nant ventricular arrhythmias. Pacing Clin. Electrophysiol. 2006; 29: complicating extradural anaesthesia for caesarean section. Br. J. Anaesth.
467â€“70. 1992; 69: 647â€“52.
5 Other disorders
249. Kalaycy, M., Cadavi, F., Altunkaya, H., Gul, S. & Ackgoz, B. Subdural 253. Bader, A. M., Gilbertson, L., Kirz, L. & Datta, S. Regional anesthesia in
empyema due to spinal anesthesia. Acta Anaesthesiol. Scand. 2005; 49: 426. women with chorioamnionitis. Reg. Anesth. 1992; 17: 84â€“6.
250. Kangwanprasert, M. & Young, R. S. Case report: spinal epidural abscess 254. Berman, R. S. & Eisele, J. H. Bacteremia, spinal anesthesia, and develop-
from Klebsiella pneumoniae. Hawaii Med. J. 2005; 64: 216â€“17. ment of meningitis. Anesthesiology 1978; 48: 376â€“7.
251. Curry, W. T. Jr., Hoh, B. L., Amin-Hanjani, S. & Eskandar, E. N. Spinal 255. Loarie, D. J. & Fairley, H. B. Epidural abscess following spinal anesthesia.
epidural abscess: clinical presentation, management, and outcome. Anesth. Analg. 1978; 57: 351â€“3.
Surg. Neurol. 2005; 63: 364â€“71. 256. Goodman, E. J., de Horta, E. & Taguiam, J. M. Safety of spinal and epidural
252. Carp, H. & Bailey, S. The association between meningitis and dural punc- anesthesia in parturients with chorioamnionitis. Reg. Anesth. 1996; 21:
ture in bacteremic rats. Anesthesiology 1992; 76: 739â€“42. 436â€“41.
Robert S. F. McKay and John E. Schlicher
discussed are very rare indeed and will receive only passing men-
tion when the anesthetic implications are trivial.
The hormonal environment during pregnancy leads to significant
changes in the integumentary system of virtually all pregnant
Integrity of skin function during anesthetic
women. In a few, skin changes may become pathologic.
Likewise, women with nonpregnancy-related skin disorders
may become pregnant, and the pregnancy may affect the course The important roles of skin during anesthesia are often neglected,
of the disease or, alternatively, the skin disorder may adversely with the anesthesiologist being especially trained to avoid disrup-
affect the mother or the fetus. This chapter will focus on (1) tion of the homeostasis of internal organs (e.g. cardiopulmonary
normal changes of the skin during pregnancy, (2) pathologic system). Yet the integrity of skin functions in the perioperative
skin disorders that occur primarily in pregnant women, (3) period is critical to good outcome and thus a plan for proper skin
other dermatologic disorders with significant effects on the care must always be part of the anesthetic management. This is
mother and/or fetus, and (4) the anesthetic considerations for particularly true when the skin is compromised by either disease
women with these dermatologic disorders. Certain diseases that or invasive techniques, in other words, in practically every anes-
affect the skin in pregnancy, such as autoimmune diseases, are thetic procedure. See Table 19.1.
discussed in detail in other chapters. These diseases may be An anesthetic plan for management of normal skin includes
mentioned only in passing in the current chapter, even though simple measures such as the avoidance of prolonged skin ische-
the degree of skin involvement may be substantial. mia through careful positioning, minimization of dermal trauma,
and avoidance of excessive heat or cold application. In skin dis-
ease, however, knowledge of the response of the damaged area to
Functions of the skin
necessary interventions may be critical. Further, careful manage-
ment may not directly involve the skin at all, for example, the
The integumentary system comprises approximately 16% of body
choice to avoid epidural morphine in patients with a history of
weight. It is a system containing multiple tissues including skin
oral herpetic lesions. Perhaps the most important preventative
itself (epidermis, dermis, and hypodermis), glands (sudoriferous
measure in skin care is skin preparation for invasive procedures,
and sebaceous), hair, nails, nervous tissue, blood vessels, and
the general guidelines of which are given in Table 19.2.
even muscle (piloerector muscles). Although considered a single
organ, the skin serves multiple discrete and interactive functions.
