RC Respirology Flashcards
What is an abnormal pulsus paradoxus?
> /10 mmHg between inspiration and expiration
DDX for abnormal pulsus
Tamponade
Asthma exacerbation
COPD exacerbation
Constrictive pericarditis
PE
Morbid obesity
Effects of hyperoxia on respiratory system
Hypercapnia, CO2 retention
Direct O2 toxicity from ROS - interstitial and alveolar edema due to leaky capillary endothelium, hyperoxic bronchitis
Absorption atelectasis
Instability of units with low V/Q ratios causing shunt
Retinopathy of prematurity (not respiratory)
Benefits of HFNC in patients with respiratory failure
Heated and humidified - reduces WOB, allows secretion clearance
Provides PEEP - decreases WOB, prevents atelectasis
Provides PEEP - prevents atelectrauma
High flows - washours out upper airway dead space, reliable FiO2 delivery due to minimal entrainment, decreases upper airway resistance
Who should have extubation to HFNC
Extubation of surgical patients
Extubation of non surgical patients at low/mod risk of extubation failure
Sources of physiological shunt
Bronchial arteries emptying into pulmonary veins
Thebesian veins emptying into left ventricle
Functional shunt: V/Q <1
Limitations/assumptions of the shunt equation
CcO2 = CAO2 = perfect diffusion between alveoli and capillaries
We assam PcO2 = PAO2 (from alveolar gas equation)
We assume that SaO2 = 1
Differences between central and mixed venous gas
ScvO2 = central line, normal is 65-70% (>80% (high PaO2 or left to right shunt) vs <65% (impaired tissue oxygenation))
SvO2 = pulmonary artery, normal is 60-65%
basically ScvO2 should have higher O2 because it doesn’t get the low O2 blood from the SVC
DDX for high O2 Extraction Ratio
Sepsis, fever
Shock
Seizures
Hyperthyroidism
Hypoxemia
Anemia
DDX for low O2 Extraction Ratio
Hypothyroidism
Hypothermia
Sedation
Mitochondrial dysfunction in sepsis
Cyanide toxicity
Hyperbaric oxygen
Hyperoxia
Polycythemia
Impact of Positive Pressure Ventilation on the heart
Decreased preload to RV and LV
Increased afterload to RV, decreased afterload to LV
Overall, decreased SV and CO, decreased cardiac work
Impact of Positive Pressure Ventilation on dead space
Increased zone 1 respiration with high V/Q areas
Increases both alveolar and anatomic dead spaces
Lung volume is raised resulting in radial traciton on the airways increasing volume of anatomic dead space
Raised airway pressures divert blood flow away from ventialated regions causing high v/q ratio or even unperfused areas
Most common in uppermost regions of the lung.
Capillaries pressures fall below airway pressure and they collapse
Different Ventilator modes and settings
Assisted= mandatory patient triggered
Controlled= mandatory Time/volume triggered
Supported= spontaneous (patient triggered) flow terminated
PCV- you set inspiratory pressure. Volume will vary
VCV - you set TV peak flor and flow pattern. Pressure will vary
PSV - (Spontaneous Pressure Support Ventilation) al breaths supported (whatever TV the patient generates)
ASV - set EPAP, PS mirrors ventilation (higher at low flow periods)
SIMV (synchronized Intermittent Mandatory Ventilation- set RR with either Volume or PRessure target), patient can do what they want in between the set breaths
APRV - airway pressure release ventilation - Bilevel ventilation where you set PEEP and plateau. rescue therapy for ARDS, helps with recruitment to help with oxygenation, spontaneous breathing (increased WOB), risk of volutrauma, risk of DH
What are PIP, Pplat, driving pressures, delta P, airway resistance
PIP: (peak inspiratory Pressure) P to overcome resistance (airways, ETT) and lung elastic properties, target <35
Pplat: P to distend alveoli, reflects compliance, target <30 cmH2O
Driving pressure: Pplat - PEEP
Delta P: PIP-Pplat, reflects resistance: both elevated within 5 means reduced lung compliance or chestwall/diaphragm/pleural. Only Elevated PIP means increased airway resistance
Airway resistance: PIP-Pplat/Flow
Types of Respiratory Maneuvers
Inspiratory hold → Pplat
Expiratory hold → intrinsic PEEP
Only in volume control
DDx of reduced peak inspiratory pressure
Air leak
Hyperventilation
What do changes to the volume pressure curve represent on a ventilator?
Slope = static compliance
Width = dynamic compliance and airway resistance
Bird beaking = over distension = turn TV down
What are Static and dynamic compliance on a ventilator?
Static: chest wall and lung tissue compliance
Dynamic: chest wall, lung tissue compliance and airway resistance
what is the DDX for sudden increase in mechanical ventilation in critically ill patients
Increased dead space - collapsed lung, mucous plug, mainstem intubation/dislodged
Increased demand - sepsis, fever
Pain, anxiety
Decreased compliance
Benefits of PEEP
Improve oxygenation -improve atelectasis/VQ, moves peripheral edema into interstitium
Lessens required FIO2 and O2 toxicity
Improves lung compliance - think of equation Compliance = delta V/Delta P
Prevent atelectrauma
Decrease WOB
Decrease LV work/afterload
Mechanisms of hypotension with PEEP
Reduced preload to RV and LV
Increased RV afterload, RV failure
Reduced LV compliance
Consequences of autoPEEP
Barotrauma
Dynamic hyperinflation
Decreased lung compliance
Decreased tidal volumes and minute ventilation
Increased WOB
Cardiac - decreased preload, decreased CO, increased PVR
Neuro - increased ICP due to reduced central venous return
DDX of increased autoPEEP
Increased airway resistance e.g. bronchospasm, kinked tube, clogged tube
Increased tidal volume
Increased respiratory rate
Increased I:E time or ratio
Decreased expiratory time
Increased inspiratory time
Decreased inspiratory flow rate
Treatment of autoPEEP
Treat bronchospasm or reason for resistance
Decrease respiratory rate
Decrease tidal volume
Decrease I:E ratio
Increase expiratory time
Increase inspiratory flow rate
Increase or add PEEP **
Permissive hypercapnia ** (reduce demand)
Sedation and paralysis if dyssynchronous, treat anxiety/pain ** (reduce demand)
Relative Contraindications to PEEP
High ICP
Hypotensive
RV failure
Right to left shunt
Barotrauma
Bronchopleural fistula
Causes for difference between PaCO2 and PETCO2
PETCO usually lower
Due to anatomical dead space
Causes of increased PETCO2
ROSC (increase by 10-20)
Effective CPR
Hyperthyroidism
Hyperthermia
Fever, sepsis
Hypoventilation
Bronchial intubation
Causes of decreased PETCO2
Hypotension, shock
Cardiac arrest
Hypothyroidism
Hypothermia
Hyperventilation
Apnea
Extubation, sudden kink
Ventilatory parameters for obstructive lung disease
Mode:volume (but no data > pressure)
FiO2: SpO2 88-92
PEEP: minimal, 5
RR: 10-12%
Vt: <8 mL/kg PBW
I:E target: 1:5
Permissive hypercapnia (pH >7.2, pCO2 <90)
Ventilatory parameters for ARDS
Mode: volume
FiO2: 88-95%
PEEP: Modest
RR: 25-35
Vt: 4-6 mL/kg/PBW
I:E target: 1:2
Permissive hypercapnia (pH >7.2)
Pplat </30 (mortality benefit)
Driving pressure </15 (mortality benefit)
Physiological benefits of permissive hypercapnia
Reduced autoPEEP
Reduce barotrauma
Decrease WOB
Rationale for permissive hypercapnia in ventilation
Obstruction - prevent autoPEEP
Restriction - low tidal volumes
Possible complications of permissive hypercapnia
Increased ICP
Decrease seizure threshold
Arrhythmias, irritable myocardium
Increased PVR 2/2 acidosis
Decreased placental flow
In addition to ventilator settings, what else do you have to take into consider in Mechanical Ventilation asthma?
Not opioids for sedation 2/2 histamine
Large ETT to reduce resistance
Consider inhaled isoflurane
Consider heliox
Consider Hodder’s maneuver
Consider ECMO
Characteristics of Heliox
Low density
Density is important in turbulent flow (large airways)
Viscosity is important in laminar flow (smaller airways)
Importance of the Winters Equation
Tells you what CO2 should be if appropriately compensated
Use this to determine goal Ve
Berlin’s criteria for ARDS - NOTE NEW CRITERIA!
Within 7 days of a known insult or worsening symptoms
Non cardiogenic pulmonary edema, not due to intravasc volume overload
Bilateral pulmonary opacities not explained by nodules, atelectasis, effusion, etc. (CXR OR CT, or lung ultrasound by trained professional) Seen in 2 quadrants (bilat or unilat)
Severity grading on PEEP 5
PaO2/FiO2<300
SpO2/FiO2 <315
Causes of ARDS
Inhalation exposures
Aspiration
Fresh water, salt water aspiration, drowning
Fat embolism
Reperfusion injury
Infections, pneumonia, sepsis
Pancreatitis
Transfusion reaction
Pathology of ARDS
- Early exudative: 1 week, high permeability pulmonary edema, proteinaceous fluid fills alveoli, hyaline membrane formation, pathology shows DAD
- Fibroproliferative: 2 weeks, interstitial inflammation, disordered healing, fibrosis
- Fibrotic: fibrosis, obliteration of normal lung architecture
Image findings of ARDS
Dependent opacities, consolidation
Bilateral, symmetrical
Ways to improve oxygenation in ARDS
Increase PEEP, mortality benefit in mod-severe
Prone positioning, 12hrs/day, PF <150 mortality benefit (It should be administered within 48 hours, evaluated daily and stopped within 48 hrs if possible)
Euvolemia
Steroids in some
Neuromuscular blockade
Inhaled NO
ECMO
Physiological benefits of prone positioning in ARDS
Improve V/Q matching
Improve secretion mobilization + drainage
Decrease compressive effects of heart
Indications for ECMO
PaCO2 >60 for >6 hours
PF <80 for >6 hours
PF <50 for >3 hours
Mechanically ventilated <7 days, BMI <40, age 18-65
Contraindications to ECMO
Disseminated malignancy
Known severe brain injury
Severe chronic organ dysfunction
Severe pulmonary hypertension
Complications of Positive Pressure Ventilation
Hypotension
Barotrauma
VALI
VAP
Airway complications e.g. stenosis, tracheobronchomalacia, fistula formation
Critical illness polyneuropathy, myopathy
Risk factors for barotrauma
High Pplat*
High PIP*
High PEEP*
Low compliance* e.g. ILD, COPD, overload
Maneuvers to reduce risk of barotrauma
Reduce RR
Reduce Vt
Increase expiratory time
Permissive hypercapnia
Increase sedation
Reduce PEEP
Benefits of tracheostomy
Reduced sedation
Phonation
Better secretion management, better mouth care
Allows mobility
Prevents laryngeal injury
Can leave ICU
Acute complications of tracheostomy
Bleeding
Surgical site infection
Dislodgement
Tube is kinged or clogged
Laryngeal nerve damage
Pneumothorax
Chronic complications of tracheostomy
Dislodgement
Trach blockage
Tracheal stenosis
Tracheobronchomalacia
Tracheoesophageal fistula
Tracheoarterial fistula
What is VALI?
