Pretreatment with steroids and an H1 atagonist such as diphenhydramine can ameliorate or prevent reactions in patients deemed to be at risk Unusual causes described in obstetric patients
Trang 1Class of agent Specifi c agents Comments
Radiocontrast media (RCM) [48 – 51] Lower osmolarity RCM presently in use have
a very low risk of inducing anaphylactoid reactions as compared to the high osmolality agents used in the past
Iso - osmolar agents make RCM reactions extremely unlikely and can be requested when a patient is felt to be at risk of such
a reaction
RCM causes anaphylactoid reactions but not true anaphylaxis The incidence of life - threatening reactions is < 0.1% Peak incidence is between the ages of 20 and 50 so it does occur in women of childbearing age Anaphylactoid reactions to RCM are more likely if it has happened before but even with a prior history of reactions to RCM, the incidence runs between 16% and 44% with a subsequent exposure Volume overload from administration of RCM can lead to cardiogenic pulmonary edema that is not a hypersensitivity response and is part of the differential diagnosis of respiratory failure in this setting [52] There is no relationship between RCM reactions and shellfi sh allergies (which are generally due to reactions to tropomyosin proteins and not iodine) The only association between these two allergies is that persons who have anaphylaxis to any agent are more likely to have anaphylaxis to other agents
Pretreatment with steroids and an H1 atagonist such as diphenhydramine can ameliorate or prevent reactions in patients deemed to be at risk Unusual causes described in obstetric
patients
Seminal fl uid Laminaria Oxytocic agents
Administration of syntocinon has been associated with anaphylactoid response but has generally been attributed to preservatives used in specifi c formulations such as chlorobutanol [55 – 59]
Methotrexate Anesthetic agents including local anesthetic [53]
Anaphylaxis to MTX used intravenously to treat cancer has been reported [60]
Colloids such as dextran, albumin Dextran use has been associated with both maternal and fetal morbidity
and mortality with an incidence of dextran - 70 solution - induced anaphylactoid reactions of 1 in 383 [61 – 64]
Exercise [54] Exertion can precipitate anaphylaxis in some individuals and this includes
the exertion of labor [65]
Blood products Whole blood, serum, plasma, fractionated
serum products or immunoglobulins can all provoke an anaphylactoid response
Blood products can cause an anaphylactoid response via type II or type III hypersensitivity reactions
Latex Exposure to hard rubbers not usually
signifi cant Latex exposure can occur with gloves, intravenous tubing, Foley catheters, endotracheal tubes, dental dams, vial stoppers, condoms, adhesive dressings, and balloons Exposure can occur through direct contact, aerosolization or inhalation
Latex allergies remain one of the leading causes of perioperative anaphylactoid reactions Widespread use of powder - free and low latex protein gloves has decreased latex sensitization but it still does occur
in healthcare workers and patients who have undergone multiple hospital procedures [26,66] Infants with spina bifi da are at increased risk of latex allergies and ideally should be delivered and cared for using non - latex materials
Table 42.2 Continued
be more common with oral ingestions and in general the delayed
second phase is less severe than the initial presentation
Diagnosis
Anaphylaxis is a clinical diagnosis Three proposed sets of criteria
for the diagnosis of anaphylaxis are reviewed in Table 42.4
Approach to a naphylaxis Acute m anagement [15 – 20]
The acute management of anaphylaxis is reviewed below and should proceed in a stepwise manner
1 Provide oxygen and assess airway Equipment for intubation
and persons experienced with intubation should be brought to
Trang 2Table 42.4 Three distinct criteria for the diagnosis of anaphylaxis [15,16,26,68]
Criterion 1
Acute onset of an illness over minutes to hours with involvement of skin,
mucosal tissue or both, e.g hives, swollen lips/tongue/uvula, fl ushing with at
least one of the following:
– respiratory compromise, e.g dyspnea, wheezing, stridor, hypoxemia
– reduced blood pressure or symptoms of end - organ dysfunction suggestive of
hypotension (e.g syncope, incontinence, collapse, hypotonia)
Criterion 2
Two or more of the following after a potentially allergenic exposure:
– mucosa/skin involvement: urticaria, fl ushing, itching, tongue, lip or uvula
swelling
– respiratory involvement: dyspnea, stridor, bronchospasm, hypoxia
– gastrointestinal involvement: abdominal pain, vomiting
– hemodynamic instability: hypotension, syncope, incontinence
Criterion 3
Drop in blood pressure (either < 90 mmHg or > 30 mmHg drop from baseline)
minutes to hours after exposure to a known allergen for that patient
Table 42.3 Manifestations of anaphylaxis [67]
Skin Itching, fl ushing, sensation that skin is being pulled or burned,
urticaria (hives) and angioedmea (88%)
Psychologic Sense of impending doom
Respiratory Shortness of breath, hoarseness, diffi culty breathing/swallowing/
