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17. Gombar S, Ahuja V, Jafra A. A retrospective analysis of obstetric patient’s outcome in intensive care unit of a tertiary care center. J Anaesthesiol Clin Pharmacol. 2014;30:502– 7.

18. Strasser SM, Kwee A, Visser GH. Spontaneous tachysystole as sign of serious perinatal conditions. J Matern Fetal Neonatal Med. 2010;23:736– 41.

19. Centre for Maternal and Child Enquiries (CMACE). Saving mothers’ lives: reviewing maternal deaths to make motherhood safer:2006– 08. e Eighth Report on Condential Enquiries into Maternal Deaths in the United Kingdom. BJOG. 2011;118:1– 203.

20. Mhyre JM, D’Oria R, Hameed AB, etal. e maternal early warning criteria:a proposal from the national partnership for maternal safety. Obstet Gynecol. 2014;124:782– 6.

21. D’Alton ME, Main EK, Menard MK, Levy BS. e national partnership for maternal safety. Obstet Gynecol. 2014;123:973– 7.

22. Ngan Kee WD. Uteroplacental blood ow. In: Chestnut DH, ed. Chestnut’s Obstetric Anesthesia: Principles and Practice. 5th ed. Philadelphia, PA:Elsevier; 2014:43– 4.

23. Boissier F, Vermersch C, Spagnolo S, Bruneel F, Brun- Buisson C, de Prost N. Septic shock complicating Plasmodium falciparum malaria in a pregnant patient with low parasitemia. Med Mal Infect. 2014;44:539– 40.

24. Ngan Kee WD, Lee SW, Ng FF, Tan PE, Khaw KS. Randomized double- blinded comparison of norepinephrine and phenylephrine for maintenance of blood pressure during spinal anesthesia for cesarean delivery. Anesthesiology. 2015;122:736– 45.

25. Pacheco LD, Saade GR, Hankins GD. Severe sepsis during pregnancy. Clin Obstet Gynecol. 2014;57:827– 34.

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49.

SEVERE PREECLAMPSIA

Uma Sasso and Emily McQuaid- Hanson

CLINICALCASE

A 32- year- old G3P2 at 36 weeks gestation presents to the labor and delivery unit for evaluation aer two blood pressure readings of 170/ 105 were observed at her scheduled obstetric clinic appointment. e patient also notes mild

TABLE49.1 CLASSIFICATION OFHYPERTENSIVE DISORDERS

OFPREGNANCY

Category Denition

Preeclampsiaeclampsia

New onset of hypertension after 20 weeks of gestation with proteinuria or any of the severe features of preeclampsia

lower extremity edema and intermittent headache for the past three days. Past medical history is notable for morbid obesity and poorly controlled asthma.

INTRODUCTION

Severe preeclampsia is part of a spectrum of hypertensive disorders of pregnancy. It is dened as new- onset hypertension aer 20 weeks of gestation in conjunction with any

Chronic hypertension Hyper tension of any cause that predates

pregnancy or is diagnosed prior to 20 weeks gestation

Chronic hypertension with superimposed preeclampsia

Gestational hypertension

Chronic hypertension in association with preeclampsia

BP elevation after 20 weeks of gestation in the absence of proteinuria or any of the severe features of preeclampsia that resolves following

delivery

severe feature, which include thrombocytopenia, liver dysfunction, renal insuciency, pulmonary edema, new- onset neurologic symptoms, or severe- range blood pressure (systolic ≥ 160 or diastolic ≥ 110).

1,2

Recent changes in nomenclature and diagnostic criteria have changed the designation of “mild preeclampsia” to “preeclampsia without severe features.” e diagnosis of preeclampsia with severe features is no longer dependent on the presence of proteinuria, and intrauterine fetal growth restriction was eliminated as a diagnostic criterion. ese changes are intended to emphasize the progressive nature of the disorder, the need for frequent reassessment, and to avoid delays in diagnosis and treatment.

2,3

Classications of hypertensive disorders of pregnancy and diagnostic criteria for severe preeclampsia are further detailed in Table 49.1 and Table49.2.

developed countries.3 ere has been a 30% increase in the incidence of severe preeclampsia in the United States over the past decade.4 e reason for this alarming increase is likely multifactorial, with contributions from an elevation in average maternal age, expanded use of assisted reproductive techniques, and increased prevalence of maternal comorbidities such as obesity, hypertension, and diabetes. Risk factors for preeclampsia are numerous and can be categorized as demographic, genetic conditions, medical conditions, obstetrical conditions, behavioral, and partner related (Table 49.3). Identifying and clarifying risk factors is an area of active research, especially with regard to genetic predisposition.

