Leela 6y2s4m

COMPARTMENT SYNDROME & SUDECK’S DYSTROPHY

LEELA SOUJANYA.M FINAL MBBS PART-2

Compartment syndrome The limbs contain muscles in compartments enclosed by bones,fascia and interosseus membranes A rise in pressure within these compartments resulting in a critical reduction of blood flow to the muscles and nerves within the compartment leads to compartment syndrome.

INCIDENCE

TYPES 

Acute compartment syndrome Elevation of I to a level and for a duration that widout decompression wil cause tissue ischemia and necrosis.

Exertional compartment syndrome Rise of I due to regular,vigorous exercise Resolution of symptoms with rest. 

ACUTE COMPARTMENT SYNDROME It is the most common type. ETIOLOGY:  Fracture  Soft tissue injury leading to edema  Crush injury  Overly tight bandaging  Burns  Prolonged compression of limb etc., 

Fracture

Injuries more prone to CS are: Supracondylar fractures of humerus Forearm bone fractures Closed tibial fractures Crush injuries to legs and forearm. 

PATHOGENESIS Primarily from increased I.  Mechanism – precipitating event.  When fluid introduced – tissue pressure rises.  When interstitial pressure exceeds P , capillary collapse and muscle ischemia occurs. 

Skeletal muscle releases histamine like substances leading to a vicious cycle of events.  Increasing critical closing pressure results in decreased blood flow.  Compartment pressure greater than 30mm of hg requires surgery 

CONSEQUENCES OF RAISED I 

Muscle Reduced blood flow to muscles Ischaemia Necrosis Duration of ischemia dictates amount of necrosis althought some fibres are more vulnerable than others.



3-4 hrs – reversible changes



6hrs –variable damage



8hrs- irreversible changes

Nerve 2 hrs- looses nerve conduction 4 hrs – neuropaxia 8hrs – irreversible changes.  Loss of neuromuscular function with raised tissue pressures at different thresholds and duration.  Mechanism uncertain.Ischaemia and toxic affects. 

BONE Nonunion is complication of ACS. It is likely that muscle ischaemia reduces capacity for development of extraosseus blood supply on which the long bone healing depends. 

CLINICAL DIAGNOSIS 5 P’s  Pain with ive stretch  Palpable swelling  Parasthesia  Paralysis  Pulses are absent- very late sign

Pain Early symptom in awake alert patient. Pain seems greater than expected for the injury. Sensitivity of 19% and specificity of 97% in diagnosis.  Palpable swelling Degree of swelling is difficult to assess,making this sign subjective. Casts or dressings obscure the swelling and prevent the assessment. 

Parasthesia – occurs in area of the nerves traversing the affected compartment. First signs of nerve ischaemia. Sensitivity 13% and specificity 98% for diagnosis. 

Paralysis – of muscle groups is late sign. Less sensitive probably due to difficulty in predicting the underlying cause of weakness, which could be due to inhibition by pain. 

Pulse  Always intact unless there is severe arterial injury or disease is in late stages.  Late sign 

Excessive pain not relieved with analgesics in pt with injury must raise an alarm. Stretch test:- earliest sign. Ischaemic muscles when stretched will cause pain. The affected muscles are stretched by ively moving the jts in direction opposite to that of damaged muscles’s action.

COMPARTMENT PRESSURE MONITORING Raised tissue pressure is the primary event in ACS,changes in I precedes the symptoms and signs. METHODS:  Needle manometer methodNeedle is introduced into the compartment and connected to a column filled partly with air and saline. 

Later it is modified to allow the infusion of saline into the compartment.I is the pressure resistance to infusion of saline.  Wick catheter method: Modification of above method.Fibrils protrude from bore of catheter and allows large surface area for measurement. It is useful for continuous measurement of pressure.

Slit catheter: Works on same principle of wick catheter.Pressure is measured through the column of saline attached to transducer.  Solid state transducer: intracompartmental catheter(pressure transducer is directly kept into the compartment. 

TREATMENT Focus on reducing dangerous pressure in compartments.  Dressings,casts or splints that are constricting the affected body part must be removed.  Surgical treatment – fasciotomy. 

Other ive treatments: Keeping body part below the level of heart. Giving oxygen through nose or mouth. Giving IV fluids. Giving pain medications. 

FASCIOTOMY Definitive surgical therapy.  If done within 6hrs – recovery, after 8hrs – controversial. Indications:  Injury at high risk of compartment syndrome.  Significant tissue injury.  When pressure difference level is below 30 mm of Hg. 

Contraindications: When diagnosis is made late. Fasciotomy after 3-4 days of onset of compartment syndrome can lead to infection and kidney failure in a setting of devascularised and necrotic muscle. 

PRINCIPLES Make early diagnosis.  Long complete incisions.  Release of all fascial compartments.  Preserve the neurovascular structures.  Debride the necrotic tissues. 

