Vascular involvement
The maternal endothelium is thought to be an important target of the placental-released factors hypothesized to drive pre-eclampsia[197].
Endothelial dysfunction can lead to reduced blood flow to organs such as the heart and kidney[133] and reduced venous blood drainage and associated venous congestion.
This contributes to organ dysfunction and can induce reflex constriction of arteries[199].
It is hypothesized that the endothelial dysfunction driven by placental-released factors initiates and drives hypertension in pre-eclampsia.
Machine learning approaches using biochemical data retrieved from electronic medical records from 11,006 women at 14–17 to 34 weeks of gestation have been documented to predict late-onset pre-eclampsia early in the second trimester[92], suggesting that early pregnancy placental vascular impairment occurs in late-onset pre-eclampsia
Pulmonary oedema
Characterized by excessive fluid accumulation in the lungs, pulmonary oedema is a rare, acute, life-threatening condition, primarily associated with severe pre-eclampsia[201,202].
Pulmonary oedema is the second most common cause of death in pregnancies complicated by hypertension[203].
There are multiple causes of pulmonary oedema, including decreased oncotic pressure, increased capillary permeability, increased hydrostatic pressure and diastolic dysfunction.
Antihypertensive medications and excessive fluid administration are risk factors for pulmonary oedema[204].
Pulmonary oedema is most common (39%) postpartum[204], when fluid sequestered in the extravascular space is mobilized into the vascular space, increasing central venous and pulmonary capillary wedge pressure
Renal involvement
The kidney is the organ most likely to be affected by endothelial injury in pre-eclampsia[198].
Renal biopsies of women with pre-eclampsia show glomerular endotheliosis that seems to be responsible for the decreased glomerular filtration rate noted in pre-eclampsia[205].
The characteristic proteinuria in pre-eclampsia is caused by high concentrations of sFLT1 inhibiting the expression of proteins of the podocyte slit diaphragm, such as synaptopodin and nephrin[206], which increases inter-podocyte separation.
The lack of vascular endothelial growth factor (VEGF) and PGF availability in the glomerular endothelium stimulates endothelin 1 expression that promotes podocyte detachment[207]
Liver involvement
Liver damage in pre-eclampsia is characterized by periportal inflammation and hepatocellular damage, subcapsular haematoma and, in rare cases, hepatic failure or rupture[208].
Widespread microangiopathy causes vasospasm of hepatic sinusoids and promotes fibrin deposition in the microcirculation[209], leading to ischaemia.
Hepatic endothelial cells are highly dependent on VEGF, and its antagonism with sFLT1 significantly alters their function given the decreased availability of nitric oxide[210].
The resulting ischaemia causes oxidative stress and inflammation that affect hepatic acini, elevating the concentration of liver enzymes in blood and contributing to the onset of HELLP syndrome.
HELLP syndrome encompasses microangiopathic haemolysis, elevation of liver enzymes and thrombocytopenia.
The most common symptoms in affected patients are right-upper quadrant pain, epigastralgia, nausea and vomiting, headache and visual changes.
In severe cases, to disseminated intravascular coagulation corroborates the worsening of the case and is diagnosed by decreased levels of fibrinogen, antithrombin, and increased prothrombin time and fibrin[212]
Neurological involvement
Neurological symptoms have been recognized as high-risk features of eclampsia for thousands of years[213].
Neurological complications are the direct cause of many maternal deaths due to pre-eclampsia, in LMICs, and include eclampsia, visual scotomata, cortical blindness, arterial ischaemic stroke, cerebral venous sinus thrombosis, subarachnoid and intracerebral haemorrhage, reversible cerebral vasoconstriction syndrome, and posterior reversible encephalopathy syndrome[213,214].
Reversible cerebral vasoconstriction syndrome and posterior reversible encephalopathy syndrome occur most commonly in the postpartum period and often with little warning[215].
The mechanisms leading to neurological complications are being uncovered; the maternal cerebral vasculature is highly sensitive to pre-eclampsia[215].
Neurovascular dysfunction is clear in pre-eclampsia, with studies showing increased sympathetic activity of the autonomic nervous system[213,216], impaired cerebral autoregulation, increased blood–brain barrier permeability[132], and vasogenic oedema, with cerebral markers, including neurofilament light chain, being dysregulated in pre-eclamptic cerebrospinal fluid, serum and plasma[218]
Fetal growth restriction
FGR occurs mainly due to placental dysfunction and is highly associated with preterm pre-eclampsia[219,220,221,222].
The ISSHP guidelines[2,13] specify that pre-eclampsia can be diagnosed after 20 weeks of gestation by new-onset hypertension in a patient previously with normotension plus one other pre-eclampsia-related symptom or sign
These can include proteinuria, acute kidney injury, liver involvement, neurological symptoms, haematological abnormalities (thrombocytopenia, disseminated intravascular coagulation, haemolysis), cardiorespiratory complications or uteroplacental dysfunction (FGR, angiogenic imbalance, placental abruption).
This new set of diagnostic criteria published in 2014 and revised in 2018 and 2021, represents a significant change compared with the previous recommendations published in 2001, which required the presence of proteinuria and new-onset hypertension in a patient with previous normotension.
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Clinical Signs and Symptoms