41: Obstetric Emergencies


CHAPTER 41
Obstetric Emergencies


Zachary D. Kuschner1 and Adel Bassily‐Marcus2


1 Northwell Health System, New York, NY, USA


2 Icahn School of Medicine at Mount Sinai, New York, NY, USA


Overview


Pregnancy results in profound physiologic changes, which are summarized in Table 41.1.


Critical care fundamentals of pregnancy


Airway management



  • Incidence of failed airway is seven times greater than in the general population.
  • Anticipate difficult airway.

Difficult airway features of the pregnant patient
















Category of complication Specific features
Anatomic Anterior larynx
Mucosal edema
Increased aspiration risk
Hypoxemic Decreased oxygen reservoir
Increased oxygen consumption
Hemodynamic Decreased cardiac reserve
Uteroplacental susceptibility to hypotension

Table 41.1 Physiologic changes in pregnancy.
















































Affected parameter Change in pregnancy Etiology
Cardiac output Increases 30–50% Increased SV and HR
SVR and MAP Decreases Endogenous vasodilators
Venous return Decreases IVC compression by uterus
Uteroplacental blood flow Increases to 1000 mL/min Decreased uterine resistance
Pulmonary functional residual capacity Decreases 10–20% Increased abdominal pressure
Minute ventilation Increases 40–70% Increased respiratory rate
Metabolic profile PaCO2 decreases; plasma bicarbonate decreases to 17–18 mEq/L Respiratory alkalosis, chronic metabolic compensation
Oxygen consumption Increases 20–33% Fetal O2 consumption
Glomerular filtration rate Increases Increased renal blood flow
Hepatic cytochrome P450 activity Increases Hormone mediated

Ventilator management



  • Titrate minute ventilation to PaCO2 30–32 mmHg to prevent fetal hypercarbia.
  • Permissive hypercapnia is not indicated.
  • Titrate FiO2 and PEEP to SpO2 >95% or PaO2 >70 mmHg to promote fetal oxygenation.
  • PaO2 <60 mmHg leads to fetal hypoxia and decompensation.
  • Minimize PEEP to avoid further reductions in venous return leading to hypotension.

Maternal cardiac arrest


Background


Incidence/prevalence



  • 1:12 000 admissions for delivery.
  • 17.8 deaths per 100 000 live births.

Common causes



  • Hypovolemia and hemorrhage.
  • Embolic phenomenon.
  • Severe pre‐eclampsia and eclampsia.
  • Sepsis.
  • Allergic reactions.
  • Medication errors and iatrogenic injuries.
  • Anesthetic complications.
  • Hypermagnesemia.
  • Pre‐existing cardiac disorders.

Prevention



  • Routine prenatal care.
  • Adequate nutrition.
  • Vaccination.
  • Treatment of pre‐eclampsia and eclampsia.
  • Optimization of comorbid conditions.

Diagnosis



  • History: solicit history of predisposing factors and conditions.
  • Physical examination: confirm pulselessness, evaluate airway, auscultate lungs, palpate abdomen, examine extremities, determine gestational age.
  • Intra‐arrest investigation:

    • Check hematocrit and blood gas.
    • Determine cardiac rhythm.
    • Cardiac ultrasound (POCUS): look for right or left ventricular strain or dilation.
    • Pulmonary ultrasound: look for unilateral absent lung sliding indicating pneumothorax, or B‐lines indicating pulmonary edema
    • Abdominal ultrasound: check for free fluid
    • Extremity ultrasound: check for a non‐compressible vein indicating deep vein thrombosis.

List of imaging techniques



  • Cardiac rhythm monitoring.
  • Cardiac ultrasound:

    • Evaluate compression depth/adequacy and location.
    • Evaluate for pulmonary embolism (PE): RV dilation, septal bowing, distended IVC.
    • Evaluate for heart failure: organized contractility with minimal LVEF.
    • Evaluate for tamponade: pericardial effusion with RA or RV diastolic collapse.

  • Pulmonary ultrasound:

    • Pneumothorax: loss of lung sliding, stratosphere sign, lung point.
    • Pulmonary edema: confluent B‐lines, pleural effusion.

  • Abdominal ultrasound:

    • Hemorrhage, placental abruption: abdominal free fluid.

  • Extremity ultrasound:

    • DVT: non‐compressible femoral, popliteal veins.

