tion should he develop an infiltrate in the irradiated area. Its occurrence is not limited to patients who have completed their course of radiation therapy. Correct diagnosis of this entity is essential because of its occasional severe morbidity, excellent response to corticosteroid therapy, and potential hazards of inappropriate antibiotic therapy. REFERENCE5
1 Whitfield AGW, Bond WH, Kunkler PB: Radiation damage to thoracic tissues. Thorax 18:371-380, 1963 2 Smith JC: Radiation pneumonitis. Am Rev Resp Dis 87: 647-655,1963 3 Castellino RA, Glatstein E, Turbow MM, et a1: Latent radiation injury of lungs or heart activated by steroid withdrawal. Ann Intern Med 80:593-599,1974 4 Bennett DE, Million RR, Ackerman LV: Bilateral radiation pneumonitis, a complication of the radiotherapy of bronchogenic carcinoma (Report and analysis of seven cases with autopsy). Cancer 23: 1001-1018, 1969 5 Case Records of the Massachusetts General Hospital (Cass 11-1971). N EnglJ Med284:603-610, 1971 6 Boushy SF, Helgason AH, North LB: The effect of radiation on the lung and bronchial tree. Am J Roentgenol 108:284-292, 1970
III-Effects of Cardiac Resuscitation: Report of Two Unusual Cases" Steven G. Atcheson, M.D.,·· Gary V. Petersen, M.D.,t and Herbert L. Fred, M.D., F.C.C.P.t
Two mishaps associated with cJosed-cbest cardiac resuscitation are presented. One-pneumoperitoneumbecame evident during Ofe, created coosiderable diagnostic difficulty, and evoked treatment that possibly hastened the patient's death. The other-cardiac puncture-appeared at autopsy and its mechanism may be unique. recently witnessed two bizarre complications of W ecardiac resuscitation. The therapeutic and philo-
sophic implications of these accidents are important and form the basis of this communication. ·From the Departments of Internal Medicine, St. Joseph Hospital, Houston, Texas and McKay-Dee Hospital, Ogden, Utah. ··Resident in Medicine, The University of Texas Medical School at Houston. tStaff Cardiologist, McKay-Dee Hospital, Ogden, Utah. Clinical Instructor, Department of Internal Medicine, University of Utah College of Medicine, Salt Lake City. tDirector of Medical Education, St. Joseph Hospital, and Professor and Vice Chairman, Department of Internal Medicine, The University of Texas Medical School at Houston. Reprint requests: Dr. Fred, St. Joseph Hospital, Houston 77002
CHEST, 67: 5, MAY, 1975
CASE REPoRTS CASE
1
At entry into the hospital, this 82-year-old woman had physical and chest roentgenographic signs of congestive heart failure. Therapy with digitalis and diuretics resulted in substantial clinical improvement. One week after admission she suddenly manifested ventricular fibrillation. External cardiac massage, electric countershock, and ventilation via face mask restored sinus rhythm and normal blood pressure in ten minutes. Midway through the procedure, progressive abdominal distension occurred. Chest roentgenogram revealed free air beneath each hemidiaphragm, but none in the mediastinum, pericardium, pleura, or subcutaneous tissues. During the next several hours, abdominal distension persisted and her rectal temperature rose to 38.9 C. Gastric perforation seemed likely, and we reluctantly proceeded with celiotomy. Operation demonstrated massive, unexplained pneumoperitoneum. Her condition then steadily worsened, and she died four days later. Autopsy established no cause of her pneumoperitoneum. She did have bronchopneumonia in both lower lobes, severe coronary atherosclerosis, and recent subendocardial infarction. Notably absent was evidence for lacerated intestine, peritonitis, fractured ribs, or intrathoracic injury. 0
Comment: This case emphasizes that pneumoperitoneum consequent to closed-chest cardiac resuscitation need not reflect perforated gut. At least five patients have displayed postresuscitative pneumoperitoneum. In two, our patient and another, 1 the site and nature of air leak defied detection. Two others2 •3 had ruptured stomach, and the fifth 4 had ruptured esophagus just proximal to the stomach. A second point commands attention. Prompt surgical intervention in all of the aforementioned patients benefited just twO. 2,4 Hence, when pneumoperitoneum complicates resuscitation, a trial of judicious medical management may be wise. CASE
2
Several hours after sustaining an acute inferior myocardial infarction, a 78-year-old man suffered cardiac standstill. Resuscitative efforts failed. Postmortem examination disclosed extensive coronary atherosclerosis and a number of exceptional abnormalities. Several sharply pointed vertebral osteophytes measuring 2 x 2 x 1 cm and resembling railroad spikes lay directly behind and impinged upon the heart. Liquid and clotted blood filled the pericardium. A half-centimeter hole extended through the pericardium and posterior wall of the left ventricle. Muscle surrounding the hole looked normal; on cut sections, however, the fibers were fragmented and incompletely striated, findings suggesting early infarction. Although the mechanism of perforation remains uncertain, we believe that during chest-wall compression an osteophyte "backstabbed" the patient, piercing his heart.
