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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