Poisoning & Environmental Exposure Flashcards by Garrett Gilbert

Ingestion of this leads to damage of the tissue lining the GI tract, manifested by necrosis, edema, scarring and severe pain. A white tongue, heavy salivation, and dysphagia are results of this process. Severe esophageal and stomach ulceration may also occur . . . NO ALTERATION in CONSCIOUSNESS

Caustic ingestion

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What should physicians monitor for in caustic ingestion

Peritonitis and mediastinitis . . potential esophageal and stomach ulceration

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hyperthermia
mydriasis (pupil dilation)
delirium
urinary retention
decreased bowel sounds
dry mouth

Anticholinergic toxicity

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CNS depression
Cardiac arrhythmias
hypotension
anticholinergic signs (hyperthermia, flushing, dilated pupils, decreased bowel sounds, urinary retention)

TCA poisoning

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Headache
vomiting
abdominal pain
flushed skin
inhalational exposure causes a bitter almond odor
highly lethal

cyanide

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AMS
Ataxia
Slurred speech

alcohol

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Bradycardia
miosis (constricted pupils)
bronchorrhea
muscle fasciculations
salivation
lacrimation
diarrhea
urination

Organophosphate poisoning . . Acetylcholinesterase is rendered non-functional leading to cholinergic excess

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What counteracts the effects of organophosphate poisoning and should be given immediately?

Atropine

- It acts by competing with acetylcholine at the muscarinic receptors

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Management of Organosphosphate poisoning

Atropine immediately
Of equal importance is the immediate removal of the patients clothing (since it is soaked with vomitus) to prevent continued absorption of organophosphates through the skin

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Obtaining an emergent ECG and analyzing the QRS complex is critical in what overdose

TCA

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Slurred speech, unsteady gait, and drowsiness are consistent with a benzodiazepine overdose (also alcohol). In the absence of coingestion, this typically presents with what vital signs and pupillary size

Normal vital signs

- Normal pupillary size (2-4 mm in bright light)

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What may develop with benzo ovedose is coingested with opioids or alcohol or when they are administered IV

Respiratory depression

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tremor
hyperreflexia
ataxia
seizures
vomiting
diarrhea

Lithium toxicity

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sedation
respiratory depression
Miosis (constricted pupils)

opioid intoxication

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horizontal nystagmus
cerebellar ataxia
confusion

phenytoin

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HTN
tachycardia
hyperreflexia
clonus
agitation

Serotonin syndrome in the setting of serotonergic drug use (eg, coprescription of antidepressant and triptan)

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headaches
nausea
vomiting
abdominal discomfort
confusion
coma
Pinkish-red skin hue

Carbon monoxide . . colorless, odorless gas emitted by automobiles, furnaces and charcoal grills
-When inhaled, it prevents the body’s tissues from utilizing oxygen effectively

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how do you diagnosis carbon monoxide poisoning

obtaining carboxyhemoglobin levels

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treatment of carbon monoxide poisoning

hyperbaric oxygen administration

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The symptoms of cyanide inhalation can be similar to those of carbon monoxide exposure, so the history is very important . . what is the difference in history and what clinical clue can help distinguish cyanide poisoning

Burning of rubber or plastic . . . NOT WOOD

- Bitter almond breath

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This presents with many similarities to carbon monoxide poisoning and it can be induced by certain drugs and environmental exposures. . . . it presents with bluish discoloration of skin and mucous membranes

Methemoglobinemia

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Garlic breath
vomiting
Watery diarrhea
QTc prolongation

ACUTE arsenic poisoning

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Hypo/Hyperpigmentation
Hyperkeratosis
Stocking-glove neuropathy

CHRONIC arsenic poisoning

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What is the mechanism of Arsenic poisoning

Binds to sulfhydryl groups

- Disrupts cellular respiration and gluconeogenesis

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Sources of arsenic

- Pesticides/insecticides - Contaminated water (often from wells) - Pressure-treated wood

Treatment of Arsenic poisoning

- Dimercaprol (British anti-Lewisite) | - DMSA (meso-2,3-dimercaptosuccinic acid, succimer)

patient who is routinely exposed to antique wood, has polyneuropathy, pancytopenia, and mild transaminase elevation, and a variety of skin lesions

Chronic arsenic toxicity

what finding on nails are characteristic of arsenic poisoning

Mees lines (horizontal striation of fingernails)

How is diagnosis of arsenic toxicity made

- History - PE - Measurement of urine arsenic levels

Acute attacks of this are triggered by a number of factors and are associated with patchy sensorimotor neuropathy and autonomic dysfunction. Severe abdominal pain is typical

Acute intermittent porphyria . . caused by a partial deficiency of porphobilinogen deaminase, an enzyme involved in heme synthesis

This can lead to sensorimotor neuropathy in a stocking-glove distribution along with microcytic anemia. Although the neuropathy is similar to arsenic toxicity, GI complaints are typical and skin changes are NOT usually seen

Chronic lead poisoning

Describe the management of TCA antidepressant overdose

- Supplemental oxygen, intubation - IV fluids - Activated charcoal for patients within 2 hours of ingestion (unless ileus present) - IV sodium bicarb for QRS widening or ventricular arrhythmia

