Serofibrinous pleural effusion

Prof. Dr. Daniela Bartoş

Definition

 The accumulation of fluid in the pleural space as a

result of a pathological process
Pathophysiology
 The pleural cavity is a virtual cavity with a negative
pressure regime
 There is a small amount of fluid in the pleural
cavity (there is a balance between the fluid
produced by the parietal pleura and the fluid
absorbed by the pleural lymph vassels)
 The presence of excess fluid in the pleural cavity is
always pathological
Pathophysiology
 Mechanisms at the origin of pleural effusion:
Pleural aggression by: infection, trauma, tumor
invasion, inflammation
 Imbalance between hydrostatic and oncotic
pressure: heart failure, kidney failure,
hypoproteinemia
Overview
 Accumulation of fluid in the pleural space secondary
to an underlying pathology
 Exudate/ Transudate Differentiation - Substance
Disease
Heart failure Pneumonia Malign PE Viral infection
process
 The exudate is always secondary to a pleural pathological
process, either locally or as an expression of a general disease that
has led to increased capillary protein permeability or lymph
obstruction
 Transudate comes from the accumulation of pleural fluid as a
result of decreasing colloid-osmotic pressure and increasing
pressure in the systemic or pulmonary circulation
TYPES of PLEURAL EFFUSION
 Exudate Pleural effusion - rich in proteins with numerous
inflammatory cells denotes pleural aggression
 Transudate Pleural effusion - poor in proteins and inflammatory
cells - shows a presumptive imbalance
 Purulent Pleural effusion - the presence of pus in the pleural
cavity as a sign of a bacterial pleural effusion
 Hemothorax - The presence of blood in the pleural cavity most
commonly following trauma
 Chylothorax - lactescent pleural effusion secondary to an obstacle or
lesion on the lymphatic pathway
Evaluation stages - First stage
Ia. History Favorable factors
• Exposure to cold / moisture
• Physical overload
• Repeated weight loss
• Co-existence of systemic diseases
Ib. Clinical exam Inspection
• Larger hemithorax
• Reduced basal hemithorax mobility
Palpation
• Voice vibrations diminished / aborted
• Apex shock moved to the left parasternal line (> 500ml) or
to the right parasternal line (> 1200ml)
Percussion – dullness
• Woody with upper horizontal edge (massive pleural
effusion)
• With the upper limit curve, the tip to the axilla (Damoiseau
curve) (average quantity 900-1200 ml)
• Only basal to costo-diafragmatic sinus (small quantities
200-300 ml)
Auscultation
• MV diminished or abolished
• Pleural friction (at the beginning of fluid accumulation)
Evaluation stages - First stage
Ib. Associated • Chest pain
Symptomatology • Cough, usually dry, irritative
• Dyspnea
• Fever
• Physical asthenia
• Nocturnal sweats
• Weight loss
• Polyarthralgia
Sign of gravity
• Rapid hemodynamic damage
• Acute respiratory failure
• Hypoxia
• Co-existence of chronic affections (HF, liver
failure)
Stages of evaluation - Second stage
II.Teste de diferentiere
Examination of the liquid by thoracentesis
<2.5g% - transudate
protein concentration
> 3.5g% - exudate
≥0.5 - exudate
ratio of pleural proteins /
serum proteins
<0.5 - transudate
Better differentiation test
transudate <1016
density of liquid
exsudat> 1016

LDH / serum LDH ≥ 0.6

concentration of LDH in
the liquid
Pleural LDH> 2/3 of serum LDH - exudate
LDH pleural <2/3 of serum LDH - transudate

Limited indication of thoracentesis

• Uncomplicated HF & viral etiology
 If the proteins in the pleural fluid are between 2.5-
3.5 g% the differentiation is based on Light’s
criteria (1972):
 transudate: LDH <200 IU / l or pleural / serum
protein <0.5 or pleural / serum LDH <0.6
 exudate: LDH> 200 or pleural / serum proteins>
0.5 or pleural / serum LDH> 0.6
Thoracentesis diagnostic use
 Neoplasia
 Empyema
 Fungal pleural effusion
 Lupus pleural effusion
 Chylothorax
 Urinothorax
 Esophageal rupture
 Hemothorax
Causes of transudation
 Heart failure
 Hepatic cirrhosis
 Nephrotic syndrome
 Myxedema
 Upper cava vein obstruction
 Peritoneal dialysis
Additional tests in case of exudate
Glucose from the <60mg% suggestive for etiology
pleural fluid • Parapneumonic
• Tuberculosis
• Malignant
• Haemothorax
• Churg Strauss syndrome
• Rheumatoid arthritis

Amylase from the Increased values in case of:

pleural fluid • Pancreatitis
• Neoplasic disease (salivary type)
• Esophagus rupture (salivary type)
Triglycerides • Chylothorax
Adenosine TB
deaminase
Cytology Larger lymphocytes - TB / neoplastic
Eosinophils> 10% - Drug allergic reaction / Churg-Strauss sdr

NTproBNP HF
 Complementary examinations
 Thoracic chest radiography and profile - liquid, density,
homogeneous opacity, declivity. Gravity sign - deflection of mediastinum by
compression
 Pleural echography allows the visualization of pleural fluid
 Standard Biological Balance
Whole blood count, ionogram, BUN, creatinine, ESR, C reactive protein, blood
culture in fever episode
 Bronchoscopy - in case of parenchymal abnormalities
Stages of evaluation - Stage three
Completing investigations
CT Exam • Tumors with pleural localization
• PE
PET-CT Specifying neoplastic etiology
Pleural biopsy The histological aspect for diagnosis:
• TB
• mesothelioma

It can be done
• Percutaneously under the CT guide
• Thoracoscopy
• Thoracotomy
Parapneumonic pleural effusion
 It usually occurs in the clinical context of a
bacterial pneumonia or a lung abscess.

