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become a rare event, lack controls, and record irrelevant data.64
sone has been successful with no apparent adverse effect on the
parturient or fetus. Neuraxial anesthesia frequently gets the blame for many neuro-
logic disorders,3 although they are about five times more likely to
Involvement of the spinal nucleus of the trigeminal (V) cranial
result from obstetric factors.65 Any form of anesthesia, signifying
nerve in the cervical cord, causing transient facial weakness, has
been reported in association with high epidural block during as it does a complicated labor, may be associated with an
labor.48,49 Because of the inverted representation of the fibers, increased incidence of neurologic sequelae.66 Transient neura-
the upper division is usually involved first, necessitating special praxia involving the femoral, lateral femoral cutaneous, obtura-
care of the eye as the corneal reflex may be lost. Trigeminal, facial, tor, peroneal, and sciatic nerves can occur after vaginal
delivery.67,68 As in earlier days, nulliparity, prolonged second
abducent (VI) and VIII nerve palsies have all been caused by loss
of cerebrospinal fluid following unintended dural puncture in stage, prolonged lithotomy position, and assisted delivery, rather
parturients,50,51 and even following puncture with a 25-gauge than neuraxial anesthesia, are associated factors.68
Sprotte needle.52 The response of these palsies to epidural blood Root damage, usually mild and causing only paresthesia, may
patch is not always encouraging.53,54,55 follow epidural analgesia, one survey detecting one case among
13 000 epidurals,65 while the incidence following spinal anesthe-
sia is probably tenfold higher.69 Peripheral mononeuropathies
Upper limb neuropathies
may be the indirect result of neuraxial anesthesia if the resultant
sensory loss allows nerve compression to go undetected.70,71,72
Brachial plexus palsy is well recognized as a neonatal problem
after difficult breech delivery, and may be seen in adults as a Many different mononeuropathies and plexopathies have been
result of arm traction, cervical rib, neoplasm, and so on. An auto- associated with pregnancy and delivery.
somal dominant familial inflammatory demyelinating form,
however, may arise de novo or be exacerbated during pregnancy
Lower limb neuropathies
or postpartum in the mother.56,57 Avoiding vaginal delivery has
not been found to alleviate the problem.56 The condition may be Lumbosacral plexus injury is the commonest cause of postpar-
tum foot drop.73 The lumbosacral plexus is formed from L4 and 5
unilateral or bilateral, and is characterized by pain and weakness
in the arm and shoulder girdle. The pain has been known to be so and sacral roots, but it is only the lumbosacral trunk (the union
severe as to prompt one mother to request sterilization to avoid of the L4 and 5 roots) that crosses the pelvic brim where it is



