Module 3: Shortness of Breath Flashcards
SOB is a common symptom of?
lung disease, myocardial ischemia or dysfunction, systemic illness (anemia, shock, sepsis, fever), obesity, deconditioning
is SOB objective or subjective?
subjective experience of breathing discomfort
what are respiratory system dyspnea
- central controller 2. ventilatory pump 3. gas exchanger
what are CV system dyspnea?
- acute ischemia 2. systolic dysfunction 3. valvular disorders 4. pericardial diseases
what is critical asthma syndrome?
umbrella term: life threatening, status asthmaticus, near-fatal asthma
what are the symptoms of critical asthma syndrome?
- inability to speak 2. reduced peak expiratory flow rate of <25% of a patient’s personal best 3. failed response to frequent bronchodilators and IV steroids 4. require emergency care 5. prone to complications 6. utilize significant resources
what is the hallmark physical examination in acute respiratory failure
- inability to speak 2. upright posture 3. use of accessory muscles of respiratory and paradoxically 4. minimal wheezing –>indicates impending loss of air movement
what is the progress to respiratory failure?
emergent airway management. lethargy, loss of wheezing, cyanosis, reduced or paradoxical respiratory efforts less obvious: early signs of respiratory exhaustion such as progressively shallow respirations, weakness, progression loss of alertness
what does a declining course look like?
- first line is bronchodialtors, failing bronchodilators > 20 minutes, increased care, worsening respirator acidosis, signs of increasing fatigue.
- acute respiratory alkalosis occurs early
- acute respiroatyr acidosis is LATE
- NIPPV - can be used selectively - reduce barotrauma, improve comfort reduce nosocomial infections
- needs to be placed early and closley monitor - if not improving need to intubate (this is not a rescue treatment)
- contraindications: vomiting, obtunded, combative, AMS
what are absolute indications for endotracheal intubation
- cardio pulmonary arrest or apnea
- imminent respiratory failure (paradoxical breathing, lethargy, hypopnea)
- acute respiratory failure with PaO2 < 60 and/or PaCO2>50
- acute on chronic respiratory failure
relative indications for ET intubation
- hypercarbia PaCO2>50 or increase > 5 mmHg/hour
- worsening respiratory acidosis
- inability to care for patient appropriately
- signs of fatigue (shallow respirations)
- failure to respond to bronchodilator therapy
how do you intubate an awake but failing patient
- awake & upright fiberoptic broncchoscopic
- induction without neuromuscular blockade
- RSI
- don’t use nasotracheal intubation d/t potential nasal polyposis
what do you do for intubation for imminent respiratory failure
- RSI
- largest ETT possible, NO over bagging
*
what are the induction agents recommended for ET intubation for imminent respiratory failure
- hypotensive/normotensive - ketamine (caution CV disease)
- hypertensive - propofol (give with volume)
- hemodynamic uncerntainty - etomidate
what are the recommendations for neuromuscular blocking agents
- succinylcoline - contraindicated in malignant hyperthermia, hyperkalemia, elevated intra-occular pressure and burns
- rocuronium or vecuronium - may have prolonged effect
what are some complications with intubation
- hypotension
- dynamic hyperinflation and increased intra-thoracic pressures may impair R-sided cardiac venous return
- arrhythmias from high dose beta-2-agonists and eletrolyte abnormalities
- barotrauma
- laryngospasm
- worsening bronchospasm
- seizures
- aspiration
- intravascular volume depletion d/t work of breathing with accompanying tachypnea and diaphoresis result in significant insensible volume loss
- post intubation PTX or pneumomediastinum - uncommon but an be fatal
physical exam cluse of pneumothorax
- tracheal deviation away from affected side
- anterior chest or neck crepitus
- unilateral loss of lung sounds
- tachycardia
- hypotension
- central cyanosis
- low pulsus paradoxus -> presence of severe hyperinflation causing extracardiac tamponade
- CT is gold standard for diagnosing PTX-> bedside ultrasound is emerging
- if US is not immediately available, and patient is deteriorating->empiric chest tube for decompression (tension PTX) before obtaining CXR
what are labs/tests you need to do?