COMPARTMENT SYNDROME 

LEG

LEG FASCIOTOMY Two techniques – 1. Double incision Two longitudinal 15-20 cm incisions are made. Anterolateral incision – to decompress anterior and lateral compartments. Posteromedial incision – to decompress superficial and deep posterior compartments. 

Single incision Single incision given just posterior to fibula. Perifibular fasciotomy. 

THIGH

THIGH FASCIOTOMY One incisionLocated over lateral thigh. Used to decompress anterior and posterior compartments. 

FOREARM 3 compartments:  Volar- superficial and deep flexors  Mobile wadbrachioradialis,Extensor carpi radialis  Dorsal- extensors 

FOREARM FASCIOTOMY Two incisions are required if both volar and dorsal compartments are involved. Volar incision- to decompress volar and mobile wad compartments. S type incision.Carpel tunnel release. 

Dorsal incision- to decompress dorsal compartment.2cm distal to lat epicondyle.

HAND     



Ten compartments One thenar One hypothenor One adductor pollicis Three dorsal interosseous Four volar interosseous

HAND FASCIOTOMY Four incisionsTwo dorsal incisionsto decompress interosseus and thumb adductor compartments 

Two volar incisionsTo decompress thenar and hypothenar compartments. 

FOOT FASCIOTOMY Two types:  Medial foot incision Below middle maleolus

Two dorsal incisionsover second and fourth metatarsal  Releases intersseoi and adductor. 

WOUND MANAGEMENT Elevate affected extremity for 24-48 hrs after surgery.  Wound is not closed upto 48 hrs.Second look debridement for consideration of coverage.  Perform dressing changes at the bedisde as per situation.  Incision usually closed after three to five days of fasciotomy. 

DRESSING TECHNIQUES Simple absorbent dressing  Semi permeable skin like membrane  Vessel loop bootlace  Vacuum assisted closure( negative pressure wound therapy) 

WOUND CLOSURE Delayed primary closure with relaxing incisions when swelling subsides.  Split skin grafting. 

COMPLICATIONS OF ACT Late sequelae Sensory loss Chronic pain Amputation Claw toes Weak dorsiflexors Volkmann’s contracture 

REFLEX SYMPATHETIC DYSTROPHY

Synonyms Causalagia syndrome  Complex regional painful syndrome 1  Sudecks atrophy  Algodystrophy  Algoneurodystrophy  Reflex neurovascular dystrophy etc., 

ETIOLOGY Exact cause is not known.  Theories include irritation and abnormal excitation of nervous tissue leading to abnormal impulses along the nerves that affect blood vessels and skin.Sympathetic system is said to be involved. 

Events that trigger RSD are:  Injuries  Postsurgical  Local disorders like arthritis  Systemic disorders like MI,stroke.  Trauma,burns.  Shoulder problems etc.

PATHOPHSIOLOGY Mechanism is unknown. Three conditions are deemed important in the development: A persistent painful lesion A predisposition to developing the syndrome. An abmormal sympathetic reflex 

SYMPTOMS Onset Is rapid or gradual.May not display al features.  Stages of symptomsAcute(stage 1) Dystrophic(stage 2) Atrophic(stage 3) 

` Acute stageBurning, flushing, blanching, sweating, swelling, pain. This stage can show early X ray changes of patchy bone thinning. Dystrophic –  Early skin changes of shiny,thickened skin and contracture with persistent pain,but diminished swelling and flushing. Atrophic –  Loss of motion and function of involved hand or foot with contracture and thinning of fatty layers under skin. 

DIAGNOSIS

INVESTIGATIONS Radiological investigations- Xray and MRI Patchy osteoporosis detected through Xray as early as two weeks after onset. A bone scan of affected limb may detect these changes even sooner. Bone densitometry can als be used to detect bone mineral density. 

TREATMENT Response is good in early stages  Cool,moist applications provides relief to burning sensations  Gradual exercise can help prevent contractures.  Medications  Nerve block  Drug pump

MEDICATIONS Antiinflammatory such as corticosteroids.  Medications for pain.  Antidepressants like amitriptyline may be of use.  Vasodilators like clonidine,  COX inhibitors  GABA analogues. 

INVASIVE TECHNIQUE Occasionally a nerve block with anesthetic injected into specialized area of involuntary nervous system.Injection of lignocaine is done.  Used in treatment and diagnosis  Results are short lasting. 

Other treatments includeSpinal cord stimulators: Neurostimulation may be surgically implanted to reduce pain by directly stimulating SC. Drug pump: Implantable drug pumps may als be used to deliver pain medication directly to CSF. Surgical sympathectomy 

PHYSIOTHERAPY For symptomatic treatment of Pain Allodynia Edema Dystrophia and t stiffness Vasomotor instability. 

THANK YOU