Module 4 SURGERY PDF

4.
Surgery
MANAGING SURGICAL
PROBLEMS AT A SECONDARY
HOSPITAL
Updated & Edited in the year 2015 by:
Dr. Vinod Shah, Department of Distance Education, CMC, Vellore
Original Authors:
Dr. Vinod Shah, Department of Distance Education, CMC, Vellore
Post Graduate Diploma in Family Medicine for recent MBBS

Graduates – 2019-20
Towards multicompetence in Secondary Level Care

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OVERVIEW
Among the essential skills required of a multicompetent practitioner at the level of
secondary care are basic surgical skills. You may be the only doctor in your
hospital and may be required to make a decision on a surgical problem. A patient
may be critically sick and in need of life-saving surgical treatment. In a situation
where the nearest referral hospital may be too far, the patient will need to be
operated upon in your hospital. In the absence of advanced diagnostic imaging,
you be required to make clinical decisions based on the available tests.
This course aims to help you develop skills in relation to the following surgical
problems.
- Acute abdominal pain:
- Intestinal obstruction
- Neck swellings
- Groin swellings
- Lower gastrointestinal bleeding
When faced with a patient with acute abdominal pain in an isolated setting, one
has to take some decisions and cannot have the luxury of referring or seeking
expert assistance. Similarly, in the case of intestinal obstruction, conservative
management like NG tube aspiration and intravenous fluids can be life-saving.
Lymph node swellings and thyroid enlargement are very common and treatment of
these can be done in a secondary hospital and is very rewarding.
Both in children and in young adults, groin swellings like hernia, hydrocoele and
inguinal nodal enlargement continue to be very common and can be managed at
your level. The ability to do a rectal examination and a proctoscopy will go a long
way in elucidating many causes of lower GI bleeding and managing them.
The common tests available to you wll be clinical pathology and biochemistry
investigations, plain X-ray and ultrasound. With these, you will be able to majority
of the above problems. During the contact course, you will learn practical
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management of these surgical problems. In contact class 2, you will gain hand-on
experience in the following procedures:
- Suturing skills
- I&D
- Hydrocoelectomy
- Injection haemorrhoids
- Lymph node biopsy
- Excision subcutaneous swellings
- Circumcision
- FNAC
We hope that you will be able to apply this learning in practice at your hospital to
help you become a comptetent medical practitioner at any secondary care centre.
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OBJECTIVES
After you complete the module you should be able to do the following in relation
to the clinical problems listed below:
 Lower GI bleeding
 Acute abdominal pain
 Neck swellings
 Leg ulcers
 Groin and abdominal swellings
1. Define important terms and describe the basic anatomy of each area of
study.
2. Outline a method of history taking and physical examination.
3. List the differential diagnoses of each of the clinical problems.
4. List the relevant investigations.
5. Describe the management of each, including when to refer.
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CONTENTS
TOPIC Minutes Page nos.
Activity 4.1 Lower GI bleeding - I
10 6
Reading Lower gastrointestinal bleeding 70 43-58
Activity 4.2 Lower GI bleeding - II 10 8
Activity 4.3 Lower GI bleeding - III 10 10
Activity 4.4 Lower GI bleeding - IV 10 12
Activity 4.5 Acute abdominal pain - I 10 14

Reading Acute abdominal pain 70 59-73
Activity 4.6 Acute abdominal pain – II 10 17
Activity 4.7 Acute abdominal pain - III 10 19
Activity 4.8 Neck swellings - I 10 21

Reading Neck swellings 70 74-95
Activity 4.9 Neck swellings – II 10 23
Activity 4.10 Neck swellings - III 10 27
Activity 4.11 Leg ulcers - I 10 31

Reading Management of chronic leg ulcers 20 96-117
Activity 4.12 Leg ulcers – II 10 34
Activity 4.13 Groin & abdominal wall swellings - I 10 37

Reading Swellings in the groin region & in the
abdominal wall 20 118-125
Activity 4.14 Groin & abdominal wall swellings - II 10 39
Additional readings 126-185
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INSTRUCTION: The first common surgical problem we will study is Lower GI

bleeding. Before you start the activity, read “Lower gastrointestinal bleeding”
(pgs.43-58) in the reader at the back of this module. Then proceed to the activity
ACTIVITY 4.1 [TIME: 10 MIN]

LOWER GI BLEEDING - I
A 62-year-old man Kolandaivelu was admitted to the Emergency Room with

the complaint of left lower quadrant pain of 4 hours' duration and several
loose stools containing bright red blood. He has had a long history of
hypertension, angina and congestive heart failure controlled by digoxin and
hydrochlorothiazide.
Physical examination showed his supine blood pressure at 100/70, pulse 104
and temperature 100.5 F. His chest was clear. The abdominal examination
revealed increased bowel sounds and tenderness over the left lower quadrant.
There was no muscle guarding or rebound tenderness.
A rectal examination revealed red bloody stool. Complete blood count
revealed hemoglobin - 9 g% and the white blood count - 12,800 with 81 polys,
15 lymphocytes, 7 monocytes and 1 eosinophil.
1. What are the possible conditions that you will think of?
2. What investigations will you order?
3. What will you see or find in the investigations?
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FE E DB AC K 4 . 1
1. What are the possible conditions that you will think of?
Diverticulosis, polyposis, angiodysplasias, ischemia, malignancy and ulcerative

colitis. However polyposis, malignancy and angiodysplasia are painless
conditions; ulcerative colitis occurs more often in the younger age group. So the
two most likely conditions are diverticulosis and ischemic colitis. The fact that the
patient has cardiac disease is in favour of ischemic colitis.
An air contrast barium enema may be the best investigation to confirm the
diagnosis.
3. What will you see or find in the investigations?
An air contrast barium enema will show irregularity of the mucosa on the sigmoid
flexure or the splenic flexure or even some narrowing. In diverticulosis, you will
see diverticulum on the left colon.
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INSTRUCTION: The next activity continues the learning on lower GI bleeding.

LOWER GI BLEEDING – II
8 year old Gnanamuthu has been brought to you for bleeding per rectum off
and on for 6 months. The bleeding is fresh and painless. This morning when
Gnanamuthu was washing himself he felt a small swelling that had come out
of the anus. By the time the mother came, the mass was not there.
1. What is the possible diagnosis?
2. How will you investigate him?
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FE E DB AC K 4 . 2
1. What is the possible diagnosis?
The history is typical of a polyp, which most often is in the rectum midline posteriorly.
2. How will you investigate him?
A rectal examination will be very helpful because the polyp can be often felt in the
midline posteriorly. Needs to be referred to a surgeon. Under anaesthesia the
swelling can be manipulated to issue out of the anus, cut and sent for biopsy.
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INSTRUCTION: The next activity is another case of GI bleeding. Revise the

readings and then attempt the activity below.

LOWER GI BLEEDING - III
62 year old Kuppuswamy comes to you with the complaint of fullness of his
lower abdomen and loss of appetite for 2/12. He has been constipated but
does pass stools once in 2 days. There is some blood mixed with the stool.
1. What are the diagnostic possibilities?
2. What investigations would you do?
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FE E DB AC K 4 . 3
1. What are the diagnostic possibilities?
 Carcinoma colon/rectum is a strong possibility considering the age, the

change in bowel habit, anorexia and bleeding per rectum
 Diverticulosis is possible and is often associated with constipation and
abdominal discomfort. However this is less common in our country.
 Ischemic colitis is also possible as he has abdominal discomfort and
bleeding. However he does not seen to be having coronary artery disease.
 Angio dysplasia is also possible but is not likely to cause abdominal
discomfort or fullness.
 Ulcerative colitis and Crohn’s disease would have started at an earlier
stage and would have had a longer history.
2. What investigations would you do?
 Rectal examination and proctoscopy to rule out local causes like hemorrhoids;
also to look for a tumour within reach of the finger.
 Barium enema - will show up the following:
 Filling defect suggesting carcinoma colon; apple core lesion will be
seen in more advanced cases and more on the left colon. This is most
likely.
 Diverticulae can be seen. It is important to remember that diverticulae
and malignancy can be associated.
 Serrated mucosa and sacculations of the antimesenteric border of the
splenic flexure and the sigmoid flexure are suggestive of ischemic
colitis.
 Colonoscopy referral will be important as besides confirming diagnosis
of carcinoma, a biopsy can also be taken. Diverticulae can be seen
clearly on colonoscopy while in Ischemic colitis, ulceration and redness
of mucosa can be seen.
Blood test for CEA (Carcino embryonic antigen) can help with the follow
up of a patient with carcinoma colon.
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INSTRUCTION: Activity 7.4 is also a case of GI bleeding. Additional reading material

for this topic is on pgs.126-185.

GI BLEEDING – IV
70 year old Ramagopal comes to you with a history of pain in the left lower
quadrant of the abdomen. He has a low grade temperature and has been more
constipated for 2 days. He is slightly obese but in good health otherwise.
However one month ago he had some bleeding per rectum mixed with stools,
which the patient attributed to “piles”.
1. What are the diagnosis possibilities?
2. How will you clinch the diagnosis?
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FE E DB AC K 4 . 4
1. What are the diagnosis possibilities?
Since he has abdominal pain one must think of the 5 “I’s” and systematically
exclude or include them –
 Intussusception – Not the age group
 Ischemic colitis – often associated with coronary artery disease. Fever
unusual, in Ischemic colitis.
 Infective causes like shigelloles and amebiasis will produce diarrhea.
 The onset of ulcerative colitis and Crohn’s is at a younger age group and
associated with diarrhea.
 Immunodeficiency (HIV) will also be associated with diarrhea.
Therefore diverticulosis is very likely as it can produce both diverticulitis and
hemorrhage.
2. How will you clinch the diagnosis?
The diagnosis can be clinched by

 Air contrast barium enema after the acute episode has subsided OR
 Colonoscopy
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INSTRUCTION: Before beginning the next activity, please read “Acute abdominal
pain” (pgs.59-73) in the reader. Then attempt the activity below.

ACUTE ABDOMINAL PAIN - I
Case 1:
Murugan is a 28-year-old rickshaw puller and he has come to you with a
history of sudden severe pain in the upper abdomen. He gives a history of
dyspepsia for the last three years. When you examine him he seems to have
muscle guarding and rigidity of the upper abdomen.
a) What is the likely diagnosis? Give reasons.
b) What investigation will you order and what will you see?
Case 2:
Madhu is a 14-year-old boy who while attending school developed severe
abdominal pain. He was sent home. The mother brings him to you the next
morning and on examination you find tenderness in the right iliac fossa. It is
likely that Madhu has acute appendicitis.
What is one question you need to ask about the pain?
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Case 7:
Raman is a 25-year-old who has been brought to you with vomiting, abdominal
pain and distension for 24 hours. You examine his abdomen and it seems
distended. There are hyperactive bowel sounds.
a) What is the diagnosis?
b) What important examination has been missed?
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FE E DB AC K 4 . 5
1.
a) What is the likely diagnosis? Give reasons.
Murugan almost certainly has a perforated duodenal ulcer. The reasons for this
diagnosis are:
o 7 year history of dyspepsia
o Guarding and rigidity in the upper abdomen
o Sudden onset (within seconds) unlike acute cholecystitis or acute
pancreatitis.
b) What investigation will you order and what will you see?
Plain X-ray abdomen - erect and left lateral decubitus - will show air under the
diaphragm. An ultrasound can rule out cholelithiasis.
2.
What is one question you need to ask about the pain?
“Where was the pain when it started and where did it shift to?”
a) What is the diagnosis?
Acute intestinal obstruction
b) What important examination has been missed?
An important examination that has been missed is looking for a groin hernia
which is the commonest cause of obstruction in a young male.
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INSTRUCTION: Two more cases with the symptom of acute abdominal pain are
detailed below. Attempt the activity after revising the relevant reading material.

ACUTE ABDOMINAL PAIN - II
1. Sunder a 55-year-old bank official comes to you with pain in the

epigastrium and projectile vomiting for the last one week. He is has lost
three kg of weight in the last one month. There is some fullness of his
epigastrium but the rest of his abdomen is not distended.
What is your suspicion?
2. A 26-year-old coolie, Murugesh has been brought to you with severe

abdominal pain. He keeps writhing and moving about on the trolley
stretcher. On examination you find it difficult to palpate as Murugesh is
very restless and you are uncertain if he has guarding or rigidity. Though
he has had two episodes of vomiting, he has no distension of the
abdomen.
Suppose you were asked to diagnose Murugesh, what possibilities would you
entertain?
3. List the danger signals in a patient with acute abdominal pain.
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FE E DB AC K 4 . 6
1. What is your suspicion?
The projectile vomiting and the fullness of the epigastrium suggest that he has pyloric
obstruction. Since he has lost weight and considering his age, Sunder may have
carcinoma stomach.
2. Suppose you were asked to diagnose Murugesh, what possibilities would

you entertain?
Since he is writhing with pain, he is unlikely to have peritonitis. Patients with

peritonitis are very still. Since he has no abdominal distension, he cannot have
intestinal obstruction of the small bowel or the large bowel.
The diagnosis could be a colic – most likely ureteric colic.
3. List the danger signals in a patient with acute abdominal pain.
a) High pulse rate (Above 100? Mt)

b) Very distended abdomen
c) Signs of guarding and rigidity
d) Absent bowel sounds or greatly increased bowel sounds
e) Yellow or feculent vomiting
f) Absolute constipation
g) Multiple fluid levels on X-ray
h) Severe hypogastric pain in a woman of childbearing age who has missed a
period.
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INSTRUCTION: In the next activity, the learning on acute abdominal pain continues.

ACUTE ABDOMINAL PAIN – III
72-year-old Thangamma has been brought to you with vomiting and

distension of abdomen for two days. She has not passed faeces or flatus for
about 40 hours. She is in pain which is colicky and central abdominal. Her
pulse is 96/mt and has no fever. No rebound tenderness felt.
1. What is your diagnosis?
2. What is the likely level of obstruction?
3. Is there gangrene associated with the obstruction?
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FE E DB AC K 4 . 7
1. What is your diagnosis?
She has intestinal obstruction as she has vomiting, distension, constipation

(absolute for 40 hours) and abdominal pain.
2. What is the likely level of obstruction?
Since she has distension, she cannot have pyloric obstruction. Colicky central
abdominal pain is more like a small bowel obstruction.
3. Is there likely to be gangrene associated with the obstruction?
She does not have features of gangrenous obstruction such as continuous

abdominal pain, tachycardia (more than 100) & fever. She has no rebound
tenderness either.
For further confirmation of your diagnosis, you can do an Hb test which may drop
in gangrenous obstruction, and a blood urea test which will show a rise.
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INSTRUCTION: The next topic is Neck swellings. The reading for this is on
pgs.74-95 at the back of the module. Please read this section before proceeding to
the activity.

NECK SWELLINGS - I
I. Gomati a 5 year old child has been brought to you with a discharging sinus
in the central part of the neck near the thyroid cartilage. The mother says that
a surgeon incised it about 6 months ago and drained some pus.
a) What do you think happened?
b) How will you further manage Gomati?
II. Raghavan is a 62-year-old man who has come to you with a swelling in the
cervical region which he noticed 7 weeks ago. He smells of tobacco smoke as
he walks in.
a) What questions will you ask in elucidating the history?
b) What is the likely diagnosis?
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FE E DB AC K 4 . 8
I.
a) What do you think happened?

Gomati had a swelling in the midline of the neck, which probably was infected and
incised. If it were, only an abscess it would have healed. Since it did not heal and
persisted as a sinus, it could be either a tuberculous sinus (cold abscess) or a
thyroglossal cyst. Tuberculous adenitis does not occur in the midline and so the
most probable cause is a thyroglossal cyst.
b) How will you further manage Gomati?
The management of a thyroglossal cyst is Sistrunk’s operation. Here the central

part of the hyoid bone is excised along with the cyst or the sinus to ensure
removing the thyroglossal tract. The latter run very close to the hyoid as it
descends.
II.
a) What questions will you ask in elucidating the history?
Have you pain and has it been growing steadily?

Have you had fever? Loss of weight? Night sweats? Have you had tuberculosis?
Do you cough? Do you have hoarseness of voice? Dysphagia? Dyspepsia?
b) What is the likely diagnosis?

The possible diagnosis –
Tuberculosis is very common and is still a possibility, but it occurs more commonly
in the young.
Secondary metastasis from a malignancy is a very likely cause and primary sites
such as larynx, naso-pharynx, and the lung should be investigated for a primary.
Smoking is a risk factor.
Lymphoma is also likely. A biopsy will be conclusive.
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INSTRUCTION: We continue the learning on Neck swellings in this activity.

Additional reading material for the topic is on pgs.126-185.

NECK SWELLINGS - II
Megala a 26-year-old woman in her post partum period comes to you with a
history of swelling in her neck for 2 months. She volunteers the information
that she is unable to sleep, and her appetite is greatly increased. On
inspection, the swelling move up on deglutition and is to the right side of the
neck. On palpation, it feels like a well-rounded nodule about 2 cms in diameter
and is not tender. The rest of the gland is normal. There are no neck nodes.
Megala’s pulse rate is 110/mt and she has no eye signs of Graves’s disease.
1. What is the diagnosis?
2. What are the eye signs of Graves’s disease? What is the significance?
7. How will you manage her?
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4. If Megala has a smooth uniform swelling of the thyroid with typical eye signs of
primary hyperthyroidism (Graves’), how will you manage her?
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FE E DB AC K 4 . 9
1. What is the diagnosis?

Megala has hyperthyroidism from the evidence that is available. She has
tachycardia, has insomnia and increased appetite. However, she does not have
primary hyperthyroidism or Graves’s disease as the thyroid gland is not uniformly
enlarged and she has no eye signs. She has a nodule in the gland which is hyper
functioning. This is a toxic nodule. It may be benign or malignant.
2. What are the eye signs of Graves’s disease? What is the significance?
 Exophthalmos (When the white of the sclera can be seen between the
limbus and the lower eyelid)
 When the upper eyelid is raised so that it is at the border of the limbus or
higher the condition is called “lid lag.”
 Chemosis or congestion of the conjunctiva
 Ophthalmoplegia, so that there is diplopia
When these eye signs are present it substantiates a diagnosis of primary
hyperthyroidism; they are not seen in secondary hyperthyroidism.
7. How will you manage her?
Order thyroid function tests to confirm that she has a hyper functioning gland.
Elevated levels of T7 and T4 and reduced levels of TSH will be confirmatory. (At this
point the family practitioner may refer to a surgeon for an FNAC and surgery.)
Perform FNAC to rule out malignancy. A follicular carcinoma of the thyroid can hyper
function causing hyperthyroidism. A surgeon will do a hemi-thyroidectomy to excise
the swelling.
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4. If Megala has a smooth uniform swelling of the thyroid with typical eye signs of
primary hyperthyroidism (Graves’), how wll you manage her?
o Since Megala is in her post partum period and probably lactating she is not fit for
radio-iodine therapy.
o She could have either surgery or anti-thyroid drug therapy.
Drug treatment has two components:
 Symptomatic- Propranolol to control the adrenergic symptoms and provide

immediate relief.
 Anti-thyroid treatment – Either Carbimazole or Propylthiouracil orally. For
details of treatment, see the table. Monitor the T4 and T7 levels. Monitor
also the blood counts, as there is risk of agranulocytosis.
 If Megala does not tolerate the drugs or has a relapse or is resistant to the
drugs, she should be referred for surgery (Sub-total thyroidectomy).
 Megala is too young for radio-iodine treatment
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INSTRUCTION: The next activity also has a case of neck swellings. Revise the
reading material before proceeding to the activity.

NECK SWELLINGS - III
Ranjita, a woman of 75, presents to you with enlarged right cervical glands
and intermittent fever. She has night sweats and feels fatigued.
On examination, she has discrete enlarged, non-tender, right cervical nodes
and large right axillary nodes. There are no other significant findings.
1. What is the differential diagnosis?
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On biopsy of the cervical node, typical Reed-Steinberg cells were seen and
there were a lot of fibrous bands histologically.
3. What is the diagnosis, pathological staging and clinical staging if no other

nodes or organs were involved after investigations?
4. How will you manage Ranjita?
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FE E DB AC K 4 . 1 0
1. What is the differential diagnosis?
The possibilities are:

Tuberculosis (as it is the commonest cause of cervical adenopathy in our
country), Hodgkin’s lymphoma and Non-Hodgkin’s; HIV infection is also
possible.
A Lymph node biopsy or an FNAC will likely give a diagnosis. Other

investigations are listed below:
 Blood counts should be done. There can be anemia, leucopenia and
thrombocytopenia. Low counts are in favor of a Non-Hodgkin’s (NHL)
though it can occur in Hodgkin’s too.
 ESR will be elevated in all the differentials listed above.
 Uric acid is often elevated in Hodgkin’s and NHL.
 Liver function to evaluate its involvement: more often involved in NHL
 Ultrasound to evaluate the nodes in the abdomen; also to see the
involvement of the liver and the spleen. This is again a possibility in
Hodgkin’s and NHL.
 X-ray chest to see the mediastinum
 Bone-marrow should be done to see if it is affected. More likely in NHL
 HIV test should be done.
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3. What is the diagnosis, pathological staging and clinical staging if no other

nodes or organs were involved after investigations?
Histo-pathologically this is consistent with Hodgkin’s lymphoma- Nodular

sclerosis (Fibrous bands are characteristic).
The clinical staging would be II B. The reasons for the staging are:
There is involvement of the cervical and axillary nodes, both on the same side
of the diaphragm. However since Ranjita has fever, loss of weight and fatigue,
she should be designated as B.
5. How will you manage Ranjita?

Since Ranjita’s clinical staging is IIB, radiotherapy cannot be given to her.
(Given only for Stages I and IIA)
She should be given chemotherapy, perhaps the ABVD regime.
Since Ranjita’s clinical staging is IIB, Radiotherapy cannot be given to her.
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INSTRUCTION: The next surgical problem is that of leg ulcers. Read carefully
“Management of chronic leg ulcers” (pgs.96-117) before proceeding to the
activity.

LEG ULCERS - I
Forty six-year-old Prakash, a bus conductor, has a vexing problem of

recurrent ulceration on his left leg for the past one year. He has no history of
trauma preceding it but complains of vague discomfort and dull ache in his
legs more towards the end of the day with mild swelling of left leg.
On examination, he has an ulcer 2x7 cms just above the left medial malleoli,
brownish pigmentation of surrounding skin, and edema of the ankle.
1. What is the probable reason for his recurrent leg ulceration?
2. What investigations will help?
3. How will you treat his condition?
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4. What advice will you give to prevent recurrence?
5. Does his job have a relation to the healing of the ulcer?
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1. What is the probable reason for his recurrent leg ulceration?
This patient has a venous ulcer due to venous hypertension. There is brownish
pigmentation of surrounding skin with oedema and varicosities on the lower leg.
This is called “lipodermatosclerosis”.
2. What investigations will help?
A Doppler ultra sound to determine the ABPI.
3. How will you treat his condition?
If the ABPI is more than 0.8, compression bandaging should be advised in addition
to limb elevation and exercise. The gravitational dermatitis should be treated with
topical steroids.
4. What advice will you give to prevent recurrence?
He must continue the compression hosiery lifelong to prevent a recurrence of

ulcers.
5. Does his job have a relation to the healing of the ulcer?
Yes. Rest and limb elevation which aids in venous return helps in healing and jobs
where the patient has to stand for long time can delay healing.
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INSTRUCTION: A second case of leg ulcers is given in the activity below.

LEG ULCERS - II
Thirty eight-year-old Chandran, a manual laborer, has come with an ulcer on

the sole of the right foot. He gives history of trauma with a splinter of wood
one month ago but did not feel much pain at that time or later, till he noticed
the foul smelling discharge from the ulcer for the past two weeks.
On examination, he has a deep ulcer under the ball of big toe with slough,
necrotic material, and purulent discharge.
1. What are the differential diagnoses in this case?
2. What clinical examinations should be done?
3. What investigations should be done?
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4. How will you manage his ulcer?
5. What other advice will you give to prevent the ulcer from recurring?
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1. What are the differential diagnoses in this case?
Chandran has a neuropathic ulcer. (The site and punched out edges with
purulent discharge are diagnostic.)
2. What clinical examinations should be done?
Tests for peripheral neuropathy should be carried out to find out the type of
sensory loss. (i.e. whether there is loss of sensation to temperature, pain, touch,
vibration etc) Examine for enlarged peripheral nerves, anaesthetic or hypo
pigmented patches of leprosy. Basic neurological examination including
reflexes.
3. What investigations should be done?
 Tests for diabetes.

 Skin smear of doubtful patches to rule out Hansen’s.
 X-ray of foot to assess degree of involvement.
 Pus swabs
4. How will you manage his ulcer?
The ulcer should be cleaned thoroughly and an appropriate antibiotic should be

given based on C&S. Offloading device must be given to allow healing of ulcer.
5. What other advice will you give to prevent the ulcer from recurring?
Advice regarding foot care, regular chiropody, avoidance of trauma, early treatment
of lesions and special foot wear.
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INSTRUCTION: The final surgical problem covered in this module is Groin &
abdominal wall swellings. Read “Swellings in the groin region & in the
abdominal wall” (pgs.118-125) before proceeding to the activity.

GROIN & ABDOMINAL WALL SWELLINGS - I
27 year old Siddhartha comes to you with a palpable swelling in the right
scrotum for an 8 week period. He has dull ache in the groin for about 7 weeks.
He had visited a local doctor who had made a diagnosis of inflammation of the
testes and epididymis; he was told that he had got the infection from his girl
friend and was put on antibiotics for a 10 day period. Siddhartha has not felt
better and he has come to you for treatment.
1. What will you look for in the physical examination?
2. What are the common testicular tumors?
3. What investigations are specific to these tumors?
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1. What will you look for in the physical examination?
Firstly determine that he has a scrotal rather than an inguino-scrotal swelling. This
can be done by trying to get above the swelling.
Then if it is an inguino-scrotal swelling, look for a cough impulse.
If it is a scrotal swelling, using the fluctuation test and the transilluminancy test, see
if it is solid or cystic. Hydrocoele is the commonest swelling and is often but not
always fluctuant.
Solid swellings can be inflammatory (tender) or neoplastic in which case it may not
be tender.
Examine for possible metastasis: the abdomen for para-aortic nodes, and the liver
and the neck for supraclavicular nodes.
2. What are the common testicular tumors?
Germinal cell tumors are the commonest, accounting for more than 95% of all
tumors. Of these, seminomas account for 40% and non-seminomas account for the
rest.
3. What investigations are specific to these tumors?
Tumor cell markers can be done not only as a possible diagnostic aid but also
for monitoring cancer recurrence. Blood tests for tumor markers: alpha-
fetoprotein (AFP), human chorionic gonadotrophin (beta HCG), and lactic
dehydrogenase (LDH). Approximately 85% of non-seminomas will have
elevations of either AFP or beta HCG. Seminomas will have elevations only in
beta HCG or LDH.
38
4. Surgery
INSTRUCTION: The last activity is also related to groin swellings. Please

undertake the activity after revising the relevant reading material Additional
readings are on pgs.118-185.

