UDK  616.24-005.6/.7:616-006.6-056.24                 

ISSN 2466-2992 (Online) (2019) br.1-2, p. 34-39

COBISS.SR-ID 46872585

PULMONARY THROMBOEMBOLISM AND CANCER - CASE REPORT

Milan Đorđević

Emergency Medical Service Jagodina

Summary:

INTRODUCTION: Pulmonary thromboembolism (PTE) is the third most prevalent disease in the cardiovascular system.

OBJECTIVE: To present an atypical scenario where malignancy manifested as PTE.

MATERIAL AND METHODS: Paper written using a descriptive method using the medical history of the Clinic for Pulmonary Diseases of the Clinical Center Niš.

CASE REPORT: 56 year old patient with pain, swelling and redness of the right eye treated for 4 weeks without significant improvement. Due to shortness of breath and cough, he was treated for pneumonia. He did an ultrasound of the heart and abdomen, CT of the chest and MR of the abdomen. Subsequently referred to a pulmonologist. Status: dyspnoic, SatO2 86%, RF 20 / min, exophthalmos of both eyeballs present. Pulmo: Auscultatory easily attenuated respiratory noise. Extremities: very pronounced varicosities with palpable hardened veins, sometimes with nodules. Laboratory on admitting LDH 1157; GGT 800,5; CRP 148; D-dimer> 5200. MSCT of the pulmonary arteries: bilateral PTE. Endocranial MSCT: Tumor alteration of the right orbit with involvement of the outer wall of the orbit and optic nerve with meta changes in the liver and lungs.

DISCUSSION: The link between cancer and hypercoagulability is known so that an unexplained case of PTE should raise the suspicion of tumor presence. The search for cancer after an episode of PTE should be limited to medical history, physical examination, laboratory and chest X-ray. Due to inadequate observation, bilateral massive PTE developed in the patient from the moment of onset of symptoms to diagnosis.

CONCLUSION: The development of PTE should be urgently treated while searching for other, unusual, causes or consequences that lead to PTE. Regardless of the obviousness of PTE and actual situation, malignancy ought to be on our mind as well.

Key words: Pulmonary thromboembolism, cancer, therapy, suspicion.

INTRODUCTION

Pulmonary thromboembolism (PTE) is the third most prevalent disease in the cardiovascular system, after acute myocardial infarction and cerebrovascular insult. [1] PTE and deep vein thrombosis (DVT) are thought to be two different clinical manifestations of the same disease, as evidenced by the fact that over 80% of patients with acute PTE also have DVT. [2] Major and minor risk factors for PTE have been revised and clearly defined in the contemporary literature. [3]

The most common symptoms of PTE are: dyspnea, chest pain, cough, syncope, hemoptysis; and in physical examination: tachypnea, tachycardia, signs of deep vein thrombosis, cyanosis and fever. The use of pulmonary artery scintigraphy and pulmonary artery angiography may be useful. PTE may occur without the first symptom and sign with a lethal outcome. Treatment of PTE includes hemodynamic and respiratory support followed by anticoagulant therapy, thrombolysis, embolectomies, surgical and percutaneous interventions, venous cava filters. Oxygen therapy is mandatory and helpful. In hemodynamically compromised patients, establishing flow through the occluded pulmonary arteries is of primary urgency. In less severe cases, treatment aims to prevent the progression of the thrombosis process and potential fatal recurrence. Based on clinical judgment, the presence or absence of a disorder of hemodynamics, patients are classified into high-risk patients with PTE and those who are not, which determines the further therapeutic procedure. [4]

OBJECTIVE

To present an atypical scenario where malignancy manifested as PTE.

MATERIJAL AND METHODS

Paper is written using a descriptive method using the medical history of the Clinic for Pulmonary Diseases of the Clinical Center Niš.

CASE REPORT

The 56-year-old patient states that the ailments began 3 months before admission, with pain, swelling and redness of the right eye. He was treated abroad for 4 weeks without significant improvement, without medical records. A few days later he complains of shortness of breath, a cough, which causes him to be treated for pneumonia. Then the patient underwent a diagnostic examination and performed heart ultrasound (dilated right heart cavity, SPDK-mean pressure in the right ventricle 87mmHg, LP-left atrial dilatation, hypokinesia of the inferior and posterior wall), abdomen ultrasound, chest CT and abdomen MRI (with spleen infarction and secondary deposits in the liver). With these analyzes and because of shortness of breath, feeling of pressure in the chest, coughing with difficulty expectoration, fatigue, loss of appetite, weight loss of 14kg for 3 months, he was admitted to pulmonology. From a personal history there was pneumonia at a young age and varicose veins. He has been a seasonal heating worker for 15 years, a longtime smoker.

Praesent status: On admission conscious, oriented, afebrile, effortless dyspnoea, cyanosis-free, cardiac compensated, normal color, difficult to move. TA 115 / 75mmHg, HR 89 / min, SatO2 86%, RF 20 / min. Head and neck: Exophthalmus present in both eyeballs, more conspicious right, right sclera with suffusion and visible capillaries and obvious lacrimation. Pulmo: Auscultatory easily attenuated respiratory murmur, basal left and lateral inspiratory crepitations. Cor: action rhythmic, tachycardic, tones clear, systolic murmur over precordium. Extremities: varicosities strongly emphasized with palpable hardened veins, sometimes with nodules up to a few cm, with trophically altered skin along the inside of the legs. Other findings normal.

