1 PLEURAL EFFUSION: PATTERN AND OUTCOME OF TREATMENT- A ONE YEAR PROSPECTIVE STUDY AT THE NATIONAL HOSPITAL ABUJA Submitted By UGWUANYI CHARLES U MBBS (Nig) 1995 A DISSERTATION SUBMITTED TO THE NATIONAL POST GRADUATE MEDICAL COLLEGE OF NIGERIA, IN FINAL FULFILLMENT OF THE REQUIREMENTS FOR THE AWARD OF THE FELLOWSHIP OF THE MEDICAL COLLEGE IN SURGERY (FMCS) NOV 2011.
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PLEURAL EFFUSION:
PATTERN AND OUTCOME OF TREATMENT- A ONE YEAR PROSPECTIVE STUDY AT THE NATIONAL HOSPITAL ABUJA
Submitted By
UGWUANYI CHARLES U
MBBS (Nig) 1995
A DISSERTATION SUBMITTED TO THE NATIONAL POST GRADUATE MEDICAL COLLEGE OF
NIGERIA, IN FINAL FULFILLMENT OF THE REQUIREMENTS FOR THE AWARD OF THE
FELLOWSHIP OF THE MEDICAL COLLEGE IN SURGERY (FMCS) NOV 2011.
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DECLARATION
It is hereby declared that this work is original, carried out under appropriate supervision,
and has not been previously submitted in part or in full to any other college(s) or
institution(s) or scientific journal for examination or publication.
Ugwuanyi Charles U.
DEDICATION To God for His infinite mercies, love and kindness in my life, to the continued gift of my
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dad Emmanuel and my mum Augustina, to the present of my darling wife, Ifeoma, and to the future of my children Chummy, Somtoo, Munny and Dodoo.
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ATTESTATION We hereby certify that we have supervised this Project on pattern and Outcome of Treatment of Pleural Effusion at The National Hospital Abuja conducted by Mr Ugwuanyi Charles U. Dr Salawu SAI, FMCS, FWACS, FICS Head of Department of Surgery, National Hospital Abuja, Nigeria Dr Yahaya Baba Adamu, FWACS, FICS Consultant Cardiothoracic Surgeon, National Hospital Abuja,Nigeria
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ACKNOWLEDGEMENTS To God almighty for sound body and mind, guidance and protection. To my Dad, Mum, Wife, Children, brothers and sisters for keeping faith during difficult moments. To Prof. Peter Obekpa, Prof. MAC Aghaji and Dr. JC Eze for inspiring me into surgical specialty To Dr. SAI Salawu and Dr Adamu Baba Yahaya for their patience, invaluable advice, support and encouragements during this work. To Dr. EA Jeje for useful advice and suggestions. To Prof. AO Adebo for his useful pieces of advice during the rudimentary stages of this work. To Dr. Tony Anigbo, for his unending words of wisdom and inspiration towards achieving excellence in surgical training for service. To all my colleagues at the National Hospital Abuja especially Dr(s) Lawal, Badejo, Ihekire, Udoye, Ekwueme for their various roles in building a solid foundation for my surgical training. To Dr. Henry Ewunonu of Histopathology Department of the National Hospital Abuja for providing me a photomicrograph of one of the pleural fluid cytology specimens from his personal collections. To my colleagues at the University College Hospital London especially Neil Kitchen, Michael Powell, Adam Meir, Mark Wilson, Chris Uff, Vivian Elwell, Pablo Goetz, Cormac Gavin who also deserve special mention for their pivotal role in my current sub-specialty training. To my secretarial staff and statistician for their invaluable input. To the National Post Graduate Medical College of Nigeria for their untiring efforts in Post Graduate Medical Training for excellence in Medicare in Nigeria.
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TABLE OF CONTENTS Title Page -------------------------------------------------------i Declaration -----------------------------------------------------ii Dedication-------------------------------------------------------iii Attestation-------------------------------------------------------iv Ethical clearance------------------------------------------------v Acknowledgement----------------------------------------------vi Table of contents-----------------------------------------------vii Summary---------------------------------------------------------ix Chapter 1- Introduction-------------------------------1 1.1- Definition of subject of study-pleural effusion------1 1.2- Historic brief in relation to pleural effusion----------2 1.3- Surgical anatomy of the pleural space---------------2 1.4- Physiology of pleural fluid turnover-------------------3 1.5- Justification of Study------------------------------------5 1.6- Scope of Study-------------------------------------------6 1.7- Inclusion criteria-----------------------------------------6 1.8- Exclusion criteria-----------------------------------------6 1.9- Limitations of study--------------------------------------6 Chapter Two-Literature Review------------------ ---8 2.1- Parapneumonic effusion-------------------------------8 2.2- Empyema thoracis-------------------------------------13 2.3- Tuberculous effusion----------------------------------16 2.4- Malignant effusion-------------------------------------17 Statement of Objectives of Study------------------22 Chapter Three-Materials and Method--------------23
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3.1- Data collection process-------------------------------23 3.2- Sample size estimation-------------------------------23 3.3- Sampling method--------------------------------------24 3.4- Data collection method and tool---------------------24 3.5- Technique of needle aspiration----------------------24 3.6- Technique of tube thoracostomy--------------------24 3.7- Subsequent patient management-------------------26 3.8- Care of chest tube-------------------------------------26 3.9- Laboratory methods-----------------------------------26 3.10- Radiological methods----------------------------------26 3.11- Data analysis and presentation----------------------26 Chapter Four-Results---------------------------------28 Chapter Five-Discussion------------------------------35 Conclusions------------------------------------------- 41 Recommendations------------------------------------42 References--------------------------------------------43 Appendix----------------------------------------------50
SUMMARY
TITLE: The pattern and outcome of surgical pleural effusion at the National Hospital
Abuja.
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STUDY OBJECTIVE: To study the etiological pattern of surgical pleural effusion and
outcome of treatment.
METHODOLOGY: Between February 2005–February 2006 some cases of surgical
pleural effusions were sampled prospectively. Study parameters were clinical symptoms
and signs, radiological features, pleural fluid analysis, primary disease condition,
treatments and outcome of treatment recorded at one and six months after treatment.
EP1- INFO Statistical Software was used and data was presented in form of tables, pie
chart and bar charts.
RESULTS: Eighty six patients participated. Fifteen declined. Breathlessness and dullness
to percussion on the affected hemithorax were found in 100% of cases. Pleural effusion
was confirmed on chest radiography. Straw colored fluid was found in 47 cases
(54.7%). Malignant pleural effusion was the commonest cause contributing 35 cases
(40.7%). Breast carcinoma was the commonest neoplasm implicated in malignant
pleural effusion contributing 23 cases (65.7%).
Chest drain was the main stay in management of surgical pleural effusions
irrespective of the cause. All patients with malignant pleural effusion had pleurodesis
while those with chronic empyema thoracis had decortication as an additional
procedure. Sixteen cases (84%) of para-pneumonic effusions made excellent progress at
one month with only three cases progressing to empyema thoracis. Second best
outcome was tuberculous effusion while malignant pleural effusion (MPE) had the
poorest outcome.
SPleurodesis was successful in 62.3% of cases of MPE at one month evaluation, but
it did not improve the overall survival in patients with MPE.
CONCLUSION: Evaluation and principled application of chest drain, pleurodesis and
decortication impacted positively on the early outcome of patients with pleural effusion.
CHAPTER ONE - INTRODUCTION
Pleural cavity is a potential space between the lungs and the chest wall. It is
lined by visceral and parietal pleura and normally contains very little lubricating
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fluid. This fluid is in dynamic equilibrium with the extra cellular fluid. In certain
pathological conditions, this equilibrium is disrupted; fluid accumulates therein
and results in pleural effusion. Among hospitalized patients, Bekele1 reported a
prevalence rate of 14.6% for pleural effusion.
Whereas some cases of pleural effusion are amenable to medical
management, others require some surgical intervention for better outcome.
These were the main focus of this study.
