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Paediatrics Royal College > Acute care/NICU > Flashcards

Acute care/NICU Flashcards

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1
Q

What tests are done as part of the IPS (integrated prenatal screen)?

A
  1. Frist trimester screen (12 week nuchal translucency +PAPP-A+ BHCG)
  2. Maternal serum screen (AFP + E + HCG)

Can detect: trisomies, open NTD, Placental insufficiency

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2
Q

When can chorionic villius sampling be completed? What does it detect?

A

9-12 weeks

Chromosome abnormalities

1% pregnancy loss

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3
Q

When can aminocentesis be completed? What does it detect?

A

>16 weeks

Chromosome AbN, lung maturation, infection, renal

0.5% pregnancy loss

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4
Q

When is the anatomic ultrasound completed?

A

18-20 weeks

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5
Q

What is the diagnosis if a baby had: transient myeloproliferative disorder, AVSD, hypotonia, absence of rectal ganglion cells?

A

T21

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6
Q

What is the diagnosis if a baby had: cutis aplsia, cleft lip and clino/polydactyly?

A

T13

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7
Q

What is the diagnosis if a baby had rocker bottom feet, interupted aortic arch, overlapping fingers, microcephaly?

A

T18

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8
Q

What is the diagnosisif a baby had extra nuchal fold and lymphedema of the hands?

A

45 X0

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9
Q

Which of the following statements is FALSE?

  1. Antenatal steriods are indicated for women presenting with the risk of PTL
  2. Antenatal steroids are used for neuroprotection and reduce CP
  3. MGSO4 is indicated forwomen
  4. MgSO4 is used for neuroprotection and decreases CP
A

2

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10
Q

What are the prenatal interventions to prevent birth defects?

A
  1. Folic acid: decreased NTD
  2. Glucose control in diabetes
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11
Q

What are the antenatal interventions to improve outcomes in prematurity?

A
  1. Antenatal steroids,
  2. MgSO4
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12
Q

What is the most common cause of SN hearing loss?

A

CMV

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13
Q

What are the main findings in congenital CMV?

A

IUGR, Microcephaly, MR, deafness, HSM

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14
Q

What are the main findings in toxoplasmosis?

A

IUD, hydrocephalus, MR, chorioretinitis

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15
Q

What are the main findins in parvovirus B19?

A

Anemia, heart failure, hydrops, IUD

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16
Q

What are the main findings of prenatal varicella?

A

Hypertrophic scars, limb deformities, brain atrophy, cataracts

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17
Q

What are the main findings of prenatal syphilis?

A

Snuffles, skin findings, metaphyseal bone lesions

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18
Q

What is the diagnosis?

A

Transient neonatal pustular melanosis

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19
Q

What is the diagnosis?

A

Erytherma toxicum

Usually not hands/feet

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20
Q

What is the diagnosis?

A

Milia

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21
Q

How does HIV present at birth?

A

Usually asymptomatic at birth

PResents with CNS, DD, growth, diarrhea in the 1st year

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22
Q

Which of the following is NOT a risk factor for neonatal hypocalcemia?

  1. Maternal Graves disease
  2. Maternal DM
  3. Maternal Vitamin D defiency
  4. Maternal hyperparathyroidism
A

Maternal Graves

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23
Q

How can maternal diabetes effect the fetus?

A

HypoGlc, macrosomia, jaundice, polycythemia, small left colon syndrome, cardiomyopathy, RDS, jaundice

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24
Q

How does pregnancy induced hypertension effect the fetus?

A

IUGR, Low Plt, Low neutro, fetal demise

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25
Q

Prenatal NSAIDS/ASA?

A

Hemorrhage

PDAclosure

PPHN

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26
Q

Carbamazepine/VPA?

A

NTD

Midface hypoplasia

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27
Q

Phenytoin?

A

Midfacial hypoplasia

Hemorrhage

Fetal hydantoin syndrome (MR/IUGR/Hypoplasia of the distal phalanges)

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28
Q

What are risk factors for preterm delivery?

A
  1. SES status: 40Y, very low SES, low BMI
  2. Past Gyne/OB Hx: Pyelo, Cx abN, multiple abortion, preterm delivery
  3. Lifestyle: >10 cig/day, heavy work
  4. Pregnancy: multiples
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29
Q

What are risk factors for IUGR?

A

Maternal:HTN, renal diseas, diabetes, APL syndrome, nutritional deficiency, smoking, substance use, maternal hypoxia

Fetal: multiple gestation, placental abnormalities, infection, congenital anomaly

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30
Q

How can you prevent hemorrhagic disease of the newborn?

A
  • Vitamin K IM at birth (0.5mg )
  • Alternative: 2mg PO with 1st feed then 2-4 wk, 6-8 wks
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31
Q

What are the presentations of hemorrhagic disease of the newborn?

A
  1. Early: 1st 24 hours, due to maternal medication
  2. Classic: 1:400, bleeding in 1st week of life, vitamin K deficiency
  3. Late: 2-12th week of life (3-8 wk in CPS statement), exclusive BG

Rx: Vitamin K, FFP

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32
Q

When will most newborns void?

A

Within the first 24 hours

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33
Q

Can babies shiver?

A

Less likely to do so

Will use brown fat thermogenesis to generate heat

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34
Q

What % of babies pass stool in the first 24 horus?

A

96%

Think: Meconiumplug, Hirschprungs, meconium ileus, imperforate anus, small left colon (IDM)

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35
Q

What are the three questions you ask at the beginning of NRP?

A
  1. Term?
  2. Crying or breathing?
  3. Tone?
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36
Q

What does MRSOPA stand for in NRP?

A

M- Mask adjust

R- reposition head

S- suction

O- open mouth

P- Pressure increase

A-Alternative airway

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37
Q

Neonatal ETT sizes?

A

>35 weeks: 3.5-4

>1 kg: 3

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38
Q

At what GA do you use a plastic bag?

A
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39
Q

What are the early onset causes of respiratory disease in newborns?

A

TTN, RDS, Severe malformations, pulmonary hypoplasia

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40
Q

What are the evolving onset causes of respiratory disease in newborns?

A

PTX, RDS, MAS, PPHN, pneumonia, loabr emphysema

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41
Q

What is the diagnosis?

A

Hyperinflated

Fluid in the fissures

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42
Q

What is the diagnosis?

A

RDS

Hypoinflated

Ground glass

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43
Q

What are the clues on history for TEF?

A

Apnea, cyanosis, forthing, choking with feeds

LOOK FOR ASSOCIATED: VACTERL

NPO, NG to suction, surgical consult

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44
Q

How does surfactant therapy help preterm babies?

A

Decreased mrotality, PTX, PIE

Decreases duration of vent support, LOS

No effect on IVH, BPD, NEC, ROP

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45
Q

What are the indications for surfactant therapy?

A

Intubated preterm with RDS

MAS FIO@ >50%, sick with pneumonia + OI >15

Natural is better

May repeat, max 3doses

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46
Q

What are the risks of surfactant therapy?

A

PTX, bradycardia, blocked tube, hemorrhage

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47
Q

What is the definition of BPD?

A

Oxygen dependence beyond 28 days or 36 weeks CGA

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48
Q

How late can apnea be considered apnea of prematurity?

A

44 wk CGA

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49
Q

When does a PDA normally close? What are the clinical features?

A
  • Closes at 5-7 days
  • Clinical features: bounding pulses, hyperdynamic precordium, loud second HS, systolic murmure
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50
Q

What are the risk factors for PVL?

A

CAN OCCUR INDEPENDENT OF IVH

PVL=CP

  • Twin-twin transfusion
  • Chorioamnionitis
  • Asphyxia
  • Severe lung disease
  • Hypocarbia
  • NEC
  • Post natal dex
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51
Q

When is the screening for ROP?

A

Who?

When? At 4weeks of age (>26+6) OR after 31 CGA (

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52
Q

What are the risk factors for ROP?

A
  1. Hypotension
  2. Prolonged ventilation
  3. Oxygen therapy
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53
Q

What are the risk factors for NEC?

A
  • Prematurity
  • Ischemia: asphxia, CHD, PDA, severe UGR, exchange transfusions
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54
Q

What are the organisms and treatment for early onset sepsis (1st week of life)?

A
  • GBS, Ecoli, Listeria
  • FSWU
  • Amp/Gent
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55
Q

What are the organisms and treatment for late onset sepsis (1 month)?

A

CONS, staph aures, enterococci

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56
Q

What are the indications for therapeutic hypothermia in HIE?

A

>36 weeks GA

Both 1&2:

1- Any 2 of APGAR 16 (Cord or one hour)

  1. Signs of moderate to severe encephalopathy
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57
Q

How do you cool?

A

Aim for temp 34+/- 0.5 degrees

Passive cooling in the community

Active cooling when in teritary centre

Method: Total body or selective cranial cooling

When? Within first 6 hours of life

Complications: hypotension, bradycardia, coagulopathy, fat necrosis

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58
Q

What is the outcome of HIE? What are the benefits of cooling?

A

Prognosis: Severe 80% morbidity, Moderate 30-50%, mild usually no deficits

Benefits of cooling: risk reduction 25% combined mortality and major NDD (NNT 11 for 1 mortality)

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59
Q

How do you calculate GIR?

A

GIR = (IV Rate (mL/hr) * Dextrose Conc (g/dL) * 1000 (mg/g))/

Weight (kg) * 60 (min/hr) * 100 (mL/dL)

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60
Q

What are red flags for neonatal jaundice?

A

Onset before 24 hours

Hemolysis

Pallor, unwell

HSM

Pale stools, dark urine

Conjugated hyperbili

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61
Q

What are the symptoms of acute bilirubin encephalopathy?

A
  • Lethargy, decreased tone and suck
  • Increased tone, opisthoclonus, retrocollis,

High pitched cry, seizure, coma

Any of these signs: EXCHANGE

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62
Q

What are the complications of exchange transfusion?

A

NEC, thrombocytopenia, anemia, hemolysis, portal vein thrombosis

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63
Q

When do you treat polycythemia?

A

Hct >70 or symptomatic: partial exchange transfusion

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64
Q

How do you calculate the volume of blood to be exchanged in partial exchange for polycythemia?

A

Volume= ((actual-desired hct) x wt x 90)/actual hct

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65
Q

What is the mechanism of TTN?

A

Pulmonary edema from delayed resorption of fluid from alveoli

Excess water =decreased pulmonary compliance therefore tachypnea used as a compensatory mechanism

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66
Q

What are the risk factors for TTN?

A

C/s, preterm birth, IDM, maternal asthma

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67
Q

What stage of lung development occurs between 16-25 weeks?

A

Canalicular stage: the transition between previable and potential viable lung occurs, as respiratory bronchioles and alveolar ducts are formed

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68
Q

What stage of lung development occurs > 25 weeks GA?

A

Saccular stage: potential for viability because gas exchange possible due to large and primitive forms of future alveoli, alveoli at 32 weeks= ZERO, term 50-150 million

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69
Q

Does alveolar growth continue after birth?

A

Yes, for at least two years!

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70
Q

What is RDS caused by?

A
  • Surfactant deficiency
  • Increase in the amount of pressure needed to open alveoli and collapse leading to V/Q mismatch and hypoxemia
  • Also leads to inflammation and epithetial injury
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71
Q

Where is surfactant produced?

A

Type II alveolar cells

Composed of 90% lipids and 10% proteins

Antenatal steroids help to stimulate surfactant synthesis

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72
Q

What are the CXR signs of RDS?

A
  • Low lung volumes
  • Reticulogranular ground-glass appearance with air bronchograms
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73
Q

What are the two main groups of diseases that lead to PPHN

A
  1. Underdevelopment: pulmonary hypoplasia (CDH, CCAM, renal agensis, IUGR)
  2. Maldevleopment: post-term delivery, meconium
  3. Maladaption: normal development of pulmonary vascular bed however acive vasoconstriction occurs
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74
Q

What are the general management guidelines for PPHN?

A
  1. Keep O2 >90%
  2. Correction of acidosis (low pH causes increased PVR)
  3. Sedation
  4. Circulatory support
  5. iNO, sildenafil, ECMO
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75
Q

What are the mechanisms that keep the PDA open?

A

Decrease sats, PGE2, increase NO

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76
Q

When does functional closure of the PDA occur?

A

50% within 24 hour, 90% within 48 hour, all within 72hour

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77
Q

What are the physiologic effects of a PDA?

A
  1. Increased PBF
  2. Decreased SBF
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78
Q

What are the clinical features of a PDA?

A

Murmur over the entire precordium, LUSB, initially systolic only however as pulmonary pressures decrease will become present in both systole and diastole

Bounding pulses

Widened pulse pressure

Tachypnea, apnea

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79
Q

What is the treatment of PDA?

A

Indomethacin or ibuprofen

SE: decreased renal, cerebral and GI blood flow

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80
Q

When does vascularization of the retinal occur?

A

No blood vessels are present before 16 weeks

Retinal vascularization begins a 15-18 weeks, starts from optic nerve and moves outward

Vascularization is complete by 34 weeks in the nasal retina and 40 weeks in the temporal retina

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81
Q

What are prevention strategies for NEC?

A

Human milk

Trophic feeds

Avoidance of H2 blockers

Probiotics

Avoidance of prolonged ABx

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82
Q

What are the ways in which meconium interferes with normal breathing?

A
  1. Airway obstruction (Ball valve effect)
  2. Chemical irritation/pneumonitis
  3. Infection (riskfactor as mec is sterile)
  4. Surfactant disruption
  5. Hypoxemia
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83
Q

What are the risk factors for BPD?

A

Prematurity, mechanical ventilation, oxygen toxicity, infection, inflammation, genetics, late surfactant deficiency

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84
Q

What are the basic toxicology investigations?

A

Point of care glucose, acetaminophen, salicylate levels, serial ECGs, pregnancy tst, AXR, core temperature

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85
Q

What toxiodromes cause tachycardia?

A
  1. Anticholinergics
  2. Sympathomimetics
  3. Ethanol
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86
Q

What toxidromes cause bradycardia?

A

Opiods

Beta blockers

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87
Q

What toxidromes cause QRS widening?

A

TCAs

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88
Q

What toxidromes cause prolonged QTc

A

Neuroleptics

Celexa

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89
Q

What are the four main types of toxidromes?

