Myoglobinuria
Acute Kidney Injury
Creatine Kinase
Heat Exhaustion
Myoglobin
Glycogen Storage Disease Type V
Water Intoxication
Acute renal impairment after immersion and near-drowning. (1/365)
Acute renal impairment (ARI) secondary to immersion and near-drowning is rarely described and poorly understood. A retrospective case-control study was performed: (1) to determine the incidence of ARI associated with near-drowning or immersion and (2) to define the clinical syndrome and to assess clinical predictors of ARI. Of 30 patients presenting after immersion or near-drowning, 50% were identified with ARI, with a mean admission serum creatinine of 0.24 +/- 0.33 mmol/L (2.7 +/- 3.7 mg/dl). These patients were a heterogeneous group: Eight had mild reversible ARI, three had ARI related to shock and multisystem failure, two had rhabdomyolysis-related ARI, and two had severe isolated ARI. Two patients required supportive hemodialysis and two died. Patients with ARI experienced more marked acidosis than control patients, as measured by serum bicarbonate (P < 0.001), pH (P < 0.001), and base excess (P < 0.001). There was also a higher admission lymphocyte count in the ARI group (P = 0.056). Dipstick hematuria on admission was significantly more common in patients with ARI (P = 0.016), and patients with 2 to 3+ of admission dipstick proteinuria had a higher peak serum creatinine than patients with less proteinuria (P < 0.05). Admission predictors of ARI by univariate logistic regression analysis included reduced serum bicarbonate (P = 0.002), pH (P = 0.001), and base excess (P < 0.001). The best predictor of ARI on multivariate analysis was a negative base excess (P = 0.01). In summary, acute renal impairment commonly occurs after immersion and near-drowning and is a heterogeneous condition. Although mild reversible renal impairment (serum creatinine < 0.30 mmol/L) (3.4 mg/dl) is usual, severe acute renal failure requiring dialysis can occur. It is recommended that any patient who presents after near-drowning or immersion should be assessed for potential ARI by serial estimations of serum creatinine, particularly when there is an increase in the initial serum creatinine, marked metabolic acidosis, an abnormal urinalysis, or a significant lymphocytosis. (+info)Non-traumatic acute rhabdomyolysis. (2/365)
A boy developed sudden severe generalized muscle stiffness, bulbar weakness and passed dark coloured urine. Laboratory tests revealed marked elevation of creatinine kinase(CK) levels and myoglobinuria. Histopathology of quadriceps muscle showed features of acute rhabdomyolysis. Patient made complete clinical recovery over a period of three weeks and CK returned to normal level. The possible aetiologies of non-traumatic rhabdomyolysis are discussed and the relevant literature reviewed. (+info)Disseminated zygomycosis due to Rhizopus schipperae after heatstroke. (3/365)
A 21-year-old woman suffered heatstroke and developed diarrhea while trekking across south Texas. The heatstroke was complicated by seizures, rhabdomyolysis, pneumonia, renal failure, and disseminated intravascular coagulation. The patient's stool and blood cultures grew Campylobacter jejuni. The patient subsequently developed paranasal and gastrointestinal zygomycosis and required surgical debridement and a prolonged course of amphotericin B. The zygomycete cultured was Rhizopus schipperae. This is only the second isolate of R. schipperae that has been described. R. schipperae is characterized by the production of clusters of up to 10 sporangiophores arising from simple but well-developed rhizoids. These asexual reproductive propagules are produced on Czapek Dox agar but are absent on routine mycology media, where only chlamydospores are observed. Despite multiorgan failure, bacteremia, and disseminated zygomycosis, the patient survived and had a good neurological outcome. Heatstroke has not been previously described as a risk factor for the development of disseminated zygomycosis. (+info)A case of acute renal failure and compartment syndrome after an alcoholic binge. (4/365)
A 25 year old man presented with anuria and bilateral leg pain two days after an alcoholic binge. He subsequently developed rhabdomyolysis causing acute renal failure, with compartment syndrome of both lower legs. This required urgent dialysis and fasciotomy respectively within six hours of admission. He remained dialysis dependent for three weeks and only after four months was he able to weight bear on both legs. Alcohol is a leading cause of rhabdomyolysis. Early recognition and prompt treatment is essential to prevent serious complications. (+info)Rhabdomyolysis and acute renal failure resulting from alcohol and drug abuse. (5/365)
