B. Modl et al., SPLENIC INFARCTS CAUSED BY PARADOXICAL EM BOLI IN SEVERE PULMONARY-HYPERTENSION, Deutsche Medizinische Wochenschrift, 121(17), 1996, pp. 556-560
History and clinical findings: A 55-year-old woman developed increasin
g shortness of breath and breath-independent pain in the left lower ch
est. 20 years previously she had had an episode of pulmonary embolism
and 10 years previously a central venous thrombosis in the left eye. N
o cause of the increased thrombogeneicity had been found. On admission
she had resting dyspnoea but a stable circulation. On auscultation th
e breath sounds were diminished over the left base and there was a dia
stolic murmur over the pulmonary area with an accentuated second sound
. There was also marked tenderness below the left costal margin. Recur
rent pulmonary embolism or left-sided pleuropneumonia was suspected. I
nvestigation: Arterial blood gases (without additional oxygen) showed
severe hypoxaemia (pO(2) 42.3 mm Hg, pCO(2) 27.8 mm Hg, pH 7.455, oxyg
en saturation 80.5%). Transthoracic and transoesophageal echocardiogra
phy showed normal left ventricular dimensions, right atrial and ventri
cular dilatation, and an atrial septal aneurysm with a right to left i
nteratrial shunt. Right heart catheterisation demonstrated severe pulm
onary hypertension. Sonography, computed tomography and scintigraphy r
evealed multiple splenic infarcts. Treatment and course: Heparinisatio
n was instituted (partial thromboplastin time 70-90 s) and overlapping
oral anticoagulation to a Quick value of 20%. Subsequently the calciu
m antagonist felodipine (15 mg daily) was given. The mean pulmonary ar
tery pressure was 61 mm Hg before and 57 mm Hg after treatment. Conclu
sion: Splenic infarction resulting from paradoxical embolisation is ra
re, but should be routinely considered in the presence of thromboembol
ic phenomena.