Marshaly Safira Masrie

405150104
Pemicu 2 KGD
LI 1. MM INTOKSIKASI &
WITHDRAWAL
 Definisi
• Intoksikasi akut:
• Ada bukti baru menggunakan zat
psikoaktif dalam dosis tinggi
• Ada keluhan & gejala intoksikasi
sesuai dengan zat psikoaktif yang
dikonsumsi
• Gangguan pada kesadaran, fungsi
berpikir, persepsi, afek, perilaku
yang bermakna klinis
• Keluhan & gejala tidak
disebabkan karena gangguan
medis, mental, dan perilaku
lainnya
• Putus obat/ withdrawal:
• Ada bukti baru menghentikan
penggunaan zat atau mengurangi
dosis zat setelah penggunaan
berulang dengan dosis tinggi
dalam jangka waktu panjang
• Keluhan & gejala sesuai dengan
gejala putus zat dari zat yang
dikonsumsi
• Keluhan & gejala tidak
disebabkan karena gangguan
medis, mental, dan perilaku
lainnya
LI 2. MM DELIRIUM
 Definition

• The essential features of delirium include disturbances of consciousness,

attention, cognition, and perception. The disturbance develops over a
short period of time (usually hours to days) and tends to fluctuate during
the course of the day.
 Etiology

• The disorders included in the DSM-IV delirium section have a common

symptom presentation of a disturbance in consciousness and cognition
but are differentiated by etiology
 FAKTOR RISIKO DELIRIUM

• Usia lanjut (> 65 tahun)

• Latar belakang disfungsi kognitif
• Demensia
• Deprivasi sensoris : riwayat gangguan pendengaran dan visual
• Riwayat imobilitas, malnutrisi, penyakit medis, atau neurologis
• Di RS : kateterisasi VU, keterbatasan fisik, deprivasi tidur dan sensoris,
penambahan 3 / > obat-obat baru
• Risiko bedah dan anestesi : bypass cardiopulmonary, tatalaksana nyeri
inadekuat / >>, anestesi inhalasi

Kasper DL, Fauci AS, Hauser SL, Longo DL, Jameson JL, Loscalzo J, editors. Harrison’s
principles of internal medicine. 19th ed. New York: McGraw-Hill Education; 2015.
Clinical Manifestation
 DIAGNOSIS DELIRIUM

• Onset akut, fluktuatif (beberapa jam / hari, dapat memburuk

pada malam hari)
• Inatensi, disertai :
– Pola pikir terdisorganisasi, atau
– Perubahan tingkat kesadaran

Kasper DL, Fauci AS, Hauser SL, Longo DL, Jameson JL, Loscalzo J, editors. Harrison’s
principles of internal medicine. 19th ed. New York: McGraw-Hill Education; 2015.
 PEMERIKSAAN FISIK DELIRIUM

• Tanda-tanda infeksi : demam, takikardia, konsolidasi paru, murmur

jantung, kaku leher
• Dehidrasi, kelebihan cairan dengan hipoksemia
• Kulit : kuning (ensefalopati hepatik), sianosis (hipoksemia), needle track
(obat IV)
• Perubahan tingkat kesadaran : hyperarousal s/d letargi, koma
• Defisit atensi : pembicaraan tangensial, fragmentary flow of ideas, tidak
mampu menuruti perintah kompleks

Kasper DL, Fauci AS, Hauser SL, Longo DL, Jameson JL, Loscalzo J, editors. Harrison’s
principles of internal medicine. 19th ed. New York: McGraw-Hill Education; 2015.
 PEMERIKSAAN PENUNJANG DELIRIUM

• Laboratorium : DPL, elektrolit, fungsi hepar dan ginjal

• Pasien usia lanjut → skrining infeksi sistemik (radiografi dada, urinalisis
dan kultur urin, kultur darah)
• Pemeriksaan pendahuluan tidak bermakna → neuroimaging

Kasper DL, Fauci AS, Hauser SL, Longo DL, Jameson JL, Loscalzo J, editors. Harrison’s
principles of internal medicine. 19th ed. New York: McGraw-Hill Education; 2015.
Treatment
PRACTICE GUIDELINE FOR THE Treatment of Patients With Delirium. WORK

GROUP ON DELIRIUM. 2010, American Psychiatric Association.

LI 3. MM ACUTE PSYCOTIVE DRUG
INTOXICATION
Psychoactive Drugs (Biopsychiatric model)
 Psychoactive Drugs

• The eight groups of abused drugs are:

1. anticholinergics,
2. Cannabinoids,
3. Dissociatives,
4. opiates,
5. psychedelics (hallucinogens),
6. sedative-hypnotics,
7. Stimulants,
8. volatiles (inhalants).

