Critical Care Medicine Unique to Pregnancy

Timothy P. Rich, M.D.

Pulmonary, Critical Care & Sleep Medicine

Outline

Epidemiology of obstetric critical careSorting out critical illness in pregnancyCritical illness unique to pregnancy– Preeclampsia and Eclampsia– HELLP Syndrome– Amniotic Fluid Embolism– Acute Fatty Liver of Pregnancy– Tocolytic-Induced ARDS

Important reminders

Incidence of Obstetric Critical Illness

Obstetrician’s perspective– 0.2 - 0.5% of deliveries require ICU

Intensivist’s perspective– ~2% of ICU admissions– ~80% are post-partum– ~50-70% require mechanical ventilation

Lapinsky SE, 2008

All very rare…

… all very serious …

… all very scary!

Sorting Out Critical Illness in the Pregnant Patient

Non-specific to pregnancy– Trauma, non-obstetric infections, etc

Aggravated by pregnancy– Gastric acid aspiration– Venous thromboembolism– Cardiopulmonary disease (PHTN, CF, Tx)– Connective tissue disease (SLE)– Diabetes

Sorting Out Critical Illness in the Pregnant Patient

Unique to pregnancy– Preeclampsia – Eclampsia– HELLP Syndrome– Amniotic Fluid Embolism– Acute Fatty Liver of Pregnancy– Tocolytic-Induced Pulmonary Edema

Preeclampsia / Eclampsia

Eclampsia was first described ~500 BC by Greek physician, Coan Prognosis Triad: HTN, proteinuria, edema >20 wksEclampsia: addition of seizure and coma

Risk factors: vascular insufficiency, preexisting HTN, renal disease, DM, lupus, antiphospholipid syndrome, BMI, multiple gestation, hydatidiform mole.

Preeclampsia/EclampsiaEpidemiology

3% of pregnancies.26 per 1000 prevalence

5-7% recurrence rate

Preeclampsia / EclampsiaPathophysiology

Unknown– Abnormal utero-placental circulation– Endothelial dysfunction (e.g., PGI2, NO)– Vasospasm– Microthrombi– Sympathetic over-activity– Immunologic dysfunction– Genetic predisposition– Many, many, many more theories…

Hypertrophic decidual vasculopathy of maternal vessels perfusing the placenta.

Preeclampsia

Preeclampsia/EclampsiaManagement

Temporizing Treatment– Anti-hypertensives- labetolol, hydralzine, nifedipine

– Magnesium sulfate to forestall seizures– Corticosteroids for fetal lung development

Definitive Treatment– Delivery of baby

Note: Post-partum preeclampsia may be ignored as simple post-delivery headache and edema.

HELLP Syndrome

Described in 1982 by Louis WeinsteinTriad: hemolysis, elevated LFT’s, low Plts

Risk factors: – 3rd trimester,– preeclampsia

Symptoms:– 90% Malaise– 65% Upper abdomen “band pain”– 30% Nausea and emesis

HELLP SyndromeEpidemiology

Incidence- 0.2 to 0.6% of all pregnancies10-20% of comorbid preeclampsia

Maternal mortality 1% with treatment

HELLP SyndromePathophsiology

Unknown:– Activation of coagulation cascade– Fibrin cross-linking of small blood vessels– Microangiopathic hemolytic anemia– Destruction of RBC’s… anemia– Platelet consumption… thrombocytopenia– Hepatic periportal necrosis… + LFTs– DIC-variant coagulopathy

HELLP SyndromeTreatment

Temporizing Management:– RBC for anemia– Platelets for thrombocytopenia– FFP for DIC-variant coagulopathy

– Anti-hypertensives (labetolol, hydralazine, nifedipine)

– Corticosteroids for inflammmation

Definitive Management:– Delivery of the baby

Amniotic Fluid Embolism

Described in 1941 by Steiner & Luschbaugh

Note: amniotic fluid components are commonly present in maternal circulation.

Triad: hypoxia, hypotension, coagulopathy

Amniotic Fluid Embolism Epidemiology

1:20,000 deliveries (1:8,000 to 1:80,000)65% with AFE present before delivery50% of first-hour deaths from hypoxia, shock70% develop ARDS80% develop DICMortality- 60%-86%

Amniotic Fluid EmbolismPathophysiology

Amniotic fluid, fetal cells, hair, etc, enter maternal venous circulation via the placental bed of the uterus.Risk factors: – Rupture of amniotic sac– Rupture of uterine or cervical vein– Pressure gradient from uterus-to-vein– Uterine manipulation, abdomen trauma (?)– Use of misoprostol for labor induction (?)

