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Table 11.5 Drug induced peripheral neuropathy
Drug Effect  Diabetic neuropathy
 Hereditary dysautonomia
Isoniazid Sensorimotor neuropathy; pyridoxine prevents
 GBS, etc.
Pyridoxine Sensory neuropathy (in large doses)
Nitrofurantoin Sensorimotor neuropathy; also caused by
 Hypoventilation due to impaired respiratory reflexes
 Vomiting and electrolyte disturbance
Vincristine Dose-related sensorimotor neuropathy; may
 Labile blood pressure, sensitive to positive pressure
develop foot drop
Cisplatin Sensory neuropathy
 Sensitivity to direct-acting vasopressors
Chloramphenicol Mild sensory; optic neuropathy associated
 Insensitivity to indirect vasopressors
Phenytoin Mild sensorimotor neuropathy
 Oxytocin can be dangerous
Dapson Motor neuropathy
 Both pain and GA may cause hemodynamic
Amiodarone Sensorimotor neuropathy in 5%
Perhexiline Sensory neuropathy
Metronidazole Mild sensory neuropathy
 Watch for hypoventilation
Lithium Sensorimotor neuropathy
 Correct fluid and electrolyte balance
Flecainide Sensory neuropathy

Chapter 11

 Uterotonic in low divided doses  Use opioids, preferably on their own, for postoperative neur-
 Good pain relief using regional techniques with very low- axial analgesia, for the same reasons
 Ensure that those caring for women receiving low-dose combi-
dose combinations
nations know that numbness or weakness should not occur,
hence such symptoms should prompt a change of position.
Bulbar weakness
 Any condition affecting relevant cranial nerves 1. Thomas P. K. Diseases of peripheral nerves. In Warrell D. A., Cox, T. M. &
Firth, J. D. (eds.), Oxford Textbook of Medicine, 4th edn. Oxford University
Press, 2005; pp. 1180“93.
 Be on the lookout for it 2. Lennox, G. G. Neurological disease in pregnancy. In Warrell, D. A., Cox,
 Metoclopramide T. M. & Firth, J. D. (eds.), Oxford Textbook of Medicine, 4th edn. Oxford
 Antacid and H2 antagonist University Press, 2005; pp. 436“9.
 Care with intubation and recovery from anesthesia 3. Turbridy, N. & Redmond, J. M. T. Neurological symptoms attributed to
epidural analgesia in labour: an observational study of seven cases. Br. J.
Obstet. Gynaecol. 1996; 103: 832“3.
Small stature, scoliosis 4. Confidential Enquiry into Maternal and Child Health. Why Mothers Die
1979“81. London: RCOG Press, 1986.
Causes 5. Reynolds, F. Scoliosis and motherhood. SOAP Newsletter 1990; 22: 4“8.
6. Rudnik-Schoneborn, S., Rohrig, D., Nicholson, G. & Zerres, K. Pregnancy and
 Condition present during growth (typically HSMN)
delivery in Charcot-Marie-Tooth disease type 1. Neurology 1993; 43: 2011“16.
 Scoliosis, skeletal disturbance
7. Byrne, D. L., Chappatte, O. A., Spencer, G. T. & Raju, K. S. Pregnancy com-
Problems plicated by Charcot-Marie-Tooth disease, requiring intermittent ventila-
 Premature labor tion. Br. J. Obstet. Gynaecol. 1992; 99: 79“80.
 Malpresentation, distorted pelvis 8. Brian, J. E. Jr., Boyles, G. D., Quirk, J. G., Jr. et al. Anaesthetic management
for cesarean section of a patient with Charcot-Marie-Tooth Disease.
 Neuraxial approach may be difficult. Find old x-rays
Anesthesiology 1987; 66: 410“12.
9. Sawicka, E. H., Spencer, G. T. & Branthwaite, M. A. Management of respira-
 Remember weight when calculating dose for regional or tory failure complicating pregnancy in severe kyphoscoliosis: a new use for
general techniques. Do not be fooled into thinking that an old technique? Br. J. Dis. Chest 1986; 80: 191“6.