Differential diagnosis in maternal cardiac arrest

























Differential diagnosis Features
Amniotic fluid embolus Rhythm: PEA
Intra‐partum sudden cardiac death
POCUS: systolic dysfunction, RV dilation
Pulmonary embolus Rhythm: PEA
Pre‐arrest shortness of breath, chest pain, palpitations, unilateral extremity edema
POCUS: RV strain/dilation
Hemorrhage Rhythm: PEA
Hypotension or hemorrhage, palpable abdominal fetus, anemia
Cardiac echocardiogram: hyperdynamic LV
Peri‐partum cardiomyopathy Rhythm: PEA or VT/VF
New heart failure symptoms
POCUS: systolic dysfunction
Hypermagnesemia Rhythm: PEA, bradycardia, prolonged PR, flattened P wave, prolonged QRS and QTc
High magnesium level, weakness, decreased muscle tone/deep tendon reflexes, bradycardia or bradypnea
POCUS: bradycardia
Ventricular fibrillation/ventricular tachycardia Rhythm: VT/VF/torsades de pointes
Sudden cardiac death, cardiac disease, electrolyte abnormalities
POCUS: fibrillation

Treatment



  • Basic life support (BLS), advanced cardiac life support (ACLS).
  • Peri‐mortem cesarean section if no return of spontaneous circulation (ROSC) within 4 minutes.
  • If hemorrhage: obstetric massive transfusion protocol (MTP).
  • Maternal monitoring does not inform the clinician about the status of the fetus:

    • Time may not permit fetal heart rate monitor to be initiated.
    • Fetal oxygenation and acid–base status must be inferred.

  • Resuscitate in supine position: manual left lateral displacement of the uterus.

Prognosis



  • Maternal rates of survival to hospital discharge after cardiac arrest are as high as 60%.
  • Maternal survival following peri‐arrest cesarean section ranges from 35% to 55%.
  • About 70% of fetal survivors of maternal cardiac arrest are delivered at 5 minutes; 95% within 15 minutes.

Post‐partum hemorrhage


Background


Definition



  • An estimated 500 mL of blood loss in a vaginal delivery.
  • An estimated 1000 mL of blood loss in a cesarean section.
  • Alternatively, any blood loss that causes hemodynamic instability in the mother.

Incidence/prevalence



  • About 3% of pregnancies.
  • About 650 deaths per year in the USA.

Etiology














  • Uterine atony.


  • Placenta previa.


  • Retained products of conception.


  • Invasive placentation.


  • Birth trauma.


  • Uterine rupture.

Predictive/risk factors




















  • Prior post‐partum hemorrhage.


  • Anemia.


  • Age >40 years.


  • Grand multiparity (≥5 births).


  • High BMI.


  • Hypertension.


  • Multiple pregnancy.


  • Prolonged placental delivery.


  • Placenta previa.


  • Instrumental delivery.

Diagnosis



  • History: syncope, anemia, pregnancy complications, prior bleeding or family history of bleeding, prolonged delivery.
  • Physical examination:

    • Primary survey: airway, ventilation, circulation, neurologic status.
    • Palpable abdomen: tenderness, peritonitis, palpable fetus.
    • Inspect vaginal introitus: birth trauma, ongoing bleeding.
    • Sterile speculum and bimanual exams: atony/retained products

  • Investigations:

    • Kleihauer–Betke test: the KB test is the standard method of quantitating fetal–maternal hemorrhage (FMH). It allows calculation of the percentage of red blood cells in the mother’s blood that are of fetal origin.
    • CBC, BMP, type and cross, coagulation panel, blood gas, Electrocardiogram.
    • FAST and cardiac ultrasound exam.

Treatment



  • Centers should have a protocol for assessment and management of post‐partum hemorrhage.
  • Quantify blood loss.
  • Monitor vital signs.
  • Uterine atony is the most common cause of post‐partum hemorrage:

    • Treat with uterotonic drugs, bimanual uterine compression, intrauterine balloon tamponade, uterine artery embolization.

  • Traumatic lacerations need to be managed surgically.
  • Retained placental tissue must be removed.
  • Coagulopathy is treated with blood products and factor concentrates.
  • Tranexamic acid is an antifibrinolytic drug that can reduce bleeding due to trauma or atony.
  • Hysterectomy for patients with uterine rupture or diffuse placenta accreta.
  • MTP for brisk bleeding, unstable patient.

