[ ]
Latest News Updates
Showing posts with label Toxicology. Show all posts
Showing posts with label Toxicology. Show all posts
By Piscean | Monday, January 30, 2012 | Posted in , , | With 0 comments

Enhanced Elimination in Toxicology 

Extracorporeal elimination
Extracorporeal elimination techniques require specialised staff, are invasive with significant risks of adverse events, and require specialised equipment and monitoring. They should only be undertaken in severe and life-threatening poisoning with appropriate toxicological and critical advice.
Haemodialysis: intermittent or continuous haemodialysis may be potentially beneficial in select poisonings based on the characteristics of the drug or toxin involved. In general, the drug or toxin needs to be a small molecule that has a small volume of distribution and slow elimination. In some cases, haemodialysis is beneficial for reasons other than removal of the drug or toxin, such as acidosis in metformin overdose where it is used to remove lactate.
Haemoperfusion: rarely used due to limited benefit in addition to haemodialysis and the limited availability of charcoal cartridges.
Plasmapheresis: despite numerous reports in the early literature there is no evidence for the use of plasmapheresis in the removal of drugs or toxins. There may be potential benefit for complications such as rhabdomyolysis.
The specific indications for extracorporeal techniques of elimination are discussed with the individual drugs and toxins and include:
  • toxic alcohols: methanol and ethylene glycol
  • anticonvulsants: valproate, carbamazepine
  • theophylline
  • lithium: chronic lithium poisoning in patients with acute renal failure
  • metformin: removal of lactate
  • methotrexate
  • salicylates.

Urinary alkalinisation
Urinary alkalinisation has a limited role, which is only in poisoning by salicylates, methotrexate and some pesticides. Use:
sodium bicarbonate 8.4% (= 1 mmol/mL) 1 mmol/kg IV as an initial bolus, then 25 to 50 mmol hourly as an IV infusion (100 mmol in 1000 mL of sodium chloride 0.9% at 250 mL/hour). The rate should be adjusted to maintain a urinary pH greater than 7.5.


PLUS EITHER

1
potassium chloride 14 to 16 mmol orally, 3 times daily (child: 1 mmol/kg/day in 2 to 4 doses) [Note 1].


OR
1
potassium chloride 10 to 20 mmol (= 0.75 to 1.5 g) IV, over 1 to 2 hours (child: 0.6 mmol/kg IV over 3 hours) preferably as a pre-mixed solution of the appropriate intravenous fluid. [Note 2].
Electrolytes should be monitored every four hours to monitor potassium and renal function. A dipstick urinalysis should be done regularly to make sure the urine remains alkaline.
Note 1: Effervescent immediate-release tablets of potassium contain 14 mmol potassium per tablet, and slow-release tablets contain 8 mmol potassium. The slow-release formulations of potassium are almost completely absorbed within one hour.
Note 2: If pre-mixed IV solution is unavailable, potassium chloride concentrate injection must be added to a large volume of parenteral fluid and mixed thoroughly before infusion. The usual maximum concentration is 40 mmol/L.
By Piscean | | Posted in , , | With 0 comments

Decontamination in Toxicology
or
How to Decontamination in Toxicology
Single-dose activated charcoal
There is limited evidence for the use of activated charcoal. The current international consensus is for its use only in significant poisoning within one hour of the estimated time of ingestion and for slow-release preparations at any time. In this situation, use:
activated charcoal 50 g (child: 1 g/kg to a maximum of 50 g) orally or via orogastric or nasogastric tube, within 1 hour of the estimated time of ingestion. Patients must be able to protect their airway or be intubated.

However, there are good theoretical reasons, and some evidence, for the use of charcoal later than one hour after ingestion. This is based on some recent studies on the effect of charcoal on clearance for particular drugs, and the fact that most studies of activated charcoal have excluded patients who have ingested severely toxic agents. Therefore the recommendation for the use of activated charcoal and the timing of its use will vary for some agents. This is described under each individual drug or toxin.
The use of activated charcoal containing sorbitol or other cathartics is no longer recommended.

Whole bowel irrigation
Whole bowel irrigation (WBI) should be considered within the first few hours for ingestions of metals or slow-release preparations. Specific examples include patients who have ingested significant iron overdose (greater than 60 mg/kg), lead, arsenic trioxide causing symptoms, lithium, slow-release potassium chloride (greater than 2.5 mmol/kg), slow-release verapamil or life-threatening doses of of slow-release diltiazem. Another group in whom whole bowel irrigation may be considered is body packers [Note 1].

Although there are good theoretical reasons for using whole bowel irrigation in these situations, there is little evidence to support its use. It is essential to carefully balance the possible benefits against the significant risk of aspiration and practical difficulties of administering whole bowel irrigation. Particular issues are the potential for vomiting and profuse diarrhoea to interfere with timely retrieval and life-saving interventions. Whole bowel irrigation is contraindicated in patients with gastrointestinal ileus. Development of ileus must, therefore, be carefully monitored by listening for bowel sounds, particularly in intubated patients and patients ingesting anticholinergic drugs. It is reasonable to discuss the use of whole bowel irrigation for individual patients with a clinical toxicologist. Use:

macrogol 3350 powder with electrolytes (ColonLYTELY) 2 sachets dissolved in 2 L of water, 1 to 1.5 L (child: 20 to 30 mL/kg/hour) in the first hour, then 1 L/hour (child: 20 to 30 mL/kg/hour) orally or via orogastric or nasogastric tube, if given within 2 hours of ingestion. Patients must be able to protect their airway or be intubated. [Note 2]


Multiple-dose activated charcoal
There is limited evidence for multiple-dose activated charcoal but it is recommended for some agents—carbamazepine, quinine, theophylline, phenobarbitone, oleander.
In adults, use:
1
activated charcoal 50 g orally or via orogastric or nasogastric tube, every 4 to 6 hours. Patients must be able to protect their airway or be intubated.


OR

1
activated charcoal 10 g orally or via orogastric or nasogastric tube, hourly. Patients must be able to protect their airway or be intubated.

In children, use:
activated charcoal 1 g/kg (to a maximum of 50 g) as an initial dose orally or via orogastric or nasogastric tube, followed by 0.5 g/kg every 4 hours. Patients must be able to protect their airway or be intubated.