Comment: This case brings into focus a fact and two questions. The fact is: Complications of successful closedchest cardiac resuscitation kill some patients.s" The questions are: 1) What kills the patient such as ours 8 ,9cardiac arrest or cardiac massage? and 2) Can one prevent catastrophes of resuscitation? Answers are conjectural at best.
ILL·EFFECTS OF CARDIAC RESUSCITATION 615
REFERENCES
2 :3
4 :; 6 7 8
9
Gordon HL, Walkup JL: Scrotal pneumatocele as an unusual sign of pneumoperitoneum: Report of a case and review of the literature. J Uroll04:441-442, 1970 Demos NJ, Poticha SM: Gastric rupture occurring during external cardiac resuscitation. Surg 55:364-366, 1964 Valtonen EJ, Hakola N: Rupture of the normal stomach during mouth-to-mouth resuscitation. Acta Chir Scand 127:427-431, 1964 McClure IN Jr. Skardasis GM, Brown JM: Cardiac arrest in the operating area. Am Surg 38:241-246,1972 Burnside J, Daggett WM, Austen WG: Coronary artery rupture by a mitral valve prosthesis after closed chest massage. Ann Thorac Surg 9:267-271, 1970 Roser LA: Cardiopulmonary resuscitation experience in a general hospital. Arch Surg 95:658-663, 1967 Tulgan H, Budnitz J: Intestinal infarction following closedchest cardiac massage. New York J Med 65:905-906, 1965 Agdal N, Jorgensen TG: Penetrating laceration of the pericardium and myocardium and myocardial rupture following ciosed-chest cardiac massage. Acta Med Scand 194:477-479, 1973 Cohn LH, Sayer WJ: Multiple complications from external cardiac massage. Calif Med 98:220-221, 1963
A Cutaneous Manifestation of Untreated Disseminated Histoplasmosis * Thomas M. O'Dorisio, M.D.,oO David A. Jasper, M.D.,t and James Sullivan, M.D.t
We present a case of histoplasmosis with skin manifestations occnrring 17 years after initial diagnosis. The cHnical manifestations of disseminated disease are discussed. Amphotericin B administered through an A-V shunt resuUed in prompt resolution of the skin lesions. treated progressive disseminated histoplasmosis is U nusually fatal.! Sarosi et al reported that 50 percent 2
FIGURE 1. Closeup of elevated, centrally cratered lesions of cutaneous histoplasmosis prior to amphotericin B therapy. cutaneous histoplasmosis, which dramatically improved with 800 mg of amphotericin B therapy. CASE REPORT
The patient was a 77-year-old black man whose first admission to the Omaha VA Hospital was May 25, 1955. Chief complaints then were chills, chest pain and epigastric pain. A diagnosis of disseminated histoplasmosis was made on the basis of positive sputum culture and a histoplasmin complement-fixation titer of 1:2045. Chest x-ray film showed upper lobe densities. There were no skin lesions or gastrointestinal involvement. Liver biopsy revealed many noncaseating granulomas. The patient received no specific treatment and histoplasmin skin tests were negative. In August, 1957, a diagnosis of Addison's disease secondary to histoplasmosis was made and he was treated with 25 mg of cortisone acetate daily. Histoplasmin complement-fixation titer at that time was 1:512 (whole yeast antigen test performed at the VA Central Mycology Laboratory). His course since 1957 was punctuated by multiple admissions for addisonian crises and pulmonary infections with spiking temperature, for which no etiology was determined. He was not treated with amphotericin B during this 17-year interval. No facial lesions or other significant abnormalities were
of their patients with disseminated histoplasmosis died within four months after diagnosis. Although the manifestations of progressive disseminated histoplasmosis are protean, cutaneous involvement is rare." In a recent study of 25 adult patients with progressive disseminated histoplasmosis;' only one patient presented with multiple subcutaneous abscesses from which Histoplasma capsulatum was cultured. We report a case of untreated progressive disseminated histoplasmosis. Seventeen years after the initial diagnosis, this patient developed secondary periorbital
°From the Veterans Administration Hospital, Omaha, Neb. oOEndocrine Fellow, Ohio State University, Columbus, Ohio. tAssistant Clinical Professor of Medicine, Creighton University. tProfessor of Medicine, Creighton University; Chief of Medicine. Omaha Veterans Administration Hospital. Reprint requests: Dr. O'Dorisio, Department of Endocrinology, 410 West Tenth, Columbus 43210
616 O'OORISIO, JASPER, SULUYAN
FIGURE 2. Comori methenamine silver (GMS) stain of lesion biopsy in Figure 3. This stain is specific for Histoplasma capsulatum which shows up as black circles.
CHEST, 67: 5, MAY, 1975