MYALGIA MYOSITIS RHABDOMYOLYSIS
SUMMARY:
RHABDOMYOLYSIS is a syndrome resulting from destruction of striate(skeletal) muscle cells with leakage of muscle intracellular toxins into the bloodstream, characterized by few symptoms, the most common being myalgia (muscle aches and cramps) and dark urine, and few sentinel laboratory findings, the most specific being a positive dipstick test for blood with few rbcs seen on microscopy, and elevated CK (creatine kinase ) in the blood. It occurs in Trauma situations, such as Crush injuries, where large quantities of muscle are destroyed. More commonly, it develops in situations where moderate to severe exercise occurs, particularly in hot humid climates, in de-conditioned individuals. Renal failure, cardiac arrhythmias, coma and death may develop. Dehydration is especially conducive to serious complication of Rhabdomyolysis. Toxins, illnesses, genetic defects (regarding ATP production) and electrolyte imbalance, are common environments where this syndrome often occurs. First and foremost is the ability to suspect rhabdomyolysis in the appropriate clinical settings. Treatment consists of treatment of the underlying condition, removal of the offending medication or toxin, rest, rehydration, and alkalinazation of the urine. Renal dialysis and treatment of Hyperkalemia may become necessary.)

When skeletal muscle is irritated or inflamed it often becomes sore and tender and the muscles ache. This MYALGIA can occur in a number of conditions. Viral Influenza is one of the more common causes of generalized muscle aches or myalgia. Certain medications, such as Statins, which are used for Hypercholesteremia, are occasionally associated with the onset of myalgia. Myalgia is most often transient, especially in it’s most common form, which is over exercise. It may resolve once the underlying illness has run it’s course, or the offending medication is stopped or simply by rest and hydration.

When myalgia intensifies, it involves the death and destruction of the skeletal muscle cells, called myo-cytes, then MYOSITIS develops. In this instance, substances, which belong within the cytoplasm of the cell, leak out into the blood. Such substances as creatine, myoglobin, aldolase, potassium, and lactate dehydrogenase are extruded into the blood stream. Myoglobin is the form of Hemoglobin found in muscle cells which transfers Oxygen and Carbon Dioxide. Myositis is characterized as exquisite tenderness of the affected muscles and the person may not be able to tolerate even the slightest pressure. The muscles may become swollen and boggy in consistency.

If the myositis is allowed to intensify, then irreversible damage may occur, generally from the muscle swelling, which, in turn, causes compression of vessels and nerves and results in massive dissolution of significant quantities of muscle. Dissolution of the myo-cytes and the subsequent release of large quantities of toxic intracellular components into the systemic circulation and the end organ consequences constitute the syndrome of RHABDOMYOLYSIS.

RHABDOMYOLYSIS may involve many organ systems, but the life threatening consequences are related to electrolyte abnormalities, i.e., acute hyperkalemia, hypocalcemia, and acute renal failure. When muscle is deprived of nutrition and circulation, intracellular-free Calcium is increased to critical levels and this triggers several degradative processes culminating in muscle cell death and in extravasation of intracellular toxins into the systemic circulation. The contraction of the extra cellular fluid volume appears to be the principal determinant of the renal toxicity of myoglobin.

Signs and Symptoms

The symptoms of Rhabdomyolysis are nonspecific and consist of an increase in ventilation, in an effort to blow off acidic CO2, and central nervous system function depression, manifesting itself as headache, lethargy, stupor and even coma, as well as severe
unexplained muscle pain, cramps and weakness. The muscles may be swollen and tender. The most commonly affected muscles are those utilized in exercise. Fever may be present, especially if associated with infections. The extremeties will demonstrate painful decreased range of motion. However, some patients are asymptomatic, necessitating the laboratory workup to suggest the diagnosis. So, it’s important that physician must maintain a high index of suspicion, which generally is tipped off by appropriate history and physical in the clinical situation, reflecting one of the many causes of Rhabdomyolysis.