A
  1. Cholinergic
  2. Anticholinergic
  3. Sympathomimetics
  4. Opiods
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90
Q

What drugs give you a cholinergic toxidrome?

A
  1. Organophosphates
  2. Carbamates: neostigmine!
  3. Alzheimers drugs
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91
Q

What is the acronym for a cholinergic toxidrome?

A

DUMBELS

Diaphoresis

Urination

Miosis

Bronchorrhea/Bradycardia

Emesis

Lacrimation

Lethargy

Salivation

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92
Q

What is the management of cholinergic exposure?

A

Early intubation, 100%

Decontamination

Atrophine until secretions and wheezing stops (muscarnic symptoms)

Inhaled atrovent/ventolin

Pralidoxime (Nicotininc symptoms)

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93
Q

What drugs give you anticholinergic toxidromes?

A

TCA

Antihistamines

Benztropine

Atropine

Lomotil

Neuroleptics

Jimson weed

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94
Q

What are the symptoms of an anticholinergic toxidrome?

A

Blind as a bat (mydriasis-dilated)

Mad as a hatter

Red as a beet

Hot as a desert

Dry as a bone

Tachycardia, absent bowel sounds

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95
Q

What is the management of anticholinergic exposures?

A

Sodium HCO3 for wide QRS
Lorazepam for agitation

Water spray and cooling fans for hyperthermia

Physostigimine is ++ toxicity

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96
Q

What drugs give you a sympathomimetic toxidrome?

A

Cocaine

Amphetamine/Meth

MDMA

Ephedrine

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97
Q

What are the symptoms of a sympathomimetic toxidrome?

A

Mydriasis

Diaphoresis

Hypertension

Tachycardia

Seizure

Hyperthermia

Psychosis

Agitation

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98
Q

What are the serious side effects of MDMA?

A

HTN

Hyperthermia: rhabdo, DIC
Hyponatremia

Serotonin syndrome

Cardiac ischemia

Hepatotoxcity

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99
Q

What is lysergic acid?

A
  • LSD
  • Rapid oral adsorption, symptoms within 30-60 min

Most of the potent hallucinogens

Mydriasis, HTN, Increased RR HR, diaphoresis

Massive OD: fever, autonomic dysregulation, vomiting, respiratory arrest, ICH

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100
Q

What is phencyclidine?

A

PCP or Angel Dust, similar to ketamine

Fluctuating behavior with delirium, paranoia, agitation

NYSTAGAMUS WHILE AWAKE

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101
Q

When do you suggest giving milk?

A

Only if toxin produces simple irritation

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102
Q

What metabolic diagnosis is represented by respiratory alkalosis?

A

Hyper NH4 until proven otherwise

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103
Q

In a baby presenting with a possible metabolic d/o with gram negative sepsis, what is the likely diagnosis?

A

Galactosemia

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104
Q

How do you calculate an anion gap?

A

AG= [Na+K]-[Cl+HCO3]

Normal

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105
Q

What are the first tests you order when suspecting a metabolic condition?

A
  1. VBG
  2. Electrolytes
  3. Glc
  4. Lactate
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106
Q

What are the three metabolic specific tests you should order?

A
  1. Urine organic acids
  2. Serum amino acids
  3. Acylcartinine profile
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107
Q

What is the difference between breastmilk and formula that effects the presentation of metabolic conditions?

A

Breastmilk 1g protein/100cc

Formula 2.5g/100cc

Therefore breastfeeding delays the presentation

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108
Q

What is the specific differential diagnoses for AG metabolic acidosis?

A
  1. Ketones
  2. Lactate
  3. Organic acids
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109
Q

What is the differential diagnosis for nonketotic hypoglycemia?

A
  1. Hyperinsulinism
  2. FAOD
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110
Q

How do you calculate BSA?

A

BSA=SqRt of Ht x Wt/3600

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111
Q

How do you calculate insensible losses?

A

300-400 ml/m2/day

(30 ml/kg/day)

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112
Q

What must you not forget with high urine outputs in water/Na dysregulation?

A

Osmotic diuresis from glucose

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113
Q

When can you give charcoal?

A

Within one hour of ingestion

Must have protected airway if low LOC

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114
Q

What can activated charcoal NOT remove?

A

PHAILS:

P:Potassium

H: Hydrocarbons

A: Alcohols

I: Iron

L: Lithium

S:Solvents

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115
Q

Is gastric lavage recommended?

A

NO- not been shown to improve outcomes

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116
Q

What is the antidote to iron?

A

DFO/Deferoxamine

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117
Q

What is the antidote to carbon monoxide?

A

Oxygen

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118
Q

What is the antidote to pesticides?

A

Atropine

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119
Q

What is the antidote to nifedipine (CCB)?

A

Glucagon, Insulin

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120
Q

What is the antidote to amitriptyline (TCA)?

A

Na HCO3

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121
Q

What is the antidote to methanol?

A

Fomepizole

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122
Q

How to hydrocarbon ingestions kill?

A

Aspiration and pulmonary toxicity

Present in: gasoline, nail polish remover, lighter fluid

Approach with STAT CXR and repeat 4-6 hours later

Rx with oxygen and bronchodilators

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123
Q

What do you see on the CXR of a hydrocarbon ingestion?

A

Perihilar infiltrates

Pneumatoceles

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124
Q

Which diabetic medication will present without hypoglycemia with Kussmaul respirations and an acidosis?

A

Metformin

Lactic acidosis

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125
Q

What drugs cause hypoglycemia?

A
  1. Glyburide (difficult to control)
  2. Beta blockers
  3. Ethanol
  4. Salicylates
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126
Q

What is the toxic metabolite of acetaminophen? What dose is toxic?

A

NAPQI

Dose 150 mg/kg

Hepatoxicity reported >90mg/kg/day

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127
Q

How will an acetaminophen overdose present?

A

AG metabolic acidosis

Acute tubular necrosis

Fulminant liver failure

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128
Q

What is the treatment of acetaminophen overdose?

A

Activated charcoal within 1 hour

Avoid AC if sedated

NAC dosing based on Rumack-Matthew nomogram

Best outcomes if NAC started within 8 hours

Follow LFTS/live function

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129
Q

What are the symptoms of a salicylate overdose?

A

Hyperpnea/tachypnea

AG metabolic acidosis

Nausea, vomiting, GI bleed

TINNITUS (progresses to hearing loss)

Hyperglycemia

Diaphoersis

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130
Q

What is the management of a salicylate overdose?

A

Charcoal up to 6 hours (to avoid bezoar formation)

Glucose to all patients

Treat hypokalemia

Alkalinize serum

Hemodialysis for CNS sypmtoms

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131
Q

What are the radio-opaque drugs?

A

COINS

Chloral Hydrate

Opiod packets

Iron and other heavy metals

Neuroleptics

Sustained release tablets

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132
Q

What is the presentation of iron?

A

10% of intentional overdoses are fatal

Stage 1 (30min-6hr): Nausea, vomiting, diarrhea

Stage 2 (6-12 hours): “Quiesent phase”

Stage 3 (12-24 hours): Metabolic acidosis, shock, GI bleed, coagulopathy, resp failure

Stage 4 (2-3 days): ARDS, liver failure

Stage 5 (3-4 weeks): GI stricture at gastric outlet

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133
Q

What are the clues to iron exposure?

A

GI symptoms

Acidosis

Multiorgan failure

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134
Q

What is the treatment of iron exposure?

A

No role for either charcoal or gastric lavage

Fluid resus

WBI if tablets seen or ,6 hours

IV deferoxamine 15mg/kg/hr until urine clears

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135
Q

What is unique about the presentation of isoproyl alcohol ingestion?

A

Ketosis without acidosis (cannot be metabolized past ketones)

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136
Q

Why is methanol so toxic?

A
  • Less inebriating than ethanol
  • Toxicity in little as one teaspoon
  • Formate causes retinal injury

Profound AG acidosis presents late

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137
Q

What substance is in antifreeze, paints, brake fluid?

A

Ethylene glycol

Colorless, ordorless, sweet taste

Inebriation without smell of ethnaol

Metabolic acidosis

Hypocalcemia (prolonged QTc)

Oxalate crystals

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138
Q

What are the clues to toxic alcohol exposures?

A

Inebriation

Odor

Osmolar gap or acidosis

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139
Q

How do you calculate osmolality?

A

Two salts and a sticky bun

OG= 2x NA + Glucose + BUN

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140
Q

How do you calculate an osmolar gap?

A

OG= Measured-Calculated Osmolarlity

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141
Q

What is the general management of toxic alcohol exposure?

A
  • Wash skin if exposed
  • Fomepizole or ethanol
  • Hemodialysis if high AG acidosis or end-organ damage
  • Cofactor therapy with folic acid
  • Thiamine and pyridoxine
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142
Q

What are the common TCAs to be ingested?

A

Amitriptyline, despiramine, imipramine

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143
Q

What are the clinical effects of TCA overdoses?

A

Inhibit NE and serotonin reuptake

Block cardiac fast Na channels- wide QRS

block muscarinic receptors-weakly anticholinergic

Block histamine receptors- sedation

Block alpha receptors- hypotension

block GABA- seizures

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144
Q

What is the treatment for a TCA overdose?

A

Activated charcoal

Intubation

NAHCO3 for QRS >100mS

NE if hypotension

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145
Q

How does carbon monoxide poisoining present?

A

Headache, dizziness, nausea, confusion, seizure, syncope, coma

Most commonly from smoke inhalation

Tasteless, odourless, non-irritating gas

240x higher affinity to Hb than O2

Dysrhythmia, cardiac arrest in up to 30%

Cherry red skin colour after excessive exposure

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146
Q

What is the treatment of a carbon monoxide exposure?

A

Remove from source and r/o smoke inhalation

Check cyanide level

Follow ECG and cardiac enzymes

Provide 100% FiO2

Hyperbaric O2 if COHb> 25%

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147
Q

What are the clues to a carbon monoxide exposure?

A

Flu-like symptoms

Fire exposure

Normal Sats

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148
Q

What is the most common cause of pediatric death in children 1-4 years?

A

Trauma

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149
Q

What preventative strategies are used to prevent submersion injury?

A
  1. Four sided self closing fence with a self locking gate (MOST EFFECTIVE)
  2. At least 4 feet high
  3. Toddlers should always be wtihin arms length of an adult, even in a tub
  4. 1 adult per baby, 1 adult per 2 young children
  5. Swimming
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150
Q

What are the risk factors for submersion injury?

A
  • Leaving children unattended
  • Alcohol or drug abuse
  • Limited swimming ability
  • Underlying medical condition: seizure disorder, toxin, prolonged QTc, syncope
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151
Q

A 14 year old male is pulled from an icy lake after being found face down. What is the most important strategy influencing survival?

  1. Imediate c-spine
  2. immediate CPR by rescuers
  3. Passive external rewarming, EMS activation and transport to a health care facility
  4. Early placement of definitive airway
A

2

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152
Q

What are GOOD prognostic indicators in submersion injuries?

A

IMMEDIATE BYSTANDER CPR is the most important factor influencing survival

ROSC in

Submersion

Pupils equal and reactive at the scene

NSR at scene

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153
Q

What are BAD prognostic indicators in submersion injuries?

A

Delayed CPR
ROSC > 25 min

Submersion >10 min

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154
Q

What do you see at different degrees of hypothermia?

A

31-32: Normal ECG, Increased HR, Increased BP, loss of shivering

28-31: Decreased HR, Decreased BP, Flipped T, afib, sluggish dilated pupils

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155
Q

What are the ECG changes you will see in hypothermia?

A
  • Marked bradycardia
  • First degree AV block
  • Osborn or J waves
  • Associated prolonged QTc and bradycardia
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156
Q

What are the principles of rewarming without a pulse?

A

>30: CPR, IV meds as needed, defibrillation as needed

Gentle intubation

Warm O2, Warm IVF

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157
Q

What is heat stroke?

A

Core temp >40 and CNS dysfuntion

Headache, disorientation, dizziness, weakness, gait disturbance

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158
Q

What are the clues to a superficial partial thickness burn?

A

Pain, moist, blisters

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159
Q

What is the initial management of burns?

A
  • Cover sterile bandages
  • Early cooling (
  • TETANUS
  • Analgesia
  • Remove shoulder clothing
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160
Q

What are indications for early intubation in burns?

A

Carbonaceous sputum

Singed nasal hairs

Soot in airway

Hoarseness

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161
Q

How do you calculate fluid management in burns?

A

Age > 9: Rule of 9s

Age

Age > 5: Parkland formula: 4cc/kg/BSA over 24 hours, 1st half in 8 hours, 2nd half in 16 hours

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162
Q

What are the physical findings of a post term infant?

A

Cracked, dry, peeling skin

Creases covering the entire sole of the foot

Mature, long fingernails

Basence of lanugo over the back

Palpable breast buds

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163
Q

What is the way to remember gastroschisis vs omphalocele?

A

Gastroschisis: Good baby, bad bowel

Omphalocele: Baby baby, good bowel

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164
Q

What is the appearance of gastroschosis?

A

Centrally located, full thickness, abdo wall defect

  1. Extruded intestine NEVER has protective sac
  2. Umbilical cord intact to the left of the defect

25% associated with bowel atresias

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165
Q

What are the risk factors for gastroschsis?

A

Young mom, EtOH abuse, ASA, ibuprofen, pseudoephedrine

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166
Q

What is the immediate management of a baby with gastrochisis?

A

Temp regulatin

Protective covering

Right lateral position and ensure bowel not kinked

NG decompression

IV fluids 2-3 maintenance

Surgical correction ASAP

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167
Q

What is the clinical appearnace of omphalocele?

A
  1. Protective membrane covered gut
  2. Cord is always attached to membrane
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168
Q

What is the likely mortality of a baby with omphalocele?

A

30%

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169
Q

What are the syndromes associated with omphalocele?

A

Beckwith-Wiedemann, conjoined twins, T18, meningomyelocele, imperforate anus

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170
Q

What are the breastfeeding benefits for baby?

A

Immunologic: IgA, lower rate of OM, LRTI, gastro,

Less allergenic

Less constipating

Better jaw/mandible development

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171
Q

What are the breastfeeding benefits for Mom?

