KGD Albert 2

An Approach to Drug Abuse, Intoxication and
Withdrawal
http://www.aafp.org/afp/2000/0501/p2763.html
An Approach to Drug Abuse, Intoxication and
Withdrawal
http://www.aafp.org/afp/2000/0501/p2763.html
Acetaminophen
• Recommended dosing 650-1000mg (adults) ; 10-
15mg in children, every 4-6 hours
• Max daily dose (adults) 4g; (children) 75mg/kg
• Complete absorption within 4 hours
Diagnosis
ACUTE CHRONIC
A single ingestion, Repeated supratherapeutic ingestion
occur within 8 hours & intentiona; occur >8hours
• Determine the patient’s risk of acute

acetaminophen exposure • Determining wether the patient is at risk for
hepatotoxicity
1 • >150mg/kg must be acutely ingested 1
• Evaluating the patient by measuring a serum

• Establish a time of ingestion
acetaminophen concentration & AST
2 2
• Determine a serum acetaminophen

• Initiating theraphy with NAC
concentration 4 hours after ingestion
3 3
Acetaminophen
http://www.ijp-online.com/viewimage.asp?img=Indian%20J%20Pharmacol_2010_42_6_412_71894_u2.jpg
Treatment
• N-acetylcysteine
- Serves as a gluthathione (binding and detoxifying NAPQI and avoiding
subsequent hepatotoxicity
- Evident of hepatotoxicity  NAC acts as a free radical scavenger & an
antioxidant and alters hepatic microcirculation and oxygen delivery
- In patients with acetaminophen-induced hepatic failure, IV
administration of NAC decreases the rates of cerebral edema,
hypotension, and death even when no acetaminophen remains
Opioid intoxication
• Opioid intoxication includes maladaptive behavioral
changes and specific physical symptoms of opioid
use
• Opioids refers broadly to all compounds related to
opium that possess analgesic and sedative
properties
• Opiate describes the opioid alkaloids found
naturally in the opium poppy plant, Papaver
somniferum
• Opioids most frequently involved in reported toxic
drug exposures were, in order of number of cases
recorded, tramadol, oxycodone, methadone,
morphine, buprenorphine, and hydrocodone
• Deaths were primarily associated with exposure to
methadone, oxycodone, and morphine
Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

Opioid intoxication
• PHARMACOLOGY
• Opioids modulate nociception in the terminals of afferent nerves in the CNS,
peripheral nervous system, and GI tract
• Opioids are agonists at the three primary opioid receptors: μ (mu), κ (kappa), and δ
(delta)
• Stimulation of the μ-receptors results in  analgesia, sedation, miosis, respiratory
depression, cough suppression, euphoria, and decreased GI motility
• Stimulation of κ-receptors results in  weaker analgesia, sedation, miosis, decreased
intestinal motility, dysphoria, and hallucinations
• Stimulation of the δ-receptors results in  some analgesia and antidepressant effect

Opioid intoxication
CLINICAL FEATURES
 The full opioid intoxication toxidrome includes
 Respiratory  slow and shallow respirations that can produce
hypercarbia, hypoxia, and cyanosis
 Mental status depression
 Analgesia
 Miosis
 Orthostatic hypotension
 Nausea and vomiting
 Histamine release resulting in localized urticaria and
bronchospasm
 Other possible findings include pulmonary edema, hypothermia,
rhabdomyolysis, compartment syndrome, myogloinuric renal
failure, and seizures associated with overdoses of tramadol,
propoxyphene, and meperidine

Opioid intoxication
DIAGNOSE
• The combination of coma, miosis, and respiratory depression strongly suggests opioid
intoxication, and in many clinical scenarios, evidence of opioid use is present
• A urine opioid screen can be positive up to 2 to 3 days after a single use of codeine,
morphine, or heroin. The methadone-specific screen can be positive up to 3 days after
ingestion
• The combination of a respiratory rate of <12 breaths/min, miosis, and circumstantial
evidence of opioid use (drug paraphernalia, needle marks, presence of a tourniquet,
bystander corroboration) was highly sensitive for opioid overdose
DIFFERENTIAL DIAGNOSIS
• The differential diagnosis of opioid intoxication includes toxicologic clonidine,
organophosphates and carbamates, phenothiazines and atypical antipsychotic
medications, sedativehypnotic medications, and carbon monoxide

