WBUHS SURGERY 1ST PAPER 2014

Group A
1. Classify shock. Discuss the pathophysiology and management of septic shock.
(3+6+6=15)
Introduction:
Shock is a systemic state of low tissue perfusion, which is inadequate for normal cellular
respiration.
Classification of shock:
Shock is classified into 5 groups based on the initiating mechanism:
1. Hypovolemic shock
2. Cardiogenic shock
3. Obstructive shock
4. Distributive shock
5. Endocrine shock.
Type Mechanism
Hypovolemic Hypovolemic shock is caused by a reduced circulating volume.
Ex.: Hemorrhage, Dehydration etc.
Cardiogenic Cardiogenic shock is due to primary failure of the heart to pump blood to the
tissues.
Ex.: MI, Cardiac arrhythmia, Valvular heart disease etc.
Obstructive In obstructive shock there is a reduction in preload because of mechanical
obstruction of cardiac filling.
Ex.: Cardiac tamponade, tension pneumothorax etc.
Distributive There is maldistribution of blood flow at a microvascular level and dysfunction
of the cellular utilisation of oxygen.
Inadequate organ perfusion is accompanied by vascular dilatation with
hypotension, low systemic vascular resistance, inadequate afterload and a
resulting abnormally high cardiac output.
Ex.: Septic shock, Neurogenic shock, Anaphylaxis etc.
Endocrine It is due to an endocrine abnormality.
Ex.: Hypo/hyper-thyroidism, Adrenal insufficiency etc.
Pathophysiology of septic shock:

Release of toxins/endotoxins from organisms like E.coli, Klebsiella, Pseudomonas and Proteus

Inflammation and cellular activation of macrophages, neutrophils and monocytes

Release of cytokines and free radicals

Chemotaxis of cells, endothelial injury, altered coagulation cascade - SIRS*

Reversible hyperdynamic warm stage of septic shock with fever, tachycardia, tachypnoea

Severe circulatory failure with MODS* (failure of lungs, liver, kidneys, heart) with DIC*

Irreversible hypodynamic cold stage of septic shock

[*SIRS: Systemic inflammatory response syndrome, MODS: Multi-organ dysfunction

syndrome, DIC: Disseminated intravascular coagulation]
Stages of Septic Shock:
1. Hyperdynamic (warm) shock:

 This stage is reversible stage. Patient is still having inflammatory response and so
presents with fever, tachycardia and tachypnea.
 Patient should be treated properly at this stage. Based on blood/ urine culture
(depending on the focus of infection), higher antibiotics like 3rd generation
cephalosporins, aminoglycosides, metronidazole are started.
 The underlying cause should be treated like draining the pus, laparotomy for
peritonitis etc.
 Ventilatory support with ICU monitoring may prevent the patient going towards
the next cold stage of sepsis.
2. Hypodynamic (cold) hypovolemic septic shock:
 Here inflammatory response is lost and patient is in decompensated shock.
 It is an irreversible stage along with MODS (Multi Organ Dysfunction Syndrome)
with anuria (renal failure), cyanosis (respiratory failure), jaundice (liver failure),
 pulmonary edema, hypoxia (lung dysfunction), cardiac depression, drowsiness;
eventually coma and death occurs.
Management of septic shock:
A. Airway:
Airway is to be protected by suction, intubation if required.
B. Breathing:
 Oxygen
 Ventilatory support: Non-invasive/ invasive.
C. C1: Circulation:
Because vasodilation and decrease in total peripheral resistance may produce
hypotension in septic shock, fluid resuscitation and restoration of circulatory volume
with balanced salt solutions is essential.
C2: Cause:
IV antibiotics will be insufficient to adequately treat the infectious episode in the
presence of an infective focus. So treat the focus of infection first. Ex:
 Drainage of an abscess;
 Laparotomy for peritonitis;
 Resection of gangrenous bowel;
 Wound excision.
D. Drugs:
 Antibiotics:
o Empirical antibiotics must be chosen carefully based on the most likely
pathogens (gram-negative rods, gram-positive cocci and anaerobes)
because the portal of entry of the offending organism and its identity may
not be evident until culture data return or imaging studies are completed.
o Antibiotics should be tailored to cover the responsible organisms once
culture data are available, and if appropriate, the spectrum of coverage
narrowed.
o Long-term, empiric, broad-spectrum antibiotic use should be minimized:
 To reduce the development of resistant organisms,
 To avoid the complications of fungal overgrowth,
 To prevent the development of antibiotic-associated colitis from
overgrowth of Clostridium difficile.
 Vasopressors:
o Vasopressors may be necessary to treat patients with septic shock.
 o Catecholamines (dobutamine/ dopamine/noradrenaline) are the most
often used vasopressors.
o Occasionally, patients with septic shock will develop arterial resistance to
catecholamines. Arginine vasopressin, a potent vasoconstrictor, is often
efficacious in this setting.
 Corticosteroids:
o Hydrocortisone therapy is not recommended as a routine adjuvant
therapy for septic shock.
o However, if SBP remains <90 mm Hg despite appropriate fluid and
vasopressor therapy, hydrocortisone at 200 mg/day for 7 days in 4 divided
doses or by continuous infusion should be considered.
Group B
2. Describe the clinical features, investigations and management of carcinoma of
stomach. (4+4+7= 15)
Clinical features:
Symptoms
Stage Common symptoms
1 (Early)  Indigestion
 Heartburn
 Loss of appetite
 Abdominal discomfort.
2 (Middle)  Fatigue
 Boating of the stomach, usually after meals.
3 (Late)  Upper abdominal pain
 Nausea and occasional vomiting*
 Diarrhoea/ constipation
 Weight loss
 Hematemesis/ melena (as the tumor bleeds frequently), which
may cause iron deficiency anemia
 Dysphagia (suggestive of a tumor at gastric cardia/ extension of
the tumor into esophagus).
[* Note: In case of pylorus involvement, symptoms of gastric outlet
obstruction may be seen, i.e., vomiting typically occurring after intake of
food, which is devoid of bile.]
 Signs
 Mass abdomen: Mass in pylorus lies above the umbilicus, nodular, hard, with
impaired resonance, mobile, moves with respiration, all border well made out.
 Features of gastric outlet obstruction may be evident i.e. +ve visible peristalsis,
+ve ausculto-percussion test, +ve succussion splash (to be checked with 4-6 hours
empty stomach).
 Along with jaundice, liver may be palpable with secondaries which are hard,
nodular with umbilication.
 Metastatic lymph nodes may be palpable, most notably in the left supraclavicular
fossa (Virchow’s node, Troisier’s sign).
 Secondaries in umbilicus, as Sister Mary Joseph’s nodules.
 Irish node (Left axillary lymph node secondaries).
 The localized gastric CA may induce a generalized hypercoagulable state in which
migratory thrombophlebitis occurs particularly in the extremities. This sign is
called Trousseau’s sign.
 Rectovesical secondaries (Blumer shelf) may be found on per rectal examination.

Investigations
General investigations:
1. Blood: Hb, TC, DC, ESR: May reveal anemia (microcytic hypochromic anemia of
iron deficiency) which may result from upper GI bleeding/ poor nutrition.
2. Renal function test: Na, K, Urea, Creatinine
3. Liver function test: Bilirubin (direct and indirect), albumin, ALT, AST: May reveal
hepatic dysfunction from liver metastasis; features of obstructive jaundice may
also be found (resulting from compression of CBD by enlarged hepatic nodes).
4. Coagulation studies: PT, aPTT, INR: Coagulation abnormalities may be found due
to liver metastasis.
5. Blood sugar: Fasting and postprandial.