- ABG essential - trend this
- describes their ability to ventilate and oxygenate
- eval for concomitant acid-base disturbances: metabolic acidosis, metabolic alkalosis (resulting from volume depletion) or respiratory alkalosis (pulmonary embolus)
- normal ABG with increasing WOB is ominous sign
- may have hypercarbia d/t airflow obstruction, hypoxemia from V/Q defects
- ECG (ischemia, arrhythmias - especially in older adults)
- CBC - infection
- chemitries
what other additional tests do you want?
- chest imaging
- CXR (most common)
- PEFR and bedside spirometry
- flow volume loops - this helps figure out the reason for the exacerbation/diagnosis
what is the treatment?
- goal is to maintain adequate perfusion and cardiac output
- rapid IVF
- mechanical ventilation
- will have some degree of hypoxemia d/t hypercapnia and V/Q mismtch
- PaO2 <55 is uncommon and should prompt search for additional processes (ex: intrapulmonary shunt from PNA or atelectasis)
- supplemental O2 (generally hypercarbic, not hypoxic)
- other causes of hypoxemia include PTX or pulmonary aspiration
treatment medications
- bronchodilators
- systemic corticosteroids
- leukotriene receptor agonists (montelukast)
- IV magnesium
- smooth muscle relaxer (bronchodilator)
- if refractory: SQ terbutaline & epi
- sedation & put on vent. if needed
what order should you think about fixing things for mechanical ventlation
- treat dynamic hyperinflation 1st & gas exchange abnormalities 2nd
does mechanical ventilation alone help the patient?
- no.
- have to watch for elevated airway resistance and mucous plugging that leads to airflow obtstruct & dynamic hyperinflation as gas is not able to escape
- inspiratory capacity and inspiratory reserve volumes fall as functional residual capacity inreases
- as IC approaches TLC inspiratory efforts are impeded by over stretched inspiratory muscles & diaphraghm flattens
- develops respiratory fatigue–>respiratory failure
- increased intra-thoracic pressure in dynamic hyperinflation leads to impaired venous return to the R heart and hemodynamic compromise
- high intra thoracic pressures may worsen dead space by reducing blood flow to alveolar units thereby worsening ventilation –> respiraotry acidosis
what happens if you increase intra-thoracic pressure?
- worsen PaCO2 d/t intrinsic PEEP –> not enough time to exhale before another vent breath is delivered
- increasing TV in order to increase the Ve (respiratory rate x tidal volume) will lead to unacceptably high airway pressures resulting in barotrauma
- strategy should be Low Ve, slow RR (8-10 bpm allowing time for full exhalation)
- extrinsic PEEP should match intrinsic PEEP and should be measured every 6-8 hours
vent settings later on?
- once Ve is accetably low and intrinsic PEEP is minimized, then improve CO2 gas exchange
how to treat refractory cases?
Heliox (helium-oxygen): decreased turbulent airflow in the large airways, has minimal toxicity
Anethetics: IV ketamine or propofol; inhaled halothane, enflurane, isoflurane, diethyl ether
Veno-veno ECHMO - helps to oxygenate the blood, the patient must have a good heart to pump, they just need help moving the air
upper airway/extra thoracic causes of wheezing
- anaphylaxis
- vocal cord dysfunction - diagnostic evaluation is laryngoscopy
- other vocal cord issues - edema
- laryngeal stenosis
- laryngocele
- tonsillar hypertrophy
- epiglottic swelling
- goiter
central airway causes of wheezing
- tracheal stenosis
- tracheo-bronchial tumors
- tracheo-bronchiomalacia
- relapsing polychrondritis
- tracheobronchial amyloid
- mucous plugging
- vascular rings
- medistinal masses
lower airway causes of wheezing
- bronchiectasis/COPD
- bronchiolotis
- bronchiolitis obliterans
- cardiac
- carcinoid
- parasitic infections
- vasculitis
- anatomic airway distortion
- focal wheezing
- myocardial ischemia
- aspirated foreign body
what are some triggers for SOB?
