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Top Ten Poisons

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Section 2-D
|Roña, Diandra Krystle B. |
|Rosales, Aileen L. |
|Rosaura, Franz D. |
|Roxas, Marie Florence S. |
|Rubio, Hannah Alexis O. |
|Rugay, Jesus Emmanuel R. |

February 1, 2012


Poisons are substances that cause disturbances in living organisms and do so by some biologic or chemical reaction in nature. For decades, the use of different substances for various applications lead to the discovery of potential toxic substances that may have caused injurious effects. Poisoning commonly occurs thru ingestion and usually, it was unintentional. Acute toxicity is the single exposure or multiple exposures for short periods to the substance causing the injury. Symptoms may be rapid and are in close relation to the toxic agent. On the other hand, chronic toxicity are caused by repeated or multiple exposure for longer periods to the poison. Signs and symptoms of chronic toxicity may appear even after several years upon the initial exposure.



Caustics are strong acids and alkali that when ingested can cause tissue injury by chemical reaction. They damage the tissues by accepting a proton (alkaline substance) or donating an proton (acidic substance) in an aqueous solution. In aqueous solutions, the hydrogen ion (H+) produces the principle toxic effects for the majority of acids, whereas the hydroxide ion (OH-) produces such effects for alkaline substances. Hydrochloric acids, sodium hypochlorite and sodium hydroxide are just a few of the more common substances that cause the injury due to their ease of access and usefulness in our daily tasks.

The potential of a substance to donate or accept protons are measured by its Ph. This relates to the strength, though not accurately the likelihood of injury. Substances with a ph of less than 2 are considered to be strong acids while substances with a ph of greater than 12 are categorized as strong alkalis. The severity of the injury caused by caustic substance are determined by the duratoin of contact, the amount and state of the substance involved (whether solid or liquid) and the substance’s inherent chemical properties. Most definitely, substances that can easily penetrat tissues are more damaging and injurious than the others. The titratable reserve can also be a factor since this predicts the amount o tissue required to neutralize or disable the effects of the poison.

According to the National Poison and Management Control Center (NPMCC) around 3,332 poisoning cases “or around 10 cases a day” were referred to their center in 2010.This is an alarming reality especially when Most of which are caused by substances or materials we utilize in our daily activities.


Ingesting bases or alkaine substances results to tissue injury characterized by liquefactive necrosis. The fats present are saponified and the proteins are solubilized. Cell death occurs from emulsification and disruption of cellular membranes. The hydroxide ion of the alkaline agent reacts with tissue collagen and causes it to swell and shorten.

Severe injury occurs rapidly after alkaline ingestion, within minutes of contact. The most severely injured tissues are those that first contact the alkali, which is the squamous epithelial cells of the oropharynx, hypopharynx, and esophagus. The esophagus is the most commonly involved organ with the stomach much less frequently involved after alkaline ingestions. Tissue edema occurs immediately, may persist for 48 hours, and may eventually progress sufficiently to create airway obstruction. Over time, if the injury was severe enough, granulation tissue starts to replace necrotic tissue. Unlike in acidic ingestions, alkali poisons produce more dangerous and deleterious effects because eschar formation is unlikely, thus, further damage spreads. Instead, scar tissue may form after 2-4 weeks, initially remodels and may thicken and contract enough to form strictures. The likelihood of stricture formation primarily depends upon burn depth.


Acid ingestions cause tissue injury by coagulation necrosis, which causes desiccation or denaturation of superficial tissue proteins, often resulting in the formation of an eschar or coagulum. This eschar may protect the underlying tissue from further damage. Unlike alkali ingestions, the stomach is the most commonly involved organ following an acid ingestion. This is attributed to the natural protection of the esophageal squamous epithelium.

After 3-4 days, the eschar sloughs off and granulation tissue fills the defect, and perforations may occur. Sometimes, a gastric outlet obstruction may occur as the resulting scar tissue contracts within a 2-4 week period.

Usual symptoms of caustics poisoning are: • Dyspnea • Dysphagia • Oral pain and odynophagia • Chest pain • Abdominal pain • Nausea and vomiting


To completely evaluate the patient, endoscopy is advised since the presence or absence of intraoral burns does not reliably indicate whether the esophagus and stomach are burned. It is indicated to check for the presence and severity of esophageal and gastric burns when symptoms or history suggests more than trivial ingestion.

