![]() Kembara Xtra - Medicine - Rhabdomyolysis The breakdown of skeletal muscle combined with the release of intracellular substances into the system. Rhabdomyolysis is characterized clinically by the presence of muscle soreness, weakness, and a urine color that is described as being tea-colored. Up to half of the patients do not exhibit any symptoms. In terms of epidemiology, there are around 26,000 hospitalizations carried out each year in the United States. Causes and effects: etiology and pathophysiology Trauma to the muscle directly (the most prevalent cause). - Trauma from being crushed - Prolonged periods of intense muscle contraction (for example, during an operation or while an individual is under the influence of alcohol). – Burns, electrocution, and lightning strikes. Muscle exertion – Intense and/or prolonged physical exercise (marathon runners, athletes, contact sports) Lightning strikes Tremors and fits – Delirium tremens Alcohol, cocaine (the most often used substance for recreational purposes), methamphetamine, phencyclidine, heroin, and bath salts; synthetic marijuana has been linked to severe rhabdomyolysis. - Antipsychotic medications (as a result of neuroleptic malignant syndrome, malignant hyperthermia, and dystonia) – Zidovudine – Malaria Preventatives – HMG-CoA reductase inhibitors, often known as statins (risk less than 0.01%, but increased with larger doses and when taken in conjunction with fibrates) In addition to Colchicine and Corticosteroids – Poisoning from snake bites – Carbon monoxide poisoning ,thrombosis, embolism, and sickle cell disease can all cause ischemic muscle damage. - The syndrome of compartments – Compression Splints ,infections that are caused by viruses include influenza A and B, coxsackievirus, HIV, and varicella. - Bacterial infections such as sepsis caused by Streptococcus or Staphylococcus, gas gangrene, necrotizing fasciitis, Salmonella, and Legionella - Autoimmune illnesses including polymyositis and dermatomyositis; metabolic and endocrinologic conditions including hypothermia and hyperthermia; – Hypothyroidism or thyrotoxicosis – Electrolyte imbalances (such as hyponatremia, hypernatremia, hypokalemia, hypocalcemia, and hypophosphatemia) – Thyroid disease (hypothyroidism) – A condition known as diabetic ketoacidosis – A hyperosmolar state Although the hereditary causes of rhabdomyolysis are uncommon, they should be suspected in children, patients with recurring episodes, or individuals who suffer attacks after minimal exercise, minor sickness, or fasting. In addition, hereditary causes of rhabdomyolysis are more likely to occur in women than in men. Disorders of lipid metabolism (such as a deficit in carnitine palmitoyltransferase, for example) – Muscular dystrophies - Problems with the way the body processes carbohydrates (such as phosphofructokinase deficiency, phosphoglycerate mutase deficiency, and myophosphorylase deficiency, often known as McArdle disease or deficiency) - Glycogen storage disorders such as phosphorylase B kinase deficiency and other glycogen storage diseases such as lactate dehydrogenase A deficiency - Problems with the mitochondria Preventive Measures in General • Refrain from engaging in strenuous activity; ensure that appropriate hydration is maintained. • Steer clear of medicines that could precipitate metabolic or electrolyte imbalances. Crush injury is diagnosed when there is direct trauma as well as prolonged compression and immobility. Accidents involving motor vehicles (MVA) and people becoming trapped in collapsing structures are two of the causes. Because of their decreased mobility and increased propensity to fall, senior citizens have a higher risk of crushing injuries. Rhabdomyolysis often takes place after one hour of immobilization; however, examples have been observed with compression lasting less than twenty minutes. A possible history of overexertion or the use of a drug or toxin (such as cocaine, amphetamine, or statins), especially in hot conditions The patient may report having symptoms such as fever, malaise, muscle aches, weakness, cramps, or exhaustion. Nausea, vomiting, and diarrhea Urine that is dark in color Agitation while patients are being restrained Extended periods of lying on a hard surface (for example, those who are inebriated or obtunded) The Patient's Clinical Examination Measurements of the patient's vital signs, including temperature, pulse, respiration rate, blood pressure, and oxygenation status On examination, the patient can have evident muscle soreness as well as evidence of a crush injury, weakness, and/or swelling. It's also possible that the muscle exam will come out perfectly normal. Myoglobinuria is indicated by urine that has a hue similar to tea, and decreased urine output may be an indicator of renal failure. Diagnosis by Differentiation Rhabdomyolysis and any