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Royal College Prep > CPS Statement Review > Flashcards

CPS Statement Review Flashcards

1
Q

What are the admission and discharge criteria for an acute asthma exacerbation?

A

Admission:

  • oxygen
  • increased WOB
  • Ventolin q<4 hr
  • deteriorating post-systemic steroids
  • social circumstances

ICU: continuous salbutamol

Discharge:

  • Ventolin q4 hours or more after 4-8hr observation
  • >93% on RA
  • minimal-no WOB
  • improving
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2
Q

Name 5 complications of procedural sedation (total 12)

A
  • Aspiration
  • Airway obstruction
  • Apnea/hypoventilation
  • Laryngospasm
  • Hypoxia
  • Hypotension
  • Bradycardia
  • Arrythmias
  • Cardiac arrest
  • seizures
  • Allergic reaction
  • Paradoxical reaction (behavioural reactions, unpleasant recovery, excitatory movements)
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3
Q

Name the ASA classifications, which are appropriate for sedation without anesthesiology, and which risk factors would indicate anesthesia consult

A
  • ASA type 1 & 2
  • Risk factors:
    • Difficult airway
    • Respiratory distress
    • Cardiac distress
    • Preterm (until 60 weeks post conception age = CGA 5 months)
    • Obese
    • OSA
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4
Q

Walk through preparation for procedural sedation (OSCE style)

  • Setting
  • Equipment
  • Rescue medications
  • Monitoring
A
  1. Adequate personnel - 2 HCPs, 1 skilled in advanced airway and resuscitation
  2. Monitoring - continuous pulse oximetry & BP q 5 mins + if possible capnography and ECG (especially for moderate to deep sedation or IV sedation)
  3. Equipment: “SOAPME”
    • S = suction catheters and apparatus
    • O = oxygen supply and delivery equipment (flow meters, tubing, prongs)
    • A = airway equipment (face masks, NPA/OPA, laryngoscope handles and blades, ETTs, stylets)
    • P = positive-pressure delivery system (bag-valve-mask ventilation)
    • M = monitors
    • E = emergency cart with alternative airways, supplies for vascular access and resuscitation drugs
  4. Rescue Medications:
    1. Atropine - prevent bradycardia (repeat x1, max 1mg child, 3mg for adolescent)
    2. Epinephrine - cardiac arrest (0.01mg/kg IV q 3-5 minutes)
    3. Succinylcholine - laryngospasm (1-2 mg/kg IV; 2-4 mg/kg IM)
  5. Antidotes
    1. Opioids → Naloxone (0.1mg/kg IV q2-3 minutes)
    2. Benzos → Flumazenil (0.01mg/kg IV, max 0.2mg q1 minute to max 0,05mg/kg or 1 mg)
  6. Monitoring
    1. During sedation q5 minutes
    2. Post sedation q15 minutes until baseline achieved
    3. For 24 hours IF EMERGENCY / COMPLICATION
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5
Q

How do you classify mild, moderate, severe and impending respiratory failure in an acute asthma exacerbation?

A
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6
Q

Name 3 general strategies to reduce procedure pain and examples of each

A
  1. Physical
    1. Infants: pacifier, swaddling, skin to skin
    2. Children: positioning
    3. Immobilization, icing
    4. Using absorbable sutures
    5. Small needle
    6. Swallowing during NG insertion
  2. Psychological
    1. Parental/caregiver presence
    2. Age-appropriate preparation (explanation of whats to come)
    3. Distraction - child life, parents, electronics etc
    4. Deep breathing
  3. Pharmacology
    1. Sucrose/breastfeeding <1 year
    2. Topical
      1. EMLA - lidocaine-prilocaine 5% - Onset 1 hour; max effect in 4 hours (1 if <3 months)
      2. Maxilene - liposomal lidocaine 4% - Onset 30 minutes; max effect 2 hours
    3. Infiltration
    4. Systemic

least invasive approach

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7
Q

How do you treat a mild asthma exacerbation?

A
  • Keep oxygen >/= 94%
  • Salbutamol q20 minutes x 1-3 doses
  • Consider inhaled corticosteroids
  • Observe in ED for minimum 2 hours
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8
Q

How do you treat a moderate asthma exacerbation?

A
  • Keep oxygen >/= 94%
  • Salbutamol q20 minutes x 3 doses, then q1hr
    • < 20kg = 5 puffs
    • > 20kg = 10 puffs
  • Consider Ipratropium q20 minutes x 3 doses
    • < 20kg = 3 puffs
    • > 20kg = 6 puffs
  • Oral steroids for 3-5 days
    • Prednisone 1-2mg/kg/day (max 50mg)
    • Dexamethasone 0.15-0.3mg/kg/day (max 10mg)
  • Observe for 4 hours in ED
  • Admit if indicated
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9
Q

How do you treat a severe asthma exacerbation?

A
  • Keep oxygen >/= 94%, consider 100% O2
  • NPO
  • Oral steroids for 3-5 days
    • Prednisone 1-2mg/kg/day (max 50mg)
    • Dexamethasone 0.15-0.3mg/kg/day (max 10mg)
  • Consider IV steroids
    • Methylprednisolone 1-2mg/kg/dose q6
    • Hydrocortisone 5-7mg/kg/dose q6
  • Salbutamol q20 minutes x 3 doses, then q1hr
    • < 20kg = 5 puffs/2.5mg neb
    • > 20kg = 10 puffs/5mg neb
    • *Continuous neb if needed
  • Ipratropium q20 minutes x 3 doses
    • < 20kg = 3 puffs/0.25mg neb
    • > 20kg = 6 puffs/0.5mg neb
  • Consider MgSO4 25-50mg/kg IV over 20 minutes
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10
Q

How do you treat an acute asthma exacerbation with impending respiratory failure?