talking, choking, lump in throat, wheezing, stridor, laryngeal edema (50%) CXR may show hyperinfl ation, pulmonary edema or ARDS [67] Intubated patients may have elevated airway pressures and increased airway resistance
Cardiovascular Faintness, palpitations, chest discomfort, syncope, tachycardia,
bradycardia, ST/T changes on EKG, multiple PVCs, hypotension due to sudden hypovolemia Shock will occur in up to 30%
Eventually fatal arrhythmias may occur
Hypotension occurs due to three factors:
1 sudden hypovolemia from third spacing of intravascular fl uid from sudden
changes in vascular permeability
2 vasodilation and
3 myocardial depression [1,15]
Although initially cardiac output may be increased, it will often decrease with progression of the syndrome Systemic vascular resistance (SVR) is typically initially reduced in anaphylaxis However, in severely hypovolemic patients vasoconstriction can occur and be so severe that there is no additional response to vasopresssors
Gastrointestinal Metallic taste in mouth, nausea, vomiting, diarrhea, incontinence,
abdominal bloating, abdominal and uterine cramping (30%)
Fetal Decreased fetal movement Fetal heart rate monitor may also
show late decelerations, tachycardia, diminished variability, bradycardia
the bedside promptly if there is any evidence of airway compro-mise or facial or neck swelling Pregnant women are diffi cult
to intubate because of pregnancy - related changes in the airway and body habitus Anaphylaxis - related airway edema may further contribute to the diffi culty in establishing an airway in
a pregnant patient Therefore, if intubation is performed it should be done by the most experienced person available and with a plan in place for what will be done should the intubation fail (including being prepared for the possibility of emergency cricothyroidotomy)
2 Administer aqueous epinephrine 0.5 mg (0.5 mL of a 1 : 1000
(1 mg/mL) solution) intramuscularly into the lateral or anterior thigh Epinephrine will both treat hypotension and help with bronchospasm and is the cornerstone of the initial medical man-agement of anaphylaxis There are no absolute contraindications
to epinephrine in the setting of anaphylaxis This dose of epinephrine may be repeated every 5 minutes as needed Subcutaneous administration is acceptable but is associated with less rapid absorption and effect than an intramuscular or intravenous injection If patient is on a β - blocker, the response
Trang 3pressor support (see below) should be introduced Cesarean delivery should rarely be necessary but should be considered if the fetus is at a gestation where delivery may lead to a viable infant and the fetus demonstrates ongoing distress despite aggressive maternal resuscitation
11 If blood pressure remains below 90/60 mmHg, begin
admin-istration of intravenous vasopressors Patients who require this level of care or who have ongoing airway concerns after the initial treatment should be transferred promptly to an intensive care unit Epinephrine can be given intravenously at a dose of 0.1 mg (1.0 mL of a 1 : 10 000 (1 mg/10 mL) solution) over several minutes and repeated every 5 – 10 minutes as needed This medication should be given with the patient on a cardiac monitor and ideally through a central line to decrease the risk of tissue damage from extravasation It can also be administered via an endotracheal tube (0.3 – 0.5 mg (3 – 5 mL of a 1 : 10 000 dilution)) if intravenous access is compromised If continued boluses of epinephrine are needed, a continuous infusion can be given: 1 mL of 1 : 1000 dilu-tion of epinephrine should be placed in 500 mL of normal saline and given at a rate of 1 – 4 micrograms per minute (0.05 – 0.1 µ g/ kg/min) and titrated to response Some concern does exist about the effects of epinephrine use in pregnancy because of both a weak association with ventral hernias when used in the fi rst tri-mester and its possible adverse effects on uterine blood fl ow Because of these concerns, some authors have suggested a trial of terbutaline subcutaneously (typically 0.25 mg subcutaneously) as
an alternative to epinephrine in pregnancy However, the data supporting the effi cacy of terbutaline in the treatment of anaphy-laxis are minimal and therefore most experts would recommend the use of epinephrine as a fi rst - line agent in treating anaphylaxis
in pregnancy given the life - threatening nature of the condition Studies in non - pregnant patients have shown that fatality rates are highest in patients in whom treatment with epinephrine is delayed [24 – 26] Other vasopressors that may be helpful in patients with anaphylactic shock when epinephrine has failed include dopamine (5 – 20 µ g/kg/min), norepinephrine (0.5 – 30 µ g/ min) or phenylephrine (30 – 180 µ g/min) Vasopressin 10 – 40 IU
IV has also been reported to be of assistance in refractory cases [15]
Management of the p atient a fter the a cute e pisode
of a naphylaxis
