COMPARTMENT SYNDROME
Overview
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Limb-threatening condition with increased pressure within an enclosed space, resulting in tissue ischaemia
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Untreated compartment syndrome leads to tissue necrosis, permanent functional impairment and if severe, renal failure and death
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Causes:
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Increased compartment volume​
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Fractures/dislocations​
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Ischaemia-reperfusion injury
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Severe soft tissue injury
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Haemorrhage into compartment
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Strenous muscle use (exercise, seizures, tetany
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Significant oedema
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Reduced compartment volume​
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Burns eschar causing constriction​
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Tight dressings/casts
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Prolonged limb positioning (eg during surgery)
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Pathophysiology
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Excess fluid or significant construction increases pressure
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Venous collapse occurs first, leading to transudation of fluid into already constricted compartment, in accordance with the Starling equation
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Leads to limb congestion and accelerating compartment pressure buildup
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When venous presure is higher than capillary perfusion pressure, capillaries collapse
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Perfusion pressure is elevated as a physiologic response, causing reduced tissue perfusion
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Hypoxia cuses tissues to undergo anaerobic metabolism
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Lactic acid accumulates​
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Cell membranes are unable to maintain osmolar gradient as ATP-dependent Na+/K+ pump fails
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Lipid peroxidation of the cell membrane stimulates inflammatory cascade, activating neutrophils and generating hypoxanthine
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Reperfusion of an ischaemic compartment brings an abundant supply of oxygen than reacts with hypoxanthine to produce superoxide​
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Iron in red blood cells react with​ hydrogen peroxide to form hydroxyl radical and other free radicals that are highly toxic
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Platelet aggregation and microvascular clotting is also promoted by these radicals causing further ischaemia
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Clinical assessment
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High index of suspicion when there is disproportionate pain in an extremity after injury at rest of with passive stretch
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Classic features (The six Ps)
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Pain​
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Pallor
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Poikilothermia (Perishingly cold)
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Pressure
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Paralysis/paraesthesia (sensory nerves affected first, then motor nerves)
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Pulselessness (very late sign!)
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Investigations
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Less helpful in diagnosis of compartment syndrome
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Usually only helpful in suspicious non-communicative patients (eg heavily sedated in ICU)
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Bloods:
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Elevated K+ and creatinine​
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Elevated creatine kinase
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Presence of urine myoglobin
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Imaging:​
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Plain radiographs (for fractures)​
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Doppler ultrasound to evaluate arterial flow and presence of deep venous thrombosis
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Compartment pressure measurement​
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Normal intracompartmental pressure (ICP) is <10 mm Hg​
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Decompression recommended when difference of ICP and diastolic blood pressure (Δp > 30 mm Hg)
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Commercial direct pressure measurement equipment
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Can otherwise be performed using wide-bore needle attached to CVP monitor​
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Both techniques require experience and know-how, and should not be performed unless confident due to risk of catastrophic missed compartment syndrome
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Management
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Early intervention is critical
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Irreversible tissue injury and muscle necrosis may start as early as 3 hours after onset of compartment syndrome​
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Fasciotomy principles
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Complete opening of all tight fascial envelopes​​
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Limited fracture fragment exposure (in fracture cases)
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Postoperative care
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Supportive care
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May require monitoring in critical care unit​
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Analgesia
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Wet-to-dry dressings
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Wound closure​
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Usually through delayed primary closure or skin grafts
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Delayed at least 48 hours​
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Can be performed provided underlying muscle healthy
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If muscle non-viable, debridement to healthy bleeding muscle is required to provide healthy wound bed for skin grafts
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Treatment of rhabdomyolysis​
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Maintain urine output at 1-2 ml/kg/hr​
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Mannitol
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Complications
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Volkmann's ischaemic contracture
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Myonecrosis and secondary contracture after prolonged muscle iscahemia​
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First step of management of known contractures is occupational therapy
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Limb loss​
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Permanent nerve damage
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Renal failure
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Death
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Scarring from fasciotomies and skin grafts