Poisoning Flashcards
(419 cards)
1
Q
A 3-year-old ingests an unknown amount of a household substance. What is the first step in management?
A
Ensure airway, breathing, and circulation (ABCs) are stable. Secure IV access, monitor vitals, and obtain a focused history and physical exam.
2
Q
What components are essential in the initial assessment of a poisoned child?
A
ABCs, vital signs, neurologic status (GCS), exposure history, time of ingestion, amount, route, and potential substances involved.
3
Q
What is the ‘coma cocktail’ and when is it used?
A
Empiric treatment for altered mental status includes oxygen, naloxone, glucose, and thiamine (in older children). Administer when diagnosis is uncertain.
4
Q
What are toxidromes and their clinical importance?
A
Toxidromes are characteristic clinical syndromes caused by specific classes of toxins, useful for narrowing down the likely agent.
5
Q
Describe the anticholinergic toxidrome.
A
Hot, dry skin, mydriasis, hyperthermia, urinary retention, dry mouth, tachycardia, and delirium. Seen in antihistamine, atropine, and TCA overdose.
6
Q
Describe the cholinergic toxidrome.
A
SLUDGE-M: Salivation, Lacrimation, Urination, Diarrhea, GI upset, Emesis, Miosis. Seen in organophosphate poisoning.
7
Q
Describe the opioid toxidrome.
A
Miosis (pinpoint pupils), respiratory depression, bradycardia, hypotension, and decreased consciousness.
8
Q
Describe the sympathomimetic toxidrome.
A
Tachycardia, hypertension, hyperthermia, mydriasis, agitation, diaphoresis. Seen with amphetamines, cocaine.
9
Q
What labs are essential in pediatric poisoning?
A
ABG, glucose, serum electrolytes, renal/liver function, coagulation, ECG, serum osmolarity, toxicology screen, specific drug levels as needed.
10
Q
What is the role of activated charcoal?
A
Given within 1 hour of ingestion of substances that are adsorbed by charcoal (1 g/kg, max 50 g). Contraindicated if airway is unprotected or corrosives/HCs ingested.
11
Q
When is gastric lavage indicated?
A
Rarely used. May be considered within 1 hour of life-threatening ingestion with no antidote, and protected airway.
12
Q
What is whole bowel irrigation and when is it used?
A
Administration of polyethylene glycol solution to flush the GI tract. Used in iron, body packers, or sustained-release drug overdose.
13
Q
What are the indications for naloxone in children?
A
Suspected opioid overdose with respiratory depression, miosis, and decreased consciousness. Start with 0.1 mg/kg IV or IM.
14
Q
When is urinary alkalinization indicated?
A
Used for salicylate and phenobarbital poisoning to enhance renal elimination. Requires careful monitoring of pH and electrolytes.
15
Q
What is the anion gap and how is it calculated?
A
AG = Na - (Cl + HCO3). Normal AG is 8–12. Elevated AG suggests metabolic acidosis due to toxin ingestion.
16
Q
What are causes of high anion gap metabolic acidosis in poisoning?
A
MUDPILES: Methanol, Uremia, DKA, Paracetamol/Propylene glycol, Iron/Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates.
17
Q
What is the osmolar gap and when is it useful?
A
OG = Measured osmolality - calculated osmolality. High OG suggests ingestion of methanol, ethanol, or ethylene glycol.
18
Q
What are common pediatric poisons requiring specific antidotes?
A
Paracetamol (NAC), iron (deferoxamine), organophosphates (atropine + pralidoxime), benzodiazepines (flumazenil, with caution), methanol (fomepizole).
19
Q
When should poison control or toxicology be consulted?
A
In any suspected moderate-to-severe poisoning, unknown substance, need for antidote or advanced management.
20
Q
What discharge criteria are used for pediatric poisoning?
A
Asymptomatic for appropriate observation period, normal mental status and vitals, no delayed-release ingestion, reliable caregivers and follow-up.
21
Q
What is the toxic dose of paracetamol in children?
A
Single ingestion >150 mg/kg or 7.5 g (whichever is lower) is considered potentially toxic and warrants evaluation.
22
Q
What is the mechanism of paracetamol toxicity?
A
Overdose depletes hepatic glutathione, leading to accumulation of NAPQI, a toxic metabolite that causes hepatocellular injury.
23
Q
What are the four clinical stages of paracetamol toxicity?
A
Stage I (0–24h): nausea, vomiting; Stage II (24–72h): right upper quadrant pain, liver enzyme rise; Stage III (72–96h): hepatic failure; Stage IV (4–14 days): recovery or death.
24
Q
When should paracetamol level be checked after ingestion?
A
Measure serum paracetamol level at 4 hours post-ingestion or as soon as possible thereafter.
25
What is the Rumack-Matthew nomogram?
A tool to assess hepatotoxicity risk from a single acute paracetamol ingestion based on serum level vs. time since ingestion.
26
When is NAC (N-acetylcysteine) indicated?
If paracetamol level is above the treatment line on nomogram, unknown time of ingestion with elevated level, or evidence of hepatotoxicity.
27
What is the mechanism of action of NAC?
NAC replenishes glutathione stores, enhances sulfate conjugation, and directly detoxifies NAPQI.
28
What are the routes of NAC administration?
Can be given orally or IV. IV is preferred in vomiting, altered mental status, or fulminant hepatic failure.
29
What is the oral NAC regimen?
140 mg/kg loading dose, followed by 70 mg/kg every 4 hours for 17 doses (total 72 hours).
30
What is the IV NAC regimen?
150 mg/kg over 1 hour, then 50 mg/kg over 4 hours, followed by 100 mg/kg over 16 hours (total 21 hours).
31
How is paracetamol toxicity managed if ingestion was <1 hour ago?
Activated charcoal (1 g/kg) may be given to reduce absorption if airway is protected.
32
What labs should be monitored during paracetamol toxicity?
LFTs (AST, ALT), INR, creatinine, glucose, electrolytes, arterial blood gas, and paracetamol levels.
33
What are signs of hepatotoxicity in paracetamol overdose?
Elevated AST/ALT, jaundice, coagulopathy, hypoglycemia, encephalopathy, and metabolic acidosis.
34
When should liver transplant be considered in paracetamol toxicity?
If pH <7.3 after fluid resuscitation, INR >6.5, creatinine >300 µmol/L, and grade III/IV encephalopathy (King’s College criteria).
35
Can chronic paracetamol overdose be toxic?
Yes. Repeated supratherapeutic dosing (e.g., >90 mg/kg/day for >1 day) can cause delayed toxicity.
36
What is the role of charcoal if NAC is given?
Activated charcoal may reduce NAC absorption if given orally; separate administration by at least 1 hour.
37
What are contraindications to NAC?
Absolute contraindications are rare. Caution with IV NAC in anaphylactoid reactions, but it can usually be restarted at a slower rate.
38
What is the prognosis after paracetamol overdose?
Excellent with early NAC. Poor prognosis in delayed treatment, massive overdose, or liver failure.
39
Is there a role for dialysis in paracetamol poisoning?
Rarely needed; may be considered in massive ingestion with high serum level, acidosis, renal failure, or altered consciousness.
40
How is paracetamol poisoning prevented in children?
Use childproof containers, proper dosing education, and limit household stockpiles.
41
What is the toxic dose of elemental iron in children?
Ingestion of >40 mg/kg elemental iron is potentially toxic; >60 mg/kg is considered severely toxic.
42
What are the common sources of iron poisoning?
Multivitamins with iron, prenatal vitamins, and iron supplements like ferrous sulfate, fumarate, or gluconate.
43
What are the clinical stages of iron poisoning?
Stage I (0–6h): GI symptoms; Stage II (6–24h): apparent improvement; Stage III (12–48h): systemic toxicity; Stage IV (2–3 days): hepatic failure; Stage V (weeks): gastric scarring.
44
What symptoms occur during Stage I of iron poisoning?
Nausea, vomiting, abdominal pain, diarrhea, hematemesis, and possible hypovolemic shock.
45
What is the hallmark of Stage III iron toxicity?
