Second Problem

Friday, 29 September 2021

Group 19_20
• Tutor : dr. Hari Darmawan, Sp. Kk FINSDV
• Ketua : Radhiyya Tsabitah Drajat (405180101) – Group 20
• Sekretaris : Billy Oktavian (405180063) – Group 20
• Notulen : Bimayuda (405180213) – Group 19

Group 19
• Oktavia Setyaningrum (405170088)
• Amirah Dea Putri Zahirah (405180007)
• Moh. Niko Fajrul Yakin (405180051)
• Jeffrey Saputra Kawi (405180117)
• Ellyta shafira (405180146)
• Devy Fransiska Susanto (405180160)
• Sylvia regina (405180212)
• Bimayuda (405180213)
Group 20
• Intan Frederika bahari (405180043)
• Billy Oktavian (405180063)
• Angelica Joanna Charity Kamalo (405180088)
• Radhiyya Tsabitah Drajat (405180101)
• Cindy Damara (405180107)
• Mohammad Jofa Rachman Putera
(405180130)
• Belinda Layrenshia (405180204)
• Arryza Fahrita Ikhsani (405180224)
 That Which Does not Kill Us Makes Us Stronger

A 20-year-old man was taken to the Emergency Department because of drowsiness and non stop vomiting. He had
been drinking and smoking weed at a club for a couple of hours before he became severely agitated which was
followed by an episode of heavy sedation. Initial physical examination results: blood pressure 90/60 mmHg, heart
rate 56 beats per minute, respiration rate 12 breaths per minutes (smells of alcohol) and body temperature 36,5 °C.
Physical examination found needle tracks on both of his lower arms and sores around his mouth and nose. During
examination, he showed pattern of repeatedly falling asleep and woke up agitated while shouting profanities to the
medical staffs. He mumbled incoherently, yanked the IV line and nasal cannula; and he also tried to climb down from
his bed several times. He shouted that the doctors were all police agents trying to throw him into jail. Because of his
agitation and failure to cooperate with medical procedures, the doctor applied physical restraint on his left hand so
that he cannot pull the IV line on his right hand. An hour later, the doctor found him breathing difficultly because the
restraint belt was wrapped several times around his neck, suggesting an attempt of suicide. His friends said that he
has history of multiple suicide attempts before. Last year he was found unconscious with half of his sleeping pill
bottle gone and three months ago he tried to jump off a bridge in an intoxicated state. His friends also stated that he
consumes multiple psychoactive substances. Laboratory result: in normal range. Liver function: AST 100 IU/L and
ALT 80 IU/L.
At the same time, a 5-year-old boy is taken by his parents to the emergency department for being unconscious.
About 3 hours beforehand, the mother found her son vomiting. An almost empty bottle containing a strong
smelling liquid and some pills were found scattered next to him. His mother suspects that his son was playing
in the kitchen again and probably mistook the liquid and pills as food. Then, the boy started to talk deliriously
and was feverish. No previous history of seizure or influenza. According to his mom, the boy is a bit late in
talking for his age. He seems weak and complains about tummy ache sometimes. There are some factories in
his neighborhood. Physical examination results: Delirious, blood pressure 90/60 mmHg, heart rate 100 beats
per minute, respiratory rate 40 breaths per minute, temperature 38 °C. Coarse crackles was heard from his
lung auscultation. Abdominal examination indicates the liver is 2 cm palpable below costal arch. Pulse
oximetry shows 90% of oxygen saturation. Laboratory result: Hb 9.5 g/dL, White blood cells (WBC)
15.000/mm3 , Ht 31%, Platelets 550.000/mm3, Na+ 128 mEq/L and K+ 3.6 mEq/L.

Identify and discuss the problems in these cases chronologically, while considering all possible differentials!

References for some lab results

Hb (children, age 1-5 yo) : 10.9-15.0 g/dl
Hematocrite : 31-45%
WBC : 5.000 – 10.000 /µL
Plateletes : 150.000 – 450.000 /µL
Natrium level : 135-153 mEq/L
Kalium level : 3.5-5.1 mEq/L
AST : 8-42 IU/L
ALT : 7-40 IU/L
Mindmap Drinking and smoking weed
Man
Suicide attempt
20 years old

Severely agitaion Drowsiness Non-stop vomiting

PHYSICAL EXAMINATION

Sore around mouth Needle tacks on

BP: 90/60 mmHg RR: 12x/minute HR: 56x/minute BT: 36,5 oC
and nose both of arms

Hypotension Sniffing Glue Normal Bradycardia Normal Drug Abuse

Morphine
Alcohol and opioid Intoxication of opioid,
Intoxication
withdrawal sedative-hypnotic and alcohol

Paracetamol
Taking Acetaminophen
Intoxication
Liver 2 cm palpable Lung Auscultation Kerosene Laboratory Result
Drinking Kerosene Tummy
below costal arch Coarse crackles Intoxication 1. Anemia
ache
2. Leukocytosis
Boy 3. Hematocrit (borderline)
BT: 36,5 oC PHYSICAL EXAMINATION Vomiting 4. Thrombocytosis
5 years old
5. Hyponatremia
BP: 90/60 mmHg Weak 6. Kalium level (borderline)
PO2 90%
RR: 12x/minute
Some factories in Carbon Monoxide A bit late in
neighborhood Metal Intoxication talking
HR: 56x/minute
Learning issues
1. Intoxication and withdrawal of psychoactive substances - (sign and symptoms, examination, treatment,
complication, prognosis)-Pediatrics and Adults
• Depresan
1.Alcohol
2.Benzodiazepin
3.Opioid
4.Barbiturat
5.Marijuana low dosage
• Stimulan
1.cocain
2.Amfetamin
3.Metamfetamin
• Hallusinogen
• 1.Marijuana high dosage
• 2.LSD
• 3.PCP
2. Intoxication and withdrawal of non-psychoactive substances (sign and symptoms, examination, treatment,
complication, prognosis) - pediatric and adult
Food
Foods containing cyanide
Drugs
1.Paracetamol
2.Digoxin
3.Salicylic acid
4.Beta blocker
Heavy Metal
1.Timbal
2.Merkuri
3.Besi
4.Arsenic

3. Other Intoxication(sign and symptoms, examination, treatment, complication, prognosis) - pediatric and adult
a.Organofosfat
b.Hidrokarbon
c.Karbon monoksida

4. ED psikiatri (sign and symptoms, examination, treatment, complication, prognosis) - pediatric and adult
a.Delirium
b.Suicide attempt
c.Agitation emergency
Alcohol intoxication

Evidence of alcohol -> smelling alcohol on the individual’s breath

PP: breath, blood (BAC) , or urine samples for toxicology analyses

kaplan dan sadocks

• Treat hypoglycemia with IV dextrose. Thiamine 100 mg IV or IM may
• be given concurrently if Wernicke encephalopathy is suspected

