0027 1.3.7.1 Clinical management of toxins version 2015 ... CRC Handouts-Dallas/0027 1.… ·...

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EMS Subspecialty Certification Review Course

Clinical management of toxins

Version Date: 2/6/2013Rev 6/5/2015

Learning Objectives

Upon the completion of this program participants will be able to:

1. Understand the common approach to prehospital evaluation of possible poisonings/toxic exposures

2. Describe the signs and symptoms associated with common toxidromes

3. List antidotes to common or emerging poisonings

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Basic Approach to Poisonings

• Unlike ED setting, more chances of exposure to rescuers• Gather history as to toxin(s) involved, route of exposure, time and mechanism(s) of exposure/ingestion

• Do not rush to assist; Avoid adding a victim to rescue• Don proper level of PPE as indicated and within training

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• Type • Time• Taken (amt)

• Route (Resp, GI, Skin, Blood)• Reason (OD, Accident, Suicide)• Routine meds /co-ingest

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General Treatment Approach• First Priority: scene safety

• Unknown potential toxicologic emergency: important to initially have broad differential dx

• History: EMS should gather as much information as possible on type of toxin(s). Pt/victim potentially unreliable

• Gather all pill bottles/prescription list/Material Safety Data Sheet (MSDS) if industrial exposure etc

• Include any medications of visitors in the home

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Treatment Considerations

• How quickly to treat versus evacuate

• Time dependent natural history versus not

– May be dangerous, slowly progressive (Fe, APAP) versus rapidly lethal, and may be dose dependent

• Rapidly reversible condition and effective antidote

– May be reasonable to give antidote before evacuation

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Common Clinical Toxidromes

• Opioids– Seda on, miosis, ↓ resp drive, ↓ bowel sounds

• Sedative‐hypnotic– Seda on, ↓respira on, NORMAL pupils and v/s

• Sympathomimetic– Agitation, mydriasis, tachycardia, hypertension, hyperthermia, diaphoresis

• Serotonin Syndrome– ALOC, tachycardia, hypertension, hyperreflexia, clonus, hyperthermia

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Cholinergic confusion

Cholinergic

• Defecation/diphoresis

• Urination

• Miosis

• Bradycardia

• Emesis

• Lacrimation

• Lethargy

• Salivation

• Bronchorrhea and spasm

Anticholinergic (anti=can’t)

• Can’t see (mydriasis)

• Can’t pee (retention)

• Can’t spit (dry mm)

• Cant’ shit (constipation)

• Can’t walk (seizures)

• Can’t talk (confusion/ams)

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Odors Associated with Toxin

ODOR

• Bitter almonds

• Fruity

• Garlic

• Gasoline

• Mothballs

• Pears

• Rotten eggs

• Freshly mowed hay

• Geraniums

What you are dying from

• Cyanide

• Isopropanol, acetone

• Organophosphates

• Petroleum distillates

• Napthalene, camphor

• Methylsalicylate

• Hydrogen sulfide

• Phosgene

• Lewisite

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General Treatment Approach

• Stabilization takes precedence over meticulous physical exam

• A complete set of vital signs may be helpful in determining type of toxin

• Note odors, presence of absence of diaphoresis, skin findings, pupils, presence of bites, bullae, IV

• Fasciculations(OPP), Rigidity(tetanus, strychnine), Tremors (Li, theiophylline), Dystonia (neuroleptics)

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General Treatment Approach

• Most hypotension can be initially treated with IV fluids

• Close monitoring of rhythms, rates and intervals using 3 and 12 lead ECG when agent suspected is cardiotoxic

• Be prepared to treat seizures

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Treatment Considerations

• Supportive care may be appropriate

• Important fact: 83% of all poisonings occur by ingestion

• Is toxin transferable to rescuers and health providers?

• Be prepared to decontaminate patient

• Activated charcoal no longer recommended11

Antidotes

Study your antidotes!

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5

AntidotesAgent• Opioids

• Beta blockers

• Cyanide

• Organophosphates

• Sulfonylureas

• Isoniazid

• Toxic Alcohol (Meth/Ethylene G)

• Methemoglobinemia

• Acetominophen

• Prolonged QRS Toxin(Sine‐Wave)

• Prolonged QT Toxin

• CO

• Benzodiazepine (Controversy)

Antidote• Naloxone

• Glucagon

• Hydroxocabalamin

• Atropine + pralidoxime

• Glucose

• Pyridoxine

• Fomepizole

• Methylene Blue

• N‐AcetylCysteine (NAC)

• Sodium Bicarbonate

• Magnesium

• HyperBaric O2

• Flumazenil

Take‐Home Points

• 1. Toxic exposures/ingestions may have wide ranging signs/symptoms, immediate or delayed onset

• 2. Gather a good history with regards to agent(s) involved, timing and route of exposure

• 3. Know how to recognize the common toxidromes and their antidotes

• 4. Do not act too hastily and endanger the rescuer(s)

• 5. Have a common approach to handling possible toxic presentations

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Common Toxidromes to Know

• Serotonin Syndrome– ALOC, tachycardia, hypertension, hyperreflexia, clonus, hyperthermia

• Sedative‐hypnotic– Seda on, ↓respira on, NORMAL pupils and v/s

• Opoids– Seda on, miosis, ↓ resp drive, ↓ bowel sounds

• Sympathomimetic– Agitation, mydriasis, tachycardia, hypertension, hyperthermia, diaphoresis

• Anticholinergic– Mydriasis, dry mucous membranes, ALOC, hallucinations, urinary retention

• Cholinergic– Miosis, lacrimation, diaphoresis, bronchospasm, bronchorrhea, vomiting,

diarrhea, bradycardia

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Caustics


Learning Objectives

Upon the completion participants will be able to:

• Define a caustic substance

• List some sources of these substances

• Describe classic differences in site and nature of injury with acid vs. alkali ingestion

• Describe the prehospital care priorities for patients with caustic ingestions

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Definitions

• Caustics and corrosives are substances which may have beneficial uses but also can be toxic because they cause tissue injury via a chemical reaction. – Caustics are capable of burning, corroding, dissolving, or eating away by chemical action (dictionary)

• A corrosive substance is one that will destroy and damage other substanceswith which it comes into contact, including metals and various organic compounds

• Vast majority of caustic chemicals are acidic or alkaline substances that damage tissue by accepting a proton (alkaline substance) or donating a proton (acidic substance) in an aqueous solution.

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Pathophysiology

• Increased risk of severe injury with pH <3 or > 11

• Severity of tissue injury also determined by the:

– Concentration and duration of contact

– Amount and state (liquid, solid) of the substance involved

– Physical properties such as tissue penetration and titratablereserve(how much acid/base to neutralize)

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Generally speaking:Solids increase risk of proximal injury (oropharynx/prox esophagus)

Liquids increase risk of distal injury(disalt esophagus/gastric)

Epidemiology

• The alkali drain cleaners and acidic toilet bowl cleaners are responsible for the most fatalities from corrosive agents.

• Approximately 10% of caustic ingestions result in severe injury requiring treatment.

• Between 1% and 2% of caustic ingestions results in stricture formation.

• Approximately 80% of caustic ingestions occur in children younger than 5 years.

• Most intentional ingestions occur in adults

Common acid‐containing sources

• Toilet bowl cleaning products

• Automotive battery liquid

• Rust removal products

• Metal cleaning products

• Cement cleaning products

• Drain cleaning products

• Soldering flux containing zinc chloride

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Common alkaline‐containing sources

– Drain and oven cleaning products

– Ammonia products(tub/tile cleaners)

– Swimming pool cleaning products

– Automatic dishwasher detergent

– Hair relaxers

– Clinitest tablets

– Bleaches(most common)

– Cement

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Alkalis

• Cause injury by liquefaction necrosis, saponification of fats and solubilization of proteins– Severe and deeper injury occurs rapidly after alkaline ingestion(min)

– Special attention paid to ocular injury

– Appear deceptively superficial

• First contact most severely affected– oropharynx, hypopharynx, and esophagus (most common).