Metabolic acidosis, shock, hepatotoxicity, lethargy, seizures, and coagulopathy.
46
Why is the initial asymptomatic phase in Stage II dangerous?
It gives a false sense of recovery while systemic absorption and toxicity continue to progress.
47
What is the most reliable lab test to assess iron poisoning?
Serum iron level measured 4–6 hours after ingestion. Levels >350 mcg/dL indicate toxicity.
48
What is the role of abdominal X-ray in iron poisoning?
Can detect radiopaque iron tablets in the stomach or intestines; helpful but not always reliable.
49
What acid-base disturbance is common in iron poisoning?
High anion gap metabolic acidosis due to lactate accumulation and mitochondrial dysfunction.
50
When is deferoxamine indicated in iron poisoning?
If serum iron >500 mcg/dL, severe symptoms (shock, acidosis), or systemic toxicity.
51
How does deferoxamine work?
It chelates free iron to form ferrioxamine, which is water-soluble and excreted in urine.
52
What is a characteristic finding during deferoxamine therapy?
Orange-red (vin rose) colored urine due to excretion of ferrioxamine.
53
What are complications of deferoxamine therapy?
Hypotension, pulmonary toxicity, Yersinia infection with prolonged use, and allergic reactions.
54
What is the role of activated charcoal in iron poisoning?
Ineffective for iron binding; not recommended. Whole bowel irrigation is preferred for decontamination.
55
When is whole bowel irrigation used in iron poisoning?
In significant ingestion with radiopaque tablets on X-ray or sustained-release iron formulations.
56
How long should serum iron be monitored?
Check initial level at 4–6 hours, and repeat if symptoms persist or treatment is ongoing.
57
What are poor prognostic indicators in iron poisoning?
Initial shock, metabolic acidosis, high serum iron >1000 mcg/dL, elevated transaminases, and coagulopathy.
58
What is the lethal dose of elemental iron in children?
>60 mg/kg elemental iron can be lethal if untreated.
59
What organ systems are primarily affected by iron toxicity?
Gastrointestinal, hepatic, cardiovascular, CNS, and metabolic (acidosis).
60
How can iron poisoning be prevented?
Keep iron-containing supplements in child-proof containers, away from children, and educate caregivers on dosage.
61
What are organophosphates and where are they found?
Organophosphates are cholinesterase inhibitors found in insecticides, pesticides, and nerve agents.
62
What is the mechanism of toxicity in organophosphate poisoning?
They inhibit acetylcholinesterase, leading to accumulation of acetylcholine at synapses and overstimulation of muscarinic, nicotinic, and CNS receptors.
63
What is the mnemonic for muscarinic symptoms of organophosphate poisoning?
SLUDGE-M: Salivation, Lacrimation, Urination, Diarrhea, GI upset, Emesis, Miosis.
64
What are nicotinic symptoms of organophosphate poisoning?
Muscle fasciculations, cramps, weakness, paralysis, hypertension, tachycardia.
65
What are CNS symptoms of organophosphate poisoning?
Anxiety, confusion, seizures, coma, respiratory depression.
66
What is the difference between muscarinic and nicotinic effects?
Muscarinic effects are due to parasympathetic overactivation; nicotinic effects are due to stimulation at neuromuscular junctions and sympathetic ganglia.
67
What is the characteristic pupil finding in OP poisoning?
Miosis (pinpoint pupils), though mydriasis can occur in mixed poisonings.
68
How is OP poisoning diagnosed clinically?
Based on history of exposure and presence of cholinergic toxidrome. Response to atropine supports diagnosis.
69
What laboratory tests assist in diagnosis of OP poisoning?
Plasma pseudocholinesterase and RBC acetylcholinesterase levels are low but not always immediately available.
70
What is the immediate management of OP poisoning?
Decontamination (remove clothes, wash skin), ABCs, oxygen, IV access, and antidotes.
71
What are the antidotes for OP poisoning?
Atropine (muscarinic symptoms) and pralidoxime (reactivates acetylcholinesterase and treats nicotinic symptoms).
72
How is atropine dosed in pediatric OP poisoning?
Start with 0.02–0.05 mg/kg IV every 5–10 minutes until secretions dry and bradycardia improves.
73
How is pralidoxime dosed in children?
Loading dose: 25–50 mg/kg (max 2 g) IV over 30 minutes; may repeat or use continuous infusion.
74
What is atropinization?
The clinical endpoint of atropine therapy: clear lungs, dry secretions, normal heart rate and blood pressure.
75
Why is early pralidoxime administration important?
It must be given before 'aging' of the phosphorylated enzyme occurs, which renders the inhibition irreversible.
76
What is intermediate syndrome in OP poisoning?
Occurs 1–4 days post-exposure, with proximal muscle weakness, cranial nerve palsies, and respiratory depression.
77
What are delayed complications of OP poisoning?
Organophosphate-induced delayed neuropathy (OPIDN) characterized by distal motor neuropathy and gait disturbances.
78
What is the role of benzodiazepines in OP poisoning?
Used to control seizures associated with CNS cholinergic excess.
79
Is gastric lavage or activated charcoal useful in OP poisoning?
Activated charcoal may be useful if administered early with intact airway. Gastric lavage is rarely used.
80
How is OP exposure prevented in children?
Secure storage of insecticides, public awareness, use of protective clothing during spraying, and regulation of toxic substances.
81
What are the main sources of lead exposure in children?
Old paint, contaminated dust or soil, leaded pipes, imported toys or cosmetics, traditional remedies, and occupational exposure brought home by caregivers.
82
Why are children more vulnerable to lead poisoning?
They absorb lead more efficiently through the GI tract, have developing nervous systems, and are more likely to engage in hand-to-mouth behavior.
83
What blood lead level (BLL) is considered elevated?
A BLL ≥5 µg/dL is considered elevated. There is no safe threshold for lead exposure.
84
What are the early clinical signs of lead poisoning?
Anorexia, abdominal pain (lead colic), irritability, constipation, and developmental delay.
85
What are the neurological manifestations of lead poisoning?
Behavioral problems, learning disabilities, decreased IQ, hearing loss, encephalopathy, seizures, and coma at high levels.
86
What are the hematologic effects of lead toxicity?
Microcytic, hypochromic anemia with basophilic stippling due to inhibition of heme synthesis.
87
What is the classic GI symptom of lead poisoning?
Lead colic – intermittent, severe abdominal pain often without specific findings on exam.
88
How does lead affect renal function?
It can cause nephropathy with proximal tubular damage and aminoaciduria, glycosuria, and low molecular weight proteinuria.
89
How is lead poisoning diagnosed?
Confirmed by venous blood lead level (BLL); fingerstick testing is used for screening but must be confirmed.
90
What is the role of radiography in lead poisoning?
Abdominal X-ray may show radio-opaque flecks (paint chips), long bone X-rays may show lead lines (dense metaphyseal bands).
91
What is the treatment for mild lead poisoning (BLL <45 µg/dL)?
Remove the source of lead, provide nutritional support (iron and calcium), and monitor BLL periodically.
92
When is chelation therapy indicated in lead poisoning?
For symptomatic children or those with BLL ≥45 µg/dL.
93
What chelating agents are used in lead poisoning?
Dimercaprol (BAL), EDTA (CaNa2-EDTA), and succimer (DMSA). The choice depends on severity and symptoms.
94
What is the preferred chelator for moderate lead poisoning (45–69 µg/dL)?
Oral succimer (DMSA) is typically used for asymptomatic patients with BLL 45–69 µg/dL.
95
What chelators are used for severe lead poisoning (≥70 µg/dL or encephalopathy)?
Start with IM dimercaprol (BAL) plus IV EDTA in a hospital setting.
96
What are the side effects of chelation therapy?
Nausea, vomiting, rash, neutropenia (DMSA), nephrotoxicity (EDTA), and hypertension (BAL).
97
What long-term complications are associated with lead exposure?
Neurodevelopmental delay, decreased academic performance, behavioral problems, and growth impairment.
98
What public health measures reduce lead exposure?
Lead-safe housing, removal of lead paint, education, screening programs, and regulations on imported goods.
