Faculty Bibliography

A 30-year-old surgical resident was admitted to the hospital with symptoms of acute hepatitis; two days later he became comatose. Hepatitis B surface antigen had been detected in his serum two days prior to admission, but it was not detected at any time thereafter. Hepatitis B e antigen, antibody to hepatitis B core antigen, and antibody to hepatitis B surface antigen were detected using sensitive radioimmunoassays at admission. Titers of antibody to hepatitis B core antigen increased over the next five weeks. Clearance of hepatitis B e antigen and subsequent appearance of antibody to hepatitis B e antigen accompanied clinical improvement and recovery. This unusual case documents that hepatitis B surface antigen can become undetectable during the course of fulminant hepatitis B and indicates the importance of tests for other serologic markers of hepatitis B virus in the evaluation of hepatitis B surface antigen-negative fulminant hepatitis

Echocardiograms were obtained in 10 normal patients and in 11 patients with respiratory insufficiency due to chronic obstructive lung disease (8) and to thoracic poliomyelitis (3). Only the eight patients with obstructive lung disease had paradoxic pulse. No patient had pericardial disease. The left ventricular internal dimension, stroke volume, and the mitral valve E-F slope and D-E excursion were measured. The inspiratory to expiratory ratio of each measurement was significantly lower in patients with obstructive lung disease than in normal subjects. The patients with thoracic poliomyelitis demonstrated almost no respiratory change in these measurements. The magnitude of the change in the measured factors probably relates to the degree of negativity of intrathoracic pressure during respiration. The inspiratory reduction of mitral valve motion and left ventricular internal dimension is not specific to tamponade but may be seen in patients who exhibit paradoxic pulse due to other conditions

Two patients with Fisher's syndrome of ophthalmoplegia, ataxia, and areflexia experienced severe weakness and respiratory distress. Both patients required tracheostomy and assisted ventilation, but both made a complete recovery. Fisher's syndrome is generally considered to be a benign variant of acute infectious polyneuropathy (the Guillain-Barre syndrome). Our two patients demonstrate that the condition is not always benign

Chest wall stimulation by electrical stimuli was employed to suppress permanent demand (ventricular-inhibited) pacemakers in two patients with competitive ventricular rhythms. The stimuli were nor perceived by either patient, and were continued until surgical intervention was effected. In selected patients with permanent pacemaker malfunction, chest wall stimulation may be appropriate and necessary initial therapy until definitive correction is performed