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| Issue 2 1998 |  |
| We
would like to extend a warm welcome to the clinicians and staff of North
Shore Private Hospital (NSPH) and wish you all the very best in your new
venture. As the preferred pathology provider to NSPH we look forward to
working with you in a successful partnership. Since the last issue of InfoLink we have launched our Intranet page which is full of helpful information about PaLMS. One of the outstanding features is our comprehensive test directory called LabInfo which is now available at your fingertips. It contains information about individual tests including collection volumes, patient preparation, availability, and reference ranges to name a few. If you do not have access to the Intranet, please ring the Service Centre on: |
| 1300 30 PALMS or 992 66066 |
| where the staff will help you with your inquiries. We anticipate our Internet page will only be a few months away with this information available to you through cyberspace. |
|
The Sydney University/PaLMS Virtual Pathology
Museum was launched on the Internet recently. It is an interactive,
educational tool which you are sure to find very interesting. Address
details and additional information are given on the back page.
Don’t forget to file this reference material in your InfoLink folder. If you have not received a folder, please contact me and I will organise one for you. As always, we are very eager to gain your feedback on this publication and any requests for specific topics you would like addressed in Info Link Kerry Heintze Marketing Manager |
| INVESTIGATION OF HYPERTENSION |
 |
Eileen DM Gallery MD(Syd) FRACP Renal Vascular Diagnostic Services phone: 61 2 9926 8948 |
| Hypertension is one of the most common medical conditions encountered in clinical practice. Some 15-20% of the adult population is affected in Australia, the prevalence increasing with age. Both women and men are affected, and in the post-menopausal population women with hypertension outnumber men. Although the majority (~85%) will have essential hypertension, this remains a diagnosis of exclusion, and can only be made after consideration and rejection of causes of secondary hypertension. Because hypertension can be the presenting feature of certain diseases which can themselves be progressive, it is of great value to look for the more common and significant causes in all hypertensive patients. The second reason for investigations in hypertensive patients is to look for co-morbid factors, or for evidence of end-organ damage. Attention to these may be of great value in prevention of complications or progression of end-organ damage. |
| Clinical Assessment - history Particular attention should be paid to a history suggestive of vascular disease (eg peripheral vascular disease, angina, cerebrovascular disease), as the morbidity associated with hypertension is increased several-fold. A history of urinary infection, kidney stones, haematuria or nocturia may suggest renal disease as the cause of the hypertension. Endocrine disorders such as diabetes mellitus may be complicated by hypertension, and thyrotoxicosis is a cause of systolic hypertension. Rare causes of hypertension such as phaeochromocytoma should be suspected if the patient gives a history of intermittent sweating, palpitations and hypertension, although phaeochromocytoma may also be associated with sustained hypertension. A history of arthritis or rash may alert you to the possibility of a collagen vascular disease. Clinical Assessment - examination The patient’s weight, height and general appearance should be recorded. Hypertension is often associated with obesity, and modest weight reduction may be of great value in treatment. Recording of the appearance may prompt recognition of certain endocrine disorders (eg hyper- or hypothyroidism, Cushing’s syndrome). The blood pressure should be taken with the patient seated comfortably, feet supported and arm resting and supported at the height of the heart. The blood pressure should be recorded in each arm (with a pre-ductal coarctation of the aorta, blood pressure will be high in the right and normal in the left arm). Equipment should be regularly calibrated - it is recommended that a mercury column sphygmomanometer be used. Examination should document or exclude evidence of end-organ damage from hypertension, in particular, left ventricular hypertrophy or enlargement, retinal vascular disease, and dipstick urinalysis abnormalities. Abdominal examination should include a search for renal enlargement, a renovascular bruit, and palpation of all peripheral pulses is mandatory. Investigations - all patients Certain investigations should be performed in all patients with hypertension when first seen. These include assessment of renal function and urinary abnormalities (since secondary causes for hypertension are most commonly found in or near the kidneys), and assessment of left ventricular function (which may be affected by hypertension), either by electrocardiogram or echocardiogram. The latter will give more accurate information about left ventricular hypertrophy, but is more invasive and expensive, and less immediately available to all practitioners. Important accompanying risk factors include hyperlipidaemia and glucose intolerance, and an initial fasting lipid profile and blood sugar can be a great help in subsequent patient management. The minimum renal functional assessment should include s.creatinine and electrolytes - sodium, potassium, chloride and bicarbonate. This will give a rough estimate of the adequacy of overall renal functional reserve, and help indicate patients who need more specialised investigations. Measurements of serum creatinine (S. creat) must be interpreted in the light of clinical information. Since the measured value is determined both by renal clearance (glomerular filtration) and by production from muscle metabolism, the relationship between the Screat and its clearance (C. creat) is affected by muscle mass - in turn affected by age and