drugs Overdose and poisoning
Definition
Acute poisoning may result from accidental self ingestion,deliberate self-harm or medical error or when a parson cross a limit of medicine or such types of drugs lets take example of alprazolam a medicine which is used for induce sleep and treat some types of anxiety .when a parson overdose from it may be death occur from that from the medicine such types of condition are know as overdose and many other drugs used as a antidotes
age effect
overdose affect all age humanIncidence/prevalence
Common presentation to A&E, commonest cause ofmedical admission of teenagers.
Clinical features
Acute poisoning should be considered in any patient presenting withaltered levels of consciousness; however, the
vast majority of patients who present are conscious. The
patient or carers may be able to give a history and bring
the containers or tablets. A full physical examination
should be made.
pathophysiology
Central nervous system: Impaired consciousness,Occasionally transient gastrointestinal upset, confusion,
dizziness and ataxia may occur
world.
Severe toxicity (usually an idiosyncratic response,
rather than dose-related) includes cardiac arrhythmias,
hypotension and shock, hyponatraemia,
seizures, increasing confusion and loss of consciousness.
A history should be taken of recent and previous
recreational drug use, including methods of administration,
alcohol intake. A psychiatric and social history
should be taken
Complications
Deaths: These appear to be due to cardiac arrhythmias,fulminant liver failure and neuroleptic malignant syndrome,
which may cause acute renal failure, disseminated
intravascular coagulation and metabolic acidosis.
Neuropsychiatric complications include memory and
concentration loss, insomnia, hallucinations and flashbacks.
how to deal when overdose
In all cases, ECG, U&Es, LFTS and creatinine kinase (CK)should be performed
how to Manage
In severe toxicity, initial management includes ensuringa clear airway, and ventilation if needed.
1 All patients should have cardiac, pulse, blood pressure
and temperature monitoring.
2 Diazepam for agitation, anxiety, significant hypertension
and seizures.
3 Continued hypertension is treated with intravenous
glyceryl trinitrate, but in refractory hypertension contact
the NPIS.
4 Symptomatic hyponatraemia is usually treated with
water restriction; however, in coexisting hypotension
normal saline infusion may be required.
Common causes of acute poisoning
Over the counter Salicylates, paracetamol, ibuprofenmedicines
Psychotropic drugs
Drugs of abuse
Opiates, cocaine, ecstasy,
amphetamines, ketamine
Garden Plants,
seeds, mushrooms,
insecticides, organophosphates
some common Drug and its Antidotes
Benzodiazepines FlumazenilParacetamol N-acetyl cysteine
Opiates Naloxone
β-blockers Atropine and glucagon
Digoxin Digoxin specific antibody
let's take some commen medicine overdosing problems and its solution
Iron overdose
Definition
Accidental or deliberate overdose of iron salts.pathophysiology
from accidental ingestion of iron-containing medications
such as vitamin preparations mistaken for sweets.
Clinical features of iron overdose
Iron causes acute necrotising gastritis. Patients may developnausea, vomiting, abdominal pain and diarrhoea.
In severe poisoning acute upper gastrointestinal bleeding,
convulsions and metabolic acidosis may occur. Late
signs in severe overdose include hypotension, coma, hypoglycaemia
and hepatocellular necrosis.
how to investigate
A serum iron level (ideally at 4 hours after ingestion) isthe best laboratory measure of severity. Abdominal Xray
may show radio-opaque tablets present in the stomach
or small bowel if taken within 2 hours of ingestion.
A raised neutrophil count and serum glucose suggests
toxicity. LFTs and blood gas measurements should be
performed.
Complications and risk factor
Gastrointestinal perforation or infarction.Management
In severe poisoning (unconscious or hypotension)intravenous fluids and desferrioxamine (a chelating
agent for iron) should be commenced immediately
before waiting for serum iron levels. Gastrointestinal
haemorrhage may require blood replacement and
metabolic acidosis should be corrected. Liver and renal
support may be required.
