bijan ziaian,md thoracic surgeon general surgeon (certified endocrine surgeon) (certified endocrine...

Bijan Ziaian,MdBijan Ziaian,Md

Thoracic surgeonThoracic surgeon general surgeongeneral surgeon

( ( certified endocrine surgeoncertified endocrine surgeon ) )

SPN-Typically recognized as a single,well

defined,spherical lesion less than 3 cm completly surrounded by normal lung

There are no associated changes of atelectasis, hilar enlargement, or pleural effusion

solitary pulmonary nodules were identified on 0.09 to 0.2% of all chest radiographs in large screening studies .

The lymphatic sump of Borrie includes the groups of lymph nodes that receive lymphatic drainage from all pulmonary lobes of the corresponding lung

The location of regional lymph node stations for lung cancer staging. Station, Description: 1, highest mediastinal lymph nodes; 2, upper paratracheal nodes; 3, prevascular, precarinal and retrotracheal nodes; 4, lower paratracheal nodes; 5, aorto-pulmonary nodes; 6, pre-aortic nodes; 7, subcarnal nodes; 8, paraesophageal nodes; 9, pulmonary ligament nodes; 10, tracheobronchial nodes; 11, interlobular nodes; 12, lobar bronchial nodes; 13, segmental nodes; 14, subsegmental nodes. Note: Stations 12, 13, and 14 are not shown in their entirety

Differential diagnosis

- malignancy:%20 to %40 risk of being malignantfor smokers the risk will be %50- infectious granuloma: arising from a

variety of organism cause of %70 to %80 of spn,s

- hamartoma: cause for about %10 of spn,s.

Factors influencing the probability of cancer in a SPN

evidence for growth over time.density of the lesion on CT scan.associated symptoms.patient age, sexcigarette smoking historyoccupational historythe prevalence of endemic granulomatousdisease

Assesment:-clinical history-physical examination-imaging-biopsy versus resection

Risk factors:Hx of smokingAge over 35HemoptysisPrior hx of neoplastic disease

Imaging:

-CXR-CT SCAN-PET SCANNodule location, size, marginmorphology, calcification pattern,growth rate, mostly recognized by ctscan

up to 50% of patients thought to have a single

lesion based on chest radiograph are proven to harbor multiple nodules when examined

byct scan.multiple nodules more likely representmetastases or granulomatous disease.

Findings suggest malignancy:

Lesion larger than 3cm regarded as mass withhigher rate of malignancy.Irregullar border,spiculated edge,corona radiate signStippled,amorphous or eccentric calcificationDoubling time between 20-400 days

Findings suggest benign lesions:Diameter smaller than 3 cm.Smooth marginCalcification within a nodulediffuse,solid,central TBlaminated or pop corn HAMARTOMAValume doubling time under 20 days andhigher than 400 days2 year size stability per cxrwhich demonstrated only a 65% positivepredictive value for chest radiographs.Thus size stability of a pulmonary mass on

chestfilms is a relatively unreliable indicator of abenign lesion

Pet scan:fluorodeoxyglucose (FDG) is used to measure

glucosemetabolism in cells imaged by PET

Can differentiate benign from malignantSensitivity %97Specificity %78

-False negative:bronchoalveolar carcinomaCacinoiedsTumors less than 1 cm -false positive: confusion with infections orinflamatoryprocesses

Biopsy:The surgeon must have an evidence-basedalgorithm for approaching the diagnosis

andtreatment of a pulmonary nodule.Only through biopsy can a pulmonary

nodulebe definitively diagnosed

Bronchoscopy %20-%80 sensetive for detecting spn,s(size,proximity to bronchialtree,prevalence of CA in population).

TTFNA

TT fna accurately identified the peipherallesions up to %95Complications may occur at a relativelyhigh rate (e.g., a 30% rate ofpneumothorax).the false-negative rate ranges from 3 to29%.

