Disease States 2 Flashcards
accumulation of fluid between parietal and visceral pleura
Pleural Effusion
MC pleural dz in US
Pleural Effusion types
excess fluid production (transudative)
decreased fluid absorption (exudative)
Pleural space fluid
typically 20 cc
maintained by hydrostatic and oncotic forces, lymphatic drainage
Pleural Effusion common etiology
- altered permeability of pleural membranes or capillaries/vascular disruption
- reduction in intravascular oncotic pressure (nephrotic syndrome, cirrhosis)
- increased capillary hydrostatic pressure (HF)
Pleural Effusion less common etiology
- reduction in pleural space (trapped lung)
- decreased lymphatic drainage or complete blockage (malignancy, trauma)
- increased peritoneal fluid with migration across diaphragm via lymphatics or structural defect
Pleural Effusion s/s
progressively worsening dyspnea (as effusion is more severe)
chest wall pain and mild, non-productive cough
general PE findings for Pleural Effusion
found at >300 cc
dullness to percussion
egophony
superior aspect and diminished/absent sounds
*** must confirm with imaging
imaging of pleural space CXR
250cc of fluid to see effusion, 500 mL will obscure diaphragm
decubitus films
decubitus films
CXR with pt lying on side
clarifies if fluid is free flowing or loculated (in pockets)
loculated = complicated/empyema
imaging of pleural space CT scan
differentiates between effusion and atelectasis
done to evaluate for presence of malignancy
imaging of pleural space US
quantifies amount of pleural fluid
guiding diagnostic and therapeutic thoracentesis
Pleural Effusion care
observation alone if suspected cause and no symptoms
unknown cause = thoracentesis
when is a thoracentesis indicated in Pleural Effusion
a new effusion of unknown cause
drain pleural fluid
therapeutic/symptoms relief
thoracentesis procedure
+/- US
done by IR, pulmonology, and CV surgery
Pulse ox monitored, no sedation, post procedure CXR and analysis
transudative pleural effusion
caused by imbalance of hydrostatic or oncotic forces
MAY BE movement of peritoneal fluid
exudative pleural effusion
caused by inflammation of the pleura or blockage of lymphatic drainage
determine type of pleural effusion
LIGHT’s criteria
evaluation of pleural fluid chemistry via thoracentesis
misclassify transudates as exudates in 15-30% of cases (diuretics HF)
LIGHT’s criteria measures
serum and pleural fluid lactate dehydrogenase (LDH) and protein
ratio of serum to pleural fluid
LIGHT’s criteria
- pleural fluid to serum protein ratio > 0.5
- Pleural fluid LDH to serum LDH ratio > 0.6
- Pleural fluid LDH > 2/3 upper limit of normal
AT LEAST 1 = Exudate (more present, more likely)
ALL NEG - transudative
tests on fluid when diagnosis unknown? (6)
- fluid glucose
- fluid pH
- cell count and differential
- cytology
- gram stain and culture
- color and consistency
specific pleural fluid test
- fluid amylase (ruptured esophagus or pancreatic origin)
- fluid triglyceride (milky - chylothorax)
- ANA/RF - collagen vascular dz/ connective tissue disorder
transudative etiologies
- HF
- Atelectasis (CA or PE)
- Hepatic hydrothorax (cirrhosis)
- hypoalbuminemia (protein calorie malnutrition, liver failure, nephrotic syndrome)
- peritoneal dialysis
- myxedema coma
- urinothorax
- migration of devices/iatrogenic
exudative pleural effusion etiologies
COMMON (7)
PNA Malignancy Tuberculosis collagen vascular disorders (SLE, RA) pancreatitis Empyema pulmonary embolus
clues of pleural effusion fluid based on appearance:
frank purulence
empyema
lung abscess
clues of pleural effusion fluid based on appearance
milky opalescent fluid
chylothorax
lymphatic CA obstruction, thoracic duct injury
clues of pleural effusion fluid based on appearance
grossly bloody fluid
trauma, CA, asbestos
must get Hct of fluid – >50% serum = hemothorax, chest tube
clues of pleural effusion fluid based on appearance
high LDH
> 1000 IU/L
empyema, malignancy, collagen vascular dz
clues of pleural effusion fluid based on appearance
glucose
<30- empyema, rheumatoid
30-50 = SLE
clues of pleural effusion fluid based on appearance
wbc
50-70% lymphs= malignancy
> 90 = TB, sarcoid, TA, chylothorax
mild pleural effusion medical tx
HF - loop diuretic
parapnumonic effusion - ABX
medical intervention prior to invasive procedure
Booerhave syndrome
esophageal rupture (forceful vomiting) causes entry of air/esophogastric fluid into mediastinum and pleural space
high amylase on analysis
tx: surgical intervention to repair rupture and IV ABX
parapneumonic effusions
caused by pneumonia
- uncomplicated
- complicated
- empyema
uncomplicated parapneumonic effusions
progressively worsening URI
exudative effusion, neutrophils
clear fluid, no organisms on GS
pH > 7.3, glucose >60
resolves gradually with appropriate ABX
complicated parapneumonic effusions
bacterial invasion (but rapid clearing) from pleural space
GS negative for organisms
pH < 7.2, glucose < 60
empyema
GS positive for organisms
pH <7.2
TB effusion
night sweats and weight loss, increasing SOB
MC in developing world
fluid will NOT show acid fast
diagnosis based on history, HIGH adenosine deaminase
tx: surgical intervention and anti-TB meds
rheumatologic effusions
rash and exposed to sun, joint pain
common complications of SLE and RA
will have high ANA titers in pleural fluid
very low pleural fluid glucose
malignant effusions
POOR prognosis
small pulmonary nodules bilaterally on CXR
most common cause of pleural effusion in > 60 yrs
must find clinical features, worsened prognosis if pH < 7.3, glucose < 60
recurrent malignant effusions
consideration for placement of tunnel pleural catheter (Pleural catheter) to drain the fluid 3
pleurodesis
obliterates pleural space to prevent recurrent pleural effusion or PTX
drains effusion or air then causes intrapleural inflammation and fibrosis
instills chemical irritant or performs mechanical abrasion during thoracoscopy
virchow’s triad
endothelial injury/damage
venous stasis (bed rest, post-op patients)
hypercoagulatbilty (factor V, malignancy)
pathogenesis of PE
start in leg as DVT
clot grows proximally causes break off that travels into pulmonary A.
