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Pediatrics- Noelle > Acute Care > Flashcards

Acute Care Flashcards

1
Q

What is the most common cause of paediatric deaths in children aged 1- 4 years?

A

trauma

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2
Q

What is the most effective strategy to prevent submersion injuries in children? how high? how many adults per baby? per child?

A

4 sided fence with self-locking, self-closing gates
must be at least 4 feet high
Toddlers should always be within arm’s length of an
adult, even in a bathtub
1 adult per baby and 1 adult per 2 young children

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3
Q

what is the most common preventable cause of death? who is at greatest risk?

A

submersion injury
children <5
typically during summer months
M>F

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4
Q

Do swimming programs for children < 4 years decrease rates of drowning?

A

NO! Swimming programs for children < 4 years do not

decrease rates of drowning

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5
Q

who is too young to wear PFD?

A

Babies who cannot sit unsupported are too young to wear PFDs

Should be worn by all infants at least 9 kg

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6
Q

what medical conditions are risk factors for submersion injuries? (4)

A

Seizure disorder
toxin (primarily ethanol)
prolonged QT
syncope

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7
Q

what are risk factors for submersion injury? (4)

A

leaving children unattended
alcohol or drug abuse (50% of adult drownings)
limited swimming ability
underlying medical condition (Seizure disorder, toxin, prolonged QT, syncope)

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8
Q

when is cervical spine immobilization recommended for submersion injuries?

A

diving
alcohol or other substances
trauma (boat, water skis)
* should not delay removal from water, can delay rescue breaths, hypoxia is the most common reason people don’t make it

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9
Q

After a submersion injury what type of ventilation if they are breathing? if they are not breathing?

A

spontaneously breathing- high flow oxygen
if they fail high flow oxygen- non invasive ventilation (CPAP)
non breathing- endotracheal intubation
decompress stomach after airway secured
avoid routine use of abdominal thrusts

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10
Q

What investigations would you order for submersion injury

A 
early arterial blood gas to assess degree of hypoxemia
electrolytes
BUN, CRE
CXR- to look for signs of ARDs
EKG
Ethanol level
Core temperature
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11
Q

what must the temperature be before you can stop resuscitation?

A

discontinue resuscitation efforts only after temp 35C

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12
Q

A 14 y.o. M is pulled from an icy lake
after being found face down. What is
the most important strategy
influencing survival

A

Immediate CPR by rescuers

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13
Q

what are good prognostic indicators after submersion injury? (4)

A
  • Return of spontaneous circulation in < 10 min
  • Submersion < 5 min
  • Pupils equal and reactive at scene
  • Normal sinus rhythm at scene
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14
Q

what are poor prognostic indicators after submersion injury? (3)

A
  • Delayed CPR
  • Return of spontaneous circulation > 25 min
  • Submersion > 10 min
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15
Q

what are some complications of submersion injury? (6)

A 
ARDS
Pulmonary edema
Pneumonia
Cerebral edema leading to increased ICP
Trauma
Hypothermia
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16
Q

what is hypothermia?

A

core temp <35C

can occur in water as warm as 21C

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17
Q

At what temperature does shivering stop?

A

core temp <32C

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18
Q

what are the 3 major metabolic disturbances associated with hypothermia?

A 
hypoglycemia
hypokalemia
hypocalcemia
metabolic acidosis
* also associated with pancreatits*
coagulopathy
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19
Q

what findings are associated with core temp:
31-32C
28-31C
<28C

A

31-32 C
- Normal ECG, ↑ HR, ↑ BP, loss of shivering
28-31 C
- ↓ HR, ↓ BP, flipped T, atrial fibrillation, sluggish,
dilated pupils, pathognomonic J wave
< 28 C
- absent pulse and BP, VF, coma, fixed dilated pupils

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20
Q

A 12 year girl was pulled from a lake and presents to the ED with a core temp of 28 C. What is the name given to the upward deflections on her ECG?

A

Osborn waves/ J wave

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21
Q

what EKG findings are associated with a T <32

A

Marked sinus bradycardia
First degree AV block
Osborn or J waves
Associated with prolonged QT and bradycardia

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22
Q

If a patient has a pulse and a core temp of 34-36 how do you rewarm them?

A

passive rewarming
remove wet clothes
dry

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23
Q

If a patient has a pulse and a core temp of 30-34 how do you rewarm them?

A 
Passive AND active external warming of
truncal areas only
• electric blanket
• overhead warmer
• hot water bottles
• heating pads
Minimizes “after-drop” or shock
associated with peripheral vasodilation
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24
Q

If a patient has a pulse and a core temp <30 how do you rewarm them?

