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",#(7),01444'9=82<.342C  2!!22222222222222222222222222222222222222222222222222}"3!1AQ"aq2BR#bS*!1"2AQa#Cq ?p1H#cֿɢU><ۖU(8oZP\.XFդ/wNqy prhY,0 큽D6t\EfHFΣϵd~ m1]ӕ 7V )Q> Nۍgj@ŀ + *qy2O:GzRG:RaOXGg#H_#ڱAj/ B*ŏr7iVF)kGĊΆG/:ɎXq2C j.)Z<ָɴJcg()@[`zQ!%IshH7F 2e`,p?Z̥SX5u=( wT,He'oQ6:zY39L^AqkpN啾ح|uv\WEc~#< IoJL*h}b;Z 3.[RA$Q2f$_CӰ#0=f%إnὨ`e,0t1iIzUKs.G?4&y,쒞m;VgH#Ůlq ~Nޤa8Q F֥RqX<a{UCNdf-GgMeߵ34)Em8c1 7!`*)9)5ݑj?hc0rVh|Fxe䬀` \ڱNŋ#?zGrɆ|9`YN]1*Q['ڴ0ipP8 2זrn|֘70:uqjPsYkilnLNvYtxt{hf? ơg[:n?Ҭe #>VU:ߙul, (eڴ2TWlQ@jN9z  ^ c'›Ug;vA17#qV@: 5g %BrT^pYEWpqM8Fv96MZkckiBifz1)dɄyUA6NKohAto\ccڟ*;?07=;n_]uoJIXw *UX_626 OǶZxc(Ie -bt,e9֮Iګ-)eV܊[L%Y;8$ oKPmqܣ8Rdk^zT|r$װ "PœMEdϻ+`pEŸ/:O#qJFޯ"qSD)mF8e`<6ҕ`Fj0(m0Jt=wh`v<4?Iag<q84ƧfJ+շWG+cX7TbҌAڣwƋFMT\ǒI8 )`h\gI}]ǁCrNԟެlb.m9TΘrv놵~,? 68@Y#qMFl/U1zULjQvlt;?U/~Lx5+sYč ֠7viLюkox'So4_˷y8e<;R)qc5Մl$n47^]?gFA;VWͬqukVUū˒<ۻԹUb5(YkI$-VdeJP9IdO1Z-k$ z4{lf UuLN޻s$<(˻N3MjF+"'eVL`2 j Cʥ˓5\Et~tEKnpu̎Xv^@JԌ|彬vI|lڴ]ֻKd'jAEc ;mFUQEU b/:SҊX%(A$b,zOlS1ʸ8) ~! ѝc_xyj/][elZKjDkCEK6dGF$xd1`Ҁ<땋f`i$$m* 7EQX0V!;$-$rL?jbe;FyhoXT ÕL`̝幎`3nCzWev+Iu xdX[RlDwRAOWj_ 'eIaD1 hA Q R Ymɹ0K.⊛Rɔ`A\;̒jqRJڋlsB`R= t.ZG5: (z@)#b +.raS;P]'&(6ĺ.?\"cWE(FF>]Ճ!]b=bgmQ;7'4A'rjD08$⮣㟐<읲}\$ձ  (j r)MfE =C AhZrU4Gp-S!qPB( / 0DTimes New Romantt} 0DArialNew Romantt} 0 DWingdingsRomantt} 0@ .  @n?" dd@  @@``  C&         !"$%()?2$y^bG"7R$\~NA3y^#7R$ vHU! 9O#  <AA@8w $ʚ;8'2ʚ;g4BdBd 00ppp@ <4!d!d@k 0t|<4dddd@k 0t|80___PPT10 ? %i;ZThe Painful Truth about Compartment Syndrome, Causalgia, and Post-traumatic Pain Syndromes[[$8Sharla Owens, M.D. Vascular Conference November 14, 2005Compartment SyndromeDefined as increased tissue pressure contained in a nonexpansile space Raised pressure within a closed fascial space reduces capillary perfusion, placing the enclosed structures at risk Most commonly observed after acute injury or ischemia in upper and lower extremities Abdominal, epidural, CHI, and angle-closure glaucoma are better defined and treated as variants of classic compartment syndromeZPathophysiology8Mechanism of: tissue volume increasing within a confined space, available tissue space decreasing, or a combination of both Space-occupying lesions such as hematoma, abscess, PSA, muscle edema/fluid Decreased space by circumstances where external devices are placed (cast, dressing) or with circumferential burns9Z9 Ischemia-Reperfusion9Ischemia results in depletion of intracellular energy stores, which, after reperfusion will generate toxic oxygen radicals. Results in cascade of activation of leukocytes/platelets, inflammatory mediators, calcium influx, disruption of cell membrane, and fluid transudation All culminate in excess fluid formation:Z: Inflammatory MediatorsReleased from ischemic skeletal muscle Produce local and systemic effects Local: increase capillary permeability, activate coagulation cascade to produce more tissue damage Magnitude of systemic response depends on amount of muscle mass involved  Consequences*Venular pressure, normally 4-7 mm Hg, increases progressively because of venous outflow obstruction from increased tissue pressure Ultimately, when intracompartmental pressure equals capillary pressure, nutrient blood flow is reduced to 0, cellular perfusion ceases, and tissue infarction commences++  Vicious Cycle Clinical PresentationdMost frequently occurs with major extremity trauma (crush or closed fractures) or reperfusion after acute arterial insufficiency Has also been reported with electrical injuries, massive volume resuscitation, and prolonged operative positioning Symptoms include severe pain, which worsens despite appropriate care for underlying injury, and neurologic signseeContinued& `Early neurologic dysfunction explained by the fact that tissues most sensitive to hypoxia are nonmyelinated type C sensory fibers (fine touch) and result in symptoms such as paresthesias. If hypoxia continues, then affects myelinated nerves, skeletal muscle, and then skin and bone. Muscle cell dysfunction fuels the progression of compartment syndromeaa Continued& Physical findings commonly include tense muscle compartments that are tender to palpation, as well as passive flexion and extension