Environmental Toxicology Flashcards by Kris Dobie

Hypothermia

hypothalamus controls thermoregulation

Heat conservation
…Peripheral vasoconstriction (less heat conduction to skin), adding clothing

Heat production
…shivering, increasing thyroxine and epinephrine.

Affects almost every system, but mostly…
Cardiovascular system and CNS

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Hypothermia Cardiovascular effects

Decreased depolarization of pacemaker cells in heart, resulting in bradycardia.

Bradycardia refractory to standard tx

MAP and Q decrease
Osborn (J) waves
…Height of wave = degree of hypothermia.

Atrial/ventricular arrhythmias.
V-fib and asystole spontaneously at core temp ~28C.

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Hypothermia CNS effects

Decreased metabolism (decreased oxygen consumption)

Core temp <33C
abnormal electrical activity

Core temp <20
EEG may show brain death

“Core temp after drop”
Occurs after rewarming has begun and cooler blood from extremities is circulated back to the core, causing patient decline.

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Hypothermia classes (mild)

Core temp 32-35C (89.6-95F)
Vigorous shivering
Possible altered judgment, dysarthria
Possible increased RR
Ataxia/apathy as temp decreases
Tachypnea/tachycardia
Cold diuresis (more renal blood flow)

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Hypothermia classes (moderate)

Core temp 28-32C (82-90F)
O2 consumption decreases
Further CNS depression
Possible stupor
Loss of shivering
Arrhythmia risk increases
Bradycardia worsens - Q reduces
Dilation of pupils
Paradoxical undressing

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Hypothermia classes (severe)

Core temp <28C (82.4F)
Susceptible to v.fib
Decreased myocardial contractility
Comatose
Pulmonary edema
Oliguria
Hypotension
Decreased/absent EEG activity

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Hypothermia treatment goals

Prevent further heat loss
Rewarm core temp
Avoid arrhythmias

Avoid excessive movement and NGT placement as they increase risk of v.fib.

Cardiac pacing and atropine are often ineffective

Typically don’t treat hyperglycemia in hypothermic patients

Hold meds if possible until warmer

Apply heat carefully

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Hyperthermia

Life-threatening condition characterized by failure of the body to regulate or dissipate heat.

Core team >38.5C (101.3F)

Heat produced endogenously or acquired from environment.

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Hyperthermia - heat cramps

Mildest form of heat illness, normal core temp.
causes painful cramps/spasms
flushed, moist skin.
Normally occurs during or after intense exercise/sweating

Treatment:
move to a cool place
remove excess clothing
hydration
stretching

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Hyperthermia - heat exhaustion

Core temp >38C (100F)

Muscle cramping
pale, moist skin
N/V/D
HA
Fatigue, weakness
Faint feeling

Treatment:
Same as with heat cramps
Humidified O2
Cool IVF (NS or LR)
Check glucose and treat as needed

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Hyperthermia - heat stroke

Core temp >40C (104F)

Life threatening, causing cell death

Hot, dry skin
Rhabdomyolysys
renal failure
Worsening CNS sx.
Oxygen demand exceeds supply

Treatment
Same as heat exhaustion
Initial rapid active cooling
Body temp should be lowered to 102
Remove pts clothing and cover with sheets soaked in room temp water or saline
Manage airway if needed

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Malignant Hyperthermia

Hypermetabolism involving skeletal muscle

Caused by the release of calcium into muscle fibers, causing sustained contraction due to depolarization.

Leads to muscle rigidity and excessive heat production.

Leads to increasing CO2 production and accelerated O2 consumption

Activation of sympathetic NS

Hyperkalemia

Can lead to DIC and multi-organ dysfunction

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Malignant Hyperthermia Symptoms

Trismus
increasing EtCO2
mixed acidosis
Rhabdomyolysis
Truncal or extremity rigidity

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Malignant Hyperthermia Treatment

Dantrolene sodium - 2.5 mg/kg, repeat until sx stop up to max of 20 mg/kg.
Cool if temp >39C
Treat dysrhythmias per ACLS guidelines
Never give calcium channel blockers with dantrolene sodium.

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Drowning

Most contributing factors are hypoxemia and acidosis

Liquid causes involuntary layngospasm initially.

Leads to inability to breath air.

Drop in PaO2 releases laryngospasm

Panic and hyperventilation can lead to increased aspiration.

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Pulmonary effects of drowning

Impaired gas exchange
pulmonary vasoconstriction
Freshwater vs saltwater: no difference in initial treatment.
Fluid-induced bronchospasm
pulmonary hypertension

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Drowning treatment

Airway management
Early intubation and PEEP application
CPAP/BiPAP in cooperative patients

ECMO

Volume expansion when indicated

NGT placement

Possible bronchoscopy

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Snake bites

2 types of poisonous snakes in US

Pit vipers, which include:
rattlesnakes, cottonmouths, copperheads
Cytotoxic and hemotoxic enzymes
Immediate pain, swelling, bleeding, vomiting, hypotension

Coral snakes (southeastern US)
neurotoxic enzymes
Minimal early signs but within 6 hrs: paresthesias, dysphagia, respiratory depression, blurred vision.

Snake bite envenomation

Mild
No signs of systemic toxicity

Moderate
Severe local pain, edema larger than 12 inches surrounding wound, systemic toxicity including N/V

Severe
Generalized petechiae, ecchymosis, blood-tinged sputum, hypotension, hyper perfusion, renal dysfunction, PT/PTT changes

Snake bite treatment

Immobilize as much as possible
Airway, ventilatory, and circulatory support
Monitor for systemic reaction
Antivenin for severe toxicity (to neutralize toxins). Monitor for anaphylaxis.

Consider anxiolytic to keep pt calm and decrease circulation of venom

Do not use compression devices.

