Cancer of the esophagus

Cancer of the esophagus is one on the most devastating and distressing cancers
there is. The inability to swallow associated with this cancer makes it rank high
among one of the most catastrophic cancers causing a lot of misery to the patients.
Patients are typically unable to swallow and wasted, while they consistently express
their desire to eat something. Therefore palliation aims to relieve the dysphagia.
Prognosis is very poor with an average survival of 6.5 months from time of onset of
dysphagia.

Epidemiology
Several regions have been noted to be high burden areas for cancer of the
esophagus. Northern China of the Honan province and the Linxian region,
Northeastern Iran of the Golestan Province, Khazakistan, South Africa in Kwazulu
natal and the Eastern Cape. And in our setting the Matebeleland region has been
noted to be a high burden area. Incedence in the high burden areas range from 10
per 100 000 and have been reported to be as high as 560 per 100 000 in areas such
as Khazakstan. In the USA incidence ranging from 4 upto 6 per 100 000 have also
been recorded. The male to female ratio ranging from 1.5 :1 upto 1.8:1 in the
developing world and 2.5:1 in the developed world . According to the national
cancer registry of Zimbabwe 2014 cancer of the esophagus had an incidence of 9.6
per 100 000 and was the 8th commonest cancer in the world in terms of incidence.
The average age at diagnosis ranges from 65 to 70 yrs. esophageal cancer mainly
has 2 histological types i.e. squamous cell carcinoma and adenocarcinoma. However
there are other histological types like adenosquamous, leiyomyoma and sarcoma.
Esophageal melanomas are also not uncommon. Squamous cell carcinoma is the
predominant histological type in the developing world and adenocarcinoma is said
to have overtaken the squamous type in the developed world to become the most
prominent type of cancer. This cancer is undergoing epidemiological transition.
Adenocarcinoma is also the predominant histological type found in lower third
esophageal cancers.

Pathophysiology
The exact cause of cancer of the esophagus is yet to be clearly elucidated. However
several risk factors have been identified and been noted to be associated with an
increased risk of developing cancer of the esophagus. The following have been noted
to have a close relationship with development of cancer of the esophagus.

Diet and lifestyle

1. Alcohol; mainly acts as a solvent for other carcinogens
2. Smoking
3. Chewing battle nuts
4. Eating smoked meat/fish; contains nitrates, nitrites and nitrosamines which are
carcinogenic

5. Eating Prickled vegetables

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6. Drinking scalding-hot beverages
7. Eating poorly stored grains which are infected with fungi e.g. Aspegillus flavus
Aspegillus parasticus and Fusurium sp. which produce aflatoxin which is a potent
carcinogen

8. Micronutrient deficiencies: micronutrients mainly act as enzyme cofactors, their

absence means the enzymes are not functional and hence accumulation of potent
carcinogens. The following nutritional deficiencies are known risk factors;
a. Zinc
b. Manganese
c. Magnesium
d. Molybedeneum
e. Selenium
f. Vitamin C/E

Premalignant conditions

1. Barrett’s esophagus
2. Achalasia
3. Plummer Vinson syndrome/ Paterson brown Kelly Syndrome
4. Tylosis palmaris et plantaris
5. Zenker’s diverticulum
6. Benign strictures secondary to ingestion of caustic/corrosive substances

Infections
1. HPV
2. CMV
3. Esophageal candidiasis

Clinical presentation

The main presenting complaint is progressive dysphagia. Patients often give a

history of difficulty to swallow hard solids which was followed weeks later with
difficulties in swallowing semi solids resulting in them resorting to trying a liquid
diet. In other cases they present after the dysphagia has progressed to a level where
they have difficulties in even swallowing their own saliva, i.e. absolute dysphagia.

Regurgitation is another common presenting complaint due to obstruction. N.B.

this is not vomiting but regurgitation. vomiting would require the esophagus to be
patent. However some patients continue trying to force food such that they
regurgitate and end up aspirating. Cough and fever therefore become presenting
complaints as a result of aspiration pneumonia. Local invasion/ metastasis into the
trachea resulting in the formation of a tracheoesophageal fistula results in
immediate coughing in a typical choking sensation as one swallows as a result of
aspiration.

