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OJHAS Vol. 10, Issue 4:
(Oct-Dec 2011) |
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Explosive
Pleuritis |
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Satish Kumar, Senior
Resident,
NM Sharath Babu, Junior
Resident,
Madan
Kaushik, Assistant Professor,
BS Verma, Associate
Professor,
SS Kaushal, Professor,
Dept.
of Medicine, Indira Gandhi Medical College,
Shimla, Himachal Pradesh, India. |
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Address for Correspondence |
Senior Resident,
Dept.
of Medicine,
Indira Gandhi Medical College,
Shimla, Himachal Pradesh, India.
E-mail:
docsatishkumar@gmail.com |
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Kumar S, Sharath Babu NM, Kaushik M, Verma BS, Kaushal SS. Explosive
Pleuritis. Online J Health Allied Scs.
2011;10(4):12 |
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Submitted: Dec 30, 2011; Accepted: Jan
6, 2012; Published: Jan 15, 2012 |
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| Abstract: |
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Pleural effusions associated
with pneumonia (parapneumonic effusions) are one of the most common
causes of exudative pleural effusions in the world. Approximately 20
to 40% of patients hospitalized with pneumonia will have an accompanying
pleural effusion. The term 'Explosive pleuritis' was originally described by Braman
and Donat in 1986 as pleural effusions developing within
hours of admission. We report a 38 years old male patient with minimal
pleural effusion which progressed rapidly within one day to involve
almost whole of the hemithorax. There were multiple loculations on ultrasonography
of thorax. Pleural fluid was sero-sanguinous and revealed gram positive
diplococcic. The patient improved with antibiotics and pigtail catheter
drainage.
Key Words:
Explosive pleuritis; Hemithorax; Loculated; Pigtail catheter.
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Pleural effusion, the
result of accumulation of fluid in the pleural space, is a common medical
problem. The term 'Explosive pleuritis' was originally described by
Braman and Donat1 in 1986 as pleural effusions developing
within hours of admission. It is the rapid development of pleural effusion
involving more than 90% of the hemithorax. We report a 38 years old male
patient with minimal pleural effusion which progressed rapidly within
one day to involve almost whole of the hemithorax with multiple septations
and required catheter drainage in addition to medical therapy. This
condition is rare and an early diagnosis and immediate treatment is
essential to reduce morbidity and mortality.
A 38 years male patient from shimla presented in medicine OPD with high
grade fever of 2 days duration and pain right side of chest and dyspnea
for one day. He was smoker and labourer by profession. Past history was
unremarkable. On examination, he was febrile and had dullness and decreased
breath sounds on right infra scapular area. Chest roentgenogram revealed
haziness over right lower zone and blunt right costo-phrenic angle (Fig.1).
The patient was started on oral amoxicillin-clavulanic acid and was
advised pleural fluid analysis. The patient did not come for pleural
tap and landed up in casualty the next day with marked dyspnea and high
grade fever. On clinical examination patient was febrile and had respiratory
distress. Chest examination revealed massive pleural effusion on right
side. Chest roentgenogram revealed homogenous opacity involving more
than 90% of right hemithorax (Fig.2).
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Figure 1: Chest X ray
PA view on day 1 showing haziness right lower zone with blunt right
CP angle
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Figure 2: Chest X ray
PA view on day 3 showing homogenous opacity involving more than 90%
of right hemithorax.