Special investigations:
1. Carcinoembryonic antigen (CEA): It is positive in 45-50% of cases
2. Cancer antigen 19-9 (CA 19-9): It is positive in 20% of cases
3. Cancer antigen 72-4 (CA 72-4): It is used to evaluate relapse cases.
Imaging studies:
1. Esophagogastroduodenoscopy/ Upper GI endoscopy:
 It has a diagnostic accuracy of 95%. This relatively safe and simple
procedure provides a permanent color photographic record of the lesion.
 This procedure is also the primary method for obtaining a tissue diagnosis
of suspected lesions.
 Biopsy of any ulcerated lesion should include at least 6 specimens taken
from around the lesion because of variable malignant transformation.
2. Barium studies (Single/ double contrast):
These studies are only 75% accurate and should be used only when upper GI
endoscopy is not feasible.
Findings:
a. Irregular filling defect
b. Loss of rugosity
c. Delayed gastric emptying
d. Dilatation of stomach in CA pylorus
e. Decreased stomach capacity in diffuse CA stomach (linitis plastica)
f. Margin of the lesion projects outward from the ulcer / into the gastric lumen
– “Carmanns meniscus sign”.
3. Chest X Ray:
To find any metastasis in lungs.
4. CT/ MRI:
CT/ MRI of the chest, abdomen and pelvis assess the local disease process as well
as evaluate potential areas of spread (i.e., enlarged lymph nodes, possible
liver/ovary metastases, ascites etc.).
5. Endoscopic ultrasound (EUS)/ Endosonography:
It is useful as a staging tool when the CT scan fails to find evidence of T3/ T4/
metastatic disease. It detects involvement of layers of the stomach, nodal status
and whether tumor is early or advanced.
6. Laparoscopy/ Laparoscopic ultrasound:
It identifies unresectable/ missed lesions in the peritoneum and used to take
peritoneal biopsy. It is also highly sensitive to detect nodal/ hepatic metastasis.
7. Combined PET-CT:
Useful to identify recurrent gastric cancer.
 Management
General treatment recommendations
Staging Recommendation
0 to 1A Endoscopic mucosal resection (EMR) or surgery
is the primary treatment.
1B to 3C, potentially resectable, Neoadjuvant chemotherapy or
medically fit chemoradiotherapy; followed by surgery.
1B to 3C, potentially resectable, Chemoradiotherapy/ chemotherapy.
medically unfit
Stage 4 Chemotherapy for metastatic disease.

Individual treatment options:

Surgery
1. Distal/ subtotal/ total gastrectomy.
2. Endoscopic mucosal resection (EMR).
Gastrectomy
Principles:

 Marginal clearance
 Nodal clearance along arteries
 Omental removal
 Removal of pancreatic lymphatic tissue.
Transection for different types of gastrectomy:
 Endoscopic mucosal resection (EMR)
 This technique is used to resect early superficial gastric CA found on screening.
 The basic steps of this technique is:
1. Identification and demarcation of the lesion
2. Submucosal injection of saline to lift the lesion
3. Endoscopic snare resection.

