British Journal of Radiology (2005) Supplement_27, 47-54
© 2005 British Institute of Radiology
doi: 10.1259/bjr/90331492
British Journal of Radiology Supplement_27 (2005),47-54 © 2005 The British Institute of Radiology
Multi-organ failure in a radiation accident: the Chinese experience of 1990
Yu Changlin, MD and
Ye GenYao, MD
Department of Radiation Medicine and Clinical Hematology, North Taiping Road Hospital, Beijing 100039, PR China
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Abstract
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On 25 June 1990 in Shanghai, two men (Shi, a 56-year-old male, and Wan, a 53-year-old male) were accidentally exposed to homogeneous high dose and high dose rate 60Co irradiation (total activity 0.85 PBq, at the time of delivery from the manufacturing factory in June 1960) up to 12 Gy and 11 Gy, respectively. Both suffered from an extremely severe haematopoietic form of acute radiation sickness. Through energetic salvage and human leukocyte antigen (HLA) haploidentical bone marrow transplantation, their survival times were prolonged to 25 days and 90 days, respectively. In the case of Wan, the implanted bone marrow resided and engrafted completely, and haematopoiesis was restored. However, the patient died of interstitial pneumonia 90 days after exposure to radiation. The clinical course of multi-organ failure and the valuable experience obtained from the management of these patients is of great significance in directing the prevention of multi-organ failure and the treatment of such patients in the future. Pathological findings from these two autopsy cases are helpful in elucidating the underlying pathogenesis of clinical multi-organ failure, the cause of death and especially, the pathogenesis and morphogenesis of lung fibrosis.
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A brief account of the accident [1]
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At 9:00 a.m. on 25 June 1990 in Shanghai, seven men entered a 60Co radiation room by mistake to transport medicine boxes and barrels where crystal glass and Chinese medicines were being irradiated.
The safety control system of the 60Co source room
Safety of any radiation system is ensured by a series of strict protective measures. There were triple protective doors from the zigzag exit to the open outside. The first door served as shelter from leaking radiation and could be opened with the key from the outside. The second door was coupled with a lifting mechanism for the radiation 60Co source, whereby the source was lowered into the well automatically when the door was opened. The button operating the door was on the control board. Unless there was an electric fault or an urgent need for maintenance, it was forbidden to open the door with the key. The third door was electrically controlled through the control board and could not be opened with a key. There was a red alarm light over the first door, which was linked with the radiation source; when the system was on the radiation position, the light flashed on. All the members working in the radiation area were equipped with a personal dose alarm FD-3007K and a radiation detector Model 70. It was the rule that anyone who was to enter the room should wear the alarm. A distance watch was also used to avoid undue proximity to the radiation source. The location of the source could also be judged by the balance hammer. Ventilation and illumination were controlled by an independent circuit. There were reflection mirrors in the zigzag passage.
Cause of the accident
The direct cause of the accident was the malpractice of Shi in disregarding the operational rules. He switched on the power for ventilation and illumination without turning on the electricity for the 60Co source system. As no power was supplied, the coupling mechanism failed to work when he forced the second door open with the key directly. Normally, the third door could not be opened manually or with a key; it could only be opened by the button on the control board. Unfortunately, the electric motors controlling the movement of the third door had been removed by Shi 2 months before the accident for mending of a defect. Without the electric motor, Shi was able to open the door manually and entered the room "smoothly". None of the seven persons who entered the radiation area carried the personal alarm with them on the day of the accident. Worst of all, the elevated 60Co source was in its working position and was entirely invisible from the outside because it was surrounded by a 30 cm diameter opaque barrel of thin white iron sheet, so that they did not see the location of the source.
Therefore, the seven men suffered acute external whole body irradiation of various high doses with high dose rate at different distances from the source over a short time. One man felt nausea 30 min after the accident. Many of them vomited a number of times within 2 h after irradiation. Some patients suffered from facial erythema and conjunctival congestion and were hospitalised at 11:00 a.m. on the same day [1]. The following is a presentation of the two most severe cases.
