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Pediatrics > BRS Emergency Medicine > Flashcards

BRS Emergency Medicine Flashcards

0
Q

2 ways to open up the airway

A

head tilt method

jaw thrust method if suspect cspine injury

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1
Q

MCC of cardiac arrest in a child is _______

A

lack of oxygen supply to the heart

heart disease is an uncommon cause in children

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2
Q

assess breathing with this method

A

look listen feel

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3
Q

where to assess pulse in infants vs. children

A

infants- brachial

children- carotid

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4
Q

compensated
decompensated
irreversible
*describe these forms of shock

A

compensated- normal BP and CO with adequate tissue perfusion, maldistributed blood flow to essential organs
decompensated- hypotension, low CO, inadequate tissue perfusion
irreversible- cell death, refractory to medical treatment

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5
Q

_____ is the MCC of shock in kids

it is commonly due to _____ or _____

A

hypovolemic

hemorrhage, dehydration

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6
Q

in hypovolemic shock, volume losses > _____ lead to decompensated shock

A

25%

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7
Q

2 phases of septic shock

A
  1. hyperdynamic stage- bounding pulses, high CO, warm extremities, wide pulse pressure
  2. decompensated stage- impaired mental status, cool extremities, diminished pulses
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8
Q

2 types of distributive shock

A

anaphylactic- acute angioedema of upper airway, bronchospasm, pulmonary edema, urticaria, hypotension

neurogenic- total loss of distal sympathetic cardiovascular tone with hypotension 2/2pooling of blood within the vascular bed

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9
Q

changes in ____ often occur before changes in BP in shock

A

HR- tachycardia occurs before hypotension

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10
Q

initial fluid management in shock

A

20 mL/kg bolus of NS or LR

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11
Q

give ______ for DIC

A

FFP

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12
Q

_____ are the leading cause of trauma in kids

A

MVA

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13
Q

special considerations in trauma in kids

A
  • they have larger heads so head injuries are more common
  • rib cage is more pliable so more energy is transmitted to lungs, liver, spleen
  • growth plates are weak and are at the highest risk of injury (ligaments are stronger than the growth plate)
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14
Q

causes of PEA

A

cardiac tamponade
tension ptx
profound hypovolemia

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15
Q

in addition to primary and secondary survey, do these tests

A

EKG
urinary cathether
NG tube
CXR

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16
Q

seizures are common after head trauma… what do you do?

A

nothing… they are self limited

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17
Q

infants are at risk for bleeding in the ______ and ______ because of open fontanelles and cranial sutures

A

subgaleal and epidural

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18
Q

epidural hematoma is tearing of the ______
on CT, you see _______
tx by _______

A

middle meningeal artery
lenticular density
surgical drainage

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19
Q

subdural hematoma is due to tearing of ______
on CT, you see _______
how to tx

A

bridging veins
crescentic density
neurosurg consult and usually surgical drainage

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20
Q

intracerebral hematoma usually occurs on _____ (side/opposite side) of trauma

A

opposite side

contrecoup injury

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21
Q

______ is an early sign of herniation in children < 4 years of age

A

bradycardia

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22
Q

cushing’s triad (late sign of herniation)

A

bradycardia
HTN
irregular breathing

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23
Q

how to manage increased ICP

A

mild hyperventilation
elevation of head
diuretics like mannitol
neurosurg consult

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24
Q

kids are prone to spinal cord injuries w/o radiographic abnormality

A

yep

SCIWORA

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25
Q

distended neck veins, decreased breath sounds, hyperresonance to percussion, displaced trachea, PEA, shock

A

tension pneumothorax

tx with needle decompression

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26
Q

occurs after injury to RUQ (esp bicycle handle bar)

  • abdominal pain and vomiting
  • bowel obstruction is found on radiographic evaluation
A

duodenal hematoma

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27
Q

lap belt injuries

A

chance fracture- flexion disruption of the lumbar spine
liver and spleen lacs
bowel perfs

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28
Q

_____ are the second MCC of accidental death in children

esp due to _____

A

burns

scalding injuries from hot liquids

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29
Q

classifying degree of burn

A

first degree- only the epidermis
-red, blanching, painful skin (ex. sunburn)

second degree (partial thickness)- epidermis and part of the dermis

  • superficial partial thickness- entire epidermis and outer portion of dermis; moist, painful, red; blister but no scar
  • deep partial thickness- entire epidermis and lower portion of the dermis; pale white; may blister and heal with scarring

third degree (full thickness)- epidermis, dermis, part of subcu tissue

  • dry, white, leathery
  • insensitive to pain b/c nerve endings are destroyed
  • skin grafts are needed
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30
Q

if you suspect someone inhaled hot gases, do this

A

intubate!!

