Common Poisoning in Medical Practice poisoning in medical... · Common Poisoning in Medical...

Preview:

Citation preview

Common Poisoning

in Medical Practiceวินัย วนานุกูล

ศูนยพิษวิทยา

ภาควิชาอายุรศาสตร

คณะแพทยศาสตร โรงพยาบาลรามาธิบดี

Common poison exposureRamathibodi Poison Center: 2001-2005

กลุมสาร จํานวน %

สารปองกันกําจัดศัตรูพืช (pesticides) 9,327 39.9

สารใชในบาน (household products) 4,421 18.9

ยา (pharmaceutical products) 4,397 18.8

สารใชในงานอุตสาหกรรม (occupational products) 2,537 10.9

พืชพิษ (plant toxins/poisonous plants) 977 4.2

สัตวพิษ (poisonous animals) 621 2.7

รวม 23,368

Outline

Pesticides

– Organophosphorus & Carbamate

Household products

– Caustic ingestion

Pharmaceutical products

– Paracetamol

– Psychotropic drugs

Common pesticide exposure and their death rateRamathibodi Poison Center: 2001-2005

สารปองกันกาํจัดศัตรูพืช จํานวนผูปวย (%) จํานวนผูเสียชีวิต อัตราการตาย

สารปองกันกาํจัดแมลง (insecticide) 4,832 50.0 470 9.7

สารปองกันกาํจัดวัชพืช (herbicide) 2,426 25.1 295 12.2

สารปองกันกาํจัดหนู (rodenticide) 1,301 13.5 27 2.1

สารปองกันกาํจัดหอย (mollusicide) 428 4.4 5 1.2

สารปองกันกาํจัดปลวก (miticide) 147 1.5 34 23.1

อื่นๆ 527 5.5 11 2.1

รวม 9,661 842 8.7

ชาย 20 ป

มีผูพบผูปวยนอนหมดสติอยูในสวน มีน้ําลายฟูมปาก พบขวดสารฆาแมลงตกอยูขางตัว

ตรวจรางกาย ที่ ER

BP 160/80 mmHg, HR 180/min., RR 20/min. shallow respiration

T 36.5 C

Unconscious, not response to pain stimuli, pupils 2 mm.

Hypersecretion with bilateral wheezes

Increased bowel sounds

ชาย 20 ป

การวินิจฉัย: ผูปวยมีภาวะเปนพิษจากสารชนิดใด?

ก. Abamectin

ข. Carbamate

ค. Organophosphate

ง. Organochlorine

จ. Pyrethroid

ACh synthesis, stroage and release

ACh- AhE Reaction

What is the mechanism of OP &CB poisoning?

Acetylcholine (Ach)

ToxidromesToxidrome Cholinergic Muscarinic Cholinergic Nicotinic

Vital signs ↓HR, ↓BP ↑HR, ↑BP

Mental Stutus Lethargy-coma

Symptoms Diarrhea, vomitting,

blurred vision

Motor weakness

Signs Salivation, diaphoresis, miosis

Fassiculation

Paralysis

Substances Pilocarpine

Mushroom

Organophosphates

Carbamates

Tobacco

Organophosphates

Carbamates

ชาย 20 ป

มีผูพบผูปวยนอนหมดสติอยูในสวน มีน้ําลายฟูมปาก พบขวดสารฆาแมลงตกอยูขางตัว

ตรวจรางกาย ที่ ER

BP 160/80 mmHg, HR 180/min., RR 20/min. shallow respiration

T 36.5 C

Unconscious, not response to pain stimuli, pupils 2 mm.

Hypersecretion with bilateral wheezes

Increased bowel sounds

CNSNicotinic

Muscarinic

ชาย 20 ป

Diagnosis:

Organophosphorus or Carbamate poisoning

Differential Diagnosis of “Unconsciousness with hypersecretion and small pupils”

– Abamectin insecticide poisoning

Abamectin

ชาย 20 ป

Diagnosis:

Organophosphorus or Carbamate poisoning

Differential Diagnosis of “Unconsciousness with

hypersecretion and small pupils”

– Abamectin insecticide poisoning

– Pyrethroid insecticide poisoning

lambda-cyhalothrin 2.5% W/V

ชาย 20 ป

Diagnosis:

Organophosphate or Carbamate poisoning

Differential Diagnosis of “Unconsciousness with hypersecretion and

small pupils”

– Abamectin insecticide poisoning

– Pyrethroid insecticide poisoning

– Chlorophenoxy herbicide poisonings

Chlorophenoxy herbicides (2,4-D)

ชาย 20 ป

Diagnosis:

Organophosphate or Carbamate poisoning

Differential Diagnosis of “Unconsciousness with hypersecretion and small pupils”

– Abamectin insecticide poisoning

– Pyrethroid insecticide poisoning

– Chlorophenoxy herbicide poisonings

– Mushroom poisoning (Amanita pantherina, เห็ดเกลด็ดาว)

– Cholinergic drugs poisoning

Classification of Insecticide Exposure(Ramathibodi Poison Center: 2001-2006)