Due to volutrauma
Alveolar overdistension
Presents with edema, hemorrhage, loss of compliance
Indicators of readiness to wean
Underlying resp condition resolved or improving/on active treatment
GCS >8
PaO2 >60 on FiO2 requirements <40% on PEEP <8
PF ratio >150
PaCO2 normal
Adequate cough
Not requiring frequent suctioning e.g. <q2 hours
Hemodynamically stable - minimal or improved pressor requirements
Abnormal RSBI (Rapid Shallow Breathing Index)
RR/TV >105
Predictive of failed extubation
Predictors of successful weaning during SBT
RR/VT = RSBI <105
Maintaining adequate ventilation
Maintaining adequate oxygenation
No signs of severe fatigue
Definition of extubation failure
Reintubation within hours-days
Risk factors for extubation failure
Age >65
Underlying cardiorespiratory disease
RSBI >105
Abundant endotracheal secretions
Weak or absent cough
Positive fluid balance in last 24 hours
Respiratory failure was for cardiac origin, PNA, neurological condition
Factors that may limit weaning
Reduced drive from over sedation or neurological problem
Underlying disease not yet resolved
Respiratory muscle weakness, deconditioning
Development of atelectasis, mucous plugging - poor/weak cough
VAP/VALI development
Oversedation
Under Sedation - anxiety, pain
Neuropathy or myopathy from prolonged intubation
Malnutrition - respiratory muscle weakness
Overnutrition - increased CO2 production
Cardiomyopathy, cardiac ischemia
Anemia
Clinical signs of failure during SBT
Anxiety, agitation, diaphoresis
Hypertension or hypotension - not between 90-180
Tachycardia - HR >140, arrhythmia
Tachypnea - RR >35 x 5 mins
Increased work of breathing - accessory muscle use, thoracoabdominal paradox
Fall in O2 (<90%), increase in CO2 - hypoxemia and hypercapnia
Stridor
What causes Right shift in the hb-dissociation curve
Increased CO2 (Bohr effect)
Increased H
Increased temperature
Increased 2,3 DPG
What causes Left shift in the hb- dissociation curve
Decreased CO2 (Bohr effect)
Decreased H
Decreased temperature
Decreased 2,3 DPG
Increased CO
Determinant of PaO2
PAO2 - POI2, PaCO2
Architecture of the lungs
Major determinants of SaO2
PaO2
Temperature
H
CO2
2,3 DPG
DDX for saturation gap
Carboxyhemoglobinemia
Methemoglobinemia
Sulfhemoglobinemia
DDX for lower SpO2 for given PaO2
Nail polish
Pigments, methylene blue
Poor circulation - Raynaud’s, peripheral vascular disease, shock
Hemoglobinemia - e.g. methemoglobinemia, sulfhemoglobinemia, thalassemia, sickle cell anemia, spherocytes etc
Motion or artifact
Technical factors
Clinical manifestations of CO poisoning
Headaches, decreased LOC, personality changes, headaches, seizures
Arrhythmias, cardiac ischemia
Cherry red skin and lips
Treatment options for CO poisoning
Supplemental oxygen
Hyperbaric oxygen
Eucapnic hyperventilation
Indications for hyperbaric oxygen in CO poisoning
Severe end organ sx e.g. MI
CO-Hb >/25%
CO-Hb >/15% if pregnant
Severe metabolic acidosis pH <7.1
Blood gas findings in CO poisoning
PaO2 normal
SpO2 normal
SaO2 decreased
CaO2 decreased
CvO2 decreased
Blood gas findings in cyanide poisoning
PaO2 normal
SpO2 normal
SaO2 decreased
CaO2 normal
CvO2 increased
Treatment for cyanide poisoning
Supplemental oxygen
Hydroxocobalamin
Nitrites
Avoid dialysis
Safe amount of lidocaine to prevent toxicity
5 mg/kg without epi
7 mg/kg with epi
Treatment of lidocaine toxicity
BZD
Lipid emulsion
At what pressure is O2 delivered at in hyperbaric O2?
2.5-3 atm
Contraindications to HyperBaric Oxygen Therapy
Pneumothorax untreated - absolute
Obstructive lung disease - relative
Blebs or bullous disease - relative
Indications for HyperBaric Oxygen Therapy
CO poisoning
Venous or arterial air embolism
Decompression sickness
Medications that can cause methemoglobinemia
Lidocaine, benzocaine
Methylene blue
Metoclopramide
Dapsone
Nitrates
Primaquine
Indications for methylene blue for methemoglobinemia
Levels >30%
Very symptomatic
Indications for intubation in someone with thermal/fire airway injury
Neck, facial burns
Laryngeal injury - Stridor
Tracheobronchial injury - cough, wheezing, melanoptysis
Paryncheal injury
Systemic toxicity e.g. CO poisoning etc
Broad categories for International Classification of Sleep Disorders
Insomnia
Sleep disordered breathing - OSA, CSA, OHS, Nocturnal Desaturation
Hypersomnolence
Parasomnias
Sleep related movement disorders
Circadian rhythm sleep wake disorders
Other
Definition of compliance with Sleep Therapy
4 hrs per night
At least 70% of nights in last month
As per CMA guide, which patients with OSA should not be driving?
Moderate-severe OSA, not compliant
Compliant but involved in MVC where they were at fault - x 1 month until compliance reassessed
Drivers admit to experiencing excessive sleepiness during major wake periods or while driving
As per the Ontario MTO, who should not be driving?
AHI >/30 in treated or untreated
As per CMA guide, which patients with narcolepsy should not be driving?
Uncontrolled cataplexy (on or off treatment) in the past 12 months
Uncontrolled daytime sleep attacks or sleep paralysis in the past 12 months
Generally no long distance commercial driving
For a commercial driver with OSA, what conditions need to be met for them to drive?
AHI <20
On effective treatment
Does not experience excess sleepiness during major wake periods
Which drivers do we screen for OSA?
Everyone should be screened with questionnaires, BMI and studies as needed
Recertified annually
When can commercial drivers be recertified?
PAP - one week, good compliance, good AHI, no sleepiness
Oropharyngeal surgery or trach - one month, good AHI, no sleepiness
Bariatric surgery - six months, good AHI, no sleepiness
Distribution of sleep
N1 - 5%
N2 - 50%
N3 - 20%
REM - 25%
Sleep spindle
Usually in N2
Fast burst 0.5-2s of 12-15 Hz activity
K complex
Usually in N2
Go up first, then down
How much theta waves do you require in N1/N2 sleep?
At least 50% of the epoch
How much delta do you need in N3 sleep?
At least 20% of the time
Other names for N3 sleep
Slow wave sleep
Deep sleep
Features of REM sleep
Low amplitude, mixed frequency
REM atonia → low chin EMG
Rapid eye movements
May see sawtooth waves
Sleep disorders during REM sleep
OSA worsens, CSA improves
Hypovent and hypoxemia in NMD or chest wall disorders (bc loss of accessory muscles during atonia) **
What does a short REM latency suggest? What are the causes of REM rebound?
- Narcolepsy
- REM Rebound
2a. Depression
2b. Medication withdrawal e.g. SSRIs, BZD, alcohol
2c. REM sleep deprivation
2d. Patients undergoing CPAP titration
Causes of REM suppression
SSRIs
Monoamine oxidase inhibitors
Sedative hypnotic drugs, barbiturates
Antiepileptics
Alcohol
Medications stimulate breathing vs suppress breathing
Stimulate: theophylline, acetazolamide, progesterone, thyroid hormone
Inhibit: BZD, barbiturates, gabapentinoids, alcohol
Effect of aging on sleep
Decrease in N3
Increase in N1 and N2
No change in REM
Increased WASO - wake after sleep onset
More arousal
Lower sleep efficiency
Body’s clock shifts earlier
Physiological changes during sleep
Decreased BP, HR, CO (increase in phasic REM)
Decreased RR, VT, VE; RR generally increase in REM
PaCO2 increase 3-5 mmHg
PaO2 decrease 5-8 mmHg; SpO2 decrease 1-2%
Increased upper airway resistance
Minimum requirements for an adequate sleep study
At least 2 hours of sleep
Other normal values (not required): 80% efficiency, <30 mins sleep onset, <90 mins REM onset
Components of a PSG
EEG
EOG
EMG
ECG
Airflow (2)
Respiratory efforts (2)
SpO2
CO2 measurement
Ways to measure airflow
Oronasal thermistor - apnea
Nasal pressure transducer - hypopnea, RERA
Ways to measure respiratory effort measured
RIP belt (respiratory inductance plethysmography)
Esophageal pressure monitoring
Diaphragmatic EMG
When should patients with sleep apnea be followed up on?
Within 4 weeks if high risk
Within 6 months for all others
Who is a level II-IV sleep study appropriate for? What are Contraindications?
