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TITLE PAGE

THE PATTERN AND OUTCOME OF TREATMENT OF PLEURAL EFFUSION IN

NATIONAL HOSPITAL ABUJA, NORTH-CENTRAL NIGERIA :

AN EVALUATION OF AETIOLOGY, DIAGNOSIS, TREATMENT AND

OUTCOME OF TREATMENT IN A 1 YEAR PROSPECTIVE

STUDY IN NATIONAL HOSPITAL.

A dissertation submitted to the National Post-Graduate Medical

College of Nigeria(NPMCN) in partial fulfillment of the

requirements for the award of the Fellowship of the

Faculty of Surgery [FMCS].

BY

DR. UGWUANYI UGOCHUKWU CHARLES P.

DEPT. OF SURGERY

NATIONAL HOSPITAL ABUJA.

NOV.2006

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DECLARATION PAGE

“It is hereby declared that this work on Pattern and Outcome

of Treatment of Pleural Effusion in National Hospital Abuja,

done under the direct supervision of Dr.S.A.I. Salawu(FMCS)

is original and has not been presented to any other college

for a fellowship, nor has it been submitted elsewhere for

publication”.

Dr.Ugwuanyi Charles Ugochukwu

ATTESTATION PAGE

I hereby certify that the work on Pattern and Outcome

of Treatment of Pleural Effusion in National Hospital by

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Dr.Ugwuanyi Charles Ugochukwu was carried out under my

supervision.

You may therefore accord it any necessary considerations.

Thank you.

Dr. S.A.I. SALAWU( FMCS, FWACS, FICS)

Chief Consultant Surgeon,

National Hospital Abuja, Nigeria.

TABLE OF CONTENTS.

Title Page i

Declaration ii

Attestation iii

Table of contents iv

Dedication v

Acknowledgement vi

Ethical Clearance vii

Summary/Abstract 1

Introduction 4

Chapter 1-Literature Review 5

Chapter 2-Materials/Method 52

Chapter 3-Results 59

Chapter 4-Discussion/conclusions 79

References 94

Proforma for Analysis 99

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DEDICATION

To Ifeoma, Chommy, Somtoo and Munny.

For being there.

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ACKNOWLEDGEMENTS

I will start by thanking the Almighty God for sound health,

guidance and protection .

My wife, Ifeoma and my children, Chommy, Somtoo and Munny

deserve special thanks for tolerating those long hours

in the office during this work.

The Chief Medical Director of National Hospital Abuja,

Dr. Z.O. Ajuwon, was very encouraging and deserves a special

appreciation.

I am also full of thanks to the Head of Department of

Surgery, National Hospital Abuja , Dr. Y.D. Abubakar

for the departmental support given to this project.

For taking the pains to supervise every stage of

this project I am most grateful to Dr. S.A.I

Salawu, Consultant Surgeon National Hospital Abuja.

Special thanks goes to Prof. Oluwole Adebo, Consultant

Cardiothoracic Surgeon, University College Hospital

Ibadan, Nigeria, for all his useful suggestions.

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Dr. Tony Anigbo, Chief Consultant Neurosurgeon in the

National Hospital, was the major source of inspiration

and deserves more thanks than I can offer.

Former Head of Department of Surgery, National Hospital

Abuja, Prof. P.O. Obekpa whom I regard as my mentor

as a Surgeon was always accessible for advice and

any form of support, and I thank him for that immensely.

All the Resident Doctors in the National Hospital

Abuja, especially in the Surgery Department were very

supportive and I remain thankful to them. Dr(S).Lawal,

Ihekire, Adamu, Udoye, Ekwueme deserve special mention.

Other members of staff of the National Hospital

Abuja, especially in the Nursing, Radiology, Chemical

Pathology, Microbiology, and histopathology ,too numerous

to mention here were very helpful and I remain very

thankful to them.

THE SUMMARY/ABSTRACT

Problem under Study – Pleural Effusion is a common cause

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of morbidity/mortality in our daily clinical practice.

There are several causes of Pleural Effusion. Whereas most

medically related causes require treatment directed

mainly at the primary cause, others require in addition

some form of surgical intervention.

Objective of the Study – To find out the common causes

of surgically important pleural effusion in the

National Hospital Abuja Nigeria, and also the

contemporary methods of diagnosis , therapy and outcome

of such.

Methodology – All cases of Pleural Effusion requiring some

form of surgical intervention , by way of tube

thoracostomy drainage at some point in their management

were sampled over a one year period spanning between

February 2005 to February 2006 in a prospective

fashion. Relevant clinical data including clinical symptoms

and signs, radiological findings, results of pleural

fluid analysis ,primary disease condition, treatments

directed at both the primary pathology as well as the

effusion , the common complications observed during

treatment and the outcome of these treatments recorded

at 6 months re-evaluation were all recorded in a

proforma.

Statistical analysis of data was done with EPI-INFO soft

ware and presented in form of pie charts, bar charts,

histogram and tables.

Results – Of the 86 cases of surgically important

pleural effusion sampled, the commonest presentation was

dyspnoea (100%) and dullness to percussion on the

affected hemithorax(100%). Thoracentasis yielded straw

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coloured fluid in (54.7%), sero-sanguinous in (27.9%),

turbid/purulent in (16.3%) and chyle in (1.2%) only. The

commonest radiological feature was the meniscus sign in

addition to the other radiological features of the

primary pathology. Chemistry analysis of the aspirate

confirmed it to be exudative effusion in 100% of cases.

Neoplastic disease was found in 35 cases (40.7%), Pulmonary

tuberculosis in 32 cases (37.2%) and Pneumonia in 19 cases

(22.1%). The commonest cause of malignant effusion was

found to be Breast Carcinoma which was recorded in

65.7% of these. Others were soft tissue sarcoma (11%), lung

carcinoma (11.4%), intra-abdominal carcinoma (8.6%), parotid

carcinoma (2.9%). Most patients had tube thoracostomy

drainage of the effusion in addition to the treatment

of the primary disease condition. Concerning outcome of

treatment, 71% of those with malignant effusion were

dead at 6 months and indeed recorded the worst prognosis

amongst the causes of primary pathology.

The commonest complication observed during treatment was

premature dislodgement of the chest tube.

Discussion/Conclusion – Neoplastic disease was the leading

cause of surgically important pleural effusion from this

study with Breast carcinoma contributing the highest

quota. It also represents the worst prognosis as well above

2/3 of all such cases were dead at 6 months. Para-pneumonic

effusions had the best outcome as 88% of them did not show

any evidence of the disease or any complication arising

there from at 6 months re-evaluation. This may be related to

availability of appropriate antibiotics and early exhibition

of such. Tuberculous effusions had a far better prognosis

than malignant ones, but not as good as the para-

pneumonic ones.

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Application of diagnostic armaments and early diagnosis is

important in the eventual outcome of treatment of pleural

effusions.

INTRODUCTION.

Pleural cavity is that potential space lined by visceral and

parietal pleura and normally contains very little fluid which

is in dynamic equilibrium with the extra-cellular fluid(ECF).

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In certain pathological conditions, this stable dynamic

equilibrium is disrupted leading to the accumulation of fluid

in the pleural space in the form of exudates or transudates.

The diagnosis, treatment and outcome of treatment of Pleural

Fluid Collection in whichever form is determined by the

specific etiologic agent.

The objective of this study was therefore to elucidate the

Pattern of Pleural Effusion commonly encountered in our

Surgical Practice here in the National Hospital, and in

clear terms define the realistic methods of diagnosis and

therapy as well as the outcome of such.

Justification of this study was based on the fact that pleural

effusion and its associated morbidity/mortality often present

a diagnostic and therapeutic challenge in our daily surgical

practice, hence the need for a study in this direction.

Scope-This is a prospective study carried out at the National

Hospital Abuja between February 2005 to February 2006.

Exclusions-All medically related causes of pleural effusions

whose treatments hardly requires any surgical intervention.All

cases of traumatic haemothorax are excluded because alteration

of Staling forces does not really play ay role in its

formation.

Limitations of this study include, patients who decline to

participate for various reasons, relatively high cost of

medical bills which affected prompt compliance to treatment

and follow up in some patients, incessant strike action in

health institutions across the country, occasional

breakdown of vital equipment, missing case notes.

CHAPTER ONE

LITERATURE REVIEW

ANATOMY OF THE PLEURAL CAVITY

EMBRYOLOGY.

At the end of the third week of intra-uterine life, the intra-

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embryonic mesoderm on each side of the midline differentiates

into 3 portions; paraxial, intermediate and lateral.

Intercellular clefts appear in the lateral mesoderm and divide

it into somatic mesoderm and splanchnic layers lining the

body wall and the yolk sac wall respectively .Hence the space

bordered by these layers forms the intra-embryonic coelom

which is initially in wide communication with the extra-

embryonic coelom .But with the cranio-caudal and lateral

folding of the body of the embryo ,this communication is lost

and a large intra-embryonic cavity extending from the thoracic

region down to the pelvic region is formed 1.

The cells of the somatic mesoderm lining the intraembryonic

coelomic cavity become mesothelial and line the outside of

the pleural ,pericardial and peritoneal cavities .Similarly,

the splanchnic mesoderm form mesothelium which line visceral

layer of lungs, heart and abdominal organs. Hence, the

different origins of parietal and visceral pleura.

The septum transversum is a thick plate of mesodermal tissue

which attempts to divide the intra-embryonic coelomic cavity

into thoracic and abdominal regions, though partially, because

it leaves a large pericardio-peritoneal canal on each side2.

When the lungs expand ,the mesoderm of the body wall is split

into a definitive wall of thorax and pleuro-pericardial

membrane which contains the common cardinal vein and phrenic

nerve.With the descent of the heart, the common cardinal veins

shift towards the midline and as a result the pleuro-

pericardial membranes are drawn out like a mesentry, and

finally fuse with each other and with the root of the lungs.

Hence the thoracic cavity is divided into a definitive

pericardial cavity and two pleural cavities, while the pleuro-

pericardial membranes persist as the fibrous pericardium in

adults.

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The pleuro-peritoneal folds which are crescent shaped extend

from the caudal border of the pleural cavities in a medial and

ventral directions and by the seventh week of intra-uterine

life ,fuses with the mesentery of the esophagus ,as well as

the septum transversum. It is at this point that the pleural

cavities are completely separated from the abdominal cavity by

this assembly of tissues from different origin called

diaphragm. Myoblasts originating from the somatic mesoderm of

the leteral and posterior chest wall penetrate the adjacent

pleuro-peritoneal membranes to form the muscular part while

the septum transversum forms the tendinous part.

GROSS ANATOMY.

The Pleural Cavity is a potential space lying between the

chest wall, lungs and mediastinum. It is lined by a two

layered membrane called pleura. The inner Visceral layer

covers the lungs including the fissures ,while the outer

Parietal layer covers the rib cage, diaphragm and mediastinum.

The Visceral pleura is absent at the hilum of the lungs where

pulmonary vessels, bronchi and nerves enter the lung tissue.

The mediastinum separates the pleural cavity into two halves.

The pleural membranes are smooth, glistening, and semi-

transparent. Despite these similarities the two membranes have

unique differences. Visceral pleura contain no pain fibres,

and has a dual blood supply from bronchial and pulmonary

vessels, while the parietal pleura is innervated by the

intercostals nerves with blood supply from systemic

intercostals vessels. The lymphatic drainage of visceral

pleura is to the sub-pleural, intra-bronchial,tracheo-

bronchial lymph nodal chain.

PHYSIOLOGY.

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The pleura produces fluid which act as a lubricant which

provide a frictionless surface between the two pleurae, in

response to changes in lung volumes during respiration. The

normal pleural space contains approximately 1ml of fluid,

representing the balance between hydrostatic and oncotic

pressure in the visceral and parietal pleural vessels on one

hand and lymphatic drainage on the other[fig.1].Disruption of

this balance results in effusions.

Normally there is a continuous circulation of fluid out of the

arterial end of the capillaries into the interstitial

space/third space, then back into the venous end of the

capillaries. In order to maintain this normal circulation of

fluid across the capillary wall, a balance between the two

main forces namely hydrostatic/capillary blood pressure and

plasma oncotic pressure, operate which controls the rate and

direction of fluid movements.

Some fluid and protein enter the lymphatics before eventually

returning to the general circulation ultimately through the

thoracic duct .This may be partly the result of tissue

pressure, and partly due to osmotic attraction of proteins in

the lymphatic system 3.

Venous capillary obstruction or any increase venous pressure

far beyond 10mmHg occur in elevated pulmonary venous pressure

due to congestive cardiac failure for instance, reduces the

quantity of fluid re-absorbed at the venous end of the

capillaries, resulting in pleural fluid accumulation

containing serum protein of less than 3g%, specific gravity of

less than 1016, and LDH usually less than 200IU, features

characteristic of a transudate.

Lymphatic obstruction as in neoplastic infiltration and

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chronic inflammation reduces the clearance of pleural filtrate

protein load along with water and hence produces pleural fluid

collection of high protein content, >3g%,specific

gravity>1016,LDH > 200IU,features in keeping with exudates.

PLEURAL EFFUSION

INTRODUCTION.

Pleural effusion is defined as an abnormal accumulation of any

type of fluid in the pleural space, as a result of the

disruption of the haemo-dynamic equilibrium that exist across

pleural membranes namely hydrothorax, sero-pus, frank pus,

blood, chyle 4.

Pleural effusion is an indicator of a pathologic process that

may be of primary pulmonary origin, related to another organ

/system or to systemic disease. Hence it may occur in the

setting of an acute or chronic disease ,but is not a diagnosis

in itself 5.

The possible mechanisms in the formation of pleural effusions

vary with different aetiologies but usually due to:

a. Altered Permeability of the Pleural Membrane

in inflammatory process, neoplstic disease,

pulmonary embolism.

b. Reduction in intra-vascular oncotic pressure

in hypo-albuminemia ,hepatic cirrhoses, syndrome.

c. Increased Capillary Permeability or Vascular

Disruption as in trauma, neoplastic disease,

inflammatory process, pulmonary infarction,

pancreatitis, uremia.

d. Increased Capillary Hydrostatic Pressure in the

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systemic/pulmonary circulation as in Superior Vena

Cava Obstruction, Congestive Cardiac Failure.

e. Reduction of Intra-Pleural Pressure and inability

Of the lung to expand in atelectasis ,mesothelioma.

f. Reduced Lymphatic Drainage/Complete Lymphatic

Lymphatic Blockade which occur in thoracic duct

obstruction/rupture following malignancy,trauma.

g. Persistent Increase in Pleural Fluid Oncotic

Pressure from an existing pleural effusion causing

accumulation of further fluid.

h. Diffusion of fluid from pulmonary edema across the

visceral pleura.