As a barrier, it protects the body from physical agents, mechanical
Normal skin changes of pregnancy
injury, dehydration, and ultraviolet radiation. The proper balance
The skin undergoes several changes during pregnancy, related pri-
of collagen and elastic fibers gives skin flexibility while preventing
marily to hormonal influences. Such changes may be marked but
overstretching. The skinâ€™s secretory glands, fat, and vascular sys-
are usually benign, nonproblematic, and/or temporary, although
tem help regulate body temperature. Likewise, when present, hair
some (such as striae gravidarum or â€˜â€˜stretch marksâ€™â€™) may persist
and the air pockets produced by piloerection may help maintain
long after the delivery. These normal skin changes, seen in many
body temperature. Skin plays a significant role in vitamin D
or most of the gravid population, are listed in Table 19.3.
production. It contains numerous receptors that interact with
the nervous system to affect the entire body. Anesthesiologists
frequently use skin as a monitor of temperature, oxygenation,
hydration, blood pressure, and even blood sugar (shivering, color,
As discussed in the first edition of this text, the labeling of derma-
tone, diaphoresis, etc.). Careful evaluation of the skin can lead to
toses in pregnant and nonpregnant patients has undergone
the detection of many systemic disease processes including con-
numerous revisions over the years. This remains the case. Many
nective tissue disease, infection, diabetes mellitus, and vascular
named diseases have been found to be identical histologically,
disease. Although skin changes themselves only rarely have anes-
representing various clinical manifestations of the same entity.
thetic implications for the pregnant woman, the underlying con-
Conversely, other entities looked alike clinically, but were later
ditions associated with such changes often have significance to the
found to be pathophysiologically distinct and thus given different
anesthesiologist. This chapter will focus on such associations and
names. Occasionally, a particular disease may have two or more
will attempt to help the clinician distinguish benign conditions
distinct etiologies yet retain a single name. As yet, no universally
from those with morbid potential. Of note, some of the 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.
5 Other disorders
Table 19.1 The effects of surgery and anesthesia on skin functions
Skin function Effects of surgery and anesthesia Potential morbidity
Sensory perception Decreases or eliminates responses to noxious input. Damage to skin itself, e.g. pressure sores.
Damage to underlying tissues, e.g. peripheral nerves.
Temperature regulation Hypercapnia and vasodilation redistribute blood. Hypo- or hyperthermia.
Anesthesia compromises vasoregulation and alters
response of sweat glands.
Infection barrier Surgery and invasive anesthesia procedures may expose Infectious morbidity.
internal tissues to environmental contamination,
Immune functions May introduce antigens. May depress immune response. Hypersensitivity reactions.
Cosmetic appeal Altered by scars/skin damage Social morbidity.
Blood vessel damage. Hematologic disruptions.
Table 19.2 Skin preparation and needle guidelines for invasive procedures
There is no universally accepted method for skin preparation.
Cutaneous antiseptics in common use include: 10% povidone-iodine, 70% alcohol, iodophor in alcohol, and 2% aqueous chlorhexidine (HibiclensÃ’).
As povidone-iodine multiuse bottles may become contaminated, it is recommended that only single-use containers of this antiseptic be used.1
Of these preparations, only chlorhexidine and iodophor in alcohol have significant residual antimicrobial activity once the skin has dried. There
are concerns that chlorhexidine, despite its use as a plaque controlling mouthwash, is toxic to various eukaryotic cells and that its use near mucous
membranes should be limited.
Although rubbing increases the antiseptic effects,2 blisters or bullae should not be vigorously scrubbed as tissue damage and spread of some types of
lesions may occur.
Topical antiseptics do dry the skin and this may exacerbate eczematous lesions. Treatment with skin moisturizers, e.g. petroleum jelly, may be
beneficial following the procedure.
Certain pathologic lesions, e.g. psoriasis and sarcoid, may be reactivated by trauma (Koebner response). Similarly, infection of the skin may be spread
by instrumentation. Thus, avoid instrumentation of blistered, raw, open, or otherwise infected skin.
Malignant melanoma lesions should not be instrumented.