Numbness and weakness in the distribution of nerves passing through compromised compartments Objective TestsObjective measurement of compartment pressure using needles/catheters was developed in the 1970s. Today, many still use needle manometry, and wick catheters Traditionally, absolute measures were used to guide therapy; pressures > 40-45 mm Hg at any point, or sustained at greater than 30 mm Hg for more than 3-4 hours mandated fasciotomy. Compartment syndrome (CS) occasionally develops at lower tissue pressures in hypotensive patientsZ 0Objective Tests, cont d.Isolated measurement of compartment pressure is neither sensitive nor specific for determining muscle ischemia Important variable is the gradient between diastolic blood pressure and compartment pressure 0Objective Tests, cont d.CS cannot exist without derangements of venous flow dynamics Jones and coworkers determined that venous duplex scanning focused on tibial veins might be an accurate means of indirectly determining presence of compartmental pressures.  0Objective Tests, cont d.Subsequent work by Ombrellaro showed that loss of normal respiratory venous phasicity correlates well with elevated tissue pressures. The finding of normally phasic tibial venous flow on duplex scanning could effectively rule out elevated tissue pressures in that compartment. 0Objective Tests, cont d.Additional noninvasive modalities include fiberoptic transducers, near-infrared spectroscopy, laser Doppler flowmetry, and tissue tonometry Above approaches are experimental, and such data should not be used independently to exclude the presence of compartment syndrome  TreatmentReactive oxygen species play a key role in the development of compartment syndrome by producing DNA damage, which triggers complex energy consuming DNA repair mechanisms, leading to more inflammatory mediators, and potentially cell death. Pretreatment with mannitol, catalase, superoxide dismutase, or other scavengers, has been shown in models to diminish cell damage after I-R injury$Treatment, cont d.MAlthough these experimental observation have implications as adjunctive therapies, surgical decompression, or fasciotomy remains the mainstay of therapy. Fasciotomy is indicated when compartment pressure is within 20-30 mm Hg of diastolic pressure Sole purpose is to release compartment HTN and prevent necrosis of compressed tissue NN$Treatment, cont d.In the lower extremity, four compartment fasciotomy of the calf can be performed through a single lateral incision, started one fingerbreadth anterior to fibula and carried out to the lateral malleolus. Access to anterior, lateral, and superficial posterior compartments is straightforward after raising narrow skin flaps. Access to deep posterior is best obtained distally where the gastrocnemius and soleus muscles become tendinous.Z$Treatment, cont d.Muscle viability is assessed by color, presence of arterial bleeding, and contraction to galvanic (electrocautery) stimulation.(Muscle relaxing anesthetic agents do not interfere with this response). Muscles that do not contract should be debrided. Myoglobinuria should be sought and treated with volume expansion, mannitol/loop diuretics as needed, and urine alkalinization by NaHCO3 to prevent renal complications.8Z  Wound ManagementEarly and complete closure of the fasciotomy wound is a critical step to maintaining a functional limb Sterile, moist dressings applied until swelling has diminished to allow closure Closure: delayed primary vs. secondary vs. skin graft vs. flap Post-traumatic Pain SyndromesThe Quick and Dirty CausalgiaXDerived from Greek causos, meaning  heat , and algos, meaning  pain . First case reported in early 16th century. Early reports from American Civil War described incomplete peripheral nerve injury secondary to penetrating trauma with subsequent burning pain, autonomic dysfunction, and  limb atrophy .R-1CRPSTerm developed at consensus committee to replace causalgia and RSD. Hallmarks of syndrome include dysfunction and pain of duration or severity out of proportion to what might have been expected from initiating event. Cause of pain and underlying pathophysiology remain obscure