Traumatic Asphyxia

MOORE, MAYER, GAGO

634 Kansas Medical Center, for reviewing the pathologic slides in these two cases. REFERENCES

2 3 4 5 6 7 8 9 10 11 12 13 14 1.'5

Templeton AW, Moffat R, Nelson D: Bronchography and bronchial adenomas. Chest .'59:.'56-61, 1971 Poirier TJ, Van Ordstrand HS: Pulmonary chondromatous hamartomas; Report of seventeen cases and review of the literature. Chest 59:50-55, 1971 Le Roux BT: Pulmonary hamartomata. Thorax 19:236243, 1964 Fraser RG, Pare lAP: Diagnosis of Diseases of the Chest. Philadelphia, W. B. Saunders, 1970, p 731 Bateson EM: Relationship between intrapulmonary and endobronchial cartilage-containing tumors ( so-called hamartomata). Thorax 20:447-461,1965 Lansden FT, Ankeney 11: Endobronchial hamartoma. Ann Thorac Surg 2:84.'5-50, 1966 Lemon WR, Good CA: Hamartoma of the lung: The improbability ot preoperative diagnosis. Radiology 5.'5:693, 1950 Munsakul N, Areechon W, Hongthiamtong P, et al: Hamartoma of the lung; Report of four cases. 1 Med Asso Thailand 53:899-903, 1970 Albrecht E: Ueber Hamartome. Verhandl Deutsch Path Geselsch 7: 153-157, 1904. Cited by Bleyer and Markst? Bleyer 1M, Marks IH: Tuberculomas and hamartomas of the lung. Amer 1 Roent 77: 1013-1022, 1957 Simon M, Bailon H: An unusual hamartoma (so-called chondroma of the lung), J Thor Surg 16:379,1947 Womack NA, Graham EA: Mixed tumors of the lung. Arch Path 26: 16.'5-206, 1934 Bateson EM: Histogenesis of intrapulmonary and endobronchial hamartomas and chondromas (cartilage-containing tumors) : A hypothesis. J Path 101 :77-82, 1970 Mason WE, Templeton AW: Bronchographic signs useful in the diagnosis of lung cancer. Dis Chest 49:284, 1966 Rinker CT, Garrotto LG, Lee KR, et al: Bronchography: Diagnostic signs and accuracy in pulmonary carcinoma. Am 1 Roent 104:802-807, 1968

CASE REPORT

On August 7, 1971, a 13-year-old boy was working under an automobile. The car slipped off the jack on which it was mounted and fell on the boy's chest pinning him between the frame of the car and the ground. The car was jacked up from his chest within 60 seconds by a friend who witnessed the accident. The patient reported later that while he was under the car he had a sensation that his head was "going to explode," after which he lost consciousness and remembered nothing until arriving at the hospital. Upon reaching the hospital he was noted to be alert, awake, oriented, and in no acute distress despite his alarming physical appearance (Fig 1). The vital signs were stable. The skin of the face, ears, and all but a small portion of the right neck was a dusky, violaceous hue which blanched slightly on pressure and resumed its color slowly. There was massive periorbital edema and the entire face had a bloated appearance. Fourplus bilateral subconjunctival hemorrhages were present in the interpalpebral areas of the conjunctivae. The left pupil was larger than the right, but both were briskly reactive to light. The right fundus showed loss of the physiologic cup of the optic disc and no spontaneous venous pulsations. The disc was surrounded by flame-shaped hemorrhages and soft exudates. No visual field of defects were present. The tympanic membranes were clear, and there were no hemorrhages in the mucous membranes of the nose and throat. Examination of the heart and abdomen was unremarkable. On neurologic examination a slight paresis of the right upper and lower extremities, and bilateral Babinski reflexes were present. The ECG was normal, and a chest roentgenogram revealed only a fractured left clavicle. Initial management of the patient consisted of the adrninis-

Traumatic Asphyxia * ]. D. Moore, M.D., John H. Mayer, M.D. and Otto Gago, M.D., F.e.C.p.

