Cardiopulmonary Rescue before Fixation: Targeted Pigtail Decompression for Hyperacute Unilateral Lung Decompensation Enabling ORIF in Bilateral Open Distal Femur Fractures

At presentation, the PaO₂/FiO₂ ratio was 92 with SpO₂ 82% on high‑flow nasal cannula 15 L/min at FiO₂ 0.80. Ultrasound‑guided 14‑Fr pigtail decompression (right 5th intercostal space, anterior axillary line) at T0 evacuated ~220 mL air with scant blood‑tinged fluid; oxygenation improved to a PaO₂/FiO₂ of 308 within 12 minutes (PaO₂/FiO₂ 308 on 3 L nasal cannula; A–a gradient 528 → 112 mmHg), and induction proceeded at T+30 minutes with ORIF commencing at T+90 minutes the same day.

Background: Hypoxemia before fracture fixation in polytrauma often derives from reversible thoracic causes. We report a case in which unilateral radiographic lung decompensation with low oxygen saturation was rapidly reversed by targeted pigtail decompression, enabling safe anesthesia and definitive fixation.

Case: A patient with bilateral open distal femur fractures (right Gustilo‑Anderson II, left I) developed acute hypoxemia with unilateral alveolar opacity on chest radiography. Ultrasound‑guided 14‑Fr pigtail decompression immediately improved oxygenation and radiographic aeration, allowing timely ORIF.

Outcome: Postoperative recovery was uneventful; long‑leg follow‑up radiographs confirmed bony healing.

Interpretation: When low SpO₂ coexists with a unilateral pattern, clinicians should not be constrained by the prior of bilateral pulmonary edema. Rapid, targeted pleural decompression (pigtail) can eliminate a reversible pleural barrier within minutes and open an anesthetic window for fracture fixation. Mechanistically, hyperacute decompensation may reflect a convergence of pleural tension‑related shunt, re‑expansion lung injury, negative‑pressure/airway factors, and fat‑embolism‑related pulmonary vascular responses.

Design: Case report with focused literature review.

In multiply injured patients, definitive fixation hinges on cardiopulmonary stability. Edema patterns are classically bilateral in hydrostatic or permeability‑driven injury; however, unilateral radiographic decompensation can occur in early re‑expansion pulmonary edema (REPE), negative‑pressure pulmonary edema (NPPE), airway malposition, and regional perfusion/ventilation imbalance. At the bedside, prompt exclusion of tension physiology and directed decompression takes priority because the benefit may be immediate and decisive for definitive orthopedic care [1].

Taken together, these changes constitute a 12‑minute rescue, with PaO₂/FiO₂ rising from 92 to 308 and hemodynamics stabilizing, thereby enabling same‑day ORIF.

A middle‑aged patient sustained bilateral open distal femur fractures in a high‑energy mechanism (right Gustilo‑Anderson type II; left type I). During pre‑operative resuscitation, the patient developed acute hypoxemia with a unilateral alveolar opacity on the right‑sided lung field. Point‑of‑care lung ultrasound and radiography favored a pleural‑compartment problem over diffuse edema. An ultrasound‑guided 14‑Fr pigtail catheter was placed for targeted decompression. SpO₂ rose promptly and a control radiograph showed re‑expansion. After stabilization, staged definitive fixation (open reduction and internal fixation) was performed. Recovery was uneventful; subsequent long‑leg alignment films demonstrated consolidating callus and functionally symmetric lower limbs.

Revision (Hemodynamics from imaging): Relief of pathologically elevated pleural pressure would be expected to reduce right‑atrial/juxtapericardial pressure, increase venous return, and promptly improve cardiac output; immediate radiographic correlates can include reversal of mediastinal shift and a lower apparent cardiothoracic ratio. Intubation and controlled ventilation improve inspiratory frame and lung inflation, further reducing the apparent silhouette; however, because AP portable cardiothoracic measurements are technique‑sensitive, we interpret these imaging changes as physiologically coherent but not proof of hemodynamic change.

Revision (discussion – evidence vs. speculation): The causal chain remains inferential. Our evidence‑based observations comprise the unilateral radiographic pattern, immediate improvement after pleural decompression, and restoration of gas exchange; by contrast, the contributions of REPE, NPPE, and fat‑embolism physiology are mechanistic hypotheses without direct confirmatory testing in this case. We therefore present these mechanisms as plausible, not proven, in accordance with contemporary reviews [2-11].

Scope of inference: Our evidence‑based elements include unilateral imaging, ultrasound evidence of pleural‑compartment tension, immediate physiologic normalization after decompression, and a durable anesthetic window enabling same‑day ORIF. Mechanistic contributors from NPPE/REPE and marrow‑fat physiology remain plausible rather than proven in this single case; we therefore present them as modifiers rather than primary causes [2-6,12,13].