Inflammatory sites may be instrumented, but like eczematous patches, they may harbor Staphylococcus aureus and therefore are best left undisturbed,
if possible. Concerns that instrumentation of tattooed skin should be avoided are based on the risk of a pigment-containing tissue core from a tattoo
being deposited into the epidural, subdural, or subarachnoid spaces, leading to later neurological complications.3 These concerns may be
unfounded because the tattoo pigments are inert dyes (red pigment may be the exception),4 which do not result in any bodily reactions once the
initial tattoo healing process has been completed. The amount of pigment that is used in the tattoo process is quite miniscule and once the tattoo has
healed, the dyes or inks are fixed in the cells within the skin, and cannot be mobilized by a needle. Thus, there is no evidence that any harm will come
from placing a clean needle through a healed tattoo.5 Shatz and coworkers reported that India ink tattooing of the colon led to no significant adverse
effects in patients studied for up to 117 months.6
Table modified from Garahan, M. B. & Licata, A. Dermatoses. In Gambling, D. R. & Douglas, M. J. (eds.), Obstetric Anesthesia and Uncommon Disorders,
1st edn. Philadelphia: W. B. Saunders, 1998, p. 353.
accepted system for naming dermatologic diseases has been Table 19.4 lists a partial differential diagnosis for pruritus and
found, and the authors are only able to use their judgment as to rash in pregnancy.
the most accurate and currently accepted nomenclature.
Pruritic dermatologic diseases seen in pregnancy
Pruritus is the leading dermatological symptom during preg-
nancy8 occurring in up to 20% of all pregnancies. Skin disorders
The most common dermatologic complaints in pregnancy are
pruritus and rash. To distinguish the various pregnancy-related peculiar to pregnancy may be called the specific dermatoses of
disorders that present with pruritus and rash, one must know the pregnancy and are usually associated with primary skin lesions.
type of lesion, its distribution, timing, and associated conditions. In contrast, pruritus gravidarum is a poorly defined condition of
pregnancy classically associated with first trimester pruritus but
Table 19.3 Normal skin changes of pregnancy7 no obvious dermatosis.9 Women with pruritus gravidarum do not
have specific lesions but only secondary skin lesions like excoria-
Hyperpigmentation of scars, nevi, and areolae are seen, along with
tion marks.10 Emollients and antihistamines can usually relieve
the midline abdominal linea nigra, and facial melasma or â€˜â€˜mask of
the symptoms of pruritus gravidarum. It is not clear whether
pruritus gravidarum is associated with another more well-defined
Striae gravidarum or stretch marks can be found on the abdomen,
condition known as intrahepatic cholestasis of pregnancy (IHCP),
breasts, arms, and thighs.
but the terms often are used interchangeably in the literature.
Vascular changes include vessel proliferation, congestion, and
Intraheptatic cholestasis of pregnancy is also associated with no
vasomotor instability. Varicosities, telangiectasias, and spinal
specific skin lesion, but it usually presents in the third rather than
angiomas are common, as well as palmar erythema, gingival
the first trimester. It is the most common liver disorder unique to
swelling, and generalized edema.
pregnancy and the diagnosis is suggested by unrelenting pruritus,
Hair growth modifications rarely include hirsutism. However, the
abnormal liver function tests (in the absence of viral or drug-
growth cycle of scalp hair changes. The growth phase (anagen) is
induced hepatitis), jaundice, and elevated serum bile acids.9
prolonged, resulting in a thick head of hair. Postpartum, a high
A full discussion of IHCP is presented later in this chapter.
percentage of the follicles simultaneously enter the resting (telogen)
phase, which results in the shedding of strands. This persists for
Polymorphic eruption of pregnancy (polymorphic
dermatitis of pregnancy, pruritic urticarial
papules, and plaques of pregnancy)
Polymorphic eruption of pregnancy (PEP) is the most common
Table 19.4 Differential diagnosis of pruritus and gestational dermatosis. It appears classically as erythematous ede-
rash in pregnancy matous papules and plaques associated with intense pruritus.11
This dermatosis is still sometimes referred to as PUPPP, the acro-
nym for pruritic urticarial papules and plaques of pregnancy,
Pruritus gravidarum Absence of skin lesions; usually which was first used descriptively by Lawley and colleagues in
1979.12 The rash generally appears after 34 weeksâ€™ gestation and
occurs in first trimester, no
occurs in approximately 1 in 200 pregnancies13 with higher incid-
change in liver enzymes e.g.
ences in twin (2.9%) and triplet (14%) pregnancies.14 Notably, a
glutathione S-transferase alpha.