1. Only six of these groups are important to family physicians involved in the
treatment of intoxication, overdose and withdrawal states. The exceptions are
cannabinoids and volatiles.
Anticholinergic
Anticholinergic Intoxication Clinical Presentation
Anticholinergic Intoxication Treatment
 Dissociative Drugs Mechanism of Action

• Dissociatives act on all six neurotransmitter systems and produce a

characteristic clinical presentation
Dissociative Drugs Clinical Presentation
Dissociative Drugs Intoxication Treatment
Dissociative Drugs Intoxication Treatment
Psychedelic Drugs (Hallucinogen)
Psychedelic Drugs Clinical Presentation
Psychedelic Drugs Intoxication Treatment
Psychedelic Drugs Intoxication Treatment
Stimulant Drugs
Stimulant Drugs Clinical Presentation
Stimulant Drugs Intoxication Treatment
Stimulant Drugs Withdrawal Treatment
Opiates
 Pharmacology

• Opioids modulate nociception in the terminals of afferent nerves in the

CNS, peripheral nervous system, and GI tract.
• Opioid receptors are transmembrane proteins that undergo
conformational change when activated by external molecules, and this
change then alters some aspect of intracellular function.
• All currently available opioid agonists possess μ-receptor activity &
result in some degree of respiratory depression.
• There is interplay between opioid receptors and other transmembrane
receptors found in the nervous system.
 Opioid Clinical Presentation

• Respiratory and mental status depression

• Analgesia
• Miosis
• Orthostatic hypotension
• Nausea and vomiting (especially in opioid-naïve patients)
• Histamine release resulting in localized urticaria and bronchospasm
• Ileus secondary to decreased GI motility
• Urinary retention secondary to increased vesical sphincter tone.
Opioid Withdrawal
Opioid Drugs Intoxication Treatment
Opioid Withdrawal Treatment
Sedative-Hypnotic Drugs
Sedative-Hypnotic Drugs (Pharmacology)
 Benzodiazepin (Introduction)

• Benzodiazepines, to varying degrees, have in common six major

pharmacologic effects: sedative, hypnotic, anxiolytic, amnestic,
anticonvulsant, and muscle relaxant.
• Benzodiazepines are commonly used for the short-term treatment of
anxiety, insomnia, seizures, and alcohol and sedative-hypnotic withdrawal.
Benzodiazepin Intoxication Clinical Manifestation
 Treatment of Benzodiazepine Intoxication

• Do not induce emesis in

benzodiazepine overdose because
mental status depression may
develop and increase the risk for
pulmonary aspiration.
• Monitor neurologic and respiratory
status and provide mechanical
ventilation if necessary.
• Benzodiazepine antagonist:
FLUMAZENIL.
• The dose of flumazenil is 0.2
milligram IV, which can be repeated
every minute, titrated according to
response or to a total dose of 3
milligrams.
Narcotic Intoxication
Narcotic Intoxication
Narcotic Intoxication
Narcotic Intoxication
Antidote and Indication For Use
Antidote and Indication For Use
LI 4. MM INTOKSIKASI KIMIA DAN
OBAT
INTOKSIKASI ALKOHOL
 Introduction
• Semua jenis alkohol menyebabkan mabuk
• Methanol dan ethylene glycolmerupakan alkohol yang toksik, yang
dapat menyebabkan morbiditas yang serius
• Jenis alkohol: ethanol, isopropanol, Methanol dan ethylene glycol
 Ethanol

• Tidak berwarna, volatile liquid, paling sering digunakan

• Toksik yang terjadi umumnya melalui konsumsi, tetapi bisa juga secara
inhalasi, atau paparan percutaneous
• Standard minuman beralkohol:
• Pathophysiology:
– Cepat diabsorbsi setelah dikonsumsi
– CNS depresanmenghambat neurotransmiter
– Dieliminasi di hepar

• Sign and Symptom:

– The hallmark of ethanol toxicity is clinical inebriation(drunkness)
– Euphoria/agitasi, intoksikasi semakin berat  slurred speech, nistagmus,
ataxia, koordinasi motorik menurun, Severe intoksikasi  depresi napas
dan koma
– Menyebabkan vasodilatasi perifer, flushed, warm skin.
– Pada anak-anak dan dewasa dengan malnutrisi, konsumsi ethanol dapat
menyebabkan hipoglikemi
• Terapi:
– Observasi hingga sadar asimptomatik
– Bila hipoglikemiaGlukosa IV 0,5-1 g/kg
– Pada long-term drinker kadang diperlukan multivitamin IV fluid
• Metadoxine
– 900 mg IV
– Mempercepat metabolisme ethanol, dan mempercepat recovery
– Indonesia belum ada
 Isopropanol

