Spring Has Sprung!

Spring Injuries, Illnesses, and Preparing for Summer 1 st By Silver Cross EMS Staff 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

Heat Emergencies

• 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 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

 Gardening  Spring 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

Drowning

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

in the SA Node

(2 of 10)

Rules of Interpretation

Rate Sinus Bradycardia

Less than 60

Rhythm

Regular

Pacemaker Site P Waves PRI QRS

SA node Upright and normal Normal Normal

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……..

• Atropine!

Drug O’ the Month

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 [email protected]

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