– stomach much less frequently

• Tissue edema occurs immediately, may persist for 48 hours, and may eventually progress sufficiently to create airway obstruction.

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Acids

• Acid ingestions cause tissue injury by coagulation necrosis– causes desiccation/denaturation of superficial tissue proteins– formation of an eschar preventing/delaying deeper injury– Dermal expaosures respond well to copious irrigation (except HF)

• The stomach is the most commonly involved organ following an acid ingestion– pyloric and antral spasm causes pooling resulting in severe injury and may induce emesis

– some natural protection of the esophageal squamous epithelium. – Small bowel exposure also occurs in about 20% of cases.– Higher mortality compared to strong alkali ingestion

Signs and symptoms of Caustic Ingestion

• The presence or absence of the following symptoms should be determined since the presence of any of these symptoms suggests the possibility of significant internal injury.

• However, their absence does not preclude significant injury.– Dyspnea– Dysphagia– Oral pain and odynophagia– Chest pain– Abdominal pain– Nausea and vomiting

Signs and symptoms• Tachycardia • Oropharyngeal burns ‐ these are important when identified, but

significant esophageal involvement may occur in the absence of oropharyngeal lesions.

• Drooling • Subcutaneous air • Acute peritonitis ‐ Abdominal guarding, rebound tenderness, and

diminished bowel sounds• Signs of impending airway obstruction may include the following:

– Stridor– Hoarseness – Dysphonia or aphonia– Respiratory distress, tachypnea, hyperpnea– Cough

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Airway Management for Caustic Ingestions

• Because of the risk of rapidly developing airway edema, immediate assessment of the patient’s airway and mental status should be performed and continually monitored.

– Equipment for endotracheal intubation and cricothyrotomy should be readily available (consider difficult airway)

– Nasotracheal intubation and BIAD should be avoided due to the increased risk of soft‐tissue perforation

• Cricothyrotomy or percutaneous needle cricothyrotomy may be necessary in the presence of extreme tissue friability or significant edema.

Treatment

• Dilution typically a home remedy for accidental (<30 min)

• Do not induce emesis or attempt to neutralize This induces an exothermic reaction, which can compound the chemical injury with a thermal injury.

– It may also induce emesis re‐exposing tissue to the caustic agent.

– NO NGT or charcoal

• Prompt evaluation of airway and vital signs as well as immediate cardiac monitoring and intravenous access.

Special Considerations

Alkali eye injury

• More severe and deeply penetrating with continued liquefaction

• Copious and continuous irrigation

Disc battery ingestion

• Most < 6yoa

• Disc battery hotline is option if reliable information

• Xray usually necessary

• Leakage(rare) risks alkali injury and toxic metals

• If airway and esophagus is involved must be removed acutely

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Take home points

• A corrosive will destroy and damage other substances, including metals, organic compounds and living tissue; caustics are toxic via a chemical reaction

• Identify acid/base to predict injury to contiguous organs

• Supportive care rather than specific antidotes– Avoid emesis or neutralization, as well as NGT or Charcoal

• Careful monitoring and management of airway considering friable/edematous tissues (high risk)

• Rapid transport to the nearest ED


Hydrofluoric acid


Learning Objectives


1. Know the major potential industrial uses for or occupational sources of HF exposure

2. Describe the pathophysiology of HF toxicity

3. List the signs, symptoms and natural history of HF exposure

4. Describe the treatment of HF exposure

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Hydrofluoric acid (HF)

• Colorless gas or fuming liquid, corrosive (hydrogen fluoride)

• When dissolved in water ishydrofluoric acid

• Used to make refrigerants, herbicides, aluminum, plastics, electrical components, fluorescent bulbs, etching, and metal/wheel cleaners, and rust removers

• The worker involved or activity is often clue on exam

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Pathophysiology

• HF dissociates and fluoride ions penetrate skin quickly and deeply without extensive coagulation necrosis (eschar formation)

• Fluoride ions react with calcium and magnesium– Systemic toxicity due to depletion of total body stores of calcium and magnesium

• Majority of deaths result from cardiac dysrhythmias secondary to hypocalcemia, hypomagnesemia, hyperkalemia, acidosis

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Hydrofluoric Acid Paradox

• Lower concentrations more severe burns because of natural history of delay in onset of symptoms– >50% immediate symptoms treatment begins quickly

– 20‐50% delayed 1‐8 hrs

– <20% up to 24 hrs: Deeper penetration of un‐dissociated HF acid, with more severe burn

• Characteristic pain out of proportion to tissue injury

• Majority of cases involve small areas usually fingers and upper extremities; look under nails as portals of entry towards bone

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Signs and symptoms

• Inhalation burns– Hypoxemia– Stridor– Wheezing– Rhonchi

• Skin burn classification– Grade 1: a white burn mark and/or erythema and pain– Grade 2: a white burn mark and/or erythema and pain + edema and blistering

– Grade 3: a white burn mark and/or erythema and pain + edema and blistering + necrosis

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Prehospital Treatment• PPE as needed to prevent exposure and rapid irrigation

• Bind fluoride– Apply calcium gluconate gel if available

– Soak digits in a magnesium hydroxide (e.g. Mylanta®)

– SQ 5‐10% CaGlu (0.5mL/cm2) if refractory

• Symptomatic management– Pain control with opioid agents

– Apply ice packs (slows diffusion of the fluoride ion)

• With any evidence of hypocalcemia, administer 10% calcium gluconate IV

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Take‐Home Points

1. HF may cause delayed symptoms

2. Treatment with topical and intravenous calcium is vital

3. Hypocalcemia is cause of lethal dysrythmias (Know cause of mortality for exam)

4. Know the major potential industrial uses for or occupational sources of HF exposure

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1.3.7.1.2 Cyanide


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Questions

1. Which of the following is true of CN poisoning? a. Interferes with cellular respiration by uncoupling phosphorylation

b. Has multiple safe antidotes

c. Renders cells less susceptible to oxidative stress

d. Results in increases in GABA effects and decreased glutamate

e. Hallmark is ongoing respiratory collapse despite oxygen therapy

2. T/F Best antidote for CN is Lilly Kit

3. T/F CN Toxicity can be mischaracterized as CO Toxicity

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Learning Objectives


1. List the potential sources of cyanide exposure

2. Understand the pathophysiology of cyanide poisoning

3. List the signs and symptoms of cyanide exposure

4. Describe the treatment of cyanide poisoning

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Chemistry of Cyanide

• Gas (hydrogen cyanide):

– Colorless with faint bitter almond smell

– Nearly 40% of the population cannot smell cyanide.

• Sodium cyanide (NaCN) and potassium cyanide (KCN) are both white powders.

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Chemistry of Cyanide

• Molecule consists of one carbon atom joined to one nitrogen atom by a triple bond.

• Cyanide anion is extremely toxic.

Cyanide

• Hydrogen cyanide is a product of combustion of certain materials.

• High in:

– Plastics

– Wool

– Silk

– Synthetic rubber

– Polyurethane

– Asphalt

Pathophysiology

• Cyanide can be inhaled, ingested or absorbed (rarely).

– Ingestion more common with suicide/murder

– “Don’t let the enemy get the information out of you”

• Toxicity depends on:

– Route

– Dose

– Duration of exposure

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Cyanide

• Toxicity varies with chemical form.

• Hydrogen cyanide (HCN) gas at concentrations of 130 ppm can be fatal within an hour.

• OSHA permissible exposure levels are 10 ppm as an 8‐hour time‐weighted average.