EPIDEMIOLOGY AND RISK FACTORS

Preeclampsia complicates 3%– 4% of pregnancies in the United States, and is a leading cause of preterm delivery and peripartum intensive care unit (ICU) admissions in

PATHOPHYSIOLOGY

Preeclampsia is a disease of endothelial dysfunction and as such impacts every organ system. While the pathogenesis of preeclampsia is not fully understood, the leading hypotheses

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TABLE49.2 DIAGNOSTIC FEATURES OFPREECLAMPSIA

resistant to vasoactive stimuli, ensuring adequate blood ow to placenta and fetus across a broad spectrum of physiologic

Preeclampsia without severe features

Severe preeclampsia

SOURCE:Adapted with permissions from Bateman B, Polley L.Hypertensive disorders.

In:Chestnut D, ed. Chestnut’s Obstetric Anesthesia, Principles and Practice. 5th ed.

Saunders/ Elsevier; 2014:825– 59.

center around the placenta as the root cause of the disorder, as evidenced by the fact that delivery of the placenta leads to resolution and that the disorder can be present in the absence of a fetus (as in molar pregnancy).3 In healthy pregnancy, remodeling of placental vascular smooth muscle facilitates formation of a low- resistance vascular bed that is

• New onset of BP ≥ 140/ 90 after 20 weeks

gestation, plus EITHER proteinuria OR any severe feature

• Proteinuria (≥ 300 mg/ 24h, protein- creatinine

ratio ≥ 0.3, or 1 + on urine dipstick)

Preeclampsia plus any one of the following features:

• BP ≥ 160/ 110 (measured on 2 occasions at

least 4 hours apart while on bedrest)

• Thrombocytopenia (platelet count < 100,000)

• Acute kidney injury (serum creatinine >1.1 mg/ dL

or >2 × baseline)

• Pulmonaryedema

• New- onset cerebral or visual disturbances

• Impaired liver function (liver enzymes > twice

normal, severe persistent RUQ or epigastric pain)

conditions. In preeclampsia, this process is disordered and incomplete, leading to a placental vascular bed that is vasoconstricted at baseline and is hyperresponsive to vasoactive stimuli. Failure of normal angiogenesis leads to supercial placentation and placental hypoperfusion that worsens throughout pregnancy. Eventually, the placenta will start to release antiangiogenic factors, cytokines, and proinammatory factors into maternal circulation, which in turn cause systemwide endothelial dysfunction and a sepsis- like reaction. As a result of chronic placental insuciency, intrauterine growth restriction and impaired fetal development may be seen, especially in cases of preeclampsia that present early in gestation.

PRESENTATION

e clinical spectrum of hypertensive disorders of pregnancy includes preeclampsia without severe features, preeclampsia with severe features, HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets), and eclampsia, which is dened by the presence of seizures. Preeclampsia with severe features is associated with signi-

TABLE49.3 RISK FACTORS FORPREECLAMPSIA

cant potential morbidity and mortality for both parturient and fetus. Maternal complications include placental abrup-

Demographic Advanced maternal age (>35years old) Black race

Hispanic ethnicity

Genetic Factors Histor y of preeclampsia in previous pregnancy

Family history of preeclampsia History of placental abruption, fetal growth

restriction, or fetaldemise

Partner who fathered a preeclamptic pregnancy in

another woman

Medical Conditions

Obesity Chronic hypertension Diabetes mellitus Chronic renal disease Antiphospholipid antibody syndrome Systemic lupus erythematosus

tion, pulmonary edema, hemorrhagic stroke, renal failure, and liver complications. Fetal complications can also be severe, up to and including fetal demise.

Preeclampsia most commonly presents late in pregnancy, aer the 34th week of gestation, and progresses slowly until delivery of the placenta. Early presentation, before 34 weeks EGA, is associated with worse maternal and fetal outcomes, and may actually represent a distinct disease process.3 Rare cases can also present postpartum, usually within 7days of delivery. Signs and symptoms of the disease, by organ system, are detailed in Table49.4.

Obstetric Conditions

Behavioral Factors (Risk reduction)

Partner- Related Factors

SOURCE:Adapted with permissions from Bateman B, Polley L.Hypertensive disorders.

In:Chestnut D, ed. Chestnut’s Obstetric Anesthesia, Principles and Practice. 5th ed.

Saunders/ Elsevier; 2014:825– 59.

