Remove Exposed Clothing-throw away it is very hard to remove the chemicals from clothing.

Wash patient with soap and water-wash time required depend on toxin

When you send the patient home DO NOT put the chemical soaked clothing back on them

Flush eyes with water or saline

Minimum time required is 10 min

Morgan lense is used in ER

Emesis with syrup of ipecac:

•  Use is declining
• Two alkaloids- works locally and centrally
• Only useful is used within 30-60 min of exposure
• Removes 20-30% of gastic contents at time of administration
• Takes 20-30 min to work
• 2+ emetic episodes over 1-2 hours
• Adverse Effects: persistent vomiting, aspiration

Gastric Lavage

• Only useful in older children and adults
• Only useful if used within 30-60 min after exposure
• Removes about 25-35% of gastric contents
• Adverse effects: vomiting, aspiration
• Not extremely useful, used less frequently

Whole Bowl Irrigation (WBI)

• Gastric administration of 1-2 liters of mixed electrolyte solution
• Golytely often used
• Given orally or NG tube
• Useful for slowly absorbed materials including sustained release products, iron preparations and drug packets
• Often used with activated charcoal
• Adverse effects: fluid/electrolyte imbalance-due to fluid loss

Activated Charcoal

• Charcoal is made with a very large surface area
• Admin usually 1 g/ kg of weight
• Supplied as a dry powder or a slurry in water or sorbitol solution (cathartic)
• Abs most toxins except:
• Metals (Pb, Li, Fe)
• Low molecular weight alcohols/glycol- methanol
• Aliphatic hydrocarbons- gas, kerosene  
• Caustics
• Can bind (remove) up to 90% of toxin in stomach
• Often used in conjunction with lavage or WBI
• Adverse effects: constipation, vomiting, aspiration
• Must confirm placement in stomach and not lungs

Cathartic

Supportive

• Seizures and cardiac toxicity are treated with usualy therapeutic maneuvers

Antidote

• N-acetylcysteine for acetaminophen
• Ethanol or 4-methylpyrazole for methanol and ethylene glycol
• Chelators for metals
• 2-PAM and atropine for organophosphates
• Digibind for digitalis glycosides

Extracorporeal Removal

• Hemodialyis
• Peritoneal dialysis
• Hemoperfusion (charcoal)
• Ultra filtration techniques
• Uncommonly used
• Useful for: methanol, ethylene glycol, salicylate, theophyline, lithium

• Lead poisoning is the most common PREVENTABLE public health problem affecting children in the industrialized world
• The human body has NO lead requirement
• Seen all over the world

Old Pain (pre-1977)

Gasoline (phased out in 1970-1980)

Ceramic glazes

Crystals

Batteries

Solder

Ethnic Medicinals (lead has a sweet taste)

Bullets-retained in body and leeches lead out

Absorption

• Rapid absorption of vapor from lungs
• Slow, partial and saturable absoprtion from small bowel

Distribution

• Distributes rapidly into soft tissue and bone
• Half life in plasma and soft tissue: 35-40 days
• Retained in bone: Half life 30-40 years
• Total body burden increases with age

Elimination

• 75% in urine
• 25% in bile, sweat, nails, hair

• Binds to nucleophilic groups (SH, NH, CO₂H)
• Enzyme inhibition
• Damages to cell membrane
• Inhibits Na/K ATPase
• Acts as calcium substitue and functions as a second messenger
• Activates protein kinase C altering neural cell development
• Alters neural cell adhesive moleule leading to poor development of neural cell interactive pathways

Anorexia

Irritability

Coma

Seizures

Neurodevelopmental defects in children

Decreased IQ

Behavorial problems (ADHD, ODD)

Abdominal Pain

Constipation

Nausea/Vomiting

Metallic taste

Anemia-with basophillic stippling

Hypertension

Limb pain

Reproductive problems-spontaneous abortion, decreased sperm counts

Bradycardia

Blood lead level (mg/dl)