A
  • Keep oxygen >/= 94%, consider 100% O2
  • NPO, get IV access, continuous monitors
  • Continuous nebulized salbutamol and ipratropium x 3 doses
  • IV steroids
    • Methylprednisolone 1-2mg/kg/dose q6
    • Hydrocortisone 5-7mg/kg/dose q6
  • Consider MgSo4, IV salbutamol, IV aminophylline, SC epinephrine
    • MgSO4 25-50mg/kg IV over 20 minutes
    • IV Salbutamol: Load: 7.5 mcg/kg over 2–5 min, followed by 1 mcg/kg/min. Titrate upwards with increments of 1 mcg/kg/min (maximum 5 mcg/kg/min)
  • Draw VBG and electrolytes (rising CO2 red flag)
  • RSI if deteriorating rapidly
  • Consult PICU
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11
Q

Discuss discharge planning for an acute asthma exacerbation (medications and follow-up)

A
  • 3-5 days of oral steroids
  • moderate - severe should go home on ICS
  • Salbutamol q4 hr at home until improved
  • Asthma action plan with inhaler techniques
  • Follow-up in 2-4 weeks
    • Respirology or allergy referral if in PICU
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12
Q

What are the main side effects of Ventolin and MgSO4?

A
  • Ventolin: hyperglycemia, hypokalemia, tachycardia
  • MgSO4: hypotension
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13
Q

What is the most frequently reported STI in Canada?

A

Chlamydia Trachomatis

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14
Q

Which HPV strains are considered high risk and what are associated risk factors?

A

16 and 18

RF: age <25, lower socioeconomic status, being an Indigenous woman

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15
Q

Name 8 risk factors for an STI

A
  • inconsistent/no condom use
  • contact with someone known to have an STI
  • new partner
  • > 2 partners in the past year
  • serial monogamy
  • no contraception/only non-barrier contraception
  • IVDU
  • any drugs (esp. if associated with sex)
  • previous STI
  • unsafe sexual practices (sharing toys/exchanging blood etc)
  • sex work/being a client
  • survival sex (exchange of sex for food/shelter/drugs)
  • street involvement/precarious housing
  • anonymous sex (met online etc)
  • experience of sexual assault/abuse
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16
Q

How often should youth be offered STI testing?

A

ALL sexually active youth under 25 years of age should be offered screening at least annually (or more if risk factors present)

***after treatment, screening should be repeated q6m if risk persists

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17
Q

Chlamydia: Screen/sample

also: what if there is a medico-legal case (ie. sexual assault)

A
  • NAAT (nucleic acid amplification test is the most sensitive and specific) - urine, urethral swab, vaginal or cervical swabs
  • Medico-legal: culture is the best (cervical or urethral)
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18
Q

Follow up testing: Chamydia

A

Test of cure at 3-4 weeks if:

  • compliance is uncertain
  • second-line/alternative treatment used
  • re-exposure is a risk
  • adolescent is pregnant
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19
Q

Gonorrhea Screen/Sample

Also, who needs a culture? What about for medicolegal purposes?

A
  • NAAT from urine, urethral/vagina/cervical swabs in both symptomatic and asymptomatic individuals
  • culture allows for antimicrobial susceptibility testing - perform if a pateint does not respond promptly to therapy
  • cultures for asymptomatic/symptomatic MSM (because increased antibiotic resistance)
  • for rectal/pharyngeal testing, discuss with the lab (generally culture is best)
  • Medico-legal: positive NAAT should be confirmed by culture/different primers or DNA sequencing
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20
Q

Follow-up testing Gonorrhea

A

Test of cure (culture 3-7 days post-treatment or NAAT 2-3 weeks later) if:

  • second-line alternative treatment
  • antimicrobial resistance is a concern
  • uncertain compliance
  • re-exposure risk if high
  • PREGNANCY
  • previous treatment failure
  • pharyngeal/rectal infection
  • disseminated infection
  • signs, symptoms persist post-treatment
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21
Q

Syphilis screening/testing in adolescents

A
  • serology is the usual test unless there are lesions compatible with syphilis.
  • treponemal-specific screens are more sensitive than non-treponemal tests
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22
Q

Syphilis F/U testing (for adolescents)

A

Depends on the nature of the infection:

Primary, secondary or early latent infection: repeat serology at 1, 3, 6 and 12 months after treatment.

Late latent infection: repeat serology at 12 and 24 months after treatment

Neurosyphilis: repeat serology at 6, 12 and 24 months after treatment

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23
Q

HIV testing

A

serology is the key diagnostic test (if positive, lab does a Western Blot).

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24
Q

HIV F/U testing:

A

antibodies may be detected at 3 weeks with fourth gen HIV antibody screening, but can take up to 6 months with older tests.

***follow up testing needs to be planned when the initial test is negative after a known exposure

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25
Q

How do you diagnose ITP?

A

Platelets < 100 x109

(usually <20)

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26
Q

What are the red flags in ITP to consider an alternative diagnosis? (History, physical and investigations)

A

Hx: constitutional symptoms, bone pain, recurrent thrombocytopenia, poor response to treatment

PE: lymphadenopathy, hepatosplenomegaly, looks unwell, signs of chronic disease

Inx: low hemoglobin, high MCV, abnormal WBC, abnormal cell morphology on smear

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27
Q

When do we screen for HSV, trichomonas and HPV?

A

Routine screening is NOT recommended for HSV and tricomonas.

screening for HPV and/or cervical cancer is not recommended before 21

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28
Q

How d you treat ITP based on the degree of bleeding?

A
  • Treatment goal: Platelets > 10-20 (if treating, to reduce bleeding risk)
  • Without active bleeding: observation 1st line
  • Moderate bleeding: IVIG 0.8-1g/kg or oral corticosteroids
  • Severe bleeding: IVIG AND IV steroids, tranexamic acid 25mg/kg/dose TID-QID
  • Relapse/non-responder: choose alternate treatment
    • ⅓ will relapse within 2-6 weeks
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29
Q

Classify mild, moderate and severe bleeding to guide treatment in ITP.

A

Mild: no bleeding, bruising, petechiae, mild epistaxis

Moderate: more severe manifestations, mucosal lesions, difficult epistaxis or menorrhagia

Severe: Any bleeding episode requiring admission (epistaxis, melena, menorrhagia, intracranial hemorrhage)

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30
Q

Discuss the principles involved with shared decision making in treatment of ITP with minimal to no bleeding.

