Pleural Perfusion

PLEURAL EFFUSIONS

Anatomy of pleural membrane and 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 

Anatomy of pleural membrane and pleural space Parietal pleura Receiving its blood supply from the systemic circulation and containing sensory nerve ending

Anatomy of pleural membrane and pleural space 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 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

Etiology from

the capillaries in the parietal pleura,

from

interstitial spaces of the lung via the visceral pleura,

from

the peritoneal cavity through small holes in the diaphragm.

Etiology This

fluid is normally removed by lymphatics in the visceral pleura, which have the capacity to absorb 20 times more fluid than is normally formed. When this capacity is overwhelmed, either through excess formation (from the interstitial spaces of the lung, the parietal pleura, or the peritoneal cavity )or decreased lymphatic absorption, a pleural effusion develops.

Mechanism of formation-resorption of pleural fluid Parietal pleura

Visceral pleura

Hydrostatic pressure(30)

Pressure of pleural space (5)

11

Permeability of systemic circulation(34)

Permeability of pleural fluid (8)

34

5+8+30-34=9

34-(5+8+11)=10

The mechanisms that lead to accumulation of pleural fluid l. Increased hydrostatic pressure in microvascular circulation (congestive heart failure) 2. Decreased oncotic pressure in microvascular circulation (severe hypoalbuminemia ) 3. Decreased pressure in the pleural space (complete lung collapse)

The mechanisms that lead to accumulation of pleural fluid

4.Increased permeability of the microvascular circulation (pneumonia) 5. Impaired lymphatic drainage from the pleural space (malignant effusion) 6. Movement of fluid from peritoneal space ( ascites )

Increased Fluid Entry Decreased

pleural pressure –i.e. Significant atalectasis, reduces pressures around nearby vessels. Decreased plasma oncotic pressure –Hypoalbuminemia alone not usually enough but can lower threshold for other factors

Increased Fluid Entry  Increased

permeability – Increase in fluid conductance or protein permeability

 Increased

microvascular pressure – Usually increased venous outflow pressure. Arterial pressures usually not transmitted due to capillary resistance. Thought to be lung interstitial fluid when hydrostatic pressure.

Decreased Fluid Exit  Reflects

a reduction in lymphatic function.  Much of how is speculative.  There are intrinsic and extrinsic factors.

Decreased Fluid Exit  Intrinsic  Prevent

ability of lymphatic vessels to transport fluid- products of inflammation, endocrine problems (hypothyroidism), direct injury (chemotherapy, radiotherapy), infiltration with cancer.

Decreased Fluid Exit  Extrinsic  Limitation

of respiratory motion (diaphragm paralysis, lung collapse), compression of lymphatics (pleural fibrosis, pleural granulomas), blockage (pleural malignancy), increased systemic venous pressure (only acutely because chronically lymphatics can adapt), decreased liquid availability (ie after pneumothorax liquid contacts fewer lymphatic openings)

Two kinds of pleural effusions Transudates 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 transudative pleural effusions in the United States are left ventricular failure and cirrhosis.

An

exudative pleural effusion occurs when local factors that influence the formation and absorption of pleural fluid are altered.  The leading causes of exudative pleural effusions are bacterial pneumonia, malignancy, viral infection, and pulmonary embolism

Clinical History  Dyspnea:

most common symptom; effusion usually at least 500mL; underlying disease may also contribute  Chest pain: sharp or stabbing; worse with deep inspiration; diminishes with increase in size of effusion; signifies pleural irritation  Other signs and symptoms dependent on underlying disease process (TB: sweats, weight loss, hemoptysis)

Physical Exam  Decreased

breath sounds  Dullness to percussion  Decreased tactile fremitus  Egophony  Pleural friction rub

 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. .

 Friction

rub: visceral and parietal pleurae become inflamed and roughened. The inflamed membranes will stick together. As the therapist auscultates 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 sticking together of the membranes and the pulling apart of those membranes with continued breathing.

Diagnosis  Pleural

effusion is usually diagnosed on the basis of the history of your family and physical exam, and confirmed by chest x-ray.  Chest films acquired in the lateral decubitus position (with the patient lying on their side) are more sensitive, and can pick up as little as 50 ml of fluid.

 At

least 300 ml of fluid must be present before upright chest films can pick up signs of pleural effusion (e.g., blunted costophrenic angles).  Once accumulated fluid is more than 500 ml, there are usually detectable clinical signs in the patient, such as decreased movement of the chest on the affected side, dullness to percussion over the fluid, diminished breath sounds on the affected side, decreased vocal fremitus and resonance, pleural friction rub, and egophony.