Vats Often use for excising and diagnosingindeterminate nudoles.Lesions suitable for Vats: Less than 3 cm in diameterLocation in outer one third of lungThe nodule must not be directlymanipulated with instruments. the visceral pleura overlying the nodulemust not be violated

the excised nodule must be extracted from

the chest within a bag .Some groups advocate proceeding

directlyto VATS in the work-up of a solitarypulmonary nodule

Lung neoplasm-Lung cancer is the leading cancer killer-Accounting for %30 leading cancer death more than CA of breast and prostate andovary combined.-3th most diagnosed cancer, behindprostate ca in men and breast ca in women-Most patient diagnosed in advance stageand therapy is rarely curative-Overall 5 years survival is %15

Epidemiology:the incidence of lung cancer in men hasbegun to decrease, while incidence hasremained stable in womenAnnual death rates for men also havedeclinedCigarette is the primary cause,esp in scc

andsclcIncrease number of cigarette, years ofsmoking and the use of unfiltered cigarette,escalate the risk of CA.%15 of lung cancers are not related withsmoking mainly adenocarcinoma

Tobacco use is the leading cause of lung cancer87% of lung cancers are related to smokingRisk related to:

amount smoked age of smoking onset gender product smoked depth of inhalation

squamous cell carcinoma and small cell carcinoma,

are extraordinarily rare in the absence of cigarette

smokingEven after smoking cessation, however, the risknever drops to that of people who never smoked,regardless of the length of abstinence.

Risk factors for lung CA Environmental tobacco smokeResidential radonCooking oil vaporsIndoor coal and wood burningGenetic factors: family history, CYP1A1Ile462Val polymorphism, XRCC1 variantsViral factors: HPV 16 and 18 

Secondhand (or passive) smoke exposure. Pre existing lung disease due to poor clearance of inhaled carcinogens, or inflammation.industrial compounds, including asbestos, arsenic,and chromium ominous combination of asbestos exposure and cigarettesmokingCOPD A previous history of tuberculosis with secondary scarformation Tobacco smoke polycyclic aromatic hydrocarbon bind to DNA inducing mutationSmoke induce cancer of : oral cavity, pharynx, larynx,

tracheobronchial tree and lung, and esophagus

Preinvasive Lesions-Squamous Dysplasia and Carcinoma In Situ(cigarette smokers) -Atypical Adenomatous Hyperplasia (stage of a stepwise evolution to BAC)-Diffuse Idiopathic Pulmonary Neuroendocrine Cell

Hyperplasiadiffuse proliferation of Neuroendocrine cells.<5mm>5mm= carcinoied tumor The term precancerous does not mean thataninevitable progression to invasive carcinoma

Invasive or Malignant Lesions

The term bronchial carcinoma is synonymous with lung cancer in general. Both terms refer to any epithelial carcinoma occurring in the bronchopulmonary tree

the pathologic diagnosis of lung cancer is based on light microscopic criteria

Immunohistochemical staining and electron microscopy are used as adjuncts in diagnosis, particularly in the assessment of potential neuroendocrine tumors.

Lung cancers are divided into two groups:

1-first group:

-non small cell lung cancer: (scc -adenocarcinoma –bronchoalveolar carcinoma

larg cell carcinoma)

-neuroendocrine tumors including: typical carcinoid,atypical carcinioid,larg cell neuroendocrine carcinoma

2-second group:small cell lung cancer

Scc

-%30 to %40 of lung CA-mostly in men and highly correlate withcigarette smoking. Histologically, cells develop a pattern ofclusters with intracellular bridges andkeratin pearls-primarily located centrally(hemoptysis,obstruction,dyspnea,pneumoia)-central necrosis makes cavity

Occasionally a more peripherally based squamous cell carcinoma will develop in a tuberculosis scar or in the wall of a bronchiectatic cavity.

Image Description: Infiltrating well-differentiated squamous cell cancer inmain-stem bronchus. The surface of the tumor is necrotic (lower right). Notebronchial cartilage at the edge of the field (upper left). The cells of this tumorare relatively well-differentiated, with a structure resembling a stratifiedsquamous pattern. The tumor has breached the basement membrane and is

extending through fibrous soft tissue toward the cartilage.