Epidemiology

The approximate annual incidence pleural effusion in

the United States is 1.3 Million. Congestive Cardiac

Failure[0.5m] , Para-pneumonia[0.3m], Malignancy[0.2m],

Pulmonary Embolism [0.15] , Tuberculous effusion [0.0025]

Internationally, the relative annual incidence of pleural

effusion is estimated at 320/100000 in industrialized

countries .Elsewhere, the distribution and causes depends

on the population such as tuberculous effusions are

common in TB prevalent areas like Sub-Saharan Africa,

with its association with HIV/AIDS prevalence.

Any age can be affected though pleural effusion is commoner in

adults. Sex incidence shows equal distribution in both

sexes, however certain causes have a sex predilection.

About 2/3 of malignant effusions occur in women

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because of association with breast and gynecological

malignancies.6

Yellow nail syndrome is also commoner in females due to

association with systemic lupus erythematosus . It is

associated with other respiratory disorders including

chronic bronchitis, pleural effusion, chronic sinusitis .

A case of Bronchiectasis in association with Yellow

Nail Syndrome was reported in Nigeria 7.

Malignant mesothelioma with effusion is common in

males due to occupational exposure of males to

asbestos.

Sympathetic effusions secondary to pancreatic problems

are commoner in males due to higher alcohol

consumption.

Rheumatoid arthritis is commoner in males, hence its

associated effusion.

CLASSIFICATION

The classification of pleural effusion is based on the

mechanism of fluid formation and pleural fluid chemistry 8.

Generally pleural effusions are classified into Transudate or

Exudate. However ,with some causes ,there exist an overlap.9.

Transudative pleural effusions - Systemic factors that govern

formation of fluid include increased systemic and or pulmonary

capillary hydrostatic pressure(elevated pulmonary capillary

wedge pressure of (10mmHg),decreased colloid osmotic pressure

in the systemic circulation or both. Pleural membranes are

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intact and not involved in the pathogenesis of the fluid

formation .The permeability of the pleural capillaries to

proteins is also normal.

Exudative effusions- Local factors govern the formation of

fluid,and these include altered permeability of pleural

membranes ,increased capillary wall permeability ,vascular

disruption ,partial or complete obstruction of the lymphatic

drainage of the pleural space. Consequently, the protein

content of an exudates is high, usually >3g%.

AETIOLOGY

THE COMMON CAUSES OF EXUDATIVE EFFUSION INCLUDE;

a. Para pneumonic secondary to bacterial, fungal,

parasitic , viral , and atypical organisms like

mycoplasma, legionella, chlamydia, rickettsiae.

b. Malignancy like carcinoma, lymphoma, mesothelio

c Tuberculosis

d. Pulmonary embolism

e. Collagen Vascular disease eg rheumatoid

arthritis, systemic lupus erythematosus,

f. Asbestos related benign inflammatory exudative

pleural effusion.

g. Gastrointestinal Disease conditions causing

sympathetic effusions such as Whipple’s disease,

intra-abdominal abscess ,acute/chronic pancreatitis,

pancreatic pseudocyst.

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h. Trauma-blunt and penetrating injury to the chest

causing haemothorax , chylothorax.

i. Post-Cardiac Injury [Dressler Syndrome], reported

after cardiac surgery, pacemaker insertion,

myocardial infarction, angioplasty, blunt

chest trauma.

j. Esophageal perforation during endoscopy

k. Drug induced primary pleural disease

Eg. nitrofurantoin, dantrolene, methysergide,

bromocriptine, amiodarone, methotrexate, oxprenolol,

practolol, minoxidil, mitomycin.

l. Meig’s Syndrome

m. Sarcoidosis

THE COMMON CAUSES OF TRANSUDATIVE EFFUSION INCLUDE;

a. Congestive Heart Failure

b. Cirrhoses[hepatic hydrothorax]

c. Atelectasis [ which may be secondary to malignancy

or pulmonary embolism]

d. Hypo albuminaemia

e. Nephrotic Syndrome

f. Peritoneal Dialysis

g. Myxedema

h. Constrictive Pericarditis

i. Superior Vena Cava obstruction

SOME CAUSES RESPONSIBLE FOR COMBINED

EXUDATIVE/TRANSUDATIVE PLEURAL EFFUSION INCLUDE:-

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a. Pulmonary embolism

b. Hypothyroidism

c. Diuresed Transudate,

d. Long Standing Transudate

e. Pericardial Disease [inflammatory,constrictive]

f. Atelectasis , amyloidosis, sarcoidosis

Despite the myriad of causes of pleural effusion

enumerated above ,by far the commonest causes include

congestive cardiac failure, pneumonias, tuberculosis,

malignancy, pulmonary embolism.

Other rarer causes of pleural effusion have been reported.

“Thoracic endometriosis was reported in a 34 year old

Ugandan female complaining of recurrent right sided chest

pain, with clinical and radiological evidence of right

sided pleural effusion 15. Subsequent management via CT

chest, chest tube drainage ,and thoracotomy confirmed

endometriosis which responded to the usual hormonal

treatment.

A case of massive hemorrhagic ascites and pleural

effusion caused by endometriosis was also reported in

Lagos , Nigeria. 16.

Pleural deposits from light chain myeloma has been

reported as another cause of pleural effusion 17

PATHOPHYSIOLOGY

Various mediators are involved in the production of

altered permeability and the evolution of pleural

effusion.

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Types of pleural effusion include hydrothorax, chylothorax,

malignant effusion, parapneumonic effusion, empyema etc. In

addition to the pathophysiologic effect of the primary

disease, pleural effusions share a common effect on

the physiological derangements of the pulmomary system.

Pleural effusion produces a restrictive defect that is

correlated with the size of the effusion. Because ,

both the air spaces and the pulmonary circulation

are compressed and because of pulmonary hypoxic

vasoconstriction , there is little shunting and only

mild hypoxaemia. In addition to lung parenchymal

compression, massive effusions pushes the mediastinum

to the contralateral side further compromising the

cardio-pulmonary function. Ventilation-perfusion mismatch

occurs, hence, tachycardia and dyspnoea are the commonest

symptoms. The accumulation of fluid in the alveoli

may occure and that predisposes to irritation of the

alveolar wall resulting in cough which is initially

dry. Tissue devitalization in chronic lung parenchymal

diseases eg pulmonary tuberculosis, malignancies, etc

predisposes the alveolar capillaries to rupture during

cough episodes resulting in occasional haemoptysis.

Pleural inflammation and metastatic deposits cause

pleuritic chest pains which decreases in intensity

as the effusion increases in size.

Removal of a large effusion can result in modest

improvement in lung function, but often, the underlying

cause of the effusion eg malignant effusion, causes

persistent functional abnormalities.

The accumulation of fluid in the hemithorax impairs the normal chest excursion and

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is responsible for the stony dullness to percussion in place of resonant note of a

hemithorax containing a fully expanded lung.

TYPES OF EXUDATIVE PLEURAL EFFUSION:

Chyliform/Pseudochylous Effusion grossly resemble frank

chylothorax .However ,the pathogenesis does not involve the

thoracic duct or indeed any lymphatic drainage system ,and it

does not contain any chylomicrons .It occurs in long standing

(mean 5 years) pleural effusions associated with Rheumatoid

arthritis ,tuberculosis ,paragonimiasis infestation . The

milky white appearance is due to the high lipid levels i.e

cholesterol crystals or lecithin-globulin complexes.10.

Malignant Pleural effusion is usually an exudate and caused

by a neoplastic disease. It accounts for 13-40% all pleural

effusions in the United States. Pleural effusion develops in

nearly 50% of patients with metastatic cancer. The most common

tumours that cause malignant pleural effusion include

adenocarcinomas and other carcinomas of the lungs, breast

cancer, lymphoma, leukaemia, accounting for about 75% of all

malignant pleural effusions .Others include ovarian carcinoma,

stomach cancer ,sarcomas and malignant melanoma. It is

usually caused by a disturbance of the normal Starling

forces regulating the re-absorption of fluid in the

pleural space, via obstruction of mediastinal lymphatics

draining the parietal pleura. Hence tumours that

metastize most frequently to these nodes such as lung

cancer, breast cancer cause most malignant effusions.

Whereas the effusion restricts ventilation, the pleural

deposits of tumour cause pleuritic chest pain.

Lymphangitic pulmonary metastases further worsen pulmonary

function. The primary lesion may also have disseminated

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to other sites such as bone, brain, further debilitating

the patient.

Fig. 1. Chest Radiographs showing massive left sided

pleural effusion and marked mediastinal shift before(A) and

after(B) tube thoracostomy drainage.

Para-pneumonic effusions complicate bacterial pneumonias .In

the United States of America,30-40% of patients with bacterial

pneumonias develop pleural effusion in-spite of their advanced

medicare .It therefore implies that the incidence of this

complication is much higher in underdeveloped third world with

the ravaging malnutrition ,poverty, HIV/AIDS, and poor access

to medicare. Streptococcus Pneumonia has a high predilection

for complications eg bacteremia ,multi-lobar involvement, and

pleural effusion. It is important to understand the

pathophysiology of parapneumonic effusions.It is most often

associated with pneumonia, particularly aspiration events

with anaerobes. But, generally, aerobic infections are

commoner than anaerobic. Similarly, gram- positive aerobic

pneumonic infections is about twice commoner than gram

negative aerobes. Commonly implicated gram positive

aerobes include Stphylococcus aureus and Streptococcus

pneumonia in about 70% of cases11.

Then, the gram negative aerobes which include

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Klebsiella, Pseudomonas, and Haemophilus species. Commonly

encountered anaerobes include Bacteroides and

peptostreptococcus species. Mixed infections do occur

sometimes in which case it is more likely to progress

to empyema . Mycobacterium tuberculosis is the commonest

cause of chronic granulomatous infection/inflammation of

the lung parenchyma and associated lymph nodes.

Following an overwhelmed host defence mechanisms, lung

tissue responds by inflammation, which can produce

tissue necrosis as in S.aureus infection , impair ciliary

action and impede phagocytosis. Inflammation may cause

exudation of fluid into the pleural space. Pleural effusion

evolves in three phases. The initial phase is the

accumulation of small but sterile fluid caused by the

infection contagious to the pleural space. Intersticial

fluid increases during pneumonic process and accumulates

in the pleural space because of increased permeability

of the interstitium as well as exceeded absorptive

capacity of the pleural space. Effusion here is

neutrophilic, with low white cell count and LDH but

normal glucose and Ph. Fortunately many para-pneumonic

effusions do not progress beyond this stage and

resolve as the pneumonia is treated, because antibiotic

penetration of the space is very good. The second

stage occurs if bacteria and polymorphs enter the

pleural space .The inflammatory response causes fibrin

to be deposited along the visceral and parietal pleura

that can lead to loculation. In association with this

is a significant rise in pleural fluid LDH level [.1000],

while the pH [.7.2] and glucose [.60mg/dl] levels fall.

The third stage occurs if the fluid is not drained

as fibroblasts move in organizing the fluid into a

pleural peel, making removal of fluid by a needle

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aspiration impossible. This pleural fluid will encase

or trap the lung permanently, impairing its ability to

function. If it is still infected, it will act as

an abscess .This abscess can drain spontaneously through

the chest wall as empyema neccesitans, or disastrously

into a bronchus forming a life threatening broncho-

pleural fistula. Hence para-pneumonic effusions can be

classified into uncomplicated effusion[exudative stage],

complicated effusion[fibrino-purulent stage], and thoracic

empyema[organization stage].

Chest trama especially penetrating and chest surgery

may also be associated with super-infection in the

pleural space. Infection via haematogenous spread or

direct contact is also possible as in subdiaphragmatic

abscess, ruptured esophagus, mediastinitis, osteomyelitis,

pericarditis, cholangitis.

Tuberculous Pleural Effusion. Mycobacterim tuberculosis is

the commonest cause chronic grnulomatous lung parenchymal

disease,which often is complicated by pleural effusion.

Effusion is usually preceeded by tuberculous pleuritis which

should be suspected in patients with history of exposure to

or mantaux positive findings. Most tuberculous effusions

result from a hypersensitivity reaction o involving the

pleural membrane and capillaries to the mycobacterium rather

than microbial invasion of the pleura, and this is

responsible for the very low yield of acid-fast bacilli in

pleural fluid analysis.

Empyema Thoracis means suppurative fluid collection in the

pleural cavity. In the pediatric age group, para-pneumonic

effusions is the most frequent etiology for empyema 12 .It is

often due to an inflammatory process in adjacent

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structures as occurs in pneumonia ,lung abscess,

,tuberculosis etc .Underlying carcinoma of the bronchus must

be suspected in any

patient over the age of 45 years presenting with pleural

effusion/empyema13. Other causes of empyema thoracis are

ruptured sub-phrenic abscess, ruptured amoebic abscess,

osteomyelitis of the spine/ribs, esophageal perforation, and

unguided instrumentation of the pleural cavity such as

aseptic pleural fluid drainage.

Pathogenesis of empyema involves an initial generalized

pleural infection and thin inflammatory exudates. It

later becomes more localized with the development of

thick pleural adhesions due to fibrin content and

thickening of the pus. The empyema may either resolve

spontaneously , rupture into the lung parenchyma, with

a resultant broncho-pleural fistula, or become chronic

with marked thickening of the pleurae and an

intervening cheesy pus akin to bread and butter

appearance. The resultant effect is restricted chest

movement, crowding of the ribs and concave scoliosis

to the affected side. It has been known that

streptococcal infection produces thin pus whereas

pneumococcus produces thick pus with a high fibrin

content of the inflammatory exudates. But with the

advent of antibiotics being used routinely in most

chest infections ,most empyema are sterile at initial

diagnosis. Indeed the advent of modern chemotherapy has

radically altered the natural history of an empyema

and has abolished the different types of empyema due

to different organisms.14. Empyema thoracis is suspected

by observing a slow rate of symptomatic improvement in

a patients general condition after chest infection and

suspicion is heightened by the typical radiographic

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features. Comfirmation of diagnosis is by aspiration of

pus with a wide bore needle such as 14G. Culture may

not be positive, though not surprising.

