Cardiovascular Journal of Africa: Vol 27 No 2 (March/April 2016)

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 27, No 2, March/April 2016

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AFRICA

The development of symptoms, an uncontrollable spike in

blood pressure or the evolution of defined organ dysfunction

signal the onset of life-threatening disease, requiring that the

focus of treatment shift from the neonatal outcome to protecting

the interests of the mother. Delivery at this point is inevitable

and the neonate will need to be cared for in the best available

circumstances. The second means of improving perinatal

outcome revolve around the use of corticosteroids, given to the

mother. These accelerate the maturation of the foetal lungs and

lessen the likelihood of neonatal intraventricular haemorrhage in

the newborn.

In addition to the necessity of effecting delivery by

either induction of labour or caesarean section, the obstetrician

plays a role in preventing complications.

The prevention of eclampsia is ensured by the use of

magnesium sulphate, given as a continuous infusion or as

intermittent intramuscular doses.

37,38

This has been shown to be

effective in reducing the risk of developing eclamptic seizures

(and recurrent seizures) without adversely sedating the foetus.

The mechanism of action is poorly understood and the use

of magnesium sulphate needs to be weighed against potential

risks. These include the development of toxicity, which is

more common in women with renal failure. Toxicity leads

to respiratory arrest, which can be reversed with intravenous

calcium gluconate.

Women who are fitting should have their seizures aborted

with intravenous benzodiazepines. Women who continue to

fit despite treatment or those who are unable to protect their

airway because of a low Glasgow coma scale need intubation

and mechanical ventilation until the pregnancy is over and the

mother’s condition shows signs of improvement.

13,39

Proper management of severe hypertension is always a

priority. Drugs used to lower the blood pressure are a variety

of agents, including direct-acting vasodilators (hydrallazine,

dihydrallazine), calcium channel blockers (nifedipine), alpha-

and beta-blockers (labetalol), and combined arterial and venous

vasodilators (nitroglycerine). Potent vasodilators such as sodium

nitroprusside or diazoxide should not be used because they are

associated with a risk of precipitous decline in blood pressure.

Specific organ failure is managed according to

specific protocols

•

Eclampsia requires attention to seizure control as outlined

above. Recurrent seizures may only be controllable by contin-

uous infusion of propofol or diazepam; this usually requires

intubation and ventilation for up to 24 hours after delivery

has been effected. The co-morbidity associated with seizures

needs individual management (see below); specific screening

and treatment of aspiration pneumonia is important. Any

focal neurological signs merit neuro-radiological investigation

to exclude haemorrhage and infarction. The differential diag-

nosis of seizure activity also merits consideration and may

extend to other possible diagnoses, including metabolic causes

for seizure activity, thrombotic thrombocytopaenic purpura,

systemic lupus erythematosis, cerebral venous thrombosis,

malaria and amniotic fluid embolus.

•

Renal failure may be manifest on the basis of diminished

preload together with peripheral, including renal, vasospasm.

Acute renal injury may also cause oliguria and azotaemia.

This is the consequence of ischaemia (due to pre-eclampsia

or pre-eclampsia complicated by hypovolaemia caused by

abruptio placentae) and haemoglobinuria. The principles

of management are those of cautious intravascular volume

expansion (no more than 300 ml of colloidal solution given

as a bolus dose) and vasodilatation.

Renal failure that fails

to respond to these measures should result in a policy of fluid

restriction, management of actual or incipient hyperkalaemia

and expectant management in anticipation of gradual recov-

ery after delivery.

In the acute phase of the illness, dialysis

may be necessary.

•

Liver injury is associated with the HELLP syndrome. This

condition needs to be distinguished from other causes of

micro-angiopathic haemolytic anaemia as well as other causes

of liver failure. The differential diagnosis therefore includes

thrombotic thrombocytopenic purpura, acute fatty liver of

pregnancy, auto-immune disease, malaria and sepsis. The

hallmark of the HELLP syndrome is that it reverses after

delivery, with the nadir of thrombocytopaenia occurring on

the third day postpartum.

The management is obstetric,

meaning delivery. Patients who do not exhibit the character-

istic resolution of the thrombocytopaenia merit investigation

for other causes of micro-angiopathic haemolytic anaemia.

The only lethal complication of the HELLP syndrome is the

development of a large subcapsular liver haematoma, which

ruptures, causing massive intraperitoneal haemorrhage.

The

liver injury itself and the elevated liver enzymes seen in

HELLP syndrome are not associated with failure of hepatic

synthetic function and do not usually lead to coagulopathy or

hypoglycaemia. These features, if present, indicate an alterna-

tive diagnosis.

•

Pulmonary oedema is the most difficult complication of severe

pre-eclampsia in which to make a specific diagnosis.

The

mechanisms of pulmonary oedema are outlined above and

the differential diagnosis will include other causes of acute

dyspnoea, commonly infection and embolus. Pulmonary

oedema itself may be the consequence of pre-eclampsia, or

pre-eclampsia complicating underlying illness. These illnesses

may include valvular heart disease and ventricular dysfunc-

tion due to cardiomyopathy. Regardless of the cause, emer-

gency management is usually the same, involving supportive

management of oxygenation and various combinations of

diuretic and vasodilator therapy with a view to reducing

both afterload and preload. This is commonly accomplished

by using direct-acting vasodilators, such as dihydrallazine,

together with intravenous furosemide. The development of

pulmonary oedema is a signal for investigation by means of

radiology, ECG and echocardiography to try to ascertain as

closely as possible what the underlying cause may be. In some

circumstances, the acute management of critically ill women

may be facilitated by the use of pulmonary artery catheters

to directly measure haemodynamic variables.

Pulmonary

oedema complicating pre-eclampsia is also an indication for

immediate delivery, to begin reversing the underlying patho-

physiology of pre-eclampsia.

Postpartum management

Delivery of the pre-eclamptic pregnant woman will trigger

reversal of the underlying disease. Generalised oedema begins

to dissipate as the capillary leak reverses and the pregnancy