219
3 Nervous system disorders


maximally vulnerable to compression from the baby™s head dur- vaginal delivery with a breech presentation, was thin and was
ing labor. There may be sciatic-type pain during labor, with kept sitting in one position during labor while her leg numbness
postpartum foot drop due to weakness of the anterior tibial and was wrongly attributed to epidural blockade. The second was
peroneal muscles, and paresthesias or numbness in the outer leg obese and suffered a period of hypotension while lying on her
and foot, for months afterwards. There is sometimes gluteal right side during preparation for elective C/S under epidural
involvement. The condition is occasionally bilateral. Sufferers anesthesia. Both experienced right-sided signs typical of sciatic
are usually primiparous, have long labors, difficult vaginal deliv- palsy: absence of movement and loss of sensation below the knee,
eries, and large babies.59,60,61,62 Recovery depends on how long with sparing of the medial side. Motor changes recovered more
the difficult labor is allowed to persist, but in one African com- quickly than the sensory changes, while occasional shooting pain
munity recovery was incomplete in 24% of women.73 A history of recurred for some years.71 Since that time two more cases of
this injury is a strong indication for C/S next time. sciatic nerve damage have been described, in women who had
Femoral nerve palsy. Transient femoral neurapraxia is fre- C/S without hypotension and with a right hip wedge, who both
quently detected after vaginal delivery, if sought.67,68 The femoral suffered left-sided sciatic nerve palsy.77,78
nerve is vulnerable to stretching injury as it passes beneath the Peroneal neuropathy results from compression of the common
inguinal ligament; it may be damaged by prolonged flexion, abduc- peroneal nerve as it winds round the head of the fibula. It may
tion, or external rotation of the hip joint. Femoral neuropathy may arise during labor as a result of incorrect and prolonged position-
follow prolonged adoption of an excessive lithotomy position,74 ing in stirrups, or compression of the lateral side of the knee
and has been reported after difficult vaginal delivery.75 Signs and against any hard object. It may result from sustained knee flexion
or prolonged squatting.79 Signs of nerve compression may go
symptoms are weakness of straight-leg raising, a diminished
patella reflex, and numbness of the front of the thigh. Some hip unnoticed or be disregarded in the presence of regional blockade.
flexion is present as function is preserved in the iliopsoas muscle; The resulting foot drop may be profound, but plantar flexion and
inversion at the ankle are preserved, unlike in an L4/5 lesion.70
walking is therefore possible but mounting stairs is not. Clearly,
prolonged use of extreme squatting and the lithotomy position Sensory impairment spares the lateral border of the foot, which
during the second stage of labor are best avoided. distinguishes it from sciatic nerve palsy.
Obturator nerve palsy. The obturator nerve may be compressed
both where it crosses the brim of the pelvis and within the obtura- Anesthetic implications
tor canal, so it would be expected to be vulnerable during difficult Neuraxial anesthesia or analgesia readily gets blamed for post-
vaginal delivery.1,46 Nevertheless, cases are rarely reported among partum neurologic disorders,3 so it is important firstly to be aware
parturients, suggesting the diagnosis may sometimes be missed. of any preexisting deficit, and secondly to make an accurate
Three cases were detected when sought prospectively by Wong diagnosis of the site of the lesion. This need not necessarily
et al.66 The mother may complain of pain when the damage occurs, involve expensive investigations such as conduction studies and
and this is followed by weakness of hip adduction and internal imaging: it is often possible to distinguish between peripheral and
rotation, with sensory disturbance over the upper inner thigh. central lesions by simple clinical means. For example, derma-
Meralgia paresthetica arises from compression of the lateral tomes (the spinal segments involved in the sensory supply to
femoral cutaneous nerve as it passes between the two divisions the skin) bear no relation to the peripheral nerve distribution to
at the lateral end of the inguinal ligament, where they attach to the skin (see Figure 11.1), while segmental motor supply also has
the anterior superior iliac spine. It is one of the most frequently a characteristic pattern (see Figure 11.2).
encountered neuropathies in childbirth.64,65,67,68 It may arise Anesthesiologists cannot wholly absolve themselves from
both during pregnancy, typically about the 30th week, and intra- responsibility for peripheral nerve injuries, if the dangers of
partum, in association with rising intra-abdominal pressure. The stretch or compression under GA or regional anesthesia are over-
presence of edema may contribute, as with the increased looked. Moreover, among those with a hereditary liability to
incidence during pregnancy of carpal tunnel syndrome and pressure palsy, even relatively brief periods of immobility or
Bell™s palsy.47 It may recur during successive pregnancies.76 pressure on any one site must be avoided.
Symptoms are unpleasant and include numbness, tingling, burn-
ing, or other paresthesias, affecting the anterolateral aspect of the
Neuropathies secondary to other conditions
thigh. The distribution is quite unlike that of a root lesion, yet
when the condition is noted de novo postpartum, it is commonly
Diabetes
attributed to neuraxial blockade by those unfamiliar with neuro-
anatomy. The symptoms can be expected to resolve following Diabetes is the commonest cause of peripheral neuropathy and is
childbirth, but if they are severe during pregnancy, they may be present in about 15% of diabetics. It does not therefore qualify
relieved by local infiltration analgesia. In severe and persistent strictly speaking as an uncommon disorder. Any type or combi-
cases, surgical release of the nerve has been advocated. nation of neuropathies may be seen in diabetes, but two types
Sciatic neuropathy has not generally been recognized as a com- predominate: (1) symmetrical combined sensory and autonomic
neuropathy, and (2) mononeuropathy, single or multifocal.1
plication of childbirth, possibly because it is mistaken for a lum-
bosacral palsy. It has, however, been described in four women Diabetes requires meticulous attention during pregnancy for
delivered by C/S.71,77,78 One woman who wished to attempt many reasons, and peripheral neuropathy, if present, can only



