Phys Clinical Cases · renal
Hypertensive Nephrosclerosis and Renovascular Disease — DCE Clinical Case
DCE short-case station: the hypertension examination with renovascular detection built in — correct measurement, fundi, bruits, kidneys and peripheral pulses — with presentation template and probing questions.
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Target exams
Approach — what the examiner is testing
This station is not "take a blood pressure". It tests whether you can measure pressure properly, stage the damage hypertension has done, and hunt for a secondary cause — in that order [1].
Measure first. Seat her rested, back supported, arm at heart level, correct cuff size; measure both arms at least once (an inter-arm difference suggests subclavian disease), and consider standing pressure if symptoms or age suggest postural drop. Say what you are doing — examiners award the measurement rigour explicitly because out-of-office and standardised readings define true resistance [1] [2].
Examination sequence
General inspection. Cushingoid facies and central adiposity; acromegalic or thyrotoxic features; uraemic tinge; anxiety and tachycardia of phaeochromocytoma — the endocrine causes hide in the first five seconds [5].
Fundi — the highest-yield two minutes. Describe what you see as a grade: arteriolar narrowing and silver wiring; AV nipping; then flame haemorrhages and cotton-wool spots; and at the top, papilloedema, which with severe pressure defines malignant hypertension and changes the urgency of everything [4].
Cardiovascular. Displaced, forceful apex and a fourth heart sound for left ventricular hypertrophy; signs of failure; auscultate the carotids; palpate radial and femoral pulses simultaneously for radiofemoral delay — coarctation is the secondary cause you can feel [5].
Abdomen — the renovascular core. Palpate for ballotable renal masses (polycystic disease, tumour) and an aortic aneurysm; then auscultate over the aorta and both renal angles, anteriorly and in the flanks, for a systolic-diastolic bruit — a lateralised renal bruit in a resistant hypertensive is renovascular disease until excluded [3]. In a young woman the same finding points to fibromuscular dysplasia [6].
Peripheral vessels and finishing. Palpate all lower-limb pulses and comment on the vascular tree — diffuse atheroma raises the pre-test probability of atherosclerotic renal artery disease; check for ankle oedema and finish with a urine dipstick and an offer to check kidney size on ultrasound [3].
Presentation template (deliver this to the examiner)
"Mrs Tran has a confirmed office pressure of 172/96 mmHg in the right arm and 168/94 in the left, measured with an appropriate cuff after rest. She has grade 2 hypertensive retinopathy with AV nipping and no haemorrhages or papilloedema, a sustained non-displaced apex with a fourth sound consistent with hypertensive heart disease, and no radiofemoral delay. Critically, she has a right renal-angle bruit, and her peripheral pulses are intact. My synthesis: severe hypertension with moderate target-organ damage and a clinical clue to right-sided renovascular disease. I would confirm true resistance with ambulatory readings and an adherence review, send secondary-hypertension screening bloods including an aldosterone-renin ratio, and image the renal arteries — duplex in a skilled laboratory, otherwise CT or MR angiography." [2] [3]
If the examiner shows you papilloedema
State immediately that severe hypertension with papilloedema is malignant hypertension — a hypertensive emergency — and that you would assess for the accompanying damage at the bedside: conscious level and neurology (encephalopathy), urine output and dipstick (AKI, haematuria), and signs of heart failure; then manage in a monitored bed with an IV titratable agent, lowering mean pressure gradually — no more than about a fifth to a quarter in the first hour — rather than crashing it [4].
Probing questions
"Your bruit — how confident are you it is renal?" — "A systolic-diastolic bruit localised to the renal angle is specific but insensitive; aortic bruits are common in vascular patients, so I present it as a clue that raises pre-test probability, then let imaging decide. The finding still changes management because it justifies the renal artery study I might otherwise not order." [3]
"She is 58 with three drugs. Why not just add a fourth?" — "Because the AHA definition of resistant hypertension obliges me to confirm it properly first — ambulatory or home readings, adherence, a genuinely adequate regimen including a diuretic — and to screen for secondary causes, of which primary aldosteronism is the commonest and renovascular disease the one her bruit suggests. Treating harder without that screen misses a potentially curable driver." [2]
"If imaging showed a mid-artery string-of-beads lesion, what then?" — "That is fibromuscular dysplasia, and the rules change: it is the young-woman, non-atherosclerotic disease treated with balloon angioplasty without a stent, which can cure or substantially improve the pressure — I would also screen her cervicocephalic vessels once, since FMD is a systemic arteriopathy." [6]
References
- [1]Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines Hypertension, 2018.PMID 29133356
- [2]Carey RM, Calhoun DA, Bakris GL, et al. Resistant Hypertension: Detection, Evaluation, and Management: A Scientific Statement From the American Heart Association Hypertension, 2018.PMID 30354828
- [3]Textor SC Current approaches to renovascular hypertension Med Clin North Am, 2009.PMID 19427501
- [4]Shantsila A, Lip GYH Malignant hypertension: not quite an obsolete diagnosis yet J Hypertens, 2019.PMID 30640869
- [5]Viera AJ, Neutze DM Diagnosis of secondary hypertension: an age-based approach Am Fam Physician, 2010.PMID 21166367
- [6]Persu A, Giavarini A, Touzé E, et al. European consensus on the diagnosis and management of fibromuscular dysplasia J Hypertens, 2014.PMID 24842696