CHAPTER 33 • HEMATOLOGY IN THE ATHLETE 197applied to rhabdomyolysis precipitated by exercise or
exertion. It is most frequently seen in running or pro-
longed exertion activity, particularly in settings of
accelerated physical training. Often it occurs with
exertional heat illness (Kark and Ward, 1994;
Baggaley; Saad, 1997; Gardner and Kark, 2002).
Biochemically, muscle injury causes a release of
myoglobin and muscle enzymes—creatine phosphok-
inase(CPK), LDH, transaminases. Severe states with
a large volume of muscle damage typically cause elec-
trolytes disturbances (potassium, phosphate, and cal-
cium) plus extracellular fluid shifts into injured tissues
(Baggaley; Saad, 1997; Vivweswaran and Guntupalli,
1999). Various extrinsic and intrinsic factors may
enhance susceptibility to rhabdomyolysis (Baggaley;
Saad, 1997; Gardner and Kark, 2002; Vivweswaran
and Guntupalli, 1999). These include the following:
a. Drug or toxin exposure (e.g., stimulants, antihista-
mines, alcohol, ephedra, and statin drugs)
b.Infection
c. Heat stroke
d. Dehydration
e. Excessive muscle overload activities (especially
eccentric loading)
f. Genetic-muscle diseases/enzyme deficiencies
g. Metabolic diseases or disorders (diabetes, thyroid
disease, chronic electrolyte disorders or acidosis)
h. Sickle cell trait
i. Autoimmune disorders (e.g., polymyositis)
j. Deconditioned state (especially with rapidly accel-
erated physical training)
•Exertional rhabdomyolysis is a spectrum condition.
Manifestations range from mild muscle injury with
negligible symptoms or systemic effects, to fulminate
cases with large muscle mass injury, severe metabolic
derangements, disseminated intravascular coagulation
(DIC), and death (Kark and Ward, 1994; Baggaley;
Saad, 1997; Gardner and Kark, 2002; Vivweswaran
and Guntupalli, 1999). Myoglobin release may cause
nephrotoxicity, but may not directly correlate with
muscle enzyme levels or metabolic disturbance.
Severity of rhabdomyolysis is gauged initially by
magnitude of symptoms and early perturbations of
blood chemistries. Collapse short of a finish line,
severe pain with inability to walk and early sustained
acidosis are ominous indicators; however, symptoms
may start off relatively mild but progress in intensity
in subsequent hours or days. Also muscle enzyme
levels may be deceptively low early on and typically
peak 1 to 2 days after the injury.
- Management thus focuses on early recognition, initi-
ating interventions appropriate to degree of injury and
monitoring for progression. Initial laboratory studies
should include basic electrolyte panel including crea-
tinine (Cr), CPK, transaminases, LDH, uric acid,
CBC, and urinalysis with microscopy. In more severe
cases, calcium, phosphate, PT, PTT, fibrinogen, and
fibrin split products should be added (Gardner and
Kark, 2000).- Positive Hgb with no RBCs on urinalysis are used as
indicators of myoglobinuria as myoglobin studies are
not quickly available in most settings (Baggaley;
Gardner and Kark, 2000). Muddy casts indicate heavy
myoglobin load and likely renal toxicity (Vivweswaran
and Guntupalli, 1999).
MILD RHABDOMYOLYSIS- Mild muscle soreness that typically resolves within
1–2 days, otherwise no complaints. - On examination has mild soreness to palpation, mini-
mal to no soreness with passive muscle stretch. - Laboratory studies reveal isolated CPK elevation
(generally ≤3000 but may be up to 5000); transami-
nases may peak slightly above normal in 1–2 days
(generally ≤ 2 ×normal values).
•Treat with oral hydration and avoidance of strenuous
exertion for 1–2 days. - Monitor for escalation or recurrence of symptoms;
educate regarding concerning preventive measures. - May return to activity the next day if these individ-
uals remain asymptomatic and laboratory studies
improved.
MODERATE RHABDOMYOLYSIS- Symptoms of moderate muscle soreness or stiffness.
- On examination has moderate muscle soreness to pal-
pation and toward extremes of passive stretch.
•Moderate elevation of CPK in first few hours with
mild increase in Cr (1.5–2 mg/dL) LDH, AST, and
ALT rise (≥ 3 ×normal) several hours to 1 day post
injury with CPK peak typically <30,000 mg/dL; uric
acid and electrolyte studies remain normal. - Initial treatment is 2 L isotonic fluids and assess
response (symptoms and studies):- Symptoms and laboratory studies improved: oral
hydration and reevaluate in 12–24 h.
2.Symptoms improved, laboratory studies little
changed: assess need for further intravenous(IV)
hydration; reassess every 4–6 h until laboratory
studies improving or refer for hospitalization if not
improving.
3.Symptoms not improving, laboratory studies
rising: refer to hospital for continued IV hydration
and monitoring (watch for developing severe or
fulminant state).
- Symptoms and laboratory studies improved: oral