Pemicu 2 KGD Sher

General management of the poisoned patient
• Clinical features
• A detailed history
• In the conscious, cooperative person, the specific agent(s), time, route,
amount, and intent of exposure need to be documented
• Environmental clues such as drug paraphernalia, empty pill bottles, odors, or
suicide notes may aid in the diagnosis
• Review hospital records for recent prescriptions or any history of psychiatric
illness
Diagnosis
• A diagnosis of poisoning is established
primarily through the history and physical
examination
• Consider empiric testing in all potentially
poisoned patients
• Consider blood glucose, an arterial blood
gas analysis, ECG, urine pregnancy test,
electrolytes, and liver function panel.
http://www.aafp.org/afp/2000/0501/p2763.html
http://www.aafp.org/afp/2000/0501/p2763.html
Treatment
• Gross decontamination should • mechanical airway and assisted
occur prior to patient entry into ventilation
the ED  Ensure that clothing • hypotension
and jewelry are removed. Wash • IV crystalloid bolus 10-20mL/kg
the skin with copious amounts of
water.
• Antidote
• further assessment of blood
Resuscitation glucose, temperature and conscious
state
• stabilization of abc
• few indicated bfore
• compromised airway patency / cardiopulmonary stabilitzation
reduced respiratory drive -> • naloxone: opiate toxicity
inadequate ventilation • cyanide antidote
• atropine: organophosphate poisoning
• Hypoglycemia
• IV dextrose • Agitation
• at risk for Wenicke’s enceph: thiamine • titrated dose of benzodiazepin
after dex
• altered mental status: indication • toxin induced: anti-psychotic as second line
• cardiac arrhythmias • hyperthermia and hypothermia

• anti-arrhythmic drugs: not first line • >39: aggresive active cooling measure
treatment • <32: active rewarming
• respond to correction of hypoxia,
metabolic/acid-base abn, administration of
antidote • Naloxone
• sodium bicab: osdium channel blocker • opioid antagonist: IV/IM/intranasal
toxicity w/ cv complication • reverse opioid-induced deleterious
• ventricular tachyarrhythmias: overdrive hypoventilation
pacing • used when RR <12
• titrated using bolus doses 0.1-0.4mg
• Seizure • large initial bolus -> volit and aspiration
• titrated to achieve desirable ventilation
• drug-induced: titrated dose of IV Benzo, and conscious state
except isoniazid-induced: need pyridoxine
• barbiturate: second line
Opioid
• agnoist at 3 receptor: mu, kappa, delta • urinary retention due to increased vesical sphincter
tone
• -bing to mu receptors in nucleus accumbens
pathway -> localized release of dopamine • opioid-induced acute lung injury: assoc. complication
w/ heroin overdose
• tachypnea, rales, decreased o2 saturation, bilateral
Clinical Features pulmo infiltrates
• intoxication: • combination of meperidine, tramadol /
• respiratory and mental status depression dextromethorphan w/ mao, ssri -> serotonin
• slow and shallow respirations -> hypercarbia, hypoxia, syndrome
cyanosis
• disorientation, hyperthermia, autonomic
• Analgesia
instability, hyperreflexia, muscle rigidity
• Miosis
• orthostatic hyoptension
• nausea and vomititing
• histamine release -> localized urticaria and
bronchospasm
• ileus due to decreased GI motility
Diagnosis Opioid Screens
• coma, miosis, respiratory depress • morphone, codeine, heroin detected
• RR <12, miosis, evidence of opioid use • hydrocodone and oxycodone
• auscultatory findings: pulmo edema • rifampin, rifampicin, quinine,
• Undress diphenhydramine: false-positive
• look for hidden drug-use paraphernalia • Dextromethorphan
• fentanyl patches • positive up to 2-3 days after use
DD Treatment
• clonidine: coma, bradycardia, hypotension, • airway protection and ventilatory maintenance
miosis, periods of apnea tht respond to
tactile/auditory stimulation • bag-valve mask ventilatory support: initially
maintain adequate oxygenation and ventilation
• organophosphate and carbamate: cholinergic
toxidrome • adequate ventilation -> naloxone
Opioid Withdrawal
• downregulation of endorphin, dynorphins and methdaone exposure
opioid receptos: long term use of opioid • precipitated by administration of antagonist:
• abrupt cessation: doesn’t allow time for naloxone / naltrexone or patrial agonist:
upregulation of receptor -> increased neuronal buprenorphine
firing and withdrawal syndrome
• peak on third day, resove by 5/6th day
Clinical Manifestation Treatment