348 SECTION B. CARDIAC CRISES

Multiple gestation Hydatidiform mole

Cigarette smoking Exercise

Nulliparity Limited preconceptional exposure to paternal

sperm (e.g., premipaternity, assisted reproductive techniques, teenage pregnancy)

OBSTETRIC MANAGEMENT OFTHE PATIENT

e only denitive cure for preeclampsia is delivery of the fetus. e timing and mode of delivery must be considered on an individual basis, weighing the risks of early delivery on fetal outcome against risk to maternal health with continued pregnancy.2 is complex obstetrical question has been studied for decades with gradually improved maternal and perinatal outcomes.

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TABLE49.4 SIGNS, SYMPTOMS, AND COMPLICATIONS OFSEVERE PREECLAMPSIA

Organ System

Central Nervous System Headache, hyperreexia (clonus), hyperexcitability

Airway Pharyngolaryngeal edema, subglottic edema Difcult intubation

Pulmonary Pulmonary edema Hypoxemia, respiratory failure

Cardiovascular Hypertension, vasospasm, attenuated response to

Hepatic RUQ/ epigastric, elevated LFTs Subscapular bleeding, hepatic rupture (35% mortality)

Renal Proteinuria, blunted increase in GFR (normally 40%- 60%

Hematologic Thrombocytopenia, hyper- or hypocoagulability, decreased

Uteroplacental Impaired perfusion, abnormal oxygen exchange Fetal growth restriction, oligohydramnios, placental

Obstetric management is focused on treatment of clinical symptoms and prevention of maternal and fetal morbidity and mortality. Intravenous magnesium infusion is used for both the prevention and treatment of seizures associated with eclampsia. Dosing of magnesium involves an intravenous bolus of 4– 6 grams given over 15 to 20 minutes, followed by 1– 2 g/ hr infusion.7 Magnesium infusion is titrated to serum magnesium level between of 5– 9 mg/ dL. Monitoring of deep tendon reexes allows early detection

Signs and Symptoms

Visual:Scotoma, amaurosis, blurred vision

vasoactive substances, hyperdynamic state

increase in pregnancy), hyperuricemia

plasma colloid osmotic pressure

as allowing for rapid anesthetic dosing for emergent cesarean delivery. Both the quality of epidural analgesia and the patient’s airway should be reexamined at frequent intervals, as the Mallampati score and the likelihood of a dicult airway can increase during the course of labor (Figure 49.1). An interdisciplinary approach with constant communication between obstetricians, anesthesia providers, and labor nurses is essential to safe care of patients with severe preeclampsia.

Sequelae

Cerebral edema, intracerebral or subarachnoid hemorrhage, ischemic stroke

End- organ ischemia, aortic dissection

Oliguria, renal failure

DIC, spontaneous hemorrhage

abruption, preterm delivery

of systemic toxicity, with loss of patellar reexes at a serum magnesium level of 12 mg/ dL.

Serum blood pressures are treated to a goal systolic pres-

LABOR ANALGESIA

sure of 140– 160mmHg, with care taken not to decrease maternal blood pressure too rapidly to avoid sudden decreases in end- organ perfusion, including placental per-

2,8

fusion.

Intravenous labetalol and hydralazine are the initial drugs of choice for eectively lowering blood pressure in this setting, although a variety of additional agents and infusions can be added for refractory pressure.

A major concern when initiating epidural labor analgesia is the risk of epidural or spinal hematoma in severely preeclamptic patients. e relative risk of complications in this population has not yet been determined compared with nonpreeclamptic parturients. While there is no consensus on lower limit of platelets for safe use of neuraxial techniques, previous requirements for platelet count

ANESTHETIC MANAGEMENT

>100,000 have largely been abandoned for more liberal standards.9 Common practice avoids placement in pre-

eclamptic patients with platelet counts less than 50,000 and Anesthesia providers should monitor patients for complications of preeclampsia and understand the implications of the disease process on the anesthetic plan. Particularly concerning can be thrombocytopenia (oen associated with HELLP syndrome) and resistant hypertension requiring aggressive management. Early epidural placement reduces pain and associated catecholamine release as well

requires careful consideration between 50,000 and 80,000.

Factors such as delivery plan, maternal airway examination,

maternal comorbidities, the rate of decline of platelets, and

the progression and severity of preeclampsia should all be

reviewed. Although coagulopathy is unlikely in preeclamp-

tic patients with normal platelet counts, coagulation stud-

ies should be obtained for patients with thrombocytopenia,

SEVERE PREECLAMPSIA 349

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Neurologic function monitoring provides information on magnesium toxicity as well as an early warning sign for potential bleeding complications.