6,740 Cases

Organophosphorus

21%

Pyrethroid

25%

Abamectin

3%

Others

5%

Combined

12%

Unknown

5%Organochlorine

4%

Carbamate

25%

Anticholinesterase-AChE Reactions

Organophosphorus VS. Carbamate Poisoning

Reversible vs. Irreversible Inhibition

– Reversible vs. Irreversible clinical poisoning

– Time to recover (duration of clinical course)

Management of

Organophosphate & Carbamate Poisoning

General Management

Specific Treatment

Management of OP & CB Poisoning

Supportive Care

– Vital signs

– Respiration: • secretion block and airway obstruction

• respiratory motor weakness

– Seizure

Specific Treatment

Airway

Skin

Parenteral

GI.

Tissues &Organs

MDAC.

Decontamination Increase Elimination

Antidotes

Hemodialysis, Hemoperfusion

Specific Treatment

Decontamination:

– NG tube irrigation

Head DownLeft Lateral

Decubitus In Awake Patient

Limit! 1 hours after ingestion only

Specific Treatment

Decontamination:

– NG tube irrigation

– Activated Charcoal 1 g/kg orally or per gastric tube

Antidotes

Antimuscarinic effects

“ Atropine”

Antinicotinic effects

“ 2 PAM ”

CNS (seizure)

“Diazepam”

Muscarinic Effects

SecretionHeart RatePupil size

Atropine

Atropine

Clinical Parameters for titration

– Secretion

– Heart rate

– Pupil diameters

Choices for administration

– intermittent iv. bolus

– continuous iv. infusion

Atropine

Endpoints:

– Minimal secretion AND/OR

– Heart rate > 60/min., or stable hemodynamics

ESTERATICSITE

Nicotinic EffectsMuscarinic Effects

(Muscle Weakness)

2-PAM

หญิงอายุ 20 ป

PI 6 ชั่วโมงกอน กินน้ํายาลางหองน้ํา “เปดโปร” ประมาณ 50 ml.

หลังกินมีอาการแสบคอมาก และปวดทองโดยเฉพาะบริเวณลิ้นป

PE P 110/min, BP 90/60, RR 24/min, T 37.8 ๐C

Erythema or soft palate and posterior pharynx, no stridor

Lung : clear

Abdomen : tender at epigastrium,

no guarding or rigidity, normal bowel sound

Hydrochloric acid 8.5%

Sodium hypochlorite 2.7%

Hydrochloric acid 15%

Caustic Agents

Irritant Corrosive (caustic) agent

SoapNonionic detergentAnionic detergent

AcidAlkali

Cathionic detergentHypochlorite

Head DownLeft Lateral

Decubitus In Awake Patient

Limit! 1 hours after ingestion only

Contraindication for Gastric Lavage

Corrosive Agents

Drugs caused rapid deterioration of consciousness

Ineffectiveness of Activated Charcoal

Strong Acid & Alkali

Alcohol

Cyanide

Elemental Metal

Management of Caustic ingestion

Mild gastroesophageal injury– Supportive treament only

Moderate to Severe (significant) gastroesophageal injury– Supportive treatment

– Endosccopy for evaluation the injury

– Parenteral nutrion (TPN, PPN)

– + steroid

– Observe for its complication• GI Bleeding

• GI perferation

• Infection

ชาย 22 ป

มีญาตพิบหมดสตใินหองนอนกอนมา รพ. ครึ่งชั่วโมง

PE BP 80/50 mmHg, HR 110/min, RR 8/min, T 36 C

Unconscious, not response to pain

Pupil 1 mm. in diameter, not react to light

No localizing sign

Lung: fine crepitation bilateral

Otherwise: normal

Therapeutic Diagnosis for Unconscious Patients

50% Dextrose in Water 50 ml.

Naloxone 2-10 mg iv

Thiamine 50 -100 mg iv.

Psychotropic Agents

Sedative Hypnotics

Benzodiazepines

Antidepressants

– Tricyclic antidepressants

– Selective serotonin reuptake inhibitors

Antipsychotics

Opiates

Barbiturates

Stimulant Hallucinogens

Amphetamine & derivatives

Cocaine

Caffeine

Marihuana

LSD

Ketamine

Volatile substance

Autonomic (ANS.) Signs

Pulse

Blood Pressure

Respiration

Temperature

Skin

Secretion

Bowel sound & Bowel

movement

Urinary Bladder

Pupils

Differentiate between Structural vs. Metabolic

– Equal in Size?

– React to light?