Chylothorax means the accumulation of chyle in the pleural

cavity .It is most commonly caused by trauma or tumor with

rupture of the thoracic duct anywhere along its course[Fig

2]. Chylothorax is usually right sided except if the

Fig.2.-Course of the thoracic duct.

The confluence of the right and left lumbar

lymphatic trunks forms the cisterna chyli which

lies on the anterior body of first lumbar

vertebra. It ascends into the posterior mediastinum to

become the thoracic duct by passing through the

diaphragm at the level of twelfth thoracic

vertebra. The thoracic duct remains on the left side

of the posterior medistinum until it ascends to the

seventh to fifth thoracic vertebra where it crosses

over to the right side where it continues its

journey towards its termination at the root of the

neck in the junction between the right subclavian and

right internal jugular veins. It can therefore be

damaged at any point in this long tortuous pathway.

_____________________________________________________________________ 27

damage to the thoracic duct is above the 5th thoracic spine

whence it becomes left sided .Gun-shot wounds, stab wounds

,iatrogenic[posterior mediastinal surgery] are the commonly

encountered causes.

The chemical content of chyle include chylomicrons and

protein and its loss in chylothorax is of immense nutritional

significance. Large volume effusions may also cause

respiratory embarrassment as well as cardiac compromise.

_____________________________________________________________________ 28

Fig.3.-Chest Radiograph showing massive left

sided pleural effusion due to chylothorax.

Haemothorax means the accumulation of blood in the pleural

cavity and is caused by trauma to the chest wall , lungs

,mediastinal structures ,diaphragm, pulmonary infarction,

neoplasm ,thoracic surgery .Bloody pleural fluid with a

haematocrit value 50% that of serum suggest haemothorax.

Pleural defibrination of blood occurs with resultant

deposition of fibrin on the pleural surfaces. A

sterile haemothorax may completely resolve , infact ,it

is expected that fibrinous deposits should peel off

the visceral pleura 3 weeks post injury, to allow

full expansion of the lungs, but an infected

haemothorax -haemothorax empyema can lead to rapid

development of fibrothorax with serious compromise of

pulmonary function. This condition is commoner in

contaminated penetrating chest injuries such as war

_____________________________________________________________________ 29

and gun-shot injuries especially when associated with

underlying lung injury. Conversely, it is less common

following clean stab injuries to the chest, and

expectedly commoner in haemo-pneumothorax than in pure

haemothorax.

Pleural cavity has the capacity to contain large

volumes of fluid /blood. In rapid bleeding into the

pleural cavity, large blood clots may occure, thus

setting the stage for a possible an imprisoning

fibrothorax later . But in slow bleed into the pleural

cavity, blood in the pleural space tends to be

defibrogenated and slow to clot. Hence auto-transfusion

can be practiced by means of a cell saver or

manually collecting the blood in a sterile drainage

system , adequate filtration and re-infusion into the

patient.

Third space loss of blood into the pleural cavity

poses a potential threat to the cardiovascular

stability of the patient, and shock may result. In

addition lung is compressed and medistinum is displaced

to the contralateral hemithorax., further compromising

both the respiratory and cardiac function. The critical

factor in this condition is tissue anoxia therefore

such patients require prompt intervention.

CLINICAL FEATURES OF PLEURAL EFFUSION.

The clinical manifestations of pleural effusion are

variable and often related to the underlying cause ,

however the commonly associated symptoms are dyspnoea ,

cough, chest pain.

Dyspnoea indicates a large effusion but usually not

_____________________________________________________________________ 30

less than 500mls. However other factors such as

underlying lung disease, cardiac dysfunction , anaemia

may contribute. It is the most common clinical presentation

of pleural effusion. 18.

Chest Pain is typically described as sharp, biting,

pleuritic. It signifies pleural irritation. It may be

localized to the chest wall or referred to the

ipsilateral shoulder or upper abdomen if diaphragm is

involved in the disease process.The pain diminishes as

the size of the effusion increases.

Cough may be non productive and is due to irritation

of the alveoli by some fluid that may accumulate

therein. It may also be productive and may even be

associated with haemoptysis especially in lung

parenchymal diseases such as tuberculosis , lung

carcinoma .

Fever of acute onset associated with chest pain,

sputum production and leukocytosis which persists after

48 hours of initiation of antibiotic treatment

complicated by dyspnoea and dullness to percussion in

the affected hemithorax is suggestive of a para-

pneumonic effusion

Other signs and symptoms are pointers to the

underlying disease process. Pedal edema , orthopnea,

paroxysmal nocturnal dyspnea ,cough productive of frothy

sputum occure in congestive cardiac failure . Haemoptysis

, night sweats, malaise, low grade fever , weight loss

occure in pulmonary tuberculosis. An acute febrile

episode , purulent sputum , pleuritic chest pain , occure

in aerobic bacterial pneumonias .

_____________________________________________________________________ 31

Physical Findings are equally variable but depends on

the volume of the pleural effusion. If the volume of

the effusion is less than 300mls,it may not be

clinically detectable .Otherwise the features are:-

-Elevated body temperature in para-pneumonic

Effusions

-Diminished chest excursion on the affected

hemithorax - Hoover’s sign

-Dullness to percussion on the affected hemithorax.

-Reduced tactile fremitus on the affected

hemithorax.

-Tracheal deviation to the contralateral side

signifies medistinal shift which is observed in

large volume effusions 1000mls. Ipsilateral

deviation may occure in obstruction of a lobar

bronchus by endobronchial tumour or less commonly

a foreign body 18.

-Diminished / inaudible breath sounds

-Pleural friction rub

-Egophony [‘e’ to ‘ a’ changes] at the most

superior aspect of effusion.

Other important physical findings that provide clues to

the cause pleural effusion include anasarca in

nephritic syndrome and hypoproteinemia ; cutanous

_____________________________________________________________________ 32

changes in liver diseases; distended neck veins , S3

gallop rhythm in congestive cardiac failure; breast

nodule, intra –abdominal mass , pelvic mass may suggest

malignant effusion.

LABORATORY INVESTIGATIONS.

Pleural fluid analysis – Thoracocentasis is done through

a selected intercostals space with a 23G needle to

sample at least 20mls of pleural fluid.

Fig.4. Thoracocentasis.

The initial step is to examine the physical

characteristics of the sampled fluid as follows:-

a. Bloody Fluids- possible causes include,

-Malignancy

-Chest Trauma

-Pulmonary Embolism

-Tuberculosis

-Infection

-Mesothelioma

_____________________________________________________________________ 33

b. Turbid Fluids- possible causes include,

-Increased cellular content as occurs

in inflammatory exudates

-Increased lipid content lipid content

c. Yellow/Whitish Turbid- possible causes include;

-Chyle

-Cholesterol

-Empyema

d. [Chcolate/ anchovy sauce] , found in:-

-Ruptured amebic liver abscess into the

pleural space[hepato-pleural fistula]

e. Black fluid, found in,

Aspergillus involvement of pleura

f. Yellow Green fluid with debris, found in

Rheumatoid pleurisy

g. Highly viscous - suggest, malignant mesothelioma

[hyaluronic acid]

h. Putrid odour- suggests

anaerobic pleural space infection

I Ammonia odour suggests,

Urinothorax

j. Purulent effusion suggest

Para-pneumonic effusion which may progress to

empyema thoracis

_____________________________________________________________________ 34

k. Yellow thick metallic sheen found in,

-long standing chyliform effusion.

CHEMICAL ANALYSIS

Initial chemical analysis of the following parameters

is mandatory; serum protein, serum LDH, pleural fluid

protein content, pleural fluid LDH.

TOTAL PROTEIN LEVELS AND DIFFERENTIALS

Pleural fluid is an exudates if one or more of the

following condition is met; ratio of pleural fluid protein

to serum level greater than 0.5 or ratio of pleural

fluid LDH to serum LDH level greater than 0.6, except

in transudative effusions caused by congestive cardiac

failure when the patient had undergone diuretic therapy

for more than 48hrs. This air can be cleared by the

use serum albumin/pleural fluid albumin ratio whereby a

gradient greater than 1.2 suggest exudates while below

1.2 suggest transudate 20.

Light’s criteria further suggests that a pleural fluid

LDH concentration greater than 2/3 of the upper limit

of normal serum reference range is most likely an

exudates.”21. It further states that if only one test

is to be performed , measurement of the total

protein concentration is the most practical in view

of its accuracy and availability.

Glucoselevel. Low levels [<60mg/dl] suggest tuberculosis,

malignancy, parapneumonic effusion, empyema , haemothorax .

LDH level is directly proportional to the degree of

inflammation, and levels greater than 1000iu/l is

_____________________________________________________________________ 35

found in parapneumonic effusion, paragonimiasis.

Amylase level. 1000 Somogyi units or pleural/serum amylase

ratio1.1 signifys a sympathetic effusion secondary to

acute pancreatitis pseudopancreatic cyst esophageal

rupture malignancy ruptured ectopic pregnancy. Assay of

pancreatic and salivary isoenzymes helps to further

narrow the diagnosis.

pH estimation , if 7.2 suggest empyema , complicated

parapneumonia , esophageal rupture , malignancy ,

paragonimiasis , tuberculosis. Worthy of note is that

pleural fluid pH is influenced by the level of

acidemia.

Cytologic analysis is strongly recommended for patients

withe a history of undiagnosed effusion, suspected

malignancy, pneumocystis carinii infection, exudative

effusion normal fluid glucose/amylase levels.

Blood Culture is necessary if the pneumonic process is

suspected to be part of a septisemic process.

Gram Staining,culture and sensitivity. Bacilli staining

with Zeil –Neelson stain, Fungal staining with potassium

hydroxide, culturing and sensitivity for aerobic /

anaerobic organisms and fungi are essential if

facilities permit.

Lipid estimation is mandatory when a milky fluid is

encountered. Triglycerides, Cholesterol, and total lipids are

estimated. The presence of chylomicrons in the fluid

confirms chylothorax while its absence in a milky fluid

confirms pseudo-chylothorax.

_____________________________________________________________________ 36

Pleural fluid creatinine /serum creatinine is done when

an effusion with an ammoniacal odour is encountered. A

ratio of greater than 1 confirms urinothorax.

Pleural fluid Haematocrit is done if a bloody pleural

fluid is encountered. When compared with serum

haematocrit and found to be greater than 50%

,haemothorax is comfirmed

CELL COUNT AND DIFFERENTIALS

a. Red Blood Cell [RBC] count > 100,000/mm3

suggest trauma, malignancy, pulmonary embolism,

post-surgery.

b. White Blood Cell [WBC] count > 10,000/mm3 suggest

parapneumonia Relative neutrophilia suggest

acute inflammatory process while eosinophilia

Suggest associated pneumothorax, haemothorax,

pulmonary infarction or Parasitic infestation

such as paragonimiasis . Pleural fluid

esinophilia commonly indicate benign disease and

a favourable prognosis when it is present in

any malignant effusion.22. Basophilia of > 10%

though uncommon indicates leukaemic infiltration.

Lymphocytic count in excess of 50% indicates

long standing chronic pleural effusion

particularly malignant disease eg lymphoma , or

tuberculosis, sarcoidosis, chylothorax. Plasma

cells suggest multiple myeloma while macrophages

suggest chronic granulomatous inflammatory

conditions.

_____________________________________________________________________ 37

c. Mesothelial cells are commonly exfoliated into

the thin pleural fluid and should not be

confused with malignant cells in view of

their histological similarities, therefore it is

the absence and not the presence that is

significant in conditions where there is

fibrosis or infiltration of the pleural surfaces

as in tuberculous effusion, empyema thoracis.

Note that the reproducibility of these test results

depends on the appropriateness of the sampling bottles.

This is discussed in more details in Chapter 2.

IMAGING STUDIES

Chest Radiograph. - Confirms the effusion as well as

helping to determine the cause of the effusion. Enlarged

cardiac silhoette, underlying lung parenchymal disease,

mediastinal shift etc when present are quite obvious.

The most common radiologic feature of pleural effusion

is the blunting of costophrenic angle and the classical

meniscus sign which occurs in advanced cases. Other

features include:-

-Generalized homogenous opacity below the meniscus

-Diffuse haziness as the fluid extends posteriorly

[ground glass appearance]

-Mediastinal shift Visibility of pulmonary vessels through

the haziness

-Absence of air bronchogram

-Obliteration of diaphragmatic silhouette

_____________________________________________________________________ 38

-Reduced visibility of lower lobe vasculature

-Widened minor fissure

-Apical capping

-Hemidiaphragmatic inversion due to weight of fluid

Noteworthy is that the usual upright postero- anterior [P-A]

view or antero-posterior [A-P] view may not show

the lateral costophrenic angle blunting until 250-

500mls of fluid has accumulated, but a lateral view

will show costophrenic angle blunting even with as

little as 175-200mls. Hence the need for additional

views. Decubitus views especially bilateral is very

useful in large effusions as hemi-diaphragmatic

elevation suggest sub-pulmonic effusion, it helps to

exclude a loculated effusion and may equally expose

an underlying pulmonary lesion .Characteristically a

decubitus view shows layering of fluid. 1cm layer

approximates 200mls of fluid 23.Supine view is only

employed in sick patients who are confined in a

recumbent position .

Fig.5.-Chest Radiographs Showing right sided empyema

_____________________________________________________________________ 39

cavity and left sided massive pleural effusion.

INTERPRETATION OF RADIOLOGICAL FINDINGS:

Bilateral pleural effusion in the absence of

congestive cardiac failure is commonly caused by

malignancy except for lung and breast carcinoma. Breast

carcinoma associated pleural effusion are typically

ipsilateral to the primary breast carcinoma in 58-70%

of cases, however 20 –26% of cases develop in the

contralateral side, while 10-16% develop bilateral

effusion 24. Other possible causes are nephritic

syndrome , pulmonary embolism , tuberculosis, esophageal

rupture , Meig’s syndrome.

Massive effusions are commonly malignant in 70% of cases.