Opioid intoxication
American Psychiatric Association. Diagnostic and statistical manual of mental disorders : DSM-5. 5th ed.
Opioid intoxication
TREATMENT
• Airway protection and ventilatory
maintenance are the most
important treatment steps for
opioid intoxications, because
respiratory depression is the
major morbidity and the cause of
essentially all the mortality

Basic Life
Support
Suspected
Opioid Overdose
Algorithm
https://www.aclsmedicaltraining.com/bls-suspected-opioid-overdose-algorithm/
Opioid WITHDRAWAL
Opioid WITHDRAWAL
• Opioid withdrawal usually starts with feelings of
anxiety, yawning, lacrimation (TABLE 186-3)
• Onset of withdrawal is usually within 6 to 12
hours of last heroin use and within 30 hours of
last methadone exposure
• Symptoms of opioid withdrawal can be rendered
more tolerable by the administration of the
central α2-agonist clonidine, antiemetics, and
antidiarrheal agents
• Daily administration of a verified dose of
methadone PO (or half the verified dose IM if
the patient cannot take oral medications) is
recommended to inhibit withdrawal symptoms
and reduce craving
• Buprenorphine, 0.3 to 1.2 milligrams IV or IM
every 6 hours, can safely be administered to a
medically ill opioid-dependent patient
experiencing withdrawal who will be admitted to
the hospital

ORGANOPHOSPHATE POISONING

ORGANOPHOSPHATE POISONING

Toxicology
Iron
 Total-body iron store averages about 4 grams in adults; the range is between
2 and 6 grams, with less iron in women than in men.
 About two thirds of the body’s iron is incorporated into hemoglobin, and the
remainder is found in other iron-containing proteins such as myoglobin,
cytochromes, and other enzymes and cofactors, or is stored as ferritin.
 The recommended daily intake of iron is about 8 milligrams for boys, adult
men, and nonmenstruating women; 18 milligrams for menstruating women;
and 27 milligrams for pregnant females.
 Because excess iron is toxic, the body uses several mechanisms to maintain
iron homeostasis: serum protein binding, intracellular storage, and, most
importantly, regulation of GI tract absorption.
 The oral bioavailability of iron depends on the formulation ingested.

Inorganic iron has <10% bioavailability, with ferrous iron (Fe2+) better
absorbed than ferric iron (Fe3+).

Toxicology

Toxicology
Iron
 Chelated iron, such as that found in meat, is more readily absorbed than the
iron in ionic preparations.
 Iron is stored within the body in the form of ferritin, a large intracellular
storage protein that can reversibly bind as many as 4500 molecules of iron.
Ferritin can also be incorporated by phagolysosomes to form hemosiderin
granules.
 In adults, about 0.5 to 1 gram of elemental iron is stored as ferritin and

hemosiderin, primarily in the bone marrow, spleen, and liver.
 There is no physiologic mechanism for removal of iron once it has entered

the body.
 Regulation of GI iron uptake and limitation of absorption by sloughing of

mucosal cell containing surplus iron are the principal mechanisms for
maintaining physiologic iron concentrations.

Toxicology
Iron
Pathophysiology
Iron is a potent catalyst for the production of oxidants such as free radicals.
Iron is a direct GI tract irritant and causes vomiting, diarrhea, abdominal pain,
mucosal ulceration, and bleeding soon after a significant ingestion. As the
mucosal surface is injured, the regulatory enterocyte barrier is compromised,
and free iron passes unimpeded into the blood, becoming systemically
available.
Freeiron disrupts critical cellular processes and induces acidosis and

widespread organ toxicity.
Itenters the mitochondria, where it inhibits oxidative phosphorylation by

disrupting the electron transport chain, which results in metabolic acidosis with
an elevated lactate.

Toxicology
Iron
Pathophysiology
 Production of toxic hydroxyl radicals, induction of membrane lipid peroxidation,

liberation of hydrogen ions from reduction of ferrous iron, and hypotension all
contribute to the metabolic acidosis seen with acute iron toxicity.
 Hepatotoxicity occurs as the portal blood supply delivers a large amount of iron to the
liver. In addition, coagulopathy unrelated to hepatotoxicity may occur through
inhibition of thrombin formation and the effect of thrombin on fibrinogen.
 Myocardial and vascular dysfunction result from vasodilation, negative ionotropic

effect, and direct myocardial iron deposition.