Two pathophysiological axes plausibly converged in this case. First, pleural‑compartment tension—air or fluid—can create a large shunt fraction by collapsing alveoli and redirecting perfusion to the dependent lung, a process that can appear unilateral on imaging; relief by small‑bore catheter is effective and supported by randomized trials and meta‑analyses in traumatic thoracic pathology [14-16]. Second, hyperacute edema in a unilateral distribution can follow sudden re‑expansion (REPE) where mechanical stress and increased capillary permeability flood the ipsilateral lung; modern case series and reviews emphasize its rarity but potential severity [2,3]. NPPE—classically bilateral—can rarely be unilateral when obstruction or malposition is regional; case reports document dependent‑lung‑predominant edema or endobronchial intubation–related unilateral patterns [4-6]. Finally, long‑bone injury can release marrow fat and free fatty acids; experimental models demonstrate acute rises in mean pulmonary arterial pressure, ventilation‑perfusion mismatch, and inflammatory endothelial injury, any of which intensify an already precarious gas‑exchange state [7-11]. These mechanisms are not mutually exclusive: transient fat‑embolism‑related pulmonary vasoconstriction may increase microvascular hydrostatic stress, while rapid lung re‑expansion adds capillary ‘stress failure’—together producing a hyperacute, side‑predominant picture that is reversible once pleural mechanics are normalized.

With oxygenation restored, fixation followed an Early Appropriate Care (EAC) paradigm—proceeding to definitive management once lactate, pH, and base‑excess criteria indicate adequate resuscitation—to minimize pulmonary and systemic complications in polytrauma [17,18]. This case underscores that cardiopulmonary rescue is a prerequisite to ‘timing’ decisions; a short, targeted decompression can convert a high‑risk physiology into an anesthetic window for safe ORIF.

Conclusion

In polytrauma, the precondition for fracture fixation is cardiopulmonary stability. When unilateral findings accompany hypoxemia, clinicians should resist anchoring bias to the prior. Rapid, ultrasound‑guided pigtail decompression can resolve a reversible pleural barrier within minutes and open a safe window for anesthesia and fixation.

Methods (practical bedside protocol)

Practical implications — Lessons learned: Protocol anchors and rationale. We anchor the bedside flow in LUS‑first triage for tension physiology [19,20]; controlled pleural off‑loading with initial water‑seal/one‑way valve to mitigate REPE [21,22]; and EAC‑aligned timing once gas‑exchange and perfusion markers normalize [17,18,23]. When a hyperacute unilateral pattern is present, a small‑bore catheter can be both diagnostic and therapeutic, rapidly restoring oxygenation without delaying orthopedics [14-16,24].

Pragmatic documentation: when feasible, record pre/post cardiothoracic ratio (CTR) on the portable CXR and a synchronized vital‑sign snapshot (HR, BP, SpO₂, ventilator settings) to anchor the physiologic turnaround in the chart.

In multiply-injured patients with hyperacute unilateral decompensation, a brief, ultrasound‑guided pleural decompression can convert a high‑risk physiology into a safe anesthetic window. Key bedside points are to (i) prioritize exclusion of tension physiology by lung/pleural ultrasound, (ii) employ controlled pigtail decompression with avoidance of early high‑suction to reduce REPE risk, and (iii) re‑evaluate oxygenation within 15–30 minutes; if normalized, proceed with definitive fixation under Early Appropriate Care thresholds [17,18] (Figures 1-4).

1) Screen physiology: bedside lung/pleural ultrasound; rule out tension; arterial blood gas.

2) Prepare: local anesthesia, sterile field; select 14-Fr pigtail; lateral/anterior axillary line at safe triangle; ultrasound to target pleural air/fluid pocket.

3) Controlled decompression: Seldinger technique; connect to one‑way valve/water seal; avoid excessive negative suction at onset to reduce REPE risk.

4) Reassess: pulse oximetry and capnography; repeat CXR within 15-30 minutes; if oxygenation normalizes and radiograph improves, proceed to anesthesia and fixation per EAC criteria.

5) Document and monitor for REPE/NPPE signs during the first 1–2 hours.

Ethics and consent

The case was managed according to institutional trauma protocols. Identifiers have been removed from images; written consent for publication was obtained.

At outpatient follow-up, the patient ambulated independently without exertional dyspnea. On examination, the bilateral knee range of motion measured 2°–110° with no extensor lag. Radiographs demonstrated progressive callus with maintained alignment; no readmissions or supplemental oxygen were required.

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