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Case reports [2]
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Case 1
Shi, a 56-year-old married male, was exposed to a 60Co source from 9:00 a.m. to 9:40 a.m. on 25 June 1990. 20 min later he complained of malaise, discomfort in the abdomen, nausea and vomiting. 1 h after the accident he attended the clinic where he was started on emergency treatment including radioprotective drugs (oestradiol benzoate, oestradiol valerate), drugs to improve the microcirculation (500 ml of dextran with low molecular weight in addition to some extracted Chinese herbal medicine intravenously), infusion of cryopreserved fetal liver cell suspension (Figure 1
) and prophylactic use of antibiotics (Figure 1). He was admitted into hospital 6 h after the accident. Physical examination revealed a temperature of 37.4°C and blood pressure of 90/60 mmHg. The patient was conscious, with the face flushing like he was inebriated. Bulbar conjunctivae were congested for 2 days. Both parotid glands were swollen for 2 days, but the superficial lymph nodes were not enlarged. There were no xanthochromia or haemorrhagic spots. The heart rate was 84 bpm and rhythmic. The heart and both lungs were normal. The abdomen was soft and the liver and spleen were not palpable. There was a temporary increase in white blood cell count from the day of accident (day 0) to day 3, which began to decrease rapidly thereafter, and the lymphocyte count dropped below 1.0 x 109 l–1 at 24 h (Table 1). Ilium and sternum punctures at day 3 and day 4 revealed stagnation of bone marrow haematopoiesis. The radiation dose was estimated to be 12 Gy.
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Figure 1. Changes in temperature and haematology, and major treatments in Shi. BMT, bone marrow transplant; WBC, white blood count count; Plt, platelet count.
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Case 2
Wan, a 53-year-old married male, was exposed to the same 60Co source (irradiation conditions: duration 15.8 min, distance to the 60Co source 125–190 cm, dose rate 0.2–1.9 Gy min–1). 10 min after exposure he complained of noticeable malaise, dizziness and nausea. At 50 min he began to have repeated vomiting and diarrhoea. 2 h after the accident he attended the clinic where he was started on emergency treatment including radioprotective drugs (oestradiol benzoate, oestradiol valerate), drugs to improve the microcirculation (500 ml of dextran with low molecular weight in addition to some extracted Chinese herbal medicine intravenously), infusion of cryopreserved fetal liver cell suspension (Figure 2) and prophylactic use of antibiotics (Figure 2). He was admitted into hospital 6 h after the accident. Physical examination revealed a temperature of 37.6°C and blood pressure of 98/60 mmHg. The patient was conscious, with facial flushing. Bulbar conjunctivae were congested for 4 days. 8 h after the accident both parotid glands became enlarged for 1.5 days. Superficial lymph nodes were not enlarged. There were no xanthochromia or haemorrhagic spots. The heart rate was 72 bpm and rhythmic. Grade II systolic blowing murmur was audible at the apex, but not conductible. Both lungs were clear, the abdomen was soft and the liver and spleen were not palpable. Changes in the haemogram from the accident (day 0) to day 3 are shown in Table 1
. The radiation dose was estimated to be 11 Gy.
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Figure 2. Changes in temperature and haematology, and major treatments in Wan. BMT, bone marrow transplant; WBC, white blood cell count; Plt, platelet count.
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Bone marrow transplantation (BMT) [2]
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Selection and preparation of the donors
The donor for Shi was his brother, and that for Wan was his daughter. The donors underwent a systematic physical examination, human leukocyte antigen (HLA)-A,B site matching, a complete set of red cell typing and isozyme test (Table 2). 4 days before bone marrow sampling, 400 ml of blood was collected from the donor, which was re-infused to the donor following bone marrow collection.
Preparation of the recipients
Blood sampling was performed on the second day of the accident for HLA-A,B site matching, a complete set of red cell typing and isozyme test (Table 2). Mixed lymphocyte culture was not performed because of the low number of lymphocytes. Wan received an intravenous drip of Cytoxan (60 mg kg–1 day–1) at day 5 (BMT –2 days), and he felt nausea and poor appetite on that evening, but did not vomit.