X-ray fluorescence of bone for total body burden (research tool)

X-ray of bone (lead lines) or abdomen (paint chips)

Delta-aminolevulinic acid in blood

Coproporphyrins in urine

• Treatment does not reverse neurologic injury
• Chelation
• BAL
• EDTA
• 2,3-dimercaptosuccinic acid (DMSA or succimer)
• D-penicillamine

Primary- identify and remove sources before exposure occurs.  Most resources are spent on primary prevention

Secondary- screen at risk populations and remove children from ptential exposures

Tertiary- treat identified cases

Organophosphates

Carbamates

Organochlorines

Chlorphenols

Pyrethrins

Arsenicals

Fumigants

Cholinesterase Inhibitors (Organophosphates and Carbamates)

Routes of Exposure

Ingestion

Dermal exposure

Respiratory exposure

Cholinesterase Inhibitors (Organophosphates and Carbamates)

Mechanism of Toxicity

• Inhibits acetylcholinesterase
• Acetylcholinesterase normally cleaves acetylcholine once it is released from neuroreceptors
• Organophosphates are irreversible inhibitors of bot acetylcholinesterase and pseudo-cholinesterase
• Carbamates reversibly inhibit acetylcholinesterase and pseudo-cholinesterase
• Clinical symptoms are caused by accumulation of acetylcholine at nerve junctions

Life Threatening symptoms are respiratory failure and cardiac dysfunction and seizures

Cardiac dysfunctions: Bradycardia or tachycardia, rare a-fib, ventricular tachycardia

Salivation

Lacrimation

Urinary incontinence

Defecation

GI-diarrhea

Emesis

+ Miosis

or

Diarrhea

Urinary incontinence

Miosis

Bronchospasm

Emesis

Lacrimation

Salivation

Levels of acetly or pseudo cholinesterase generally correlated with the severity of symptoms but are not readily available

• Stabilization
• Decontamination
• Atropine- works by blocking the acetylcholine receptor at the nerve ending
• Organophosphates
• Carbamates
• 1st line treatment
• Large and repeated doses are needed
• Pralidoxime (2-PAM)-works by reversing the binding of organophosphate to cholinesterases
• May also have some atropine like action
• Chemically degrades some organophosphates
• NOT used to treat Carbamate
• Used early on b/c organophosphate irreversibly binds over time

Organocholrine Compounds

Routes of Exposure

DDT, Chlordane, and Lindane

Ingestion

Dermal exposure

Inhalation exposure

These agents affect the brain by interfering with axonal transmission.

Myocardial irritability

Stimulate hepatic enzymes

• CNS-behavioral changes, sensory disturbances, involuntary muscle activity, seizures
• Cardiac- dysrhythmias
• Liver and kidney damage
• Rashes
• Carcinogenicity

• Symptomatic after appropriate decontaminatin
• Cholestyramine has been used following large acute exposures to increase clearance of these agents
• All of these agents are lipophilic and accumulate in body fat.  Fat levels are more indicative of exposures than serum levels and often remain elevated for very long periods after exposure.

Chlorophenols

Routes of Exposure

Agents: Pentacholorphenol (PCP)- used as a herbicide, wood preservative, germicide, fungicide, and molluscicide

Dermal

Ingestion

Chlorophenols

Mechanism of Toxicity

PCP is an irritant to mucous membranes

Uncouples oxidative phosphorylation leading to stimulation of cellular oxidatvie metabolism

Chlorophenols

Signs and Symptoms

• Skin/Mucous membranes- ittitation, contact dermatitis
• CNS- headache, weakness, fever, sweating, decreased alertness, thirst
• Cardiac- tachycardia
• GI- abdominal pains, nausea

Chlorophenols

Treatment

• First isolated from chrysanthemums
• Most are now made synthetically
• Mechanism- Pyethrins paralzye the nervous system of insects but have limited effects in humans
• Signs and Symptoms- Idiosyncratic allergic reaction

