LABORATORY/DIAGNOSTIC DATA: CBC normal. Chemistry showed sodium 152, potassium 4.2, chloride 102, bicarbonate 26, BUN 19, creatinine 0.9, glucose 92. Upon discharge, sodium 134, potassium 4.3, chloride 102, bicarbonate 24, BUN 19, creatinine 0.7, glucose 88. Liver function is normal. Troponin less than 0.5. Magnesium 1.9, calcium 8.8. Urinalysis unremarkable. Urine culture negative. Sedimentation rate 10. CRP 0.3. TSH 5.7. CK-MB normal.
Left shoulder x-ray showed degenerative changes, mild intracapsular effusion. Adenosine Cardiolite stress test showed moderate size reversible ischemia in the inferolateral wall, ejection fraction 50%. Chest x-ray showed cardiomegaly, no infiltrates. Urinalysis unremarkable. CT angiogram showed left ventricular ejection fraction of 55%, left main artery 40% stenosis in the distal LAD. All grafts were patent. LAD occluded in the distal portion. First diagonal also occluded. Left circumflex, nondominant diffuse small vessel distal disease as well as moderate disease in ostium. Moderate biatrial enlargement. Pulmonary artery dilatation of 3.7 cm. EKG showed normal sinus rhythm, right bundle branch and new T-wave inversion in V3 to V6 leads. Left ribs, no fracture or dislocation.
LABORATORY/DIAGNOSTIC DATA: CBC: WBC 8.8, hemoglobin 13.2, hematocrit 39.4, MCV 93.4, platelets 128,000. Protime 10.6, INR 1.04, aPTT 27.7. Heparin antibody was negative. Chemistry profile, through the emergency room, glucose 132, BUN 18, creatinine 1.2, sodium 142, potassium 4.6, chloride 106, CO2 of 26, calcium 8.7, total protein 6.8, and albumin 4.1. SGOT 38, SGPT 72, alkaline phosphatase 89, total bilirubin 0.7, and magnesium 2.2. Troponin was less than 0.5 x2; one troponin was 0.67. BNP was 118. Homocysteine level was 12. ANA was negative. Cardiolipin antibodies were all negative. Urinalysis was within normal limits. Stool for occult blood was negative x2. Protein S was 128, antithrombin III was 60, protein C was 109. Anticardiolipin antibodies were negative. Prothrombin G mutation was unremarkable. Factor V Leiden mutation was negative.
CT scan of the chest revealed resolution of the pulmonary emboli previously seen. Bullous emphysema was present. Portable chest x-ray at the time of admission revealed stable chest findings with no active pulmonary disease. Venous duplex scan of the bilateral lower extremities reveal bilateral deep venous thrombosis. Echocardiogram revealed no significant pericardial effusion. There was normal left ventricular size with uniformly normal left ventricular wall motion. Left ventricular ejection fraction was greater than 55%. The mitral and tricuspid valves appeared to open well. The aortic valve was trileaflet and opened well. The pulmonic valve was not seen. There were no intracardiac masses present. There was trivial tricuspid regurgitation. Normal left ventricular systolic function without any evidence of right ventricular enlargement or pulmonary hypertension. The aortic root was upper limits of normal at 3.7 cm. A preliminary report from the CT scan of the chest revealed bilateral pulmonary embolism.
LABORATORY DATA: CBC: WBC 5.5, hemoglobin 14.6, hematocrit 43.2, MCV 95.4, platelets 182,000, polys 59, bands 6, lymphs 28, monocytes 6, eosinophils 1. Atypical lymphs were seen. Prothrombin time 10, INR 0.94, aPTT 27.2, D-dimer 0.76. Chemistry profile: Sodium 141, potassium 4.3, chloride 104, CO2 of 26, BUN 13, creatinine 0.7, glucose 96, calcium 8.6, magnesium 1.9. Total bilirubin 0.3, SGOT 25, SGPT 37. Troponin less than 0.4. Total protein 7.5, albumin 3.7, globulin 3.8. Alkaline phosphatase 74. Carbamazepine level was 10.2 initially and later 11.5, normal range reported 12.
