DVT & PE Flashcards
Prevention
Goals of therapy:
Prevent thrombus extension & early & late recurrences of VTE
Clinical Manifestations of DVT include
May be asymptomatic, nonspecific
Leg Edema
Tenderness
Discoloration/erythema
Difficulty walking
Clinical Manifestations of DVT include
May depend on size of clot- larger clots tend to?
produce more pronounced symptoms
Clinical Manifestations of DVT include
Most clinically significant PEs orginate from?
LE DVTs. Can have minor S&S & have extensive clot.
Diagnosing DVT
DVT unlikely what test?
Positive?
Negative?
D-DImers
Positive complete venous US
Negative = no DVT
Diagnosing DVT
DVT likely what test?
complete venous US
Treatment for Proximal DVT
At least 3 mo AC; DOAC in noncancer pts if no contraindications
Reassessment of Proximal DVT occurs when?
may extend for how long? and why?
3mo
May extend AC to yearly evaluation d/t risk/benefit, compliance, and patients preference
Treatment of Isolated Distal DVT with High risk recurrence?
3 mo AC
Treatment of Isolated Distal DVT with High risk recurrence?
Treatment or surveillance 4-6 wk AC (full or lower dose) or venous US surveillance
Modified Wells Criteria: Clinical Assessment for PE
What factors are assessed?
Clinical symptoms of DVT (leg swelling, pain with palpation)
Other diagnosis less likely than PE
HR > 100
Immobilization (>/= 3 days) or surgery in the previous four weeks
Previous DVT/PE
Hemoptysis
Malignancy
Prox DVT/PE, no cancer can be treated w/ what?
For how long?
Dabigatran
Rivaroxaban
Apixaban
Edoxaban
3mo
DVT provoked by surgery can be treated w/ what?
For how long?
Dabigatran
Rivaroxaban
Apixaban
Edoxaban
3mo
DVT with no surgery can be treated w/ what?
For how long?
Dabigatran
Rivaroxaban
Apixaban
Edoxaban
3mo
1st unprovoked DVT can be treated with?
for how long?
Rivaroxaban - reduced dose
Apixaban - reduced dose
Extended treatment
Active CA & + VTE/PE can be treated with? for how long?
Rivaroxaban
Apixaban
Edoxaban
LMWH - may be preferred if luminal GI malignancy
If unprovoked DVT & DCing anticoag use what?
ASA
Isolated distal DVT of LE + no symptoms or risks of extension use what?
serial dopplers
Drugs that are Factor Xa inhibitors?
Rivaroxaban
Apixaban
Edoxaban
Drugs that are Thrombin inhibitors?
Dabigatran
Drugs that are Factor Xa/Thrombin Inhibitors?
LMWH
Complications of DVT: Post-thrombotic syndrome
Occurs in up to what % of patients with proximal DVT, within how long, despite anticoagulation?
Results from?
Duration?
Symptoms?
50%
~ 1-2yrs
valvular incompetence &/or residual obstruction
Chronic & progressive
Pain, edema, sometimes ulcerations
Complications of DVT: Venous Ulceration
From what?
Usually appears where?
Prevent by use of?
post-thrombotic syndrome
usually appear perimalleolar area
compression stockings
What type of PE can be life-threatening in normal persons?
What type of PE can be life-threatening in person with impaired physiologic reserves?
Massive emboli
Submassive
2/3 of those who die from PE will do so w/n how long?
1st hour of presentation
In those with HD instability, mortality increases by how much?
7 fold
Heart Failure d/t PE results from?
Vascular resistance to RV output increased RV pressure leading to ventricular wall stress increase leading to cardiac ischemia.
In early phase of Heart Failure d/t PE what compensatory mechanisms maintain flow?
Which leads to?
Tachycardia & RV dilation
RV output falls d/t wall stress & ischemia leading to decreased LV preload
RV dilation causes interventricular septal shift leading to?
decreased LV compliance leading to decreased LV output leading to hypotension
Increased pulmonary vascular resistance is d/t?
thrombus itself & neural reflexes, humoral factor release from platelets/endothelium, & hypoxia
Hypoxia in PE is common d/t
V/Q mismatch
intracardiac shunting thru patent foramen ovale in r/t elevated R heart pressures
Intrapulmonary shunting thru areas of atelectasis & decreased CO
all leading to decreased mixed venous O2 sat
Increased deadspace in PE occurs d/t
ventilated but underperfused areas of lung leading to decreased etCO2 compared to arterial CO2.
