Tuesday, 24 June 2008

Bedside Better Than MRI

Dear Bloggers

There is too much reliance on machinery to try and help us as physicians make a diagnosis. 

The next case, which as always has been anonymised, demonstrates that a simple history and bedside examination was all that was needed to establish a firm diagnosis.

A 70 year old female was admitted to a hospital in North Japan with dizziness on standing, weakness of her legs and blurring of her vision.

She had been otherwise well one week before admission and had been started on hypertensive medication by a local doctor for newly diagnosed hypertension. The patient had been taking the drug according to directions. However, she began to experience dizziness on standing and leg weakness. All symptoms resolved when she was lying flat at night time. She denied collapse or loss of consciousness and there was no history of chest pain. However, when she stood up, she did experience a rapid heart beat but without chest discomfort.

There was no previous medical history of note.

She was a non-smoker and only drank occasional alcohol. She lived with her husband in a ground floor apartment.

On examination the patient looked well and was alert and fully conversant.

General: Afebrile. No jaundice, anaemia, clubbing, cyanosis, oedema or lymphadenopathy (JACCOL)

CVS: Pulse 72 regular, BP 190/90 (lying), JVP not elevated, Heart sounds S1 normal, loud S2. No added sounds or murmurs. No carotid bruits. No peripheral oedema.

RESP: RR 16/min, Sats 98% breathing ambient room air, trachea central, expansion  normal, percussion resonant bilaterally, auscaultation normal vesicular breath sounds.

ABDO: Soft, flat, non-tender, no rebound or guarding. No organomegaly or masses. Bowel sounds normal. Rectal exam normal and no faecal occult blood.

CNS- Cranial nerves II-XII within normal limits.

PNS- tone, power, reflexes, coordination, sensation all within normal limits.

The resident was uncertain of the cause of the symptoms and the patient underwent several tests.

ECG- revealed slight sinusoidal T wave abnormalities in the lateral chest leads but there was no ST elevation or depression.

Lab Data- revealed elevated liver function with AST and ALT being 3x normal. The bilirubin and ALP were normal. All other blood results were normal including the CBC, Renal function and Cardiac enzymes (CK and Troponin-T).

CXR- was within normal limits.

CT head scan was performed which revealed only age-related cerebral atrophy.

MRI head scan again revealed no pathological problem.

In this case, the history is extremely important. The patient had started a new anti-hypertensive drug and had begun to develop what appeared to be postural-related symptoms which resolved on lying flat.
Unfortunately, the history had not been fully appreciated by the resident. Despite a normal neurological examination, the patient still underwent cranial scanning, twice, which was unnecessary.

An astute physician reviewed the patient at the bedside and obtained further history which again supported the likely diagnosis of postural hypotension. A simple bedside test was performed which gave the diagnosis.

Initially, the patient was laid flat and the blood pressure was 193/92mmHg. The patient was then elevated to about 50 degrees sitting and at one minute the blood pressure was rechecked and was 189/87mmHg and there were no symptoms. At two minutes with still no symptoms present, the blood pressure was 180/79mmHg. By three minutes, the patient was developing blurred vision and the blood pressure was 178/77mmHg. It was decided to stand the patient with her being held on either side by a physician and with a third physician checking the blood pressure. Full resuscitation equipment was available in case of collapse.

On standing, the patient developed the full set of dizziness symptoms but was fully conversant with no loss of consciousness. The blood pressure at one minute was 150/69mmHg. Pulse rate had not risen appreciably.

On lying the patient flat, the symptoms completely resolved.

Hence, this patient had confirmed postural (orthostatic) hypotension likely to be drug-induced.

A blood pressure drop of more than 20 mmHg of the systolic and / or 10 mmHg of the diastolic (20/10 mmHg) are consistent with the diagnosis of postural hypotension.

Other problems to consider are autonomic failure (pure autonomic failure, diabetes, multisystem atrophy, Parkinson's disease), hypovolaemia (e.g. dehydration, haemorrhage etc), adrenal failure, pituitary failure, baroreceptor dysfunction etc.

However, with such a strong history of starting a new drug and developing postural hypotension, the drug was the likely offender and in addition, it may well have been the cause of the mild liver dysfunction.

In this case, a simple bedside test would have sufficed to make the diagnosis. Cranial scanning was not necessary especially as the thorough neurological examination was within normal parameters.

You may be saying to yourself, 'Hang on a minute, the blood pressure is still high but the patient has hypotensive symptoms?!' Yes, that is correct. This patient despite not having what we would all regard as true hypotension nevertheless has a sufficient drop in both systolic and diastolic blood pressure on standing to cause symptoms. This is a relative hypotension and is still relevant and should not be ignored just because the systolic blood pressure remains above 100mmHg !

