pleural perfusion
TRANSCRIPT
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PLEURAL EFFUSIONSPLEURAL EFFUSIONS
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Anatomy of pleural membraneAnatomy of pleural membrane
and pleural spaceand pleural space
Pleural membrane consists of parietal
pleura and visceral pleura A space situated between parietal and
visceral pleura is called pleural space
It is normally filled with 5 - 10 milliter
of serous fluid
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Parietal pleura
Receiving its blood supply from thesystemic circulation and containing
sensory nerve ending
Anatomy of pleural membrane
and pleural space
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Visceral pleura
Receiving its blood supply from the low
pressure pulmonary circulation and
containing no sensory nerve fibers
Anatomy of pleural membrane
and pleural space
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Pleural space
A potential space that is situated
between parietal and visceral pleura
and normally filled with 5-10 ml of
serous fluid,which serves as a coupling
system
Anatomy of pleural membrane
and pleural space
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EtiologyEtiology
from the capillaries in theparietal pleura,
from interstitial spaces of the lung
via the visceral pleura,
from theperitoneal cavity through
small holes in the diaphragm.
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EtiologyEtiology
This fluid is normally removed bylymphatics in the visceral pleura, whichhave the capacity to absorb 20 times morefluid than is normally formed.
When this capacity is overwhelmed,either through excess formation (from theinterstitial spaces of the lung, the parietal
pleura, or the peritoneal cavity )ordecreased lymphatic absorption, a pleuraleffusion develops.
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Mechanism of formation-resorptionMechanism of formation-resorption
of pleural fluidof pleural fluid
Parietal Visceralpleura pleura
Hydrostaticpressure(30)
Permeabilityof systemic
circulation(34)
Pressure of pleuralspace (5)
Permeability of pleural
fluid (8)
11
34
34-(5+8+11)=105+8+30-34=9
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The mechanisms that lead to accumulationThe mechanisms that lead to accumulation
of pleural fluidof pleural fluid
l. Increased hydrostatic pressure in microvascular
circulation(congestive heart failure)
2. Decreased oncotic pressure in microvascularcirculation(severe hypoalbuminemia )
3. Decreased pressure in the pleural space (complete lung collapse)
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The mechanisms that lead to accumulation ofThe mechanisms that lead to accumulation of
pleural fluidpleural fluid
4.Increased permeability of themicrovascular circulation(pneumonia)
5. Impaired lymphatic drainage from thepleural space (malignant effusion)
6. Movement of fluid from peritoneal space( ascites )
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Increased Fluid EntryIncreased Fluid Entry
Decreased pleural pressure
i.e. Significant atalectasis,
reduces pressures around nearbyvessels.
Decreased plasma oncotic pressure
Hypoalbuminemia alone notusually enough but can lowerthreshold for other factors
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Increased Fluid EntryIncreased Fluid Entry
Increased permeability
Increase in fluid conductance or
protein permeability
Increased microvascular pressure
Usually increased venous outflowpressure. Arterial pressures usuallynot transmitted due to capillaryresistance. Thought to be lung
interstitial fluid when hydrostaticpressure.
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Decreased Fluid ExitDecreased Fluid Exit
Reflects a reduction in lymphatic function.
Much of how is speculative.
There are intrinsic and extrinsic factors.
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Decreased Fluid ExitDecreased Fluid Exit
Intrinsic
Prevent ability of lymphatic vessels to
transport fluid- products of inflammation,
endocrine problems (hypothyroidism),
direct injury (chemotherapy, radiotherapy),
infiltration with cancer.
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Decreased Fluid ExitDecreased Fluid Exit
Extrinsic
Limitation of respiratory motion (diaphragm
paralysis, lung collapse), compression oflymphatics (pleural fibrosis, pleural granulomas),
blockage (pleural malignancy), increased systemic
venous pressure (only acutely because chronically
lymphatics can adapt), decreased liquidavailability (ie after pneumothorax liquid contacts
fewer lymphatic openings)
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Two kinds of pleural effusionsTwo kinds of pleural effusions
Transudates and exudatesTransudates and exudates
A transudative pleural effusion occurs
when systemic factors that influence the
formation and absorption of pleural
fluid are altered.
The leading causes of transudativepleural effusions in the United States
are left ventricular failure and cirrhosis.