Other possibilities include congestive cardiac failure ,

tuberculosis , liver cirrhoses , transdiaphragmatic rupture

of huge liver abscess, paragonimiasis, pancreatic

pseudocyst, Meig’s syndrome. Massive effusion is often

accompanied by mediastinal shift. If not or if shifted the

ipsilateral side it suggests narrowing of ipsilateral

mainstream bronchus probably due to carcinoma .It may

also be due to atelectasis, or fixation of the

mediastinum due to fibrosis of chronic inflammation or

tumour infiltration of the mediastinal nodes of

ipsilateral lungs.

The localization of the fluid also provide diagnostic

clues eg isolated right sided effusion occure in

cirrhoses , sub-phrenic/liver abscess, hydatid disease of

the liver, Meig’s syndrome, endometriosis while left

sided effusion points to esophageal rupture pancreatic

disease left sub-phrenic , transdiaphragmatic rupture of

_____________________________________________________________________ 40

splenic abscess.

Atypical radiologic presentations include sub pulmonic

effusions typical of nephrotic syndrome.

Fig .6.- Chest RadiographS showing a homogenous opacity

on the right hemithorax(A) and meniscus sign on the right

hemithorax(B)

ULTRASONOGRAPHY-

Can detect as low as 50mls of pleural fluid.

It is rapid and available at bedside

It can identify a loculated / encysted effusion

It can also differentiated pleural fibrosis thickening and

parenchymal consolidation

COMPUTERISED TOMOGRAPHIC SCANNING [C-T SCAN]

Permits simultaneous imaging of the entire pleural

space, lung parenchyma, and mediastinum, as well as

the lesion contained therein, and the anatomical

relationships.

_____________________________________________________________________ 41

Fig.7. C-T scan of the chest showing right sided empyema

thoracis.

MAGNETIC RESONANCE IMAGING [MRI]

MRI has a limited role , but it is useful and better

than C-T SCAN in depicting tumour extension to the

chest wall , brachial vessels, subclavian vessels,

vertebral bodies, and spinal canal.

NUCLEAR IMAGING

With gallium labeled leukocytes is occasionally employed

to rule out lung parenchymal infection

CONTRAST ENHANCED STUDY OF ESOPHAGUS

This can be done with the patient in a lateral

decubitus position .A water soluble contrast agent like

hexabrix is preferred for this test and is useful in

investigating for esophageal perforation.

VENTILATION – PERFUSION SCANNING [V-P SCAN]

This test is mandatory if pulmonary embolism is

suspected, but the associated pleural effusion should

first be drained so that it does not affect the

interpretation of the result.

_____________________________________________________________________ 42

MANAGEMENT OF PLEURAL EFFUSION

COMMON PROCEDURES;

1. Thoracocentasis- This is the first line and least

invasive of all diagnostic procedures. It may also be

therapeutic and relatively safe. An appropriate sized needle

is placed into the appropriate intercostals space to sample

the fluid.

2. Tube Thoracostomy- The placement of a thoracostomy

into a designated intercostals space usually suffice for

evaluation and treatment of most pleural fluid

collection.

3. Per-cutanous Biopsy- This is a non invasive method

employed to biopsy pleural , lung parenchymal or

mediastinal lesions, with accuracy enhanced by image

guidance.

4. Open Biopsy- Involves at least a mini-thoracotomy such

that a visual assessment of the lesion and the extent

can equally be made.

5. Thoracoscopy/Biopsy-Allows an endoscopic assessment of

pleural cavity and mediastinum and enhances accuracy of

biopsy ,through a minimally invasive approach.

6. Other Ancillary Procedures like bronchoscopy, perfusion

lung scanning, pulmonary arteriography are complementary.

TREATMENT OF PLEURAL EFFUSION

Pre-hospital care- involves recognition of the cardio-

pulmonary instability in such patients and taking

prompt measures aimed at initial resuscitation in

_____________________________________________________________________ 43

line with standard principles of basic life

support(BLS), while making prompt arrangements to

evacuate such patients to a well set emergency

department outfit.

Emergency Room Care- Based on the presentation, the

patient is classified into three:-

1. stable patient , not requiring hospital admission

2. stable patient , but requires hospital admission

3. unstable patient, requires immediate intervention

Stable patients include pleural effusion secondary to

viral pleurisy, free fluid thinner than 10mm on a

lateral decubitus , asymptomatic effusion secondary to

medical conditions like Congestive Heart Failure, Renal

Disease, Liver Cirrhoses and also any post surgical

effusion thinner than 10mm. Such patients need no

admission , but must be re-evaluated 2-3 days later

while on medication for the primary disease, and if

the effusion is worsening, thoracocentasis for fluid

analysis is indicated.

Stable patients requiring admission have an effusion

more than 10mm thickness on decubitus view. Such include

parapneumonic effusions with no toxic features, recurrent

effusions with a change in symptomatology. Admission is

for further evaluation via diagnostic thoracocentasis. Para

pneumonic effusions should be promptly treated with

antibiotics because of the tendency to complications

such as empyema thoracis even before any invasive

procedures.

Unstable patients are toxic with cardio- pulmonary

_____________________________________________________________________ 44

instability as in life threatening traumatic or medical

conditions, hydropneumothorax, massive effusion with

mediastinal shift, ruptured thoracic duct, esophageal

perforation.

Such patients are made to sit up so as to increase

tidal volume and reduce work of breathing. Then an

immediate diagnostic/therapeutic thoracocentasis is done.

Chest tube placement with tube directed postero-

inferiorly for liquids and superiorly for air. Traumatic

Haemothorax and Empyema Thoracis requires large bore

thoracic catheter size 34-40F.

Radiographs play an essential role in the management

of pleural effusion. However, in very unstable and

severely distressed patients, in the emergency department

thoracocentasis and thoracostomy tube insertion play a

leading role in stabilizing such patients , while

radiographs is reserved for monitoring. Note that

critically distressed patients have been lost in the

radiograph bukky because this simple rule was

neglected.

In view of the possibility of an evolving pathology

especially in chest trauma, a repeat chest radiograph

should be obtained 3-6hrs later.

The need to evaluate the the patient from head to toe

cannot be overemphasized because it helps to address

other life threatening conditions.

When the patient is stabilized, continued management in

the ward involves accurate diagnosis, as per the cause

of the cause and treatments channeled to that. Medical

_____________________________________________________________________ 45

cases are referred accordingly, while surgical patients

are managed accordingly.

This research mainly focuses on surgically related

pleural effusion, where procedures like thoracocentasis,

thoracostomy, ribresection , thoracotomy, pleurodesis, are

fairly routine procedures.

The commonest procedure in the management of pleural

effusion are thoracocentasis, tube thoracostomy, and

pleurodesis.

Thoracocentasis can be done in the emergency unit,

consulting room, or in the ward with local anasthetic

infiltration on the appropriate intercostals space.21g

needle is then inserted and directed through the upper

border of the rib of the selected intercostals space

to sample the fluid, which is sent for analysis.

Chest tube is inserted by asking the patient to sit

on a chair , edge of the bed, or lying at 45 degrees

on the bed. Intercostal space , usually the 5th

intercostals space in the mid axillary line is selected

because it can afford an easy and safe access to the

pleural space for the drainage of both liquid and

air. It is infiltrated with 1% xylocaine. Incision is

made through skin, subcutaneous plane, and intercostals

muscles parted, staying very close to the upper border

of the adjacent rib.

_____________________________________________________________________ 46

Fig.8. Diagramatic illustration of dissection through an

intercostal space during tube thoracostomy.

On breaching the parietal pleura a gush of fluid is

is noted ,which may require an indwelling thoracic

catheter retained for a couple of days to ensure a

smother and complete drainage and usually connected to

an underwater seal drainage system to eliminate the

leakage of air into the pleural cavity. The area of

skin incision is neatly sutured, purse string placed

and then dressed. Patient may be given some

analgesics and antibiotic. The chest tube is connected

to a closed pleural drainage system which ranges from

simple to the very complex depending on the specific

clinical problem. A sound understanding of the

principles of the chest drainage system by both the

attending physician and nursing staff is of primary

importance and time spent communicating this to the

understanding of the attending nursing staff is well

spent. 25. When little or no continuing air leakage is

expected, and only liquid drainage is expected, a

simple underwater seal drainage system or a rubber

flutter valve with a plastic bag arrangement is

adequate. [fig.9].

_____________________________________________________________________ 47

Fig.9. Diagramatic illustration of a patient with right

sided tube-thoracostomy with underwater seal connection.

From Ibadan Nigeria, Adebo et al reported that their

preferred method of chest drainage in traumatic

haemothorax consist of insertion under anaesthesia of

the tubular end of of an Aldon`s Urobag equivalent

to number 34 Argyle chest tube, beveled, multifenestrated

and placed within the 5th or 6th intercostals space in

the mid - axillary line.26. It is also important to

note that some previous study has confirmed the

efficacy of this valved system in the evacuation of

fluid and or air from the pleural space.27. In the

past a two bottle system with the first being a dry

tap provides separate reservoir for collection of

fluid, then the second bottle which contains the

underwater seal specification, but this arrangement

added to the dead space between the pleural space and

the water seal surface. When large air leaks are

expected , large glass bottles with rubber stoppers and

glass tubes have been replaced by compact plastic

_____________________________________________________________________ 48

drainage that require less space and are unlikely to

be damaged and may be used as a simple underwater

seal or attached to a vacuum source. The three

compartment system comprises a collection chamber ,

water seal , and vacuum regulator with a long tube

open to the air and extending under the water level.

Pumps with a low air flow capacity should not be used

when large air leaks either continous or intermittent

is expected. The drainage system should function to

prevent ingress of air into the pleural cavity, even

when the vacuum apparatus fails, also the system should

allow egress of large volume of air suddenly, whether

the vacuum system is functioning or not. Needless to

mention , the drainage bottles should be placed at a

level below the chest always even when the patient

being wheeled to other parts of the hospital.

The correct placement and completeness of drainage are

both comfirmed on chest radiographs .Complete re-

expansion of the lungs is an indication for removal

of the chest tube, during which the purse string is

neatly tied to forestall the leakage of air into the

pleural cavity.

Large effusions are drained in aliquots of say

500mls every 4hours,so as to avert the development of

pulmonary edema, a potentially fatal condition that

may complicate drainage of massive effusions in one

swoop Some patients may experience violent cough which

may result in rupture of some fragile blood vessels

in the lung parenchyma such that an initially non

haemorrhagic effusion becomes so and patient may also

develop haemoptysis. A sudden release of pressure in

the chest can also cause a drop blood pressure.28.

_____________________________________________________________________ 49

Treatment of Parapneumonic Effusion. For community acquired

pneumonia, a 2nd or 3rd generation cephalosporin and a

macrolide antibiotic is quite effective. In severe

community-acquired pneumonia and hospitalized patients, a

3rd generation cephalosporin with antipseudomonal activity

and a macrolide is preferred. Parenteral route is

preferred and is continued until afebrile for 7-10 days

then continued orally for 1-3 weeks. For uncomplicated

parapneumonic effusions, complete resolution with

antibiotics alone is expected. However, serial physical

examination and radiography may necessitate repeat

thoracentasis if patients condition worsens ,especially

if effusion increases in size or patient remains or

becomes afebrile. For complicated effusion, there is a

variable response to antibiotic alone and since gram

stain is positive, tube thoracostomy is recommended. For

empyema initial management involves tube thoracostomy.

If there is no noticeable improvement following tube

thoracostomy, an ultrasound scan or computerized

tomographic scan of the chest is performed to detect

loculated fluid as well as the position of the tube.

In the presence of multiple loculi, thrombolytic therapy

is administered intrapleurally. The thombolytic agents

must be administered early to be more effective and

studies suggest that treatment group required less

surgical intervention and fewer days of hospital stay

29. Streptokinase and urokinase are equally effective

although streptokinase may lead to sensitization with

production of an antibody response and subsequent

allergic reaction. Loculations in the pleural space

can also be disrupted and pleural space drained

completely via Video-Assisted Thoracoscopy[VATS] or open

_____________________________________________________________________ 50

thoracostomy/decortication which also helps to evacuate

any abscess collection.

Open drainage of an abscess cavity via rib resection

is only recommended in patients who are too ill to

tolerate a major decortication surgery. 1 to 3 ribs

overlying the lower part of the empyema cavity is

resected to allow open drainage.

Tuberculous Pleural Effusion usually disappears with prompt

exhibition of standard anti-Koch’s regimen. The aim of anti-

tuberculous chemotherapy include, to cure the patient of the

disease with minimum interference with their living in as

short a time as possible whatever the initial drug

susceptibility of the causative organisms, to prevent death

from active disease or its late effects, to prevent relapse

of the disease and emergence of acquired drug resistance and

finally to protect the community from transmission of the

disease. Properly applied short course chemotherapy is

guaranteed to yield the desired results especially in the

context of control programmes recommended by under the

National Tuberculosis Programme of the World Health

Organization. For associated Pleural effusion, a closed system

needle aspiration helps to relieve associated mild respiratory

distress but situations where there is severe respiratory

distress due to massive pleural effusion and respiratory rate

above 40 cycles per minute, a standard tube thoracostomy

drainage of the pleural space is indicated. Therefore tube

thoracostomy drainage of a tuberculous pleural effusion is

best avoided unless when absolutely indicated to avoid the

risk of empyema necessitants.

Malignant Pleural Effusion tend to be massive and recurrent,

hence presents a therapeutic challenge. Treatment directed at

_____________________________________________________________________ 51

the primary mitotic lesion in form of surgery, chemotherapy

and radiotherapy are usually employed early in the disease

management. The appearance of malignant pleural effusion

therefore indicates an advancement of the mitotic lesion in

spite of any previous treatments. Hence, the presence of

malignant effusion is a poor prognostic sign with a mean

survival after diagnosis of 3-11 months in most series

30.

In recurrent pleural effusion there may be need for

pleurodesis. Following complete drainage and re-expansion

of the lungs, and daily chest tube drainage of less

than 100mls, it may just be possible to approximate

the two pleural surfaces in order to forestall further

re- accumulation of fluid. Historically, many chemical

agents have been instilled into the pleural space and

shown to have some effectiveness in controlling

effusions, including tetracycline, oxycycline, minocycline,

bleomycine, cisplatine, doxorubicine, etoposide,

fluorouracil, mitomycine, mitoxanthrone, interferone,

corynebacterium parvum, mepacrine, methylprednisolone, and

talc. 31.

