Summary:
The authors present a novel 2-staged approach for complex dorsolumbar wound reconstruction in a multioperated spine patient with limited local flap options and contraindications for free flap reconstruction due to arteriosclerosis and cardiac issues. A delayed dorsal propeller flap was first autonomized to enhance perfusion, followed by elevation and mobilization 4 weeks later. This approach combined the historic delay phenomenon with modern propeller flap techniques, achieving durable coverage and infection control. The case highlights the value of integrating traditional and innovative surgical methods for complex reconstructions.
Complex back wounds from repeated spinal procedures and recurrent infections demand meticulous multidisciplinary management. Local and regional flap options are often limited. Free flap closure with microsurgical anastomosis may be contraindicated in patients with significant comorbidities or poor recipient vessels. This case illustrates how blending historical techniques such as the delay phenomenon with modern reconstructive principles enables safe, tailored solutions for complex defects where conventional options are limited. We opted for a staged, delayed extended propeller flap1 to optimize perfusion and surgical outcomes.
MEDICAL AND SURGICAL HISTORY
A 78-year-old woman with multiple lumbar spine procedures, chronic infections, arteriosclerosis, osteoporosis, arthritis, hypertension, dyslipidemia, hyperthyroidism, and class 2 obesity presented with significant wound dehiscence and exposed spinal hardware. The patient’s vascular status, infection risk, arteriosclerosis, and cardiac disease rendered free flap reconstruction unfeasible. Due to previous flap use and limited local tissue, an alternative approach was required.
Seven years earlier, the patient underwent oblique lumbar interbody fusion from L2 to L5, followed by D10-S1-V fusion for degenerative scoliosis. Postoperatively, she developed a large epidural hematoma and wound dehiscence, requiring multiple revisions, debridement, and flap coverage. Cultures grew extended spectrum beta-lactamase-producing Escherichia coli, treated with meropenem and long-term trimethoprim-sulfamethoxazole suppressive therapy.
One year later, hardware failure and infection with the same pathogen necessitated multistage revision, including osteotomy and extended fusion. Two years afterward, she developed another epidural abscess, requiring hardware exchange and lumbosacral fusion. Cultures revealed E. coli and Candida albicans, managed with meropenem, fluconazole, and suppressive trimethoprim-sulfamethoxazole.
Nine months later, noncompliance with antibiotics led to infection recurrence, which was treated surgically with multilevel fixation and local fasciocutaneous flap closure. Lifelong antibiotics were reinstated.
After 2 years of infection control, the patient presented with paraplegia and instrumentation failure. Stabilization was achieved using an anterior thoracolumbar approach. Three months postoperatively, a large (15 × 20 cm) wound dehiscence with exposed hardware developed, requiring extensive debridement, hardware removal, dorsal bone grafting, and targeted antibiotics for Enterobacter cloacae, coagulase-negative Staphylococcus, and Staphylococcus epidermidis.
The patient was referred to our plastic surgery team. Given her complex history, a staged approach was planned: first, stabilization and debridement, followed by delayed wound closure. (See figure, Supplemental Digital Content 1, which displays the patient’s initial presentation: extensive infected wound dehiscence with osteosynthesis material exposure, https://links.lww.com/PRSGO/E427.)
SURGICAL STRATEGY
During the first stage, in the left lateral decubitus position, a lateral perforator was identified using Doppler ultrasound. Regional anesthesia was provided via an intercostal block and infiltration of Klein solution with a double dose of lidocaine. The solution was injected across the right hemiback. The extension was delayed by creating 3 incisions—medial paravertebral, lateral vertical (posterior axillary line), and distal horizontal (at the iliac crest level, deep to the fascia). These incisions were made following random flap design principles to ensure adequate perfusion. An antimicrobial, medicated gauze dressing impregnated with 1% mupirocin (Bactigras) and wet gauze was placed between the donor site and the elevated distal part of the flap, creating a barrier to prevent direct contact between the tissues to ensure proper hydration and protection of the flap and donor site, fixed with separated stiches (Fig. 1). This initial dressing protocol was followed by a protective sterile dressing, which was changed every 2 days in the early postoperative period (first stage).
Fig. 1.
First stage of delayed surgery: 3 distal incisions.
The second stage was performed a month later in a prone position under general anesthesia. Surgical screw revision from D3 to L3 was conducted, with extensive debridement. Rod insertion was done by sliding them under the skin to preserve the flap site. The rods were then bent, compressed, and secured in place, and fluoroscopy confirmed appropriate kyphosis and scoliosis correction. Bone graft harvested from the pelvis was mixed with allograft and placed at the surgical site. Antibiotic-loaded beads were placed to prevent infection at the surgical site (Fig. 2).
Fig. 2.
Second stage of delayed surgery: wound debridement with antibiotic-loaded beads.
For wound closure, the subfascial layer was carefully dissected to identify and preserve perforators. A flap delay technique was used through precise incisions, resulting in significant tissue expansion. A key perforator, located at 23 cm, was dissected transmuscularly and transformed into a fully vascularized island flap. The remaining portion of the flap was elevated in a subfascial and subtrapezial plane, extending to the contralateral side to maximize coverage (Fig. 3).
Fig. 3.
Second stage of delayed surgery: propeller flap elevation including perforator dissection.
