OVERVIEW

What is Crush Syndrome?

Crush syndrome refers to a clinical condition characterized by prolonged compression of muscle-rich areas in the limbs or trunk, leading to rhabdomyolysis. This causes the leakage of muscle cell contents into extracellular fluid and circulation, resulting in electrolyte imbalances. Symptoms include limb swelling, necrosis, hyperkalemia, myoglobinuria, and acute kidney injury.

How does Crush Syndrome occur?

• When human muscles are subjected to prolonged pressure, they become ischemic and necrotic, leading to localized swelling—this is known as crush injury, typically occurring in muscle-rich areas of the limbs or trunk.

• After the destruction and breakdown of blood and tissue proteins at the injury site, large amounts of toxic substances are produced. Once pressure is relieved and blood flow resumes, these toxins are released and spread throughout the body, causing systemic damage—primarily manifesting as renal failure symptoms like oliguria or anuria. This condition is called crush syndrome.

SYMPTOMS

What are the common symptoms of crush syndrome?

It can be divided into local and systemic symptoms.

• Local symptoms: Limb pain, swelling, skin induration, hardening, subcutaneous bruising, skin tightness, and blister formation around the compressed area. In severe cases, compartment syndrome (a sign of ischemic necrosis) may occur.

• Systemic symptoms: Varies depending on the organs affected by toxins and the severity of the condition. Patients may generally experience fatigue, dizziness, loss of appetite, pale complexion, chest tightness, abdominal distension, and constipation. Some may also have fever, flushed face, dark yellow or tea-colored urine, and increased heart rate. Severe cases may involve palpitations, shortness of breath, anuria, and even shock symptoms such as pallor, cold extremities, and profuse sweating.

What are the manifestations of compartment syndrome after crush syndrome?

Compartment syndrome is a condition that occurs in specific fascial compartments of the limbs after injury. The main symptoms include localized limb swelling, pain, and restricted movement. Classic compartment syndrome can be described by the "5 P's":

• Pain (Pain), which may later diminish or disappear due to sensory abnormalities (Painless);

• Pallor (Pallor) in the extremities;

• Paralysis (Paralysis) of the limb;

• Paresthesia (Paresthesia) of the skin;

• Pulselessness (Pulselessness).

Compartment syndrome can lead to ischemic necrosis of the affected limb and, in severe cases, acute kidney failure or even multiple organ dysfunction, which can be life-threatening.

Why does crush syndrome, which affects the limbs, harm the entire body?

This is determined by the key features of crush syndrome:

• Shock: Some patients may not show early signs of shock, or the shock phase may be too brief to detect. Others may experience severe neural stimulation, extensive tissue damage, and rapid blood pressure drop due to massive blood loss, leading to worsening shock that affects the whole body.

• Myoglobinuria: Within 24 hours after pressure is relieved, urine changes may appear, ranging from pinkish, tea-colored, brown, to dark brown or soy-sauce-colored. This is a hallmark of crush syndrome, caused by the release of necrotic muscle breakdown products into the bloodstream, damaging the kidneys.

• Hyperkalemia: Due to muscle necrosis, large amounts of intracellular potassium enter circulation. Combined with impaired renal potassium excretion, potassium accumulates dangerously, potentially reaching fatal levels that cause cardiac arrest within 24 hours. Hyperkalemia is often accompanied by hyperphosphatemia, hypermagnesemia, and hypocalcemia, worsening cardiac toxicity.

• Acidosis and azotemia: Ischemic muscle necrosis releases acidic substances, causing metabolic acidosis. Severe trauma also increases catabolism, leading to toxin buildup. Patients may exhibit confusion, deep breathing, agitation, extreme thirst, nausea, and other symptoms.

These combined effects result in systemic damage.

Why might crush syndrome patients have soy-sauce or tea-colored urine? Is a urine test necessary?

Because urine status reflects injury severity, testing is essential. Key observations include:

• Crush syndrome patients often exhibit urine color changes, with myoglobin-rich urine appearing reddish-brown, dark brown, tea-colored, or soy-sauce-colored.

• Acute kidney injury may reduce urine output: <400 mL/day indicates oliguria, while <100 mL/day indicates anuria.

• Urinalysis (e.g., urine volume, specific gravity, sodium, creatinine, protein, and casts) helps assess disease severity.

What is myoglobinuria in crush syndrome?

Healthy individuals have minimal myoglobin in urine. However, acute muscle damage in crush syndrome releases large amounts of myoglobin. Due to its small molecular weight, myoglobin easily enters urine, forming myoglobinuria.

