Download Rhabdomyolysis

Heat Illness
Rhabdomyolysis
Sudden Cardiac Death
Sickle Cell Trait
October 14th, 2015
James Leinhart, MD
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AGENDA
Definition
Stats
Mechanism
Pathophysiology
Risk Factors
Diagnosis
Management
Recovery
Prevention
Questions
Heat Illness - Definition
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Heat Cramps
Heat Tetany
Heat Edema
Heat Syncope / Exercise Associated
Collapse (EAC)
• Heat Exhaustion / Exertional
Hyperthermia
• Exertional Heat Stroke (EHS)
Heat Illness - Definition
• Heat Cramps
– Abdomen, lower extremities
– Often yelling in pain
– Fluid/electrolyte deficiency
– Fatigue, faulty neuromuscular communication
• Heat Tetany
– Carpopedal spasm
– Hyperventilation
• Heat Edema
– Hands, feet
Heat Illness - Definition
• Heat Syncope / Exercise Associated
Collapse (EAC)
– Immediately upon cessation
– Decreased vasomotor tone
– Venous pooling
– Dehydration
Heat Illness - Definition
• Heat Exhaustion / Exertional
Hyperthermia
– Temperature < 104°F
– No mental status changes
– Weakness, dizziness, syncope, cramps, N/V
• Exertional Heat Stroke (EHS)
– Temperature > 104°F
– AMS
– Absent sweating
– Seizures
– Coma
Exertional Heat Stroke
• Defined by hyperthermia
(> 40°C) with CNS
disturbances and
multiorgan failure.
• Almost all exhibit sweat
soaked and pale skin at
time of collapse
• In contrast, non-exertion
related heatstroke
presents with dry, hot and
flushed skin.
Exertional Heat stroke
• Predisposing factors
– Strenuous exercise in a hot
humid environment
– Lack of heat acclimatization
– Poor physical fitness
• Greatest risk when the wet bulb
globe temperature exceeds 28°C
(82°F) during high intensity
exercise (>75% VO2max) and/or
strenuous exercise that lasts
longer than 1 hour.
• EHS can occur in cool to moderate
environments
Heat Illness - Stats
• Incidence
– Varies based on event
– Highly dependent on environmental
conditions
– Limited reporting on non-fatal EHS
• Football
– Since 1995, average 3 deaths/year
– 1/350,000
• Marathon
– 1/10,000 finishers
Exertional Heat Stroke
• Factors that increase risk
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Obesity
Low physical fitness
Lack of heat acclimatization
Dehydration
Previous history of EHS
Sleep deprivation
Sweat gland dysfunction
Sunburn
Viral illness
Diarrhea
Alcohol/drugs
Certain medications
Heat Illness –
Mechanism/Pathophysiology
• As a cell is heated above it’s thermal threshold (about 40°C)
• Cellular damage
– Protein denaturation
– Cell dysfunction->organ dysfucntion
• Inflammatory Cytokines / Heat Shock Proteins
– Circulatory collapse / shock
– Systemic / end organ damage
• Vascular Endothelium Damage
– coagulopathies
Exertional Heat Stroke
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Recognition
– Immediate recognition is paramount
to survival
– Signs and symptoms generally
nonspecific.
• Disorientation, confusion,
dizziness, irrational or unusual
behavior, inappropriate
comments, headache, irritability,
loss of balance and muscle
function, vomiting, collapse,
hyperventilation, seizures and
coma
– Rectal Temperature should be
measured: >40°C (104°F)
– SBP<100mm Hg, Tachycardia,
hyperventilation and shock-like
appearance are common.
Heat Illness – Diagnosis
• Signs/Symptoms
– Core (rectal, foley) temperature > 104°F
– Impaired cardiac output
• Hypotension, tachycardia, tachypnea
– AMS
• Irritability, ataxia, confusion, disorientation, syncope,
hysteria, psychosis, seizure, coma
– Diminished peripheral cooling
• Decreased perspiration, hot skin
– DIC
• Bleeding, ecchymosis, pulmonary edema
– ARF  metabolic abnormalities
Exertional Heat Stroke
• Treatment
– A life- threatening medical
emergency that requires immediate
whole body cooling.
