rhabdomyolysis compartment syndrome n.
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RHABDOMYOLYSIS & COMPARTMENT SYNDROME. Trevor Langhan PGY-1 May 20, 2004. OBJECTIVES. Compartment syndrome review Review rhabdomyolysis Controversies in management Measuring compartments. CASE. 24 Y Male fell 20 feet while rock climbing isolated right leg tib/fib fracture

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    2. OBJECTIVES • Compartment syndrome review • Review rhabdomyolysis • Controversies in management • Measuring compartments

    3. CASE • 24 Y Male fell 20 feet while rock climbing • isolated right leg tib/fib fracture • injury at 14:00 near Canmore • transport time one hour • Arrives in department at 15:45

    4. Compartment syndrome • A limb and life threatening condition • Perfusion pressure falls below tissue pressure in a closed anatomic space • Untreated leads to: • tissue necrosis • permanent functional impairment • possible renal failure • death

    5. Compartment syndrome • 1872 - Richard vonVolkmann • documented nerve injury and contracture following supra-condylar fracture • known now as Volkmann’s contracture • Usually associated with long bone fractures • May be secondary to vascular injury

    6. Compartment syndrome • 1930’s Jepson described ischemic contractures in dog hind legs after limb hypertension 20 to venous obstruction • 1941 Bywaters and Beall reported crush injuries after London Blitz • 1970’s began to measure compartmental pressures

    7. Compartment syndrome • Elevated pressures can be noted wherever a compartment is present: • hand • forearm • upper arm • abdomen • buttock • entire lower extremity

    8. Compartment syndrome • Similar to herniation syndromes in cranium • Fascial compartment acts as a closed space • Fluid is introduced into fixed volume, so pressure rises • As tissue pressure increases, perfusion pressure decreases • Oxygen unavailable for cellular metabolism

    9. Increased fluid content: intensive muscle use (tetany, seizures, exercise) burns Intra-arterial injection envenomation hemorrhage decreased serum osmolarity Decreased compartment size: burns casts military anti-shock trousers Compartment syndrome

    10. Compartment syndrome • Tissue perfusion determined by: • CPP - IFP = 18 mmHg • Cell metabolism needs 5-7 mmHg • Usual cap perf pressure 25 mmHg • Interstitial fluid pressure 4-6 mmHg • With rising interstitial pressure compromise of perfusion pressure

    11. Compartment syndrome • Matsen et al. Diagnosis and management of compartmental syndrome. J Bone Joint Surg 1980; 62A:286-91. • Intra-compartmental pressure rises • Venous pressure rises • Venous P > CPP = capillary collapse • Intervention indicated if compartment pressure > 30 mmHg

    12. Compartment syndrome • Capillaries collapse and oxygen delivery compromised • Hypoxic cell injury causes cells to release vasoactive substances (histamine, serotonin) • Increases endothelial permeability • Continued fluid leakage from capillaries into compartment • pH falls due to anaerobic metabolism

    13. Compartment syndrome • Mortality/morbidity related to time of injury to intervention • Rorabeck and Macnab reported almost complete recovery of limb function if fasciotomy within 6 hours • Matsen et al. found necrosis after 6 hours of ischemia - considered upper limit of tissue viability • Multiple studies looking at limb function with delayed fasciotomy • High incidence of sepsis and amputation • Creates open wound from a closed one • Necrotic tissue in fascia is in sterile environment • Don’t do fasciotomy after 6 hours

    14. Compartment syndrome • Suspect CS whenever significant pain occurs following an injury • Pressure increases and ischemia begins - nerves malfunction • Pain typically out of proportion to exam findings • Burning sensation or tightness

    15. Compartment syndrome • Traditional signs are not reliable • Symptoms assume a conscious patient with normal sensorium • 5 P’s • pain • parasthesia • pallor • poikilothermia • pulselessness

    16. Compartment syndrome • Determine mechanism • long bone fractures • high-energy trauma • penetrating injuries - arterial injury • venous injuries - don’t be misled by pulses • crush injuries

