HYPERTENSIVE DISEASE IN PREGNANCY
Hypertensive disorders complicating pregnancy are common and form one of the deadly triad, along with hemorrhage and infection that result in a large number of maternal deaths.
Classification of Hypertensive disorders complicating pregnancy
Pregnancy induced Hypertension: Hypertension that develops as a consequence of pregnancy and regresses postpartum. Divided into;
1. Hypertension without proteinuria or pathological edema
2. Pre-eclampsia – with proteinuria and/or pathological edema
3. Eclampsia – proteinuria and/or pathological edema along with convulsions
Coincidental hypertension: Chronic underlying hypertension that antecedes pregnancy or persists post partum
Pregnancy-aggravated hypertension: Underlying hypertension worsened by pregnancy
– Superimposed pre-eclampsia
– Superimposed eclampsia
Transient Hypertension: Hypertension which develops after the mid trimester of pregnancy and is characterized by mild elevations of blood pressure that do not compromise the pregnancy. This form of hypertension regresses after delivery (within 12wks), but may return in subsequent gestations.
Major predisposing factors;
familial history of pre-eclampsia or eclampsia
chronic vascular disease
Multipara with multifetal pregnancy or fetal hydrops
. 35 yrs
. Multiparas with vascular disease, including chronic essential hypertension and diabetes, or those with coexisting renal disease
Diagnosis of Pregnancy-induced Hypertension
The diagnosis is made when blood pressure is ≥140/90 mm Hg.
Pre-eclampsia = hypertension plus;
– proteinuria defined as ≥300 mg of urinary protein per 24 hours, or ≥100 mg/dL in at least two random urine specimens collected ≥6 hours apart
– Edema which is pathological and not just dependent; it usually involves the face and hands and persists even after arising. A useful indicator of nondependent edema is that rings have become too tight
– Diastolic BP <100mmHg – Proteinuria – Trace – 1+ – Normal serum creatinine – Minimal liver enzyme elevation Severe pre-eclampsia Systolic ≥ 160mmHg and Diastolic >110mmHg
Persistent proteinuria of ≥3+, or 24-hour urinary excretion of ≥4 g
Epigastric or RUQ pain frequently accompanied by marked elevated serum liver enzymes likely results from hepatocellular necrosis, edema, and ischemia that stretches Glisson’s capsule. It usually is a sign to terminate the pregnancy. The pain presages hepatic infarction and hemorrhage as well as catastrophic rupture of a hepatic subcapsular hematoma especially in older and multiparous women.
Thrombocytopenia (<100*109/L) is characteristic of worsening pre-eclampsia, and probably is caused by microangiopathic hemolysis induced by severe vasospasm. Evidence of gross hemolysis such as hemoglobinemia, hemoglobinuria, or hyperbilirubinemia is indicative of severe disease.
Cardiac dysfunction with pulmonary edema
Fetal growth restriction
Impaired GFR Oliguria <400mL/d Plasma creatinine may rise >1.2mg/dL
Eclampsia is diagnosed when grand mal convulsions appear before, during, or after labor, usually preceded by headache, visual disturbances, or epigastric pain, are precipitated by pregnancy-induced or aggravated hypertension.
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Theories about the Cause of Pregnancy-induced Hypertension
1. Immunological Mechanisms – The risk of pregnancy-induced hypertension is appreciably enhanced in circumstances where formation of blocking antibodies to antigenic sites on the placenta might be impaired. This may arise;
– During immunosuppressive therapy to protect a renal transplant
– Where effective immunization by a previous pregnancy is lacking, as in first pregnancies
– Where the number of antigenic sites provided by the placenta is unusually great compared with the amount of antibody, as with multiple fetuses
2. Genetic Predisposition
3. Dietary Deficiencies – incidence increases with calcium deficiency, obese women, and with pre-pregnancy weight
4. Vasoactive Compounds – Nitric oxide, previously termed endothelium-derived relaxing factor (EDRF), a potent vasodilator whose absence or decreased concentration might play a role in the etiology of pregnancy-induced hypertension. Cigarette smoking has been reported to reduce the incidence of pregnancy-induced hypertension
5. Endothelial Dysfunction – Damaged endothelium activates endothelial cells to promote coagulation, and increases sensitivity to vasopressor agents.
