Critical Care and Tox

Question 1

Sepsis Defined

Answer 1

“Life threatening organ dysfunction
secondary to dysregulated host response
to infection”

Use your clinical acumen, measure lactate,
and a screening tool to diagnosis sepsis

SIRS is easiest tool to memorise for oral exam :

HR >90
Temp >38 or <36
RR >20 or PaCO2 <32
WBC >12 or <4 or 10% bands
2 or more = positive screen

Septic Shock = Sepsis +
-adequate volume resuscitation
-Persistent ↓BP requiring
vasopressors to keep MAP ≥ 65
-actate > 2 mmol/L

Question 2

A quick word on differentiation of
cardiogenic vs septic shock

Answer 2

ScvO2 helps differentiate
cardiogenic vs septic shock
* > 80% corresponds with high
flow states (eg. sepsis).
Mitochondrial dysfunction
leads to reduced O2 utilization
* < 65% indicates poor forward
flow: cardiogenic shock
* Here, the heart isn’t strong
enough to pump the
oxygen out to the cells

Question 3

Sepsis: IMMEDIATE Initial Resuscitation

Answer 3

• If sepsis induced hypotension/shock, begin rapid administration of at least
  30ml/kg (ideal body weight) crystalloid within the first 3h (2021 = Suggestion)
• See next slide for guiding fluid resuscitation
• Use vasopressors if patient is hypotensive during or after fluid resuscitation
  to keep MAP≥65
  – Norepinephrine (“levophed”) is first line vasopressor
• Give broad spectrum antibiotics within 1 hour
  – Obtain blood cultures prior to antibiotics if possible

Question 4

Sepsis: Antibiotic Choice

Answer 4

Broad spectrum antibiotics recommended (e.g. piperacillin-tazobactam) and
consider individual risk of:

– MRSA coverage empirically if high risk
* High risk: known MRSA colonized, recurrent skin/soft tissue infxn, PWID, central lines, dialysis

– Multi-Drug Resistant (MDR) organism – **double (2 antibiotic) GN coverage if high risk
* High risk: previous abx within 3 months, known MDR colonization, local prevalence, travel to endemic
country or hospitalization abroad
**This is a weak recommendation with low quality evidence

– Fungal coverage if high risk
* High risk: neutropenia, immunocompromised, TPN, dialysis, chronic lines, PWID, HIV, Heme or solid organ
transplant, emergency GI surgery or anastomotic leak

• Daily assessment for de-escalation of antibiotics
• Rapidly identify if infection requires source control, remove source (including vascular access device) as soon as possible

Question 5

Sepsis: Guiding Resuscitation

Answer 5

Use DYNAMIC VARIABLES over physical examination and static
parameters alone to guide resuscitation
– Response to fluid bolus
– Response to passive leg raise (45o raise x 30-90sec = 15% increase in stroke volume)
– Pulse pressure variation (PPV) (>10%)
– Echocardiography
* Stroke volume or Stroke volume variation (SVV)
* IVC
– Intubated, fully ventilated-Distensibility Index >15-20% likely to be fluid responsive
– Intubated breathing spontaneouslyà cannot use
– Spontaneously breathing not intubated IVC <2cm and respiratory variation>50%àlikely fluid responsive
* Lactate levels – if elevated aim to reduce with resuscitation
* Capillary refill à Abnormal >3sec, Normal <3sec

Question 6

Sepsis: IV Fluids

Answer 6

WHICH ONE?
✓ Recommend Crystalloid first line
✓ Suggest using balanced crystalloid over
NS (SMART trial)
– Decreases major adverse kidney events at 30
days (death, new renal replacement,
Cr>200% above baseline)
? Suggest albumin in patients who received
large volumes of crystalloid over crystalloid
alone
- Costly, no mortality benefit, did not define
“large volume” – weak recommendation only

❌
Do not use starches (34 deaths per 1000)

❌
Do not use gelatin

Question 7

Hemodynamic Management and Vasopressors

Answer 7

Doses
Norepinephrine/Epinephrine
0.05-0.5mcg/kg/min
Vasopressin 2.4 units/hr
Dobutamine 2.5-10 mcg/kg/min
Add vasopressin when
Norepinephrine approx 0.25 –
0.5 mcg/kg/min

Question 8

Steroid recommendations

Answer 8

Theory: may help immune dysregulation, relative adrenal insufficiency
* Consider for septic SHOCK with ongoing requirement for vasopressor
– Hydrocortisone 200mg/d (typically 50 mg IV q6h)
– Consider when norepinephrine 0.25mcg/kg/min for > 4hrs
– Not recommended in sepsis without shock
* Duration unclear (caution if prolonged àmay need to taper)
* No mortality benefit – considered a vasopressor sparing agent
* Risks include potential hyperglycemia, hypernatremia,
neuromuscular weakness

dont give liberal oxygen:
(target 94-96%, a sat >96% increases mortality incritically ill)

Question 9

When to not use HFNC?