Occurs when thrombus occupies >25% of pulmonary vasculature
S&S of PE
Non-specific/asymptomatic
Dyspnea
Tachypnea
Pleuritic pain
Pre-syncope/sycope
Cough
Orthopnea
Wheezing
Tachycardia/afib
Crackles on lung exam (21%)
Hypoxemia
Hypocapnia
Clinical manifestations of Massive PE
Acute cardiopulmonary S&S r/t RV failure or ischemia
Sudden cardiopulmonary arrest, often with bradyarrhythmias, PEA
Significant anxiety, impending doom
Substernal CP - sudden, unrelenting, nonradiating
Syncope d/t low CO or bradycardia
Shock
Acute cor pulmonale -
EKGs - nonspecific but may reveal signs of R heart strain (new R axis deviation or new RBBB) or ST
CXR - nonspecific but pt’s w/ PE in PIOPED-I study were more likely to have elevated R diaphragm, pleural based
PE may lead to acute cor pulmonale which is shown by?
distended neck veins, prominent component of 2nd heard sound
PE may cause EKG changes such as?
signs of R heart strain (New R axis deviation or new RBBB) or ST
PE may cause CXR changes such as?
elevated R diaphragm
Pleural based opacities,
Westermark’s sign (dilation of pulm. vessels & sharp cutoff)
EKG suspicious for PE will Show S1Q3T3 meaning?
S-waves in lead I
Q-waves in lead III
Inverted T-waves in lead III
Differential Dx of PE can include?
MI
Pericarditis
Heart Failure
Pneumonia
Asthma
COPD
PTX
Rib Fx
Musculoskeletal pain
Intrathoracic CA
Sepsis
Diagnosing PE
Need what?
May Utilize objective clinical assessments such as?
Clinical suspicion
Wells, Geneva, revised Geneva
Diagnosing PE
Why use CXR?
may have nonspecific findings of?
utilized in general evaluation of pts w/ possible PE to exclude other causes of clinical presentation
Elevated diaphragm, pleural based infiltrates, focal oligemia (Westermark’s sign), hypovascularity
Echocardiography (TTE) may show?
greater RV diameter & evidence of RV strain & failure
McConnell’s sign: regional RV dysfunction w/ akinesia of mid free wall but normal motion
May actually identify PE
Echo does not r/o presence of PE
Suspected PE in patient w/o hemodynamic instability
Assess clinical probability of PE
Low or intermediate clinical probaility or PE unlikely what test(s)?
D-dimer: if negative no treatment
D-dimer: If positive CTPA
CTPA: no PE no treatment
CTPA: PE confirmed treatment
Suspected PE in patient w/o hemodynamic instability
Assess clinical probability of PE
High clinical probability or PE likely what test(s)?
CTPA: no PE no treatment or investigate further
CTPA: PE confirmed Treatment
Suspected PE in a patient w/ hemodynamic instability
Perform what test?
If signs of PE are present, what test(s)?
Bedside TTE looking for RV dysfunction
CTPA if immediately available. If not initiate treatment of high-risk PE
CTPA if positive initiate treatment of high-risk PE
CTPA if negative investigate other causes of shock or instability
Definition of hemodynamic instability, which delineates acute high-risk PE
Cardiac Arrest
Obstructive shock
Persistent Hypotension
Need for CPR
SBP < 90 mmHg or vasopressor required to achieve a BP >/= 90 mmHg despite adequate filling status AND End organ hypoperfusion (AMS, cold, clammy skin, oliguria/anuria; increased serum lactate)
SBP < 90 mmHg or SBP drop >/= 40 mmHg, lasting longer than 15 min and not caused by new-onset arrhythmia, hypovolemia, or sepsis
Risk Stratification
Clinical findings?
RV failure (TTE, CT)
tachycardia
hypotension
respiratory insufficiency
syncope
Risk Stratification
Lab indicators
troponin
BNP
Lactate
hyponatremia
PE O2 for sats > 90%
high flow NC
NIV
Invasive MV
Tx of RV failure
Volume optimization
Dose?
