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In pre-eclampsia: (1) There is an imbalance in different components of prostaglandins - relative or absolute deficiency of vasodilator prostaglandin (PGI2) from vascular endothelium and increased synthesis of thromboxane (TXA2), a potent vasoconstrictor in platelets. (2) There is increased vascular sensitivity to the pressor agent angiotensin-II. Angiotensinase activity is depressed, following proteinuria with elimination of α₂ globulin (see Flowchart 18.1). (3) Nitric oxide: It is synthesized in the vascular endothelium and syncytiotrophoblast from L-arginine. It significantly relaxes vascular smooth muscle, inhibits platelet aggregation and prevents intervillous thrombosis. Deficiency of nitric oxide contributes to the development of hypertension. (4) Endothelin-1 is synthesized by endothelial cells, and it is a potent vasoconstrictor compared to angiotensin-II. Endothelin-1 also contributes to the cause of hypertension. (5) Inflammatory mediators: Cytokines [tumor necrosis factor (TNF-α), interleukins (IL-6) and others] derived from activated leukocytes cause endothelial injury. (6) Abnormal lipid metabolism - results in more oxidative stress. Lipid peroxides, reactive oxygen species (ROS) and superoxide anion radicals - cause endothelial injury and dysfunction. Platelet and neutrophil activation, cytokines, superoxide radical production and endothelial damage are in a vicious cycle. (7) Imbalance of angiogenic and antiangiogenic proteins in placental vascular bed - there is overproduction of two antiangiogenic factors from the trophoblastic tissue. These two antiangiogenic factors are: (a) soluble fms-like tyrosine kinase 1 (SFlt-1) and (b) soluble endoglin. SFlt-1 binds with VEGF and placental-like growth factor (PLGF) and causes endothelial cell dysfunction. (8) Others - mutation of factor V Leiden increases the risk.

Hence pre-eclampsia is characterized by endothelial dysfunction and vasospasm. Endothelial dysfunction is due to oxidative stress and the inflammatory mediators. Vasospasm results from the imbalance of vasodilators (PGI2, nitric oxide) and vasoconstrictors (angiotensin-II, TXA2, endothelin-1). Both are in a vicious cycle.

EDEMA: The cause of excessive accumulation of fluids in the extracellular tissue spaces is not clear. Probable explanations are: Increased oxidative stress → endothelial injury → increased capillary permeability. On this basis, the leaky capillaries and decreased blood osmotic pressure are the probable explanations.

PROTEINURIA: The probable chain of events is as follows. Spasm of the afferent glomerular arterioles → anoxic change to the endothelium of the glomerular tuft → glomerular endotheliosis → increased capillary permeability → increased leakage of proteins. Tubular reabsorption is simultaneously depressed. Albumin constitutes 50-60% and α-globulin constitutes 10-15% of the total proteins excreted in the urine.

While the question as to why the syndrome occurs still remains unsolved, the pathological changes are well documented, especially in severe pre-eclampsia or in eclampsia.

Uteroplacental bed: There is increased evidences of premature aging of the placenta. Areas of occasional acute red infarcts and white infarcts are visible on the maternal surface of the placenta.

Villi: Syncytial degeneration, increased syncytial knots, basement layer, and proliferative endarteriis are evident in varying degrees.

In pre-eclampsia, the normal endovascular invasion of cytotrophoblast into the spiral arteries fails to occur beyond decidua-myometrial junction (see p. 28). As a result, the musculoelastic media in the myometrial segment remains responsive to vasoconstrictor stimuli resulting in decreased blood flow (see Fig. 3.7). There is acute atherosis of spiral arteries with obliteration of lumen.

Intervillous circulation: The blood flow is impaired to the extent of about one-third, secondary to the changes in the maternal blood vessels. This results in placental changes, anatomical and functional, which are responsible for fetal jeopardy.

Kidney: The changes are conspicuous in the glomerulus which becomes enlarged (glomerular endotheliosis). Endothelial cells swell up and fibrin-like deposits occur in the basement membrane. The lumen may be occluded. Interstitial cells in between the capillaries proliferate. There is associated spasm of the afferent glomerular arterioles. Patchy areas of damage of the tubular epithelium due to anoxia are evident. The net effects are reduced renal blood flow and glomerular filtration rate (25%), and impaired tubular reabsorption or secretory function. Recovery is likely to be complete following delivery. In severe cases, intense anoxia may produce extensive arterial thrombosis leading to bilateral renal cortical necrosis.