Answer 9

Post extubation for patients at a high risk
of extubation failure: NIV over HFNC
(unless relative or absolute CI)

• Acute hypercapnic resp failure
  secondary to COPD (pH < 7.35): trial NIV
  before HFNC

Question 10

When to use HFNC?

Answer 10

• Hypoxemic resp failure (adults): HFNC
  over Conventional O2 Therapy (COT) or
  NIV
• Patients taking Non-Invasive Ventilation
  (NIV) breaks: HFNC over COT
• Post extubation (non-surgical patients)
  that are at a low/mod risk of extubation
  failure: HFNC over COT
• Post-operative patient at low risk of
  respiratory complications: HFNC or COT
• Post-operative patient at high risk of
  respiratory complications: HFNC or NIV

Question 11

NIV Should Definitely be Used For:

Answer 11

BiPAP for mild-severe acidotic COPD patients (RR
>20-24, pH≤7.35, and PaCO2>45)
* BiPAP/CPAP for Cardiogenic pulmonary edema*
(not cardiogenic shock and acute MI)

Question 12

NIV Should Probably Not be Used For:

Answer 12

• Treatment of post-extubation resp failure
• Prevention of post-extubation resp failure if
  not high risk
• Hypercapneic COPD patients who are NOT
  acidotic

Question 13

Contraindications to NIV

Answer 13

• Facial surgery, facial trauma, airway
  obstruction
• Decreased LOC (*relative)
• Inability to clear secretions
• Respiratory arrest
• Hemodynamic instability (reduces preload)
• Other Indication for intubation (e.g. airway
  protection)

Question 14

Ventilator Hacks

Answer 14

How to decrease PaCO2
increase RR
increase tidal volume
(minute ventilation = RR * Vt)

How to increase SpO2
(PaO2)

Increase FiO2
increase PEEP
increase inspiratory time
Stop pulm vasodilators (eg nitroprusside)

Example of Vent settings:

RR 10-12, VT 6-8ml/kg (6 if ARDS)

PEEP 5-20, PC 5-25

Question 15

Lung and Airway Pressures

Answer 15

Peak inspiratory pressures (PIP) – Reflects airway resistance + lung compliance – Target <35cm H2O

• Plateau pressure (Pplat) – The pressure in the lungs when no air is moving, reflects lung compliance
  – This is the pressure that the alveoli are seeing – Target <30 cm H2O in any vented patient * >30 = risk of barotrauma causing pneumothorax/lung
  injury
  – May be confounded by chest wall restriction (ie. Obesity)
• Positive End Expiratory Pressure (PEEP)
  -Pressure at end of Resp cycle
  -increases solubility of oxygen
  -splits airways , decreased WOB

Question 16

ARDS diagnosis

Answer 16

Timing Within 1 week of known clinical insult or worsening respiratory symptoms

Pulmonary edema -Not cardiogenic pulmonary edema or due to intravascular volume overload

Chest Imaging Bilateral infiltrates on CXR or CT
Or on LUNG ULTRASOUND by trained professional
*not explained by nodules, pleural effusions or atelectasis

Hypoxemia SpO2/FiO2 ≦315 with SpO2 ≦ 97%

MILD
PaO2/FiO2 **

201-300 with
NIV/CPAP PEEP ≧ 5 or
HFNC >30l/min

MOD

101-200
PEEP ≧ 5

Severe

≦ 100
PEEP ≧ 5

Question 17

ARDS Causes and Pathophysiology

Answer 17

DIRECT LUNG INJURY
* Pneumonia
* Aspiration pneumonitis
* Drowning
* Thoracic trauma/pulmonary contusion
* Smoke or toxic inhalation
* Fat emboli
* Reperfusion injury (post lung transplant)

SYSTEMIC INFLAMMATION
* Severe sepsis
* Transfusion reaction (TRALI)
* Shock
* Pancreatitis

Pathophysiology:
* Proteinaceous fluid fills alveoli
* Neutrophils flood alveolar space
* Hyaline membranes form on epithelial
basement membrane
* Microthrombi form
* Fibrosis develops (late stage)

Treatment:
1. Ventilation Strategies
2. Prone positioning
3. Neuromuscular Blockade
4. ECLS/ECMO
5. Corticosteroids
6. Inhaled Pulmonary Vasodilators

Question 18

ARDS: Ventilation

Answer 18

Mode: Volume Control
Tidal volume (Vt): Initial Vt at 6ml/kg PBW - target 4-8 ml/kg PBW

Plateau pressure: ≤ 30 cm H2O, Driving pressure (Pplat - PEEP) target < 15 cm H2O

PEEP: target higher PEEP in mod/severe ARDS, based on FiO2-PEEP Tables SpO2:
target 88-93% or PaO2 55 - 80 mmHg (avoid hyperoxia – ↑s harm)

CO2: permissive hypercapnia allowed, target pH > 7.25

• Deep sedation to achieve the above parameters

Question 19

ARDS Treatment Modalities Summary

Answer 19

High PEEP -Recommended for in mod/sev ARDS. Mortality benefit in moderate-severe

Prone positioning Strong recommendation for severe ARDS. Mortality benefit if P/F < 150 (PROSEVA trial). Duration > 12hrs per day.

