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Patient with weakness, decreased appetite, unsteady gait and palpable abdominal mass

An 82 year old lady developed weakness which settled gradually over a period of about 3 weeks. At the same time she noticed a decrease in appetite. Gradually the weakness became so severe that she could hardly get out of bed and shortly before asking for our help she developed instability in walking. Her medical history included hypertension, anaemia (for which she had been tested 3 years ago in hospital with no documented diagnosis), hypothyroidism and atrial fibrillation. Her treatment included anti-hypertensive drugs (3 classes), antiarrhythmic drugs, thyrolimon, and osteoporosis drugs.


On clinical examination, the patient had the appearance of a sufferer, her skin had a yellow tinge (jaundice), and her conjunctivae were pale, suggesting severe anaemia. On neurological examination there was diffuse weakness in both movement and coordination of movements. At the same time, she had great difficulty getting up from both a prostrate and sitting position. Finally, on palpation of her abdomen there was a round, semi-hard formation at the bottom, about the size of a child's head.


Due to the patient's condition, admission to the hospital was recommended where tests revealed hypokalemia (K=2.9 mEq/L) and hyponatremia (Na=113 mEq/L) (two components called electrolytes that regulate the function of the nerves and the heart), an increase in bilirubin (2. 5 mg/dl), anemia (hematocrit 28 that gradually with hydration dropped to 22), increase in lactate dehydrogenase, an enzyme that is mainly increased in liver, heart or blood diseases, and increased C reactive protein and erythrocyte sedimentation rate. CT scan showed distension of the bladder with no obvious signs of obstruction or tumor in the area (urinary retention).


The screening showed that the hyponatraemia and hypokalemia were due to the use of diuretics (a class of anti-hypertensive drugs). This was followed by their replenishment by intravenous administration, discontinuation of diuretics and reduction of oral fluids. Correction of electrolytes was achieved in one week. A myelogram was performed which showed myelodysplastic syndrome (refractory anemia). The patient was transfused with 2 units of red blood cells. A urinary catheter was inserted with which 3 liters of urine was removed from the patient's bladder in a short time. The catheter was removed after 2 days of insertion, but due to a flaccid bladder and recurrence of retention it was reinserted. Cyst medications were administered and the catheter was removed without problems after 3 days.


The combination of hyponatremia, hypokalemia and anemia in this patient exacerbated the weakness, instability and urinary retention. The patient gradually began to regain her strength and on the day of discharge from the hospital she was able to get out of bed and out of the chair with ease. Her anti-hypertensive treatment was adjusted, instructions were given for transfusion again in case of a drop in haematocrit and instructions for bladder exercise. On re-examination after a few days the patient felt that she had fully recovered her strength.


Hyponatraemia is a potentially fatal condition because of the swelling it causes in the brain. It is a relatively common cause of weakness and can present with noisy symptoms such as confusion, irritability or even seizures or coma if it settles rapidly. Its aetiology is varied but can be summarised in 3 main categories:

1) Hyperglycemia due to fluid retention in the body in severe heart or liver failure or nephrotic syndrome.
2) Isovolemic due to antidiuretic hormone over-secretion as a result of cancer or infections, primary polydipsia, renal or adrenal insufficiency and hypothyroidism.
3) Hypovolemia due to fluid loss from vomiting, diarrhea or excessive sweating, acute kidney damage, hypoaldosteronism or medications such as diuretics.

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