PULMONARY EMBOLISM, A RARE BUT DEADLY COMPLICATION OF CO POISONING

Abstract

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Carbon Monoxide (CO) is a colorless, odorless gas found in fumes produced from carbon fuels in engines, stoves, and fireplaces. CO binds to hemoglobin forming a molecule called carboxyhemoglobin (CO-Hb), which has higher affinity to O2 than hemoglobin itself which leads to symptoms of hypoxia and ischemia. Given an adequate history, clinicians can quickly initiate treatment but differentials for shortness of breath (SOB) must be sought and ruled out. Our case report will discuss the importance of CO poisoning and its involvement in thrombus formation and development of a pulmonary embolism (PE). CASE PRESENTATION: 62 year old female with history of COPD was brought to ED due to acute SOB and lethargy. Upon EMS arrival, CO level was 800. While in transport in EMS, the patient's CO-Hb level was 34 (trended to 11.4). The patient was found to have sp02 of 86% on room air (RA), and was placed on 10L nonrebreather mask. Patient was hemodynamically stable and afebrile. Labs revealed WBC 17.96, platelet 409k (clumped), troponin 0.08 ng/mL, LDH 405 units/L, and CRP 22.3 mg/L. Patient was deemed not a candidate for hyperbaric oxygen therapy. CT Head without contrast ruled out intracranial pathology and UA ruled out UTI. Chest X-ray revealed bilateral hazy opacities. CTPE revealed RUL/RML segmental and subsegmental PE as well as bilateral GGO reflecting interstitial edema in the setting of CO poisoning. Echo revealed EF of 65% with no wall motion abnormalities. COVID PCR test resulted negative making PE more likely as cause for SOB and patient was started on therapeutic Lovenox and empiric Azithromycin and Ceftriaxone. Within 24 hours, patient clinically improved and was discharged on Xarelto. DISCUSSION: PE in patients with CO poisoning should be suspected if the patient does not clinically improve with initial treatment. CO toxicity has been known to cause inflammatory and obstructive changes to arterioles and venules. Furthermore, it may induce vasospasms and increase platelet aggregation, leading to venous thrombus formation. CO poisoning may also increase oxidative stress with nitric oxide and oxygen free radicals causing further damage to endothelial lining1 and leading to further platelet dysfunction. 2 This combination of vessel wall injury and stasis in blood flow are important for development of thrombus. Treatment of given thrombus will lead to moderate resolution of symptoms. CONCLUSIONS: Treatment may be delayed in patients with coexisting PE and CO poisoning as it may be misdiagnosed. It is especially difficult to identify PE in patients with stable O2 saturation. However, the combination of endothelial damage and eventual increased platelet aggregation plays a critical role in thrombus formation in patients with CO toxicity. As a result, it is an important differential for patients with CO poisoning especially when symptoms do not respond to initial treatment. REFERENCE #1: Ruth-Sahd LA, Zulkosky K, Fetter ME. Carbon monoxide poisoning: case studies and review. Dimens Crit Care Nurs. 2011 Nov-Dec;30(6):303-14. doi: 10.1097/DCC.0b013e31822fb017. PMID: 21983502. REFERENCE #2: Ikeda H, Koga Y, Oda T, Kuwano K, Nakayama H, Ueno T, Toshima H, Michael LH, Entman ML. Free oxygen radicals contribute to platelet aggregation and cyclic flow variations in stenosed and endothelium-injured canine coronary arteries. J Am Coll Cardiol. 1994 Dec;24(7):1749-56. doi: 10.1016/0735-1097(94)90183-x. PMID: 7963124. REFERENCE #3: Sevinc A, Savli H, Atmaca H. An interesting cause of pulmonary emboli: acute carbon monoxide poisoning. Clin Appl Thromb Hemost. 2005 Jul;11(3):353-7. doi: 10.1177/107602960501100317. PMID: 16015424. DISCLOSURES: no disclosure on file for Jagadish Akella; No relevant relationships by Javed Iqbal, source=Web Response No relevant relationships by Vaishali Mehta, source=Web Response No relevant relationships by Najia Sayedy, source=Web Response