• feelings of anxiety, yawning, lacrimation,
diaphoresis, rhinorrhea, diffuse myalgias • iv fluid, electrolyte replacement, antiemetic
• -> piloerection, mydriasis, nausea, profuse • clonidine: suppress sympathetic hyperactivity,
vomiting, diarrhea, abdominal cramping shorten duration of withdrawal
• very uncomfortable but not life-threatening • daily administration of methadone PO: inhibit
and rarely fatal withdrawal symptoms
• vomiting and aspiration of gastric contents -> • not administered until withdrawal symptoms
pneumonitis and dehydration appear
• onset: 6-12h of last heroid use, w/in 30h of
Cocaine, Amphetamine
• CNS stimulant and local anesthetic, release of
dopamine, epi, nore, serotonin
• excess -> sympathetic activation -> mydriasis,
tachycardia, hypertension, diaphoresis ->
dysrhythmias, seizures, hyperthermia
• euphoria assoc. w/ enhanced alertness
• block conduction of nerve impulse: blck fast
sodium channels
• QRS-complex widening and QT-interval
prolongation
• large dose: direct toxic effect on myocardium ->
negative inotropy
Clinical Feature Pulmo
• result of sympathomimetic, vasoconstrictive, psychoactive, • smoke crack cocaine
local anesthetic
• pulmo hemorrhage, barotrauma, pneumonitis, ashtma, pulmo
edema
CV • pneumomediastinum, pneumothorax, bronchospasm
• dysrhythmias, myocarditis, cardiomyopathy, acute coronary
syndrome
GI
• vasocontriction in coronary a. ->cocaine-induced chest pain
• ischemia bowel necrosis, ischemic colitis, splenic infaction
• STEMI/NSTEMI, atypical chest pain
• ulceration, bleeding, peroration
• ECG appearance of Brugada pattern
• advanced tooth decay: meth user
• Takotsubo syndrome: apical ballooning of left ventricle • poor oral hygiene, persistent dry mouth, jaw clenching
CNS Endocrine
• seizures, intrcranial infarction, hemorrhages • mdma -> hyponatremia
• severe transient hypertension, cerebral vasoconstriction
• choreoathetosis and repetitive movements Renal
• paranoid psychosis: long term amphetamine abus eand • Rhabdomyolysis
withdrawal
• hyperthermia, vasoconstriction, hypotension, hypovolemia
Lab
• creatine kinase: in pt w/ agitation / elevated temp ->
possible metabolic acidosis, renal failure or rhabdomyolysis
• hyponatrmia: often w/ altered mental status, after use of
amphetamine
• chest pain: eck and serum level of cardiac biomarkers
• hyperthermic: coagulation and liver function
• altered mental status: ct of head
• urine amphetamine
Treatment
• IV access
• O2 administration for hypoxia
• monitor of vital signs, treatment of medical complication,
supportive care, adequate sedation to prevent self-harm,
testing and iimaging
• Hyperthermia cool-mist spray and fans / cooling blankets
• rhabdomyolisis: aggresive IV hydration
• seizure: Benzo
Acetaminophen
• pt >6 years old ingest • Treatment
• >10 grams / 200mg/kg as single ingestion • antidote acetylcysteine
• >10 gr / 200mg/kg over 24h period • glutathione substitute  binding
• >6 gr / 150mg/kg per 24h for at least 2 the toxic metabolite as it is
consecutive days produced
• children <6y • most effective when given early
• >200mg/kg as single ingestion
and should be started within 8–
10 hours if possible
• 150mg/kg per 24h for 48h • Liver transplantation for patients with
fulminant hepatic failure
• Manifestations
• Asymptomatic, mild gastrointestinal
upset (nausea, vomiting)
• elevated aminotransferase levels and
hypoprothrombinemia (24–36 hours)
• fulminant liver failure occurs  hepatic
encephalopathy and death
• Renal failure may also occur
Patfis
• Acetaminophen-induced liver damage initially occurs in hepatic zone III (centrilobular)
because oxidative metabolism is concentrated in this area. With severe toxicity, necrosis
of the entire liver parenchyma may occur. The clinical effects of severe acetaminophen
toxicity are the result of severe fulminant liver failure rather than a direct acetaminophen
effect. These effects include multiorgan failure, systemic inflammatory response
syndrome, hypotension, cerebral edema, and death.
• The principal therapy for acetaminophen toxicity is N-acetylcysteine (NAC), which is
effective via two separate mechanisms. Soon after overdose, NAC serves as a glutathione
precursor and a sulfur-containing glutathione substitute binding to, and thereby
detoxifying NAPQI and avoiding subsequent hepatotoxicity. In addition, NAC may
decrease NAPQI formation by enhancing acetaminophen conjugation with sulfate to
nontoxic metabolites.
• Even after acetaminophen hepatotoxicity is evident, NAC acts as a free-radical scavenger
and an antioxidant and alters hepatic microcirculation and oxygen delivery. In patients
with acetaminophen-induced hepatic failure, IV NAC decreases the rates of cerebral
edema, hypotension, and death even when no detectable acetaminophen remains in the
serum
Digitalis
• treatment of atrial fibrillation and symptomatic congestive heart
failure
• Inhibits Na-K ATPase -> increased intracellular na and extracell k ->