Transplantation
BMT was performed on day 11 for Shi, and on day 7 for Wan. Bone marrow collection was conducted according to routine procedures under epidural anaesthesia. The filtered bone marrow was infused to the recipients intravenously. The amount of bone marrow infused, the number of nucleated cells and the number of granulocyte–macrophage colony-forming units (CFU-GM) are shown in Table 3.
Prevention of rejection and graft-versus-host disease (GVHD)
Both patients were started on infusion of cyclosporin A (CsA) (Sandoz, Switzerland) 2 days before BMT. The dosage was regulated from 1 mg kg–1 day–1 to 3 mg kg–1 day–1 based on daily CsA concentration in the blood (30–600 ng ml–1). Methotrexate 10 mg m–2 was administered at days 1, 3, 6 and 11 of BMT. Five doses of antilymphocyte globulin (Merieux Institute, France) 0.5 ml kg–1 day–1 was infused intravenously on alternative days starting from day 5 of BMT.
Routine supporting treatment and symptomatic management
Both patients were subjected to total environmental protection, including skin sterilisation, laminar flow (Grade 100) isolation, intestinal disinfection using oral berberine, Nivemycin, SMZ-Co and Mycostatin, and sterile nursing of the oral cavity, skin and perianus. During the agranulocytic period, there were signs of infection and full doses of combined antibiotics were started. The type and dosage of the antibiotics were adjusted over time with the results of the constitutional pathogenic cultures. When mycotic infection was suspected, imidazoles such as ketaconizole and fluconazole, and 5-fluorocytosines were used; when mycotic infection was strongly suspected or when pathogenic cultures showed evidence of deep infection, amphotericin B was used in Wan. Intravenous infusion of acyclovir, intravenous infusion of human globulin at a daily dose of 3–6 g on alternative days, and intramuscular injection of cytomegalovirus (CMV) hyperimmune serum were used for prevention of infection.
At day 4 after exposure, a Hickman two-way catheter was inserted via the right subclavicular vein to ensure fluid infusion. High protein, high vitamin, low fecula diet sterilised by microwaves was given. When the patients showed lower intake and presented with pronounced gastrointestinal symptoms, deep vein high nutrition, milky fat and 50% glucose were infused to maintain the daily calorie intake over 8368 J (2000 kcal). Water, potassium, magnesium, calcium and other electrolytes and trace elements were supplemented based on daily output and plasma electrolyte levels. When haemorrhagic tendency was likely or when the platelet count was below 20 x 109 l–1, single platelet suspension (CS-3000 plus, Fenwall) was infused. Erythrocyte suspension was given when needed. All blood products to be used were irradiated at 25 Gy before infusion.
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Clinical manifestations and the course of therapy [2]
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Case 1: Shi
The body temperature, haemogram and major treatments of Shi are shown in Figure 1.
On the day of exposure, the patient had noticeable nausea and vomited five times, totalling 5000 ml, which contained gastric content and mucus. On subsequent days he had two to four episodes of vomiting and frequent diarrhoea of yellowish or dark-greenish soft faeces, until 1 week later when diarrhoea became less frequent, although the quality and consistency remained abnormal. At day 12, a 0.3 cm x 0.5 cm ulcer on the palate was seen, which was covered with a pseudomembrane, and an ulcerative blood bulla was seen at the root of the tongue. From day 13, head, axillary and pubic hair began to fall off, and at day 21 the patient was almost epilated. At day 20 the patient had a cough with production of blood sputum. At day 21 the patient began to have persistent fever up to 39°C, more bloody sputum, coffee-coloured fluid vomitus and microhaematuria. Use of high dose antibiotics and antimycotics, platelet suspension and haemostatics did not help. By midday of day 22 the patient suddenly had shortness of breath, cyanosis and progressive reduction of oxygen saturation. Blood gas analysis showed partial pressure of oxygen (PaO2) of 3.2 kPa (24 Torr). Emergency endotracheal intubation and auxillary respiration using an artificial respirator were performed in the afternoon. At day 23 the patient had decreased blood pressure, oliguria and anuria, and failed to respond to a large dosage of furosemide. The patient had elevated blood urea nitrogen and creatinine, icteric sclera and elevated blood bilirubin up to 102.6 µmol l–1. At day 24 the patient received peritoneal dialysis, and at 1:15 p.m. of day 25 the patient died in cardiac arrest. Autopsy showed extensive haemorrhage in multiple organs, massive haemorrhage of both lungs, mycotic septicaemia and adult respiratory distress syndrome (ARDS). The peripheral haemogram showed that the patient's total white blood cell (WBC) count increased temporarily between day 0 and day 4, decreased rapidly afterward, and reached the minimum (0.075 x 109 l–1) at day 9. At day 11 the WBC count rose to1.05 x 109 l–1 and remained at that level for 3 days, which might be owing to fetal liver cell infusion. At day 14 the WBC count began to decrease gradually and dropped to the minimum (0.022 x 109 l–1 from day 17 to the last day of life. Of the four bone marrow punctures performed at days 0, 3, 4 and 11, three (days 3, 4 and 11) showed a myelogram of poor proliferation and haematopoietic stasis. At day 24 (BMT +13 days), monocytes amounted to 37% (Table 4).