Squamous Carcinoma of Lung (Medium Power)

This low power view of lung is centered on a sheet of neoplastic cells outlinedby yellow arrows. • The surrounding stroma is composed of desmoplastic fibrotic tissue heavilyinfiltrated by lymphocytes. • The neoplastic cells show hyperchromatic nuclei and an increased N:C. • Higher power will allow histologic typing

Adenocarcinoma -%25 to %40 of all lung cancers-Adenocarcinoma is the most frequent

histologic type found in women and occurs more frequently in females than in males

-most often is a peripherally based tumor-frequently discoverd incidentally-symptom of chest wall invasion and

pleural effusion dominate.

Histologically, adenocarcinoma is composed of glands with or without mucin production, combined with destruction of contiguous lung architecture.

• This is a close view of a peripheral adenocarcinoma (yellow arrow).

• The neoplasm is yellowish-tan with a well-circumscribed lobulated periphery. • The overlying pleura (white arrow) is puckered.

Pulmonary Adenocarcinoma (External View) •This is the pleural surface of the lung. •Note the puckering of the pleural surface with surrounding hemorrhage at the arrow. •The carcinoma cannot be identified in this picture but lies directly beneath the puckered area.

• This low power view of a poorly differentiated adenocarcinoma shows nests (arrows)of tumor cells embedded in dense fibrous (desmoplastic) stroma. • Some nuclei are extremely large and hyperchromatic. • There are no central lumens in the nests nor are there well-defined intercellular bridges. • The intervening stroma contains scattered lymphocytes

Adeno carcinoma of lung,mucinous type.This is a view of a mucicarmine stain on an adenocarcinoma of the lung. • Despite the lack of central lumens in the nests of neoplastic cells (black arrows)there is vivid intracellular mucin staining (yellow arrows to magenta globules) . • Such extensive positivity identifies this neoplasm as an adenocarcinoma

This low power view of an adenocarcinoma shows nests (arrows)of tumor cells embedded in dense fibrous (desmoplastic) stroma. • Some nuclei are extremely large and hyperchromatic. • There are no central lumens in the nests nor are there well-defined intercellular bridges. • The intervening stroma contains scattered lymphocytes

Adenocarcinoma with focal clear cellchange

Bronchoalveolar carcinoma(BAC)-relatively rare, %5 of all lung cancers-Growth pattern is unique, rather than

invading lung parenchyma, tumor cells fill the alveolar spaces

-aerogenously seed in other part of lung-there are 3 XR patterns: single nodule,

multiple nodule, diffuse form mimicking pneumonia

-air bronchogram can be seenFor a tumor to be classified as a pure BAC,

there can be no evidence of destruction of surrounding lung parenchyma.

Bronchoalveolar cell carcinomaThe view is of the pleural surface of the lung. • The pleural lymphatics are full of anthracotic laden macrophages. • A small portion of the lung has been incised to reveal a poorly demarcated yellowish tumor indicated by arrows

Bronchoalveolar carcinoma.This neoplasm iscomprised of columnar cells (arrows). The nuclei are densely hyperchromatic and vary insize. The cytoplasm contains occasional vacuoles

Large cell Carcinoma of the lung:account for %10 to %20 of all lung ca, can be

bothcentrally or peripherally

They are often admixed with other cell types suchas squamous cells or adenocarcinomaLarge cell carcinoma can be confused with a

largecell variant of neuroendocrine carcinoma, IHC canbe diagnosticThe tumor is composed of sheets of poorlydifferentiated large tumor cellsThe cells containround to oval nuclei and prominent nucleoli. There is marked cellular atypia and an increasedmitotic activity.

This is a view of a large cell neoplasm of the lung. • The green arrows point to the extensive necrosis. • The blue arrows demonstrate large, hyperchromatic, anaplastic cell. • All other cells on the slide are neoplastic as well

Larg cell CA of the lung:The blue arrows point to typical examples of neoplastic cells. • The green arrows demonstrate the necrotic debris. • No gland formation or intercellular bridges are seen.

