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	<title>negative-pressure wound therapy &#8211; Science</title>
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	<title>negative-pressure wound therapy &#8211; Science</title>
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		<title>Two-Stage Surgery With Biologic Mesh Offers New Hope for Contaminated Hernia Repair</title>
		<link>https://scienmag.com/two-stage-surgery-with-biologic-mesh-offers-new-hope-for-contaminated-hernia-repair/</link>
		
		<dc:creator><![CDATA[Ophelia Keating]]></dc:creator>
		<pubDate>Sat, 03 Oct 2026 00:53:09 +0000</pubDate>
				<category><![CDATA[Medicine]]></category>
		<category><![CDATA[abdominal wall reconstruction]]></category>
		<category><![CDATA[biologic mesh]]></category>
		<category><![CDATA[biologic mesh in abdominal surgery]]></category>
		<category><![CDATA[bridging underlay biologic mesh]]></category>
		<category><![CDATA[case report]]></category>
		<category><![CDATA[chronic fistula repair]]></category>
		<category><![CDATA[complex abdominal wall reconstruction]]></category>
		<category><![CDATA[component separation technique]]></category>
		<category><![CDATA[contaminated hernia repair]]></category>
		<category><![CDATA[contaminated surgical field]]></category>
		<category><![CDATA[enterocutaneous fistula]]></category>
		<category><![CDATA[general surgery]]></category>
		<category><![CDATA[hernia recurrence]]></category>
		<category><![CDATA[hernia recurrence prevention]]></category>
		<category><![CDATA[incisional hernia]]></category>
		<category><![CDATA[infected surgical field management]]></category>
		<category><![CDATA[innovative surgical strategies]]></category>
		<category><![CDATA[mesh-based hernia repair challenges]]></category>
		<category><![CDATA[negative-pressure wound therapy]]></category>
		<category><![CDATA[recurrent incisional hernia treatment]]></category>
		<category><![CDATA[two-stage hernia reconstruction]]></category>
		<category><![CDATA[underlay mesh placement]]></category>
		<category><![CDATA[XenMatrix]]></category>
		<guid isPermaLink="false">https://scienmag.com/?p=229867</guid>

					<description><![CDATA[A new case report describes a two-stage abdominal wall reconstruction combining component separation with bridging underlay biologic mesh that kept a high-risk patient hernia-free at twelve months despite a heavily contaminated surgical field.]]></description>
										<content:encoded><![CDATA[<p>Surgeons have long struggled with one of the most stubborn problems in abdominal surgery: how to rebuild a weakened abdominal wall when the surgical field is already contaminated with infection. A newly published case report in BMC Plastic and Reconstructive Surgery describes a dual-stage reconstruction strategy that combined component separation with a bridging underlay biologic mesh, and the outcome offers a cautiously optimistic data point in an area of surgery where consensus has remained elusive. The patient, a 73-year-old woman with a massive recurrent incisional hernia, hidden infection, and a chronic fistula buried inside old surgical mesh, has shown no recurrence at twelve months and remains independent in her daily activities.</p>
<p>The scale of the underlying problem is considerable. Incisional hernias, which occur when tissue pushes through a healed surgical scar, affect an estimated 10 to 50 percent of patients after open abdominal surgery. Even after repair, recurrence rates between 8.7 and 32 percent have been reported. Simple suture repair of the fascia, the tough connective tissue layer that holds the abdominal contents in place, carries recurrence rates as high as 60 percent according to long-term randomized trial data. Adding mesh to reinforce the repair reduces that figure to around 24 percent, which is why mesh has become a standard part of modern hernia surgery. But mesh introduces its own dilemma when the surgical field is contaminated.</p>
<p>Synthetic prosthetic mesh, typically made of permanent polymer materials, performs well in clean surgical environments and reduces recurrence effectively. In contaminated fields, however, it carries serious long-term risks: mesh infection, wound dehiscence, and the formation of enterocutaneous fistulas, in which bowel abnormally connects to the skin. Biologic mesh, made from processed collagen scaffolds of human or animal origin, was developed partly to address this. Because the material is decellularized collagen rather than plastic, it is far more resistant to infection and can become integrated into the patient&#8217;s own tissue through revascularization and cellular ingrowth. The trade-off is cost: biologic mesh can cost up to 200 times more than a synthetic equivalent, a disparity that has fueled an ongoing debate about whether the clinical benefits justify the expense.</p>