    17. Compartment syndrome • DVT prophylaxis? • Anticoagulation significantly increases the risk of CS • Case report of fasciotomy after simple venous puncture in anti-coagulated patient • CS found in athletes and soldiers without overt trauma • Injury secondary to vigorous exercise

    18. Compartment syndrome • Pain and burning, decreased strength and eventually paralysis • Limb may feel tense or hard • Pain at rest or with passive movement are red flags • Sensory nerves lose conductive ability before motor nerves • Ant. compartment of lower leg • check superficial peroneal nerve • lost sensation to web of 1st two toes

    19. Compartment syndrome • Clinical diagnosis in most cases • Obtunded patients or equivocal physical exam may warrant pressure measurement • Typically diagnoses at pressures between 30-40 mmHg • Only recognized treatment is fasciotomy and release of pressure • Delay leads to necrosis and permanent disability • Vaillancourt et al. 2001 published in CJEM mean time of injury to ED presentation was 9 hours

    20. Compartment syndrome • Old belief that muscle was OK until 6 hours after ischemia • Based on tourniquet extrapolated studies • Animal research in dogs • Experimental ACS versus ischemia from a tourniquet showed greater level of muscle necrosis

    21. Compartment syndrome Vaillancourt C et al. Acute compartment syndrome: How long before muscle necrosis occurs? Can J Emerg Med 2004;6(3):147-54. • Historical cohort analysis of all fasciotomies done for ACS • Clinical Dx or by measured compartment pressures • Pathologic Dx of necrosis by path reports and surgeon OR protocols • N = 76 (most young men with trauma 82%) • 49% suffered some muscle necrosis (1/3 of these lost >25% of muscle belly) • 2/4 cases that had OR within 3 hours of injury had necrosis, and 11 had necrosis within 6 hours • But 11 had injury to OR time >24 with no necrosis • Fancy stats showed that 37% of ACS develop necrosis within 3 hours

    22. Compartment syndrome Hope MJ, McQueen MM. Acute Compartment Syndrome in the Absence of Fracture. J Orthop Trauma. 2004 Apr;18(4):220-4. • N = 164 (13 excluded) • Compared presence of a fracture • time to fasciotomy and patient demographics • 38 of 151 had no fracture • ACS with no fracture were: • Older (p <0.05) • More co-morbidities (p<0.001) • Greater time to OR (mean 12.4 hours, p<0.05) • 20% had muscle necrosis vs. 8% in # group

    23. Compartment syndrome

    24. Compartment syndrome

    25. Compartment syndrome

    26. Compartment syndrome Uliasz A, Ishida JT, Fleming JK, Yamamoto LG. Comparing the methods of measuring compartment pressures in acute compartment syndrome. Am J Emerg Med. 2003 Mar;21(2):143-5. • (1) Stryker • (2) manometric IV pump • (3) Whitesides method • “standard pressure” model using column of water and beef muscle • 22, 33, 44, 55, and 66 mmHg • 3 separate days using a different muscle slab • 9 measurements for each method at each “standard pressure” level (45 measurements for each device)

    27. Compartment syndrome

    28. Compartment syndrome • Unable to reliable measure pressure with Whitesides method (9 step process) • Stryker instrument and IV pump • both found to be fairly accurate and reliable methods of measuring the intramuscular pressure of our model • The Stryker instrument is expensive • $1575, plus $66 disposable unit per use

    29. STRYKER METHOD (1) Fill the Stryker instrument with normal saline (2) zero the Stryker instrument (3) insert the needle into the area of measurement (4) inject 0.3 cc normal saline (5) read the pressure measurement IV PUMP METHOD (1) Set the IV pump to manometry mode (2) zero the IV pump (3) insert the needle into the tissue being measured (4) infuse 0.3 cc normal saline at a slow infusion rate (5) read the pressure measurement. Compartment syndrome