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Metastatic effects of the tumor at times involves paralysis of the vocal cords as
result of involvement of the recurrent laryngeal nerve resulting in patients having
hoarness of the voice. Liver metastasis will result in the patient having jaundice.
Rarely mets to the lung resulting in hemoptysis. Hematemesis and odynophagia are
also rare findings seen at times when the tumor ulcerates. Pseudo achalasia
following invasion of tumor into the myenteric plexus has also been reported.

These patients are wasted and dehydrated as a result of not eating and because of
cachexia of malignancy

Investigations

1. FBC and U+E

In the full blood count these patients might have a low Hb as a result of anamia of
chronic illness. Hct can be raised as a result of dehydration causing
hemoconcetration. The WCC can be raised as a result of infection from aspiration
pneumonia.
For the urea and electrolytes. Because of the dehydration the urea is raised.
Hypokalaemia is a common finding in patients with absolute dysphagia who are
constantly spitting their saliva. (Saliva is the main source of potassium and
approximately 1-1.5L of saliva is produced per day.)

2.CXR
As a prerequisite ca esophagus patients must have a chest x ray. This will rule out
an evidence of aspiration pneumonia and it may also detect mets to the lung. Mets to
the lung can be seen as coin/canon ball lesions and in other cases as miliary
mottling as in the case of lymphagitis carcinomatosa.

3.Barium swallow
A barium swallow though falling out of favor in same centers as the prime
investigation gives us a guide about the anatomy and physiology of the esophagus
and the related tumor. This is of prime importance when planning intervention esp.
When one plans to dilate the stricture or stent insertion or the surgical approach if
esophagectomy is to be considered.
Findings of a barium swallow include:
a. The anatomy of the tumor and its location whether is in the upper, middle or
lower third ( cervical, thoracic or abdominal)
b. irregularities of the esophageal walls
c. Shouldering
e. axis change/deviation
f. Filling defect
g. Evidence of spillage into the tracheobronchial tree ( tracheoesophageal fistula)

4.Esophagoscopy and biopsy (upper G.I. Endoscopy and biopsy)

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These are the investigations which will give you the definitive diagnosis after
histology from the biopsies.

5. Endoscopic ultrasound
This is important when staging and assessing the T stage of the tumor. The
following are the T stages
T1 tumor confined to the mucosae
T2 tumor extending upto the muscularis
T3 tumor extending upto the adventitia
T4 tumor extending upto the paraesophageal and mediastinal structures

6. CT scan of the chest and abdomen

This is mainly important in assessing nodal involvement
No no nodal involvement
N1 nodal involvement

7. PET/CT scan
Important in assessing metastasis. It involves use of radioactive substance
(fludeoxyglucose). Metastasis detected as hyper metabolic lesions. Important in
determining the M stage of the tumor as well.
Mo no metastasis
M1 metasstasis

Management.

Traditionally management of Ca esophagus has put much emphasis on palliative

care. However with an increasing incidence of ca esophagus in young patients and
with improved diagnostic abilities and screening in other regions, the management
of this malignancy has significantly changed resulting in many cases where we aim
for cure. The management therefore now depends on the stage of the tumor, with
the N status and the M status proving more important than the T status in
determining the mode of treatment. In many cases patients with Ca esophagus
present late because the tumor only presents with dysphagia when 60% or more of
the lumen is occluded. The fact that the tumor grows longitudinally following the
lymphatics rather than growing out as an endoluminal tumor meaning significant
growth has to take place before luminal occlusion. The fact that the esophagus
doesn't have a serosa having adventia only makes the esophagus to be a distensible
hallow tube this also leads to late presentation of dysphagia. Above all pain is not an
early presenting feature hence patients do not come so seek medical attention early.

For palliative care the following can be done:

1. Serial dilatation using bougies e.g Hurst bougie, Mallorney bougie etc
2. Stenting e.g self expandable stents and fixed diameter stents which can be
metallic or plastic. In our setting the Procter -Livingstone tube is currently being
used other examples include Celestine tube and Artikinson tube
3. Radiotherapy ( brachytherapy )

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4. Photodynamic therapy
5. Laser Therapy
6. Argon photo coagulative therapy
7. Radio frequency ablative therapy

Surgery with curative intent;

The fact that the lymphatic drainage is longitudinal makes it difficult to have a
consensus of what a clear margin is in terms of resection. Distances of 5 cm upto as
much as 10cm have been quoted in literature.
Esophagectomy is the surgical procedure usually done for esophageal cancer
Surgical approaches are dependent on the anatomical location of the tumor whether
upper middle or lower third. The following are the surgical approaches for an
esophagectomy:
1. Ivor-Lewis
2. Modified Mckeon
3. Transhiatal
4. Transabdominal

Neoadjuvant therapy :
chemotherapy, radiotherapy or chemoradio therapy then surgery
Have been shown to produce a better outcome, compared to surgery alone for Ca
esophagus patients.however radiotherapy before surgery makes surgery to be
more technically challenging because of difficulties in identifying tissue plans as
result of radiotherapy induced fibrosis.

