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- ARDS
- connective tissue disease-associated lung disease
- interstitial fibrosis
- systemic disease and lungs
Case presentation: the trainee
A 56-year-old woman of South Indian origin presented with 2 weeks of cough, fever, malaise and dyspnoea ,with no response to amoxicillin. She was generally well with mild hypertension, type 2 diabetes controlled with metformin, hypothyroidism and vitamin D deficiency. There were no other relevant exposures, previous imaging, lung function or other investigations.
Initial observations: temperature 38.2°C, blood pressure 112/76 mm Hg, RR 24, SpO2 94% on 3 L/min of O2 via nasal cannulae. Examination of the chest revealed bilateral crackles.
Chest X-ray on admission showed bilateral patchy consolidation to the mid zones (figure 1A).
Initial test results are shown below:
White cell count 8.8×109/L (4–10).
C-reactive protein 141 (<5).
HIV negative.
Throat swab PCR negative for respiratory viruses.
With a working diagnosis of community-acquired pneumonia, treatment was initiated promptly with intravenous amoxicillin/clavulanic acid and clarithromycin, O2 via nasal cannulae, intravenous crystalloids and paracetamol, and the patient was admitted to the acute admissions unit. Despite this, the patient failed to improve. Amoxicillin/clavulanic acid was changed to piperacillin/tazobactam, and she was transferred to the high dependency unit (HDU) 4 days after admission due to increasing O2 requirements. Sputum examination was positive for Candida sp only.
Intensive care assessment
This patient deteriorated despite appropriate medical therapy. She was initially managed on HDU with high flow nasal O2. However, her respiratory failure progressed rapidly, requiring invasive mechanical ventilation 5 days after admission. CT scan of the chest showed features consistent with ARDS (Acute Respiratory Distress Syndrome) (figure 1B).
There was little change over the following 4 days despite treatment with meropenem, clarithromycin and fluconazole. Ten days after admission, on day 5 of mechanical ventilation, gas exchange and lung mechanics rapidly deteriorated with a severe hypoxaemic respiratory acidosis (FiO2 …
Footnotes
Contributors All authors treated the patient and co-wrote the manuscript. GT is responsible for the overall content as guarantor.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.