Chemotherapy
 Neoadjuvant chemotherapy:
 Downstaging of disease to increase resectability
 Decrease disease burden prior to surgery
 Determine chemotherapy sensitivity
 Reduce local and distant recurrences and improve survival.
 Adjuvant chemotherapy:
 Increase survival rate and decrease relapse rate
 Combination chemotherapy is recommended with the following agents:
 5 Fluro-uracil (5-FU)
 Leucovorin
 Doxorubicin
 Mitomycin.
 Palliative therapy
 Indication: Distant metastasis, carcinomatosis, unresectable hepatic metastases,
pulmonary metastases or direct infiltration into organs that cannot be resected
completely.
 Radiotherapy along with following palliative surgeries are done:
 Wide local excision
 Partial gastrectomy
 Total gastrectomy
 Gastrointestinal anastomosis
 Bypass.
OR
A 50 year old male patient presents with bleeding per rectum. How will you investigate
and manage this patient. (7+8=15)
Please refer to the 2006 surgery paper 1 group B 2nd question.
Group C
3.a. Breast biopsy.
Introduction:
A biopsy is a procedure used to remove tissue or cells from the body for examination
under a microscope. A breast biopsy is a procedure in which samples of breast tissue are
removed with a special biopsy needle or during surgery to see if cancer or other
abnormal cells are present.
Types of breast biopsies:
Name of technique Description in brief
Fine needle aspiration A very thin needle is placed into the lump/ suspicious area to
biopsy (FNAB) remove a small sample of fluid/ tissue. No incision is necessary. A
FNAB may be done to see if the suspicious area is a cyst or a lump.
Core needle biopsy A large needle is guided into a lump/ suspicious area to remove a
small cylinder of tissue (also called a core). No incision is necessary.
Surgical biopsy/ The surgeon removes part/ all of a lump/ suspicious area through an
Open biopsy incision into the breast. There are 2 types of surgical biopsies. During
an incisional biopsy, a small part of the lump is removed. During an
excisional biopsy, the entire lump is removed.
 Stereotactic biopsy Stereotactic biopsy finds the exact location of a breast lump/
suspicious area by combining a mammogram and a computer results
to create a 3D image of the breast. A sample of tissue is removed
with a needle that is guided to the right area using that 3D image.
Vacuum-assisted A type of tube or probe is inserted into the breast lump/ mass
biopsy through a small cut made in the skin. The breast tissue is gently
suctioned into the tube, and a rotating knife inside the tube removes
the tissue.
Ultrasound-guided A technique that uses a computer and a transducer that sends out
biopsy ultrasonic sounds waves to create images of the breast lump/ mass.
This technique helps to guide the needle to the exact biopsy site.

3.b. Incarcerated hernia:

Definitions:
A hernia is a protrusion of a viscus or part of a viscus through an abnormal opening in
the walls of its containing cavity.
When the lumen of that portion of the colon occupying a hernial sac is blocked with
faeces, it is called incarcerated hernia.
Risk of an incarcerated hernia:
 There is a risk of the hernia being strangulated at any time.
 The hernia becomes strangulated when the blood supply of its contents is
seriously impaired, rendering the contents ischemic.
 In a strangulated hernia, gangrene can occur within 6 hours.
 If the strangulation is unrelieved, perforation of wall of small intestine occurs and
peritonitis spreads from the sac to peritoneal cavity.
Clinical features:
Clinical features of incarcerated hernias:
 Painful enlargement of a previous hernia or defect
 Cannot be manipulated (spontaneously/ manually) through the fascial defect
 Nausea, vomiting and symptoms of bowel obstruction (possible).
Clinical features of strangulated hernias:
 Sudden pain: At first situated over the hernia, is followed by generalized
abdominal pain, colicky in character and often located mainly at the umbilicus
 Nausea and subsequent vomiting
 An increase in hernia size
 On examination the hernia is tense, extremely tender and irreducible and there is
no expansile cough impulse.
Management:
Urgent surgical repair is required in strangulated hernia. Steps are:
1. Open the skin, subcutaneous tissue and external oblique
2. Divide the inguinal ring in case of inguinal hernia and divide inguinal ligament in
case of femoral hernia to relieve obstruction
3. Open the hernial sac and carefully inspect the sac contents for visibility:
 Apply warm, wet packs to the gut for a few minutes. Gangrenous or
nonviable gut will be black or deep blue without peristalsis
 Note: If bowel falls back into the abdomen prior to assessment of its
viability, perform a laparotomy
4. Resect any gangrenous loop of bowel and make an end-to-end anastomosis.

