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4.2. Resultados de las encuestas y entrevistas

4.2.6. Encuesta dirigida a estudiantes

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-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

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.

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

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.

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.

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.

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

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

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

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.

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

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

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

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.

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1. Jan Langman, Formation of body cavities and

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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

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

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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:

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