The mitral valve area was 0

The mitral valve area was 0.6 cm2, and the other cardiac valves were normal. response to tissue injury or infection. Activation of leukocytes, K252a platelets, complement, and factor XII by contact with the bypass circuit and surgical trauma is followed by the systemic secretion of cytokines and other inflammatory mediators. The induced expression of adhesion molecules on activated leukocytes and endothelial cells can result in the sequestration of white cells within tissues and a clinical syndrome, the systemic inflammatory response syndrome (SIRS), which differs quite widely among patients. In its extreme form, it can lead to multiple organ failure that often includes the adult respiratory distress syndrome, a condition associated with massive leukocyte infiltration in the lung and high mortality.1The locked-in syndrome is a rare clinical entity consisting of quadriplegia, paralysis of the lower cranial nerve, mutism, and bilateral paresis of horizontal gaze and is associated with unaltered consciousness, with intact vertical eye movements and blinking allowing some form of human communication by way of eye codes. Furthermore, there is usually cranial nerve weakness with the sparing of only the more laterally placed nuclei.2The locked-in syndrome results most commonly from a lesion in vertical pons, although extensive bilateral destruction of cortical-bulbar and cortico-spinal tracts in the pedunculi cerebri may be responsible. Sensory impairment due to medial lemniscuses involvement and damage to the decussating fibers from the spinal tract of trigeminal nerve are inevitable. The lesion at the basis pontis spares the pathways for somatic sensation and the non-specific ascending system of neurons and fibers K252a responsible for arousal and wakefulness; nevertheless, it interrupts the cortico-bulbar and cortico-spinal pathways, depriving the patient of speech and the ability to respond in any other way. The locked-in syndrome has been reported after ventral pontine infarction following basilar artery occlusion, air embolism,3,4pontine hemorrhage,5tumor, trauma, heroin abuse, encephalitis,6hypoglycemia,7and Basilar artery ectasia.8We add here a new cause, which is severe inflammatory reaction due to cardiopulmonary bypass with the gangrene of the distal extremity or the blue toe syndrome. == Case Report == A 45-year-old woman was admitted to our heart center with severe mitral stenosis and left atrial clot. The patient gave a history of shortness of breath on minimal exertion for one week and no cerebral symptoms, Rabbit Polyclonal to Smad1 including headache, dizziness, transient ischemic attacks, or strokes. She was found to be fully conscious, alert, and oriented with stable vital signs. Blood pressure was 110/80 mmHg, and diastolic murmur was audible over the mitral area. Physical examination revealed intact cranial nerves, motor power, and sensation. There was no evidence of vasculitis such as Oslers nodes, Jane way pad, palmer erythema, or cyanosis of fingers. Blood investigation showed an erythrocyte sedimentation rate (ESR) of 4 mm with no leukocytosis and a white blood cell (WBC) of 10.000 mm3. The electrolytes and kidney and liver function were within normal limits. Chest X-ray showed prominence of the left cardiac border due to left atrial enlargement. Electrocardiography was indicative of no change, but twodimensional echocardiography revealed a large bulky non-mobile thrombosis in the left atrium with severe mitral stenosis. The mitral valve area was 0.6 cm2, and the other cardiac valves were normal. Pre- and postoperative laboratory measurements included negative antinuclear antibodies and rheumatoid factor, and elevation of C4 & C3 components of complement; in addition, HBS Antigen (especially in polyarteritis nodosa) was negative. The patient underwent open heart surgery via the ascending aorta K252a and bicaval cannulation. The aorta was cross-clamped, and the heart was arrested with cold cardioplegia by achieving systemic hypothermia at 30C on the cardiopulmonary bypass. Intraoperatively, the stenotic mitral valve was found to have a bulky clot attached to the valve and wall of the left atrium. The diseased mitral valve and the clot were excised, and the left atrial cavity was irrigated with copious amounts of normal saline and a valve was thereafter implanted. The left ventricle was then filled completely with saline and blood and fully deaired. The patient was weaned successfully off cardiopulmonary bypass with inotropic support and K252a transferred to the intensive care unit. After 6 hours, blood pressure dropped and central venous pressure elevated and the extremity became.