3.c. Blood substitutes

Introduction:
Blood substitutes are an attractive alternative to the costly process of donating,
checking, storing and administering blood, and they may avoid the immunogenic and
potential infectious complications associated with transfusion.
Types:
Blood substitutes are of 2 types:
 1. Biometric: These substitutes mimic the standard oxygen-carrying capacity of the
blood and are haemoglobin based.
2. Abiotic: These substitutes are synthetic oxygen carriers and are currently
primarily perfluorocarbon based.
Characteristics of an ideal blood substitute:

 It should have a reasonable amount of oxygen delivery, when compared to

human RBCs
 It should lack antigenicity
 It should have a substantially reduced ability to transmit infections
 It should be readily available
 It should have a long half life
 It should be capable of being stored at room temperature.
Adverse effects:
Adverse effects associated with Hb-based oxygen carriers include:

 Diarrhea DJ
 Jaundice
 Hypertension
 Abdominal pain HAS
 Skin rash
 Fever
FSH
 Stroke
 Hemoglobinuria
 Oliguria OL
 Laboratory anomalies such as an elevation in lipase levels.
- Although most of these side effects were transient and clinically asymptomatic, many
clinical trials involving these agents have been discontinued or held due to these
associated adverse effects.
3.d. Volvulus neonatorum:
Introduction: Stages of normal rotation of midgut:
Stage Time Events taking place
1 4 -8th week
th
Midgut supplied by superior mesenteric artery (SMA)
grows rapidly. As coelomic cavity cannot accommodate the
 growing midgut during that period, it protrudes into the
umbilical cord as physiological hernia.
th th
2 10 -12 week Midgut migrates into coelomic cavity in following steps:
1. Small bowel returns towards the left side of abdomen.
2. The caecocolic loop first returns to left lower abdomen
and then it rapidly rotates 270° anticlockwise to reach
right iliac fossa.
3. The duodeno-jejunal segment rotates 270°
anticlockwise to reach left of SMA and behind the
colon.
3 Beyond 12 Fusion of different parts of mesentery and posterior
weeks peritoneum

(Please see www.youtube.com/watch?v=AscKR_cQExY for 3D animation)

Volvulus neonatorum/ midgut volvulus arises from a case of classical intestinal

malrotation. In this, there is failure in the 2nd stage; leading to a right DJ flexure and a
central caecum; creating a narrow base for the small bowel mesentery; which
predisposes to midgut volvulus.
Clinical features:
 Malrotation with volvulus is life-threatening and typically presents with bilious
vomiting. Bile-stained vomiting in the infant is a sign of intestinal obstruction
until proved otherwise.
 As the gut strangulates, the baby may pass bloodstained stools and becomes
progressively sicker.
Diagnosis:
An upper GI contrast study confirms the malrotation.
Treatment:
 Resuscitation and urgent surgery are needed. It is called Ladd’s procedure.
 The steps are:
1. Untwist the volvulus
2. Widen the base of the small bowel mesentery
3. Straighten the duodenum
4. Position the bowel in a non-rotated position
5. Remove the appendix.
3.f. Amoebic liver abscess:
Causative agent: Entamoeba histolytica
Risk factors:
 Alcoholics
 Cirrhotics.
Pathogenesis:

Inflammation of Superior
Portal vein Liver
the caecum mesenteric vein

Inflammation of Inferior
Portal vein Liver
the sigmoid colon mesenteric vein

Liver
Release of histiolysin
(Right lobe is affected Amoebic hepatitis
by the trophozoites
more)

Formation of “Anchovy Liquefaction necrosis,

sauce’ pus which is
chocolate brown
coloured and odourless
Multiple sterile micro-
thrombosis of blood
abscess, which may be
vessels, hemolysis of
secondarily infected
RBCs

Location:
Amoebic liver abscess is more common in right posterior-superior region (80%) because
of streamline effect, i.e., the portal vein is in direct continuation with the right branch.
Complications of amoebic liver abscess:
 Site of rupture Complications
Lung (commonest) Expectoration of chocolate-coloured sputum (amoebic pus)
Pleural cavity Empyema thoracis/ Broncho-pleural fistula: Right lower
chest pain associated with persistent cough
Skin Amoebiasis cutis
Peritoneal cavity Generalized peritonitis
Intestine, CBD Diarrhoea and discharge of pus in the stools
Pericardium Cardiac tamponade (most dangerous and fatal complication)
Bare area of liver Retro-peritoneal abscess

