COVID-19 is an independent risk factor for pulmonary embolism (PE). Little is known about alteplase therapy in this patient group. A retrospective study analyzed 74 patients with PE and acute respiratory distress syndrome (ARDS) due to COVID-19 who were hospitalized in the intensive care unit in 2021. Patients with or without confirmed right heart thrombi (RHT) were treated with unfractionated heparin or alteplase. The mortality rate in patients with RHT treated with heparin was 100% compared to 37.9% and 55.2% in those treated with alteplase without RHT and alteplase with RHT, respectively. The risk of death in the alteplase group increased with delayed thrombolysis (p = 0.009, odds ratio (OR) = 1.73 95% CI (confidence interval) 1.14–2.62), increased D-dimer concentration (p = 0.02, OR = 1.43 95% CI 1.06–1.93), and decreased PaO₂/FiO₂ ratio (p = 0.001, OR = 0.56 95% CI 0.41–0.78). The receiver operating characteristic method determined that a 1-day delay in thrombolytic treatment, D-dimer concentration >5.844 mg/L, and PaO₂/FiO₂ <144 mmHg predicted a fatal outcome. The risk of death in patients with severe COVID-19 with ARDS and PE increases with higher D-dimer levels, decreased PaO₂/FiO₂, and delayed thrombolytic treatment. Thrombolysis seems to be treatment of choice in severe COVID-19 with PE and RHT. It should be carried out as soon as possible after the diagnosis is established.

Background. Serotonin syndrome is a life-threatening condition that may be caused by an unanticipated interaction of serotonergic drugs. Medications of this category are routinely prescribed during treatment of blast injury. Their effect on serotonin receptors should be taken into account to prevent the development of serotonin syndrome. Case description. A patient was transported from another hospital directly to the ICU to continue treatment of consequences of multiple blast injuries of lower limbs and abdomen, complicated by wound infection and clinical depression. Treatment with linezolid and duloxetine combined with repeated surgical interventions with opioid-based anesthesia has resulted in development of the serotonin syndrome, manifesting as tremor and frequent clonic seizures. Complete revision of the prescribed pharmacological therapy as well the approach to sedation and anesthesia has led to a complete resolution of clinical symptoms of this complication. Conclusion. In this case, improvement was achieved through discontinuation of fluoxetine and linezolid. All unfavorable drug interactions must be taken into account in management of complex blast injury. Limiting opioid use through regional anesthesia and prescription of sedative agents that do not promote serotonin accumulation may prevent the development of serotonin syndrome in such patients.