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1.

Mengapa didapatkan penurunan kesadaran?

2. Mengapa pasien tampak sesak dan sianosis?

3. Mengapa takipneu, hipotensi, dan takikardi?

4.

Mengapa didapatkan hematom pada temporal kanan?

5.

Mengapa dada asimetris, suara nafas hemithorax kanan menghilang?

6. Mengapa akral dingin dan pucat?

7. Mengapa diberikan oksigen dengan face mask?

8.

Apakah tindakan dokter menutup luka dengan perban sudah benar?

9.

Mengapa kondisi penderita semakin menurun?

10.Bagaimana penanganan pasien di skenario?

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If the case is a pneumothorax:

Finally, venous obstruction leading to shock may be seen with tension pneumothorax. In this condition,

elevated intrapleural pressure from an injury to the lung or airways collapses the intrathoracic great veins,

resulting in inadequate venous filling and shock. Tension pneumothorax should be diagnosed by physical

examination and not chest radiography. Needle decompression often restores venous filling sufficiently to

reverse the shock state until a thoracostomy tube can be placed. In many patients, the length of some

venous cannulas may be insufficient to reach the pleural space. If suspicion of the diagnosis is significant, a

lack of response to needle decompression should prompt immediate tube thoracostomy.

Pathophysiology

With reference to the atmospheric pressure, the pleural space normally has negative pressure during the

complete respiratory cycle. This negative pressure is created by the chest wall which tends to expand, and

the lungs which tend to collapse. As such, the alveolar pressure is more than the pleural pressure. As a

result, if a leak develops between an alveolus and the potential pleural space, air moves from the alveolus

to the pleural space till the pressure equalises on both sides. As a consequence, the lung volume

decreases, and the thoracic cavity volume increases.

A pneumothorax results in a decrease in the vital capacity as also a decrease in the PaO2. A healthy person

is likely to easily cope with this reduction in lung function. But in patients with underlying lung disease, the

reduced vital capacity progresses to respiratory insufficiency with alveolar hypoventilation and respiratory

acidosis as a result of reduced PaO2 and an increase in alveolar-arterial oxygen difference (AaDO2).

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CLASSIFICATION AND TERMINOLOGY OF THE PNEUMOTHORAX

It is usually classified on the basis of its causes. Pneumothoraces are classified as traumatic and

nontraumatic (spontaneous). Nontraumatic pneumothoraces are further subdivided into primary

(occurring in persons with no known history of lung disease) and secondary (occurring in persons with a

known history of lung disease, such as chronic obstructive pulmonary disease).

Pneumothoraces may also be further described as simple pneumothorax (no shift of the heart or

mediastinal structures) or tension pneumothorax. It can also be classified as open (sucking chest wound)

and closed (intact thoracic cage).

PATHOPHYSIOLOGY OF PNEUMOTHORAX

In normal people, the pressure in pleural space is negative with respect to the alveolar pressure during the

entire respiratory cycle. The pressure gradient between the alveoli and pleural space, the transpulmonary

pressure is the result of the inherent elastic recoil of the lung. During spontaneous breathing the pleural

pressure is also negative with respect to atmospheric pressure.

When communication develops between an alveolus or other intrapulmonary air space and the pleural

space, air flows from the alveolus into the pleural space until there is no longer a pressure difference or

until the communication is sealed.

Tension pneumothorax

Tension pneumothorax develops when a disruption involves the visceral pleura, parietal pleura, or the

tracheobronchial tree. The disruption occurs when a one-way valve forms, allowing air inflow into the

pleural space, and prohibiting air outflow. The volume of this nonabsorbable intrapleural air increases witheach inspiration. As a result, pressure rises within the affected hemithorax; ipsilateral lung collapses and

causes hypoxia. Further pressure causes the mediastinum shift toward the contralateral side and

compresses both, the contralateral lungand the vasculature entering the right atrium of the heart.This

leads to worsening hypoxia and compromised venous return. Researchers still are debating the exact

mechanism of cardiovascular collapse but, generally the condition may develop from a combination of

mechanical and hypoxic effects. The mechanical effects manifest as compression of the superior and

inferior vena cava because the mediastinum deviates and the intrathoracic pressure increases. Hypoxia

leads to increased pulmonary vascular resistance via vasoconstriction. If untreated, the hypoxemia,

metabolic acidosis, and decreased cardiac output lead to cardiac arrest and death.

Traumatic pneumothorax

A traumatic pneumothorax can result from either penetrating or nonpenetrating chest trauma. With

penetrating chest trauma, the wound allows air to enter the pleural space directly through the chest wall

or through the visceral pleura from the tracheobronchial tree. With non penetrating trauma, a

pneumothorax may develop if the visceral pleura is lacerated secondary to a rib fracture, dislocation.

