Junior Surgery Clerkship Notes

MBBS Class of 2017

2
Table of Contents

3
4
 Theoretical Basis of Practical Sessions- Dr. East 28-09-09

IV Therapy
- Water
- Sodium
- Potassium
- Calcium
- Magnesium
- Phosphate
- Chloride

Note: K+, Ca2+, Mg2+, PO4, Cl- IV therapy are only important in special
circumstances
- Eg: prolonged NPO, pyloric stenosis
- Water, sodium and potassium are the routine electrolytes that are monitored
and replaced

Water
- 100 ml/kg for the first 10 kg
- 50 ml/kg for the next 10 kg
- 20 ml/kg for the remainder of the body weight

Note: About 1500 ml of urine is lost daily

- 1000 ml of daily insensible losses

Electrolytes
1- Sodium- 1-2 mmol/kg/day (approximately 70-140 mmol/day)
2- Potassium- 0.5 -1 mmol/kg/day
- Note: the kidney cannot conserve potassium, therefore potassium has to be
added to the maintenance regime
- The first sign of hypokalemia in a post-surgery patient is ileus

Hypokalemia:
** Hypokalemia may be due to a total body deficiency of potassium as a result of
the following:

5
- Prolonged NPO
- Long-term diuretic or laxative use
- Chronic diarrhea
- Hypomagnesiumia

** Acute causes of potassium depletion include:

- Diabetic ketoacidosis
- Severe GI losses due to vomiting and diarrhea
- Dialysis
- Diuretic therapy

** Hypokalemia may also be the result of large potassium shifts from the
extracellular to the intracellular space as seen with:
- Alkalosis
- Insulin
- Catecholamines
- Sympathomimetic
- Hypothermia

** The short-term results of hypokalemia include:

- GI hypomotility (ileus)
- Cardiac dysrythmia
- Muscle weakness or cramping

** Additional Losses:
- Additional 500 ml for insensible losses
- Additional 250 ml of water per degree Celsius

Third Space
Third Space Losses- This is fluid that moves into the third space and are no longer
physiologically available to the intravascular space
- Therefore this fluid, once lost to the third space, cannot be absorbed
physiologically

6
** If an IV fluid is administered, the fluid will distribute itself according to its
relative osmotic and Oncotic pressures
- Isotonic fluids- will distribute evenly between the intravascular and
interstitial spaces according to their relative volumes
- The interstitial space is approximately twice as large as the vascular space,
therefore redistribution of isotonic fluids favor hydration of the interstitial space
- Therefore isotonic fluids are inefficient intravascular volume expanders
and may cause significant edema in large doses
- Hypotonic Fluids- cause a decrease in intravascular tonicity and will also
hydrate the interstitial space to a greater extent than the vascular space
- Therefore hypotonic fluids tend to cause even more edema than the isotonic
crystalloids
- Colloids- are crystalloids with suspended large molecules, therefore they
expand the vascular space because of their ability to exert an Oncotic pressure

** As a result of surgery and inflammation there will be changes to net filtration

within the spaces
- Due to the inflammatory response of surgery there is an increased tendency
for fluid to move OUT of the vascular space
- Albumin leak has been estimated at about 5-15% per hour during major
surgery

Note: The larger, longer and more invasive the surgery, the greater the
inflammatory response
- Also the greater chance that capillary leak will be severe

** Therefore the combination of invasive surgery and excessive crystalloid

administration will cause interstitial volume expansion and edema
- The operative site is the most vulnerable to the edema
- Because this will be the area of greatest capillary leak

http://www.acaciasasa.co.za/articles/pdfs/007Robertson.pdf

Note: An acceptable urine output is 0.5-1ml/kg/hr

7
Writing the Fluid Regime:
Once the amount of fluid has been calculated based on maintenance fluid + fluid
losses divide:
24/# of 500 ml bottles

Note: The maximum rate of KCl administration in an unmonitored patient is

10mmol/hr
- The maximum concentration of KCl should be 60mmol/L

** IV therapy for hypovolemia and hemorrhagic shock should include 2L of

crystalloid for every 500ml of blood loss

Dressings
** The surgical incision should be dressed for 2-3 days to absorb blood and serum
that would be leaking from the site

Chemical Debriding Agents:

- EUSOL- calcium hypochloride
- Hydrogen peroxide
- Used to remove dead cells

NG Tube
** The main purpose is to remove swallowed air
- Insertion causes a predisposition to reflux because the GE junction is forced
open to allow passage of the tube
- Another complication is edema of the ary-epiglottic folds

CVP Monitoring
- Reflects the balance between venous return and cardiac output

8
28-09-09- COLORECTAL CANCER
** Iron deficiency anemia NOT secondary anemia is a feature of colorectal cancer

Sister Mary Joseph Nodule- a palpable nodule bulging into the umbilicus as a
result of metastasis of a malignant cancer in the pelvis or abdomen
- GI malignancies account for about 50% of the underlying sources
- Most commonly are gastric cancer, colonic cancer, pancreatic cancer
- Gynecological cancers account for about 25%- primarily ovarian and
uterine cancers

** The cancer cells may spread to the umbilicus via direct transperitoneal
spread. Other theories include:
- Via the lymphatics that run alongside the obliterated umbilical vein
- Hematogenous spread
- Via remnant structures such as the falciform ligament, median umbilical
ligament or a remnant of the vitelline duct

** SJM nodule is associated with a poor prognosis

Colon Tumors
** Can be classified into benign or malignant

Benign:
- Adenomatous polyp
- Papilloma
- Lipoma
- Neurofibroma
- Hemagioma

Malignant:
1- Primary- carcinoma, lymphoma, carcinoid tumor
2- Secondary- invasion from adjacent tumors
- EX: stomach, bladder, uterus, ovary

Carcinoma

9
** Large bowel carcinomas are the second commonest cause of death from
malignant disease
- Next to lung cancer (males) and breast cancer (females)

** The sigmoid is the commonest site in the colon

- The rectum accounts for 1/3 of all large bowel cancers
- 5% of tumors of the large bowel are (multiple) synchronous

Predisposing Factors:
- Pre-existing polyps
- Ulcerative colitis
- Inherited colorectal cancer syndromes- Familial adenomatous polyposis
(FAP), hereditary non-polyposis colon cancer

Familial Adenomatous Polyposis- invariable proceeds to colon carcinoma unless

treated
- Accounts for 0.5% of all colon cancers
- Autosomal dominant inheritance
- Associated with a mutation in the FAP gene
- Polyps first appear in adolescence
- Symptoms of diarrhea and bleeding at age 21 years
- Malignant change occurs between 20-40 years

Note: Affected individuals have hypertrophy of the retinal pigment layer

- This is a useful non-invasive screening test
- Congenital hypertrophy of retinal pigment epithelium- is best seen by slit-
lamp examination
- The flat pigmented lesions are usually multiple and bilateral

** Variants of FAP include Gardner’s Syndrome

- Gardner’s syndrome is characterized by the presence of multiple polyps of
the colon along with extra-colonic tumors
- The extra colonic tumors include: desmoid tumors, osteomas of mandible
+skull,

10
- The polyps in the colon predispose the individual to colon cancer
- Polyps can also grow in the duodenum, small bowel or stomach

** FAP is a result of a germline mutation in the adenomatous polyposis coli gene

(APC gene)
- The APC gene is a tumor suppressors gene
- Normal APC protein promotes apoptosis in colonic cells
- Sequesters the growth stimulatory effects of b-catenin
- The loss of APC function after mutation prevents apoptosis and allows b-
catenin to accumulate intracelluarly
- This stimulates cell growth and there is a consequent development of
adenomas
- The result is alterations in the expression of genes that affect the
proliferation, differentiation, migration and apoptosis of cells
- Ultimately enough genetic events happen that allow the adenomatous
polyps to become malignant

Treatment: Endoscopic surveillance

- Once polyps are detected colonscopic surveillance is recommended to
remove large polyps
- Surgery (colectomy) is usually delayed until an appropriate psychological
age is reached
- However surgery just be done before the onset of cancer
- Colectomy with mucosal proctectomy and ileoanal pouch pull-through-
allows retention of rectal function

Hereditary Non-Polyposis Colon Cancer- HNPCC)- accounts for about 5% of

colorectal cancers
- Results from a gene mutation affecting DNA mismatch repair
- This leads to genomic instability
- Tumors tend to occur in the right colon and arise before age 50

Colon Cancer- Pathology

** These tumors are adenocarcinomas. There spread can be varied:

11
1- Local Spread- encircling the wall of the bowel and invading coats of the
colon
- Eventually involving adjacent viscera- small intestine, stomach, duodenum,
ureter, bladder, uterus, abdominal wall

2- Lymphatic Spread- to the regional lymph nodes. Eventually spreading via

the thoracic duct. May involve supraclavicular nodes in late cases
3- Hematogenous Spread- to the liver via the portal vein and then to the lung
4- Transcoelomic Spread- producing malignant nodules throughout the
peritoneal cavity

** Carcinoma of the colon is staged according to the Dukes Classification

- Depends on the extent of transmural extension and lymph node spread

** The manifestation of colon carcinoma can be divided into those:

- Produced by the tumor
- Arising from the presence of secondaries
- General effects of the tumor

Local Effects
1- Change in Bowel Habit- most common symptom. Either constipation,
diarrhea or the two alternating
- The diarrhea may be accompanied by mucus or bleeding