- pulmonary infections - viral/bacterial
- sepsis
- pulmonary aspiration
- GERD
- inhaled foreign body
- ischemic cardiac disease
- anaphylactoid or anaphylactic reactions to drugs/food
- once intubated-mucous plugs
what is pleural effusion
excess of fluid in pleural cavity
transudative pleural effusion
- cardiac (HF) most common
- renal
- hepatic
exudative (inflammatory) causes of pleural effusion
- malignancy
- infection
what is most likely cause of exudative effusion?
PNA - most will not require interventions
Malignancy is the most important and will need follow-up
*an undiagnosed unilateral pleural effusion w/o a history suggestive of acute infection should be considered malignant until proven otherwise
how should transudative effusions be treated?
bilateral effusions are usually d/t cardiac/renal/hepatic impairment –>treatment of cause will usually improve effusions w/o need for intervention
how do you diagnose cardiac effusions
- shortness of breath and one or more of the following
- previous h/o HF
- paroxysmal nocturnal dyspnea
- orthopnea
- S3 gallop
- jugular venous distention
- positive abdomino-jugular test
- displaced apical impulse
- radiological cardiomegaly, cephalization of the vessels and interstitial or alveolar edema
duration of development of pleural effusion
- rapidly: over hours to days
- injury to chest wall
- recent chest infection
- slow over weeks to months
- empyema
- malignancy
- TB pleuritis
clinical findings of PE
- asymptomatic
- SOB vs DOE
- fever
- pleuritic chest pain
- “stony” dullness to percussion
- reduced chest expansion on affected side of the hemithorax
- reduced BS over thee effusion
- bronchial breathing-area superior to the fluid
improtant history points
- focus on severity & rate of onset
- dyspnea
- cough (non-productive)
- pleuritic chest pain
- constitutional symptoms
- fever
- sweats
- weight loss
- recent injury or interventions to chet
- recent illness, especialy r/t chest
- recent hospitalizations or operations such as cardiac surgery
- current or h/o malignancy
- previous exposure to TB
- full occupational history (including asbestosis)
- smoking/tobacco history
- drugs, including recent changes to Rx and use of any anti-coagulation)
- assessment/evidence of uncontrolled cardiac, hepatic, renal failure
how do you diagnose pulmonary effusion
- CXR 1st
- ct scan is standard of care and tells you size and location and if it’s loculated
- CBC tells you infection? blood loss? platelet abnormality? liver/renal function? also look for hypoalbuminemia as this can cause effusion
- TTE/BNP for those with bilateral effusion to evaluate for heart failure
- can exclude HF if BNP is lower than 100 pg/mL
do you need to do throacentesis in acute decompensated HF?
no, unnecessary unless:
- chest pain
- fever
- unilateral pleural effusion (especially left sided)
- absence of cardiomegaly on CXR
- no response to diuretics
- when aspirated pleural fluid is usually yellowish or seirous, can also be watery
pleural fluid analysis in acute decompensated HF
- serum to pleural fluid albumin gradient (serum albumin - pleural fluid albumin) >1.2 g/dL
- LDH < 2/3 of upper normal limit for serum
- pleural fluid to serum LDH ratio < 0.6
- cholesterol < 45 mg/dL
- pleural fluid to serum protein ratio < 0.5
- serum to pleural fluid protein gradient > 3.1 g/dL
- protein levels lower than 3 g/dL
*
when do you see effusion w/ acute decompensated HF
45% of patients on CXR
% icreased when more sensitive techniques (u/s ct)
CXR:
BL 60%
right 30%
left 10%
loculated means?
defined borderes
light’s criteria for lab diagnosis of exudative effusion
- > 3gm protein
- PL/Sr protein > 0.5
- LDH > 200 IU
- glucose > 1
- WBC > 25,000
- Sp Gr > 1.016
- pH low, < 7.2 = empyema
light’s criteria for lab diagnosis of transudative effusion
- < 3 gm protein
- PL/Sr pro < 0.5
- LDH < 200 IU
- glucose < 1
- WBC very low
- Sp Gr < 1.016
- pH high > 7.3
pleural fluid analysis
- color
- clear = normal/transudate
- anchovy = exudate
- white = chylothorax/lymph/exudate
- chemistries
- protein LDH, glucose
- cell count
- pH
- cytology
what is symptom management?