Management after an anaphylactic reaction typically involves ongoing vasopressor support until the blood pressure no longer requires it The acute symptoms and danger should usually have begun to resolve within 6 hours of the onset of the event Steroids and antihistamines are typically continued for 72 – 96 hours and then can be discontinued
Once the patient has been stabilized, a careful history should
be taken to identify all exposures in the hours prior to the reac-tion The patient should also be asked about any exertion prior
to the onset of the event, including sexual activity
Laboratory fi ndings that may be drawn as soon as possible after the event to help confi rm the diagnosis of an anaphylactoid
to epinephrine may be dampened, and the patient may be given
glucagon 1 mg intravenously as an alternate if epinephrine
does not produce the desired effect This dose of glucagon
may be repeated as needed every 1 minute until a total of 5 mg
has been given Glucagon has chronotropic and inotropic
effects on the heart that are not mediated through the β -
receptors [21]
3 Ensure the patient has two large - bore (14 – 16 G) peripheral
intravenous lines in place for fl uid and medication
administra-tion and prepare to obtain central venous access Typically
5 – 10 mL/kg of normal saline or Ringer ’ s lactate should be
admin-istered in the fi rst minutes of treatment although this will warrant
monitoring in patients with renal or cardiac disease [22] Pregnant
women have a predisposition to pulmonary edema that also
war-rants extra attention to overall fl uid balance Use fl uid boluses to
maintain blood pressure above 90/60 mmHg, especially if the
patient has not responded to epinephrine Anaphylaxis is often
associated with sudden and massive extravasation of fl uid into
the third space and patients may have profound intravascular
volume depletion In severe cases of anaphylaxis up to 7 L of fl uid
may need to be given to support blood pressure [23]
4 Remove the inciting antigen when possible Consider use of a
tourniquet to obstruct venous return from a limb that was
exposed to the probable precipitating antigen when appropriate
The tourniquet should be released every 15 minutes to prevent
ischemia
5 Place the patient in the reverse Trendelenburg position lying
on her left side to improve venous return
6 Initiate cardiac and frequent blood pressure monitoring
Initially, these parameters should be measured no less frequently
than every 5 minutes
7 Administer an intravenous histamine H 1 blocker (typically
diphenhydramine 25 mg IV over 3 – min) and histamine H 2
blocker (typically ranitidine 1 mg/kg IV over 10 – 15 min)
8 Administer intravenous steroids (typically hydrocortisone
100 mg every 6 hours or methylprednisolone 1 – 2 mg/kg per day)
These agents do not treat the acute symptoms of anaphylaxis but
may have a role in preventing late - phase reactions Because there
are rare reports of biphasic reactions occurring as late as 72 hours
after the initial exposure, many experts would continue steroids
at a dose equivalent to this dose for a total of 4 days (typically
prednisolone 50 mg daily)
9 If wheezing is present, administration of bronchodilators such
as albuterol (2.5 – 5 mg in 3 mL saline via nebulizer) should be
considered
10 Place a fetal monitoring device on the patient Several
anec-dotal reports of fetal injury or death in the setting of anaphylaxis
despite prompt maternal blood pressure control have suggested
that maternal blood pressure in anaphylaxis may be maintained
at the expense of uterine (or splanchnic) fl ow Evidence of fetal
distress should be addressed by improving oxygen delivery
through increasing oxygen administration, changing position of
the mother, and increasing fl uid administration If there is
ongoing evidence of maternal or fetal compromise, then
Trang 4Table 42.5 The differential diagnosis of anaphylaxis
Vasovagal response Should generally be associated with bradycardia and pallor and no fl ushing, rash, itch, hives or wheezing
Anxiety Hives and hypotension should not be present
Amniotic fl uid embolism (AFE) Initial presentation may be similar but AFE should not be associated with rash, itch or hives and is generally associated with
DIC Pulmonary edema in pregnancy Pulmonary edema can occur in pregnancy in association with fl uid overload, pre - eclampsia, infection or tocolytic
administration Onset will generally be gradual over several hours and not be associated with rash or hypotension Medication effects other than allergies Vancomycin, nicotinic acid, ACE inhibitors and alcohol can all cause fl ushing in susceptible individuals
Pulmonary embolism or any other cause
of acute respiratory failure
Can cause sudden - onset tachycardia, respiratory failure (with or without wheeze) and hypotension but should not cause rash
or itch Scromboid poisoning [68] Histamine - producing bacteria in fi sh such as spoiled tuna, mackerel and skipjack can cause gastrointestinal symptoms,
fl ushing, headache, dizziness but not usually hives This can be diffi cult to distinguish from anaphylaxis but is suggested by
a clustering of cases related to a particular meal/restaurant Vocal cord dysfunction Young women can present with acute inspiratory stridor related to paradoxic vocal cord motion This is more often seen in