But it appears that talc is a better option

than the rest as suggested by a large single arm

comparative studies and very small randomnized studies

suggest advantages for talc as the sclerosing agent

compared to tetracycline and bleomycine in greater

than 90% and 50% respectively 32. In our practice

tetracycline is more accessible compared to the rest

sclerosing agents. Dissolved in sterile water tetracycline

has shown a good promise as a sclerosing agent for

pleurodesis. ”33.

_____________________________________________________________________ 52

TECHNIQUE OF PLEURODESIS

Before removal of the chest tube after drainage, a

reconstituted solution of the chosen agent is injected

into the pleural cavity after which the tube is double

clamped for at least 2 hours, while the patient is

asked to turn from side to side to ensure even

distribution of the agent in the pleural cavity.

Thereafter it is unclamped and may be connected to a

low suction if necessary. Chemical pleurodesis can also

be done via a video-assisted thoracoscopy in the

operating room, under general anaesthesia, during which

the surgeon may access any biopsy 34.

The chest tube is removed when there is both clinical

and radiological indication. Securing nylon suture is

severed, tube pulled out, while the purse string is

tied simultaneously to avoid sucking in air. Air tight

dressing is now applied.

Patient may experience fever and chest pain due to

the inflammatory process in the pleural cavity. Aspirin

tablets are quite helpful should this complication arise.

There are reported cases of failure to pleurodesis

usually due to loculation , inaccurate tube placement,

lung entrapment by visceral peel , all hampering the a

complete drainage of the the pleural cavity. These

factors are more important than the choice of a

sclerosing agent. Surgical decortication has been advocated

for this problem but it is potentially dangerous and

has resulted in broncho-pleural fistula and empyema.

Placement of a pleuro-peritoneal shunt has also been

attempted but it is often complicated by fibrinous

obstruction of the stoma. A pleural spigot has

_____________________________________________________________________ 53

recorded some success in fourteen published cases but

the potential complication is infection which may

worsen an already bad situation. Radiation therapy may

be indicated in pleural effusion secondary to lymphoma

though with limited success and also the potential

danger of lung damage.

Malignant pleural effusion are still an unresolved clinical

problem inspite of the above measures. Current trials

with interleukin 2 injected into the pleural space

have been documented. The efficiency of intra-pleural

interleukin 2 has never been related to lesion

location or cancer histotype. This observation

demonstrates that treatment with intra-cavity interleukin

2 avoids repeated accumulation of fluid , not only with

an anti-neoplastic mechanism but mainly inducing

fibrosis process.35.

Treatment of Empyema Thoracis , depends on the stage

in the natural history of the disease.

In Stage 1 Disease[acute stage], the pus is thin and

remains thin. When collected in in a test tube, it

contains less than one third sediment after 24hrs

standing. Treatment here involves aspiration and

instillation of heavy doses of antibiotic done every

2-3 days. Chest tube insertion can also be done, but

patient must also receive systemic antibiotics.

In Stage 2 Disease [sub-acute stage], the pus is thick

with a high fibrin content. On 24hrs standing, the

sediment greater than one third basically due to a

high fibrin content. Chest tube placement may be done

initially especially in an acutely ill patient

_____________________________________________________________________ 54

moreso when there is an associated broncho-pleural

fistula, ruptured esophagus, lung abscess. This

procedure is usually temporary because even the widest

bore tube easily gets blocked by fibrin. Decortication

should be offered to fit patients while tube

thoracostomy should

be maintained as long as there is fear of lung

collapse. Rib resection [fig 10] is the preferred

modality of treatment when the pus is thick

especially after a failed aspiration and intercostals

tube drainage. To avoid chronicity, rib resection

drainage must not be delayed too long and it must

be adequate and dependent.

Fig.10 Diagrammatic

illustration of rib

resection drainage

procedure in

empyema thoracis.

In Stage 3

Disease [chronic], there is a marked adhesive fibrin

deposits on both visceral and parietal pleural

surfaces, with some little intervening insipissated pus.

The drainage method employed earlier may have been too

late or grossly inadequate. Decortication is the

procedure of choice at this stage and it involves

the complete removal of the fibrous wall of the

empyema cavity from both the lung, chest wall and

_____________________________________________________________________ 55

diaphragm in order to allow the the previously

imprisoned lung to expand and fill up the space

previously occupied by the empyema. This

operation is a major undertaking and should only be

done if the patient was previously fit and the

general condition is still reasonably good and is not

adviced in the elderly.

Other associated or predisposing disease conditions

should equally be treated on their own merits , at

the same time the empyema thoracis is being treated.

Treatment of chylothorax may be conservative initially,

by decompressing the thoracic lymphatics with parenteral

hyper-alimentation or oral medium chain triglycerides

and adequate drainage with intercostals tube. Talc

pleurodesis may be tried after 3-4 weeks. If the above

measures fail, thoracotomy is nessecitated and it is

aimed at ligating the thoracic duct at the site of

leakage, whose identification is facilitated a fatty

meal just prior to surgery.

Pleuro-peritoneal shunts have been used successfully for

refractory chylothorax in infants following surgery for

congenital heart disease.

For adults with malignancies, surgical intervention may

not be effective but in trauma cases, conservative

decompression as outlined above usually suffices and

surgical intervention is usually unnecessary.

The management of haemothorax depends on the rate of

bleeding, volume of blood already lost, associated

haemodynamic derangement, as well as the underlying

_____________________________________________________________________ 56

cause. If haemothorax is small [<250mls] and bleeding had

stopped, as evidenced by clinical status, only

observation may suffice. For moderate blood loss [500mls]

a tube thoracostomy with an underwater seal drainage

system is adviced because it allows complete evacuation

of blood from the pleural space as well as ensuring

adequate monitoring of any continued bleed. Serial chest

roentgenogram helps to monitor lung re-expansion. Needle

aspiration is discouraged because of the risk of

introducing infection, but if considered necessary at

any point, all aseptic procedures must be adhered to.

If there is a continued bleeding of volumes

>200mls/hr, or an initial loss of >1500mls of fresh

blood, or presence of massive clots, or clinical signs

of haemodynamic instability, there is an overwhelming

indication for an emergency exploratory thoracotomy with

concomitant vigorous correction of haemodynamic

instability. Because blood in the pleural space tends

to be de-fibrinogenated, and slow to clot, it can be

collected via a sterile drainage system into a sterile

container, filtered and re-infused into the patient.36.

To prevent the the development of an imprisoning

fibrothorax and to gain re-expansion of a lung

compressed by blood clot, early evacuation of clotted

haemothorax and decortication are sometimes recommended .

It is however expected that fibrinous deposits on the

pleural surfaces should peel off 3 weeks post injury,

so as to allow full re-expansion of the lungs.

_____________________________________________________________________ 57

CHAPTRE TWO-MATERIALS AND METHOD

OVERVIEW

This was a prospective study involving all patients who

presented to National Hospital Hospital Abuja between February

2005 and February 2006 with pleural effusion requiring some

form of surgical intervention in the course of their

management.

_____________________________________________________________________ 58

STUDY CENTRE.

The Department of Surgery, National Hospital Abuja wass the

study center. Is located in the central business district of

the Federal Capital Territory(FCT) Abuja.

FCT is located in the North Central Geo-Political zone of

Nigeria.

National Hospital Abuja was established by Decree 36 of

1999 by the then Military Government.

Its operations has remained under the supervision of

Presidency via the office of the Secretary to the

Federal Government since the current democratic

dispensation.

It was designed to serve as an apex referral hospital

for Nigerians as well as neighboring countries, so

as to stem the tide towards seeking medical treatment

abroad hence its endowment with the state of the art

equipment.

STUDY POPULATION

FCT settlers who are heterogeneous in nature constitute

the bulk of the patients that attend National Hospital

for treatment. The rest were from neighboring states and

countries.

Inclusion Criteria-Only patients with clearly defined clinical

and radiological evidence of pleural effusion who in addition

will benefit from surgical intervention constituted the

study group. Random sampling was done over a period of 1 year

_____________________________________________________________________ 59

spanning from February 2005-February 2006.

Exclusion Criteria-Any other patient including those with

pleural effusion with medically related causes. All cases of

traumatic haemothorax whose formation does not depend on the

alteration of starling forces.

Sample Size-A total of 86 cases fulfilled the stipulated

requirements for sampling and were available for sampling

during the study period between February 2005 to February

2006.

Whereas some of these patients presented through the accident

and emergency unit , others were referred from

oncology, Internal Medicine, Pediatrics departments of the

hospital or from neighboring hospitals.

DATA COLLECTION PROCESS

Patients that met the criteria were sampled randomly

during the stipulated study period.

A pre-designed proforma was employed as a tool to

document the relevant demographic ,clinical , radiological,

biochemical, bacteriological, cytological data as well as

treatment modality, outcome of treatment, and complication

of treatment peculiar to any sampled case.

PATIENT HANDLING PROTOCOL

Except in dire emergencies with severe life threatening

respiratory distress, all selected patients were

subjected to thorough history, physical examination and

radiological assessment , followed by consent for

thoracocentasis which yielded the pleural fluid itself,

providing an opportunity to assess its physical

appearance such as purulent/turbid, serosanguinous, straw

coloured, milky etc. Thoracocentasis was done through the

5th intercostals space mid-axillary line under sterile

condition. The sampled fluid was accordingly stored in

their respective ideal containers as follows:

_____________________________________________________________________ 60

-Plain tube for protein, LDH, glucose, triglycerides, and

Cholesterol estimation

-Ethylene diamine tetra acetic acid bottle for cell count

and packed cell volume

-Heparin treated blood gas syringe for ph

-Sterile container for Gram stain/culture, acid-fast

bacilli and fungal studies

-50 millilitre heparin treated container for cytology.

Following a successful thoracocentasis, patient’s consent

was further sought and a thoracostomy tube was

inserted through the appropriate intercostal space ,

usually the 5th or 6th space mid-axillary line, and

tightly secured in place with nylon 2 suture, ensuring

that at least all the fenestrations at the thoracic

end of the chest tube were well insinuated into the

pleural cavity. The thoracostomy tube which all along

was double clamped with strong artery forceps to

prevent sucking air into the chest was then connected

to the under-water seal drainage system and the clamps

removed.

Immediate observation of an oscillatory movement of a

column of fluid in the tube indicates a correct

placement of tube in the pleural space. This was

further confirmed by a post- intubation check X-ray of

the chest.

For patients who presented with massive pleural

effusion, the fluid was only allowed to drain in

aliquots of 200-300mls/hr to avoid complications like acute

onset severe cough which may provoke haemoptysis, rebound

pulmonary edema.

CARE OF THE CHEST TUBE

Constant reassurance of the patient was mandatory.

Thoracostomy site wound was inspected regularly and any

_____________________________________________________________________ 61

sepsis treated accordingly. Oscillation of fluid column was

checked regularly to ensure that tube remained in-situ

Daily recording of output from the chest tube was

done and when less than 50cc ,indicated that extubation

was due.

Extubation was effected by asking the patient to

inhale maximally and to hold the breath, while the

sutures holding the tube were severed and tube pulled

out quickly and a pre-positioned purse string

tightened to secure an air-tight seal of the chest

wall. A neat dressing was then applied.

LABORATORY METHODS

CHEMISTRY

Electrolyte estimation was by the use of ion-selective

electrode method in an automated machine.

Lipid estimation was done by automated enzymatic colorimetrc

test.

Protein level was estimated by turbimetry/precipitation

or colorimetric method(Biuret’s test)

Microbiology

Initial Gram- Stain, followed by culture in chocolate,

blood and Ma Conkey medium, and then antibiotic

sensitivity.

Acid- Fast Bacilli x3 was done on the sediment of the spun

fluid.

Fungal Test can be done with seaboard agar.

CYTOLOGY

_____________________________________________________________________ 62

Pap smear of the spun sediment was made on a

slide and fixed with 90% alcohol, then stained with

Haematoxylene-Eosin solution before reading.

RADIOLOGY

A postero-anterior chest radiograph was usually done and

it often defines the features of the effusion as

well as any associated mediastinal shift/pathology.

Other views may be quite useful in certain circumstances such

as,

Lateral view defines minimal collection (<175cc) in

the costo-phrenic angles, supine views for moribund/bed

confined patient, and decubitus for investigating other

associated pathology in the lung which may have been

masked by the effusion.

Chest radiographs were also used to monitor the

progress of drainage of the effusion.

Computerized Tomographic Scanning and Magnetic Resonance

Imaging are other modalities of investigating chest

pathologies.

SUBSEQUENT PATIENT MANAGEMENT

In most patients, nothing more need be done. However

in some, associated pathology or the outcome of

investigations dictated further treatment such as

pleurodesis for recurrence prone malignant effusion,

decortication for complicated empyema thoracis.

_____________________________________________________________________ 63

ETHICAL CONSIDERATIONS

Ethical clearance was sought from the ethical committee of the

National Hospital. Only patients who willfully consented

were included in this study and reserved the right

to withdraw at any stage if they felt so.

An information sheet was given to all subjects stating

all that was required of them and providing opportunity

to clear their doubts, before consent was given.

DATA ANALYSIS-was done using the EPI-INFO statistical soft

ware package and presented in the form of pie charts, bar

charts, histogram and tables.

SAMPLE OF INFORMATION SHEET FOR PATIENTS/RELATIVES

Fluid can accumulate in the space inside the chest called

pleural cavity. This condition is abnormal and in certain

quantity leads to breathlessness and impaired quality of life.

There are various causes such as trauma, tumor, infection

which may be revealed in the course of investigation.

A structured in management has a direct effect on the outcome

of treatment. This study is mostly carried out by the patient

bedside in the wards where they are normally admitted such as

the Surgical, Medical, pediatric wards under strict

supervision.

With your consent, we believe that your enrolment in this

study will benefit not only you but also others with similar

problems. It will also afford us yet another opportunity for

the advancement of surgical research.

We are also quite willing to furnish you with any further

explanations on demand.

_____________________________________________________________________ 64

Thank you

Dr.Charles Ugwuanyi

Dept. of Surgery

National Hospital Abuja.

SAMPLE OF CONSENT FORM FOR PATIENTS.

