It is impossible to resuscitate a pre-eclamptic woman without proper knowledge of the underlying pathophysiology.
Whereas all hypertensive disorders in pregnancy (pre-eclampsia, essential hypertension, 'secondary' hypertension) share high blood pressure as a common theme (probably mediated by inappropriate vasoconstriction), pre-eclampsia is the only disorder with multisystem abnormalities (1).
The triad of physiological derangements in pre-eclampsia is:
1. Intense vasospasm,
2. Local or disseminated intravascular coagulation,
3. Plasma volume contraction.
Although the cause of pre-eclampsia is unknown the placenta appears to be the culprit - delivery of the placenta is the only known cure and the disorder is more frequent with large placental mass, eg. twins (2), or abnormal placentae (3). Current hypotheses propose release of a toxic factor from the placenta which alters maternal endothelial cell functions (4), though this is unproven.
Vasospasm follows due to excess production or sensitivity to vasoconstrictors (angiotensin II, serotonin and endothelin are the most popular candidates) and/or decreased production or sensitivity to vasodilators (prostacyclin and nitric oxide are the current candidates here). This issue is by no means resolved.
Intravascular coagulation is associated with platelet activation (5), thrombocytopenia and, often, reduced production of anti-thrombin III (6).
Plasma volume contraction follows vasospasm, capillary leakage (7) and, in more severe cases, reduction in plasma oncotic pressures (8). There is redistribution of fluid from the intravascular to interstitial fluid spaces so that total extracellular fluid volume remains unaltered (9). These are important considerations as intravascular volume correction may result in pulmonary oedema when capillary permeability is high and plasma oncotic pressure low.
The net result of this triad of abnormal physiology is organ hypoperfusion. Systems most commonly affected are the kidney (manifested by reduced GFR, proteinuria, hyperuricaemia and occasionally oliguria), the liver (manifested by elevated aspartate transaminase with or without epigastric and right upper quadrant pain), the brain (manifested most commonly by transient visual scotomata due to occipital lobe ischaemia, severe headaches and rarely convulsions, ie. eclampsia) and the placenta (manifested by intrauterine fetal growth retardation and less commonly placental abruption (Table E.3) or fetal death in utero). Peripheral oedema is common but is not a useful clinical sign; pulmonary oedema is rare and when it occurs is usually iatrogenic.
References:
1. Brown MA, Pregnancy induced hypertension: pathogenesis and management. Aust. NZ J Med. 1991; 21: 257-273.
2. Long PA, Oats JN. Pre-eclampsia in twin pregnancy -severity and pathogenesis. Aust. NZ Obstet Gynecol. 1987; 27: 1-5.
3. Newman RB, Eddy GL. Association of eclampsia and hydatidiform mole. Obstet Gynecol Survey. 1988; 43: 185-190.
4. Roberts JM, Redman CWG. Pre-eclampsia: more than pregnancy -induced hypertension. Lancet. 1993; 341: 1447-1450.
6. Horn EH. Platelets in normal and hypertensive pregnancy. Platelets. 1991; 2:183-195.