scholarly journals Double Bolus Thrombolysis for Suspected Massive Pulmonary Embolism during Cardiac Arrest

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Gerard O’Connor ◽  
Gareth Fitzpatrick ◽  
Ayman El-Gammal ◽  
Peadar Gilligan

More than 70% of cardiac arrest cases are caused by acute myocardial infarction (AMI) or pulmonary embolism (PE). Although thrombolytic therapy is a recognised therapy for both AMI and PE, its indiscriminate use is not routinely recommended during cardiopulmonary resuscitation (CPR). We present a case describing the successful use of double dose thrombolysis during cardiac arrest caused by pulmonary embolism. Notwithstanding the relative lack of high-level evidence, this case suggests a scenario in which recombinant tissue Plasminogen Activator (rtPA) may be beneficial in cardiac arrest. In addition to the strong clinical suspicion of pulmonary embolism as the causative agent of the patient’s cardiac arrest, the extremely low end-tidal CO2suggested a massive PE. The absence of dilatation of the right heart on subxiphoid ultrasound argued against the diagnosis of PE, but not conclusively so. In the context of the circulatory collapse induced by cardiac arrest, this aspect was relegated in terms of importance. The second dose of rtPA utilised in this case resulted in return of spontaneous circulation (ROSC) and did not result in haemorrhage or an adverse effect.

2020 ◽  
Vol 13 (4) ◽  
pp. e234083 ◽  
Author(s):  
John Edward Ashbridge Taylor ◽  
Chen Wen Ngua ◽  
Matthew Carwardine

Massive pulmonary embolism (PE) is a leading cause of maternal death and may require intra-arrest thrombolysis as well as resuscitative hysterotomy. The case presented is a primigravida in her mid-30s at 28 weeks gestation. The patient presented to the emergency department after out-of-hospital cardiac arrest. Return of spontaneous circulation (ROSC) was achieved but not sustained. Episodic cardiopulmonary resuscitation with epinephrine boluses was required. Resuscitative hysterotomy was performed intra-arrest. Echocardiography revealed a dilated right heart consistent with massive PE and thrombolysis was administered. ROSC was obtained thereafter and output was sustained. Subsequent CT brain revealed irreversible hypoxic injury. Treatment was withdrawn with the support of family. Postmortem examination confirmed massive PE. Thrombolysis can restore and improve cardiovascular status in cardiac arrest caused by massive PE. Thrombolysis is not contraindicated in maternal resuscitation where resuscitative hysterotomy may also be required.


2018 ◽  
Vol 2018 ◽  
pp. 1-4
Author(s):  
Abdullah E. Laher ◽  
Muhammed Moolla ◽  
Feroza Motara ◽  
Fathima Paruk ◽  
Guy Richards

Introduction. It is estimated that the diagnosis of pulmonary embolism (PE) is missed in as many as 84% of all cases of PE. Cardiac arrest following PE is generally associated with poor outcomes. Case Report. A 43-year-old man presented to the Emergency Department (ED) in cardiac arrest. Swelling of his right lower limb was noted on arrival. Point of care ultrasound was performed during ongoing cardiopulmonary resuscitation (CPR) and showed a thrombus in the right iliofemoral vein as well as dilatation of the right ventricle. Fibrinolytic therapy was initiated immediately and a return of spontaneous circulation (ROSC) was achieved 30 minutes later. The diagnosis of PE was finally confirmed on computed tomography pulmonary angiography once haemodynamic stability was achieved. The patient was thereafter transferred to the intensive care unit for postresuscitation care and further management. Several days later, he was discharged home neurologically intact and fully recovered. Discussion. Since outcomes after cardiac arrest following PE are generally dismal, available and potentially life-saving interventions to restore pulmonary circulation should be rapidly implemented when PE is the likely cause of cardiac arrest.


2017 ◽  
Vol 18 (4) ◽  
pp. 342-347 ◽  
Author(s):  
Alister Seaton ◽  
Luke E Hodgson ◽  
Ben Creagh-Brown ◽  
Adrian Pakavakis ◽  
Duncan LA Wyncoll ◽  
...  

A 59-year-old man was diagnosed with a massive pulmonary embolism. Despite thrombolysis there were two episodes of cardiac arrest and following recovery of spontaneous circulation profound cardiorespiratory failure ensued. An extracorporeal membrane oxygenation retrieval team initiated veno-venous extracorporeal membrane oxygenation on site to facilitate transfer to the extracorporeal membrane oxygenation centre. An excellent outcome is reported in the short term. This represents one of the few published cases of veno-venous extracorporeal membrane oxygenation for a massive pulmonary embolism following thrombolysis.


2020 ◽  
Vol 121 (1) ◽  
pp. 42-48
Author(s):  
Elisavet Kaitalidou ◽  
Dimitrios Karapiperis ◽  
Vasileios Makrakis ◽  
Maria Kipourou ◽  
Dimitrios Petroglou

A male patient with a history of immobilization due to motor weakness, was transferred to our emergency department after syncope during physiotherapy, with recorded hypotension. Transthoracic echocardiography showed severe dilatation of the right ventricle (RV), with apex hypercontractility and almost akinetic RV free wall. The above findings, in addition to the unexpected visualization of a large, free-floating, right atrial thrombus, a rare finding associated with high mortality, readily confirmed the clinical suspicion of acute pulmonary embolism (PE) causing circulatory collapse. Intravenous fibrinolysis and vasopressor therapy were successfully administered, and hemodynamic instability was soon alleviated.


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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