Treatment of caustic poisoning is supportive. Gastric emptying by emesis or lavage is contraindicated because it can reexpose the upper GI tract to the caustic substance.Likewise, attempts to neutralize a caustic substance by correcting pH is also not advised because severe exothermic reactions may result. Activated charcoal is contraindicated because it may infiltrate burned tissue and interfere with endoscopic evaluation. Oral fluids are started when they can be tolerated.


Jewelry cleaner contains various chemicals which can cause serious symptoms if ingested or other types of exposure occur. The chemicals cause damage to the gastrointestinal lining and the damage may continue for weeks after the poison was ingested. Death can result in severe cases. The type and severity of symptoms varies depending on the amount of chemical involved and the nature of the exposure.

General toxicity Poisonous ingredient includes ammonia, corrosive alkali, detergent and soap

Signs and Symptoms • Eye irritation • Skin irritation • Skin burns • Burning mouth sensation • Skin necrosis • Headache • Cough • Sleepiness • Dizziness • Abdominal pain • Nausea • Vomiting • Blood in stool • Blood in vomit • Reduced blood pressure • Throat pain • Mouth pain • Loss of vision • Gastrointestinal burns • Breathing difficulty • Throat swelling • Respiratory system • irritation

Treatment and Management • Decontamination, symptomatic and supportive measures • Exposure Route For Chemical poisoning o Inhalation, eye, skin, ingestion • Jewelry cleaner can cause severe burns to the inside of the gastrointestinal tract. • Extensive damage to the mouth, throat, eyes, lungs, esophagus, nose, and stomach are possible. • The ultimate outcome depends on the extent of this damage. • Damage continues to occur to the esophagus and stomach for several weeks after the poison was swallowed, and death may occur as long as a month later.

A. Home Care

Seek immediate medical help. Do not make a person throw up unless told to do so by poison control or a health care professional. If the chemical is on the skin or in the eyes, flush with lots of water for at least 15 minutes. If the chemical was swallowed, immediately give the person water or milk, unless instructed otherwise by a health care, breathing rate, and blood pressure. Symptoms will be treated as appropriate.

B. Hospital care • The patient may receive: o Breathing tube o Bronchoscopy -- camera down the throat to see burns in the airways and lungs o Endoscopy -- camera down the throat to see burns in the esophagus and the stomach o Fluids through a vein (IV) o Oxygen o Surgical removal of burned skin (skin debridement) o Washing of the skin (irrigation) -- perhaps every few hours for several days o Outlook (Prognosis) o How well a patient does depends on the amount of poison swallowed and how quickly treatment was received. The faster a patient gets medical help, the better the chance for recovery.

3. Ethanol poisoning • Ethanol is a 2-carbon–chain alcohol. • The chemical formula is CH2 CH3 OH. • Pure ethanol is a colourless liquid with a burning taste. • It is used industrially as a solvent and in the manufacture of detergents, cosmetics and perfumes.
Figure 1. The pathway of ethanol metabolism. Disulfiram reduces the rate of oxidation of acetaldehyde by competing with the cofactor nicotinamide adenine dinucleotide (NAD) for binding sites on aldehyde dehydrogenase (ALDH)

Toxicity • Ethanol is rapidly absorbed from the GI tract. • Adults - absorb 80-90% of ingested alcohol within 1 hour and metabolize it at a rate of 7-15 g per hour (reducing blood concentrations by approximately 150-200 mg/L (15-20 mg/dL) per hour) • fatal dose in adults - approximately 5-8 g/kg body weight (6-10 mL/kg absolute ethanol) • fatal dose in children - approximately 3 g/kg body weight (4 mL/kg absolute ethanol) • A blood concentration of 1.8 g/L (0.18 g/dL, 180 mg/dL, 39 mmol/L) would usually cause intoxication and concentrations of 3.5 g/L (0.35 g/dL, 350 mg/dL, 76 mmol/L) are associated with stupor and coma. • Concentrations of > 4.5 g/L (0.45 g/dL, 450 mg/dL, 98 mmol/L) are often fatal. • Inhalation is not likely to cause problems unless concentrations are high. o Irritating to eyes and skin.
A. Ingestion • Mild - concentration 4.5g/L (0.45 g/dL, 450 mg/dL, 98 mmol/L) • Deep coma, respiratory depression or arrest and circulatory failure.
D. Inhalation • Ethanol inhalation causes irritation of the nose and throat with choking and coughing at higher concentrations. • Eyes: Stinging, burning and lacrimation. • Skin: Burning and stinging.