• Volatile liquid, bitter, burning taste and aromatic odor

• Ditemukan pada produk rumah tanggacontoh alkohol 70% (sebagai
disinfektan), detergent, produk rambut, dll
• 2x lebih potent dibanding ethanol pada depresi CNS
• Pathofisologi:
– Cepat diabsorbsi di GI Tract
– Metabolisme: liverdi metabolisme menjadi keton
– Ketosis dan osmolar gap tanpa asidosisciri khas isopropanol toxicity
– Lethal dose pada dewasa: 2-4 ml/kg
• Sign and symptom:
– Symptom utama: depresi CNS
– Gastric irritationmual, muntah, nyeri abdomen, pankreatitis akut
hingga hemorrhagic gastritis
– Onset terjadinya gejala : 30-60 menit setelah konsumsi
– Hipoglikemi
– Severe: koma, depresi napas dan hipotensi
– Pada anak-anak, penggunaan di kulit, dapat menyebabkan luka bakar.
• Diagnosis:
– Fruity odor of acetone/ smell of rubbing alcohol pada napas
– Osmolar gap, ketonuria, ketonemia tanpa asidosis
– Kadar intoksikasi isopropanol, biasanya 50 mg/dL
• Terapi:
• Suportif
• Monitoring: depresi napas (intubasi dan ventilasi bila perlu), hipotensi
(biasanya cukup diberikan IV fluid)
• Hemodialisis kalau kadar isopropanol >400 mg/dLJarang digunakan
 Methanol dan Ethylene Glycol

• Metabolisme dari kedua zat inimenghasilkan metabolit toksik yang

dapat menyebabkan asidosis metabolik dan kerusakan end- organ.
• Pathophysiology
• Methanol
– Dosis yang dapat menyebabkan gangguan visual permanen pada
dewasa: 24 gr / 30 mL
– Formic acid is the metabolite responsible for the toxicity and metabolic
acidosis that occurs with methanol poisoning
• Ethylene glycol
– End organ damage oleh ethylene glycol, dikarenakan sitotoksik oleh
glycolic acid
• Diagnosa:
– Lab: kadar ethanol darah, AGD, anion dan osmolar gap, serum
osmolarity, kadar kreatinin kinase, keton
• Terapi:
– Prinsip dasar terapi: initial resusitasi, cardiopulmonary support, koreksi
asidosis, mencegah pembentukan metabolit toksik, meningkatkan
clearance
Tatalaksana Intoksikasi Methanol dan Ethylene
Glycol
 Referensi
• Tintinalli Judith E, et al. Tintinalli’s Emergency medicine. 8th
ed. 2011
• A. James Giannini, M.D., Chemical Abuse Centers, Inc.,
Austintown, Canton and Columbus, Ohio Am Fam Physician.
2000. May;61(9):2763- 2774.
INTOKSIKASI KIMIA
 Kerosene (paraffin)

Tintinalli JE, Stapczynski JS, Ma OJ, Yealy DM, Meckler GD, Cline DM. Tintinalli’s

emergency medicine 8th edition. 2016. New

 Hydrocarbons

Tintinalli JE, Stapczynski JS, Ma OJ, Yealy DM, Meckler GD, Cline DM. Tintinalli’s

emergency medicine 8th edition. 2016. New

 Diagnosis

• Diagnosis of hydrocarbon toxicity incorporates the findings of the

history, physical examination, bedside cardiac and pulmonary
monitoring, laboratory tests, and chest radiography.
• Determine the specific hydrocarbon-containing product
• Pulse oximetry, arterial BGA, ECG, chest radiograph
• Hepatic function, ammonia serum, prothrombine time (ingest/inhale
halogenated hydrocarbons)
• Catecholamines may cause dysrhythmias, especially after exposure to halogenated
hydrocarbons and aromatic hydrocarbonsAVOID
• There is no benefit to gastric lavage because risks of aspiration far outweigh any
theoretical benefits.
 Disposition and follow-up

• In cases of inhalation or aspiration of nonhalogenated aliphatic

hydrocarbons, asymptomatic patients may be discharged home after
about 6 to 8 hours of observation with instructions to return if delayed
symptoms develop.
• Hospitalization is also recommended for those who ingest hydrocarbons
capable of producing delayed complications (e.g., halogenated
hydrocarbons causing hepatic toxicity) or hydrocarbons with toxic
additives (organophosphates and organic metal compounds).
 Organophosphate

