Airway patency

Ventilatory status

Evaluate for shock

Rapidly identify injuries

Prioritize mmanagement

Reverse life-threatening conditions

Airway

Breathing

Circulation

Disability

Exposure

Secondary Survery:

History:

Secondary Survey

Phsyical exam

Skin

Head

Spine

Chest

Abdomen

Pelvis

GU system

Extremities

CNS

Burns

Hypothermia

Heat stroke and heat related illness

Drowning

Animal and human bites

Insect and spider stings

Poisoning

Epidemiology:

Toddlers are the most affected group

Boys> girls

Hot water or food

Appliances- irons, heaters

Flames

Grills

Vehicle-related burns

Curling irons

___: sub-grouped as superficial or deep depending on appearance

Superficial partial thickness burns

Deep partial thickness burns

Rarely indicated

With extensive partial- and full thickness burns:

baseline CBC, BMP, and creatine kinase

ABG and carboxyhemoglobin levels

Complications:

Scarring, infection, loss of function, contractures, compartment syndrome, renal failure

Burn Management

Superficial and non-Extensive Partial Thickness Burns

Refer to burn surgeon- wounds with potential to cause disfigurement or function impairment

Analgesia

Initial treatment of superficial or non-extensive partial thickness burns

Saline irrigation followed by antibiotic ointment and non-adherent dressing, leave small blisters intact

Burn Management

Full thickness, Deep or Extensive Partial-Thickness, and Subdermal Burns

ABC's

Perform Primary survey

Consider toxicity

Perform secondary survery

Initial fluid resuscitation

Parkland formula for fluid therapy is 4mL/kg/% BSA for 24 hrs (goal urine output is 1-2mL/kg/h

Admit- burns > 10% BSA, suspicion for abuse, associated with inhalational injury, explosion, fractures or requiring parental analgesia

Burns > 20% BSA for full-thickness burns >2% BSA admit to children's hospital or burn center

Subdermal burns- immediate hospitalization at a burn center

Small airways/lungs more prone to smoke and thermal injury

Small bodies more prone to hypothermia from epithelium loss

Electrical Burns

Conduct Burn

Burns to the commissure of lips from biting electrical cords

Late complication: labial artery hemorrhage

Hot liquids should be placed as far as possible from counter edges

Water heater thermostats should be turned less than 120 degrees F

Irons and electrical cords should be kept out of reach

Barriers around fireplaces are crucial

Children >6 months should wear sunscreen and hats when outdoors

Core themperature <35 degree C

Sepsis, metabolic derangements, ingestions, CNS disorders, and endocrinopathies

Neonates, trauma victims, intoxicated, and chronically disabled are high risk

Physical Exam:

Cool mottled skin

Shivering

Bradycardia

Physical Exam:

Declining mental status

Pale or cyanotic, pupils fixed or dilated, muscles or rigid, may be no palpable pulse

Diagnostics:

CBC

Electrolytes

Coagulation studies

Glucose

Blood gas studies

CXR if ___

Hypothermia

Submersion

General supportive measures

Rewarming

Monitor core body temp

Observe for arrhythmias

If ventricular fibrillation or asystole- PALS

Correct hypoglycemia

Passive external- cover with blankets (mild cases 33-35C)

Active external- warming lights, thermal mattresses or electric warming blankets, warm bath immersion

Be aware for "after-drop"

Active core- warmed humidified oxygen, warmed IV fluids, warmed peritoneal and pleural lavage

Heat related illness

2 Forms:

Exertional Heat Stroke

Nonexertional Heat stroke

Heat related illness

Risk Factors

Environment

Medical

Drugs/medications

Behaviors

Pathophysiology:

Heat production is incrased 10-20 times by strenous exercise

Pathophysiology:

When environmental temp is greater than body temp, body gains heat by conduction an radiation and can lose heat by evaporation

Pathophysiology:

Child have greater surface-to-mass ration, higher metabolic rates, inability to increase cardiac output, decreased sweat production, and inability to independently change environments

Miliaria rubra (prickly heat)- heat rash

heat cramps/spasm

Heat tetancy

Heat Syncope

Heat Edema

Heat exhaustion

Heat Stroke

History:

Weakness, lethargy, thirst, malaise, diminished ability to work or play, HA, N/V, myalgias, pale skin, dizziness

History:

History of CNS dysfunction in environment consistent with, or predisposing condition conductive to, development of heat-related ilness

Physical Exam:

Visual disturbances, syncope, mild CNS dysfuntion, impaired judgment, cramps, vertigo, hypotension

Physical Exam:

Tachycardia, hyperventilation, paresthesias, agitation, ataxia, psychosis, temperature <40C, sweating environmental exposure

Physical Exam:

Temp >40C, altered level of consciousness, ataxia, posturing, incontinence, seizures, coma, purpura or petechiae, 2/3 with constricted pupils; may have muscle rigidity with tonic contractions and dystonia that mimic seizures

Physical Exam:

Shock

Hot,dry, or clammy skin, pink or ashen color

Weakness, N/V, anorexia, HA, dizziness

Diagnostics:

Heat cramps

Decreased levels of serum and urine sodium and chloride

BUN level normal or slightly increased

Diagnostics:

Heat exhaustion

Hyponatremia or hypernatremia (free water loss)

Hypochloremia

Low uring sodium

Chloride hemoconcentration

Normal LFTs

Diagnostics:

Heat Stroke

Electrolyte abnormalities: sodium chloride level norm or high hypokalemia, incrased BUN/creatinine; low K+, Ca, P; hypoglycemia

Hematologic: hemoconcentration, leukocytosis, thrombocytopenia

Preenel azotemia

Elevatied AST/ALT

Metabolic Acidosis

Coagulopathy

Prevention:

Avoid enclosed spaces

Reduce activity levels, keep cools, use shaded areas

Cool or tepid baths

Increase fluid levels

loose light colored clothing

Acclimatization via gradual conditioning

Liberal dietary sodium

Avoid caffeine and alcohol

Avoid prolonged standing in hot envronments

Heat Related Illness

Management

Medications: Chlorpromazine, benzodiazepine

Fluid replacement

Cooling and support of cardiovascular system

Electrolyte replacement

Prognosis:

Heat related illnesses

Prognosis:

Heat stroke

Epidemiology:

2nd only MVA are the most common cause of death from unintentional injury in childhood

Drowning

Epidemiology:

<5 years of age and 15-19 years of age

Males, African Americans, low socioeconomic status, residents of southern states

Risk Factors:

Children <5

Boys

Direct access to swimming pools

use of alcohol or illicit drugs

Risk Factors:

Inadequate adult supervision

Children with seizure disorders

Children with primary cardiac arrhythmias

Drowning:

Prognostics indicators: (poor prognosis)

<3 years

Length of submersion >5 min

time to effective CPR >10 min

Lack of vital signs at scene

Length of resuscitation > 25min

Warm water

Pathophysiology:

Begins with a loss of normal breathing as panic ensues and subsequent apnea, laryngospasm or aspiration occurs

Pathophysiology:

Water aspirated into the trachea and lungs washes out surfactant and leads to atelectasis, intrapulmonary shunting, poor lung compliance, increased capillary permeability, and hypoxemia ultimately resulting in ARDS

Pathophysiology:

Severe hypoxemia is the final and common pathway and results in multisystem organ failure

Pathophysiology:

Cerebral hypoxia results in cerebral edema and increased ICP

History:

Mechanism: diving or high-impact injury, intoxication, seizure disorder, cardiac arrhythmia, child abuse

Physical Exam:

Vital signs with core temp

Neuro: pupillary response, cranial nerve findings, GCS, gag reflex

Respiratory: rales, tachypnea, wheezing, retractions, nasal flaring

Phsyical Exam:

Circulation: perfusion, strength of distal pulses, capillary refill, urine output

GI tract: abdominal distention

MSK: neck injuries

Lab:

ABG

Electrolytes

Blood glucose

Toxicology

Anticonvulsant levels

Imaging:

CXR

Cervical spine films

Neuroimaging

ABC's

Protect cervical spine

Supplemental oxygen

Reduce ICP

Raise body temperature

Complications:

Pneumonia or pneumothorax

Brain injury

Pulmonary injury

ARDS

Metabolic acidosis

Ischemic injury to organs

DIC

Hypothermia

75% recover

Duration and severity of initial hypoxic insult are most important determinants of brain injury and death

Boys > Girls

Younger children- head and neck wounds

School age- upper extremities

Physical exam:

Abrasions, lacerations and puncture wounds. May tear skin, subcutaneous tissue, muscle or cause bone fxs

Pathogens:

Pasteurella cansis

Pasteurella multocida

Streptococc Staphylococci

Anaerobes

Debride devitalized tissue and remove foreign matter

Irrigate using NS with high pressure

Consider tetanus prophylaxis

Dress and provide wound care instructions

Do not suture wound closed (unless on face)

Bites involving joint, periosteum, or associated with fx require prompt otho consultation

Augmentin- if infection

Complications:

Scarring

CNS infections

Septic arthritis

Osteomyelitis

Endocarditis

Sepsis

Post traumatic stress

Girls > Boys

Higher risk of infection

Physical exam:

Abrasion or puncture wound

Diagnostics:

Serologic test for Bartonella henselae, CRP and sed rate

Same as dog bit

Might soak wound in dilute povidone-iodine solution for 15 min

Consider tetanus prophylaxis or radies

Only close when absolutely necessary

Prophylactic antibiotics with Augmentin 80mg/kg/day divided in 3 doses

Complications:

Cellulitis

Tenosynovitis

Septic arthritis

Cat scratch disease

Pathogens:

Streptococci

Staphylococci

Anaerobes

Eikenella corrodens

Physical Exam:

Cresent Shaped

Treat hand and deep wounds with antibiotic prophylaxis- Augmentin

WOund management same as dog bites

Suture wounds involving severe face injuries only

Refer to hand surgeon if extensor tendon injury or joint involvement

Complications:

Infection of the metacarpophalangeal joints

Dog, cat, wild omnivore, carnivore, and bat bites may require it, check with Animal control or local veterinarian

RIG (rabies immune globulin) first then HDCV

(human diploid cell vaccine)

No initial local reaction except minor pain and swelling then severe local pain within 24 hrs

Cyanosis, morbilliform rash, fever chills, malaise, N/V, weakness, joint pains, hemolytic reaction with hemoglobinura, jaundice and delirium

Fatalities rare

Cold compress to bite site

Tetanus prophylaxis

Total wound excision ASAP to level of fascia

Dexamethasone 4mg IV QID during acute phase (not shown to be helpful)

Fever, sweats, chills, abdominal pain, N/V, HA, hypertension, parenthesis, shock

Death extremely rare

Cold compress to bite site

Pain control with benzodiazepines and opioids or opiates

IV calcium gluconate relieves muscle spasms, diazepam may also be used

Antivenin available for severe cases (may cause anaphylaxis)

Painful but usually not dangerous

Death from anaphylaxis might occur

Insect Stings

Hemolysis

Rhabdomyolysis

Shock

Remove stinger

For allergic reaction: Epi 1:1000 solution, 0.01mL/kg, should be administered IV or SQ above the sting

Ancillary drugs- Isoproterenol aerosol inhaler, corticosteroids, and diphenhydramine

Cold compresses

Fourth-leading cause of child death

Over 1/2 million cases/yr

Peak age 2 yr (accidental vs attempted)

Incidents less after age 5

Over 90% at home

Most non-fatal

Frantic phone calls:

Obtain information: pts name, age, weight, address, and telephone number

Name of substance, time taken, amount, pt's condition

Emergency exists if: if self-poisoning was intentional or ingestant is high risk (caustic solutions, hydrogen fluoride, drugs of abuse or medications such as a CCB, opioid, hypoglycemia agent or antidepressant

Instruct them to bring poison container to ER!