Toxicology

Toxicology
Iron
Clinical Features
 Five stages of clinical toxicity are traditionally described, although in more practical
terms, acute iron toxicity can be considered to manifest in two clinical stages: local GI
tract toxicity and systemic toxicity.
 Stage 1
 Is characterized by abdominal pain, vomiting, and diarrhea.
 Iron is directly irritating and corrosive to the GI tract and typically induces vomiting within the
first few hours following ingestion.
 Vomiting is the clinical sign most consistently associated with acute iron toxicity. Patients with
symptoms of gastric irritation may either recover over several hours or progress to systemic
toxicity.
 The absence of GI symptoms within 6 hours of ingestion essentially excludes a significant iron
ingestion.

Toxicology
Iron
 Stage 2 (Latent Stage)
 Does not always occur.
 If present, this stage is a 6- to 24-hour interval following ingestion during which GI
symptoms may resolve and falsely reassure the patient and physician.
 However, this is not a truly quiescent phase.
 Patients with significant toxicity have ongoing clinical illness and progressive
systemic deterioration because of volume loss and worsening metabolic acidosis,
despite the absence of GI symptoms.
 Alternatively, the resolution of GI findings may signal the end of mild poisoning, and
in such a circumstance, the results of the patient’s laboratory studies should be
normal.
 Stage 3
 Is characterized by systemic toxicity from iron-induced disruption of cellular
metabolism with resultant shock and lactic acidosis.
 Iron-induced coagulopathy may worsen bleeding and hypovolemia.
 The coagulopathy may be biphasic, with prolonged prothrombin time and partial
thromboplastin time within the first 24 hours.
Toxicology
Iron
 This initial coagulopathy appears to be reversible with chelation therapy, because it
is free iron that initially interferes with the activity of factors in the coagulation
cascade.
 Subsequent coagulopathy is from iron-induced hepatic injury that reduced
coagulation factor production.
 During stage 3, renal failure, cardiomyopathy, and failure of other critical organ
systems may also occur.
 Stage 4 (Hepatic Stage)

 Develops 2 to 5 days following ingestion.
 It results from iron uptake by the reticuloendothelial system with local lipid
peroxidation; it manifests as elevation of aminotransferase levels and may progress
to hepatic failure.
 Stage 5
 Refers to delayed sequelae, including gastric outlet obstruction secondary to the
corrosive effects of iron on the pyloric mucosa.
 Delayed sequelae are rare and occur 4 to 6 weeks after ingestion.
Toxicology
Iron
Diagnosis
 laboratory testing
 Laboratory tests should include CBC, determination of serum electrolyte levels, renal
and liver function studies, coagulation function tests, serum glucose, and serum iron
levels, with the understanding that these results are to assess the overall condition of
the patient, because iron toxicity is largely a clinical diagnosis.
 In general, serum iron levels measured within 4 to 6 hours after an acute ingestion
correlate with the severity of toxicity, but low serum iron levels do not necessarily
mean absence of toxicity.
 Serum iron levels may be low because of variable times to peak level following
ingestions of different iron preparations, and treatment with deferoxamine can
artificially lower serum iron levels.
 Serum total iron-binding capacity has little value in the assessment of iron-poisoned
patients.
 It becomes falsely elevated in the presence of elevated serum iron levels or
deferoxamine, and significant organ damage occurs despite exceeding the serum
iron level.

Toxicology
Iron
Diagnosis
 Imaging
 Standard ferrous sulfate tablets and reduced iron are radiopaque and frequently visible on
routine radiographs and this may help guide GI decontamination when present.
 However, many iron preparations are not routinely detected, including pediatric chewable and
liquid preparations, and absence of radiopaque material on radiographs does not exclude iron
ingestion.

