household toxicity, pesticides, hydrocarbons and rodenticides

compare between acids and alkalis toxicity type, mechanism and depth

acids: coagulative necrosis, forms eschae limits penetration, self limiting, located in Stomach

alkali: liquefactive necrosis, saponification of fats allowing continued penetration, deeper, located in esophagus

mention phases of lesion development of corrosives

inflammation 24-48 hrs; acute cellular necrosis

sloughing phase:4-7days: cells slough off leaving ulcers and perforations

granulation phase 2 weeks: collagen deposition, new tissue formation

cicatrization phase 2-4 weeks: dense fibrous tissue formation and potential stricture development

menyion acute complications of corrosives

upper airway obstruction larynx edema

GIT hemorrhage

esophageal or gastric perforation

shock: neurogenic or hypovolemic

delayed complications of corrosives

mediastinitis

pericarditis

esophageal stricture

tracheoesophageal fistula

mpyloric stenosis

malnutrition, dehydration and cachexia

investigations to diagnose GIT lesions in corrosives and CONTRAINDICATIONS

upper GI endoscopy

CI:

1. airway obstruction

2. clinical signs of perforation

3. severe hemodynamic instability

severity grading and prognosis

Grade I: mucosal erythema and edema, excellent prognosis

grade II: mucosal ulcer, hemorrhage and pseudomembranes, good with treatment

grade Iii: deep ulcers, necrosis, high complications

mention complications of corrosives and how to diagnose them

pneumomediastinum in esophageal perforation - chest X-ray

free air under diaphragm, gastric perforation - abdominal X-ray

esophageal stricture - barium swallow after 21 days

extent of injury - CT scan of chest/abdomen

anemia- CBC

acid base status - ABG

assess renal function - electrolytes and BUN, and serum creatinine

blood glucose levels

emergency treatment of corrosives

1. secure airway immediately

2. dilute carefully

3. areange early endoscope

4. monitor closely for complications

5. provide adequate pain relief

6. anti shock measures

7. no otal intervention

supportive treatment of corrosives

1. nutritional support

2. acid suppression

3. antibiotics

4. corticosteroids

surgical intervention and indications for corrosives

emergency: sever hemorrhage, perforation and grade Iii injury

elective: delayed,

1. esophageal stricture dilatation: stricture

2. esophageal stenting: refractory stricture

3. esophageal replacement: in case of severe non-dilatable strictures

long term follow up for corrosives

for grade II and III injuries:

1. regular follow up for 1 year

2. serial esophagogram to detect stricture formation

3. endoscopic surveillance

4. nutritional assessment

button batteries mechanism of injury

1. corrosive effects: alkaline content

2. pressure necrosis

3. heavy metal toxicity

treatment of button batteries

1. airway assessment

2. location based management: remove in trachea or esophagus and symptomatic stomach,

3. for asymptomatic stomach: stool examination, x ray in 4-7 days, return if symptoms develop

4. if battery in intestine: monitor, if battery stops moving or becomes symptomatic, remove, most batteries beyond stomach pass spontaneously

pathophysiology of phenol

general protoplasmic poison:

1. cell membrane disruption

2. protein coagulation

3. coagulative necrosis

4. systemic absorption leading to multiorgan toxicity

routes of ingestion of phenol

1. ingestion

2. inhalation

3. skin exposure(rapid and extensive)

4. eye exposure(vision loss)

characteristic symptoms of phenol

phenol odor

distinctive painless skin lesions

dark olive green urine

characteristic presentation of corrosives

spontaneous vomiting

hoarseness and stridor

dysphagia and drooling

hemetamesis and melena

investigations for phenol toxicity

1. urine studies

2. renal function

3. hematological: CBC, methemoglobin(cyanosis), decreased hemoglobin and RBCs(hemolysis)

4. liver function test

5. ECG for arrhythmia

6. chest x ray if inhalation exposure

treatment of phenol

emergency: ABCD

decontamination:

1. for ingestion: gastric lavage within 1 hour

2. inhalation: remove victim, expose to fresh air, administer oxygen and monitory respiratory complications

3. skin: immediate and prolonged washing, remove contaminated clothing, avoid scrubbing

4. eye exposure: flush and irrigate for 15-30 mins, check corneal pH, urgent opthalmology consultation

specific treatment:

1. for methemoglobinemia: methylene blue

2. acute kidney injury: hemodialysis, alkalinize urine if myoglobinuria, aggressive fluid resuscitation

kerosene toxicity mechanism

pulmonary:

1. direct chemical injury to repsiratory epithelium

2. surfactant disruption- alveolar collapse

3. increased capillary permeability => pulmonary edema

4. risk of secondary bacterial infection

CVS depression

cardiac sensitisation to catecholamines - arrhythmia

GI mucosal irritation

timeline of kerosene toxicity

0-2 hrs: GI and initial resp. symptoms(tachypnea)

2-6 hours: peak resp symptoms, distress and dyspnea

6-24 hours: chest x ray changes appear

more than 48 hrs: possible secondary bacterial infection

investigations of kerosene

pulse oximetry

chest x ray(4-6hrs)

ABG

CBC

tests for toxic additives

critical rules of management of kerosene

no vomiting

no GL or AC

no prophylacatic antibiotics

critical points of management of corrosives

no vomiting, GL, AC or neutralising agents

treatment of kerosene

emergency: ABCDE

decontamination:

1. remove contaminated clothes

2. wash skin and eye irrigation

supportive treatment:

1. bronchodilators

2. ventilatory support

3. antibiotics: not prophylactic, only with 2ry infection

4. #corticosteroids: not recommende

discharge criteria for kerosene toxicity

asymptomatic 6 hrs

normal vitals and chest exam

normal oxygen saturation

routes of exposure for organophosphates (pesticides)

dermal(slower but common in farmers) 1-4 hrs

ingestion(suicidal, fastest and most severe) 30 mins to 2 hours

inhalation(intermediate in farmers) 15 mins-1 hour

pathophysiology of OPC(pesticides)

irreversible inhibition of acetyl choline esterase by phosphorylation

accumulation of acetyl choline at netve endings

continuous overstimulation of receptors

affects true cholinesterase (RBC AChE) and pseudocholinesterase (plasma AChE)

aging occurs after 24-48 hours

most important clinical manifestations of OPCs

DUMBELS

bronchospasm, bronchorrhea

respiratory failure: most common cause of death

anxiety

fasciculations

investigations for OPC toxicity

specific: cholinesterase enzyme levels:

1. pseudocholinesterase: easier, better and more available

2. true AChE: more accurate indicator

ECG

ABG

serum electrolytes(hypokalemia)

serum glucose(hyperglycemia

Liver and kidney function tests

chest X-ray

treatment of OPCs(pesticides)

stabilisations: ABCD

decontamination:

dermal:

1. healthcare worker protection is essential: wear gloves, gowns and avoid contact with contamination clothing

2. remove all contaminants, wash skin thoroughly, pay attention to hair, nails and skin folds, cut hair if it retains odor

oral: gastric lavage(1-2 hrs and protect airways first) and AC(1-2 hrs)

antidote:

1. atropine comp for muscarinic only, doesn't affect nicotinic effects and doesn't reactivate AchE

2. oximes(before aging): reactivates AchE, reverse all effects, (obidoxime)

supportive treatment: respiratory support, seizure control(BZDs, fluid management, electrolyte balance and monitoring

atropine dosing and endpoints for OPCs

adults: 1-2mg IV every 10-20 mins, continue till atropinisation

pediatric: 0.03-0.05mg/kg IV(min 0.1 mg) every 10-20 minutes

Endpoints:

1. clear lung fields on auscultation

2. adequate oxygenation >90%

3. reduction in bronchial secretions

complications of OPC poisoning

1. intermediate syndrome: 24-96 hours after apparent initial recovery, not responsive to antidotes, after cholinergic crisis resolves, overall weakness(neck, palsy, tendon reflex and limbs and respiratory ms.

2. organophosphorus induced delayed neuropathy: 2-3 weeks after exposure due to neuropathy target esterase(NTE), unresponsive to antidotes, not related to AChE inhibition partial recovery(months to years), may cause permanent disability. , starts with burning in fret, progressive weakness, tendon reflexes loss and sensory loss

routes of absorption and mechanism of carbamates

dermal, ingestion, inhalation.

reversible inhibition AchE by carbamylation, hydrolyzes within hours,

carbamates vs OPCs

treatment of carbamates

same as OPCs

EXCEPT: no oximes but considered if OPC and carbamate congestion

phosphides modes of toxicity and mechanism

suicidal, accidental and occupational

chemical reaction: on contact with water, phosphides liberate phosphine gas

Toxic mechanism: rapidly absorbed

inhibits cytochrome c oxidase enzyme in mitochondrial ETC blocking aerobic metabolism, resulting in:

1. decreased ATP

2. lactic acid accumulation (metabolic acidosis

3. cellular death

mention phases of phosphides toxicity and main problems

acute phase(1-24 hrs): GIT (black vomitus with rotten fish or garlic odor) , respiratory(ARDS, dyspnea and resp failure) and cardiovascular (most serious), (arrhythmia, cardiac arrest(most common cause of early death). neurology(coma(bad prognosis)), metabolic acidosis

phase 2: apparent recovery(may be absent) 24-48 hrs)

phase 3: delayed toxicity phase 36 hrs- 7 days:

1. severe hepatotoxicity: prolonged PT/INR, acute liver failure, jaundice

2. renal toxicity

3. multiorgan failure: DIC, death from cardiovascular collapse of multi organ failure

investigations of rodenticides(phosphides)

1. ECG

2. ABG

3. serum electrolytes

4. cardiac markers

5. liver function tests(AST, ALT, PT/INR(crucial), serum billirubin)

6. renal function test

7. blood glucose

8. chest x ray

treatment of phosphide poisoning

ABCD,

decontamination: GL with paraffin or coconut oil to neutralise gastric acid, reduce phosphine gas liberation,

AC is contraindicated

specific:

1. magnesium sulfate: cardioprotective

2. N-acetylcysteine: antioxidant, hepatoprotective, free radical scavenger

3. IV sodium bicarbonate: sever metabolic acidosis pH<7.2

supportive treatment:

1. fluid management

2. correct electrolyte abnormalities

3. cardiovascular support

4. hepatic support(vit K and FFP)

5. hemodialysis in renal failure