Chest x-ray in the emergency room revealed no significant change. The cardiac silhouette was stable and no focal consolidation or pleural effusion was appreciated. Head CT scan revealed no intracranial hemorrhage, mass effect, extraaxial fluid collections or fracture. The visualized sinuses and the mastoid air cells were aerated. Pulmonary CT angiogram with the pulmonary embolism protocol revealed a left upper lobe mass suspicious for neoplasia. It was associated with mediastinal and bilateral hilar adenopathy. Also noted was a bilateral lower lobe atelectasis and interstitial change. Brain MRI was unremarkable. Cervical spine MRI revealed intervertebral disk degenerative changes present within the cervical spine. Maxillofacial CT in the axial plane with coronal reconstruction views revealed no acute abnormality. There was a deviated nasal septum.
CT scan of the chest revealed resolution of the pulmonary emboli previously seen. Bullous emphysema was present. Portable chest x-ray at the time of admission revealed stable chest findings with no active pulmonary disease. Venous duplex scan of the bilateral lower extremities reveal bilateral deep venous thrombosis. Echocardiogram revealed no significant pericardial effusion. There was normal left ventricular size with uniformly normal left ventricular wall motion. Left ventricular ejection fraction was greater than 55%. The mitral and tricuspid valves appeared to open well. The aortic valve was trileaflet and opened well. The pulmonic valve was not seen. There were no intracardiac masses present. There was trivial tricuspid regurgitation. Normal left ventricular systolic function without any evidence of right ventricular enlargement or pulmonary hypertension. The aortic root was upper limits of normal at 3.7 cm. A preliminary report from the CT scan of the chest revealed bilateral pulmonary embolism.
LABORATORY DATA: CBC: WBC 5.5, hemoglobin 14.6, hematocrit 43.2, MCV 95.4, platelets 182,000, polys 59, bands 6, lymphs 28, monocytes 6, eosinophils 1. Atypical lymphs were seen. Prothrombin time 10, INR 0.94, aPTT 27.2, D-dimer 0.76. Chemistry profile: Sodium 141, potassium 4.3, chloride 104, CO2 of 26, BUN 13, creatinine 0.7, glucose 96, calcium 8.6, magnesium 1.9. Total bilirubin 0.3, SGOT 25, SGPT 37. Troponin less than 0.4. Total protein 7.5, albumin 3.7, globulin 3.8. Alkaline phosphatase 74. Carbamazepine level was 10.2 initially and later 11.5, normal range reported 12.
Chest x-ray in the emergency room revealed no significant change. The cardiac silhouette was stable and no focal consolidation or pleural effusion was appreciated. Head CT scan revealed no intracranial hemorrhage, mass effect, extraaxial fluid collections or fracture. The visualized sinuses and the mastoid air cells were aerated. Pulmonary CT angiogram with the pulmonary embolism protocol revealed a left upper lobe mass suspicious for neoplasia. It was associated with mediastinal and bilateral hilar adenopathy. Also noted was a bilateral lower lobe atelectasis and interstitial change. Brain MRI was unremarkable. Cervical spine MRI revealed intervertebral disk degenerative changes present within the cervical spine. Maxillofacial CT in the axial plane with coronal reconstruction views revealed no acute abnormality. There was a deviated nasal septum.
LABORATORY STUDIES: The patient has a myoglobin level of 484, which is elevated. White count is 10.8, hemoglobin is 9.8, platelets are 192,000. BUN 66 and creatinine 2.8. Sodium 137 and potassium 5.4. Total bilirubin is 2.3. Urinalysis shows rbc's 206 in high power field and wbc's of 142 per high power field. Leukocyte esterase large.
CT scan of the head shows a small to moderate subdural hemorrhage on the right, greatest along the tentorium but also extending laterally along the posterior temporal and parietal lobes. Chest x-ray shows possible early pneumonia adjacent to the left heart border, pulmonary nodule in the right upper lobe medially. He has a urine culture, which shows Klebsiella, Enterococcus and Serratia greater than 100,000 colony-forming units.