    30. Compartment syndrome Heemskerk J, Kitslaar P. Acute compartment syndrome of the lower leg: retrospective study on prevalence, technique, and outcome of fasciotomies. World J Surg. 2003 Jun;27(6):744-7. Epub 2003 May 13 • August 1994 to August 2000, a total of 36 patients were treated for the clinical diagnosis of acute compartment syndrome • Fracture • blunt trauma • reperfusion after treatment for acute arterial obstruction • excessive physical training • long-term surgery in the lithotomy position • after use of an intra-aortic balloon pump

    31. therapy-associated data number of opened compartments prophylactic or therapeutic fasciotomy Complications significant wound infection Hematoma nerve damage postoperative pain laboratory parameters (serum CK and creatinine) clinical outcome (death, amputation, leg dysfunction analyzed for patient characteristics Sex Age admission periods cause of the compartment syndrome Compartment syndrome

    32. Compartment syndrome • 18/40 had limb with good function at 1 year • 11/40 dysfunctional limb • After fasciotomy, mortality rates of 11%–15% • amputation rates of 11%–21% • creatinine over 120 mol/l (normal 53–110 mol/l) at the time of fasciotomy was a predictor of poor outcome (p = 0.026) • Older age also a predictor of bad outcome

    33. RHABDO • Clinical syndrome caused by injury to skeletal muscle • Release of cellular contents into ECF and circulation • Diagnosis by measuring cellular contents in plasma and urine • ARF is most serious complication • 5-15% of U.S. pts with ARF needing admission have rhabdo as an etiology

    34. RHABDO • Bywaters’ and Beal’s description of trapped WWII victims • Five victims all entrapped below rubble • Extremity injuries • All five presented in shock with dark urine • Progressed to ARF • Histology showed tubular necrosis and pigmented casts • Bywaters and Stead identified myoglobin as the urinary pigment in 1944

    35. RHABDO • Tonnes of anecdotal mass casualty case reports of ARF after earthquakes, beatings, collapse of mines • U.S. most common cause of rhabdo is prolonged muscle compression following alcohol bingeing • Creatine Kinase (CK) levels correlate with degree of muscle injury • ARF may occur in 4-33% of cases with a mortality ranging from 3-50% • 5-7% of ARF admissions in the U.S.

    36. RHABDO • Several studies to predict who’s at risk of progressing to ARF from crush injuries Oda et al. Analysis of 372 patients with crush syndorme caused by the Hanshin-Awafi earthquake. Journal of Trauma-Injurey Infection & Critical Care 1997;42(3):470-5. • Significant correlation between CK levels and number of limbs crushed • CK > 75 000 U/L higher rate of ARF and mortality (84% vs. 39%, p<0.01, and 4% vs. 17%) Ward MM. Factors predictive of acute renal failure in rhabdomyolysis. Ardch Intern Med 1988;148(7):1553-7. • Peak serum CK >16 000 U/L highest risk of ARF and death • 90% of pts had peak CK level within 24 hours

    37. RHABDO • By definition: is the liberation of components of injured skeletal muscle into circulation • Direct compression of muscle leading to local crush injury • Don’t forget vascular causes – thrombus, embolus, traumatic interruption or external compression • Tissue pressure > capillary perfusion pressure • With relief of compression – re-perfusion of muscle • Fundamental pathophysiology is ischemia followed by re-perfusion

    38. RHABDO • Other etiologies: • Direct compression (ischemia/re-perfusion) • Multi-trauma • Prolonged immobility • Seizures • Lightning strike • Vascular compromise • Steroids • Neuromuscular blockade • Congenital enzyme disorders • Prolonged exercise • Soft tissue infections

    39. RHABDO • Muscle compression leads to mechanical stress • Opens stretch reactive channels that allow influx of fluid and lytes into cell (including Na+ and Ca++) • Cells swell and intra-cellular Ca++ rises • Causes increased activity of proteases and degradation of myofibrillar proteins • Ca++ dependant phosphorylases are activated and cell membranes degraded • ATP production lowered b/c anaerobic not aerobic • Neutrophil migration into cells and release of proteolytic enzymes and free radicals • Causes micro-vascular vasoconstriction and worsening ischemia


