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| CASE REPORT |
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| Year : 2014 | Volume
: 4
| Issue : 1 | Page : 88-90 |
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Benefits of thrombolytics in prolonged cardiac arrest and hypothermia over its bleeding risk
Raghav Gupta1, Aditi Jindal2, Hope Cranston-D'Amato1
1 Department of Internal Medicine, Critical Care Medicine and Infectious Disease, St. Luke's Hospital, Chesterfield, Missouri, USA
2 Department of Pediatric Dentistry, Tufts University School of Dental Medicine, Boston, Massachusetts, USA
| Date of Web Publication | 3-Mar-2014 |
Correspondence Address:
Raghav Gupta
14463, Greencastle Dr., Apt. #6, Chesterfield, 63017, MO, USA.St. Luke's Hospital, 232, South Woods Mill Road, Chesterfield, 63017, MO
USA
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2229-5151.128021
 Abstract | | |
A 52-year-old non-smoking Caucasian male, who was admitted to our emergency room after he was found unconscious in the bathroom, went into cardiac arrest requiring prolonged cardiopulmonary resuscitation (CPR) and hypothermia therapy. Cardiac catheterization showed non-obstructive coronary arteries and further bedside echocardiogram suggested probable pulmonary embolism (PE) as an underlying cause of cardiac arrest. Although thrombolytic therapy is an effective therapy for PE, it is not routinely given during prolonged CPR for its life- threatening bleeding complications. Many reported cases have suggested a beneficial effect of empiric thrombolytic in cardiac arrest, but unrelated to duration of resuscitation and adjuvant treatments that imposes bleeding risk. We suspect that tissue plasminogen activator (tPA) should be promptly given to prolonged cardiac arrest patients, even when bleeding risk is high with the concurrent hypothermia treatment, keeping the benefits over risk strategy. Our patient received thrombolytic, tPA and showed remarkable clinical, physiological and radiographical improvement. Keywords: Hypothermia, prolonged cardiac arrest, thrombolytics
How to cite this article:
Gupta R, Jindal A, Cranston-D'Amato H. Benefits of thrombolytics in prolonged cardiac arrest and hypothermia over its bleeding risk. Int J Crit Illn Inj Sci 2014;4:88-90 |
How to cite this URL:
Gupta R, Jindal A, Cranston-D'Amato H. Benefits of thrombolytics in prolonged cardiac arrest and hypothermia over its bleeding risk. Int J Crit Illn Inj Sci [serial online] 2014 [cited 2023 Mar 21];4:88-90. Available from: https://www.ijciis.org/text.asp?2014/4/1/88/128021 |
| Introduction | |  |
Sudden cardiac arrest is linked more with structural heart disease; however it is also associated with pulmonary embolism (PE). The conventional treatment of PE is anticoagulation but the risk of bleeding is high in the situations where patients undergo prolonged cardiac arrest and hypothermia management. We hereby, present the unique case of pulmonary embolism diagnosed on the basis of clinics and bedside echocardiogram during a prolonged cardiopulmonary resuscitation (CPR), needing hypothermia management, and associated with rapid and remarkable recovery after administration of a loading dose of tissue plasminogen activator (tPA) without any complication of bleeding.
| Case Report | | |
A 52-year-old non-smoking Caucasian male, who is allergic to shrimps, presented to the emergency room (ER) after he was found unconscious in the bathroom. At 6 days before presentation, patient had symptoms of severe cough with streaks of blood and dyspnea on exertion and was treated with azithromycin antibiotic for presumed upper respiratory tract infection. The day before presentation, patient's symptoms of cough and dyspnea started getting worse. Patient reported taking benzonatate antitussive, which caused tingling and numbness around his mouth and cheeks, which resolved spontaneously after 30 min. Patient did not report of hives, swelling of the face or tongue and difficulty in swallowing. Subsequently, patient got extremely agitated and short of breath leading to state of unconsciousness. Emergency medical services were activated, 100% oxygen was initiated and patient was transferred to our ER.
