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Background The effect of venoarterial extracorporeal membranous oxygenation (V‐A ECMO), plasma exchange (PE), and direct hemoperfusion (DHP) for fatal cibenzoline succinate poisoning is unclear. We report a rare case of severe cibenzoline succinate poisoning along with cardiac arrest, wherein the patient was managed with V‐A ECMO, PE, and DHP. We also measured the blood levels of cibenzoline succinate frequently. Case Presentation A 51‐year‐old woman had a refractory cardiac arrest after cibenzoline succinate ingestion. We initiated V‐A ECMO, PE, and DHP. Plasma exchange did not improve clinical manifestations. Her clinical condition improved during DHP, but there was no evidence about removal of drugs. On day 3, DHP and ECMO were terminated. On day 9, she was transferred to another hospital without arrhythmia recurrence. Conclusion Venoarterial ECMO is effective in cases of cibenzoline succinate poisoning‐related cardiac dysfunction or cardiac arrest. No evidence was obtained for the effects of PE and DHP., A case report of cibenzoline succinate poisoning treated with extracorporeal cardiopulmonary resuscitation and direct hemoperfusion.

In blunt cerebrovascular injury, reported traumatic basilar artery occlusions have involved dissection of the basilar artery, distal embolization due to traumatic vertebral artery dissection, or entrapment of the basilar artery into the clivus fracture. To date, however, there are no reports of traumatic basilar artery entrapment without a clivus fracture. Here, we report the first case of traumatic basilar artery occlusion caused by entrapment into an originally existing bone defect. A 67-year-old man with a history of treatment for intracranial aneurysm suffered multiple traumatic injuries in a fall. On arrival at our hospital, he presented with neurogenic shock with quadriplegia. Computed tomography (CT) showed small epidural hematoma, C4-6 cervical spinous process fracture, and Th2-3 vertebral body fracture. CT angiography revealed occlusion of the basilar artery trunk. As vertebrobasilar artery dissections and clivus fracture were not observed; however, we could not elucidate the pathology of the basilar artery occlusion. On day 4, after surgery for the cervical and thoracic lesions, he exhibited consciousness disturbance. Diffusion-weighted imaging on day 5 showed hyperintensities in the brainstem and cerebellum. Basi-parallel anatomic scanning magnetic resonance imaging showed that the basilar artery, while lacking vascular wall injuries, was tethered into the clivus. Antithrombotic therapy was performed, but the patient progressed to a locked-in state. Previous head CT before the trauma revealed a bone defect already present in the clivus. We speculated basilar artery entrapment into this preexisting bone defect. We must look for basilar artery injury in trauma patients even in the absence of clivus fracture.

Case Sibutramine is a weight loss agent that was withdrawn from the market in the USA and European Union because it increases adverse events in patients with cardiovascular diseases. However, non-prescription weight loss pills containing sibutramine can be still easily purchased over the Internet. A 21-year-old woman without history of cardiovascular diseases developed cardiac arrest. She was a user of a weight loss pills, containing sibutramine and hypokalemia-inducing agents, imported from Thailand over the Internet. Outcome She was successfully resuscitated without any neurological deficits by using extracorporeal membrane oxygenation for refractory ventricular fibrillation. Conclusion This case indicates that sibutramine can cause cardiac arrest even in subjects without pre-existing cardiovascular disease when combined with agents that promote QT prolongation.

In multiple trauma, blunt carotid artery injuries (BCAIs) have occasionally been reported. However, bilateral blunt carotid artery occlusions (Grade 4 BCAIs) associated with multiple trauma are rare, and delays in diagnosis and treatment result in a lethal outcome. Here, we report our experience with bilateral carotid artery occlusions. A 76-year-old female suffered multiple traumas in a motor vehicle accident. On arrival at our hospital, she presented in a coma, with left mydriasis and unreactive pupils. Computed tomography (CT) showed bifrontal intracranial epidural hematoma and fractures of the facial bone and anterior skull base, and osteoplastic craniotomy was urgently undertaken for the epidural hematoma. However, the comatose state and unreactive pupils persisted during the post-operative course. Serial head CT findings showed progressive bilateral ischemic changes, and radiological examinations revealed bilateral internal carotid artery occlusions. We speculated that bilateral Grade 4 BCAIs had induced progressive cerebral infarctions. The patient partially responded to anticoagulation therapy with heparin infusion, but died of multiple organ failure on day 15. When bilateral progressive ischemic changes are observed in a patient with severe traumatic brain injury, bilateral Grade 4 BCAIs should be considered in the differential diagnosis. CT angiography as part of whole-body CT at admission may be effective for preventing delays in diagnosis and treatment of bilateral Grade 4 BCAIs.