Laboratory elevation of the CK (Creatine Kinase) is a key to the diagnosis, and is the most sensitive indicator. The CK is usually 5 times or more greater than the normal level and can be greater than 100,000 IU/L. Exercise to near exhaustion, is associated with a CK rise of only about 10,000 IU/L. Still, there is poor correlation between CK elevations and the morphologic degree of muscle damage. Urinalysis, initiated because the urine will darken (often the first clue) with the increased excretion of myoglobin, will demonstrate a positive test for hemoglobin, but the microscopic exam will show only a few red blood cells, suggesting Rhabdomyolysis. Microscopic urine exam may demonstrate “Muddy casts”, which re diagnostic of myoglobin or hemoglobin in the renal tubular fluid.

Once suspected, from the clinical symptoms, the clinical setting, especially the history of the illness, and the initial lab. tests, then measuring the Myoglobin in the urine and serum may confirm the diagnosis. Once the renal threshold for myoglobin is reached, myoglobin is cleared at 75 per cent of the glomerular filtration rate. If there is marked muscle breakdown, the serum myoglobin lever may be elevated.

Abnormal electrolyte findings may trigger off the premonition suggesting Rhabdomyolysis, by he presence of Hypernatremia, Hyperkalemia, Hyperuricemia (secondary to enhanced release of purine precursors), and Lactic acidosis (secondary to glycogen depletion and anaerobic mertabolism).

As the renal status deteriorates, the urine output may fall suggesting oliguric renal failure.

CAUSES OF RHABDOMYOLYSIS

Traumatic damage to large quantities of muscle was recognized during Crush Injuries in the Second World War and the diagnosis of Rhabdomyolysis was anticipated and recognized frequently.

Since then, Non-traumatic causes of Rhabdomyolysis are now recognized as being more frequent than the traumatic causes. It may occur after moderate to severe exercise in otherwise healthy people. This is reported to occur among young unconditioned military recruits, particularly in hot and humid military training. The heat generated during exercises encourages shunting of the blood to the surface for heat dissipation, depriving the kidneys and gastrointestinal tract of blood. This causes deterioration of the gut wall, allowing invasion of intestinal bacteria and bacterial toxins into the blood stream. This transient septicemia in the environment of a contracted body fluid volume can lead to myoglobin-induced renal failure.

Some genetic enzyme deficient conditions are associated with muscle necrosis even after minimal exercise.

Chronic Alcoholics are particularly susceptible to Rhabdomyolysis in certain situations. After binge drinking, there are significant electrolyte concentration changes in he muscle cells causes by direct injury from alcohol. These people often have deficiencies in potassium and phosphorus homeostasis, as well as easy susceptibility to infection, which may intensify the toxic effects of alcohol. In cirrhosis of the liver, phosphorus and potassium are shifted from the blood into the intracellular compartment, rendering the alcoholic more susceptible to rhabdomyolysis.

Recently Rhabdomyolysis has been associated with viral , bacterial and rickettsial Infections. It appears that the these organisms may attack the muscle directly or may lead to muscle-specific toxin generation. It occurs most commonly with influenza virus type A and B. It is seen in HIV patients as a sequelae to acute myositis, especially as part of the febrile illness that precedes seroconversion after infection. Certain bacteria, such as Lenionella species, Streptococcus species, Tularensis and Salmonella species have been incriminated. Several reports confirm the association between Q fever and Rocky Mountain spotted fever, rickettsial infections, to Rhabdomyolysis.

Chronic electrolyte imbalances, such as hypokalemaia and hypophophatemia may precipitate rhabdomyolysis. This has been reported also, in patients who drink excessive quantities of fluid, especially water, lowering their sodium (hyponatremia). Low potassium conditions which may potentiate the possibility of Rhabdomyolysis are seen with chronic administration of long-acting thiazide diuretics, certain antibiotics, and even ingestion of mineral corticoid-like substances, such as licorice. Hypomagnesemia, and even hypernatremia have been incriminated. Diabetic ketoacidosis has been reported to cause Rhabdomyolysis.

Heatstroke has been incriminated, as has hypothermia. This is especially susceptible when the addition of exercise is added. Once again, this appears to be do to shifts in intracellular Calcium and Phosphorus.

Miscellaneous Causes include Cocaine abuse, carbon monoxide poisoning, neuroleptic malignant syndrome, and prolonged coma in a fixed position (Saturday night Palsy).

