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After a massive transfusion and trauma, the clotting cascade is altered both intrinsically and extrinsically by alterations of thrombomodulin-protein C which increases coagulation activation and impairment, and increased fibrinolysis (Vernon, Morgan & Morrison, 2019). The alterations in pathways from massive transfusion is due to dilution and thrombocytopenia from the blood products and their preservatives themselves (Vernon, Morgan & Morrison, 2019). This process is jump-started due to the massively increased fibrinolysis from plasminogen binding to fibrin, then tPA activates and turns plasminogen into plasmin, as a systemic result of dilution and thrombocytopenia after blood product administration (Vernon, Morgan & Morrison, 2019).

Some specific assessment findings on a patient would be blood oozing or hemorrhage from any insertion site that was previously performed, which indicates that there is fibrinolysis occurring (Latif et al., 2016). This would prompt an emergent lab work for a PT and PTT as well as fibrinogen levels, fibrinogen degradation products, platelet count, hemoglobin and hematocrit, and peripheral smear looking for schistocytes or fragmented erythrocytes (Latif et al., 2016). In DIC, a Pt and PTT would be increased, fibrinogen decreased, thrombocytopenia and low hematocrit, and presence of schistocytes or fragmented erythrocytes indicating mechanical shearing from a possible clot (Latif et al., 2016). These positive findings would indicate a higher ISTH score which is indicative of DIC (Hayakawa, 2020).

In this scenario, it is most likely that the patient is in the Bleeding Phase of DIC and has essentially skipped the clotting phase of DIC (Hayakawa, 2020). There is a two-part process in the management of this scenario, first how much is the patient bleeding or oozing from the site, second what are the lab values of platelets in conjunction with the bleeding or not bleeding values (Hayakawa, 2020). For example, If the patient is actively bleeding then a transfusion of platelets would be indicated when the platelets drop below 50, and if they are not bleeding then when the platelets drop below 20 (Hayakawa, 2020). There is the option to use cryoprecipitate but it is reserved for those who are bleeding (Hayakawa, 2020).

For this patient in particular, since DIC is a dynamic disease of massive coagulation and fibrinolysis, we have to be aware of the patient’s ability to clot pre and post-transfusion (Hayakawa, 2020). It is possible to send the patient into a hypercoagulable state with too much administration of clotting factors (Hayakawa, 2020). It is important to go “low and slow” as in ordering one unit of replacement at a time of FFP or Platelets and rechecking the labs post-transfusion, reassessing, then deciding if another dose is required (Hayakawa, 2020).


Hayakawa, M. (2020). Management of disseminated intravascular coagulation: current insights on antithrombin and thrombomodulin treatments. Open Access Emergency Medicine, 1, 25. https://doi-org.lopes.idm.oclc.org/10.2147/OAEM.S135909

Latif, E., Adam, S., Rungruang, B., Al-Hendy, A., Diamond, M. P., Rotem, E., Cannell, J., & Browne, P. C. (2016). Use of uterine artery embolization to prevent peripartum hemorrhage of placental abruption with fetal demise & severe DIC. Journal of Neonatal-Perinatal Medicine, 9(3), 325–331. https://doi-org.lopes.idm.oclc.org/10.3233/NPM-16915108

Vernon, T., Morgan, M., & Morrison, C. (2019). Bad blood: A coagulopathy associated with trauma and massive transfusion review. Acute medicine & surgery, 6(3), 215–222. https://doi.org/10.1002/ams2.402


Disseminated Intravascular- Coagulability is defined as a widespread of intravascular fibrin formation in response to an excess blood protease activity that overcomes the natural anticoagulant mechanisms (Arruda & High, 2018, p. 834). Patients with DIC will show signs and symptoms of bleeding from the venipuncture sites, petechiae, ecchymoses, to severe hemorrhage from the gastrointestinal tract, lung and into the CNS. A prolonged prothrombin time, aPTT, platelets of 100,000 /uL or a rapid decline in platelet numbers in the presence of schistocytes in the blood smear and an elevated levels of fibrin degradation product are some of the most common laboratory findings in patient with DIC (Arruda & High, 2018, p. 835).

Patients who are actively bleeding or those who at high- risk of bleeding or those who have a platelet count of less than 10000 to 20000/uL should receive fresh frozen plasma or platelet concentrates (p. 836). According to the prothrombin time of more than 1.5 times the normal is a good indicator of the severity of clotting factor consumption this patient may need a replacement of fresh frozen plasma. Patients who have a low fibrinogen or a brisk hyperfibrinolysis may need a cryoprecipitate. Some of the risk factors that providers need to consider when treating patients with DIC is to whether give an anticoagulation such as heparin, antithrombin III concentrates or anti-fibrinolytic drugs. Providers need to avoid giving antifibrinolytic agents such as tranexamic acid (TXA), epsilon-aminocaproic acid (EACA) or aprotini and prothrombin complex concentrates (PCC) in patients with DIC due to a blockage of the fibrinolytic system that can increase the risk of thrombotic complications (Leung, 2021).


Arruda, V.R. & High, K.A. (2018). Coagulation Disorders. J.L. Jameson, D.K. Kasper, D.L., Longo, A.S.Fauci, S.L. Hauser & J.Loscalzo (Eds). Harrison’s Principles of Internal Medicine (20th ed, Vol. 1, pp. 830-838). Library of Congress Catagaloging- in publication data.

Leung, L.L.K. (2021). Disseminated intravascular coagulation (DIC) in adults: Evaluation and management. Retrieved from https://www.uptodate.com/contents/disseminated-intravascular-coagulation-dic-in-adults-evaluation-and-management?search=dic&sectionRank=2&usage_type=default&anchor=H4101269295&source=machineLearning&selectedTitle=1~150&display_rank=1#H1274217204


CC: Shortness of breath with chest pain.

