CASE REPORT

PIOPNEUMOTHORAX


Created By :
Nicky C Hasyimzoem, S.Ked
Mutia A Maharani, S.Ked
Octaria Anggraini, S.Ked



Perceptor:
Dr. DEDY ZAIRUS, Sp.P



CLINICAL WORK OF INTERNAL MEDICINE, SMF. PULMONOLOGY
OCTOBER 2013
ABDUL MOELOEK HOSPITAL, BANDAR LAMPUNG
SECTION 1
st

The history taking and physical examination were done on August 16
th

2013 in Pulmonary Ward (Melati) Dr. Hi. Abdul Moeloek General Hospital,
Bandar Lampung.

Identification of Patient
Name : Mr. R
Age : 36
Gender : Male
Address : Pidada Panjang, Bandar Lampung
Profesion : Entrepreneur
Education : Senior High School
Marriage status : Mariage
Religion : Moslem
Admission date : October 4
th
2013

History
Anamnesis : Autoanamnesa
Chief Complaint : Shortness of breath
Secondary Complaint : chest pain, cough

History of Present Illness :
Os came with complaints of left chest pain through to the back and
abdomen, accompanied by shortness, and productive cough. Chest pain
felt since 2 months before entering the hospital but patients do not care
and continued to work. Os feel chest pain severe increasingly since 2
days. Os feel nauseous and he vomit since 2 days before entering the
hospital. Os complained of shortness. Tightness is felt if he in activity. He
can not work as usual. Tightness has been felt since 2 days before entering
the hospital. Tightness is reduced when at rest but he was still difficult to
breathe. Os also complained of productive cough, cough has been felt
since first week before entering the hospital. Cough is persistent with
sputum and the colour is yellowish, now he is not cough anymore. He did
not notice any wheezing or weird breath sounds. He also said that he
never been sweaty night, low appetite, and weight loss. Him weight is
same with he has illness. Os came to the clinic and recommended to get x-
rays examination . X-rays examination results illustrated there was fluid in
the lungs. Os has a history of intermittent fever and the fever still common
when taking the stall medicine. Os did not has a long cough history. Os did
not has a history of ATD (Anti Tuberculosis Drug). Os did not has a history
of dibetes melitus. Os did not has a history of hypertension.
History of Past Illness
Os has a history of intermittent fever and the fever still common
when taking the stall medicine. Patient has not diabetes Melitus. He
never had asthma or severe breathlessness before, and never had
traumatic in chest.

History of Family Illness
There was no family member who diagnosed as tuberculosis, or
having wet cough more than 2 weeks.

Lifestyle and Activity
The patient was not an active smoker. The patient is a rubber
farmer, and still able to do his work before the worsening of his
breathlessness.
Physical Examination
General appearance : Moderate ill
Consciousness : Compos mentis, E4V5M6
Average weight (kg) : 65 kg
Height (cm) : 170 cm
Present weight (kg) : 63 kg
BMI : 22,49 kg/m
2

Blood Pressure : 110/70 mmHg
Pulse : 74 bpm , regular
Temperature : 38.7
0
C
Respiration Rate : 36 x/minute

Head : Normocephali, atraumatic, normal hair
distribution, hair not easily revoked
Eye : isochor pupils, anemic conjuctiva +/+, icteric
sclera -/-
visual field intact,
Nose : Symmetrical, septum deviation (-), discharge (-),
concha oedem (-)
Mouth : caries , stomatitis (-)
Throat : tonsil T1-T1 calm, hyperemis pharing (-)
Neck : thyroid gland normal size, lymph nodes not
palable, deviation of trachea (-)

Thorax
Lung
Inspection : asymmetrical shape, asymetrical
chest movement, decreased left hemithorax
movement, accessory muscle use (-),
Palpation : absent vocal fremitus on the left
hemithorax, no tenderness.
Percussion : hypersonor on left hemithorax
Auscultation : absent breathe sounds of the left
hemithorax, vesicular breath sound on the right
hemithorax. Wheezing (-), Crackles (+).

