Muscle Necrosis Research Articles

Chronic Wound Infection Model of Acinetobacter baumannii in Outbred Mice.

We established a murine wound infection model with doxycycline treatment against multidrug-resistant Acinetobacter baumannii (AB5075) in Institute of Cancer Research (ICR) outbred mice. Using three groups of neutropenic ICR mice, two full-thickness dorsal dermal wounds (6 mm diameter) were made on each mouse. In two groups, wounds were inoculated with 7.0 × 104 colony-forming units of AB5075. Of these two groups, one received a 6-day regimen of doxycycline while the other was sham treated with phosphate-buffered saline as placebo control. Another uninfected/untreated group served as a control. Wound closure, clinical symptoms, bacterial burden in wound beds and organs, and wound histology were investigated. Doxycycline-treated wounds completely healed by day 21, but untreated, infected wounds failed to heal. Compared to controls, wound infections without treatment resulted in significant reductions in body weight and higher bacterial loads in wound beds, lung, liver, and spleen by day 7. Histological evaluation of wounds on day 21 revealed ulcerated epidermis, muscle necrosis, and bacterial presence in untreated wounds, while wounds treated with doxycycline presented intact epidermis. Compared to the previously developed BALB/c dermal wound model, this study demonstrates that the mouse strain selected impacts wound severity and resolution. Furthermore, this mouse model accommodates two dorsal wounds rather than only one. These variations offer investigators increased versatility when designing future studies of wound infection. In conclusion, ICR mice are a viable option as a model of dermal wound infection. They accommodate two simultaneous dorsal wounds, and upon infection, these wounds follow a different pattern of resolution compared to BALB/c mice.

RABDOMYOLYSIS CAUSED BY EXERCISE

INTRODUCTION: Rhabdomyolysis is a clinical and paraclinical syndrome characterized by the presence of skeletal muscle necrosis that leads to the consequent release of intracellular muscle components with a variable clinical presentation and complications that put life at risk such as acute kidney injury
 METHODS: We present a case report of a patient with a rhabdomyolysis with a severe elevation of muscle enzymes and secondary acute kidney injury who was subsequently documented (initial Total CK 189,000 u/L) after extreme physical activity (CrossFit), who developed multiple complications and the need for support in the Intensive Care Unit (ICU) with satisfactory outcome.
 RESULTS: Patient with and kidney failure, receiving renal therapy with a favorable evolution and survival at discharge from the intensive care unit of a third-level hospital in the city of Pereira, Risaralda, Colombia.
 CONCLUSIONS: Rhabdomyolysis is a clinical and paraclinical syndrome characterized by the presence of skeletal muscle necrosis. The main cause is a severe direct traumatic injury or crushes injuries, however, other conditions such as infections, intoxication, muscle ischemia, neuroleptic malignant syndrome, malignant hyperthermia, metabolic disorders, and genetic pathologies can also cause it, and particularly the Prolonged rest or immobilization or strenuous exercise. The clinical presentation and complicatios are variable.

The Past, Present, and Future of Deep-Tissue (Pressure) Injury.

The Past, Present, and Future of Deep-Tissue (Pressure) Injury.

Unfathomed Dangers from Aluminum — Alzheimer’s? Autism? Multiple Sclerosis?

