Pemicu

Elfind
180
APPROACH TO THE POISONED
PATIENT
Rosen's Emergency Medicine-Concepts and Clinical Practice,2-Volume Set, 9e (Jun 1, 2017)_(0323354793)_(Elsevier)

Toxidromes
• constellations of S/S based on 1. Sympathomimetic
autonomic & neurochemical – Sympathomimetic excess  ‘fight
processes  suggest a particular or flight rx”
class of exposure and direct – Patients altered, delusional,
management and therapy especially w/ ingestion of
substituted amphetamines
– Sympathomimetics
– Vital signs ⬆⬆ HT, tachycardia,
– Anticholinergics tachypnea
– Cholinergic – ⬆metab rate  hyperthermia
– Sedative/hypnotic – Mydriasis, diaphoresis
– Opioid – Severe overdose  ⬇diastolic
filling time + arrhythmogenesis 
circulatory collapse + shock 
REFRACTORY TO PRESSOR / FLUID
RESUSCITATION

3. Cholinergic
2. Anticholinergic
– Bc overstimulation of parasympathetic
– Antimuscarinic  blocks portion of ANS
cholinergic tone  alter normal – “fluids coming from every orifice” bc
homeostatic balance between ⬆gl. secretion  diaphoresis,
sympathetic & parasymphatetic urination, miosis, bronchorrhea,
emesis, lacrimation, lethargy,
– This allows sympathetic side fx salivation
unopposed, generates state of – Agents of concern are primarily
relative sympathomimesis  anticholinesterase agents, such as
delirium, hyperthermia, organophosphates and carbamate
mydriasis, cutaneous flushing insecticides.
– Ps. can die from excessive
– Secretory gl. of skin & mucosa
bronchorrhea drowning in their own
are cholinergically innervated secretions, unless timely antidotal
 dry & not diaphoretic therapy and cholinesterase
regenerators can be given.

4. Sedative / hypnotic 5. Opioid
– hallmark: sedation – Similar to
– Severe ingestion  general sedative/hypnotics
anesthesia + loss of tone & -Sedation + diminished
airway protective reflexes
respiratory drive
– Hypothermia bc muscle metab
– Causes miosis, except
suppression
– Ethanol frequently seen,
pentazocine &
Other agents such as propoxyphene
barbiturates and – Responsive to naloxone,
benzodiazepines will also direct opioid-receptor
cause a similar picture, as will antagonist
illicit substances such as gamma-
hydroxybutyrate (GHB)

Differential Dx Diagnostic testing
• Frequently, poisoned • diagnostic studies routinely checked :
patients have some level - complete blood count,
of delirium as part of their - serum chemistry with renal function,
presentation. - liver function tests,
• As such, excluding other - urinalysis (w/ pregnancy test if appropriate),
causes of altered mental - urine toxicology screen,
status while initiating - serum alcohol concentration,
appropriate toxicologic - serum lactate,
therapy should be - bedside glucose.
considered
• Based on these results, 
other tests such as
specific serum
concentrations may be
obtained

• ABG if metab acidosis
 calculate anion gap
[Na] – ([HCO3] + [Cl])
N: 8-12 mEq/L
• Ingestion toxic alcohol (such as,
methanol, ethylene glycol, or
isopropanol) suspected 
calculating the osmole gap may be
helpful;
• Urine toxicology  confirmatory,
shouldn’t supplant clinical eval &
judgement
• ECG if ps tachy /bradycardic,

prolonged QRS / QT intv

Management
The general management of a
poisoned patient involves
• Supportive care
– ABCs
– Vascular access 
intraosseus line
• Decontaminate /
enhance limitation
• Antidotal th/

