Acute Care CPS Flashcards

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1
Q

3 ways to diagnose anaphylaxis

A
  1. Acute illness with involvement of skin and/or mucosal tissue (hives, pruitis, flushing, swollen tongue/uvula) and ONE OF resp compromise or reduced BP/end organ dysfunction (hypotonia, syncope, incontinence)
  2. 2+ of involvement of skin/mucosa, resp compromise, reduced BP/end organ dysfunction, persistent GI symptoms that occurs after exposure to LIKELY allergen
  3. Reduced BP after exposure to known allergen
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2
Q

What weights should use
1. EpiPen Jr
2. EpiPen

A
  1. 10 to 25 kg
  2. > 25 kg
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3
Q

How does epi work in anaphylaxis

A

Alpha effects: increase PVR, reverses vasodilation, decreases angioedema and urticaria
Beta effects: B1 chronotropy and ionotropy on the heart, B2 bronchodilation and reduction of inflammatory mediators

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4
Q

What epi formulation is used in anaphylaxis? And what is the dose?

A

1:1000
Dose is 0.01 mg/kg with max of 0.5 mg

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5
Q

Why are H1 and H2 antagonists used in anaphylaxis?

A

H1 can releive the cutaneous symptoms of anaphylaxis
H2 helps with cutaneous in combination with H1

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6
Q

Meds that can be used in anaphylaxis

A

Epi (first line)
H1 and H2 antihistamines
Corticosteroids
Inhaled medications (salbutamol, inhaled epi)

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7
Q

When do we use
1. IV epi
2. Glucagon
in anaphylaxis?

A
  1. Persistent hypotension
  2. For patients who regularly take beta blockers
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8
Q

When do biphasic reactions occur in anaphylaxis?

A

1 to 72 hours

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9
Q

Which patients are more likely to have biphasic anaphylactic reactions?

A

Delayed administration of epi
More than one dose of epi required
More severe symptoms on presentation

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10
Q

How long do you need to observe someone post anaphylaxis

A

4 to 6 hours (most biphasic reactions occur in this time)

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11
Q

Who should be admitted to hospital for observation post anaphylaxis?

A

Repeated doses of epi
More severe symptoms
Biphasic reaction
Consider high risk features too: peanut allergy, asthma, beta blocker use

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12
Q

Shock dosing for VF

A

Initial dose is 2-4 J/kg

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13
Q

Post ROSC care goals for
1. Oxygenation
2. BP
3. Temp
4. Seizures

A
  1. Oxygen therapy 94-99% (avoid hyperoxemia)
  2. Fluids/inotropes to keep SBP > 5th % for age
  3. 5 days of normothermia OR 32-34 for 2 days, then 3 days of 36 to 37.5 deg
  4. Prophylactic meds not needed routinely, but treat clinical seizures. EEG in the first 7 days
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14
Q

Why can you use adenosine in a wide complex tachycarida?

A

Can distinguish between ventricular or supraventricular rhythms
BUT, avoid in WPW

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15
Q

Sizing ETTs for children
1. < 1 year old
2. 1-2 years old
3. > 2 years old

A
  1. 3 mm cuffed
  2. 3.5 mm cuffed
  3. 3.5+ age/4

Add 0.5 for uncuffed tubes

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16
Q

When/how does CCHD screening occur?

A

Between 24 and 36 hours after birth
Using right hand and either foot

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17
Q

Cardiac lesions that are USUALLY CYANOTIC and are detectable using pulse ox screening (7)

A

Hypoplastic left heart syndrome
Pulmonary atresia with intact ventricular septum
Total anomalous pulmonary venous return
Tetralogy of Fallot
Transposition of the great arteries
Tricuspid atresia
Truncus arteriosus

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18
Q

Cardiac lesions that MAY BE CYANOTIC and are detectable using pulse ox screening (5)

A

Coarctation of the aorta
Double outlet right ventricle
Ebstein’s anomaly
Interrupted aortic arch
Defects with single ventricle physiology

19
Q

What is a
1. Abnormal
2. Borderline
result when using pulse ox screening for CCHD

A
  1. < 90% in right hand or foot
  2. 90-94% in right hand and foot OR > 3% difference

3 borderline readings 1 hour apart = fail

20
Q

Triad of lab findings in DKA

A

Hyperglycemia (> 11)
Serum ketosis (beta-hydroxybutyrate 3 or more) and/or ketonuria (moderate or large)
Acidosis (pH <7.3 or bicarb < 18) with AG > 12

21
Q

Risk factors for DKA (13)