CESAREAN DELIVERY

Box 49.1 summarizes the key steps to consider in the event of cesarean delivery. If a labor epidural is in place, it can be dosed to obtain surgical anesthesia for urgent and nonurgent cesarean delivery. In the absence of an epidural in situ, for nonemergent deliveries a spinal anesthetic is oen used,

despite unfounded historical concerns of maternal hypotension.

14,15

However, general anesthesia may be required for cesarean delivery due to time constraints in a true emergency or due to contraindications to neuraxial techniques such as coagulopathy, hemodynamic instability, or patient refusal. If general anesthesia is required, major anesthetic concerns in severely preeclamptic patients include airway management, hypertensive response to direct laryngoscopy, and postpartum hemorrhage. Higher incidence of dicult airway in this population is related to airway edema and friability.16 Oropharyngeal edema may worsen during long labor and additionally complicate endotracheal intubation.

Figure49.1 Airway pictures prelabor (Samsoon modication of Mallampati

class 1 airway; A) and postlabor (Samsoon modication of Mallampati class 3 airway; B). SOURCE:Kodali BS, Chandrasekhar S, Bulich LN, Topulos GP, Datta S.Airway

Changes during Labor and Delivery. Anesthesiology. 2008 Mar;108(3):357– 62.

Furthermore, a moderately dicult airway may become impossible if repeated attempts to secure the airway result in pharyngeal bleeding and impair use of advanced airway equipment such as videolaryngoscopy and beroptic

elevated liver enzymes, eclampsia, or evidence of clinical bleeding (venipuncture sites, vaginal bleeding). romboelastography (TEG) or rotational thromboelastometry (ROTEM) may help provide a real- time image of combined eect of thromobocytopenia and coagulopathy on clot formation.

10,11

When neuraxial labor analgesia is contraindicated or declined by the patient, parenteral opioid medications such as low- dose remifentanil via patientcontrolled analgesia (PCA) can be used for labor analgesia.

During initiation of neuraxial analgesia, providers should recognize the patient’s hydration status and anticipate the possibility of volume depletion despite elevated blood pressures. Given the potential benets of decreased intravenous uid in this setting,

7,12

the practice of volume coloading needs to be made on a case- by- case basis. Dosing an epidural aer conrmation of negative test dose should be judicious and slow, to avoid relative hypotension and organ underperfusion.13 Epidural infusions should be programmed to avoid motor blockade not only to improve the likelihood of successful vaginal delivery but also to allow for continuous monitoring of lower- extremity reexes.

bronchoscope.

Hypertension during major surgical events, but particularly during direct laryngoscopy (DL) can increase the risk of cerebral vascular injury under anesthesia. Frequent blood pressure evaluation is warranted, and in the case of uncontrolled hypertension, placement of a preinduction arterial line may be of benefit if time and maternal- fetal status permits. Multiple pharmacologic combinations to prevent hypertension associated with DL have been studied and can be used, including esmolol bolus of 1– 2 mg/ kg with or without lidocaine, nitroglycerin bolus, and remifentanil bolus.17 Other studies have identified issues with some calcium channel blockers due to interaction with magnesium therapy and with sufentanil and remifentanil use being associated with the need for administration of naloxone to the neonate. Many vasodilator infusions will not be readily available on the labor and delivery unit if needed urgently, and these should be planned for ahead oftime.

Cesarean delivery may place patients with severe preeclampsia at increased risk for postpartum hemorrhage

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BOX 49.1 KEY STEPS INPREPARING FORAND PERFORMING

ANESTHESIA FORCESAREAN DELIVERY INTHE PARTURIENT

WITHPREECLAMPSIA

1. Preoperative evaluation and preparation

a. Airway:Reexamine— may have changed over the

course oflabor

b. Hemodynamics

i. Insure adequate IVaccess

ii. If poorly controlled hypertension is present,

consider invasive monitoring (art line, centralline)

iii. Have fast- acting vasoactive drugs drawn up

andready

c. Laboratory

i. Most recent platelet count ( + / − coags),LFTs

ii. Type andscreen

iii. Consider crossmatch if clinical risk factors for

uterine atony are present

d. Drugs

i. Induction agents and paralytics forRSI

ii. Short- acting vasoactive medications (seeabove)

iii. Uterotonics

1. Oxytocin 10– 40 units in 250– 500 mL or IM,

then carboprost 250mcgIM

2. Avoid methylergonovine due to risk of

exacerbating hypertension

2. Intraoperative management

b. If epidural insitu

i. “Dose up” the epidural (convert to surgical

anesthetic)

