Rhabdomyolysis is a condition characterized by the breakdown of muscle fibers which releases muscle fiber contents into the bloodstream. This can lead to kidney damage or failure. Causes include crush injuries, prolonged immobilization, infections, certain drugs, and toxins. The breakdown of muscle fibers leads to electrolyte abnormalities and an overload of breakdown products in the kidneys which can impair kidney function. Early treatment involves aggressive fluid resuscitation and monitoring for complications like hyperkalemia or renal failure. Outcomes depend on early recognition and intervention to prevent further kidney damage.

1. Rhabdomyolysis
…a big word for big problEMS
Reappropriated from the
internet… SORT OF

2. Causes of Rhabdomyolysis
• In US: alcohol abuse and subsequent immobility and coma,
direct myotoxic effects of alcohol
• Crush injuries, long surgeries in lithotomy or lateral decub,
surgery on morbidly obese patients (gluteal), contact sports,
burns, lifting heavy weights
• Vascular compromise – compartment syndrome, embolus and
subsequent reperfusion
• DT’s, NMS, hyperthermia, long-term vecuronium
• Electrolyte disturbances
• Drugs (HMGCoA red. inh., psychedelic)
• Infections-Legionella, strep, influenza, HIV

3. Hemlock (Conium maculatum )
•Old Testament Book of Numbers 11
(31-35): Israelites suffered a “mass
plague” during their exodus following
ingestion of quail.
• In the Mediterranean, quails eat
hemlock during spring migration, and
rhabdo from eating the birds is a
recognized phenomenon.
Rhabdomyolysis
• Release of intracellular components from injured
myocytes into the circulation
Poison hemlock was used to execute Socrates.

4. Pathophysiology of ARF
• “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%

5. Myocyte Injury
Hours of
ischemia
0 2 4 6
Tolerable-no
permanent
histological
changes
Irreversible
anatomic and
functional changes
Muscle
necrosis

6. Cell Ion Physiology
intracellular
extracellular

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

8. Patient Will Develop:
• Hypovolemia
• Hyperkalemia (too much Potassium)
• Hyperphosphatemia
• Hypocalcemia

9. 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

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

11. Pathophysiology of ARF
Not reabsorbed
Binds Tamm-
Horsfell proteins
Kidneys just cannot handle it !
Myoglobin – 1-3% of
wet mm weight

12. Diagnosis:
(above my pay grade, but still interesting)
• Serum CKMM
– Correlates w/severity of rhabdo
– Normally 145-260 U/L
– Levels peak w/in 24h
– >5000 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
(+) for blood
uric acid
crystals

13. Malinoski, et al. (2004)
Treatment
Algorithm for
preventing renal
failure
WAY ABOVE MY
PAY GRADE

14. EMS TREATMENT
• Rapid Transport
• Airway Mgmt / ECG
• Normal Saline (not LR)
• Sodium Bicarb?
• Calcium Chloride?
• D50/Insulin?
• Albuterol neb treatment?
• Diuretics?

15. Hyperkalemia = peaked T-waves

16. LCEMS CRUSH INJURY PROTOCOL
ALS LEVEL 1: PARAMEDIC ONLY
PRE-EXTRICATION
1. Establish two large bore IVs of NS (or LR). 2 liters NS bolus, followed by
500 ml/hr (limit fluid bolus for pediatric (20 ml/kg) and patients with
history of cardiac or renal dysfuction
2. Pain control per Pain Protocol 2.1.5. Fentanyl is preferred to Morphine.
a. Fentanyl 50 – 100 mcg IV or IM
b. Morphine 4 mg initial then 2 mg increments prn up to 10 mg
3. IMMEDIATELY PRIOR TO EXTRICATION: Give Sodium Bicarbonate
1 mEq/kg up to 100 mEq IVP
4. Extrication
POST-EXTRICATION
5. Continue cardiac monitoring and assess for hyperkalemia; i.e. widening of
QRS (>0.12 seconds) and peak T waves, hypotension
6. If hyperkalemic changes on monitor, give; Calcium Chloride 1 gm IV slow
(over 5 minutes)
7. Give an Albuterol (only) Neb 2.5 mg
8. Dress/splint wound/extremity
9. Call Trauma Alert if criteria are met

17. Early Treatment: HOSPITAL
• FLUIDS
– Begin early, even on the field
• Damaged muscles attract a lot of fluid
– Up to 10L/day
• Ideally ½ NS with 100mmol/L bicarb
– prevents tubular precipitation
– reduces risk of hyperkalemia from damaged mm
– corrects acidemia
– not proven beneficial however not deleterious
• 10ml/h 15% mannitol
– renal vasodilator
– free radical scavenger
– Forced diuresis w/in 6 hrs of admission

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

19. Studies
• Many done after earthquakes,
mass beatings, other natural
disasters
– Spitak earthquake of 1988 in
Armenia 600 required dialysis
– Marmara earthquake Turkey
1999 n=462 on dialysis, 19%
mortality which was much
better than before
– 1995 International Society of
Nephrology created Disaster
Relief Task Force to prev/treat
crush injury-induced ARF
The causes of death in 50 patients with the crush syndrome
following the Hanshin–Awaji Earthquake. Deaths from
hypovolemia and hyperkalemia were the most common in the
early period, while sepsis leading to multiple organ failure was
responsible for most of the late deaths