esophageal cancer

CHAPTER 1
THEORY: ESOPHAGEAL CANCER
1.1 Introduction
The American Cancer Society's estimates for esophageal cancer in the United States for 2013 are
about 17,990 new esophageal cancer cases diagnosed (14,440 in men and 3,550 in women),and
about 15,210 deaths from esophageal cancer (12,220 in men and 2,990 in women).
This disease is 3 to 4 times more common among men than among women. The lifetime risk of
esophageal cancer in the United States is about 1 in 125 in men and about 1 in 435 in women.
Overall, the rates of esophageal cancer in the United States have been fairly stable for many
years. It was once much more common in African Americans than in whites. But it is now about
equally as common, as rates have fallen in African Americans and increased slightly in whites
over the past few decades. Squamous cell carcinoma is the most common type of cancer of the
esophagus among African Americans, while adenocarcinoma is more common in whites. Cancer
of the esophagus is much more common in some other countries. For example, esophageal cancer
rates in Iran, northern China, India, and southern Africa are 10 to 100 times higher than in the
United States. The main type of esophageal cancer in these countries is squamous cell carcinoma.
Although many people with esophageal cancer will go on to die from this disease, treatment has
improved and survival rates are getting better. During the 1960s, fewer than 5% of patients
survived at least 5 years after diagnosis. Now, about 20% of patients survive at least 5 years after
diagnosis. This includes patients with all stages of esophageal cancer at the time of diagnosis.
Survival rates for people with early stage cancer are higher.
1.2 Anatomy of Esophagus
The esophagus is a hollow, muscular tube that connects the throat to the stomach. It lies behind
the trachea (windpipe) and in front of the spine. Food and liquids that are swallowed travel
through the inside of the esophagus (called the lumen) to reach the stomach. In adults, the
esophagus is usually between 10 and 13 inches long and is about ¾ of an inch across at its
smallest point.

1.3 Histology of Esophagus
Mucosa: This is the layer that lines the inside of the esophagus. The mucosa has 3 parts:
• The epithelium forms the innermost lining of the esophagus and is normally made up
of flat, thin cells called squamous cells. This is where most cancers of the esophagus
start.
• The lamina propria is a thin layer of connective tissue right under the epithelium.
• The muscularis mucosa is a very thin layer of muscle under the lamina propria.
Submucosa: This is a layer of connective tissue just below the mucosa that contains blood vessels
and nerves. In some parts of the esophagus, this layer also contains glands that secrete mucus.
Muscularispropria: This is a thick band of muscle under the submucosa. This layer of muscle
contracts in a coordinated, rhythmic way to push food along the esophagus from thethroat to the
stomach.
Adventitia: This is the outermost layer of the esophagus, which is formed by connective tissue.
The upper part of the esophagus has a special area of muscle at its beginning that relaxes to open
the esophagus when it senses food or liquid coming toward it. This muscle is called the upper
esophageal sphincter.
The lower part of the esophagus that connects to the stomach is called the gastroesophageal (GE)
junction. A special area of muscle near the GE junction, called the lower esophageal sphincter,
controls the movement of food from the esophagus into the stomach and it keeps the stomach's
acid and digestive enzymes out of the esophagus.
Reflux and Barrett’s Esophagus
The stomach has strong acid and enzymes that digest food. The epithelium (inner lining) of the
stomach is made of gland cells that release acid, enzymes, and mucus. These cells have special
features that protect them from the stomach's acid and digestive enzymes.

In some people, acid escapes from the stomach back into the esophagus. The medical term for
this is gastroesophageal reflux disease (GERD), or just reflux. In many cases, reflux can cause
symptoms such as heartburn or a burning feeling spreading out from the middle of the chest. But
sometimes, reflux can occur without any symptoms at all.
If reflux of stomach acid into the lower esophagus continues for a long time, it can damage the
lining of the esophagus. This causes the squamous cells that usually line the esophagus to be
replaced with gland cells. These gland cells usually look like the cells that line the stomach and
the small intestine and are more resistant to stomach acid. The presence of gland cells in the
esophagus is known as Barrett's (or Barrett) esophagus. People with Barrett's esophagus are much
more likely to develop cancer of the esophagus. These people require close medical follow-up in
order to find cancer early. Still, although they have a higher risk, most people with Barrett's
esophagus do not go on to develop cancer of the esophagus
1.4 Esophageal Cancer
Cancer of the esophagus (also referred to as esophageal cancer) starts in the inner layer (the
mucosa) and grows outward (through the submucosa and the muscle layer). Since 2 types of cells
can line the esophagus, there are 2 main types of esophageal cancer: squamous cell carcinoma
and adenocarcinoma.
The esophagus is normally lined with squamous cells. The cancer starting in these cells is called
squamous cell carcinoma. This type of cancer can occur anywhere along the esophagus. At one
time, squamous cell carcinoma was by far the more common type of esophageal cancer in the
United States. This has changed over time, and now it makes up less than half of esophageal
cancers in this country.
Cancers that start in gland cells are called adenocarcinomas. This type of cell is not normally part
of the inner lining of the esophagus. Before an adenocarcinoma can develop, gland cells must
replace an area of squamous cells, which is what happens in Barrett's esophagus. This occurs
mainly in the lower esophagus, which is the site of most adenocarcinomas. Cancers that start at
the area where the esophagus joins the stomach (the GE junction), which includes about the first
2 inches of the stomach (called the cardia), tend to behave like esophagus cancers (and are treated
like them, as well), so they are grouped with esophagus cancers

1.4.1 Risk Factor
There are several risks factor such as:
Age: Less than 15% of cases are found in people younger than age 55.
Gender: Compared with women, men have more than a 3-fold higher rate of esophageal cancer.
Gastroesophageal reflux disease
Barrett's esophagus: The risk of cancer is highest if dysplasia is present or if other people in
family also have Barrett’s.
Tobacco and alcohol: The link to squamous cell esophageal cancer is even stronger. Drinking
alcohol also increases the risk of esophageal cancer. The chance of getting esophageal cancer
goes up with higher intake of alcohol.
Obesity: This is in part explained by the fact that people who are obese are more likely to have
esophageal reflux.
Diet: A diet high in fruits and vegetables is linked to a lower risk of esophageal cancer. Drinking
very hot liquids frequently may increase the risk for the squamous cell type of esophageal cancer
due to long-term damage the liquids do to the cells lining the esophagus. Overeating, which leads
to obesity, increases the risk of the adenocarcinoma of the esophagus.
Achalasia: People with achalasia have a risk of esophageal cancer that is many times normal. On
average, the cancers are found about 15-20 years after the achalasia is diagnosed.
Tylosis: This is a rare, inherited disease that causes excess growth of the top layer of skin on the
palms of the hands and soles of the feet. People with tylosis need to be watched closely to try to
find esophageal cancer early. Often this requires regular monitoring with an upper endoscopy
Esophageal webs: A web is a thin membrane extending out from the inner lining of the
esophagus that causes an area of narrowing. Most esophageal webs do not cause any problems,
but larger webs may cause food to get stuck in the esophagus, which can lead to problems
swallowing. When an esophageal web is found along with anemia, tongue irritation (glossitis),
brittle fingernails, and a large spleen it is called Plummer-Vinson syndrome. Another name for

this is Paterson-Kelly syndrome. About 1 in 10 patients with this syndrome eventually develop
squamous cell cancer of the esophagus.
Workplace exposures: Exposure to chemical fumes in certain workplaces may lead to an
increased risk of esophageal cancer. For example, exposure to the solvents used for dry cleaning
may lead to a greater risk of esophageal cancer. Some studies have found that dry cleaning
workers may have a higher rate of esophageal cancer.
Injury to the esophagus: Lye is a chemical found in strong industrial and household cleaners
such as drain cleaners. Lye is a corrosive agent, meaning it can burn and destroy cells. Sometimes
small children mistakenly drink from a lye-based cleaner bottle. The lye causes a severe chemical
burn in the esophagus. As the injury heals, the scar tissue can cause an area of the esophagus to
become very narrow (called a stricture). People with these strictures have an increased rate of the
squamous cell type of esophageal cancer as adults. The cancers occur on average about 40 years
after the lye was swallowed.
History of certain other cancers:People who have had certain other cancers, such as lung
cancer, mouth cancer, and throatcancer have a high risk of getting squamous cell carcinoma of
the esophagus as well. This may be because all of these cancers can be caused by smoking.
Human papilloma virus: Genes from human papilloma virus (HPV) have been found in up to
one-third of esophagus cancer tumors from patients living in Asia and South Africa. Signs of
HPV infection have not been found in esophagus cancers from patients living in the other areas,
including the US. HPV is a group of more than 100 related viruses. They are called papilloma
viruses because some of them cause a type of growth called a papilloma (or wart). Infection with
certain types of HPV is linked to a number of cancers, including throat cancer, anal cancer, and
cervical cancer
1.4.2 Diagnosis of Esophageal Cancer
1.4.2.1 Sign and Symptoms
Dysphagia: The most common symptom of esophageal cancer is a problem swallowing. This is
often mild when it starts, and then gets worse over time as the opening inside the esophagus gets
narrower. Dysphagia is commonly a late symptom caused by a large cancer. When swallowing

becomes difficult, people often change their diet and eating habits without realizing it. They take
smaller bites and chew their food more carefully and slowly. As the cancer grows larger, the
problem gets worse. People then may start eating softer foods that can pass through the
esophagus more easily. They may avoid bread and meat, since these foods typically get stuck.
The swallowing problem may even get bad enough that some people stop eating solid food
completely and switch to a liquid diet. If the cancer keeps growing, at some point even liquids
will not be able to pass. To help pass food through the esophagus, the body makes more saliva.
This causes some people to complain of bringing up lots of thick mucus or saliva.
Chest Pain: Sometimes, people complain of pain or discomfort in the middle part of their chest.
Some people describe a feeling of pressure or burning in the chest. These symptoms are more
often caused by problems other than cancer, such as heartburn, and so they are rarely seen as a
signal that a person may have cancer. Swallowing may become painful when the cancer is large
enough to limit the passage of food through the esophagus. Pain may be felt a few seconds after
swallowing, as food or liquid reaches the tumor and has trouble getting past it.
Weight Loss: About half of patients with esophageal cancer lose weight (without trying to). This
happens because their swallowing problems keep them from eating enough to maintain their
weight. Other factors include a decreased appetite and an increase in metabolism from the cancer.
Other symptoms are: Hoarseness, chronic cough, hiccups, pneumonia, bone pain, and bleeding
into the esophagus.
1.4.2.2 Imaging Tests
Barium Swallow: A barium swallow test can show any irregularities in the normally smooth
surface of the inner lining of the esophagus. Even small, early cancers can often be seen using
this test. Tumors grow out from the lining of the esophagus and stick out into the lumen (the open
area of the tube). They cause the barium to coat that area of the esophagus unevenly. Early
cancers can look like small round bumps or flat, raised areas (called plaques), while advanced
cancers look like large irregular areas and cause a narrowing of the width of the esophagus. This
test can also be used to diagnose one of the more serious complications of esophageal cancer
called a tracheo-esophageal fistula.