Neuromuscular blockade -No mortality benefit. Consider in severe ARDS after optimizing PEEP and ventilator settings. Reduces ventilator desynchrony,

Inhaled INO No mortality benefit. May improve oxygenation by improving VQ mismatching and
reducing shunting. Bridge therapy.

Diuresis Decreases duration on ventilator.

ECMO No clear mortality benefit, acts as a bridge therapy. (EOLIA trial).

Steroids No benefit for ARDS. May be clinically indicated depending on underlying cause (ie.
Covid pneumonia, concern of COP).

Question 20

ECMO Respiratory Considerations

Answer 20

Consider ECMO

• Severe ARDS
• Hypercapneic respiratory failure
• Bridge to lung transplantation
• Primary graft dysfunction after lung transplantation
• Status asthmaticus

Do NOT Consider ECMO

Absolute
* Disseminated malignancy
* Known severe brain injury
* Prolonged CPR without adequate tissue perfusion
* Severe chronic organ dysfunction
* Severe chronic pulmonary hypertension
* Non-recoverable advanced comorbidity (ie. CNS
damage or terminal malignancy)

Call for ECMO referral if:
* P/F < 80 mmHg for > 6 hours OR P/F < 50 mmHg for > 3 hours
* PaCO2 > 60 mmHg for > 6 hours (despite optimization of vent)
* Mechanically ventilated < 7 days
* BMI < 40 or weight < 125 kg
* Age 18 - 65

Question 21

Weaning from Mechanical Ventilation

Answer 21

Assess readiness for weaning from ventilator
1. Reversal of underlying reason for intubation
and ventilation
2. Improvement of oxygenation
(PaO2 > 60 mmHg, FiO2 < 40%, PEEP < 8)
3.Ability to perform work of breathing
(Normal/compensated Co2, pH, adequate
cardiac function, adequate diaphragm
function)

Assess readiness for extubation
1. Adequate cough
2. Minimal secretions, ability to manage secretions
3. Awake/Alert, following commands, no sedation
4. No increased risk of airway obstruction – post-op
swelling resolved, ETT cuff leak present

Question 22

Spontaneous Breathing Trial (SBT)

Answer 22

• Mimics patient’s own ability to breathe independently
• Perform on PSV for 30 minutes
  – PSV 5/5 vs. 0/0 vs. 5/0 à variable practices
  – Toronto standardized practice is 0/0
• Failure of SBT - tachypnea, increased work of
  breathing, tachycardia, hypotension, desaturation
  – Always ask ‘why’, and try to correct underlying cause of failure
• Rapid shallow breathing index (RSBI) à respiratory rate (breaths/min)/tidal volume
  (L/min)
  – RSBI > 105 is a predictor of extubation failure

Question 23

Sedation

Answer 23

SCCM 2018 Guidelines:
* Target RASS -2 to +1 (light sedation)
* Daily sedation interruptions and nurse
titrated protocols can help achieve this
* Propofol or dexmedetomidine are
preferable to benzodiazepines
– Reduced LOS, duration of IMV, delirium
– Beware of bradycardia and hypotension
* Do not use dexmedetomidine if deep
sedation is required

Question 24

Delirium

Answer 24

Treatment of delirium in the ICU
– Nonpharmacologic therapy:
* Optimize mobility, sleep, hearing, vision
* Frequent orientation
* Minimize modifiable risk factors – medications,
transfusions

– Pharmacologic therapy
* Pharmacological agents (statin, anti- psychotics) should not be used to
prevent delirium in ICU patients
* Do not routinely use Haldol, atypical
antipsychotic or statin to treat delirium except
if significant hallucinations, distress, agitation
* Consider dexmedetomidine for intubated
patients with delirium to help facilitate
extubation/weaning

Question 25

Pain in the ICU

Answer 25

Multimodal approach to pain management
* Opioids are mainstay, especially post-op, but associated with side effects (respiratory depression, delirium, dependence)

• Adjuncts should be used to reduce opioid requirements
  – Acetaminophen, NSAIDS (where appropriate)
  – Low dose ketamine (0.5 mg mg/kg bolus then 1-2 mcg/kg/min infusion) in post-operative patients
  – Gabapentin, pregabalin, carbamazepine for neuropathic pain
  – Do not routinely use lidocaine, local anesthetics or inhaled volatiles for painadjuncts (may be effective for special circumstances – postoperative, trauma)
• Others recommended: cold therapy, relaxation techniques, music,massage