A

ABCDEFGH

Allergic conidtions reduced

Best food for infant

Close relationship with mother

Development of IQ, jaws, mouth

Economical

Fitness

Guards against cancers for mother (breast, ovary, uterus)

Hemorrhage reduced postpartum

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172
Q

How does breastmilk compared to cow milks?

A

67kcal/100cc

Lower portein content

Greater whey

Both lactose based

More fat!

Richer in A

Lower FE

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173
Q

What are the metabolic complications of TPN?

A

Electrolyte Ab

Glucose AB

Ca/PO4 abN

Cholestasis

Line infection

Bone D/o

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174
Q

What is the differential diagnosis for ambiguous gentalia?

A
  1. Undervirilization of males
  2. Virilization of females
  3. True hermphroditism
  4. Incomplete gonadal dysgenesis
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175
Q

What does VACTERL stand for?

A

Verterbal

Anal

Cardiac (VSD)

TEF

Eo Atresia

Renal

Limb

NORMAL DEVELOP AND INTELLIGENCE

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176
Q

What does CHARGE stand for?

A

Coloboma

Heart d/s

Atresia (chonal)

Retarded growth and developemtn

Gential AbN

Ear abN

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177
Q

How does galactosemia present?

A

Within first few days after bith

Jaundice, vomiting, HSM, FTT, poor feeding, lethargy

E coli sepsis!

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178
Q

What are the causes of early onset hemorhhagic disease of the newborn?

A

0-24 hours

Maternal drugs

Inherited coagulopathy

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179
Q

What are the causes of classic hemorhhagic disease of the newborn?

A

Vitamin K deficiency

BF

(

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180
Q

What are the causes of late onset hemorhagic disease of the newborn?

A

Cholestatis

Warfarin

ABLP deficiency

Lack of Vitamin K

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181
Q

What are the components of the APGAR scores?

A

Appearance

Pulse

Grimace

Activity

Respiratory effort

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182
Q

When should rH negative moms receive rHoGAM?

A

28 weeks

Invasive procedures

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183
Q

What is the most common cause of severe thrombocytopenias in the first day of life?

A

Neonatal alloimmune thrombocytopenia (NAIT)

Maternal alloimmune antibodies against HPA on fetal platelets results in NAIT

Can occur in first pregnancy

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184
Q

What is the treatment of NAIT?

A

Need to administer a specific HPA type to avoid continued destruction of transfused platelets.

Subsequent pregnancies: weekly IVIG to minimize the incidence of thrombocytopneia and ICH.

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185
Q

Which infants have a set-up for ABO incompatilibility?

A

Mom O, Infants A or B

Individuals with type A or B have naturally occuring Anti-A and anti B isoantibodies that are frequently igM and do not cross the placenta

Individuals with type O have isoantibodies that are IgG and can cross the placenta.

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186
Q

What are the contraindications to a lumbar puncture?

A
  1. Low platelets
  2. Infections of the skin at the puncture site
  3. Lumbosacral anomalies
  4. Cardioresp instability
  5. Increased ICP
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187
Q

What are the contraindications to breastfeeding?

A

HIV

HTLV

Galactosemia

Active TB

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188
Q

What does cryo contain?

A

Plasma thats been spun: fibringoen, factors V,VIII, XIII, VWF

1 unit/5 kg (1 unit=15mL)

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189
Q

What is the dose of FFP?

A

10 ml/kg

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190
Q

Should you never glue a hand?

A

NO

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191
Q

Which is more likely to cause infection: dog or cat bites?

A

CAT >50% will get infected

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192
Q

When is antimicrobial therapy indicated for bite wounds?

A
  • Moderate or severe bite wounds
  • Puncture wounds
  • Facial bites
  • Hand and foot bites
  • Wounds in IC and asplenic people
  • Wounds with signs of infection
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193
Q

What would be your first choice of antibiotic for human and animal bites?

A

Amoc/Clav

194
Q

What are the exclusions for organ donation?

A
  • Severe untreated systemic sepsis
  • AIDS
  • Active HBV, HCV, CMV
  • Active extracranial malignancy
  • CJD
  • Active disseminated TB
  • HIV
195
Q

What are the confounders of NDD?

A
  • Unresusciated shock
  • Hypotension
  • Severe metabolic disorders
  • Neuromuscular blockade
  • Significant drug intoxication
196
Q

What type of current in present in high voltage burns?

A

AC pulls victim towards source, tetany prevents release

Deep muscle injury is common

197
Q

What type of current is lightning burns?

A

DC, short duration that throws victim from source

198
Q

What are the different types of arrests for high voltage vs. lightning burns?

A

high voltage:VF

Lightning: asystole

199
Q

When should you expect inhalational injury?

A

Carbonaceous sputum

Singed nasal hairs, eyebrows

Hoarseness/stridor

COHB> 10-50%

SOB, CP

Burn in closed space/fireworks

200
Q

What is the most common form of abuse?

A

NEGLECT

201
Q

What fractures are concerning for non-accidential trauma?

A

Metaphyseal clip #, bucket handle

Spiral # of femur/humerus

Posterior rib #

Skull #

Scapula, sternum

Spinal processes

202
Q

What is the PCP triad?

A

Halluications

Nystagmus

Rigidity

203
Q

What is the triad for an ASA overdose?

A
  1. Tinnitus
  2. Hyperventilation
  3. Resp Alkalosis
204
Q

What 3 medications can kill with one pill?

A
  1. Oral hypoglycemics
  2. TCAs
  3. Calcium channel blockers
205
Q

What are the clinical features of TCA overdose? (think triad)

A

Overall blocks Na channels and inhibition of GABA reuptake

  1. CNS:
    - seizures
  2. CVS
    - prolonged PR/QRS/QT
    - arrhythmias
    - hypotension
    - LOOK at AVR = positive R’ wave in AVR
  3. Anticholinergic
    - hot as hell (hyperthermia has very bad prognostic effect)
    - blind as bat
    - mad as hatter
    - red as beet
    - dry as bone
    - bowel and bladder lose their tone
206
Q

In a TCA overdose, what is a predictor of toxicity?

A

Widened QRS –> get ECG asap: if widened, this is predictive of seizures and ventricular dysrhythmias
-nothing else is predictive besides QRS (not drug level, not symptoms)

207
Q

What is the management for TCA overdose?
-how long should you monitor them for if asymptomatic?

A

Charcoal: give even if > 1 hr since gastric emptying may be delayed (due to anticholinergic effect)

If decreased LOC: intubate asap

Bicarb: for QRS > 100 msec, arrhythmias, hypotension, acidosis
-NaHCO3 1-2 mEq/kg bolus, then start infusion

Pressors: norepinephrine for hypotension always!

Active cooling if hyperthermic

Monitor x 6 hours

208
Q

How to treat seizures secondary to toxic ingestion?

A

Use benzos ONLY! Do not use phenytoin since this may worsen Na channel blockade (most drugs cause Na blockade)

209
Q

What are the toxic doses for:

  • acetaminophen
  • ibuprofen
  • ASA
A

Acetaminophen: 150 mg/kg
Ibuprofen: 100 mg/kg
ASA - 150 mg/kg

210
Q

What is the progression of acetaminophen overdose?

A

0-24 hrs: GI irritation or asymptomatic
24-48 hrs: liver involvement, increased PTT is the earliest marker, than rise in AST
72-96 hrs: fulminant hepatic failure, renal failure
4-14 days: recovery or death

211
Q

What are signs of salicylate overdose? Treatment?

A

Tinnitus is often 1st symptom
GI upset (vomiting), confusion/cerebral edema, impaired plt function, pulmonary edema, central hyperventilation (tachypnea)
(Causes uncoupling of oxidative phosphorylation)
-give bicarb for urine alkalination
-call nephro (may need dialysis)
-need to order salicylate levels q2h until they peak and then document at least 2 decreasing ones

212
Q

What are the steps to clearing C-spine on xray film?

A
  1. Ensure adequacy of film
    - need to see C1-C7 and space between C7 and T1 on lateral film to qualify as adequate film
    - if cannot see space between C7 and T1, need swimmers view
  2. Assess vertebral alignment
    - anterior vertebral line, posterior vertebral line, spinolaminar line, posterior spinal line
  3. Assess bony integrity
  4. Assess disc spaces
  5. Odontoid view
    - look for disruptions in odontoid and atlas
  6. Soft tissues
    - prevertebral soft tissue should be
213
Q

What is the most common arrthythmia associated with halogenated hydrocarbon abuse?

A

VT and VF

214
Q

What are the steps of RSI?

A

AMPLE
Preparation: SOAP-ME (suction, oxygen, airway assessment & equipment, position, medications, environment)
Preoxygenation
Premedication
Sedation
Sellick Maneuver
Paralysis
Intubation & confirmation

215
Q

What are the main differences between adult and pediatric airway? (5)

A

For pediatric airway:

  1. Large head and occiput
  2. Large, floppy epiglottis
  3. Larynx is more anterior
  4. Cricoid is narrowest portion of airway
  5. Small oropharynx with large tongue
216
Q

What are the 4 contraindications to rapid sequence intubation?

A
  1. Anticipated difficult airway and unsuccessful attempt
  2. Significant facial or laryngeal trauma
  3. Upper airway obstruction
  4. Cardiopulmonary arrest
217
Q

What are the indications for use of atropine as premedication in rapid sequence intubation?

A

Neonate

218
Q

What are the actions of atropine in rapid sequence intubation? (2)

A
  1. Minimizes vagal stimulation (prevents bradycardia)
  2. Decreases oral secretions
219
Q

What is evidence for use of lidocaine as premedication in rapid sequence intubation?

A

Used in head injury
and thought to reduce rise in ICP associated with laryngoscopy

No evidence to support use in 2001 literature review (no improvement in neurological outcome)

220
Q

What are the effects of the following when used in rapid sequence intubation:

  • Fentanyl
  • Midazolam
  • thiopental
  • etomidate
  • ketamine
  • propofol
A
  1. Fentanyl: sedation, analgesia
    - little hemodynamic effect
  2. Midazolam: sedation, amnesia, NO ANALGESIA EFFECT
    - respiratory and hemodynamic depression
  3. Thiopental: sedation with NO ANALGESIA
    - respiratory and hemodynamic depression
    - laryngospasm and bronchospasm
    - reduces ICP
  4. Etomidate: sedation with NO ANALGESIA
    - minimal respiratory and hemodynamic depression
    - decreases cerebral blood flow, metabolic rate and ICP
    - suppresses cortisol production and may produce myoclonus
    - do NOT use in sepsis!
  5. Ketamine: dissociative sedation, amnesia AND analgesia!
    - minimal hemodynamic effects
    - bronchodilation
    - may cause laryngospasm
    - increases oral secretions
    - no longer thought to increase ICP (multiple studies)
  6. Propofol: sedation, rapid onset and offset
    - hypotension
221
Q

What are the biggest concerns with use of etomidate in rapid sequence intubation for critically ill patients? (2)

A
  1. Adrenal suppression
  2. Hypotension

***Most studies show there is little evidence to support this though

222
Q

What are the adverse effects of succinylcholine and subsequent relative contraindications?

A
  1. Hyperkalemia –> do not use in renal failure
  2. Increased intraocular pressure –> do not use in patients with open globe injury
  3. Malignant hyperthermia
  4. Rhabdomyolysis and myoglobinuria –> do not use in trauma or burns > 48 hrs after injury
  5. Neuromuscular disease
223
Q

What is the onset and half life of:

  • succinylcholine
  • rocuronium
A

Succinylcholine:

  • onset 15-30 secs
  • duration: 5-15 minutes

Rocuronium:

  • onset 30-60 secs
  • duration: 30-45 mins
224
Q

How do you reverse rocuronium?

A

Neostigimine

225
Q

What is an alternative to neuromuscular blockade in RSI if contraindicated?

A

Propofol + Fentanyl may be just as effective in some studies

226
Q

What medication choices for RSI would be appropriate for an infant with tracheomalacia, croup, severe stridor, previous difficult intubation?

A

Do NOT paralyze!
Propofol 3 mg/kg (rapid onset and offset) and topical lidocaine sprayed on the vocal cords
-this will allow you to bag
-will wear off quickly if difficult intubation

227
Q

What medication choices for RSI are appropriate for a patient in status epilepticus?

A

Propofol - anti-epileptic properties
Succinylcholine - short acting
(caution with rocuronium as you may not be able to tell if they’re still seizing or not)

NOT KETAMINE

228
Q

What are the most important steps in sepsis guidelines that affects mortality? (3)

A
  1. Need 20 cc/kg NS bolus within first 10 minutes
  2. Need 60 cc/kg NS bolus within first 60 minutes
  3. Need antibiotics in within first 60 minutes
229
Q

Why does ketamine have minimal effect on blood pressure in sepsis?

A

Causes catecholamine surge to maintain blood pressure
-however, in children who are catecholamine deplete (severe sepsis), may still get hypotensive with ketamine since there are no catecholamines left

230
Q

What are the indications for abdo CT in trauma patients?

A
  1. Seat belt sign
  2. Hx or mechanism suggestive or distracting injuries
  3. AST > 200 or ALT > 125
  4. Gross or microhematuria > 50 RBCs
  5. Decreasing HCT or HGB
231
Q

What are the 3 components of abdominal compartment syndrome?

A
  1. Hypotension (from IVC compression)
  2. Respiratory distress (from increased intraabdominal pressure)
  3. Decreased urine output (from bladder compression and from hypotension)
232
Q

How do you estimate ETT size?

A

(Age/4) + 4 CUFFED

233
Q

How do you estimate a patient’s weight based on age?

A

(Age x 2) + 9

234
Q

What are anatomical considerations in pediatric patients that influence effect of abdominal trauma? (4)

A
  1. Less fat and muscle for protection
  2. Flexible ribs = less likely to fracture but underlying structures can still be injured
  3. Multiple injuries more common since organs are in close proximity
  4. Increased risk for gastric distention (aspiration risk, can be mistaken for abdo distension as result of trauma)
235
Q

In abdominal trauma, in general terms, which structures are more likely to be injured in a crush injury?

A

Midline structures since they are compressed against the spine

236
Q

What are the 3 most commonly injured organs in abdominal blunt trauma?

A
  1. Spleen
  2. Liver
  3. Bowel
237
Q

What is Waddell’s triad?

