Post on 11-Jan-2016
Spring Has Sprung!
Spring Injuries, Illnesses, and Preparing for Summer
By Silver Cross EMS Staff1st Trimester March 2012 CME
Our Agenda Today
• Review illnesses/injuries more common in the spring/early summer months.
• Review heart rhythm of the month – Bradycardia
• (ALS) Review drug of the month – Atropine
So What Does Spring Bring?
• Heat• Bugs/Allergies• Sports injuries• Gardening/landscaping chemicals• Spring cleaning chemicals• Drowning• Lightening
Heat
Heat
• Given our mild winter, it’s a strong possibility that this spring will be warmer as well.
• 2010 was Illinois’s warmest spring to date.– High temperature hit 83 in April 2010
• Measures to prevent heat injury• Avoid long periods of exposure• Drink plenty of clear fluids• Use shade to reduce heat• Avoid using diuretics• Avoid using amphetamines• Limit alcohol intake
Heat Emergencies
Heat Cramps
– Muscle spasms – Poor fluid level– Overexertion with fatigue– Sodium and electrolyte loss– Extended exertion in heat
Heat Cramps
– Physical findings• Cramps in fingers• Arms• Legs• Abdomen
Heat Cramps
– Differential diagnosis• Tetany – hypocalcemia-related muscle cramps• Other heat emergency• Simple muscle cramps
– Therapeutic interventions • Remove from heat• Oral hydration of electrolytes• IV bolus
Heat Emergencies
• Heat exhaustion– Dehydration & compensated hypovolemia – Sweating– Sodium & electrolyte loss– Vasodilation with venous pooling– Extended exertion in heat
Heat Exhaustion
– Physical findings• Rapid shallow breathing• Weak rapid pulse• Flushed or pale skin• Cool clammy skin• Heavily sweating• Normal core temp which can rise to 100-105° F• May present with dehydration
Heat Exhaustion
– Differential diagnosis• Uncomplicated dehydration• Hypoglycemia• Infection• Intoxication• Fatigue
Heat Exhaustion
– Therapeutic interventions• Similar to heat cramps• Remove from heat• Supine• Oral hydration of fluids/electrolytes• IV bolus• Manage core temp
Heat Emergencies
• Heat stroke– Increase in core temp over 105°F with decreased LOC– Hypothalamic temperature regulation lost– Chain reaction within tissue – Cellular death of brain, kidneys, liver– Hallmark is altered mental status– Metabolic acidosis– Hyperkalemia – Multiple Organ Dysfunction (MODS)
Heat Stroke
– Classic heat stroke• Long periods of heat and humidity exposure• Affects very young, very old, diabetics,
alcoholism and cardiac history• Risks from diuretics, psychotropics, anticholinergics• Late sign – hot red dry skin
Heat Stroke
– Exertional heat stroke• Sudden rise in core temp during exertion • All age groups susceptible• Patient not fluid deprived• Skin may be sweaty
Heat Stroke
– Physical findings• Altered LOC – disorientation, combative, unconscious• Lack of sweating• Hallucinations• Seizures• Core temp above 40.6°C or 105°F• Red, hot, wet or dry skin• Tachycardia that slows near death• Tachypnea progressing to bradypnea• Hypotension often lacking diastolic
Heat Stroke
– Differential diagnosis• CVA• Hypoglycemia• Infection• Uncomplicated dehydration• Intoxication• Neuroleptic malignant syndrome
Heat Stroke
– Therapeutic interventions• Goal -cooling core temperature• Goal –replenish fluid• Airway management• Cardiac monitoring
Insects/Allergies
Spring Critters
• Gardening, outdoor sports, spring picnics, all attract insects.
• While some are friendly, others can be life threatening.
