Acute Care Flashcards
Name some types of cholinergics
Organophosphates (pesticides such as sarin “nerve” gas, dursban in RaidTM and malathion)
Carbamates (neostigmine, pyridostigmine, pesticides
such as aldicarb)
Alzheimer’s drugs (DonepezilTM)
Name some symptoms of cholinergic exposure
Diaphoresis Urination Miosis Bronchorrhea / Bradycardia Emesis Lacrimation Lethargy Salivation
Secretions everywhere
Treatment for cholinergic syndrome
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
Examples of Anticholinergic Drugs
TCAs (weakly anticholinergic)
Antihistamines (diphenhydramine, hydroxyzine) Benztropine (CogentinTM)
Atropine and cyclopentolate (mydriatic eyedrop) Diphenoxylate-atropine (LomotilTM)
Many neuroleptics (chlorpromazine, olanzapine)
Signs and Symptoms of anticholinergic syndrome
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)
Management of anticholinergic overdose
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
What are examples of sympathomimetic drugs
Cocaine
Amphetamine / Methamphetamine
MDMA (ecstasy)
Ephedrine
What are the symptoms pf sympathomimetic drug exposure
Mydriasis Diaphoresis (MAIN DIFFERENCE FROM ANTICHOLINERGICS) Hypertension Tachycardia Seizures Hyperthermia Psychosis Severe agitation
Ecstasy specific Symptoms
HTN (HTN emergencies, ICH) Hyperthermia (rhabdo, DIC) Hyponatremia (seizures) Serotonin syndrome Cardiac ischemia Hepatotoxicity
Ecstasy Management
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
LSD Specific Symptoms
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
PCP specific symptoms
seizures and delirium
Fluctuating behavior with delirium, paranoia, agitation Nystagmus while awake
Dystonic posturing, muscle rigidity, myoclonus
Serotonin syndrome Symptoms
Serotonin Syndrome
< 12 hours
Increased: BP,RR,HR,T
Pupils: Enlarged
Mucosa: Sialorrhea
Skin: Diaphoresis
Neurologic: Increased Reflexes (LE), increased Tone
Mental Status: Agitation
NMS Symptoms
Time course: 3-4 days
< 12 hours
Increased BP,RR,HR,T
Pupils: Normal
Mucosa: Sialorrhea
Skin: Diaphoresis
Neurologic: Rigid
Mental Status: Stupor
Opioid Toxidrome Symptoms
Bradycardia Hypotension Respiratory depression Miosis Coma
Treatment of Opioids
Naloxone (IV or IN)
Should see an effect in seconds
Ensure patent airway and adequate ventilation
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
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
When should you NOT use charcoal?
Avoid in severe caustic ingestion
Compromised airway reflexes
>1hr from ingestion
What ingestions is charcoal not effective for?
Potassium Hydrocarbons Alcohols Iron Lithium Solvents
Treatment for lidocaine overdose?
Lorazepam and 20% intralipid
What can you use IV lipid for?
For life-threatening overdoses of local anesthetics (iatrogenic), bupropion, amitriptyline
Antidote for Iron?
Deferoxamine
Antidote for carbon monoxide?
oxygen
Antidote for pesticide?
atropine
cholinergic
Antidote for Nifedipine?
Glucagon
Antidote for Amitripytline?
Sodium Bicarb…for QRS >100
Antidote for methanol?
Fomepizole
Antidote for glyburide?
Glucose
What are some examples of Hydrocarbons?
Gasoline, nail polish remover, lighter fluid common
Main complication of hydrocarbon ingestion?
Aspiration is common and pulmonary toxicity accounts for most fatalities
Changes seen 2-8 hours post
Deterioration in 24-48 hours
Perihilar infiltrates
Pneumatoceles
Treatment of Hydrocarbon Ingestion?
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
Metformin ingestion can cause what complication?
Lactic Acidosis
Usually normal Glucose
List 4 drugs that cause hypoglycemia
Glyburide
Beta blockers
Ethanol
Salicylates
Acetaminophen toxic ingestion occurs at what dose?
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
What complications can occur secondary to Tylenol ingestion?
Anion gap metabolic acidosis
Acute tubular necrosis
Fulminant liver failure
What are the stages of Tylenol ingestion?
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
Treatment of Acetaminophen Ingestion
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
What are examples of salicylates?
