Introduction: Genetic risk factors that increase venous thromboembolism risk are disorders in the synthesis or activity of coagulation factors. Factor V Leiden, prothrombin (20210-A), antithrombin deficiency, protein C and protein S deficiency, and hyperhomocysteinemia are the most common venous thromboembolism-related gene mutations. When genetic factors are combined with non-provoking risk factors (obesity, psoriasis, smoking and previous venous thromboembolism) the result is increased venous thromboembolism risk for each factor individually. Previous venous thromboembolism is one of the strongest risk factors, even in patients actively treated with anticoagulants. Patients are more likely to have recurrent venous thromboembolism with longer duration. Psoriasis is a complex immune-mediated disease, associated with cardiovascular risk, hypercoagulability markers and elevated homocysteine. Lots of observational reports suggest increased incidence of venous thromboembolic events in patient with psoriasis. Case presentation: We present patient with inherited thrombophilia and chronic diffuse plaque psoriasis complicated with deep venous thrombosis and pulmonary embolism. DNA analysis indicates the presence of homozygosis for Factor V Leiden mutation as well as heterozygosis for Factor XIII V34L, PAI-1 5G/4G and MTHFR A1298C polymorphism. Dermatological anamnesis is positive for plaque psoriasis since 12 years ago. Conclusion: The presentation of this case indicates an association between venous thromboembolism and chronic psoriasis. All patients with recurrent thromboembolism, hereditary thrombophilia, and moderate to severe psoriasis should be considered to be at higher risk for venous thromboembolism and appropriately treated.
Post-pneumonectomy syndrome is a rare, late complication of pneumonectomy, caused by a mediastinal shift, rotation and deviation of the remaining lung into the contralateral hemithorax, most commonly resulting in symptomatic central airway compression. Case reportRecurrent syncope following a left pneumonectomy was described in a 63 year-old man, forty years after the initial treatment. Four years physician visit including the family doctor, a neurologist, neurosurgeon, physiatrist, radiologist, psychiatrist and finally a cardiologist made the diagnosis hard to establish and the treatment delayed.The post-pneumonectomy syndrome is a complex constellation of symptoms, following previous lung pneumonectomy, with various presentations mimicking different pathologies.Its diagnosis is often misleading, making the treatment and prognosis hard to predict.
With no ideal specific therapy confirmed by the science community, and many low income countries barely being able to obtain a sufficient number of vaccines, as well as the long-term mental health impact, the COVID-19 infection makes for a worldwide health and global problem.Case report A COVID-19 positive patient was admitted due to poor condition, malaise and bilateral interstitial pneumonia with borderline oxygen saturation of 94%, hypoxemia with pO2 of 64mmHg, and elevated C reactive protein (CRP) of 70. The patient was put on oxygen support of 3l/min, and started parenteral antibiotic and LMWH in prophylactic doses -a combination that primarily improved the patient's condition. Three days after hospitalization marked shortness of breath with a drop in oxygen saturation of 62% referred. With further increasing of the oxygen flow, and a transfer to ICU, gas pressures showed significant worsening and the patient was put on mechanical support with a CPAP mask.Despite adding pulsed doses of potent corticosteroid, rapid acting insulin for blood glucose control, and administerring convalescent plasma and parenteral nutrition, the CRP levels were increasing and oxygen was decreasing. Hypotensive, tachycardic and with reduced urine output, the patient was intubated and set up on IPPV mechanical support. Vasopressor stimulation didn't improve the diuresis and elevation of degradation products followed, as well as elevation of the troponin and cardiospecific enzymes -non of which was caused by sepsis.Eight days after admission, the left arm presented as pale, cool and cyanotic. Fully deteriorated laboratory findings of multiple organ system failures (MOFS) were undoubtable; with the oxygen levels incompatible of life, and a CT scan with ARDS presentation, a continuous heparin infusion was the only solution. At the beginning, nothing indicated the deleterious outcome; however, with a highly unusual presentation of arterial thrombosis, the upper limb gangrene became too much and the patient died.COVID-19 is primary a respiratory infection, but the virus can affect other organs and systems, with some very rare presentations and deleterious outcomes.
Case report of a 33-year-old male SARS-CoV-2 positive patient admitted to hospital because of hemoptysis, dyspnea, fever, oxygen saturation of 60%, hypoxemia, elevated C-reactive protein (CRP). The patient was not vaccinated and it was his first infection with the virus. The symptoms started 10 days before with headache, fever, and cough. Chest radiography on hospital admission detected diffuse interstitial pneumonia in both lungs. Initial CT (Computed Tomography) presented extensive lung involvement with bilateral wide areas of consolidation with air bronchogram, the non-consolidated area showing patchy ground glass infiltration. The patient was hospitalized in ICU (Intensive Care Unit), oxygen support was started immediately with non-invasive ventilation (NIV), CPAP (Continuous Positive Airway Pressure) mode, FiO2 (Fraction of inspired Oxygen) 100%, PEEP (Positive end-expiratory pressure) 8, and the saturation started to increase. Therapy consisted of parenteral antibiotic, low-molecular weight heparin (LMWH) in prophylactic doses, pulsed dose of corticosteroid (methylprednisolone), Remdesivir, tocilizumab (Actemra), albumin, protein-pump inhibitor, antipyretics, fluids, physical therapy. Microbiology results from sputum detected MRSA (methicillin-resistant Staphylococcus aureus) and therapy with Vancomycin was started according to recommendations. After three days of vancomycin therapy, the patient manifested profuse epistaxis and tamponade was necessary. Hemostasis result was normal, but severe thrombocytopenia was noticed in the blood count. Platelets and plasma were administered and the bleeding stopped. Vancomycin was replaced with Linezolid. In the next days of follow up, the platelets increased, and the corticosteroid dose was slowly reduced. During the treatment as the health status of the patient improved, the CPAP therapy was replaced with routine oxygen support, gradually lowering the oxygen flow until saturation of 94% was achieved at ambient air. The COVID-19 pandemic is still evolving and the medical fraternity is posed with a huge challenge. COVID-19 is primary a respiratory viral infection, but the virus can affect many organs and systems, presenting various signs, symptoms and outcomes.