Barium swallow demonstrating stricture due to
cancer
Barium swallow demonstrating an endoluminal
mass in the mid esophagus
Computed Tomography (CT) Scan: CT scans are not usually used to make the initial diagnosis
of esophageal cancer, but they can help see how far it has spread. CT scans often can show where
the cancer is in the esophagus. These scans can also show the nearby organs and lymph nodes
(bean-sized collections of immune cells to which cancers often spread first), as well as distant
areas of cancer spread.
Magnetic resonance imaging (MRI) scan: Like CT scans, MRI scans provide detailed images
of soft tissues in the body. But MRI scans use radio waves and strong magnets instead of X-rays.
The energy from the radio waves is absorbed and then released in a pattern formed by the type of
tissue and by certain diseases. A computer translates the pattern of radio waves given off by the
tissues into a very detailed image of parts of the body. A contrast material might be injected into
a vein. MRI scans are very helpful in looking at the brain and spinal cord, but they are not often
needed to assess spread of esophageal cancer.
Positron emission tomography (PET) scan: For a PET scan, a form of radioactive sugar
(known as fluorodeoxyglucose or FDG) is injected into the blood. The amount of radioactivity
used is very low. Cancer cells in the body are growing rapidly, so they absorb large amounts of

the radioactive sugar. The picture is not finely detailed like a CT or MRI scan, but it provides
helpful information about whole body.
Endoscopy
Upper endoscopy: Performing esophagogastroduodenoscopy allows direct visualization and
biopsies of the tumor.
Endoscopy demonstrating intraluminal
esophageal cancer
Chest CT scan showing invasion of the trachea
by esophageal cancer
Endoscopic ultrasound: This is actually a type of imaging test that involves the use of endoscopy.
Ultrasound tests use sound waves to take pictures of parts of the body. They use no radiation and
are very safe. For an endoscopic ultrasound, the probe that gives off the sound waves is at the end
of an endoscope, which is passed down the throat and into the esophagus. This allows the probe
to get very close to the cancer. This is done with local anesthesia and light sedation.
This test is very useful in determining the size of an esophageal cancer and how far it has grown
into nearby tissues. It can also help determine if nearby lymph nodes might beaffected by the
cancer. If enlarged lymph nodes are seen on the ultrasound and not beside the tumor, the doctor
may use a thin, hollow needle to get biopsy samples of them. This helps to decide if the tumor
can be surgically removed.
Bronchoscopy: This exam may be done for cancer in the upper part of the esophagus to see if it
has spread to the windpipe (trachea) or the tubes leading from the trachea into the lung (bronchi).

If abnormal areas are seen, small instruments can be passed down the bronchoscope to take
biopsy samples.
Laparoscopy and thoracoscopy have a greater than 92% accuracy in staging regional nodes.
Lab testing of biopsy samples
An area seen on endoscopy or on an imaging test may look like cancer, but the only way to know
for sure is to do a biopsy.This is most often done during an endoscopy exam. A doctor called a
pathologist then looks at the tissue under a microscope to see if any cancer cells are present. If
there is cancer, the pathologist will determine the type (adenocarcinoma or squamous cell) and
the grade of the cancer (how abnormal the patterns of cells look under the microscope).
HER2 testing: If esophageal cancer is found but is too advanced for surgery, samples may be
tested for the HER2 gene or protein. Some people with esophageal cancer have too much of a
protein called HER2 on the surface of their cancer cells, which helps the cells grow. However, a
drug that targets the HER2 protein, known as trastuzumab (Herceptin®), may help treat these
cancers when used along with chemotherapy. Only cancers that have too much of the HER2 gene
or protein are likely to be affected by this drug, which is why doctors may test tumor samples for
it.
Other tests are: blood test, complete blood count (CBC) to look for anemia (which could be
caused by internal bleeding). A stool sample may be checked to see if it contains occult (unseen)
blood. Also check for liver and kidney functions are normal.
1.4.3 Staging
Esophageal cancer staging was changed in the last edition of the Union for International Cancer
Control/American Joint Cancer Committee (UICC/AJCC) manual in 2009. All esophageal
tumors and tumors with epicenters within 5 cm of the esophagogastric junction that also extend
into the esophagus are classified and staged according to the esophageal scheme. All other tumors
with an epicenter in the stomach greater than 5 cm from the esophagogastric junction or those
within 5 cm of the esophagogastric junction without extension into the esophagus are staged
using the gastric carcinoma scheme.

Conventional staging tools such as esophagoscopy or barium esophagogram can demonstrate
only intraluminal disease extent, and CT scan of the chest is relatively insensitive, except for the
presence of extensive local disease. Esophageal ultrasound allows the visualization of both the
esophageal wall and local lymph nodes. As such, it allows a clinical determination of both T and
N stage in most patients.
Survival rates are not readily available for each stage in the AJCC staging system for esophageal
cancer. The survival rates below come from the National Cancer Institute's Surveillance,
Epidemiology, and End Results (SEER) database, and are based on patientswho were diagnosed
with esophageal cancer between 2002 and 2008. The SEER database does not divide survival
rates by AJCC stage. Instead, this database divides cancers into 3 larger, summary stages:
• Localized means that the cancer is only growing in the esophagus. It includes AJCC
stage I and some stage II tumors (such as those that are T1, T2, or T3, N0, M0). Stage
0 cancers are not included in these statistics.
• Regional means that the cancer has spread to nearby lymph nodes or tissues. This
includes T4 tumors and cancers with lymph node spread (N1, N2, or N3).
• Distant means that the cancer has spread to organs or lymph nodes away from the
tumor, and includes all M1 (stage IV) cancers.
Stage 5-Year Relative Survival Rates are: Localized 38%, regional 20% and distant 3%
These survival rates for esophageal cancer do not separate squamous cell carcinomas from
adenocarcinomas, although adenocarcinomas are generally thought to have a slightly better
prognosis (outlook) overall.

1.4.4 Treatment of Esophageal Cancer
General treatment information
The main options for treatment of cancer of the esophagus include:
• Surgery
• Radiation
• Chemotherapy
• Targeted therapy
• Endoscopic treatments
Endoscopic treatments, such as endoscopic mucosal resection, radiofrequency ablation, and
photodynamic therapy, may be used for early cancers and pre-cancers of the esophagus. Some of

these treatments can also be used as palliative treatment when all the cancer cannot be removed.
Palliative treatment is meant to relieve symptoms, such as pain and trouble swallowing, but it is
not expected to cure the cancer.
Esophagectomy: Often a small part of the stomach is removed as well. The upper part of the
esophagus is then connected to the remaining part of the stomach. Part of the stomach is pulled
up into the chest or neck to become the new esophagus. How much of the esophagus is removed
depends upon the stage of the tumor and where it's located. If the cancer is in the lower part of
the esophagus (near the stomach) or at the place where the esophagus and stomach meet (the
gastroesophageal or GE junction), the surgeon will remove part of the stomach, the part of the
esophagus containing the cancer, and about 3 to 4 inches of normal esophagus above this. Then
the stomach is connected to what is left of the esophagus either high in the chest or in the neck.
If the tumor is in the upper or middle part of the esophagus, most of the esophagus will need to be
removed to be sure to get enough tissue above the cancer. The stomach will then bebrought up
and connected to the esophagus in the neck. If the stomach cannot be used to replace the
esophagus, the surgeon may use a piece of the intestine instead. When a piece of intestine is used,
it must be moved without damaging its blood vessels. If the vessels are damaged, not enough
blood will get to that piece of intestine, and the tissue will die.
Esophagectomy may be done using either of 2 main types of techniques. The standard, open
technique uses one or more large incisions (cuts) in the neck, chest, or abdomen to perform the
surgery. In minimally invasive surgery, the surgeon operates through several smaller incisions
using special long, thin surgical instruments.
Open esophagectomy: Many different approaches can be used in operating on esophageal cancer.
For a transthoracic esophagectomy, the esophagus is removed with the main incisions in the
abdomen and the chest. If the main incisions are in the abdomen and neck, it is called a
transhiatalesophagectomy. Some approaches use incisions in the neck, chest, and abdomen.
Minimally invasive esophagectomy: For some early (small) cancers, the esophagus can be
removed through several small incisions instead of 1 or 2 large incisions. The surgeon puts a
scope (like a tiny telescope) through one of the incisions to see everything during the operation.
Then the surgical instruments go in through other small incisions. In order to do this type of