Properties and use?
Caveats?
Cautious volume loading use NS or LR </= 500 ml over 15-30 min
Consider in patients with low CVP
Volume loading can over-distend the RV worsening ventricular interdependence and reduce CO
Tx of RV failure
Vasopressors and inotropes
Norepi
Dose?
Properties and use?
Caveats
0.2-1.0 nanogram/kg/min
Increases RV inotropy and systemic BP, promotes positive ventricular interactions, and restores coronary perfusion gradient
Excessive vasoconstriction may worsen tissue perfusion
Tx of RV failure
Vasopressors and inotropes
Dobutamine
Dose?
Properties and use?
Caveats?
2-20 nanogram/kg/min
Increases RV inotropy, lowers filling pressures
May aggravate arterial hypotension if used alone, w/o a vasopressor; may trigger or aggravate arrhythmias
Tx of RV failure
Mechanical circulatory support
Strategy?
Properties and use?
Caveats?
Veno-arterial ECMO/extracorporeal life support
Rapid short-term support combined w/ oxygenator
Complications w/ use over longer periods (>5-10 days), including bleeding and infections; no clinical benefit unless combined with surgical embolectomy; requires an experienced team
Anticoagulation for high or intermediate probability includes?
LMWH, fondaparinux, UFH, NOACs
If anticoagulation is initiated parenterally, what is recommended for most patients?
LMWH or fondaparinux over UFH
When oral anticoagulation is started in patient w/ PE who is eligible for NOAC (which drugs?) a NOAC is recommended in preference to?
apixiaban, dabigatran, edoxaban or rivaroxaban
VKA
When patients are treated w/ a VKA overlapping w/ what?
Until a INR of what is reached?
parenteral anticoagulation
2.5 (range of 2-3)
Rescue thrombolytic therapy is recommended for patients with what?
hemodynamic deterioration or anticoagulation treatment
Systemic Thrombolytic is recommended for?
high-risk PE
Anticoagulation dosing
Enoxaparin
1mg/kg q12 hr
1.5mg/kg once daily
Anticoagulation dosing
Tinzaparin
175 IU/kg once daily
Anticoagulation dosing
Dalteparin
100 IU/kg q 12 hr
200 IU /kg once daily
Anticoagulation dosing
Nadroparin
86 IU/kg q12 hr
171 IU/kg once daily
Anticoagulation dosing
Fondaparinux
Body weight < 50kg
Body weight 50-100 kg
Body weight > 100 kg
5mg once daily
7.5 mg once daily
10 mg once daily
Thrombolytic dosing
rtPA
100 mg over 2 hr
0.6 mg/kg over 15 min (max dose of 50 mg)
Thrombolytic dosing
Streptokinase
250,000 IU as a loading dose over 30 min, followed by 4400IU/kg/hr over 12-24 hr
Accelerated regimen: 1.5 million IU over 2 hr
Thrombolytic dosing
Urokinase
4400 IU/kg as a loading dose over 10 min, followed by 4400 IU/kg/hr over 12-24 hr
Accelerated regimen: 3 million IU over 2 hr
Special circumstances
If IV dye allergy:
D-dimer w/ clinical assessment to exclude PE
If mild allergy, pretreat w/ steroids
Venous u/s & VQ scan if severe allergy
Special Circumstances
If impaired renal function:
D-dimer w/ clinical assessment
venous u/s
VQ scan if u/s (-)
Medication tips
LMWH dosing in obesity
VKA monitoring after adjustment
VKA monitoring stable dose
No anti Xa levels in which patients
No monitoring of DOACs when?
use actual body weight
</= 4 wks
6-12 wks
obesity or CrCl < 30 ml/min
during bleeding
Medication tips
INR w/ VKA 4.5-10 & no bleeding
Elevated INR + life-threatening bleeding
Bleeding on Xa inhibitor
Bleeding on dabigatran
Bleeding on LMWH or UFH
Resume anticoagulation w/n how long of bleed?
no intervention
PCC + vit K
+/- PCC or Xa (recombinant), inactivated-zhzo
idarucizumab
protamine
90 days
Elderly considerations for anticoagulation
no bid differences in timing or dosing
pay attention to renal function
