Venous insufficiency causing congestion and inflammationCellulitisMuscle or tendon injuryBaker cyst (including ruptured synovial membrane)HematomaArterial insufficiency and claudicationAsymmetrical edema (e.g., due to congestive heart failure or liver disease)

74. PE and DVT Flashcards by Tegan Turner

<span>while PE and DVT can occur in any age group, older patients have a much higher incidence, at 1/10,000 in people 20 to 30 years old and 1/100 in people greater than 80 years old.</span>

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P<span>E and DVT are frequently on the differential diagnosis for patients who present with chest pain, dyspnea, syncope, tachycardia, hypoxemia, leg pain, edema, and other nonspecific complaints. </span>

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<span>venous thrombosis occurs when the propensity of blood to coagulate overwhelms endogenous anticoagulant and fibrinolytic systems</span>

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<span>Numerous factors associated with the classic triad of venous injury, venous stasis, and hypercoagulability have been associated with an increased risk of VTE in epidemiologic studies</span>

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<span>might increase a patient’s propensity to clot and should consider these factors when determining whether a patient’s clinical presentation warrants an evaluation for VTE. Important factors include older age, prior history of VTE, active cancer, recent surgery or trauma, recent hospitalization longer than three days, limb immobility, and estrogen use (especially if initiated in the past three months).</span>

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<span>As many as 50% of patients diagnosed with PE have no apparent clinical risk factors for PE or DVT at the time of diagnosis. </span>

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<span>The superficial venous system consists primarily of the greater and short saphenous veins and perforating veins.</span>

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<span>Distal greater saphenous vein thrombi are often referred to as superficial thrombosis, but greater saphenous clots near the connection with the femoral vein should be referred to as DVT. </span>

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<span>he deep venous system includes the anterior tibial, posterior tibial, and peroneal veins, collectively called the calf veins.</span>

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<span>he calf veins join together at the knee to form the popliteal vein, which extends proximally and becomes the femoral vein at the adductor canal. Venous thrombi in the popliteal or more proximal veins are referred to as proximal DVT. T</span>

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<span>The femoral vein (previously known as the superficial femoral vein), is joined by the deep femoral vein and then the greater saphenous vein to form the common femoral vein, which subsequently becomes the external iliac vein at the inguinal ligament. Venous thrombi in the proximal femoral and iliac veins are known as iliofemoral DVT.</span>

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<span>Compression ultrasound, including point-of-care ultrasound, is typically limited to the common femoral, femoral, and sometimes popliteal veins.</span>

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<span>DVT formation typically begins when monocytes expose blood to tissue factor on their surfaces. This process overwhelms natural anticoagulant and fibrinolytic mechanisms and leads to the aggregation of red blood cells, platelets, and fibrin in the venous sinuses or cusps of the lower extremity deep veins. </span>

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<span>A PE can be described as saddle if the clot is visualized across the bifurcation of the main right and left pulmonary arteries </span>

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<span> Increased right ventricular (RV) afterload (i.e., when the pulmonary artery systolic pressure exceeds 40 mm Hg) can lead the thin-walled right ventricle to dilate and become hypokinetic. </span>

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<span>More than 90% of upper extremity DVT occur in the presence of an indwelling catheter or similar device.</span>

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<span>In the absence of a device, upper extremity DVT tends to occur in the dominant arm of young athletes, a condition known as Paget-Schroetter syndrome. Paget-Schroetter syndrome is an effort-induced form of thoracic outlet syndrome</span>

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UE DVT <span>Repetitive motion of the arm in the setting of hypertrophied scalene muscles or congenital cervical ribs causes compression of the subclavian vein and DVT.</span>

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DDX dvt

<ul><li><div>Venous insufficiency causing congestion and inflammation</div></li><li><div>Cellulitis</div></li><li><div>Muscle or tendon injury</div></li><li><div>Baker cyst (including ruptured synovial membrane)</div></li><li><div>Hematoma</div></li><li><div>Arterial insufficiency and claudication</div></li><li><div>Asymmetrical edema (e.g., due to congestive heart failure or liver disease)</div></li></ul>

