Acute Care Flashcards

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1
Q

Name some types of cholinergics

A

Organophosphates (pesticides such as sarin “nerve” gas, dursban in RaidTM and malathion)

Carbamates (neostigmine, pyridostigmine, pesticides
such as aldicarb)

Alzheimer’s drugs (DonepezilTM)

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2
Q

Name some symptoms of cholinergic exposure

A
Diaphoresis
Urination
Miosis
Bronchorrhea / Bradycardia 
Emesis
Lacrimation 
Lethargy 
Salivation

Secretions everywhere

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3
Q

Treatment for cholinergic syndrome

A

100% oxygen
Early endotracheal intubation (avoid succinylcholine!)

PPE, remove clothing and vigorously irrigate skin

Atropine 0.05 mg/kg IV/IM/IO bolus Q5min until
secretions and wheezing stops

Inhaled iptratropium (AtroventTM)

Pralidoxime (2-PAM) 25 mg/kg IV with atropine

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4
Q

Examples of Anticholinergic Drugs

A

TCAs (weakly anticholinergic)
Antihistamines (diphenhydramine, hydroxyzine) Benztropine (CogentinTM)
Atropine and cyclopentolate (mydriatic eyedrop) Diphenoxylate-atropine (LomotilTM)
Many neuroleptics (chlorpromazine, olanzapine)

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5
Q

Signs and Symptoms of anticholinergic syndrome

A

tachycardia first symptom
absent bowel sounds

Dry as a Bone (dry mouth, urinary retention)
Hot as a desert (hyperthermia)
Blind as a bat (mydriasis-dilated pupils)
Red as a beet (flushed skin)
Mad as a hatter (confused)

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6
Q

Management of anticholinergic overdose

A

Sodium bicarbonate if prolonged QRS (TCAs)

Lorazepam for agitation

Water spray and cooling fans for hyperthermia

Consider activated charcoal 1 g/kg (max 50 g) PO

Consider physostigmine if both peripheral and
central toxicity (delirium) is present
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7
Q

What are examples of sympathomimetic drugs

A

Cocaine
Amphetamine / Methamphetamine
MDMA (ecstasy)
Ephedrine

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8
Q

What are the symptoms pf sympathomimetic drug exposure

A
Mydriasis 
Diaphoresis (MAIN DIFFERENCE FROM ANTICHOLINERGICS)
Hypertension 
Tachycardia 
Seizures 
Hyperthermia
Psychosis 
Severe agitation
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9
Q

Ecstasy specific Symptoms

A
HTN (HTN emergencies, ICH)
Hyperthermia (rhabdo, DIC) 
Hyponatremia (seizures) 
Serotonin syndrome
Cardiac ischemia 
Hepatotoxicity
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10
Q

Ecstasy Management

A

HTN: lorazepam 1 mg IV or phentolamine (you don’t give anti-hypertensives)

Hyponatremia (Fluids restriction or 3% NS)

Activated charcoal if within 1 hour

Agitation: lorazepam 1 mg IV

Hyperthermia: cool water mist and fans

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11
Q

LSD Specific Symptoms

A

Rapid oral absorption with symptoms appearing at 30-60 min and lasting up to 12 hours

One of the most potent HALLUCINOGENS
Mydriasis
HTN
↑RR
↑HR
diaphoresis
hyperreflexia 

Massive overdose results in hyperthermia, autonomic dysregulation, vomiting, respiratory arrest, ICH

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12
Q

PCP specific symptoms

A

seizures and delirium
Fluctuating behavior with delirium, paranoia, agitation Nystagmus while awake
Dystonic posturing, muscle rigidity, myoclonus

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13
Q

Serotonin syndrome Symptoms

A

Serotonin Syndrome

< 12 hours

Increased: BP,RR,HR,T

Pupils: Enlarged

Mucosa: Sialorrhea

Skin: Diaphoresis

Neurologic: Increased Reflexes (LE), increased Tone

Mental Status: Agitation

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14
Q

NMS Symptoms

A

Time course: 3-4 days
< 12 hours

Increased BP,RR,HR,T

Pupils: Normal

Mucosa: Sialorrhea

Skin: Diaphoresis

Neurologic: Rigid

Mental Status: Stupor

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15
Q

Opioid Toxidrome Symptoms

A
Bradycardia 
Hypotension 
Respiratory depression 
Miosis
Coma
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16
Q

Treatment of Opioids

A

Naloxone (IV or IN)
Should see an effect in seconds
Ensure patent airway and adequate ventilation

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17
Q

What drug ingestion causes these symptoms?
Promoted online as a treatment for opioid withdrawal (?)
Produces euphoria in overdose
Prolongs QT and QRS intervals
Respiratory depression
Highly toxic to young child in overdose
Not detected in urine drug screen

A

Loperamide (Kratom)…Immodium

anticholinergic
but also binds to opioid mu receptors
very toxic to young children
in therapeutic doses does not cross BBB - overdose will cross and hit mu receptors

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18
Q

When should you NOT use charcoal?

A

Avoid in severe caustic ingestion
Compromised airway reflexes
>1hr from ingestion

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19
Q

What ingestions is charcoal not effective for?

A
Potassium 
Hydrocarbons 
Alcohols
Iron
Lithium 
Solvents
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20
Q

Treatment for lidocaine overdose?

A

Lorazepam and 20% intralipid

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21
Q

What can you use IV lipid for?

A

For life-threatening overdoses of local anesthetics (iatrogenic), bupropion, amitriptyline

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22
Q

Antidote for Iron?

A

Deferoxamine

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23
Q

Antidote for carbon monoxide?

A

oxygen

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24
Q

Antidote for pesticide?

A

atropine

cholinergic

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25
Q

Antidote for Nifedipine?

A

Glucagon

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26
Q

Antidote for Amitripytline?

A

Sodium Bicarb…for QRS >100

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27
Q

Antidote for methanol?

