Unraveling Complexities: Rhabdomyolysis, Acute Renal Injury, and Compartment Syndrome Following a Wasp's Sting.

This study delves into the rare occurrence of rhabdomyolysis induced by wasp stings, emphasizing its toxic systemic repercussions. Drawing parallels with documented instances of insect bites worldwide, including those by honey bees and Africanized bees, the research explores the correlation between multiple wasp stings and acute renal failure associated with rhabdomyolysis. The venom's active components, such as amines, kinins, and histamine-releasing peptides, underpin toxic systemic reactions, leading to hemolysis, coagulopathy, and severe cytotoxicity-induced acute renal failure. Noteworthy is the emergence of blackish necroses at the sting site, suggesting intense cytotoxicity. The study also highlights skin necrosis as a prognostic indicator for toxic systemic reactions. The presented case manifests an anaphylaxis-like reaction, revealing insights into toxic responses devoid of IgE-mediated allergic reactions. Timely intervention, encompassing hydration, transfusion, and dialytic support, proves imperative in scenarios involving multiple wasp stings, offering successful outcomes documented through plasma exchange in severe cases. This research prompts considerations beyond anaphylaxis, urging exploration of severe toxic systemic reactions in the context of multiple wasp stings.

Profound Rhabdomyolysis and Viral Myositis Due to SARS-CoV-2: A Case Report.

The novel SARS-CoV-2 introduced several new inflammatory conditions including SARS-CoV-2-associated rhabdomyolysis and viral myositis. We present a 22-year-old man who noted a week of cough followed by myalgias, dark-colored urine, and decreased oral intake. He was found to have acute nontraumatic rhabdomyolysis after an acutely positive SARS-CoV-2 test. Initial creatine kinase (CK) level was above the reference range as were liver enzymes reflective of muscle breakdown. Treatment involved fluid resuscitation and pain control, with close monitoring of kidney, liver, and skeletal markers over five days of hospitalization till there was clinical and symptomatic improvement.

Exercise induced muscle weakness in a young adult: McArdle's disease unusual presentation.

McArdle's disease (Glycogen storage disease type V) is a rare inherited autosomal recessive disease involving defect in enzyme, glycogen phosphorylase (PYGM) which results in accumulation of glycogen mainly affecting skeletal muscles. It commonly presents in childhood and rarely in adults with symptoms like exercise intolerance, muscle weakness, cramps and fatigue. Herein, we report an unusual case of a 22 years old male in Pakistan with probable McArdle's Disease presenting with repeated episodes of generalized cramping muscle pain, exercise intolerance and haematuria. The diagnostic approach to identifying this disease as well as the differentials of other rare types of skeletal muscle disorders that should be kept in mind while dealing with a similar clinical picture, irrespective of the age of presentation, have been discussed.

Myopathic Carnitine Palmitoyltransferase II (CPT II) Deficiency: A Rare Cause of Acute Kidney Injury and Cardiomyopathy.

Carnitine palmitoyltransferase II (CPT II) deficiency is a long-chain fatty acid (LCFA) oxidation disorder. There are three main types classified by symptoms and age of onset: the neonatal form, the infantile hepatocardiomuscular form, and the adult or myopathic form. The first two are early-onset severe disorders presenting with marked hypoketotic hypoglycemia, cardiomyopathy, and liver dysfunction. The latter is characterized by muscle pain and weakness and stiffness, typically triggered by exercise or febrile illnesses and occasionally associated with myoglobinuria. One of the most common complications is acute kidney injury (AKI) following massive rhabdomyolysis, which is managed with aggressive fluid therapy; crystalloid solutions are preferred. We report an otherwise healthy 38-year-old patient who presented with severe myalgia, cramps, fatigue, low-grade fever, and transient myoglobinuria, after intense physical training. Significant recurrent muscle pain was reported. Family history was unremarkable. Imaging studies showed no abnormalities. Echocardiogram showed a left ventricle ejection fraction (LVEF) of 40%. Acetylcarnitine analysis with tandem mass spectrometry and molecular tests confirmed the diagnosis. Fluid resuscitation was started. Acute kidney injury was diagnosed and managed with plasmapheresis and five sessions of hemodialysis. The patient was discharged upon the improvement of renal function with lifestyle modification recommendations. In otherwise healthy young adults presenting with myalgia and rhabdomyolysis triggered by physical activity or infection, CPT II deficiency should be considered, and genetic testing should be initiated to provide an opportunity for patients to modify their daily lifestyle, preventing future attacks and the development of complications.