Question 26

Sleep

Answer 26

Use non-pharmacologic component to improve sleep
– Limit noise (ear plugs)
– Light reduction (eye shades)
– Avoid sleep disruption

• Do not use Propofol to promote sleep
  – Unable to make recommendations for dexmedetomidine or melatonin
  to promote sleep
• Consider assist-control over pressure support at night to
  improve sleep in appropriate (ventilated) patients

Question 27

Post Arrest Targeted Temperature Management

Answer 27

1. Continuous monitoring of core temperature in comatose
   patients after ROSC.
2. Actively prevent fever (T < 37.7oC) with antipyretics and
   cooling blankets set to 37.5oC.
3. Actively prevent fever for at least 72 hours.
4. Do not actively rewarm patients with mild hypothermia to
   achieve normothermia after ROSC.

Question 28

Neurologic Outcomes

Answer 28

● Brain Death:
○ Irreversible cessation of cerebral and brainstem function

● Persistent Vegetative State:
○ Severe anoxic brain injury progressing to a state of wakefulness without
awareness
○ No purposeful responses, sleep wake cycles intact

● Minimal Conscious State:
○ Limited interaction with environment with visually tracking +/- simple commands
○ Intelligible verbalization or sometimes yes/no but not always appropriate

● Locked In:
○ Retained alertness, cognitive abilities, can move eyes and blink voluntarily,
paralysis of the limbs and oral structures

Question 29

Criteria for Determination of Death

Answer 29

• Death = Permanent cessation of brain function
  – Absence of consciousness
  – Absence of brainstem reflexes
• Death caused by cessation of blood flow to brain, due to:
  1. Circulatory Arrest – Death by Circulatory Criteria (DCC)
  2. Devastating brain injury – Death by Neurological Criteria (DNC)
• Donation can occur after follow:
  1. DNC
  2. DCC
• Controlled circumstances – WLSM, MAiD
• Uncontrolled circumstances – i.e. unanticipated arrest. NPOD

Question 30

Donation after Death by Circulatory Criteria (DCC)

Answer 30

• DCC = absence of extracranial circulation leads to permanent absence of intracranial circulation
• Use invasive arterial BP and continuous ECG for monitoring
  – Don’t use other monitoring of circulation – i.e. Echo, palpation, US
• Absence of circulation when pulse pressure < 5mmHg
• Observation time after cardiac arrest to confirm permanence
  – 5 minutes in controlled circumstances (WLSM, MAiD)
  – 10 minutes in uncontrolled circumstances

Question 31

Death by Neurologic Criteria (DNC)

Answer 31

3 pre-requisites before conducting DNC assessment
1. Mechanism causing devastating brain injury leading to death
2. Neuroimaging to support cause
3. Absence of confounders
– Temperature: core ≥ 36 celsius (rectal, esophageal, bladder, arterial, bladder, central venous)
– Time: wait ≥ 48hrs after arrest (unless imaging shows devastating injury)
– Drugs: Wait 5 half lives if drug is known (e.g. sedatives, neuromuscular blockers,
– Shock: Must be resuscitated appropriately (i.e. not un-resuscitated)
– Metabolic disorders*: Na 125-159, PO4 >0.4, Glucose 3-30, pH 7.28-7.5, PaCO2 < 60, Urea
< 40 (if available), Cr < 400, bilirubin < 100

“If these derangements cannot be corrected and are judged to be potentially contributing to the loss of
brain function, ancillary investigation should be considered. ”
– Severe weakness: myasthenia, ALS, spinal cord injury
– Decompressive craniectomy

Question 32

DNC Assessment

Answer 32

3 criteria to confirm DNC

1. Absence of consciousness – no wakefulness or response to stimuli
2. Motor examination

• Central stimulation (supra-
  orbital notch)
• Peripheral stimulation

2. Absence of brainstem function – no brainstem reflexes
3. Brainstem Reflexes
   - Pupillary response to light
   - Corneal response
   - Cough
   - Gag
   - Vestibulo-ocular (cold calorics.
   Don’t use oculo-cephalic – dolls
   eyes)
4. Absence of capacity to breathe
5. Apnea testing
   - No respiratory effort
   - pH < 7.28, pCO2 > 60 AND
   pCO2 increase ≥20

DNC: Ancillary Testing

• Required if DNC examination cannot be completed (i.e. confounder cannot
  be reversed, trauma to one eye prevents pupillary/corneal/vestibulo-ocular reflex testing)
• Ancillary tests used to support theory of cessation of brain function
• Several modalities can be used
  – CT angiography (CTA)
  – CT perfusion (CTP)
  – Transcranial Doppler
  – Radionuclide lipophillic perfusion study