I-----------------------------hereby give consent for

myself/my child to participate in this on pleural effusion.

I have been furnished with the information sheet which has

been fully explained to me. I also understand that that no

additional expenses will be incurred by me as a result of

this study other than the routine expenses associated with my

healthcare and follow-up.

I hereby make this declaration willingly.

Signature of patient/Gourdian Signature of witness

CHAPTER THREE-RESULTS

A total of 86 cases of pleural effusion requiring some

sort of surgical intervention were sampled in this 1

year prospective study spanning February 2005 to

February 2006 in the National Hospital Abuja.

Sex Distribution.[fig 11]

There were 48 males [55.8%] and 38 females [44.2%]

Male: Female ratio is therefore 1.26: 1.

_____________________________________________________________________ 65

Fig. 11.- Sex distribution of patients.

Age Distribution [fig 12]

Age range was from 1 year to 80 years.

Peak age was 30 years with a frequency of 9 representing

40.7% of all cases.

Youngest age was 1 year with a frequency of 2

representing 2.3% of all cases sampled.

Oldest patient was 80 years with a frequency of 1

representing 1.2% of cases.

The cluster age incidence was between 17 years and 66

years.

_____________________________________________________________________ 66

Fig. 12.- Age distribution of patients.

City of Residence of Patients. (fig 13)

Cases residing within Abuja and environs

constitute 67 [81.7%] of all cases sampled, while

were spread across the other parts of Nigeria.

Fig. 13.- City of residence of patients.

Clinical Presentation of Cases Studied. (fig 14)

_____________________________________________________________________ 67

Breathless

ness

Coug

h

Chest

pain

Feve

r

Weight

Loss

86 83 78 42 50

.Fig 14.-Clinical Presentation of Cases Studied.

Breathlessness was present in all the 86 (100%) patients

studied.

Cough was present in 83 (96.5%) of cases.

Chest Pain occurred 78(90.69%) of cases.

Fever was present in 42(48.8%) of cases.

Weight loss was present in 50(58.13%) of cases.

Physical signs in keeping with right sided

pleural effusion was found in 54(62.79%) of

cases while signs of left sided pleural

effusion was found in 28(32.55%) of cases. The

chest signs were bilateral in 49(4.6%) of

cases studied.

Physical Appearance of Pleural Fluid

0

10

20

30

40

50

60

70

80

90

Breathlessness Chest pain Weight Loss

_____________________________________________________________________ 68

sampled via Thoracocentasis.(fig.15)

1

14

24

47

0

5

10

15

20

25

30

35

40

45

50

Frequency

Chyle

Pus

Sero-

sanquinous

Straw colour

liquid

Fig.15.-Physical Appearance of Pleural Fluid

Straw coloured fluid was found in 47(54.7%) of cases,

Sero-sanguinous in 24(27.9%) , purulent/turbid fluid in

14(16.3%) and milky/chylous fluid in only one case

representing 1.2% of cases.

Pathology Associated with Pleural Effusion (fig. 16)

_____________________________________________________________________ 69

1

Fig.16.-Pathology Associated with Pleural Effusion.

Neoplastic Disease was present in 35(40.72%)

of cases , Pulmonary Tuberculosis in 32(37.2%)

of cases and Pneumonia in 19(22.1%) of cases.

Distribution of malignant causes.(fig. 17)

Fig. 17.-Disstribution of malignant causes of pleural

effusion.

Breast carcinoma made up 23(65.7%) , Intra-abdominal

_____________________________________________________________________ 70

malignancy 3 (8.6%) , Lung carcinoma 4(11.4%) , Soft

Tissue Sarcoma 4(11.4%) and Parotid Tumour1(2.9%).

Chemical Analysis of Pleural Effusion.

a. Specific Gravity- ranged from 1016 to 1018

in all cases.(fig. 18)

1016 1017 1018

13 39 340

200

400

600

800

1000

1200

Values and freq.

Specific Gravity No. Of Patients

Datasets

Frequencies of Specific Gravity

Fig. 18.- Specific Gravity Ranges.

b. Protein Content- ranged from 39mg/dl to 72

mg/dl in all the 86 samples.

c. Glucose level- ranged from 21mg/dl to 67mg/dl(Table 1)

Gl

ucose

No. Of

Patients

Pe

rcent

21 4 4.

7%

23 6 7.

0%

24 1 1.

2%

26 1 1.

2%

27 4 4.

7%

28 2 2.

3%

29 1 1.

2%

30 1 1.

2%

_____________________________________________________________________ 71

31 8 9.

3%

32 8 9.

3%

34 8 9.

3%

35 1 1.

2%

36 1 1.

2%

37 6 7.

0%

38 2 2.

3%

39 1 1.

2%

41 3 3.

5%

42 6 7.

0%

43 6 7.

0%

44 1 1.

2%

45 4 4.

7%

47 5 5.

8%

51 1 1.

2%

55 1 1.

2%

62 1 1.

2%

63 1 1.

2%

67 2 2.

3%

T

otal 86

1

00.0%

Table 1 Glucose Levels

_____________________________________________________________________ 72

d. Triglycerides ranged from 86mg/dl to 300 mg/dl.(Table 2)

T

G

No. of

Patients

Pe

rcent

8

6 1

1.

2%

8

7 2

2.

3%

8

9 1

1.

2%

9

0 1

1.

2%

9

5 4

4.

7%

9

6 1

1.

2%

9

7 1

1.

2%

9

8 15

17

.4%

1

01 4

4.

7%

1

02 12

14

.0%

1

03 5

5.

8%

1

04 5

5.

8%

1

05 3

3.

5%

1

07 1

1.

2%

1

08 2

2.

3%

1

09 3

3.

5%

1

12 2

2.

3%

1

15 1

1.

2%

1

20 1

1.

2%

1

23 13

15

.1%

1

24 1

1.

2%

1

25 2

2.

3%

1

32 1

1.

2%

_____________________________________________________________________ 73

1

34 1

1.

2%

1

45 1

1.

2%

1

52 1

1.

2%

3

00 1

1.

2%

T

otal 86

1

00.0%

Table .2.- Triglyceride

Levels in fluid sample

e. Lactate Dehydrogenase (LDH) ranged from 350 iu to

4120iu.(Table.3)

L

DH

No. Of

Patients

Pe

rcent

3

50 1

1.

2%

4

00 3

3.

5%

8

42 1

1.

2%

8

50 1

1.

2%

8

67 1

1.

2%

8

97 1

1.

2%

9

50 1

1.

2%

_____________________________________________________________________ 74

9

74 1

1.

2%

9

80 2

2.

3%

9

83 3

3.

5%

9

86 1

1.

2%

1

080 1

1.

2%

1

100 1

1.

2%

1

120 2

2.

3%

1

132 1

1.

2%

1

181 1

1.

2%

1

186 1

1.

2%

1

278 1

1.

2%

1

420 1

1.

2%

1

489 1

1.

2%

1

589 1

1.

2%

_____________________________________________________________________ 75

1

789 1

1.

2%

1

816 1

1.

2%

1

823 1

1.

2%

1

830 1

1.

2%

1

848 2

2.

3%

1

856 1

1.

2%

1

875 1

1.

2%

1

880 1

1.

2%

1

934 1

1.

2%

1

974 1

1.

2%

1

980 2

2.

3%

1

984 1

1.

2%

2

085 1

1.

2%

2

102 1

1.

2%

_____________________________________________________________________ 76

2

116 1

1.

2%

2

120 1

1.

2%

2

167 1

1.

2%

2

168 2

2.

3%

2

170 1

1.

2%

2

180 4

4.

7%

2

186 1

1.

2%

2

188 1

1.

2%

2

240 2

2.

3%

2

246 1

1.

2%

2

281 1

1.

2%

2

467 1

1.

2%

2

678 1

1.

2%

2

750 1

1.

2%

_____________________________________________________________________ 77

2

810 1

1.

2%

2

812 1

1.

2%

2

830 1

1.

2%

2

840 1

1.

2%

2

845 1

1.

2%

2

864 1

1.

2%

2

870 1

1.

2%

2

896 1

1.

2%

3

120 4

4.

7%

3

121 1

1.

2%

3

124 1

1.

2%

3

140 1

1.

2%

3

180 1

1.

2%

3

310 2

2.

3%

_____________________________________________________________________ 78

3

320 1

1.

2%

3

340 1

1.

2%

3

380 1

1.

2%

3

720 1

1.

2%

3

812 1

1.

2%

4

120 1

1.

2%

T

otal 86

1

00.0%

Table 3 Lactate Dehydrogenase (LDH) Levels

f. Cholesterol level ranged from 96mg/dl to 188mg/dl.

(Table 4)

Choles

terol

No. Of

Patients

Pe

rcent

96 1 1.

2%

108 1 1.

2%

109 1 1.

2%

110 1 1.

2%

115 1 1.

2%

123 2 2.

3%

124 1 1.

2%

_____________________________________________________________________ 79

125 1 1.

2%

127 2 2.

3%

128 2 2.

3%

129 1 1.

2%

130 1 1.

2%

132 1 1.

2%

134 1 1.

2%

135 3 3.

5%

142 1 1.

2%

143 2 2.

3%

145 3 3.

5%

146 3 3.

5%

147 1 1.

2%

149 1 1.

2%

154 6 7.

0%

156 14 16

.3%

160 1 1.

2%

162 1 1.

2%

163 4 4.

7%

164 2 2.

3%

165 2 2.

3%

167 12 14

.0%

168 2 2.

3%

168.9 2 2.

3%

169 1 1.

2%

171 1 1.

2%

173 2 2.

3%

174 2 2.

3%

_____________________________________________________________________ 80

178 1 1.

2%

187 1 1.

2%

188 1 1.

2%

Total 86 1

00.0%

Table .4.- Cholesterol Levels

g. Sodium level ranged from 130mg/dl to

140 mg/dl.(Table 5)

_____________________________________________________________________ 81

Table .5.- Sodium Levels

h. Potassium level ranged

from 2.9mg/dl to

4.1mg/dl.(Table 6)

N

a+

No. Of

Patients

Pe

rcent

1

30 1

1.

2%

1

31 3

3.

5%

1

32 2

2.

3%

1

35 3

3.

5%

1

36 2

2.

3%

1

37 11

12

.8%

1

38 8

9.

3%

1

39 6

7.

0%

1

40 5

5.

8%

1

41 15

17

.4%

1

42 3

3.

5%

1

43 12

14

.0%

1

45 3

3.

5%

1

47 12

14

.0%

T

otal 86

1

00.0%

_____________________________________________________________________ 82

Table.6.-

Potassium

Levels

i. Chloride level ranged from 95mg/dl to

Potassium No. Of Patients Perce

nt

2.9 1 1.2%

3.1 7 8.1%

3.2 3 3.5%

3.4 1 1.2%

3.5 7 8.1%

3.6 1 1.2%

3.7 13 15.1%

3.8 10 11.6%

3.9 10 11.6%

4.1 15 17.4%

4.2 8 9.3%

4.3 4 4.7%

4.4 1 1.2%

4.5 2 2.3%

4.6 1 1.2%

4.7 2 2.3%

Total 86 100.0

%

_____________________________________________________________________ 83

114mg/dl.(Table 7)

Fig. 19-Chloride Levels

j. Ph ranged from 7.0 to 7.2 (Fig. 20)

7 7.1 7.212

68

6

010203040506070

Value and

Freq.

pH No. Of Patients

Data set

pH Chart of Patients

fIg.20 Ph range Levels

K. Bicarbonate ranged from 18mg/dl to 25mg/dl.(Table 9)

_____________________________________________________________________ 84

Table

.9.-

Bicarbonate Levels

CYTOLOGICAL ANALYSIS OF PLEURAL FLUID.

Of the 35 cases of neoplastic disease associated

pleural effusion, 24(68.6%) did not yield any positive

cytology while 11(31.42%) yielded positive cytology.

ACID FAST BACILLI(AFB) ANALYSIS OF PLEURAL FLUID

Of the 32 cases of Tuberculous effusion, positive

AFB yield was found in Only 2(6.25%) but negative in

30(93.75%) of cases.

White Cell Count- In the tuberculous cases, 24 out of the

32(75%) had relative lymphocytosis while the rest (25%) had

neutrophilia most probably due to secondary infection. All

HCO

3- No. Of Patients

Percen

t

18 5 5.8%

19 19 22.1%

20 23 26.7%

21 17 19.8%

21.

2 1 1.2%

22 19 22.1%

23 1 1.2%

25 1 1.2%

To

tal 86

100.0

%

_____________________________________________________________________ 85

(100%)of the cases of para-pneumonic effusions had

neutrophil lymphocytosis

Microscopy Culture and Sensitivity of Pleural Fluid

Of the 19 cases of parapneumonic effusion, 14(73.68%)

yielded negative growth while 5(26.3 %) yielded positive

culture.

CHEST X-RAY FINDINGS

4(4.6%) cases had radiologically confirmed bilateral

pleural effusion of varying degree.

1(1.16%) case had a radiological evidence of right

sided hydro-pneumothorax

28(32.55%) cases had a radiological evidence of left

sided pleural effusion of varying degree.

53(60.22%) cases had radiological evidence of right

sided pleural effusion of varying degree.

62 cases (72.09%) had radiologically confirmed

Mediastinal shift,usually to the opposite side of

the lesion.

TREATMENT OF PLEURAL EFFUSIO IN NATIONAL HOSPITAL. (FIG.V)

Treatment of the primarily associated pathology was initiated

and or consolidated.

Tube- thoracostomy with an underwater seal drainage system, was

offered to 81(94.1%) of all cases.

_____________________________________________________________________ 86

Pleurodesis was offered as an additional treatment to 32(37.2%)

of these.

Exploratory Thracotomy was offered to 6 patients

representing 6.9% of all, while

Tube thoracostomy with under-water seal drainage and low

suction was offered to 4 patients (4.65%)only.

OUTCOME OF TREATMENT AT 6 MONTHS EVALUATION

a. Neoplastic Disease Associated Pleural Effusion.

25 cases(71.4%) of malignant effusion progressed to death at

six months check up in-spite of all treatments given.

9 cases (25.7%) had partial recovery and still battling with

the disease at six months.

Only 1 case representing 2.9% of all malignant effusion showed

clinical evidence of complete recovery at six months.

b. Para-Pneumonic Pleural Effusion

16 cases (88.9%) of all para-pneumonic effusions showed

clinical and radiological evidence of complete recovery.