Cor
Inspection : ictus cordis is not visible
Palpation : ictus cordis is palpable in the 4
th

ICS of left Mid clavicula.
Percussion :
Right boundary : ICS V linea parasternal dextra
Left boundary : ICS V linea midclavicula sinistra
Upper limit : ICS III linea parasternal sinistra

Auscultation : S1/S2 heart sounds, regular ,
murmur (-), gallop(-)
Abdomen
Inspection : abdomen flat, no tension, no dilated
veins
Palpation : no percussion pain, no defense
muscular, no enlarged liver
Percussion : timpanic, percussion pain (-), shifting
dullness (-)
Auscultation : bowel movement (+), normal

Extemity : warm , oedem regio dorsum pedis dextra et
sinistra (+), oedem regio antebrachii dextra (+), cyanosis (-)

Laboratory and Imaging (RSAM July 23
rd
2013)

Hb 14.0 g/dl (N : 13,5-18 gr% )
ESR 40 mm/jam (N : 0-10 mm/jam)
Leucocyte 96.000/ml (N : 4500-10.700)
Diff count 0/0/0/60/34/6 (N : 0-1/ 1-3/2-6/50-70/20-40/2-
8)
Trombocyte 460.000 /ul (N : 150.000-400.000/ul)

Chemical Blood
OT/PT 19/23 ul (N : 6-30/6-45 ul)
Ureum 19 u/l (N : 10-40 u/l)
Creatinin 23 u/l (N : 0,7-1,3 u/l)
GDS 151 mg/dl (N : 70-200 mg/dl)



WSD fluid : types of discharge is seroxantochrome fluid (Pus)
undulations +, bubbles +


Bacterioligy Culture Test (October 10
th
2013)

Kind of examination : Resistensi Test / Kultur
Sample : Pus
Result : The result of bactery culture found gram-negative
rods bacteria (Alkaligenes Sp)


Sensitivity Test :

Postero-anterior chest Roentgen ( July 8
th
2013)










Conclusion : Hidropneumothoraks dextra with
colaps in right lung field
Interpretation :

Bones and joints (clavicula, scapula,
costae, vertebrae) are intact
Trachea deviasi (-)
Avascular and hyperluscent area in
left lung field
Blunting of right costophrenic angle
(air fluid level form)
Invisible infiltrat in left lung field
Size of cor is normal
RESUME
Os came with complaints of left chest pain through to the back and abdomen,
accompanied by shortness, and productive cough. Chest pain felt since 2 months
before entering the hospital but patients do not care and continued to work. Os
feel chest pain severe increasingly since 2 days. Os feel nauseous and he vomit
since 2 days before entering the hospital. Os complained of shortness. Tightness is
felt if he in activity. He can not work as usual. Tightness has been felt since 2 days
before entering the hospital. Tightness is reduced when at rest but he was still
difficult to breathe. Os also complained of productive cough, cough has been felt
since first week before entering the hospital. Cough is persistent with sputum and
the colour is yellowish, now he is not cough anymore. He did not notice any
wheezing or weird breath sounds. He also said that he never been sweaty night,
low appetite, and weight loss. Him weight is same with he has illness. Os came to
the clinic and recommended to get x-rays examination . X-rays examination results
illustrated there was fluid in the lungs. Os has a history of intermittent fever and
the fever still common when taking the stall medicine. Os did not has a long cough
history. Os did not has a history of ATD (Anti Tuberculosis Drug). Os did not has a
history of dibetes melitus. Os did not has a history of hypertension.

Physical examination revealed the patient looks ill but not
in acute distress, compos mentis, Pulse 74 bpm, regular,
Temperature 38.7
0
C, Respiration Rate 36 x/minute, BMI
22,49 kg/m
2
, Ananemic conjunctiva +/+. Chest examination
revealed WSD tube inserted into fifth intercostal space, left
axillary line. Decreased left side thoracic expansion and
absent breath sound on the left side. Laboratory findings
revealed mild anemia (Hb 14 g/dl), total leucocyte count of
26.000. The posteroanterior chest x ray revealed a left
pneumothorax with left lung infiltrat.