GROIN & ABDOMINAL WALL SWELLINGS - II
22 year old Ganeshan comes to you with sudden onset of pain in the right
testis. He also has some abdominal ache and vomiting. He gives no history
of trauma.
1. What are the possibilities?
2. How will you resolve the differential diagnoses?
39
4. Surgery
1. What are the possibilities?
There are two common reasons for pain in the scrotum: infection (epididymo-
orchitis) and torsion.
2. How will you resolve the differential diagnoses?
Very sudden onset of pain, higher level of the affected testes as compared to the
opposite side, horizontal position of the opposite testes and vomiting are in favour
of torsion; evidence of pus cells in the urine and tenderness of the prostate are in
favour of epididymo-orchitis. Other differences between the two are tabled in the
section on torsion of the testes.
40
4. Surgery
NOTES
41
4. Surgery
READINGS
42
4. Surgery
LOWER GASTRO INTESTINAL BLEEDING
Definitions –
Lower gastrointestinal bleeding is defined as bleeding that issues from that part of
the gastro Intestinal tract distal to the ligament of Treitz. (duodenal jejunal flexure).
Massive or acute lower gastrointestinal bleeding - Bleeding of less than 72 hours

duration which causes hemodynamic instability with a drop in Hb levels; and
requiring transfusion of at least 2 units of packed cells.
Moderate or Chronic Bleeding – Bleeding that has continued for 7 days to a week
without causing hemodynamic instability. This group may present with history of
bleeding PR with signs and symptoms of anemia.
Occult bleeding - Where the patient presents with another complaint but where
occult blood has been found in the stools e.g. presents with anemia or some
abdominal discomfort or diarrhea or during a checkup.
43
4. Surgery
CHARACTERISTICS & CAUSES OF

LOWER GI BLEEDING
Massive Moderate Occult

bleeding bleeding bleeding
Characteristics
 Older  Any age

 Any age
 Bright red blood from  No obvious blood
 Mixed with stool
rectum  Stool positive for
 Haematochezia or occult blood
 Hemodynamically Malena
unstable  Hemodynamically
 Hb ↓ stable
 Hb ↓
Common causes
 Medical causes like DIC,  Hemorrhoids  Hookworm

Coagulopathy  Fissure in ano  Malignancy
 Angiodysplasia  Polyps  U colitis
 Diverticular disease  Intussception specially infants  Ischemic colitis
(rare in our country)  Infections – Shigella, Entamoeba  Multiple polyps
 Colitis inflammatory  Inflammatory - U colitis, Crohn’s  Diverticulosis
 Meckel’s (in younger  Carcinoma  Angiodysplasia
age group)  Ischemic colitis – (splenic flexure,
Rectosigmoid older age)
 Meckel’s
44
4. Surgery
Symptoms
1. Bleeding - nature and duration
Nature:
o Bright red blood not mixed with stools; usually comes from the
anorectum. In fissure bleeding is mild and may streak the stool
surface. In haemorrhoids, the bleed may be dripping or jet-like after
defaecation.
o Bright red blood mixed with stools; usually comes from the lower GI
tract, as bleeding from the upper GI tract shows up as malena,
(However, rapid bleeding from oesophageal varices can show up as
fresh blood per rectum.)
Duration:
o In hemorrhoids, diverticulosis, fissure-in-ano, ulcerative colitis, Crohn’s
disease and polyposis, the history may go back to months.
o In amoebic colitis, Meckel’s diverticulum, colonic malignancy and
ischemic colitis, the history may go back to days or weeks.
o In A.V. malformation, DIC, enteric fever (typhoid ulcer bleed), and
diverticulosis, the history of acute massive bleeding may go back only
hours or days.
2. Associated problems
(i) Hemetemesis – In 20% of upper GI bleeds, there is malena or maroon
colored or even bright red blood per rectum
(ii) Fever – In amoebic colitis or shigellosis, enteric fever or acute fulminant
ulcerative colitis, the patient can have associated fever.
(iii) Abdominal pain – There is associated abdominal pain in infective
diarrhea, intussusception, ischemic colitis, inflammatory bowel disease,
and HIV.
(iv) Diarrhea – Is a feature of infective diarrhea, inflammatory bowel disease
and HIV.
(v) Pain in the ano-rectum during defecation – Fissure-in-ano; thrombosed
piles; proctitis as in ulcerative colitis
45
4. Surgery
7. Changes in bowel habits -

Often in carcinoma of the colon and rectum there are changes in the patient’s
bowel habits. (Instead of one stool/day, 7 to 4 stools/day; instead of constipation,
diarrhea, etc.)
4. History of mass issuing out of the rectum -
Possibilities in this case include hemorrhoids, intussusception, polyp and
prolapse rectum.
5. Family history of polyposis – is seen in familial polyposis coli.
6. History of drugs - Aspirin, NSAIDs, chemotherapeutic drugs, and anticoagulant
use.can produce bleeding per rectum.
7. History of malignancy and radiation – Malignancy and radiation colitis can both
cause bleeding.
Clinical features to look for

1. Age
Infancy - Intussception, fissure-in-ano are some important causes; however mal-
rotation, gangrene bowel and volvulus can occur in neonates.
Necrotizing enterocolitis, allergy and lymphoid hyperplasia are other
causes in infants.
Young - Meckel’s diverticulum, enteric and amoebic infections, fissure-in-ano,
inflammatory bowel disease, HIV causing diarrhea and bleeding per
rectum
Older - Malignancy hemorrhoids, ischemic bowel disease, diverticulum,
angiodysplasia of colon
2. Evidence of anemia - Chronic visible and occult blood loss can sometimes
produce congestive cardiac failure secondary to anemia.
7. Rectal examination –
o Ulcer or tumour can be felt in carcinoma of the rectum.
o A polyp can be felt sometimes specially midline posteriorly in infants.
o Fissure-in-ano can be seen by spreading the anal opening by gently
separating the buttocks.
o Hemorrhoids can be seen on proctoscopy and
o Intussception can sometimes emerge out of the anorectum specially in
infants.
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4. Surgery
4. Abdominal examination -
 Evidence of portal hypertension should be looked for such as ascites,
splenomegaly, gynecomastia and testicular atrophy. Bleeding
hemorrhoids secondary to cirrhosis of the liver can have these
problems.
Note: Right colonic bleeding can present as malena if the bleeding is slow.
Stomach or upper GI bleeding can present as bright red blood if the transit
time is rapid.
Lower gastro intestinal bleeding and abdominal pain

Remember the 5 I’s
o Infective – Shigella, Amoeba, Campylobacter, Clostridia
o Inflammatory bowel disease – Ulcerative colitis
o Intussusception in infants
o Ischemic colitis in older age group
o Immuno deficiency - HIV
47
4. Surgery
INVESTIGATIONS
Type Rationale
Hb, PCV
To estimate quantity of bleeding
To rule out bleeding disorder

Bleeding time / clotting
time, Platelet count,
Prothrombin
To rule out hepatic dysfunction

Liver function tests
Atherosclerotic disease may

suggest ischemic colitis
Blood sugar, BP, ECG
In a patient with unexplained

anemia
Occult blood
Amoebic colitis
Stool for amoeba
If associated fever and abdominal

symptoms - to rule out Salmonella
Blood culture
Hemorrhoids, fissure-in-ano, polyp

(Inflammatory polyp can often be
PR & Proctoscopy felt in the rectum in the midline
posteriorly.)
48
4. Surgery
Carcinoma Colon as a cause of lower GI bleeding

Colorectal malignancy is a group that comprises of malignant tumors from the
rectum, colon and the appendix. (from Wikipedia, the free encyclopedia)
Symptoms
Symptoms of colorectal cancer may include:
 Change in bowel habits (e.g. constipation, diarrhoea, change in the caliber of
stools)
 Blood in stools (malena, hematochezia)
 Bowel obstruction (rare) by the tumor
Often, the symptoms are much less specific:
 Anemia, with symptoms such as tiredness, malaise, pallor
 Unexplained weight loss
 Tumor in the abdomen for example - Hepatomegaly (enlargement of the liver)
due to spreading of the tumor
It is also possible that there will be no symptoms at all. This is one reason why many
organizations recommend periodic screening for the disease with fecal occult blood
testing.
TUTOR SAYS
Left sided colonic malignancy = Frank bleeding/ Bowel obstruction
Right sided colonic malignancy = Usually change in bowel habit/ Anemia/
Occult bleeding/ palpable mass
Predisposing factors-
Certain factors increase a person's risk of developing the disease. These include:
 Age. The risk of developing colorectal cancer increases with age. Most cases
occur in the 60s and 70s, while cases before age 50 are uncommon unless a
family history of early colon cancer is present.
 History of cancer. Women who have had cancer of the ovary, uterus, or
breast are at higher risk of developing colorectal cancer.
 Heredity:
o Family history of colon cancer, especially in a close relative before the
age of 55 or multiple relatives
49
4. Surgery
o Familial adenomatous polyposis (FAP) carries a near 100% risk of

developing colorectal cancer by the age of 40 if untreated
o Hereditary nonpolyposis colorectal cancer (HNPCC) or Lynch
syndrome
 Long-standing ulcerative colitis or Crohn's disease of the colon, approximately
70% after 25 years if the entire colon is involved
 Smoking. Smokers are more likely to die of colorectal cancer than non-
smokers.
Diet. Studies show that a diet
o high in red meat (Chao et al 2005) and
o low in fresh fruit, vegetables,
o low in poultry and fish
increases the risk of colorectal cancer.
 Physical inactivity. People who are physically active are at lower risk of
developing colorectal cancer.
 Virus. Exposure to some viruses (such as particular strains of HPV- human
papilloma virus) may be associated with colorectal cancer.
Normal air contrast barium enema
Diagnosis, screening and monitoring
Identification of malignancy
Colorectal cancer can take many years to develop
and early detection of colorectal cancer greatly
improves the chances of a cure. Therefore,
screening for the disease is recommended in
individuals who are at increased risk. There are
several different tests available for this purpose.
 Digital rectal exam (DRE): The doctor
inserts a lubricated, gloved finger into the
rectum to feel for abnormal areas. It only
detects tumors large enough to be felt in the distal part of the rectum and is
not really a screening test.
 Fecal occult blood test (FOBT): a test for microscopic amounts of blood in the
stool.
50
4. Surgery
 Double contrast barium enema (DCBE): First, an overnight preparation is

taken to cleanse the colon. An enema containing barium sulfate is
administered, then air is insufflated into the colon, distending it. The result is a
thin layer of barium over the inner lining of the colon which is visible on X-ray
films. A cancer or a precancerous polyp can be detected this way. This
technique can miss the (less common) flat polyp.
 Endoscopy: Sigmoidoscopy: A lighted probe (sigmoidoscope) is inserted into
the rectum and lower colon to check for polyps and other abnormalities.
 Colonoscopy: A lighted probe called a colonoscope is inserted into the rectum
and the entire colon to look for polyps and other abnormalities that may be
caused by cancer. A colonoscopy has the advantage that if polyps are found
during the procedure they can be immediately removed. Tissue can also be
taken for biopsy.
 Standard computed axial tomography is an x-ray method that can be used to
determine the degree of spread of cancer, but is not sensitive enough to use
for screening. Some cancers are found in CAT scans performed for other
reasons.
 Specialized blood tests: Measurement of the patient's blood for elevated
levels of certain proteins, called tumor markers can give an indication of
tumor load. In particular, high levels of carcino-embryonic antigen CEA in the
blood can indicate metastasis of adenocarcinoma. These tests are frequently
false positive or false negative, and are not recommended for screening but
for follow up.
Pathology
The most common colon cancer cell type is
 adenocarcinoma which accounts for 95% of cases.
Other, rarer types include
 lymphoma and
 squamous cell carcinoma.
Cancers on the right side (ascending colon and cecum) tend to be exophytic, that is
the tumour grows outwards from one location in the bowel wall. This very rarely
causes obstruction of feces, and present with symptoms such as anemia. Left-sided
tumours tend to be circumferential, and can obstruct the bowel causing a stricture.
51
4. Surgery
Histopathology: Adenocarcinoma is a malignant epithelial tumor, originating from

glandular epithelium of the colorectal mucosa. It invades the wall, infiltrating the
muscularis mucosae, the submucosa and thence the muscularis propria.
Sometimes, tumor cells are discohesive and secrete mucus which invades the
interstitium producing large pools of mucus/colloid (optically "empty" spaces)-
mucinous (colloid) adenocarcinoma, poorly differentiated.
If the mucus remains inside the tumor cell, it pushes the nucleus at the periphery -
"signet-ring cell".
Depending on glandular architecture, cellular pleomorphism and mucosecretion of
the predominant pattern, adenocarcinoma may present 7 degrees of differentiation:
well, moderate and poorly differentiated.
Staging
TNM or Dukes
Colon cancer staging is an estimate of the condition of a particular cancer for
diagnostic and research purposes. The systems for staging colorectal cancers
largely depend on the extent of local invasion, the degree of lymph node
involvement and whether there is distant metastasis.
The most common currently used system for staging is the TNM system, though
many doctors still use the older Dukes system. The TNM system assigns a number:
 T - The degree of invasion of the intestinal wall
o T0 - no evidence of tumor
o Tis- cancer in situ (tumor present, but no invasion)
o T1 - tumor present but minimal invasion
o T2 - invasion into the submucosa
o T7 - invasion into the muscularis propria
o T4 - invasion completely through the wall of the colon
Large “apple core” lesion-

Sigmoid carcinoma
52
4. Surgery
 N - the degree of lymphatic node involvement

o N0 - no lymph nodes involved
o N1 - one to three nodes involved
o N2 - four or more nodes involved
 M - the degree of metastasis
o M0 - no metastasis
o M1 - metastasis present
Treatment
The treatment depends on the staging of the cancer. When colorectal cancer is
caught at an early stage (with little spread) it can be curable. However when it is
detected at a later stage (when distant metastases are present), it is less likely to be
curable.
Surgery remains the primary treatment while chemotherapy and/or radiotherapy may
be recommended depending on the individual patient's staging and other medical
factors.
Surgery
Surgical treatment is by far the most likely to result in a cure of colon cancer if the
tumor is localized. Very early cancer that develops within a polyp can often be cured
by removing the polyp at the time of colonoscopy. More advanced cancers typically
require surgical removal of the section of colon containing the tumor leaving
sufficient margins to reduce likelihood of re-growth. If possible, the remaining parts
of colon are anastomosed together to create a functioning colon. In cases when
anastomosis is not possible, a stoma (artificial orifice) is created. While surgery is
not usually offered if significant metastasis is present, surgical removal of isolated
liver metastases is common. Improved chemotherapy has increased the number of
patients who are offered surgical removal of isolated liver metastases.
Laparoscopic assist resection of the colon for tumour can reduce the size of painful
incision and minimize the risk of infection.
As with any surgical procedure, colorectal surgery can in rare cases result in
complications. These may include infection, abscess, fistula or bowel obstruction.
Chemotherapy
Chemotherapy is used to reduce the likelihood of metastasis developing, shrink
tumor size, or slow tumor growth. Chemotherapy is often applied after surgery
53
4. Surgery
(adjuvant), before surgery (neo-adjuvant), or as the primary therapy if surgery is not

indicated (palliative). The treatments listed here have been shown in clinical trials to
improve survival and/or reduce mortality and have been approved for use by the US
Food and Drug Administration.
 Adjuvant (after surgery) chemotherapy. One regimen involves the
combination of infusional 5-fluorouracil, leucovorin, and oxaliplatin (FOLFOX).
o 5-fluorouracil (5-FU)
o Leucovorin (LV)
o Oxaliplatin (Eloxatin®)
o Capecitabine (Xeloda®)
 Chemotherapy for metastatic disease. Commonly used first line regimens
involve the combination of infusional 5-fluorouracil, leucovorin, and oxaliplatin
(FOLFOX) with bevacizumab or infusional 5-fluorouracil, leucovorin, and
irinotecan (FOLFIRI) with bevacizumab.
o 5-fluorouracil (5-FU)
o Leucovorin
o Irinotecan
o Oxaliplatin
o Bevacizumab
o Cetuximab
Radiation therapy
Radiation therapy is not used routinely in colorectal cancer, as it could lead to
radiation enteritis, and is difficult to target specific portions of the colon, but may be
used on metastatic tumor deposits if they compress vital structures and/or cause
pain. There may be a role for post-operative adjuvant radiation in the case where a
tumor perforates the colon as judged by the surgeon or the pathologist. However, as
the area of the prior tumor site can be difficult (if not impossible) to ascertain by
imaging, surgical clips need to be left in the colon to direct the radiotherapist to the
area of risk.
Prognosis
Survival is directly related to detection and the type of cancer involved. Survival
rates for early stage detection is about 5 times that of late stage cancers.
54
4. Surgery
Prevention
Most colorectal cancers should be preventable, through
o increased surveillance,
o improved lifestyle.
Surveillance
Most colorectal cancers arise from adenomatous polyps. These lesions can be
detected and removed during colonoscopy. Studies show this procedure would
decrease by more than 80% the risk of cancer death, provided it is started by the
age of 50, and repeated every 5 or 10 years (Winawer et al 1997). However since
this form of cancer is not common in our country and therefore may not be cost
effective, it is not recommended for India.
Lifestyle modification
The comparison of colorectal cancer incidence in various countries strongly
suggests that
* A sedentary lifestyle
* Smoking
* Overeating (i.e. high caloric intake)
* Diet high in meat (red or processed)
could increase the risk of colorectal cancer.
In contrast, physical exercise, and eating plenty of fruits and vegetables would
decrease cancer risk. Fruits and vegetables contain protective phytochemicals.
Eating whole apples, including the skin, offers some anticancer benefits (Liu et al).
Accordingly, lifestyle changes could decrease the risk of colorectal cancer as much
as 60-80% (Cummings and Bingham 1998).
Diverticulosis
Diverticulosis is very common in the west, and it is
getting to be more common in India too. The
frequency of diverticulosis in barium studies in India
increased from 0.7% among subjects in the third
decade to 72.4% in patients above 60 years. Most
patients were city dwellers, vegetarians and belonged to the upper socio-economic
stratum.
55
4. Surgery
Many people have small pouches in their colons that bulge outward through weak
spots; the mucosa and the sub mucosa herniates through weaknesses in the muscle
layer forming pouches called diverticula. This fragility occurs in the regions where
the arterial vessels penetrate trough the muscular stratum. Each pouch is called a
diverticulum and the condition of having diverticula is called diverticulosis. The
condition becomes more common as people age. About half of all people over the
age of 60 have diverticulosis.
Etiology
Age: Diverticuli are more common with age when the bowel muscle weakens.
Constipation is the most common cause of diverticulosis. Increased intra-colonic

pressure secondary to the constipation leads to weaknesses in the colon walls
giving way to diverticula.
Other causes may include a colonic spasm which increases pressure, which may be
due to dehydration or low-fiber, high fat diets; although this may also be due to
constipation. Fiber causes stools to retain more water and become easier to pass
(either soluble or insoluble fiber will do this).
A diet without sufficient fiber makes the stools small, requiring the bowel to squeeze
harder to remove the smaller stool.
Symptoms Most people with uncomplicated diverticulosis do not have any

discomfort or symptoms. However, symptoms may include
 Mild cramps,
 Bloating, and
 Change in bowel habits : more constipation but sometimes even diarrhea.
 Symptoms related to anemia like lightheadedness and weakness.
Complications of diverticulosis Infection

Occurs in 10-20 % of patients with diverticulosis. Infection of a diverticulum often
occurs as a result of stools collecting in a diverticulum. An attack of diverticulitis can
56
4. Surgery
develop suddenly and without warning. This is the most

common complication. The symptoms include -
* tenderness around the left side of the lower
abdomen.
* fever, nausea, vomiting, chills, cramping, and
constipation may occur as well.
* The severity of symptoms depends on the extent of the infection and
complications.
Bleeding
Small bleeds are more common than large ones. Bleeding diverticula are caused by
a small blood vessel in a diverticulum that weakens and finally bursts. Bleeding can
be in very small amounts and may stop by itself, not requiring treatment. In case of
severe bleeding, the patient needs to be referred to the emergency surgical section.
Abscess, Perforation, and Peritonitis
The infection causing diverticulitis often clears up after a few days of treatment with
antibiotics. If the infection occurs slowly over a few days then, an abscess may form
around the diverticulum in the colon and may be palpable per abdomen. This can be
treated conservatively or referred to the surgeon.
If the infection is overwhelming and rapid and large, then peritonitis results and the
whole abdomen becomes tender and guarded. Peritonitis requires immediate
surgery and will need quick referral. Without surgery, peritonitis can be fatal.
Fistula
The most common type of fistula occurs between the bladder and the colon. It
affects men more than women. This type of fistula can result in a severe, long-
lasting infection of the urinary tract. The problem will need referral to the surgeon for
colectomy and fistulectomy.
Intestinal obstruction in large and / or small bowel
The scarring caused by infection may cause partial or total blockage of the large
intestine. Also when there are adhesions between the large bowel diverticular mass
and the small bowel, then kinking may occur and small bowel obstruction may be the
result.
Diagnosis
Barium Enema will show up the diverticula; however this should not be done on a
patient who has acute abdominal pain.
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4. Surgery
Colonoscopy is probably the most useful test as it can rule out other lesions as
well.
CT scan and MRI also will help when the patient has a mass in the left colon region;
this may be ordered by the surgeon.
Treatment
In the absence of any complication no treatment is necessary except some
conservative measures.
* Increasing the fibre content of foods (20-75 grams each day),
* Fibre supplements like bran and Isabgul
Removing factors that may be causing constipation- like dehydration and
drugs.
* Foods with large seeds such as nuts, popcorn hulls, and sunflower, pumpkin,
caraway, and sesame seeds should be avoided. They can get caught in the
diverticulum. The seeds in tomatoes, zucchini, cucumbers, strawberries, and
raspberries, as well as poppy seeds, are generally considered harmless.
Treatment of Diverticulitis
 An attack of diverticulitis without complications may respond to antibiotics
within a few days if treated early (Gentamycin with Ampicillin and
Metronidazol)
 To help the colon rest, bed rest and intravenous fluids for 24 hours may be
prescribed.
 Later a liquid diet, along with a pain reliever like an anti-spasmodic like Tab.
Dicyclomine may be prescribed.
Indications for referral for surgery:
If you do not have facilities for admission then any patient with acute diverticulitis will
have to be referred.
If you have admitted a patient with diverticulitis, then he should be referred to the
surgeon for any of the following reasons:
 Increasing pain that is spreading to the whole of the abdomen
 Increasing pulse rate
 Bleeding that is more than a few drops
 Distension of abdomen
 Recurrent attacks of abdominal pain
(Additional readings on Lower GI bleeding are on pgs.179-161)
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4. Surgery
ACUTE ABDOMINAL PAIN
CAUSES OF ABDOMINAL PAIN

Process Organ involved Disorder
Inflammation Bowel Inflammatory bowel disease
Appendix Appendicitis
Gall bladder Cholecystitis
Pancreas Pancreatitis
Fallopian tube Salpingitis
Colonic diverticulae Diverticulitis
Perforation Duodenum Perforated duodenal ulcer
Stomach Perforated gastric ulcer
Colon (diverticula or Faecal peritonitis
carcinoma)
Gall bladder Biliary peritonitis
Appendix Appendicitis
Obstruction Gall bladder Biliary colic
Small intestine Acute small bowel obstruction
Large bowel Acute large bowel obstruction
Ureter Ureteric colic
Urethra Acute urinary retention
Mesenteric artery Intestinal infarction
occlusion
Haemorrhage Fallopian tube Ruptured ectopic pregnancy
Spleen or liver Ruptured spleen or liver
(haemoperitoneum)
Ovary Ruptured ovarian cyst
Abdominal aorta Ruptured AAA
Torsion Sigmoid colon Sigmoid volvulus
(ischaemia) Ovary Torsion ovarian cyst
Testes Torsion of testes
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4. Surgery
HISTORY TAKING
a) Site of pain – Often this can give a clue to the diagnosis.
Epigastric pain Duodenal ulcer perforation
Acute pancreatitis
Right Hypochondrium Gall bladder disease / Cholecystitis
Umbilical region Intestinal obstruction / early
appendicitis
Loin Pyelonephritis or renal colic
Hypogastrium Cystitis
Tubal pregnancy
Salpingo – Oophoritis
b) Mode of onset –
if the pain is very sudden then it is likely to be perforation of a duodenal ulcer;
perforation of the ileum (in typhoid), volvulus, torsion, ureteric and biliary colic can
also produce sudden abdominal pain.
Stereotypes of Pain Onset and Associated Pathology
Sudden onset (full pain in Rapid onset (initial Gradual onset (hours)
seconds) sensation to full pain
over minutes or hours)
Perforated ulcer Strangulated hernia Appendicitis
Mesenteric infarction Volvulus Strangulated hernia
Ruptured abdominal aortic Intussusception Chronic pancreatitis
aneurysm Acute pancreatitis Peptic ulcer disease
Ruptured ectopic pregnancy Biliary colic Inflammatory bowel disease
Ovarian torsion or ruptured Diverticulitis Mesenteric lymphadenitis
cyst Ureteral and renal colic Cystitis and urinary
Pulmonary embolism retention
Acute myocardial infarction Salpingitis and prostatitis
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4. Surgery
c) Shifting
The pain of early appendicitis is felt around the umbilicus as it is mediated by the
visceral peritoneum. However, as the organ becomes inflamed the pain shifts to the
right iliac fossa because the parietal peritoneum overlying the inflamed appendix
becomes involved.
d) Character of the pain
COLICKY pain is present when a hollow viscus is blocked therefore
(i) Intestinal pain can be colicky when there is intestinal obstruction.
(ii) When the common bile duct is blocked by a stone it also produces colicky
pain.
(iii) If the ureter or pelvic calyceal system is blocked by a stone, again there
will be colicky pain.
e) Aggravating and relieving factors –
When there is involvement of the parietal peritoneum as in appendicitis, cholecystitis
or general peritonitis any movement like walking, jolting can produce much pain.
Fatty foods can precipitate pain in cholecystitis.
Vomiting relieves the pain in peptic ulcer. In acute pancreatitis, just sitting up can
ameliorate pain.
f) Vomiting
Character of the vomitus
Projectile – Forceful ejection of large quantities of vomitus happens in obstruction of
the pylorus or the duodenum.
What does the vomitus contain?
Non-bilious vomiting indicates pyloric obstruction.
Bilious vomiting denotes obstruction beyond the sphincter of ODDI.
Blood in the vomitus is seen in duodenal ulcer, carcinoma stomach, Mallory Weiss
syndrome (longitudinal tear of the lower esophagus) or some systemic condition
such as uraemia.
Frequency
Vomiting is not a feature of a perforated peptic ulcer.
It is frequent in intestinal obstruction.
It is to be noted that pain comes first before vomiting in acute appendicitis, peptic
ulcer and in the colics.
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4. Surgery
g) Constipation / Diarrhoea
In intestinal obstruction there may be one passage of stool early in the course of the
disease; however there is absolute constipation later (Absolute constipation means
no passage of gas or stools).
In all intra abdominal emergencies there will be constipation except under the
following conditions –
a) Ileal appendix can sometimes produce irritation of the ileum and precipitate a
few stools.
b) A pelvic abscess or pelvic inflammation secondary to general peritonitis can
also produce irritation of the rectum and tenesmus.
Past History
In perforation of a peptic ulcer there may be a history of epigastric burning pain.
There may be past history of pain in ureteric or biliary colic.
A woman who has missed her period and has severe lower abdominal pain can
have a ruptured ectopic gestation.
Physical Examination
Inspection
(i) It is important to inspect all the hernial orifices.
(ii) Look for distension and locate where it is maximally present. In high
obstruction the distension is mainly in the upper abdomen; in large bowel
obstruction, the distension is also seen the flanks.
(iii) Look for visible peristalsis – in dynamic intestinal obstruction before
paralytic ileus sets in there is a step ladder pattern of peristalsis.
Still patient indicates peritonitis.

Writhing patient indicates colic or bowel obstruction.
Palpation
Tenderness over the abdomen and over which quadrant in particular, should be
noted.
When there is involvement of the parietal pleura, there is reflex contraction of the
abdominal muscles and on palpation the abdomen appears “tight”.
This involuntary tightening of muscles is rigidity, and is a sign of intra abdominal
inflammation.
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4. Surgery
Voluntary tightening of the muscles because of fear of pain is called guarding.