Another classification of Rhabdomyolysis divides the types into 1.) Pure exertional, 2.) Exertion in those with genetic enzyme deficiencies, and 3.) Exertion in Nonhereditary forms. The first type is the typical heavy exertional type. The second category occurs in those individuals, who have defects in the pathways by which ATP is generated. These defects in the environment of exercise will contribute to Rhabdomyolysis. The third category includes those precipitating factors such as drugs, toxins, or infections, in which, the addition of exercise will cause muscle breakdown. Therefore exercise in patients who are alcoholic or have ingested cocaine (especially if they have an associated potassium and phosphate deficiency) places them at exceptional risk for Rhabdomyolysis.

DIFFERENTIAL DIAGNOSIS

The major physical clue to Rhabdomyolysis is the presence of painful, aching, and tender muscles. But this can also occur in primary muscular disorders, such as: Polymyositis, dermatomyositis, rheumatoid arthritis, fibrositis, polymyalgia rheumaica, tendonitis, localized infection and even with some medications (steroids, diuretics).

The other major clue, i.e., dark brown urine, can be seen in: hemoglobinuria, porphyria, uorbilinogen, medications (nitrofurantoin, priqmaquine, metronidazole, rifampin).

KIDNEY FAILURE

Renal failure appears to occur form the direct toxic effects of the excessive myoglobin. Myoglobin’s toxic effects appear to be enhanced by a diminution in extra cellular fluid volume, which is especially seen in trauma, where large volumes of fluid may extravasate into the lower extremities, resulting in severe ECF volume contraction. Renal failure is one of the most common cause of death in this condition.

Myoglobin, through it’s metabolites, is directly cyto-toxic to the renal cells. The production of oxygen and non-oxygen free radicals, because of the excess of free iron, lead to oxidant stress and injury to the renal cells. There is evidence that the alterations in the intracellular glutathione may contribute to the pathogenesis of pigment-induced renal failure.

Myohemoglobin may form tubular casts in the renal tubules, especially in an acid urine, which, once formed, may cause intra-tubular obstruction and increase in pressure and resultant diminished glomerular filtration rate, aggravating the already ongoing kidney damage.

TREATMENT

Irrespective of the etiology of the breakdown of the muscle cells, Rhabdomyolysis is potentiated if the extra cellular fluid volume is contracted, such that the urine output is diminished. So, the first and most important goal in treatment is to increase the urine output. This is most expeditiously done by giving IV normal saline, from 4 to 6 liters within the first 24 hrs.

Since the nephrotoxic effects of myoglobin are potentiated in an acidic urine setting, giving of Bicarbonate to alkalinize the urine is very beneficial. Maintenance of the urine pH greater than ki6 prevents disassociation of the myoglobin.

Since diuresis of the excessive Myoglobin is one of the goals, the giving of an osmotic diuretic such as Mannitol is very helpful. Lasix also can be given for it, fast diuretic action and it’s acidification of the urine.

Treatment of the underlying condition, such as a Compartment Syndrome, where increased intercompartmental pressure is elevated with deprivation of blood flow and death of tissue, by a fasciotomy is crucial.

Treatment is continued until the urine dipstick is negative for blood, creatinine is normal and the other laboratory tests indicative of Rhabdomyolysis are returned to normal.

COMPLICATIONS

Acute Renal Failure–This is the most serious complication, and may require renal dialysis, hopefully for the short haul, only.

Cardiac Arrhythmias– Because of the electrolyte imbalances commonly encountered, the heart muscle may become irritable and potentially fatal rhythms may ensue. Checking for and treating these imbalances are mandatory.

Disseminated Intravascular Coagulopathy (DIC)–This is a condition combining bleeding and excessive clotting simultaneously, resulting in death of vital organs. It must be anticipated and treated expeditiously and aggressively.

Cardiomyopathy and respiratory failure may ensue.

PREVENTION

Since excessive exercise is the more common culprit in the enviroment of predisposing factors, such as Substance Abuse, genetic enzymatic defects, or de-conditioning, it is wise to recommend gradual increase in exercise activity, particularly in the proper temperature and humidity, and to encourage adequate hydration.

References:

Bobby Adcock;Rhabdomyolysis: XIV Musculoskeletal/Connective Tissue Diseases);

P. Visweswaran M.D., J. Guntupalli, M.D.;Rhabdomyolysis; Critical Care Clinics, Vol 15. No. 2. April 1999, (Pg. 415-427).