Blood vessels: There is intense vasospasm. Circulation in the vasa vasorum is impaired leading to damage of the vascular walls, including the endothelial integrity.

Liver: Periportal hemorrhagic necrosis of the liver occurs due to thrombosis of the arterioles. The necrosis starts at the periphery of the lobule. There may be subcapsular hematoma. Hepatic insufficiency seldom occurs because of the reserve capacity and regenerative ability of liver cells. Liver function tests are specially abnormal in women with HELLP syndrome.

HELLP syndrome: This is an acronym for hemolysis (H), elevated liver (EL) enzymes and low platelet (LP) count (<100,000/mm³). Microangiopathic hemolytic anemia is the hallmark of the triad of HELLP syndrome. This is a rare complication of pre-eclampsia (10-15%). HELLP syndrome may develop even without maternal hypertension. This syndrome is manifested by nausea, vomiting, epigastric or right upper quadrant pain, along with biochemical, and hematological changes. Abnormal peripheral smear (schistocytosis, burr cells) is observed. Parenchymal necrosis of liver causes elevation in hepatic enzymes (AST and ALT >70 IU/L, LDH >600 IU/L) and bilirubin (>1.2 mg/dL). There may be subcapsular hematoma formation (which is diagnosed by CT scan) and abnormal peripheral blood smear. Eventually liver may rupture to cause sudden hypotension, due to hemoperitoneum.

Management: Principles of management are same as that of pre-eclampsia and eclampsia (see p. 214). Antiseizure prophylaxis with magnesium sulfate (see p. 221) is started. Careful assessment of maternal and fetal status followed by delivery is done. Administration of corticosteroids (see p. 296) improves perinatal (↑ pulmonary maturity, ↓ IVH and ↓ necrotizing enterocolitis) and maternal (↑ thrombocyte count, ↑ urinary output) outcome. Cesarean section is the common mode of delivery. Epidural anesthesia can be used safely if the platelet count is >1,00,000/mm³. Platelet transfusion should be given if the count is <50,000/mm³. Patient should be managed in an ICU until there is improvement in platelet count, urine output, BP and liver enzymes. Recurrence risk of HELLP syndrome is 3-19%.

Expectant management has been carried out selectively when pregnancy is less than 34 weeks, with bed rest, plasma volume expansion (infusion of 5-25% albumin), antithrombotic agents (dipyridamole), immunosuppressive agents (steroids) and others (fresh frozen plasma). In HELLP syndrome perinatal mortality ranges between 5 and 60% and maternal mortality may be up to 25%.

Complications: Maternal: Abruptio placenta, DIC, acute renal failure, severe ascites, pulmonary edema, pleural effusions, cerebral edema, laryngeal edema, retinal detachment, subcapsular liver hematoma, ARDS, sepsis and death. Perinatal: Morbidity and mortality are significantly increased. This is due to preterm delivery, prematurity, RDS and sepsis (see p. 429).

Posterior reversible encephalopathy syndrome presents (occipital and posterior parietal lobes) reversible encephalopathy syndrome (PRES) is a transient neuroradiological entity characterized by the features of hypertension, generalized seizures, altered mental status, headache and vision changes. The hallmark of diagnosis is bilateral symmetrical vasogenic edema in the occipital and posterior parietal lobes. It is evident on T2-weighted MRI images.

Underlying pathology is thought to be cerebral edema and vasospasm of cerebral and retinal vessels. PRES is usually reversible with prompt diagnosis and treatment. Rarely, it may lead to cortical infarction and irreversible ischemic damage and even death.

Neuroradiologic imaging should be done in a patient with persistent headache, hypertension, seizures or visual changes (blindness) even in the postpartum period.

Heart: Subendothelial hemorrhages may occur. Focal necrosis and hemorrhage in the myocardium may affect the conducting system leading to heart failure.

Lungs: There is evidence of edema or hemorrhage from chylous pneumonia and ARDS. This is due to low oncotic pressure.

Brain: Neuroimaging (CT, MRI) studies revealed: thrombosis areas in the cortex, cerebral edema, capillary thrombosis, infarction, and necrosis. Clinical manifestations of headache, scotomas, blindness, convulsions are due to PRES (Fig. 18.1).