2- Intestinal Obstruction- due to constricting neoplasm, usually found in the

left colon
3- Perforation- of the tumor into the general peritoneal cavity
- Or locally with the formation of a pericolic abscess

Secondary Effects- jaundice, abdominal distention due to ascites or hepatomegaly

General Effects of Malignant Disease- Presenting features may be anemia,

anorexia or weight loss
- Tumors of the left side of the colon, where the contained stool is solid are
typically constrictive growths

12
- Therefore obstructive features predominate
- Tumors of the right side tend to be proliferative and the stools here are
semi-liquid
- Therefore obstructive symptoms are uncommon on the right
- Patients with a carcinoma of the caecum or ascending colon usually presents
with anemia and weight loss

Examination
1- Presence of a mass palpable either per abdomen or per rectum
2- Clinical evidence of intestinal obstruction
3- Evidence of spread- hepatomegaly, ascites, jaundice, supraclavicular nodes
4- Clinical evidence of anemia or weight loss

Investigations
1- Sigmoidoscopy- demonstrates tumors in the rectosigmoid region
2- Colonoscopy- allows higher inspection of the colon
3- Barium enema- can reveal the growth as either a stricture or filing defect
(apple=core deformity)
- However a negative barium enema does not definitely exclude the presence
of a small tumor, especially in the presence of extensive diverticulosis
- CT Scan-

Differential Diagnosis:
- Diverticular disease
- Ulcerative colitis
- Dysentery- and other causes of constipation and diarrhea

Treatment
Pre-operative: bowel is cleansed by enemas and oral stimulant laxatives
- Metronidazole + gentamicin are given at the time of surgery

Operative: Wide resection of the growth along with its regional lymphatics
- Bowel prep is contraindicated in obstructed cases

Post-operative- Chemotherapy with 5-fluorouracil

13
Dukes A Tumors- are usually curable with over 90% 5-year survival
Dukes B Tumors- disease is till confined to the bowel wall- 65%
Dukes C Tumors- involves lymph nodes metastases

Colonic Surgery
** The different colonic resections are based on the blood supply to the colon
coming from the:
i- Superior Mesenteric Artery- supplies the midgut components
ii- Inferior Mesenteric Artery- supplies the hindgut components

** Survival of colonic cancer (Dukes C disease) is dependent on the adequacy of

resection (clearing all affected lymph nodes)
- Therefore surgery involves taking as much of the lymphatic drainage as
possible
- Resecting as far down the principal artery as possible because lymphatic
drainage runs alongside arterial inflow

Radical Colectomy- removal of the lymph nodes up to the origin of the arteries
that supply the bowel being resected
Non-radical Colectomy- lymph nodes are preserved

http://www.answers.com/topic/colectomy

Anterior Resection
- Anterior resection of the rectum done for cancers of the proximal 2/3rds of
the rectum
- Use a stapled anastomosis with a per circular staples

Abdominal Perineal Resection- done for cancers in the lower third of the rectum
- Removal of the anus, rectum, part of the sigmoid colon along with the
associated lymph nodes
- Incisions are made in the abdomen and perineum
- The end of the remaining sigmoid colon is brought out permanently as a
colostomy

14
- APR result in a lower quality of life as compared to anterior resections

Aspirin Chemoprophylaxis
** Studies have shown that aspirin chemoprophylaxis (81mg daily) can reduce the
incidence of colorectal adenomas in people at risk
- Especially in colon cancers that demonstrate over expression of COX-II
- COX-2 promotes inflammation and cell proliferation and certain colorectal
cancers tend to over express this enzyme
- Randomized trials have demonstrated that selective inhibitors of COX-2
reduce the risk of adenomas in persons at high risk
- COX 2 is progressively over expressed during the sequence of development
from adenoma to carcinoma

http://ebm.bmj.com/cgi/reprint/8/6/178
http://content.nejm.org/cgi/content/full/356/21/2131

Diverticular Disease- DR TITUS

** Diverticula of the colon consist of out-pouching of mucus membranes through

the muscle wall of the bowel
- They lack the normal muscle coats, they are examples of false diverticula
- In the colon, diverticula are found most commonly in the sigmoid and
descending colon
- Diverticulae become rare in passing from the left to the right side of the
coon
- Diverticula re unusual before the age of 40 years
- Sex distribution is roughly equal
- Colonic diverticula are common in the West but rare in people of developing
countries

** Diverticular disease of the colon refers to diverticulosis and its complications

** A diverticulum is a false, pulsion diverticulum consisting of a herniation of
mucosa through the muscle wall of the colon

15
Etiology
** Low fiber diet
** Inefficient, intense contractions required to mix and propel small volume stool,
therefore resulting in muscle hypertrophy
- Results in generation of high intraluminal pressures during non-propulsive
segmentation contractions
- Therefore pulsion diverticula forms

** Diverticular disease is common in all populations with a refined, low fiber diet
- Affects 50% of 60 year olds and 80% of 80 year olds
- Equal in both sexes

** The diverticulae are false diverticula with only mucosa, submucosa and serosa
in the wall
- Occur only at points of weakness in the colonic wall. These points are:
- Where nutrient vessels penetrate
- Where longitudinal muscle is deficient i.e. between taeniae
- Therefore only occur on the mesenteric side of the ante-mesenteric taeniae
- Diverticulae almost NEVER occur in the rectum

** Hypertrophy of the muscle of the sigmoid colon produces high intraluminal

pressures

16
- This causes herniation of the mucosa at the sites of potential weakness in the
bowel wall
- These points corresponds to the points of entry of the supplying vessels to
the bowel

** Diets that are low in bulk tend not to distend the sigmoid colon, which allows
high intramural pressures to develop
- High fiber diets distend the colon and reduce intraluminal pressure

Note: Muscle hypertrophy, especially of the sigmoid colon, may precede

diverticulum formation
- Causes shortening of affected colon

Terminology
i- True Diverticulum- An out pouching covered by all the layers of
the bowel wall
- EX: Meckel’s diverticulum, jejunal diverticulum

ii- False Diverticulum- Lacking the normal muscle coat of the bowel
- Ex: colonic diverticulum

iii- Diverticula- Plural of diverticulum

- Majority are in the sigmoid colon

iv- Diverticulosis- The presence of usually colonic diverticula

- May be asymptomatic

v- Diverticular disease- complicated diverticulosis

vi- Diverticulitis- inflammation of a diverticulum
- Also known as pericolitis
- Inflammation around the colon in the fat
- If it continues it can become perforation that is either localized or
generalized

17
Uncomplicated Diverticulosis
- Most asymptomatic
- May present with colicky lower abdominal pain
- May present with altered bowel habit (alternating diarrhea + constipation)

Complicated Diverticular Disease

Massive Bleeding:
- Erosion of adjacent nutrient artery
- Complicates 5% of cases of diverticulosis
- Responsible for 55% of cases of lower GI bleeding
- Most of the rest of lower GI bleeding are due to angiodysplasia especially
in younger patients
- Massive bleeding occurs from right-sided diverticulae more commonly than
on the left
- Almost never associated with diverticulitis
- Stops spontaneously in more than 90% of cases
- High recurrence rate

18
Perforation:
- Diverticulitis
- Abscess
- Free perforation
- Fistula
- Bowel obstruction
- Stricture

** Clinical features of diverticular disease of the colon:

1- Diverticulitis- results from infection of one or more diverticula. An
inflamed diverticulum may do one of three things:
i- Perforate: into either
- General peritoneal cavity to cause generalized peritonitis
- Into the pericolic tissues with formation of a pericolic abscess
- Into adjacent structures (bladder, small bowel, vagina) forming a fistula
(colovesical, colovaginal, colo-intestinal or colo-cutaneous)

ii- Produce chronic infection- with inflammatory fibrosis, resulting in

obstructive symptoms (acute, chronic, or acute on chronic)
- Colicky lower abdominal pain and change in bowel habits
- Frank bowel obstruction

iii- Hemorrhage- as a result of erosion of a vessel in the bowel wall. The

bleeding varies from acute and profuse to a chronic occult loss

Acute Diverticulitis
** Characterized by an acute onset of low central abdominal pain
- The pain shifts to the left iliac fossa (LIF)
- Accompanied by fever, vomiting, local tenderness + guarding
- Vague mass may be felt in the LIF and on rectal examination
- Perforation into the general peritoneal cavity produces signs of general
peritonitis

Note: A pericolic abscess is akin to an appendix abscess BUT on the left side
- A tender mass accompanied by a swinging fever and leukocytosis

19
Note: Stool in the diverticulae may predispose to the onset of acute Diverticulitis
BUT the exact triggering factor is unknown
** A typical history includes a patient with an age of >40 years
- Pain initially periumbilical and moves to LIF
- Lower abdominal bloating
- Alteration of bowel habit
- Fever
- Tenderness in the lower abdomen
- Ill appearance
- Fever
- Abdominal distention
- Tenderness + guarding
- Decreased bowel sounds

Note: Doing a barium enema is contraindicated in acute diverticular disease

because of the possibility of inducing a perforation

Chronic Diverticular Disease

** Mimics the local clinical features of colon carcinoma
1- Change in bowel habit- with diarrhea alternating with constipation
2- Large bowel obstruction- with vomiting, distension, colicky abdominal pain
and constipation
- Small bowel obstruction from adhesion of a loop of small intestine to the
inflammatory mass is not uncommon