procedure well, the surgeon needs to be highly skilled and have a great deal of experience
removing the esophagus this way. Because it uses smaller incisions, minimally invasive
esophagectomy may allow the patient to leave the hospital sooner and recover faster.
Lymph node removal: For either type of esophagectomy, nearby lymph nodes are removed
during the operation as well. These are then checked to see if they contain cancer cells. If the
cancer has spread to lymph nodes, the outlook is not as good, and the doctor may recommend
other treatments (like chemotherapy and/or radiation) after surgery.
Radiation therapy for cancer of the esophagus: Radiation therapy is the use of high-energy
radiation to kill cancer cells. It is often combined with other types of treatment, such as
chemotherapy (chemo) and/or surgery, to treat esophageal cancer. Radiation therapy may be
used:
• As part of the primary (main) treatment of esophageal cancer in some patients,
typically along with chemo. This is often used for people who can't have surgery due
to poor health.
• Before surgery (usually along with chemo), to try to shrink the cancer and make it
easier to remove (called neoadjuvant treatment).
• After surgery (usually along with chemo), to try to kill any areas of cancer cells that
may have been left behind but are too small to see. This is known as adjuvant therapy.
• To ease the symptoms of advanced esophageal cancer such as pain, bleeding, or
trouble swallowing. This is called palliative therapy.
There are 2 main types of radiation therapy:
External-beam radiation therapy: This type of treatment focuses radiation from outside the
body on the cancer. This is the type of radiation therapy most often used when the intent is to try
to cure esophageal cancer.. Radiation therapy is much like getting an x-ray, but the radiation is
stronger. The procedure itself is painless. Each treatment lasts only a few minutes. Most often,
radiation treatments are given 5 days a week for several weeks.
Internal radiation therapy (brachytherapy): For this type of treatment, the doctor places
radioactive material very close to the cancer through an endoscope. The radiation travels only a

short distance, so it reaches the tumor but has little effect on nearby normal tissues. The
radioactive source is then removed a short time later. Brachytherapy can be given 2 ways;for
high-dose rate (HDR) brachytherapy, the doctor leaves the radioactive material near the tumor for
a few minutes at a time, which may require several treatments. In low-dose rate (LDR)
brachytherapy, a lower dose of radiation is put near the tumor for longer periods (1 or 2 days) at a
time. This requires that the patient stay in the hospital during treatment, but it can usually be
completed in only 1 or 2 treatments. Brachytherapy is most often used with more advanced
esophageal cancers to shrink tumors so a patient can swallow more easily. This technique cannot
be used to treat a very large area, so it is better used as a way to relieve symptoms (and not to try
to cure the cancer).
Chemotherapy for cancer of the esophagus: Chemotherapy (chemo) uses drugs that are given
through a vein or by mouth to treat cancer. These drugs enter the bloodstream and reach all areas
of the body, making this treatment useful for cancer that has spread. Depending on the type and
stage of esophageal cancer, chemo may be given:
• As part of the main (primary) treatment, along with radiation therapy.
• Before surgery (usually along with radiation therapy) to try to shrink the cancer and
make it easier to remove. This is called neoadjuvant treatment.
• After the cancer has been removed by surgery (usually along with radiation therapy)
to try to kill any small areas of tumor cells that may have been left behind. This is
known as adjuvant treatment.
• Alone or with radiation to help control symptoms like pain or trouble swallowing
when the cancer can't be cured. This is called palliative treatment.
Chemo by itself rarely cures esophageal cancer. It is often given together with radiation therapy.
This combination (called chemoradiation or chemoradiotherapy) can be useful for large tumors
that couldn't be removed otherwise. It can shrink the tumor enough for surgery to be an option.
Chemoradiation is also often used before surgery for smaller tumors. Using chemoradiation
before surgery can help people live longer than using surgery alone. Chemoradiation is also
sometimes given after surgery, but it isn’t clear that it is as helpful as giving it before surgery.

In some cases, chemoradiation may be used as the only treatment. This may be a good choice for
patients who cannot have surgery because they have other major health problems. Thismay also
be an option for some patients who could have surgery.
Chemo is given in cycles, with each period of treatment followed by a rest period to allow the
body time to recover. Each chemo cycle typically lasts for a few weeks. Many different chemo
drugs can be used to treat esophageal cancer. Common regimens are:
• Carboplatin and paclitaxel (Taxol®) (which may be combined with radiation)
• Cisplatin and 5-fluorouracil (5-FU) (often combined with radiation)
• ECF: epirubicin (Ellence®), cisplatin, and 5-FU (especially for gastroesophageal
junction tumors)
• DCF: docetaxel (Taxotere®), cisplatin, and 5-FU
• Cisplatin with capecitabine (Xeloda®)
Other chemo drugs that have been used to treat cancer of the esophagus include oxaliplatin,
doxorubicin (Adriamycin®), bleomycin, mitomycin, methotrexate, vinorelbine (Navelbine®),
topotecan, and irinotecan (Camptosar®). For some esophagus cancers, chemo may be used along
with the targeted drug trastuzumab(Herceptin®).
Targeted therapy for cancer of the esophagus: As researchers have learned more about the
changes in cells that cause cancer, they have been able to develop newer drugs that specifically
target these changes. Targeted drugs work differently from standard chemotherapy drugs. They
often have different (and less severe) side effects. A small number of esophagus cancers have too
much of a protein called HER2 on the surfaceof their cells. This protein may help the cancer cells
to grow. Having too much of this protein is caused by having too many copies of the HER2 gene.
A drug that targets the HER2 protein, known as trastuzumab (Herceptin), may help treat these
cancers when used along with chemotherapy. If you have esophageal cancer and cannot have
surgery, your doctor may have your tumor biopsy samples tested for the HER2 protein or gene.
Only cancers that have too much of the HER2 protein or gene are likely to be affected by this
drug.

Trastuzumab is given by injection into a vein (IV) once every 3 weeks along with chemo. The
optimal length of time to give it is not yet known. Most of the side effects of trastuzumab are
relatively mild and may include fever and chills, weakness, nausea, vomiting, cough, diarrhea,
and headache. These occur less often after the first dose. Less often, this drug can cause heart
damage, leading to the heart muscle becoming weak. That is why this drug is not often given with
certain chemo drugs called anthracyclines, such as epirubicin (Ellence) or doxorubicin
(Adriamycin), because it may further increase the risk of heart damage if they are given together.
Endoscopic treatments for cancer of the esophagus: Several types of treatment for esophageal
cancer can be done by passing an endoscope (a long, flexible tube) down the throat and into the
esophagus. Some of these treatments may be used to try to cure very early stage cancers, or even
to prevent them from developing by treating Barrett's esophagus or dysplasia. Other treatments
are used mainly to help relieve symptoms from more advanced esophageal cancers that can't be
removed. Endoscopic mucosal resection
Endoscopic mucosal resection (EMR) is a technique where the inner lining of the esophagus is
removed with instruments attached to the endoscope. EMR can be used for dysplasia (precancer)
and some very early focal (single, small tumors) cancers of the esophagus. After the abnormal
tissue is removed, patients take drugs called proton pump inhibitors to suppress acid production
in the stomach. This can help keep the disease from returning.
Photodynamic therapy: Photodynamic therapy (PDT) is a method that can be used to treat
esophageal pre-cancer (dysplasia) and some early esophageal cancers. These may be found when
Barrett's esophagus is biopsied. PDT can also be used to help with symptoms for some cancers
thatare too advanced to be removed. For this technique, a light-activated drug called porfimer
sodium (Photofrin®) is injected into a vein. Over the next couple of days, the drug is more likely
to collect in cancer cells than in normal cells. A special type of laser light is then focused on the
cancer through an endoscope. This light causes changes in the drug that has collected inside the
cancer cells, changing it into a new chemical that can kill cancer cells. The dead cells may then
be removed a few days later during an upper endoscopy. This process can be repeated if needed.
The advantage of PDT is that it can kill cancer cells with very little harm to normal cells. But
because the chemical must be activated by light, it can only kill cancer cells near the inner

surface of the esophagus – those that can be reached by the light. This light cannot reach cancers
that have spread deeper into the esophagus or to other organs.
Radiofrequency ablation (RFA): This procedure can be used to treat dysplasia in areas of
Barrett's esophagus. It may lower the chance of cancer developing in that area. In this procedure,
a balloon containing many small electrodes is passed into an area of Barrett's esophagus through
an endoscope. The balloon is then inflated so that the electrodes are in contact with the inner
lining of the esophagus. Then an electrical current is passed through it, which kills the cells in the
lining by heating them. Over time, normal cells will grow in to replace the Barrett's cells. The
patient needs to stay on drugs to block stomach acid production after the procedure. Endoscopy
(with biopsies) then is done periodically to watch for any further changes in the lining of the
esophagus. RFA rarely causes strictures (narrowing) or bleeding in the esophagus.
Laser ablation: This technique can be used to help open up the esophagus when it is blocked by
an advanced cancer. This can help improve problems swallowing. In this treatment, a laser beam
is aimed at the cancer through the tip of an endoscope. The laser opens up the esophagus by
vaporizing and coagulating cancerous tissue. The laser used is called a neodymium: yttrium-
aluminum-garnet (Nd:YAG) laser. Most patients will benefit from laser endoscopy, but the
cancer often grows back, so the procedure may need to be repeated every month or two.
Argon plasma coagulation: This technique is similar to laser ablation, but it uses argon gas and
a high-voltage spark delivered through the tip of an endoscope. The spark causes the gas to reach
very high temperatures, which can then be aimed at the tumor. This approach is used to help
unblock the esophagus when the patient has trouble swallowing. Electrocoagulation
(electrofulguration).This method involves passing a probe down into the esophagus through an
endoscope and then burning the tumor off with electric current. In some cases, this treatment can
help relieve esophageal blockage.
Esophageal stent: A stent is a device made of mesh material. Most often stents are made out of
metal, but they can also be made out of plastic. Using endoscopy, a stent can be placed into the
esophagusacross the length of the tumor. Once in place, it self-expands (opens up) to become a
tube that helps hold the esophagus open. The success of the stent depends on the type of stent that

is used and where it is placed. Stents will relieve trouble swallowing in most patients that are
treated. They are often used after other treatments to help keep the esophagus open.
References:
1. American Cancer Society. Cancer Facts and Figures 2013. Atlanta, Ga: American Cancer
Society; 2013.
2. American Joint Committee on Cancer. AJCC Cancer Staging Manual. 7th ed. New York,
NY: Springer; 2010:103–111
3. National Cancer Institute. Physician Data Query (PDQ). Esophageal Cancer Treatment.
7/13/2012. Accessed at
www.cancer.gov/cancertopics/pdq/treatment/esophageal/HealthProfessional on May 17,
2013.
4. Keith M Baldwin, DO. Esophageal cancer. Attending Surgical Oncologist, Roger
Williams Medical Center, Boston University School of Medicine. Accessed at
http://emedicine.medscape.com/article/277930

