Pneumothorax/PE Flashcards
Pneumothorax
General
Life-threatening condition
Air collects in the pleural space, causing partial or full collapse of the lung which can impair ventilation and/or oxygenation
Classification
Traumatic:
Resulting from blunt or penetrating chest trauma
Open: a connection through thechest wall
Closed: no connection to the outside air
Spontaneous:
Occurs without any apparent cause or inciting event
Primary: no underlying disease or event identified
Secondary: known pre-existing lung condition or inciting event
pneumothorax
Epidemiology
Traumatic:
Occurs more frequently than spontaneous pneumothorax
Spontaneous:
Primary spontaneous pneumothorax:
More common in youngerpatients (20–30 years old)
Patientsare typically tall and slim (Marfan syndrome)
Men > Women
Smokers > Non-smokers
Secondary spontaneous pneumothorax:
Occurs in middle-aged and olderpatients
Men > Women
Smokers > Non-smokers
Pneumothorax
Etiology
Blunt orpenetrating injury
Rib fracturescausing lunglaceration
Disruption of the tracheobronchial tree
Gunshot or stab wound
Iatrogenic- medical introduction
Lung surgery
Central venous catheterinsertion
Thoracentesis
Mechanicalventilation
Esophageal procedures
Primary (idiopathic)
Ruptured apical subpleuralblebsorbullae
Secondary
Chronic obstructivepulmonary disease (COPD) accounts for 50% of spontaneous cases
Bronchiectasis
Lung malignancies
Lunginfections
Genetic diseases
Cysticfibrosis, Marfan’s syndrome, Ehlers-Danlos syndrome
(Pressure within the pleural space is established by two main opposing forces:
One is the muscle tension of the diaphragm and chest wall which contract and expand the thoracic cavity outwards, and the other is the elastic recoil of the lungs, which try to pull the lungs inward
The two pull on each other creating a balance between the forces that creates a slight vacuum in the pleural space
The pleural space normally has a pressure of -5 centimeters of water relative to the pressure of 0 centimeters of water in both the thoracic cavity and the lungs)
pneumothorax
patho
As air enters thepleural space, there is a loss of the negative pressure
The normal opposing forces no longer pull on each other
Theelasticrecoil in the lung tissues causes either a partial or full lung collapse
The chest wall simply springs outward slightly
Tension pneumothorax
Patho, Sx
Life threatening condition that can develop from any type of a pneumothorax
One-way valve for air to flow into the pleural space
Air accumulates in thepleural spacewith each inspiratory phase → ↑pleural spacepressure → shifting of themediastinum→compressionof the contralateral lung →hypoxia, hypercapnia
Eventualcompressionof the vena cava and atria → ↓ venous return to the heart and ↓ cardiac function → rapid cardiopulmonary collapse
Develops similarly to a spontaneous pneumothorax or a traumatic pneumothorax - with the one difference being that it creates a one-way valve for air to flow into the pleural space
Timely diagnosis and treatment are crucial for patient survival
Pneumothorax
Clin Man
Radiating pain?
