Download Supportive management of poisoning

Supportive management
of poisoning in ICU
Goals of Treatment
• Support of vital signs
• Prevention of further poison
absorption
• Enhancement of poison elimination
• Administration of specific antidotes
• Prevention of reexposure
Phases of Poisoning &
Treatment priorities
• Pre toxic-Prior to the
onset of poisoning
• Decontamination,
Sampling, Observation
• Toxic- Time between
onset and it’s peak
effect
• Resuscitation and
stabilization, Enhance
poison elimination
• Supportive,
monitoring, Watch
toxic effect of
metabolite,
redistribution of
poison
• Resolution
Supportive care-Goals
• To maintain physiologic homeostasis until
detoxification is accomplished
• To prevent and treat secondary
complications such as
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aspiration, pneumonia
bedsores
cerebral and pulmonary edema
rhabdomyolysis, renal failure
thromboembolic disease, coagulopathy
Sepsis & generalized organ dysfunction due to
hypoxia or shock.
Indications for admission
in ICU
• Respiratory
• Cardio vascular
• CNS:
• Respiratory depression
Pulmonary edema,
Intubation, Aspiration
pneumonia
• Cardiac arrhythmias,
hypotension AV block (2 or
3rd degree ) TCA or
Phenothiazine over dosage
showing QTc>0.5sec or
QRS >0.12 sec
• Unresponsiveness to verbal
stimuli Seizures Drug over
dosage with CNS
depression Cerebral edema
Indications-Contd
• Metabolic
• Extra corporeal
management
• Others
Hyperkalemia, Hypo or
Hyperthermia and NMS
Severe metabolic acidosis
Emergent dialysis or
hemoperfusion, AV
hemofiltration, Need for
extracorporeal membrane
oxygenation, Exchange
transfusion
Administration of drugs- Fab
fragments, naloxone as infusion
Anti snake venom administration
Enhancement of Poison
Elimination
• Multiple-dose activated charcoal
• Forced diuresis and Alteration of urine
Ph Diuresis and ion trapping via alteration of
urine pH may prevent the renal absorption of
poisons that undergo excretion by glomerular
filtration and active tubular secretion.
• Extracorporeal removal
– Peritoneal dialysis, hemodialysis, charcoal or
resin hemoperfusion, hemofiltration,
plasmapheresis, and exchange transfusion are
capable of removing any toxin from the
bloodstream.
Forced diuresis
• Saline diuresis -Enhance the renal
excretion of
alcohols, bromide, calcium, chromium,
fluoride, isoniazid, lithium, meprobamate,
potassium, and thallium.
• Alkaline diuresis (producing a urine pH 7.5
and a urine output of 3 to 6 mL/kg body
weight per hour by adding sodium
bicarbonate to an intravenous solution)
enhances the excretion of chlorpropamide,
fluoride, ethotrexate, phenobarbital,
sulfonamides, and salicylates.
Limitations
• Contraindicated in congestive heart
failure, renal failure, and cerebral
edema.
• Acid-base, fluid, and electrolyte
imbalance can occur which should be
monitored carefully.
EXTRACORPOREAL
REMOVAL
• Dialysis is effective in
– acetone, atenolol, barbiturates, bromide,
chloral hydrate, ethanol, ethylene glycol,
isopropyl alcohol, lithium, methanol,
procainamide, theophylline,salicylates, sotalol,
and possibly heavy metals.
• Hemoperfusion
– poisoning due to caffeine, carbamazepine,
carbon tetrachloride, chloramphenicol,
dapsone, disopyramide, hypnotic-sedatives
,methotrexate,
Mushrooms, paraquat, phenytoin, procainamide,
theophylline, and valproate.
Limitations
• Both techniques require central venous
access and systemic anticoagulation and
often result in transient hypotension.
• Hemoperfusion cause hemolysis,
hypocalcemia, and thrombocytopenia.
• Peritoneal dialysis and exchange
transfusion when other procedures are
either not available, contraindicated, or
technically difficult
General Supportive Care
• Airway protection
• Oxygenation/ventilation
• Hemodynamic support
• Treatment of seizures
• Correction of temperature
abnormalities
• Correction of metabolic
derangements
• Treatment of arrhythmias
Respiratory care
• Endotracheal intubation: For protection against the
aspiration, done prophylactically when unable to drink
or speak
• Mechanical ventilation: For respiratory depression
or hypoxia, therapeutic sedation or paralysis in
neuromuscular hyperactivity.
