HTLH 2501 Case Study: IBD's Impact on Pulmonary Embolism Risk

This case study explores the relationship between Inflammatory Bowel Disease (IBD) and Pulmonary Embolism (PE), focusing on a 33-year-old male with a history of ulcerative colitis. The study investigates the question of how active IBD contributes to the development of PE. The hypothesis proposed is that prolonged IBD increases the risk of PE due to inflammation and disruption of the coagulation factors equilibrium. The discussion is supported by two peer-reviewed journal articles, examining the role of hypercoagulability, endothelial dysfunction, and the impact of steroid treatments on PE risk. The analysis highlights the increased risk of DVT and PE in IBD patients, the activation of the coagulation cascade, and the influence of pro-inflammatory cytokines. The study concludes that chronic IBD, especially when treated with steroids, significantly elevates the vulnerability to PE, emphasizing the importance of understanding the underlying mechanisms to improve patient outcomes.

Running head: CASE STUDY
CASE STUDY
Name of the Student
Name of University
Author’s note

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Introduction
Inflammatory bowel disease (IBD) is defined as a group of inflammatory situation of the
small intestine and the colon. The Crohn’s disease (CD) and ulcerative colitis (UC) are two
different types of idiopathic IBD that is presented with chronic progressive and relapsing
inflammation affecting the entire gastrointestinal tract and colonic mucosa respectively (Loddo
& Romano, 2015). Pulmonary embolism (PE) is a life threatening condition that involves
embolic and thrombotic occlusion of the pulmonary arterial system (Piazza, Hohlfelder &
Goldhaber, 2015). The case study of choice (case study 8) represents a 33-year old man with
previous history of IBD and at present suspected with PE. The following paper will help to
answer one question in relation to the pathophysiology highlighted in the selected case study.
The paper will initiate with the selected research question followed by the hypothesis and a
critical discussion of two peered reviewed journals in order to answer the question of choice.
Question
What is the role of active inflammatory bowel disease in the development of pulmonary
embolism?
Hypothesis
The presence of IBD for a prolong period of time increases the vulnerability of
developing pulmonary embolism. The IBD lead to inflammation, hampering the normal process
of secretion of cytokines and coagulation factor. Hamper in the equilibrium of the coagulation
factor leads to the development of pulmonary embolism.

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Discussion
In the case study the patient has a previous reported case of IBD. The clinical
presentation of IBD includes passage of pus or mucus, bloody diarrhoea and abdominal pain
(Loddo & Romano, 2015). In the case study, the 33-year old man was diagnosed with UC 4
years before and was present to the primary healthcare physicians with chronic diarrhoea,
extreme weight loss and anaemia arising from iron-deficiency. The thrombotic occlusion during
pulmonary embolism (PE) mainly occurs due to the development of deep vein thrombosis
(DVT). DVT is defined as the formation of blood clot in more than one deep vein. The
formations of progressive clots results in clot to break loose from the walls of the veins. The clot
then travels through the blood stream of the veins and lodge in the lungs resulting in the
development of PE. This is the reason why PE is popularly known as pulmonary
thromboembolism (Piazza, Hohlfelder & Goldhaber, 2015). The clotting in the lungs might be
responsible for symptoms displayed by the 33-year old man in the case study like pain in right
chest, increase in pain during inspiration while lying down.
Chung Lin, Hsu and Kao (2015) reported that IBD related with the chronic inflammation
might increase the vulnerability of developing PE and DVT however, there are poor
epidemiological evidences suggesting their relationships. Thus in order to address this concern,
Chung Lin, Hsu and Kao (2015) conducted a longitudinal nationwide cohort study in the Taiwan
healthcare field. The analysis of the results showed that the risk of DVT and PE are significantly
higher in the population that is suffering from IBD for a prolong period of time in comparison to
the general population. The underlying pathophysiology for this is highlighted as follows. Chung
Lin, Hsu and Kao (2015) are of the opinion that basic mechanism of thromboembolism includes
formation of hypercoagulability along with generation of endothelial dysfunction as represented