 Clinical exam: Para or meta-pneumonitis pleural

effusion as it is classically defined, accompanied
by fever, pleural pain, and cough accentuation.
 The objective clinical examination highlights:
 the presence of condensation syndrome
 Sign: dullness, abnormal vibration transmition
Incriminated germs
S. Pneumoniae Pneumonia is complicated with pleural effusion in ~ 50% of
cases
para / metapneumonic
Germs - isolated from the liquid in 5% cases
S. Aureus Germs isolated 80% of the cases in the pleural fluid
(especially in children)
Gram negative Pseudomonas
E. Coli
Legionella

 The amount of fluid in the case of parapneumonic effusion

is generally low
 It tends to resorb with curing the pneumonic process
 In cases diagnosed late, there may be a process of
loculation or transformation into pleural empyema.
 Pleural Puncture:
- clear, sterile liquid, rich in PMN

N.B. Unfavorable risk factors requiring emergency

evacuation: pH <7.20; LDH> 1000UI / l, low
glycose, positive bacteriological tests
Parapneumonic effusion
 Paraclinically:
 Xray identifies the liquid +/- pulmonary
condensation
 Ex. pleural fluid:
 exudate with a high amount of fibrin, citrine or dense
appearance
 Cytological exam shows a high proportion of
polynuclear neutrophils or lymphocytes
 the cultures in the liquid are sterile
Parapneumonic effusion
 Pathophysiology:
 The visceral pleura in the vecinity of the pneumonic
process - inflammatory process
 Interstitial fluid crosses the visceral pleura - pleural
space
 Accumulation rate> lymphatic drainage capacity
 When germs invade pleura – empyema
Treatment:
 is the same as for parenchymal disease to which
anti-inflammatory treatment and fluid evacuation are
added if it is a more important pleural effusion
Parapneumonic effusion in viral
pneumonia
 Real incidence is unknown
 Adenoviruses, influenza virus, CMV, HS, VEB
 Small amount of liquid
 The fluid is exudate with leukocytes between 100-
6000 / mm3 usually lymphocytes
 Evolution is short, self-limiting, less than a week,
with healing without pleural effusions with anti-
inflammatory treatment
Parapneumonic effusion in
fungal pneumonia
 1% pleural effusions
 Aspergillus fumigatus - invades pleura (fistula, TB
reactivation)
 Dg - Positive skin reaction to Aspergillus or serum
antibodies
 Treatment
 evacuating the pleural cavity
 Excision of the fistula
 Amphotericin B parenterally
Parapneumonic effusion in
fungal pneumonia
 Coccidioides immitis associates in 20% pleural effusion
cases
 Fever
 Nodal erythema
 Erythema multiform
 Pleural pain
 Normal Glucose in Liquid
 Cytological examination - predominant lymphocyte -
eosinophils
 Requires systemic antifungal therapy

 Histoplasmosis associates in 1% cases of pleural effusions

that spontaneously reabsorbes within a few weeks
Parasitic pleural effusion
 Amoebiasis - the most common
 Complicate an amoeba liver abscess (through diaphragm
erosion)
 Clinical - cough + pleuritic pain + dyspnea
 Liquid
 Appearance "chocolate sauce"
 Entamoeba histolytica is isolated
 Mortality ↑↑↑
 Treatment
 Metronidazole 750 mg x 2 / day - 5-10 days
 Diloxamid furoate 500 mg x 3d
Parasitic pleural effusion
 Hepatic / lung hydatid cyst may complicate with pleural
effusion by breaking it into the pleural space
 Clinical - anaphylactic shock
 Severe chest pain
 Dyspnea
 Liquid Exam - Daughters
 Treatment - Surgical: Removal & Drainage
Post-embolic pleural effusion
 usually accompanies multiple or bulky lung infections. It is
possible to occur as a result of sub-inflated mood infarction
and non-specific inflammation in the adjacent pleural area.
 Clinically - classic picture when the triad is present:
 Deep vein thrombosis
 Clinical picture of thoracic thrombosis, subfebrility,
hemoptysis, suggestive radiographic image
 small or medium fast progression of serum
hemorrhage or serocitrin fluid
 post-embolic pleural effusion is in most cases unilateral
and accompanies feverish, chest pain with pleural effusion,
dyspnea
Post-embolic pleural effusion
 Sometimes venous thrombosis is missing, with only the risk
factors of it being present: prolonged immobilization, heart
failure in valvular or elderly, myocardial infarction, fractures,
neoplasia, surgery
 Paraclinically :
 signs of fluid discharge can be associated with a
condensation image suggesting lung infarction
 the pleural fluid is exsudate serum hemorrhagic or
serocitrin rich in fibrin
 the leukocytes in the fluid are mainly neutrophils; the
appearance of pleural effusion with eosinophils
Post-embolic pleural effusion
 Evolution is regressive in 7-14 days except in
cases where the embolism is recurrent.
 The treatment is similar to that of TEP
 Anticoagulation medication will consist
 Initially, heparin was given
 Later antivitamin K is given for 3-6 months

