CHEST TRAUMA

Chest trauma is basically divided into blunt chest trauma and penetrating chest
trauma. Thoracic injuries, like with all traumas, can result from blunt or penetrating
mechanism. Fractures and soft tissue injuries are common. Compromised breathing
remains a particularly urgent concern in these patients, which is unique to thoracic
injuries and demonstrates common physiologic signs regardless of cause. Structures
that can be injured include the protective bony thorax (ribs, sternum, scapula, and
spinal column). The diaphragm inferiorly, and the soft tissue content of the thorax
(heart, lungs, esophagus, and great vessels). Severe cardiovascular compromise can
also result from injury to the chest. By far the most morbidity and mortality as a
result of blunt chest trauma is caused by Motor Vehicle Crashes. 40 % of patients in
motor vehicle crashes sustain blunt chest trauma and 20% of all trauma patients
have chest trauma. The spectrum of disease occurring in blunt Chest trauma ranges
from rib fractures, pulmonary contusion complicating to Acute Respiratory Distress
Syndrome (ARDS) simple pneumothoraces, hemothoraces and surgical emphysema
(tissue pneumomatosis) to life threatening conditions like tension pneumothorax
and tension hydrothorax as well as cardiac tamponade as a result of
hemopericardium.

Pneumothorax
Pneumothorax is air in the pleural cavity. Anatomically the pleural cavity is a
potential space between the parietal pleura and visceral pleural. The two pleurae
are usually in apposition with only a thin film of fluid separating the 2.

Causes of pneumothorax
The commonest cause of pneumothorax is chest trauma either blunt or penetrating.
These types of pneumothoraces fall under traumatic pneumothoraces. The trauma
at times can be iatrogenic for examples barotrauma in mechanical ventilation and
when one attempts to put a central line in the neck e.g. in the subclavian vein. Other
causes include the shearing forces of trauma which will subsequently cause lung
parenchymal damage as well. Rib fractures can also cause parenchymal lung
damage and subsequent pneumothorax.

Spontaneous pneumothorax
Can be divided into primary spontaneous pneumothorax ( PSP) and secondary
spontaneous pneumothorax ( SSP).

In primary spontaneous pneumothorax the cause is not apparently known. It

usually occurs in tall young men, with ruptured pleural blebs. An association with
smoking has been reported in many cases, this may be associated with the
emphysematous- like changes which occurs in smokers resulting in subpleural
blebs.

Dr R Kanyongo Dept. Of Cardiothoracic Surgery 2015 Page 1

In secondary spontaneous pneumothorax, there is underlying lung parenchymal
disease (bullous lung disease). The pneumothorax is usually a result of ruptured
bullae in a diseased lung. e.g.
1. Pulmonary tuberculosis
2. COAD/COPD e.g. Emphysema, alpha1 anti trypsin deficiency
3. Cystic fibrosis
4. PneumoCystis jirovicei Pneumonia (PCP)
5. Connective tissue disorders Marfan’s syndrome, Ehler’s Danlos syndrome

Tension Pneumothorax
This is when air accumulates in the pleural cavity via a one way valve mechanism
such that air accumulates in the space but cannot exit. Each subsequent breath
results in pressure building up within the pleural cavity resulting in the patient
having increasing respiratory distress, as a result of lung collapse from the
increased pleural pressure. This also causes a shift in the mediastinum further
causing cardiovascular compromise as well. Tension pneumothorax is a surgical
emergency. Emergency surgical decompression can be done using a large bore
needle in the second intercostal space mid clavicular line, and the classical "hiss"
(characteristic sound of decompression usually from a valve released/opened for a
gas under pressure) can be heard after decompression. A chest drain can then be
put following emergency decompression.

Clinical findings

Symptoms
1. Shortness of breath
2. Chest pain

Signs
1. Restless
2. Alar flaring, use of accessory muscles of respiration, tachypnea (respiratory
distress)
3. Tracheal deviation to the contralateral side, distended neck veins, raised JVP
hypotension tachycardia and tachypnea in tension pneumothorax (similar in cardiac
tamponade)
4. Chest asymmetry, reduced expansion ipsilateral side
5. Affected side hyper resonant/tympanic to percussion
6. Reduced/ no air entry on affected side.