Depends on the etiology and size of the pneumothorax
Asymptomatic (small) – incidental finding
Symptoms
Dyspnea- severtity depends on how much air
Can range from mild to severe
May be gradual or sudden
Sudden sharppainon the affected side; may radiate to the ipsilateral shoulder
Pleuritic chestpain
Anxiety
Tension pneumothorax
Associated with rapid clinical deterioration
In primary spontaneous pneumothorax, the severity of pain can decrease after 24 hours, possibly due to gradual spontaneous resolution
Pneumothorax
vitals/PE findings
Vital signs:
Tachypnea
Tachycardia
Hypotension
Hypoxia-both more likely in tension pneumo
Respiratory:
Reduced or absent breath sounds on the affected side
↓Tactile fremitus
Hyper-resonance topercussion
↓ Chest expansion
Tracheal deviation - more likely in tension pneumo
Cutaneous:
Evidence of trauma
Subcutaneous emphysema
Cyanosis
pneumothorax
CXray
Suspected based on the clinical presentation and confirmed by imaging
Chest radiograph:
Performed in the upright position (when possible)
Small pneumothorax will typically not show on anX-ray
General findings:
White visceral pleural line defining the lung and pleural air
Bronchovascular markings are not visible beyond the pleural edge
Deep sulcus sign (gas outlines the costophrenic sulcus)
Ipsilateral hemidiaphragm elevation
Tension pneumothorax findings:
Potential mediastinal shift and/or tracheal deviation to the contralateral side
Ipsilateral hemidiaphragm flattening
Ribsare spread apart
Pneumothorax
small vs large
Small vs. large pneumothorax
Small – the presence of a visible rim of < 2 cm between the lung margin and the chest wall
Large – the presence of a visible rim of > 2 cm between the lung margin and the chest wall
pneumothorax
ultrasound
Ultrasound
E-FAST(Extended Focused Assessment With Sonography in Trauma) allows clinicians to rapidly diagnose traumatic thoracoabdominal injuries at the bedside
Initial test to rule in dangerous diagnoses such as hemoperitoneum, pericardial effusion, hemothorax, and pneumothorax
Includes views of:
Hepatorenal recess (Morison pouch)
Perisplenic area
Suprapubic window (Douglas pouch)
Subxiphoid pericardial window
Subxiphoid pericardial window
Bilateral hemithoraces and the upper anterior chest wall
Pneumothorax
CT
Computed tomography (CT):
The most sensitive
Used if the diagnosis remains uncertain after radiographs
Can provide additional information about associated causes
Findings:
Air in thepleural space
Can evaluate for loculations, pleural pathology, and lung disease
pneumothorax
Tx
Depends on the amount of air collected in thepleural cavityand the stability of the patient
Interventions:
Supplemental oxygen-encourages reexpansion of the lung.
For symptomatic pts :
Needle decompression
14- or 16-gauge needle is inserted through thechest wall
2nd intercostal space in the midclavicular line or 5th intercostal space in the anterior ormidaxillary line
Should be followed by chesttube placement
Chesttube thoracostomy
A catheter inserted into thechest wall
Placed in the 4th to 5th intercostal space at themidaxillary line
pneumothorax
patients are deemed stable if (5)
Patientsare deemed stable if:
Respiratory rate< 24 breaths per minute
Heart rateis between 60–120 beats per minute
Blood pressure is normal
Oxygen saturation> 90% on room air
Patient is able to speak in full sentences
Stable patients
Small pneumothorax:
Supplemental oxygen
Monitor the patient for a minimum of 6 hours
Serial radiographs are performed to monitor for progression
pneumothorax
Tx of large pneumo
if primary or secondary
Traumatic pneumothorax: chesttube placement
Primary spontaneous pneumothorax (not recurrent)
Needle aspiration to remove pleural air is the 1st step
If there is no improvement, or the pneumothorax recurs, a chest tube is placed
Secondary spontaneous pneumothorax
Chesttube placement
Treatment for the underlying disease
Thoracic surgeryconsultation for definitive management (due to a high likelihood of recurrence)
Pneumothorax
Complications
Respiratory failure
Cardiac arrest
Pneumomediastinum(air is present in themediastinum)
Pneumoperitoneum(air is in theperitoneal cavity)
Re-expansionpulmonary edema
Occurs with rapid expansion of the lung
Higher risk if the lung has been collapsed for several days
Procedure complications:
Infection
Fistulaformation and air leaks
Intercostal nerve damage
Bleeding
Recurrence – 20-60% rate in the next 3 years after the initial episode
Hemothorax
general
Collection of blood in the pleural cavity
Source of blood may be thechest wall, lung parenchyma, heart, or great vessels
Can result from traumatic and non-traumatic causes
Hemothorax
Clin Man
Clinical Presentation
Similar to pneumothorax, but patients can show signs of hemorrhagicshock (large hemothorax)
Hypotension
Tachycardia
Tachypnea
↓Jugular venous pressure
Diagnosis: CXR or Ultrasound; CT scan (definitive imaging choice)
hemothorax