A

Pattern of injury when a child is struck by a car while crossing the street

  1. Fractured femur (impact from car)
  2. Head injury (thrown a distance and hit their head on ground)
  3. Intra-abdominal or intra-thoracic injury (thrown a distance)
238
Q

What 4 organs are commonly injured in bike handlebar injury?

A
  1. Liver
  2. Spleen
  3. Pancreas
  4. Duodenal injury
239
Q

What are contraindications to a foley catheter in a trauma? (4)

A
  1. Blood at the urethral meatus
  2. Pelvis injury (high risk for associated GU injury)
  3. Rectal injury
  4. High riding prostate
240
Q

What are contraindications to CT scan in a trauma patient?

A

UNSTABLE or indication for emergent OR
-CT should NOT be used for screening; should be used for characterizing and staging of suspected injuries

241
Q

What are the general management principles for a hemodynamically stable patient with:

  1. Lower penetrating chest wounds
  2. Anterior penetrating abdominal wounds
A
  1. Lower penetrating chest wound: serial chest exams, thoracoscopy, laparoscopy, CT scan to look for diaphragm injury
  2. Anterior penetrating abdo wound: FAST, wound exploration, DPL, serial exams, laparoscopy

****remember not to miss diaphragmatic injuries = commonly missed and never heal on their own leading to diaphragmatic herniation

242
Q

What are indications for laparotomy in abdominal trauma? (4)

A
  1. Hemodynamically unstable patient with positive FAST or DPL
  2. Free air on AXR
  3. Peritonitis
  4. Positive CT scan
243
Q

Which structures are commonly injured with pelvic fractures? (3)

A
  1. Urethra
  2. Bladder
  3. Rectum

***ALWAYS do a GU/rectal/vaginal exam in these patients

244
Q

What are the reversal agents for the following:

  • benzos
  • non-depolarizing muscle blocking agents (ie. rocuronium)
  • depolarizing muscle blocking agents (ie. succinylcholine)
A
  • Benzos: flumazenil (gaba receptor antagonist)
  • rocuronium: neostigmine (acetylcholinesterase inhibitor)
  • succinylcholine: no reversal agent, just TIME
245
Q

What are the management steps in TBI?

A

Maintain normal:

  1. O2 sats
  2. PCO2 (35-40)
  3. BP (>5th percentile)
  4. Temp (no hyperthermia, do not cool)

Avoid:

  1. Hypoglycemia
  2. Seizures

**Treat elevated ICP + impending herniation with hyperosmolar therapy

246
Q

What are 3 things that increase risk of mortality in TBI?

A
  1. Hypoxia
  2. Hypo or hypercarbia
  3. Hypotension
247
Q

What is TBI management stps in PICU?
-what are indications for hyperventilation?

A
  1. ICP probe if 20 x 5 mins, then:
    - give sedation
    - muscle relax
    - hyperosmolar therapy
    - drain EVD if present
    - elevate HOB

**Only hyperventilate (PCO2 25-30) if impending herniation (Cushing’s triad, blown pupil) = this is the fastest way to decrease ICP in a herniating patient

248
Q

What is a normal ICP?

A
249
Q

Criteria for pediatric brain death?

A
  1. Established etiology capable of causing neurological injury in absence of reversible conditions
  2. No confounders including: unresuscitated shock, hypothermia ( 60 mmHg AND rise > 20 mm Hg
  3. Ancillary tests: ONLY do this if cannot perform an element of clinical NDD (angiography [CT-angio] or nuclear med, NO MORE EEG IS ALLOWED)
250
Q

What personnel can perform neurological determination of death?

A

Any licensed physician with the requisite knowledge and skill
-should be done by 2 physicians

251
Q

What are side effects of ketamine? (6)

A
  1. Hypertension
  2. Tachycardia
  3. Amnesia
  4. Analgesia
  5. Bronchorrhea
  6. Bronchodilation

***causes endogenous release of catecholamines
-great for kids who are hemodynamically unstable

252
Q

What is systemic vascular resistance in cold shock?

A

Increased!

253
Q

Why do we need O2? (on a biochemical level)

A

Glycolysis = 2 ATP + pyruvate
-then pyruvate can either combine with O2 in Kreb’s cycle to make 32 ATP
OR
-pyruvate can under anaerobic metabolism and create lactate and only 2 ATP
-lactate = acidotic, cells don’t like acidosis and thus they stop working and they die

254
Q

What are the characteristics of warm shock vs. cold shock?

A

Warm shock:

  • vasodilators > vasoconstrictors
  • warm, flash cap refill, wide pulse pressure, bounding pulses
  • shock because of low preload and loss of autoregulation

Cold shock:

  • vasoconstrictors > vasodilators
  • cold, poor pulses, prolonged cap refill, narrow pulse pressure
  • shock because of myocardial depression + increased afterload (possible effect of endotoxin on myocardium)
255
Q

What are the definitions of:

  • SIRS
  • Sepsis
  • Severe sepsis
  • Septic shock
A

SIRS: 2+ hyper/hypothermia, increased heart rate and/or RR, low or high WBC

  • sepsis = SIRS + presumed infection
  • severe sepsis = sepsis + organ dysfunction
  • septic shock = sepsis + refractory hypotension
256
Q

What are the effects of epinephrine in shock?

  • low dose
  • high dose
A

Epinephrine:

  • low dose: decreases alpha 1, increases beta 1, beta 2, decreases SVR (reduces vasoconstriction)
  • high dose: alpha 1, beta 1, beta 2, increases SVR
257
Q

Causes of cardiogenic shock? (5)

  • signs/symptoms?
  • investigations?
  • treatment?
A
  1. Cardiomyopathy
  2. Viral myocarditis
  3. Post bypass
  4. Coronary artery anomalies
  5. Arrhythmias
    - signs and symptoms: cold shock, poor perfusion, heart failure
    - investigations: CXR, EKG, 4 limb BPs, ABG, lytes, lactate, echo
    - treatment:
  6. Increase oxygen delivery (fluid and or lasix, afterload reduction, inotropic support with milrinone for ex)
  7. Decrease oxygen demand (positive pressure ventilation, sedation, etc)
258
Q

What are signs of neurogenic shock?

A

Spinal cord injury at level of sympathetic chain (T1 to L2)

  • loss of sympathetic output to heart, vessels, etc.
  • signs: inappropriately normal HR in hypotension
259
Q

What is the management for shockable rhythm (ie. VT/VF)?

A

Shock as SOON as you can with 2J/kg –> then CPR x 2 mins, then shock again at 4 J/kg if able + epi –> CPR x 2 mins, recheck rhythm and pulse q2mins, epi q3-5mins

  • coordinate 15:2 if no advanced airway, no need to coordinate once intubated
  • epi dose = 0.01 mg/kg 1:10000 IV

***Remember that CPR is your first priority, THEN defibrillation, then epi is your last resort (don’t have great evidence about whether it helps or not)

260
Q

What are 3 things you can tell the team to ensure good quality CPR?

A
  1. Compress 1/3 of AP diameter of chest
  2. Aim for 100 compressions/min
  3. Allow complete recoil
  4. Minimize interruptions
  5. No leaning (stool if needed)
  6. Change CPR providers q2min
261
Q

What is the treatment for ventricular tachycardia?

  • stable?
  • unstable?
A
  • Stable: call cardio and may start amio, lidocaine, etc.
  • Unstable = refer to pulseless arrest (shock + CPR)
262
Q

When would you consider an epinephrine infusion in anaphylaxis?

A

After 3 doses of epi IM needed

263
Q

What are the 2 divisions of the lung?

A

Conducting zone = rigid passageways from oropharynx to terminal bronchioles = physiologic dead space
-respiratory zone = from respiratory bronchioles and alveoli = sites of gas exchange

264
Q

What are the equations for oxygenation and ventilation?

A

Oxygenation: PaO2 = [(Atm - humidity) x FiO2] - (CO2/0.8)
ie. [(760-47) x 0.21] - (CO2/0.8)
-ventilation: RR x TV
(this is minute ventilation)

265
Q

What are the 3 causes of hypercapnea?

A
  1. Hypoventilation (eg. CCHS, drugs)
  2. Obstructive lung disease (eg. asthma, OSA)
  3. Neuromuscular disease (low tidal volumes)
266
Q

Cs of confirmation of intubation

A
  1. Clinical by auscultation
  2. Clinical by direct laryngoscopy
  3. CO2 detected
  4. CXR
  5. Condensation in the ETT
267
Q

Burns

A

1, Remove clothes and other exposures
2. ABCDEs (100% FiO2) + rapid trauma assessment ALWAYS (increased risk of having secondary trauma)
3. Wash burns with tepid water, flush chemical burns, cool minor burns with cool saline
4. Estimate %BSA involved with partial/full thickness
5. If > 10%, then at risk for SIRS response and fluid resuscitate with:
Parkland formula = 4 cc/kg/% BSA + maintenance crystalloid (1/2 in first 8 h, 1/2 in 16 h)
-monitor urine output with foley

268
Q

What are risk factors for airway involvement in burns?

A
  1. Closed space
  2. Any respiratory distress
  3. Singed hairs
  4. Soot around face
  5. Burns involving steam/combustibles, etc
  6. Carbanaceous sputum
269
Q

What are the clinical features of organophosphate toxicity?

  • pathophysiology?
  • treatment and 2 antidotes?
A

Think DUMBBELS (tells you effects at muscarinic receptors)
Diarrhea
Urination
Miosis
Bradycardia
Bronchospasm/bronchorrhea
Emesis
Lacrimation
Salivation
-at nicotinic receptors: muscle weakness, fasciculations and eventually paralysis, delirium
=these are all cholinergic symptoms (ie. the opposite of anticholinergic signs)

Pathophysiology:
-organophosphates bind to and inhibit the action of acetylcholinesterase THUS nothing to break down acetylcholine at the NMJ (muscarinic receptors) so you can a lot of parasympathetic activation

Treatment:

  1. Basic decontamination = washing all exposed skin with soap and water and immediately removing all exposed clothing
  2. Supportive care with intubation if decreased LOC/risk of aspiration

Antidotes for treatment:

  1. Atropine boluses or continuous infusion = competitive antagonist for muscarinic receptors so less acetylcholine can bind to the receptors; target to resolve respiratory secretions
    - controversial whether you should give activated charcoal if ingested insecticides
  2. Pralidoxime: breaks the bond between the organophosphate and the enzyme reactivating acetylchoinesterase (only effective if used before bond ages and becomes permanent)
270
Q

What is the action of neostigmine?

A

Acetylcholinesterase inhibitor = thus increases acetylcholine action at the muscarinic receptors

271
Q

How can pupillary findings assist in the diagnosis of toxic ingestions?

  • miosis? (5)
  • mydriasis? (2)
  • nystagmus? (3)
A

Miosis:

  1. opioids
  2. organophosphates
  3. clonidine
  4. barbiturates
  5. ethanol

Mydriasis:

  1. anticholinergics (atropine, antihistamines, TCAs)
  2. sympathomimetics (amphetamines, caffeine, cocaine, LSD, nicotine)

Nystagmus:

  1. Ketamine
  2. Phenytoin
  3. Barbiturates
  4. PCP (think darting eyes)
272
Q

What are 2 commonly used insecticides?

  • how do they differ in action and clinical features?
  • antidotes?
A
  1. Organophosphates
    - bind irreversibly to acetylcholinesterase if left untreated and permanently inactivates the enzyme (known as AGING)
    - takes weeks to months to regenerate inactivated enzymes
  2. Carbamates
    - form temporary bond only, allows reactivation of acetylcholinesterase within 24 hrs

Antidotes:

  1. Atropine (competitive antagonist of muscarinic receptors)
  2. Pralidoxime (reverses binding of organophosphate to acetylcholinesterase)
    - not needed in carbamate poisoning since the bond degrades spontaneously
273
Q

What is the dose for chloral hydrate?
-possible side effects?

A

20-75 mg/kg/dose 60 minutes prior to procedure
-side effects: possible resp depression, unreliable absorption, unreliable in children > 3 yo

274
Q

What are advantages of ketamine over other sedatives?
-side effects?

A
  1. Maintains upper airway muscle tone and does not cause resp depression (maintains spontaneous breathing)
  2. Does NOT cause hypotension = causes endogenous catecholamine release so maintain blood pressure and heart rate
  3. Provides sedation, analgesia, amnesia all at once
  4. Rapid onset and short duration of action

Side effects:

  1. Increased secretions
  2. Post-sedative vomiting
  3. Hypertension
  4. Unpleasant hallucinations
  5. Laryngospasm (rare)
275
Q

What are the underlying cause of Reye syndrome?

  • clinical features? (3)
  • what is ONE distinguishing feature that helps you differentiate between Reye syndrome vs. liver failure?
  • treatment?
A

Precipitated in a genetically susceptible person by the interaction of a viral infection (influenza and varicella) and ASA use = secondary mitochondrial hepatopathy

Clinical features: overall, acute onset of vomiting and encephalopathy

  1. Neurologic symptoms: can progress to seizures, coma and death
  2. Liver dysfunction (coagulopathy, transaminitis, hyperammonemia) BUT NORMAL SERUM BILIRUBIN LEVELS (unlike in liver failure)
  3. Increased intracranial pressure and resultant herniation = very important contributor to morbidity and mortality

Treatment: no effective therapy except supportive care
-may need liver transplant

276
Q

What are 3 types of electrical burns?

A
  1. Minor electrical burns (ie. result of biting an extension cord)
  2. High-tension electrical wire burn
  3. Lightning burn
277
Q

Clinical features seen in minor electrical burns?
-treatment?

A

Usually from biting an electrical cord

  1. Localized burns to mouth
  2. Hospital admission is not necessary since these are nonconductive injuries (do not extend beyond site of injury)
  3. Treat with topical antibiotic cream until the patient can be seen by plastics
278
Q

What are clinical features of high-tension electrical wire burns?
-treatment?