women with a preceding diagnosis of asthma Stridor in this setting is typically only inspiratory which distinguishes it from the stridor seen with true airway edema which is typically both inspiratory and expiratory Hypotension, uvular edema, rash should not be seen in these patients
Acute myocardial infarction, congestive
heart failure
Less likely in this patient population but it is reasonable to obtain EKG, CXR and serial cardiac enzymes (troponin) in patients presenting with probable anaphylaxis If concern exists for a cardiac cause, an echocardiogram should be ordered acutely Miscellaneous Flushing syndromes (carcinoid syndrome, medullary carcinoma of the thyroid, perimenopausal symptoms) pheochromocytoma
Hemorrhagic/hypovolemic shock Septic shock
Epiglottitis Status asthmaticus Foreign body aspiration Panic attacks Systemic mastocytosis
response include serum levels of histamine and tryptase, both of
which will be elevated in anaphylaxis [18,27] Histamine will be
elevated for up to 60 minutes and tryptase for up to 6 hours
Typically, several specimens should be obtained in the 6 - hour
period following the onset of anpahylaxis so that a pattern of
elevation followed by decline may be observed The assay for
histamine can be falsely elevated from basophil activation of
clotted blood in the test tube and has a very short half - life that
limits its clinical use at many instructions Therefore a 24 - hour
urine sample looking for the histamine metabolite N - methyl
his-tamine may be a useful additional test to consider Assays showing
elevated levels of histamine or tryptase and its metabolites are
indicative of anaphylaxis; however a normal assay does not
pre-clude the diagnosis
All patients who have had an anaphylactic event should be
educated as to the seriousness of their condition and its
propen-sity to recur Patients should be provided a prescription for an
epinephrine autoinjector and educated as to its use The
impor-tance of this should be emphasized to the patient, as many
patients will not fulfi l their prescription or be willing to self - inject
unless they clearly understand the nature of their condition [15,28,29] Preloaded auto - injectors marketed in the US include EpiPen © and Twinject © Twinject © has the advantage of offering two - dose devices that may be necessary to treat more severe reac-tions in adults
Ideally, all patients who have had an episode of life - threatening anaphylaxis should be referred to an allergist for care and coun-seling regarding their condition Allergists will often do skin and serum IgE tests to confi rm or identify inciting antigens and con-sider the need for immunotherapy Skin testing should only be done by allergists and should be delayed for at least 4 weeks so that mast cells in the skin have a chance to replenish their infl am-matory mediators Serum testing can, however, be done imme-diately [15]
Patients who have had anaphylaxis should be told to wear a MedicAlert bracelet or a similar device to avoid inadvertent expo-sure to a precipitating allergen Patient with anaphylaxis who have been on a β - blocker should generally be switched to an alternate medication if at all possible because the β - blocker may decrease the effi cacy of epinephrine given in a subsequent attack
Trang 513 Brazil E , MacNamara AF “ Not so immediate ” hypersensitivity – the
danger of biphasic anaphylactic reactions J Accid Emerg Med 1998 ;
15 : 252
14 Douglas DM , Sukenick E , Andrade P , Brown JS Biphasic systemic
anaphylaxis: an inpatient and outpatient study J Allergy Clin Immunol
1994 ; 93 : 977
15 Yocum MW , Khan DA Assessment of patients who have experienced
anaphylaxis: a 3 - year survey Mayo Clin Proc 1994 ; 69 : 16
16 Sampson HA , Munoz - Furlong A , Campbell RL , et al Second sympo-sium on the defi nition and management of anaphylaxis: summary report – Second National Institute of Allergy and Infectious Disease/
Food Allergy and Anaphylaxis Network symposium J Allergy Clin
Immunol 2006 ; 117 : 391
17 Atkinson TP , Kaliner MA Anaphylaxis Med Clin North Am 1992 ; 76 :
841
18 Fisher M Treatment of acute anaphylaxis BMJ 1995 ; 311 : 731
19 Zaloga GP , Delacey W , Holmboe E , Chernow B Glucagon reversal of
hypotension in a case of anaphylactoid shock Ann Intern Med 1986 ;
105 : 65
20 Lieberman P , Kemp SF , Oppenheimer J , et al The diagnosis and
management of anaphylaxis: an updated practice parameter J Allergy
Clin Immunol 2005 ; 115 : S483
21 Fisher MM Clinical observations on the pathophysiology and
treat-ment of anaphylactic cardiovascular collapse Anaesth Intens Care
1986 ; 14 : 17
22 Clark S , Long AA , Gaeta TJ , Camargo CA Jr Multicenter study of
emergency department visits for insect sting allergies J Allergy Clin
Immunol 2005 ; 116 : 643
23 Sampson HA , Mendelson L , Rosen JP Fatal and near - fatal
anaphy-lactic reactions to food in children and adolescents N Engl J Med
1992 ; 327 : 380
24 Clark S , Bock SA , Gaeta TJ , et al Multicenter study of emergency
department visits for food allergies J Allergy Clin Immunol 2004 ; 113 :