CHAPTER 2
THEORY: DOUBLE-LUMEN ENDOTRACHEAL TUBE AND GENERAL
ANESTHESIA
2.1 Double-Lumen Endotracheal Tube
2.1.1 Introduction
Double-lumen endotracheal tube placement is performed to achieve lung separation.
However, thoracic surgeons may require lung separation and one-lung ventilation to perform
certain procedures and provide optimal surgical exposure.
For double-lumen endotracheal tube placement, the anesthesiologist places a tube with
two lumens through which to ventilate the lungs. This double-lumen tube is placed in the trachea,
with one lumen in either the left or right bronchial main stem; the other lumen remains in the
trachea. This allows the clinician to ventilate both lungs or the right/left lung independently. The
operative lung is referred to as the surgical lung or nondependent lung. The image below depicts
a double-lumen endotracheal tube.
Double-lumen endotracheal tube
Of the three methods of lung separation—double-lumen endotracheal tube placement,
bronchial blocker, and single-lumen endobronchial tube placement—double-lumen endotracheal
tube placement is the most common way of separating the two lungs. It is not only quicker than
the other two methods, but it allows for access into an isolated lung, suctioning from the isolated
lung, and application of continuous positive airway pressure if required to improve oxygenation.
Ventilation of either or both lungs can be easily achieved. In addition, even though a

fiberopticscope is very helpful with double-lumen endotracheal tube placement, it is not
absolutely required, which can also be an advantageous in some situations.
However, double-lumen endotracheal tubes may be challenging to place in patients with
difficult airways. Double-lumen endotracheal tubes are not meant for postoperative ventilation. In
addition, because of their significantly larger size and stiffness, they have a higher propensity for
trauma after insertion, which may result in postoperative hoarseness and/or vocal cord lesions.
2.1.2 Indication
a. Absolute Indications
Separation of the two lungs for any of the absolute indications discussed here should be
considered a lifesaving maneuver because failure to separate the lungs under any of
these conditions could result in a life-threatening complication or situation. Absolute
indications are as follows:
Isolation of each lung to prevent contamination of a healthy lung (eg, infection,
massive hemorrhage)
Control of distribution of ventilation to only one lung (eg,
bronchopleural/bronchopleural cutaneous fistulas, unilateral cyst or bullae, major
bronchial trauma/disruption)
Unilateral lung lavage
Video-assisted thoracoscopic surgery (VATS)
b. Relative Indications
There are a large number of relative indications for separation of the lungs, and they are
all for the purpose of facilitating surgical exposure by collapsing the lung in the
operative hemithorax. Relative indications are as follows:
Thoracic aortic aneurysm
Pneumonectomy
Lung volume reduction
Minimally invasive cardiac surgery

Upper lobectomy
Esophageal procedures
Lobectomy (middle and lower lobes)
Mediastinal mass resection
Thymectomy
Bilateral sympathectomies
2.1.3 Technique
a. Tube Insertion
• Several methods can be used to insert the double-lumen endotracheal tube: under
direct laryngoscopy, via tube exchanger, or over fiberoptic bronchoscope.
• During placement, a curved laryngoscope blade is used to intubate the airway. The
distal, bronchial (blue) tube is held with the tip directed upward. As it passes
through the glottis, the stylet is removed. At this point, the tube is advanced and
rotated 90 degrees (towards the side to be intubated) and advanced until resistance is
felt; this depth is usually between 28-30 cm.
• At this point, the tracheal (white) cuff is inflated, breath sounds are auscultated, and
end-tidal CO2 is noted on the capnogram to tell the clinician that the tube is in the
airway. At this point, correct tube placement is confirmed by direct visualization via
bronchoscopy.
• The flexible, fiberoptic bronchoscope is passed down the tracheal lumen. The
clinician will deflate the tracheal cuff and pull back until the carina is seen. At this
point, tracheal cartilaginous rings are anterior and the tracheal membrane is
posterior. Advance the tube until the bronchial blue tip enters the left main stem.
• At this point, inflate the blue balloon with 1-3 mL of air until the blue cuff is visible
in the left main stem. A portion of the blue cuff should be seen seated in the left
main stem.
• After placement, the patient is positioned laterally on the operating room table.
After positioning, the tube should be checked again to validate that it has not
moved. The tube can either become malpositioned by coming out or advancing to a
deeper level.

• When patient position is changed to lateral, the tube can be displaced, mainly due to
extension of the neck.
• The clinician should check position periodically throughout the surgery.
b. Position Verification
• There are multiple methods available to confirm placement, including radiographic
verification, auscultation, fiberoptic visualization, and various clinical tests such as
selective capnography and use of underwater seal. Auscultation and fiberoptic
examination are used most commonly.
Auscultation
• Auscultation is a widely available first-line test. After placement of the double-
lumen endotracheal tube, the tracheal cuff is inflated and ventilation is attempted.
The patient should have bilateral breath sounds and end-tidal CO2 should be noted
on capnogram. This tells the clinician that the tube is in the airway.
• Next, the tracheal lumen is clamped and opened. The bronchial cuff is inflated with
minimal volume to stop the leak (usually about 2 mL of air). At this point,
confirmation of separation of lungs can be done with air bubble leak test. One-sided
breath sounds should be heard, only over the desired lung field.
• Next, with the bronchial cuff up, the tracheal lumen is unclamped and reconnected,
the bronchial lumen is clamped, and ventilation is attempted through tracheal
lumen. If the tube is positioned correctly, breath sounds should be heard over
contralateral hemithorax. Then the bronchial lumen is unclamped and reconnected
and bilateral breath sounds should be audible again. This concludes auscultation for
correct placement.
Fiberoptic Bronchoscope
• The fiberoptic bronchoscope first is advanced through the tracheal lumen to confirm
that the bronchial tube is placed in the desired bronchus. For the left bronchus, the
cuff should be ideally placed 5 mm below the carina. It is crucial to identify the
right bronchus. The right main bronchus gives off the right upper lobe bronchus,
which is the only one that has 3 orifices in it. Then examination through the

bronchial tube is done to assure tube patency and determine margin of safety.
Therefore, orifices to both upper and lower lobes must be identified. Identification
of those bronchi confirms correct placement of a left-sided tube.
2.2 General Anesthesia
General anesthesia uses intravenous and inhaled agents to allow adequate surgical access
to the operative site. A point worth noting is that general anesthesia may not always be the best
choice; depending on a patient’s clinical presentation, local or regional anesthesia may be more
appropriate.
Anesthesia providers are responsible for assessing all factors that influence a patient's
medical condition and selecting the optimal anesthetic technique accordingly. Attributes of
general anesthesia include the following:
Advantages
• Reduces intraoperative patient awareness and recall
• Allows proper muscle relaxation for prolonged periods of time
• Facilitates complete control of the airway, breathing, and circulation
• Can be used in cases of sensitivity to local anesthetic agent
• Can be administered without moving the patient from the supine position
• Can be adapted easily to procedures of unpredictable duration or extent
• Can be administered rapidly and is reversible
Disadvantages
• Requires increased complexity of care and associated costs
• Requires some degree of preoperative patient preparation
• Can induce physiologic fluctuations that require active intervention
• Associated with less serious complications such as nausea or vomiting, sore throat,
headache, shivering, and delayed return to normal mental functioning
• Associated with malignant hyperthermia, results in acute and potentially lethal
temperature rise, hypercarbia, metabolic acidosis, and hyperkalemia
Nowadays, the risk caused by anesthesia to a patient undergoing routine surgery is very
small. Mortality attributable to general anesthesia is said to occur at rates of less than 1:100,000.
Minor complications occur at predicable rates, even in previously healthy patients.

2.2.1 Preparation for General Anesthesia
Safe and efficient anesthetic practices require certified personnel, appropriate medications
and equipment, and an optimized patient.
Minimum infrastructure requirements for general anesthesia include a well-lit space of
adequate size; a source of pressurized oxygen (most commonly piped in); an effective suction
device; standard ASA (American Society of Anesthesiologists) monitors, including heart rate,
blood pressure, ECG, pulse oximetry, capnography, temperature; and inspired and exhaled
concentrations of oxygen and applicable anesthetic agents.
Beyond this, some equipment is needed to deliver the anesthetic agent. This may be as
simple as needles and syringes, if the drugs are to be administered entirely intravenously. In most
circumstances, this means the availability of a properly serviced and maintained anesthetic gas
delivery machine.
An array of routine and emergency drugs, including Dantrolene sodium (the specific
treatment for malignant hyperthermia), airway management equipment, a cardiac defibrillator,
and a recovery room staffed by properly trained individuals completes the picture.
2.2.2 Preparing the patient
Preoperative evaluation allows for proper laboratory monitoring, attention to any new or
ongoing medical conditions, discussion of any previous personal or familial adverse reactions to
general anesthetics, assessment of functional cardiac and pulmonary states, and development of
an effective and safe anesthetic plan. It also serves to relieve anxiety of the unknown surgical
environment for patients and their families. Overall, this process allows for optimization of the
patient in the perioperative setting.
Physical examination associated with preoperative evaluations allow anesthesia providers
to focus specifically on expected airway conditions, including mouth opening, loose or
problematic dentition, limitations in neck range of motion, neck anatomy, and Mallampati
presentations. By combining all factors, an appropriate plan for intubation can be outlined and
extra steps, if necessary, can be taken to prepare for fiberoptic bronchoscopy, video
laryngoscopy, or various other difficult airway interventions.

