Transcript EVALUATION OF THE ENVENOMED PATIENT Assessment of type

EVALUATION OF THE ENVENOMED
PATIENT
Assessment of type and extent of
envenoming Neurotoxic paralysis
'Sleepy' or drooping eyelids
Difficulty swallowing, dysarthria and
drooling
Limb weakness
Respiratory distress
Excitatory neurotoxicity
• Sweating, salivation, piloerection
• Tingling around mouth, tongue or muscle
twitching
• Dyspnoea (pulmonary oedema)
Myolysis
•
Muscle pain or weakness
Coagulopathy
•
•
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Blood oozing from bite site and/or gums
Bruising
Melaena, haematemesis
Local effects
•
Pain, sweating, blistering, bruising etc.
Taking a history in envenoming
• When was the patient exposed to a bite/sting?
• Was the organism causing it seen and what did it look
like (size, colour)?
• What were the circumstances (on land, in water etc.)?
• Was there more than one bite/sting?
• What first aid was used, when and for how long?
• What symptoms has the patient had (local and
systemic)?
• Are there symptoms suggesting systemic envenoming
(paralysis, myolysis, coagulopathy etc.)?
• Past medical history and medications?
• Past exposure to antivenom/venom and allergies
• Acute poisoning is common, accounting for about
10% of hospital admissions in the UK. In developed
countries, the most frequent cause is intentional
drug overdose in the context of self-harm and
usually involves prescribed or 'over-the-counter'
medicines. Accidental poisoning is also common,
especially in children and the elderly .Toxicity also
may occur as a result of alcohol or recreational
substance use, or following occupational or
environmental exposure. Poisoning is a major
cause of death in young adults, but most deaths
occur before patients reach medical attention, and
mortality is much lower than 1% in those admitted to
hospital.
• In developing countries, the frequency of
self-harm is more difficult to estimate
because patients may be reticent in
admitting to deliberate poisoning. Household
and agricultural products such as pesticides
and herbicides are more freely available, are
common sources of poisoning and are
associated with a much higher case fatality.
In China and South-east Asia, pesticides
account for about 300 000 suicides each
year.
Important substances involved in poisoning
Analgesics, e.g. paracetamol and non-steroidal
anti-inflammatory drugs (NSAIDs)
• Antidepressants, e.g. tricyclic antidepressants
(TCAs), selective serotonin re-uptake inhibitors
(SSRIs) and lithium
• Cardiovascular agents, e.g. β-blockers, calcium
channel blockers and cardiac glycosides
• Drugs of misuse, e.g. opiates, benzodiazepines,
stimulants (e.g. amphetamines, MDMA, cocaine)
• Carbon monoxide*
• Alcohol
In South and South-east Asia
• Organophosphorus* and carbamate
insecticides
• Aluminium and zinc phosphide
• Oleander
• Snake venoms
• Antimalarial drugs, e.g. chloroquine
• Antidiabetic medication
Poisoning in old age
• Aetiology: commonly results from accidental
poisoning (e.g. due to confusion or dementia) or
drug toxicity as a consequence of impaired renal or
hepatic function or drug interaction. Toxic
prescription medicines are more likely to be
available.
• Psychiatric illness: self-harm is less common than
in younger adults but more frequently associated
with depression and other psychiatric illness, as
well as chronic illness and pain. There is a higher
risk of subsequent suicide.
• Severity of poisoning: increased morbidity and
mortality result from reduced renal and hepatic
function, reduced functional reserve, increased
sensitivity to sedative agents and frequent
comorbidity
GENERAL APPROACH TO THE POISONED
PATIENT
Triage and resuscitation
s Patients who are seriously poisoned must be
identified early so that appropriate management is
not delayed. Triage involves:
• immediate measurement of vital signs
• identifying the poison(s) involved and obtaining
adequate information about them
• identifying patients at risk of further attempts at selfharm and removing any remaining hazards from
them.
Those with possible external contamination with
chemical or environmental toxins should undergo
appropriate decontamination .Critically ill patients
must be resuscitated
Substances of very low toxicity
• Writing/educational materials
• Decorating products
• Cleaning/bathroom products (except
dishwasher tablets which are corrosive)
• Pharmaceuticals: oral contraceptives, most
antibiotics (but not tetracyclines and
antituberculous drugs), H2-blockers, proton
pump inhibitors, emollients and other skin
creams, baby lotion
• Miscellaneous: plasticine, silica gel,
household plants, plant food
• The Glasgow Coma Scale (GCS) is commonly employed to assess
conscious level, although it has not been specifically validated in poisoned
patients. The AVPU (alert/verbal/painful/unresponsive) scale is also a rapid
and simple method. An electrocardiogram (ECG) should be performed and
cardiac monitoring instituted in all patients with cardiovascular features or
where exposure to potentially cardiotoxic substances is suspected.