Polymorphic eruption of Papules and plaques start in stria on number of differing entities with similar clinical aspects, nonspe-
pregnancy (polymorphic abdomen; occurs in third cific histology, and negative immunoflurescence have been called
PUPPP (for example, Aronson et al. listed three types of PUPPP).15
dermatitis of pregnancy, trimester after 34 weeksâ€™
pruritic urticarial papules gestation; involvement of face, Given this confusion among dermatologists, the designation â€˜â€˜poly-
and plaques of pregnancy, palms, or soles unusual. morphic eruption of pregnancyâ€™â€™ (PEP) has generally replaced the
term PUPPP.16 The usual plaque and papules begin on the lower
late onset prurigo)
Intrahepatic cholestasis Elevated bile acid; absence of skin abdomen, particularly within striae, and spread to the back and
of pregnancy (obstetric lesions; occurs in third trimester, proximal extremities (see Figure 19.1). Involvement of face, palms,
and soles is unusual,17,18 but may be a significant source of distress
hepatosis) glutathione S-transferase alpha
to the patient.17 Dyshidrosis may occur occasionally.19 It has been
Pemphigoid gestationis Vesicles and bullae involve skin but suggested that primiparity, multiple pregnancy, and excessive
(herpes gestationis) usually not mucous membranes; weight gain are associated features. Although intensely pruritic,
occurs in second and third the rash resolves within a few weeks after pregnancy and the con-
trimesters; skin biopsy with dition usually does not recur. Further work-up may be indicated for
immunofluorescent microscopy atypical presentations, bullous or pustular lesions, or in a patient
shows subepidermal blistering with systemic symptoms. Of clinical importance, the rash of PEP
with basement membrane deposits can be difficult to distinguish from that of pemphigoid gestationis,
of C3 complement and IgG. an autoimmune bullous disorder with potential fetal consequences
Pruritic folliculitis Small red pustules with acne-like that may recur with subsequent pregnancy, menses, or hormonal
therapy.17 A direct immunofluorescent skin biopsy (positive in
appearance; intensely pruritic;
pemphigoid) may be used to distinguish the two conditions.20
benign; treated with benzoyl
peroxide and antihistamines.
Eczema Significantly underreported in Anesthetic implications
pregnancy; history of atopy/ It is unlikely that PEP would have a significant impact on the
allergies/asthma. anesthetic management of the patient, although the avoidance
of agents that release histamine seems logical. Likewise, affected
IgG Â¼ immunoglobulin G
skin should probably be avoided during instrumentation,
5 Other disorders
Figure 19.1 Pruritic urticarial papules and plaques of pregnancy.
# Deanna Poirier, Dermatlas: www.dermatlas.org. Used with
permission. (See color plate section.)
particularly since scratching of lesions by the patient might intro- first symptom in 97%), and elevated serum bile acids in the absence
of other pathological conditions.25 Notably, pruritus occurs in the
duce bacteria at the site. It is important that the anesthesiologist
does not mistakenly identify bullous diseases (the implications of absence of skin lesions. Although elevation of plasma bile salts is
which are discussed later in the chapter) as PEP. associated with itching, there is no correlation between the concen-
tration of bile salts and severity of the itch.26 The cause of intra-
hepatic cholestasis may be dysfunction of bile secretion by active
Intrahepatic cholestasis of pregnancy
hepatocellular transporters.27 The result is the intracellular accu-
(obstetric hepatosis) see also Chapter 14
mulation of toxic bile acids that leads to cholestatic liver cell injury.
