Heart failure and breast enlargement suggesting cancer.

(figure). Capillary loops were not thickened and no trichrome positive deposits were seen. The tubules, interstitium, and blood vessels were all normal. Immunofluorescence studies were negative for all immunoglobulins, fibrin, and g-IC. Electron microscopy showed diffuse foot process fusion of the podocytes (see figure) with no electron dense deposits. The basement membrane was normal. He received corticosteroids, and his oedema decreased dramatically in two weeks. He again defaulted follow up. Comment Our patient clearly had mild decompression sickness with substernal pain, dizziness, headache-usual symptoms of the decompression syndrome'-and niinimal change 'glomerulonephritis. 'Any association between the two conditions is difficult to ascertain. Rapid ascent to the surface after diving causes decompression sickness because inert gases, mainly nitrogen, which are dissolved in the blood and tissues, come out of solution and form bubbles that produce embolism. The protean manifestations of decompression sickness cannot be completely explained by the physical effects ofthe bubbles. Interface ofblood and bubbles causes protein denaturation, increases platelet adhesiveness, produces red cell sludging in the microcirculation, and promotes the formation oflipid emboli.' Localised oedema occurs in 90/o of patients with acute decompression sickess,2 although we know of no reports of generalised oedema. Minial change glomerulonephritis might be the result of rapid change in environmental pressure, especially if the glomerular basement membrane is regarded as a thixotropic gel.3 The occurrence ofthe nephrotic syndrome with decompres-sion sickness might have been coincidental. The change in environmental pressure on rapid ascent after diving, therefore, probably accelerates and aggravates oedema, perhaps the reverse of what occurs in up to the neck immersion in water. Unilateral or asymmetric pleural effusions are a well recognised clinical finding in moderate cardiac failure.' We should like to add breast enlargement mimicking malignancy to the unilateral manifestations of congestive cardiac failure. An 81 year old woman presented with a three week history of general malaise with swelling of the right arm and right breast and increasing abdominal girth. Nine months previously she had been admitted with episodic dyspnoea. Clinically she had had right basal consolidation and mild congestive cardiac failure. Chest radiography had suggested pulmonary infcion. She was not given anticoagulants but responded to antibiotics and diuretics. At outpatient follow up at eight months she was well. At her second presentation she was short of breath at rest and had massive pitting oedema to the sacrum, over the right flank, and over the whole ofthe right arm. The right …