Peri‐partum cardiomyopathy


Background


Definition



  • Heart failure in the last month of pregnancy or within 5 months post‐partum, characterized by left ventricular systolic dysfunction without an alternative etiology.

Incidence/prevalence


The incidence varies by geographic region:



  • USA: 1:1000–4000 live births.
  • South Africa: 1:1000 live births; Haiti: 1:300 live births.

Etiology



  • Myocardial insufficiency: proposed mechanisms include oxidative stress and prolactin upregulation.
  • 16 kDa fragment of prolactin promotes apoptosis.
  • Proposed insults: low selenium levels, viral, cytokines, hemodynamic stress.

Predictive/risk factors














  • Multiparity.


  • Prolonged tocolytics.


  • Maternal age >30 years.


  • Cocaine use.


  • Pre‐eclampsia.


  • Black race/ethnicity.

Diagnosis



  • Criteria:

    • Onset during the last month of pregnancy or 5 months post‐partum.
    • LV systolic dysfunction (EF <45%).
    • No alternative cause identified.
    • No preceding cardiac disease.

  • History: shortness of breath, orthopnea, paroxysmal nocturnal dyspnea, fatigue, decreased exercise tolerance, bilateral lower extremity swelling.
  • Physical examination: rales, S3 heart sound, bilateral lower extremity edema.
  • Investigations: rule out alternative etiologies

    • CBC, BMP, troponin, BNP, TFTs.
    • Cardiac ultrasound.
    • Rarely cardiac MRI (gadolinium contraindicated ante‐partum) or endomyocardial biopsy.

Differential diagnosis of peri‐partum cardiomyopathy
















Differential diagnosis Features
Existing cardiac disease Symptoms prior to pregnancy
Pulmonary embolism History of VTE, sudden onset, unilateral lower extremity swelling
Viral myocarditis Fever, viral illness

Treatment


Stable cases: outpatient management



  • Prevent cardiac remodeling: angiotensin‐converting enzyme inhibitor (ACEI)/angiotensin receptor blocker (ARB) versus hydralazine and nitrate if ante‐partum.
  • Diuresis.
  • Anticoagulation if EF <35%.

Unstable cases: inpatient management



  • Treatment of pulmonary vascular congestion.
  • Fetal cardiac monitoring: delivery if decompensation.
  • Preload, afterload optimization.
  • Vasopressors if needed to maintain SBP >90 mmHg:

    • Monitor for utero‐fetal insufficiency.

  • Inotropes and inodilators if needed for low cardiac output:

    • Consider monitoring urine output, serial cardiac US, placement of pulmonary artery catheter.

Agents for treating peri‐partum cardiomyopathy




























Focus of therapy Medication regimen Notes
Prevention of cardiac remodeling Captopril 6.25–50 mg three times daily
Ramipril 1.25–5mg twice daily
Enalapril 1.25–0 twice daily
Candesartan 2–32 mg daily
Varsartan 40–160 mg twice daily
Metoprolol tartrate .125–.25 mg daily
Hydralazine 10–40 mg three times daily
Nitroglycerin 10–20 ug/min then titrated to BP
ACEI and ARB contraindicated in ante‐partum patients
Beta‐blockers should be continued up to 6 months after resolution
Management of preload and pulmonary vascular congestion Hydrochlorothiazide 12.5–50 mg daily
Furosemide 20–80 mg once or twice daily
Spironolactone 12.5–50 mg daily
Norepinephrine 8–12 μg/kg/min
Institute in all hemodynamically stable patients
Inotropic support Milrinone 0.125–0.5 μg/kg/min
Dobutamine 2.5–10 μg/kg/min
Indicated for poor perfusion and SBP <90 mmHg
Prolactin inhibition Bromocriptine 2.5 mg twice daily for 2 weeks, then 2.5 mg daily for 2 weeks Requires concomitant anticoagulation due to thrombotic risk
Definitive end‐stage therapy Ventricular assist device
Cardiac transplant
End‐stage heart failure without recovery after 6 months

Prognosis



  • Full recovery in 25–85% of cases.
  • Progression to end‐stage heart failure in 13–25% of cases.
  • Mortality at 6 months: 3–30%.