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31
Q

for burns, fluid resuscitation is critical

A

yep

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32
Q

skin care for burns

A

1st degree
-moisturizers, analgesics
2nd degree
-opiates, debridement of dead skin to prevent infection
3rd degree
-skin grafting, hydrotherapy, escharotomy

abx in the form of topical 1% silver sulfadiazine for 2nd and 3rd degree

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33
Q

victims of near drowning may suffer from aspirating liquid (_____) or from laryngospasm (______)

A

wet drowner

dry drowner

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34
Q

near drowners might cough up ______

in the next few days, monitor for these things

A

pink frothy material
aspiration pneumonia
deterioration of pulmonary function

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35
Q

bruises on fleshy or protected areas (face, cheek, back, chest, abdomen, buttocks, genitalia) suggest______

A

child abuse

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36
Q

what do nonaccidental burns look like

A

clear line of demarcation

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37
Q

aging of bruises by color

A

red blue: 0-3 days
blue purple: 3-5 days
green: 5-8 days
yellow brown: 8-14 days

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38
Q

top 2 causes of death in child abuse cases

A

head injuries

visceral injuries

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39
Q

fxs of first or posterior rib, sternum, scapula, vertebral spinous processes
bucket handle or corner fxs

A

child abuse!

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40
Q

what to do if you suspect child abuse

A

call CPS
skeletal survey
dilated ophtho exam to look for retinal hemorrhages

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41
Q

what postmortem finding is common in SIDS pts

A

intrathoracic petechiae

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42
Q

most cases of poisoning in children are 2/2 child abuse

A

F

90% are accidental

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43
Q

poisoning: bitter almond odor

A

cyanide

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44
Q

poisoning: garlic odor

A

arsenic

organophosphates

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45
Q

poisoning: acetone odor

A

salicylates

isopropyl alcohol

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46
Q

poisoning: wintergreen odor

A

methylsalicylate

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47
Q

poisoning: moth ball odor

A

camphor

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48
Q

poisoning skin finding: cherry red color

A

carbon monoxide

cyanide

49
Q

poisoning skin finding: sweaty

A

organophosphates

sympathomimetics

50
Q

poisoning skin finding: dry skin

A

anticholinergics

51
Q

poisoning skin finding: urticaria

A

allergic reaction

52
Q

poisoning skin finding: gray cyanosis

A

methemoglobinemia

53
Q

poisoning miosis

A

opiates
phencyclidine
organophosphates
phenothiazines

54
Q

poisoning mydriasis

A

amphetamines
cocaine
TCAs
atropine

55
Q

poisoning nystagmus

A

dilantin

phencyclidine

56
Q

poisoning retinal hemorrhages

A

CO

methanol

57
Q

in a poisoning situation, radio-opaque stuff in the stomach on imaging may indicate:

A 
CHIPE
chloral hydrate and calcium
heavy metals
iodine and iron
phenothiazines
enteric-coated tablets
58
Q

in AMS, always give these

A

dextrose and naloxone

59
Q

ipecac

  • what does it do
  • is it effective
A

rapidly induces emesis

does not really improve clinical outcome

60
Q

gastric lavage can be performed if it’s within _____ of ingestion of a toxin

A

1 hour

61
Q

activated charcoal improves clinical outcome but is ineffective for the following:

A 
iron
lithium
alcohols
ethylene glycol
iodine
K
arsenic
62
Q

whole bowel irrigation is a rapid and complete emptying of the intestinal tract with ______ and ______

A

polyethylene glycol and an electrolyte solution

63
Q

pathophys of acetaminophen poisoning

A

depletion of glutathione (a cofactor used during metabolism of acetamionphen by the cytochrome P-450 system) –> accumulation of toxic intermediates –> hepatocellular necrosis

