CHAPTER 450 POISONING AND DRUG OVERSE Flashcards
it refers to the development of dose-related adverse effects following exposure to chemicals, drugs, and other xenobiotics
poisoning
age prone to poisioning
<6 years old
major reason for increased number of poisoning deaths
opoids
unintentional exposures include
improper use of chemicals at work or play label misleading product mislabel mistaken identification unlabeled chemicals uninformed self medication dosing errors elderly
most common reported reason for intentional poisoning
recreational use of ethanol
pharmaceutical agent most often implicated in fatal poisoning
acetaminophen
leading cause of death from poisoning
carbon monoxide
correct diagnosis established by
history, physical examination, routine and toxicologic laboratory evaluations and clinical course
history includes:
time route duration circumstances the name and dose chemical involved the time of onset nature and severity of symptoms time and type of first aid used medical and psychiatry history
if the px is confused or comatose suspect?
history of psychiatry problems
recent changes of economic and relationship status
work with chemicals
what is body packing or body stuffing
ingesting or concealing drugs in the body cavity
relevant information may be available from
family friends paramedics police pharmacist physicians employers
it focuses the vital signs, and the systems
physical examination
neurologic status includes the:
documentation of the neuromuscular abnormalities such as dyskinesia, dystonia, fasciculations, myoclonus, rigidity and tremors
examine the eye for:
nystagmus and pupil size and reactviity
examine the abdomen for:
bowel activity and bladder size
examine the skin for:
burns bullae color warmth moisture pressure sores puncture marks
what to do when history is unclear?
examine all the orifices for the presence of chemical burns, and drug packets
it also provide important diagnostic clues
odor of breath
vomitus
color of the nails and skin and urine
how to diagnose a poisoning in cases of unknown etiology
relies on pattern recognition
how to detect pattern recognition to diagnose poisoning in unknown etiology
first: assess the pulse, blood pressure and respiratory rate and temperature and neurologic status and characterized the overall physiologic state as stimulated, depressed, discordant or normal
second: identify the pathophysiologic patterns or toxic syndrome (toxidrome)
third: identify the particular agent involved by looking at the unique poison specific physical or ancillary test abnormalities
most reliable prognosticator of poor outcome in poisoning from stimulants
temperature elevation
what are the 4 physiologic state
stimulated
depressed
discordant
normal
stimulated physiologic state is characterized by
increased pulse, bp rr, temp and neuromuscular activity
stimulated physiologic state reflects the
symphathetic, anticholinergic or hallucinogen poisoning or drug withdrawal
feature of all stimulants and is most marked in anticholinergic poisoning since the pupillary reactivity relies on muscarinic control
mydriasis
anticholinergic syndrome is characterized by:
hot dry flushed skin
decreased bowel sounds
urinary retention
other: diaphoresis, pallor and increased bowel activity with nausea, diarrhea
findings that suggest sympathetic poisoning
increased vital signs and organ ischemia
selective alpha adrenergic stimulants such as decongestants can cause
reflex bradycardia
selective beta-adrenergic stimulants such as asthma therapeutics can cause
hypotension
ergot alkaloids can cause
limb ischemia
phencylidine and ketamide can cause
rotatory nystagmus
cocaine can cause
delayed cardiac contraction
what do seizures suggest
sympathetic etiology
state characterized by mixed vital signs and neuromuscular abnormalities
discordant physiologic state
cause of depressed physiological state
functional sympatholytics (agents that decrease cardiac function and vascular tone)
cholinergic such as muscarinic and nicotinic agents
opiods
sedatives
feature that is most pronounced in opiods and cholinergic poisoning
miosis
other clues that may suggest physiologic depressed state
cardiac arrhythmias conduction disturbances mydriasis nystagmus seizures
what can cause arythmias and conduction disturbances
antiarrhythmias calcium channel blocker digitalis glycosides propoxyphene cyclic antidepressants
what can cause mydriasis