 Heals without pleural effusions

Pancreatitis pleural effusion
 20% of pancreatitis associates pleural effusion
(unilateral left)
 Pancreatic enzyme contact with transdiaframatic
lymphatic plexus
 Clinically - Pancreatic affection predominates
 Serum-sanguinous / haemorhagic fluid with
PMN 1000-50,000 / mm3; possibly no increased
eosinophils
 Liquid Glucose - Normal
 Liquid Amylase >>> Blood Level (6: 1)
 Treatment - similar to pancreatitis
Pleural effusion secondary to
esophageal perforation (Boerhaave
syndrome)
 Esophageal perforation - in 2/3 second cases EDS
for foreign body removal / stenosis dilatation
 Followed by inflammatory acute mediastinum -
severe chest pain
 In 60% cases (usually left)
 Exudate liquid
 Increased amylase (salivary origins) and low pH <6
 +/- food remnants
 Severe evolution-riskof empyema
 Treatment - surgical + drainage
Pleural effusion secondary to
subdiaphragmatic abscesses
 Secondary surgeries
 Week 1-3 postoperative
 80% are associated with pleural fluid reaction
 Exudate with predominant PMN
 Leukocytosis (up to 50,000 / mm3)
 Normal Glucose
 pH> 7.2
 Secondary to a liver abscess (20% cases)
 Clinical abdominal pain, fever, abnormal liver function tests
 CT Confirmation
 Surgical treatment - abscess resection & pleural drainage
 SEL with pleural effusion
 Pleural effusion 40% of patients. Isolated or in the context
of polyserositis - exudative pericarditis. It is usually small or
medium, bilateral.
 The pleural fluid is exudate -> serous.
 Cytology is mixed with lymphocytes and numerous PMNs.
The lupus cells are inconsistently found in the fluid.
Glucose in the liquid has normal values. The complement is
low and antinuclear antibodies are present.
 Treatment - corticosteroids
Rheumatoid arthritis pleural
effusion
 More often in men and patients with ↑ RF titres or with
subcutaneous nodules
 the onset is marked by fever, pleural pain, cough
 otherwise evolves with afebrility
 the liquid efflux is of medium volume, unilateral, and
rarely bilateral
 may be accompanied by granulomatous pulmonary
lesions, infiltrative or diffuse interstitial fibrosis, lesions
that appear as an expression of pulmonary rheumatoid
determinations
Rheumatoid arthritis pleural
effusion
 The pleural fluid is usually exudate, serous or opalescent.
Cytology is uncharacteristic, with predominant lymphocyte
or mixed cellularity (lymphocytes, mesothelioma and fewer
red blood cells). Glucose in the liquid is very low (20-30 mg
%). LDH over 700 IU. There may be rheumatoid factors
consistent or not with their presence in serum or articular
fluid.
 The positive diagnosis is on the combination of
polyarthritis with unremitting pleural effusion.
 Treatment: NSAID and lower proportion of corticosteroids
Churg-Strauss sdr pleural effusion
 30% of CS sdr patients
 Pleural fluid
 exudate
 high LDH concentration
 Low pH & glucose level
 Mixed cellularity with numerous eosinophils
 Treatment - corticosteroid
Drug-related pleural effusion
 It often associates acute symptoms with a few
hours / days after treatment
 Shivers
 Fever
 Cough
 Dyspnoea
 Blood eosinophilia in pleural fluid also
 Described after Nitrofurantoin and Procarbazine
 Methysergide & Dantrolene - chronic pleural effusion fluid
with changes to fibrosis - changes occurring 2-3 years after
the start of treatment and resolved 6 months after
discontinuation
Postoperative pleural effusion
 In patients who have undergone upper abdominal
surgery or heart surgery.
 Pleural fluid appears probably due to pleura or
pericardial trauma during surgery.
 does not require special treatment, it resolves
spontaneously.
Dressler's Syndrome
 Pleuro-pericarditis & fever 3-4 weeks after a
myocardial or pericardial disease (myocardial
infarction, heart surgery, chest trauma with heart
damage)
 Immunological response - antibodies against
cardiac structures.
 The pleural fluid serous, small amount, one side
 or bilaterally. Glucose & pH - normal.
Uncharacteristic cellularity.
 Diagnosis - Exclusion
 Treatment - NSAIDs
Exposure to asbestos
 Rate of occurrence - correlation with exposure
level
 In the first 10 years of exposure, serum / serum-
sanguinolent pleural effusion occurs.
 PMN, mononuclear leukocytes & eosinophils are
predominant in the fluid.
 Sometimes pleural biopsy is required to exclude
mesothelioma or bronchogenic carcinoma.
 usually resolves spontaneously in 1-2 years.
Uremic pleural effusion
 Occurs in 20% of patients with chronic renal
failure.
 Chest pain & pleural friction.
 In a small number of patients pleural effusion may
be sero-sanguinous or haemorrhagic
 Glycopleuria is normal
 Cellularity is predominantly lymphocyte.
 The choice of treatment is dialysis.
Yellow nail syndrome
 Rare pathologies that associate nail changes
(become thin, curved, yellow) and important
lymphedema
 Pleural effusion, chronic pulmonary infections &
bronchiectasis.
 Pleural effusion occurs in 1/3 of patients & bilateral
 Exudate, serous, normal glucose & predominant
lymphocyte
 There is no specific treatment.
 If pleural effusion is massive, pleurodesis may be
done
Meigs Syndrome
 Pelvic Tumor (Fibroma or Ovarian Tumor) with
 pleural effusions and ascites.
 Citrine exudate, less serohaemoragic
 Mixed cytology, predominantly lymphocyte.
 The structure of pleural fluid and ascites is similar.
 After thoracentesis, quickly re-occurs and
disappears after the surgical cure of the pelvic
tumor.
Eosinophilic pleural effusion
 Proportion of eosinophils in pleural effusions of at
least 10%.
Etiology
Diseases that associate Löffler syndrome
pleural effusion with - Periarteritis Nodosa
eosinophils and blood - Pulmonary or extrathoracic hydatid cyst
eosinophilia - Hodgkin's lymphoma