– Cold water cooling provides the
fastest whole body cooling rate and
the lowest morbidity and mortality.
– If unavailable-> ice water,
towels/sheets with ice on head, trunk
extremities etc…
– Hematological and serum chemistry
should be obtained if possible.
– Fluids to preserve intravascular
volume, improves renal flow and
protects kidneys from
Rhabdomyolysis
Exertional Heat Stroke
• Return to play
– Refrain from exercise for at least 7 days.
– Follow up in one week for physical exam and repeat
lab testing or diagnostic imaging of affected organs.
– When cleared, begin exercise in a cool environment
and gradually increase duration, intensity, heat
exposure for 2 weeks to acclimatize and demonstrate
tolerance
– If return to activity is difficult, consider a laboratory
exercise-heat tolerance test about 1 month postincident.
– Clear the athlete for full competition if heat tolerance
exists after 2-4 weeks of training.
Heat Illness – Recovery
• Increased susceptibility to EHS after acute event
– Impaired central thermoregulation up to several
months
• At least 7 days asymptomatic rest
• Graduated return to activity protocol
– Stepwise over two weeks
– Supervised
Heat Illness - Question
• During the second football practice of the day on
day three of the college preseason football camp,
an offensive lineman is found sitting on the ground,
unwilling to stand up. He states his left calf is
cramping and that he feels lightheaded and
exhausted. You suspect possible exertional heat
stroke. Which of the following statements about this
condition is true?
A. Axillary, oral, or a rectal temperature greater than 104F (40C)
establishes the diagnosis of exertional heat stroke
B. This condition occurs randomly without warning and cannot be
predicted
C. Cold/ice water immersion is an effective way to treat exertional
heat stroke
D. There are two patterns of presentation: sodium depletion and
water depletion
Heat Illness - Question
• During the second football practice of the day on
day three of the college preseason football camp,
an offensive lineman is found sitting on the ground,
unwilling to stand up. He states his left calf is
cramping and that he feels lightheaded and
exhausted. You suspect possible exertional heat
stroke. Which of the following statements about this
condition is true?
A. Axillary, oral, or a rectal temperature greater than 104F (40C)
establishes the diagnosis of exertional heat stroke
B. This condition occurs randomly without warning and cannot be
predicted
C. Cold/ice water immersion is an effective way to treat exertional
heat stroke
D. There are two patterns of presentation: sodium depletion and
water depletion
Rhabdomyolysis
• In athletics most cases exertional but can be caused by crush
injuries, burns and multiple other causes.
• Prolonged, heavy repetitious exercise leads to breakdown of
skeletal muscle and leakage of cellular contents.
• Etiology: local tissue hypoxia leading to failure of cellular function
and potassium efflux and calcium influx
• Common predisposing factors: Heat, humidity, dehydration, poor
conditioning.
Rhabdomyolysis
• Presentation: Muscle pain and tenderness, muscle swelling, muscle
cramps, reddish brown urine.
• Most cases are subclinical and never diagnosed
• Labs: CK is the most important diagnostic enzyme. Rhabdo defined
as greater than 5 times the upper limit of normal or 1000.
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<200= nml
>600= subclinical to mild
>10,000= most clinical cases
>200,000= severe
Rhabdomyolysis
• Mild to moderate
– Respond well to aggressive hydration
– Damage not persistent
• Severe cases
– Acute Tubular Necrosis: Caused by renal hypoperfusion,
acidosis, and myoglobin sludging in renal tubules.