Rhabdomyolysis is a common cause of acute renal failure (ARF) associated with drug misuse. Abuse of the gel formulation of temazepam has been a particular problem in the West of Scotland. We performed a retrospective review of dialysis-dependent ARF from rhabdomyolysis and drug misuse in the West of Scotland, 1986-1997. We identified 76 patients, of whom 87% were male. Seventeen cases occurred in the first 6 years, compared with 59 in the subsequent 6 years. Median age was 32. Thirty cases followed intravenous drug misuse, 46 followed oral drug misuse. The substances most frequently misused were alcohol (54%), heroin (24%) and parenteral temazepam (17%). The temazepam cases all followed the introduction of the gel formulation. Three out of 4 patients requiring limb amputation had injected temazepam. Of intravenous drug misusers tested, 72% were hepatitis-C-positive. Some 43% of patients had deprivation scores in the worst category. ARF due to rhabdomyolysis from substance misuse is increasing in our area. Alcohol is frequently responsible. The introduction of the gel formulation of temazepam has contributed to the increase. Those at risk in this study were young, male, had a high incidence of hepatitis C and lived in the most deprived areas. (+info)Atorvastatin compared with simvastatin-based therapies in the management of severe familial hyperlipidaemias. (6/365)
We compared atorvastatin with simvastatin-based therapies in a prospective observational study of 201 patients with severe hyperlipidaemia. Atorvastatin 10 mg therapy was substituted for simvastatin 20 mg, 20 mg for 40 mg, 40 mg for simvastatin 40 mg plus resin, and 80 mg for simvastatin-fibrate-resin therapy. Lipid and safety profiles were assessed. Atorvastatin reduced total cholesterol by 31 +/- 11-40 +/- 14% vs. 25 +/- 12-31 +/- 11%; LDL by 38 +/- 16-45 +/- 18% vs. 31 +/- 18-39 +/- 18% and geometric mean triglycerides by 29.3-37.3% vs. 16.6-24.8%, but reduced HDL 11% +/- 47% at 80 mg compared with a 16% +/- 34% increase with simvastatin-based therapy. Target LDL < 3.5 mmol/l was achieved more often with atorvastatin (63% vs. 50%; p < 0.001). Atorvastatin increased geometric mean fibrinogen by 12-20% vs. a 0-6% fall with simvastatin (p << 0.001). Side effects were noted in 10-36% of patients, including one case of rhabdomyolysis, and 36% discontinued therapy. These data suggest that atorvastatin is more effective than current simvastatin-based therapies in achieving treatment targets in patients with familial hypercholesterolaemia but at the expense of a possible increase in side-effects. This issue needs further study in randomized controlled trials. (+info)Acute myoedema: an unusual presenting manifestation of hypothyroid myopathy. (7/365)
We describe a patient with primary hypothyroidism due to autoimmune thyroiditis, presenting with acute myoedema and spontaneous rhabdomyolysis. During his hospital stay, he developed altered sensorium due to hypo-osmolal hyponatraemia and later developed bilateral foot drop that responded to appropriate treatment. (+info)Unusual consequences of heroin overdose: rhabdomyolysis, acute renal failure, paraplegia and hypercalcaemia. (8/365)
A 29-yr-old man, known to be a heroin addict, was found at home totally unrousable, bent on his hips in the lotus position. On admission, he required frequent ventricular defibrillation, external pacing and infusion of calcium. A diagnosis of rhabdomyolysis caused by heroin and cocaine overdose was made. He developed paraplegia below T12, acute renal failure, acute compartment syndrome in one leg and a coagulation defect. Despite a fasciotomy, a through-knee amputation of the leg was required. Haemodialysis was required for 26 days, and this period was complicated by increased serum calcium concentrations, which was treated with disodium pamindrate. Calcium deposits were palpable in the muscles and could be seen in vessels on limb x-rays. After 34 days, he was eventually discharged to a general surgical ward and subsequently into the community. (+info)Rhabdomyolysis is a medical condition characterized by the breakdown and degeneration of skeletal muscle fibers, leading to the release of their intracellular contents into the bloodstream. This can result in various complications, including electrolyte imbalances, kidney injury or failure, and potentially life-threatening conditions if not promptly diagnosed and treated.