347
25 Kill C , Wranze E , Wulf H Successful treatment of severe anaphylactic
shock with vasopressin Two case reports Int Arch Allergy Immunol
2004 ; 134 : 260
26 Bochner BS , Lichtenstein LM Anaphylaxis N Engl J Med 1991 ; 324 :
1785
27 Fisher M Treatment of acute anaphylaxis BMJ 1995 ; 311 : 731
28 Weiss ME , Adkinson NF Immediate hypersensitivity reactions to
penicillin and related antibiotics Clin Allergy 1998 ; 18 : 515
29 Riedl MA , Casillas AM Adverse drug reactions: types and treatment
options Am Fam Physician 2003 ; 68 ( 9 ): 1781
30 Pumphrey R Anaphylaxis: can we tell who is at risk of a fatal reaction?
Curr Opin Allergy Clin Immunol 2004 ; 4 : 285
31 Barnard JH Studies of 400 Hymenoptera sting deaths in the United
States J Allergy Clin Immunol 1973 ; 52 : 259
32 Novembre E , Cianferoni A , Bernardini R , et al Anaphylaxis in
chil-dren: clinical and allergologic features Pediatrics 1998 ; 101 : E 8
33 Porsche R , Brenner ZR Allergy to protamine sulfate Heart Lung
1999 ; 28 : 418
34 Ditto AM , Harris KE , Krasnick J , et al Idiopathic anaphylaxis: a series
of 335 cases Ann Allergy Asthma Immunol 1996 ; 77 : 285
35 Kemp SF , Lockey RF , Wolf BL , Lieberman P Anaphylaxis: review of
266 cases Arch Intern Med 1995 ; 155 : 1749
36 Horan RF , Sheffer AL Exercise - induced anaphylaxis Immunol
Allergy Clin North Am 1992 ; 3 : 559
37 Ewan PW Anaphylaxis BMJ 1998 ; 316 : 1442
Differential d iagnosis
The differential diagnosis of anaphylaxis is broad and is
sum-marized in Table 42.5
Conclusions
Anaphylaxis and anaphylactoid reactions are common in
hospi-talized patients They are a medical emergency which warrant
prompt administration of oxygen, intravenous fl uids,
epineph-rine and removal of the inciting agent when possible Management
in pregnancy is unchanged from that for non - pregnant patients
The life - saving nature of epinephrine in this setting justifi es its
use even if there are concerns about its effects in general on
pla-cental fl ow Patients who have had anaphylactic responses should
be observed for at least 8 hours and placed on steroids because
of a risk of a biphasic response in 48 – 72 hours With prompt
identifi cation and management, both mother and fetus can
expect to do well
References
1 Sampson HA , Munoz - Furlong A , Bock SA , et al Symposium on the
defi nition and management of anaphylaxis: summary report J Allergy
Clin Immunol 2005 ; 115 : 584
2 Winbery SL , Lieberman PL Anaphylaxis Immunol Allergy Clin North
Am 1995 ; 15 : 447
3 DeJarnatt AC , Grant JA Basic mechanisms of anaphylaxis and
anaphylactoid reactions Immunol Allergy Clin North Am 1992 ; 12 :
501
4 Lieberman P , Camargo CA Jr , Bohlke K , et al Epidemiology of
ana-phylaxis: fi ndings of the American College of Allergy, Asthma and
Immunology Epidemiology of Anaphylaxis Working Group Ann
Allergy Asthma Immunol 2006 ; 97 : 596
5 International Collaborative Study of Severe Anaphylaxis An
epide-miologic study of severe anaphylactic and anaphylactoid reactions
among hospital patients: methods and overall risks Epidemiology
1998 ; 9 : 141
6 Thong BY , Cheng YK , Leong , KP et al Anaphylaxis in adults referred
to a clinical immunology/allergy centre in Singapore Singapore Med
J 2005 ; 46 : 529
7 Webb LM , Lieberman P Anaphylaxis: a review of 601 cases Ann
Allergy Asthma Immunol 2006 ; 97 : 39
8 Fisher MM , Doig GS Prevention of anaphylactic reactions to
anaes-thetic drugs Drug Saf 2004 ; 27 : 393
9 Reisman RE Insect sting anaphylaxis Immunol Allergy Clin North Am
1992 ; 12 : 535
10 Pumphrey R Anaphylaxis: can we tell who is at risk of a fatal reaction?
Curr Opin Allergy Clin Immunol 2004 ; 4 : 285
11 Stark BJ , Sullivan TJ Biphasic and protracted anaphylaxis J Allergy
Clin Immunol 1986 ; 78 : 76
12 Lieberman P Biphasic anaphylactic reactions Ann Allergy Asthma
Immunol 2005 ; 95 : 217
Trang 653 Slater RM , Bowles BJM , Pumphrey RSH Anaphylactoid reaction to
oxytocin in pregnancy Anesthesia 1985 ; 40 : 655
54 Hofmann H , Goerz G , Plewig G Anaphylactic shock from
chlorobu-tanol - preserved oxytocin Contact Derm 1986 ; 15 : 241
55 Morriss WW , Lavies NG , Anderson SK , Southgate HJ Acute respira-tory distress during cesarean section under surgery from spina bifi da