DSM 5
Alcohol withdrawal
• Classic sign –> tremulousness (6-8 hours after cessation)
• psychotic and perceptual symp­toms (e.g., delusions and hallucina­tions)
begin in 8 to 12 hours
• seizures in 12 to 24 hours
• delirium tremens (DTs)/alcohol delirium (anytime during the first 72 hours )
• Other symptoms: general irritability, gastrointestinal symptoms (nausea and
vomiting) and sympathetic autonomic hyperactiv­ity, including anxiety,
arousal, sweating, facial flushing, mydria­sis, tachycardia, and mild
hypertension
• Generally alert
European journal of
internal medicine 19
(2008) 561-567
DSM 5
Alcohol withdrawal
• control alcohol withdrawal symptoms -> benzodiazepines (PO,IV,IM)
diazepam, chlordiazepoxide
• carbamazepine 800 mg
• Beta-adrenergic receptor antagonists and clonidine -> block the
symptoms of sympathetic hyperactivity

kaplan and sadocks

Benzodiazepine intoxication
• The classic presentation -> CNS depression (ranging from mild
drowsiness to a coma-like, stuporous state) with normal vital signs or
near normal
• Many patients will still be arousable and even provide a reliable
history
• Classic symptoms include slurred speech, ataxia, and altered mental
status.
• respiratory depression and airway compromise
• In children -> Ataxia is the most common sign

https://www.ncbi.nlm.nih.gov/books/NBK482238/
Evaluation
• Airway
• Breathing
• Circulation

• PP: urine drug screen

Treatment:
• supportive (endotracheal intubation to provide definitive airway management)
• Flumazenil

https://www.ncbi.nlm.nih.gov/books/NBK482238/
Benzodiazepine withdrawal
• Anxiety, agaitation, insomnia
• Muscle aches and headaches
• Numbness, tingling, parasthesia, hypersensitivity to noise, light and taste, smell, dizziness
• Impaired concentration and memory
• Depersonalisation and derealisation
• Depression, paranoid, psychosis
• Withdrawal seizures are more likely to occur after abrupt cessation of long-term use of
high doses, in particular short acting drugs such as alprazolam

• short acting -> 1-2 days of last use, peak at 7-14 days
• Long acting -> 2-7 days, peaking around 20 days

https://www.sahealth.sa.gov.au/wps/wcm/connect/public+content/sa+health+internet/resources/benzodiazepine+withdrawal+dacas+factsheet
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1711840/?page=1
Opioids
Introduction
• Opioids include therapeutic agents and illicit substances.
• Toxicity occurs as a result of an intentional overdose, intentional abuse, or
adverse effect of therapeutic use.
• Opioids are well absorbed after gastrointestinal (oral and rectal), and it
depends on its lipid solubility.
• Heroin is usually abused through intravenous and subcutaneous routes,
but it is also absorbed after nasal administration because it is lipid soluble.
• Heroin peaks in the serum within 1 minute of intravenous injection, 3 to 5
minutes of intranasal administration, and 10 minutes of subcutaneous
injection.
• Withdrawal symptoms occur 4 to 6 hours after discontinuation of heroin
and 24 to 48 hours after discontinuation of methadone.

Rosen’s emergency medicine: concepts and clinical practice, 9 th Edition.

 signs and symptoms
- CNS depression
- Respiratory depression effects on the
respiratory medullary center via suppression
of hypercapnic sensitivity & overriding
hypoxic impulses
- Miosis due to stimulation of receptors in the
Edinger-Westphal nucleus of the oculomotor
nerve
- Acute lung injury may be seen in overdose.
Pulmonary edema failure of oxygenation
desaturated pulse oximetry despite adequate
RR & rales on lung auscultation
- Bradycardia, mild hypotension, pruritus,
flushing, nausea, vomiting, dysfunction
- “Skin popping” at the subcutaneous injection
site is a sign of illicit opioid use

Rosen’s emergency medicine: concepts and clinical practice, 9 th Edition. Philadelphia:

Elsevier, 2018.
Diagnosis & PP
• Diagnosis: clinical signs of Treatment
toxidrome and rapid response to • Stabilisasi & Suportif
naloxone. • Airway, oksigenasi, ventilasi
• Acute lung injury  bi-level positive airway
• PP  not always reliable : pressure, continuous positive airway pressure,
mechanical ventilation
- ECG,
• Antidotum
- monitor end-tidal carbon dioxide • The competitive opioid antagonist naloxone; very
and oxygen saturation, fast (onset 2 minutes, duration 20 minutes – 2
hours). Not effective via IV, SC, IM, inhalation,
- Hypoglycemia endotracheal. Typical dosage: 0.04 – 15 mg IV

- urine test : positive within 72 hours

after use

Rosen’s emergency medicine: concepts and clinical practice, 9 th Edition. Philadelphia:

Elsevier, 2018.
BARBITURAT
• Toxicity: depression of CNS activity by amplifying the activity of gamma-aminobutyric
acid (GABA), a major central inhibitor, decreased transmission of autonomic ganglia,
myocardium, GI tract and inhibition of acetylcholine responses at the neuromuscular
junction
• Clinical Symptoms: drowsiness, slurred speech, ataxia, unsteady gait, nystagmus,
emotional lability, decreased cognition. Severe Intoxication coma & respiratory arrest,
hypotension, increased HR/N.
• DD: intoksikasi ethanol, benzodiazepin, antiepilepsi (carbamazpin, fenitoin, asam
valproat); hipoglikamia, iskemia serebral

Diagnostic Testing:
• Serum levels (>50 g/mL coma; 80 g/mL
fatal respiratory depression; N: 15 to 40
g/mL)
• Positive urine test qualitative
• CXR  detection of
pulmonary edema
• CT head  patient in coma with trauma,
focal neurologic signs, papilledema
Rosen’s emergency medicine: concepts and clinical practice, 9 th Edition. Philadelphia: Elsevier, 2018.
Tatalaksana
• No specific antidote  supportive
• Mild – moderate overdose  oxygen,
intubate
• Careful fluid replacement  maintain
systolic BP >90 mmHg and adequate urine
noncardiogenic output
• Dopamine or norepinephrine  if fluid
bolus fails to treat hypotension
• Activated charcoal 50 – 100 g PO (1 g/kg in
children)  patient is conscious
• Hemodialysis  in poor condition despite
treatment, but only effective against
phenobarbital toxicity
Cannabis-related disorders
• Street names: weed, grass, pot, ganja, skunk
• Forms of preparation (most commonly smoked, vaporized; ingested orally
via pill, capsules, oil, food)
• Medical marijuana (e.g., dronabinol)
• Mechanism of action: tetrahydrocannabinol (THC) interacts w/
CB1 and CB2 → inhibition of adenylate cyclase
• Low dose (depressant), high dose (hallucinogen)
• Cannabinoid effects  limbic system, affecting memory, cognition and
psychomotor performance, mesolimbic pathway, impacting the reward
pathway and areas of pain perception
Harrisons Principles of Internal Medicine.20th Edition
Rosen’s Emergency Medicine.9 ed, 2018
Neural circuitry of depression and addiction
• 3 major pathologic adaptations
• Tolerance and dependance in reward
circuits
• Sensitization to the rewarding effect
• Impaired executive function