A

Clinical features:

  1. Deep muscle injury that cannot be readily assessed initially from high voltage = look for points of entry of current through the skin and exit site (usually current enters through upper extremity with exit through lower extremity onto the ground and injuries any organ or tissue in its path)
  2. Cardiac abnormalities: arrythmias, asystole
  3. Resp: resp arrest, aspiration
  4. Renal: acute renal failure from rhabdomyolysis and myoglobinuria
  5. Neurologic: motor paralysis, loss of consciousness
  6. Abdominal: viscus perforation and solid organ damage
  7. MSK: compartment syndrome from deep burns

Treatment goals: supportive basically with focus on AGGRESSIVE hydration in order to wash out the kidneys, ALWAYS admit for observation given you don’t know the extent of the injury, early debridement of wounds, tetanus prophylaxis

279
Q

What are possible internal complications from lightning burns? (3)

A
  1. Cardiac arrest (asystole, PVCs, VF, MI)
  2. CNS: cerebral edema, hemorrhage, seizures
  3. Renal: rhabdomyolysis and renal failure
280
Q

What is the most important complication of hydrocarbon toxicity?
-baseline investigations (2)?

A

Aspiration pneumonitis due to inactivation of type II pneumocytes and resulting surfactant deficiency (aspiration occurs during coughing and gagging at time of ingestion or vomiting after ingestion)
-baseline investigation: blood gas and CXR, monitor for 6 hours

281
Q

How does the viscosity of a hydrocarbon determine risk of aspiration pneumonitis?

A

The LESS viscous, the MORE chance of aspiration pneumonia (think that if it’s thin, it can spread out more in the lungs to cover larger surface area)
-ie. gasoline, lamp oil, kerosene

282
Q

What is “sudden sniffing death?”
-treatment?

A

Volatile hydrocarbons that are commonly abused by inhalation (ie. halogenated ones) can sensitize the myocardium to the effects of endogenous catecholamines = increased risk of Vtach and Vfib (usually refractory to conventional management)

Treatment: still follow PALS algorithm but consider treatment with beta blocker to block effects of endogenous catecholamines on sensitized myocardium

283
Q

What is the treatment of hydrocarbon ingestion?

  • main complication of hydrocarbon ingestion?
  • main complication of hydrocarbon inhalation?
A

Observation and supportive care for respiratory symptoms!!!

  • emesis and lavage are CONTRAINDICATED given the risk of aspiration
  • activated charcoal is NOT useful because it does not bind the common hydrocarbons and can also induce vomiting
  • main complication of ingestion:
    1. ARDS (some require intubation and ECMO) from aspiration pneumonitis
  • main complication of inhalation:
    1. Arrhythmias and cardiac arrest
284
Q

What are the antidotes for the following:

  • acetaminophen
  • anticholinergics
  • benzos
  • beta-blockers
  • calcium channel blockers
  • ethylene glycol/methanol
  • iron
  • methemoglobinemia
  • organophosphates
  • salicylates
  • sulfonylureas
  • TCAs

A.

  • acetaminophen: N-acetylcysteine
  • anticholinergics: neostigmine or physostigmine
  • benzos: flumazenil
  • beta blockers: glucagon
  • calcium channel blockers: insulin and calcium salts
  • ethylene glycol/methanol
  • iron: deferoxamine
  • methemoglobinemia: methylene blue
  • organophosphates: atropine & pralidoxime
  • salicylates: sodium bicarb
  • sulfonylureas: octreotide
  • TCAs: sodium bicarb
A
  • acetaminophen: N-acetylcysteine
  • anticholinergics: neostigmine or physostigmine
  • benzos: flumazenil
  • beta blockers: glucagon
  • calcium channel blockers: insulin and calcium salts
  • ethylene glycol/methanol
  • iron: deferoxamine
  • methemoglobinemia: methylene blue
  • organophosphates: atropine & pralidoxime
  • salicylates: sodium bicarb
  • sulfonylureas: octreotide
  • TCAs: sodium bicarb
285
Q

What are methods of GI decontamination after ingestions? (4)
-Which two are the only ones likely to have significant clinical benefit in management of poisoned patient?

A
  1. Activated charcoal
  2. Whole bowel irrigation
    (THESE ARE THE ONLY TWO THAT ARE RECOMMENDED FOR USE)
  3. Gastric lavage
  4. Syrup of ipecac to induce vomiting
286
Q

Is activated charcoal recommended for use in poisonings?

  • how does it work?
  • when should it be given?
  • contraindications? (10)
A

YES!!! Thought to be potentially the most useful

  • activated by heat and creates network of pores that have large absorptive area, thus adsorbing toxins onto its surface and preventing absorption from GI tract
  • should be given within 1 hr of ingestion!!!!!
  • can cause vomiting

Contraindications: CHEMICAL CamP
Cyanide
Hydrocarbons
Ethanol
Metals
Iron
Caustics
Airway unprotected
Lithium
Camphor
Potassium

287
Q

What is the dose of activated charcoal?
-common side effects? (2)

A

1 g/kg in children and 50-100 g in adolescents and adults

  • common side effects:
    1. vomiting (20%)
    2. constipation
288
Q

What is whole bowel irrigation?
-what are the usual indications? (3)

A

Whole bowel irrigation: instill large volumes through NG tube (35 ml/kg/hr in children or 1-2 L/hr in adolescents) of GoLYTELY to cleanse the entire GI tract until rectal effluent runs clear

  • indications:
    1. For slowly absorbed substances (sustained release preparations)
    2. Substances not well absorbed by charcoal
    3. Drug packets (ie. heroin or cocaine)
289
Q

What fractures should raise suspicion of child abuse? (5)

A
  1. Spiral fractures
  2. Posterior rib fractures
  3. Spinal fractures
  4. Metaphyseal fractures
  5. Femoral fractures in non mobile child
  6. Scapular fractures
290
Q

Up to what age should a skeletal survey be ordered?

A

Up to age of 2 years (yield is lower after that)

291
Q

What are clinical features of osteogenesis imperfecta? (5)

A
  1. Blue sclera
  2. Wormian bones (extra bones in between sutures)
  3. Dentinogenesis imperfecta (poorly developed, discolored teeth)
  4. Hearing loss
  5. And of course, frequent fractures with little force
292
Q

After initial ED visit for sexual assault, what follow-up care should be offered to the patient? (4)

A
  1. Supportive counselling
  2. HIV follow up and counselling with ID/HIV team in 3-5 days
  3. Follow up gyne exam in 1-2 wks
  4. Repeat serologic tests for syphilis and HIV in 6 wks, 3 mo and 6 mo
293
Q

What 4 infections are diagnostic for sexual abuse in a non-sexually active child?

A
  1. HIV
  2. Syphilis
  3. Gonorrhea
  4. Chlamydia

(other infections such as trichomonas, condyloma acuminata, herpes, BV is less clear)

294
Q

What is the most common physical finding in sexual abuse?

A

Normal examination

295
Q

What organ systems are affected in patients suffering from heat stroke?

A
  1. CNS: confusion, seizures, LOC
  2. Cardiac: hypotension due to hypovolemia and peripheral vasodilation, myocardial dysfunction
  3. Renal: ATN and renal failure from hypoperfusion
  4. Hepatocellular injury
  5. Heme: abnormal hemostasis (DIC usually)
  6. Muscle: rhabdomyolysis from high temp
296
Q

What bloodwork should be ordered for a patient in a housefire?

A
  1. CBC: look for signs of bleeding
  2. Lytes: look for hyperkalemia
  3. Renal function to rule out renal failure
  4. BLOOD CARBOXYHEMOGLOBIN (HbCO = rule out carbon monoxide poisoning)
  5. Gas
  6. Urinalysis for myoglobin
297
Q

What is the criteria for transfer to burn centre? (8)

A
  1. Partial thickness and full thickness burns of greater than 10% BSA
  2. Partial thickness and full thickness burns involving face, eyes, ears, hands, feet, genitalia, joints
  3. Full thickness burns of any size in any age group
  4. Significant electrical burns
  5. Burns suspicious for abuse
  6. Significant chemical burns
  7. Inhalation injury
  8. Burn injury in patients with preexisting illness that could complicate treatment
298
Q

Why are alkali burns worse than acid burns in the eye?

A

Alkali = causes liquefactive necrosis (eats through tissue leaving more extensive injury) whereas acid = coagulation necrosis (buffered by tissue and limited penetration)

299
Q

What lacerations should not be sutured? (4)

A
  1. Puncture wounds
  2. Mucosal surface lacerations (mouth, vagina)
  3. Contaminated wounds that cannot be reliably cleaned
  4. Human bites

****Some authorities recommend that wounds > 12 hrs on arms and legs and > 24 hrs on face should not be sutured and left to heal by secondary intention

300
Q

What are key questions to ask on history for a patient coming in with an animal bite?

A
  1. Circumstances surrounding the bite
    - type of animal (domestic or wild)
    - provoked or unprovoked
    - immunization status of child (tetanus) and animal (rabies)
301
Q

When should you consider ordering an xray in a patient presenting with an animal bite? (2)

A
  1. Penetrating injury over bone or joint for suspected fracture
  2. Foreign body inoculation
302
Q

Which animal bites are most likely to become infected? (2)
-which should be cultured? (cat? human? dog?)

A
  1. Human bites (regardless of mechanism of injury, ie. bite vs. closed fist against tooth) = high risk of infection, especially anaerobes
  2. Cat bites = at least 50% even if early medical attention is received
    Thus need to culture ALL cat and human bites!
    -culture dog bite IF deep and extensive, > 8 hrs old, early signs of infection, or immunosuppresed patient
303
Q

What are risk factors for infection after an animal bite? (7)

A
  1. Immunocompromised patient
  2. Crush or deep puncture wounds
  3. Delay in treatment > 24 hrs
  4. Human and cat bites
  5. Bites on hand, foot, genitals
  6. Perforation of bone or tendons
  7. Presence of foreign material
304
Q

Which microorganisms are associated with bites:

  • dog?
  • cat
A

Dog: staph, strep, pasteurella, capnocytophaga, anaerobes

Cat: pasteurella (higher carriage in cats than dogs), staph, strep

305
Q

What is the initial management of ALL animal bites?
-what about hand bites?

A
  1. If needed, obtain culture
  2. Apply local anesthetic
  3. Clean and vigorously irrigate with copious amounts of normal saline
    -no evidence for antibiotic containing solutions over saline and can actually cause local irritation
  4. Debride devitalized tissue
  5. MAY be able to do primary closure on facial bite wounds 24 hrs old
    ***Hand bites: all need to be immobilized until follow up assessment 3 days later
306
Q

Which animal bites require operative debridement and exploration? (3)

A
  1. Cranial bites by large animal
  2. Closed fist injury (involvement of metacarpophalangeal joint aka knuckle)
  3. extensive wounds with a lot of devitalized tissue
307
Q

What are the indications for antibiotic therapy in a patient presenting with a bite? (7)

  • oral vs. IV?
  • first choice for abx coverage?
A
  1. Moderate or severe bite wounds (especially if edema or crush injury present)
  2. Puncture wounds (especially if penetration of bone, tendon or joint)
  3. Facial bites
  4. Hand and foot bites
  5. Genital area bites
  6. Wounds in immunocompromised
  7. Wounds with signs of infection
  8. All human and cat bites (dog = controversial)

***Oral vs. IV depends on the wound, signs of infection, and immune status

1st line: PO amoxi-clav for empirical therapy or IV ampicillin/sulbactam
(do NOT use first gen cephalosporins since they don’t have good coverage for oral microbes)
-if pen allergic: azithromycin

308
Q

Which patients require tetanus after an animal bite?

A

ALL patients who are incompletely immunized or if it’s been longer than 10 years since last immunization
-tetanus immunization schedule: 2, 4, 6, 18 mo, 4 yo and q10 years after that

309
Q

What emergency drugs can be given through an ETT? (5)

A

LEAN-V

  1. Lidocaine
  2. Epinephrine
  3. Atropine
  4. Naloxone
  5. Vasopressin

**Epi = 10x IV dose
**other meds = 2x IV dose

-need to follow administration with a 5 ml NS flush and PPV to bag it in

310
Q

What are 4 contraindications to the use of an IO?

A
  1. Placement in fractured bone
  2. Placement through dirty or infected skin
  3. Use in patients with bone disorders (osteopetrosis or osteogenesis imperfecta)
  4. Repeat attempt into the same bone
311
Q

What are possible complications of IOs? (4)

A
  1. Extravasation of fluid
  2. Superficial skin infection
  3. Osteomyelitis (rare)
  4. Theoretical risk for bone growth arrest, fat embolism but these have not been reported
312
Q

What are the 6 Hs and 4 Ts?

A
  1. Hydrogen ion
  2. Hypoglycemia
  3. Hypovolemia
  4. Hyper/hypokalemia
  5. Hypothermia
  6. Hypoxemia
  7. Toxins
  8. Tension pneumothorax
  9. Tamponade
  10. Thromboembolism
313
Q

What are predictors for good outcome in pediatric cardiac arrest? (6)

A
  1. Initiation of prompt CPR
  2. Witnessed event
  3. Out of hospital arrest
  4. Short interval to EMS
  5. Short duration of CPR
  6. Initial rhythm of VT or VF
314
Q

What two ingestions are treated with urinary alkalinization with sodium bicarb?

A
  1. TCA overdose
  2. Salicylate overdose
315
Q

What ingestions are radioopaque on abdominal radiograph?

A

CHIPS

  1. Chloral hydrate
  2. Heavy metals (iron, lead, arsenic)
  3. Iodides
  4. Phenothiazines, psychotropics (TCAs)
  5. Slow release capsules (enteric coated tablets)
316
Q

What are the key distinguishing clinical features of ingestion of the following:

  • ethanol (triad)
  • methanol
  • isopropyl alcohol
  • ethylene glycol
A
  • Ethanol triad: hypoglycemia, hypothermia, coma
  • methanol: severe metabolic acidosis and permanent retinal damage leading to blindness (due to formic acid formation = blocks mitochondria, thus metabolic acidosis)
  • isopropyl alcohol: gastritis, hyperglycemia, hypotension
  • ethylene glycol: severe metabolic acidosis, cranial nerve palsies and cause renal damage by precipitation of calcium oxalate crystals
317
Q

What arterial blood gas pattern is classic for salicylate poisoning?

A

Metabolic acidosis with respiratory alkalosis!

  • salicylates directly stimulate the medullary respiratory drive center causing tachypnea
  • also cause lactic acidosis due to uncoupling of oxidative phosphorylation
318
Q

What is water intoxication?