A

Fomepizole

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28
Q

Antidote for glyburide?

A

Glucose

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29
Q

What are some examples of Hydrocarbons?

A

Gasoline, nail polish remover, lighter fluid common

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30
Q

Main complication of hydrocarbon ingestion?

A

Aspiration is common and pulmonary toxicity accounts for most fatalities

Changes seen 2-8 hours post
Deterioration in 24-48 hours
Perihilar infiltrates
Pneumatoceles

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31
Q

Treatment of Hydrocarbon Ingestion?

A

Stat CXR and repeat in 4-6 hours post-ingestion…
If both look good you can send them home
Oxygen
+/- bronchodilators
Can d/c at 4-6 hours if asymptomatic and normal CXR
Supportive Care

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32
Q

Metformin ingestion can cause what complication?

A

Lactic Acidosis

Usually normal Glucose

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33
Q

List 4 drugs that cause hypoglycemia

A

Glyburide
Beta blockers
Ethanol
Salicylates

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34
Q

Acetaminophen toxic ingestion occurs at what dose?

A

Toxic metabolite is NAPQI

Toxic dose is 150 mg/kg (7.5 grams in adult)

Hepatoxicity reported in children given > 90 mg/ kg/day for more than 1 day

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35
Q

What complications can occur secondary to Tylenol ingestion?

A

Anion gap metabolic acidosis
Acute tubular necrosis
Fulminant liver failure

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36
Q

What are the stages of Tylenol ingestion?

A
Stage I (0-24 hrs): Asymptomatic or nausea/ vomiting
Stage II (24-72 hrs): Right upper quadrant pain and onset of hepatocellular injury
Stage III (72-96 hrs): Maximal hepatoxicity; Most deaths occur during this phase
Stage IV (> 4 days): Recovery
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37
Q

Treatment of Acetaminophen Ingestion

A

Activated charcoal within 1 hour
NAC dosing based on Rumack-Matthew nomogram (nomogram only works for up to 8h)
Best outcomes if NAC started within 8 hours
Follow transaminases, INR/PTT, RFTs, lipase

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38
Q

What are examples of salicylates?

A
ASA
Bismuth salicylate (antidiarrhoeal agent)
Methyl salicylate (Rub A535TM)
Salicylic acid (wart removal)
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39
Q

What are the symptoms of salicylates overdose?

A

Hyperpnea / tachypnea….respiratory alkalosis
AG metabolic acidosis…pulmonary/cerebral edema Nausea, vomiting, gastrointestinal bleed
Tinnitus (early) or hearing loss
Hyperglycemia…hypoglycemia
Diaphoresis

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40
Q

Management of salicylate overdose

A

Charcoal up to 6 hours (bezoar formation)

Glucose to all patients with altered mental status regardless of peripheral glucose

Treat hypokalemia: because it can impair alkalinization

Alkalinize serum to urine pH between 7.5 - 7.6 to “trap”
salicylate anions in blood and renal tubule

Hemodialysis - indicated for CNS symptoms

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41
Q

Investigations for Iron Ingestion

A

Toxic quantity calculated as elemental iron
Ferinsol bottle and “gummy bears” not toxic
Serum iron within 4-6 hours of ingestion
Abdominal x-ray suggestive
If no opacities are seen, patient is unlikely to benefit from gastric decontamination

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42
Q

Examples of radiopaque drugs

A
Chloral hydrate
Opioid packets (latex)
Iron and other heavy metals
Neuroleptics (early)
Sustained-release tablets / Salicylates (early)
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43
Q

Stages of Iron Toxicity

A
Stage I (30 min-6 hrs): Nausea, vomiting, diarrhea
Stage II (6-12 hrs):“Quiescent” phase
Stage III (12-24 hrs): Metabolic acidosis: Shock, GI haemorrhage, coagulopathy, respiratory failure
Stage IV (2-3 days): ARDS, liver failure
Stage V (3-4 wks): GI strictures at gastric outlet
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44
Q

Clues to iron ingestion

A

GI symptoms
Acidosis
Multiorgan failure

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45
Q

Iron Management

A

No role for either charcoal or gastric lavage

Fluid resuscitation essential

WBI if tablets seen on AXR or if < 6 hours from ingestion (textbook answer only!)

IV deferoxamine (DFO) is the antidote of choice
  and must be given early

Dose is 15 mg/kg/hr until urine color clears

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46
Q

Isopropyl Alcohol Ingestion Symptoms

A

The most common toxic alcohol ingested

Hallmark is ketosis without acidosis

As little as 2 cc can lead to symptoms

Mainly causes inebriation that peaks in 1-2 hours

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47
Q

Management of Isopropyl Alcohol ingestion

A

Rule out co-ingestion with ethanol, methanol or ethylene glycol ingestion
No role for activated charcoal
No role for ADH inhibition with fomepizole or ethanol
Discharge after 2 hours if asymptomatic

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48
Q

List some things methanol is found in

A

windshield wash, bingo dabbers

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49
Q

Signs and Symptoms from methanol ingestion

A

Less inebriating than ethanol
Toxicity associated with as little as one teaspoon!
Formate causes retinal injury (blurring, central scotoma, blindness)
Normal methanol level doesn’t rule out ingestion Profound AG acidosis presents late (> 24 hrs)

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50
Q

What is ethylene glycol found in?

