1. Crush Injuries and Rhabdomyolysis Dr.M.Mortazavi Nephrologist

2. INTRODUCTION 
Rhabdomyolysis is a syndrome characterized by muscle necrosis and the release of intracellular muscle constituents into the circulation.
The severity of illness ranges from asymptomatic elevations in serum muscle enzymes to life-threatening cases associated with extreme enzyme elevations, electrolyte imbalances, and acute renal failure

3. “Crush syndrome” first recorded in bombing of London during WWII: 5 people who were crushed presented in shock with swollen extremities, dark urine.
Later died from renal failure.
5-35% of patients with rhabdomyolysis develop ARF
mortality is 3-50%

4. Cause of Rhabdomyolysis
Traumatic muscle injury
Drugs and toxins
Infections
Genetic disorders
Excessive muscle activity
Ischemia
Electrolyte and endocrine
Immunologic disease

5. Pathophysiology of Rhabdomyolysis

6. Myocyte Injury Tolerable-no permanent histological changes
Muscle necrosis
Hours of ischemia
Irreversible anatomic and functional changes

7. Cell Ion Physiology
intracellular
extracellular

8. Pathogenesis of Myocyte Injury
Ca++
compression
Protease activation
Membrane degradation
Nuclease activation
Lipid peroxidation
ischemia
Influx of Ca++, Na+ and fluids
Attraction of PMN’s
Decreased ATP production
cell lysis
More Ca++ influx

9. Pathophysiology of ARF
CONTRIBUTORS:
Dehydration (hypovolemia)
Aciduria
Renal vasoconstriction
Cast formation
Heme-induced toxicity to tubule cells
Not reabsorbed
Binds Tamm-Horsfell proteins
Myoglobin – 1-3% of wet mm weight

11. Synergistic tubular damage
Rhabdomyolysis
Myoglobinemia
Endotoxin
cascade
3,rd spacing
NO scavenging
Myoglobinuria
Volume depletion
Acidemia
Proxmial tubule
Fe loading
Aciduria
Renal hypoperfusion/
Ischemia
Cast formation
Luminal stasis
Synergistic tubular damage
ARF
ATN

13. Diagnosis

14. CLINICAL MANIFESTATIONS AND DIAGNOSIS
The classic presentation of rhabdomyolysis includes myalgias, red to brown urine due to myoglobinuria, and elevated serum muscle enzymes (including creatine kinase)

15. When to Suspect Rhabdo
Occurs in up to 85% of patients with traumatic injuries.
Those with severe injury who develop rhabdomyolysis-induced renal failure have a 20% mortality rate
Multiple orthopedic injuries
Crush injury to any part of the body (eg: hand)
Laying on limb for long period of time –patient “found down”
Long surgery
Brown urine

16. What to Watch for if you suspect Rhabdo:
Clinical: Mm pain, weakness, dark urine
Hypovolemia, shock
Electrolyte abnormalities : ↑K+, ↓ Ca++ (sequestered in injured tissues), acidemia upon reperfusion

17. Clinical and laboratory features of rhabdomyolysis
History and physical examination
Urinalysis
Serum potassium concentration
Creatine kinase
Acid –Base balance
Uric acid
BUN/Cr
Ca/Ph methabolism
DIC

18. Diagnosis Serum CKMM Serum myoglobin Ca++ UA-myoglobinuria
Correlates w/severity of rhabdo
Normally U/L
Levels peak w/in 24h
>3000 high correlation with renal failure
#’s in 100,000’s not uncommon
high t(1/2): 1.5 days
Serum myoglobin
t(1/2) 2-3 h
Excreted in bile
Ca++
UA-myoglobinuria
dipstick will be (+) for hemoglobin, RBC’s and myoglobin
Microscopy: no RBC’s, brown casts, uric acid crystals
Other measures: carbonic anhydrase III, aldolase
sample UA
uric acid crystals
(+) for blood

19. Approach to the patient with red or brown urine
                                                                            
Electrolyte abnormalities 

20. Muscle enzymes 
The hallmark of rhabdomyolysis is an elevation in serum muscle enzymes. Serum CK levels may be massively elevated to above 100,000 IU/L.
Elevations in serum aminotransferases are common and can cause confusion if attributed to liver disease.

21. Electrolyte abnormalities

23. Prevention and Treatment

24. MANAGEMENT
Plasma volume expansion with intravenous isotonic saline should be given as soon as possible, even while trying to establish the cause of the rhabdomyolysis.
Treatment of the underlying cause of the rhabdomyolysis.

25. Monitoring with serial measurements of serum potassium, calcium, phosphate, and creatinine ,CPK is recommended.

26. MANAGEMENT
The metabolic consequences of and renal functional impairment due to rhabdomyolysis should be anticipated, particularly potentially life-threatening hyperkalemia.
Hypocalcemia? Should be treated?

27. Early Treatment FLUIDS Begin early, even on the field
Damaged muscles attract a lot of fluid
Up to 10L/day
Ideally NS with bicarb
prevents tubular precipitation
reduces risk of hyperkalemia from damaged mm
corrects academia
mannitol
renal vasodilator
free radical scavenger

28. Late Treatment Dialysis – intermitted preferred to continuous
Reduce use of anticoagulants in trauma patients