Skin decontamination
Patients who have been doused in, or who have ingested with associated spillage of, hazardous materials should have all of their clothes removed and then be washed in a shower with soapy water. Once this has been done there is then no risk of secondary contamination or poisoning by toxic agents in persons looking after these patients. An Australian consensus statement on nosocomial risk in organophosphate poisoning has been published. [Note 3]

Gastric lavage
Gastric lavage is no longer recommended, except in rare circumstances where a single aspiration of the stomach contents may be attempted early in potentially life-threatening poisoning and only if the airway is protected. A safe option is to simply suction out the contents of the stomach if the patient has been intubated but instillation of fluid in the stomach is not recommended.

Induced emesis
Inducing emesis by any means is not recommended due to the risks of aspiration. Syrup of Ipecac is not recommended at all and ipecacuanha is no longer available in this formulation in Australia. This is due to lack of effectiveness and the risks of aspiration if the patient becomes sedated and then begins to vomit.

Ocular decontamination
Ocular decontamination requires copious irrigation with either water or normal saline. For substances that are irritant and minimally corrosive then irrigation for 15 to 20 minutes is usually sufficient. For corrosive agents irrigation should continue longer, see Eye trauma: chemical burns.
Note 1: Body packing refers to the swallowing of plastic- or latex-wrapped packages of illicit drugs for concealment from inspection. Presentation to the emergency department is often long after swallowing the packages, which have therefore usually entered the small or large intestine.
Note 2: Macrogol is the recommended International Nonproprietary Name (rINN) for polyethylene glycol.
Note 3: Little M, Murray L. Consensus statement: risk of nosocomial organophosphate poisoning in emergency departments. Emerg Med Australas 2004;16(5-6):456-8.
By Piscean | | Posted in , , | With 0 comments

Resuscitation in Toxicology

Supportive care
Initial resuscitation should be based on the assessment of the patient and not the particular toxin involved and standard advanced life support (ALS) guidelines should be followed (see Figure 14.4 and Figure 14.5). Specific instances where treatment may differ are indicated below.

The majority of patients taking overdoses or with drug toxicity are young and healthy, so cardiac and respiratory support should be continued for much longer periods of time in patients with a toxicity-related cardiorespiratory arrest.

If there is any doubt, cardiac compression and ventilatory support should be continued until the situation has been discussed with a clinical toxicologist. There has been survival with normal neurological function in patients receiving cardiopulmonary resuscitation (CPR) for hours.

Airway
There are no specific differences from Resuscitation except for caustic and corrosive ingestions . CNS depression is a common effect of drugs, so regular and careful assessment of airway protection and patency is important.

Breathing
Toxicology patients rarely have hypoxia unless they develop aspiration pneumonitis. The commonest problem is hypoventilation secondary to respiratory depression.

Circulation

Inotropic support
The use of intravenous fluid therapy and inotropic support should be based on patient haemodynamics and the specific toxins ingested.
Although specific inotropes or or other drugs are suggested in toxicology patients, the initial management of cardiogenic shock should be the same as for any other cause  unless there are specific contraindications to particular inotropes. The initial inotrope of choice is adrenaline unless its vasopressor actions are contraindicated, such as in beta blocker overdose. Administration of an inotrope should only be undertaken in consultation with a toxicologist or cardiologist.

Other inotropes are used in toxicology, but should usually be used in consultation with a clinical toxicologist. Usual doses of these are given in Box 14.24.

Prolonged cardiopulmonary resuscitation is essential because unlike in arrests due to cardiovascular disease, the majority of patients are healthy prior to the overdose, and survival with normal neurological function after long periods (hours) of cardiopulmonary resuscitation is well documented.


Adult doses of other inotropes used in toxicology (Box 14.24)
Milrinone (phosphodiesterase inhibitor)
milrinone 50 micrograms/kg IV, slowly over 10 minutes, followed by 0.375 to 0.75 micrograms/kg/minute IV, adjusting according to clinical and haemodynamic response, up to a maximum of 1.13 mg/kg daily.
Insulin euglycaemia
1
short-acting insulin 1 unit/kg  IV bolus, followed by 1 unit/kg/hour. The dose can be increased to 2 units/kg/hour or further but this should be discussed with a clinical toxicologist


PLUS


glucose 10% or 50% IV infusion

OR

2
glucagon 5 to 10 mg (= 5 to 10 units) IV bolus, then continue at 5 to 10 mg/hour.
Dobutamine
dobutamine 2.5 to 10 micrograms/kg/minute IV.


Drug-induced arrhythmias
QT prolongation and torsades de pointes: QT prolongation should be monitored and any other precipitating factors should be determined and treated if possible. Electrolytes, including magnesium and calcium, should be checked and deficiencies corrected.
Patients with hypomagnesaemia should have magnesium replacement. [Note 1]
In adults, use:
magnesium sulfate 50% 5 to 10 mL (= 2.5 to 5 g or 10 to 20 mmol) IV over 30 to 60 minutes.

In children, use:
magnesium sulfate 50% 0.1 mL/kg (= 50 mg/kg or 0.2 mmol/kg) IV over 20 minutes [Note 2], followed by 0.06 mL/kg/hour (= 30 mg/kg/hour or 0.12 mmol/kg/hour) IV infusion.

Patients with hypocalcaemia should have calcium replaced. Use:
In adults, use:
calcium gluconate 10% 10 to 20 mL (= 1 to 2 g or 2.2 to 4.4 mmol) IV, over 10 to 30 minutes.

In children, use:
calcium gluconate 10% 2 to 5 mL/kg/day (= 200 to 500 mg/kg/day) IV infusion.

Patients with hypokalaemia should have potassium replaced. If the patient is able to take and absorb oral potassium, use:
potassium chloride 14 to 16 mmol orally, 3 times daily (child: 1 mmol/kg/day in 2 to 4 doses) [Note 3].

If the serum potassium is less than 3 mmol/L or the patient is unable to take or absorb oral potassium, use:
potassium chloride 10 to 20 mmol (= 0.75 to 1.5 g) IV, over 1 to 2 hours (child: 0.6 mmol/kg IV over 3 hours) preferably as a pre-mixed solution of the appropriate intravenous fluid. [Note 4].
Isoprenaline or transvenous pacing should be considered in patients with a prolonged QT interval and bradycardia. In adults, use:
isoprenaline 20 micrograms IV, repeat according to clinical response, and commence an infusion at 1 to 4 micrograms/minute, but the rate may need to be rapidly increased to give double, quadruple or higher doses as required to overcome the beta blockade.

Torsades de pointes may resolve spontaneously within a minute but if not, first-line treatment is a 200 J DC shock or equivalent. If there is no response to an initial DC shock this can be repeated with increasing voltage shocks. Magnesium should also be given (except in torsades de pointes resulting from beta blocker overdose, see Toxicology: beta blockers).
In adults, use:
magnesium sulfate 50% 2 to 4 mL (= 1 to 2 g or 4 to 8 mmol) IV as a slow injection over 2 to 5 minutes.

