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Y3R2 - Toxicology ☠️ > L3: Caustics > Flashcards

L3: Caustics Flashcards

1
Q

Def of Corrosives

A
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2
Q

Classification of Corrosives

A
  • Mineral acids
  • Organic acids
  • Alkalies
  • Corrosive salts
  • Button batteries
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3
Q

Examples of corrosive Organic acids

A

Carbolic Acid “Phenol”
Oxalic Acid
Acetic Acid.

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3
Q

Examples of corrosive mineral acids

A

Sulphuric Acid
Nitric Acid
Hydrochloric Acid.

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3
Q

Examples of corrosive salts

A

Mercuric Chloride.

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3
Q

Examples of corrosive alkalis

A

Caustic Potash
Na Hydroxide
Ammonium Hydroxide.

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4
Q

what do button battries contain?

A
  • Contain in mercuric chloride
  • used in watches and calculators.
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5
Q

manner of poisoning by Corrosives

A

In children: 85% accidentally ingested in children between 1-3 years.

In adult: Intentional exposures by adults are more significant (done by suicidal patients).

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5
Q

what are forms of corrosives?

A

bleach, household cleaners, paint and rust removers and strong lyes.

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6
Q

Clinical picture of Corrosive Toxicity

A
  • Patients who have ingested alkaline or acid agents have similar initial. presentations
  • They most commonly affect gastrointestinal, respiratory, eye and skin.
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7
Q

GIT manifestations in Corrosive Toxicity

A
  • Pain
  • Dysphagia
  • Others
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8
Q

GIT Pain in Corrosive Toxicity

A
  • Corrosions and burning pain of of lips and oral cavity.
  • Severe chest or abdominal pain (in esophageal or gastric perforation)
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9
Q

what is the most common symptom of Corrosive Toxicity?

A

Acute dysphagia

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10
Q

Dysphagia in Corrosive Toxicity

A
  • Dysphagia (inability to tolerato oral fooding)

Acute dysphagia: The most common symptom

Chronic dysphagia: Stricture formation

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11
Q

Other GIT Symptoms in Corrosive Toxicity

A
  • Drooling
  • Hypersalivation
  • Vomiting
  • Hematemesis
  • Shock
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12
Q

Does Presence or absence of oral lesions predict severity of burn?

A

No

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13
Q

Mechanism of Respiratory manifestations in Corrosive Toxicity

A
  • By Direct exposure of upper respiratory tract to corrosive substance, inhalation of corrosive gases

(e.g. chlorine and ammonia) and aspiration of vomitus

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14
Q

respiratory Manifestations of Corrosive Toxicity

A
  • Injury in Upper respiratory tract: (Epiglottitis, laryngeal edema & ulceration)
  • Stridor & Hoarseness.
  • Dysphonia & Aphonia
  • Dyspnea, Wheezing & Coughing.
  • Pneumonitis “Impaired gas exchange & Pulmonary edema “Non-cardiogenic”
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15
Q

Systemic manifestations of Corrosive Toxicity

A
  • Can occur after inhalation, skin exposure or ingestion of agents with systemic effects.
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16
Q

what are corrosives that cause systemic manifestations?

A
  • Hydrofluoric acid, Oxalic acid and Carbolic acid.
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17
Q

Complications of Corrosive Toxicity

A
  • Early
  • Late
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18
Q

Early complications of Corrosive Toxicity

A
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19
Q

Late Compliacations of Corrosive Toxicity

A
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20
Q

Laboratory Investigations of Corrosive Toxicity

A
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21
Q

Radiological investigations of Corrosive Toxicity

A
  • X-rays of the chest and abdomen
  • CT scans
  • Endoscopy.
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22
Q

X-ray of the chest & abdomen in Corrosive Toxicity

A
  • Free mediastinal and intraperitoneal air adjacent to liver
  • Pulmonary aspiration and Chemical pneumonitis.
  • Impacted button batteries
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23
Q

what does Free mediastinal and intraperitoneal air adjacent to liver denote in Corrosive toxicity?

A

esophageal or gastric perforation

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24
Q

what CT Scans are done in Corrosive Toxicity?

A

Barium swallow CT scan

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25
Q

Time of doing Barium swallow CT Scan in Corrosive Toxicity

A

Follow-up contrast studies 3-4 weeks after the injury if dysphagia is present.

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25
Q

when sould EGD by Done in Corrosive Toxicity?