ASA Bismuth salicylate (antidiarrhoeal agent) Methyl salicylate (Rub A535TM) Salicylic acid (wart removal)
What are the symptoms of salicylates overdose?
Hyperpnea / tachypnea….respiratory alkalosis
AG metabolic acidosis…pulmonary/cerebral edema Nausea, vomiting, gastrointestinal bleed
Tinnitus (early) or hearing loss
Hyperglycemia…hypoglycemia
Diaphoresis
Management of salicylate overdose
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
Investigations for Iron Ingestion
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
Examples of radiopaque drugs
Chloral hydrate Opioid packets (latex) Iron and other heavy metals Neuroleptics (early) Sustained-release tablets / Salicylates (early)
Stages of Iron Toxicity
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
Clues to iron ingestion
GI symptoms
Acidosis
Multiorgan failure
Iron Management
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
Isopropyl Alcohol Ingestion Symptoms
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
Management of Isopropyl Alcohol ingestion
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
List some things methanol is found in
windshield wash, bingo dabbers
Signs and Symptoms from methanol ingestion
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)
What is ethylene glycol found in?
antifreeze, paints, brake fluid
What is the management of ethylene glycol ingestion
Colorless, odorless, sweet taste Inebriation with no odor of ethanol Metabolic acidosis:cardiac decompensation Hypocalcemia: prolonged QTc Oxalate crystals appear late
Clues to Toxic Alcohol Exposure
Inebriation
Odor
Osmolal gap or Acidosis
Treatment of Toxic Alcohol Ingestion
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
Symptoms of TCA ingestion
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
What is the management of TCA ingestion
Activated charcoal
Frequently require intubation because obtunded
NaHCO3 for QRS > 100 because of significant morbidity and mortality
Norepinephrine infusion if hypotensive
Physostigmine contraindicated
Symptoms of Carbon Monoxide Poisoning
Initially headache, dizziness, nausea, confusion, seizure, syncope, coma but don’t correlate with COHb level
Dysrhythmia and cardiac arrest in < 30%
Diagnosis of Carbon Monoxide Poisoning
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
Management of CO exposure
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)
When should you THINK of cyanide poisoning?
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
Management of Cyanide poisoning
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
Examples of CCB
Dihydropyridines: amlodipine, nifedipine
Non-dihydropyridines: verapamil, diltiazem (high glucose)
Signs and Symptoms of CCB ingestion
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
Management of CCB ingestion
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
Laundry Detergent Capsules Symptoms
Vomiting, drooling, respiratory distress
Airway compromise and esophageal perforation
Skin burns
Management of ingestion of laundry detergent capsules
supportive
ave them drink a glass of water
Symptoms of nicotine overdose
Onset of vomiting, diaphoresis, confusion within 2 hrs Seizures, initial ↑BP, ↑RR, ↑HR ⇒ ↓BP, ↓RR, ↓HR
Who is most at risk for a submersion injury
Males > Females
Children < 5 years at greatest risk
Usually during the summer months
Associated with hypothermia and trauma
Most common cause of death in children aged 1-4
Trauma
Most effective strategies for preventing submersion injuries.
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
Who should wear a PFD?
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
Risk Factors for Submersion injury
Leaving children unattended
Alcohol or drug abuse (50% of adult drownings) Limited swimming ability
Underlying medical conditions(?):
- Seizure disorder, toxin, prolonged QT, syncope
Factors for good prognosis after submersion injury
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
What are poor prognostic factors for submersion injury
What are poor prognostic indicators?
- Delayed CPR
- Return of spontaneous circulation > 25 min
- Submersion > 10 min
What are complications of submersion injury?
ARDS Pulmonary edema Pneumonia Cerebral edema leading to increased ICP Trauma Hypothermia
Definition of Hypothermia
Defined as core temp < 35 C
Metabolic disturbances from hypothermia
Shivering stops at core temp < 32 C
Accompanied by hypoglycemia, hypocalcemia, hypokalemia, metabolic acidosis
Associated with pancreatitis
Features of hypothermia at 31-32 C
- Normal ECG, ↑ HR, ↑ BP, loss of shivering
Features of hypothermia at 28-31 C
- ↓ HR, ↓ BP, flipped T, atrial fibrillation, sluggish, dilated pupils
Features of Hypothermia at <28C
- absent pulse and BP, VF, coma, fixed dilated pupils
EKG findings in hypothermia
Marked sinus bradycardia
First degree AV block
Osborn or J waves Associated with prolonged QT and bradycardia
Seen in core T < 32 C
Special CPR Considerations with hypothermia
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!