weight does not affect neuraxial dose requirement. It cer- 10. Antognini, J. F. Anaesthesia for Charcot-Marie-Tooth disease: a review of 86
tainly does affect maximum safe dose.98 cases. Can. J. Anaesth. 1992; 39: 398“400.
11. Reah, G., Lyons, G. R. & Wilson, R. C. Anaesthesia for caesarean section in a
patient with Charcot-Marie-Tooth disease. Anaesthesia 1998; 53: 586“8.
Neuraxial blockade and defensive medicine 12. Patrick, J. A., Meyer-Whiting, M., Reynolds, F. & Spencer, G. T. Perioperative
care in restrictive respiratory disease. Anaesthesia 1990; 45: 390“5.
It would be poor practice to avoid the use of regional techniques 13. Scull, T. Epidural analgesia for labour in a patient with Charcot-Marie-
Tooth disease. Can. J. Anaesth. 1996; 43: 1150“2.
in the presence of a neuropathy, simply for fear of litigation. It is
14. Hahn, A. F., Brown, W. F., Koopman, W. J. & Feasby, T. E. X-linked dominant
therefore wise to ensure that any preexisting neurologic deficit is
motor and sensory neuropathy. Brain 1990; 113: 1511“25.
fully mapped, and the patient understands that any exacerbation
15. Viet, H. R. Refsum disease. N. Engl. J. Med. 1947; 236: 996.
of her condition should not automatically be attributed to 16. Lepski, G. R. & Alderson, J. D. Epidural analgesia in labour for a patient with
anesthesia. Remember it is much harder to produce chemical or hereditary neuropathy with liability to pressure palsy. Int. J. Obstet. Anesth.
2001; 10: 198“201.
irritative nerve damage in the epidural than in the subarachnoid
17. Peters, G. & Hinds, N. P. Inherited neuropathy can cause postpartum foot
space. Nevertheless, beware of concealing signs of nerve com-
drop. Anesth. Analg. 2005; 100: 547“8.
pression or attributing them to anesthesia.
18. Sweeney, B. P., Jones, S. & Langford, R. M. Anaesthesia in dysautonomia:
further complications. Anaesthesia 1985; 40: 783“6.
19. Porges, R. F., Axelrod, F. B. & Richards, M. Pregnancy in familial dysauto-
Safeguards to minimize peripheral nerve
nomia. Am. J. Obstet. Gynecol. 1978; 132: 485“8.
compression 20. Robertson, D., Haile, V., Perry, S. E. et al. Dopamine beta-hydroxylase
deficiency. A genetic disorder of cardiovascular regulation. Hypertension
(Particularly important in those with HNPP, but see more pre-
1991; 18: 1“8.
cautions earlier under Hereditary neuropathy with liability to 21. Scurrah, N. J., Ross, A. W. & Solly, M. Peripartum management of a patient
pressure palsies.) with dopamine beta-hydroxylase deficiency, a rare congenital cause of
 Watch for signs of nerve compression; do not automatically dysautonomia. Anaesth. Intens. Care 2002; 30: 484“6.
22. Dell™oste, C., Vincenti, E. & Torre, G. Multiple and various anaesthetics,
attribute them to regional blockade
ketamine included, in a young patient with familial dysautonomia: case
 Avoid prolonged use of the lithotomy position, or else ensure
report. Minerva Pediatrica 1996; 48: 113“16.
that hip flexion and abduction are reduced to a minimum 23. Challands, J. F. & Facer, E. K. Epidural anaesthesia and familial dysautonomia
 Avoid prolonged positioning that may cause compression of (the Riley Day syndrome). Three case reports. Paed. Anaesth. 1998; 8: 83“8.
sciatic or peroneal nerves 24. Lieberman, J. R., Cohen, A., Wiznitzer, A., Maayan, C. & Greemberg, L.
Cesarean section by local anesthesia in patients with familial dysautono-
 Use low-dose local anesthetic/opioid combinations during
mia. Am. J. Obstet. Gynecol. 1991; 165: 110“11.
labor to minimize numbness and allow maximum mobility