1. Ensure a clear airway and adequate ventilation, particularly in obtunded patients. Ventilation may be required for respiratory depression.
2. Gut decontamination is unlikely to be of benefit since ethanol is rapidly absorbed and activated charcoal does not significantly reduce the rate of absorption.
3. Observe for at least 4 hours if >0.4 mL/kg body weight of absolute ethanol had been ingested in a child (i.e. 1 mL/kg 40% spirit, 4 mL/kg 10% wine or 8 mL/kg 5% beer). • Observe adults with features of moderate or severe toxicity for a minimum of 4 hours.
4. Monitor pulse, blood pressure and body temperature.
5. Monitor blood glucose in all patients.
6. Measure urea, electrolytes, arterial blood gases and blood ethanol concentration in patients with features of moderate to severe toxicity and perform 12 lead ECG.
7. Correct hypoglycaemia as quickly as possible. • If the patient is awake give oral glucose. • If the patient is drowsy or unconscious give up to 500 mL 5% or 250 mL 10% dextrose IV (titrated to patient responsiveness). • 50 mL 50% dextrose IV may be given but is irritant to veins and can cause skin necrosis in cases of extravasation. 5% or 10% is equally effective. • Smaller quantities of glucose (0.5-1 g/kg) are required in children (e.g. 5-10 mL/kg of 10% dextrose IV. • Glucagon is rarely effective. • NB Chronic alcohol abusers must also be given thiamine intravenously.
8. Correct hypotension by raising the foot of the bed and/or by expanding the intravascular volume. • If severe hypotension persists despite the above measures consider use of inotropes such as dopamine (2-10 micrograms/kg body weight/minute) or dobutamine (2.5-10 micrograms/kg body weight/minute).
9. If hypothermic, rewarm slowly using conventional means.
10. Control convulsions with intravenous diazepam (0.1-0.3 mg/kg body weight) or lorazepam (4mg in an adult and 0.05 mg/kg in a child). Correct acid base and metabolic disturbances. • Phenytoin (loading dose 15mg/kg IV infusion in adults and children) may be useful if fits are unresponsive to above measures. • If seizures persist consider the need for intubation, paralysis and ventilation (remember that there may continue to be cerebral activity and measures to control this will require active management).
11. Consider hemodialysis if blood ethanol concentration > 5g/L (0.5 g/dL, 500 mg/dL, 108.5 mmol/L) or if arterial pH 100 nmol/L).
12. Inhalation: Symptomatic and supportive treatment only.

ALCOHOL WITHDRAWAL SYNDROME • When a person with alcoholism stops drinking, withdrawal symptoms begin within 6-48 hours and peak about 24-35 hours after the last drink. • During this period, the inhibition of brain activity caused by alcohol is abruptly reversed. • Stress hormones are overproduced, and the central nervous system becomes overexcited. • Common symptoms include: o Anxiety o Irritability o Agitation o Insomnia • Additional symptoms may include: o Extremely aggressive behavior o Fever o Rapid heartbeat o Changes in blood pressure (either higher or lower) o Mental disturbances • Seizures occur in about 10% of adults during withdrawal. • In about 60% of these patients, the seizures are multiple. • The time between the first and last seizure is usually 6 hours or less. • Delirium tremens (DTs) are withdrawal symptoms that become progressively severe and include altered mental states (hallucinations, confusion, severe agitation) or generalized seizures. o DTs are potentially fatal. o They develop in up to 5% of alcoholic patients, usually 2 - 4 days after the last drink, although it may take 2 or more days to peak. • It is not clear if older people with alcoholism are at higher risk for more severe symptoms than younger patients. However, several studies have indicated that they may suffer more complications during withdrawal, including delirium, falls, and a decreased ability to perform normal activities.