From WSD fluid we found secret like pus, and the result of
bactery culture found gram-negative rods bacteria
(Alkaligenes Sp)

Diagnosis
Piopneumothoraks

Treatment
O2 2 Litres/minute
IVFD RL gtt X/minute
Ceftriaxone 1 g/ 12 hours (IV)
Metronidazol / 12 hours (IV)
Ambroxol sirup 3x1C
Observe the development of WSD till the undulations and
Bubble negative
Chest X-Ray if the lug re-expands, then off WSD

Prognosis
Quo ad vitam : dubia
Quo ad functionam : dubia
Quo ad sanationam : dubia ad bonam

Recommended Examination
Lipid profile, uric acid serum
ECG
Acid-resistant bacteria
Sitology bacteria
SECTION 2
nd

REFERENCE
A. PLEURAL EFFUSION

1.1 Etiology
Although the etiologic spectrum of pleural
effusion is extensive, most pleural effusions
are caused by congestive heart failure,
pneumonia, malignancy, or pulmonary
embolism.


The following mechanisms play a role in the formation of
pleural effusion:

Altered permeability of the pleural membranes (eg, inflammation,
malignancy,pulmonary embolus)
Reduction in intravascular oncotic pressure (eg, hypoalbuminemia, cirrhosis)
Increased capillary permeability or vascular disruption (eg, trauma, malignancy,
inflammation, infection, pulmonary infarction, drug hypersensitivity,
uremia, pancreatitis)
Increased capillary hydrostatic pressure in the systemic and/or pulmonary
circulation (eg, congestive heart failure, superior vena cava syndrome)
Reduction of pressure in the pleural space, preventing full lung expansion (eg,
extensive atelectasis, mesothelioma)
Decreased lymphatic drainage or complete blockage, including thoracic duct
obstruction or rupture (eg, malignancy, trauma)
Increased peritoneal fluid, with migration across the diaphragm via the lymphatics
or structural defect (eg, cirrhosis, peritoneal dialysis)
Movement of fluid from pulmonary edema across the visceral pleura
Persistent increase in pleural fluid oncotic pressure from an existing pleural
effusion, causing further fluid accumulation

Pleural effusions are generally classified as
transudates or exudates, based on the
mechanism of fluid formation and pleural fluid
chemistry.
Transudates result from an imbalance in oncotic and
hydrostatic pressures, whereas
exudates are the result of inflammation of the pleura
or decreased lymphatic drainage.
In some cases, the pleural fluid may have a
combination of transudative and exudative
characteristics.

1.2 Clinical Presentation
A detailed medical history should be obtained from all
patients presenting with a pleural effusion, as this may
help to establish the etiology.

For example, a history of chronic hepatitis or alcoholism
with cirrhosis suggests hepatic hydrothorax or alcohol-
induced pancreatitis with effusion.
Recent trauma or surgery to the thoracic spine raises the
possibility of a CSF leak.
The patient should be asked about a history of cancer,
even remote, as malignant pleural effusions can develop
many years after initial diagnosis.
An occupational history should also be obtained, including
potential asbestos exposure, which could predispose the
patient to mesothelioma or asbestos pleural effusion.

1.3 Clinical Manifestations
The clinical manifestations of pleural effusion
are variable and often are related to the
underlying disease process.
The most commonly associated symptoms are
progressive dyspnea,
cough, and
pleuritic chest pain.

1.4 Physical Examinations
Physical findings in pleural effusion are variable
and depend on the volume of the effusion.
Generally, there are no physical findings for
effusions smaller than 300 mL.
With effusions larger than 300 mL, findings may
include the following:
asymmetrical chest expansion, with diminished or
delayed expansion on the side of the effusion,
decreased tactile fremitus, and
Dullness to percussion,


Mediastinal shift away from the effusion - This is
observed with effusions of greater than 1000 mL;
Displacement of the trachea and mediastinum toward
the side of the effusion is an important clue to
obstruction of a lobar bronchus by an endobronchial
lesion, which can be due to malignancy or, less
commonly, to a nonmalignant cause, such as a foreign
body.
Diminished or inaudible breath sounds
Egophony ("e" to "a" changes) at the most
superior aspect of the pleural effusion
Pleural friction rub

Other physical findings, as follows, may suggest
the underlying cause of the pleural effusion:
Peripheral edema, distended neck veins, and S
3
gallop
suggest congestive heart failure. Edema may also be a
manifestation of nephrotic syndrome; pericardial
disease; or, combined with yellow nails, the yellow
nail syndrome.
Cutaneous changes with ascites suggest liver disease
Lymphadenopathy or a palpable mass suggests
malignancy.