    41. RHABDO • Cell membrane function is impaired • Further influx of Na+ and Ca++ • Water follows Na+ into cell causing edema and finally complete lysis of cell releasing contents into circulation • Large volumes of intra-vascular fluid sequestered in injured extremities • Hypovolemia 1st manifestation of crush syndrome Bywaters and Popjak Experimental crushing injury: peripheral circulatory collapse and other effects of muscle necrosis in the rabbit. Surg Gynecol Obstet 1942;75:612-27. • showed ischemia in animal limbs using a touniquet • injury was tolerated by the animals without causing hypovolemia and systemic effects until reperfusion • Rabbits then died of hypovolemic shock

    42. RHABDO Oda et al. Analysis of 372 patients with crush syndrome caused by the Hanshin-Awaji earthquake. Journal of Trauma-Injury Infection & Critical Care 1997;42(3):470-5. • 35 deaths out of 372 crush syndrome victims • 23/35 (66%) cause of death was hypovolemic shock • Most common cause of death in first 4 days • Additionally to hypovolemia • Subject to large toxin load • May develop life-threatening electrolyte abnormalities

    43. RHABDO

    44. RHABDO • 4-33% of pts with rhabdo develop ARF (mortality 3-50%) • Three main mechanisms • Decreased renal perfusion • Cast formation with tubule obstruction • Direct toxic effect of myoglobin

    45. RHABDO • Decreased renal perfusion • From hypotension • Renin-angiotensin • Myoglobin causes release of endothelins • Decrease GFR by vasoconstriction of af and ef arterioles • Rat model showed giving bosentan (endothelin-R antagonist prevent ARF, no human trials)

    46. RHABDO • Myoglobinemia and subsequent myoglobinuria • Respiratory pigment comprising 1-3% of wet weight of skeletal muscle • Single heme group in centre • Low circulating levels easily bound by haptoglobin and cleared by reticuloendothelial system • At elevated levels binding capacity is saturated – free myoglobin levels rise • Plasma levels >0.5 to 1.5 mg/dL filtered by KD – measurable in urine (dipstick +ve RBC/microscopy 0 RBC) • Myoglobin is not reabsorbed in the tubueles • H20 reabsorbed as pt is hypovolemic • Results in dark pigmented urine

    47. RHABDO • Cast formation and tubular obstruction occur in acidic urine with high myoglobin concentration • Reacts with Tamm-Horsfell protein and ppts forming casts • Animal models have shown alkaline urine reduces cast formation • Hypothesis that casts obstruct urine flow in tubules

    48. RHABDO • Direct toxic effect of myoglobin main component of renal failure • Increasing evidence of free radical mediated injury • Endogenous renal scavenging agents depleted in myoglobinuria-induced renal failure • In acidic urine myoglobin dissociated to protein and ferrihemate • Iron catalyzes the formation of free radicals • This reactivity is decreased in an alkaline environment • Animal model has shown desferrioxamine (chelating agent) protects vs. renal failure in rhabdo

    49. RHABDO • Early diagnosis is crucial in pts with rhabdo • Significant soft-tissue injuries or ischemia-reperfusion injuries are at highest risk • Present often with painful, swollen limbs and should be observed for compartment syndrome • Phys exam more difficult in the intoxicated, CNS injured patient • Dark, tea-colored urine dipstick +ve for blood with absence of RBC on microscopy is suggestive • Cheap screen test is serum CK level • Monitor urine output and do serial CK

    50. RHABDO • Several studies to predict who’s at risk of progressing to ARF from crush injuries Oda et al. Analysis of 372 patients with crush syndorme caused by the Hanshin-Awafi earthquake. Journal of Trauma-Injurey Infection & Critical Care 1997;42(3):470-5. • Significant correlation between CK levels and number of limbs crushed • CK > 75 000 U/L higher rate of ARF and mortality (84% vs. 39%, p<0.01, and 4% vs. 17%) Ward MM. Factors predictive of acute renal failure in rhabdomyolysis. Ardch Intern Med 1988;148(7):1553-7. • Peak serum CK >16 000 U/L highest risk of ARF and death • 90% of pts had peak CK level within 24 hours