Burns & Poisoning

Made by: Ibtihal Ahmad

Supervised by:
Dr. Hisham Dweik
Dr. Mohammed Skafi
Burns
Epidemiology
• >100,000 children\ year sustain a burn injury
• Fatalities from burns are decreasing, but burns remain a significant cause
of morbidity.
• Boys are more likely to sustain a burn injury, as are children age 4 and
under.
• >40% of deaths from burns occur in this age group.

• Thermal burns secondary to scald or flame are the most common type of
burn.
• Not all burns are accidental, and child abuse should be considered
Pathophysiology of burn injury

• Caused by disruption of the three key functions of the skin:

1. Regulation of heat loss
2. Preservation of body fluids
3. Barrier to infection
• Burn injury releases inflammatory and vasoactive mediators➡⬆
capillary permeability, ⬇plasma volume and ⬇ CO
• The body then becomes hypermetabolic with ⬆ resting energy
expenditure and protein catabolism (may continue for up to a year
after injury)
Classification of burns
Burns usually are classified based on four criteria:
• Depth of injury
• Percent of body surface area involved
• Location of the burn
• Association with other injuries
Clinical Manifestations
1. Superficial (first-degree) burns
• involve only the epidermis (Superficial layers)
• characterized by red, blanching on pressure w/ rapid refill, painful and dried
out skin that heals in 2-5 days without scarring (e.g., sunburn or mild scald
injuries)
• require only moisturizers and analgesics
2. Partial-thickness (second-degree)

a. Superficial partial-thickness burns involve the entire epidermis and outer portion of the dermis (papillary
dermis). After debridement, the underlying dermis appears moist, painful and red. They blister but usually
do not scar. Healed within 1–3 weeks with hypopigmentation/hyperpigmentation

b. Deep partial-thickness burns involve destruction of the entire epidermis and deeper layers of the dermis
(papillary and reticular dermis). Burns are mottled skin with red, pink and/or pale white. They may blisters
(fragile >>rupture easily) and heals with scarring. Healing takes ≥3 weeks

• Manegement
• require appropriate analgesics (e.g., opiates), debridement of dead skin to prevent
infection and grafting
• Intact bullae (large blisters)>> not removed
• Bullae that have ruptured>> should be removed
3. Full-thickness (third-degree and fourth-degree)

a. Third-degree burns involve the complete destruction of the epidermis, dermis, and
part of the SQ tissue.
b. Fourth-degree burns involve underlying fascia, muscle, or bone

• Painless
• Tissue necrosis with black, waxy-white, or gray leather-like skin (eschar)
• Dried out, inelastic appearance
• Skin grafts are needed (doesn't heal by it self) and hydrotherapy. Escharotomy may be needed.
Fourth-degree burns may require reconstruction in addition to grafting
Inhalation injuries should be suspected if there are:

• facial burns
• singed nasal hairs
• carbonaceous sputum
• Hoarseness on vocalization also is consistent with a supraglottic injury.
• may result in bronchospasm, airway inflammation, and impaired pulmonary
function
Rule of nines
LABORATORY AND IMAGING
STUDIES
• Initial laboratory testing, including CBC, type and cross match,
coagulation studies, basic chemistry profile, ABG, and chest
radiograph
• A carboxyhemoglobin assessment should be performed for any
suspected inhalation exposure
• Cyanide levels should be considered in children who sustain smoke
inhalation and have altered mental status.
• Unusual patterns of burns may increase suspicion of child abuse and
result in appropriate evaluation to assess for nonaccidental trauma to
the skeleton or CNS.
CHILD ABUSE
Burns often have distinguishable patterns.

1. Immersion burns (M/C in infants)

– Glove-stocking pattern of extremity
– Dipping into bathtub hot water:
° Appear on buttocks
° Demarcation is uniform and distinct
° Flexion creases spared; hands and feet spared
° No splash burns
° Incompatible with falling into tub or turning on hot water while in tub
2. Contact burns: objects used to burn may be branded to the skin (e.g cigarette/curling iron)
• Cigarette burns → circular, punched-out lesions of uniform size
Management

1. Initial resuscitation should include the ABCs.

a. Endotracheal intubation should be performed in any victim suspected of
inhaling hot gases
b. Assess oxygenation by pulse oximetry. Administer 100% oxygen and assess
for carbon monoxide inhalation
c. IV access
2. Fluid resuscitation is critical

a. Lactated Ringer solution is the isotonic crystalloid fluid of choice in burn resuscitation.
b. Children with a significant burn should receive a rapid bolus of 20 mL/kg of lactated Ringer solution.
c. Thereafter, the resuscitation formula for fluid therapy is determined by the percent of body surface
burned. Total fluids are 2-4 mL/kg per percent burn per 24 hours
d. Fluids should be titrated to achieve adequate perfusion, and one marker of which is urine output greater
than 1 mL/kg per hour.
3. Skin care depends on the degree of burn.