胸腔积液 X 线

Ultrasound  Ultrasound – Aids in identification of loculated effusions – Aids in differentiation of fluid from fibrosis – Aids in identification of thoracentesis site – Available at bedside

B 超

CT Scan – Aids in differentiation of  Lung consolidation vs. Pleural effusion  Cystic vs. Solid lesions  Peripheral lung abscess vs. Loculated emypema – Aids in identification of  Necrotic areas  Pleural thickening, nodules, masses  Extent of tumor

thoracentesis.  Once

a pleural effusion is diagnosed, the cause must be determined. Pleural fluid is drawn out of the pleural space in a process called thoracentesis. A needle is inserted through the back of the chest wall into the pleural space.

thoracentesis.  Only

symptomatic pleural effusions or effusions larger than 50% of hemithorax require thoracentesis or chest tube drainage.  Most resolve spontaneously.

thoracocentesis

Two kinds of pleural effusions Transudates and exudates Transudate           

Cause Apperance Specific gravity Coagulability Revalta test Protein content P. To serum Pre LDH P. To s Cell count Differential cell

non-inflammatory light yellow <1.018 unable negative <30g/L < 0.5 < 200 I U/ L < 0.6 < 100×10 6/ L Lymphocyte

Exudate flammatory,tumor yellow, purulent >1.018 able positive >30g/L > 0.5 > 200 I U / L > 0.6 > 500×10 6 / L Different

Transudative and exudative pleural effusions  distinguished

by measuring the lactate dehydrogenase (LDH) and protein levels in the pleural fluid. Exudative pleural effusions meet at least one of the following criteria, whereas transudative pleural effusions meet none:

Light'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-thirds

normal upper limit for serum

The above criteria misidentify ~25% of transudates as exudates. If one or more of the exudative criteria are met and the patient is clinically thought to have a condition producing a transudative effusion, the difference between the protein levels in the serum and the pleural fluid should be measured. If this gradient is greater than 31 g/L (3.1 g/dL), the exudative categorization by the above criteria can be ignored because almost all such patients have a transudative pleural effusion.

 If

a patient has an exudative pleural effusion, the following tests on the pleural fluid should be obtained: description of the fluid, glucose level, differential cell count, microbiologic studies, and cytology

 Glucose

is decreased with cancer, bacterial infections, or rheumatoid pleuritis. If cancer is suspected, the pleural fluid is sent for cytology. If cytology is negative, and cancer is still suspected, either a thoracoscopy, or needle biopsy of the pleura may be performed.

Effusion Due to Heart Failure  The

most common cause of pleural effusion is left ventricular failure. The effusion occurs because the increased amounts of fluid in the lung interstitial spaces exit in part across the visceral pleura. This overwhelms the capacity of the lymphatics in the parietal pleura to remove fluid.

A

diagnostic thoracentesis should be performed if the effusions are not bilateral and comparable in size, if the patient is febrile, or if the patient has pleuritic chest pain, to verify that the patient has a transudative effusion. Otherwise the patient is best treated with diuretics.

Parapneumonic Effusion  associated

with bacterial pneumonia, lung abscess, or bronchiectasis and are probably the most common cause of exudative pleural effusion in the United States. Empyema refers to a grossly purulent effusion.

 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 (<60 mg/dL)  positive Gram stain or culture of the pleural fluid  the presence of gross pus in the pleural space

Effusion Secondary to Malignancy  lung

carcinoma, breast carcinoma, and lymphoma.  The pleural fluid is an exudate, and its glucose level may be reduced if the tumor burden in the pleural space is high.  The diagnosis is usually made via cytology of the pleural fluid.

Tuberculous Pleuritis  usually

associated with primary TB and are thought to be due primarily to a hypersensitivity reaction to tuberculous protein in the pleural space  Patients with tuberculous pleuritis present with fever, weight loss, dyspnea, and/or pleuritic chest pain.  The pleural fluid is an exudate with predominantly small lymphocytes. The diagnosis is established by demonstrating high levels of TB markers in the pleural fluid

Hemothorax  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

Pneumothorax  Pneumothorax

pleural space.

is the presence of gas in the

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 of air in the pleural space.  The communications can occur through rather the chest wall or the lung. According to this, pneumothorax was divided into three types.

Pneumothorax = Free Air Within the Pleural Space

Category   

Closed pneumothorax Open pneumothorax Tension pneumothorax

Closed pneumothorax

Introductory Remarks    



In most cases(86%),pneumothorax is closed. Closed pneumothorax is usually the result of a small pulmonary laceration by a fracture rib. It can develop immediately,or after a delay. In most instances,uncomplicated pneumothorax is limited by the spontaneous closure of the air leak as the lung collapsed. Increased pressure in the pleural space collapse the lung.

Pathophysiology

Size of Pneumothorax  Rhea

and associates :



A = Maximal apical interpleural distance B = Interpleural distance at midpoint of upper half of lung C = Interpleural distance at midpoint of lower half of lung  Average interpleural distance = A+B+C/3  Small (<20%) , moderate (20 to 40%) , large (>40%) .