CRPSVComplex- dynamic/varied presentation, autonomic, cutaneous, motor, inflammatory, and dystrophic changes Regional- wide distribution beyond the area of lesion; distal part of limb usually affected Pain- out of proportion to initiating event, hallmark of condition. Refers to spontaneous burning and thermally or mechanically induced allodynia.XW _T)#CPRS, cont d.Type I (RDS) follows inciting event Pain and allodynia beyond territory of single nerve disproportionate Edema/abnormal skin blood flow in region "ZZ Type II (Causalgia) results from specific nerve injury Pain and allodynia beyond territory of single nerve Edema/abnormal skin blood flow in region EtiologyTraumatic- fractures, dislocations, sprains, burns, crush injuries (Majority of cases) Nontraumatic- prolonged bed rest, neoplasms, metabolic bone disease, MI, CVA (15% of pts s/p MI develop persistent pain in the UE during their recovery) Idiopathic L N  ! PathogenesisNot well understood Most popular theory is that of  artificial synapses occurring at site of injury, where a short circuit occurs at the point of partial nerve interruption that allows efferent sympathetic impulses to be relayed back along afferent somatic fibers. Stimulation of a sensory nerve may make the nerve more sensitive to the usual types of sensory stimuli. This theory has difficulty explaining similar pain without over nerve injury (CRPS I)Z"Presentation and DiagnosisStage I, acute: warmth, erythema, burning, edema, hyperalgesia, hyperhidrosis, patchy osteoporosis. Good result with chemical sympathectomy, spontaneous resolution possible. Stage II, dystrophic: Coolness, mottling of skin, cyanosis, brawny edema, brittle nails, diffuse osteoporosis. Good response to sympathetic block, symptoms present for fixed interval, spontaneous resolution rare.6#Presentation and DiagnosisStage III, atrophic- Pain always extends beyond area of injury, florid trophic changes, atrophy of skin, fixed joint contractures, severe demineralization and ankylosis on plain films. Diagnosis of CRPS II certain when clinical presentation includes superficial burning pain in distribution of single somatic sensory nerve, hyperesthesia, vasomotor abnormalities, radiographic evidence of osteoporosis, and a good response to local sympathetic blockade."Z$Diagnostic Sympathetic BlockValidity of clinical diagnosis can be strengthened by a positive response to sympathetic block Patients should quantify the degree of pain relief experienced (e.g., 100%, 50%) Degree of pain relief is an excellent predictor of how much relief can be expected from surgical sympathectomyZ% TreatmentxDepends on clinical stage of development, severity of symptoms, and degree and duration of relief by sympathetic block Disabling pain, several month duration, relief from block for typical duration, should be considered candidates for surgical sympathectomy Pain of recent onset, with relief from blockade that lasted beyond duration of anesthetic, continue with nonoperative  xy& $Treatment, cont d.Nonoperative therapy relies on early mobilization for susceptible patients, drug therapy (phenytoin, amytriptyline, and carbamazepine), intermittent sympathetic blocks, and physiotherapy. TENS (Transcutaneous electrical nerve stimulation) Steroids Neuromodulation   '!$Treatment, cont d.nStage I: PT +/- TENS, sympathetic block for severe pain or pts unable to undergo PT. If above fails, possible course of steroids. Stage II: PT, TENS, steroid therapy combined. Sympathetic blocks and surgical sympathectomy considered if measures fail. Stage III: Steroid or sympathetic block and surgical sympathectomy should be considered, but may be unsuccessful.  no("SummaryKey to Compartment Syndrome is a high index of suspicion, and early intervention CRPS- no one really knows what it is, or what causes it, but once diagnosed, the patient should seek therapy, get on medication, and potentially have surgery.   0` f3f3` ff̙` ___` ff` 3ff3f>?" dd@,?lPd@   Z l<@ d`"  n?" dd@   @@``@n?" dd@  @@``PR    @ ` ` p>>  (  VF y  "yZ  S B7 C DEHFPv @?q 6 6 n(dx  G b q %(@"B y2   `G1?"  TԒgֳgֳ ?"P  T Click to edit Master title style! !  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