Adive to Parents

Inhaled poisons

Adive to Parents

Poisons on skin

Remove clothing if necessary to flood involved part with water.

Wash with soapy water and rinse thoroughly

Call doctor or poison control center

If medicine, give nothing

Call poison control center

Copious irrigation

Pour water (plain tap water) into the eye using drinking glass or pitcher for 15-20mins. Then, go to the hospital

Corrosives

Volatile hydrocarbons (examples: toluene, methylene chloride, and acetone)

Absent gag reflex, comatose

Probably not useful >2 hrs after ingestion

Biggest possible OG tube

Lavage until clear fluid returns

Nasogastric or PO

1-2g/kg (mx 100g) may repeat for those agents with slow passage

When multiple doses are given, repeated doses sorbital or slaine cathartics must be given

Repeat charcoal dosing every 2-6 hrs until charcoal is passed

Do not use with ingestion of heavy metals, may be harmful in hydrocarbons, caustics and solvent ingestions

Emesis common

Use has decreased dramatically over the past 10 yrs and is reserved for those instances when medications have been taken within 30-60 min prior

It can be given orally w/in 1 hr of ingestion

Dose: 15ml; may repeat in 20min

Very safe

0.1mg/kg IV, up to 1mg (IV)

< 1 yr: 1 amule (0.4mg). If no response 5 more ampules (2mg) should be given rapidly

Over 1yr: 2 amps, repeat dose (2-4mg/dose)

Caution: narcan short acting (<1hr)

Can produce severe hepatotoxicity

Children <5 years

Acetaminophen Poisoning

3 Stages of Toxicity

2-24hrs

24-48hrs

48+ hrs

Acetaminophen Poisoning

2-24 hrs

N/V

Malaise

Diaphoresis

Acetaminophen Poisoning

24-48hrs

Acetaminophen Poisoning

48+ hrs

Necrosis signs

Jaundice

Coagulopathy

Hypoglyemia

Coma

Encephalopathy

2 to 4% mortality if untreated

Ipecac or lavage, charcoal

Administer acetylcycteine (IV or oral)

Serum acetaminophen level

Obtain blood levels at 4 hrs after ingestion, if toxic treat

Rumack-Matthew nomogram-predicts severity and need for management in overdose

Children > 40kg: IV acetylcycsteine (Acetadote)

Loading dose 150mg/kg adminstered over 15-60min; followed by a second infustion of 50mg/kg over 4 hrs, and then a third infusion of 100mg/kg over 16hrs

Children < 40 kg: Iv acetylcysteine must have less dilution to avoid hyponatremia

Oral dose is 140mg/kg diluted to a 5% solution in sweet fruit juice or carbonated soft drink with loading dose of 70mg/kg and then administered every 4 hrs for 72 hrs

Common sources:

Alcoholic beverages, tinctures, cosmetics, mouthwashes, rubbing alcohol, hand sanitizers

Manage hypoglycemia and acidosis

Start IV drip of D5W or D10W if blood glucose is <60mg/dL

Death cuased by respiratory failure

Common Sources:

diet pills, ectasy, speed, crank, crystal and ice, methylphenidate, spice, bath salts

Symptoms:

CNS stimulation

Anxiety

Hyperpyrexia

Diaphoresis

HTN

Abdominal cramps

Symptoms:

N/V

Inability to void

Hypernatremia

Seizures

Rhabdomyolysis

Toxic psychosis

Diasepam

Control Hyperthermia

Absorbed rapidly and metabolized by the liver, lungs and kidneys

Potentially toxic dose is 10-50mg/kg

Antihistamines

Antitussives

Expectorants

Decongestants

May cause CNS depression or child may react paradoxically with excitement, hallucinations, delirium, ataxia, tremors and convulsions followed by CNS depression, repiratory failure or cardiac collapse