Question 33

Management of Neurological Injuries

Answer 33

Types: traumatic brain injuries, subarachnoid hemorrhages, stroke, hypoxic injuries, etc.
Principles of ICU management (Neuro lecture for specifics):
* Intubation for airway protection (if GCS < 8)
* Keep head of bed > 45 degrees
* Target normothermia, euglycemia, normocapnia
* Preferentially use normal saline for fluid management to avoid significant sodium
shifts and avoid hyponatremia
Increased ICP management: (in addition to above)
* Hypertonic 3% saline (250 cc bolus) or mannitol (0.25 – 1 g/kg/dose, may repeat
every 6-8 hrs)
* Hyperventilation (target CO2 of 26 – 30)
* ICP monitoring (goal to keep ICP < 20 mmHg)
* Increase sedation (make sure airway is secured)
* Blood pressure control (to maintain cerebral perfusion pressure > 60)
* Avoid restrictive neck taping or excessive rotation/flexion of the neck
* Treat seizures with anticonvulsant therapy if suspected
* Surgical consultation for consideration of EVD placement (if hydrocephalus) or
decompressive craniectomy

Question 34

Tox Quick Approach

Answer 34

• History:
  – What did the patient take? How long ago? How much?
• Co-ingestions (EtOH? ASA? Acetaminophen? Toxic alcohols?)
  – Environmental exposures : Carbon monoxide risk factors
  – Past Medical History, Meds, Allergies, Social
• Physical: look for toxidromes
  – Vitals, GCS, capillary blood glucose
  – Pupils (mydriasis, mioisis)
  – Neuro (Reflexes, clonus, rigidity)
  – Skin (dry, sweating, hot)

Question 35

Management- acute tox

Answer 35

• ABC, IV access, Continuous Cardiac Monitors, O2, Foley
• C-collar if unwitnessed LOC
• Consider – Dextrose, oxygen, naloxone, thiamine
• Tox specific treatment (see next slide)
  – Decrease Absorption
  – Increase Elimination
  – Antidotes
• Call Poison Control (ALWAYS!)
  – And Psychiatry if intentional overdose, once pt is stable and talking
  – And Addictions medicine if applicable

Question 36

TCA Overdose-presentation and dx

Answer 36

Signs and Symptoms * CVS – Hypotension – Arrhythmias * Sinus tach * VF/VT as QRS
widens

• CNS – Dec LOC, agitation,
  psychosis, delirium
  – Seizures

Anticholinergic Toxicity
RED as a beet
DRY as a bone

urinary retention

MAD as a hatter
sedation, confusion,
delirium, hallucination

BLIND as a bat (mydriasis)
dilated pupils that
DON’T respond to light

HOT as a desert
hyperthermic
STUFFED as a turnip

absent bowel sounds
SEIZURES (since acts on GABA)

TCA serum levels are not helpful
– Urine tox can detect TCA use, but beware of false positives
(carbamazepine, diphenhydramine, cyclopenzaprine, quetiapine)
* Would expect to see a respiratory acidosis from decrease LOC
* ECG is very helpful

Diagnosis is made based on:
1. History of ingestion or TCA use
2. Physical findings of anticholinergic toxidrome
3. Characteristic ECG findings (see next slide)

Question 37

Treatment if TCA OD

Answer 37

• ABCs, IV, O2, Monitors, Foley, Acute care area, Poison control
• Decontamination
  – Can consider activated charcoal (1g/kg, max 50g) if present within 1-
  2hours unless they have a decreased LOC, gut perforation, bowel
  obstruction
• No increased elimination
• No antidote
• DO NOT use Physostigmine to counteract anticholinergic toxicity
  (will worsen cardiac instability, increases risk of cardiac arrest)

Symptom Specific Management

LOC
– GCS 8, intubate
– Agitation: benzodiazepines (Ativan or diazepam at 5 – 10 min intervals)
– Seizures
* Start with Ativan or diazepam, add midazolam infusion if refractory
* Then propofol infusion if refractory
* Then Barbiturates
* DO NOT USE PHENYTOINà Enhances Cardiac Toxicity

• Hypotension
  – NS or Na Bicarb bolus (up to 30ml/kg)
  – Norepi or phenylephrine if refractory
  – Consider hypertonic saline boluses 100 mg IV if refractory despite vasopressors

