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
Delivery room
Operating room
Intensive Care Unit
Post Anesthesia
Care Unit
The cause of preeclampsia is unknown
Primary placental causes
Secondary maternal systemic illness
Ill-defined links between the two (maternal
systemic inflammatory response?)


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
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


Low cardiac filling pressures (CVP, PCWP),
decreased plasma volume
Vasoconstriction - increased SVR
Low cardiac output
Tissue oxygen extraction impaired
Inadequate oxygen delivery
and consumption
Inadequate cellular oxygenation
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
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
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
Fetal complications of severe preeclampsia
Intrauterine growth retardation
Premature delivery
Abruptio placentae
Fetal distress/fetal demise
Associated maternal risks
General/regional anesthesia
DIC
Hemorrhage
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)

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
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
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)

Cardiac failure?

Untreated preeclamptic women almost always
have low filling pressures and a hyperdynamic
circulation


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

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


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

Lancet 1995: 345: 1455-1463
Lancet 2002: 359: 1877-1890
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!



Impending eclampsia
Severe preeclampsia with signs of cerebral affection
like visual disturbancies, headache, increased reflexes,
and clonus

BJA 1996: 76: 133-148
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