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presence of PTE with associated hemodynamic instability. e aPTT should be maintained at one and one- half to two and one- half times the normal range.

Fondaparinux is the preferred anticoagulant in patients who develop heparin- induced thrombocytopenia, or severe cutaneous reactions to heparin, as there is minimal crossreactivity with UFH.29 If a thromboembolic event results in acute hemodynamic instability, supportive measures should be initiated as described above forAFE.

FOLLOW- UP

Anticoagulation has implications for the initiation of neuraxial analgesia; as does timing of postpartum anticoagulation. e 2010 Guidelines for the American Society of

3. e patient has been switched to heparin at 36 weeks gestation and is receiving 10,000 U twice a day. She is now 38.5 weeks. How long must you wait prior to placement of neuraxial labor analgesia? Would thistimeframe change if she were on therapeutic heparin?

4. e patient is requesting neuraxial labor analgesia 8 hours aer her last dose of heparin. What laboratory values would you obtain?Why?

5. e patient never converted to heparin therapy and remains on theraputic LMWH. When would placement of neuraxial labor analgesia be appropriate? What would the timing be if she had only been on prophylacticLMWH?

Regional Anesthesia (ASRA) provide recommendations for the timing of neuraxial anesthesia in anticoagulated patients.36 If a patient has been anticoagulated with UFH for > 4days, ASRA recommends a platelet count, given the risk of heparin- induced thrombocytopenia. Measurement of aPTT is not necessary in patients receiving prophylactic doses of UFH. ASRA does not recommend a delay in the initiation of neuraxial anesthesia in women receiving subcutaneous, prophylactic doses of UFH, or in women receiving twice- daily dosing with a total daily dose of <10,000 units. No laboratory tests apart from a platelet count are necessary prior to neuraxial anesthesia in women receiving LMWH. A delay of 10– 12 hours is recommended in women with prophylactic dosing of LMWH, and 24 hours in women receiving therapeutic doses. Any patient receiving UFH or LMWH in addition to aspirin should not receive a neuraxial procedure for at least 24 hours. Aer delivery, the ASRA guidelines dier from the guidelines of the American Congress of Obstetricians and Gynecologists with regard to the timing of reinitiation of anticoagulation in the setting of recent neuraxial procedure; therefore, a multidisciplinary discussion of anticoagulation plans is usually necessary.

VENOUS AIR EMBOLISM

CASE

32YO G1P0 undergoing cesarean delivery for breech presentation under spinal anesthesia. e anesthesiologist places the operating room table in Trendelenburg positioning to facilitate the rise of surgical blockade and does not return it to neutral position prior to the start of surgery. Shortly aer you arrive to take over the case the patient complains of intense chest pressure and her SpO2 drops to83%.

MECHANISM

Venous air embolism (VAE) is a common occurrence during cesarean delivery. e incidence varies widely, ranging from 10%, to 65% depending on the study.

37– 41

Apressure gradient as small as - 5 cmH2O between the atmosphere and vasculature can allow a signicant amount of air to be entrained into the venous circulation. Air is entrained typically aer placental separation occurs, and the endo-

CASE- BASED DISCUSSION

1. Despite leg swelling, there is no evidence of DVT on ultrasonography. What would your next diagnostic test be? Would any laboratory values be helpful? What riskfactors does this patient have for thromboembolism?

2. On V/ Q scan there is evidence of small basilar PTE. What would be your pharmacologic agent of choice for anticoagulation? Would you change agents at any point during her pregnancy?

metrial surface is exposed.40 Uterine position, that is uterine exteriorization during repair, and possibly maternal Trendelenburg position, may increase pressure gradient between the right side of the heart and open venous sinuses in the surgical eld.

40– 42

Most air emboli are small, but even small volumes of air can precipitate pulmonary vasospasm.43 Vasoactive mediators or mechanical obstruction of small vessels cause pulmonary vasoconstriction that results in V/ Q mismatch, hypoxemia, right- sided heart failure, arrhythmias, and hypotension. Fluid resuscitation and increased hydrostatic

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pressure may provoke interstitial pulmonary edema. Large volumes of air (>3 mL/ kg) can result in cardiovascular collapse by creating an “air lock” that causes potentially fatal right ventricular outow tract obstruction.

RISK FACTORS

TABLE47.3 METHODS TODETECT VENOUS AIR EMBOLISM

Method of Detection

Transesophageal echocardiography

Precordial Doppler High 0.05

Pulmonary artery catheter High 0.25

Sensitivity

High 0.02

Volume of Air Detected (mL/ kg)

Venous air embolism is more likely to occur during cesarean delivery, especially when the uterus is exteriorized prior to hysterotomy closure. However, it can occur during vaginal delivery as well. Patients with known intracardiac shunt are at risk for paradoxical embolus, and extra care should be

Expired CO

Expired nitrogen Moderate 0.5

SOURCE:Modied from Mirski MA, Lele AV, Fitzsimmons L, Toung TJK. Diagnosis and

treatment of vascular air embolism. Anesthesiology. 2007;106:164– 77.