Toxicology

Toxicology
Iron
Treatment
 Patients with clinical toxicity should first be stabilized with attention to airway,
breathing, and circulation, after which GI decontamination and chelation therapy with
deferoxamine may proceed.
 Antiemetics such as metoclopramide or ondansetron should be used for repetitive

vomiting.
 Patients with persistent vomiting and abnormal vital sign values or other signs of poor
perfusion or shock should undergo aggressive fluid resuscitation and treatment with
deferoxamine.
 Coagulopathy should be treated with parenteral vitamin K and/or fresh frozen plasma,
as indicated.
 Significant blood loss may require transfusion.

Toxicology
Mercury
 Elemental mercury is absorbed primarily by vapor inhalation.
 Vacuuming elemental mercury, as from a broken thermometer or fluorescent

light bulb, causes volatilization due to both the heat and the airflow through
the canister.
 Absorption by the GI tract is usually negligible so that swallowing mercury

contained in a glass thermometer (elemental mercury) does not produce
adverse effects unless the mucosa is damaged.
 Elemental mercury can be absorbed dermally.
 IM injections of mercury can induce abscess and granuloma formation.
 Slow absorption and delayed systemic toxicity after IM injections of

elemental mercury have been reported.
 IV injections have produced mercury pulmonary and systemic emboli.

Toxicology
Mercury
 Elemental mercury crosses the blood–brain barrier, where it is ionized and
trapped in the CNS.
 Inorganic mercury salts are absorbed primarily through the GI tract, but
they may also be absorbed across intact skin. Mercuric salts deposit in the
ionized form primarily in the kidney, followed by the liver and spleen.
Mercury salts do not enter the CNS in consequential amounts nor do they
cross the placenta.
 Organic mercury compounds are also primarily absorbed by the GI tract.

The highly lipid-soluble short-chained alkyls easily cross membranes,
accumulating in red blood cells, the CNS, liver, kidney, and fetus. Longer-
chained alkyl and the aryl compounds are biotransformed into inorganic
mercuric ions in the body. Therefore, toxicity with these compounds more
closely resembles inorganic mercury toxicity.
 Inorganic and the aryl organic mercurials are eliminated in the urine and
feces. The short-chained alkyl compounds are excreted primarily in the bile,
where they undergo significant enterohepatic circulation.

Toxicology
Mercury
Pathophysiology
 Mercury binds with sulfhydryl groups, affecting a diverse number of enzyme and
protein systems.
 Methyl mercury also inhibits choline acetyl transferase, which catalyzes the final step
in the production of acetylcholine and may produce symptoms of acetylcholine
deficiency.
 Mercuric salts produce proximal renal tubular necrosis

Toxicology
Mercury
Clinical Features
 The clinical effects of mercury poisoning depend on the form and, in some cases, the
route of administration. In general, the neurologic, GI, and renal systems are
predominantly affected.
 Elemental Mercury
 Acute symptoms following inhalation of elemental mercury vapor include shortness of breath,
fever/chills, cough, nausea, vomiting, diarrhea, metallic taste, headaches, weakness, and blurry
vision.
 In severe cases, patients may develop acute lung injury and severe respiratory distress.
 Following metabolism of ingested or injected elemental mercury to inorganic salts, patients
may also develop signs of inorganic mercury toxicity, including tremor and renal failure.

Toxicology
Mercury
Clinical Features
 Inorganic Mercury
 Mercury salts are caustic, and an acute ingestion produces a severe hemorrhagic gastroenteritis
with abdominal pain often associated with a characteristic graying of the oral mucosa and
metallic taste.
 Shock and cardiovascular collapse may rapidly ensue.
 Acute kidney injury results from both direct toxicity of the mercury ions and from decreased
renal perfusion due to shock.
 GI symptoms of chronic inorganic mercury toxicity include metallic taste, burning sensation in
the mouth, loose teeth, mucosal lesions and fissures, excessive salivation, and nausea.
 Hallmarks of chronic neurologic toxicity include tremor, neurasthenia, and erethism.
 Neurasthenia is characterized by fatigue, depression, headaches, and difficulty concentrating.
Erethism refers to behavioral changes characterized by shyness, emotional lability, irritability,
insomnia, and delirium.
 Chronic renal toxicity ranges from reversible proteinuria to the nephrotic syndrome.