Anesthesiology 1990 ; 73 : 556
56 Kawarabayashi T , Narisawa Y , Nakamura K , Sugimori H , Oda M , Taniguchi Y Anaphylactoid reaction to oxytocin during cesarean
section Gynecol Obstet Invest 1988 ; 25 ( 4 ): 277
57 Maycock EJ , Russell WC Anaphylactoid reaction to syntocinon
Anaesth Intens Care 1993 ; 21 : 211
58 Cohn JR , Cohn JB , Fellin F , Cantor R Systemic anaphylaxis from low
dose methotrexate Ann Allergy 1993 ; 70 ( 5 ): 384
59 Barbier P , Jonville AP , Autret E Fetal risks with dextrans during
delivery Drug Saf 1992 ; 7 : 71
60 Ring J Anaphylactoid reactions to intravenous solutions used for
volume substitution Clin Rev Allergy 1991 ; 9 : 397
61 Berg EM , Fasting S , Sellevoid OFM Serious complications with dextran - 70 despite hapten prophylaxis Is it best avoided prior to
delivery? Anesthesia 1991 ; 46 : 1033
62 Paull J A prospective study of dextran - induced anaphylactoid
reac-tions in 5475 patients Anaesth Intens Care 1987 ; 15 : 163
63 Smith HS Delivery as a cause of exercise - induced anaphylactoid
reac-tion: case report Br J Obstet Gynaecol 1985 ; 92 ; 1196
64 Ahmed SM , Aw TC , Adisesh A Toxicological and immunological
aspects of occupational latex allergy Toxicol Rev 2004 ; 23 : 123
65 Allmers H , Schmengler J , John SM Decreasing incidence of occupational contact urticaria caused by natural rubber latex
allergy in German health care workers J Allergy Clin Immunol 2004 ;
114 : 347
66 Edde RR , Burtis BB Lung injury in anaphylactoid shock Chest 1973 ;
63 : 637
67 Fisher MM Clinical observations on the pathophysiology and
treat-ment of anaphylactic cardiovascular collapse Anaesth Intens Care
1986 ; 14 : 17
68 Lehane L Update on histamine fi sh poisoning Med J Aust 2000 ; 173 :
149
38 Tejedor A , Sastre DJ , Sanchez - Hernandez JJ , et al Idiopathic
anaphy-laxis: a descriptive study of 81 patients in Spain Ann Allergy Asthma
Immunol 2002 ; 88 : 313
39 Dykewicz MS Cough and angioedema from angiotensin - converting
enzyme inhibitors: new insights into mechanisms and management
Curr Opin Allergy Clin Immunol 2004 ; 4 : 267
40 Idsoe O , Guthe T , Willcox RR , de Weck AL Nature and extent of
penicillin side - reactions, with particular reference to fatalities from
anaphylactic shock Bull World Health Organ 1968 ; 38 ( 2 ): 159
41 Brown AF , McKinnon D , Chu K Emergency department
anaphy-laxis: a review of 142 patients in a single year J Allergy Clin Immunol
2001 ; 108 : 861
42 Stevenson DD Approach to the patient with a history of adverse
reactions to aspirin or NSAIDs: diagnosis and treatment Allergy
Asthma Proc 2000 ; 21 : 25
43 Brown SG , Blackman KE , Stenlake V , Heddle RJ Insect sting
anaphy-laxis; prospective evaluation of treatment with intravenous adrenaline
and volume resuscitation Emerg Med J 2004 ; 21 : 149
44 Clark S , Bock SA , Gaeta TJ , et al Multicenter study of emergency
department visits for food allergies J Allergy Clin Immunol 2004 ; 113 :
347
45 Bock SA , Munoz - Furlong A , Sampson HA Fatalities due to
anaphy-lactic reactions to foods J Allergy Clin Immunol 2001 ; 107 : 191
46 Novembre E , Cianferoni A , Bernardini R , et al Anaphylaxis in
chil-dren: clinical and allergologic features Pediatrics 1998 ; 101 : E8
47 Bush WH Treatment of systemic reactions to contrast media Urology
1990 ; 35 : 145
48 Lieberman P Anaphylactoid reactions to radiocontrast material
Immunol Allergy Clin North Am 1992 ; 12 : 649
49 Bush WH , Swanson DP Acute reactions to intravascular contrast
media: types, risk factors, recognition, and specifi c treatment AJR
1991 ; 157 : 1153
50 Lieberman P , Kemp SF , Oppenheimer J , et al The diagnosis and
management of anaphylaxis: an updated practice parameter J Allergy
Clin Immunol 2005 ; 115 : S483
51 Browne IM , Birnbach DJ A pregnant woman with previous
anaphy-lactic reaction to local anesthetics: a case report Am J Obstet Gynecol
2001 ; 185 ( 5 ): 1253
52 Tarlo SM Natural rubber latex allergy and asthma Curr Opin Pulm
Med 2001 ; 7 : 27
Trang 7Critical Care Obstetrics, 5th edition Edited by M Belfort, G Saade,
M Foley, J Phelan and G Dildy © 2010 Blackwell Publishing Ltd.