Insects
– Honeybees signs/symptoms• Local pain, itching• Swelling, edema• Anaphylactic shock• Headache, weakness• Nausea, vomiting• Respiratory distress• Respiratory failure• Renal failure
Insects
– Honeybees treatment• ABCs• Rapid removal of stinger• Ice pack to bite site• Detailed patient history, including allergies• Analgesics• Anaphylactic shock, IV access• Epinephrine/Benadryl• Rapid transport
Insects
• Wasps, yellow jackets, fire ants– Signs/symptoms
• Local pain, itching• Swelling, edema• Anaphylactic shock• Headache, weakness• Nausea, vomiting• Respiratory distress• Respiratory failure• Renal failure
Insects
• Wasps, yellow jackets, fire ants– Treatment
• ABCs• Ice pack to bite site• Detailed patient history, including allergies• Analgesics
Spiders
• Black widow spider signs/symptoms– Severe pain at bite site– Swelling at bite site– Piloerection– Diaphoresis– Tachycardia
– Hypertension– Hypertension– Fever,
hyperthermia– Muscle spasms– Abdominal pain
Spiders
– Black widow spider treatment
• ABCs• Detailed patient history,
including ID• Ice back to bite site• Cardiac monitoring
Spiders
• Brown recluse spider signs/symptoms
– Local: itchiness at site bite– Erythema, edema– Papule formation– Necrotic lesion– Bull’s-eye rash– Systemic: fever, chills– Malaise, weakness
– Nausea, vomiting– Rash– Seizures– Hypotension– Disseminated
intravascular coagulation
Spiders
• Brown recluse spider treatment– ABCs– Detailed patient history, including ID– IV fluids
Spiders
• Brown recluse spider bite
• Top, bite of brown recluse spider after 6 hours
• Middle, 24 hours• Bottom, 48 hours
Ticks
• Tick diseases• Rocky Mountain spotted
fever• Fever, headache, abdominal pain,
vomiting, muscle pain, rash.
• Lyme disease• Fever, headache, fatigue,
characteristic skin rash.• Can spread to joints, heart,
nervous system.
– Tick paralysis
Ticks
• Treatment• Remove tick• Treat neurologic symptoms• Clean wound with soap & water, dress
Sports
In Spring, Sports are the Thing
• Weekend warriors• Kids and parents outside after long winter• Baseball, softball, soccer tryouts, etc
Common Sports Injuries
• Broken bones• Sprains• Strains• Cuts• Bruises• Back/spine injuries
• We handle most of these very, very well already.
Concussion in Sports
• New attention turning to concussion in sports• More than any other sports injury, can have
life-long consequences• EMS ability to recognize possible concussion
helps athletes heal under a doctor’s care
The American Academy of Neurology
Concussion is a trauma-induced alteration in mental status that may or may not be associated with loss of consciousness.
The Third International Conference on Concussion in Sport (2008)
Concussion is a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces.
How Common?
• 2-4 million concussions in all age groups yearly.
–300,000 head injuries yearly in high-school sports.
•30% of high-school and collegiate athletes return to play same day, 70% after 4 days.
•80 – 90% of concussions resolve within 7 to 10 days.
Males account for 70%.
Problem is…..
In study of high-school football players with concussion, 53% did not report injury because:
-They did think their injuries were serious enough to report.-They did not realize symptoms consistent with concussion.-They did not want to be held out of play.-Their parents didn’t want them held out of play (!)
Why Did it Happen?
Concussion: a result of sudden acceleration, deceleration, or rotational forces imparted to brain.
With or without direct impact.
Mechanism of injury may be subtle and not obvious. Magnitude of impact doesn’t correlate with injury.
Concussion can also occur in noncontact sports.
What Happened?
Concussion: dysfunction of brain metabolism rather than structural injury or damage. On cellular level: disruption, increased permeability, and depolarization of neuronal cell membranes. Decreased blood flow to brain creating mismatch between metabolic demands and supply.
Neuronal dysfunction can last from 1 to 10 days or more following the concussion.
Brain more vulnerable to further injury during this time.
Second Impact Syndrome
Second concussion in athlete who has not fully recovered from first concussion. Unclear whether Second Impact Syndrome is a new brain injury or a complication of initial injury. Characterized by:
Rapidly progressive brain edema.Brain stem herniation.High mortality, often within minutes.
