Download Leiszler General Medical Emergencies 2014

GENERAL MEDICAL
EMERGENCIES
Matt Leiszler, MD
Primary Care Sports Medicine
University of Colorado Hospital
August 8, 2014
OBJECTIVES
• Review case-based examples of
some serious medical
emergencies
• Understand the signs/symptoms,
diagnosis of these emergencies
• Discuss on field management of
life threatening emergencies
• Evaluate your own preparation
for such emergencies
CASE 1, FOOTBALL
• 19 year old male football player
• Known sickle cell trait
• Running 300 m interval conditioning
test
• Hot weather
• After finishing  collapsed, unable to
stand under own power  cramps and
profuse sweating
CASE 1, FOOTBALL
• Cooled with cool towels
• Oral hydration initiated
• Assisted to the training room
via stretcher
• Paraparesis in upper and
lower extremities
• Symptoms persist  Started
IVF  called paramedics
CASE 1, FOOTBALL
• Cooled with cool towels
• Transferred to ED
• Oral hydration initiated
• Pulse 110
• Assisted to the training room
via stretcher
• Oral Temp 99 F
• Paraparesis in upper and
lower extremities
• Symptoms persist  Started
IVF  called paramedics
• Rectal temp 101.5 F
• BP 147/80
• Unable to void
CASE 1, FOOTBALL
• Admitted with severe myalgias,
unable to raise foot/leg, abdominal
tenderness.
• CK 200,000 initially
• MRI Spine normal
• Weakness felt to be related to
rhabdo, not spinal cord injury
• Required hemodialysis
• Finally d/c’d after 17 days with
improving acute rhabdo
CASE 1, FOOTBALL
• Diagnosis:
• Heat exhaustion with heat cramps
and acute rhabdomyolysis
HEAT ILLNESS
• High school sports: approximately 9,237 time-loss heat
illnesses nationally per year
• Probably underestimation (results based on missing
at least one day of practice)
• 70.7% in football players
• 66.3% in August
• 1995-2011: 31 high school football players died from
heat stroke
STAGES OF HEAT ILLNESS
Increasing Severity
Heat Stress
Heat Exhaustion
Heat Stroke
Heat cramps can occur anywhere along the spectrum
STAGES OF HEAT ILLNESS
HEAT CRAMPS
• Painful muscle spasms associated with
weakness, fatigue, nausea/vomiting,
tachycardia
• Can occur during or hours after exercise
• Etiology:
• Unopposed Ca in presence of salt
depletion?
• Changes in motor neuron excitability?
• Accumulation of nitrous oxide in muscle?
STAGES OF HEAT ILLNESS
HEAT STRESS
• Increased HR and BP
• Dizziness
• Restlessness
• Fatigue
• Emotional lability
STAGES OF HEAT ILLNESS
Increasing Severity
Heat Stress
Heat Exhaustion
Heat Stroke
Heat cramps can occur anywhere along the spectrum
STAGES OF HEAT ILLNESS
HEAT EXHAUSTION
•
•
•
•
•
•
•
Weakness and exhaustion
Dizziness or syncope
Muscle cramps
Nausea/Vomiting
Excessive sweating
Flushed appearance
Dilated pupils
STAGES OF HEAT ILLNESS
HEAT STROKE
• Sweat-soaked and pale skin
in exertional heat stroke
• Usually do NOT see dry,
hot, flushed skin as in
classic non-exertional heat
stroke in elderly
STAGES OF HEAT ILLNESS
HEAT STROKE
• Medical emergency
• Potential for mortality
• Clumsiness
• Stumbling
• Headache
• Nausea
• Dizziness
• Apathy
• Confusion
• Impairment of consciousness
• Core temp >40° C
• Central nervous system changes
STAGES OF HEAT ILLNESS
HEAT STROKE
• May also see changes in personality or performance
• Easy to confuse with concussion in contact sports
STAGES OF HEAT ILLNESS
HEAT STROKE
• May rapidly progress to hypotension, seizures, coma, death
• Complications
• Rhabdomyolysis
• Myonecrosis
• Acute renal failure
• DIC
• ARDS
CORE BODY TEMPERATURE
• Measurement:
• MUST be done by rectal thermometer (other locations can be
spuriously lowered by temp of air, skin, liquids)
• Heat Exhaustion:
• Usually Temp <40° C (104° F)
• Heat Stroke
• Usually Temp >40° C (104° F)
PATHOPHYSIOLOGY
• Core temp increases 0.15-0.20o C for every 1% body
weight loss during sweating
• Rise in core temp. stimulates sweating
• More difficult to “keep up”
PREVENTING HEAT ILLNESS
• Education
• Acclimatization
• Diet: no restriction of sodium
• Hydration
• Prehydration
• 7-10 oz fluid every 10-20 mins
• Weight measurements
• Practice schedules
RISK FOR DEHYDRATION
Watts, AJMS, 2001.