99
What nutritional interventions help reduce lead absorption?
Adequate intake of calcium, iron, and vitamin C lowers lead absorption from the gut.
100
How is lead poisoning monitored over time?
Regular follow-up with BLL measurements, developmental assessments, and home environment evaluation.
101
What are common sources of hydrocarbon exposure in children?
Kerosene, gasoline, lamp oil, lighter fluid, paint thinners, and mineral spirits.
102
What is the primary route of toxicity in hydrocarbon poisoning?
Aspiration into the lungs during ingestion or vomiting, leading to chemical pneumonitis.
103
Why are hydrocarbons particularly dangerous for children?
Low viscosity and high volatility promote aspiration even with small ingestions.
104
What are the early symptoms of hydrocarbon ingestion?
Coughing, choking, gagging, vomiting, and respiratory distress within 30 minutes of exposure.
105
What are pulmonary complications of hydrocarbon aspiration?
Chemical pneumonitis, hypoxia, ARDS, pulmonary edema, and respiratory failure.
106
What systemic effects can hydrocarbons cause?
CNS depression, arrhythmias (especially with halogenated hydrocarbons), hepatotoxicity, and renal damage.
107
What is the role of chest X-ray in hydrocarbon poisoning?
Indicated if the child is symptomatic; may show infiltrates or consolidation within 2–6 hours.
108
When should a child be admitted after hydrocarbon ingestion?
If symptomatic (cough, vomiting, respiratory distress), abnormal vitals, or abnormal chest X-ray.
109
Is activated charcoal useful in hydrocarbon poisoning?
No. Charcoal does not adsorb hydrocarbons effectively and increases aspiration risk.
110
Is gastric lavage recommended in hydrocarbon ingestion?
Generally contraindicated due to aspiration risk. May be considered if co-ingestants are life-threatening.
111
What is the mainstay of treatment for hydrocarbon poisoning?
Supportive care: oxygen, monitoring, and treatment of respiratory symptoms. No specific antidote.
112
What cardiovascular complications can occur?
Sensitization of myocardium to catecholamines leading to arrhythmias, particularly with halogenated hydrocarbons.
113
What are red flag signs indicating severe hydrocarbon toxicity?
Cyanosis, tachypnea, wheezing, hypoxia, altered mental status, and persistent vomiting.
114
How soon do pulmonary symptoms appear after aspiration?
Usually within 30 minutes to 2 hours; may worsen over 6–12 hours.
115
When can a child be safely discharged after hydrocarbon ingestion?
If asymptomatic for at least 6 hours with normal vitals and chest exam.
116
What are examples of hydrocarbons with systemic toxicity?
Aromatic hydrocarbons (e.g., benzene) and halogenated hydrocarbons (e.g., carbon tetrachloride, trichloroethylene).
117
What labs are helpful in severe cases of hydrocarbon poisoning?
ABG, chest X-ray, CBC, liver and renal function, ECG (for arrhythmias), and lactate.
118
What is the role of bronchodilators in hydrocarbon poisoning?
May be used in cases with bronchospasm or reactive airway symptoms.
119
Why is vomiting induction contraindicated in hydrocarbon ingestion?
Increases risk of aspiration and chemical pneumonitis.
120
How can hydrocarbon poisoning be prevented?
Proper labeling, childproof containers, secure storage away from food or drink, and caregiver education.
121
What are caustic substances and where are they found?
Caustics are strong acids or alkalis found in household cleaners, drain openers, toilet bowl cleaners, and industrial products.
122
What are the two main types of caustic agents?
Acids (e.g., sulfuric, hydrochloric acid) and alkalis (e.g., sodium hydroxide, potassium hydroxide).
123
How do alkalis cause tissue damage?
They cause liquefactive necrosis, penetrating deeply into tissues and increasing risk of perforation.
124
How do acids cause tissue injury?
They cause coagulative necrosis, often limited to the stomach, forming eschar that may limit depth of injury.
125
What are the early symptoms of caustic ingestion?
Oral burns, drooling, dysphagia, odynophagia, vomiting, and chest or abdominal pain.
126
What signs indicate severe esophageal or gastric injury?
Stridor, dyspnea, hematemesis, abdominal rigidity, and signs of perforation or shock.
127
Is vomiting or neutralizing agents recommended after caustic ingestion?
No. Inducing emesis or neutralizing agents increases risk of re-exposure and heat generation.
128
Is activated charcoal useful in caustic ingestion?
No. It is not effective and can obscure endoscopy or worsen injury.
129
What is the role of endoscopy in caustic ingestion?
Diagnostic endoscopy within 12–24 hours is recommended to assess the extent of esophageal and gastric damage.
130
When is endoscopy contraindicated in caustic ingestion?
Absolute contraindications: signs of perforation, severe respiratory distress, and hemodynamic instability.
131
What imaging is indicated in caustic ingestion?
Chest and abdominal X-rays if perforation is suspected. CT scan may assess extent of injury or complications.
132
What is Zargar’s classification in caustic injury?
A grading system (0–3b) used to classify mucosal injuries on endoscopy; grades 2b and 3 have high risk of stricture.
133
What is the management of mild caustic ingestion?
Supportive care with NPO status, IV fluids, and observation. Advance diet as tolerated if no injury.
134
When are corticosteroids considered in caustic ingestion?
Controversial. May be considered in grade 2b esophageal injury to reduce stricture risk, but benefit is uncertain.
135
What are long-term complications of caustic ingestion?
Esophageal strictures, pyloric stenosis, increased risk of esophageal carcinoma, and feeding difficulties.
136
What is the role of antibiotics in caustic injury?
May be used if there is evidence of perforation, infection, or severe injury requiring steroids.
137
When is surgery indicated in caustic ingestion?
In cases of perforation, necrosis, or uncontrolled bleeding. Emergency laparotomy or esophagectomy may be needed.
138
What is the risk of delayed complications?
Strictures may develop weeks after ingestion, and patients may require dilation or surgical intervention.
139
What precautions should be taken to prevent caustic ingestion?
Store chemicals in original containers, use child-resistant caps, and keep out of reach of children.
140
What are signs of perforation requiring urgent intervention?
Sudden severe pain, abdominal rigidity, subcutaneous emphysema, hypotension, or sepsis.
141
What are benzodiazepines and their clinical uses?
CNS depressants used for anxiety, seizures, sedation, muscle relaxation, and insomnia. Common agents include diazepam, lorazepam, and midazolam.
142
How do benzodiazepines cause toxicity?
By enhancing GABA-A receptor activity, leading to CNS depression, respiratory depression, and hypotonia.
143
What are typical clinical features of benzodiazepine overdose?
Drowsiness, slurred speech, ataxia, hypotonia, respiratory depression (rare with monotherapy), and coma.
144
What is the typical time course of benzodiazepine toxicity?
Symptoms appear within 30 minutes to 2 hours and can last longer depending on the agent’s half-life.
145
How is benzodiazepine overdose diagnosed?
Primarily clinical; confirmatory testing via urine drug screens can detect class but not severity.
146
What are risk factors for severe benzodiazepine toxicity?
Co-ingestion with alcohol, opioids, or other sedatives; young age; and pre-existing respiratory compromise.
147
Is gastric decontamination recommended in benzodiazepine overdose?
Activated charcoal may be used within 1 hour in significant, isolated ingestion if airway is protected.
148
What is the antidote for benzodiazepine poisoning?
Flumazenil, a GABA receptor antagonist, reverses CNS effects but must be used with caution.
149
When is flumazenil contraindicated?
History of seizures, benzodiazepine dependence, co-ingestion of pro-convulsant agents (e.g., TCAs), or suspected raised ICP.
150
What is the risk of using flumazenil?
Can precipitate seizures or withdrawal symptoms in dependent patients or with pro-convulsant co-ingestions.
151
How is flumazenil administered?
Initial dose is 0.01 mg/kg (max 0.2 mg) IV over 15 seconds, may repeat at 1-minute intervals to a max dose of 1 mg.
152
What is the mainstay of treatment for benzodiazepine overdose?
Supportive care: airway protection, oxygen, IV fluids, and close monitoring until symptoms resolve.