Pathogenic findings
Fecal culture at day 6 revealed Candida albicans. From day 15 the patient had persistent positive fungal reaction. At day 21, sputum smear and culture revealed positive Candida albicans, and blood and urine cultures showed positive results.
Case 2: Wan
The body temperature, haemogram and major treatments of Wan are shown in Figure 2.
On the skin mucosa at day 2 following exposure there appeared diffuse herpes simplex at the upper left lip and nasal vestibule, which began to scab at day 8 and to heal at day 15 after intravenous and topical application of acyclovir, and the use of interferon-
. Palate ulceration was seen 2 days after exposure and increased in number thereafter. At day 12 the patient had extensive mucous erosion and ulceration in the oral cavity, and congested sore throat. The erosion and ulceration were covered with pseudomembranes, and propagated to congestion of the throat and pain, which propagated to lip mucosa and vestibule of the mouth. By day 21 the signs of mucositis subsided but erosion of both lips and checks remained apparent. At day 25, erosion of the mouth began to heal, and necrotic mucosa and pseudomembrane began to fall off and were covered with fresh epithelial mucosa. By day 35 the ulceration of the mouth had healed completely.
Epilation (hair of head, axillary and pubic hair, and moustache) began at day 11, and by day 17 the patient was almost epilated. At day 16, dark red congestive patchy examthemas maculosum were seen at the neck and prosternum regions, which gradually became fused and larger. Blisters first appeared at the neck and developed constitutionally from the neck, face and prothorax to the armpit, from the upper abdomen to bilateral groins, from the cubital fossae to middle abdomen, and from the lumbodorsal region to proximally distal extremities. There was burning pain and tenderness in the affected skin, which underwent the following stages: erythema—darkening—xerosis, pigmentation—dry desquamation. There was a small number of blisters on the prothoracic skin. Healing of the skin was effected at day 56 by cleaning protection and application of fluocinolone acetomide ointment, although there still was local desquamation.
Gastrointestinal symptoms
The patient had nausea and vomiting on the day of the accident, which were greatly relieved 36 days later, but he had poor appetite for a month. With the healing of oral ulceration, his appetite gradually improved. Diarrhoea was frequent and persisted for 16 days, the maximum reaching seven times daily with a total amount of 1700 ml. The stools were yellow–green or dark brown in colour and watery in consistency. Occult blood in stool was ++ to +++. From day 3 to day 6, diarrhoea was accompanied by dull pains in the upper abdomen, and began to improve from day 17, occurring one to two times daily although the stool was deformed. When diarrhoea became frequent, internal haemorrhoids prolapsed, accompanied by bleeding and severe pain, but there was no tenderness around the anus. Gastrointestinal symptoms subsided by day 30.