A
  • Minimal risk of bleeding
  • Inpatient (IVIG) vs. outpatient (steroids) treatment
  • Child returning to regular activities sooner with IVIG
  • Risks of blood products
    • transfusion reactions
    • aseptic meningitis
    • N/V
    • fever
    • rash
  • Side effects of steroids
    • Mood changes
    • increased appetite/weight
    • Gastritis
    • HTN
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31
Q

What discharge counselling would you provide to a patient with ITP (follow-up, activity, health care precautions)?

A
  • Counsel on signs of bleeding
  • Follow-up with physical exam and platelet check until recovered
  • Avoid contact sports or activities with injury risk (esp. head) while platelets low or evidence of bleeding
  • Avoid anti-platelet meds
  • Remind all health care providers
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32
Q

For which STI is combination treatment recommended (and why)?

A

Gonorrhea: increasing resistance to cephalosporins and azithromycin

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33
Q

What samples should be collected (STI testing): Asymptomatic male with risk factors.

A
  1. First catch urine for C &G
  2. pharyngeal/rectal swabs for C&G if history or unprotected receptive oral or anal exposure)
  3. Serology for: Syphyllis and HIV
  4. Consider: Hep A, B, C (serologies)
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34
Q

STI testing: When do you consider Hep A testing in an asymptomatic individual?

A

History of oral-anal contact

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35
Q

STI testing: When do you consider Hep B testing in an asymptomatic individual?

A

no history of Hep B vaccine (or an uncertain history)

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36
Q

STI testing: When do you consider Hep C testing in an asymptomatic individual?

A

you can always consider, but especially if there is a history of drug injection in the patient or their partners

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37
Q

What samples (STI testing) should be collected for an asymptomatic female with risk factors?

A
  1. First catch urine OR vaginal swab for C &G
  2. pharyngeal/rectal swabs for C&G if history or unprotected receptive oral or anal exposure)
  3. Serology for: Syphyllis and HIV
  4. Consider: Hep A, B, C (serologies)
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38
Q

What samples (STI testing) should be collected for a male with symptoms of urethritis?

A
  1. Urethral swab for gram stain for gonorrhea and culture (NAAT can be used when available)
  2. first-catch urine for chlamydia (NAAT)
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39
Q

What samples (STI testing) should be collected for a female with symptoms of cervicitis?

A
  • Vaginal or cervical swab for gram stain, N gonorrhoeae (culture or NAAT if culture unavailable) and C trachomatis (NAAT or culture)
  • swab of cervical lesions (if present) for HSV
  • vaginal swab for wet mount
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40
Q

What samples (STI testing) should be collected for an individual with suspected pharyngeal gonoccocal infection?

A
  • swab the posterior pharynx and the tonsillar crypts.
  • use the swab to directly inoculate the appropriate culture medium, or place it in a transport medium
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41
Q

What samples (STI testing) should be collected for an individual with genital ulcer disease?

A
  • swab of ulcerative, erosive, pustular or vesicular lesions for HSV culture or HSV polymerase chain reaction (PCR)
  • AND
  • swab serology for syphillis
  • refer to an ID/STI clinic for patients iwth HIV, immunosuppression, systemic symptoms, history of travel (?test for other pathogens), MSM, atypical or nonhealing lesions
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42
Q

What features of a genital ulcer make you worried for syphillis? how do you test?

A

painless ulcer.

serology, swab from ulcer for dark-field exam, direct/indirect fluorescent antibody or NAAT if available

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43
Q

What samples (STI testing) should be collected for symptoms of vaginitis?

A
  • collected pooled vaginal secretions if available.
  • if no secretions available, swab the vaginal wall in the posterior fornix to prep a smear (or put in a transport medium)
  • if high risk for STI, do swabs (vaginal or cervical) for C&G
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44
Q

how can you test for trichomonas and non-STI causes of vaginitis?

A

wet-mount and gram stain smears from the vagina

when possible, also send NAAT for Trichomonas

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45
Q

When do you need to involve an ID doc in STI management?

A
  • HIV, syphillis (urgently)
  • for the other STIS, when recommended tratments are not tolerated or pathogens are resistant
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46
Q

What is the recommended treatment of C and G anogenital (urethral, endocervical, vaginal, rectal) co-infection:

A
  1. Ceftriaxone 250 mg IM x1 AND azithromycin 1g PO x1
  2. Cefixime 800 mg PO x1 AND Azithromycin 1g PO x1
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47
Q

What is the recommended treatment of C and G pharyngeal co-infection:

Preferred and alternative

A

Preferred: Ceftriaxone 250 mg IM x1 AND azithromycin 1 g POx1 (ie. same as anorectal)

Alternative:

  1. Cefixime 800 mg PO x1 AND azithromycin 1g PO x1
  2. Azithromycin 2 g PO x1
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48
Q

Treatment of Genital/perianal HSV infection: first episode

A

3 options:

  1. Valacyclovir 1000 mg PO BID for 10 days
  2. Famciclovir 250 mg PO TID x5 days
  3. Acyclovir 200 mg PO 5x/day for 5-10 days (don’t pick this one)
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49
Q

Treatment of Genital/perianal HSV infection: recurrent lesions

A

3 options:

  1. Valacyclovir 500 mg PO BID or 1000 mg PO OD x3 days
  2. Famciclovir 125 mg PO BID x5 days
  3. Acyclovir 200 mg PO 5x/day for 5 days (800 mg PO TID for 2 days may be the same)
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50
Q

Treatment of Trichomonas

A

Metronidazole 2 g PO in a single dose OR metronidazole 500 mg PO BID for 7 days

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51
Q

Name 4 primary prevention strategies against STIs.

A
  1. vaccines against HPV
  2. vaccines against Hep B
  3. condomes
  4. behavioural change
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52
Q

Give an approach for taking a sexual and reproductive health history.

A

7 Ps:

  • Partners
  • Practices
  • Protection (from STIs)
  • Past history of STIs
  • Prevention (of Pregnancy)
  • Permission (Consent)
  • Personal (gender) identity
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53
Q

What should be recommended to youth who are ambivalent about contraception or considering pregnancy?