A. Rule out alternative diagnoses • This is particularly true when the presentation includes altered mental status and fever. Conditions, such as infection (eg, meningitis), trauma (eg, intracranial hemorrhage), metabolic derangements, drug overdose, hepatic failure, and gastrointestinal bleeding, can mimic or coexist with alcohol withdrawal. • A premature diagnosis of alcohol withdrawal can lead to inappropriate use of sedatives, which can further delay accurate diagnosis.
B. Control of symptoms and supportive care • Benzodiazepines are used to control psychomotor agitation and prevent progression to more severe withdrawal. • Supportive care, including intravenous fluids, nutritional supplementation, and frequent clinical reassessment including vital signs, is important.

1. Benzodiazepines
a. Selection • Benzodiazepines are used to treat the psychomotor agitation most patients experience during withdrawal and to prevent progression from minor withdrawal symptoms to major ones. • Diazepam (Valium), lorazepam (Ativan) and chlordiazepoxide (Librium) are used most frequently to treat or prevent alcohol withdrawal, but other benzodiazepines may be used. • In general, long-acting benzodiazepines with active metabolites (eg, diazepam) are preferred because they seem to result in a smoother course with less chance of recurrent withdrawal or seizures. • Lorazepam (Ativan) or oxazepam (Serax) for the treatment of patients with advanced cirrhosis. • The shorter half-life of lorazepam and the absence of active metabolites with oxazepam may prevent prolonged effects if oversedation occurs. • In contrast, chlordiazepoxide has a relatively long half-life and may lead to oversedation in patients with severe liver disease. Treatment with agents available in parenteral form (eg, lorazepam,diazepam) may be necessary in patients who cannot receive oral medications.
b. Route • All patients with seizures or DT require intravenous (IV) therapy with benzodiazepines. • IV therapy is appropriate for the initial management of most patients with tremulousness from alcohol withdrawal because of guaranteed absorption and rapidity of onset. • It is important to have IV access in all patients at risk of severe withdrawal. • Intramuscular administration should be avoided because of variable drug absorption. • Oral formulations are preferred in most outpatient settings and for the prevention of withdrawal in asymptomatic patients known to be at risk.
c. Dosing • Titration of medications should be based upon a given patient's risk factors for and ability to tolerate DT. • As an example, a patient younger than 45 years with no comorbid illnesses should be lightly sedated to a degree that insures safety and comfort but does not obscure the neurologic examination. • In contrast, an older patient with preexisting cardiopulmonary disease may benefit from heavier sedation, but must be closely monitored due to the greater risk imposed by the high systemic stress of major withdrawal or oversedation. Explicit criteria for ICU admission are provided. • IV diazepam, 5 to 10 mg IV every 5 to 10 minutes, until the appropriate level of sedation is achieved. • Lorazepam, 2 to 4 mg IV every 15 to 20 minutes, can also be used. • In severe withdrawal, select patients may require massive doses (>500 mg diazepam) to achieve initial control of symptoms, and continued aggressive use of benzodiazepines thereafter (>2000 mg diazepam over 48 hours).

Refractory delirium tremens • Some patients have refractory delirium tremens despite treatment with high-dose benzodiazepines, possibly because of low endogenous GABA levels or acquired conformational changes in the GABA receptor. • It may be present if more than 50 mg of diazepam or 10 mg of lorazepam is required to control the symptoms of severe withdrawal during the first hour of treatment, or if doses greater than 200 mg of diazepam or 40 mg of lorazepam fail to adequately control symptoms during the initial three to four hours of treatment. • In patients with refractory delirium tremens, barbiturates (specifically phenobarbital) can be very effective when given with benzodiazepines • phenobarbital 130 to 260 mg IV, repeated every 15 to 20 minutes, until symptoms are controlled. • Another reasonable alternative is propofol, which can act to open chloride channels in the absence of GABA, and may also antagonize the excitatory amino acids that are upregulated during alcohol withdrawal. • Endotracheal intubation and mechanical ventilation are frequently necessary if phenobarbital or propofol are used.