Peripheral haemogram
Total WBC count increased temporarily from day 0 to day 4, and then decreased gradually until day 6 when it dropped below 1.0 x 109 l–1, and reached the minimum (0.011 x 109 l–1) at day 15 (BMT +8 days). It began to pick up at day 19 (BMT +12 days) until it reached above 0.5 x 109 l–1 at day 26 (BMT +19 days), above 1.0 x 109 l–1 at day 28 (BMT +21 days) and above 3.0 x 109 l–1 at day 43 (BMT +36 days).
Myelogram
The results of the myelogram at days 1, 4, 42 (BMT +35 days), 67 (BMT +60 days) and 89 (BMT +82 days) are shown in Table 4. The myelogram at day 4 showed extremely low proliferation, with juvenile leukocytes rarely seen. At day 44 (BMT +37 days), proliferation of bone marrow became apparently active, with more juvenile leukocytes, indicating a good recovery of haematopoiesis (Table 4).
Engraftment evidence of BMT
Peripheral HLA converted into donor's type at day 31 (BMT +24 days). At day 42 (BMT +35 days) and day 67 (BMT +60 days), peripheral blood and bone marrow lymphocyte chromosomes completely converted to the karyotype of the donor, and polymerase chain reaction of in vitro amplifier for bone marrow cell Y-specific DNA sequence showed negative results, indicating that bone marrow of the donor had been engrafted.
Graft-versus-host disease (GVHD)
Scattered rose-coloured erythemas were seen at day 26 (BMT +19 days) over the palmar finger ends of both hands and soles. At day 29 (BMT +22 days), skin eruptions increased markedly, which were propagating to the greater and lesser thenars of the palmar sides, post back and thoracoabdominal region. Differentiation of this condition was difficult because of complicated radiation injury to the skin. Icteric sclera and impaired liver function were also noticed. Total bilirubin was 32.44 µmol l–1 and alanine aminotransferase (ALT) was 62 U. The patient had persistent high fever up to 40°C, although gastrointestinal symptoms were not aggravated. Abdominal skin biopsy at day 37 (BMT +30 days) suggested there was GVHD of degree I according to the Seattle criteria. Methylprednisolone 3 mg kg–1 day–1 was started at day 30 (BMT +23 days), and at day 35 (BMT +28 days), skin eruptions over the fingers, toes and palms began to subside, becoming xerotic and desquamated. At day 43 (BMT +36 days), skin eruptions over the back and chest improved, the body temperature subsided, and liver function became normal with bilirubin below 17.1 µmol l–1.
Interstitial pneumonia
At day 47 (BMT +40 days), the patient began to run a fever accompanied by cough. Coughing was not productive but became progressively worse. Chest radiography at day 57 (BMT +50 days) showed diffuse reticular change over the middle and lower fields of both lungs. The patient began to have irritable dry coughs, increased respiratory rate, decreased oxygen saturation and a temperature of 39°C at day 59 (BMT +52 days). Oxygen inhalation at 1–4 l min–1 did not help much. Blood gas analysis at day 60 (BMT +53 days) showed PaO2 of 6.13 kPa (46 Torr). The patient's condition became worse at day 61 (BMT +54 days). Nasal intubation and face-masked oxygen inhalation could not improve the difficult respiration of the patient. PaO2 decreased to 5.07 kPa (38 Torr) and the patient developed decompensatory metabolic acidosis. Tracheotomy and positive expiratory end pressure (PEEP) were performed at 0:10 a.m. of day 62 (BMT +55 days). The patient's condition improved for a time, but irritable coughs antagonised the mechanical respiration. As the patient did not respond to morphine and diazepam, an intravenous drip of midazolam and muscle relaxants pipecurium bromide (Arduan) or atracurium besilate was started at day 66 (BMT +59 days). Although irritable coughing was brought under control when the maximum dose of tracurium reached 2.6 mg kg–1 h–1, pulmonary pathology continued to deteriorate. Chest radiography showed that the reticular nodular change was spreading to the upper lungs, which was accompanied by parenchymatous exudative change. Culture of the alveolar lavage showed positive CMV, in which CMV inclusion bodies were seen. Respiratory parameters elevated gradually. At day 80 the patient began to inhale oxygen of over 60% concentration. PEEP was 0.196 kPa. Dropsy of chest and generalised oedema were present at day 85, followed by rapid deterioration of respiratory function. The patient died of respiratory failure at day 90. The pathological autopsy report confirmed the diagnosis of radiation pneumonia complicated by CMV infection and diffuse fibrosis of lung.
