Extracorporeal Membrane Oxygenation Haemoperfusion for Leptospirosis Pulmonary Hemorrhagic Disease: Report of 1 Case

ABSTRACT

Severe pulmonary leptospirosis (SPFL), characterized by diffuse alveolar haemorrhage (DAH) and acute respiratory distress syndrome (ARDS), carries a high mortality, often due to diagnostic delays and complex management. We report a case of a 42‐year‐old male with outdoor occupational exposure who presented with fever and hemoptysis, rapidly progressing to severe respiratory failure and thrombocytopenia. Chest imaging confirmed DAH/ARDS. For refractory hypoxemia, veno‐venous extracorporeal membrane oxygenation (VV‐ECMO) was initiated without systemic anticoagulation due to active pulmonary haemorrhage. Metagenomic next‐generation sequencing (mNGS) of bronchoalveolar lavage fluid rapidly identified Leptospira interrogans , enabling targeted antimicrobial therapy alongside multidisciplinary support. The patient gradually improved, was successfully weaned from ECMO and ventilator support, and was discharged without residual organ dysfunction. This case demonstrates that early application of anticoagulation‐free VV‐ECMO combined with mNGS‐based rapid diagnosis and multidisciplinary care can improve outcomes in SPFL, highlighting the importance of considering this diagnosis in febrile patients with DAH and environmental exposure.

We present a case of a 42‐year‐old male with severe pulmonary leptospirosis who developed diffuse alveolar haemorrhage and was successfully managed with venovenous extracorporeal membrane oxygenation without systemic anticoagulation.

1. Introduction

Leptospirosis is a zoonotic disease caused by pathogenic Leptospira spirochetes, transmitted via contact with environments contaminated by infected animal urine [1]. Pulmonary involvement, occurring in most cases, can rapidly progress to diffuse alveolar haemorrhage (DAH) and acute respiratory distress syndrome (ARDS). This severe pulmonary form poses a significant diagnostic and therapeutic challenge due to its nonspecific early presentation. Recent advances, particularly metagenomic next‐generation sequencing (mNGS), enable rapid pathogen identification and have improved clinical decision‐making in critically ill patients [2]. For managing the resulting refractory respiratory failure, extracorporeal membrane oxygenation (ECMO) has emerged as a potentially life‐saving intervention, even in the context of active pulmonary haemorrhage [3].

2. Case Report

On September 8, 2025, a 42‐year‐old male presented with a 7‐day history of fever, myalgia, and cough, followed by 1 day of hemoptysis. Coarse bilateral breath sounds were noted.

Initial labs indicate active infection, systemic inflammation, and renal impairment. Arterial blood gas under FiO₂ 90% showed hyperoxemia and hypocapnia (Table 1). Chest radiography demonstrated bilateral diffuse infiltrative shadows (Figure 1), and subsequent computed tomography revealed multifocal areas of increased attenuation throughout both lungs, consistent with pneumonia and possible pulmonary edema (Figure 2). Despite initial consideration of severe pneumonia with sepsis, the early prominence of myalgia and alveolar haemorrhage, combined with key epidemiological clues (outdoor occupational exposure and rodent contact), leptospirosis emerged as the leading clinical suspicion.

TABLE 1.

Evolution of the patient's clinical parameters during the hospital stay.

Parameter	Value						Reference range
	Day1	Day2	Day3	Day4	Day9	Day12
Hb	110	99	85	89	110	108	130–175 g/L
WBC	13.6	20.75	12.95	21.19	17.75	5.87	3.5–9.5X109/L
NE	10.03	11.91	11.21	20.47	14.63	3.51	1.8–6.3X109/L
LYM	0.25	0.32	0.26	3.21	1.55	1.17	1.1–3.2X109/L
PT	12.6	14.8	15.1	13.9	11.2	10.3	10–14 s
APTT	31.2	34.4	35.3	27.5	20.2	22.6	24–32 s
FIB	6.99	7.36	6.69	5.59	3.32	2.34	1.8–3.5 g/L
BUN	12.09	13.5	14.6	15.88	97.1	6.86	3.1–9.5 mmol/L
Cr	133	266	282	196.1	65.6	71.7	57‐111 mmol/L
ALB	21.5	19.5	21.1	33.2	32.6	38	35–50 g/L
Tbil	9.4	22.6	26.1	32.9	8.5	5.8	3.4–20.5 mmol/L
AST	24	29	22	64.7	296	35.6	15–40 U/L
ALT	11	12	12	44.2	195.1	43.9	9–50 U/L
CRP	206	214	182	58.5	18.5	3.7	0‐10 mg/L
K	3.05	—	3.13	—	3.68	3.68	3.5–5.3 mmol/L
CK	80	51	—	44	56	—	50‐310 U/L
CK‐MB	27	10	9	—	12.5	—	0‐24 U/L
Lac	2.2	1.6	1.7	1.4	0.7	0.7	0.5–1.7 mmol/L
pH	7.45	7.38	7.39	7.56	7.41	7.43	7.35–7.45
PaO2	162	147	134	169	179	153	80–100 mmHg
FiO2	90	80	50	50	40	30
PaO2/FiO2	180	183.75	268	338	447.5	510	> 300
PaCO2	28	38	42	46	37	40	35–45 mmHg
HCO3—	22.9	26.8	31.7	30.5	24.1	25.5	22–27 mmol/L