Harrisons Principles of Internal Medicine.20th Edition

Cannabis intoxication
• DSM-V requires the following features to be present: 
• Any of the following behavioral/mental disturbances must occur during or shortly after cannabis consumption
• Euphoria
• Perceptual disturbances 
• Impaired reaction time, concentration, and motor coordination
• Social detachment
• Impaired judgment
• Joviality, anxiety, panic
• At least two of the following symptoms must be present within two hours after cannabis consumption:
• Tachycardia
• Conjunctival injection (red eyes), mydriasis
• Increased appetite
• Dry mouth
• Additionally, the following features may be present 
• Paranoid delusions, hallucinations
• Increased or decreased blood pressure

Sadock, Benjamin J. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. 11 th Edition. Philadelphia: Lippincott Williams & Wilkins; 2015.
Cannabis withdrawal
• Clinical features of withdrawal: DSM-V requires ≥ 3 of the following features
to occur within one week following cessation of prolonged cannabis use 
• Irritability, aggression
• Anxiety
• Depression
• ↓ Appetite and/or weight loss
• Restlessness
• Sleep disturbances
• Anorexia
• At least one of the following physical symptoms must also be
present: headaches, tremors, abdominal pain, fever, chills, sweating.

Sadock, Benjamin J. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. 11 th Edition. Philadelphia: Lippincott Williams & Wilkins; 2015.
• History
• What agent
• Time of exposure
• Quantity
• Method of usage
• Signs and symptoms
• Previous rehabilitation
• HIV/AIDS
• Stressor
• Physical exam and essential workup
• Vital signs, neurologic and psychiatric exam, ECG, determination of risk of
rhabdomyolisis

Rosen’s Emergency Medicine.9 ed, 2018

• Diagnostic test
• Lab
• Electrolytes, BUN, creatinine, glucose levels, coagulation screen, arterial, or venous blood gas

• Urine toxicology screen (rare)

• Imaging
• Xray, CT
• Ddx
• Hypoglycemia
• Meningitis, encephalitis
• Sepsis
• Intracranial bleeds or lesions
• Withdrawal (ethanol, sedative–hypnotic, baclofen)
• Serotonin syndrome
• Psychiatric illnesses

Rosen’s Emergency Medicine.9 ed, 2018

• PRE-HOSPITAL
• Benzodiazepines are generally preferred
• For hyperthermic patient: Use sedation rather than physical restraint
• INITIAL STABILIZATION/THERAPY
• Management of ABCs
• Aggressive cooling if hyperthermic
• IV access/rehydration  for significant fluid loss/ rhabdomyolysis
• Naloxone, Accu-Chek, dextrose, and thiamine if patient has altered mental
status

Rosen’s Emergency Medicine.9 ed, 2018

• ED TREATMENT/PROCEDURES
• Cooling measures:
• – Cool mist and fans
• – Benzodiazepines if agitated
• – Paralytics with intubation if needed
• Sedate for agitation or autonomic signs:
• – Benzodiazepines
• – Rarely neuroleptics
• Activated charcoal (AC)
• Place in a quiet, calm environment
• Maintain urine output of 2–3 mL/kg/hr and consider urine alkalinization for
treatment of rhabdomyolysis

Rosen’s Emergency Medicine.9 ed, 2018

• MEDICATION
• Benzodiazepines (diazepam): 5–10 mg IV (peds: 0.2–0.5 mg/kg) IV or lorazepam:
1–4 mg IV/IM (peds: 0.02–0.05 mg/kg) IV/IM, may repeat as needed
• Dextrose (D50W) for hypoglycemia: 1 ampule: 25 g/50 mL (peds: D 25W, 0.5–1
g/kg or 2–4 mL/kg) IV, may repeat as needed
• Haloperidol (Haldol): 2.5–5 mg IV or IM may repeat every 30–60 min until calm,
usual max. dose is 10–20 mg
• Naloxone (Narcan): Initial dose: 2 mg (peds: 0.01–0.1 mg/kg) IV or IM, may
repeat as needed
• Sodium bicarbonate infusion for rhabdomyolysis: 3 ampules in 1 L of D5W;
infuse at 1.5–2 times maintenance rate (keep urine pH > 7.5)
• Thiamine (vitamin B1): 100 mg (peds: 25 mg) IV or IM × 1 dose

Rosen’s Emergency Medicine.9 ed, 2018

• DISPOSITION
• Admission Criteria
• Severely intoxicated
• Atypical presentation
• Prolonged symptoms (>12 hr after exposure)
• Prolonged periods of agitation and hyperthermia
• Discharge Criteria
• Asymptomatic.
• Pediatric Considerations
• Suspected cases of child abuse or neglect require referral to child protective services.
• FOLLOW-UP RECOMMENDATIONS
• Upon discharge, patients should receive follow-up care from their PCP,
psychiatrist, or drug counseling facility.

Rosen’s Emergency Medicine.9 ed, 2018

• PEARLS AND PITFALLS
• Do not delay in the diagnosis and treatment of hyperthermia.
• Use appropriate physical and chemical restraints to control violent and
agitated patients to protect the patient and staff from physical injury.
• Conduct serial exams and vital signs (especially temperature). Do not assume
once a violently agitated patient is calm that the patient is recovering. The
patient may be progressing to serious illness.

Rosen’s Emergency Medicine.9 ed, 2018

Rosen’s Emergency Medicine.9 ed, 2018
• Complications 
• Cannabis-induced psychosis with paranoia, delusional thoughts,
and/or hallucinations
• Cannabis-induced anxiety disorder
• Cannabis-induced sleep disorder
• Higher lifetime probability of other substance use disorders
• Cannabinoid hyperemesis syndrome 
• Pathophysiology: overridden antiemetic properties due to cannabis accumulation with chronic
use, hepatic biotransformation of cannabis to proemetic metabolites, splanchnic vasodilation, and
inhibition of GI motility and disruption of hypothalamic activity
• Cyclical vomiting
• Relieved w/ hot bath decrease mesenteric congestion
• Resolved w/ its discontinuation

Rosen’s Emergency Medicine.9 ed, 2018

• Complications 
• Cannabis use disorder: DSM-V requires ≥ 2 of the following features to occur within
a 1-year period of cannabis use, accompanied by agitation and severe impairment of
functioning
• in larger amounts or over a longer period
• Persistent desire to cut down or repeated unsuccessful efforts to stop using it
• A large amount of time is spent using cannabis, trying to acquire it, or recovering from its effects
• Strong craving
• Cannabis use has a negative impact on social and professional function Continued cannabis use
despite social or interpersonal problems
• Loss of interest
• Recurrent use of cannabis in situations in which its use is associated with the risk of physical
harm

Sadock, Benjamin J. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. 11 th Edition. Philadelphia: Lippincott Williams & Wilkins; 2015.
 • Continued cannabis use despite persistent or recurrent psychological or physical problems that
can most likely be attributed directly to the use of cannabis
• Tolerance, which can manifest as:
• The need to markedly increase the amount of cannabis to achieve the desired effect/intoxication
and/or
• A reduced effect over time when the same amount of cannabis is used
• Withdrawal
• Long-term effects include pulmonary problems, immunosuppression,
and sex hormone imbalance.
• No deaths have been solely attributed to marijuana.
• Pediatric exposures  may lead to hypothermia, ataxia, nystagmus,
tremor, tachycardia, injected conjunctiva, and labile affect.
• Oral ingestion of potent marijuana in children  rapid onset of drowsiness,
hypotonia, and lethargy, which can lead to coma and airway obstruction.

