Low attenuation areas in necrotizing soft tissue infection.

Necrotizing Soft Tissue Infection can be challenging to differentiate from abscesses based on computed tomography imaging findings only, so it is crucial to perform surgical debridement as early as possible.

Monensin poisoning outbreak in free-ranging and captive birds.

Monensin poisoning is uncommon and has been rarely reported in birds. This work aimed to described clinical-pathological aspects of an outbreak of monensin poisoning in captive and free-ranging birds. Thirty-seven of 600 captive birds fed a diet containing 893.19 mg/kg of monensin died within 10 days (mortality 6.17%). There was no ionophore antibiotics on the feed label supplied to captive birds, which established an error in feed production. Necropsies were performed on twelve animals: Muscovy duck (Cairina moschata) (2/12), greater rhea (Rhea americana) (2/12), black-necked swan (Cygnus melancoryphus) (2/12), garganey (Anas querquedula) (1/12), ostrich (Struthio camelus) (1/12), and common pigeon (Columbus livia) (4/12). These four common pigeons were free-ranging birds and died after eating the same contaminated feed. Birds were mainly found dead, however in animals which clinical signs were observed (Columba livia, Rhea americana, Cairina moschata, Anas querquedula, and Struthio camelus), they included incoordination, inability to stand, and intense prostration, that ranged from 24 to 72 h until death. Grossly, five birds had focally extensive pale firm areas in the myocardium and two had in the skeletal muscles, one being concomitant lesions. Histologically, muscle necrosis and degeneration were observed in striated musculature (skeletal and/or heart) in all birds analyzed. Monensin poisoning outbreaks can affect free-ranging birds that are fed on external feeders, as well as captive birds, due to an error in the feed formulation.

Considering the Promise of Vamorolone for Treating Duchenne Muscular Dystrophy.

This commentary provides an independent consideration of data related to the drug vamorolone (VBP15) as an alternative steroid proposed for treatment of Duchenne muscular dystrophy (DMD). Glucocorticoids such as prednisone and deflazacort have powerful anti-inflammatory benefits and are the standard of care for DMD, but their long-term use can result in severe adverse side effects; thus, vamorolone was designed as a unique dissociative steroidal anti-inflammatory drug, to retain efficacy and minimise these adverse effects. Extensive clinical trials (ongoing) have investigated the use of vamorolone for DMD, with two trials also for limb-girdle muscular dystrophies including dysferlinopathy (current), plus a variety of pre-clinical trials published. Vamorolone looks very promising, with similar efficacy and some reduced adverse effects (e.g., related to height) compared with other glucocorticoids, specifically prednisone/prednisolone, although it has not yet been directly compared with deflazacort. Of particular interest to clarify is the optimal clinical dose and other aspects of vamorolone that are proposed to provide additional benefits for membranes of dystrophic muscle: to stabilise and protect the sarcolemma from damage and enhance repair. The use of vamorolone (and other glucocorticoids) needs to be evaluated in terms of overall long-term efficacy and cost, and also in comparison with many candidate non-steroidal drugs with anti-inflammatory and other benefits for DMD.

Pterygoid Muscle Necrosis Caused by Radiation and Intra-Arterial Cisplatin Infusion Chemotherapy (RADPLAT): A Case Report.

Introduction: Radiation and intra-arterial cisplatin infusion chemotherapy (RADPLAT) for advanced maxillary sinus cancer has accumulated evidence as a treatment with fewer complications and better 5-year survival rates. In this study, we report a case in which pterygoid muscle necrosis occurred 6 months following RADPLAT treatment for maxillary sinus cancer. Case Presentation: The 45-year-old woman had a long history of taking immunosuppressants against rheumatoid arthritis (RA) prior to treatment. Although achieving complete response (CR) to RADPLAT, the patient developed trismus (1 fingerbreadth or less) 6 months following treatment. Abscess formation and recurrence were suspected from the imaging findings; however, the biopsy with endoscopy indicated necrotic tissue. Currently, 18 months have passed without cancer recurrence. Although trismus temporarily improved with rehabilitation, the width of the mouth opening is currently a few millimeters, so the patient can only take liquid food. Conclusion: Pterygoid muscle necrosis should be recognized as a new major complication.

Spontaneous Development of Immune-Mediated Necrotizing Myopathy (IMNM) After Chronic Use of Statins: A Case Report.