<p>The case report centers on a 73-year-old woman who arrived with nausea, vomiting, and abdominal pain. Her history was complicated: hypertension, high cholesterol, a heart attack two decades earlier treated with stenting, coronary bypass surgery, and a hysterectomy thirty years before that had been complicated by infection and a temporary colostomy. On examination, she had a large, non-reducible hernia in her left lower abdomen with what surgeons call loss of domain, meaning so much bowel had migrated into the hernia sac that returning it to the abdominal cavity would be difficult. Her laboratory values told a worrying story: an elevated white blood cell count of 15.5 thousand per microliter, impaired kidney function, and a prealbumin level of 10 milligrams per deciliter indicating significant malnutrition. A CT scan revealed a 7.8-centimeter abdominal wall defect packed with loops of small and large bowel.</p>
<p>What the surgical team found in the operating room was worse than the imaging suggested. After beginning the procedure robotically and encountering dense adhesions, they converted to an open laparotomy. The hernia contained the entire cecum and roughly 140 centimeters of small intestine. Buried within the defect was old permanent mesh from a repair the patient did not know she had received, and stuck to that mesh was a chronic fistulous tract surrounded by infectious material. The team resected the diseased segment of bowel, created a side-to-side anastomosis to restore continuity, removed necrotic hernia sac and ulcerated skin, and irrigated the field copiously. With a 15-centimeter fascial defect remaining and the patient becoming hemodynamically unstable on vasopressor medications, definitive reconstruction was judged too risky. Instead, they placed an AbThera negative pressure dressing, a temporary wound vacuum system, and transferred her to the surgical intensive care unit, intubated and sedated.</p>
<p>Two days later, with her white blood cell count improving and her ventilator requirements minimal, the team returned to the operating room for the second stage. This is the technical heart of the report. Because the bowel could not be reduced through the fascial defect, the surgeons performed a left-sided anterior component separation, a technique first described by Ramirez and colleagues in 1990. The procedure involves releasing the external oblique muscle from the internal oblique along the lateral abdominal wall, which allows the rectus abdominis muscles to slide medially and gain several centimeters of closure. In this patient, releasing the external oblique yielded roughly 8 centimeters of immediate fascial mobilization. Even so, the fascial edges could not be brought together without tension, so the team bridged the gap with a 20 by 25 centimeter piece of XenMatrix, a porcine-derived, non-crosslinked collagen mesh, sutured in an underlay position beneath the fascia using running absorbable sutures, with the skin loosely approximated over a wound vacuum.</p>
<p>The choice of underlay placement and non-crosslinked material reflects deliberate biomechanical reasoning. Underlay mesh, positioned beneath the abdominal wall, distributes forces across a larger area than mesh placed on top of the fascia, and published series report recurrence rates of 7 to 30 percent with this configuration. The Rives-Stoppa retrorectus technique, in which mesh is sandwiched between well-vascularized tissue planes, may be more durable but is often technically impossible in patients with multiple prior surgeries because those planes have been obliterated by scar tissue. The absence of cross-linking in XenMatrix allows tissue integration within about two weeks and, critically, permits safe direct contact with bowel. In this case, the mesh lay directly on the intestine with no fistulization at twelve-month follow-up, a feared complication that did not materialize.</p>
<p>The recovery was not smooth, and the report is candid about that. The patient required wound vacuum changes three times weekly for a month, an operative debridement of necrotic skin edges three weeks after the index operation, temporary dialysis through a permacath, intravenous antibiotics, and total parenteral nutrition to optimize healing. Her kidney function eventually normalized, the dialysis catheter was removed, and she tolerated a low-fiber diet without nutritional supplementation before discharge to a skilled nursing facility. At outpatient follow-up, her wound shrank progressively with granulation tissue filling in under a portable wound vacuum, and she has had no readmissions for postoperative infection. She remains ambulatory and satisfied with her quality of life.</p>
<p>The authors situate their result within a genuinely contested literature. A randomized trial by Rosen and colleagues found a 20.5 percent recurrence rate with biologic mesh versus 5.6 percent with synthetic mesh at two years in contaminated single-stage repairs, alongside the stark cost differential, leading some surgeons to argue synthetic mesh remains preferable. Carbonell and colleagues, by contrast, found nearly identical mesh-removal rates for infection, around 4 to 5 percent, between the two materials. Studies of bridging repairs consistently show higher recurrence than repairs achieving fascial closure, because biologic mesh stretches under prolonged tension due to its inherent elasticity. Here, even after component separation, a 3 to 4 centimeter midline gap remained, so the surgeons recreated a pseudo-midline by suturing the anterior sheath to the mesh with at least 5 centimeters of overlap, a recognized salvage maneuver. Multistaged approaches, such as removing infected mesh, treating with antibiotics, and repairing later, have produced recurrence rates around 19 percent at 32 months.</p>
