Episode 1.46 Download 2021
Patricia Strawbridge
We report a 96-year-old Japanese man who developed a sudden onset of left hemiplegia and coma. He was found to have diabetes mellitus, hypertension, and atrial fibrillation since 1996 with occasional episodes of congestive heart failure. He was otherwise apparently well until July 5 of 1997 when he developed a sudden onset of unresponsiveness and convulsion involving his right hand and was admitted to our hospital. On admission, his BP was 210/120 mmHg, heart rate 76/min and irregular, BT 36.5 degrees C, and Cheyne-Stokes respiration. General medical examination was otherwise unremarkable. Neurologic examination revealed semicoma, conjugated deviation to the right, loss of oculocephalic response, left facial paresis of central type, flaccid left hemiplegia, and bilateral Babinski sign. Pertinent laboratory findings are as follows: BUN 47 mg/dl, creatinine 1.46 mg/dl, GPT 69 IU/l, LDH 1,142 IU/l, and CK 385 IU/l. A chest x-ray film revealed cardiac enlargement and EKG showed left ventricular hypertrophy and atrial fibrillation. Cranial CT scan revealed low density areas involving the right anterior cerebral and the right posterior cerebral artery territories. He was treated with an intravenous osmotic agent and short course of intramuscular steroid. He remained unconscious despite these treatment and developed sudden cardiopulmonary arrest three weeks after the admission. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had suffered from cerebral embolism of cardiac origin. The cause of the death was ascribed to acute subendocardial myocardial infarction. Most of the participants agreed with this conclusion. Postmortem examination revealed an old subendocardial myocardial infarction involving the posterior septal region and posterolateral wall of the left ventricle. Neuropathologic examination revealed hemorrhagic infarctions involving the territories of the right anterior cerebral, right middle cerebral, right posterior cerebral, and left anterior cerebral arteries. The left A1 portion of the anterior cerebral artery was hypoplastic, and the left pericallosal artery appeared to have been receiving blood supply from the right anterior cerebral artery through the anterior communicating artery. The large arteries in the base showed marked arteriosclerosis; particularly, the initial portion of the right posterior artery showed near complete arteriosclerotic occlusions. These characteristic arterial changes appeared to be the reason why this patient suffered from an extensive infarction from what appeared to have been a single episode of cerebral embolism probably initially involving the right internal carotid artery.
There are few studies evaluating the effect of fever on the bioavailability of oral antimicrobials. Owing to the growing interest in early conversion of febrile hospitalized patients from intravenous to oral therapy to reduce costs and avoid line sepsis, we evaluated the absorption of a single 500 mg dose of ciprofloxacin in 12 patients during an acute febrile episode and following defervescence. Patients able to take medication by mouth, oral temperature > or = 38.9 degrees C, and no known gastrointestinal disease were enrolled. Medications known to interact with the test agent were discontinued. Serum samples were obtained prior to and up until 12 h postdose. Pharmacokinetic parameters were obtained from the concentration-time profile using noncompartmental methods. The mean values for C(max) were 2.45 +/- 0.77 and 2.31 +/- 1.26 microg/ml, for T(max) 1.48 +/- 0.75 and 2.48 +/- 1.46 h, AUC(0-->infinity) 10.91 +/- 3.64 and 11.05 +/- 4.41 microg/ml h, and T (1 2 ) 4.05 +/- 0.65 and 4.08 +/- 0.76 h, respectively, for the febrile and afebrile periods. No statistically significant differences were observed between these parameters. We conclude that oral ciprofloxacin is well absorbed and is a suitable alternative to intravenous therapy in selected patients during an acute febrile illness.
To test the utility and safety of percutaneous transluminal coronary angioplasty (PTCA) after recombinant tissue plasminogen activator (t-PA), we performed the procedure in all suitable candidates with acute myocardial infarction (MI) who had successful t-PA mediated coronary thrombolysis. Twenty consecutive patients with MI received t-PA after coronary angiographic conformation of total occlusion. Successful recanalization with t-PA was achieved in 13 patients, leaving a residual obstruction of 84 +/- 6% in the nine patients for whom PTCA was attempted at a mean of 21.6 h. Success was achieved in seven patients, leading to a residual lesion of 29 +/- 7%. In the two patients for whom PTCA was unsuccessful, total reocclusion occurred prior to the attempt despite therapy with heparin, aspirin, dipyridamole, and nifedipine. All PTCA procedures were uncomplicated. Serial two-dimensional echocardiography at 10 days, compared to admission, demonstrated infarct zone wall motion index improvement in the patients with successful PTCA (group A, 0.83 +/- 0.36 to 1.46 +/- 0.49) as compared to the 13 patients without thrombolysis or successful PTCA (group B, 0.61 +/- 0.26 to 0.66 +/- 0.39), (P less than 0.05). One patient of group A sustained a massive stroke at 2 weeks after hospital discharge. In the remaining six patients, follow-up exercise testing and/or coronary arteriography demonstrated a negative treadmill test and/or patent infarct vessel, respectively. After successful PTCA, no patient had clinical signs of reocclusion, reinfarction, postinfarction angina, or congestive heart failure. At 9.4 +/- 2 months, all six patients are asymptomatic and have returned to work. Thus, sequential PTCA after t-PA can be performed safely and successfully in patients with MI and this approach may be associated with improved regional function and a favorable post-MI course.
As Part III of a comprehensive evaluation of CMAQ for the summer 1999 Southern Oxidants Study episode, the observed number ( N), volume ( V), surface area ( S), and size distributions of accumulation-mode particles during the Aerosol Research Inhalation Epidemiological Study (ARIES) are used to evaluate CMAQ's capability in reproducing PM size distributions. CMAQ underpredicts V, S, and geometric number mean diameter (by a factor of 1.24-1.54), and overpredicts N, geometric standard deviation, and geometric volume mean diameter (by a factor of 1.46-2.2) on most days. In addition to inaccurate meteorology and emissions, insufficient condensational growth of PM and uncertainty in the initial size distribution may contribute to the underpredictions in V and S. An overestimation of the PM number emission rates (by a factor of 3-5.3) and several other model assumptions/treatments may contribute to the PM number overpredictions. Among the factors that we studied, the floor value of K zz, the boundary conditions (BCONs) of O 3, the emissions of gaseous precursors such as NO x and NH 3 and primary PM species such as POM, and the assumed initial PM size distribution and emission fractions have been identified to be the most influential factors that affect the overall model performance. Sensitivity simulations with a floor value of K zz of 0.1 cm 2 s -1, adjusted emissions of NO x, NH 3, and POM, and adjusted initial PM size distribution and emission fractions provide moderate-to-significant improvements. Further investigation into the uncertainties/deficiencies in model treatments for PM such as gas-to-particle mass transfer will identify additional causes for discrepancies between observations and predictions.
Subjects with more than 3 episodes of acute respiratory infections/year had a statistically significant lower value of plasma concentration of zinc as compared to those who had less than 3 episodes/year (14.230.76 μmol/L versus 15.891.46 μmol/L, p
There are no significant differences between those who had an episode of acute diarrhea/year compared with more than 1 episode/year (15.491.44 μmol/L versus 15.091.56 μmol/L, p=0.480, Student's t test).
dd2b598166