Compartment syndrome
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COMPARTMENT SYNDROME CRUSH INJURIES
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Compartment syndrome
- 1. COMPARTMENT SYNDROME & CRUSH INJURY 7TH MAY 2018 PRESENTED BY: NASRI
- 2. Presentation outline Compartment syndrome ◦ Definition ◦ Compartments of upper and lower limb ◦ Clinical symptoms & signs ◦ Management Crush injury ◦ Introduction ◦ Pathophysiology ◦ Clinical features ◦ management
- 4. INCREASE INOSTEOFASCIAL compartment PRESSURE. Compartments are groupings of bone, muscles, nerves, and blood vessels in upper and lower limbs Each compartment is covered by fascia respectively. ∆P <30 mmHG between diastolic blood pressure (DBP) and fascial pressure DEFINITION
- 5. ETIOLOGY
- 6. FRACTURES OF ELBOW, FOREARM, PROXIMAL 1/3 OF TIBIA & MULTIPLE FRACTURES OF HAND & FOOT CASCADE OF EVENT : LOCAL TRAUMA AND SOFT TISSUE DESTRUCTION> BLEEDING AND EDEMA > INCREASED COMPARTMENT PRESSURE > VASCULAR OCCLUSION > MYONEURAL ISCHEMIA (AFTER 12 HOURS OR LESS)
- 9. CLINICAL PRESENTATION PAIN (EARLY SYMPTOM) OUT OF PROPORTION TO EXPECTATION STRETCH PAIN TENSE SWELLING NOT RELIEVED BY ADEQUATE ANALGESIA Sigamoney, K., Khincha, P., Badge, R., & Shah, N. (2015). Compartment syndrome: challenges and solutions. Orthopedic Research and Reviews, 7, 137-148.
- 10. CLASSIC FEATURES 6 P’s PAIN PARAESTHESIA PALLOR PARALYSIS PERISHINGLY COLD PULSELESSNESS
- 12. ARM
- 13. Arm Compartment Muscle Nerve Anterior Biceps brachii Coracobrachialis Brachialis Musculocutaneous nerve Posterior Triceps Radial nerve
- 14. FOREARM
- 15. ForearmCompartment Muscles Nerve Anterior • Superficial • Middle • Deep Pronator teres, Flexor carpi radialis, Palmaris longus, Flexor carpi ulnaris Flexor digitorum superficialis Flexor digitorum profundus, flexor pollicis longus, pronator quadratus Median nerve Ulnar nerve Posterior • Superficial • Deep Aconeus, Ext digital communis, Ext digital minimi, Ext carpi ulnaris Supinator,Abductor pollucis longus, Ext pollicis brevis, Ext pollicis longus, Ext indicis proprius Posterior interosseous nerve Lateral (Mobile web compartment) Brachioradialis Extensor carpi radialis longus Extensor carpi radialis brevis
- 17. Hand Compartment Content Thenar Abductor pollicis brevis, Flexor pollicis brevis, Opponens pollicis Hypothenar Abductor digit minimi, Flexor digitiminimi brevis, Opponens digiti minimi Adductor Adductor pollicis Palmar interosseous (3) Palmar interosseous muscles Dorsal interosseous (4) Dorsal interosseous muscles
- 18. LOWER LIMB
- 19. THIGH
- 20. Thigh Compartment Muscle Nerve Anterior Quadriceps Sartorious Femoral nerve Posterior Hamstrings Sciatic nerve Adductor Adductor Gracilis Obturator nerve
- 21. LEG
- 22. LegCompartment Muscle Nerve Action Anterior Tibialis anterior Extensor hallucis longus Extensor digitorum longus Peronues tertius Deep peroneal nerve Dorsiflexion Extension of great toe Extension of 4 other toes Deep Posterior Tibialis posterior Flexor hallucis longus Flexor digitorum longus Popliteus Tibial nerve Plantarflexion Flexion of great toe Flexion of other 4 toes Superficial Posterior Gastrocnemius Plantaris Soleus Tibial nerve Lateral Peoneus longus Peronus brevis Superficial peroneal nerve Evert foot
- 23. FOOT