DEFINITION OF SUBJECT OF STUDY
Surgical pleural effusion is a pathological accumulation of exudative fluid into the
pleural cavity. Common predisposing pathological conditions include bacterial
pneumonias, pulmonary tuberculosis, and lung tumors. This fluid compresses the
lungs and mediastinum with a resultant derangement of cardio-respiratory
function. This condition is potentially fatal but often amenable to surgical
intervention. It is therefore important to define its pattern in our environment as
a guide to appropriate management of similar cases in the future.
HISTORICAL BRIEF
Long before the physiology of pleural fluid turnover was understood,
pathologic conditions of the pleural cavity have been described. In one of his
classic quotations, Hippocrates described the management of empyema thoracis
as follows: When empyemata are opened by the cautery or knife and the pus
flows pure and white, the patient survives but if it is mixed with blood, muddy
and foul smelling, the patient dies.2 Though this ancient statement may not
stand modern scientific scrutiny, it shows that empyema is an age long disease
of mankind.
The high incidence of empyema complicating pneumonia and death arising
there from during the World War I provided an opportunity for the Empyema
Commission of the United States Army to develop the principles of management
of empyema thoracis in an era long before the advent of antibiotics. This
principle hinged on the use of under water seal drainage rather than open
drainage system as previously practiced. It is on record that almost two-thirds of
all deaths during that war were related to pneumonia and empyema.3 The World
War II provided yet another opportunity to perfect this invaluable surgical
principle which remains accepted to this day.
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Following the discovery of antibiotics in 1929 by Fleming and subsequent
widespread availability and use, the hazards of pulmonary infection, its
complications and need for surgical intervention were greatly reduced.4
On the other hand, the increase in cigarette smoking after the World War
II was associated with an increased incidence of lung cancer and associated
malignant pleural effusions in developed countries. Lung cancer contributes 35%
of all malignant pleural effusions.5 Increase in the incidence of malignant pleural
effusion is also accounted for by rising incidence of breast cancer as well as
other malignant conditions.
Physiology of the pleural fluid turn-over has become clearer now. This is
due to the accumulated experimental data over the past 30 years6,7 as well as
the pioneering work of Starling and Tubby8. Consequently pathophysiology of
common diseases affecting the pleura is better understood, thereby providing a
guide to rational treatment and improved outcome.
SURGICAL ANATOMY OF THE PLEURAL SPACE
The development of the pleural cavity begins in the third week of intra-
uterine life. The mesodermal layer of the trilaminar germ disc differentiates into
three portions on each side of the midline namely paraxial, intermediate and
lateral. Intercellular clefts appear in the lateral portion and later coalese to form
intra-embryonic coelom. This forms a space which separates the splanchnic and
somatic mesoderm.
This space initially is in wide communication with the extra-embryonic
coelom, but with the cranio-caudal and lateral folding of the embryo, this
communication is lost, leaving a large intra-embryonic cavity which extends from
the thoracic down to the pelvic region9.
The diaphragm which separates this communication into a definitive chest
and abdominal cavity is formed subsequently from four structures namely:
septum transversum, pleuro-pericardial membranes, pleuro-peritoneal folds and
myoblasts originating from the somatic mesoderm of the lateral and posterior
chest wall. These penetrate the adjacent pleuro-peritoneal membranes to form
the muscular part of the diaphragm while the septum transversum forms the
tendinous part.
The cells of the somatic mesoderm lining the intra-embryonic coelom
become mesothelial and form the parietal pleura as well as the parietal
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pericardium and peritoneum, while that of the splanchnic mesoderm form the
visceral pleura, pericardium and peritoneum. It is the space in between the
visceral and parietal pleurae that forms the pleural cavity.
The mediastinum which houses the heart and great vessels, separate the
pleural cavities into two halves. The parietal membrane of each half lines the rib
cage, diaphragm and mediastinum while the visceral membrane line the lungs
and its tissues, but is deficient at its hila.
The visceral pleura is deficient in pain fibres but is richly innervated by
autonomic fibres from the vagus and sympathetic nerves. It has a dual blood
supply from bronchial and pulmonary vessels. The parietal pleura derive
innervation from branches of intercostal nerves and blood supply from intercostal
vessels whose tributaries run in the extra-parietal pleural space. This space is
equally ramified by lymphatic channels that form the major drainage conduit of
pleural fluid.
PHYSIOLOGY OF PLEURAL FLUID TURNOVER
A sound knowledge of the physiology of pleural fluid dynamics is pivotal in
understanding the various pathological conditions arising from its derangement.
Physiologic concepts of pleural fluid turnover dates back to 192710. The old
hypothesis claiming that pleural fluid filters at parietal pleura and reabsorbed at
the visceral pleura is rather too simplistic. This is because it would imply that
protein concentration of the pleural fluid will continue to increase indefinitely
since protein which is continuously filtered at the parietal pleura would not be
reabsorbed at the visceral end. The diagram below illustrates the present view of
pleural fluid turnover.
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Parietal Interstititum Lymphatics
Parietal
interstititum
Systemic Capillary
Fig. i- Illustration of Pleural Fluid Turnover.
The acceptable description of water flux (Jv) between two compartments labeled
1 and 2 is captured in the revised Starling law:
JV = Kf [ ( pH1 pH2) σ ( 1 2)]
KF = Filtration coefficient
PH = Hydrostatic pressure of capillaries in each compartment.
= Colloid osmotic pressure
σ = solute reflection coefficient of the membrane.
For solute flux, the description is rather different as it occurs partly via the
water flux and partly down a diffusion concentration gradient11. Pleural fluid (water
flux + solute flux) is normally filtered at the parietal pleural level from systemic
vessels onto the pleural space down a relatively small pressure gradient.
The parietal mesothelium has few but large pores as reflected in a low σ value
of 0.3 but also low solute permeability coefficient12. The effect of this endowment
is efficient sieving of proteins so that the protein concentration of pleural fluid is
low (1g/dl) compared to that of the parietal pleural interstitial space (2.5g/dl).
Since absorption through the visceral pleura is almost negligible, most of the
filtered pleural fluids are drained through the parietal pleural lymphatics12. Pleural
fluid volume is controlled within a narrow limit 0.3ml/kg with a protein
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concentration of 1g/dl. The only mechanism assuring this control on minimal
pleural liquid volume is represented by the lymphatic drainage13. Hence there is
compensatory increase in lymphatic flow in response to an increased pleural fluid
volume in a negative feedback manner.
The major function of this minimal pleural fluid is to ensure a frictionless
interface between the pleurae. Filtration and absorption is a continuous process
and up to 700mls daily turnover is normal. Disruption of this normal physiology of
pleural fluid turnover results in accumulation of fluid in the pleural space. This is a
common event in most cases of pleural effusion. When the filtration rate exceeds
the potential re-absorption or when the absorbing mechanism is primarily altered,
the compensatory mechanisms are overwhelmed.
Several conditions disturb the equilibrium of forces involved in fluid transfer
across the pleura leading to pleural effusion. These may be subdivided into three
main categories, the ones that change trans-pleural pressure balance, impair
lymphatic drainage, or produce increase in mesothelial and capillary endothelial
permeability14. Pleural effusion resulting from changing transpleural pressure
balance alone usually does not have high protein content but in the latter two
conditions, the protein content is usually high. In addition cellular content may be
high in conditions leading to increased mesothelial and capillary permeability. This
is the basis for classification of pleural effusion into exudates with high
protein/cellular content and transudates with low protein content.
In the clinical setting, differentiating exudative from transudative effusion is
generally achieved by the criteria presented by Light15. Pleural fluid protein/serum
protein 0.5, pleural fluid LDH 2/3 of the upper limit of the normal serum level
and pleural fluid LDH/ serum LDH 0.6 favor exudative effusions. Most of the
surgically important pleural effusions are exudative, for example para-pneumonic
effusion, while most medically important effusions are transudative for example
congestive cardiac failure.
JUSTIFICATION OF STUDY
The Surgical unit of National Hospital has been challenged with a large
number of cases of pleural effusion requiring surgical intervention. Some of these
patients were referred from the oncology unit and others from medical and
pediatric units. There hasn’t been an articulated management protocols for the
different types of commonly encountered pleural effusion. Therefore appropriate
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classification of the etiological patterns and adoption of sound management
protocols based on evidence is hoped to guide future management of similar
cases.