Clinical Diagnosis of Rhabdomyolysis without Myoglobinuria or Electromyographic Abnormalities in a Dog.

A 2-year-old female neutered Old German Shepherd was presented for acute non-ambulatory tetraparesis. Upon presentation to the emergency department, hematology and biochemical blood tests revealed no abnormalities aside from mildly elevated C-reactive protein levels (22.5 mg/L, reference range 0.0-10.0) and immeasurable creatine kinase (CK) activity. Neurological evaluation the next day revealed ambulatory tetraparesis, general proprioceptive deficits, mild ataxia and dubious diffuse myalgia. Withdrawal reflexes were weak on both thoracic and pelvic limbs. The CK was determined to be significantly elevated at that point (32.856 U/L, ref. range 10.0-200.0). Urinalysis revealed no abnormalities. An electromyographic (EMG) study of thoracic limb, paraspinal and pelvic limb muscles revealed no abnormalities. A magnetic resonance imaging (MRI) study of the cervicothoracic spinal cord was performed and revealed no abnormalities. A presumptive clinical diagnosis of rhabdomyolysis without myoglobinuria or EMG abnormalities was formed. Muscular biopsies were declined due to the rapid clinical improvement of the dog. A follow-up showed the progressive decline of CK activity to normal values and clinical remission of signs. A diagnosis of rhabdomyolysis was concluded based on clinical signs, consistent CK activity elevations and the response to supportive treatment for rhabdomyolysis, despite the absence of myoglobinuria and EMG abnormalities. Rhabdomyolysis should not be excluded based on the lack of EMG abnormalities or myoglobinuria in dogs.

[Diagnostic approach to rhabdomyolysis]. / Vignette diagnostique de l'étudiant. Approche diagnostique de la rhabdomyolyse.

Rhabdomyolysis is a clinical syndrome related to the damage of skeletal muscle. The symptomatology is often poor, but it classically includes muscle weakness, myalgia and red-brown urine. The causes may be multiple but are most frequently traumatic : the so-called "crush syndrome". The diagnosis is based on the increase in serum creatine kinase, which is sometimes associated with myoglobinuria. Rhabdomyolysis may cause severe complications, such as ionic disorders or acute kidney injury which can lead to the death of the patient.

La rhabdomyolyse est un syndrome clinique lié à la destruction du muscle squelettique. La symptomatologie est souvent pauvre et associe classiquement une faiblesse musculaire, des myalgies et des urines noirâtres. Les causes peuvent être multiples, mais sont le plus fréquemment traumatiques et regroupées sous le terme anglophone de «crush syndrome¼. Le diagnostic repose sur la majoration sérique de la créatine kinase, à laquelle s'associe parfois une myoglobinurie. Rarement bénigne, la rhabdomyolyse peut engendrer des complications sévères, telles que des troubles ioniques ou une insuffisance rénale pouvant mener au décès du patient.

Juvenile-Onset Recurrent Rhabdomyolysis Due to Compound Heterozygote Variants in the ACADVL Gene.

Very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency is a rare autosomal recessive long-chain fatty acid oxidation disorder caused by mutations in the ACADVL gene. The myopathic form presents with exercise intolerance, exercise-related rhabdomyolysis, and muscle pain, usually starting during adolescence or adulthood. We report on a 17-year-old boy who has presented with exercise-induced muscle pain and fatigue since childhood. In recent clinical history, episodes of exercise-related severe hyperCKemia and myoglobinuria were reported. Electromyography was normal, and a muscle biopsy showed only "moth-eaten" fibers, and a mild increase in lipid storage in muscle fibers. NGS analysis displayed the already known heterozygote c.1769G>A variant and the unreported heterozygote c.523G>C change in ACADVL both having disease-causing predictions. Plasma acylcarnitine profiles revealed high long-chain acylcarnitine species levels, especially C14:1. Clinical, histopathological, biochemical, and genetic tests supported the diagnosis of VLCAD deficiency. Our report of a novel pathogenic missense variant in ACADVL expands the allelic heterogeneity of the disease. Since dietary treatment is the only therapy available for treating VLCAD deficiency and it is more useful the earlier it is started, prompt diagnosis is essential in order to minimize muscle damage and slow the disease progression.