Differentiate Among the Causative Agents

– Nonspecific

– Interpretation with Precaution

ชาย 22 ป

มีญาตพิบหมดสตใินหองนอนกอนมา รพ. ครึ่งชั่วโมง

PE BP 80/50 mmHg, HR 110/min, RR 8/min, T 36 C

Unconscious, not response to pain

Pupil 1 mm. in diameter, not react to light

No localizing sign

Lung: fine crepitation bilateral

Otherwise: normal

Suspected CNS Suppression Intoxication

Anticholinergic Signs

Respiratory Suppression

Constricted Pupils

Opiates

Yes

Yes

No

Opiod Overdose

Diagnostic Tools

– Therapeutic Diagnostic: Naloxone

– Urine opiod

Suspected CNS Suppression Intoxication

Anticholinergic Signs

Respiratory Suppression

Constricted Pupils

Opiates

Barbiturate

Yes

Yes

No

No

Barbiturate Overdose

Diagnostic Tools

– Can mimic brain death

– Skin Blisters (6%)

Barbiturate Overdose

Diagnostic Tools

– Can mimic brain death

– Skin Blisters (6%)

– Blood & urine barbiturate

– Therapeutic diagnostic: None,

– But need to R/O opiate toxicity

Drugs Eliminated by

Multiple Doses of Activated Charcoal

Phenobarbital

Phenytoin

Theophylline

Salicylates

Carbamazepine

Dapsone

Choice of Hemodialysis & Hemoperfusion

Hemodialysis

Lithium

Bromide

Ethanol

Methanol

Ethylene Glycol

Salicylates

Hemoperfusion

Barbiturate

Theophylline

Disopyramide

Meprobamate

Suspected CNS Suppression Intoxication

Anticholinergic Signs

Respiratory Suppression

Constricted Pupils

Benzodiazepine

Opiates

Barbiturate

Yes

Yes

No

No

No

Benzodiazepine Overdose

Diagnostic Tools

– Blood & Urine Benzodiazepine

– Therapeutic Diagnostic: ?? Flumazenil

Suspected CNS Suppression Intoxication

Anticholinergic Signs

Respiratory Suppression

Constricted Pupils

Dilated PupilsTCA

Benzodiazepine

Opiates

Barbiturate

YesYes

Yes

Yes

No

No

No

Tricyclic Antidepressants (TCA) Overdose

Diagnostic Tools

– Blood & Urine TCAs

– EKG: Widening of QRS complexes

R in aVR

– Therapeutic Diagnostic: None

QRS Complexes As a Predictor for TCAs Toxicity

QRS Duration Risk

> 0.10 sec Seizure

>0.16 sec Ventricular Arrhythmias

Suspected CNS Suppression Intoxication

Anticholinergic Signs

Respiratory Suppression

Constricted Pupils

Dilated PupilsTCA

Phenothiazine

Benzodiazepine

Opiates

Barbiturate

YesYes

Yes

Yes

NoNo

No

No

หญงิ 20 ป นักศึกษา

6 ชั่วโมงกอน รับประทานยาพาราเซทตามอล 60 เม็ด

2 ชั่วโมงกอน มีอาการคลื่นไสอาเจยีนหลายครั้ง ญาตจิึง

นําสง รพ.

ตรวจรางกายไมพบความผิดปกตใิดๆ

OH

NHCOCH3

Glucoronide

NHCOCH3

Sulfate

NHCOCH3

O

NHCOCH3

OH

NHCOCH3

OH

NHCOCH3

X

Glutathione

GSH

+

Cell Death

KIDNEYS

NAPQI

PARACETAMOL

Clinical Stages of Paracetamol Poisoning

Stage 1 (12 - 24 hours post-ingestion):

nausea, vomiting, anorexia, diaphoresis

Stage 2 ( 24 - 48 hours):

Clinically improved,

↑Transaminase enzymes, ↑ Bilirubin, ↑ Prothrombin Time

Stage 3 (72 - 96 hours):

Peak hepatotoxicity

Stage 4 (7 - 8 days):

Recovery

What should predict the risk to develop paracetamol

induced hepatic injury in the early phase?

The blood paracetamol level

4 248 12 16 20 Hours after ingestion

200150

90% of cases will have enzyme > 1,000 if no Treatment

60% of cases will have enzyme > 1,000 if no Treatment

300

Recommending of Treatment

From Rumack BH, et al. Arch Intren Med 1981;141:380-5.

OH

NHCOCH3

Glucoronide

NHCOCH3

Sulfate

NHCOCH3

O

NHCOCH3

OH

NHCOCH3

OH

NHCOCH3

X

Glutathione

GSH

+

Cell Death

KIDNEYS

NAPQI

N-Acetylcysteine

PARACETAMOL

N-acetylcysteine regimens

Oral Regimen

– LD 140 mg/kg

– MD 70 mg/kg every 4 hours 17 doses

IV. Regimen

– LD 150 mg/kg iv drip in 15 -30 min.

– MD 50 mg/kg iv. drip in 4 hours followed by

100 mg/kg iv. drip in 16 hours

Hepatic injury and Dead in patients treated with NAC(Line 200)

Treatment group N % of liver

injury

% Dead from

liver failure

Supportive treatment only 57 58.0 5.3

Time of delayed NAC treatment

< 10 hrs 527 6.1 0.0

10 -24 hrs 953 26.4 1.1

< 24 hrs 1,462 19.1 0.7

สายดวน: 1367, 1330โทร: 02-201-1083, 02-354-7272

Recommended