3- Blood + mucus per rectum- episodes of pain in the LIF, passage of mucus or
bright red blood per rectum
- Melena
- Anemia due to chronic occult bleeding

** More unusual presentations include:

- Sudden severe rectal hemorrhage
- Colovesical fistula- fistula into the bladder with the passage of gas bubbles
(pneumaturia) and fecal debris in the urine

20
Note: Diverticulitis is the commonest cause of colovesical fistula
- Other causes include: Colon CA, Bladder CA, Crohn’s disease + trauma

Investigations
** The diagnosis of symptomatic uncomplicated diverticulosis include the use of:
- Barium enema
- Colonoscopy

** In the case of bleeding other cause of rectal bleeding should be ruled out by
sigmoidoscopy:
- Rule out upper GI bleeding by NG tube or gastroscopy
- Try to localize bleed point by selective angiography, radionuclide scan or
colonoscopy

** Note: Rigid sigmoidoscopes only view the rectum and therefore do not
visualize colonic diverticulae
- Flexible sigmoidoscopes have a better utility in these conditions

** Barium enema demonstrates diverticula as globular out-pouchings

- Show a signet ring appearance because of the filling defect produced by
contained pellets of feces
- Edema and thickening produce a saw-tooth appearance of a narrowed
segment of sigmoid colon

Note: Barium enema should not be done in the setting of acute disease because of
the risk of iatrogenic perforation of the friable and inflamed bowel

** The diagnosis of diverticulitis (acute) is made clinically or with the use of CT

or MRI
- Therefore cancer should be ruled out by barium enema or colonoscopy after
the acute phase
- These investigations done at least 3 weeks later

** The diagnosis of an abscess is made clinically or with CR or MRI

21
- In diverticulitis with abscess formation there is walling-off and localization
of the inflammation
- Therefore associated with severe symptoms BUT localized signs
- The abscess may be pericolic or pelvic

Note: Ultrasound can be used to diagnose the presence/absence of fluid (abscess)

** The diagnosis of free perforation is also made clinically

- Plain X-rays of the abdomen can be done to rule out perforation by looking
for free air under the diaphragm
- Laparotomy

** The diagnosis of a fistula is made:

- Clinically
- Contrast study from high pressure viscus
- Endoscopy both involved organs

** The diagnosis of acute bowel obstruction:

- Clinical
- Plain x-rays
- CT
- Water soluble contrast enema

** Stricture with abdominal pain is diagnosed via barium enema and/or

colonoscopy

Treatment
** Surgery is only indicated if:
1- The patient has generalized peritonitis
2- Patient remains in shock despite fluid resuscitation
3- Patient who re-bleeds in hospital
4- If blood is not available for conservative management

** Surgery involves resection of the entire colon and an ileo-rectal anastomosis

- This type of anastomosis has an increase degree of leakage and abscess formation

22
Note: The commonest cause of massive GI bleeding in patients over age 60 is
diverticular disease
- BUT in younger patients the cause is more likely to be angiodysplasia

** The treatment of uncomplicated, symptomatic diverticulosis is a high fiber diet

- The bleeding usually settles spontaneously 90% of the time
- Resection of affected segment if localization is successful
- Total Colectomy and ileo-rectal anastomosis of localization is unsuccessful
or unwise

Note: Diverticular disease with bleeding is RARELY a cause of chronic blood

loss BUT it is a common cause of acute blood loss

** Acute diverticulitis is usually managed conservatively

- Patient is placed o a fluid died
- Antibiotics- metronidazole with penicillin and gentamicin or a cephalosporin

Diverticulitis + Abscess <2cm

- Antibiotics
- Pass an NG tube to relieve the ileus that may have been caused by
abdominal distention due to accumulation of fluid
- Almost never acute resection
- Elective resection if there are recurrent episodes of diverticulitis or if
colostomy was performed for acute obstruction

Abscess >2cm
- Drainage- US or CT guided or open
- Resection as above

Free Perforation
- Resection of involvement segment, colostomy and Hartman procedure or
mucus fistula

Fistula

23
- Treatment should not be attempted until fistula is mature (6 months after
onset)
- Disconnection of the viscid, resection of the colon and closure of defect
- Defunction the bowel by loop ileoostomy to allow anastomotic healing

Acute Bowel Obstruction

- Requires Laparotomy to establish the diagnosis
- Affected segment of colon is resected and bowel brought out as an end-
colostomy

29-09-09- Skin Coverage + Burns

** The aim in skin coverage is to use autograft. However alternatives include:

vii- Xenograft
viii- Homograft/Allograft- cadaver skin

Split Thickness Skin Graft- is a graft that include two skin layers of the body
- The full epidermal skin layer and part of the dermal skin layer
- Epidermis + papillary dermis
- Advantages- offers a higher rate of graft survival, minimizes donor site
damage
- Disadvantage- tends to contract more than full thickness skin grafts
- Usually taken from the lateral thigh

Full-Thickness Grafts- consists of both the epidermis and complete dermal skin
layers
- Used when skin flap surgery is nor available
- Has better cosmetic outcome than STG
- Less contracture, increased resistance to trauma and less deformation both
functionally and cosmetically

http://www.burnsurvivorsttw.org/burns/grafts.html

** Epidermal appendages play a critical role in re-epitheliazation after

epidermal or superficial dermal injuries

24
- Including the healing of split-thickness skin graft donor sites

Note: The choice between full and split thickness grafting depends on wound
condition, location, thickness, size and aesthetic concerns
- STSG require less ideal conditions for survival and have more broader range
of applications than FTSG
- STSG are used to resurface large wounds, line cavities, resurface mucosal
deficits, close flap donor sites and resurface muscle flaps
- BUT STSG are more fragile, especially if placed over areas with little
underlying soft tissue support

** The graft initially survives on plasma exudate form the wound (plasmatic
imbibition)
- Neo vascularization occurs day 3 post grafting

** Grafts must be left intact 5-7 days to allow vascular connections

- The donor site heals via re-epitheliazation
- Covered with an occlusive dressing

Full Thickness Skin Graft

- Used when cosmesis is a concern
- Ex: facial defects
- The donor site for FTSG has to be closed via suturing

** The recipient site usually requires more healing time

- Therefore the size of the graft must be smaller than STSG

Flaps
- Used to cover deeper defects
- Involving nerves, vessels, joints etc
- Consists of both skin and subcutaneous tissue

Note: All blood supply to the skin is derived from the perforating arteries from
the underlying musculature

25
- Therefore skin flaps are taken with the muscle underlying forming a
myocutaneous flap
- Flaps are named according to what tissue is taken:
- EX: pec major, lat dorsi, tran-flap, osteomyocutaneous flap

Advantage: more tissue is available and more vascularized tissue that can be
moved further is available

Free Flaps- with microvascular transfer require at least 1 artery and 2 veins for
grafting

Burns
** Can be classified according to the causative agent:
1- Thermal (Flame) Burn- due to direct contact with a hot object or to hot
vapor or hot liquid
- Scalds are commonest types of burns in Jamaica usually to toddlers

2- Chemical Burns- may be from strong acids or alkali

3- Electrical Burns (Injuries)-
4- Contact burns- with hot objects
5- Radiation Burns- due to exposure by radiation.
- Chronic Radiation exposure- results in a chronic injury that is an end
arteritis
- Flaps are appropriate for treating these injuries because it vascularized
tissue needs to be introduced into the area

** Burns can also be classified according to the depth:

1- Partial Thickness- the underlying germinal epithelium is still intact.
Complete healing takes place within a few days
- Usually relatively superficial with erythema due to capillary dilation
- +/- Blistering produced by exudation of plasma beneath the coagulated
epidermis
- Deeper partial thickness burns extend down to the germinal layer and may
partially destroy it
- With these burns there is intense blistering

26
2- Full Thickness- Destroy the entire skin layers including the germinal
epithelium
- Very small deep burns may heal from an ingrowth of epithelium from
adjacent healthy skin
- More extensive burns, unless grafted, heal by dense scar tissue with
consequent contracture and deformity

i- First Degree Burns- Involving the epidermis. Can only become

complicated if they become associated with infection
ii- Second Degree Burns- usually seen with scalds. Has a blistered or a pink-
shiny painful appearance
- Involves any layer of the dermis (papillary or reticular)

iii- Third Degree- Dull, painless, leathery appearance. Thrombosed veins

may be visible. Involves the full thickness of the dermis
iv- Fourth Degree- involves subcutaneous tissue, muscle and bone. Usually
seen in electrical injuries

Clinical Features
Pain- due to stimulation of numerous nerve endings in the damaged skin
- Superficial burns tend to be MORE painful than deep burns
- Deeper burns may be relatively painless due to extensive destruction of
nerve endings

Plasma Loss- Loss of the epidermis, along with the exudation of plasma through
the damaged capillaries
- Plasma loss is most marked in the first 24 hrs after burning
- By the time a coagulum has formed (within 48 hrs) this plasma loss ceases
- The amount of plasma loss is proportional to the area of the burn NOT the
depth

Hypovolemic Shock- is a direct result of plasma loss

- The intravascular volume is rapidly depleted as plasma is lost from the
surface of the burn