Signs and Symptoms
–Amnesia– Retrograde / Anterograde–Confusion or disorientation–Feeing Drowsy, Stunned or Foggy–Impaired Level of Consciousness/LOC–Inappropriate Play Behaviors–Poor Concentration and Attention–Seeing Stars or Flashing Lights–Slow to Answer Questions or Follow Directions
Loss of consciousness only occurs in 10% of concussions.
More Signs and Symptoms
•Ataxia or Loss of Balance•Vision changes•Dizzy/ Lightheaded/Syncope•Fatigue Weakness•Headache•Nausea/Vomiting•Ringing in the Ears•Seizures•Slurred or Incoherent Speech•Vacant stare/Glassy Eyed/Unequal pupils
Behavioral Signs and Symptoms
• Anxiety / Nervousness • Depression (May be Long Term)• Emotional Lability• Irritability• Low Frustration Tolerance• Personality Changes
On-Field Evaluation – Differential Diagnosis
Many symptoms of concussion not specific to concussion. Differential Diagnosis in athletes include:
Heat-related Illness
Dehydration
Hypoglycemia
Acute Exertional Migraine
Multiple Concussions
•Adverse effects of repeated concussions cumulative–Greater as interval between concussions is shorter.
•Cumulative effects on cerebral function, cognition.–Including early onset memory disturbances and dementia.
•How many concussions should disqualify athlete? –Some experts have suggested as few as three.
Spring Poisoning Risks
GardeningGardening Spring CleaningSpring Cleaning
Poisonings
• Household products & industrial chemicals– Corrode metal, destroy tissue on contact– Corrositivity measured by pH, 0-14 scale
• Acid low <2• Base high >12.5
– When acids & bases mix, toxicity
Household products & industrial chemicals
– Acids• Cleaning solutions, toilet bowl cleaners, drain openers,
metal polishers• Foods• Soap & water most effective decontaminate• Internal decontamination – emetics never used.
Household products & industrial chemicals
– Acids• Eye decontamination immediate
– Becomes necrotic sore, eschar forms– Thin layer of cells on cornea destroyed– Denatures proteins in cornea– Visual impairment
Poisonings
– Acids• GI damage
– Mouth, esophagus & stomach burns• Ulceration• Perforation• Vasculature absorption• Acidosis
Household products & industrial chemicals
• Acids– Hydrofluoric acid
• Acute & systemic toxicity• Penetrates deeper than most acids• Dermal burns show white/yellow-white underneath skin• Systemic hypocalcemia – pulls calcium from bones• Cardiac dysrhythmias • Antidote: Topical calcium gluconate for skin burns
• IV calcium gluconate for systemic burns• Eye irrigation with normal saline for eye exposure
Household products & industrial chemicals
– Bases• Alkaline materials• Caustics• Toilet bowl cleaners, drain openers, household bleach• Burns produce tissue liquification necrosis
• Breakdown, dissolution of cell membrane, form soap• Slick, slimy skin• Pain delayed
• Burns penetrate deeper
Household products & industrial chemicals
– Bases• Rapid external decontamination • Burns to stomach more severe, dissolves protective
mucous layer that lines stomach• Ulceration• Perforation• Ammonia
• Fertilization on farms• Refrigerants in industrial setting• Chief ingredient in methamphetamine production
Poisonings
• Household products & industrial chemicals– Pesticides & nerve agents
• Organophosphates• Carbamates• Insect sprays• Ingestion, absorption, inhalation• More toxic by ingestion/contact
Poisonings
• Household products & industrial chemicals– Pesticides & nerve agents
• Nerve signal travels alon neiron through electrochemical mechanism
• Stops at synapses• At synapse, chemical neurotransmitter released from
neuron, travel across junction
Poisonings
• Household products & industrial chemicals– Pesticides & nerve agents
• Acetylcholine normally binds to cholinergic receptor.• Electrochemical pulse continues in next neuron or
contraction starts in muscle• Nerve agents inhibit enzyme acetylcholinesterase
– Suppose to help releases acetylcholine from its receptors– If it doesn’t, you end up with muscular paralysis
Poisonings
– Organophosphates commonly found in the home/at work – fertilizer, malathion, parathion
• Signs/symptoms of organophosphate poisoning– “Wet” patient presenting with SLUDGEM symptoms– Sweating & muscle fasciculations– Respiratory arrest– Airway management is priority
A Spring Swim
• Water is colder in the spring than many people realize – hypothermia a risk.
