Thoracic outlet syndrome in a throwing athlete diagnosed with MRI and MRA

Thoracic outlet syndrome comprises the clinical manifestations in the arm caused by compression of the neuro-vascular bundle as it leaves the thoracic inlet. The neuro-vascular bundle is composed of the subclavian artery, the subclavian vein, and the bra-chial plexus. The symptoms of thoracic outlet or inlet syndrome are most often caused by compression of the nerves of the brachial plexus, which is involved in up to 98% of cases; the remainder are due to vascular compression. MRI with MRA demonstrates well the anatomy of the brachial plexus as well as any vascular compression or occlusion. The relationship of the axillary and subclavian vein to the first rib and subclavius muscle also can be demonstrated. We present a college baseball player who presented with numbness in the fingers of his throwing hand when throwing a baseball. Evaluation with spin-echo and two-dimensional time-of-flight MR angiographic (MRA) imaging of the thoracic outlet region revealed obstruction of the subclavian vein with the arm abducted. To our knowledge, no such cases have been diagnosed previously with MRI.     

Optimum lead positioning for recording bipolar atrial electrocardiograms during sinus rhythm and atrial fibrillation

Background: To date, Holter monitoring has been predominantly utilized in the investigation and monitoring of ventricular arrhythmias and myocardial ischemia. Whether currently employed lead configurations are optimal for recording atrial electrocardiograms (ECGs) is unknown. Hypothesis: This study was undertaken to determine which conventional and novel lead configurations are optimal for recording atrial electrical activity during sinus rhythm and atrial fibrillation. Methods: Recordings were performed on eight healthy volunteers in sinus rhythm and four patients in atrial fibrillation. Each subject had 10 ECGs of three bipolar and three augmented unipolar leads recorded during supine rest, while rising to upright, and during standing rest, yielding a total of 60 leads (30 bipolar leads). Each tracing was inspected by two observers, and parameters such as P-wave amplitude and duration, whether the P-wave onset was clearly seen, atrial fibrillatory-wave amplitude, and amplitude of noise during standing were scored. Results: Leads recording interiorly and leftward orientated bipoles provided the best registration of sinus P waves. The Pwave amplitude in the standard bipolar C5 lead (0.12 d? 0.02 mV) was, however, inferior to others such as recordings between Cl and C6 positions (P-wave amplitude 0.16 d? 0.02 mV) or from below the right clavicle to the left upper quadrant of the abdomen (0.16 d? 0.01 mV). Optimal recording of fibrillatory waves was from different leads, such as a bipole from below the left clavicle to a low C1 position (fibrillatory wave amplitude 0.27 d? 0.03 mV). Conclusion: When Holter recordings are performed for the investigation of atrial arrhythmias, nonstandard lead configurations provide superior recording of atrial electrical activity. We advocate the use of electrodes positioned from C1 to C6, from below the left clavicle to a low C1 position, and a vertically orientated lead from the manubium to the twelfth vertebra or the xiphisternum.     

Reflections on the anesthesia-neurosurgical alliance

This is an uncommon article for a modern scientific journal in that it contains no data, it is written in the first person, and it recounts only the personal experiences of a clinical neurosurgeon about the evolution of neurosurgery, anesthesiology, and neuroanesthesiology in Philadelphia from 1939 to 1988, when the surgeon retired from the operating room. The surgeon, Fred Murtagh, practiced neurosurgery during an extraordinarily formative time for American medicine and neurosurgery. He was on the faculty of Temple University for many years and currently is Emeritus Professor of Neurosurgery at the University of Pennsylvania. His observations are from the point of view of a man who has been in the operating room continuously since the early 1940s grappling with the practical problems confronting the neurosurgeon. In addition, he is a highly observant individual and considered by many to be an extraordinary teacher. With respect to the genesis of this article, the neuroanesthesia group at the University of Pennsylvania invited Dr. Murtagh to one of their monthly meetings. A tape recorder was placed in front of him and we were privileged to listen to 2 h of reminiscence about his career and relationships between anesthesiologists and neurosurgeons. Over a several year period, Fred Murtagh and D. S. Smith extracted that tape and wrote the following article. It is my belief that this article, despite its unorthodox format, contains observations of import to clinicians in general and to those who practice the subspecialty of neurosurgical anesthesia.     

Two ＇fishy＇ tales

1 病例1:患儿"死了" 我在一个农村医院值班的时候,抢救室接诊了1个病情离奇的2岁越南裔女孩.患儿没有自主呼吸,靠急救工作人员给她人工送气.急救工作人员叙述说,他们接到电话,对方让他们去接1个即将分娩的孕妇.然而当急救工作人员到达现场时,没有发现孕妇,反而发现1个年轻的越南裔妇女,怀里抱着"睡着的"女儿.工作人员发现患儿没有呼吸,估计她可能已经"死了",但奇怪的是可以清楚地摸到她的脉搏.工作人员立即给患儿人工送气,她的面色有所好转,在急救车送其回医院的路上,她的情况一直比较稳定.     

Haemodynamic effects of glucagon

The central and peripheral vascular haemodynamic effects of glucagon were studied in 29 patients. With a single dose method of 2 or 5 mg. glucagon intravenously the inotropic action of the drug produced immediate increased myocardial contractility with significant increase in cardiac output and enhanced cardiac performance, and lowering of pulmonary arterial pressure and pulmonary vascular resistance. No primary peripheral vascular effect was evident, and the increased systemic pressure and lowered systemic resistance appear to be secondary to the central action of the drug. With the dosage used there were no undesirable side-effects apart from a feeling of slight nausea. Though the haemodynamic effects are abrupt, reaching their maximum values in the first 10 minutes after injection, they tend to be dissipated within half an hour, presumably due to the very rapid destruction of the drug. Repeated booster doses rather than continuous infusion may be the method of choice to maintain an increased cardiac output. The positive chronotropic action of the drug may cause transient palpitations. Glucagon increased the cardiac output in the acute phase of myocardial infarction by 42 per cent. The haemodynamic effects in chronic rheumatic heart disease are more varied, and it may increase left atrial pressure in mitral stenosis, which is undesirable. Hyperglycaemia results from liver glycogenolysis but blood sugar levels rarely exceeded 200 mg./100 ml. These results warrant further study of the value of glucagon as a positive inotropic agent in low output heart failure, especially in acute myocardial infarction with cardiogenic shock, or after cardiac surgery, or in unrelieved chronic congestive heart failure.     

Use of amiodarone and digoxin specific Fab antibodies in digoxin overdosage.

A 61 year old man with mild aortic stenosis and chronic depression took 12.5 mg digoxin in a suicide attempt. Ventricular tachycardia and fibrillation were resistant to lignocaine and to phenytoin but responded to intravenous amiodarone, with restoration of pacing. Because of persistent hyperkalaemia he was also treated with Fab fragments of digoxin specific antibody, which bound most of the ingested digoxin. It is suggested that the treatment of choice in severe digoxin poisoning is amiodarone for ventricular arrhythmias followed by pacing if necessary and the use of Fab antibody fragments if hyperkalaemia persists.