It is helpful to talk to the patient throughout the examination, which serves to relax
and distract him or her and thus allows more accurate findings. While palpating the
abdomen, the physician should carefully note the area of greatest tenderness,
judging either by indications of discomfort or the patient's subjective impression.
Unilateral abdominal wall muscle spasm is always involuntary.
Sign Finding Association
Cullen's sign Bluish periumbilical Retroperitoneal hemorrhage

discoloration (hemorrhagic pancreatitis,
abdominal aortic aneurysm
rupture)
Kehr's sign Severe left shoulder Splenic rupture

pain Ectopic pregnancy rupture
McBurney's Tenderness located Appendicitis

sign 2/7 distance from
anterior iliac spine to
umbilicus on right side
Murphy's sign Abrupt interruption of Acute cholecystitis

inspiration on palpation
of right upper quadrant
Iliopsoas sign Hyperextension of right Appendicitis

hip
causing abdominal pain
Obturator's Internal rotation of Appendicitis

sign flexed right hip causing
abdominal pain
Grey-Turner's Discoloration of the Retroperitoneal hemorrhage

sign flank (hemorrhagic pancreatitis,
abdominal aortic aneurysm
rupture)
Chandelier Manipulation of cervix Pelvic inflammatory disease

sign causes patient to lift
buttocks off table
Rovsing's sign Right lower quadrant Appendicitis

pain with palpation of
the left lower quadrant
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4. Surgery
Rebound tenderness
It can be elicited in the following way-
Very gently depress the abdominal wall with your hand and then suddenly remove it.
The patient will wince with pain. This again denotes involvement of the parietal
peritoneum, because of intra abdominal inflammation whether it is due to
appendicitis or strangulated bowel or peritonitis.
Auscultation –The abdomen should be auscultated prior to palpation, with close
attention paid to the presence and tone of bowel sounds. It is necessary to listen for
at least one minute over various parts of the abdomen before concluding that bowel
sounds are absent.
Increased bowel sounds indicate dynamic intestinal obstruction. Absence of bowel
sounds indicate paralytic ileus. Normal bowel sounds rule out general peritonitis.
Steps in physical examination for acute abdomen

(1) Inspection (6) Guarding or rigidity
(2) Palpation (7) Punch tenderness
One-finger examination Costal area
Rebound tenderness Costo-vertebral area
Deep
(7) Percussion (see under obliteration (8) Special signs
of liver dullness)
(4) Auscultation (9) External hernias and male genitalia
(5) Cough tenderness (10) Rectal and pelvic examination
Percussion
Obliteration of liver dullness
As you percuss on the mid-axillary and come down, normally there is a dullness
corresponding to the liver. This is obliterated in perforation of a peptic ulcer.
Rectal examination
It will be possible to elicit tenderness if there is pelvic appendicitis. If there is a
pelvic abscess, a bulge can be felt per rectum.
Vaginal examination
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4. Surgery
In a ruptured ectopic gestation, one can elicit tenderness on movement of the cervix.
Tenderness in both the fornices indicates salpingitis
Abdominal pain mimics
Lower lobe pneumonia may present with upper abdominal pain and it is important to
auscultate the chest in all cases of abdominal pain.
Important: Pleuritic pain can mimic upper abdominal pain
Tuberculosis of the spine with some involvement of the intercostals nerves will
produce referred adnominal pain.
Torsion of the testis or strangulated hernia can be missed if not routinely looked for.
Diabetic crisis and uraemia can also present with abdominal pain.
ASSESSMENT AND DIAGNOSIS

Referred Pain
 Fore gut pain (stomach, duodenal, gall bladder) is referred to the upper
abdomen
 Mid gut pain (small intestine, appendix, right colon is referred to the mid
abdomen
 Hind gut pain (mid transverse. Descending, sigmoid colon and rectum)
occurs in lower abdomen)
 Diseased retroperitoneal organs (kidney, pancreas) may present with
back pain
 Ureteric pain radiates to the testicle or labia
 Diaphragmatic irritation presents as shoulder tip pain.
Structure irritated Location of referred pain

Diaphragmatic Shoulder area (Kehr’s sign)
Ureteral Hypogastrium, groin, inner thigh
Cardiac pain Epigastrium, jaw, shoulder
Appendix Periumbilical via T 10 nerve
Duodenum Umbilical region via greater thoracic
splanchnic nerve
Hiatal hernia Epigastrium via T7 and T8 nerves
Pancreas or gallbladder Epigastrium
Gallbladder and bile duct Epigastric pain that wraps around to the
scapular region
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4. Surgery
Investigations
a) WBC – Total & differential counts – to look for leucocytosis
b) Serum Lipase and Serum Amylase (Normal 50-150 somogyi units) can be
raised to 400 or more.
c) Blood sugar and serum creatinine to rule out concomitant diabetes and
chronic renal failure.
Urine May show RBC and WBC if the inflamed appendix is in proximity to it.
RBC may also be seen in ureteric colic.
X-ray An X-ray should be taken with the patient sitting up.
Multiple fluid levels indicate intestinal obstruction. Gas under the diaphragm
indicates perforation of the duodenum, ileum or stomach.
In intussuception, a barium enema will outline the colon till it reaches a pincer
shaped filling defect.
Ultrasonography is excellent in evaluating the gallbladder and abdominal aorta and

for detecting pelvic pathology such as ectopic pregnancy or tubo-ovarian abscess.
Approach to a patient with acute abdomen
Look for danger signals
a) High pulse rate (above 100/min)

b) Very distended abdomen
c) Signs of guarding and rigidity
d) Absent bowel sounds or greatly increased bowel sounds
e) Yellow or feculent vomiting
f) Absolute constipation
g) Multiple fluid levels on X-ray
h) Severe hypogastric pain in a woman of child bearing age who has
missed a period.
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4. Surgery
If danger signals are present then refer to a surgeon.
WHO can be kept for observation?

A patient with none of the above danger signals
and
whose X-ray abdomen (erect)
and
ultrasound are normal
and
whose blood sugar, blood urea and serum amylase are normal.
Algorithm for acute abdominal pain
Acute Abdominal Pain
Colicky pain Non-Colicky pain
 Abdomen soft Abdomen distended No Guarding  Guarding +

 No Guarding ↑ bowel sounds No Rigidity Rigidity
 No Rigidity No Guarding No Distension present
 No distension No Rigidity Pulse normal  Pulse ↑
 Bowel sounds Blood sugar  Intra
 Normal normal abdominal
Blood urea normal inflammation
Secreting normal
Renal or Ureteric Uncomplicated Observe Refer

Colic bowel obstruction
Can treat at clinic Insert NG tube

start IV Refer
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4. Surgery
Duodenal ulcer perforation:

Usually (but not always) a male patient with past history of epigastric pain presents
with sudden onset of severe upper abdominal pain. Usually there is no history of
vomiting. The patient lies very still and resents any sudden movement. On
examination there is guarding and rigidity in the upper abdomen and on auscultation,
there are no bowel sounds. An X-ray taken in the erect posture will show gas under
the diaphragm. If the amount of gas is minimal, an X-ray taken in the left lateral
decubitus position will pick up free air in the peritoneal cavity. A Ryle’s tube should
be inserted and stomach contents emptied. Intravenous fluids should be started and
the patient referred quickly to a surgeon.
Renal / Ureteric Colic-

When a stone enters the pelviureteric junction and travels down, severe colicky pain
ensues. This is due to ureteric spasm.
The pain occurs in the age group 70-50 years of age and is more common among
men. The pain radiates from the loin to the groin and onto the testes or the labia.
The patient is in great agony. A few episodes of vomiting is common. Usually lasts
about 8-12 hours and the urine is often smoky due to microscopic haematuria.
Investigations in a patient with ureteric colic -
1) Urine – Micro will show microscopic haematuria
2) Plain X-ray abdomen will also show the stone as most stones are radio
opaque.
3) Ultrasound will also show a stone and pick up dilatation of the pelvicalyceal
system.
4) An IVP is not required unless planning for surgery.
Management of a patient with ureteric colic-
 The patient can be kept nil by month
 An intravenous line should be started and kept well hydrated.
 Inj. Diclofenac Sodium 75 mg IM followed by 50 mg thrice daily – orally
 Inj. Pethidine 100 mg IM or Inj. Morphine 15 mg IM may also be given.
Outcome
Most stones will pass spontaneously as they are less then 5 mm in diameter. If the
patient does pass the stone then it should be retrieved for analysis. In rare cases
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4. Surgery
the stone does not pass and causes obstructive hydronephrosis. This is an
indication for referral to a urologist. The following are the other indication for referral:
 If the patient has a single kidney
 If he also has diabetes
 If he develops high fever suggestive of infection.
Intestinal obstruction:
The four cardinal signs of intestinal obstruction are:
 Abdominal pain
 Vomiting
 Obstipation (no stools or gas)
 Distension
Once a diagnosis of intestinal obstruction is made it will be necessary to determine
three things:
a) Site of obstruction
b) Simple obstruction or gangrenous obstruction
c) The exact cause of obstruction
CLINICAL GUIDE TO SITE OR LEVELOF OBSTRUCTION
If vomiting and pain without distension

High obstruction such as in pyloric
Constipation – later
stenosis or pyloric tumour
If vomiting early with pain and later

Small bowel obstruction
constipation with central abdominal
distension
If constipation early, with pain but later

vomiting and distension of flanks as Large bowel obstruction
well as central abdomen
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4. Surgery
High Obstruction as in Pyloric or Duodenal

 Frequent vomiting
 Abdominal pain relieved by vomiting
 No distension
 Constipation late feature
 Plain X-ray erect – stomach bubble only in pyloric obstruction. “Double
bubble” in duodenal stenosis
 Visible gastric peristalsis from left to right
Small Bowel Obstruction

 Starts with vomiting
 Colicky central abdominal pain
 Central abdominal distension
 Constipation later
 Several small bowel fluid levels seen on X-ray (identified with valvulae
conniventes running across the full breadth of the loop)
 Step ladder pattern of visible peristalsis in the central abdomen
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4. Surgery
CAUSES OF SMALL BOWEL INTESTINAL OBSTRUCTION
Pyloric stenosis due

to duodenal ulcer
Carcinoma
Adhesions
External hernia
Round worm bolus
Meckel’s
diverticulum
with band
Tuberculous
stricture
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4. Surgery
Large Bowel Obstruction:-

 Constipation early
 Pain in lower abdomen
 Enormous distension
 Vomiting late feature
 Maximum number of fluid levels
b) Is this obstruction simple or gangrenous?
If there is gangrene then -
 The pain will be continuous rather than colicky
 There will be tachycardia and fever
 There will be rebound tenderness
 The haemoglobin would have dropped and WBC count will be very
high
 Blood urea will rise above normal
Presence of gangrene is an indication for immediate surgery.
Causes of obstruction
The following are the usual causes of obstruction –
Mechanical
 Pyloric obstruction - as a
I. Complication of duodenal ulcer
II. Pyloric “tumour” (Hypertrophic pyloric stenosis) in neonates
III. Pyloric malignancy
 External herniae – Inguinal and femoral
 Adhesions post operative
 Round worm obstruction
 Meckel’s diverticulum with band
 Tuberculous stricture – usually in Ileum
 Large bowel –
I. Carcinoma colon
II. Intussception
III. Volvulus of the sigmoid colon
Often the exact cause is only definitely known at surgery.
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4. Surgery
Non-mechanical causes
 Paralytic Ileus after surgery
 Peritonitis and followed by Ileus
 Drugs and hypokalemia can also cause Ileus
Management of intestinal obstruction

Simple non gangrenous obstruction should be treated conservatively to start
with.
a) Administer intravenous fluids using normal saline or Ringer’s lactate.
b) Insert NG tube and commence aspiration
c) Insert urethral catheter so that you can monitor hydration.
d) Relieve pain with narcotic analgesics
e) Monitor distension, pulse and aspiration amounts
Failure of conservative management at 48 hours (increasing distension) is an
indication for surgery. Obstruction due to adhesions and bands often settle with
conservative management.
(Additional readings on Acute abdominal pain are on pgs.162-169)
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4. Surgery
NECK SWELLINGS
Neck swellings are not uncommon in family practice.
1. Neck swellings occur in children more often than in adults.
2. Lymph nodes are the commonest cause of enlargement and
3. Infections are the commonest reason for the lymphadenopathy.
4. Viral and bacterial infections including tuberculosis are the important
causative agents.
Causes of neck swellings
Swellings superficial to the deep fascia resemble swellings anywhere else in the
body. (Example- Lipoma, hemangioma, furuncle etc.). Other swellings peculiar to the
neck can be subdivided into:
 Swellings in the midline and
 Swellings that are laterally placed
Swellings in the midline include:
 Thyroglossal cyst
 Sublingual dermoid cyst
 Plunging ranula
 Carcinoma of the larynx and trachea
 Pharyngeal Pouch
 Laryngocoele Uncommon and will not be discussed.
 Subhyoid Bursa
Swellings placed laterally in the neck include:
 Lymph node enlargement

 Thyroid swellings
 Salivary gland tumours
 Branchial Cysts
 Sternomastoid Tumour
 Cervical Rib
 Cystic Hygroma
 Tuberculous spinal Abscesses
 Carotid Artery Aneurysms
 Arteriovenous Fistula
Uncommon and will not be discussed.
 Carotid Body Tumour
 Actinomycosis
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4. Surgery
History taking:
History Significance
Age Think of infective and congenital causes in children

Think malignancy in the older age group
Tuberculosis and lymphoma in any age group
Neuroblastoma, lymphosarcoma, rhabdomyosarcoma,
and Hodgkin’s are the most frequent tumor types in
children under the age of 6 years.
Hodgkin and lymphosarcoma occur with almost equal
frequency in preadolescent children, followed by thyroid
malignancies and rhabdomyosarcoma.
Hodgkin’s disease is the most common malignancy in
adolescents.
Older age group (India); Squamous cell carcinoma
metastases from carcinoma nasopharynx/oral cavity or
larynx.
Has it been there from birth? Cystic hygroma, Sternomastoid tumor, congenital goiter
and ectopic thyroid
Multiple swellings favour a diagnosis of lymph node
How many swellings
pathology
Midline or lateral See table above for significance
Short history (less than 2-7 weeks) favors a diagnosis of
infection.
Duration of the swelling
Longer duration favors other causes including
tuberculosis.
Tenderness and fever less

Obviously this is in favour of an infection
than 7 weeks
Fever/loss of weight for longer

Tuberculosis/Lymphoma/Leukemia
than 7 weeks
Tuberculous node or a branchial fistula; if in the midline
Discharging sinus
a thyroglossal fistula
Symptoms of
cough/smoking/loss of Older age group: Think of a primary site that could have
weight/hoarseness of metastasized to the neck nodes
voice/dysphagia/dyspepsia
Has it been growing without
Think malignancy
pain?
Has it been growing with
Infection/abscess
associated pain?
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4. Surgery
A simplified method of diagnosis of a neck swelling in 7 easy steps:

 Was it present at birth or did it come on afterwards?
 Is it in the anterior triangle or the posterior triangle?
 If in the anterior triangle, is it in the midline, lateral or in the

submandibular region?
Neck swellings
Swellings
present at birth Swellings that
come on later
See list below
Posterior
Anterior triangle triangle
See list below
Laterally placed Midline

See list below See list below
Submandibular
region
See list below
Category
Swelling present at birth Swellings present later in life:
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4. Surgery
Diagnosis table
Possible nature of swelling Features
Swellings present at birth

Supraclavicular region:
 Cystic hygroma Diffuse
Fluctuant and transilluminant
 Sternomastoid tumor Firm swelling on the middle third of the sternomastoid
muscle; may be associated with distortion of the neck:
lateral flexion of the neck towards the side of the
swelling.
Swellings present later in life

Anterior triangle region:
 Congenital thyroid
swelling Iodine deficiency or dyshormogenetic goiter.
 Ectopic thyroid Both the goiter and the ectopic thyroid will move up
on deglutition
Posterior triangle region Likely to be tuberculous or malignant metastasis from
 Supraclavicular nodes the lung/stomach or the testis.
 Cystic hygroma Can appear later in infancy

 Swellings higher up in the Usually likely to be lymph nodes with an infective
posterior triangle including focus the scalp (lice)
the occipital region
 Bony hard swelling Cervical rib (incidental finding)

Anterior triangle region: Submandibular gland can be enlarged
Submandibular region- Because of a stone in the duct causing sialectasis or
can be a mixed tumor of the gland.
 Enlargement of the
submandibular gland Plunging ranula is a cystic swelling in the floor of the
 Plunging ranula mouth that can be seen in the submandibular region
Both the above can be felt bimanually with a finger in
the mouth.
Likely to be lymph nodes
 Enlargement not bimanually Dermoid cyst

palpable
 Cystic swelling freely mobile
Anterior triangle swellings:

Midline
 Thyroglossal cyst Moves up on protrusion of the tongue
 Tumor arising from the
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4. Surgery
larynx Older age group; typically a smoker and can be

malignant
Lateral placed anterior triangle Upper deep cervical nodes are the commonest cause
swellings: of swellings in both children and adults and the
causes are infective- viral, bacterial or Tuberculous.
 Lymph Node Enlargement
 Thyroid Swellings Thyroid swellings can be clinically diagnosed by the
 Branchial Cysts fact that they move up on deglutition.
 Cold Abscesses
 Carotid Artery Aneurysms Branchial cysts appear in adolescence and are
 Carotid Body Tumour placed at the junction of the upper third and the lower
two thirds of the sternomastoid muscle.
Cold abscesses are due to tuberculosis of the lymph

nodes or rarely the cervical spine.
Rarely pulsatile swellings occur in the neck in older

individuals and they may be either carotid body tumor
(transmitted pulsations) or aneurysm of the carotid
artery. Both of these occur under the cover of the
sternomastoid muscle.
Thyroglossal cyst
 May present as a painless small swelling (2cms.) anytime after birth.

 May get infected and present as an inflamed painful midline swelling and
 May present as a fistula in the midline that is discharging; this is the result of it
becoming an abscess.
The thyroglossal duct is the forerunner of the thyroid gland and it grows downwards
from the foramen caecum of the tongue. The
lower end becomes the thyroid gland and the
upper part atrophies. If a portion of this upper part
of the duct remains patent it can form a cyst - a
thyroglossal cyst. The cysts are usually found
anywhere between the isthmus of the thyroid
gland and the hyoid cartilage, or just above the
hyoid cartilage. They occur at any age but the
majority is seen in patients between 15 and 70
years of age. Ion ex
Note: Thyroglossal cysts are not present at birth. If a midline swelling is present at
birth in the line between the isthmus and the foramen cecum, it is likely to be an
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4. Surgery
ectopic undescended thyroid, rather than a thyroglossal cyst. If this needs to be

excised for cosmetic reasons or suspicion of malignancy, thyroxine replacement is
required.
Clinically the cyst can be diagnosed as follows:
 Moves up with deglutition like the thyroid

 Moves up with the protrusion of the tongue unlike a thyroid (because of
its attachment with the hyoid bone).
 Moves from side to side but not up and down.
 Is usually fluctuant.
The treatment of the thyroglossal cyst is surgical and the operation is called
Sistrunk’s operation where the mid portion of the hyoid bone is excised along with
the thyroglossal cyst to ensure non-recurrence.
Cervical lymphadenopathy
The four kinds of lymph-nodal enlargement are: Acute localized, Persisting localized,
Acute generalized, and Persisting generalized.
1) Acute localized lymphadenopathy: usually due to local infection from head or

neck (See table for drainage sites)
2) Persisting localized lymphadenopathy: usually due to tuberculosis and
malignancy from the drainage sites (See table for drainage sites) Secondary
tumour deposits from:
o Squamous carcinoma and melanoma of the skin of neck, face, scalp

and ear
o Squamous carcinoma of the mouth and tongue
o Squamous carcinoma of the nasopharynx, oropharynx, larynx and
paranasal sinuses
o Adenocystic carcinoma of the major or accessory salivary glands
o Papillary (and occasionally medullary) carcinomas of the thyroid
3) Generalized acute lymphadenopathy e.g. Infectious mononucleosis, secondary

syphilis and HIV. (Rubella, Cat scratch disease, Toxoplasmosis, CMV are rarer
causes.)
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4. Surgery
4) Generalized persisting lymphadenopathy- Lymphomata, leukemia
Table of drainage sites
Group of nodes Please examine

Submental nodes Infective or malignant lesions in chin, central part of lip,
gingiva, floor of mouth and tip of tongue
Submandibular nodes Infective or malignant lesions in palate, tongue, floor of

mouth, lower lip, cheek, gingiva, and maxillary antrum
Jugular chain nodes Infective or malignant lesions in tongue, mouth, pharynx,
(Deep cervical) larynx, upper esophagus and thyroid gland.
Tonsillar node Tonsils
Supraclavicular nodes Primary malignancy from lungs, breast, testis and arm
Superficial posterior Scalp infection
triangular and occipital
nodes
Post auricular and pre- Pinna and possible external otitis media
auricular nodes
Indirect laryngoscopy: No examination of a patient with lymph node swellings is

complete without an examination of the larynx and the pharynx. An indirect
laryngoscopy should be done on all such patients. The technique will be
demonstrated during the contact program.
Tuberculous lymphadenitis
Tuberculosis is the commonest cause of cervical lymphadenopathy next to reactive

hyperplasia. The pathology of Tuberculous adenitis can be divided into four stages:
Stages in Tuberculous lymphadenitis:

 Stage of adenitis and enlargement
 Stage of periadenitis and matting
 Stage of caseation and liquefaction
 Sinus formation and “collar stud” abscess.
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4. Surgery
Four stages in the pathology of TB adenitis
Clinical features in patients with cervical tuberculous

lymphadenopathy
 Typically a young patient (10-70 years)

 Neck swelling (Unilateral more common)
 Malaise
 Weight loss
 Fever
 Cough
 Discharging sinus
 Haemoptysis
Examination of cervical lymph nodes:
 Multiple matted nodes is the commonest presentation.
 Discrete nodes also occur very frequently.
 Multiple non-matted nodes also is a possible presentation.
 Cervical sinus and discharging abscesses is also seen though less frequently.
 Unilateral presentation is far more common than bilateral.
The most common group to be involved are:
 Upper deep cervical including Jugulo-digastric
 Lower deep cervical including Jugulo-omohyoid
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4. Surgery
 Submandibular
 Supraclavicular group of lymph nodes
Investigations warranted include:
 ESR which is usually raised
 Mantoux test which is more often positive
 Rarely an X-ray chest may show an active lesion or pleural effusion
 Fine needle aspiration cytology (FNAC) is a rapid, cheap, simple, and

effective method of diagnosis for cervical lymphadenopathy. This will be
described at the end of the module as an appendix. Your tutor believes that
all family practitioners should perform FNAC for a cheaper and a quicker
diagnosis. It can reduce the need for open biopsies. With practice the
majority of tuberculous adenitis cases can be picked up with this technique.
Treatment: Most of the patients can be managed with a six month daily
chemotherapy regimen. Surgery is rarely needed.
Reactive hyperplasia:
In our country we see a category of lymphadenitis that is called “reactive

hyperplasia”. When there is repeated infection say in the scalp and in the external
auditory canal etc. the lymph nodes undergo repeated enlargement and regression;
however after several episodes of these even when the infection is controlled the
nodes do not go back to its original size. This condition is called “reactive
hyperplasia and is very common among the families with poor hygiene.
When a child has many discrete nodes, has no other systemic symptoms, has a
normal growth pattern and the nodes are in the upper part of the posterior triangle or
involving the tonsillar node, then a course of antibiotic treatment may be offered. If
there is significant reduction in size of the nodes then no further treatment is offered
except follow up.
If the nodes continue to be the same or increase in size then a FNAC should be
done for diagnosis. Some surgeons always do an open biopsy of these nodes to be
sure that they are not missing tuberculosis. However, with this approach a very large
number of children will get unnecessarily biopsied every OP day.
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4. Surgery
Infectious mononucleosis or Glandular fever:
While there is no doubt that this occurs in India, the exact incidence is not known.
The infective agent is the Epstein Barr Virus (EBV) which has probably a part to play
in the etiology of Hodgkin’s.
The infection is spread by sputum through kissing and perhaps droplet infection. The
incubation period is about 4 weeks. The virus attacks the B cell lymphocytes and the
body responds by a proliferation of the T cell lymphocytes.
Clinical symptoms:
Sore throat, fever, malaise and anorexia are some constitutional symptoms. There
is lymphadenopathy especially of the cervical region. Other serious complications
can ensue- hepatitis, splenomegaly, pericarditis, encephalitis, hemolytic anemia and
petechial hemorrhages.
Laboratory diagnosis: One can suspect this infection if there is lymphocytosis (more
than 20%) and abnormal lymphocytes with large irregular nuclei.
Paul-Bunnel test is more specific but may be unavailable in smaller laboratories.
Treatment:
Bed rest and avoidance of alcohol is recommended.
Steroids may be given for serious complications like hepatitis and pericarditis etc.
Ampicillin should be avoided as it can precipitate a rash.
It is a self limiting condition.
Thyroid swelling
This is a major subject and the objective of our module will be to define the two
important areas that concern the family practitioner and leave the rest to the
specialist.
These two areas are:
 Primary thyrotoxicosis or Graves’ disease and
 Hashimoto’s thyroiditis causing myxedema(Covered in the module on
edema).
Once the swelling moves up on deglutition, it is a thyroid swelling and more specific
history questions and physical examination is indicated.
The history questions can be classified as follows:
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4. Surgery
1) General questions
2) Questions relating to thyrotoxicosis (thyroid hyper function)
3) Questions relating to thyroid deficiency
4) Questions relating to pressure effects and possible metastasis
General questions:
Age:
Young women tend to have iodine deficiency goiters and primary thyrotoxicosis.
Hashimoto’s thyroiditis occur in middle aged women
Papillary carcinoma occurs in the young, follicular in the 20-40 age group and
anaplastic in the older age group.
Pain:
Most of the time thyroid conditions are painless but acute thyroiditis and sub acute
thyroiditis can be painful. Both of the above are rare conditions. Bleeding into an
adenoma or into a goitrous nodule can produce pain.
Duration:
Often goiters are present for decades; some dyshormogenetic goiters (due to faulty
metabolism) are present from a very young age. Papillary and follicular
malignancies can be present for a few years before they begin to metastasize.
Anaplastic malignancy has a shorter history.
Questions relating to thyrotoxicosis:

Loss of weight inspite of an increased appetite
Excessive sweating
Intolerance to heat
Anxiety, insomnia, irritability, palpitations and fine tremor of the hand.
Menstrual changes –amenorrhea
Questions regarding thyroid deficiency:

Loss of appetite and increase in weight
Intolerance to cold
Dryness of skin, loss of hair including the eyebrows
Fatigue, somnolescence, constipation and oligomenorrhea/
Change in voice (hoarseness)
Questions regarding pressure effects :

Hoarseness of voice due to involvement of the recurrent laryngeal nerve
Very rarely a huge enlargement of the thyroid can produce some dysphagia and
some discomfort in breathing.
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4. Surgery
Any bone pain or any new swellings in the neck (asking for metastasis)
Tips for clinical examination of the thyroid:

This should be done standing behind the patient and palpating the thyroid gland
with both hands. After confirming that it moves up on deglutition, tenderness, size
and consistency is noted. Hard areas are often cystic and soft areas are often
solid. Look for the following in the thyroid gland:
 Is it enlarged on one or both sides?
 Is there one nodule or many?
 If the whole gland is enlarged, is there one big nodule?
 Is it tender?
 Palpate for the cervical nodes.
 Does the thyroid feel fixed to the trachea?
Causes of thyroid enlargement: Classification

 Nontoxic enlargement: (euthyroid or hypothyroid)
o Diffuse enlargement- Colloid goiter
o Multinodular goiter- Often this is iodine deficiency
o Single nodular goiter- This can be a solitary nodule of a multi-nodular
goiter or a benign tumor or a malignant tumor. With the help of
FNAC, Ultrasound scan (cysts are less likely to be malignant) and
by radioactive scans (a cold nodule that does not take up
radioiodine is more likely to be malignant) a tentative diagnosis
can be made. Refer this category.
o If signs of myxedema are present, the thyroid swelling is likely to be
Hashimoto’s thyroiditis.
 Toxic goiters- (Hyperthyroidism)
o If the thyroid swelling is uniform, patient a young woman, has pretibial
edema and has eye signs then the diagnosis is likely to be
Graves’s disease.
o If the thyroid swelling is nodular and not uniform or if there is a single
nodule then medical treatment is unlikely to help and the patient
should be referred to a surgeon.
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Which category can you handle?
Swelling thyroid
Look for signs of toxicity
Toxicity present Toxicity absent

Smooth uniform swelling? If no, Single nodule or multiple?
Single nodule or multiple? Painful or painless?
Single adenoma Multi-nodular

