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Radiation Death from Cardiovascular Shock Following a Criticality Accident Report of a Second Death from a Newly Defined Humaii Radiation Death Syndrome

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Radiation Death from Cardiovascular Shock Following a Criticality Accident Report of a Second Death from a Newly Defined Humaii Radiation Death Syndrome 446; Reprinted from the Archives of Pathology May 1967, Volume 83 Copyright 1967, American Medical Association 704636 Radiation Death From Cardiovascular Shock Following a Criticality Accident Report of a Second Death From a Newly Defined Humaii Radiation Death Syndrome Herbert Fanger, MD, Providence, RI, and Clarence C. Lushbaugh, MD, Oak Ridge, 7env Two case histories of nuclear radiation victims sidered secondary to cerebral and cerebellar are similar and reflect radiation-induced hypoten- damage. After exposure to more than 5.000 sion, vascular damage, shock, and death within R, most animals manifest a neurologic syn- Case K two days. Pathologic changes in one patient are drome; malaise, weakness, ataxia, and pros- Fig 1.-Position: described which show these two cases to repre- tration are progressive. Finally, such ani- ring tanks (approx sent a lethal subsyndrome the acute radiation criticality excursior of mals become unresponsive and die with con- the activities and syndrome, occurring in the dosage range between vulsive manifestations.2 Pathologic changes epicenters of the c the acute gastrointestinal and neurologic sub- tirnated distances fl syndromes. Because meningeal and cortical in such instances include meningeal leuko- face of the heart arc of changes occur as part of the vascular damage, cytic exudates, necrosis of cerebellar gran- tion the neutro exposure in patient terminal neurologic symptoms occur that lead io ular cells, oligodendroglial and cortical the suspicion of neurologic damage. Only mini- neurone lysis, and progressive cerebral deaths of some 1 mal neuronal damage and glial reaction were edema.3.4 This syndrome and its pathologic tims may pos~ present, however, and death apparently resulted basis has been defined in monkeys5 but not manner, clinic: from increased intracranial pressure, cerebral in man. first two days a anoxia, cardiac failure, and massive peripheral In man the hematologic syndrome has during the first edema. been documented by clinical and pathologic were not made studies of cases of intentional1 and acciden- Until the dea tal exposure to ionizing radiation.l.6 The in this report, ( THREEMAJOR mechanisms of fatal ter- sequence of hematologic events is almost mination have been recognized in humans identical with that in animals, except for had been jnvoh which exposure after lethal radiation exposure: central nerv- temporal differences in the nadir and recov- rads, and had ous system injury; gastrointestinal mucosal ery of peripheral while lolood cell counts. manifest clinic. loss; and hematopoietic failure.1 At radia- There phenomena are delayed in man, so death syndromc tion exposure levels (300 to 800 R) which that his acute hematologic syndrome lasts Idaho Falls Re, are known to result in death of animals 60 days instead of 30 davs.6 3 These observa- received instan within 30 days or man within 60 days, death tions have been verified in normal man by rads or more occurs as a result of hemorrhage, infection, extensive study of the Hiroshima and Naga- u or died short11 and anemia secondary to hematopoietic in- saki atom bomb casual tie^,^ and the Los them.14 The 19, jury. Radiation between 1,000 and 3,000 R Alamos,5Jo Oak Ridge,l* and the Vinca ac- tim (patient I denudes the mucosa of the smal,l intestine, cidents.12 failed to manifa and results in septicemia and electrolyte im- The occurrence of the gastrointestinal age until imme balance causing death within five days in syndrome, on the other hand, is documented though he h: animals and within two weeks in man. At in man by only two cases: Accident Case exposures higher than 3,000 R, deaths in ani- LA-36 and the 1960 Russian suicide.l3 In 10,000 rads expl Just before des mals or man within 24 to 48 hours are con- these instances the total-body depth-dose tional, uncontrt distribution of 1,350 and 1,910 rads, respec- Accepted for publication Jan 27. 1967. movements. In From the Pathology Department, Rhode Island tively, was extremely uneven, but death OC- course and bec: Hospital, Providence, RI, and the Medical Division. curred in nine to ten days as predicted, coin- Oak Ridge Institute of Nuclear Studies, a unit of whole-body dos Oak Ridge Associated Universities, Tnc., Oak Ridge, cidental with intestinal mucosal denudation. topsy findings Tenn. No human deaths have been attributed Reprint requests to Oak Ridge Institute of Nu- syndrome werc clear Studies, Oak Ridge, Tenn 37830 (Dr. Lush- per se to the neurologic syndrome as it is minimal changl baugh). known in animals. Although the early tis and perivasc Arch Path-Vol 83, May I967 io05435 RADIATION DEATH-FANGER & LUSHBAUGH 447 P‘ 34- ,,‘ GWNKOCYTES 0 CASE K M- 26 - 22 - I I- 510- e--- ”?