That aluminum is fatally toxic is beyond doubt, demonstrated by mass human poisoning at Camelford in Cornwall in Britain in 1988 (chapter 18) and by occasional fish kills (p. 49). Aluminum may also be a contributing factor in a number of human diseases, in particular those involving brain and nerves (p. 124) — autism, Alzheimer’s disease (AD) (chapter 14), Parkinson’s disease, multiple sclerosis. Aluminum salts used in kidney dialysis may be responsible for dialysis-related encephalopathy (pp. 38, 79).
 Aluminum adjuvants in vaccine can cause macrophagic myofasciitis (MMF: inflammation and associated microscopic muscle necrosis at the injection site) as well as such whole-body ailments as chronic fatigue syndrome and marked cognitive deficits (Rigolet et al. 2014); one middle-aged individual injected with five aluminum-adjuvanted vaccines within 4 weeks became work-disabled (pp. 72-73).
 Studying the possible dangers associated with aluminum adjuvants in vaccines is complicated by the fact that aluminum acts as an antigen as well as an adjuvant — the immune system generates antibodies against aluminum itself, so that later exposures to aluminum might produce an antibody cascade capable of damaging any of the tissues in which aluminum had accumulated (pp. 73-76).
 Christopher Exley has studied aluminum in relation to human health for some 35 years. This book summarizes his work and cites the pertinent primary publications (some 200) in appropriate peer-reviewed journals. The book also offers quite convincing evidence of the determined efforts by a variety of vested interests to disparage and suppress Exley’s work and findings.
 In my opinion, the published work summarized in this book makes a plausible case based on empirical evidence that aluminum may be a contributing causative factor in neurological and nerve diseases. Further, Exley suggests fully detailed mechanisms and quite plausible for how that comes about. Beyond that, he points to a quite fundamental a priori reason why aluminum, among all the other elements and metals, might be so uniquely dangerous. It is the third most abundant element in the Earth’s crust (after oxygen and silicon), yet there are no known biological uses of aluminum. By contrast, several other metals and non-metals are essential components of some biological systems, for example, iron in hemoglobin in blood (pp. 5-6, 11). Those two facts make it far from implausible that absorption of aluminum could be biologically harmful, by competing with or replacing other metals, or perhaps just because of its chemically oxidative properties.
 But if all that is so, how has the Earth’s biosphere flourished for billions of years without succumbing to the toxicity of the super-abundant aluminum?

A Case of Left Ventricular Free Wall Rupture with Suspected Posterior Papillary Muscle Necrosis

A Case of Left Ventricular Free Wall Rupture with Suspected Posterior Papillary Muscle Necrosis

High prevalence of necrotising myopathy pattern in muscle biopsies of patients with anti-Jo-1 antisynthetase syndrome.

Until now, researchers have not provided a well-defined muscle histological pattern for antisynthetase syndrome (ASSD). Therefore, we aimed to analyse the muscle biopsies of patients with anti-Jo-1 ASSD. This study included 26 patients with anti-Jo-1 ASSD admitted for investigation of the disease and obligatorily with muscle impairment, from 2010 to 2021, whose serial frozen muscle sections were analysed. Patients' mean age at disease diagnosis was 42.8±11.6 years, and the female gender was most predominant. Concerning muscle biopsies, cell infiltrates were present in 76.9% of the samples, and they were mainly located at the endomysium area (70%), with a predominance of macrophages (92.9%). Fiber muscle necrosis was present in 92.3% and was diffused in 54.2%. Expression of MHC-I was seen in all samples. Samples were mostly marked by the presence of CD68+ and discreet/low CD4+ and CD8+ staining, which is consistent with a higher predominance of observed necrosis and macrophage cell infiltrates. In general, 38.5% of patients had a necrotising myopathy pattern in muscle biopsies, whereas 34.6% and 26.9% had a general inflammatory myopathy pattern and nonspecific myopathy, respectively. This necrotising myopathy pattern was not associated with the demographic, clinical, or laboratory data. Our data show that almost 40% of patients with well-defined anti-Jo-1 ASSD with objective muscle impairment have a necrotising myopathy pattern in their muscle biopsies. Although this pattern is more classically related to immune-mediated necrotising myopathies, in association with clinical manifestations and the presence of anti-Jo-1 autoantibodies, this characteristic may lead to ASSD diagnosis.

Macrophage plasticity in Duchenne muscular dystrophy: a nexus of pathological remodelling with therapeutic implications.

Duchenne muscular dystrophy (DMD) is characterized by chronic skeletal muscle necrosis, leading to muscle regeneration failure and fibrosis. Although macrophages (MPs) are normally essential for muscle regeneration, dysregulated MP function promotes pathological muscle remodelling. Infiltrating MPs can be predominantly pro-inflammatory (M1 biased), anti-inflammatory (M2 biased) or of a mixed phenotype and can originate from the adult bone marrow (monocyte dependent) or embryonic precursors (monocyte independent). In mdx mice (genetic model of DMD) lacking either Toll-like receptor (Tlr) 2 or Tlr4, it is found that MP infiltration of dystrophic muscle is significantly reduced and that the MP phenotype is shifted toward a more anti-inflammatory profile. This is accompanied by significant improvements in muscle histology and force production. Lack of the chemokine receptor CCR2, which impedes monocyte release from the bone marrow, leads to similar beneficial effects in mdx mice. Evidence was also found for Tlr4-regulated induction of trained innate immunity in MPs cultured from the bone marrow of mdx mice before their entry into the muscle. These MPs exhibit epigenetic and metabolic alterations, accompanied by non-specific hyper-responsiveness to multiple stimuli, which is manifested by potentiated upregulation of both pro- and anti-inflammatory genes. In summary, exaggerated recruitment of monocyte-derived MPs and signs of trained innate immunity at the level of the bone marrow are features of the immunophenotype associated with dystrophic muscle disease. These phenomena are regulated by Toll-like receptors that bind endogenous damage-associated molecular pattern (DAMP) molecules, suggesting that DAMP release from dystrophic muscles modulates MP plasticity at the bone marrow level through Toll-like receptor-driven mechanisms.