Uniform enlargement Not uniform enlargement (Toxic If painful think of acute or sub
Can be benign or malignant Can be iodine deficiency or
Usually a young woman: single or multi-nodular goiter) acute thyroiditis.
FNAC/Ultrasound malignant. (FNAC/ scan)
Graves’s disease Refer to surgeon (Can treat with analgesics)
Refer to surgeon Refer
This category belongs to the

family practitioner!
Choose mode of treatment
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Thyrotoxicosis
Primary-
Graves’ disease is the most common cause of hyperthyroidism and is an

autoimmune disorder. The IgG antibodies stimulate the TSH receptors evoking
increased thyroid production. Eye signs are unique to Graves’s disease and do
not occur in secondary hyperthyroidism.
Secondary-
When hyperthyroid state complicates an adenoma or a multi-nodular goiter then

the label “secondary” applies. This occurs in older women.
The clinical features to look for in all hyperthyroid states are:
 Tachycardia
 Diaphoresis (often profuse)
 Warm, moist skin
 Widened pulse pressure
 Congestive heart failure (may be a high output failure)
 Thyroid enlargement
o Nontender, diffuse enlargement in Graves disease (Primary

thyrotoxicosis)
o Tender, diffusely enlarged gland in thyroiditis
o Thyroid nodules, either single or multinodular goiter
 Eye signs: (Unique to Graves’s disease)
 Exophthalmos (When the white of the sclera can be seen between the
limbus and the lower eyelid)
 When the upper eyelid is raised so that it is at the border of the limbus
or higher the condition is called “lid lag.”
 Chemosis or congestion of the conjuctiva
 Ophthalmoplegia, so that there is diplopia
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 Atrial fibrillation
o Typically in elderly patients
o May be refractory to digitalis
o Converts after antithyroid therapy in 20-50% of patients
 Myopathy
 Thyroid bruit - Relatively specific for thyrotoxicosis
 Fine, resting tremor
Investigations:
 Perform Thyroid function studies to confirm the diagnosis.
o Elevation of free T4 and low to undetectable TSH levels are

diagnostic of thyrotoxicosis.
o Excessive TSH levels in the setting of elevated free T4 indicate

hyperthyroidism of pituitary origin.
 Hyperglycemia (may be found)
 Hypokalemia (in thyrotoxic periodic paralysis)
Management of primary thyrotoxicosis-
Three modalities of treatment available include antithyroid drugs, radio-active

Iodine and surgery.
Each of the three has advantages and disadvantages.
 Those patients with primary hyperthyroidism (Graves’ disease) who are

unfit for surgery or who may be economically unable to afford surgery, are
good candidates for the medical anti-thyroid drug therapy. Secondary
hyperthyroidism due to a toxic nodule or toxic multi-nodular goiter is not an
indication for anti-thyroid drug treatment as the results are poor. The
recurrence rate of thyrotoxicosis after medical treatment is about 50%.
 Surgery has a very good success rate but the surgery is fraught with some
complications like injury to the recurrent nerve and parathyroid glands;
thyroid storm can occur during the surgery. Depending on how much
88
thyroid has been left behind, hypothyroidism or recurrent thyrotoxicosis is
a likely postoperative complication. Surgery is the best option for
secondary hyperthyroidism due to a toxic nodule or a toxic multi-nodular
goiter.
 Radioactive is a very efficient method of treatment but is a contraindication
in young women in their reproductive age group and in those who are
lactating. Too little radio-iodine will allow some persistence of toxic
symptoms needing anti-thyroid drugs; too much will result in long term
hypothyroidism requiring replacement therapy.
As a family practitioner, you should be able to choose the modality of treatment

for your patients and initiate medical management if that has been the decision.
Medical management:
Symptomatic treatment:
The adrenergic symptoms that can be so distressing for the patient can be
rapidly controlled by the use of Propranolol. The dose is 40-80 mgm/day in
three divided doses. Asthma is a contraindication but can be used with care in
congestive failure.
Specific treatment:
Carbimazole and Propylthiouracil are the two common drugs used as anti-thyroid
agents. They prevent hormone synthesis by inhibiting both the organification of
iodine to tyrosine residues and the coupling of iodotyrosines. These drug must be
given orally. Propylthiouracil has the added benefit of inhibiting peripheral
conversion of T4 to T7.
Methylcellulose eye drops will aid in lubrication and comfort when the eye
symptoms of Graves’ disease are significant. Tape the eyelids shut during sleep,
to prevent exposure keratitis.
The details of anti-thyroid treatment are given in the table on the following page:
89
o Carbimazole is a commonly used drug and give it for a start in the dosage of
20-40 mg/day in 2-4 divided doses for a period of 4-6 weeks.
o Monitor Thyroid function (T4 and T7: TSH takes a long time to come down
and so is not useful) and usually in about 4 week’s time it (T4 and T7)
tends to come down; as the TFT returns to normal levels, the drug dosage
is correspondingly reduced.
o When the patient feels euthyroid, stop the beta-blockers, which are
symptomatic relief agents.
o Review again after 8-12 weeks and if the T4 and T7 has come down further,
reduce the dose of carbimazole again; repeat this titration of the drug till
you can reduce the dosage to 5 mgm/day.
o Continue dosage of 5mgm/day for at least 6 months but preferably for 18
months.
o Discontinue Carbimazole when the patient has been euthyroid for several
months.
o Rash, nausea, vomiting, and agranulocytosis are some side effects.
o Monitor the white cell count every month for 4 months to pick up
agranulocytosis. This complication is rare (one in 1000) and occurs usually
in the first 7 months.
o Propylthiouracil is the drug of choice for anti-thyroid therapy in pregnancy
and the dosage in mild to moderate thyrotoxicosis is 150-450 mg/day
Lymphomas
These are proliferations of lymphoid system and can occur either in the lymph
nodes or in organs containing lymphoid tissue. There are two broad categories:
o Hodgkin’s lymphoma and
o Non-Hodgkin’s lymphoma (More common)
The role of the family physician is to accurately diagnose, counsel and refer
these patients.
HODGKIN’S LYMPHOMA
This disease is characterized histo-pathologically by the presence of Reed-

Sternberg cells (with mirror image nuclei).
Etiology
Not fully known but previous infection with EBV (Epstein Barr virus causing
infectious mononucleosis) may have a role.
90
More common in men and has two peaks of
incidence; once in early adult life and another at
45-75 years of age.
Clinical features:
Most common presentation is with enlarged

painless nodes in the cervical region (50%),
mediastinal (25%), axillary nodes (18%), inguinal
(16%), abdominal (9%). The consistency is
rubbery.
The spleen and the liver may also be enlarged. Sites of nodal enlargement in
Hodgkin's
Constitutional symptoms include fever (25%), drenching night sweats, and weight
loss of more than 10% of body weight. Other less common include pruritus,
fatigue, anorexia and alcohol induced pain at the lymph node sites.
Investigations recommended:
 Blood counts- May find anemia, lymphopenia and eosinophilia.

 ESR is an indicator of disease activity.
 Liver function may be deranged especially if the liver is involved.
 Uric acid is raised
 Chest X-ray may show mediastinal widening.
 CT scans are used for staging of the disease and
 Lymph node biopsy is necessary for confirmation of diagnosis and for a
pathological classification.
 Bone marrow biopsy and liver biopsy may be needed in advanced cases.
Pathological classification Histopathology- Prognosis

Predominant cell
Types type
1. Lymphocyte Small lymphocytes Very Good
predominant
2. Nodular sclerosis Nodular bands present Good
3. Mixed cellularity Lymphocytes, Eosinophils, Fair

Neutrophils and Histiocytes
4. Lymphocyte depleted Few cells; plenty of Reed- Poor
Steinberg giant cells
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Management is based on the clinical staging: the Ann Arbor classification.
Staging Description
I Involvement of a single lymph node region (I) or extra nodal
site (E)
II Involvement of two or more lymph node sites (II) or an extra

nodal site +lymph node site, on the same side of the
diaphragm (IIE).
III
Involvement of lymph node regions on both sides of the

diaphragm (III), which may also be accompanied by
involvement of the spleen (IIIS) or by localized involvement of
one extra nodal site (IIIE) or both (IIISE)
IV Diffuse involvement of one or more extra nodal organs or

tissues with or without associated lymph-node involvement.
All the above get
designated as B if they  If there is fever more than 78 degrees C,
have these symptoms  drenching night sweats,
for example: I B, II B  unexplained loss of weight of more than 10% of body
etc. If they do not have weight within the last 6 months.
these symptoms the
designation is A-
(IA,IIA)
Management: Radiotherapy
o Radiotherapy is indicated for stages IA and IIA.

o Also given for pressure symptoms
o Another indication is for debulking a tumor.
Management: Chemotherapy
o Indicated for all B symptoms

o Stage II disease when there are three sites involved
o Stage III and IV
Chemotherapy is usually given with ABVD or the older MOPP and MVPP
regimens.
ABVD: Adriamycin, Bleomycin, Vinblastine, Dacarbazine. (This last regime

carries no risk of acute leukemia later). This is presently the “gold standard” in
treatment. A total of 6-8 cycles; given each month blood counts permitting.
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MOPP: Mustine, Oncovin (Vincristine), Procarbazine, and Prednisolone.
MVPP: Mustine, Vinblastine, Procarbazine, Prednisolone
ChlVPP: Chlorambucil, Vinblastine, Procarbazine, Prednisolone
All can cause myelo-toxicity and so monitor blood counts.
Note: The reason for including this information about management of Hodgkin’s
is to help you counsel your patient intelligently before referral.
Prognostic indicators
 Mediastinal mass greater than a third of the chest

 More than 40 years of age and male sex
 B Symptoms and increased ESR
 More than 2-4 nodal sites
 Extra nodal disease
 Histology: Lymphocyte depletion and mixed cellularity.
Non-Hodgkin’s Lymphoma (NHL)
There is malignant monoclonal proliferation of lymphoid cells majority of which

are B-cells (90%) and the rest are T cells.
Clinical features:
Lymphadenopathy is the main form of presentation.

Extra-nodal disease is more common than in Hodgkin’s and the following sites
can get involved:
 Gastro-intestinal tract including the liver and the spleen
 Testis
 Lung and the mediastinum with superior vena cava obstruction
 Brain
 Thyroid and the Skin.
 Naso-pharyngeal region
Bone marrow involvement is frequent and can lead onto anemia and leucopenia.
Mesenteric nodes get involved more commonly than in Hodgkin’s and infection is
common.
“B” symptoms are more common than in Hodgkin’s.
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Investigations:
 Blood counts should be done, as there can be anemia, leucopenia and
thrombocytopenia.
 ESR will be elevated.
 Serum creatinine as the ureter could get involved.
 Uric acid is often elevated.
 Liver function to evaluate its involvement
 Ultrasound to evaluate the nodes in the abdomen; also to see the liver and
the spleen.
 X-ray chest to see the mediastinum.
 Bone-marrow should be done to see if it is affected.
 Immunoglobulins are reduced.
 HIV test should be done.
 Lymph node biopsy should be done to get a good histo-pathological
picture.
STAGE DESCRIPTION OF INVOLVEMENT

I Single lymph node region or a single extra nodal organ or
site
II 2 or more nodal sites on the same side of the diaphragm
III Nodal sites on both sides of the diaphragm
IV Diffuse involvement of one or more extra-lymphatic
organs
“B” if:  There is fever more than 78 degrees C,
 Drenching night sweats,
 Unexplained loss of weight of more than 10% of
body weight within the last 6 months.
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Management:
Radiotherapy is used for stage I and II A and for de-bulking the tumor.
Chemotherapy is used for IIB, III and IV. Single drug therapy is used and
Chlorambucil is the drug of choice (20mg/sq.metres/day). Once response has
been achieved, drug therapy can be discontinued for a number of years.
In high grade lymphomas CHOP regime is used (Cyclophosphamide, adriamycin,
vincristine and prednisolone).
Clinical differences between Hodgkin’s and Non-Hodgkin’s Lymphoma
Hodgkin’s Non-Hodgkin’s
Cell of origin unclear B-cell proliferation (90%),T-cell(10%)
More likely to be localized Less likely
Spreads by contiguity Non-contiguous spread
Mesenteric nodes affected less often Commonly
Extra-nodal lesions less common Common
Bone-marrow involved rarely Common
Remission rate 75% Less than 70-40%
(Additional readings on Neck swellings are on pgs.170-174)
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MANAGEMENT OF CHRONIC LEG ULCERS
(See Additional readings on this topic for more details - pgs.175-181)
SPECIFIC CONDITIONS
1. Venous Leg Ulceration
Incompetent valves can produce venous hypertension in the lower limbs.
Chronic venous leg ulceration is defined as an area of discontinuity of the
epidermis, persisting for four weeks or more, as a result of venous
hypertension.
 It accounts for about 70% of lower limb ulceration.
 Incompetent venous valves result in an increase in capillary
pressure with subsequent stasis or pooling of blood, capillary
damage, fibrosis, and a poorly nourished skin which is easily
damaged.
 Ulcers are usually found within the “gaiter” region of the lower limb
i.e. below the bulge of the gastrocnemius and above the malleoli of
the ankle.
The Gaiter Area (Below the calf bulge and above the malleolus)
 Ulcers are shallow with ragged, irregular bluish edges.

 There is often pigmentation of the surrounding skin, with hardening
which is called lipodermatosclerosis.
 Ankle-brachial pressure index (ABPI), as determined by Doppler
ultrasound is in excess of 0.8 in venous ulcers. (ABPI is the ratio of
systolic pressure at the ankle to that in the arm. Generally, the
higher of the recordings of pressure in the dorsalis pedis /posterior
tibial arteries serves as numerator with the higher systolic pressure
96
between the brachials serving as denominator. The resting ABPI
is about 1; values below 0.8 indicate some degree of associated
arterial obstruction. A value of less than 0.7 suggests imminent
necrosis. Values between 0.5 -0.8 suggests a combination of
arterial and venous disease.)
The figure below shows the technique for measuring the ABPI. (The cuff is tied to
the calf and the systolic pressure in the dorsalis pedis is noted. Where access to
Doppler facility is difficult, manual palpation of the systolic pressures should be
tried as that also can give a rough estimate of the ABPI.)
Measuring ABPI
using Doppler
(use manual
method if Doppler
unavailable)
Other features are venous flare (dilatation of superficial venules), telangiectasia

(dilated and tortuous vessels) and atrophie blanche (It occurs when capillaries
are destroyed and looks like a white patch on the skin resembling a scar. An
ulcer in this area is extremely painful.)
Malignant transformation can occur in long standing venous ulcers. These ulcers
are called “Marjolin’s ulcer” and most often they are squamous cell carcinoma on
histopathology. Any change in the nature of ulcers that fail to heal should evoke a
suspicion of malignant transformation.
97
Treatment
Graduated compression bandaging, properly applied, and combined with
exercise, is the treatment of choice in venous ulceration.
MANAGEMENT OF VENOUS ULCERS COMPRISES OF THE FOLLOWING
STEPS
Compression bandaging
Ulcer care
Ulcer dressings
Treatment of infection
Pain relief
Treatment of venous eczema/dermatitis
Other measures to accelerate wound healing
Surgical interventions
Compression Bandaging
 High compression bandages have a higher healing rate than low
compression bandages.
 Padding to protect bony prominences is recommended under high
compression bandage systems.
98
 Arterial insufficiency is a contra-indication to the use of compression
except in a modified form under specialist supervision.
 Congestive cardiac failure is also a contraindication as it increases the
venous return to the heart and can aggravate the failure.
ACTION RATIONALE
Compression
Venous ulceration should be treated with Aids venous return and reduces venous
high compression bandaging to achieve a hypertension.
pressure between 70-40mmHg at ankle
graduating to half at calf in a normal
shaped limb.
Arterial insufficiency (<0.8) is usually a Compression on an arterially compromised
contra-indication to high compression limb may lead to ischemia.
except under specialist supervision.
Protect bony prominences with cotton To prevent pressure necrosis
padding.
Use compression with caution in diabetic These patients are more susceptible to
patients and those with connective tissue small vessel disease.
disease.
Bandaging Technique for Venous Ulceration
Guide to a Good Bandaging Technique

 Psychological Preparation: Patients must be committed to receiving
treatment and understand the significance of compression as the central
treatment modality.
 Elastic bandages are preferred. (Non-elastic material will initially
provide high pressure; however with a slight reduction of oedema, this
pressure will decrease significantly. On the other hand elastic material will
maintain its compression for a much longer period.) It is important to
maintain sufficient pressure for sufficient time.
 Each turn of the bandage should be of equal tension (50% extension).
 The ankle circumference measurement will determine the need for any
modification of the bandaging technique. (The pressure generated by any
bandage is determined principally by the tension in the fabric, the number
of layers applied and the degree of curvature of the limb. The relationship
between these factors is governed by Laplace’s law, which states that the
applied pressure is directly proportional to the tension in the bandage but
99
inversely proportional to the radius of the curvature of the limb to which it
is applied. The natural cone shape of the lower limb is therefore a major
factor in achieving a correct pressure gradient. Where the patient’s ankle
circumference or limb shape is outside the normal range, modifications
can be made to the system to achieve adequate sub-bandage pressures.
Thin limbs with a circumference of less than 18cm require additional
padding to increase protection and artificially increase the circumference
of the limb.
 Only use bandages of 10cm width.
 Protect all bony prominences and areas of at risk of high pressure (foot,
ankle, Achilles tendon, tibial crest) with padding with cotton or orthopedic
wool. Due to the increased skin sensitivity in venous disease, the padding
layer should cover all vulnerable areas and just be visible at the toes and
top of the bandage.
 Bandaging should be done in the morning, before the patient becomes
ambulant and when the edema has decreased (Elevation of the limb to
empty the veins prior to bandaging may be advised), and bandage should
be removed only after the patient is in bed.
 On the foot, begin extension from base of toes with 2 anchoring turns at
50% extension.
 On the angle apply figure of 8 using a high and then low turn to avoid
excess layers over dorsum of foot.
 On the limb, apply in a figure of 8 or spiral with 50% extension and 50%
overlap. Bandaging should extend over the upper portion of the
gastrocnemius muscle to prevent slippage.
 As rapid loss of edema may occur in the first few weeks of treatment, thus
reducing the ankle circumference, the patient should be reviewed regularly
and be advised to return if pain or edema increases.
Note: Incorrect bandaging technique may be harmful.
Studies have proved beyond doubt that the careful design of original Charring
Cross four – layer bandaging system is much more effective in the treatment of
100
venous ulcers. Its high cost limited availability restricts its usage in India. For
those who can afford to purchase it, the four-layer bandaging kit (Profore R
Regular, System 4) should he recommended. It is available as a kit with four
separate bandages.
The 1st layer made of orthopedic wool which is used to absorb exudates and
redistribute pressure around the ankle is applied in a loose spiral.
The 2nd layer is a crepe bandage which increases absorbency and smoothes the
orthopedic wool layer and is applied in a spiral.
The 7rd layer is a light compression bandage applied in a figure of 8 with 50%
extension and overlap.
The 4th layer is an elastic cohesive bandage which maintains the 4 layers in
place and is applied using 50% extension 50% overlap spiral technique.
Ulcer Care
An effective skin care policy is important to protect the surrounding skin.
ACTION RATIONALE
Cleansing Therapeutic for patient and removes debris
Immerse or irrigate with warm tap water, from the wound.
avoiding antiseptics. Antiseptics are unnecessary and may
An emollient (oil, Liquid paraffin) may be delay wound healing.
added to the water. Moisturizes the surrounding skin.
Care of surrounding skin To prevent dryness, scaling and eczema.
Moisturize with emollient( white petroleum Scales act as a focus for infection and can
jelly i.e. Vaseline) cause pressure necrosis under
Remove scale by soaking, moisturizing compression bandaging.
and/ or mechanical removal. Protects surrounding skin from exudates.
Barrier products such as Zinc oxide cream

may be necessary.
Debridement (removal of slough and dead Presence of necrotic tissue may delay
tissue) healing and encourage bacterial growth.
101
Ulcer Dressings
Note: No specific dressing has been shown to improve healing rates in venous
ulcers.
ACTION RATIONALE
Dressings – Type and Technique Most chronic wounds are colonized
A clean technique is enough. Can use therefore an aseptic technique is
warm tap water to wash the wound unnecessary.
instead of normal saline and can dry it
with a clean cloth rather than sterilized
cotton.
A ‘simple’ non-adherent permeable Removal of an adherent dressing
dressing (Vaseline gauze) is damages healing tissue.
recommended.
Exudative wounds may require a more Impermeable dressings allow
absorbent dressing. accumulation of exudates which may
macerate skin.
Dressings may be left in place for one Frequent dressing change may delay
week if not soaked or dirty. wound healing.
Treatment of Infection
Important:
 Systemic antibiotics should be used to treat clinical infection.
 Topical antibiotics and antibacterial agents are frequent sensitizers
to the skin and should be avoided.
102
ACTION RATIONALE
Routine swabbing of ulcers for Culture To assist in the identification of the
& Sensitivity (C & S) is unnecessary infecting organism and selection of the
most appropriate antibiotic based on
A wound swab should be taken for the laboratory tests. Gram staining
gram staining and culture and helps to correlate the results of C & S
sensitivity if clinical signs of infection tests.
are present.
Systemic antibiotics should be Infection may delay the healing
prescribed when the clinical signs of process. Topical antibiotics should not
infection are present. be used as they lack efficacy,
Treatment of cellulitis may require a encourage resistance, and may cause
prolonged course of high dose contact allergy.
antibiotics.
Note: Cephalexin can be used as the first line of treatment till C&S results are
available. In rural areas Septran can be given as a first drug.
Additional points:
 The presence of bacteria in a leg ulcer does not mean that it is infected as
all chronic ulcers can be colonized by micro-organisms which are not
producing any inflammatory reaction.
 A diagnosis of infection should therefore be made on clinical evidence,
e.g. cellulitis.
 Odour or increased exudates does not necessarily indicate infection and
can be managed with selective dressings.
 Treatment of cellulitis may require a prolonged course of high-dose
antibiotics.
103
Pain relief: Pain may be a feature of venous ulcers and should be relieved. Pain
is a feature of approximately 60% of all venous ulcers. Increased pain levels or
new episodes of pain may indicate infection.
ACTION RATIONALE
Assess site, frequency and level of To relieve distress and aid compliance
pain and treat appropriately. with treatment.
Treatment of Venous Eczema/ Dermatitis

Venous eczema presents as an itchy, inflammatory condition of the skin
characterized by erythema, weeping and scaling usually in the gaiter area with or
without ulceration. It is discussed here since it can precede or coexist with
ulceration.
 Graduated compression is the main treatment for venous eczema.
 A high percentage of patients with venous disease display contact allergy
to topical applications especially to topical antiseptics and topical
antibiotics.
 Patients with contact allergy should be referred for patch testing. Patch
testing is a non-invasive procedure where patches of probable allergens
are placed on an area of the patient’s body, preferably the back, and the
response is evaluated.
ACTION RATIONALE
Emollients or barrier preparations are used Soothing to patient and alleviates
for mild eczema dryness and irritation.
Ointments are generally preferable to Ointments are better for a chronic dry
creams. eczema and are less sensitizing than
creams.
Mild to moderate topical steroids such as Anti-inflammatory effect.
fluticasone or betamethasone are used in
more severe cases or unresponsive
eczema. Avoid using very potent steroids
such as clobetasol.
104
Other measures to accelerate wound healing
Elevation, Exercise, and Mobility
 Progressive loss of ankle joint movement can accompany venous
ulceration.
 Good calf muscle pump function is an important aspect of ulcer healing.
 Walking and passive ankle exercises should be encouraged.
 When resting, elevation of the limb above chest level is beneficial.
ACTION RATIONALE
Encourage mobility. Improves venous return by activating
calf muscle pump and avoids stiffening
of joints.
Elevate limbs. Aids venous return and reduces
edema.
Avoid long periods of standing and Standing increases venous
encourage limb elevation while resting. hypertension.
Surgical Intervention
 Skin grafting-
 indicated for ulcers that fail to heal within 12 months.
 May be indicated earlier for large ulcers.
 Vein surgery- superficial vein surgery (such as vein stripping or ligation
of perforators), has been shown to be effective only if the deep venous
system is competent.
Note: Patients with venous ulceration should have the opportunity for
assessment of deep venous competency by Duplex Ultrasound to determine
suitability for superficial venous surgery.
105
PREVENTION OF VENOUS ULCERATION
Primary Prevention
 DVT is a common cause of venous disease. The use of compression

hosiery (Class II) worn peri-operatively and during pregnancy may reduce
the incidence.
 For people predisposed to venous ulceration and or engaged in work
which demands standing for long periods, advise walking / sitting in
between regular periods.
 People with varicose vein with oedema of the limb should be advised to
use compression stockings (Class II) when they are ambulant.
 Advise lower limb elevation while resting and while in bed.
Secondary Prevention of Ulcer Recurrence
 Chronic venous leg ulcers almost always recur unless preventative

measures are maintained.
 Graduated compression hosiery is the single most effective intervention in
preventing leg ulcer recurrence and should be prescribed for life.
Failure to comply leads to a great chance of recurrence (80% to 100%)
ACTION RATIONALE
Use suitable compression hosiery. To increase venous return and reduce
venous hypertension
Moisturize skin regularly with bland To help maintain integrity of the skin.
emollient.
Avoid prolonged standing. Standing increases venous
hypertension.
Weight reduction. Obesity reduces mobility and hinders
elevation of the legs.
106
REFERRAL FOR SPECIALIST ADVICE
Patients in the following categories may require referral:
 Peripheral vascular disease with an ABPI of less than 0.8.

