Crush syndrome

Crush syndrome and proteinuria

Massive destruction of muscle tissue in crush syndrome leads to the release of myoglobin into the systemic circulation. This triggers the mechanism of extrarenal (overflow) proteinuria.

Normally, urinary protein is virtually undetectable (up to 30–50 mg/day, maximum 150 mg). During compression, prerenal (overflow) proteinuria develops. Low-molecular-weight proteins (myoglobin) freely pass through the intact renal filter, but their amount is so vast that the tubules cannot cope with reabsorption. A similar overflow mechanism is observed in intravascular hemolysis (hemoglobin release) and multiple myeloma (Bence Jones protein).

For comparison, other types of proteinuria have a different nature:

• Renal glomerular: damage to the filter itself (albumin is lost).
• Renal tubular: impaired reabsorption in the tubules.
• Hemodynamic: due to blood congestion in heart failure.
• Postrenal: admixture of exudate from the urinary tract due to inflammation.

Visceral compression in lymphocytic leukemia

The concept of "compression syndrome" is also applicable in hemato-oncology. In lymphocytic leukemia, pathologically enlarged lymph nodes act as a space-occupying lesion, causing compression syndrome:

1. Mediastinal compression: affected lymph nodes compress the heart, trachea, and esophagus, disrupting their functions.
2. Abdominal compression: enlargement of mesenteric and porta hepatis lymph nodes leads to portal vein compression. This directly results in portal hypertension and fluid accumulation in the abdominal cavity (ascites).

Spinal nerve compression syndromes

Compression of neural structures and vessels in osteochondrosis causes a cascade of pain and visceral disorders.

Thoracic region: Radicular syndrome presents as intercostal neuralgia. Interscapular back compression is characteristic—the "iron vice" sign, which intensifies at night. Compression at the $Th_{6} - Th_{11}$ level mimics gastralgia (intensifies after physical labor, subsides at night, independent of food intake). Lesions of the upper segments produce a pseudocardiac syndrome with shallow breathing and a sense of dread.

Cervical region: Compression manifests as a visceral syndrome ("cervical angina"). Pain begins in the interscapular area and radiates to the heart. Unlike true angina, the pain lasts up to 2 hours, depends on posture, is not relieved by nitroglycerin, and does not alter the ECG. Axial load on the head causes characteristic pain radiation (Spurling and Jackson tests), while neck traction reduces it (Bärtschi test).

Traumatic compression of the pelvic bones

Severe injuries are often associated with direct or indirect mechanical compression of the pelvic ring. Lateral pelvic compression or a blow to the greater trochanter causes an acetabular floor fracture with central hip dislocation.

Diagnosis is based on clinical presentation (instruments are not always used due to shock):

• Positive signs of "compression" and "distraction" stress (pain upon pressure on the iliac wings).
• Pelvic asymmetry and hematomas (in the perineum in anterior pelvic ring injuries).

Important nuance: trauma can cause pseudo-abdominal syndrome. A growing retroperitoneal hematoma irritates the peritoneum, causing muscle rigidity. To differentiate from a real organ rupture, Joyce's sign is checked (the percussion dullness does not shift when the body position changes) along with diagnostic paracentesis.

Class and exam questions

What else to study on this topic

• Hemolytic states in lymphocytic leukemia (hemolytic jaundice, hemosiderosis)
• Vasomotor disorders in thoracic osteochondrosis (decreased oscillatory index)
• Types of renal proteinuria (glomerular, tubular, hemodynamic)
• Classification of acetabular fractures (rim, displaced and undisplaced floor)

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.