*Chest X ray shows an area of hyperlucency with loss of lung markings. (Air appears
dark/black on a plain radiograph.)*

Management

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Management of all trauma patients must follow the ABC protocol. After insuring
airway patency and that the patient is breathing and that there is adequate
circulation;
1. Oxygen per face mask
2. Chest drain - inserted anyway between the 4th or 5th intercostal space between
the anterior and mid axillary line.
The chest drain in an underwater seal for a patient with pneumothorax will be
bubbling. Bubbling stops when the pneumothorax has been drained.
3. Post drainage/ post tube thocostomy/ post ICD chest X ray to ensure correct
placement of drain and to see if the lung has re expanded.

An air leak which persists beyond 48-72 hrs. (seen as continuous bubbling in the
underwater seal) suspect a bronchial leak or bronchopleural fistula and might need
surgical repair. If conservative management is considered free drainage via a one
way Heimlich valve can be considered.

Cardiac tamponade
Can occur in blunt chest trauma. Also myocardial contusion can occur in the same
setting.
*Homework read on difference in clinical findings in cardiac tamponade and tension
pneumothorax*

Catemenial pneumothorax/ hemothorax

Occurs in women and occurs with each menstrual cycle. Believed to be a result of
ectopic endometrial tissue within the pleural cavity (endometriosis) and can occur
as a pneumothorax, hemothorax or hemopneumothorax.

Pulmonary contusion
Following blunt chest trauma some patients present in respiratory distress with
evidence of hypoxia low SpO2 and CXR showing infiltrates (in patient who had no
other pre morbid disease of the lung) this shows that there is pulmonary contusion
which at times complicates into ARDS

Acute Respiratory Distress syndrome

ARDS is the pulmonary component of the systemic inflammatory response
syndrome (SIRS). It can be caused by direct (contusion, near drowning, aspiration,
smoke inhalation) or indirect (trauma, sepsis, pancreatitis) insults.
Criteria for its diagnosis include:
1. Known cause
2. Acute onset of symptoms
3. Hypoxia refractory to O2 / FEV1/FVC less than 200
4. New bilateral fluffy’ infiltrates on chest X-ray
5. No evidence of cardiac failure (pulmonary artery wedge pressure<18mmHg).

ARDS develops in two phases:

1. Acute exudative phase
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 The insult(director/indirect) leads to neutrophil activation and the release of
inflammatory mediators such as tumor necrosis factor (TNF), platelet activating
factor(PAF),interleukin IL-1 and IL-6; there is also the release of proteases and toxic
oxygen radicals that damage the lung parenchyma. This lung damage leads to
increased capillary permeability and allows protein-rich exudates to fill the alveoli
and form hyaline membranes There is thrombosis in alveolar capillaries and
hemorrhage into the alveoli. This leads to alveolar collapse and decreased surfactant
production, leading to increased lung compliance

2. Late organization phase

There is regeneration of typeII pneumocytes; the hyaline membranes organize with
pulmonary fibrosis, leading to interstitial fibrosis and obliteration of alveolar spaces
and alveolar microvasculature.

Hemothorax.
Accumulation of blood in the pleural cavity. This usually follows blunt or
penetrating chest trauma.

Symptoms
1. Chest pain
2. Shortness of breath

Signs
1. Restlessness
2. Alar flaring, use of accessory muscles of respiration (respiratory distress)
3. Tracheal deviation to contralateral side, distended neck veins raised JVP
hypotension tachycardia and tachypnea (occurs when there is tensioning)
4. Chest asymmetry (reduced expansion affected side)
5. Stony dullness on affected side
6. Reduced air entry/ no air entry on affected side.
Hemothorax can be confirmed clinically by attempting aspiration using a needle.