Pathophysiology of pre-eclampsia-eclampsia
Vasospasm – Vascular constriction causes resistance to blood flow and accounts for the development of arterial hypertension. It also exerts a damaging effect on vessels. Angiotensin II causes endothelial cells to contract. These changes lead to endothelial cell damage and interendothelial cell leaks through which blood constituents, including platelets and fibrinogen, are deposited subendothelially. The vascular changes, together with local hypoxia of the surrounding tissues, presumably lead to hemorrhage, necrosis, and other end-organ disturbances that have been observed at times with severe preeclampsia. With this scheme, fibrin deposition is then likely to be prominent, as seen in fatal cases.
Increased Pressor Responses in women with early pre-eclampsia. Roll Over Test/Supine pressor response – A hypertensive response with increased diastolic pressure of at least 20 mm Hg is induced by having the woman especially at 28 to 32 weeks assume the supine position after lying laterally recumbent
Maternal and fetal consequences of pre-eclampsia-eclampsia
a) Maternal consequences
Normal left ventricular filling pressures
High systemic vascular resistances
Hyperdynamic ventricular function
Blood Volume – Hemoconcentration due to vasoconstriction made worse by increased vascular permeability
Decreased plasma clotting factors
Erythrocytes may be so traumatized that they display bizarre shapes and undergo rapid hemolysis
Endocrine Changes – With sodium retention, hypertension, or both, renin secretion by the juxtaglomerular apparatus decreases. Because renin catalyzes the conversion of angiotensinogen to angiotensin I (which is then transformed into angiotensin II by converting enzyme), angiotensin II levels decline, resulting in a decrease in aldosterone secretion.
Fluid and Electrolyte Changes – Commonly, the volume of extracellular fluid in women with severe pre-eclampsia-eclampsia has expanded beyond the normally increased volume that characterizes pregnancy.
The Kidney – renal perfusion and glomerular filtration are reduced
– Plasma uric acid concentration is typically elevated
– Plasma creatinine may be elevated two to three times over nonpregnant normal values due to a reduction in plasma clearance
– Proteinuria develops late in pregnancy
– Anatomical Changes – glomerular capillary endotheliosis – the glomeruli were enlarged with glomerular capillary endothelial swelling, and subendothelial deposits of fibrillary protein material
– Acute renal failure characterized clinically by oliguria or anuria and rapidly developing azotemia develops from;
tubular necrosis – it is invariably induced by hypovolemic shock, usually associated with hemorrhage at delivery, for which adequate blood replacement is not given
renal cortical necrosis develops when the major portion of the cortex of both kidneys undergoes necrosis
The Liver – Periportal hemorrhagic necrosis in the periphery of the liver lobule
Bleeding from these lesions may cause hepatic rupture or they may extend beneath the hepatic capsule and form a subcapsular hematoma
– HELLP Syndrome. Liver involvement in pre-eclampsia- eclampsia is serious and is frequently accompanied by evidence of other organ involvement, especially the kidney and brain, along with hemolysis and thrombocytopenia – Hemolysis, Elevated liver enzymes, and Low Platelets.
The Brain – edema, hyperemia, focal anemia, thrombosis, and hemorrhage
A regular finding was fibrinoid changes in the walls of cerebral vessels. The lesions sometimes appeared to have been present for some time, as judged from the surrounding leukocytic response and hemosiderin-pigmented macrophages. These findings are consistent with the view that prodromal neurological symptoms, visual disturbances and convulsions may be related to these lesions.