tricyclic antidepressants and some antiarrhymics, meperidine and diphenocylate atropine such as lomotil
what can cause nystagmus
sedative hypotics
what can cause seizures
cholinergic agents
propoxyophene
cyclic depressants
physiologic state characterized by decreased pulse, bp, rr, and temp and neuromuscular activity
depressed physiologic state
cause of normal physiologic state
non-toxic exposure
psychogenic illness
poisoning of toxic time bombs that are slowly absorbed and slowly distributed and require metabolic activation
laboratory result most common in advanced methanol, ethylene glycol and salicyate intoxication
increased anion gap metabolic acidosis
what happens when there is increased blood levels of bromide, calcium, iodide, lithium or magnesium
abnormally low anion gap
a difference of >10 mmol per liter between serum osmality suggests the presence of low molecular weight solute such as acetone, alcohol , glycol, and ether, or sugar
a difference of >10
ketosis suggest of
acetone, iso alcohol, salicylate poisoning or alcoholic ketoacidosis
hypokalcemia suggest of
beta-adrenergic blocker, caffeine, diuretics, theophylline, toleune
hyperkalcemia suggest of
poisoning of alpha adrenergic agonist
beta adrenergic blocker
cardiac glycosides
fluoride
hypocalcemia suggest of
ethylene glycol
fluoride
oxalate poisoning
result of ECG in px poisoned with alpha adrenergic agonist, beta blockers, calcium channel blockers and cholinergic agents
bradycardia and atrioventricular block
QRS and QT interval prolongation is caused by
hyperkalemia
antidepressants
membrane active drugs
ventricular tacycardia suggests
poisoning with cardiac glycosides
fluorides
membrane active drugs
radiologic result in px with posoining of carbon monoxide, cyanide and opiods
pulmonary edema
aspiration pneumonia is common in px with
coma
seizures
petroleum distillate aspiration
what can be used to rule out and confirm suspected poisoning
toxicologic analysis
what can be used to rule out and confirm suspected poisoning
toxicologic analysis
screening test that should not be used because it cannot confirm the exact identity of the detected substance
rapid qualitative hospital-based urine test
useful for diagnostic purposes
response to antidotes
resolution of altered mental status and abnormal vital signs within minutes of IV administration of dextrose, naloxone, or flumazenil is diagnostic of
hypoglycemia
opoid poisoning
benzodiazepine intoxication
grade of physiologic stimulation that is anxious, irritable but the vital signs are normal with diaphoresis with flushing and pallor, mydriasis and hyperflexia sometimes present
grade 1 physiologic stimulation
grade of physiologic stimulation that is agitated may have confusion or hallucinations but can converse and follow commands but the vital signs are mild to moderately increased
grade 2 physiologic stimulation
Grade of physiologic stimulation that is delirious, unintelligible speech, uncontrollable motor hyper-activity moderately increased vital signs and tachyarrhythmias are possible
grade 3 f physiologic stimulation
grade of physiologic stimulation that is in coma, seizures and in cardiovascular collapse
grade 4 physiological stage stimulation
grade of depressed if the px is awake, lethargic or sleeping but arousable by voice or tactile stimulation and able to converse and follow commands but may be confused
Grade 1 physiologic depression
grade of physiologic depression if the px responds to pain but not to voice can vocalize but not converse with the spontaneous motor activity present with brainstem reflexes intact
grade 2 physiologic depression
grade of physiologic depression that is unresponsive to pain, spontaneous motor activity absent with brainstem reflexes depressed, motor tone, respirations and temperature decreased
grade 3 physiologic depression
grade of physiologic depression that is unresponsive to pain, flaccid paralysis, brainstem reflexes and respirations absent with cardiovascular vital signs decreased
grade 4 physiologic depression
what are the treatment goals for poisoning and drug overdose
support of vital signs prevention of further poisoning absorption enhancement of poison elimination administration of specific antidotes prevention of re-exposure
what is the highest priority in the pre-toxic phase?
decontamination and treatment are solely based on history and pe
when history is not obtainable and poison is causing delayed toxicity what is the appropriate best thing to do?