- diuresis
- oxygen
- determine cause
- help locating
- tap–> thoracentesis
- chest tube
- thoracoscopic surgery
what is pneumothorax?
air in pleural cavity (interspersed between the lung and chest wall)
- generally associated with physical exertion
- presences/absence of breathlessness influences management strategy
how are PTX categorized?
PSP - spontaneous pneumothorax
SSP secondary pneumothorx
what is suggestive of a tension pneumothorax?
severe symptoms & signs of respiratory distress
are signs of dyspnea/CP typically present ?
not always, need high index of suspicion
signs & symptoms of pneumo
- sudden
- ipsilateral pleuritic pain
- sometimes extreme SOB
- labored respirations
- anxiety
- SQ emphysema
- tension
- JVD
- traceal deviation away
- medistinal shift away
physical signs of pneumothorax
- after procedure (central line placement)
- reduced lung expansion, hyper-resonance
- diminished breath sounds on side of PTX
- clicking are cardiac apex, occassionally heard
- cyanosis, sweating, severe tachypnea, tachycardia, hypotension –> might indiate tension PTX
diagnostic tests for pneumothorax
- standard erect PA CXR is gold stsandard for 1st test
- lateral CXR may provide additional information
- expiratory films do not provide additional benefits
- supine and lat. decub XR are good for trauma patients or those that can’t be moved, but aren’t as accurate
- US main value added is management of supine trauma patients
- digital imaging - magnification, measurement & contrast manipulation, ease of transmission, storage & repordution
- CT is gold standard in detection of small PTX and size estimation
what should you do first for diagnostic tests for PTX
CXR, inspiration & look for displacement of pleural line
- CXR is the main stay but has severe limitation when quantifying size (then need CT)
- presence of bullous lung disease can lead to erroneous diagnosis
what other differential diagnosis can you have with PTX
myocardial infarction
pulmonary emboli
pleural effusion
pericarditis
background on primary spontaneous PTX (PSP)
- greater liklihood in men
- sub-pleural blebs and bullae at lung apices in up to 90% of cases
- small airway obstruction, mediated by influx of inflammatory cells, often characterizes PTX and may manifest in smaller airways at an earlier stage with ‘empysema like changes’
- health male smokers have a 12% vs non smokers have 0.1% risk
- taller men have > risk since negative pleural presure gradient increases –> lung base to apex
- alveoli at lung apex have a significantly greater distending pressure
- predisposed to development of apical sub-pleural blebs
what are risk for recurrence of PSP?
< 4 years since last PSP, smoking, height, > 60 y/o
do patients stop smoking after first PSP?
no they continue despite counseling
symptoms of PSP
can be minimal or absent
symptoms are greater in SSP, even if the PTX is relatively small
many patients present several days after onset, the longer the timer period the greater the risk of re-expansion pulmonary edema (patient gets used to PTX, so when its fixed it brings on problems)
background of secondary PTX - SSP
- associated w/ underlying lung disease (most common COPD)
- elderly w/ unrecognized lung disease tolerate them less well
*
risk factors for recurrent SSP
age, pulmonary fibrosis, empysema
what has higher morbidity & mortality, PSP or SSP?