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<span>The Wells DVT score has not been validated in pregnant women, but the LEFt score has been validated in a study of 157 pregnant women. It consists of 1 point in case of left ( </span><i>L</i><span> ) leg suspicion, 1 point for edema ( </span><i>E</i><span> ), and 1 point if the suspicion occurred during the first trimester ( </span><i>Ft</i><span> ) of pregnancy. A LEFt score of 0 or 1 indicates low PTP. Although not validated, an approach that substitutes the LEFt score for the Wells score in pregnant women is reasonable.</span>

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The D-dimer test measures the enzymatic breakdown of cross-linked fibrin from any intravascular thrombus

What other than a dvt can cause + ddimer results?

Female sex
•
Advanced age
•
Black or African American race
•
Cocaine use
•
Immobility (general, limb, or neurologic)
•
Hemoptysis
•
Hemodialysis
•
Malignancy (active)
•
Rheumatologic disease (rheumatoid arthritis, systemic lupus erythematosus)
•
Sickle cell disease
•
Pregnancy and postpartum state
•
Recent surgery (within 1 month)

ddimer adjusted for age normal limit?

age x5 in mb

Bedside point-of-care ultrasound (POCUS) performed by a trained emergency clinician is 90% to 95% accurate compared to radiology-performed US. 789 Test characteristics are highest for femoral veins and lowest for saphenous and popliteal veins. POCUS of the upper extremity is not well studied and should be performed by radiology when necessary.

Ultrasound cannot be used to rule out iliac or pelvic vein thrombosis. For this, venography (typically CT) is needed. When duplex ultrasound is not available, the decision to empirically anticoagulate while awaiting the availability of ultrasound imaging should be based on the PTP of DVT, and the risk anticoagulation poses to the patient. Generally, patients with low PTP do not need empirical anticoagulation while they wait for diagnostic imaging.

The DOACs rivaroxaban and apixaban do not require bridging with low-molecular-weight heparin (LMWH) and are the first-choice anticoagulants for most patients with DVT

Concern about the ability to reverse anticoagulation should not dissuade an emergency clinician from starting DOAC therapy.

However, DOACs are either contraindicated or not studied for the treatment of DVT associated with pregnancy, severe renal failure, liver failure, antiphospholipid antibody syndrome, and high-risk PE.

Absolute contraindications to anticoagulation include:

- •
  Active bleeding into a critical organ or uncontrolled site
- •
  Severe bleeding diathesis
- •
  Recent, planned, or emergency high-bleeding-risk surgery or procedure
- •
  Recent major trauma
- •
  Recent intracranial, spinal or ocular hemorrhage

Relative contraindications to anticoagulation include:

- •
  History of gastrointestinal major bleeding
- •
  Intracranial or spinal tumors
- •
  Previous bleeding into a tumor
- •
  Large abdominal aortic aneurysm with concurrent severe hypertension
- •
  Stable aortic dissection
- •
  Recent, planned, or emergent low-bleeding-risk surgery/procedure

VTE BLEED score components and points

•
Active cancer, 2 points
•
Male patient with uncontrolled hypertension, 1 point
•
Anemia, 1.5 points
•
History of bleeding, 1.5 points
•
Renal dysfunction (creatinine clearance 30–60 mL/min), 1.5 points
•
Age ≥60 years, 1.5 points

Distal superficial vein thrombophlebitis can adequately be treated with nonsteroidal antiinflammatory drugs and warm compresses. The rate of DVT or PE within three months of superficial thrombophlebitis is about 3%, so patients with superficial vein thrombosis should be scheduled for a repeat ultrasound in 7 days to rule out progression.

If a greater saphenous vein clot is proximal (within 3 cm of the connection with the femoral vein; see Fig. 74.2 ), the risk of extension to the deep venous system is about 25% so therapeutic (full dose) anticoagulation is warranted for at least 30 days.