Adjuvant therapy
Chemotherapy/radiotherapy or chemoradio therapy after surgery.

For further reading :

1. Esophageal cancer in young patients;

To date the youngest patient to be diagnosed of esophageal cancer in Zimbabwe
was an 18 year old female patient ( chimuka d,muteweye w et al). The youngest
patient recorded in literature was an 8 year old in India ( Paymaster et al) The
largest case series to date was from western Kenya with 109 young Ca esophagus
patients, with the youngest patient being 14years( young described as any patient
who is 30 yrs or younger) recorded at Tenwek hospital in western Kenya over a
period of 13.5 years i.e from January 1996 to June 2009. The findings proved Ca
esophagus to be a unique cancer. The findings proved genetics and environmental
factors to play a significant role in cancers of the esophagus in this population. 80%
of the 109 patients were of the Kalenjin tribe. 70% of this population had a family
history of a malignancy and 49 % had a family history of cancer of the esophagus.
The male to female ratio in this population was just like in any other populations at
1.4:1 and 80 percent of the cases the histology was squamous cell carcinoma.
Overally 6% of the cases of Ca esophagus were diagnosed in young patients during
this 13.5 year period as compared to an average 1.5% in other high burden areas.

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The results also highlighted the fact of shared genetic and environmental risk
factors ( food and traditional medicines). Only 15% had a history of either using
alcohol or having a history of smoking.

2. HIV and cancer of the esophagus

A recent study of 600,000 AIDS patients demonstrated a 69% increase in the risk of
esophageal carcinomas, compared to matched non-AIDS individuals ( Peerson et al
gastric and esophageal malignancies in HIV 2012) This increase was consistent
before and after the Highly Active Antiretroviral Therapy (HAART) era. These
results were consistent with other studies demonstrating the same association.
Theories as to why this is so have proposed associated immunosuppression,
infections, increased prevalence of tobacco and alcohol use, as well as other factors,
as the reasons behind this association. However, comparing HIV patients to other
immunosuppressed populations, and the discrepancies between observed
pathological types among HIV-infected patients compared to the expected
pathological types related to alcohol and smoking do not indicate that these are the
only causes. The exact mechanism remains controversial and is likely multi-
factorial. Demographics of different Esophageal cancers among the HIV-infected,
proposed theories, and means of prevention are heavily discussed in the literature.
However, very little material approaches clinical aspects of the HIV-infected patient
with potential or proven Esophageal Cancer. The growing burden of non-AIDS
defining cancers highlights the importance of early detection and management
among the HIV-infected. However, the risk of esophageal cancer with HIV, while
elevated, would not justify a cost-effective screening of all the HIV-infected
population.

Definitions

1. Achalasia a Greek word meaning failure to relax. Achalasia is a condition

characterized by a triad of failure of the lower esophageal sphincter (LES) to relax,
increased LES tone/ hypertension and aperistalsis. It is a result of neuronal
degeneration of the myenteric plexus.

2. Barrett’s esophagus is a condition in which there is metaplastic change in the

epithelium in the lower esophagus (squamocolumnar junction) which normally has
stratified squamous and columnar epithelium, changing to intestinal type columnar
epithelium which contains mucus and secretory glands. This is a result of chronic
gastroesophageal reflux disease ( GERD). The change is an adaptation to the chronic
insult.

3. Plummer Vinson Syndrome/ Paterson Brown Kelly

The association of postcricoid dysphagia, upper esophageal webs, and iron
deficiency anemia is known as Plummer-Vinson syndrome (PVS) in the United
States and Paterson-Brown Kelly syndrome in the United Kingdom. The term
sideropenic dysphagia has also been used, because the syndrome can occur with
iron deficiency (sideropenia), but it is not associated with anemia. Other

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associations are atrophic glossitis, kolionychia and angular chelitis.the syndrome is
extremely rare. Most of the patients are white middle-aged women, in the fourth to
seventh decade of life but the syndrome has also been described in children and
adolescents. The dysphagia is usually painless and intermittent or progressive over
years, limited to solids and sometimes associated with weight loss. Symptoms
resulting from anemia (weakness, pallor, fatigue, tachycardia) may dominate the
clinical picture. Enlargement of the spleen and thyroid may also be observed.