• Or they may feel that remaining ice on some bodies of water is thick enough to hold them.
• Also children eager to swim after a long winter may not abide by safety rules.
Submersion Injuries: Drowning & Associated Cautions
• Immersion syndrome• Sudden cardiac arrest caused by massive vagal
stimulation after sudden exposure to cold water• Stimulates parasympathetic nervous system, decreases
heart rate
• Post-immersion syndrome• Delayed deterioration of a previous asymptomatic or
minimally symptomatic patient
Submersion Injuries: Drowning & Associated Cautions
• Shallow water blackout– Unconsciousness after submersion– Common with adolescent boys “goofing off”
Submersion Injuries: Drowning & Associated Cautions
• Epidemiology & demographics– Second leading cause of accidental death in US– Leading cause of accidental pediatric death – Teenagers second major group– Elderly third highest group
Risk factors
• Black children 3 fold higher risk than white children• Male/female ration of 5:1• Male/female boating related drowning ratio 12:1• Fresh water drowning in majority• Alcohol use a common denominator• 67% of pediatric bathtub drowning attributed to
abuse/neglect
Submersion Injuries: Drowning & Associated Cautions
• Etiology – Classic sequence starts with panic
• Victim can no longer hold breath, reflexively takes a breath, and water enters mouth
• Victim takes several violent intakes of air and water while flailing
Submersion Injuries: Drowning & Associated Cautions
• Etiology– Water intake hits posterior oropharynx
• Laryngospasm• Bronchospasm• Severe hypoxia• Acidosis• Cardiac disturbances• CNS anoxia• Coma
Submersion Injuries: Drowning & Associated Cautions
• Physical findings– Often accompanied by trauma
• Assess for spinal trauma• When in doubt, treat for c-spine injury
– Cardiac disturbances common– Hypothermia common
Submersion Injuries: Drowning & Associated Cautions
• Differential diagnosis– Trauma– Spinal injury– Cardiac disturbances– Hypothermia– Hypoglycemia– CNS disturbances– Metabolic abnormalities
Submersion Injuries: Drowning & Associated Cautions
• Therapeutic interventions– Priority is reversing hypoxia– If any resuscitation is required, patient must be
transported
Submersion Injuries: Drowning & Associated Cautions
• Complications– Sudden respiratory arrest– ARDS/MODS– Release of fluid into alveoli– Inflammation of alveoli and lung tissue– Loss of surfactant– Atelectasis– Aspiration pneumonia– Pneumothorax
Lightning
Lightning Injury
• Definition: Injuries from transmission of electricity between sky & ground
• Strikes injure 500-1000 per year and kill 100• Most common in spring and early summer,
between 3:00PM and 6:00PM
Lightning Injury
• Physical findings– Minor injury
• Tympanic membrane rupture• Confusion• Amnesia – may deny event occured• Brief loss of consciousness• Temporary deafness• Blindness• Paresthesia or dysesthesias in extremities
Lightning Injury
• Physical findings– Moderate injury
• Disorientation• Combativeness (hypoxia)• Coma• Motor paralysis• Absent pulses due to
arterial spasm• Sympathetic instability
(cardiac irritability)• Hypotension• Vascular trauma• Spinal shock• Seizures• Burns
Lightning Injury
• Physical findings– Severe injury
• Cardiac arrhythmia• Cardiac arrest• Pulmonary edema• Pulmonary contusion• Ortho injuries
Lightning Injury
• Differential diagnosis– High voltage injury
• Therapeutic interventions– Pulseless victims are treated first– Symptomatic interventions– Prevention
Break
• Let’s take five.• Then we will resume with the rhythm and
drug o’ the month.