Toxicology
Mercury
Clinical Features
 Acrodynia, also known as pink disease, is an immune-mediated reaction
characterized by a generalized rash; edema and erythema of the palms, soles, and
face; excessive sweating; fever; irritability; splenomegaly; and generalized hypotonia
with particular weakness of the pelvic and pectoral muscles.
Organic Mercury
 The short-chained alkyl compounds, methyl, dimethyl, and ethyl mercury, have the
most devastating effects on the CNS.
 After a latent period of weeks to months, orofacial paresthesias are a common initial
symptom, followed by headache, tremor, and fatigue. In severe cases, patients may
develop ataxia, muscle rigidity and spasticity, blindness, hearing deficits, and
dementia.
 Although less prominent than the neurotoxicity, mild GI, renal, and pulmonary
abnormalities may develop with organic mercury poisoning.

Toxicology
Mercury
Diagnosis
 An occupational exposure history, in either the index patient or a house- hold

member, along with typical physical findings, especially tremor or a constellation of
signs and symptoms suggesting erethism or acrodynia, suggests mercury toxicity.
 Ingestion of mercuric chloride can produce a rapidly fatal course and should be
considered in a patient presenting with a corrosive gastroenteritis.
 Often, however, the diagnosis of mercury toxicity is subtle, arrived at only after many
other diagnoses have been investigated.
 For poisoning from all forms of mercury, except short-chained alkyls, a 24-hour urinary
measurement of mercury should be performed after a 5-day seafood-free diet.
 A seafood meal (contaminated with mercury) can temporarily elevate the mercury
level to the toxic range until the mercury is eliminated. Most unexposed individuals
will have 24-hour urine mercury levels <10 to 15 micrograms/L (<0.05 to 0.075
micromol/L).

Toxicology
Mercury
Diagnosis
 A level >20 micrograms/L (>0.1 micromol/L) may indicate meaningful exposure.
 Short-chained alkyl mercury compounds are excreted predominantly by the bile,

rendering urinary measurements invalid to assess toxicity from these agents.
 Laboratory diagnosis after this exposure rests on finding elevated whole-blood

mercury levels, because these compounds concentrate in erythrocytes.
 Whole-blood mercury levels are normally <5 micrograms/L (<0.025 micromol/L).
 Although elevated blood or urine values are necessary to confirm the diagnosis, they
correlate poorly with toxicity and are unable to distinguish the asymptomatic exposure
from mercury poisoning.

Toxicology
Mercury
Diagnosis
MRI findings in methyl mercury toxicity from ingestion of contaminated

seafood include marked atrophy of the visual cortex, cerebellar vermis and
hemispheres, and postcentral cortex.
Behavioral changes or tremor similar to those caused by mercury can be seen

with hypothyroidism, apathetic hyperthyroidism, metabolic encephalopathy,
senile dementia, adverse effects of therapeutic drugs (such as lithium,
theophylline, or phenytoin), Parkinson’s disease, delayed neuropsychiatric
sequelae of carbon monoxide poisoning, lacunar infarction, cerebellar
degenerative disease or tumor, and ethanol or sedative-hypnotic drug
withdrawal.
Corrosive gastroenteritis can be caused by iron, arsenic, phosphorus, acids,

or alkali ingestion.
Cerebral palsy, intrauterine hypoxia, and teratogenic effects of therapeutic

and illicit drugs and environmental contaminants should be considered when
evaluating an infant thought to be affected in utero by short-chained alkyl
mercury compounds. Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8 th edition. 2016
Toxicology
Mercury
Treatment
General therapeutic measures include removal from exposure and sup-

portive therapy, including supplemental oxygen and IV hydration.
Hemodialysis does not enhance mercury clearance but may be indicated for
treatment of acute kidney injury.
For elemental mercury, the severe respiratory failure following inhalation of

volatilized elemental mercury or aspiration of elemental mercury may require
endotracheal intubation and positive-pressure ventilation.
For ingestion of inorganic mercury salts, treat with aggressive IV hydration

and GI decontamination, including gastric lavage if the patient has not had
significant emesis, and consider activated charcoal. Given the profuse diarrhea
that may ensue, a cathartic is not indicated.
For organic mercury toxicity, institute gastric decontamination in the setting of

acute ingestion. Neostigmine may improve motor function in methyl mercury–
poisoned patients by improving acetylcholine levels at the neuromuscular
junction. Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8 th edition. 2016
Toxicology
Mercury