Decontamination
• Syrup of ipecac – not recommend @ED
• Gastric lavage
– Within 1hr of ingestion of potentially
life-threatening poison which doesn’t
adsorb to actv charcoal / no antidotes
exist
• Single-dose activated charcoal (10-25gr)
– The activated charcoal is administered
within one hour post-ingestion, and
– The ps. is alert, able, and willing to
cooperate with administration,
anticipated to remain alert, protective
of airway reflexes
– The substance ingested has high
toxicity (eg, verapamil, colchicine), or
is a toxic, sustained–release agent (eg,
bupropion SR), or
– There is evidence of a massive
ingestion of a toxic agent
(eg,salicylates)
Enhanced Elimination
Certain substances are amenable to
enhancing these elimination pathways
- ex vivo with hemodialysis and its related
therapies, Hemodialysis and its
- in vivo with multipledose activated related therapies are best
charcoal (MDAC) and urinary alkalinization. suited to remove poisons of
low molecular weight, low
protein binding, and high
water solubility;
When MDAC indicated

Initial loading dose of ActCharcoal:xenobiotics = 10:1
+ 50% initial dose every 4-6hr for up to 24 hrs

Substance Abuse
Cannabis-Related Disorders
• Cannabis sativa • Cannabis use disorder
• Clinical features: – Earlier age of first use, more
– dilation of conjunctival blood often cannabis has been used
vesels (red eyes) & mild  higher risk of dependence
tachycardia • Cannabis intoxication
– ⬆appetite – the munchies – & – ⬆users’ sensitivity to external
dry mouth  cannabis stimuli, reveals new details,
intoxication
makes colors brighter&richer
– Long term usage: cerebral
– High dose  depersonalization
atrophy, seizure susceptibility,
& derealization
chromosomal dmg, birth defect,
impaired immune reactivity, – Motor skills impaired, and
alteration in testosterone []. remains after subjective,
Dysregulation of menstrual cycle euphoric effects have resolved
• Cannabis intoxication delirium • Cannabis-induced psychotic
– Marked impairment on disorder
cognition & performance tasks – Florid psychosis  in high potency
• Cannabis withdrawal cannabis user
– Psychotic episode referred as
– Daily use  withdrawal sx
“hemp insanity”
within 1-2wk of cessation
– Irritability, cannabis cravings,
• Cannabis-induced anxiety
nervous, anxiety, insomnia, disorder
disturbed/vivid dreaming, – Acute cannabis intoxication
⬇appetite, weight loss, – Panic attacks may be induced
depressed mood, restlessness, – Appearance of anxiety sx is
headache, chills, stomach pain, correlated w the dose & is the
sweating, tremors most common adverse rx to mod
use of smoked cannabis
Treatments
• Abstinence
– Direct intervention (hospitalization)
– Monitoring: urine drug screen, detect cannabis for
up to 4 wk after use
• Support
– Family, group psychotherapy
Hallucinogen-Related Disorder
• Lysergic acid diethylamide
(LSD) • LSD  hallucinogenic
• Natural, synthetic substances prototype
• Produce loss of contact w/ – Well absorbed after oral
reality and heightened ingestion
consciousness – Tolerance develops rapidly
• Psilocybin (from mushrooms), & virtually complete after 3
mesaline (peyote cactus); or 4 days of continuous use
harmine, harmaline, ibogaine, – Tolerance reverses in 4-7
dimethyltryptamine (DMT), days
phencyclidine (PCP)  angel – Physical dependence /
dust withdrawal sx  don’t
occur with hallucinogens
Diagnosis
• Hallucinogen use disorder
– Dulled thinking, decreased
reflexes, loss of memory, loss of
impulse control, depression,
lethargy, impaired concentration
• Hallucinogen intoxication
– Maladaptive behavioral and
perceptual changes
– DD: anticholinergic &
amphetamine intoxication &
alcohol
– Tx: talking down the pt.
– Severe cases: dopaminergic
antagonist (haloperidol, diazepam)
• Hallucinogen persisting • Hallucinogen
perception disorder
– Long after ingesting hallucinogen, intoxication delirium
person experience flashback of
hallucinogenic sx
• Hallucinogen induced
– Visual distortions, geometric psychotic disorders
hallucinations, false perceptions of
movement, flashes of color, trails of – “bad trip”, experience
images from moving objects, +ve resembling acute panic
afterimages & halos, macropsia,
micropsia, time expansion, physical sx
rx to cannabis
– Last few sec-min – Ends when the
– Complication: suicidal behavior, immediate effect of
major depressive disorder, panic
disorder hallucinogen wear off
INHALANT-RELATED DISORDERS
• Inhalant drugs – volatile • Ppl like to inhale these products
substances / solvents  volatile for their intoxicating effect
hydrocarbons that vaporize to • Conduct disorder, mood disorder,
gaseous fumes @ room temp, suicidalitym physical & sexual
inhaled to enter bloodstream via abuse / neglect
transpulmonary route • Inhalant = CNS depressants
• 4 commercial classes
– Effect appear within 5 mins
– Solvents for glues & adhesives and can last for 30 min-hr,
– Propellants (aerosol paint depending on the inhalant
sprays, hair sprays, shaving substance & dose
cream)
– Thinners (paint products,
correction fluids)
– Fuels (gasoline, propane)
Diagnosis
• Inhalant intoxication delirium
• Inhalant intoxication – Bc pharmacodynamic interaction