153
Do all benzodiazepines have the same toxicity profile?
No. Long-acting agents (diazepam) may have prolonged effects; some (midazolam) have faster onset and shorter duration.
154
How is pediatric accidental ingestion of benzodiazepines managed?
Assess airway, monitor vitals, observe for 6–12 hours depending on agent; rarely requires antidote unless severe.
155
What are withdrawal symptoms of benzodiazepines in chronic users?
Anxiety, agitation, insomnia, tremor, and seizures; can be life-threatening.
156
How does flumazenil affect chronic benzodiazepine users?
May precipitate acute withdrawal and seizures; use only in non-dependent, acute ingestion cases.
157
What supportive care is needed for severe benzodiazepine overdose?
Airway protection (may require intubation), respiratory support, IV fluids, and ICU monitoring.
158
What is the prognosis of isolated benzodiazepine overdose?
Generally excellent with supportive care; rarely fatal unless co-ingestants are involved.
159
What is the role of observation in benzodiazepine poisoning?
Observation for respiratory depression, mental status changes, and supportive care until resolution.
160
How can benzodiazepine poisoning be prevented?
Keep medications in childproof containers, away from children, and avoid overprescribing or unsupervised access.
161
What is carbon monoxide (CO) and how is it produced?
A colorless, odorless gas produced by incomplete combustion of carbon-containing fuels such as wood, gas, coal, and car exhaust.
162
What is the mechanism of CO toxicity?
CO binds to hemoglobin with 200–250 times the affinity of oxygen, forming carboxyhemoglobin (COHb) and impairing oxygen delivery to tissues.
163
Why is CO poisoning dangerous?
It causes cellular hypoxia despite normal oxygen saturation, leading to CNS and cardiac ischemia.
164
What are common sources of CO exposure in children?
Faulty heaters, enclosed fires, car exhaust in garages, gas stoves, generators, and charcoal grills.
165
What are the early symptoms of CO poisoning?
Headache, dizziness, nausea, vomiting, fatigue, and flu-like symptoms.
166
What are signs of severe CO poisoning?
Confusion, syncope, seizures, coma, hypotension, arrhythmias, myocardial ischemia, and lactic acidosis.
167
What is the diagnostic test of choice for CO poisoning?
Measurement of carboxyhemoglobin (COHb) level via co-oximetry on arterial or venous blood.
168
What is a normal COHb level?
Non-smokers: <2%; smokers: up to 10%. Levels >10% suggest exposure; symptoms often correlate poorly with levels.
169
What is the role of pulse oximetry in CO poisoning?
It is unreliable as it cannot differentiate oxyhemoglobin from COHb, giving falsely normal readings.
170
How is CO poisoning treated?
Immediate 100% oxygen via non-rebreather mask to displace CO from hemoglobin, reduce COHb half-life.
171
What is the half-life of COHb on room air and oxygen?
Room air: 4–6 hours; 100% O2: ~60–90 minutes; hyperbaric O2: ~20–30 minutes.
172
When is hyperbaric oxygen therapy (HBOT) indicated?
COHb >25%, neurologic symptoms, cardiovascular instability, pregnancy with COHb >15–20%, or loss of consciousness.
173
What are the neurological complications of CO poisoning?
Delayed neuropsychiatric syndrome (DNS): memory loss, personality changes, parkinsonism, and cognitive impairment.
174
How long after exposure can DNS appear?
Typically within 2–40 days after initial recovery.
175
What are ECG and cardiac findings in CO poisoning?
Myocardial ischemia, arrhythmias, elevated troponins, especially in high-risk or older children.
176
How is pediatric CO exposure different from adults?
Children are more vulnerable due to higher metabolic rate and smaller body mass; symptoms may develop faster.
177
What environmental clues suggest CO exposure?
Multiple family members with symptoms, winter heating use, indoor generators, or enclosed fires.
178
How is CO poisoning confirmed in an unconscious child?
Consider COHb level and environmental history. Treat empirically with 100% oxygen if suspected.
179
Can CO cross the placenta?
Yes. Fetal hemoglobin binds CO more avidly, increasing risk of fetal hypoxia and death.
180
How can CO poisoning be prevented?
Proper ventilation, regular maintenance of heating devices, CO detectors at home, and public education.
181
What is the source of salicylate poisoning in children?
Aspirin (acetylsalicylic acid), oil of wintergreen (methyl salicylate), and other over-the-counter medications.
182
What is the toxic dose of aspirin in children?
Acute ingestion of >150 mg/kg is potentially toxic; >300 mg/kg can be severe or life-threatening.
183
What is the mechanism of salicylate toxicity?
Uncouples oxidative phosphorylation, stimulates respiratory center, disrupts glucose metabolism, and causes metabolic acidosis.
184
What are early symptoms of salicylate poisoning?
Tinnitus, nausea, vomiting, hyperventilation, abdominal pain, and sweating.
185
What acid-base disturbance is characteristic of salicylate poisoning?
Mixed respiratory alkalosis (early) and high anion gap metabolic acidosis (later).
186
How does salicylate poisoning affect the CNS?
Confusion, agitation, hallucinations, seizures, cerebral edema, and coma in severe cases.
187
What are signs of severe salicylate toxicity?
Hyperthermia, metabolic acidosis, pulmonary edema, seizures, renal failure, and cardiovascular collapse.
188
What labs are essential in suspected salicylate poisoning?
Serum salicylate level, ABG, electrolytes, glucose, renal function, and anion/osmolar gap.
189
What is the therapeutic and toxic salicylate level?
Therapeutic: 10–30 mg/dL; Toxic: >30 mg/dL; Severe: >100 mg/dL (acute).
190
How often should salicylate levels be monitored?
Every 2 hours until levels decline and clinical stability is achieved due to delayed peak absorption.
191
What is the role of activated charcoal in salicylate poisoning?
Effective if given within 1 hour of ingestion. Multiple doses may be useful in sustained-release forms.
192
What is the role of urinary alkalinization?
Enhances renal clearance of salicylates. Use sodium bicarbonate to maintain urine pH 7.5–8.0.
193
When is hemodialysis indicated in salicylate poisoning?
Severe toxicity, salicylate level >100 mg/dL, refractory acidosis, renal failure, altered mental status, or fluid overload.
194
What are complications of salicylate poisoning?
Pulmonary edema, renal failure, seizures, cerebral edema, and cardiovascular collapse.
195
Why is glucose important in salicylate toxicity?
Glucose should be administered to symptomatic patients even with normal serum glucose due to neuroglycopenia.
196
What are contraindications to intubation in salicylate poisoning?
Avoid intubation unless absolutely necessary; can lead to abrupt CO2 rise and worsening acidosis.
197
What ECG changes may be seen in salicylate poisoning?
Nonspecific ST/T changes; QT prolongation may occur but arrhythmias are uncommon.
198
What are risks of using acetazolamide in salicylate poisoning?
It may worsen systemic acidosis and is not recommended.
199
What is the prognosis in salicylate poisoning?
Good with early recognition and treatment; delayed care or massive ingestion can be fatal.
200
How can salicylate poisoning be prevented?
Proper storage of aspirin-containing products, parental education, and use of child-resistant packaging.
201
What are common tricyclic antidepressants (TCAs)?
Amitriptyline, nortriptyline, imipramine, desipramine, clomipramine.
202
What is the mechanism of TCA toxicity?
Inhibition of norepinephrine and serotonin reuptake, sodium channel blockade, anticholinergic effects, and GABA antagonism.
203
What is the toxic dose of TCA in children?
As little as 10–20 mg/kg can cause severe toxicity; even one adult tablet may be dangerous.
204
What are the early symptoms of TCA poisoning?
Drowsiness, agitation, dry mouth, tachycardia, mydriasis, and urinary retention.
205
What are the anticholinergic effects seen in TCA poisoning?
Hyperthermia, flushed dry skin, mydriasis, tachycardia, ileus, urinary retention, and altered mental status.
206
What are the life-threatening effects of TCA toxicity?
Seizures, hypotension, arrhythmias, and coma.