A
  • multivitamin containing folic acid should be recommended
  • optimal immunization with MMR, varicella and hep B should be ensured.
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54
Q

Name 4 adverse health issues that are increased among LGBTQ+ youth. Name 2 protective factors against SI/suicide in trans youth

A

Adverse Health Issues

  • STI aquisition
  • bullying
  • depression
  • anxiety
  • low self-esteem
  • substance use
  • suicide attempts
  • insecure housing

Protective Factors (against suicide among trans youth)

  • parental support of sexual orientation/gender identity
  • timely access to gender-affirming treatments
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55
Q

Name 4 complications of untreated STIs?

A
  • Pelvic inflammatory disease
  • prostatitis
  • chronic pelvic pain
  • infertility
  • effects on developing fetus/neonate
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56
Q

What is the difference btn PrEP and PEP?

A

PrEP: HIV pre-exposure prophylaxis. Taken daily and long-term, BEFORE exposure to HIV.

PEP: post-exposure prophylaxis. Taken AFTER high-risk exposure to prevent HIV seroconversion after a high-risk exposure has occurred.

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57
Q

Recommended STI screening for asymptomatic immunocompetent youth

A

NAAT for C and G via any of:

  1. first catch urine
  2. urethral/cervical swab
  3. vaginal swab (may be self-collected)

AND Serology for HIV and syphillis

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58
Q

What STI testing can you do for someone who has performed oral sex?

A

pharyngeal swab: culture for C and G (and/or NAAT when available)

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59
Q

What and how do you do STI testing for people who report receptive anal intercourse (including MSM)

A

anal swab - culture for C and G (and/or NAAT if available)

**insert swab 2-3 cm into the anal canal and press laterally to sample epithelium.

If visible fecal contamination, discard the swab and try another.

60
Q

What is your approach to consenting youth for HIV and syphillis testing?

A
  • use an “opt out” approach
  • consider, “Urine and blood testing are part of the routine screening that we offer to all sexually active teens. Even though the risk of HIV and syphilis may be low, treatments are available, and so it is important to identify infections that can be there even without symptoms. Is that ok with you?
  • also inform the teen that they may be contacted by public health if positive
61
Q

What are the main triggers of anaphylaxis?

A

⅓ have an identifiable trigger

  • Food (nuts, fish, dairy, eggs, fish)
  • Bee/wasp stings
  • Medications
62
Q

Describe the potential presenting symptoms of anaphylaxis (5 systems)

A

Cutaneous (80-90%)

  • urticaria
  • pruritus
  • angioedema
  • flushing

Respiratory (60-70%)

  • stridor/upper airway obstruction
  • hoarsness
  • oropharyngeal/laryngeal/uvular edema
  • swollen lips.tongue
  • Sneezing
  • Rhinorrhea
  • Coughing
  • SOB
  • Bronchospasm
  • Tachypnea
  • Respiratory arrest

Cardiovascular

  • Dizziness
  • Hypotension
  • Syncope
  • Tachycardia/arrythmia/cardiac arrest
  • Diaphoresis/pallor/cyanosis

GI

  • Nausea/vomiting
  • Diarrhea
  • Abdominal pain

CNS

  • Fussiness/irritability
  • Drowsiness/lethargy
  • reduced LOC/somnolence
63
Q

Define Anaphylaxis

A
  1. Acute onset of illness (within minutes to hours) with involvement of skin/mucosal tissues PLUS:
    1. Respiratory compromise
    2. Reduced BP or associated end organ dysfunction
  2. Two or more of the following after exposure to a likely allergen for the patient:
    1. Skin-mucosal involvement
    2. Respiratory compromise
    3. Reduced BP or associated end organ dysfunction
    4. GI symptoms
  3. Reduced BP after exposure to a known allergen.
64
Q

What is the outpatient treatment of anaphylaxis?

A

EpiPen JR (0.15mg) <25kg

  • *can consider weight dosed if < 10kg, but parents must be competent to draw up dose in syringe

EpiPen (0.3mg) > 25kg

Epi (1:1000) 0.01mg/kg IM

65
Q

What is the first-line inpatient treatment for anaphylaxis?

A

ABCs

IM epinephrine (1:1000) 0.01mg/kg

Prepare for airway management (consider RSI)

66
Q

What are the second line treatment options for anaphylaxis?

A

Antihistamines: relief of cutaneous symptoms

  • H1 and H2 antihistamines
  • Ranitidine can be synergistic with H1

Corticosteroids: no proven benefit

Salbutamol: for bronchospasm/wheeze

Epi neb: for stridor

Epi infusion: for persistent hypotension (0.1-1 ug/kg/min)

Glucagon IV for refractory anaphylaxis: stimulates overrides beta and alpha agonist

67
Q

Discuss the disposition of patients with anaphylaxis.

A
  • Observe for 4-6 hours in ED (longer if from rural/distant location)
  • Admit if severe, repeat epi or biphasic reaction
  • Consider admission if high risk (peanut, asthma, beta blockers)
  • PICU if airway management, IV epi or glucagon
  • Discharged patients need epi + teaching
    • Consider 3 days of steroids or antihistamines
    • medic alert bracelet
    • refer to allergy or immunology
68
Q

Describe a biphasic reaction in anaphylaxis

A
  • Recurrent anaphylaxis within 1-72 hours after onset of symptoms (most in 4-6 hours)
  • Occurs in 5-20% of patients
  • 3% have a serious reaction requiring treatment
  • Might be associated with delayed epi, severe symptoms or requiring multiple doses of epi
69
Q

Describe indications and contraindications for ondansetron use in ED for gastro.

A
  • Highly potent selective serotonin 5-HT3 receptor antagonist
  • Indicated as a single dose (no benefits with multi-dose therapy) for kids > 6 months with vomiting, mild-mod dehydration and failure or oral rehydration
  • Follow-up with oral therapy 15-30 minutes post dose
  • Not recommended if primarily diarrheal
70
Q

What is the dose of ondansetron for gastroenteritis and what are common side effects?