Statin medications, in addition to lifestyle modifications, have been the regimen of choice for addressing dyslipidemia in the general population. Its widespread use has been justified by increasing evidence that hyperlipidemia is a strong risk factor for the development of atherosclerotic disease resulting in myocardial infarction and other cardiovascular events. Unfortunately, this medication is not tolerated by some patients as it causes uncomfortable side effects such as myalgias, arthralgias, and headaches to name a few.  On rare occasions, some patients may develop immunity against the medication itself resulting in a condition known as immune-mediated necrotizing myopathy (IMNM). In such instances, patients carry antibodies against 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) or signal recognition particle (SRP). A small subset of patients may develop IMNM even in the absence of these two antibodies and they are termed seronegative. In this care report, we review the case of a 55-year-old Hispanic male with a history of Hashimoto's thyroiditis and hyperlipidemia who presented to an outpatient rheumatology office for severe proximal muscle weakness after being asymptomatic on rosuvastatin for over 20 years. The patient was stabilized with high-dose steroids and was subsequently given a regimen of mycophenolate and intravenous immunoglobulin (IVIG). He was able to regain approximately 75%-80% of his baseline muscle strength.

Missense mutation of c.635 T > C in CAPN3 impairs muscle injury repair in a Limb-Girdel Muscular Dystropy Model.

Limb-girdle muscular dystrophy recessive 1 (LGMDR1), previously known as LGMD2A, is a specific LGMD caused by a gene mutation encoding the calcium-dependent neutral cysteine protease calpain-3 (CAPN3). In our study, the compound heterozygosity with two missense variants c.635 T > C (p.Leu212Pro) and c.2120A > G (p.Asp707Gly) was identified in patients with LGMDR1. However, the pathogenicity of c.635 T > C has not been investigated. To evaluate the effects of this novel likely pathogenic variant to the motor system, the mouse model with c.635 T > C variant was prepared by CRISPR/Cas9 gene editing technique. The pathological results revealed that a limited number of inflammatory cells infiltrated the endomyocytes of certain c.635 T > C homozygous mice at 10 months of age. Compared with wild-type mice, motor function was not significantly impaired in Capn3 c. 635 T > C homozygous mice. Western blot and immunofluorescence assays further indicated that the expression levels of the Capn3 protein in muscle tissues of homozygous mice were similar to those of wild-type mice. However, the arrangement and ultrastructural alterations of the mitochondria in the muscular tissues of homozygous mice were confirmed by electron microscopy. Subsequently, muscle regeneration of LGMDR1 was simulated using cardiotoxin (CTX) to induce muscle necrosis and regeneration to trigger the injury modification process. The repair of the homozygous mice was significantly worse than that of the control mice at day 15 and day 21 following treatment, the c.635 T > C variant of Capn3 exhibited a significant effect on muscle regeneration of homozygous mice and induced mitochondrial damage. RNA-sequencing results demonstrated that the expression levels of the mitochondrial-related functional genes were significantly downregulated in the mutant mice. Taken together, the results of the present study strongly suggested that the LGMDR1 mouse model with a novel c.635 T > C variant in the Capn3 gene was significantly dysfunctional in muscle injury repair via impairment of the mitochondrial function.

A biomaterial-based therapy for lower limb ischemia using Sr/Si bioactive hydrogel that inhibits skeletal muscle necrosis and enhances angiogenesis.

Muscle necrosis and angiogenesis are two major challenges in the treatment of lower-limb ischemic diseases. In this study, a triple-functional Sr/Si-containing bioceramic/alginate composite hydrogel with simultaneous bioactivity in enhancing angiogenesis, regulating inflammation, and inhibiting muscle necrosis was designed to treat lower-limb ischemic diseases. In particular, sodium alginate, calcium silicate and strontium carbonate were used to prepare injectable hydrogels, which was gelled within 10 min. More importantly, this composite hydrogel sustainedly releases bioactive Sr2+ and SiO3 2- ions within 28 days. The biological activity of the bioactive ions released from the hydrogels was verified on HUVECs, SMCs, C2C12 and Raw 264.7 cells in vitro, and the therapeutic effect of the hydrogel was confirmed using C57BL/6 mouse model of femoral artery ligation in vivo. The results showed that the composite hydrogel stimulated angiogenesis, developed new collateral capillaries, and re-established the blood supply. In addition, the bioactive hydrogel directly promoted the expression of muscle-regulating factors (MyoG and MyoD) to protect skeletal muscle from necrosis, inhibited M1 polarization, and promoted M2 polarization of macrophages to reduce inflammation, thereby protecting skeletal muscle cells and indirectly promoting vascularization. Our results indicate that these bioceramic/alginate composite bioactive hydrogels are effective biomaterials for treating hindlimb ischemia and suggest that biomaterial-based approaches may have remarkable potential in treating ischemic diseases.