Activated Charcoal

Whole bowel irrigation

Physostigmine (0.5-2.0 mg IV, slowly adminstered)

Benzodiasepines (0.1mg/kg IV)

Treat cardiac dysrhythmias and hypotension

Absorbed through GI, respiratory tracts and skin

Causes death in 65% of victims

Arsenic Poisoning

Acute poisoning Early Signs

Abdominal pain

Vomiting

Watery and blood diarrhea

Cardiovascular collapse

Parasthesias

Neck pain

Garlic odor on breath

Arsenic Poisoning

Acute poisoning Late signs

Convulsions

Coma

Anuria

Exfoliative dermatitis

Arsenic Poisoning

Acute poisoning

Death as a result of___

Arsenic Poisoning

Chronic Poisoning

Anorexia

Generalized weakness

Giddiness

Colic

Abdominal pain

Polyneuritis

Dermatitis

Nail changes

Alopecia

Anemia

Arsenic Poisoning Management

Acute poisoning

Arsenic Poisoning

Chronic Poisoning Management

Collect 24hr baseline urine specimen >50mch/L is elevated

If treatment is initiated, continue chelation for 5 days. After 10 days repeat 5 day cycle once or twice

Prognosis:

Complete recovery, vegetative state, or any degree of mental injury

Iron

Iron poisoning

Iron

Hemorrhagic gastroenteritis

Phase of improvement

Delayed Shock

Liver Damage with hepatic failure

Pyloric stenosis 3-4 weeks post ingestion

Iron poisoning Stages

Hemorrhagic gastroenteritis

Iron poisoning

Phase of improvement

Iron poisoning

Delayed shock phase

Up to 50% mortality

Ipecac or lavage if early

Supportive care for severe symptoms such as shock

Deferoxamine 15 mg/kg/hr or more for 6hrs, repeat q 12hrs or 90mg/kg IM q 8hrs (contraindicated with renal failure)

Hemodialysis, exchange transfusion

Insidious onset

Children < 5 yrs of age

Sources: leaded paint, fruit tree sprays, solder, brass alloys, home-glazed pottery, fumes from burning batteries

History and physical exam: weakness, irritability, weight loss, vomiting, personality changes, ataxia, constipation, HA, colicky abdominal pain

Late symptoms: developmental delay, convulsions, coma

Diagnostics: Blood level levels

CBC and serum ferritin concentration

Glycosuria, proteinuria, hematuria, and aminoaciduria

Hypochromic anemia with basophilic stripping of the red cells

Reticulocytosis

Blood lead levels >80mcg/dL in symptomatic pts

Succimer- initated at blood levels >45mcg/dL

Initial dose 10mg/kg q8h x 5 days

Then given every 12hrs for 14days

High Calcium, high phosphorus diet and large doses of Vit D

Presentation:

Hyperventilation

N/V, dehydration

Fever w/o obvious cause

Lethargy

Sweating

Delirium, shock, coma

Follow Done's nomogram

If first sampl in non-toxic range, repeat level at 6 hrs

Ipecac, lavage, charcoal, supportive

Forced alkalinization of urine with IV D5NS, bicarbonate, potassium,diuretic

Hemodialysis if acid-base abnormalities very severe

Injuries (trauma, mainly MVAs)

Suffocation (foreign-body aspiratio, drowning, plastic bags, refrigerators)

Smoke inhalation

SIDS

Infections of Respiratory Tract

Severe dehydration

Poisoning

About 40 to 50% survive respiratory- only arrest

Only 2 to 10% survive associated cardiac arrest

Pediatric Advanced Cardiac Life support (PALS or ACLS)

Epi is the first-line drug for smptomatic bradycardia in children, 0.01mg/kg (for adults, atropine)