Pulmonary embolic disease


Background


Definition



  • Embolic occlusion of a pulmonary artery by venous thrombus or leaked fetal amniotic fluid that may result in hemodynamic changes due to mechanical obstruction, vasoconstriction, or inflammatory mediated myocardial depression.

Incidence/prevalence



  • Venous thromboembolism (VTE) incidence: 5–12 events per 10 000 pregnancies ante‐natally, 3–7 events per 10 000 pregnancies post‐partum.
  • VTE risk in pregnancy is increased 7–10× relative to the general population. The risk returns to baseline at 6 weeks post‐partum.
  • Amniotic fluid embolism (AFE) complicates 2–7 per 10 000 pregnancies

Etiology



  • VTE: inhibition of fibrinolysis, venous stasis, endothelial activation.
  • AFE: leakage of amniotic fluid into systemic circulation, resulting in endovascular dysfunction, mechanical obstruction, and myocardial depression.

Diagnosis



  • VTE:

    • History: prior VTE, shortness of breath, chest pain, unilateral lower extremity erythema, edema, erythema. May present as sudden cardiac arrest.
    • Physical examination: tachypnea, unilateral lower extremity edema/erythema/tenderness.
    • Imaging: ECG or cardiac rhythm monitor, cardiac ultrasound, lower extremity venous ultrasound, CXR, CT angiogram (more diagnostic than V/Q scan).

  • AFE:

    • History: intra‐partum cardiac arrest. Alternatively sudden onset symptoms of heart failure.
    • Physical examination: sudden loss of pulses. Rales, bilateral lower extremity edema.
    • Imaging: POCUS TTE or TEE if available.

  • Lab work, AFE and PE: blood gas, troponin, BNP, CBC, CMP, magnesium, INR, aPTT. d‐dimer is not as useful in pregnant patients.

Treatment



  • Cardiac arrest: follow ACLS guidelines.
  • Shock: tPA 100 mg over 2 hours for PE; ECMO if rapidly available.

    • Optimize preload: crystalloid infusion, inotropic support.
    • Consider expedited caesarean section in unstable patients.

  • VTE:

    • Stable patients: enoxaparin 1 mg/kg twice a day, dalteparin 200 U/kg each day or 100 U/kg twice a day, tinzaparin 175 U/kg each day. Titrate to factor Xa level: target range 0.5–1.1 U/mL.
    • Unstable patients or near delivery: heparin 80 U/kg bolus, infusion of heparin 18 U/kg, titrate to aPTT. Hold heparin 4 hours prior to delivery, resume 6 hours after vaginal delivery or 12 hours after cesarean.

  • AFE: perfusion is rarely intact. Manage via BLS, ACLS, inotropic support, airway management.

    • Avoid excessive fluids.
    • After ROSC: immediate delivery in the case of viable fetus (>23 weeks).
    • If no ROSC: perimortem cesarean section at 4 minutes.
    • Evaluate for coagulopathy and treat if present.

Prognosis



  • AFE: mortality is greater than 60%. Cardiac arrest survival <10%.
  • PE: 15–18% mortality at 3 months.

Pre‐eclampsia and eclampsia


Background


Definition



  • Pre‐eclampsia: new hypertension after >20 weeks of gestational age.
  • Severe pre‐eclampsia: pre‐eclampsia with organ dysfunction.
  • Eclampsia: seizure or acute neurological deficits in a patient with pre‐eclampsia.

Incidence/prevalence



  • Pre‐eclampsia:

    • 2–8% of all pregnancies.
    • 25% progress to severe pre‐eclampsia.

  • Eclampsia: 1–3 per 1000 pregnant women.

Etiology



  • Pre‐eclampsia: endovascular dysfunction, possibly due to placental hypoxemia and inflammation. Can occur in the absence of placental abnormalities.
  • Eclampsia: cerebral vasospasm, arterial insufficiency, local ischemia, disruption of the blood–brain barrier with cerebral edema.

Predictive/risk factors



  • Pre‐eclampsia: history of pre‐eclampsia, primiparity, obesity, family history of pre‐eclampsia, multiple pregnancies, history of hypertension or diabetes. Smoking decreases risk.