SSP
does smoking minimize risk of SSP?
yes
how is breathlessness compared to size of PTX in SSP
breathlessness is out of proportion to PTX size
unreliable indiator of PTX size
symptoms are greater in SSP
when should you consider tension PTX vs SSP
when severe symptoms are accompanied by signsof cardiorespiratory distress
what is more important for ptx, size of ptx or degree of clinical compromise?
degree of clinical compromise
how are accurate ptx sizes calculated, what exam?
ct scan
how do you differentiate large from small ptx?
visible rim of > 2 cm between lung margin and chest wall at the level of the hilum
what does breathlessness tell you in ptx?
need for active intervention as well as supportive treatment (including O2)
what determine sthe rate of resolution and relative indication for active intervention?
size of ptx
how long would a complete ptx take to resolve?
up to 6 weeks and if a persistent air leak even longer
what do you do w/ significant breathlessness
undergod immediate interventions
when is obseration the treatment of choice in ptx?
for small PSP w/o significant symptoms
some asymptomatic patients w/ large PSP
conservative management with small ptx is safe
what types of ptx are life threatening?
tension ptx & bilateral ptx
the require immediate chest tubes
what should you consider if the patient has marked breathlessness with a small psp?
possible tensio ptx
should you give supplemental high flow O2?
when possible!
should you treat hypoxemia?
yes - you can get a four fold increase in rate of resolution!
what should need decompression happen
w/ a 14-16 gauge
2nd intercostal space at mid clavicular line
may reduce length of stay
should not be repeated unless there were technical difficulties
following failed needle aspiration, small bore <14 french chest tube insertion is recommended
do people go home with chest tubes?
some people do for PTX that won’t go away
should suction be used?
not routinely
risk of re-expansion pulmonary edema
if you do, use high volume low pressure suction systems
a persistent air leak w/ or w/o incomplete re-expansion of the lung is the usual reason for consideration of the use of suction
what is optimal suction pressure
10 to 20 cm H2O
what else should you do if you need to use suction?
think about referral to thoracic surgeon
what is SQ emphysema
- a well recognized complication of chest tube
- usually seen w/ malpositioned, kinked, blocked or clamped chest tubes
- can happen with large air leak and small bore chest drain
- sometimes acute airway obstruction/thoracic compression may lead to respiratory compromise leading to thacheostomy, skin incision decompression and insertion of large bore chest drain
typical clinical situations where tension ptx arises
- ventilated patients in ICU
- trauma
- resuscitaiton (cpr)
- lung diease, acute presentaitons of asthma/copd
- blocked, clamped/displaced chest drains
- non-invasive ventilation
- hyperbaric O2 treatment
*
what does venous thromboembolism vte include?
dvt (deep vein thrombosis) & pulmonary embolism (PE)
statistics on PE
60K-100K americans die of VTE each year
10-30% of people will die w/in one month of diagnosis
incidence increases exponentially w/ age
sudden death is the first symptom in ~ 25% w/ PE
acquired risk factors for 1st episode of vte
increasing age
cancer
antiphospholipid
infections (HIV/sepsis, etc)
inflammatory disorders (SLE, IBD, vasculitis)
nephrotic syndrome
obesity
smoking
environmental risk factors for 1st episode of vte
surgery
tramua
immobilization
central venous catheter
pregnancy/post-partum
hormonal therapy
chemotherapy
travel
genetic risk factors for 1st episode of VTE (much less common)
- antithrombin deficiency
- protein C deficiency
- protein S deficiency
- factor V leiden
- prothombin gene mutation
- non-O ABO blood group
- dysfibrogenemia
- elevated factor VIII, IX, XI
- hyperhomocysteinemia (including homocystinuria)
types of emboli
- thromboembolism
- air from catheters, surgery
- fat (long bone fx)
- amniotic fluid
- septic (endocarditis)
- foreign bodies (IVDA)
DVT symptoms
- extremity swelling
- pain/cramp ache in calf or thing
- warmth
- erythema
- >50% will have long term complications post thrombotic (swelling, pain, discoloration & scaling in the affected limb)
PE symptoms
- dyspnea even at rest/SOB