In children, use:
magnesium sulfate 50% 0.05 to 0.1 mL/kg to a maximum of 4 mL (= 0.025 to 0.05 g/kg or 0.1 to 0.2 mmol/kg to a maximum of 8 mmol/dose) IV as a slow injection over 10 to 15 minutes.

If there is deterioration to ventricular fibrillation or asystole, standard advanced life support protocols should be followed, see Figure 14.4 and Figure 14.5.
Note 1: In toxicology patients, the correction of magnesium deficiency, if required, needs to be done rapidly while the patient has a prolonged QT interval and is at risk of torsades de pointes.
Note 2: Magnesium can be given intramuscularly in infants or children if urgent IV access not possible.
Note 3: Effervescent immediate-release tablets of potassium contain 14 mmol potassium per tablet, and slow-release tablets contain 8 mmol potassium. The slow-release formulations of potassium are almost completely absorbed within one hour.
Note 4: If pre-mixed IV solution is unavailable, potassium chloride concentrate injection must be added to a large volume of parenteral fluid and mixed thoroughly before infusion. The usual maximum concentration is 40 mmol/L.
By Piscean | Friday, January 27, 2012 | Posted in , , | With 0 comments
By Piscean | | Posted in , , | With 0 comments

Arterial blood gases in Toxicology

Arterial blood gases are an important investigation in overdose patients for two major conditions.
Respiratory depression: many drugs in overdose cause CNS depression and respiratory depression. The most sensitive test for respiratory depression is a pCO2 on an arterial blood gas. An arterial blood gas should be undertaken in any drug overdose where there is evidence of respiratory depression (respiratory rate less than 12), or where the ingested drug(s) are known to cause profound respiratory depression (eg opioids).
Metabolic acidosis: this is an important complication for a number of drug/toxins in overdose and an arterial blood gas (including a lactate level) will help determine the severity and aetiology of any metabolic acidosis
By Piscean | | Posted in , , | With 0 comments

Radiological imaging in Toxicology

Chest X-ray is important for patients with hypoxia (not secondary to hypoventilation) and in patients who have suspected aspiration pneumonitis. It may also be important in patients who develop pulmonary oedema, and if there is any type of inhalational injury.
A brain CT may be occasionally required to exclude other diagnoses in patients with central nervous system depression, coma or in patients with a suspected hypoxic brain injury following an overdose
By Piscean | | Posted in , , | With 0 comments

Pathology tests in Toxicology

In general patients with poisoning do not require routine blood tests and only in specific cases, or for particular drugs, is testing required. Renal function tests may be useful in patients who have ingested drugs that may cause renal impairment (eg NSAIDs) or, more importantly, drugs that are renally eliminated (eg lithium, digoxin). Liver function tests are essential with paracetamol poisoning and other instances where liver injury is suspected (eg colchicine). Specific blood tests are listed as key investigations for individual drugs.
By Piscean | | Posted in , , | With 0 comments

Drug concentrations in Toxicology

Serum concentrations of the drug are rarely available for the clinical management of patients and are only necessary in a number of notable exceptions, namely:
paracetamol
most common anticonvulsants, eg phenytoin, carbamazepine, phenobarbitone, valproate
aspirin
digoxin
iron
lithium
methotrexate
potassium
theophylline
toxic alcohols: methanol, ethylene glycol, ethanol.
By Piscean | | Posted in , , | With 0 comments
Electrocardiography


QRS widening
QRS widening on the ECG is a sodium channel effect, most commonly seen with tricyclic antidepressants, but also with a number of other medications. A QRS duration greater than 120 msec (0.12 seconds) is generally regarded as abnormal. A list of drugs associated with QRS widening is provided in Table 14.29.

Drugs associated with QRS widening and sodium channel blockade (Table 14.29)
Antidepressants
tricyclic antidepressants
venlafaxine
Antihistamines
diphenhydramine
Antipsychotics
thioridazine
Cardiovascular drugs
flecainide
propranolol
quinidine
Local anaesthetics
bupivacaine
ropivacaine
Others
bupropion
chloroquine
cocaine
dextropropoxyphene
dolasetron
hydroxychloroquine
quinine

QT prolongation
QT prolongation on ECG is a potassium channel effect associated with torsades de pointes. The assessment of the QT interval remains problematic, but a QT nomogram, see Figure 14.21, has been suggested as a useful way to determine if the QT/HR pair is abnormal (at risk of torsades de pointes). To use the nomogram (Figure 14.21), the QT interval should be measured manually on a 12-lead ECG from the beginning of the Q wave to the end of the T wave in multiple leads (namely, six leads including limb and chest leads) and the median QT calculated. The median QT interval is plotted on the nomogram against the heart rate recorded on the ECG. If the point is above the line, then the QT/HR is regarded as 'at risk'.
Drugs known to cause this effect are listed in Table 14.30.

Drugs associated with QT prolongation and torsades de pointes (Table 14.30)
Antiarrhythmics
amiodarone
disopyramide
dofetilide
procainamide
quinidine
sotalol
Other cardiovascular drugs
bepridil
enalapril
propranolol
Antidepressants
citalopram
escitalopram
fluoxetine
moclobemide
tricyclic antidepressants [NB1]
Antihistamines
loratadine
Antimicrobials
ciprofloxacin
clarithromycin
erythromycin
fluconazole
moxifloxacin
pentamidine
sparfloxacin
voriconazole
Antipsychotics
amisulpride
droperidol
haloperidol
pimozide
thioridazine
ziprasidone
Chemotherapeutic agents
arsenic
Other drugs
caesium
chlorpromazine
cisapride
cocaine
methadone
NB1: QT prolongation is usually due to QRS widening and there is no true lengthening of the JT interval
A full list with continuing updates can be found at http://www.qtdrugs.org/medical-pros/drug-lists/drug-lists.htm

QT interval nomogram to assess risk of torsades de pointes (Figure 14.21)

The QT interval should be measured manually on a 12-lead ECG from the beginning of the Q wave to the end of the T wave in multiple leads (six leads including limb and chest leads) and the median QT calculated. The median QT interval is plotted on the nomogram against the heart rate recorded on the ECG. If the point is above the line, then the QT-HR combination implies a risk of torsades de pointes.