Airway management
Presence of obesity, large breasts, short muscular neck, receding jaw, prominent upper incisor
and high arched palate suggest difficult intubation.
Predictive tests
a. Mallampati Classification : indicatiors of difficult intubation
Mallampati classification
b. Cormack and Lehane Grading : used to grade the view at laryngoscopy
c. Thyromental distance : measured form upper edge of thyroid cartilage to the chin with the
head fully extended
d. Cervical spine movement : Assesment of the full range of motion at atlanto-occipital joint
(flexion, extension and rotation)
When suspicion of an adverse event is high but a similar anesthetic technique must be
used again, obtaining records and previous anesthetic records from previous operations or from
other institutions may be necessary.
Other requirements
The need for coming to the operating room with an empty stomach is to reduce the risk of
pulmonary aspiration during general anesthesia when a patient loses his or her ability to
voluntarily protect the airway.
Patients should continue to take regularly scheduled medications up to and including the
morning of surgery. Exceptions may include the following:

Anticoagulants to avoid increased surgical bleeding
Oral hypoglycemics (For example, metformin is an oral hypoglycemic agent that is
associated with the development of metabolic acidosis under general anesthesia.)
Monoamine oxidase inhibitors
Beta blocker therapy (However, beta blocker therapy should be continued perioperatively
for high-risk patients undergoing major noncardiac surgery)
2.2.3 The process of anesthesia
a. Premedication
This is the first stage of a general anesthetic and usually conducted in the surgical
ward or in a preoperative holding area. The goal of premedication is to have the patient arrive
in the operating room in a calm, relaxed frame of mind.
The most commonly used premedication is midazolam, a short-acting benzodiazepine.
In anticipation of surgical pain, nonsteroidal anti-inflammatory drugs or acetaminophen can
be administered preemptively. When a history of gastroesophageal reflux exists, H2 blockers
and antacids may be administered. Drying agents (eg, atropine, scopolamine) are now only
administered routinely in anticipation of a fiberoptic endotracheal intubation.
b. Induction
This is the critical part of the anesthesia process. This stage can be achieved by
intravenous injection of induction agents (drugs that work rapidly, such as propofol), by the
slower inhalation of anesthetic vapors delivered into a face mask, or by a combination of
both.
In addition to the induction drug, most patients receive an injection of an opioid
analgesic, such as fentanyl (a synthetic opioid many times more potent than morphine).
Induction agents and opioids work synergistically to induce anesthesia. In addition,
anticipation of events that are about to occur, such as endotracheal intubation and incision of
the skin, generally raises the blood pressure and heart rate of the patient. Opioid analgesia
helps control this undesirable response.

The next step of the induction process is securing the airway. This may be a simple
matter of manually holding the patient's jaw such that his or her natural breathing is
unimpeded by the tongue, or it may demand the insertion of a prosthetic airway device such
as a laryngeal mask airway or endotracheal tube. The major decision is whether the patient
requires placement of an endotracheal tube. Potential indications for endotracheal intubation
under general anesthesia may include the following:
• Potential for airway contamination (full stomach, gastroesophageal [GE] reflux,
gastrointestinal [GI] or pharyngeal bleeding)
• Surgical need for muscle relaxation
• Predictable difficulty with endotracheal intubation or airway access (eg, lateral or
prone patient position)
• Surgery of the mouth or face
• Prolonged surgical procedure
Not all surgery requires muscle relaxation. If surgery is taking place in the abdomen
or thorax, an intermediate or long-acting muscle relaxant drug is administered in addition to
the induction agent and opioid. This paralyzes muscles indiscriminately, including the
muscles of breathing. Therefore, the patient's lungs must be ventilated under pressure,
necessitating an endotracheal tube.
Persons who, for anatomic reasons, are likely to be difficult to intubate are usually
intubated electively at the beginning of the procedure, using a fiberoptic bronchoscope or
other advanced airway tool.
c. Maintenance phase
At this point, the drugs used to initiate the anesthetic are beginning to wear off, and
the patient must be kept anesthetized with a maintenance agent. Anesthetic gas must be
provided. These may be inhaled as the patient breathes spontaneously or delivered under
pressure by each mechanical breath of a ventilator.
The maintenance phase is usually the most stable part of the anesthesia. As the
procedure progresses, the level of anesthesia is altered to provide the minimum amount of
anesthesia that is necessary to ensure adequate anesthetic depth. Traditionally, this has been a

matter of clinical judgment, but new processed EEG machines give the anesthesia provider a
simplified output in real time, corresponding to anesthetic depth.
If muscle relaxants have not been used, inadequate anesthesia is easy to spot. The
patient moves, coughs, or obstructs his airway if the anesthetic is too light for the stimulus
being given. If muscle relaxants have been used, then clearly the patient is unable to
demonstrate any of these phenomena. In these patients, the anesthesia provider must rely on
careful observation of autonomic phenomena such as hypertension, tachycardia, sweating,
and capillary dilation to decide whether the patient requires a deeper anesthetic. This requires
experience and judgment.
Excessive anesthetic depth, on the other hand, is associated with decreased heart rate
and blood pressure, and, if carried to extremes, can jeopardize perfusion of vital organs or be
fatal. Short of these serious misadventures, excessive depth results in slower awakening and
more adverse effects.
As the surgical procedure draws to a close, the patient's emergence from anesthesia is
planned. Experience and close communication with the surgeon enable the anesthesia
provider to predict the time at which the application of dressings and casts will be complete.
In advance of that time, anesthetic vapors have been decreased or even switched off entirely
to allow time for them to be excreted by the lungs. Excess muscle relaxation is reversed using
specific drugs and an adequate long-acting opioid analgesic to keep the patient comfortable in
the recovery room. If a ventilator has been used, the patient is restored to breathing by
himself, and, as anesthetic drugs dissipate, the patient emerges to consciousness.
Removal of the endotracheal tube or other artificial airway device is only performed
when the patient has regained sufficient control of his or her airway reflexes.
d. Reversal
It is a process of discontinuation of anesthetic agents at the end of surgery to allow
return of consciousness and recovery from muscle paralysis while maintaining analgesia.
Volatile agents are discontinued first and later the nitrous oxide. Patient is given 100%
oxygen. Wait for return of spontaneous breathing; this can be observed on capnography and
can also be felt with reservoir bag if patient is manually ventilated.

Administer reversal agent such as neostigmine (anticholinesterase) or glycopyrrolate
to counteract non-depolarizing muscle relaxant; atropine is usually given to counteract the
parasympathetic effects of anticholinesterase.
Reversal agent is given when there is evidence of spontaneous breathing effort.
Patient’s tidal volume has to be ensured that it is adequate and able to control own airway
before attempting extubation.
2.2.4 Postoperative Care
The anesthesia should conclude with a pain-free awakening and a management plan for
postoperative pain relief. This may be in the form of regional analgesia, oral, transdermal or
parenteral medication. Minor surgical procedures are amenable to oral pain relief medication
such as paracetamol and NSAIDs such as ibuprofen. Moderate levels of pain require the addition
of mild opiates such as tramadol. Major surgical procedures may require a combination of
modalities to confer adequate pain relief.
Parenteral methods include patient-controlled analgesia (PCA) involving a strong opiate
such as morphine, fentanyl or oxycodone. To activate a syringe device, patient will press a button
and receive a preset dose or bolus of the drug (eg: 1mg of morphine). The PCA device then locks
out for a preset period to allow drug to take effect. If the patient becomes too sleepy or sedated,
they make no more morphine requests.
Shivering is a frequent occurs in the post operative period. Apart from causing discomfort
and exacerbating post operative pain, shivering has been shown to increase oxygen consumption,
cathecolamine release, cardiac output, heart rate, blood pressure and intra ocular pressure. There
are number of techniques used to reduce this occurrence, such as increasing the ambient
temperature in theatre, using conventional or forced warm air blankets and using warmed
intravenous fluids.
2.2.5 Common Anesthetic Drugs
The main group of drugs commonly used in general anesthesia are broadly classified into
induction agents, muscle relaxants, analgesics and reversal agents.
Induction agents then are further classified into inhalational and parenteral/
a. Inhalational Anaesthetic Agents

It exists as gaseous form (nitrous oxide) or volatile liquids (isoflurane). Halothane
is a halogenated alkane derivative. Other modern volatile agents are halogenated methyl
ether derivatives (enflurane, isoflurane). Controllability is by pulmonary administration
and is delivered via vaporizers. The commonly used inhalational agents are liquids at
room temperature and therefore they need to be converted to the gaseous state for
administration to patients. Vaporizers is a device for producing a clinically useful and
stable concentration of an anesthetic vapour in a carrier gas ( oxygen and nitrous oxide).
The aim of inhalational anaesthesia is the development of an appropriate tension or partial
pressure of anesthetic agent within the brain.
Gaseous anaesthetic agents
 Nitrous oxide
 It is stored in steel cylinders as a liquid under pressure in equilibrium with the
gas phase at normal room temperature.
 N2O is a colorless gas without appreciable odour or taste and non explosive.
 It is a potent analgesic but a weak anaesthetic agents
 It cause depress hematopoietic function ( megaloblasticanemia,
thrombocytopenia and leucopenia), thus not advisable for administration of more
than 24 hours.
 It is widely used as an adjuvant to lower the MAC of volatile anesthetics. With
inhalation of 70% N2O / 30% O2 MAC value are reduced (~35%- 45%)
Volatile Anesthetic agents
 Halothane
Halothane is a haloalkane and has a MAC value of 70%. It can be used for
induction of anesthesia in children. Halothane is a non specific Ca2+
influx inhibitor and it
may cause bradycardia. It increases the automaticity of the heart and when combined with
adrenaline it may cause tachyarrythmias. One of the important side effects is ha;othane
hepatotoxicity. The diagnosis of halothane hepatitis is by exclusion. This may progress
into fulminant hepatic failure with a high mortality. Obese middle aged women having

repeat halothane exposures are at risk. Halothane hepatitis may occur following a single
exposure.
 Isoflurane
It causes a dose dependent reduction in blood pressure. The decrease in blood
pressure is due to vasodilatation and decreased total peripheral resistance. The heart rate is
increased via reflex mechanisms but arrhythmias are uncommon. Isoflurane does not
affect ventricular conduction and does not increase the excitability of ventricular
myocardium. Induction of anesthesia is difficult with isoflurane due to its pungent odour
and preanesthetic concentration of isoflurane may cause an airway reflex stimulation, with
increased secretions and/or coughing and laryngospasm.
 Sevoflurane
It is a new inhalational agent and more expensive than others. It has pleasant
odour and can be used as induction agents in paediatric and adult patients. It has rapid
onset of induction and recovery of anesthesia because it is less soluble in blood than
isoflurane. It has a mild negative inotropic effect. It also decreases systemic vascular
resistance but does not cause reflex tachycardia. Sevoflurane is less arrythmogenic when
compared to halothane and it is suitable for daycare surgery.
b. Intravenous induction agents
Criteria for ideal intravenous anesthetic agents:
 Induction of anesthesia should be rapid, smooth and safe
 It should have limited effects on cardiovascular and respiratory systems
 It should possess analgesic activity.
 Consciousness should return rapidly, smoothly and predictably.
i. Sodium thiopental (Pentothal)
Thiopental is the only intravenous barbiturate being used today and is classified
under an ultra short acting barbiturate. It is prepared as a 2.5% solution, water soluble,
pH of 10.5 and stable for up to 1-2 weeks if refrigerated.