The process of rhabdomyolysis typically involves three key components:
1. Muscle injury: Direct trauma, excessive exertion, prolonged immobilization, infections, metabolic disorders, toxins, or medications can cause muscle damage, leading to the release of intracellular components into the bloodstream.
2. Release of muscle contents: When muscle fibers break down, they release various substances, such as myoglobin, creatine kinase (CK), lactate dehydrogenase (LDH), aldolase, and potassium ions. Myoglobin is a protein that can cause kidney damage when present in high concentrations in the bloodstream, particularly when it is filtered through the kidneys and deposits in the renal tubules.
3. Systemic effects: The release of muscle contents into the bloodstream can lead to various systemic complications, such as electrolyte imbalances (particularly hyperkalemia), acidosis, hypocalcemia, and kidney injury or failure due to myoglobin-induced tubular damage.
Symptoms of rhabdomyolysis can vary widely depending on the severity and extent of muscle damage but may include muscle pain, weakness, swelling, stiffness, dark urine, and tea-colored or cola-colored urine due to myoglobinuria. In severe cases, patients may experience symptoms related to kidney failure, such as nausea, vomiting, fatigue, and decreased urine output.
Diagnosis of rhabdomyolysis typically involves measuring blood levels of muscle enzymes (such as CK and LDH) and evaluating renal function through blood tests and urinalysis. Treatment generally focuses on addressing the underlying cause of muscle damage, maintaining fluid balance, correcting electrolyte imbalances, and preventing or managing kidney injury.
Myoglobinuria is a medical condition characterized by the presence of myoglobin in the urine. Myoglobin is a protein found in muscle cells that is released into the bloodstream when muscle tissue is damaged or broken down, such as during intense exercise, trauma, or muscle diseases like muscular dystrophy and rhabdomyolysis.
When myoglobin is present in high concentrations in the blood, it can damage the kidneys by causing direct tubular injury, cast formation, and obstruction, which can lead to acute kidney injury (AKI) or even renal failure if left untreated. Symptoms of myoglobinuria may include dark-colored urine, muscle pain, weakness, and swelling, as well as symptoms related to AKI such as nausea, vomiting, and decreased urine output.
Diagnosis of myoglobinuria is typically made by detecting myoglobin in the urine using a dipstick test or more specific tests like immunoassays or mass spectrometry. Treatment may involve aggressive fluid resuscitation, alkalization of the urine to prevent myoglobin precipitation, and management of any underlying conditions causing muscle damage.
Acute kidney injury (AKI), also known as acute renal failure, is a rapid loss of kidney function that occurs over a few hours or days. It is defined as an increase in the serum creatinine level by 0.3 mg/dL within 48 hours or an increase in the creatinine level to more than 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days, or a urine volume of less than 0.5 mL/kg per hour for six hours.
AKI can be caused by a variety of conditions, including decreased blood flow to the kidneys, obstruction of the urinary tract, exposure to toxic substances, and certain medications. Symptoms of AKI may include decreased urine output, fluid retention, electrolyte imbalances, and metabolic acidosis. Treatment typically involves addressing the underlying cause of the injury and providing supportive care, such as dialysis, to help maintain kidney function until the injury resolves.
Creatine kinase (CK) is a muscle enzyme that is normally present in small amounts in the blood. It is primarily found in tissues that require a lot of energy, such as the heart, brain, and skeletal muscles. When these tissues are damaged or injured, CK is released into the bloodstream, causing the levels to rise.
Creatine kinase exists in several forms, known as isoenzymes, which can be measured in the blood to help identify the location of tissue damage. The three main isoenzymes are:
1. CK-MM: Found primarily in skeletal muscle
2. CK-MB: Found primarily in heart muscle
3. CK-BB: Found primarily in the brain
Elevated levels of creatine kinase, particularly CK-MB, can indicate damage to the heart muscle, such as occurs with a heart attack. Similarly, elevated levels of CK-BB may suggest brain injury or disease. Overall, measuring creatine kinase levels is a useful diagnostic tool for assessing tissue damage and determining the severity of injuries or illnesses.