Possibility of Multiple Drug-Drug Interactions in Patients Treated with Statins: Analysis of Data from the Japanese Adverse Drug Event Report (JADER) Database and Verification by Animal Experiments.

Adverse drug events due to drug-drug interactions can be prevented by avoiding concomitant use of causative drugs; therefore, it is important to understand drug combinations that cause drug-drug interactions. Although many attempts to identify drug-drug interactions from real-world databases such as spontaneous reporting systems have been performed, little is known about drug-drug interactions caused by three or more drugs in polypharmacy, i.e., multiple drug-drug interactions. Therefore, we attempted to detect multiple drug-drug interactions using decision tree analysis using the Japanese Adverse Drug Event Report (JADER) database, a Japanese spontaneous reporting system. First, we used decision tree analysis to detect drug combinations that increase the risk of rhabdomyolysis in cases registered in the JADER database that used six statins. Next, the risk of three or more drug combinations that significantly increased the risk of rhabdomyolysis was validated with in vivo experiments in rats. The analysis identified a multiple drug-drug interaction signal only for pitavastatin. The reporting rate of rhabdomyolysis for pitavastatin in the JADER database was 0.09, and it increased to 0.16 in combination with allopurinol. Furthermore, the rate was even higher (0.40) in combination with valsartan. Additionally, necrosis of leg muscles was observed in some rats simultaneously treated with these three drugs, and their creatine kinase and myoglobin levels were elevated. The combination of pitavastatin, allopurinol, and valsartan should be treated with caution as a multiple drug-drug interaction. Since multiple drug-drug interactions were detected with decision tree analysis and the increased risk was verified in animal experiments, decision tree analysis is considered to be an effective method for detecting multiple drug-drug interactions.

A Biomaterial-Based Therapy for Lower Limb Ischemia Using Sr/Si Bioactive Hydrogel by Inhibiting Skeletal Muscle Necrosis and Enhancing Angiogenesis

A Biomaterial-Based Therapy for Lower Limb Ischemia Using Sr/Si Bioactive Hydrogel by Inhibiting Skeletal Muscle Necrosis and Enhancing Angiogenesis

Olanzapine Induced Rhabdomyolysis in A Schizophrenic Adult: Case Report

Rhabdomyolysis is a syndrome characterized by acute necrosis of skeletal muscle and subsequent release of its cellular contents into the circulation. It can occur due to trauma, exercise, infections and some metabolic diseases, as well as secondary to the use of various drugs. A 34-year-old male patient with a diagnosis of schizophrenia for 2 months was brought to our emergency department by his relatives because of the intake of 350 mg of olanzapine for suicide. The patient whose extrapyramidal system findings were present and whose creatine kinase (CK) was found to be 42670 U / L in laboratory tests was hospitalized to our service because of the secondary rhabdomyolysis for the use of olanzapine. During the hospitalization period, only the medical treatment returned normalcy to the CK level, and the kidney and liver dysfunction did not develop, and the patient was discharged by psychiatric outpatient clinic control. Rhabdomyolysis is a rare and potentially serious adverse drug reaction to antipsychotic drugs. The patients should be evaluated for side effects and in terms of rhabdomyolysis facilitating factors. Especially in high doses, patients should be monitored for rhabdomyolysis, which is a serious complication, such as acute renal damage.

Cholesterol absorption blocker ezetimibe prevents muscle wasting in severe dysferlin-deficient and mdx mice.