 Uncontrolled diabetes mellitus.
 Severe unresponsive cellulitis.
 Diagnostic uncertainty with a suspicion of malignancy.
 Ulcer is part of autoimmune diseases such as Rheumatoid arthritis, SLE and
involving organs such as the kidney, lung, and heart.
 Eczema/dermatitis failing to respond to moderate potency topical steroid.
 Failure to improve at 12 weeks despite adequate compression bandaging or
failure to heal completely in 12 months.
 Suspicion of primary lymphedema i.e. Ulceration without evidence of chronic
venous insufficiency.
2. Arterial Leg Ulceration

Definition
Arterial ulcers are caused by insufficient blood supply to the lower limb, with
resultant tissue ischaemia and necrosis.
Causes
 Accounts for about 10% of leg ulcers.
 Risk factors include smoking, hypertension, hyperlipidemia, and
diabetes.
 There is usually underlying atherosclerosis or a vasculitis such as
Buerger’s disease. Buerger’s disease is most often seen in young men
who smoke. And it mainly affects the arteries that supply the feet while
atherosclerosis affects the larger vessels also.
Clinical Features
 There is often a history of intermittent claudication. This is a cramp-like
pain felt in the muscles that is
* brought on by walking
107
* not present on taking the first steps (contrast with osteoarthritis)
* is relieved by standing still (contrast with lumbar intervertebral disc
compression where pain is present on walking and is not relieved with rest)
The distance walked before the onset of pain is called the claudication
distance (a variable distance which is altered by walking up hill, against a
wind, the speed of walking or by changes in general health such as anemia or
heart failure). It is a clinical measure of the severity of arterial obstruction.
 Patient may complain of rest pain (a severe pain felt in the foot at rest,
made worse by lying down or elevation of the foot). Pain is worse at night
and interferes with sleep; it may be relieved by hanging the foot out of bed
or by sleeping in the chair. It suggests a high degree of arterial
obstruction.
 Skin is cold and atrophic and there may be loss of hair. In the presence of
ischaemia the limbs become blanched on elevation and develop a purple
discoloration on dependency (more visible in fair skinned individuals). The
angle of elevation at which blanching first occurs gives a rough guide to
the degree of ischemia.
 Pre-gangrene is a combination of rest pain, color changes, oedema and
hyperaesthesia, with or without ischemic ulceration.
 Peripheral pulses are feeble or absent. Where peripheral pulses are
apparently normal, exercising the patient to the point of claudication may
unmask the effect of an arterial obstruction by causing the previously
palpable pulse to disappear. After a minute or two the pulse reappears.
 Buerger’s Test: The legs of a normal individual, even if they be raised by
90 degree remain pink. In case of an ischaemic limb elevation to a lesser
degree will cause marked pallor.
 Ulcers have a punched out appearance, are often multiple and may
involve both feet, on the shins, and around the malleoli. They are often
extremely painful.
108
Relationship of clinical findings to site of disease
Aortoiliac Claudication in buttocks, thighs and calves. Femoral and
obstruction distal pulses absent in both limbs. Bruit over aorto-iliac
region. Impotence common
Iliac obstruction Unilateral claudication in thigh and calf and sometimes
buttock. Bruit over iliac region. Unilateral absence of
femoral and distal pulses
Femoro-popliteal Unilateral claudication in calf. Femoral pulse palpable with
obstruction absent unilateral distal pulses.
Obstruction Femoral and popliteal pulses palpable; dorsalis pedis and
beyond the posterior tibial not so.
popliteal
Only ankle pulses Claudication in calf and foot
absent
Management of Arterial Ulceration

Treatment of arterial ulcer is symptomatic.
 Advise stopping smoking immediately particularly for patients with
Buerger’s disease. If the patient keeps smoking, the disease will continue
to proceed and become more severe.
 Regular exercise within the limits of pain. Patients are worried by the
presence of pain on walking. They must be assured that walking is not
doing any harm. Spontaneous improvement occurs over few months as
collaterals develop.
 Diet control for reducing weight in the obese and in the treatment of
hyperlipidemia.
 Vasodilator drugs are found to be ineffective. Drugs such as
pentoxiphylline (Trental) help to some extent.
 Lumbar sympathectomy may be indicated in intractable cases. It may
relieve rest pain and ulceration.
 Systemic antibiotics must be given if there is cellulitis.
109
 Control of diabetes, hyperlipidemia and hypertension.
 Care of feet by keeping it warm and modified foot wear (Claudication
distance can be increased by raising the heels of shoes by 1 cm)
 Pain relief with analgesics and elevation of the head of the bed (Buerger’s
position).
 Compression bandaging should not be applied as severe damage to the
leg can result.
 All patients with arterial ulceration should be referred for a vascular
opinion. If ABPI is less than 0.5 this referral should be urgent.
 All patients with an ABPI less than 0.6 without active ulceration should
also be referred for a vascular opinion.
 If ulcers do not heal or if gangrene develops then amputation may be
necessary.
Local Ulcer Management

The general principles of wound management apply, with some specific
provisions.
ACTION RATIONALE
Dressing Technique
Use an aseptic technique. Patients with arterial ulcers are more
prone to infection.
Debridement
In dry necrotic wounds, debridement In a poorly vascularized foot, an open
should be used with caution. wound can become infected.
Infection
If organisms are isolated, treat with In a poorly vascularized limb, a higher
high dose antibiotics for at least two blood serum level of antibiotics is
weeks. If cellulitis present, intravenous needed for a longer period of time in
antibiotics should be used. order to eradicate the bacteria.
110
Observe wound more frequently. Deterioration can be rapid.
Oedema
In an edematous limb, do not Will effect tissue perfusion.
encourage elevation above level of
heart.
Pain
Control pain. To relieve distress.
Opiates may be necessary.
Mobility
Encourage walking. Walking will encourage development of
Encourage limb dependency if no collateral circulation.
oedema present. To aid perfusion of the limb.
Encourage patient to keep limb warm. Smoking reduces oxygen levels in
Advise to stop smoking. blood and destroys vitamin C.
Ensure shoes are good fit. To prevent damage to foot.
Note: About half of arterial ulcers have a previous venous component; the ulcers are of
mixed etiology.
Management of Mixed Ulcers
Arterial insufficiency is a contraindication to the use of compression except in a
modified form under specialist supervision.
In the presence of chronic venous insufficiency plus an abnormal ABPI of less
than 0.8, compression therapy may be appropriate but should be carried out
under specialist supervision.
Patients with diabetes have a higher risk of peripheral vascular disease and as a
result ABPI readings may be unreliable (greater than 1.2) due to arterial
calcification.
111
In the presence of diabetes or rheumatoid disease, compression bandaging may
be appropriately and safely carried out. However, in these circumstances
specialist advice should be sought before compression bandaging is used.
7. Diabetic ulcers
Clinical features
Diabetic foot examination

Deformity Charcot's, pes cavus, claw toes, hammer toes
Infection Crepitus, fluctuation, deep tenderness
Atrophic nails Also fungal infection/subungual ulcers
Breakdown of skin Ulcers, fissures, blisters
Edema Pitting oedema lower limbs
Temperature  Cold - ischaemic
 Hot - infection
Ischaemia Pulses may be weak/absent
Callosities Plantar surface, metatarsal heads
Skin color  Pale - ischaemia
 Pink with pain and absent pulses - ischaemia
 Diabetic ulcers precede 85% of non-traumatic amputation
Causes
 The etiology of diabetic foot ulcers is multifactorial. Majority of diabetic
ulcers are due to the clinical triad of
*peripheral sensory neuropathy
*trauma
*deformity
Other factors
 Ischemia
 Infection
 Callus formation resulting in focal areas of high pressure
 Edema
 Previous ulcer
 Obesity
 Autonomic neuropathy causing decreased sweating and dry, fissured skin.
 Limited joint mobility due to co-existing Charcot’s joints
 Poor glucose control leading to impaired wound healing
112
 Ill-fitting foot wear that causes skin breakdown or inadequate protection
from high pressure and shear forces.
 Poor vision which increases the likelihood for trauma and failure to detect
early lesions.
Pathophysiology
Fissures  Infection  Abscess  Ulcer

Shearing forces  Dermal callus  Dermal  Ulcer hematoma
 15% diabetics develop foot ulcers

 Diabetic ulcer is an example of neuropathic ulcer where there is
generalized sensory impairment and often a history of minor trauma
precedes the development of ulcer.
 4% diabetics have deep-seated ulcers
 Typically a diabetic ulcer is deep, painless and infected and has a
‘punched out’ appearance. These ulcers are known as ‘perforating
ulcers’ .Tissue surrounding the ulcer is well perfused and peripheral
pulses are often palpable.
 Ulcers decrease quality of life of the patient.
 74% below knee amputees are dead at the end of 2 years.
Sites predisposed to
ulceration in a
neuropathic/diabetic
foot.
Ulceration is particularly
likely to occur over the
dorsal portion of the
toes and on the plantar
aspect of the metatarsal
heads and the heel.
113
Investigations for a neuropathic ulcer
o Pus swabs for gram staining and C & S from deep within the
ulcer
o X-rays of the limb for detecting the presence of underlying
Osteomyelitis and or joint deformities due to Charcot joints.
o Blood tests –fasting blood sugar, TPHA (a specific test for
syphilis) or VDRL
o Skin smears of doubtful patches to rule out leprosy.
Limb threatening infections (Indications for referral)
 Cellulitis extending beyond 2 cm
 Deep ulcer
 Osteomyelitis
 Critical ischaemia (rest pain , gangrene)
Depth- Ischemia Classification for diabetic ulcer
To determine the depth of the ulcer, it should be probed with a blunt sterile
probe. This helps to detect sinus tract formation, undermining of ulcer
margins and dissection of the ulcer into tendon sheaths, bone or joints. A
positive probe to bone finding has a high predictive value for osteomyelitis.
Failure to diagnose underlying osteomyelitis often results in failure of wound
healing.
 0- At risk foot, no ulcer A- Not ischaemic

 1- Superficial ulcer B- Ischemia without
gangrene
 2- Deep ulcer exposing C- Forefoot gangrene
tendon, joints
 7- Extensive ulceration, D- Complete foot gangrene
abscess
114
Management of Diabetic/ Neuropathic ulcer
 The primary goal in the treatment of diabetic foot ulcers is to obtain
wound closure.
 Management of ulcer is largely determined by its severity and
vascularity and the presence of infection.
 Control of hyperglycemia is basic to the treatment of diabetic ulcers.
Treatment (according to depth)
 0- Patient education, proper footwear
 1- Offloading or decreasing pressure (TCC, special footwear), Antibiotics
 2- Debridement, Antibiotics, Offloading
 7- Debridement, Amputation, Offloading
Offloading devices such as total contact cast help to relieve pressure from
the pressure-bearing areas.
Treatment (according to ischemia)

 A- No treatment
 B- Non invasive vascular investigations
 C- Vascular consultation
 D- Major amputation, vascular consultation
Debridement
 Remove all necrotic and fibrous tissue
 Until bleeding from the wound occurs
 Lay open all tracks, sinuses
 Done in theatre
Dressing of wounds
 Saline dressings best
 Topical enzymes cannot replace debridement
 Topical antiseptics toxic to healing wounds
115
Antibiotics
 Based on C&S from deep within the wound
 Start on broad spectrum antibiotics
 In osteomyelitis, 4-6 weeks of culture directed antibiotic therapy, after
appropriate surgery
Prevention
A diabetic patient with a history of previous ulceration or amputation is at
increased risk for further ulceration, infection and subsequent amputation.
Alteration in foot dynamics due to ulceration, joint deformity or amputation can
cause the abnormal distribution of plantar pressures and result in formation of
new ulcers.
 Patient education- instruction on foot hygiene, daily inspection
 Proper foot wear ( with pressure-relieving insoles )
 Pick up early lesions
 Prompt treatment
Footwear
Preventive footwear with insole made of materials such as microcellular
rubber (MCR) has a cushioning effect as well as resilience and is an essential
element of ulcer prevention and have been associated with significant
reductions in their development. The commonly designed footwear is a
sandal with a backstrap (with no toe rings).
On the following page is a protocol or algorithm for leg ulcers based on

the chart devised by D.G. MacLellan for the Wound Foundation of
Australia.
116
HISTORY
Initiating factors, Medical history,
Family history, Drug history, Ulcer treatment
EXAMINATION INVESTIGATIONS
Peripheral pulses Ankle-brachial index (ABI)
Varicose veins or venous stigmata Full blood examination
Ulcer site, size and character Urea and electrolytes
Neurological examination of limbs Serum albumin and glucose
Signs of connective tissue disease Wound biopsy
DETERMINATION OF PROBABLE AETIOLOGY
Mixed
Venous Arterial Vasculitic
Venous duplex scan
Venous duplex Consult vascular Neuropathic
+
scan Surgeons Infective
Consult vascular
surgeon Neoplastic
MANAGEMENT
1 .Septic ulcer treatment (most would need)
Venous 2. Underlying aetiology

Superficial Valvular
incompetence Neoplastic
Graduated compression Arterial Treat according to lesion
Stockings Management directed towards
Bandages reperfusion
Infective
Surgery Debridement / antibiotics
Deep Valvular as indicated
incompetence
Graduated compression
Stockings Vasculitic
Bandages Control underlying condition
(physician input)
7. Medical management 4. Allied health management

Control diabetes, cardiac Podiatrist
failure etc., and Systemic Orthotist as
antibiotics for cellulitis Physiotherapist appropriate
Analgesia Nutritionist.
117
SWELLINGS IN THE GROIN REGION AND IN THE ABDOMINAL WALL
Causes
Conditions that produce swellings in the groin region and scrotum-
Differential diagnosis of a mass in the groin region:-

 Malgaigne’s bulges
 Hernia – femoral and inguinal
 Undescended testis – unilateral or bilateral
 Spermatic cord swellings (Encysted hydrocoele)
 Lymph nodes
 Post femoral artery puncture haematoma
 Subcutaneous neoplasm – e.g. Lipoma
 Psoas abscess (Tuberculous and pyogenic)
 Saphena Varix
Differential diagnosis of a mass in the scrotum:-

 Hydrocoele
 Haematocoele – Traumatic
 Cyst of the epididymus
 Chronic epididymo Orchitis – Tuberculous and filarial
 Varicocoele
 Carcinoma
 Testicular torsion
Groin swellings can be

(i) Inguinal (above the inguinal ligament)
(ii) Inguino – scrotal (when it extends into the scrotum)
(iii) Femoral – situated below the inguinal ligament
(iv) Inguino – femoral – situated both above and below the
inguinal ligament.
118
History
AGE Congenital hydrocoele, hernia and umbilical hernia are
common in children.
Varicocoele and indirect inguinal hernia occur in young
adults.
Direct inguinal hernia occurs in the older age group.
SEX Inguinal hernias are commoner than femoral hernia in
both the sexes. However, femoral hernia and para-
umbilical hernias are more common in women.
AREA Filarial funiculitis, epididymo–orchitis is more common in
Orissa, South Gujarat and Kerala.
MODE OF ONSET & Hernia starts insidiously; however, inflammatory lesions
DURATION will be accompanied by pain. Torsion of the testes
starts very suddenly. Hernias, which get incarcerated
and strangulated, become very painful.
Clinical features
VARIATION When a swelling becomes visible on standing and
disappears on lying down, it is likely to be a direct
inguinal hernia or a varicocoele.
A congenital hydrocoele is small in the morning and
becomes filled up by the evening.
PHYSICAL Examine the patient standing up – This will facilitate the
EXAMINATION examination of a hernia which sometimes is not visible
lying down.
TRY TO GET ABOVE If you are able to do this, the lump is purely a scrotal
THE SWELLING swelling such as a hydrocoele. If you are unable to get
above the swelling then it is an inguino-scrotal swelling
such as an inguinal hernia.
119
The usual facts about a lump should be ascertained such as
 Position
 Temperature
 Tenderness
 Shape
 Size
 Fluctuation
 Transilluminancy
Examination of the Scrotum - Cough impulse and reducibility

All hernias (except when they are strangulated or incarcerated) will have an
impulse on coughing and this is a cardinal sign.
It is important to make sure that the hernia is reducible. All hernias that become
irreducible should be immediately operated upon.
How to test for reducibility?
Often as soon as the patient lies down, the hernia reduces.
If it does not reduce then the following method should be employed –
a) Flex the thigh and keep it adducted
b) The left hand guides the contents into the direction of the superficial
inguinal ring
c) The right hand gently squeezes the fundus
No force should be applied. This method, also called “taxis” should not be used
if there are signs of intestinal obstruction or signs of inflammation (gangrene).
120
First decide the answers to these four questions
1. Can you get above the swelling? 7. Is the swelling translucent?

2. Can you identify the testis and 4. Is the swelling tender?
epididymis
Swellings confined to the scrotum
Swellings not confined to the scrotum

Testis and epididymis not definable
Testis and epididymis definable
Cough impulse No cough impulse

Reducible Not reducible Opaque Translucent
Testis Palpable Testis not palpable
Opaque Translucent
Translucent
Opaque
Internal ring
Cyst of epididymis
Vaginal hydrocele
Tender
Not tender
Hernia Infantile
hydrocele Not tender
Tender
Tuberculous
Tumour Acute epididymo-
epididymis
Chronic Haematocele, orchitis
Gumma, Tumour
Torsion, Severe epididymo- 121
Orchitis, Acute haematocele
Determine the relationship of the swelling to the inguinal ligament and the pubic
tubercle.
An inguinal hernia is above the inguinal ligament and medial to the pubic tubercle. A
femoral hernia is below the inguinal ligament and lateral to the pubic tubercle.
When inguinal nodes are enlarged, the areas of drainage should be examined –
 Scrotal skin
 Penis including the prepuce
 Perianal region
 Foot including the web spaces
Web space infection, perianal inflammation and penile ulcers or balanoposthitis can
produce inguinal lymphadenopathy.
When testicular swellings are being examined the epigastrium and the left
supraclavicular areas should be examined for secondaries.
The lumbar spine can be the focus of tuberculous infection with a resultant psoas
abscess pointing in the groin, just lateral to the femoral artery.
Differences between Direct and Indirect Inguinal Hernia
Features Direct Indirect

Age Occurs in older men Children and young adults
Extent Very rarely enters the Often does
scrotum
Reduction of hernia Very rapidly reappears on Reduction and
and reappearance standing and disappears on reappearance is slow
lying
Pressure over the Cannot prevent emergence Can prevent emergence
internal ring
Strangulation Very uncommon Is a dreaded complication
Repair Requires the use of a mesh to Herniotomy is often enough
strengthen the posterior wall
Management
The following advice should be given to patients with hernia:
1. If the hernia is irreducible it is urgent that he be referred to a surgeon.
2. Childhood hernias –
122
 General rule is “As soon as possible”
 For reducible herniae – the “6.2” rule can be applied
Birth to 6 weeks - surgery in 2 days
6 weeks to 6 months – surgery in 2 weeks
Over 6 months – surgery in 2 months
3. Direct hernias in very old patients with medical conditions may be managed
conservatively. Fit patients with direct hernia should be operated upon.
Signs of strangulation or obstruction –
These are the same signs as for intestinal obstruction namely –
 Severe colicky abdominal pain,
 Vomiting,
 Distension and
 Constipation.
Guarding, rigidity and severe tachycardia would mean that besides intestinal
obstruction, there is gangrenous bowel as well.
Examination of the scrotum
Inspection
 The left testes usually hangs a little lower.
 Oedema of the scrotum is seen in congestive failure and nephrotic syndrome.
 Any redness of the skin should be noted. Cellulitis of the scrotum is often
painless.
 Swellings should be noted. Hernias produce an inguino scrotal swelling;
Varicocoele, cyst of the epididymis and tumours of the testes can often be
seen on inspection.
Palpation
 The scrotum should be palpated with the patient standing.
 The testes and epididymis should be palpated on each side and compared.
 The spermatic should be felt with the thumb and forefinger and from medical
to lateral. The vas deferens can be felt like a whipcord on each side. It is
usually the size of a “match-stick”. Any enlargement or irregularity should be
noted as it becomes “beaded” in tuberculosis and thickened in filariasis.
123
 If the testes is not palpable in the normal region then an attempt should be
made to palpate with just two fingers in the inguinal region, femoral region and
rarely in the peritoneum.
 Transillumination test for seeing if the swelling of the testes is transilluminant
or not. Hydrocoele is usually transilluminant. However, a haematocoele or a
tumour is not.
 Regional lymph nodes including the para aorta nodes and left supraclavicular
nodes should also be palpated.
Swellings of the testis can be classified as follows:
With pain or tenderness Without pain or tenderness
Sudden pain Pain for Transilluminant

of few hours more than a
duration day + Urine
Urine micro micro – pus
normal cells
Hydrocoele or cyst of
epididymis
Torsion of Acute epididymo
testes orchitis
Refer to surgeon Conservative

after confirming treatment after
with Doppler confirming with
ultrasound Doppler ultrasound
Not transilluminant
Tuberculous Malignancy Haematocoele Varicocoele

epididymitis
is often
painless
124
Differentiation between Torsion of Testes and Acute Epididymo-Orchitis
Clinical feature Torsion Epididymo-Orchitis

acute
Age Early teens – average Sexually active adults or
age 5-15 years Elderly
Onset Sudden Gradual
Severity of pain Very severe Moderate
Associated symptoms Vomiting, abdominal pain Fever
Angell’s Sign The opposite testes lies
horizontal because of a
long mesentry between
the testes and epididymis
Position of testes Lies at a higher level No difference
because of torsion
Palpation The epididymis and the Might be able to do so.
testes cannot be
palpated separately
Effect of gentle scrotal No change or even worse Some relief
elevation
Doppler ultrasound Blood flow interrupted Not so
(Additional readings for this topic on pgs.182-199)
125
ADDITIONAL READINGS
126
Additional readings for Lower GI bleeding
PROBABLE SOURCE OF BLEEDING BASED ON SOME CLINICAL INDICATORS
Upper GI Fissure Gastroenteritis Malignancy Piles Ulcerative Polyp

G/O rectum Colitis
Symptom or clinical
indicator
Hematemesis Almost certainly No No No No No No
Malena Most likely No No Possible-right No No Possible-right
colon colon
Hematochezia (Bright red Possible if No Possible Yes Yes Yes Yes
blood in stool) bleeding is very
brisk
Blood streaked stool No Yes No No No No Yes
Occult blood 50% likely No No Yes No Yes Yes
Abdominal pain or Yes Yes Yes Only if Only if Yes No
perianal pain obstructed thrombosed
Diarrhoea No No Yes Yes No Yes No
Mass per rectum No No No Yes Yes No Yes if
Intussception
Sentinel skin tag No Yes No No No No No
127
ALGORITHM FOR MILD TO MODERATE BLEEDING IN LOWER GI TRACT
Mild to Moderate bleeding lower GI

tract
Abdominal pain No abdominal pain

 Infection
 Inflammatory
 Intussception
 Ischaemia
 Immune deficiency (HIV) Pain anal canal No pain
 Hemorrhoids
 Carcinoma
 Polyps
Fissure-in-ano  Meckel’s
Prolapsed piles /  Liver disease
Thrombosed piles  Diverticular
disease
HIV test Biopsy rectum Ba enema Stool exam (Amebic colitis)
Intussception – “pincer” deformity

Ulcerative colitis Pipe stem colon – Ulcerative colitis
Stenosis spl. Flexure – Ischemic
colitis
 Meckel’s in  Proctoscopy  Barium enema  Ultrasound  Colonoscopy if

Children - rare  Hemorrhoids  Diverticulosis  Cirrhosis possible will
in our country  Proctitis  Carcinoma  Splenomegaly show –
(Homosexually Varices  Polyposis
active)
 Polyp - children  Carcinoma
 Diverticulum
128
ALGORITHM FOR MANAGEMENT OF OCCULT BLEEDING
A test for occult bleeding in the stool has been found to be positive.
How will you manage further?
History of Aspirin or NSAID or steroids or Anti

coagulants
Negative
Positive Stop & see
No diarrhea Change in bowel habit or

Diarrhoea associated
Rectal exam & Colonoscopy

proctoscopy
Positive findings in Negative Malignancy

 Fissure-in-ano Inflammatory
 Hemorrhoids bowel disease
 Rectal malignant
ulcer
 Rectal Colonoscopy
inflammatory
polyp
Malignancy Polyp Angiodysplasia

Colon (Biopsy to Diverticular disease
be taken) Ischemic colitis
129
ALGORITHM FOR MASSIVE ACUTE BLEEDING
Massive acute bleeding
Stabilize – blood transfuse
Insert NG tube to rule out upper GI bleeding
Blood found Blood not found
Treat for upper GI bleeding Fever & toxicity
No. Prepare bowel for Colonoscopy Yes, consider
Lesion not found Lesions Enteric – typhoid Acute fulminant

or Visibility poor visible ulcer bleeding ulcerative colitis
Celiac Diverticulosis less Angiodysplasia – Malignancy – Ulcerative

angiography common in India geriatric age group over 40 biopsy colitis biopsy
Lesion detected Embolise Not detected
Consider Technician nuclear

scan. If not available –
intraoperative endoscopy
130
ANATOMY OF HAEMORRHOIDS
Prolapsed "rosette” of internal hemorrhoids
 The anal canal has a triradiate lumen lined by three fibrovascular cushions of
submucosal tissue.
 The cushions are suspended in the canal by a connective tissue framework derived
from the internal anal sphincter and longitudinal muscle.
 Within each cushion is a venous plexus that is fed by arteriovenous communications.
These specialised vascular structures allow for enlargement of the cushion to
maintain fine continence.
 In health as in disease the anal cushions appear in the right anterior, right posterior,
and left lateral positions.7
Pathogenesis-The theory of sliding anal lining:
o Fragmentation of the connective tissue supporting the cushions leads to their

descent. This occurs with age and the passage of hard stools, which produce
a shearing force on the framework.
o
Straining produces an increase in venous pressure and engorgement.
o The prolapsed cushion has an impaired venous return, which results in
dilation of the plexus and venous stasis.
o
Inflammation occurs with erosion of the cushion's epithelium, resulting in
bleeding.
131
Thus haemorrhoids result from the pathological changes in prolapsed anal cushions.
This mechanism was proposed as the theory of sliding anal lining and has
superseded notions that piles were a form of varicose veins.
Evolution of haemorrhoids and classification:
 Internal haemorrhoids originate from the internal haemorrhoidal venous plexus above
the dentate line;
 External haemorrhoids originate from the external plexus below the dentate line. This
line lies at 2 cm from the anal verge and demarcates the transition from the upper
anal canal, lined with columnar epithelium, and the lower anal canal, lined with
sensate squamous epithelium.
Internal haemorrhoids may be classified according to the degree of prolapse, although this
may not reflect the severity of a patient's symptoms.
 First degree haemorrhoids bleed but do not prolapse.

 Second degree haemorrhoids prolapse on straining and reduce
spontaneously.
 Third degree haemorrhoids prolapse on straining and require manual
reduction.
 Fourth degree haemorrhoids are prolapsed and incarcerated.
Symptoms vary with conditions such as pregnancy, repeated straining, or changes in diet or
work patterns. Sufferers may undergo periods of remission and relapse or heightened
awareness of symptoms.
 Haemorrhoidal bleeding is bright red and usually noticed on wiping or in the toilet
bowl. Prolapse occurs with a bowel movement and is associated with an
uncomfortable sensation of fullness and incomplete evacuation;
 Patients complain of a lump at the anal verge.

Soiling may occur in third and fourth degree haemorrhoids as a result of impaired
continence or production of mucus discharge.
 Discharge can cause perianal irritation and itching.
 Third degree haemorrhoids can prolapse and cause discomfort because of the
reflex spasm of the sphincter complex. This discomfort can be relieved by reduction.
 Fourth degree haemorrhoids may become "strangulated" and present with acute
severe pain by prolapsing and causing spasm of the sphincter complex.
 Progressive venous engorgement and incarceration of the acutely inflamed
haemorrhoids leads to thrombosis and infarction.
 When the external haemorrhoids also get strangulated there is concomitant
cutaneous pain.
External hemorrhoids cause symptoms in 2 ways:
First, acute thrombosis of the underlying external hemorrhoidal vein can occur. Acute
thrombosis is usually related to a specific event, eg, physical exertion, straining with
constipation, a bout of diarrhea, or a change in diet. These are acute, painful events. Pain
results from rapid distension of innervated skin by the clot and surrounding edema. The pain
lasts 7-14 days and resolves with resolution of the thrombosis. With resolution of the
thrombosis, the stretched anoderm persists as excess skin or skin tags.
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Secondly the external thromboses can occasionally erode the overlying skin and cause
bleeding. Recurrence occurs approximately 40-50% of the time, at the same site. This
occurs at the same site because the underlying damaged vein remains present. Simply
removing the blood clot and leaving the weakened vein in place, compared with excision of
the offending vein with the clot, will predispose to recurrence.
Physical Examination:
Inspection and examination of the entire perianal area.
Warn the patient before any probing or poking.
Patient apprehension is great prior to any anal examination. Go to great lengths to
reassure the patient.
Gentle spreading of the buttocks allows easy visualization of most of the anoderm
including the distal anal canal.
Anal fissures and perianal dermatitis (pruritus ani) are easily visible without internal
probing.
Note the location and size of skin tags and the presence of thromboses.
Normal corrugation of the anoderm and a normal anal wink with stimulation confirms
intact sensation.
Digital examination of the anal canal in the left lateral position can identify any
indurated or ulcerated areas. Be sure to palpate the prostate in all men.
Note: Hemorrhoids are not palpable on rectal examination unless they

are thrombosed.
Because internal hemorrhoids are soft vascular structures, they are usually not
palpable.
Anoscopy is mandatory for viewing internal hemorrhoids. The anoscope

should be a side-viewing scope.
When angled well by the examiner, the side-viewing anoscope allows the
soft hemorrhoidal tufts to fill the beveled end of the scope and to be
appropriately evaluated.
o
The hemorrhoidal cushions can be viewed by using the
anoscope in the left lateral, right anterior, and right
posterior positions (7 o'clock, 7 o'clock, 11 o'clock
positions).
o Haemorrhoidal size, severity of inflammation, and bleeding
should be assessed.
o Prolapse can be observed when the patient performs a
Valsalva maneuver. Having a patient strain while sitting on
a toilet may reproduce prolapse most accurately.
Flexible/rigid sigmoidoscopy is performed to exclude proximal disease. Side Viewing Anoscope
Colonoscopy, virtual colonoscopy, and
Barium enema are reserved for cases of bleeding without an identified anal source.
These symptoms are not attributable to hemorrhoids and are considered non–outlet-type
bleeding.
Dietary and lifestyle modification