It is rare for a woman with eclampsia not to awaken after a seizure. It is also rare for a woman with severe pre-eclampsia to become comatose without an antecedent seizure.
b) Placental effects
Compromised placental perfusion from vasospasm is almost certainly a major culprit in the genesis of increased perinatal morbidity and mortality associated with pre-eclampsia.
c) Fetal effects
The major cause of fetal compromise occurs as a consequence of reduced uteroplacental perfusion.
Prematurity – IUGR
Symptoms of hypertension – headache – often frontal but may be occipital, and is resistant to relief from ordinary analgesics
– Epigastric or right upper quadrant pain – probably due to hepatic ischemia or to stretching of the hepatic capsule, possibly by edema and hemorrhage and may be indicative of imminent convulsions.
– Visual disturbances are also ominous
Diastolic pressure of ≥90 mm Hg that persists
A sudden increase in weight exceeding > 2 pounds in any given week, or 6 pounds in a month due almost entirely to abnormal fluid retention (weight gain of 1 pound per week is normal)
Visible signs of nondependent edema such as swollen eyelids and puffy fingers
Proteinuria almost always develops later than hypertension and usually later than excessive weight gains
Prophylaxis and Early Treatment
Rapid weight gain any time during the latter half of pregnancy – Normally before 20 wks, net weight gain is 2Kg and may even have lost 2-3Kg in early pregnancy due to vomiting and poor appetite; after 20wks, weight increases by ½ Kg/wk
An upward trend in diastolic blood pressure
Early prophylactic treatment with aspirin 75-100mg/d reduces incidence of pre-eclampsia due to selective suppression of thromboxane synthesis by platelets and sparing of endothelial prostacyclin production.
Antioxidants Vitamin C & E
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Basic management objectives for any pregnancy complicated by pregnancy-induced hypertension are;
termination of pregnancy with the least possible trauma to mother and fetus
birth of an infant who subsequently thrives
complete restoration of health to the mother
Manage conservatively until labor commences
Hospital Management -Hospitalization is considered for women with pregnancy-induced hypertension if there is a persistent or worsened elevation in blood pressure or development of proteinuria. With hospitalization, a systematic study should be instituted that includes the following:
A detailed medical examination followed by daily searches for development clinical findings such as headache, visual disturbances, epigastric pain, and rapid weight gain.
Admittance weight monitoring twice weekly thereafter
Admittance analysis for proteinuria and at least every 2 days thereafter
Blood pressure readings with an appropriate-size cuff every 4 hours, except between midnight and morning, unless the midnight pressure has increased
Measurements of plasma creatinine, hematocrit, platelets, and serum liver enzymes, the frequency to be determined by the severity of hypertension
Frequent evaluation of fetal size and amniotic fluid volume by the same experienced examiner and by serial sonography if remote from term Doppler Ultrasound for resistance umbilical artery Biophysical profile weekly fetal kick chart every morning at 8(mother)
The aim of therapy is to maintain BP at about 130/90 mmHg
Sedatives – Phenobarbitone – 30mg TDS
– Valium – 5mg TDS
– These are also anticonvulsants
Vasodilators – Aldomet – 250mg TDS/750mg/d QID
– Hydralazine – 25-50mg/d TDS
CCB – Nifedipine – 20mg BD
No role of diuretics & salt restriction
Severe Pre-eclampsia – cf Eclampsia
Termination of Pregnancy
Delivery is the cure for pre-eclampsia.
Indications for termination of pregnancy;
No fetal growth
Uncontrolled BP despite antihypertensive drug use
Deteriorating maternal condition – Renal, Liver and CNS
Eclampsia is characterized by generalized tonic-clonic convulsions that develop in some women with hypertension induced or aggravated by pregnancy. Coma without convulsions has also been called eclampsia; however, it is better to limit the diagnosis to women with convulsions and to regard fatal non-convulsive cases as due to severe pre-eclampsia.
