We report the case of a 62-year-old man who suffered from central thoracic pain, vomiting sensation in hands and nausea.
A week before she had had a similar episode without requiring medical assistance.
45 minutes after the symptoms appeared, the patient was assisted in the hospital of her area, diagnosed with a lower infarction, and started fibrinolysis with Streptokinase 1,500,000 IU.
The patient was also treated with Solinitrina, Aspirin and Zantac, and was referred to the Regional Hospital because there were no beds available in the Coronary Care Unit.
Half an hour after admission to the Regional Hospital (about 4.30 hours after symptoms), she begins with pain in both lower limbs, accompanied by intense sensitivity and absence of pulse.
Computerized Axial Tomography (CAT) was performed, ruling out aortic dissection and when embolism was suspected, the patient was referred to the Provincial Hospital.
A chest CT scan showed no pathology in the thoracic aorta and an ultrasound scan of the lower limbs showed bilateral occlusion at the poplite level.
She underwent surgery, performing bilateral embolectomy, obtaining coloration, but coldness persists.
Histopathological examination revealed fibrotic stenosis.
After the first hours the patient shows hemodynamic instability, with appearance of lice in the lower limbs, renal failure and shock, and finally death occurred 24 hours after the onset of symptoms.
The external examination of the cadaver showed violated red coloration in the lower third of thighs, knees, genital area and lower abdomen.
The lungs were increased in size and consistency, pressure is perceived crepitation, fingerprint remains after pressure (Fova) and cutting, after compressing, foam.
The right lung weighed 850 grams and the left lung weighed 640 g.
After the pericardial sac was infiltrated, a slight cardiomegaly weighing 390 grams was observed.
The left ventricle was hypertrophic with a maximum thickness in its free wall of 2 cm. Histopathological analysis of the heart shows chronic ischemic heart disease, on which lies an old infarction and a recent one, from 1 to 3 weeks of evolution.
The thoracic aorta shows a large ruptured atherosclerotic plaque, with intraplaque hemorrhage and adhering material below the cay.
The abdominal aortic endothelium is occupied by clotted reddish material.
The liver disease looks like this.
Liver and lung examination confirmed the macroscopic diagnosis of steatosis and pulmonary edema.
1.
Many emboli originating from ruptured atheromatous plaques that cause ischemic necrosis of the muscle fibers are found in arterioles responsible for irrigating the skeletal musculature of asbestos.
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Histologically, the kidneys present acute tubular necrosis, myoglobin pigment in tubules and emboli in arterioles resulting from rupture of atheroma plaques.