blockage of blood flow to lung
blockage of blood flow to lung causes
- hypoxia (ventilation-perfusion mismatch)
- increased strain on R heart to overcome resistance
- decreased preload to left heart causing low output heart failure
PE s/s
abrupt onset of dyspnea
pleuritic chest pain
tachypnea, tachycardia, hypoxia*
syncope
fever cough
asymptomatic
steps determining PE
- Well’s criteria to determine likelihood
- D -dimer assay ( < 500 no PE), >500
- CTA to diagnose
modified wells
3 pos, 1.5 pts, 1 pt
PE likely if >4 points (unlikely <4 points)
D- DImer
given to pt’s with LOW probably of PE
reliably excludes PE if not suspected
positive D Dimer means CTA
CT angiography
imaging study of choice for PE
must consider risk of AKI
definitive choice
VQ scan
measures discordance between perfusion (technetium labeled albumin) and ventilation (xenon or technetium)
no perfusion but ventilation suggests PE
Low prob. = < 20% chance
Intermediate = 20-80@ chance
high probability >80%
additional diagnosis PE
CXR, troponin, EKG
cxr - abnormal bu non specific, can’t be used
troponin - elevated in 50%, R heart strain
EKG - sinus tach, non specific changes
additional diagnostics in PE
echo, venous u/s, ABG
echo - not used, but can evaluate strain
venous US - look for DVT
ABG_ hypoxemia, hypocapnea, respiratory alkalosis
alveolar arterial gradient
content of O2, typically 5-10
NO increased if lack of O2 due to respiratory
INCREASED if lack of O2 due to low blood flow (PE)
tx of pE
anticoagulation and hospital admission
telemetry bed, ICU
NOACs, warfarin, LMWH have NO effect on embolus, they prevent extension of formed clot and further embolism
NOACS
req. loading dose, no pre tx
rivaroxaban/xarelto
apaxiban/eliquis
dabigitran/pradaxa
edoxaban/savaysa (not good if CrCL is high/low)
LMWH is preferred in who? PE tx
pts w/ malignancy
pts who can’t take coumadin/NOACS (malignancy, preg)
warfarin
jantoven
UFH, LMWH, or fondaparinox dc after INR is 2.0 BUT after 5 days of warfarin initiation to prevent skin necrosis
unstable pt tx PE
persistent HoTN, elevated troponin
thrombolysis and surgical thromobectomy if life threatening
stable pt PE, cannot anticoagulant
IVC/greenfield filter
removable filter placed, should be removed as soon as patient is no longer at risk or can take anticoagulant
duration of anticoagulation PE
3 months
if first PE
due to reversible, precipitating factor
duration of anticoagulation on PE
3+
first PE, unprovoked
3 months then reassess risk/benefit (likely 6 months)
PE duration of anticoagulation
indefiniate
recurrent PE or first PE with irreversible risk factor
accumulation of air in pleural space
penumothroax
via ruptured bleb or thru external chest wall
lung becomes compressed – collapsed
pneumothorax types
primary spontaneous
secondary spontaneous
iatrogenic
traumatic
tension
primary spontaneous pneumothorax
occurs without known lund dz or inciting event
18-40, tall thin, smoking
ass. w/ genetic factors, inherited disorders (marfan;s), pregnancy
secondary spontaneous pneumothorax
underlying pulmonary dz alters normal lung structure
enters via distended, damaged, compromised alveoli
iatrogenic pneumothorax
accidentally caused during chest procedures (pleural or lung nodule biopsy, thoracentesis, central line insertion)
pulmonary blebs/bullae
large tissue in lung that can easily rupture
seen in COPD and other lung dz (margin, congential/genetic)
destruction of connective tissue
traumatic pneumothorax
blunt or penetrating trauma to chest wall, barotrauma (PEEP_
=/- rib fractures
tension pneumothorax
LIFE THREATENING
draws air into space via ruptured bleb, but air can’t escape so it accumulates
compression of heart, vena cava, decreased blood flow and CO, = shock, death
tension PTX tx
emergent chest tube placement
s/s PTX
acute onset dyspnea and chest pain
tachypnea, tachycardia, decreased/absent breathe sounds
HoTN, JVD, tracheal deviation
subcutaneous emphysema
air under skin that is a sign of pneumothorax
feels like rice crisps
PTX dz
CXR imaging of choice, may miss trauma (so do a CT)
can asses underlying contributors and determine severity
PTX Tx
observation +/- O2
simple aspiration
emergency needle decompression
tube throacostamy
surgical
pleurodesis
too for all PSP >15% and secondary spontaneous PTX
tube throacostamy
air removed via continuous suction