TRANSUDATIVE PLEURAL EFFUSION
Dr.Naresh Kumar
Junior Resident
Dept. of Pulmonary Medicine
TYPES OF PLEURAL EFFUSION
• 1 EXUDATIVE
• 2 TRANSUDATIVE
TRANSUDATIVE PLEURAL EFFUSION
• Transudative pleural effusion are defined as
effusion that are caused by systemic factors
that alter the pleural equilibrium or starling
forces
• Components of starling forces :
-Hydrostatic pressure
- Permeability
- Oncotic pressure
CAUSES OF TRANSUDATIVE PLEURAL
EFFUSION
Common causes
Generalized salt and water retention
• Congestive heart failure
• Nephrotic syndrome
Ascites
• Cirrhosis
• Peritoneal dialysis
Other Causes
• Myxedema
• Hypoalbuminemia
• Urinothorax
• CSF leakage
• obstruction of brachiocephalic vein
• Pulmonary veno-occlusive disease
•
Fontan procedure
•
Glomerulonephritis
Characteristics of Transudative
Pleural fluid
•
•
•
•
•
•
Straw coloured
Non Viscous
Odorless
WBC < 1000 mononuclear predominant
Sugar > 60 mg/dl (except urinothorax )
Ph 7.45-7.55
Light’s criteria
Light's criteria are nearly 100 percent sensitive at
identifying exudates
but approximately 20 percent of patients with pleural
effusion caused by heart failure may fulfill the criteria for
an exudative effusion after receiving diuretics
In these circumstances, the pleural effusion is
transudative if :
– the difference between protein levels in the serum and the
pleural fluid is greater than 3.1 g/dL
– A serum-effusion albumin gradient greater than 1.2 g/dL
CONGESTIVE HEART FAILURE
• Most common cause of Transudative pleural
effusion
• CHF accounts for 90 percent of transudative
effusion
• Usually small ,bilateral effusion
• Unilateral effusion can occur ( 12 percent )
• More on right side by ratio of 2:1
PATHOPHYSIOLOGY
CHF
Pleural effusion
Fluid moves from the pulmonary
interstitial spaces across the
visceral pleura into pleural space
Increased Pressure in
pulmonary capillaries
Increased amount of fluid enter
the interstitial spaces of lung
Increased interstitial pressure
in subpleural interstitial spaces
Signs and symptoms
• H/O Increasing dyspnea on exertion
• Increase in peripheral edema
• Orthopnea or paroxysmal nocturnal
dyspnea
•
: Dyspnea is frequently out of propotion
to the size of effusion
• Signs of both r/l side heart failure
• Signs of pleural effusion
CHEST XRAY
• Cardiomegaly and
usually b/l pleural
effusion
DIAGNOSIS
If patient has
• Cardiomegaly
• b/l pleural effusion
• Afebrile
• No pleuritic chest pain
• No need for thoracentesis
• Treatment of CHF is started and observe the
patient to determine whether the fluid is
reabsorbed
INDICATIONS FOR THORACENTESIS
•
•
•
•
Effusions are not b/l and comparably sized
Pleural chest pain
Febrile
Effusions do not rapidly disappear after
starting treatment of CHF
EFFECT OF THORACENTESIS IN CHF
• Between the first and third thoracentesis , the
mean protein level increased from 2.3 to 3.5
gm/dl
• and the mean lactate dehyrogenase level
increased from 176 to 262 IU/l
PRO BRAIN NATRIURATIC PEPTIDE
• It based on ,when the ventricles are subjected to
increased pressure or volume ,BNP
is released
• Biologically active BNP and larger amino terminal
part N terminal probrain netriuratic peptide ( NTProBNP) are released in equimolar amounts in
circulation
PLEURAL FLUID (NT-ProBNP)
• Levels below 100 pg/ml  CHF unlikely
• Levels above 1500 pg/ml  Diagnostic of CHF
TREATMENT
Aims of treatment
• Decrease the venous hypertension
• Control of heart failure
• Treat heart failure with digitalis,diuretics
• Therapeutic thoracentesis indicated in patient’s
with heart failure and large pleural effusion
refractory to treatment
• In rare cases , pleurodesis with minocycline or
tetracycline will be helpful.
NEPHROTIC SYNDROME
• Nephrotic syndrome is a triad of proteinuria ,
hypoalbuminemia and edema
• It is a non specific disorder in which the kidneys are
damaged ,causing them to leak large amounts of
protein (proteinuria at least 3.5 gm/day /1.7mtsquare
body surface area ) from the blood into the urine.
• Pleural effusion due to nephritoc syndrome are usually
b/l and are frequently infrapulmonary in location
• Pleural effusion occur in 1/5th of cases
• Pleural effusion often associated with peripheral
edema.