To achieve a 2-layer closure of the defect, the flap was translated and advanced into the cervicodorsal region to ensure coverage of both the exposed osteosynthesis material and a portion of the donor site. A lateral decompression triangle at the thoracolumbar level was intentionally left for secondary healing and managed with an incisional vacuum-assisted closure system to optimize tissue integration and wound healing (Fig. 4).
Fig. 4.
Second stage of delayed surgery: inset of the flap.
POSTOPERATIVE COURSE
Postoperative care included meticulous wound management with structured dressing changes and targeted antibiotic therapy. A protective sterile dressing changed every 2 days was applied in the early postoperative period. A vacuum-assisted closure system was applied to the secondary healing area at the thoracolumbar level to optimize granulation tissue formation and wound contraction.
Antibiotic therapy (vancomycin, co-trimoxazole, ciprofloxacin) was guided by intraoperative cultures and the patient’s clinical history. By the 11-month follow-up, the patient demonstrated complete wound closure, with stable soft tissue coverage and no further complications. (See Supplemental Digital Content 2, which displays the patient’s postoperative outcome with complete wound closure with stable soft tissue coverage, https://links.lww.com/PRSGO/E428.)
DISCUSSION
Spine reoperations frequently create complex wound closure challenges due to large defects, high-tension anatomy, prior surgery, compromised vascularity, and recurrent infections. We present a 2-stage reconstructive approach for a multioperated dorsolumbar defect, highlighting the collaboration between spine orthopedics and plastic surgery.
A key element is the delay phenomenon2—a time-tested yet underused strategy that improves flap viability by inducing vascular remodeling through preconditioning.3 In this case, the delay enhanced the reliability and reach of a propeller flap, avoiding microsurgical free flaps in a high-risk patient with arterial disease and cardiac comorbidities.
A crucial question is whether the traditional 1-month delay can be shortened without increasing necrosis risk. Experimental studies, such as Holzbach,4 suggest early improvements, though human data remain limited. Emerging approaches—including rheological modulation,5 hypoxia preconditioning,6 growth factor therapies,7 and bioengineered solutions8–11—may further reduce delay time.12 This case demonstrates how blending classic techniques with modern perforator-based flaps can address extensive dorsolumbar defects.
DISCLOSURE
The authors have no financial interest to declare in relation to the content of this article.
Supplementary Material
Footnotes
Published online 21 October 2025.
Disclosure statements are at the end of this article, following the correspondence information.
Related Digital Media are available in the full-text version of the article on www.PRSGlobalOpen.com.
REFERENCES
- 1.Pignatti M, Ogawa R, Hallock GG, et al. The “Tokyo” consensus on propeller flaps. Plast Reconstr Surg. 2011;127:716–722. [DOI] [PubMed] [Google Scholar]
- 2.Ghali S, Butler PEM, Tepper OM, et al. Vascular delay revisited. Plast Reconstr Surg. 2007;119:1735–1744. [DOI] [PubMed] [Google Scholar]
- 3.Zhang F, Waller W, Lineaweaver WC. Growth factors and flap survival. Microsurgery. 2004;24:162–167. [DOI] [PubMed] [Google Scholar]
- 4.Holzbach T, Neshkova I, Vlaskou D, et al. Searching for the right timing of surgical delay: angiogenesis, vascular endothelial growth factor and perfusion changes in a skin-flap model. J Plast Reconstr Aesthet Surg. 2009;62:1534–1542. [DOI] [PubMed] [Google Scholar]
- 5.Pearl RM. A unifying theory of the delay phenomenon—recovery from the hyperadrenergic state. Ann Plast Surg. 1981;7:102–112. [DOI] [PubMed] [Google Scholar]
- 6.Izadpanah A, Jansen DA, Chaffin AE, et al. Nontopical nitrates in flap perfusion and delay phenomenon. Plast Reconstr Surg Glob Open. 2024;12:e5918. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Hayward PG, Alison WE, Carp SS, et al. Local infiltration of an angiogenic growth factor does not stimulate the delay phenomenon. Br J Plast Surg. 1991;44:526–529. [DOI] [PubMed] [Google Scholar]
- 8.Bayati S, Russell RC, Roth AC. Stimulation of angiogenesis to improve the viability of prefabricated flaps. Plast Reconstr Surg. 1998;101:1290–1295. [DOI] [PubMed] [Google Scholar]
- 9.Zhang H, Zhang T, Chen H, et al. The effects of inactive platelet-rich plasma at different injection time on prefabricated flap viability in rabbits. Ann Plast Surg. 2021;86:701–706. [DOI] [PubMed] [Google Scholar]
- 10.Zan T, Li Q, Dong J, et al. Transplanted endothelial progenitor cells increase neo-vascularisation of rat pre-fabricated flaps. J Plast Reconstr Aesthet Surg. 2010;63:474–481. [DOI] [PubMed] [Google Scholar]
- 11.Yi C, Xia W, Zheng Y, et al. Transplantation of endothelial progenitor cells transferred by vascular endothelial growth factor gene for vascular regeneration of ischemic flaps. J Surg Res. 2006;135:100–106. [DOI] [PubMed] [Google Scholar]
- 12.Lese I, Graf DA, Tsai C, et al. Bioactive nanoparticle-based formulations increase survival area of perforator flaps in a rat model. PLoS One. 2018;13:e0207802. [DOI] [PMC free article] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.