Organophosphorus (OP) pesticide poisoning is a leading cause of morbidity and mortality in the developing world, affecting an estimated three million people annually. Much of the morbidity is directly related to muscle weakness, which develops 1-4 days after poisoning. This muscle weakness, termed the intermediate syndrome (IMS), leads to respiratory, bulbar, and proximal limb weakness and frequently necessitates the use of mechanical ventilation. While not entirely understood, the IMS is most likely due to persistently elevated acetylcholine (ACh), which activates nicotinic ACh receptors at the neuromuscular junction (NMJ). Thus, the NMJ is potentially a target-rich area for the development of new therapies for acute OP poisoning. In this manuscript, we discuss what is known about the IMS and studies investigating the use of nicotinic ACh receptor antagonists to prevent or mitigate NMJ dysfunction after acute OP poisoning.

Organophosphorus (OP) pesticide poisoning is a significant problem worldwide. Research into new antidotes for these acetylcholinesterase inhibitors, and even optimal doses for current therapies, is hindered by a lack of standardized animal models. In this study, we sought to characterize the effects of the OP pesticide parathion on acetylcholinesterase in a Wistar rat model that included comprehensive medical care.Methods. Male Wistar rats were intubated and mechanically ventilated and then poisoned with between 20 mg/kg and 60 mg/kg of intravenous parathion. Upon developing signs of poisoning, the rats were treated with standard critical care, including atropine, pralidoxime chloride, and midazolam, for up to 48 hours. Acetylcholinesterase activity was determined serially for up to 8 days after poisoning.Results. At all doses of parathion, maximal depression of acetylcholinesterase occurred at 3 hours after poisoning. Acetylcholinesterase recovered to nearly 50% of baseline activity by day 4 in the 20 mg/kg cohort and by day 5 in the 40 and 60 mg/kg cohorts. At day 8, most rats’ acetylcholinesterase had recovered to roughly 70% of baseline. These data should be useful in developing rodent models of acute OP pesticide poisoning.

Background In cases of severe accidental hypothermia, it was recommended that resuscitation should be continued until the patient has rewarmed, as hypothermia itself can preserve cerebral function, and hypothermic cardiac arrest is reversible. During cardiopulmonary resuscitation for normothermic patients, muscle rigidity suggests the initiation of postmortem changes such as rigor mortis and can lead to the termination of resuscitation. Currently, the prognosis of cardiac arrest due to severe accidental hypothermia accompanied by rigidity is unknown. Case presentation A 29-year-old woman was found unresponsive near a snowy mountain trail. Upon discovery, she was found to be in cardiac arrest with an initial asystole rhythm and exhibited mandibular rigidity. On admission, her core temperature was 22 °C. Although cardiac arrest continued, and she showed no response to normal resuscitation, blood gas analysis revealed that her initial serum potassium level was 5.4 mmol/L. Extracorporeal membrane oxygenation (ECMO) for systemic perfusion and rewarming was initiated. After ECMO was introduced, return of spontaneous circulation was achieved. She showed no neurological impairments at discharge. Conclusions Muscle rigidity does not rule out the possibility of resuscitation in patients with severe accidental hypothermia under cardiac arrest. Serum potassium levels may assist in deciding whether ECMO should be introduced, even if a patient is in asystole. This knowledge may help emergency physicians to save the lives of such patients.

Pancreatic damage is commonly observed as a consequence of accidental hypothermia (core body temperature below 35 °C). We aimed to investigate the risk factors for pancreatic damage and the causal relationship in patients with accidental hypothermia.This retrospective, single-center, observational case-control study was conducted in the emergency department of a tertiary care medical center. We investigated patients who were admitted for accidental hypothermia over a course of ten years (January 2008 to December 2017).Of the 138 enrolled patients, 70 had elevated serum amylase levels (51%). We observed a correlation between initial core body temperature and serum amylase level (Spearman's rank correlation coefficient -0.302, p 0.001). Patients who developed acute pancreatitis had a significantly lower initial core body temperature than those who did not develop it (odds ratio = 0.76; 95% confidence interval [CI] = 0.61-0.94; p = 0.011). Receiver operating characteristic analysis showed that a body temperature lower than 28.5 °C at the time of visit was predictive of acute pancreatitis (area under the curve = 0.71, 95% CI = 0.54-0.88, sensitivity = 0.67, specificity = 0.69, p = 0.017).We concluded that an initial core body temperature lower than 28.5 °C was a risk factor for acute pancreatitis in accidental hypothermia cases. In such situations, careful follow-up is necessary.