Need to know how much time has elapsed since bite occurred, mark area of bite.

Hydrofluoric acid toxicity

H+ ions cause initial superficial burns (may not appear to be dramatic)

Fluorid penetrates the underlying tissues, causing necrosis

Strong reaction with calcium and magnesium - rendering them neutral.

Caustic ingestions or exposures

Cause tissue injury by altering state of molecules and covalent bonds.

H+ ions cause majority of effects in acids

OH- (hydroxide) ions cause majority of effects in alkalines

Acidic exposure

Cell death occurs from coagulation necrosis.
Formation of eschar
>4” should be admitted for evaluation
May protect underlying tissue from further damage.

Alkaline exposure

Cell death occurs from disruption of cell membranes
…liquefaction necrosis
Ongoing penetration into tissues.

Caustic ingestions treatment

Airway control DO NOT administer emetics (may expose esophageal mucosa to more toxin) Gastric lavage contraindicated NGT suctioning (may reduce toxin exposure to small bowel) Activated charcoal contraindicated Supportive care ...antibiotics, PPIs, pain management

**Acetaminophen toxicity**

Common overdose substance in adults Ingestion of 7.5g or 150mg/kg is toxic 4 phases of acetaminophen toxicity Phase 1: 0-24 hrs Phase 2: 24-72 hrs Phase 3: 72-96 hrs Phase 4: 4 days - 3 weeks

Acetaminophen toxicity phase 1

0-24 hrs May be asymptomatic or report N/V, anorexia, malaise, pallor, diaphoresis Subclinical rise in transaminase levels begins approximately 12 hrs after acute ingestion

Acetaminophen toxicity phase 2

RUQ pain/tenderness, anorexia, N/V, tachycardia, hypotension Continued rise in transaminase Increased liver enzymes, serum bilirubin and PT Oliguria as a result of acute tubular necrosis (ATN)

Acetaminophen toxicity phase 3

72-96 hrs. Most dangerous phase N/V abdominal pain, tender hepatic edge jaundice, hepatic encephalopathy coagulopathy (DIC), hypoglycemia, Death due to fulminate hepatic necrosis Peak for liver function abnormalities

Acetaminophen toxicity phase 4

4 day - 3 weeks Complete resolution of symptoms and organ failure

Acetaminophen toxicity treatment

N-acetylcisteine (NAC) When to give: >140mcg/kg at 4 hrs >70 mcg/kg at 8 hrs GI decontamination (activated charcoal)

Aspirin toxicity

Phase 1: Hyperventilation (resp alkalosis) Alkaluria (potassium and bicarb excreted in urine. Phase 1 may last up to 12 hrs. Phase 2: Continued resp alkalosis switching to metabolic acidosis with paradoxic acuduria due to potassium loss from kidneys. Lasts 12-24 hrs. Phase 3: Dehydration, hypokalemia, and progressive metabolic acidosis. Phase 3 may begin 24 hrs after ingestion.

Aspirin toxicity symptoms

N/V Diaphoresis tinnitus vertigo hyperventilation, tachycardia Depressed DTRs

Aspirin toxicity treatment

GI decontamination (activated charcoal) Sodium bicarbonate Gastric, systemic, and urinary alkalinizer ...1-2 mEq/kg LR or NS for urinary excretion and alkalinization. ...10-20 mL/kg/hr until urine output = 1mL/kg/kr. Ventilatory support Prevent acidemia via hyperventilation Ve - 240 mL/kg/min

Beta blocker toxicity symptoms

Bradycardia, hypotension Hypothermia Arrhythmias Hypoglycemia Seizures May see respiratory compromise can range from asymptomatic to shock

beta blocker toxicity treatment

Fluid resuscitation (20 mL/kg) inotropes and chronnotropes Glucagonn 5mg IVP milronone 200 mcg/kg gastric lavage cardiac pacing / CPR Insulin - high dose (1U/kg bolus, 1-10 U/kg/hr)

Calcium channel blocker toxicity

Verapamil, nifedipine, diltiazem, amlodipine Symptoms: Hypotension, bradyarrhythiias, hyperglycemia, potential for cardiac arrest. Treatment: Gastric decontamination Calcium loading glucagon, insulin Atropine vasopressors cardiac pacing

Digitalis / digoxin

Used in tx of CHF, afib Narrow therapeutic level (0.5-2 ng/mL) Yellow oleander and foxglove are plants with cardiac glycoside toxicity (mimics digitalis toxicity) Digitalis toxicity symptoms Yellow-green visual aberration PVCs, bradyarrhythiias, VTach, heart blocks EKG changes Treatment: Digibind Gastric lavage, activated charcoal Tx of electrolyte imbalances Antidysrhythmics ...NO quinidine, procainamide, or calcium Temporary pacing for blocks Cardioversion only if absolutely necessary

**Toxin / antidote chart**

Carbon monoxide: Oxygen Cyanide: Amyl nitrate Na thiosulfate Organophosphates: Atropine, 2-PAM Methemoglobinemia: Methylene blue Anticholinergic: Physostigmine Coumadin: Vitamin K, FFP Heparin: Protamine sulfate Beta blockers + CCB: Glucagon, calcium

In fire victims, increased respiratory distress and coughing after administration of high flow oxygen could be caused by?

cyanide ...Cyanide is found in everyday items such as insulation, furniture coverings, and carpets which can release cyanide if they catch fire.

In hypothermia, withheld meds until core temp reaches?

30C (86f)

**What acid-base imbalances would you anticipate in salicylate toxicity?**

Respiratory alkalosis and metabolic acidosis. salicylate toxicity results in stimulation of the respiratory center in the brain leading to hyperventilation, which leads to respiratory alkalosis early. AND...As toxicity worsens, there is a loss of potassium which eventually leads to metabolic acidosis.