– Presence of maladaptive behavioral w/ other substances
changes & at least 2 physical sx – Hypoxia that may be associated
– Intoxicated state: apathy, diminished w/ inhalant or its method of
social & occupational functioning, inhalation
impaired judgment,
impulsive/aggressive behavior – If delirium results in severe
– + nausea, anorexia, nystagmus, behavioral disturbance  short
depressed reflexes, diplopia term tx w/ dopamine receptor
– High doses & long exp: stupor & antagonist (haloperidol) might be
unconsciousness necessary
– Rashes around pt’s nose & mouth,
– Avoid benzodiazepine bc ⬆pt’s
unusual breath odors, residue of
inhalant substances on pt’s face, respiratory depression
hand or clothing • Inhalant-induced persisting dementia
– Irritation of eye, throat, lungs, nose – Bc neurotoxic effect of inhalant
– Prolonged period of hypoxia
Clinical features Treatment
• Small initial dose inhalant • Resolves spontaneously
disinhibiting & produce feelings of • Effect of intoxication: coma,
euphoria & excitement, pleasant bronchospasm, laryngospasm,
floating sensation cardiac arrhythmias, trauma, or
• High dose  fearfulness, sensory burns need treatment.
illusions, auditory & visual
• Course & tx of inhalant-induced
hallucinations, distortion of body size
– Neurological sx: slurred speech,
psychotic disorder is brief
decreased speed of talking, ataxia • Confusion, panic, psychosis 
• Long term use: irritability, emotional mandate special attention to pt
lability, impaired memory safety
• Withdrawal syndrome: sleep • Severe agitation haloperidol (5
disturbance, irritability, jittery, N/V, mg IM per 70 kg body weight)
tachycardia, (sometimes) delusion & • Avoid sedative bc can aggravate
hallucinations psychosis
OPIOID-RELATED DISORDERS
• Cluster of physiological,
behavioral, cognitive symptoms
• WHO: “The use of a drug takes
on a much higher priority for a
given person than other
behaviors that once had a
higher value”
• Opioid abuse: pattern of
maladaptive use of opioid drug
leading to significant
impairment / distress and
occuring within 12 month
period
Diagnosis
• Heroin (most commonly • Opioid use disorder
abused opioid)  more – Pattern of maladaptive
lipid soluble than morphine use of opioid drug, leading
– Cross BBB faster, rapid to significant impairment /
pleasurable onset than distress, occuring within
morphine 12 month period
• Codeine, absorbed through • Opioid intoxication
GI tract  transformed to – maladaptive behavioral
morphine in the body changes and specific
• All opioid  ⬇cerebral physical symptoms of
blood flow opioid use.
• Morphine & heroin withdrawal syndrome
– Begins 6-8hr after last dose, after 1-2wk
period of continuous exposure or after
adm of narcotic antagonist
– Peaks during 2nd/3rd day
– Subside during the next 7-10 days
– Sx may persist for 6 months/longer
• Meperidine
– Peaks 8-12 hr, ends in 4-5days
• Methadone
– Begins 1-2 days after last dose, ends in
10-14 days
• Symptoms: severe muscle cramps, bone
aches, profuse diarrhea, abd cramps,
rhinorrhea, lacrimation, piloerection (cold
turkey), yawning, fever, pupillary dilation,
HTN, tachycardia, temp dysregulation
SELDOM DIE
• Residual sx: insomnia, bradycardia, temp
dysregulation  persist for months after
withdrawal
Clinical features
• Adverse effects
– Potential transmission of
• Mode of entry: oral, intranasal
hepatitis & HIV through
(snorted), injected IV/SC contaminated needles
• Addictive bc euphoric high that users – Idiosyncratic allergic rx to opioid
experience (esp IV)  anaphylactic shock, pulmo
• Associated symptoms: feeling of edema, death
warmth, heaviness of extremities, – Mephedrine x MAOIs  gross
dry mouth, itchy face (esp the nose), autonomic instability, severe
facial flushing) behavioral agitation, coma,
• Initial euphoria  sedation ‘nodding seizure, death
off’ • Opioid overdose
• Physical effect: respiratory – Death bc respiratory arrest
depression, pupillary constriction, – Sx: marked unresponsiveness,
smooth muscle contraction (incl coma, slow RR, hypothermia,
ureters & bile duct), constipation, hypoTN, bradycardia
change in BP, HR, temp, RR – Triad: coma, pinpoint pupils,
resp depression
– Inspect needle tract
Treatment & rehab
• Overdose treatment • Pregnant woman w opioid
– Ensure adequate airway dependence
– Tracheopharyngeal secretion – Neonatal withdrawal: low
 aspirated dose methadone (10-40 mg
– Ventilate pt daily)
– Naloxone IV at slow rate – 0.8 – Fetal AIDS transmission:
mg per 70kg body weight zidovudine + other anti-HIV
medication to decrease
– Signs of improvement: ⬆RR,
incidence of HIV in newborns
pupillary dilation
• Psychotherapy
• Medically supervised withdrawal
& detoxification
– Methadone
– Opioid substitute:
levomethadyl, buprenorphine
– Opioid antagonists
ALCOHOL-RELATED DISEASE
Acute intoxication - ALCOHOL
• slurred speech, CNS depression, dis inhibition, lack of coordination
• nystagmus, diplopia, dysarthria, ataxia  may progress to coma
• hypotension (peripheral vasodilation)
• if obtunded, rule out
– head trauma/intracranial hemorrhage
– associated depressants/street drugs, toxic alcohols