207
What ECG findings are characteristic of TCA overdose?
Prolonged QRS (>100 ms), right axis deviation, QT prolongation, and terminal R wave in aVR >3 mm.
208
Why is QRS duration important in TCA poisoning?
QRS >100 ms predicts seizures; >160 ms predicts ventricular arrhythmias.
209
What is the first-line treatment for cardiac toxicity in TCA overdose?
IV sodium bicarbonate to narrow QRS and correct acidosis.
210
What is the mechanism of bicarbonate in TCA poisoning?
Alkalinizes serum (reducing TCA binding to sodium channels) and increases sodium concentration to overcome blockade.
211
What is the dosing of sodium bicarbonate in TCA poisoning?
1–2 mEq/kg bolus, repeated as needed; goal pH 7.45–7.55.
212
When are benzodiazepines used in TCA toxicity?
To treat seizures; avoid phenytoin due to possible cardiac depression.
213
Is charcoal useful in TCA overdose?
Yes, if given within 1 hour and if airway is protected.
214
When is intubation indicated in TCA poisoning?
For coma, seizures, or inability to protect airway; premedicate to avoid sympathetic surge.
215
Is dialysis useful in TCA overdose?
No. TCAs are highly protein-bound and not dialyzable.
216
How long should a child be monitored after TCA ingestion?
At least 6–12 hours; longer if symptomatic or if ECG changes persist.
217
What is the prognosis in TCA poisoning?
Potentially fatal, especially with seizures, coma, or arrhythmias. Rapid treatment improves outcomes.
218
What are signs of worsening toxicity despite therapy?
Refractory hypotension, wide QRS despite bicarbonate, arrhythmias, and persistent acidosis.
219
What adjuncts may be used for refractory hypotension?
Lipid emulsion therapy, norepinephrine or phenylephrine infusion.
220
How can TCA poisoning be prevented?
Keep medications out of children’s reach, use child-resistant containers, and monitor for intentional ingestion.
221
What are toxic alcohols and examples of each?
Methanol (found in windshield washer fluid), ethylene glycol (antifreeze), and isopropanol (rubbing alcohol).
222
What is the toxic mechanism of methanol and ethylene glycol?
Both are metabolized by alcohol dehydrogenase into toxic metabolites: formic acid (methanol) and glycolic/oxalic acid (ethylene glycol), leading to metabolic acidosis and organ damage.
223
What is the lethal dose of methanol or ethylene glycol in children?
As little as 0.5–1 mL/kg can be fatal without treatment.
224
What are the early signs of methanol poisoning?
Headache, dizziness, nausea, vomiting, visual disturbances ('snowfield vision'), and metabolic acidosis.
225
What are the key signs of ethylene glycol poisoning?
CNS depression, metabolic acidosis, calcium oxalate crystals in urine, renal failure, and hypocalcemia.
226
What acid-base disturbance is seen in toxic alcohol poisoning?
High anion gap metabolic acidosis with high osmolar gap.
227
How is osmolar gap calculated?
OG = Measured osmolality – Calculated osmolality; >10–15 mOsm/kg suggests toxic alcohol ingestion.
228
What is the role of calcium oxalate crystals in ethylene glycol poisoning?
Seen on urine microscopy; associated with renal tubular damage.
229
What is the antidote for methanol and ethylene glycol poisoning?
Fomepizole or ethanol (both inhibit alcohol dehydrogenase).
230
What is the dosing of fomepizole?
Loading dose 15 mg/kg IV, then 10 mg/kg every 12 hours. Increase to 15 mg/kg every 12 hours after 48 hours.
231
When is ethanol used as an antidote?
If fomepizole is unavailable; competes with toxic alcohols for alcohol dehydrogenase.
232
What is the role of hemodialysis in toxic alcohol poisoning?
Indicated for severe acidosis, renal failure, visual symptoms, or high serum methanol/ethylene glycol levels.
233
What labs support the diagnosis of toxic alcohol poisoning?
ABG (acidosis), elevated osmolar and anion gap, serum creatinine, calcium (↓), and serum levels of methanol or ethylene glycol.
234
What are fundoscopic findings in methanol toxicity?
Optic disc hyperemia and retinal edema, potentially leading to blindness.
235
Why is folinic acid or folic acid given in methanol poisoning?
Enhances metabolism of formic acid into CO2 and water, reducing toxicity.
236
Why is thiamine and pyridoxine given in ethylene glycol poisoning?
They promote conversion of toxic metabolites into non-toxic products.
237
What supportive treatments are used in toxic alcohol ingestion?
Airway management, bicarbonate for acidosis, IV fluids, seizure control, electrolyte correction.
238
What is the role of urine testing in ethylene glycol poisoning?
Fluorescence under UV light may suggest ingestion if product contains fluorescein; calcium oxalate crystals support diagnosis.
239
How is toxic alcohol ingestion confirmed?
Direct measurement of methanol or ethylene glycol levels (may be delayed), or clinical suspicion with high anion/osmolar gap.
240
How can methanol/ethylene glycol poisoning be prevented?
Proper labeling, child-resistant packaging, public awareness, and supervised use of automotive/industrial products.
241
What are common venomous snakes in pediatric envenomation?
Vipers (e.g., Russell’s viper), elapids (e.g., cobras, kraits), and sea snakes in endemic regions.
242
What are the major effects of viper bites?
Local tissue necrosis, coagulopathy, hemorrhage, hypotension, and renal injury.
243
What are the effects of elapid (cobra/krait) envenomation?
Neurotoxicity, ptosis, ophthalmoplegia, respiratory muscle paralysis, minimal local swelling.
244
What clinical signs suggest systemic envenomation?
Progressive swelling, bleeding, hypotension, neurotoxicity (ptosis, bulbar weakness), dark urine.
245
What is the first aid for snakebite?
Immobilize limb, remove constrictive clothing, avoid incision, suction, or tourniquet. Transport to hospital quickly.
246
What are contraindicated first aid measures for snakebite?
Tourniquet, incision, suction, ice packs, or oral remedies.
247
What is the role of antivenom in snakebite treatment?
Administered for systemic signs or significant local progression. Polyvalent antivenoms are commonly used.
248
What are indications for antivenom administration?
Neurotoxicity, coagulopathy, spontaneous bleeding, hypotension, renal failure, or rapidly spreading swelling.
249
How is the dose of antivenom determined?
Based on severity, not age or weight. Initial dose typically 10 vials; repeat based on clinical/lab response.
250
What are complications of antivenom therapy?
Anaphylaxis, serum sickness (delayed hypersensitivity), and pyrogenic reactions.
251
What premedication is recommended before antivenom?
Adrenaline (SC or IM), antihistamines, and corticosteroids may be considered in high-risk patients.
252
How is neurotoxicity from elapid bites managed?
Antivenom plus neostigmine with atropine may be tried in postsynaptic neurotoxicity (e.g., cobra).
253
What lab tests are important in viper bites?
Clotting time, PT/INR, platelet count, hemoglobin, renal function, urinalysis (hematuria/myoglobin).
254
How is coagulopathy monitored in viper bite victims?
20-minute whole blood clotting test (WBCT); failure to clot indicates coagulopathy.
255
When is dialysis needed in snake envenomation?
In cases of acute kidney injury, refractory hyperkalemia, or severe metabolic acidosis.
256
What is scorpion sting syndrome?
Neurotoxic envenomation leading to autonomic storm: hypertension, tachycardia, salivation, vomiting, and pulmonary edema.
257
What are signs of severe scorpion envenomation in children?
Restlessness, excessive salivation, hypertension followed by hypotension, respiratory distress, myocarditis.
258
What is the management of scorpion sting?
Supportive care, prazosin (alpha-blocker) for autonomic symptoms, and scorpion antivenom if available.
259
What is the mechanism of prazosin in scorpion sting?
It counteracts the alpha-adrenergic overactivation responsible for vasoconstriction, hypertension, and pulmonary edema.
260
How can envenomation be prevented?
Wear protective clothing, avoid walking barefoot, use bed nets, shake out shoes, and educate communities in endemic areas.
261
What are common beta-blockers involved in pediatric poisoning?