Does crush syndrome have long-term complications?

Yes, patients may experience sequelae:

• Prolonged compression or decompressive surgery may cause muscle necrosis, leading to impaired or lost limb function.

• Some acute kidney injury patients may progress to chronic kidney failure, requiring long-term dialysis.

• A few critically ill patients may develop multi-organ dysfunction syndrome or severe infections, resulting in permanent organ damage.

CAUSES

In what situations does crush syndrome commonly occur?

Crush syndrome typically occurs in the following situations:

• Building collapses caused by natural disasters such as earthquakes;

• Being crushed or trapped by heavy objects in accidents like landslides, car crashes, or fires;

• Other scenarios (e.g., drug overdose, carbon monoxide poisoning, elderly individuals living alone falling accidentally) where patients, due to unconsciousness or inability to control their bodies, end up compressing their limbs under their own weight.

Why does compartment syndrome occur after crush syndrome?

The fascia in muscles forms enclosed compartments. In crush syndrome, prolonged compression or trauma from heavy objects causes tissue ischemia. Once the pressure is relieved, blood flow resumes, leading to bleeding and swelling in the injured tissues (primarily muscle tissue). This increases the volume and pressure within the compartment (fascial space), triggering the condition.

The elevated pressure further damages the muscles, exacerbating swelling and creating a vicious cycle that results in muscle necrosis.

What are the causes of death in crush syndrome patients?

• Primarily complications of acute kidney failure, such as hyperkalemia, severe acidosis, heart failure, or hypovolemic shock.

• Or death caused by concurrent conditions like multiple organ dysfunction syndrome (MODS), acute respiratory distress syndrome (ARDS), pulmonary embolism, disseminated intravascular coagulation (DIC), or severe infections (at the injury site or other organs).

DIAGNOSIS

How to determine muscle necrosis after crush syndrome? Is creatine phosphokinase testing necessary?

Creatine phosphokinase (CK or CPK) is an enzyme released during muscle injury, which helps assess the extent of muscle damage. Blood tests at different time points can track its rise and fall, making it a crucial indicator for diagnosing muscle damage in crush syndrome and evaluating its severity.

How to detect crush syndrome early?

• On-site assessment: Medical responders should suspect crush syndrome in patients with a history of limb compression, mark them accordingly, and transfer them promptly for further treatment.

• For suspected cases:

  • Obtain detailed information on the cause and mechanism of injury, duration of limb compression and swelling, and any history of reddish-brown, dark brown, or tea-colored urine post-injury, along with urine output.

  • Measure blood pressure and pulse to assess blood/fluid loss and shock.

• Urine tests: Include routine analysis, specific gravity, and myoglobin detection.

A positive result confirms the diagnosis and warrants immediate intervention. If the first two criteria are positive but urine tests are negative, monitor closely as a suspected case.

How is crush syndrome diagnosed?

Diagnostic criteria for crush syndrome include:

• Prolonged compression by heavy objects.

• Persistent oliguria or anuria unresponsive to fluid therapy.

• Reddish-brown or dark brown (tea- or soy sauce-colored) urine.

• Protein, red/white blood cells, and casts in urine.

• Elevated serum myoglobin, creatine kinase, and lactate dehydrogenase levels.

• Acute kidney injury (oliguria/anuria or progressive rise in serum creatinine).

What blood tests are needed for crush syndrome?

• Complete blood count (CBC) and blood type: Assess infection, blood/plasma loss, fluid overload in oliguric phase, and coagulation status; prepare for potential transfusions.

• Electrolytes, acid-base balance, and blood gas analysis: Detect life-threatening conditions like hyperkalemia, hypermagnesemia, hypocalcemia, acidosis, or hypoxia.

• Liver and kidney function tests: Evaluate organ damage.

• Coagulation profile and D-dimer: Identify severe coagulopathy to prevent fatal spontaneous bleeding; monitor for hypercoagulability, which may progress to bleeding due to depleted clotting factors.

• Serum myoglobin, troponin, and enzyme panels: Assess muscle necrosis and cardiac injury.

• Lactate, C-reactive protein (CRP), and procalcitonin: Evaluate organ perfusion, systemic inflammation, and infection.

How to assess the severity of crush syndrome?

Crush syndrome is classified into three grades based on injury severity, muscle damage extent (CPK levels), and lab results:

• Grade I (Mild): Myoglobinuria positive, CPK >10,000 U/L (normal: 130 U/L), no systemic symptoms like acute kidney failure.