A

antifreeze, paints, brake fluid

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51
Q

What is the management of ethylene glycol ingestion

A
Colorless, odorless, sweet taste
Inebriation with no odor of ethanol
Metabolic acidosis:cardiac decompensation
Hypocalcemia: prolonged QTc 
Oxalate crystals appear late
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52
Q

Clues to Toxic Alcohol Exposure

A

Inebriation
Odor
Osmolal gap or Acidosis

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53
Q

Treatment of Toxic Alcohol Ingestion

A

Wash skin if exposed
Fomepizole or ethanol based on ingestion history, OG, serum level
Hemodialysis if high AG acidosis or end-organ damage
Cofactor therapy with folic acid or leucovorin
Thiamine 100 mg and pyridoxine 50 mg

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54
Q

Symptoms of TCA ingestion

A

Inhibit norepinephrine 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 receptors- seizure

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55
Q

What is the management of TCA ingestion

A

Activated charcoal
Frequently require intubation because obtunded

NaHCO3 for QRS > 100 because of significant morbidity and mortality

Norepinephrine infusion if hypotensive

Physostigmine contraindicated

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56
Q

Symptoms of Carbon Monoxide Poisoning

A

Initially headache, dizziness, nausea, confusion, seizure, syncope, coma but don’t correlate with COHb level

Dysrhythmia and cardiac arrest in < 30%

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57
Q

Diagnosis of Carbon Monoxide Poisoning

A

Standard pulse oximetry and arterial pO2 normal

COHb < 5% (non-smokers) and < 10% (smokers)

Carboxyhemoglobin (COHb) level > 3% consistent with toxic inhalation

Check cyanide level

Follow ECG and cardiac enzymes

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58
Q

Management of CO exposure

A

Remove from source and rule out smoke inhalation
Treat if COHb > 10% if 100% FiO2

Hyperbaric oxygen (best if < 6 hrs of exposure) if:
- COHb > 25% (> 15% in pregnant female or child)
- Neurologic Symptoms (loss of consciousness,
seizure, cardiac ischemia, cerebellar deficits)

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59
Q

When should you THINK of cyanide poisoning?

A

House fire
CO poisoning
Persistent lactic acidosis with CO poisoning

Cerebral edema, seizures, coma
House fire (wool, plastics), stone fruit pits, cassava root, nitroprusside infusion
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60
Q

Management of Cyanide poisoning

A

Antidote is hydroxycobalamin kit

Indicated if increased lactate or decreased BP

Transiently reddening of skin and urine (chromaturia)

Adequate oxygenation necessary often with mechanical ventilation

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61
Q

Examples of CCB

A

Dihydropyridines: amlodipine, nifedipine

Non-dihydropyridines: verapamil, diltiazem (high glucose)

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62
Q

Signs and Symptoms of CCB ingestion

A

Ingestion of at least 5x normal dose can develop severe intoxication

Hypotension and bradycardia can be profound and refractory

May maintain pristine mental status despite hypotension

Precipitous deterioration is common so early aggressive therapy is needed

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63
Q

Management of CCB ingestion

A

Atropine (0.02 mg/kg) 0.5-1.0 mg IV Q2-3 minutes

Calcium gluconate bolus or infusion

Glucagon 5 mg IV but causes severe N/V

Norepinephrine is initial vasopressor of choice

High dose insulin euglycemic therapy (has positive inotropic effects)

Insulin 1 unit/kg bolus —> 1-10 units/kg/hr + K Must add 2.5 mL/kg of IV D10W

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64
Q

Laundry Detergent Capsules Symptoms

A

Vomiting, drooling, respiratory distress
Airway compromise and esophageal perforation
Skin burns

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65
Q

Management of ingestion of laundry detergent capsules

A

supportive

ave them drink a glass of water

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66
Q

Symptoms of nicotine overdose

A

Onset of vomiting, diaphoresis, confusion within 2 hrs Seizures, initial ↑BP, ↑RR, ↑HR ⇒ ↓BP, ↓RR, ↓HR

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67
Q

Who is most at risk for a submersion injury

A

Males > Females
Children < 5 years at greatest risk
Usually during the summer months
Associated with hypothermia and trauma

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68
Q

Most common cause of death in children aged 1-4

A

Trauma

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69
Q

Most effective strategies for preventing submersion injuries.

A

Most effective prevention strategy is a four-sided self-closing fence with a self-locking gate
Toddlers should always be within arm’s length of an adult, even in a bathtub
1 adult per baby and 1 adult per 2 young children
Swimming programs for children < 4 years do not
decrease rates of drowning

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70
Q

Who should wear a PFD?

A

Should be worn by all infants at least 9 kg
Babies who cannot sit unsupported are too young to wear PFDs
Water wings, inflatable undies, pool noodles are not safety devices

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71
Q

Risk Factors for Submersion injury

A

Leaving children unattended

Alcohol or drug abuse (50% of adult drownings) Limited swimming ability

Underlying medical conditions(?):
- Seizure disorder, toxin, prolonged QT, syncope

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72
Q

Factors for good prognosis after submersion injury

A

Immediate bystander CPR is most important factor influencing survival
What are other good prognostic indicators?
- Return of spontaneous circulation in < 10 min
- Submersion < 5 min
- Pupils equal and reactive at scene
- Normal sinus rhythm at scene

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73
Q

What are poor prognostic factors for submersion injury

A

What are poor prognostic indicators?

  • Delayed CPR
  • Return of spontaneous circulation > 25 min
  • Submersion > 10 min
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74
Q

What are complications of submersion injury?

A
ARDS
Pulmonary edema
Pneumonia
Cerebral edema leading to increased ICP 
Trauma
Hypothermia
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75
Q

Definition of Hypothermia

A

Defined as core temp < 35 C

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76
Q

Metabolic disturbances from hypothermia

A

Shivering stops at core temp < 32 C

Accompanied by hypoglycemia, hypocalcemia, hypokalemia, metabolic acidosis

Associated with pancreatitis

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77
Q

Features of hypothermia at 31-32 C

A
  • Normal ECG, ↑ HR, ↑ BP, loss of shivering
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78
Q

Features of hypothermia at 28-31 C

A
  • ↓ HR, ↓ BP, flipped T, atrial fibrillation, sluggish, dilated pupils
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79
Q

Features of Hypothermia at <28C

A
  • absent pulse and BP, VF, coma, fixed dilated pupils
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80
Q

EKG findings in hypothermia

A

Marked sinus bradycardia
First degree AV block
Osborn or J waves Associated with prolonged QT and bradycardia
Seen in core T < 32 C

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81
Q

Special CPR Considerations with hypothermia

A

Avoid CPR in T < 28 and good pulse
If pulseless → CPR
If VF → defibrillation x 3 but no more until T > 30
Drugs rarely effective until T > 30
Can trigger dysrhythmia if T < 30 just by bumping bed!

