Interventional therapy for a case of Mycoplasma pneumoniae pneumonia complicated by upper extremity arterial embolism in a child: a case report

Abstract

Background

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Mycoplasma pneumoniae pneumonia complicated with arterial embolism in children is rare but progresses rapidly, potentially leading to severe limb ischemia and disability. This study reports a case of MPP complicated with upper limb arterial embolism and reviews relevant literature to explore its pathogenesis, treatment strategies, and clinical management principles.

Case presentation

On January 9, 2025, Hebei Provincial Hospital of Traditional Chinese Medicine admitted an Asian male pediatric patient with upper limb arterial embolism. The patient developed acute limb ischemia secondary to Mycoplasma pneumoniae pneumonia and was diagnosed with upper limb arterial embolism. Endovascular thrombectomy was performed, followed by postoperative anticoagulation, anti-infective therapy, and traditional Chinese medicine treatment. After comprehensive management, the ischemic condition of the affected limb significantly improved, with no obvious functional impairment, achieving satisfactory therapeutic outcomes.

Conclusion

The risk of thrombosis in children with Mycoplasma pneumoniae pneumonia is often overlooked by clinicians. Due to its rapid progression and potentially severe consequences, early identification of thrombotic risk is crucial. A multidisciplinary approach should be adopted to determine the most appropriate treatment strategy for each patient, aiming to improve prognosis and reduce the risk of disability.

Background

Mycoplasma pneumoniae (MP), a predominant pathogen of community-acquired pneumonia in preschool and school-aged children, not only causes respiratory system damage but has also been shown to activate the coagulation cascade through multiple pathways, thereby predisposing patients to thrombotic complications. Epidemiological data demonstrate that MP infections account for 26.5% of pediatric thromboembolic events, with a higher incidence in males than females [1]. Notably, refractory Mycoplasma pneumoniae pneumonia (RMPP) [2] carries an elevated thrombotic risk compared to uncomplicated Mycoplasma pneumoniae pneumonia (MPP) [3]. When thromboembolism occurs in limb arteries, it may precipitate acute limb ischemia (ALI), defined as tissue hypoperfusion secondary to acute interruption of arterial blood flow. Without prompt intervention, ALI can progress to limb necrosis or life-threatening complications [4]. Herein, we present a pediatric case of acute upper limb ischemia admitted to our department on January 9, 2025, supplemented by a systematic review of published literature.

Case presentation

An Asian male patient aged 3 years and 7 months was admitted to the Department of Respiratory Medicine on January 5, 2025, with a 5-day history of fever, cough, and productive sputum. Chest CT revealed consolidation with a high-density shadow in the right middle lobe and patchy infiltrates in the right lower lobe with blurred margins (Fig. 1). On January 6, 2025, pathogen-targeted metagenomic sequencing of bronchoalveolar lavage fluid (BALF) obtained via fiberoptic bronchoscopy under intravenous anesthesia revealed a high-priority drug resistance gene, Mycoplasma pneumoniae (23 S RNA), with a sequence count of 99,885 (99.93%), indicating macrolide resistance. The respiratory team administered oral doxycycline treatment to the patient. During hospitalization, the child developed progressive pallor and coolness in the right hand, which caregivers initially overlooked. He was discharged on January 8, 2025. On January 9, 2025, the patient presented to the Department of Vascular Surgery with exacerbated pallor and coldness in the right hand. Emergency upper extremity arterial ultrasound revealed hypoechoic thrombi in the distal brachial artery, proximal radial artery, and ulnar artery (Fig. 1). The patient’s family denied any relevant medical, family, and psycho-social history including relevant genetic disorders history. The vascular team admitted him with the following presentation: cold, pale right hand with intermittent numbness and normal respiratory and gastrointestinal function.

The relevant auxiliary examinations are as follows:

• 1) Before intervention (January 9, 2025):Hemoglobin was 124 g/L, and the platelet count was 387 × 10⁹/L. D-dimer was elevated at 2214 ng/mL. Biochemical results showed creatinine at 26 µmol/L (≈ 0.29 mg/dL), uric acid at 153 µmol/L (≈ 2.57 mg/dL), lactate dehydrogenase (LDH) at 419 U/L, and creatine kinase (CK) at 30 U/L.