Abbreviations: ALB, albumin; ALT, alanine aminotransferase; APTT, activated partial thromboplastin time; AST, aspartate aminotransferase; BUN, blood urea nitrogen; CK, creatine kinase; CK‐MB, creatine kinase‐MB; Cr, serum creatinine; CRP, C‐reactive protein; FIB, fibrinogen; Hb, haemoglobin; K, potassium; LYM, lymphocyte percentage; NE, neutrophil percentage; PT, prothrombin time; Tbil, total bilirubin; WBC, white blood cell count.

FIGURE 1.

Chest X‐ray examination. Bilateral alveolar interstitial syndrome.

FIGURE 2.

Chest computed tomography. Multiple patchy, hazy ground‐glass opacities and areas of consolidation bilaterally, with predominant involvement of the subpleural regions in the dorsal segments of both lower lobes.

Empirical antimicrobial therapy was initiated with intravenous levofloxacin (500 mg daily) alongside supportive measures. Fiberoptic bronchoscopy performed on admission revealed diffuse mucosal haemorrhage throughout the trachea and bronchial tree(Figure 3). Bronchoalveolar lavage fluid was collected for mNGS analysis.

FIGURE 3.

Electronic bronchoscope. Both lungs are infected and bleeding.

However, on the second day of hospitalization, the patient's condition deteriorated rapidly. Despite receiving high‐flow oxygen support, progressive dyspnea and declining oxygen saturation persisted. Laboratory parameters indicated worsening systemic inflammatory response and acute renal impairment. Consequently, the patient was transferred to the intensive care unit (ICU) for further management. Within a few hours, endotracheal intubation was performed due to refractory hypoxemia. Mechanical ventilation was initiated in pressure‐assist/control mode with lung‐protective settings at FiO₂ of 100%.

Despite lung‐protective ventilation strategies, oxygenation remained inadequate. In view of extensive bilateral alveolar infiltrates on imaging and clinical evidence of diffuse alveolar haemorrhage confirmed by bronchoscopy, venovenous extracorporeal membrane oxygenation (VV‐ECMO) was initiated to ensure adequate oxygen delivery and minimize ventilator‐induced lung injury. Given the risk of active pulmonary haemorrhage, systemic anticoagulation was withheld during ECMO support. To prevent and early detect circuit thrombosis, a multimodal monitoring strategy was implemented: transmembrane pressure (ΔP) was monitored hourly, with a progressive increase (> 40–50 mmHg considered abnormal) indicating oxygenator thrombosis; pre‐ and post‐oxygenator blood gases were assessed three times daily to evaluate oxygenator gas exchange efficiency; and systematic visual inspection of the circuit, particularly the transparent oxygenator housing and centrifugal pump head, was performed each shift by dedicated nurses to identify fibrin deposition or blood flow abnormalities. Oxygenator exchange was promptly performed upon evidence of persistently elevated ΔP, deteriorating oxygenator function, or visible thrombus formation. In this patient, the oxygenator was electively replaced on day 7 of support without circuit occlusion or interruption of blood flow.