In the ER, patient presented with grey colored skin and symptoms of severe dyspnea. As per the patient's wife, he had no calf pain and/or swelling recently. There were no recent hospitalizations, prolonged immobilization or history of pulmonary embolism (PE) and/or deep vein thrombus (DVT). He had no other medical procedures and/or surgeries performed in the recent past. Patient's father has a history of PE secondary to extensive airplane travel and stroke. Patient has no history of familial clotting disorders. Consequently, patient developed complete heart block and received intravenous atropine and epinephrine. An electrocardiogram showed a right bundle branch block and ST-segment elevations in the inferior leads with elevated troponins of 13.5 ng/ml (normal <0.03 ng/ml). Cardiac monitor showed pulseless electric activity and patient was intubated and cardiopulmonary resuscitation (CPR) was initiated immediately. The cardiac arrest was presumed from ST elevation myocardial infarction and the patient was transferred to cardiac catheterization laboratory. Patient intermittently remained in cardiac arrest requiring intra-aortic balloon pump and temporary pacemaker. Short episodes of CPR were performed. Cardiac catheterization showed non-obstructive coronary arteries and a hyper-dynamic left ventricle. Patient's blood pressure remained low and so patient was continued on epinephrine, dopamine drips. Patient was then transferred to the intensive care unit and he remained intubated with mechanical ventilation and ongoing CPR. On physical examination, the patient was noted to have respiratory rate of 30 breaths/min, fixed and dilated pupils of 7 mm and endotracheal tube in place. His neck was supple without jugular vein distention. Chest examination revealed distant lung sounds, with no wheezing. Cardiac auscultation was tachycardia with no murmurs, gallops and rubs. On neurologic al examination, the patient's Glasgow coma scale was <9 with no gag reflex and response to Babinski. Rest of the examination was unremarkable. Laboratory data revealed white cell count of 11.7 × 10 9 /L (normal 4.3-10 × 10 9 /L) with the normal differentials, creatinine of 2.4 mg/dl (normal 0.7-1.3 mg/dl), ionized calcium of 4.0 mg/dl (normal 4.6-5.1 mg/dl) bicarbonate of 15 mmol/L (normal 22-30 mmol/L), serum osmolality of 322 mOsm/kg (275-295 mOsm/kg), anion gap of 21 mmol/L (normal 8-16 mmol/L) and lactic acid of 16 mmol/L (normal 0.7-2.1 mmol/L) and D-dimer of 6.68 μg/ml (normal <0.49 μg/ml). Other blood cell counts, liver function tests, alcohol, salicylate, methanol levels and urine toxicology screen were unremarkable. An arterial blood gas showed a pH of 6.8, pCO 2 of 70 mmHg, pO 2 of 90 mmHg on mechanical ventilation, consistent with mixed respiratory and metabolic acidosis. Electrocardiogram showed sinus tachycardia with occasional premature ventricular complexes and right bundle branch block. Chest X-ray showed bilateral basilar infiltrates and cardiomegaly. Stat bedside echocardiogram revealed moderate hypokinesis and enlargement of the right ventricle. Patient's clinical symptoms, laboratory investigations, negative cardiac catheterization of obstructive coronary arteries, electrocardiogram showing sinus tachycardia and echocardiogram proving hypo kinesis and enlargement of right ventricle suggested presumed diagnosis of PE causing cardiac arrest. At the same time, alteplase, tissue plasminogen activator (tPA) was administered immediately with the dose of 0.6 mg/kg over 2 min in a bolus form and heparin drip was started. During the course of the intensive care stay, patient was treated with hypothermic protocol for cardiac arrest with no bleeding complications. Intravenous sodium bicarbonate and calcium chloride were given, cardiac arrest was eventually terminated and patient got extubated. The blood pressure got stabilized and dopamine, epinephrine drips were stopped. Furthermore, intravenous hydrocortisone, benadryl was administered for possible anaphylactic reaction.