• Large number of cmpds usually gasses or liquids, bubbled into the soil prior to planting to eliminate a variety of pests.
• Methylbromide, ethylene oxide, carbon disulfide, formaldehyde, phosphine, and various chlorinated and brominated hydrocarbons
• Mechanism of Toxicity-cmpds act by a variety of mechansims
• Irritants to the mucous membranes most notable in the lung
• Many are CNS depressants
• Signs and Symptoms- Variable
• Respiratory distress
• GI irritation
• CNS depression
• Methyl bromide and carbon disulfide are capable of causing long lasting or permanent neurological damage
• Treatment- Remove exposure, decontamination and supportive care

• In therapeutic doses abs is rapid, reaching a peak in 30-120 min
• Abs may be delayed in overdose, therefore blood levels should not be drawn before 4 hours
• Most of the drug is metabolized in the liver to a non-toxic metabolites by glucuronidation or sulfation.
• A small percentage is metabolized by the cytochrome P450 mixed function oxidase to an active intermediate: N-acetly-p-benzoquinone-imine (NAPQI)
• Under normal circumstances NAPQI is detoxified by glutathione
• In overdose glutathione is depleted and the active intermediate binds to hepatocytes causing hepatic necrosis
• Normal half-life of acetaminophen is 2-3 hours

• Live is the primary organ effected by toxicity
• Renal damage may occur, in general in conjunction with hepatic failure
• Myocardial damage and pancretitis have also been reported

• 0-24 hours
• Symptoms are often absent
• May see anorexia, nausea, pallor, vomiting, diaphoresis, lethargy
• Coma and metabolic acidosis have been reported rarely in severe cases

• 24-72 Hours
• Initial symptoms when present become less pronounced
• Right upper quadrant pain may be present
• Chemical evidence of hepatic dysfunction
• ↑ AST
• ↑ ALT

• 72-96 hours
• Frank hepatic failure develops with characteristic effects such as encephalopathy and coagulopathy

• 4 days - 2 weeks
• Recovery Phase
• In those that recover, long-term hepatic sequelae are unlikely

In general children are less likely to develop toxicity than adults (etiology? different metabolism?)

• In acute ingestions acetaminophen levels should be drawn > 4 hours post-ingestion
• Nomogram is used with acute ingestions only
• Nomogram has two line.  There is potential for toxicity if the acetaminophen level falls above the line. Treatment is recommended if the level falls on or above the lower line. The lower (dotted) line represents a 25% allowance for errors in estimates of time of ingestion,
• Silent killer-consider obtaining acetaminophen levels in all overdose situations.  

• Mechanisms of action of N-acetylcysteine (NAC) (antidote) is inclear- enhances glutathione stones? Anti-oxidant effect?
• NAC is most effective when given within 8 hours of ingestion but may be of benefit up to 224 post-ingestion. In selected cases use after 24 hours post-ingestion may be advisable
• IV- NAC approved for use in 2004- 21 hour course of IV
• Oral NAC- 140 mg/kg loading dose, followed by 70 mg/kg every 4 hours times 17 doses
• should be diluted to 5% to increase palatability
• Side effects of oral NAC-emesis and nausea
• Foul tasting and smelling

• Decreased glutathione store-malnourished, AIDS, chronic alcholism
• Form more NAPQI
• P450 induction-anticonvulsants
• Form more NAPQI
• Chronic ingestion
• Can't use nomogram
• APAP level, LFTs, GI symptoms
• Give antidote if increased acetophine leve or if increased AST and ALT
• Tyenol Extened Relief
• Acute Ingestion, time of ingestion unknown

• Helium, methane, ethane, nitrogen and carbon dioxide
• Displacement of oxygen from the environment
• Exposure usually in confined spaces or concentrated forms of the gas
• Signs and Symptoms- related to hypoxemia
• Confusion
• CNS depression
• Seizures
• Arrhythmias
• Treatment centers on removal from source, supplemental oxygen and supporeive care