Sudden chest compression abruptly increases the alveolar pressure, which may cause alveolar rupture.

Once the alveolus is ruptured, air enters the interstitial space and dissects toward either the visceral pleura

or the mediastinum. A pneumothorax develops when either the visceral or the mediastinal pleura

ruptures, allowing air to enter the pleural space.

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(http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2700561/)

Pathophysiology

The lung is surrounded by two layers, the parietal pleura, which lines the interior of the chest wall, and the

visceral pleura, which covers the lungs. They are separated by a thin layer of lubricating fluid within thepleural space. A small negative pressure within the pleural space helps keep the lung inflated and the

two layers closely apposed. With inspiration, the negative intrathoracic pressure increases and leads to

expansion of the lung from an influx of air. If the pleural space is disrupted, air, blood, or other fluid can

accumulate in between the two layers of the pleura and the normal pressure gradient is compromised.

This interferes with normal inspiratory-induced inflation and leads to collapse of the lung. As the amount

of fluid or air increases, respiratory function worsens and symptoms of dyspnea are produced, often with

pleuritic chest pain and anxiety. The degree of respiratory compromise depends on the volume of fluid or

air in the pleural space, the patients age, baseline pulmonary status, and the integrity of the chest wall.

The positive pressure accumulation of air associated with tension pneumothorax leads to severe

respiratory dysfunction and cardiovascular compromise.

https://www.inkling.com/read/roberts-hedges-procedures-emergency-medicine-6th/chapter-

10/pathophysiology

If the case is a haemothorax:

Pathophysiology

Thoracic trauma injuries are divided between blunt injuries such as those sustained in auto crashes andpenetrating injuries such as stab or gunshot wounds. Penetrating injuries such as those suffered by our

patient produce lung lacerationsand often result in hemothoraces. The first concern is hemorrhage, which

can quickly lead to hypovolemic shock. This condition is defined as systolic blood pressure of less than

100mmHg.

The pathophysiology of shock is basically a failure of cellular function. As blood is lost, leaking into the

thoracic cavity, blood pressure drops and results in loss of tissue oxygenation. The cells convert oxygen

and nutrients into high energy ATP through hydrolysis. When this mechanism breaks down, the body

begins anaerobic respiration with the by product of lactate,a fixed acid. Anaerobic respirations can only

synthesize ATP at a rate of 5-10% of normal for the bodys needs. This produces excess proteins that leakinto extracellular compartments. This is facilitated by the damage to membrane permeability due to

trauma. As excess proteins are bound by bicarbonate the blood pH drops and metabolicacidosis ensues

along with the central chemoreceptor response of hyperventilation, which compensates by reducing

carbon dioxide levels.

In our patients case the right middle and lower lobes were too badly damaged to save. Their removal

further complicated the high peripheral vascular resistance that accompanies shock. Our slide presentation

shows the algorithm for dealing with hypovolemic shock. I agree with the treatment of a lobectomy in this

case. The organ was beyond repair, the patient is young with no previous respiratory issues so the

remaining lung space should be able to adequately ventilate the patient. Hypovolemic shock effects four

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2700561/http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2700561/http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2700561/https://www.inkling.com/read/roberts-hedges-procedures-emergency-medicine-6th/chapter-10/pathophysiologyhttps://www.inkling.com/read/roberts-hedges-procedures-emergency-medicine-6th/chapter-10/pathophysiologyhttps://www.inkling.com/read/roberts-hedges-procedures-emergency-medicine-6th/chapter-10/pathophysiologyhttps://www.inkling.com/read/roberts-hedges-procedures-emergency-medicine-6th/chapter-10/pathophysiologyhttps://www.inkling.com/read/roberts-hedges-procedures-emergency-medicine-6th/chapter-10/pathophysiologyhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2700561/

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major systems; hematological, cardiovascular, renal and neuroendocrine. The following is an overview of

the effects on each system.

In the blood, injury results in the activation of the coagulation cascade and constriction of the blood

vessels. Platelets, involved in clotting, are activated early inthe process. Exposed collagen subsequently

causes fibrin deposition and stabilization of the clot. This entire process is complete within 24 hours after

the onset of injury.

The cardiovascular system initially responds by increasing the heart rate and myocardial contractions

while constricting peripheral blood vessels. Later the response continues due to increased release of

norepnephrine and decreased baseline vagal tone which is regulated by baroreceptors . Through this

mechanism the blood is redistributed to the brain, heart and kidneys causing a decrease in perfusion to

less critical body functions such as skin, muscle and the GI tract.