• may also contribute to respiratory/cardiac depression
– hypoglycemia (screen with bedside glucometer)
– hepatic encephalopathy: confusion, altered LOC, coma
• precipitating factors: GI bleed, infection, sedation, electrolyte
abnormalities, protein meal
– Wernicke’s encephalopathy (ataxia, ophthalmoplegia, delirium)
– post-ictal state, basilar stroke
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Withdrawal - ALCOHOL
• beware of withdrawal signs
• Common deficiencies : Thiamine, Niacin, Folate, Glycogen,
Magnesium, Potassium
• Treatment
– diazepam 10-20 mg IV/PO or lorazepam 2-4 mg IV/PO q1h until
calm
• frequency of dosing may have to be increased depending on
clinical response
– may use CIWA protocol and give benzodiazepines as above until
CIWA <10
– thiamine 100 mg IM/IV then 50-100 mg/d
– magnesium sulfate 4 g IV over 1-2 h (if hypomagnesemic)
– admit patients with DT or multiple seizures
Cardiovascular complications - ALCOHOL
• HTN
• cardiomyopathy: SOB, edema
• dysrhythmias (“holiday heart”)
• AFib (most common), atrial utter, SVT, VTach
(especially Torsades if hypomagnesemic/
hypokalemic)
Metabolic abN - ALCOHOL
alcoholic ketoacidosis
• AG metabolic acidosis, urine ketones, low glucose, and normal
osmolality
• history of chronic alcohol intake with abrupt decrease/cessation
• malnourished, abdominal pain with N/V
• treatment: dextrose, thiamine (100 mg IM/IV prior to dextrose),
volume repletion (with NS)
• generally resolves in 12-24 h
other alcohols
• ethylene glycol CNS, CVS, renal findings
• methanol
– early: lethargy, confusion
– late: headache, visual changes, N/V, abdominal pain, tachypnea
• both ethylene glycol and methanol produce severe metabolic
acidosis with anion gap (as the
• alcohol is metabolized) and osmolar gap (initially a er ingestion but
before metabolism)
• EtOH co-ingestion is protective
• Treatment
– urgent hemodialysis required
– fomepizole 15 mg/kg IV bolus OR EtOH 10% IV bolus and
infusion to achieve blood level of 22 mmol/L (EtOH loading may
be done PO)
– consider folic acid for methanol, and pyridoxine and thiamine
for ethylene glycol – both help reduce conversion to active
metabolites
• other abnormalities associated with alcohol: hypomagnesemia,
hypophosphatemia, hypocalcemia, hypoglycemia, hypokalemia
GI abN - ALCOHOL
Gastritis
• common cause of abdominal pain and GI bleed in chronic alcohol
users
Pancreatitis
• serum amylase very unreliable in patients with chronic pancreatitis,
may need serum lipase
• hemorrhagic form (15%) associated with increased mortality
• fluid resuscitation very important
Hepatitis
• AST/ALT ratio >2 suggests alcohol as the cause as well as elevated
GGT with acute ingestion
peritonitis/spontaneous bacterial peritonitis
• leukocytosis, fever, generalized abdominal pain/tenderness
• occasionally accompanies cirrhosis
• paracentesis for diagnosis (common pathogens: E. coli, Klebsiella,
Streptococcus)
GI bleeds
• most commonly gastritis or ulcers, even if patient known to have
varices
• consider Mallory-Weiss tear secondary to retching
• often complicated by underlying coagulopathies
• minor: treat with antacids
• severe or recurrent: endoscopy
Disposition - ALCOHOL
• before patient leaves ED ensure stable vital signs, can walk
unassisted, and fully oriented
• offer social services to nd shelter or detox program
• ensure patient can obtain any medications prescribed and can
complete any necessary follow-up
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DRUG INDUCED
Acetaminophen
• Acetaminophen is absorbed
rapidly, with peak plasma
concentrations generally
occurring within 1 hour and
complete absorption within
4 hours.
• Mechanism of action :
Absorbed inhibits
prostaglandin E2 (PGE2)
synthesis  antipyresis and
analgesia.
• Acetaminophen-induced liver damage initially
occurs in hepatic zone III (centrilobular)  severe
toxicity  necrosis of the entire liver parenchyma
• Effects :
– multiorgan failure,
– SIRS,
– hypotension,
– cerebral edema,
– Death.
Clinical Features
Differential Dx
• Px with ↑ aminotransferases, bilirubin, partial thromboplastin
time (PTT)/international normalized ratio (INR), or creatinine;
– including acute tubular necrosis,
– rhabdomyolysis,
– ischemic hepatitis,
– alcoholic hepatic disease,
– cyclopeptide-containing mushroom toxicity,
– viral hepatitis,
– Wilson disease,
– other hepatic toxicities (eg, valproic acid, isoniazid [INH], statins,
herbal medications, vinyl chloride, and polychlorinated biphenyls).
Dx testing
• Goals patient assessment:
(1) the determination of the patient’s risk,
(2) diagnostic testing,
(3) treatment with the antidote NAC when appropriate.
• classified as acute or chronic
• acute  single ingestion or a series of ingestions that are arbitrarily
defined to occur within an 8-hour period.
• Chronic  All other ingestions, including accidental repeated
supratherapeutic ingestions and intentional ingestions spread over
longer than 8 hours.
1. Determine the patient’s risk of acute
acetaminophen exposure
2. diagnostic testing,
3. treatment with the antidote NAC when
appropriate
Clinical presentation
• History • Physical Examination