1.5 Distinguishing Transduates from Exudates
The fluid is considered an exudate if any of the
following applies:
Ratio of pleural fluid to serum protein greater
than 0.5
Ratio of pleural fluid to serum LDH greater than
0.6
Pleural fluid LDH greater than two thirds of the
upper limits of normal serum value

These criteria require simultaneous
measurement of pleural fluid and serum protein
and LDH. However, a meta-analysis of 1448
patients suggested that the following combined
pleural fluid measurements might have sensitivity
and specificity comparable to the criteria from
Light et al for distinguishing transudates from
exudates

:
Pleural fluid LDH value greater than 0.45 of the upper
limit of normal serum values
Pleural fluid cholesterol level greater than 45 mg/dL
Pleural fluid protein level greater than 2.9 g/dL

Transudates are caused by a small, defined group
of etiologies, including the following:
Congestive heart failure,
Cirrhosis (hepatic hydrothorax),
Atelectasis
Which may be due to malignancy or pulmonary
embolism, Hypoalbuminemia, Nephrotic syndrome,
Peritoneal dialysis, Myxedema, Constrictive
pericarditis, Urinothorax - Usually due to obstructive
uropathy,
Cerebrospinal fluid (CSF) leaks to the pleura
Generally in the setting of ventriculopleural shunting
or of trauma or surgery to the thoracic spine,
Duropleural fistula - Rare, but may be a complication
of spinal cord surgery, Extravascular migration of
central venous catheter, Glycinothorax
The more common causes of exudates include the
following:
Parapneumonic causes,
Malignancy (most commonly, lung or breast cancer,
lymphoma, leukemia; less commonly, ovarian carcinoma,
stomach cancer, sarcomas, melanoma)
[9]
, Pulmonary
embolism, Collagen-vascular conditions (rheumatoid
arthritis, systemic lupus erythematosus

),
Tuberculosis (TB),
Pancreatitis,
Trauma,
Postcardiac injury syndrome,
Esophageal perforation,
Radiation pleuritis, Sarcoidosis, Fungal infection,
Pancreatic pseudocyst, Intra-abdominal abscess, Status-
post coronary artery bypass graft surgery, Pericardial
disease, Meigs syndrome (benign pelvic neoplasm with
associated ascites and pleural effusion),
Ovarian hyperstimulation syndrome,
Drug-induced pleural disease (see Pneumotox On
Line for an extensive list of drugs that can cause
pleural effusion),
Asbestos-related pleural disease, Yellow nail syndrome
(yellow nails, lymphedema, pleural effusions),
Uremia,
Trapped lung (localized pleural scarring with the
formation of a fibrin peel prevents incomplete lung
expansion, at times leading to pleural effusion),

1.6 Radiography
Effusions of more than 175 mL are usually apparent as
blunting of the costophrenic angle on upright
posteroanterior chest radiographs.
On supine chest radiographs, which are commonly used in
the intensive care setting, moderate to large pleural
effusions may appear as a homogenous increase in density
spread over the lower lung fields.
Apparent elevation of the hemidiaphragm, lateral
displacement of the dome of the diaphragm, or increased
distance between the apparent left hemidiaphragm and
the gastric air bubble suggests subpulmonic effusions. (See
the images below.)


1.7 Pleural Fluid examinations
Normal pleural fluid
Clear ultrafiltrate of plasma that originates from the
parietal pleura
A pH of 7.60-7.64, Protein content of less than 2% (1-2
g/dL)
Fewer than 1000 white blood cells (WBCs) per cubic
millimeter
Glucose content similar to that of plasma
Lactate dehydrogenase (LDH) less than 50% of plasma

1.8 Differential Diagnoses
Liver or lung transplantation, upper
genitourinary trauma, and abdominal trauma
are among the conditions to consider in the
differential diagnosis of pleural effusion, but
note they are rare.

1.9 Treatment and Management
Transudative effusions are usually managed by treating the
underlying medical disorder. However, whether transudates
or exudates, large, refractory pleural effusions causing
severe respiratory symptoms, even if the cause is
understood and disease-specific treatment is available, can
be drained to provide relief.