Question 38

Treatment of Arrhythmias TCA OD

Answer 38

• Wide complex (ventricular) tachy OR prolonged QRS > 100
  – Na Bicarb 1-2mEq/kg IV àif QRS narrows start infusion (3amps in a bag of
  D5W) at 250ml/h
  – If fails, give magnesium sulfate
  – If fails, lidocaine (class IB) 1.5mg/kg bolus then 1-4mg/min
• Class IA, 1C, and III anti-arrhythmic are C/I
  – If fail and unstableà lipid emulsion, VA ECMO
• Sodium Bicarb
  – Indication
• QRS>100, ventricular arrhythmia, or hypotension
  – Goal pH 7.50-7.55
  – Bolus 1-2 amps then run as an infusion at 250ml/h

Question 39

Toxic Alcohols- presentation

Answer 39

Ethylene Glycol
Found in Antifreeze, wiper fluid, cleaners, fuels, moonshine, solvents, hand sanitizer

-Decreased LOC
-Frank hematuria, flank pain, oliguria
-HypoCa

PE -Cranial Nerve palsies
-Tetany

Methanol

-Decreased LOC
-Retinal injury leading to blindness

-Afferent pupillary defect
-Mydriasis (dilation)
-Retinal sheen
-Hyperemia of the optic disc

Labs -Classically high AG and OG *see next slide
-Lytes, Creatinine and Urine R&M
-ECG (Watch QTc for ethylene glycol–> hypoCa -Prolonged QT)

Question 40

Treatment-Toxic Alcohols

Answer 40

ABCs, IV, O2, CCM, Foley, Monitored setting
* Decontaminate
–No role (can try NG aspirate if within 60min)
* Enhanced elimination
–Acidemia allows toxic metabolites to penetrate end-organ
tissue, so give bicarb!
–Give 1-2meq/kg then set up an infusion at 150-250 cc/h
– The goal pH=7.35

-Inhibition of alcohol dehydrogenase
– Inhibition of alcohol dehydrogenase blocks degradation of the parent
alcohol into its toxic metabolites
– Fomepizole or ethanol with:
* Folic acid 50 mg IV q6h for methanol
* Thiamine 100 mg IV and pyridoxine 50 mg IV for ethylene glycol

– Indications
* Serum methanol >6.2mmol/L or ethylene glycol >3.2mmol/L OR
* Documented recent history of ingestion of toxic amounts of methanol or ethylene glycol
and an osmolar gap>10 OR
* Suspicion of ingestion and 2 of the following:
–pH <7.3 OR Bicarb <20 OR OG>10 OR urine oxalate crystals

Hemodialysis
– This is the definitive therapy
– Will clear both the alcohol and their toxic metabolites
– Indications for HD - any 1 of…
* End organ dysfunction
(eg. Coma, Seizure, Visual defects, Renal failure)
* pH≤7.15
* Persistent metabolic acidosis
* High AG metabolic acidosis
* Very high level of parent alcohol

• No antidote

Question 41

A quick word on the other alcohols….

Answer 41

• Ethanol
  – Intoxication level is 4-10
  – We can account for ethanol in Osmolar gap calc:
  Osmolar gap=Sosm-CalcOsm
  Calculated Osm=2Na+gluc+bun+(1.25xEtOH)
• Isopropyl alcohol
  – Treatment is just supportive

Question 42

Salicylate Toxicity-presentation

Answer 42

Early Findings
(1-2h post-ingestion)

-Tinnitus
-Nausea, vomiting
-Hyperventilation
-Fever

Late Findings

-Coma/seizures
-Non-cardiogenic pulmonary edema
-Arrhythmia
-Thrombocytopenia
-AKI

Salicylate level
– Toxicity with serum levels greater than 2.9-3.6mmol/L
– Order levels q 2-4 hours
* ABG/VBG
– Respiratory alkalosis - direct stimulation of the resp centre
– Anion gap metabolic acidosis -uncoupling of oxidative phosphorylation
– Common to see a mixed acid-base disturbance with 2 primary problems
– If concurrent respiratory acidosis, consider:

– Acute lung injury
– CNS depression
– Mixed overdose

Question 43

Salicylate Toxicity-Treatment

Answer 43

Decontaminate
* Activated charcoal (1g/kg up to 50g PO/NG) within 2 hours
(or longer if enteric coated or bezoar)
* Can consider whole bowel irrigation (ask Poison control)

Enhanced Elimination
* Alkalinize the urine and blood
– Aim to have a blood pH 7.4-7.5, do not go above 7.55 and urine pH 7.5-8
– Give 1-2mEq/kg IV bicarb then start an infusion at 250ml/h
* Watch K, Na and Ca
– Correct hypokalemia before alkalinization
* In hypokalemia, the renal tubules will absorb K and excrete H+, preventing alkalinization

Enhanced Elimination

– Salicylate Levels >7.2mmol/L
– Hypoxemia requiring supplemental O2
– A change in mental status
– Renal failure (and salicylate level >6.5mmol/L)
– Progressive deterioration of vital signs
– Severe acid –base or electrolyte imbalance despite
appropriate treatment (pH <7.2)
– Hepatic compromise with coagulopathy
– Volume overload preventing admin of sodium bicarb

