key: cord-0693011-hrd65s1w authors: Siddiqui, Saquib Navid; Jayasekhar, Roland; Tshering, Sonam; Jugjali, Ranjana; Shanmugavadivel, Devipangaj; Jawed, Asheer; Rahman, Mohammed Mostafizur title: A Unique Tale of COVID-19 Induced Concomitant Overt DIC and Acute Bi-lateral Pulmonary Embolism date: 2021-01-21 journal: Int J Infect Dis DOI: 10.1016/j.ijid.2021.01.040 sha: c4404b7c0d27dacd9ea166431315491ebae33b1d doc_id: 693011 cord_uid: hrd65s1w Severe Acute Respiratory Syndrome - CoronaVirus - 2 (SARS-COV-2), a novel coronavirus resulted in the beginning of a new chapter in human history. Initially originating as an epidemic respiratory illness in Wuhan, China, COVID-19 eventually spread to almost all countries of the world and has now been declared as a global pandemic disease by the WHO. With each passing day, our understanding of the patho-physiology of COVID-19 continues to evolve. A plethora of research has been conducted to explore the dynamics of various different clinical entities related to SARS COV-2 and in particular, COVID-19 associated coagulopathy. A large scale of patients have been reported to have developed pulmonary embolism without any other standard triggers or risk factors. This has led to widespread speculation that the COVID-19 virus by itself is an independent risk factor for VTE. In addition to the development of thromboembolic complications like pulmonary embolism, COVID-19 has also been reported to have triggered disseminated intravascular coagulation (DIC). At this instance, it is unclear to state if pulmonary embolism was induced by COVID-19 induced thrombosis or if it was precipitated as a result of coagulopathy secondary to DIC. In this case report, we describe a unique case of a COVID associated coagulopathy in a patient with confirmed pulmonary embolism along with an overt DIC. Following the diagnosis, the challenge faced by us was the appropriate treatment modality with regard to this unique situation. The patient was then treated with anticoagulants and steroids along with blood products. The patient markedly improved and was clinically stable on discharge. Dr. Saquib Navid Siddiqui 1 , Dr. Roland Jayasekhar 2, Dr. Sonam Tshering 3 , Dr. Ranjana Jugjali 4 , Dr. Devipangaj Shanmugavadivel 5 , Dr. Asheer Jawed 6 , Dr. Mohammed Mostafizur Rahman 1) Specialist Registrar, William Harvey Hospital, UK 2) SHO, William Harvey Hospital, UK 3) IMT Trainee, Southend Hospital, UK 4) SHO, William Harvey Hospital, UK. 5) Pathologist, Gunam Multispeciality Hospital, Tamilnadu, India 6) Specialist Registrar, William Harvey Hospital, UK 7) SHO, William Harvey Hospital, UK Corresponding author: Dr. Saquib Navid Siddiqui, specialist registrar, respiratory medicine, William Harvey Hospital. Email id: sns.saquib@gmail.com Informed Consent: Written informed consent for the paper to be published (including case history, image) was obtained from the patient for publication of this paper.  Full therapeutic LMWH should be considered if the platelet count above 50,000  Patients with active bleeding with overt DIC should receive blood products  Anti-coagulation dose should be half of the therapeutic dose if platelets are <50,000  Only prophylactic dose if the platelet count is below 30,000.  Platelet transfusion and an IVC filter to consider if platelet count below 30,000. In this case report, we describe a unique case of a COVID associated coagulopathy in a patient with confirmed pulmonary embolism along with an overt DIC. Following the diagnosis, the challenge faced by us was the appropriate treatment modality with regard to this unique situation. The patient was then treated with anticoagulants and steroids along with blood products. The patient markedly improved and was clinically stable on discharge. Keywords: thromboembolism, disseminated intravascular coagulation, sars-cov-2, covid-19 J o u r n a l P r e -p r o o f A priority call was initiated in the emergency triaging area when the paramedics brought in a 65-years-old lady who was saturating at 65% on room air. She was then initiated on full flow oxygen at 15 litres non breathing mask, which then elevated her saturations to about 92-95%. Upon stabilizing the patient, history revealed that for the past 7 days, the patient has been experiencing viral prodrome. Her symptoms