Introduction: COPD patients are at high risk for PE and DVT due to immobility, inflammation, comorbidities. Prevalence of PE during AECOPD is uncertain and often under-diagnosed. Material and methods: Single-center, prospective, an observational trial of 100 hospitalized patients with AECOPD, diagnosed according to GOLD criteria, 40-75 years, stratified according to airflow limitation (I-IV), divided into subgroups (PE-diagnosed/non-PE and with known/ undetermined exacerbation etiology). Investigations: clinical risk assessment, electrocardiogram (ECG), laboratory, spirometry, gas-analysis, D-dimer (DD), chest X-ray, thoracic ultrasonography (TUS), Doppler-ultrasonography of deep-veins of lower-extremities (DULE). Patients with high DD and DVT or high DD and abnormal TUS underwent computed-tomography pulmonary-angiography (CTPA). Results: PE was diagnosed in 26 (26.0%), DVT in 5 (5.0%) of hospitalized AECOPD patients. There was a positive correlation between COPD-severity and PE. Frequencies of PE in GOLD-stages I, IV, were 0 (0.0%), 3 (11.5%), 8 (30.7%), 15 (57.7%) respectively. Patients with pleuritic chest-pain, TUS abnormality, phlebitis and high DD were more likely to develop PE. Localization was subsegmental in 9 (34.6%), in one of the main pulmonary arteries 7 (26.9%), lobar and interlobar arteries in 10 (38.5%). DD was significantly higher among patients with PE than those without (3.34 ± 1.1 μg/mL vs. 2.2 ± 0.8μg/mL, P < 0.0001). There was positive correlation between the presence of PE and elevated DD > 2.0 μg/mL (P = 0.02). There was no statistically significant difference between patients with PE and without, according to age, gender and comorbidities (P > 0.05). Immobility and obesity were significantly higher among PE patients, P = 0.032 and P < 0.0001 respectively. Conclusion: AECOPD associated with pleuritic chest pain, immobility, high DD, should be considered for PE. Chest-ultrasound, as a low-cost and safe procedure, can be a very helpful investigation.
GPA is a systemic, necrotizing, small-vessel vasculitis associated with circulating anti-neutrophil cytoplasmic autoantibodies (ANCA), and so called ANCA-associated vasculitis (AAV). A white woman in her early thirties, was sent to hospital because of hemoptysis, dyspnea, fever, cough, general fatigue, swollen joints. Chest radiography on hospital admission detected diffuse small nodules in both lungs. Laboratory tests: white blood cells 13.9…16.7…18.2×10 9 /L, hemoglobin 91…80…110g/L, hematocrit 30…25..35%, erythrocytes 3.7…3.1…4.2×10 12 /L, platelet count 4.45…5.5…5.7×10 9 /L, sedimentation rate 72…60…45mm/h per first hour, C-reactive protein 111…80…35mg/L, D-dimer 4100…3500…1250 ng/ml. Biochemistry analysis: kidney function tests (blood urea nitrogen 10.4…7.4…5.6 mmol/L, creatinine 110…95…87 μmol/L, liver tests normal, albumin 28g/L, total protein 58 g/l. Urinalysis: mild proteinuria (+), 16-18 red blood cells, epithelial cells (++), 24-hour proteinuria 0,52g/L. Gas analyses: partial oxygen pressure 7.6…8.9…9.3 kPa, partial pressure of carbon dioxide 3.7…4.2…4.6 kPa, oxygen saturation 90…93…95%. She was febrile 38.5∘C, heart rate 122 beats/minute, swollen ankles, pale skin, conjunctival hyperemia, coagulated blood in both nostrils. Lung auscultation sound normal. Lung CT scan detected diffuse, bilateral, small nodules, some of them with areas of cavitation and pseudo-cavitation. Autoimmune antibody tests: positive c-ANCA 95U/ml, negative p-ANCA, negative RF 158IU/ml, positive antiproteinase-3 900 U/ml. Renal ultrasonography normal. IL-6 serum level normal 5 pg/ml, also C3 level 1.2 g/L and C4 level 0.3 g/L. Lung ultrasonography: bilateral, irregular, subpleural, hypoechogenic changes, with different size and central necrosis. Tracheobronchial mucosa was vulnerable, inflamed and edematous, bronchial lavage negative for malignancy and infection. Bronchial biopsy detected necrotic granulomas with multinucleated giant and inflammatory cells confirming the diagnosis of PGA. Cyclophosphamide combined with corticosteroids was given four months until the time of remission. The corticosteroid dose was slowly reduced and cyclophosphamide was switched to azathioprine to maintain remission. The treatment duration of the maintenance immunosuppressive medication after 10 months follow up is still ongoing with continuous monitoring of side effects.
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