- P ‘4- VI- Lwmocym usf K sbellar a 5,000 :.‘tL;.-hhC,, , Case cm Case IC syn- K P 02 6 10 14- I8 -22 TIME POST EXPOSURE IHJURSI I pros- Fig 1.-Positions of the two men, relative to stir. h ani- ring tanks (approximate relative scale) in which the Fig 2.-Changes in peripheral white blood cell count xiticality excursions accidentally occurred, showing and differentials in the two patients showing the early ;h con- the activities and bodily orientation of the men to complete disappearance of lymphocytes and extreme 9anges epicenters of the criticality excursions (asterisks). Es- leukocytosis. timated distances from the reaction to the anterior sur- leuko- face of the heart are shown. There was greater modera. gran- tion of the neutron flux by water in the total-body severe cardiovascular changes and general- ortical exposure in patient K. ized edema seemed to account for his death ?rebra1 and to explain the protracted irrevocable rologic deaths of some Hiroshima and Nagasaki vic- shock from which this man suffered.15 The ut not tims may possibly have occurred in this absence in patient K of definitely primary manner, clinical observations during the neurologic injury similar to that previously le has first two days and postmortem examinations described in animals after massive doses of lologic during the first week after the detonations radiation2,.”,5 suggested that the two-day :ciden- were not made.9 death syndrome in man might be cardio- The Until the death of the man (P) described vascu1ar.l0 in this report, only one other person (K)10 almost Pathologic Details pt for had been involved in a radiation accident in recov- which exposure was known to exceed 4,000 The pathologic details of the Rhode Island :ounts. rads, and had survived sufficient time to radiation accident victim of 196416 are report- an, so manifest clinical symptoms of a two-day ed here at length, because they support the hy- lasts death syndrome.10 (The three victims of the pothesis that the neurologic syndrome in man, if it exists as such at all, is a terminal or sec- serva- Idaho Falls Reactor Test Site accident who received instantaneous doses of 1,000 kilo- ondary event in another death syndrome in- Ian by volving the cardiovascular system. A primary Naga- rads or more were killed instantly by blast or died shortly after medical aid reached neurologic radiation death syndrome in man :e Los apparently requires an integrated total-body them.14 The 1958 Los Alamos accident vic- ca ac- dose in excess of 10,000 rads and such a death is tim (patient K) survived 34 hours and yet to be observed. The Rhode Island patient ?stinal failed to manifest signs of neurologic dam- (P) received an estimated integrated whole- iented age until immediately before his death, al- body dose of about 8,800 rads,l7 roughly twice ; Case though he had received approximately as much as the Los Alamos man (K),IO more radiation than considered necessary to produce :.I3 In 10,000 rads exposure to the front of the head. h-dose Just before death he suddenly became irra- cerebellar granule cell necrosis in experimental tional, uncontrollable, and made convulsive animals within 24 hours of exposure.lJ0 ‘espec- The accidents in which the two men were in- Ith OC- movements. In spite of hypotensive clinical course and because of an estimated average volved were basically similar criticality excur- , coin- sions, which occurred when fissionabIe material whole-body dose in excess of 4,500 rads, au- iation. in process of being reclaimed was unintention- topsy findings of the so-called neurologic ibuted ally caused to flow into unsafe geometric vol- syndrome were anticipated. Instead, only s it is umcs (Fig 1).In both accidents the man was minimal changes of mild meningeal vasculi- early close to a tank containing the extracting fluid. tis and perivascular edema were seen, while In Rhode Island, the tank was open at the top, I Arch Path-Vol 83, May 1967 448 RADIATION DEATH-FANGER & LUSHBAUGH 104, on into a sapling - though the twiligl quate for the othe About 30 minutes an ambulance ar CASE I( a CbSE P speaking coherent1 during violent crar -1 YI - L., -606 himself onto the st IW I Y Y ambulance. At ti HMCT _-----A -5c a r facilities and stafl rC4SEK the largest general aCASEP ? he arrived about Z -30 y 98- C4SE K ;L 2 OCAS P g - trip he suffered w“e IIIIIIlIIIIlillllflIfII0 0 4 8 12 16 20 24 28 32 36 43 44 nausea, vomiting, ( 97 III’lf11 1~~1~1~1111111 4 8 12 16 20 24 28 32 36 40 44 TIME POST EXPOSURE IHOURSI The details of his TIME POST EXPOSURE [HOURS) Fig 4.-Parallel changes in peripheral blood hemato- and therapy has E Fig 3.-Fluctuations in rectal temperatures of the crit and hemoglobin values in the two patients. An : men. The early high fevers rapidly subsided.
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