Sadock, Benjamin J. Kaplan & Sadock’s synopsis of psychiatry : behavioral sciences/clinical psychiatry. 11 th Edition. Philadelphia: Lippincott Williams & Wilkins; 2015.
Rosen’s Emergency Medicine.9 ed, 2018
Cocain
• Cocain : alkaloid found in E.coca • Diagnostic :
– Laboratory : chemistry panel, creatine
• PE : dysrhythmias, myocarditis,
cardiomyopathy, ACS, seizures, kinase level, urine drug screens
cerebral infactions and – ECG
hemorrhages, local airway • Treatment :
bronchospasm, hyperthermia,
vasoconstriction, hypotension and
hypovolemia

Tintinalli's Emergency Medicine Ed.9

Physical problem
- Snorting: runny nose, sinusitis, epistaxis, wounds, nasal septal
perforation
- Injections: local skin infection to systemic
- Smoking: sore throat, melanoptysis
Psikiatri problem
-Tolerance and dependence
-Agitation, depression, fatigue, high craving, anxiety, angry outbursts,
sleep disturbances
Social problem
- Marriage separation to divorce
- Damage to self-productivity Detained,
- convicted
Cause of death
-Overdose
-Respiratory paralysis
-SIDS in babies
AMPHETAMINE POISONING SIGNS AND SYMPTOMS
• Increased release of norepinephrine, • CNS:
dopamine, and serotonin – Agitation
• Decreased catecholamine reuptake – Delirium
• Direct effect on α- and β-adrenergic receptors – Hyperactivity
– Tremors
– Dizziness
ETIOLOGY
– Mydriasis
– Headache
• Prescription drugs:
– Choreoathetoid movements
– Amphetamine (Benzedrine)
– Hyperreflexia
– Dextroamphetamine (Dexedrine)
– Cerebrovascular accident
– Diethylpropion (Tenuate)
– Seizures and status epilepticus
– Fenfluramine (Pondimin)
– Coma
– Methamphetamine
• Psychiatric:
– Methylphenidate (Ritalin)
– Euphoria
– Phenmetrazine (Preludin)
– Increased aggressiveness
– Phentermine
– Anxiety
– Hallucinations (visual, tactile)
– Compulsive repetitive actions
• Cardiovascular:
– Palpitations
– Hypertensive crisis
– Tachycardia or (reflex)
bradycardia
– Dysrhythmias (usually
tachydysrhythmias)
– Cardiovascular collapse
HISTORY
• Determine the type, amount, timing, and route of amphetamine exposure
• Assess for possible coingestions_x0002_
• Evaluate for symptoms of end organ injury:
– Chest pain
– Shortness of breath
– Headache, confusion, and vomiting
Physical Exam
Common findings include:
– Agitation
– Tachycardia
– Diaphoresis
– Mydriasis
Severe intoxication characterized by:
– Tachycardia
– HTN
– Hyperthermia
– Agitated delirium
– Seizures
– Diaphoresis
_x0002_
Hypotension and respiratory distress may precede
cardiovascular collapse
_x0002_
Evaluate for associated conditions:
– Cellulitis and soft tissue infections
– Diastolic cardiac murmurs or unequal pulses
– Examine carefully for trauma
– Pneumothorax from inhalation injury
– Focal neurological deficits
Rosen’s Emergency Medicine.9 ed, 2018
DIAGNOSIS TESTS & INTERPRETATION Treatment
Lab PRE-HOSPITAL
_x0002_ • Patient may be uncooperative or violent.
• Urinalysis: • Secure IV access.
– Blood
• Protect from self-induced trauma.
– Myoglobin
_x0002_ INITIAL STABILIZATION/THERAPY
• Electrolytes, BUN/creatinine, glucose: • ABCs
– Hypoglycemia may contribute to altered mental • Establish IV 0.9% NS access.
status. • Cardiac monitor
– Acidosis may accompany severe toxicity. • Naloxone, dextrose (or Accu-Chek), and
– Rhabdomyolysis may cause renal failure. thiamine if altered mental status
– Hyperkalemia—life-threatening consequence of
acute renal failure _x0002_ ED TREATMENT/PROCEDURES
• Coagulation profile to monitor for potential DIC: _x0002_
– INR, PT, PTT, platelets Decontamination:
_x0002_ – Administration of activated charcoal
• Creatine phosphokinase (CPK): – Whole-bowel irrigation with
– Markedly elevated in rhabdomyolysis polyethylene glycol
solution for body packers _x0002_
• Urine toxicology screen: Hypertensive crisis:
– For other toxins with similar effects (e.g., cocaine) – Initially administer benzodiazepines if
– Some amphetamine-like substances (e.g., agitated.
methcathinone) may not be detected. _x0002_ – α-blocker (phentolamine) as second-line
• Aspirin and acetaminophen levels if suicide attempt agent
is a possibility – Nitroprusside for severe, unresponsive
hypertension
• Arterial blood gas (ABG) – Avoid β-blockers, which may exacerbate
hypertension.
Agitation, acute psychosis:
– Administer benzodiazepines.
Hyperthermia:
– Benzodiazepines if agitated
– Active cooling if temperature
>40◦C:
◦ Tepid water mist
◦ Evaporate with fan.
– Paralysis:
◦ Indicated if muscle rigidity
and hyperactivity
contributing to persistent
hyperthermia
◦ Nondepolarizing agent (e.g.,
vecuronium)
◦ Avoid succinylcholine.
◦ Intubation; mechanical
ventilation
– Apply cooling blankets.
_x0002__x0002_
Hypotension:
– May be late finding due to
catecholamine depletion
– Initially bolus with isotonic
crystalloid solution
– If no response, administer
norepinephrine.
– Dopamine may not be effective
Rosen’s Emergency Medicine.9 ed, 2018
MEDICATION
• Activated charcoal: 1–2 g/kg up to 100 g PO
• Dextrose: D50W 1 amp: 50 mL or 25 g (peds: D25W 2–4 mL/kg) IV
• Diazepam (benzodiazepine): 5–10 mg (peds: 0.2–0.5 mg/kg) IV
• Lorazepam (benzodiazepine): 2–6 mg (peds: 0.03–0.05 mg/kg) IV
• Nitroprusside: 1–8 μg/kg/min IV (titrated to BP) _x0002_
• Phenobarbital: 15–20 mg/kg at 25–50 mg/min until cessation of seizure activity
• Phentolamine: 1–5 mg IV over 5 min (titrated to BP)
• Vecuronium: 0.1 mg/kg IVP

Rosen’s Emergency Medicine.9 ed, 2018

 Hallusinogen
High Dose Marijuana Lysergic Acid Diethylamide Phencyclidine
(LSD) (PCP, “angel dust”)
Typically Hallucinogen 5-15 milligrams of 20-80 mikrograms (8-12h) 1-9 milligrams (4-6h)
Dose tetrahydrocannabinol (THC)