blood and urine samples were sent for toxicologic screening and quantitative analysis
what is toxic phase
interval between the onset of poisoning and its peak effect
management during toxic phase
based on laboratory and clinical findings
when does the effect of overdose manifested
begin sooner and peak later and last longer than they do after a therapeutic dose
what is the first priority
resuscitation and stabilization
what to give in px with altered mental status that has come and seizures
intravenous glucose
naloxone
thiamine
measures that enhance the decontamination of salicylates
urinary alkanization
enhance decontamination in metals
chelation therapy
what is the goal of supportive therapy
maintain the physiologic homeostasis until detoxification is accomplished and to prevent and treat secondary complications
indications for admission in intensive care unit
patients with severe poisoning (coma, respiratory depressionm hypotension, cardiac conduction abnormalities, cardiac arrythmias
those needing close monitoring
respiratory care to prevent aspiration of gastrointestinal contents especially in those with CNS depressions and seizures
endotracheal intubation
respiratory care for px with respiratory depression or hypoxemia and for facilitation of therapeutic sedationn or paralysis of patients in order to prevent or treat hyperthermia, acidosis and rhabdomyolysis associated with neuromuscular hyperactivity
mechanical ventilation
oxygenation and ventilation is best determined by
pulse oximetry and arterial blood gas analysis
not a reliable indicator for the need of intubation
gag reflex
if the px hypotension is unresponsive to volume expansion and appropriate next step is?
treatment with norepinephrine and epinephrine and high dose dopamine
what should be considered in px with severe but reversible cardiac failure
intraaortic balloon pump counterpulsation
venoarterial or cardiopulmonary perfusion techniques
treatment for sympathetic hyperactiviity
benzodiazepine
treatment for anticholinergic posoining
physostigmine
treatment for ventricular arrhythmia
sodium bicarbinate
lidocaine
phenytoin
treatment in px with torsades de pointed and prolonged QT intervals
magnesium sulfate and overdrive pacing
treatment for severe cardiac glycoside poisoning
magnesium and anti digoxin antibodies
seizures caused by excessive stimulation of catecholamine receptors is treated with
agents that enhance GABA activity such as benzodiazepine and barbiturates
seizures caused by isoniazid are treated with
pyridoxine
what is contraindicated in toxicologic seizures
phenytoin
serotonergic receptor overstimulation is serotonin syndrome is treated with?
cyproheotadine
the average time from ingestion to presentation of adults
> 3 hours
the average time of ingestion to presentation of children
> 1 hour
preferred method of gastrointestinal decontamination that has fewer contraindications and complications
activated charcoal
mechanism of action of charcoal
the charcoal adsorbs ingested poisons within the gut lumen allowing the charcoal toxin complex to be evacuated in stool
what compounds that are not well absorb in charcoal
charged ionized chemicals such as mineral, acid, alkalis, and highly dissociated salts of cyanide, fluoride, iron, lithium and other inorganic compounds
side effects of charcoal
nausea, vomiting, and diarrhea or constipation and prevents the absorption off orally administered therapeutic agents
complications of charcoal
mechanical obstruction of airway, aspiration, vomiting, and bowel obstruction and infarction caused by inspissated charcoal
when is charcoal not recommended
ingested corrosives because it will obscure endoscopy
what method is preferred for life-threatening poisons that cannot be treated with other method
gastric lavage
how is gastric lavage performed?