• Wound care starts with cleaning and debriding the wound.

• Effective pain control is important to allow for complete debridement.
• Topical agents (1% silver sulfadiazine) and dressings are then applied to
control bacterial colonization, decrease evaporative losses, and aid in pain
control.
• Various grafts, such as cadaver allografts, porcine xenografts, or skin
substitutes, have been used initially to cover wounds.
4. Hospitalization
For severe burns care is best managed by a MDT in a qualified burn
center. The American Burn Association criteria for patients who should
be transferred to a burn center are as follows:
Criteria for Transfer
The following types of burn injuries typically require transfer to a burn center:
1. Partial-thickness burns on >10% TBSA.
2. Partial and full-thickness burns involving the face, hands, feet, genitalia, perineum, and major
joints
3. Full-thickness burns in any age group
4. Electrical burns, including lightning injury
5. Chemical burns
6. Inhalation injury
7. Burn injury in patients with preexisting medical disorders that could complicate management,
prolong recovery, or affect mortality (e.g., diabetes, renal failure)
8. Any patient with burns and concomitant trauma (e.g., fractures) in which the burn injury poses the
greatest risk of morbidity or mortality.
9. Burned children in hospitals without qualified personnel or equipment for pediatric care
10. Burn injury in patients who will require special social, emotional, or rehabilitative intervention,
including child abuse cases.
Children with significant burns require immediate nutritional support.
• Enteral feeds should be started early unless there is a specific
contraindication.
o may require parenteral nutrition if unable to tolerate full enteral feeds
• Consider supplementation of vitamins and trace elements.
• Other factors that may improve the hypermetabolic state include:
o pain control
o blood glucose control
o use of medications including anabolic steroids such as oxandrolone and β blockers such
as propranolol
PROGNOSIS
• Most children who sustain burns recover without significant disability
• Physical scarring and emotional impact of disfiguring burns are long-term consequences of burn
injuries

PREVENTION
• Most burns occur in the home.
• Prevention is possible by using:
o smoke and fire alarms
o having identifiable escape routes and a fire extinguisher
o reducing hot water temperature to 49°C (120°F)
Carbon monoxide poisoning
Epidemiology.
Carbon monoxide (CO) is a by-product of incomplete combustion of carbon-containing
material. It is odorless, tasteless, and colorless.
• Excessive exposure may occur from fires, tobacco, faulty home heaters, car exhaust, and
industrial pollution.

Pathophysiology.
CO interferes with oxygen delivery and utilization.
1. CO displaces oxygen from the hemoglobin molecule, forming carboxyhemoglobin (CO-Hb),
which can no longer carry oxygen.
2. The oxygen–hemoglobin dissociation curve is shifted to the left.
3. Carbon monoxide also interferes with cellular oxidative metabolism.
Clinical features depend on the CO-Hb level.

1. Low levels are associated with nonspecific symptoms such as headache, flulike
illness, dyspnea with exertion, and dizziness.
2. High levels are associated with visual and auditory changes, vomiting,
confusion and later syncope, slurred speech, cyanosis, myocardial ischemia,
coma, and death.
3. Classic PE findings, although uncommon, include cherry red skin and retinal
hemorrhages. Tachycardia and tachypnea may be present.
4. Young children (<8 years) have more symptoms at lower CO-Hb levels.
• Young children are also more likely to have GI symptoms (e.g.,vomiting and diarrhea)
instead of neurologic symptoms.
5. Delayed permanent neuropsychiatric syndrome, consisting of memory loss,
personality changes, deafness and seizures, may occur in some victims up to 4
weeks after CO exposure.
Diagnosis is made by measuring the CO-Hb level.
• REMEMBER that CO-Hb levels are not always indicative of the degree of CO exposure
• OTHER abnormal findings:
• anion-gap metabolic acidosis
• low oxygen saturation (however, PaO2 may be normal)
• evidence of myocardial ischemia on ECG or elevated cardiac enzymes