increase intracellular ca -> delayed after-depol -> premature
ventricular contraction and dysrhythmias
• shorten atrial and ventricular repolarization
• increase vagal tone
• toxic concentration -> increase sympathetic tone
DIGITALIS GLYCOSIDES
• syncope, dysrhythmia
• GI distress, dizziness, headache, delirium,
malaise, confusion
• acute toxicity
• abrupt onset of symptoms
• early manife: GI symptoms
• increased central vagal tone -> bradydysrhythmias
/ av block
• neuro: weakness / confusion
• viewing yellow-green halos around objects:
xanthopsia
• Hyperkalemia
• Chronic
• often result of drug-drug interaction / declining
renal function
• diuretic -> mild dehydration and hypokalemia ->
reduce clearance of digoxin
• neuro: weakness, fatigue, confusion, delirium
Diagnosis
Diagnosis
• single ingestion of 1-2mg in adult
• acute ingestion of 10mg in adult, 4mg in child
• ecg: premature ventricular contraction
• Lab: markedly elevated serum k toxicity
Treatment
• general supportive care
• treatment of specific complication
• prevention of further drug absorption
• enhancement of drug elimination
• antidote when indicated : digoxin-Fab
• continuous cardiac monitoring, IV access
Sherman SC, Weber JM, Schindlbeck MA, Patwari RG. Clinical Emergency Medicine. USA: McGraw-
Hill; 2014.
Warfarin Intoxicate
• Anticoagulant, could cause • The toxic dose of warfarin is highly
serious bleeding variable. chronic or repeated
ingestion of even small amounts of
• Monitoring warfarin with INR warfarin (2-5 mg/day) eventually
• Inhibit vitamin K dependant can lead to significant
procoagulant factors (II, VII, anticoagulation, especially in the
IX, X) presence of interacting drugs.
Patients with hepatic dysfunction,
• Maintain INR 2.0-3.0 malnutrition, or a bleeding
• Exceeds INR leads to increase diathesis are at the greatest risk of
risk of bleeding toxicity from warfarin use.
• Life-threatening complications include • If the PT is elevated, treatment with
massive GI bleeding and intracranial
hemorrhage. More common findings of vitamin K1 is appropriate. Ten
excessive anticoagulation are ecchymoses, milligrams orally is a reasonable daily
subconjunctival hemorrhage, epistaxis, dose and the duration of therapy may
vaginal bleeding, bleeding gums, or be many weeks.
hematuria. • Active, serious hemorrhage should be
• In all patients, if prolongation of the PT is treated with FFP A volume of 15 mL/kg
observed after an acute ingestion, it may is typically sufficient to completely
appear in as early as 8-12 hours; however,
reverse coagulopathy.
peak effects commonly are delayed until
at least 1-2 days postingestion.
Sherman SC, Weber JM, Schindlbeck MA, Patwari RG. Clinical
Emergency Medicine. USA: McGraw-Hill; 2014.
Cyclic Anti-Depressants
• Cyclic antidepressants inhibit • Treatment
reuptake of norepinephrine and • Obtain IV access and initiate cardiac
serotonin and antagonize rhythm and ECG monitoring
postsynaptic serotonin receptors • Patients should receive 1 gram/kilogram
of activated charcoal PO
• Clinical features  altered mental • Hypotension is treated with isotonic
status, seizures, cardiac conduction crystalloids
or rhythm disturbances, hypotension, • Treat conduction disturbances and
respiratory depression, and, in severe ventricular dysrhythmias with sodium
cases, coma. bicarbonate .
• Diagnosis  ECG changes include • Synchronized cardioversion may be
sinus tachycardia; right axis deviation indicated for unstable patients
of the terminal 40 milliseconds; PR, • Control agitation & seizures with
QRS, and QT interval prolongation; benzodiazepines
right bundlebranch block; A-V blocks;
and the Brugada pattern.
Anticholinergic
Toxicity
Diagnosis
• Electrolytes, glucose, creatine phosphokinase, and pulse oximetry
should be obtained
• DD  viral encephalitis, Reye syndrome, head trauma, other
intoxications, neuroleptic malignant syndrome, delirium tremens,
acute psychiatric disorders, and sympathomimetic toxicity.
Treatment
• Cardiac monitor and intravenous or intraosseus access
• Activated charcoal  ecrease drug absorption
• Temperature monitoring
• Treat dysrhythmias, widened QRS complexes, and hypotension from
sodium blocking agents (eg, cyclic antidepressants) with IV sodium
bicarbonate 1 mEq/kg
• Treat agitation with benzodiazepines ( lorazepam )
• Treat seizures with benzodiazepines (lorazepam 2 milligrams IV).
• Physostigmine  indicated if conventional therapy fails to control
seizures, agitation, unstable dysrhythmias, coma with respiratory
depression, malignant hypertension, or hypotension
HALLUCINOGENS
• Treatment
• Obtain IV access and initiate cardiac rhythm and ECG monitoring
• Patients should receive 1 gram/kilogram of activated charcoal PO
• Hypotension is treated with isotonic crystalloids
• Treat conduction disturbances and ventricular dysrhythmias with sodium
bicarbonate .
• Synchronized cardioversion may be indicated for unstable patients
• Control agitation & seizures with benzodiazepines
TRAZODONE
