Poisoning & Environmental Exposure Flashcards
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
What should physicians monitor for in caustic ingestion
Peritonitis and mediastinitis . . potential esophageal and stomach ulceration
- hyperthermia
- mydriasis (pupil dilation)
- delirium
- urinary retention
- decreased bowel sounds
- dry mouth
Anticholinergic toxicity
- CNS depression
- Cardiac arrhythmias
- hypotension
- anticholinergic signs (hyperthermia, flushing, dilated pupils, decreased bowel sounds, urinary retention)
TCA poisoning
- Headache
- vomiting
- abdominal pain
- flushed skin
- inhalational exposure causes a bitter almond odor
- highly lethal
cyanide
- AMS
- Ataxia
- Slurred speech
alcohol
- Bradycardia
- miosis (constricted pupils)
- bronchorrhea
- muscle fasciculations
- salivation
- lacrimation
- diarrhea
- urination
Organophosphate poisoning . . Acetylcholinesterase is rendered non-functional leading to cholinergic excess
What counteracts the effects of organophosphate poisoning and should be given immediately?
- Atropine
- It acts by competing with acetylcholine at the muscarinic receptors
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
Obtaining an emergent ECG and analyzing the QRS complex is critical in what overdose
TCA
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)
What may develop with benzo ovedose is coingested with opioids or alcohol or when they are administered IV
Respiratory depression
- tremor
- hyperreflexia
- ataxia
- seizures
- vomiting
- diarrhea
Lithium toxicity
- sedation
- respiratory depression
- Miosis (constricted pupils)
opioid intoxication
- horizontal nystagmus
- cerebellar ataxia
- confusion
phenytoin
- HTN
- tachycardia
- hyperreflexia
- clonus
- agitation
Serotonin syndrome in the setting of serotonergic drug use (eg, coprescription of antidepressant and triptan)
- 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
how do you diagnosis carbon monoxide poisoning
obtaining carboxyhemoglobin levels
treatment of carbon monoxide poisoning
hyperbaric oxygen administration
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
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
- Garlic breath
- vomiting
- Watery diarrhea
- QTc prolongation
ACUTE arsenic poisoning
- Hypo/Hyperpigmentation
- Hyperkeratosis
- Stocking-glove neuropathy
CHRONIC arsenic poisoning
What is the mechanism of Arsenic poisoning
- Binds to sulfhydryl groups
- Disrupts cellular respiration and gluconeogenesis
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
