Rhabdomyolysis: CrossFit, Frankenstein's Children & The Treatment Conundrum

Viet Tran

'Rhabdo' is one of those things that we don't often see in the emergency setting. Occasionally we'll see the post-inebriated patient who happened to sleep in the wrong position with a high CK or someone who had the unfortunate combination of an epiphany and a personal trainer with a vigorous work ethic. Suzanne Kenny took us through what Rhabdo is all about, when we should be worried and the evidence currently floating about.

SUMMARY

• Definition of rhabdomyolysis is ambiguous in the clinical setting
  
• Exercise induced rhabdomyolysis is unlikely to lead to AKI and in the absence of risk factors consider oral rehydration & discharge
• BACM is a clinical diagnosis – bloods and admission not required
  
• Mainstay of rhabdomyolysis if treatment required is aggressive fluid resuscitation
  

Definition

Rhabdomyolysis is a syndrome charecterized by muscle necrosis and the release of intracellular muscle constituents into the circulation. CK levels are typically markedly elevated and muscle pain and myoglobinuria may be present. The severity of illness ranges from asymptomatic elevations in the serum muscle enzymes to life threatening disease associated with extreme enzyme elevations, electrolyte imbalances and acute kidney injury

UpToDate 2015

The Problems with Rhabdomyolysis

• Hyperkalemia (early)
• Shock (from 3rd spacing)
• Renal Failure from myoglobin release (late)

The Haem Pigment - Giving Myoglobin a bad wrap in Rhabdo

• The Haem pigment in myoglobin causes AKI
• Its smaller and not strongly protein bound = rapidly filtered/excreted = more likely to cause AKI (vs Haemaglobin)
• Urine dipstick doesn't discriminate from haem in myoglobin or haemaglobin

How Haem Causes AKI

• Tubular obstruction by forming casts
• direct proximal tubular cell injury
• Vasoconstriction reducing outer meduullary flow and therfore ischaemia

Co-factors to AKI

• Volume depletion (more vasoconstirction, more cast formation)
• Acidosis (more cast formation)
• Ischaemia

Causes

TRAUMATIC

• Crush Injuries
• Prolonged immobilisation

EXERTIONAL

• Marked exertion (esp untrained)
• Hyperthermia
• Metabolic myopathies

DRUGS

• Immobilisation
• Direct myotoxins (statins, colchicine)
• Excess muscle energy demands (cocaine, amphetamines)

OTHER

• Toxins
• Infections
• Electrolyte disorders
• Endocrine disorders

Grey Areas

CK Level
Paucity of evidence exists (so take the following with a grain of salt)

• AKI uncommon if CK < 10,000
• CK < 5,000 only need oral rehydration
• Levels peak at 24-72 hrs post insult
• Look for signs of compartment syndrome if CK continues to rise > 72hrs

Clinical Diagnosis (The Triad)

1. Muscle Pain (NB in a methodically borderline study < 50% with raised CK had muscle pain)
2. Weakness
3. Dark urine or +ve dipstick (same findings as point 1)

When Should We Be Suspicious? (When Sx are Vague or Absent)

• Muscle pain
• Pressure areas
• Multitrauma or Large Injuries
• Electrolyte abnormalities
• AKI

Clinical Translation

[Own Opinion] Consider Outpatient Treatment IF

• No risk factors (eg dehydration,d rugs, sickle cell etc)
• Normal baseline renal function
• No suspiscion of compartment syndrome
• CK levels less then < 15,000 to 20,000

If they need inpatient management

• CK probably  > 5000
• Early and aggressive fluid resus is mainstay (normally start 1-2 litres saline/hr aiming for UO >200ml/hr)
• Alkalinisation of urine may help prevent (danger is if becoming anuric may become severely alkalotic)
• Diuretics – no good evidence they  prevent AKI, but may be needed if overdo fluid resus!
• Dialysis
  
• Compartment release

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BACM: Benign Acute Childhood Myositis

• Young school age usually 4-10 years old (can generally localise pain)
  
• M:F = 4:1
  
• Usually 24-48 hrs after the resolution of the viral symptoms (ie convalescent phase)
  
• CK (if done) virtually always raised (into the 10,000s)
  
• Hallmark is spontaneous and complete resolution within a week

Gait is ALMOST pathognomonic:

• Frankenstein = wide based gait with flexed hips and extended knees
  
• Toe walking
  
• Bottom shuffling or crawling
  

Sequelae

• No documented cases clinically consistent with BACM resulted in renal impairment
  
• Many papers mentioned “rare” cases of AKI in cases of viral myositis (appeared to be cases with features not consistent with BACM eg ongoing fevers, generalised muscle pains, unwell)
  

Therefore

• BACM is a clinical diagnosis
• It's reasonable not to do any bloods
  
• Review only if doesn’t improve or unwell
  

Viral Myositis - not to be confused with BACM

• More diffuse muscle involvement
  
• May even have abdo pain secondary to abdominal wall muscle involvement
  
• Muscles can be boggy as well as tender – a compartment syndrome can even develop
  
• They are UNWELL
  

If you're thinking BACM or Viral Myositis, also think about...

• Guillain-Barré syndrome: abnormal neurologic examination, with absent or decreased deep tendon reflexes in the lower extremities
  
• Other: hip causes eg septic arthritis, osteomyelitis
  

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