<p>The report&#8217;s honest limitations are as instructive as its success. Twelve months is a short follow-up interval; most hernia recurrences appear within two to four years, so the absence of recurrence so far is encouraging but not definitive. The authors themselves note that in hindsight, definitive closure might have been delayed further to allow a longer antibiotic course in the contaminated field. They conclude that non-crosslinked porcine biologic mesh combined with anterior component separation is a safe and reasonable option for high-risk patients with contaminated wounds, particularly those too unstable for a single-stage repair, and they call for prospective randomized trials with larger samples and longer follow-up to settle the questions of mesh type, placement, and cost-effectiveness. For now, the case adds a practical, well-documented template: achieve source control first, let the infection clear, then rebuild with a technique that respects both the biology of healing and the mechanics of the abdominal wall.</p>
<p><strong>Subject of Research:</strong> Dual-stage abdominal wall reconstruction for contaminated incisional hernia using component separation and biologic mesh</p>
<p><strong>Article Title:</strong> Dual-stage abdominal wall reconstruction using component separation and bridging underlay biologic mesh in a contaminated incisional hernia: a case report and literature overview</p>
<p><strong>Article References:</strong> Bland, S., &amp; Wood, B. (2025). Dual-stage abdominal wall reconstruction using component separation and bridging underlay biologic mesh in a contaminated incisional hernia: a case report and literature overview. <em>BMC Plastic and Reconstructive Surgery, 1</em>(1), Article 4. <a href="https://doi.org/10.1186/s44452-025-00003-7" rel="noopener noreferrer">https://doi.org/10.1186/s44452-025-00003-7</a></p>
<p><strong>Image Credits:</strong> AI Generated</p>
<p><strong>DOI:</strong> <a href="https://doi.org/10.1186/s44452-025-00003-7" rel="noopener noreferrer">10.1186/s44452-025-00003-7</a></p>
<p><strong>Keywords:</strong> incisional hernia, abdominal wall reconstruction, component separation technique, biologic mesh, XenMatrix, contaminated surgical field, enterocutaneous fistula, underlay mesh placement, negative pressure wound therapy, hernia recurrence, case report, general surgery</p>
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		<post-id xmlns="com-wordpress:feed-additions:1">229867</post-id>	</item>
		<item>
		<title>When Vasculitis Masks a Flesh-Eating Infection: Rare Case Reveals Diagnostic Traps</title>
		<link>https://scienmag.com/when-vasculitis-masks-a-flesh-eating-infection-rare-case-reveals-diagnostic-traps/</link>
		
		<dc:creator><![CDATA[Ophelia Keating]]></dc:creator>
		<pubDate>Fri, 02 Oct 2026 01:36:33 +0000</pubDate>
				<category><![CDATA[Medicine]]></category>
		<category><![CDATA[case report]]></category>
		<category><![CDATA[clinical judgment versus scoring systems]]></category>
		<category><![CDATA[corticosteroids]]></category>
		<category><![CDATA[cyclophosphamide]]></category>
		<category><![CDATA[diagnostic challenges in vasculitis]]></category>
		<category><![CDATA[differential diagnosis of necrotizing infections]]></category>
		<category><![CDATA[fasciotomy]]></category>
		<category><![CDATA[flesh-eating infection]]></category>
		<category><![CDATA[immunosuppression]]></category>
		<category><![CDATA[immunosuppressive therapy complications]]></category>
		<category><![CDATA[life-threatening soft tissue infections]]></category>
		<category><![CDATA[LRINEC score]]></category>
		<category><![CDATA[necrotizing fasciitis]]></category>
		<category><![CDATA[negative-pressure wound therapy]]></category>
		<category><![CDATA[polyarteritis nodosa]]></category>
		<category><![CDATA[polyarteritis nodosa diagnosis]]></category>
		<category><![CDATA[rare case report on vasculitis and fasciitis]]></category>
		<category><![CDATA[soft tissue infection in vasculitis patients]]></category>
		<category><![CDATA[soft-tissue infection]]></category>
		<category><![CDATA[surgical debridement]]></category>
		<category><![CDATA[vasculitis]]></category>
		<category><![CDATA[vasculitis and infection overlap]]></category>
		<guid isPermaLink="false">https://scienmag.com/?p=224902</guid>

					<description><![CDATA[A case report describes a 38-year-old woman with polyarteritis nodosa whose necrotizing fasciitis was missed by standard scores, highlighting the diagnostic challenges in immunosuppressed patients.]]></description>