220
Chapter 11


L1 L2 L3 L4 L5 S1 S2 S3 S4
Hip flexion
Anterior cutaneous branches
T10
extension
(intercostal nerves)
abduction
Lateral cutaneous branches
adduction
(intercostal nerves)
T12 medial rotation
Subcostal nerve lateral rotation
Femoral branch Knee flexion
S
L1 (genitofemoral nerve)
4 extension
Ilioinguinal nerve Ankle dorsiflexion
Lateral femoral plantar flexion
L2 cutaneous nerve
Big toe dorsiflexion
Obturator nerve Levator ani
Coccygeus
L3
Anterior
Figure 11.2 The spinal segments involved in the movements of joints in the leg.
cutaneous
(Reproduced from Reynolds, F. & Bromage, P. Neurologic sequelae of childbirth
nerve
and regional anesthesia. In Chestnut, D. (ed.), Obstetric Anesthesia: Principles and
Femoral nerve
L4
Practice, 3rd edn.), St Louis: Mosby, 2004, pp. 579“60164; by permission of the
publisher. Data from Russell, R. Assessment of motor blockade during epidural
Saphenous
analgesia in labour. International Journal of Obstetric Anesthesia 1992; 4: 230“4.)
nerve
Lateral
L5
cutaneous
nerve
Management
Where there is a hint of peripheral neuropathy in a diabetic
Common peroneal nerve
pregnant woman, autonomic function must be assessed. Heart
rate variability in response to rising from lying to standing, to
deep breathing, and coughing can demonstrate a < 5 beats/min
Superior peroneal
rise, compared with the normal rise of > 15 beats/min.81,82
nerve
S
Sural nerve/ Pupillary and lacrimal dysfunction, impaired sweating and vas-
1
tibial nerve
cular reflexes, postural hypotension, and atonicity of bowel and
Deep peroneal
bladder also signify autonomic neuropathy.
nerve
In addition to the need for assiduous blood glucose control, the
Figure 11.1 The segmental (right leg) and peripheral (left leg) sensory nerve main factors that require consideration when contemplating
distributions useful in distinguishing central from peripheral nerve injury.
anesthesia in the pregnant diabetic with a peripheral neuropathy
(From Redick, L. F. Maternal perinatal nerve palsies. Postgrad. Obstet. Gynecol.
are given earlier (see Anesthetic considerations for parturients
1992; 12: 1“6; by permission of the author and publisher.)
with dysautonomia).
Epidural, spinal, or combined spinal“epidural anesthesia have
all been recommended for both labor analgesia with vaginal
benefit from this. Diabetic autonomic neuropathy, however, is
particularly dangerous in pregnancy.80,81 It may be associated not delivery and C/S, and may be suitable provided low-dose LA/
opioid combinations are used. Any procedure that might produce
only with postural hypotension and disordered baroreceptor
sudden hemodynamic changes should be avoided. Gastroparesis
reflexes, but also with diarrhea, gustatory sweating, bladder dys-
function,82 and above all gastroparesis,80 which may lead to may be treated with metoclopramide.
severe intractable vomiting and electrolyte disturbance in preg-
nancy. Respiratory reflexes may also be impaired, leading to
Porphyria
hypoventilation, while respiratory arrest has been described
among diabetic women of childbearing age.82 No wonder, then, Acute attacks in acute intermittent and variegated porphyria and
coproporphyria may be accompanied by a predominantly motor
that diabetic dysautonomia may be considered a relative contra-
indication to pregnancy.80,81 neuropathy, but there may also be sensory and autonomic fea-
tures. Facial paralysis, dysphagia, and ocular palsies are typical;
Nevertheless, in a prospective comparison of pregnant diabetic
the most severe cases may progress to respiratory paralysis. Mild
women with nonpregnant diabetics and nondiabetic pregnant
cases regress in a few weeks, but severe cases and slowly progres-
women, Lapolla et al. found that pregnancy did not induce or
sing cases can leave a severe sensorimotor paralysis that takes
worsen peripheral nerve dysfunction in insulin-dependent dia-
months to improve. Pregnancy may provoke an attack.84,85 The
betes.83 Diabetes was in all cases well controlled using home
porphyrias are addressed fully in chapter 13.
glucose monitoring and a team approach.