Clinical Features • Smoking marijuana: alteration of • Mydriasis • Small or midsizes pupils

mood and usually relaxation and • Tachycardia • Nystagmus
euphoria • Anxiety • Muscle rigidity
• Mild increase in heart rate and • Muscle Tension • Hypersalivation
conjunctival injection • Agitation
• Other acute peripheral changes: • Catatonia
urinary retention, decreased
testosterone levels, and decreased
intraocular pressure
• Short-term memory is impaired, and
the ability to perform complex tasks
may be adversely affected
• Oral ingestion of marijuana: ataxia,
vomiting, agitation, anxiety, and CNS
depression
• Pediatric exposures to marijuana:
hypothermia, ataxia, nystagmus,
tremor, tachycardia, injected
conjunctiva, and labile affect
• Oral ingestion in children: rapid
onset of drowsiness, hypotonia, and
lethargy  coma and airway
obstruction and respiratory
compromise

Tintinalli's Emergency Medicine Ed.9

 High Dose Marijuana Lysergic Acid Diethylamide Pneumocystis Jirovecii
(LSD) Pneumonia (PCP)
Diagnostic Testing • Urinary metabolites : detactable • LSD can be detected in urine test for 2-4 days • No laboratory tests are specific for PCP
within 1 hr after smoking after last use, in a blood test for 6-12 hrs after last intoxication, but, in addition to hypoglycemia,
marijuana use, and in a hair test for up to 90 days elevation in WBC count and BUN and creatinine
• Marijuana cigarettes can be levels may be seen.
detacted for 72 hr, cut off lvl :
100ng/m
Management • Prevention of injury and • Reassurance • Benzodiazepines
reassurance for those who have • Benzodiazepines • Hydration
panic reactions • Active cooling
• Extremely agitated patient : oral
or parenteral administration of
benzodiazepines or
antipsychotics
• Antiemetics (eg : ondansetron 4-
8mg IV, or metoclopramide 10-20
mg IV)  treat nausea and
vomiting e.c. cannabinoid
hyperemesis syndrome (CHS)
• Synthetic cannabinoids and
heavy, daily marijuana use
• Hot showers : rapid reduction in
the symptomps of CHS
• Children : admission for a 24-
hour observation period

Complications • Acute psychosis (rare) • Coma • Coma

• Panic reactions (rare) • Hyperthermia • Seizures
• Coagulopathy • Hyperthermia
• Persistent psychosis • Rhabdomyolysis
• Hallucinogen persisting perception disorder • Hypertension
• Hypoglycemia

Tintinalli's Emergency Medicine Ed.9

 Intoxication: Paracetamol
• Toxic exposure to APA is likely
when patient >6 years old ingest
either:
a) >10 gr or 200 mg/kg in single
ingestion or over a 24 hour
period
b) >6 g or 150 mg/kg/day for two
consecutive days would be 8
hours
• For children <6 years, either:
a) >200 mg in a single ingestion or
over an 8 hours period
b) 150 mg/kg/day for two
consecutive days would be
considered toxic https://www.ncbi.nlm.nih.gov/books/NBK441917/
 Intoxication: Paracetamol

• The clinical course of acetaminophen toxicity is divided into four stages:

a) During the first stage (30 min to 24 hours), the patient may be asymptomatic
or may have emesis.
b) In the second stage (18 hours to 72 hours), there may be emesis plus right
upper quadrant pain and hypotension.
c) In the third stage (72 hours to 96 hours), liver dysfunction is significant with
renal failure, coagulopathies, metabolic acidosis, and encephalopathy.
Gastrointestinal (GI) symptoms reappear, and death is most common at this
stage.
d) The fourth stage (4 days to 3 weeks) is marked by recovery.

https://www.ncbi.nlm.nih.gov/books/NBK441917/
Intoxication: Algorithm
Digoxin Toxicity
• Digoxin is derived from the Balkan foxglove
plant, Digitalis lanata  belongs to a class of
medications known as cardiac glycosides
• These agents function to increase myo­cardial
contractility and slow AV nodal conduction
and are commonly used for the treatment of
congestive heart failure and various cardiac
dysrhythmias including atrial fibrilla­tion.
• With toxic concentrations
digoxin paralyzes the Na+,K+,-ATPase pump, potassium
cannot be transported into cells, and serum potassium
concentration can rise as high as 13.5 mmol/L.
digoxin can directly block the generation of impulses in
the SA node, depress conduction through the AV node,
and increase the sensitivity of the SA and AV nodes to
catecholamines..

Rosen Barkin’s 5 Minute Emergency Medicine Consult

Rosen’s Emergency Medicine. 9th edition.
Digoxin Toxicity
• The most common symptoms, in more than 80% of cases, are
nausea, anorexia, and fatigue; but a variety of gastrointestinal,
neurologic, and ophthalmic disturbances also occur

Diagnosis
• ECG dysrhythmia
• Digoxin level:
– Normal range: 0.5–2 ng/mL
– Distribution after oral intake not complete until 6 hr;
therefore, >6-hr level is most accurate steady state
concentration.
– False elevations possible with spironolactone use,
pregnancy, hyperbilirubinemia, chronic renal failure,
liver failure, CHF
– May be falsely elevated after digoxin-specific Fab
fragments given

Rosen’s Emergency Medicine. 9th edition.

Digoxin Toxicity

Rosen’s Emergency Medicine. 9th edition.

Tintinalli’s Emergency Medicine Manual 8th Edition
salicylic acid intoxication

• As a food preservative: manufacture of methyl salicylate, acetyl

salicylate, or other salicylates.
a. Exposure routes Short term exposure:
• Inhalation: Irritation
• Skin contact : Irritation
• Eye contact : Irritation
• Ingestion: nausea, vomiting, diarrhea, dizziness, difficulty breathing,
headache, drowsiness, disorientation, hearing loss, visual disturbances,
pulmonary congestion, kidney damage, convulsions, coma
Tintinalli’s Emergency Medicine Manual 8th Edition
b. Long term exposure
• Inhalation There is no information on significant side effects.
• Skin contact: Burns, ringing in the ears, nausea, vomiting, diarrhea,
dizziness.
• Eye contact : Irritation
• Ingestion: Ringing in the ears, nausea, vomiting, diarrhea, dizziness,
difficulty breathing, headache, drowsiness, disorientation, hearing
loss, visual disturbances, pulmonary congestion, kidney damage,
convulsions, coma.