Alternative and contraindicated agents • Drugs other than phenobarbital and propofol have been used with benzodiazepines or, rarely, alone to treat alcohol withdrawal. • These agents are less well studied than benzodiazepines and may mask the hemodynamic signs of withdrawal, which can precede seizures. • The following should not be used routinely in the treatment of moderate or severe alcohol withdrawal: o Ethanol o Antipsychotics (eg, haloperidol) o Anticonvulsants (eg, carbamazepine) o Centrally acting alpha-2 agonists (eg, clonidine) o Beta blockers (eg, propranolol) o Baclofen
C. Prophylaxis • patients with a history of seizures, delirium tremens, or prolonged, heavy alcohol consumption, who are minimally symptomatic or asymptomatic and are admitted to the hospital for other reasons, can be prophylactically treated with oral chlordiazepoxide. • For prophylaxis, 50 to 100 mg every six hours for one day, followed by 25 to 50 mg every six hours for an additional two days. • Monitoring is no different from patients in active withdrawal. • Patients should be reassessed frequently and additional 25 to 50 mg doses of chlordiazepoxide administered each hour if a score of 8 or greater is achieved on the Clinical Institute Withdrawal Assessment for Alcohol Scale (CIWAS-Ar).
|Cumulative Score | |
|0-8 |No medication is necessary |
|9-14 |Medication is optional for patients with a score of 8–14 |
|15-20 |A score of 15 or over requires treatment with medication |
|>20 |A score of over 20 poses a strong risk of Delirium tremens |
|67 |Maximum possible cumulative score |

• Asymptomatic or minimally symptomatic patients at lower risk for seizures or delirium tremens who are being admitted to the hospital for other reasons should be closely monitored and may be treated with oral chlordiazepoxide 25 to 50 mg every hour as needed when a score of 8 or greater is achieved on the CIWAS. • After acute treatment, all patients should be screened for alcohol dependence and should be considered at risk for recurrent episodes of withdrawal.

WERNICKE’S ENCEPHALOPATHY • Thiamine (vitamin B-1) deficiency can result in Wernicke encephalopathy, a serious neurologic disorder. • Korsakoff amnestic syndrome is a late neuropsychiatric manifestation of Wernicke encephalopathy with memory loss and confabulation; sometimes, the condition is referred to as Wernicke-Korsakoff syndrome or psychosis. • Wernicke encephalopathy may develop in nonalcoholic conditions, such as prolonged starvation, hyperemesis gravidarum, bariatric surgery, and human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS), and can even develop in healthy infants given the wrong formulas.

Treatment • as little as 2 mg of thiamine may be enough to reverse symptoms, the dose of thiamine required to prevent or treat Wernicke encephalopathy in most alcoholic patients may be as high as greater than 500 mg given once or, preferably, 2 or 3 times daily parenterally • Treat all poorly nourished patients with large doses of parenteral thiamine, particularly if intravenous glucose administration is necessary, even in the absence of symptoms and signs of Wernicke encephalopathy. • Administering dextrose to an individual in a thiamine-deficient state exacerbates the process of cell death by providing more substrate for biochemical pathways that lack sufficient amounts of coenzymes. • Start thiamine prior to or concurrently with treatment of intravenous glucose solutions, and continue until the patient resumes a normal diet. • The administration of dextrose or other carbohydrates in this setting can be hazardous, because glucose oxidation is a thiamine-intensive process that may drive the last reserves of circulating vitamin B-1 toward the intracellular compartment, thereby aggravating neurologic damage. • Patients with Wernicke encephalopathy are likely hypomagnesemic and should be treated empirically with parenteral magnesium sulfate, as they may be unresponsive to parenteral thiamine in the presence of hypomagnesemia. • After correction of hypomagnesemia in conjunction with thiamine repletion, the blood transketolase activity can return to normal and clearing of the clinical signs of Wernicke encephalopathy may occur. • The cornerstone of therapy for prevention or treatment of Wernicke encephalopathy in most alcoholic patients is thiamine until the patient resumes a normal diet. Administer daily oral thiamine (100 mg) on a long-term, outpatient basis.

