Delayed onset of impaired consciousness complicated with ketoacidosis after disulfiram overdose

Abstract Background We report a case of disulfiram overdose that caused a delayed onset of impaired consciousness and ketoacidosis. Case presentation A 61‐year‐old man was transferred to our hospital following a suicide attempt. The patient lost consciousness after an overdose of disulfiram and brotizolam. He was diagnosed with acute drug intoxication and was intubated. On day 2, he showed an improved consciousness response and was successfully extubated. On day 5, the state of consciousness worsened again, and ketoacidosis progressed. The patient required hemodialysis and suffered from impaired consciousness for the following 2 weeks. Eventually, he recovered gradually and was discharged to the rehabilitation ward. Conclusions The delayed appearance of symptoms after the disulfiram overdose was thought to be related to the slow metabolism of disulfiram in the body. Our case suggests the necessity of careful follow‐up for delayed impaired consciousness

Peripheral VA-ECMO and pericardial drainage connected to the ECMO circuit for cardiac tamponade from blowout rupture: a case report

Abstract Background Left ventricular free wall rupture, particularly the blowout type, is still one of the most lethal complications of myocardial infarction and can cause catastrophic cardiac tamponade. Extracorporeal membrane oxygenation (ECMO) is often used to treat haemodynamic instability due to cardiac tamponade. However, elevated pericardial pressure can cause collapse of the right atrium, resulting in inadequate ECMO inflow and preventing the stabilisation of the circulation. Further, it can interfere with the venous return from the superior vena cava (SVC), increasing the intracranial pressure and reducing cerebral perfusion levels. Case presentation A 65-year-old man was hospitalised for out-of-hospital cardiac arrest. We used ECMO for cardiopulmonary resuscitation. After the establishment of ECMO, transthoracic echocardiography and left ventriculography revealed massive pericardial effusion. The treatment was supplemented with pericardial drainage since ECMO flow was frequently hampered by suction events. However, the blowout rupture led to the requirement of constant drainage from the pericardial catheter. To tend to this leak, we connected the venous cannula of ECMO and the pericardial drainage catheter. The surgery was performed with stable circulation without suction failure of ECMO. During the course of the intensive care management, the neurological prognosis of the patient was revealed to be poor, and the patient was shifted to palliative care. Unfortunately, the patient died on day 10 of hospitalisation. Conclusion We present a case wherein the combination of pericardial drainage and ECMO was used to maintain circulation in a patient with massive pericardial effusion due to cardiac rupture

Klebsiella pneumoniae sepsis complicated with central nervous system involvement: A case series

Abstract Central nervous system (CNS) infection with Klebsiella pneumoniae can be a complication of invasive liver abscess syndrome; however, CNS infections due to K. pneumoniae without liver abscesses are rare. We report three fatal cases of CNS infection due to K. pneumoniae that lacked liver abscesses during the initial investigation

Purpura fulminans with Lemierre’s syndrome caused by Gemella bergeri and Eikenella corrodens: a case report

Abstract Background Gemella bergeri is one of the nine species of the genus Gemella and is relatively difficult to identify. We herein describe the first case of septic shock due to a Gemella bergeri coinfection with Eikenella corrodens. Case presentation A 44-year-old Asian man with a medical history of IgG4-related ophthalmic disease who was prescribed corticosteroids (prednisolone) presented to our hospital with dyspnea. On arrival, he was in shock, and a purpuric eruption was noted on both legs. Contrast enhanced computed tomography showed fluid retention at the right maxillary sinus, left lung ground glass opacity, and bilateral lung irregular opacities without cavitation. Owing to suspected septic shock, fluid resuscitation and a high dose of vasopressors were started. In addition, meropenem, clindamycin, and vancomycin were administered. Repeat computed tomography confirmed left internal jugular and vertebral vein thrombosis. Following this, the patient was diagnosed with Lemierre’s syndrome. Furthermore, he went into shock again on day 6 of hospitalization. Additional soft tissue infections were suspected; therefore, bilateral below the knee amputations were performed for source control. Cultures of the exudates from skin lesions and histopathological samples did not identify any pathogens, and histopathological findings showed arterial thrombosis; therefore it was concluded that the second time shock was associated with purpura fulminans. Following this, his general status improved. He was transferred to another hospital for rehabilitation. The blood culture isolates were identified as Gemella bergeri and Eikenella corrodens. Gemella bergeri was identified by matrix-assisted laser desorption ionization-time of flight mass spectrometry and confirmed by 16S rRNA gene sequencing later. The primary focus of the infection was thought to be in the right maxillary sinus, because the resolution of the fluid retention was confirmed by repeat computed tomography. Conclusions Gemella bergeri can be the causative pathogen of septic shock. If this pathogen cannot be identified manually or through commercial phenotypic methods, 16S rRNA gene sequencing should be considered