Presentation on theme: "Compartment Syndrome and the Stryker Intra-Compartmental Pressure Monitor System."— Presentation transcript:
Compartment Syndrome and the Stryker Intra-Compartmental Pressure Monitor System
Compartment Syndrome When pressure is elevated within a confined space, capillary blood flow is compromised. The resulting edema within the soft tissue from ischemia results in further swelling and increased pressure.
Terms Acute compartment syndrome: An elevation of intercompartmental pressure to a level and for a duration that without decompression will cause tissue necrosis. Exertional compartment syndrome: Elevation of intercompartmental pressure during exercise causing ischemia, pain, and possibly neurologic symptoms and signs. There is resolution with rest, but it may progress to acute compartment syndrome. Volkmann ischemic contracture: Irreversible muscle necrosis leading to ischemic contractures. Crush syndrome: The systemic result of muscle necrosis commonly caused by prolonged external compression of an extremity. Muscle necrosis is established by the time of presentation, but intracompartmental pressure may rise as a result of intracompartmental edema, causing a superimposed acute compartment syndrome.
History 1850: First report attributed to Hamilton by Hildebrand 1881: Richard von Volkmann published a summary of his findings: paralysis and contractures occurred after tight bandaging and were caused by prolonged blocking of arterial blood. He recognized that muscle cannot survive for longer than six hours with complete occlusion of blood and not for longer than 12 hours with partial occlusion. 1888: Peterson recognized that ischemic contracture can occur in the absence of bandaging. Early twentieth century: The first description of fasciotomy and the importance of its early application were suggested.
World War I: The belief propagated that compartment syndrome was result of arterial injury and spasm. The excision of the “damaged” artery yielded successful results. Of course, the fascia was released during the exposure. So….can you have compartment syndrome and normal peripheral pulses? History
Seddon 17 challenged the arterial injury theory as the sole cause of compartment syndrome, noting normal pulses. In 1966, early and gross swelling in the compartments and pressure that was released with fasciotomy were noted. Nolan and McQuillan 18 described a vicious circle of increasing tension in an enclosed compartment causing venous outflow obstruction and subsequent reduction in arterial inflow. They concluded that delay in fasciotomy was the single cause of failure of treatment.
Compartment Syndrome Etiology Compartment Size Tight dressing (bandage or cast) Localized external pressure, lying on limb Closure of fascial defects Compartment Content Bleeding, fixation, vascular injury, bleeding disorders Capillary permeability: ischemia, trauma, burns, exercise, snake bite, drug Injection, in vitro fertilization
Compartment Syndrome Etiology Fractures ( closed and open) Blunt trauma Temporary vascular occlusion Cast or dressing Closure of fascial defects Electrical burns Exertional states Gunshot wound Intravenous A lines Hemophilia and coagulation Intraosseous infusion (infant) Snake bite
Measurement of pressures with the Stryker Intra-Compartmental Pressure Monitor Turn on. Assemble the needle, transducer, and syringe. Seat into chamber and close lid. Tilt 45° and purge chamber and needle of air. Prep skin (not on pig). Just before the needle enters the skin, zero the Stryker Intra-Compartmental Pressure System, and don’t change the angle after this. Inject <1/3 mL of fluid provided by the manufacturer in the syringe to clear the side port. Allow time for the reading to stabilize; it may take 15 to 20 seconds.
Compartment Syndrome Pathophysiology Normal tissue pressure – 0 to 4 mm Hg – 8 to 10 mm Hg with exertion Absolute pressure theory – 30 mm Hg (Mubarak et al. 20 ) Pressure gradient theory – <20 mm Hg of diastolic pressure (Whitesides et al. 8 and McQueen and Court-Brown 21 )
Compartment Syndrome: A Clinical Diagnosis Pain out of proportion Palpably tense compartment Pain with passive stretch Paresthesia or hypoesthesia Paralysis Pulselessness or pallor
Medical Management Make sure that the patient is normotensive. Hypotension reduces perfusion pressure and facilitates further tissue injury. Remove the circumferential bandages and cast. Maintain the limb at the level of the heart as elevation reduces the arterial inflow and the arteriovenous pressure gradient on which perfusion depends. Administer supplemental oxygen.
Compartment Syndrome Pressure Measurements Suspected compartment syndrome Equivocal or unreliable examination Clinical adjunct ONLY after discussing it with the attending physician
When NOT to check pressures Compartment syndrome is diagnosed on a clinical basis.
Threshold for Decompression 30 mm Hg: close to capillary blood pressure 20,25 40 mm Hg 13,26 50 mm Hg in tibia fixation and normotensive 27 <10 to 30 mm Hg: difference between diastolic and tissue pressure (delta P) 8 Difference between mean arterial pressure and tissue pressure of <30 mm Hg in normal muscle or <40 mm Hg in traumatized muscle 22-24,28
Fasciotomy Principles Make an early diagnosis. Make long extensile incisions. Release all fascial compartments. Preserve neurovascular structures. Debride necrotic tissues. Provide coverage within seven to ten days.
Compartment Syndrome Lower Leg Four compartments – Lateral: peroneus longus and peroneus brevis (PB) – Anterior: extensor hallucis longus, extensor digitorum longus (EDL), tibialis anterior (TA), peroneus tertius – Superficial posterior: gastrocnemius (G), soleus (S) – Deep posterior: tibialis posterior (TP), flexor hallucis (FH) longus, flexor digitorum longus
Compartment Syndrome Forearm Three anatomical compartments – Mobile wad: brachioradialis, extensor carpi radialis longus, and extensor carpi radialis brevis – Volar: superficial and deep flexors – Dorsal: extensors The pronator quadratus is described as a separate compartment.