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Pleural tap was done but only
50ml of sero-sanguinous fluid could be tapped. Ultrasonography thorax
was suggestive of multiple septations in pleural effusion. Pig tail
catheterization was done under ultrasonographic guidance and fibrinolytic
therapy with streptokinase was injected through the catheter and sero-sanguinous
fluid was drained. CT thorax after 2 days revealed loculated right
pleural effusion with mediastinal lymph node (8.4mm) with alveolitis
right lung field (Fig.3). On detailed work up, investigations revealed:
Pleural fluid: ADA- 24.8U/L, Cytology- 180 WBC (N-70%, L-30%) second
time repeated pleural fluid analysis revealed 480 cells mostly neutrophils,
protein- 5.2mg%, culture - sterile, Gram stain- gram positive diplococci, AFB- negative, glucose- 39.4mg/dl(40-60), LDH- 1963u/l
(more than 3
times serum LDH value of 448.7). Haemogram: TLC- 16050/cmm, Polymorphs 84%,
lymphocytes 15%,(repeated after 5 days of treatment - 11810/cmm with P-80%,L-19%),
Hemoglobin - 12.1g%, Platelets- 209000/cmm, ESR- 50mm 1st
hour. Biochemistry: Random blood sugar – 101mg%, Urea-36mg/dl,
creatinine- 1.0mg/dl, sodium- 137meq, potassium- 4.5meq, chloride- 101meq.
Liver function tests were normal. Blood culture was sterile. No organisms
were detected on gram staining of sputum, sputum culture was sterile
and it was negative for AFB. On these evidences it was diagnosed to
be a case of explosive pleuritis probably caused by streptococcal infection.
Patient was started with injectable amoxicillin-clavulanic acid and
levofloxacin was added. After streptokinase fibrinolysis about 500-700
ml of sero-sanguinous pleural fluid was drained daily for 5 days, later
the volume gradually decreased (fig.4). The pigtail catheter was removed
and the patient was discharged on 14th day with advice
to follow up.
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Figure 3: CT Thorax showing
pleural effusion with loculations and septations on the right side (after
pig tail catheter drainage).
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Figure 4: Chest X ray
on day 7 after pig tail catheter drainage of right pleural effusion.
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Pleural effusions associated
with pneumonia (parapneumonic effusions) are one of the most common
causes of exudative pleural effusions in the world. Approximately
20 to 40% of patients hospitalized with pneumonia will have an accompanying
pleural effusion.2 The term 'Explosive pleuritis' was originally
described by Braman and Donat1 in 1986 as pleural effusions
developing within hours of admission. In their original article, clinical
and roentgenographic evidence for two cases of explosive pleuritis caused
by group A beta-hemolytic streptococci, in the absence of bronchopneumonia,
were presented .They proposed that the pathogenesis of explosive pleuritis
relates to the observation that streptococcal infections have a unique
propensity to cause blockage of the peribronchial and subpleural lymphatics
with cellular and necrotic debris.1 Jasdeep K Sharma et al3
in their article defined explosive pleuritis as the rapid development
of pleural effusion involving more than 90% of the hemithorax within
24 hours, causing the compression of pulmonary tissue and a mediastinal
shift to the contra lateral side.
The bacteriology
of pleural infection differs somewhat from that of pneumonia. In one
study of 434 patients with pleural infection, of whom nearly 60% achieved
a microbiological diagnosis using standard conventional methods, the
most prevalent organisms cultured in community-acquired pleural infections
were streptococcal species (Streptococcus milleri [32%], Streptococcus pneumoniae
[13%], other streptococci [7%]) followed by anaerobes (16%) and staphylococci
(11%).4 More than 40% of patients with pleural effusion do
not ever have a positive bacterial culture. This may be partly dependent
on the use of antibiotics prior to pleural fluid sampling and the care
with which the sample is handled and cultured, On the other hand, blood
cultures are positive in only a few cases of pleural infection (12%).5
IIn our patient, bacteriological
diagnosis could not be achieved as both blood culture and pleural
fluid culture samples were taken after antibiotics were started. Though there were gram positive diplococci in the pleural fluid
smears and serum LDH levels were markedly raised.
The organisms implicated
in explosive pleuritis include the broad spectrum of organisms responsible
for major causes of pulmonary infection. These include gram-positive
cocci such as Streptococcus pneumoniae, Streptococcus pyrogenes and other
streptococci and staphylococci. Gram- negative cocci such as Neisseria
meningitides and Moraxella catarrhalis are also included.3
Laboratory results may reveal elevated polymorphonuclear leucocytes.