A 
Active external and internal rewarming
• Warmed IV or intraosseous (IO) fluid
(without K+) at 43 C
• Warm humidified oxygen at 42-46 C
• Peritoneal lavage, ECMO, esophageal
warming tubes
Do not delay advanced airway placement
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25
Q

If a patient has NO pulse with temp >30 what should you do? <30?

A

> 30: CPR, IV meds as needed, defibrillation as needed
<30: CPR, NO IV meds, limit defibrillation to 3 shocks!
warm with cardiopulmonary bypass
nelsons says give one shock at max power and then warm 1-2 degrees or until >30 for additional shocks
Be-Low 3-0?
Just Push
No Do (pamine or Epi)
NO VASOACTIVE DRUGS UNTIL TEMPERATURE >30

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26
Q

Defibrillate all cases of pulseless VT or VF to max of

______ shocks if temperature < 30 C

A

3!!

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27
Q

How should you treat frostbite in ER

A

In ER, 42 C water bath, do not rub,
keep rewarmed areas open, dry, and
sterile

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28
Q

What is the metabolic disturbance associated with hyperthermia

A

loss of NaCl

acute tubular necrosis seen in 30% of cases of heat stroke

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29
Q

what are heat cramps? tx?

A

exercise-associated muscle cramps
intense painful muscle contractions
due to excess water (hypotonic fluids) resulting in salt depletion
tx: oral electrolyte solution or IV fluids, salt replacement

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30
Q

what happens with heat exhaustion? what are the two types of heat exhaustion

A

Temp >39C but neurologic status intact
excessive peripheral vasodilation
inability to deliver sufficient blood volume
muscle fatigue
profuse sweating
excessive water and/or sodium losses
TYPE 1: water depletion type- temp >39, water depletion= hypernatremia
TYPE 2: salt depletion type- hyponatremia (CF patients at risk)

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31
Q

what is heat stroke?

A

core body temp >40 with CNS dysfunction

  • headache
  • DISORIENTATION
  • dizziness
  • weakness
  • GAIT DISTURBANCE
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32
Q

what is the management of heat stroke?

A

Remove clothing
Active cooling: ice packs in groin, axillae, neck, cooling
fans over body sprayed with tap water at 15 C
Stop cooling when T < 38.5
Coma may persist for > 24 hours after normothermia
Fluid AND salt replacement orally
diuresis for rhabdomyolysis

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33
Q

what are the complications of heat stroke? (5)

A 
Hyponatremia
Seizure
Rhabdomyolysis
DIC
Multi-system organ failure
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34
Q

what are the 4 types of burns?

A

superficial
superficial partial thickness
deep partial thickness
full thickness

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35
Q

what is a superficial burn?

A

epidermis only
reddness, pain, no blisters
heals in 3-5 days

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36
Q

what is a superficial partial thickness burn?

A 
epidermis + 1/2 dermis
red/pink
pain
moist
BLISTERS
heals in 2 weeks
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37
Q

what is deep partial thickness burn?

A 
epidermis + >1/2 dermis
pale
dry
less tender
speckled appearance
GRAFTING OFTEN NEEDED
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38
Q

what is full thickness burn?

A 
subcutaneous tissue
pale
charred
leathery appearance
non-tender
most require grafting
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39
Q

What is the initial management for burns?

A 
Cover with sterile bandages
Early cooling ( < 30 min) prevents further injury
TETANUS (DIRTY WOUND)
analgesia
remove smoldering clothes
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40
Q

what are some indications for early intubation for burn patients? (4)

A
  • Carbonaceous sputum
  • Singed nasal hairs
  • Soot in airway
  • Hoarseness
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41
Q

what is the Parkland formula? what type of fluid do you use?

A

Age > 5: Parkland formula = 4 cc/kg/BSA over 24
hours (1st half in 8 hours, 2nd half in 16 hours)
add maintenance to Parkland
Use Normal Saline or Ringer’s Lactate (no albumin)

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42
Q

what is the admission criteria for burns?

A 
Suspected non-accidental injury
> 10% BSA partial thickness
> 2 % BSA full thickness
> 1% BSA of hands/feet/face/perineum
Circumferential burn
Enclosed space fire or evidence of inhalation injury
Electrical injury with high tension wire
(rhabdomyolysis)
Associated trauma
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43
Q

what complications are associated with burns

A

Children < 20 kg at risk of hypoglycemia
No role for prophylactic broad spectrum antibiotics
Early infection: Staph aureus, GAS
Late infection: Pseudomonas, Bacteroides
Daily dressing change with topical antibiotic BID until
re-epithelialization

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44
Q

what type of current is seem with lightening? what type of pattern do we see? what is the main thing we watch for?