Diseases with pleural Pulmonary thromboembolism -Asbestos

effusion with eosinophils, - Bronchial neoplasm
without blood eosinophilia - Chest trauma
- Bacterial pneumonia
- LES, PR
- Mycosis
- Reaction to drugs(nitrofurantoin,gliclazid,dantrolene
Eosinophilic pleural effusion
 Causes of eosinophils presence in the pleural fluid
are not known.
 It is possible to involve local and general
immunological mechanisms.
 The etiologic diagnosis sometimes involves
complex explorations.
 The treatment does not contain any special
features other than etiological treatment.
Haemothorax
 Blood in the pleural space
 The most common cause of thoracic trauma
 Iatrogenic procedures (central venous catheters)
 The bleeding source can be :
 pulmonary parenchymal dilaceration
 damage to intercostal vessels
 rupture of pleural adhesions
 In 60-80% of cases, pneumothorax is associated
 Treatment of hemothorax evacuation & stop bleeding
 Chylothorax
 Lymph accumulation in pleural cavity due to thoracic duct
rupture.
 The pleural liquid has a milky aspect, opalescent &
contains chylomicrons, TGL & lymfocites.
 Chylothorax is heavy and tends to recur after draining

Causes
• tumors which invade the thoracic duct, among this the
lymphomas are on the first place
• Trauma of the thoracic duct
• Subclavian vein thrombosis with thrombi occluding the
thoracic duct
• Pulmonary limfangiomatosis
Chylothorax
 Symptomatology ~ volume of fluid
 Chest pain & fever are missing
 Post-trauma is set in 2-10 days
 The pleural fluid is milky white, odorless
 ! Differentiation with pleural empyema - centrifuges.
 Adding 1-2 ml of ethyl ether to the pleural fluid. If the liquid
contains a lot of cholesterol, it clears up.
 The best method of diagnosis is triglyceride dosing - level>
110mg% = chylothorax
Chylothorax
 ! Measures for lymph decrease: continuous gastric
aspiration, bed rest & parenteral nutrition
 Chylothorax traumatic injury to the chest can generally
resolve spontaneously. If after 7 days the chest canal lesion
is not closed, the surgical ligation will be done.
 Lymphoma or other cancers are involved in chemotherapy
and mediastinal irradiation.
 Pleurodesis is an option
 Chest canal ligation is not effective in neoplasia
Neoplastic pleural effusion
 When in fluid or pleural biopsy - neoplastic cells
 Paramalignant pleuresy - there are no atypical cells
 secondary
 lymphatic & blood metastases from a receiving cancer
 Expansion from a tumor in the vicinity of the pleura

• Lung cancer
• Cancer san
• Gastric cancer
secondary • Ovarian cancer
• lymphomas
• Pleural mesothelioma
 Neoplastic pleural effusion
 In paramalignant pleuresies is not a direct invasion of the
pleura.
 Cause - lymphatic obstruction, local or systemic tumor
effect or a complication of irradiation or chemotherapy.
 A pulmonary tumor may cause lymph / bronchial
obstruction - the fluid is transuded
 May occur due to the systemic effects of a lung tumor
• adenocarcinomas induce a hypercoagulation state that
can lead to a pulmonary embolism with pleural effusion
 Hypoalbuminemia is another cause of paramalignant
effusion
Neoplastic pleural effusion
 Radiotherapy can lead to pleural effusion 6 weeks
to 6 months after the cure ends.
 Chemotherapy also has the potential to cause
pleural effusion, especially if methotrexate,
procarbazine, cyclophosphamide, mitomycin or
bleomycin are used.
 Clinical manifestations of neoplastic pleural
effusion are due to the amount of fluid
accumulated in the pleura. They are cough &
dyspnea.
 Sometimes - asymptomatic & dg - clinical
Neoplastic pleural effusion
 Serous / serum hemorrhagic / hemorrhagic pleural fluid
 Cytological: lymphocytes, macrophages & mesothelial cells
 Exudate fluid, protein> 4 g%
 If transduced
 HF Associated
 atelectasis through obstructive bronchial tumor
 Early stage of lymphatic obstruction.

 Glucose & pH of the pleural fluid can be N / ↓

 Neoplastic cells present - test of certainty
neoplastic etiology
 Neoplastic pleural effusion
Additional investigations
Chest X ray It shows besides fluid opacity that can be unilateral or bilateral
and the presence of a parenchymal lesion suggestive of lung
cancer.
CT lung It is especially useful for pulmonary neoplastic processes and
less for the determination of the etiology.
Pleural biopsy It has diagnostic value only if it is positive. In some
cases - negative because pleural lesions are nodular, and they
do not affect the entire pleural surface.
Tumor markers Carcinoembrionic antigen (CEA)
carbohydrate antigens CA 15-3, CA 19-9.
CA 72-2, enolase play a role in establishing the neoplastic origin
Calretinin & cytokeratin 5/6 are the best markers for
pleural mesothelioma
Male, aged 35;

 Nonsmoker
 DVT left limb 2 years ago
Reasons for hospitalization
 Fever - 39 ° C with chills
 Dry cough
 Scarred right thorax
 Dyspnea to minimal effort