Juha P. Kokko:Rhabdomyolysis: IX Critical Care Medicine; Pg. 522-525;

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Blunt trauma to the chest principally occurs from deceleration accidents. So falls, motor vehicle accidents and sports are the areas where this type of injury most frequently occurs. There are 5 major injuries that may occur in blunt chest trauma. These may occur singly or in cohorts. They are: 1.) Myocardial contusions, 2.) Traumatic Aortic dissection or tear, 3.) Flail chest, 4.) Tracheobronhial disruption, and 5.) Sternal fracture. In one study, ” Of 142 blunt trauma patients, 38 had Myocardial contusion 36 had traumatic aortic dissection, 33 had flail chest, 28 had sternal fracture, 7 had tracheobronchial disruption, and 3.5% had coexisting injuries”.

The primary aims of management of chest trauma are:
1.) Prompt restoration of normal cardiorespiratory function
2.) Control of Hemorrhage
3.) Treatment of associated injuries
4.) Prevention of sepsis

The diagnosis of the more serious of these injuries require diagnosis at or soon after triage and admission to the Emergency Room, because, while many of these people die at the accident scene, many more die soon after reaching the hospital. Most of these injuries can and must be suspected
and confirmation of their presence diligently sought for. This is accomplished by testing and close observation.

TRAUMATIC AORTA RUPTURE

Patients with Traumatic Aortic Rupture overwhelmingly used to die before reaching the hospital (80-85%), but now, only 40-70% die at the scene, and it had been determined that only 25% will die if the blood pressure is controlled. Therefore, with suspected or proven TAR, keeping the BP less than 120 mm. Hg., or the mean arterial BP less than 80 mm. Hg. is efficacious in preventing further tearing or rupture. This makes hemodynamic sense, since there is less peripheral arterial resistance from a lower, yet
effective, blood pressure.

More than 80% of injuries rupture through the intima, media and adventia (the three layers of the arterial wall), resulting in exsanguinations and death at the accident site. Patients who survive have maintained the integrity of the adventitia, but are at risk of complete rupture. 30% of survivors, from the accident, will die within 6 hrs.; another 20% by 24 hrs. if diagnosis is delayed. The abnormal blood containing space of the aorta between the inner and middle arterial layer (intimamedia) and the outer layer (adventitia) of the Aorta is referred to as a “pseudoaneurysm”. This is the first stage in the natural history of aortic rupture. This pseudoaneurysm then proceeds to grow, either slowly or rapidly, and can last for a few seconds to several years. In the final phase, the outer layer ruptures, resulting in free blood from the pseudoaneurysm pouring into the surrounding tissue.

Even then, in some few cases, the blood from the ruptured aorta may remain contained in the cylindrical space surrounding the Aortic vessel. This space is the supporting connective structure, which hold the Aorta, along with its branches, in place. Ultimately, this temporary barrier is breached by the pressure of the blood and the blood pours into the rest of the mediastinum or into the lung area and the patient exanguinates (bleeds out).

Diagnosis: Taking the BP in both upper extremities can often suggest the diagnosis. Remember, shock is not a one arm diagnosis. Taking the BP in all 4 extremities is an excellent way to pick of a TAR rupture, which might, otherwise, be missed.

Suspicion of a TAR should arise by the presence of cohort injuries, which attest to the severity of the accident. Other findings frequently associated with a TAR are Lt. Hemothorax, First rib fracture and Sternal fracture.

Routine chest x-ray arises suspicion of a TAR by the presence of a widened mediastinum. The pseudoaneurysm causes the aortic shadow on x-ray to expand laterally and occupy a larger central space on routine anterior-posterior chest films. A CAT Scan will confirm the presence, very quickly. Echocardiograms, which have recently become available for use in the ER can non-invasively
illustrate the dilated aorta, if sought for.

Treatment: The gold standard is still to take the patient, immediately, to surgery, in order to prevent further blood loss and abrupt rupture of the pseudoaneurysm. This approach has been fairly successful, often with other areas of bodily trauma attendant to simultaneously.