Normal Blood Pressure Homeostasis

When initially standing up, approximately 0.5-1.0 litres of venous blood pools in the capacitance vessels. Baroreceptors sense a drop in blood pressure and result in reflex vasoconstriction, increased heart rate and return of venous blood to the heart. These effects are immediate and without appreciable symptoms to a normal individual. Longer  term changes include increased renin output to increase angiotensin II and aldosterone to increase vessel tone and sodium reabsorption respectively. Other changes include the increased output of ADH which leads to vasoconstriction and increased water absorption from the kidneys.

Pathological Causes

Hypovolaemia- in states of severe hypovolaemia e.g. bleeding, approximately 3o% of the blood volume can be lost before postural blood pressure drops can be seen. This is especially relevant in young patients. Hence, asking questions about bleeding and searching for possible unseen causes e.g. abrutio placenta, GI haemorrhage are mandatory.

Drugs- the elderly are very sensitive to drugs. Even seemingly innocuous drugs can have adverse side effects such thiazide diuretics, tricyclic antidepressants, beta-blockers, neuroleptic medications. As I always say, take a decent drug history and look up the side-effects (if you don't already know them) and check for drug-drug interactions!

Adrenal Failure- steroids are required to allow the vascular smooth muscle to be responsive to circulating catecholamines to maintain vascular tone. Hypocortisolaemia leads to vascular collapse and hence, patients with no obvious hypovolaemia and no offending drugs, should have this easily treatable condition ruled out. Other possible signs might be a low sodium and high potassium in addition to fasting hypoglycaemia. However, patients with a normal K level can still have hypocortisolaemia.

Pituitary Failure- Absence of ACTH leads to a similar problem of hypocortisolaemia. Whereas adrenal failure is associated with raised ACTH levels and hyperpigmentation, panhypopituitarism, and hence low ACTH output, is not. Checking anterior pituitary hormones would be advisable and should be part of the work-up for patients in whom the immediate cause of postural hypotension is not clear.

Other conditions are associated with autonomic failure and include diabetes mellitus, and hence, checking a fasting glucose and a 75 gram oral glucose tolerance test would be appropriate. HbA1c is not part of the British or American Diabetes Association guidelines for making the diagnosis of diabetes as it can be misleading.

Multi-System Atrophy (MSA) which includes the famous Shy-Drager and Parkinsonism etc should be considered but such abnormalities of cerebellar dysfunction, tremor, bradykinesia and cog-wheel rigidity should be unmasked during the physical examination (if performed correctly!) 

Autonomic failure can be examined for by doing the postural blood pressure testing and checking compensatory changes in heart rate. If the heart rate fails to increase by more than 10  beats per minute during the postural test, then this suggests autonomic failure. Heart rate increase > 100 / min suggests hypovolaemia. If symptoms develop without hypotension, then this suggests Postural Orthostatic Tachycardia Syndrome (POTS); this is usually evident in younger patients.

Investigations for autonomic failure include the measuring of the R-R interval on ECG with the patient doing slow breathing. The ratio of the R-R interval of expiration to inspiration should be more than 1.15. If less, it suggests autonomic failure.

Baroreceptor dysfunction paradoxically occurs in patients with hypertension which thereby predisposes elderly patients to orthostatic hypotension. The commonest cause in the elderly is decreased baroreceptor responsiveness plus impaired arterial constriction.

  1. This involved removing / treating the underlying cause
  2. Postural manoeuvres such as getting out of bed slowly in the morning, taking sufficient fluid and salt in the diet (as long as their is no hypertension or heart failure), using compression stockings to improve venous return, addition of fludrocortisone to mimimise symptoms in those individuals with sufficient salt intake, midodrine to cause vasoconstriction and non-selective beta-blocker Propranolol which leads to uninhibited alpha-vasoconstrictive effects.

Lessons to be Learned
  • Avoid cranial scanning unless it is absolutely necessary; just because you can scan someone does not mean that you have to or that you should. A thorough history and examination may be sufficient to give all the necessary information. Only if there is a neurological abnormality e.g. upper motor neurone signs, should the patient be scanned.
  • Patients with a history of postural related symptoms should have a bedside measurement of blood pressure. An initial lying blood pressure should be performed and then repeating the measurements at 1, 2 and 3 minutes in the sitting position (if the patient cannot stand) or standing. If the patient is stood up, they should be supported in case of potential collapse with full resuscitation equipment being available. Blood pressure measurements should then be performed at 1, 2 and 3 minutes.  
  • A blood pressure drop of more than 20 mmHg of the systolic and / or 10 mmHg of the diastolic (20/10 mmHg) is consistent with the diagnosis of postural hypotension.
 In this case, there was a hint of dropping blood pressure at 3 minutes when sitting and this  was confirmed after just 1 minutes of standing.
  • Patients without a supportive drug history and in whom there is no clear cut cause, should have a rectal examination to check for gastrointestinal haemorrhage. Consider other potential causes in the elderly as listed above.
Have a great week !

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