Intrahepatic cholestasis of pregnancy is a pregnancy-specific liver Liver biopsy shows dilated bile canaliculi, minimal inflammatory
response, and nonspecific cholestasis.28 The measurement of glu-
disease associated with minimal maternal risk but a significant risk
of perinatal mortality, preterm delivery, fetal distress, and meco- tathione S-transferase alpha (GSTA, a specific marker of hepatocel-
nium staining.21 The disease reportedly occurs in approximately 1% lular integrity) provides a test of liver dysfunction that distinguishes
of pregnancies at a median gestational age of 34 weeks22 and women with IHCP from those with benign pruritus gravidarum.29
accounts for 20% of cases of jaundice in pregnancy. Intrahepatic Serum bilirubin is also typically elevated. Although transaminases
cholestasis of pregnancy is a genetic disorder predisposing a may increase, moderate to severe elevations suggest the possibility
woman to increased cholestasis during each pregnancy or while of other hepatic disease such as drug-induced or viral hepatitis.
taking oral contraceptives.23 Among women noted to develop jaun- Gamma-GT is usually normal (see Table 14.5 in Chapter 14).
dice with oral contraceptives, 50% previously had intrahepatic Although usually benign for the mother, evidence associates
cholestasis of pregnancy.24 The diagnosis is based on pruritus (the IHCP with poor fetal prognosis resulting from increased transfer
of bile acids from mother to fetus. This leads to an accumulation of pregnancy (PP) is an autoimmune pregnancy-associated sub-
of bile acids in the cord blood serum, meconium, and amniotic epidermal blistering disease and must be differentiated from
fluid and may account for diminished fetal well-being and sudden bullous pemphigoid, epidermolysis bullosa acquisita, dermatitis
intrauterine death by IHCP. Fisk and Storey30 found low birth- herpetiformis, linear IgA dermatosis, cicatricial pemphigoid
weight and prematurity (44%) in the more severe cases; meco- (mucous membrane pemphigoid [MMP]), porphyria cutanea
nium occurred in 45%. Perinatal mortality was 0.35% although tarda, and drug reactions (i.e. toxic epidermal necrolysis,
this incidence did not differ from that of the general population. Lyell syndrome, Stevens-Johnson syndrome). (See Table 19.5).
When IHCP is diagnosed, ursodeoxycholic acid (UDCA) Pemphigoid of pregnancy usually affects skin and, rarely,
coupled with close maternalâ€“fetal surveillance is indicated. mucous membranes. The disorder occurs in approximately
Delivery should be effected near term following confirmation of one in 50 000 pregnancies and usually begins in the second or
fetal lung maturity, or earlier if fetal compromise is identified.21 third trimester and occasionally in the postpartum period.
Ursodeoxycholic acid treatment reduces the bile acid content in Pemphigoid of pregnancy may occur in trophoblastic disease
the mother and in turn, in the fetal compartment.31 In addition, and with oral contraceptive use.38 The disease appears to be
UDCA administered to the mother lowers the amount of bile mediated by immunoglobulins G1, G3, and A (IgG1, IgG3, and
acids present in colostrum. Treatment with UDCA is especially IgA) that specifically target the 180-kD component (BP 180) of
useful in severe forms of IHCP, or when there is a history of hemidesmosomes (collagen XVII). The terms pemphigoid gesta-
sudden fetal death in a previous pregnancy.32 In a series reported tionis or pemphigoid of pregnancy reflect the immunopathologic
by Davies and colleagues,33 twelve pregnancies were managed similarity to bullous pemphigoid, a disease of the elderly that
expectantly and perinatal morbidity and mortality resulted in also involves antibodies to the 180-kD hemidesmosomal anti-
eight stillbirths, two premature deliveries complicated by fetal gen but that does not appear to show reactions to hormonal
distress with one perinatal death, and one cesarean section stimulation. The membrane proximal NC16A domain of this
[C/S] for fetal distress. Subsequently, these investigators treated autoantigen contains key epitopes of autoantibodies and T
three women who had IHCP with UDCA. No perinatal morbidity cells and plays an essential role in the pathogenesis of both
diseases as well as other blistering diseases (see Table 19.5).39
or mortality occurred. Intrahepatic cholestasis of pregnancy
starts to resolve spontaneously within 24 hours of delivery, Abnormal expression of class II major histocompatibility com-
plex (MHC) also occurs in the placental villi of women with PP,40
although jaundice and abnormal liver function tests may persist