Moderate-high pretest probability
Do not suspect other sleep disorders
Do not have other comorbid diseases
Not a titration study
Criteria for moderate-high pretest probability of OSA
Excessive Daytime Sleepiness on most days with 2 of the following:
Snoring
Witnessed apneic episodes
Witnessed choking during sleep
Witnessed gasping during sleep
Diagnosed HTN
Criteria for comorbid/complicated disease
Cardiorespiratory disease
History of stroke
Respiratory muscle weakness, NMD
Suspicion for hypoventilation
Levels of Home Sleep Apnea Testing
II: Full PSG but done at home
III: airflow, effort, ECG, pulse oximetry
IV: pulse oximetry
Requirements that need to be met to be able to do split night study
Moderate-severe OSA based on at least 2 hours of recordings
3 hours available for titration
Definition of apnea vs hypopnea
Apnea: decrease in flow >/90% from baseline x >/10 seconds
Hypopnea: decrease in flow >/30% from baseline x >/10 seconds and accompanied by desaturation of SaO2 by 3% or arousal
Definition of obstructive vs central HYPOPNEAs
Obstructive: snoring, thoracoabdominal paradox, increased insp flattening of nasal pressure compared to baseline
Central: None of the above
Definition of mixed apneas
Starts out as central, then obstructive
Definition of a RERA
Increase in resp effort or flattening of nasal pressure waveform
Event causes arousal or desaturation without meeting appropriate criteria x 10 s
Definition of hypoventilation
Increase in PaCO2 >55 mmHg x 10 mins
Increase in PaCO2 by >/10 mmHg to a value above 50 mmHg x 10 mins
AHI vs RDI
AHI = Apnea + hypopnea/total sleep time
RDI = Apnea + hypopnea + RERA/total sleep time
DDX for EDS
Insufficient sleep
Sleep disordered breathing - OSA, CSA, Narcolepsy, etc.
Neurologic disorders - Parkinson’s, dementia, stroke, MS
Hypothyroidism
Adrenal insufficiency
Anemia, iron deficiency
CKD, renal failure, hepatic encephalopathy
Depression, other psychiatric conditions
Medications, substances
What medical conditions should make you think about screening for OSA?
OHS
Difficult to control HTN
Recurrent atrial fibrillation post cardioversion or ablation
Pulmonary Hypertension
Neurological control of upper airway muscles
Cranial nerves 5,7,9,10,11,12
Risk Factors for OSA
Smoking
Elevated BMI
Family history
Increased age
Male, post menopausal
Increased mallampati score
Tonsil or adenoid hypertrophy
Increased neck circumference
Retrognathia
Micrognathia
Macroglossia
Nasal abnormalities
Low lying palate
Hypothyroidism
Acromegaly
Neuropathy or myopathy
Mechanism of hypoxemia in OSA
Underlying lung disease
Baseline supine SaO2
Low FRC (e.g. obesity)
Duration of apneic/hypopneic episodes
Frequency of apneic /hypopneic episodes
Respiratory efforts in between apneic/hypopneic episodes
Possible complications of OSA
Hypertension
Coronary artery disease
Arrhythmias
Stroke
Heart failure
PH if concomitant OHS
Diabetes
Erectile dysfunction
Depression
Cognitive deficits
MVCs
Screening questionnaires for OSA
Berlin questionnaire
STOP-Bang questionnaire
Diagnostic criteria for OSA
Symptoms/complications + AHI >/5
AHI >/15
Severity of OSA
Mild: >/5 - 14.9
Moderate: 15 - 29.9
Severe: >/30
Positional sleep apnea definition
Supine AHI is at least double non supine AHI
Indications for PAP treatment in OSA
Moderate to severe OSA/ AHI >/15
Mild but symptoms (e.g. EDS), reduced QOL, or hypertension
Critical occupation
Starting pressure and max pressure for PAP
Start at 4 cm H2O
Switch to BPAP 15 cm H2O
Absolute max 20 cm H2O
Min and max pressures for BPAP
Min difference of 4 cm H2O
Max difference of 10 cm H20
Min pressure 4 cm H2O, Max pressure of 30 cm H2O
How to progress titrating to next pressure during titration study
> /2 apneic events
/3 hypopneic events
/5 RERAs
/3 mins snoring
Any of this within a 5 min period
Want >/ 30 mins without breathing event
Criteria for optimal titration
- Optimal: RDI <5 for at least 15 mins, supine sleep observed, REM sleep not interrupted by spontaneous arousals
- Good: RDI </10 or by 50% of baseline RDI if baseline <15, supine sleep observed, REM sleep not interrupted by spontaneous arousals
- Adequate: RDI not </10 but reduced by 75% from baseline or one in which above met but supine REM did not occur at selected pressure
- Unaccepted: None of the above are met
Causes of persistent sleepiness in OSA despite treatment
Non adherence/compliance
Additional medical condition
Additional sleep disorder
Treatment emergent central sleep apnea
Inadequate pressures/not fully controlled
Sleep deprivation/insufficient sleep
Once the other causes are ruled out, how can you treat patients with OSA who still have EDS?
Modafinil
Solriamfetol
Indications for modafinil in OSA
Ongoing EDS despite appropriate treatment
Concomitant narcolepsy
Concomitant circadian rhythm disorder
Certain occupations - shift workers (Temporary)
Methods to increase adherence to PAP therapy
Education
Humidity
Nasal mask vs. full face mask
Treatment of nasal congestion
Polypectomy
Oral appliance
APAP
Benefits of treatment (PAP, OA, MMA)
Improved AHI (all stages)
Improved symptoms: Definitely moderate-severe, unclear mild
Decreased BP: moderate-severe
PAP also improves responsiveness of Afib to tx, ?improve outcome after stroke
Contraindications to APAP
Chronic lung disease e.g. COPD
Previous UPPP (Uvulopalatopharyngoplasty)
Heart failure
Central sleep apnea
OHS/hypoventilation syndrome
Medications causing hypoventilation e.g. chronic opioid use
Neuromuscular disease, chest wall disorder
Treatments for OSA other than PAP
Positional therapy
Oral appliances
Surgery
Hypoglossal nerve stimulation
Weight loss
Indications for oral appliance
Primary snoring disorder without OSA
OSA but intolerant of or unwilling to try PAP (vs. no treatment)
To reduce PAP pressures
Not responsive to CPAP
Complications associated with OA
Dental malocclusion
TMJ pain
Gum pain
Drooling or dry mouth
Surgical options in OSA
UPPP (Uvulopalatopharyngoplasty)
Mandibular advancement
Tonsillectomy, adenoidectomy
Tracheostomy
Reasons to consider tracheostomy for sleep disordered breathing
Intolerant of PAP/high pressures
Cannot achieve control with other treatment
Other abnormalities prevent adequate mask fitting
Other reasons for tracheostomy e.g. craniofacial weakness
Patient preference
Main things you should assess on overnight oximetry
Mean nocturnal saturation (92)
Nadir SpO2
Time spent </88% (5 mins)
% of study spent <90% (20%)
Cutoffs for the Oxygen Desaturation Index
<10
10-30
>30
What is considered an oxygen desaturation for an ODI?
Reduction in SpO2 >/4% for >/10 seconds
Components of insomnia
Difficulty sleeping or maintaining sleep
Adequate opportunities for sleep
Affect functioning
PSG findings of insomnia
Increased WASO
Increased sleep latency >/30 minutes
Reduced sleep efficiency
Reduced sleep time <6-6.5 hours
Medical causes of insomnia
Medications e.g. stimulants, coffee
Psychiatric e.g. depression, anxiety
Neurologic e.g. parkinsons, dementia
Chronic pain, diabetes, HTN, cancer
Classification of central sleep apnea
- Primary central sleep apnea
- Primary central sleep apnea of infancy or prematurity
- CSA with Cheyne stokes
- CSA due to medical disorder without Cheyne Stokes
- 4a. Central insult e.g. tumour, stroke, encephalitis, polio
- 4b. Respiratory muscle weakness e.g. NMD, chest wall disease
- 4c. Renal failure
- 4d. Atrial fibrillation - High altitude periodic breathing
- Treatment emergent central sleep apnea
- Medication or substance related
Medications that can cause CSA
Opioids
Benzodiazepines
Gabapentinoids
Antidepressants
PSG findings in general CSA
Cessation or reduction in ventilatory effort x >/10 seconds
Most common in N1/N2
No effort via RIP belt or diaphragmatic EMG
>/5 central events per hour and >50% of total events
Snoring and desats are less prominent than OSA
PSG definition of Cheyne Stokes Respiration
- > /5 central apneas/hypopneas per hour associated with crescendo,decrescendo breathing in between
- Number is >50% of total apneas/hypopneas
- > /3 consecutive apnea/hypopneas
- Cycle length 40-90 seconds
- Recorded over min 2 hours
Diagnostic criteria of Cheyne Stokes Respiration (CSR)
Symptoms/predisposing condition (HF, neurologic dz, AF)
PSG criteria
Not better explained by other disorder
Cheyne Stokes Respiration vs. Central Sleep Apnea
Cycle length longer >40 seconds
Period of hyperpnea is longer
O2 saturation nadir is more delayed (prolonged circulation time)
Arousals during hyperpnea whereas at end of apnea with CSA
Causes of Cheyne Stokes Respiration
Heart failure
Renal failure
Central disease e.g. stroke, tumors
Medications e.g. sedatives
Pathophysiology of Cheyne Stokes Respiration
- Apnea
- Increased circulatory time
- Increased chemoreceptor responsiveness to CO2
- Increased loop gain - increase in response size
- Apnea
Pathophysiology of other CSAs
TESCA: obstruction relieved, CO2 falls, apnea, high loop gain
Altitude: increased vent due to O2, CO2 falls, apnea, high loop gain
Opioids: hypoventilation
Impact of CSR on HF
Increased mortality
Occurs in 30% of patients with HF
Treatment options for CSR
GDMT of HF, transplantation
Nocturnal oxygen
CPAP therapy - (not the other OSA tx) - BPAP used with caution bc can have same effect as ASV, so avoid
Phrenic nerve stimulation
?Acetazolamide, theophylline [limited evidence]
Benefits of CPAP in CSR
Improve AHI
Improve arrhythmias
May improve LV function
SERVE-HF trial
adaptive servoventilation (ASV) increased all cause mortality in HFrEF <45%
Contraindicated
Management of general CSA
Idiopathic → BPAP-ST, ASV, CPAP
CSA 2/2 hypoventilation → BPAP-ST, ASV > CPAP
Altitude → descend, oxygen, acetazolamide
Treatment emergent → expectant, ASV > BPAP-ST, oxygen, acetazolamide
Biot’s breathing
Hyperpnea mix with apnea
Associated with meningitis
Changes that occur to the sleep architecture with altitude
Increased WASO (Wakefullness after sleep onset)
Increased N1, N2
Decreased N3
Kind of like aging
Mechanism of action of acetazolamide
Carbonic anhydrase inhibitor
Leads to increased bicarbonate excretion
Causes metabolic acidosis, stimulates breathing
Classification criteria for sleep related hypoventilation
Idiopathic central alveolar hypoventilation syndrome
Congenital central alveolar hypoventilation syndrome
Obesity hypoventilation syndrome
Sleep related hypoventilation due to disorder, medication, substance
Cause of congenital central hypoventilation syndrome
Autosomal dominant
PHOX2B gene mutation → loss of RTN
Role of obesity in OHS
Fat produces more CO2
Leptin suppresses respiratory drive
Altered respiratory mechanics
Indications for screening for OHS
BMI >30 with OSA (known or suspected)
BMI >30 with:
- Unexplained dyspnea
- Unexplained awake hypoxemia
- Pulmonary hypertension, signs of it
- Polycythemia, sx of it (e.g. facial plethoraX)
- Elevated bicarbonate
How do you screen for OHS?
