Quiz 2

Acetaminophen

— levels should be obtained in all cases of reported or suspected poisoning, regardless of history and physical exam. It is readily available and patients can initially present without signs or symptoms even with toxic levels.

pregnancy test

A — should be performed in all females of childbearing age, as women may attempt suicide due to an unwanted pregnancy.

Routine urine screening for drugs of abuse

Often, this testing is requested by the receiving psychiatric facility for admission purposes, long-term care planning or diagnosis

activated charcoal

Previously, — was not routinely recommended in treatment of ingestions that occurred greater than one hour prior to presentation; however newer data regarding acetaminophen ingestions suggests that the half-life of this drug in the stomach is markedly increased in overdose settings and that there may be some therapeutic benefit to its administration past the traditional one hour mark. Other circumstances that may warrant charcoal administration past the one hour mark include massive overdoses, poisoning with sustained release preparations and ingestion of agents that slow gastrointestinal motility. or acetaminophen, it may offer some benefit when used up to four hours post ingestion.

Rumack Matthew nomogram

is a semi-logarithmic graph used in emergency medicine to assess the potential risk of liver toxicity after a single, acute acetaminophen (paracetamol) overdose

Decontamination

— should accompany stabilization of the airway, breathing and circulation. The patient should have all clothing removed and copious aqueous irrigation performed

Chromic Acid

is a strong acid that contains the hexavalent (CrVI3), or most hazardous, form of chromium. Acute skin exposure may cause burns and chronic exposure may result in skin and nasal ulcer formation. These skin ulcers are round or oval growths with reddish edges and necrotic centers and are often referred to as “chrome holes” or “chrome sores

Chromic Acid

—inhalation may be associated with upper respiratory irritation and bronchospasm, manifested by cough, chest pain and dyspnea. Pulmonary congestion visible on radiographs, interstitial pneumonia and delayed, non-cardiogenic edema have been reported.

• Renal failure secondary to acute renal tubular acidosis

• Liver damage

• Hemolysis

• Non cardiogenic pulmonary edema

Systemic effects of chromic acid exposure

Ascorbic Acid (Vitamin C)

— has been recommended for cases of ingestion and skin exposure to reduce absorption of chromium by oxidizing it from the hexavalent to trivalent form, which does not cross cell membranes as rapidly.

2 hours

Vitamin C intervention for chromium exposure should be performed within —

• Hemodialysis

• Exchange transfusion

• Chelation therapy

What therapies are ineffective for chromic acid exposure

Arsenic

It is a naturally occurring metalloid element. Acute poisoning predominantly affects the gastrointestinal system, causing nausea, vomiting, abdominal pain and diarrhea

• Severe encephalopathy

• Rhabdomyolysis

• Acute renal failure

Other systemic complications of arsenic poisoning

• crystalloid fluids

• pressor

Hypotension should be treated with —; however, — agents may be required. Fluid status should be carefully monitored, as cerebral and pulmonary edema may occur.

Arsenic

Although a symmetrical sensorimotor peripheral polyneuropathy may develop 1-3 weeks following ingestion, some patients may develop symptoms within 24 hours. Sensory symptoms usually occur first with patients complaining of “pins and needles” or electrical shock-like pains in the lower extremities.

What poisoning is this

Arsenic

Early examination may demonstrate isolated, diminished or absent vibratory sense. Motor weakness may later develop and can sometimes mimic Guillain-Barré syndrome. Reversible pancytopenia and hepatitis can occur within one week after the initial illness. Dermatologic lesions, a dry, hacking cough and Mees lines (horizontal 1-2 mm white lines on the nails) can also develop after severe acute and chronic exposures.

What poisoning is this

• Potassium

• Calcium

• Magnesium

Arsenic poisoning

• what concentrations should be maintained in the normal range and urine output should be maintained.

• lidocaine and electrical defibrillation

Arsenic poisoning

• Ventricular dysrhythmias may occur. Ventricular tachycardia and ventricular fibrillation are treated with —

• Class IA

• Class IC

• Class III

Because arsenic is associated with prolongation of the QTc, agents that prolong the QTc should be avoided (—). Bicarbonate therapy may be effective

• Unithiol

• Dimercaprol

• DMSA

Arsenic poisoning

• Chelation therapy should be initiated as soon as possible with —

airway and respiratory status

Any patient presenting with possible foreign body ingestion should have a complete assessment of his —, including pulse oximetry readings when indicated.

• Electrical discharge

• Pressure necrosis

• Obstruction/leakage of battery contents

Button battery ingestion

• Complications may occur for several reasons, including

Mercury

Systemic absorption of heavy metals from broken or fragmented batteries is a common concern but has been rarely reported. — batteries may pose a particular hazard if they break.

Endoscopy

This battery requires emergent removal because of its location in the esophagus. Esophageal injury from button batteries has been reported in less than two hours. what is the removal method of choice

• Foley catheters (risk for aspiration)

• Magnetized probes

What are other methods of battery removal

phenytoin

CNS effects are the most common symptoms of acute — ingestion.