Chan A, Isbister GK, Kirkpatrick CM, Dufful SB. Drug-induced QT prolongation and torsades de pointes: evaluation of a QT nomogram. QJM 2007;100(10):609-15 by permission of Oxford University Press.
By Piscean | | Posted in , , | With 0 comments

Risk assessment of Toxicology

A careful risk assessment is the most important step in managing the poisoned patient after the initial resuscitation. A sensible approach that balances the risks of toxicity in the individual patient will make it much easier to institute decontamination, specific treatments and decide on the appropriate disposition. Early recognition of a low-risk patient will prevent unnecessary decontamination and expensive retrieval of patients in remote locations. Conversely, early recognition of severe toxicity will allow the institution of early decontamination and life-saving treatment, as well as early retrieval to appropriate critical care services and/or specialised toxicological units. In difficult cases, it is advisable to contact a clinical toxicologist or the Poisons Information Centre.

A risk assessment should be based on:
  1. toxin/drug:
  • type of drug or chemical (intrinsic toxicity)
  • dose (amount of drug/chemical ingested)
  • route of exposure (ingestion, contact, inhalation, parenteral)
     2. individual patient: age, sex, comorbidities
     3. time since ingestion
     4. clinical effects.
It is essential to get a good patient history as well as corroborating history (eg relatives, ambulance officer). Patients very rarely lie but may not recall events accurately.
By Piscean | | Posted in , , | With 0 comments

Poisons information centers

Seek expert advice for all serious poisonings or those that are unfamiliar. Poisons information centers in Australia are:
  • on 24-hour access throughout Australia
  • contacted by telephoning 13 11 26
  • staffed by pharmacists, able to refer to clinical toxicologists for medical advice.
When calling the Poisons Information Center have available the following useful information:
  • name of product: the exact name and spelling of the product makes finding information on it easier. Having the product at hand when calling makes this easier, and there may be additional information on the packaging. Active constituents can be useful if there is no record of the product name
  • age and weight of the patient
  • details of the exposure: time and type of ingestion (eg swallowed, licked container lid), ocular, skin contact
  • immediate action by the parents or carers
  • clinical effects: symptoms will influence what treatment is recommended.
In New Zealand the National Poisons Center is located in Dunedin and can be contacted by calling 0800-POISON / 0800 764766
By Piscean | Wednesday, November 2, 2011 | Posted in , , , | With 0 comments


Naltrexone

Naltrexone is an opioid antagonist used in the prevention of relapse in alcohol and opioid dependence. It is thought that alcohol ingestion causes the release of endogenous opioids, reinforcing the drinking behaviour. By blocking central opioid receptors, naltrexone prevents the reinforcing effects of alcohol and continued use inhibits the craving for alcohol. In opioid dependence, blockade of opioid receptors markedly weakens or completely blocks the euphoria and other effects of opioids. It is important that naltrexone is only used as an adjunct to psychological and social treatments.
Naltrexone is almost completely absorbed after oral administration, and reaches peak plasma concentrations within 1 hour. Bioavailability ranges from 5% to 40% because of extensive first-pass hepatic metabolism. The major active metabolite, 6-beta-naltrexol, reaches peak plasma concentrations 2 to 10 times higher than naltrexone, which probably contributes to the long duration of action. Naltrexone should not be used in patients with hepatitis or liver failure.

Patients should be warned that naltrexone can accelerate the loss of tolerance that occurs with abstinence from opioids. As a result, use of opioid agonists after cessation of naltrexone administration can place the person at high risk of fatal overdose.

Administration of naltrexone to an opioid-dependent person precipitates withdrawal within minutes. This persists for up to 48 hours, and is difficult to reverse. Nausea, vomiting, severe diarrhoea, confusion, irritability and hallucinations may occur. Therefore, naltrexone should not be administered until the withdrawal process is complete and the person has remained opioid-free for 7 to 10 days, or longer if a longer-acting opioid such as methadone has been used.

The most commonly reported adverse effects are nausea and headache.


Naloxone

Naloxone acts as a pure antagonist at opioid receptors. It is rapidly metabolised by the liver and has a half-life of approximately 1 hour. It is used to reverse sedation and respiratory depression after opioid overdose and intoxication.

Reversal of opioid analgesia by naloxone can lead to a recurrence of pain and to signs of withdrawal, so it is advisable not to use the drug unless the clinical situation warrants it.

Patients should be monitored frequently and repeat doses may need to be given at a later time because naloxone has a shorter half-life than most of the commonly used opioids. Too rapid reversal can precipitate acute withdrawal, hypotension, acute pulmonary oedema and/or a recurrence of pain. Dose requirements are extremely variable, depending on the dose of opioid to be antagonised.

To avoid re-emergence of opioid adverse effects, ensure that patches are removed before reversal, and determine what long-acting formulations have been administered, so that treatment with naloxone can be adjusted accordingly.
It may be possible to avoid a patient relapsing into narcosis after overdose by the use of an infusion of naloxone; this is particularly useful when long-acting drugs or formulations have been taken.
Emergency setting
Naloxone should not be used routinely in undifferentiated coma. It should only be used if opioid intoxication is suspected based on the clinical history and examination. Naloxone may result in severe withdrawal and aggression in chronic narcotic abusers. Uncooperative patients may not be willing to undergo further observation upon waking. The aim should be to avoid dangerously depressed levels of consciousness or respiration that may require intubation, rather than achieving full alertness. In the hospital setting where there are staff with advanced airway skills, careful observation may be the best management. Where these skills do not exist, full reversal is preferred. In all cases, initial basic life support measures, must still take priority over naloxone administration.

Postoperative setting
For reversal of opioid sedation and respiratory depression in adults in the postoperative setting, naloxone can be given in 100 microgram increments intravenously, every 2 minutes until the desired effect is obtained (more frequent injection may be required if the patient is apnoeic) or, by diluting 1 ampoule (400 micrograms/mL) to 10 mL with sterile normal saline, it can be given in 1 mL (ie 40 micrograms) increments and titrated against response. This may avoid the severe pain occurring when the analgesic effect of the opioid is suddenly reversed.

Opioid-induced pruritus
Naloxone appears to be the most reliable and cost-effective form of treatment for opioid-induced pruritus. A dose of 120 micrograms subcutaneously is used.
By Piscean | Monday, October 3, 2011 | Posted in , , , | With 0 comments

Toxicology: calcium channel blockers

For pharmacological information, see Calcium channel blockers in 'Getting to know your drugs'.
Indicators of toxicity
Dose ingested
The toxic dose varies in adult deliberate self-poisoning and unintentional poisoning. Toxicity may develop with just two to three times the normal daily dose in elderly patients. In children, ingestion of less than 12 mg/kg verapamil, or less than 2.7 mg/kg nifedipine, is unlikely to cause toxicity.