condition that produces acute tubular necrosis have the potential to be confused with one another. Inflammatory myopathie,bacterial or viral infection,Guillain-Barré syndrome,myocardial infarction,Inflammatory myopathies,Phosphorylase, phosphofructokinase, carnitine palmityl transferase, and phosphoglycerate deficiency. Results From the Laboratory Initial Examinations (in the lab and with imaging) The most essential diagnostic test is the creatine kinase (CK) measurement, which should be increased to >5 times the upper limit of normal or >1,000 U/L. CK levels that are greater than 5,000 U/L are linked to the development of acute renal failure (ARF), which should trigger intensive fluid resuscitation. CK levels reach their maximum in less than twenty-four hours and return to normal in three to five days; as a result, CK is a more sensitive diagnostic than myoglobin. Myoglobin is to blame for the damage done to the kidneys, and C. After a few hours, serum myoglobin levels reach their maximum, and they return to normal after around 24 hours. Due to the quick clearance, even normal levels of myoglobin do not exclude the possibility of rhabdomyolysis. A positive dipstick test for blood in the sediment of the urine that does not contain erythrocytes is indicative of an injury caused by either hemoglobin or myoglobin. Acute renal failure (ARF) might exacerbate elevated serum potassium levels caused by muscular damage. Initial hypocalcemia: Calcium reaches the injured muscle cells where it precipitates as calcium phosphate, which ultimately results in calcification of the ischemic muscle cells. Initial hypocalcemia should only be treated if the patient is experiencing symptoms or has ECG alterations; otherwise, it will resolve itself throughout the renal recovery phase. 20–30% of patients will experience hypercalcemia during the renal recovery phase. This complication is unique to rhabdomyolysis-induced ARF. As renal function returns to normal, there is a mobilization of the calcium that had precipitated, an increase in calcitriol, and the disappearance of hyperphosphatemia. It is possible that you are suffering from extreme hyperuricemia, which can lead to acute uric acid nephropathy. The presence of elevated BUN and creatinine levels is suggestive of ARF. It is possible for hepatic impairment to be reversible. On the other hand, an injury to the muscle may be the cause of elevated levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactic dehydrogenase, rather than an injury to the liver. Increases in coagulation times, fibrin degradation products, and D-dimer, in conjunction with decreases in platelets and fibrinogen, are suggestive of the presence of disseminated intravascular coagulation (DIC). Electrocardiogram with 12 leads because hyperkalemia might cause deadly arrhythmias Additional Assessments, as well as Other Important Factors Notwithstanding normal initial levels, there is a risk of delayed renal failure and electrolyte problems Creatine phosphokinase (CPK) levels that are steadily rising are a sign of ongoing muscle damage. Findings from renal imaging are consistent with those found in other ARF mechanisms. Diagnostic Methods and Other Procedures If compartment syndrome is suspected, the pressures inside the muscles' compartments should be checked. The Interpretation of Tests Necrosis of the muscle Myoglobin-related renal damage may have similarities to acute tubular necrosis brought on by other causes. Management Deal with the underlying cause (such as discontinuing a drug, regulating the temperature, treating an injury, or treating an infection). In many cases, it is vital to drink a lot of water. It is possible for up to 12 liters of fluid to become sequestered in the muscles following severe muscle trauma, often known as crush injuries. Ensure proper monitoring of renal function, CK levels, and electrolytes. Due to the possibility of arrhythmias, it is important to monitor your potassium levels. • Administer the necessary treatment for DIC or hepatic impairment. Recognize the symptoms of compartment syndrome and treat it as soon as possible. The First Line Of Defense Is Medication The most critical strategy is aggressive fluid resuscitation, which consists of normal saline (NS) and 5% glucose solution with a goal urine output of 200 to 300 mL/hr. In order to avoid a volume overload, it is advisable to alternate between NS and 5% glucose. The rate of infusion ought to be set at 500 mL per hour. Sodium bicarbonate to boost urine pH over 6.5 may be used to achieve urine alkalinization, which may reduce the amount of myoglobin-induced nephrotoxicity in the tubules. – Use is fraught with debate. – One of the potential adverse effects is a worsening of hypocalcemia. – Patients who have acidosis, very high CK levels, or both acidosis and concomitant hyperkalemia may benefit from taking