 Symptomatology started 2 days before admission

Clinical examination
 Fever - 38.5 ° C
 Dermatitis the right lower limb
 Respiratory system
 Vibrations diminished basal right
 Right basal dullness
 Swollen vesicular murmur and rare rhizome basaltic
rallies
 Cardiovascular system - regular, tachycardic
(110bpm)
EKG
X ray
Diagnosis?
1. Right basal pneumonia with right
parapneumonic pleural effusion
Therapeutic attitude
 Antibiotic treatment is initiated with
 Augmentin 1.2 g x 2 / day iv
 Gentamicin 80 mg x 3 / day iv
 Unfavourable evolution
 Persistent fever
 the occurrence of a diarrhea syndrome
Pleural liquid examination
 Biochemistry - Exudate

 Cytology - poorly differentiated carcinoma

Chest tomography
Bronchoscopy
 It does not directly highlight the tumor - located
peripherally

 Bronchial brush - inflammatory cells

Evolution
 4 days after admission – distal DVT right lower limb
 Doppler ultrasound - thrombosis
 Deep vein of the right lower limb
 iliac vein
 The vena cava up to the renal vein

 Anticoagulant treatment has been initiated

 In this contextinterpreted as paraneoplastic syndromes

 Diarrheal syndrome
 DVT
Evolution
 Twelve days after admission, the CT scan is repeated

 The increase in tumor volume is highlighted

 No secondary determinations are highlighted

 Fever gradual remission (under antibiotic treatment)

 Dx
1. Pulmonary thromboembolism with right pleural
effusion

2. Pulmonary neoplasm with right pleural effusion

Subsequent attitude
 Pleural fluid is harvested
 the morphopathological examination in 2 hospital units
reconfirmed the diagnosis
 Oncological consultation decides to initiate
cytostatic treatment
 The patient performs the first two cytostatic
treatments
Differential diagnosis
 in favor arguments
 Three anatomopathological examinations with
concordant results
 The presence of associated manifestations that could
be classified as paraneoplastic syndromes
 Against arguments
 Lack of a direct anatomopathological evidence
 Young patient without risk factors for lung cancer
Dx approach
 Repeat the bronchoscopic exam
 Direct detection of lung injury is achieved
 Macroscopic Inflammatory Aspect
 Biopsy material is taken

Morphopathological exam

Diagnosis aspect for PULMONARY INFARCTION

Final diagnosis
 Subsequent dosages: Protein C and S deficiency

 Symptoms of hypercoagulability of the plaque

complicated with
 Pulmonary infarction (possibly over-infected)
 Deep vein thrombosis recurrence
Tuberculous pleural effusion
Prof. Dr. Daniela Bartoş
Definition
Fluid accumulation in the pleural cavity due to the
localization of TB-specific lesions in the pleura.

 The incidence of tuberculous pleural effusion has

decreased in the recent years to 6.8 per 100,000
inhabitants. The TB pleural effusion rate, as a
manifestation of respiratory tuberculosis, is 11%.
 The gender distribution is 2/1 in favor of male sex.
Incidence rate
 -One third of the world’s population is infected
 -Almost 9 million cases annually
 -Nearly 9 million positive microscopic cases
 -50 % under diagnosis !!!!!!
 -Over 2 million deaths annually (≈ 3 mill !!!)
 -Decreased incidence rates but there are 1% more
cases each year
 -450.000 cases in the European area
 -70.000 deaths
 -Eastern states +++
 -Romania ≈ 110 cases /100.000
Pathogeny
 should be considered as a form of adult TB. The
disease occurs mainly in the young adult, being
considered as an expression of TB first infection.
Coexistence with other active or inactive
pulmonary determinations suggestive of secondary
stage TB.
 Pleura can be contaminated by:
 Haematogenic way
 Lymphatic way
 By contamination or by the intrusion of a casual lesion
from a subpleural outbreak
 Pathogeny
 Studies have shown that the presence of BK in the pleura does not
cause the forming of pleural effusion unless the pleural effusion has a
state of hypersensitivity.
 Koch Bacillus causes a neutrophilic reaction, then accumulations of
macrophages and lymphocytes.

 The number of T lymphocytes is higher in the pleural fluid than in

the blood. They are helper T cells (CD4 +, CD29 +) that proliferate and
produce interferon gamma.
 All these suggest a hypersensitivity mechanism
Pathogeny
 In most of the cases, considered to be a manifestation of sensitivity
to BK and to bacillary proteins (tuberculoproteins). Arguments for
this hypothesis:
 The presence of a time interval (3-7 months), present in 75% of the
cases, from the moment of tuberculin installation to the
development of the pleural exudate.
 Bacteriological criterion: reduced number of bacilli in the fluid and
their quick disappearance.
 The intense reaction to tuberculin and its fluctuations.
 All of these suggest a hypersensitivity mechanism
Pathogeny
 Can accompany parenchymal TB, affecting the pleura
in several ways:
 Opening into the pleural cavity of a caseated
subpleural node
 Pleural infection through contiguity lesion - through
close contact of the pleura with TB parenchymal
lesion
 By retrograde lymphatic way from bronchial trachea
nodes
 The pleural effusion accompanying parenchymal TB
is attested by miliary nodes found in pleural biopsy
Morfophopathology
 The main morphopathological element is the tuberculous follicle
accompanied by an important pleural inflammatory reaction.
 Macroscopic:
 Usually the entire pleural cavity affected predominantly on
the right (45%) and the parietal pleura is thicker
 the pleura is hyperemic, non-glossy, with fibrous plaques or
fibrilar character which gives it a vilous-rugged appearance
(cat's tongue). Deposits are friable and make false
membranes
 under the fibrous deposits the pleura is thickened and
adherent to the lung, sometimes very thick (neo-membranes)
 after removal of false membranes, miliar nodes or large
prominent granules that sometimes ulcerate are seen
 the fibrous deposits on the two pleural effusions sometimes
join together to form pleural symphysis
 Morphopathology
 Microscopic:
 Partial or total fade away of the epithelial layer
 On cross-section:
 the first layer is made-up of fibrin, floating endothelial cells,
neutrophils, erythrocytes. Over time, areas in this layer become
hyalinized
 layer II is the neomembrane, which is the pleura becoming
thickened by a granulation tissue with serous corium as a starting
point
 layer III – the subserous corium which is edematous, hyperemic
and infiltrated with follicles
 the lung participates with a congestive neighborhood reaction
translated by: edema and interstitial congestion, desquamation
and minimal alveolar exudative reaction
Morfopathology