SCOPE OF STUDY
The scope of this study is limited to consenting patients who suffered pleural
effusion amenable to surgical intervention and presented to the Surgical
Department of the National Hospital Abuja over a 13 months period spanning
February 2005 - February 2006). During this study period, a total of 101 patients
presented with surgical pleural effusion out of 1,908 admissions into the surgical
ward. Out of these, 86 consenting ones were sampled consecutively for this study.
INCLUSION CRITERIA
All consenting surgically treatable pleural effusions such as para-
pneumonic, tuberculous, malignant effusions.
EXCLUSION
All medically related pleural effusions such as in congestive cardiac failure were
excluded because their treatment does not involve any surgical intervention.
Similarly, all cases of traumatic hemothorax were also excluded because their
formation does not involve any prior derangements in the Starling forces,
although chest tube drainage is equally pivotal in their management.
LIMITATION
o Some patients declined participation for personal reasons
o High cost of medical treatment excluded some important cases.
o Occasional strike action in the Hospital, disrupted timely follow up in
some cases.
o Limited availability and high cost of some diagnostic equipment at the
time of this study such as computerized tomographic scans and magnetic
resonance imaging.
o Similarly, non availability of anerobic culture was another limiting factor.
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Ethical clearance was obtained from the ethical committee of the National
Hospital before the project commenced (copy attached). Only patients who
willfully consented were included in this study. They also reserved their right to
withdraw at any stage.
Information sheet (appendix)-Clearly indicated as much information as the
patient needed to make an informed consent.
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CHAPTER TWO - LITERATURE REVIEW
PATHOLOGY AND MANAGEMENT OF SURGICALLY IMPORTANT PLEURAL EFFUSION.
Pleural effusion as previously noted is an abnormal accumulation of any type of
fluid in the pleural space as a result of the disruption of the haemodynamic equilibrium
that exists across the pleural membranes. Such conditions include hydrothorax, sero-
pus, frank pus, blood and chyle16.This haemodynamic equilibrium is a function of the
normal physiology of pleural fluid turnover, which is determined by Starling forces as
previously discussed. It has been stated that pleural effusion is an indicator of a
pathologic process that may be of primary pulmonary origin, related to another organ,
system or a systemic disease. Hence it is not a diagnosis in itself17.
The surgically important pleural effusions include para-pneumonic effusions,
empyema thoracis, malignant pleural effusions (MPE), tuberculous effusions. In 1972,
Maher18 reviewed 84 cases, out of which 67% were malignant, and 33% were non-
malignant (para-pnemonic, tuberculous). Later, Pedro de Lelis 19 reviewed 84 cases, out
of which 71% were malignant and 29% non-malignant. Jose20 in a ten year
retrospective study sampled 766 cases (average 76 per year) also revealed the leading
role of malignant pleural effusion.
PARA-PNEUMONIC EFFUSION
This is a recognized complication of bacterial pneumonia. Research shows that
approximately 20%-60% of patients with bacterial pneumonia develop a
radiographically demonstrable pleural effusion.21 Abrahamian22 reported 30%-40% in
similar patients in the United States. In the South Eastern part of Nigeria Anyanwu 23
after studying 120 cases in children over a period of four years at UNTH Enugu,
concluded that para-pneumonic effusion is a common condition seen in Nigerian
children. In another study involving 60 children aged between one month to sixteen
years, he categorized pleural sepsis in children into three; pyothorax 40(66.6%),
pyo-pneumothorax 15(25%) and localized empyema 5(12.3%) 24. Edewor25 from
UBTH Benin, Nigeria reports that pleural disease is a frequent occurrence in children
with a frequency of 12.8% in all childhood radiographs and accounting for 1.48% of
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all pediatric admissions. A dissenting view however came from Asuquo26 in Calabar,
the South-Southern part of Nigeria, as his seven years study yielded only 48 cases,
constituting only 0.2% of all childhood admissions at UCTH Calabar. A similar study
in Ethiopia clearly shows that 60% of all para-pneumonic effusions were found in
children less than five years27. From the foregoing discussion, it appears that
majority favor the position that para-pneumonic effusion is commoner in children.
Both aerobic and anaerobic organisms are implicated in the etiology of bacterial
pneumonia. Among the aerobic organisms, Gram-positive infection is about twice as
common as the Gram-negative ones and the commonly implicated gram positive
aerobes include staphylococcus aureus and streptococcus pneumonia in about 70%
of cases28. Gram negative aerobes include klebsiella, pseudomonas, haemophilus
species. Anaerobes that are commonly encountered include bacteroides, and
peptostreptococcus species. In a study at UNTH Enugu involving 40 children aged
between three weeks to thirteen years, Anthony29 found that of the ten culture
positive cases, streptococcus pneumonia was isolated in three cases, staphylococcus
aureus in two cases, coliforms in two cases while haemophilus influenza, proteus
mirabilis and pseudomonas aeruginosa in one case each. Asuquo26 found
staphylococcus aureus most predominant in his study. In certain instances, both
aerobic and anaerobic infections occur in a mixed fashion in which case progression
to empyema is more likely.
Following overwhelmed host defense mechanisms, lung tissue respond by
inflammation which causes micro vascular vasodilatation involving lung parenchyma
and adjacent pleurae. The resultant effect is the exudation of fluid and widening of
intercellular junctions in between the mesothelial cells of the pleura. Consequently,
fluid accumulates in the pleural space in excess of the normal turnover. There is also
associated exudation of acute inflammatory cells such as neutrophils alongside the
pleural fluid. Other aspects of the lung pathological process in pneumonia include
lung consolidation, necrosis and abscess. There are three stages of development of
para-pneumonic pleural effusion. In the first stage, there is an accumulation of small
but sterile fluid in excess of the absorptive capacity of the parietal pleura. The
effusion here is neutrophilic with low lactate dehydrogenase (LDH) level but normal
glucose content and PH. It is not likely to progress beyond this stage if the
pneumonic process is promptly and adequately treated. This is because antibiotic
penetration of the space through the porous membrane is good. The second stage
occurs if bacteria and polymorphs enter the pleural space and render the fluid
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accumulated therein infected. The sustained inflammatory process cause fibrin
deposition on the pleurae and can predispose to loculation of fluid. There is an
associated increase in pleural fluid LDH and levels greater than 1000iu can be
reached. LDH normally catalyses the reversible inter-conversion of pyruvate and
lactate and is liberated when cells containing the enzyme are lysed during
inflammatory activities. Similar situation is also found in conditions of high tissue
turnover such as cancer. The pH drops to acidic levels ( 7.2) due to accumulation
of acidic products of inflammation. Glucose is used up by inflammatory cells whose
metabolism is accelerated, hence the level drops. (60mg/dl). The third stage
happens when the fluid is not drained and fibroblasts move in and organize the fluid
into a pleural peel thus making the removal of the fluid by needle aspiration
impossible. This peel will encase and trap the lung permanently thus restricting its
compliance and function. An abscess could be encased in between the visceral and
parietal fibrous peel and this is called empyema thoracis. Stage one para-pneumonic
effusion can be said to be uncomplicated since they remain sterile and resolve with
effective antibiotic therapy of the underlying pulmonary infection while stage two
and three are complicated due to the propensity to form pleural loculations and
fibrosis especially if prompt and adequate drainage is not carried out soon after the
appearance of the effusion30. Penetrating chest injury,chest surgery, rupture of
hepatic and sub-diaphragmatic abscesses, perforation of esophagus, rib
osteomyelitis are other possible causes of infection of the pleural space.
Clinical features include fever of acute onset associated with chest pain,
productive cough and leucocytosis which persist after 48hrs of antibiotic treatment.
Dyspnoea and dullness to percussion in the affected hemi thorax results.