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Autopsy findings [3]
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In the case of Shi, the main pathological findings were: extremely hypoplastic bone marrow in which only a few plasma cells and immature haematopoietic cells remained; radiation pneumonia and massive haemorrhage in both lungs; spot haemorrhage in the skin and internal organs; and haemopyelectasis. In addition, the autopsy showed bile stasis in the liver cells and small bile ducts, slight fibrosis of the portal tract in the liver, exfoliation of the mucosa of the gastrointestinal tract, dermatitis and alopecia, parotitis, and atrophy of the testes. The terminal septicaemia was of fungal origin. In the case of Wan, there was severe atrophy of lymphoid tissues in general, but after successful BMT, red marrow was seen, and the granuloeythroid series of haematopoietic cells was observed. However, no megakaryocytes were found. Multiple foci of extra-bone marrow haematopoiesis were seen in some organs. The main pathological findings in the lungs were fibrosis, local haemorrhage and fibrinotic exudate in the alveolar cavity, bronchopneumonia and possibly virus infection (immunohistochemical staining showed that CMV and herpes simplex virus antigens were present). The pathological findings in the lungs led to hypertrophy and dilatation of the right heart. Additionally, alopecia, CMV infection of the parotid gland, gastritis and enteritis, fibrotic proliferation in the liver, bile stasis and jaundice of the skin were noted. Atrophy of the testes was observed as well as spot haemorrhage in some organs. An acute bacterial verrucous endocarditis of the aortic valve was noted, and exfoliation of verruca leading to infarct formation of the spleen and kidney was found.
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Discussion
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Cause of death [4]
In these two cases of acute radiation sickness, the haematopoietic system in the bone marrow was damaged, especially hypoplasia of the magakaryocytic series. The mechanisms of coagulation and anticoagulation were destroyed and led to widespread haemorrhagic lesions of the whole body. Haemorrhage was the main cause of death. In the case of Shi, radiation pneumonia and massive haemorrhagic lesions were seen in both lungs, so that the respiratory crisis was seen rapidly. A fungal septicaemia also contributed to the death of Shi. In the case of Wan, owing to success of BMT, his survival period was longer than Shi and haemorrhagic lesions were also mild. The cause of death of Wan was owing to the severe fibrosis of the lung. Secondary bacterial and viral infections accelerated pulmonary damage, then induced to respiratory failure. In addition, fibrosis of the lung led to intrapulmonary blood vessel obliteration and thickened walls following irradiation. This caused pulmonary hypertension along with hypertrophy of the right heart, complicated by cardiac failure.
Aetiological factors and morphogenesis of the lungs
From a literature review [5], a radiation dose over 30 Gy may cause fibrosis of the alveolar cavity after 5 months, but 45 Gy may take only 65 days. If the dosage was increased, pulmonary fibrosis may occur rapidly. In the case of Wan, with only 11 Gy, pulmonary fibrosis was severe after 3 months, so we believe that radiation damage was just one factor in the formation of pulmonary fibrosis. In addition, in the case of Wan, although BMT has been successful, interstitial pneumonia and diffuse alveolar damage appeared and accelerated fibrosis. According to reports of Nash et al [6], if the oxygen inspirated from artificial respiration is overdosed with partial oxygen pressure, this would increase lung oedema and congestion, haemorrhage, fibrinous exudate, and hyaline membrane formation. During the later stage, proliferation of fibroblast and fibrosis in the alveolar walls could be observed evidently. From a report of Klein [7], overdosage of oxygen inspiration could induce type II alveolar epithelium and fibroblast proliferation and fibrosis of stroma. We therefore suggest that high concentration of oxygen inspiration in the long-term might act as another aetiological factor for fibrosis. Intrapulmonary ghost giant cell formation indicates the presence of a viral infection. This, as the authors have mentioned previously, based on radiation damage of the lung, severe lung fibrosis was formed due to multiple aetiological factors.