Predictors of muscle necrosis in patients with acute compartment syndrome.

PURPOSE: The predictors of muscle necrosis after acute compartment syndrome (ACS) remain debated. This study aimed to investigate the predictors for muscle necrosis in ACS patients. METHODS: We collected data on ACS patients following fractures from January 2010 to November 2022. Patients were divided into the muscle necrosis group (MG) and the non-muscle necrosis group (NG). The demographics, comorbidities, and admission laboratory indicators were computed by univariate analysis, logistic regression analysis, and receiver-operating characteristic (ROC) curve analysis. RESULTS: In our study, the rate of MN was 37.6% (83 of 221). Univariate analysis showed that numerous factors were associated with muscle necrosis following ACS. Logistic regression analysis indicated that crush injury (p = 0.007), neutrophil (NEU, p = 0.001), creatine kinase myocardial band (CKMB, p = 0.047), and prothrombin time (PT, p = 0.031) were risk factors. Additionally, ROC curve analysis identified 11.415 109/L, 116.825 U/L, and 12.51 s as the cut-off values for NEU, CKMB, and PT to predict muscle necrosis, respectively. Furthermore, the combination of NEU, CKMB, and PT had the highest diagnostic accuracy. CONCLUSIONS: Our findings showed that crush injury and the level of NEU, CKMB, and PT were risk factors for muscle necrosis after ACS. Additionally, we also identified the cut-off values of NEU, CKMB, and PT and found the combination of crush injury, PT, and NEU with the highest diagnostic accuracy, helping us individualize the assessment risk of muscle necrosis to manage early targeted interventions.

High prevalence of necrotizing myofibers in adult dermatomyositis muscle biopsies.

INTRODUCTION/OBJECTIVES: This study aimed to analyze the presence, grade, and relevance of myofiber necrosis in the muscle tissues of patients with adult dermatomyositis. Second, these parameters were associated with the patients' demographic, clinical, and laboratory data. METHOD: This was a retrospective study, from 2001 to 2021, which included 89 muscle biopsies of patients with definite dermatomyositis performed at the time of diagnostic investigation. Immunohistochemical analysis was performed on serially frozen muscle sections. The presence and degree of endomysial/perifascicular myofiber necrosis were also analyzed. The degree of necrosis was semi-quantitatively coded as absent/mild, moderate, or severe. The presence or absence of perifascicular atrophy and also perivascular lymphomononuclear infiltration was also evaluated. RESULTS: Muscle biopsies from 89 patients, the majority of whom were Caucasian women, were evaluated. Both perifascicular atrophy and perivascular lymphomononuclear infiltrates were observed in 76 (85.4%) samples. Moderate or intense areas of myofiber necrosis in endomysial/perifascicular areas were found in 30/89 (33.7%) and 14/89 (15.7%) muscle biopsies, respectively, with a predominance of macrophagic infiltrate in relation to lymphomononuclear cells in these regions. The degree of muscle weakness in the limbs (upper and lower) was associated only with areas of intense myofiber necrosis. CONCLUSIONS: A high prevalence of myofiber necrosis was observed, which patients resembled the initial clinical feature of patients with immune-mediated necrotizing myopathies. Key Point • A high prevalence of myofiber necrosis was observed in muscle biopsies of patients with dermatomyositis.

Statin-induced necrotizing autoimmune myopathy: a systematic review.

Statins are a class of lipid-lowering medications used worldwide by millions of people and are safe for frequent use in most patients. However, they cause necrotizing autoimmune myopathy in some patients. We reviewed case reports of 80 patients from 2010 to present diagnosed with statin-induced necrotizing autoimmune myopathy (SINAM), aiming to analyze the clinical, physiological, serologic characteristics and outcomes of SINAM. The mean age of these patients was 66 ±9.4, the majority being male (61.3%). All patients reported proximal muscle weakness, and a few had myalgias, extra muscular symptoms such as dysphagia, and pulmonary complications. Most of the patients were on atorvastatin, simvastatin, or rosuvastatin. The mean creatine kinase was 10,094.2 ±7,351.7 U/l, and anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase enzyme was positive for 93.8% of patients. The majority of patients were started on steroids; other treatments were also used. Prompt cessation of statins and initiation of immunosuppressants reduced morbidity and mortality.

