CLINICAL THERAPEUTICS

RHEA BERNADETTE R. DANGUILAN

MD-III B
Case:
A 22 yr old man presents to the ER complaining of
severe chest pain and shortness of breath. PE
reveals tall thin man with decreased breath sounds,
decreased tactile fremitus and hyperresonance to
percussion over the right chest. His EKG appears
normal but CXR reveals pleural line and a deep
sulcus sign over the right lung. You immediately
place him on oxygen and prepare him for a minor
surgical procedure.
General data: 22 yr old man
chief complaint: severe chest pain
shortness of breath
Physical Exam: tall thin man
decreased breath sounds
decreased tactile fremitus
hyperresonance to percussion over the right lung
Lab Exam: EKG is normal
CXR: pleural line
deep sulcus sign over the right lung
DIAGNOSIS:

PNEUMOTHORAX
 INTRODUCTION
PNEUMOTHORAX
- is the presence of air within the pleural space
- - is considered to be one of the most common forms of
thoracic disease.
- Air can enter the intrapleural space through a
communication from the chest wall (ie, trauma) or through
the lung parenchyma across the visceral pleura.
- Pneumothorax can occur spontaneously or result from
trauma or medical procedures.
CLASSIFICATION:
1. Spontaneous pneumothorax- many observations suggest that
spontaneous pneumothorax often results from rupture of a subpleural
bleb.
A. primary
B. secondary
2. Traumatic pneumothorax - is caused by penetrating or blunt trauma to
the chest
3. Iatrogenic pneumothorax - results from a complication of a diagnostic
or therapeutic intervention
Etiology
Primary spontaneous pneumothorax- occurs in patients
without underlying pulmonary disease

- classically in tall, thin young men in their teens and 20s. It is

thought to be due to spontaneous rupture of subpleural apical
blebs or bullae that result from smoking or that are inherited.
Risks factors for primary spontaneous pneumothorax (PSP):
Smoking
Tall, thin stature
Marfan syndrome
Pregnancy
Familial pneumothorax

Secondary spontaneous pneumothorax- occurs in patients

with underlying pulmonary disease.
ANATOMY AND PHYSIOLOGY
The lungs consist of airways (trachea and bronchi) that divide
into smaller and smaller branches until they reach the air
sacs, called alveoli.

The lung itself is covered with a membrane called the visceral

(or pulmonary) pleura.
> parietal pleura - lining of the thoracic cavity.
> Between the two membranes is a thin, serous fluid which acts
as a lubricant – reducing friction as the two membranes slide
across one another when the lungs expand and contract with
respiration.
 RESPIRATION

Respiration is a passive, involuntary activity.

When the diaphragm, the major muscle of
respiration, is stimulated- it contracts and moves
downward.
Inhalation-the external intercostals move the rib cage up and out.
The chest wall and parietal pleura move out, pulling the visceral
pleura and the lung with it.
- As the volume within the thoracic cavity increases, the pressure
within the lung decreases.
Exhalation- When the diaphragm returns to its normal, relaxed state,
the intercostal muscles also relax and the chest wall moves in.
The lungs, with natural elastic recoil, pull inward and air flows out of
the lungs
The negative pressure between the two pleurae maintains partial
lung expansion by keeping the lung pulled up against the
chest wall.
- During inhalation, the pressure is approximately –8 cm H2O
- duringexhalation, approximately –4 cm H2O
Under normal conditions, the mechanical attachment of the pleurae,
plus the residual volume, keep the lungs from collapsing.
- The pleura is a thin serous layer, which covers the lungs (visceral
pleura) and is reflected, by way of the lung hila, on to the chest
wall and pericardium (parietal pleura).
- Only a thin layer of pleural fluid separates the parietal and
visceral pleura. The parietal layer secretes 2400 ml of fluid
daily, which is resorbed by the visceral layer
PATHOPHYSIOLOGY
The alveolar walls and visceral pleura form a barrier that
separates the intrapleural and intra-alveolar spaces and
maintains the pressure gradient.
> If a defect occurs in this barrier, air enters the pleural space
until either the pressures equalize or the communication seals.
With the loss of negative intrapleural pressure in one
hemithorax, the ipsilateral lung collapses.
> A large pneumothorax results in restrictive ventilation
impairment. Shunting of blood through nonventilated lung
tissue may result in acute hypoxemia, although over time this
effect is mitigated by compensatory vasoconstriction in the
collapsed lung.
In primary spontaneous pneumothorax, disruption of the alveolar-
pleural barrier occurs when a subpleural bullae (or bleb), typic
ally located at the lung apex, ruptures into the pleural space.
>Etiology of these bullae-
related to degradation of elastic fibers within the lung and an imb
alance in the protease antiprotease and oxidant-
antioxidant systems.
>In secondary spontaneous pneumothorax,the underlying lung
disease weakens the alveolar -pleural barrier.
>In patients with pneumonia, the cytotoxic effects of repeated episode
s of inflammation lead to bullous and cystic changes.
>In patients with COPD, chronic exposure to cigarette smoke results i
n the development of large, thin walled bullae
that areat an increased risk for rupture.
CLINICAL PRESENTATION
Small pneumothoraces are asymptomatic