• Asphyxiant of tissue occurs by various mechanisms, including binding of the toxin to hemoglobin and cytochrome oxidase
• Carbon monoxide is the most common cause of death in the US.  Sources include incomplete combustion of carbonaceous fuels ( fires, auto exhaust, heating equipment)
• Cyanide-decreases oxygen delivery to tissue
• Sources include photography, electroplating, chemical labs, pitted fruits such as apricots, cherries, peaches, and bitter almonds
• Hydrogen sulfate occurs as a byproduct of bacterial decomposition of protein (sewer gas)
• Signs and symptoms often reflective of hypoxemia
• "However other poorly elucidated mechanisms (e.g. binding to various enzymes) are likely invovled and play a role in the clinical picture"
• Treatment in all cases centers on removal from source, supplemental oxygen, and supportive care
• High flow oxygen and in some cases hyperbaric oxygen for carbon monoxide toxicity
• Cyanide Antidotes: amyl nitrate, sodium nitrate, sodium thiosulfate, hydrocobalanine
• Hydrogen sulfide antidotes- amyl nitrite, sodium nitrite

Irritant Gases

High solubility gases

• Ammonia, chloramine, hydrogen chloride
• Highly irritating, producing rapid onset of clinical side effects
• As a result patients may be prompted to escape
• Symptoms may include oral, nasal, and throat pain, conjunctival irritation, cough, and stridor
• Lower respiratory tract injury is also possible in significant exposures 
• Bronchospasm
• Pulmonary edema
• Treatment centers on removal from source, supplemental oxygen, and supportive care
• Nebulized sodium bicarbonate may improve symptoms in acid (hydrogen chloride) inhalations and inhalations which result in acid formation (chloramine)
• No evidence of improve outcome

Irritant Gases

Intermediate Water Solubility Gases

• ex. Chlorine
• Sources include swimming pools, industry,
• Results in both upper and lower respiratory effects
• Wheezing-may use bronchodilators
• Less irritation which results in the possibility of delay in onset of symptoms for a few hours
• Treatment centers on removal from source, supplemental oxygen, and supportive care
• Chlorine inhalation results in acid formation-nebulized sodium bicarbonate may improve symptoms
• No evidence of improved outcomes

Irritant Gases

Low Water Solubility

• Phosgene (carbonyl chloride)
• Used in WWI
• Terrorism concern
• Has industrial applications
• Lack of irritating properties tends to result in delayed onset of symptoms (several hours) and lower respiratory tract effects
• Treatment centers on removal from source, supplemental oxygen, and supportive care
• Patients generally kept for observation overnight due to delay in symptom onset

• Chemicals containing hydrogen and carbon
• Availability: Industrial and household products
• Kerosene
• Gasoline
• Lighter fluid
• Furniture Polish
• Insecticide
• Used as solvents, fuels, degreasers, pesticides "Decor"

• Toxicity is related to volatility and viscosity
• Kerosene and Gasoline
• Highly volatility and low viscosity
• Capable of causing aspiration pneumonia and acute respiratory distress syndrome (ARDS)
• Crude oil, petroleum, mineral oil
• Low volatility, high viscosity
• Low risk of injury
• Systemic toxicity following ingestion
• Aromatics
• Xylene or toluene
• Benzene based on ring structure
• Complex Hydrocarbons
• Solvents for other agents (pesticides)
• Organophosphates
• Halogenated hydrocarbons
• Not all are toxic
• Contain chlorine, fluoride, or bromine
• Carbon tetrachloride
• Aromatic and halogenated
• CNS depression
• Sedation
• Lethargy
• Coma
• Confusion
• Ataxia
• Headache
• Seizures
• Cardiac dysrhythmias
• Less toxic agents usually do not see systemic effects but may be at risk for aspiration/complications
• Kerosene/Gasoline
• Paint thinners/turpentine/Charcoal and lighter fluids
• Mineral seal oil
• Furniture Polish