Anesthetic Management of a Patient With McArdle Disease: A Case Report and Review of the Literature.

McArdle disease (glycogen storage disorder type V) is a rare inherited condition resulting in impaired energy metabolism. Challenges in anesthetized patients with McArdle disease include hypoglycemia, rhabdomyolysis, myoglobinuria, acute renal failure, and postoperative fatigue. We review the literature and discuss a successful anesthetic that had no perioperative complications for a patient with McArdle disease undergoing robotic-assisted lung wedge resection. Preoperatively, we obtained a complete blood count, chemistry panel, and creatine kinase level. Intraoperatively, we proceeded with general endotracheal anesthesia and monitored point-of-care electrolytes, hemoglobin, and blood glucose. The patient had an uneventful postoperative recovery and was discharged home on postoperative Day 3. Patients with McArdle disease can undergo safe surgery with appropriate perioperative planning and a well-managed anesthetic. Efforts should focus on mitigating the risks of hypoglycemia, rhabdomyolysis, myoglobinuria, acute renal failure, and postoperative fatigue.

Fatal rhabdomyolysis caused by COVID-19 infection: a case report.

COVID-19 is a systemic viral disease complicated with medical conditions. Severe rhabdomyolysis during the COVID-19 course is not until now well known. Case presentation: The authors presented a 48-year-old female with fatal rhabdomyolysis caused by COVID-19 infection. She was referred to us with cough, generalized myalgia and arthralgia, and fever during the last week. Laboratory results showed an elevated erythrocyte sedimentation rate, elevated C-reactive protein level, and elevated creatine kinase. The nasopharyngeal swab confirmed the diagnosis of coronavirus 2 RNA infection. She was managed initially in the COVID-19 isolation department. Three days later, she was transferred to the intensive care unit and mechanically ventilated. Laboratory results were consistent with rhabdomyolysis. She died because of cardiac arrest due to continuous hemodynamic deterioration. Clinical discussion: Rhabdomyolysis is a serious condition that can be fatal or cause disability. Rhabdomyolysis cases have been reported in COVID-19 patients. Conclusion: Rhabdomyolysis cases have been reported in COV19 patients. Further studies are needed to understand the mechanism and to optimize the treatment.

NGS-Based Genetic Analysis in a Cohort of Italian Patients with Suspected Inherited Myopathies and/or HyperCKemia.

Introduction/Aims HyperCKemia is considered a hallmark of neuromuscular diseases. It can be either isolated or associated with cramps, myalgia, weakness, myoglobinuria, or rhabdomyolysis, suggesting a metabolic myopathy. The aim of this work was to investigate possible genetic causes in order to help diagnose patients with recurrent hyperCKemia or clinical suspicion of inherited metabolic myopathy. Methods A cohort of 139 patients (90 adults and 49 children) was analyzed using a custom panel containing 54 genes associated with hyperCKemia. Results A definite genetic diagnosis was obtained in 15.1% of cases, while candidate variants or variants of uncertain significance were found in a further 39.5%. Similar percentages were obtained in patients with infantile or adult onset, with some different causative genes. RYR1 was the gene most frequently identified, either with single or compound heterozygous variants, while ETFDH variants were the most common cause for recessive cases. In one patient, mRNA analysis allowed identifying a large LPIN1 deletion missed by DNA sequencing, leading to a certain diagnosis. Conclusion These data confirm the high genetic heterogeneity of hyperCKemia and metabolic myopathies. The reduced diagnostic yield suggests the existence of additional genes associated with this condition but also allows speculation that a significant number of cases presenting with hyperCKemia or muscle symptoms are due to extrinsic, not genetic, factors.