Management

1. Administer high-flow 100% oxygen immediately via nonrebreather facemask. 

2. If available, HBOT (more rapid)

3. Hospitalization is indicated for:

 CO-Hb levels > 25%

 CO-Hb levels > 10% during pregnancy
 history or presence of neurologic symptoms
 presence of metabolic acidosis or ECG changes
Poisoning
Epidemiology
a. 60% of all poisonings occur in children <6 years old.
• with a male predominance in children under 13, but a female predominance
in adolescence.
b. 90% of poisonings are accidental.
• The majority of poisonings occur at home when the child’s caregiver is
distracted.
c. Most poisons are ingested, although poisons may also be inhaled,
spilled on the skin or into the eyes, or injected intravenously.
d. Mortality is < 1%.
Etiology
• The M/C toxic exposures involve commonly used household products.
a. Cosmetics and personal care products (M/C toxic exposure)
b. Cleaning agents
c. Cough and cold preparations
d. Vitamins, including iron
e. Analgesics (e.g., acetaminophen, NSAIDS, aspirin)
f. Plants (6–7% of all ingestions)
g. Alcohols (e.g., ethanol) and hydrocarbons (e.g., gasoline, paint thinner,
furniture polish)
h. Carbon monoxide
i. Prescription medications
Evaluation
When to Consider poisoning?
>> in patients presenting with unexplained, nonspecific signs and symptoms,
such as:
• Seizures*
• severe vomiting and diarrhea
• metabolic derangement
• A.M.S
• cardiovascular compromise/ dysrhythmias**/ shock
• abnormal behaviors
• trauma
2. History obtained from caregivers typically identifies the poison.

A. Information about the toxin should include the type or name of toxin, toxin
concentration/ amount (if known), and the route of exposure.
1. Potential poison dose is calculated for the worst-case scenario. Toxicity is typically on the
basis of the amount ingested per kilogram of body weight.
2. Consider multiple agents in adolescents.
B. Information about the environment should include location of victim when
discovered, and medications, plants, vitamins, herbs, and chemicals in the
home.
C. Time of exposure is crucial in directing interventions.
** Available data often are incomplete or inaccurate, requiring a careful physical
examination and laboratory approach.

3. Physical examination should be comprehensive and may provide

additional clues to the identity of the toxin.
4. Investigations:

a. Screening laboratory tests include:

• osmoles, serum glucose, electrolytes, ABG and calculation of the anion or osmolar gap
• Quantitative toxicology assays (serum and urine toxicology screens)
• identifying the specific drug
• providing guidance for therapy
• anticipating complications
• estimating the prognosis
b. A full 12-lead ECG should be part of the initial evaluation in all patients suspected
of ingesting toxic substances.
C. Radiographic imaging of the abdomen (KUB) may reveal radiopaque
substances (CHIPED)

• Chloral hydrate and Calcium

• Heavy metals(lead, zinc, barium, arsenic, lithium, bismuth as in Pepto-Bismol)
• Iodine and Iron
• Phenothiazines, Play-Doh, potassium chloride
• Enteric-coated tablets
• Dental amalgam
TREATMENT
• The four foci of treatment for poisonings are supportive care,
decontamination, enhanced elimination, and specific antidotes.
• Supportive Care
• mainstay of treatment in most cases
• Takes precedence over other diagnostic or therapeutic procedures
• ABC
• If the level of consciousness is depressed and a toxic substance is suspected,
glucose (1 g/kg IV), 100% oxygen, and naloxone should be administered
Gastrointestinal Decontamination
AIM: prevent the absorption of a potentially toxic ingested substance>> prevent the poisoning

• Syrup of ipecac & Gastric lavage

• Single-dose activated charcoal
• An adsorbent agent
• Usually only effective for substances 100–1000 daltons in size that were ingested less than 1 hour prior to administration.
• contraindicated in patients with altered consciousness who do not have a protected airway.
** Charcoal is ineffective against caustic or corrosive agents, hydrocarbons, heavy metals,alcohols, ethylene glycol, iodine,
potassium and water-insoluble compounds.