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82
Q

Rewarming for 34-36 degrees

A

Passive rewarming:
Remove wet clothes
Dry

83
Q

Rewarming 30-34C

A

Passive AND active external warming of truncal areas only
electric blanket

use Bair Hugger
overhead warmer
hot water bottles heating pads

84
Q

Rewarming < 30C

A

Active external and internal rewarming

Warm humidified oxygen at 42-46 C
warming tubes
Warmed IV or intraosseous (IO) fluid (without K+) at 43 C

Peritoneal lavage, ECMO, esophageal

85
Q

CPR at T >30

A

T > 30
Continue CPR
IV meds as needed
Defibrillation as needed

86
Q

CPR at T <30

A

T < 30
Continue CPR but no IV meds
Limit defibrillation to 3 shocks

87
Q

Treatment of Frostbite

A

En route avoid warming if significant time to ER

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

88
Q

What is Heat Exhaustion

A

Excessive peripheral vasodilation then
Inability to deliver sufficient blood volume then
Muscle fatigue

Profuse sweating
Excessive water and/or sodium losses

89
Q

What are heat cramps

A

Exercise-associated muscle cramps
Intense painful muscle contractions
Due to excess water and electrolyte losses

Highly conditioned athlete post-exercise

Painful muscles
Labs
↓ Na,↓ Cl

people who don’t hydrate properly with water and salt

90
Q

What is heat stroke?

A
Core T > 40 with CNS symptoms
Headache
Disorientation
Dizziness
Weakness
Gait disturbance

**think tourists at a resort who don’t drink enough water

Heat Wave
Infants left in vehicles

T > 40
Hot skin, CV collapse, rhabdo, ARF, severe CNS
dysfunction

Normal/↑ NaCl ↑ CK
↓ Ca

91
Q

Heat exhaustion, water depletion

A

Unacclimatized in hot climate with inadequate water intake (tourists)

T < 40 Lethargy, N/V, headache,

↓ BP, ↑ HR
↑ Na,↑ Cl

92
Q

Heat Exhaustion, NaCl depletion

A

Unacclimatized in hot climate with inadequate salt intake (CF)

T > 38 Above with severe muscle cramps

↓ Na

93
Q

Management of Heat Stroke

A

Remove clothing

Active cooling: ice packs in groin, axillae, neck, cooling fans over body sprayed with tap water at 15 C

Stop cooling when T < 38.5

Coma may persist for > 24 hours after normothermia
Fluid AND salt replacement orally

94
Q

Complications of Heat Stroke

A
Hyponatremia
Seizure
Rhabdomyolysis
DIC
Multi-system organ failure
95
Q

What is a superficial burn

A

Superficial

Epidermis only

Redness, pain, no blisters Heals in 3-5 days

96
Q

What is a Superficial partial thickness burn

A

Epidermis + 1/2 Dermis
Red/pink, pain, moist, blisters
Heals in 2 weeks

97
Q

What is deep partial thickness burn

A

Epidermis + > 1/2 Dermis
Pale, dry, less tender, speckled appearance
Grafting often needed

98
Q

What is full thickness burn

A

Subcutaneous tissue
Pale, charred, leathery appearance, non-tender
Most require grafting

99
Q

Management of burns

A
Cover with sterile bandages
Early cooling ( < 30 min) prevents further injury 
Tetanus (dirty wound)
Analgesia
Remove smoldering clothing
Measure carboxy-hemoglobin
100
Q

What are the indications for early intubation with burns

A

Need to know this!

  • Carbonaceous sputum
  • Singed nasal hairs
  • Soot in airway
  • Hoarseness
101
Q

What is the parkland formula

A

Age > 5: Parkland formula = 4 cc/kg/BSA over 24

hours (1st half in 8 hours, 2nd half in 16 hours)

102
Q

BSA calculation for children

A

Age > 9: Rule of 9’s

Age < 9: Child’s palm = 1% BSA (not superficial)

103
Q

What types of infections do you see with burns

A

No role for prophylactic broad spectrum antibiotics

Early infection: Staph aureus, GAS
Late infection: Pseudomonas, Bacteroides
Daily dressing change with topical antibiotic BID until re-epithelialization

104
Q

Who do you need to admit with burns?

A
Suspected non-accidental injury
> 10% BSA partial thickness
> 2 % BSA full thickness
> 1% BSA of hands/feet/face/perineum
Circumferential burn
Enclosed space fire or evidence of inhalation injury
Electrical injury with high tension wire (rhabdomyolysis)
Associated trauma
  • Admission criteria (Per Nelson’s)
  • > 15% BSA
  • Full thickness (“3rd degree”)
  • Electrical burns caused by high-tension wires/lightening
  • Chemical burns
  • Inhalation injury
  • Social concerns
  • Suspected abuse
  • Burns to hands/feet/face/perineum/genitals/major joints • Complex underlying medical conditions
  • Underlying fractures
  • Pregnancy
105
Q

High tension wire injury complications

A

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

CLUES: Entrance/exit wounds
Rhabdomyolysis
VF/arrest

106
Q

Lighting side effects

A
Cerebral edema (delayed), ICH, seizure 
Rhabdomyolysis
Asystole and respiratory failure
Monitor for delayed cerebral edema and arrhythmia
107
Q