• Clinical features
• Central nervous system depression
• Ataxia
• Dizziness
• Seizures
• Orthostatic hypotension
• Vomiting and abdominal pain
• ECG abnormalities include QT interval prolongation, sinus bradycardia and
tachycardia, and torsades de pointes.
• Treatment
• Initiate cardiac rhythm monitoring and obtain a 12-lead ECG
• Single-dose activated charcoal is recommended
• Treat hypotension with isotonic IV fluids, followed by norepinephrine
• Treat torsades de pointes with IV magnesium sulfate
• Discharge patients who remain asymptomatic for at least 6 hours, with
psychiatric evaluation as indicated.
• Admit those with neurologic and/or cardiac symptoms for > 6 hours after
ingestion to a monitored bed
BUPROPION • Treatment
• Clinical features • Start a peripheral IV line and
initiate cardiac rhythm monitoring.
• Agitation, dizziness, tremor,
vomiting, drowsiness, and • GI decontamination is
tachycardia recommended if done within 1
hour of ingestion
• Seizures
• Treat seizures with
• ECG changes include sinus benzodiazepines , followed by
tachycardia, QRS interval phenobarbital
widening, and QT interval
prolongation • Observe asymptomatic patients
for 8 hours
MIRTAZAPINE • Treatment
• Clinical features  sedation, • Isolated overdoses can generally
be managed with supportive care
confusion, sinus tachycardia, and
hypertension. • Single-dose activated charcoal is
recommended for GI
• Coma and respiratory decontamination.
depression are seen in severe • Admit symptomatic patients to a
cases or with coingestion of monitored bed. Discharge
other sedatives. asymptomatic patients after 6
hours
SELECTIVE-SEROTONIN REUPTAKE • Treatment
INHIBITORS • Establish IV access and initiate cardiac
monitoring.
• Clinical features  vomiting,
sedation, tremor, sinus tachycardia, • Single-dose activated charcoal is
appropriate for most ingestions
mydriasis, seizures, diarrhea, and • Seizures  Benzodiazepines
hallucinations • Observe patients for at least 6 hours.
• Sinus bradycardia is more common Admit patients who are tachycardic,
with fluvoxamine than with other lethargic, or have conduction
SSRIs. abnormalities on ECG 6 hours after
ingestion
• QRS and QT interval prolongation
has been reported in citalopram
ingestions
SEROTONIN/NOREPINEPHRINE • Treatment
REUPTAKE INHIBITORS • Initiate peripheral IV access and
• Venlafaxine, duloxetine, and cardiac monitoring
desvenlafaxine • Single-dose activated charcoal
• Seizures  Benzodiazepines
• Overdose  hypertension, • Treat hypotension with fluids and
diaphoresis, tremor, mydriasis, a direct-acting α-agonist
sedation, and seizures. • All patients require at least 6
• ECG changes include sinus hours of observation, longer for
tachycardia and QRS or QT those ingesting extended-release
preparations. Admit symptomatic
interval widening patients to a monitored bed.
NSAID
Antihipertensive
Insecticides
• Organophosphorus insecticides include diazinon, acephate,
maalthion, parathion, and chlorpyrofos.
• Most patients become symptomatic within 8 hours of dermal
exposure, though some fat-soluble agents (eg, fenthion) can cause
delayed symptoms
Herbicides
• Herbicides are agents used to kill weeds
Rodenticides
• The most commonly used rodenticides are superwarfarins, including
bordifacoum, diphenacoum, and bormadoline
• Coagulopathy typically develops within 48 hours and lasts for weeks
to months due to the long half-lives of these agents
• Acute intentional or repeated ingestions  delayed hemorrhage,
including hematuria, gastrointestinal hemorrhage, or epistaxis
• Diagnosis  screening for toxic effect can be performed with an INR
obtained 24 to 48 hours after ingestion
Treatment
• If the INR is elevated (> 2), then start oral vitamin K1 , typically at
doses of 20 milligrams a day in adults (1 to 5 milligrams for children)
and continue for up to 10 months.
• Acute hemorrhage requires more aggressive therapy with fresh frozen
plasma, IV vitamin K1, and addition of prothrombin complex or
recombinant activated factor VII for refractory hemorrhage
Iron
• direct GI tract irritant -> vomitting,
diarrhea, ab pain, mucosal ulceration,
bleeding soon after significant ingestion
• mucosal surface injured -> free iron
passes to blood -> dirsupts cellular
processes -> induce acidosis and
widespread organ toxicity
• enters mitochondria -> inhibit oxidative
phophorylation -> metabolic acidosis w/
elevated lactate
• hepatotoxicity, coagulopathy, myocardial
and vascular dysfunction
• Clinical features  5 stages
1. First few hours of ingestion  abdominal pain, vomiting, and diarrhea.
2. Up to 24 hours following ingestion  While patients may be asymptomatic,
they often appear ill, and may have abnormal vital signs reflecting hypovolemia
and metabolic acidosis.
3. Appear early or develop hours after the second stage as shock and a metabolic
acidosis evolve  Iron-induced coagulopathy may cause bleeding and worsen
hypovolemia. Hepatic dysfunction, cardiomyopathy, renal failure may also
develop