Clinical features:
 The typical patient with amoebic liver abscess is a young adult male with a history
of pain and fever and insidious onset of non-specific symptoms such as anorexia,
fever, night sweats, malaise, cough and weight loss, which gradually progress to
more specific symptoms of pain in the right upper abdomen, shoulder tip pain,
hiccoughs and a non-productive cough.
 A past history of bloody diarrhoea or travel to an endemic area raises the index of
suspicion.
 Examination reveals a patient who is toxic and anemic. The patient will have
upper abdominal rigidity, tender hepatomegaly, tender and bulging intercostal
spaces, overlying skin edema, a pleural effusion and basal pneumonitis – the last
usually being a late manifestation.
 Occasionally, a tinge of jaundice or ascites may be present.
 Rarely, the patient may present as an emergency due to the effects of rupture
into the peritoneal, pleural or pericardial cavity.
Investigation:
General investigations:
1. Blood: Hb, TC, DC, ESR: Anemia, leukocytosis and elevated ESR may be present
2. Renal function: Na+ K+ Urea Creatinine
3. Liver function: Bilirubin (direct and indirect), Albumin, AST, ALT, ALP: Altered
levels of albumin and liver enzymes, high level of ALP
4. Coagulation profile: PT, aPTT: PT may be high.
Special investigations: Serological tests:
These tests are highly specific but reliable only in non-endemic areas:
 1. Indirect haemagglutination
2. Indirect immunofluorescence
3. ELISA.
Imaging studies:
1. USG abdomen:
It will show altered echogenicity and will also assess the size, location, number of
abscess, nature of liver.
2. CT scan:
CT scan shows raised diaphragm; abscess cavity – its size, location, number;
presence of pleural effusion; changes in the lung.
3. Chest X Ray:
It may show a pleural effusion or raised fixed diaphragm (tenting).
4. Sigmoidoscopy/ Colonoscopy:
They can identify flask shaped active ulcers in large intestine. Immediate
microscopic examination of scrapings from the ulcer will show trophozoites.
Treatment:
1. Medical management:
 It is very effective and should be the first choice.
 Metronidazole 500-800 mg TDS for at least 10 days is the drug of choice
for amoebic liver abscess.
 After treatment with metronidazole, a full course of luminal amoebicide
like Diloxanide furoate 500 mg TDS for 10 days should be added to
eradicate cysts.
 Aspiration is carried out when rupture of an abscess is expected.
Aspiration also helps in the penetration of metronidazole, and so reduces
the morbidity when carried out with drug treatment in a patient with a
large abscess. If there is evidence of secondary infection in aspiration,
appropriate drug treatment is added.
2. Surgery:
 Surgery is reserved for complicated cases only (rupture into pleural/
peritoneal/ pericardial cavities) and should be done in ICU.
 Resuscitation, drainage and appropriate lavage with vigorous medical
treatment are the key principles.
 In large abscesses, repeated aspiration is combined with drug treatment is
effective.
  In rare complications like toxic megacolon and severe intestinal
hemorrhage, intensive supportive therapy is followed by resection and
exteriorization.
Group D
4.a. Fractures occurring due to fall on outstretched hand (FOOSH)
Depending on where the forces from FOOSH are applied, fractures and dislocations can
occur at the wrist, forearm or elbow.
Wrist fractures
Mechanism:
When falling on outstretched hand, palm strikes the ground with the wrist in
hyperextension.
Diagram shows lateral view of bones of
forearm and wrist: humerus (HUM),
which includes capitulum (CAP); radius
and radial head articulating with
capitulum; ulna and olecranon wrapping
around trochlea; and scaphoid (S)
articulating with distal articular surface of
radius.