Increasing intake of fibre is useful for
 softening motions,
 relieving constipation, and thus
 reducing straining;
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 to reduce episodes of bleeding and discomfort in patients with internal haemorrhoids,
but
 it does not improve the degree of prolapse.
 Can relieve the symptoms of non-prolapsing haemorrhoids, but it may take six weeks
for a significant improvement.
 Lifestyle advice on avoiding straining and reading on the toilet should be emphasized.
High fibre foods can be found in most food groups. Fibre generally is divided into two
categories.
Note: Non-prolapsing haemorrhoids can be managed adequately in primary care with the
above measures.
* Insoluble fibre is found in wheat bran and in celluloses from vegetables and fruits.
* Soluble fibre is commonly found in oatmeal, oat bran (the best source), guar gum,
psyllium seed, fruit pectin and gum arabic. When mixed with water, it produces a
gelatinous mucous gel.
Different types of food should be selected to get the benefits of them all.
Fruit Name Total dietary fiber
Apple 7.2 ± 0.21
Jackfruit 7.5 ± 0.08
Jambu 7.5 ± 0.02
Pear 4.7 ± 0.25
Fig 5.0 ± 0.21
Custard apple 5.5 ± 0.20
Amla 7.7 ± 0.10
Dates 7.7 ± 0.46
Guava 8.5 ± 1.07
Sapota (chickoo) 10.9 ± 0.44
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Dietary Fibre
Food Items gm per 100g
Bajra 20.7
Ragi 18.6
Wheat 17.6
Sorghum 14.7
Black gram dhal 14.7
Red gram dhal 14.1
Bengal gram dhal 17.6
Green gram dhal 17.5
Dry coconut 8.9
Rice 7.6
Medical treatment
A range of ointments is available that contain
*
local anaesthetics,
* mild astringents, or
* steroids.
 These agents may be used to provide short term relief from discomfort, but
there is a lack of evidence to support their widespread use.
 They do not affect the underlying pathological changes in the anal cushions.
 Continuous application can cause eczema and sensitization of the anoderm;
rectal absorption can lead to systemic side effects.
The major dietary sources of flavonoids include fruit and fruit products, tea, and soya
beans.
A number of flavonoids have been shown to have anti-inflammatory effects and/or to

strengthen blood vessels. These effects could, in theory, be beneficial for people with
hemorrhoids. Most, but not all, double-blind trials using a group of semisynthetic flavonoids
(hydroxyethylrutosides derived from rutin) have demonstrated significant improvements in
itching, bleeding, and other symptoms associated with hemorrhoids when people used
supplements of 600–4,000 mg per day.
Diosmin is one flavonoids containing drug that is commonly used and is useful.
Outpatient treatment
Interventional procedures are performed in clinic to treat first degree haemorrhoids that do
not respond to dietary modification as well as second and third degree haemorrhoids.
Treatment is directed at the asensate origin of the haemorrhoid lying above the dentate line.
If performed correctly these procedures should not be painful.
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Rubber band ligation
The technique was originally described by Barron in 1967 and is the most commonly used
outpatient treatment. Anoscopy is performed to identify the haemorrhoid's origin, which is
grasped by using a forceps or suction device. A band is then applied at its base. The
strangulated haemorrhoid becomes necrotic and sloughs off, while the underlying tissue
undergoes fixation by fibrotic wound healing.
Banding equipment
 If the procedure is well tolerated up to three piles can be banded at one visit. This
increases the risk of
 discomfort (29% in multiple banding versus 4.5% in single banding),
 vaso-vagal symptoms (5.2% in multiple bandings versus 0% in single bandings), and
urinary symptoms (12.7% in multiple bandings versus 0% in single bandings).
 Multiple banding does not increase the risk of major complications.
 Injection of a local anaesthetic does not reduce the discomfort associated with
multiple banding.
 If application of the first band causes discomfort then repeat sessions of single
banding are advised.
Post banding , complications included
 urinary retention,
 rectal bleeding,
 pelvic sepsis, and perianal abscess occurred in 2.5% (17 patients) of
procedures and required admission to hospital.
Minor complications including haemorrhoid thrombosis, band displacement, mild bleeding,
and formation of mucosal ulcers occurred in 4.6% (24 patients).
Band ligation is the most effective outpatient procedure for haemorrhoids, providing a cure in
79% of patients with first to third degree haemorrhoids. Eighteen per cent of patients have a
relapse requiring repeat banding, and 2.1% fail to respond. The addition of fibre supplements
will increase the long term cure rate after banding.
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Injection sclerotherapy
Injection sclerotherapy is an alternative to band ligation in first and
second degree haemorrhoids. Injection of phenol in oil into the pedicle
leads to tissue fibrosis. Rare complications include pelvic infection and
impotence as a result of incorrectly sited injections. Sclerotherapy may
provide a short term benefit, but long term follow up shows
sustained improvements in only 28% of patients. After six months
outcome after injection sclerotherapy is comparable to treatment with fibre supplementation
alone in bleeding haemorrhoids.
Algorithm for management of hemorrhoids
Patient presents to general practitioner with symptoms
Assessment includes anoscopy and other tests if required
Non prolapsing piles Prolapsing piles
Fibre supplements Refer to colorectal surgeon
First and second degree Third degree Fourth degree
Band ligation and Band ligation and Surgical

fibre supplements fibre supplements Haemorrhoidectomy
Stapled haemorrhoidopexy
depends on surgeon’s
experience
Referral for Surgery

Haemorrhoidectomy
Surgery is advised for symptomatic third degree haemorrhoids not responding to banding
and for fourth degree haemorrhoids. Less than 10% of patients referred for specialist
treatment will require surgery. Only symptomatic haemorrhoidal tissue should be excised
("limited haemorrhoidectomy"). This conserves the sensory anoderm for continence and
decreases postoperative pain and anal stenosis.
Milligan-Morgan haemorrhoidectomy is one very popular technique. This entails grasping

and everting the haemorrhoid, then dissecting it off the anal sphincter. The vascular pedicle
is ligated, and the wounds are left open to granulate, separated by bridges of skin and
mucosa. Ferguson haemorrhoidectomy is another popular technique. The haemorrhoid is
exposed in the anoscope, and excision and ligation are performed in its anatomical position.
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The wound is closed with a continuous suture. Both methods are effective forms of
treatment; in theory wound closure should offer faster healing, but this has not been shown
consistently. Wound dehiscence after excision of three piles prolongs healing after closed
surgery (6.9 weeks in closed operation versus 4.9 weeks in open operation).
 Some surgeons may prefer to do a stapled haemorrhoidectomy which has been
claimed to have a shorter hospital stay, less pain but may have a higher recurrence
rate. .
 Traditionally patients would stay in hospital after surgery until their first postoperative
bowel motion.
 Laxatives will reduce pain during the first postoperative motion, and
 Restricting perioperative intravenous fluid will minimize the risk of urinary retention.
 Successful day surgery is dependent on adequate community nursing, to encourage
the appropriate use of analgesics and reassure patients; up to nine home visits may
be required.
 The addition of prophylactic metronidazole reduces pain and convalescence after day
surgery and increases patients' satisfaction
Anal Fissure
Anal fissures are among the most common anorectal disorders in the pediatric population;
however, adults also are affected.
Definition: An anal fissure is a superficial linear tear distal to the dentate line in the anoderm
most commonly caused by passage of a large, hard
stool.
Pathophysiology: In anal fissures, anus distal to

dentate line is involved. About 90% of anal fissures
occur in the posterior midline where skeletal muscle
fibers that circle the anus are weakest. The remaining
10% are found in the anterior midline. Anal canal
hypertensioncaused by high resting tone of the anal
sphincter is considered to cause ischemia of the anal
canal critical to the pathogenesis of the fissure.
Causes:
 Passage of hard stool
 Chronic diarrhea
 Habitual use of cathartics
 Anal trauma (can occur with anal intercourse or a rectal examination using a
speculum or digit)
 Anal fissures can be seen in patients with syphilis and other sexually transmitted
diseases, tuberculosis, leukemia, inflammatory bowel disease such as Crohn’s
disease, previous anal surgery, HIV, and other conditions or diseases.
 Incidence of anal fissures in patients with leukemia is approximately 24%.
Sex: Anal fissures affect both sexes equally; however, an anterior fissure is more likely to
develop in women than in men.
Age: Although anal fissures are the most common cause of rectal bleeding in infants, they
are primarily seen in young adults.
Anal fissures in children may indicate sexual abuse.
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History:
Rectal pain, usually described as burning, cutting, or tearing
* Pain with bowel movements
* Bloody stools
o Typically, bright-red blood appears on surface of stools. Blood usually is not
mixed into stool.
o Occasionally, blood is found on toilet paper after wiping.
o Patient may report no bleeding.
* Mucoid discharge
* Pruritus
Physical:
 Place patient in left lateral decubitus position with knees drawn up toward chest.
 Examine patient carefully to avoid infliction of further pain or sphincter spasm.
Examination may be facilitated by application of a topical anesthetic, such as
Lidocaine jelly, prior to digital rectal examination.
 Most fissures are visible externally when patient bears down as if having a bowel
movement.
 Examination of anus reveals a linear tear in fissure-in-ano.
 Note depth of fissure and its orientation to the midline, often described using clock
orientation of hour hand.
 Majority of tears are found in the posterior midline.
 Rectal examination is generally difficult to tolerate because of sphincter spasm and
pain.
 Acute fissures are erythematous and bleed easily.
 With chronic fissures, classic fissure triad may be seen.
 Deep ulcer
 Sentinel pile, which forms when base of fissure becomes edematous and
hypertrophic
 Enlarged anal papillae
Lab Studies:
 Diagnosis of anal fissure primarily is based on history and physical examination.
 If Syphilis or Chlamydia infection is in the differential, a VDRL test may be necessary
for syphilis. Lab test for Chlamydia is difficult and empirical treatment will be
necessary.
Treatment:
Anal fissures can cause a vicious cycle in which the patient, in anticipation of pain
associated with bowel movement, resists the urge to defecate, causing stools to become
larger and harder; more pain with defecation results.
 Use WASH regimen in treatment of acute anal fissures.
 Warm water; shower or Sitz bath after bowel movement
 Analgesics- In the case of severe pain a topical anesthetic may be applied.
 Stool softener- Psyllium / Isab Gul (Isogel) is very useful.
 High fiber diet- Increase fruits and vegetables in diet.
 Most uncomplicated fissures resolve in 2-4 weeks with supportive care.
However when an acute fissure does not heal it becomes a chronic fissure.
Chronic anal fissures frequently require surgical treatment.
Management of a chronic fissure
Application of 0.20% Gylceryl trinitrate ointment has been shown to be quite effective
in the treatment of chronic anal fissure and it acts by relaxing the internal sphincter and
thus increasing the blood supply locally.
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 Application should be twice a day
 to the fissure directly
 for a period of 4-6 weeks. (About 75% of fissures will heal in this way. However
there is a small recurrence rate and a 25% failure rate. These should be referred
to the surgeon.)
 Headache is a side effect and if the patient is unable to comply he/she should be
offered surgery.
Injection of Botulism toxin for chronic fissure in ano:
 Injection of Botulinum toxin 20 units on either side of the fissure into the internal
sphincter provides definite relief and cure. Botox causes denervation of the
internal anal sphincter. The toxin acts rapidly and paralysis occurs within a few
hours. If there is not enough relief re-treatment should be given after 4 weeks. At
the end of re-treatment about 70% enjoy total healing and an additional 25%
experience major relief from symptoms. Side effects like lack of “gas” control can
occur but are temporary.
Surgery- The lateral internal sphincterotomy:
The most common surgical procedure is lateral internal sphincterotomy or "LIS." In an LIS,
the surgeon actually divides the internal sphincter muscle, which prevents that muscle from
going into spasm, reduces the pressure in the anal canal and increases the blood flow.
Usually, the fissure heals within a couple of days, even though the surgeon does nothing to
the fissure itself. The operation is based upon the interesting research finding 15 years ago
that patients with chronic fissures tend to have excessive anal canal pressure (tightness)
and that by reducing the pressure a bit, the fissure can heal. It is quite an amazing little
operation and for those who have had serious pain after each bowel movement, sometimes
for months or years, it can be a godsend.
The following post operative surgical complications may occur:

o Urinary retention
o Bleeding
o Abscess formation
o Flatus and liquid incontinence
o Recurrence of fissures
Prognosis:
 Most uncomplicated fissures resolve in 2-4 weeks with supportive care.
 Chronic anal fissures do very well after surgery.
TUTOR SAYS- “NO, NO!”

Although anal stretching (Lord’s procedure) can also be helpful, the recurrence rates are
higher.
Posterior sphincterotomy is not indicated and
Fissurectomy is not advised.
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Management algorithm for anal fissure
Anal fissure
Acute
Chronic
WASH
REGIME
2% Glyceryl trinitrate
ointment for 4-6 weeks
twice a day
No Yes
70% healed 70% not healed
Botox injection
Rest healed 9% not healed
LIS
1% some Rest healed without

incontinence for complication
flatus
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INTUSSUSCEPTION
Definition: Intussusception is the telescoping or prolapse of one portion of the bowel into an
immediately adjacent segment.
Pathophysiology: Intussusception most commonly occurs at the terminal ileum (ie,

ileocolic). The telescoping proximal portion of bowel (ie, intussusceptum) invaginates into the
adjacent distal bowel (ie, intussuscipiens).
The mesentery of the intussusceptum is compressed, and the ensuing swelling of the bowel
wall quickly leads to obstruction. Venous engorgement and ischemia of the intestinal
mucosa cause bleeding and an outpouring of mucous, which results in the classic
description of red "currant jelly" stool.
Most cases (90%) are idiopathic, with no identifiable lesion acting as the lead point or
pathological apex of the intussusceptum.
Features-
 Intussusception is the predominant cause of intestinal obstruction in infants. The
estimated incidence is 1-4 per 1000 live births.
 Most patients recover if treated within 24 hours.
 Mortality with treatment is 1-7%. If left untreated, this condition is uniformly fatal in 2-
5 days.
 Recurrence is observed in 7-11% of cases. Most recurrences involve
intussusceptions that were reduced with contrast enema.
 Overall, the male-to-female ratio is approximately 7:1.
Age: Intussusception is most common in infants aged 7-12 months, with an average age of
7-8 months.
* Two thirds of the cases occur before the patient's first birthday.
* Intussusception occurrence is rare in persons younger than 7 months, and
becomes less common in persons older than 76 months.
Symptoms:
 The typical presentation is a previously healthy infant boy aged 6-12 months with
sudden onset of colicky abdominal pain with vomiting.
 Paroxysms of pain occur 10-20 minutes apart with drawing up of legs.
 Initially, loose or watery stools are present concurrent with vomiting and, within 12-24
hours, blood or mucous is passed rectally.
 Early in the course, the patient appears completely well between the episodes of
abdominal pain.
 Lethargy may dominate the initial presentation. However, lethargy usually occurs
later in the process.
 The classic triad of colicky abdominal pain, vomiting, and red currant jelly stools
occurs in only 21% of cases.
Physical:
 Usually, the abdomen is soft and non-tender early, but it eventually becomes
distended and tender.
 A sausage shaped mass may be palpable in the right upper quadrant.
 Currant jelly stools are observed in only 50% of cases.
 Most patients (75%) without obviously bloody stools have stools that test positive for
occult blood.
 Fever is a late finding and is suggestive of enteric sepsis.
Causes:
 Most cases are idiopathic.
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 In adults and in children older than 7 years, a mechanical lead point usually can be
found.
Caecal Intussception Ileo Ileal Intussception
 Predisposing factors
o Enlargement of the Peyer’s patches in the ileum due to
Recent upper respiratory illness
Recent diarrheal illness
o Cystic fibrosis causing change in motility
o Chronic indwelling GI tubes
 Mechanical causes- more often in older children
o Intestinal polyp (eg, Peutz-Jeghers syndrome, familial polyposis coli, juvenile
polyposis)
o Meckel diverticulum
o Enlargements of the Peyer’s patches
o Small tumors like Intestinal lymphosarcoma, Hemangioma
o Blunt abdominal trauma with intestinal or mesenteric hematomas
o Henoch-Schönlein purpura
 See the section on intestinal obstruction for emergency management-.

 Laboratory- Packed cell volume, electrolytes, Blood urea and Serum creatininine.
X-ray studies-
 Plain abdominal x-ray findings may be normal early in the disease or may show
perforation, typical obstructive pattern, or soft tissue mass of the intussusception on
the right side. A paucity of gas in the right upper quadrant may be present.
Note: An X-ray contrast study for Intussusception is both a diagnostic as well as a

therapeutic maneuver. Should be done jointly by the family practitioner and the
surgeon.
 If Intussusception is strongly suspected, perform a contrast enema without delay.

This is contraindicated in patients with an obvious surgical abdomen (eg, signs of
peritonitis or perforation) and in unstable patients. Before a contrast is performed, a
143
surgeon should be informed so that he could be available for reduction using the
contrast medium.
 Ultrasound has been used to diagnose Intussusception. A target sign is
characteristic.
Management:
Admission is indicated for all patients because up to 10% of those with successful
radiologic reduction have a recurrence, usually in the first 24 hours.
 Provide rehydration and stabilization as needed.
 Contrast enema is diagnostic in approximately 95% of intussusception cases. It is
therapeutic and curative in most cases with less than 24-hour duration.
Referral: Indications:
The family practitioner could take the responsibility of radiological reduction only if the
radiologist and the surgeon are present. If this fails it may be best if he is immediately
referred for surgical reduction.
Complications:
 Continued bleeding
 Gangrene and bowel perforation
 Dehydration, shock and sepsis
 Recurrence often when reduction achieved using contrast.
Prognosis:
Prognosis is excellent if diagnosed and treated early; otherwise, the resultant intestinal
obstruction can produce gangrene and death.
ANGIODYSPLASIA
Definition:
Angiodysplasia of the colon is a condition of dilated and fragile blood vessels in the colon
that results in intermittent loss of blood from the gastrointestinal tract. The condition is mostly
related to the aging and degeneration of the blood vessels, as it occurs in older adults.
Etiology:
There are several theories about the cause of angiodysplasia of the colon.
o The most likely is that normal contractions of the colon result in dilation
(stretching) of colonic veins, venules, and capillaries.
o The dilation becomes so severe that a small direct passageway develops
between the artery and vein (arteriovenous fistula). It is in this area of the colon
wall that the patient is at risk for bleeding. Angiodysplasia of the colon has been
seen in about 7% of "nonbleeding persons" and in about 5% of patients evaluated
for blood in the stool, anemia, or hemorrhage.
o Men and women are equally at risk for developing angiodysplasia of the
colon.
o Most patients are older than 50 years.
o In the western world this is the commonest cause of bleeding after
diverticulosis.
Pathology:
The angiodysplastic lesions (smaller than 0.5cms.) are most often situated in the caecum
and the ascending colon. They tend to be small and never palpable abdominally.
Clinical features-
o Bright blood mixed with stool (Hematochezia)
144
o Maroon colored blood
o Malena
o Occult bleeding: In this case the presentation is likely to be one of anemia
and features related to chronic anemia.
o One in six may present with massive hemorrhage.
o Bleeding from angiodysplasia usually is self-limited, but it can be chronic,
recurrent, or even acute and life threatening.
o Approximately 90% of bleeding angiodysplasias spontaneously cease
bleeding.
o Mortality is related to the severity of bleeding, hemodynamic instability, age,
and the presence of co-morbid medical conditions.
Investigations:
One must have a high index of suspicion when a patient older than 60 bleeds small amounts
in his stool regularly causing a microcytic anemia.
A Haemoglobin estimation,
Stool examination (to rule out infections),
Examination of the anal region for fissures and prolapsed piles,
an anoscopy to visualize hemorrhoids and
an air-contrast enema should be done to rule out malignancy should be done.
Angiodysplasia will not be picked up by any of these tests.
Colonoscopy is probably the most reliable test for diagnosing angiodysplasia.
However a mesenteric angiogram will help localize the lesion and the quantum of the
malformation. The angiogram will show pooling of dye in the colon as well as a
“vascular tuft”. The indication for this test is when the visibility in the colon has been
compromised for colonoscopy because of the bleeding.
Management:
Conservatively: When the patient is hemodynamically stable he should be treated with blood
and intravenous fluids till the bleeding stops. Most often it does.
In the rare event that the bleeding continues he should be referred to a gastroenterologist so
that the diagnosis can be confirmed by colonoscopy and a electro coagulation or a
photocoagulation of the dysplastic lesion can be done.
ISCHEMIC COLITIS
Definition
Ischemic colitis involves an area of
inflammation of the colon caused by
mesenteric vessel disease leading to
ischemic damage. The areas affected tend to
be the splenic flexure and the sigmoid
flexure.
Causes, incidence, and risk factors
 Affects people over 60
 Patients often have associated
coronary artery disease with angina
 Associated- Peripheral vascular
disease
 Associated diabetes
 Have a history of stroke
 Have low blood pressure /congestive
cardiac failure- leading to poor bowel
perfusion
 If the symptoms occur in a younger
female patient the cause is most likely
145
to be oral contraceptives.
Symptoms
 Abdominal pain
 Fever
 Vomiting
 Bright red blood via the rectum (blood in the stool)
 Diarrhea
Signs and tests
ECG/Blood sugars/Serum lipids may need to be evaluated.

Arrhythmia of the heart needs to be ruled out.
Barium enema- Findings on barium enema examination may include the following:
 Serrated mucosa
 Sacculations of the wall of the colon usually the anti-mesenteric side.
 Tubular narrowing
 Long stricture
Colonoscopy or flexible sigmoidoscopy may show inflamed mucosa or ulcers in the colon.
Treatment
Mild, transient ischemic colitis is treated by maintaining

o good blood pressure
o good hydration
o Good hemoglobin
o Correcting congestive failure and arrhythmia.
o Most cases of ischemic colitis are mild, self-limited, and do not require
therapy.
Chronic ischemic colitis leading to stricture formation is treated by surgical removal of the
stricture. Therefore needs to be referred to the surgeon if the symptoms do not improve.
INTESTINAL POLYPOSIS
An important cause of rectal bleeding is the polyps. A polyp is a small growth of tissue
shaped like the head or stalk of a mushroom.
The easiest way to understand and classify this very confusing subject is to categorize it into
four important types-
I. Hyperplastic polyps- This is the commonest group.

 Usually less than 0.5 cm in diameter,
 Hyperplastic polyps represent 90% of all epithelial polyps
 Hyperplastic polyps most commonly occur in the rectosigmoid colon,
 Most commonly diagnosed in those aged 50-70 years.
 Histologically have glands, nonmalignant epithelial cells and lymphoid tissue.
 Have no malignant potential.
 Can bleed and present with anemia.
II. Hamartomatous polyp-

 These are also called “inflammatory polyps”
 Commonest form of polyp in children
 Can occur throughout large bowel but are most common in the rectum
 Usually presents before 12 years
 Present with prolapsing lump or rectal bleeding
 Not pre-malignant
 Treated by local endoscopic resection
 The child does not need to be followed up.
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III. Adenomatous polyps- Adenomas are traditionally divided into 7 types: tubular,
tubulovillous, and villous. Tubular adenomas are the most common of the 7 types (75%) and
can be found anywhere in the colon. They may pedunculated (with a stalk) or sessile
(without a stalk). Adenomatous polyps comprise approximately
 10% of all colonic polyps.
 More than 90% are smaller than 1.5 cm in diameter and have a small
potential for malignancy.
 Larger adenomatous polyps have a greater (10%) potential for malignant
change.
 The risk of malignant potential is related to the size of the adenoma.
 The degree of villous component of these polyps is correlated with the risk of
progression to carcinoma.
 Villous adenomas are associated with the highest morbidity and mortality
rates of all polyps.
IV. Polyposis syndromes

A variety of polyposis syndromes can affect Suspect malignancy in a polyp which is
the GI tract. The adenomatous polyposis
syndromes include the o Larger than 1.5 cms.
o classic familial adenomatous o When is multiple
polyposis (FAP), o That which is a familial syndrome
o Gardner syndrome, and o That is villous rather than tubular
Turcot syndrome. o Has many extraintestinal
o Hamartomatous familial manifestations
polyposis syndromes include
Peutz-Jeghers syndrome, juvenile polyposis syndrome,
o Cowden disease, and
o Ruvalcaba-Myhre-Smith syndrome.
These syndromes need to be recognized - because these polyps are premalignant.
Relax! You do not have to remember all these syndromes!! Only recognize that if
polyposis is familial then there is a greater danger of malignancy.
Familial adenomatous polyposis (FAP)- This is the most important of the group.
 Aetiological factor in 1% of colorectal cancers
 It has an autosomal dominant inheritance
 Develop colonic polyps in teens or early 20’s
 Untreated progresses to cancer by 70’s
 Screening – by rigid or flexible sigmoidoscopy is a safe alternative to colonoscopy as
rectal sparing rarely seen; start late teens and continue until 40 yrs and polyp free.
 Extra-colonic manifestations:
o Osteomas. epidermoid cysts = Gardener’s Syndrome
o Gastroduodenal polyps
o Desmoid tumours
o Congenital hypertrophy of retinal pigmented epithelium
 Surgical options:
o Panproctocolectomy and ileostomy
o Restorative panproctocolectomy
o Subtotal colectomy and ileorectal anastomosis
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 Suspect juvenile polyp or an inflammatory polyp in children with bleeding. Do a
rectal examination to feel for it and also do a sigmoidoscopy to confirm.
 Suspect hyperplastic polyp in older folk above 60 and similarly do a
sigmoidoscopy to confirm.
 Always submit them to a biopsy so as to rule out adenomatous polyp.
 Suspect a familial syndrome if a child or an adult has-
 Multiple polyps
 History of colonic malignancy in the family
 Has extraintestinal tumors,
 Has massive bleeding per rectum and diarrhea
Investigations and diagnosis-

Besides checking blood for Hemoglobin, the investigations that will clinch the diagnosis are-
Sigmoidoscopy-
Colonoscopy and
Air Contrast Barium enema.
It is important to remember that all polyps should be subjected to a biopsy so that if
necessary they can be followed up for possible malignant change.
.
MECKEL’S DIVERTICULUM as a cause of lower GI bleeding
A Meckel's diverticulum is a
o true congenital diverticulum since it has all the bowel wall layers unlike in
diverticulosis.. It is a
o vestigial remnant of the omphalomesenteric duct, and is
o the most frequent malformation of the gastrointestinal tract. It is present in
o approximately 2% of the population, with an equal distribution between males
and females, although
o males more frequently experience symptoms.
o Also can be present in an indirect hernia, where it is known as "Hernia of
Littre." Furthermore, it can be attached to the umbilicus, with the possibility of
local cysts, torsions of intestine around the intestinal stalk, leading to
obstruction, ischemia, and necrosis.
Symptoms
Approximately 98% of people afflicted with Meckel's diverticulum are asymptomatic. If
symptoms do occur, they typically appear before the age of two.
The most common presenting symptom is
 Intestinal obstruction, followed by
 Painless rectal bleeding,
 Volvulus and
 Intussusception. Occasionally,
 Meckel's diverticulitis may present with all the features of acute appendicitis. Also,
severe pain in the upper abdomen is experienced by the patient along with bloating
of the stomach region. At times, the symptoms are so painful such that they may
cause sleepless nights with extreme pain in the abdominal area.
 Rarely perforation and peritonitis.
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Meckel’s diverticulum presents more often as intestinal obstruction in India as against
the western context where it presents more often as painless massive bleeding. The
reason is that in Indian patients, ectopic gastric mucosa which causes the peptic
ulceration and bleeding is much less common.
Complications of Meckel’s diverticulum include

 Intestinal Obstruction due to bands or Intussusception or volvulus
 Inflammation
 Perforation of the peptic ulcer in the ileum
 Bleeding per rectum
Diagnosis
Most of the time in our country since the patient presents with intestinal obstruction, all that
is needed is to make a diagnosis of Meckel’s diverticulum is to suspect it in all young people
with small bowel obstruction.
 In case of small bowel obstruction, put in a naso-gastric tube, start intravenous fluids
and then refer to a pediatric surgeon or a general surgeon.
Complication of Indian Western

Meckel’s statistics statistics
Obstruction 87% 40%
Bleeding 5% 50%
 Note: If a child presents with painless moderate to severe

bleeding suspect Meckel’s bleeding and refer.
 A technetium-99m (99mTc) pertechnetate scan is the investigation
of choice to diagnose Meckel's diverticula when bleeding is the
presenting symptom. This is possible only in places where this
facility is available.
 This scan detects gastric mucosa; since approximately 20% of
Meckel's diverticula have ectopic gastric (stomach) cells contained
within them, this is displayed as a spot on the scan distant from the
stomach itself. Patients with these misplaced gastric cells may
experience peptic ulcers as a consequence. Other tests such as
 colonoscopy and screenings for
 bleeding disorders should be performed, and
 angiography can assist in determining the location and severity of
bleeding.
Treatment
Treatment is surgical, consisting of a resection of the affected portion of the bowel.
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Additional readings for Acute abdominal pain
We shall look at some conditions in detail -

Acute appendicitis
This is a disease of the young and most patients are below 25. The pain starts in the
epigastrium or around the umbilicus and after several hours moves to the right iliac fossa.
Vomiting and fever follow. There is usually some constipation.
On examination there is no distension of abdomen. However, there is muscle guarding and
some rigidity in the right iliac fossa. Rebound tenderness is present also but is confined
initially to the right iliac fossa.
Diagnosis depends on
 History of shifting pain
 Some form of gastrointestinal disturbance – loss of appetite, nausea, vomiting
 Guarding and rebound tenderness in the right iliac forsa
 Mild leucocytosis and fever
Appendicitis in the elderly may not cause enough guarding or rigidity and therefore there is
often a delay in diagnosis.
Appendicitis is uncommon before five years of age. In older children the constitutional
symptoms are greater.
Acute Salpingo-oophoritis
The pain is felt in the suprapubic region and in the iliac fossae in sexually active women. It
usually starts at or just after menstruation and is associated with some white discharge and
dysuria. Usually there is no muscle guarding or rigidity. On vaginal examination, movement
of the cervix is very painful.
Ruptured ovarian follicle (mittelschmerz/ mid-cycle pain)
The pain is felt as a sudden pelvic pain in young menstruating women around the mid-cycle
period. It is maximal at onset, movement is painful, lasts for a few hours to a couple of days.
There may be diffuse tenderness in the lower abdomen and nothing abnormal is noted on
ultrasound.
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Flow chart for right lower abdominal pain
Right lower abdominal pain
WBC Yes RBC Yes
Right pyelonephritis Urinalysis Right renal colic
Normal
Shift of pain + tenderness Acute appendicitis