The renal system stimulates an increase of rennin, which converts angiotensin to angiotensin I. This is

later converted to angiotensin II by the lungs and liver. The two main effects of Angtiotensin II arevasoconstriction of arterial smooth muscle and stimulation of alodsterone secretion by the adrenal

cortex. Aldosterone actively reabsorbs sodium and thus causes water retention. The neuroendocrine

system responds by causing an increase in antidiuretic hormone (ADH). This indirectly leads toan

increase in the reabsorption of NaCl and water.

The early acute lung injury and more advanced ARDS observed following shock and trauma are widely

believed to result from pathologic neutrophil-endothelial cell interactions. These mechanisms injure the

pulmonary capillary endothelial membranes, leading to interstitial and alveolar edema and resulting in

diminished pulmonary compliance and diffusion capacity.

As time passes the bodys inflammatory response to lung injury gives the appearance of a generalized

rather than local response. In many cases, the deterioration of pulmonary function after chest trauma will

result as much or more from the systemic response of inflammation than the original injury.

In a hemothorax the pleural space and lung parenchyma have been compromised, allowing blood from the

thoracic vessels to enter the pleural space. It takes at least 200-300ml of blood in the pleural space to be

visible on x-ray. A massive hemothorax is a collection of more than 1500ml of blood in the pleural space.

The presence of this much fluid dramatically reduces the affected lungs ability to ventilate by damaging

the normal elastic recoil produced between the lungs and chest wall. In response the chest wall recoils

outward and the lung collapses inward.

A pneumothorax is a condition in which air has entered the pleural space resulting in similar physiological

complications. In a tension pneumothorax, as air escapes from the lung into the pleural space, it gathers

increasing positive pressure.As the air space increases, more collapse occurson the affected side along

with a mediastinal shift.This, in turn, may cause a kinking of vascular structuressuch as the vena cava. As

the cascade continues, venous return to the right side of the heart decreases and hemodynamic

instability results.

(http://www.smccd.net/accounts/hernandezr/rpth485/chest_trauma.pdf)

http://www.smccd.net/accounts/hernandezr/rpth485/chest_trauma.pdfhttp://www.smccd.net/accounts/hernandezr/rpth485/chest_trauma.pdfhttp://www.smccd.net/accounts/hernandezr/rpth485/chest_trauma.pdfhttp://www.smccd.net/accounts/hernandezr/rpth485/chest_trauma.pdf

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Physiology/Pathophysiology

Penetrating chest trauma frequently creates serious or fatal injury because of the vital structures and

processes that are housed within the chest cavity. Maintaining adequate intrapleural and intrapulmonic

pressures within the chest cavity is essential for adequate breathing.

The lungs are surrounded by thin, durable membranes called pleura. The parietal pleura lines the chest

wall. The visceral pleura is attached to the surface of the lung. Between the two pleural layers is a small

amount of fluid,which serves both as a lubricant and a means to provide surface tension to keep the

lungs inflated.A fluid bond between the visceral and parietal pleura creates a steady pull between the two

pleural layers, which leads to a constant intrapleural negative pressure.The fluid bond is analogous to a

water glass being placed upside down on a wet countertop. When the glass is pulled straight upward, the

fluid bond creates a suction (negative pressure) and the glass can t be pulled upward off the countertop

unless the fluid bond seal is broken. The lung is comprised of elastin fibers that have a natural recoil

tendency. This recoil property wants to pull the lung inward away from the thoracic wall; however, the

fluid bond in the pleural space overcomes the elastin recoil and keeps the lungs from completely

collapsing. If the fluid bond were eliminated, the lungs would collapse to approximately 5% of their

normal resting size. The integrity of the pleural layers and appropriate pressure within the chest are

essential for adequate breathing. A break in the continuity and integrity of the pleural layer would reduce

the fluid bond and allow the elastin recoil to collapse the lung.

It is believed that the pleural space can hold between 34 liters of blood or air. Air will cause a dramatic

reduction in surface tension when the pleura lose contact with each other, resulting in the inability to

expand the affected lung. The volume of blood that can collect in the pleural space is enough to cause

exsanguination. Blood or other fluids in the pleural space can also cause alveolar collapse in the areas

where these substances are present.

Hemothoraxis a collection of blood in the pleural space. As noted above, this space will hold between 34

liters of blood. Although blood in this capacity will prevent gas exchange due to alveolar collapse, it also

can cause death from blood loss without one drop of blood ever leaving the body. This means that

hemothorax can affect the body in two ways: hemodynamically and by impeding alveolar gas exchange.

