1 / 30

Critical care management of preeclampsia and eclampsia

Critical care management of preeclampsia and eclampsia. Gunnar Dahlgren, MD, PhD Department of Anesthesia and Intensive Care Karolinska University Hospital Stockholm. gunnar.dahlgren@karolinska.se. The obstetric ICU patient. Intensive Care Unit. Delivery room. Post Anesthesia Care Unit.

alpha
Download Presentation

Critical care management of preeclampsia and eclampsia

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Critical care management of preeclampsia and eclampsia Gunnar Dahlgren, MD, PhD Department of Anesthesia and Intensive Care Karolinska University Hospital Stockholm gunnar.dahlgren@karolinska.se

  2. The obstetric ICU patient Intensive Care Unit Delivery room Post Anesthesia Care Unit Operating room

  3. The cause of preeclampsia is unknown • Primary placental causes • Secondary maternal systemic illness • Ill-defined links between the two (maternal systemic inflammatory response?)

  4. Primary changes in the vasculature • Impaired endothelial production of prostacylin, and possibly NO • Release of platelet-derived factors as thromboxane and serotonin • Release of endothelial procoagulant factors Vasoconstriction Low grade DIC

  5. Pathology • Placenta: Spiral arteries fail to undergo physiological dilatation and show luminal disease similar to acute atherosis in non-pregnant patients • Kidney: Glomerular capillary endotheliosus. Might progress to ATN or acute cortical necrosis • Placenta, kidney, brain, and liver show features consistent with chronic ischemia

  6. Inadequate cellular oxygenation • Low cardiac filling pressures (CVP, PCWP), decreased plasma volume • Vasoconstriction - increased SVR • Low cardiac output • Tissue oxygen extraction impaired Inadequate oxygen delivery and consumption

  7. Hypertension in pregnancy • Pre-existing hypertension (3-5% of pregnancies) • Pregnancy-associated hypertension (12%) (occurring de novo after the 20th week of pregnancy and settling within 6 weeks after delivery) • Gestational hypertension (6-7%) • Preeclampsia (5-6%) • Superimposed preeclampsia (25% of women with pre-existing hypertension) Lancet 2000: 356: 1260-1265

  8. Preeclampsia/eclampsia definitions • Preeclampsia: Hypertension >140/90 with proteinuria of at least 0.3g/24h • Severe preeclampsia: Preeclampsia with hypertension >160/110 or proteinuria >5g/24h or multiorgan involvement • Eclampsia: Convulsions in any woman who has, or then presents with, hypertension in pregnancy of any cause

  9. Symptoms other than hypertension and proteinuria in severe preeclampsia • Oliguria (<400 ml/24h) • Cerebral signs (headache, blurred vision, altered consciousness) • Pulmonary edema, cyanosis • Epigastric or right upper quadrant pain • Impaired liver function • Hepatic rupture • Trombocytopenia • HELLP syndrome

  10. Fetal complications of severe preeclampsia • Intrauterine growth retardation • Premature delivery • Abruptio placentae • Fetal distress/fetal demise Associated maternal risks General/regional anesthesia DIC Hemorrhage

  11. Maternal complications of severe preeclampsia • Cardiovascular dysfunction (cardiac failure, hypertension) • Renal dysfunction (oliguria, reduced GFR, elevated creatinine, acute tubular necrosis, cortical necrosis) • Respiratory dysfunction (ARDS, pulmonary edema) • Hepatic dysfunction (elevated liver enzymes, subcapsular hematoma, HELLP syndrome) • Cerebral dysfunction (encephalopathy, ischemia, cortical blindness, retinal detachment, infarction, hemorrhage, edema, eclampsia)

  12. ”Delivery of the fetus and placenta is the definitive management of severe preeclampsia. Once severe disease has been established and is progressing, delivery of the fetus and placenta must be accomplished to limit maternal risk.” Int Care Med 1997: 23: 248-255

  13. Invasive hemodynamic monitoring • There are no data from randomized controlled clinical studies illustrating the usefulness of PA-catheters or echocardiographic techniques in patients with preeclampsia • Echocardiography shows good agreement with PA-catheter measurements of cardiac output • CVP may be misleading and needs cautious interpretation, particularly in patients treated with vasoactive agents or plasma volume augmentation • Invasive monitoring could still be considered in patients with persistant oliguria, pulmonary edema and significant blood loss in order to guide therapy Best Pract Res Clin Obst Gyn 2001: 15: 605-622