Moderate 0.5

taken in these instances. An air embolus that reaches the arterial circulation (by means of a patent foramen ovale or atrial/ ventricular septal defect) can lead to cardiovascular and neurologic sequelae and morbidity. Loss of resistance to air during epidural placement should also be avoided in these patients.

below the level of the heart, as tolerated. Nitrous oxide should be discontinued and 100% oxygen administered. Endotracheal intubation should be performed with supported ventilation as needed. Central line placement may be indicated to deliver potent vasopressors.43 e use of the Valsalva maneuver and positive- end expiratory pres-

ASSESSMENT (PRESENTING SIGNS AND SYMPTOMS)

sure should be avoided, because an increase in right atrial pressure may result in a paradoxical embolism. Circulatory support should be provided with chest compressions, intra-

Most air emboli are subclinical.44 Awake patients may expe-

vascular volume expansion, and vasopressors as needed.

rience transient episodes of hypoxemia, dyspnea, or chest pain during uterine repair. be limited to hypoxemia and a slight decrease in end- tidal CO2 in patients undergoing general anesthesia.43 Clinically signicant air emboli may be associated with hypotension, heart rate or rhythm changes, evidence of right- sided heart strain on the electrocardiogram, an increase in central venous pressure, or an increase in pulmonary artery pres-

37,38,40,41

Evidence of VAE may

FOLLOW- UP

In patients with delayed emergence from anesthesia, computed tomography or magnetic resonance imaging may be considered to evaluate for intracerebral air. Hyperbaric oxygen may improve neurologic outcomes if instituted within 6 hours of intracerebral air embolism.

sure. Aprecordial stethoscope may detect a pathognomonic “millwheel murmur.” Transesophageal echocardiography may reveal air in the right atria or the pulmonary artery.

CASE- BASED DISCUSSION

MANAGEMENT OFPATIENT

As most VAE are subclinical and hemodynamically insignicant, routine precordial Doppler monitoring, while recommended by some experts,43 is rarely used. ere are multiple methods to detect VAE (Table 47.3). Transthoracic or transesophageal echocardiography may help to conrm a diagnosis of VAE and to guide appropriate clinical management.

TREATMENT

Upon recognition of VAE, the surgical eld should be ooded with saline and the surgical eld should be lowered

PERIPARTUM EMBOLISM 337

1. Why should the operating room table be placed in neutral position prior to the start of surgery?

2. What is the most sensitive method of detection ofVAE?

3. Discuss the mechanism of paradoxical air embolism.

CONCLUSION

While incidence and maternal implication vary depending on the embolic class, presenting signs and symptoms oen overlap. Similarly, initial treatment with oxygen and

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vasopressor support is similar to all embolic disorders of pregnancy. Patients who suer VAE will rarely become symptomatic, while AFE carries a high risk for signicant maternal morbidity and mortality. Providers should rule out embolism in patients who suer acute dyspnea, hypoxemia, and hemodynamic instability.

REFERENCES

1. Clark SL. Amniotic uid embolism. Clin Obstet Gynecol. 2010;53:322– 8.

2. Knight M, Tunell D, Brocklehurst P, Spark P, Kurinczuk JJ. Incidence and risk factors for amniotic- uid embolism. Obstet Gynecol. 2010;115:910– 7.

3. Abenhaim HA, Azoulay L, Kramer MS, Leduc L. Incidence and risk factors of amniotic uid embolisms:a population- based study on 3 million births in the United States. Am J Obstet Gynecol. 2008;199:49e1– 8.

4. Kramer MS, Rouleau J, Liu S, Bartholomew S, Joseph KS. Amniotic uid embolism:incidence, risk factors, and impact on perinatal outcome. BJOG. 2012;119:874– 9.

5. Kramer MS, Rouleau J, Baskett TF, Joseph KS. Amniotic- uid embolism and medical induction of labour: a retrospective, population- based cohort study. Lancet. 2006;368:1444– 8.

6. Clark SL, Hankins GD, Dudley DA, Dildy GA, Porter TF. Amniotic uid embolism: analysis of the national registry. Am J Obstet Gynecol. 1995;172:1158– 67.

7. Olcott Ct, Robinson AJ, Maxwell TM, Grin HA. Amniotic uid embolism and disseminated intravascular coagulation aer blunt abdominal trauma. J Trauma. 1973;13:737– 40.

8. Cromey MG, Taylor PJ, Cumming DC. Probable amniotic uid embolism aer rst- trimester pregnancy termination. Acase report. J Reprod Med. 1983;28:209– 11.

9. Kelly MC, Bailie K, McCourt KC. A case of amniotic uid embolism in a twin pregnancy in the second trimester. Int J Obstet Anesth. 1995;4:175– 7.

10. Margarson MP. Delayed amniotic uid embolism following caesarean section under spinal anaesthesia. Anaesthesia. 1995;50:804– 6.

11. Davies S. Amniotic uid embolism and isolated disseminated intravascular coagulation. Can J Anaesth. 1999;46:456– 9.

12. Stanten RD, Iverson LI, Daugharty TM, Lovett SM, Terry C, Blumenstock E. Amniotic uid embolism causing catastrophic pulmonary vasoconstriction:diagnosis by transesophageal echocardiogram and treatment by cardiopulmonary bypass. Obstet Gynecol. 2003;102:496– 8.