2 cases (11.1%) only showed evidence of partial recovery and

progression to empyema thoracis.

c.Pulmonary Tuberculous Effusion

15 cases (51.7%) of all tuberculous effusion showed both

clinical and radiological evidence of complete recovery at 6

months.

_____________________________________________________________________ 87

9 cases (31%) showed partial recovery.

5 cases (17.22%) progressed to further complications culminating

in death.

COMMON COMPLICATIONS OBSERVED IN TREATMENT OF PLEURAL EFFUSION

IN NATIONAL HOSPITAL.

a. Premature Dislodgement of thoracostomy tube was

observed in 29 cases representing 33.72% of all

cases studied.

b. Progression to infection in a previously sterile

fluid was observed in 9 cases(10.4%).

c. Pneumothorax was observed in 8 cases (9.30%).

d. Wound sepsis at the thoracostomy site was

observed in 29 cases (33.7%)

e. Recurrence of effusion was observed in 35

cases (40.7%).

TREATMENT OF COMPLICATIONS

All cases of premature dislodgement of thoracostomy tube

and pneumothorax were treated satisfactorily by proper

re-positioning/ securing of the tube and antibiotic cover.

Wound sepsis was treated by daily wound dressing and

wound swab culture and sensitivity directed antibiotic therapy.

_____________________________________________________________________ 88

Recurrent Effusion was treated by repeat tube thoracostomy

in 21(60%) of recurrent cases with additional pleurodesis

in 13(37.1%) of cases. Only one case of recurrence had

thoracotomy and decortication.

_____________________________________________________________________ 89

CHAPTER 4-DISCUSSIONS AND CONCLUSIONS

Though males were more affected than females in this

study, certain associated pathologies were commoner in

females , for example, carcinoma of the breast in females

was responsible for 65% of all malignant effusions in

this series.

All age groups were affected but the cluster age

incidence was 17 to 66 years. Very few cases were seen at the

extremes of life.

Most patients (81.7%) involved in this study reside within

Abuja, Nigeria and its environs, which constitute the

major catchments area for National Hospital. The rest

were spread across other parts of Nigeria and beyond.

CLINICAL PRESENTATION

All the 86 patients (100%) sampled, presented with dyspnoea. It

is the most common presentation of pleural effusion as

clearly documented by Abrahamian et al. 18.

Pleural effusion produces a restrictive defect on the

lungs, alveolar sacs, and pulmonary circulation is thus

compromised. Massive effusion further pushes the mediastinum

to the contralateral side . There is also a decreased

ipsilateral lung volume modulated by neurogenic reflexes

from the lungs , all contributing to compromised cardio-

_____________________________________________________________________ 90

pulmonary function. The resultant clinical effect of all

these is dyspnoea as well as tachycardia.

It is not likely that an effusion not sufficient to

produce clinically detectable dyspnoea to be surgically

important. About 500mls of pleural fluid is required to

produce clinically detectable dyspnoea. It is important to

note that other associated pathologies both in the lungs

and elsewhere may contribute to dyspnoea.

Cough was the second commonest symptom encountered in

this series, present in 96.5% of cases. It was initially

unproductive ,caused by irritation of the alveolar walls

by some fluid accumulation . In a few cases it later

became productive and infact was associated with

haemoptysis. Studies have shown that this situation

arises in the chronic lung parenchymal diseases such as

pulmonary tuberculosis, malignancies, whereby the

sorrounding alveolar blood vessels are sufficiently

devitalized by this underlying pathology and are rendered

prone to rupture easily especially with violent coughs,

hence precipitating haemoptysis.

Chest pain was recorded in 78% of cases. It was typically

described as sharp, biting, or pleuritic initially. This is

due to pleural irritation caused by inflammation or

malignant deposits around the pleura, and localized to

the ipsilateral chest wall or referred to to the

ipsilateral shoulder if the shoulder is involved.

Weight loss was recorded in a little above half the

cases (58.1%). It is not usually caused by the effusion,

but related to the underlying pathological condition such

_____________________________________________________________________ 91

as malignant cachexia of advanced neoplastic disease,

chronic debilitating diseases.

Fever was found in just below half the cases

studied(48.8%), mostly observed in parapneumonic cases,

or secondary to septic instrumentation of the pleural

space in a previously sterile effusion.

The aforementioned symptoms occurred in various combinations

in different patients, in addition to other symptoms directly

related to the primary pathology.

Physical signs elicited on chest examination in keeping

with right pleural effusion was found in 62.8%. These

signs include reduced chest excursion, dullness to

percussion, reduced tactile fremitus, egophony.

The same signs were elicited on the left hemothorax in

32.5% of cases, while in 4.6% of cases they were

bilateral.

Therefore, this study demonstrates that pleural effusion

was commoner in the right hemithorax.

Thoracocentasis which was carried out to sample pleural

fluid in all cases studied yielded straw-coloured fluid

in 54.7% of cases, followed by serosanguinous fluid in

27.9% , pus in 16.3% and milky in 1.2%.

Straw coloured fluid was therefore the commonest, while

chylous fluid was the least common.

_____________________________________________________________________ 92

Straw coloured fluids are commonly found in tuberculous

pleural effusions, but can also be found in some

malignant pleural effusions as well as para-pneumonic

effusions and sympathetic effusions.

Serosanguinous fluids are commonly seen in malignant pleural

effusions, but can also be seen in tuberculous pleural

effusion, pulmonary embolism.

Frank haemothorax are usually caused by chest trauma,

blood dyscrasias, but are excluded from this study since

they are not strictly speaking effusions.

Purulent/turbid effusions are almost always diagnostic of

an exudates due to parapneumonic condition, but it can

also be found in other types of effusion following a

septic instrumentation of the pleural space. It may

therefore indicate a progression to empyema thoracis.

Milky effusion is almost always associated with chylothorax,

but in some cases of long standing transudative

effusions, the cholesterol content increases, thus giving

a milky appearance in a condition called pseudochylous

effusion.

No cases of brown/chocolatey fluid suggesting ruptured amebic

abscess, or black fluid suggesting aspergillosis was

encountered in this study.

PLEURAL FLUID ANALYSIS.

The assessment of pleural aspirate was guided to some

extent by the clinical context in which the effusion

_____________________________________________________________________ 93

occurred. In most cases the cause of the pleural

effusion was already known at this stage from clinical

and radiological evaluation. However laboratory evaluation

of pleural aspirate may either buttress an already known

diagnosis or provide an inroad into the elucidation of a

pleural effusion whose cause was not already known.

Measurement of total protein and lactate de-hydrogenase

concentrations, microbiologic and cytologic analysis are

among the myriad of tests that can be conducted for

these purposes.

In this study , the total protein concentration of

pleural fluid ranged from 39g/dl to 72g/dl. This was way

above 3g/dl which is generally used as the reference

point for distinguishing exudates from transudates,

though this may result in misclassification in about 15%

of cases. This is where Lights criteria comes in, with

a sensitivity of 99% and specificity of 98%.21. It

employs parameters such as a combination of serum

protein, pleural fluid LDH, serum LDH estimation in

various permutations.

A 1997 meta-analysis of the diagnostic value of tests

used to distinguish transudates from exudates did not

find any test or combination of tests to be clearly

superior.20 Hence the choice of tests is individual

preference, but if choice narrows to one, measurement of

the total protein concentration is the most practical

choice in view of high accuracy and availability.

_____________________________________________________________________ 94

Protein level was high due to increased pleural

permeability resulting from complex inflammatory mediators

interacting between the mesothelium whose cells play an

active role in inflammation, phagocytosis, leucocyte

migration, tissue repair, antigen presentation, coagulation

and fibrinolysis and the endothelium. Lymphatic blockade

aqually plays a role especially in malignant effusions.

So, all the samples studied were clearly exudative, and

was therefore not surprising that all pleural fluids

sampled in this study had a high specific gravity which

ranged from 1016 to 1018, due to the high protein

and/or cellular content.

The lactate dehydrogenase levels were also clearly elevated

well above the upper limit of normal in most of the

samples.

Conversely, most of the sampled fluids had relatively low

level of glucose which ranged from 21 to 67mg/dl. This

is in line with findings in tuberculous effusions,

malignant effusions , parapneumonic effusions etc.It is

believed that the high cellular metabolic activity in these

conditions use up the available glucose.

Trigyceride was mostly within normal range except in one

case which recorded 300mg/dl. That was the only case of

chylothorax in this study and was secondary to iatrogenic

rupture of the thoracic duct in a patient that had

decortication for stage 3 empyema thoracis.

_____________________________________________________________________ 95

High pleural fluid triglyceride levels is most commonly

caused by rupture of thoracic duct due to tumour ,

trauma , whereby chylous fluid high in chylomicrons and

protein content is lost into the pleural cavity

usually the right. This is of immense nutritional importance,

and such patients sooner tips to severe nutritional

deficiency.

Though the electrolyte picture was found to be similar

to that of serum in most cases, the ph were

slightly acidic .Again this is attributable to an avalanche of

products of anerobic cellular respiration such as lactic acid.

Acidic pleural effusion suggests parapneumonic

effusion/empyema, malignancy, tuberculosis.

The diagnostic yield of cytological analysis in this

study was only 24%. In some other studies it is

generally in the range of 50 to 60 % . It is even

higher in patients with bulky pleural tumour, and a

repeat cytological testing may increase the yield to

more than 70%. Similarly, testing of 3 or more samples

may increase the yield to 90%. The low yield in this

study may be attributed to a number of factors such as

observer dependent error, poor tissue sampling and

handling, inadequate sampling , laboratory limitations.

Out of the 32 cases of pulmonary tuberculosis

encountered in this study, positive pleural fluid acid-

fast bacilli was found in only 2 cases representing

6.25%. This is indeed a very low yield.

_____________________________________________________________________ 96

Based on a study by Seibert A.F. et al, where he reviewed

1,738 cases, of pulmonary tuberculosis, between 1968 to

1988,in Mobile, Alabama, 70 cases of tuberculous pleural

effusion were identified. Diagnostic modality used was to

culture mycobacterium in sputum, pleura, or pleural

fluid, backed up with clinical/radiologic features. But

this diagnosis could also be made in the absence of a

positive culture and acid-fast bacilli if the patient

had a lymphocytic exudates in addition to all clinical

and roentgenographic abnormalities, which improved on

anti-tuberculous medications. It is there fore not unusual

not to have a very low yield of acid-fast bacilli in

pleural fluid in cases of tuberculous pleural effusion.

Tuberculous pleuritis should therefore be suspected in

patients with a history of exposure to or mantaux

positive findings and in patients with lymphocytic

effusions, especially if less than 5% mesothelial

cells are detected on diffrential count. Because most

tuberculous effusions probably result from a

hypersensitivity reaction to the mycobacterium, rather

than from microbial invasion of the pleura, acid-fast

bacilli stains of the pleural fluid are rarely

diagnostic (<10% of cases) , and pleural fluid cultures

grow mycobacterium in less than 65% of cases.40.

The combination of histology and culture of pleural

tissue biopsy further increases the diagnostic yield to

90%. This was one major limitation of this study due

to the absence of Abrams pleural biopsy needle.

Adenosine deaminase activity(ADA) whereby a level in

pleural fluid greater than 43u/u, interferon-gamma

_____________________________________________________________________ 97

concentration in pleural fluid greater than 140pg/ul all

support tuberculous pleuritis, but since both were not

available for this study, that was another limitation

of this study.

Only 26.3% of the parapneumonic effusions yielded a positive

culture. This is rather not surprising since with the

advent of antibiotics most of these patients have

already been exposed to various antibiotics before

presentation, hence sterilizing the pleural fluid. This is

the same reason why the natural history of empyema

thoracis has been more or less abolished , and very

few cases of empyema complicating parapneumonic are seen

nowadays.

Concerning radiological findings, only 4.6% of cases

studied showed an evidence of bilateral pleural effusion

by way of blunting of costophrenic angles, classical

meniscus sign, and homogenous opacity below the meniscus.

Commonly employed is the P-A view where by a minimum of

250-500mls of fluid must accumulate before the

costophrenic angles could be blunted. Other views such

as A-P , decubitus were not commonly employed in this

study. Bilateral pleural effusion in the absence of

congestive cardiac failure is commonly caused by a

malignancy excluding breast and lung carcinoma. This is

because breast/lung carcinoma associated pleural effusion

are typically ipsilateral to the primary lesion in 58

to 70% of cases, however 20 to 25% of cases develop

an effusion in the contralateral side, while 10 to 16%

develop bilaterally 22. Other causes of bilateral

_____________________________________________________________________ 98

pulmonary effusion include pulmonary tuberculosis, Meig’s

syndrome, pancreatic pseudocyst.

Hydropneumothorax was recorded in 1.16% of cases studied. The

most likely cause is a ruptured subpleural bleb in

pulmonary tuberculosis. Other causes include previous chest

intubation, and malpositioned chest tube.

Left sided effusion was recorded in 32.55% of cases

while right sided effusions was found in 53%. Hence

right sided effusions were far commoner in this series.

Certain pathologies have a predeletion to a specific

sided effusion , for example, whereas esophageal rupture,

trans-diaphragmatic rupture of splenic abscess produce a

left sided effusion, sub-phrenic and liver abscess ,

hydatid disease will rupture into the right pleural

space. None of these cases were however encountered in this

study.

Mediastinal shift was recorded in 72% of cases, usually

to the contralateral side, and mainly observed in

massive effusions. But in some cases, either no shift

is observed or an ipsilateral shift may even be

observed. This occurs if there if there is narrowing of

ipsilateral mainstream bronchus, which can be caused by

carcinoma, atelectasis, fixation of the mediastinum due

to fibrosis of chronic inflammation or tumour

infiltration of the mediastinal nodes of ipsilateral

lungs,

The pathologic condition responsible for pleural effusion

in each case was nearly always identified following

_____________________________________________________________________ 99

structured application of clinical methods via history,

physical examination , laboratory and radiological

evaluation.