Other indicators of toxicity
Severity of poisoning is highly dependent on the type of calcium antagonist, with the most severe effects from cardioselective calcium antagonists, verapamil and diltiazem. Only massive ingestions of peripherally selective agents (nifedipine, felodipine, amlodipine) will result in severe poisoning.
Patients with underlying cardiac disease are likely to have more severe effects.

Clinical presentation
The main presenting features include:
cardiovascular effects: hypotension (combination of peripheral vasodilatation and myocardial depression) progressing to cardiogenic shock; bradycardia, first degree heart block progressing to junctional bradycardia (no P wave), idioventricular rhythms and asystole; pulmonary oedema 
 
central nervous system: drowsiness, confusion, rarely seizures Coma is usually secondary to hypotension/hypoxia from cardiovascular collapse.
gastrointestinal effects: nausea, vomiting
metabolic effects: hyperglycaemia; lactic acidosis. 
 
Key investigations
ECG: should be done in all patients
blood glucose level and electrolytes
blood gases. 
 
Treatment
Airway and breathing
Ensure that there is an adequate airway and breathing. However, intubation and ventilation is usually only required with severe poisoning where a decreased level of consciousness is multifactorial (hypoxia, hypotension, direct drug effect).

Circulation
Hypotension should be treated with a fluid bolus of 20 mL/kg of normal saline. Use:
sodium chloride 0.9% 20 mL/kg IV over 10 to 30 minutes.

This should be repeated if there is no response, or only a partial response. Persistent hypotension will need to be treated with inotropes.
Serial ECGs and ECG monitoring should be done in all but minor poisoning with calcium channel blockers. Bradycardia can be treated initially with atropine if there is hypotension, use:
atropine 0.5 to 1.5 mg IV as a bolus, repeat after 15 minutes if necessary (child: 0.02 mg/kg to a maximum of 0.5 mg/dose IV, repeated in 5 minutes if required to a total maximum of 1 mg).

Severe bradycardia with persistent hypotension may require temporary transvenous pacing, but ventricular rather than atrial pacing will be required due to atrioventricular (AV) nodal blockade.
Inotropic support
The choice of inotrope will depend partly on the particular calcium channel blocker ingested. Hypotension will usually result from a combination of myocardial depression, heart block and peripheral vasodilatation. Calcium therapy, see Antidotal therapy should be considered early before the use of inotropes. The following inotropes are recommended based on animal studies and anecdotal experience. Use:
1
adrenaline 1 to 20 micrograms/minute IV infusion, see Box 14.4


OR


1
short-acting insulin 1 unit/kg (see Table 5.30) IV as an initial bolus, followed by an infusion of 1 unit/kg/hour IV. The dose can be increased to 2 units/kg/hour or further but this should be discussed with a clinical toxicologist



PLUS
glucose 50% 50 mL (child: glucose 10% 2.5 mL/kg) IV as an initial bolus, followed by an infusion according to Box 14.26

OR

2
dopamine 10 to 20 micrograms/kg/minute (child: 5 to 20 micrograms/kg/minute) IV infusion, see Box 14.6.

The use of a combination of inotropes such as dobutamine and noradrenaline may be an appropriate option, but should be done in consultation with a critical care specialist. Vasopressors such as metaraminol or low-dose adrenaline may be useful in the short term for hypotension. Use:
1
metaraminol 0.5 to 1 mg (child: 0.01 mg/kg) IV as a bolus; this can be repeated if there is clinical response


OR

2
adrenaline 0.1 to 1 mg (child: 0.01 mg/kg) IV as a bolus; this can be repeated every 2 to 5 minutes depending on clinical response. An adrenaline infusion should then be commenced, see Box 14.4.

In patients in cardiac arrest the following should be used in addition to normal advanced life support protocols (see Figure 14.4 and Figure 14.5):
1
adrenaline 1 mg (child: 0.01 mg/kg) IV as a bolus; this can be repeated every 2 to 5 minutes depending on clinical response. An adrenaline infusion should then be commenced see Box 14.4


PLUS EITHER [Note 1]
1
calcium gluconate 10% 60 mL (child: 1.0 mL/kg) IV; if there is no response this dose can be repeated every 2 to 5 minutes


OR

2
calcium chloride 10% 20 mL (child: 0.2 mL/kg) IV; if there is no response this dose can be repeated every 2 to 5 minutes.

Prolonged cardiopulmonary resuscitation should be undertaken in these patients (4 to 8 hours), as prior to the overdose these patients are usually healthy individuals. Cardiac assist devices and/or extracorporeal circulatory support should be considered if available.
Decontamination
Consider an initial dose of charcoal up to 4 hours after severe poisoning with calcium channel blockers, if the patient has a protected airway. Calcium channel blockers can cause ileus, which is a contraindication to charcoal. Use:
activated charcoal 50 g (child: 1 g/kg to a maximum of 50 g) orally or via orogastric or nasogastric tube, up to 4 hours after the estimated time of ingestion. Patients must be able to protect their airway or be intubated.

Whole bowel irrigation should be considered for ingestions of slow-release preparations. However, evidence of benefit is based on single case reports and this must be weighed against the risk of aspiration in sedated patients and the availability of resources to administer whole bowel lavage. Use:
macrogol 3350 powder with electrolytes (ColonLYTELY) 2 sachets dissolved in 2 L of water, 1 to 1.5 L (child: 20 to 30 mL/kg/hour) in the first hour, then 1 L/hour  (child: 20 to 30 mL/kg/hour) orally or via orogastric or nasogastric tube, if given within 2 hours of ingestion. Patients must be able to protect their airway or be intubated. [Note 2]
Specific pharmacological therapies
Antidotal therapy
A specific antidote does not exist for calcium channel blocker overdose. However, the administration of calcium to increase extracellular calcium appears to partially reverse the heart block and arrhythmias induced by calcium channel blocker overdose—usually found with verapamil or diltiazem. In patients with heart block or cardiac dysrhythmias, use [Note 1]:
1
calcium gluconate 10% 30 mL (child: 0.6 mL/kg) IV, over 10 minutes; if there is no response this dose can be repeated every 5 minutes


OR

2
calcium chloride 10% 10 mL (child: 0.2 mL/kg) IV, over 10 minutes; if there is no response this dose can be repeated every 5 minutes.