13. Shechtman M, Ziser A, Markovits R, Rozenberg B. Amniotic uid embolism: early ndings of transesophageal echocardiography. Anesth Analg. 1999;89:1456– 8.

14. Clark SL, Cotton DB, Gonik B, Greenspoon J, Phelan JP. Central hemodynamic alterations in amniotic uid embolism. Am J Obstet Gynecol. 1988;158:1124– 6.

15. Clark SL, Montz FJ, Phelan JP. Hemodynamic alterations associated with amniotic uid embolism:a reappraisal. Am J Obstet Gynecol. 1985;151:617– 21.

16. Clark SL. New concepts of amniotic uid embolism: a review. Obstet Gynecol Surv. 1990;45:360– 8.

17. Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ, Jeejeebhoy FM, Gabrielli A. Part12:Cardiac arrest in special situations:2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2010;122:S829– 61.

18. Kaneko Y, Ogihara T, Tajima H, Mochimaru F. Continuous hemodialtration for disseminated intravascular coagulation and shock

due to amniotic uid embolism: report of a dramatic response. Intern Med. 2001;40:945– 7.

19. McDonnell NJ, Chan BO, Frengley RW. Rapid reversal of critical haemodynamic compromise with nitric oxide in a parturient with amniotic uid embolism. Int J Obstet Anesth. 2007;16:269– 73.

20. Nagarsheth NP, Pinney S, Bassily- Marcus A, Anyanwu A, Friedman L, Beilin Y. Successful placement of a right ventricular assist device for treatment of a presumed amniotic uid embolism. Anesth Analg. 2008;107:962– 4.

21. Hsieh YY, Chang CC, Li PC, Tsai HD, Tsai CH. Successful application of extracorporeal membrane oxygenation and intra- aortic balloon counterpulsation as lifesaving therapy for a patient with amniotic fluid embolism. Am J Obstet Gynecol. 2000;183:496– 7.

22. James AH, Jamison MG, Brancazio LR, Myers ER. Venous thromboembolism during pregnancy and the postpartum period: incidence, risk factors, and mortality. Am J Obstet Gynecol. 2006;194:1311– 5.

23. Jacobsen AF, Skjeldestad FE, Sandset PM. Incidence and risk patterns of venous thromboembolism in pregnancy and puerperium: a register- based case- control study. Am J Obstet Gynecol. 2008;198:233e1– 7.

24. Liu S, Rouleau J, Joseph KS, et al. Epidemiolog y of pregnancyassociated venous thromboembolism:a population- based study in Canada. J Obstet Gynaecol Can. 2009;31:611– 20.

25. Gerbasi FR, Bottoms S, Farag A, Mammen E. Increased intravascular coagulation associated with pregnancy. Obstet Gynecol. 1990;75:385– 9.

26. Gerbasi FR, Bottoms S, Farag A, Mammen EF. Changes in hemostasis activity during delivery and the immediate postpartum period. Am J Obstet Gynecol. 1990;162:1158– 63.

27. James AH, Tapson VF, Goldhaber SZ. rombosis during pregnancy and the postpartum period. Am J Obstet Gynecol. 2005;193:216– 9.

28. Knight M. Antenatal pulmonary embolism:risk factors, management and outcomes. BJOG. 2008;115:453– 61.

29. American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 123. romboembolism in pregnancy. Obstet Gynecol. 2011;118:718– 28.

30. Sipes SL, Weiner CP. Venous thromboembolic disease in pregnancy. Semin Perinatol. 1990;14:103– 18.

31. Stein PD, Beemath A, Matta F, et al. Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II. Am J Med. 2007;120:871– 9. 2071924:2071924.

32. Hollingsworth H, Pratter M, Irwin R. Acute respiratory failure in pregnancy. J Intensive Care Med. 1989;4:11– 34.

33. Leung AN, Bull TM, Jaeschke R, et al. An ocial American oracic Society/ Society of oracic Radiology clinical practice guideline: evaluation of suspected pulmonary embolism in pregnancy. Am J Respir Crit Care Med. 2011;184:1200– 8.

34. Bates SM, Greer IA, Middeldorp S, Veenstra DL, Prabulos AM, Vandvik PO. VTE, thrombophilia, antithrombotic therapy, and pregnancy: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidencebased clinical practice guidelines. Chest. 2012;141:e691S- 736S. 3278054:3278054.

35. Greer IA, Nelson- Piercy C. Low- molecular- weight heparins for thromboprophylaxis and treatment of venous thromboembolism in pregnancy: a systematic review of safety and ecacy. Blood. 2005;106:401– 7.

36. Horlocker TT, Wedel DJ, Rowlingson JC, etal. Regional anesthesia in the patient receiving antithrombotic or thrombolytic therapy:American Society of Regional Anesthesia and Pain Medicine evidence- based guidelines (third edition). Reg Anesth Pain Med. 2010;35:64– 101.