Intravascular fetal squames present

Amniotic Fluid Embolism

Amniotic Fluid EmbolismPathophysiology

Two Effects-– Mechanical obstruction – minor

Pulmonary arterial vascular obstruction– Acute pulmonary HTN , RV failure and hypoxemia

– Anaphylactoid reaction – majorHumoral, systemic response

– Leukotrienes, endothelin, IL-1, TNF-alpha, PG, collagen, tissue factor III, thromboxane A2, etc

DIC and hemorrhageBiventricular failure and hypotension

Amniotic Fluid Embolism Management

Temporizing treatment– Intubation, mechanical ventilation

ARDS Protective Lung Protocol

– PA catheter (rather than CVP monitor)STAT echocardiogramInotropic support

Definitive treatment– Delivery by Caesarean section decreases

fetal mortality

Acute Fatty Liver of Pregnancy

Described in 1941 by H.L Sheehan– “acute yellow atrophy of the liver”

Triad: abdomen pain, anorexia, jaundiceRisk factors:– Late 3rd trimester with clinical triad– Moderately elevated LFTs (e.g., 300-600)

Acute Fatty Liver of PregnancyEpidemiology

1:7000 to 1:15,000 pregnanciesOlder literature-– fulminant hepatic failure… high mortality

Recent literature-– early recognition… lower mortality

Maternal mortality 18%Fetus mortality 23-47%

Acute Fatty Liver of PregnancyPathophysiology

Maternal mitochondrial fatty acid metabolism disorder

LCHAD Deficiency: long-chain 3-hydroxyacyl-coenzyme A dehydrogenase

Deficiency leads to accumulation of medium and long chain FA in the fetus which re-enters the maternal circulation overwhelming the beta-oxidation enzymes

Acute fatty Liver of Pregnancy

23yo female, 34-wks gestation with “acute yellow atrophy”.

23yo female 34wks gestation with microvesicular steatosis… liver tx.

Acute fatty Liver of Pregnancy

Acute Fatty Liver of Pregnancy Genetics

LCHAD gene has been isolatedMissense mutation- E474Q

Autosomal recessive inheritanceMaternal heterozygous for mutation

Acute Fatty Liver of Pregnancy Treatment

Temporizing management– Consider a liver biopsy (r/o viral hepatitis)– Supportive care

Definitive management– Delivery… stress of FA overload is removed– May require a liver transplant

Tocolytic -InducedPulmonary Edema

Described in 1988 by Milos and Pisani

Beta-adrenergic agonists used to arrest premature contractions.

Tocolytics increase intracellular cAMP, thus relaxing smooth muscleTriad: hypoxemia, infiltrates, normotensiveRisk factors: – recent (<24hrs) or current po/IV tocolytic therapy

Tocolytic-Induced Pulmonary EdemaEpidemiology

Incidence 0-4.4% <24-hrs after useMortality < 5%

Tocolytic-Induced Pulmonary EdemaPathophsiology

Noncardiac > Cardiac etiology– Beta-adrenergic agonist activity– Increased ADH and renin release– Enhanced Na+ and water resorption– Volume overload– Increased hydrostatic pressure

In the setting of lower oncotic pressureUnlikely direct toxic effect or increased permeability

Pisani RJ, Ann Intern Med 1989, May 1; 110(9): 714-8La Chapelle A, A&A 2002, June; 94(6):1593-1594

Tocolytic-Induced Pulmonary EdemaTreatment

Temporizing Management– Ventilatory support:

CPAP Intubation and ventilation

– Gentle diuresis and fluid restriction

Definitive Management– Discontinue tocolytic medication

All very rare…

… all very serious…

… all very scary…

… but remember…

Critical Care is a Team Sport

Intensivist-PulmonologistCritical Care Nurse PractitionersCritical Care Registered NursesCritical Care PharmacistsRespiratory TherapistsNutrition ServicesSocial Work, Chaplaincy

Important Reminders

Eternal vigilanceKeep your differential broad

Use the “triads” for pattern recognitionManage the patient in the ICUAnd remember you are not alone…Consult– Intensivist, Cardiology, Pulmonary,

Gastroenterology, etc

Thank you