3 Nervous system disorders

25. Hirsch, N. P., Murphy, A. & Radcliffe, J. J. Neurofibromatosis: clinical pre- 52. Chohan, U., Khan, M. & Saeed-uz-zafar. Abducent nerve palsy in a par-
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353: 1114“16. 53. Heyman, H. J., Salem, M. R. & Klimov, I. Persistent sixth cranial nerve par-
27. Sakai, T., Vallejo, M. C. & Shannon, K. T. A parturient with neurofibroma- esis following blood patch for postdural puncture headache. Anesth. Analg.
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Obstet. Anesth. 2005; 14: 332“5. 54. Dunbar, S. A. & Katz, N. P. Failure of delayed epidural blood patching
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labour in a parturient with neurofibromatosis. Can. J. Anaesth. 1995; 42: 420“2. 55. Szokol, J. W. & Falleroni, M. J. Lack of efficacy of an epidural blood patch in
29. Spiegel, J. E., Hapgood, A. & Hess, P. E. Epidural anesthesia in a parturient treating abducent nerve palsy after an unintentional dura puncture. Reg.
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Guillain-Barr´ syndrome. Anaesthesia 2000; 55: 894“8.
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37. van der Meche, F. G. & Schmitz, P. I. Dutch Guillain-Barr´ Study Group. A
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42. Alici, H. A., Cesur, M. & Erdem, A. F. Repeated use of epidural anaesthesia 69. Holloway, J., Seed, P. T., O™Sullivan, G. & Reynolds, F. Paraesthesiae and
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44. McCombe, P. A., McManis, P. G., Frith, J. A. et al. Chronic inflammatory 71. Silva, M., Mallinson, C. & Reynolds, F. Sciatic nerve palsy following child-
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45. Dorsey, D. L. & Camann, W. R. Obstetric anesthesia in patients with idiopathic Anaesth. 1997; 44: 313“16.
facial paralysis (Bell™s palsy): a 10-year survey. Anesth. Analg. 1993; 77: 81“3. 73. Bademosi, O., Osuntokun, B. O., Van der Werd, J. H. et al. Obstetric neuro-
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Saunders, 1989. 74. Warner, M. A., Warner, D. O., Harper, M., Schroeder, D. R. & Maxson, P. M.
47. Farrar, D. & Raoof, N. Bell™s palsy, childbirth and epidural analgesia. Int. J. Lower extremity neuropathies associated with lithotomy positions.
Obstet. Anesth. 2001; 10: 68“70. Anesthesiology 2000; 93: 938“42.
48. Collier, C. B. Bilateral trigeminal nerve palsy during extensive lumbar epi- 75. Gherman, R., Ouzounian, J. G., Incerpi, M. H. & Goodwin, T. M. Symphyseal
dural block. Int. J. Obstet. Anesth. 1997; 6: 185“9. separation and transient femoral neuropathy associated with the
49. Sprung, J., Haddox, D. & Maitra-D™Cruze, A. M. Horner™s syndrome and McRoberts maneuver. Am. J. Obstet. Gynecol. 1998; 178: 609“10.
trigeminal nerve palsy following epidural anaesthesia in obstetrics. Can. J. 76. Van Diver, T. & Camann, W. Meralgia paresthetica in the parturient. Int. J.
Anaesth. 1991; 38: 767“71. Obstet. Anesth. 1995; 4: 109“12.
50. Carrero, E. J., Agusti, M., Fabregas, N. et al. Unilateral trigeminal and facial 77. Umo-Etuk, J. & Yentis, S. M. Sciatic nerve injury and caesarean section
nerve palsies associated with epidural analgesia in labour. Can. J. Anaesth. (letter). Anaesthesia 1997; 52: 605“6.
1998; 45: 893“7. 78. Roy, S., Levine, A. B., Herbison, G. J. & Jacobs, S. R. Intraoperative position-
51. Martin-Hirsch, D. P. & Martin-Hirsch, P. L. Vestibulocochlear dysfunction ing during cesarean as a cause of sciatic neuropathy. Obstet. Gynecol. 2002;
following epidural anaesthesia in labour. Br. J. Clin. Pract. 1994; 48: 340“1. 99: 652“3.