A

direct current
feathering or arborescent pattern common
monitor for delayed cerebral edema, ICH, seizure, arrhythmia, rhabdomyolysis, asystole and respiratory failure

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45
Q

What is the most common cause of morbidity and

mortality in burn patients?

A

Infection!!

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46
Q

what complications are seen with high tension wires? what must you do for monitoring?

A 
Muscle damage → Compartment syndrome,
rhabdomyolysis → ARF
CNS injury common
VF/arrest common
Must monitor with urinalysis and ongoing ECG
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47
Q

After bitting electrical injury what should you warn the parents about

A

eschar can detach and cause significant bleeding from labial artery 1-3 weks later

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48
Q

what should you do for a patient with a low voltage electrical injury?

A

EKG and look for an exit wound
can still cause arrhythmia and seizure if contact is near chest or head
if exit wound or tender compartment, rule out rhabdomyolysis

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49
Q

what are 3 cholinergic drugs

A

organophosphates (sarin “nerve” gas
carbamates (neostigmine, pyridostigmine, aldicarb)
Alzheimer’s drugs (donepezil)

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50
Q

what is the main difference between organophosphates and carbamantes

A

organophosphates bind IRREVERSIBLY to inhibit acetylcholinesterase at 24-48h
carbamates transiently inhibit acetylcholinesterase so symptoms are REVERSIBLE within 48 hours

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51
Q

Cholinergic toxidrome

A

DUMBELLS

D- diaphoresis
U- urination
M- miosis
B- bronchorrhea/bradycardia
E- emesis
L- lacrimation
L- lethargy
S- salivation
  • organophosphates and carbamates
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52
Q

what is the treatment for cholinergic toxidrome

A

atropine (q5min)
pralidoxime (2-PAM) with atropine

100% oxygen
early intubation
PPE, remove clothing and vigorously irrigate the skin

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53
Q

what type of toxidrome is seen with Jimsonweed

A

ANTICHOLINERGIC

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54
Q

what are the features of anticholinergic toxidrome

A 
mad as a hater
red as a beet
dry as a bone
blind as a bat
hot as a desert

*dry skin, agitation, flushing

dilated pupils
confused
dry mouth
flushed skin
tachycardia
shaking
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55
Q

what is the treatment for TCA with prolonged QT

A

sodium bicarbonate

if QRS >100msec administer sodium bicarb

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56
Q

what is the treatment for agitation seen with anticholinergic toxidrome?

A

lorazepam

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57
Q

when should you consider physostigmine for anticholinergic toxidrome?

A

consider if both peripheral and central toxicity (Delirium) is present

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58
Q

what are examples of sympathomimetic drugs? (4)

A

cocaine
amphetamine/methamphetamine
ETDA
ephedrine

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59
Q

what is the main difference between anticholinergic and sympathomimetic toxidrome?

A

sympathomimetic- diaphoresis

antiperspirants keep you dry and so do anticholinergics!!

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60
Q

what are 2 clues to amphetamine (sympathomimetic) exposure

A

diaphoresis

agitation

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61
Q

How do you diagnoses MDMA overdose?

A

diagnose with MDMA screen in urine

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62
Q

what symptoms do you see with MDMA (6)

A 
HTN
Hyperthemia
Hyponatremia
Serotonin syndrome
cardiac ischemia
hepatotoxicity
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63
Q 
what is the management for MDMA
HTN
Hyponatremia
agitation
hyperthermia
A 
HTN- lorazepam 1mg IV
Hyponatremia- fluid restrict or 3% NS if seizing
Activated charcoal within 1 hour
agitation- lorazepam 1mg IV
hyperthermia- cool water mist and fans
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64
Q

how low does sodium have to be before there is a risk of seizures

A

typically <120

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65
Q

what is the key presentation associated with LSD or “Acid”

A

HALLUCINATIONS
one of the most potent hallucinogens putting patient as risk of severe injury
common to have co-injestion with MDMA at raves

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66
Q

what is the key presentation associated with PCP or “angel dust”

A

nystagmus while awake*
structurally similar to ketamine
dystonic posturing, muscle rigidity, myoclonus, hyperreflexia fluctuating behavior with delirium, paranoia and agitation

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67
Q

what is the difference between serotonin syndrome and neuroleptic malignant syndrome

A 
Serotonin syndrome:
<12h
increase bp, RR, HR, T
pupils: ENLARGED
mucosa: sialorrhea
skin: diaphoresis
neurologic: INCREASED REFLEXES (LE) AND TONE
mental status: agitation
Neuroleptic Malignant syndrome:
3-4d
increase bp, RR, HR, T
pupils: NORMAL
mucosa: sialorrhea
skin: diaphoresis
neurologic: RIGID
mental status: STUPOR
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68
Q

What SSRI should you worry about most in overdose?