A
  • Should be performed within 12 to 24 hours after ingestion.
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26
Q

Endoscopy in Corrosive Toxicity

A

Esophagogastroduodenoscopy (EGD)

  • Flexible endoscopy is the standard diagnostic tool in symptomatic patients.
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27
Q

Aspects of TTT in Corrosive Toxicity

A
  • Observation
  • Emergency and supportive measures
  • Decontamination
  • Symptomatic treatment
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28
Q

Observation in Corrosive Toxicity

A

Asymptomatic & Symptomatic

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29
Q

Observation of asypmtomatic patients in Corrosive Toxicity

A
  • Asymptomatic case with unintentional caustic ingestions should be subject to close observation and monitoring for 4 hours, without the need for endoscopy.
  • If the patient remains asymptomatic and able to eat and drink, he can be discharged with appropriate follow-up.
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30
Q

Observation of sypmtomatic patients in Corrosive Toxicity

A
  • All symptomatic cases require admission to the intensive care unit should avoid any oral intake because of risk of perforation.
31
Q

Emergency TTT in Corrosive Toxicity

32
Q

Decontamination in Corrosive Toxicity

A
  • Inhalation
  • Skin & Eyes
  • Ingestion
33
Q

RESP Decontamination in Corrosive Toxicity

A
  • Remove from exposure
  • Give supplemental oxygen if available.
34
Q

Skin & Eyes Decontamination in Corrosive Toxicity

A
  • Remove all clothing
  • Wash skin and irrigate eyes with copious water or saline.
35
Q

Gastric Decontamination in Corrosive Toxicity

A

Prehospital & Hospital

36
Q

Prehospital gastric Decontamination in Corrosive Toxicity

A
  • DO Dilution: With 1-2 cups of milk or water
  • Early & Late
  • Do not do Neutralization
37
Q

Hospital Decontamination in Corrosive Toxicity

37
Q

Early dilution in Corrosive Toxicity

A

(Recommended)

  • Within the first few minutes after ingestion.
  • In alert patients who are not vomiting, can tolerate liquids, have no airway compromise and not complaining chest or abdominal pain.
37
Q

Late dilution in Corrosive Toxicity

A
  • not recommended because vomiting may occur.
38
Q

Neutralization in Corrosive Toxicity, Is it indicated?

A

No

  • Do not give pH-neutralizing solutions (diluted vinegar or bicarbonate), As it worsen tissue damage by forming gas and exothermic reaction.
39
Q

Symptomaic TTT in Corrosive Toxicity

A
  • Parental nutrition
  • Gastric acid reduction
  • Antiemetics
  • Analgesic
  • Corticosteroids
  • Antibiotics
  • Surgical consultation
  • Endoscopy
40
Q

Is oral intake Recommended in Corrosive Toxicity?

A

No, Withholding oral intake until the condition stabilized

41
Q

Parentral nutrition in Corrosive Toxicity

A

Total parenteral nutrition should be instituted rapidly.

42
Q

Gastric acid reduction in Corrosive Toxicity

A

H2 Antagonists, and/or Proton Pump Inhibitors.

43
Q

Antiemetics in Corrosive Toxicity

A

In children to prevent additional esophageal injury from emesis

44
Q

analgesics in Corrosive Toxicity

A

Narcotic analgesics to reduce the pain.

45
Q

Corticosteroids in Corrosive Toxicity

A

Recommended:

  • In patients with circumferential superficial ulcers in esophagus after corrosive ingestion, Intravenous dexamethasone should be administered for a short period (3 days),
  • To prevent the development of esophageal stricture.

Not recommended:

  • In a patient with perforation
  • Corticosteroid may be harmful because they mask early signs of inflammation.
46
Q

Surgical consultation in Corrosive Toxicity

A

Immediate surgical consultation in esophageal and gastric perforation.

46
Q

Antibiotics in Corrosive Toxicity

A
  • Broad spectrum antibiotics (Cephalosporin) indicated in:
  • If their evidence of a superficial and deep ulcers in esophagus
  • If there is evidence of perforation.
  • If there is evidence of mediastinitis or peritonitis.
    If corticosteroid therapy is used.
47
Q

Endoscopy TTT in Corrosive Toxicity

A

Endoscopic dilation
- For esophageal stricture and gastric outlet obstruction.

Endoscopic removal
- “immediately” for any lodged Button Batteries in / esophagus or trachea.