Pathophysiology• Cyanide stops aerobic production of ATP

– Cyanide poisoning is a form of histotoxic hypoxia because the cells of an organism are rendered unable to use oxygen

– Cyanide inhibits mitochondrial cytochrome(a3) oxidase of electron transport chain Oxidative phosphorylation inhibitor (Phenols “uncouple”)

• Inhibits other enzymes leading to:– Increased susceptibility to oxidative stress– Increased glutamate and excitatory neurotoxicity– Decreased GABA (inhibitory receptors) leading to seizures

• Tissues that primarily depend on aerobic respiration are particularly affected:– Heart– Central nervous system

Signs and Symptoms

Low levels

• Dyspnea

• Headache

• Nausea

• Anxiety

• Altered mental status

High levels

• Hyperpnea

• Loss of consciousness

• Seizures

• Apnea

• Death within minutes

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High oxygen consumption tissues are most susceptible

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Consider CN Toxicity

• At various stages, the symptoms of CN poisoning are similar to those experienced when hiking or climbing at altitudes

• Classic scenario is hemodynamic and respiratory compromise not responsive to oxygen despite expectation

• History is key: Suspect co‐inhalation with any smoke inhalation

• Markedly elevated lactate– Some suggest > 10

• Unreliable indicators:– Cherry red skin/flushing

– Bright red venous blood52

Cyanide Treament

• Antidotes available:

– Cyanide Antidote Kit:*

• Amyl nitrite

• Sodium nitrite

• Sodium thiosulfate

– Hydroxycobalamin

Review this for historical interest

Cyanide Antidote Kit

• Nitrites administered to form methemoglobin.

– Cyanide has a greater affinity for methemoglobin (MET‐Hb) and frees cytochrome oxidase

– Amyl nitrite (inhaled q 30s); Sodium nitrite (300mg IV)

• Sodium thiosulfate (12.5g IV) binds cyanide and forms thiocyanate.– Thiocyanate much less toxic than cyanide anion and excreted through the kidneys

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Cyanide Antidote Kit

• Problems (related to nitrites):

– MET‐Hb does not transport O2.

– The conversion of HB to MET‐Hb changes the state of the heme molecule where O2 binds.

– MET‐Hb has heme in the ferric (Fe3+) state and not the ferrous state (Fe2+).

– O2 can only bind to heme when in the Fe2+ state.

Cyanide Treatment Caveat

• Concomitant CO and CN poisoning is more common than once thought

• CO‐Hb and CN treatment induced MET‐HB reduce the O2‐carrying capacity of the blood.

• Children are particularly at risk for hypotension and adverse effects from methemoglobinemia.

• Once useable Hgb reaches crucial level CV Collapse

100% Hb

20% CO-Hb

20% MET-Hb

O2-carrying capacity

nearly halved!

Hydroxocobalamin

• Precursor to cyanocobalamin (a form of Vitamin B12).– Hydroxocobalamin combines with cyanide forming renallyexcreted cyanocobalamin

– Does not inhibit Hgb function

• Minimal side effect profile– Reddish skin and urine

– Allergic reaction

– Hypertension

• Prohibitively expensive for some systems– Especially to replace multiple expired doses

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CO and Cyanide Poisoning

• Parts of cyanide antidote kit (amyl nitrite, sodium nitrite) induce methemogloninemia.

• Cyanide antidotes and CO poisoning can lead to elevated CO‐Hb and MET‐Hb significantly reducing O2 capacity of blood.

• Sodium nitrite should be avoided for combination cyanide/CO poisonings when SpCO >10%.

• Hydroxycobalamin converts cyanide to cyanocobalamin(Vitamin B12) which is renally‐cleared.

• Hydroxycobalamin is the antidote of choice for mixed CO and cyanide poisoning.

Take‐Home Points

• Cyanide is a cellular poison which blocks cellular respiration via inhibition of Cytochrome

• Cyanide exposure usually leads to rapid loss of conscious, respiratory failure and cardiovascular collapse

• Nitrite‐based antidotes are contraindicated in the presence of hypoxia and concomitant CO poisoning

• Important to consider CN in smoke exposure

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Carbon Monoxide and Cyanide

• Cyanide more common in fires than once thought.

– CO and CN often released in structure fires from burning plastic materials resulting in severe toxicity

• Symptoms of cyanide toxicity often attributed to CO because of lack of a high index of suspicion.

– Cyanide and CO both primarily affect the heart and CNS thus multiplying the ill‐effects

– The effects of CO and cyanide are cumulative.

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Cyanide Poisoning

• Amyl nitrite is administered via inhalation or ventilation.

• Sodium nitrite is administered intravenously.

• Sodium thiosulfate is administered intravenously.

Cyanide Treatment

Cyanide Treatment

• Concomitant CO and CN poisoning therapy can significantly decrease the O2‐carrying capacity of the blood.

• Combination of CO‐Hb and MET‐HB can significantly reduce the O2‐carrying capacity of the blood.

• Children are particularly at risk for hypotension and adverse effects from methemoglobinemia.

100% Hb

20% CO-Hb

20% MET-Hb

O2-carrying capacity

nearly halved!

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Cyanide Treatment

• Hydroxycobalamin

– Precursor to cyanocobalamin (Vitamin B12).

– Hydroxycobalamin combines with cyanide to form cyanocobalamin which is excreted through the kidneys.

– FDA approval in US obtained in December 2006.

– Marketed as Cyanokit™.

Toxins

Carbon Monoxide


Carbon MonoxideWhat is the likely SPO2 level on an obtunded victim suspected of CO poisoning with a Hgb‐CO of 30 and

placed on a non‐rebreather mask?

a) 70

b) 80

c) 90

d) 100

Version Date: 2/6/2013

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Learning Objectives


1. Understand the pathophysiology of carbon monoxide (CO) poisoning

2. Describe the signs and symptoms of CO poisoning

3. Understand the methods of CO detection, and its sometimes elusive diagnosis

4. Describe the treatment and disposition of patients with CO poisoning

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Chemistry of Carbon Monoxide

• Gas:– Colorless

– Odorless

– Tasteless

– Nonirritating

• Results from the incomplete combustion of carbon‐containing fuels.

• Stable Molecule: Triple Bond

• Some ambient

CO Pathophysiology

• Affinity for heme 2‐300x O2

– displaces O2 from binding sites.

– prevents O2 from binding.

• Shifts oxy‐Hgb curve to left preventing release of O2

• Essentially induces relative (functional) anemia

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Pathophysiology

• CO also binds to other iron‐containing proteins:– Myoglobin (dysrhythmias and cardiac dysfunction)

– Cytochrome oxidase (met acidosis)

• Direct injury to endothelium releases nitric oxide– Peripheral vasodilation and hypotension

– Inflammatory response

– Increased free radical injury

Epidemiology

• CO is leading cause of poisoning deaths in industrialized countries.

• CO may be responsible for half of all poisonings worldwide.

• ~5,000–6,000 people die annually in the United States as a result of CO poisoning.

• ~40,000–50,000 emergency department visits annually result from CO poisoning.

Incidence

• Significant increase in CO poisoning seen following disasters.

• Primarily relates to loss of utilities and reliance on gasoline‐powered generators and use of fuel‐powered heaters.

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Incidence and Epidemiology

• Most accidental deaths are due to:– House fires.

– Automobile exhaust.

– Indoor‐heating systems.

– Stoves and other appliances.

– Charcoal grills.

– Camp stoves.

– Water heaters.

– Boat exhausts.

Seasonal and Demographic Variation

• Increased accidental CO deaths:– Patient > 65 years of age.

– Male

– Ethanol intoxication.

• Accidental deaths peak in winter:– Use of heating systems.

– Closed windows.

Clinical Features of CO Poisoning• Presentation resembles other diseases

– Often dubbed the great imitator• Often misdiagnosed as:

– Viral illness (e.g., the “flu”)– Acute coronary syndrome– Headache/Migraine– Other Toxic Ingestions

• Misdiagnosis may occur in 30-50% of CO-patients presenting to the ED, often due to failure to consider

• Key is to suspect the diagnosis in first place

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Signs and Symptoms

• CNS– Confusion

– Altered mental status

– Drowsiness

– Visual disturbances

– Gait disturbance

– Agitation

– Seizures

– Coma

– Death

• Cardio‐pulmonary– Chest pain– Palpitations/Dysrhythmias– Non‐cardiogenic pulmonary

edema– Hypotension– DOE/SOB– Syncope

• Other– Abdominal pain– Nausea/vomiting– Renal failure– rhabdomyolysis

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Signs and Symptoms (Chronic)

• Same as with acute CO EXCEPT that onset and severity may be extremely varied.