Thoracocentesis helps to confirm the diagnosis and predict the need for chest tube or
surgical drainage3. Physical, chemical and microbiological examination as well as white
blood cell count confirms the exudative nature of the effusion. The color and turbidity of
the fluid may help in determining the stage of effusion for example, a frankly purulent
effusion suggests stage three (empyema thoracis) while a thin serous exudate suggests
stage one (uncomplicated) effusion. A frankly haemorrhagic effusion may suggest an
underlying malignant lesion. Relevant chemical analysis includes pH, glucose, LDH and
protein levels. In para-pnemonic effusions, pH is low ( 7.1), glucose is low ( 40), LDH
is high (1000iu) and protein is high (3.5g/dl). 31
Gram-stain and culture will be negative in stage one disease but may be positive in
stages two and three. The offending organism could be isolated and antibiotic sensitivity
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determined. White blood count will show leucocytosis with preponderance of
polymorphs. It has been posited that diagnostic thoracocentesis provides essential
information for the management of patients with para-pneumonic effusion32.
Radiological evaluation of para-pneumonic effusion involves chest radiographs,
ultrasound and computerized tomographic scanning. Under normal circumstances, the
pleural space contains between seven and 14mls of fluid33. This small amount of fluid
does not show on chest radiograph. Chest radiographs can fail to detect small effusions
and do not attain 100 percent sensitivity, even when decubitus views are included, until
the amount of pleural fluid exceeds 500ml34. Abrahamian 22 believe that a decubitus view
showing a one centimetre thickness of opacity approximates 200mls of fluid.
Radiological features include blunting of costo-phrenic angle, classical meniscus sign,
homogenous opacity below the meniscus, mediastinal shift to the contralateral side in
large effusions and obliteration of diaphragmatic silhoette. In most cases, conventional
chest radiography with lateral decubitus views will show the presence and location of
pleural effusion. When additional imaging is required to detect, localize and guide
thoracocentesis, ultrasound is a preferred technique for reasons of cost, availability,
safety and portability35. Ultrasound can detect the presence of as little as 5-50mls of
fluid and is 100% sensitive for effusions of 100mls and above34. Computerized
tomographic scan of the chest is superior but for cost and enormous radiation exposure.
Treatment is stage dependent. For stage one (uncomplicated), complete
resolution is expected with prompt and adequate antibiotics administration. Parenteral
route is preferred and it is continued until patient is afebrile for seven to ten days.
Thereafter oral medication continues for twenty one days. There is usually no need for
chest drainage at this stage. However some studies have shown that some patients with
stage one (uncomplicated) para-pneumonic effusions even when treated as above will
eventually require chest tube drainage36. If fever and other chest signs persists in-spite
of appropriate antibiotic administration, repeat chest radiography and diagnostic
thoracocentesis is indicated. Progression to stage two para-pneumonic effusion requires
chest drainage as an additional treatment modality to prevent development of fibro
thorax and to control infection37. This position has been challenged by Berger38 with
some data showing that some patients with complicated para-pneumonic effusion may
not need chest tube drainage. If no improvement occurs, fluid loculation and
progression to empyema thoracis occurs. Further imaging such as computerized
tomographic scanning of the chest confirms the diagnosis. The presence of loculation is
a predictor of increased morbidity independent of fluid characteristics39. There is an
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argument in favor of draining effusions that may not have required drainage than to
leave un-drained some effusions that will later become complicated. This will reduce
morbidity, mortality and length of hospital stay40. In the presence of multiple loculi,
thrombolytic therapy administered intra-pleurally has been tried with varying successes
but must be administered early to be more effective. Studies have shown that patients
treated with intra-pleural thrombolysis required less surgical intervention and fewer days
of hospital stay41.Steptokinase and Urokinase are thrombolytic agents and both are
equally effective although streptokinase has more allergic property. The addition of a
lytic agent was first suggested in 194942 and the result was reported impressive.
Adverse systemic reactions have outweighed their benefits43. Success rates of up to
80% have been reported with streptokinase44. Studies by Henke45 have further
supported the efficacy of streptokinase in these conditions.
Fig ii- Chest X-ray showing left sided massive pleural effusion with
mediastinal shift before and after drainage
Although favorable results have been reported as stated above, the indications,
timing, dose and duration of fibrinolytic therapy are still to be determined46. Continued
search for an early and effective way to guarantee complete drainage of the pleural
space and discourage progression to chronic empyema thoracis, early surgical
intervention was proposed47. The advent of minimally invasive video assisted
thoracoscopic surgery is appealing, as it led to effective destruction of loculated
collections and more effective drainage. Following their reported long experience with
thoracoscopy, Baimbridge48 have found it to be effective in only 60% of patients in their
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study. However, these procedures are not widely available in developing countries.
Open thoracotomy and decortication are major procedures that are reserved for chronic
cases because it not only evacuates the abscess, but also removes the imprisoning
fibrous peel that restrict the pulmonary function.
Adjuvants to treatment include chest physiotherapy and adequate nutritional
support49. All causes of reversible immunosurpression should be addressed accordingly.
The prognosis of para-pneumonic effusion is good especially if early intervention is
made to prevent the progression of the disease process to the more advanced stages
which are more difficult to manage.
EMPYEMA THORACIS
Empyema thoracis is a sequel to para-pneumonic and tuberculous effusion and
simply means pus in the pleural space. Some authors include all pleural effusions with a
positive gram stain or culture regardless of the gross appearance of the fluid in the
definition50. It was noted earlier that 20-60% of para-pneumonic effusions are
complicated by empyema. It was also noted that the advent of antibiotic use in 1929 as
well as the experiences of the World War I and II, as regards treatment have all
contributed to a significant decline in the incidence of the disease and an associated
increase in the favorable outcome of the disease. In the pediatric age group, para-
pneumonic effusions are the most frequent etiological factor for empyema51. Other
documented causes include rupture of esophagus, extension of sub-diaphragmatic
infection, direct inoculation from trauma or thoracocentesis, direct extension from
paravertebral abscess. Of particular note is underlying carcinoma of the bronchus which
must be suspected in any patient over the age of 45 years presenting with empyema52.
Bacteriology of empyema has changed with antibiotic advances and improved
culture techniques. Before the penicillin era, streptococcus pyogenes and streptococcus
pneumonia were the most common isolates, but with the advent of penicillin,
staphylococcus aureus has become more common50. Since 1970, anaerobic infections
have been recognized with increasing frequency. Fusiform bacilli, bacteroides, anaerobic
streptococci and clostridium species are all implicated. Currently, with the increasing
prevalence of hospital acquired pneumonia especially in the intensive therapy unit, gram
negative aerobic bacilli are now commonly isolated.
Empyema includes both the complicated stages two and three of the para-
pneumonic process. Only stage one is excluded since there is no demonstrable bacterial
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contamination of the fluid at this stage. The evolution of the pathological process in
empyema thoracis has been conveniently divided into three stages for the purposes of
therapeutic guidance. The exudative phase has thin and watery pus. In the fibrino-
purulent stage, the empyema becomes thick and tenacious and there is accompanying
fibrin deposition on the pleural surfaces and within the empyema cavity with a resultant
multiple loculations, and finally the chronic phase or organizing phase, a thick fibrous
peel coats the chest wall, diaphragmatic, mediastinal and pulmonary surfaces. The
enlarging empyema progressively entraps and collapses the lung thereby leading to
functional compromise. It can also rupture into the lung parenchyma with a resultant
broncho-pleural fistula or through the chest wall as empyema necessitans.
The clinical presentation of empyema generally blends with that of the underlying
pneumonic process. Pleuritic chest pain, dyspnoea and chest pain are frequent. In the
chronic phase, weight loss and anaemia are more prominent than fever and chest pain.
Radiographic investigation involves a postero-anterior and lateral chest X-ray, which
shows the characteristic appearance of lower lung zone opacification, blunting of
costophreric angle and a lateral meniscus which is concave upward. Sub-pulmonic
effusion which may be confused with an elevated diaphragm may be noted occasionally.
Chest X-ray can help to distinguish between an empyema and lung abscess, a distinction
which has a very important therapeutic bearing. Lung abscesses are usually treated
medically whereas empyemas require a combined surgical and medical therapy.