64
Q

4 phases of acetaminophen poisoning

A 
stage 1
-30 min-24 hours
-asymptomatic, or N/V/D
stage 2
-24-72 hours
-GI sxs resolve; hepatic transaminases begin to increase 
stage 3
-72-96 hours
-hepatic necrosis, jaundice, hypoglycemia, hepatic encephalopathy, renal failure, etc
stage 4
-4 days-2 weeks
-resolution of sxs, progressive liver damage, or death
65
Q

how to tx acetaminophen poisoning

A
  • gastric lavage
  • activated charcoal
  • get serum acetaminophen levels 2-4 hours after ingestion –> Matthew-Rumack nomogram –> if hepatitis, give NAC (give it within 8 hours of ingestion)
66
Q

respiratory alkalosis with anion gap metabolic acidosis indicates ______ poisoning

A

salicylate (aspirin)

67
Q

pathophys of salicylate poisoning

A
  • directly stimulates respiratory center –> respiratory alkalosis
  • uncouples ox phos –> lactic acidosis
68
Q

fever, diaphoresis, flushed appearnace, tinnitus, etc

poisoning by _____

A

salicyclate

69
Q

how to tx salicylate poisoning

A

gastric lavage
activated charcoal
get serum salicylate level 6 hours after ingestion –> Done nomogram
alkalinize the urine with sodium bicarb, IV fluids

70
Q

antidote for acetaminophen

A

NAC

71
Q

antidote for anticholinergic agents

A

physostigmine

72
Q

antidote for benzos

A

flumazenil

73
Q

antidote for black widow spinder

A

antivenin lactrodectus mactans

74
Q

antidote for CO

A

oxygen

75
Q

antidote for coral snake

A

antivenin micrurus fulvius

76
Q

antidote for cyanide

A

CN antidote kit

hydroxocobalamin (vitamin B12)

77
Q

antidote for digitalis

A

digoxin specific Fab antibodies

78
Q

antidote for heavy metals

A

D-penicillamine
dimercaprol
DMSA
EDTA, Ca

79
Q

antidote for inducers of dystonia

A

diphenhydramine

benztropine

80
Q

antidote for inducers of mehemoglobinemia

A

methylene blue

81
Q

antidote for iron

A

deferoxamine

82
Q

antidote for isoniazid

A

pyridoxine (vitamin B6)

83
Q

antidote for methanol and ethylene glycol

A

ethanol

fomepizole

84
Q

antidote for narcotics

A

naloxone

85
Q

antidote for organophosphates; carbamate pesticides

A

atropine

pralidoxime

86
Q

antidote for beta blockers; CCBs

A

glucagon

87
Q

antidote for sulfonylurea oral hypoglycemic agents

A

octreotide

glucagon

88
Q

pathophys of iron poisoning in children

A

direct damage to GI tract –> hemorrhage
hepatic injury and necrosis
third spacing and pooling of blood in the vasculature
interference with ox phos

89
Q

stages of iron toxicity

A

stage 1: 1-6 hours
-abd pain, N/V/D, GI bleeding, shock, fever, leukocytosis
stage 2: 6-12 hours
-resolution of stage 1 sxs
stage 3: 12-36 hours
-metabolic acidosis, circulatory collapse, hepatic and renal failure, DIC, neuro deterioration
stage 4: 2-6 weeks
-pyloric or intestinal scarring with stenosis

90
Q

how to tx iron poisoning

A
  • gastric lavage **note: activated charcoal doesn’t work
  • obtain serum iron level 2-6 hours after ingestion
  • give IV deferoxamine if serum iron levels > 500, severe GI sxs, more than 100 mg/kg of iron was ingested
  • can also do deferoxamine test dose… if urine turns pink/red, give it
91
Q

lead poisoning is typically _____ in timeline

A

chronic

92
Q

sxs of lead poisoning

A

abdominal- colicky pain, constipation, anorexia, vomiting
neuro- irritabliilty, seizures, listlessness
peripheral blood smear- microcytic anemia with basophilic stippling
dense metaphyseal bands on xrays of the knees and wrists (lead lines)