221
3 Nervous system disorders


Infection
Table 11.2 Peripheral nerve syndromes in HIV infection
Leprosy
Type Comment
With the ever-increasing use of air travel, leprosy has become a
worldwide problem. It is a chronic infection of cool tissues and Distal symmetric Most commonly painful
produces a multiple mononeuropathy that tends to affect super- polyneuropathy Etiology “ cytomegalovirus
ficial nerves,86 particularly the median, ulnar, peroneal, and facial. “ dideoxycytidine
Transmission is by direct contact or through respiratory mucosa, “ dideoxyinosine
with low infectivity and a long incubation period of 3“5 years. The “ Vitamin B12 deficiency
condition is slowly progressive, but periodically the immune sys- Inflammatory Similar to Guillain-Barr´ syndrome or
e
tem mounts a sudden massive and destructive increase in activity demyelinating chronic inflammatory demyelinating
against M. leprae. Ultimately, nerve damage may become perma- peripheral neuropathy neuropathy
nent. Lupus antibodies may be present. Dapsone, a folate antago- Mononeuritis multiplex Associated with cytomegalovirus
nist, is the mainstay of therapy. It is inexpensive and is considered infection
safe in pregnancy, but may provoke fever, leukopenia, anemia, and Progressive Associated with cytomegalovirus
hemolysis and may itself cause a dose-related motor neuropathy; polyradiculopathy infection, CD4 < 50
rifampicin and clofazimine are alternatives. Treat with ganciclovir
In women with leprosy, even though apparently cured, nerve Autonomic Treatment: fluid/electrolyte
function may deteriorate in pregnancy.87 Relapse and exacerbation management; fluorocortisone; may
are maximal in late pregnancy. Fortunately the fetus is not infected. require antiarrhythmic medication
A case is described in which CSE anesthesia was used success-
fully.86 It is recommended that a patch of skin on the back that is
not affected by the condition is selected for needle insertion. Table 11.3 Some vasculitic neuropathies

Proportion with peripheral
Human immunodeficiency virus
Syndrome neuropathy
Many types of peripheral neuropathy are seen in the HIV-infected
patient.88 They are caused by the infection itself, or by the rather Polyarteritis nodosa 50“75%
toxic drugs that may be used in its treatment (see Table 11.2). The Churg-Strauss disease 50%
condition and its management are discussed more fully in Rheumatoid arthritis 1“5%
chapter 18. Systemic lupus erythematosus 10%
Wegener granulomatosis 20%
Diphtheria
This is now a rare cause of peripheral neuropathy. The exotoxin
produces segmental demyelination. Palatal weakness may follow
Pulmonary infiltration results in restrictive lung disease with a
2“3 weeks after pharyngeal diphtheria, and local muscle paralysis
decreased vital capacity. Myocardial involvement may produce
a similar interval after cutaneous diphtheria.1 The condition may
heart block, heart failure, paroxysmal dysrhythmias, and cor pul-
then spread to cranial nerves followed by generalized, predomi-
monale. Uveitis, keratoconjunctivitis sicca, parotitis, hepato-
nantly motor, neuropathy. In severe cases the respiratory muscles
splenomegaly, lupus pernio of the skin, and generalized
may be affected.
lymphadenopathy also occur. Hypercalcemia develops in 10%
of patients. Steroids are used to treat progressive lung disease
and other serious manifestations.
Vasculitis
Sarcoidosis is occasionally exacerbated by pregnancy.
Peripheral nerve damage is encountered in many vasculitic syn- Obstetric and anesthetic management are dictated by the cardio-
dromes (see Table 11.3)89 and may be related to necrotizing pulmonary status of the mother.91 Good maternal and fetal out-
angiitis of the vasa nervorum.1 There may be a multifocal mono- comes are possible in women with sarcoidosis.92
neuropathy, a distal sensory neuropathy sometimes restricted to
the digitial nerves, or, in rheumatoid arthritis, an entrapment
Poisoning with heavy metals and solvents
neuropathy. Most of these conditions are multisystem diseases
that may interact with pregnancy.90 (See Chapter 23.) Heavy metals accumulate in the body and exert their toxic effects
by combining with one or more of the reactive groups essential
for physiological function.93,94 They produce a variety of periph-
Sarcoidosis
eral neuropathies (see Table 11.4). Exposure may come from high
Sarcoidosis is a rare cause of subacute or chronic asymmetrical concentrations in soil or water, leaching from utensils and cook-
polyneuropathy, which may be associated with polymyositis, or ware, industry and mining, use of pesticides and therapeutic
of mononeuropathy, often facial palsy. In some cases, multiple agents, burning fossil fuels containing heavy metals, and the
cranial nerves are affected successively. addition of tetraethyl lead to gasoline.