Tx
Airway, breathing, andcirculation(ABC) assessment→ administer100% oxygen→ establish intravenous (IV) access
Stabilize the patient (fluidresuscitationand blood transfusion as necessary)
Reverseanticoagulants, if necessary
Provideanalgesiaappropriate to the level of the patient’spain
Insert a chest tube (thoracostomy) for large hemothorax or in an unstable patient
Used to drain the hemothorax
Monitor output of the hemothorax
Hemothroax
Surgical intervention (thoracotomy)
indication
is indicated when:
Evacuating > 1,500 mL of blood directly after inserting a chest tube
Continued high output → collecting of > 1 L (1,000 mL) of blood over 4 hours or > 200 mL/hour for 3 consecutive hours
hemothorax
complications
Impairedventilationon the affected side
Leads to respiratory distress
May requireintubation
Empyema
Retained blood collection develops a bacterial infection
5% of cases
Fibrothorax
Formation of scar tissues within thelungsdue to blood irritation
1% of cases
Pulmonary Embolism
general
Intraluminal obstruction of a mainpulmonary arteryor any of its branches
Common, potentially fatal condition
Epidemiology:
Incidence: approximately 112 per 100,000 in the United States
Slight male predominance
Relationship of PE withDVT
> 90% ofPEsare due to DVTs of the lowerleg
50% of untreated proximal DVTs lead to PE within 3 months
3 primary factors that contribute toVTE
Virchow’s triad
Venous stasis
Hypercoagulability
Vascular endothelial damage
PE
etiology
Any condition that worsens 1 (or more) of the 3 factors increases the risk ofPE as well as DVT
Dislodged DVT is the most common cause for PE
Rare causes: fat embolism (long bone fractures), tumor embolism, infected clots (right-sided endocarditis), sickle cell disease
PE
RF
genetic/acquired/medical conditions
Genetic:
Factor V Leidenmutation (most common genetic)
Prothrombingene mutation
Protein C andProtein Sdeficiencies
Acquired: (most are aquired)
Immobilization
Recent surgery(especially orthopedic surgery)
Malignancy
Trauma
Obesity
Smoking (with Birthcontrol is very high risk)
Estrogenexposure:
Pregnancy
Hormonal contraception
Hormone replacement therapy
Medical conditions:
Hypertension
Congestiveheart failure
Autoimmune disease
Nephrotic syndrome
Covid-19
never prescribe birth control to a smoker for this reason.
Anatomic Locations of PE
Most emboli move beyond the bifurcation to smaller branches of apulmonary artery:
Lobar branches
Segmental branches
Subsegmental branches
Saddle embolus:
At the bifurcation of the mainpulmonary trunk
May extend into the right or left mainpulmonary artery
Usually have multiple emboli, with bilateral involvement in the lower lobes more frequently than the upper lobes
PE
Patho
PE causes impaired gas exchange due to obstruction of the pulmonary vascular bed→ ventilation/perfusion (V/Q) mismatch
Alveolar ventilation remains the same
Pulmonary capillary blood flow decreases
Decreased blood flow leads to dead space and hypoxemia; decreases oxygen signals the brain to increase breathing
Blood pumped from the RV to the pulmonary arteries cannot pass the clot → increased pulmonary artery pressure (PAP) and increased pulmonary vascular resistance (PVR) = right heart strain and potential right-sided heart failure
Ventilation/Perfusion (V/Q) mismatch
↑ PAP
↑ PVR
Right heart strain
PE
Pulmonary infarction:
Pathophysiology
Pulmonary infarction:
Occurs in about 10% ofpatients
Associated with small emboli in the segmental and subsegmental branches, causingischemiaof lung tissue
Produces:
-An intense inflammatory response which leads to:
-Vasoconstrictionand bronchoconstriction in unaffected nearby areas → further decreasesblood flow(Q) and airflow(V)
-Decreasedsurfactantproduction +atelectasis→ shunting (perfusion withoutventilation) → worsens V/Q mismatch
-Intra-alveolar hemorrhage is possible (hemoptysis)
PE
Sx
Presentation varies significantly
High suspicion must be maintained given the risks of complications andmortality
Can be asymptomatic (incidentally found on imaging)
Massive PEpresents with hemodynamic instability/shock
Symptom:
Dyspneaat rest and/or during exertion (most common
tachycardia
Pleuritic chestpain
Cough
Hemoptysis
Near syncope/Syncope-rare
Symptoms ofDVT
Calfpainand/or tenderness
Extremityswelling
Palpable cord
Erythema
Warmth
PE
PE findings
Physical exam findings
Tachypnea
Tachycardia
Ralesand/or decreased breath sounds
Hypoxia
Hypotension
Loud second heart sound (P2)
Jugular vein distension - evidence of R heart strain more chronic
PE
Dx
Made through imaging studies
Decision to obtain imaging is based on:
Clinical suspicion
Pretestprobability assessment (Modified Wells criteria)
D-dimerlevels
PE Dx
if high probability straight to imaging
intermediate start with D dimer
low probability do PERC score, then D dimer
PE
Clinical suspicion
Pulse oximetry:room-airoxygen saturation (O2sat) < 95%- the lower it gets the higher the suspicion.