Schachter53 listed three criteria for distinguishing empyema from abscesses. Extension of
air fluid level to the chest wall, tapering border of the air fluid collection, extension of
the air fluid collection across fissure lines are all in keeping with an empyema. An
abscess tends to be spherical in shape and further from the ribs and the air fluid has
similar length on both anterior-posterior and lateral films54. Kumar and Clark55 agree that
a chest X-ray showing air-fluid level in the absence of tuberculosis is in keeping with an
abscess. Computerized tomographic scanning is definitely superior to simple radiographs
in evaluation of empyema thoracis56. For example, the radiographic thickness of contrast
enhanced pleural membranes and the presence of edema in extra-pleural tissues can
assist in the differential diagnosis of empyema from a transudative or malignant
effusion57.
Treatment of empyema thoracis starts with a broad spectrum antibiotic, which
may be modified according to Gram stain, culture and sensitivity results although most
are often already sterilized by the prior administration of antibiotics4.
24
Fig. iii-Chest X-ray, C-T scan of the chest and intra-operative image showing
empyema thoracis.
Chest tube drainage is the initial treatment of choice. If difficulty in drainage is
encountered, rib resection provides a viable alternative provided drainage is obtained in
the most dependent portion of the cavity. Rib resection provides an additional
opportunity to break down loculations.
In the chronic organized stage, the treatment modality includes chronic drainage
via an Eloesser flap which involves rib-resection that allows the fashioning of an
anteriorly based skin flap, which is drawn over the edge of the wound and sewn to the
parietal pleura, thus creating an epithelized stoma that will not close spontaneously. The
added advantage is that it provides an excellent opportunity for long term drainage,
irrigation, debridement and packing of the empyema cavity. Pleurectomy/decortication is
usually reserved for patients with a chronic cavity and thick fibrous peel, which may
have resulted from inadequate treatment or the late recognition of the disease process.
This is a major procedure that requires a thoracotomy with excision of the thick fibrous
peel which encases and restricts the normal function of the chest wall, diaphragm,
mediastinum and lung. Occasionally a concomitant pulmonary resection is required to
remove an underlying pulmonary pathology which in the face of active infection in the
empyema space is associated with an increased incidence of morbidity and mortality50.
This operation is a major undertaking and is reserved as a last option even in
reasonably fit patients. It is not advised in the elderly. Prognosis depends on the stage
of the disease.
25
TUBERCULOUS (TB) EFFUSION
This is caused by pulmonary tuberculosis. Mycobacterium tuberculosis is the
commonest cause of chronic granulomatous infection of the lung parenchyma and
associated lymph nodes. Tuberculosis afflicts a third of the world’s population and it is
estimated that ninety five percent of TB cases and ninety eight percent of TB related
deaths occur in developing countries57. This explains why effusion associated with
pulmonary tuberculosis is a very important clinical condition.
It is usually preceded by a tuberculosis pleuritis which is a hypersensitivity
reaction involving the pleural membranes and capillaries. It is rather not due to a direct
invasion of the pleural membranes by the mycobacterium. This is the reason why there
is usually a very low yield of acid fast bacilli in the pleural fluid. There is a marked
exudation of protein rich fluid from inflamed capillaries of pleural membranes into the
pleural space in excess of its drainage capacity. Consequently fluid accumulates in the
pleural space. There is also an associated exudation of mono-nuclear cells such as
lymphocytes, some of which are lysed to release high level of lactate
dehydrogenase(LDH) into the pleural fluid. This is what accounts for the high level of
LDH in tuberculous effusions. An increased metabolic activity in the pleural space is
responsible for low glucose level as well as low pH which is due to build up of metabolic
bye-products such as lactic acid. These patients usually have a history of chronic cough,
contact with chronic cough patients and may be Mantoux positive. Some are already on
treatment for pulmonary tuberculosis, but compliance is questionable.
Thoracocentesis yields a straw colored fluid though it may occasionally be
hemorrhagic. Onadeko58 reports that tuberculosis is the second commonest cause of
haemorrhagic effusion in Nigeria after malignant effusion. When subjected to further
analysis, it shows high protein content, high LDH, low pH, low glucose, high lymphocyte
count. Measurement of adenosine deaminase activity (ADA) as well as interferon gamma
concentration when available is quite specific for tuberculous effusion. Acid-fast bacilli
stain of pleural fluid as well as culture of mycobacterium from the pleural fluid are useful
but of low diagnostic yield. Chest X-ray shows the typical features of effusion which may
be massive and opacifies the whole hemithorax. Any associated lung lesion can only be
seen after drainage of the fluid. Computer scanning of the chest may be indicated to
resolve any associated pulmonary lesion.
Treatment involves strict compliance with standard anti-tuberculous drugs. The
aims of therapy are as follows: To cure the patient of the disease with minimum
interference with their living, in as short a time as possible whatever the initial drug
26
susceptibility of the causative organism, 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. Various regimens
exist but short course treatment with two months of isoniazid (5-10mg/kgmax,
300mg/day), rifampicin (10mg/kg, max, and 600mg/day), pyrazinamide (35mg/kg-max,
1500mg/day), ethambutol (15mg/kg), and a further four months of isoniazid and
rifampicin is widely used. It is efficient and favors compliance. Patient is considered
cured at six months but a relapse rate of 2-3% has been reported57. Mild to moderate
cases of pleural effusion disappear without any need for chest tube drainage except in
situations where massive effusion is present. This is to prevent unnecessary empyema
necessitans. Prognosis is good if treatment is administered early. If HIV infection was
detected in the routine work up, co-administration of appropriate anti-retroviral drugs is
highly recommended and is quite beneficial.
MALIGNANT PLEURAL EFFUSION (MPE)
This is fluid exudation into the pleural cavity as a result of neoplastic disease
process. It may be the presenting sign of cancer especially extrapulmonary cancers in
some patients, but in others, it is a mark of recurrent, disseminated or advanced
disease59. MPE accounts for 25% of all pleural effusions encountered in a General
Hospital setting60.
Almost all forms of cancer are reported to cause pleural effusion. In one series,
Hausheer61 found that over two thirds of all malignant pleural effusions were attributed
to carcinomas of the lung (35%), breast (23%) and Lymphoma (10%). Abrahamian22
also documented that the most common causes of pleural effusion include
adenocarcinomas and other carcinomas of the lungs, breast, lymphoma and leukaemia,
which account for 75% of all cases. However, in some cases, the cause of the malignant
effusion is unknown and this accounts for about 12% in Hausheer’s series. Given the
prevalence of breast and lung carcinoma today, it is not surprising that some
investigators report that up to 50% of patients afflicted with these malignancies will
develop effusion at some time during the disease process62. But with the recent
advances in oncology management of cancer such as breast carcinoma, above position
credited to Greenwald remains debatable today. Some argue that the increased survival
occasioned by the recent advances in oncology management provides enough time for
effusions and recurrences63.
MPE may arise from a variety of cancer-related events. Parenchymal tumors
27
(primary or metastatic) may erode the visceral pleura spilling cells and disrupting the
normal resorptive flow of fluid from the visceral to the parietal pleura. Alternatively, the
pleurae are themselves common sites of metastatic seeding. The presence of tumor
seeds here results in increased capillary permeability due to inflammation or overt
endothelial disruption. There is also disruption of lymphatic drainage due to tumor
seeding in the lymphatic channels. The existence of co-morbid factors in the patient,
though not directly related to cancer related pleural pathology can exacerbate the
pleural effusive process. Such factors as documented by Ruckdeschel63, include
mediastinal node involvement by tumor, co-existent obstructing pneumonia, prior
confirmed effusion into the chest cavity, while needle aspiration provided a sample for
physical, microbiological, biochemical and cytologic analysis. This process was applied in
all 86 patients who consented to participate in this study. It was helpful in defining the
exact patterns which guided appropriate treatment.
Sample Size Estimation
From, Bekele’s1 study, the prevalence of pleura effusion among hospital admission was
14.6%. The minimum sample size is calculated using the formula for proportion. When
N > 10,000,
N = Z2 pq/d2.