BackgroundMuscular dystrophy (MD) causes muscle wasting and is often lethal in patients due to a lack of proven therapies. In contrast, mouse models of MD are notoriously mild. We have previously shown severe human‐like muscle pathology in mdx [Duchenne MD (DMD)] and dysferlin‐deficient limb‐girdle MD type 2B (LGMD2B) mice by inactivating the gene encoding for apolipoprotein E (ApoE), a lipid transporter synthesized by the liver, brain and adipocytes to regulate lipid and fat metabolism. Having recently established that human DMD is a novel type of primary genetic dyslipidaemia with elevated cholesterol, we sought to determine whether cholesterol could exacerbate the muscle wasting process observed in severe rodent MD.MethodsSevere mdx and dysferlin knock‐out mice lacking ApoE were treated with ezetimibe (15 mg/kg/day), a clinically approved drug exhibiting few pleiotropic effects. In separate studies, dietary cholesterol was raised (from 0.2% to 2% cholesterol) in combination with experimental micro‐injury and direct cholesterol injection assays. Muscles were assessed histologically for changes in collagen and adipocyte infiltration and both transcriptomic and cellular changes by RNA‐seq and fluorescence‐activated cell sorting analysis.ResultsTreatment of severe DMD and LGMD2B mice with ezetimibe completely prevented clinical signs of ambulatory dysfunction (0% incidence vs. 33% for vehicle treatment; P < 0.05). Histological analyses revealed that ezetimibe‐reduced fibro‐fatty infiltration up to 84% and 63% in severely affected triceps (P ≤ 0.0001) and gastrocnemius (P ≤ 0.003) muscles, resulting in a respective 1.9‐fold and 2.2‐fold retention of healthy myofibre area (P ≤ 0.0001). Additionally, raising dietary cholesterol and thus concentrations of plasma low‐density lipoprotein‐associated cholesterol (by 250%; P < 0.0001) reduced overall survivability (by 100%; P < 0.001) and worsened muscle damage in the LGMD2B triceps by 767% (P < 0.03). Micro‐pin‐induced mechanical injury in LGMD2B mice fed a high cholesterol diet exacerbated muscle damage by 425% (P < 0.03) and increased macrophage recruitment (by 98%; P = 0.03) compared with those injured on a chow diet. Parallel RNA‐seq analyses revealed that injury in cholesterol‐fed mice also modulated the expression of 3671 transcripts (1953 up‐regulated), with fibrogenic, inflammatory and programmed cell death‐associated pathways among the most enriched. Mice lacking dysferlin also displayed heightened muscle necrosis (by 123%; P < 0.0001) following a direct intramuscular injection of cholesterol compared with control mice.ConclusionsCholesterol exacerbates rodent MD. Specific inhibition of cholesterol absorption with ezetimibe may safely attenuate human MD severity and delay death.

Influence of Methomyl (Copter 90%) on certain biochemical activities and histological structures of land snails Monacha cartusiana

This manuscript was conducted to spotlight the toxic effect of two sub-lethal concentrations of Methomyl (Copter) LC20 (0.075 g/L) and LC40 (0.180 g/L) on some biochemical parameters and histological alterations for land snail Monacha Cartusiana (Muller, 1774). Land snails belong to the class Gastropoda and Phylum Mollusca. This study cleared that both the used concentrations (of Copter) caused a significant increase for activities of three enzymes: alkaline phosphatase (ALP), alanine amino transaminase (ALT), and Aspartate amino transaminase (AST) after 24, 48, and 72 h from exposure starting. In contrast, a total protein (TP) activity decreased at exposure for two concentrations at all lethality periods. Both concentrations of Copter (0.0.75 g/L and 0.180 g/L) have shown histological changes for land snail tissues after 96 h of exposure; digestive gland, hermaphrodite gland, foot, and mantle. Degeneration, rupture, and vacuolization for digestive cells have been shown; furthermore, hemolytic infiltration in connective tissue will be recognized for the digestive gland. The Oocyte and sperm show degenerated with deformation in the connective tissue of the hermaphrodite gland. Likewise, deformation in the muscle fiber layer of the foot in the land snail distorts the epidermis and mucus gland suffering from necrosis. Moreover, mantle shows rapture in epidermis layer, deformed in muscle fiber layer, and vacuolization and necrosis take place in mucus gland.