Propranolol, atenolol, metoprolol, labetalol, carvedilol, and sotalol.
262
What is the mechanism of beta-blocker toxicity?
Beta-blockade leads to decreased heart rate, contractility, and conduction velocity, and may cause hypotension, bradycardia, and cardiogenic shock.
263
Which beta-blockers are particularly dangerous in overdose?
Propranolol (lipophilic, CNS toxicity), sotalol (QT prolongation), and labetalol (alpha-blocking effects).
264
What is the toxic dose of beta-blockers in children?
As little as 1–2 tablets of propranolol can cause serious toxicity in toddlers.
265
What are early symptoms of beta-blocker overdose?
Bradycardia, hypotension, hypoglycemia (especially in infants), fatigue, nausea, and lethargy.
266
What are severe manifestations of beta-blocker poisoning?
Cardiogenic shock, AV block, seizures, coma, bronchospasm (especially in asthmatics).
267
How does propranolol cause CNS toxicity?
Its high lipid solubility allows it to cross the blood-brain barrier, causing seizures and coma.
268
What is the initial management of beta-blocker poisoning?
ABCs, IV access, cardiac monitoring, glucose levels, and activated charcoal if within 1 hour.
269
What is the antidote for beta-blocker toxicity?
High-dose glucagon is the first-line antidote.
270
How does glucagon work in beta-blocker poisoning?
It activates adenylate cyclase independently of beta-receptors, increasing intracellular cAMP and improving heart rate and contractility.
271
What is the dose of glucagon for beta-blocker toxicity?
Initial bolus: 50–150 mcg/kg IV (max 10 mg), followed by infusion 2–5 mg/hour.
272
What if glucagon is ineffective?
Use high-dose insulin-euglycemia therapy (HIET) to support myocardial metabolism and improve contractility.
273
What is high-dose insulin therapy in beta-blocker poisoning?
Insulin 1 unit/kg IV bolus, followed by infusion of 0.5–1 unit/kg/hour with dextrose to maintain euglycemia.
274
What other treatments are used in severe cases?
Vasopressors (epinephrine, norepinephrine), lipid emulsion therapy, pacing (external or transvenous), ECMO.
275
What is the role of calcium in beta-blocker toxicity?
Calcium may help support myocardial contractility but is more effective in calcium channel blocker toxicity.
276
When is intralipid therapy considered?
For lipophilic beta-blockers like propranolol, particularly in refractory cardiovascular collapse.
277
What monitoring is needed during beta-blocker poisoning?
Continuous ECG, blood pressure, glucose, potassium, and frequent neurological assessment.
278
What are poor prognostic signs in beta-blocker overdose?
Refractory hypotension, bradycardia, prolonged QRS or QT, seizures, coma, and poor response to glucagon.
279
How long should a child be observed after beta-blocker ingestion?
At least 6–12 hours; longer if symptomatic, depending on the specific agent’s half-life.
280
How can beta-blocker poisoning be prevented?
Educate caregivers, use child-resistant packaging, and store medications out of children's reach.
281
What are common calcium channel blockers (CCBs)?
Verapamil, diltiazem (non-dihydropyridines), and amlodipine, nifedipine (dihydropyridines).
282
What is the mechanism of CCB toxicity?
Inhibition of L-type calcium channels leads to decreased cardiac contractility, bradycardia, vasodilation, and impaired insulin secretion.
283
Which CCBs primarily cause bradycardia and heart block?
Non-dihydropyridines: verapamil and diltiazem.
284
Which CCBs primarily cause vasodilation and hypotension?
Dihydropyridines: amlodipine and nifedipine.
285
What are the signs of severe CCB toxicity?
Hypotension, bradycardia, AV block, shock, hyperglycemia, and lactic acidosis.
286
Why does CCB poisoning cause hyperglycemia?
Inhibition of insulin release from pancreatic beta-cells due to calcium channel blockade.
287
What is the toxic dose of CCBs in children?
Varies by agent, but ingestion of even one pill (especially extended-release) can be serious.
288
What is the initial management of CCB poisoning?
Supportive care: airway management, IV fluids, cardiac monitoring, and glucose monitoring.
289
Is activated charcoal indicated in CCB poisoning?
Yes, if ingestion occurred within 1 hour and airway is protected.
290
What is the antidote for CCB poisoning?
There is no specific antidote, but high-dose calcium is used to overcome calcium channel blockade.
291
How is calcium administered in CCB poisoning?
Calcium gluconate (60 mg/kg IV) or calcium chloride (20 mg/kg IV) over 5–10 minutes, repeat or continuous infusion.
292
What is the role of high-dose insulin therapy (HIET) in CCB poisoning?
Enhances myocardial carbohydrate uptake and improves inotropy. Dosing: 1 unit/kg bolus, then infusion with dextrose.
293
Why is glucose infused with HIET?
To prevent hypoglycemia and support insulin's metabolic effects.
294
What are additional treatments for CCB toxicity?
Vasopressors (epinephrine, norepinephrine), lipid emulsion therapy, atropine, pacing, ECMO.
295
What is the role of glucagon in CCB poisoning?
May improve cardiac output, but effect is variable; more useful in beta-blocker toxicity.
296
What monitoring is essential during treatment?
Cardiac rhythm, blood pressure, serum glucose, potassium, acid-base status.
297
How does extended-release CCB ingestion affect management?
Delayed toxicity, need for prolonged observation (at least 24h), and consider whole bowel irrigation.
298
When is lipid emulsion therapy indicated?
In severe CCB toxicity unresponsive to calcium, insulin, and vasopressors.
299
What are signs of improvement in CCB poisoning?
Improved heart rate, blood pressure, mental status, urine output, and resolution of acidosis.
300
How can CCB poisoning be prevented?
Caregiver education, safe medication storage, and use of child-resistant packaging.
301
What is clonidine and its clinical uses?
Clonidine is an alpha-2 adrenergic agonist used for hypertension, ADHD, and opioid withdrawal management.
302
What is the mechanism of clonidine toxicity?
Clonidine causes excessive central sympathetic inhibition, leading to hypotension, bradycardia, respiratory depression, and CNS depression.
303
What is the toxic dose of clonidine in children?
A dose of 0.5–1 mg can be toxic, with severe toxicity occurring in doses >1 mg in children.
304
What are early signs of clonidine poisoning?
Bradycardia, hypotension, miosis, lethargy, and mild sedation.
305
What are severe symptoms of clonidine poisoning?
Severe CNS depression, respiratory depression, hypotension, bradycardia, and coma.
306
What is the first-line treatment for clonidine overdose?
Supportive care: IV fluids, airway protection, and monitoring vital signs.
307
What is the role of naloxone in clonidine poisoning?
Naloxone may help in some cases as clonidine toxicity may cause respiratory depression through opioid-like effects on the brainstem.
308
Is activated charcoal useful in clonidine poisoning?
Yes, if given within 1 hour of ingestion and the airway is protected.
309
What is the role of intravenous fluids in clonidine poisoning?
IV fluids are used to maintain perfusion and support blood pressure in hypotensive children.
310
What medications can be used to treat severe bradycardia in clonidine poisoning?
Atropine or isoproterenol can be used to treat bradycardia if it is symptomatic or persistent.
311
What are the ECG findings in clonidine toxicity?
Bradycardia, prolonged QT interval, and potential heart block.
312
What role does norepinephrine infusion play in clonidine toxicity?
Used for refractory hypotension in severe cases where fluids and other measures fail.
313
What is the prognosis for clonidine poisoning?
Good with early intervention; toxicity typically resolves within 6–12 hours after supportive care.
314
When is naloxone used in clonidine toxicity?
If respiratory depression is present, administer naloxone to reverse central CNS effects.
315
What are the risks of clonidine toxicity in children?
Children are more vulnerable due to smaller body mass, and even small overdoses can lead to significant toxicity.
316
When should children be monitored after clonidine ingestion?
At least 6–12 hours; longer in severe cases or if multiple ingestions are suspected.
317
What is the role of blood pressure monitoring in clonidine poisoning?
