A 56-year-old woman was admitted with a 3 week history of increased bilateral lower limb swelling. Past medical history included chronic obstructive pulmonary disease (COPD), secondary pulmonary hypertension, right heart failure and paroxysmal atrial tachyarrhythmias.
Her medications at the time of admission were warfarin 3 mg once daily, ramipril 5 mg twice daily, bisoprolol 7.5 mg once daily, diazepam 5 mg three times daily, spironolactone 25 mg once daily, furosemide 40 mg twice daily, amiodarone 200 mg once daily, and fluoxetine 20 mg once daily. There had been no recent alterations to her medication regimen. She denied any non-compliance with treatment.
On examination the patient was hypertensive, with a blood pressure 204/106 mm Hg, and oxygen saturations of 82% on air. She had evidence of worsening right heart failure with bilateral pitting oedema to her knees and features of tricuspid regurgitation, jugular venous pressure (JVP) being elevated to the angle of the jaw, along with pulsatile hepatomegaly and ascites. Auscultation of her chest revealed hyper-expansion with decreased breath sounds.
Initial investigations included urea and electrolytes (U&Es): serum potassium 2.5 mmol/l, sodium 148 mmol/l, urea 4.9 mmol/l, creatinine 104 mmol/l, chloride 107 mmol/l, and bicarbonate 48 mmol/l.
Chest x-ray showed cardiomegaly with upper lobe diversion and a small effusion at the left base. Her electrocardiogram (ECG) showed sinus rhythm with no new changes. Arterial blood gas (ABG) on 40% inhaled oxygen revealed a metabolic alkalosis, hypercapnia and hypoxia (pH 7.52, pCO2 8.81 kPa, pO2 9.12 kPa, and HCO3– 52 mmol/l).
The patient was given intravenous potassium replacement therapy initially, followed by oral potassium supplements. She also received intravenous furosemide 40 mg twice daily for several days, to relieve her peripheral oedema, and higher oral doses of spironolactone. After 5 days her oedema had greatly improved, serum potassium was 4.5 mmol/l, she was normotensive, and her acid–base balance had corrected. She was discharged home.
She was readmitted 2 weeks later with reduced level of consciousness, hypertension, and signs of right heart failure. Her U&Es on admission were sodium 143 mmol/l, potassium 2.2 mmol/l, urea 12.6 mmol/l, and creatinine 175 mmol/l. Her potassium concentration had decreased despite an increase in her spironolactone dose. The serum bicarbonate was again grossly elevated at 59 mmol/l, while chloride was 68 mmol/l. ABG on admission on 28% oxygen revealed a metabolic alkalosis, hypercapnia and hypoxia.
On further questioning about additional medication, the patient admitted to drinking around 25 100 ml bottles of kaolin and morphine mixture over the previous 72 h due to her feeling depressed. She had been buying the mixture from her local chemist for approximately 5 years for relief of diarrhoea due to irritable bowel syndrome. She developed an addiction to the mixture and, despite no continued diarrhoeal symptoms, steadily increased the amount she was ingesting to a current amount of 5–8 bottles per week.