were primarily fever, chest pain, cough with clear expectoration, and intermittent shortness of breath on exertion. She had been diligently monitoring her oxygen saturations at home and noted them to be hovering around 60-65% on room air. On further exploration, it was noted that she neither had gastro-intestinal symptoms nor smell/ taste alterations that were common with SARS-COV2. Also, her past medical history included Type II Diabetes Mellitus and is on oral hypoglycemics. She added that she is otherwise fit and well and is a non-smoker and is independent. During general examination, she was noted to have pleuritic sounding chest pain and was also markedly dyspnoeic, tachycardic, tachypnoeic, and was constantly saturating around 92-95% on 15 litres non rebreathing mask. She was unable to speak in full sentences due to breathlessness. Auscultation during chest examination revealed pleural rub along with bi-basal crackles without any wheeze. Other systemic examinations were normal. A 12 lead ECG showed a right bundle branch block (RBBB) with sinus tachycardia (Figure 01) . A bedside echocardiogram ruled out RV strain. Arterial blood gas showed hypoxic respiratory failure. The working diagnosis for this patient was now two-fold, i.e. she had bi-lateral pulmonary embolism and an overt disseminated intravascular coagulation, which essentially made the decision of treatment a tricky one. It is interesting to note that the patient has no previous history or other risk factors for thromboembolic disorders other than COVID-19 and has no family history of similar ailments. She was treated with therapeutic Low Molecular Weight Heparin (LMWH) at a 50% dose reduction after discussion with haematology. Initially, no blood products were transfused as she was clinically monitored continuously and was found to have no signs of any active bleeding. However, further blood tests revealed that her platelet count had a progressive decline from 32×10^9/l to 18×10^9/l (repeated 6 hours post initial baseline platelet count), which then subsequently dropped to 8×10^9/l (repeated 3hours after the second blood sample was taken to follow up platelet count), still without any bleeding manifestations. Though she was clinically not bleeding, as protocol dictated, she was then transfused with 1 unit of single donor platelet as clinically mandated. This eventually elevated the platelet count to 52×10^9/l, which relatively remained stable during the remainder of her stay in the hospital which was eventually 212×10^9/l during the day of her discharge with normalization of the clotting screen. Her anti-coagulation dose was increased to full therapeutic dose (1.5mg/kg body weight) on the third day of treatment as her platelet count remained above 50,10^9/l after 1unit platelet apharesis. D-dimer came down to 0.35mg/L on the day of discharge (after 9 days of treatment in the hospital). Regular monitoring of her blood levels was done to ensure that no untoward clinical events be manifested. Other supportive measures that were given to the patient along with the aforementioned treatment modalities were that supplementary oxygen was provided as needed, which was titrated according to her oxygen needs, antibiotics were administered as her infective markers were elevated and also to cover for any secondary bacterial infections. Oral dexamethasone 6 mg was prescribed once a day during the entire stay in the hospital. Non-Invasive Ventilation requirements J o u r n a l P r e -p r o o f were negligible as she improved clinically. She was given chest physiotherapy and received regular input from the nutritionist to keep her nutritional status optimal. After a 9-day ordeal, she was discharged following her improved clinical condition with improved breathing and blood parameters. Although her case was unique, the patient had declined to participate in any of the ongoing national recovery trials. We will discuss the factors that led to the development of Disseminated Prevalence of venous thromboembolism in patients with severe novel coronavirus pneumonia Systemic endothelial dysfunction: a common pathway for COVID-19, cardiovascular and metabolic diseases Acute pulmonary embolism and COVID-19 pneumonia: a random association? 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