Symptoms of pneumothorax include:

- acute onset of chest pain ( severe and/or stabbing)
- shortness of breath ( sudden in onset)
- diaphoresis
- cyanosis (in the case of tension pneumothorax)
- decreased alertness and/or consciousness (a rare finding)
Respiratory findings:
- Respiratory distress (considered a universal finding)
- Tachypnea (or bradypnea as a preterminal event)
- Distant or absent breath sounds: Unilaterally decreased or absent
lung sounds
-Hyperresonance on percussion
- Decreased tactile fremitus
- visceral pleural line is observed clearly
- deep sulcus sign on a supine chest radiograph
Cardiovascular findings:
-Tachycardia: This is the most common finding
-Pulsus paradoxus
-Hypotension
- Jugular venous distention
DIFFERENTIAL DIAGNOSIS
Condition Differentiating signs/symptoms
ASTHMA, acute Expiratory wheeze and chest tightness
Exacerbation Therapeutic trial of bronchodilators relieves
symptoms

COPD, acute Fever, increased cough, and change in

Exacerbation sputum colour suggest an infective
exacerbation
PULMONARY Presence of risk factors forthromboembolism,
EMBOLISM such as obesity, prolonged bed rest,
pregnancy/postpartum period, inherited
thrombophilias, active malignancy, recent trauma/fracture
WORK UP AND LABORATORY

- History and physical examination

- Chest radiography
- Chest computed tomography (CT)
- Arterial Blood Gas (ABG)
- CONTRAST- ENHANCED ESOPHAGOGRAPHY
TREATMENT
- restore lung volume and an air-free pleural space and to
prevent recurrences
- supplemental oxygen- at 3 L/min nasal canula
- simple aspiration
- chest tube drainage
- vacuum-assisted thoracostomy (VATS) with pleurodesis and/or
closure of leaks and bullectomy
- open surgical procedures such as thoracotomy for
pleurectomy or pleurodesis.
- In patients with repeated pneumothoraces who are not good
candidates for surgery, sclerotherapy with talc or doxycycline
may be necessary.
MEDICATIONS:
- Lidocaine hydrochloride is a local anesthetic- used for
analgesia for thoracentesis and chest tube placement.
> adverse effect: allergic reactions
- Opiate analgesic agents are used for pain control. important in the
initial placement of thoracostomy tubes
> Morphine- practically the regimen is 1-2 mg IV
- Benzodiazepines are used for conscious sedation. These
agents are useful for premedication before
pleurodesis/sclerotherapy or placement of a thoracostomy
tube.
> Midazolam, Lorazepam (Ativan)- administer 0.05 mg/kg IV,
not to exceed 4 mg/dose.
THANK YOU!