- abrupt onset, central PE will be acute and severe
- small peripheral PE is often mild and may be transient
- if pre-existing HF or pulmonary disease can have worsening dyspnea and that may be the only symptom
- hemoptysis
- tachypnea
- accessory muscle use
- hypoxemia
- chest/pleural pain: irriation d/t distal emboli causing pulmonary infarction
- central PE - typical anginal character, possibly d/t RV ischemia
- requires DDx with ACS or aortic dissection
- changes in MS/anxiety
- pre-syncope/syncope
- tachycardia
- fever
- hypotension
initial testing for DDx r/t dyspnea
ABG
CRX - lateral can show RV enlargement/failure
ECG - more severe PE can show chagnes indicative of RV strain such as inversion of T waves in leads V1-V4, incomplete/complete RBBB
Milder: only sign is tachycardia
Artial arrhythmias, most frequently is AF by may be assocaited w/ acute PE
differential diagnoses of dyspnea
- pericardial tamponade
- acute MI/ACS
- tension PTX
- aortic dissection
- PNA
- atelectasis
- aspiration
- pulmonary edema
- asthma
key assessment in patient’s thrombosis risk factors
- history
- wells’ criteria for DVT PE diagnosis
- geneva score for PE diagnosis
- PERC - tool identifies outpatients present with chest pain who are thought to be low risk for PE in whom further diagnositc testing can be avoided
D dimer
- elevated in acute thrombosis d/t simultaneous actiation of coagulation and fibrinolyss
- negative predictive value of D dimer is high and normal levels renders acute PE/DVT unlikely
- if you have a negative D dimer you can say the patient most likley doens’t have a DVT, but if it’s positive then they need to get a scan
- D dimer test is not useful for confirmation of PE
diagnostic approach for patient’s with low pre-test porbability of PE
- PERC criteria should be applied
- in those who meet all PERC criteria the risk for PE is lower than the risk of testing
- those who do not meet all of the criteria should be further stratified by using a plasma d dimer test
diagnostic approach for patients with intermediate pretest probability of PE
- do not apply PERC
- d dimer testing is warranted
- a normal d dimer level provides sufficient negative predicitive value for PE - no imaging studies are indicated
- elevated plasma d dimer should prompt imaging studies
- CTA
- VQ scan if not able to do CT scan
diagnostic approach for patients with high pretest probability of PE
- do not apply PERC
- high pretest probability of PE according to clinical perspetive or prediction tool imaging studies should be performed
- CTPA is the preferred method of diagnosis when available
- V/Q lung scanning should be used with CTPA is unavailable / contraindicated
- d dimer assay should not be obtained in patients with a high pretest probability of PE b/c a negative value will not obviate the need for imaging
classificaiton of PE
- high risk (massive) PE: life threatening condition
- hypotension, cardiogenicshock, circulatory collapse
- intermediate risk (sub massive) PE
- echo evidence of RV dysfunction or pulmonary HTN or presence of increased markers of myocardial injury (troponin)
- low risk (non massive) PE
- no evidence of RV dyfunction, pulmonary HTN, increased troponin
why does RV fail with PE
- acute PE interferes w/ both circulation and gas exchange
- RV failure and obstructive shock due to pressure overload is the primary cause of death in severe PE
- RV fails to maintain enough blood flow through pulmonary circulation to achieev adequate LV filling
PE assocaited RV failure diagnosis
- PE evidence of RV dysfunction
- JVD, distened neck veins
- parasternal heave
- accentuated pulmonary component of 2nd heart sound
- systolic murmur consistent with TR (heard at RSB), severe TV insufficiency
- peripheral edema - generally late
- diagnosis
- 4 chamber cardiac view chest CT that can identify RV pressure overload
- TTE: RV dilation, interventricular septal flattening w/ paradoxic motion, increased RV/LV ratio, RV hypokinesis, pulmonary hypotension, increased TR
massive PE/ RV failure managment
- systemic thrombolysis is first line treatment
- surgical pulmonary embolectomy
- catheter direction thrombectomy
- treatment goals:
- optimizing pre-load, RV contractility and coronary perfusion pressure and minimizing afterload