A

citalopram- risk of seizures and qt prolongation

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69
Q

what is the most popular opioid with teens?

A

fentanyl

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70
Q

what is the most popular opioid overdose in toddlers?

A

methadone (prolongs QT interval)

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71
Q

What synthetic opioid is 100 times more potent then fentanyl

A

W-18 is 100 times more potent than fentanyl

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72
Q

What are the features of opioid toxidrome? (5)

A 
bradycardia
hypotension
respiratory depression
miosis
coma
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73
Q

what is the treatment for opioid overdose?

A

Naloxone

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74
Q

what is promoted online as a treatment for opioid withdrawal?

A

Imodium (loperamide)

NOT detected in urine drug screen

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75
Q

what are the signs of loperamide overdose?

A 
euphoria
prolonged QT, QRS
respiratory depression
highly toxic to young children in overdose
*not detected in urine drug screen
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76
Q

what is the usual time frame for activated charcoal?

A

typically within 1 hour of ingestion

1g/kg (max 50g)

77
Q

when does activated charcoal FAIL?

A 
P- potassium
H- hydrocarbons
A- alcohols
I- iron
L- lithium
S- solvents
if it is used to make something shiny it doesn't work!
avoid if compromised airway/caustic ingestion/patient non compliant
78
Q

when do we consider intralipids?

A

for life-threatening overdoses of local anesthetics, bupropion, amitriptyline

79
Q 
what is the antidote for:
iron
carbon monoxide
pesticide
nifedipine
amitriptyline
methanol
glyburide
A 
iron- desferoxamine
carbon monoxide- oxygen
pesticide- atropine
nifedipine- glucagon
amitriptyline- sodium bicarbonate
methanol- fomepizole
glyburide- glucose
80
Q

what do we worry about for hydrocarbons? what is the initial investigation?

A

we worry about pulmonary aspiration
aspiration is common and pulmonary toxicity account for most fatalities
CXR on arrival and repeat 4-6h post ingestion (can see perihilar infiltrates and pneumatoceles)
Can d/c after 4-6 h if asymptomatic and normal CXR

81
Q

what are common hydrocarbons

A

gasoline, nail polish remover, lighter fluid

82
Q

what can be seen on bloodwork with metformin ingestion?(2)

A

normal glucose

lactic acidosis

83
Q

what would be seen with glyburide ingestion?

A

hypoglycaemia that is difficult to control

Glieburide….lies are bad…. hypoglycemia that is difficult to control

84
Q

List 4 drugs that cause hypoglycemia

A

salycilates
ethanol
glyburide
beta blockers

85
Q

what is the toxic metabolite of acetaminophen

A

NAPQI

86
Q

what is the toxic dose of acetaminophen?

A

150mg/kg

7.5g in adults

87
Q

what are 3 complications of acetaminophen overdose

A

anion gap metabolic acidosis
acute tubular necrosis
fulminant liver failure

88
Q

what are the 4 stages for acetaminophen overdose

A

stage 1: 0-24h, asymptomatic or nausea/vomiting
stage 2: 24-72h, right upper quadrant pain and onset of hepatocellulr injury
stage 3: 72-96h, maximal hepatotoxicity; most deaths occur during this phase
stage 4: >4d, recovery
** peak hepatic injury 3 days post ingestion **

89
Q

what is the treatment for acetaminophen overdose?

A

activated charcoal within 1 hour (Avoid if sedated or suspected GI obstruction)
NAC (N-acetylcysteine) dosing based on Rumack- Matthew nomogram

90
Q

what time frame is associated with the best outcome for NAC

A

best outcomes if NAC started within 8 hours

91
Q

when do you start NAC if a patient has ingested a toxic dose of acetaminophen

A

start IV NAC protocol immediately

92
Q

what is the minimum level above which toxic effects are seen on Rumack- Matthew nomogram

A

1000umol/L is the minimum level above which toxic effects are seen
nomogram applies to acute ingestions only
nomogram begins at 4 hours

93
Q

List 3 examples of salycilates

A

ASA
bismuth salicylate (antidiarrheal agent)
methyl salicylate “Rub A535”

94
Q

what is the treatment of salicylate overdose? 4

A

charcoal up to 6 hours (risk of bezoar formation)
***glucose to all patients with altered mental status REGARDLESS of peripheral glucose
treat hypokalemia
alkalinize serum to urine pH between 7.5-7.6 to “trap salicylate anions in blood and renal tubule

95
Q

how is the toxic quantity of iron calculated? can iron be seen on xray

A

toxic quantity calculated as elemental iron
measure a serum iron within 4-6 hours of ingestion
iron can appear on xray

96
Q

what are the radio-opaque drugs

A 
C- chloral hydrate
O- opioid packets (latex)
I- iron and other heavy metals
N- neuroleptics (early)
S- sustained- release tablets/ salicylates (Early)
97
Q

what is the treatment for iron overdose?