• 2) After intervention (January 11, 2025):Hemoglobin decreased to 102 g/L, and the platelet count increased to 480 × 10⁹/L. D-dimer slightly decreased to 1998 ng/mL. Creatinine decreased to 22 µmol/L (≈ 0.25 mg/dL), uric acid increased to 217 µmol/L (≈ 3.65 mg/dL), LDH decreased to 305 U/L, and CK rose to 80 U/L.

• 3) Re-examination (January 16, 2025):Hemoglobin rose to 115 g/L, and the platelet count further increased to 581 × 10⁹/L. D-dimer decreased to 737 ng/mL. Creatinine stabilized at 26 µmol/L (≈ 0.29 mg/dL), and uric acid was 186 µmol/L (≈ 3.13 mg/dL). Thrombin-antithrombin III complex (TAT) and plasmin-α₂-plasmin inhibitor complex (PIC) levels remained unchanged at 17.7 ng/mL and 4.0 µg/mL, respectively. Autoimmune antibody tests, including lupus anticoagulant (dRVVT/SCT), anticardiolipin antibodies (IgA/IgG/IgM), and anti-β₂-glycoprotein I antibodies (IgA/IgG/IgM), were all negative.

The therapeutic outcomes and follow-up are as follows: Immediate anticoagulation with enoxaparin (75 IU/kg/day once daily) and anti-infective therapy with doxycycline hyclate (2.5 mg/kg/day divided twice daily) were initiated upon admission, followed by scheduled interventional procedures the next morning.

On January 10, 2025, under combined general and regional anesthesia, the patient underwent upper extremity arteriography, thrombectomy, and balloon angioplasty. Positioning supine, the right common femoral artery was accessed via a modified Seldinger technique after standard disinfection and draping. A 5 F radial sheath was inserted, followed by systemic heparinization. A 150 cm hydrophilic guidewire and 5 F VER catheter were advanced into the right brachial artery, with angiography revealing the absence of contrast opacification in the right brachial artery, proximal ulnar artery, and radial artery, along with poor digital perfusion (Fig. 1).Thrombus aspiration was performed via a 5 F Navien RFX058-125-08 intracranial support catheter over a microguidewire, yielding a minimal dark-red thrombus. A microcatheter (LMC-21-153) and thrombectomy stent (CRD-4-20) were subsequently deployed, extracting substantial thrombi. Balloon angioplasty (Passeo-18 2/150/150) restored brachial artery patency, although persistent nonvisualization of the ulnar artery and suboptimal distal radial artery perfusion were noted (Fig. 1). Further angiography of the deep palmar arch revealed filling defects, suggesting the need for additional thrombectomy to remove the residual thrombus. Final angiography demonstrated restored palmar arch perfusion and improved digital staining. The sheath and guidewires were withdrawn, with hemostasis achieved via a vascular closure device and compression bandaging.

Fig. 1

Imaging findings of pulmonary CT, vascular ultrasonography, and intraoperative angiography. (A) Chest CT image demonstrating patchy consolidation in the right middle and lower lung lobes, indicating pulmonary inflammation. (B) Doppler ultrasonography revealing a high-resistance spectral waveform in the right brachial artery. (C) Absence of flow signals in the right radial artery on ultrasonography. (D) Intraoperative contrast angiography image showing nonvisualization of the right brachial artery, proximal ulnar artery, and radial artery. (E) Postthrombectomy angiography documenting restored patency of the brachial artery, with persistent nonvisualization of the ulnar artery and suboptimal distal radial artery opacification. (F) Follow-up ultrasonography demonstrating a reduced luminal diameter and compromised flow perfusion in the right radial artery