• Cherry red skin color is unreliable, not always present

– May be a late finding‐ typically at post mortem

• CO‐Hb may not correlate with symptoms/sequelae.

Long‐Term Complications

• Delayed Neurologic Syndrome (DNS):– Recovery seemingly apparent.

– Behavioral and neurological deterioration 2‐40 days later.

– True prevalence uncertain (estimate range from 1‐47% after CO poisoning).

– Patients more symptomatic initially appear more apt to develop DNS.

– More common when there is a loss of consciousness in the acute poisoning.

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Delayed Neurologic Syndrome

• Signs and Symptoms:

– Memory loss

– Confusion

– Ataxia

– Seizures

– Urinary incontinence

– Fecal incontinence

– Emotional lability

• Signs and Symptoms:

– Disorientation

– Hallucinations

– Parkinsonism

– Mutism

– Cortical blindness

– Psychosis

– Gait disturbances

– Other motor disturbances

Non‐combustion Source

• Don’t forget methylene chloride (for the test)

– Look for in the patient using paint thinner/stripper

• Transdermal absorption

• Is metabolized to CO

• Carboxyhemoglobin levels may continue to rise

– Unlike inhaled ‐should decline once source removed

– Also could be utilized on a test scenario

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Diagnosis

• Lab determination of carboxyhemoglobin

– Suspicion primarily based on history

– Treatment primarily based on symptoms in setting of CO

• Now have co‐oximetry capable of detecting

– Carboxyhemoglobin

– Methemoglobin

• May have value as screening tool

• Fire/EMS units often have RAD‐57 (Massimo)

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Carbon Monoxide Detection

• New generation oximeter/CO‐oximeter can detect 4 different hemoglobin forms.– Deoxyhemoglobin (Hb)– Oxyhemoglobin (O2‐Hb)– Carboxyhemoglobin (CO‐Hb)– Methemoglobin (MET‐Hb)

• Provides:– SpO2

– SpCO– SpMET– Pulse rate

• Pitfalls– SpO2 level falsely high in CO poisoning (? Test question)– High ambient light

Patient Groups at Higher Risk

• Children

• Pregnant women – Fetal hemoglobin has greater affinity for CO

– may exhibit milder symptoms with high fetal toxicity

• Elderly and underlying disease, co‐morbidity in any ages

– Cardiopulmonary diseases

– Anemia

Treatment

• Supportive

– ABC

– Cardiac monitor

– Symptomatic management

• Early high concentration oxygen reduces T 1/2:

– Room air: 240‐360 minutes

– O2 (100%): 80‐90 minutes

– Hyperbaric O2: 22 minutes

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Treatment

• Efficacy of hyperbaric oxygen therapy (HBO) is a matter of conjecture although still commonly practiced.

• Generally reserved for severe poisonings.

• May aid in alleviating tissue hypoxia.

• Significantly decreases half‐life of CO‐Hb.

• Specialists believe mitigates sequelae

Indications for HBO Therapy

• Syncope

• Altered mental status

• Coma

• Focal neurologic deficits

• Acute myocardial ischemia

• Seizures

• Pregnant CO‐Hb>15% or fetal distress

• CO‐Hb>25%

Take‐Home Points

• CO poisoning is the great imitator.

• Early high flow O2 is critical to reducing half‐life

• CO‐Hgb may not correlate with symptoms

– Beware young, old and pregnant

– Non‐invasive CO monitoring is available

• Use of HBO therapy is controversial

– Use in severe/refractory symptoms

• Immediate and long term effects from CO poisoning

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CO Poisoning

• Remember, CO poisoning is the great imitator.

• Missed CO exposure often leads to death and disability.

• CO is a particular risk for firefighters.

Treatment

• Administer high‐concentration oxygen.

– Maximizes hemoglobin oxygen saturation.

– Can displace some CO from hemoglobin.

– Associated with improvements in neurological and cardiac complications.

Indications for HBO Therapy

• Possibly consider for:–Cardiovascular compromize (i.e., ischemia, dysrhythmias).

–Metabolic acidosis

–Extremes of age

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Sources of Carbon Monoxide

• House fires

• Automobile (gasoline engine) exhaust

• Space heaters

• Indoor grills/barbeques

• Camp stoves

• Cigarette smoke

Environmental CO Exposure

• Environmental exposure typically <0.001% (10 ppm).

• Higher in urban areas.

• Sources:

– Volcanic gasses

– Bush fires

– Human pollution

CO Exposure

Source Exposure (ppm)

Fresh Air 0.06-0.5

Urban Air 1-30

Smoke-filled Room 2-16

Cooking on Gas Stove 100

Actively Smoking a Cigarette 400-500

Automobile Exhaust 100,000

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Firefighter Risks

• CO is a significant and deadly occupational risk factor for firefighters.

• Sources:

– Structure fires

– Apparatus fumes

– Portable equipment fumes

– Underground utility fires

– Closed‐space rescue situations

Pathophysiology

• Pathophysiology of CO poisoning first described by French physician Claude Bernard in 1857.

• CO poisoning actually very complex.

• CO binds to hemoglobin with an affinity ~ 250 times that of oxygen.

• The combination of CO and hemoglobin is called carboxyhemoglobin (CO‐Hb).

Normal CO‐Hb Levels

Source CO-Hb (%)

Endogenous 0.4-0.7

Tobacco Smokers:

1 pack/day

2-3 packs/day

cigars

5-6

7-9

Up to 20

Urban Commuter 5

Methylene chloride (100 ppm for 8 hours) 3-5

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Pathophysiology

• Impact of CO on major body systems:

– Neurologic:

• CNS depression resulting in impairment:– Headache

– Dizziness

– Confusion

– Seizures

– Coma

• Long‐term effects:– Cognitive and psychiatric problems

Pathophysiology


– Cardiac:

• Decreased myocardial function:– Hypotension with tachycardia

– Chest pain

– Dysrhythmias

– Myocardial ischemia

– Most CO deaths are from ventricular fibrillation.

• Long‐term effects:– Increased risk of premature cardiac death

Pathophysiology

• Impact of CO on major body systems:– Metabolic:

• Respiratory alkalosis (from hyperventilation)

• Metabolic acidosis with severe exposures

– Respiratory:• Pulmonary edema (10‐30%)

– Direct effect on alveolar membrane

– Left‐ventricular failure

– Aspiration

– Neurogenic pulmonary edema

34

Pathophysiology


– Multiple Organ Dysfunction Syndrome (MODS):

• Occurs at high‐levels of exposure

• Associated with a high mortality rate.

Pathophysiology Summary

• Limits O2 transport:

– CO more readily binds to Hb forming CO‐Hb.

• Inhibits O2 transfer:

– CO changes structure of Hb causing premature release of O2 into the tissues.

• Tissue inflammation:

– Poor perfusion initiates an inflammatory response.

Pathophysiology Summary

• Poor cardiac function:– O2 delivery can cause dysrhythmias and myocardial dysfunction.

– Long‐term cardiac damage reported after single CO exposure.

• Increased activation of nitric oxide (NO):– Peripheral vasodilation.

– Inflammatory response.

35

CO Poisoning

• Signs and symptoms closely resemble those of other diseases.

• Often misdiagnosed as:

–Viral illness (i.e., influenza)–Acute coronary syndrome

–Migraine

• Estimated that misdiagnosis may occur in up to 30‐50% of CO‐exposed patients presenting to the ED.

CO POISONING SIGNS & SYMPTOMS

• Signs and symptoms usually vague and non‐specific.

• You must ALWAYS maintain a high index of suspicion for CO poisoning!

CO Poisoning

• Classifications:

– Acute

• Results from short exposure to a high level of CO.