37. Karuparthy VR, Downing JW, Husain FJ, etal. Incidence of venous air embolism during cesarean section is unchanged by the use of a 5 to 10 degree head- up tilt. Anesth Analg. 1989;69:620– 3.

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38. Malinow AM, Naulty JS, Hunt CO, Datta S, Ostheimer GW. Precordial ultrasonic monitoring during cesarean delivery. Anesthesiology. 1987;66:816– 9.

39. Fong J, Gadalla F, Pierri MK, Druzin M. Are Doppler- detected venous emboli during cesarean section air emboli? Anesth Analg. 1990;71:254– 7.

40. Vartikar JV, Johnson MD, Datta S. Precordial Doppler monitoring and pulse oximetry during cesarean delivery:detection of venous air embolism. Reg Anesth. 1989;14:145– 8.

41. Handler JS, Bromage PR. Venous air embolism during cesarean delivery. Reg Anesth. 1990;15:170– 3.

42. Cluver C, Novikova N, Hofmeyr GJ, Hall DR. Maternal position during caesarean section for preventing maternal and neonatal complications. Cochrane Database Syst Rev. 2010:CD007623.

43. Mirski MA, Lele AV, Fitzsimmons L, Toung TJ. Diagnosis and treatment of vascular air embolism. Anesthesiology. 2007;106:164– 77.

44. Epps SN, Robbins AJ, Marx GF. Complete recovery aer near- fatal venous air embolism during cesarean section. Int J Obstet Anesth. 1998;7:131– 3.

45. Blanc P, Boussuges A, Henriette K, Sainty JM, Deleie M. Iatrogenic cerebral air embolism: importance of an early hyperbaric oxygenation. Intensive Care Med. 2002;28:559– 63.

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48.

SYSTEMIC INFLAMMATORY RESPONSE SYNDROME AND SEPSIS INTHE PREGNANT PATIENT

Daria M. Moaveni

CLINICALCASE

end of the century shows increasing incidence in the United

Kingdom (UK) and United States. e rate of OB sepsis in A 37- year- old otherwise healthy P3G3 woman is 2 hours postpartum from an uneventful CD with epidural anesthesia following a 15- hour induction of labor for postdates and subsequent arrest of active phase. She is currently in the postanesthesia recovery unit (PARU), and the nurses are asking you to discharge her to the postpartum oor. Her current vital signs are T 38.3, HR 104, RR 25, BP90/ 50.

Maryland increased from 10.1 to 16.6 per 100,000 deliveries

from 1999 to 2008.5 Maternal severe sepsis and sepsis- related

death doubled in the United States from 1998 to 2008.2 Sepsis-

related maternal mortality appears to be increasing 10% per

year.2 In the UK, from 2009 to 2012, 23% of maternal deaths

were secondary to sepsis.8 Potential causes for this alarming

trend include an increased incidence of invasive streptococcal

infections, particularly a reemergence of hypervirulent Gram-

INTRODUCTION

positive Streptococcus pyogenes, or group Astreptococcus.7 e

rates of cesarean delivery (CD) and obesity have also increased,

both of which increase peripartum infection risk. Risk factors Pregnant patients are generally healthy women who undergo uneventful labors and deliveries and proceed home within

for maternal morbidity and mortality from sepsis

marized in Table48.1.

7– 11

are sum-

a few days postpartum. However, the incidence of sepsis and sepsis- related death is increasing among parturients. In 2013, sepsis was the sixth leading cause of maternal mortality worldwide and accounted for 9.7% of maternal deaths.1 In the United States the most recently reported incidence of sepsis during pregnancy was 1:3333.2 Although only

0.3%– 0.6% of patients with sepsis are pregnant,3 sepsis is the reason for 4.8%– 7.1% of all obstetric (OB) intensive care unit (ICU) admissions,

4,5

and the mortality rate for septic shock among obstetric patients admitted to an ICU has been reported as high as 33%.6 Most importantly, it is a preventable cause of maternal morbidity and mortality.

DIAGNOSIS

DEFINITIONS

e current denitions for systemic inammatory response syndrome (SIRS), sepsis, severe sepsis, and septic shock in nonpregnant adults were last updated in 2012 by the Surviving Sepsis Campaign Guidelines Committee.12 In 1992, SIRS was dened at the ACCP/ SCCM Consensus Conference;13 it was then reviewed as an unclear denition in the 2001 International Sepsis Denitions Conference,14 and was not included in the 2012 International Guidelines

HISTORY AND EPIDEMIOLOGY

for Management of Severe Sepsis and Septic Shock.12 AVenn diagram proposed by Bone in 1992 depicts the relationship among the terms13 (Figure48.1).

e sepsis- related maternal mortality rate in England and Wales decreased dramatically aer the introduction of antibiotics, particularly penicillin in the 1940s to treat group A streptococcus infections.7 Despite the dramatic decrease in maternal mortality due to the introduction of antibiotics and aseptic techniques in the mid- 20th century, data from the

DIAGNOSTIC CRITERIA

Although the denitions for SIRS and sepsis in adults are specied, there are currently no parameters that dene sepsis in pregnant or postpartum women. For parturients, normal

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TABLE48.1 RISK FACTORS FORMATERNAL MORBIDITY

AND MORTALITY FROMSEPSIS

High- Income Countries Low- Income Countries

7– 11

us, the diagnosis and treatment of sepsis may be delayed in the obstetric population and may contribute to maternal mortality.