TREATMENT OF HEAT CRAMPS
• If in single extremity:
• If in multiple sites:
• Evaluate on sideline
• Move to cool, shaded area
• Institute stretching
• Remove uniform
• Massage with ice
• Institute stretching
• Give copious fluids
• Massage
• Oral NaCl ingestion in fluids
or foods
• Give copious fluids
• Consider IV
TREATMENT OF HEAT EXHAUSTION
• Remove from practice/game
• Remove uniform/equipment
• Move to cool, shaded area
• Elevate legs
• Monitor core temperature
• Give copious fluids (PO if able)
• Aggressive cooling—Use cool, wet towels and fans vs ice bath
• Monitor closely
TREATMENT OF HEAT STROKE
• Activate EMS immediately
• Remove from play
• Remove uniform
• Cold water or ice bath
immersion immediately
TREATMENT OF HEAT STROKE
• IMMEDIATE aggressive cooling to 39oC
• High flow O2, pulse ox, intubate prn
• IV NS 250-300cc/hr
• Cardiac monitor
• Continuous core temperature monitoring
• Foley
• ABG, CBC, SMA 18, PT/PTT, UA, urine myoglobin, UDS
• EKG, CXR
• Benzodiazepines or chlorpromazine for shivering
TEMPERATURE-DURATION AREA
• Severity of illness related to duration of temperature
above a critical level—main determinant of survival
• Not necessarily the absolute temperature
• Therefore rapid cooling is paramount
COOLING MEASURES
• Mist spray with fan
COOLING MEASURES
• Ice water towels/sheets and ice packs in groin, axillae, neck
COOLING MEASURES
• Ice water bath immersion (preferred)
MONITORING COOLING
• Cold-water or ice immersion provides greatest cooling rate—
should start as quickly as possible
• Monitor heart rate, blood pressure, respiratory rate, mental
status, and especially core temperature
• Important not to overcool past 38.6° C
• Should not usually exceed 15-20 minutes
PROGNOSIS OF HEAT STROKE
• 90% survival with proper treatment
• Morbidity directly related to duration of hyperthermia
• Poor prognosis
• Prolonged hyperthermia
• Hyperkalemia, ARF, elevated LFTs
• Persistence of coma with normal temperature
RETURN TO PLAY
• Same-day RTP not advised
• Recovery may take 1-3 days for heat exhaustion; longer for
heat stroke
• Do not allow return if still symptomatic
• Increased risk of recurrence if symptoms still present
• Correct underlying cause:
• Lack of acclimatization vs poor fitness level
EXERTIONAL RHABDOMYOLYSIS
• Relatively rare, but high morbidity and mortality
• Breakdown and necrosis of striated skeletal muscle after
physical activity
• Overproduction of heat 
• Depletion of ATP 
• Increase in intracellular calcium from direct injury and
rupture of the cellular membrane 
• Death of skeletal muscle cells 
• Necrosis causing pain, swelling, potential end organ damage
EXERTIONAL RHABDOMYOLYSIS
• Risk factors:
• Sickle cell trait
• Infection
• Autoimmune disorders
• Drug/toxin exposure
• Metabolic disease
• Low fitness levels
• Contact sports
• Dehydration
• Heat/Cold illness
• Crush syndromes
Black football players with SCT: 37x higher risk of
exertional-related death vs non-SCT counterparts
EXERTIONAL RHABDOMYOLYSIS
• Diagnosis
• Pain, tenderness,
weakness, and swelling in
muscles
• Elevated CK
• 5x upper limit of
normal
EXERTIONAL RHABDOMYOLYSIS
• May see elevated creatine kinase in asymptomatic athletes
• Ultramarathon (161 km) finishers:
• Median CK: 20,850 IU/L
• Mean CK: 32,956 IU/L
• Range: 1,500 to 264,300 IU/L
Hoffman, Wilderness
Environ Med, 2012
EXERTIONAL RHABDOMYOLYSIS
• Treatment:
• Mild cases  may go undiagnosed
• Oral hydration, rest
• Severe symptoms and CK > 5x upper limit normal
• Hospital admission
• IVF: NS to maintain urine output of 200 mL/hr
• Track CK, Renal Function, Electrolytes
• May need hemodialysis
• Avoid diuretics
EXERTIONAL RHABDOMYOLYSIS
• Return to sport
• No evidence-based
guidelines
• Consider testing in
high-risk athletes:
• Low-risk athletes—return
depends on:
• Afebrile
• Symptom-free; no
muscle pain
• EMG
• Well-hydrated
• Genetic testing
• Normal CK levels
• Muscle biopsy
• Myoglobin negative
• Exercise challenge
CASE 2, SOCCER
• 25 y/o male Hungarian soccer player, Miklos Feher
• Professional game in Portugal
CASE 2, SOCCER
• Soon they determine the player is pulseless and CPR is
begun
• No AED is available
• Ambulance arrives on the field, rushed to the hospital
• CPR for over an hour, then pronounced dead
• Cause of death: cardiac arrhythmia
• Hypertrophic cardiomyopathy (HCM)
THE DOWNED ATHLETE
• Sudden cardiac death
• A leading cause of death in
the US
• 350,000 cardiac arrests in
the US OUT of the
hospital
• Over half of these < 65
y.o.