Tintinalli’s Emergency Medicine Manual 8th Edition

Treatment
• Stabilization Airway management, which frees the airway to ensure air
exchange.
• Management of respiratory function to improve ventilation function
by providing artificial respiration to ensure adequate oxygen demand
and carbon dioxide expenditure.
• Circulation management, aims to restore the function of blood
circulation.
• Management includes activated charcoal (if the patient presents within
1 hour of poisoning), alkalinisation of serum and urine, and
management of fluids and hypokalaemia.
Tintinalli’s Emergency Medicine Manual 8th Edition
Decontamination

• Aims to reduce exposure to toxins, prevent damage and reduce

absorption. Decontamination done as early as possible can prevent
harm and save lives
• Eye decontamination
• Decontamination of skin (including hair and nails)

Tintinalli’s Emergency Medicine Manual 8th Edition

 Eye decontamination

• The patient's position is sitting or lying with the head held back and
tilted to the side of the eye that is affected or worst.
• Gently open the affected eyelid and apply a gentle amount of cold
clean water or 0.9% NaCl solution for 15-20 minutes.
• Avoid washing water marks on the face or other eyes.
• If you're still not sure it's clean, wash it again for another 10 minutes.
• Do not let the patient rub his eyes.
• Cover your eyes with sterile gauze and immediately send/consul to an
ophthalmologist
Tintinalli’s Emergency Medicine Manual 8th Edition
 Decontamination of skin, hair and nails

• Take the patient immediately to the nearest shower.

• Wash the affected skin immediately with cold or warm running water and
soap for at least 10 minutes.
• If water is not available, gently wipe the patient's skin and hair with a cloth
or paper. Don't rub.
• Remove contaminated clothing, watches and shoes or their vomit and
dispose of them in a closed plastic/container container.
• Rescuers need to be protected from splashes, for example by wearing
gloves, a nose mask and an apron. Be careful not to inhale it.
• Dry with a dry and soft towel.
Tintinalli’s Emergency Medicine Manual 8th Edition
 Intoxication Beta-Blocker
• Beta-blockers antagonize beta-adrenergic receptors and are used mainly in the
treatment of cardiovascular disorders also used in the management of anxiety,
migraine headache, glaucoma, tremor, and various other disorders.

• Absorption  1 to 4 hours except for sustained-release preparations.

• Excretion  the liver most frequently and some in renal

• most of the beta-blockers are moderately lipophilic  blood-brain barrier and

may cause seizures in overdose cases.

https://www.ncbi.nlm.nih.gov/books/NBK448097/
 Examination
• History of drug used
• Monitor vital sign
• EKG
• Propanolol -> causes natrium
channel blockade -> QRS
widening, positive R’ wave in
aVR
• sotalol -> causes potassium efflux
blockade -> QT prolongation

https://www.ncbi.nlm.nih.gov/books/NBK448097/
Tintinalli's emergency medicine : a comprehensive study guide
https://litfl.com/beta-blocker-overdose/ 
 Management
• Airway management
• Atropine
• Albuterol
• Decontamination : activated charcoal if <1 hour
• Bowel irrigation
• Benzodiazepine
• Sodium bicarbonate  QRS widening & QTc prolongation
• Glucagon 50mcg/kg up to 10mg
• Euglycemia (HIE) high dose 1 U/kg of regular insulin bolus + 0.5 g/kg
dextrose intravenously (IV)
• Vasopressor
• Calcium salt

https://www.ncbi.nlm.nih.gov/books/NBK448097/
 Prognosis
• The outcomes after beta-blocker toxicity depend on when the patient presents and
the amount ingested.
• Individuals with underlying heart and lung disease are most susceptible to the
toxic effects of beta-blockers. The outcomes are worse in people who are also
consuming other cardioactive and psychotropic agents.

https://www.ncbi.nlm.nih.gov/books/NBK448097/
 Lead poisoning
 Lead has multiple mechanisms of toxicity:
 Binds sulfhydryl groups  multiple enzymatic processes
 Resembles Ca 2+  interfering with Ca 2+-dependent processes
 May have mutagenic potential
• Distribution:
 Up to 99% of lead is bound to erythrocytes after initial absorption.
 Ultimately redistributed into bone:
o 95% of total body lead in adults
o 70% of total body lead in children
 High lead levels result in lead entry into the CNS and neurotoxicity.
• Often coexists with iron deficiency
• Impairs heme synthesis  FEP with zinc ZPP
• Associated with drops in IQ and violent behavior
Rosen & Barkin’s 5 Minute Emergency Medicine Consult 5th edition
 Etiology
• Acute toxicity: Pottery glaze, folk remedies,cosmetics ,jewelry , weights , home-
distilled alcoholic beverages , lead dust from ammunition and primer
• Chronic toxicity:
• Occupational exposures: Battery manufacturing/recycling, bridge painting , construction
workers , de-leading, electronic waste recycling, firing range instructors , mining and smelting
, pottery workers , welders
• Home exposures (pediatric poisoning): Lead-based paint inhalation/ingestion from toys and
walls, contaminated water from old pipes , lead dust from the clothing of a parent exposed at
work, imported foods , folk medicines

Rosen & Barkin’s 5 Minute Emergency Medicine Consult 5th edition

 Signs and symptoms
Neurologic: GI: Cardiovascular:
o Seizures o Hypertension
o Colicky abdominal
o Encephalopathy pain o Myocarditis and conduction defects
o Learning disabilities o Ileus Renal: Chronic renal insufficiency
o Psychiatric Hematologic:
o Nausea/vomiting
disturbances o Burton Lines o Anemia
o Cerebral edema o Increases RBC fragility
o Hepatitis/pancreatitis
o Peripheral motor Musculoskeletal: Lead lines from increased Ca
neuropathy 2+ deposition at epiphyse

Rosen & Barkin’s 5 Minute Emergency Medicine Consult 5th edition

 Treatment

Essential Workup:Blood lead

level (BLL)

Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. Eight edition.

Mercury Poisoning
• Mercury poisoning can result from exposure to elemental, inorganic,
or organic mercury compounds
Clinical features:
• Elemental mercury exposure is most likely to occur after contact with
a broken thermometer, and mercury is primarily absorbed via
inhalation. Vapor exposure result in cough, fever, dyspnea, vomiting,
and headache.
• Ingestion of inorganic mercury result in corrosive injury to the GI
tract, with vomiting, diarrhea, abdominal pain, and GI bleeding
followed by acute renal failure
Tintinalli’s Emergency Medicine Manual 8th Edition
Clinical features:
• Organic mercury is found in some fungicides and pesticides and can
be absorbed when ingested. Poisoning tends to occur with chronic
exposures and results in profound central nervous system dysfunction

Diagnosis:
A history of exposure to mercury is key to diagnosis and is confirmed
by an elevated 24-hour urine mercury level when toxicity is due to
elemental or inorganic mercury; an elevated whole blood mercury level
is necessary in cases of organic mercury exposure

Tintinalli’s Emergency Medicine Manual 8th Edition

Tintinalli’s Emergency Medicine Manual 8th Edition
Iron Toxicity
Iron poisoning is one of the most common toxic ingestion and one of
the most deadly among children. Failure to diagnose and treat iron
poisoning can have serious consequences including multi-organ failure
and death