- preload: give volume challenge, may initialy increase CO but continued fluid may result in RV volume overload, watch CVP
- inotropic agents: dobumatine, may require other pressors
- afterload reduction: inhaled nitric oxide, milrinone
- ECMO & VAD
anticoagulation treatment phases
- 5-10 days
- acute, IV heparin, SQ LMWH, SQ fondaparinux
- 3-6 months
- short term, warfarin, SQ LMWH
- > 3-6 monhts
- long term, warfarin, SQ LMWH (in cancer) ASA, nothing
acute phase management of PE/DVT
- catheter directed thrombolysis w/ mechanical thrombectomy is considered for:
- life/limb threatening thrombosis or significant thrombus burden
- systemic (massive PE)
- perform ASAP as thrombus has not yet had time to become better organized which means more difficult to lyse/fragment
- the longer you wait, the less favorable benefit risk ratio in short term phase
- thrombolytic therapy
- used for acute exensive proximal LE DVT or with proximal DVT that fails to respond with initial anti-coagulation
why is UFH or LMWH good for acute phase PE management
shorter half life
facilitates peri-procedural management
why is UFH good for acute phase management
high bleeding risk - shorter half life and complete reversibility
morbidly obese and underweight and patients w/ severe renal impairment/unstable renal function
needs close monitoring w/ frequent blood draws
UFH 8-10 fold higher risk for HIT than LMWH
why is LMWH good for accute phase PE management?
can be perferred outside of special hospitalized populations
use of fondaparinux in acute phase management
extremely low incidence of HIT
can be used instead of warfarin
has long half life w/ normal renal function
lack of antidote
use of warfarin in acute phase management
delay use until all planned invasive procedures are completed
begin once therapeutic levels of UFH/LMWH are achieved
should be 5 days overlap and until INR of 2 or more is achieved for 24 hours
information on direct oral anti-coagulants
- no rotine monitoring, not easily reversible
- have longer half life than UFH/LMWH
- can accumulate in impaired renal/hepatic funciton
- caution w/ low platelets as high bleeding risk, potent drug/drug interactions
- limited experience w/ peri-operative managment
- Pradaxa needs 5 days of parenteral AC
- Xarelto/Eliquis can be used w/o initial parenteral therapy
- Xarelto - risk for GIB in elderly
management of cvc associated dvt
AC w/o CVC removal
removal can be considered if symptoms don’t resolve
AC for at least 3 months or duration of CVC whichever is longer
at least 3 months of AC for pacemaker wire associated CTE
management of AC for DVT/PE
ambulation is safe after therapeutic AC is achieved
SCD - do not increase risk of recurrent VTE, do not have any beneficial effect on leg discomfort associated w/ DVT
active cancer is a potent risk fator continue AC as long a underlying cancer is active
unprovoked VTE - high risk for recurrence, need long term AC, reassess anually
contraindications to outpatient anticoaguation treatment
- active or high risk of bleeding recent surgery (7 days)
- cardiopulmonary instability
- severe symptomatic venous obstruction
- high risk pulmonary embolism, SBP<90, hypovolemia, sepsis
- thrombocytopenia (<50000)
- other medical/surgical condition requiring inpatient management
- medical non-compliance
- geographical or telephone inaccessibility
- poor hepatic function (INR 1.5)
- unstable renal function
- poor home health care support environment
diagnosis of dvt not able to anticoagulate
if contraindicated to anticogulation placement of a vena cava filter can be considered in patients at risk for PE
distal calf DVT, serial duplex studies can be considered to determine clot extension, which would place the patient at risk for PE. filter would be warranted if AC is contraindicated –> after duplex survelliance in 1 week
- recommended AC vs. observation, 3 months of therapy
dvt prevention
- hospitalized patients especially high risk
- vital to have patients OOB and ambulating
- SQ heapring Q8H
- surgical service may want weight based
- lovenox for high risk patients, lower bleeding and HIT
- SCD
when should you put in a vena cava filter
within 4 weeks of VTE
if contraindicated for AC (active bleeding, risk for major bleeding)
filter is not recommended for distal LE DVT, superficial venous thrombophlebitis, VTE oler than 1 month, or UE DVT
