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Open Veterinary Journal Apr 2024Bloody urine is classified in farm animals as hematuria, hemoglobinuria, and myoglobinuria. In small ruminants, discolored urine is reported due to several etiologies...
BACKGROUND
Bloody urine is classified in farm animals as hematuria, hemoglobinuria, and myoglobinuria. In small ruminants, discolored urine is reported due to several etiologies which is sometimes fatal. Of these causes are babesiosis, bacillary hemoglobinuria, copper toxicity, and hypophosphatemia.
AIM
This study was designed to investigate the clinical, etiological, hematobiochemical, ultrasonographic, and pathological findings in rams and bucks with red urine syndrome.
METHODS
Eighteen male animals (nine rams and nine bucks) of 6 months to 3 years were examined. Parallel, 10 healthy controls were used. They were admitted due to red urine, voiding of only urine drops, straining during the act of urination, grunting during urination, ventral abdominal edema, and abdominal distension. The duration of the disease ranged from 2 to 30 days. A history of chronic copper toxicosis was informed in two bucks and a ram. Two blood samples were collected from diseased as well as from controls in EDTA tubes (for complete blood count testing) and in plain tubes (for serum collection).
RESULTS
Hematuria was found in 11 animals (seven bucks and four rams) while hemoglobinuria was detected in seven animals (five bucks and two rams). Sonographic findings in diseased animals included ruptured urinary bladder in 3, ruptured urethra in 5, penile calculi, uroperitoneum in 6, distended urinary bladder in 7, hydronephrosis in 5, echogenic deposits in the bladder in 3, and ventral urine accumulation in four animals. Laboratory evaluation of a Geimsa-stained blood smear confirmed the infection with Babesia in three bucks and a ram. Hemolytic anemia was marked in two bucks and a ram due to chronic copper toxicity. Biochemical abnormalities included hypoalbuminemia, hyperglobulinemia, increased blood urea nitrogen and creatinine concentration, and hyperglycemia. Postmortem examination was carried out on six animals (four rams and two bucks).
CONCLUSION
Discolored urine in rams and bucks in this study resulted from hematuria due to urinary calculi and pelvic abscessation or from hemoglobinuria due to Babesia infection or due to copper toxicity. Hemolytic anemia was the outstanding hematological finding and hypoalbuminemia, hyperglobulinemia, increased blood urea nitrogen (BUN) and creatinine, and hyperglycemia were the characteristic biochemical findings. Sonography of the urinary tract was very helpful in assessing the renal parenchyma, urinary bladder, and abdominal cavity for the verification of urolithiasis, hydronephrosis, intact or ruptured urinary bladder, uroperitoneum, and perforated urethra.
Topics: Animals; Male; Goat Diseases; Sheep Diseases; Sheep; Goats; Ultrasonography; Hematuria; Hemoglobinuria
PubMed: 38808288
DOI: 10.5455/OVJ.2024.v14.i4.13 -
Clinical Medicine (London, England) May 2024Statin-induced immune-mediated necrotising myopathy (IMNM) is an inflammatory myopathy that can present as proximal muscle weakness and, in some cases, as dysphagia and...
Statin-induced immune-mediated necrotising myopathy (IMNM) is an inflammatory myopathy that can present as proximal muscle weakness and, in some cases, as dysphagia and respiratory distress. In this report, we present a case of statin-induced IMNM in a 78-year-old male. The patient had significantly high levels of creatinine kinase and myoglobinuria and experienced gradual weakness in the proximal muscles for 1 month after initiating a 20 mg dose of Atorvastatin 10 months before admission. Rapid clinical improvement was observed with the use of high-dose glucocorticoids in conjunction with methotrexate.
PubMed: 38710328
DOI: 10.1016/j.clinme.2024.100217 -
Journal of Orthopaedic Case Reports Jan 2024The association between rhabdomyolysis secondary to traumatic crush injuries and the resultant acute kidney injury has been well described . The pathway of opioid...