Pathophysiology
Pleural effusion in nephrotic syndrome is due to
combination of :
• Decrease plasma oncotic pressure (because of
protein loss)
• Increase hydrostatic pressure (because of salt and
water overload
• Thromboembolic episodes of pulmonary vessels
due to increase renal vein thrombosis or due to
protein S deficiency may be another cause of
pleural effusion
Investigations
Diagnostic thoracentesis 
Should be perform to ascertain that
the pleural fluid is transudate
Lung scan or ct angiography should be done to
rule out pulmonary embolism
Treatment
Aims of Rx
• Decreasing the protein loss in urine to increase the plasma
protein
• Decrease the increased extra cellular volume
Rx
• Diuretics
• Low sodium diet
• ACE inhibitors
• Serial therapeutic thoracentesis should not be performed
because they only further deplete the protein stores
HYPOALBUMINEMIA
• Albumin ,the body’s predominant serum
binding protein ,comprises 75-80 percent of
normal plasma colloid oncotic pressure and 50
percent of protein content
• Hypoalbuminemia caused by various
conditions including nephrotic syndrome
,hepatic cirrhosis ,heart failure & malnutrition
• According to starling equation hypoalbuminemia would
decrease the oncotic pressure of the blood and increase
the rate of pleural fluid formation
• But study done in patients with different serum albumin
levels , no significant difference of plasma oncotic pressure
between patients with or without pleural effusion
• Thus ,hypoalbuminemia is an uncommon cause of pleural
effusion
• The recognition of pleural effusion in patients of low serum
albumin levels should prompt careful clinical evalution to
identify the other potential causes for effusion .
CIRRHOSIS
• Incidence of pleural effusion in cirrhosis of liver
about 6 percent
• Pleural effusion usually occur only when ascitic
fluid is present
• Pleural effusion in patients with cirrhosis and
ascitis usually right sided (67 percent) left sided
(16 percent )and b/l in (16 percent)
• Right side is more involved because the right
hemidiaphragm is more likely to have
embryological developmental defects
Pathophysiology
• Pleural effusion occur due to movement of the
ascitic fluid from the peritoneal cavity into the
pleural cavity
• In patients with tense ascitis and increased
intra abdominal pressure, the diaphragm may
be stretched ,causing microscopic defects, the
increased hydrostatic pressure in the ascitic
fluid results in one way transfer of fluid from
the peritoneal to the pleural cavity
Diagnosis
• Both paracentesis and thoracentesis should be performed
to ascertain that the ascitis and pleural fluid are compatible
with the diagnosis and do not have high
polymorphonuclear cell counts
• Pleural fluid protein level is usually higher than the ascitic
fluid protein level but is still below 3gm/dl &the pleural
fluid LDH level is low
• Occasionally blood tinged or frankly bloody pleural fluid is
not much significant because it may occurs due to the
patients poor coagulation status
• Amylase level should be determine & cytological
examination performed on both fluid specimens to rule out
pancreatic ascitis or malignant disease .
• In patients with cirrhosis, ascites, and pleural effusion there
is possibility of spontaneous pleural infection, which is
analogous to the spontaneous bacterial peritonitis
• Spontaneous bacterial peritonitis diagnosed if they have
cirrhosis along with a positive bacterial culture of the
pleural fluid and a neutrophil count greater than 250
cells/mm3 or a negative culture and a neutrophil count
greater than 500 cells/mm3.
• Patients with spontaneous bacterial pleuritis have worse
liver disease
• The treatment of choice is an antibiotic to which the
cultured bacteria are susceptible.
• Tube thoracostomy is usually not indicated
Treatment
• The management of pleural effusions associated with cirrhosis and
ascites should be directed toward treatment of the ascites because
the hydrothorax is an extension of the peritoneal fluid.
• The patient should be put on a low-salt diet, and diuretics should be
given.
• The best diuretic therapy appears to be the combination of
furosemide and spironolactone.
• The initial starting dose is 40 mg of furosemide and 100 mg of
spironolactone.
• The doses can be increased up to 160 mg of furosemide and 400
mg of spironolactone daily.
• Serial therapeutic thoracenteses are not indicated because the
pleural fluid rapidly reaccumulates.
Other treatment options
• Liver transplantation patients refractory to salt
restriction and diuretics and remain symptomatic from
the presence of the large pleural effusion.
• Transjugular intrahepatic portal systemic shunt (tips).
• Shunt are frequently ineffective because of the
pressure differences between the peritoneal cavity, the
pleural space, and the systemic veins. Because the
pleural pressure is less than the central venous
pressure, fluid will preferentially move to the pleural
space rather than to the central veins.
• Video-thoracoscopy with closure of the diaphragmatic
defects and pleurodesis
Peritoneal Dialysis
• Peritoneal dialysis is a well established means
of renal replacement therapy.