Describe the pathophysiology of TCA overdose causing cardiac toxicity

- TCAs inhibit fast sodium channels in the His-Purkinje system and myocardium - This decreases conduction velocity, increases duration of repolarization, and prolongs absolute refractory periods - This results in hypotension, QRS prolongation, and Ventricular arrhythmias (eg, Vtach, Vfib)

QRS interval > 100 msec in the setting of TCA overdose is an indication for sodium bicarb therapy. Describe the mechanism behind how this helps

- Increased serum pH and extracellular sodium - Increased pH (goal 7.50-7.55) decreases drug avidity for sodium channels - Elevate extracellular sodium concentration increases the electrochemical gradient across cardiac cells and affects the ability of TCSs to bind to fast SODIUM channels

Describe the mechanism by which sodium bicarb helps in aspirin overdose

Urine alkalinization increases salicylate excretion

Treatment of acute opioid intoxication

- Naloxone (may need repeated dosings) - Airway management and ventilation - Exclude other AMS causes (eg, hypoglycemia)

Describe the clinical findings of Frostbite

- Superficial pallor and Anesthesia - Blistering, eschar formation - Deep tissue necrosis and mummification

Management of frostbite

- Rapid rewarming in 37-39 C (98.6 - 102.2 F) WATER bath - analgesia and wound care - Thrombolysis in severe, limb-threatening cases

This is used to reverse life-threatening delirium caused by anticholinergic agents (eg, atropine, diphenhydramine)

Physostigmine

What are used to treat seizures due to TCA overdose

Benzodiazepines

Management of Caustic ingestion

- Secure ABCs - Decontamination: remove contaminated clothing and visible chemicals; irrigate exposed skin - Chest x-ray if respiratory symptoms - Endoscopy within 24 hours

This can decrease systemic absorption of poisons and is used for many types of toxic ingestions

Activated charcoal

Miosis and acute opioid intoxication

Many do have miosis, but its absence does not exclude the diagnosis. -Normal or even enlarged pupils may be seen in patients who have co-exposures to other agents that conteract miosis (eg, methamphetamine)

This is an alternate opioid agonist used in long-term management of opioid addiction, but it is not useful in acute intoxication

buprenorphine

Hypothermia and acute opioid intoxication

Hypothermia results from environmental exposure and impaired themogenesis and can occur even at room temperature in severely intoxicated patients

This is administered in cases of beta blocker intoxication, which presents with bradycardia and hypotension

Glucagon

What is the most reliable and predictive sign of opioid intoxication

Decreased respiratory rate

Patient brought to emergency department 2 hours after ingesting a potentially toxic dose (single dose of > 7.5 g) of acetaminophen. Describe the progression of Acetaminophen intoxication

- in early stage can by asymptomatic (first 24 hours) or may have only nonspecific symptoms such as nausea, vomiting, and anorexia - After 24 hours, patients may develop severe liver injury

Describe the management of Acetaminophen toxicity

- Intitial management should be focused on gastric decontamination with activated charcoal if the patients presents within 4 hours of ingestion - Acetaminophen levels should be obtains at same time - The Rumack-Matthew nomogram provides the likelihood of hepatotoxic effects of acetaminophen overdose after a single ingestion based on plasma levels . . used to guide administration of N-acetylcysteine in patients with dangerous levels . . first point begins at 4 hours

Methanol's immediate effects are similar to those of alcohol, causing disinhibition. However, within 24 hours of ingestion, methanol can lead to headache, nausea, vomiting, and epigastric pain. What is the most severe consequence of methanol intoxication?

- vision loss | - coma

Physical exam and labs in methanol poisoning

- Optic disc hyperemia - Anion gap metabolic acidosis - Increased osmolar gap is often seen as well

Normal anion gap

8-12

Ethylene glycol and methanol poisoning share similarities. Both are sometimes ingested as a substitute for ethanol and both can cause anion gap metabolic acidosis and inceased osmolar gap . . describe the difference in damage organs?

- Methanol damages eyes | - Ethylene glycol damages kidneys

this presents with anion gap metabolic acidosis along with Tinnitus, fever, and hyperventilation

Aspirin overdose

what dipstick and UA finding is consistent with Rhabdomyolysis

-Large blood on dipstick with no RBCs by microscopy

uncontrolled efflux of calcium from the sarcoplasmic reticulum is the underlying pathophysiology of what?

malignant hyperthermia

Inadequate sodium and water replacement during physical activity can lead to head EXHAUSTION (not stroke) because of the body's inability to maintain what?

- adequate cardiac output - Core body temp is usually < 40 C (104 F) - Significant CNS dysfunction (eg, seizure, delirium) is NOT present

All patients with smoke inhalation should be suspected for this and treated with what?

- Acute carbon monoxide poisoning | - 100% oxygen via a nonrebreather facemask

What are the early symptoms of CO poisoning

typically neurological and include agitation, confusion, somnolence

These are the proper antidotes for patients with anticholinesterase toxicity, as seen in organophosphate poisoning. These patients presents with cholinergic toxicity characterized by bradycardia, miosis, and salivation

Atropine and pralidoxime