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Deutsche Medizinische Wochenschrift 1996-Apr

[Splenic infarction caused by paradoxical emboli in severe pulmonary hypertension].

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala
Ingia / Ingia
Kiungo kimehifadhiwa kwenye clipboard
B Mödl
N Reuter
C Pfafferott
A Wirtzfeld

Maneno muhimu

Kikemikali

METHODS

A 55-year-old woman developed increasing shortness of breath and breath-independent pain in the left lower chest. 20 years previously she had had an episode of pulmonary embolism and 10 years previously a central venous thrombosis in the left eye. No cause of the increased thrombogenesis had been found. On admission she had resting dyspnoea but a stable circulation. On auscultation the breath sounds were diminished over the left base and there was a diastolic murmur over the pulmonary area with an accentuated second sound. There was also marked tenderness below the left costal margin. Recurrent pulmonary embolism or left-sided pleuropneumonia was suspected.

METHODS

Arterial blood gases (without additional oxygen) showed severe hypoxaemia (pO2 42.3 mm Hg, pCO2 27.8 mm Hg, pH 7.455, oxygen saturation 80.5%). Transthoracic and transoesophageal echocardiography showed normal left ventricular dimensions, right atrial and ventricular dilatation, and an atrial septal aneurysm with a right to left interatrial shunt. Right heart catheterisation demonstrated severe pulmonary hypertension. Sonography, computed tomography and scintigraphy revealed multiple splenic infarcts.

METHODS

Heparinisation was instituted (partial thromboplastin time 70-90 s) and overlapping oral anticoagulation to a Quick value of 20%. Subsequently the calcium antagonist felodipine (15 mg daily) was given. The mean pulmonary artery pressure was 61 mm Hg before and 57 mm Hg after treatment.

CONCLUSIONS

Splenic infarction resulting from paradoxical embolisation is rare, but should be routinely considered in the presence of thromboembolic phenomena.

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