sex. Additionally, the S. creat will not rise clearly out of the normal range until approximately 50% of the kidney’s function is lost - this is shown clearly in Figure 1 - the glomerular filtration rate (Ccreat) is halved by the time the Screat is 0.12mmol/L, the upper limit of normal). Renal imaging should be performed in the majority of patients with hypertension - usually a plain X-ray of the abdomen (KUB) together with renal ultrasound will suffice, but more specialised imaging may be necessary (for instance to exclude renovascular disease). Investigations - selected patients The accompanying table lists the more common causes of secondary hypertension, their clinical features and investigations to make the diagnosis. Young patients with severe hypertension in whom no cause is found by the tests listed above, should be considered for more extensive investigations. In addition, certain clinical and biochemical features detected in initial assessment of the patient may suggest a secondary cause for hypertension. Remember that patients who have underlying stable chronic hypertension may develop a secondary problem (eg the patient with polycystic renal disease, who post renal transplantation develops primary hyperaldosteronism, or the patient with longstanding chronic essential hypertension who develops secondary atherosclerotic renal artery stenosis). This should be suspected if there is a sudden increase in the severity of pre-existing hypertension. Renovascular hypertension Fibromuscular dysplasia of the renal arteries should be considered particularly in young women with severe hypertension, while secondary atherosclerotic renal artery stenosis should be contemplated in older patients with recent exacerbation of previously stable hypertension, recent deterioration in renal function, or evidence of vascular disease in other organs. A high plasma renin activity is common in this situation due to relative renal ischaemia of the affected kidney. A nuclear medicine renal scan is of value as a screening test for unilateral disease, but renal angiogram is the definitive investigation to show the stenosis, and allow assessment of its severity and most appropriate corrective procedure. Primary hyperaldosteronism Unexplained hypokalaemia, or nocturia in the absence of significant renal functional impairment, should suggest the presence of primary hyperaldosteronism. This diagnosis is pursued by concomitant measurement of plasma renin activity (PRA) and plasma aldosterone. Interpretation of the values requires consideration of sodium, hormonal and volume homeostasis, and knowledge of the patient’s intake of a number of pharmacologic agents. The diagnostic specificity is enhanced by estimation of concurrent 24h urinary aldosterone, creatinine and sodium excretion. As shown in Figure 2 (a-c), from the PaLMS reporting form devised by Professor Stokes at Royal North Shore Hospital, the relationship amongst PRA, P aldosterone and U aldosterone is clarified by examination in light of sodium balance. The values depicted by (x) show the presence of secondary hyperaldosteronism, as might be seen in sodium deprivation, or in renal ischaemia (eg in renal artery stenosis). They are clearly distinguishable from those depicted by (o), which is classical for primary hyperaldosteronism, with suppression of PRA, and aldosterone levels above the normal range. Once the diagnosis is made, manipulation of sodium balance, adrenal imaging by CT scan, and selective adrenal vein aldosterone measurements will allow distinction between bilateral adrenal hyperplasia and unilateral adrenal adenoma. Renal disease A low serum bicarbonate suggests acidosis, and should direct attention to renal tubular function. At RNSH, this is measured by means of the One Day Renal Function Test (ODRFT) which allows simultaneous assessment of glomerular, proximal and distal renal tubular functions, with detailed urinary micriscopy. The patient with proteinuria and cast excretion may have primary or secondary glomerulonephritis. Immunological tests should include ANA, DNA, anticardiolipin and antineutrophil cytoplasmic antibodies, and renal biopsy may be necessary. Imaging tests may include, in addition to renal ultrasound, CT scan, retrograde pyelography, micturating cystourethrogram according to the suspected diagnosis. Phaeochromocytoma Patients with episodic hypertension (+sweating, tachcardia) and/or unexplained arrhythmias should have measurement of 24h urinary catecholamine excretion to exclude phaeochromocytoma. The majority of patients will be detected by a single measurement, but since the secretion of catecholamines can be intermittent, it is often useful to perform two consecutive estimations, or to repeat the estimation at a time when the patient experiences episodic symptoms. The majority of phaeochromocytomas will be detected by measurement of adrenaline, noradrenaline and dopamine, but in cases where the clinical suspicion is high and these measurements normal, it is of value to collect another sample for measurement of extra metabolites - particularly metanephrine and normetanephrine. The majority of phaeochromocytomas will be situated within the adrenal gland, and of sufficient size to be visible on CT scan or MRI. However, localisation may require the performance of a nuclear medicine functional scan with MIBG (met-iodo benzyl guanidine). |
| On the Internet at http://blackburn.med.usyd.edu.au/palms/pathology_museum The virtual Museum is a joint project of Anatomical Pathology, PaLMS and the Northern Clinical School. The Virtual Museum, as well as showing images of the "Pot" specimens situated in the "Real" Pathology Museum (Vindin House, RNSH), has descriptions of specimens, clinical history, microscopic images and descriptions and final diagnoses. Please let us know what you think of our Virtual Pathology Museum. We plan major expansions over the next few months, so visit the site regularly to see our new material. |
| Barbara Young Anatomical Pathology, PaLMS phone: 61 2 9926 7085 email: young1@med.usyd.edu.au |