Dark urine as the initial manifestation of COVID-19: a case report

BackgroundRhabdomyolysis is defined as a syndrome consisting of muscle necrosis and the release of intracellular muscle components into the bloodstream. Although rhabdomyolysis has been previously reported as an initial presentation or late complication of COVID-19, the data on it is still limited, and currently, there is no single case of COVID-19 in the literature that describes creatine kinase levels of more than 30,000 IU/L.Case presentationA 50-year-old African–American male presented to the hospital with decreased urine output, dark urine color, and constipation for the past couple of days. He was found to have acute kidney injury, liver injury, and creatinine kinase of 359,910 IU/L, for which aggressive intravenous fluid therapy was given. Infectious workup resulted in positive severe acute respiratory syndrome coronavirus 2 polymerase chain reaction. Two days after admission, the patient became symptomatic from a coronavirus disease 2019: he developed fever and hypoxia, and was placed on supplemental oxygen and started on a 10-day course of dexamethasone. The patient responded well to the treatment and supportive care for coronavirus disease 2019 and was successfully discharged.ConclusionClinicians should be cognizant of atypical coronavirus disease 2019 presentations. The spectrum of damage of coronavirus disease 2019 is still an evolving topic, and more research is required to reveal the exact mechanisms by which severe acute respiratory syndrome coronavirus 2 leads to rhabdomyolysis.

Histopathological characteristics of cervical extensor tissue in patients with dropped head syndrome

BackgroundTo date, the histopathologic characteristics of dropped head syndrome (DHS) have not been reported sufficiently. The present study investigates the histopathology of biopsy specimens from the cervical paravertebral region in patients with DHS.MethodsHistopathological parameters were evaluated in biopsy specimens of the cervical paravertebral soft tissue from 15 patients with DHS.ResultsAmong the 15 cases of DHS examined, skeletal muscle was identified in 7 cases, all of which showed necrosis, microvessel proliferation and atrophy. The ligament was identified in 12 cases, 8 of which showed degeneration. The lag time between the onset of symptoms and the performance of a biopsy in all 8 cases, which showed degeneration was over 3 months. Microvessel proliferation in the ligament was observed in 1 of the 4 cases, in which the lag time between the onset of symptoms and the performance of a biopsy was less than 3 months (acute or subacute phase), and in 7 of the 8 cases, in which the lag time between the symptoms and the performance of a biopsy was over 3 months (chronic phase). Chronic inflammation in the ligament was identified in 1 of the 12 cases.ConclusionsThe identification of necrosis, microvessel proliferation, and atrophy in the skeletal muscle of patients with DHS and the presence of ligament degeneration and microvessel proliferation in the chronic but not acute or subacute phases may suggest that persistent skeletal muscle damage of the cervical paravertebral region causes subsequent ligament damage in patients with DHS.

Abstract 10279: Altered Myocardial Gene Expression in H2-kbm1 Mice with Orexinergic Dysfunction and Heart Failure

Introduction: Mice carrying a homozygous frameshift mutation of the class I major histocompatibility antigen H2-K1 (H2-Kbm1) exhibit impaired development of hypothalamic orexinergic neurons. Similar to mice lacking the hypocretin (orexin) 2 receptor, H2-Kbm1 mice develop dilated cardiomyopathy and systolic heart failure (HF) from an early age. Previous studies suggest response to orexinergic signaling is predictive of patient response to current HF pharmacotherapeutic regimes. Our goal was to characterize the myocardial gene expression profiles of H2-Kbm1 mice. Methods: RNA was isolated from mice hearts (wild type n=5, mutant n=7) via the Qiagen RNeasy Mini Kit. DNase treatment was done to limit contamination of genomic DNA. Gene expression was measured using Illumina nexteq500 and 550 sequencing systems from a DNA library generated via the NuGene library kit (10 ng RNA). RNA-seq data analyses including comparisons, volcano and heatmap plots were completed. Results: H2-Kbm1 mice differentially express 398 myocardial genes compared to control mice. Ingenuity pathway analysis indicates that these genes are involved in necrosis of cardiac muscle (z-score -1.8), cell death (z-score 1.6), and cardiac contractility (z-score -4). Upstream signaling analysis suggest regulation by Mir-122 (z-score 2.4), DNMT3 A and B (z-score 3.3 and 2.5), VEGF (z-score 4.6) and rosiglitazone (z-score -6.8). Canonical pathway analysis is shown in Figure 1. Conclusion: H2-Kbm1 mice develop heart failure with marked myocardial transcriptional abnormalities that lead to impaired cardiac contraction and cell death. Differentially expressed genes are predominantly involved in mitochondrial function, oxidative phosphorylation, sirtuin signaling and the TCA cycle. Regulation of these genes is associated with miR-122, DNA methylations by DNMT3 A &amp; B, VEGF and rosiglitazone signaling. The orexin pathway is a potential target for heart failure therapeutics.