A Sepsis in Obstetrics Score (SOS) was recently devel-

Cesarean delivery Emergency cesarean delivery Prolonged rupture of membranes Retained products of conception Earlylabor Multiple vaginal examinations(>5) Obesity Diabetes Anemia Low socioeconomicstatus Wintermonths Inuenza Pneumococcal disease Group Astreptococcus Failure to recognize severity Increased susceptibility to severe

infection:

Sickle cell disease, congenital

immunodeciency syndromes, hyposplenism, chronic organ diseases (lung, musculoskeletal, cardiac, liver, renal), immunosuppressive therapies,

connective tissue disease, malignancy Advanced maternalage Cerclage Amniocentesis Fetal or placental surgery

Poverty Unhygienic birth conditions Lack of skilled birth

assistants

Long distance to healthcare

facility

Unavailable medical

supplies Youngage Primiparity Anemia HIV, tuberculosis, malaria Failure to recognize severity

oped based on retrospective data from pregnant and postpartum patients presenting to the emergency department of a tertiary care hospital with a clinical suspicion of sepsis.16 e sepsis scoring system was modied based on normal physiologic parameters for healthy pregnant women for temperature, systolic blood pressure, heart rate, respiratory rate, oxygen saturation, WBC, proportion of immature neutrophils, and lactic acid16 [Table 48.2]. Abnormal parameters receive a score of +1 to +4, with a maximum total score of 28 [Table 48.3]. Ascore ≥ 6 was associated with an increased risk of ICU admission, and the positive predictive value of the SOS was 16.7%.

ETIOLOGY

e etiology of sepsis among pregnant and postpartum women includes pyelonephritis, pneumonia, H1N1 inuenza, chorioamnionitis, endometritis, mastitis, urinary tract infections, ulcerative colitis with bowel perforation,

Crohn’s disease with abscesses, ruptured appendicitis, vascuphysiologic changes in heart rate, respiratory rate, carbon dioxide level, and white blood cell count (WBC) during the second trimester, third trimester, labor, and 48 hours postpartum continue to overlap with sepsis criteria.

12,13,15

lar access infections, pancreatitis due to acute fatty liver dis-

ease of pregnancy, septic abortion, and bacterial meningitis

with epidural abscess.

include E. coli, staphylococcus, streptococcus (especially

2,6,8,9,16

e most common organisms

Trauma

Bacteremia

Sepsis

Infection

Figure48.1 The interrelationship between systemic inammatory syndrome (SIRS), sepsis, and infection. SOURCE:Adapted from Bone RC, Balk RA, Cerra FB, etal.

Denitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/ SCCM Consensus Conference Committee. American College of Chest

Physicians/ Society of Critical Care Medicine. Chest. 1992;101:1645, Figure1.

SYSTEMIC INFLAMMATORY RESPONSE SYNDROME ANDSEPSIS 341

Fungemia

Parasitemia

Severe Sepsis

Viremia

Other

SIRS

Septic Shock

Other

Burns

Pancreatitis

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TABLE48.2 COMPARISON OFDIAGNOSTIC CRITERIA FORSEPSIS BYTHE SURVIVING

SEPSIS CAMPAIGN GUIDELINES COMMITTEE TOTHE SEPSIS INOBSTETRICSSCORE

Parameter

Temperature (°C)

Respiratory rate (breaths per minute) Tachypnea > 24 or < 12

PaCO2 (mmHg) - - - - -

Heart rate (beats per minute) > 90 > 119

White blood cell count (× 109/ L)

Immature neutrophils (%) > 10%

Systolic blood pressure (mmHg) < 90

SpO2 (%) - - < 92%

Lactic acid (mmol/ L) > 1

Italics:Normal values in pregnantwomen

Surviving Sepsis Campaign [12]

> 38.3 or <36 > 38.4 or <36

> 12 or < 4 > 16.9 or < 5.7

Lanceeld group A beta- hemolytic Streptococcus), fusobacterium, and Gram- negative organisms.

2,10,16

respiratory distress syndrome was reported in 70% of obstetric patients admitted to the ICU.6 In the obstetric

Sepsis in Obstetrics Score [16]

≥ 10%

≤ 90

≥ 4

population, respiratory, cardiovascular, and renal failure

MULTIPLE ORGAN DYSFUNCTION SYNDROME AND MORTALITY

are associated with higher mortality compared with failure of the liver, central nervous system, and hematologic system.17 Puerperal sepsis and intrauterine death with

coexisting sepsis has been reported to have a higher morSepsis may rapidly progress to multiple organ dysfunction syndrome (MODS) without treatment. Acute

tality rate compared to hypertensive disorders and hem-

orrhage in developing countries.

