Pneumothorax/PE Flashcards

(58 cards)

1
Q

Pneumothorax

General

A

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

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2
Q

pneumothorax

Epidemiology

A

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

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3
Q

Pneumothorax

Etiology

A

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

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4
Q
A

(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)

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5
Q

pneumothorax

patho

A

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

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6
Q

Tension pneumothorax
Patho, Sx

A

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

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7
Q

Pneumothorax

Clin Man
Radiating pain?

A

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

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8
Q

Pneumothorax

vitals/PE findings

A

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

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9
Q
A
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10
Q

pneumothorax

CXray

A

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

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11
Q
A

Tension pneumothorax findings:
Potential mediastinal shift and/or tracheal deviation to the contralateral side
Ipsilateral hemidiaphragm flattening
Ribsare spread apart

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12
Q

Pneumothorax

small vs large

A

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

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13
Q

pneumothorax

ultrasound

A

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

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14
Q

Pneumothorax

CT

A

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

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15
Q

pneumothorax

Tx

A

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

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16
Q
A
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17
Q

pneumothorax

patients are deemed stable if (5)

A

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

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18
Q

pneumothorax

Tx of large pneumo
if primary or secondary

A

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)

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19
Q

Pneumothorax

Complications

A

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

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20
Q
A
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21
Q

Hemothorax

general

A

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

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22
Q

Hemothorax

Clin Man

A

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)