4. 2 to 5 days after ingestion and is characterized by elevation of
aminotransferase levels and possible progression to hepatic failure
5. Occurs 4 to 6 weeks after ingestion, reflects the corrosive affects of iron on the
pyloric mucosa and may cause gastric outlet obstruction
Lead
• Most exposures  inhalation of • Symptoms of chronic, mild lead
lead dust / fumes / ingestion of poisoning are slow in onset &
contaminated substances, such as nonspecific.
paint chips ; Less often direct skin • Acute exposure  symptomatic 
contact “Lead colic”  cramping abdominal
pain with nausea, vomiting,
• no known physiologic need for lead. constipation,
diarrhea.
&, occasionally,
• Lead binds to sulfhydryl groups & • Other  fatigue, anemia, peripheral
other ligands  interferes with neuropathy, renal impairment, &
critical enzymatic reactions.
• toxic effects  most prominent in • hepatic & CNS dysfunction (mild
headache / personality changes to
the hematopoietic, neurologic, & full-blown
renal systems
Arsenic poisoning
• Arsenic is used in a variety of insecticides
and herbicides as well as mining and
smelting processes
• Acute Toxicity
• Nausea, ab pain vomiting, diarrhea (rice water-
like) within hours of exposure.
• Hypotension and tachycardia may develop
secondary to hypovolemia and direct
myocardial dysfunction.
• Encephalopathy, pulmonary edema, and acute
renal failure have been described.
• Chronic
• peripheral neuropathy, malaise, and confusion.
• Skin findings include alopecia,
hyperpigmentation, keratoses, and transverse
white nail lines (Mees lines).
Management
•The initial management  address life
threatening condition with supportive
management of shock, dysrhythmias, &
seizures
•Hemodialysis removes arsenic in the
setting of acute renal failure
•Chelation  Intramuscular
dimercaprol
•Workers should modify their habits to
avoid further absorption, & repeated
monthly 24-hour urine collections can
follow arsenic excretion.
Treatment
Mercury poisoning
• Elemental mercury exposure
• occur after contact with a broken thermometer
• absorbed via inhalation (especially with heating or vacuuming)  normal GI tracts,
cough, fever, dyspnea, vomiting, and headache.
• Acute lung injury can progress to respiratory failure.
• Inorganic mercury
• used as a disinfectant and in manufacturing  corrosive injury to the GI tract
• vomiting, diarrhea, abdominal pain, and GI bleeding early, followed by acute renal
failure
• Organic mercury
• found in some fungicides and pesticides
• can be absorbed when ingested.
• tends to occur with chronic exposures and results in profound central nervous
system dysfunction.
Hydrocarbon
• Organic compound tht contain
hydrogen and carbon
Marx JA, Hockberger RS, Walls RM, et al, editors. Rosen’s Emergency Medicine Concepts & Clinical Practice. 9th ed. Philadelphia: Elsevier; 2017.
CO Intoxication
• CO is generated through incomplete combustion of virtually all carbon-
containing products
• Structure fires (e.g., wood), clogged vents for home heating units (e.g.,
methane), and use of gasoline powered generators indoors
• CO interacts with deoxyhemoglobin
carboxyhemoglobin (COHb)
• Hemoglobin binds CO tightly
• In muscle, CO binds myoglobin atraumatic
rhabdomyolysis
• CO inhibits the final cytochrome complex involved
in mitochondrial oxidative phosphorylation 
switch to anaerobic metabolism and ultimately in
cellular death
• Delayed-onset neurologic complications hypoxic
insult; reperfusion injury and lipid peroxidation
related to platelet-induced nitric oxide release
• By alteration of the platelet-associated nitric oxide
cycle, the microvascular endothelium of the central
nervous system undergoes free radical–mediated
injury  localized inflammation and dysfunction
https://www.cdc.gov/disasters/co_guidance.html
Clinical features :
• Asphyxia  altered mental status, including coma and seizures; hypotension, cardiac arrest;
metabolic acidosis
• Mild CO poisoning  headache, nausea, vomiting, dizziness, myalgia, confusion
• Neurologic assessment  normal or focal findings or subtle perceptual abnormalities
• The often-touted cherry-red skin color  postmortem finding
Diagnosis :
• Lab  CO-oximetry, ABG, COHb levels, Serum lactate, Serum cardiac marker, Creatine
phosphokinase level
• ECG, Chest Xray, head CT
http://www.emed.ie/Toxicology/CO.php
https://www.cdc.gov/disasters/co_guida
nce.html
Hydrogen Cyanide Intoxication
• Hydrogen cyanide is a gas with many commercial uses, particularly in
synthetic fiber manufacture and fumigation
• Odor of bitter almonds
• When cyanide salts are dissolved in water, hydrogen cyanide can leave the
surface, under acidic conditions
• Tissue hypoxia dysfunction of the heart, CNS  coma, seizures,
dysrhythmias, cardiovascular collapse
• Diffuse cellular dysfunction  elevated serum lactate concentration 
metabolic acidosis
Diagnosis  low arterial-venous oxygen difference, pulse oxymetri, ABG, lactate
concentration
Marx JA, Hockberger RS, Walls RM, et al,