– Chronic:

• Results from long exposure to a low level of CO.

36

Signs and Symptoms (Acute)

• Malaise

• Flu‐like symptoms

• Fatigue

• Dyspnea on exertion

• Chest pain

• Palpitations

• Lethargy

• Confusion

• Depression

• Impulsiveness

• Distractibility

• Hallucination

• Confabulation

• Agitation

• Nausea

• Vomiting

• Diarrhea

• Abdominal pain

Signs and Symptoms (acute)

• Headache

• Drowsiness

• Dizziness

• Weakness

• Confusion

• Visual disturbances

• Syncope

• Seizures

• Fecal incontinence

• Urinary incontinence

• Memory disturbances

• Gait disturbances

• Bizarre neurologic symptoms

• Coma

• Death

CO ppm Duration Symptoms

50 8 hours OSHA minimum

200 2-3 hours Mild headache, fatigue, nausea, dizziness

400 1-2 hours Serious headache—other symptoms intensify. Life-threatening > 3 hours

800 45 minutes Dizziness, nausea and convulsions. Unconscious within 2 hours. Death within 2-3 hours.

1,600 20 minutes Headache, dizziness and nausea. Death within 1 hour.

3,200 5-10 minutes Headache, dizziness and nausea. Death within 1 hour.

6,400 1-2 minutes Headache, dizziness and nausea. Death within 25-30 minutes.

12,800 1-3 minutes Death

37


CO Myocardial Injury Patients (n)

Died

(%)

5-year Survival

(%)

Myocardial injury from CO 85 37.6 71.6

No Myocardial injury from CO

145 15.2 88.3

• Cardiac Complications:

– 230 sequential patients with moderate to severe CO poisoning treated with HBO.

Myocardial injury and long-term mortality following moderate to severe carbon monoxide poisoning. Henry CR, et al. JAMA. 2006;295:398-402


• Depression and anxiety can exist up to 12 months following CO exposure.

• Higher at 6 weeks in patients who attempted suicide by CO.

• No differences in rates between accidental and suicide‐attempt at 12 months.

Carbon Monoxide Detection

• Biological CO detection previously required hospital‐based ABGs or venous sample to measure CO‐Hb.

• Technology now available to detect biological CO‐Hb levels in the prehospital and ED setting.

• Referred to as CO‐oximetry

38

CO‐Oximetry

Treatment Algorithm

Treatment

• Continue to monitor SpO2 and SpCO levels throughout treatment.

• Obtain 12‐lead ECG (if ALS) and monitor ECG.

39


1.3.7.1.5 Organophosphates


Questions

1. Which of the following is true of OPP poisoning? a. Gives a dry OD toxidrome similar to that of anti‐cholinergics

b. Has no safe antidotes

c. Usually causes miosis

d. Is a nerve agent because it effects the adrenergic receptors

e. All organophosphates are nerve agents

2. T/F The dose of Atropine for OP Poisoning is 0.04/kg

3. T/F Diazepam has no role in OPP poisoning

116

Learning Objectives


1.Understand the pathophysiology of organophosphate (OPP) poisoning as basis for the term “nerve agents”

2.List some better‐known nerve agents

3.List potential sources of OPP exposure

4.Describe the effects, signs and symptoms of OPP

5.Discuss and understand the basis for treatment of OPP poisoning

117

40

Nerve Agents

• Nerve agents are essentially OPP agents

• Tabun (GA), Sarin (GB), Soman (GD), VX

• Above 4 are most toxic of the chemical agents

• Penetrate skin, eyes, lungs

• Other sources of OPP include insecticides and herbicides: Most common suicide in agrarians

• Diagnosis made clinically; confirmed in laboratory

Chemistry of Nerve Agents

• Nerve agents are liquids at normal ambient temperatures

• G‐agents volatile, non‐persistent; vapor and liquid threat

• VX fairly non‐volatile, persistent; liquid threat

• Vapor heavier than air Sarin = C4H10FO2P

Methylphosphofluoridic acid, 1-methylethyl ester, orIsopropylmethanefluorophosphonate

ysiology

• Work at receptors

• Anti‐Cholinesterase

• Potentiate Ach

41

Pathophysiology at Muscarinic Sites

• SLUDGE: salivation, lacrimation, urination, defectation, GI symptoms, emesis

OR

• DUMBBELSS: diarrhea, urination, miosis/muscle weakness, bronchorrhea, bradycardia, emesis, lacrimation, salivation/sweating

Pathophysiology at Nicotinic Sites

• Skeletal muscles

• – Fasciculations

• – Twitching

• – Weakness

• – Flaccid paralysis

• Other (ganglionic)

• – Tachycardia

• – Hypertension

Overall Symptoms

Neuromuscular

• Twitching

• Weakness

• Paralysis

• Respiratory failure

• Long term sequalea

• Psych symptoms

• Brain damage

Autonomic• Reduced Vision• Small pupil size• Drooling• Sweating• Diarrhea• Nausea• Abdominal pain• Vomiting

Central Nervous• Headache• Convulsions• Coma• Respiratory arrest• Confusion• Slurred speech• Depression• Respiratory depression

42

Differential Symptoms

• Toxicity varies with chemical form and amount.

• Vapor effects occur within seconds, peak minutes (no delaymay be test question)

• Low exposure

– Miosis (dim vision, eye pain)

– Rhinorrhea

– Dyspnea

• High exposure

– Immediate loss of consciousness, seizures, apnea,

– flaccid paralysis


Low levels

• Localized sweating

• Fasciculations

• No likely miosis

• Anxiety

Moderate amount < LD50

• GI effects

• Uncommonly miosis

High levels

• Effect in less than 30‐60 minutes

• Sudden Loss of consciousness

• Seizures

• Flaccid

• Dyspnea to Apnea

• Death within minutes

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Liquid exposure can be delayed up to 18 hours

Treatment

• Self‐protection ‐ respiratory protection via PAPR or

• SCBA or properly fitted gas mask with appropriate filter

• Airway/ventilation

– Often High resistance

• Antidotes Kits available = Mark 1

– Nerve agent Antidote Kit:*

• Duodote auto‐injector

• Atropine +

• Pralidoxime

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Nerve Agents TreatmentAtropine

• Antagonizes muscarinic effects

• Dries secretions; relaxes smooth muscle

• Given IV, IM, ET

– No effect on pupils (test?)

– No effect on skeletal muscle

– IV in hypoxic patient

• Starting dose ‐ 2 mg• Maximum cumulative dose ‐ 20 mg– Insecticide poisoning requires much more• Side effects in normal people– Mydriasis– Blurred vision– Tachycardia– Decreased secretions and sweating

Treatment Caveat

• Atropine should be administered before other measures to reduce muscariniceffects and therefore facilitate adequate ventilation.

• Given IV, IM, ET

• Dries secretions; relaxes smooth muscle

• May cause cardiac arrhythmias when given IV in the hypoxic patient

• No effect on pupils or skeletal muscle ( ? test Question)

• How much to give?– Until secretions are drying or dry– Until ventilation is “easy”• If conscious or casualty is comfortable– Do not rely on heart rate/pupil size (might be in Test question)

Antidote Kit‐ Pralidoxime

• Also called 2‐PAM Chloride

• Removes nerve agent from AChE in absence of aging

– 600 mg IM or 1 gram slowly (20‐30) in IV infusion

– Hypertension with rapid infusion

• No effects at muscarinic sites

• Helps at nicotinic sites

• New research controversial

44

Pre‐hospital Treatment

• If no signs or symptoms: Observe 1 (Vapor) – 18 hours (liquid)• Symptomatic: Earliest Tx is DuoDote (Atropine 2.1mg+ 2PAM)• Parenteral Atropine will not dilate: Only Homatropine drops• Severe Exposure: Increasing Doses of Atropine IV q 5 min• Maintain airway and ventilation as necessary• Administer 2 PAM 1 g IV asap• Diazepam 2‐5 mg IV to prevent seizures• Repeat 2 PAM in one hour‐ the antidote of choice • All beneficial effects for enhancing survival are peripheral

