Critical Care Obstetrics part 62 docx

Anaphylactic Shock in Pregnancy 599 Class 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 Chapter 42 600 Table 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] . Affected system Symptoms/signs Comments 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 Anaphylactic Shock in Pregnancy 601 pressor 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 se veral 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 – 5 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 vaso- Chapter 42 602 Table 42.5 The differential diagnosis of anaphylaxis. Alternative diagnoses Comments 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. Anaphylactic Shock in Pregnancy 603 13 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 . Chapter 42 604 53 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 . 605 Critical 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 intrapartum 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 Chapter 43 606 hypoxic 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 probably 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 - reactivity, 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. 607 Figure 43.1 Admission FHR of this term pregnancy with spontaneously ruptured membranes exhibits a baseline rate around 120 bpm and numerous FHR accelerations or a reactive FHR pattern. Figure 43.2 Some time later, the fetus exhibits an FHR tachycardia around 160 bpm, repetitive FHR decelerations and non - reactivity. Chapter 43 608 Fetal 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. . 27 . 605 Critical 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. 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. 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