Admission Laboratory: Le 12.2; Er 3.47; Hgb 103; Hct 31%; Tr 198; AST 85; ALT 88; LDH 1157; GGT 800,5; CRP 148; D-dimer> 5200; other parameters within the reference limits. Laboratory on release: Le 13.2; Er 3.55; Tr 104; AST 163; ALT 137; ALP 1070; LDH 1038; GGT 789; Alb 27; CRP 110; D-dimer 525; AFP (alpha

Figure 1

Figure 2

Figure 3

feto protein) 3.38; Blood gases: partial respiratory failure with pO2 51-56 mmHg.

Multi-slice CT of the pulmonary arteries: bilateral PTE with a few nodular changes. (Figures 1,2 and 3) Multi-slice CT of endocranium and orbits: Tumor alteration of the right orbit with involvement of the outer wall of the orbit and optic nerve, without spreading intrabulbar. In the right bulb, intrabulbar hyperdense content. Lacunar infarcts endocranially supratentorial.

The patient was presented to the Maxillofacial Consilium that indicated biopsy and histopathological verification of the retrobulbar tumor.

During hospitalization, the patient underwent a diagnostic procedure to determine the existence of a retrobulbar tumor with involvement of the outer wall of the right orbit and subsequent meta changes in the liver and lungs. He also developed paraneoplastic syndrome, which is manifested as bilateral massive PTE as well as spleen infarction and lacunar infarcts in the endocranium. It is a patient with an extended primary neoplastic process of the maxillofacial region and is further treated in the domain of oncologists and maxillofacial surgeons. As the lungs developed massive bilateral pulmonary thromboembolism with manifest partial respiratory failure, undergoing the patient to general endotracheal anesthesia and any invasive procedure was highly contraindicated.

DISCUSSION

Thromboembolism is a significant cause of intrahospital morbidity and mortality. The link between cancer and hypercoagulability has been known for over a century, so the unexplained case of PTE should raise the suspicion of tumor presence. [5]

Activation of the coagulation process in cancer has a multifactorial background. Tumors can express prothrombotic molecules. Some cancerous cells produce substances such as cysteine protease and / or serine that directly contribute to coagulation by activating factor X. It is also possible that the tumor produces a tissue physiological factor responsible for the activation of the extrinsic coagulation pathway. Tumor cells can also promote coagulation indirectly by secreting tumor necrosis factor and endothelial-like proteins and mononuclear cells, stimulating the secretion of prothrombotic molecules, which in turn may play a role in platelet activation. [6]

The incidence of PTE in patients with neoplasms is significantly increased on autopsy findings. In the literature, the most commonly associated cancers with PTE have been described as pancreatic, gastric, colon, and ovarian cancers. [5] The risk of developing venous thromboembolism in cancer patients is four times higher than in the general population. [7] Although the highest number of PTE episodes has been reported in patients with lung, colon and prostate cancers, the relatively high risk of PTE is in multiple myeloma, brain and pancreatic cancers. When it comes to metastases, the most associated cases of PTE are cancer of the stomach, bladder, kidney and lung. [8] About 10% of PTE patients will develop cancer within the next 5-10 years, with the highest number of cases within the first two years of being diagnosed with PTE. [9] Sorensen and coworkers suggest that cancer has a higher incidence of occurrence of idiopathic PTE compared to PTE that occurs postoperatively. [10] In a five-year study in Taiwan, the incidence of cancer after or at the same time as PTE was 47.37%, significantly higher than in previous reports. [11]

PTE is often accidentally detected in cancer patients during the staging and follow-up. [5,7,11,12] A prospective cohort study was conducted in a study published in July 2019 to analyze the rate of recurrent thromboembolism, major bleeding, and all-cause mortality in 695 patients with solid tumor or hematologic malignancy and incident PTE. The results showed that recurrence rates in cancer patients with incidental PTE were significant, despite anticoagulant therapy. [12]

Cancer screening in patients with PTE is without justification. Di Nisio et al suggested the most effective approach in such patients is to have an abdomen and pelvis CT in combination with mammography and sputum cytology. However, when such an approach was compared with the baseline clinical evaluation at the 5-year follow-up, no benefit was found. [13,14] Therefore, the search for cancer after an episode of PTE should be limited to medical history, physical examination, laboratory, and chest X-ray. [15]

Due to inadequate observation and a long period of time from the onset of the first symptoms until diagnosis, patient developed a bilateral massive PTE. In our case, it is particularly interesting that this is a tumor that could not be pathohistologically verified because invasive procedures and general anesthesia were contraindicated due to PTE. Since the retroorbitally biopsy of the tumor was impossible to do, it was thought to do a biopsy of meta changes in the liver,both delayed for the same reason.

CONCLUSION

The described case report showed how inadequate observation of the patient led to late diagnostics and forwarding to the appropriate specialists according to the indications. Bilateral massive PTE was a problem for further diagnostics and timely oncology therapy. Had the scenario been different, the development of paraneoplastic manifestations might not have occurred. It ought to be recognized that PTE is to be urgently treated while looking for other, unusual, causes or consequences that lead to PTE. PTE can be both a consequence and a cause of cancer so that regardless of the obviousness of PTE and the situation, we must think about malignancy as well.

REFERENCES

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