4. Tylosis Palmaris et plantaris

A genetic disorder characterized by thickening (hyperkeratosis) of the palms and
soles, white patches in the mouth (oral leukoplakia), and a very high risk of
esophageal cancer. This is the only genetic syndrome known to predispose to
squamous cell carcinoma of the esophagus. The risk of developing esophageal
cancer is 95% by age 70. The syndrome is inherited in an autosomal dominant
manner. The gene has been mapped to chromosome 17q25 but has not been
identified. The syndrome is also called nonepidermolytic palmoplantar
keratoderma/ Howel-Evans Syndrome.

5.Zenker's diverticulum.
Zenkers diverticulum is an esophageal pouch that develops in the upper esophagus
that causes debilitating dysphagia and regurgitation of food. It is a pulsion
diverticulum of the hypopharynx i.e an outpouching of the sbmucosa and mucosa
through Killian's triangle, an area of weakness between the transverse fibers of the
cricopharyngeus muscle and the oblique fibers of the inferior constrictor muscles.
Zenker's diverticula are lined with stratified squamous epithelium with a thin
lamina propria. No muscular layer exists. Fibrosis surrounding the diverticulum is
common.It is named after Friedrich Albert von Zenker (1825-1898) who in 1877
published a series of patients with this disorder and described its anatomic
pathophysiology.

Reference books
1. John Hopkins manual of Cardiothoracic surgery
2. Shawartz principles of surgery
3. Pearsons surgery of the esophagus
4. Robins an Coltrans pathological basis of disease
5. Mastery in Cardiothoracic surgery
6. Sabiston and spencer chest surgery
7. General thoracic surgery.

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Bronchogenic carcinoma
Lung cancer is a leading cause of preventable death attributed to smoking and
environmental exposure. Its highest incidence is in men but recent trends have
shown a significant increase in women paralleling the trend of smoking prevalence
in different genders. Bronchogenic carcinoma is mainly divided into non-small cell
carcinoma (NSCC) and small cell carcinoma (SCC). Non-small cell carcinoma makes
up 80% of all bronchogenic carcinomas.

NSCC has three main histological types

1. Squamous cell carcinoma (mainly central)
Has a strong association with smoking as compared to adenocarcinoma.
Macroscopically it appears as a white or grey tumor growing from bronchial
epithelium
Histology shows keretinazation and pearl formation
Immunohistochemistry shows cytokeratin 5 and 6 (CK5 and CK6) carcinoembryonic
antigen and keratin

2. Adenocarcinoma (mainly peripheral)

Is the common histological type found in non-smokers. Also arises in areas of
previous scarring/fibrosis it has an association with tuberculosis scarring and
bronchiectasis and is also common histological type in women. Macroscopically it
appears as a white fleshy solid tumor. Immunohistochemistry reveals TTF-1
(Thyroid transcription factor 1) Cytokeratin 7 (CK7)

3. Large cell carcinoma

is a poorly differentiated epithelial tumor consisting of sheets or nests of large
polygonal cells with vesicular nuclei and prominent nucleoli. Large cell carcinoma is
usually diagnosed by excluding other tumor types during histopathologic
examination. Most large cell carcinomas are located in the peripheral lung and
invade the visceral pleura, chest wall, or adjacent structures.

Other histological types like adenosquamous carcinoma, adenoid cystic carcinoma,

epithelial- myoepithelial carcinoma and epidermoid cystic carcinoma make up 2%
of NSCC.

Adenocarcinoma is also further divided into

a. bronchoalveolar carcinoma ( usually presents as a solitary pulmonary nodule
with a diffuse intestinal infiltrative pattern resembling a pneumonia)
b. papillary
c. Acinar
d. Mucinous

SCC
Small cell carcinoma previously known as oat cell carcinoma has the greatest
association with paraneoplastic syndromes. It is very aggressive with a fast
progression. However it is very much chemo sensitive but has a high recurrence
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rate. Because of its aggressive nature SCC is usually staged into stages; extensive
disease and limited disease.