Diagnosis



  • Pre‐eclampsia: BP >140 mmHg on two separate readings more than 4 hours apart with either >300 mg urine protein/24 hours or protein : creatinine ratio ≥0.3.
  • Severe pre‐eclampsia: hypertension with proteinuria (as above) or organ system failure.

    • Vascular hypertension: BP >160 mmHg systolic or 110 mmHg diastolic on two readings more than 4 hours apart.
    • CNS: cerebral dysfunction or visual symptoms.
    • Hepatic: right upper quadrant pain or transaminases more than twice the upper limit of normal.
    • Hematologic: thrombocytopenia <100 000 platelets/μL.
    • Renal: serum creatinine >1.1 mg/dL or doubled above baseline.
    • Pulmonary: pulmonary edema.

  • Eclampsia: Grand mal seizure after 20 weeks gestation with hypertension.

Treatment



  • Pre‐eclampsia:

    • Mild: control hypertension.
    • Severe: seizure prophylaxis, control hypertension, supportive care, delivery.

  • Eclampsia: magnesium infusion, supportive care, delivery.

Table of treatment of severe pre‐eclampsia
















Focus of treatment Intervention
Hypertension Hydralazine: 5–20 mg IV every 30 minutes
Labetalol: 10–20 mg IV every 10 minutes, double dose with re‐dosing up to 80 mg per dose and total maximum of 220 mg
Seizure prophylaxis First line: magnesium sulfate IV piggyback 4–6 g loading dose over 30 minutes with 2 g/h infusion. May load IM. Goal: serum magnesium level 4.8–8.4 mg/dL
Continue through delivery
Monitor for magnesium toxicity
Delivery Definitive management for all viable fetuses
Early viable gestations: may delay delivery for corticosteroid administration

Prevention/management of complications



  • Monitor closely for magnesium toxicity.
  • If patient suffers cardiac arrest while receiving magnesium, in addition to resuscitation, stop magnesium and treat toxicity empirically with calcium.

Prognosis



  • Pre‐eclampsia: 0.2% mortality with 5% risk of significant morbidity; 50 000–70 000 deaths worldwide annually.
  • Eclampsia: 2–3 deaths per 10 000 live births in developed countries; 16 – 69 deaths per 10 000 live births in developing countries.

Reading list



  1. Dulu A, Ragsdale ES, Goffman D. Critical care issues in pregnancy. In: Oropello JM, Pastores SM, Kvetan V (eds), Critical Care. New York: McGraw‐Hill, 2017, pp. 829–50.
  2. Einav S, Kaufman N, Sela HY. Maternal cardiac arrest and perimortem caesarean delivery: evidence or expert‐based? Resuscitation 2012; 83(10):1191–200.
  3. Hegewald MJ, Crapo RO. Respiratory physiology in pregnancy. Clin Chest Med 2011; 32:1–13.
  4. Lam MTC, Dierking E. Intensive care unit issues in eclampsia and HELLP syndrome. Int J Crit Illn Inj Sci 2017; 7(3) 136–41.
  5. Papazian J, Kacmar RM. Obstetric hemorrhage: prevention, recognition, and treatment. Adv Anesth 2017; 32(1):119–35.
  6. Troiano NH, et al. AWHONN High‐Risk and Critical Care Obstetrics, 3rd edition. Philadelphia: Wolters Kluwer Health, 2013.

Guidelines


National society guidelines
























Title Source Date and reference
Cardiac Arrest in Pregnancy: A Scientific Statement from the AHA American Heart Association 2015
Jeejeebhoy FM, et al. Circulation 2015;132(18):1747–73
Management of Pulmonary Embolism American College of Cardiology 2016
Konstantinides SV, Barco S, Lankeit M, Meyer G. J Am Coll Cardiol 2016;67(8):976–90
Hypertension in Pregnancy American College of Obstetricians and Gynecologists 2013
American College of Obstetricians and Gynecologists; Task Force on Hyptertension in Pregnancy. Obstet Gynecol 2013;122:1122–31
Amniotic Fluid Embolism: Diagnosis and Management Society for Maternal‐Fetal Medicine 2016
Society for Maternal‐Fetal Medicine (SMFM) with the assistance of Pacheco LD, et al. Am J Obstet Gynecol 2016;215:B16–24
Nov 20, 2022 | Posted by in ANESTHESIA | Comments Off on 41: Obstetric Emergencies
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