Masahiro Kashiura

Amiodarone and lidocaine for shock refractory ventricular fibrillation or ventricular tachycardia in out-of-hospital cardiac arrest: are they really effective?

In 2015, the American Heart Association and European Resuscitation Council updated the guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care according to the International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations (1-3). The guidelines recommend administration of amiodarone for sustained ventricular fibrillation (Vf) and ventricular tachycardia (VT) refractory to CPR, defibrillation, and vasopressor in out-of-hospital cardiac arrest. Lidocaine is recommended as an alternative to amiodarone. However, these recommendations remain weak and are based on the two previous randomized controlled trials (RCTs) performed more than 10 years ago. In these trials, compared with both placebo and lidocaine, amiodarone improved the rate of return of spontaneous circulation (ROSC) but not the survival to hospital discharge and neurological outcome (4). However, these studies were not statistically powered to investigate survival and neurological outcome, so the actual efficacy of amiodarone therapy remains undetermined.

Chest compression-related fatal internal mammary artery injuries manifesting after venoarterial extracorporeal membrane oxygenation: a case series

BackgroundCardiopulmonary resuscitation-related bleeding, especially internal mammary artery injuries, can become life-threatening complications after initiating venoarterial extracorporeal membrane oxygenation owing to the frequent involvement of concomitant anticoagulant treatment, antiplatelet treatment, targeted temperature management, and bleeding coagulopathy. We report the cases of five patients who experienced this complication and discuss their management.Case presentationWe retrospectively evaluated five patients with cardiopulmonary resuscitation-related internal mammary artery injuries who were treated between February 2011 and February 2016 at our institution. All five patients were Asian men, aged 56 to 68-years old, who had received concomitant intravenously administered unfractionated heparin (3000 units) with antiplatelet therapy. Four patients received targeted temperature management. The injuries and hematomas were detected using contrast-enhanced computed tomography in all cases. Three patients were treated using transcatheter arterial embolization within 6 hours following cardiopulmonary arrest, and two were resuscitated and received appropriate treatment following early recognition of their injuries. Two patients died of hemorrhagic shock with delayed intervention. Four of the five patients had excessively prolonged activated partial thromboplastin times before their interventions.ConclusionsComputed tomography should be performed as soon as possible after the return of spontaneous circulation to identify injuries and consider appropriate treatments for patients who have experienced cardiac arrest. Delayed bleeding may develop after treating hypovolemic shock and relieving arterial spasms; therefore, transcatheter arterial embolization should be performed aggressively to prevent delayed bleeding even in the absence of extravasation. This approach may be superior to thoracotomy because it is less invasive, causes less bleeding, and can selectively stop arterial bleeding sooner. A 3000-unit intravenous bolus of unfractionated heparin may be redundant; heparin-free extracorporeal cardiopulmonary resuscitation may be a more appropriate alternative. Unfractionated heparin treatment can commence after the bleeding has stopped.

Unilateral cardiogenic pulmonary edema associated with acute mitral regurgitation

Two cases of cardiogenic unilateral pulmonary edema are reported. Both patients presented to the emergency department with dyspnea, and chest radiography revealed unilateral infiltration, which mimics pulmonary disease. However, the patients were diagnosed with cardiogenic pulmonary edema, because echocardiography showed severe mitral regurgitation with an eccentric jet.

A case of circumferential type A aortic dissection with intimal intussusception diagnosed using repeat transthoracic echocardiography examination

Sometimes it is difficult to diagnose circumferential aortic dissection with enhanced computed tomography alone. A 58‐year‐old woman presented with sudden‐onset chest discomfort and loss of consciousness. Transthoracic echocardiogram showed mild aortic regurgitation. Enhanced computed tomography scans showed no obvious intimal tear or flap at the proximal ascending aorta, but an intimal flap was observed from the aortic arch to both common iliac arteries. Stanford type B dissection was tentatively diagnosed. Repeat detailed transthoracic echocardiography examination showed an intimal tear and flap at the ascending aorta; prolapse into the left ventricle caused severe aortic regurgitation. Type A aortic dissection was definitively diagnosed; emergent operation showed a circumferential intimal tear originating from the ascending aorta.

Hemodialysis for removal of dabigatran in a patient with gastric hemorrhage

An 82‐year‐old man taking dabigatran was admitted with syncope. Computed tomography showed extravasation from the stomach. Laboratory data revealed renal insufficiency and prolonged activated partial thromboplastin time. The gastric endoscopy showed a gastric ulcer with an exposed vessel. However, an endoscopic hemostatic procedure failed to completely stop the bleeding. The patient experienced cardiac arrest from hypotensive shock. Spontaneous circulation returned after 5 min of resuscitation. After endoscopy, computed tomography showed a gastric perforation. For dabigatran removal, the patient underwent a 6‐h hemodialysis session. Thrombin activity and thrombin–antithrombin complex increased during hemodialysis, while activated partial thromboplastin time decreased.

Diverticulitis-induced pylephlebitis possibly misdiagnosed as biliary duct obstruction

A 59‐year‐old Asian man presented to our emergency department with hypogastrium pain, loss of appetite, and diarrhea. On admission, he was hypotensive and jaundiced. Laboratory test results revealed thrombocytopenia, hypercreatininemia, and hyperbilirubinemia. Color Doppler sonography showed no blood flow in the right and left branches of the portal vein, which seemed similar to biliary obstruction. Enhanced computed tomography showed portal vein thrombi, consistent with pylephlebitis; a broad‐spectrum antibiotic and an anticoagulant were administered.