Mechanism of action: Depress the reticular activating system, reflecting the ability
of barbiturates to decrease the rate of dissociation of the inhibitory neurotransmitter
GABA from its receptors
Pharmacokinetics
 Short duration of action (5-10 minutes) following IV bolus reflects high lipid
solubility and redistribution from the brain to inactive tissues.
 Protein binding parallels lipids solubility, decreased protein binding increases drug
sensitivity.
 Fat is the only compartment in which thiopental continues to accumulate 30
minutes after injection
 Thiopental is metabolized in the liver slowly. Its hepatic excretion ratio is 0.15
It has an anticonvulsant effect and is a useful drug for cerebral protection in head
injury. It also has an analgesics effect. In the presence of inadequate anaesthesia, airway
manipulation may result in bronchospasm and laryngospasm. Cardiovascular effects of
barbiturate include decrease in blood pressure due to vasodilatation and direct myocardial
depression. There is a compensatory increased in heart rate.
It should be used cautiously in haemodynamically unstable patients and is
contraindicated in hypovolaemia and hypotensive patients. Induction dose is 3-5mg/kg in
a healthy adult.
ii. Propofol
It is 2,6-diisopropyl-phenol, under group of hindered phenol, an alkylphenol
derivative. Formulated in a solution with 10% soy bean oil, hydrophobic nature. It has
rapid onset and short duration of action. Emergence and awakening are prompt and
complete after even prolonged infusions.
Mechanism of action: Propofol increases the inhibitory neurotransmission
mediated by gammaaminobutyric acid.

It has extensive metabolism by hepatic and extrahepatic. It has no cumulative
effects, has antiemetic property and suitable for daycare surgery. It does not
hasantianalgesic activity.
Propofol is an ideal drug for total intravenous anesthesia. The target controlled
induction (TCI) and maintenance of anesthesia can be achieved nowadays with propofol
by a special TCI pump. Propofol also can be used to provide sedation in ICU, for minor
procedures or in combination with regional anesthesia.
Effects on organ system
Cardiovascular: decrease in arterial blood pressure secondary to a drop in systemic
vascular resistance, contractility, and preload. Hypotension is more pronounced than with
thiopental. Propofol markedly impairs the normal arterial baroreflex response to
hypotension.
Respiratory: propofol causes profound respiratory depression. Propofol induced
depression of the upper airway reflexes exceeds that of thiopental
Cerebral: decreases cerebral blood flow and intracranial pressure.
Induction dose: 1.5-3 mg/ kg in a healthy adult.
iii. Ketamine
It is a phenicyclidine derivative. It produces dissociative anesthesia resulting in
catatonia, amnesia and analgesia. Patient may appear awake and reactive but does not
response to sensory stimuli
Mechanism of action: It acts on NMDA receptor. It blocks polysynaptic reflexes in
the spinal cord, inhibiting excitatory neurotransmitter effects. It has both anesthetic and
analgesic properties. It causes postoperative psychic phenomena- emergence delirium,
vivid dreams, hallucination. Therefore it is not suitable for adults. These effects can be
minimized by combination with benzodiazepines.
Clinical usage:
Induction of anesthesia in poor risk patients (eg: hypotension or bronchial asthma)
As sole agent in dressing of burns, radiological procedures in children, mass
casualties in the field.
In the management of unresponsive severe bronchospasm

It is contraindicated in raised intracranial pressure, perforating eye surgery,
hypertension, heart failure, recent myocardial infarction, aneurysm and valvular heart
disease.
Dosage:
o IV 1.5-2 mg/kg, onset 30 sec. duration 5-10min.
o IM 10 mg/kg, onset 3-8min, duration 10-20min
Systemic effects:
Increase intracranial and intraocular pressures
Postoperative nausea and vomiting
Increased salivation. An antisialagogue is recommended before used
Preservation of airway reflexes and produces brochodilatation
Increased in cathecolamines secretion
Ketamine has cardiovascular effects: increases heart rate, blood pressure and
pulmonary arterial pressure. It is most likely due to direct stimulation of the sympathetic
nervous system.
c. Neuromuscular blocking agents
Muscle relaxants are generally classified into two groups(depolarizing and non-
depolarizing), depending on their mechanism of action.
Depolarizing muscle relaxants
Used to provide skeletal muscle relaxation to facilitate tracheal intubation and
optimal surgical condition. Ventilation must be provided as the diaphragmatic muscle
would also be paralysed. There is no CNS activity and the problem of awareness begin
with introduction induction of muscle relaxants.
Factors that influence inclusion of muscle relaxants in general anesthesia are types
of surgical procedures (anatomic location and patient position), anesthetic techniques and
patient factors (ASA class, obese, exreme of age).
Succinylcholine
The only depolariser drug that is used clinically. It consists of two molecules of
acetylcholine linked together. It acts on nicotinic receptors at neuromuscular junction

(NMJ) to cause sustained depolarization that prevents propagation of action potential. The
net effect of SCh induced depolarization is uncoordinated skeletal muscle activity that is
seen as fasciculation.
It remains a useful muscle relaxants because of its rapid onset and short duration
of muscular relaxation that cannot be achieved by any other available nondepolarising
muscle relaxants.
A dose of 1-2 mg/kg produces profound muscle relaxation within one minute. Full
recovery is 10-12 minutes. It is used in emergency surgery as rapid sequence induction
technique and in situation of difficult airway management.
Side effects
 It may cause cardiac dysarryhmias such as bradycardia especially in children.
 Hyperkalemia – at risk patients (burns, extensively trauma, unrecognized muscular
dystrophy and denervation injuries.
 Increased intragastric pressure (offset by even greater increase in lower
oesophageal sphincter)
 Increased intraocular pressure (due to cycloplegic action of succinylcholine)
 Prolonged response in presence of atypical cholinesterase
 Increased intracranial pressure
 Muscle pain and myoglobinuria
Non depolarizing muscle relaxant
Acts on nicotinic receptors in a competitive fashion to produce neuromuscular
blockade- absence od depolarization. Can be antagonized by anticholinesterase drugs.
They are used to facilitate endotracheal intubation, controlled ventilation and maintenance
of muscle relaxation during surgical procedures.
a. Atracurium
It is an intermediate acting benzyliso-quinolinium type NDMR. The
intubation dose is 0.5-0.6mg/kg. It presents as 10mg/ml solution in 25mg or 50mg
glass ampoules and is stored at 4 °C. Histamine release may occur in susceptible
patients but anaphylactoid reaction is very rare.
b. Vecuronium

It is an aminosteroid group and presents as freezed dried powder and
diluted with sterile water before used. There is no histamine release and devoid of
cardiovascular side effects. It does not antagonize fentanyl induced bradycardia. It
is metabolized by liver and also excreted unchanged in bile. The intubation dose is
0.08-0.1 mg/kg.
c. Rocuronium
It is an aminosteroid group. Its rapid onset of action makes it a potential
replacement for SCh when rapid tracheal intubation is needed. Its duration of
action is similar to vecuronium and has similar pharmacokinetic characteristic. It
has minimal cardiovascular side effects and very low potential for histamine
release. Dosage for endotracheal intubation is 0.6 mg/kg.
d. Pancuronium
It is a long acting NDMR with a steroid structure (Bisaminoquaternary
steroid). It increases heart rate and blood pressure and cardiac output due to
cardiac vagal blockade. Histamine release is very rare and bronchospasm is
extremely uncommon.
Assessment of neuromuscular blockade
1. Clinical assessment
a. Ability to lift up head for 5 second
b. Hand grip for 5 second
c. Ability to produce vital capacity breath > 10 ml/kg
d. Tongue protrusion
2. Responses to electrical stimulation of a peripheral nerve stimulator
Anticholinesterase
Anticholinesterase is used to reverse non depolarizers. It inhibits the action of
acetylcholinesterase and increase the concentration of acetylcholine at the neuromuscular
junction. It also acts at parasympathetic nerve endings. Anticholinesterase increases acetylcholine
at both nicotinic and muscarinic receptors. Muscarinic effects can be blocked by administration
of atropine or glycopyrolate.

d. Opioid analgesics
Few examples of this drugs are morphine, pethidine, fentanyl and nalbuphine.
This drugs act on opioid receptors and classified as full agonist, antagonist, or mixed
agonist-antagonist depending on the actions on the opioid receptors. Three main receptors
are mu, kappa and delta.
Morphine pharmacokinetics:
Elimination halftimes for morphine following bolus administration is about 1.7-4.5
hours. Following bolus administration onset time is relatively slow (15-30 minutes)
because:
1. morphine exhibits relatively low lipid solubility about 2.5% of fentanyl
(Sublimaze)
2. at physiological pH, morphine, a weak base with the pKa of about 8.0, is
primarily ionized. The ionized form does not favor passage through the lipid
membrane; accordingly, only about 10%-20% of molecules are un-ionized.
Relatively high plasma clearance (15-40 ml/kg/minute) has implicated extrahepatic
clearance mechanisms, most likely renal.
Fentanyl (Sublimaze) pharmacokinetics:
Fentanyl (Sublimaze) is significantly more lipid-soluble, compared morphine and,
relative to morphine, has a more rapid onset of action (fentanyl (Sublimaze) is also a
weak base and at physiological pH only about 10% of molecules are un-ionized).
Clearance of about 10-20 ml/kg/minute is consistent with a primary hepatic
mechanism. Fentanyl (Sublimaze)'s short duration of action following bolus
administration is explained by rapid redistribution from brain to other compartments
such as skeletal muscle and fat. If, however, fentanyl (Sublimaze) is administered by
continuous IV infusion or multiple IV dosing, other non-CNS compartments will
saturated and remaining CNS fentanyl will contribute to postoperative ventilatory
depression.