27
Airway- Smoke inhalation or thermal injury of the respiratory tract may rapidly
result in respiratory obstruction from pharyngeal or laryngeal edema
- Inhalational injury causes a chemical injury to the lung
- Intubate immediately to prevent respiratory failure
- Leave intubated for 4-5 days because there will be swelling and edema in
the lungs

Stress Reaction- the adrenocortical response of sodium and water retention,

potassium loss and protein catabolism occurs as in any severe injury
- Peptic ulceration (Curling’s ulcer) may occur as a reaction to the stress

Treatment
1- Immediate First Aid Treatment- the immediate treatment of any burn is to
stop the burning process immediately
- Remove the patient from the source of the burn
- Apply cold running water to cool the area

2- Subsequent Treatment- management of the local condition- prevent infection

and promote healing
3- General Treatment- mitigate the effects of burns

** Circumferential full thickness burns affecting the chest or limb contract and
may restrict breathing and impair blood flow to the limbs
- This contracts much be increased acutely to save the limb (escharotomy)

** Inhalational burns are indicated by burnt skin and soot around the face
- Burns to the airway produce edema
- May necessitate intubation or tracheosotmy

** Skin grafting is carried out immediately if the eyelids are involved

- To prevent ectropion with the risk of corneal ulceration
- The face, hands + joint flexures are next in priority for skin grafting
procedures
- Scarring in these site will produce deformity and disability

28
** Relieve pain with intravenous opiates

** Rapid fluid loss occurs, and the rate of loss is quickest in the first 12 hours
- Aggressive replacement of fluid is essential
- Burn shock occurs due to the increased capillary permeability
- As a result fluid shifts from the IV space to the interstitial space

Note: In 30% + burns, the edema can be generalized because the increased
permeability affects the entire body now

Note: There are two underlying principles in this replacement:

1- The correct amount of fluid to be replaced
2- The correct type of fluid

** The amount of fluid to be replaced depends on the total area burnt (%TBSA)
- Rule of 9’s

Percentage Surface Area

- Head & neck = 9
- Each arm = 9
- Each leg = 2x9 = 18
- Front of trunk = 2x9 = 18
- Back of trunk = 2x 9 =18
- Perineum = 1

Note: Infants the had and neck are 17%

** The rate of fluid replacement must take into account that most fluid is lost in the
first few hours after the burn, before a coagulum forms

** Burns greater than 10% in children and 20% in adults are severe burns
- These require intravenous fluid replacement

Parkland Formula:
- 4 X persons weight (kg) x %burn

29
- Fluid is lactated ringers with ½ given in the first 8hrs of the onset of the burn
and the remainder given over r the next 16 hrs.

** Stop the intense fluid therapy at 24 hrs because the increased capillary
permeability is self-limiting
- Therefore after 24 hrs give dextrose water

** Protein losses are calculated as:

½ x weight in kg x % burns = amount of protein/colloid to be given. Usually as
FFP after 24 hrs

Note: If the burns are full thickness, about 50% of the fluid replacement should be
given as blood to replace the extensive red cell destruction that occurs within the
affected area

Burn Shock Treatment:

1- Insert 2 large bore IV
2- Ascertain time of burn
3- Monitor urine output
4- Pain management- always IV not IM
5- Antibiotic prophylaxis- risk of invasion from skin commensals
6- Cover wound- with silver sulfadiazine which is a common topical burn agent
- Disadvantages- allergy, unexplained leucopenia (2-3 weeks after),
thrombocytopenia
7- Put in an NG tube
8- Give PPIs to prevent Curling’s ulcers

Note: Burn infections tend to spread in the skin via lymphatics

Electrical Injuries
1- Heart
2- Kidney- the myoglobinuria due to the extensive muscle death leads to
damage to the kidney as the myoglobin is filtered
- Give large amounts of fluids to flush the kidneys and prevent renal failure
- Osmotic diuretic (mannitol) can be given to help flush the kidneys

30
Note: Electrical injuries are also associated with occult muscle damage
- Damage to the intimal vessels
- Use CPK to monitor

Flash Burn- flame component + electrical burn

Note: Calculate evaporative losses as ¼ of Parklands formula
- Therefore it would be 1 x weight (kg) x %burn

** The burn patient in general gradually drops their hemoglobin because the half-
life of red blood cells is reduced (10 days – 2 weeks)
- Monitor and transfuse as necessary to maintain Hb at 12 g/dl

Nutrition
** Burn injures induce a hypermetabolic state. Therefore if enteral nutrition is not
possible, parenteral feeding should be instituted early (within 24hrs of injury_
- Patients rapidly become catabolic
- Adequate calorie and protein replacement are necessary to avoid a negative
nitrogen balance

25 (patients weight +40) x % burn = gives the kilocalories/day needed

Note: Burn scar contracture is prevented by grafting, splinting, physiotherapy

Post- Operative Complications

1- Local or general Complications-
- Local- involves the operation site itself
- General- affecting any of the other systems of the body (respiratory,
urological, cardiovascular complications)

2- Time of Occurrence Postoperatively

- Immediate- within the first 24 hrs
- Early- within the first 3 weeks

31
- Late- any subsequent period, usually long after the patient has left the
hospital

Wound Infection
** The incidence of wound infection after surgical operations is related to the type
of operation. The common classifications of risk groups are:
1- Clean- infection rate of <1%
- Ex: hernia repair

2- Clean Contaminated- where a viscus is open but with little or no spillage

- Infection rate is <10%

3- Contaminated- where there is obvious spillage or inflammatory disease

- EX: a gangrenous appendix

4- Dirty- in the presence of frank pus or gross soiling

- Ex: perforated large bowel
- Infection rate as high as 40%

** The principal causes of wound infection are the:

- Penicillin resistant staph aureus
- Streptococcus fecalis
- Pseudomonas
- Coliform bacilli

Examination of Lumps & Bumps- Dr. Fray

1- Site
2- Size
3- Shape
4- Surface
5- Consistency- fluctuant, hard, nodular
6- Temperature
7- Transillumination
8- Pulsation
9- Mobility

32
10- Fixation
11- Presence or absence of a punctum- opening that suggests the swelling may
be a sebaceous cyst

** The differential diagnosis for a swelling includes:

- Sebaceous cysts
- Dermoid Cysts
- Lipoma
- Neurofibromatoma
- Hematoma
- Lymphadenopathy
- Keloid
- Neoplasm
- Exoctosis?
- Ganglion- wrist
- Neuroma

Biliary Tract Disease

** A diverticulum grows out from the ventral wall of the foregut (primitive
duodenum), which differentiates into the hepatic ducts and the liver
- A lateral bud from this diverticulum becomes the gallbladder and the
cystic duct

** The principal developmental abnormalities include:

1- The long cystic duct traveling alongside the common hepatic duct to open
near the duodenal orifice (10%)
2- Congenital absence of the gallbladder
3- Reduplication of the gallbladder
4- Congenital obliteration of the ducts (Biliary atresia)
5- Absence of the cystic duct with the gallbladder opening directly into the
side of the common bile duct
6- Long mesentery to the gallbladder which allows acute torsion of the organ
to occur with consequent gangrene and rupture

33
Bile Composition & Function
** Bile is a combination of cholesterol, phospholipids (principally lecithin), bile
salts (chenodeoxycholic acid and cholic acid) and water

** Bile also contains conjugated bilirubin

- Which is the breakdown product of hemoglobin

** In the gut, bile salts act as a detergent, by breaking up and emulsifying fats to
facilitate their absorption
- The bile salts are resorbed back into the gut
- Pass back via the portal venous drainage to the liver
- And are then re-secreted into bile

** Diversion or absence of bile from the gut, results in malabsorption of fat and
the fat-soluble vitamins (ADEK)

Gallstones
** There are 3 common varieties of stones:
1- Cholesterol- 20%- occur as solitary oval stone, or as two stones (one
indenting the other) or multiple mulberry stones associated with a strawberry
gallbladder
- The surface is yellow and greasy to the touch
- May be associated with high blood cholesterol
- Positive correlation between cholesterol stones and OCP and pregnancy and
increasing age
- Family history, obesity and low dietary fibers are also risk factors
- The supersaturated bile from these patients is known as lithogenic (stone-
forming bile)
- Bile may also become supersaturated with cholesterol due to a deficiency of
bile salts
- This may occur as a result of interruption of the enterohepatic circulation
- EX: resection of the terminal ileum in Crohn’s disease treatment

34
** Cholesterol stones form in the gallbladder when supersaturated bile is further
concentrated
- As the cholesterol precipitates on the gallbladder wall (cholesterosis) it
forms yellow submucosal aggregations of cholesterol with an appearance like
strawberry skin (strawberry gallbladder)

2- Bile Pigment (5%)- small, black, irregular, multiple, gritty and fragile
- Are made up of calcium bilirubinate with some calcium carbonate
- Occur in the hemolytic anemias (sickle cell, hereditary spherocytosis)
- In the hemolytic anemias there is excess of circulating bile pigment
deposited in the biliary tract

3- Mixed (75%)- Cut surface is has alternate dark and light zones of pigment
and cholesterol
- Most have the same metabolic origin as cholesterol stones
- That is there is some slight alteration in the composition of bile which
allows precipitation of cholesterol together with bile pigment

** Gallstones may have several effects:

1- Silent- gallstones lying free in the lumen of the gallbladder produce no
pathological disturbance of the wall. The patient is symptom-free