1. 2% lidocaine with epinephrine 1:200,000

+ bicarb (onset 5– 10 minutes)– OR- 3%

chloroprocaine with bicarb (onset 3– 8 minutes)

2. Expected volume to achieve T4 level:15– 30cc

ii. Preoxygenate while dosingup

iii. If feasible, document fetal heart rate (FHR) while

dosing epidural

iv. Be prepared to treat hypotension

c. If no epidural insitu

i. Perform spinal anesthetic if maternal/ fetal

conditionallows

1. Conrm no maternal contraindications

2. While performingspinal

a. Preoxygenate

b. Monitor FHR if able

c. Consider lateral positioning to facilitate above

d. Be prepared to treat hypotension

ii. If spinal is not possible due to urgency or maternal

contraindications, proceed withGA

1. RSI— note:blunt sympathetic reex (e.g.,

lidocaine, esmolol, or remifentanil)

2. Minimize systemic narcotics/ benzodiazepines

until after delivery

a. In allcases

i. Communicate with obstetricians— clarify urgent vs.

emergent need for delivery

ii. Continue magnesium infusion except in case of

severe uterineatony

iii. Positioning:15°– 20° of left lateral displacement

ofuterus

iv. Be prepared to treat hyper- and hypotension

v. Be prepared to treat to respond to bleeding

SEVERE PREECLAMPSIA 351

due to thrombocytopenia or coagulopathy as well as uterine atony as a result of magnesium therapy. Patients should have at least a type and screen in the blood bank, and there should be uterotonics available. If general anesthesia is used, volatile anesthetic concentration should be decreased aer delivery. Both the anesthesiologist and obstetrician should frequently estimate blood loss to identify the need for transfusion. Continuation of intravenous magnesium for severe preeclampsia is recommended intraoperatively.2 In the setting of ongoing postpartum hemorrhage due to refractory uterine atony, magnesium should be discontinued until uterine tone improves and the patient is resuscitated. Early

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placement of additional vascular access is advised, although

CASE- BASED LEARNING DISCUSSION

the use of central vascular access including pulmonary artery catheterization has not been shown to improve outcomes in this setting.

18– 20

1. e patient’s past medical history includes

hypertension, well- controlled asthma, and cigarette smoking. She recently remarried to a man who had

ECLAMPSIA

had a vasectomy, and they underwent intrauterine insemination with donor sperm to achieve this

pregnancy. What is the incidence of preeclampsia, and For patients who progress to eclampsia, immediate goals are treatment of the seizure, airway support, and optimization of fetal status. Place the patient in le lateral decubitus position to decrease the risk of aspiration as well as improve uterine perfusion. Supplemental oxygen (15 L/ min, or FiO2 1.0 if intubated) should be provided and ventilation assisted as needed. e patient should be monitored with pulse oximetry, blood pressure, and EKG (if available) as well, and fetal heart rate should be continuously traced. Treatment of signicant hyper- or hypotension and arrhythmias should be rapid. Abolus dose of 4– 6 grams of intravenous magnesium should be given, followed by continuous infusion of 1– 2 g/ hr if not already infusing.

Once the patient has been stabilized, the patient’s neurological function should be carefully assessed, and electrolytes, including magnesium, checked. Intravenous fluids should be used sparingly to decrease the risk of cerebral edema. While a seizure does not necessitate immediate emergency delivery of the fetus, the obstetrician and anesthesiologist should discuss the planned timing and mode of delivery as well as review the differential diagnosis for seizures in parturients to ensure an alternate process is not missed.

what are risk factors? Are any behaviors protective? Is there any way to prevent the development of preeclampsia in parturients who are high- risk?

2. Given the patient’s gestational age and severity of preeclampsia, the obstetric team begins an induction of labor. Prior to planned articial rupture of membranes, the patient requests a labor epidural. What are your anesthetic concerns? How will you manage the patient’s uids? What, if any, laboratory studies are needed? Her platelets return at a level 75,000. Do you require additional laboratory analysis at this time? Would you place an epidural?

3. Aer epidural placement, you are called back to the labor and delivery suite. e patient has suered an observed tonic- clonic seizure. What is the dierential diagnosis? How would you manage the patient?

4. Two hours aer the magnesium infusion is initiated, the nurse notes that the patient has lost patellar deep tendon reexes. What are common side eects of magnesium infusion? What are the signs and symptoms of magnesium toxicity, and at what serum blood levels do they develop? What are the anesthetic implications of taking a patient on a magnesium infusion to theOR?