Most common cause of paediatric cardiac arrest

A

respiratory failure

108
Q

CPR one rescuer compression:breath ratio

A

30:2

109
Q

CPR two rescuer compression:breath ratio

A

15:2

110
Q

CPR compression breath ratio once patient is intubated

A

Asynchronous 100:10

Breaths and compressions happening independently of each other

111
Q

Describe good quality compressions

A

Compressions:
Lower sternum at nipple line
On a firm surface
1/3 anterior diameter of the chest (4cm infant; 5cm child) 100-120 times per minute, allowing for full chest recoil

112
Q

Treatment for poor perfused bradycardia

A

(must have hypotension, altered mental status, signs of shock)

Epinepherine 0.01mg/kg of the 0.1mg/mL solution
Repeat every 3-5 minutes
Pacing if needed

113
Q

How do you manage PEA

A

NO SHOCKING
CPR
Epinephrine 0.01mg/kg of the 0.1mg/mL solution
Give every 3-5 minutes

114
Q

Stable SVT management

A

Vagal maneuvers
Adenosine 0.1mg/kg (max 6mg)
Second dose 0.2mg/kg (max 12mg)

Need expert consultation for amiodarone and procainamide

115
Q

Unstable SVT management

A

Synchronized cardio version 0.5-1 J/kg
If ineffective then do 2J/kg

Can used adenosine 0.1mg/kg (max 6mg)
Second dose 0.2mg/kg (max 12mg)
ADENOSINE SHOULD NOT DELAY CARDIOVERSION

116
Q

Vtach with a pulse treatment

A

Adenosine 0.1mg/kg (max 6mg)
Second dose 0.2mg/kg (max 12mg)

Need expert consultation for amiodarone and procainamide

Synchronized cardio version 0.5-1 J/kg
If ineffective then do 2J/kg

117
Q

Pulseless Vtach/Vfib treatment

A
shock
shock
epi (0.01 mg/kg of the 0.1mg/mL solution
shock
Amiodarone/lidocaine
repeat

Shock 2, 4, 6, 8, 10J/kg

118
Q

What are the H’s and T’s

A
Hypovolemia
Hypoxia
Hydrogen Ions
Hypoglycemia
Hypothermia
Hypo/Hyperkalemia
Tension Pneumo
Tamponade (cardiac)
Toxins
Thrombosis, pulmonary
Thrombosis, coronary
119
Q

Are compressions only ok for children?

A

noooooo
compression only CPR isn’t appropriate for children
etiology in kids is mostly resp failure! so doesn’t make sense to just do compressions

120
Q

When using an AED, whence you stop using the paediatric dose attenuator?

A

Use pediatric dose attenuator up to 25 kg or eight years of age

121
Q

What should you avoid in patients with WPW?

A

Avoid adenosine in patients with known WPW

122
Q

Who gets atropine with intubation?

A

Infants <30 days

If >30 days shouldn’t use it automatically

123
Q

With ROSC, do you aim for hypo, hyper or norm thermal?

A

If comatose after out of hospital cardiac arrest, its reasonable to maintain 5d of normothermia (36.5-37.5C)

124
Q

What is your target O2 sat with ROSC?

A

With ROSC target O2 sat >94 and <100%, maintain normotension

125
Q

What are your indications for intubation?

A

Reduction of LV afterload
Need to decrease demand or regular physiology
Patient can’t ventilate or oxygenate
Impending resp failure
Impending failure of: lungs, airway, MSK, CNS, PNS

126
Q

What equipment do you need for intubation?

A
S = suction
O = oxygen
A = airway equipment
     • Laryngoscopeandblade 
     • ETT above and below
     • Stylette
     • BVM–well fitting mask 
      • Back-up option

P = Pharmaceuticals
• Atropine +/-
• Ketamine/fentanyl/midazolam/propofol
• Rocuronium/succinylcholine

ME = monitoring equipment

127
Q

ETT sizes

A

• <1 y: 3.0, 1-2: 3.5 ETT

• 2 years and older
4 + (age/4) uncuffed
3.5 (age/4) microcuffed

128
Q

How do you confirm ETT position?

A

Look for bilateral chest movement and listen for equal breath sounds
• Listen for gastric inflation over stomach
• Check exhaled carbon dioxide with CO2 detector or capnography
• check oxygen saturation with a pulse oximeter
• In hospital: perform a chest x-ray to verify that the tube is in the mid trachea

129
Q

What are normal tidal volumes?

A

Healthy lung: age appropriate respiratory rate, tidal volumes (VT) of 7- 10 ml/kg healthy lung

130
Q

What is the usual starting ventilator setting

A

PIP 20 cmH2O, PEEP 5 cmH2O, VR 25 FiO2 0.5

131
Q

What is the consequence of ventilator asynchrony?

A

Patient’s respiratory pattern does not match what is set on the ventilator
• Affects VT delivery
• Excessive intrathoracic pressures can lead to barotrauma, discomfort and affect cardiac output

132
Q

What is one way you could treat ventilator asynchrony?

A

increase patient sedation

133
Q

How do you change VENTILATION on a vent

A

Increase PIP and ventilator rates if you want to increase CO 2 clearance

134
Q

How do you change OXYGENATION on a vent?

A

Increase PEEP and FiO2 if you need to improve oxygenation

135
Q

What is the first sign of shock?

A

Hypovolemic shock is characterized primarily by fluid loss and decreased preload.
Tachycardia and an increase in systemic vascular resistance are the initial compensatory responses to maintain cardiac output and systemic blood pressure.”

136
Q

What is the difference between COMPENSATED and UNCOMPENSATED shock?

A

Blood pressure!

Compensated: normal NP
Uncompensated: Hypotension

137
Q

Types of hypovolemic shock

A
Diarrheal  illness 
Hemorrhage 
Burns
Vomiting 
Volume  depletion

Decreased PRELOAD!

