Case report

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Case report

• Intern ???

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Basic data

• Name ? x x
• Sex male
• Age 55 y/o
• admission date 92-11-26
• chart No.

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Chief complaints

• Hemoptysis from one day before admission

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Present illness (1)

• Patient is a 55 year-old male with a past history
  of TB s/p complete treatment, Right zona
  granulosa nodular hyperplasia s/p laparoscopic
  adrenalectomy on 91-5-15.
• According to patients statement ,he felt
  weakness about ten years ago. Then hypertension
  was noted since fifty years old and he had
  regular followed up at LMD and our hospital at
  the first beginning.

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Present illness (2)

• But blood pressure was still under poor control.
  Besides hypokalemia and hyperaldosteronism were
  noticed at that time. Then he was transferred to
  Dr.???. NaCl challenge test ,Postural test , and
  abdominal CT were arranged. Aldosterone producing
  adenoma was suspected. Later, right adrenalectmy
  was arranged and pathology showed adrenal nodular
  hyperplasia.
• But he had already discontinued the
  antihypertensive agents for one year. He also
  took the herbal medicine for the blood control
  but in vain.

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Present illness (3)

• He is now admitted from ER to our CHESTMEDICINE
  division service because of hemoptysis from one
  day before admission .At ER, bronchoscope showed
  bloody clot and bleeding tendency from left
  lingular or lower lobe.
• Besides ,high bloody pressure(220/120) and
  hypokalemia were also noted. There is no
  leukocytosis or left shift. Under the impression
  of hemoptysis and hypokalemia,he was admitted to
  chest ward and combined with Dr.??? for further
  care.

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Postural test

• Aldosterone decrease aldosterone producing
  adenoma
• Aldosterone increase idiopathic hyperaldosteroism

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Pathology

• The specimen submitted consists of adrenal gland
  with soft tissue measuring 8.5x4.5x2.1 cm in
  size, fixed in formalin
• Glossly ,the adrenal gland measures 10gm in
  weight and 6x3x1cm in size. It is golden
  yellowish in color. The cut surface reveals a
  dominant yellow cortical nodule and several
  smaller nodules.
• Zona glomerulosa nodular hyperplasia

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Personal history

• Smokingnil
• Alcohol drinkingnil
• Drug allergynil
• Hypertension
• Diabetes mellitusnil

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Past history

• Old TB s/p complete treatment about 30years ago
• Right zona granulosa nodular hyperplasia s/p
  laparoscopic adrenalectomy on 91-5-15

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PE

• Cons clear
• conj not pale sclera aniceric
• neck supple
• chest symmetric expasion
• BS bil clear HS RHB
• abd soft and obese
• bowel sound hypoactive
• Ext freely movable but weakness

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Lab data
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Lab data
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Lab data
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Lab data
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Impression

• Hemoptysis r/o old TB related
• Hypokalemia r/o adrenal gland related
• Secondary hypertension

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Plan

• Arrange bronchoscope.
• Arrange Abdominal CT r/o adrenal gland
  hyperplasia
• Spironolactone or ACE inhibitor to control blood
  pressure

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Primary aldosteronism

• aldosterone-producing adrenal adenoma (Conn's
  syndrome)
• idiopathic hyperaldosteronism (bilateral
  cortical nodular hyperplasia)

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aldosterone-producing adrenal adenoma

• Most cases involve a unilateral adenoma, which is
  usually small and may occur on either side.
• Aldosteronism is twice as common in women as in
  men, usually occurs between the ages of 30 and
  50, and is present in approximately 1 of
  unselected hypertensive patients.

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Idiopathic hyperaldosteronism

• In many patients with clinical and biochemical
  features of primary aldosteronism, a solitary
  adenoma is not found at surgery.
• Instead, these patients have bilateral cortical
  nodular hyperplasia.
• In the literature, this disease is also termed
  idiopathic hyperaldosteronism, and/or nodular
  hyperplasia. The cause is unknown.

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Signs and symptoms

• Most patients have diastolic hypertension.
• Potassium depletion is responsible for the muscle
  weakness and fatigue.
• The polyuria results from impairment of urinary
  concentrating ability and is often associated
  with polydipsia.
• Proteinuria may occur in as many as 50 of
  patients with primary aldosteronism, and renal
  failure occurs in up to 15.
• Thus, it is probable that excess aldosterone
  production induces cardiovascular damage.

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Diagnosis

• The criteria for the diagnosis of primary
  aldosteronism are
• (1) diastolic hypertension without edema,
• (2) hyposecretion of renin (as judged by low
  plasma renin activity levels) that fails to
  increase appropriately during volume depletion
  (upright posture, sodium depletion), and
• (3) hypersecretion of aldosterone that does not
  suppress appropriately in response to volume
  expansion.

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Diagnosis

• the ratio of serum aldosterone to plasma renin
  activity is a very useful screening test.
• A high ratio (gt30), suggests autonomy of
  aldosterone secretion. Aldosterone levels need to
  be gt500 pmol/L (gt15 ng/dL) and the salt intake
  not be restricted in making this assessment.

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Diagnosis

• aldosterone-producing adenomas should be
  localized by abdominal CT scan.
• If the CT scan is negative, percutaneous
  transfemoral bilateral adrenal vein
  catheterization with adrenal vein sampling may
  demonstrate a two- to threefold increase in
  plasma aldosterone concentration on the involved
  side.
• In cases of hyperaldosteronism secondary to
  cortical nodular hyperplasia, no lateralization
  is found.
• In a patient with an adenoma, the
  aldosterone/cortisol ratio lateralizes to the
  side of the lesion.

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Differential diagnosis

• The most common problem is to distinguish between
  hyperaldosteronism due to an adenoma and that due
  to idiopathic bilateral nodular hyperplasia.
• This distinction is of importance because
  hypertension associated with idiopathic
  hyperplasia is usually not benefited by bilateral
  adrenalectomy, whereas hypertension associated
  with aldosterone-producing tumors is usually
  improved or cured by removal of the adenoma.
• An anomalous postural decrease in plasma
  aldosterone and elevated plasma
  18-hydroxycorticosterone levels are present in
  most patients with a unilateral lesion. However,
  these tests are also of limited diagnostic value
  in the individual patient, because some adenoma
  patients have an increase in plasma aldosterone
  with upright posture, so-called renin-responsive
  aldosteronoma.
• A definitive diagnosis is best made by
  radiographic studies, including bilateral adrenal
  vein catheterization, as noted above.

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Treatment

• Primary aldosteronism due to an adenoma is
  usually treated by surgical excision of the
  adenoma. Where possible a laparoscopic approach
  is favored.
• Spironolactone, are effective in many cases.
  Hypertension and hypokalemia are usually
  controlled by doses of 25 to 100 mg
  spironolactone every 8 h.
• When idiopathic bilateral hyperplasia is
  suspected, surgery is indicated only when
  significant, symptomatic hypokalemia cannot be
  controlled with medical therapy, e.g., by
  spironolactone, triamterene, or amiloride.
• Hypertension associated with idiopathic
  hyperplasia is usually not benefited by bilateral
  adrenalectomy.