Bicarbonate >27
Straight to PaCO2 if high pretest probability
Diagnostic criteria for OHS
BMI >30
Awake PaCO2 >45
Hypoventilation not explained by another disorder e.g. lung disease
(PSG is required to assess for OSA, not absolutely needed for diagnosis but almost always done)
Treatment of OHS
AHI >30 → CPAP first
AHI <30 → BIPAP-ST
No OSA → BiPAP-ST
Weight loss (25-50%), not sole treatment
If admitted with resp failure → BIPAP-ST> APAP until sleep study
Treatments that are associated with HARM in the management of OHS
Oxygen
Respiratory stimulants
Classification criteria for hypersomnolence
Primary
- Idiopathic hypersomnia
- Kleine Levin syndrome
- Narcolepsy
Secondary
- Genetic disorder
- CNS disorder e.g. stroke
- Parkinsons
- Post traumatic
- Metabolic encephalopathy
DDX of Sleep Onset REM Periods
Narcolepsy
Idiopathic hypersomnolence
Due to PD, post traumatic, genetics, central tumour, metabolic
REM rebound:
- Depression
- Medication withdrawal e.g. SSRIs, BZD, alcohol
- REM sleep deprivation
- Patients undergoing CPAP titration
Requirement prior to MSLT
PSG the night before (NOT split night)
>/ 6 hours of sleep on PSG
Withhold REM suppressing medications x 2 weeks
Causes of narcolepsy
Idiopathic
Autoimmune, post infectious
Neurosarcoid
CNS - strokes, tumors
Features of narcolepsy
Sleep attacks during the day and EDS
Hypognogic
Sleep paralysis
+/- cataplexy
PSG/MSLT features of narcolepsy
Mean sleep onset latency </8 minutes
>/2 SOREMPs </15 mins
Loss of REM atonia
Increased N1 sleep
Reduced sleep efficiency, spontaneous awakenings
Drug categories used in treatment of narcolepsy
Selective DA reuptake inhibitor
- Modafinil
Selective NE and DA reuptake inhibitor
- Methylphenidate
- Solriamfetol
Other
- Sodium oxybate: GHB
- Venlafaxine for cataplexy
Conditions that are associated with REM sleep behavior disorder
Parkinsons
MSA, other forms of dementia
Stroke, tumour
Narcolepsy
SSRIs
Treatment for REM sleep behavior disorder
Changes to make sleeping area safe
Melatonin
Clonazepam
Sleep disorders can occur secondary to Parkinsons Disease
Insomnia
Hypersomnolence
REM sleep behavior disorder
Restless leg syndrome
Excessive daytime sleepiness
Examples of opioid related disorders
Central sleep apnea
Hypoventilation
Obstructive sleep apnea
Insomnia
Causes of RLS
Iron deficiency
Pregnancy
Uremia
Parkinson disease, spinal cord disease, prolonged immobility
SSRIs + other meds
Family history
Scoring a PLM (periodic leg movement)
4 consecutive leg movements, 5-90 s apart
The movement is 0.5-10 s, 8mV in amplitude above resting EMG
Diagnosis of PLMD (periodic leg movement disorder)
Periodic leg movement index (PLMI) >/15 per hour
Not explained by another cause e.g. other sleep disorder
Diagnostic criteria for RLS
Uncomfortable sensation in legs/urge to move
Worse when lying down to rest
Worse at night
Made better/relieved by movement
Can cause concern/affect functioning
Treatment of RLS
Iron replacement (ferritin <75 → treat)
Gabapentinoid - pregabalin, gabapentin
DA agonist - pramipexole, ropinirole
DA analogue - carbidopa-levodopa
Opioids
Examples of circadian rhythm disorders
Advanced sleep phase syndrome
Delayed sleep phase syndrome
Irregular sleep-wake rhythm
Criteria for sleep related hypoxemia
SpO2 </88% x 5 mins
No hypoventilation
What innervates the respiratory muscles?
Diaphragm - C3/4/5
Intercostals - thoracic nerves
Abdominal - lumbar nerves
Upper airways - cranial nerves
Levels of neuromuscular disease
Cerebral cortex - stroke, cancer
Brain stem/basal ganglia - stroke, cancer
Spinal cord - trauma, MS
Anterior horn cell - polio, post polio, ALS
Motor nerves - ALS
NMJ - MG, LEMs
Muscles - muscular dystrophy
DDX for elevated Residual Volume
ALS
Mid-low c-spine injury
DDX for low ERV
Obesity
T spine injury
Measures of respiratory muscle strength
Sitting and supine VC
MIP, MEP
SNP
Sniff esophageal pressure
Phrenic nerve EMG
Sniff transdiaphragmatic pressure
Clinical manifestations of ALS
Bulbar symptoms
UMN symptoms: spasticity, hyperreflexia, extensor plantar
LMN: atrophy, fasciculations
Causes of nocturnal hypoxemia in ALS
Concomitant OSA (?CSA, mixed>OSA)
Concomitant hypoventilation - resp muscle weakness
Central hypoventilation (loss of cortical drive to breath)
Underlying lung (e.g. VQ mismatch due to microatelectasis), heart, PVD disease
Upward shift in ventilatory setpoint for PaCO2 by 2-3 mmHg
In hypoventilation due to muscle weakness, what is the progression of symptoms?
REM → NREM → daytime
Loss of accessory muscles in REM
What Monitoring every 2-6 months in ALS
Clinical symptoms
FVC sitting
Supine FVC, MIPS, MEPS, SNPs
Cough hx, PCF
Arterial blood gas/TcCO2 if hypercapnia suspected, or bulbar sx preclude PFT
Nocturnal oximetry/PSG if SDB suspected
Indications to start NIV in ALS
Orthopnea
FVC <50% predicted
Sitting or supine FVC <80% predicted with sx and other indicator of resp muscle weakness
MIPS or SNPS <-40 cm
Daytime PaCO2 >45 mmHg
SDB criteria (see figure)
Best predictors of death at 6 months in ALS
FVC <50% predicted
SNP <-40
MIP <-40
Benefits of NIV in ALS
HrQOL
Some physiological parameters e.g. slowing VC decline, daytime PaCO2
Mortality
What does not yet have a clear goal in ALS treatment?
Respiratory muscle training
Diaphragmatic pacing
Benefits of tracheostomy in ALS
HrQOL
Mortality
Medications should be avoided in myasthenia
Fluoroquinolones
Aminoglycosides
Macrolides
Beta blockers
Procainamide
Checkpoint inhibitors
Iodinated contrast
Treatment of MG
Maintenance - pyridostigmine
Flare - steroids, PLEX, IVIG
Lambert Eaton Syndrome vs. MG?
More proximal muscle weakness
More ANS abnormalities
Less bulbar muscle involvement
Respiratory risks/manifestations associated with GBS
Weak cough
Bulbar dysfunction - Aspiration pneumonitis, aspiration pneumonia
Respiratory muscle weakness - hypoventilation, atelectasis
Sleep disordered breathing
Dysautonomia and bronchospasm
Predictors of respiratory failure in GBS requiring mechanical ventilation
FVC <60% predicted
Onset to admission <7 days
Inability to stand, life arms up, life head off pillow
Presence of facial weakness
Inability to cough
Indications for intubation in GBS
20-30-40 rule (each as separate point) :
VC<20
MIP < -30
MEP < 40
Severe bulbar weakness, cannot protect airway
Respiratory rate sustained >30
Hypoxemia/SpO2 <92%
Hypercarbia >50mmHg
Hemodynamic instability
Treatment of GBS
IVIG, PLEX
What are the types of muscular dystrophy?
BMD (Becker)
DMD (Duchenne)- worse
Predictors of nocturnal hypoventilation in muscular dystrophy?
VC <40% in DMD
VC <60% in other muscular dystrophies
Therefore, screening PaCO2 in those with VC <40%
What are causes of unilateral vs bilateral diaphragmatic paralysis?