Arrow indicates hyperextension of wrist

that occurs during fall on outstretched
hand. Inset shows enlargement of area
indicated by outline and rotated to
typical orientation of wrist radiographs.
Lightning bolts represent common sites
of fractures due to falls on outstretched
palm:

Fractures caused: A = Colles, B = Dorsal

Barton, C = Scaphoid.

Examples of wrist fractures resulting from FOOSH:

Example General description
Colles fracture Transverse fracture through the distal metaphysis of radius
Dorsal Burton fracture Fracture through the dorsal rim of distal articular surface of radius
Scaphoid fracture Usually non-displaced fracture of the scaphoid
 Forearm and elbow fractures
Mechanism:
Not only does a FOOSH cause hyperextension of the wrist, but it also transmits an axial
load along the length of the forearm, from wrist to elbow, which may result in specific
patterns of fractures.

Diagram shows frontal view of bones of

forearm: humerus (HUM), which
includes capitulum (CAP) and trochlea
(TRO); radius with head articulating
with capitulum; ulna with olecranon
wrapping around trochlea; and carpus
as one unit. Falling on outstretched
hand (downward arrow) results in
transmission of axial forces up forearm
(upward arrows).

Examples of forearm and elbow fractures resulting from FOOSH:

(See pictures on next page)
Example General description
Both Bone Forearm Fracture Transverse fractures of the shafts of both the radius and ulna,
particularly seen in children
Monteggia Fracture- Ulnar shaft fracture with radial head dislocation
Dislocation
Galeazzi Fracture- Radius fracture with dislocation of the distal ulna at the distal
Dislocation radioulnar joint
Radial head fractures Simple radial head fractures are common and usually are
isolated injuries. Severely comminuted radial head fractures
are uncommon; ex.: Essex-Lopresti fracture.
 ① Monteggia Fracture-Dislocation
② Galeazzi Fracture-Dislocation
③ Essex-Lopresti fracture:

I. Application of axial load to

① ②
radius alone, impacting radial
head into capitulum (CAP) and
causing comminuted radial
head fracture.
II. Asymmetric axial load between
radius and ulna causes tearing
along length of interosseous
membrane (IOM) and disrupts
distal radioulnar joint (DRUJ).
③

4.b. Osteochondroma
Introduction:
This is the commonest benign tumor of the bone. This is not a true neoplasm because its
growth stops with cessation of growth of epiphyseal plate.
Special growth pattern of this tumor:
 It starts as a small overgrowth of cartilage at the edge of the physeal plate.
 Then it develops by endochondral ossification into a bony protuberance still
covered by the cap of cartilage. For this reason, this tumor is also called
“cartilage capped exostosis”.
 Any bone that develops in cartilage may be involved; the commonest sites are
the fast-growing ends of long bones and the crest of the ilium.
 It may go on growing but at the end of the normal growth period for that bone it
stops enlarging.
 Any further enlargement after the end of the growth period is suggestive of
malignant transformation.
Clinical features:
 The patient, usually around adolescence, presents with a painless swelling
around a joint (commonly around the knee).
 Occasionally there is pain due to inflammation of an overlying bursa (bursitis) or
impingement on soft tissues, or, rarely, paresthesia due to stretching of an
adjacent nerve.
Diagnosis:
The X Ray appearance is diagnostic. It shows:
 A well-defined exostosis emerging from the metaphysis
 Its base co-extensive with the parent bone
 It looks smaller than it feels because the cartilage cap is usually invisible on X Ray
 However, large lesions undergo cartilage degeneration and calcification and then
the X Ray shows the bony exostosis surrounded by clouds of calcified material.
 Multiple lesions may develop as part of a heritable disorder – hereditary multiple
exostosis.