performed by sequentially administering and aspirating 5 ml of fluid per kilogram of body weight through a no.40 French orogastric tube (no. 28 for children)
preferred solute used in gastric lavage in infants
normal saline and tap water
the positon of px when doing gastric lavage to prevent aspiration
trendelenburg and left lateral decubitus
lavage absoprtion within 5 mins, 30 mins and 60 mins of ingestion
decreases as time lengthens
common complication of gastric lavage
aspiration
serious complication of gastric lavage
esophageal and gastric perforation and tube misplacement
contraindicated in gastric lavage
corrosive
petroleum distillate ingestions because the risk of gastroesophageal perforation and aspiration pneumonitis
compromised airway
risk of hemorrhage or perforation due to esophageal or gastric pathology
recent surgery
px who refuse
emetogenic agent that is once used in decontamination but no longer used in decontamination
syrup of ipecac
chronic use of ipecac complications
electrolyte and fluid abnormalities, cardiac toxicity, and myopathy
another method for gastric decontamination that is performed by administering bowel cleansing solution that contains electrolytes and polyethylene glycol
whole bowel irrigation
whole bowel irrigation is appropriate in px with
ingested foreign bodies
packets of ilicit drugs
and heavy metals
salts given together with charcoals to promote the rectal evacuation of gastrointestinal contents
cathartics
side effects of cathartics
abdominal pain
nausea
occasional vomitting
complications of repeated doses of cathartics
severe electrolytes disturbances and excessive diarrhea
contraindications of cathartics
ingested corrosives and with preexisting diarrhea
when is dilution recommended
only after the ingestion of corrosives
technique used in rare situations such as ingestions of potentially toxic foreign bodies
endoscopic or surgical removal
initial treatment for for topical exposures
immediate copious flushing with water and saline
preferred for eye irrigation
saline
treatment for inhlational exposures
supplemental oxygen or fresh air
treatment for inhlational exposures
supplemental oxygen or fresh air
treatment for dermal decontamination
triple wash
removal of liquids in cavities such as vagina and rectum
irrigation
when is multiple-dose of charcoal therapy considered
ingestion of theophyline, phenobarbital, carbamazepine, dapsone and quinine
complications of multiple-dose charcoal therapy
intestinal obstructions, pseudo-obstruction and nonoccluisive intestinal infarction in px with decreased gastric motility
how urinary alkalinization works
ion trapping via alteration of urine ph may prevent the renal absorption of poisons that undergo excretion by glomerular filtration and active tubular secretion
what ions are trapped in the membrane
acidic are ionized and trapped in alkaline urine whereas basic become ionized and trapped in acid urine
urine alkalinization urine ph
ph >7.5 and urine output of 3-6 ml of body weight per hour by the addition of sodium bicarbonate to an IV solution
contraindication of urinary alkalinization
congestive heart failure, renal failure and cerebral edema
agents most amenable to enhance elimination bu dialysis
low molecular mass <500 high water solubility low protein binding small volumes of distirbutio (<1l) prolonged elimination (long half life) high dialysis clearance relative to total body clearance
when is dialysis considered
severe poisoning due to carbamazepine, ethylene glycol, isoprophyl alcohol, lithium, methanol, theophyline, salicylates and valproate
candidates for extracorporeal removal
px with severe toxicity whose condition deteriorates despite the aggressive supportive therapy, those with potentially prolonged irreversible or fatal toxicity, those with dangerous blood level of toxins, those who lack capability for self detoxification because of liver or renal failure and those with serious underlying illness or complication that will adversely affect recovery
how do antidotes work
counteract the effect of poisons by neutralizing them or by antagonizing their physiologic effect by activation of opposing nervous system activity, provision of competitive metabolic or receptor substance
how to prevent re-exposure
limit their access to poisions
fundamentals of supportive care in poisoning management
airway protection oxygenation/ventilatiom treatment of arrythmias hemodynamic support treatment of seizures correction of temperature and abnormalities correction of metabolic derangement prevention of secondary complications
fundamentals in prevention of further poisoning absoprtion
gastrointestinal decontamination such as gastric lavage, activated charcoal, whole bowel irrigation,dilution and endoscopic surgical removal and decontamination of other sites such as eye, skin and body decontamination