Massive iliofemoral vein occlusion results in swelling of the entire leg, with extensive vascular congestion and associated venous ischemia, producing a painful cyanotic extremity. There may be associated arterial spasm resulting in phlegmasia alba dolens (painful pale leg), which may mimic an acute arterial occlusion. Elevated compartment pressures can also lead to limb ischemia. Phlegmasia is a limb-threatening emergency.

Upper extremity DVT can cause PE, and all patients with DVT above the elbow require definitive treatment with anticoagulation prescribed at the same doses as lower extremity DVT

The most common symptom of PE is dyspnea

Chest pain is the second most common symptom of PE.

When PE causes pulmonary infarction, symptoms can be clinically similar to lobar pneumonia, including pleuritic chest pain, cough, hemoptysis, and fever

Pulseless electrical activity ([PEA], >20 depolarizations/min, without palpable pulses) is the most common electrocardiographic (ECG) finding in patients with cardiac arrest due to PE

The most common vital sign abnormality in PE is tachycardia, and about half of all patients with PE have a heart rate greater than 100 beats/min

Pulmonary embolism can produce hypoxemia (pulse oximetry reading <95% at sea level or <92% at higher elevations), but the degree of hypoxemia is unpredictable

Alternative diagnoses include pneumonia, acute coronary syndromes, aortic dissection, pericarditis, pleural or pericardial effusion, pulmonary hypertension, pneumothorax, acute decompensated congestive heart failure, asthma, chronic obstructive pulmonary disease, gastroesophageal reflux, dyspepsia, musculoskeletal pain, and nonspecific chest pain.

The most common finding of PE on the ECG is tachycardia.

Symmetric T-wave inversion in the anterior leads (V ₁ –V ₄ ), the McGinn-White S1Q3T3 pattern, and incomplete or complete right bundle branch block ( Fig. 74.9 ) indicate acute cor pulmonale and are associated with more severe PE

omarkers including cardiac troponin, B-type natriuretic peptide (BNP)/N-terminal pro-B-type natriuretic peptide (NT-pro-BNP), and lactate can all be elevated in PE. An elevated troponin indicates myocardial injury and is associated with higher mortality after PE

when false-negative D-dimer results do occur, it may be because the PE is subacute or chronic. The half-life of circulating D-dimer is less than 8 hours. However, the clinical relevance of the circulating half-life is unknown, because large PE continue to release D-dimer as they lyse over time. False-negative D-dimer measurements may also be seen with severe lipemia and ongoing warfarin therapy

Most centers use CTPA as the primary imaging method for evaluating possible PE.

Due to this confusion, the term high-risk PE is a preferred term to describe the PEs resulting in hemodynamic instability.

many institutions now recommend shielded, low-radiation CTPA rather than V./Q.V./Q. scanning as the first test for pregnant women.

One reason a small proportion of women can be ruled out with noninvasive testing is that D-dimer levels fluctuate and steadily increase throughout pregnancy until they peak on the first day after delivery

The average dose of naturally occurring background radiation is 0.5 to 1.0 mSv over a normal gestation. Exposure to radiation doses lower than 50 mSv has not been shown to be associated with different pregnancy outcomes

Factors independently associated with clinical deterioration after PE diagnosis include ED hypotension, hypoxemia, prior coronary artery disease, residual deep vein thrombosis, and right heart strain on echocardiogram. Clues to oncoming cardiopulmonary decompensation include worsening respiratory distress and hypoxemia, increasing tachycardia and shock index, or a change in mental status. Deterioration in the ECG from a narrow-complex tachycardia to an incomplete right bundle branch block to a complete right bundle branch block also suggests life-threatening pulmonary hypertension

PE are classified as high risk, or “massive,” intermediate risk or “submassive,” and low risk. These risk categories are defined by the hemodynamic status of the patient and the presence of right ventricular dysfunction, not by the size of the thromboembolism.

