hypokalaemia an overview

Hypokalaemia: an overview

Presented by:Dr. Muhammad Humayun Kabir

MBBS, FCPS (Surgery), MRCS (Edin)BSMMU, Dhaka, Bangladesh

Hypokalaemia

• Aetiology and clinical assessment

• Patients with mild hypokalaemia (plasma K 3.0–3.3 mmol/L) are generally asymptomatic, but more profound reductions in plasma potassium often lead to muscular weakness and associated tiredness.

• Ventricular ectopic beats or more serious arrhythmias may occur and the arrhythmogeniceffects of digoxin may be potentiated.

• Typical ECG changes occur, affecting the T wave in particular.

• Functional bowel obstruction may occur due to paralytic ileus.

• Long-standing hypokalaemia causes renal tubular damage (hypokalaemic nephropathy) and interferes with the tubular response to ADH resulting in polyuria and polydipsia.

• Generally, hypokalaemia is indicative of abnormal potassium loss from the body, either through the kidney or the gastrointestinal tract.

• When there is no obvious clinical clue to which pathway is involved, measurement of urinary potassium may be helpful;

• if the kidney is the route of potassium loss, the urine potassium is high (> 30 mmol/day), whereas if potassium is being lost through the gastrointestinal tract, the kidney retains potassium, resulting in a lower urinary potassium (generally < 20 mmol/day).

• Treatment of hypokalaemia involves first determining the cause and then correcting this where possible.

• Mild hypokalaemia: slow-release potassium chloride tablets or syrup supplimentation.

• Severe cases:– IV supplimentation is needed.– The rate of administration depends on the severity of

hypokalaemia and the presence of cardiac or neuromuscular complications, but should generally not exceed 10 mmol of potassium per hour.

• In patients with severe, life-threatening hypokalaemia, the concentration of potassium in the infused fluid may be increased to 40 mmol/L if a peripheral vein is used, but higher concentrations must be infused into a large ‘central’ vein with continuous cardiac monitoring.

• ‘Rule of 40’:

• If magnesium depletion is also present, replacement of magnesium may also be required for hypokalaemia to be corrected since low cell magnesium can enhance the mechanism for tubular potassium secretion, causing ongoing urinary losses.

A Close Look at the Adrenal Glands

Adrenal glands hyperfunction:

Primary hyperaldosteronism

• Excessive production of aldosterone, due mostly to aldosteronoma or to spontaneous bilateral hyperplasia of the zona glomerulosa of the adrenal cortex, leads to the combination of hypertension, hypokalemia, nocturia, and polyuria.

• A syndrome resembling nephrogenic diabetes insipidus may occur as a result of reversible damage to the renal collecting tubules. The alkalosis may produce tetany

• Primary hyperaldosteronism (PHA) is defined by hypertension, as a result of hypersecretion of aldosterone.

• Among patients with hypertension the incidence of PHA is approximately 2 per cent.

• Recent studies have revealed that up to 12 per cent of hypertensive patients have PHA with normal potassium levels, thus potassium levels are an inconsistent diagnostic feature of this disease, and cannot be relied on to confirm or exclude it.

Primary Hyperaldosteronism

(Conn's syndrome)1. Solitary adrenal adenomas (80-90%)

2. Bilateral adrenal hyperplasia (10-20%)

3. Adrenal Carcinoma (rare)

4. Unilateral Adrenal Hyperplasia (very rare)

Diagnosis

• The key feature of the biochemical diagnosis is the assessment of potassium level and the aldosterone to plasma renin activity ratio.

• Withdrawal of following medications for 1 week is mandatory before proceeding for biochemical tests:

– Antihypertensive and diuretic therapy, which cause hypokalaemia and influence the renin–angiotensin–aldosterone system.

– oral contraceptives or other estrogen preparations: these may increase renin and angiotensin levels and therefore aldosterone levels, thus raising the blood pressure artificially.

– If the patient is following a salt-restricted diet, aldosterone is normally elevated.

• In true aldosterone excess, serum sodium is slightly elevated and CO2 increased, whereas serum potassium is very low, for example, 3 mEq/L or less.

• Urine and serum potassium determinations while the patient is receiving good sodium replacement provide a screening test.

• Potassium wasting is established if the urinary potassium level is >30 mEq/L/24 h but the serum potassium level is low (3 mEq/L or less).

• Once the biochemical diagnosis is confirmed, MRI or CT should be performed to distinguish unilateral from bilateral disease.

• Conn’s adenomas usually measure between 1 and 2 cm and are detected by CT with a sensitivity of 80–90 per cent.

• Micronodular changes and small adenomas are often underdiagnosed.

• An apparent unilateral mass could be a non-functioning tumour in a patient with bilateral micronodularhyperplasia.

Fig. 20.22 Aldosterone-producing adenoma causing Conn’s syndrome. A CT scan of left adrenal adenoma (arrow). B The tumour is ‘canary yellow’ because of intracellular lipid accumulation

• Selective adrenal vein catheterisation can help before a decision on non-surgical or surgical treatment is made.

• During selective adrenal vein catheterisation, samples are obtained from the vena cava and from both adrenal veins and the aldosterone to cortisol ratio (ACR) is determined in each sample.

• A significant difference in the ACR ratio on one side indicates unilateral disease.

Treatment

ALDOSTERONOMA

• If the site of the tumor has been established, only the affected adrenal need be removed.

• The procedure of choice is laparoscopic unilateral adrenalectomy.

BILATERAL NODULAR HYPERPLASIA

Medical treatment is recommended.

MEDICAL TREATMENT: Indications:• If surgery not possible due to comorbidity, • if the hypertension is mild in an older person, or• if bilateral hyperplasia is the cause

• Drugs used: – spironolactone (Aldactone), 25–50 mg orally four times daily. – Amiloride, a potassiumsparing diuretic, may be given in doses of

up to 20–40 mg/day. – Other antihypertensive agents may also be necessary.

• Hypertension remains in as many as 70% of cases, probably because of irreversible damage to the systemic microcirculation.