138
Q

Clinical Presentation of hypovolemic shock

A
Tachycardia
 Orthostatic  hypotension
 dry  mucous  membranes
decreased  urine  output,
perfusion  normal->  impaired
139
Q

Causes of cardiogenic shock

A

CHD
Myocarditis
Arrhythmia

Left ventricular failure, impaired myocardial function Decreased contractility

140
Q

Clinical Presentation of cardiogenic shock

A

Tachycardia, cool extremities, delayed capillary refill time, poor perfusion, decreased urine output

141
Q

Obstructive shock causes

A

Pericardial Tamponade
Tension pneumothorax
Pulmonary embolism
Congenital heart disease lesions that are dependent on PDA for systemic blood flow and duct closes

Reduced SV due to pathology that prevents adequate LV preload “mechanical barrier”

142
Q

Presentation of Obstructive shock

A
Tachycardia
cool  extremities
 delayed  capillary  refill  time
 poor  perfusion 
 decreased  urine  output 

SIGNS OF THE UNDERLYING ETIOLOGY

143
Q

Causes of distributive shock

A

Anaphylaxis
Neurogenic shock
Pharmacologic

Inadequate vasomotor tone, capillary leak, reduced intravascular volume

144
Q

Clinical presentation of distributive shock

A
Tachycardia  or  bradycardia
peripheral  vasodilation
 flash  capillary  refill
bounding  pulses
poor  urine  output
145
Q

Definition of mild blood loss and vital signs you would see with it

A
<30% blood loss
Increased HR
thready peripheral pulse
normal SBP
normal Pulse pressure
Anxiety, irritability, confusion
Cool, mottled, prolongs cap refill
low to very low U/O
146
Q

Definition of moderate blood loss and the vital signs you would see with it

A
30-45% blood loss
Increased HR
thready central pulse
Peripheral pulses absent
normal SBP
lethargic, poor response to pain
cyanotic, markedly prolongs cap refill
very low U/O
147
Q

Definition of Severe blood loss and the vital signs you would see with it

A
>45% blood loss
Increased HR followed by decreased HR
weak or absent central pulse
Peripheral pulses absent
Hypotension, DBP may be undetectable
Coma
pale and cold
no U/O
148
Q

Initial steps of septic shock

A

bolus NS 20ml/kg,
correct hypoglycemia/hypocalcemia
start antibiotics

149
Q

Glascow Coma Scale….go

A

Eye Opening Response
• Spontaneous–open with blinking at baseline 4 points
• To verbal stimuli, command, speech 3 points
• To pain only (not applied to face) 2 points
• No response 1 point

Verbal Response
• Oriented 5 points
• Confused conversation, but able to answer questions 4 points
• Inappropriate words 3 points
• Incomprehensible speech 2 points
• No response 1 point

Motor Response
• Obeys commands for movement 6 points
• Purposeful movement to painful stimulus 5 points
• Withdraws in response to pain 4 points
• Flexion in response to pain (decorticate posturing) 3 points
• Extension response in response to pain (decerebrate posturing) 2 points
• No response 1 point

150
Q

What are the three different levels of severity for TBI based on GCS?

A

Severity:
Mild GCS 14-15
Moderate GCS 9-13
Severe GCS <9

151
Q

Things that will worsen secondary brain injury

A
  • Increased CSF pH/decreased CO2: vasoconstriction cerebral arterioles and can lead to inadequate perfusion and ischemia

o Hyponatremia: worsen cerebral edema

o Hypotension and hypertension: affect cerebral blood flow is cerebral autoregulation impaired by the injury

o Hyperthermia increases cerebral metabolic demand

o Hypoglycemia leads to neuronal apoptosis, seizures increase cerebral metabolic demand and can result in loss of airway control and hypoxemia

152
Q

Summarize the Canadian CATCH rules for head CT in children

A

CT of the head is required for children with a minor head injury* plus any one of the following findings:

High risk (need for neurological intervention)

  • Glasgow Coma Scale score <15 at 2 h after injury
  • Suspected open or depressed skull fracture
  • History of worsening headache
  • Irritability on examination

Medium risk (brain injury on CT scan)

  • Any sign of basal skull fracture (eg, hemotympanum, ‘raccoon’ eyes, otorrhea or rhinorrhea of cerebrospinal fluid, Battle’s sign)
  • Large, boggy hematoma of the scalp
  • Dangerous mechanism of injury (eg, motor vehicle collision, fall from a height ≥3 feet (≥91 cm) or down five stairs, falling from a bicycle without a helmet)

*Minor head injury is defined as an injury sustained within the past 24 h associated with witnessed loss of consciousness, definite amnesia, witnessed disorientation, persistent vomiting (more than one episode) or persistent irritability (in a child younger than two years of age) in a patient with a Glasgow Coma Scale score of 13 to 15.

153
Q

Management of mild TBI

A

• Mild: discharge with WRITTEN anticipatory guidance,

Observe in hospital if: headache, repeated vomiting or GCS <15 after period of observation

154
Q

Management of moderate TBI

A

•Moderate: CT head, consult neurosurgery, supportive care and likely admission to ICU

155
Q

Management of Severe TBI

A

• Severe: intubation and ventilation, supportive care (prevent secondary injury): normothermia, normal blood pressure, normal sodium, normal CO2, normal glucose, head of bed 30 degrees, head midline, ensure c-spine collar not obstructive cerebral venous drainage, adequate analgesia/sedation, consider seizure prophylaxis (efficacy unproven)

156
Q

Management of coning

A

•Suspected conning (dilated pupils, hypertension, bradycardia, extensor posturing, abnormal respirations: hyperventilate (CO2 25-35), FiO2 1, hyperosmolar therapy

157
Q

Signs of conning

A

• Conning: hypertension, bradycardia, irregular respirations, signs of 6th or 3rd CN palsy

158
Q

What must be present to diagnose brain death

A
  • Established etiology capable of causing neurologic death
  • Absence of reversible conditions that can mimic brain death AND absent confounders: unresuscitated shock, hypothermia (<34 °C), severe metabolic disorders that can cause reversible coma: glucose, electrolytes, IEM, liver and renal dysfunction, peripheral nerve or neuromuscular dysfunction, drug intoxications
  • Deep, unresponsive coma ABSENCE of motor responses EXCLUDING spinal reflexes and ABSENT brain stem reflexes: cough, gag, corneal, pupils, vestibulo-occular
  • (Apnea Test) Patient does not breathe, PaCO2 at least 60mmHg and at least 20 mmHg above pre apnea test level and pH 7.28 following apnea test
159
Q

When is time of death?