There is a four fold rise in ASO (antistreptolysin-O) titres over
several weeks or a single titre of more than 250 Todd units. Our patient
had leucocytosis but ASO titres could not be obtained as it was not
being done currently in the hospital. The clinical presentation and
physical findings in our patient were consistent with variable degrees
of respiratory distress and respiratory system findings of pleural effusion
as described by Jasdeep k Sharma et al3 in their patient
having explosive pleuritis.
In streptococcal pneumonia
there is a high frequency of pleurisy and pleural effusion that rapidly
progresses to loculated empyema called explosive pleuritis.6
This process can occur over a period of hours. Similar picture was there
in our patient and the pleural effusion rapidly progressed in about
24 hours. Pathologically severe sero-sanguinous pleural effusion, hemorrhagic
edema of the lung and dilated lymphatics in the interlobular septa are
present.6 The fluid drained in our patient was also sero-sanguinous
and exudative.
The diagnosis and
treatment of this condition make thoracotomy essential. Thoracentesis
alone is ineffective. Although rapidly developing pleural effusions
are best treated by early chest tube drainage because of a tendency
toward early loculation, it is not unusual to have only minimal fluid
drained from the pleural space.7 In our patient also only
a small amount of fluid could be aspirated initially. It is only after
pigtail catheter drainage the fluid could be drained. In addition the
antibiotics (amoxicillin-clavulanic acid and levofloxacin) were started
and the patient improved with the combined treatment.
In a trial by Nicholas
A. Maskellet al8, intrapleural streptokinase had a modest
adverse-event profile in patients with pleural infection but was ineffective
in reducing mortality, the need for surgical drainage, or the length
of the hospital stay. Studies conducted earlier had established that
fibrinolytic agents do lead to macroscopically effective in vivo lysis
of intrapleural fibrin adhesions9and reduce the volume of
infected pleural-fluid collections. Thus, there may still be a role
for fibrinolytic agents in treating the small subgroup of patients who
have an exceptionally large, loculated collection of pleural fluid that
causes substantial dyspnea, hypoxemia, or hypercapnia by the mechanical
impairment of lung function.8 In our patient also the pleural
fluid drainage increased substantially after streptokinase was injected
in the pleural cavity and patient had marked symptom relief.
Our patient had clinical
deterioration over a short period of time (about 24 hours) and
rapid progression of radiological findings characteristic of explosive
pleuritis though we could not arrive at a bacteriological diagnosis.
The condition should be treated as a medical emergency and the patients
usually require surgical intervention in addition to medical therapy.
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Braman SS, Donat WE.
Explosive pleuritis. Am J Med.1986;81:723-726.
- Light RW. Pleural Diseases.
Fifth Edition. Lippincott, Williams and Wilkins, Baltimore. 2007.
- Sharma JK, Marrie TJ.
Explosive pleuritis. Can J Infect Dis. 2001 Mar-Apr;12(2):104–107.
- Maskell NA, Batt S, Hedley
EL, Davies CW, Gillespie SH, Davies RJ. The bacteriology of pleural infection
by genetic and standard methods and its mortality significance. Am. J
Respir Crit Care Med. 2006;174:817-823
- Foster S, Maskell N.
Bacteriology of complicated parapneumonic effusions. Curr Opin Pulm Med.2007;13:319-323
- Johnson JL. Pleurisy, Fever
and rapidly progressive pleural effusion in a healthy 29 year old physician.
Chest 2001;119;1266-1269.
- Thomas DF, Glass JL, Baisch
BF. Management of streptococcal empyema. Ann Thorac Surg
1966;2;658-664.
- Maskell NA. U.K. Controlled
Trial of Intrapleural Streptokinase for Pleural Infection. N Engl J Med
2005;352:865-874.
- Maskell NA, Gleeson FV.
Effect of intrapleural streptokinase on a loculated malignant pleural
effusion. N Engl J Med 2003; 348:e4-e4
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