Question 44

Acetaminophen Toxicity

Answer 44

Toxicity:
* Likely to occur with single ingestions > 250 mg/kg or over 12g in 12 hour period
* Severe liver toxicity occurs in doses greater than 350 mg/kg
(AST and ALT > 1000) unless appropriately treated

Signs and Symptoms:
* Stage I (0.5 0 24 hrs) – nausea, vomiting, diaphoresis, pallor, lethargy, malaise, or
asymptomatic
* Stage II (24-72 hrs) – RUQ pain, jaundice, oliguria, rise in ALT & AST
* Stage III (72 – 96 hrs) – jaundice, confusion (hepatic encephalopathy), marked
elevation in AST & ALT, prolonged INR/PTT, bili > 68, hypoglycemia, lactic acidosis,
hyperammonemia, bleeding diathesis, renal failure
* Stage IV (96 hrs – 14 days) – recovery phase where hepatic necrosis may develop

Question 45

Treatment Acetaminophen Toxicity

Answer 45

Acetaminophen levels
should be drawn 4 hours
after ingestion ideally and
plotted on modified
Rumack Matthew
nomogram
* Not applicable in repeated
supratherapeutic ingestion

NAC protocol indications:
* Serum concentration above treatment line on RM nomogram
* Single ingestion > 7.5 g (150 mg/kg)
* Unknown time of ingestion + concentration > 66 umol/L
* History of ingestion + liver injury
* Delayed presentation (>24 h) with evidence of liver injury
* Consider in acute undifferentiated liver failure

Target INR < 1.3, ALT < 100
U/L, acetaminophen < 132 before stopping

Mild flushing/urticaria – continue infusion with
antihistamine/steroid.

Question 46

Assessing Risk of Hepatotoxicity in Acetaminophen Toxicity

Answer 46

If ANY of the following occur:
* Ingestion of greater than 7.5 – 10 g in 24 hours
* Ingestion of greater than 4g in 24 hours AND increased risk of
susceptibility to hepatotoxicity (ie. Chronic ETOH use)
* Abdominal pain, liver tenderness, nausea, vomiting, jaundice
* Supratherapeutic serum acetaminophen concentrations
(> 130 mmol/L)
* Elevated ALT or AST (> 50 U/L) on presentation

Question 47

Carbon Monoxide poisoning Treatment

Answer 47

Sample scenario:
“Confused elderly man comes with headache in
winter from remote cabin with normal BP and
unexplained AGMA lactic acidosis …”
Treatment
1. Remove source, move to well ventilated area
2. 100% FiO2 – HFNC or Intubate (i.e. Coma)
* COHb half lives
– Room air: 250-320 minutes
– 100% FiO2: 90 mins
– Increased atmospheric pressure (2.5ATA): 20 mins
1. Consider Hyperbaric O2
– Conflicting evidence – expert consensus
– Potential indications
* If within 6h of exposure is best
* CoHb > 25%
* Seizure or Coma
* Syncope
* Pregnant woman with >15% COHb or Fetal distress in
pregnancy

• If they are suffering CO poisoning after a smoke
  inhalation, treat for concurrent cyanide poisoning

Question 48

Cyanide (CN) Poisoning- Treatment

Answer 48

Treatment
1. Supportive
* Control airway (intubate), 100% FiO2
* Crystalloids and vasopressors for shock
* Bicarb for acidosis
2. Hydroxycobalamin
* Binds CN forming cyanocobalamin -> Urine
* 5g IV over 15mins, repeat x1 if needed
* A/E:anaphylactoid reaction, HTN
3. Nitrites
* MetHb higher affinity for CN than Hb -> induce
methemobloginemia
* Pre-hospital: amyl nitrate
* Na nitrite 3% 10ml over 2-4mins IV
* A/E: Hypotension, hypoxia (don’t give if COHb)
4. Sodium thiosulfate
* Enhances renal excretion
* 150-200mg/kg over 10-20mins
* A/E: hypernatremia
1 and 2 are mainstay of management. 3 and 4 only
if hydroxycobalamin unavailable

Question 49

Methemoglobinaemia Treatment

Answer 49

• Early recognition
  – Stop offending agent
  – Draw MetHb level, ABG
• Supportive
  – Coma: Airway protection, intubation
  – Cyanosis: Provide high-flow oxygen (if responds then unlikely MetHb)
• Methylene blue
  – 1-2mg/kg, repeat at 30 mins if no response
  – Relative Contraindications: G6PD deficiency (may cause hemolysis), serotonin syndrome
  (serotonergic)
  – No clear cut off for when to use - potentially if symptomatic or MetHb > 30%. Liaise with poison
  centre.
• Cimetidine – can be used for dapsone induced MetHb
• Ascorbic acid – Theoretically can be used if no response to methylene blue,
  although not typically used

Question 50

Lithium Overdose

Answer 50

Pharmacokinetics
● Lithium does not bind to proteins and is
distributed freely throughout the body
● Therapeutic window 0.6-1.2mmol/L
○ However, can get sx of overdose in
therapeutic window as well!