- 24. FOOT Compartment Medial Abductor hallucis Flexor hallucis brevis Flexor hallucis longus tendon Lateral Abductor digiti minimi Flexor digiti minimi Superficial central Flexor digitorum brevis Lumbricals (4) Flexor digitorum longus tendon Deep central (Calcaneal) Quadratus plantae Posterior tibial neurovascular bundle Adductor Adductor hallucis Interosseus (1-2) Dorsal interosseous muscles Interosseus (2-3) Dorsal and plantar interosseous muscles Interosseus (3-4) Dorsal and plantar interosseous muscles Interosseus (4-5) Dorsal and plantar interosseous muscles
- 26. MEASURE THE INTRACOMPARTMENTAL PRESSURRE - A slit catheter is introduced into the compartment and the pressure is measured - ΔP = general diastolic pressure – compartment pressure if <30 mmHg, need immediate compartment decompression
- 27. If no facilities to measure pressure: ≥ 3 classical signs (6Ps) – diagnosis is almost certain If signs are equivocal, limbs examined at 15 minutes intervals & if no improvement within 2 hours of splitting the dressings, fasciotomy should be done. Muscle will be dead after 4-6 hours of total ischemia! APPLEY’S CONCISE ORTHOPAEDICSAND FRACTURES 3RD EDITION 2005
- 28. Treatment DECOMPRESSION Casts/bandages/dressing completely removed. Limb is nursed flat (elevating limb cause further decrease in end-capillary pressure and aggravates muscle ischemia) ΔP <30 mmHg : immediate open fasciotomy Fasciotomy Example: In leg – opening all 4 compartments through medial & lateral incisions, wounds left open and inspected 2 days later - if muscle necrosis debridement - if tissues are healthy wound suture OR skin graft
- 29. FasciotomyTechnique Anterolateral incision ◦ identify and protect the superficial peroneal nerve ◦ fasciotomy of anterior compartment performed 1cm in front of intermuscular septum ◦ fasciotomy of lateral compartment performed 1cm behind intermuscular septum Posteromedial incision ◦ protect saphenous vein and nerve ◦ incise superficial posterior compartment ◦ detach soleal bridge from back of tibia to adequately decompress deep posterior compartment
- 30. CRUSH INJURY
- 31. INJURY CAUSED AS A RESULT OF DIRECT PHYSICAL CRUSHING OF MUSCLES DUETO SOMETHING HEAVY ◦EARTHQUAKE ◦MOTOR-VEHICLE ACCIDENT ◦TRAUMA -ENTRAPMENT
- 32. 80% of crush injury patients die due to severe head injuries or asphyxiation.Of 20% that reach hospital, 10% make an uneventful recovery. Another 10% go into crush syndrome (Bywater & beall,1941) Crush syndrome series of metabolic changes produced due to an injury of skeletal muscles of such a severity as to cause a disruption of cellular integrity and release of its content into circulation (rajagopalan,2010) ◦ Life & limb threatening condition
- 33. PATHOPHYSIOLOGY ONCETISSUETENSION RELEASEDREPERFUSIONTO ISCHEMIC DAMAGED MUSCLE DISRUPTS NA⁺/K⁺ -ATPASE MECHANISM THUS, MYOGLOBIN DEGRADATION PRODUCTS IE, LACTIC ACID, URIC ACID, MUSCLES ENZYMES LIKE CREATININE PHOSPHOKINASE AND ALDOLASE, LACTATE DEHYDROGENASE, IONS LIKE POTASSIUM AND PHOSPHATE RELEASED INTO CIRCULATION RELEASED OF SUCH SUBSTANCE RAISED MUSCLEVOLUME ANDTENSION NITRIC OXIDE SYSTEM IS ACTIVATED AGGRAVATING MUSCLE VASODILATATION AND HYPOTENSION
- 34. METABOLIC DERANGEMENT Hypovolemia (fluid sequestration in damaged muscle) Hyperkalemia Hypocalcemia (due to calcium deposition in muscle), corrected only presence of symptoms Hyperphosphatemia Metabolic acidosis Myoglobinemia / myoglobinuria OBSTRUCTION & DESTRUCTIONOF RENALTUBULES
- 35. CLINICAL FEATURES PETECHIAE BLISTERS BRUISES MYALGIA MUSCLE PARALYSIS SENSORY DEFICIT ARRTHYMIA OLIGURIA Sever, M. S.,Vanholder, R., & Lameire, N. (2006). Management of crush-related injuries after disasters. New England Journal of Medicine, 354(10), 1052-1063.