The management of exudative effusions depends on the
underlying etiology of the effusion.
Pneumonia, malignancy, or TB causes most diagnosed exudative
pleural effusions, with the remainder typically deemed
idiopathic.
Complicated parapneumonic effusions and empyemas should
be drained to prevent development of fibrosingpleuritis.
Malignant effusions are usually drained to palliate symptoms
and may require pleurodesis to prevent recurrence.

Medications cause only a small proportion of all pleural
effusions and are associated with exudative pleural
effusions.
However, early recognition of these iatrogenic causes
of pleural effusion avoids unnecessary additional
diagnostic procedures and leads to definitive therapy,
which is discontinuation of the medication.
Implicated drugs include medications that cause drug-
induced lupus syndrome (eg, procainamide,
hydralazine, quinidine), nitrofurantoin, dantrolene,
methysergide, procarbazine, and methotrexate.

B. PNEUMOTHORAX

2.1 Background
Pneumothorax is defined as the presence of air or
gas in the pleural cavity (ie, the potential space
between the visceral and parietal pleura of the
lung). The clinical results are dependent on the
degree of collapse of the lung on the affected
side. Pneumothorax can impair oxygenation
and/or ventilation.
2.2 Classification of Pneumothorax

Primary and secondary spontaneous pneumothorax
Spontaneous pneumothorax is a commonly
encountered problem with approaches to treatment
that vary from observation to aggressive intervention.
Primary spontaneous pneumothorax (PSP) occurs in
people without underlying lung disease and in the
absence of an inciting event (see the images below).
[1]


Iatrogenic and traumatic pneumothorax
Iatrogenic pneumothorax is a traumatic
pneumothorax that results from injury to the
pleura, with air introduced into the pleural
space secondary to diagnostic or therapeutic
medical intervention (see the following
image).
Traumatic pneumothorax results from blunt
trauma or penetrating trauma that disrupts
the parietal or visceral pleura.
Tension pneumothorax
A tension pneumothorax is a life-threatening
condition that develops when air is trapped in
the pleural cavity under positive pressure,
displacing mediastinal structures and
compromising cardiopulmonary function.
Pio Pneumothorax
Pio Pneumothorax is Pneumothorax with
empiema in one field of lung, the common
etiology of pio pneumotorax is that from the
lungs like pneumonia, lungs abces, fistula
bronkopleural, tuberculosa, and from extra
pulmonal is thorax injury, thorax surgery,
thorakocentecis in pleural effusion, etc.

2.3 Pathophysiology
Spontaneous pneumothorax
In normal respiration, the pleural space has a negative
pressure.
As the chest wall expands outward, the surface
tension between the parietal and visceral pleura
expands the lung outward.
The lung tissue intrinsically has an elastic recoil,
tending to collapse inwards.
If the pleural space is invaded by gas from a ruptured
bleb, the lung collapses until equilibrium is achieved
or the rupture is sealed.
As the pneumothorax enlarges, the lung becomes
smaller. The main physiologic consequence of this
process is a decrease in vital capacity and partial
pressure of oxygen.

2.4 Risk Faktor
A wide variety of disease states and circumstances may
result in a pneumothorax.
Primary and secondary spontaneous pneumothorax
Risks factors for primary spontaneous pneumothorax (PSP)
include the following:
Smoking
Tall, thin stature in a healthy person
Marfan syndrome
Pregnancy
Familial pneumothorax

Diseases and conditions associated with secondary
spontaneous pneumothorax include the following:

Chronic obstructive lung disease (COPD) or emphysema:
Increased pulmonary pressure due to coughing with a
bronchial plug of mucus or phlegm bronchial plug may play
a role.
Asthma
Human immunodeficiency virus/acquired
immunodeficiency syndrome (HIV/AIDS) with PCP infection
Necrotizing pneumonia
Tuberculosis
Sarcoidosis
Cystic fibrosis
Bronchogenic carcinoma or metastatic malignancy

Iatrogenic and traumatic pneumothorax
Causes of iatrogenic pneumothorax include the following:
Transthoracic needle aspiration biopsy of pulmonary nodules
(most common cause, accounting for 32-37% of cases)
Transbronchial or pleural biopsy
Thoracentesis
Central venous catheter insertion, usually subclavian or internal
jugular
[15]