ALCOHOL DEPENDENCE It is a psychiatric diagnosis (a substance related disorder DSM-IV) describing an entity in which an individual uses alcohol despite significant areas of dysfunction, evidence of physical dependence, and/or related hardship, and also may cause stress and bipolar disorder.
|Medication |Dosage |Side effects |Contraindications* | |
|Acamprosate |333-mg enteric coated tablets Adults |Diarrhea, headache, flatulence, nausea, |Severe renal impairment (creatinine| |
|(Campral) |≥ 132 lbs (60 kg): two tablets three |vomiting, dyspepsia |clearance < 30 mL per minute [0.5 | |
| |times per dayAdults < 132 lbs: two | |mL per second]) | |
| |tablets with the morning meal,one | | | |
| |with the midday meal, and one with | | | |
| |the evening meal | | | |
|Disulfiram |Begin with 250 mg once per day; |Disulfiram–alcohol interaction: palpitations,|Alcohol, metronidazole (Flagyl), or| |
|(Antabuse) |increase to 500 mg once per day. |flushing, nausea, vomiting, headache |paraldehyde use psychosis; | |
| | | |cardiovascular disease | |
|Fluoxetine (Prozac)|Begin with 20 mg per day; may |Nausea, headache, sedation, anxiety, sexual |Use of an MAOI, mesoridazine | |
| |increase to 60 mg per day as needed. |dysfunction |(Serentil), or thioridazine | |
| | | |(Mellaril) | |
|Nalmefene (Revex) |Available only in an injectable form |Nausea, tachycardia, vasodilation, dizziness,|None | |
| |(outside of research) to treat opiate|headache, chills, vomiting | | |
| |overdose. | | | |
|Naltrexone (Trexan)|50 mg once per day |Nausea, headache, anxiety, sedation |Narcotic use, acute opioid | |
| | | |withdrawal, acute hepatitis, liver | |
| | | |failure | |
|Ondansetron |4 mcg per kg twice per day |Malaise, fatigue, headache, dizziness, |None | |
|(Zofran) | |anxiety | | |
|Topiramate |Begin with 25 mg morning dose and |Recent FDA warning of metabolic acidosis, |None | |
|(Topamax) |increase to a total of 300 mg given |especially with renal or liver | | |
| |twice a day in divided doses. |diseaseDizziness, somnolence, ataxia, | | |
| | |impaired concentration, confusion, fatigue, | | |
| | |paresthesias, speech difficulties, diplopia, | | |
| | |nausea | | |

4. Pesticides


DEET (N,N-diethyl-3-methylbenzamide) was developed by the military as an insect repellent in 1946 and introduced for public use in 1957. It has broad-spectrum activity and effectively repels most mosquitoes, biting flies, chiggers, fleas and ticks. It is the most effective insect repellent available for human use. Currently, DEET is formulated in aerosols, pump sprays, lotions, creams, liquids, sticks, roll-ons and impregnated towelettes, with concentrations ranging from 5% to 100%. There is widespread use of products containing DEET due to the increasing incidence of West Nile Virus in the United States and recommendations by the Centers for Disease Control that it is the preferred insect repellant. It is estimated that 30% of the population in the United States applies DEET each year. The widespread use, concern for mosquito-borne viruses, and media attention have rekindled interest in DEET and its potential toxicities.

Mechanism of action

DEET is absorbed through the skin. Dermal absorption depends on the concentration and solvents in the formulation. Dermal absorption of DEET may also vary by age and body mass. Infants less than 2 months of age have a larger surface area to body mass ratio and can more easily attain elevated plasma concentrations. Absorption can also be increased when DEET is applied to broken skin. When DEET is formulated with ethanol, absorption may also be increased as ethanol enhances permeability of the skin.

Absorption decreases under conditions of perspiration and elevated body temperature. DEET distributes into skin and fatty tissues but does not accumulate in the superficial layers of the skin. Following removal of DEET from the surface of the skin, the remaining product in the lower layers of the dermis is absorbed, metabolized and excreted in the urine.

The rate of elimination of DEET after topical application is faster than the rate of absorption, and elimination has been found to be complete within 12 hours of removal. The primary route of elimination is through the urine, with negligible elimination in the feces. The metabolism of DEET may change in response to large exposures; more of the parent compound is excreted unchanged in the urine and several additional metabolites may be present in the urine.

There is little information available about oral absorption. Severe symptoms have appeared within 30 minutes of ingestion, which implies rapid GI absorption.

Signs and Symptoms

DEET has few adverse effects when applied as directed. The most common problem is local skin irritation, including erythema and pruritis, at the site of application. One case of anaphylaxis after brief exposure to DEET has been reported. When the patient was re-exposed to DEET in an emergency department she experienced similar symptoms of anaphylaxis. Many people, including military and forest service personnel, apply high concentrations of DEET on a daily basis and have developed more severe adverse effects due to chronic exposure. These adverse effects included insomnia, muscle cramps, mood disturbances and rashes.