• Agent
• Route of Exposure
• Aspiration
• Ingestion
• Inhalation
• Vomiting
• Dermal (Gas vs. organophosphates)
• Amount of exposure
• Chemical structure
• Viscosity and volatility
• Age of patient

• Population
• Pediatrics-common
• Adults- less common
• Intentional
• Need to distniguish between ingestion and exposure
• With ingestion it is usually not systemically toxic

• Ocular
• Irritation and Burning
• Corneal Injury
• Dermal
• Irritation and 1º burns
• GI irritation → vomiting → aspiration
• Nausea, vomiting, diarrhea
• GI bleeding
• Renal Tubular Damage
• Highly volatile compounds
• Pulmonary effects are most common
• Aspiration during ingestion and or vomiting
• Low surface tension and viscosity allows a small amount to spread over a large pulmonary surface
• Hydrocarbons with the lowest viscosities produce the greatest lung injury
• Clinical pneumonitis → ARDS
• Alteration of destruction of surfactant
• Inflammatory reaction

• Immediate Symptoms
• Highest risk for aspiration and pneumonia
• Coughing
• Gasping
• Choking
• Sputtering
• Chest Pain
• Dyspnea
• Cyanosis
• Progression of symptoms
• Cough
• Tachypnea
• Wheezing
• Changes in respiration
• Evidence for pneumonitis
• Does not appear on CXR for 6-12 hours
• Secondary bacterial pneumonia is usually a late finding
• Chronic respiratory disease

• Medical and Social History
• Substance exposure
• Treatment interventions
• Clinical examination-lung and cardiac are the most important
• Pulse oximetry
• ABG
• CXR
• CMP-LFT's and renal function

• Do not induce emesis
• Most simple hydrocarbons-no need to remove from the stomach
• Only indicated if a mixed ingestion or a very large dose of an aliphatic hydrocarbon
• Aromatic or complex hydrocarbons may necessitate lavage because of their potent toxities
• Protect the airway-place cuffed EET before the lavage tube passed
• Activated Charcoal is not useful for aliphatic and alicyclic hydrocarbons
• May bind significant quantities of some aromatic and substituted hydrocarbons
• Remove contaminated clothing and wash exposed skin with soap and water
• Remember to protect yourself and staff especially if it is an organophosphate
• Irrigate exposed eyes with water or saline
• Fluorescein examination to determine if corneal injury.

• Call the regional poison center for adivce
• Carbon tetrachloride antidote is acetycysteine
• Methemoglobin formers antidote is methylene blue
• Chelation for leaded hydrocarbons
• Antidotes for pesticides- 2-Pam, Atropine

• ABC
• Hospitalize symptomatic patients
• Seizures-treat with BZD
• Peumonitis
• Treat the patient not the CXR (May shot appear for 6-12 hours)
• O₂ if indicated
• DO NOT give antibiotics
• ARDS-Mechanical ventilation- O₂ and PEEP
• GI- symptoms
• Usually self-limiting but may persist for 2-3 days
• Vomiting may lead to further aspiration
• Death may occur despite aggressive supportive care

• Intentional inhalation of a volitile substance for the purpose of achieving a euphoric state or alteration in the state of consciousness or perception
• About 20% of high school seniors have experimented inhalation
• About 19% of 8th graders have experimented with inhalation
• Affects children as young as 2 years of age
• Significant morbidity and mortality
• Peak age: 13-16 yrs old
• Most common cause of death is "sudden sniffing death syndrome"
• Volatile substances
• Capable of rapidly producing a pleasurable sensory experience
• Readily available
• Inexpensive
• "Legal"

• Any hydrocarbon can have mind-altering effects when inhaled in large doses
• Liquids- model glue, adhesives, Gas, Contact cement, Lacquers, Dry-cleaning fluids
• Aerosols-Compressed air, Paints, Butane fuel, Cooking sprays, Cosmetics, Toiletries, Cool Whip
• Air freshners
• Fire extinguishers