Subsequently, patient rapidly improved with decreased requirement of oxygen. Repeated arterial blood gases within an hour were improved and revealed pH of 7.15, pCO 2 of 47 mmHg and pO 2 of 404 mmHg. Repeated echocardiogram noted normal size and function of the right ventricle. Venous Doppler's of the lower extremities showed DVT in the left distal femoral vein, gastrocnemius, peroneal vein and normal right lower extremity. The inferior vena cava filter was placed to prevent further occurrence of life-threatening clots or pulmonary embolus and heparin drip was continued. The renal failure secondary to the cardiogenic shock improved with 2 mg of bumetanide, oral diuretic therapy. During the hospital course, heparin was discontinued due to patient's low platelet count and positive heparin induced thrombocytopenia panel. Rivaroxaban, the oral anticoagulant was initiated and patient was transferred to floor with oxygen saturation of 95% on room air. On the medical floor, patient was walking and moving around, could talk in full sentences, was able to feed himself. Within 3 days of the hospital stay, he showed remarkable clinical and functional improvement and was discharged to home in a stable condition.
| Discussion | | |
Sudden cardiac arrest (SCA) and sudden cardiac death (SCD) is defined as a sudden termination of cardiac activity with hemodynamic instability requiring immediate CPR. It has become a serious clinical and public health issue. Despite advancement in the clinical and research medicine, United States (US) vital statistics mortality data due to SCA and SCD has been expanding. The published death data reports that 15% of the total mortality in the US and other industrialized countries is secondary to SCA. [1] Sudden death, in majority of the cases comprise of lethal coronary heart disease, which account for 70% of the total and approximately 10-15% of the cases are secondary to other structural heart disease including cardiomyopathies, arrhythmias and valvular abnormalities. [2],[3] Rest of the non-cardiac causes of SCA are attributed to bleeding, infections and familial SCD of uncertain cause. [3] PE is also a possible non-cardiac cause of SCA associated with very high mortality and often revealed by autopsy. [4]
CPR with skillful chest compressions and early defibrillation remains the cornerstone of basic and advanced cardiac life support. Furthermore, important is the identification and treatment of all possible reversible causes. The mechanism of SCA and its outcome largely depends on the underlying cause, hypoxemia, severe acid base imbalance and the duration of resuscitation (usually prolonged if it is more than 4 min). [5] SCA mortality is largely associated with brain death and most of the reported data justifies the role of mild therapeutic hypothermia with its neuroprotective effect. [6] The risk of bleeding is highly associated with hypothermia management, especially if thrombolysis or cardiac intervention has to be done. [7],[8] Bedside echocardiogram is a useful diagnostic tool to determine heart valve and pericardium integrity, ventricular function and to differentiate kinds of shock. [9] Coronary catheterization and emergency percutaneous coronary intervention remains the principal approach for the resuscitated patients presenting with ST-segment elevation and high troponins. [10] Important is to consider pulmonary emboli, which can be the underlying cause of the same presentation.
Although, SCA is linked more with structural heart disease, association with PE remain under high suspicion. Acute PE is an extremely fatal disease, if not early diagnosed and treated appropriately. Clinical presentation is highly variable and is often associated with sinus tachycardia in electrocardiogram and arterial blood gases showing hypoxemia, hypocapnia and respiratory alkalosis. Serum troponin I and troponin T are found elevated in 30-50% of patients with PE. [11] Though, confirmed diagnosis is attained by angiography, chest computed tomography with contrast if not contraindicated or ventricular perfusion scan, bedside echocardiogram has a remarkable role in emergency cases. [9] Prompt anticoagulation is initiated, unless contraindicated. There are several reported cases of favorable outcomes associated with thrombolysis in presumed or confirmed diagnosis of PE during cardiac arrest. [12],[13],[14]
We hereby, present the unique case of PE diagnosed on the basis of clinics and bedside echocardiogram during a prolonged CPR, needing hypothermia management and associated with rapid and remarkable recovery after administration of a loading dose of tPA without any complication of bleeding.
| Conclusion | | |
In this patient, the presence of clinical signs of dyspnea and hemoptysis, sinus tachycardia on electrocardiogram, elevated troponins and bedside echocardiogram showing enlargement and hypokinesis of the right ventricle, suggested the diagnosis of PE as an underlying cause of prolonged cardiac arrest, which prompted to start tPA, despite the risk of bleeding associated with the hypothermia management. Patient showed rapid clinical, physiological and radiographical improvement with the anticoagulation therapy. This case illuminates the precedence of early initiation of tPA with the expeditious diagnosis of PE, along with prolonged CPR and hypothermia treatment. The risk of bleeding remains low with the benefits attained by the given management.
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