• Drug-induced pulmonary edema is usually noncardiac
rather than cardiac.
– e.g- inhalation of poisonous gases, increased
bronchial secretions in ChEase inhibitors poisoning,
Overdosage of opiates
Respiratory care
• Extracorporeal measures for severe
but reversible respiratory failure
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membrane oxygenation,
venoarterial perfusion,
Cardiopulmonary by pass,
partial liquid(perfluorocarbon)
ventilation
– hyperbaric oxygen therapy
Cardio vascular System
• Hypotension- Shock:
I or Vasovagal- by nitrites, anesthetic
II – Severe poisoning, corrosives,
depressant drugs
• Treatment: volume expansion
– norepinephrine, epinephrine, or high-dose
dopamine
- Intraaortic balloon pump counter
pulsation ,Venoarterial or
cardiopulmonary perfusion techniques
should be considered for severe but
reversible cardiac failure.
– Correction of metabolic abnormalities,
replacement of blood
Specific Therapy
Hypotension & Brady arrhythmia:
Beta blocker and calcium channel
blocker poisoning: Glucagon, calcium,
and high-dose insulin with dextrose.
– cardiac glycoside poisoningAntibody therapy
Specific Therapy
• Supra ventricular tachycardia with hypertension
Mild to moderate- Observation, Benzodiazepines
Severe with sympathetic hyperactivity- combined alpha
and beta blocker (labetalol), a calcium channel blocker
(verapamil or diltiazem), or a combination of a beta
blocker and a vasodilator (esmolol and nitroprusside) is
preferred.
– Anticholinergic poisoning- physostigmine
• Supraventricular tachycardia without
hypertension:
– secondary to vasodilatation or hypovolemia -responds to fluid
administration.
Tachyarrhythmia
• Of any etiology: Lidocaine and phenytoin.
• TCA or other membrane active
agents:NaHCO3
• Torsades de pointes and QT prolongation:
Magnesium sulfate and overdrive pacing.
• Severe cardiac glycoside poisoning:
Magnesium and anti-digoxin antibodies.
• If the patient is hemo dynamically stable:
Observation
• Correction of underlying acid-base, electrolyte,
oxygenation, and temperature derangements
Congestive Cardiac
Failure
• Poisons producing myocardial damage
causes CCF
• Digitalis doesn’t have any role
• Other measures for CCF helps viz.,
preload and afterload reduction,
diuretics, O2 therapy
Cardiac Arrest
• Causes:
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Inhalation of GA agents
CO poisoning and asphyxiation
LA injections
Over dosage of cardiac drugs
Idiosyncrasy to drugs
• Management:
• As per ACLS protocol
CENTRAL NERVOUS
SYSTEM
• Seizures: Major cause of morbidity
and mortality as it results in anoxia,
coma , aspiration, and serious
metabolic derangement.
• Management:
Quiet, darkened environment,
ABC, Temperature control, Drugs
Drug treatment
• Thiamine, Dextrose, Naloxone
• Anticonvulsants-Benzodiazepines,
Barbiturates( Phenytoin is CI)
• Specific antidotes whenever
Appropriate
• Management of secondary
complications
Specific Antidotes
• By excessive
stimulation of
catecholamine
receptors –( e.g.,
sympathomimetic or
hallucinogen poisoning and
drug withdrawal) Isoniazid,
Strychnine
• Isoniazid, Beta
blocker, TCA
• OPC,OC
• Benzodiazepines,
Barbiturates
• Pyridoxine (GABA
enhancer)
• P2AM,Atropine
• For poisons with
central dopaminergic
effects- phencyclidine
(psychotic behavior)
• Treatment of seizures
secondary to cerebral
ischemia or edema or
to metabolic
abnormalities
• Haloperidol-dopamine
antagonist
• Correction of the
underlying cause
Delirium or Psychosis
• Causes: Fever, metabolic derangement,
anticholinergic and antihistamines, neurological
medications, recreational abuse of drugs, alcohol
and other withdrawal syndromes, oral
hypoglycemics, thiamine deficiency
• Management
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Prevent injury
Place in quiet, dark room
