Ventilator-associated cavitary pneumonia after lung contusion: a case report

Abstract

Background and Aim

Ventilator-associated cavitary pneumonia is common with Streptococcus pneumoniae, Staphylococcus aureus, Klebsiella pneumoniae, Haemophilus influenzae, and Pseudomonas aeruginosa. Escherichia coli-associated cavitary pneumonia is a rare condition primarily observed in immunocompromised patients.

Case presentation

This report details a case of ventilator-associated cavitary pneumonia caused by multidrug-resistant Escherichia coli in a 27-year-old man of Iranian Baluch ethnicity who developed pulmonary contusion and subdural/subarachnoid hemorrhage after trauma.

Conclusion

E. coli is an emerging cause of ventilator-associated pneumonia and should be included in the differential diagnosis of cavitary pneumonia.

Introduction

Ventilator-associated pneumonia (VAP) is a common hospital-acquired infection in patients with mechanical ventilation. The aspiration of organisms from the oropharynx and stomach is the primary cause. [1]. E. coli is a frequent cause of VAP, but it is a rare cause of community-acquired pneumonia (CAP), primarily seen in patients with human immunodeficiency virus (HIV) and those receiving immunosuppressive treatments. Necrotic pneumonia (NP) or cavitary pneumonia caused by this organism has been observed rarely in patients with HIV and recipients of immunosuppressive treatments [2]. We present a specific case of ventilator-associated cavitary pneumonia (VACP) caused by Escherichia coli in a 27-year-old man with no prior medical history.

Case report

A 27-year-old Iranian Baluch ethnicity man was admitted to the emergency room of Khatam Al-Anbia Hospital in Zahedan (Sistan and Baluchestan Province, Iran) with decreased consciousness and respiratory distress. The patient’s companions report a long-time opium addiction and a recent minor car accident 3 days ago, along with a 3-day history of opium overuse. They did not mention any other medical history for the patient. On clinical examination, the patient’s GCS was 7. No signs of trauma, such as bruising, swelling, abrasions, lacerations, or deformities, were observed on the body surface. Bilateral crackles were audible on lung auscultation. The abdomen was soft and non-tender. The pelvis and limbs were stable, and the pulses were symmetrical and palpable in all limbs. Pupils were pinpoint and poorly reactive to light. His blood pressure was 90/45 mmHg, heart rate was 134 beats/minute, respiratory rate was 30 breaths/minute, temperature was 37 °C, and SpO₂ was 70% when breathing ambient air. The patient’s blood sugar level was measured at 96 mg/dL via a glucometer. Therefore, opium poisoning was strongly suspected. The patient received 100% oxygen via Mapleson mask. Two intravenous lines were established, and a 2 L normal saline infusion was initiated. Despite four intravenous administrations of 0.4 mg naloxone and one vial of 50% glucose, the patient remained unresponsive. The patient was immediately intubated and mechanically ventilated with AC/VC + (PRCV), TV = 500 mL, RR = 12, Ti = 1.3, PEEP = 5, and FiO₂ = 100–40%. The patient underwent CT scans of the lungs, brain, abdomen, and pelvis. CT scans revealed bilateral lung hyperdensities and a small frontal subdural/subarachnoid hematoma with frontal bone fracture; the abdomen and pelvis were normal (Figs. 1 and 2).

Fig. 1.

A chest showed bilateral lung consolidation and ground-glass opacities, most prominent in the right middle lobe

Fig. 2.

A brain computed tomography showed a 5 mm right subdural hematoma expanded into the interhemispheric fissure, a left frontal subarachnoid hemorrhage, a 2 mm midline shift, and a frontal bone fracture (red arrow). According to the neurosurgeon’s opinion, the patient did not require surgery. A follow-up computed tomography scan 24 hours later showed no change in the amount of hemorrhage

The patient’s initial test results were as follows.

WBC = 2/4 × 10³ / /µl, RBC = 4/1 mil/ /µl, HB = 10/6 g/dL, HCT = 34/9%, PLT = 123 × 1000, PT = 17/second, PTT = 46/second, INR = 1/6, BS = 50 mg/dl, BUN = 47 mg/dl, CR = 1/2 mg/dl, K = 3/9 meq/l, Na = 139 meq/l, ABG (PH = 7/24, PaCO₂ = 47/9, HCO₃ = 20/1, BE = -7/2, PaO₂ = 48/8, O₂Sat = 84/8).

Given the patient’s history of trauma (pulmonary contusion, SDH, SAH), leukopenia, and decreased consciousness, tracheal secretions, blood, and urine were cultured. The patient was transferred to the intensive care unit (ICU). Empiric antibiotic therapy with ceftriaxone 2 g twice a day and clindamycin 600 mg twice a day was initiated to cover aspiration pneumonia. He was also symptomatically treated with bronchodilators, N-acetylcysteine and dexamethasone.

Despite negative culture results after 48 h, the patient developed a fever of 39°C and leukocytosis. We empirically changed the antibiotic regimen to meropenem 2 g twice a day and levofloxacin 750 mg daily. However, the patient remained febrile with leukocytosis. We added vancomycin 1 g twice a day to the antibiotic regimen for MRSA coverage, and we sent blood, urine, and tracheal secretions sample cultures again. Blood and urine cultures were negative, but E. coli grew in tracheal secretions, which were sensitive to tobramycin, amikacin, gentamicin, and colistin; it was resistant to ceftriaxone, levofloxacin, ciprofloxacin, meropenem, cefepime, ceftazidime, piperacillin/tazobactam, trimethoprim/sulfamethoxazole, and others. Accordingly, colistin 4 million units TDS and amikacin 1.5 g daily were added to the patient’s antibiotic regimen. Following antibiotic administration, the patient’s fever and leukocytosis resolved, and consciousness improved. A follow-up lung CT scan revealed multiple large cavities in both lungs, predominantly in the right lung (Fig. 3).