McBurney’s point
No
Female sex?
Yes No
Consider: PID, ectopic pregnancy, ruptured Consider torted right testis

follicle, torted ovarian cyst.
If diagnosis unclear may need ultrasound,
or laparoscopy to differentiate
Consider – if longer history (>2 days)

- Crohn’s disease
- Appendix abscess
Ultrasound useful to differentiate.
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Acute non-specific mesenteric adenitis
This is a disease of children below six years of age. Unlike in appendicitis there is no
shifting pain and the pain tends to be around the umbilicus. Absence of guarding and rigidity
is another feature to distinguish it from appendicitis. Treatment of this condition is
conservative. A course of antibiotics( ampicillin, septran) may be given.
Acute cholecystitis
Most often this is a result of stones in the gall bladder. Though it is often said that this is
common in fat, fertile, females over forty, it occurs in both sexes and in different age groups.
Dyspeptic symptoms often precede an acute attack. The pain is precipitated because of the
stone blocking the neck of the gall bladder. Severe pain in the right hypochondrium that may
radiate to the back of the scapula may be present. The patient looks ill and guarding will be
present in the right hypochondrium.
If the stone shifts then drainage is re-established and the pain gradually subsides. If it does
not, then empyema of the gall bladder follows.
More and more surgeons prefer to operate in the acute phase itself and perform a
cholecystectomy. However, the patient needs to be referred early (within 48 hours) if
surgery has to be performed.
Acute Pancreatitis
Usually two causes of acute pancreatitis namely
1. Alcohol use and
2. Gall stone disease of the biliary tract account for 80% of all cases of acute
pancreatitis.
Clinically patients with acute pancreatitis may be as young as 70 or in the older age group
(60 and above). Alcohol is the likely cause in the young while gall stone disease is more
likely in the older age group. (The average intake of alcohol is usually 150gm per day for 5-7
years.
Presentation is with acute upper abdominal pain more in the epigastrium,vomiting or
retching, tachycardia, sometimes jaundice and hiccups. Cyanosis and shock can occur in
more severe cases. The pain in pancreatitis is referred to the back and the left loin and is
relieved by sitting up and forwards and made worse on lying down supric. Pancreatitis pain
is considered one of the most severe forms of abdominal pain.
On examination, tenderness is maximum just above the umbilicus. While there is no board
like rigidity, some guarding of the upper abdominal muscles may be felt. The left loin is also
tender on palpation on account of the tail of the pancreas. (Retroperitoneal bleeding will
produce Cullen’s sign.)
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The diagnosis is based on the following.
Blood Tests:
S. Amylase (2-12 hours later and peaks at 24 – 76 hours)
S. Amylase lacks sensitivity and specificity (20 – 60%) but is easy to do. However many
other conditions also increase S. Amylase. S. Lipase increases within 4-8 hours and peaks
at 24 hours. The sensitivity (90%) and the specificity (90%) are better than S. Amylase.
S. Trypsin levels are the most accurate but since it is difficult to do, it is not recommended.
Other tests:
PCV (Haemo concentration) and S. Calcium (Hypocalcaemia) should also be done.
Plain X-ray abdomen may show a gas filled duodenum secondary to ileus and is called “the
sentinel loop sign”.
Ultrasound is an acceptable form of study and can see the gall stones as well as edema of
the pancreas and peripancreatic fluid collection. However, in about 70% of patients the
pancreas is not visible because of bowel gas.
Raising the threshold to atleast three times the normal value can increase the specificity of
S. Amylase and Lipase.
CT: It is very important to accurately make a diagnosis of acute pancreatitis as the patient
can be spared a laparotomy. The treatment of acute pancreatitis is conservative and so
sometimes CT might be necessary to confirm a diagnosis of acute pancreatitis. The
pancreas can be seen as an edematous structure with loss of definition of its borders, loss of
peripancreatic fat, fluid collection or a psuedocyst formation.
Complications of acute pancreatitis include –
a) Hypovolemia and shock
b) Acute renal shutdown
c) A dynamic ileus with abdominal distension
d) Acute respiratory distress and cyanosis
e) Pancreatic neurosis and abscess formation (1-5%)
f) Psuedocyst formation occurs in 8% of cases
Treatment
a) Treat shock – give 6-8 litres / day
b) Though NG aspiration and nil by mouth will keep the patient comfortable.
c) Manage pain using Meperidine. Morphine should not be used. Pethidine or
Pentazocine are used alternatively.
d) Prevent hypocalcemia and hypomagnesemia
e) Broad spectrum antibiotic cover may be given.
f) Inj. Ranitidine may be given to keep the stomach pH close to neutral.
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It is possible that patients with acute pancreatitis need critical care specially if they have
been in shock; it is best to refer them after BP and pulse are steadied.
Morphine should not be used to treat the pain of acute pancreatitis as it causes a
spasm of the sphincter of Oddi.
Algorithm for management of Intestinal Obstruction
Is it simple or gangrenous  Continuous Pain?

 Tachycardia &
Fever?
 Rebound
tenderness?
 ↓ Hb ↑ WBC
 ↑ Blood urea
Gangrenous Simple
Surgery Adynamic Dynamic

Obstruction Exaggerated tinkling
(No bowel sounds) Bowel sounds
Check serum + K if low correct Conservative management

Septicemia in children (give
antibiotics)
Distension not settling, Distension

Pulse rate rising
Gastric aspirate ↑
Surgery
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INTUSSUCEPTION
Intussception is common in children under two years of age and most often occurs in infants
between 6-12 months of age.
Symptoms
 The onset is sudden and the child screams withdrawing the legs upwards. The colic
comes on every 10-20 minutes.
 Vomiting comes on later and so also distension.
 Passage of bright red blood with mucus has been called “red current jelly” stools.
On gentle palpation, a sausage shaped mass that contracts with every colic can be felt.
Rectally if the intussception has traveled far enough, the apex can be felt. Most often no
cause for this can be found in infants.
Causes
In older children and in adults, intussception often is directed because of a mechanical lead
point in the form of,
 Meckel’s diverticulum
 Intestinal polyp
 Intestinal lymphosarcoma
 Haemangeoma of the bowel
 Henoch – Schonlein purpura
Investigations
 A contrast enema should be performed if the diagnosis is suspected. However if

there has been perforation or gangrene, a contrast study is contra indicated.
 An ultrasound can also pick up the intussusception.
 A pincer shaped shadow is seen by barium contrast.
Treatment
The contrast enema can also be the time to effect hydrostatic reduction. The enema can
should be kept at three feet height above the child and reduction confirmed under
fluoroscopy. Since this reduction is best done with a standby surgeon, the GP is advised to
refer the patient with intussusception to a surgeon.
In older children and adults a hydrostatic reduction is not advised as it is likely that a cause
might be missed. It is best to advise surgery.
SIGMOID VOLVULUS
This is the most common form of volvulus and is responsible for eight percent of all intestinal
obstructions. This is particularly common in elderly persons and persons with neurological
condition. The narrow mesentry of the sigmoid mesocolon approximates the two limbs of
the sigmoid colon thereby favoring torsion.
Symptoms
Can present sub-acutely as chronic abdominal distension, constipation and abdominal
discomfort. However more often presents acutely with colicky lower abdominal pain,
massive distension, constipation and later on vomiting. A palpable mass may be present.
Shock and high fever, guarding and rigidity are indicative of sigmoid gangrene.
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Plain X-ray abdomen will show a grossly dilated sigmoid.
Grossly dilated sigmoid seen on

plain X-ray abdomen.
Barium enema will show an abrupt pointed cut off – so called “bird of prey” sign.
“Bird of Prey” sign in

Sigmoid volvulus
Contrast study
Treatment
Decompression of the sigmoid can be achieved by introduction of a stiff tube per rectum
(aided by endoscopy, where possible). If there has been gangrene or perforation, surgical
resection is indicated and the patient should be referred.
If conservative decompression fails, refer him for surgical decompression and corrective
surgery.
Twisted Ovarian Cyst
An ovarian cyst is usually asymptomatic. However 70% of women develop small to large
cysts. This is seen as an incidental finding on ultrasound.
However, an ovarian cyst is liable to the following complications-
a) Twisting or Torsion of the cyst

b) Haemorrhage within the cyst
c) Rupture of the ovarian cyst
d) Infection of the cyst
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Of these, twisting of the ovarian cyst is the most painful. Cysts larger than 4cms are more
likely to cause torsion. It is a little more common on the right side. It produces severe lower
abdominal colicky pain with vomiting.
Investigations
On palpation a cyst is often large enough to be palpable per abdomen. It can also be felt per
vagina and moving the cervix can be tender.
It needs to be differentiated from rupture of an ectopic pregnancy. This can be done as

follows –
a) A large palpable mass is likely to be an ovarian cyst
b) Ultrasound examination will show that the mass is connected with the ovary and
is cystic
c) Pregnancy test will be negative in a patient with twisted ovarian cyst.
A patient with a twisted ovarian cyst needs emergency surgery.
Additional readings for Neck swellings
DEFINITIONS
Anterior triangle of the neck: This is the part bounded by the anterior border of the sterno-
mastoid, lower border of the jaw and the midline. However, the structures under cover of the
sterno-mastoid may be considered to belong to
the anterior triangle, i.e. the jugular chain of
lymph nodes.
Submandibular triangle is that part of the anterior
triangle that is bounded by the digastric muscle
and the lower jaw.
Posterior triangle: Is that part of the neck

bounded by the anterior edge of the trapezius
muscle, posterior border of the sterno-mastoid
muscle and the clavicle.
Cystic Hygroma (Lymphatic cyst)
This is likely to present to the family practitioner who delivers babies or sees new born
children and infants.
This is a congenital malformation of the lymphatic system where there is a failure of the
connection of the peripheral lymphatics in the neck to the main lymphatic pathway. There is
a collection of many small and large lymphatic cysts which contain colorless lymph. For this
reason this swelling is brilliantly transilluminant.
The majority present at birth or soon afterwards and sometimes the size is massive and
causes disfigurement.
157
They usually occur in the posterior triangle but may communicate with similar swellings in
the axilla or in the retropharyngeal space, where
lymph node groups occur.
They can get infected and then can cause

reddening of the skin and can go onto septicemia.
They usually occupy the subcutaneous space but
may send ramifications into the deeper tissues
making surgery very tedious.
The treatment of this condition is surgery; there

may be a place for prophylactic penicillin if the
surgery is delayed and there is fear of re-
infection.
Prenatal ultrasound can often pick up this defect if

it large.
Sternomastoid tumor
Infarction of the middle segment of the sternomastoid

muscle in utero causes an area of swelling in the
muscle that can be felt at birth. This heals by fibrosis
and depending on the volume of infarction there is a
disability, often called “torticollis”. This consists of
flexion and lateral rotation of the head towards the
tumor. If the area of fibrosis is extensive then
physiotherapy should be instituted; often this is all that
is required. However if there is no improvement
surgery is required.
The role of the family practitioner is to recognize the

condition and institute physiotherapy as soon as
possible or refer to a pediatric surgeon.
Branchial cyst
This is usually the remnant of the second branchial cleft. Normally the second branchial arch
grows downwards and fuses with the 5th arch and the intervening clefts disappear. However
if the second cleft remnant persists then a cyst forms.
The characteristics of the cyst are as follows:
 Appears usually during adolescence or before 25 years of age.

 The position is usually at the junction of the upper third and the lower two thirds
of the sternomastoid muscle and is partly under cover of the anterior border of
that muscle.
 Is about 2-7 inches in length and lies obliquely with the long axis forwards and
downwards.
 Has some lymphoid tissue in the wall and so can get infected.
 Is not transilluminant but is fluctuant.
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 There are no related enlarged nodes and
if present they may indicate a cold
tuberculous abscess.
 Can be bilateral.
 Aspirate contains cholesterol crystals
which are characteristic under the
microscope; can use as diagnostic test.
 Ultrasound will confirm a cystic mass.
The management of this swelling is surgery which is a

fairly simple operation and can be done as a day care
operation.
Branchial fistula
There is yet another abnormality associated with the branchial cleft and that is the branchial
fistula. Here the second branchial cleft persists and opens to the surface usually at the
junction of the lower third and the upper two thirds of the sternomastoid at its anterior edge.
(The second branchial arch fuses incompletely with the 5th arch.)It discharges mucus and
pus every now and then when the tract becomes full of pus. The inner opening is found on
the anterior aspect of the posterior pillar of the tonsils in the oro-pharynx. However often the
upper end closes off and the condition should then be called branchial sinus.
This can be differentiated from a Tuberculous sinus by the fact that the latter often is situated
in the upper one third of the sternomastoid and will have associated lymphadenopathy.
The treatment of this condition is surgery, again a day care procedure. The parents should
be told that more than one incision may be needed for complete removal.
Ranula
A ranula is a transparent retention cyst in the floor of the mouth arising from the sublingual
salivary glands. Ranula means a small frog and the cyst is so-called because of a blue-grey,
dome-like swelling beneath the tongue, supposed resemblance to a small frog.
 The cyst enlarges slowly, and wraps itself around the free border of the mylo-hyoid
muscle, penetrating the deep structures of the floor of the mouth. (When it extends
into the submandibular space then it is called a plunging ranula)
 It is more common in neonates and children and potentially can cause respiratory
embarrassment if it gets infected.
 It is highly transilluminable.
 It may burst spontaneously, discharging its contents and collapsing, but almost
invariably recurring.
 Is bimanually palpable from one finger inside the floor of the mouth.
Treatment depends on size. Small ranulae are excised; larger ones are marsupialized, i.e.
de-roofed so that the cyst opens into the floor of the mouth.
FINE NEEDLE ASPIRATION CYTOLOGY
The “biopsy” till recently has been the only tool available for the clinician when tissue has to
be examined for a diagnosis to be made. Over the last two decades however, FNAC has
been used to make a diagnosis in both superficially and deeply located masses, the latter
159
being approached with radiological guidance. This technique originated in Sweden but has
since been very popular as a diagnostic test in the rest of the world. The designation “fine”
implied the use of a needle which is less than 1 mm in diameter.
Note: For the family medicine practitioner, the FNAC should be confined to the superficial
swellings especially lymph nodes.
ADVANTAGES
FNAC is
 Far less traumatic than a conventional biopsy, besides, it being a
 Rapid
 Safe and
 Inexpensive test.
 Its accuracy in many situations, when applied by experienced practitioners, can
approach that of histopathology in providing an unequivocal diagnosis.
INDICATIONS
To be suitable for FNAC the disease process must be localized and clearly defined by
clinical examination.
Sites which are most often aspirated are:
 Lymph nodes
 Thyroid
 Salivary gland tumors
 Breast
 Soft tissue swellings
 Abdominal tumors under radiological or ultrasound guided aspiration can be done.
ASPIRATION PROCEDURE
Equipment
Standard disposable needles, 27-22g. (0.6-0.7mm) which are 70-50mm long are generally
useful for most palpable lesions.
A standard disposable plastic syringe of 10-20 ml capacity made of rigid material is sufficient
to produce a good negative pressure.
Sterility
Simple skin disinfectant is adequate for superficial palpable lesions. Sedation and local
anesthesia is hardly required when 22-27g needles are used.
Aspiration Technique
 When aspirating better control of the needle is achieved by supporting the barrel of
the syringe with the free (left) hand. Near vertical approaches are less painful and
allow better appreciation of depth.
 The aspirating technique is basically simple and is illustrated in a stepwise manner in
Figure 1.
 To obtain the best yield of tissue, the needle showed should be moved back and
forth along the same track, while maintaining negative pressure.
 For aspiration of thyroid nodules suction need not be applied on the syringe, to avoid
too much blood in the sample. After aspiration, pressure should be applied over the
aspirated site to minimize haematoma formation.
Preparation of smear
Smearing Technique
The smearing technique is illustrated in Figure 2.
A “dry” aspirate, that which contains mainly tissue and little fluid or blood is best smeared
gently with the flat of a slide as shown in the figure.
A “wet” aspirate, that which contains fluid or blood, is smeared in two steps. The first step
uses a slide held at an angle which drags the cells to the middle of the slide, to get rid of
160
excessive fluid. The second step involves gently smearing of the cells with the flat of a slide,
as for the “dry’ aspirate.
Fixation of Smear
At least two smears in each case are fixed immediately (while wet) in 95% ethyl alcohol or
PAP fixative (equal parts of rectified spirit and ether) for 70 minutes. Immediate staining of
smears is done at the bed side by the Diff – Quick method on at least one slide. The
technician reads these smears, while wet, under the microscope and is able to inform the
doctor if the smears are adequate.
The other slides are air-dried and fixed in acetone free methanol for 70 minutes.
Staining of Smear
Air dried smears, fixed in Methanol 1 minute.
DQ Solution I - 5 dips (5 seconds)
DQ Solution II - 5 dips (5 seconds)
Distilled H2o - 5 dips (5 seconds)
After distilled H2O – These slides are examined under the microscope while wet.
Air Dried Smears

After the air dried smears are fixed in acetone free methyl alcohol for 70 minutes, the slides
are dried and stained by the MGG staining procedures.
May-Grunwald Stain … 5 mts
Giemsa Stain … 15 mts
Buffer Water … 15 mts
The smears are then air dried, cleared in Xylene for 5 minutes and mounted using Gum
Damar.
Wet Fixed Smears

After wet smears are fixed in 95% alcohol or PAP fixative (equal parts of rectified spirit and
ether) for. 70 minutes. Haematoxylin Eosin staining is done.
Haematoxyllin and Eosin Staining Procedure

i. Slides are washed in running tap water
ii. Dipped in staining jar containing Harris Haematoxylin: 15-20 seconds.
iii. Washed in running tap water
iv. Dipped once in 20% Ammonia water
vi. Washed in Distilled water
Smears are then air dried in xylene for 5 minutes and mounted using Gum Damar.
Dispatch of slides
After staining slides can then be packed in an appropriate manner to prevent breakage and
sent to relevant pathologist experienced in the field for interpretation.
FNA is not a substitute for conventional histopathology but a valuable complement to it. The
demand for FNA cytology has grown in our hospital as a result of requests in particular from
general surgeons, physicians, radiotherapists and otorhinolaryngeal surgeons. We are sure
161
that this technique will find a useful place in the peripheral hospital too, just as exfoliative
cytology has done.
Additional readings for Management of chronic leg ulcers
Introduction
About one to two percent of the population get leg ulcers. Caring for these patients is a
significant part of the workload of primary health care professionals. Recurrence rates are
high, so any management plan must include a strategy to tackle prevention.
A number of pathological conditions are associated with lower limb ulceration, some acting
through more than one mechanism.
Definitions
 A chronic leg ulcer is defined as an area of breakdown in the skin on the lower limb,
of four weeks duration or more.
 Acutely inflamed ulcers have an outer rim of cellulitis.
Causes
While the underlying problem is usually
 vascular in western countries,
 trauma and infections are more common in India.
1. Principal Causes
 Chronic venous hypertension, usually due to incompetent valves in deep and
perforating veins.
 Arterial disease e.g. atherosclerotic occlusions of large vessels leading to tissue
ischaemia.
 Combined chronic venous hypertension, arterial disease
162
2. More unusual causes (10% in total)
 Neuropathy e.g. associated with diabetes mellitus, spina bifida, leprosy
 Vasculitis e.g. associated with Rheumatoid arthritis, SLE, polyarteritis nodosa
 Malignancy e.g. squamous cell carcinoma, melanoma, basal cell carcinoma,
Kaposi’s sarcoma, Marjolin’s ulcer
 Infection e.g. tuberculosis, leprosy, syphilis, fungal infections.
 Blood disorders e.g. sickle cell disease, polycythemia, thalassemia
 Metabolic disorder e.g. Pyoderma gangrenosum, pretibial myxedema.
 Lymphedema
 Trauma e.g. laceration, burns, irradiation injuries.
 Iatrogenic e.g. over-tight bandaging , ill-fitting plaster cast
 Self inflicted
 Tropical ulcer
SPECIFIC CONDITIONS (contd.)
4. Traumatic Ulcers
Where there is an underlying vascular problem, minor trauma can lead to an intractable
ulcer. In this case, the minor traumatic event, which could be a minor knock to the leg or an
insect bite, is merely a final trigger leading to tissue breakdown.
In people who do not have an underlying vascular problem, more major trauma can lead to a
period of ulceration. The skin overlying the tibia and around the malleolus is poorly
vascularised even in healthy people and traumatic lacerations in these areas can take a long
time to heal, especially if there is tissue loss or care is not taken to remove contaminating
debris or haematoma.
Treatment- Rest and encasing the limb in POP cast might often be necessary in managing
intractable ulcers.
5. Vasculitic Ulcers
Some factors of particular relevance to ulcer healing in Rheumatoid Arthritis (RA) are
considered here.
 Deformity and disability in these patients increase the risk of traumatic injury.
 Many patients are on high dose steroid therapy which can have cutaneous effects,
making the skin more susceptible to trauma and impairing some aspects of healing.
 Malnutrition is a common problem for people with RA who may have a poor appetite,
thereby delaying wound healing.
 Vasculitis can lead to local ischaemia which impairs healing.
 Edema may become an intractable problem for the people with coexisting peripheral
vascular disease who cannot tolerate limb elevation.
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Management
a) Regular ankle and foot exercises are important as with venous ulcers.
b) Attention should be paid to reducing pressure over heels and to preventing even the most
minor traumatic injuries.
c) The skin should be kept supple and the cracks treated
with emollients.
d) Special foot wear may be required.
e) The success rate for skin grafting is poor.
6. Tropical Ulcers
These ulcers were common in the tropics, but as living standards rise their incidence has
decreased.
 Start as small infected cuts from the sharp grasses (which explain their distribution
anteriorly on the leg, becoming more lateral lower down).
 Some consider them as primarily infective (which would explain why they sometimes
occur in epidemics in the wet season).
 Tropical ulcers develop through three stages.
Stage-1 A pustule or neglected cut, containing
Vincent’s and fusiformis organisms (both are pencillin sensitive). This stage is not seen in
the hospital.
Stage-2 Progress to form an acutely painful ulcer with raised, thickened and slightly
undermined edge. This ulcer grows rapidly for several weeks. A bloody discharge covers the
grey slough on its floor, skin around is dark and swollen. Bone, muscle and tendon
occasionally lie exposed in its base. After about a month, ulcer either improves and heals or
goes on to next stage.
Stage-7 It becomes a chronic ulcer and resembles any other long standing indolent
ulcer. Osteomyelitis is rare, but a reactive periostitis may raise the ulcer above the skin.
Sometimes its edge is thickened and everted and resembles a carcinoma.
Treatment
In stage-2 i) When an ulcer is <6cm, antibiotics in the penicillin group and moist dressings
will help to cure it. The ulcer should be cleaned thoroughly. And dressings should be
changed every day. If granulations are abundant, then scrape the base of the ulcer with a
scalpel. Scraping reduces the fibrosis under the graft later and so makes it more stable.
ii) If larger than 6 cm, then the epithelium from its edges will take a long time to grow across
it, and ulcer needs grafting. Most grafting should be done at the acute or sub acute stage.
Stage-7 Split skin grafts do not take well on long standing fibrotic ulcers or they may take
initially and breakdown later. Ideally they need a muscle or myocutaneous flap.
Chronic ulcers cause longstanding morbidity and become malignant in which case it may be
advisable to refer the patient.
7. Malignant Ulcers
A small proportion of leg ulcers are of malignant origin. Squamous cell carcinoma (SCC) and
basal cell carcinoma (BCC) are the most frequent cause of leg ulceration due to neoplasm.
Occasionally malignant melanomas are also found. Inguinal lymphadenopathy may indicate
metastatic spread of neoplasm.
Rarely squamous cell carcinoma develops in burn scars, non-healing venous ulcers,
osteomyelitic sinuses and other scar tissues and is recognized by proliferative changes at
the ulcer margin. These are known as “Marjolin’s ulcer”.
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Treatment
A biopsy is indicated in all chronic ulcers failing to respond to treatment and having
proliferative nature at their margins. When confirmed, wide excision with a margin of normal
tissue should be done.
Infiltrated lymph nodes in SCC are treated with radiotherapy or sometimes block dissection.
Marjolin’s Ulcer (squamous cell carcinoma developing in a long standing burn scar)
PATIENT ASSESSMENT GUIDELINES

Assessment of patients presenting with lower limb ulceration
It is essential that an accurate assessment of the cause and contributory factors of the ulcer
is determined before the onset of treatment.
Clinical history for the record RATIONALE

Patient Details Incidence of leg ulceration increases with
age. Male/Female ratio 1:2
Age/Sex
Diabetes Diabetic patients are at risk of large and
small vessel disease
Rheumatoid Arthritis May develop vasculitis which causes
Connective Tissue Disease occlusion of small vessels leading to tissue
ischaemic.
Trauma May be the primary causative factor with or

without an underlying disease process.
Smoking Risk factor of arterial disease.
Current Medication May be an indicator of current medical
status. Steroids and cytotoxic drugs delay
healing
History of exposure For syphilitic ulcers
History of neurological symptoms, spine Seen in spina bifida, Tabes dorsalis
surgery
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Vascular history for the record RATIONALE
History of D.V.T/Phlebitis/Varicose Indicative of venous disease.
veins/previous leg ulceration.
Intermittent claudication Indicative of arterial disease, of limited
value in immobile patients.
Night Cramps Calf cramps are common in chronic

venous insufficiency.
Rest pain in lower leg Indicative of advanced arterial disease.

Ischaemic heart disease Arterial disease affects all arterial systems.
Hypertension. CVA
Previous venous surgery Indicative of venous disease.
Examination of Lower Limb

Palpable pulses alone are not always an accurate indication of arterial status.
RECORD RATIONALE
Oedema All signs of chronic venous insufficiency
Brown pigmentation, purple/red
Eczema/Dermatitis
Presence of lipodermatosclerosis
Ankle flare
Atrophie blanche
Assess mobility and degree of ankle Immobility, limited or fixed ankle joint will
movement affect efficiency of calf pump.
Palpable pulses. Not always an accurate indicator of arterial
status.
Tissue necrosis fore foot or toes Indicative of arterial disease.
Decreased temperature
Hair loss
Buerger’s test positive
Sensory impairment Diabetic ulcers have decreased vibration
sensation. The temperature and pain
sensations are initially lost in leprosy.
Hypo pigmented anaesthetic patches and Indicative of leprosy.
enlarged peripheral nerves with or without
nerve palsy.
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INITIAL WOUND ASSESSMENT A non-healing or atypical leg ulcer should be
considered for biopsy.
RECORD RATIONALE
Measurement of Ulcer Area Serial measurement of the ulcer is useful
for monitoring healing.
Ulcer Depth May indicate arterial insufficiency.
(i) Superficial – skin loss only
(ii) Deep- subcutaneous tissue
(iii) Underlying structures i.e.
tendon deep fascia, bone
Ulcer edge Generally an unreliable determinate of
ulcer etiology.
Flat sloping edge Often these ulcers are venous and skin
around the ulcer is red –blue (due to
haemosiderin deposition)
Often seen in neuropathic (diabetes,
Punched out edge syphilis, etc), arterial and vasculitic ulcers.
Seen in tuberculosis.
Seen in squamous cell carcinoma.
Classically seen in basal cell carcinoma.
Undermined edge An atypical leg ulcer should be considered
for biopsy.
Everted edge
Rolled edge
Ulcer Base Aid to choice of dressing and indicator of

Epithelialization progress.
Granulation
Slough
Eschar
Level of exudates Will influence dressing choice and
Minimal/moderate/high frequency of dressing change
Odour May indicate colonization.

Site of ulcer Venous ulcers are usually confined to the
Gaiter gaiter area.
Fore foot or heel May indicate ischemia or diabetes.
Pain To relieve distress and aid compliance with
Assess level, frequency and duration of treatment. Vasculitic and arterial ulcers are
pain. extremely painful.
Position Venous ulcers are seen in ‘Gaiter’ area.
Vasculitic and neuropathic ulcers are
common on the food.
Temperature Limb is cold in arterial disease.
Warmth indicates active infection/cellulites.
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Laboratory Investigations
 There is no routine bacteriological swabbing of venous ulcers.