sodium bicarbonate. – Infuse at a rate of 200 mL per hour 1 liter of D5W containing 150 mEq (3 ampules) of NaHCO3. Second in line IV mannitol as a bolus if urine production continues to be low, 1 to 2 g/kg, with a maximum of 200 g in 24 hours and a cumulative dosage of 800 g should be administered. It is only used to prevent ARF in cases where diuresis is insufficient (less than 200 mL/hr), notwithstanding the administration of fluid treatment. - Causes an increase in the production of prostaglandin, which in turn causes renal vasodilation and diuresis, hence lowering the risk of myoglobin damage. Mannitol, which acts as an osmotic agent and is filtered by the tubules but is not reabsorbed by them, enhances sodium delivery and diuresis. It is possible that this will remove debris from necrotic cells and avoid an increase in compartment pressures. – There is debate regarding the use of mannitol. There is little data to support the claim that it improves outcomes more than vigorous IV hydration does. Mannitol, which acts as a free-radical scavenger, can protect the kidneys from damage if it is administered prior to tubular blockage. – If you find that you need to force diuresis, think about adding furosemide (40 to 120 mg per day). – In cases with anuric renal failure, diuretics should not be used; older patients and those with cardiovascular disease should also exercise caution. Hyperkalemia can occur as a direct consequence of the extensive release of intracellular potassium reserves or ARF. Treatment is necessary when ECG alterations are present (such as tall, thin T waves, PR prolongation, QRS widening, and P wave flattening), as severe hyperkalemia can pose a threat to a patient's life. - Calcium gluconate, intravenous 1 to 2 ampules (0.5 mL 10% calcium gluconate equals 4 mg elemental calcium; provide 4 mg/kg/hr for 4 hours) to stabilize the cardiac membrane. - If acidosis is evident, administer one to two ampules, or two to three milliliters per kilogram, of sodium bicarbonate intravenously. The condition of hypocalcemia can be made worse by sodium bicarbonate. – If it is safe to do so, an enema containing up to 20 grams of oral sodium polystyrene sulfonate (Kayexalate) at a dose of one gram per kilogram of the patient's body weight may be administered. – Insulin and albuterol both have a short-term effect of temporarily driving potassium into the cells. The effects of insulin on low blood sugar can be counteracted by the administration of glucose. - Caution: constant monitoring of potassium levels to avoid overcorrection, which could result in hypokalemia and arrhythmias Symptomatic and refractory hyperkalemia (ECG) is one of the indications for dialysis, as are oliguria (0.5 mL/kg over a 12-hour period), anuria, volume overload, and chronic acidosis (pH 7.1). Referral; often treated as an inpatient; a diagnosis of compartment syndrome warrants surgical consultation for the possibility of fasciotomy; a diagnosis of acute renal failure (ARF) may warrant dialysis treatment. Extra Medical Interventions During the oliguric phase, intravenous calcium gluconate may be beneficial for treating symptomatic hypocalcemia, which is uncommon. Surgical Treatments Available for Patients Suffering from Muscle Entrapment and Compartment Syndrome Admissions and enrollments Patients whose CK levels have risen significantly should be admitted to the hospital for hydration through an IV and clinical observation. Volume expansion with NS to raise urine production to at least 150 mL/hr. CK typically peaks between 24 and 36 hours after a muscle injury, therefore monitoring should establish that the CK is going downward. The function of the kidneys ought to be steady or improving. Electrolytes ought to be within typical ranges. Patients who have a little elevated creatinine kinase level but otherwise normal renal function may be allowed to leave the hospital following the observation phase if their CK level is falling. Keep in Touch Repeat the CK, electrolyte, and renal function tests within a few days as part of your follow-up care. Monitoring of the Patient Dependant on the disease: necessary for metabolic myopathies.Myotoxic medicines should be stopped and monitored regularly. Myopathologies can be fatal. Diet When you have renal failure, you should limit your protein consumption to bring down your BUN level. Reduce the amount of potassium you consume. It is vital to limit fluid consumption while suffering from anuria. The prognosis will depend on the primary cause of the rhabdomyolysis as well as the patient's ability to recover from ARF without experiencing any complications. Complications: Death, most commonly as a result of hyperkalemia or renal failure The prognosis is excellent if the patient receives dialysis and other forms of supportive care.
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