N = the desired sample size (when population is greater than 10,000)
Z = the standard normal deviate set at 1.96 which corresponds to the 95% confidence interval. P = Prevalence as a proportion q= 1-p d= error margin (5%= 0.05) Therefore, using p=14.6%, N = (1.96)2 *0.146*0.854. 0.052. = 191.59.
Thus, n = 191. However, the estimated population size based on hospital records the year preceding
this study showed that 78 patients with surgical pleural effusions were admitted into the
surgical wards. This was found to be less than the desired sample size.
33
Consequently, all consecutive patients with pleural effusion who met the inclusion
criteria were included in this study for the one year period (February 2005-February
2006). During this period, 86 out of 101 patients who were admitted to the surgical
wards for surgical pleural effusion consented and participated in this study
Sampling method All eligible participants who met the inclusion criteria, admitted into the surgical wards
and willfully consented during the stated one year study period were sampled
consecutively for the study.
Data collection method and tool Data collection was done using interviewer administered questionnaire that was
administered to the consenting 86 patients only. With the help of two of my well
informed colleagues who were equally involved in managing these patients, these
patients were successfully sampled during the stated study period.
Technique of Needle Aspiration
Usually, the 5th or 6th intercostal space in the mid-axillary line was first identified and
marked for this procedure. Under sterile conditions, a needle puncture was made
perpendicularly through the skin into the pleural space with a 21G needle.
Approximately 20 cc of aspirate was taken. At the end of procedure, the needle
puncture site was again cleaned and dressing applied. Specific sample containers were
selected for this purpose as follows: Plain tube for protein, LDH, glucose, triglycerides
and cholesterol estimation. Ethylenediamine tetra-acetic acid bottle (EDTA) for cell
count. Heparin treated blood gas syringe for Ph. Sterile container for Gram stain/ culture
and acid fast bacilli. Heparin treated container for cytology.
Technique of Tube Thoracostomy
After explaining the procedure to the patients, reassuring them and gaining their
confidence, a supine position with bed inclined at about 45o was adopted. Intranasal
oxygen at 5 liters/min was a standard precaution. A mounted chest X-ray was reviewed
to confirm laterality and avoid a costly mistake of operating on the wrong side. This is in
keeping with WHO pre-operative checklist. The fifth intercostal space in the mid-axillary
line was identified and a one centimeter transverse mark on the skin was made with a
with a surgical pen. After a standard skin preparation and draping to expose only the
marked spot, local anesthesia was provided with local infiltration of about 5-10mls of
1% xylocaine. After a few minutes wait for its effect to kick in, a one centimeter
transverse skin incision down to the subcutanous plane was made. Gentle blunt
34
dissection was made at the upper border of the sixth rib to avoid the sub-costal vessels
and nerves which run in the groove on the lower border of the fifth rib. The intercostal
muscles were parted to reach the parietal pleura. Gently perforation usually yielded a
gush of fluid. Appropriate sized, double clamped chest tube was selected and carefully
positioned into the pleural cavity to a length of about 8cm. Thereafter the tube was
firmly secured to the surrounding skin with strong nylon one suture, after suturing the
skin incision. A purse string around the stoma was also pre-positioned to be secured
tight on removal of the tube at a later date. The wound was neatly dressed, tube
connected to an under water seal bottle, and the clamps removed. An immediate
oscillatory movement of the air-fluid column in the tube confirmed correct tube
placement in the pleural cavity. The drainage bottle was always placed below the chest
level so as to prevent reverse drainage. In transit from one part of hospital to another
the nursing staff was advised to double clamp the tube. A check chest X-ray after each
procedure was mandatory.
Check chest radiograph is equally mandatory in confirming completeness of drainage
and re-expansion of the lungs. This signifies that the chest drain was no longer needed,
hence indication for removal or for any further procedure such as pleurodesis, if
required.
For removal, under sterile precautions, the skin anchoring Nylon one stitch was severed
and the patient asked to take a deep breath. Very quickly the tube was pulled while an
assistant immediately tightened the pre-positioned purse string. Sterile air-tight dressing
was applied immediately to prevent sucking air into the pleural cavity.
For pleurodesis, a paste of tetracycline was prepared by dissolving 4grams of
tetracycline (eight capsules of 500mg each) into 40cc of normal saline in a sterile
gallipot. Making sure that the lungs are fully re-expanded on check chest X-ray and that
daily output was less than 50 cc, this solution was injected through the chest tube into
the pleural cavity. The tube was double clamped and the patient asked to shift from side
to side to prevent premature egress and ensure even distribution. The tube was
clamped for two hours during which time the sclerosant effect of tetracycline kicks in.
During tetracycline induced pleuritis, some patients may feel feverish but usually
responded to simple antipyretics such as paracetamol. The tube was subsequently
removed in a similar fashion as outlined above after 24hrs followed by a check post
extubation chest x-ray.
35
Subsequent Patient Management.
For tuberculous effusions, the infectious diseases physicians were consulted for advice
on enforcing compliance with recommended anti-tuberculosis regimen (usually short
course) as well as follow-up. Similarly a strict compliance with appropriate antibiotic
medications for para-pneumonic cases was ensured. A one week course of intravenous
Augmentin (1.2g 8hrly) and a further three weeks of oral augmentin (375mg 8hrly)
were found to be quite effective. In pediatric patients, dosage was adjusted accordingly
in consultation with the paediatricians. The aim was to prevent recurrence and
progression to further complications such as empyema thoracis.
Care of the chest tube:
Patients were constantly reassured. The thoracostomy sites were daily inspected for
evidence of sepsis and premature/accidental tube dislodgement, and managed
accordingly. Daily output was noted, and when less that 50cc, a check X-ray was carried
out to confirm completeness of drainage and re-expansion of the lung, and if
satisfactory, chest tube was removed.
Laboratory methods:
Chemistry: Electrolyte estimation was by use of automated ion selective electrode
method. Lipid estimation was by automated enzymatic colorimetric method. Protein
estimation was by turbimetry/precipitation or colorimetric (Biuret’s test).
Microbiology tests were initial Gram – stain, followed by culture in chocolate and
MaConkey medium, then antibiotic sensitivity. Acid – fast bacilli stain was done on the
sediment of the spun fluid.
Cytology: A pap smear of spun sediment on a slide was fixed with 90% alcohol, and
stained with haematoxylin–eosin solution, and read.
Radiological methods:
Postero-anterior chest radiograph was employed to define the features of the effusion,
as well as any associated mediastinal shift, and any other lesion. In moribund bed
confined patients, supine view was employed. Decubitus view was used to delineate any
associated lung pathology which may have been masked by the effusion. These
radiographs were not only useful in diagnosis, but also in monitoring progress of
treatment. Computerized tomographic scanning was employed in only a few patients to
properly delineate mass lesion, and its anatomical relations.
Data Analysis / Presentation
36
Epi-info statistical software package was used to analyze data, which was presented in
the form of pie charts, bar charts, histogram, and tables as well as in simple narrative
terms. The mean, variance, standard deviation and standard error of the mean of some
variables were equally presented.
37
CHAPTER FOUR-RESULTS
A total of 101 surgical pleural effusions were seen during this study period
out of 1,908 admissions into the surgical wards at the National Hospital(5.2%).
86/101(85.1%) consented to participate in the study. There were 38 females and
48 males making a ratio of 1.26: 1 in favour of the males (Table 1).
There were nineteen para-pneumonic cases (22%) with a M: F 2.8:1, thirty
two of tuberculous (37%) with M: F 4.3:1 and thirty five of malignant effusions
(40.2%) with M: F 1:3.7.
Pleural effusion was observed in all age groups. Youngest was in a one year
old with parapneumonic effusion while the oldest was an 81 year old male with
malignant effusion. The mean age was 37.36 years, standard error of mean 1.7,
standard deviation 15.75.