FOLLOW- UP

5. e patient is taken to the operating room for a STAT cesarean delivery for nonreassuring fetal heart rate.

Patients with severe preeclampsia should be observed closely aer delivery. Magnesium is continued for at least 24 hours, hypertension should be tracked and treated as needed, and providers should monitor for complications such as cerebrovascular accident or pulmonary edema, which are more likely to occur postpartum. Unlike the typical course of gestational hypertension, preeclampsia may cause elevated blood pressures for weeks aer delivery, though improvement to baseline is oen seen within 5days aer delivery. e patient should be counseled on implications for future deliveries and general preventative health, since preeclampsia has been linked to future higher risk of ischemic heart disease, congestive heart failure, end- stage renal disease, and

8,21,22

stroke.

e epidural has been dosed for surgery, but patient does not have adequate block when tested by the surgeons. How would you manage? What are some of the anesthetic concerns of general anesthesia for preeclamptic patients? How will you induce the patient? How will you manage blood pressure during surgery?

6. Aer delivery of the baby, the obstetric team reports poor uterine tone. What risk factors does the patient have for uterine atony? How will you adjust your anesthetic? What uterotonics will you use, and which will you avoid in this patient? What are their mechanism of action and side eects? Should magnesium be continued?

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7. Shortly aer extubation and transport to the PACU, the patient complains of dyspnea, particularly in the supine position. She is now requiring high- ow oxygen by facemask. What is the dierential diagnosis? How will you evaluate further?

REFERENCES

1. Report of the National High Blood Pressure Education Program

Working Group on high blood pressure in pregnancy. American Journal of Obstetrics and Gynecology. 2000;183:S1– S22.

2. American College of Obstetricians and Gynecologists. Hypertension

in pregnancy:report of the American College of Obstetricians and Gynecologists’ Task Force on Hypertension in Pregnancy. Obstetrics and Gynecology. 2013;122(5):1122– 31.

3. Bateman B, Polley L. Hypertensive disorders. In:Chestnut D, ed.

Chestnut’s Obstetric Anesthesia, Principles and Practice. 5th ed. Saunders/ Elsevier; Philadelphia, PA; 2014:825– 59.

4. Kuklina EV, Ayala C, Callaghan WM. Hypertensive disorders and

severe obstetric morbidity in the United States. Obstet Gynecol. 2009;113:1299– 306.

5. Repke JT. What’s new in preeclampsia? Best articles from the past

year. Obstet Gynecol. 2013;121:682– 3.

6. American College of Obstetricians and Gynecologists. ACOG

committee opinion no.560:medically indicated late- preterm and early- term deliveries. Obstet Gynecol. 2013;121(4):908– 10.

7. Steegers EA, von Dadelszen P, Duvekot JJ, Pijnenborg R. Pre-

eclampsia. Lancet. 2010;376:631– 44.

8. Melchiorre K, Sharma R, ilaganathan B. Cardiovascular implica-

tions in pregnancy:an overview. Circulation. 2014;130(8):703– 14.

9. Vlessides M. Regional anesthesia found safe for low- platelet parturi-

ents. Clinical Anesthesiology. 2015;41:1.

10. Orlikowski CE, Rocke DA, Murray WB, etal. rombelastography

changes in pre- eclampsia and eclampsia. Br J Anaesth. 1996;77(2):157– 61.

11. de Lange NM, van Rheenen- Flach LE, Lancé MD, etal. Peri- partum reference ranges for ROTEM thromboelastometry. Br J Anaesth. 2014;112(5):852– 9.

12. Ganzevoort W, Rep A, Bonsel GJ, etal. A randomised controlled trial comparing two temporizing management strategies, one with and one without plasma volume expansion, for severe and early onset pre- eclampsia. BJOG. 2005;112(10):1358– 68.

13. Vricella LK. Epidural- associated hypotension is more common among severely preeclamptic patients in labor. Am J Obstet Gynecol. 2012; 207:335.e1– 335.e7

14. Henke VG. Spinal anesthesia in severe preeclampsia. Anesth Analg. 2013;117:686– 93.

15. Aya AG, Mangin R, Vialles N, etal. Patients with severe preeclampsia experience less hypotension during spinal anesthesia for elective cesarean delivery than healthy parturients: a prospective cohort comparison. Anesth Analg. 2003;97(3):867– 72.

16. Munnur U, de Boisblanc B, Suresh MS. Airway problems in pregnancy. Crit Care Med. 2005;33(10 Suppl):S259– 68.

17. Pant M, Fong R, Scavone B. Prevention of peri- induction hypertension in preeclamptic patients: a focused review. Anesth Analg. 2014;119:1350– 6.