Expanded Dengue Syndrome Presenting as Intracranial Hemorrhage, Fever, and Rhabdomyolysis: A Case Report.

Rare clinical manifestations of dengue are included under the expanded dengue syndrome (EDS), with intracranial hemorrhage (ICH) being one of them. We discuss an uncommon presentation of dengue with basal ganglia hemorrhage, hyperthermia, and rhabdomyolysis in a 53-year-old hypertensive female who presented with sudden onset syncope, left-sided weakness, and altered sensorium for days, with high-grade fever and vomiting. The Glasgow coma scale (GCS) score was 5, and the patient was intubated. Noncontrast computerized tomography (NCCT) of the brain revealed right basal ganglia bleeding with intraventricular hemorrhage. Electrocardiography (ECG) revealed sinus tachycardia. The patient had spikes of high-grade fever, rhabdomyolysis, stage III acute kidney disease, and coagulopathy. Dengue IgM antibodies were positive. Treatment was started, and the patient was in the intensive care unit (ICU) for six months, following which she was discharged. Given this, one can speculate on the importance of viral diseases presenting with ICH as these are rare and are diagnosed quite late, which can also prove to be fatal.

Rhabdomyolysis and myoglobinuria following single induction dose of propofol in a dog.

OBJECTIVE: To report a case of rhabdomyolysis and myoglobinuria following single induction dose of propofol in a dog. CASE SUMMARY: A 5-year-old intact male Shih-Tzu dog was presented for pigmenturia occurring a few hours following anesthesia for comprehensive oral health assessment and treatment. After premedication with IV diazepam (0.5 mg/kg), anesthesia was induced with IV propofol (4 mg/kg) and maintained with isoflurane vaporized in oxygen. A few hours following recovery from anesthesia, the dog developed rhabdomyolysis and myoglobinuria associated with increased serum alanine aminotransferase and C-reactive protein concentrations, as well as mild hypokalemia and euglycemic glycosuria. Approximately 48 hours after IV fluid therapy, the dog was clinically normal, and myoglobinuria progressively resolved. NEW OR UNIQUE INFORMATION PROVIDED: This is the first case description of rhabdomyolysis and myoglobinuria following a single dose of injectable propofol.

Rhabdomyolysis Associated With Semaglutide Therapy: A Case Report.

This report describes the case of a 47-year-old woman with myalgias, weakness, and elevated creatine kinase associated with semaglutide therapy prescribed for weight loss. Her symptoms and laboratory markers were consistent with rhabdomyolysis and resolved after discontinuation of semaglutide. Upon rechallenge at a lower dose, symptoms recurred, and urinalysis was consistent with myoglobinuria. Symptoms again rapidly resolved upon discontinuation of the medication. It is imperative for physicians to recognize semaglutide as a possible cause of myalgias and rhabdomyolysis in clinically suspected patients. To the best of our knowledge, this is the first reported case in the literature and may be specific to semaglutide rather than a class effect of glucagon-like peptide 1 (GLP-1) agonists.

Myoglobinuria-induced Acute Kidney Injury Secondary to CovishieldTM Vaccination.

Vaccination is the best strategy for the development of herd immunity and for the control of the SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) pandemic. As the number of immunizations across the globe reaches a record number, random cases of diverse adverse effects of the vaccines are being documented. We report a case of renal biopsy-proven myoglobin-induced acute tubular injury requiring dialytic support post-CovishieldTM vaccination. Awareness of this rare complication is necessary so that it can be recognized early, and renal injury avoided.

A case of sub-acute compartment syndrome of bilateral pectoralis major, deltoid and triceps muscles.

A 19-year-old healthy bodybuilder presented to the emergency department with gradually worsening pain in both his upper arms and shoulders and inability to fully flex his elbows. The haematological investigations revealed a markedly raised Creatinine Kinase (74,400 U/L) and myoglobinuria. The patient required an emergency surgical decompression of the pectoral and the anterior and posterior compartments of arms of both upper limbs with secondary closure after 48 h. The patient had an uneventful post-op and recovery of his functions with some initial restriction of full flexion of his left elbow and some weakness in his triceps, all of which gradually improved.