20 mg/kg

What is the minimum oral toxic dose of phenytoin

• 10-20 mg/L,

• 20-30 mg/

• 30-40 mg/L

• 40-50 mg/L

• 50 mg/L

Phenytoin levels

• At levels — mild nystagmus may be present

• At levels between —L nystagmus is common, and ataxia may occur.

• At levels between —patients often develop ataxia and slurred speech.

• At levels between —patients may develop lethargy, confusion and combativeness.

• At levels above — patients also develop choreoathetoid movements and opisthotonic posturing

albumin

In some instances, the patient's serum phenytoin level may seem discordant with their symptoms. In these situations, a serum — level might be helpful as higher free phenytoin concentrations are seen in the setting of hypoalbuminemia.

gingival hyperplasia

Patients on long term phenytoin therapy can develop —, which is the most common adverse effect in adults and children

Phenytoin encephalopathy

chronic phenytoin toxicity may result to

isopropanol

The major effects of acute — ingestion are on the central nervous system, mimicking the inebriation caused by ethanol, and gastrointestinal systems. The usual signs and symptoms include CNS depression, slurred speech, ataxia, lethargy, weakness, nausea and headache

isopropyl alcohol

Death from — use is rare but can occur secondary to coma with untreated airway compromise, injury resultant from ataxia or stupor, or rarely, hypotension caused by vasodilation and possible myocardial depression after massive overdose.

• 250 mL

Isopropanol

• Some sources give an estimated lethal dose of — in adults; however with treatment, adults and children have survived much larger ingestions.

• methanol

• ethylene glycol

Isopropanol toxicity

• Initial management should be focused on stabilizing the airway, breathing and circulation. If exposure is by the cutaneous route, skin decontamination should be extensive as significant absorption and toxicity can occur, especially in infants. It is important to ensure that no — or — were coingested

100 mg/dL

Serum isopropanol levels are mostly used to substantiate the diagnosis and treatment is supportive. Levels greater than — can cause a decreased level of consciousness.

hemodialysis

Rarely, — is needed for massive ingestions. It effectively removes isopropyl alcohol and acetone from the circulation. Indications for it include isopropanol levels exceeding 400-500 mg/dL, renal failure, hypotension and coma in patients unresponsive to supportive care (intravenous fluids or vasopressors).

• Euglycemia

• Ketosis

• Little or no acidosis

• Increased osmolality

It is crucial to differentiate isopropyl alcohol poisoning from that of ethylene glycol or methanol, as the latter are more dangerous. Characteristic laboratory findings include

acetone

Isopropanol is metabolized by alcohol dehydrogenase to —, which can worsen CNS depressant effects and accounts for the marked ketosis seen in these patients

anion gap metabolic acidosis

Isopropanol can be distinguished from methanol and ethylene glycol because it does not produce an elevated —

Methanol

— can be found in multiple industrial products, including antifreeze, solvents, disinfectants, de-icing solutions, windshield wiper fluid, and fuels. Exposure by ingestion is associated with the most negative effects, while cutaneous and inhalational exposures rarely cause toxicity.

• inebriation and gastrointestinal discomfort.

Methanol toxicity

• The initial effects of methanol are —

formic acid

Methanol

• Due to metabolism of the parent alcohol to —, a potent and specific neurotoxin, patients develop edema of the optic nerve with resultant visual changes, and ultimately, permanent blindness.

afferent papillary defect

An — is an ominous sign in methanol poisoning. A funduscopic exam may reveal disc hyperemia and papilledema.

True

True or false

• Methanol itself is of limited toxicity, but its metabolites produce toxicity. If methanol exposure is suspected, a stat blood level should be obtained.

• ethanol

• fomepizole

Methanol toxicity

• In any patient who has ingested more than a sip, has a metabolic acidosis and/or an osmolal gap, ADH inhibiting therapy with — should be started immediately. The agent of choice is generally institution specific but a knowledge of each is important

Ethanol

—, in sufficient concentrations, (greater than 100 mg/dL), competitively inhibits the formation of the toxic metabolites, as it has a greater affinity for ADH than methanol. This allows the unchanged parent alcohol (methanol) to be excreted by the pulmonary and renal routes

Fomepizole

It also has higher affinity for alcohol dehydrogenase than methanol and as such acts similar to ethanol to prevent the formation of toxic metabolites. It is becoming the antidote of choice in most institutions.

hemodialysis

After ADH blocking therapy, the elimination of methanol via the pulmonary and renal routes becomes first order and is drastically slowed (t 1/2 of approx 48 - 54 hours). Because of this, non-emergent — is generally performed to remove methanol and avoid the excess cost associated with prolonged hospital stays and prolonged use of ADH inhibitors

folic acid

Methanol toxicity

• Cofactor therapy with — is sometimes used to expedite elimination of formic acid, which is partially dependent on tetrahydrofolate.