A

Swallowing lots of water and thus getting hyponatremia and secondary seizures
-can see in babies who go swimming and swallow a lot of water

319
Q

What are the changes in your lungs during air transport? (2)

A
  1. Decreased pressure and thus increased gas expansion
  2. Decreased PaO2
320
Q

What baseline investigations will you order for an ingestion?

A
  1. Glucose
  2. Lytes
  3. Renal Function
  4. LFTs
  5. EKG
  6. Serum osmolality
  7. Blood gas
  8. Urine tox screen
  9. Ethanol level
  10. Other alcohol levels
  11. Acetaminophen, salicylate level
321
Q

What is the treatment for isopropyl alcohol ingestion?

A

Supportive care

322
Q

What is oil of wintergreen?

A

A salicylate!!!

323
Q

A patient presents with an ingestion but won’t tell you what they took and are asymptomatic. What is your management plan?

A
  1. Supportive management
  2. Observe 4-6 hours if asymptomatic
    - if you do eventually find out what they took, need to figure out half life and observe for at least that long
324
Q

A patient overdoses on cocaine is extremely agitated and a danger to himself and others. What immediate treatment would you start?

A

Benzos (used for agitation or hallucinations)

325
Q

Which 4 organs are most commonly injured with blunt abdo trauma?

A
  1. Liver
  2. Spleen
  3. Kidneys
  4. Pancreas
    OCCASIONALLY bowel (seatbelt injuries, handlebars)
326
Q

Indications for laparotomy in abdo trauma?

A
  1. Persistent hemodynamic instability with evidence of abdo injury
  2. Penetrating injury to abdo
  3. Pneumoperitoneum
  4. Multisystem trauma and they need other OR procedures if evidence of abdo injury
327
Q

What is the management of carbon monoxide poisoning?

A

Think about this in the winter time!!! May have CO leak in house while heat is on. Whole family may present with flu like symptoms, delayed neuropsychiatric syndrome (can happen up to weeks after poisoning)
1. Order carboxyhemoglobin level on blood gas

Treatment:
1. 100% oxygen until levels

328
Q

What temperature should you rewarm to in resuscitation of a hypothermic patient?

A

34 degrees

329
Q

What are the clinical features of lower abdominal lap belt injuries? (3)

A
  1. Bladder rupture
  2. Chance fracture: L1 & L2
  3. Bowel rupture
330
Q

What are the indications for imaging prior to LP?

A
  1. Papilledema
  2. Focal neuro signs
  3. Decreased LOC or coma
331
Q

What is the treatment for methanol overdose? (2)

A
  1. Fomepizole
  2. Folate
332
Q

What are two coingestions you should ALWAYS check for in a patient with suspected ingestion?

A

Acetaminophen and salicylate

333
Q

What is the treatment for cyanide toxicity?

A
  1. 100% oxygen
  2. You have two options:
    a) Cyanide antidote kit:
    - sodium nitrite (produces methemoglobin which then reacts with cyanide to form cyanmethemoglobin)
    - sodium thiosulfate (increases metabolism of cyanmethemoglobin to hemoglobin and less toxic thiocyanate)
    b) Hydroxocobalamin (vitamin B12) (reacts with cyanide to form nontoxic cyanocobalamin which is then excreted in urine) = superior to cyanide antidote kit so is now the preferred antidote
334
Q

What are the clinical features of iron toxicity?
-toxic dose?

A

Think GI symptoms! Iron is directly corrosive to the GI mucosa:

  1. GI bleed from ulceration and perforation–> hematemesis, melena
  2. Hypotension: due to massive volume losses from increased permeability of capillaries
  3. Accumulation of iron in liver and heart = liver toxicity, cardiac dysfunction
  4. Anion gap metabolic acidosis due to hypotension and hypovolemia
    - toxic dose: > 40 mg/kg
335
Q

What are the 4 stages of iron toxicity?

A
  1. Initial stage: 30 min - 6 hr post ingestion
    - profuse vomiting and bloody diarrhea
    - volume losses
  2. Second stage: 6-24 hrs post
    - quiescent phase, GI symptoms resolve
  3. 3rd stage: 12-24 hrs post
    - multisystem organ failure, shock, hepatic and cardiac dysfunction, ARDS, metabolic acidosis
    - death occurs most cmomonly during this stage
  4. 4th stage: 4-6 wks post
    - GI strictures and obstruction
336
Q

What is the management of iron toxicity?

A
  1. Draw serum iron levels 4-6 hrs after ingestion along with gas, CBC, glucose, liver enzymes, LFTs
  2. AXR to look for iron tablets
  3. Monitor closely for hypotension with aggressive fluid support
  4. Whole bowel irrigation!!!! (remember that activated charcoal does NOT absorb iron)
  5. Deferoxamine for moderate to severe iron intoxication
    - IV infusion at 15 mg/kg/hr until urine runs clear (deferoxamine iron complex colors urine red)
337
Q

What is the antidote for lead toxicity?

A

2,3-dimercaptosuccinic acid

338
Q

What are the clinical features of foxglove or lily of the valley poisoning?

A

CARDIAC effects! = nausea, vomiting, bradycardia, AV block, hyperkalemia

339
Q

What is the definition of heat stroke vs. heat exhaustion?

A

Heat stroke: temp > 40 with neurologic symptoms
-heat exhaustion: T 38-40 without neurologic symptoms

340
Q

What are ECG findings in a patient with hypothermia?

A
  1. J wave (pathognomonic) = after R wave, see a rounded bump (kind of like RSR’ but rounded contour)
  2. PR, QRS, QT elongation
341
Q

Indications for dialysis? (5)

A

AEIOU

  • Acidosis
  • Electrolyte imbalance (hyperkalemia)
  • Ingestion
  • Overload (fluid)
  • Uremia
342
Q

What are side effects of lasix? (4)

A
  1. Hyponatremia
  2. Hypokalemia
  3. Nephrocalcinosis
  4. Metabolic alkalosis
343
Q

What toxidrome does gravol cause?

A

Anticholinergic

344
Q

What are the side effects of NSAID use in neonates? (ie. treatment of PDA)?

A
  1. Transient increase in GFR
  2. Platelet dysfunction
  3. Increased NEC (slight mesenteric vasoconstrictor = decreased blood flow to gut)
  4. Hypoglycemia
345
Q

What are side effects of risperidone? (7)

A
  1. Acute dystonic reaction
  2. Neuroleptic malignant syndrome
  3. Diabetes
  4. Weight gain
  5. Seizures
  6. Hepatotoxicity
  7. Prolonged QT
346
Q

What are the clinical features of increased ICP in an infant?

A
  1. Sunsetting sign
  2. Shrill cry
  3. Irritability
  4. Bulging AF
347
Q

What is the management of a 13 yo who was just sexually assaulted?

A
  1. History and physical, document findings
  2. Report to CAS
  3. Pregnancy test and emergency contraception
  4. STI screen and prophylaxis
  5. Forensic kit if
348
Q

What are 3 side effects of anthracyclines?

A
  1. Cardiomyopathy
  2. Red urine
  3. Myelosuppression
349
Q

A patient has hypopigmented scar after minor trauma and vesicular rash in sun exposed areas. This is most likely due to which medication?

A

NSAIDs = pseudoporphyria

350
Q

What cardiac medication taken during pregnancy increases risk of hypothyroidism in baby?

A

Amiodarone = has a lot of iodide in it!
-amiodide :)

351
Q

What are the points in GCS?

A

EVM!!!!

Eyes:
1 - no eye opening
2 - eye opening to painful stimuli
3 - eye opening to verbal stimuli
4 - spontaneous eye opening

Verbal:
1 - none
2 -incomprehensible sounds
3 - incoherent words
4 - disoriented conversation
5 - normal conversation

Motor:
1 - None
2 - decerebrate posturing (extension)
3 - decorticate posturing (flexion)
4 - withdrawal to pain
5 - localizes pain
6 - follows commands/normal

352
Q

What is the most common bacterial etiology of spontaneous bacterial peritonitis?

A

Strep pneumo!!!

353
Q

What are the clinical features of serotonin syndrome?

A

SHIVERS

  1. Shivering
  2. Hyperreflexia
  3. Increased temperature (hyperthermia)
  4. Vitals: increased HR, RR, labile BP
  5. Encephalopathy (agitation, delirium, confusion)
  6. Restlessness
  7. Sweating
354
Q

How much should TFI be increased by in order to ensure feed safety?

A

20-30 ml/kg/d –> if calculating this for oral feeds, divide by 8 for q3h feeds

355
Q

What is the definition of polycythemia?

A

Hct > 65% or Hgb > 220

356
Q

What are the differences between gastroschisis and omphalocele?

A

Omphalocele:

  • midline
  • protective cover (guts herniating through umblical cord)
  • 25-40% have congenital anomalies (Beckwidth Wiedemann, Trisomy 13 & 18)

Gastroschisis:

  • not midline (right sided most common)
  • no protective cover (full thickness abdo wall defect)
  • 10-15% have intestinal atresia
357
Q

What is the Kleihauer-Betke test?

A

Tests mom for baby’s blood

  • bleeding from the fetal into the maternal circulation (fetomaternal hemorrhage)
  • put mom’s blood into some filter thing and it breaks down mom’s beta chains but not fetus’ gamma chains
358
Q

What are the causes of apnea in:

  • prems
  • terms
  • both
A

Prem:

  • apnea of prematurity
  • IVH
  • eye exams
  • PDA
  • RDS
  • anemia

Term:

  • cerebral infarct
  • polycythemia

Both:

  • infection
  • NEC
  • cardiac
  • asphyxia
  • hypothermia
  • aspiration
  • seizure
359
Q

Differential diagnosis for neonatal hematuria?

A
  1. Vascular: renal artery or venous thrombosis (common in infants of diabetic moms)
    - both can be caused by umbilical catheterization
  2. Coagulation disorder: vitamin K deficiency
  3. Renal:
    - renal cortical necrosis
    - neonatal glomerulonephritis (seen in maternal syphillis)
  4. Trauma: birth, iatrogenic, perinatal asphyxia
  5. Infection
  6. Neoplasm
    - Wilms
    - Neuroblastoma
    - Nephroblastoma
    - Rhabdomyosarcoma
    - Polycystic kidney disease
360
Q

Complications seen in infants of diabetic mothers?

A
  1. Large for gestational age
  2. Hypoglycemia
  3. Congenital anomalies (neural tube, renal, cardiac malformations
  4. Polycythemia –> hyperbilirubinemia
  5. Shoulder dystocia/birth trauma
  6. Renal vein thrombosis
  7. Hypocalcemia
  8. Hypomagnesemia
  9. Congenital anomalies (neural tube, renal, cardiac malformations
361
Q

What are prenatal signs of TEF (3)?

A
  1. Frequent fetal hiccups
  2. Polyhydramnios
  3. Microgastria
362
Q

What is the most common type of TEF?
-second most common?

A

Think from most common to least common: CAE-BD (It’s CAE’S BIRTHDAY!)
C (85%) = Esophageal atresia with distal TEF
-on CXR after insertion of NG tube, will see coiling
-esophageal atresia
-distal tracheoesophageal fistula
-gastric distension
-respiratory distress/aspiration secondary to GERD

Second most common: type A (9%) = isolated esophageal Atresia (think A for ATRESIA!)

  • esophageal atresia without tracheoesophageal fistula
  • no gas in abdomen
  • scaphoid abdomen

Third most common: type E (6%) = isolated TEF (no esophageal atresia)

  • presents later in life
  • recurrent pneumonias/persistent cough due to aspiration

Fourth most common: type B (1%) = Proximal TEF with esophageal atresia

Fifth most common: Type D (!) = Double TEF with esophageal atresia (tracheoesophageal fistula between proximal and distal esophageal ends)

(Esophageal atresia: presents in neonate because they can’t eat and the food comes back up!)

363
Q

What are the risk factors for neonatal polycythemia? (10)

A
  1. IDM
  2. SGA
  3. Graves disease
  4. Neonatal hypothyroidism
  5. Maternal hypertension
  6. Postmature
  7. Recipient of twin-twin transfusion
  8. Delayed cord clamping
  9. Beckwith-Wiedemann syndrome
  10. Trisomy 13, 18, 21
364
Q

What are the clinical manifestations of neonatal polycythemia? (8)

What are the complications of neonatal polycythemia? (6)

A

***Many affected infants are asymptomatic
***Symptoms and complications secondary to stasis and hyperviscosity in vasculature

Clinical manifestations:

  1. Irritability
  2. Lethargy
  3. Poor feeding
  4. Hypoglycemia
  5. Hyperbilirubinemia
  6. Thrombocytopenia
  7. Respiratory distress
  8. Cyanosis

Complications:

  1. Seizures
  2. Stroke
  3. Renal failure
  4. Renal vein thrombosis
  5. Pulmonary hypertension
  6. Necrotizing enterocolitis
365
Q

What are the indications for partial exchange transfusion in neonatal polycythemia?

A

Should be considered if:

  1. Hct > 70-75%
  2. S/S of hyperviscosity
366
Q

In partial exchange transfusion for neonatal polycythemia, what is the formula for volume to be exchanged?

A

Volume of exchange (ml) = blood volume x (Observed-desired hematocrit)/observed hematocrit

***withdraw the blood slowly and replace with crystalloid (NS)

367
Q

Describe the hyperoxic test.

A

Arterial gas is obtainedi n the right radial artery prior to placing the patient on 100% O2 via oxygen hood or I&V. Leave 100% O2 on for 10 minutes. Then repeat the art gas.

  • PaO2 > 150 post hyperoxic test: pulmonary disease
  • PaO2
368
Q

What are the side effects of PGE1 (6)?

A
  1. Apnea
  2. Hypotension
  3. Fever
  4. Bradycardia or tachycardia
  5. Seizures
  6. Cutaneous flushing
369
Q

What is the cause of hemolytic disease of the newborn aka erythroblastosis fetalis?

A

Rh incompatibility: pre-natal transplacental passage of maternal IgG antibodies active against paternal RBC Rh antigens on the fetus’ RBC

ABO incompatability: post-natal destruction of fetal RBCs by maternal IgM antibodies

370
Q

What is RhoGAM?