222
Chapter 11



Table 11.4 Poisoning with heavy metals

Effects

Substance CNS Peripheral nerve Fetal Other Treatment

Lead Mental retardation, Motor (lead palsy) Danger assumed GIT Remove source
headache “ wrist drop Renal Chelation (EDTA)
“ foot drop Hematological
“ extraocular
Thallium Late convulsions Painful sensory GIT Prussian blue
and coma followed by motor, dermatological Mannitol
ocular, and Magnesium
KCl " renal excretion
autonomic palsies
Thiocarbamate
Arsenic Headache, Sensorimotor Chromosomal GIT, hair loss, all Sulfur, ipecac
confusion and neuropathy breaks organs Gastric lavage
convulsions CVS support
Dimercaprol
Penicillamine
Hemodialysis
Mercury Tremor, irritability, Sensorimotor Cortical/cerebellar Gingivitis, GIT Chelation (DMPS,
memory loss, neuropathy atrophy Renal damage DMSA, or EDTA)
etc.

GIT ¼ gastrointestinal tract; KC1 ¼ potassium chloride; CVS ¼ cardiovascular system; CNS ¼ central nervous system


Lead poisoning produces effects on the gastrointestinal, neuro- neuritis usually affecting the legs more than the arms. Acute treat-
muscular, central nervous, hematological, and renal systems. The ment includes ipecac or gastric lavage, cardiovascular stabilization,
neuromuscular syndrome (lead palsy) is now rare. The well-used dimercaprol, d-penicillamine, and hemodialysis, as indicated.
muscles of the forearm, wrist, and fingers and extraocular muscles Mercury poisoning may produce a sensorimotor neuropathy simi-
are commonly involved, more often those on the dominant side. lar to that caused by arsenic, although it primarily affects the CNS.
Wrist drop and, to a lesser extent, foot drop are characteristic of lead Organic or methyl mercury is highly lipid soluble and readily crosses
poisoning. There is no sensory involvement. Evidence of perma- the blood“brain barrier and placenta and into breast milk. Elemental
nent neurological sequelae from levels of lead previously thought mercury is poorly absorbed by the gastrointestinal tract, but is readily
safe raised fears of damage to the fetus and newborn, and led to the absorbed as a vapor via the lungs. Inorganic mercury salts are
prohibition of organic lead-salt additives in gasoline and consumer absorbed through the gastrointestinal tract and skin. Prenatal poison-
products. Treatment of lead poisoning consists of removal from the ing produces cerebral palsy due to cortical and cerebellar atrophy.
source of exposure and administration of chelating agents (EDTA About 6% of American women have blood mercury concentrations
and penicillamine). Increased levels of lead in maternal blood have above the safe reference level of 5.8 mg/l. Those intending to become
been associated with hypertension in pregnancy.95 pregnant should follow official advice about eating fish.96
Thallium is used as an insecticide and rodenticide, a catalyst in A distal symmetric, predominantly sensory, axonopathy may
fireworks, in the manufacture of optical lenses, in industry as an follow exposure to certain hexacarbon industrial solvents such as
alloy, and in cardiac perfusion imaging. Immediate symptoms of n-hexane (in contact cement), methyl-n-butyl ketone (in plastic-
thallium toxicity are gastrointestinal with nervous system invol- coated and color-printed fabrics), dimethylaminoproprio-
vement (peripheral sensory, motor, and, less frequently, auto- nitrile (DMAPN) used in the manufacture of polyurethane foam,
nomic) beginning within a week of ingestion. Symptoms include methyl bromide (fumigant), and ethylene oxide (gas sterilant).
paresthesias, myalgia, weakness, tremor, ataxia, and, less com- Treatment of the multisystem disturbances, including periph-
monly, tachycardia, hypertension, and salivation. Treatment eral neuropathy, associated with heavy metal and solvent poison-
includes Prussian blue and mannitol or magnesium sulfate for ing is directed at life-threatening acute complications. Anesthetic
gut decontamination, and potassium chloride (KCl) to enhance management of the parturient is determined by the obstetric
renal excretion. Avoid administration of systemic chelating situation and degree of organic dysfunction present.
agents, as they may worsen the neurologic symptoms.
Inorganic arsenic does not cross the blood“brain barrier, but does
Deficiency states
cross the placenta. It causes chromosomal breaks in cultured human
leukocytes, and teratogenetic effects in hamsters. Manifestations of In the Western world, nutritional polyneuropathy is usually asso-
chronic arsenic poisoning include sensory and peripheral motor ciated with alcoholism. Mothers who have significant systemic