High-risk PE result in hemodynamic instability, defined as a systolic arterial pressure (SBP) less than 90 mm Hg that is sustained for 15 minutes and not caused by dysrhythmia or other etiology. ⁵⁷ Patients who have a drop in their baseline SBP of greater than 40 mm Hg, who require vasopressors, or who have profound bradycardia (<40 bpm) can also be considered high-risk PE. It is also reasonable to require that the patient’s PE be large enough to conceivably cause the patient’s hemodynamic instability.

Intermediate-risk PE requires that the patient be hemodynamically stable and have evidence of RV dysfunction on echocardiogram or a positive troponin. Echocardiographic evidence of RV dysfunction includes RV dilatation, hypokinesis, or bowing of the intraventricular septum toward the left ventricle (LV). RV dilatation on CT (defined as an RV : LV ratio >1) is 88% sensitive for RV dysfunction on echocardiogram, but is only 39% specific. ⁵⁸ CT evidence of RV dysfunction should, therefore, be confirmed with echocardiography. Some guidelines also use a clinical risk model (i.e., the pulmonary embolism severity index [PESI]) and troponin values to subcategorize patients as intermediate-low or intermediate-high ris

Low-risk PE are hemodynamically stable with no evidence of RV dysfunction. These risk categories are important because the mortality increases from less than 1% to 3% (low risk) to 3% to 15% (intermediate risk) to 15% to 50% (high risk). Accordingly, advanced therapies like thrombolysis or thromboembolectomy are not recommended for low-risk patients, sometimes recommended for intermediate-risk patients, and recommended for high-risk patients.

Absolute contraindications to thrombolysis include: (1) gastrointestinal bleeding within previous 30 days; (2) active hemorrhage in any of the following sites at the time of enrollment—intraperitoneal, retroperitoneal, pulmonary, uterine, bladder, or nose; (3) head trauma causing loss of consciousness within previous 7 days; (4) any history of hemorrhagic stroke; (5) ischemic stroke within the past year; (6) history of intraocular hemorrhage; (7) known or suspected intracranial metastasis; (8) liver failure with prothrombin time abnormal (international normalized ratio [INR] > 1.7); (9) surgery that required opening of the chest cavity, peritoneum, skull, or spinal canal within the previous 14 days; (10) subacute bacterial endocarditis under treatment; (11) pregnancy; (12) large pericardial effusion.

Relative contraindications to thrombolysis include: age > 75 years; dementia; surgery more than 30 days but less than 60 days prior; any prior stroke; symptoms suggesting transient ischemic attack in the past 30 days; any prior gastrointestinal bleeding; concurrent use of a thienopyridine (e.g., clopidogrel); INR > 1.7 from warfarin use; any metastatic cancer, recent fracture, recent fall with head strike, history of hematuria, recent dental extraction, or orthopedic surgery.

Systemic thrombolysis dosing regimens: alteplase (recombinant tissue plasminogen activator, rtPA) 100 mg IV over two hours

However, intubation and positive-pressure ventilation increase intrathoracic pressure, lower preload, and can worsen RV compression of the LV. This may precipitate hemodynamic collapse and cardiac arrest in patients with severe PE. Intubation should, therefore, be avoided whenever possible. When intubation is necessary, the emergency clinician should optimize pre-intubation hemodynamics, including with vasopressors, prior to induction. ⁵³

For patients who present with actual or pending hemodynamic instability, the first priority is resuscitation. For hypotensive patients, small volume boluses (such as 250–500 mL) can improve cardiac output

HD resus of pe pts:
If the administration of intravenous fluids is contraindicated or no longer beneficial, vasopressors should be administered, and norepinephrine should be the initial agent in blood pressure support. ¹² Dobutamine is useful as an adjunct but may worsen hypotension unless coadministered with norepinephrine.