– Always attempt to identify the exact – Hemodynamic instability:
formulation, amount, and timing of the poisoning
ingestion
– Tachypnea: compensate for an
– Ask about any coingestants (eg,
ethanol) that might impact the
ongoing metabolic acidosis
metabolism of APAP & clarify the – Coingestions/ combination
number and frequency of ingestions to products (eg, APAP+opiod or
rule out chronic toxicity. APAP+diphenhydramine):
– Ask about risk factors for increased abnormalities due to con current
toxicity: chronically & alcoholic patients opiod/ anticholinergic toxidromes
and those taking medications that – Diffuse abdominal tenderness:
activate the cytochrome P450 system
overdose
(eg, anticonvulsants, antituberculosis)
– Ask about the presence of any – Tender hepatomegaly: latent stage
abdominal pain, nausea, and vomiting – Skin & sclera: looking signs of
jaundice
Diagnostic studies: Lab
• Determine treatment • Check a baseline complete
Rumack-Matthew nomogram blood count and follow serial
• Check a full panel of liver hemoglobin levels in patients
studies ( aspartate who develop coagulopathies
aminotransferase, alanine • Order a metabolic panel asses
aminotransferase, albumin, electrolyte abnormalities &
bilirubin) calculate the anion gap
• Order a coagulation profile • Confirm the degree of acidosis
(prothrombin time [ PT] , with blood gas sampling.
international normalized ratio • Check the renal function in all
and partial thromboplastin patients as acute kidney injury is
time) determine the degree common secondary to intra-
of liver synthetic dysfunction. renal NAPQI production.
• Patient w/ acute ingestions of reliable timing plot
their 4-hour APAP level on the Rummack-Matthew
normogram
• Rummack-Matthew normogram:
– Cannot be used if either the time of ingestion is unknown/
ingestion is chronic
– Unreliable in cases of coingestion w/ product that alter
APAP absorption & pharmacokinetics
• King’s college liver transpant criteria estimate the
severity & identify which patients may require transfer
– Patients w/ pH <7.3 after fluid resuscitation/ a combination
of PT > 100
– creatinine >3.3 mg/dL
– grade 3 or 4 encephalopathy
Treatment
Start NAC in
patients with
1. Acute ingestions
and 4-hour
levels that lie
above the
nomogram
Cutoff
2. in patients who
report
significant
ingestions if
obtaining a level
will be
significantly
delayed
3. In those with
evidence of
hepatoxicity
presumed
secondary to
SULFONAMIDE INTOXICATION
• The sulfonamides are synthetic
antimicrobial agents with a
wide spectrum encompassing
most gram-positive and many
gram-negative organisms.
• Range of toxicity :
– Since many of the adverse
effects appear to be
hypersensitivity reactions, there
is no specific toxic dose.
– The incidence of the adverse
effects appears to increase with
increased sulfonamide dosage.
Gx
• DERMATOLOGIC: • GASTROINTESTINAL:
– including rash, – Nausea
– vomiting are common.
– pruritus,
– • HYPERSENSITIVITY REACTION:
erythema nodosum,
– Transient myopia,
– Quite severe and often
– conjunctivitis,
fatal erythema multiforme
– hepatic injury,
of the Stevens-Johnson
– keratitis.
type have been reported.
– Lyell's Syndromes are • NEUROLOGIC:
– Headache,
usually associated with the
– depression,
use of a long-acting
sulfonamides – hallucinations
• GENITOURINARY : Adverse effects increase in renal
failure without dose reduction
• FLUID-ELECTROLYTE:
– Hyperkalemia has been reported following therapeutic use of
trimethoprim/sulfamethoxazole.
• HEMATOLOGIC :
– Hematologic effects are uncommon, but several have been
reported.
– These include acute hemolytic anemia, agranulocytosis,
thrombocytopenia, aplastic anemia, and
methemoglobinemia.
PP
• lab tests
– liver function : ↑ ALT dan AST
– kidney function : ↑ BUN Kreatinin
– Hematopoietic should be monitored
Treatment
• ORAL/PARENTERAL EXPOSURE
• A) Treatment : symptomatic and supportive. There is no specific
antidote for sulfonamide intoxication.
• B) ACTIVATED CHARCOAL:
– Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose:
25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years),
and 1 g/kg in infants less than 1 year old.
• C) HYPERSENSITIVITY REACTION
– The drug should be immediately discontinued and the patient observed
for the possibility of anaphylactic shock.
– In this situation the normal treatment for anaphylaxis is carried out with
the establishment of an open airway, epinephrine, and diphenhydramine.
D
• D) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid  persists,
administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT:
begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1
mcg/kg/min); titrate to desired response.
• E) DIURESIS: If kidney function is normal, consider administration of
D5/0.45 NaCl with a diuretic such as furosemide 1 mg/kg to a maximum of
40 mg/dose to obtain a urine flow of 3 to 6 mL/kg/hr.
• F) anuria or agranulocytosis,  dialysis and/or isolation should be
considered. Obtain a baseline CBC, hepatic and renal function test.
• G) CHRONIC THERAPY: Discontinue the use of the drug; provide
symptomatic and supportive care.
• H) SEIZURES:
– Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to