										<content:encoded><![CDATA[<p>A rare and treacherous collision of two serious diseases has been documented in a new case report published in Clinical Case Reports, describing a 38-year-old woman with polyarteritis nodosa who developed necrotizing fasciitis, the rapidly progressive soft tissue infection often described in the public imagination as a flesh-eating disease. The case is striking not only because of the rarity of the combination, but because the underlying vasculitis and the patient&#8217;s immunosuppressive treatment created a clinical picture so ambiguous that standard diagnostic scores and laboratory markers pointed in the wrong direction. The report offers a detailed account of how clinicians navigated the overlap between chronic inflammatory disease and acute life-threatening infection, and why the authors argue that clinical judgment must sometimes override scoring systems when a patient is deteriorating in front of the medical team.</p>
<p>Polyarteritis nodosa, or PAN, is a necrotizing vasculitis that attacks medium-sized and small arteries. The inflammation of the vessel walls can lead to occlusion of the arteries, cutting off blood supply to the tissues they serve and producing ischemia, ulceration, and tissue death. In this patient, the disease had already announced itself in dramatic fashion: for a month before her acute deterioration, she had suffered recurring necrotic, weeping sores across her feet, thighs, arms, and torso. An earlier histopathological evaluation had confirmed the diagnosis, showing prominent involvement of small and medium-sized vessels with acute inflammation and fibrinoid necrosis, the characteristic pattern of vessel wall destruction seen in PAN, with no granulomas or malignancy to suggest an alternative explanation. Her lesions were further complicated by what the treating team described as diffuse pyoderma gangrenosum, another ulcerating condition that can accompany systemic disease and that further muddied the diagnostic waters.</p>
<p>The acute crisis began with burning pain, redness, and swelling in the third and fourth digits of her right hand. She had already completed fourteen days of vancomycin and sulzone therapy without any improvement in her ulcers, an early warning that something beyond ordinary cellulitis was at work. Over the following four days, the symptoms spread relentlessly from the fingers to the entire hand and forearm. When clinicians examined her, they found erythema, swelling, severe pain, skin discoloration, fluid-filled bullae, and frank necrosis covering the hand and forearm, with ulcers on the palm leaking pus. This constellation of findings, particularly the pain that appeared disproportionate to the visible findings and the rapid tissue destruction, raised the immediate suspicion of necrotizing fasciitis, an infection of the fascial planes that can advance by the hour and cause systemic toxicity and multi-organ failure if not treated urgently.</p>
<p>The differential diagnosis in such a presentation is broad and unforgiving. The team considered severe cellulitis, a pyoderma gangrenosum flare in the setting of active PAN, compartment syndrome, clostridial myonecrosis, and even chronic conditions such as hypopigmented mycosis fungoides, though the acute tempo made the latter unlikely. Compartment syndrome was initially entertained because of the marked swelling and pain in the limb, but the clinical course and operative findings pointed instead toward a necrotizing soft tissue infection. Gas gangrene was judged less likely because there was no crepitus and imaging did not suggest gas in the soft tissues. Severe cellulitis, too, fell away as a leading explanation once the disproportionate pain, the bullae, and the intraoperative appearance of devitalized tissue were weighed together. The decisive combination was the severe acute onset, the purulent material, the systemic inflammatory reaction, and the prompt improvement that followed emergency surgery and broad-spectrum antibiotics.</p>
<p>Laboratory investigations told a deliberately confusing story. Her erythrocyte sedimentation rate was elevated at 59 millimeters per hour, and her white blood cell count showed striking leukocytosis at 28.8 times ten to the ninth per liter, a figure that fell after surgery and antimicrobial therapy in keeping with clinical improvement. Yet her C-reactive protein remained largely within the normal range despite the severity of the infection, and her LRINEC score, a laboratory risk indicator designed to identify necrotizing fasciitis, was only 3, well below the threshold that would suggest the diagnosis. Complement levels were normal, blood cultures showed no bacterial growth after five days, and immunofluorescence studies for IgG, IgA, IgM, C1q, and C3 were negative. Doppler ultrasound demonstrated subcutaneous edema in the affected limb, and ultrasound findings were supportive of necrotizing fasciitis. The authors emphasize that these results highlight a critical lesson: individual inflammatory markers may be nondiagnostic, and necrotizing fasciitis should not be excluded solely on the basis of a normal CRP or a low LRINEC score when the clinical presentation is concerning.</p>