A

0.15mg/kg (max 8mg)

8-15kg = 2mg

15-30kg = 4mg

>30kg = 6-8mg

S/E: diarrhea, arrhythmia (do not need ECG or electrolyte screen unless high risk factors)

71
Q

Name 8 ddx for wheeze in child <2y

A

Asthma

Viral bronchiolitis

laryngotracheomalacia

Pneumonia

Foreign body aspiration

GERD

Congestive heart failure

Vascular ring

allergic reaction/anaphylaxis

mediastinal mass

tracheal esophageal fistula

Cystic fibrosis

72
Q

List evidence based investigations in typical bronchiolitis

A

NONE!

Consider: CXR, CBC, blood culture, NPS if unclear diagnosis or severe

73
Q

Name 4 risk factors for severe disease in bronchiolitis

A
  1. Prematurity < 35 weeks GA
  2. <3 months at age of presentation
  3. Hemodynamically significant cardiopulmonary disease
  4. Immunodeficiency
74
Q

List admission criteria for bronchiolitis (6)

A
  1. Signs of severe respiratory distress (WOB, RR>60/min)
  2. O2 required to keep sats >90%
  3. Dehydration
  4. Cyanosis or apnea
  5. High risk for severe disease
  6. Family unable to cope

Discharge:

  1. Improved WOB/tachypnea
  2. O2 sats >90% without oxygen or on home oxygen supports
  3. adequate oral feeding
  4. education provided & follow up arranged
75
Q

Name 2 recommended interventions and 5 NOT recommended interventions for bronchiolitis management

A

Recommended: hydration (NG or IV), oxygen, frequent reassessment

NOT recommended: ventolin, steroids, antimicrobials, 3% saline nebs, cool mist therapy, chest physio

Can consider: epinephrine nebs, nasal suctioning, combined epi neb & oral dex, avoid continuous monitoring if possible (prolongs hospital stay; indicated if high risk in early course of disease)

76
Q

Children are at higher risk of intracranial head lesion compared to adults–

Name the 3 physiological reason for higher risk & the typical pattern of injury

A
  1. Larger head to body size
  2. Thinner cranial bones
  3. Less myelinated neural tissue

Pattern → diffuse axonal injury and secondary cerebral edema

77
Q

Which signs associated with a head trauma increase the risk for intracranial injury

A
  1. Prolonged LOC
  2. Disorientation, confusion, amnesia
  3. Worsening headache
  4. repeated or persistent vomiting
78
Q

Head trauma can be classified by GCS - name the GCS associated severities

A

Mild: GCS 14-15

Moderate: GCS 9-13

Severe: GCS <9

79
Q

In initial management of head trauma (ABCs) name the factors to avoid that would contributing to secondary injury

A
  1. Hypoxia
  2. Hypotension
  3. Hypothermia
  4. Raised ICP
80
Q

In the initial assessment and stabilization, name the specific ABCD considerations in suspected head trauma

A

A: consider possibly C-spine injury

B: maintain c-spine precautions

C: hemodynamic instability UNLIKELY due to intracranial injury alone → consider extracranial lesion

D: GCS, pupils, tone, reflex, fontanelles → look for signs of basal skull fracture

81
Q

Name the signs of basal skull fracture & what should be avoided in managing acute respiratory decompensation

A

Periorbital ecchymosis (“raccoon eyes”)

ecchymosis over mastoid bone (battle’s sign)

leakage of CSF from nose/ears/hemotympanum

AVOID nasal intubation

82
Q

Name indications for CT scan in suspected head trauma

A

Absolute:

  1. Focal neurological deficit
  2. suspected open or depressed kull fracture, widened diastatic skull fracture on xray

Relative:

  1. GCS <14, <15 2 hours after injury
  2. Symptoms worsen over 4-6 hours
  3. Signs of basal skull fracture
  4. Large/boggy scalp hematoma if >2y (if <2y consider skull xray first)
  5. Mechanism suspicious for severe injury
  6. Persistent irritability <2 years of age
  7. Seizure at any time
  8. Known coagulation disorder
83
Q

Name 3 risk associated with poor prognosis with documented intracranial injury

A
  1. GCS <6 or severity at presentation
  2. Raised ICP
  3. Severity of other injuries present
  4. Pre-injury ADHD
  5. Low socioeconomic status
84
Q

Name observation recommendations for mild head trauma (GCS 14-15)

A

Asymptomatic → d/c home with clear RTC instructions (worse H/A, persiste V+, difficulty awakening)

History of LOC, persistent V+ or H/A → observe in ED → if improved d/c home; if persistent admit for monitoring/IVF if V+

<2 yo → observe in ED with frequent reassessment; admit if concern for inflicted injury; ambulatory asymptomatic toddler can be d/c

Patients with impact seizures (immediately after injury or shortly after) with normal neurological exam and normal CT head are at low risk for further complications and can be discharged

85
Q

Name initial management and disposition of moderate head trauma (GCS 9-13)

A
  1. CT head
  2. Admit to hospital
  3. Neurosurgical/truama consult, consider PICU if GCS 9-10
86
Q

Name initial management and disposition of severe head trauma (GCS <9)

A
  1. Stabilize and intubate
  2. CT head
  3. Continuous vitals and CO2 monitoring
  4. Mechanical ventilation to maintain O2/ventilation
  5. Maintain normothermia
  6. Adequate sedation & analgesia
  7. Fluids to AVOID hypotension & maintain normovolemia

Transport to centre with neurosurgical and PICU services

87
Q

State epidemiology of post-traumatic seizures after traumatic brain injury and 5 risk factors to develop

A

most occur <24 hours but up to 7 days post injury; incidence 5-7% → 30-35% in severe head injury

Risk factors: young age, severe head trauma, cerebral edema, subdural hematoma, open or depressed skull fractures

Patients with impact seizures (immediately after injury or shortly after) with normal neurological exam and normal CT head are at low risk for further complications and can be discharged

88
Q

What are the 2 most significant brain injuries that can affect the preterm brain?