Rewarming for 34-36 degrees
Passive rewarming:
Remove wet clothes
Dry
Rewarming 30-34C
Passive AND active external warming of truncal areas only
electric blanket
use Bair Hugger
overhead warmer
hot water bottles heating pads
Rewarming < 30C
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
CPR at T >30
T > 30
Continue CPR
IV meds as needed
Defibrillation as needed
CPR at T <30
T < 30
Continue CPR but no IV meds
Limit defibrillation to 3 shocks
Treatment of Frostbite
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
What is Heat Exhaustion
Excessive peripheral vasodilation then
Inability to deliver sufficient blood volume then
Muscle fatigue
Profuse sweating
Excessive water and/or sodium losses
What are heat cramps
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
What is heat stroke?
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
Heat exhaustion, water depletion
Unacclimatized in hot climate with inadequate water intake (tourists)
T < 40 Lethargy, N/V, headache,
↓ BP, ↑ HR
↑ Na,↑ Cl
Heat Exhaustion, NaCl depletion
Unacclimatized in hot climate with inadequate salt intake (CF)
T > 38 Above with severe muscle cramps
↓ Na
Management of Heat Stroke
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
Complications of Heat Stroke
Hyponatremia Seizure Rhabdomyolysis DIC Multi-system organ failure
What is a superficial burn
Superficial
Epidermis only
Redness, pain, no blisters Heals in 3-5 days
What is a Superficial partial thickness burn
Epidermis + 1/2 Dermis
Red/pink, pain, moist, blisters
Heals in 2 weeks
What is deep partial thickness burn
Epidermis + > 1/2 Dermis
Pale, dry, less tender, speckled appearance
Grafting often needed
What is full thickness burn
Subcutaneous tissue
Pale, charred, leathery appearance, non-tender
Most require grafting
Management of burns
Cover with sterile bandages Early cooling ( < 30 min) prevents further injury Tetanus (dirty wound) Analgesia Remove smoldering clothing Measure carboxy-hemoglobin
What are the indications for early intubation with burns
Need to know this!
- Carbonaceous sputum
- Singed nasal hairs
- Soot in airway
- Hoarseness
What is the parkland formula
Age > 5: Parkland formula = 4 cc/kg/BSA over 24
hours (1st half in 8 hours, 2nd half in 16 hours)
BSA calculation for children
Age > 9: Rule of 9’s
Age < 9: Child’s palm = 1% BSA (not superficial)
What types of infections do you see with burns
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
Who do you need to admit with burns?
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
High tension wire injury complications
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
Lighting side effects
Cerebral edema (delayed), ICH, seizure Rhabdomyolysis Asystole and respiratory failure Monitor for delayed cerebral edema and arrhythmia
Most common cause of paediatric cardiac arrest
respiratory failure
CPR one rescuer compression:breath ratio
30:2
CPR two rescuer compression:breath ratio
15:2
CPR compression breath ratio once patient is intubated
Asynchronous 100:10
Breaths and compressions happening independently of each other
Describe good quality compressions
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
Treatment for poor perfused bradycardia
(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
How do you manage PEA
NO SHOCKING
CPR
Epinephrine 0.01mg/kg of the 0.1mg/mL solution
Give every 3-5 minutes
Stable SVT management
Vagal maneuvers
Adenosine 0.1mg/kg (max 6mg)
Second dose 0.2mg/kg (max 12mg)
Need expert consultation for amiodarone and procainamide
Unstable SVT management
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
Vtach with a pulse treatment
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
Pulseless Vtach/Vfib treatment
shock shock epi (0.01 mg/kg of the 0.1mg/mL solution shock Amiodarone/lidocaine repeat
Shock 2, 4, 6, 8, 10J/kg
What are the H’s and T’s
Hypovolemia Hypoxia Hydrogen Ions Hypoglycemia Hypothermia Hypo/Hyperkalemia
Tension Pneumo Tamponade (cardiac) Toxins Thrombosis, pulmonary Thrombosis, coronary
Are compressions only ok for children?
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
When using an AED, whence you stop using the paediatric dose attenuator?