TABLE48.3 THE SEPSIS INOBSTETRICSSCORE

Variable

Score +4 +3 +2 +1 0 +1 +2 +3 +4

Temperature (°C)

Systolic blood pressure (mmHg) >90 70– 90 <70

Heart rate (beats per minute) >179 150– 179 130– 149 120– 129

Respiratory rate (breaths per minute)

SpO2 (%)

White blood cell count (μ/ L)

% Immature neutrophils

Lactic acid (mmol/ L)

The Sepsis in Obstetrics Score was developed to improve the diagnostic accuracy of sepsis in pregnant patients. Ascore ≥ 6 is associated with an increased risk of ICU admission.

SOURCE:Adapted from Albright CM, Ali TN, Lopes V, Rouse DJ, Anderson BL. The Sepsis in Obstetrics Score:a model to identify risk of morbidity from sepsis in pregnancy. Am J Obstet

Gynecol. 2014;211:39.e2, Figure1.

High Abnormal Range Normal

>40.9 39– 40.9 38.5– 38.9 36– 38.4 34– 35.9 32– 33.9 30– 31.9 <30

≤119

>49 35– 49 25– 34 12– 24 10– 11 6– 9

≥92%

>39.9 25– 39.9 17– 24.9 5.7– 16.9 3– 5.6 1– 2.9 <1

≥10%

≥4

<10%

Low Abnormal Range

90–91% 85–89% <85%

≤5

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OBSTETRIC IMPLICATIONS

sepsis initiatives, including the Surviving Sepsis Campaign

management guidelines from 2004, 2008, and 2012; an Pregnant women with sepsis have a higher rate of preterm labor, preterm delivery, neonatal sepsis, perinatal hypoxia and acidosis, fetal death, and neonatal death compared with parturients without sepsis.11 Purulent myometritis may cause uterine irritability and subsequent tachysystole,18 and continuous fetal monitoring may reveal fetal tachycardia due to maternal fever, minimal or absent baseline variability, absent accelerations, and possibly decelerations.11 e fetal mortality rate in these cases has been reported as high as 21.19%.17 Although a diagnosis of sepsis itself is not necessarily an indication for prompt delivery, worsening

emergent CMACE brieng on genital tract sepsis; Health

Protection Agency guidelines for prevention and control

of Group A Streptococcal infection in acute healthcare

and maternity settings in the UK; and Royal College of

Obstetricians and Gynaecologists guidelines on bacte-

rial sepsis in pregnancy and bacterial sepsis following

pregnancy.

Antibiotic prophylaxis is recommended for the following obstetric conditions:periabortion, CD, preterm or prolonged rupture of membranes, and third- or fourth- degree perineal tear.

maternal respiratory or hemodynamic condition and nonreassuring fetal status may lead to emergency CD.6 However, early, aggressive treatment for the mother is the rst priority and will oen improve fetal status.11 Sepsis secondary to chorioamnionitis and/ or intrauterine fetal demise may be other indications for delivery, since the source of infection will be present as long as the pregnancy continues.

10,11

Timing of early delivery is dependent on maternal condition, gestational age, and fetal status.11 In a retrospective review of 30 obstetric patients treated in an ICU setting for severe sepsis and septic shock, the mean gestational age at diagnosis of severe sepsis was 25.6 (±8.7) weeks, and patients delivered at a mean age of 33.5 (±7.6) weeks; 9/ 15 antepartum patients were treated for sepsis, discharged home, then readmitted for delivery.6 In contrast, the mean gestational age of parturients diagnosed with septic shock was 28.3 (±5.5) weeks, and they were all delivered during the same admission at a mean gestational age of 28.4 (±5.9) weeks.

PRESENTATION AND MANAGEMENT OFTHE

PARTURIENT WITHSEPSIS

PRESENTING SIGNS AND SYMPTOMS

e signs and symptoms of sepsis may present at any gestational age, during labor, in the operating room, recovery room, or postpartum. Alow index of suspicion for sepsis is important in diagnosing the condition early and establishing prompt treatment. Patients may present with vomiting, diarrhea, malaise, myalgia, headache, productive cough, urinary symptoms, vaginal discharge, abdominal pain, abdominal aches between contractions, pelvic pain, and breast pain.10 Patients may also present with altered mental status. Asking about a history of sore throat or sick contacts may assist in diagnosis.

In 2014, the Maternal Early Warning Criteria were dened by the National Partnership for Maternal Safety in order to reduce maternal morbidity and mortality associated with critical illnesses, including hemorrhage, hypertensive crisis, sepsis, venous thromboembolism, and heart failure.

20,21

e purpose of the parameters is to identify abnormal vital signs and promote early and prompt bedside evaluations of patients who may be deteriorating. Implementing the Maternal Early

PREVENTION

Warning Criteria may facilitate early diagnosis and treatment of sepsis, although no randomized control trials have evaluated

e Centre for Maternal and Child Enquiries (CMACE) reported that mothers who died from Group Astreptococ-

whether this warning system improves outcomes in obstetrics (Table48.4).

cal sepsis from 2006 to 2008 had been in contact with children, who commonly have infections due to this organism, or had had a recent respiratory infection or sore throat.19 (e Centre for Maternal and Child Enquiries [CMACE] has been renamed to Mothers and Babies:Reducing Risks through Audits and Condential Enquiries across the United Kingdom [MBRRACE- UK].) In the most recent report, the mortality rate from genital tract sepsis more than halved between 2006– 2008 and 2010– 2012 (RR

0.44; 95% CI 0.22– 0.87, p=0.016).8 e report notes that the reduction may have been due to the implementation of

TREATMENT

INITIAL RESUSCITATION

Maternal mortality due to sepsis has been attributed to failures in three areas:diagnosis, administration of antibiotics, and proper uid management.19 Due to the potential for rapid decompensation, early, aggressive, goal- directed treatment should not be delayed.

