Case 34 A hypertensive 38-year-old woman

Diana had her second child at the age of 32. Her blood pressure was first noted to be slightly high towards the end of this pregnancy. At the postnatal check her blood pressure was 140/90 mmHg. Over the subsequent two years her blood pressure was measured on a few occasions. The readings showed systolic pressures of 150–160 mmHg and diastolic pressures of 90–100. Diana’s creatinine and cholesterol were normal.

Dr Williams decided to treat her with atenolol.

What would you do now?

During the next four years, follow-up was rather intermittent and Diana’s compliance with medication somewhat erratic. Blood pressure readings ranged between 160–180 mmHg and 90–105 mmHg.

In 2009, at the age of 38, Diana had a sudden onset of severe headache and collapsed at home. She was admitted to hospital and found to have had a right middle cerebral artery haemorrhage. Diana had a craniotomy and evacuation of the cerebral haematoma. Unfortunately she only made a partial recovery and was left with a severe left hemiparesis. She is only able to walk up to 100 yards with a stick and requires a wheelchair for longer distances. Subsequent investigation revealed that her hypertension was secondary to polycystic kidneys.

It was alleged that Dr Williams should have investigated Diana to determine if there was a secondary cause for her hypertension in view of her young age. It was alleged that if she had been investigated she would have been found to have polycystic kidneys and that this would have prompted referral to a nephrologist. This would have resulted in earlier and better control of her hypertension. In addition it was alleged that Diana’s hypertension was inadequately treated.

Expert comment

The Health Survey for England 2009 showed that 32 % of men and 27% of women over the age of 35 have a BP of 140/90 or more or are on treatment for hypertension (NHS, 2009). At least 95% of cases are ‘primary’, or ‘essential hypertension’. Secondary cause of hypertension should be considered in those who are aged 35 or less, in patients with difficult to control hypertension, and in those who have features of an underlying cause.

At the time of this case the British Hypertension Society advised that hypertension should be diagnosed if there were three readings of a blood pressure ≥ 160/100 (Williams et al., 2004). If the blood pressure was between 140/90 and 160/100 the patient’s cardiovascular risk should be assessed and the patient treated if this was greater than 20% in 10 years.

These guidelines have been superseded by those published in August 2011 by NICE. In this case it was not clear on what basis the diagnosis of hypertension was made. The choice of antihypertensive medication was appropriate because Diana was of child-bearing age. Dr Williams could have chosen an ACEI in view of her age but would have had to warn her about the need to discontinue the medication should she become pregnant. The latest guidance is that ACE inhibitors, angiotensin receptor blockers and chlorothiazide are teratogenic and should not be used in pregnancy. The limited evidence available does not show an increase in congenital abnormalities with any other antihypertensive treatment (NICE, 2011).

The most problematic issue is that Dr Williams does not seem to have appreciated the need to investigate Diana. Had he done so, the diagnosis of polycystic kidney disease (PKD) would have been made four or five years before Diana had the subarachnoid haemorrhage.

Autosomal dominant PKD is an inherited condition that will affect 50% of the children of a parent who is affected. It is one of the commoner of the inherited diseases and affects between 1 in 400 and 1 in 1000 individuals (Gabow, 1993). Many general practitioners will have one or more patients with the condition.

The condition is usually diagnosed after a renal ultrasound shows multiple cysts in both kidneys. An ultrasound may be requested for several reasons: for the investigation of loin pain (which occurs with PKD), because a relative has the condition, for the investigation of asymptomatic haematuria or to investigate causes of secondary hypertension (Gabow, 1993).

The commonest complication of PKD is the development of hypertension. 60% of adults develop hypertension before they begin to lose any measurable degree of renal function (Gabow, 1993). Cerebral ‘Berry aneurysms’ are also associated with PKD. The frequency with which berry aneurysms are found in patients with PKD is quoted as anything between 0% and 40%. Three studies which together screened a total of 273 patients with PKD for asymptomatic berry aneurysms found aneurysms in 13 patients (a prevalence of 5%) (Gabow, 1993).

Treatment of hypertension reduces the risk of stroke and heart disease in all patients (whether they have PKD or not). The evidence is that treatment of mild to moderate hypertension (blood pressures of 140 to 180 mmHg systolic and 90 to 110 mmHg diastolic) in patients with ‘essential hypertension’ (as opposed to those with hypertension secondary to PKD) reduces the risk of stroke by between 30% and 43% (MRC, 1985; Wood et al., 1998). The percentage reduction is likely to be greater for haemorrhagic strokes. However, to ‘prove’ causation in civil litigation the risk of stroke would have to be reduced by more than 50% (such that the stroke would be more likely than not to have been prevented). Causation experts would be likely to argue this issue in this case.

A further issue, with regard to both breach of duty and causation, is that it can be difficult to adequately treat hypertension. A BMJ review in 2004 commented that, with the introduction of newer stringent targets, blood pressure was controlled adequately in only a third of patients (Campbell & Murchie, 2004).

A study among UK general practitioners found widespread scepticism about the evidence base, desirability and achievability of tighter blood pressure target levels (Heneghan et al., 2007). In addition up to 40% of patients treated for hypertension fail to take their medication as prescribed (Vrijens et al., 2008).

However, realistically, breach of duty could not be defended.

Even in the light of the difficulties outlined above the doctors in the practice did not manage Diana’s blood pressure adequately. Diana’s blood pressure was checked infrequently and was always above a target level of 140/85. Usual practice would have been for her to have had her blood pressure taken every 6 months once it was adequately controlled.

Furthermore, Diana should have been investigated for secondary causes of hypertension because she was very young to have essential hypertension.

Had the diagnosis of PKD had been made earlier Diana should have been referred to a nephrologist. In these circumstances the blood pressure may well have been more aggressively managed with a view to slowing the deterioration of renal function. The target level for blood pressure would have been 130/80. In addition Diana might have been more motivated to take her medication regularly.

Legal comment

It will prove difficult to defend Dr Williams’s standard of care. At the end of the day, the causation experts are likely to conclude that with appropriate treatment, Diana would not have suffered her stroke. However, causation is not straightforward. There are a number of arguments (surrounding the difficulties in controlling hypertension) that Dr Williams’s lawyers will be able to use to negotiate a discounted settlement.

The level of damages will depend largely on how badly Diana’s disability affects her life. Damages could easily be in the high hundreds of thousands of pounds.

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