Etilogy:
Ingestion of less than 20 mg/kg of elemental iron is non-toxic. Ingestion
of 20 mg/kg to 60 mg/kg results in moderate symptoms. Ingestion of
more than 60 mg/kg can result in severe toxicity and lead to severe
morbidity and mortality. 
https://www.ncbi.nlm.nih.gov/books/NBK459224/
History & physical

https://www.ncbi.nlm.nih.gov/books/NBK459224/
Treatment:

https://www.ncbi.nlm.nih.gov/books/NBK459224/
 ARSENIC POISONING
• Sources :
• Smelting Industry
• Electronic Industry
• Herbicides / Pesticides
• Signs & Symptoms : • Diagnostic Studies :
• Nausea • Hematemesis • CBC : leukocytosis
• Vomiting • Peripheral Neurohathy • Imaging : radiopaque sing on abdominal
• Diarrhea • Hypotension • Urinary : arsenic >68 mcmol/L
• Abdominal pain • Garlic odor • Serum Arsenic : >0.9mcmol/L
• Delirium • Gum lines • Arsenic in hair or nails
• Seizures • ECG :
• Prolong QT interval • ST depression
• Alopecia
• Broadening QRS • T-wave flattening
• Mees’ Lines
Nelson Textbook of Pediatrics 21st Edition Harrison’s Principles of Internal Medicine 19th Edition Tintinalli’s Emergency Medicine Manual 8th Edition Buku Ajar Ilmu Penyakit Dalam Jilid 1 Edisi VI
 ARSENIC POISONING – EMERGENCY DEPARTEMENT
• Primary Survey • Chelating Therapy
• Airways : (+/-) Endotracheal intubation • Dimercarpol IM
• Breathing : oxygen • Succimer PO
• Circulation • CaNa2EDTA
• 1-2 ampules/day for 5 days
• DMPS
• IV access • 1-2 capsules for 12 times
• Cristaloid : Ringer lactate / normal saline
• (+/-) Vasopressors
• Vitamin C & E supplement

• Whole-bowel irrigation
• Polyethylene glycol solution

Nelson Textbook of Pediatrics 21st Edition Harrison’s Principles of Internal Medicine 19th Edition Tintinalli’s Emergency Medicine Manual 8th Edition Buku Ajar Ilmu Penyakit Dalam Jilid 1 Edisi VI
Nelson Textbook of Pediatrics 21st Edition Tintinalli’s Emergency Medicine Manual 8th Edition
 Organofosfat
• Organophosphates are used as medications, insecticides. Symptoms include increased
saliva and tear production, diarrhea, nausea, vomiting, small pupils, sweating, muscle
tremors, and confusion.

https://www.ncbi.nlm.nih.gov/books/NBK470430/
Tintinalli Judith E, et al. Tintinalli’s Emergency medicine. 8th ed. 2011
 • With supportive care, these patients can have a complete return to normal neurologic
function within 2 to 3 weeks. Another later complication is neuropathy. Most commonly
this starts as stocking-glove paresthesia and progresses to symmetric polyneuropathy with
flaccid weakness that starts in the lower extremities and progresses to include the upper
extremities.
• Those who survive may also develop the following neuropsychiatric deficits:
o Confusion
o Impairment in memory
o Lethargy
o Psychosis
o Irritability
o Parkinson like symptoms

https://www.ncbi.nlm.nih.gov/books/NBK470430/
Tintinalli Judith E, et al. Tintinalli’s Emergency medicine. 8th ed. 2011
 Physical examination
• Some organophosphates have a distinct garlic or petroleum odor that may help in diagnosis. there is
a portable test that can measure AChE in red blood cells within minutes.
• Other blood work that should be ordered includes CBC, glucose levels, troponin, liver and renal
function, and arterial blood gas. The ECG will reveal sinus bradycardia due to the parasympathetic
activation
Management
• The first step in the management of patients with organophosphate poisoning is putting on personal
protective equipment. Secondly, you must decontaminate the patient. In the case of ingestion,
vomiting and diarrhea may limit the amount of substance absorbed but should never be induced.
• Airway control is vital. In some patients, intubation may be required due to bronchospasm, seizures
or bronchorrhea. During intubation, succinylcholine must be avoided as it may prolong the
paralysis. Good intravenous access, cardiac monitoring, and pulse oximetry are the standard of care.

https://www.ncbi.nlm.nih.gov/books/NBK470430/
Tintinalli Judith E, et al. Tintinalli’s Emergency medicine. 8th ed. 2011
Intoksikasi hidrokarbon

Rosen’s Emergency Medicine. 2017

Tintinalli JE. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Edition. 2011
Hydrocarbons fall into two broad categories:
• aliphatic (straight chain structure eg: propane)
• aromatic (cyclic structure eg: toluene)
Exposure to hydrocarbons can be through inhalation, oral (risk of aspiration), and dermal.
• Inhalation is usually due to accidental or occupational exposure
• Oral is common in children and accidental. Caution can occur aspiration and pneumonitis
Ordinary
• dermal due to exposure from work

Rosen’s Emergency Medicine Concepts and Clinical Practice 9e

Patofisiologi

• Acute hydrocarbon
intoxication usually affects
3 main organs, namely the
lungs, heart, and CNS.
• Oral hydrocarbon
intoxication usually only
causes local symptoms in
the GI tract such as
abdominal pain, vomiting,
and diarrhea.

Rosen’s Emergency Medicine Concepts and Clinical Practice 9e

Diagnosis and management

• History of exposure and characteristic bad

breath
• Lab tests such as electrolytes, complete
blood count, and liver function are used to
determine symptoms related to renal
tubular acidosis, hypokalemia, bone
marrow/liver injury that can be caused by
hydrocarbons.
• ECG if there is a history of use of
halogenated hydrocarbons, dysrhythmias,
syncope, and hemodynamic instability.
• Chest X-ray if there are lung-related
complaints
• Plain abdominal radiographs can show
radio opaque images due to certain
substances (eg chlorinated hydrocarbons).
• CHAMP

Rosen’s Emergency Medicine Concepts and Clinical Practice 9e

Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8th ed
Carbon monoxide
• CO exposure produces toxicity by 3 major pathways.
1. inhibition of systemic O2 delivery CO binds to hemoglobin (Hb) with an
affinity roughly 240 times greater than O2
2. The ability of CO to inhibit normal cellular respiration
3. The binding of CO to myoglobin  Myoglobin binds to CO with an affinity
40 times that of 02
Carbon monoxide
• Clinical presentation
- Vague headache (most common complaint), followed by fatigue, malase,
nausea, cognitive difficulties (memory impairment), paresthesias, weakness,
altered mental status and lethargy
- Cardivascular symptomps  ischemic chest pain, shortness of breath and
palpitations
• History of CO exposure
- Fire victims
- Faulty furnances during winter in older houses
- In enclosed spaces with eunning automobiles
- Recent use of any paint stripper or solvents (may contain methylene chloride)

Sherman SC. Clinical Emergency Medicine. Tintinalli’s Emergency Medicine 8 . 2016 pg 1439
th
• Pysical examination
• Laboratory & imaging
- Tachypneic may be attempting to
compensate for underlying metabolic - COHb level (help confirm
acidosis diagnosis and estimate the severity
of the exposure)
- Acute CO poisoning  “cherry red”
appearance to their skin due to the bright - Metabolic panel
red color of carboxyhemoglobin - CXR  in shortness of breathor
- Altered mental status history of smoke inhalation as
chemical injury to the lung
- Loss of coordination
- CT of the brain  altered mental
- Retinal flame hemorrhages
status or focal neurologic deficits
- Auscultate the lungs  inspiration to rule out alternative etiologies
crackles (may be indicatve of chemical
injury to the lung parenchyma with • Diagnostic Test
secondary acute respiratory distress Co-oximetry : distinguish between normal
syndrome) hemoglobin and COHb (and MetHb)
- Thermal injury in the skin (fire victims)

Tintinalli’s Emergency Medicine 8 th. 2016 pg 1438 Sherman SC. Clinical Emergency Medicine.
 Algorithm
• Supportive care in the form of
airway management, oxygen
therapy, and intravenous fluids
remains the most important
intervention.
• Normobaric O2 via
a nonrebreather facemask should be
administered until the
COHb level is <5% and the patient
is clinically stable.