Antepartum eclampsia – convulsions appear before labor
Intrapartum eclampsia – convulsions appear during labor
Postpartum eclampsia – convulsions appear after labor. Most cases of postpartum eclampsia develop within 24 hours of delivery, but otherwise typical cases are seen up to 10 days postpartum. Other diagnoses should be considered in women with the onset of convulsions > 48 hours postpartum.
a) Pre-eclampsia – Headache, visual disturbance, and epigastric or right upper quadrant pain – precedes the onset of eclamptic convulsions
b) The convulsive movements usually begin about the mouth in the form of facial twitchings. After a few seconds, the entire body becomes rigid in a generalized muscular contraction. The face is distorted, the eyes protrude, the arms are flexed, the hands are clenched, and the legs are inverted. All muscles are now in a state of tonic contraction. This phase may persist for 15 to 20 seconds.
c) Suddenly the jaws begin to open and close violently, and soon after, the eyelids as well. The other facial muscles and then all muscles alternately contract and relax in rapid succession. Foam, often blood tinged, exudes from the mouth. The face is congested and the conjunctivae are injected. This phase, in which the muscles alternately contract and relax, may last about a minute.
d) Gradually, the muscular movements become smaller and less frequent, and finally the woman lies motionless. Throughout the seizure the diaphragm has been fixed, with respiration halted. For a few seconds the woman appears to be dying from respiratory arrest, but just when a fatal outcome seems almost inevitable, she takes a long, deep, stertorous inhalation, and breathing is resumed
e) Occasionally, coma or substantively altered consciousness follows a seizure, or may even accompany pre-eclampsia without convulsions. At least in some cases, this is due to extensive cerebral edema
She will not remember the convulsion or, in all probability, events immediately before and afterward.
Post convulsive complications
Fever of 39°C or more is a very grave sign, because it is probably the consequence of a central nervous system hemorrhage which is more likely in older women with underlying chronic hypertension or rarely may be due to a ruptured berry aneurysm or arteriovenous malformation and may lead to sudden death synchronously with a convulsion or follows shortly thereafter.
Pulmonary edema, which is a grave prognostic sign, may follow eclampsia convulsions. There are at least two sources:
– Aspiration pneumonitis may follow inhalation of gastric contents if simultaneous vomiting accompanies convulsions;
– Cardiac failure may be the result of a combination of severe hypertension and vigorous intravenous fluid administration.
Blindness may follow a seizure, or it may arise spontaneously with pre-eclampsia. There are at least two causes:
– varying degrees of retinal detachment
– Occipital lobe ischemia or infarction
Whether due to cerebral or retinal pathology, the prognosis for return of normal vision is good and usually complete within a week
Rarely, eclampsia is followed by psychosis, and the woman becomes violent. This usually lasts for several days to 2 weeks, but the prognosis for return to normal is good, provided there was no preexisting mental illness.
Other signs and symptoms
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As with severe pre-eclampsia, after delivery;
an increase in urinary output is usually an early sign of improvement
Proteinuria and edema ordinarily disappear within a week
Blood pressure returns to normal within 2 weeks after delivery. The longer hypertension persists postpartum, the more likely that it is the consequence of chronic vascular or renal disease.
Until other causes are excluded, however, all pregnant women with convulsions should be considered to have eclampsia.
ruptured cerebral aneurysm
Control of convulsions with magnesium sulfate, using an intravenously administered loading dose and periodic intramuscular injections standardized in dose and frequency of administration.
Intermittent intravenous injections of hydralazine to lower blood pressure whenever the diastolic pressure is 110 mm Hg or higher.
Avoidance of diuretics and hyperosmotic agents.
Limitation of intravenous fluid administration unless fluid loss is excessive.
Delivery – Emergency CS
A large percentage of women who develop recurrent hypertension during subsequent pregnancies will develop chronic hypertension
Outcome for children of pre-eclamptic mothers is usually good if they are not born hypoxic or acidotic