A

After first determination of brain death

160
Q

Who can declare brain death

A

Two fully licensed physicians with skills in the management of severe brain injury and neurologic determination of death

161
Q

When can brain death be declared?

A

24h after a hypoxic ischemic brain injury,
term neonates >48h old,
cerebral perfusion study

162
Q

Indication for ancillary testing?

A

Impossible to complete brain death testing

OR unresolved confounding factors in a patient with etiology capable of causing brain death in a deep, unresponsive coma Eg cerebral radiocontrast angiography, radionuclide angiography

163
Q

What about declaring death in neonates?

A
  • must be> 36 weeks GA,
  • assessment must also include occulocephalic and suck reflexes
  • must be at least 36 °C
  • must be at least 48h old
  • assessed by 2 physicians at least 24h apart
164
Q

What is different about declaring death in infants 30d to 1 year

A
  • Assess the occulocephalic reflex instead of vestibulo- occular reflex
  • two full separate exams by different physicians
165
Q

Leading cause of unintentional death from injury is

A

MVA

then submersion injury

166
Q

How long to observe a child who is now stable post brief submersion event?

A

Observe in hospital minimum 6-8h for signs of pulmonary edema,
many with mild respiratory symptoms at first return to normal by 4-6h

167
Q

Submersion injury- prophylactic antibiotics or no

A

No indication for prophylactic antibiotics

168
Q

How fast can you rewarm someone?

A

Warm by 1-2°C per hour

169
Q

Best prognostic factor following submersion injury

A

Neurologic examination during the first 24-72h is the best prognostication of long term outcome

170
Q

Are swimming lessons good for children?

A

• Swimming programs <4 years of age isn’t an effective prevention strategy

171
Q

How o prevent childhood drowning?

A
  • Residential pools fenced on all 4 sides with self closing, self latching gate
  • Constant arms-length adult supervision
  • Government approved personal flotation devices should be used for children who cannot swim+ constant supervision
  • Parents and pool owners need to know CPR and have an emergency action plan
172
Q

What should you do with a pneumothorax pre transfer

A

CHEST TUBE

Physiologic considerations: gasses expand 10-15%, sounds of the transport may make physical exam more challenging by obscuring assessment, motion and vibration can lead to increased metabolic rate, fatigue, shortness of breath

173
Q

Pros/Cons of ground transport

A

Ground/ambulance: more spacious, can handle more weight than a helicopter, able to make stops if patient deteriorates and procedures are needed, slowest

174
Q

Pros/Cons of airplane transport

A

• Airplane gas expansion > 30%, decrease in arterial oxygen saturation (93% vs 100% at sea level)
So what?: blood loss or shock should receive supplementary oxygen, NG for ileus and chest tube for pneumothorax MUST be inserted first, Change ETT cuff from air to saline because of changes on the plane!

175
Q

Pros/Cons Helicopter transport

A

• Helicopter: LOUD, faster than ground, lower altitude than airplane and only works in certain weather conditions

176
Q

Management of Asthma Exacerbation

A
3 x salbutamol with ipratropium bromide 
• Steroids (Dex/Methylpred/hydrocortisone) 
• Magnesium sulfate
• IV salbutamol
• Don’t forget to phone a friend...
WITH PICU:
• Aminophylline
• Heliox
• Mechanical support • Ketamine
• Epinephrine
• Above should only be done with ICU support!!!!
177
Q

When should you intubate with Asthma?

A

Ideally NEVER

Only two indications
• Decreased LOC not maintaining ventilation drive
• Refractory, severe hypoxemia
• Never based on a gas!!!!!!

178
Q

Major virus for bronchiolitis?

A

RSV is the major culprit

  • RSV season usually 4-5 months long, starts Nov-Jan
  • 10-30% have multiple viruses
179
Q

Who is at higher risk for severe bronchiolitis Disease?

A
  • Infants born prematurely (<35 weeks’ gestation)
  • <3 months of age at presentation
  • Hemodynamically significant cardiopulmonary disease - - Immunodeficiency
180
Q

Who to admit with bronchiolitis

A
  • Signs of severe respiratory distress (eg, indrawing, grunting, RR >70/min)
  • Supplemental O2 required to keep saturations >90%
  • Dehydration or history of poor fluid intake
  • Cyanosis or history of apnea
  • Infant at high risk for severe disease (Table 4)
  • Family unable to cope
181
Q

Treatment for bronchiolitis

A

Recommended:

  • Oxygen Hydration
  • Epinephrine nebulization

Evidence Equivocal:

  • Epinephrine nebulization
  • Nasal suctioning
  • 3% hypertonic saline nebulization
  • Combined epinephrine and dexamethasone
182
Q

Who should get RSV palivizumab vaccine?

A

Recommended for:
• Hemodynamically significant CHD or CLD <12m at start of season
• Preterm before GA30 at start of season
• GA <36 now <6months in remote communities
• Immunodeficiencies, T21, C.F., upper airway concerns, chronic pulm disease other than CLD should not be routinely offered
• Considerforseveredisease/homeO2
• Not recommended to continue it break through disease

183
Q

What conditions respond to HHFNP

A
  • Obstructive sleep apnea
  • Bronchiolitis
  • Asthma
  • Pneumonia/Pneumonitis
  • Heart failure
184
Q

Main virus for croup?