 In the final stage the fibrous masses can be joined

together, making symphyses or a compact,
pseudo-cartilaginous coating. In case of a proper
treatment, the recovery of pleural lesions is
complete.
The clinical picture
 The onset can be:
 sudden: in full apparent state of health, with thoracic pain of
variable intensity and high fever, accompanied by chills. The
chest pain is accentuated by respiratory movements.
 signs of bacillary impregnation, asthenia, weight loss, subfebrile
condition, night sweats
 slowly, progressive, staggered in 1-2-3 weeks with signs of
bacillary impregnation, progressive fever, progressive chest pain
 with an intercostal neuralgia, which precedes the occurrence of
fluid
 asymptomatic - the liquid is accidentally discovered
Pleural effusion symptoms
 General signs:
 the overall condition is generally good
 Fever is always present (remittent or irregular),
accompanied by small and repeated chills,
especially in the first week of illness. Sometimes the
fever increases progressively to 39° C and then
gradually decreases, in 3-6 weeks the patient is
apyretic
 pallor, sometimes with congested cheeks on the
side of the pleura
 asthenia
 weight loss
 Pleural effusion symptoms
 Functional signs:
 - extrapulmonary:
 digestive disorders, sickness, vomiting, feeling full especially in
left abundant efusions
 tachycardia with fever
 − pulmonary:
 chest pain: strong at the begining, but tends to diminish
according the fluid accumulation
 The patients may adopt an antalgic position on the affected
side
 Irritating cough, generally (dry, short, painful, appearing in
seizures)
 dyspnea –according to the amount of accumulated liquid
Pleural effusion symptoms
physical signs:
 inspection:
 bulging hemithorax – large amount of liquid
 mydriasis may appear on the affected side by
sympathetic chain irritation
 reduced mobility or even immobility of the basal
region of the chest wall
 palpation:
 the vocal vibrations are diminished or may even
disappear depending on the amount of liquid
 the top of the heart moves to the left parasternal line
(500 ml) up to the right parasternal line (1200 ml)
Pleural effusion symptoms
 the percussion:
 if less than 500 ml liquid, the opacity can not be clinically
detected
 woody opacity with upper right edge if large quantities of
liquid
 the classic Damoiseau curve - is oblique towards the
axilla- if quantities between 800-1200 ml
 opacity of Traube space in left pleurisies
 the auscultation:
 pleuretic sound – hearable at the upper limit of the opacity
 Diminution or abolishing of the vesicular whispering
 pleural frictions, many of them at the beginning , can be
heard on a large area, harsh, diminishes when fluid
accumulates and reoccurs when the volume of fluid
decreases
 egophony: the voice perception is modified ‘goat voice’
 PECTORILOCVIA AFONA: whispered voice perception
Paraclinic examinations
 Chest Xray:
 For a radiological opacity to be seen, 200-400 ml of
liquid are required
 The diaphragm’s contour is pale
 The costodiafragmatic sinus becomes opaque
 Homogeneous opacity, costal intensity, moves to lateral
movements of the chest
 Large amounts of fluid opacifies the whole hemithorax,
move the mediastinum, usually keep clear the peak of
the lung.
Paraclinic examinations

 IDR to tuberculine:

 Moderate or poor response within the first 2 weeks after

testing with 2U PPD
 10-30% of TB effusions evolve with negative IDR due to
the presence of suppressive T lymphocytes in excess.
Paraclinic examinations
 Pleural fluid examination:
 -Serocitrin aspect (90%) rarely haemorhagic or purulent
 -Rivalta positive reactivity with albumin 3g%
 - Low in glucose - below 0.8 g%
 -Increased pleural LHD > 500UI / I
 - Rich in neutrophils at first and later in lymphocytes (80%)
 - BK isolation can only be done in cultures in Lowenstein-
Jensen environment or by inoculation on lab rats. The
result is positive in only 2/3 of cases
 -NAP (nucleic acid amplification) test with high specificity
98% but with low sensitivity -62%
Paraclinic examinations
- adenosine deaminase (ADA) is elevated in case of
TB. A value above 45 U / l is highly suggestive for
the bacillary ethiology.
- a pleural lysozyme increased over 15 mg% - may
suggest tuberculosis etiology in 80% of cases.
Increased values of pleural lysozyme are also
found in non-tuberculous pleural empyema or in
some cases in malignant pleurisy.
- an increased pleural concentration of interferon
gamma (IFN-gamma) may also suggest TB
Paraclinic examinations
 Pleural biopsy:
 It has the best diagnostic performance and
highlights tuberculous follicles in 80% of cases
 Thoracoscopy or thoracotomy
 When the other methods were irrelevant for the
diagnosis process
 Positive diagnosis
 is based on histological and bacteriological confirmation
 the arguments for diagnosis are:
 The age between 35-30 years
 Serous fluid with lymphocytic predominance
 IDR-positive tuberculin or positive after 4-6 weeks
 Pleural ADA increased
 Pleural lysozyme / plasma lysozyme is over 2
 Healing with no sequelae
 Positive response to tuberculostatic treatment
 Differential diagnosis
1. With other forms of effusions, of which the most
important is neoplastic
Differentiation elements:
 Large amount of fluid, often hemorrhagic, that
recovers after puncture
 No fever
 Cytology often highlights altered mesothelioma
and neoplastic cells
 Tuberculosis ineffective treatment
 Disease progresses to progressive aggravation,
possibly with progressive pain
 Differential diagnosis
2. With other effusions
 Infectious (Mycoplasma pn., Chlamidia, Rickettsii)
- It grows insidious with not too abundant fluid and with lymphocytes in
the fluid
- Favorable evolution under tetracycline or erythromycin
- Serology positive for mycoplasma
 Heart