Chest X ray can show blunting of the costophrenic angles, a meniscus or an air fluid
level or complete homogenous opacification (complete white out)
* liquid substances appear as an opacity or is white on a plain radiograph*

Management
Follows ABC protocols establishing i.v. access cannot be overemphasized
1. Oxygen per face max.
2. Two large bore cannulation
3. I.V. Fluid resuscitation
4. FBC and U+E
5. Group and retain (cross match as guided by hemodynamic assessment or Hb)

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6. Chest drain (massive hemothorax = >1500mls of blood drained instantly on ICD
insertion or > 300mls drained /hr for 4 consecutive hours. This is an indication for
an emergency thoracotomy)

Pleural effusion
Accumulation of a liquid in the pleural space e.g blood (hemothorax), chyle (
(chylothorax) serous liquid ( hydrothorax).

Malignant pleural effusions

Accumulation of a liquid within the pleural space as a result of an underlying
malignancy, in the strictest sense a malignant pleural effusion contains malignant
cells within the pleural fluid. The fluid is usually hemorrhagic. Management usually
involves drainage, thoracscopy and biopsy. For a known primary with confirmed
histology, pleurodesis is also part of the management when the lung has re
expanded.

*pleurodesis = obliteration of a pleural space by inducing inflammation so that the

parietal and visceral pleura are in apposition (closing up the space so that there is
no room for anything to accumulate within the space)

Agents for pleurodesis

1. Chemical
a. Talc powder (slurry/poudrage)
b. Bleomycin
c. Tetracycline

2. Mechanical (traumatic pleural abrasions to induce inflammation)

3. Biological (use of corynebacterium )

Empyema Thoracis
An empyema is collection of pus in a visceral cavity e.g. Subdural empyema, gall
bladder empyema, hypopyon (pus in the anterior chamber of the eye)
Accumulation of pus in the pleural cavity is known as Empyema Thoracis.
The commonest cause of empyema is following a para pneumonic effusion. The
commonest cause being strep pneumo followed by staph aureus other infective
organisms commonly isolated include hemophilus influenza, klebiseilla and
peptostreptoccoci. Other causes include; pulmonary TB, iatrogenic following chest
drain insertion and esophageal perforations, sub phrenic abscess, hepatic abscess
lung abscess etc.
Empyema Thoracis formation generally follows 3 stages
1. Exudative Phase
An exudate is a fluid which has a protein content >30g/L. In the exudative phase
there is inflammation of the pleura leading to increased permeability of the pleurae
resulting in intestinal fluid moving into the pleural space. The fluid is often cloudy or
clear at times. This fluid is sterile and has glucose levels, pH and LDH within normal
Dr R Kanyongo Dept. Of Cardiothoracic Surgery 2015 Page 5
ranges. During this stage treatment is usually with antibiotics and rarely is there a
need for drainage

2. Fibrinopurulent stage
This stage follows the exudative phase there is increasing white cells (usually
polymophonucleocytes) and there is also bacterial colonization within the fluid.
There is also migration of fibroblasts to the pleural cavity. Pleural fluid pH goes
down glucose levels go down LDH levels increase and cultures are usually positive.
In this stage drainage using an intercostal stage is usually employed. There is also a
tendencies to form loculations and septation in the end stage of the fibrinopurulent
stage hence use of fibrinolytics alteplase streptokinase etc. together with ICD
drainage can be considered

3. Organizing Stage
In this stage there is proliferation of fibroblasts leading to the formation of a pleural
peel or a cortex. Surgery is usually indicated at this stage in the form of a
decortication. In an untreated patient, pleural fluid may drain spontaneously
through the chest wall (i.e., empyema thoracis necessitatis).