• Whole-bowel irrigation (WBI)

• rapid, complete emptying of the intestinal tract accomplished using polyethylene glycol (an osmotic agent) and an
electrolyte solution (to prevent electrolyte imbalance).
• May be effective for toxic ingestion of sustained-release or enteric-coated drugs.
• There is theoretical benefit in its use for potentially toxic ingestions of iron, lead, zinc, or packets of illicit drugs
• The AACT does not recommend the routine use WBI
Enhanced Elimination
• Multiple-dose activated charcoal should be considered only if a patient has
ingested a life-threatening amount of carbamazepine, dapsone, phenobarbital,
quinine, or theophylline.

• Alkalinization of urine may be helpful for salicylate or methotrexate ingestion.

• Dialysis may be used for substances such as methanol, ethylene glycol, salicylates,
theophylline, bromide and lithium, that have:
• low volume of distribution
• low MW
• low protein binding
• high degree of water solubility
PROGNOSIS
• Most poisonings result in minimal or no toxicity, or have minor effects.
• Intentional ingestions result in a much higher rate of major effects or death
compared with unintentional ingestions.
• Adolescents are more likely to have a moderate, major, or fatal effect from
ingestion compared to younger children.

PREVENTION
• Properly educating parents regarding safe storage of medications and
household toxins
• If a child has ingested poison, a poison control center should be called.
Acetaminophen

• One of the M/C medications ingested by children and adolescents.

• Doses >150 mg/kg are associated with toxicity.
• Pathophysiology
 Exhaustion of hepatic metabolic pathways causes increased formation of a
toxic metabolite of acetaminophen, N-acetyl-p-benzoquinoneimine (NAPQI).
 Glutathione initially inactivates NAPQI, but its reserves are eventually depleted, leading
to NAPQI build-up.
 NAPQI → irreversible oxidative hepatocyte injury →hepatocellular  necrosis
Clinical features
Management
• Activated charcoal administered < 4 hours after ingestion

• Measure serum acetaminophen (APAP) levels 2-4 hours after ingestion (or immediately,

if ingestion occurred > 4 hours prior to presentation)
• The level should be plotted on the Matthew–Rumack nomogram to determine the potential for
hepatitis.

• Antidote: N-acetylcysteine (NAC)
 Administered 4–24 hours after ingestion (Most effective within 16 hr of ingestion)
 NAC ,a glutathione precursor, replenishes glutathione stores in the liver
 140 mg/kg PO initial dose, then 70 mg/kg PO q4hr × 17 doses
 150 mg/kg IV over 1 hr, followed by 50 mg/kg IV over 4 hr, followed by 100 mg/kg IV over 16 hr
• Treatment of liver failure
• Liver transplant in severe cases
Salicylates
• Salicylates are an ingredient in many OTC compounds, such as Pepto-
Bismol, Ben-Gay, and oil of wintergreen.
• Doses >150 mg/kg are associated with toxicity.

• Pathophysiology
 Salicylates (weak acid) directly stimulate the respiratory center of the brain → CO2
washout → primary respiratory alkalosis.
 Salicylates are uncouplers of mitochondrial oxidative phosphorylation → inhibition
of TCA cycle and ATP production → accumulation of lactic acid and ketones →
increased anion gap metabolic acidosis.
Clinical features. \
•Early symptoms: tinnitus, nausea, vomiting, tachypnea, hyperpnea
•Late symptoms: hyperthermia, agitation, delirium, seizures, noncardiogenic pulmonary edema

** Clinical presentation is variable and may not always correlate with

serum salicylate levels.
Laboratory findings

• ABG: mixed respiratory alkalosis and increased anion gap metabolic

acidosis
• Serum salicylate level:
• Because salicylate levels are not always elevated initially and do not
necessarily correlate with clinical presentation, a high index of suspicion
should be maintained when caring for a patient with symptoms of salicylate
toxicity. Rapid treatment is essential!
• BMP: Hyperglycemia, followed later by hypoglycemia, ↑ BUN, ↑
creatinine & hypokalemia
• Toxicology screen: evaluate for concurrent ingestions
Management
1. Stabilization of VSs: adequate oxygenation, IV fluids, IV glucose, and correction
of hypokalemia. Tepid sponging for hyperthermia
2. Activated charcoal is effective and may be readministered every 4 hours in
severe poisonings.
3. Obtain serum salicylate level at least 6 hours after ingestion.
• The level should then be plotted on the Done nomogram to assess for potential toxicity.
4. Alkalinization of serum & urine with IV sodium bicarbonate to a urine pH > 7
and large volume IV fluids
To enhance renal excretion of salicylates.
5. Dialysis may be required for life-threatening ingestions.
• Indicated in patients with severe acidosis, very high levels of serum salicylate,
cerebral/pulmonary edema, or RF
Metal Toxicity
Iron
• Epidemiology
• Iron is one of the M/C and potentially fatal childhood poisonings.
• As little as 20 mg/kg of iron is toxic.