A

NO role for either charcoal or gastric lavage
fluid resuscitation is essential
whole bowle irrigation if tablets seen on AXR or if <6h from ingestion
IV deferoxamine (DFO) is the antidote of choice and MUST be given early
continue deferoxamine until urine color clears

98
Q

what are 3 clues to iron exposure

A

gi symptoms
acidosis
multiorgan failure
cardiovascular collapse happens at 12 hour mark

99
Q

what is the only toxic alcohol that will result in an increase in serum ketones

A

isopropyl alcohol

100
Q

what is the most common toxic alcohol ingested?

A

isopropyl alcohol
the hallmark is KETOSIS without acidosis
mainly causes inebriation that peaks in 1-2 hours

101
Q

what should you do if patient presents with isopropranol ingestion

A

rule out co-ingestion with ethanol, methanol or ethylene glycol
no role for activated charcoal
discharge after 2 h if asymptomatic

102
Q

Methanol

A

highly toxic- toxicity associated with as little as one teaspoon
less inebriating then ethanol
formate causes retinal injury (blurring, central scotoma, blindness) (formic acid= metabolic acidosis= retinal injury)
profound AG acidosis presents late (>24h)

103
Q

what are the 2 drugs you give for methanol ingestion

A

fomepizole or ethanol

folic acid or leucovorin

104
Q

can you rule out an ingestion based on a normal osmolar gap?

A

No!
increases only in the presence of the parent alcohol so insensitive in late presentations
not sufficiently sensitive to exclude small ingestion

105
Q

what is the treatment for TCA overdose?

A

activated charcoal
NaHCO3 for QRS >100 because of significant morbidity and mortality
NOREPINEPHRINE if hypotensive
physostigmine is CONTRAINDICATED

106
Q

what is the treatment for canabinoid hyperemesis

A

standard antiemetics INEFFECTIVE
TOPICAL CAPSAICIN has shown consistent benefit
haloperidol has also shown promise
volume assessment and rehydration necessary
CEASE USE

107
Q

what is seen with synthetic cannabinoid use in children <12

A

acute psychosis in children <12
more potent then THC but less pleasurable and more toxic
supportive therapy and benzodiazepines if agitated

108
Q

why do we worry about carbon monoxide

A

240x higher infitinity to Hb than O2- hypoxemia
initially HEADACHE, dizziness, nausea, confusion, seizure, syncope, coma but don’t correlate with COHb level
worry about DSYARRHYTHMIA AND CARDIAC ARREST (<30%)

109
Q

what is the treatment for carbon monoxide

A

treat if COHb level >10% with 100% FiO2

110
Q

what carboxyhemoglobin level is consistent with toxic inhalation

A

> 3%

111
Q

when is hyperbaric oxygen recommended for carbon monoxide poisoning

A

COHb >25% (>15% in pregnant female or child)

ANY neurologic symptom! (loss of consciousness, seizure, cardiac ischemia, cerebellar deficits)

112
Q

what is the management of cyanide exposure

A

antidote is HYDROXYCOBALAMIN KIT
indicated if increased lactate or decreased blood pressure
transiently see reddening of skin and urine (chromaturia)

113
Q

what lab finding is suggestive of cyanide exposure

A

LACTIC ACIDOSIS- prevents aerobic metabolism

primarily seen with house fires!

114
Q

what is seen with calcium channel blocker ingestion?

A

hypotension and bradycardia- can be profound and refractory!

ex of calcium channel blockers- verapamil, diltiazem, amlodipine, nifedipine

115
Q

what is the treatment for calcium channel blocker ingestion?

A

atropine 0.5-1mg IV q2-3minutes
calcium glucagon bolus or infusion
glucagon 5mg IV
norepinephrine is the vasopressor of choice
HIGH DOSE INSULIN EUGLYCEMIC THERAPY HAS POSITIVE INOTROPIC EFFECTS

116
Q

in children what type of trauma predominates?