2- Impaction in Gallbladder- either at the exit of the gallbladder or in the

cystic duct
- Water is absorbed from the contained bile
- The bile becomes concentrated and produces a chemical cholecystitis
- The cholecystitis is initially sterile BUT may become secondarily infected
from organisms secrete from the liver into the bile stream
- If a stone impacts in the outlet of the empty gallbladder, the walls of the
organ may continue to secrete mucus and the gallbladder distends to form a
mucocele

35
3- Choledocholithiasis- gallstones that migrate into the common bile duct.
This may be silent or produce an intermittent or complete obstruction of the
common bile duct with pain and jaundice
4- Gallstone ileus- occurs when there is ulceration through the wall of the
gallbladder into the duodenum or colon
- The large gallstone may become impacted in the distal ileum and produce an
intestinal obstruction
- Therefore gallstone ileus is a mechanical obstruction by an intraluminal
stone and not a paralytic ileus

** The presence of gallstones in the biliary tree is associated with:

- acute + chronic pancreatitis
- carcinoma of the gallbladder

Clinical Features

Biliary Colic
- Produced by impaction of the stone in the gallbladder outlet (Hartmann’s
Pouch) or the cystic duct
- The impaction may occur for a short period and after which the calculus
wither falls back into the organ or is passed along the duct
- Contractions of the smooth muscle wall of the gallbladder and cystic duct
produce severe pain
- The pain usually lasts for a few hours
- Usually found in the right subcostal region BUT it may also be epigastric
or spread as a band across he upper abdomen
- Radiation of the pain to the lower angle of the right scapula is common
- Usually accompanied by vomiting and sweating

Acute Cholecystitis
- If the stone remains impacted in the gallbladder outlet, the wall becomes
inflamed
- Due to the irritation of the concentrated bile
- Gallbladder fills with pus
- Fever (38-39 deg C)

36
- Upper abdomen is extremely tender and often a palpable mass develops in
the region of the gallbladder
- The mass is the distended, inflamed gallbladder wrapped in inflammatory
adhesions to adjacent organs
- 95% of cause of acute cholecystitis are associated with gallstones

** Complications include:
- Empyema of the gallbladder
- Jaundice- caused by the swollen gallbladder pressing against the common
bile duct
- Gallbladder perforation

** Differential diagnosis
- acute appendicitis
- perforated duodenal ulcer
- acute pancreatitis
- right-sided basal pneumonia
- coronary thrombosis

Chronic Cholecystitis
** Almost ALWAYS associated with gallstones. Repeated episodes of
inflammation results in chronic fibrosis and thickening of the entire gallbladder
wall
- Patient has recurrent bouts of abdominal pain due to mild cholecystitis
which may or may not be accompanied by fever
- Discomfort after fatty meals because fats stimulate the release of CCK
which causes the gallbladder to contract onto the stones

** Differential diagnosis:
- Other causes of chronic dyspepsia including peptic ulceration and hiatus
hernia
- Coronary insufficiency

Choledocholithiasis

37
Defn: Stones in the common bile duct
- May be symptomless
- Often associated with attacks of biliary colic accompanied by obstructive
jaundice
- With clay colored stools and dark urine
- Attacks last for hours or several days
- The attack stops when either the small stone is passed through the sphincter
of Oddi or when it disimpacts and falls back into the dilated CBD

Note: If the obstruction is NOT relieved either spontaneously or by operation, the

back pressure in the biliary system results in secondary biliary cirrhosis and liver
failure

** Secondary biliary cirrhosis- is produced by obstruction of extra hepatic biliary

ducts
- Characterized by regeneration nodules surrounded by fibrous septa

Ascending Cholangitis
** Infection of the CBD, which leads to jaundice and pain along with rigors, high
intermittent fever and severe toxemia
- The duct system is severely inflamed and filled with pus
- Liver may contain multiple small abscesses
- Treatment is antibiotics and urgent drainage

** Differential diagnosis of stones in the CBD

With Jaundice- 75% of cases
i- Carcinoma of the pancreas or other malignant obstructions of the CBD
ii- Acute hepatitis

Without Jaundice- 25% of cases

i- Renal colic
ii- Intestinal obstruction
iii- Angina pectoris

38
http://emedicine.medscape.com/article/774352-overview

Complications of Cholelithiasis
1- Cholecystitis
2- Empyema of the gallbladder
3- Mucocele of the gallbladder
4- Choledocholithiasis- stones in the CBD
5- Ascending cholangitis
6- Gall stone ileus
7- Gangrene perforation with biliary peritonitis
8- Secondary biliary cirrhosis
9- Pancreatitis
10- Fistulae

Choledochoenterostomy- The surgical formation of a communication between the

common bile duct and any part of the intestine
- Usually done with the duodenum (second part)
- A good operation when combined with a papillotomy for sicklers who are
prone to developing stones, because then the stones fall easily into the small
intestine and are passed out in the stool

Note: The electrolyte concentration of bile is the same as blood BUT the
bicarbonate content is bile is higher

** What 3 things are absorbed in the terminal ileum?

- oxalic acid
- Secondary bile salts
- Vitamin B12

** Predisposing conditions to cholelithiasis are:

i- High fat diet
ii- Diet high in carbohydrates- because bile gets supersaturated because the
gallbladder is not emptying due to the lack of fats in the diet
iii- Biliary dyskinesia
iv- Pregnancy- due to the increased levels of progesterone

39
v- Any disease of the terminal ileum
vi- Hemoglobinopathies- SS, HS (pigment stones)
vii- Drugs- tamoxifen

Breast

** Breast Ca is the most common malignancy in females in the world

- Incidence is about 100/100,000 women in the US
- Lifetime risk in the US = 1/8 women
** There are 5 common symptoms of breast disease that require urgent attention:
1- A new discrete lump
2- Nipple discharge
3- Nipple retraction or distortion of recent onset
4- Altered breast contour or dimpling
5- Suspected Paget’s disease

** 95% of all lumps in the breast will be one of the following

- Carcinoma
- Cyst
- Fibroadenoma
- Fibroadenosis

** The following less common causes should also be considered:

1- Trauma- fat necrosis
2- Other cysts- galactoceles, abscess, cystadenoma, retention cyst of the glands
of Montgomery
3- Other tumors- duct papillomas, sarcoma, hamartoma, lipomas

** The diagnosis of discrete breast lumps is based on the following modalities:

1- Clinical examination
2- Radiological Imaging:
- Mammography- usually in older patients over 35 years
- Ultrasound- usually in younger patients
- MRI

40
3- Biopsy- FNAC or core biopsy

Mastalgia
** Breast pain can be separated into cyclical and non-cyclical mastalgia
- Cyclical mastalgia is the most common

** Causes of non-cyclical mastalgia include:

- Breast abscess
- Carcinoma of the breast
- Tietzes Syndrome- chondritis of the costal cartilage
- Chest wall lesions

Benign Breast Disease

1- Cystic Disease- cysts are common in the perimenopausal age group but
uncommon after the menopause
- Cysts present as a painful, tender swelling in the breast
- The lump may be fluctuant but occasionally may mimic a solid lump if the
cyst is tense
- Appear as well-defined, rounded opacities on mammography
- BUT ultrasound will distinguish a cyst from a solid lump

2- Sclerosing Adenosis- may present with pain or lumpiness in the breasts.

May have areas of increased density or micro calcification on mammography

Non-Neoplastic Breast Lumps

1- Fibroadenoma- arises from an entire lobule. Has both stromal and epithelial
components
- More common in the 3rd decade
- Usually presents as a discrete, firm, mobile lump
- Lump is not attached to skin
** Investigate with US or mammogram
- Core biopsy for larger lumps

41
2- Hamartoma- are rare lesions that present as a breast lump or as an
incidental finding
- They appear as a breast within a breast
- Have a well-defined capsule
- Comprise a variable mixture of breast lobules, stroma and fat

3- Gynecomastia- proliferation of male breast tissue. Thought to be due to an

imbalance in estrogens and androgens. Causes of gynecomastia include:
- Drugs- digoxin, spironolactone, cimetidine, estrogens or androgens
- Cirrhosis of the liver
- Renal failure
- Hypogonadism
- Suprarenal tumors
- Testicular tumors
- Idiopathic

Breast Tumors
Benign:
- Intraduct papillomas-
- Phyllodes tumor

Carcinoma:

** Breast cancers arise in the terminal duct lobular unit (TDLU)

- The commonest type of breast cancer is invasive ductal carcinoma

** Ductal carcinoma in situ and Lobular carcinoma in situ

** Breast carcinoma tends to spread by direct extension

- Involvement of skin and subcutaneous tissues leads to skin dimpling,
retraction of the nipple and eventually ulceration

** Blockage of dermal lymphatics leads to cutaneous edema pitted by orifices

Cystosarcoma Phyllodes

42
- Clinically mimic large fibroadenomas
- Arise from breast stroma (connective tissue)
- Demonstrate a range of neoplastic behavior from benign to malignant
- Note: Most are benign

** The malignant variety behave like sarcomas

- Have local spread and local recurrence
- Hematogenous spread to lungs and bone
- Lymph node spread is rare

Treatment:
- Wide local excision (1 cm margin)
- OR simple mastectomy without axillary lymph node dissection (ALND)