Recent articles have explored delayed surgery for suspected TAR. One article suggested that in this group, the “survival depends on the severity of other associated injuries. This means that the timing of surgical intervention in the stable (covered) aortic rupture with serious associated injuries should preferably be deferred, unless surgery has to be performed in cases of symptomatic transection in the hemodynamically unstable condition, including simultaneous surgery of concomitant lesions”. In one study, “7 patients had surgery postponed to allow for treatment or resolution of concomitant severe injuries. The non-operated group of patients avoided surgery because: A. Premorbid cardiac risk factors, B. Multiple complex intraabdominal injuries with coagulopathy. On the other hand, concomitant injuries, in particular, intra-abdominal solid injuries associated with frank bleeding, often take prescidence over immediate repair of the aortic injury”.
” It is clear that select patients with TAR can be managed without operation. They include concomitant cardiac, pulmonary, head or intra-abdominal injuries with or without premorbid symptoms”. “Patients who will develop life threatening complications from blunt cardiac injury can be identified in an emergency room setting. Think of aortic disruption in patients with hypotension
unexplained by other injuries”.

MYOCARDIAL CONTUSION

High speed/rapid-deceleration thoracic impact can cause damage to the heart muscle lying just below the inner chest wall. This impact can contuse the heart muscle leading up to a series of events that can be life threatening. Contused heart muscle, often, will not contract with it’s previous vigor, causing a transient fall in cardiac output. This results in a fall in the blood pressure and diminished delivery of oxygen to the periperal tissues. In other words, Shock may ensue. In addition, this muscle, which is now in disarray, may contribute to electrical disturbances in the heart rhythm, resulting in
arrhythmias, often associated themselves, with shock and subsequent death.

Because myocardial contusion is an important cause of rapid death after blunt chest trauma, it should be suspected at triage in the ER. It should be sought for, because there is no second chance. Two problems exist, however. Firstly, there is no standard diagnosis for this disorder, except at autopsy, and secondly, there is no definite protocol to identify patients at high risk for contusion. Myocardial contusion has been reported to occur in 8% to 71% of patients after blunt chest trauma. Other studies report an incident of 7-17% and suggest that only one third of these patients present with significant morbidity. One article suggests that 15% of those suspected of having MC died, 14% having died in the ER and 1% after leaving the ER. Of those suspected of MC, 20% developed arrhythmias, and of those, 20% had serious arrhythmias.

The pathology of MC varies from obvious tissue damage to the naked eye to, only microscopic hemorrhage, scattered sparsely throughout the heart muscle. Yet, it is hemodynamic con-sequences do not always follow the pathological picture. Even “stunned” myocardium can be associated with a fall in blood pressure or myocardial arrhythmias. Many patients with contused hearts have a transient decrease in cardiac output which resolves, spontaneously, within several hours, if shock and it’s associated complications do not or are not allowed to occur.

The triage in the emergency department must determine if a myocardial contusion is likely. Although no definite criteria exists for a definitive diagnosis, a likelihood of the condition is to be suspected from the history, the physical examination, the associated other injuries, and ancillary studies. The history of a deceleration injury with a bent or broken steering wheel; the presence of a bruised, contused or tender chest wall; chest wall abrasions, or a broken sternum, numerous ribs, or the 1st rib, by physical examination, along with abnormal vital signs, such as hypotension or tachycardia and EKG abnormalities, all dictate the level of suspicion, of the presence of an MC. The extent of other injuries, such as a broken pelvis, pneumothorax, intra-abdominal bleeding, all testify to the intensity of
the accident and should alert the triage personnel to the associated possibility of this condition. Persons older than 60 years old are candidates for this complication.

A high ISS (Injury Severity Score), used by the Emergency Paramedics is a good indicator for the possible presence of MC. Tachycardia is the most common physical sign, and is probably due to the reduced cardiac output (myocardial injury) and may be associated with a normal blood pressure early in the scenario. The presence of hypotension, on the other hand, suggests either hypovolemia, usually from blood loss, or myocardial dysfunction with diminished cardiac output, or both, and early volume resusitation may prevent further myocardial damage.

Hypotension from hemothorax or cardiac tamponade may occur associated with thecontusion or from some other injury.

