Major bleeding complications in cardiopulmonary resuscitation: the place of thrombolytic therapy in cardiac arrest due to massive pulmonary embolism

Resuscitation ◽  
2003 ◽  
Vol 57 (1) ◽  
pp. 49-55 ◽  
Author(s):  
Karin Janata ◽  
Michael Holzer ◽  
Istepan Kürkciyan ◽  
Heidrun Losert ◽  
Eva Riedmüller ◽  
...  
2014 ◽  
Vol 34 (03) ◽  
pp. 233-236
Author(s):  
C. Martin ◽  
F. Alt ◽  
A. Wingerter ◽  
G. Staatz ◽  
H. Schinzel ◽  
...  

SummaryAcute pulmonary embolism (PE) is a serious complication in association with malignant diseases. We describe the successful treatment of PE applying a systemic thrombolytic therapy in a 4-year-old boy with acute lymphoblastic leukaemia.The thrombolytic therapy with recombinant tissue plasminogen activator (rtPA) 0.1 mg/ kg bodyweight per hour for six hours was continued for six days without important side effects. In particular no bleeding complications were observed. Computed tomography with contrast revealed a remarkable regression of the central PE. Without further delays the chemotherapy was resumed.


2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Hafiz B. Mahboob ◽  
Bruce W. Denney

Massive pulmonary embolism (PE) frequently leads to cardiac arrest (CA) which carries an extremely high mortality rate. Although available, randomized trials have not shown survival benefits from thrombolytic use. Thrombolytics however have been used successfully during resuscitation in clinical practice in multiple case reports and in retrospective studies. Recent resuscitation guidelines recommend using alteplase for PE related CA; however they do not offer a standardized treatment regimen. The most consistently applied approach is an intravenous bolus of 50 mg tissue plasminogen activator (t-PA) early during cardiopulmonary resuscitation (CPR). There is no consensus on the subsequent dosing. We present a case in which two 50 mg boluses of t-PA were administered 20 minutes apart during CPR due to persistent hemodynamic compromise guided by bedside echocardiogram. The patient had an excellent outcome with normalization of cardiac function and no neurologic sequela. This case demonstrates the benefit of utilizing bedside echocardiography to guide administration of a second bolus of alteplase when there is persistent hemodynamic compromise despite achieving return of spontaneous circulation after the initial bolus, and there is evidence of persistent right ventricle dysfunction. Future trials are warranted to help establish guidelines for thrombolytic use in cardiac arrest to maximize safety and efficacy.


2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
H Shiota ◽  
E Kagawa ◽  
M Kato ◽  
N Oda ◽  
E Kunita ◽  
...  

Abstract Introduction Paradoxical cerebral infarction is a mechanism of acute ischemic stroke; however, definitive images to diagnose paradoxical embolism are not often obtained. We report a case of paradoxical cerebral embolism complicated with cardiac arrest due to massive pulmonary embolism. Case report A 40-year-old man presented due to sudden-onset chest pain, and was admitted to our hospital. He was restless and had cold sweat; we could not measure blood pressure. Electrocardiography showed wide QRS complex with right bundle branch block, and T wave inversion in leads V1 and III. Transthoracic echocardiography showed diffuse severe left ventricular hypokinesis, with slightly better inferior wall motion compared to other segments. Few minutes after arriving, he experienced cardiac arrest; chest compression was initiated. He was transported to the catheter laboratory, and veno-arterial extracorporeal membrane oxygenation was initiated subsequently. To diagnose the cause of arrest, we performed coronary angiography, which revealed no occluded coronary artery. Pulmonary angiograms showed bilateral proximal pulmonary artery occlusion with massive thrombi (panel A). Surgical embolectomy was performed after cardiac team discussion. After ICU admission post-surgery, pericardial effusion was increased, and the blood drained continuously from the chest tube; a large amount of blood transfusion was required. Reopen chest haemostasis was utilised. After the second ICU admission, anisocoria was observed; subsequent computed tomography showed low density and midline shift in almost the entire left cerebral hemisphere (Panel B). Carotid duplex ultrasound revealed a large thrombus saddled at the left carotid artery bifurcation (Panel C and D). We rechecked the transthoracic echocardiogram at arrival to reveal the cause of the cerebral infarction, which showed the thrombus to be at the ascending aorta (Panel E). We thought that the thrombi had moved from the lower limb to the right atrium. The massive pulmonary embolism increased the pulmonary artery and right atrial pressure, resulting in the lower pressure of the left atrium compared to that of the right atrium. The thrombi passed through the patent foramen ovale into the left atrium, moved into the left ventricle, and embolised the left internal carotid artery (Panel F). He expired due to severe neurologic injury from brain herniation. Conclusion In this case, although the pulmonary embolism was massive and led to cardiac arrest, the deteriorated haemodynamics improved by extracorporeal cardiopulmonary resuscitation and surgical embolectomy. However, we could not rescue the patient because of the severe neurological injury due to paradoxical embolism. Paradoxical cerebral infarction in pulmonary embolism is rare; however, we should pay careful attention to early detection of paradoxical cerebral infarction in pulmonary embolism and treatment for return of the patient to the former lifestyle. Abstract P684 figure


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