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Clinical HistoryClinical History
Dyspnea: most common symptom; effusionusually at least 500mL; underlying disease may
also contribute
Chest pain: sharp or stabbing; worse withdeep inspiration; diminishes with increase in
size of effusion; signifies pleural irritation
Other signs and symptoms dependent onunderlying disease process (TB: sweats,
weight loss, hemoptysis)
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Physical ExamPhysical Exam
Decreased breath sounds
Dullness to percussion
Decreased tactile fremitus
Egophony
Pleural friction rub
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Usually not present until >300mL of pleural fluid
Egophony: Egophony is the Greek word for"Voice of the Goat". This sound is the "EEEEE" to
"AAAAA" conversion that a person will make
when being asked to say "EEEEE" while the
auscultator listens to the lungs which is heard by
the auscultator as "AAAAA" through the
stethoscope. .
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Friction rub: visceral and parietal pleurae become
inflamed and roughened. The inflamed
membranes will stick together. As the therapistauscultates the chest wall, the rubbing together of
the inflamed membranes will cause the patient to
experience pain and stop breathing - a maneuver
called splinting. The pain is caused by the stickingtogether of the membranes and the pulling apart of
those membranes with continued breathing.
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DiagnosisDiagnosis
Pleural effusion is usually diagnosed on the
basis of the history of your family and
physical exam, and confirmed by chestx-ray.
Chest films acquired in the lateral decubitus
position (with the patient lying on theirside) are more sensitive, and can pick up as
little as 50 ml of fluid.
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At least 300 ml of fluid must be present beforeupright chest films can pick up signs of pleuraleffusion (e.g., blunted costophrenic angles).
Once accumulated fluid is more than 500 ml, thereare usually detectable clinical signs in the patient,such as decreased movement of the chest on theaffected side, dullness to percussion over the fluid,diminished breath sounds on the affected side,decreased vocal fremitus and resonance, pleuralfriction rub, and egophony.
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XX
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UltrasoundUltrasound
Ultrasound
Aids in identification of loculated effusions
Aids in differentiation of fluid from fibrosis
Aids in identification of thoracentesis site
Available at bedside
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CT ScanCT Scan
Aids in differentiation of
Lung consolidation vs. Pleural effusionCystic vs. Solid lesionsPeripheral lung abscess vs. Loculated emypema
Aids in identification of
Necrotic areasPleural thickening, nodules, massesExtent of tumor
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thoracentesisthoracentesis..
Once a pleural effusion is diagnosed, the
cause must be determined. Pleural fluid is
drawn out of the pleural space in a processcalled thoracentesis. A needle is inserted
through the back of the chest wall into the
pleural space.
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thoracentesisthoracentesis..
Only symptomatic pleural effusions or
effusions larger than 50% of hemithorax
require thoracentesis or chest tube drainage.Most resolve spontaneously.
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thoracocentesis
T ki d f l l ff iT ki d f l l ff i
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Two kinds of pleural effusionsTwo kinds of pleural effusions
Transudates and exudatesTransudates and exudates
Transudate Exudate Cause non-inflammatory flammatory,tumor
Apperance light yellow yellow, purulent
Specific gravity 1.018
Coagulability unable able
Revalta test negative positive
Protein content 30g/L
P. To serum Pre < 0.5 > 0.5
LDH < 200 I U/ L > 200 I U / L
P. To s < 0.6 > 0.6
Cell count < 10010 6/ L > 50010 6 / L
Differential cell Lymphocyte Different
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Transudative and exudativeTransudative and exudative
pleural effusionspleural effusionsdistinguished by measuring the lactate
dehydrogenase (LDH) and protein levels in
the pleural fluid. Exudative pleuraleffusions meet at least one of the following
criteria, whereas transudative pleural
effusions meet none:
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Light's criteriaLight's criteria
Previously criteria proposed by Light for an
exudative effusion are met if at least one of
the following exists (Light's criteria) 1. pleural fluid protein/serum protein >0.5
2. pleural fluid LDH/serum LDH >0.6
3. pleural fluid LDH more than two-thirdsnormal upper limit for serum
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The above criteria misidentify ~25% of transudatesas exudates. If one or more of the exudativecriteria are met and the patient is clinically thought
to have a condition producing a transudativeeffusion, the difference between the protein levelsin the serum and the pleural fluid should bemeasured. If this gradient is greater than 31 g/L
(3.1 g/dL), the exudative categorization by theabove criteria can be ignored because almost allsuch patients have a transudative pleural effusion.
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If a patient has an exudative pleural
effusion, the following tests on the pleural
fluid should be obtained: description of thefluid, glucose level, differential cell count,
microbiologic studies, and cytology
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Glucose is decreased with cancer, bacterial
infections, orrheumatoid pleuritis. If cancer
is suspected, the pleural fluid is sent forcytology. If cytology is negative, and
cancer is still suspected, either a
thoracoscopy, or needle biopsy of the pleuramay be performed.