• Pesticides include insecticides, herbicides, and rodenticides

• Six major classes of insecticides are in common use
• Commonly used organophosphates include diazinon, acephate,
malathion, parathion, and chlorpyrifos
• Systemic absorption of organophosphates occurs by inhalation and after
mucous membrane, transdermal, transconjunctival, and GI exposure.
Manifestasi
• Diagnosis and treatment are based on history and the presence of a suggestive
toxidrome; laboratory cholinesterase assays and reference laboratory testing for
specific compounds take time and have limitations, and waiting for results delays
administration of potentially life-saving therapy.
• Miosis and muscle fasciculations are considered reliable signs of organophosphate
toxicity.
• Therapy should not be withheld
pending determination of cholinesterase
levels.
• Atropin (Pupillary dilatation is not a
therapeutic end point)
• The end point of therapy is determined
by the absence of signs and symptoms
on withholding pralidoxime therapy.
• Following an acute exposure, the patient
may have neurologicsequelae, such a
paresthesias or limb weakness, along
with nonspecificsymptoms lasting days
to months.
HEAVY METAL POISONING
Heavy Metal Poisoning
 Arsenic

In fact, before penicillin was discovered arsenic was one of the primary treatments for
syphilis
 Arsenic Poisoning Clinical Manifestation
• Acute
• The clinical features initially are GI,
including nausea, vomiting, abdominal
pain, and bloody rice water diarrhea •
Hypovolemic shock may follow in severe
cases as a result of endothelial damage
and third spacing of fluid
• Hematologic abnormalities, including
bone marrow depression, pancytopenia,
anemia, and basophilic stippling, usually
appear within 4 days of large ingestions
• Neurologic manifestations include a distal
symmetric peripheral neuropathy
commonly presenting with burning and
numbness in the hands and feet
• Chronic
• Dermatologic changes include
hyperpigmentation and keratosis on the
palms and soles, The nails may exhibit
transverse white bands known as Mees
lines
• Cardiovascular effects include an
increased incidence of hypertension and
peripheral vascular disease. Sporadic
outbreaks of peripheral vascular gangrene
known as black foot disease have occurred
in Taiwan and have been linked to high
levels of arsenic in the drinking water
• Chronic arsenic exposure has been
associated with various malignancies
including skin, lung, liver, bladder, and
kidney
Arsenic poisoning and Mees lines

• Mees lines are the result of

interruption of the nail matrix,
can be seen in acute and chronic
poisoning, and are not specific to
arsenic.
• They may not be evident until
weeks after the exposure and
may not be present in all
patients
Diagnosis of Arsenic Poisoning
 Management of Arsenic Poisoning

• Treatment of arsenic poisoning begins with the removal from the exposure
source
• Supportive measures and chelation therapy are the mainstays of
management. Volume resuscitation is of paramount importance in the
severely poisoned patient
• Chelation with dimercaprol or succimer (2,3- dimercaptosuccinic acid,
DMSA) should be considered in patients who have symptoms or increased
body burden of arsenic. Hemodialysis maybe considered for patients who
have renal failure
Mercury
 Mercyry Poisoning Clinical Manifestation
• Acute
• Acute toxicity may manifest
within hours of a large exposure
with GI upset, chills, weakness,
cough, and dyspnea, with severe
cases developing adult
respiratory distress syndrome
and renal failure
• Chronic
• Chronic mercury toxicity may
develop over a period of weeks to
months, depending on the level of
exposure.
• Initial symptoms commonly include
GI upset, constipation, abdominal
pain, and poor appetite, and may
mimic a viral illness. Other
symptoms include dry mouth,
headache, and muscle pains.
• Chronic exposure results in two
distinct clinical syndromes,
acrodynia and erethism.
• Acrodynia is a complex of symptoms
occurring in chronic toxicity from
elemental and inorganic mercury. It
occurs more commonly in infants and
children, but has been reported in adults
• Characteristic findings include sweating,
hypertension, tachycardia, pruritus,
weakness, poor muscle tone, insomnia,
anorexia, and an erythematous,
desquamating rash to the palms and soles
• Oral findings including reddened, swollen
gums, subsequent mucosal ulcerations,
and possible tooth loss .By an unknown
mechanism, mercury may result in
proximal weakness primarily involving
the pelvic and pectoral girdle
Erethism
Heavy metal & toxic inhalation
Heavy metal & toxic inhalation
Heavy metal & toxic inhalation
 Referensi
• Ibrahim D, Froberg B, Wolf A, Rusyniak DE. Heavy Metal
Poisoning: Clinical Presentations and Pathophysiology. Clinics
in Laboratory Medicine. 2006 Mar;26(1):67–97.
• Kasper DL, editor. Harrison’s principles of internal medicine.
19th edition / editors, Dennis L. Kasper, MD, William Ellery
Channing, Boston, Massachusetts [and five others]. New York:
McGraw Hill Education; 2015.
INTOKSIKASI OBAT
Acetaminophen Toxicity (Epidemiology)
Acetaminophen Toxicity
Acetaminophen Toxicity Clinical Manifestation
Acetaminophen Toxicity Treatment
Digitalis Glycosides (Digoxin)
Tatalaksana
LI 5. PSYCOTIC BREAK
 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