A

Rho (D) immunoglobulin: IgG anti-D antibodies
-given to Rh negative mothers at approxiamtely 28 weeks and the Rho (D) immunoglobulin will remove any anti-D positive fetal RBCs before the maternal immune system can respond to them (prevents maternal sensitization)

371
Q

During what events can maternal sensitization occur in hemolytic disease of the newborn caused by Rh incompatibility?

A
  1. Blood transfusion: if Rh-positive blood is infused into an Rh-negative woman through error
  2. During pregnancy: when fetal blood enters mom’s circulation through spontaneous or induced abortion
  3. At delivery: fetal blood enter’s mom’s circulation
372
Q

Why is hemolytic disease of the newborn caused by Rh incompatibility worse in subsequent pregnancies?

A

In first pregnancy, usually the mother is exposed to fetal blood during delivery. Initially IgM antibodies are produced which are then later replaced by IgG antibodies over time (baby has already been delivered at this point). In subsequent pregnancies, smaller amounts of antigen can stimulate IgG production which can then cross the placenta and cause hemolytic disease in subsequent pregnancies
-this is why RhoGAM should be given to Rh negative moms at 28 weeks and also immediately post-partum

373
Q

What are the complications of hemolytic disease of the newborn caused by Rh incompatibility? (4)

A
  1. Severe anemia –> heart failure –> hydrops fetalis
  2. Extramedullary hematopoiesis: hepatosplenomegaly
  3. Bone marrow hyperplasia with increased erythropoiesis and subsequently, thrombocytopenia
  4. Severe hyperbilirubinemia (within 1st day of life)
374
Q

What lab test is the best predictor of severity of hemolytic disease of the newborn caused by Rh incompatibility of the newborn at delivery?

A

Cord blood bilirubin level: indicates severity of hemolysis in utero

  • Cord blood Hgb is less reliable since it can be normal if baby has compensatory bone marrow and extramedullary hematopoiesis
  • Mom’s anti-Rh titers correlate poorly to severity of disease
375
Q

Describe the steps in antenatal diagnosis of hemolytic disease of the newborn caused by Rh incompatbility.

A
  1. Determine whether mom is Rh-negative or Rh-positive.
  2. If Rh-negative, take history of previous transfusions, abortion or pregnancies
  3. Test dad’s blood type to check for incompatibility
  4. Measure maternal titer of IgG antibodies to D antigen at 12-16, 28-32, 36 wks of gestation
    - presence of elevated antibody titers at the beginning of pregnancy, rapidly rising titers or titer of 1:64 or greater suggests significant hemolytic disease
376
Q

What antenatal monitoring should occur for Rh negative mothers found to have Rh positive fetus?

A

If IgG antibodies to D antigen is found at a titer of 1:16 or more, monitor by Doppler US of middle cerebral artery flow, real time US for signs of hydrops and then percutaneous umbilical blood sampling if needed.

377
Q

What is the antenatal treatment for hemolytic disease of the newborn secondary to Rh incompatibility?
-indications?

A

In utero transfusion of PRBCs through the umbilical vein

  • maternal/fetal sedation with diazepam and fetal paralysis with pancuronium
  • may need to be repeated every 3-5 wks
  • indications:
    1. Hydrops
    2. Fetal anemia (Hct
378
Q

What is the postnatal treatment for hemolytic disease of the newborn secondary to Rh incompatibility?

A
  1. . Resuscitation if severe hemolytic anemia is present
  2. IVIG
  3. May require exchange transfusion if severe hyperbilirubinemia
379
Q

What is the cause of the classic form of galactosemia?

A

Galactose-1-phosphate uridyl transferase deficiency (GALT)

  • enzyme responsible for metabolizing galactose-1-phosphate
  • autosomal recessive
  • without this enzyme, galactose-1-phosphate accumulates and causes injury to kidney, liver and brain
380
Q

What is the dietary source of galactose?
-when do infants with classic galactosemia typicaly present and why?

A

Milk and dairy products - lactose is converted to glucose & galactose in our bodies!
-infants with classic galactosemia present usually within the 1st week of life since they are receiving high amounts of lactose through breast milk or formula

381
Q

What are the clinical features of galactosemia?

  • acute (7)
  • if untreated, chronic complications? (5)
A

Newborn or young infant with:

  1. Jaundice
  2. Hepatomegaly
  3. Vomiting
  4. Hypoglycemia
  5. Seizures
  6. Lethargy/poor feeding
  7. E coli sepsis (thought to be secondary to phagocytic and neutrophil dysfunction due to impaired glycolysis secondary to galactosemia)

Later in infancy or childhood if untreated:

  1. Mental disability
  2. Cataracts
  3. Renal failure
  4. Vitreous hemorrhage
  5. Hypergonadotrophic hypogonadism

***Galactose-1-phosphate accumulates in liver, brain and kidney!

382
Q

What are the diagnostic tests for galactosemia (2)?

A
  1. Urine for reducing substances: galactosuria is present
  2. Direct enzyme assay for GALT in RBCs - will be deficient
383
Q

What is the treatment for galactosemia?

A

Elimination of galactose from the diet

  • galactosemia is a contraindication for breastfeeding
  • will need lactose free formulas
384
Q

What are the acute issues seen in babies born with maternal heroine use?

A
  1. Respiratory depression
  2. RDS
  3. Lower birth weight
  4. Jaundice
385
Q

What are the 3 main categories of neonatal coagulopathy?
-what are the 3 forms of hemorrhagic disease of the newborn?

A
  1. Hemorrhagic disease of the newborn: secondary to vitamin K deficiency
  • early form (within 1st 24 hrs): maternal meds affecting vitamin K levels
    1. Phenytoin
    2. Isoniazid
    3. Rifampin
    4. Barbituates
    5. Warfarin
  • classic form (DOL 2-7): vitamin K injection not given at birth
  • late form (weeks 2-6): decreased vitamin K intake secondary to breastfeeding or hepatobiliary disease
    2. Congenital coagulopathy: bleeding in deep tissues
  • hemophilia A or B
    3. DIC: bleeding everywhere
  • decreased fibrinogen
  • increased PTT
  • increased INR
  • decreased platelets
386
Q

What maternal meds may lead to early hemorrhagic disease of the newborn? (5)

A
  1. Phenytoin
  2. Isoniazid
  3. Rifampin
  4. Barbituates
  5. Warfarin
387
Q

What are the causes of neonatal DIC?

  • maternal (2)
  • infant (4)
A

Maternal

  1. Eclampsia
  2. Placental abruption

Infant:

  1. Sepsis
  2. Asphyxia
  3. Severe acidosis
  4. NEC
388
Q

How long does it take umbilical cord to slough off?

A

2 weeks
-worry if it takes longer than 1 month since it might indicate neutrophil chemostatic defects

389
Q

What is 2 vessel umbilical cord associated with? (4)

A
  1. Renal abnormalities
  2. Congenital malformations
  3. IUGR
  4. Trisomy 18
390
Q

What are the recommendations for safe sleep practices (7)?

A
  1. Sleep in a crib that meets government standards
  2. Crib in parent’s room for 6 months
    - room sharing protects against SIDS
  3. Back to sleep
  4. No heavy blankets, toys, etc. Can have thin blanket and baby can be in a sleeper
  5. Decreased second hand smoke
  6. Baby should not be in a non-crib surface (water bed, couch)
  7. In hospital, baby and mom should not share a bed
391
Q

What are the risk factors for contracting RSV bronchiolitis? (8)

A
  1. Prematurity
  2. Less than 2 years old with cardiac issues
  3. Second hand smoke
  4. Underlying lung pathology
  5. IUGR/SGA
392
Q

What are the etiologies of polyhydramnios? (5)

A
  1. GI obstruction: esophageal, duodenal, intestinal obstruction
  2. Hypotonia (difficulty with swallowing): anencephaly, neural tube defects
  3. GDM
  4. Non-immune fetal hydrops
  5. Idiopathic (most common)
  6. Bartter syndrome
393
Q

What is Bartter syndrome?
-clinical features

A

Chloride channel abnormality

  • polyuria, hypokalemia, hyponatremia, hypercalcemia
  • often presents with seizures secondary to hyponatremia
394
Q

What are the indications for exchange transfusion? (4)

A
  1. Severe hyperbilirubinemia
  2. Hemolytic disease of the newborn
  3. Polycythemia
  4. Hyperkalemia
395
Q

What are the side effects of exchange transfusion? (6)

A
  1. NEC
  2. Death
  3. Hyperkalemia
  4. Infection
  5. Thrombosis/air embolism
  6. Volume overload
396
Q

Distinguish between G6PD, alpha, and beta thalassemia in terms of clinical presentation

A

G6PD: presents at 1 week
Alpha thalassema: presents at birth with hydrops and death in neonate
Beta thalassemia: presents at 2-3 months

397
Q

How is G6PD inherited?

A

X-linked recessive

398
Q

What is Erb palsy?
-associated complication?

A

C5-C6 nerve palsy: waiter’s tip

  • assymetric moro
  • palmar grasp present
  • shoulder won’t move but hand can move
  • associated complication: 5% can ipsilateral diaphragmatic paralysis (C5 keeps you alive)
399
Q

What is Klumpke’s palsy?
-associated complication?

A

C8-T1 nerve palsy: Klumpke’s Klaw
-associated complication: 33% have Horner’s syndrome

400
Q

How do you treat brachial plexus palsy?

A

Immobilize x 7-10 days, then physiotherapy for mobilization

401
Q

What are favorable prognostic signs for brachial plexus palsy?

A
  1. Recovery within 2 wks
  2. Only involvement of proximal upper extremity
402
Q

What percentage of babies with brachial plexus will have residual deficits?

A

20-30%

403
Q

What is the most common cause of neonatal conjugated hyperbilirubinemia?

A

Neonatal hepatitis

404
Q

What are the causes of conjugated hyperbilirubinemia? (8)

A

**Top 3 most common:

  1. Biliary atresia
  2. Cholestasis
    - Alagille
    - congenital
  3. Idiopathic neonatal hepatitis
  4. Choledochal cyst
  5. Infections
  6. TPN
  7. Galactosemia
  8. Alpha-1-antitrypsin
405
Q

What is the pathophysiology of congenital lobar emphysema?
-what are the CXR findings?

A

unilateral enlargement due to accumulation of air and/or fluid

  • valve effect, hyperexpansion and air trapping
  • left upper lobe most commonly affected
  • on CXR: hyperlucency, hyperinflation of one lobe with mediastinal shift and compression of remaining lung
406
Q

What are the 4 categories of lung bud abnormalities?

A
  1. Congenital lobal emphysema
  2. Congenital pulmonary adenomatoid malformation (CPAM) (used to be known as CCAM)
  3. Pulmonary sequestration
  4. Bronchogenic cyst
407
Q

What is the pathophysiology of CPAM?
-CXR findings?

A

Congenital pulmonary adenomatoid malformation

  • Proliferation of bronchiole structures but no alveoli
  • a bunch of cysts of lung tissue that communicates with tracheobronchial tree
  • CXR findings: cysts (white)
408
Q

What is the pathophysiology of pulmonary sequestration?

  • CXR findings?
  • most common location?
A

Lung tissue not connected to bronchi and trachea

  • blood supply is from systemic circulation and not pulmonary circulation
  • most common location: left costophrenic sulcus
409
Q

What is the major complication of subcutaneous fat necrosis?

A

Hypercalcemia

410
Q

Differentiate between jiterriness and seizures.

A

Eye movements:

  • normal in jitteriness
  • horizontal deviation, nystagmus and staring and blinking in seizures

Movement:

  • fine movements in jitteriness
  • coarse movements in seizures

Able to stop movements:

  • yes in jitteriness
  • no in seizures
411
Q

How long does erythema toxicum last for? What do the papules contain?
-what about pustular melanosis? What do the pustules contain?

A

Erythema toxicum = develops 1-3 d after birth, lasts up to 1 week, contains eosinophils
Pustular melanosis = present at birth, lasts 2-3 d, contains neutrophils

412
Q

What are some conditions associated with a large anterior fontanelle?

A
  1. Hypothyroidism
  2. Apert syndrome
  3. Trisomy 13, 18, 21
  4. Hydrocephaly
  5. Osteogenesis imperfecta
413
Q

Where is the position of a cephalohematoma vs. subgaleal hematoma vs. caput?

A
  • Cephalohematoma: subperiosteal hemorrhage (doesn’t cross suture lines)
  • Subgaleal: collection of blood BELOW the aponeurosis that covers the scalp and the entire length of the occipito-frontalis muscle = can lead to extensive bleeding, develop a consumptive coagulopathy leading to hypotension
  • Caput: soft tissue swelling of the scalp (crosses suture lines)
414
Q

What is Mobius syndrome?

A

Absence of hypoplasia of the facial nerve leading to symmetrical facial palsy

415
Q

if retinal hemorrhages occur during delivery from instrumentation or C-section, when should they resolve by?

A

5% resolve by 2 weeks, they should ALL resolve by 4 weeks

416
Q

What is the management of gastroschisis?

A
  1. Temperature monitoring since can lose heat from exposed bowel
  2. NG decompression
  3. Surgical intervention ASAP
  4. IV fluids
  5. Protective covering and keep bowels in right lateral position to protect kinking of bowel until surgical repair
  6. NPO = TPN
  7. Broad spectrum antibiotic coverage
417
Q

What are the main differences between breast milk and cow’s milk? (5)

A

Breast milk:

  1. Lower protein content
  2. Greater whey:casein ratio (70:30 as opposed to 60:40)
  3. Higher fat content (30-50% compared to 3-4%)
  4. Richer in Vitamins A, C, E; lower in Vitamins D and K
  5. Lower iron but better absorption
418
Q

What is the calculation for determining umbilical catheter length?

  • UVC
  • UAC
A

UVC: (3 x wt in kg) + 9
UAC: (0.5 x UVC insertion depth) + 1

419
Q

What are the increased risks of twin pregnancies? (8)

A
  1. Prematurity
  2. Growth restriction
  3. Spontaneous abortion
  4. Placental abnormalities (abruption, previa)
  5. Increased perinatal mortality
  6. Birth asphyxia
  7. Fetal malposition
  8. Polyhydramnios
420
Q

If maternal drug abuse is suspected, which specimen from the infant is most accurate for detecting exposure?