Frequent monitoring is essential to detect and treat hypotension promptly, which may require vasopressor support.
318
What is the role of atropine in clonidine poisoning?
Atropine is used to treat severe bradycardia when symptoms are clinically significant or associated with hypotension.
319
How can clonidine poisoning be prevented?
Store medications in child-proof containers and educate caregivers on proper dosing and storage.
320
What is digoxin and its clinical uses?
Digoxin is a cardiac glycoside used for heart failure, atrial fibrillation, and supraventricular tachycardia.
321
What is the mechanism of action of digoxin?
Inhibits Na+/K+ ATPase, increasing intracellular calcium, which enhances myocardial contractility and slows conduction at the AV node.
322
What is the toxic dose of digoxin in children?
Toxicity can occur with doses as low as 3–5 mcg/kg; fatal doses are usually >10 mcg/kg.
323
What are the early symptoms of digoxin toxicity?
Nausea, vomiting, anorexia, abdominal pain, confusion, fatigue, and blurred vision (yellow-green halos).
324
What are cardiac manifestations of digoxin toxicity?
Bradycardia, AV block, ventricular arrhythmias, and atrial tachycardia with block.
325
What is the most serious complication of digoxin toxicity?
Life-threatening arrhythmias, including ventricular fibrillation and complete heart block.
326
How is digoxin toxicity diagnosed?
Clinical symptoms along with elevated digoxin blood levels, ECG findings, and confirmation with serum electrolytes.
327
What is the normal therapeutic digoxin level?
0.5–2 ng/mL; levels >2 ng/mL are considered toxic.
328
What is the role of the ECG in digoxin toxicity?
Classic findings: 'reverse tick' sign, atrial tachycardia with block, and a long PR interval.
329
What is the treatment for digoxin toxicity?
Discontinuation of digoxin, supportive care, correcting electrolytes (especially hypokalemia), and antidote administration if necessary.
330
What is the antidote for digoxin toxicity?
Digoxin-specific antibody (ovine-derived digoxin immune fab).
331
How is digoxin-specific antibody administered?
Dose is based on the severity of toxicity and digoxin levels. Typical dosing is 40 mg vial for 0.5–3 mg/L of digoxin toxicity.
332
When is digoxin-specific antibody indicated?
In life-threatening arrhythmias, severe toxicity (e.g., >10 ng/mL), or when other therapies fail.
333
What is the role of potassium in digoxin toxicity?
Hypokalemia potentiates digoxin toxicity by increasing digoxin binding to the Na+/K+ ATPase. Correct potassium levels before using digoxin.
334
How does magnesium help in digoxin toxicity?
Magnesium helps stabilize the cardiac membrane, especially in cases of digoxin-induced arrhythmias.
335
What is the management of bradycardia due to digoxin toxicity?
Atropine or temporary pacing if symptomatic bradycardia persists. Avoid beta-blockers or calcium channel blockers.
336
How is potassium supplementation used in digoxin poisoning?
Increases extracellular potassium, which competes with digoxin for binding to the Na+/K+ ATPase pump.
337
What are the long-term management strategies for digoxin toxicity?
Prevent recurrence by monitoring serum digoxin levels, correcting underlying electrolytes (especially potassium), and tapering or discontinuing digoxin if indicated.
338
What are the contraindications to digoxin in pediatric patients?
In children with congenital heart disease or renal impairment, digoxin should be used cautiously or avoided if possible.
339
How can digoxin poisoning be prevented?
Proper dosing, monitoring serum levels regularly, use of child-resistant packaging, and educating caregivers about signs of overdose.
340
What are common household products that can cause poisoning in children?
Household cleaning products (bleach, ammonia), batteries, alcohol, detergents, antifreeze, and personal care products.
341
What are the symptoms of bleach poisoning?
Vomiting, nausea, abdominal pain, and possible burns to the mouth, throat, and stomach.
342
What is the management of bleach ingestion?
Dilute with water or milk if ingestion is small and asymptomatic. Avoid neutralizing agents. Seek medical evaluation if large amounts are ingested.
343
What is the toxic dose of bleach?
Ingestion of large amounts (1-2 mL/kg) can cause significant esophageal and gastric irritation.
344
What complications can arise from bleach ingestion?
Esophageal and gastric burns, respiratory distress, aspiration pneumonia, and metabolic alkalosis.
345
What is the role of activated charcoal in bleach poisoning?
Activated charcoal is not recommended as bleach is highly caustic and charcoal will not neutralize it.
346
What is the management of battery ingestion in children?
Remove the battery promptly (within 2 hours of ingestion). Endoscopy may be required if the battery is stuck in the esophagus.
347
What are the risks of button battery ingestion?
Button batteries can get lodged in the esophagus and cause severe tissue damage due to electrical current and alkaline leakage.
348
What is the management of button battery ingestion?
Immediate removal of the battery, ideally within 2 hours. X-ray for localization, endoscopic retrieval if lodged in the esophagus.
349
What are the complications of button battery ingestion?
Esophageal perforation, fistula formation, vocal cord paralysis, and long-term esophageal or airway damage.
350
What are the symptoms of detergent poisoning?
Nausea, vomiting, abdominal pain, drooling, and possible chemical burns to the mouth and throat.
351
What is the management of detergent poisoning?
Rinse mouth with water, give small sips of water or milk if non-caustic. Avoid inducing vomiting, and monitor for respiratory distress.
352
What are the signs of antifreeze poisoning in children?
Initial signs include vomiting, lethargy, and abdominal pain. After 12–24 hours, signs of renal failure and CNS depression may develop.
353
What is the toxic dose of ethylene glycol (antifreeze) in children?
Toxicity may occur after ingestion of as little as 1.5–2 mL/kg of ethylene glycol.
354
What is the antidote for ethylene glycol poisoning?
Fomepizole or ethanol inhibit alcohol dehydrogenase, preventing the formation of toxic metabolites (glycolic acid, oxalic acid).
355
What is the role of hemodialysis in antifreeze poisoning?
Hemodialysis is used for severe toxicity (e.g., high levels of ethylene glycol, metabolic acidosis, renal failure, or altered mental status).
356
What is the management of alcohol poisoning in children?
Supportive care: IV fluids, airway management, glucose, and thiamine. Naloxone may be needed if opioids are co-ingested.
357
What is the role of gastric lavage in household product poisoning?
Gastric lavage may be considered if ingestion occurred within 1 hour and the airway is protected, but not recommended in caustic or corrosive ingestions.
358
What preventive measures can be taken to reduce household poisoning risk?
Proper storage of cleaning products, medications, and chemicals in child-proof containers. Educating caregivers and using child-resistant packaging.
359
What are common causes of bacterial food poisoning in children?
Salmonella, Escherichia coli (E. coli), Campylobacter, Shigella, Listeria, and Vibrio species.
360
What is the most common cause of bacterial gastroenteritis in children?
Rotavirus, but bacterial infections such as Salmonella and E. coli are also common causes.
361
What are the typical symptoms of food poisoning?
Nausea, vomiting, diarrhea, abdominal pain, fever, and dehydration.
362
How does Salmonella infection present in children?
Fever, abdominal cramping, diarrhea (which may be bloody), vomiting, and sometimes septicemia.
363
What is the typical presentation of E. coli O157:H7 infection?
Bloody diarrhea, abdominal cramps, and fever. Can lead to hemolytic uremic syndrome (HUS), causing kidney failure.
364
What is the pathophysiology of E. coli O157:H7?
Produces shiga toxin that damages endothelial cells in the kidneys, causing HUS and potential renal failure.
365
What is the management of Salmonella food poisoning?
Supportive care (hydration, electrolyte balance). Antibiotics are not recommended for uncomplicated cases due to increased resistance.
366
What are the signs of dehydration in children with food poisoning?
Dry mucous membranes, decreased urine output, lethargy, sunken eyes, and poor skin turgor.
367
What are the risk factors for developing hemolytic uremic syndrome (HUS) after E. coli infection?
Young age, immunocompromised status, and severe bloody diarrhea.
368
What are the complications of HUS?
Acute renal failure, thrombocytopenia, hemolytic anemia, and CNS involvement (seizures, encephalopathy).