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79. Babayev, M., Bodack, M. P. & Creatura, C. Common peroneal neuro- 88. Simpson, D. M. & Olney, R. K. Peripheral neuropathies associated with
pathy secondary to squatting during childbirth. Obstet. Gynecol. 1998; 91: human immunodeficiency virus infection. Neurol. Clin. 1992; 10: 685“711.
830“2. 89. Kissel, J. T. & Mendell, J. R. Vasculitic neuropathy. Neurol. Clin. 1992; 10:
80. MacLeod, A. F., Smith, S. A., Sonksen, P. H. & Lowy, C. The problem of 761“81.
autonomic neuropathy in diabetic pregnancy. Diabetic Medicine 1990; 7: 90. Ramsey-Goldman, R. The effect of pregnancy on the vasculitides. Scand. J.
80“2. Rheumatol. 1998; 107: 116“17.
81. Hagay, Z. & Weissman, A. Management of diabetic pregnancy complicated 91. Haynes de Regt, R. Sarcoidosis and pregnancy. Obstet. Gynecol. 1987; 70: 369“72.
by coronary artery disease and neuropathy. Obstet. Gynecol. Clin. N. 92. Cohen, R., Talwar A. & Efferen, L. S. Exacerbation of underlying respiratory
America 1996; 23: 205“20. disease in pregnancy. Crit. Care Clin. 2004; 20: 713“30.
82. Page, M. M. & Watkins, P. J. Diabetic autonomic neuropathy. Lancet 1987; i 93. Klaassen, D. Heavy metals and heavy-metal antagonists. In Hardman, J. G.
(8054): 14“16. & Limbird, L. E. (eds.), Goodman and Gilman™s The Pharmacological Basis
83. Lapolla, A., Cardone, C., Negrin, P. et al. Pregnancy does not induce or of Therapeutics, 9th edn., New York, NY: McGraw-Hill, 1996, p. 1649.
worsen retinal and peripheral nerve dysfunction in insulin-dependent dia- 94. Graef, J. W. Heavy metal poisoning. In Isselbacher, K. J., Braunwald, E.,
betic women. J. Diabetes and its Complications 1998; 12: 74“80. Wilson, J. D. et al. (eds.), Harrison™s Principles of Internal Medicine, 13th
84. Brodie, M. J., Moore, M. R., Thompson, G. G. et al. Pregnancy and the acute edn., New York, NY: McGraw-Hill Inc, 1994, p. 2461.
porphyrias. Br. J. Obstet. Gynaecol. 1977; 84: 726“31. 95. Sowers, M., Jannausch, M., Scholl, T. et al. Blood lead concentrations and
85. Bancroft, G. H. & Lauria, J. I. Ketamine induction for cesarean section in a pregnancy outcomes. Arch. Environ. Health 2002; 57: 489“95.
patient with acute intermittent porphyria and achondroplastic dwarfism. 96. Centers for Disease Control and Prevention (CDC). Blood mercury levels in
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1997; 25: 168“70. system. N. Engl. J. Med. 1989; 321: 442“54.
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23“34. cause of confusion. Reg. Anesth. Pain Med. 2005; 30: 314“16.

Hector J. Lacassie and Holly A. Muir

Introduction results from the interaction of circulating levels of progesterone
and estrogen and the activation of two relatively minor opioid
Pain is defined as a sensory and emotional experience associated
analgesic systems (delta and kappa) by the endogenous opioids
with actual tissue damage or described in terms of such damage.1
dynorphin and enkephalin.12,13 These opioids are felt to be quies-
This definition has endured through time; however, the classifi-
cent under basal conditions. Modulation of these systems is con-
cation of the different types of pain is evolving. Original descrip-
trolled by descending noradrenergic pathways using stimulation
tions of pain were based on a temporal evolution, where the
of spinal a2 receptors to amplify synergistically the antinocicep-
distinction between acute and chronic pain was that if it lasted
tive response.13 Benefits from this association are a decreased
for more than six months it was considered chronic. Another
need of either agent to achieve a certain level of antinociception,
more conservative and innovative view proposed one month as
coupled with the low likelihood of developing tolerance for each
the defining criterion.2 These early definitions did not account for
receptor type.13 Even though the aforementioned mechanisms
the mechanisms involved in the development of the pain. The
control some forms of pain during labor and delivery, break-
prevailing contemporary view is to classify pain according to
through pain can still occur, depending on the magnitude or
the primary pathology involved in the cause of pain, namely:
even the nature of the labor pain.
inflammatory (acute) or neuropathic (chronic).3 The latter can
Several painful disease states are of particular interest during
be considered a disease of the nervous system and not merely a
pregnancy due to their high prevalence, intensity of symptoms,
symptom of some other condition.4 Furthermore, poorly treated
and/or impact on daily activity. As maternal pain can potentially
acute pain can lead to neuropathic chronic pain.5 The current
interfere with fetal development and growth14 it is important to be
temporal cutoff value for chronic pain is three months.
aware of these conditions and to alleviate pain where possible to
During pregnancy, acute inflammatory pain, usually arising from
the benefit of mother and fetus. Headache, orthopedic problems,
labor and delivery, is the most common type of pain. However,
and fibromyalgia are more prevalent during pregnancy and so will
other pain syndromes (chronic neuropathic or acute inflammatory
be discussed in this chapter in addition to postpartum chronic pain.
evolving to chronic neuropathic) have been recognized throughout
pregnancy. In this chapter we will discuss painful entities encoun-
tered during pregnancy, focusing on the chronic pain states and
recurrent inflammatory pain that may lead to chronic pain.
Migraine is a common disorder, with an overall prevalence
greater in women than in men (18% vs. 6%), and the highest
prevalence concentrated between the ages of 25 and 55 years,
Gender, pregnancy and antinociceptive pathways
which are the most productive and reproductive years of life.15
According to the World Health Organization, migraine is one of
Reviews of gender and pain have noted that the prevalence of
the most disabling chronic disorders.16
most pain conditions appears to be higher in women.6 This
Migraine is the first category in the classification of headaches
higher prevalence may be related to pain from sex-specific vis-
and it is further subdivided in two major subtypes: migraine with
ceral organs, with the female pelvic region being more complex
aura (MA) and migraine without aura (MO).17 The prevalence of
and the greater number of pathophysiological conditions directly
migraine during pregnancy is around 15 to 20%.18,19 Retrospective
or indirectly linked to female reproductive functions.2 Much
studies,19,20 and one prospective study,18 found that in over 80% of
investigation has concentrated on somatic sensitivity; however,
cases MO improves during pregnancy (see Figure 12.1) while MA is
increasing knowledge about sex and hormonal differences has
less likely to improve.20 These studies strongly support the role of
produced a better understanding about pain from pelvic organs.7
estrogen as well as endogenous opioids, which progressively
When sex differences are analyzed in terms of response to
increase during pregnancy, in the genesis and modulation of
analgesic treatments, women respond better than men to opioid
migraine attacks.18,21
analgesia (both mu agonists and kappa agonists)8 and cholinergic
analgesia (mainly through the nicotinic component of choliner-
gic analgesia at the spinal level)9 in normal and chronic pain
subjects.10 Men, in contrast, respond better to nonsteroidal
anti-inflammatory drugs (NSAIDs).8 Migraine is a primary disorder of the brain, in which neural events
Gender and hormonal status are factors in antinociception cause dilation of blood vessels. This vasodilatation produces pain
during pregnancy.11 Antinociception associated with pregnancy and further nerve activation, mainly through the ophthalmic