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Effusion Due to Heart FailureEffusion Due to Heart Failure
The most common cause of pleural effusion
is left ventricular failure. The effusionoccurs because the increased amounts of
fluid in the lung interstitial spaces exit in
part across the visceral pleura. Thisoverwhelms the capacity of the lymphatics
in the parietal pleura to remove fluid.
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A diagnostic thoracentesis should be
performed if the effusions are not bilateral
and comparable in size, if the patient isfebrile, or if the patient has pleuritic chest
pain, to verify that the patient has a
transudative effusion. Otherwise the patientis best treated with diuretics.
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Parapneumonic EffusionParapneumonic Effusion
associated with bacterial pneumonia, lung
abscess, or bronchiectasis and are probably
the most common cause of exudativepleural effusion in the United States.
Empyema refers to a grossly purulent
effusion.
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Factors indicating the likely need for a procedure
more invasive than a thoracentesis (in increasing
order of importance) include: loculated pleural fluid
pleural fluid pH < 7.20
pleural fluid glucose < 3.3 mmol/L (
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Effusion Secondary to MalignancyEffusion Secondary to Malignancy
lung carcinoma, breast carcinoma, and
lymphoma.
The pleural fluid is an exudate, and itsglucose level may be reduced if the tumor
burden in the pleural space is high.
The diagnosis is usually made via cytologyof the pleural fluid.
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Tuberculous PleuritisTuberculous Pleuritis
usually associated with primary TB and arethought to be due primarily to ahypersensitivity reaction to tuberculousprotein in the pleural spacePatients with tuberculous pleuritis present
with fever, weight loss, dyspnea, and/orpleuritic chest pain. The pleural fluid is an exudate with
predominantly small lymphocytes. Thediagnosis is established by demonstrating
high levels of TB markers in the pleural fluid
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HemothoraxHemothorax
Most hemothoraces are the result of trauma;
other causes include rupture of a blood
vessel or tumor.Most patients with hemothorax should be
treated with tube thoracostomy
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PneumothoraxPneumothorax
Pneumothorax is the presence of gas in the
pleural space.
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..Introductory remarks
Pneumothorax, like chest wall injury, is a common
sequel of blunt thoracic injury.
Because the intrapleural pressure is normally
negative during inspiration, any communication
with atmospheric pressure cause accumulation o
air in the pleural space.
The communications can occur through rather thechest wall or the lung. According to this,
pneumothorax was divided into three types.
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Category Closed pneumothorax
Open pneumothorax Tension pneumothorax
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PathophysiologyPathophysiology
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Size of PneumothoraxSize of PneumothoraxRhea and associates :
A = Maximal apical interpleural distance
B = Interpleural distance at midpoint ofupper half of lung
C = Interpleural distance at midpoint of
lower half of lung
Average interpleural distance = A+B+C/3
Small (40%) .
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Introductory RemarksIntroductory Remarks
As the lung collapsed, the hole on its surface decreases in
size and ultimately closes.
When the patient inspires, the hole in the lung surface
reopens as the lung expands, but with expiration the holeagain closes. As pressure in the pleural space increase, the
hole in the pulmonary surface is less and less likely to
open with inspirating effort.
In most cases, when the lung collapses to the point atwhich intrapleural air no longer accumulates with
inspiration, the pneumothorax is stable.
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Clinical FeaturesClinical Features
In slight pneumothorax (lung collapses is less
than 30%), both circulation and respiration are
little impaired, and most patients have no
symptoms.
As the pressure in the ipsilateral pleural cavity
increases (lung collapses is more than 30%), the
patients have the symptoms of chest distress,short of breath, chest pain.
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Clinical featuresClinical features
Physical examination shows that trachea is
pushed toward the other side (normal side),
decreased or diminished breath sound.
The X-ray examination indicates that the lung is
collapsed and air accumulated in the pleural
space, sometimes with little pleural effusion.
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TreatmentTreatment
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TreatmentTreatment
1. Slight (5 to 10%) pneumothorax can be treated
conservatively. The rapid reabsorption of the
air should be verified radiologically. (About 1-2 weeks)
2. Moderate (10 to 30%) pneumothorax often can
be evacuated through needle puncture, but, ifrecurrence occur, it should be drained through
an intercostals tube.
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TreatmentTreatment
Complete pneumothorax quickly can
become compressive.
Intercostals tube drainage is indicated. In the same times, patients with chest
tube placed for trauma should
routinelyreceive antibiotics to prevent infection.