Electrocardiography(ECG)may show:
Arrhythmia:
Sinustachycardia(anything over 100)
Atrial fibrillation
Right heart strain pattern:- not on boards
Newright bundle branch block
Right axis deviation
Dominant R waveinleads V1 and V2
S1Q3T3pattern (rare):
Prominent S wave in lead I
Q wave in lead III
InvertedT wavein lead III
PE
PE
Modified Wells Criteria
KNOW THIS
score > 4 : PE likely (intermediate/high)
Score <= 4 : PE unlikely (low)
PE
High-sensitivity D-dimer
Byproduct of crosslinkedfibrindegradation → indicating thrombus breakdown
> 95% sensitivity when negative
A negative test effectively rules outVTEin low-risk and moderate-risk cases
Low specificity → a positive test (elevated value) doesnotconfirmVTE since any condition that causes clots to form can elevateD-dimerlevels (recent surgery, cancer, orsepsis)
Specificity of d-dimer decreases steadily with age; use age-adjusted cut-offs for patients over 50 years
PE
Pulmonary Embolism Rule-out Criteria (PERC)
for low probability
Created to reduce testing in patients who have a very low probability of PE
Pre-test probability < 15%
Includes 8 components that must be absent to rule out PE
Interpretation
If the patient is deemed low risk and all criteria are absent, then there is no need for further PE workup
If the patient is deemed low risk but is positive for ANY criteria, ad-dimershould be considered
If a d-dimer is positive, further investigation such as CTPA or V/Q scan may be indicated
PE
Modified wells track
PEprobabilityassessment andD-dimerlevels guide diagnostic workup
If PE is unlikely (ModifiedWells Score≤ 4):
D-dimernormal (< 500): PE excluded
D-dimerelevated: Order computed tomographic angiography(CTA) of the chest with contrast or V/Q scan
If PE is likely (ModifiedWells Score > 4): OrderCTAof the chest with contrast
PE
CTA of the chest w contrast
Current “gold standard” in diagnosing PE
Best initial test if modifiedWells score> 4
Showsfilling defectsin the pulmonary vasculature
PE
Ventilation-perfusion (V/Q) scan
for people with poor renal function(cant handle contrast), or if CTA is inconclusive. Used if CTA of the chest is contraindicated, not available, or inconclusive
Compares distribution of air in thelungs via inhalation of radioactive xenon gas (theventilationscan) and perfusion via labeled serum markers (the perfusion scan)
PE shows areas of perfusion defects withnormalventilation
Scored as normal, low-, intermediate-, or high-probability of PE
Major limitation: most individuals have indeterminate scans
PE
CTA with Saddle PE
V/Q mismatch
PE
anticoagulation Tx
& options
Anticoagulation: initial treatment
Medication is selected based onpatientcomorbidities and patient preferences
Administered for 3‒6 months to prevent recurrence (somepatientsmay require lifelong therapy)
Options:
Low molecular weight heparin (LMWH)
Enoxaparin (Lovenox): 1 mg/kg every 12 hours or 1.5 mg/kg daily
Unfractionated heparin(UFH) - *preferred inpatientswithrenal failure or pregnancy and it costs less than DOACs *
Follow hospital protocol
Indirect factor Xa inhibitor:fondaparinux (Arixtra) - not commonly used
< 50 kg: 5 mg daily
50–100 kg: 7.5 mg daily
> 100 kg: 10 mg daily
Direct factor Xa inhibitors/DOAC - no monitoring required