• Survival rate: 3-5%
• About 10K-15K “saves”
SUDDEN CARDIAC DEATH
• Athletes—INCIDENCE??
• Prior U.S. estimates (Maron): 1/164,000
• Italy: 1/28,000
SUDDEN CARDIAC DEATH
INCIDENCE OF
SUDDEN CARDIAC DEATH
 Harmon, et al, 2011
 SCD 2004-2008 in National Collegiate Athletic Association
Athletes (NCAA)
 400,000 athletes per year, age 17-23, 40 sports, 3 divisions
 NCAA SCD database/memorials, insurance claims, Parent
Heart Watch, media reports
 Incidence SCD 1/44,000 per year in NCAA athletes.
INCIDENCE OF
SUDDEN CARDIAC DEATH
INCIDENCE OF SCD BY SPORT
HIGH RISK GROUPS
 Athletes (3x risk vs non athletes)
 Sex: Males (2.5 x risk)
 Race: African Americans (3x risk)
 Sport: BB, FB, Swimming, Track, Soccer
SUDDEN CARDIAC DEATH
• Risk factors:
• Less than 30 years old: Structural heart disease
• Hypertrophic Cardiomyopathy
• Anomalous coronary artery
• Marfan’s syndrome
• Aortic Stenosis
• Myocarditis/Pericarditis
• Over 30 years old: Atherosclerotic coronary artery disease
• This should always be a consideration
SUDDEN CARDIAC ARREST
• If you watch an athlete drop to the ground while
exercising, suspect the worst and react quickly
• Agonal breathing and gasping  occurs in more than
50% of patients with primary cardiac arrest
• May be mistaken for breathing, CPR/defibrillation
delayed
SUDDEN CARDIAC ARREST
• Acute Treatment:
• Suspected SVT may respond to valsalva and other vagal
maneuvers, these athletes are awake and anxious…but
alive
• If unresponsive, begin CPR and use the AED as soon as
possible  there is life in electricity
• Know where the AED is, better yet, have it available
• Long-Term Management:
• Will require thorough evaluation including: Echo, EP studies,
heart cath and possible ablation
CARDIAC ARREST
HIGHLIGHTS OF THE AHA 2010
GUIDELINES
• “Push hard, push fast”
• Continuous chest compressions
• Minimize interruptions
• Health care professional rescuers
• No more than 10 seconds for
pulse check
• Single untrained rescuers
• Chest compression-only CPR
• Excellent CPR and early defibrillation
DEFIBRILLATION SUCCESS:
DEPENDENT ON SPEED OF
APPLICATION
AUTOMATIC EXTERNAL DEFIBRILLATOR
• Public access defibrillator programs
• Casino study
• Outcomes of rapid defibrillation
by security officers after cardiac
arrest in casinos
• Survival rate 74% in those who
received first shock within 3
minutes
• Survival rate 49% in patients who
received first shock after 3 minutes
Valenzuela, N Engl J Med 2000: 343:1206
AUTOMATIC EXTERNAL DEFIBRILLATOR
• Public access defibrillator programs
• Airport study
• Airport personnel and non-trained
members of the public at Chicago
O’Hare airport
• 21 cardiac arrests
• 18/21 were in ventricular fibrillation
• 10/18 survived neurologically intact
to hospital discharge
Caffrey, N Engl J Med 2002: 347:1242
Survival to hospital discharge in students and adults with sudden
cardiac arrest on a high school campus.