- 36. MANAGEMENT FLUID RESUSCITATION ◦EARLIER IV FLUID COMMENCE IS BETTER (EVEN BEFORE THE EXTRICATION) ◦NORMAL SALINE IS PREFERRED ◦TARGETTED U/O exceeds 300cc/hour once hospitalized ◦Diuresis (by mannitol, diuretics or IV fluids ) should be prompted to increase the tubular flushing and eliminate the proteinaceous material
- 37. Hyperkalemia in crush syndrome Can occur soon after extrication fatal arrhythmia May occur before manifestations of renal failure
- 38. Urgent hemodialysis May be needed following persistent hyperkalemia Persistent metabolic acidosis Oliguric AKI
- 39. Antibiotics: broad spectrum non nephrotoxic abx may be needed Surgery: fixation over fractures. Conservative amputations may have to be performed as emergencies or elective measures. fasciotomy (any increase in compartmental pressure) Sever, M. S.,Vanholder, R., & Lameire, N. (2006). Management of crush-related injuries after disasters. New England Journal of Medicine, 354(10), 1052-1063.
- 40. REFERENCES APPLEY’S CONCISEORTHOPAEDICSAND FRACTURES 3RD EDITION 2005 Rajagopalan, S. (2010). Crush injuries and the crush syndrome. MedicalJournal Armed Forces India, 66(4), 317-320. Sever, M. S.,Vanholder, R., & Lameire, N. (2006). Management of crush-related injuries after disasters. New EnglandJournal of Medicine, 354(10), 1052-1063. Sigamoney, K., Khincha, P., Badge, R., & Shah, N. (2015). Compartment syndrome: challenges and solutions. Orthopedic Research and Reviews, 7, 137-148. http://www.orthobullets.com//
Editor's Notes
- Compartment syndrome may occur acutely, or as chronic syndrome Acute compartment syndrome (ACS) most often develops soon after significant trauma, particularly involving long bone fractures. However, ACS may also occur following minor trauma or from non-traumatic causes. ACS is seen more often in patients under 35 years of age. Young men appear to have the highest incidence.
- Sigamoney, K., Khincha, P., Badge, R., & Shah, N. (2015). Compartment syndrome: challenges and solutions. Orthopedic Research and Reviews, 7, 137-148.
- Compartment syndrome occurs when the pressure within a closed osteo-fascial muscle compartment rises above a critical level. This critical level is the tissue pressure which collapses the capillary bed and prevents low-pressure blood flow through the capillaries and into the venous drainage. Normal tissue pressure is 0-10 mm Hg. The capillary filling pressure is essentially diastolic arterial pressure. When tissue pressure approaches the diastolic pressure, capillary blood flow ceases. A number of studies have shown that if diastolic arterial pressure is not more than 30 mm Hg above tissue pressure, compartmental capillary blood flow is significantly obstructed and severe hypoxia occurs in muscle and nerve tissue. Nerve Nerve will function for about 2-4 hours Following loss of function peripheral nerve have the potential to recover Muscle Warm ischemia time for muscle is 6-8 hours Muscle tissue subject to prolonged ischemia can never recover and is replaced by inelastic fibrous tissues and results in Volkmann’s ischemic contracture later Eaton and Green Cycle for compartment Syndrome Vicious circle of Volkmann/s Ischemia Skeletal muscle responds to ischemia by releasing histamine like substances that increase vascular permeability. Plasma leaks out of the capillaries, and relative blood sludging in the small capillaries occurs, worsening the ischemia. * histamine is a vasodilator The myocytes begin to lyse, and the myofibrillar proteins decompose into osmotically active particles that attract water from arteria l blood. A relatively small increase in osmotically active particles in a closed compartment attracts sufficient fluid to cause a further rise in intramuscular pressure. When tissue blood flow is diminished further, muscle ischemia and subsequent cell edema worsen. This vicious cycle of worsening tissue perfusion continues to propagate.
- COINCIDE WITH LIMB ISCHEMIA
- Anterior/Volar most commonly affected
- Anterior compartment -> Dorsiflexion, extension of toes -> To test anterior compartment, do the opposite
- Bywater n beall- british medical journal Rajagopalan- MJAFI 2010
- RUBINSTEIN ET AL J. CLIN INVEST 1998
- GUNA- 300 cc/hour-require 12 litres of fluid per day (4-6 L contain bicarb), usually, intake > due to accumulation of fluid in muscle(may exceed 4L) until myoglobinuria disappear However, fluid administration should be individualised