Carbon Monoxide
information
Carbon Produced by the incomplete combustion of materials - carbon-
Monoxide containing materials from machinery and motor vehicles
Poisoned •through inhalation

•Limit exposure to <1000 ppm
Symptom •Dyspnea
•Headache, weakness, blurred vision, nausea, vomiting, red
mucous membranes, respiratory rate, and pulse increase,
convulsions, coma subsequent shock, respiratory depression,
arrhythmias, and death
•> 1000 ppm: unconsciousness, respiratory failure, and death if
inhaled> 1 hour
Complicatio Cerebral and pulmonary edema, myocardial infarction / stroke,
n mental disorders, and personality deterioration
prevention •Levels of carbon monoxide inside, the air around us must be
below exposure limits
Carbon Monoxide
information
Emergency •Avoid contact later, the patient had to be removed
action •Oxygen 100%
Antidote oxygen
Common •Keep the body temperature normal
Actions •Notice TD patients
•Reduce cerebral edema :1g/kg mannitol as a solution
of 20%
•Overcoming edema : sererbral prednisolone 1 mg.kg
IV or IM every 4 hours
•nflammation of the lungs caused by bacterial
infection specific chemotherapy drugs
•Reduce neurological complications : 2-4 week break
•Overcome convulsions :diazepam 0.1 mg / kg IV
slowly
Delirium
• Kriteria delirium yang disebabkan intoksikasi zat (DSM-IV)
A. Gangguan kesadaran
B. Hambatan dalam fungsi kognitif
C. Awitan tiba”, perjalanan penyakit singkat & berfluktuasi sepanjang hari
D. Menemukan 1/2
1. Gejala pada kriteria A dan B berkembang selama iintoksikasi
2. Pengganaan intoksikasi disini untuuk mengatasi penyebab yang ada hubngan dengan
ganggannya.
• Kriteria delirium yang disebabkan pts zat (DSM-IV)
D. Menemukan kriteria A dan B. keadaan ini berkembang selama/dalam waktu
singkat sesudah sindroma putus obat
• Terapi
• Bila penyebabnnya toksisitas
antikolenergik→physostigmin salisilat 1-2mg IV/IM
boleh ulang 15-30 menit jika perlu
• Haloperidol 2-10mg IM boleh diulang 1 jam jika
pasien masih menunjukkan agitasi
• Lorazepam 1-2mg sebelum tidur
• Prognosis
• Bila penyebabnya telah diketahuui dan dapat
dihalangkan maka gejala akan menghilang dalam
wakt 3-7 hari dan hilang seluruhnya dalam waktuu 2
minggu
PSYCHOTIC BREAK
• Psychotic brief
• Gangguan berlangsung singkat (DSM kurang dari 1 bulan, tp sekurangnya 1
hari)
• Gangguan mungkin berkembang sbg terhadap respon stresor psikososial yg
parah atau kelompok stresor
• Faktor resiko :
• Peristiwa kehidupan yg besar yang dapat menyebabkan kemarahan
emosional, cth: kematian anggota keluarga, kecelakaan kendaraan
• Efek akut penyalahgunaan obat cth: LSD, opiates
Gejala karakteristik
• Onset tiba-tiba
• Perubahan emosional
• Pakaian atau perilaku aneh berteriak-teriak atau diam membisu
• Gangguan daya ingat utk peristiwa yg belum lama terjadi
• Prognosis baik, 50%-80% pasien tidak memiliki masalah psikiatrik
berat lanjut
Criteria diagnostic
A. Presence of one (or more) of the following symptoms.
At least one of these must be (1), (2), or (3):
1. Delusions.
2. Hallucinations.
3. Disorganized speech (e.g., frequent derailment or
incoherence).
4. Grossly disorganized or catatonic behavior
Note: Do not include a symptom if it is a culturally sanctioned
response.
B. Duration of an episode of the disturbance is at least 1
day but less than 1 month, with eventual full return to
premorbid level of functioning.
C. The disturbance is not better explained by major
depressive or bipolar disorder with psychotic features
or another psychotic disorder such as schizophrenia or
catatonia, and is not attributable to the physiological
effects of a substance (e.g., a drug of abuse, a
medication) or another medical condition
Terapi
• Perawatan di RS: mungkin diperlukan untuk pemeriksaan dan
perlindungan pasien
• Farmakoterapi: obat antipsikotik antagonis reseptor dopamin dan
benzodiazepin
• Psikoterapi: individual, keluarga, kelompok mungkin diindikasikan
DIAGNOSTIC MARKERS
• Kokain :
• Metabolit kokain (benzoylecgonine) terdeteksi di urine
selama 1-3 hari setelah pemakaian dosis tunggal; 7-12 hari
pada pemakaian berulang
• MDMA, metamfetamin, amfetamin :