Rhabdomyolysis-induced acute kidney injury and concomitant apoptosis induction via ROS-mediated ER stress is efficaciously counteracted by epigallocatechin gallate.

Rhabdomyolysis induced acute kidney injury (RIAKI) is a life-threatening condition responsible for approximately 19-58% of AKI cases worldwide. We performed an intramuscular injection of glycerol (10 mL/kg) in male wistar rats to induce AKI. Epigallocatechin gallate (EGCG) was administered for 3 consecutive days to evaluate its protective effects. We observed significant downregulation in serum creatinine, blood urea nitrogen (BUN) and LDH at different time points on EGCG treatment groups in a dose-dependent manner. Similarly, H&E staining also revealed that EGCG was able to reduce the formation of damaged tubules and tubular necrosis which was prominently spread throughout the kidney tissue of glycerol treatment group. Concomitantly, we observed upregulated inflammation, ER stress and elevated oxidative stress in the glycerol treated group only, which was significantly normalized upon EGCG treatment in both in vitro and in vivo studies. The occurrence of apoptosis in kidney tubules was found to be relatively higher in glycerol treated group and H2O2 treated HEK-293 cells. The results obtained after EGCG treatment revealed a significant decrease in apoptotic cell population, which was further validated by immunofluorescence staining against p53 and comet assay in HEK-293 cells and p53 IHC in kidney tissues. Western blotting also revealed a systemic downregulation of intrinsic mitochondrial apoptotic pathway markers such as bax, bcl-2, pro and cleaved caspase 3, caspase 9 and PARP1. Additionally, the results for flow cytometry analysis and TUNEL assay corroborated apoptotic equilibrium. Conclusively, we reckon EGCG as a multi-therapeutic natural product that can be used the for treatment of AKI.

Cardiac arrest as a manifestation of unknown Type V glycogenosis: a case report.

Few cases have been reported to date, in which a massive rhabdomyolysis causes a cardiac arrest in a male adult suffering from undiagnosed McArdle disease. Veno-arterial extracorporeal membrane oxygenation and cytokine adsorption filter (CytoSorb®) were required to reach a complete and successful recovery.

[Biochemical analysis of an uncommon monoclonal peak on urine protein electrophoresis: a case report]. / Analyse biochimique d'un pic insolite d'allure monoclonale en électrophorèse des protéines urinaires: à propos d'un cas.

Urine protein electrophoresis is often required for diagnosis and monitoring of urological or renal diseases and lymphoid hemopathies. We here report an uncommon urine protein electrophoresis result. The test was performed using agarose gel electrophoresis and capillary electrophoresis. It was a monoclonal peak of unknown significance migrating with gammaglobulins. Scientific literature and the tests performed demonstrated that it was myoglobin. In fact, myoglobin (17 kDa) is freely filtered by the glomerulus and normally reabsorbed by the tubules. If tubule capacity for reabsorption is exceeded, its presence results in overcharging proteinuria. Myoglobinuria helped diagnose rhabdomyolysis in our patient. Thus, the analysis of unknown peaks, can provide information on symptoms but also underlying pathologies, which may be of clinical interest.

Discolored Urine in Horses and Foals.

This article describes the most common causes of urine discoloration. The review includes a description of the most common disorders causing hematuria, highlighting clinical presentation, treatments, and pathophysiology. Causes of hemoglobinuria and myoglobinuria together with their mechanisms of renal injury are also reviewed.

Whole-exome sequencing detects PYGM variants in two adults with McArdle disease.

McArdle disease is a debilitating glycogen storage disease with typical onset in childhood. Here, we describe a former competitive athlete with early adult-onset McArdle disease and a septuagenarian with a history of exercise intolerance since adolescence who was evaluated for proximal muscle weakness. Exome sequencing identified biallelic variants in the PYGM gene for both cases. The former athlete has the common, well-known pathogenic variant p.(Arg50Ter) in trans with a novel missense variant, p.(Asp694Glu). The second individual has a previously described homozygous missense variant, p.(Arg771Gln). Here, we describe the clinical course, enzyme-testing results using muscle tissue, and molecular findings for the individuals and add to the knowledge of the genotypic spectrum of this disorder.