Neuro endocrine neoplasm:

Neuroendocrine tumors form aspectrum of lesions ranging from verywell differentiated neuroendocrinetumors (carcinoied tumors) to

differentiated malignancies with endocrinefeatures, typified by small cell carcinoma

divided into 2 groups 1- hyperplasia 2-three separate groups of carcinomaGI- typicall cacinoiedGII-atypical carcinoiedCIII-large cell type or small cell type

Grade I:low grade ,primarily in central airwaysonly %20 peripheralaccur in youngersHemoptysis, obstruction, pneumoniaVery vascullarLymph node metastasis is in %15Rarely spread systemic

Grade II:Aggresive clinical behaviorUnlike gradeI, linked to cigarette smokingMore likely peripherally located Much higher malignant potentialLymph node metastasis in %30-%50%25 remote metastasis at the time of

diagnosis

Grade III:large cell tumore accure in heavy smokersOccur in middle or peripheral field of lungTheir neuroendocrine nature is revealed

bypositive immunohistochemical staining forat least one neuroendocrine marker.

Grade III small cell type:Is the most malignant necAccount for %25 of all lung cancersLeading producer of para neoplastic

syndromes

Salivary Gland–Type Neoplasm The tracheobronchial tree hassalivary-type submucosal bronchialGlandsThe two most common areadenoid cystic carcinoma andmucoepidermoid carcinomaBoth tumors occur centrally due totheir site of origin. Adenoid cystic carcinoma is a slowGrowing. Mucoepidermoid carcinoma consists of squamous andmucous cellsand is graded as low or high grade, depending

Clinical presentation:

There are wide variety of symptomesClinical symptomes and signes are

related to1-histologic feature2-location of tumor in the lung3-biologic features and production of

para neoplastic syndromes4- presence or absence of metastasis

Tumor histology:-Scc and sclc are mostly centrally locatedThen cough, hemotysis,wheezing,Dyspnea,Pneumonia are common.In contrast adeno ca are often locatedperipherally and discovered incidentallysymptomes due to pleural or chest wallinvasion

Tumor locationPulmonary symptoms: Cough secondary to irritation ,compressionDyspnea due to obstructionWheezing due to narrowing of an airway morethan %50HemoptysisPneumoniaLung abscess

Non pulmonary symptoms: mostly because of direct tumor invasionChest wall: pleuritic pain, localized chestwall pain, radicullar painpancoast syndrom in superior sulcusTumorhorner syndrom,arm pain, chest wall painphrenic nerve and recurrent nerveinvolvment

Svc syndrom:Mostly occurs with sclc,produce bulkyenlargment of mediastinal lymph nodesand compress svcSymptoms: swelling ofhead,neck,arm,headache, edema ofconjuctiva-Direct invasion of vertebral body: localizeback pain

Tumor biologyBoth sclc and nsclc can produce para neoplasticsyndroms.May produce symptomes even before symptoms

ofprimary tumor appear.Symptomes abate with treatment of tumor.-HPO-hypercalcemia(%10), because of metastasis orsecretion of PTH (%15) most often in scc-endocrinopathy most often in sclc

Paraneoplastic Syndromes in Patients with Lung Cancer:

Endocrine : Hypercalcemia (ectopic parathyroid hormone) Cushing's syndrome Syndrome of inappropriate secretion of

antidiuretic hormone Carcinoid syndrome Gynecomastia Hypercalcitoninemia Elevated growth hormone level Elevated levels of prolactin, follicle-

stimulating hormone, luteinizing hormone Hypoglycemia

Neurologic : Encephalopathy Subacute cerebellar degeneration Progressive multifocal

leukoencephalopathy Peripheral neuropathy Polymyositis Autonomic neuropathy Eaton-Lambert syndrome

Skeletal : Clubbing Pulmonary hypertrophic osteoarthropathyHematologic : Anemia Leukemoid reactions Thrombocytosis Thrombocytopenia Eosinophilia Pure red cell aplasia Leukoerythroblastosis Disseminated intravascular coagulation

Cutaneous : Hyperkeratosis Dermatomyositis Acanthosis nigricans Hyperpigmentation Erythema gyratum repens Hypertrichosis lanuginosa acquistaOther : Nephrotic syndrome Hypouricemia Secretion of vasoactive intestinal peptide with

diarrhea Hyperamylasemia Anorexia or cachexia

Metastatic symptoms

Most commonly at-vertebral bodies-bones-brain(%10 at time of diagnosis)-liver-adrenal glands-lung-skin-soft tissue