18. Li YH, Novikova N. Pulmonary artery ow catheters for directing management in pre- eclampsia. Cochrane Database Syst Rev. 2012;6:CD008882.

19. Dennis AT. Management of pre- eclampsia:issues for anaesthetists. Anaesthesia. 2012;67:1009– 1020.

20. Siddiqui N, Goldszmidt E, Haque SU, Carvalho JC. Ultrasound simulation of internal jugular vein cannulation in pregnant and nonpregnant women. Can J Anaesth. 2010 Nov;57(11):966– 72.

21. Smith GN, Pudwell J, Walker M, Wen SW. Ten- year, thirty- year, and lifetime cardiovascular disease risk estimates following a pregnancy complicated by preeclampsia. J Obstet Gyneaecol Can. 2012;34:830– 5.

22. Aukes AM, De Groot JC, Wiegman MJ, Aarnoudse JG, Sanwikarja GS, Zeeman GG. Long- term cerebral imaging aer pre- eclampsia. BJOG. 2012;119:1117– 22.

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50.

SEVERE PERIPARTUM HEMORRHAGE

Joy L. Hawkins

CLINICALCASE

can we do better? For example, although protocol- driven

care has been shown to improve outcomes in emergency A 30- year- old G4P3 at 28 weeks gestation presents to your labor and delivery (L&D) triage with painless, bright red vaginal bleeding. She has had limited prenatal care, and an ultrasound exam on arrival reveals complete placenta previa. Her prior obstetric history is signicant for three cesarean deliveries. On further examination, her bleeding has stopped and she is hemodynamically stable. Vital signs:BP 110/ 60, HR 90 and hematocrit30%.

situations, a survey of academic obstetric anesthesia units

found that at least 20% had no postpartum hemorrhage

protocol.

Which mothers are most at risk of signicant hemorrhage? A review of 8.5 million deliveries in the National Inpatient Sample from 1999 to 2008 found the incidence of postpartum hemorrhage doubled over the time reviewed to 4.2 per 1,000 deliveries.7 Signicant risk factors for severe hemorrhage included placenta previa or abruption

EPIDEMIOLOGY

(adjusted odds ratio [aOR] 7.0), preeclampsia (aOR 3.1), amnionitis (aOR 2.9) and multiple pregnancy (aOR 2.8) (Table 50.1). A similar review of deliveries in NewYork

Hemorrhage at delivery is commonly dened as ≥ 500 mL for a vaginal delivery and ≥ 1000 mL for a cesarean delivery. e Centers for Disease Control and Prevention (CDCP) report on pregnancy- related mortality in the United States found that hemorrhage accounted for 11.4% of maternal deaths,1 and hemorrhage remains the most common cause of maternal mortality worldwide.2 Additionally, a study looking at 115,502 women at 25 hospitals in the MaternalFetal Medicine Units (MFMU) Network found that severe

State found the risk factors most strongly associated with massive transfusion (dened as requiring 10 or more units of blood) included abnormal placentation such as placenta previa, accreta, increta, or percreta (adjusted odds ratio [aOR] 18.5); placental abruption (aOR 14.6); severe preeclampsia (aOR 10.4); and intrauterine fetal demise (aOR

5.5).8 Women with one or more of these risk factors should be informed of the possibility of hemorrhage and transfusion, deliver in a hospital with resources to manage massive

maternal morbidity occurred in 2.9/ 1,000 births, and that severe postpartum hemorrhage was responsible for approximately half of the cases.3 In their population, severe morbidity was 50 times more common than maternal mortality.

e American Society of Anesthesiologists’ (ASA) Closed Claims Project reviewed closed anesthesia malpractice claims related to hemorrhage from all causes and found that obstetric patients accounted for the largest group of claims (30%).4 Common elements of these cases were delayed diagnosis of severe hemorrhage, delayed transfusion, and poor team communication. Although postpartum hemorrhage is a leading cause of maternal morbidity and mortality, care is oen suboptimal in terms of diagnosis and management. Many series have found a high level of preventability in maternal deaths due to hemorrhage.5 How

TABLE50.1 RISK FACTORS FORSEVERE OBSTETRIC

HEMORRHAGE

Obstetric Condition Adjusted Odds Ratio

Abnormal placentation

Placental abruption

Severe preeclampsia

Placenta previa or abruption

Intrauterine fetal demise

Amnionitis

Multiple pregnancy

7,8

aOR 18.5

aOR 14.6

aOR 3.1/ 10.4

aOR 7.0

aOR 5.5

aOR 2.9

aOR 2.8

354

https://t.me/medicina_free

355

transfusion, and have adequate intravenous access and type and cross- matched blood available prior to delivery.