• Patients with accidental

exposures who are clinically
well with COHb levels <5%
after 100% O2 treatment can be
safely discharged.
Sherman SC. Clinical Emergency Medicine.
Treatment
• Hyperbaric O2 :
• Oxygen: • 300 min in
Dose:
• Administer ambient air
100%O2 at 3atm
100% • 90 min in 100%
May be repeated
normobaric O2 : normobaric O2 Benefits:
• ◦ Via face • 20 min at 3 atm May reduce delayed neurologic
mask or (hyperbaric O2) sequelae
endotracheal
tube Decreases half-life of
• Continue O2 carboxyhemoglobin
therapy until Potential adverse effects:
carboxyhemoglo Tympanic membrane rupture
bin level <10%. Pneumothorax
Seizure
• Half-life of Decompression sickness
carboxyhemoglo Pulmonary edema
bin:
 Rosen’s Emergency Medicine Concepts and Clinical Practice 9e pg 1933

• The true benefit of treatment with HBO

is most likely to limit the prevalence of
delayed neurologic symptoms.
• The only absolute contraindication to
HBO is an untreated pneumothorax

Tintinalli’s Emergency Medicine 8 th. 2016 pg 1439

 DELIRIUM
The clinical hallmarks of delirium are decreased attention or awareness and a change in
baseline cognition.
•Clouding of consciousness
•Difficulty maintaining or shifting attention
•Disorientation
•Illusions
•Hallucinations
•Fluctuating levels of consciousness
•Dysphasia
•Dysarthria
•Tremor
•Asterixis in hepatic encephalopathy and uremia
•Motor abnormalities
https://emedicine.medscape.com/article/288890-overview
Diagnostic criteria
The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) diagnostic
criteria for delirium is as follows [1] :
• Disturbance in attention (ie, reduced ability to direct, focus, sustain, and shift attention) and
awareness.
• Change in cognition (eg, memory deficit, disorientation, language disturbance, perceptual
disturbance) that is not better accounted for by a preexisting, established, or evolving
dementia.
• The disturbance develops over a short period (usually hours to days) and tends to fluctuate
during the course of the day.
• There is evidence from the history, physical examination, or laboratory findings that the
disturbance is caused by a direct physiologic consequence of a general medical condition, an
intoxicating substance, medication use, or more than one cause.

https://emedicine.medscape.com/article/288890-overview
The most common medications
used are antipsychotic medications
• Haloperidol (Haldol)
• Risperidon (Risperdal)
• Benzodiazepin
• Lorazepam (Ativan)
Hypnotic, Miscellaneous
Agents in this class may be useful in
the prevention and management of
delirium.
• Melatonin (Herb/Suppl)
• Ramelteon

Vitamin
• Tiamin

https://emedicine.medscape.com/article/288890-overview
Sadock, Benjamin J. Kaplan & Sadock’s synopsis of psychiatry : behavioral
sciences/clinical psychiatry. 11th Edition. Philadelphia: Lippincott Williams &
Wilkins; 2015.
 Sign on Patient with Suicide attempt Risk and Violent

Kaplan & Sadock's Synopsis Of Psychiatry. 11th ed.

2. Identification
• Get rid of any accessories that can be used to harm themselves (Necklace,
belt)
• Always accompanied by staff or family
3. Evaluation
• Trigger/Risk Factor
• Comorbid
• Drug or Alcohol abuse
• Neurological examination
• Mental status examination

Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. 2011

Mental Status Examination

Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. 2011

Kaplan & Sadock's Synopsis Of Psychiatry. 11th ed.
Treatment
• Psychotherapy
• Emphaty
• Patient accompanied by their family
• Building your trust with the patient
• Pharmacotherapy:
• Give Antipsychotic if the patient have heavy agitation, schizophrenia, acute
mania, anxiety
• Sudden and episodic desire to hurt theirself or others: haloperidol, β-
adrenergic receptor antagonists, carbamazepine, lithium

Kaplan & Sadock's Synopsis Of Psychiatry. 11th ed.

Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. 2011
 EMERGENCY AGITATION

Vieta,et.al. Protocol for the management of psychiatric patients with psychomotor agitation. Spain: BMC Psychiatry. 2017
VERBAL DE-ESCALATION
• A variety of other approaches have been
recommended for the treatment of agitated
patients. Perhaps the most common
recommendation is the use of verbal de-escalation
or “talking down” the patient. Use of verbal de-
escalation is standard in many psychiatric settings
and may even be useful in patients with dementia.
• The goal of verbal de-escalation is to help the
patient regain control. Verbal de-escalation likely
does not need to be provided for long periods of
time and may allow PO medication over IM
injections. In some clinical trials of agitation, a
high proportion of patients have been ineligible
for medication treatment after successful verbal
calming.

Tintinalli’s Emergency Medicine A Comprehensive Study Guide 7th Ed

• PHYSICAL RESTRAINT

https://emcrit.org/emcrit/human-bondage-chemical-takedown/
https://emupdates.com/danger/

Tintinalli’s Emergency Medicine A Comprehensive Study Guide 7th Ed

 Suicidal
Attempts
Suicidal attempt

Multiple Psychoactive Substances

Intoxication
Smoking Weed Laboratory Test : Alcohol
- Alcohol serum
Alcohol Consumption - Psychoactive substances serum levels
- Liver Function Intoxication
Cannabis
Primary Survey Clinical History

Diagnostic Confirmed
Man 20 y.o. Treatment
Studies Diagnosis

IV Access Physical
Examination
Intoxication
Opioid
Needle tracks

Sores around his Drug Abused

mouth & nose Psychotic

Smells of alcohol
Delirium
Paranoid idea

Yanked IV Line &

Nasal Cannula

Climb down
from bed
 Factories in neighboorhood Hydrocarbon
Laboratory Test : Poisoning
- Heavy Metals Serum
Eat unknown pills
- Liver Function
- Renal Function
Drink unknown liquid Paracetamol
- Coagulation Profile
Poisoning
- Blood gas
- CBC
Primary Survey Clinical History

Diagnostic Confirmed
Boy 5 y.o. Treatment
Studies Diagnosis

Physical
IV Access
Examination
Other Test:
- Plain Radiograph Heavy Metal
- ECG Poisoning
Coarse crackles

Liver palpable Carbon Monoxide

Poisoning

SatO2 : 90 %