Diagnosis,evaluation,staging1-assessment of primary tumor2-presence of metastatic disease3-functional status

Assessmen of primary tumor-CXR-CT SCAN-MRI-Bronchoscopy-pet scan.Assess primary tumor, relationship with

other structures,invasion.Proof of invasion may require thoracoscopy

or even thoracotomy .MRI not for evaluating lung but for defining

relationship to major vessels

.Tissue diagnosis can be obtain through bronchoscopy or needle biopsy

.thoracotomy for diagnosis and staging of primary tumor, up to %5 of cases.

.chest ct scan is the most effective and non invasive method to assess mediastinal and hilar node for enlargment.

.node more than 1 cm in diameter, %70 metastasis and %30 inflammation

.pet scan

Treatment :

Only %15 percent of lung cancersdiagnose in early stage(t1,t2_+n1 )(t3-n1)-standard of treatment is surgery-surgery as a single treatment modaltyis disappointing-RT and CH are other modalties oftreatment

Early stage disease: Early-stage disease typically is defined as stages I and

II. In this group are T1 and T2 tumors.N1+_ ,T3N0.this is a small group. The current standard of treatment is surgical resection.

Survival is suboptimal, and surgery alone is disappointing.

Patient in stage 1a without any treatment have med survival of 14 months. 5 years survival about 22%

After lung resection 5 y survival will be 67%. For stage ll it will be 41% Advanced age at diagnosis, male sex, low

socioeconomic status, nonsurgical treatment, and poor histologic grade are associated with increased mortality risk on multivariate analysis.

Appropriate surgical procedures for patients with early-stagedisease include lobectomy, sleeve lobectomy, and occasionallypneumonectomy with mediastinal lymph node dissection orSampling.Any tumor of the superior sulcus, including tumors withoutevidence of involvement of the neurovascular bundle, is nowcommonly known as Pancoast's tumor.Chest wall involvement at or below the second rib should not

beconsidered Pancoast's tumor. Treatment involves aMultidisciplinary approach The recommendation for resection of Pancoast's tumors ,depends on the results of mediastinal lymph node analysis .In N2 spread patients surgery has no role. For this reason,resection should always be preceded by mediastinoscopy.Now the choice of treatment is induction chemoradiation

thrapyfollowed by surgical resction. With complete surgical resction 5years survival will be 54% and

Surgical excision is performed via thoracotomy with en bloc resection of the chest wall, vascular structures, and anatomic lobectomy. A portion of the lower trunk of the brachial plexus and the stellate ganglion are also typically resected

En bloc resection also is used for other locally advanced tumors (T3) with direct invasion of the adjacent chest wall, diaphragm, or pericardium. If a large portion of the pericardium is removed, reconstruction with thin Gore-Tex membrane will be required to prevent cardiac herniation and venous obstruction

If a patient is deemed medically unfit for major pulmonary resection due to inadequate pulmonary reserve or other medical conditions, then options include limited surgical resection and radiotherapy

. Limited resection, defined as segmentectomy or wedge resection, can be used only for more peripheral T1 or T2 tumors.

studies suggest decreased long-term survival rate for tumor size >3 cm but not for smaller tumors

Another option for patients who are poor operative candidates isdefinitive radiotherapy. dose of 60 to 65 Gy. 5years survival of 30%forstage I. tomotherapy and robotic radiosurgery are modern technique Withminimize toxicity.Postoperative adjuvant chemotherapy previously was found to be of

no

Benefit in multiple prospective randomized trials.potential benefit for preoperative (or induction) chemotherapy has

beenproved.induction chemotherapy may result in increased perioperative

morbidity Mortality.however, except in patients undergoing right-sided pneumonectomyafter induction chemotherapy, the incidence of perioperative

morbidityand mortality is not different for the two groups

Locoregional Advanced Disease:

Surgical resection as sole therapy has a limited role in treatment of

stage III disease. T3 N1 tumors can be treated with surgery alone but

with 5 years survival of 25%. Patients with N2 disease have 5 yearssurvival of 5% to 10% with surgery alone. Post op N2,s have 30% 5 yearssurvival.Surgery is occasionally appropriate for select patients with T4, N0 orN1, M0 primary tumors (e.g., tumors invading the superior vena caval,carinal or vertebral body involvement, or satellite nodules in the sameLobe.Surgery has no role in any T,N3 or in T4 and N2. SURVIVAL RATEREMAIN LOW IN THESE PATIENTS.Definitive radiotherapy is predominantly used for palliation ofsymptoms in patients with poor performance status, because the curerate of radiotherapy as a single modality in patients with N2 or N3disease is <7%

Such poor results for patients with stage IIIA lung cancer reflect thelimitations of locoregional therapy in treating a disease process thatresults in death because of systemic metastatic spread. Definitive treatment of stage III disease (when surgery is not felt to

befeasible at any time) is usually a combination of chemotherapy andradiotherapy

Preoperative (Induction) Chemotherapy for Non–Small Cell Lung Cancer

The use of chemotherapy before possible surgical resection has a number of potential advantages:

    1. The tumor's blood supply is still intact, which allows better chemotherapy delivery and avoids tumor cell hypoxia (in any residual microscopic tumor remaining postoperatively), which would increase radioresistance.

2. The primary tumor may be downstaged with enhanced resectability.

3. Patients are better able to tolerate chemotherapy before surgery and are more likely to complete the prescribed regimen than when chemotherapy is given after surgery.

4. Preoperative chemotherapy functions as an in vivo test of the primary tumor's sensitivity to chemotherapy.

5. Response to chemotherapy can be monitored and used to guide decisions about additional therapy.

6. Systemic micrometastases are treated. 7. Patients who have progressive disease

(non-responders) are identified and spared a pulmonary resection.

Potential disadvantages include the following:     1. In theory the perioperative complication rate may

increase (predominantly in patients requiring right pneumonectomy after induction chemotherapy).

2. While the patient is receiving chemotherapy, potentially curative resection is delayed; if the patient does not respond, this delay could result in tumor spread.

Metastatic lesion to the lungCan be resected but:1-the primary tumor must already be

controlled2-the patient must be able to tolerate the

surgery3-the metastasis must be compeletly

resectable according to CT scan4-no evidence of extrapulmonary tumor

burden5-alternative superior therapy must be

unavailable

Final Thought

“If you explain something sosimply that even a fool can understand it, then only afool will understand it."

Lung infections

1-lung abscess, empyema2-mycobacterial infections3-pulmonary mycoses

Localized area of pulmonary paranchymal necrosis,at least 2 cm in diameter.

Lung abscess is the result of a lower respiratory tract infection only by organisms that cause necrosis

Primary:Immunocompromisd patientsHighly virulent organismAspiration

1. I. Primary2.   A. Necrotizing pneumoni.

Staphylococcus aureus, Klebsiella, Pseudomonas, Mycobacteriu 2. Bacteroides, Fusobacterium, Actinomyces     . Entamoeba, Echinococcus   B. Aspiration pneumonia

. Anesthesia    2. Stroke3 Drugs or alcohol  1. C. Esophageal diseae2. . Achalasia, Zenker's diverticulum,

gastroesophageal reflux  D. Immunodeficiency   Cancer (and chemotherapy)    . Diabetes   . Organ transplantation   . Steroid therapy    . Malnutrition

II. Secondary  A. Bronchial obstruction    1. Neoplasm     2. Foreign body  B. Systemic sepsis    1. Septic pulmonary emboli    2. Seeding of pulmonary infarct  C. Complication of pulmonary trauma    1. Infection of hematoma or contusion    2. Contaminated foreign body or penetrating injury  D. Direct extension from extraparenchymal infection    1. Pleural empyema    2. Mediastinal, hepatic, subphrenic

Clinical features

Productive coughFeverChillsLeukocytosis over 15000Weight lossFatigueMalaisePleuretic chest painDyspnea

Indolent fashion: Weeks or months of :coughMalaiseWeight lossLow grade fevernight sweetLeukocytosisanemia

After aspiration 2 weeks elapse before cavitation occurs.