A

BLUNT trauma

in adolescents penetrating trauma increases accounting for 15% of trauma and higher mortality

117
Q

what does SOAPME stand for

A 
S- suction
O- oxygen
A- airway equipment
      - laryngoscope and blade
      - ETT above and below
      - stylette
      - BVM- well fitting mask
      - Back up such as LMA, video laryngoscopy
P- pharmaceuticals (ex: ketamine and rocuronium/succinylcholine)
ME- monitoring equipement
118
Q

what are the absolute contraindications to succinylcholine (3)

A

DO NOT give in any circumstance where you may have elevated CK or potassium or risk of malignant hyperthermia

  • muscular dystrophies and myopathies
  • burns, crush, trauma (48-72h later)
119
Q

what are the relative contraindications to succinylcholine (3)

A
  • increased ICP
  • increased intraocular pressure
  • known pseudocholinesterase deficiency (risk for prolonged duration of action)
120
Q

what are signs of tension pneumothorax and what are the treatment options?

A

absent breath sounds on one side
tracheal deviation AWAY from affected side
hypotension
TREAT WITH NEEDLE DECOMPRESSION FIRST AND THEN CHEST TUBE
need chest tube prior to transport

121
Q

What are the landmarks for needle decompression

A

2nd intercostal space mid clavicular line

ABOVE THE 3RD RIB- neurovascular bundle is below

122
Q

What is the treatment for massive hemothorax

A

large bore chest tube (4x ETT)

123
Q

what is Beck’s triad for cardiac tamponade

A

muffled heart sounds
distended neck veins
hypotension

124
Q

what is the treatment of cardiac tamponade

A

fluid resuscitation
pericardiocentesis
thoracotomy

125
Q

what are the sights of major hemorrhage

A

floor and 4 more!

  • chest
  • pelvis
  • abdomen
  • long bones (teens)
126
Q

what are the signs with class 1, 2, 3 and 4 hemorrhage

A 
class 1: <15%, normal vitals apart from tachypnea
class 2: 15-30%, tachypnea, tachycardia, BP NORMAL (see narrowing of pulse pressure)
class 3: 30-40%, see signs of hypotension * consider fluid replacement with crystalloid and blood
class 4:>40%, very comatose
127
Q

what is massive hemorrhagic protocol (3)

A

start with o negative blood 15ml/kg
tranexamic acid (TXA) if within 3 hours of traumatic injury
then activate MTP if need more blood
2:1:1 (pRBC’s: FFP: platelets)

128
Q

what is the key complication associated with massive hemorrhage protocol

A

hyperkalemia- peaked t waves on EKG

129
Q

what is AVPU

A

A- awake/alert
V- responds to verbal stimulation
P- responds to painful stimulation
U- the patient is unresponsive

PU= equivalent to GCS <8

130
Q

What is GCS eyes

A

4- spontaneously
3- to voice
2- to pain
1- no eye opening

131
Q

what is GCS verbal

A 
5- oritented
4- confused
3- inappropriate words
2- incomprehensible sounds
1- none
132
Q

what is GCS motor

A 
6- obeys commands
5- localizes to pain
4- withdrawal to pain
3- flexion to pain
2- extension to pain
1- none
133
Q

what is lab belt complex

A

hyperflexion leads to CHANCE FRACTURE (fracture L1-L2) (compression fracture of lumbar spine)
compression of intra-abdominal organs (duodenal perforation messenteric disruption, pancreatic, bladder injuries)

134
Q

what are the indications for CT for abdominal trauma

A 
low BP
abdominal tenderness
femur fracture
elevated liver enzymes
microscopic hematuria
initial hematocrit <30%
135
Q

what does the cps recommend for trampoline use in homes and playgrounds

A

CPS recommends AGAINST ALL at home/playground
fractures most common in the upper limb
most occur on mat, some by falling off
most occur when >1 person on trampoline

136
Q

what does cps recommend for ATV

A

<16yo should NOT operate any ATV including youth model
>16yo should have license/training course, helmet, eye protection, boots, gloves, long pants; restrict passengers to number ATV designed for

137
Q

what does cps say about bicycle helmet use in canada

A

helmets reduce risk of head injury by 70%

legislation increases rate of helmet use

138
Q 
car seats:
rear facing?
front facing?
booster seat?
seat belt?
A

rear facing: <1<10kg
front facing: >1, >10 kg
booster (typically 5-9): at least 18kg (40lb)
seat belt: at least 36kg (80lb) and 145cm tall

139
Q

what GCS is associated with mild, moderate and severe head injury

A

mild: GCS 14-15
moderate: 9-13
severe: GCS <8

140
Q

what are the high risk criteria for CATCH

A

W- worsening headache
I- irritability on exam
G- GCS <15 at 2h after injury
S- suspected open or depressed skull fracture

141
Q

what are the medium risk criteria for CATCH

A

S-sign of basal skull fracture
D- dangerous mechanism of action (MVA, fall >3 feet or 5 stairs, fall off bike with no helmet)
H- hematoma (large boggy hematoma of the scalp)

142
Q

what are the signs of basal skull fracture (4)

A 
raccoon eyes
otorrhea or rhinorrhea of CSF
battle sign
hemotypmpanum
if there are signs of basal skull fracture then no tube by nasal route!!
143
Q

why are children more prone to intracranial injury

A

large head: body ratio
thinner cranial bones
less myelinated neural tissue
more likely: diffuse axonal injury with cerebral swelling or subdural in infants
less likely: epidural, parenchymal intracranial hemorrhages

144
Q

what is primary injury with head trauma? seocndary injury?