…
Most common cause of unilateral hemidiaphragm
Trauma
Idiopathic
Clinical manifestations of diaphragmatic paralysis
Exertional dyspnea
Orthopnea
Bendopnea
Sleep disordered breathing symptoms
Physical examination findings in diaphragmatic paralysis
Paradoxical motion in unilateral
Paradoxical abdominal wall retraction
Diagnostic tests to assess for paralysis
Imaging
Sniff test - ultrasound, fluoroscopy
Sitting and supine test
MIP, SNP
EMG of diaphragm, transdiaphragmatic pressure
Values of MEP/MIP that are concerning for diaphragmatic paralysis
MEP/MIP >1.5 for unilateral
MEP/MIP >3 for bilateral
Complications of diaphragmatic paralysis
Unilateral: occasional hypoventilation, atelectasis
Bilateral frequent hyperventilation, atelectasis, PNA, resp failure
Treatment of diaphragmatic weakness
Unilateral: plication
Bilateral: NIV, pacing
Indications for NIV for NMD in general
- FVC < 80% associated with symptoms such as tachypnea and use of accessory muscles, tachypnea, excessive fatigue, excessive daytime sleepiness
- SNIP < 40 mmHg
- MIP < 60 mmHg
- Daytime hypercapnia PCO2 > 45 mmHg
- Nocturnal saturation < 88% for 5 consecutive minutes
Causes of kyphoscoliosis
Idiopathic
Congenital - spinal/vertebral malformations at birth
Cartilage disorders - Marfan syndrome, EHD
Bony disorders - e.g. osteopenia, osteoporosis
Neuromuscular disorders - e.g. muscular dystrophy, cerebral palsy, Charcot Marie Tooth
Post thoracoplasty
Risk factors for respiratory failure in kyphoscoliosis
Cobb’s angle >110 degrees
VC <45 degrees in surgically untreated (we start monitoring at VC <50%)
Concomitant NMD
Concomitant lung disease
Screening for NIV needs in patients with kyphoscoliosis
Once FVC <50%, we look for hypercapnic resp failure
Treatment of respiratory failure in kyphoscoliosis
Nocturnal NIV +/- O2
Nocturnal O2 if just hypoxemia
Benefits of airway clearance
Secretion clearance
Reduce airway resistance
Improve respiratory system compliance
Prevent atelectasis
Prevent pneumonia
Prevent respiratory failure, prevent need for trach or intubation
Decrease work of breathing
Markers of a weak cough
PCF <270 L/minute
MEP <60 cm H2O
Bulbar dysfunction
Expiratory cough flow tracing - absence of transient increase in expiratory flow (cough spikes)
Secretion management strategies in DMD
Atropine
Scopolamine
Botox injection into salivary glands (submandibular and parotid)
Salivary gland RT
Indications to start a cough support device in NMD
PCF <270 L/minute
Methods to enhance cough in NMD
Lung volume recruitment - glossopharyngeal breathing, bag valve mask
Manually assisted cough
Mechanical insufflation and exsufflation device
Contraindications to lung recruitment in NMD
Unconscious or unable to communicate
Increased ICP, severe TBI
SIgnificant hypotension
Pneumothorax, risk for barotrauma e.g. bullous disease
Hemoptysis
?Cannot protect their airway e.g. severe bulbar weakness
Contraindications to NIV
Loss of consciousness, unable to protect airway
Requiring intubation
Hemodynamic instability
Facial trauma or deformity
Hemoptysis
Upper GI bleeding, perforation or recent surgery
Causes of hypercapnia in patient with NMD on BPAP?
Non compliance or low duration
Pressures are not optimal
Disease progression
Underlying lung disease
Compensation for metabolic alkalosis
Other than BiPAP, other ways to optimize respiratory status in NMD
Cough assist
Secretion mobilization and volume
Daytime mouthpiece ventilation
Smoking cessation
Vaccination
DDX for a lymphocyte predominant BAL pattern
Lymphoproliferative disorders
Connective tissue diseases
Cryptogenic organizing pneumonia
Radiation pneumonitis
Sarcoidosis
Hypersensitivity pneumonitis
NSIP
Drug induced pneumonitis
DDX for an eosinophilic predominant BAL pattern
Infections - fungal, PJP, helminthic
ABPA
Hodgkin’s lymphoma
Eosinophilic pneumonia
Asthma, bronchitis
EGPA
Drug induced pneumonitis
Bone marrow transplant
DDX for a neutrophil predominant BAL pattern
Infection
Bronchitis
Aspiration pneumonia
UIP/IPF
Asbestosis
ARDS, DAD
Connective tissue diseases
What BAL value of lymphocytes is suggestive of granulomatous inflammation?
> 25%
50% is especially suggestive of HP or cellular NSIP
Pulmonary manifestations of drug induced disease
Eosinophilic pneumonia
Hypersensitivity pneumonitis
Organizing pneumonia
Occupational asthma
Diffuse alveolar hemorrhage
ARDS
Drug induced sarcoid reaction, vasculitis and lupus
Bronchiolitis - obliterative bronchiolitis
Fibrosing mediastinitis
Pleural effusions
Pulmonary hypertension
Alveolar hypoventilation
RFs for development of amiodarone induced lung toxicity
Older age
>/2 months of therapy
>/400 mg oral daily
Total cumulative dose
High FiO2 administration
Underlying lung disease
RFs for development of bleomycin induced lung toxicity
Older age
Cigarette smoking
Higher doses (>400 units)
Concomitant radiation
Concurrent cisplatin or cyclophosphamide
High FiO2 administration
Underlying lung disease
RFs for development of nitrofurantoin lung toxicity
Older age
Female
Renal impairment
Medications that cause mediastinal lymphadenopathy
Phenytoin
Methotrexate
Benefits of O2 therapy in ILD
Resting hypoxemia: dyspnea, QOL, ?PH
Ambulatory hypoxemia: Exercise tolerance
DDx for ILD with preserved lung volume
CPFE*
Chronic sarcoidosis*
Chronic HP*
RB-ILD*
LAM
PLCH
Lymphangitic carcinomatosis
Heart failure
Important studies in the treatment of ILD
INPULSIS 1 and 2: nintedanib in ILD
ASCEND: Pirfenidone in ILD
SENSIS: Nintedanib in SSc-ILD
INBUILD: Non IPF fibrosing ILD
PANTHER: Steroids had increased mortality in IPF
Numerical cutoffs for surgical lung biopsy
FVC <55%
DLCO <35%
Possible adverse events post surgical lung biopsy
Prolonged air leak
Pneumothorax, hemothorax, pleural effusion
Infection
Delayed wound healing
ILD exacerbation
Requirement for intubation
Benefits of PR in ILD
Improved dyspnea
Improved QOL
Management of refractory dyspnea in ILD
Breathing retraining
Relaxation techniques
Fans
Body positioning
Low dose opioids
RFs for IPF
Genetics - TERC/TERT/MUC5B
Smoking
Environmental pollution
?Microaspiration
Definitions of familial pulmonary fibrosis
Fibrotic ILD in at least 2 related family members
Conditions are associated with UIP pattern
IPF
Familial IPF
CTD-ILD (SARD- ILD)
Drugs
Asbestosis
Chronic hypersensitivity pneumonitis
Radiographic pattern of UIP + associated level of confidence
Confident - 90%
Probable - 70 to 90
Indeterminate - 50 to 70
Alternative - <50%
Mediastinal findings that would suggest an alternative diagnosis to UIP
Esophageal dilatation
Pleural plaques
Type of biopsy is recommended for IPF
Surgical lung biopsy
Cryobiopsy
Histopathological findings in IPF
Subpleural and/or paraseptal predominance
Patchy involvement
Dense fibrosis with architectural distortion +/- honeycombing
Fibroblastic foci
Absence of features suggesting alternative diagnosis e.g. granulomas
Poor IPF prognostic factors on initial diagnosis
Older age
Male
FVC <50%
DLCO <35%
Greater extent of fibrosis on CT
Hypoxemia at rest or with exertion
Low 6MWT, especially <250 meters
Lower BMI
Certain comorbidities e.g. PH
Poor IPF prognostic factors on follow up
Absolute reduction in FVC by 10%
Absolute reduction in DLCO by 15%
Worsening fibrosis on HRCT
Worsening level of dyspnea
Poor UIP prognostic factors
IPF as opposed to secondary dx
Male
Older age
Heavy smoking
Poor baseline FVC
Poor baseline DLCO
Decline in FVC by 10%, DLCO by 15% over 6 months
CPFE
PH
“Appropriate clinical setting” for IPF?