 All patients with leg ulceration should have a fasting blood glucose recorded to
exclude diabetes.
RECORD RATIONALE
Full Blood Count (FBC) Anemia may delay healing. Sickle cell
disease may present as ulceration.
Urea and Electrolytes Patients in renal failure have an increased
risk of arterial disease.
Glucose To exclude diabetes.
Auto-immune Screen If rheumatoid or other connective tissue
disorders are suspected.
Wound Swab Not done routinely. All chronic wounds
colonized by bacteria. Swab only if clinical
signs of infection present, delayed healing
or rapid development or breakdown of
ulcer.
X-ray For perforating ulcers to assess degree of
involvement.
Specific test for syphilis To rule out syphilis
Note: Other blood and biochemical investigations will depend on the patient’s clinical history
and local protocols.
Measurement of Ankle Brachial Pressure Index (ABPI) is the most reliable way to
detect arterial insufficiency
RECORD RATIONALE
Locate by palpitation and Doppler the To confirm presence/absence of arterial
dorsalis pedis and posterior tibial pulses at disease.
the ankle.
Record Systolic Pressures on two foot Not reliable in patients with diabetes and
pulses and calculate the ABPI other processes where calcification of the
vessels may be present.
Additional readings for Groin & abdominal wall swellings
Definitions
HERNIA is a protrusion of an organ through its containing wall.

While hernia can refer to protrusion of a muscle through its fascia and brain through the
foramen magnum, we are confined to the discussion of abdominal herniae.
STRANGULATED HERNIA when the blood supply to the contents of a hernia is cut off, it is
termed strangulated.
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INCARCERATED when the hernia becomes irreducible and bowel is not obstructed or
strangulated, it is termed incarcerated.
ANATOMY: The inguinal region encompasses two distinct areas:
 The inguinal canal

 The femoral triangle
The inguinal canal:-
The canal is simply the medial half of the thickened lower free edge of the external oblique
aponeurosis (also called the inguinal ligament) which curls back on itself to form a ‘U’
shaped gutter called the inguinal canal. The canal contains the spermatic cord in the male
and the round ligament in the female.
Deep to the external oblique aponeurosis are the lowermost fibres of the internal oblique
muscle arising from the lateral third of the inguinal ligament. They run medially in an arch,
convex upwards to the edge of the rectus abdominis where they join the aponeurosis of the
transverses abdominis muscle to form the rectus sheath. At this point the united
aponeurosis is called “the conjoint tendon”.
The half-moon gap beneath the arch of the internal oblique muscle is the weak spot and is
covered by a derivative from the transverses muscle called the transversalis fascia. The
inferior epigastric artery runs upwards and medially towards the rectus sheath. There is
entry of the vas deferens and testicular vessels just lateral to the inferior epigastric artery
through an opening called the internal ring. Indirect inguinal hernia passes through the ring
and through the inguinal canal and emerges through the external ring. Direct hernia just
pushes the transversalis fascia medial to the artery.
As the vas deferens enters the deep inguinal ring it is invested by a covering from the
transversalis fascia and is called the internal spermatic fascia. It collects another covering
from the internal oblique and is called the cremasteric fascia and finally it gets a coating of
external spermatic fascia from the external oblique.
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Anatomy of the inguinal hernia
Deep inguinal canal
Femoral nerve
Femoral artery
Femoral vein
Pubic tubercle
Superficial ring
Indirect inguinal hernia
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The femoral triangle:-
This region is conceptually simpler than the inguinal canal. Its borders are as follows – the
inguinal ligament (superior); medial border of the adductor muscle (medial) the medial
border of the Sartorius muscle (lateral); Iliopsoas and pectineus and the long adductor
muscle (floor).
The major feature of this triangle is the femoral sheath, which is a condensation of the deep
fascia and contains from lateral to medial, the femoral artery, femoral vein and the femoral
canal. The femoral canal is the space medial to the vein and contains the lymph node of
Cloquet. Other features of the femoral triangle include the femoral nerve lateral to the sheath
and the great saphenous vein, which passes through a hole in the deep fascia (saphenous
opening) to join the femoral vein.
Umbilical Anatomy:-
The umbilical cicatrix represents the following structures that normally close and cicatrizes –
1. Umbilical vein
2. Two hypogastric arteries
3. Allantois which forms the bladder
4. Omphalo mesenteric duct, which is connected to the ileum
THE HERNIAS –
Two generic features of all hernias are that they

 Have an expansile impulse on coughing
 Are reducible
Following are the common herniae –
(1) Inguinal - Direct

Indirect
 Congenital
 Acquired
(2) Umbilical - True umbilical as in infants
Paraumbilical as in adult women
7) Epigastric
(4) Femoral
(5) Incisional hernia
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Common Hernia
Epigast
ric
Umbilic
al
Incision
al
Inguinal
Femor
al
The following are the uncommon herniae. They are worth remembering because some day
you might diagnose one and save a life –
 Spigelian
 Obturator
 Lumbar
 Gluteal
Uncommon Hernia
Lumbar
Spigelian
Gluteal
Obturator
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Inguinal Hernia –
The indirect inguinal hernia is most common in the young and occurs in a preformed sac that
travels through the deep inguinal ring, inguinal canal and the external ring. Males are more
affected than females. A little manipulation is often required for its reduction and after
reduction, it tends to reappear gradually. It is best seen with the patient standing up and
coughing. Depending on the degree of patency of the processes vaginalis the indirect
inguinal hernia can be divided into-
 Bubonocoele- Where the sac is patent just beyond the internal ring.
 Funicular type –
In the funicular type the sac is patent right down to the testis. This is the commonest
form of adult hernia.
 Complete type (Congenital type):

This is where the procession vaginalis is completely patent and is often the case in young
children.
Direct inguinal hernia:
This comes through the weak posterior wall of the triangular area called the Hasselbach’s
triangle bounded by the inguinal ligament, inferior epigastric artery and the border of the
rectus abdominis. It does not come through the internal ring and it has a wide “mouth”.
Therefore the chances of strangulation and irreducibility are much less than in an indirect
inguinal hernia. Direct hernia is very rarely seen in women and usually affects older men. It
pops out quickly on standing and disappears as rapidly when lying down.
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ANATOMY OF THE COMPLICATIONS OF HERNIA
A B
(A) Neck of Sac. This tight ring

of peritoneum is usually the site
of any strangulation.
(B) A strangulated hernia. The blood supply of the

contents of the hernia is cut off. When a loop of
gut is strangulated there will also be intestinal
obstruction.
C D
(C) A strangulated hernia. If the sac is (D) When two adjacent loops of
small, a knuckle of bowel can be bowel are in the sac, the intervening
caught in the sac and strangled without portion in the abdomen is the first to
causing intestinal obstruction. This is suffer if the neck of the sac is tight,
called a Richter’s hernia. because it is the centre of the whole
loop involved. Thus the strangulated
piece is intra-abdominal. This is a
rare variety of strangulation. It is
called a Maydl’s hernia
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E F
(E) Sliding hernia. If bowel which is

normally extra peritoneal forms one side
of the sac, it is thought to have slid down (F) Incarceration: the contents
the canal pulling peritoneum with it, are fixed in the sac because of
hence the name hernia-en-glissade. The their size or adhesions. The
sac can contain other loops of bowel, hernia is irreducible but the
and the gut forming the wall of the sac bowel is not strangulated or
can be strangled by the external ring. obstructed.
G H
(G) Reduction-en-masse. It is possible to push a hernia back through the abdominal

wall, so apparently reducing it, without actually pushing the contents out of the sac. If
they were strangulated in the first position they will still be strangulated in the second.
(H) Never push hard when trying to reduce a hernia.
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FEMORAL HERNIA
A femoral hernia occurs through the femoral canal. Sometimes only the extra peritoneal fat
and the peritoneum herniate but often the bowel also gets herniated as the canal expands.
This is more common in females and is more common on the right side. It may be bilateral
in 20% of cases. It may remain asymptomatic for a long time and then suddenly present
with signs of obstruction or strangulation. At other times the patient may present with a
dragging abdominal pain.
Note: In all patients with abdominal pain, the groin should always be examined for a hernia
Femoral hernia is notorious for producing a Richter’s hernia – wherein only one
circumference of the bowel becomes devascularized because of pressure. Therefore signs
of intestinal obstruction will be delayed and then present with perforation and peritonitis.
The reason strangulation is more common in femoral hernia is because on three sides of
the femoral canal there is either bone or a ligament thereby giving no room for expansion.
Differential diagnosis:
I. Femoral hernia can be differentiated from an inguinal hernia as follows:
 Femoral hernia when it is traced backwards originates lateral to the pubic tubercle,
while an inguinal hernia traverses medial to it.
 Invaginate the inguinal canal by introducing the little finger through the external ring; it
will be seen that in femoral hernia, this is empty.
 Femoral hernia is ten times more likely to be irreducible than an inguinal hernia.
II. Femoral hernia can be distinguished from Saphena Varix (varicosity of the sapheno femoral junction
area) as follows –
 A Saphena Varix has a bluish tinge
 Associated with the varicosity of the long saphenous vein
 Saphena Varix quickly reduces and quickly pops out. However, a femoral hernia is
often irreducible and if it is not, then it reduces with some manipulation.
a) A thrill can be felt in the long saphenous vein when the Saphena Varix is percussed.
III. Femoral hernia can be distinguished from inguinal lymph nodes very easily as there is
no cough impulse and reducibility in the latter.
Besides the lymph nodes are situated along the inguinal ligament, are nodular and often
very mobile.
UMBILICAL LESIONS
The umbilicus is an inverted cicatrized button placed equidistant from the xiphisternum and
the pubic symphysis. If it is displaced upwards or downwards, it indicates that, there is a
tumour or a cyst in the lower or upper abdomen respectively.
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Umbilical Granuloma –
Often a neonate is brought to the doctor for a pale red protuberance in the umbilicus that
discharges. Usually this disappears with two or three applications of silver nitrate. This is
called an umbilical granuloma. If it does not disappear after this, the child may be referred
to a pediatric surgeon, for this may turn out to be a patent Vitello – intestinal duct remnant
and may need surgery.
Other lesions of the umbilicus –

Omphalitis – Among poorer communities where deliveries are not conducted with aseptic
measures, there are increased chances of the umbilical region of the newborn to get
infected. When this happens, serious consequences may follow such as septicaemia
(spreading through the umbilical vein) jaundice and death. Therefore, umbilical sepsis
should be treated with a course of injection Gentamycin 5 mg / kg in 7 or 4 divided doses.
Sometimes by the time the child is brought to you an abscess of the abdominal wall may
already have formed. This abscess should be drained forth with and antibiotics given as
above.
Discharges from the umbilicus –
 Urine discharge – When the urachus is patent, the bladder contents discharge in
small amount through the umbilicus. This needs to be referred for surgical
correction.
 Fecal discharge –
When the omphalo mesenteric duct is fully patent, contents of the ileum will leak
through the umbilicus. This also needs surgical referral.
 Mucus discharge-
A mucus discharge from the umbilicus could indicate that the umbilical end of the
omphalo mesenteric duct is patent while the intestinal end is closed. This mucus
membrane in the umbilicus is sometimes called an umbilical adenoma and should
be differentiated from an umbilical granuloma. The latter will disappear with silver
nitrate stick cauterization while the mucus membrane (umbilical adenoma) will keep
discharging. The latter condition needs surgical referral.
Umbilical Fistulae
A patent vitello intestinal duct

discharge: intestinal contents
A patent urachus discharge:

Urine
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Abdominal Cysts Related to Umbilical Development
A vitello intestinal
duct cyst
A urachal cyst
Congenital umbilical hernia

This comes right through the umbilicus and the umbilical scar is at the centre of it. In the
neck of the sac, the umbilical ring can be felt all round being continuous with the linea alba.
Features of a Congenital Umbilical Hernia –

Usually the defect is 1-2cms and there is a soft round swelling, which has an impulse on
crying and is reducible.
Note: This is a very common problem in our country. No treatment is required and the
defect will close before the child is two years of age. Hypothyroidism however, should
always be ruled out.
In children with hypothyroidism, umbilical hernia is often present and so thyroid function
tests (T4 and TSH) may be ordered if there is any clinical suspicion.
Indications for referral to a surgeon are-
a) When the defect is more than two cms

b) When the hernia becomes irreducible. The parents must be told that this
complication is rarely possible and at any time, if the swelling does not reduce,
they must report to a surgeon.
c) When the hernia is still present after two years of age.
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Para umbilical Hernia-
This is a herniation of abdominal contents through an opening in the linea alba just above
the umbilicus. Therefore, the hernia is covered by the umbilicus at its base while the rest of
it is covered by skin above it.
This is common in obese women above 40 and there are chances of strangulation.
Therefore surgery is advised, in all cases.
This condition must be distinguished from an “unfolding of the umbilicus” that occurs in
ascites or in tumours that distend the abdomen. In this condition the umbilical cicatrix is
stretched. There is no cough impulse and there is no swelling that can be reduced.
Epigastric Hernia
An epigastric hernia, sometimes called the fatty hernia of linea alba can often be seen if the
patient is thin. It mostly contains fat and no bowel but because they often have symptoms
of abdominal pain, can be mistaken for the pain of an ulcer. However if you slide your
forefinger from the Xiphisternum to the umbilicus a small “button” like swelling will be
palpable.
If the symptoms are significant, surgery may be advised.
Incisional Hernia
This is also called a “Ventral hernia” and occurs in people who have had an abdominal
operation. There may or may not be history of abdominal dehiscence or history of wound
infection.
The hernia will depend on the size or the length of the incision and the degree to which it
has not healed. If the defect is very narrow say the size of two finger tips chances of
strangulation are high. Conversely, if the incision admits the whole hand the risk of
strangulation is much less.
If the swelling is not obvious, it can be made to pop out by raising the head and the legs
with the patient lying supine.
Surgery is necessary for all small incisional hernias and it may be necessary to operate on
the large ones too for cosmetic reasons. Therefore, patients with incisional hernias can all
have a surgical opinion.
Spigelian Hernia
It occurs through the linea semilunaris, 4cms above the inguinal ligament. It is reducible
and seldom causes symptoms. However occasionally, the patient has symptoms of
intestinal obstruction, because of strangulation of a loop of bowel. In the latter case, the
patient will present with a tender mass which is irreducible.
This should be differentiated from a haematoma of the inferior epigastric artery as it occurs
in almost the same place. In spigelian hernia when it becomes irreducible, symptoms of
intestinal obstruction will be present.
Note: Malgaigne’s bulges are seen in old individuals with poor musculature. They are
diffuse swellings of the lower abdomen and are found on both sides.
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Undescended Testis:-
The way undescended testis can be differentiated from other groin swellings-
1. The hemiscrotum on that side will be hypoplastic and testis will not be
palpable, in the scrotum.
2. If there is a cough impulse then there is an associated hernia.
3. An ultrasound can locate this testis.
Saphena Varix is a dilatation at the top of the long saphenous vein due to valvular
incompetence. It may reach the size of a golf ball or even larger. It is a soft bluish
reducible swelling and associated with varicosities of the rest of the saphenous vein.
Saphena Varix
Tapping the saphenous vein will transmit a thrill to the Saphena Varix. This along with the
bluish color and its quick reducibility will differentiate it from a femoral hernia. This is
treated surgically with high saphenous ligation.
Lymph nodes of the Groin –
The superficial groin lymphnodes are arranged like a T. The horizontal group is
below and parallel to the inguinal ligament and the vertical group is along the femoral
vessels. Both groups should be palpated on each side and their enlargement can be
because of infection or tumour in the following drainage area-
 Leg and the toes (including the web spaces)

 Perianal region
 Genitalia including the prepuce
 Abdominal wall (lower part)
 Buttocks
It must be remembered that the inguinal nodes are normally palpable but never more than 1
cm in size.
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VARICOCOELE:-
A varicocoele is a dilatation and tortuosity of the pampiniform plexus and the internal
spermatic vein. Is a common occurrence and 15% of all males but 40% of infertile males
are affected.
There is a relationship between semen quality and varicocoele. It is thought that a
varicocoele interferes with the quality of semen through alteration in the thermoregulatory
process of the testes. This is in turn due to back flow of blood from the renal vein into the
testicular vein.
The semen may have the following abnormalities:-

 Sperm count can be low but rarely can produce azoospermia.
 The percentage of motile sperms may go down.
 The percentage of morphological abnormal sperms may go up.
 The testes may undergo a little atrophy in the long term.
Etiology:-
 More common on the left side probably because of the angle at which the left
testicular vein enters the renal vein
 The lack of anti-reflux valves at the junction of the left testicular vein and renal vein.
One-sided varicocoele can affect the spermatogenesis on both sides.
Varicocele
Clinically they may present as follows:-
 Routine evaluation of an infertile couple.

 Dragging pain in the scrotum
Varicocoeles can vary in size and can be classified into these 7 groups –
Large Varicocoele that is obvious on inspection.
Moderate Varicocoele that is palpated as a “bag of worms” with the patient standing.
181
Small Varicocoele that is palpable only on raised abdominal pressure.
A high resolution color Doppler ultrasonography is the gold standard for diagnosis. In any
infertile couple, if the semen quality is not optimal, varicocelectomy must be advised and
should be referred to a surgeon.
A transinguinal approach is best and using optical magnification, visualize and ligate all
contributory veins. The improvement in semen quality may take 7-4 months after surgery.
Note: Presume torsion in a young man unless otherwise proved.
Torsion of the Testes
This usually occurs in a boy or a young man and has a sudden onset of severe pain in the
groin and scrotum. The spermatic cord may be thickened in the early stages and even
twists may be felt. The torsion is always away from the midline – that is the right testes
rotates clockwise and the left testes rotate in the anti – clockwise direction. The
corresponding side of the scrotum may become red.
Urine microscopy will help in differentiating it from an epididymo-orchitis. In the latter pus
cells will be found and on rectal examination, the prostate will be tender. Another way of
differentiating between epididymo-orchitis and torsion is to do Doppler ultrasound. Venous
blockade can often be picked up in torsion of the testes on an ultrasound.
However if doubts exist, then the patient should be referred to a surgeon for immediate
exploration. One cannot assume that it is epididymo-orchitis without enough evidence, as it
may be possible to salvage the testes in the case of torsion of the testes.
Epididymo-orchitis – This can occur in a patient who has urinary infection or arthritis or
prostatis. Blood borne infection also can occur. The treatment is with broad-spectrum
antibiotics and elevation of the scrotum when the patient is lying down.
The spread to the epididymis may be secondary to a venereal infection and so the spouse
should also be examined.
Testicular tumours – risk factors
Although testicular cancer accounts for 1% of all cancers in men, it is the most common
form of cancer in young men 15 to 40 years old. Although the exact cause of testicular
cancer is unknown, several factors seem to increase risk.
o Undescended testicle(s),
o Klinefelter's syndrome (a sex chromosome disorder characterized by low levels
of male hormones, sterility, development of breasts, and small testes).
o Exposure to certain chemicals and
o Infection with the human immunodeficiency virus (HIV).
o A family history of testicular cancer may increase risk. White American men
have about five times the risk of African-American men and more than twice
the risk of Asian men.
182
Testicular cancers may be classified as follows:
 Seminomas account for about 70-40% of all testicular tumors. These are usually
found in men in their 70s and 40s. The condition is usually localized to the testes,
although in about 25% of cases it spreads to lymph nodes.
 Non-seminomas account for 60% of all testicular tumors; subcategories of these
tumors are listed below. Non-seminoma tumors often contain more than one of the
following cell types:
o Embryonal carcinoma (about 20% of testicular cancers) occurs in 20-70 year
olds and is highly malignant. It grows rapidly and spreads to the lung and
liver.
o Yolk sac tumor (about 60% of all testicular cancers in young boys).
o Teratomata (about 7% of testicular cancers in adult men and 40% in young boys).
o Choriocarcinoma (rare).
Symptoms:
Note: There may be no symptoms in some individuals - while in others, there may be:
o Dull ache in the back or lower abdomen

o Gynecomastia (excessive development of male breast tissue), this can also
occur normally in adolescent males, in whom it is not a symptom of testicular
cancer.
o Testicular discomfort/pain or a feeling of heaviness in the scrotum
o Occasionally, the initial symptoms are related to the spread of the cancer to
other parts of the body, such as the lungs, abdomen, pelvis, or brain.
Signs and tests
A physical examination typically reveals a firm, non-tender testicular mass that does not
"trans-illuminate". Other tests include:
 Scrotal ultrasound used to confirm solid mass.

 Blood tests for tumor markers: alpha-fetoprotein (AFP), human chorionic
gonadotrophin (beta HCG), and lactic dehydrogenase (LDH). Approximately 85% of
non-seminomas will have elevations of either AFP or beta HCG. Seminomas will
have elevations only in beta HCG or LDH. These tests can also be used to monitor
the response to treatment.
 A chest X-ray done to look for potential metastasis to the lungs.
Painless, non-transilluminant, unilateral enlargement of the testis – presume

malignancy unless otherwise proved.
 An abdominal CT scan may also be done to look for potential metastasis.
Differential diagnosis will include a haematocoele and tuberculous epididymo-orchitis. In a

haematocoele a history of severe trauma is present and the swelling comes on immediately
and then does not grow in size. Malignancy of the testes the patient may give a history of
gradual growth of the swelling.
183
In Tuberculous epididymis, there will be beading of the vas deferens and the seminal
vesicles will be enlarged and palpable.
Often the diagnosis may be in doubt and the best way out of it is to explore the testes
surgically.
Differences between Teratoma and Seminoma
Teratoma Seminoma
History Short Long
Age 2-7rd decade 4th decade
Spread Mainly vascular Mainly lymphatic
Consistency Solid and cystic Solid
Prognosis Good Very good
Therapy Radio-resistant Radio-sensitive
Treatment: Tissue biopsy is usually by orchidectomy.
Treatment depends on the type of tumor, the stage of the tumor, and the extent of the
disease. Most patients can be cured.
Histologically the cells can be seminoma or non-seminoma. If both types of seminoma and
non-seminoma cells are found in a single tumor, the tumor is treated as a non-seminoma.
The next step is to determine how far it has spread to other parts of the body to help in
"staging."
 In Stage I, the cancer has not spread beyond the testicle.

 In Stage II, the cancer has spread to the retroperitoneal lymph nodes in the
abdomen.
 In Stage III, the cancer has spread beyond the lymph nodes to the liver, lungs or
bones.
There are three types of treatment that can be used based on the staging:
1. Surgical treatment includes orchiectomy and removal of associated lymph nodes

(lymphadenectomy). This is usually performed in the case of both seminoma and
non-seminoma testicular tumors.
2. Radiation therapy using high-dose X-rays or other high-energy rays may be used
after surgery for patients with seminomas to prevent the tumor from recurring. The
use of radiation therapy is usually limited to the treatment of seminomas.
3. Chemotherapy -- using drugs such as cisplatinum, bleomycin, and etoposide, has
greatly enhanced the survival rate of both seminomas and non-seminomatous
testicular tumors.
The cure rate for Stage I seminoma tumor is over 95% and for Stage III is 90%.
184
The cure rate for a Stage I nonseminoma tumor is over 95% and Stage III is 70%.
Tuberculous Epididymo-Orchitis :
Clinical features
 Relatively painless swelling
 Epididymis involved more than the testes
 Beaded vas deferens
 Thickening of the seminal vesicle
 Scrotal skin – loss of rugosity and in later stages, a sinus which is adherent to the
testes may develop.
 Concomitant renal tuberculosis likely
Investigations
A chest X-ray may show active pulmonary tuberculosis.
An ultrasound may show renal involvement by tuberculosis.
An ESR should be done to monitor treatment.
Urine - 7-5 samples should be obtained to look for AFB. Urine-micro may also have
pus cells. However, on routine culture of the urine, no organisms will grow.
This is called “sterile” pyuria and is characteristic of tuberculosis.
If the diagnosis is in some doubt, fine needle aspiration may be done by the GP for a
diagnosis. This skill will have to be learnt. Often the fine needle aspiration is inconclusive;
then the patient should be referred to a surgeon for exploration.
Treatment
However if the diagnosis is definite, then chemotherapy may be started. If the lesion
continues to discharge through a sinus, then again orchiectomy should be done.
Hydrocoele:-
This is the commonest swelling of the scrotum in our country. Typically, the onset is
gradual and painless. It is transilluminant. Can get above the swelling and there is no
cough impulse. Testes cannot be felt separately and the cord structures are normal.
Usually no obvious cause is found and this is the commonest form of hydrocoele – also
called primary hydrocoele. Hydrocoele can be secondary to many other conditions such as
acute epididymo-orchitis, tuberculosis, and malignancy. These hydrocoele are called
secondary hydrocoeles. Secondary hydrocoeles are usually lax and not very big.
The best way to manage a primary hydrocoele is surgery. Aspiration is not recommended
as fluid may recollect afterwards and there is a danger of introducing infection. Another
advantage of surgery is that you can make sure that the testes and epididymis are normal
and there is no underlying tumours or tuberculosis, as would be the case in a secondary
hydrocoele.
If there is a transilluminant swelling attached to the testes and if the testes can be felt
separately, then the condition may be a cyst of the epididymis. The treatment of this
condition is to wait till the man has had children and then it can be excised.
185

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Updated & Edited in the year 2015 by:

Dr. Vinod Shah, Department of Distance Education, CMC, Vellore

Dr. Vinod Shah, Department of Distance Education, CMC, Vellore

Post Graduate Diploma in Family Medicine for recent MBBS

Towards multicompetence in Secondary Level Care

Activity 4.2 Lower GI bleeding - II 10 8

Activity 4.3 Lower GI bleeding - III 10 10

Activity 4.4 Lower GI bleeding - IV 10 12

Activity 4.5 Acute abdominal pain - I 10 14

Activity 4.6 Acute abdominal pain – II 10 17

Activity 4.7 Acute abdominal pain - III 10 19

Activity 4.8 Neck swellings - I 10 21

Activity 4.9 Neck swellings – II 10 23

Activity 4.10 Neck swellings - III 10 27

Activity 4.11 Leg ulcers - I 10 31

Activity 4.12 Leg ulcers – II 10 34

Activity 4.13 Groin & abdominal wall swellings - I 10 37

Activity 4.14 Groin & abdominal wall swellings - II 10 39

Additional readings 126-185

INSTRUCTION: The first common surgical problem we will study is Lower GI

ACTIVITY 4.1 [TIME: 10 MIN]

A 62-year-old man Kolandaivelu was admitted to the Emergency Room with

2. What investigations will you order?

3. What will you see or find in the investigations?

Diverticulosis, polyposis, angiodysplasias, ischemia, malignancy and ulcerative

2. What investigations will you order?

3. What will you see or find in the investigations?

INSTRUCTION: The next activity continues the learning on lower GI bleeding.

ACTIVITY 4.2 [TIME: 10 MIN]

1. What is the possible diagnosis?

2. How will you investigate him?

1. What is the possible diagnosis?

2. How will you investigate him?

INSTRUCTION: The next activity is another case of GI bleeding. Revise the

ACTIVITY 4.3 [TIME: 10 MIN]

1. What are the diagnostic possibilities?

2. What investigations would you do?

1. What are the diagnostic possibilities?

 Carcinoma colon/rectum is a strong possibility considering the age, the

2. What investigations would you do?

INSTRUCTION: Activity 7.4 is also a case of GI bleeding. Additional reading material

ACTIVITY 4.4 [TIME: 10 MIN]

1. What are the diagnosis possibilities?

2. How will you clinch the diagnosis?

1. What are the diagnosis possibilities?

2. How will you clinch the diagnosis?

The diagnosis can be clinched by

ACTIVITY 4.5 [TIME: 10 MIN]

a) What is the likely diagnosis? Give reasons.

What is one question you need to ask about the pain?

a) What is the diagnosis?

b) What important examination has been missed?

a) What is the diagnosis?

Acute intestinal obstruction

b) What important examination has been missed?

ACTIVITY 4.6 [TIME: 15 MIN]

1. Sunder a 55-year-old bank official comes to you with pain in the

What is your suspicion?

2. A 26-year-old coolie, Murugesh has been brought to you with severe

3. List the danger signals in a patient with acute abdominal pain.

1. What is your suspicion?

2. Suppose you were asked to diagnose Murugesh, what possibilities would