editors. Rosen’s Emergency Medicine
Concepts & Clinical Practice. 9th ed.
Philadelphia: Elsevier; 2017.
Industrial toxins and cyanide
RESPIRATORY TOXINS • Diagnosis  chest
radiography and laboratory
studies (arterial blood gas,
carboxyhemoglobin,
methemoglobin, and
lactate)
• Management
• Administer 100% oxygen,
usually humidified, along
with bronchodilators as
needed
• Prophylactic steroids and
antibiotics are generally not
indicated
CYANIDE
• Cyanide exposure most commonly
results from fires that involve
synthetic materials, wool, or plastics,
but may also be associated with
vermicidals, precious metal
reclamation, chemical laboratories,
and Prunus seeds.
• Diagnosis  Because delays in
treatment can lead to death, cyanide
poisoning is usually diagnosed
clinically at the bedside. Blood
cyanide levels are not rapidly
available
• Management
• Administer 100% oxygen and secure the airway. Administer crystalloids and
vasopressors for hypotension.
• Consider decontamination with activated charcoal if the airwa
HYDROGEN SULFIDE
• Hydrogen sulfide is a colorless gas used in the petrochemical industry
and can emanate from sewage or manure.
• Hydrogen sulfide causes cellular asphyxia that leads to lactic acidosis
• In high concentrations, rapid loss of consciousness, seizures, and
death can occur after only a few breaths
• Treatment  100% oxygen, followed by administration of sodium
nitrite IV, as with cyanide poisoning
Herbal and vitamins
Herbal Symptoms
Nutmeg Hallucinations, agitation, gastrointestinal upset, miosis, coma, and hypertension.
Ephedra, used for weight loss, Sympathomimetic toxicity, leading to strokes, seizures, and cardiac ischemia and
contains ephedrine dysrhythmias
Yohimbine (α2 –adrenergic Hallucinations, weakness, hypertension, and paralysis
receptor antagonist)
Pennyroyal oil Hepatotoxicity
Absinthe (wormwood) Psychosis, intellectual deterioration, ataxia, headache, and vomiting
contains volatile oils
Black (or blue) cohosh, used to Nausea, vomiting, dizziness, and weakness
treat menopause
Juniper, used as a diuretic Renal toxicity, nausea, and vomiting
Lobelia, used for asthma Anticholinergic syndrome
Garlic, ginkgo, and ginseng Bleeding in patients on warfarin
(have antithrombotic activity)
Diagnosis
• Diagnosis is usually made clinically.
• A history of massive acute ingestion or chronic supratherapeutic use
should be sought.
• Laboratory studies that may be helpful include a basic metabolic
panel, hepatic enzymes, coagulation studies, bleeding time,
toxicology screen, and urine pregnancy test.
• An ECG may be indicated with signs of sympathomimetic stimulation.
Treatment
1. Consider activated charcoal 1 gram/kilogram PO for large vitamin A or
vitamin D overdoses.
2. Treat hypercalcemia from vitamin A or D overdose with normal saline,
furosemide, and prednisone (to reduce GI absorption).
3. Consider diagnostic and therapeutic lumbar puncture to treat increased
intracranial pressure of pseudotumor from hypervitaminosis A.
4. Administer diphenhydramine 25 to 50 milligrams IV (1 milligram/
kilogram in children) or PO to patients with “niacin flush” symptoms.
5. Consider N-acetylcysteine 140 milligrams/kilogram PO or IV for treating
severe hepatotoxicity from herbal preparations such as pennyroyal oil.
Alcohol-Related Disease
• The oxidation of alcohol -> complex process involving three enzyme
systems, all contained in the hepatocyte.
• Acetaldehyde -> converted to carbon dioxide and water, primarily

