Rhabdo

Question 1

Describe Rhabdo

Answer 1

Potentially life threatening condition characterized by the breakdown of skeletal muscle and the relase into the circulatory system of intracellular contents including CK, AST, LDH and electrolytes.

Although the cuases of rhabdo are diverse the pathogenesis appears to follow a final common pathway - increased cytoplasmic calcium conentration leading to myocyte destruction with the release of muscle components into the ciruclation. There are two primary mechanisms whereby calcium pathologically accumulates in the cell

1) direct cell membrane damage
2) ATP depletion.

Rhabdo is classified into 4 basic pathophysiological processes

1) impairment of the muscles production or use of ATP at the cellular level. ATP concnetration within the cell fall; energy dependant mechanisms falter including Na/K atpase pumps leading to disruption of chemical gradients sarcolemma and cell membrane compromise and cell destruction
2) impairment of delivery of o2, glucose and other nutrients to skeletal muscle
3) increased in metabolic demands beyond the ability of the organism to deliver o2 and nutrients
4) Direct myocyte damage.

Question 2

Give DDX of Rhabdo

Answer 2

1) prolonged immobilisation
- Pressure injury and direct myocyte damage

2) excessive muscle activity
- ATP deleoption

3) Muscle ischaemia
- ATP production is imited
- Muscle cell hypoxia leads to muscle damage in as little as 2 hours with irreversible anatomic and functional changes within 4 hours

4) Temp extremes
- Heat stroke
- NMS
- malignant hyperthermia
- serotonin syndrome

5) Electrical current

6) electrolyte abnormalities
- hypokalaemia

7) Drugs - illicit
- opiods
- antipsychotics
- beno
- amphetamines
- ectasy
- LSD
- synthetic cannabinoids

8) Medications
- statin induced rhabdo is well documented

9) infections
10) metabolic myopathies
11) Connective tissue disorders
12) Rheumatological disorders

13) endo
- hypohtyroidism

Question 3

Discuss early complications of rhabdo

Answer 3

Early

1) Compartment syndrome
- The massive influx of Calcium and sodium in rhabdomyolysis leads to the accumulation of large amounts of extracellular fluid in the muscles cells causing local oedema and raised intracompartmental pressure.
- This leads to tissue ischaemia
- Volkamans contracture
- Intra-compartmental pressure above 50mmhg or sustained pressures of more than 30m HG during max 6 hour period are indications for fasciotomy

2) electrolyte and acid disturbances
- Hyperkalamia
- Acidemia - exacerbates hyperkalaemia and itself can be exacerbated by renal impairment.
- Disruption of muscle cells releases large amounts of phosphoric components into circulation leading to hyperphosphataemia and ectopic calcification. Calcium phosphate crystal deposition can lead to hypocalcaemia further increasing chance of arrythmia/ malignant dysthymia

3) Hypovolaemia
- fluid moves from intravasuclar compartment into damaged muscle causing profound intravascular fluid depletion. THe shift may exceed 15L

4) heaptic dysfunction
- Large elevation in serum live enzyme levels may occur
- not fully understood

Question 4

Discuss late complications of rhabdo

Answer 4

1) Myoglobin induced AKI
- -Myoglobin cast formation
- -direct cytotoxic action of myoglobin on the epithelial cells of the PCT
- -intra-renal vasoconstriction and ischaemia - fluid shift and renal dysufnction leads to activation of the RAS and sympathetic nervous system producing vasocontriction.

2) DIC

Question 5

Discuss ix of rhabdo

Answer 5

CK - has a half life of 1.5 days, its elevarted in the first 12 hours and peaks during the first 3days and normalises at around 5 days

In the past myoglobin levels were used to diagnose rhabdo - however myoglobin has a half life of 1-3 hours and is completely absent after 24 hours.

Urine dipstick
-positive for blood –> myoglobin filtered into the urine

U&E for electrolyte disturbances
COAG- DIC

Question 6

Discuss management of rhabdo

Answer 6

Fluid expansion is the mainstay of treatment. Can need very large amounts with titration of urine output to 300ml/hr in adults 2-3ml/kg

Alkalinsations - controversial
Principles of benifit of alkalinisations
1) myoglobin precipirtation is increased in acidic urine
2) Reduction-oxidation cycling of myoglobin and lipi peroxidation and thus tubule injury are inhibited in alkaline urine
3) myoglobin induces renal vasoconstirction only in an aicdic medium
Consideration for Hco3 – nil firm evidence for the same

Diuretics - controversial

• Benifit of mannitol in rhabdo is not established. Stuides suggest that it might be protective by cuasing diuresis which minimises intratubular pigment deposition and cast formation. Also free radical savenger - bulk of benefit is from the osmotic diuretic affect rather than direct effect.
• Large doses of mannitol may be detrimental by causing renal vasoconstrction and tubular toxicity.
• Loop diuretics only used in fluid overload

Dialysis may be needed depending on severity of AKI

• Unmanageable metabolic acidosis
• hyperkalaemia refractory to medical treatment
• uremia
• fluid overload