A case of traumatic asphyxia is reported, followed by a discussion of the etiologic, pathogenetic, and systemic manifestations of the syndrome. A brief discussion of the treatment and prognosis is included.

T

he clinical picture of traumatic asphyxia is characterized by an intense violaceous hue of the skin of the head and neck, bilateral subconjunctival hemorrhages, and varying degrees of facial edema. It results from severe compression of the thorax with reflux of blood from the right heart into the great veins of the head and neck. For those who are unfamiliar with this syndrome, it is a striking and unforgettable picture. "From the Department of Surgery, Section of Thoracic Surgery, University of Michigan Medical Center, Ann Arbor. Reprint requests: Dr. Gago, University Hospital, Ann Arbor 48104

FIGURE 1. The patient on admission to the hospital.

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TRAUMATIC ASPHYXIA tration of nasal oxygen, clevation of the head of the hed 30· and a figure-of-eight dressing for the fractured clavicle. Administration of oxygen had no effect on the color of the patient's face and neck. After 12 hours of hospitalization the color in the head and neck began to fade, and the periorbitul edema had decreased significantly. The right-sided paresis had disappeun-d as had the Babinski reflexes, and the pupils were equal and reactive to light. On the fourth hospital day the patient was discharged. The papilledema, hemorrhages, and exudates in tilt' right disc were gone, and the chest x-ray film was clear. The purple color of the face was scarcely perceptible. Examination thn-e weeks after till' injury was unrernarkahle and the patient stated that the subconjunctival hemorrhages had cleared one week earlier. (Fig 2 and 3) ETIOLOGY

The etiology of traumatic asphyxia is related to severe compression of the thorax with reflux of blood from the right heart retrograde through the valveless superior vena cava and the great veins of the head and neck. This massive back pressure is transmitted to the capillaries of the head and neck which become engorged with blood. Capillary atony and dilatation result in stagnation. The stagnant blood desaturates and produces the characteristic color changes. Animal experiments perfaimed to determine the pathogenesis of traumatic asphyxia have failed to produce the clinical picture. Williams, Minken, and Adams' investigated the possibility that a "fear response" consisting of a split second of forewarning of impending trauma and closure of the glottis with thoraeoabdominal splinting contributed to the production of the clinical picture. Pneumatic tourniquets were placed on the chest and abdomen of anesthetized dogs. A cuffed endotracheal tube kept the lungs in complete expansion. With the abdominal cuff inflated and simulating splinting of the musculature, markedly elevated cave-jugular pressures were noted as the thoracic tourniquet was inflated. This pressure increase was greater than the pressure found in the animals undergoing thoracic compression alone. It was concluded that warning, splinting of the musculature, and thoracic compression produced the pressure rise and therefore the clinical picture. However, the investigators were never able to produce this picture in their subjects.

FICU!U;

2. Subconjunctival hemorrhages.

Associated Iniuries Associated injuries are common in traumatic asphyxia. The most frequent of these is injury to the chest wall and lungs. Rih fractures, pulmonary contusion. pneumothorax and hemothorax head the list. Injury to the heart and great vessels is rare. There is only one reported case of cardiac injury: pericurdial effusion with tamponade." Visual disturbances are fairly common." Immediate permanent loss of vision was attributed to retinal hemorrhage and immediate transient loss to retinal edema. As in our case, anisocoria of a transient nature may be present. Papilledema, hemorrhage into the retina or vitreous exudates and retinal edema may he noted on

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:3. The patient three weeks post injury.

636

DOHNER, WARD, STANDORD

fundoscopic exam. These may be unilateral or bilateral. Subconjunctival hemorrhage with or without conjunctival edema is a constant feature of the clinical picture. Neurologic findings are frequent with about one-third of the patients manifesting unconsciousness, which usually develops at the time of injury. Intracranial or intracortical hemorrhages are rare even in injuries that result in fatality. This is probably due to the rigid structure of the cranium which resists the sudden increase in venous pressure, and to the large venous sinuses at the base of the brain which damp the transmission of pressure. Skeletal injuries are common and include fractures of the clavicle, humerus, radius, ulna, facial bones, vertebrae, metatarsals and tibia. Skull fracture is rare. Treatment The clinical syndrome by itself requires no specific treatment, and efforts should be directed toward the management of any associated injuries.