<p>The reasons this patient was so vulnerable to such an infection form a central thread of the report. Her long-term corticosteroid therapy with prednisolone for active arthritis suppressed her immune system, and she had also received cyclophosphamide, a potent immunosuppressant, as part of her PAN treatment, with monthly injections and methylprednisolone among the medications that may have predisposed her to severe soft tissue infection. She additionally had a history of treated hepatitis C. The vasculitis itself had damaged her peripheral veins to the point that intravenous drugs had to be delivered through a central venous catheter to ensure reliable access. Together, these factors created what the authors describe as an ideal setting for necrotizing fasciitis to develop, underscoring the need for close monitoring in high-risk populations whose immune defenses have been deliberately or pathologically blunted.</p>
<p>Treatment proceeded along the lines that guidelines for necrotizing fasciitis demand, and the sequence mattered. Because of the marked limb swelling and concern about rising compartment pressures, an emergency fasciotomy was performed first to relieve tissue pressure, followed by surgical debridement of devitalized tissue, the acknowledged cornerstone of therapy for this infection. Broad-spectrum intravenous meropenem and levofloxacin were continued postoperatively, with tramadol for pain control and enoxaparin to prevent thrombosis during the recovery period. Negative-pressure wound therapy, commonly known as VAC therapy, was instituted to promote healing and granulation tissue formation, and once healthy granulation tissue had developed and the infection was controlled, the wound was closed by secondary closure without the need for skin grafting. The patient also received clotrimazole for vaginal thrush, a reminder of how immunosuppressed patients can acquire secondary infections even as the primary crisis is being managed.</p>
<p>The outcome was favorable, and the trajectory is instructive. The patient remained clinically stable throughout her postoperative course, was discharged after a five-day hospital stay with instructions for continued wound care, and achieved complete wound healing within approximately three weeks, with no evidence of recurrent infection at follow-up. At her ten-day follow-up she showed significant improvement and no signs of infection. The authors note that the good clinical response to prompt surgical intervention and antimicrobial therapy supports the accuracy of the clinical diagnosis, even though the workup had important gaps. Tissue culture and susceptibility testing were not available, so the causative pathogen was never microbiologically confirmed and therapy remained empiric. Advanced cross-sectional imaging with CT or MRI to delineate the extent of fascial involvement was also not performed, because the team judged that in a patient deteriorating this quickly, delaying definitive management for advanced imaging would have been the greater risk.</p>
<p>Necrotizing fasciitis remains rare, with an estimated incidence of roughly one to two cases per 100,000 person-years, though reported rates vary geographically. The most commonly implicated pathogens are Group A Streptococcus and Staphylococcus aureus, including methicillin-resistant strains, and the infection can be monomicrobial or polymicrobial. Large bullae filled with bloody or yellowish fluid can occur, as in this patient, although the blackened necrotic lesions classically associated with the disease are not always present, and skin darkening is another hallmark. Untreated infection can spread to deeper structures including nerves, causing nerve damage and reduced sensation, and blisters with gas formation suggest Clostridium species. Skin and blood cultures remain critical for pathogen identification, although they may fail, as they did here. The case stands as a vivid reminder that in immunocompromised patients with underlying vascular disease, histological evidence, early clinical recognition, vigorous surgical care, and targeted antimicrobial therapy together form the difference between recovery and catastrophe, and that no laboratory score should be allowed to overrule an experienced clinician&#8217;s alarm.</p>
<p><strong>Subject of Research:</strong> Necrotizing fasciitis occurring in a patient with polyarteritis nodosa</p>
<p><strong>Article Title:</strong> Rare Case of Necrotizing Fasciitis With Polyarteritis Nodosa in a Multi‐Comorbid Patient</p>
<p><strong>Article References:</strong> Hassan, S. M. S., Shahab, S. H., Raza, M., Saleem, S., Hussain, M. F., &amp; Habib, F. (2026). Rare Case of Necrotizing Fasciitis With Polyarteritis Nodosa in a Multi‐Comorbid Patient. <em>Clinical Case Reports, 14</em>(10), Article e73624. <a href="https://doi.org/10.1002/ccr3.73624" rel="noopener noreferrer">https://doi.org/10.1002/ccr3.73624</a></p>
<p><strong>Image Credits:</strong> AI Generated</p>
<p><strong>DOI:</strong> <a href="https://doi.org/10.1002/ccr3.73624" rel="noopener noreferrer">10.1002/ccr3.73624</a></p>
<p><strong>Keywords:</strong> necrotizing fasciitis, polyarteritis nodosa, vasculitis, immunosuppression, fasciotomy, surgical debridement, LRINEC score, soft tissue infection, cyclophosphamide, corticosteroids, negative-pressure wound therapy, case report</p>
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