Neoplastic disease was identified in 40.7% of all cases

studied, followed by pulmonary tuberculosis in 37.2% and

pneumonia in 22.1% of all cases. This showed that

malignant pleural effusions was almost twice commoner

than para-pneumonic pleural effusion. Further analysis of

the causes of malignant pleural effusions showed that

breast carcinoma was responsible for 65% ,about 2/3 of

all cases of malignant effusion , while the rest

encountered including, lungs, intra-abdominal, soft tissue

sarcoma and parotid carcinoma constituted the rest 1/3.fig

16.

All the medical causes of pleural effusion such as

congestive cardiac failure as well as traumatic

haemothorax were excluded from this study. Other surgical

causes of pleural effusion were not encountered in this

study, probably due to their rarity in this environment.

Treatment directed at the primarily associated pathology

was either initiated and/or consolidated.

In most tuberculous and parapneumonic pleural effusions,

the aim of surgical intervention via chest intubation is

to alleviate life threatening cardio-respiratory

insufficiency while allowing adequate time for the

chemotherapeutic agents to act towards curing the

patient.

_____________________________________________________________________ 100

This contrasts sharply with the situation in malignant

effusion.To improve the quality of life of the patient,

the least invasive, least morbid, and least costly therapy

should be employed in managing malignant effusions. This

is because most of these patients have limited survival.

Hospitalization should be minimized, so that patients are

not unnecessarily removed from the family.

In this study, 94% of all cases had tube thoracostomy

and underwater seal drainage , while an additional low

suction was applied in 4.6% cases, the aim of which

was to encourage completeness of drainage. 37% of these

case required further pleurodesis which is aimed at

discouraging fluid re-accumulation, a situation which

applied mostly in malignant pleural effusions. The

diagnosis of a malignant pleural effusion signifies a

poor prognosis because it is usually a manifest of far

advanced disease. In a meta-analysis of 417 patients with

malignant effusion, the survival period was 4 months.

Hence treatment should not be heroic but directed at

alleviating and improving the quality of life as much

as possible. Exploratory thoracotomy was offered to only

6.9% of patients , indicated only in cases that required

decortication.

The outcome of treatment in malignant pleural effusion

was uniformly fatal as up to 71% were dead at 6

months of diagnosis, while 25% were seriously battling

the disease at 6 months check-up, despite all treatment

modalities. Only one case (2.9%) showed a clinical

evidence of absence of disease at 6 months check-up.

This high mortality/morbidity seen in malignant effusions

_____________________________________________________________________ 101

comfirms Heffner .J.E. et al position that the diagnosis of

malignant pleural effusion signifies a poor prognosis

because it is usually a manifest of a far advanced

disease, with a median survival of 4 months.

Conversely, 51.7% of tuberculous pleural effusions showed

both clinical and radiological evidence of complete

recovery at 6 months check-up, while 31% were still

battling the disease and 17.2% had progressed to further

complication and death in-spite of all treatment. It was

however not clear if the co-morbid conditions which was

found in some of these cases contributed to this

mortality, but this is outside the scope of this

study, and indeed is worth futher researching into.

88% of the parapneumonic cases recovered completely,

while 11% had partial recovery at 6 months check.

Some of the latter indeed progressed to empyema

thoracis. This high rate of complete recovery and very

low rate of progression to empyema thoracis can be

attributed to availability and early exhibition of

antibiotics.

This study therefore confirmed that parapneumonic effusions

had the best outcome , followed by tuberculous and

malignant ones having an abysmally low outcome.

Common complications observed in the course of treatment

include premature dislodgement of chest tube which was

observed in 33.72% of all cases intubated. Closely

related to that is pneumothorax which was observed in

9.3% of all cases. This complication was directly

_____________________________________________________________________ 102

related to poor surgical technique even as some patients

have been blamed for pulling on the tube. Treatment was

directed to improving surgical technique by employing the

appropriately trained personnel and ensuring that tube is

positioned or repositioned and tightly secured with

appropriate sutures. Contamination and infection of a

previously sterile pleural effusion was observed in 10.4%

of cases while wound sepsis around the thoracostomy

site was observed in 33.7% of cases. Both were directly

related to non adherence to strict aseptic technique

during the procedure of chest tube insertion, especially

during emergencies. Treatment here was by preventive

measures and the use of appropriate antibiotics.

Recurrent effusion was recorded in 40.7% of cases

especially in malignant and tuberculous pleural effusions.

In malignant pleural effusions, recurrence is due to

persistent and indeed the progression of the primary

disease in spite of the exhibition of multimodality

treatment especially in advanced/metastatic diseases. In

tuberculous pleural effusion it is mainly due to

persistence of infection following drug resistance and/or

non-compliance to medication. It may also be related to

advanced disease state. Treatment of recurrence was by

repeat chest intubation and pleurodesis for malignant

effusions . In tuberculous cases, repeat chest drainage,

review of anti-koch’s medication were the hallmarks of

treatment. Exploratory thoracotomy and/ decortication were

indicated in very few cases.

In conclusion, this study was able to expose the common

causes of pleural effusion requiring surgical intervention in

National Hospital Abuja. The diagnostic armaments and

_____________________________________________________________________ 103

their uses , treatment modalities and limitations , the

outcome of treatment as it applies to the different

diseases and the common complications of treatment

observed were equally exposed, hence providing a platform

for improvement in the management of patients suffering

from this disease.

_____________________________________________________________________ 104

REFERENCES

1. Jan Langman, Formation of body cavities and

Serous Membrane; Medical Embryology, Fourth

Edition, Page 144. 1984.

2. Jan Langman, Formation of Diaphragm and Thoracic

Cavity; Medical Embryology, Fourth Edition, Page

144. 1984.

3. Bhattachariya S.K., Surgical Physiology of

Rate and Directionof Fluid Movements; ShortCases

in Surgery, Fourth Edition, Page191, 1978.

4. Anyanwu C.H., Pleural Effusions, Thoracic

Surgery; Principles and Practice of Surgery and

Pathology in the Tropics, Third Edition, Page 427

5. Friedrick M.A., Pleural Effusion; e-medicine,

http://www.e-medicine.com/emerg/topic462.htm,

page 6 of 32.

6. Ibid.

7. Adegboye V.O., Ladipo J.K., Adebo O.A., Yellow

_____________________________________________________________________ 105

Nail Syndrome and Bronchiectasis; Nigerian

Journal of Surgical Research, Volume 4, No 3,

2002, page 115 – 118.

8. Anyanwu C.H., Thoracic Surgery , Principles and

Practice of Surgery and Pathology in the Tropics,

Third Edition, Page 427.

9. Abrahamian F.M., Pleural Effusion; e-medicine,

http://www.e-medicine.com/emerg/topic462.htm.

Page 6 of 32.

10. Ibid.

11. John.A.H., Parapneumonic effusions in pediatrics,

http://www.pediatrics uchicago.edu/chiefs/am

report/parapneumonic effusion-files/slide

0006.htm.

12. Alkrinawi .S. Respiratory Infection in

Children;emedicine,http://www.ipeg.org/guidelines

/empyema.ht.ml.

13. Kussabe R.B.,Rare Causses of Pleural Effusion:

African Health Science,2001 (2) : 97-98.

14. Raymond.H., Michael .B., Empyema: Essentialss of

Thoracic Surgery: page 105,1996.

15. Kusabe .R.B., Rare Causes of Pleural Effusion:

African Health Science, 2001 (2) 97-98.

_____________________________________________________________________ 106

16. Lesi O.A., Kehinde M.O., Massive Haemorrhagic

Pleural Effusion-an unusual presentation of

endometriosis, Nigerian Medical Practitioner,

volume 44 (1) 2003, 22-44.

17. Basssey . J.A, Graham .A. Gould, Pleural

Deposits from Light Chain Myeloma- an unusual

cause of pleural effusion: Archives of Ibadan

Medicine, volume3 (2) 2002, 64-65.

18. Abrahamian.F.M.,PleuralEffusion

e-medicine,http://www.emedicine.com/emerg/

topic462.htm.Page15 of 32.

19. Robbins.J.,Pleural Effusion,e-medicine,

http://www.e-medicine.com/med/topic 1843 html.

20. Abrahamian .F.M.,Pleural Effusion,

e-medicine,http://www.e-medicine.com/emerg/topic

462. htm. Page 15 of 32.

21. Rafel.S. et al., Management of Pleural effusion,

http://www.medscape.com/viewarticle/535594

22. Abrahamian.F.M.,PleuralEffusion,

e-medicine,http://www.e-medicine.com/emerg/topic

462.htm.page 15 of 32.

23. Ibid

24. Robbins Jeffery,Pleural Effusion,

_____________________________________________________________________ 107

e-medicine,http://www.e-medicine.com/emerg.

PAGE 3 of 18.

25. Heimlich,H.J., Valve Drainage of Pleural Cavity;

Diseases of the Chest. 53:282,1968.

26. Oluwole Adebo,The Value of Chest Intubation In

The Initial Management of Chest Trauma In a

Developing Country; African Journal of Trauma;

May 2004 – Nov 2004, Vol 2(no 2-4) .page 76-79.

27. Adegboye V.O, Adebo O.A, Ossinowo .O., Brimmo:

Closed Chest Drainage Without an Underwater

Seal. African Journal of Medical Sciences 1996,

25 (4) 353-5.

28. Cancer Bacup- Management of Pleural Effusion,

http://www.cancerbacup.org.uk/resources support.

29. Snow.J.A.Parapneumoniceffusions in children.

http://pediatrics uchicago.edu/chief/AM

report/parapneumonic effusion

30. Indu,D,Aprim, YY; Surgery on CD Rom, Johnson and

Johnson Professional Export. African Health Care

Services.jjpex@ethgb.com.

31. Walker RPB,Voughan LM, Sahn SA, chemical

pleurodesis for malignant pleural effusions.

Annals of Internal Medicine 120(1): 56-64;1994.

32. Hartman DL, Gaither J.M, Kesler K.A et al.

_____________________________________________________________________ 108

Comparison of insufflated Talc under

laparoscopic guidance with standard tetracycline

and bleomycin for control of malignant pleural

effusion .Journal of Thoracic and CardioVascular

Surgery,105(4):743-748,1993.

33. Ezeome E.R. et al. Use of tetracycline

capsules for pleurodesis in breast cancer

patients with malignant pleural effusion.Journal

of College of Medicine, University of Nigeria

Nsukka,2005:9(2) :82-84 .Published in African

Journal On Line (AJOL).

34. Carolyn Clary-Macy,Chemical pleurodesis for

pleural effusion, UCSF, Thoracic Surgery http:

//www.cancersupportivecare.com/pleural

html.pg2/2. 2005.

35. Arigoni C ,Tisi E, Ballabio D, Cassina E

et al.Neoplastic Pleural Effusion.

Our Therapeutic Progress . page 5/13

http:// www.chirurgia

thoracica.org/pleuri-effusion-maligne-htm.

36. Jacobs L.M, Hsieh J.W.,A Clinical Review

Of auto-transfusion and its role In trauma,

Journal of American Medical Association

251:3283,1984.

_____________________________________________________________________ 109

Proforma for Analysis

(A) Bio-data

Name

Age

Sex

Hospital No.

Tribe

Town / City of Residence

Occupation

Marital Status

(B) Presenting Complaints

YES NO

Breathless

Cough

Chest Pain

Fever

Wt Loss

Others

_____________________________________________________________________ 110

(C) Associated Pathology

Present Absent

Neoplastic disease

Tuberculosis (PTB)

Pneumonia

Connective Tissue

Disease

Recurrence

Others (Pls specify)

D. Type of Neoplastic Disease

Present Absent

Breast CA

Lungs CA

Soft Tissue Sarcoma

Intra Abdominal Malignancy

Parotid CA

Others.

E. Findings on Physical Examination

Parameters present Absent

Pallor

Cynosis

Features of respiratory distress e.g., RR,

Flaring of alar nasi, sweating etc

Trachea Deviation

Increased Chest Excursion

Decreased Chest Excursion

Increase Percussion Note

Decreased Percussion Note

Normal air entry

Any Added sounds

Abnormal Heart sound

Distended Neck Veins

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F. Investigative findings

Pleural Fluid Collection – Physical Characteristics

Yes No

Air -

Liquid: - blood:

- Straw colored

liquid

- Pus

- Chyle

- Clear Liquid

- Sero - Sanguinous

G. Pleural Fluid Aspirate Analysis

Chemistry Control Level

Specific Gravity

- glu

- Prot

- LDH

- Serum LDH

- P. LDH/S.LDH

- PH

- TG

Cholesterol

TG / cholesterol

Na+

- Cl-

- K+

-HCo3-

Transudate

Exudate

Microbiology

Present

Absent

- AFB

- MCS

- Pus Cell

- Fungal

Cytology

Present

Absent

- WBC

- RBC

- Malignant Cells

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H. Radiological Findings

Chest X-ray – PA View <25% 25-50% >50%

Normal Study

(R) Hydrothorax

(L) Hydrothorax

Bilateral Hydrothorax

(R) Pneumothorax

(L) Pneumothorax

Bilaterial Pneumothorax

Hydropneumothorax

Mediastinal shift

CT - chest

State Findings (If any, pls) Yes

No

I. Treatment Modality

Yes No

- Observation

(Serial chest X-ray)

- Needle Aspiration

- Tube thoracostomy +

Under – Water Seal Drainage

- Tube Thoracostomy +

Under – Water Seal Drainage + Low

Suction

- Rib – resection + Eloesser Window

- Thoracotomy (Exploratory)

- Pleurodesis

- Decortication

- Pneumonectomy

- Pleuro – peritoneal shunt

- Video thoracoscopy with debridement of

pleural

Instillation of streptokinase

Others (Pls. specify)

J. Treatment of Other Concomitant disease Condition

Please specify Yes ……… Or No ………….

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K. Outcome of Treatment

Complete Recovery Complication

Pneumonia

Pulmonary tuberculosis

Neoplastic Diseases

Constrictive Pericaditis

Chronic Liver Disease

Congestive Cardiac

Failure

Chest Trauma

Connective tissue

Disease

Others (pls. specify)

L. COMMON COMPLICATION OBSERVED

Present Absent

Premature Dislodgement of Tube

Pneumothorax of Tube

Wound Sepsis E.g., Meleny’s

Gangrene

Progressive Empyema Thoracis

Recurrence

M. Treatment of Recurrence

Yes No.

Needle Aspiration

Tube Thoracostomy

Eleasar Window

Pleurodesis

Decortication