Breast Cancer Risk Factors

- Increasing age- peak in 6th + 7th decades
- Family history- first degree relative with pre-menopausal breast cancer
- History of benign breast disease
- Gene carriage (BRAC1 + 2)- the presence of the gene carries a lifetime risk
- Gender- women 100 x more than men
- Early menarche + late menopause- long exposure to menstrual cycling of
hormones
- Nulliparity and first child > 30 years old
- HRT

** If the breast cancer is benign use the Gail Model as a risk assessment tool
- Scores risk factors
- Used to make a decision if breast prophylaxis is needed in women aged 35-
55 years
- Prophylaxis with tamoxifen or raloxifene is recommended if the Gail score
indicates a 5 year risk of 1.7% or greater

Symptoms & Signs

** History of a lump palpated by the patient, partner or doctor
- The lump increase in size over time and never decreases

43
- Lump is almost always painless
- May have been present for up to years

** The history may also include:

- Bloody nipple discharge
- Unilateral eczema

** Symptoms of metastatic disease include:

- Enlarged axillary and or supraclavicular lymph nodes
- Bone pain
- Shortness of breath

Note: Anorexia and weight loss are NOT usual features of advanced breast cancer

** Inspection of the breast may demonstrate:

- Marked asymmetry
- Obvious lump
- Nipple retraction
- Nipple distortion
- Dimpling
- Skin infiltration

** Ask the patient to raise the arms over the head slowly
- This allows for exaggeration of nipple distortion and dimpling
- The mass may also become visible or more prominent

** On palpation the lump may be hard with ill-defined edges

- Immobile within breast tissue
- Test lump for fixation to skin and pectoralis major
- Check for axillary lymphadenopathy

Preclinical Detection
** Encourage monthly self examination of breasts
- Mammography plus ultra sound initially at 35 years
- Start earlier if there is a strong family history

44
- BUT use ultrasound instead of mammography in women under age 35 years

Abnormalities:
- Microcalcifications
- Architectural distortion
- Mammography alone misses 10-15% of cancers, especially in dense breasts

Note: Mammography is not done in younger women because the breast tissue is
too dense
Treatment

** Surgery followed by adjuvant therapy for stages 1 and II

** Neo-adjuvant treatment followed by surgery for stages III and IV

Early Breast Cancer ( Stages I + II)

1- Breast Conserving Surgery (BCS) with sentinel lymph node biopsy or
axillary lymph node dissection
- Tumor < 5cm or the breast: tumor volume ratio is high

2- Mastectomy with SLNB or ALND

45
** The purpose of sentinel lymph node biopsy is to indicate when lymph nodes are
negative for metastases
- Therefore SLNB makes ALND unnecessary
- ALND should be avoided because of high morbidity (pain, paresthesiae,
lymphedema)

** The sentinel lymph node is the first node to collect combined lymphatic
drainage from the entire breast before distribution to other nodes
- There may be more than 1 SLN but usually not more than 2

Note: SLNB is indicated only for patients with clinically normal axilla and
primary tumor <5cm
- If it is done for more advanced disease, there is a high false-negative rate

** Methylene blue is used and injected into the sub-areolar tissue

- If negative no further dissection is needed
- If it is positive proceed to ALND

ALND
** The aim is to remove at least 10 nodes from Berg’s levels I & II
- Avoid level III
- Can result in lymphedema of the ipsilateral arm, pain syndromes and
paresthesiae

** However ALND serves 3 objectives:

i- Prognostication
ii- Indication for chemotherapy + radiotherapy
iii- Therapeutic removal of involved nodes

Note: The breast cancer specimen is routinely sent for

- Histology

46
- ER/PR receptor assay
- HER-2 overexpression assay

Note: There is an increased incidence of ER +ve tumors in post-menopausal

women

Note: Micrometastases can still be present without having palpable nodes

Clinical Staging
** The Manchester System is a type of staging system

Stage I:
- Lump found in the breast without palpable nodes
- Mobile tumor less than 2cm

Stage II:
- Lump that is 2-5 cm and mobile nodes

Stage III:
- Lump >5cm and fixed nodes

Stage IV:
- Distant metastases

** The TNM system is a clinico-pathological system of staging

Tumor:
- 1- <2 cm
- 2- 2-5 cm
- 3- >5 cm

Nodes:
- 0- No nodes
- 1- Mobile nodes

47
- 2- Fixed Nodes

Metastases:
- 0- None
- 1- Mets present

Note: Early breast cancer is considered to be Stage I or II (T2N1M0)

** General principles of treatment include:

- Surgery followed by adjuvant therapy for stages I + II
- Neo-adjuvant treatment (primary systemic therapy) followed by sugery for
stages III and IV
- The purpose of neo-adjuvant therapy is to attempt to downstage the size of
the breast tumor

Biopsy
1- Fine Needle Aspiration Cytology
2- Core Needle
3- Incisional
4- Excisional

Note: Cannot get information on hormone receptor status with FNAC

Treatment
** There are two forms of treatment for local disease:
1- Lumpectomy + Axillary lymph node dissection- for small lesions and
post-surgery the remaining breast tissue must be irradiated
- There are two main indications to avoid doing lumpectomy even with a
small lesion
i- Size of breast- in a very small breast it may be better to do a mastectomy
because the result will be disfiguring because of the low breast:tumor ratio
ii- Central lesion- near the nipple
2- Modified Radical Mastectomy-

48
Pathology
** Breast cancer arises from the terminal duct lobular unit. There are two types
by way of origin
- Ductal carcinoma
- Lobular carcinoma
Ductal Carcinoma In-situ
i- Comedo- central necrosis
ii- Cribriform- spaces between cells
iii- Solid
iv- Papillary

Note: Comedo forms are more aggressive than non-comedo

- Significant percentage of DCIS is associated with occult invasion
- DCIS should be considered a precursor lesion and should be treated like
invasive breast cancer

Ductal Carcinoma- Infiltration of

i- Schirrhous- 80%- productive fibrosis
ii- Medullary- lymphocytic infiltrate and has better prognosis than
schirrhous
iii- Papillary- blood filled cystic lesions with papillary formations
iv- Tubular- glandular patterns
v- Colloid (mucinous)-
vi- Inflammatory- signs of inflammation without lymphocytic or leukocytic
reaction. Extensive vascular and lymphatic invasion
vii- Extensive Intraductal Component- >25% of cells in-situ, adjacent to or
mixed in with infiltrative cancer. Hich local recurrence rate after BCS

Lobular Carcinoma In-Situ

- Often found incidentally in biopsy specimen
- Often bilateral (20%)
- Associated with neighborhood calcifications rather than calcifications in
the lesion itself
- Most subsequent carcinomas are ductal in origin

49
- Therefore LCIS is considered a marker for risk (20-30% lifetime risk)
rather than a precursor lesion

Note: Invasive ductal Ca is a part of the sequelae of LCIS and it may develop in
the opposite breast

** LCIS is treated by one of 4 options:

i- Follow up
ii- Chemoprophylaxis
iii- Mastectomy + mirror image biopsy of other breast
iv- Bilateral mastectomy

Note: A gene study should be done and if positive for BRCA 1+2 a skin-sparing
mastectomy should be done

Infiltrating Lobular
- 10% of breast cancer
- High incidence of bilaterality
- Similar prognosis to infiltrating ductal
- Usually treated by mastectomy and mirror image biopsy

Adjuvant Therapy
Radiotherapy- should be started not less than 1 month post surgery and not more
than 3 months
Indications:
- After Mastectomy if the tumor is near to the posterior margin or near to
skin margins
- If after mastectomy axillary lymph nodes are involved

Note: Done after all cases of breast conservation surgeries

** Complications include burns and cardiac injury

- Radiotherapy like surgery is aimed at local control of the disease

50
Chemotherapy- should be started not less than 1 month post surgery and nor more
than 3 months post surgery
** Indications for chemotherapy vary from institution and are based on:
- Axillary mets
- Tumor size
- Tumor grade
- Age
- ER status

** Regimes:
- CMF- cyclophosphamide + methotrexate + fluoruracil

Hormonal Treatment
- All ER/PR positive patients should receive hormonal manipulation

Tamoxifen
- Used in ER positive patients for 5 years, regardless of age
- Complications- weight gain, decreased libido, hot flashes, endometrial
cancer, thromboemobolic diseases, cataracts

Aromatase Inhibitors- Femara, Arimidex

- Used in ER positive post-menopausal patients instead of tamoxifen
- However it has NO effect in pre-menopausal women with intact ovaries
- Can be used in post-menopausal ER positive patients with advanced disease
but only after castration
- Complications include hot flashes, bone pain and osteoporosis

Follow-Up
** Physical examination every 6 months after the end of therapy for 5 years and
then annually
- Examine affected breast or mastectomy site for local recurrence
- Examine regional lymph node drainage
- Examine contralateral breast
- Auscultate and percuss lungs for pleural effusion and examine abdomen for
hepatomegaly

51
- Annual mammogram

Note: Blood work, chest x-rays and bone scans are not recommended in the
absence of symptom or signs

SURGICAL ITEMS

Foley Catheter- is a thin, sterile tube that is designed to be inserted into the
bladder to drain urine
- Held in place with a balloon filled with sterile water at the end
- The urine drains into a bag