20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum
of 10 mg/dose.
– May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV
initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1
mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15
minutes as needed, if seizures continue).
• I) METHEMOGLOBINEMIA:
– Determine the methemoglobin concentration and evaluate the
patient for clinical effects of methemoglobinemia (ie, dyspnea,
headache, fatigue, CNS depression, tachycardia, metabolic
acidosis).
– Symptomatic methemoglobinemia with methylene blue (this
usually occurs at methemoglobin concentrations above 20% to
30%, but may occur at lower methemoglobin concentrations in
patients with anemia, or underlying pulmonary or
cardiovascular disorders).
– Administer oxygen while preparing for methylene blue therapy.
J) METHYLENE BLUE: INITIAL DOSE/ADULT OR CHILD: 1 mg/kg
IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be
given 1 hour after the first dose if methemoglobin levels remain
greater than 30% or if signs and symptoms persist.
Warfarin
• Activated charcoal is empirically used to minimize systemic absorption of the toxin.
• Vitamin K1 is used in the management of poisoning and overdose, in the prevention of toxic effects,
and in metabolic disorders in which toxic substances accrue.
• Activated charcoal (Actidose-Aqua, Char-Caps, Kerr Insta-Char)
– Activated charcoal is the emergency treatment used for poisoning caused by drugs and
chemicals. A network of pores present in activated charcoal adsorbs 100-1000 mg of drug per
gram of charcoal. Activated charcoal does not dissolve in water.
– Administer activated charcoal to patients who present 1-2 hours postingestion or to patients in
whom co-ingestants may delay gastric emptying or gut motility; minimal benefit is expected if
more than 4 hours have passed since the ingestion.
• Phytonadione (MEPHYTON)
– Phytonadione (Vitamin K1) can overcome competitive block produced by warfarin and other,
related anticoagulants. (Note that vitamin K3 [menadione] is not effective for this purpose.)
The clinical effect is delayed for several hours while liver synthesis of clotting factors is initiated
and plasma levels of clotting factors II, VII, IX, and X are gradually restored.
– Vitamin K1 is not to be administered prophylactically; use only if evidence of anticoagulation
exists. The required dose varies with the clinical situation, including the amount of
anticoagulant ingested and whether it is a short-acting or long-acting anticoagulant.
• Blood Components
– Fresh frozen plasma (FFP) has been the mainstay for urgent anticoagulation
reversal in patients taking vitamin K antagonists (eg, warfarin). FFP requires blood
group typing and thawing before use. Unlike plasma, human prothrombin complex
concentrate does not require blood group typing or thawing and is administered in
a significantly lower volume than plasma. Prothrombin does have a slightly higher
risk for thromboembolic (TE) events compared with plasma, particularly in patients
with a history of TE events.
• Fresh frozen plasma
– Each unit provides all plasma proteins and clotting factors to support adequate
hemostasis to treat bleeding.
• Prothrombin complex concentrate, human (Kcentra)
– Contains Factors II, VII, IX, X, Protein C and S. It is indicated for urgent reversal of
acquired coagulation factor deficiency induced by vitamin K antagonist therapy in
adults with acute major bleeding
Abuse of New Psychoactive Substances
• There has been an explosive increase in the non-medical use of so-called ‘designer drugs' or
‘new psychoactive substances' (NPS), which are synthetic alternatives to illicit drugs of abuse (
Baumann et al, 2014).
• NPS are easy to obtain, inexpensive, and not detected by standard toxicology screens.
• Products containing NPS are often given deceptive names and labeled ‘not for human
consumption' to circumvent laws prohibiting the sale and use of psychoactive drugs.
• There are well known examples of NPS that mimic most types of abused drugs—stimulants
(‘bath salts'), cannabinoids (‘spice'), hallucinogens (‘N-bombs'), and opioids (‘MT-45’)
—but the pharmacology and toxicology of these substances have not been well characterized.
• Although NPS can elicit subjective effects that resemble their progenitors, potential off-target
sites of action are unknown and adverse medical consequences are common.
Life-threatening toxidromes have been described for each type of NPS  with symptoms
including agitation, hallucinations, psychosis, violent behaviors, and coma.
• In the United States, an alarming spike in toxic exposures and fatalities associated with abuse
of synthetic cannabinoids has occurred during the past year (Trecki et al, 2015).
• Patients intoxicated with NPS present a significant burden to healthcare professionals,
especially those involved with emergency medical care, and the long-term neuropsychiatric
consequences of NPS exposure are not known.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4707839/
Fact file on new psychoactive substances
March 2016
• The public health risks of new psychoactive substances

