4.1. Pregnancy induced hypertension 

4.1.1. Definition: 

Pregnancy- induced hypertension or pre-eclampsia is a multisystem disease occurring after the 20th week of pregnancy. 

Pre-eclampsia complicates 7-10% of all pregnancies. It is characterised by: 

• Hypertension > 140/90 (mild-diastolic > 90, severe-above 160/100) 
• Oedema
• Proteinuria > 0.3 gm/l in 24 hours 

Eclampsia is further complicated by tonic/clonic convulsions which may lead to coma. 

4.1.2. Pathophysiology 

The underlying cause is not known but it is thought it may be due to substances released from the placenta affecting endothelial cells. This endothelial cell damage disrupts capillary integrity

throughout the body. Pre-eclampsia is a multi system disease. The following pathological changes have been described: 

• Vasoconstriction leading to hypertension and tissue hypoxia. 
• Retention of sodium and water above that found in normal pregnancy. 
• Localised intravascular coagulation especially in the placenta and kidneys. Pre-eclampsia is categorised as mild, moderate or severe. 

4.1.3 Factors differentiating mild from severe pre-eclampsia*

Pre-eclampsia is more common in: first pregnancies, diabetics, patients with polyhydramnios and multiple pregnancies. 

4.1.4. Maternal changes 

Cardiovascular 

• Vasoconstriction causing hypertension and hypoperfusion. 
• Reduced blood volume (relative to normal). 
• Oedema secondary to leaky capillaries and salt retention. The oedema usually presents peripherally but pulmonary oedema may also occur. 

Renal 

• Decreased renal blood flow. 
• Decreased urine output. 
• Protein urea. 

Haematological 

There is increased fibrinogen, fibrin and platelet turnover. 

• Platelet count may be reduced. If less than 100,000 x 109/L check coagulation profile, i.e. INR or prothrombin time. If less than 75,000 x 109/L it is best to avoid a spinal anaesthetic as there may be an increased risk of spinal haematoma. 
• Platelet function may be impaired. 
• HELLP Syndrome (Haemolysis, elevated liver enzymes, low platelets). 

Neurological 

There is hyper-excitability and hyper-reflexia. Visual symptoms and headache suggest severe pre-eclampsia and the possibility of an impending convulsion (eclampsia). 

Placenta 

Decreased blood flow and possible infarcts leading to intra-uterine growth retardation and increased incidence of fetal distress. 

Note: Pre-eclampsia is an unpredictable condition. Eclampsia can develop without severe hypertension. 

The changes of pre-eclampsia continue for up to 48 hours after delivery and may peak in the first 24 hours after delivery. The highest risk for severe complications such as pulmonary oedema, eclampsia and thrombocytopaenia occur in the first 24 hours post partum. 

4.1.5. Treatment of toxaemia

The aim of treatment in pre-eclampsia is to control blood pressure, prevent eclampsia and plan delivery of the fetus at the appropriate time. Good communication between the obstetric, anesthetic and pediatric teams is important. After assessment of the patient, including history, examination and appropriate blood tests where available (full blood picture, urea, electrolytes,  creatinine, clotting profile if platelet count is less than 100,000 x 109 ). The principles of treatment are: 

Management of hypertension 

The aim here is to protect the mother from the complications of extreme hypertension. To control an acute hypertensive episode where the systolic blood pressure is greater than 170 or the diastolic is greater than 110 (or both), drugs such as nifedipine, labetalol, atenolol, methyldopa or hydralazine are used depending on what is available. Labetolol and hydralazine can be given IV in hypertensive crises. The management of severe hypertension should be in a controlled setting, in hospital with appropriate close BP monitoring. 

Seizure prophylaxis 

Magnesium sulphate is the drug of choice for seizure prophylaxis in the following settings: 

• After an eclamptic seizure, to prevent further seizures. 
• In severe pre-eclampsia with signs of cerebral irritability, i.e. headaches, visual disturbance, etc. 

Dosage: 

• Magnesium sulphate is usually given IV (4g load over 15 minutes), followed by a continuous infusion of 1g/hr. Therapeutic levels of magnesium are 4-6mEq/L. Levels can be monitored but toxicity is extremely unlikely with this regime and clinical monitoring would be sufficient (see below). Magnesium also has an anti-hypertensive effect and prolongs the effect of muscle relaxants. 
• Magnesium can be given intramuscularly (4 grams deep IM into each buttock as a loading dose – total 8 grams). This can be monitored clinically using assessment of the patella deep tendon reflexes. The point at which the deep tendon reflex is abolished is equivalent to a blood level of 10mEq/L which is above the therapeutic range but lower than levels causing more serious side effects (i.e. arrhythmias and severe muscle weakness). If the tendon reflexes are abolished the next IM dose (4 grams deep IM into 1 buttock) is given when the reflexes return. This will usually be about 4 hours after the loading dose. Therefore, magnesium can be given intramuscularly with regular monitoring of tendon reflexes to monitor toxicity. Magnesium toxicity is treated with IV calcium. 

The management of convulsions 

• Protection of the airway: This may be achieved by placing the patient in the left lateral position with high flow oxygen. If the seizure is prolonged and unresponsive to IV treatment (see below), endotracheal intubation using a rapid sequence induction may be necessary. 
• The treatment of convulsions: Give IV diazepam (2.5mg /30 secs up to 20mg). Thiopentone in small doses can also be used. 
• The prevention of further convulsions. Give magnesium sulphate (as described under Seizure prophylaxis, earlier). 

Fluid management 

Patients with pre-eclampsia have a relative hypovolemia and require careful fluid management. The fluid management is guided by urine output to maintain a urine output of 1ml/kg/hr. Careful IV hydration with Hartmann’s solution (or 0.9% saline) is used to maintain an adequate urine output. These patients are at higher risk of developing pulmonary oedema, therefore their fluid management must be frequently reassessed. 

Foetus 

Delivery of the foetus must be timed carefully. The main reason for delivery is either foetal distress or intrauterine growth retardation. There are some maternal relative and absolute indications for delivery also. See specialised textbooks