Intercostal nerve block
Tracheostomy
Cardiopulmonary resuscitation (CPR): Consider the possibility of
a pneumothorax if ventilation becomes progressively more
difficult.
Acute respiratory distress syndrome (ARDS) and positive
pressure ventilation in the ICU: High peak airway pressures can
translate into barotrauma in up to 3% of patients on a ventilator
and up to 5% of patients with ARDS.
[16]

Nasogastric feeding tube placement

Causes of traumatic pneumothorax include the
following:
Trauma: Penetrating and nonpenetrating injury
Rib fracture
High-risk occupation (eg, diving, flying)

Traumatic pneumothoraces can result from both
penetrating and nonpenetrating lung injuries.
Complications include hemopneumothorax and
bronchopleural fistula. Traumatic
pneumothoraces often can create a 1-way valve
in the pleural space (only letting in air without
escape) and can lead to a tension pneumothorax.

2.5 Physical Examination
The presentation of a patient with pneumothorax
may range from completely asymptomatic to life-
threatening respiratory distress.
Symptoms may include diaphoresis, splinting chest
wall to relieve pleuritic pain, and cyanosis (in the case
of tension pneumothorax).
Findings on lung auscultation also vary depending on
the extent of the pneumothorax.
Affected patients may also reveal altered mental
status changes, including decreased alertness and/or
consciousness (a rare finding).

Respiratory findings may include the following:
Respiratory distress (considered a universal finding) or
respiratory arrest
Tachypnea (or bradypnea as a preterminal event)
Asymmetric lung expansion: A mediastinal and tracheal
shift to the contralateral side can occur with a large
tension pneumothorax.
Distant or absent breath sounds: Unilaterally decreased or
absent lung sounds is a common finding, but decreased air
entry may be absent even in an advanced state of the
disease.
Lung sounds transmitted from the unaffected hemithorax
are minimal with auscultation at the midaxillary line
Hyperresonance on percussion: This is a rare finding and
may be absent even in an advanced state of the disease.
Decreased tactile fremitus
Adventitious lung sounds (crackles, wheeze; an ipsilateral
finding)
Cardiovascular findings may include the following:
Tachycardia: This is the most common finding. If the heart
rate is faster than 135 beats per minute (bpm), tension
pneumothorax is likely.
Pulsus paradoxus
Hypotension: This should be considered as an
inconsistently present finding; although hypotension is
typically considered a key sign of a tension pneumothorax,
studies suggest that hypotension can be delayed until its
appearance immediately precedes cardiovascular collapse.
Jugular venous distention: This is generally seen in tension
pneumothorax, although it may be absent if hypotension is
severe.
Cardiac apical displacement: This is a rare finding.
2.6 Diagnostic Considerations
Spontaneous Pneumothorax
Because patients with primary spontaneous
pneumothorax (PSP) will have apical emphysematous
pulmonary disease on computed tomography (CT)
scanning or thoracoscopy,

2.7 Differential Diagnoses
Acute Coronary Syndrome
Acute Respiratory Distress Syndrome
Aortic Dissection
Congestive Heart Failure and Pulmonary Edema
Esophageal Rupture and Tears
Myocardial Infarction
Pericarditis and Cardiac Tamponade
Pulmonary Embolism
Rib Fracture

2.8 Approach Considerations

Arterial Blood Gas Analysis

Chest Radiography
A linear shadow of visceral pleura with lack of lung markings
peripheral to the shadow may be observed, indicating collapsed lung.
An ipsilateral lung edge may be seen parallel to the chest wall.
In supine patients, deep sulcus sign (very dark and deep costophrenic
angle) with radiolucency along costophrenic sulcus may help to
identify occult pneumothorax. The anterior costophrenic recess
becomes the highest point in the hemithorax, resulting in an unusually
sharp definition of the anterior diaphragmatic surface due to gas
collection and a depressed costophrenic angle
Small pleural effusions commonly are present and increase in size if
the pneumothorax does not reexpand.
Mediastinal shift toward the contralateral lung may also be apparent.



Figure 2.1 Radiograph of a patient with a small spontaneous primary pneumothorax
Figure 2.2 Close radiographic view of patient with a small spontaneous primary pneumothorax (same patient as from the previous image).