Abstract 9162: Increased Ratio of B2/B1-like Lymphocytes in the Perivascular Adipose Tissue Could Contribute to Plaque Destabilization in Human Coronary Arteries: Preliminary Results

Introduction: B-lymphocyte density in the pericoronary adipose tissue (PvAT) was correlated with plaque size in human coronary arteries. However, the subtypes of B cells in the PvAT and atherosclerotic plaque composition have not investigated yet. Hypothesis: We hypothesized that B2 and the ratio of B2/B1-like lymphocytes in the PvAT will correlate with an increase in components related to plaque destabilization and a decrease in components related to plaque stabilization. B1-like lymphocytes will correlate with an increase of components related to plaque stabilization. Methods: Coronary arteries were freshly dissected with adjacent PvAT. The most important atherosclerotic plaque was selected from each main coronary artery. From 107 artery segments, we calculated the percentage of arterial obstruction, intima-media thickness, the minimum fibrous cap thickness, and the percentage of collagen, smooth muscle cells, fibrous cap, calcification, lipid, necrosis, and intraplaque hemorrhage. We considered B2-lymphocytes as CD20 + CD43 - and B1-like lymphocytes as CD20 + CD43 + using the immunohistochemistry double staining technique. The densities of B2, B1-like, and the ratio of B2/B1-like lymphocytes were correlated with plaque composition using linear, negative binomial, or Poisson regressions models with clustering for multiple measures in the same individual and adjusted for age, sex, hypertension, diabetes, body mass index, sedentary lifestyle, smoking, and alcohol consumption. Results: B2 and B1-like lymphocyte density in the PvAT were not correlated with plaque components. However, the increase of the ratio of B2/B1-like lymphocytes was associated with a decrease in intraplaque collagen (β= -0.19, 95%CI= -0.35; -0.03, p=0.01), calcification (β= -0.15, 95%CI= -0.28; -0.02, p=0.01), hemorrhage (β= -0.08, 95%CI= -0.15; -0.02, p=0.009), minimum fibrous cap thickness (β= -0.03, 95%CI= -0.04; -0.01, p&lt;0.001), and an increase in the number of vasa vasorum in adventitia layer (β= 0.006, 95%CI=0.001; 0.01, p=0.006). Conclusions: An increase in the ratio of B2/B1-like lymphocytes in the PvAT could contribute to plaque destabilization by the decrease of atherosclerotic plaque components related to plaque stabilization.

A RARE CASE OF AN EXTENSIVE SUBCUTANEOUS NECROSIS IN THE LEFT TEMPORAL REGION CAUSED BY ORANGE OIL INJECTION AND ITS MANAGEMENT

Orange oil (isoparaffin C11-C15) is a solvent material that dissolves tooth filling materials effectively. A 29-year-old male who had extensive subcutaneous left temporal necrosis after an inadvertent orange oil injection is presented. Due to the injection, an immediate oedema and cellulitis formed in the left buccal, zygomatic, and temporal region. After a prompt drainage and antibiotherapy, the patient’s complaints were resolved. Due to partial temporal muscle necrosis and fibrosis, the interincisal mouth opening (IIO) was 15 millimeters. With a precise physical medicine and rehabilitation regimen, the IIO became 35 millimeters at the postoperative first year

A RARE CASE OF AN EXTENSIVE SUBCUTANEOUS NECROSIS IN THE LEFT TEMPORAL REGION CAUSED BY ORANGE OIL INJECTION AND ITS MANAGEMENT

Orange oil (isoparaffin C11-C15) is a solvent material that dissolves tooth filling materials effectively. A 29-year-old male who had extensive subcutaneous left temporal necrosis after an inadvertent orange oil injection is presented. Due to the injection, an immediate oedema and cellulitis formed in the left buccal, zygomatic, and temporal region. After a prompt drainage and antibiotherapy, the patient’s complaints were resolved. Due to partial temporal muscle necrosis and fibrosis, the interincisal mouth opening (IIO) was 15 millimeters. With a precise physical medicine and rehabilitation regimen, the IIO became 35 millimeters at the postoperative first year