Regarding the morphogenesis of pulmonary fibrosis, Dunnill [8] divided it into three stages: the first or the acute or exudate stage, where its change mainly includes oedema of the alveolar cavity or hyaline membrane formation. At the second or proliferative stage, a large amount of fibroblasts and fibrocytes and type II pulmonary epithelium proliferation were seen in the alveolar walls and cavity. Sometimes, metaplasia may also be seen. At the third stage, alveolar reconstruction and severe local fibrosis occurred. In the case of Wan, all three stages of the lesion listed as above may be seen simultaneously. It is believed that different parts of the lung might have different pathological aetiologies.
Pathogenesis of jaundice
According to a literature review [5], high dose radiation may induce hepatic damage; there appeared diffuse hepatic necrosis and hepatic function disturbance that led to the appearance of jaundice. After low to middle dosage irradiation, hepatic pathological findings are as follows: congestion of central vein and sinus, hepatocyte compressed and atrophic; and at a later stage, owing to interlobular vascular lesions, some of the hepatocytes may degenerate. In these two cases, the patients had fibrous tissue proliferation in the portal area, thickened blood vessels, epithelium swelling of the bile duct and stasis and narrowing of bile duct. In these two cases, no abnormal hepatic functions (as judged by serum glutamic pyruvic transaminase (sGPT), thymol turbidity test, zinc turbidity test, and albumin/globulin ratio) were found clinically. Zhang Pu et al [3] believed that bile stasis occurred by intrahepatic fibrosis and complicated with small bile duct damage then secondary jaundice, so that direct bilirubin was increased. Of course, BMT can induce GVHD, because liver is also a target organ. Bombi et al [9] mentioned, in their autopsied BMT cases, that small bile duct stasis of the liver may have occurred, and we also agree with this opinion.
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References
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- Min Rui, Meng Xianshun, Chen Qi, et al. Shanghai June 25 radiation accident: report of the process and analysis of the causes. In: Liu Benti, Ye Genyao, editors. Collected papers on diagnosis and emergency treatment of the victims involved in Shanghai June 25 60Co radiation accident. Beijing, China: Military Medical Science Press, 1996:1.
- Meng Pelin, Cao Luxian, Huang Long'an, et al. Extremely severe degree bone marrow form of acute radiation sickness: clinical report of 2 cases. In: Liu Benti, Ye Genyao, editors. Collected papers on diagnosis and emergency treatment of the victims involved in Shanghai June 25 60Co radiation accident. Beijing, China: Military Medical Science Press, 1996:39.
- Zhang Pu, Yu Hongyu, Dong Rongchun, et al. Pathological analysis of two cases of extremely severe degree bone marrow form of acute radiation sickness. In: Liu Benti, Ye Genyao, editors. Collected papers on diagnosis and emergency treatment of the victims involved in Shanghai June 25 60Co radiation accident. Beijing, China: Military Medical Science Press, 1996:195.
- Ye Genyao. Analysis and evaluation on the management of seven victims in the 60Co radiation accident of the June 25, 1990. In: Liu Benti, Ye Genyao, editors. Collected papers on diagnosis and emergency treatment of the victims involved in Shanghai June 25 60Co radiation accident. Beijing, China: Military Medical Science Press, 1996:283.
- Shipman TL, et al. Acute radiation death resulting from an accidental nuclear critical excursion. J Occup Med 1961;3:146.
- Nash G, Blennerhassett JB, Pontoppidan H. Pulmonary lesions associated with oxygen therapy and artificial ventilation. N Engl J Med 1967;276:368–74.[Medline]
- Klein J. Normobaric pulmonary oxygen toxicity. Anesth Analg 1990;70:195–207.[Free Full Text]
- Dunnill MS. Pulmonary fibrosis. Histopathology 1990;16:321–9.[Medline]
- Bombi JA, Cardesa A, Llebaria C, Rives A, Carreras E, Granena A, et al. Main autopsy findings in bone marrow transplant patients. Arch Pathol Lab Med 1987;111:125–9.[Medline]
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Abstract
A brief account of...