Rhythm O’ the Month
• Bradycardia
Dysrhythmias Originating Dysrhythmias Originating in the SA Node in the SA Node (2 of 10)(2 of 10)
NormalQRS
NormalPRI
Upright and normalP Waves
SA nodePacemaker Site
RegularRhythm
Less than 60Rate
Sinus Bradycardia
Rules of Interpretation
Sinus Bradycardia
• Clinical Significance– May be caused by
• Excessive inhibitory vagal tone
WHAT PART OF THE AUTONOMIC NERVOUS SYSTEM IS INERVATED?
Sinus Bradycardia - Causes
• Decrease in sympathetic tone on the AV node (increase in parasympathetic tone)
• Pressure on fontanels in infants• Intracranial swelling• Glottic irritation from ET tubs, gagging, emesis• Disease of the SA node• Hypothermia, Hypoxia
Sinus Bradycardia
• Administration of digitalis, propranolol (Inderal), verapamil, and quinidine
• Common in acute inferior AMI - Involves the right coronary artery which supplies the SA node with blood
Sinus Bradycardia
Treat the patient, not the monitor!
Bradycardia is also common during sleep, rest and in trained athletes!
Sinus Bradycardia
• Ultimate clinical significance…..– Decreased heart rate/BP which leads to decreased
CARDIAC OUTPUT
Sinus Bradycardia
• Treatment Modalities– Asymptomatic – pulse and adequate BP (>100
systolic)Routine Medical Care IV, O2, monitor Position of Comfort
Sinus Bradycardia
• Symptomatic– Hemodynamic Instablity (BP <100 systolic)
• Syncope, hypotension, altered mentation• Chest pain, palpitations, diaphoresis• Difficulty in breathing• Poor skin vitals and perfusion
Sinus Bradycardia
• Hypotension– Leads to decreased cardiac output
– Palpitations• Because of SA node’s increased relative refractory
period permits refractory firing
Sinus Bradycardia
– Chest Pain• Heart disease already exists• Coronary blood flow is decreased
Sinus Bradycardia
• Bottom Line: TREAT THE UNDERLYING CAUSE TO ABOLISH THE DYSRHYTHMIA AND INCREASE THE RATE
Sinus Bradycardia
• After treating an identified underlying cause and rate remains BELOW 60 bpm………..
It’s time for drugs……..
Drug O’ the Month
• Atropine!
Atropine Indications
• Symptomatic bradycardia. • NO LONGER USED: asytole or PEA• Nerve agent exposure• Organophosphate poisoning
Adverse Reactions
• Dry mouth, hot skin, intense facial flushing• Blurred vision or dilation of the pupils with
subsequent photophobia• Tachycardia• Restlessness• May cause paradoxical bradycardia if the dose
administered is to low or pushed to slowly
Contraindications
• Acute MI• Myasthenia Gravis• GI Obstruction• Closed angle glaucoma • Known sensitivity to atropine, belladonna
alkaloids or sulfates (NOT sulfa)
How Atropine Works
• Increases firing of the SA node.• Increases conduction through the AV node.• Opposes the action of the vagus nerve.• Blocks acetylcholine receptor sites• Decreases bronchial secretions.
Atropine Dosage
Symptomatic Bradycardia• Adult: 0.5 mg IV/IO every 3 to 5 minutes to a
max dose of 0.04 mg/kg. Don’t delay pacing for Atropine.
• Peds: Epi First! Then 0.02 mg/kg (min of 0.1 mg/dose; max of 0.5 mg/dose). Repeat once in 5 minutes
Dosage
Nerve Agent or Organophosphate Poisoning• Adult: 2 mg IVP repeated if needed every 5
minutes until symptoms dissipate• Peds: 0.02 mg/kg IV/IM every 5 minutes as
needed until symptoms dissipate
Questions?
• If you are watching live, just type in the text box!
• If you are watching the pre-recorded version or the Power Point, address questions to afinkel@silvercross.org
• Stay safe out there!
References
• Aehlert, Barbara, “Paramedic Practice Today,” Volume 1, 2010
• The 3rd International Conference on Concussion in Sport, held in Zurich, November 2008