Treatment of DEET exposure consists of decontamination and supportive care. After ocular exposure the eyes should be irrigated from the eye with lukewarm water for 15 minutes. Patients with persistent eye irritation or pain should be evaluated for corneal injury or chemical conjunctivitis.

Following large dermal exposure, the area should be washed 2-3 times with soap and water or an alcohol-detergent solution such as “green soap”.

Inducing emesis is not recommended, but gastric aspiration via nasogastric tube followed by activated charcoal may be of benefit if large quantities are ingested and the patient presents within one hour of ingestion. Ingestion or dermal application of DEET rarely causes seizures, but when seizures occur diazepam or another benzodiazepine should be utilized.

Other supportive therapies such as anti-emetics for nausea and vomiting, intravenous fluids and vasopressors for hypotension, and antihistamines for severe skin irritation may be useful. There is no specific antidote available for treatment of DEET toxicity.


Carbamate insecticides are derivatives of carbamic acid, HOC(O)NH2. They have the general formula shown below where R is an alcohol, oxime or phenol and R1 is hydrogen or a methyl group.

O H || | R-O-C-N-R1 Carbamates vary in their spectrum of activity, mammalian toxicity and persistence. They are relatively unstable compounds that break down in the environment within weeks or months. Carbamates are commonly used as surface sprays or baits in the control of household pests.

Mechanism of action

Carbamate insecticides inhibit cholinesterase enzymes. Their inhibitory effect on cholinesterase is brief.
The reversal of the effect of carbamates is so rapid that measurements of blood cholinesterase levels in human beings or other animals exposed to carbamates are likely to be inaccurate and always in the direction of appearing to be normal. To assess exposure to carbamates, it is necessary that the blood sample is collected on the same day as the exposure occurred and that the analysis is performed as soon as possible to minimise any reversal in the collected specimen.

Signs and Symptoms

Carbamates may be absorbed through the skin as well as by ingestion and inhalation. Spontaneous recovery without medical treatment occurs generally within 4 hours of an exposure which has produced symptoms and signs of headache, light-headedness or dizziness, weakness, excessive salivation, nausea, or vomiting. More severe symptoms and signs generally prompt medical treatment. Individuals have recovered from poisoning that produced such symptoms and signs as visual disturbances, profuse sweating, abdominal pain, incoordination, muscle fasciculations, breathing difficulties or changes in the pulse rate.

There is no evidence of carbamates causing delayed neurotoxicity. There is no clear evidence that carbamates have adverse health effects from long-term exposure at levels that do not affect acetylcholinesterase levels. Carbamates are not regarded as mutagenic, carcinogenic or teratogenic substances.


If a carbamate insecticide is ingested, vomiting should be induced. If absorbed through the skin, contaminated clothing should be removed and the skin washed thoroughly with soap and water. In carbamate poisoning, the use of atropine is indicated, but oximes are contra-indicated. It is very important to note that the absorption of a small amount of relatively non-toxic carbamate by a person who was recently exposed to organophosphates, but who does not show evidence of clinical poisoning, may precipitate an acute toxic state. This may occur because about a 70% depression of cholinesterase activity may be tolerated without clinical signs. Any further depression can result in an acute poisoning.

Generally, a depression of cholinesterase activity lasting longer than 48 hours is unlikely to be caused by carbamates. A detailed history of pesticides used recently should be taken whenever possible to ascertain the total exposure of the patient to cholinesterase inhibiting and other pesticides.

5. Paracetamol

Paracetamol is the most common single agent involved in poisonous ingestions in young children. While there is potential for serious liver damage if a large dose is ingested, in practice, it is rare for a child to achieve toxic blood levels by ingesting paracetamol elixir (syrup).

Paracetamol is also commonly involved (often mixed with other drugs) in episodes of intentional selfharm by teenagers. In this situation, relatively large amounts of paracetamol may have been ingested and this may not be disclosed in the history. It is much more likely that a toxic level will be achieved under these circumstances. Paracetamol exhibits analgesic action by peripheral blockage of pain impulse generation. It produces antipyresis by inhibiting the hypothalamic heat-regulating centre. Its weak anti-inflammatory activity is related to inhibition of prostaglandin synthesis in the CNS.


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