Injuries and poisoning Flashcards
Leading cause of death and disability among kids and young adults?
- trauma (age 1-44)
When do unintentional injury deaths peak?
- during toddler years (1-4)
- adolescence and young adulthood (15-24)
Leading cause of unintentional injury?
- falls
- MVA/traffic
- poisoning
How can we as providers prevent injuries in children?
- at every well-child visit counsel parents on age appropriate injury prevention
Leading cause of accidental death in kids?
- motor vehicle injuries
Peak incidence of motor vehicle injuries?
- 15-24: adolescent drivers more likely to be involved in fatal MVA than adults
- due to alcohol, excess speed and no seat belts
How can we prevent motor vehicle injuries?
- safe driving habits
- driver’s ed
- safer cars
- safer roads
- restraints: age approp, properly installed and used
Child safety restraint guidelines?
- infants less than 1 and weighing less than 35 lbs should be in infant only rear facing child safety seat in back seat
- 1-4 and weighing 20-40 lbs can be in forward facing only or convertible child safety seat, installed in back seat of vehicle
- ages 4-6 need booster seat installed in back seat (booster seat for kids under 6 or less than 60 lbs in MT)
Submersion injuries are common in what age groups?
prevention?
- # 1 cause of unintentional injury/death ages 1-4
- # 2 cause of unintentional injury/death ages 5-9
- M:F ratio - 5:1
- locations: pools, lakes, streams, oceans, bathtubs (age 1)
- prevention: supervision near water, 2 seconds left alone is too long
- fence unguarded pools with self closing gates, swimming lessons, and diving safety
Risks of burns?
- house fires
- scalding burns: hot water, keep pan handles out of reach, keep water heater set below 125 F
- electrical burns: cords/plugs
- contact burns: hot appliances, wood stoves
- never leave a clothes iron or curling iron unsupervised while it is on
Scalding burns - how quickly they can occur?
- hot water causes 3rd degree burns in: 1 sec at 156 2 sec at 149 5 sec at 140 15 sec at 133
Most common cause of non-fatal injury? Peak incidence?
prevention?
- falls
- peak incidence: toddler years
- more than 700,000 hospitalizations a year
- 3rd leading cause of death from injury (all persons)
- prevention: home safety:
barriers, pointed corners, sharp edges, closed doors, inaccessible windows, bars on apt windows - no infant walkers!!
Pedestrian injuries highest risk in what age group? Prevention?
- highest risk: 10-15 years old
prevention: - pedestrian education
- look both ways
- walk on side walks or against flow of traffic
- adequate lighting, bright reflective clothing
- guardian supervision (esp under 9)
- traffic management:
observe/enforce speed limits and traffoc signs/lights - school bus stops away from high traffic areas
When are bike injuries highest risk of death?
- boys age 5-14
- head trauma most serious injuries
- most deaths involve crash with motor vehicle
- prevention: bike helmets
- bike safety education
- bike paths versus shoulder of road
Greatest risk period for FB/choking?
Prevention?
- 1st yr of life
- prevention:
age approp toys, food prep, liquid meds under 3 yrs, small objects out of reach
Common toy related injuries?
- aspiration and ingestion dangers
- burns and electric shock
- lacerations
- projectile injuries
- skateboards, rollerblades, other high speed devices
Most common sports injuries?
- sprains, strains, and contusions
- re-injury is a major problem
Types of life-threatening sports injuiries?
- severe head/neck injury
- cardiac or respiratory arrest
- severe hemorrhage or shock
- heat stroke
Differences in musculokseletal system in ped pts?
- ped bone has higher water content and lower mineral content: so less brittle than adult bone, thick periosteum in kids, rich blood supply
- physis (growth plate): cartilagionous structure that is weaker than bone predisposed to injury
Most commonly fractured bone in kids?
- clavicle
- younger kids fracture upper extremities
- get older, more risk for lower extremity fractures
- closed reductions of fractures more common in kids
Why are kids at risk for head trauma?
- large heads
- thin skulls
- poor muscle control
- diffuse edema more common than intracranial hematomas
When should you consider the possibility of serious injury in a child?
- if injured child has altered mental status or appears to have inappropriate behavior
- sig mechanism regardless of whether there are obvious injuries
- injured child has evidence of poor systemic perfusion
Guidelines for neuroimaging in head trauma?
- imaging recommended if LOC greater than 1 min, evidence of skull fx, or focal neuro findings
- consider imaging or observation if brief LOC
There is an increased likelihood of intracranial injury if what sxs and signs are present?
- immediate seizures
- HA
- vomiting
- lethargy
GCS of 13 or 14, what should be done?
- emergent neuro imaging
GCS of 15 with LOC or PTA, what should be done?
- warrants strong consideration for neuro-imaging
What are signs of elevated ICP?
- AVPU (alert, voice, pain, unresponsive)
- pupils
- vomiting
- cushing response (HTN, bradycardia, apnea)
- controlled hyperventilation if IICP
- resuscitate hypovolemic shock aggressively
Concussion definition?
- in children generally defined as sx head injury with no intracranial injury identified with CT (mild TBI)
Presentation of a concussion?