for months. However, if symptoms of liver disease persist beyond suggesting ongoing immunologic stimulation. This has led some
this time then chronic hepatopathy must be ruled out. investigators to believe that the primary immunologic event takes
place within the placenta and that the skin is an immunologic
bystander.41 Pemphigoid of pregnancy is found primarily in
Concerns for the anesthesiologist in IHCP include the degree of whites as one of the specific human lymphocyte antigens asso-
hepatic disease and the possibility of planned near-term obstetric ciated with the disease (HLA-DR4) is seldom seen in the black
population.42 Paternal human lymphocyte antigen (HLA) type
interventions (e.g. early induction of labor). Decreased small
may also be associated with the development of PP.43 Other
intestinal bile acid concentrations can lead to impaired absorp-
tion of fats and fat-soluble vitamins, resulting in steatorrhea and autoantibodies may occur in association with PP. Shornick and
deficiencies in vitamins A, D, E, and K.34 Although unusual, coag- Black found an increased frequency of Graves disease in women
with a history of PP.44
ulopathy may occur with IHCP and a case of epidural hematoma
complicating cholestasis of pregnancy has been reported.35 Pemphigoid of pregnancy is characterized by intensely pruritic
Injection of vitamin K and fresh frozen plasma can prevent coag- urticarial lesions that usually begin on the abdomen and may, at
ulopathy. If cholestyramine is used then prophylactic vitamin K first, resemble PEP. Within days, vesicles and bullae on erythe-
should be used in a dose of 10 mg/day. There is an increased risk of matous bases develop. The polymorphic plaques migrate out-
postpartum hemorrhage so the patient should have blood cross- ward, typically starting from the periumbilical region and
matched and large bore intravenous (i.v.) lines inserted. spreading to the abdomen, trunk, buttocks, and extremities.
Other causes of pruritus should be ruled out including thyroid Facial and oral lesions are rare. Diagnosis may be confirmed by
disease, renal failure, lymphoma, anemia, and drug reactions. skin biopsy with immunofluorescent microscopy showing sub-
Physical examination should be normal in IHCP, with the excep- epidermal blistering with basement membrane deposits of C3
tion of possible skin excoriation from scratching. Ondansetron complement and IgG. The condition may resolve late in preg-
may be effective treatment for IHCP-associated pruritus.36 nancy, but, unlike PEP, classically flares up again at delivery then
Opioids, especially neuraxial opioids, may exacerbate the prur- slowly resolves over weeks to months. There may also be non-
itus, but effective pain management should be used. gestational recurrences triggered by oral contraceptives and
The disease mostly leads to maternal discomfort, but fetal and
Pemphigoid of pregnancy (herpes gestationis)
neonatal complications, including preterm delivery and low
birthweight, have been reported.54,55 Although Shornick and
Milton,37 in 1872, designated this intensely pruritic rash that
may follow a viral-like prodrome as herpes gestationis, but the Black confirmed these complications, they found no increase in
disorder is autoimmune in origin rather than viral. Pemphigoid
5 Other disorders
Table 19.5 Immunopathology of specific subepidermal bullous dermatoses
Target site(s) a,45,46 and/or pathologic findings
Disease Clinical features
I. Autoimmune â€“ circulating autoantibodies against basement membrane zone
Pemphigoid of pregnancy (PP) BP 180 (type XVII collagen) NC16A domain Characteristic skin lesions.
Bullous pemphigoid (BP) N-terminal 45 amino acids of the NC16A domain of Occurs primarily in elderly; otherwise similar
BP 180 (type XVII collagen). Intracellular regions â€“ to pemphigoid of pregnancy.
less frequent IgG and/or C3 along the basement
Epidermolysis bullosa acquisita Type VII collagen. Bullae over areas of trauma; laryngeal stenosis
(EB) may occur from dense scarring.
Dermatitis herpetiformis IgA granular deposits in the dermal papillae of Characterized by variable degrees of enteropathy
noninvolved skin. and increased intestinal permeability;
otherwise similar to bullous pemphigoid.
Linear IgA dermatosis (LAD) BP 180 (type XVII collagen); linear pattern of Similar to bullous pemphigoid; less frequent in
granular IgA along the basement membrane. females; normal intestinal findings.
Cicatricial pemphigoid BP180 (type XVII collagen) NC16A domain and the Mucosal involvement with little skin involvement.
(CP) also called mucous C-terminus that projects into the dermal- Frequent eye involvement with risk of
membrane pemphigoid epidermal junction; linear binding of IgG and blindness.