Figure 2.4Radiograph of a patient with spontaneous primary pneumothorax due to a left upper lobe bleb

Figure 2.6 Radiograph of a patient with a large spontaneous tension pneumothorax.
2.9 Treatment
Pharmacotherapy
Observation without oxygen
Supplemental oxygen
Simple aspiration
Chest tube placement
One-way valve insertion (portable system)
Thoracostomy with continuous wall suction

SECTION 3
rd

DISCUSSION
How is the mechanism of piopneumothoraks in this patient?

Many mechanisms can result in abnormal amounts of pleural fluid, including:
Increased hydrostatic pressures in the microvascular circulation.
Decreased oncotic pressures in the microvascular circulation.
Decreased pleural space pressure (resulting from lung collapse).
Increased permeability of the microvascular circulation.
Obstruction of lymphatic drainage
Pleural effusion is a secondary disease being related to tuberculosis or other lung disease such as TB,
pneumonia, trauma, etc., because there is irritation on the lining of pleural cavity, thus altering the
permeability of the membrane and decreasing the oncotic pressure needed to drain the excess fluid in the
pleural space. normally there is a small amount of pleural fluid in the pleural space that lubricates the
parietal and visceral pleura during expiring and inspiring.

If the primary lesion enlarges, pleural effusion is a distinguishing finding. This effusion develops because
the bacilli infiltrate the pleural space from an adjacent area. Dullness to percussion and a lack of breath
sounds are physical findings indicative of a pleural effusion because excess fluid has entered the pleural
space.
Pio Pneumothorax is Pneumothorax with empiema in one field of lung, the common etiology of pio
pneumotorax is that from the lungs like pneumonia, lungs abces, fistula bronkopleural, tuberculosa, and
from extra pulmonal is thorax injury, thorax surgery, thorakocentecis in pleural effusion, etc.

What are the problems of the patient ?
The problem of the patient that we found including :
Piopneumothorax
The patient was admitted to the hospital because complaints of left chest
pain through to the back and abdomen, accompanied by shortness, and
productive cough. Chest pain felt since 2 months before entering the
hospital but patients do not care and continued to work. Os feel chest
pain severe increasingly since 2 days. Os feel nauseous and he vomit since
2 days before entering the hospital. Os complained of shortness. Tightness
is felt if he in activity. He can not work as usual. Tightness has been felt
since 2 days before entering the hospital. Tightness is reduced when at
rest but he was still difficult to breathe. Os also complained of productive
cough, cough has been felt since first week before entering the hospital.
Cough is persistent with sputum and the colour is yellowish, now he is not
cough anymore. Besides, the absence of weird breath sounds (like
wheezing) and no history of asthma attack make asthma is unlikely. The
absence of high fever makes pneumonia is unlikely too.

Then, it could be confirmed by physical examination.
The absence of breath sound in one side of the
chest along with decreased expansion movement ,
decreased vocal fremitus, and hypersonor percussion
could lead to the pneumothorax diagnosis.
Pneumothorax itself is one of the complication of
empiema.
Is the management of the patient ?
O2 2 Litres/minute
IVFD RL gtt X/minute
Ceftriaxone 1 g/ 12 hours (IV)
Metronidazol / 12 hours (IV)
Ambroxol sirup 3x1C
Observe the development of WSD till the
undulations and Bubble negative
Chest X-Ray if the lug re-expands, then off WSD

What is the complications that may in this
patient?
Complications of pleural effusions include collapse
of the lung; pneumothorax, or air in the chest
cavity, which is a common side effect of the
thoracentesis procedure; and empyemas
(abscesses) caused by infection of the pleural
fluid, which require drainage of the fluid.

A pleural effusion may cause or worsen a lung infection, such as
pneumonia. The extra fluid may get infected and form a pocket of
pus, which is called empyema (em-peye-EE-ma). You may have
other problems, such as a collapsed lung. The problems you may
have depend on what is causing your pleural effusion. Talk to your
caregiver about any concerns you may have about your illness or
treatment.

Pio Pneumothorax is Pneumothorax with empiema in one field of
lung, the common etiology of pio pneumotorax is that from the
lungs like pneumonia, lungs abces, fistula bronkopleural,
tuberculosa, and from extra pulmonal is thorax injury, thorax
surgery, thorakocentecis in pleural effusion, etc, the common
complication from piopneumothorax is syok septic and it will be
caused of death for this patient.