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by the Virchow’s triad. Both in the case of UC and CD, there is a localised manifestation of the
formation of systemic inflammation. This systemic inflammation activates the coagulation
cascade like thrombin-antithrombin complexes, D-dimers and prothrombin fragments. Wu
(2015) reported high levels of coagulation factor in the blood of the patients who are suffering
from IBD for a prolong period of time. Inflammation formed as a result of the IBD disease
activates for the pro-inflammatory cytokines. The increase in the secretion of the pro-
inflammatory cytokines stimulation to secretion of the coagulation cascade while decreasing the
overall execution of the fibrolysis. Chung Lin, Hsu and Kao (2015) stated that increase in the
coagulation cascade leads to the generation of the blood clots resulting in the formation of the PE
resulting in chest pain. In relation to the DVT and IBD it can be said that the patient in the case
study was experiencing swelling in the lower parts of the leg due to the manifestation of DVT.
Min et al. (2016) stated that the manifestation of DVT first occurs in the lower extremities of the
body and the clot first appears to occur in the deep veins of the lower parts of the leg. This is the
reason why the patients in the case study was suffering from pain in the lower parts of the leg
(for the past several weeks) much before he encountered pain in chest (last 5 days for
admission). Chung Lin, Hsu and Kao (2015) also concluded at the end that probability of
developing DVT or PE in case of IBD increases with age and the tenure for which a person is
suffering from the disease. In relation to the case study, it can be said that age is not the major
concern for the patients as he is only 33 years old. The main concern here included his long
exposure to the IBD. Chung Lin, Hsu and Kao (2015) highlighted in the pathology discussion
that the IBD for a prolong period of time leads to the generation of endothelial dysfunction and
frailty. Endothelial dysfunction means a condition in which the endothelial layer of the small
arteries that is the inner lining of the arteries fails to function normally leading to improper flow

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of the blood through the arteries. Gaps in the flow of the blood through the arteries lead to the
generation of the blood clot and thus leading to the formation of PE.
Bollen et al. (2016) conducted a study in order to evaluate the risk of patients of IBD in
developing thromboembolic events like PE in comparison to the healthy population. A
retrospective study was conducted with 84 IBD patients with thrombo-embolic events (TE). The
analysis of the results showed that there is a significant association with the disease activity of
IBD and the co-occurrence of TE. In the discussion, Bollen et al. (2016) reported that both the
venous and the arterial sites can be affected in the IBD. However, venous events occur more
often in comparison to the arterial events in patients with IBD. In spite of siting endothelial
dysfunction directly like Chung Lin, Hsu and Kao (2015), Bollen et al. (2016) stated that there
occurs changes in the components of the blood corpuscles in the endothelial vessels of the
patients with IBD leading to formation of clot. In accordance with the justification given by
Chung Lin, Hsu and Kao (2015), Bollen et al. (2016) stated that active or chronic IBD leads to
the formation of severe inflammation leading to the up-regulation of the coagulation factors like
Factor V, VIII and XI along with prothrombin fragment F1 +2 and fibrinogen. This up-
regulation of the coagulation factor shifts the endothelial surface towards more pro-coagulant
state and facilitating the development of PE. Furthermore, inflammatory cytokines cytokines and
cells are important parts of the atherosclerotic plaque leading to the generation of arterial events
and development of PE and subsequent pain in chest. Bollen et al. (2016) also reported in their
retrospective study that patients who have active IBD are more vulnerable in developing PE. In
the concerned case study, the 33-year old main was suffering from active IBD it is evident from
the fact that he has a history of ulcerative colitis for the past 4 years. During the time of the
disease identification (4 years ago), he was reported with chronic diarrhea. The specimen of

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biopsy of the colon showed that he is having chronic yet active from of colitis. He was treated
with mesalamine for combating the symptoms associated with IBD. However, he has stopped
taking medication for several months. The study conducted by the Majewski and Piotrowski
(2015) highlighted that 5-aminosalicylate agents (5-ASA), mesalazine (5-aminosalicylic acid),
sulfasalazine, that are used for the treatment of IBC results in the development of the pulmonary
lesions. The prolong use of these medications result in the change in the underlying clinical
pathology. The frequently reported change in the clinical pathology includes eosinophilic
exudative pleuritis and interstitial pneumonitis along with the high predominance of lymphocytes
or eosinophils. In some cases poorly formed non-necrotizing granulomas are also detected in the
biopsy of the lungs obtained from the patients with IBC complaining of chest pain. This
infiltration of eosinophil results in the development of the non-productive cough, followed by
shortness of breath and fever. This is in accordance with the findings of Bollen et al. (2016) that
showed that the IBD patients who have been treatment for 5-aminosalicylic acids are 36% more
likely to develop pulmonary embolism or other pulmonary complications. However, the
symptoms highlighted by Majewski and Piotrowski (2015) does not directly co-elated with the
symptoms of the patients represented in the case study. The symptoms of the patients represented
in the case study reported no visible representation of cough, shortness of breath, fever, chills or
hemoptysis. Thus it in relation to the research findings highlighted by Bollen et al. (2016) it can
be said that the patients’ who are treated with 5-aminosalicylic acid ( a form of steroids) is
associated with increases risk of the cardiovascular disease as prolong use of the medication
hampers the arterial and venous network. The treatment of IBD with the help of steroids induces
a hypercoaguable state thus inflicting an increase in the secretion of the coagulation factors
(FVII, VIII and XI). The increase in the coagulation factor is associated with decrease in the