Use pediatric dose attenuator up to 25 kg or eight years of age
What should you avoid in patients with WPW?
Avoid adenosine in patients with known WPW
Who gets atropine with intubation?
Infants <30 days
If >30 days shouldn’t use it automatically
With ROSC, do you aim for hypo, hyper or norm thermal?
If comatose after out of hospital cardiac arrest, its reasonable to maintain 5d of normothermia (36.5-37.5C)
What is your target O2 sat with ROSC?
With ROSC target O2 sat >94 and <100%, maintain normotension
What are your indications for intubation?
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
What equipment do you need for intubation?
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
ETT sizes
• <1 y: 3.0, 1-2: 3.5 ETT
• 2 years and older
4 + (age/4) uncuffed
3.5 (age/4) microcuffed
How do you confirm ETT position?
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
What are normal tidal volumes?
Healthy lung: age appropriate respiratory rate, tidal volumes (VT) of 7- 10 ml/kg healthy lung
What is the usual starting ventilator setting
PIP 20 cmH2O, PEEP 5 cmH2O, VR 25 FiO2 0.5
What is the consequence of ventilator asynchrony?
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
What is one way you could treat ventilator asynchrony?
increase patient sedation
How do you change VENTILATION on a vent
Increase PIP and ventilator rates if you want to increase CO 2 clearance
How do you change OXYGENATION on a vent?
Increase PEEP and FiO2 if you need to improve oxygenation
What is the first sign of shock?
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.”
What is the difference between COMPENSATED and UNCOMPENSATED shock?
Blood pressure!
Compensated: normal NP
Uncompensated: Hypotension
Types of hypovolemic shock
Diarrheal illness Hemorrhage Burns Vomiting Volume depletion
Decreased PRELOAD!
Clinical Presentation of hypovolemic shock
Tachycardia Orthostatic hypotension dry mucous membranes decreased urine output, perfusion normal-> impaired
Causes of cardiogenic shock
CHD
Myocarditis
Arrhythmia
Left ventricular failure, impaired myocardial function Decreased contractility
Clinical Presentation of cardiogenic shock
Tachycardia, cool extremities, delayed capillary refill time, poor perfusion, decreased urine output
Obstructive shock causes
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”
Presentation of Obstructive shock
Tachycardia cool extremities delayed capillary refill time poor perfusion decreased urine output
SIGNS OF THE UNDERLYING ETIOLOGY
Causes of distributive shock
Anaphylaxis
Neurogenic shock
Pharmacologic
Inadequate vasomotor tone, capillary leak, reduced intravascular volume
Clinical presentation of distributive shock
Tachycardia or bradycardia peripheral vasodilation flash capillary refill bounding pulses poor urine output
Definition of mild blood loss and vital signs you would see with it
<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
Definition of moderate blood loss and the vital signs you would see with it
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
Definition of Severe blood loss and the vital signs you would see with it
>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
Initial steps of septic shock
bolus NS 20ml/kg,
correct hypoglycemia/hypocalcemia
start antibiotics
Glascow Coma Scale….go
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
What are the three different levels of severity for TBI based on GCS?
Severity:
Mild GCS 14-15
Moderate GCS 9-13
Severe GCS <9
Things that will worsen secondary brain injury
- 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
Summarize the Canadian CATCH rules for head CT in children
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.
Management of mild TBI
• Mild: discharge with WRITTEN anticipatory guidance,
Observe in hospital if: headache, repeated vomiting or GCS <15 after period of observation
Management of moderate TBI
•Moderate: CT head, consult neurosurgery, supportive care and likely admission to ICU
Management of Severe TBI
• 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)
Management of coning
•Suspected conning (dilated pupils, hypertension, bradycardia, extensor posturing, abnormal respirations: hyperventilate (CO2 25-35), FiO2 1, hyperosmolar therapy
Signs of conning
• Conning: hypertension, bradycardia, irregular respirations, signs of 6th or 3rd CN palsy
What must be present to diagnose brain death
- 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
When is time of death?
After first determination of brain death
Who can declare brain death
Two fully licensed physicians with skills in the management of severe brain injury and neurologic determination of death
When can brain death be declared?
24h after a hypoxic ischemic brain injury,
term neonates >48h old,
cerebral perfusion study
Indication for ancillary testing?
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
What about declaring death in neonates?