Upon procedure completion, the patient’s palm and entire thumb/index finger exhibited a restored pinkish hue, with partial recovery in proximal segments of the middle/ring/little fingers and significantly improved temperature. Postoperative anticoagulation was adjusted to enoxaparin (75 IU/kg twice daily) alongside continued doxycycline hyclate (2.5 mg/kg twice daily). During afternoon rounds, the affected hand showed comparable warmth to the contralateral hand, although persistent pallor was noted. Palpable radial and brachial artery pulses were documented, with a diminished ulnar artery pulse. Normal muscle strength, unrestricted mobility, and intact physiological reflexes were observed. The following day, recurrent coldness in the right index finger and a weakened radial pulse prompted supplemental therapy: papaverine hydrochloride (4.5 mg/kg/day divided three times daily) and urokinase (1500 IU/kg once daily). Subsequent clinical improvement ensued without relapse. After 9 days of treatment, the patient was discharged on rivaroxaban (0.5 mg/kg twice daily) and an herbal decoction promoting blood circulation (one daily dose). One-month follow-up upper extremity ultrasound revealed a reduced diameter and suboptimal flow in the right radial artery, whereas brachial/ulnar arterial hemodynamics remained normal (Fig. 1). Bilateral hands showed no discernible discrepancy in function or appearance.

Discussion and conclusions

Recent studies have demonstrated a direct association between Mycoplasma pneumoniae (MP) infection and thrombosis. Among thromboembolic complications, pulmonary thromboembolism is the most common, while cerebral artery embolism and cardiac thrombosis are the most frequent extrapulmonary thromboembolic events [5].

To further explore extrapulmonary thrombosis associated with MP infection, we conducted a retrospective review of case reports published between January 2000 and January 2025. Literature was retrieved from PubMed and Ovid using the keywords “Mycoplasma pneumoniae” AND “embolism” OR “thrombosis,” with the patient age restricted to 0–18 years. A total of 38 articles were included, involving 110 pediatric patients. Pulmonary embolism cases were excluded from this summary.Among the included cases, some lacked specific information on age and sex. Based on available data, there were 36 male and 27 female patients. The youngest was 3 years old and the oldest 13 years and 10 months, with a median age of 7 years. The time from onset of pneumonia symptoms to the detection of thrombosis ranged from 4 to 26 days, with a median of 11 days.A total of 128 thrombotic sites were reported. Cerebral artery embolism was the most frequently affected site (26 cases, 20.31%), while mesenteric vein and inferior vena cava thromboses were the least common (1 case each, 0.78%). Arterial thrombosis accounted for 68 cases (53.1%), venous thrombosis for 35 cases (27.3%), and intracardiac thrombosis for 25 cases (19.5%). Given the focus of this report on MP-associated upper limb arterial embolism, it is noteworthy that arterial involvement represents the most common type of extrapulmonary thrombosis, highlighting the need for early vascular assessment in affected children.

The systemic inflammatory response induced by MP infection may play a key role in thrombosis formation [6].Although the exact mechanisms remain unclear, three widely recognized pathways have been proposed. First, MP infection may activate the coagulation system by inducing vasculitis and a hypercoagulable state via molecular mimicry and immune complex deposition [7]. Mycoplasma surface proteins share structural similarities with human proteins such as β2-glycoprotein I, which can trigger autoimmune responses, leading to thrombosis formation [8,9,10]. Second, MP infection may stimulate the production of antiphospholipid antibodies, increasing the risk of arterial and venous thrombosis [11, 12]. Third, tissue factor, a key initiator of coagulation, is significantly upregulated following MP infection, leading to the activation of the coagulation cascade [13].

In the present case, anticoagulation therapy was the primary treatment to prevent further thrombus formation and progression. Low-molecular-weight heparin (LMWH) is recommended as the first-line anticoagulant for pediatric patients due to its proven safety and efficacy [14]. For patients requiring long-term anticoagulation, warfarin remains a commonly used medication [15]. In recent years, direct oral anticoagulants (DOACs) such as rivaroxaban and dabigatran have been increasingly used in pediatric venous thromboembolism (VTE), though their efficacy and safety in MP-associated thrombosis require further investigation. Additionally, MP infection may promote thrombosis by activating platelet aggregation pathways. In certain cases, antiplatelet therapy (e.g., aspirin or clopidogrel) may serve as an adjunctive treatment. For patients with severe vascular obstruction or inadequate response to anticoagulation therapy, thrombolytic therapy can be considered. Studies have shown that tissue plasminogen activator (tPA) is effective in treating large thrombi in children, though its bleeding risk must be carefully weighed [16].