• Grade II (Moderate): Myoglobinuria positive, CPK >20,000 U/L, elevated creatinine/urea without oliguria, but with significant plasma leakage, hypovolemia, and hypotension. Risk of kidney failure.

• Grade III (Severe): Myoglobinuria positive, markedly high CPK, oliguria/anuria, shock, metabolic acidosis, and hyperkalemia. Life-threatening kidney failure.

TREATMENT

What are the on-site first aid measures for crush syndrome?

• Rescuers should quickly enter the scene and strive to relieve the pressure of heavy objects as soon as possible to reduce the chances of this condition occurring.

• Avoid moving the injured limb to minimize the absorption of tissue breakdown toxins and reduce pain. Especially for injured individuals who can still move, explain the dangers of movement.

• Cool the injured limb with cold water or expose it to cool air. Massage and heat application are prohibited to avoid worsening tissue hypoxia.

• Do not elevate the injured limb to prevent lowering local blood pressure and affecting blood circulation.

• For open wounds and active bleeding on the injured limb, stop the bleeding, but avoid using pressure bandages or tourniquets.

• All individuals with crush injuries should consume alkaline beverages (8 g of sodium bicarbonate dissolved in 1,000–2,000 mL of water, with added sugar and salt). This promotes diuresis and alkalizes urine, preventing myoglobin deposition in renal tubules and kidney damage. If oral intake is not possible, administer 5% sodium bicarbonate intravenously.

Is a tourniquet used for crush syndrome?

Generally, no.

Improper use of a tourniquet or prolonged application may lead to local muscle damage, necrosis, and even worsen crush syndrome. Therefore, tourniquets should generally be avoided for crush injuries.

However, if the injured person has been trapped for an extended period with little hope of limb salvage or cannot receive fluid therapy, a tourniquet may be considered before rescue to prevent sudden death due to a rapid drop in blood volume and toxin absorption into circulation after rescue.

Once reliable venous access is established, adequate fluid resuscitation is provided, and close monitoring is in place, the tourniquet can be released or amputation performed.

Why does crush syndrome require incision of the injured limb?

Severe swelling occurs in limbs subjected to prolonged pressure. The fascia, which normally protects muscles, is tough and tight. As it continues to perform its role, the internal swelling pressure cannot be relieved.

Early decompression involves incising the injured limb on-site, with simple debridement of necrotic tissue and drainage if necessary. This reduces compartment pressure, preventing or mitigating crush syndrome.

Even if muscles are already necrotic, drainage can prevent harmful substances from entering the bloodstream, reducing systemic toxicity. It also removes non-viable tissue, lowering the risk of infection.

What are the systemic treatment measures for crush syndrome?

• Anti-shock measures with large-volume fluid resuscitation. Provide adequate volume resuscitation under monitoring to correct shock.

• Alkalize urine. Intravenous sodium bicarbonate is typically administered to increase the solubility of acidic methemoglobin in urine, aiding excretion and preventing myoglobin deposition in renal tubules. This protects kidney function and prevents acidosis.

• Diuresis and dehydration. After sufficient volume resuscitation, diuresis and dehydration help increase renal blood flow, prevent kidney failure, and reduce compartment pressure, potentially avoiding fasciotomy in some patients.

• Anti-infection measures. Administer broad-spectrum antibiotics and tetanus antitoxin.

Under what circumstances should amputation be considered for crush syndrome?

Amputation should be considered in the following situations:

• The injured limb has no or severely insufficient blood flow, with little hope of functional recovery.

• Severe systemic toxicity symptoms persist despite decompression and other treatments, endangering the patient's life.

• The injured limb develops specific infections, such as gas gangrene.

How to manage acute kidney failure in crush syndrome patients?

• Strictly control fluid intake. Follow the doctor's dietary instructions and avoid excessive water intake.

• Treat metabolic acidosis.

• Correct water and electrolyte imbalances, especially hyperkalemia.

• Prevent and control infections.

• Promote kidney function recovery.

• Enhance nutrition.

• Implement blood purification measures, including hemodialysis and continuous hemofiltration, to save the patient's life. Continuous renal replacement therapy should be initiated early in the following cases:

  • Multiple organ injuries or multiple organ dysfunction syndrome (MODS).

  • Hemodynamic instability.

  • Volume overload unmanageable by hemodialysis or peritoneal dialysis.

  • Severe infection or sepsis.

  • Hypercatabolic state: daily increase in serum creatinine >44.2 μmol/L, urea nitrogen >3.57 mmol/L, potassium >1 mmol/L.

  • Refractory electrolyte and acid-base imbalances.