93
Q

how to dx and tx lead poisoning

A

dx with elevated lead level or elevated erythrocyte protoporphyrin
tx for significant toxicity with dimercaprol, BAL, EDTA

94
Q

____ cause coagulation necrosis that produces superficial damage to the mouth, esophagus, and stomach

A

acids (toilet bowl cleaner)

95
Q

_______ cause liquefaction necrosis that produces deep and penetrating damage

A

alkalis (oven and drain cleaners, bleach, laundry detergent)

96
Q

gastric perforation and peritonitis may follow ______ ingestion

A

acid

97
Q

esophageal perforation with mediastinitis may follow _____ ingestion

A

alkali

98
Q

how to manage caustic ingestions

A

no ipecac, gastric lavage, or activated charcoal

do an endoscopy

99
Q

pathophys of CO poisoning

A
  • CO displaces oxygen from hemoglobin, creating carboxyhemoglobin (CO-Hb)
  • oxygen hemoglobin dissociation curve is shifted to the left (they are bound tighter… impaired release of oxygen to tissues)
  • CO interferes with cellular oxidative metabolism
100
Q

low levels: HA, flulike illness, dizziness

high levels: visual and auditory changes, vomiting, confusion, slurred speech, cyanosis, MI, coma, death

A

CO poisoning

101
Q

cherry red skin and retinal hemorrhages suggest ______

A

CO poisoning

102
Q

CO poisoning can cause delayed permanent neuropsych syndrome (memory loss, personality change, deafness, seizures, etc)

A

yep

103
Q

how to dx CO poisoning

A

dx CO poisoning by measuring CO-Hb levels

104
Q

how to tx CO poisoning

A

100% oxygen
hyperbaric oxygen if available
hospitalization for CO-Hb > 25% or > 10% if there are other problems

105
Q

management of bite wounds

A

copious irrigation
wounds on face, large wounds, wounds < 12 hours old- suture it!
abx like augmentin
tetanus ppx if needed

106
Q

cat bites are at high risk of infection with ____

A

P multocida

you might also get cat scratch disease

107
Q

human bites are especially serious if at the MCP joint

likelihood and organisms of infection

A

high risk of infection

strep viridans, staph aureus, bacteroides, peptostreptococcus, eikenella corrodens

108
Q

spider with red or orange hour glass marking on the ventral surface
what kind of toxin is the venom

A

black widow spider

neurotoxin

109
Q

black widow spider bite sxs

A

few local sxs
severe HTN and muscle cramps
nonspecific sxs

110
Q

how to tx black widow bite

A

local wound care
benzos for muscle camps
latrodectus antivenin

111
Q

spider with a brown violin-shaped marking on the dorsum of the thorax

A

brown recluse/fiddleback spider

112
Q

brown recluse spider bite clinical features

A
  • initial bite not bad… after 1-8 hours, painful itchy papules that increases in size and discolors
  • some pts develop necrotic and ulcerated deep lesion
  • systemic rxns within 24-48 hours: fever, chills, weakness, vomiting, joint pain, DIC, renal failure
113
Q

how to tx brown recluse spider bite

A

local wound care, tetanus ppx
steroids, skin grafting, dpasone, hyperbaric oxygen
no antivenin available

114
Q

most snake bites are via the _____

A

pit viper snakes (rattlesnake, cottonmouth, copperhead)

115
Q

venom of the pit viper snakes

clinical features

A

proteolytic enzymes

  • paresthesias of the scalp, periorbital fasciculations, weakness, metallic taste in mouth
  • coagulopathy, thrombocytopenia, hypotension, shock
116
Q

how to tx pit viper snake bite

A

crotalidae polyvalent antivenin within 4-6 hours
children require more of the antivenin
can also give crotalidae polyvalent immune Fab

117
Q

coral snakes- how to know if they’re dangerous

tx for their bites

A

red next to yellow, kill a fellow
red next to black, venom lack
neurotoxic venom causes severe systemic sxs… there is antivenin for the Eastern US and Texas coral snakes

118
Q

GCS < ____ signifies severe head injury

A

8

119
Q

infection with pasteurella is more common in cat/dog bites than human bites (T/F)

A

T

120
Q

ingestion of prenatal vitamins puts kids at risk for ____ poisoning

A

iron

Pediatrics (14 decks)

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