223
3 Nervous system disorders


Summary: general notes on management of
disease related to alcohol abuse are usually more than 30 years of
parturients with peripheral neuropathies
age. A distal symmetric sensorimotor polyneuropathy occurs in
alcoholics and is clinically indistinguishable from those due to
Restrictive respiratory insufficiency
diabetes mellitus, malnutrition, and HIV infection. Neuropathy in
alcoholics may result from poor nutrition with deficiency of thia- Causes
mine, pyridoxine, pantothenic acid, folic acid, or a combination of i. Neuropathy affecting muscles of respiration
the B vitamins.97  HSMN
The neuropathy has no effect on the course of pregnancy, but  Guillain-Barre syndrome (GBS)
´
other alcohol-related organ dysfunction places the mother at  Any neuropathy
increased risk. Alcohol abuse results in a myriad of acute and ii. Scoliosis
chronic complications, such as withdrawal seizures, aspiration  Conditions affecting trunk muscles during growth
pneumonitis, cardiomyopathy, liver dysfunction, peptic ulcer,  Typically HSMN (any type)
malabsorption, pancreatitis, esophageal varices, coagulopathy, Signs
endocrine effects, and immunologic suppression.  Restlessness
The adverse fetal effects of alcohol have long been recognized.  Difficulty sleeping, orthopnea, headache
As well as the fetal alcohol syndrome, high rates of prematurity  Tachycardia
and infant mortality, and adverse perinatal outcomes have been  Breathless during speech
linked to maternal alcohol abuse.  FVC grossly reduced (FEV1 is misleading when FVC is low)
Obstetric and anesthetic considerations are not determined by Problems
the neuropathy although, as usual, the deficit must be documen-  Pregnancy increases need for mechanical ventilation
ted. The presence of dysfunction in other organs should deter-  Sedation, anesthesia, and analgesia poorly tolerated
mine management. Coagulopathy may preclude regional  Hypotension may produce cynanosis
anesthesia, while anxiety and acute intoxication may dictate GA.  Anemia and blood loss poorly tolerated
Nevertheless, general anesthesia may need to be modified to take  Neuraxial approach may be difficult
account of the altered pharmacokinetics and pharmacodynamics  Cannot lie flat for awake C/S
associated with chronic alcoholism. Management
 Not like obstructive respiratory insufficiency
 Noninvasive respiratory support may be needed sooner or
Drug-induced neuropathies
later in pregnancy and postpartum if FVC < 1 L at outset
Many drugs are known to produce neuropathy (see Table 11.5).
 Do not mistake tachycardia and cyanosis for a cardiac
The major problem is diagnosis and, once it is established, further
condition. Provide mechanical ventilation. Oxygen alone
exposure must be avoided. Once the neurologic deficit is accu-
is not the answer
rately documented, anesthetic options are governed by the obste-
 Give GA if needed
tric, maternal, and fetal needs.
 Requirement for NMB and analgesics are minimal
 Low threshold for blood replacement

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