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anticoagulant mechanism leading the synthesis of fibrinolysis inhibitor plasminogen activator
inhibitor-1 and ultimately development of blood clot. Bollen et al. (2016) also stated that the
treatment done with steroid increases the risks of PE by five fold in comparison to the treatment
done with any other biological factors. Thus in case of the patient the treatment of steroids in the
form of 5-aminosalicylic acid made him more vulnerable to PE.
that steroid treatment is independently, corrected for disease activity, associated with an
almost five-fold increase in risk for venous TE compared with treatment with only a biological
agent. In this study, only 33% of the IBD patients developed an unprovoked TE when they were
treated successfully with biological treatment versus 67% when treated with CS therapy.
Conclusion
Thus from the above discussion, it can be stated that people who are suffering from the
IBD for a prolong period of time are susceptible towards the development of PE. This is because,
IBD causes inflammation. The inflammation within the body increases the secretion of pro-
inflammatory cytokines. The pro-inflammatory cytokines hampers the equilibrium of the
secretion of the coagulation factor. This results in the generation of the blood clots in the
pulmonary arteries. The prolong clots in arteries, hampers the blood flow, leading to the
development of pain and ultimate development of PE. The patients who are on steroids for
treating IBD are more vulnerable in developing PE in comparison to the general population. This
is because steroids hampers the secretion of the coagulation factor and thus disrupts the normal
process of blood clotting. The PE in some cases manifests as DVT like clot in the lower portion
of the limbs and if this is left untreated, the chances of developing PE accelerates. The
hypothesis framed is correct that IBD increases the risk of developing PE.

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References
Bollen, L., Casteele, N. V., Ballet, V., Van Assche, G., Ferrante, M., Vermeire, S., & Gils, A.
(2016). Thromboembolism as an important complication of inflammatory bowel
disease. European journal of gastroenterology & hepatology, 28(1), 1-7. doi:
10.1097/MEG.0000000000000495
Chung, W. S., Lin, C. L., Hsu, W. H., & Kao, C. H. (2015). Inflammatory bowel disease
increases the risks of deep vein thrombosis and pulmonary embolism in the hospitalized
patients: a nationwide cohort study. Thrombosis research, 135(3), 492-496.
https://doi.org/10.1016/j.thromres.2014.12.025
Loddo, I., & Romano, C. (2015). Inflammatory bowel disease: genetics, epigenetics, and
pathogenesis. Frontiers in immunology, 6, 551.
https://doi.org/10.3389/fimmu.2015.00551
Majewski, S., & Piotrowski, W. (2015). Pulmonary manifestations of inflammatory bowel
disease. Archives of medical science: AMS, 11(6), 1179. doi: 10.5114/aoms.2015.56343
Min, S. K., Kim, Y. H., Joh, J. H., Kang, J. M., Park, U. J., Kim, H. K., ... & Choi, S. Y. (2016).
Diagnosis and treatment of lower extremity deep vein thrombosis: Korean practice
guidelines. Vascular specialist international, 32(3), 77. doi: 10.5758/vsi.2016.32.3.77
Piazza, G., Hohlfelder, B., & Goldhaber, S. Z. (2015). Pathophysiology of Deep Vein
Thrombosis and Pulmonary Embolism: Beyond Virchow’s Triad. In Handbook for
Venous Thromboembolism (pp. 15-20). Springer, Cham. https://doi.org/10.1007/978-3-
319-20843-5_3

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Wu, Y. (2015). Contact pathway of coagulation and inflammation. Thrombosis journal, 13(1),
17. https://doi.org/10.1186/s12959-015-0048-y