Rivaroxaban (Xarelto): 15 mg 2 times daily (with food) for 21 days, followed by 20 mg daily (with food)
Apixaban (Eliquis): 10 mg 2 times daily for 7 days, followed by 5 mg 2 times daily
Direct thrombin inhibitor:dabigatran (Pradaxa)
Can be administered after 5–10 days of initial treatment with LMWH orUFH
150 mg 2 times daily
PE
Contraindications for anticoagulation
Contraindications:
Active bleeding
Acuteintracranial hemorrhage
Major trauma
Severebleeding disorders
PE
general Tx
Assess and treat any hemodynamic instability
Address the ABCs
Airway
Breathing/respiratory support:
Supplemental oxygentherapy to improve O2sat > 95%
Circulation/hemodynamic support:
Small amount ofIV fluids(avoid fluid overload, which worsens the effects ofright-sided heart failure)
Vasopressors- if hypotensive
Cardiac medications based on the presence and severity ofheart failure and hemodynamics
PE
Timeline of anticoags
lifelong treatment if unprovoked or multiple clot incedents
3-6 months if provoked
PE
Reperfusion therapy
indications
Thrombolytic therapy
Infusion of a lytic agent -
tissue plasminogen activator (tPA)
Routes:
Systemic therapy
Catheter directed: a catheter tip directed at the embolus in an attempt to lyse the thrombus
Indications:
Hemodynamically unstable patientswith a massive embolus
Hemodynamically stable patientswith adverse outcomes (RV dysfunction)
Individuals unresponsive to systemic anticoagulantswith clear deterioration
good for people who cant take anticoags and large clots
PE
Embolectomy
Embolectomyconsists of removal of the embolus:
Catheter-based or surgical procedure
Indications:
Hemodynamically unstable patientswith massive emboli, who are not suitable candidates for thrombolytic therapy (e.g., active bleeding)
In cases of failed thrombolytic therapy
PE
Prophylaxis against recurrent PE
Anticoagulation: secondary prevention ofVTE
Options:
LMWH
Vitamin Kantagonists:warfarin (Coumadin)
Requiresregularmonitoring of theprothrombin time(PT)
Numerous drug interactions
Contraindicated inpregnancy(teratogenic)
Direct factor Xa inhibitors:rivaroxaban,apixaban,edoxaban
Monitoring generally not required
More expensive
Thrombininhibitors:dabigatran
Requires monitoring of the activatedpartial thromboplastin time(aPTT)
Often used inpatientswith a history of HIT
Depending on the initial and secondary therapies, “bridging” may be required to ensure fullanticoagulation during transition of therapy (continuing LMWH untilwarfarinis effective based on the PT)
PE
Prophylaxis against recurrent PE
Inferior vena cava (IVC) filter
Used to prevent recurrent PE in patients with DVT in the lower extremities
Barrier placed within theIVCto prevent passage of the migratory thrombus into the pulmonary arterial system
Indications:
Contraindicationstoanticoagulants
Complications from or failed systemic anticoagulants
PE prophylaxis
lifestyle changes
Lifestyle/other options
Exercise
Weight loss
Smokingcessation
Control ofhypertension
Avoidestrogen(combined oral contraceptive pills) in high-riskpatients
Compressionstockings
PE
Prognosis
Prognosis
Estimatedmortality
Untreated PE: approximately 30%
Treated PE: 2%‒11%
Poor prognostic indicators
RV dysfunction
Shockduring presentation
Recurrence
More likely inpatientswith unresolved risk factors (cancer)
Highest in the 1st 2 weeks after presentation
