What is viral myositis?
Acute myositis caused by a DNA or RNA virus can be a localized self-limiting process or a lethal systemic severe lesion. The severity of the disease is related to the type of virus and the immune status of the patient. The common ones are acute benign myositis, epidemic chest pain, and acute rhabdomyolysis. The clinical manifestations are fever, diarrhea, cough, sputum, localized muscle or generalized myalgia, and myalgia, which is mostly dull and often occurs after exercise.
I. Acute benign myositis in children
Etiology
Acute benign myositis in children may be a viral infection associated with viral infections such as coxsackievirus, influenza A or B virus and parainfluenza virus types 1 and 3, especially group B influenza virus infections. In recent years, it has been reported to be associated with EBV, HIV virus, etc.
Clinical presentation
The children were in good health and had fever, runny nose, nasal congestion, paroxysmal cough and other symptoms of upper respiratory tract infection at the beginning of the disease. Myalgia is mostly dull, often after exercise, and can be relieved after rest. On examination, there was tenderness in both calf muscles, but no skin sensory abnormalities, no redness or swelling in appearance, and negative neurological pathology. The myalgia recovered quickly after treatment and disappeared rapidly, and the time of symptom relief in this group was 2-4 days.
Laboratory examination
The peripheral blood leukocytes were all in the normal range, and the peripheral blood picture was dominated by elevated lymphocytes. Serum creatine kinase (CK) was high, ranging from 394 u/L to 2,759 u/L. Lactate dehydrogenase (LDH), creatine kinase isoenzyme CK-MB) and alpha hydroxybutyrate dehydrogenase (HBDH) were also mildly elevated, but CK was significantly elevated.
Diagnosis and differential diagnosis
The diagnosis is generally easy based on clinical manifestations and laboratory tests, but must be differentiated from other diseases. Myalgia seen in the course of influenza: myalgia at the beginning of influenza is soreness, weakness and widespread pain, the site is not fixed, CK is not significantly elevated; epidemic myalgia: caused by coxsackievirus, echovirus, characteristic performance in fever headache prodromal symptoms followed by sudden onset of severe intolerable episodic pain on both sides of the chest or at the attachment of the diaphragm, deep inspiration or position change can make the pain worse; polymyositis or Dermatomyositis: slow progression, lesions mainly involving the proximal muscle groups of the limbs, often complicated by skin damage, without severe myalgia and tenderness; acute myoglobinuria: more acute onset, occurring in the high fever phase of viral infection, manifested as severe myalgia and muscle spasms, muscle swelling, tenderness is obvious, urine is soy sauce, urine occult blood test is negative, myoglobin in the urine, severe cases lead to acute renal failure, muscle biopsy can be seen Myofibrillar necrosis, sometimes with phagocytosis, usually without obvious inflammatory cell infiltration, poor prognosis.
Treatment
Restriction of activity, bed rest for severe pain. Treatment is mainly antiviral, mainly with virazole or diflucan, supplemented with (Vit)B1, VitB6, VitC, etc., and bacterial infection is treated with sodium penicillin. Myalgia was relieved in 1 d of treatment, and walking was not difficult, and myalgia disappeared completely in 4 to 5 d. The more severe cases should be treated with hormones such as hydrocortisone or prednisone. The total course of treatment was about 7-10 d. All the patients walked on the ground in 3-6 d, and the pain disappeared and the body temperature was normal.
II. Epidemic chest pain
Epidemic myalgia, also known as epidemic chest pain, Bornholm disease, the pathogenic microorganisms are enteroviruses, mostly caused by coxsackievirus group B type 1-6, but also by group A type 1, 4, 6, 9, 10 and echovirus type 1, 2, 6, 9, although infectious and epidemic, but clinically uncommon.
Clinical manifestations
The main clinical manifestation is sudden onset of muscle pain, which is paroxysmal and increases with muscle activity. In a few cases, the disease may be accompanied by viral meningitis and myocarditis. Most of them have a good prognosis and resolve within 3-10 days.
Acute rhabdomyolysis
Many drugs can cause rhabdomyolysis (bony muscle) damage, the mild manifestations of muscle pain and weakness, serious rhabdomyolysis, acute renal failure, and even life-threatening.
1. Drugs that cause rhabdomyolysis?
1.1 Lipid-lowering drugs?
Lovastatin, simvastatin and pravastatin and other hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors have a direct toxic effect on the rhabdomyolysis. All 38 cases reported in the domestic and international literature occurred at therapeutic doses, but the time of appearance ranged from 36h to 24 months, with most occurring after 3 months. The incidence of muscle lesions with muscle pain and elevated creatine kinase (CK) was less than 0,5%. Patients taking concomitant drugs affecting the cytochrome P450 enzyme system such as cyclosporine, nicotinic acid derivatives, itraconazole, erythromycin, clarithromycin, azithromycin and mibefradil are more likely to develop them.
Fibric acid derivatives can also cause muscle damage. Long-acting phenoxyacetic acid drugs such as benzafibrate (bezafi-brate) have a risk of causing renal impairment and rhabdomyolysis.