Fiber optic Raman spectroscopy for the evaluation of disease state in Duchenne muscular dystrophy: An assessment using the mdx model and human muscle.

INTRODUCTION/AIMS: Raman spectroscopy is an emerging technique for the evaluation of muscle disease. In this study we evaluate the ability of in vivo intramuscular Raman spectroscopy to detect the effects of voluntary running in the mdx model of Duchenne muscular dystrophy (DMD). We also compare mdx data with muscle spectra from human DMD patients. METHODS: Thirty 90-day-old mdx mice were randomly allocated to an exercised group (48-hour access to a running wheel) and an unexercised group (n = 15 per group). In vivo Raman spectra were collected from both gastrocnemius muscles and histopathological assessment subsequently performed. Raman data were analyzed using principal component analysis-fed linear discriminant analysis (PCA-LDA). Exercised and unexercised mdx muscle spectra were compared with human DMD samples using cosine similarity. RESULTS: Exercised mice ran an average of 6.5 km over 48 hours, which induced a significant increase in muscle necrosis (P = .03). PCA-LDA scores were significantly different between the exercised and unexercised groups (P < .0001) and correlated significantly with distance run (P = .01). Raman spectra from exercised mice more closely resembled human spectra than those from unexercised mice. DISCUSSION: Raman spectroscopy provides a readout of the biochemical alterations in muscle in both the mdx mouse and human DMD muscle.

Rhabdomyolysis, myoglobinuric nephrosis, and crystalline nephropathy in a captive bottlenose dolphin.

A 5-y-old female bottlenose dolphin (Tursiops truncatus) from an aquarium in Japan had clinical signs of anorexia, vomiting, and bradykinesia. Enrofloxacin and lactated Ringer solution were administered for treatment of bacterial infection and for rehydration. Elevations of creatine kinase and aspartate aminotransferase activities were detected on day 4 of treatment, indicating that rhabdomyolysis had developed on day 3. On day 5, serum creatinine and urea concentrations increased and remained high throughout the remaining treatment; the dolphin died on day 16. Postmortem examination revealed massive necrosis of the longissimus dorsi muscles. Histologic examination revealed extensive necrosis of skeletal myofibers, multifocal renal tubular necrosis with intratubular casts and crystals, and suppurative bronchopneumonia. The renal casts labeled positively with anti-myoglobin antibody; expression of aquaporin-1 was decreased in renal tubules compared to normal kidney tissue. To our knowledge, this description of clinicopathologic findings of rhabdomyolysis leading to acute kidney injury with concomitant crystalline nephropathy has not been reported previously in a bottlenose dolphin.

Biomarkers for Duchenne muscular dystrophy: myonecrosis, inflammation and oxidative stress.

Duchenne muscular dystrophy (DMD) is a lethal, X-linked disease that causes severe loss of muscle mass and function in young children. Promising therapies for DMD are being developed, but the long lead times required when using clinical outcome measures are hindering progress. This progress would be facilitated by robust molecular biomarkers in biofluids, such as blood and urine, which could be used to monitor disease progression and severity, as well as to determine optimal drug dosing before a full clinical trial. Many candidate DMD biomarkers have been identified, but there have been few follow-up studies to validate them. This Review describes the promising biomarkers for dystrophic muscle that have been identified in muscle, mainly using animal models. We strongly focus on myonecrosis and the associated inflammation and oxidative stress in DMD muscle, as the lack of dystrophin causes repeated bouts of myonecrosis, which are the key events that initiate the resultant severe dystropathology. We discuss the early events of intrinsic myonecrosis, along with early regeneration in the context of histological and other measures that are used to quantify its incidence. Molecular biomarkers linked to the closely associated events of inflammation and oxidative damage are discussed, with a focus on research related to protein thiol oxidation and to neutrophils. We summarise data linked to myonecrosis in muscle, blood and urine of dystrophic animal species, and discuss the challenge of translating such biomarkers to the clinic for DMD patients, especially to enhance the success of clinical trials.