Action of opioid drugs:
A. Central nervous system: Analgesia, sedation, euphoria, nausea, vomiting, miosis,
depression of ventilation, pruritus and skeletal muscle rigidity.
B. Respiratory system: bronchospasm in susceptible patients and depressed cough reflex
C. Cardiovascular system: bradycardia (fentanyl) or tachycardia ( pethidine)
D. Skin: pruritus may be due to histamine release or action on opioid receptor.
E. Gastrointestinal tract: constipation, delays gastric emptying, increased tone of the
common bile duct and sphincter of Oddi.
F. Urinary tract: increased sphincter tone and retention of urine.
Use of opioids in anesthesias
Premedication drugs
Induction of anaesthesia
Blunt haemodynamic reactions to noxious stimulation
Intraoperative analgesia
Postoperative analgesia
Used in ICU as analgesia to facilitate mechanical ventilation
Drug Doses
Morphine 2.5 - 5 mg (IV), 15 - 30 mg (oral)
Pethidine 50 to 100 mg S.C., I.M or in reduced doses I.V.
repeated every 3 to 4 hours
Fentanyl 25 - 50 µg (IV), 150 - 300 µg (oral)
Naloxone
It is an antagonist at all opioid receptors of pure opioid antagonist. It reverse all opioid
actions including analgesia. It has short duration of action ( 1-4 hours) and has limited action
against partial or mixed actions opioids. Abrupt reversal of opioid analgesia can result in
sympathetic stimulation (tachycardia, ventricular irritability, hypertension and pulmonary
oedema).

Dosage :
 Bolus:
o Adult: 0.04 mg IV in titrated bolus every 23 minutes until the desired
effects
o Child: 1-4mcg/kg titrated
 Continuous infusion: 5mcg/kg/hr IV will prevent respiratory depression without
altering the analgesia produced by neuraxial opioids.
Tramadol
It is an opioid agonist at mu receptor and inhibits noradrenaline reuptake and release of 5-
hydroxytryptamine (monoaminergic pathways). It is given intravenously with the dose of 1-2
mg/kg and also can be given orally (good bioavailability). It produces less respiratory depression
in equivalent dose if compared with morphine.
Non opioids
Use of non steroidal anti-inflammatory drugs as analgesics (eg: Ketorolac, Diclofenac). It
block synthesis of prostaglandins by inhibiting cyclooxygenase enzyme. It reduces pain by
peripheral action and centrally by reducing input of nociceptive information in spinal cord.
Ketorolac and Ketoprufenhas opioid sparing effects.
Side effects:
 Reduced platelet aggregation may increase bleeding – it is not advisable for neurosurgical
and ophthalmic surgery.
 It may cause damage to gastric mucosa causing ulceration and bleeding.
 Bronchospasm – patients with asthma have an increased incidence of sensitivity to aspirin
 Renal failure- inhibition of renal prostaglandin synthesis may interfere with maintenance
of renal blood flow.
Drug Doses
Voltaren (Diclofenac) 100-200 mg daily
Paracetamol 2 x 500mg 4-6 hourly
Synflex Initially 550 mg then 275 mg
6-8 hrly

CHAPTER 3
CASE: PERIOPERATIVE ASSESSMENT
3.1. Preoperative Assessment
3.1.1. Case History
IDENTIFICATION DATA
Name : Rosli bin Ahmad Tajudin
Sex : Male
Age : 45 years old
Nationality/Tribe : Malaysian/Malay
Religion : Islam
Address : Kangar, Perlis
Marital Status : Married
Occupation : Government Officer
Admission Date :14th
May 2013
CHIEF COMPLAINT
This 45-year old malay gentleman presented with a chief complaint of difficulty in
swallowing for the past two months, worsening last week.
HISTORY OF PRESENTING ILLNESS
Patient suddenly developed difficulty in swallowing since two months ago. This is the
first episode. Patient’s condition is progressively worsening. Initially, he was unable to take solid
food but later on, he could not tolerate fluid as well. He vomited out food particles and fluid after
each meal. Patient also had loss of appetite and he lost around five to six kilogram body weight in
two months period.

Gastroscopy (OGDS) and tissue biopsy was done on 8th
May 2013 with the impression of
esophageal carcinoma. CT Scan done on 9th
May 2013 shows soft tissue mass at the mid
esophagus (2.8 cm length) which is causing stenosis of its lumen. On 13th
May 2013, Barium
Swallow Test was carried out with the impression of persistent narrowing of distal esophagus
with irregular wall outline suggesting esophageal tumour.
Otherwise, he has no regurgitation, no cough, no choking and aspiration, no painful
swallowing, no heartburn, no fever, no alteration of bowel habit, no shortness of breath, no
hoarseness of voice, no abdominal pain, no upper respiratory tract infection and no urinary tract
infection.
PAST MEDICAL HISTORY
He has no known of other medical condition.
PAST SURGICAL HISTORY
Patient had undergone oesophagogastroduodenoscopy (OGDS) on 8th
May 2013.
ANAESTHETIC HISTORY
Patient has never gone through any anaesthetic procedures.
DRUG HISTORY
Patient is not on any medication. There’s no history of drug or food allergy. Patient
claimed he is not taking any traditional medication or over the counter drugs.
FAMILY HISTORY
There is no history of malignancy in the family. However, patient’s father has diabetes
mellitus and his mother has hypertension.
SOCIAL HISTORY
Patient is a government officer, married with 4 children. Currently, he lives with his wife
and children. He is able to carry out activity of daily life independently. He is an active smoker

(20 sticks/day) for 20 years. He is non-alcoholic. There is no recent travel. He denied any high-
risk behavior.
3.1.2. Physical Examination
GENERAL EXAMINATION
Patient is alert and conscious, lying comfortably on the bed. He does not look ill, not in
pain, and not in respiratory distress. He has normal body build, and his hydration and nutritional
status is fair. There’s no gross deformity, no involuntary or abnormal movement, and there’s a
branula attached at his left hand.
VITAL SIGNS
HEAD, NECK & EXTREMITIES EXAMINATION
On general examination (extremities), the palm is moist, no pallor, no palmar erythema
and the temperature was normal. There’s no clubbing finger, and no bluish discoloration of the
nail. No leukonychia or koilonychia noted. There’s no fine tremor or flapping tremor. There’s
also no pedal edema at both lower extremities.
Examination of the head did not reveal pallor of the conjunctiva, no jaundice of the sclera,
no exophthalmus, no arcussenilis and no xanthelasma. There’s also no bluish discoloration of the
lips and the tongue. The dental hygiene is good.
Vital signs Value Interpretation
Temperature 37°C Afebrile
Blood pressure 135/80 mmHg Normal
Pulse rate 78 bpm Normal
Respiratory rate 18x/minute Normal
Pain score 0/10 Not in pain
Height 170 cm -
Weight 61 kg -
Body Mass Index 21 kg/m2
Normoweight

For neck examination, on inspection, there’s no redness, no skin changes, no discharge,
no surgical scar and no prominent vein and no increase in jugular venous pressure. On palpation,
there is no increase in temperature and no palpable lymph nodes and no trachea deviation. On
auscultation, there’s no bruit can be heard.
RESPIRATORY SYSTEM EXAMINATION
From airway assessment, patient was classified as Mallampati class I, and the thyromental
distance was 6.5 cm or three fingers wide.
Patient has no history or symptoms of upper respiratory tract infection. On examination;
on inspection, the chest moved symmetrically with respiration, with abdominal-thoraco breathing
pattern. The chest shape was normal and there was no deformity or scar noted on both anterior
and posterior chest wall. There were also no signs of respiratory distress. On palpation, the chest
expansion and tactile vocal fremitus were symmetrical on both anterior and posterior chest. On
percussion, it was a symmetrical resonance sounds. On auscultation, no wheezing or crepitation
heard. Air entry was equal on both sides.
CARDIOVASCULAR SYSTEM EXAMINATION
The peripheral pulses were palpable, equal and regular. There was no surgical scar seen
on the chest. There was neither heave nor thrill can be palpated. Apex beat was palpable at left
midclavicular line between 4th
and 5th
intercostal space. Normal 1st
and 2nd
heart sounds were
heard and there were no additional sounds or murmurs heard in the mitral, tricuspid, aortic and
pulmonary area.
ABDOMINAL EXAMINATION
On inspection, the abdomen was not distended, moves with each respiration. The
umbilicus is centrally located. Otherwise, there is no surgical scar, no visible peristalsis or
pulsation, no skin discolouration and no cough impulse.
On palpation, the abdomen is soft and non-tender. No mass can be appreciated and no
hepatomegaly or splenomegaly. The kidney was not ballotable.