HD instability and resus in a pe pt failed fluids, vasopressors:
Extracorporeal membrane oxygenation (ECMO) can unload the right ventricle, increase cardiac output, and provide a bridge to thrombolysis or thromboembolectomy for patients with high-risk PE. ⁵⁴ ECMO requires institutional infrastructure and expertise which is only available in specialized centers. Survival of patients with PE who require ECMO is about 70%. ⁵⁴ ^, ⁵⁵

Patients with a high PTP, no contraindication to anticoagulation, and evidence of hemodynamic instability, including recent syncope, hypotension, hypoxemia, or right heart dysfunction, should receive empirical anticoagulation while awaiting pulmonary vascular imaging

DOAC medications have not been extensively tested in patients with severe PE, pregnant women with PE, or in patients with hypercoagulable states like antiphospholipid antibody syndrome. For these patients, LMWH is preferred.

For patients in whom thrombolysis, surgery, or another advanced intervention is being considered, intravenous unfractionated heparin may be preferable because it has a short half-life, and anticoagulation should be discontinued prior to thrombolysis or a procedure. However, intravenous heparin provides unreliable anticoagulation, and many patients remain subtherapeutic throughout the first 24 to 48 hours of treatment.

All anticoagulants commonly used in the ED, including the DOACs, now have effective reversal agents. The anticoagulant effect of unfractionated heparin can be almost completely and rapidly reversed with protamine sulfate, whereas LMWH can only be 50% neutralized with protamine. Protamine has no effect on fondaparinux, rivaroxaban, or apixaban. Andexanet alfa, a modified recombinant inactive form of human factor Xa, is now available to reverse anticoagulant effect (anti-factor Xa activity) in patients with life-threatening or uncontrolled bleeding on rivaroxaban and apixaban.

Thrombolytic therapy in PE remains a controversial treatment. It is generally agreed that patients with arterial hypotension (systolic blood pressure < 90 mm Hg or > 40-mm Hg drop from baseline) should receive thrombolysis

Thrombolytic in a seriously hypotensive pe pt:
Appropriate regimens for full-dose thrombolysis include alteplase (recombinant tissue plasminogen activator, rtPA) given as a 100-mg IV bolus over two hours, reteplase given as 10 units IV over two minutes and then repeated 30 minutes later, and tenecteplase given as a single weight-based bolus dose over 5 to 10 seconds. Practically speaking, two IV boluses of 50 mg separated by 15 minutes may be more realistic than a two-hour infusion of alteplase for an unstable patient.

PE Surgical thromboembolectomy can be life-saving for patients with severe refractory hypotension or free-floating thrombi in the right heart (“clot-in-transit”), especially if the clot crosses a patent foramen ovale

Surgical embolectomy may be the best option for patients who have severe PE with a contraindication to fibrinolysis; however, extracorporeal perfusion requires intensive heparin anticoagulation, and the patient’s mental status cannot be monitored during surgery—a key concern in patients with a high risk of intracranial hemorrhage.

For the vast majority of ED patients, placement of an inferior vena cava (IVC) filter is not indicated. However, for a patient diagnosed with PE in the presence of an absolute contraindication to anticoagulation, such as a recent cerebral hemorrhage, large cerebral infarction, or brain metastases, the appropriate consultant should be contacted for urgent placement of an inferior vena cava filter.

Hestia criteria for outpt tx PE:

Low-risk PE safe for outpatient treatment if:

•
Systolic blood pressure > 100 mm Hg
•
No thrombolysis needed
•
No active bleeding
•
Oxygen required to maintain oxygen saturation > 94%
•
Not already anticoagulated
•
Absence of severe pain requiring > two doses of intravenous narcotics
•
Other medical or social reasons to admit
•
Creatinine clearance > 30 mL/min
•
Not pregnant, severe liver disease, or heparin-induced thrombocytopenia

Coma is a state of depressed consciousness in which a patient is not aware, is not awake, and does not respond to vigorous stimulation. This stands in contrast to stuporous or lethargic patients, who also may have a decreased level of awareness or consciousness but can be aroused with external stimuli.

