PE, DVT, Pneumothorax, & Atelectasis

True or False: there are a lot of PEs that can break off and become DVTs

true

What are PEs/DVTs?

complication of thrombus formation in deep vein circulation

What will 50-60% of proximal DVTs do?

embolize to pulmonary circulation

What are the PE statistics?

third leading cause of death among hospitalized patients

Who is most likely to have a DVT?

>40 years old, caucasians and black people with more complications

What is the pathophysiology of DVTs?

• virchow’s triad

• formation of fibrin clot

What are the s/sxs of DVTs?

• edema

• erythema/warmth

• pain

• homan’s sign may be positive

• palpable indurated cord-like vein (rope-like structure)

Can deep veins usually be palpated?

no, but in DVTs it can get to a point where it becomes a palpable indurated cord-like vein

What is virchow’s triad?

endothelial injury, venous stasis, and hypercoagulability

How is homan’s sign performed?

provider dorsiflexes the foot ont he affected side, and if pain is produced, that is a positive homan’s sign, but it is well-known to be inaccurate

What are the potential endothelial injuries that can contribute to 1/3 of Virchow’s triad?

• surgery

• IV drug users

• trauma

What are the potential causes of venous stasis that can contribute to 1/3 of Virchow’s triad?

• imobility

• traveling

• hyper-viscosity

• increased central venous pressure

What are the potential causes of hypercoagulability that can contribute to 1/3 of Virchow’s triad?

• medications

• disease

• inherited genetic defects

What are medications that can lead to hypercoagulability?

oral contraceptives or estrogen replacements

What are inherited genetic defects that can lead to hypercoagulability?

clotting deficiencies or abnormalities (ex. Factor V, antithrombin 3 defieincey, Protein C or S deficiencies)

What are the reasons someone may have increased central venous pressure, leading to venous stasis?

pregnant people and people with truncal obesity will have downward pressure on the femoral veins and can lead to a DVT because it blocks the blood trying to get up and out of the legs

True or False: hyperlipidemia leads to hypercoagulability, but one of the things that doesn’t is malignancies

false; both can lead to hypercoagulability states

What is used for DVT risk stratification?

well’s scoring

What is the first imaging test done in a suspected DVT?

US of affected limb with doppler

Even though US is the preferred test, what is the gold standard?

venography

What labs can we get when we suspect a DVT?

• D-dimer

• coagulation studies

• anti-thrombin III

• CRP

• ESR

Why is venography gold standard but not always preferred?

it takes longer, is more invasive, and there’s the potential of a rxn to the dye

True or False: Everyone has a little D-dimer in their body because of their natural degradation processes

True

Why can D-dimers support the diagnosis of a clot?

it will be more elevated than usual in cases of large or multiple small clots

When can’t you trust a D-dimer

When people have smaller, insignificant clots that are not creating oclusions (no edema, erythema, etc), then it’s unclear; if someone has less RFs and the levels are elevated, it’s much more likely to be DVT (even if not symptomatic)

What are CRP and ESR?

non-specific inflammatory markers

What is the only part of the well’s score that isn’t given a +1 if present?

Alternative diagnosis to DVT is more likely to get a -2

How does Well’s scoring work in cases where DVTs are unlikely (<2)?

a D-dimer is done; negative → no DVT, positive → do US, positive US → anti-coagulate, negative → no DVT

How does Well’s scoring work in cases where DVTs are unlikely (>2)?

First, get a D-dimer; if negative or positive → US, if no DVT, you could still do venography, or repeat US in 1 wk, then no DVT again confirms, if positive → anticoagulate

When do we automatically do an US for DVTs?

If they have 3 or more criteria from well’s scoring

What score of Well’s criteria do you take action, and what do you do?

What is the goal of DVT treatment?

prevent embolus, prevent recurrent DVT, prevent post-thrombotic syndrome that can lead to permanent venous valve damage

What are the treatment types of DVTs?

anticoagulation, thrombolytic therapy, surgical extraction

What are the DVT treatments in order of preference?

direct oral anticoagulant → warfarin → heparin

What are the direct oral anticoagulants?

• apixaban (eliquis)

• rivaroxaban (Xarelto)

• edoxaban (savaysa)

• dabigatran (pradax)

What is the MOA of apixaban (eliquis)?

inhibits factor Xa

What is the MOA of rivaroxaban (Xarelto)?

inhibits factor Xa

What is the MOA of edoxaban (Savaysa)?

inhibits factor Xa

What is the MOA of dabigatran (pradax)?

direct thrombin inhibitor

What is Warfarin (Coumadin)?

a vitamin K antiagnoist

What does warfarin (Coumadin) do?

inhibits clotting factors II, VII, IX, X

What should be monitored while patients are on warfarin (coumadin), and what should the results be?

monitor INR (2.0-3.0 levels)

How would you reverse the effects of Warfarin (Coumadin)?

vitamin K

What is the MOA of LMWH?

binds to and accelerates antithrombin III

What are the types of LMWH?

• dalteparin (Fragmin)

• enoxaparin (lovenox)

When is LMWH CI?

in renal insufficiency

What are the 2 types of heparin?

1. LMWH

2. unfractioned heparin

How is unfractionated heparin different from LMWH?

more specific for inactivation of thrombin

What will the aPTT of patients on unfractioned heparin be?