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0pen0pen pneumothoraxpneumothorax
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Introductory RemarksIntroductory Remarks
The incidence of open pneumothorax in peacetime is low while in wartime generallyhigher but varies to some extent according to
the weapons used.Open pneumothorax is usually produced by a
stab or gunshot wound, or by some other sharpobject.
Open or communicating pneumothorax isreferred to as a sucking wound.
The pleural cavity communicates directly with
the atmosphere.
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PathophysiologyPathophysiology
Open pneumothorax mdiastinal flutter is a form o
internal paradoxical motion where the
mediastinum swings to one side or the other
according to the phase of respiration.
During inspiration, air is more easily aspirated
through the wound than through the glottis, and
the mediastinum is attracted towards the particallyinflated healthy lung; this increases the
pneumothorax.
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PathophysiologyPathophysiology
During expiration, on the other hand, air escapes
more quickly through the wound than through the
glottis consequently, the mediastinum shifts in
the other direction.
The repercussions of mediastinal flutter are often
aggravated both by the increased dead space
created by rebreathing and by the cyclical torsionof the vascular pedicles.
Symptom and examination.
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PathophysiologyPathophysiology
DURING INSPIRATION--air enters more easily through the wound than through the glottis
--pulmonary collapse increase
--air passes from the collapsed to the intact lung
--the mediastinum sways towards the intact lung
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ManagementManagement
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ManagementManagement
Open pneumothorax should be closed with sterile
dressing and then drained.
Drainage must be immediate andeffective;otherwise the patients condition will
deteriorate soon after the chest wall is closed.
The patient must be in full expiration at the
moment the wound is occluded.
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M
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ManagementManagement
It can be minimized by:
1) removing the occlusive dressing from
time to time and asking the patient tocough loudly or by
2) covering the wound with a valve made
from a colostomy bag with an open
corner. Immediate underwater seal or
suction drainage is indicated in every
case .
M t
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ManagementManagement
The patient should then be intubated and,if necessary, ventilated with positive
pressure.
When the patients were sent to thehospital, progressive management is thatventilation and blood transfusion toantishock.
The thoracic wound should then bedebrided and explored, and all foreign
bodies and clots moved from the pleuralcavity.
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ManagementManagement
It may be necessary to enlarge the wound to give
access to intrathoracic injuries found during
routine exploration .
The pleural cavity should be cleaned thoroughly
and topically effective antibiotics applied before
closure. It should be use antibiotics to prevent
infection;Asking the patient to cough and sputum and move
early.
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Tension pneumothoraxTension pneumothorax
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Introductory RemarksIntroductory Remarks
In tension pneumothorax, air continues to
accumulate in the pleural space with each
inspiratory effort.
The fact that the hole opens with
inspiration and closes with expiration
produces a valve-like mechanism that
causes the pneumothorax to increase in sizewith each respiratory cycle and produces a
tension pneumothorax.
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PathophysiologyPathophysiology This pathophysiology is easily and
quickly reversed with decompression
of the pneumothorax Some of the
physical findings associated with
tension pneumothorax are the same asthose seen with any pneumothorax,
but may be more pronounced.
There are no breath sounds on the
injured side, and subcutaneous airmay develops in face, neck and chest.
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ManagementManagement
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ManagementManagement
The trachea may be deviated away from the side
of the injury.
Shock may also be present and, because there isinterference with venous retun to the right atrium,
neck veins may be distended.
Immediate pleural drainage is mandatory in all
case of tension pneumothorax ;sometimes it mustbe performed even before X-ray .
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ManagementManagement
If the necessary equipment is unavailable,
temporary decompression can be obtained and
venous return restored by implanting several
large-bore needles into the upper chest wall and
asking the patient to cough;
this opens the pneumothorax ,while large enough
to ease tension , the needles are of sufficientlysmall caliber (compared with the glottis )not to
induce mediustinal flutter.
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ManagementManagement
Alternatively a large-lore needle can be
implanted through a finger cot.
These ploys are largely expedient. Under normal circumstance, the basic
maneuver is to evacuate the thorax through an
intercostal tube (with suction if possible).
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Definitive TreatmentDefinitive Treatment
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Definitive TreatmentDefinitive Treatment
Needle puncture or drainage with underwater
seal or, in most instances, suction drainage
followed by:
1)X-ray to verify pulmonary expansion,
2)investigation of the cause if the lung has not re-
expand,
3) thorcotomy in the even of a massive air leak .
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52
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52
80% 1200
l
2 Male,52y, abruptly chest pain , dyspnea,for 4days ,spontaneous pneumothorax on right chset wall lung
compression 80%, air exhaust about 1200ml
soon
cough
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