  14. Maternal complications of severe preeclampsia • Cardiovascular dysfunction (cardiac failure, hypertension) • Renal dysfunction (oliguria, reduced GFR, elevated creatinine, acute tubular necrosis, cortical necrosis) • Respiratory dysfunction (ARDS, pulmonary edema) • Hepatic dysfunction (elevated liver enzymes, subcapsular hematoma, HELLP syndrome) • Cerebral dysfunction (encephalopathy, ischemia, cortical blindness, retinal detachment, infarction, hemorrhage, eclampsia)

  15. Cardiac failure? • Untreated preeclamptic women almost always have low filling pressures and a hyperdynamic circulation

  16. Untreated pre-eclampsia Best Pract Res Clin Obst Gyn 2001: 15: 605-622

  17. Cardiac failure? • Untreated preeclamptic women almost always have low filling pressures and a hyperdynamic circulation • The situation in treated preeclamptic patients is more variable and unpredictable

  18. Treated pre-eclampsia Best Pract Res Clin Obst Gyn 2001: 15: 605-622

  19. Cardiac failure? • Untreated preeclamptic women almost always have low filling pressures and a hyperdynamic circulation • The situation in treated preeclamptic patients is more variable and unpredictable • In patients with pulmonary edema a significant part of the women has a depressed cardiac performance

  20. Pulmonary edema Best Pract Res Clin Obst Gyn 2001: 15: 605-622

  21. Cardiac failure? • Untreated preeclamptic women almost always have low filling pressures and a hyperdynamic circulation • The situation in treated preeclamptic patients is more variable and unpredictable • In patients with pulmonary edema a significant part of the women has a depressed cardiac performance • Diastolic dysfunction, estimated with echocardiography, is not uncommon in preeclamptic patients with pulmonary edema • There is an association between preeclampsia and peripartem cardiomyopathy

  22. Hypertension • Untreated severe hypertension increases the risk for cerebral hemorrhage, renal/liver dysfunction, pulmonary congestion, decreased placental perfusion, placental detachment • Treatment indicated in severe hypertension • Hydralazine less effective than nifedipine and equally effective as labetalol for reducing blood pressure* • Side-effects (eg maternal hypotension, placental abruption, cesarean section) more frequent with hydralazine than with labetalol and nifedipine* * BMJ 2003: 327: 955-964

  23. Oliguria • Decreased plasma volume • Decreased renal perfusion and glomerular filtration • Pre-renal oliguria may develop to acute tubular necrosis, most often with a good prognosis • Acute cortical necrosis is rare; poor prognosis Diuresis <100 ml/4h Plasma volume expansion if CVP is <5 mmHg Furosemide if fluid balance is positive Echocardiography PA catheter to optimize left ventricular preload (PCWP 12-14 mmHg) and reduce afterload appropriately

  24. Pulmonary edema • Incidence 6% in severe preeclampsia • Reduced COP (from 22 in normotensive patients at term to 15 mmHg in severe preeclampsia), a further reduction in COP after delivery. • A COP-PCWP difference of 4 mmHg or less is associated with pulmonary edema in critically ill non-pregnant patients (Chest 1977: 72: 709) • Increased capillary permeability • Possible left ventricular dysfunction (systolic and/or diastolic) • Increased risk during the first day(s) post partem

  25. HELLP syndrome • Microangiopathic hemolytic anemia, consumptive thrombocytopenia, liver dysfunction • 4-12% of patients with severe preeclampsia, 30% occur postpartum • DIC often secondary to placental abruption, sepsis or fetal death • Platelet count indirectly proportional to severity of disease • Differential diagnoses: TTP, HUS, SLE, sepsis, acute fatty liver of pregnancy • Complications: ARF, ARDS, hemorrhage, placental abruption, rarely liver hematoma with rupture

  26. Lancet 1995: 345: 1455-1463

  27. Lancet 2002: 359: 1877-1890

  28. Eclampsia • The treatment of choice for eclampsia and prophylaxis against recurrent convulsions is magnesium sulphate (Lancet 1995: 345: 1456-1463) • Magnesium sulphate is also the drug of choice for seizure prophylaxis in patients with preeclampsia (Lancet 2002: 359: 1877-1890) • Prophylaxis in patients with preeclampsia is however in many departments limited to patients with severe preeclampsia or impending eclampsia • Stabilize maternal condition before vaginal or cesarean delivery!

  29. Impending eclampsia Severe preeclampsia with signs of cerebral affection like visual disturbancies, headache, increased reflexes, and clonus BJA 1996: 76: 133-148

  30. Summary • Preeclampsia is a syndrome of unknown etiology with multiorgan involvement • It presents with a wide spectrum of symptoms • It is sometimes difficult to distinguish from other systemic diseases • Severe cases may progress to MOF and death • Delivery of the child and placenta is the only specific treatment – other lines of teatment are only supportive • There are several issues regarding diagnostic techniques and treatment options that need further evaluation

More Related