Autopsy of the bilateral lungs. (A) A large thrombosis was found in the right pulmonary artery (arrows). Scale bar = 2.0 cm. (B) A thrombosis was also found in the left pulmonary artery (arrows). Scale bar = 2.0 cm. (C) Histopathology showed thromboses in the pulmonary arteries (H&E, 20 × ). 

Contexts in source publication

Context 1

... insipidus (DI) is a well-recognized complication of traumatic brain injury (TBI). 1–3 Recently, in a retrospective study of 102 patients Agha et al. reported an incidence of DI of 21.6% in the immediate period following TBI. 4 In this series, the occur- rence of DI was related to the severity of the traumatic insult, but it was unrelated to the development of anterior pituitary abnor- malities. The majority of patients with post-traumatic DI had not recovered when they were revaluated with the water deprivation test 6–36 months post injury; therefore, the majority of patients with persistent DI suffer from partial antidiuretic hormone (ADH) deficiency. We encountered a pulmonary embolism associated with replacement therapy due to secondary DI after multiple traumas including TBI in a 23-year-old man at 37 days after the trauma. Here, we report a case of pulmonary embolism during vasopressin replacement treatment due to secondary DI. A 23-year-old man, who had previously been in good health, was admitted to our emergency room after having been struck by an automobile. Before his arrival at the hospital, his consciousness level was E1V3M5 according to the Glasgow coma scale. After his arrival at the hospital, we performed artificial respiration as he was in shock. Radiologic and computer tomography (CT) scans demon- strated multiple traumas (TBI, pelvis fracture, right femur fracture, and bilateral pulmonary contusions) (Fig. 1) and a chest burn. We performed external fixation for the pelvis fracture, direct traction for the right femur fracture, and catheter drainage for the bilateral pulmonary contusion, and he was admitted to our intensive care unit. From five days after the accident, polyuria appeared (about 3500–5000 ml/day). His urine and blood tests showed low spe- cific urine value (1.000–1.006), low urinary osmotic pressure (229 mOsm/kg), and low serum ADH (0.9 pg/ml) and so vasopressin replacement treatment was started due to DI related to the TBI. After his dyspnea had improved, osteosynthesis was performed to repair the fractures (pelvis and right femur fractures). Although he was transferred to a wheelchair from 10 days after the operation, dyspnea occurred, and he suffered sudden cardiopulmonary arrest at 23 days after the operation (at 37 days after the accident) from which he died. In the autopsy, large thromboses were found in the bilateral pulmonary arteries (Fig. 2), and lymphocyte infiltration into the posterior pituitary was also detected (Fig. 3). DI is a well-recognized complication of TBI. The majority of patients with post-traumatic DI will require ADH replacement therapy and tend to suffer from dehydration. 4 On the other hand, some negative effects of ADH on blood coagulation, such as increased platelet cohesion and the promotion of von Willebrand factor release, have been reported. 4 In this context, it is necessary to monitor patients receiving ADH replacement therapy for DI after TBI for thromboses. However, the incidence of thrombosis during ADH replacement therapy is disputed. Several studies into thrombosis and ADH replacement therapy have been reported. Doepker et al. reported that there was no significant relationship between thrombosis and ADH replacement therapy in patients with DI (not only secondary DI after TBI). 5 In contrast, Yoshida et al. reported that ADH is a factor affecting thrombosis, since serum osmotic pressure fluctuations are induced by ADH replacement therapy. 6 In our case, we think that there were three factors that may have contributed to the observed thrombosis. First, a high degree of dehydration occurred due to the DI after TBI and chest skin burn. In cases in which sufficient fluids cannot be supplied by drinking alone, water needs to be supplied via an intravenous drip. Next, this patient was instructed to take bed rest for a long period because he had multiple traumas and TBI. To prevent thrombosis, elastic stockings and intermittent pneumatic compression were used. Moreover, osteosynthesis was performed to repair the pelvis and right femur fractures and aimed to ensure early ambulation. Finally, he required ADH replacement therapy due to DI after TBI. ADH has the effect of increasing platelet cohesion and promoting von Willebrand factor release, 4 and as serum osmotic pressure fluctuations are also induced by ADH replacement therapy, 6 we think that intravenous thromboses will tend to form. In the management of DI patients after TBI, we believe that controlling urinary output and monitoring urinary and serum osmotic pressure are necessary. In particular, we must take care during the management of patients undergoing ADH replacement ...

Context 2

... (pelvis and right femur fractures). Although he was transferred to a wheelchair from 10 days after the operation, dyspnea occurred, and he suffered sudden cardiopulmonary arrest at 23 days after the operation (at 37 days after the accident) from which he died. In the autopsy, large thromboses were found in the bilateral pulmonary arteries (Fig. 2), and lymphocyte infiltration into the posterior pituitary was also detected (Fig. ...