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Acute compartment syndrome
This document provides a history and overview of compartment syndrome. It discusses how compartment syndrome was first described in 1881 and the early studies identifying the condition and need for fasciotomy. It defines compartment syndrome as elevated tissue pressure within a closed space, describes the pathophysiology and risk factors. Diagnosis involves symptoms like pain out of proportion and tense compartments. Treatment is fasciotomy to release pressure if symptoms don't improve after conservative measures. Complications include contractures if not treated promptly.
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Acute compartment syndrome
- 1. DR. SIDHARTH YADAV DEPT.OF ORTHOPAEDICS NKPSIMS ACUTE COMPARTMENT SYNDROME
- 2. Compartment Syndrome Definition Elevated tissuepressure within a closed osteofascial space Reduces tissue perfusion – ischemia Results in cell death - necrosis
- 3. History Volkmann 1881 Richard vonVolkmannpublished an article in which he attempted to describe the condition of irreversible contractures of the flexor muscles of the hand to ischemic processes occurring in the forearm Application of restrictive dressing to an injured limb
- 4. History Hildebrand 1906 First usedthe term Volkmann ischemic contracture to describe the final result of any untreated compartment syndrome. First to suggest that elevated tissue pressure may be related to ischemic contracture.
- 5. History Thomas 1909 Reviewed the112 published cases of Volkmann ischemic contracture and found fractures to be the predominant cause. Also, noted that tight bandages, an arterial embolus, or arterial insufficiency could also lead to the problem
- 6. History Murphy 1914 First tosuggest that fasciotomy might prevent the contracture. Also, suggested that tissue pressure and fasciotomy were related to the development of contracture
- 7. History Ellis 1958 Reported a2% incidence of compartment syndrome with tibia fractures, and increased attention was paid to contractures involving the lower extremities
- 8. History Seddon, Kelly, andWhitesides 1967 Demonstrated the existence of 4 compartments in the leg and to the need to decompress more than just the anterior compartment. Since then, compartment syndrome has been shown to affect many areas of the body, including the hand, foot, thigh, and buttocks
- 9. Types of compartmentsyndrome 9 Compartment syndromes can be classified as : Acute compartment syndrome (ACS) Chronic compartment syndrome (CCS) depending on the cause of increased intra-compartmental pressure and the duration of symptoms
- 10. Sites of AcuteCompartment Syndrome 10 Acute compartment syndrome can develop anywhere a skeletal muscle is surrounded by a substantial fascia. ACS may occur in foot, leg, thigh, buttocks, lumbar paraspinous muscles, hand, forearm, arm and shoulder.
- 11. Compartments 11 Foot 9 Leg 4(anterior,lateral, sup & deep posterior ) Hand 4 Thigh 3 (anterior, posterior, medial ) Forearm 4 (sup &deep volar,dorsal, mobile wad of Henry)
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- 16. Pathophysiology of ACS 16 CSdevelops after prolonged elevated intra-compartmental pressure , which results from either externally applied or internally expanding pressure forces. Increased tissue pressure will decrease capillary blood flow leading to local tissue necrosis caused by O2 deprivation . Local blood flow (LBF) =Pa-Pv/R.
- 17. Pathophysiology of ACS 17 Theelevated intra-compartmental pressure increases the local venous pressure leading to narrowed arteriovenous perfusion gradient and compartment tamponade, resulting -if uncontrolled - in nerve injury and muscle ischemia
- 18. Etiology of ACS External Restriction of Compartment Size : - casts - tight dressings - splints - lying on limb for long period - burn eschar - closure of fascial defect - lithotomy position
- 19. Etiology of ACS 19 •Factures (the most common are) : In adults --- closed and open tibial shaft fracture , distal radial fracture In children --- radial head or neck fracture , supracondylar fracture , forearm fractures
- 20. Etiology of ACS 20 Hemorrhage(e.g. due to vascular injury ) Coagulopathy (e.g. hemophilia , thrombolytics , sickle cell disease or trait ) Muscle edema (e.g. severe exercise , crush injury, trauma with or without fx )
- 21. Etiology of ACS 21 Surgicallyrelated (e.g. knee arthroscopy , tibial osteotomy without drainage , after epidural anesthesia ) Massive crystalloid infusion Ruptured Backer’s cyst Muscle hypertrophy ( androgens )
- 22. Etiology of ACS 22 Intracompartmentalfluid infusion (interosseosus infusion) Capillary leak syndrome Intra-arterial injections of sclerosing agents Post –ischemic reperfusion
- 23. Compartment Syndrome Tissue Survival Muscle 3-4 hours - reversible changes 6 hours - variable damage 8 hours - irreversible changes Nerve 2 hours - looses nerve conduction 4 hours - neuropraxia 8 hours - irreversible changes
- 24. Compartment Syndrome Pathophysiology Normal tissuepressure 0-4 mm Hg 8-10 with exertion Absolute pressure theory 30 mm Hg - Mubarak 45 mm Hg - Matsen Pressure gradient theory < 20 mm Hg of diastolic pressure – Whitesides McQueen, et al
- 25. Compartment Syndrome Diagnosis Painout of proportion Palpably tense compartment Pain with passive stretch Paresthesia/hypoesthesia Paralysis Pulselessness/pallor
- 26. Pain Classically out ofportion to injury Exaggerated with passive stretch of the involved muscles in compartment Earliest symptom
- 27. Paresthesia Also early sign Peripheralnerve tissue is more sensitive than muscle to ischemia Permanent damage may occur in 75 minutes Difficult to interpret Will progress to anesthesia if pressure not relieved
- 28. Paralysis Very late finding Irreversiblenerve and muscle damage present Paresis may be present early Difficult to evaluate because of pain
- 29. Pallor & Pulselessness Rarelypresent Indicates direct damage to vessels rather than compartment syndrome Vascular injury may be more of contributing factor to syndrome rather than result