– Acute Compartment Syndrome:
– Rhabdo causes muscle swelling which increases intramuscular
pressure
– Athletes with chronic compartment syndrome: increased
pressures and decreased tissue perfusion leads to Rhabdo
Treatment
• Aggressive early hydration
– Maintains renal perfusion, clears myoglobin and prevents ATN.
– May require 4-12L NS in first 24 hours.
– Urine output goal 3ml/kg/hr
• Alkalinization of urine with bicarbonate
– Myoglobin is less nephro toxic in alkaline urine
• Correct electrolyte abnormalities
– Caution hyperkalemia and cardiac dysrhythmias
• Fasciotomy if necessary
Rhabdomyolysis
• Ongoing care
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Repeat CK, elctrolytes and renal function in a few days
CK goal below 1000
Discontinue myotoxic drugs if any
Activity as tolerated after normalization of labs
• Diet
– When rhabdo causes renal failure restrict protein intake to lower
BUN
– Limit potassium intake if renal failure
Sudden Cardiac Death - Question
• A 19-year-old female tennis player comes to you for her
preparticipation examination. She denies any cardiac
symptoms and has always kept up with her peers.
There is no history of heart disease or early death in the
family. Examination is unremarkable except for a
systolic ejection murmur that increases with Valsalva
and standing, and decreases with fist clenching and
squatting. Which of the following is the most significant
predictor of sudden cardiac death in this athlete?
A.
B.
C.
D.
E.
Sudden death in her brother
Muscle fiber disarray on biopsy
Septal thickness > 1.8 cm
Paroxysmal atrial fibrillation on Holter monitoring
Resting BP 120/75, and BP 95/70 after six minutes of exercise
Sudden Cardiac Death - Question
• Which of the following is a current American
Heart Association (AHA) recommendation
regarding cardiac evaluation during the
preparticipation exam?
A.
B.
C.
D.
Auscultate for heart murmur during provocative maneuvers
Palpate bilateral brachial pulses
Obtain bilateral brachial blood pressure with the athlete standing
Perform electrocardiogram on all athletes
Sudden Cardiac Death - Definition
• An unexpected death due to cardiac causes
occurring in a short time period (generally
within 1 h of symptom onset) in a person with
known or unknown cardiac disease.
Cardiac
Sudden Cardiac Death
• Structural
– HOCM (25-36%)
– CCA (19%)
– MVP
– Aortic Rupture
(marfans)
– AS
– myocarditis
– CAD (age >30)
• Electrical
– LQTS
– SQTS
– WPW
– Brugada
– AV blocks
• Traumatic
– Commotio Cordis (20%)
Cardiac
• In a collapsed athlete, cardiac arrest should be assumed
until proven otherwise
• Time from arrest to defibrillation is the single greatest
factor affecting survival
– Survival rates decrease 10% for every minute
defibrillation is delayed w/o CPR.
– Decreases to 3-4% if CPR is administered.
• Drezner et al
– Demonstrated high survival rates for sudden cardiac
deaths for high schools with AED programs.
– 16/18 (89%) student athletes and 8/9 (89%) adults
who arrested during physical therapy
– Survival wo AED’s is approximately 8%
Cardiac
• Presentation
– Brief seizure-like activity with
myoclonic movements have been
reported in over 50% of athletes
with cardiac arrest.
– Agonal respirations or gasps are
often mistaken for normal
breathing
• Treatment
– Activate EMS, attach AED if
available
– ABC vs CAB
• More emphasis on chest
compressions (30:2) rather than
rescue breathing.