Laboratory Diagnosis and Aging

• RBC Cholinesterase levels

– Blood levels do not necessarily correlate with symptoms

• Military uses RBC‐ChE > 80% of baseline

– Levels increase after 2 PAM administration

– Depends on exact agent

• “Aging process” occurs when Nerve agent irreversibly bound to Enzyme AChase

– VX occurs 60 hours after exposure, Sarin 4‐6 hours

– Soman is most potent at 2 minutes

Concept of Pre‐Treatment

• Carbamates (Prototype Pyridostigmine)

– Inhibits AChE

– Bind to active site of cholinesterase

– Spontaneously reversible – No aging with Pyridostigmine

– Blocks the OPP from attaching; FDA approved for Soman

– No oxime re‐activators will be needed to recover the AChE

– Marketed as Mestinon™. A medicine for Myesthenia

45

Take‐Home Points

• All Nerve Agents are OPP but not vice versa

• Most common OPP are used in agriculture

• Four common nerve agents: GA, GB, GD, VX

• Pathophysiology is binding AChE, potentiating ACh

• Receptors effected are cholinergic

• Symptoms are skeletal, autonomic or central=SLUDGE

• Antidotes are peripheral, pretreatment may help GD

• Atropine doses may be very large, aimed at secretion

– Avoid relying on pupils for titration133

For test

• Remember: SLUDGE pneumonic

• Less to no delay with vapor, delay with liquid

• Remember: Miosis not automatic, but if preset probably toxic

• Do not use miosis to gauge response

• May need way more Atropine than other applications – until secretions clear or easier to ventilate

• Know Mark 1 Kit and doses


1.3.7.1.6 Mustards and Blistering Agents


46

Questions

1. Which of the following is true of OPP poisoning? a. Gives a dry OD toxidrome similar to that of anti‐cholinergics

b. Has no safe antidotes

c. Usually causes miosis

d. Is a nerve agent because it effects the adrenergic receptors

e. All organophosphates are nerve agents

2. T/F The dose of Atropine for OP Poisoning is 0.04/kg

3. T/F Diazepam has no role in OPP poisoning

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Learning Objectives


1. Understand the pathophysiology of mustards and other blistering agents (BA)

2. List some better‐known agents

3. List potential sources of such agents and exposure

4. Describe the effects, signs and symptoms of BA exposure

5. Discuss and understand the basis for treatment of BA poisoning

137

Blistering Agents

• Blistering agents are also called vesicants

• Mustards ‐ Sulfur Mustard = Mustard Gas (H), Distilled Mustard (HD), Lewisite, Mustard T (HT)

• Above 4 are most known of those chemical agents

• Odor: H,HD, T smells like garlic, onions, mustard

• Sources: WW I Chemical weapon manufacture

• Source: Stockpiles in Iran‐Iraq War (1982‐88

• No useful purpose, nor natural occurence

• Diagnosis made visually

47

Chemistry of Mustards

• Vesicants are chemicals that attack cells

• Can bind proteins in living organisms

• Destroy and damage DNA (like Radiation)

• Alter cellular structure and health

• 5% of WW I soldiers who were exposed died of such estimated 45,000 casualties

• Again, used in Iran‐Iraq war

Pathophysiology

• Agents work at cellular level

• Vapor inhalation and liquid threat

• Topical skin, eye and mucous membrane threat

• Latent periods may elapse between exposure and some effects

– Skin, eye, oral mucosa immediate

– Organ System may be more delayed: respiratory, GI

• Systemic toxicity ‐ like radiation

Target OrgansSkin Effects

• Redness

• Itching

• Eventual Blister

• Eyes

• Conjunctivitis

• Corneal Burns

• Blurred vision

Respiratory Effects

• Coryza, Clear

• Cough

• Sore throat

• Dyspnea

• Hemoptysis

• Chest tightness

Gastrointestinal Effects

• Nausea

• Vomting

• Abdominal pain

• Diarrhea

• Hematemesis

Cardiovascular

• A‐V Block

• Hypotension (high

Lewisite exposure)

48


• Mustard Toxicity varies with chemical form and amount

• Effects occur within 1‐2 h in severe vapor exposure

• Low exposure: 12‐24 hours

– Respiratory symptoms start

– Nausea and vomiting with Cholinergic effects

– Dyspnea

• Delayed symptoms at level of organ tissue are possible

– 3‐5 days: destruction of GI or lung mucosa

– Marrow: anemia, bleeding, pancytopenia, immunosuppression

Treatment‐Mustards

• Respiratory protection as needed

• Rapid decontamination

– Remove clothes

– Flush skin rapidly

• Decon within 2 minutes after exposure is only way to prevent tissue damage

• Over hydrating not helpful because not thermal burn

• Supportive respiratory care always a mainstay

Special Mention‐ Lewisite

• Severe damage to same targets organs, but immediate

– Pain and irritation within secs to mins, redness < 30 mins

• Vesicant with Skin irritation >> Mustards

– Known for Tissue necrosis with Pseudomembranes

• Odor =“Geraniums”

• Same damage to tissues with main differences (test)

– “Lewisite shock”: Low BP, life‐threat

– No effect in Marrow

– Sores known to heal faster than mustards

49

Lewisite‐ Treatment

• Rapid Decontamination (ASAP)

• Copious flushing of eyes

• Do not induce vomiting in ingestions

• Same attention to ABCs

• Other main difference: Antidote exists

– British Anti‐Lewisite = Dimercaprol

– Marketed as BAL™.

– Chelating Agent

Take‐Home Points

• All Blistering agents/vesicants are potent chemicals

• Sources are warfare and serve no useful purpose

• Four common agents

• Pathophysiology: destroys tissue at cellular level (DNA) then can damage multiple organ systems

• Principles of treatment are PPE, Decon and supportive

• Lewisite only has more immediate effects

• Only lewisite has an antidote for chelation

– BAL = Dimecaprol146

For test

• Remember odors

• Lesser delay with vapor, some delay with liquid

• Remember: Exception to delay is Lewisite

• Know Lewisite not effect marrow but does cause lewisite Shock

• Know lewisite has an antidote

50


1.3.7.1.3.2 Phosgene


Learning Objectives


1. Know the basic properties of pulmonary irritants and potential sources of exposure to Phosgene

2. Describe the differences between patients with Phosgene exposure as opposed to other irritants

3. Describe the pre‐hospital treatment and disposition of patients exposed to Phosgene

149

Pulmonary Irritants

• Properties

• Inhalant substances cause direct respiratory tract damage

• Some more delayed than others

• Hallmark symptom is dyspnea

– Initially might be Exertional, then at rest

• Cough is prevalent

– Initially may be dry, later frothy or pink‐tinged (non‐cardiogenic pulmonary edema)

51

Phosgene Properties

Phosgene• White Gas at Temp 47F

• Smell = Fresh Mown hay

• Cough

• Dyspnea

• Onset delayed: 2‐24h

• May hug floors upon release

Ammonia

• Colorless, water soluble, alkaline gas, pungent odor, immediate irritation to eyes

Chlorine• Greenish‐Yellow

• Smell = Pungent Odor

• Stridor

• Onset immediate to eyes, nose

• Onset : <12 hrs to respiratory tract

•

151

Sources of Phosgene

• Phosgene is not found naturally in the environment.

• Used to produce other chemicals such as pesticides.