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23
Q

hemothorax

Tx

A

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

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24
Q

Hemothroax

Surgical intervention (thoracotomy)
indication

A

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

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# hemothorax complications
Impaired ventilation on the affected side Leads to respiratory distress May require intubation Empyema Retained blood collection develops a bacterial infection 5% of cases Fibrothorax Formation of  scar  tissues within the lungs due to blood irritation 1% of cases
26
# Pulmonary Embolism general
Intraluminal obstruction of a main pulmonary artery or 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 with DVT **> 90% of PEs are due to DVTs of the lower leg 50% of untreated proximal DVTs lead to PE within 3 months**
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3 primary factors that contribute to VTE
**Virchow’s triad** Venous stasis Hypercoagulability Vascular endothelial damage
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# PE etiology
Any condition that worsens 1 (or more) of the 3 factors increases the risk of PE 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
29
# PE RF genetic/acquired/medical conditions
**Genetic**: Factor V Leiden mutation (most common genetic) Prothrombin gene mutation Protein C and Protein S deficiencies **Acquired:** (most are aquired) Immobilization Recent surgery (especially orthopedic surgery) Malignancy Trauma  Obesity Smoking (with Birthcontrol is very high risk) Estrogen exposure: Pregnancy Hormonal contraception Hormone replacement therapy **Medical conditions:** Hypertension Congestive heart failure Autoimmune disease Nephrotic syndrome Covid-19 ## Footnote never prescribe birth control to a smoker for this reason.
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Anatomic Locations of PE
Most emboli move beyond the bifurcation to smaller branches of a pulmonary artery: Lobar branches Segmental branches Subsegmental branches Saddle embolus: At the bifurcation of the main pulmonary trunk May extend into the right or left main pulmonary artery ## Footnote Usually have multiple emboli, with bilateral involvement in the lower lobes more frequently than the upper lobes
31
# 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**
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Ventilation/Perfusion (V/Q) mismatch ↑ PAP ↑ PVR **Right** heart strain
33
# PE Pulmonary infarction: Pathophysiology
Pulmonary infarction: Occurs in about 10% of patients Associated with small emboli in the segmental and subsegmental branches, causing ischemia of lung tissue Produces: -An intense inflammatory response which leads to: -Vasoconstriction and bronchoconstriction in unaffected nearby areas → further decreases blood flow (Q) and air flow (V) -Decreased surfactant production + atelectasis → shunting (perfusion without ventilation) → worsens V/Q mismatch -Intra-alveolar hemorrhage is possible (hemoptysis)
34
# PE Sx
Presentation varies significantly High suspicion must be maintained given the risks of complications and mortality Can be asymptomatic (incidentally found on imaging) Massive PE presents with hemodynamic instability/shock Symptom:  **Dyspnea** at rest and/or during exertion (most common tachycardia **Pleuritic chest pain** Cough Hemoptysis Near syncope/Syncope-rare **Symptoms of DVT** Calf pain and/or tenderness Extremity swelling Palpable cord Erythema Warmth
35
# PE PE findings
Physical exam findings Tachypnea **Tachycardia** Rales and/or decreased breath sounds Hypoxia Hypotension *Loud second heart sound (P2) Jugular vein distension* - evidence of R heart strain more chronic
36
# PE Dx
Made through imaging studies Decision to obtain imaging is based on: Clinical suspicion Pretest probability  assessment (Modified Wells criteria) D-dimer levels
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# PE Dx
if high probability straight to imaging intermediate start with D dimer low probability do PERC score, then D dimer
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# PE Clinical suspicion
Pulse oximetry: room-air oxygen saturation (O2 sat) < 95%- the lower it gets the higher the suspicion. Electrocardiography (ECG) may show: Arrhythmia: **Sinus tachycardia** (anything over 100) Atrial fibrillation Right heart strain pattern:- not on boards New right bundle branch block Right axis deviation Dominant R wave in leads V1 and V2 **S1Q3T3 pattern (rare):** Prominent S wave in lead I Q wave in lead III Inverted T wave in lead III
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# PE
40
# PE Modified Wells Criteria ## Footnote KNOW THIS
## Footnote score > 4 : PE likely (intermediate/high) Score <= 4 : PE unlikely (low)
41
# PE High-sensitivity D-dimer
Byproduct of crosslinked fibrin degradation → indicating thrombus breakdown **> 95% sensitivity when negative** A negative test effectively rules out VTE in low-risk and moderate-risk cases **Low specificity** → a positive test (elevated value) does not confirm VTE since any condition that causes clots to form can elevate D-dimer levels (recent surgery, cancer, or sepsis) Specificity of d-dimer decreases steadily with age; use age-adjusted cut-offs for patients over 50 years
42
# PE Pulmonary Embolism Rule-out Criteria (PERC) ## Footnote 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, a d-dimer should be considered** If a d-dimer is positive, further investigation such as CTPA or V/Q scan may be indicated
43
# PE Modified wells track
PE probability assessment and D-dimer levels guide diagnostic workup If PE is unlikely (Modified Wells Score ≤ 4): D-dimer normal (< 500): PE excluded D-dimer elevated: Order computed tomographic angiography (CTA) of the chest with contrast or V/Q scan If PE is likely (Modified Wells Score > 4): Order **CTA** of the chest **with contrast**
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# PE CTA of the chest w contrast
Current “**gold standard**” in diagnosing PE Best initial test if modified Wells score > 4 Shows filling defects in the pulmonary vasculature
45
# 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 the lungs via inhalation of radioactive xenon gas (the ventilation scan) and perfusion via labeled serum markers (the perfusion scan) PE shows areas of perfusion defects with normal ventilation Scored as normal, low-, intermediate-, or high-probability of PE Major limitation: most individuals have indeterminate scans
46
# PE ## Footnote CTA with Saddle PE
## Footnote V/Q mismatch
46
# PE anticoagulation Tx | & options
**Anticoagulation:** initial treatment Medication is selected based on patient comorbidities and patient preferences Administered for **3‒6 months** to prevent recurrence (some patients may 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 in patients with renal 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 or UFH 150 mg 2 times daily
46
# PE Contraindications for anticoagulation
Contraindications: Active bleeding Acute intracranial hemorrhage Major trauma Severe bleeding disorders
46
# PE general Tx
Assess and treat any hemodynamic instability Address the ABCs **Airway Breathing/respiratory support:** Supplemental oxygen therapy to improve O2 sat > 95% **Circulation/hemodynamic support:** **Small** amount of IV fluids (avoid fluid overload, which worsens the effects of right-sided heart failure) Vasopressors- if hypotensive Cardiac medications based on the presence and severity of heart failure and hemodynamics
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48
# PE Timeline of anticoags
lifelong treatment if unprovoked or multiple clot incedents 3-6 months if provoked
49
# 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 patients with a massive embolus Hemodynamically stable patients with adverse outcomes (RV dysfunction) **Individuals unresponsive to systemic  anticoagulants with clear deterioration** good for people who cant take anticoags and large clots
50
# PE Embolectomy
Embolectomy consists of removal of the embolus: Catheter-based or surgical procedure Indications: Hemodynamically unstable patients with massive emboli, who are not suitable candidates for thrombolytic therapy (e.g., active bleeding) In cases of failed thrombolytic therapy
51
# PE Prophylaxis against recurrent PE
Anticoagulation: secondary prevention of VTE Options: LMWH Vitamin K antagonists: warfarin (Coumadin) Requires regular monitoring of the prothrombin time (PT) Numerous drug interactions Contraindicated in pregnancy (teratogenic) Direct factor Xa inhibitors: rivaroxaban, apixaban, edoxaban Monitoring generally not required More expensive Thrombin inhibitors: dabigatran Requires monitoring of the activated partial thromboplastin time (aPTT) Often used in patients with a history of HIT Depending on the initial and secondary therapies, “**bridging**” may be required to ensure full anticoagulation during transition of therapy (continuing LMWH until warfarin is effective based on the PT)
52
# 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 the IVC to prevent passage of the migratory thrombus into the pulmonary arterial system Indications: Contraindications to anticoagulants Complications from or failed systemic anticoagulants
53
# PE prophylaxis lifestyle changes
Lifestyle/other options Exercise Weight loss Smoking cessation Control of hypertension Avoid estrogen (combined oral contraceptive pills) in high-risk patients Compression stockings
54
# PE Prognosis
Prognosis Estimated mortality Untreated PE: approximately 30% Treated PE: 2%‒11%  Poor prognostic indicators RV dysfunction Shock during presentation Recurrence More likely in patients with unresolved risk factors (cancer) Highest in the 1st 2 weeks after presentation 
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