• Less emphasis on checking pulses
HOCM – Mechanism/
Pathophysiology
• Asymmetric LV hypertrophy
– Septum
– Thickness > 15 mm
– Septum:Free Wall > 1.3
– Nondilated LV
– Disorganized cellular architecture
– 1/3 cases with coronary intramural tunneling
– LV diastolic dysfunction
– Dynamic outflow obstruction
– Ventricular arrhythmias
HOCM – Mechanism/
Pathophysiology
• Genetics
– 11 mutated sarcomeric genes
– 55% autosomal dominant
– 45% sporadic
HOCM – Diagnosis
• Symptoms
– Usually asymptomatic until death
– Only 21% have prior symptoms
• Exertional CP, lightheadedness, dyspnea, syncope
• PPE
– Athlete Hx
– FH SCD in family members < 35 years old
– PE
• Harsh systolic ejection murmur
– Increases with decreased venous return (valsalva, standing)
– Diminishes with increased venous return (supine, squatting)
HOCM – Diagnosis
• ECG
– 95% abnormal
• Prominent Q waves
• Deep inverted T waves
• Increased QRS voltage
• Echocardiography
– Gold standard
HOCM – Diagnosis
HOCM – Diagnosis
HOCM – Diagnosis
HOCM – Management
• PPE
– Hx, FH SCD, PE
– ECG, TTE if indicated
• Class IA sports only (low-static, low-dynamic)
– Bowling, golf, etc.
• Informed consent
• AED
• ICD
Commotio Cordis
Sudden Cardiac Death - Question
• A 19-year-old female tennis player comes to you for her
preparticipation examination. She denies any cardiac
symptoms and has always kept up with her peers.
There is no history of heart disease or early death in the
family. Examination is unremarkable except for a
systolic ejection murmur that increases with Valsalva
and standing, and decreases with fist clenching and
squatting. Which of the following is the most significant
predictor of sudden cardiac death in this athlete?
A.
B.
C.
D.
E.
Sudden death in her brother
Muscle fiber disarray on biopsy
Septal thickness > 1.8 cm
Paroxysmal atrial fibrillation on Holter monitoring
Resting BP 120/75, and BP 95/70 after six minutes of exercise
Sudden Cardiac Death - Question
• A 19-year-old female tennis player comes to you for her
preparticipation examination. She denies any cardiac
symptoms and has always kept up with her peers.
There is no history of heart disease or early death in the
family. Examination is unremarkable except for a
systolic ejection murmur that increases with Valsalva
and standing, and decreases with fist clenching and
squatting. Which of the following is the most significant
predictor of sudden cardiac death in this athlete?
A.
B.
C.
D.
E.
Sudden death in her brother
Muscle fiber disarray on biopsy
Septal thickness > 1.8 cm
Paroxysmal atrial fibrillation on Holter monitoring
Resting BP 120/75, and BP 95/70 after six minutes of exercise
Sudden Cardiac Death - Question
• Which of the following is a current American
Heart Association (AHA) recommendation
regarding cardiac evaluation during the
preparticipation exam?
A.
B.
C.
D.
Auscultate for heart murmur during provocative maneuvers
Palpate bilateral brachial pulses
Obtain bilateral brachial blood pressure with the athlete standing
Perform electrocardiogram on all athletes
Sudden Cardiac Death - Question
• Which of the following is a current American
Heart Association (AHA) recommendation
regarding cardiac evaluation during the
preparticipation exam?
A.
B.
C.
D.
Auscultate for heart murmur during provocative maneuvers
Palpate bilateral brachial pulses
Obtain bilateral brachial blood pressure with the athlete standing
Perform electrocardiogram on all athletes
Sickle Cell Trait – Question
• Which of the following statements regarding
sickle cell trait athletes is true?
A. Sickle cell trait, in contrast to sickle cell disease, has
little to no mortality in athletes
B. Any cramping, struggling, or collapse in a sickle-trait
athlete must be considered sickling – a medical
emergency – until proven otherwise
C. The symptoms of exertional sickling and heat illness
are not distinguishable
D. Acclimation to intense training, increased hydration,
and increased rest afford no protection to sickling in
athletes
Sickle Cell Trait – Question
• A 20 year-old-male football player with known
sickle cell trait slumps to the ground
complaining of diffuse muscle fatigue. His
ABCs are intact and his core temperature is
101°F. What is the best initial form of
treatment?
A.
B.