* The chest drain with a large swing:

The normal swing of a chest drain is usually 1cm up to 2cm. A large swing signifies
that there is formation of a pleural space which may be due to;
1. Formation of a cortex
2. Blockage of a bronchus
3. Parenchymal lung disease

Penetrating chest trauma

Penetrating chest trauma is usually classified as high velocity or low velocity
trauma. Gunshot wounds e.g. Rifle or pistol are typically high velocity and have
entry wounds typically small and exit wounds (may not be present) which are
typically larger than the entry wound. Typical low velocity injuries result from stab
wounds e.g. from knives, screw drivers and spears and arrows. A shot gun can either
be low velocity or high velocity depending on the range/distance from which it is
fired from (has multiple pellets or fragments) . Penetrating trauma can also be from
ballistics bombs grenades land mines etc. penetrating trauma can cause
transmediastinal trauma if high velocity. Commonly penetrating trauma affects the
soft tissue, lung, heart, esophagus, trachea and great vessels respectively. The
majority of patients with penetrating 1ung injury can be managed with tube
thoracostomy alone. However, 20 per cent of those that require thoracotomy will
need some form of lung resection. Management of penetrating trauma is mainly
centered on exploration of the wound, maintance of hemodynamic stability ensuring
that there is no respiratory compromise and prevention of sepsis. Hence every stab
wound anti tetanus toxoid injection and prophylactic antibiotics are advocated for.
(Read further as home work)

Dr R Kanyongo Dept. Of Cardiothoracic Surgery 2015 Page 6

Penetrating cardiac trauma remains a highly lethal but potentially salvageable
injury. Most patients die of exsanguination before reaching the hospital. Aortic
injury is also lethal with the same risk as penetrating cardiac trauma

Surgical emphysema/Tissue pneumatosis.

Presence of air under the subcutaneous tissue typically felt as crepitus or crepitance
on palpation is a common finding in trauma patients. Many students have described
the feel as a sandy feel some as spongy others as pebbly bubbly feel. This
unmistakably characteristic feel is medically described as crepitus. It's a result of air
entering the tissue from air leaking from the tracheobronchial tree. This air is
atmospheric air and the main component is nitrogen which is poorly absorbed by
tissuees as well as being less soluble than O2, therefore principles of management
depends on displacing the nitrogen by creating a concentration gradient which
replaces the Nitrogen with 100% oxygen which is more soluble and readily
absorbed by tissues. Placement of a chest drain is part of the management since
these injuries are invariably accompanied by a pneumo or hemothorax.

Rib fractures
Simple rib fractures are generally well tolerated. In the absence of underlying
pathology, the treatment consists of pain control, incentive spirometry (IS), and
aggressive pulmonary toilet. However, multiple rib fractures pose a greater
challenge with pain control and can result in major morbidity in the older trauma
patient. Morbidities include the need for intubation, development of pneumonia,
and prolonged ventilator support

Flail chest
A segment of chest wall that is fractured in multiple places, resulting in an area of
the bony thorax that is "free" from rigid fixation, is termed a flail chest. It can be a
result of a fracture of more than two consecutive ribs in two places, fracture of more
than 2 ribs along their axis and their corresponding cartilage or a floating sternum
(not attached to the corresponding ribs on either side). Usually this segment
produces “paradoxical breathing" i.e. the flial segment is sucked in during
inspiration and it moves out with expiration. Small flail segments may be tolerated
with good analgesia. Posterior flail segments benefit from several natural points of
fixation (such as the overlying scapula) and do not contribute to respiratory
embarrassment. However, larger flail segments, especially those encountered
anteriorly and laterally, may compromise pulmonary function by blunting the
negative inspiratory force of spontaneous inspiration. The negative pressure of the
descending diaphragm preferentially collapses the chest wall, preventing aeration of
the lung. In these cases, the treatment is positive pressure ventilation (PPV)
(pneumatic stabilization) until the chest wall mechanics improves. Often,
oxygenation is additionally impaired by the underlying pulmonary contusion that
nearly always accompanies such an injury. The underlying pulmonary contusion
and the protracted recovery usually govern the length of time needed for
mechanical ventilation. Occasionally, the flail segment requires fixation to maintain
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the integrity of the chest wall to allow ventilation and healing and re-establish lung
volume. In addition, some ribs, fractured inward, may pose a threat to intrathoracic
structures from sharp edges.