• Gauging the public health risks, prevalence and incidence of abuse of
new psychoactive substances is extremely difficult, because of their
number, and the rapid modifications in chemical structures.
• However, many so-called ‘research chemicals’ have been associated
with death and serious toxic consequences for users, including
respiratory depression, unconsciousness, nerve damage, balance and
vision disturbances, and hearing loss.
• In England and Wales, the number of deaths involving new
psychoactive substances are low compared with deaths involving
opiates or cocaine, however, they have risen from 60 deathsin 2013 to
67 in 2014. These deaths were predominantly associated with
methcathinones such as mephedrone.
Substances under surveillance
WHO Expert Committee on Drug Dependence http://www.who.int/medicines/access/controlledsubstances/
http://www.who.int/medicines/access/controlled- Substances_under_surveillance.pdf?ua=1
substances/ecdd/en/
• Categories of NPS sold in the market
• The main substance groups of NPS are aminoindanes (e.g. 5,6-
methylenedioxy-2-aminoindane (MDAI)), synthetic cannabinoids
(e.g. APINACA, JWH-018), synthetic cathinones (e.g. 4-
methylethcathinone (4-MEC) and α-pyrrolidinopentiophenone
(α –PVP)), phencyclidine-type substances (e.g. methoxetamine
(MXE)), phenethylamines (e.g. 2C-E and 25H-NBOMe),
piperazines (e.g. benzylpiperazine (BZP) and 1-(3-chlorophenyl)
piperazine (mCPP)), plant-based substances (e.g. kratom
(mitragyna speciosa Korth), salvia divinorum and khat (Catha
edulis)), tryptamines (e.g. α-methyltryptamine (AMT)), and other
substances (e.g. 1,3-dimethylamylamine (DMAA)).
https://www.unodc.org/LSS/Page/NPS