** A Foley catheter can be used for the following:

i- Retention of urine leading to urinary hesitancy, straining to urinate,
decreased in size and force of urinary stream, incomplete emptying
ii- Obstruction of the urethra by an anatomical condition that makes
urination difficult
- Prostate hypertrophy, prostate cancer, narrowing of the urethra

iii- Urine output monitoring in a critically ill or injured person

iv- Collection of a sterile urine specimen for diagnostic purposes
v- Nerve-related bladder dysfunction (after spinal trauma)
vi- Imaging study of the lower urinary tract
vii- Post-surgery for monitoring

Complications:
- Balloon can break while the catheter is being inserted
- Balloon does not inflate after it is in place
- Urethral bleeding
- Catheter introduces an infection into the bladder
- If the balloon opens before the catheter is completely inserted, there can be
bleeding, damage and rupture of the urethra leading to long-term scarring and
urethral strictures

52
NG-Tube
** Gastric intubation via the nasal passage is a procedure that provides access to
the stomach for diagnostic and therapeutic purposes
- NG tube can act as a closed active or passive drain

Diagnostic Indications
- Evaluation of an upper GI bleed
- Aspiration of gastric fluid content
- Identification of the esophagus an stomach on chest x-ray
- Administration of radiographic contrast to the GI tract

Therapeutic Indications
- Gastric decompression-
- Relief of symptoms and bowel rest in the setting of small bowel obstruction
- Aspiration of gastric content from recent ingestion of toxic material
- Administration of medication
- Feeding
- Bowel irrigation

Absolute Contraindications
- Severe mid-face trauma
- Recent nasal surgery
- Basal skull fracture

Relative Contraindications
- Coagulation abnormality
- Esophageal varices or stricture
- Recent cautery of esophageal varices
- Alkaline ingestion

Sizes:
- Adult 16-18 F
- Pediatric- the correct tube varies with the patients age
- To find the correct size, add 16 to the patients age in years and then divide
by 2

53
http://www.ics.ac.uk/downloads/2008112340_GIFTASUP%20FINAL_31-10-
08.pdf
IV THERAPY GUIDELINES

Diathermy
- Device used for heating body tissues by the passage of high frequency
electrical current
- Results in coagulation, desiccation or cutting of tissues
- Used for surgical dissection as a bloodless knife and for hemostasis
- NOT used for circumcision, brain surgery, plastic surgery and
ophthalmology cases
- Because of the danger of coagulation of blood in these areas supplied by end
arteries

Complications:
- Burns
- Damage to adjacent tissues
- Increased susceptibility to infection and seromas
- Ischemia

Contraindications: Persons with pacemakers

Fleet Enema
- Phospho sodium enema
- Osmotically active agent
- Used for clearing/preparing bowel for procedures involving the lower GI
tract
- EX: left sided bowel resection and anastomosis, IVP or lower GI endoscopy
- Complications: Elderly patients may get fluid and electrolyte imbalance.
Therefore avoid in old patients and those with cardiac + kidney problems

Colostomy Bag

54
** A colostomy is an artificial opening made between the large bowel and the skin
outside to divert feces and flatus
- The stool and wind is then collected by an external bag
- Temporary or permanent

** A temporary (loop) colostomy is most commonly done to defunction an

anastomosis after an anterior resection
- To prevent fecal peritonitis developing after traumatic injury to the rectum
or colon
- To facilitate the operative treatment of a high fistula
- Most loop colostomies are made in the transverse colon but the sigmoid
colon can also be used

** A double-barreled colostomy is a type of temporary colostomy

- The colon is divided and both ends are brought up separately to the surface
- This ensures that the distal segment is completely defunctioned

** An end-colostomy is formed by bringing the distal end of the divided colon to

the surface in the left iliac fossa, where it is sutured in place.

Complications:
- Prolapse
- Retraction
- Necrosis of the distal end
- Stenosis of the orifice
- Colostomy hernia
- Bleeding- usually from granulomas around the margin of the margin
- Colostomy diarrhea

Sigmoidoscopy

55
- Flexible sigmoidoscopy allows visualization of the inside of the large
intestine from the rectum through the sigmoid or descending colon (65cm)
- Tumors, hemorrhoids, polyps, ulcers etc can be visualized and biopsied
- Bleeding, inflammation, abnormal growths, and ulcers can be noted
- Complications include hemorrhage and perforation of the colon

T-Tube
- Closed, passive drain
- One end inserts into the CBD and the opposite end into the common hepatic duct
(transverse) and the vertical portion fits into the cystic duct
- Used for drainage of bile after CBD exploration
- Allows or decompression of the biliary system
- Formation of tract for radiologic instrumentation (cholangioagram) and stone
removal
- Drains percutaneously, therefore allows free drainage and passage of small
stones

** Removed if:
- There is a normal T-tube cholangiogram
- The bilirubin levels are not increasing
- There is decreased drainage

Pg 56

Head Injuries- Dr. Fray 12/10/09

Types of Injury
- skull vs scalp vs brain parenchyma
- Mechanism of injury: blunt, penetrating
- Acceleration/deceleration or rotational

Scalp Injuries
** Most scalp injuries are simple penetrating injuries
- Manage by debridement and suture

56
Skull Injuries
** The skull fractures along its weakest plane, which varies according to the
position of the injuring force
- A skull fracture is most important as an indicator of the force of the injury
AND the risk of intracranial hemorrhage

** Fractures that extend thorough any of the paranasal air sinuses (frontal,
ethmoid, sphenoid) communicate with the outside
- Therefore these are known as compound (open) fractures
- Must be treated with anaerobic antibiotic coverage as well as gram positive
and gram negative
- External communication may manifest as a runny nose
- However the clear fluid is CSF

Note: Compared to normal nasal secretions CSF is rich in glucose and low in
mucin content
- Normal nasal secretions have no sugar and are rich in mucin

** This external connection may be indicated by intracranial air (aerocele) or

fluid in one of the sinuses on a CT or skull x-ray

** Fractures through the petrous temporal bone may result in CSF otorrhea
- CSF passes through into the external auditory meatus directly or via the
mastoid air cells

Depressed Fractures
- A localized blow drives a fragment of bone below the level of the
surrounding skull vault
- Depressed fractures should be elevated because the result will be damage to
the underlying parenchyma and eventual fibrosis
- This fibrosis may lead to the formation of an epileptic foci

Orbital Hematoma:

57
- Fractures of the anterior and middle cranial fossae are frequently associated
with orbital hematoma
- Blood tracks forward into the orbital tissues, into the eyelids and behind the
conjunctiva
- Note: A black eye is a superficial hematoma of the eyelid and surrounding
soft tissues produced by direct injury

Brain Injuries
** Brain injury can be divided into:
1- Primary- is the direct result of trauma
- Due to the direct penetrating trauma
- Also the result of the fact that the brain is relatively mobile within the skull,
therefore it can become injured after being forced into sudden acceleration and
deceleration
- Results are both diffuse and local effects

2- Secondary- occurs after the initial event and is the result of hypoxia,
hypercapnia, hypotension (ischemia), intracranial hemorrhage or meningitis

Diffuse Brain Injury- diffuse neuronal injury occurs as a result of shearing

movements
- The worse is rotational shearing, which occurs when a blow is delivered off
center
- The result is axon damage and rupture of the small vessels
- Often results in brainstem injury

Localized Brain Injury- local brain damage occurs as the brain impacts against the
skull
i- Coup Injury- is the direct impact of the brain on the skull at the site of
injury
ii- Countre Coup- occurs as the brain rebounds against the opposite wall of
the skull resulting in edema and bruising at the site of impact
- Common sites of impact are the frontal lobes in the anterior fossa and
temporal lobes within the middle fossa
- With contrecoup to the occipital lobes

58
Cerebral Perfusion
** Cerebral perfusion is normally auto regulated by the vasoactive cerebral
arterioles to maintain constant cerebral blood flow over a wide range of systemic
blood pressures
- If systemic arterial pressure falls, cerebral vasodilation occurs to
compensate
- If it falls further and exceeds the arterioles ability to compensate, cerebral
ischemia occurs

Note: A rise in ICP will reduce the cerebral perfusion pressure

- Cerebral perfusion pressure = BP –ICP
- The flow of blood pressure to the brain is auto regulated until the perfusion
pressure is around 40 mmHg

Note: An increase in ICP coupled with hypotension in head injury victims reduces
cerebral blood flow
- As a result the ischemia affecting the cardio respiratory centers in the
floor of the 4th ventricle leads to a reflex increase in systemic pressure and
bradycardia (Cushing’s reflex)

Management of Head Injury

- Initial assessment
- Immediate management
- Delayed Management

Initial Assessment:
1- History: Important points to note in the history are:
i- Mechanism of injury- nature of the force and direction relative to the
recipient are important
ii- Immediate condition of the injured person- level of consciousness (GCS),
vital signs (pulse, RR, BP), size + reactivity of pupils, recorded limb movements
iii- Change in the condition of the injured persons
iv- Prior condition of the injured person

59
2- Examination- should reassess the patients conscious level to decide whether
the condition has worsened or improved
- Look for associated injuries (eg tension pneumothorax or fractured spine)
- ABC + cervical spine
- Full CNS exam
-
3- Special Investigations-
i- Skull X-ray- indicated wherever a period of LOC has occurred
ii- Cervical spine x-ray-
iii- CT scan