Ventilator and ECMO parameters were adjusted dynamically during support (Table 2), with mechanical ventilation minimized to facilitate lung rest while maintaining adequate CO₂ clearance and oxygenation through extracorporeal support. Concurrent acute kidney injury prompted initiation of continuous renal replacement therapy (CRRT) using regional citrate anticoagulation, with parameters adjusted based on daily fluid and metabolic balance. Given the high clinical suspicion of leptospirosis, empirical antimicrobial therapy was transitioned to intravenous penicillin G (0.96 g every 6 h) combined with oral doxycycline (100 mg every 12 h). Subsequent mNGS of bronchoalveolar lavage fluid confirmed Leptospira interrogans infection, leading to discontinuation of doxycycline and continuation of penicillin G monotherapy. The q6h dosing interval of penicillin G was selected based on the patient's acute kidney injury and ongoing CRRT, ensuring therapeutic efficacy while avoiding drug accumulation. Penicillin G was administered from September 19 to October 1 (12 days), while doxycycline was given for only 3 days (September 19 to 22). With multimodal organ support, the patient's condition gradually stabilized. CRRT was discontinued on September 24 following sustained improvement in hemodynamic status and renal function. VV‐ECMO was successfully weaned and withdrawn after a period of stable oxygenation during circuit‐off trials, with cannulas removed and haemostasis achieved (Table 3).

TABLE 2.

ECMO parameters, and medication dosages during ECMO.

	Day2	Day3	Day4	Day5	Day6
Ventilatory parameters
Respiratory rate	10	10	10	12	12
Ventilation mode	PC	PC	PC	PC	PC
FiO2 (%)	40	40	40	40	40
PEEP(cmH2O)	5	8	8	8	5
Oxygen saturation(%)	40	40	40	40	40
ECMO record
Blood flow (L/min)	3.8	3.85	3.8	3.8	3.8
Gas flow (L/min)	2.5	2.5	2.5	0.5	0.5
Motor RPM	3500	3510	3510	3510	3510
FiO2 (%)	100	100	100	60	50

TABLE 3.

Metagenomic next‐generation sequencing (mNGS) for pathogen detection.

Name	Sequence reads	Confidence
Leptospira interrogans	86	86%

On the following day, the patient passed a spontaneous breathing trial and was successfully extubated, transitioning to high‐flow nasal oxygen. Follow‐up laboratory tests (Table 1) and chest CT (Figure 4) showed marked resolution of inflammation and pulmonary infiltrates.

FIGURE 4.

Chest CT scan reveals improvement in lesion absorption.

The patient remained clinically stable, with no fever, cough, or dyspnea, and was discharged after 20 days of hospitalization. He was sent home with oral antibiotics and close outpatient follow‐up, having achieved full functional recovery without residual respiratory or multi‐organ impairment. The treatment timeline is summarized in Figure 5.

FIGURE 5.

Treatment process of Case.

3. Discussion

The rapid progression to DAH and ARDS in severe leptospirosis portends a poor outcome, with fatality rates exceeding 50% in affected patients [4]. The use of venovenous extracorporeal membrane oxygenation (VV‐ECMO) in this setting remains challenging due to the coexistence of life‐threatening respiratory failure and a bleeding diathesis. A critical aspect of management in our patient was the decision to withhold systemic anticoagulation given ongoing pulmonary haemorrhage—a strategy supported by recent reports demonstrating that ECMO can be safely maintained without heparin for several days, particularly in the early phase of DAH [5]. While anticoagulation increases bleeding risk, its absence may predispose to circuit thrombosis; however, this concern was effectively mitigated through a rigorous multimodal monitoring protocol. These observations align with evidence that anticoagulation‐free ECMO strategies do not significantly increase [6]. Concurrently, ECMO facilitated ultra‐protective ventilation, minimizing ventilator‐induced lung injury.

These findings underscore that VV‐ECMO, when applied early and tailored to the individual bleeding‐risk profile, can be a life‐saving intervention in severe leptospirosis complicated by DAH.

Author Contributions

Qigang Zeng and Longyun Xie (co‐first authors, marked with*) were responsible for collecting and organizing the clinical data of the case, and drafting the original manuscript (contributions: Investigation, Data curation, Writing, original draft). Wenshan Dai and Feilong Xu conducted literature review and analysis, and participated in revising and polishing the manuscript (contributions: Literature review, Writing, review and editing). Yong Dai supervised the study design, reviewed the scientific validity of the clinical data, and finalized the manuscript (contributions: Conceptualization, Supervision, Writing, review and editing).

Funding

The authors have nothing to report.

Ethics Statement

The authors declare that written informed consent was obtained for the publication of this manuscript and accompanying images using the consent form provided by the Journal.

Conflicts of Interest

The authors declare no conflicts of interest.

Zeng Q., Xie L., Dai W., Xu F., and Dai Y., “Extracorporeal Membrane Oxygenation Haemoperfusion for Leptospirosis Pulmonary Hemorrhagic Disease: Report of 1 Case,” Respirology Case Reports 14, no. 5 (2026): e70565, 10.1002/rcr2.70565.

Data Availability Statement

The data that supports the findings of this study are available in the Supporting Information of this article.