- Appear in the context of advanced cardiac disease

-Usually bilateral
-They disappear from cardiotonic or diuretic treatment
 From collagenosis

- Typically with little liquid

- Immunological tests confirm diagnosis
 Differential diagnosis
 Lower lobar pneumonia
- condensation syndrome with accentuated vocal vibrations, tubular
sound, ralles
- an accompanying pleural reaction may occur
 Lower lobar atelectasis

- alveolar condensation syndrome with auscultatory silence

 Pleural sclerosis cu pahipleuritis

- The hemithorax is retractable, diminished vocal vibrations, less dull with

percusion
 Broncho-pulmonary neoplasm
 Subfrenic abscess

- It causes confusion (chest pain and dyspnea)

 giant lung hydatid cyst
 Congenital or acquired diaphragmatic relaxation - free sinuses
Evolution
 Correctly treated, generally evolves favorably, fever drops
after 2-6 weeks, as well as other signs of general infection.
The fluid begins to spontaneously resorbes after 3 weeks.
 Untreated, the disease represents a remarkable risk, 25-
30% of patients developing pulmonary TB in the next 2
years
 Complications:
 The purulent transformation of the fluid (pleural
empyema) with chronic evolution
 Parietal abscesses, osteitis, parietal muscle atrophy
 Pulmonary fibrosis, respiratory failure
 Pachypleuritis, pulmonary symphysis
Treatment

 Objectives:
 Fast fluid resorbtion
 Prevention of sequelae and pulmonary
tuberculosis or in other organs
 Providing a normal pulmonary function
Tuberculostatic treatment

The treatment of TB pleural effusion is the same for tuberculosis

The current treatment scheme:
 Rifampicin (R), Isoniazid (H), Pirazinamide (Z), Etambutol (E) for 2
months followed by 4-month R + H combination in bi-weekly
administration
 If associated with other tuberculous pulmonary or extrapulmonary
determinations, the therapeutic scheme will be:
 R + H + Streptomycin + pyrazinamide administered bi-weekly (2/7 for
3 months) followed by another 3 months with the R + H combination
in bi-weekly administration
 Will be given in a DOT manner - directly observed therapy
 Anti-inflammatory treatment
 In cases where the etiology is definitely tuberculous, it
is useful to use corticosteroids. If the diagnosis is
uncertain, the corticosteroid therapy is not
recommended because the initial evolution is
favorable anyway.
 The accepted dose is 30-40 mg / day prednisone with
a decrease of 5 mg every 3-4 days, the total duration
of treatment being 3-4 weeks.
 It is also necessary to evacuate almost entirely the
pleural fluid to prevent the formation of pleural
symphysis.
 NB. The duration of treatment is 6 months, over this period relapses
are very rare
Kinesiotherapy

 It may have comparable effects with the corticoid

 It starts as soon as the acute phenomenon have
been remitted and the resorption of the fluid is
obvious and continues for 2-3 weeks after the
liquid resorption
Symptomatic treatment
 For pain analgesics or even opiates in rare cases
can be used
 Dyspnea will be controlled using the evacuation
puncture. The liquid is drained until the patient
begins to cough or feels chest tightness. The
evacuation above this limit alters the pleural
pressure, possibly favoring a fluid increase.
 Rest as long as the patient has fever
 The diet will be balanced, hypercaloric, rich in
fresh food
Pneumothorax
Prof. Dr. Daniela Bartoş
Definition
 The presence of air in the pleural cavity

 Source:
1. Pulmonary – most often
2. Digestive – ruptured esophagus
3. External – continuity
Classification
 spontaneous:
 Primary – without previously known lung disease
 Secondary – cause by a previously known lung disease

 provoked:
 Trauma
 Iatrogenic (dg / therapy)
Pathogeny
 Spontaneous primary idiopathic :

 In young subjects (20-40 years) asthenic stature (tall,

thin) more frequent in male smokers
 Effraction of small gaseous subpleural spaces pleural
blebs – predominantly situated in the apical region
 Effraction of an emphysema subpleural bullae
(homogeneous distruction of all lung parenchyma in a
specific region)
Pathogeny
 Neonatal spontaneous pneumothorax
 1-2% of term neonates, especially after laborious
births, 2x in males
 More frequent in neonatal ARDS pts
 Secondary to mechanic issues during the first lung
expansion, especially when bronchial obstruction by
meconium, mucus or thrombus
Pathogeny
 Catamenial pneumothorax
 Very rare, in young females, discrete symtoms, after
24-48h of menstruation
 Usually right hemithorax, tends to recur
 Possibly as a result of pleural endometriosis
Pathogeny
 Spontaneous secondary pneumothorax
 More severe because it complicates a pre-existing
pathology