In absence of symptoms, serum levels are monitored
every 2 hours until levels fall or symptoms develop.
Symptomatic patients with moderate (3–5 mg/L or
55–90 μmol/L) or severe (>5 mg/L or 90 μmol/L)
poisoning may require treatment with i.v. desferrioxamine.
Patients who have not developed symptoms
by 6 hours following ingestion are unlikely to have
had a significant overdose and do not require further
monitoring.
Within an hour of ingestion of large doses of iron,
gastric lavage or endoscopic removal of tablets may be
performed.
Tricyclic antidepressant overdose
Definition
Accidental or deliberate overdose of tricyclic antidepressantdrugs.
Incidence/prevalence
Almost 1.8% of poisoning cases, but 18% of all deaths
by poisoning.
Pathophysiology
Tricyclic antidepressants have anticholinergic, alpha adrenergicblocking, and adrenergic uptake inhibiting
properties. They also have a quinidine like effect on the
myocardium. Alcohol and other psychotropic drugs increase
the toxicity.
Clinical features
Common features include hot, dry skin, dry mouth,dilated pupils and urinary retention.
Cardiovascular consequences include sinus tachycardia,
vasodilation, hypotension and cardiac arrhythmias.
Neurological consequences include ataxia, nystagmus
and altered levels of consciousness including coma,
hypothermia and respiratory depression. There may
be increased tone, increased deep tendon reflexes and
extensor plantar responses. If the patient is comatose,
all reflexes may be absent.
Convulsions occur in over 5%.
Confusion, agitation and visual hallucinations may
occur during recovery.
Complications
Pulmonary oedema due to decreased cardiac contractilityand fluid overload.
Investigations
Arterial blood gases to check both pH and bicarbonate
levels. ECG may reveal prolonged PR interval and QRS
complexes or bizarre changes in severe toxicity.ContinuousECGmonitoring
is essential. U&Es and urine output
should be monitored
Lithium overdose
Definition
Lithium poisoning usually results from chronic drug accumulation,accidental or deliberate overdose of lithium
carbonate
pathophysiology
Lithium has a narrow therapeutic index (the levels atwhich it becomes toxic are only marginally higher than
those needed to be therapeutic). Impaired renal excretion
such as with dehydration or renal failure may induce
toxicity, as may concomitant use of nonsteroidal
anti-inflammatory drugs or ACE-inhibitors
Clinical features
There is good correlation between symptoms and plasmaconcentration.
Mild toxicity: Nausea, diarrhoea, blurred vision,
polyuria, fine resting tremor, muscle weakness and
drowsiness.
Moderate toxicity: Confusion, faints, muscle fasciculation,
hyperreflexia, myoclonus, incontinence, restlessness
or decreased consciousness.
Severe toxicity: Depressed conscious level, convulsions,
arrhythmias including conduction block, hypotension
and renal failure.
Investigations
Serum Lithium levels should be measured if chronic toxicityis suspected. Therapeutic concentration between 0.4
and 1 mmol/L. Serious toxicity and significant mortality
in levels above 2 mmol/L. In acute overdose, levels
should be taken 6 hours post-ingestion and 6–12 hourly
thereafter. Symptomatic patients require ECG monitoring.
Management
In chronic accumulation, stopping lithium is often allthat is needed to alleviate symptoms; however, patients
may require other treatments for bipolar disorder.
In acute severe toxicity, airway and ventilatory support
may be required if unconscious. All patients should be
observed for a minimum of 24 hours post-ingestion.
Ensure adequate hydration and correct any electrolyte
imbalance. In refractory hypotension, inotropes may
Prognosis
The mortality in chronic poisoning is 9%, but as highas 25% in acute overdose. Clinical symptoms may persist
after the serumlithium levels have fallen and 10% of
patients with chronic poisoning have long-term neurological
sequelae.
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