• Source: Adult-strength ferrous sulfate tablets and iron supplement in pediatrics and prenatal care and in the
management of anemia

• Pathophysiology
 Iron-mediated toxicity and cell death is caused by:
 Free radical formation
 Lipid peroxidation
 Disruption of oxidative phosphorylation and mitochondrial function
CONSEQUENCES
1. Direct damage to the GI tract leading to hemorrhage (hemorrhagic gastroenteritis)
2. Hepatic injury and necrosis
3. Third spacing and pooling of blood in the vasculature leading to hypotension
Management
1. Activated charcoal does not bind to iron. However, if a polyingestion is
suspected, activated charcoal should be given.
2. Hypovolemia, blood loss, and shock should be anticipated and treated.
3. WBI should be considered for life-threatening ingestion.
4. Serum iron level should be obtained 2–6 hours after ingestion.
5. Intravenous deferoxamine, an iron-binding ligand, should be given if any
of the following condition exists:
a. If serum iron levels > 500 µg/dL, or if > 300 µg/dL and acidosis, hyperglycemia, or
leukocytosis are present
b. If severe GI symptoms are present
c. If >100 mg/kg of iron is ingested
**Test dose of deferoxamine may be administered
Lead poisoning

• Sources of exposure include: ingestion of lead-based paint chips, water carried by outdated
lead pipes, improperly glazed or foreign-made ceramic food or water containers, and pica
(compulsive eating of nonnutrient substances such as dirt, paint, and clay).
• Clinical features.
Lead poisoning is typically a chronic ingestion; however, children may also present with acute
lead intoxication.

1. Abdominal complaints include colicky pain, constipation, anorexia, and vomiting.

2. CNS complaints include listlessness, irritability, seizures, and decreased consciousness with
encephalopathy.
3. Peripheral blood smear may show microcytic anemia, basophilic stippling, and red blood cell precursors.
4. Radiopacities may be seen on abdominal radiographs, and dense metaphyseal bands may be seen on
radiographs of the knees and wrists (lead lines).
Pathophysiology
Diagnosis.
• An elevated lead level or elevated erythrocyte protoporphyrin is the
basis of diagnosis.
Management.
• Treatment for significant toxicity includes:
dimercaprol, British antilewisite (BAL), or calcium disodium
ethylenediaminetetraacetic acid (EDTA)
Caustic agents.
• These are acids or alkalis with corrosive potential.
Pathophysiology
 Acids (e.g., toilet bowl cleaner) cause coagulation necrosis that leads to superficial damage to the
mouth, esophagus, and stomach. More severe injury results from compounds that have a Ph<2
 Alkalis (e.g., oven and drain cleaners, bleach, laundry detergent) cause liquefaction necrosis that
produces deep and penetrating damage, most commonly to the mouth and esophagus. More
severe injury results from compounds that have a pH >12.
Clinical features
1. Immediate burning sensation with intense dysphagia, salivation, retrosternal chest pain, and
vomiting
2. Obstructive airway edema (especially with acid ingestion)
3. Gastric perforation and peritonitis may follow acid ingestion.
4. Esophageal perforation with mediastinitis may follow alkali ingestion.
Management. Treatment initially includes the ABCs.
1. No attempt should be made to neutralize the caustic agent, because
the combination of acid and alkali will generate an exothermic reaction
and worsen any burn.
2. Activated charcoal is contraindicated because it interferes with
endoscopy.
3. Endoscopy is performed to assess the degree of damage.
4. Household bleach has less corrosive potential and generally does not
require treatment.
References
• Marcdante, Karen, and Robert M. Kliegman. Nelson Essentials of
Pediatrics. Saunders, 2018.
• Brown, Lloyd J., and Lee Todd Miller. BRS Pediatrics. 2018.
• AMBOSS