A

parainfluenza

185
Q

Management of croup

A
  • Mild croup: consider dexamethasone
  • Mod-severe: humidified O2, NPO, neb epi, observe for at least 2 hrs after neb epi to ensure continued improvement, administer dex, consider use of heliox for severe
  • Impending failure: high conc O2 (NRB mask), assist ventilation, administer IV/IM dex, ETT (smaller tube – half size smaller than predicted for age), prepare for surgical airway if needed
186
Q

Indications for dialysis

A
  • Refractory volume overload
  • Persistent hyperkalemia
  • Severe, refractory metabolic acidosis
  • Uremia
  • Calcium/phosphorus imbalance
  • Neurologic symptoms
  • Certain toxins
187
Q

Management of Hyperkalemia

A

Management
• Remove iatrogenic causes

Stabilize
• Calcium

Shift
• Sugar/insulin
• Bicarb
• Ventolin

Remove
• Furosemide
• Dialysis

Confirm
• Repeat tests
• ECG

188
Q

Hyperkalemia EKG changes

A

Peaked T waves
long QRS
Long PR

then becomes a sinusoidal wave

189
Q

SIADH diagnosis

A
  • Diagnosis
  • Euveolmic/hypervolemic
  • Hyponatremia, low serum osmoles
  • High urine osmoles
  • High urine sodium
190
Q

How to calculate free water deficit

A

• Total body water x (Serum sodium – desired sodium)/desired sodium
• = (0.6L/kg x Wt(kg)) x (Serum Sodium – desired sodium)/desired
sodium
• Ex = (0.6 x 20) (160-140)/140)

• = 1.7 L

191
Q

Definition of liver failure

A

Defined as:
INR>1.5, uncorrectable by Vit K, with encephalopathy or INR > 2 uncorrectable by Vit K

  • Evidence of acute liver injury
  • No evidence of chronic liver disease
192
Q

When should an intubation be done by anesthesia/ENT

A
  • Upper airway obstruction
  • Mediastinal mass
  • Known difficult airway
193
Q

Pulmonary Hypertension you would want WHAT type of acid base balance?

A

patients with PHTN need alkalosis for pulmonary vasodilatation

194
Q

Main causes of Hypoxemia

A
Causes of Hypoxemia:
 1. Low FIO2
2. Hypoventilation
3. V/Q mismatch
4. Shunt (intracardiac or intrapulmonary)
= most common...good blood flow, but alveoli obstructed, etc.
5. Impaired alveolar-capillary diffusion
emphysema, asthma, etc.
195
Q

Bad prognostic factors on history for an asthma exacerbation

A

Medical

  • Previous attack with rapid/severe deterioration
  • Previous PICU admission
  • Previous mechanical ventilation
  • Syncope/seizure during attack

Psychosocial

  • Denial, non-compliance
  • Depression or other psychiatric disorder
  • Dysfunctional family
  • Inner city resident
196
Q

Severe Asthma warning signs

A
SEVERE ASTHMA WARNING SIGNS:
• Cyanosis, PaO2 <70 in 40% oxygen
• Absent breath sounds
• Marked expiratory wheeze
• Maximal accessory muscle use
• Altered level of consciousness
• Inability to speak
• Marked pulsus paradoxus
197
Q

Management of Status Epilepticus

A

AIRWAY AND BREATHING:
– POSITION patient on side +/- chin lift/jaw thrust
– PATENCY: Suction secretions
– APPLY 100% OXYGEN
– Assist ventilation if signs of respiratory depression or if saturations low despite 100% oxygen by face mask

CIRCULATION:
– Cardiorespiratory monitor – IV access

CHECK Bedside blood glucose level
– Give IV dextrose 10% 5ml/kg if <2.6mmol/L
- CHECK sodium, calcium

GIVE ANTICONVULSANTS (ALL MUST BE IN WITHIN 45 min)
– IV Lorazepam 0.1mg/kg (max4mg) OR IV Midazolam 0.1mg/kg
– Give benzodiazepines within the first 5 minutes
– IV fosphenytoin 20mg/kg over 20 minutes
– IV phenobarbital 20mg/kg over 20minutes
– If no resolution, IV midazalom infusion
– Consult neuro

198
Q

How to decrease intracranial hypertension

A

Reducing the space occupied by any of the four components:

  • Reduce brain size (hyperosmolar therapy)
  • Reduce CSF by drainage
  • Reduce blood by vasoconstriction *only when showing signs of brainstem compression
  • Surgical removal of hematoma
  • Open the skull to allow expansion of the structures (?)
199
Q

What is Cushings Triad

A

Increased BP, Decreased HR, Abnormal RR
Altered LOC
Pupillary changes

200
Q

Risk Factors for Cerebral Edema with DKA

A

Clinical
• New onset
• Age <5

Lab
• Initial pH < 7.1
• High Urea
• Initial corrected Na > 145

Treatment
• Failure of Na to rise as glucose decreases
• Bicarbonate use

201
Q

When can you declare brain death in neonates?

A

Newborns: < 30 days and ≥ 36 wks gestation
– 2 full exams with apnea tests with ≥ 24h interval between exam
– Must be ≥ 48h after birth

202
Q

When can you declare brain death in infants 30d-1year

A

Infants: 30 days ≥ and ≤ 1 year

– Full, separate exams must be performed, but no fixed interval

203
Q

When can you declare brain death in children >1

A

Children ≥ 1 year old to adults
– Still need two physicians, but can perform exam, including apnea testing concurrently
– In the setting of hypoxic-encholapathic injury, exam must be delayed ≥ 24h post injury.
- If examined separately, apnea test must be repeated

204
Q

What is a positive Apnea Test

A

A POSITIVE Apnea Test is present when:
PaCO2 ≥ 60mmHg AND is 20mmHg greater than pre-apnea value AND

pH ≤ 7.28 AND

Patient remained apneic (respiratory reflex is absent.)