A

Meconium = greater sensitivity than urine with positive findings persisting longer
-contains metabolites gathered over as much as 20 weeks (as opposed to urine with more recent exposure)

421
Q

What is the best way to assess gestational age in the fetus?

A

***Historically Nagele’s rule is the best way: 1st day of last menstrual period

If this is not available:

  • before 12 weeks gestation: crown-rump length on US
  • beyond 12 weeks: biparietal diameter on US
422
Q

What are the 5 components of the biophysical profile?

A
  1. Fetal breathing movements
  2. Gross movements
  3. Amniotic fluid level
  4. Fetal HR
  5. Fetal tone

***2 points each for possible total of 10 points

423
Q

At what gestational age does pupillary reaction to light develop?

A

As early as 29 weeks but not consistently present until 32 weeks

424
Q

When do premature infants “catch up” on growth charts?

A

Most catch up growth occurs during the 1st 2 years of life with most catching up by 3 years of age

425
Q

What are risk factors for NEC in preterm infants? (5)
-one protective risk factor against NEC?

A
  1. Prematurity
  2. Low birth weight
  3. Use of steroids or NSAIDs
  4. Requiring ventilator support
  5. Symptomatic PDA requiring surgery

Protective risk factor: breast milk

426
Q

How long should infants with NEC receive nothing by mouth?

A

Infants with true confirmed NEC (radiographic or surgical evidence): NPO + TPN x 2-3 wks
-infants with suspected NEC can be fed after 3-7 days of bowel rest

427
Q

What are the 3 stages of NEC?

A

Stage 1: suspected NEC

  • clinical signs: abdo distention, bloody stools, emesis, gastric residuals, apnea, lethargy
  • radiological signs: ileus, distension

Stage 2: Proven NEC

  • clinical signs + abdo tenderness +/- metabolic acidosis, thrombocytopenia
  • radiological signs: pneumatosis intestinalis, portal venous gas

Stage 3: Advanced NEC

  • clinical features in stage 2 + hypotension, significant acidosis, DIC, neutropenia
  • radiological features: stage 2 findings with pneumoperitoneum
428
Q

When should iron supplementation be initiated for preterm babies?

A

4-8 weeks of age and maintained x 12-15 months

429
Q

A newborn presents with thrombocytopenia. What is the most likely etiology in each of the following if present?

  • blueberry muffin rash
  • absence of radii
  • palpable flank mass and hematuria
  • large hemangioma
  • abnormal thumbs
A
  • blueberry muffin rash: think TORCH or viral infection
  • absence of radii: think TAR (thrombocytopenia with absent radii)
  • palpable flank mass and hematuria: renal vein thrombosis
  • large hemangioma: Kasabach-Merritt syndrome
  • Abnormal thumbs: Fanconi syndrome
430
Q

What are the lab findings of DIC?

A
  1. Decreased fibrinogen
  2. Increased PT/PTT
  3. RBC fragmentation on peripheral smear from microangiopathic hemolytic anemia
431
Q

What is the differential diagnosis of hypocalcemia in the neonate?

  • early (first 3 days of life) (3)
  • late (after 1st week of life) (8)
A

Early:

  1. Premature infants
  2. Infants with birth asphyxia
  3. Infants of diabetic moms

Late:

  1. High phosphate cow milk formula
  2. Intestinal malabsorption
  3. Postdiarrheal acidosis
  4. Hypomagnesemia
  5. Neonatal hypoparathyroidism
  6. Rickets
  7. Citrate (from exchange transfusion)
  8. Alkalosis
432
Q

What is the treatment for hypocalcemia in an infant presenting with seizures?

A

10% calcium gluconate, 2 ml/kg over 10 minutes

433
Q

What is the most common pathogen causing late-onset sepsis in the prem infant in NICU?
-treatment?

A

Coag negative staph (nosocomial infection)
-treatment: vancomycin

434
Q

What is the classification of IVH?

A

Grade 1: germinal matrix hemorrhage
Grade 2: IVH without ventricular dilatation
Grade 3: IVH with ventricular dilatation
Grade 4: IVH with parenchymal involvement

435
Q 
# Fill in the blank: in more than 90% of cases, IVH in prem infants occurs during the first \_\_\_\_ days of life.
-what is a common complication of severe IVH?
A

3!
-complication: posthemorrhagic hydrocephalus

436
Q

What are the benefits of breastfeeding? (9)

A
  1. Fewer episodes of otitis media, resp, GI illness
  2. Human milk facilitates growth of beneficial, nonpathogenic flora
  3. Increased immune protection
  4. Improved neurodevelopment
  5. Reduction in diabetes mellitus
  6. Economic
  7. Mom returns to pre pregnancy weight faster
  8. Protective for mom against certain cancers (ovarian, breast)
  9. Improved maternal-child bonding
437
Q

What are contraindications to breastfeeding? (4 major categories)

A
  1. Metabolic d/o: galactosemia, PKU, urea cycle defects
  2. Infections: HIV, TB before treatment, Human t-cell lymphotropic viruses, HSV if present on breast
  3. Substance use by mom
  4. Medications: chemotherapy, radiation, lithium,
438
Q

What are 3 clinical features of vitamin E deficiency?

A
  1. Hemolytic anemia (vitamin E is important for stabilizing the RBC membrane)
  2. Peripheral edema
  3. Thrombocytosis (increased platelets!!!)
439
Q

In utero exposure to cocaine results in increased risk of which complications?

A
  1. Preterm labor
  2. Placental abruption
  3. Neonatal irritability
  4. SGA
  5. Microcephaly

***Usually requires no treatment

440
Q

What is the timing of amniocentesis during pregnancy?
-what about CVS?

A
  • Amniocentesis: between 15-17 wks typically
  • CVS: after 10 wks
441
Q

What causes the following?

  • early decels
  • variable decels
  • late decels
A
  • Early decels: head compression during contractions = not concerning
  • Variable decels: most common, due to cord compression, may be concerning
  • late decels: MOST concerning, due to uteroplacental insufficiency
442
Q

When is the onset of neonatal acne?

A

At around 3 weeks of life = from sebaceous gland stimulation by maternal androgens
-usually resolves by 4 mo of age

443
Q

What are the manifestations of neonatal lupus erythematous? (4)

A
  1. Cardiac: congenital heart block (usually 3rd degree), occurs during 18-30th week gestation, can lead to fetal hydrops
  2. Skin: annular erythematous scaling plaques on sun exposed areas during first 2 weeks of life and spontaneously disappears by 6 months when maternal abs are decreasing
  3. Thrombocytopenia
  4. Hepatitis
444
Q

What is commonly seen in infants born to moms who were on the following medications during pregnancy?

  • lithium
  • phenytoin
  • tetracycline
A
  • phenytoin: digit and nail hypoplasia
  • lithium: ebstein anomaly
  • tetracycline: yellow-brown discoloration of teeth
445
Q

Why do babies grunt in resp distress?

A

They are closing their glottis to maintain lung volume and gas exchange during exhalation

446
Q

What is the most common neonatal cystic lung malformation?

A

Congenital lobar emphysema

447
Q

What is the most common form of spina bifida?

A

Myelomeningocele: failure of the posterior neural tube to close

448
Q

What is VACTERL syndrome?

A

Vertebral abnormalities
Anorectal malformations
Cardiac anomalies
TEF
Renal or radial anomalies
Limb malformations

449
Q

What is the double bubble sign?

A

Represents duodenal atresia
-the 1st bubble on the left is the gas in the stomach and the 2nd bubble on the right is gas in the duodenum since it cannot pass through the atresia (no gas in the small or large bowel distal to the level of the obstruction)

450
Q

What is the management of meconium ileus?

A

Diagnostic gastrografin enema (hypertonic, water soluble) = washes out meconium
-OR surgical management if this doesn’t work

451
Q

What is the underlying pathophysiology of Hirschsprung disease?
-associated with what conditions? (3)

A

Failed migration of neural crest cells = affected bowel fails to relax causing a functional obstruction (dilated proximal colon, distal small caliber lumen)

  • associated with:
    1. Trisomy 21
    2. Smith-Lemli-Opitz syndrome
    3. Congenital central hypoventilation syndrome
452
Q

What is the most severe complication of neonatal immune-mediated thrombocytopenia?

A

IVH (can occur in utero)

453
Q

What are clinical features of congenital toxoplasmosis infection?
-treatment?

A

Hallmark is CNS involvement!!

  1. Chorioretinitis
  2. Diffuse intraparenchymal calcifications
  3. Hydrocephalus
    - treatment:
  4. Pyramethamine
  5. Sulfadiazine
  6. Leucovorin
454
Q

The mother of a newborn baby develops varicella shortly after birth. What is the timing for which you should give VZIG to the infant?

A

Give VZIG if mother develops varicella 5 days before or 2 days after delivery

455
Q

What is the most common cardiac defect seen in infants of diabetic moms?

A

Hypertrophic cardiomyopathy

456
Q

What is the classic triad of congenital rubella syndrome?

A
  1. Sensorineural hearing loss
  2. Cataracts
  3. Congenital heart disease
457
Q

Which infection is prevented by newborn eye prophylaxis with 0.5% erythromycin, 1% silver nitrate or 1% tetracycline?

A

N. gonorrhea!
-these reduce the incidence of C. trachomatis but does not PREVENT infection

458
Q

What is the difference between neonatal alloimmune thrombocytopenic purpura vs. neonatal autoimmune thrombocytopenic purpura?
-treatment of each?

A

Neonatal alloimmune thrombocytopenic purpura: maternal antibodies directed against paternal antigen on baby’s platelets = see low plts in baby, normal plts in mom.

  • tx:
    1. planned C section to decrease risk of intracranial hemorrhage
    2. Maternal IVIG prenatally
    3. Washed maternal plts given to baby postnatally

Neonatal autoimmune thrombocytopenic purpura: maternal ITP with autoantibodies crossing placenta and destroying baby’s plts = see low plts in baby, low plts in mom.

  • tx:
    1. Maternal steroids prenatally
    2. IVIG/steroids for baby postnatally
459
Q

In electrical injury, is alternating or direct current more hazardous?

A

At low voltages (e.g., those found in household electrical devices), alternating current is more dangerous than direct current. Exposure to alternating current can provoke tetanic muscle contractions so that the victim who has grasped an electrical source is unable to let go, thereby prolonging the exposure and producing greater tissue injury. Direct current or high-voltage alternating current typically causes a single forceful muscular contraction that will push or throw the victim away from the source.

460
Q

ETT depth?

A

Age/2 +12

461
Q

Hs and Ts?

A

H’s: Hypoxemia, hypovolemia, hypothermia, hyper/hypokalemia, hypoglycemia, and hydrogen ion (acidosis)

T’s: Tamponade, tension pneumothorax, toxins, and thromboembolism

462
Q

Blood loss= volume

A

25% of blood volume equals 20 mL/kg,

463
Q

Newborn shock

A

The misfits

Trauma (nonaccidental and accidental)

Heart disease and hypovolemia

Endocrine (e.g., congenital adrenal hyperplasia)

Metabolic (electrolyte)

Inborn errors of metabolism

Sepsis (e.g., meningitis, pneumonia, urinary tract infection)

Formula mishaps (e.g., underdilution or overdilution)

Intestinal catastrophes (e.g., volvulus, intussusception, necrotizing enterocolitis)

Toxins and poisons

Seizures

464
Q

Antidotes

A
465
Q

Ingestion odours

A
466
Q

What additional recommendations have been made regarding the most ideal sleep environment for infants?

A

In addition to supine positioning, recommendations to decrease the risk for SIDS or suffocation include”

use of a firm sleep surface

breastfeeding

room-sharing without bed-sharing

routine immunization

consideration of a pacifier

avoidance of soft bedding,

overheating, and exposure to tobacco smoke, alcohol, and illicit drugs.

467
Q

MRSOPA

A

M = Mask adjustment

R = Repositioning

S = Suctioning

O = Open the mouth

P = Increase the pressure

A = Alternate airway

468
Q

ETT Size Neonate

A
469
Q

APGAR

A
  • Appearance (pink, mottled, or blue)
  • Pulse (> 100, < 100, or 0 beats/minute)
  • Grimace (response to suctioning of the nose and mouth)
  • Activity (flexed arms and legs, extended limbs, or limp)
  • Respiratory effort (crying, gasping, or no respiratory activity)
470
Q

Jaundice

A
471
Q

Head bleeds

A
472
Q

Breastmilk to cows milk comparison

A

67 kcal/100cc

ower portien content

Greater whey:casein ratio

CHO: both lactose

Fat 30-50% vs. 3-4%

Vitaimins: more ACE, lower DK

Minerals: lower Fe, better absorption

473
Q

When does the suck-swallow reflex become coordinated?

A

32 weeks

474
Q

TPN complications

A

Electrolyte ABN

Glucose AbN

Cholestasis

Line infections

Bone d/o

475
Q

When do infants acquire most of their passive transplacental immunity?

A

After 32 weeks

476
Q

NEC RF?

A

Prematurity

Asphyxia

Enteral feedins

Polycythemia and hypervisocity

Exchange transfusions

477
Q

16 yo female on surgical ward in traction for femoral fracture and splenic rupture. She develops sudden onset CP, cough and O2 sats 84%. Give 3 of the most likely causes of the sudden distress. Give 3 investigations to do to confirm diagnosis.

A

Fat embolus, PE, pneumothorax. CT angiogram, CXR, Ultrasound of lower limb, EKG,D-dimer

478
Q

4 “medical reasons” why brain dead patient may not be able to be an organ donor.

A
  • Sepsis untreated
  • HIV positive
  • CMV active infection
  • Malignancy
479
Q

Polycythemic newborn. Hb 240, Hct 0.75. Wt 2000g. Child requires a partial exchange transfusion. What fluid do you use as the diluent? How much blood to you replace to decreae the Hct to 0.5?

A
  • Exchange transfusion if Hct > 70 – 75% on venous sample
  • Use normal saline, albumin or plasma
  • Blood volume to be exchanged = [(Observed Hct – Desired Hct)/Observed Hct)]x blood volume (80cc/ kg)
    = [(.75-0.5)/0.75] x 80mL/kg x 2 kg = 0.33 x 160
    = 52.8 mL
480
Q
A

Paediatrics Royal College (11 decks)

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