Introductory 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 hole again 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 at which intrapleural air no longer accumulates with inspiration, the pneumothorax is stable.

Clinical 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.

Clinical 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.

Treatment

Treatment 1. Slight (5 to 10%) pneumothorax can be treated conservatively. The rapid reabsorption of the air should be verified radiologically. (About 12 weeks)  2. Moderate (10 to 30%) pneumothorax often can be evacuated through needle puncture, but, if recurrence occur, it should be drained through an intercostals tube. 

Treatment  Complete

pneumothorax quickly can become compressive.  Intercostals tube drainage is indicated.  In the same times, patients with chest tube placed for trauma should routinely receive antibiotics to prevent infection.

0pen pneumothorax

Introductory Remarks  The

incidence of open pneumothorax in peacetime is low while in wartime generally higher 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 sharp object.  Open or communicating pneumothorax is referred to as a sucking wound.  The pleural cavity communicates directly with the atmosphere.

Introductory Remarks  



Open pneumothorax can be categorized according to the size of the parietal wound: When the wound is smaller than the glottis, the pneumothorax is usually moderate, and abnormal side lungs are still have part of lung function When the wound is larger than the glottis, pulmonary collapse is more significant even though the pneumothorax remains uncompressive, and abnormal side lungs will lose lung function.

Pathophysiology  Open

pneumothorax mdiastinal flutter is a form of 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 partically inflated healthy lung; this increases the pneumothorax.

Pathophysiology 





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 torsion of the vascular pedicles. Symptom and examination.

Pathophysiology

DURING EXPIRATION --air escapes more easily through the wound than through the glottis --the lung partially expands --air from the intact lung is rebreathed into the partially collapsed lung --the mediastinum sways towards the injuried side

Pathophysiology

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

Management

Management  Open

pneumothorax should be closed with sterile dressing and then drained.  Drainage must be immediate and effective;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.

Management If for any reason drainage equipment is unavailable,wound closure is sometimes dangerous.  It creates the risk of tension pneumothorax.this risk is particularly high in cases of pulmonary laceration(e.g.gunshot wounds). 

Management It can be minimized by:  1) removing the occlusive dressing from time to time and asking the patient to cough 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 .

Management 





The patient should then be intubated and, if necessary, ventilated with positive pressure. When the patients were sent to the hospital, progressive management is that ventilation and blood transfusion to antishock. The thoracic wound should then be debrided and explored, and all foreign bodies and clots moved from the pleural cavity.

Management  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.

Tension pneumothorax

Introductory 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 size with each respiratory cycle and produces a tension pneumothorax.

Introductory Remarks 





.

According to this, if the pressure in the pleural space with tension pneumothorax becomes high enough, both respiration and homodynamic are impaired. High intrapleural pressures on the side of injury minimize effective expansion of the lungs. As the pressure in the ipsilateral pleural cavity increases, the heart is pushed toward the other side of the chest; venous return is compromised, and cardiac output decreases.

Pathophysiology 



This pathophysiology is easily and quickly reversed with decompression of the pneumothorax Some of the physical findings associated with tension pneumothorax are the same as those seen with any pneumothorax, but may be more pronounced. There are no breath sounds on the injured side, and subcutaneous air may develops in face, neck and chest.

Management

Management  The

trachea may be deviated away from the side of the injury.  Shock may also be present and, because there is interference 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 must be performed even before X-ray .

Management  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 sufficiently small caliber (compared with the glottis )not to induce mediustinal flutter.

Management   

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).

Definitive Treatment

Definitive Treatment  Once

the pneumothorax has been drained, the next step is to elucidate its cause; a significant leak through the drain signals an injury to the upper airways; the drain should be clamped to avoid asphyxia, and thoracotomy should be performed immediately.  Treatment of closed, simple or tension pneumothorax.

Definitive 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 reexpand,  3) thorcotomy in the even of a massive air leak .

Definitive Treatment Treatment of closed,simple or tension pneumothorax:  No treatment (death shortly after arrival)  Needle puncture or conservative treatment  Intercostal tube drainage only  Drainage followed by thoractomy for repair of causal injury or other severe injury  Immediate thoractomy

男， 52 岁，四天前抬一重后突然出现胸 痛、气急、呼吸困难。急诊检查发现有右 侧 胸壁自发性气胸，肺压缩 80% ，气管 明显左移，当即给与抽气 1200 毫升，患 者初觉症状缓解，但抽气后不久反而出现 逐渐加重的咳嗽、胸闷、呼吸困难、咯多 量泡沫痰。 （ l ）病人抽气后发生了什么现象？ （ 2 ）如何解释。 Male,52y, abruptly chest pain , dyspnea,for 4days , spontaneous pneumothorax on right chset wall ， lung compression 80%, air exhaust about 1200ml ， soon ， cough 、