A

Younger age
Lower SES
Delayed diagnosis in new patients
Previous DKA
Poor glycemic control
Unrecognized insulin pump malfunction
Infection
Certain meds (atypical antipsychotics, steroids, etc)
Ethnicity
Limited access to care
Co-existing mental health or social and family issues
Peripubertal stage
Adolescence

22
Q

DKA severity definitions

A

Mild: pH 7.2-7.29, bicarb 10- <18
Moderate: 7.1 to 7.19, bicarb 5 to 9
Severe: pH < 7.1, bicarb < 5

23
Q

Risk factors for cerebral edema in DKA (10)

A

New onset diabetes
Longer duration of symptoms
Age < 5
Severe acidosis
Lab evidence of severe dehydration (elevated urea, hematocrit)
Hypocapnia (CO2 < 21)
Insulin therapy in first hour and/or insulin bolus
Rapid administration of hypotonic fluids
Use of sodium bicarb
Failure of sodium to rise

24
Q

Goal rate to decrease glucose in DKA

A

No more than 5 an hour to 15-17

25
Q

When do you start insulin for DKA patients?

A

After the first hour of fluid therapy AND when K is > 3.3

26
Q

When (and how much) K should be added to IV fluids in DKA?

A

K of 40
When measured K is <5.5 and after recent urine output

27
Q

When do we replace phosphate in DKA

A

Measured levels < 0.5 OR concerns of cardiac dysfunction, resp failure, GI dysmotility, or metabolic encephalopathy

28
Q

Treatment of cerebral edema from DKA

A

Minimize patient movement and agitation
HOB to 30 deg
Head in midline position
Isotonic fluids (change if using 0.45%)
Reduce rate of IV to 75% of calculated hourly rate
3% saline or mannitol
PCCU consultation

29
Q

What age range is most common in ITP? And how long does it usually take to resolve?

A

2-5 years
Resolution within 6 months

30
Q

Recommended treatment options for ITP with
1. No active bleeding
2. Moderate bleeding
3. Severe bleeding

A
  1. Observation first line, oral steroids or IVIG second line
  2. Active therapy with single dose IVIG or short course corticosteroids
  3. IV steroids and IVIG, may need TXA but discuss with hematology, PLT transfusion only if acute life threatening bleeds or needing immediate surgery
31
Q

When do children with ITP typically relapse?

A

One third of children will relapse within 2 to 6 weeks

32
Q

Definition of
1. No/mild
2. Moderae
3. Severe
bleeding in ITP

A
  1. None or at most bruising, petechiae, or mild epistaxis, no interference with daily living, may have some mild oozing of petechiae
  2. More severe skin manifestations, some mucosal lesions, more troublesome epistaxis or menorrhagia
  3. Bleeding episodes (epistaxis, melena, menorrhagia, or ICH) needing hospitalization
33
Q

2 options for length of treatment of steroids in ITP

A

4 mg/kg/day (BID to QID) for 4 days with no taper
2 mg/kg/day orally for 1-2 weeks, with taper
No evidence to support one over other

34
Q

Which treatment for ITP should be used if rapid increase is required?

A

IVIG
Increase in platelets within 24 hours, peak response at 2 to 7 days
Steroids have increase within 48 hours

35
Q

2 definitions of convulsive status epilepticus

A

Continuous GTC activity with loss of consciousness for longer than 30 mins
2 or more discrete seizures without return to baseline mental status

36
Q

Definition of early/impeding status epilepticus

A

Continuous or intermittent seizures lasting longer than 5 mins without full recovery of consciousness between seizures

37
Q

For children seizing because of toxic ingestions or drug withdrawals (specifically theophylline and TCA ingestions) which second line med should you NOT give? What should you give instead?

A

NOT phenytoin or fosphenytoin
Phenobarbital is better choice

38
Q

Best seizure med to treat status in children <6 mo, prolonged febrile seizures, and seizures caused by toxic ingestions/drug withdrawals?

A

Phenobarbital

39
Q

When should you avoid giving valproate?

A

In children with known or suspected mitochondrial disease
Including children <2 years with unexplained dev delay

40
Q

When is pyridoxine (B6) helpful in status?

A

Children <18 mo with seizures that may be caused by an undiagnosed metabolic disorder

41
Q

Most common cause of convulsive status epilepticus

A

Prolonged febrile seizure

42
Q

When should you consider non-convulsive status?

A

LOC not improving as expected after the convulsions have stopped
Neuromuscular paralysis being used

43
Q
A