1.5-3x the upper limit of the normal range

What are the potential complications of unfractionated heparin?

hemorrhage, HIT

What is the MOA of fondaparinux?

indirectly inhibits factor Xa

What is the most preferred DVT anticoagulantion regimen in low-risk patients?

direct oral anticoagulation alone

What is a PE?

thrombus that has broken off and travels to the pulmonary vasculature

How does a air emboli occur?

air introduced into the venous system, then the air creates a bubble and the bubble itself travels, lodges somewrhere and cuts off everything

How does an embolus form due to amniotic fluid?

amniotic fluid has a different density, so it can rise and move and has the opportunity to block something

How does a fat emboli occur?

usually trauma related, a blood vessel could be opened and teared, and little particles can be introduced to the vein

How can foreign body emboli occur?

common with trauma and IV drug users

How can a septic emboli form?

usually from vegetative plaque of endocarditis that originates in the heart

What are the types of emboli?

• thrombus

• air

• amniotic fluid

• fat

• foreign body

• septic

What is the pathophysiology of PEs?

clot travels and lodges in part of the pulmonary arterial circulation or systemic artery

What are respiratory consequences of PEs?

• increased alveolar dead space

• hyperventiliation

• hypoxemia (ventiliation-perfusion mismatch)

• decreased regional surfactant

What is surfactant needed for?

needed for proper lung tissue function, for it to contract and inhale with inhalaltion and exhalation

What are the hemodynamic consequences of PEs?

• reduces cross sectional area of pulmonary vascular bed

• increases right ventricular afterload

• may results in right-sided HF or ventricular failure

• potential pulmonary arterial vasoconstriction from neurohormonal reflexes

What are the signs of PEs?

• dyspnea

• cough

• pleuritic chest pain

What may be found on PE in patients with a pulmonary embolus?

• tachypnea

• hypoxia

• rales

• fever

• accentuated S2

• tachycardia

• signs related to underlying cause (thrombophlebitis, pregnnacy, drug use)

What is the gold standard test to diagnose a PE?

pulmonary angiography, specifiically helical CT pulmonary angiography

What lab is taken for suspected PEs?

D-dimer is used to exclude PE in a low-probability patient

What test can be done if a CT is not avaliable or CI to diagnose a suspected DVT?

ventilation-perfusion lung scan (VQ)

What are the findings of an ECG in a patient with a PE?

sinus tachycardia and nonspecific ST segment, and wave changes

What are the wave changes seen on ECG in potential PE patients?

Deep S wave in lead 1, significant Q wave and T wave inversion in lead 3

What are the treatments for PE?

• anticoagulation (IN STABLE PATIENTS)

• thrombolytic therapy

• inferior vena cava filter

• surgical extraction (embolectomy)

What is the last resort treatment in a PE?

surigcal extraction (embolectomy) due to high risk of mortality

What are the types of anticoagulation used in PE treatment?

• direct oral anticoagulants (preferred agent)

• warfarin

• heparin

• fondaparinux

What type of heparin is preferred in PE treatment?

LMWH over unfractionated heparin

True or False: direct oral anticoagulants should be used with another anticoagulant in PE treatment

false; direct oral anticoagulants can be used as monotherapy

What is a CI of a inferior vena cava filler in PE treatment?

anticoagulants

When is an inferior vena cava filter in PE treatment indicated?

• recurrent thromboembolism despite adequeate anticoagulation

• chronic recurrent pulmonary emboli with pulmonary hypertension

What are the ways to prevent PEs?

• ambulation

• hydration

• anticoagulation

• compression stockings (30-40 mmHg)

What is a pneumothorax?

accumulation of air in the pleural space (potential space between the visceral and parietal pleurae)

How can a pneumothorax present?

spontaneous or traumatic

How does a primary spontaneous pneumothorax occur?

no underlying lung disease or trauma

How does a secondary spontaneous pneumothorax occur?

complication of preexisting lung disease that alters normal lung structure

How does a traumatic pneumothorax occur?

penetrating or blunt trauma

How does a iatrogenic pneumothorax occur?

during/following a medical procedure

How does a tension pneumothorax occur?

penetrating trauma, infection, CPR, mechanical ventilation; most dangerous kind

Who can have a primary spontaneous pneumothorax?

• tall, thin male

• age 10-30 y/o, younger people

What are the potential RFs of a primary spontaneous pneumothorax?

± history of smoking or FH of pneumothorax

What causes a primary spontaneous pneumothorax?

subpleural apical blebs/bullae rupture

What is the pathophysiology of a pneumothorax?

pleural space fills with gas from a ruptured bleb → gas pressure outside lung overcomes gas pressure inside lung → lung collapses until the rupture is sealed

What are the s/sxs of a pneumothorax?

• sudden chest pain on affected side

• sudden dyspnea

• tachycardia

What may we find on PE when checking the affected side?

• decreased breath sounds on auscultation

• hyperresonance on percussion

• decreased tactile fremitus

• decreased movement of chest

How do people with a tension pneumothorax present?

• hypotension and mediastinal/trachel shift

• hyperressoance on affected side

• hpyoxia

• respiratory failure

What is the best way to diagnose a pneumothorax?

chest radiograph

What may be seen on a chest radiograph in a patient with a pneumothorax?

• visceral pleural line with no lung markings beyond affected lung portion (“companion line”)

• pleural effusion

• “deep sulcus” sign (supine)

What might be seen in a tension pneumothorax on chest radiograph?

• large amount of air in affected side

• shift of mediastinumm toward unaffected side

What is a complication of a pneumonthorax?

• pneumomediastinum

• subcutaneous emphysema

Where would we expect air to leak out in a pneumomediastinum?

air leaks out of skin overlying the chest wall

What is the treatment for an asymptomatic pneumothorax patient?

supportive care and treat depending on risk of recurrence

How is a tension pneumothorax treated?

• needle aspiration in 2nd intercostal space at MCL

• chest tube placement