Fig. 3.

Chest computed tomography showed bilateral lung cavities (predominantly right), pulmonary fibrosis, and a mild right pleural effusion

Re-cultures of blood, urine, and pulmonary secretions were performed, all of which were negative. The patient’s level of consciousness also increased, and his respiratory function was acceptable based on ventilator data. Therefore, we extubated the patient. The intravenous antibiotic therapy continued for two weeks. After that, the patient’s general condition was excellent. A follow-up chest X-ray revealed persistent lung cavities. The patient was discharged with bronchodilators, antibiotics, and a follow-up appointment (Fig. 4).

Fig. 4.

The patient’s chest X-ray demonstrates persistent pulmonary cavities

Discussion

Necrotizing pneumonia (NP) is a rare but fatal complication of lung infections. Acute necrotizing pneumonia is commonly caused by S. aureus, S. pneumoniae, K. pneumoniae, H. influenzae, and P. aeruginosa. Community-acquired methicillin-resistant S. aureus is a particularly concerning cause, often leading to rapid respiratory failure and shock [3]. Mycobacterium tuberculosis is also a common cause of cavitary pneumonia [4]. Less common causes of NP include S. viridans, anaerobic bacteria, and fungi [4, 5].

Risk factors for acute necrotizing pneumonia include old age, smoking, chronic alcohol abuse, diabetes mellitus, chronic lung diseases or liver disease and prolonged corticosteroid use [3, 6]. NP begins with local inflammation, progressing to lung destruction and cavities. Alveolar congestion promotes clots and vascular occlusion, disrupting lung structure and forming abscesses resistant to antibiotics [5]. The process of alveolar destruction depends on the ability of the microorganism and the underlying predisposition of the host. Capsular polysaccharides’ buildup overwhelms macrophages via antigenic properties, while toxins such as hemolysin/leukocidin worsen lung damage. Clindamycin administration likely helps by reducing pyogenic substance release and increasing bacterial susceptibility to immune system killing through membrane changes [4]. Disease severity and delayed diagnosis increase morbidity/mortality from necrotizing pneumonia. A definitive diagnosis of this type of pneumonia typically takes about nine days [5].

E. coli is a Gram-negative bacterium transmitted via the fecal–oral route and rarely causes NP except in immunocompromised patients or with bloodstream infections [2]. Khalafi et al. reported a case of necrotizing Escherichia coli community-acquired pneumonia resistant to trimethoprim/sulfamethoxazole in a 44-year-old Hispanic man. The infection was successfully treated with ampicillin-sulbactam. After 9 days of antibiotic therapy, the patient was extubated and discharged in stable condition [7]. The Escherichia coli isolates in these two cases showed different antibiotic susceptibility and resistance patterns. In this case, multidrug resistance was likely due to hospital-acquired pneumonia. Organisms’ drug susceptibility and resistance profiles in intensive care units are unique; healthcare providers should continuously monitor common ventilator-associated pneumonia pathogens and their antibiotic susceptibility patterns within each hospital to inform empirical antibiotic prescriptions [8].

Hosseini et al. reported a fatal community-acquired necrotizing pneumonia caused by Escherichia coli in a patient with uncontrolled diabetes; the infection led to severe hemoptysis and patient death [2]. In another case report, a 55-year-old smoker and multi-drug abuser with seizures and drug-induced rhabdomyolysis developed cavitary pneumonia caused by Escherichia coli [9]. Case reports showed that E. coli-induced cavitary pneumonia was more commonly seen in community-acquired pneumonia, where the patient had a significant risk factor. We did not find any reports of E. coli-induced cavitary ventilator-associated pneumonia.

Escherichia coli pneumonia, while more frequent in ventilated patients, carries a higher risk of necrosis, cavitation, and mortality when community-acquired. Prompt identification of the causative organism via culture or polymerase chain reaction (PCR), along with antibiotic sensitivity testing, is crucial for appropriate antibiotic selection and treatment [10].

Conclusion

Escherichia coli is a dangerous pathogen that can cause necrotizing pneumonia. Therefore, clinicians should consider this organism’s potential for multidrug resistance in the empirical antibiotic regimen whenever a cavity is observed on a chest CT or x-ray of a mechanically ventilated patient.

Generative AI disclosure

No generative AI was used in the writing of this case report.

Abbreviations

VAP

Ventilator-associated pneumonia

PCR

Polymerase chain reaction

HIV

Human immunodeficiency virus

BD

Twice in a day

TDS

3 Times in a day

PEEP

Positive end-expiratory pressure

ICU

Intensive care unit

AC/VC + (PRCV)

Assist control/ volume control + (pressure regulated volume control)

RR

Respiratory rate

TV

Tidal volume

Ti

Time inspiration

SDH

Subdural hematoma

SAH

Subarachnoid hematoma

Author contributions

AK: Providing care, following up on the patient’s treatment process, writing case reports, and final editing. ARD: Follow up on the patient’s treatment progress and edit the case report.

Funding

The authors did not receive any funding for this work.

Data availability

All patient file data, radiographs, and CT scans will be available upon request by contacting the corresponding author of the case report.

Declarations

Ethics approval and consent to participate

The study protocol was approved by the ethics committee of Zahedan University of Medical Sciences (ethical code: IR.ZAUMS.REC.1404.064).

Consent for publication

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare that they have no competing interests.