Male
Smoker
>60 years old
Comorbidities that need to be managed in IPF
GERD
Pulmonary hypertension
Obstructive sleep apnea
Lung cancer
Therapies that improve survival in IPF
Antifibrotics: nintedanib and pirfenidone
Lung transplantation
Benefits of antifibrotics
Improve QOL
Reduce the decline of FVC
Reduce rate of exacerbation and hospitalization
Reduce the mortality
Requirements for antifibrotic initiation/who would benefit
Age >40
FVC >/50
DLCO >/30
Overall prognosis for IPF
Death within 4-5 years of diagnosis
Possible triggers for an IPF flare
Bad disease at baseline - low FVC, DLCO, 6MWD
Infection
Pulmonary embolism
Aspiration
Lung biopsy, bronchoscopy, other procedures
Immunosuppressive therapy
Prognosis of an IPF flare
50-90% in hospital mortality
Median survival 3-4 months
Diagnostic criteria for IPF flare
Acute respiratory deterioration
<1 month in duration
Bilateral GGO with or without consolidation on background of fibrosis
Not explained fully by another cause e.g. volume overload
Criteria for progressive pulmonary fibrosis
Need two of the three criteria
Need them to be occurring in the past year
1. Progression of symptoms
2. Decline in PFTs
- FVC >5% within one year
- DLCO >10% within one year
3. Worsening radiographic progression
DDX of PPFE (pleuroparynchymal fibroelastosis)
Idiopathic
CTD e.g. scleroderma
Chronic HP
Occupational exposures
Chemotherapy
Post HSCT, bone marrow, lung
Imaging findings in PPFE
Pleural thickening
Associated subpleural fibrosis
Concentrated in the upper lobes
Histopathological findings in PPFE
Upper zone pleural fibrosis
Subjacent intra alveolar fibrosis and alveolar fibroelastosis
Radiographic findings of CPFE
Emphysema in upper lobes
Fibrosis (usually UIP pattern) in lower lobes
Notable complications of CPFE
Lung cancer
Pulmonary hypertension
Diagnostic criteria for IPAF
Presence of interstitial pneumonia (imaging or pathology)
Does not meet CTD criteria
Exclusion of other etiologies
At least 2 of: clinical criteria, serological criteria, morphological criteria
Secondary causes of NSIP
Idiopathic
Connective tissue diseases
Drugs/medications
Exposures - hypersensitivity pneumonitis
Infections, including HIV
Radiographic features of NSIP
Basilar, peripheral OR diffuse
Cellular is GGO dominant
Fibrotic is reticulation, traction, bronchovascular bundle thickening +/- honeycombs
Subpleural sparing
Causes of drug induced sarcoidosis
TNF alpha inhibitors
Immune checkpoint inhibitors
HAART
Interferons
Pulmonary manifestations of sarcoidosis
Interstitial lung disease
Progressive massive fibrosis
Alveolar sarcoid
Tracheal stenosis, subglottic stenosis
Lower airway obstruction
Lymphadenopathy
Pulmonary hypertension
Mechanisms of PH in sarcoidosis
Interstitial lung disease
Cardiac disease e.g. cardiomyopathy
PVOD like lesions
Granulomatous inflammation and involvement of vessels → intrinsic sarcoid vasculopathy
Fibrosing mediastinitis
External compression of PA by lymphadenopathy
Portal hypertension
Non pulmonary manifestations of sarcoidosis
Neuro - hydrocephalus, aseptic meningitis, facial nerve palsy, small fiber neuropathy, optic neuritis, encephalopathy, psychosis
Ocular sarcoidosis - anterior uveitis
Cardiac sarcoid - cardiomyopathy, heart block, arrhythmias
Renal sarcoid - nephrolithiasis
Hepatic sarcoid - transaminitis, cholestasis
Hypercalcemia, hypercalciuria
Rashes
Other: spleen, bone marrow
Clinical features that make diagnosis of sarcoidosis highly probable
Uveitis
Optic neuritis
Lofgren’s syndrome
Lupus pernio
Erythema nodosum
Hypercalcemia or hypercalciuria
Bilateral hilar adenopathy
Perilymphatic nodules
Gadolinium enhancement
Parotid uptake
Osteolysis, cysts/punched out lesion
DDX for erythema nodosum
Medications e.g. OPC, TNF alpha inhibitors
Infections e.g. hepatitis B, streptococcus, fungal
Inflammatory e.g. sarcoidosis, IBD
Malignancy
Pregnancy
How does small fiber neuropathy present?
Paresthesias
Numbness
Pain
Autonomic dysfunction - palpitations, orthostasis, sexual dysfunction
How is Erdheim Chester syndrome differentiated from sarcoidosis?
BRAF V600 somatic mutation
CD68 marker on biopsy
Pulmonary manifestations of IgG4 disease
Lymphadenopathy
Nodules or masses
Interstitial lung disease
Fibrosing mediastinitis
Subglottic stenosis, tracheal stenosis
Pleural thickening
Pleural effusions
Diagnosis of IgG4 disease
Serum and BAL IgG4 can be suggestive
Biopsy definitive
Manifestations of cardiac sarcoidosis
Conduction e.g. AV block, BBB, tachyarrythmias, sudden death
Cardiomyopathy
Coronary artery disease from vasculitis
How do you investigate cardiac sarcoidosis?
Cardiac MRI (ATS suggests this first line)
Cardiac PET
Transthoracic echocardiogram
Lab findings in sarcoidosis
Anemia, thrombocytopenia, leukopenia
Hypergammaglobulinemia
Hypercalcemia, hypercalciuria
Elevated rheumatoid factor
DDX for elevated serum ACE
Sarcoidosis
Hypersensitivity pneumonitis
Silicosis
Berylliosis
Asbestosis
Tuberculosis
Coccidioidomycosis
Hodkin’s lymphoma
Gaucher’s disease
Hyperthyroidism
PBC
Imaging findings in sarcoidosis
Perilymphatic distribution of nodules
Miliary nodularity
Lymph node enlargement, can have eggshell calcification
Galaxy sign
Garland sign
Progressive massive fibrosis
Signs of fibrosis - reticulation, traction, volume loss
Alveolar sarcoidosis
Lambda sign
Panda sign (parotid uptake)
Patterns of calcification often seen in sarcoidosis LN
Eggshell
Icing sugar
Cutoffs for CD4-CD8 count for sarcoid
<1 → highly unlikely
>4 → highly likely
Staging criteria for sarcoidosis ( and spontaneous remission %)
I: LN → 90%
II: LN and parenchymal changes → 70%
III: parenchymal changes →20%
IV: fibrosis → 0%
Diagnosis of sarcoidosis
Compatible clinical and radiographic hx
Non caseating granuloma
No other cause of non caseating granuloma
Pathological finding in sarcoidosis
Non caseating granuloma
Discrete, well organized granulomas composed of giant cells, histiocytes and surrounded by lymphoblasts
Granulomas distributed along lymphatics and bronchovascular bundles
Sparse surrounding lymphocytic infiltrate
Difference between HP and sarcoidosis pathology
Non caseating granulomas
Poorly formed, small, loosely arranged
Distribution around bronchioles
Inflammatory infiltrates found at interstitial sites distant from granuloma
Who can forgo lymph node sampling in suspecteted sarcoid?
Heerfordt’s syndrome
Lofgren’s syndrome
Lupus pernio
DDX for non caseating granulomas
Sarcoidosis
Sarcoid like reactions to malignancies
Lymphoma
Hypersensitivity pneumonitis
Berylliosis
IgG4 disease
PLCH
Erdheim Chester disease
GI diseases e.g. PBC, IBD
DDX for usually necrotizing granuloma
Tuberculosis, fungal infections, syphilis
Vasculitis
Rheumatoid nodules
GLILD
Bronchocentric granulomatosis
Sensitivity and specificity of biopsies in sarcoidosis
Endobronchial - 70% sensitive
EBUS - 80% sensitive; highest yield
Transbronchial
RFs for difficult to treat sarcoidosis
African american
Age >40
Progressive pulmonary involvement
Neuro, cardiac, eye involvement
Good prognostic indicators of sarcoid
Erythema nodosum
Lofgren’s syndrome
Stage I disease
Spontaneous improvement or resolution
Benefits of treatment in sarcoid
Improve sx/accelerate remission
Improve imaging
Increases risk of recurrence
Things need to be screened at baseline in sarcoid
CBC
Crea
ALP
Calcium, urine calcium, albumin
ECG
Eye examination
Things need to be followed up on in sarcoid BW
CBC
Crea
ALP
Calcium
Indications for treatment of pulmonary sarcoidosis
Reduced FVC, reduced DLCO
Moderate to severe pulmonary fibrosis
Precapillary pulmonary hypertension
Deterioration in symptoms, lung function or imaging on follow up - as per BTS, DLCO <65% or drop by >/15%, FVC >70%, or drop by >/10%
Indications for treatment of extra pulmonary sarcoidosis
Ocular
Neuro
Renal
Hypercalcemia
Cardiac
Treatment options for sarcoidosis
Glucocorticoids
Methotrexate
TNF-alpha inhibitors
Other: MMF, AZA, lef, JAK inhibitor, rituximab
Immune Suppressive Therapies that have RCT level of evidence in sarcoidosis
Steroids
MTX
Infliximab
How much steroids do you give them in Sarcoid treatment?
Steroid 20-40 x 4-6 weeks (0.25-0.5mg/kg) evidence 20 as good as 40.
Taper 6-18 months
Indications to add on second Immune Suppressive Therapy in sarcoid treatment
Progression of disease despite steroids
Steroid intolerant
Unable to tolerate steroids below 10-15 mg oral daily
Strong patient aversion to steroids
Presence of major comorbidities made worse by steroids e.g. DM, osteoporosis
Agents treat hypercalcemia in sarcoidosis
Steroids
Ketoconazole
Possibly TNF alpha inhibitors
Management of fatigue in sarcoidosis
Exercise training
Inspiratory muscle training
Methylphenidate, modafinil
Treatment of the skin manifestations of sarcoidosis
Topical steroids
Oral steroids, MTX (ok evidence)
Infliximab* best evidence
Treatment of Small Fiber Neuropathy in sarcoid
Symptomatic - gabapentin
TNF alpha or IVIG
Treatment of neurosarcoidosis
Steroids
MTX
Infliximab
Treatment of cardiac sarcoidosis
Steroids
Other IST, but not RCT
Poor prognostic variables in cardiac sarcoidosis that would help management decisions
Age >50
Ventricular tachycardia
NYHA III-IV
LVEF <40%
Echo evidence of abnormal global longitudinal strain
Interventricular septal thinning
Elevated BNP or trop
Cardiac inflammation by PET
Late gadolinium enhancement by MRI
Symptoms that would trigger cardiac work up in Sarcoid
Palpitations
Chest pain
Syncope, near syncope
Tachycardia, bradycardia
New ECG findings
Vision changes that would trigger a vision work up in Sarcoid
Floaters
Blurry vision
Visual field loss
Who would be “suspected” to have PH in Sarcoid?
Fibrotic lung disease
Exertional chest pain
Syncope
Prominent P2, S4
Reduced 6MWD
Desaturation with exercise
Increased PA diameter on CT
Elevated BNP
DDX of dyspnea disproportionate to lung function impairment
Cardiac sarcoidosis
Pulmonary hypertension
Benefits of steroids in pulmonary sarcoidosis
Improve symptoms (accelerate remission but increase risk of recurrence)
Improve or preserve QOL
Improve or preserve FVC
Improve radiographic disease burden
Clinical features are highly suggestive of HP
Female, non smoker
Relevant exposure history
Hx getting worse with exposure (4-8 hrs), better away.
