In the busy clinical work, we often fail to
pay enough attention to some seemingly simple cases, which leads to our neglect
of the most basic clinical foundation, that is, the collection of medical
history and the interpretation of test results. Here, I would like to share
with you a recent clinical encounter in the cause of hypertension.
The patient is an elderly male with
repeated dizziness for more than 20 years and a history of hypertension for
more than 20 years. He has been hospitalized in our hospital and is now taking
"Nifedipine Controlled-Release Tablets 30mg QD" to control his blood pressure. His blood pressure is
usually on the high side and generally fluctuates between 160 and 180/80 and
100 mmHg. This time I have been sent to our department for treatment due to
dizziness. When entering the department, the main symptom is dizziness, showing
drowsiness, without dizziness, recent sleep is still acceptable, accompanied by
headache, showing blood vessel distension, and pain. Physical
examination: blood pressure 192/80 mmHg, neurological examination,
cardiopulmonary examination, and abdominal examination were not special.
Then treat it first according to primary
hypertension, and then urgently check the biochemical, coagulation, and other
indicators to see if there is any need for emergency treatment. Biochemical
return on the day, serum potassium 3.01 mmol/L, did not think so much at that
time, gave immediate oral potassium supplement, at the same time the next day
biochemical review.
The director rounds the next day, the
director asks: how much blood potassium checks? 2.95mmol/L, still low. Have
secondary hypertensive expression at ordinary times? After immediately asking
the medical history, I learned that I was accompanied by sweating, elevated
blood pressure, and no facial flushing or palpitation when I had dizziness and
headache in the afternoon. At the same time, the patient's previous
hospitalization data were consulted, and it was found that there were also low
levels of serum potassium. The director immediately instructed that 4 items of
hypertension and 3 items of adrenal function should be improved. At the same
time, the head MRI+MRA should be improved to detect cerebrovascular and substantive
problems. Besides, aldosterone should be added and potassium should be
supplemented appropriately.
Sure enough, after a few days, four
hypertension (in the decubitus position) were reported: aldosterone/renin
activity ratio 43.36, adrenal function 3, and no significant abnormality in
cranial MR. Abdominal CT was arranged to locate the adrenal gland immediately.
Results: Multiple adrenal nodules were found in bilateral adrenal glands and
adenomas were considered. After years of perplexing patients with dizziness and
high blood pressure, the cause has finally been found: primary aldosteronism.
Primary aldosteronism is caused by
hyperplasia or tumor of the adrenal cortex resulting in excessive voluntary
secretion of aldosterone, resulting in increased potassium excretion in the
distal convoluted tubule of the kidney, sodium and water retention in the body,
and thus increasing the effective blood volume and blood pressure. Clinically,
it is characterized by long-term hypertension with hypokalemia, and some
patients have normal serum potassium. Symptoms may include muscle weakness,
periodic paralysis, dysphoria, polyuria, and other symptoms. Most of the blood
pressure is mild to moderate elevation, about 1/3 of the performance of
intractable hypertension. Laboratory tests showed hypokalemia, hypersodium,
metabolic alkalosis, decreased plasma renin activity, and hyperaldosteronism in
plasma and urine. The increase of plasma aldosterone/plasma renin activity
ratio has higher diagnostic sensitivity and specificity. Ultrasound,
radionuclide, CT, and MRI can determine the nature and location of the lesion.
This simple case of hypertension, also to
our front-line clinicians put forward some "warning". First,
attention should be paid to the integrity of the medical history collection,
and should not ignore the detailed collection of relevant differential medical
history because of the simple disease and mild disease. Second, the
abnormal laboratory indicators should be more interpreted, do not miss the
"small" indicators that may point to the information. At the same time, if
the patient has previous hospitalization history, the abnormal information at
that time should be examined in detail for our reference and to make an
accurate judgment on the condition.