 Classically seen in:

 Pts with emphysema – difficult to interpret Xray
 During asthma attacks – pneumomediastinum alone is
possible
 Pts with bronchiectasis (especially in cystic fibrosis)
Pathogeny
 Spontaneous secondary pneumothorax
 Can complicate other lung diseases:

 Bronchial cancer or primitive/secondary pleural cancer

 Sarcoidosis
 Diffuse interstitial fibrosis
 Histiocitosis X
 Infection:
 TB , Staf (piopneumothorax)
 Pneumocystis jirovecii
Pathogeny
 Traumatic pneumothorax

 Pleural injury:
 Direct (penetration thoracic trauma)

 Indirect
 Alveolar rupture by sudden increase in alveolar pressue as
a result of hitting shock
 Air reaches in and dissects interstitial spaces towards
visceral pleura which is dilacerated
Pathogeny
 Iatrogenic pneumothorax

 As a result of a medical procedure:

 Pleural puncture
 Pleural/transthoracic lung biopsy
 Subclavian vein catheter placement
 Transbronchial biopsy
 Mechanical ventilation
Pathogeny

Spontaneous primary pneumothorax

 In young males (~ 20 years, rare after 40 years), without an
obvious trigger.
 May be preceeded by increased effort (physical effort,
coughing etc).
 It is currently considered that those who develop it have a yet
undiagnosed lung disease
Risk factors
 Smoking: risk is proportional to no cigarettes/day,
larger in males
 Family history: reported a family aggregation;
genetic determinism has not be elucidated
 Marfan Syndrome
 Homocisteinuria
Tablou clinic
 Chest pain, dispnea
 Clinical exam:
 Affected hemithorax:
 Diminished chest expansion
 Absence of vocal vibration transmission
 Hyperresonance
 Absent/diminished vesicular sounds
 Cardiovascular:
 Tachycardia
 Arterial hypotension (in tension PTX)
Chest Xray
 Rapid & easy dx

 Characteristics:
 Transparency in the
periphery
 Clear pleural separation
line
 Mediastinum shift in Linie pleurala

tension PTX

Tension PTX
Lung CT
 Not routinely used
 Identifies small
localized PTX
 Dx underlying
pathology
Differential Dx
 Similar clinical manifestations:
 Acute myocardial infarction
 Pulmonary embolism
 Acute aortic dissection

 Other pathology

–Pleural effusion –Gastric ulcer

–Pneumonia –Pancreatitis
–Angina –Colecistitis
Evolution
 Spontaneous:
 Healing – spontaneous resorbtion
 Chronic - hidro- or pio-pneumotorax
 Primary spontaneous PTX– 1st year recurrence
rate 25-50%
 Higher risk in females, smokers, longilin individuals
Clinical form
 Tension pneumothorax:
 Surgical emergency
 Cyanosis, anxiety, dyspnea, tachycardia, arterial
hypotension
 Chest Xray: collapsed lung shifting the mediastinum in
the opposite direction
 Emergency treatment: emergency aspiration
Clinical form
 Bilateral pneumothorax :
 Rare occurrence
 Successive rather than simultaneous
 Hemopneumothorax:
 In relapses, by rupture of previous aderency
 In trauma:
 Penetration rib fracture
 Stabbing, shot wounds
Treatament
 Objective
 Removal of air from pleural cavity
 Prevent recurrence

 Initial approach:
 Oxygen-therapy (in all circumstances)
 Differs according to quantity
 Clinically stable at first event of primary
spontaneous with small air volume PTX (≤ 3 cm
between pleural line and thoracic wall)
conservator: observation ≥ 6, then check Xray.
 If no progression may be seen in ambulatory care.
 Clinically stable at first event of primary
spontaneous with medium-large air volume PTX:
 Needle aspiration (18-22 gauge)
 Pleural tube insertion if needle aspiration is ineffective
 Clinically stable primary spontaneous recurrent
PTX or hemopneumothorax – pleural tube and
thoracoscopy
 If unstable – pleural drainage. Bridge therapy -
18G needle in II-III intercostal space on
midclavicular line.
 In the case lung re-expansion > 90% is not
obtained in first 3 days – video-assisted
thoracoscopy or thoracotomy
Treatment – primary spontaneous PTX
PSP
Dyspnea
YES
Aspiration Pleural
and/or > drainage
2cm
NO
Successful? Successful?

NO
YES YES NO

• Pneumology consultation
Removal of tube 24h
after complete lung after 48h
expansion • Thoracic surgery
Monitoring or consultation after 5 days
Discharge
Treatment – secondary spontaneous PTX

PSS
Dyspnea +
YES Pleural
> 50 years + drainage
> 2cm

NO NO
Pneumology
Aspiration Successful? Aspiration consultation

Successful? Successful?
YES YES NO

Admission
24h
Removal of tube 24h
• Thoracic surgery
after complete lung consultation after 3 days
expansion
Discharge
Pleural drainage kit
Pleural drainage

Security region
Control chest Xray

Pleural drainage with incomplete lung re-expansion

Preventing recurrence
 PSP – only in those having needed thoracoscopy:
 Pleurodesis by talc infusion or abrasion

 SSP – all pts require recurrence prevention

measures:
 Ablation of emphysema bullae
 Pleurodesis by talc infusion or abrasion