Drezner J A et al. Br J Sports Med 2013;47:1179.
Survival to hospital discharge in students and adults with sudden
cardiac arrest on a high school campus.
• The survival rate
was 79% in schools
with an established
emergency action
plan for SCA versus
44% in those
without
HEMODYNAMIC PHASE
• 2010 AHA Guidelines
• At least 100 compressions per minute
• 1 compression per 0.6 seconds
• Allow the chest to recoil completely after each
down-stroke
• Minimize the frequency and duration of any
interruptions
HEMODYNAMIC PHASE
• Compression takes priority over defibrillation initially during
this phase (4-10 minutes)
• Defibrillation of the globally ischemic heart beyond about 4
minutes may be detrimental
• Outcomes improved when defibrillation is briefly delayed
• May be related to partial restoration of oxygen, or
washing out deleterious metabolic factors accumulated
during ischemia
VENTILATIONS IN CPR
• Animal studies:
• Excess ventilations  increased intrathoracic pressure and
decreased perfusion pressures
• Human studies:
• Patients receive more ventilations than recommended
• Single rescuer CPR—Ventilation—Time for 2 breaths:
• Lay public: 16 seconds (Assar, Resus, 2000)
• Medical Students: 14 seconds (Heidenreich,
• EMS: 10 seconds (Higdone,
Resus, 2006)
Resus, 2004)
• Can we eliminate mouth-to-mouth rescue
breathing and still get the same survival?
CARDIOCEREBRAL RESUSCITATION
• Delays endotracheal intubation
• Emphasizes minimal interruptions of
chest compressions
• Deemphasizes positive-pressure
ventilations
• Prioritizes defibrillation according to
the 3-phase time-sensitive model of
ventricular fibrillation
• Encourages early administration of
epinephrine
CARDIOCEREBRAL RESUSCITATION
• NOT for:
• Respiratory arrest (ie, drowning)
• Children and infants
• Drug overdose (alcohol)
CARDIOCEREBRAL RESUSCITATION
Bobrow, JAMA, 2008
Figure 2. Survival to hospital discharge of patients out-of-hospital cardiac arrest (OHCA) in
Arizona from January 1, 2005, to December 31, 2009, a time when chest compression-only
CPR was advocated and taught to the public.
Ew y G A , and Bobrow B J J Intensive Care Med
2014;0885066614544450
METABOLIC PHASE
• Therapeutic hypothermia
• When should this begin? EMS?
• How long?
• Best method?
• Non-VF arrest?
• Cardiac catheterization
CARDIOCEREBRAL RESUSCITATION
ON THE SIDELINES
• Minimize interruptions
• Chest compression rate: 100 compressions/minute
• Chest compression depth:
• 2 inches in adults
• 1/3 AP diameter in children
• Full chest recoil—No residual leaning
• Eliminate excessive ventilations
• Goal: Provide adequate oxygen to blood without impeding
function
CASE 3, SOCCER
• 19 y/o male starting forward
• Has allergic rhinitis and known allergy to bee
stings
• During a game, late in the first half while
sitting on the bench he is stung by a bee on
the neck
• He jumps and attempts to swat the bee, who
stings him again
• Witnessed by teammates and ATC
CASE 3, SOCCER
• He has a frightened look of impending doom on his
face and reminds the trainer he is allergic to bee stings
• The trainer starts digging though her bag looking for
the epinephrine syringe – which is not there
• The patient is now audibly wheezing and straining to
breath
• Signs of urticaria and angioedema are becoming
noticeable
CASE 3, SOCCER
• Assistant trainer has run to training room where she
thinks the bee sting kit is located
• Player is now on his knees and begins to vomit
• Physician is looking for laryngoscope and endotrachial
tube to intubate the patient
• In less than 5 minutes from the first bee sting, the
player’s breathing has become labored and he is now
laying on the ground near the bench and appears dusky
blue
ANAPHYLAXIS
• Signs and symptoms
• Begins within seconds to
minutes after contact with
offending antigen
• Respiratory:
Bronchospasm and
laryngeal edema
• CV: Hypotension,
dysrhythmia
• GI: Nausea, vomiting and
diarrhea
• Cutaneous: Urticaria,
angioedema
• Neurological: Seizures
• Hematological:
Activation of intrinsic
coagulation pathway
leading to DIC
• Death
ANAPHYLAXIS
• Mechanism/Description
• Acute widely distributed form of shock occurs within
minutes after exposure to antigen
• Rapid release of bioactive molecules such as histamine,
leukotrienes and prostaglandins from inflammatory cells
producing:
• Increased vascular permeability, vasodilatation,
smooth muscle contractions
• Manifested in a decrease of total vascular resistance
and reduced cardiac output
ANAPHYLAXIS
• Acute Treatment
• Remove stinger (credit card, straight edge)
• ABC’s
• Assure adequate ventilation
• Endotrachial intubation is paramount, but is difficult due to
laryngeal edemaon if done quickly
• King Airway
• LMA
• Transtrachial jet insufflation and cricothyrotomy may be
necessary
ANAPHYLAXIS
•
Key Medications
•
Epinephrine: 0.3-0.5 mg (1:1,000 dilution) SQ, administered immediately (Epipen
0.3mg 1:1000)
• Peds dosing
• <30 kg, 0.15mg 1:1000 (Epipen Jr)
• >30 kg, 0.3 mg 1:1000 (Epipen)
• Repeat after 15 minutes
ANAPHYLAXIS
•
Key Medications
• Epinephrine: 0.3-0.5 mg (1:1,000 dilution) SQ, administered
immediately (Epipen 0.3mg 1:1000)
• Peds dosing
• <30 kg, 0.15mg 1:1000 (Epipen Jr)
• >30 kg, 0.3 mg 1:1000 (Epipen)
• Repeat after 15 minutes
• Direct injection into the venous plexus at the base of the tongue may
be necessary
• Diphenhydramine (Benadryl): 50 mg IV in adults, 1-2 mg/kg in Peds
• Methylprednisolone (Solumedrol): 125mg IV in adults, 1-2 mg/kg in Peds
ANAPHYLAXIS
• Transport
• Airway compromise  CALL 911
• Significant generalized reaction  Hospital admission ,
observe for 24 hours
• Follow-up
• Follow-up appointment with allergist
• Patients MUST carry Epipen in the future
• Avoid known triggers
SUMMARY
• Medical Emergencies will happen, so expect them and
be prepared
• Know your athletes; who has Sickle Cell Trait, a history
of Asthma, Anaphylaxis, etc…
• ABC’s are the first step in emergency management
• If an athlete collapses during exercise, suspect the
worst and carry your AED to the field
• Good chest compressions vital
REFERENCES
•
Tietze, David C (07/2014). "Exertional rhabdomyolysis in the athlete: a clinical review". Sports health (19417381), 6 (4), p. 336.
•
Harmon KG, Drezner JA, Klossner D, Asif M. Sickle cell trait associated with a RR of death of 37 times in
National Collegiate Athletic Association football athletes: a database with 2 million athlete-years as the
denominator. Br J Sport Med. 2012;46:325-330.
•
O’Connor FG, Campbell WW, Heled Y, et al. Clinical practice guideline for the management of exertional
rhabdomyolysis in warfighters. CHAMP USU Consortium for Health and Military Performance.
http://www.usuhs.mil/mem/pdf/ExertionalRhabdomyolysis.pdf.
•
Armstrong L, Casa D, Millar-Stafford M, et al. Exertional Heat Illness during Training and CompetitionMedicine &
Science in Sports & Exercise. 3/2007; 39(3):556-572
•
Center for Disease Control and Prevention—Morbidity and Mortality Weekly Report. Heat Illness Among High
School Athletes --- United States, 2005—2009. 8/2010; 59(32);1009-1013
•
Gagnon D, Lemire B, Casa D, et al. Cold-Water Immersion and the Treatment of Hyperthermia: Using 38.6 oC as a
Safe Rectal Temperature Cooling Limit. Journal of Athletic Training 2010; 45(5):439-444.
•
Hoffman MD, Ingwerson JL, Rogers IR, et al. Increase creatine kinase concentrations at the 161-km Western States
Endurance Run.
Wilderness Environ Med. 2012 Mar;23(1):56-60.
•
Ewy, Gordon A (07/30/2014). "Cardiocerebral Resuscitation: An Approach to Improving Survival of Patients With Primary Cardiac Arrest". Journal of
intensive care medicine (0885-0666)
THANK YOU