369
What is the treatment for HUS?
Supportive care (IV fluids, dialysis, blood transfusions), careful monitoring of kidney function, and avoidance of antibiotics (which may worsen the condition).
370
What are common viral causes of food poisoning?
Norovirus, rotavirus, adenovirus, and astrovirus.
371
What is the management of viral gastroenteritis?
Supportive care, including hydration and electrolytes. Antiemetics and antidiarrheals are used cautiously in children.
372
What is the role of antibiotics in food poisoning?
Antibiotics are only indicated for specific bacterial infections (e.g., severe Shigella or Salmonella), but they should not be used for viral or uncomplicated cases.
373
How can food poisoning be prevented?
Proper food handling, cooking meat thoroughly, handwashing, avoiding unpasteurized products, and good hygiene practices.
374
What is the role of probiotics in food poisoning management?
Probiotics may help restore gut flora and reduce the duration of diarrhea, but evidence is mixed and they are not a first-line treatment.
375
When should a child with food poisoning be hospitalized?
If there is severe dehydration, high fever, blood in stools, persistent vomiting, or signs of sepsis.
376
What is the role of antidiarrheal medications in food poisoning?
Generally avoided in children with bacterial infections, as they can worsen symptoms. In viral gastroenteritis, they can be used to manage symptoms.
377
What is the clinical presentation of Norovirus infection?
Sudden onset of vomiting, diarrhea, and abdominal cramps. Typically self-limited and resolves within 1–3 days.
378
What is the role of hydration in food poisoning?
Critical in preventing dehydration, especially in young children and infants. Oral rehydration solutions are preferred over plain water.
379
What is botulism and what causes it?
Botulism is a rare, life-threatening condition caused by the neurotoxin produced by Clostridium botulinum.
380
What are the sources of botulism toxin?
Foodborne botulism (improperly canned foods), wound botulism (from infected wounds), and infant botulism (due to ingestion of spores, typically in honey).
381
What is the mechanism of botulism toxicity?
The botulinum toxin blocks acetylcholine release at neuromuscular junctions, causing flaccid paralysis.
382
What are the early symptoms of botulism poisoning?
Symmetrical descending paralysis, difficulty swallowing, dry mouth, blurry vision, ptosis, and muscle weakness.
383
What are the hallmark signs of botulism?
Cranial nerve involvement (e.g., ptosis, diplopia), descending muscle weakness, and autonomic dysfunction (dry mouth, constipation).
384
What is the pathophysiology of botulism?
The botulinum toxin cleaves SNARE proteins, preventing vesicle fusion and acetylcholine release, leading to muscle paralysis.
385
How is botulism diagnosed?
Clinical diagnosis based on symptoms (e.g., descending paralysis), confirmed by detecting botulinum toxin in serum, stool, or food.
386
What is the management of botulism poisoning?
Administer botulism antitoxin as soon as possible, supportive care, and mechanical ventilation if necessary.
387
When should botulism antitoxin be given?
As soon as the diagnosis is suspected, even before confirmation by lab tests, to reduce the severity of symptoms.
388
What is the role of botulism antitoxin?
It neutralizes free botulinum toxin in the bloodstream, preventing further progression of paralysis but cannot reverse existing paralysis.
389
What are the side effects of botulism antitoxin?
Risk of serum sickness, anaphylaxis, and allergic reactions, particularly in individuals previously exposed to equine-derived products.
390
What is the prognosis of botulism with treatment?
With early antitoxin administration and supportive care, the prognosis is good, though recovery can take weeks to months.
391
What are complications of botulism?
Respiratory failure, aspiration pneumonia, and prolonged paralysis.
392
What is the role of mechanical ventilation in botulism?
Used for respiratory failure and airway protection due to paralysis of respiratory muscles.
393
What is the role of antibiotics in foodborne botulism?
Antibiotics are not recommended for foodborne botulism, as they do not affect the botulinum toxin. They may be used in wound botulism.
394
What is the role of antibiotics in wound botulism?
Penicillin or metronidazole may be used to treat the underlying Clostridium infection but will not reverse toxin effects.
395
What is the role of wound debridement in wound botulism?
Surgical debridement is used to remove contaminated tissue and reduce toxin load in wound botulism.
396
How can botulism be prevented?
Proper canning techniques, avoiding honey in infants under 1 year old, and wound care to prevent contamination.
397
What are the risk factors for infant botulism?
Ingestion of spores, often from honey or dust, in infants under 12 months of age.
398
What is the clinical presentation of infant botulism?
Constipation, poor feeding, hypotonia (floppy baby), ptosis, and respiratory distress in severe cases.
399
What are the most common bacterial causes of foodborne illness?
Salmonella, Escherichia coli (E. coli), Listeria monocytogenes, and Campylobacter jejuni.
400
What are the typical symptoms of Salmonella infection?
Abdominal cramps, diarrhea (often bloody), fever, nausea, vomiting, and occasionally septicemia.
401
What is the pathophysiology of Salmonella infection?
Ingestion of contaminated food leads to intestinal invasion by the bacteria, causing inflammation and systemic spread, including bacteremia in vulnerable hosts.
402
What are the complications of severe Salmonella infection?
Sepsis, bacteremia, osteomyelitis, endocarditis, and meningitis.
403
What is the treatment for mild Salmonella gastroenteritis?
Supportive care (hydration, electrolyte replacement). Antibiotics are not routinely recommended in uncomplicated cases.
404
When are antibiotics indicated in Salmonella infections?
Invasive disease (e.g., bacteremia, meningitis), immunocompromised patients, or severe prolonged illness.
405
What is E. coli O157:H7 and how does it cause harm?
A strain of E. coli that produces Shiga toxins, causing bloody diarrhea, abdominal cramps, and potentially hemolytic uremic syndrome (HUS).
406
What is the hallmark complication of E. coli O157:H7 infection?
Hemolytic uremic syndrome (HUS), which causes acute renal failure, thrombocytopenia, and hemolytic anemia.
407
How is E. coli O157:H7 infection diagnosed?
Stool culture and detection of Shiga toxin-producing E. coli (STEC) or stool PCR for toxin genes.
408
What is the management of E. coli O157:H7 infection?
Supportive care for diarrhea. Avoid antibiotics as they may increase the risk of HUS.
409
What are the signs of hemolytic uremic syndrome (HUS)?
Hemolysis (anemia, jaundice), thrombocytopenia (petechiae, bruising), and acute kidney injury (oliguria, anuria).
410
What is Listeria monocytogenes and who is most at risk for infection?
Listeria is a foodborne pathogen causing meningitis, septicemia, and encephalitis, particularly in neonates, pregnant women, the elderly, and immunocompromised individuals.
411
What are the typical symptoms of Listeria infection?
Fever, headache, myalgia, gastroenteritis, and in severe cases, meningitis or septicemia.
412
How is Listeria monocytogenes diagnosed?
Blood cultures, cerebrospinal fluid (CSF) cultures, or stool PCR, depending on the clinical presentation.
413
What is the treatment for Listeria infection?
Empiric antibiotics (e.g., ampicillin or penicillin with gentamicin) are started promptly, especially in neonates and immunocompromised patients.
414
What is the primary source of Listeria infection?
Contaminated food, particularly unpasteurized dairy products, deli meats, and ready-to-eat meals.
415
What are the risk factors for Listeria infection in pregnancy?
Pregnant women are 10 times more likely to contract Listeria, leading to miscarriage, stillbirth, or neonatal infection.
416
How is foodborne toxin-related illness prevented?
Proper food handling, cooking meat to the appropriate temperature, avoiding raw or undercooked foods, and hand hygiene.
417
What are common viral causes of foodborne illness?
Norovirus, rotavirus, and hepatitis A.
418
What is the role of probiotics in foodborne infections?
Probiotics may help reduce the duration of diarrhea in some viral or bacterial infections but are not a substitute for medical treatment.
419
What is the role of antibiotics in foodborne infections?
Antibiotics are not routinely used for viral gastroenteritis but may be necessary for bacterial infections like Salmonella or Listeria.