SP5.2.5 A 4-year single-centre cohort study assessing outcomes in vascular surgery patients undergoing calf fasciotomies

Abstract Aims Acute compartment syndrome (ACS) is a surgical emergency. Delayed diagnosis and fasciotomy can result in irreversible muscle necrosis causing permanent disability and major amputation. This study compared patient outcomes following calf fasciotomies to prevent ACS (prophylactic) versus treat ACS (therapeutic) and early (within 6 hours of ACS diagnosis) versus delayed fasciotomies (beyond 6 hours) at a single vascular centre. Methods All patients undergoing calf fasciotomies between 1st January 2017 and 31st December 2020 were identified from a prospectively collected departmental database. Caldecott-approved data collection was conducted. The primary outcomes were wound infection, foot drop, muscle debridement, split-skin graft (SSG) requirement, vacuum dressing, 30-day amputation and death rates. Statistical analysis was performed using Fisher’s exact test. Results 73 patients (51 men, 22 women; median age 67, IQR 56-75 years) underwent calf fasciotomies (44 therapeutic and 29 prophylactic) mainly following acute thromboembolic ischaemia. Higher complication rates occurred among delayed (15) versus early (29) fasciotomy patients: wound infection (13.3% vs 3.4%), foot drop (20.0% vs 3.4%), muscle debridement (40.0% vs 24.1%), loss of anterior compartment (13.3%, 3.4%) need for SSG (29.5% vs 17.2%), vacuum dressing (46.7% vs 20.7%) and 30-day amputation rate (20.0% vs 13.8%) but lower 30-day death rate 13.3% vs 17.2%). None of these results were statistically significant. 34.1% of delayed fasciotomies were due to awaiting emergency theatre availability. Conclusion ACS patients undergoing calf fasciotomies are at high risk of complications including amputation and death. Ongoing education on mortality risk and early communication with emergency theatres are critical in their management.

Acute Myocardial Injury and Rhabdomyolysis in COVID-19 Patients: Incidence and Mortality.

BackgroundMyocardial injury has been defined as an elevated troponin level. The frequency of acute myocardial injury of hospitalized coronavirus disease 2019 (COVID-19) patients ranges from 7% to 36%. COVID-19 patients with cardiovascular disease (CVD) have a four-fold higher risk of mortality (odds ratio, 4.33; CI 95%, 3.16-5.94). In COVID-19 hospitalized patients’ study showed mortality rate was 18.5%. Rhabdomyolysis is considered as muscle necrosis and the release of intracellular muscles elements and enzymes into blood. In one of retrospective cohort study of COVID-19 hospitalized patients, incidence of rhabdomyolysis was 16.7%.Materials and methodsThis retrospective observational study consisted of 413 COVID-19 hospitalized patients. Patients with rhabdomyolysis was defined as creatine kinase level greater than 1,000 U/L and acute myocardial injury was defined as serum high-sensitivity troponin-T for males greater than 30 ng/l and for female greater than 20 ng/l. The primary outcome was in-hospital mortality of COVID-19 patients with acute myocardial injury and rhabdomyolysis. ResultsThe incidence of acute myocardial injury and rhabdomyolysis in hospitalized COVID-19 patients was 23.9% (99) and 15.7% (65), respectively. The mortality rate of in hospitalized COVID-19 patients who developed acute myocardial injury (28.3%) was significantly higher in comparison to patients who developed rhabdomyolysis (13.8%).DiscussionThe binding of SARS-CoV-2 virus to the angiotensin-converting enzyme 2 (ACE2) is a critical step in the pathophysiology in patients with COVID-19. There may be diverse direct and indirect mechanisms of acute myocardial injury in COVID-19 including ischemic injury, hypoxic injury (MI type 2), direct viral myocarditis, stress cardiomyopathy and systemic cytokine storm. Musculoskeletal injury may be caused by direct viral myositis or indirectly by host immune hyperinflammatory cytokine storm response that leads to skeletal muscle fiber proteolysis and fibrosis.ConclusionsAcute myocardial injury and rhabdomyolysis were underreported in COVID-19 patients. The incidence and mortality of acute myocardial injury are higher than that of rhabdomyolysis in COVID-19 hospitalized patients. The outcome was worse in COVID-19 patients with severe acute myocardial injury. Patients with acute myocardial injury and rhabdomyolysis may get benefits from rehabilitation programs.