through aldehyde dehydro- genase (ALDH).
• Alcohol is a central nervous system depressant.

• increases the release of γ-aminobutyric acid (GABA) in the brain, and it
inhibits postsynaptic N-methyl-d-aspartate glutamate receptor activity.
Alcohol Withdrawal Syndrome
• Alcohol withdrawal syndrome (AWS) -> continuum of syndromes that
begins after a decrease in the amount of intake of ethanol.
• AWS is often divided into three sets of symptoms.

• The first set consists of autonomic hyperactivity, which appears within hours of the
last drink and usually peaks within 24 hours. Common presenting characteristics
include trembling, sweating, nausea, vomiting, anxiety, and agitation.
• The second symptom set includes additional neuronal excitation, with epileptiform
seizures and global confusion, usually occurring within 24 to 48 hours of abstinence.
• The third feature set comprises delirium tremens or alcohol withdrawal delirium
(AWD), with auditory and visual hallucinations, confusion and disorientation,
clouding of consciousness, impaired attention, and pronounced autonomic
hyperactivity.
Marx JA, Hockberger RS, Walls RM, et al,
editors. Rosen’s Emergency Medicine
Concepts & Clinical Practice. 9th ed.
Philadelphia: Elsevier; 2017.
Clinical Features
• Minor alcohol withdrawal (6 hr)
• mild autonomic hyperactivity—nausea, anorexia, coarse tremor, tachycardia,
hypertension, hyperreflexia, sleep disturbances (eg, insomnia, vivid dreams),
and anxiety.
• Major alcohol withdrawal (>24 hr)
• anxiety, insomnia, irritability, tremor, anorexia, tachycardia, hyperreflexia,
hypertension, fever, decreased seizure threshold, auditory and, more
commonly visual hallucinations, and finally delirium.
Diagnostic Testing
• Mental Status
• Serum alcohol level or measure alcohol level by breathalyzer.
• Laboratory test results (eg, toxicology screen, electrolyte levels)
• Glucose level
• Oximetry
• AST & ALT
• A ratio of AST to ALT higher than 2, especially if concentrations of these
enzymes do not exceed 400 units/L, suggests alcoholic hepatitis
Treatment
• Benzodiazepines.
• Lorazepam (1-4 mg IV every 5-15 minutes)
• Diazepam (5 mg IV every 5-10 minutes)
• Butyrophenones.
• Haloperidol, a dopamine antagonist, can be considered in patients with major alcohol
withdrawal or delirium tremens not responding to IV benzodiazepines.
• Thiamine (100 mg IV)
• Magnesium (2 g IV)
Delirium
• Acute or subacute state of cognitive
dysfunction caused by an underlying
physiologic condition
• Three types of delirium
-Hyperactive
-Hypoactive
-Mixed
• Drug intoxication or withdrawal are
the most common cause of delirium
in younger adults
Drug induced delirium Clinical features
• Caused by imbalance of noradrenergic, • Natural history : patient’s with
serotoninergic, dopaminergic, cholinergic delirium can progress from apathy to
homeostasis marked agitation in the course of
hours
• Anticholinergic drugs • The hallmark of delirium is fluctuating
• Tricylic antidepressants course of symptoms and inattention
• Sedative-hypnotics • Short term memory impairment
• Narcotics • Disturbance sleep-wake cycle
• Psychedelic drugs LSD • Perceptual disturbances, delusion,
• Phenyclidine hallucination
• Often exhibits autonomic nervous
system abnormalities
• Brief psychotic disorder is defined as a
psychotic condition that involves the
sudden onset of:
1. psychotic symptoms, which lasts 1 day
or more but less than 1 month.
2. Remission is full, and the individual
returns to the premorbid level of
functioning.
Brief psychotic disorder is an acute and