fundamentals in enhancement of poison elimination
multiple dose activated charcoal
alteration of urine ph
chelation
extracorpeal removal
causes of stimulated physiologic condition
sympathetic such as sympathomimetics, ergot alkaloids, methylxanthines, monoamide oxidase inhibitors
anticholinergics such as antihistamines, antipsychotics and belladona alkaloids, cyclic depressants and mushroom and plants
examples of sympathomimetics
a1 adrenergic agonist and b2 adrenergic agonist
mechanism of action of sympathomimetics
stimulation of central and peripheral sympathetic receptor directly or indirectly (release and inhibit release of norepi and dopamine)
mechanism of action of sympathomimetics
stimulation of central and peripheral sympathetic receptor directly or indirectly (release and inhibit release of norepi and dopamine)
clinical features of sympathomimetics
a1- reflex bradycardia
b- hypotension and hypokalemia
treatmen of sympathomimetics
phentolamine-severe hypertension
labetalol-hypotension and tacycardia
examples of ergot alkaloids
ergotamine
methysergide
bromocriptine
pergolide
mechanism of action of ergot alkaloids
stimulation and inhibition of serotonergic and a adrenergic receptors
simulation of dopamine receptors
clinical features of ergot alkaloids
formication and vasospasm with limb, myocardial and cerebral ischemia to gangrene and involuntary movements
treatment for ergot alkaloids
nitroprusside or nitroglycerine for vasopasm
prazosin, captopril- limb ischemia
dopamine for movement disorders
examples of methyxanthines
caffeine and theophylline
mechanism of action of methylxanthines
inhibition of adenosine synthesis and adenosine receptor antagonism
stimulation of epi and norepi release
inhibition of phosphodiesterase-increased intracellular cyclic adenosine and guanosine monophosphate
clinical features of methylxanthines
pronounced gastrointestinal symptoms
toxicity occur at lower drug level in chronic than in acute
treatment of methylxanthines
propranolol for tacycardia with hypotension
beta blocker for supraventricular or ventricular tacycardia
indications for hemoperfusion and hemodialysis
unstable vital signs
seizures
theophylline level of 80-100 after acute overdose and 40-60 with chronic exposure
example of monoamide oxidase inhibitors
phenelzine
tranycypromine
selegiline
mechanism of action of monoamine oxidase inhibitors
inhibition of monoamide oxidase resulting in impaired metabolism of endogenous catecholamines and exogenous sympathomimetic agent s
clinical feature of monoamine oxidase inhibitors
delayed and slowly progressive
terminal hypotension and bradycardia in severe cases
treatment of monoamine oxidase inhibitors
short acting agents such as nitroprusside and esmolol for severe hypotension and tacycardaia
direct acting sympathomimetic: norepi and epi for hypotension and bradycardia
examples of anticholinergic agents
antihistamines antipsychotics belladonna alkaloids cyclic antidepressants mushrooms and plant s
examples of anti-histamines
diphenydramine
doxylamine
pyrilamine
mechanism of action of antihistamines
inhibition of central and postganglionic parasympathetic muscarinic cholinergic receptors
clinical features of anti-histamines
dry skin mucous membranes decreased bowel movements flushing urinary retention myoclonus picking activity
treatment of antihistamines
physostigmine for delirium and neuromuscular hyperactivity
examples of antipyschotics
chlorpromazine
olanzapine
quetiapine
thioridazine
mechanism of action of antipsychotics
inhibition of alpha adrenergic dopaminergic histaminergic muscarinic and serotonegic receptors
inhibit sodium, pottasium and calcium channles
clinical features of antipsychotics
miosis
anticholinergic effects
extrapyramidal effects
tachycardia
treatment for antipsychotics
sodium bicarbonate for ventricular tachydysrhymias
magnesium, isoproterenol in torsades des pointes
examples of belladonna alkaloids
atropine
hyoscyamine
scopolamine
mechanism of action of belladonna alkaloids
inhibition of central and pots-ganglionic parasympathetic muscarinic cholinergic receptors
clinical features of belladonna alkaloids
dry skin mucous membrane decreased bowel sounds flushing urinary retention myoclonus picking activity
treatment for belladonna alkaloids
physostigmine
examples of cyclic depressants
amitriptyline
dexopine
imipramine
mechanism of action of cyclic depressants
inhibition of alpha adrenergic dopaminergic , histaminergic and muscaranic and serotonergic receptors
inhibition of nore and epi
inhibition of serotonin reuptake
clinical features of cyclic antidepressants
seizures tachycardia cardiac conduction delays anticholinergic toxidrome
treatment of cyclic depressants
hypertronic sodium bicarbonate