Hypertensive Disorders of Pregnancy

Chapter 14 Hypertensive Disorders of Pregnancy


Hypertension is the commonest medical condition encountered in pregnancy, complicating approximately 5% of all pregnancies; it is a significant cause of maternal and fetal/neonatal morbidity and mortality. Pregnancy may induce hypertension in women who have been normotensive prior to pregnancy, or may aggravate existing hypertensive conditions.



Definition and classification


The definition and classification of the hypertensive disorders are complex (Box 14.1). It is important to recognise the distinction between:



image a woman whose hypertension antedates pregnancy (pre-existing or chronic hypertension)


image a woman who develops an increased blood pressure during pregnancy (new, gestational or pregnancy-induced hypertension).



Box 14.1 Classification and definition of hypertensive disorders in pregnancy



Chronic hypertension




• Hypertension before pregnancy or a diastolic blood pressure of 90 mmHg or more before 20 weeks’ gestation, and persisting 6 weeks after delivery



New, gestational or pregnancy-induced hypertension




• Development of hypertension without other signs of pre-eclampsia


• Diagnosed when, after resting, the woman’s blood pressure rises above 140/90 mmHg, on at least two occasions, no more than 1 week apart after the 20th week of pregnancy in a woman known to be normotensive


• Hypertension diagnosed for the first time in pregnancy, which does not resolve postpartum, is also classified as gestational hypertension



Pre-eclampsia




• Diagnosed on the basis of hypertension with proteinuria, when proteinuria is measured as > 1 + on dipstick or > 0.3 g/L of protein in a random clean catch specimen or an excretion of 0.3 g protein/24 hours


• In the absence of proteinuria, pre-eclampsia is suspected when hypertension is accompanied by symptoms including:


image headache

image blurred vision

image abdominal/epigastric pain, or

image altered biochemistry: specifically, low platelet counts, abnormal liver enzyme levels

• These signs and symptoms, together with blood pressure above 160 mmHg systolic or above 110 mmHg diastolic and proteinuria of 2 + or 3 + on a dipstick, demonstrate the more severe form of the disease



Eclampsia




• The new onset of convulsions during pregnancy or postpartum, unrelated to other cerebral pathological conditions, in a woman with pre-eclampsia



Pre-eclampsia superimposed on chronic hypertension




• This may occur in women with pre-existing hypertension (under 20 weeks’ gestation) who develop:


image new proteinuria (> 0.3 g/24 hours)

image sudden increases in pre-existing hypertension and proteinuria

image thrombocytopenia (platelet count < 100 × 109/L)

image abnormal liver enzymes

An incremental rise in blood pressure is not included in this classification system. However, it is considered that women who have a rise of 30 mmHg systolic or 15 mmHg diastolic blood pressure require close observation especially if proteinuria and hyperuricaemia (raised uric acid level) are also present.



Pathological changes




Blood


Hypertension, together with endothelial cell damage, affects capillary permeability. Plasma proteins leak from the damaged blood vessels, causing a decrease in the plasma colloid pressure and an increase in oedema within the extracellular space. The reduced intravascular plasma volume causes hypovolaemia and haemoconcentration, which is reflected in an elevated haematocrit. In severe cases the lungs become congested with fluid and pulmonary oedema develops, oxygenation is impaired and cyanosis occurs. With vasoconstriction and disruption of the vascular endothelium the coagulation cascade is activated.



Coagulation system


Increased platelet consumption produces thrombocytopenia. Disseminated intravascular coagulation (DIC) is characterized by low platelets and fibrinogen and prolonged prothrombin time. As the process progresses, fibrin and platelets are deposited, which will occlude blood flow to many organs, particularly the kidneys, liver, brain and placenta.



Kidneys


In the kidney, hypertension leads to vasospasm of the afferent arterioles, resulting in a decreased renal blood flow, which produces hypoxia and oedema of the endothelial cells of the glomerular capillaries. Glomeruloendotheliosis (glomerular endothelial damage) allows plasma proteins to filter into the urine, producing proteinuria. Renal damage is reflected by reduced creatinine clearance and increased serum creatinine and uric acid levels. Oliguria develops as the condition worsens, signifying severe and renal vasoconstriction.



Liver


Vasoconstriction of the hepatic vascular bed will result in hypoxia and oedema of the liver cells. In severe cases oedematous swelling of the liver causes epigastric pain and can lead to intracapsular haemorrhages and, in very rare cases, rupture of the liver. Altered liver function is reflected by falling albumin levels and a rise in liver enzyme levels.