• Dapat terdeteksi di urine selama 1-3 hari, dan mungkin
bisa lebih dari 4 hari (tergangung dosis dan metabolisme)
• Hair sample : > 90 hari
Tatalaksana Amphetamine Toxicity
ALCOHOL INTOXICATION
ALCOHOL WITHDRAWAL
• TIMELINE ALCOHOL WITHDRAWAL SIGNS AND SYMPTOMS
• Alcohol withdrawal syndrome can occur as early as 6 hours after alcohol cessation,
usually peaks after 2-3 days, and can persist up to 7days after alcohol cessation
The Ohio State University Wexner Medical Center. Alcohol withdrawal.

ALCOHOL WITHDRAWAL

ALCOHOL WITHDRAWAL

ALCOHOL WITHDRAWAL

ALCOHOL WITHDRAWAL

ALCOHOL WITHDRAWAL

KGD Albert 2

Transféré par

Informations du document

Titre original

Copyright

Formats disponibles

Partager ce document

Partager ou intégrer le document

Options de partage

Avez-vous trouvé ce document utile ?

Ce contenu est-il inapproprié ?

Droits d'auteur :

Formats disponibles

KGD Albert 2

Transféré par

Droits d'auteur :

Formats disponibles

An Approach to Drug Abuse, Intoxication and

• Determine the patient’s risk of acute

• Evaluating the patient by measuring a serum

• Determine a serum acetaminophen

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

 The oral bioavailability of iron depends on the formulation ingested.

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

 In adults, about 0.5 to 1 gram of elemental iron is stored as ferritin and

 There is no physiologic mechanism for removal of iron once it has entered

 Regulation of GI iron uptake and limitation of absorption by sloughing of

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

Freeiron disrupts critical cellular processes and induces acidosis and

Itenters the mitochondria, where it inhibits oxidative phosphorylation by

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

 Production of toxic hydroxyl radicals, induction of membrane lipid peroxidation,

 Myocardial and vascular dysfunction result from vasodilation, negative ionotropic

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

 Stage 4 (Hepatic Stage)

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

 Antiemetics such as metoclopramide or ondansetron should be used for repetitive

 Significant blood loss may require transfusion.

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

 Vacuuming elemental mercury, as from a broken thermometer or fluorescent

 Absorption by the GI tract is usually negligible so that swallowing mercury

 Elemental mercury can be absorbed dermally.

 IM injections of mercury can induce abscess and granuloma formation.

 Slow absorption and delayed systemic toxicity after IM injections of

 IV injections have produced mercury pulmonary and systemic emboli.

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

 Organic mercury compounds are also primarily absorbed by the GI tract.

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

 Mercuric salts produce proximal renal tubular necrosis

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

 An occupational exposure history, in either the index patient or a house- hold

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

 A level >20 micrograms/L (>0.1 micromol/L) may indicate meaningful exposure.

 Short-chained alkyl mercury compounds are excreted predominantly by the bile,

 Laboratory diagnosis after this exposure rests on finding elevated whole-blood

 Whole-blood mercury levels are normally <5 micrograms/L (<0.025 micromol/L).

Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th edition. 2016

MRI findings in methyl mercury toxicity from ingestion of contaminated

Behavioral changes or tremor similar to those caused by mercury can be seen

Corrosive gastroenteritis can be caused by iron, arsenic, phosphorus, acids,

Cerebral palsy, intrauterine hypoxia, and teratogenic effects of therapeutic

General therapeutic measures include removal from exposure and sup-

For elemental mercury, the severe respiratory failure following inhalation of

For ingestion of inorganic mercury salts, treat with aggressive IV hydration

For organic mercury toxicity, institute gastric decontamination in the setting of