Squawks on examination
Poor prognostic markers/increased mortality
Older age
Male
Smoker
Unidentified exposure
Ongoing exposure
Low FVC, low DLCO
Evidence of fibrosis, extent of fibrosis
UIP pattern on imaging, histology
Fibrotic NSIP pattern
Lower BAL lymphocytosis (<20%)
Difference of HP from silo filler’s disease and organic dust toxic syndrome
HP is granulomatous disease
ODTS and Silo Filler’s disease cause obliterative bronchiolitis
Inorganic causes of HP
Isocyanates - spray paints, polyurethane foam, insulation
HFA-134a - coolants
Drug induced - MTX, bleo, nitro
Organic causes of HP
Infectious - Mycobacterium avium, thermophilic actinomyces, aspergillus, bacillus subtilis
Animal proteins - bird serum proteins, droppings, feathers
Plants - wood dust, flour dust, seaweed
Usual lab findings in HP
Lymphocytosis (in BAL)
Neutrophilia, lymphopenia
Usually no eosinophilia
Usual radiographic findings in non fibrotic HP
parynchemal infiltration (GGOs, mosaic attenuation)
small airway disease (ill defined centrilobular nodules, air trapping)
Distribution (diffuse with possible basal sparing)
What are the usual radiographic findings in fibrotic HP
- irregular linear opacities/coarse reticulations with lung distortion (may have some mild traction bronchiectasis and honeycombing)
- distribution (random or mid lung zone predominante with sparing in the lower lobes)
- ill definied centrilobular nodules/GGOs
- 3 density pattern often in lobular distribution
Features of pathology for non-fibrotic and fibrotic HP
Preferred mode of biopsy in HP
Transbronchial in HP
Cryobiopsy in fibrotic HP
Surgical in both when the others fail
When is BAL for assessment of lymphocytosis recommended in HP
Recommended in non fibrotic HP
Suggested in non fibrotic HP
Depends on ATS vs. Chest
Treatment of HP
Observation- Antigen removal
Prednisone 0.5 - 1 mg/kg/day x 4-6 weeks then taper over 3 months
Steroid sparing agent
Antifibrotics
Steroid sparing agents that are used in HP
MMF
Azathioprine
Antifibrotics
Normal composition of pleural fluid
75% macrophages
23% lymphocytes
1% mesothelial cells
Rare PMNs and eosinophils
pH usually 7.6
Pressure of the pleura at FRC and at TLC
- 5 cm
-30 cm
Causes of transudative and exudative effusions
What are the 2 and 3 test rules for pleural fluid
Pleural LDH >0.45 ULN
Pleural Cholesterol >45
+/- Pleural protein >29
Note light’s (LDH>0.6 ULN, PleurProtein>0.5 SerumProtein, PleurLDH>0.6 SerumLDH)
Ddx for eosinophilic pleural effusion.
Blood or air in the pleural space
Medications
Fungal infections, parasitic infections e.g. paragonimiasis
ABPA
Malignancies
EGPA
BAPE
PE
Ddx for lymphocytic pleural effusion.
Post CABG, PCIS
Pseudochylothorax, chylothorax
Malignancy (including mesothelioma), lymphoma
Tuberculosis
Rheumatoid arthritis
Sarcoidosis
Uremic pleuritis
Cardiac failure
What is the difference between lymphocytic and very lymphocytic?
> 50% vs >80%
Especially TB, lymphoma, RA
Ddx for neutrophilic pleural effusion
Empyema
Esophageal rupture
Acute or chronic pancreatitis
Pulmonary embolism
SLE can start out neutrophilic
TB can start out neutrophilic
Causes of low pH/glucose in pleural fluid
Empyema
Paragonimiasis
RA/SLE effusion
Malignancy related effusion
Esophageal rupture
Hemothorax
Causes of elevated pleural protein
Tuberculosis
MM, WM
How can you tell apart an exudative from pseudoexudative?
P:S albumin <0.6
S-P albumin >12 g/L
S-P protein >31 g/L
Medication causes of pleural effusion
Methotrexate
Nitrofurantoin
Amiodarone
Phenytoin
Ergot alkaloids e.g. bromocriptine
Dasatinib
Beta blockers
DDX for pleural thickening
Benign and malignant masses
Pleural infections
CTD causes
Pleural plaques
Post hemothorax
Post pleurodesis
DDX for pleural calcification
Pleural plaques, previous asbestos exposure
Mesothelioma (~20%)
Malignancy e.g. extraskeletal osteosarcoma of the pleura
Previous radiation
Previous infection e.g. TB, empyema
Previous pleurodesis
Previous hemothorax
DDX for positive pleural PET?
Malignancy
Infection
Autoimmune
Previous talc pleurodesis
Etiology of fibrothorax
Previous infection, empyema
CTD - e.g. RA or SLE related effusion
BAPE
Previous hemothorax
Previous pleurodesis
Drug reactions
Features of trapped lung
Transudate or borderline exudate fluid
Drainage results in pneumothorax ex vacuo
Initial (-) intrapleural pressure
Pressure falls rapidly bc extremely high elastance
No improvement in dyspnea with drainage
Management of Hepatic Hydrothorax
Salt and fluid restricted diet
Diuresis e.g. furosemide, spironolactone
TIPS
Transplantation
?Thoracentesis
Causes of pleural effusions post CABG
Early post CABG effusion
Late post CABG effusion
Post cardiac injury syndrome
Hemothorax
Chylothorax
Pneumothorax/hydropneumothorax
Parapneumonic effusion
Infectious mediastinitis
HF related effusion
How do you differentiate between early and late nonspecific pleural effusions?
Both are usually left sided
Both exudative
Early usually bloody, eosinophilic (or neuts)
Late usually lymphocytic
pH and glucose normal
How does PCIS present? (Post Cardiac Injury Syndrome)
Fever, pleuritis, pleural effusion
Exudative, lymphocyte predominance
Anti myocardial antibodies
pH and glucose normal
Pleural fluid characteristics of RA
Exudative
Glucose <1.6
Pleural to serum glucose <0.5
pH <7.3
LDH >700
Protein >30
Lymphocyte predominant
Cholesterol >5.18 mmol/L
RF elevated >1:320
C3/C4 reduced
Cytology shows multinucleated giant cells (tadpole sign)
How is SLE related fluid different from RA related fluid?
More symptomatic - almost always has pleuritis
Association with lupus flare
More likely to be bilateral
Requires tx with NSAIDs or prednisone
Causes of chylothorax
Idiopathic
Trauma
Surgery, especially esophageal
Lymphoma, metastatic adenocarcinoma
Tuberculosis
LAM
Yellow nail syndrome
Chylous ascites
Lymphatic malformations
Pleural fluid features of chylothorax
Milky white
Exudative
Lymphocyte predominant
TG >124 mmol/L or evidence of chylomicrons (lipoprotein electrophoresis)
pH, glucose, LDH normal
Pleural fluid features of pseudochylothorax
Milky white
Exudative
Lymphocyte predominant
Cholesterol >5.18 mmol/L or presence of cholesterol crystals
Causes of pseudochylothorax
Tuberculosis
Helminth infection e.g. paragonimiasis
Rheumatoid arthritis
Hemothorax
Treatment of chylothorax
Dietary changes (low fat, high protein)
Fat soluble vitamins
Chest tube (unless v small and asx)
May need somatostatin/octreotide
Sirolimus in LAM
Intervention/surgical
Triad in yellow nail syndrome
Yellow nails
Lymphedema
Pulmonary symptoms - sinusitis, bronchiectasis, recurrent PNA, effusions
Microbiology of pleural effusions
Staph aureus
Strep pneumo
GNB (pseudomonas, acinetobacter, klebsiella, enterobacteria)
Anaerobic bacteria (baceroides, fusobacterium, etc.)
Signs of pleural infection on CT scan
Lentiform shape
Split pleura sign (most reliable to differentiate from abscess)
Does compress surrounding lung
Obtuse angle with the pleura
Contrast enhancement
Hypertrophy of extrapleural fat
If you do not have pleural pH available, what else can you use as guide?
Pleural glucose <3.3
Things that affect the clinical outcome (need for sx, mortality) in pleural infections
RAPID score components
CT/US septations
Pleural contrast enhancement
Size >400 cc
Pleural fluid microbubbles
Increased attenuation f extrapleural fat
Things do not affect clinical outcomes in pleural infections
Size of tube
Causative organism
Components of the RAPID score for pleural fluid evaluation
Renal function
Age
Purulent - yes or no
Infection source
Diet - albumin
What does the RAPID score correspond with?
Mortality at 3 and 12 months
Indications for chest tube insertion
Empyema - pus, positive gram stain, positive culture
Very loculated
Very septated
Massive effusion (>50% of hemithorax)
pH <7.2
Intermediate pH but LDH >900
Complications of pleural infections
Bronchopleural fistula
Pleural calcifications
Pleural thickening
Empyema necessitans (pus extending into the chest wall, common with TB)
Fibrothorax
Antibiotic for treatment of parapneumonic effusion
Beta lactam + beta lactamase inhibitor
Ceftriaxone/FQ + metronidazole
Carbapenems
Clindamycin
Carbapenem + vanco if HAP
Duration 2-6 weeks
If needed, when is surgery ideally performed RE: pleural effusion?