EVALUATION OF LOCALIZED INFLAMMATORY REACTIONS SECONDARY TO INTRAMUSCULAR INJECTIONS OF ENROFLOXACIN IN STRIPED BASS (MORONE SAXATILIS).

Enrofloxacin is a fluoroquinolone widely used in animals including fish. Intramuscular (IM) injection of enrofloxacin is a feasible and efficacious option for drug delivery. In many species IM injection has been associated with injection site reactions and increases in serum muscle enzymes. Injection site reactions have not been well characterized in fish. Three groups of striped bass (Morone saxatilis) received an IM injection of enrofloxacin 2.27% in the right epaxial musculature 24, 48, or 96 hr prior to evaluation. Mean dose was 7.69 mg/ kg (6.14-9.69 mg/kg). The 24- and 48-hr groups received an injection of equal-volume 0.9% saline in the left epaxial musculature. A corresponding noninjected tissue sample was designated in the left epaxial musculature from each fish of the 96-hr group. Fish were euthanized and injection sites and noninjection control sites were evaluated grossly and histologically. Grades 1-4 were assigned to samples, with grade 1 corresponding to normal tissue and grades 2, 3, and 4 corresponding to mild, moderate, and severe inflammation and/or necrosis respectively. Externally, all control and injection sites appeared visually unremarkable. On cut surface, epaxial muscle of the enrofloxacin-injected tissue appeared moderately to severely hemorrhagic compared to saline and noninjected tissue, which was normal or mildly hemorrhagic. Histologically, eight of eight noninjected tissues were grade 1. For saline-injected tissues, 14 of 16 tissues were grade 2 and 2 samples were grade 3 when 24- and 48-hr groups were combined. For enrofloxacin-injected tissues, 8 of the 8 24-hr samples were grade 3 and 16 of the 16 48- and 96-hr samples were grade 4. These data show that IM injection of enrofloxacin 2.27% is associated with severe hemorrhage, necrosis, and inflammation in striped bass, and may negatively affect animal welfare.

Potentially serious adverse effects from application of a circumferential compression device for pelvic fracture: A report of three cases.

Pelvic circumferential compression devices (PCCDs) have gained wide acceptance in the management of patients with pelvic fracture. These devices are considered safe due to their noninvasive nature and significant hazards associated with the use of PCCDs have not been reported previously. However, we present herein the cases of three patients who received PCCD application and eventually developed major complications presumably caused by PCCDs. As a result, one patient developed surgical site infection following internal fixation and required several debridements. Another patient ended up with a walking disability. The remaining patient eventually died from exsanguination following application of the PCCD. Clinicians should be aware of the potential for deleterious effects, including bladder rupture, muscle necrosis, and vessel injuries. In particular, application for acetabular fractures and prolonged application of PCCDs should be avoided.

Necrotizing myositis: highlighting the hidden depths - case series and review of the literature.

BACKGROUND: Necrotizing myositis (NM) is a life-threatening emergency. It causes focal muscle necrosis without abscess formation or extensive involvement of the overlying fascia and soft tissue. It is a clinical diagnosis requiring a high index of clinical suspicion. Usual presentation can readily be mistaken to represent more benign pathologies such as muscular injury, viral myopathy or deep venous thrombosis. The clinical course following initial misdiagnosis is rapid deterioration into profound sepsis and progressive multiorgan failure. Prompt treatment is associated with favourable outcomes, but early diagnosis is challenging due to initial absence of cutaneous signs and symptoms. Delayed referral to surgeons with appropriate expertise results in higher morbidity and mortality. The cornerstones to treatment are complete surgical debridement, intensive care management and accurate antimicrobial therapy. METHODS: We report four cases of NM demonstrating classical scenarios of initial misdiagnosis, delays in referral and review by an experienced surgeon. A review of the current literature to aid with overall management is also included. RESULTS: Review of literature that revealed the most common presentation was antecedent prodromal flu-like symptoms followed by rapidly progressing focal muscle pain. Patients were initially misdiagnosed followed by rapid deterioration into profound sepsis before surgical opinion was obtained. CONCLUSION: NM is a rare and potentially fatal disease that must be considered in the differential diagnoses of the young, healthy patient with acute limb pain and fever. A high index of suspicion will facilitate earlier management and reduce morbidity and mortality.

Predicting factors of muscle necrosis in acute compartment syndrome of the lower extremity.