C.
D.
Intravenous fluids
Stretching and massage of affected muscles
Cold/ice water immersion
Oxygen 15L via NRB
Sickle Cell Trait – Definiton
• Condition in which normal hemoglobin A and
abnormal hemoglobin S are produced
Sickle Cell Trait – Stats
• More common in people
of African American and
Mediterranean descent
• Originally spontaneous
mutation
– Possible protective
benefit against malaria
• 5% to 8% African
American population
– About 1 in 12
– 2 million people in US
Sickle Cell Trait – Mechansim/
Pathophysiology
• No effect on exercise capacity
• Extreme exercise conditions can induce sickling,
increase deoxygenated hemoglobin levels, impair
RBC perfusion, lead to ischemia
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Acidosis
Hypoxia
Dehydration
Altitude
Asthma
Illness
Sickle Cell Trait
Sickle Cell Trait – Diagnosis
• NCAA mandated testing (2010)
– Hemoglobin electrophoresis
• Signs/Symptoms
– Muscle fatigue with +/- cramping
• Usually early in workout
• Characteristic slump to the ground – “sickling collapse”
– Abdominal pain
• Splenic infraction
– Hematuria
– Rhabdomyolysis
– ARF
– Metabolic abnormalities
Sickle Cell Trait – Management
• Prevention
– Acclimitization
– Gradual work-out progression
– Hydration
• Treatment
– ABCs
– High flow oxygen – 15L NRB
– Cool the athlete
– IVF
– Transport to ED
Sickle Cell Trait – Question
• Which of the following statements regarding
sickle cell trait athletes is true?
A. Sickle cell trait, in contrast to sickle cell disease, has
little to no mortality in athletes
B. Any cramping, struggling, or collapse in a sickle-trait
athlete must be considered sickling – a medical
emergency – until proven otherwise
C. The symptoms of exertional sickling and heat illness
are not distinguishable
D. Acclimation to intense training, increased hydration,
and increased rest afford no protection to sickling in
athletes
Sickle Cell Trait – Question
• Which of the following statements regarding
sickle cell trait athletes is true?
A. Sickle cell trait, in contrast to sickle cell disease, has
little to no mortality in athletes
B. Any cramping, struggling, or collapse in a sickle-trait
athlete must be considered sickling – a medical
emergency – until proven otherwise
C. The symptoms of exertional sickling and heat illness
are not distinguishable
D. Acclimation to intense training, increased hydration,
and increased rest afford no protection to sickling in
athletes
Sickle Cell Trait – Question
• A 20 year-old-male football player with known
sickle cell trait slumps to the ground
complaining of diffuse muscle fatigue. His
ABCs are intact and his core temperature is
101°F. What is the best initial form of
treatment?
A.
B.
C.
D.
Intravenous fluids
Stretching and massage of affected muscles
Cold/ice water immersion
Oxygen 15L via NRB
Sickle Cell Trait – Question
• A 20 year-old-male football player with known
sickle cell trait slumps to the ground
complaining of diffuse muscle fatigue. His
ABCs are intact and his core temperature is
101°F. What is the best initial form of
treatment?
A.
B.
C.
D.
Intravenous fluids
Stretching and massage of affected muscles
Cold/ice water immersion
Oxygen 15L via NRB
Algorithm for Collapsed Athlete
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Wen et al, 2014
Conclusion
• Cardiac
- Very sudden, no cramping, usually unresponsive, +/- Seizure
activity.
• Rhabdo
– Cramping, muscle aches, reddish urine, normal mental status
• Exercise-associated collapse
– Athlete collapses either immediately upon crossing the finish line or
within a few moments after finishing
• Heat Illness
– CNS changes (confusion, delerium, stupor, seizures or coma)
– Often with heat cramping- rock hard muscles, writhing and yelling in
pain
• Sickling
– Usually early in workout, increasing pain and weakness in working
muscles
References
References
References
Questions?