• Fumes of the product may be inhaled directly from a container, plastic bag, or saturated rag
• May spray directly into mouth-Laryngospasm b/c the liquid is cold
• Inhalation is usually through the mouth and several deep inspirations are required to produce euphoria
• May heat agent to increase vaporization
• Exhaled air is frequently rebreathed
• Hypercarbia
• Hypoxia

• Solvent vapors are readily absorbed from the lungs and reach high concentrations in the CNS (lipid solubility)
• Inhalants are depressants and are pharmacologically related to anesthetic gases
• User is initially stimulated, uninhibited, and prone to impulsive behavior then speech becomes slurred and gait-ataxia
• Euphoria with/without hallucinations is followed by drowsiness and sleep
• Coma is unusual because drowsy and terminates inhalant exposure
• Sudden sniffing death syndrome
• Result of hydrocarbon induced myocardial sensitivity to epinephrine
• Sudden surge of epinephrine secondary to the startle reflex with a resultant fatal cardiac dysrhythmia
• About 20% of deaths occur during their first exposure
• Common with Butane

• Deliquency
• School failure
• Social Maladjustment
• Unusual location of products of abuse
• Child's room, book bag, under bed

• Vivid hallucinations
• Appearance of intoxication
• Euphoria
• Feeling of ominpotence
• Clouding of consciousness
•  Seizures
• Tinnitus
• Slurred Speech
• Headache- Increased CO₂ Decreased O₂ in blood
• Sedation
• Coma
• Dermal-perioral pyoderma
• Chest pain, dysrhythmias
• Laryngospasms
• Conspicuous odor of the inhalant
• Asphyxia or pneumonitis
• Stained Clothing
• Flecks of paint or glitter on face
• Odor on Clothes

• CNS damage with dementia and cerebellar damage
• Lodd of congnitive and other higher functions
• Gait disturbance
• White matter degeneration and loss of brain mass

Deafness

Meatabolic acidosis

Decreased visual acuity

Toxic hepatitis

Embryopathy

Asphyxia-negligible

Aspiration-15%

Suffocation-15%

Dangerous Behavior-15%

Sudden Sniffind Death Syndrome-55%

• Symptomatic Treatment
• ABC
• Oxygen
• Anticonvulsants
• Antidysrhythmics
• Decontamination

• Synthetic cathinone drug of abuse
• Contain a ketone group of the Β carbon which causes decreased CNS penetration and less potency
• May lead to overdose or adverse effects
• Product usually contains methyelnedioxypyrovalerone (MDVP) or 4-methylmethcathion (Mephedrone) which release and inhibit the reuptake of serotonin, dopamine, and norepinephrine
• Purchased legally on internet, smoke houses, gas station, and convenience stores
• Marketed as bath salts, plant food, and insect repellants
• Evades illegal status of methamphetamines
• DEA made illegal in 2011
• Taken orally, nasally, or IV
• Sympathomimetic toxidrome: clinical effects mimic drugs that are structurally similar to methamphetamines
• Symptoms:
• Euphoria
• Empathy
• Bruxism-grinding of teeth
• Agitation
• Tachycardia
• Delusions
• Increased sexual desire
• Panic
•  Hallucinations
• Treatment for hyperthermia, cardiac toxicity, liver toxicity, and CNS changes
• Use benzodiazepines for seizures

• Available as supplements containing:
• Iron only
• In combination with multiple vitamins and other minerals
• Indication
• Treatment of anemai
• Prenatal supplementation
• Toxicity of iron is based on the amount of elemental iron in the preparation
• Usually reported as mg of elemental iron on bottle
• Multivitamins-usually have 15-18 mg elemental Fe/tablet
• Prenatal vitamins- 65 mg elemental Fe/tablet
• Mild Toxic Dose: 20-60 mg/kg
• Moderate/Severe Toxic Dose: 60-100 mg/kg
• Life Threatening Toxic Dose: > 100 mg/kg
• Lethal Toxic Dose: > 180 mg/kg