Within day 3
Should not be favored over chest tube initially
VATS is preferred over medical pleuroscopy and thoracotomy
Surgical options
Drainage
Debridement
Decortication
Benefits of intrapleural enzyme therapy
Reduces volume on imaging
Reduces LOS
Reduces requirement for thoracic surgery
Indications for giving a reduced dose
Very hemorrhagic fluid at baseline
Disease with hemorrhage risk e.g. RCC with lung mets
Anticoagulation that cannot be stopped
Note: Anticoagulation increases risk to 10% (overall risk 4%) but half dose did not change risk
RFs for enzyme related bleeding
Concurrent administration of anticoagulation
Elevated RAPID score
Plt count <100,000
Sites of pneumomediastinum
Alveolar sacs (most common)
Tracheobronchial tree
Esophageal
Bowel rupture
Physical examination findings of pneumomediastinum
Hamman’s crunch (crunching with each heart beat or mediastinal crunch)
Subcutaneous emphysema
High pitched voice
Image findings of esophageal rupture
Pneumomediastinum - air around the mediastinum
Widened pneumomediastinum
Pneumothorax
Pleural effusion
Subcutaneous emphysema
Air under the diaphragm
Causes of primary pneumothorax
Asthenic body habitus
Subpleural blebs
Smoking - cigarettes, marijuana, snorting cocaine
Diving
Causes of secondary pneumothorax
Bullous lung disease
LAM
PLCH
COPD
Asthma
Bronchiectasis
Thoracic endometriosis
Ehler Danlos, Marfans
RF for tension pneumothorax development
Traumatic pneumothorax
Post CPR pneumothorax
On NIV or mechanical ventilation
Blocked or kinked chest tube
Hyperbaric oxygen treatment
Underlying lung disease
Mechanisms of hypotension in tension pneumothorax
IVC compression → reduced RV preload
RV compression → reduced LV preload
Increased LV afterload
Increased RV afterload
Imaging findings in a tension pneumothorax
Visible lung edge
Shifting of mediastinum, deviated trachea
Splaying of the ribs
Adequate size for intervention for a pneumothorax
> /2 cm laterally or apically on CXR
If using CT, any size that can safely be accessed with imaging support
Borders of the triangle of safety
Lateral edge of pectoralis muscle
Lateral edge of latissimus dorsi
Fifth intercostal space/nipple line/breast line
Base of axilla
High risk features in the treatment algorithm of pneumothorax
Underlying lung disease aka Secondary pneumothorax
Age >/50, smoking history
Bilateral pneumothorax
Hemopneumothorax
Tension pneumothorax/hemodynamic compromise
Significant hypoxemia
Indications of applying suction for a pneumothorax
The pneumothorax increases in size despite chest tube insertion
Fails to improve after 24-48 hours
There is persistent air leak
Percentage of pneumothorax that resolves per day
1.25 - 2.2% per day
Increased by 4-6X via oxygen
Indications for a surgical consultation in pneumothorax
Recurrent pneumothorax, ipsilateral or contralateral
First pneumo BUT:
- SSP and significant physiological compromise
- Tension pneumothorax/hemodynamic compromise
- Spontaneous hemothorax
- Bilateral pneumothorax
- Persistent air leak 5-7 days, or lung fails to re expand
- Pregnant
- High risk occupation
What surgical technique is preferred for pneumothorax
VATS > thoracotomy
Can do any: bullectomy, pleurectomy, mechanical pleurodesis, chemical pleurodesis
When would you consider non surgical but definitive management, e.g. talc slurry?
Unwilling to do surgery
Unable to do surgery
This is because surgical options more effective
Recurrence rate for pneumothorax
PSP → 33%
SPS → 13-39%
After first recurrence → 60%, after second recurrence → 80%
Causes of persistent air leak
Conditions: Pneumothorax, Barotrauma, Infections, Malignancies
Procedures: wedge biopsies, lobectomy, LVRS, trauma
Treatment options for persistent air leak
Treat underlying infection
Add suction
Second chest tube or bigger chest tube
Blood patch
Chemical pleurodesis
Surgical options
Recommendations re: activities post pneumothorax
No PFTs x 2-4 weeks
No flying until resolved at least x 1 week
No diving ever
Management of bronchopleural fistula volume of leak in a vented patient
Reduce Pplat
Reduce autoPEEP → increase expiratory time, reduce Vt, permissive hypercapnia
Causes of malignant pleural masses
Mesothelioma
Metastases
Lymphoma
Malignant fibrous tumour
Askin tumour
Sarcoma
Extraskeletal osteosarcoma
What type of malignancy is primary effusion lymphoma?
Usually diffuse large b cell lymphoma
Usually no associated lymphadenopathy
DDX for malignant effusions in patients with HIV
Lymphoma
Primary effusion lymphoma
Kaposi sarcoma
Other cancers
Most common causes of pleural metastases
Lung (adeno)
Breast
Lymphoma
GI/GU
Where in the pleural do malignancies usually start?
Mets - visceral pleura
Meso - parietal pleura
Non malignant causes of pleural masses
Solitary fibrous tumour of the pleura
Lipoma
Mesothelial cyst
Pleural endometriosis
Pleural plaques, thickening (not really masses)
What are the associated paraneoplastic syndromes with solitary tumour of the pleura?
Hypoglycemia, Doege-Potter syndrome (elevated IGF)
Hypertrophic pulmonary osteoarthropathy
Concerning features of pleural malignancy on imaging
Thickness > 1 cm
Circumferential thickening
Involvement of the mediastinal pleura
Diaphragmatic thickening > 7
Nodular thickening
Sensitivity of pleural fluid for malignancy
Overall, 60%, increase by 15% with the second tap
Adenocarcinoma 80%
Breast 70%
Small 50%
Mesothelioma 30%
Squamous cell 20%
Definition of non expandable lung in MPE
> /25% of the lung is not opposed to the chest wall
Is based on CXR
Treatment for MPE
Aspiration has shorter LOS but more need for intervention
IPC vs chest tube with talc slurry or poudrage
Management of MPE in mesothelioma
Talc poudrage preferred
Other options IPC, slurry, PP
Benefit of MPE management
Improved dyspnea
Improved QOL
Agents for pleurodesis
Talc
Doxycycline
Bleomycin
Rate of spontaneous pleurodesis once an IPC is inserted
25%
Clinical factors suggest will gain improvement with IPC
Improvement after therapeutic thoracentesis
Rapid reaccumulation
Prognosis is >1 month
Supports to have home care
Possible side effects from pleurodesis
Chest pain
Fever
ARDS
Treatment of infected/loculated MPE with IPC inserted
Abx
Intrapleural enzymes
Intrapleural normal saline
Extra chest tube
Surgical - VATS, decortication
How long after asbestos exposure does mesothelioma occur?
~40 years after exposure
3 main subtypes of mesothelioma
Epithelioid
Biphasic
Sarcomatoid
Causes of mesothelioma
Asbestos (+ dose response)
Erionite fibers
Thoracic radiation
SV40 infection, other viral infections
Chronic pleural disease
Imaging features are concerning for mesothelioma
Pleural thickening with concerning features (see previous)
Presence of asbestos exposure
Local invasion - chest wall, mediastinum, diaphragm, ribs
Usually unilateral changes, usually right side predominance
Spreads along pleura and fissures
Starts at parietal pleura
Diagnosis of mesothelioma
Image guided biopsy
Medical pleuroscopy
Surgical pleuroscopy/VATS
Management of mesothelioma
- Double immunotherapy - ipilimumab + nivolumab (previously was chemo, but studies show immunotherapy better)
- Debulking surgery if candidate
- Both improve survival
Poor prognostic markers in mesothelioma
Histology
Stage
Age
Poor performance status
Malignant causes of lymphangitic carcinomatosis
Cervical
Colon
Stomach
Breast
Prostate, pancreas
Thyroid
Lung
Diagnosis of lymphangitic carcinomatosis
Biopsy - TBBx or surgical
Histological findings of lymphangitic carcinomatosis
Obstruction and distension of lymphatics by tumour cells
Treatment of lymphangitic carcinomatosis
Treat underlying cancer
Steroids, but no clear data
Opioids for symptom control
How many segments are there in each lobe of the lung?
RUL: 3
RML: 2
RLL: 5
LUL: 5
LLL: 5
Equations for PPO lobectomy and pneumonectomy
Lobectomy PPO FEV1 = FEV1 x [1 - (resected segments/19)]
Pneumonectomy = PPO FEV1 = FEV1 x [1 - fraction of perfusion to resected lung]
Examples of important post operative complication predictors
VO2 max
FEV1
DLCO
In post operative planning, what are the cutoffs for SWT and stair climbing? Low technology exercise test.
SWT <400 m
Stair climb <22m
In post operative planning, what are the cutoffs for VO2 max?
<10 mL/kg/minute (<35%)→ high
10-20 → moderate
>20 (>75% predicted) → low
Patient factors that increase post op complications from non-pulmonary surgery
Age
Smoking
ASA class
OSA
COPD (especially if FEV1 <60%)
Pulmonary hypertension
Low albumin
Obesity is not a risk factor
Surgical factors that increase post op complications from non-pulmonary surgery
Aortic > intrathoracic > upper abdominal > abdominal
Duration of surgery
Emergency surgery
General anesthesia (epidural better)
Paralytics
How can post operative complications be prevented?
Optimize underlying lung disease prior to surgery
Smoking cessation (>8 weeks previous surgery)
Avoid GA if possible; regional blocks if possible
Avoid long acting neuromuscular blockade
Shorter surgery (<3 hours)
Laparoscopic
CPAP if OSA
Lung expansion techniques
Pain control
Physiological changes that occur after a pneumonectomy
FEV1, FVC, lung volumes, DLCO decrease
Decrease compliance
Increased resistance
Dead space can increase or decrease
RV EF reduces, LV function does not change
No change in blood gasses
What normally happens to the post pneumonectomy space?
Fills with air, then with fluid
Complete opacification takes 4 months
Post pneumonectomy complications
Post pneumonectomy syndrome
Post pneumonectomy empyema
Bronchopleural fistula
Esophagopleural fistula
Pulmonary embolism
Pneumothorax
Hemorrhage
Arrhythmias, MI
When does post pneumonectomy syndrome occur?
After 6 months following surgery
Almost exclusively after right sided pneumonectomy
(it is excessive mediastinal shift resulting in compression and stretching of the tracheobronchial tree and the esophagus)
When does post pneumonectomy pulmonary edema occur?
Within 72 hours
Non cardiogenic edema/ARDS
More common during right vs left
RFs for post pneumonectomy pulmonary edema
Right sided resection
Large perioperative fluid load
Single lung ventilation
High inspired O2 concentrations
Inclusion criteria for NSLT?
Age 55-74
Current smoker or quit within the last 15 years
Has at least 30 pack year smoking history
Experienced centers
Exclusion criteria for NSLT?
Lung cancer
Hemoptysis
Lost >/15 lb in the last 1 year
Chest CT in the prior 18 months
Key differences between the NLST and NELSON trials
Different proportion of males/females
Inclusion criteria
Nodule management protocol - diameter vs volume
Control comparison - CXR vs nothing
Follow up - different # and intervals