A

intracranial hemorrhage and white matter insult

89
Q

What is the (very basic) pathogenesis of IVH?

A
  1. fragility of the germinal matrix (which is a highly vas ularized region of the brain, and is extremely fragile and the primary source of bleeding in the cerebral ventricles causing IVH)
  2. fluctuations in cerebral blood flow (during a period of physiologic instability and limited cerebral autoregulation)
90
Q

Name 7 risk factors for fluctuations in the fluctuation of cerebral blood flow in prems:

A
  1. variation in systemic BP
  2. anemia
  3. hypo- or hyper-carbia
  4. acidosis
  5. PDA
  6. severe RDS
  7. pneumothorax
91
Q

What is Periventricular hemorrhagic infarction (PVHI)

A
  • parenchymal lesion, usually associated with severe IVH
  • represents a venous hemorrhagic infarct in the drainage area of the periventricular terminal veins
  • **typically leads to to cystic changes in periventricular white matter (porencephalic cyst)
92
Q

After what period EGA does the incidence of IVH become very low? Why?

A
  • After about 34-36 weeks, IVH becomes quite infrequent.
  • ***the germinal matrix involutes overtime and is almost absent by 34-36 weeks
  • But rates are much higher in infants born before 32 weeks EGA
  • Both the severeity and risk of GMH-IVH increase with decreasing of EGA
93
Q

Describe the Papile IVH grading system (it’s the one we usually use):

A

Grade 1: IVH is limited to the GM

Grade 2: IVH involves blood in the ventricles

Grade 3: IVH has blood filling and distending the ventricular system

Grade 4: parenchymal involvement with hemorrhage

Grades 1 and 2: mild

Grade 3 and 4: severe

**does not specifically include white matter lesions in brain locations other than periventricular areas or lesions in the cerebellum, basal ganglia and brainstem

**in this grading system, grade 4 is quite broad. depending on the locus and extent of the bleed, the severity and extent can vary quite greatly

94
Q

What do grades 1-4 of PVL on HUS represent?

A

Grade 1: transient periventricular areas with increased echogenicity for 7 days or more

Grade 2: small, localized fronto-parietal cysts

Grade 3: extensive periventricualr cystic lesions

Grade 4: areas of increased echogenicity in deep white matter which are evolving into extensive cystic lesions

95
Q

Name 5 risk factors for IVH

A
  1. prematurity (predominant)
  2. low birth weight (esp <1000g)
  3. lack of maternal prenatal corticosteroid use
  4. birth outside of a tertiary care centre
  5. histological chorioamnionitis
96
Q

What are 5 RF for abnormal brain imaging in the LATE AND MODERATELY preterm infants?

A
  1. lower EGA
  2. head circumference below the 3rd %ile
  3. need for resus at birth or critical care out of keeping with the usual neonatal course (mechanical ventilation/inotropes)
  4. complicated monochorionic twin pregnancy (IUGR/fetal demise)
  5. postnatal complications (sepsis, NEC etc)
97
Q

Neonatal HUS:

  • what views in prems?
  • what is it good at detecting (3)
    • what is 1 disadvantage?
A

Views: anterior and mastoid fontanelles

  • Ideal at detecting: GMH-IVH, large cerebellar bleeds and large cysts/echogenic areas in white matter
  • Disadvantage: operator dependent (and therefore, can miss subtle lesions)
98
Q

CT-head in neonates:

  • when do we use it?
    • what can it detect?
A
  • really just for emergencies now (otherwise, we use MRI)
  • can detect calcifications, hemorrhage, brain injury and edema secondary to hypoxia-ischemia, venous sinus thrombosis, masses and structural abnormalities

***obvious there is ionizing radiation…

99
Q

MRI head for neonates:

what does it detect?

what are the issues?

A

Highest resolution of:

  1. white matter injury
  2. low grade IVH
  3. cerebral malformation
  4. posterior fossa abnormalities

**can also help to diagnose inborn errors of metabolism

It is very expensive, time-consuming etc

100
Q

what are the 3 strongest predictors of abnormal neuromotor function:

  • on neonatal HUS?
  • neonatal MRI (at term-equivalent age)?
A

HUS:

  1. severe IVH (Papile grades 3 and 4)
  2. cystic PVL
  3. PHVD (posthemorrhagic ventricular dilatation)

MRI:

  1. Moderate to severe white matter injury
  2. cerebral injury
  3. abnormal myelination in the posterior limb of the internal capsule

**any combo of these increases the risk for adverse motor outcomes, that said there is only moderate sensitivity and specificity

However, in infants with grade 4 IVH, the absence of myelin in the PLIC has been shown to be strongly predictive of future hemiplegia

*remember that other neonatal complications of prematurity (BPD, ROP, sepsis etc), genetics and socio-familial factors also affect outcomes

101
Q

Name ROUTINE first imaging, repeat imaging and term-corrected imaging for:

infant born less than 32 weeks (ie. 31+6 and lower)

A

First imaging: HUS 4-7 days post-birth (detects GMH-IVH and early ventricular dilatation)

Repeat imaging: 4-6 weeks post-birth (detects white matter injury)

Term-corrected imaging:

  • routinely for neonates born before 26 weeks
  • not routine if born btn 26+0 and 31+6 (unless previous moderate to severe anomalies like grade 3 or 4 IVH, post-hemorrhagic ventricular dilation, or other risk factors like critical illness, vasopressors, NEC etc)
102
Q

Name ROUTINE first imaging, repeat imaging and term-corrected imaging for:

infant born 32 weeks to 36+6 with additional risk factors

A

First imaging: HUS 4-7 days post birth

Repeat imaging: 4-6 weeks post-birth, and only if the first image is abnormal

Term-corrected imaging: not routine

103
Q

What abnormality detected on routine head imaging would trigger repeat HUS sooner than the usual repeat schedule? When should you repeat?