• Abs is a 1st order process as elemental Fe
• Transported to RES bound to transferrin
• Excreted via desquamation of the skin, blood loss, and excretion into bile
• Fixed daily loss: 1mg; can be up to 2mg in iron overload
• Serum iron normal range is 0-100 mcg/dl

Stomach and Small Intestine

• Corrosive mucosal damage initially
• Hydrogen ion production
• Generation of vasoactive substances- histamine, serotonin, ferritin
• End result is vasodialtion with subsequent venous pooling, low cardiac output, and shock
• May cause hemorrhagic necrosis and perforation of stomach and small intestines

Circulating Free Iron

• Disrupts mitochondrial function and cellular metabolism
• Uncouples oxidative phosphorylation
• Interferes with electron transport system
• Lactic acidosis may develop
• Free radical formation can damage membranes via peroxidation
• Due to irons capacity for oxidation/reduction reactions
• Iron is a direct CNS depressant
• Pyloric stenosis-late finding as a result of scarring
• Gastric outlet obstruction may develop

• 0-6 hours after ingestion
• Abdominal pain, Nausea, Vomiting
• Hematemesis
• Hemorrhagic diarhea
• melna
• Tachycardia
• Hypotension
• Pallor
• Fever
• Hyperglycemia
• Leukocytosis
• Acidosis
• Massive fluid loss → shock, renal failure and death
• Poor prognostic signs: shock, coma,l or hypotension in this period
• If no symptoms within 6 hours of ingestion very unlikely the patient will develop symptoms

• 6-24 hours
• Temporary recovery for 2-24 hours
• Metabolic Acidosis
• Lethargy
• Debate about existence of this latency thase

• 8-14 hours after ingestion
• Abrupt relapse of symptoms
• Persistent GI symptoms
• Hepatic Necrosis
• CNS-obtundation, coma, seizures
• Changes in mental status
• Pulmonary Edema
• Hemorrhage
• Shock
• Metabolic-Refractory metabolic acidosis
• Hypoglycemia
• Renal Tubular dysfunction
• Clotting abnormalities-depresses activity of factors V, VII, IX, X

• 2 days to 3 weeks after ingestion
• ARDS
• Cirrhosis
• Sepsis (Y, entercolitica)
• Gastric scarring with pyloric stenosis

• Serum Iron
• Obtained 4-6 hours after ingestion can predict severity of poisoning
• Repeat serum level in 8-12 hours after initial level to detemine if there is delayed absorption
• Iron levels DO NOT correlate with phases of toxicity
• TIBC-not reliable in overdose
• Intracellular iron burden produces systemic toxicity NOT iron in the blood
• Not Toxic < 350 mcg/dl
• Mildly Toxic: 350-500 mcg/dl
• Mod-Severel Toxic: 500-1000mcg/dl
• Life Threatenig: > 1000 mcg/dl
• Metabolic Acidosis with high anion gap
• Blood glucose > 150 mg/dl
• WBC > 15K/mm
• Coagulation studies: PT/PTT
• Abdominal XR
• Radiopaque pill (Iron only not multivitamins)
• Paint chips
• Follow up barium swallow-late in course
• Patients with significant GI symptoms
• Patients with prolonged GI exposure to iron

• Decontamination
• Emesis or lavage are NOT usually indicated
• Cathartic or WBI may be of value
• Especially in large ingestions to expel undissolved tablets
• Risk of bezoar
• Chelation with Deferoxamine (desferal)
• IV antidote (protein) which chelaes iron
• May produce vin rose' urine (~30%)
• Adverse effects: Hypotension if infused to rapidly
• Allergic reaction
• Indication: Serum iron > 500 mcg/dl
• Significant systemic signs/symptoms evident regardless of level
• Mechanism of action: Pulls iron out of mitochondria and cells by mass action
• Forms water-soluble ferrioxamine (renally excreted)
• Discontinue when urine color returns to normal
• Serum iron < 100-150 mcg/dl