48
Q

Characters of Phenol (Carbolic acid)

A
  • Phenol has characteristic odor.
49
Q

Uses of Phenol (Carbolic acid)

A
  • It is one of the oldest antiseptic agents.
  • Currently it is used as a disinfectant.
50
Q

Forms of Phenol (Carbolic acid)

A

Phenolic compounds include

  • Dinitrophenols
  • Hydroquinone
  • Hexachlorophone
  • Creosol
  • Chloroxylenol (in Detlol)
51
Q

Execretion of Phenol (Carbolic acid)

A
  • Its elimination half-life is 0.5-4.5 hours.
52
Q

Absorbtion of Phenol (Carbolic acid)

A
  • Rapidly absorbed following inhalation, skin exposure and ingestion.
53
Q

CP of Phenol (Carbolic acid)

A

It can give both local and systemic effects

53
Q

Manifestation due to local actions of Phenol (Carbolic acid)

A
  • Skin exposure
  • Eye exposure
  • Lung exposure
  • GIT exposure
54
Q

Skin exposure to Phenol (Carbolic acid)

A
  • It produces painless deep white patches that turn erythematous (red) and finally brown.
  • Phenol appears to have local anesthetic properties and can cause extensive damage before pain is felt.
55
Q

Eye exposure in Phenol (Carbolic acid)

A
  • Contact with eyes produces irritation and severe corneal damage.
56
Q

Lung exposure in Phenol (Carbolic acid)

A
  • Inhalation produces respiratory tract irritation, tracheobronchitis and chemical pneumonia.
57
Q

GIT Exposure in Phenol (Carbolic acid)

A
  • Ingestion causes diffuse local corrosions, pain, nausea, vomiting and diarrhea.
58
Q

Cardiac manifestations due to Phenol (Carbolic acid)

A
  • Hypotension and arrhythmias.
58
Q

Manifestations due to systemic action of Phenol (Carbolic acid)

A
  • Cardiac
  • Metabolic
  • Neural
  • Renal
  • Hematological
59
Q

Neural manifestations due to Phenol (Carbolic acid)

A

1st:
- Initial, transient CNS stimulation
(Agitation, confusion & seizures).

2nd:
- Followed rapidly by CNS depression.
(Lethargy or coma & respiratory arrest).

60
Q

Metabolic manifestations due to Phenol (Carbolic acid)

A
  • Acidosis and shock
61
Q

Renal manifestations due to Phenol (Carbolic acid)

A
  • Acute toxic glomer/onephritis which causes acute renal failure.
  • Oliguria (scanty urine) and albuminuria.
  • Urine Contains red cast and turns green if exposed to air (Due to presence of oxidative product of phenol).
62
Q

Hematological manifestations due to Phenol (Carbolic acid)

A

Hemolysis and methemoglobinemia in some phenolic compounds (eg, dinitrophenol and hydroquinone).

63
Q

TTT of Phenol (Carbolic acid) Toxicity

A
  • Emergency and supporlive measures
  • Decontamination
  • Antidote
  • Enhanced elimination
64
Q

Emergency TTT of Phenol (Carbolic acid) Toxicity

65
Q

Decontamination in Phenol (Carbolic acid) Toxicity

A
  • Inhalation
  • Skin and eyes
  • Ingestion
66
Q

RESP decontamination in Phenol (Carbolic acid) Toxicity

A
  • Remove victims from exposure and administer supplemental oxygen.
67
Q

Ingestion decontamination in Phenol (Carbolic acid) Toxicity

67
Q

Skin & Eyes decontamination in Phenol (Carbolic acid) Toxicity

A
  • Remove contaminated clothes and wash exposed skin with soapy water or olive oil.
  • Immediately flush exposed eyes with water or saline for at least 15 minutes.
68
Q

When to consider Gastric lavage in Phenol (Carbolic acid) Toxicity?

A

if:

  • A large dose has been ingested.
  • The patient’s condition is evaluated within 30 minutes.
  • The patient has oral lesions or persistent esophageal discomfort.
69
Q

When to avoid Gastric lavage in Phenol (Carbolic acid) Toxicity?

A
  • Gastric lavage is not necessary after small to moderate ingestions if activated charcoal can be given promptly.
70
Q

Caution during gastric lavage in Phenol (Carbolic acid) Toxicity

A

Care must be taken when placing the nasogastric tube

71
Q

Antidote in Phenol (Carbolic acid) Toxicity

A
  • No specific antidote is available.
  • Methylene blue: If methemoglobinemia occurs, administer it.
72
Q

Enhanced Elimination in Phenol (Carbolic acid) Toxicity

A
  • Repeated dose activated charcoal in hexachlorophene (excreted in the bile).

Y3R2 - Toxicology ☠️ (15 decks)

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