A review of existing literature revealed that among reported cases of MP-associated thrombosis with poor prognosis, including fatal cases, cerebral artery embolism was predominant [17,18,19,20]. Most of these patients received anticoagulation therapy alone, which was significantly less effective than treatments used for thromboembolism in other locations. Clinicians should recognize the higher risk associated with cerebral artery embolism and adopt a more comprehensive therapeutic approach.

Surgical treatment options include endovascular and traditional open surgical approaches, typically reserved for cases in which anticoagulation or thrombolysis fails. Endovascular techniques such as mechanical thrombectomy and catheter-directed thrombolysis are preferable for acute cases (within 72 h of thrombosis formation) with well-defined anatomical lesions (e.g., pulmonary artery trunk, intracranial venous sinuses, or deep veins of the lower limbs) and no contraindications due to bleeding risks. These techniques offer advantages of minimal invasiveness and real-time imaging guidance. Traditional open surgical procedures, such as surgical thrombectomy and vascular bypass surgery, are more commonly used in cases of chronic organized thrombi causing vascular occlusion, anatomical anomalies limiting endovascular access, or failed endovascular interventions.

A literature review identified 11 pediatric cases of MP-associated thromboembolism treated surgically. Four cases underwent endovascular interventions: (1) deep vein thrombosis of the lower limb [21], treated with anticoagulation, filter placement, and catheter-directed thrombolysis, with a good prognosis; (2) celiac artery, hepatic artery, and splenic artery embolism [22], treated with anticoagulation, volume expansion, and endovascular thrombolysis, with a moderate prognosis (splenic artery remained occluded at 1-year follow-up); (3) pulmonary artery, superior mesenteric vein, inferior vena cava, and common iliac vein thrombosis [23], treated with anticoagulation, filter placement, and endovascular thrombolysis, with a good prognosis; (4) lower limb arterial embolism [24], treated with catheter-directed thrombolysis, with a good prognosis.

Six cases underwent open surgical interventions: (1) cardiac thrombosis [25], treated with anticoagulation, antiplatelet therapy, and surgical thrombectomy, with a good prognosis; (2) lower limb arterial embolism [26], treated with open thrombectomy and thrombolysis, with a good prognosis; (3) cardiac thrombosis [27], treated with anticoagulation and surgical thrombectomy, with a good prognosis; (4) lower limb artery and intracranial venous sinus thrombosis [28], treated with anticoagulation, volume expansion, and open thrombectomy, with a good prognosis; (5) lower limb arterial embolism [18], treated with anticoagulation, antiplatelet therapy, and open thrombectomy, with a good prognosis; (6) cardiac thrombosis [29], treated with surgical thrombectomy, with a good prognosis. One patient underwent a hybrid intervention: superior mesenteric artery, celiac artery, and splenic artery embolism [30], treated with anticoagulation, endovascular thrombolysis, and open surgery (exploratory laparotomy, bowel resection, and anastomosis). The patient was stable at discharge, though long-term follow-up data were not reported.

Surgical interventions in pediatric thrombosis face multiple challenges. First, pediatric blood vessels are small, limiting maneuverability. Mismatches between catheter size and vascular structure increase the risk of vascular injury or thrombus fragmentation. Second, long-term anticoagulation is required to prevent recurrence, but MP-related antiphospholipid antibodies may interfere with anticoagulant metabolism, increasing the risk of bleeding or recurrent thrombosis. Third, current evidence is primarily based on case reports or small retrospective studies, and no pediatric-specific risk stratification models have been established. In the present case, selecting an appropriate surgical approach was challenging due to the unavailability of pediatric-specific endovascular devices. After multidisciplinary discussions, a decision was made to use certain neurointerventional devices beyond their intended scope. Although the surgery was successful, this case highlights the urgent need for pediatric-specific interventional equipment and standardized surgical protocols.

Although MP infection-associated thrombosis is becoming increasingly recognized, further research is needed to elucidate its precise mechanisms and optimize individualized treatment strategies. Future studies should focus on refining clinical management guidelines to improve patient outcomes.