Large doses of calcium may be required and up to 10 g has been used as an initial dose in severe toxicity. If there is a response to calcium then an infusion is recommended. Use:
1
calcium chloride 10% 1 to 10 mL/hour (0.02 to 0.2 mL/kg/hour in children) IV infusion, by a central line


OR

2
calcium gluconate 10% 3 to 30 mL/hour (0.06 to 0.6 mL/kg/hour in children) IV infusion.

Serum calcium needs to be measured in all patients. The aim is to produce hypercalcaemia and generally patients have minimal adverse effects. It is reasonable to aim to maintain the ionised serum calcium above 2 mmol/L.
Correction of acidosis
Sodium bicarbonate should be administered to patients with severe acidosis provided they have adequate ventilation (either spontaneous or mechanical ventilation). To rapidly change blood pH, use:
sodium bicarbonate 8.4% (= 1 mmol/mL) 1 to 2 mmol/kg IV boluses every 3 to 5 minutes, titrated to a narrowing of the QRS complex or resolution of arrhythmias.

Bicarbonate infusions are not appropriate because the body will buffer the change. Repeat boluses may be required over a period of four to six hours.

Monitoring and disposition
Criteria for discharge: All patients ingesting slow-release formulations must be observed for 24 hours. If no clinical or ECG effects develop they can be discharged.
Criteria for admission: All patients who have ingested more than twice the daily dose or who have evidence of toxicity must be admitted to a critical care unit for close observation.
By Piscean | | Posted in , , , | With 0 comments

Toxicology: beta blockers

For pharmacological information, see Beta blockers in 'Getting to know your drugs'.
Indicators of toxicity
Dose ingested
No clear toxic dose has been identified except for propranolol where ingestions of more than 2 g are associated with seizures.

Other factors determining toxicity of beta blockers
There are a number of important risk factors in beta blocker poisoning:
type of beta blocker:
propranolol: CNS effects, class IA anti-arrhythmic properties
sotalol: more severe cardiac effects and QT prolongation
patient's age or underlying heart disease
co-ingestion of calcium antagonist or digoxin.
Clinical presentation
The presenting features include:
central nervous system effects: seizures, delirium and coma occur with lipophilic beta blockers such as propranolol 
 
cardiovascular effects: Hypotension is due to a combination of myocardial depression and bradycardia. The most common arrhythmia is sinus bradycardia. In severe cases there can be 1st to 3rd degree heart block, junctional bradycardia, ventricular bradycardia and asystole.
metabolic effects: hypoglycaemia. 
 
Key investigations
ECG: QRS widening can occur with propranolol poisoning, (see QRS widening) and QT prolongation with sotalol (see QT prolongation).
blood glucose level.
Treatment
Airway and breathing
Ensure that there is an adequate airway and breathing. However, intubation and ventilation are usually only required with severe poisoning, where a decreased level of consciousness is multifactorial (hypoxia, hypotension, direct drug effect).
Coma and seizures are common with severe propranolol poisoning and will require early intervention.

Circulation
Hypotension should be treated with a fluid bolus of 20 mL/kg of normal saline. Use:
sodium chloride 0.9% 20 mL/kg IV, over 10 to 30 minutes.
This should be repeated if there is no response or only a partial response. Persistent hypotension will need to be treated with inotropes, see Inotropic support.
Serial ECGs and ECG monitoring should be done in all but minor poisonings with beta blockers. Bradycardia can be treated with atropine if there is hypotension, use:
atropine 0.5 to 1.5 mg IV as a bolus; repeat after 15 minutes if necessary (child: 0.02 mg/kg to a maximum of 0.5 mg/dose IV, repeated in 5 minutes if required to a total maximum of 1 mg).

Severe bradycardia with persistent hypotension may require temporary transvenous pacing.
Torsades de pointes may occur with sotalol poisoning and the QT interval should be measured regularly. Torsades de pointes should be treated with a 200 J DC shock and then isoprenaline or transvenous pacing, but magnesium should be avoided due to its potential to cause calcium channel blockade. In adults, use:
isoprenaline 20 micrograms IV, repeat according to clinical response, and commence an infusion at 1 to 4 micrograms/minute (see Box 14.5). The rate may need to be rapidly increased to give double, quadruple or higher doses as required to overcome beta blockade. 


Inotropic support
There is considerable controversy over inotropes in beta-blocker poisoning and advice from a clinical toxicologist should be obtained early. Although glucagon is often recommended there is no evidence to support its effectiveness, and there is rarely enough glucagon kept in hospitals to maintain treatment for over an hour. Recent animal evidence suggests vasopressors do not improve outcomes, so adrenaline, noradrenaline and vasopressin should be avoided in isolation. The following inotropes are recommended based on animal studies and anecdotal experience. In adults, use:
1
isoprenaline 20 micrograms IV, repeat according to clinical response (up to 100 micrograms), and commence an infusion at 2 to 4 micrograms/minute (see Box 14.5). The rate may need to be rapidly increased to give double, quadruple or higher doses as required to overcome beta blockade. Isoprenaline can be given via a peripheral line


OR


1
short-acting insulin 1 unit/kg (see Table 5.30) IV as an initial bolus, followed by an infusion at 1 unit/kg/hour IV. The dose can be increased to 2 units/kg/hour or further but this should be discussed with a clinical toxicologist



PLUS

glucose 50% 50 mL (child: glucose 10% 2.5 mL/kg) IV as an initial bolus, followed by an infusion according to Box 14.26

OR


2
glucagon 5 to 10 mg (= 5 to 10 units) IV as an initial bolus, followed by an infusion at 5 to 10 mg/hour IV

OR

2
milrinone 50 micrograms/kg IV, slowly over 10 minutes, followed by an infusion of 0.375 to 0.75 micrograms/kg/minute IV, adjusting according to clinical and haemodynamic response, up to a maximum of 1.13 mg/kg daily [Note 1].

Vasopressors such as metaraminol or low-dose adrenaline may be useful in the short term if there is evidence of reduced systemic vascular resistance with the use of insulin or isoprenaline. However, they should not be used in patients with the poor perfusion typical of untreated beta blocker poisoning. In adults, use:
1
adrenaline 1 mg IV as a bolus; this can be repeated every 2 to 5 minutes depending on clinical response. An adrenaline infusion should then be commenced. See Box 14.4.


OR
2
metaraminol 0.5 to 1 mg IV as an initial bolus; this can be repeated if there is a clinical response.