A

primary injury- occurs at the time of injury
we cannot do anything about this
secondary injury- occurs later (hours-days)
process of cerebral edema developing and affecting autoregulation

145
Q

what is the formula for CPP

A

CPP- MAP-ICP
target 50-70
if you have increased ICP then need higher MAP to maintain CPP

146
Q

What is the management of secondary injury for head trauma (7)

A 
ICP peaks 2-3 days later (48-72h)
Normal MAPs
Normal CO2
Normal temperature
Normal glucose
Normal saturation
no seizures
no infections
147
Q

what are the signs of herniation

A 
hypertension
bradycardia
irregular respiration
3rd or 6th nerve palsy
3rd- eyes down and out, dilated pupil, ptosis (seen with uncal herniation)
6- lateral rectus palsy
148
Q

what is the management for herniation?

A

intubate and hyperventilate (CO2 30-35 with FiO2 100%)
head of bed to 30 degrees
head midline
mannitol (1g/kg) or 3% hypertonic slaine (3-5mL/kg) or both
sedation
if seizing- loading dose of phenytoin or phenobarb

149
Q

what are the most common c spine injuries in kids

A

upper c spine injuries C1-C3

c spine injuries are rare in kids (<3% of blunt trauma)

150
Q

what x rays do you order for cpsine

A

ap
lateral
odontoid
CT of c-spine NOT routine

151
Q

what is SCIWORA

A

spinal cord injury without radiologic abnormality
related to ligamentous injury
need MRI
have an abnormal MRI

152
Q

what are the 6 steps for return to play concussion guidelines

A
  1. No activity * children should remain at this step until symptom-free for several days (optimally 7-10 days) must be fully back to school before return to play
  2. Light aerobic exercise
  3. sport specific exercise
  4. non-contact training drills
  5. full-contact practice
  6. return to play
153
Q

what are common etiologies of convulsive status epilepticus in children (10)

A 
Acute CNS infection (bacterial meningitis, viral meningitis, encephalitis)
metabolic derangement
antiepileptic drug non compliance
antiepileptic drug overdose
non-antiepileptic drug overdose
prolonged febrile seizure
remote:
cerebral dysgenesis
perinatal HIE
progressive neurodegenerative disorders
cerebral migrational disorders
154
Q

what are the treatment options for status epilepticus

A

benzos x 2 then phenytoin/fosphenytoin then phenobarb, then midazolam

155
Q

what is the dose for lorazepam for status epilepticus

A

0.1 mg/kg IV/IO/buccal/PR max 4 mg

156
Q

what is the dose for midazolam for status epilepticus

A
  1. 5mg/kg buccal (max 10mg)

0. 2mg/kg IN/IM max 10mg (5mg/nostril)

157
Q

what is the dose for diazepam for status epilepticus

A

0.5mg/kg PR (max 20mg/dose)

158
Q

what loading doses/medications can you give for status epilepticus if you cannot get IV access

A

fosphenytoin IM- 20mg/kg
paraldehyde PR- 400mg/kg
phenytoin IO- scant evidence- 20mg/kg (max 1000mg)

159
Q

what is the definition of a BRUE

A 
child <1 year old with >1 of the following:
cyanosis or pallor
absent, decreased or irregular breathing
marked change in tone
altered level of responsiveness
NO other explanation
160
Q

what is low risk criteria for BRUE

A

age <60 days
gestational age >32 weeks and postconceptual age >45 weeks
occurrence of only 1 BRUE (no prior BRUE ever and not occurring in clusters)
duration of BRUE <1 minute
no CPR required
no concerning historical features/physical examination findings (ie cardiac, seizures)

161
Q

what should you do with a low risk patient with a BRUE prior to sending them home? what MAY you consider

A

educate the caregivers about BRUEs offer resources for CPR training to caregiver

May consider:
EKG
pertussis test
observe in ER

162
Q

what should you NOT do for BRUE

A

should NOT

  • obtain WBC count, blood culture, CSF, serum sodium, potassium, chloride, BUN, creatinine, calcium, ammonia, blood gases, urine organic acids, plamsa amino acids, chest radiograph, echo, EEG, studies for GER
  • initiate home cardio-respiratory monitoring
  • prescribe acid suppression therapy for anti-epileptic medications