Specifically, para-pneumonic effusions were also observed in all age groups
but mean age dropped to 26.6 years. Standard error of the mean was 4.1 while
Standard deviation was.17.57. Malignant effusions were observed mainly from
the third decade of life with mean age=42.14 years, standard error of
mean=1.89, Standard deviation=11.03. Tuberculous effusion were also observed
from the third decade of life with mean age=38.72 years, standard error of
mean=2.8 Standard deviation=15.86
Table 1: Sex distribution
a) General
Sex Freq. Percentage
F 38 44.2%
38
M 48 55.8%
Total 86 100%
General M: F =1.26:1
The commonest presenting symptom observed in all effusions (Table 2)
was shortness of breath (100%) It was associated with cough (96.5%), chest
pain (90.6%), fever (48.8%) and weight loss (58.13%).
Specifically, all the para-pneumonic effusions had breathlessness, cough,
chest pain and fever but only 15.7% had weight loss at presentation. For the
tuberculous effusions, fever and weight loss were observed in 71.8% and 17%
respectively while breathlessness, cough and chest pain were recorded in all.
The malignant effusions recorded breathlessness in all cases, but cough in
94.1%, chest pain in 77.1% and weight loss in 85.7%. No fever was recorded
amongst the malignant effusions as a presenting symptom.
Table 2 : General symptoms at initial presentation
Symptoms Freq. Percentage (%)
Breathlessness 86 100
Cough 83 96.5
Chest pain 78 90.69
Fever 42 48.8
Wt. loss 50 58.13
39
Positive physical signs including reduced chest excursion, dull percussion note on
the affected hemi-thorax, as well as reduced air entry were observed more on the right
side (62.9%) than on the left (32.55%). In 4.6%, it was observed bilaterally (Table 3)
Radiograph appearance including blunting of costo-phrenic angle, opacification of the
hemi-thorax followed a similar pattern to confirm the distribution of the effusions.
Table 3: General signs at initial presentation (Reduced chest excursion, stony
dullness to percussion, reduced air entry)
Signs Freq. Percentage %
Positive on right hemi-
thorax
54 62.79%
Positive on left hemi-thorax 28 32.55%
Positive bilaterally 4 4.6%
Total N=86 100%
Following test aspiration of the effusion the general physical appearance displayed straw
colour in 54.7%, sero-sanguinous in 27.9%, and frankly purulent in 17.4%. Specifically
straw colour was observed more in tuberculous effusion (84.3%) than in para-
pneumonic (36.8%) and malignant (37.1%) effusions. Sero-sanguinous was observed
more in malignant effusions (62.9%) than in para-pneumonic (5.3%) and
tuberculous(3.1%) effusions. Purulent aspirate was mainly seen in para-pneumonic
effusions (57.9%) but was also seen in a few tuberculous cases (12.5%)
40
Clearly outlined in the table 4 is the result of chemical analysis which confirmed
that all surgical effusions were found to be exudative in nature with high protein and
lactate dehydrogenase levels as well as a high specific gravity.
Table 4: Chemical analysis of fluid
Mean values Para-pneumonic Tuberculous Malignant
Specific gravity 1018 1017 1016
Prot. Conc.(g/L) 44 41 40
Glu. Conc.(mg/dl) 30 32 46
LDH 1502 1706 1304
Cholesterol(mg/dl) 148 156 1502
Na+(mg/dl) 139 140 144
K+(mg/dl) 4.0 3.6 3.8
PH 7.1 7.0 7.2
HCO3-(mg/dl) 18 18 21
Para-pneumonic effusions showed marked neutrophil leucocytosis with a mean
value of 18,200. Tuberculous effusions showed relative lymphocytic leucocytosis with a
mean value of 14,700, while malignant effusions did not show any remarkable changes
in leucocytes.
Three was a very low yield of acid-fast bacilli on ZN stain of aspirates of
tuberculous effusion as only two out of thirty two cases yielded positive results (6.2%).
A relatively low yield of bacteria was also recorded on Gram-stain of para-
pneumonic effusions as only five out of nineteen was positive (26%).
Chest tube drainage was performed on all cases studied as the initial procedure.
Additional tetracycline pleurodesis was performed on all cases of malignant effusions to
prevent recurrence, while decortication was performed for six cases that progressed to
empyema thoracis.
As outlined in the table 5, premature dislodgement of tube was the commonest
complication of chest tube drainage observed in this study. It was recorded in 29 out of
41
86(33%) while others such as stoma infection, pneumothorax, and empyema were
equally observed. Of note is a single case of chylothorax which was observed following
decortication.
Table 5:-Complications of Chest Intubation for drainage
Complication Para-pneumonic Tuberculous Malignant
Premature chest tube
dislodgement(Total=29)
5 9 15
Infection in a previously
sterile fluid(Total=9)
_ 2 7
Pneumothorax(Total=8) 2 3 3
Stoma site
infection(Total=19)
11 5 3
Empyema(Total=6) 3 3 _
Post -op
chylothorax(Total=1)
_ 1 _
In terms of outcome of treatment, at one month evaluation, a persisting or rather
recurrent effusion was recorded in 13 out of 35 (37%) of malignant effusions while the
rest 22 out of 35 (62.8%) were cured of their effusions and were in a reasonably good
quality life. At 6 months re-evaluation-Malignant effusion
Of the 13 previously noted with persisting/recurrent effusions at one month
follow–up, three were dead from various cancer complications. Of the surviving ten,
seven (70%) responded to further pleurodesis and enjoyed reasonably good quality life,
while three(30%) still suffered from the disease.
For para-pneumonic effusions, outcome of treatment at 1 month evaluation
revealed that excellent results were recorded in most cases of parapneumonic effusions
as 16 out of 19(84.2%) responded well to treatment. Unfortunately three cases
progressed to empyema.
For tuberculous effusions, evaluation revealed that 25 out of 32 cases(78%)
responded well to treatment at 6 months evaluation, four had persisting/recurrent
effusion while three had further progressed to empyema.
42
Neoplastic disease was by far the commonest primary predisposing condition to pleural
effusion observed in this study followed by pulmonary tuberculosis and pneumonia (Fig
VI)
Fig. vi- Primary pathology
Breast carcinoma was observed to be the commonest mitotic lesion involved in
malignant effusions (66.7%) while others include lung, parotid, intra-abdominal and soft
tissue sarcomas.
Fig. vii- Specific neoplastic cases
43
More than 2/3 of patients studied lived in Abuja and its environs (Fig viii)
Fig. viii- City of residence
Abuja
Others
Abuja - 67 - 81.7%
Others - 19 - 18.3%Total - 86 - 100%
There was a relatively low yield of cancer cells on cytological analysis of aspirated
malignant effusions as only 11 out of 35 were positive (31%). In those with a positive
yield, the photomicrograph below displays a characteristic increased nuclear–cytoplasmic
ratio, hyperchromasia and pleomorphism.
Fig.ix- Photomicrographs of positive cytology pleural effusion with H/E and Leishman
stains-Mag.X200 (courtesy Dr Henry Ewunonu) Histopathology department .National
Hospital Abuja.)
44
CHAPTER FIVE- DISCUSSION
Pleural effusion is an important surgical problem as it accounted for about 5% of all
admissions into the surgical ward during the study period. Results show that it affects all
age groups and sex. This study identified three major categories of effusions of surgical
interest namely parapneumonic, tuberculous and malignant. Occasionally the
parapneumonic and tuberculous progress to empyema if not properly treated. As
general as the statement above might seem, this study showed some group
predilection. For instance, parapneumonic effusions were observed more in the younger
age group, while tuberculous and malignant effusions were observed more in the older
age group. Malignant effusions were also observed more in female sex. The reason is
that carcinoma of the breast which is basically a female gender problem was responsible
for more than two thirds of the malignant effusion. Although carcinoma of the male
breast has been reported it accounts for less than 2% of all breast carcinoma cases83
and not a single case was recorded in this study. All the cases of pleural effusion
observed in children below 10 years were para-pneumonic, a finding which is in line with
previous ones by Anyanwu16 and Edenwor25. This is probably because complicated
pneumonias are commoner in the pediatric age group.
Residents of Abuja and its environs constituted 81.7% of the study population (Fig
viii). This is simply due to proximity to the referral centre.