If the patient has a cardiac arrest, prolonged cardiopulmonary resuscitation should be undertaken (4 to 8 hours), as prior to the overdose these patients are usually healthy individuals. Cardiac assist devices and/or extracorporeal circulatory support should be considered if available.
Decontamination
Consider an initial dose of charcoal up to two hours after the estimated time of ingestion in severe poisoning if the patient has a protected airway. Use:
activated charcoal 50 g (child: 1 g/kg to a maximum of 50 g) orally or via orogastric or nasogastric tube, within 2 hours of the estimated time of ingestion. Patients must be able to protect their airway or be intubated.

Caution: In the setting of beta blocker overdose, atropine should be administered prior to the insertion of a nasogastric tube to prevent further bradycardia due to vagal stimulation. Use:
atropine 300 to 600 micrograms (child: 0.02 mg/kg to a maximum of 0.5 mg/dose) IV.

Specific pharmacological therapies
Anticonvulsant therapy
Treat underlying hypoglycaemia, see below.
Persistent seizures seen in propranolol poisoning should initially be treated with benzodiazepines. For drug and dosing recommendations, see Anticonvulsant therapy.
Treatment of hypoglycaemia
Hypoglycaemia should be treated. Use:
glucose 50% 50 mL (child: glucose 10% 2.5 mL/kg) IV, as an initial bolus.
Monitoring and disposition
Criteria for admission: All patients with deliberate self-poisoning or patients unintentionally ingesting more than the daily dose of beta blockers should be assessed initially and observed for at least six hours.
By Piscean | Friday, September 9, 2011 | Posted in , , | With 0 comments
Toxicology
Poisoning

Definition

Poisoning occurs when any substance interferes with normal body functions after it is swallowed, inhaled, injected, or absorbed. The branch of medicine that deals with the detection and treatment of poisons is known as toxicology.

Description

Poisonings are a common occurrence. About 10 million cases of poisoning occur in the United States each year. In 80% of the cases, the victim is a child under the age of five. About 50 children die each year from poisonings. Curiosity, inability to read warning labels, a desire to imitate adults, and inadequate supervision lead to childhood poisonings.
The elderly are the second most likely group to be poisoned. Mental confusion, poor eyesight, and the use of multiple drugs are the leading reasons why this group has a high rate of accidental poisoning. A substantial number of poisonings also occur as suicide attempts or drug overdoses.
Poisons are common in the home and workplace, yet there are basically two major types. One group consists of products that were never meant to be ingested or inhaled, such as shampoo, paint thinner, pesticides, houseplant leaves, and carbon monoxide. The other group contains products that can be ingested in small quantities, but which are harmful if taken in large amounts, such as pharmaceuticals, medicinal herbs, or alcohol. Other types of poisons include the bacterial toxins that cause food poisoning, such as Escherichia coli; heavy metals, such as the lead found in the paint on older houses; and the venom found in the bites and stings of some animals and insects. The staff at a poison control center and emergency room doctors have the most experience diagnosing and treating poisoning cases.

Causes and symptoms

The effects of poisons are as varied as the poisons themselves; however, the exact mechanisms of only a few are understood. Some poisons interfere with the metabolism. Others destroy the liver or kidneys, such as heavy metals and some pain relief medications, including acetaminophen (Tylenol) and nonsteroidal anti-inflammatory drugs (Advil, Ibuprofen). A poison may severely depress the central nervous system, leading to coma and eventual respiratory and circulatory failure. Potential poisons in this category include anesthetics (e.g. ether and chloroform), opiates (e.g., morphine and codeine), and barbiturates. Some poisons directly affect the respiratory and circulatory system. Carbon monoxide causes death by binding with hemoglobin that would normally transport oxygen throughout the body. Certain corrosive vapors trigger the body to flood the lungs with fluids, effectively drowning the person. Cyanide interferes with respiration at the cellular level. Another group of poisons interferes with the electrochemical impulses that travel between neurons in the nervous system. Yet another group, including cocaine, ergot, strychnine, and some snake venoms, causes potentially fatal seizures.
Severity of symptoms can range from headache and nausea to convulsions and death. The type of poison, the amount and time of exposure, and the age, size, and health of the victim are all factors which determine the severity of symptoms and the chances for recovery.
Common Household, Industrial, And Agricultural Products Containing Toxic Sustances
Alcohol (rubbing) FuelAntifreeze Floor/furniture polish
Arsenic Gasoline Art and craft supplies
Glues/adhesives Automotive fluids Hemlock
Batteries, automotive Kerosene Batteries, household
Mercury Building products Metal primers
Cleaning products Metalworking materials Cosmetics/personal care items
Mothballs Cyanide Oven cleaners
Daffodil bulbs Paint strppers/thinners Dieffenbachia
Paints, oil-based or alkyds Disinfectants/air fresheners Paints, water-based or latex
Drain openers Pesticides Flea collars/insect repellent
English nightshade Stains/finishes Ethanol
Strychnine Foxglove Wood preservatives

Plant poisoning

There are more than 700 species of poisonous plants in the United States. Plants are second only to medicines in causing serious poisoning in children under age five. There is no way to tell by looking at a plant if it is poisonous. Some plants, such as the yew shrub, are almost entirely toxic: needles, bark, seeds, and berries. In other plants, only certain parts are poisonous. The bulb of the hyacinth and daffodil are toxic, but the flowers are not; while the flowers of the jasmine plant are the poisonous part. Moreover, some plants are confusing because portions of them are eaten as food while other parts are poisonous. For example, the fleshy stem (tuber) of the potato plant is nutritious; however, its roots, sprouts, and vines are poisonous. The leaves of tomatoes are poisonous, while the fruit is not. Rhubarb stalks are good to eat, but the leaves are poisonous. Apricots, cherries, peaches, and apples all produce healthful fruit, but their seeds contain a form of cyanide that can kill a child if chewed in sufficient quantities. One hundred milligrams (mg) of moist, crushed apricot seeds can produce 217 mg of cyanide.
Common houseplants that contain some poisonous parts include:
  • Aloe
  • Amaryllis
  • Cyclamen
  • Dumb cane (also called Dieffenbachia)
  • Philodendron
Common outdoor plants that contain some poisonous part include:
  • Bird of paradise flower
  • Buttercup
  • Castor bean
  • Chinaberry tree
  • Daffodil
  • English ivy
  • Eucalyptus
  • Foxglove
  • Holly
  • Horse chestnut
  • Iris
  • Jack-in-the-pulpit
  • Jimsonweed (also called thornapple)
  • Larkspur
  • Lily-of-the-valley
  • Morning glory
  • Nightshade (several varieties)
  • Oleander
  • Potato
  • Rhododendron
  • Rhubarb
  • Sweet pea
  • Tomato
  • Wisteria
  • Yew
Symptoms of plant poisoning range from irritation of the skin or mucous membranes of the mouth and throat to nausea, vomiting, convulsions, irregular heartbeat, and even death. It is often difficult to tell if a person has eaten a poisonous plant because there are no tell-tale empty containers and no unusual lesions or odors around the mouth.
Many cases of plant poisoning involve plants that contain hallucinogens, such as peyote cactus buttons, certain types of mushrooms, and marijuana. A recent case of plant poisoning in France concerned Datura, or moonflower, a plant that has become popular with young people trying to imitate Native American puberty rites.
Other cases of plant poisoning result from the use of herbal dietary supplements that have been contaminated by toxic substances. The Food and Drug Administration (FDA) has the authority to monitor herbal products on the market and issue warnings about accidental poisoning or other adverse affects associated with these products. For example, in 2002 a manufacturer of nettle capsules found to contain lead recalled the product following a warning from the FDA. Other dietary supplements have been found to contain small quantities of prescription medications or even toxic plants.