Need NOT

  • obtain viral respiratory test, urinalysis, blood glucose, serum bicarbonate, serum lactic acid, neuroimaging, eval for anemia
  • admit to hospital solely for cardiorespiratory monitoring
163
Q

what is the definition of DKA

A

blood glucose >11
pH< 7.3 or bicarb <15
ketonemia or ketonuria

164
Q

what are some clinical manifestations of DKA

A 
tachypnea, deep sighing Kussmaul respiration
dehydration
nausea
vomiting
abdominal pain
confusion
drowsiness
progressive obtundation
loss of consciousness
fuity breath odour
polyuria
polydipsia
weight loss
165
Q

what is mild hypothermia? moderate? severe?

A

mild 32-35
moderate 28-32
severe <28

166
Q

At what potassium level would you terminate CPR

A

terminate CPR if potassium >12

167
Q

what is the equation for osmolarity

A

2 x Na + glucose + urea

2 salts and a sticky bun

168
Q

what is osmolar gap? what is normal

A

measured osmolarity- calculated osmolarity

normal: 0-5

169
Q

what is anion gap?

A

Na - Cl- HCO3

Normal 8-12

170
Q

what are some things that cause an anticholinergic toxidrome? (7)

A 
jimsonweed
scopolamine
atropine
glycopyrrolate
diphenhydramine
dimenhydrinate
olanzapine
171
Q

what drug should be avoided with anticholinergic toxidrome?

A

phenytoin!!

can cause FATAL ARRHYTHMIAS!

172
Q

what drugs should you NOT give with TCA

A

physostigmine- leads to complete heart block
phenytoin- fatal arrhythmia
flumazenil- worsens seizures
hemodialysis is not useful because the drug is highly protein bound with a large Vd

173
Q

what is the antidote for benzodiazepine?

A

flumazenil

174
Q

what are the signs and symptoms of salicylates? what is the one key feature?

A 
nausea/vomiting
fever
TINNITUS **
diaphoresis
tachypnea
seizures
175
Q

what is the key bloodwork feature for ASA overdose

A

respiratory alkalosis and metabolic acidosis
dehydration
intracellular hypoglycemia

176
Q

what is Reye syndrome? what do we see on bloodwork?

A

rapidly progressive encephalopathy, associated with liver toxicity. It usually begins shortly after recovery from a viral infection. About 90% of cases in children are associated with aspirin (salicylate) use

On bloodwork:
elevated AST/ALT
low glucose
elevated ammonia
fatty acid infiltration of liver
increased ICP
177
Q

what is a common co-ingestant with ASA

A

acetaminophen

don’t forget to order an acetaminophen level!

178
Q

what is the main side effect seen with NAC

A

anaphylactoid type reaction
stop infusion
treat with benedryl/epi/ventolin as needed

179
Q 
which of the following is NOT expected with an iron overdose
ileum
hypovolemia
an asymptomatic period
metabolic acidosis
A

ILEUS!

180
Q

List 4 signs of recent marijuana use

A 
Conjunctival injection
Dry mouth
Increased appetite
Euphoric mood
Paranoia
Perceptual changes
Depersonalization
Agitation
Impaired reaction time
Impaired concentration
Tachycardia
Hypertension
Ataxia
181
Q

Left shoulder pain

A

small splenic capsular tears may cause abdominal or referred left shoulder pain

182
Q

Give the 4 fracture findings that are specific in non-accidental trauma:

A 
Posterior rib fracture
Femoral metaphyseal corner fractures
Scapula spinous process fracture
Femur fractures in non-ambulatory children
Proximal humeral fractures

corner fractures in the metaphysis are the most classic.
Transverse fractures in long bones are the most prevalent

183
Q

lap belt fracture

A

chance fracture

184
Q

What 3 things would you go Red Man Syndrome

A

stop infusion
It can be prevented by slowing the vancomycin infusion (1/2 the original rate) rate or by pre-administration of H1-receptor blockers

185
Q

Treatment for Acute Dystonic Reactions

A

Benadryl

186
Q

Iatrogenic cause of methemoglobinemia

A

Inhaled Nitric Oxide

187
Q

what are two treatment options for hypertensive emergency?

A

nicardipine
labetalol
esmolol
sodium nitroprusside

188
Q

What is the long term complication of methanol toxicity

A

blindness

189
Q

what are two treatments that you should start for Kawasaki disease

A

ASA 3-5mg/kg PO daily

IVIG 2g/kg IV now

Pediatrics- Noelle (28 decks)

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