- HA
- confusion and disorientation
- difficulties with memory
- inattentiveness
- dizziness
Management of a concussion?
- physical and cognitive rest primary interventions
- assessment for concomitant injuries
- may use meds for HA and nausea short term
- gradual return to activity after sxs have resolved
- return to play only after pt is asx and has progressed through increasing levels of exertion w/o sxs
Common causes of poisoning in peds?
- cosmetic and personal care products
- cleaning substances
- analgesics
- plants
- cough and cold meds
risk of ingestion:
-improper or dangerous storage practices (cupboard locks), changes in normal home routines, visiting grandma
Dangerous Rxs for kids?
- antidepressants (TCAs especially, not so much SSRIs)
- sedatives and antipsychotics
- stimulants and ilicit drugs
- cardiac meds
Assessment of acetaminophen overdose?
- # tabs or syrup ingested? strength?
- toxic exposure is suggested when greater than 140 mg/kg ingested in single dose when greater than 7.5 g is ingested within 24 hr period
- serum acetaminophen levle: draw 4 hrs following ingestion in anyone suspected of overdose
- toxicity nomogram to determine need for tx
APAP overdose presentation over time?
- variable and depends on length of time following ingestion
- stage 1: first 24 hrs - often minimal signs and sxs of toxicity, perhaps anorexia, N/V, pallor, malaise
- stage 2: 2-3 days - signs of hepatotoxicity including RUQ pain and tenderness, elevated LFTs nad bilirubin
- stage 3: 3-4 days - some pts will progress to fulminant hepatic failure, findings: metabolic acidosis, coagulopathy, renal failure, encephalopathy, and recurrent GI sxs
- stage 4: pts who survive stage 3
What is happening to body during Acetaminophen overdose?
- initially liver breaks it down to non-toxic form
- shortly after however because of high acetaminophen load - glutathione levels are depleted
- when glutathione stores decrease to less than 30% of nomral, hepatic necrosis ensues (if sufficient amt of acetaminophen remaining)
- N-acetylcysteine (mucomyst) works to counteract hepatic toxicity by replenishing glutathione
Management of acetaminophen overdose?
- GI decontamination with early admin of activated charcoal orally or through NG tube
- Mucomyst: 140 mg/kg then maintenance dose (70 mg/kg) q 4 hrx 17 doses
- supportive care
- no ipecac to induce vomitng - this will delay admin of mucomyst
Why has number of exposures to aspirin decreased?
- fear of Reyes
- lower dose of chewable forms (81 mg)
- restriction on number of tabs/bottle
Presentation of Aspirin overdose?
- typically: tinnitus and vomiting
- hyperpnea, fever, lethargy, confusion, convulsions, coma, resp/cardiac failuire
- sx onset within few hrs following ingestion
- dx: plasma salicylate concentrations
Tx of aspirin overdose?
- no specific antidote
- activated charcoal
- alkalinization with IV bicarb
- dialysis may be necessary
Iron is toxic to what body systems?
- GI, cardiovascular and CNS
- will cause metabolic acidosis
Presentation of iron overdose?
- initial GI sxs: vomiting, abdominal pain, GI bleed, diarrhea
- stable period (after 6 hrs and up to 24 hrs sxs may resolve, which may falsely reassure you)
- resolution of GI sxs is presumed to occur as circulatting free Fe is redistributed into reticuloendothelial systems
- can progress to circulatory shock
Dx of Fe overdose?
- abdominal xray: can see pure Fe, but vitamins won’t show up
- serum Fe concentrations
Tx of Fe overdose?
- whole bowel irrigation
- don’t use ipecac, may obscure initial signs of clinical toxicity and it isn’t thought to be more effective than gastric emptying than Fe-induced vomiting
- activated charcoal not recommended, doesn’t absorb sig amounts of Fe
- blood levels to determine toxicity
- deferoxamine IV (chelating agent) for severe cases
Amt of Fe ingestion and sxs?
- pts who ingest less than 20 mg/kg of elemental Fe are usually asx
- 20-60 mg/kg may or may not produce sxs of serious toxicity
- small # of pts who have taken 40-60 mg/kg of Fe are sx
- ingestions of more than 60 mg/kg can be assoc with serious toxicity
- death from Fe toxicity has been reported from wide range of doses (60-300 mg/kg)
Lead poisoning? Causes?
aka: plumbism
- insidious disorder but may have acute episodes (repetitive ingestions of small amts far more serious and common than single massive exposure)
- paint/paint chip ingestion
- contaminated household dusts in old homes
- living near lead smelter
- lead contaminated soils
Presentation of lead poisoning?
Tx?
- vague sxs: weakness, irritability, wt loss, vomiting, personality changes, ataxia, constipation, HA, colicky abdominal pain, developmental delay, behavioral disorders, seizures, peripheral neuropathy
- blood disorders: anemia
- tx: interrupt ingestion
chelation therapy with succimer (in sx children) - SCREEN appropriately!!
key intervention for APAP overdose? Why?
- N-acetlycystein (mucomyst), replenishes glutathione which reduces APAP to nontoxic form
