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Flashcards in Injuries and poisoning Deck (47)
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1
Q

Leading cause of death and disability among kids and young adults?

A
  • trauma (age 1-44)
2
Q

When do unintentional injury deaths peak?

A
  • during toddler years (1-4)

- adolescence and young adulthood (15-24)

3
Q

Leading cause of unintentional injury?

A
  • falls
  • MVA/traffic
  • poisoning
4
Q

How can we as providers prevent injuries in children?

A
  • at every well-child visit counsel parents on age appropriate injury prevention
5
Q

Leading cause of accidental death in kids?

A
  • motor vehicle injuries
6
Q

Peak incidence of motor vehicle injuries?

A
  • 15-24: adolescent drivers more likely to be involved in fatal MVA than adults
  • due to alcohol, excess speed and no seat belts
7
Q

How can we prevent motor vehicle injuries?

A
  • safe driving habits
  • driver’s ed
  • safer cars
  • safer roads
  • restraints: age approp, properly installed and used
8
Q

Child safety restraint guidelines?

A
  • 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)
9
Q

Submersion injuries are common in what age groups?

prevention?

A
  • # 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
10
Q

Risks of burns?

A
  • 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
11
Q

Scalding burns - how quickly they can occur?

A
- hot water causes 3rd degree burns in:
1 sec at 156
2 sec at 149
5 sec at 140
15 sec at 133
12
Q

Most common cause of non-fatal injury? Peak incidence?

prevention?

A
  • 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!!
13
Q

Pedestrian injuries highest risk in what age group? Prevention?

A
  • 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
14
Q

When are bike injuries highest risk of death?

A
  • 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
15
Q

Greatest risk period for FB/choking?

Prevention?

A
  • 1st yr of life
  • prevention:
    age approp toys, food prep, liquid meds under 3 yrs, small objects out of reach
16
Q

Common toy related injuries?

A
  • aspiration and ingestion dangers
  • burns and electric shock
  • lacerations
  • projectile injuries
  • skateboards, rollerblades, other high speed devices
17
Q

Most common sports injuries?

A
  • sprains, strains, and contusions

- re-injury is a major problem

18
Q

Types of life-threatening sports injuiries?

A
  • severe head/neck injury
  • cardiac or respiratory arrest
  • severe hemorrhage or shock
  • heat stroke
19
Q

Differences in musculokseletal system in ped pts?

A
  • 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
20
Q

Most commonly fractured bone in kids?

A
  • clavicle
  • younger kids fracture upper extremities
  • get older, more risk for lower extremity fractures
  • closed reductions of fractures more common in kids
21
Q

Why are kids at risk for head trauma?

A
  • large heads
  • thin skulls
  • poor muscle control
  • diffuse edema more common than intracranial hematomas
22
Q

When should you consider the possibility of serious injury in a child?

A
  • 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
23
Q

Guidelines for neuroimaging in head trauma?

A
  • imaging recommended if LOC greater than 1 min, evidence of skull fx, or focal neuro findings
  • consider imaging or observation if brief LOC
24
Q

There is an increased likelihood of intracranial injury if what sxs and signs are present?

A
  • immediate seizures
  • HA
  • vomiting
  • lethargy
25
Q

GCS of 13 or 14, what should be done?

A
  • emergent neuro imaging
26
Q

GCS of 15 with LOC or PTA, what should be done?

A
  • warrants strong consideration for neuro-imaging
27
Q

What are signs of elevated ICP?

A
  • AVPU (alert, voice, pain, unresponsive)
  • pupils
  • vomiting
  • cushing response (HTN, bradycardia, apnea)
  • controlled hyperventilation if IICP
  • resuscitate hypovolemic shock aggressively
28
Q

Concussion definition?

A
  • in children generally defined as sx head injury with no intracranial injury identified with CT (mild TBI)
29
Q

Presentation of a concussion?

A
  • HA
  • confusion and disorientation
  • difficulties with memory
  • inattentiveness
  • dizziness
30
Q

Management of a concussion?

A
  • 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
31
Q

Common causes of poisoning in peds?

A
  • 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
32
Q

Dangerous Rxs for kids?

A
  • antidepressants (TCAs especially, not so much SSRIs)
  • sedatives and antipsychotics
  • stimulants and ilicit drugs
  • cardiac meds
33
Q

Assessment of acetaminophen overdose?

A
  • # 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
34
Q

APAP overdose presentation over time?

A
  • 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
35
Q

What is happening to body during Acetaminophen overdose?

A
  • 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
36
Q

Management of acetaminophen overdose?

A
  • 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
37
Q

Why has number of exposures to aspirin decreased?

A
  • fear of Reyes
  • lower dose of chewable forms (81 mg)
  • restriction on number of tabs/bottle
38
Q

Presentation of Aspirin overdose?

A
  • typically: tinnitus and vomiting
  • hyperpnea, fever, lethargy, confusion, convulsions, coma, resp/cardiac failuire
  • sx onset within few hrs following ingestion
  • dx: plasma salicylate concentrations
39
Q

Tx of aspirin overdose?

A
  • no specific antidote
  • activated charcoal
  • alkalinization with IV bicarb
  • dialysis may be necessary
40
Q

Iron is toxic to what body systems?

A
  • GI, cardiovascular and CNS

- will cause metabolic acidosis

41
Q

Presentation of iron overdose?

A
  • 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
42
Q

Dx of Fe overdose?

A
  • abdominal xray: can see pure Fe, but vitamins won’t show up
  • serum Fe concentrations
43
Q

Tx of Fe overdose?

A
  • 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
44
Q

Amt of Fe ingestion and sxs?

A
  • 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)
45
Q

Lead poisoning? Causes?

A

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

46
Q

Presentation of lead poisoning?

Tx?

A
  • 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!!
47
Q

key intervention for APAP overdose? Why?

A
  • N-acetlycystein (mucomyst), replenishes glutathione which reduces APAP to nontoxic form