INTRODUCTION
The association between rhabdomyolysis secondary to traumatic crush injuries and the resultant acute kidney injury has been well described . The pathway of opioid overdose and acute kidney injury (AKI) has been documented but not fully elucidated. This process is believed to be multifactorial in its pathophysiology, but it remains obscure. Acidosis, systemic hypoxia, hypothermia, muscle compression, immunologic, or direct toxic effects have been identified as contributing factors to opioid-induced AKI. Musculoskeletal crush injuries account for one of the most common causes of rhabdomyolysis leading to AKI. However, the vast majority of crush injuries documented involve large regions of the body and most commonly involve the lower extremity. This is hypothesized to be due to the need for a considerable amount of muscle necrosis and sufficient myoglobinuria to cause AKI. There is a paucity of literature describing isolated upper extremity crush injuries severe enough to cause AKI. The case described herein outlines a patient who developed isolated right upper extremity compartment syndrome and resultant rhabdomyolysis leading to AKI in the setting of an opioid overdose.
CASE REPORT
Rhabdomyolysis may be caused by a variety of metabolic events. The pathophysiology of rhabdomyolysis secondary to acute crush injuries with resultant AKI is well documented. However, the literature describing cases of acute kidney injury caused by upper extremity compartment syndrome-induced rhabdomyolysis is limited. We present the case of a 33-year-old male who developed right upper extremity compartment syndrome after being incapacitated following an opioid overdose. He subsequently underwent emergent fasciotomies and was found to have an AKI secondary to rhabdomyolysis in the acute post-operative period.
CONCLUSION
This case describes a patient who was found to have isolated right upper extremity compartment syndrome and subsequent rhabdomyolysis, which resulted in AKI following an opioid overdose. This case highlights that an isolated incidence of upper extremity rhabdomyolysis is sufficient to cause acute kidney injury. The literature describing this pathology in isolated upper extremity injuries is limited as this phenomenon is typically encountered in the setting of lower extremity compartment syndrome.The pathophysiology and mechanism of this pathology are of particular importance to the fields of orthopedic surgery, nephrology, and internal medicine. This case highlights the need for early and adequate fluid resuscitation in patients with isolated upper extremity injuries to minimize the risk of subsequent AKI.
PubMed: 38292112
DOI: 10.13107/jocr.2024.v14.i01.4174 -
Cureus Dec 2023This report describes the case of a 47-year-old woman with myalgias, weakness, and elevated creatine kinase associated with semaglutide therapy prescribed for weight...
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.
PubMed: 38192938
DOI: 10.7759/cureus.50227 -
Indian Journal of Nephrology 2023Acute kidney injury can complicate rhabdomyolysis in 10-40% patients. Myoglobinuria and elevated creatine kinase (CK) form the basis of diagnosis. When associated with...
Acute kidney injury can complicate rhabdomyolysis in 10-40% patients. Myoglobinuria and elevated creatine kinase (CK) form the basis of diagnosis. When associated with azotemia and/or oliguria, intermittent hemodialysis is a treatment option. 31-year-old young man came with lower limb pain after doing 800 sit ups. At the presentation, blood pressure was high, serum creatinine was 15.7mg/dl and creatine kinase(CK)>20000 IU/L. Intermittent dialysis was initiated. He developed posterior reversible encephalopathy syndrome, generalized tonic clonic convulsions and a further rise in CK. He underwent extracorporeal removal of myoglobin with medium cut-off (MCO) membrane. After 3 sessions with MCO membrane, myoglobin and CK levels reduced. He was transitioned to conventional dialysis and discharged in a stable condition with complete renal recovery. Medium cut-off membrane effectively removes circulating myoglobin without significant albumin loss and is cost effective.
PubMed: 38174295
DOI: 10.4103/ijn.ijn_151_22 -
Neuromuscular Disorders : NMD Jan 2024Obscurin, encoded by the OBSCN gene, is a muscle protein consisting of three main splice isoforms, obscurin-A, obscurin-B, and obscurin kinase-only protein (also known...