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.
3 Nervous system disorders

risks of prophylactic or treatment medications.21 Acetaminophen,
a Food and Drug Administration (FDA) category B drug,28 is
commonly recommended for headache in pregnancy. Other
FDA category B medications for headaches include NSAIDs, pred-
nisone, and metoclopramide. Opioids, caffeine, and beta-block-
ers are FDA category C.28 Recent trials addressing the usefulness
and safety of sumatriptan (FDA category C) in pregnancy have
yielded promising results with no evidence of untoward effects in
the newborn.29,30 Recommended drugs and dosages are depicted
in Table 12.1.

Back pain
Back pain is one of the most common pain conditions in the
general population, with a lifetime prevalence of 58“84% of all
Figure 12.1 Attack frequency during the three months preceding pregnancy
adults6 and a peak at younger ages.31 During pregnancy, the
and during the trimesters of pregnancy in 47 women affected by migraine
without aura. & ¼ No attacks; & ¼ less than one attack/month; hatched ¼ 1“3 most common orthopedic complaint is backache, with a nine
attacks/month; double hatched ¼ 1“3 attacks/week. First trimester vs. month prevalence close to 50%,32,33 a stable point prevalence
pregravid period, P ¼ 0.0001; second vs. first trimester, P ¼ 0.0001; third vs. throughout pregnancy of 25%,33 and a true incidence rate of
second trimester, P ¼ 0.02. Reprinted from Sances, G. et al.18 with permission.
Ostgaard et al. subdivided back pain into three categories: high
back pain, low back pain, and sacroiliac pain.33 This last group is
branch of the trigeminal nerve (see Figure 12.2).22 This trigemi-
referred to as posterior pelvic pain in some publications and
novascular system acts as a network extending in the walls of all
seems to be closely related to the anterior or symphyseal
major vessels and projects widely throughout the cortex, dura,
pain,33,34 which is discussed later in this chapter. This differentia-
and midbrain.23 The originating event generating the neurovas-
tion into three categories has prognostic value since posterior
cular cascade that ends up in pain is unknown. However, evi-
pelvic pain increases as pregnancy advances,33 and it is more
dence suggests that activation of trigeminal sensory neurons and
prevalent and more intense than back pain.35 However, after
release of mediators that modulate inflammation, vasodilatation,
delivery, posterior pelvic pain is usually less frequent and less
and extravasation of plasma proteins ultimately leads to pain.15
intense than back pain.35 Risk factors that have been consistently
Estrogen and other reproductive hormones interact with the tri-
linked to back pain are: presence of back pain before pregnancy,
geminovascular system, possibly explaining why headache can
multiparity, and heavy workload.32,33,35
be influenced by pregnancy.23

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