11.3 Musculoskeletal

Compartment Syndrome: A Time-Critical Surgical Emergency

Compartment syndrome occurs when pressure within a closed fascial compartment rises high enough to collapse capillary perfusion, producing ischemia and, if untreated, irreversible muscle and nerve necrosis within hours. Common causes are fractures (the tibia is the most frequent site), crush injuries, reperfusion after vascular repair, tight casts or dressings, burns, and infiltration/extravasation of fluids. The clinical picture is summarized by the 6 Ps, but their timing is crucial - the early signs drive the decision, and waiting for the late signs means the limb is already lost.

Pain out of proportion to the injury and pain on passive stretch of the muscles in the compartment are the earliest and most sensitive findings. Distal pulses are frequently present until late, so a palpable pulse never rules out compartment syndrome. When the exam is equivocal or the patient is obtunded, compartment pressure is measured: normal is under 10-12 mmHg, an absolute pressure above 30 mmHg is concerning, and a delta (perfusion) pressure - diastolic blood pressure minus compartment pressure - below 30 mmHg is a strong indication for surgery. The definitive treatment is emergent fasciotomy. Supportive measures include removing constrictive casts and dressings and keeping the limb at the level of the heart - NOT elevated, because elevation lowers the arterial-to-compartment perfusion gradient and worsens ischemia. Abdominal compartment syndrome is the analogous process in the abdomen: sustained intra-abdominal hypertension (measured via bladder pressure) above about 20 mmHg with new organ dysfunction (oliguria, rising peak airway pressures) is treated with decompressive laparotomy.

Rhabdomyolysis

Rhabdomyolysis is the breakdown of skeletal muscle with release of intracellular contents - myoglobin, creatine kinase (CK), potassium, phosphate, and uric acid - into the circulation. Causes include crush and trauma, prolonged immobilization or a long "down time," seizures, limb ischemia, statins and other drugs, extreme exertion, and hyperthermic states (heat stroke, neuroleptic malignant syndrome, malignant hyperthermia). The danger is acute kidney injury (AKI) from myoglobin, which is nephrotoxic, obstructs renal tubules, and causes renal vasoconstriction - so-called pigment nephropathy.

The cornerstone of treatment is early, aggressive intravenous isotonic crystalloid to restore renal perfusion and flush myoglobin, targeting a urine output of roughly 200-300 mL/hr. Electrolytes are monitored closely and hyperkalemia is treated urgently because it is the most immediate life threat. Sodium bicarbonate to alkalinize the urine and mannitol are sometimes used but remain controversial and secondary to volume resuscitation. Because the same crush injuries cause both problems, patients must be monitored for coexisting compartment syndrome and for AKI severe enough to require renal replacement therapy.

Fractures and Fat Embolism Syndrome

Major fractures carry risks beyond the bone itself: hemorrhage (femur and pelvic fractures can sequester large blood volumes), infection, venous thromboembolism, and fat embolism syndrome (FES). FES arises most often after long-bone (femur) or pelvic fractures, when fat globules enter the circulation and lodge in the lungs and brain. The classic triad is hypoxemia/respiratory distress, neurologic change (confusion, agitation), and a petechial rash over the axillae, chest, and conjunctivae, usually appearing 24-72 hours after injury. Care is supportive - oxygenation and ventilatory support - and the best prevention is early fracture stabilization. FES is distinguished from pulmonary thromboembolism partly by timing and by the petechial rash, which is not seen with clot embolism.

Immobility Complications and Prevention

Critical illness and orthopedic injury enforce immobility, which drives predictable complications. Venous thromboembolism (VTE) - deep vein thrombosis and pulmonary embolism - is prevented with pharmacologic prophylaxis (low-molecular-weight heparin such as enoxaparin, or unfractionated heparin) and mechanical prophylaxis (sequential compression/intermittent pneumatic compression devices) when anticoagulation is contraindicated. ICU-acquired weakness (critical illness polyneuropathy and myopathy) is diffuse, symmetric weakness from prolonged ventilation, immobility, sepsis, hyperglycemia, deep sedation, corticosteroids, and neuromuscular blockers. Additional immobility hazards include pressure injuries, contractures, atelectasis and pneumonia, and constipation.

The evidence-based countermeasure is the ABCDEF bundle: Assess and manage pain, Both spontaneous awakening and breathing trials, Choice of light, goal-directed sedation, Delirium monitoring (CAM-ICU), Early mobility and exercise, and Family engagement. Early mobility is safe in appropriately screened patients and reduces delirium, ventilator days, and ICU-acquired weakness - making mobilization an active therapy, not merely comfort care.

Crush syndrome and integrated monitoring

The musculoskeletal emergencies of this chapter overlap and reinforce one another, and the CCRN rewards candidates who see the connections. Crush syndrome is the classic example: a prolonged crush injury simultaneously produces rhabdomyolysis (with hyperkalemia and myoglobinuric acute kidney injury), compartment syndrome (from swelling within the fascial envelope), and hypovolemia (from fluid sequestration into damaged muscle). A dangerous surge of potassium can occur at the moment of extrication or after reperfusion, so continuous cardiac monitoring and pre-emptive fluid resuscitation are begun early. Pressure injuries are staged 1 through 4 (plus unstageable and deep-tissue injury) and are prevented by repositioning at least every 2 hours, offloading heels, managing moisture, and using specialty support surfaces for high-risk patients. Because immobilized critical-care patients are at once at risk for bleeding and for clotting, VTE prophylaxis is continually reassessed against surgical and hemorrhagic risk, with mechanical devices bridging any period when pharmacologic prophylaxis must be held. The unifying theme is anticipatory, protocol-driven prevention: the complications of immobility are largely predictable, and the ICU nurse who bundles pain control, minimal sedation, daily awakening and breathing trials, delirium screening, and early mobility measurably shortens the road to recovery.