Heat exhaustion is a condition characterized by excessive loss of water and salt, typically through heavy sweating, leading to physical symptoms such as weakness, dizziness, cool moist skin with goose bumps when in a hot environment, and a rapid, weak pulse. It can also cause nausea, headache, and fainting. Heat exhaustion is less severe than heat stroke but should still be treated as a medical emergency to prevent progression to the more serious condition. The primary treatment for heat exhaustion includes restoring water and salt balance through oral or intravenous rehydration, cooling the body with cold compresses or a cool bath, and removing the person from the hot environment.
Myoglobin is a protein found in the muscle tissue, particularly in red or skeletal muscles. It belongs to the globin family and has a similar structure to hemoglobin, another oxygen-binding protein found in red blood cells. Myoglobin's primary function is to store oxygen within the muscle cells, making it readily available for use during periods of increased oxygen demand, such as during physical exertion.
Myoglobin contains heme groups that bind to and release oxygen molecules. The protein has a higher affinity for oxygen than hemoglobin, allowing it to maintain its bound oxygen even in low-oxygen environments. When muscle cells are damaged or undergo necrosis (cell death), myoglobin is released into the bloodstream and can be detected in serum or urine samples. Elevated levels of myoglobin in the blood or urine may indicate muscle injury, trauma, or diseases affecting muscle integrity, such as rhabdomyolysis or muscular dystrophies.
Glycogen Storage Disease Type V, also known as McArdle's disease, is a genetic disorder that affects the body's ability to break down glycogen, a complex carbohydrate stored in muscles, into glucose, which provides energy for muscle contraction.
This condition results from a deficiency of the enzyme myophosphorylase, which is responsible for breaking down glycogen into glucose-1-phosphate within the muscle fibers. Without sufficient myophosphorylase activity, muscles become easily fatigued and may cramp or become rigid during exercise due to a lack of available energy.
Symptoms typically appear in childhood or adolescence and can include muscle weakness, stiffness, cramps, and myoglobinuria (the presence of myoglobin, a protein found in muscle cells, in the urine) following exercise. Diagnosis is usually confirmed through genetic testing and enzyme assays. Treatment typically involves avoiding strenuous exercise and ensuring adequate hydration and rest before and after physical activity. In some cases, dietary modifications such as high-protein or high-carbohydrate intake may be recommended to help manage symptoms.
Medical Definition of Water Intoxication:
Water intoxication, also known as hyponatremia, is a condition that occurs when an individual consumes water in such large quantities that the body's electrolyte balance is disrupted. This results in an abnormally low sodium level in the blood (hyponatremia), which can cause symptoms ranging from mild to severe, including nausea, headache, confusion, seizures, coma, and even death in extreme cases. It's important to note that water intoxication is rare and typically only occurs in situations where large amounts of water are consumed in a short period of time, such as during endurance sports or when someone is trying to intentionally harm themselves.
Muscular diseases, also known as myopathies, refer to a group of conditions that affect the functionality and health of muscle tissue. These diseases can be inherited or acquired and may result from inflammation, infection, injury, or degenerative processes. They can cause symptoms such as weakness, stiffness, cramping, spasms, wasting, and loss of muscle function.
Examples of muscular diseases include:
1. Duchenne Muscular Dystrophy (DMD): A genetic disorder that results in progressive muscle weakness and degeneration due to a lack of dystrophin protein.
2. Myasthenia Gravis: An autoimmune disease that causes muscle weakness and fatigue, typically affecting the eyes and face, throat, and limbs.
3. Inclusion Body Myositis (IBM): A progressive muscle disorder characterized by muscle inflammation and wasting, typically affecting older adults.
4. Polymyositis: An inflammatory myopathy that causes muscle weakness and inflammation throughout the body.
5. Metabolic Myopathies: A group of inherited disorders that affect muscle metabolism, leading to exercise intolerance, muscle weakness, and other symptoms.
6. Muscular Dystonias: Involuntary muscle contractions and spasms that can cause abnormal postures or movements.
It is important to note that muscular diseases can have a significant impact on an individual's quality of life, mobility, and overall health. Proper diagnosis and treatment are crucial for managing symptoms and improving outcomes.