Patients who may need antidotes should be weighed when this is feasible,
so that appropriate doses can be prescribed. Substances that are unlikely
to be toxic in humans should be identified so that inappropriate admission
and intervention are avoided
•
Clinical assessment and investigations. Occasionally, patients may be unaware
or confused about. what they have taken, or may exaggerate (or less commonly
underestimate) the size of the overdose, but rarely mislead medical staff
deliberately. In some parts of the world, such as Asia, patients may not readily
admit to deliberate self-poisoning.. The patient may have a cluster of clinical
features ('toxidrome') suggestive of poisoning with a particular drug Poisoning is
a common cause of coma, especially in younger people, but it is important to
exclude other potential causes unless the aetiology is certain. Urea, electrolytes
and creatinine should be measured in most patients. Arterial blood gases should
be checked in those with significant respiratory or circulatory compromise, or
when poisoning with substances likely to affect acid-base status is suspected
.Calculation of anion and osmolar gaps may help to inform diagnosis and
management
Causes of acidosis in the poisoned patient
• Cause Normal lactate*High lactateToxic
Salicylates, Metformin, Methanol, Iron ,Ethylene
glycol, Cyanide ,Paraldehyde, Sodium
valproate , Carbon monoxide Other ,Renal failure
Shock Ketoacidosis , Severe diarrhoea
*Unless circulatory shock is present, when it will
be high in any case
• Anion and osmolar gaps in poisoning
•
Anion gap Osmolar gap Calculation
[Na+ + K+] - [Cl- + HCO3-
]Osm (measured) - [2Na + K + Urea + Glucose]Normal range12-16
mmol/L< 10 mOsm/kg Common toxic causes of elevation *Ethanol
Ethylene glycol
Methanol
Salicylates
Iron
Cyanide Ethanol
Ethylene glycol
Methanol
Psychiatric assessment
• All patients presenting with deliberate drug
overdose should undergo psychosocial evaluation
by a health professional with appropriate training
prior to discharge.This should take place once the
patient has recovered from any features of
poisoning, unless there is an urgent issue such as
uncertainty about his or her capacity to decline
medical treatment
General management
•
Patients presenting with eye or skin contamination should
undergo appropriate local decontamination procedures
.Gastrointestinal decontamination .Laboratory analysis in
poisoning
Acetylcholinesterase
• Plasma cholinesterase is reduced more rapidly but is less
specific than red cell cholinesterase in organophosphorus
poisoning
• Antidote use should not be delayed pending results
Carboxyhaemoglobin
• > 20% indicates significant carbon monoxide exposure
Digoxin
• Therapeutic range usually 1-2 μg/L
• Concentrations > 4 μg/L usually associated with toxicity,
especially with chronic poisoning
Ethanol
• Toxicity at concentrations > 1.8 g/L
Iron
• Take sample at least 4 hrs after overdose or if there are
clinical features of toxicity
• Concentrations > 5 mg/L suggest severe toxicity
Lithium
• Take sample at least 6 hrs after overdose or if there are
clinical features of toxicity
• Usual therapeutic range 0.4-1.0 mmol/
Methaemoglobin
• Methaemoglobinaemia associated with toxicity due to nitrites, benzocaine,
dapsone, chloroquine, aniline dyes
• Concentrations > 20% may require treatment with methylthioninium chloride
(methylene blue)
Paracetamol
• Take sample at least 4 hrs after overdose
• Use nomogram to determine need for antidotal treatment Salicylate
• Take sample at least 2 hrs (symptomatic patients) or 4 hrs (asymptomatic patients)
after overdose
• Concentrations > 500 mg/L suggest serious toxicity
• Repeat after 2 hrs if severe toxicity is suspected
Theophylline
• Take sample at least 4 hrs after overdose or if there are clinical features of toxicity
• Repeat after 2 hrs if severe toxicity is suspected
• Concentrations > 60 mg/L suggest severe toxicity
• Patients who have ingested potentially life-threatening quantities of toxins may be
considered for gastrointestinal decontamination if poisoning has been recent).
Induction of emesis using ipecacuanha is now never recommended
Activated charcoal
• Use of gastric decontamination methods Single-dose
activated charcoal ‘
The administration of activated charcoal may be considered
if a patient has ingested a potentially toxic amount of a
poison (which is known to be adsorbed to charcoal) up to
1 hr previously.
Multiple-dose activated charcoal
1.'Multiple-dose activated charcoal should be considered
only if a patient has ingested a life-threatening amount of
carbamazepine, dapsone, phenobarbital, quinine or
theophylline
.'2.Gastric lavage 'Gastric lavage should not be employed
routinely, if ever, in the management of poisoned patients.
'3.Whole bowel irrigation (WBI)
• 'WBI should be considered for potentially toxic
ingestions of sustained-release or enteric-coated
drugs, particularly for those patients presenting
more than 2 hrs after drug ingestion. WBI should
be considered for patients who have ingested
substantial amounts of iron, as the morbidity is
high and there is a lack of other options for
gastrointestinal decontamination. The use of WBI
for the removal of ingested packets of illicit drugs
is also a potential indication
• Given orally as slurry, activated charcoal absorbs toxins in the bowel
as a result of its large surface area. If given sufficiently early, it can
prevent absorption of an important proportion of the ingested dose
of toxin. However, efficacy decreases with time and current
guidelines do not advocate use more than 1 hour after overdose in
most circumstances However, use. after a longer interval may be
reasonable when a delayed-release preparation has been taken or
when gastric emptying may be delayed. Some toxins do not bind to
activated charcoal .so it will not affect their absorption. In patients
with an impaired swallow or a reduced level of consciousness, the
use of activated charcoal, even via a nasogastric tube, carries a risk
of aspiration pneumonitis. This risk can be reduced but not
completely removed by protecting the airway with a cuffed
endotracheal tube.