Diagnosing Renal Artery Stenosis- Look for Cardio-renal Syndrome and Flash Pulmonary Oedema

We all know renovascular hypertension exists. But how does it present clinically? Are their any distinguishing features that set it apart from other causes of hypertension and from subjects with essential hypertension?

Renovascular hypertension has two principal aetiologies. By far the commonest aetiology is atherosclerotic narrowing of the proximal renal artery. This can be predominantly unilateral or bilateral.

A much less common cause is fibromuscular dysplasia, affecting young females often in the 30-50 year range. This typically affects the distal renal artery, and for some reason, tends to be predominantly right sided.

So how does renovascular disease present? There are two terms often used to describe this condition, without realising that this is in fact the underlying aetiology. The first is cardio-renal syndrome and the second is flash pulmonary oedema.

Probably the most characteristic presentation of atherosclerotic renal artery stenosis is rapidly worsening hypertension, worsening renal impairment and incremental heart failure. This is often erroneously interpreted as cardio-renal syndrome, particularly in subjects with pre-existing heart failure, but the key finding is the hypertension. Subjects with longstanding heart failure, the cohort who develop cardio-renal syndrome, often have low or low-normal BP. They should not show a trend for a recent increase in BP.

This classical presentation has been somewhat tempered in the last decade or two by the widespread use of ACE inhibitors and direct angiotensin blockers for treating both hypertension and heart failure, but when present, is strongly suggestive of severe renal artery stenosis.

Some physicians measure serum renin and aldosterone levels to make a suggestive diagnosis of renovascular hypertension, before considering imaging studies such as CT angiogram. However, this could be misleading. While renin and aldosterone levels would be expected to be high in predominantly unilateral renal artery stenosis, these hormones are normal in bilateral renal stenosis and in subjects who have renal artery stenosis in a single surviving kidney.


The other, albeit, less common presentation is flash pulmonary oedema. Far too often, clinicians invoke the rare diagnosis of phaeochromocytoma in such subjects, when the blame lies with a much more common condition. Renal artery stenosis should always be suspected in subjects who have one or more episodes of "flash" pulmonary oedema.

Trautmann's Triangle & Otogenic Brain Abscess

A 64 year old woman presents with fever, headache and a discharging right ear.

A CT scan shows appearances consistent with a large right cerebellar abscess. This is later confirmed on a MR scan. You start antibiotics to cover S. aureus, gram negatives and anaerobes and given the discharging ear, decide to send off an ENT consult.

What putative diagnosis would you put on the consult request? Acute otitis media? Chronic suppurative otitis media?

Surprising though it may seem, in a case series of 40 otogenic abscesses, acute otitis media was not implicated even once. In all but one case, the predisposing factor was a cholesteatoma.

With otogenic brain abscesses affecting the temporal lobe, spread occurs through the tegmen tympani.

For abscesses affecting the cerebellum, spread from the affected ear occurs through the Trautmann's triangle, an area bounded by the sigmoid sinus posteriorly, bony labyrinth anteriorly, superior petrosal sinus superiorly and the internal jugular vein inferiorly.

On CT, an abscess may be confused with a necrotic tumour. The best arbiter is a diffusion weighted MR scan.

In the above case, a combined neurosurgical and ENT approach would be favoured. Most experts would drain the cerebellar abscess first, followed by a radical mastoidectomy.

Reference

Mandalà M, Muzzi E, Trabalzini F. Giant Cerebellar Lesion in a Patient With Purulent Ear Drainage. JAMA Otolaryngol Head Neck Surg 2016. doi:10.1001/jamaoto.2016.0014

Postural BP- You Are Looking At The Wrong Metric

How common is this? An elderly man is admitted to an inpatient facility following a fall at home. During his consultation, you find out that he felt "giddy" before falling. It's happened a few times in the past as well.

Quite reasonably, you instruct the nurse to measure supine and standing blood pressure. You specifically request the nurse to measure the BP after the patient has been lying or standing for a full three minutes.

The nurse informs you that the BP fell by 10/5 mm Hg when the gentleman stood. You are reassured and leave it at that.

But have you missed the diagnosis here?

The normal response to being stood is for the systolic BP to fall slightly and for the diastolic BP to rise slightly. Therefore, the pulse pressure narrows.

More importantly though, the pulse rate speeds up slightly. Apart from the vasoconstriction involved in raising the standing BP, the heart beats slightly faster to maintain the systolic BP at a nearly constant level.

In autonomic failure, be it peripheral, i.e. diabetes, amyloid, or central, as in Parkinsons and Parkinkons plus syndromes and much less commonly in primary autonomic failure, both systolic and diastolic BP fall. More significantly, the pulse rate, instead of rising, remains invariant. It neither rises nor falls. Most patients with autonomic failure also have postprandial hypotension.

Vasovagal syncope is more common than autonomic failure, with two principal types- cardioinhibitory- due to excessive parasympathetic activity, and vasodepressor- due to interruption of sympathetic outflow.

In cardioinhibitory syncope, the pulse rate actually falls on standing. The BP falls too. Some patients may develop asystole.

In vasopdepressor syncope, there is sinus tachycardia. The BP falls.

In postural orthostatic tachycardia sydrome (POTS), the patient's pulse rate increases by >30 beats per minute upon standing. The BP does not fall.

Therefore, the following is a guide to using the blood pressure & pulse rate to differentiate between various types of syncope- standing BP and pulse compared with supine.

Old subject- BP falls by >20/10, pulse rate remains unchanged- autonomic failure

Old or young subject- BP falls, pulse rate falls or becomes asystolic (ECG may show 1st degree block in other cases)- cardioinhibitory syncope

Young subject- BP falls, becomes tachycardic- vasodepressor syncope

Young subject- BP does not fall, pulse rate increases by >30/minute- POTS

Any age- BP does not fall, pulse rate increases by <30/minute- normal response.