Treatment: Then if a myocardial contusion is suspected, the possibilities of subsequent complications, consisting mostly of cardiogenic shock, or arrhythmia, must be anticipated and carefully monitored to diagnose. Hypotension is first resusitated with fluid replacement. If volume replacement is not satisfactory to reverse the hypotensive state, then inotropic agents and even IABP (Intra Aortic Balloon Pump) or even a MAST (Military Anti Shock Trousers) or PASG (Pneumatic anti-shock garment) have been utilized with success. Surgery may have to be delayed in patients with cardiogenic shock until stabilization is accomplished. Arrhythmias are watched for by heart monitoring and treated as they occur. The majority of patients with myocardial contusion do extremely well and the few serious ones, if anticipated and monitored are also salvagable. ” The coexistence of myocardial contusion and torn descending thoracic aorta occurs in a small percentage of cases, but is not surprising in view of a probable common injury mechanism; i.e., high-speed/rapid-deceleration thoracic impact”. An IABP(Intra-Aortic Balloon Pump) is very helpful, in this instance, for post operative cardiac support.

FLAIL CHEST

A Flail Chest consists of sequential Fractures of 3 or more adjacent ribs, or one or more rib fractures with an associated costochondral seperation or with a fracture of the sternum.This causes an unstable or “floating” segment of the chest wall that moves “paradoxically” during respiration. This simply means that the chest wall moves inward instead of the usual outward direction, during inspiration. This is a common injury associated with Blunt Chest Trauma, but the mortality is attributed to the occurence of pulmonary contusion, massive hemothorax and later to the occurence of ARDS(Aduklt Respiratory Distress Syndrome). A case of penetrating aortic Innjury by a detached rib fragment has been reported.
Of significance, is that the presence of a flail chest is to serve as a marker of other more significant intrathoracic injuries, which, as mentioned above, consist of pulmonary contusion, pneumothorax or hemothorax or both. Its presence, did not seem, in one study, to be a marker for great vessel, tracheobronchial or diaphragmatic injury, amplifiling why the case of aortic penetration, mentioned above, was a reportable case.

Flail Chest is especially important as a marker for the recognition of high kinetic energy absorbsion, which could result in life threatening thoracic, as well as non-thoracic injuries.

TRACHEOBRONCHIAL DISRUPTION

Although this injury is one of the more infrequent injuries in Blunt Chest Trauma, this injury can be life threatening and should be sought for if the following symptoms and signs are present. They include 1.) Subcutaneous emphysema, 2.) A shortness of breath, 3.) Sternal tenderness and, 4.) coughing up of blood. The X-ray will most often show air in the chest cavity or the mediastinum and clavical or rib fractures. Teracheobronchial disruptions are a marker for high-energy impact-type injuries suggesting the presence of other associated life-threatening injures.

If a tracheobronchial disruption is suspected, a bronchoscopy should be done to confirm visually the disruption . Therapy is directed towards the definite abnormality, which usually involves the use of surgery. Mechanical ventilation is often necessary.

In one study, disruptions involved the trachea in 3 patients, the right bronchus in 5 patients, and the left bronchus in 2 patients.

STERNAL FRACTURES

Sternal fractues constitute from 8-10% of admissions to trauma centers. Isolated sternal fractures are associated with low morbidity and mortality but do require management of pain. Often, they serve as a marker for cardiac and concomitant injuries. With the inception of mandatory seatbelt legelation, there has been a rise in this type of injury.
When confronted with a sternal fracture, it is important to access the heart via an EKG and cardiac serum enzkymes and have the patient evaluated by a cardiologist. Although an Isolated Sternal Frature has a good prognosis, careful evaluation and clinical observation are useful.

Bibligraphy
Blunt Chest Trauma
Emerg Med Clin North Am 1993 Feb; 11 (1):81-96
J Trauma 2001 Nov;51 (5):970-4
Thoracic Aortic Rupture
J Trauma 1990 Vol.30, No.12: 1606-8
Ann Thorac Surg 2002; 73: 1149-54
Myocardial Contusions
Am Surg 1999 Feg;65 (2):181-5
Semin Thorac Cardiovasc Surg
1992 Jul; 4(3): 195-202
Sternal fractures
World J Surg 2002 Oct;26(I10): 1243-6
Asian Cardiovasc Thorac Ann 2002 Jun; 10(2): 145-9
Flail Chest
J Am Coll Surg 1994 May; 178(5): 466-70
Eur J Cardiothorac Surg 1999 Sep; 16(3):374-7
Tracheobronchial Disruption
Ann Thorac Surg 1990 Oct;50(4): 569-74

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