40% to 75% of patients produce a foul-smelling sputum.

Rare but severe complications:Massive hemoptysisEndobronchial spreadRupture into plueral cavitySeptic shockRespiratory failure

Why rare?Because of modern antibotic era.Mortality rate about 5% to 10%In immunosuppresive cases rates range

from 9-28%

Cxr shows a density or massThin wall and air-fluid levelCT-scan will clarify the diagnosisEndobronchial obstrucation or associated

mass must rule out.A cavitary lung CA is frequently mistaken

for a lung abscess

Managment:Systemic antibiotics are the mainstay of

therapyCommunity-acquired: penicillin,ampicillin

or amoxicillinB latamase inhibitor or metronidazol

should be added

Failure of medical therapyAbscess under tensionAbscess increasing in size during

appropriate treatmentContralateral lung contamination Abscess >4–6 cm in diameter Necrotizing infection with multiple

abscesses, hemoptysis, abscess rupture, or pyopneumothorax

Inability to exclude a cavitating carcinoma

Empyema:

Definition: purulent pleural effusionWhat are the causes?-parapnumonic -post pnumonic-post surgical-post trumatic

At the bedside:Grossly purulent, foul-smelling pleural

fluidMakes the diagnosis at bedside.diagnosis is confirmed by a combination

of clinical scenario with positve pleural fluid culture.

Pathophysiology:

The spectrum of organisms involved in the development of parapnumonic empyema is changing.

-pneumococci ,staphylococci still are the most common cause

-gram negative aerobics and anaerobics are becoming more prevalent.

-mycobacteria and fungi are rare.-multiple organisms may be found in 50%

of cases.Why cultures may be negative?-antibiotics are initiate before antibiotics-culture process is not efficient.Therefore ,it is better that the antibiotic of

choice be guided by the clinical scenario

And not just the organisms found on culture.

Broad spectrum antibiotics may be still required even when the cultures have failed, or if the single organism is grown, when the clinical picture is more consistent with a multiorganism process.

What are the most common gram-negative organisms cause empyema?

Escherichia coliKlebsiella Pseudomonas Entrobacter These organismsmay be fastidious or

difficult to document by culture

What are the conditions can cause gram negative empyema?

Periodontal disease Aspiration syndromsAlcholismGeneral anesthesia Drug abuseGe reflux

What are the route of organism entry into the pleural cavity?

Contiguous spread from pneumoniaLung abscessLiver abscessThoracocentesis Thoracic surgical proceduresEsophageal injurytruma

Stages of the disease:

The early stage:The effusion is wateryIt is free in pleural cavityPh is above 7.3, glucose level greater

than 60mg/dl, LDH is lower than 500u/l

Treatment:.Antibiotic and a type of drainageThe goal is complete lung expansion

Ph lower than 7.2 and a low glucose level means that a more aggressive approach of drainage should be pursued.

Second stage(fibrinopurulent):Thick and loculated fluid associated with

fibrinous adhesion.DrainageThoracoscopy Antibiotics

Third stage:Formation of pleural peel, trapped lung.In this stage surgical decortication would

be necessary.

Managment:

If there is a residual space, persistent pleural infection is likely to occur.

Causes?Contracted lungSurgical lung resection

Small space that can be drained by a chest tube = conservative managment

In the face of pleural symphysis, chest tube can be DC.

If the cavity persist, chest tube can be converted to open.

Patient,s can be followed by serial CT-scan.

Larger space may require open thoracotomy.

Massive hemoptysis

Expectoration of more than 600ml of blood within 24-hour

.mortality rate is %30 to %50

Chest wall mass

Chest wall neoplasm

Benign:ChondromaOsteochondroma Desmoid tumor

Primary chest wall tumorsBone origin:Chodrosarcoma Osteosarcoma Ewing,s sarcoma

Malignant chest soft tissue sarcoma

Final Thought

“If you explain something sosimply that even a fool can understand it, then only afool will understand it."