Neuroendocrine cells

1. Atypical carcinoid
2. Typical carcinoid
3. Neuroendocrine large cell carcinoma
4. Neuroendocrine small cell carcinoma

Risk factors
Smoking
Asbestos
Occupational exposure to radon, polycyclic aromatic hydrocarbons in dyes
Arsenic
Radiation
Nickel
Chromates
TB scarring

Pathophysiology

Development of lung cancer is considered as a series of genetic changes induced by

environmental factors, which leads a normal cell to develop into a cancer. These
genetic changes are mutations of the tumor oncogenes and tumor suppressors as
well as the change in the tumor microenvironment that allows the tumor to grow
and metastasize into other organs. Known mutations in adenocarcinoma are of the
K-RAS oncogene EGFR and the tumor suppress genes p53 and p16. Similar
multistage mutations also occur in invasive squamous cell carcinoma but less than
2% mutations of K-RAS and EGFR mutations but with about 60% in p53 mutations.
Small cell carcinoma has ~ 90 p16/RB gene mutations and 30% mutations in Myc
oncogene.

Clinical presentation
Cough
Hemoptysis
Chest pain
Dyspnea
Weight loss

Metastatic effects
1. Pancoast tumor; apical lung tumour invading the cervical sympathetic
ganglia causing Horner’s syndrome. Pancoast syndrome occurs when there is
Horner’s syndrome plus invasion of the lower roots of the brachial plexus

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 causing pain in the medial aspect of the arm and wasting of the thena
muscles of the hand.

2. Horner’s syndrome: ptosis, miosis, enopthalmous and anhidrios

3. Pathological bone fractures
4. Paraplegia ( mets to the spine
5. Stroke/ neurological deficits ( mets to the brain)

Non metastatic effects/ Para neoplastic syndromes

1. Clubbing
2. Hypertrophic osteoathropathy
3. Acanthosis Nigrans
4. Dermatomyositis
5. Lambert Eaton syndrome

Neuroendrocrine symptoms
1. Cushing syndrome
2. Syndrome of inappropriate ADH secretion
3. Hypercalcaemia (secretion of Parathormone like hormone)
4. Hyperglycaemia
5. Hypercalcinotanaemia
6. Hyperthyroidism
7. Carcinoid syndrome

Investigations.
1.CXR ( after FBC and U+E)
2. Bronchoscopy and biopsy/ bronchoalveolar lavage with bronchial Washings for
cytology
3. CT scan chest Abdomen and pelvis ( brain in suspected mets)

Staging
Tx Malignant cells in bronchial secretions, no other evidence of tumour
Tis carcinoma in situ
T0 None evident
T1 <3cm
T2 3cm -7cm tumor or any tumor which is >2cm distal from carina/ any tumor
size with visceral pleural involvement , partial atelectasis from tumor
T3 tumor >7cm tumor involving the chest wall. Tumor less than 2cm from carina
T4 tumor invading heart, aorta and esophagus and other mediastinal structures
presence of malignant pleural effusion

No no nodal involvement
N1 peribrochial nodes ipsilateral hilar nodes
N2 contralateral hila ipsilateral mediastinal and subcarinal lymph nodes
N3 contralateral mediastinal nodes, scalene and supraclavicular nodes

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Mo no metastasis
M1 distant metastasis
M1a separate tumor nodule(s) in contralateral lobe, pleural nodules malignant
pleural and pericardial effusion
M1b distant metastasis

From the TNM classification Bronchogenic cancer can be staged from Stage I -IV
Management will thus depend on the stage of the tumor
* read on the various stages for interest *

In general there is good outcome for surgery for stage I upto stage II b. however
surgery can be performed for tumors upto stage IIIb. Surgery is either a lobectomy
or a pneumectomy. However the cardiopulmonary reserve has to be assessed before
undertaking these operations to assess whether or not a patient will be able to
withstand surgery. Surgery remains the mainstay in treatment of lung cancers.
Radiotherapy can be offered to patients who can not withstand surgery. For
advanced disease chemotherapy is offered.

Prognosis
Overall, the prognosis for lung cancer is poor. The estimated overall 5-year survival
rate for all of the patients with lung cancer is about 16 percent; however, patients
with resected pathologic early stage lung cancer can achieve a 5-year survival rate
of 70 to 80 percent. The type and pathologic stage of lung cancer is the best
predictor for prognosis

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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.

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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
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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)

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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)
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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
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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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