43 Fetal Considerations in the Critically Ill
Gravida
Jeffrey P Phelan 1 & Shailen S Shah 2
1 Department of Obstetrics and Gynecology, Citrus Valley Medical Center, West Covina and Clinical Research, Childbirth
Injury Prevention Foundation, City of Industry, Pasadena, CA, USA
2 Maternal - Fetal Medicine, Virtua Health, Voorhees, NJ and Thomas Jefferson University Hospital, Philadelphia, PA, USA
Introduction
Unlike any other medical or surgical specialty, obstetrics deals
with the simultaneous management of two – and sometimes
more – individuals Under all circumstances, the obstetrician must
delicately balance the impact of each treatment decision on the
pregnant woman and her fetus, seeking, when possible, to
mini-mize the risks of harm to each person Throughout this text, the
primary focus has been on the critically ill obstetric patient and,
secondarily, her fetus Although the fetal effects of those illnesses
were reviewed in part, the goal of this chapter is to highlight,
especially for the non - obstetric clinician, the important clinical
fetal considerations encountered when caring for these
compli-cated pregnancies To achieve that objective, this chapter reviews:
(i) current techniques for assessing fetal well - being; (ii) fetal
assessment in the intensive care unit; (iii) fetal considerations in
several maternal medical and surgical conditions; (iv) the
con-temporary management of the gravida who is brain - dead or in a
persistent vegetative state; and (v) the role of perimortem
cesar-ean delivery in modern obstetrics
Detection of f etal d istress in the c ritically i ll
o bstetric p atient
More than four decades ago, Hon and Quilligan [1]
demon-strated the relationship between certain fetal heart rate (FHR)
patterns and fetal condition by using continuous electronic FHR
monitoring in laboring patients Since then, continuous
elec-tronic FHR monitoring has become a universally accepted
method of assessing fetal well - being during labor [2,3] with the
goal of permitting the clinician to identify those fetuses at a
greater likelihood of intrapartum fetal death [4] and to intervene
when certain FHR abnormalities are present
In addition to the intrapartum assessment of fetal well - being, the fetal monitor has been used to assess fetal health before labor [5] and attempt to identify those fetuses at risk for intrauterine death and convert those fetuses so identifi ed from outpatient to inpatient care Once in labor and delivery, continuous fetal moni-toring is used to determine whether continued expectant man-agement or delivery by induction of labor or cesarean is the next form of intervention It is this area of fetal monitoring, antepar-tum rather than intraparantepar-tum fetal assessment that is used more frequently in the arena of the critically ill gravida Regardless, the focus of this chapter will be on applications of fetal monitoring
to assess fetal status both in the intensive care unit setting and intrapartum during labor
Although the presence of a reassuring FHR tracing is virtually always associated with a well - perfused and oxygenated fetus [5,6] , an “ abnormal tracing ” is not necessarily predictive of an adverse fetal outcome While it was anticipated that the detec-tion of abnormal FHR patterns during labor and expeditious delivery of such fetuses would impact the subsequent develop-ment of cerebral palsy, this expectation has not been realized because the number of fetuses injured during labor was highly overestimated and the number of fetuses injured before labor were highly underestimated [7] However, with the ubiquitous use of electronic FHR monitoring during labor and a rise in the cesarean delivery rate for the past two decades from 5% to over 25%, a decline in the rate of asphyxia - induced cerebral palsy among singleton term infants has been observed [8,9] For example, Smith and associates [9] documented a 56% decline over two decades in the incidence of hypoxic ischemic encepha-lopathy (HIE) among singleton term infants During this time, the incidence of HIE dropped from 1 per 8000 to 1 per 12 500 births
While the specifi c entity of cerebral palsy is, in most cases, unrelated to the events associated with labor and delivery, it is more often related to prenatal developmental events, infection,
or complications of prematurity Nevertheless, the basic physio-logic observations relating to specifi c FHR patterns remain, for the most part, valid The critically ill mother will necessarily shunt blood from the splanchnic bed (including the uterus) in response
Trang 8hypoxic event, such as those depicted in Table 43.1 , the FHR suddenly drops and remains at a lower level unresponsive to remedial measures and/or terbutaline therapy In the critical care setting, a sudden, rapid, and sustained deterioration of the FHR
or a prolonged FHR deceleration may arise from a partial or complete abruption in cases of markedly elevated maternal blood pressures or an aggressive lowering of maternal BP with antihy-pertensive agents [17] This type of FHR pattern may also herald
a sudden maternal hypoxic event, such as amniotic fl uid embolus syndrome [18] , acute respiratory insuffi ciency, or an eclamptic seizure [17,19] Prolonged FHR decelerations have also been associated with maternal operative procedures such as cardiopul-monary bypass with inadequate maternal fl ow rates [20,21] , and brain surgery during hypothermia [22]
In a patient with a prior normal baseline FHR, the abrupt occurrence and persistence of a fetal heart rate of less than
110 bpm for an extended period of time unresponsive to remedial measures and/or terbutaline therapy constitutes an obstetric emergency Under these circumstances, and assuming the preg-nant woman is hemodynamically and clinically stable and the fetus is potentially viable, these patients should be managed as if the fetus has had a cardiac arrest and be delivered as rapidly as it
is technically feasible for the level of the institution
Tachycardia
