A forty-year-old man presented with a two-month history of exertional dyspnoea and intermittent palpitations. The symptoms had worsened significantly in the few days preceding admission and he complained of orthopnoea and a persistent dry cough. He denied any antecedent infections but admitted to occasional cocaine and alcohol use. Examination at this time was unremarkable except for a persistent tachycardia of 126 beats per minute. Electrocardiography confirmed sinus tachycardia. Chest X-ray showed an increased cardiothoracic ratio and a globular heart.
His past history was significant for bilateral total hip replacement 4 years prior to presentation for a 2-year history of hip pain and inability to weight bear. Avascular necrosis was suspected. The procedure on the right was complicated by loosening of the acetabular cap which required reoperation one day postoperatively. The DePuy Corail  Total Hip System (cementless femoral stem without collar) was used bilaterally.
A bedside echocardiogram during this admission revealed severely impaired left ventricular systolic function in the absence of gross dilatation. The left ventricle also appeared hypertrophied. In addition, a circumferential pericardial effusion of significant size was noted. Ejection fraction was estimated at 40-45% by Simpson's biplane method on echocardiography.
Pericardiocentesis was carried out: a total of 1.32 L of straw-coloured clear pericardial fluid was aspirated and sent for testing. Bacterial culture (including Mycobacterium tuberculosis PCR) and cytology were negative. Biochemistry was compatible with a transudate.
He underwent extensive workup for possible causes: EBV; CMV; HEP screen (HBsAg, HAV IgM, and anti-HCV antibody); Rickettsia conorii IgM, M. pneumoniae, ANA, total ENA, RF, ANCA, total IgM, IgA, and IgG, all tested negative.
Following pericardiocentesis the cardiac contractility was observed to improve significantly on serial echocardiography; however ejection fraction did not improve. Speckling of the myocardium was, however, noted. Endomyocardial biopsy was performed which revealed no evidence of amyloid deposition on Congo red staining. Mild perivascular fibrosis around a few intramural vessels and mild vacuolation of a few cardiomyocytes was seen.
A repeat bedside echocardiogram showed reaccumulation of the pericardial effusion and the patient was subsequently started on colchicine 500 micrograms BD. His antifailure treatment was optimized. The pericardial effusion continued to recur, so definitive management of the pericardial effusion with a pericardial window was performed.
The patient was referred back to hospital from primary healthcare in view of a vague epigastric discomfort together with tachycardia. ECG confirmed new onset atrial flutter at 176 beats/min. He was anticoagulated with heparin and warfarin and urgent DC electrocardioversion was performed at 100 J under general anaesthetic, restoring sinus rhythm without any complications.
On this occasion, echocardiography showed severely impaired biventricular function with an LVEF 20% using Simpson's biplane method and advanced diastolic dysfunction with restrictive transmitral filling and raised filling pressure and a small localised pericardial effusion (inferolateral/inferior aspect of LV).
Right and left heart studies showed normal coronary arteries. Cardiac output was estimated at 3.5 L/min by temperature haemodilution method.
Given the past history of bilateral hip arthroplasty and persistent right-sided hip pain, the possibility of cardiomyopathy secondary to cobalt heavy metal poisoning due to a metal-on-metal (MoM) reaction from the hip prostheses was discussed. Whole blood cobalt levels were 4174 nmol/L (reference range < 5 nmol/L). The case was brought to the attention of the orthopaedic surgeon who performed the hip replacements and who confirmed that a cobalt-chromium alloy component was present (reference numbers provided below).
Ultrasound imaging of the right hip demonstrated an inhomogenous, generally hypoechoic fluid collection with internal scattered echogenic debris measuring 8 cm x 3 cm x 2.5 cm located between the skin and the right greater trochanter. The reporting radiologist suggested that this may represent an aseptic lymphocyte-dominated vasculitic-associated lesion reaction.
The left hip appeared largely unremarkable.
The need for right hip revision was discussed with the patient who understood and agreed.
Eight months later, revision of right total hip replacement was performed. Blackening of the gluteal muscle and greater trochanter secondary to metallosis was noted. The femoral stem was solid; however the head was dislocated. Thorough capsulotomy and synovectomy were performed. Postoperatively he was managed on ITU in view of his cardiomyopathy. Histology demonstrated reparative and inflammatory changes with metallosis.
Five months later, he had a much better exercise tolerance (NYHA class III improved to class I) and estimated left ventricular ejection fraction on echocardiography improved to 45-50%.