Reassure
Monitoring of vitals
Treatment of complications like hyperthermia
Benzodiazepines
Hypoglycemia
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Situations
• Alcohol / Anesthesia following starvation
• Plant poisoning like mushroom
• Acetyl cholinesterase inhibitors like OPC
• Edetates chelating zinc from slow release
formulations of insulin
• Salicylate over dosage
Management:
– Recognition of the problem and treatment in
standard lines
Acute Renal Failure
• Causes:
• Direct toxicity: Amino glycosides, NSAIDs,
Mushroom, Cyclosporin,CCl4, heavy metals, arsenicals,
sulfonamides, ethylene glycol
• Hemolytic substrates: Castor beans, abrus,
Naphthalene, Benzene
• Myoglobinuria: Stimulants, convulsants, hyperthermic
agents
• Prolonged hypovolemia, hypotension
• Multifactorial as in snakebite
• Treatment:
• Treatment of shock, specific antidote for the
poison, FAD for rhabdomyolysis, Dialysis along with
general measures for treatment of ARF
Metabolic Abnormalities
• As the result of vomiting, diarrhea, kidney
damage and other procedures
• If renal function and thirst is normal can
be replaced orally or IV
• Acidosis
• Respiratory depression, methanol, ethylene glycol,
paraldehyde poisoning , lactic acidosis
• Treatment:
• Elimination of the cause, Alkali administration as
temporary measure- To alkalinize the urine
(salicylate poisoning), to raise the overall pH to
prevent arrhythmia (TCA Poisoning)
Hyperthermia
• Leads to Increased O2 requirement and
metabolism
• Causes:
• Side effect/Drug interaction: MAO+SSRI
( Serotonin syndrome)
• Seizures or rigidity:TCA, Amphetamine, Cocaine,
• Disrupted thermo regulation: Anticholinergic agents,
Malignant Hyperthermia ,NMS,
• Increased metabolic rate: Thyroxin over dosage,
• Treatment:
• General measures, Neuro muscular paralysis,
Dantroline sodium, Bromocryptine in specific
situations
Hypothermia
• Though decreases the metabolic rate,
circulation is impaired , detoxification and
elimination of poisons are slowed
• Causes: Vasodilatation by alcohol and
calcium channel blockers, barbiturates, oral
hypoglycemic agents
• Treatment: Slow warming, warm blankets,
extracorporeal circulation, peritoneal and
gastric lavage with warm liquids
Liver Damage
• Direct cell injury-Acetyl salicylic acid,
amanita phylloids,CCl4,Chloroform
• Delayed cell injury-Alcohol
• Hemolytic anemia overwhelming hepatic
capacity-Castor bean, Primaquin
• Hepatic vein thrombosis-bush tea
(Pyrazolidine alkaloids)
• Cholestasis and portal inflammation
Investigations
• Cell injury- Raised bilirubin, ALT,
AST, LDH, A:G reversal, Low plasma
prothrombin level after 24 hrs of
Vit k
• Obstruction: Increased Sr bilirubin
and Alk.Po4ase,Sr. Cholesterol,
Decreased urine and fecal
urobilinogen
Treatment
• D/C drugs
• Prevent further damage
• Avoid Anesthetic/ Surgical
provocation
• Vit K
• Supportive treatment
Methaemoglobinemia
• Formed by oxidation of ferrous to
ferric ion in Hb by chemicals which is
a poor carrier of O2
• Agents:
• Phenazopyridine, Phenacetin
• Anesthetic agents: Benzocaine, Lidocaine
• Antibiotics:Primaquin, sulfones,
trimethoprim
• Organic nitrates & nitrites, aniline, bromate,
chlorate
Clinical Features
Level of MethHb
– 15%
– 30-40%
– 60% and more
Symptoms
• cyanosis,
asymptomatic
• Dizziness,
Headache,
Weakness,Dyspnea,
Chocolate cyanosis
• Stupor,
Respiratory
distress
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Investigations&
Treatment
Pulse oxy metry- Unreliable
Spectrophotometer Analysis: For level
ABG- Normal PO2& Normal Saturation
Management:
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100% O2 by mask
Removal of poison by lavage, emesis
Methylene blue-1% solution 0.1-0.2ml/kg IV over 10 mts
Ascorbic acid 1g IV if methylene blue NA
Exchange transfusion
Thank You