Brain


Hypertension, combined with cerebrovascular endothelial dysfunction, increases the permeability of the blood–brain barrier, resulting in cerebral oedema and microhaemorrhaging characterised by the onset of headaches, visual disturbances and convulsions. Where the mean arterial pressure (MAP – i.e. the systolic blood pressure plus twice the diastolic pressure divided by 3) exceeds 125 mmHg, the autoregulation of cerebral flow is disrupted, resulting in cerebral vasospasm, cerebral oedema and blood clot formation. This is known as hypertensive encephalopathy; if left untreated, it can progress to cerebral haemorrhage and death.



Fetoplacental unit


In the uterus, vasoconstriction caused by hypertension reduces the uterine blood flow which can result in placental abruption and placental scarring. The amount of oxygen that diffuses through the cells of the syncytiotrophoblast and cytotrophoblast into the fetal circulation within the placenta is diminished, the placental tissue becomes ischaemic, the capillaries in the chorionic villi thrombose and infarctions occur, leading to fetal growth restriction.



The midwife’s role in assessment and diagnosis


As the hypertensive disorders are unlikely to be prevented, early detection and appropriate management can minimise the severity of the condition. A comprehensive history will identify:



image adverse social circumstances or poverty, which could prevent the woman from attending for regular antenatal care


image the mother’s age and parity


image primipaternity and partner-related factors


image a family history of hypertensive disorders


image a past history of pre-eclampsia


image the presence of underlying medical disorders: for example, renal disease, diabetes, systemic lupus erythematosus (SLE) and thromboembolic disorders.


The two essential features of pre-eclampsia, hypertension and proteinuria, are assessed for at regular intervals throughout pregnancy. Diagnosis is usually based on the rise in blood pressure and the presence of proteinuria after 20 weeks’ gestation.




Blood pressure measurement


The mother’s blood pressure is taken early in pregnancy to compare with all subsequent recordings, taking into account the normal pattern in pregnancy. It is important to consider several factors in assessing blood pressure.



image Blood pressure machines should be calibrated for use in pregnancy and regularly maintained.


image Blood pressure can be overestimated as a result of using a sphygmomanometer cuff of inadequate size relative to the arm circumference. The length of the bladder should be at least 80% of the arm circumference. Two cuffs should be available with inflation bladders of 35 cm for normal use and 42 cm for large arms.


image Rounding off of blood pressure measurements should be avoided and an attempt should be made to record the blood pressure as accurately as possible to the nearest 2 mmHg.


image The use of Korotkoff V (disappearance of sound) as a measure of the diastolic blood pressure has been found to be easier to obtain, more reproducible and closer to the intra-arterial pressure; therefore this reading should be used unless the sound is near zero, in which case Korotkoff IV (muffling sound) should be used instead.



Urinalysis


Proteinuria in the absence of urinary tract infection is indicative of glomerular endotheliosis. The amount of protein in the urine is frequently taken as an index of the severity of pre-eclampsia. A significant increase in proteinuria, coupled with diminished urinary output, indicates renal impairment. A 24-hour urine collection for total protein measurement will be required to be certain about the presence or absence of proteinuria and to provide an accurate quantitative assessment of protein loss.



image A finding of > 300 mg/24 hours is considered to be indicative of mild to moderate pre-eclampsia.


image A finding of > 3 g/24 hours is considered to be severe.



Oedema and excessive weight gain


These are variable findings and nowadays are usually considered only when a diagnosis of pre-eclampsia has been made based on other criteria. The sudden severe widespread appearance of oedema is suggestive of pre-eclampsia or some underlying pathology and further investigations are necessary. This oedema pits on pressure and may be found in non-dependent anatomical areas such as the face, hands, lower abdomen, and vulval and sacral areas.



Laboratory tests


The alterations in the haematological and biochemical parameters listed in Box 14.2 are suggestive of pre-eclampsia.



Box 14.2 Laboratory findings in pre-eclampsia




• Increased haemoglobin (Hb) and haematocrit levels


• Thrombocytopenia


• Prolonged clotting times


• Raised serum creatinine and urea levels


• Raised serum uric acid level


• Abnormal liver function tests, particularly raised transaminases

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Related posts:

  1. The Placenta
  2. Prolonged Pregnancy and Disorders of Uterine Action
  3. The Third Stage of Labour
  4. Problems of Pregnancy

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Jul 11, 2016 | Posted by in MIDWIFERY | Comments Off on Hypertensive Disorders of Pregnancy

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