Obscurin, encoded by the OBSCN gene, is a muscle protein consisting of three main splice isoforms, obscurin-A, obscurin-B, and obscurin kinase-only protein (also known as KIAA1639 or Obsc-kin). Obscurin is located at the M-band and Z-disks and interacts with titin and myomesin. It plays an important role in the stability and maintenance of the A- and M-bands and the subsarcolemmal organization of the microtubule network. Furthermore, obscurin is involved in Ca2+ regulation and sarcoplasmic reticulum function and is connected to several other muscle proteins. OBSCN gene variants have been reported to be relatively common in inherited cardiomyopathies. Here we reported two young patients with a history of cramps, myalgia, exercise intolerance, rhabdomyolysis, and myoglobinuria without any evidence of concomitant cardiomyopathy in association with novel OBSCN variants (c.24822C>A and c.2653+1G>C). Obscurin-deficient muscle fibers seem to have increased susceptibility to damage triggered by exercise that may lead to rhabdomyolysis. More studies are needed to clarify the diverse clinical phenotypes and the pathophysiology of OBSCN gene variants.
Topics: Humans; Muscle Proteins; Muscle Fibers, Skeletal; Sarcomeres; Sarcoplasmic Reticulum; Rhabdomyolysis; Protein Serine-Threonine Kinases; Rho Guanine Nucleotide Exchange Factors
PubMed: 38159459
DOI: 10.1016/j.nmd.2023.10.013 -
The American Journal of Emergency... Feb 2024Caffeine poisoning can cause fatal ventricular arrhythmias. In this report, we describe a case of severe caffeine poisoning with extraordinarily high blood caffeine...
Caffeine poisoning can cause fatal ventricular arrhythmias. In this report, we describe a case of severe caffeine poisoning with extraordinarily high blood caffeine levels. Despite developing refractory ventricular fibrillation, the patient was successfully treated with intermittent hemodialysis (IHD) under circulatory support by venoarterial extracorporeal membrane oxygenation (VA-ECMO). A 22-year-old male was transported to our hospital approximately 2.5 h after ingesting 200 highly caffeinated tablets (200 mg/tablet) (40 g caffeine total) in a suicide attempt. On arrival, the patient vomited frequently with a Glasgow Coma Scale score E3V2M5, heart rate 185 beats/min, and a blood pressure of 97/62 mmHg. Shortly after arrival, the patient developed ventricular fibrillation which was refractory either to three electrical defibrillations or antiarrhythmic drugs, resulting in endotracheal intubation for mechanical ventilation and VA-ECMO. Starting from 2 h after arrival, intermittent hemodialysis (IHD) was performed for 11 h, which markedly improved clinical symptoms and circulatory parameters. Serum caffeine level was 454.9 mg/dL upon arrival at the hospital, but it decreased to 55.5 mg/dL by the end of IHD treatment. Renal replacement therapy (RRT) including intermittent hemodiafiltration, continuous hemodiafiltration, and IHD was continued because of rhabdomyolysis with myoglobinuria and secondary caused acute kidney injury. The patient was weaned off VA-ECMO on hospital day 7, extubated on hospital day 18, weaned from RRT on hospital day 46, and was transferred to another hospital for physical rehabilitation on hospital day 113. IHD under circulatory support by VA-ECMO should be considered in severe caffeine poisoning causing potentially fatal arrhythmias.
Topics: Male; Humans; Young Adult; Adult; Caffeine; Ventricular Fibrillation; Cardiovascular System; Extracorporeal Membrane Oxygenation; Arrhythmias, Cardiac; Renal Dialysis
PubMed: 38129271
DOI: 10.1016/j.ajem.2023.12.014 -
JPMA. the Journal of the Pakistan... Dec 2023McArdle's disease (Glycogen storage disease type V) is a rare inherited autosomal recessive disease involving defect in enzyme, glycogen phosphorylase (PYGM) which...
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.
Topics: Humans; Male; Young Adult; Adult; Glycogen Storage Disease Type V; Muscle, Skeletal; Muscle Weakness; Fatigue; Muscle Cramp
PubMed: 38083936
DOI: 10.47391/JPMA.8401 -
Cureus Oct 2023Carnitine 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...
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.
PubMed: 37933340
DOI: 10.7759/cureus.46595