HPI: – A 28-year Darrin, a white male patient came to ED c/o SOB for the last 2 hours and was admitted to the hospital. Started off with Cough and SOB on walking. Started Rt. Sided chest pain worsens with cough and deep breath. No relieving factors. Denies any fever, chills, malaise, and general weakness.

PMH: -R. flank pain with kidney stone 2 years ago Hernia repair at age of 6, nosebleed as a child and knee trauma. Mom diet at 50 with unknown cause, Dad is 58 with ischemic heart disease and CAD with CABG 2 yrs. ago, sister had multiple spontaneous abortions, positive family history of maternal grandfather died at 65 age following Abdominal surgery, nose bleeds and recurrent thrombophlebitis, chest pain, PE and was on coumadin.

Physical exam: – VS- HR-120, BP-120/80, TEMP-98.6, RR-30 shallow, Rhythm-regular, HT-7’3’’. Weight-150 lbs. Chest: Dullness to percussion at posterior right lung base and resonant to percussion otherwise.

Diagnostic tests to be ordered.

My differential diagnosis will be.

1. Pulmonary embolism.

2. pneumothorax.

3. Pneumonia. 

1. CBC was within normal limits: To evaluate any infectious inflammatory cause which is evidenced by leukocytosis and presence of anemia or any platelet disorders. Leukocytosis is present in this patient can be of pneumonia, atelectasis, lung cancer, pulmonary tuberculosis. Sickle cell anemia may present with chest pain most prevalent in middle eastern and African descent populations. Since it is absent these conditions may be ruled out with other tests. In the later stage of pulmonary embolus, the patient may show up with leukocytosis.

2. ABG: pH-7.49, PO2-60, pCO2-32, O2 sat 75%, Bicarbonate-25 nmol/L on RA. And on O2 100% pH-7.45, pO2-80, pCO2-35, O2 sat-85%, Bicarb-24 mEq/L. The patient has hypoxia and respiratory alkalosis, on room air and 100% Oxygen his hypoxia is corrected, and pH and back to normal. In PE because the part of the lung was affected with embolism, with possible lung infarction and that part of the lungs is not participating with air exchange make the patient, tachyonic, hypoxia leading to respiratory alkalosis. Respiratory worsening and relevant increase of D-dimer may enhance clinical suspect. 

1. Chest X-ray; Negative for infiltrates or other acute abnormalities. 

1. CT chest: Significance noted involving right lower lobe: Which is not confirmatory for the cause but can be suggestive of pulmonary embolus when you clinically correlate with patients’ symptoms and dullness in the right lung. According to Faggiano et al (2020), thrombosis of segmental/subsegmental arteries within lung infiltrates was occasionally seen on CT 

1. CT Chest spiral with PE protocol: There are intra-arterial filling defects in multiple vessels and segmental peripheral areas of consolidation (Lung infarcts) involving the right lower lobe. There are very confirmatory findings of right lower lobe filling defect in the intra-arterial in multiple vessels and area of consolidation in the diagnosis of pulmonary embolism in the right lower lobe. 

1. D-dimer: 850 ng/ml. Patients with pulmonary embolism usually have elevated D-dimer above 250ng/ml. This high level places the patient at high risk for any thromboembolic condition such as DVT and PE., stroke, or MI. This patient may have a clot in his lungs affecting his right lower lobe and probable infarction. A normal D-dimer level allows the safe exclusion of PE in outpatients with a low or intermediate clinical probability of PE (Bompard al, 2020) 

1. Covid-19: SARS COV: Which was not available. 

1. EKG Sinus tachycardia with occasional atrial premature contractions: This can be a finding in pulmonary embolus which causes stress to the heart causing tachycardia and atrial premature contractions. Right ventricular strain shows with sinus tachycardia and atrial arrhythmias is a common finding in PE (Thomson, Kourounis, Trenear, Messow, Hrobar, Mackay, & Isles, 2019). 

1. TEE (Transesophageal echocardiogram): Patients’ findings were normal position, size, and movement of the heart muscle, valves, and heart chambers. According to Bikdeli et al (2018), early TEE is commonly performed for acute PE, the right heart enlargement, right ventricular hypokinesis, and right heart thrombi are predictive of worse outcomes.

The primary diagnosis after diagnostic study is right lower lobe pulmonary embolism.


Bikdeli, B., Lobo, J. L., Jiménez, D., Green, P., Fernández‐Capitán, C., Bura‐Riviere, A., … & Quintavalla, R. (2018). Early use of echocardiography in patients with acute pulmonary embolism: Findings from the RIETE registry. Journal of the American Heart Association, 7(17), e009042. Retrieved from https://www.ahajournals.org/doi/full/10.1161/JAHA.118.009042

Faggiano, P., Bonelli, A., Paris, S., Milesi, G., Bisegna, S., Bernardi, N., … & Maroldi, R. (2020). Acute pulmonary embolism in COVID-19 disease: Preliminary report on seven patients. International journal of cardiology, 313, 129-131. Retrieved from https://www.sciencedirect.com/science/article/abs/pii/S016752732031901X

Bompard, F., Monnier, H., Saab, I., Tordjman, M., Abdoul, H., Fournier, L., … & Revel, M. P. (2020). Pulmonary embolism in patients with COVID-19 pneumonia. European Respiratory Journal, 56(1). Retrieved from https://erj.ersjournals.com/content/56/1/2001365.short

Thomson, D., Kourounis, G., Trenear, R., Messow, C. M., Hrobar, P., Mackay, A., & Isles, C. (2019). ECG in suspected pulmonary embolism. Postgraduate medical journal, 95(1119), 12-17. Retrieved from https://pmj.bmj.com/content/95/1119/12.abstract

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