6,11

Early transfer to an ICU

SYSTEMIC INFLAMMATORY RESPONSE SYNDROME ANDSEPSIS 343

344

https://t.me/medicina_free

TABLE48.4 MATERNAL EARLY WARNING CRITERIA

FORCRITICAL ILLNESS INPARTURIENTS

Parameter Abnormal Values

treatment of septic shock. Epinephrine can be added and can substitute for NE. Vasopressin can also be added to norepinephrine to either increase mean arterial pressure (MAP) or decrease NE dose. e systemic circulation

Systolic blood pressure (mmHg) < 90 or > 160

Diastolic blood pressure (mmHg) > 100

Heart rate (beats per minute) < 50 or > 120

of pregnant women is less responsive to norepinephrine and epinephrine, whereas the uterine circulation is more responsive.22 us pregnant women may require higher doses of vasopressor agents to increase MAP at the cost of

Respiratory rate (breaths per minute) < 10 or > 30

SpO2 (%)on room air at sea level < 95%

Oliguria, mL/ hr for ≥ 2 hours

Maternal agitation, confusion, or unresponsiveness; Patient with preeclampsia reporting a nonremitting headache or shortness of breath

< 35

decreased uteroplacental perfusion. Norepinephrine use has been reported for treatment of shock in a pregnant woman at 6months gestation without fetal complications.23 It has also been used in healthy pregnant women to maintain blood pressure during spinal anesthesia for CD at term24 without signicant dierences in Apgar scores at 1 minute and 5 minutes nor in umbilical arterial blood gases compared with patients receiving phenylephrine.24 Umbilical

may be warranted. e 2012 Surviving Sepsis Campaign provides guidelines for management of severe sepsis and septic shock.12 But, considerations for pregnant women are not specically addressed. Box 48.1 summarizes a workup more specic for parturients.

venous blood pH (7.35 [7.34– 7.37] vs. 7.34 [7.32– 7.36], p=0.031) and oxygen content (12.7 mL/ dL [11.3– 14.4] vs. 11.8 mL/ dL [9.6– 13.7], p=0.047) were higher in the norepinephrinegroup.

No studies are available regarding use of vasopressin for

septic shock in pregnant women. Atheoretical risk is acti-

VASOPRESSOR THERAPY

According to the Surviving Sepsis Campaign Guidelines,12

vation of uterine V1a receptors, leading to uterine contractions, thus caution is recommended if vasopressin is used during pregnancy.

norepinephrine (NE) is the rst- line vasopressor for

BOX 48.1 WORKUP FORDIAGNOSIS OFMATERNAL

10,11

SEPSIS

Cultures

Blood, urine,sputum

Consider vaginal discharge, amniotic ﬂuid, breastmilk

Throat, perineal, abdominal woundswabs

Labs

CBC, CMP, lactate, ABG, PT/ INR/ PTT/ ﬁbrinogen if DIC is suspected

Fetal Assessment

Cardiotocography

Pelvic ultrasound

Retained products of conception

Consider CXR, CT, echocardiography

Exploratory laparotomy if abscess if suspected

CBC=complete blood count; CMP=complete metabolic prole; ABG=arterial blood gas; PT=prothrombin time; INR=international normalized ratio; PTT=partial thromboplastin time; DIC=disseminated intravascular coagulation; CXR=chest xray; CT=computerized tomography

ANTIMICROBIAL THERAPY

Multiple factors inuence the choice and dosing of antibiotics for an obstetric patient with sepsis. ese include the increased volume of distribution in pregnancy, increased renal blood ow due to pregnancy, and uid and vasopressor administration.10 Medications safe to give during pregnancy and for mothers who are breastfeeding also aect choice of antibiotics. In general, broad- spectrum antibiotics cover Gram- positive, Gram- negative, and anaerobic bacteria.11 Recommended empiric antibiotics administered within 1 hour of sepsis diagnosis include gentamicin, clindamycin, and penicillin11 (Box 48.2). Antimicrobial agents can then be adjusted when culture results are available. Early consultation with an infectious disease physician and with the pharmacy is essential to proper antibiotic management for sepsis in obstetric patients.