Generally, dyspnoea was the commonest presenting symptom. The explanation is
that pleural effusion induces restrictive effect on the lungs and alveolar sacs, thus
compromising the pulmonary function. A massive effusion also displaces the
mediastinum to the opposite side, which further compromises cardio-respiratory
functions. Dypnoea is the body’s attempt to compensate and maintain the oxygen
saturation of the blood for effective tissue oxygenation. In addition, carbon dioxide is
not effectively cleared from the compromised lung, resulting in a raised PCO2. This
45
situation over drives the respiratory centre in the medulla and thus manifests as
shortness of breath.
Fever, a constant problem in para-pneumonic effusions, was observed in low grade
in some cases of tuberculous effusions but none in the malignant cases. Fever and chest
pain can be explained by the on-going inflammatory process. As documented by
Herbert27, pleuritic chest pain, fever and cough are the clinical presentation of
empyema, which normally blends with the pneumonic process.
Weight loss was a major problem in the malignant effusions. Cachexia has
been documented as the commonest cause of cancer death. Toxohomone and
cytotoxic polypeptides have been postulated as the cause, although with no clear
evidence yet84. It is also believed that interleukins play a very important role in
cancer cachexia. Chronic empyema is associated with both anaemia and
anorexia, which contribute to the weight loss.
The major physical signs on the chest were reduced chest excursion, stony
dullness to percussion, and reduced air entry to the hemithorax. As noted earlier, right
sided effusion was found to be almost double that of the left in this study. The reason
for this may be related to the anatomical disposition of the right major bronchus as a
direct continuation of the trachea. Furthermore, the predisposing lesions such as lung
malignancy, pulmonary tuberculosis, pneumonia were commoner on the right. Bilateral
cases were due to a diffuse pulmonary pathology such as tuberculosis,
bronchopneumonia, or bilateral dissemination of secondary malignant lesion.
Radiological features were blunting of costo-phrenic angle, opacification of the
hemithorax, and classical meniscus sign in some cases. Radiological confirmation is
mandatory because it helps to plan appropriate treatment. The radiological findings
usually confirmed the clinical suspicion of pleural effusion.
Pleural fluid aspiration is very helpful in initial assessment of physical and
biochemical characteristics of pleural effusions. The physical appearance noted in this
study were straw colour, serosanguinous and purulent. Whereas purulent fluid was
commoner in the para-pneumonic effusions, the straw colored fluid was commoner in
the tuberculous effusions while the sero-sanguinous fluid was commoner in the
malignant effusions.
Physical appearance of pleural fluid however, is not specific and the finding of
straw colored or sero-sanguinous effusion, demands for a more detailed assessment of
the patient and further analysis of the fluid.
46
Mean values for the specific gravity, protein concentration, and LDH were
elevated. This is in keeping with the criteria presented by Light15 for exudative
conditions. The mean glucose concentration of 30mg/dl and 32mg/dl in para-
pneumonic and tuberculous effusions respectively were much lower than that of the
malignant effusions (46mg/dl). Lipid estimation was basically within normal range
except for the lone case of chylothorax complicating thoracotomy for empyema
thoracis, where the triglyceride level was 300mg/dl. Loss of this high volume of
triglycerides in chylothorax is of major nutritional significance. The sodium and
potassium levels were similar to that of serum, while the bicarbonate level of
18mg/dl each in para-pneumonic and tuberculous effusions were slightly more acidic
than the malignant ones which showed an average bicarbonate level of 21mg/dl.
High LDH level, as earlier explained is due to high cellular turnover and lyses which
releases this enzyme into the fluid. Specifically, the mean LDH concentration in
tuberculous effusions (1706IU) was found to be higher than that of para-pneumonic
(1504IU) and the malignant ones (1304IU). The average glucose was 36 mg/dl. This
relatively low level is attributed to the high metabolic activity in the pleural space which
utilizes the available glucose. The low concentration of glucose was noted more
specifically in the para-pneumonic (30mg/dl) and the tuberculous (32mg/dl) ones. The
low PH, averaging 7.1 in this study is also attributed to high metabolic activity and its
products such as lactic acid especially in a relatively anerobic environment of the pleural
fluid. The lowest PH of 7.0 was found in the tuberculous effusions.
Cytological analysis was relevant only in malignant pleural effusion. Positive
results were recorded in only one third of cases. The features of a positive result
were pleomorphic cells with increased nuclear cytoplasmic ratio as well as
nuclear hyperchromicity. There was indeed a low cytology yield in this study
compared to the findings of Erozan 67 whereby initial cytology yield was up to
63%, and rising to 77% in subsequent samples. Perhaps what is important is
that a negative yield could become positive on subsequent sampling and since
false positive cytology almost never occurs according to Hausheer77, it is
therefore possible that a second and even a third sampling could have improved
the yield. Seeding of malignant cells into the pleural fluid is responsible for this
finding.
Cell count confirms lymphocytosis of the pleural fluid which is in keeping with
tuberculous effusion. These are chronic inflammatory cells in contrast to the relative
47
neutrophilia found in para-pneumonic and empyematous effusions.
Acid-Fast Bacilli test was conducted on tuberculous effusions only. It was positive in
only two cases (6.25%). The reason is captured in the pathogenesis which involves
tuberculous pleuritis. This is a hypersensitivity reaction involving the pleural membranes
and capillaries and not due to a direct invasion of the pleura by the mycobacterium. It is
possible that biopsy of the pleural tissue may increase the yield of mycobacterium but
we have not specifically biopsied the pleura in this study.
About a third of the para-pneumonic effusions (26.3%) yielded a positive result on
Gram staining. The high rate of negative Gram-stain in para-pneumonic effusion and
empyema (73.68%) is difficult to explain in this study, but some scholars believe that
self antibiotics medication and abuse before and during presentation, could be
responsible.4
Neoplastic disease was observed to be the commonest cause of pleural effusion
and closely followed by tuberculosis with para-pneumonic cases as least common. That
malignant pleural effusion assumes this position was supported by Leff 60 whose study
showed that malignant pleural effusion accounts for 25% of all cases of pleural effusion
(including medical causes) in a General Hospital setting. Rising incidence of neoplastic
diseases and late presentation is responsible for this. Breast carcinoma stands out as the
commonest cause of malignant pleural effusion in this study contributing 65% of cases
followed by lung cancer and soft tissue sarcoma both contributing. Intra-abdominal
malignancies and parotid carcinoma contributed a little. This is in sharp contrast to the
findings of Hausheer77in United States, where lung carcinoma was the commonest with
35% and breast second commonest with 23%. The rising incidence of smoking and its
direct relationship with lung cancer in their environment and the rising incidence of
breast cancer and late presentation in our environment is probably responsible for this
disparity. It was stated earlier in the review that some investigators report that up to
50% of patients afflicted with cancer will develop malignant pleural effusion sometime
during their disease62.
All cases involved in this study were treated with tube- thoracostomy drainage as
part or all of the treatment required. A sound understanding of the basic principles of
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 spent85. In their five year retrospective study involving 65 patients,
Ekwunife86 affirmed that though tube-thoracostomy is a simple and efficacious
procedure for the treatment of pleural space collection, premature tube dislodgement
48
was the commonest complication observed accounting for 50% of all complications, and
advised that safety of procedure should be improved by adequate training. Various
modifications of this drainage system have been adapted to suit different circumstances.
From Ibadan Nigeria, Adebo87 reported that their preferred method of chest drainage
consists of insertion under local anesthesia of the tubular end of an Aldon’s Urobag
equivalent to number 34 Argyle chest tube, beveled, fenestrated and placed within the
fifth or sixth intercostal space in the mid–axillary line. Similar studies in the past had
confirmed the efficacy of this system in the evacuation of fluid from the pleural space88.
Tube-thoracostomy/underwater seal drainage system was pivotal in the treatment of
these cases and proved to be quite reliable in the relief of symptoms, consequently all
the patients benefited from it. In-fact 84.2% of all the para-pneumonic effusions needed
no further treatment except antibiotics. A recognized sequel of untreated or
unresponsive parapneumonic and tuberculous effusions is empyema thoracis. Indeed,
three cases each progressed to empyema thoracis at one month evaluation in this study.
For tuberculous effusions, standard anti-tuberculous drugs include 600mg rifampicin