A

Abnormality: grade 2 or higher IVH/white matter injury is detected on first imaging, a repeat HUS should be performed 7-10 days later

**if ventricular dilation or worsening IVH/white matter injury is detected, the frequency of HUS should be intensified (at least weekly initially)

repeat HUS should also be conducted in the weeks following acute illness (NEC/sepsis etc)

104
Q

What are the risk factors which would trigger “routine” head imaging for late and moderately late prems (ie. 32-36+6 weeks)

A
  • need for critical care out of keeping with the usual neonatal couse
  • complicated monochorionic twin pregnancy (IUGR, fetal demise)
  • microcephaly
  • complicated postnatal course: sepsis, NEC, major surgery, abnormal neuro symptoms
105
Q

Which EGA neonates automatically qualify for routine head imaging?

A

HUS is recommended for all infants born at or before 31+6 weeks in the first 4-7 days post birth to detect GMH-IVH and early ventricular dilatation.

106
Q

Which prems require an additional HUS at term-corrected age?

A
  • Prems born before 26 weeks
  • prems born 26+0 - 31+6: if additional risk factors or previous moderate to severe anomalies no HUS (grade 3 or higher IVH, post-hemorrhagic ventricular dilation, grades 3-4 PVL)
107
Q

When should you consider head imaging for late and moderately prem infants (32+0 - 36+6):

A

they aren’t routinely required, but consider when risk factors have been identified:

  • need for resus or critical care out of keeping with the usual neonatal course for GA, complicated monochronionic twin pregnancy, microcephaly, or a postnatal course compliactred by sepsis, NEC, major surgery or abnormal neuro signs)
108
Q

When should you consider term-corrected MRI?

A
  • not currently a routine recommendation
  • consider if moderate to severe anomalies on HUS (grade 3 or higher IVH, hemorrhagic ventricular dilatation, or grades 3-4 PVL), clinical risk for white matter injurry or for parental reassurance
  • also consider, cost, transport, stability and relevance for treatment
109
Q

Define neonatal brachial plexus palsy (NBPP)

A

weakness or flaccid paralysis of the upper extremity, diagnosed soon after birth

resulting from injury of one or more cervical and thoracic nerve roots (C5-T1)

110
Q

Name 7 risk factors for brachial plexus palsy

A

Strong association:

  • humeral fracture
  • shoulder dystocia (this one is modifiable - with “time-outs” pre-op, risk assessments etc)
  • clavicular fracture

Moderate:

  • pre-existing maternal diabetes
  • forceps/vacuum-assisted delivery
  • episiotomy
  • fetal/birth asphyxia
  • macrosomia (>4.5 kg)
  • LGA

twin/multiples and c/s seem to reduce the rates

111
Q

Name and Number (but don’t describe) the classes of neonatal brachial plexus palsy

A

Group 1: Classic Erb’s Palsy

Group 2: Extended Erb’s Palsy

Group 3: Total palsy WITHOUT Horner’s syndrome or oculosympathetic paresis (miosis, ptosis, ipsilateral facial anhidrosis)

Group 3: total palsy WITH Horner’s syndrome

112
Q

Name and describe the roots injured and site of weakness/paralysis for a Group I NBPP.

A

Group 1: Classic Erb’s Palsy

Roots: C5 or C6

Site of Weakness/Paralysis: Absent shoulder abduction, external rotation, elbow flexion and forearm supination

113
Q

Name and describe the roots injured and site of weakness/paralysis for a Group II NBPP.

A

Group 2: Extended Erb’s Palsy

Roots: C5 to C7

Site of Weakness/Paralysis: Classic Erb’s palsy findings (Absent shoulder abduction, external rotation, elbow flexion and forearm supination)

AND absence of wrist and digital extension

114
Q

Name and describe the roots injured and site of weakness/paralysis for a Group III NBPP.

A

Group III: Total Palsy without Horner’s Syndrome or oculosympathetic paresis

Roots: C5-T1

Site of Weakness/Paralysis:

Complete flaccid paralysis (flail extremity) involving all plexus roots

**absence of miosis, ptosis and ipsilateral facial anhidrosis

115
Q

Name and describe the roots injured and site of weakness/paralysis for a Group IV NBPP.

A

Group IV: Total palsy with Horner’s syndrome

Roots: C5-T1 and sympathetic chain involvement

Site of Weakness/Paralysis: Complete flaccid paralysis (flail extremity) with Horner’s syndrome indicating sympathetic chain involvement and avulsion injury

(Horner’s syndrome: miosis, ptosis and ipsilateral facial anhidrosis)

***can have phrenic nerve palsy and an elevated ipsilateral diaphragm as well

116
Q

Which groups of infants with NBPP will require surgical intervention?

A

Infants with total plexus injury (groups III and IV) with no signs of recovery need reconstructive microsurgery to repair the injured plexus and to improve outcomes

Gray zone:

infants with a deficit that has been managed conservatively but who may be considered for surgery based on select criteria like no recovery of bicep function at 3 months of age or a failed cookie test at 9 months

117
Q

Name 3 long-term consequences of persistent NBPP

A
  1. weakness
  2. development of skeletal malformations (contractures, limb length discrepancy)
  3. cosmetic deformities
118
Q

identify parts of a focused history/physical for NBPP?

A

History: risk factors for NBPP from the maternal and/or delivery history (like shoulder dystocia/fractures etc)

Exam: detailed MSK/neuro examine including active and passive ROM and normal reflexes.

***assess for humeral and/or clavicular fractures (as this can minic NBPP due to pain limiting ROM)

119
Q

If you suspect a neonatal clavical/humerus fracture what do you need to assess on the baby right away?

A

resp status and symmetry of chest movements to r/o a phrenic nerve injury (you might also see an elevated hemi-diaphram on CXR/U/s as well

120
Q

Name 4 conditions on a DDx for a neonatal brachial plexus palsy

A
  1. pseudoparesis (pain due to fracture, or infection of the bone, joint, soft tissue, vertebra etc)
  2. myotonia congenita (form of arthrogryposis multiplex congenita - AMC)
  3. anterior horn cell injury (ie. congenital cervical spinal atrophy, congenital varicella syndrome)
  4. pyrimidal tract or cerebellar lesions
121
Q

What features are predictive of severe NBPP?