transient psychotic syndrome.
Diagnosis As with other acutely ill psychiatric
patients, the history necessary to make
A diagnosis of brief psychotic disorder is the diagnosis may not be obtainable
solely from the patient.
appropriate when psychotic symptoms last
at least 1 day but less than 1 month and are
not associated with a mood disorder, a Although psychotic symptoms may be
obvious, information about prodromal
substance-related disorder, or a psychotic
disorder caused by a general medical symptoms, previous episodes of a mood
disorder, and a recent history of
condition. ingestion of a psychotomimetic
substance may not be available from
the clinical interview alone.
There are three subtypes of brief psychotic In addition, clinicians may not be able
disorder: (1) the presence of a stressor, (2) to obtain accurate information about
the absence of a stressor, and (3) a the presence or absence of precipitating
postpartum onset. stressors. Such information is usually
best and most accurately obtained from
a relative or a friend.
Clinical Features
• The symptoms of brief psychotic disorder always include at least one major
symptom of psychosis, such as hallucinations, delusions, and disorganized
thoughts, usually with an abrupt onset, but do not always include the entire
symptom pattern seen in schizophrenia.
• Some clinicians have observed that labile mood, confusion, and impaired
attention may be more common.
the onset of brief psychotic disorder than at the onset of eventually
chronic disorders. Characteristic symptoms in brief psychotic disorder
include:
1. emotional volatility, strange or bizarre behavior, screaming or
muteness, and impaired memory of recent events.
2. Some of the symptoms suggest a diagnosis of delirium and warrant
a medical workup, especially to rule out adverse reactions to drugs.
3. The symptom patterns include acute paranoid reactions and
reactive confusion, excitation, and depression. Some data suggest
that, in the United States, paranoia is often the predominant
symptom in the disorder.
Precipitating Factor
• The clearest examples of precipitating stressors are major life events that would
cause any person significant emotional upset.
• Such events include the loss of a close family member or a severe automobile
accident. Some clinicians argue that the severity of the event must be considered
in relation to the patient’s life.
• Others have argued that the stressor may be a series of modestly stressful
events rather than a single markedly stressful event, but evaluating the amount
of stress caused by a sequence of events calls for an almost impossibly high
degree of clinical judgment.
Hospitalization
• A patient who is acutely psychotic may need brief hospitalization for
both evaluation and protection. Evaluation requires close monitoring of
symptoms and assessment of the patient’s level of danger to self and others. In
addition, the quiet, structured setting of a hospital may help patients regain their
sense of reality. While clinicians wait for
• the setting or the drugs to have their effects, seclusion, physical restraints, or
one-to-one
• monitoring of the patient may be necessary.
Antipscyhotic drug
• antipsychotic drug is chosen, a high-
potency antipsychotic drug, such as • Alternatively, benzodiazepines can be
used in the short-term treatment of
haloperidol, or a psychosis. Although benzodiazepines
serotonin dopamine agonist such as have limited or no usefulness in the
ziprasidone may be used. In patients longterm
who are at high risk for • Anxiolytic medications, however, are
often useful during the first 2 to 3
the development of extrapyramidal weeks after the resolution the
adverse effects (e.g., young men), a psychotic episode.
serotonin dopamine • Clinicians should avoid long-term use of
antagonist drug should be any medication in the treatment of the
administered as prophylaxis against disorder.
medication-induced movement • If maintenance medication is necessary,
a clinician may have to reconsider the
disorder symptoms. diagnosis
Psychotherapy
• Psychotherapy is of use in providing an opportunity to discuss the
stressors and the psychotic episode.
• major topics in psychotherapy. Associated issues include helping
patients deal with the loss of self-esteem and to regain self-
confidence.
• An individualized treatment strategy based on increasing problem-
solving skills while strengthening the ego structure through
• psychotherapy appears to be the most efficacious.
• Family involvement in the treatment process may be crucial to a
successful outcome.
References
• Sadock BJ, Sadock VA, Ruiz P. In Pataki CS, Sussman N, editors. Kaplan
& Sadock’s synopsis of psychiatry: behavioral sciences/clinical
psychiatry. 11th ed. Philadelphia: Lippincott Williams & Wilkins; 2015.
• Cecil RL, Goldman L, Schafer AI. Goldman's Cecil medicine. 24th ed.
Philadelphia: Elsevier/Saunders; 2012.

Pemicu 2 KGD Sher

Hochgeladen von

Dokumentinformationen

Originaltitel

Copyright

Verfügbare Formate

Dieses Dokument teilen

Dokument teilen oder einbetten

Freigabeoptionen

Stufen Sie dieses Dokument als nützlich ein?

Sind diese Inhalte unangemessen?

Copyright:

Verfügbare Formate

Pemicu 2 KGD Sher

Hochgeladen von

Copyright:

Verfügbare Formate

General management of the poisoned patient

• cardiac arrhythmias • hyperthermia and hypothermia

Clinical Manifestation Treatment

Marx JA, Hockberger RS, Walls RM, et al,

• Acetaldehyde -> converted to carbon dioxide and water, primarily

• Alcohol is a central nervous system depressant.

• AWS is often divided into three sets of symptoms.

Brief psychotic disorder is an acute and

Das könnte Ihnen auch gefallen