Household chemicals

Many products used daily in the home are poisonous if swallowed. These products often contain strong acids or strong bases (alkalis). Toxic household cleaning products include:
  • ammonia
  • bleach
  • dishwashing liquids
  • drain openers
  • floor waxes and furniture polishes
  • laundry detergents, spot cleaners, and fabric softeners
  • mildew removers
  • oven cleaners
  • toilet bowl cleaners
Personal care products found in the home can also be poisonous. These include:
  • deodorant
  • hairspray
  • hair straighteners
  • nail polish and polish remover
  • perfume
  • shampoo
Signs that a person has swallowed one of these substances include evidence of an empty container nearby, nausea or vomiting, and burns on the lips and skin around the mouth if the substance was a strong acid or alkali. The chemicals in some of these products may leave a distinctive odor on the breath.

Pharmaceuticals

Both over-the-counter and prescription medicines can help the body heal if taken as directed. However, when taken in large quantities, or with other drugs where there may be an adverse interaction, they can act as poisons. Drug overdoses, both accidental and intentional, are the leading cause of poisoning in adults. Medicinal herbs should be treated like pharmaceuticals and taken only in designated quantities under the supervision of a knowledgeable person. Herbs that have healing qualities when taken in small doses can be toxic in larger doses, or may interact with prescription medications in unpredictable ways.
Drug overdoses cause a range of symptoms, including excitability, sleepiness, confusion, unconsciousness, rapid heartbeat, convulsions, nausea, and changes in blood pressure. The best initial evidence of a drug overdose is the presence of an empty container near the victim.

Other causes of poisonings

People can be poisoned by fumes they inhale. Carbon monoxide is the most common form of inhaled poison. Other toxic substances that can be inhaled include:
  • farm and garden insecticides and herbicides
  • gasoline fumes
  • insect repellent
  • paint thinner fumes

Diagnosis

Initially, poisoning is suspected if the victim shows changes in behavior and signs or symptoms previously described. Hallucinations or other psychiatric symptoms may indicate poisoning by a hallucinogenic plant. Evidence of an empty container or information from the victim are helpful in determining exactly what substance has caused the poisoning. Some acids and alkalis leave burns on the mouth. Petroleum products, such as lighter fluid or kerosene, leave a distinctive odor on the breath. The vomit may be tested to determine the exact composition of the poison. Once hospitalized, the patient may be given blood and urine tests to determine his or her metabolic condition.

Treatment

Treatment for poisoning depends on the poison swallowed or inhaled. Contacting the poison control center or hospital emergency room is the first step in getting proper treatment. The poison control center's telephone number is often listed with emergency numbers on the inside cover of the telephone book, or it can be reached by dialing the operator. The poison control center will ask for specific information about the victim and the poison, then give appropriate first aid instructions. If the patient is to be taken to a hospital, a sample of vomit and the poison container should be taken along, if they are available.
Most cases of plant poisoning are treated by inducing vomiting, if the patient is fully conscious. Vomiting can be induced by taking syrup of ipecac, an over-the-counter emetic available at any pharmacy.
For acid, alkali, or petroleum product poisonings, the patient should not vomit. Acids and alkalis can burn the esophagus if they are vomited, and petroleum products can be inhaled into the lungs during vomiting, resulting in pneumonia.
Once under medical care, doctors have the option of treating the patient with a specific remedy to counteract the poison (antidote) or with activated charcoal to absorb the substance inside the patient's digestive system. In some instances, pumping the stomach may be required. This technique, which is known as gastric lavage, involves introducing 20-30 mL of tap water or 9% saline solution into the patient's digestive tract and removing the stomach contents with a siphon or syringe. The process is repeated until the washings are free of poison. Medical personnel will also provide supportive care as needed, such as intravenous fluids or mechanical ventilation.
If the doctor suspects that the poisoning was not accidental, he or she is required to notify law enforcement authorities. Most cases of malicious poisoning concern family members or acquaintances of the victim, but the number of intentional random poisonings of the general public has increased in recent years. A case reported in 2003 involved the use of nicotine to poison 1700 pounds of ground beef in a Michigan supermarket. Over a hundred persons fell ill after eating the poisoned beef.

Prognosis

The outcome of poisoning varies from complete recovery to death, and depends on the type and amount of the poison, the health of the victim, and the speed with which medical care is obtained.

Prevention

Most accidental poisonings are preventable. The number of deaths of children from poisoning has declined from about 450 per year in the 1960s to about 50 each year in the 1990s. This decline has occurred mainly because of better packaging of toxic materials and better public education.
Actions to prevent poisonings include:
  • removing plants that are poisonous
  • keeping medicines and household chemicals locked and in a place inaccessible to children
  • keeping medications in child-resistant containers
  • never referring to medicine as "candy"
  • keeping cleaners and other poisons in their original containers
  • disposing of outdated prescription medicines
  • not purchasing over-the-counter medications with damaged protective seals or packaging
  • avoiding the use of herbal preparations not made by a reputable manufacturer

Key terms

Antidote — A medication or remedy for counteracting the effects of a poison.
Emetic — A medication or substance given to induce vomiting.
Gastric lavage — A technique for washing poison out of the stomach by instilling water or saline solution through a tube, removing the stomach contents by suction, and repeating the process until the washings are free of poison. It is also called stomach pumping.
Toxicology — The branch of medicine that deals with the effects, detection, and treatment of poisons.
 
Reference: http://medical-dictionary.thefreedictionary.com/Poisoning