The percussion gives tympanic sound, and there’s no shifting dullness. On auscultation,
the bowel sound was present and no renal bruit heard.
CENTRAL NERVOUS SYSTEM EXAMINATION
Patient was alert, and well oriented to person, time and place. Glasgow Coma Scale was
15/15. Facial expression was symmetry. All cranial nerves were intact.
MUSCULOSKELETAL SYSTEM EXAMINATION
Patient has a normal muscle bulk, strength, tone and power for both upper and lower
extremities. The shape of vertebral spine is normal. No deformities noted. Gait was normal.
PHYSICAL STATUS
ASA score is 1. Patient was healthy with no systemic disease, and the surgery was an
elective surgery.
3.1.3. Investigation
• Full blood count:

• Renal profile
Components Value Normal Range Interpretation
Sodium 138 (mmol/L) 135 – 145 Normal
Potassium 3.7 (mmol/L) 3.3 – 5.3 Normal
Urea 3.7 (mmol/L) 1.7 – 8.3 Normal
Creatinine 61 (umol/L) <97 Normal
• Coagulation:
Prothrombin time 11.7 (sec) 10.4 – 13.2 Normal
INR 0.99 0.9 – 1.1 Normal
APTT test 28.5 (sec) 20.1 – 34.9 Normal
APTT ratio 1.0
White blood cell 8.8 (109
/L) 4.0 – 11.0 Normal
Red blood cell 4.7 (106
/L) 3.8 – 4.8 Normal
Haemoglobin 13.0 (g/dL) 12.0 – 15.0 Normal
Haematocrit 38.8 (%) 36.0 – 46.0 Normal
Mean cell volume 82.0 (fL) 83.0 – 101.0 Normal
MCH 29.4 (pg) 27.0 – 32.0 Normal
MCHC 31.7 (g/dL) 31.5 – 34.5 Normal
Platelet 298 (103
/uL) 150 – 450 Normal
Differential:
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
4.75 (103
/uL)
2.90 (103
/uL)
0.35 (103
/uL)
0.30 (103
/uL)
0.05 (103
/uL)
2.0 – 7.0
1.0 – 3.0
0.2 – 1.0
0.02 – 0.50
0.02 – 0.10
Normal
Normal
Normal
Normal
Normal

EKG:
• Sinus rhythm
• No ischemic changes
• Interpretation: Normal
Chest X-Ray:
• Lung: Normal
• No cardiomegaly
• Bones: Intact
• Soft tissues: Normal
• Trachea is not deviated
Indirect Laryngoscope:
• Both vocal fold mobile equally
• No anterior compression
• Impression: Normal vocal cord
3.1.4. Summary
A 45 years old malay gentleman, an active smoker, presented with difficulty in
swallowing since the past 2 months, worsening one week before admission to the hospital.
Initially he was unable to tolerate solid food but later on he could not take fluid as well. This is
accompanied by loss of appetite and weight loss. On physical examination, patient is clinically
stable and not dehydrated. Gastroscopy and tissue biopsy, CT scan, Barium Swallow Test results
are suggestive of esophageal carcinoma. Otherwise, there’s no significant finding in any other
system.

3.1.5. Preoperative Diagnosis
• Esophageal Carcinoma
3.1.6. Plan
• Lower Esophagectomy + thoracotomy + pyloroplasty
• To keep nil by mouth by 12 midnight (8 hours prior to surgery)
• To inquire informed consent for the surgery and anaesthetic procedures
• Send blood for blood crossmatch
• To plan for general anaesthesia/intermittent positive pressure volume (double lumen
intubation).
3.2.Intraoperative Assessment
Anaesthesia : Balanced general anaesthesia with intermittent positive pressure ventilation
(double lumen intubation)
Fasting : Patient was kept nil by mouth 8 hours prior to operation.
Premedication : Patient was given tablet midazolam 7.5 mg night before operation and in the
morning prior to operation.
3.2.1. AnaesthesiaProcedures :
I. Preoperative assessment was done and consent was taken from the patient.
II. GA machine was checked and anaesthetic drug was prepared before patient was
entered into the operation room.
III. Intravenous assessed was established by inserting IV catheter 18G and patient was
preloaded with normal saline.
IV. Procedures were done in a full aseptic technique, scrubbed, gloved and gowned.
V. Patient was preoxygenated with 100% oxygen for 3 minutes at 8am.
VI. Administration of intravenous Fentanyl 100mcg and intravenous Propofol 100mg.
VII. Loss of consciousness was assessed by loss of eyelash reflex.
VIII. Test ventilate before give muscle relaxant.

IX. Then, IV rocuroniumbromide 50mg was given and mask ventilate with oxygen and
volatile gas Sevoflurane 2% for 3minutes.
X. Laryngoscopy and intubation were then performed by using double lumen
endobronchial tube size 39mm, Cormack Lehane I, anchored at 29mm.
XI. Post intubation, both lungs were tested for one sided lung ventilation and tube was
confirmed further by fibreoptic bronchoscopy visualization.
XII. Arterial line was inserted at right radial artery.
XIII. Triple lumen catheter was inserted at right internal jugular vein.
XIV. Other IV access available: right hand 16G branula, left hand 18G branula
XV. The vital sign which are oxygen saturation, brain tissue carbon dioxide, respiratory
rate, blood pressure, heart rate, any blood loss and urine output was monitored during
the operation.
XVI. Estimated blood loss is 500ml. Patient was given 7 pint fluid; 2 pint IV Voluven, 2
pint IV Nacl 0.9%, 3 pint IV Hartman Solution. No blood transfusion was done during
the operation.
XVII. Anaesthesia was maintained with Sevoflurane and morphine 12mg.
XVIII. Intra operatively patient was also given IV Ranitidine 50mg, IV Cefobid 1g, and IV
Flagyl 500mg
XIX. Post operatively, double lumen endobronchial tube was exchanged with portex ETT
size 8.0 mm, anchored at 21 mm.
XX. Patient was sent to intensive care unit (ICU) for weaning, transfer by manual bagging.

3.2.2. Drugs :
3.2.2.1. Intravenous :
a. Fentanyl 100mcg
b. Propofol 140 mg
c. Rocuronium bromide 50g
d. Morphine 12mg
e. Ranitidine 50mg
f. Cefoperazone 1g
g. Metronidazole 500mg
h. Ephedrine 6mg
i. Phenylephrine 100 mcg
3.2.2.2. Gases :
1. Oxygen / air (L/min) 1:2
2. Volatile : Sevoflurane MAC 1.0
3.2.3. Monitoring :
Time 930a
m
10.00a
m
10.30a
m
11.00a
m
11.30a
m
12.00p
m
12.30p
m
1.00p
m
1.30p
m
2.00p
m
O2 Sat
(%)
100 100 99 100 100 100 98 100 100 100
Resp
(x/min)
12 12 12 13 15 12 12 12 14 12
CVP
(mmHg
)
9 6 9 8 8 12 12 9 9 10
Urine
(ml)
100 500 500
Temp
(°C)
35.6 35.6 35.6 35.1 35.0 34.7 34.7 34.6 35.0 35.1

Blood Pressure and Heart Rate :
Blood pressure was monitored every 5 minutes during the whole operation procedure. The
systole reading range was between 90 – 150 mmHg and diastolic pressure was between
50 – 90mmHg. Heart rate was monitored every 5minutes and noted to be in normal range
which was within 70 – 90 beats per minutes.
3.2.4. Summary:
Patient was hemodynamically stable throughout the operation with 500ml
estimated blood loss but no blood transfusion was needed. There is a tumor at the lower
esophagus noted 1 cm above cardia measuring 3 X 3 cm. Proximal gastrectomy was done.
Due to limited space over superior resectable margin, surgeon proceed with thoracotomy
and single lung ventilation initiated. Lower end esophagectomy was done and proceed with
proximal gastric and lower end esophagus anastomosis. Air leak test done – no
leaking.Vagus nerve is preserved. Chest tube size 32 Fr was inserted. Right chest wall
incision closed layer by layer. Patient was transferred to intensive care unit.
3.3. Post Operative Assessment
After the operation, double lumen endobronchial tube was exchanged with endotracheal
tube size 8 mm anchored at 21 mm.
Patient was sent to the intensive care unit (ICU) for weaning, transferred with manual
bagging.
Non-invasive blood pressure (NIBP) monitor, ECG monitoring, pulse oximeter and DVT
venocuff prophylaxis were set-up.
Patient was keep nil by mouth, put below radiant warmer to prevent hypothermia.
Pain was minimal and there were no complaints of headache, nausea or vomiting.
Otherwise, no other post-operative complications noted.

Vital Signs Reading Interpretation
Blood pressure 111/89 mmHg Normal
Pulse rate 65 x/min Normal
Respiratory rate 20x/ min Normal
Temperature 37°C Afebrile
SpO2 100% Normal
Pain score 2/10 Mild pain
Post-operative anaesthesia recovery score
Parameters Signs Score
Activity Able to lift the head or has a good hand grip
None of the above
1
0
Respiration Able to breathe and cough easily
Dyspnoeic or apnoeic
1
0
Circulation BP within 20% of pre-operative level
BP above or below 20% of pre-operative
level
Pulse regular rate, within 20% of pre-
operative level
Pulse irregular, above or below 20% of pre-
operative level
1
0
1
0
Consciousness Arousable
Not responding
1
0
Colour Pink
Dusky
1
0
Total score 3/6
Note:
Score 5 or more may be coming home with the conditions of operation/ action possible
Score 4 to the treatment room when the breathing value is 1

Score 3 or less to ICU
Operative findings:
Tumor at the lower esophagus noted 1 cm above cardia measuring 3 X 3 cm.
Proximal gastrectomy was done.
Thoracotomy and single lung ventilation initiated due to limited space over superior
resectable margin.
Lower end esophagectomy was done and proceed with proximal gastric and lower end
esophagus anastomosis. Air leak test done – no leaking.
Vagus nerve is preserved.
Noted multiple metastatic lymph nodes involving caeliac lymph nodes and metastatic
nodules over the pancreas. No liver nodules.
Plan:
i. To put patient on CPAP PEEP setting.
ii. To give IV morphine 3 mg/hour
iii. To give IV Dexmedetomidine (Precedex) 0.4 mcg/kg/hour
iv. To give IV pantoprazole 40 mg
v. To give IV Sulfaperazone 2g twice daily
vi. Infuse 2 pints of dextrose 5% and 3 pints normal saline 0.9% in 24 hours
vii. Keep nil by mouth for 6-8 hours

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