with no cases of AFE attributed to infusion of cell- salvaged blood. If banked blood cannot be cross- matched or the patient refuses transfusion, the use of cell salvage can be

GENERAL MANAGEMENT OFPERIPARTUM HEMORRHAGE

life- saving. Its use in obstetric hemorrhage is supported in practice guidelines from national bodies in the United States and Great Britain. While cell salvage may be useful,

availability may limit its use in many acute or emergency e American College of Obstetricians and Gynecologists (ACOG) has a Patient Safety Checklist to guide management once estimated blood loss (EBL) following vaginal delivery is greater than 500 mL.9 Unfortunately, caregivers on L&D are not accurate when visually estimating blood loss during delivery, and postpartum blood loss is signicantly underestimated. Use of a visual aid such as a pocket card with examples of known blood volumes can improve accuracy of EBL aer delivery.10 Weighing sponges and other blood- containing materials will also improve accuracy while keeping an ongoing estimation of bloodloss.

Once the diagnosis of severe hemorrhage is made, management may include cell salvage, interventional radiology techniques, transfusion protocols that follow a 1 PRBC:1 FFP: 1 platelet unit strategy, and medications to manage coagulopathy such as recombinant Factor VIIa and tranexamic acid (Table 50.2). Peripartum resuscitation should always follow traditional hemorrhage guidelines of maintenance of normal acid- base status and avoidance of hypothermia, but there are some unique considerations for the peripartum patient.

Concern for amniotic uid embolism (AFE) syndrome and for alloimmunization due to fetal red blood cell contamination has limited the use of red blood cell salvage during cesarean delivery. However, a comparison of maternal central venous blood with cell salvage blood aer washing and with use of a leukocyte depletion lter showed no difference in particulate contaminants,11 and over 400 case reports of cell salvage in parturients have been reported

situations on the L&Dunit.

Consultation with interventional radiology provides another therapeutic technique for real or potential uncontrolled hemorrhage. Balloon catheters for occlusion or embolization can be placed into the iliac vessels by a femoral route either preoperatively12 or when life- threatening hemorrhage has not responded to other treatments.

13,14

e technique is less eective in the presence of coagulopathy or during acute massive hemorrhage, and should not replace ongoing resuscitation or delay proceeding with hysterectomy when necessary. However, serious complications can occur with this technique, including leg ischemia, tissue necrosis, pseudoaneurysms, and even paraplegia,15 and the technique should be used (if at all) as part of a multimodal management plan.

Despite the lack of randomized controlled trials in obstetric patients, many obstetric units have adopted massive transfusion protocols similar to those used for military trauma cases and other types of traumatic injury.17 ese protocols focus on early administration of fresh frozen plasma and platelets with red blood cells to achieve a set ratio. ere is limited data in obstetric patients, but one study of 142 women with PPH found a higher FFP:RBC ratio was associated with a lower requirement for advanced interventional procedures such as embolization, B- Lynch suture, or hysterectomy.18 An obstetric massive transfusion protocol will expedite release of blood products and facilitate an organized provider response with the goal of improving patient safety.

Laboratory studies are an integral part of resuscitation. Fibrinogen levels and thromboelastography may

TABLE50.2 ADVANCED MANAGEMENT TECHNIQUES

FORSEVERE POSTPARTUM HEMORRHAGE

be particularly helpful in obstetric hemorrhage. Several studies have shown that a low brinogen level in the early phase of obstetric hemorrhage is an important predictor

Strategy References

Cell salvage 11– 13

Interventional Radiology 14– 18

of severe postpartum hemorrhage.20 Fibrinogen levels less than 2 g/ L are independently associated with an increased risk of severe postpartum hemorrhage (OR 12.0, 95% CI

2.6– 56.1).21 Obstetric hemorrhage is oen associated with

1:1:1 Transfusion protocols 19– 22

Fibrinogen levels, TEG or ROTEM, and emergency hemostasis panel

Tranexamic acid 28– 29

Recombinant Factor VIIa 30– 33

23– 27

increased brinolytic activity that can be diagnosed with a thromboelastogram (TEG).22 Reference ranges specic to the peripartum period have been established for ROTEM thromboelastometry.23 A criticism of standard coagulation tests has been their slow turnaround times, however, one institution described the multidisciplinary development of

SEVERE PERIPARTUM HEMORRHAGE 355

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