When do crush syndrome patients require blood purification therapy?

Blood purification therapy should be considered in the following cases:

• Prolonged crush injury with oliguria, anuria, or azotemia.

• Hyperkalemia, acidosis, or other electrolyte and acid-base imbalances unresponsive to fluid therapy.

• No urine output after >3L of fluid resuscitation, with cardiac or circulatory overload.

What is the purpose of blood purification therapy for crush syndrome patients?

• For crush syndrome patients, myoglobinemia is the primary cause of acute kidney failure. Even if systemic circulation (e.g., blood pressure, heart rate) improves, failure to clear excess myoglobin can still lead to acute kidney failure. Blood purification effectively removes myoglobin, reducing kidney damage.
  
  
• Crush syndrome often involves hyperkalemia, azotemia, and acidosis. Blood purification precisely controls fluid balance, provides better nutritional support, and stabilizes the internal environment, correcting water, electrolyte, and acid-base imbalances.
  
  
• Early in crush injuries, toxins and inflammatory cytokines cause systemic inflammation. Blood purification clears these inflammatory factors, reducing organ damage.

DIET & LIFESTYLE

What should patients with crush syndrome pay attention to in their diet?

In terms of diet, patients with crush syndrome should pay attention to:

• During the acute phase, the diet should be light, typically low-fat, high-carbohydrate, high-calorie, high-quality low-protein (high-quality protein mainly refers to animal protein, such as milk, eggs, etc.), low-salt, and low-potassium. If undergoing dialysis treatment, dietary restrictions can be appropriately relaxed. Insufficient calorie intake in the diet can lead to protein breakdown, worsening azotemia and hyperkalemia.

• During the oliguric phase, high-potassium foods (such as bananas, oranges, grapes, potatoes, mushrooms, etc.) should be avoided. Alkaline beverages, such as sodium bicarbonate, should also be provided. Fluid intake should be carefully controlled to prevent water intoxication. After kidney function improves, high-protein foods can be gradually increased.

What should patients with crush syndrome pay attention to in daily life?

In daily life, patients with crush syndrome should pay attention to:

• Monitor the swelling, color, firmness, and peripheral blood circulation of the injured limb, as well as any bleeding or fluid leakage, arterial pulses, and sensation in the affected limb.

• Restrict movement of the injured area, which is especially critical for patients who can still move the affected limb.

• Avoid applying heat to the injured area, do not use compression bandages, and do not elevate the limb.

• Engage in functional rehabilitation exercises for the limb to prevent paralysis caused by prolonged inactivity.

How should patients with crush syndrome exercise after improvement?

• Functional rehabilitation of the injured limb. For patients with stable limb injuries and stable vital signs, muscle training for the affected limb should begin as early as possible to prevent muscle atrophy and promote functional recovery. Systematic functional training should be conducted once the condition stabilizes to restore physical function as much as possible.

• Prosthesis fitting and training. For amputees, prostheses should be fitted as early as possible, followed by professional functional rehabilitation training to help them regain daily living abilities quickly.

PREVENTION

How to Prevent Crush Syndrome?

Since the mortality rate of this condition is high, prevention is crucial. General preventive measures include:

• Administering saline and colloidal solutions after injury: Replenish fluids as soon as possible post-injury. On the first day, calculate the required amount based on the compressed area, duration of compression, and body weight, adjusting later as needed. However, if acute renal failure has already occurred, fluid replacement should not follow this protocol, and infusion volume must be controlled.

• Alkalinizing urine: Since crush syndrome often involves acidosis, alkaline medications should be used early to alkalinize urine, preventing acidosis and stopping myoglobin from depositing in renal tubules due to acidic urine. Oral sodium bicarbonate solution or intravenous 5% sodium bicarbonate can be administered.

• Diuresis: Once blood pressure stabilizes, diuresis can be performed to allow more alkaline urine to pass through renal tubules before kidney damage occurs, increasing the excretion of harmful substances like myoglobin. Intravenous 20% mannitol can be used rapidly and should be applied early.

• Relieving renal vasospasm: After crush injury, the concentration of vasoconstrictors like renin and histamine in the blood increases, causing renal vasoconstriction and reduced blood flow. Early use of mannitol can be combined with vasodilators to relieve renal vasospasm and improve renal blood flow.

• Fasciotomy decompression: Release exudates to improve circulation. The incision should extend beyond the most severely swollen muscle area, with no need for deep exploration. For limbs with necrotic muscles, amputation should be performed decisively once myoglobinuria or other early signs of renal failure appear.