CT scan of the head shows a small to moderate subdural hemorrhage on the right, greatest along the tentorium but also extending laterally along the posterior temporal and parietal lobes. Chest x-ray shows possible early pneumonia adjacent to the left heart border, pulmonary nodule in the right upper lobe medially. He has a urine culture, which shows Klebsiella, Enterococcus and Serratia greater than 100,000 colony-forming units.
LABORATORY DATA: CBC: WBC 7.9, hemoglobin 13.4, hematocrit 40.8, MCV 97.8, platelets 134,000, lymphs 11.5, polys 79.6, monocytes 6.5, eosinophils 1.9, basophils 0.5. Protime 11.8, INR 1.13, aPTT 28.4, repeat was 42.8. Chemistry profile through the emergency room revealed glucose 132, BUN 37, creatinine 1.6, sodium 142, potassium 3.9, chloride 110, CO2 of 26, calcium 9.4, total protein 6.6, albumin 3.8, SGOT 36, SGPT 41, alkaline phosphatase 56, total bilirubin 1.6, magnesium 2.1. Troponin less than 0.5 x4, myoglobin 67. Cholesterol 88, triglyceride 126, HDL cholesterol 30, LDL cholesterol 33. BNP was 729. Hemoglobin A1c was 5.9. Urinalysis was within normal limits. Stool for occult blood was negative.
Myocardial perfusion imaging with Cardiolite revealed irreversible perfusion defect in the inferior wall, presumably due to underlying infarct. The left ventricle was markedly dilated. Ejection fraction of the left ventricle was 25%. Portable chest x-ray at the time of admission revealed bilateral infiltrates and mild vascular congestion, most likely representing congestive heart failure. EKG revealed an electronic ventricular pacemaker with premature ventricular complexes. When compared with a previous EKG, ventricular rate had decreased by 18 beats per minute. There was limited echocardiographic study and Optison was used to improve endocardial visualization. Mild left atrial enlargement with normal right atrial size. Mild left ventricular chamber enlargement with decreased left ventricular contractility. Estimated ejection fraction was in the 40% range. There was global hypokinesia; however, the inferior wall did appear more hypokinetic than the remainder of the ventricle, as does the posterior wall. There was a small pleural effusion. Normal aortic root dimension. Mild thickening of the mitral valve with normal opening and closure. Mild thickening of the aortic valve with normal opening and closure. Normal appearance of the tricuspid valve. Doppler exam showed mild tricuspid regurgitation with no tricuspid stenosis. There was moderate pulmonary hypertension and estimated pulmonary pressures of approximately 50 to 55. Normal function of the aortic valve with no regurgitation or stenosis. Normal function of the pulmonic valve. Trace mitral regurgitation with no mitral stenosis.
Myocardial perfusion imaging with Cardiolite revealed irreversible perfusion defect in the inferior wall, presumably due to underlying infarct. The left ventricle was markedly dilated. Ejection fraction of the left ventricle was 25%. Portable chest x-ray at the time of admission revealed bilateral infiltrates and mild vascular congestion, most likely representing congestive heart failure. EKG revealed an electronic ventricular pacemaker with premature ventricular complexes. When compared with a previous EKG, ventricular rate had decreased by 18 beats per minute. There was limited echocardiographic study and Optison was used to improve endocardial visualization. Mild left atrial enlargement with normal right atrial size. Mild left ventricular chamber enlargement with decreased left ventricular contractility. Estimated ejection fraction was in the 40% range. There was global hypokinesia; however, the inferior wall did appear more hypokinetic than the remainder of the ventricle, as does the posterior wall. There was a small pleural effusion. Normal aortic root dimension. Mild thickening of the mitral valve with normal opening and closure. Mild thickening of the aortic valve with normal opening and closure. Normal appearance of the tricuspid valve. Doppler exam showed mild tricuspid regurgitation with no tricuspid stenosis. There was moderate pulmonary hypertension and estimated pulmonary pressures of approximately 50 to 55. Normal function of the aortic valve with no regurgitation or stenosis. Normal function of the pulmonic valve. Trace mitral regurgitation with no mitral stenosis.