- 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
What is different about declaring death in infants 30d to 1 year
- Assess the occulocephalic reflex instead of vestibulo- occular reflex
- two full separate exams by different physicians
Leading cause of unintentional death from injury is
MVA
then submersion injury
How long to observe a child who is now stable post brief submersion event?
Observe in hospital minimum 6-8h for signs of pulmonary edema,
many with mild respiratory symptoms at first return to normal by 4-6h
Submersion injury- prophylactic antibiotics or no
No indication for prophylactic antibiotics
How fast can you rewarm someone?
Warm by 1-2°C per hour
Best prognostic factor following submersion injury
Neurologic examination during the first 24-72h is the best prognostication of long term outcome
Are swimming lessons good for children?
• Swimming programs <4 years of age isn’t an effective prevention strategy
How o prevent childhood drowning?
- 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
What should you do with a pneumothorax pre transfer
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
Pros/Cons of ground transport
Ground/ambulance: more spacious, can handle more weight than a helicopter, able to make stops if patient deteriorates and procedures are needed, slowest
Pros/Cons of airplane transport
• 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!
Pros/Cons Helicopter transport
• Helicopter: LOUD, faster than ground, lower altitude than airplane and only works in certain weather conditions
Management of Asthma Exacerbation
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!!!!
When should you intubate with Asthma?
Ideally NEVER
Only two indications
• Decreased LOC not maintaining ventilation drive
• Refractory, severe hypoxemia
• Never based on a gas!!!!!!
Major virus for bronchiolitis?
RSV is the major culprit
- RSV season usually 4-5 months long, starts Nov-Jan
- 10-30% have multiple viruses
Who is at higher risk for severe bronchiolitis Disease?
- Infants born prematurely (<35 weeks’ gestation)
- <3 months of age at presentation
- Hemodynamically significant cardiopulmonary disease - - Immunodeficiency
Who to admit with bronchiolitis
- 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
Treatment for bronchiolitis
Recommended:
- Oxygen Hydration
- Epinephrine nebulization
Evidence Equivocal:
- Epinephrine nebulization
- Nasal suctioning
- 3% hypertonic saline nebulization
- Combined epinephrine and dexamethasone
Who should get RSV palivizumab vaccine?
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
What conditions respond to HHFNP
- Obstructive sleep apnea
- Bronchiolitis
- Asthma
- Pneumonia/Pneumonitis
- Heart failure
Main virus for croup?
parainfluenza
Management of croup
- 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
Indications for dialysis
- Refractory volume overload
- Persistent hyperkalemia
- Severe, refractory metabolic acidosis
- Uremia
- Calcium/phosphorus imbalance
- Neurologic symptoms
- Certain toxins
Management of Hyperkalemia
Management
• Remove iatrogenic causes
Stabilize
• Calcium
Shift
• Sugar/insulin
• Bicarb
• Ventolin
Remove
• Furosemide
• Dialysis
Confirm
• Repeat tests
• ECG
Hyperkalemia EKG changes
Peaked T waves
long QRS
Long PR
then becomes a sinusoidal wave
SIADH diagnosis
- Diagnosis
- Euveolmic/hypervolemic
- Hyponatremia, low serum osmoles
- High urine osmoles
- High urine sodium
How to calculate free water deficit
• 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
Definition of liver failure
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
When should an intubation be done by anesthesia/ENT
- Upper airway obstruction
- Mediastinal mass
- Known difficult airway
Pulmonary Hypertension you would want WHAT type of acid base balance?
patients with PHTN need alkalosis for pulmonary vasodilatation
Main causes of Hypoxemia
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.
Bad prognostic factors on history for an asthma exacerbation
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
Severe Asthma warning signs
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
Management of Status Epilepticus
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
How to decrease intracranial hypertension
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 (?)
What is Cushings Triad
Increased BP, Decreased HR, Abnormal RR
Altered LOC
Pupillary changes
Risk Factors for Cerebral Edema with DKA
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
When can you declare brain death in neonates?
Newborns: < 30 days and ≥ 36 wks gestation
– 2 full exams with apnea tests with ≥ 24h interval between exam
– Must be ≥ 48h after birth
When can you declare brain death in infants 30d-1year
Infants: 30 days ≥ and ≤ 1 year
– Full, separate exams must be performed, but no fixed interval
When can you declare brain death in children >1
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
What is a positive Apnea Test
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.)
