there have been a few reports of patients who experienced cerebral infarctions after hemorrhagic shock . we herein report a rare case of a schizophrenic patient with cerebral infarctions after hemorrhagic shock , and discuss the mechanism underlying its occurrence . a 33-year - old male , who had been diagnosed with schizophrenia and given a prescription for 7.5 mg olanzapine , was discovered to have multiple sites of self - inflicted bleeding after cutting his wrists . he had a past history of kawasaki disease , which had completely resolved when he was a child . when the emergency medical technicians checked him , he was conscious , but in shock . he could understand what was being said , but he could not speak . his vital signs were : blood pressure , 86/50 mmhg ; pulse rate , regular at 110/minute ; saturation of peripheral oxygen in room air , 98% ; and tympanic temperature , 36.4c . he could write his name slowly using his right hand , but his characters were poorly formed . he was suspected to be in hemorrhagic shock , so he received rapid infusion of 500 ml of lactate ringer 's solution , and his wounds were closed . his vital signs returned to within the normal range after this treatment , without the need for a transfusion . the abnormal results of his blood biochemical analyses were as follows : white blood cell count , 21900/l ; glucose , 239 mg/ dl ; blood urea nitrogen , 25 mg / dl ; creatinine , 2.23 mg / dl , and hba1c was 5.0% . a computed tomography ( ct ) scan of the head revealed a low density area in the right insular and external putamen . an electrocardiogram and sonography for evaluation of the heart , coronary artery , and carotid artery were negative for any pathological finding . magnetic resonance imaging ( mri ) of the head demonstrated multiple small high intensity areas in the right frontotemporoparietal lobe and left thalamus , in addition to the head ct findings [ figure 1 ] . a transcranial doppler examination did not show any evidence of microemboli , even when using microbubble infusion with the valsalva maneuver . the patient subsequently received a diagnosis of speech apraxia , motor aphasia , and dysgraphia due to multiple cerebral infarctions . his deficits gradually improved , and he could speak again beginning on the fourth hospital day . as his d - dimer level had increased from 1.7 on arrival up to 12 g / ml on the tenth day , warfarin and aspirin were prescribed . the results of the biochemical analyses of his blood were as follows : antithrombin iii , 105.0% ; protein c , 93% ; protein s , 79.8% ; lupus anticoagulant , 0.8 seconds ; anti - nuclear antibodies x 40 ; anti - cardiolipin igg antibodies , 8 u / ml ; von willebrand factor , 200% ( 50  150% ) ; x - factor , 94% ; myeloperoxidase - anti - neutrophil cytoplasmic antibodies , negative ; and cytoplasmic - anti - neutrophil cytoplasmic antibodies , negative . after his mental state was considered to have sufficiently stabilized , he was discharged on the twenty - fifth hospital day . the mri of the head , on arrival ; the diffusion - weighted image showed multiple small high intensity areas in the right frontotemporoparietal lobe and left thalamus ( arrow ) this is the fourth case of cerebral infarction concomitant with hemorrhagic shock in english literature . generally , isolated hemorrhagic shock itself does not result in the occurrence of cerebral infarction . for children , there is a clinical association between hemorrhagic shock and encephalopathy syndrome , however , this syndrome is due to the cerebrovascular injuries induced by disseminated intravascular coagulopathy triggered by infection , making this clinical entity different from cerebral infarction concomitant with hemorrhagic shock . reported three adult cases of cerebral infarction after severe hemorrhagic shock , who required a large amount of blood via transfusion , ranging from 5 to 12 l. they hypothesized that the mechanism responsible for these complications was a cerebral infarction induced by hemodynamic insufficiency triggered by hemorrhagic shock , because the location of the cerebral infarctions coincided with the boundary zones where functional anastomoses between the two arterial systems existed . however , two of the three cases had lung injures , so an air embolism could also have caused the cerebral infarction . the other patient had a past history of pulmonary embolism and already had a high d - dimer level on arrival , so paroxysmal cerebral infarction could have been the cause . their hypothesized mechanism underlying these complications was thromboembolic events induced by multiple large infusions of coagulants , such as , thrombocyte concentrates , fresh frozen plasma , antithrombin iii , prothrombin complex , and recombinant factor viia , to obtain hematemesis . the present case did not undergo any treatment with coagulants , and his hemorrhagic shock was mild , so the previous theories did not apply to this case . one of possible causes of cerebral infarction was as a side effect of olanzapine therapy . olanzapine had a high affinity for the serotonin receptor 2a , and the serotonin - induced platelet aggregation could be affected following treatment . metabolic abnormalities such as dyslipidemia , hyperhomocysteinemia , and hyperglycemia were observed in subjects treated with olanzapine , and were all associated with decreased fibrinolytic activity . there is a controversy on whether olanzapine is a risk factor for the occurrence of cerebral infarction , and in a meta - analysis to evaluate atypical antipsychotic medications , including olanzapine , the odds ratio concerning cerebrovascular accidents was 1.50 ( confidence interval 0.33  7.44).[68 ] accordingly , hemorrhagic shock and olanzapine could be considered weak causative factors for cerebral infarction , but working together , they might have been responsible for the present patient 's infarctions . the plasma d - dimer levels were neither sufficiently sensitive nor specific to be utilized in stroke diagnostics , but numerous studies showed that patients with various strokes and stroke - related diseases had acutely increased plasma d - dimer levels on arrival . although a high d - dimer level on arrival suggested cardioembolic stroke , the possibility of such a diagnosis was considered to be low in this case . generally , the mean d - dimer levels were slightly elevated during the first week and then increased during the next two weeks , after an ischemic stroke , possibly due to activated thrombin formation induced by the infarcted brain . in addition , the high plasma d - dimer levels during the course of acute stroke suggested complications of deep vein thrombosis . however , the d - dimer levels were markedly elevated on the day of admission , and thereafter , gradually decreased by day four in the trauma setting . accordingly , the delayed increase observed in the d - dimer values , in this case , may have been induced by either the natural course after a stroke or may signify a complication of deep vein thrombosis . we have herein reported the fourth known case of cerebral infarction concomitant with hemorrhagic shock , and discussed the possible underlying mechanism .
we herein report the fourth case of cerebral infarction , concomitant with hemorrhagic shock , in english literature . 
 a 33-year - old male , who had been diagnosed with schizophrenia and given a prescription for olanzapine , was discovered with multiple self - inflicted bleeding cuts on his wrist . on arrival , he was in hemorrhagic shock without verbal responsiveness , but his vital signs were normalized following infusion of lactate ringer 's solution . 
 the neuroradiological studies revealed multiple cerebral ischemic lesions without any vascular abnormality . 
 he was diagnosed with speech apraxia , motor aphasia , and dysgraphia , due to multiple cerebral infarctions . as there was no obvious causative factor with regard to the occurrence of cerebral infarction in the patient 
 , the hypoperfusion due to hemorrhagic shock , and the thromboembolic tendency due to olanzapine , might have acted together to lead to the patient 's cerebral ischemia .