S&S
● GI-n/v/diarrhea is the earliest symptom CVS-T
wave flattening in the precordial leads, QT
prolongation, brady, unmask Brugada
● Heme-Increases WBC (15-20)
● CNS (late finding)-Dizzy, lightheaded,
orthostatic, lethargy, slurred speech, ataxia,
tremor, myoclonic jerks
Diagnosis
● Li levels should be obtained on presentation +
serially after ingestion of sustained release.

Treatment
1. Decontamination-Li is NOT absorbed by activated
charcoal. Can try whole bowel irrigation if there is:
- Sustained release ingestion
-Symptomatic patients
-Unknown amounts ingested
->40 mg/kg ingested, or <6h from ingestion
-Increasing lithium levels

2. Enhanced elimination-IHD is indicated for patients with

-Arrhythmias
-seizures or severely abnormal mental status
-serum lithium levels ≥5mmol/L
-serum lithium levels ≥4mmol/L w/ Cr >176umol/L

3. Restore fluid balance (NS at 1.5 maintenance)
4. Do NOT enhance elimination with forced diuresis -Get
   a small increase in elimination but then get salt/water
   depletion that leads to increased Li retention

Question 51

Organophosphate Poisoning- treatment

Answer 51

A/B
* 100% FiO2
* Intubate (constant reassessment of ability to
protect airways and resp insufficiency from
diaphragmatic weakness)
* Avoid succs as it is cleared by
acetylcholinesterase (which is inhibited by
OP)
* Can use roc, but will need high doses
C-Usually hypotension and brady-fluids
* Can cause HTN and Tachy with sympathetic
stimulation

D-Decontaminate-Wash patient, medical personnel
should wear full protection, be in well vented area

Antidote

• Atropine
• Atropine competes for acetylcholine, preventing
  cholinergic activation
• Fixes muscarinic symptoms
• Indications:
• Miosis
• Excessive sweating
• Hypotension
• Resp distress (poor air entry, bronchorrhea,
  bronchospasm/wheeze)
• Bradycardia
• Start at doses 2mg IV, double dose q3-5 minutes until
  pulmonary signs and symptoms are alleviated
• Once atropinization, start infusion 10-20% of total
  dose required to atropinize patient per hour (to
  max 3g/h)
• S/E
• Agitation, urinary retention, ileus, hyperthermia,
  tachy causing MI if pre-existing heart disease
• Tachy is NOT a C/I to cholinergic toxicity-may be
  tachy from hypoxia…which will resolve!

Question 52

Acute Desaturation/Hypoxia in ICU

Answer 52

1. Check the ventilator – all connections intact? Is the oxygen connected?
2. Disconnect ETT from vent
   àBag-ventilate – is there increased resistance?
   – AIRWAY = blocked ETT, bronchoconstriction
   – Airspace = Blood, Pus, Water, Cells, Protein
   – Pleura = Pneumothorax, effusion, hemothorax
   – Vascular = Pulmonary Embolism
3. Deep suction
4. Auscultate, check that trachea is midline**
5. Check other vitals – hypotension, tachycardia = could it be hypoperfusion?
6. Chest X-ray à check ETT placement (right mainstem intubation?)
7. Review history: New Line? (pneumo]) New blood? (TRALI/TACO) ACS/bolus?
   (acute pulmonary edema) Off DVT proph? (PE) Fevers? (VAP)

Question 53

Gas Trapping

Answer 53

Aka auto-peep or intrinsic-peep
* What is it
– Occurs when the expiratory time on the vent is shorter than the actual
time needed to fully deflate the lungs
* How to detect
– Do an end-expiratory breath hold

Signs and Symptoms
* Increased work of breathing
* Wheeze
* Increased chest distension
* Decreased chest expansion
* Bilateral decreased air entry
* Increased CO2
* Increased intrathoracic pressures
– Dec venous return and
hemodynamic instability

Causes

• Machine factors
  – Kinked ETT
  – ETT clogged by sputum
  – Patient biting on ETT
• Vent settings
  – High RR
  – High I:E ratio
• Patient
  – Bronchospasm
  – Increased RR

Vent changes
* Need long I:E ratio (1:4 or 1:5) (i.e. give
more time to exhale)
* Lower the resp rate
* Decrease the Vt
* Apply PEEP to counter the increased work
of breathing
* Last line measures
– Disconnect from vent and press on chest
– Heliox
– ECCOR2
– High frequency oscillation