PERIOPERATIVE MANAGEMENT OFTHE PARTURIENT WITHSEPSIS

Management of sepsis in the pregnant or postpartum woman is multifaceted, and communication among the

344 SECTION B. CARDIAC CRISES

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345

4. What is your plan for workup?

BOX 48.2 EMPIRIC ANTIBIOTIC THERAPY FORSEPSIS INTHE

PREGNANT PATIENT

1. Gentamicin 1.5 mg/ kg IV, then 1 mg/ kgIVQ8H

2. Clindamycin 900 mgIVQ8H

3. Penicillin 3million unitsIVQ4H

5. What is your initial treatmentplan?

6. What are the possible etiologies of her infection?

7. Who else should be involved in this patient’scare?

1. Vancomycin 15 mg/ kg IV then dosing by pharmacy

2. Piperacillin and tazobactam 4.5gIVQ6H

IV=intravenous; Q=every; H=hour

obstetrician, neonatologist, infectious disease physician, critical care physician, and anesthesiologist allows for complete care of the mother and fetus. For the pregnant woman, fetal monitoring may direct timing and route of delivery. Neonates may require resuscitation at delivery, admission to a neonatal ICU, and/ or administration of antibiotics.10 Anesthesiologists may be involved in the management of a septic patient on the labor and delivery oor, in the operating room, or recoveryroom.

CONCLUSION

Sepsis is a preventable and treatable cause of maternal morbidity and mortality. e incidence of maternal sepsis is increasing in developing countries and may be due to an increase in streptococcal and inuenza infections, delays in recognition and diagnosis, and delays and inadequacy in treatment. e Sepsis in Obstetrics Score may provide more appropriate criteria for diagnosing sepsis in parturients. Early, goal- directed therapy with uids, antibiotics, and vasopressors if necessary, as well as involvement of a multidisciplinary team enhances care of both the mother andfetus.

CASE- BASED LEARNING DISCUSSION

1. Would you discharge this patient from the PARU? Why or why not? What are your concerns?

2. What additional information would you like to know? What is your dierential diagnosis?

3. Does this patient meet criteria for a diagnosis of sepsis?

REFERENCES

1. Kassebaum NJ, Bertozzi- Villa A, Coggeshall MS, et al. Global, regional, and national levels and causes of maternal mortality during 1990– 2013:a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2014;384:980– 1004.

2. Bauer ME, Bateman BT, Bauer ST, Shanks AM, Mhyre JM. Maternal sepsis mortality and morbidity during hospitalization for delivery: temporal trends and independent associations for severe sepsis. Anesthesia & Analgesia. 2013;117:944– 50.

3. Martin GS, Mannino DM, Eaton S, Moss M. e epidemiology of sepsis in the United States from 1979 through 2000. N Engl J Med. 2003;348:1546– 54.

4. Pollock W, Rose L, Dennis CL. Pregnant and postpartum admissions to the intensive care unit:a systematic review. Intensive Care Med. 2010;36:1465– 74.

5. Wanderer JP, Leert LR, Mhyre JM, Kuklina EV, Callaghan WM, Bateman BT. Epidemiology of obstetric- related ICU admissions in Maryland:1999– 2008. Crit Care Med. 2013;41:1844– 52.

6. Snyder CC, Barton JR, Habli M, Sibai BM. Severe sepsis and septic shock in pregnancy:indications for delivery and maternal and perinatal outcomes. J Matern Fetal Neonatal Med. 2013;26:503– 6.

7. Acosta CD, Knight M. Sepsis and maternal mortality. Curr Opin Obstet Gynecol. 2013;25:109– 16.

8. Saving lives, improving mothers’ care: lessons learned to inform future maternity care from the UK and Ireland condential enquiries into maternal deaths and morbidity 2009– 2012. MBBRACEUK: Mothers and Babies: Reducing Risks rough Audits and Condential Enquiries across the United Kingdom. https:// www. npeu.ox.ac.uk/ mbrrace- uk/ reports. Accessed October 23,2015.

9. Freedman RL, Lucas DN. MBRRACE- UK:saving lives, improving mothers’ care— implications for anaesthetists. Int J Obstet Anesth. 2015;24:161– 73.

10. Ford JM, Scholeeld H. Sepsis in obstetrics:cause, prevention, and treatment. Curr Opin Anaesthesiol. 2014;27:253– 8.

11. Barton JR, Sibai BM. Severe sepsis and septic shock in pregnancy. Obstet Gynecol. 2012;120:689– 706.

12. Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign:international guidelines for management of severe sepsis and septic shock:2012. Crit Care Med. 2013;41:580– 637.

13. Bone RC, Balk RA, Cerra FB, etal. Denitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. e ACCP/ SCCM Consensus Conference Committee. American College of Chest Physicians/ Society of Critical Care Medicine. Chest. 1992;101:1644– 55.

14. Levy MM, Fink MP, Marshall JC, et al. 2001 SCCM/ ESICM/ ACCP/ ATS/ SIS International Sepsis Denitions Conference. Intensive Care Med. 2003;29:530– 8.

15. Bauer ME, Bauer ST, Rajala B, etal. Maternal physiologic parameters in relationship to systemic inammatory response syndrome criteria: a systematic review and meta- analysis. Obstet Gynecol. 2014;124:535– 41.

16. Albright CM, Ali TN, Lopes V, Rouse DJ, Anderson BL. e Sepsis in Obstetrics Score:a model to identify risk of morbidity from sepsis in pregnancy. Am J Obstet Gynecol. 2014;211:39.e1– 8.

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