Most cases of depressed consciousness or coma are the result of a metabolic derangement, usually a glucose disorder, drug overdose, or adverse drug effect,

Other common causes include:

traumatic brain injury, systemic or central nervous system (CNS) infection, ischemic or hemorrhagic stroke, intracranial mass, and, less commonly, a psychiatric illness

Consciousness consists of two domains: arousal and awareness. Arousal ranges from fully awake, to arousable with verbal or tactile stimulation, to unarousable. Anatomically, arousal is maintained by the subcortical structures, including the brainstem nuclei, thalamus, basal forebrain, hypothalamus and, most notably, the ascending reticular activating system (ARAS).

the ascending reticular activating system (ARAS). ARAS neurons are located predominately in the pons and midbrain, connect to the thalamus, and project to the cortex. Awareness consists of the content of consciousness, ranging from self-aware and coherent to confused, inattentive, or perhaps delusional.

Toxicologic, metabolic, infectious, and other disorders causing diffuse brain injury or neuronal dysfunction cause 65% of coma cases; of these, toxins are the most common

adrenal crisis labs: hyponatremia, hyperkalemia, and hypoglycemia

Critical dx coma/decreased consciousness for toxins

hypoglycemia
opioids
simple asphyxiants
co
historic hypoxia with confusion/seizure/collapse/H sulfide smells like rotten eggs, cyanid (bitter almond smell)
methemoglobinemia

Emergent dx coma or decreased consciousness

sedatives
toxic alcs
inhalants
psych meds with wide qrs
anticonvulsants
anticholi
clonidine
beta blocker
salicyclates
NMS
Serosyndr

Structural critical dx of coma or decr loc

ICH
cortical infarct
cerebellar infarct
basilar a occlusion

An abrupt onset of coma suggests a stroke, seizure, or cardiac event, whereas a more gradual onset of symptoms suggests an infectious or inflammatory process, metabolic disorder, or enlarging intracranial mass.

The combination of hypertension and bradycardia, known as the Cushing reflex , suggests severe ICP elevation.

The main objectives of the neurologic examination are to determine the depth of coma, identify lateralizing deficits, and assess for brainstem dysfunction. The examination should proceed systematically and include an evaluation of the patient’s level of consciousness, cranial nerves, brainstem reflexes, and motor responses

Seizures can also cause horizontal eye deviation, typically away from the cerebral lobe generating the epileptiform activity

Nystagmus in an unresponsive patient may be a sign of nonconvulsive status epilepticus (NCSE), brainstem dysfunction, drug overdose (e.g., anticonvulsants, lithium, ketamine, ethanol, phencyclidine), or envenomation (scorpion sting)

Disconjugate gaze in the vertical plane, also known as skew deviation, strongly suggests a cerebellar or brainstem lesion.

Forced deviation of the eyes, usually in the horizontal plane, may indicate an ipsilateral hemispheric or contralateral pontine lesion.

Brainstem function is evaluated through the various brainstem reflexes, including the oculocephalic reflex (doll’s eyes), oculovestibular reflex (cold caloric testing), corneal reflex, and gag reflex

Conscious patients can usually suppress the oculocephalic reflex.

The oculovestibular reflex is a more sensitive test for brainstem dysfunction and cannot be resisted voluntarily. After cerumen impaction and tympanic membrane perforation have been excluded, the patient’s head is elevated to 30 degrees up from the horizontal and ice water is infused into the external auditory canal. In a comatose patient with an intact brainstem, the stimulus results in sustained conjugate deviation of the eyes toward the ear being irrigated. Absence of a response to the irrigation should raise suspicion for brainstem dysfunction. In response to cold water caloric testing, conscious patients experience not only tonic deviation of the eyes toward the stimulated ear but also nystagmus (with the fast phase away from the side of irrigation), vertigo, nausea, and vomiting. The presence of nystagmus is suggestive of wakefulness and psychogenic unresponsiveness.

74. PE and DVT Flashcards

(108 cards)