Background Time is a crucial factor for the successful early management of the multi-trauma patient. Hybrid operating theaters, which support the integration of surgical treatment and interventional radiology, provide opportunities to reduce the time-to-surgery for life threatening conditions. Case presentation We describe the early successful treatment of a 54-year-old male who sustained multiple injuries when he was hit by a 1000 kg bale of wheat that fell from a height. He was admitted with hemorrhagic shock due to intra-abdominal bleeding, an unstable fracture of the pelvis, and blunt aortic injury, which was considered to be at high risk of rupture. External fixation was applied to the pelvis in the resuscitation bay, and the patient was transferred to a hybrid operating theater for treatment of both the intra-abdominal hemorrhage and blunt aortic injury. Damage control laparotomy and thoracic endovascular aortic repair were performed uneventfully. Conclusions Hybrid treatment, which combines emergency surgery and intraoperative interventional radiology, provides a prompt and appropriate management approach for the treatment of patients with severe multiple trauma and may improve patient outcomes.

Background Tension gastrothorax is a kind of obstructive shock with prolapse and distention of the stomach into the thoracic cavity. Progressive gastric distension leads to mediastinal shift, reduced venous return, decreased cardiac output, and ultimately cardiac arrest. Therefore, it is crucial to decompress the stomach distension for the initial resuscitation of tension gastrothorax. Case presentation A 75-year-old female was transported to our resuscitation bay due to motor vehicle crash. At the time of arrival to our hospital, the patient developed cardiac arrest. While undergoing cardiopulmonary resuscitation, an unstable pelvic ring was recognized, so we performed a resuscitative thoracotomy to control hemorrhage and to perform direct cardiac massage. Once we performed the thoracotomy, the stomach and omentum prolapsed out of the thoracotomy site and through the diaphragm rupture site and spontaneous circulation was recovered. Neither the descending aorta nor the heart was collapsed. Although we had continued the treatment for severe pelvic fracture (including blood transufusions), the patient died. Given that (1) the stomach prolapsed out of the body at the time of the thoracotomy; (2) at the same timing, spontaneous circulation returned; and (3) the descending aorta and heart did not collapse, we hypothesized that the main cause of the initial cardiac arrest was tension gastrothorax. Conclusions Recognition of tension gastrothorax pathophysiology, which is a form of obstructive shock, makes it possible to manage this injury correctly.

We report a case of absolute vitamin K deficiency (VKD) diagnosed by measuring serum VK levels in an elderly woman undergoing warfarin therapy. A 78-year-old woman was admitted to our hospital because of dyspnea and sore throat diagnosed as pharyngitis 1 week before admission. On admission, the sore throat had exacerbated and dyspnea developed. She had history of atrial fibrillation, for which warfarin 1.5 mg/d was started approximately 10 years prior and her international normalized ratio (INR) had been maintained at an acceptable therapeutic level. Blood results revealed unmeasurable INR and abnormally prolonged activated partial thromboplastin time (APTT). She was diagnosed with adenoiditis and warfarin-related coagulopathy and administered intravenous VK (20 mg) and fresh frozen plasma (FFP; 4 U), which improved INR and APTT. Since the coagulopathy responded to intravenous VK administration, the patient was clinically diagnosed with warfarin-related relative VKD. Approximately 1 month later, she returned with complaints of sore throat. Blood results indicated abnormal INR (7.22) and APTT (N80.0 s). She was diagnosed with recurrent adenoiditis and VK deficient coagulopathy. The patient’s serum VK levels were low (VK1 level, 0.13 ng/mL; VK2 levels, 0.85 ng/mL). Initial treatment of VK (20 mg) and FFP followed by intravenous VK (20 mg/d) for 6 days, her symptoms dissipated. Warfarin was suspected to have caused absolute VKD. Severe coagulopathy in patients undergoing warfarin therapy is primarily caused by, relative VKD. However, the possibility of warfarin-related absolute VKD should be suspected when INRis not sufficiently improved by intravenous VK administration.