• Phosgene can be formed when chlorinated hydrocarbon compounds are exposed to high temperature source

Treament

• Remove from source of exposure

• ABCs

• Flush skin and eyes with copious amounts of water

• O2, cool mist, bronchodilators may assist

• Airway management may be necessary (intubation, PEEP)

• Hydration

• Transport even if improved: observation under medical supervision for 48 hours is recommended

52

Take‐Home Points

• Removal of patient(s) from source of exposure is key

• Primary problem is respiratory irritant and effects on pulmonary tissue

• Supportive care includes attention to airway and ventilation

• Always consider delayed effects

154


1.3.7.1.3 Chlorine


Learning Objectives


1. Know the basic properties and potential sources of exposure to chlorine

2. Describe the signs and symptoms of patients with Chlorine exposure

3. Describe the pre‐hospital treatment and disposition

156

53

Chlorine

• Properties

• Greenish‐yellow gas

• Less alkaline than ammonia

• Chlorine + water = HCl + Free O2 radicals

– 30x more irritating to lungs than HCl

Sources of Chlorine

• Significant irritant to the eyes and respiratory tract

• Characteristic pungent odor

• Used in swimming pools and laboratories

• Industrial exposures may produce large numbers of casualties

Signs and Symptoms

Low levels

• Very irritated eyes

• Nausea

• Anxiety

• Cough

• Dyspnea

High levels

• Hyperpnea

• Wheezing

• Stridor

• Altered consciousness

• Apnea

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54

Treament

• Remove from source of exposure

• ABCs


• O2, cool mist, bronchodilators

• Airway management (intubation, PEEP)

• Hydration

Take‐Home Points

• Removal of patient(s) from source of exposure is key

• Primary problem is respiratory irritant and effects on pulmonary tissue

• Supportive care includes attention to airway and ventilation

161


1.3.7.1.8 Hydrocarbons


55

Learning Objectives


1. Know the basic properties and potential sources of Hydrocarbons

2. Describe the signs and symptoms of hydrocarbon exposure, and targets of toxicity

3. Know the major factors involved in toxicity

4. Describe the pre‐hospital treatment and disposition of patients exposed to hydrocarbon

163

Chemistry of Hydrocarbons

• Organic Substances contain carbon and hydrogen molecule (CxHy)

• CDC describes Total petroleum (TPH) and Polycyclic Aromatic (PAH)

– TPH originally come from crude oil, vary from clear liquid that evaporate, to thick liquids or semi‐solids that do not evaporate

– PAH formed during incomplete burning of coal, oil/gas waste, or other organics, may look like soot and do not dissolve in H2O

• Sources

– TPH in any distillates (gasoline, kerosene, fuel oil, mineral oil, lamp oil, asphalt, solvent for other products like pesticides)

– PAH may be used in plastics or pesticides

Causes of Exposure• Occupational (Could be vignette in test)

– Manufacturing: May be subclinical over time (Toluene)

– More likely with halogenated hydrocarbons

• Accidental

– Ingestion most common in kids < 5

• Intentional

– Suicide attempts are possible

• Recreational

– Inhalation Common in adolescents (huffing for a high)

– Refrigerants or propellants in aerosols

56

Toxicity Target and Factors

Target Organs• Primarily Lung (acute)

• GI Tract

• Central Nervous System

• Skin, Eyes

• Liver, Kidney, Immune (delay)

• Cardiovascular

Example of Low and High

• Low viscosity: Turpentine

• High: Mineral Oil

Main Factors• Viscosity = resistance to flow

• Low viscosity = High aspiration

• Above single most important

• Volatility = tendency for liquid to evaporate/vaporize

• High volatility = High aspiration

• Test question

166

Signs and Symptoms• Respiratory symptoms consistent with aspiration

– Cough, may be transient or prolonged

– Gagging or choking sensation (acute or delayed)

– Respiratory distress can develop

• Cardiovascular (Most prominent with inhalation)

– Syncope (usually prior to arrival), possible V‐fib w/o warning (test)

• CNS: At first may cause a transient euphoria (Huffing)

– Headache, altered mental status, then lethargy

• GI

– Nausea and vomiting, burning in epigastric area

• Skin and Eyes: Burning

Treatment

• Mostly supportive, treat dysrythmias

• ABCs

• May need decontamination by removing clothing and


• Airway management may be necessary (intubation, PEEP)

• Ongoing symptoms warrant observation beyond 6 hours

– Need to have negative chest X‐Ray at 6 hours

57

Take‐Home Points

• Primarily affects lungs

• Primary problem is aspiration

• Know factors for worse toxicity: Viscosity, volatilily

• Care supportive

• Always consider delayed effects, prolonged coughing

• Kids ingest, workers inhale over time, teens huff

• Do not forget V‐fib without warning

169

Toxins

1.3.7.1.9 Effects of radiation exposure

Version Date:6/7/15

Learning Objectives


1. Define Radiation, and classify the types

2. Describe the effects and stages of radiation exposure

3. Describe means of exposure and differences in result

4. Discuss the initial approach to self protection and decontamination after a radiation incident

171

58

Radiation

• Radiation is energy transmitted in the form of electromagnetic waves or energetic particles.

• Well‐known forms of electromagnetic radiation include radiowaves, microwaves, infrared, visible light, ultraviolet light, x‐rays, and gamma rays.

172

Types of radiation

• Non‐ionizing‐Cause excitement of atoms/molecules

– Radio/microwave, invisible and visible spectrum light

• Ionizing radiation‐removes electrons breaks bonds

– Alpha, beta, gamma and X‐ray

– Causes gross surface and subsurface damage(DNA)

– Impairs ability to repair those injuries

– Greatest effect on rapidly dividing, renewing tissue

173

Background• Only x‐rays and gamma rays contain sufficient energy to cause ionization.

• The principal pathologic effect of ionizing radiation results from damage to DNA.

• In turn, DNA damage is the principal cause of the biologic effects of radiation

• Tissues with a high turnover rate are more sensitive to the toxic effects of radiation than cells differentiated.

• Early effects of radiation are seen after large doses of radiation are delivered over short periods and especially affect rapidly dividing, self‐renewing organs – skin, bone marrow, and gut epithelium.

174

59

Means of Exposure

• Contamination

– Radioactive materials on outside of person

– Removed with clothing and washing

• Ingestion

– MOST dangerous

– Radioactive materials concentrated by tissues

• Irradiation

– Radiation passing through body

175

176

Clinical syndromes

• Localized exposure to high doses of radiation may cause cutaneous injury similar to burns.

• Blistering, erythema, desquamation, and ulceration often present about 12‐20 days after irradiation with the onset and severity related to the magnitude of exposure.

177

60

Acute radiation syndrome

• The acute radiation syndrome (ARS) occurs after whole‐body exposure to a large dose of ionizing radiation.

• This syndrome includes a number of characteristic signs and symptoms whose severity depends on magnitude of dose and duration of exposure.

• Does not occur at low radiation doses (<1 Gy) and is uniformly fatal at doses >10 Gy.

178

179

Exposure burns

• Caused by irradiation(radioactive source of activity sufficient to damage cells)

• Caused by a strong, concentrated “capsule” or contamination of the skin over a significant period of time

180

61

Radiation burns

• Burn is not perceived by patient at time of occurrence (think sunburn)

• Damages ability of cells to regenerate

• Takes weeks/months to be manifest

181

Ingestion injury

• May be highly lethal even in small amounts

• Symptoms usually take days to weeks to appear

182

Acute Radiation Sickness(Stages)

• Prodromal Stage

– N/V, anorexia, diarrhea if severe

• Latent Stage

– Duration is dose dependent (hrs‐wks)

• Manifest Illness Stage

– ARS syndromes

• Recovery or death

183

62

ARS Syndromes

• Bone marrow syndrome(hematopoietic)

– Infection and hemorrhage

• Gastrointestinal syndrome

– Infection, dehydration, electrolyte abnormalaties

• Cardiovascular/CNS syndrome

– ALOC, ataxia, sz

– Cardiovascular collapse

184

Irradiation Protection Principles

• Time ‐Minimize time spent near radioactive source– Linearly cumulative (5hrs with 1or 1hr with 5)

• Distance – inverse square law– Exposure decreases as square of distance (test)

– 1000mrem/hr is 2.5mrem at 20 ft (1000/400)

• Shielding ‐ Place physical shields around source– Alpha rays stopped by paper/clothing/skin

– Beta blocked by FF turnout gear (1cm skin unprotected)

– Gamma : good luck

185

Take‐Home Points

• Ionizing radiation is the type of EMW that breaks bonds and causes tissue (DNA) damage, inability to regenerate

• Effects of radiation are delayed and dose dependent

• Modes of exposure = contaminate, irradiation, ingestion

– Radioactive ingestion most dangerous, but more delayed

• Exposure to ionizing radiation is function of time, distance and shielding Protection is based upon latter

• Irradiation burns, ingestion causes ARS in stages

– Multiple organ systems, dividing cells vulnerable186

63

Toxins

1.3.7.2 Approach to initial decontamination in radiation incidents

Version Date:6/7/15

Management principles and axioms

• Radioactive contamination is not immediately dangerous to life/health. Use airborne and infection control practices. Little risk unless inhaled or ingested.