Prognosis Ninety percent of the patients who survive the first few hours after injury will recover from traumatic asphyxia when it occurs as a single entity. The survival rate is directly related to the extent of associated injuries. REFERENCES

Williams JS, Minken SL, Adams JL: Traumatic asphyxiareappraised. Ann Surg 167:384-392, 1968 2 Fred HL, Chandler FW: Traumatic asphyxia. Am J Med 29:508-0517, 1960 3 Heuer GJ: Traumatic asphyxia; with especial reference to its ocular and visual disturbances. Surg Gynec Obstet 36: 686-696, 1923 4 Conwell HE: Traumatic asphyxia, report of four cases. J Bone Joint Surg 9:106-110,1927

tion of therapy resulted in rapid recovery. This patient is compared with others treated with busulfan, methotrexate and cyclophosphamide.

M

any drugs have been implicated in toxic and hypersensitive effects on the Iung.>" Several cytotoxic agents, including busulfan, methotrexate, and cyclophosphamide have been reported.v? In one of these reports, primary or additive effects of cytosine arabinoside, 6-mercaptopurine, vincristine, sarcolysin and procarbazine were suggested.' The purpose of this article is to present a well-documented alveolitis secondary to chemotherapy in a patient with lymphosarcoma. Sequential roentgenograms and pulmonary function tests demonstrated severe alveolar-capillary block that quickly resolved with cessation of therapy. Lung biopsy documented acute alveolitis without fibrosis. CASE REPORT

A 50-year-old steel worker was hospitalized at the Denver Veterans Administration Hospital in August, 1969 because of complaints of malaise, fever, sweating, and a 20 pound weight loss. In September, 1966, he was diagnosed as having lymphocytic lymphosarcoma and had received 3000 r irradiation to an abdominal mass. In July 1967, because of right pleural effusion, hepatomegaly and lymphadenopathy in the inguinal, axillary and supraclavicular regions, he had received 15 mg nitrogen mustard intravenously and four injections of quinacrine (Atabrine) into the right pleural space. There had been rapid clearing of the pleural effusion and regression of all palpable lymph nodes. In June, 1968, he received 2000 r to both axillary areas for enlarging painful lymphadenopathy; there was rapid regression of the masses. He was started on 20-30 mg of prednisone daily at this time. In April, 1969, he developed symptoms and signs of right distal brachial plexus involvement plus enlargement of lymph nodes in all previously noted areas. Right supraclavicular node biopsy showed lymphoblastic lymphosarcoma. Following 1200 r 60Co therapy to his brachial plexus, his symptoms cleared rapidly.

Alveolitis during Procarbazine, Vincristine and Cyclophosphamide Therapy* V. Alton Dohner, M.D.,oO Harry P. Ward, M.D., and Ray E. Standard, M.D.

A 47-year-old man with lymphosarcoma developed severe dyspnea, radiographic pulmonary infiltrates, restrictive lung disease and diffusion impairment during therapy with procarbazine, vincristine and cyclophosphamide. Open lung biopsy demonstrated alveolitis. Cessa°From the Departments of Medicine and Pathology, The Webb-Waring Institute for Medical Research, Veterans Administration Hospital, and University of Colorado Medical Center, Denver. oOFHPS-USPHS Postdoctoral Fellow in Pulmonary Diseases. Reprint requests: Dr. Dohner, PHS Indian Hospital, PO Box 2143, Billings, Montana 59103

FIGURE 1. Chest radiograph of August 15, 1969 demonstrating pleural thickening in the right costophrenic area.

CHEST, VOL. 62, NO.5, NOVEMBER, 1972