1,2 β2 agonists
Terbutaline and other β2 agonists can cause rhabdomyolysis and acute renal failure, which may be related to the hyperdynamic effects of these drugs such as tremor and agitation that cause rhabdomyolysis.
1,3 Amphetamines?
Amphetamine (amphetamine) causes nerve endings to release norepinephrine which has a significant a-adrenergic-mediated vasospastic effect and is one of the pathogenic mechanisms causing rhabdomyolysis.
1,4 Drug abuse
Non-pharmacological use of many drugs can cause muscle damage, and the mechanism of action is related to drug-induced coma or activity transition. Phencyclidine is a pain reliever and is often abused. It has been reported that 25 cases of rhabdomyolysis were found in 1000 patients with phencyclidine poisoning, and up to 40% with acute renal failure. This is associated with muscle overactivity, toxic coma and direct rhabdomyolysis. Opioids such as diacetylmorphine (heroin) and methadone, barbiturates and benzodiazepines overdose causing coma muscle compression can occur with rhabdomyolysis and acute renal failure.
1,5 Drugs that cause hypokalemia?
Hypokalemia is a predisposing factor for rhabdomyolysis. Therefore, many of the drugs that cause hypokalemia can cause muscle damage, especially when other susceptibility factors are present at the same time. Drugs that cause acute potassium loss such as amphotericin B, strong diuretics, light laxatives, glyburic acid (raw gastric ketones) and long-term use of glyburic acid can cause rhabdomyolysis. Diabetic ketoacidosis, hyperosmolar nonketotic coma or lithium toxicity can cause rhabdomyolysis and acute renal failure.
1, 6 Malignant hyperthermia and neuroleptic malignant syndrome (NMS)
Many clinical and pathological features of acute rhabdomyolysis are associated with fever and dysautonomia, or NMS. Haloperidol, chlorpromazine, haloperidol, and risperidone have been reported to cause NMS associated with a rapid decrease in CNS dopamine function. Certain patients with genetic defects in muscular drugs, the use of isoflurane, enflurane and succinylcholine can induce a malignant hyperthermia-like disorder.
1,7 Ethanol
Acute rhabdomyolysis is associated with ethanol in at least 20% of cases. Asymptomatic CK elevation and histologic myopathy may occur in healthy individuals who consume large amounts of ethanol. Subclinical manifestations or overt rhabdomyolysis are commonly seen in alcoholics.
2. Clinical manifestations
Rhabdomyolysis usually occurs with acute muscle pain, muscle spasms, muscle edema, a “watery” feeling on palpation of the muscle, and systemic manifestations including nausea and vomiting and soy sauce-colored urine. Severe muscle pain and rhabdomyolysis are characterized by elevated serum CK activity, which can reach more than 10 times the normal value. Blood myoglobin concentration is elevated. Acute renal failure occurs in about 1/3 of cases, with early hyperkalemia, hyperuricemia and hyperphosphatemia.
Hypocalcemia is more pronounced than in other types of renal failure, and hypercalcemia can occur later and is a feature of some cases. The presence of “blood” in the urinalysis, but the absence of red blood cells under the microscope, is an important diagnostic clue.
Urine myoglobin concentration is elevated. Other associated manifestations of acute rhabdomyolysis are: compartment syndrome with localized muscle damage; hyperkalemic arrhythmias and diffuse intravascular coagulation with the release of muscle components into the circulatory system with systemic effects.
Dehydration, fever, acidosis and depletion of muscle energy stores due to starvation are predisposing factors for rhabdomyolysis.
3. Diagnosis
History of use of drugs that cause rhabdomyolysis and their precipitating factors.
Clinical manifestations such as muscle pain, weakness, muscle spasm, muscle swelling, muscle “watering sensation” and acute renal failure should be suspected as rhabdomyolysis. Serum CK is 10 times higher than normal; elevated blood myoglobin concentration, non-erythrocytic sauropuria and myoglobinuria can confirm the diagnosis. Other cofactors should also be considered.
4. Prevention and treatment
There are more than 150 kinds of drugs that cause severe muscle damage. More than 80% of the cases of rhabdomyolysis are caused by drugs, especially in drug abusers. Long-term drinkers should be careful with drugs that can cause rhabdomyolysis.
If you do need to use them, you should regularly observe the changes in your condition and make the necessary examinations for early detection, early discontinuation and early treatment to avoid acute renal failure. If the disease is mild, it can be restored to normal soon after timely discontinuation of the drug, and no special treatment is necessary. For more serious cases, supportive therapy is mainly adopted. Early infusion of large amounts of fluid to maintain adequate urine volume. Intravenous sodium bicarbonate to correct acidosis alkalinize the urine to reduce tubular embolic damage of myoglobin. Active prevention of complications and hemodialysis treatment for impaired renal function. For statin-induced rhabdomyolysis, oral ubiquinone (CoQ10) 254 mg/d can completely relieve the symptoms after 3 months.