Achalasia
Achalasia is a Greek word which means failure to relax
Achalasia is failure of the lower esophageal sphincter to relax. It is also
characterized by increased lower esophageal sphincter tone/ esophageal
hypertension and aperistalsis (triad of achalasia). Achalasia is a functional
obstruction. It is caused by neuronal degeneration or loss of the ganglia in the
myenteric plexus /Aubach's plexus which is between the inner circular muscles and
outer longitudinal muscles
*meisner plexus is submucosal*

Clinical presentation

1. Chronic dysphagia; patients give a long history of dysphagia (even as long as 5 to

20 years. Different from a short history in Ca esophagus ~2 to 3 months on average)
The dysphagia is to both solids and liquids but at times the effect of gravity and the
mass effect makes the dysphagia to be less to solids as compared to liquids
(different from Ca esophagus in which dysphagia is typically progressive from solids
to liquids)
Dr R Kanyongo Dept. Of Cardiothoracic Surgery 2015 Page 8
2. Regurgitation

3. Other common symptoms include chest pain and heartburn. Heartburn can
complicate the picture of achalasia and may be present in up to 48 per cent of
patients. Invariably, these patients are misdiagnosed and treated with PPis that are
usually unsuccessful (reason for late diagnosis)

4. Aspiration pneumonia

5. Halitosis (increased bacterial activity in the stagnat food bolus /chyme)

Investigations

1. Barium swallow
A barium swallow is often the first study performed for patients with dysphagia. It is
diagnostic, showing a dilated esophagus with an air-fluid level and the
pathognomonic finding of a "bird's beak'' with advanced achalasia.

2. Upper GI Endoscopy/ esophagoscopy

At endoscopy, a dilated esophagus with a tight LES that "pops" open with gentle
pressure is seen. Other endoscopic findings include retained food and saliva, but
most importantly, endoscopy rules out strictures and obstruction unrelated to
achalasia. However, normal endoscopy may be present in 40 percent of patients.

3. Esophageal manometer is the gold standard diagnostic modality: Classic

manometric abnormalities can be identified including hypertensive LES (resting
pressure >45 mmHg)

Management
Management can be medical, surgical or interventional/endoscopic

1. Medical
Medical treatment options include oral nitrates ( GTN) and calcium channel blockers
( nifidipine) in an attempt to facilitate LES relaxation. Therapy is usually ineffective
since most patients are unable to tolerate the side effects that include headaches,
hypotension, and tachyphylaxis. Therefore, medical therapy is generally reserved
for patients who are not candidates for surgical intervention.

2. Endoscopy
a. Endoscopic botulinum toxin injection
b. Endoscopic Pneumatic dilatation
c. Per oral endoscopic myotomy

Endoscopically injected botulinum toxin blocks the release of acetylcholine,

resulting in lower resting and basal LES pressures. Although botulinum toxin is
Dr R Kanyongo Dept. Of Cardiothoracic Surgery 2015 Page 9
effective in approximately half of the patients at 6 months, the rest require multiple
injections. Repeated injections of botulinum toxin results in an inflammatory
response at the LES, making later surgical intervention difficult. Most surgeons
agree that botulinum toxin should be reserved for patients who are not surgical
candidates. Pneumatic dilation is aimed at fracturing the muscularis propria;
however it also carries a slight risk of esophageal rupture.

c. Per Oral endoscopic Myotomy (POEM)

It's a fairly new modality of treatment popularized by the Chinese (read further as
home work)

3. Surgery
Surgical myotomy is the procedure of choice in patients diagnosed with achalasia
who do not have multiple medical co morbidities. The Heller myotomy was first
introduced in 1913 by Ernest Heller. The original Heller myotomy was performed
using both an anterior and a posterior longitudinal myotomy, disrupting the LES.
More recently, the procedure has been modified and is limited to an anterior
longitudinal myotomy (modified Heller Myotomy). It can be performed
laparoscopically or open surgery via a thoracotomy or laparatomy. Nearly 50
percent of patients develops GERD after a Heller myotomy. As result other surgeons
also fashion an antireflux mechanism ( fundoplication) e.g a Dor,Tupert or Neisen
Fundoplication and others prefer to deal with the GERD later and manage it
medically( H2 blockers and PPIs)

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