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Rosen's Emergency Medicine-Concepts and Clinical Practice,2-Volume Set, 9e (Jun 1, 2017)_(0323354793)_(Elsevier)

Rosen's Emergency Medicine-Concepts and Clinical Practice,2-Volume Set, 9e (Jun 1, 2017)_(0323354793)_(Elsevier)

Rosen's Emergency Medicine-Concepts and Clinical Practice,2-Volume Set, 9e (Jun 1, 2017)_(0323354793)_(Elsevier)

Rosen's Emergency Medicine-Concepts and Clinical Practice,2-Volume Set, 9e (Jun 1, 2017)_(0323354793)_(Elsevier)

Rosen's Emergency Medicine-Concepts and Clinical Practice,2-Volume Set, 9e (Jun 1, 2017)_(0323354793)_(Elsevier)

• ECG if ps tachy /bradycardic,

Rosen's Emergency Medicine-Concepts and Clinical Practice,2-Volume Set, 9e (Jun 1, 2017)_(0323354793)_(Elsevier)

Rosen's Emergency Medicine-Concepts and Clinical Practice,2-Volume Set, 9e (Jun 1, 2017)_(0323354793)_(Elsevier)

When MDAC indicated

Rosen's Emergency Medicine-Concepts and Clinical Practice,2-Volume Set, 9e (Jun 1, 2017)_(0323354793)_(Elsevier)

• The public health risks of new psychoactive substances

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