The blood from hemothorax can come from two general areas: extrapleural and intrapleural, which

includes the great vessels of the body in the mediastinum. The most common and often most profuse

bleeding is caused by laceration of the extrapleural intercostal or internal mammary arteries. On the

underside of each rib, and slightly toward the inside, is a vein, artery and nerve. This is important toremember in regards to placement of decompression needles.

Intrapleurally, bleeding from damage to the lung parenchyma is usually limited because of self-

compression and the relative low pressures in these vessels. Of course, a rupture of the great vessels

contained in the mediastinum, including the aorta and the superior and inferior venae cava, will cause a

massive hemothorax.

When assessing the patient with a hemothorax, you will likely find signs of hypo-volemic shock and a

mechanism of injury consistent with penetrating chest injury to include GSW, stabbing or even a closed

chest injury, if it causes injuries to blood vessels. In hemothorax, you would find a dull sound on percussion

over affected areas. It is important to note that many of these patients are placed supine on a backboard,

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which may diminish the accuracy of auscultation or percussion, especially in minor to moderate

hemothorax, by causing a distribution of the blood over a greater area, masking pertinent physical

findings.

(http://www.emsworld.com/article/10324543/penetrating-chest-trauma)

Pathophysiology

Bleeding into the pleural space can occur with virtually any disruption of the tissues of the chest wall and

pleura or the intrathoracic structures. The physiologic response to the development of a hemothorax is

manifested in two major areas: hemodynamic and respiratory. The degree of hemodynamic response is

determined by the amount and rapidity of blood loss.

Hemodynamic response

Hemodynamic changes vary, depending on the amount of bleeding and the rapidity of blood loss. Blood

loss of up to 750 mL in a 70-kg man should cause no significant hemodynamic change. Loss of 750-1500 mL

in the same individual will cause the early symptoms of shock (ie, tachycardia, tachypnea, and a decrease

in pulse pressure).

Significant signs of shock with signs of poor perfusion occur with loss of blood volume of 30% or more

(1500-2000 mL). Because the pleural cavity of a 70-kg man can hold 4 L of blood or more, exsanguinating

hemorrhage can occur without external evidence of blood loss.

Respiratory response

The space-occupying effect of a large accumulation of blood within the pleural spacemay hamper normal

respiratory movement. In trauma cases, abnormalities of ventilation and oxygenation may result,

especially if associated with injuries to the chest wall.

A large enough collection of blood causes the patient to experience dyspneaand may produce the clinical

finding of tachypnea. The volume of blood required to produce these symptoms in a given individual varies

depending on a number of factors, including organs injured, severity of injury, and underlying pulmonary

and cardiac reserve.

Dyspnea is a common symptom in cases in which hemothorax develops in an insidious manner, such asthose secondary to metastatic disease. Blood loss in such cases is not so acute as to produce a visible

hemodynamic response, and dyspnea is often the predominant complaint.

Physiologic resolution of hemothorax

Blood that enters the pleural cavity is exposed to the motion of the diaphragm, lungs, and other

intrathoracic structures. This results in some degree of defibrination of the blood so that incomplete

clotting occurs. Within several hours of cessation of bleeding, lysis of existing clots by pleural enzymes

begins.

Lysis of red blood cells results in a marked increase in the protein concentration of the pleural fluid and anincrease in the osmotic pressure within the pleural cavity. This elevated intrapleural osmotic pressure

http://www.emsworld.com/article/10324543/penetrating-chest-traumahttp://www.emsworld.com/article/10324543/penetrating-chest-traumahttp://www.emsworld.com/article/10324543/penetrating-chest-traumahttp://www.emsworld.com/article/10324543/penetrating-chest-trauma

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produces an osmotic gradient between the pleural space and the surrounding tissues that favors

transudation of fluid into the pleural space. In this way, a small and asymptomatic hemothorax can

progress into a large and symptomatic bloody pleural effusion.

Late physiologic sequelae of unresolved hemothorax

Two pathologic states are associated with the later stages of hemothorax: empyema and fibrothorax.

Empyema results from bacterial contamination of the retained hemothorax. If undetected or improperly

treated, this can lead to bacteremia and septic shock.

Fibrothorax results when fibrin deposition develops in an organized hemothorax and coats both the

parietal and visceral pleural surfaces. This adhesive process traps the lung in position and prevents it from

expanding fully. Persistent atelectasis of portions of the lung and reduced pulmonary function result from

this process.

(http://emedicine.medscape.com/article/2047916-overview#a0104)

http://emedicine.medscape.com/article/2047916-overview#a0104http://emedicine.medscape.com/article/2047916-overview#a0104http://emedicine.medscape.com/article/2047916-overview#a0104http://emedicine.medscape.com/article/2047916-overview#a0104