- 30. Compartment Pressure Technique Whiteside infusion Stictechnique: side port needle Wick catheter Slit catheter
- 31. Whiteside Technique Simple technique Readilyavailable supplies With 18 gauge needle least accurate More accurate if use side port needle
- 32. Stryker Stic System Easyto use Can check multiple compartments Different areas in one compartment
- 33. Management of ACS 33 Removal of the possible cause (release of tight dressings or circular constrictive bandages, splitting of casts) Correction of coagulopathy Positioning of the limb at the level of the heart
- 34. Management of ACS 34 Ifsymptoms don’t resolve in 30 to 60 min after appropriate treatment ,pressure measurement should be repeated,and,if equivocal, fasciotomy is indicated
- 36. Management of ACS 36 Thedefinitive treatment of acute compartment syndrome is FASCIOTOMY Procedure is done without a tourniquet,each potentially limiting envelope is opened over the entire length of the compartment, all muscle groups should be soft to palpation at the end of the procedure Muscle debridement should be kept to a minimum
- 37. FACIOTOMY OF LOWERLIMB FOR THIGH Make a lateral incision distal to intertrochantric line extending to the lateral epicondyle. Expose the iliotibial band & make aa straight incision in line with skin incision Reflect the vastus lateralis off the intermuscular septum
- 38. • FOR LEG Singleincision faciotomy Double incision faciotomy fibuloectomy
- 41. Chronic Compartment Syndrome 41 Alsoknown as exertional CS, recurrent CS and subacute CS Exercise –induced pain Occur mainly in the lower limb Typical patient is young (20-30s) athlete (long distance runner)or military recruits pushed past normal limits of functional tolerance
- 42. Pathophysiology of CCS 42 Notyet fully understood Probably occurs from increased muscle relaxation pressure during exercise , which causes decreased muscle blood flow, leading to ischemic pain and impaired muscle function
- 43. COMPLICATION OF COMPARTMENT SYNDROME Reperfusioninjury Volkmann’s contracture Weak dorsiflxors Claw toe Sensory loss Chronic pain Amputation
- 44.
Editor's Notes
- #12 Mobile wad of Henry (brachioradials,ECRL & ECRB)
- #16 —Forearm compartments. ECRB = extensor carpi radialis brevis, ECRL = extensor carpi radialis longus, BR = brachioradialis, FCU = flexor carpi ulnaris, PL = palmaris longus, FCR = flexor carpi radialis, FDS = flexor digitorum superficialis, ED = extensor digitorum, EDM = extensor digiti minimi, ECU = extensor carpi ulnaris, FDP = flexor digitorum profundus, FPL = flexor pollicis longus, PT = pronator teres, S = supinator, APL = abductor pollicis longus, EPB = extensor pollicis brevis, EPL = extensor pollicis longus, EI = extensor indices, R = radius, U = ulna.A, Drawing of proximal forearm.
- #24 Studies have shown that nerve tissue is the most sensitive to ischemic changes. Nerve conduction is lost in 1-2 hours of total ischemia and survive up to 4 hrs with only neuropraxia changes, while axonotmesis and irreversible changes occur after 8 hrs. Muscle may survive up to 4 hours with reversible changes, variable damage occurs by 6 hrs, and irreversible changes after 8 hrs under conditions of warm ischemia.
- #25 Normal resting muscle tissue pressure is up to 4 mm Hg and 8-10 with exertion. Exercise induced CS may have a resting based line of 10-15 mmHg. Many studies utilizing clinical evaluations and animal models by Whitesides, Mubarak, Matsen, Heckman, Heppenstall and Matava have help to establish a better understanding of the pathophysiology and thresholds of ischemia. Two schools of though prevail: 1. The Absolute Pressure Theory of Murbarak and Matsen who suggest surgical decompression in CS with pressures that reach or exceed these thresholds. 2. The Perfusion Theory of Whitesides who demonstrated in animal models and human subjects the relationship of tissue perfusion and diastolic blood pressure. His group recommends surgical decompression when the tissue pressure is within 20mm Hg of the DBP. McQueen suggested a differential &lt;30mmHg of the diastolic pressure and the intramuscular pressure as a threshold for release as being more reliable. Mean arterial pressure can also serve as a benchmark with a release suggested when intramuscular pressure is within 45 mm Hg. Caution must be exercised in traumatized tissue and especially in hypotensive patients
- #26 These physical findings have been described as the clinical hallmarks of CS. They are not very sensitive and if seen in the later stages it may be too late to change the underlying pathology. CS may be present with good pulses and no pallor and loss of pulses rarely occur unless arterial damage is present. Pain out of proportion and pain with passive stretch of a muscle in the compartment in question may be the most sensitive clinical finding before the onset of ischemic dysfunction of the nerves and muscles. These findings are useful only in a conscious cooperative patient and once paresthesia begin the pain may decrease. One important point to make is of CS is a possibility then regional anesthesia, continuous epidurals and PCA intravenous opiate analgesia should be avoided since they may mask the symptoms of compartment syndrome. Otherwise monitoring of the tissue pressure is warranted. There exist reports of missed compartment syndrome in tibia fracture and other surgical patients at risk managed postoperatively with these techniques and therefore they are generally avoided.
- #31 Confirm clinical exam Regional anesthetic Vascular injury
- #34 By colloid infusion,blood replacement,platelet transfusion. Because this position will produce the highest arteriovenous gradient .on the other hand elevation of the limb decreases the arterial inflow without significantly increasing the venous outflow,thus increasing local ischemia.
- #35 Removal of one side of the cast can reduce the ICP by 30% , bivalving can produce additional 35% & cutting the webril 10%