Treatment:
 When symptomatic, the tumor should be excised.
 The excision includes the periosteum over the exostosis; since leaving it may
result in leaving a few cartilage cells which will grow again and may cause
recurrence of the swelling.
4.c. Greenstick fracture
Introduction:
Greenstick fracture is a special type of pediatric incomplete long bone fracture.
Because a child's bones are much more flexible than adult bone, an incomplete, or
'greenstick' fracture may occur. A "greenstick fracture" means that one side of the
fracture has broken and one side is bent.
Pathophysiology and mechanism of injury:
 Greenstick fractures occur when the force applied to a bone results in bending of
the bone such that the structural integrity of the convex surface is overcome,
resulting in fracture of the convex surface.
 However, the bending force applied doesn't break the bone completely and the
concave surface of the bent bone remains intact.
 This can occur following an indirect trauma following a fall on an outstretched
arm/ a direct blow.

Clinical features:
Similar to a classical long bone fracture:
 Pain at the injured area
 There may be swelling and redness at fracture site
 The child may cry inconsolably
 As Greenstick fractures are stable (continuity of bone intact), they only causes a
bend at the injured part, rather than a deformity.
Diagnosis:
X Ray is diagnostic. It shows a fracture which is usually:
  Mid-epiphyseal
 Incomplete
 Angulated.

Treatment:
 Most fractures of the arms and legs require a cast to keep the bones in good
alignment while the break heals. If the bones are in a poor alignment, they may
need to be repositioned, typically under sedation.
 X-rays are required in a few weeks to make sure the fracture is healing properly,
to check the alignment of the bone, and to determine when a cast is no longer
needed. Most fractures or breaks require 4-8 weeks for complete healing.
 After the cast is removed, the child should avoid high-impact activities for
another 1-2 weeks to keep from re-injuring the arm or leg.
4.d. Fracture of patella
Introduction:
Patella fracture is one of the most common knee injuries.
Mechanism of injury:
 The mechanism of injury may be direct or indirect.
 In a direct injury, as may occur by a blow on the anterior aspect of the flexed
knee, usually a comminuted fracture (a fracture causing formation of >2
separated bone components) results. The comminution may be limited to a part
or whole of the patella. The latter is also called a stellate fracture.
 In an indirect injury, a sudden violent contraction of the quadriceps in a flexed
knee gives rise to a fracture with the fracture-line running transversely across the
patella, dividing it into 2; the so-called two-part fracture.
 Types of patella fractures:

a) Two-part fracture

b) Stellate fracture

Clinical features:
Symptoms:
 Pain and swelling over the knee (main symptoms)
 Additional symptoms may include:
a. Inability to straighten the knee
b. Inability to walk.
Signs:

 Bruising (a sign of direct trauma)

 Knee may be swollen (due to hemarthosis resulting from trauma)
 Crepitus may be felt (in case of comminuted fracture)
 Gap between fracture fragments may be felt (in case of displaced fracture)
 Extensor lag: The patient will not be able to lift his leg with the knee in full
extension; it remains in a position short of full extension (due to disruption of the
extensor apparatus).
Diagnosis:
X Ray (A-P and Lateral view of knee joint) will show a fracture with wide separation of
fracture fragments. A sunrise/ skyline view may be required.
Treatment:

1. Initially:
 Ice application,
 Cylinder plaster slab (from above ankle to the groin).
2. Non-operative:
Indicated for closed fractures + minimum displacement (≤2 cm) + intact extensor
retinaculum.
 Cylinder plaster cast for 6-8 weeks
 Isometric quadriceps exercises
 Encouragement of early weight bearing
 After cast removal, gradual knee flexion and isotonic quadriceps exercises
are started.
3. Operative:
Indicated for fracture with ≥2 cm displacement/ extensor retinaculum tears/
open fractures.
Operative options are:
 Tension band wiring
 Circumferential wiring
 Partial patellectomy.
4.e. Spina bifida: Please see from 2009 Surgery Paper 1 Question no. 4.e.