This is a 76-year-old male patient with a history of hypertension and Crohn's disease treated with prednisone (30mg daily) and tablezalin, who came to the emergency room of another center for fever of 5 days of evolution and arthralgia.
Presence of hypotension with a mean arterial pressure (MAP) <55mmHg and hyponatremia (129mEq/l) was suspected due to adrenal insufficiency due to deprivation (with methylprednisone administration 48h before)
Arthralgias are also attributed to a sprout of inflammatory bowel disease by abrupt cessation of medication.
In the following 24h, the patient complained of dyspnea with progressive desaturation (76%), without cyclophosphamide.
A thoracic computerized axial tomography was performed, which showed a nonspecific bilateral ground glass pattern.
The diagnostic suspicion at that time corresponds to interstitial lung disease versus community-acquired pneumonia, and treatment with cyclophosphamide, levofloxacin and methylprednisolone is initiated.
The patient was admitted to our hospital with the main diagnosis of acute hypoxemic respiratory failure.
When presenting 4 signs of severity of the British Thoracic Society4 for community-acquired pneumonia, he was admitted to our Critical Care Unit: tachypnea >30 breaths per minute, urea >42mg/dl, bilateral lung disease.
Chest X-ray showed signs of diffuse bilateral interstitial pneumonia, which was accompanied by extensive manifestations of exudative alveolitis with upper mediastinal widening, compatible with left-sided lymphadenopathy.
In the complete blood count, leukocytes and leukocytes were not detected, which could be expected in a parasitic infection.
Pneumococcal antigen was positive in urine analysis. Treatment with linezolid and cefoxime alternative fluconazole was initiated, with non-invasive ventilation with continuous positive pressure of +7 cmH2O and inspiratory therapy assistance.
Progressively, the patient presented a general deterioration with severe sepsis and multiorgan dysfunction, with the presence of shock, need for inotropes and vasopressors to achieve a MAP >60mmHg and acute respiratory failure requiring continuous orotracheal ventilation.
This deterioration was due to infection caused by the existence of concomitant bacterial or fungal infections, which led to the change of antibiotic treatment (imipenem, bacterial anhydride, new antibiotics), and microbiological isolates.
It was in this last BAS that larvae of S were observed, so that the treatment was restricted to the elimination phase (16.5mg/24h) by nasogastric tube (NGT).
After repeating the biological cultures at 48h and showing the presence of Ss larvae still active in BAS, gastric juice and feces, it was associated with albendazole treatment (400mg/24h) by SNG.
A subsequent microbiological control was performed 48h after the combined treatment, and the lesions were observed in BAS Ss.
However, the subsequent evolution was acute respiratory distress syndrome (ARDS) with severe hypoxemia and septic shock refractory to vasoconstrictor and inotropic support.
The patient died 17 days after admission to our unit.
