Cause: Unknown; genetic component, incid incr × 2 if maternal or paternal h/o preeclampsia (Nejm 2001;344:867)
Pathophys:
(Nejm 1996;335:1480) Multifactorial
Sympathetic vasoconstrictor hyperactivity that abates w delivery (Nejm 1996;335:1480)
Normally, pregnancy induces a decrease in peripheral vascular resistance mediated by increased resistance to angiotensin; somehow this effect is lost via a trophoblast-dependent process w platelet dysfunction (Nejm 1990;323:478). Vasodilating prostacyclin (PGI2) level suppression present even in 1st trimester (Jama 1999;282:356)
CNS sx assoc w reversible brain edema and leukoencephalopathy, also seen in immunocompromised and renal failure pts (Nejm 1996;334:494)
Incidence 4-6% in primips who represent 85% of all pts with PIH/eclampsia, 1.8% in subsequent pregnancies, though risk gradually returns to primip rate as interval between pregnancies incr to 10 yr; not correlated w partner change (Nejm 2002;346:33); 25% in patients with chronic hypertension (Nejm 1998;339:667). 2nd most common cause of maternal deaths after pulmonary embolus, causes 15%
Sx: Pregnant, weight gain, edema, headache, *visual changes,*acute onset, abdominal pain, *esp epigastric
Si:
300 mg/24 h or 1+ proteinuriaAll sx disappear (in 95%) by 72 h postpartum; a small percentage may persist for weeks. If occurs in 1st trimester, must be mole or trophoblastic tumor. Risk of end-stage renal disease decades later is incr by 4-6× (Nejm 2008;359:800)
Preeclampsia: HT + proteinuria after 20-wk gestation, most in 3rd trimester; associated when severe but short of eclampsia, w a 1% maternal and 10% prenatal infant mortality; when severe evolves to eclampsia, without rx, in 25-50%
Eclampsia (toxemia; defined by seizures) risk increased by each* finding by hx, pe and lab noted: renal failure; CHF; CNS bleed; DIC; Sheehan's syndrome; fetal demise; hepatic hemorrhage and rupture (Nejm 1985;312:424); HELLP syndrome (HELLP Syndrome (Hemolysis, Elevated Liver Function Tests, Low Platelets)); newborn neutropenias, transient in 50%, associated with sepsis (Nejm 1989;321:557)
Fetal growth retardation
r/o other causes of hypertension in pregnancy: pheochromocytoma; more benign TRANSIENT HYPERTENSION OF PREGNANCY; and chronic hypertension in pregnancy
Lab:
Chem:Uric acid elevated; creatinine elevations*; eventually perhaps measurements of anti-angiogenic factors like tyrosine kinase and placental growth factor (Nejm 2006;355:992, 1056; 2004;350:672) to predict women at high risk, urinary placental growth factor levels significantly low 4-8 wk before onset (Jama 2005;293:77)
Hem:Hemolytic anemia*and thrombocytopenia*which may be mild; platelet intracellular calcium markedly elevated by vasopressin in susceptibles (Nejm 1990;323:434); polycythemia indicating hypovolemia
Path: Renal, bx or at postmortem shows ATN, occasionally bilateral cortical necrosis, swollen glomerular endothelial cells with fibrin in them. Placenta shows spotty necrosis with small vessel disease
Urine: 24 h protein >300 mg, may be >2 gm*; creatinine clearance decreased (normally in pregnancy is 100-150 cc/min). 24-h calcium <100-150 mg, unlike benign hypertensives who excrete more calcium
Rx:
Preventive w: ASA 60-100 mg po qd by wk 12? (Bmj 2000;322:329 vs Nejm 1998;338:701); not vit C or vit E (Nejm 2006;354:1796); calcium (Nejm 1997;337:69 vs 1991;325:1399)
of HT during pregnancy (Can Med Assoc J 1997;157:1245): 
-Methyldopa (Aldomet) alone; or propranolol (Nejm 1981;305:1323); or -methyldopa + hydralazine; or clonidine + hydralazine (Med J Aust 1991;154:378). But rx of PIH, unless severe, does not improve outcome. Avoid ACEIs, which are teratogenic (Jama 1997;277:1193) even in first trimester (Nejm 2006;354:2443)
of preeclampsia (Can Med Assoc J 1997;157:1245): bed rest; deliver when fetus mature or if severe, even if fetus not mature; hospitalize for failure of home bed rest, diastolic BP 110, or proteinuria 2+ by dip or 500 mg/24 h; avoid diuretics and salt restriction; hydralazine 5-10 mg q20min iv to get diastolic BP <105; or labetolol 10-20 mg iv q10min; or perhaps nifedipine 10 mg sl then po q 6 h (Obgyn 1991;77:331); follow with po hydralazine, -methyldopa, or 
-blockers. Rx does not improve fetal outcome but does protect maternal CNS (Am J Obgyn 1990;162:960)
of eclampsia (seizures): stabilize, then deliver within 4-5 h of onset, may need D+C to get rid of all placenta; MgSO4 if inducing for preeclampsia; give 4 gm iv over 20 min, then 2 gm/h iv, or can give im, eg, 10-gm load then 5 gm q 4 h (Nejm 1995;333:201); follow Mg levels, 5-7 mg/cc is therapeutic range; continue 12-24 h postpartum; unknown mechanism of action but better than all other drug options (Nejm 2003;348:275, 304); may cause fatal newborn respiratory depression, helped by iv calcium gluconate gm for gm