low free T4 serum level and
potential for significant airway obstruction exists, an awake
an elevated TSH.
fiberoptic intubation is the airway management technique of
choice.5 Hypothyroidism is associated with an increased risk of pre-
eclampsia, placental abruption, intrauterine growth restriction
Nonpharmacologic methods to reduce patient anxiety should
(IUGR), prematurity, stillbirth, emergency C/S for nonreassuring
be used preferentially. However, patient anxiety may contribute
FHR pattern, acquired von Willebrand (VW) syndrome,12 and
to hemodynamic lability, and small, titrated doses of midazolam
postpartum hemorrhage. The blood dyscrasia appears to be
may be necessary. In doses less than 0.02 mg/kg, midazolam does
related to an impaired release of VW factor that resolves once
not appear to produce neonatal sedation or respiratory depres-
the hypothyroidism is corrected. No case reports have linked
sion, or maternal amnesia for delivery.
hypothyroidism to epidural hematoma. Other serious maternal
Preoperative twelve-lead electrocardiogram (EKG) and peri-
end-organ effects include anemia, cardiomegaly, cardiomyopa-
operative cardiac rhythm monitoring are recommended. Invasive
thy, conduction abnormalities, bradycardia, and cardiac stroke
cardiovascular monitoring may be helpful to guide fluid manage-
volume reduction. Maternal thyroid hormones play a significant
ment and adrenergic blockade, particularly if high-output CHF or
role in early neurologic development, and maternal hypothyroid-
significant dysrhythmias are present. Drugs that promote tachy-
ism between the 7th and 20th week of gestation places the fetus at
cardia should be avoided including ketamine, anticholinergics,
sympathomimetics, and pancuronium.6 A perioperative esmolol risk for impaired neurologic development and neonatal mental
retardation.13
infusion may be useful to control cardiovascular responses to



276
Chapter 16


Thyroid replacement therapy with levothyroxine 0.1 mg/day Neurologic examination prior to block placement may reveal
has no known adverse fetal effects if euthyroid hormone levels any preexisting neurologic weakness or paresthesias. If acquired
are achieved.14 The aim is to lower TSH levels to 0.5“1.5 mIU/l.11 VW disease is suspected, desmopressin 0.3 mg/kg given i.v. over
Excess thyroid supplementation may increase risk for sponta- ten minutes has been shown to acutely correct the coagulation
neous abortion or IUGR.15 Both levothyroxine and endogenous defect. Metabolism of amide local anesthetics may be slowed,
T4 and T3 cross the placental barrier to enter the fetal circulation; and some authors have speculated an increased risk for local
however, there are marked maternal to fetal gradients of all three. anesthetic toxicity, although none has been demonstrated. The
At delivery, maternal serum free T4 and T3 concentrations are stress of labor or surgery may unmask reduced adrenal cortical
twice those in cord serum. In cases of fetal thyroid agenesis, function, warranting steroid supplementation.
intrauterine neurologic development is often normal because
the small amount of maternal T4 transferred to the fetus contri-
Thyroid dysfunction and drugs
butes to T3 concentrations in the fetal brain minimizing the
effects of fetal hypothyroidism. Various drugs affect thyroid function through their actions on
Subclinical hypothyroidism refers to early or mild thyroid production, secretion, transport, and metabolism of thyroid hor-
mones (see Table 16.2).19
hypofunction with slightly high TSH (4“10 mIU/l) and normal
T4 and T3 levels.11,16 The consequences of subclinical hypothy- Long-term therapy with cytokines in patients with chronic
roidism in the general population are minimal.17 However, preg- inflammatory disorders or tumors may result in thyroid dysfunc-
nancies in women with subclinical hypothyroidism are three tion. Interferon alpha has been associated with antithyroid micro-
times more likely to have placental abruption and two times somal antibodies in 20% of patients, and transient hypothyroidism,
more likely to have preterm labor (< 34 weeks).16 hyperthyroidism, or both may result.
Amiodarone is not recommended in the first trimester of preg-
Anesthetic implications nancy because it has the potential to cause hypothyroidism and
Laboring women who begin their pregnancy with severe hyperthyroidism in the neonate in addition to congenital defects
hypothyroidism are at increased risk for urgent C/S for nonreas- (see Chapter 2). Amiodarone causes characteristic changes in
suring FHR pattern, regardless of their thyroid status at term. thyroid function in euthyroid individuals because of its iodine
content and a direct toxic effect on thyroid parenchyma.20
Therefore, epidural placement in labor may be helpful in facil-
itating a rapid transition to surgical delivery. For patients ren-
dered euthyroid during the antepartum period, no major
Neonatal thyroid dysfunction
modifications of either general or regional anesthesia are
required. Neonatal hyperthyroidism develops in 1“5% of the offspring of
Patients who remain severely hypothyroid present a number of women with Graves disease, as a consequence of the trans-
potential anesthetic problems. Firstly, there may be excess sensi- placental passage of thyroid-stimulating immunoglobulin (TSI).
tivity to induction agents, opioids, and sedatives. Minimal doses Women rendered euthyroid by thyroid gland ablation before
of sodium thiopental or ketamine are given for emergency C/S pregnancy may continue to produce TSI. The fetus exposed to
using GA. In some women, nitrous oxide alone may cause uncon- TSI may experience IUGR, goiter, and tachycardia, and as a neo-
sciousness. Secondly, cardiac depression and bradycardia may be nate, may demonstrate tachycardia, irritability, weakness, and
worsened by the effects of depressant drugs such as induction hyperactivity. Neonatal hyperthyroidism is usually transient, last-
agents and volatile anesthetics. Fortunately, hypothyroid patients ing one to five months, and resolves in proportion to the half-life
appear to respond normally to i.v. fluids and exogenous catecho- of immunoglobulin (IgG).
lamines. Nevertheless, invasive hemodynamic monitoring may Neonatal hypothyroidism without goiter can occur when
be indicated, particularly in the presence of hypovolemia and women with Graves disease produce TSH-binding inhibitory
abnormal baroreceptor reflexes. Thirdly, reduced skeletal muscle immunoglobulin (TBII). These antibodies cross the placenta,
activity may impair postoperative respiratory effort and may bind fetal TSH, and cause transient fetal hypothyroidism.
increase sensitivity to neuromuscular blocking agents. A peri- Affected neonates are at risk for bradycardia and IUGR.
pheral nerve stimulator may not be reliable in the severely Neonatal hypothyroidism with goiter can result when mater-
hypothyroid patient.18 Fourthly, abnormal respiratory control nally administered antithyroid drugs including propylthiouracil,
mechanisms and impaired central neurologic responses to methimazole, and iodine, cross the placenta, suppress the fetal
hypoxia and hypercarbia mandate monitoring of oxygen satura- thyroid gland, and stimulate fetal TSH.

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