A

incomplete recovery by 1 month of age (ie. active elbow extension/flexion remain absent) as assessed by an HCP with expertise in MSK/neuro exams

**incomplete recovery at 1 month suggests nerve injury beyond neuropraxia and assessment by a specialist team is needed.

often, primary care providers can overestimate recovery -→ not enough referrals

122
Q

what feature of NBPP necessitates referral to a brachial plexus multi-D team? What should you include in the referral?

A

incomplete recovery of any upper extremity movement at 1 mo

referral should include info on risk factors, severity of injury and course of recovery

123
Q

who should be a part of a multi-D team for NBPP?

A
  • PT or OT
  • peds surgery (plastics, ortho or equivalent)
124
Q

Can infants have non-operative therapy for NBPP in their community (ie. not at a tertiary centre)?

A

Yes!

but there should be a continuous dialogue btn the multi-D team at the tertiary center, community health care provides and non-operative therapists to identify issues of growth, development and specialized assessments

125
Q

What is the “critical window” for acute brain injury in prems?

A

the first 72 hours post-birth = highest risk period for acute preterm brain injury

**95% of IVH or parenchymal lesion cases are detected by day 5

126
Q

When the CPS talks about neuroprotective measures for prems, what EGA are they referring to?

A

32+6 and below

this is a pain in the neck, because the paper they have on imaging prem heads states that you need routine head imaging if under 31+6

127
Q

describe the relationship btn chorioamnionitis and preterm premature rupture of membranes (PPROM) and neuro outcomes

A
  • chorioamnionitis is a primary risk factor for prem labour/delivery (incidence increases with decreasing age)
  • ? risk factor for IVH/PVL/CP
128
Q

What is the SOGC suggested antimicrobial approach to any mother presenting with PPROM and expected to deliver at 32+6 or earlier?

A

penicillin and macrolide (or just macrolide if penicillin allergic)

***also provides GBS coverage

This is thought to prolong pregnancy and reduce morbidity for both mother and newborn

129
Q

Which neonates born at/under 32+6 weeks GA need to be started on empiric antibiotics?

A

any neonate (at or under 32+6) born to a mother with suspected or confirmed chorioamnionitis, PPROM, preterm labour or an unexplained onset of nonreassuring fetal status

***this is regardless of their initial clinical status as they can be asymptomatic initially (treat for 36-48 hours pending cultures)

also need to be evaluated and have blood cultures drawn

130
Q

Does prolonged ROM affect the neonatal brain?

A

if ruptured for >72 hours, there is an increased risk of IVH/intraparenchymal hemorrhage in prems

131
Q

At which gestation do we offer mothers at risk of delivery antenatal corticosteroids?

A

mothers at 34+6 weeks with a risk of delivery in the next 7 days should get antenatal corticosteroids (or at least be offered)

132
Q

When do we consider intrapartum MgSO4?

A

Mothers at risk for imminent delivery (within 24 hours) of an infant at or less than 33+6 weeks GA

133
Q

at what gestational age do we recommend AGAINST umbilical cord milking? Why?

A

Not recommended if very prem (ie. less than 32 weeks) due to an increased risk for SEVERE IVH

Just do delayed cord clamping instead!

134
Q

Describe thermoregulation techniques in prems.

What age do we use this?

A

All infants less than 32 weeks EGA

To prevent hypothermia:

  • polyethylene bag/wrapping,
  • a thermal mattress
  • a preheated radiant warmer with servo-control
  • a hat
  • other precautions:
    • keep the temp of the delivery room at 25-26 degrees C
135
Q

When do you consider starting inotropes in prems (for hypotension)?

A

Avoid inotropes to treat hypotension unless a combo of other clinical signs are present such as:

  • elevated lactate
  • prolonged cap refill
  • decreased u/o
  • low cardiac output

Avoid iatrogenic causes of hypotension

136
Q

Name 2 iatrogenic causes of hypotension in prems

A
  1. lung hyperinflation
  2. dehydration

so, before starting inotropes, consider a CXR and a slowly infused bolus

137
Q

who are the targets for PROPHYLACTIC indomethacin?

A

high-risk, extreme prems. And the decision to treat should be based on combined risk factors (GA, exposure to antenatal steroids, birth site)

138
Q

What is the target pCO2 range for neuroprotection in prems?

What value is concerning for causing PVL?

What value is concerning for causing IVH?

A

Goal pCO2: 45-55 mmHg (Max of 60 mmHg)

Risk of PVL: pCO2 <35 mmHg

Risk of IVH: pCO2 >60 mmHg

139
Q

What ventilation approach should be used for all prems in the first 72 hours postdelivery?

A

Volume-Targeted Ventilation

140
Q

Describe neuroprotective positioning for a prem? How long should this be the case?

A

in the first 72 hours post delivery, a prem’s head should be in a NEUTRAL, MIDLINE POSITION, HEAD OF BED AT 30 DEGREES

141
Q

What is the optimal interval of antenatal corticosteroid administration prior to delivery?

A

Over 48 hours

142
Q

how do antenatal corticosteroids help in prem neuroprotection?

A

vasoconstriction in the fetal brain (and in animal models, they accelerate organ system maturity)

143
Q

What is the best route (ie. vaginal vs. c/s) of delivery for prems at risk for mortality or IVH?

A

there is no evidence that one is better than the other, EXCEPT when they are breech

144
Q

For women in preterm labour, is it better to do expectant management or immediate delivery? (with respect to neuro outcomes)

A

no difference in neonatal brain injury

145
Q

What are the guidelines for umbilical cord management?

A

All infants who do not need immediate resus should receive delayed cord clamping of 60-120 seconds

DCC is preferred over umbilical cord milking because the studies assessing milking are few

146
Q

What is the relationship btn delayed cord clamping and neuro outcomes?

A

Delayed cord clamping (or cord milking) reduces overall risk for acute brain injury and appears to protect against motor disabilities later in life

147
Q

What is considered to be hypotension in a prem?

A

No consistent definition exists, but often accepted are:

  1. MAP
  2. <30 mmHg

***for 2 consecutive measurements

Royal College Prep (4 decks)

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