• Do not withhold treatment for decontamination. Conventional injuries are greater acute hazard than radiation exposure and contamination

• Special skills are not required to manage radioactive patient. Need radiation detection devices but decon is clothing removal and soap and water

188

Protection

• Prevent ingestion at all costs

• Focus on time, distance and shielding when responding to an event

• Time of exposure is linearly cumulative but exposure is reduced by the square of the distance

• Decon is mechanical removal of materials.(most eliminated with removal of clothing)

189

64

Approach to initial decontamination

• Radioactive materials (contamination) that collect on the outside of a person may be removed by simple mechanical means (often 80%)

• Most contamination is removed by removing/disposing of clothing

• Exposed skin may be cleaned with soap and water

• Key is to prevent accidental ingestion or inhalation of radioactive particles

190

Initial approach

• Secure the scene, don PPE and attempt to rescue injured or ill victims while minimizing exposure

• Conventional injuries and illnesses present a much greater acute hazard to patients than radiation exposure and contamination

• Standard medical treatment should be initiated as soon as feasible and not delayed to assess contamination status

191

Decontamination

• Remove the victims clothing and wrap in clean sheets

• Do not delay resuscitative care.

• In contrast, if a contaminated patient has a non–life‐threatening or serious condition, they should be decontaminated prior to definitive medical treatment.

• In a mass casualty event, individuals who are neither contaminated nor ill or injured should be instructed to go home and take a regular shower with soap and shampoo. They should bag and store their potentially contaminated clothing in a safe place.

192

65

Take‐Home Points

• 1. Effects of radiation are typically delayed

• 2. Time, distance and shielding are key

• 3. Do not delay time‐critical medical interventions in order to perform decontamination

• 4. Know Management Axioms; Medical hazards worse

• 5. Remove and bag clothing

• 6. Skin decon with soap and water

193

194

195

Types of Radiation in the Electromagnetic Spectrum

66

Toxins

1.3.7.4 Decontamination (Hazards)


Learning Objectives


1. Describe the general principles of decontamination

2. List the different types of decontamination

197

General Principals of Decon

• Avoid becoming another victim (“Don’t get DEAD”)

• Reduce exposure

– Remove from source

– Remove clothing

• Reduce absorption

– If dry DON’T wet it

– If wet make it more wet (soap and water)

• If unknown agent look for toxidrome

198

67

“Not Getting Dead”

• Starts with situational awareness

• Distance is your friend; stop and observe from afar

– Position vehicle uphill and upwind

– Look for containers, solids, liquids, visible vapors

– Look for dead things with no injuries (buzzard, not possum)

– Look for placards

• CHEMTREC System: On‐line and Round the clock 800#

• IF unknown assume the worst

199

PPE as defined by OSHA

• Level A

– Self contained environment (SCBA)

– Gases, liquids and solids

• Level B

– Self contained air supply

– Splash protection/chemical resistant clothing

• Level C

– Full faced mask with filter canister (PAPR)

– Splash protection/chemical resistant clothing

• Level D

– Bunker gear

200

201

A

B

C

D

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Hot Zone

• Life threatening levels of toxin

– Level A PPE if unknown

– Agent appropriate PPE

• Rapid evacuation from area

• Care limited to BLS measures

– Airway, hemorrhage control, antidote (PRN)

– Analogous to some principles of TCCC (LE)

202

Warm Zone

• Contamination reduction zone, upwind from hot– Min Level B if unknown

• Where clothing removed (reduce exposure up to 90%)

• Where decon takes place– Dry: brush off with non‐abrasive brush or towel

– Wet: large volume, LOW pressure, warm water

• “Solution to pollution is dilution!”

203

Cold Zone

• Support zone

• Full assessment and triage

• Staging

• Additional treatment as needed

• Transport

204

69

Patient Specific Decon

• 80% of poisonings are by ingestion

• Dermal decon

• Ocular decon

• GI decon

205

Decontamination

• 1. Remove patients from IDLH (immediate danger to life and health area)

• 2. Initiate triage

• 3. Remove clothing‐this removes ~80% of contaminants

• 4. Bag and tag removed clothing

206

Dermal‐ GENERAL Rules

• Gases and vapors low risk of secondary exposure

– Clothing may contribute to off‐gassing

• Liquids/solids

– Work head to toe copious warm water for 10‐15 min

– Do not abrade the skin!

– Avoid spread to mouth and nose mucosa, and eyes

– Wounds get additional 5‐10 min

207

70

Ocular‐GENERAL Rules

• Begin ASAP

• Irrigation with NS or LR

– Min 15‐30 min

– Caustics end point is normalization of pH

– Irrigation throughout transport (EMS)

• Direct away from medial canthus

• Don’t forget surrounding soft tissues

208

GI‐GENERAL Rules

• Charcoal use is controversial(particularly EMS)

– Ipecac is not‐ Default to DON’T

– Gastric lavage – Default to DON’T

• Where it might be useful in selected few:

– < 1 hr or delayed release product

– Life threatening amounts

• Where it is clearly NEVER

– Unprotected airway, especially with charcoal

– Caustics or hydrocarbon ingestion: Re‐injures upper airway

209

General principles

• Dry decontamination

– Removal of contaminants from the skin and clothing without use of water

• Wet decontamination

– Involves use of (soap and) water

210

71

Mass Casualty Decon

• Shower or hose victims after ‐or not‐clothing removal (especially for liquid exposures)

• Use high volume, low pressure, tepid water

• 30 secs to 3 min

– Longer may increase skin absorption

• Direct to observation for late Sx

• Secondary with soap

211

Take‐Home Points

• Avoid Hazard, Proper PPE, remove from IDLH, decon– Clothing removal results in removal of ~ 80% of contaminants

• Treatment only life threat/antidote until in cold zone

• General rules of decon : when in doubt flush it out– Dry agents: decon without water

• Mass decon 30s‐3min ASAP post clothing off if poss

• Warm zone decon tepid water, low pressure– Soap and gentle friction for liquid agents

212

Decon principles for responders

• Life‐saving interventions implemented prior to decon should be limited to airway support, hemorrhage control, and administration of appropriate antidotes

• Non‐ambulatory pts should be decon’d in this order:

– Airway, open wounds, then front and back from head to toe

213

72

Post‐decon

• Move patients to cold zone/support zone

• Full medical assessment, treatment and transport

214

Technical decon

• Deliberate, time‐consuming, 9 step technical process

• Decon of rescue personnel who may be contaminated with powders, aerosols, or liquids

• Establishment of technical decon corridor

• Water supply, soap, brushes, pools

• Once decon is complete, personnel go to warm/cold zone to remove PPE in systematic fashion to minimize chance of cross contamination

215

Emergency decon

• Responder in PPE has a suit breech or suddenly becomes ill or injured

• Quickly rinse with soap and water and then take to warm (contamination) zone‐ cold (support) zone border to remove PPE and receive medical treatment

• If technical decon area not readily accessible, use high volume water from hoses

216

73

Medical monitoring of responders

• Paramedics on scene to monitor HAZ MAT personnel

• Report to rehab officer

• Medical monitoring pre‐ and post‐entry into the hot zone for all personnel wearing PPE

217

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