BACKGROUND: Acute physiologic compartment syndrome (ACS) is a disorder of increased intra-compartmental pressure leading to decreased tissue perfusion and muscle necrosis. Tissue ischemia can result in irreversible muscle and nerve injury and requires urgent fasciotomy. The aim of this study was to determine the factors associated with the presence of necrotic muscle in patients undergoing leg fasciotomy. METHODS: This is a retrospective cohort study of all patients undergoing fasciotomies for ACS of the leg at two level 1 trauma centers from 2000 to 2015. We found 1,028 patients who underwent leg fasciotomies. We excluded ACS at other sites than the leg, the index fasciotomy performed at an outside institution, prophylactic fasciotomy with no clinical signs of ACS, and patients with inadequate medical records. A total of 357 patients were included in the final analysis. We used bivariate analysis to assess which explanatory variables are associated with the main outcome measure, the presence of necrotic muscle at fasciotomy. We used multivariable regression analysis to determine association accounting for any confounding. RESULTS: Of 357 cases of ACS of the leg, 14.6% of patients presented with an open fracture and 21.3% of patients were multiply injured. Overall, 14.3% of cases had muscle necrosis at the time of fasciotomy. Fifty-nine percent of patients with necrotic muscle required more than 3 debridements. Open fracture was the only statistically significant predictor of muscle necrosis (OR=2.8). Crush injury (OR=3.1) and soft tissue injuries (OR=2.8) were at an increased odds of necrotic muscle, but only marginally significant. CONCLUSION: ACS is a potentially limb threatening condition often associated with poor outcomes, particularly when the diagnosis is delayed. Patients with open fracture have a three-fold increase in odds of necrotic muscle at the time of fasciotomy.

Outbreak of monensin poisoning in cattle due to supplementation error / Surto de intoxicação por monensina em bovinos devido a erro de suplementação

ABSTRACT: Iatrogenic intoxications occur in domestic animals. Mortality was observed in a group of calves, reaching 20 deaths until the day of the technical visit, with or without sudden clinical signs, on a farm in the city of Pires do Rio, State of Goiás, Brazil. Deaths after the visit were not accounted systematically. Clinical signs included muscle weakness, ataxia, recumbency, bilateral jugular distention, and death. Suspected diagnosis of poisoning by ionophore antibiotics was made based on clinical and laboratory findings from nine animals, which included high plasma CK and LDH levels, as well as on anatomopathological findings of a recently dead calf, which showed myocardial and skeletal muscle degeneration and necrosis. Monensin overdose (25.5 µg/kg in skeletal muscle and 209.4 µg/kg in the liver) was detected by liquid-chromatography and mass-spectrophotometry analysis, contributing to the confirmation of ionophore poisoning diagnosis.

RESUMO: Intoxicações iatrogênicas ocorrem em animais domésticos. Um lote de bezerros apresentou mortalidade, chegando a 20 mortes até o dia da visita técnica, após sinais clínicos súbitos ou ausência destes, em uma propriedade rural do município de Pires do Rio, estado de Goiás, Brasil. As mortes após a visita não foram sistematicamente contabilizadas. Os sinais incluíam fraqueza muscular, ataxia, decúbito, distensão bilateral da veia jugular e morte. Baseado nos achados clínicos e laboratoriais de nove bovinos, que incluíram níveis de CK e LDH elevados no plasma, assim como degeneração e necrose miocárdica e na musculatura esquelética à avaliação anatomopatológica em um dos bezerros mortos, que apresentou degeneração e necrose em miocárdio e músculo esquelético. Uma sobredosagem de monensina (25,5 µg/g no músculo esquelético e 209,4 µg/g no fígado) foi detectada com análise por cromatografia líquida e espectrofotometria de massas, contribuindo para a confirmação do diagnóstico de intoxicação por ionóforos.

Modified bridle tendon transfer procedure following a complete musculature loss of the anterior leg compartment: Case report and literature review.

The complete musculature loss of the anterior compartment of the leg is a rare complication that occurs as a result of local tissue damage, intracompartmental bleeding and ischemia-reperfusion events. It causes foot drop and equinovarus deformity that negatively impact the quality of life of affected patients. This report describes a modified bridle tendon transfer procedure to correct this defect in a case of extensive muscle necrosis secondary to local hemorrhage. A review of the literature was carried out to elucidate the benefits and risks associated to this technique.