• Hydrothorax mostly on right side is a well
known complication of peritoneal dialysis
• It is observed in approximately 2 percent of all
peritoneal dialysis patients
• Pleural effusions can result from CAPD by the
movement of the dialysate from the peritoneal cavity
into the pleural cavity through a mechanism similar to
that of cirrhosis and ascites.
• The effusion developed within 30 days of initiating the
dialysis in 50% of the patients, but 18% had been on
dialysis for more than a year before the effusion
developed.
• The pleural effusion occurs on the right side
approximately 90% of the time, but it can be bilateral
or left sided.
Diagnosis :
• Pleural fluid have glucose level intermediate
between that of the dialysate and the serum.
• Protein level below 3 g/dl
• low LDH level (<100 IU/L) which is higher than
that in the ascitic fluid.
Treatment :
• Dialysis must be stopped
• Dialysis should be stopped for 2 to 6 weeks
• 50 percent of patients have resolution of
hydrothorax after temporary cessation of PD
for 2 – 6 weeks.
Other treatment options :
• Pleurodesis :
It should be done if there is recurrence after
temporary cessation of PD.
• VATS
Diaphrgm can be examined for areas of
leaking and can be clipped.
MYXEDEMA
• Mxedema rarely presented by pleural effusion
• Myxematous pleural effusion is more frequent in women
• The cause of myxematous pleural effusion is increased
capillary permeability with leakage of plasma proteins
• Isolateral pleural effusion secondary to hypothyriodism can
be either an exudate or a transudate
• The diagnosis of myxedema should always be considered in
older patients with pleural effusion when there are no
pathognomic findings
Treatment : effusions are resistant to treatment with digitalis
and diuretics but disappear after treatment with thyroid
harmone therapy
URINOTHORAX
• Pleural fluid that accumulate due to
retroperitoneal leakage secondary to urinary
obstruction , trauma ,retroperitoneal
inflammation,malignancy ,failed nephrostomy
or kidney biopsy is called urinothorax
• This is rare cause of pleural effusion
• Pleural effusion develop within hours of the
precipitating event and disappears rapidly
once the obstruction is relived
Diagnosis :
• Pleural fluid looks and smells like urine
• Protein level < 1 gm/dl
• LDH level high
• pH below 7.2 but can be normal
• Glucose can be normal or reduced
Conformation of the diagnosis can be obtained with
simultaneous measurements of pleural fluid and serum creatinine
levels
• Pleural fluid creatinine has been greater than the serum creatinine
in all cases of urinothorax
• Ratio higher than 1 and in most cases greater than 10
Brachiocephalic Vein obstruction
• Obstruction of the brachiocephalic vein can
lead to a pleural effusion.
• Causes :
– intrathoracic goiter
– thrombosis of the vein due to a central venous
catheter
– hemodialysis catheter
– pleural fluid is borderline transudate.
CSF leakage
• Rare cause of pleural effusion.
• Causes :
– Ventriculopleural shunting,
– Trauma
• Diagnosis :
– fluid is clear and colorless
– protein level is very low.
– Measurement of the pleural fluid b2 transferrin.
• Diagnosis can be made by radionuclide
cisternography.
Pulmonary Veno-Occlusive Disease
• Rare disease
• Characterized pathologically by evidence of
repeated pulmonary venous thrombosis.
• The characteristic histologic feature of
pulmonary veno-occlusive disease is
obstruction of pulmonary venules and veins
by intimal fibrosis; intravascular fibrous septa
are nearly always present.
• The etiology of this disease is unknown.
Mechanism :
• Increased interstitial fluid that results from obstruction of the
pulmonary veins
Sign and symptoms :
• Slowly progressive dyspnea and orthopnaea
• Signs of pulmonary hypertension
• Pleural effusion in a patient with pulmonary hypertension is
suggestive of the diagnosis of pulmonary veno-occlusive disease
Diagnosis :
• Pulmonary veno-occlusive disease can be definitively diagnosed by
surgical lung biopsy.
Treatment :
• lung transplantation
Fontan Procedure
• In Fontan procedure, the right ventricle is
bypassed by an anastomosis between the
superior vena cava, the right atrium, or the
inferior vena cava and the pulmonary artery.
• The procedure is typically performed for
tricuspid atresia or univentricular heart.
• Pleural effusion is a significant problem after
the Fontan procedure.
• The pathogenesis of the formation of the large
amounts of pleural fluid postoperatively in
these patients is not definitely known.
• It is probably related to the increased systemic
venous pressure.
Characteristic of pleural fluid :
• Pleural fluid is transudate
• Pleural fluid reveals primarily lymphocytes.
Rx :
• Diuretics
• Fluid restriction
• Ace inhibitors
• Low fat diet
• Oxygen
Other treatment options :
• Pleuroperitoneal shunt
• Pleurodesis
• Ligation of thoracic duct