Fetal tachycardia is defi ned as a baseline FHR of 160 bpm or greater Most commonly, this type of baseline FHR abnormality can be associated with prematurity, maternal pyrexia, or chorio-amnionitis In addition, betamimetic administration, hyperthy-roidism, or fetal cardiac arrhythmias may also be responsible The clinical observation of a FHR tachycardia, in and of itself, is prob-ably not an ominous fi nding but probprob-ably refl ects a normal physi-ologic adjustment to an underlying maternal or fetal condition Although operative intervention is rarely required, a search for the underlying basis for the tachycardia and a reanalysis of the admission FHR pattern may be helpful
For example , the patient with a previously reactive FHR pattern with a normal baseline rate (Figure 43.1 ) who develops the Hon pattern of intrapartum asphyxia or ischemia [11] which is char-acterized by a substantial rise in the baseline rate often to a level
of tachycardia (Figures 43.2 & 43.3 ) in association with an inabil-ity to accelerate or non - reactivinabil-ity, repetitive FHR decelerations,
to shock Because of this and the fact that the fetus operates on
the steep portion of the oxyhemoglobin dissociation curve, any
degree of maternal hypoxia or hypoperfusion may fi rst be
mani-fested as an abnormality of the FHR In this sense, the late
second - and third - trimester fetus serves as a physiologic oximeter
and cardiac output computer Observation of FHR changes, thus,
may assist or alert the clinician to subtle degrees of physiologic
instability, which would be unimportant in a non - pregnant adult
but may have potentially detrimental effects to the fetus [10]
The next few pages present an overview of FHR patterns
per-tinent to the critically ill gravida Interpretations of FHR patterns,
like all diagnostic tests, depend on the index population, and
consequently, certain of these observations may not be applicable
to the laboring but otherwise well mother For a more detailed
description of antepartum and intrapartum FHR tracings
associ-ated with fetal brain injury the reader is referred to the classic
descriptions by Phelan and Ahn [11] , Phelan and Kim [12] ,
Phelan [13] and Phelan and associates [14]
Baseline f etal h eart r ate
The baseline FHR is the intrinsic heart rate of the fetus A normal
baseline FHR is between 110 beats per minute (bpm) and
160 bpm A baseline FHR below 110 bpm is termed a bradycardia
and 160 bpm or higher is considered a tachycardia
Bradycardia
Bradycardia is defi ned as the intrinsic heart rate of the fetus of
less than 110 bpm, as opposed to a sudden, rapid, and sustained
deterioration of the FHR from a previously normal or tachycardic
rate that lasts until delivery As such, a FHR bradycardia may be
associated with an underlying congenital fetal abnormality, such
as a structural defect of the fetal heart In addition, congenital
bradyarrhythmias may involve fetal heart block secondary to a
prior maternal infection, a structural defect of the fetal heart, or
systemic lupus erythematosus with anti - Ro/SSA antibodies [15]
In these circumstances, the FHR bradycardia is not usually a
threat to the fetus But, alternative methods of fetal assessment,
such as the fetal biophysical profi le (FBP) [16] , are necessary in
this select group of patients to assure fetal well - being before
and during labor Given the inherent diffi culties in providing
continuous fetal monitoring and assuring fetal well - being in
fetuses with a bradyarrhythmia, cesarean delivery may well
rep-resent the preferred route of delivery for these patients Obviously,
the decision to proceed directly to a cesarean will depend on the
overall clinical circumstances and appropriate patient informed
consent
Prolonged f etal h eart r ate d eceleration or a s udden,
r apid and s ustained d eterioration of the f etal h eart r ate
Prolonged FHR deceleration is distinctly different from a
brady-cardia In the former, the fetal monitor strip is typically reactive
with a normal or tachycardic baseline rate; but, due to a sentinel
Table 43.1 Sentinel hypoxic events associated with a sudden, rapid, and
sustained deterioration of the fetal heart rate that was unresponsive to remedial measures and/or terbutaline lasting until delivery from a previously reactive fetal heart rate
Umbilical cord prolapse Uterine rupture Placental abruption Maternal arrest, e.g AFE syndrome Fetal exsanguination
AFE, amniotic fl uid embolus
Trang 9Figure 43.2 Some time later, the fetus exhibits an FHR tachycardia around 160 bpm, repetitive FHR decelerations and non - reactivity
Trang 10Fetal h eart r ate v ariability
Fetal heart rate variability (FHRV) is defi ned as the beat - to - beat variation in the FHR resulting from the continuous interaction
of the parasympathetic and sympathetic nervous systems on the fetal heart For clinical purposes, normal FHRV may be viewed
as a beat - to - beat variation of the FHR of 6 bpm or more above and below the baseline FHR
Currently, two approaches, the National Institutes of Child Health and Human Development (NICHD) [25] and the Childbirth Injury Prevention Foundation (CIPF) [11,14] are available to classify FHRV The NICHD and CIPF approaches subclassify FHRV into 4 and 2 categories, respectively This means that the CIPF classifi cation incorporates the NICHD cri-teria of undetectable (absent FHRV) and minimal (more than
and usually a loss of FHR variability, fl ags fetal brain injury [23]
and the fetus is at risk for hypoxic ischemic brain injury [11 – 13]
In this clinical setting, assessment of the usual causes of FHR
tachycardia should be undertaken If the mother does not have a
fever to account for the change in fetal status, assessment of fetal
acid – base status with scalp or acoustic stimulation [6,12] or
delivery as soon as it is practical, in keeping with the capability
of the hospital, should be considered If the gravida has a fever,
she should be cultured, and treated with antibiotics and
anti-pyretics If the FHR pattern does not return to normal (i.e the
same FHR pattern the fetus had on admission – normal baseline
FHR and reactive) within approximately an hour of the initiation
of medical therapy and regardless of whether the fetal heart rate
variability is average [11 – 13,24] , the patient should be delivered
as expeditiously as possible
Figure 43.3 Later in the labor, the baseline FHR reaches 180 bpm and continues to exhibit repetitive FHR decelerations, non - reactivity, and diminished variability The
fetus was born with spastic quadriplegia due to hypoxic ischemic encephalopathy