** Following the initial brain injury, further deterioration may be due to:
i- Increasing cerebral edema as the brain swells
ii- Intracranial hemorrhage- extradural, subdural or intracerebral
iii- Hypoxia- due to impaired ventilation or ischemia
iv- Infection- secondary to compound fractures, including fractures
involving the temporal bone or paranasal sinuses
v- Hydrocephalus- communicating or non-communicating

Pupil Size and Response:

- If a cerebral hemisphere is pressed on by an enlarging blood clot, the third
cranial nerve on that side becomes compressed by descent of the uncus over the
edge of the tentorium cerebelli
- Occulomotor transmits parasympathetic pupilloconstrictor fibers
- Third nerve palsy results in dilatation of the corresponding pupil due to
intact unopposed sympathetic supply
- Also the failure of the pupil to react to light
- However the consensual light reflex is preserved
- Eventually the contralateral third nerve becomes compressed and the
opposite pupil in turn dilates and becomes fixed to light

Traumatic Intracranial Bleeding

** Hemorrhage within the skull following injury may be classified as
1- Extradural

60
2- Subdural- acute, chronic
3- Subarachnoid
4- Intracerebral
5- Intraventricular

Extradural
- History: minor head injury with temporary concussion, lucid period
development of headache and progressively deeper coma due to cerebral
compression by the extradural clot
- May have a dilated purple, hemiparesis or hemiplegia which indicates
contralateral compression, or a boggy scalp hematoma, overlying the extradural
clot

Note: CT scan is diagnostic

Acute Subdural Hematoma

- Results from bleeding into the subdural space from the lacerated brain or
torn vessels
- Usually part of a severe head injury
- Treatment: Release of the subdural clot through a craniotomy

Chronic Subdural Hematoma

- Usually follows a trivial injury usually in an elderly patient
- Injury may have occurred weeks or months before
- Causes a small tear in a cerebral vein as it traverses the subdural space
- Whenever the patient, coughs, strains, or bends over a little blood
extravascates

Clinical Features: Mental deterioration, headaches, vomiting, drowsiness which

progresses to coma
- Moderate papilloedema is seen in about 50% of cases
- Contrast CT will demonstrate the outline of the clot
- Treatment: evacuation of clot or fluid collection through burr holes

Subarachnoid Hemorrhages

61
- Blood in the CSF after head injury gives a clinical picture of meningeal
irritability with headache, neck stiffness and a positive Kernig’s sign
- Treatment: Analgesic, bed rest

Intracerebral Hemorrhage
- Small hemorrhages throughout the brain substance

Intraventricular Hemorrhage
- Hemorrhage into a ventricle may occur from tearing of the choroid plexus
at the time of injury
- OR rupture of an intracerebral clot into the ventricle
- Occurs partly in childhood

Anatomy of the Great Vessels

Arch of the Aorta

** The ascending aorta approaches the manubrium and then at the level of the
manubriosternal joint becomes the arch
- The arch passes backwards over the left bronchus to reach the body of T4
vertebrae just to the left of the midline

Peripheral Arterial Disease- Bedside Teaching Dr. East

** When assessing a patient with arterial disease, the disease is rarely localized to
the peripheries
- Therefore involvement of other organs, especially the heart, CNS, and
abdominal viscera have to be kept in mind
- Artherosclerosis is a generalized disease, therefore cerebral circulation is
often affected un addition to circulation to the legs
- Therefore there may be a history of intermittent loss of consciousness,
blindness, hemiparesis etc
- Other signs related to generalized artherosclerosis include angina or
previous MI, history of TIAs or stroke, abdominal aortic aneurysm or previous
repair

62
Etiology:
i- Artherosclerosis
ii- Thomboangiitis obliterans- (Buerger’s Disease)- found
exclusively in smokers. Tends to affect younger patients than artherosclerosis
- Has distal to proximal progression
- Remits on smoking cessation
iii- Diabetic micro-angiopathy
iv- Thromboembolism
v- Raynaud’s phenomenon
vi- Ergot poisoning

Major Risk Factors:

- Hypercholesterolemia
- Cigarette smoking
- Hypertension
- Diabetes mellitus

Relative Risk Factors

- Advanced age
- Male gender
- Hypertriglyceridemia
- Sedentary lifestyle
- Family history

Note: There are 3 components of the serious effects of smoking in artherosclerotic

disease
i- Nicotine- induces vasospasm
ii- Carbon monoxide- is found in inhaled smoke and becomes taken up by
hemoglobin to form carboxyhemoglobin. This dissociates slowly and is
unavailable for oxygen carrying, resulting in relative tissue hypoxia
iii- Increased platelet stickiness- with increased risk of thrombosis formation

** The symptoms and signs are related to loco regional disease

63
- The symptoms develop from intermittent claudication of the calves over a
period of months/years to the acute onset of ischemia following an embolus

Note: Sudden onset of pain in the leg suggestive of an embolus should prompt an
investigation into the source
- EX: atrial fibrillation, recent MI, aortic aneurysm
- Acute deterioration in a patient with claudication is suggestive of
thrombosis on the background of artherosclerotic occlusive disease

Rest Pain- is the next level of severity of PAD from claudication

- Felt in the forefoot, constant
- Relieved by leg dependency and aggravated by elevation

** Signs of critical limb ischemia are:

- Presence of gangrene
- Rest pain
- Non-healing ulcerations on the tips of the toes or dorsum of the foot

Examination

Ankle Brachial Pressure Index (APBI)

- A Doppler probe is held over the brachial artery and a BP cuff is inflated to
occlude the blood flow
- As the cuff deflates a Doppler signal reappears and a systolic pressure is
recorded
- Similar pressure readings are taken from the dorsalis pedis and posterior
tibial arteries with a cuff just above the ankle
- The ABPI is the ratio of pressure at the foot pulse to that at the brachial
artery
- Values less than 0.5 indicate significant ischemia
- <0.4 = critical limb ischemia
- < 0.7 = claudication

Note: Heavily calcified vessels may be incompressible and give false high
readings

64
- EX: diabetes mellitus

Limb Inspection
- Skin pallor, absence of hairs
- Ulcers usually on the lateral malleolus and in the interdigital clefts
- Gangrene
- Fixed staining is purpuric areas that do not blanch on pressure. In a context
of an acutely ischemic limb, fixed staining
- Hyperpigmentation of the distal leg
- Venous guttering- the veins of the foot + leg may be empty therefore they
appear as shallow grooves or gutters

Skin Temperature:
- A clearly marked change of temperature may reveal the site of blockage of a
main artery

Peripheral Pulses
- Absent or diminished pulses (from femoral to dorsalis pedis) distal to
obstruction and compare to the other side
- The abdomen should be examined for any evidence of abnormal aortic
pulsations
- If distal pulses are absent there is possibility that no aortic pulsation will be
felt due to thrombosis of the terminal aorta

Investigations of PAD
1- Urine for sugar and blood glucose- to exclude diabetes
2- Hb estimation- to exclude anemia or polycythemia. Anemia may sometimes
precipitate angina or claudication
3- ESR + CRP- raised in inflammatory or mycotic aneurysms
4- Serum cholesterol- raised in artherosclerosis
5- ECG- to exclude associated coronary disease
6- Echocardiogram- to confirm valvular lesions, mural thrombus, ventricular
aneurysms

65
7- Chest X-ray- bronchial carcinoma is a common finding in end-stage vascular
disease. Also to assess the cardiac silhouette
8- Doppler ultrasound-/Ultrasonography- measuring flow patterns can
quantify the degree of stenosis of a vessel because blood velocity increases as it
crosses a stenosis to maintain the same flow rate
9- Arteriograpjy- used to determine the site and extent of a blockage.
Performed to identify the severity and distribution of the disease. This information
can be used to see if reconstructive surgery would be useful

Note: Classical angiography should never be performed on claudicants

- This is because it is an invasive test and claudicants are NOT treated
surgically

** However all patients with critical ischemia who are otherwise fit for surgery
should be investigated with a view to performing corrective surgery

** Complications of classical angiography include:

- Hemorrhage
- False aneurysm
- AV fistula
- Dissection
- Thrombosis
- Embolus
- Anaphylaxis
- Renal failure

** Candidates for surgery are persons with critical ischemia with a lesion that is
amenable to surgical bypass

** Surgery should only be considered for claudication if it seriously impairs

quality of life
- Claudication is usually controlled by conservative management
- Adjust risk factors (lifestyle changes), address co-morbidities, improve
exercise tolerance

66
** The criteria for a successful surgery are:
1- Localized- as opposed to extensive obstruction
2- Good Inflow- good blood supply up to the area of blockage
3- Good outflow- good patent vessels distal to the area of blockage to receive
the conduit

Note: Good inflow and poor outflow is not reconstructable by bypass

- However poor inflow and good outflow may be correctable by extra-
anatomic bypass)

Medical Treatment of Chronic Occlusive Disease

1- Risk factor modification
2- Use of statins- this medications have an anti-inflammatory effect that is
independent of cholesterol lowering
- Therefore statins may have positive effects even in the absence of elevated
cholesterol levels

3- Weight reduction
4- Smoking cessation
5- BP control
6- Glycemic control
7- Anti-platelet agents- aspirin or clopidogrel or cilostazol
8- Exercise- 30 mins for at least 3-4 times per week. Walking may also
encourage the growth of collaterals and may lead to increase in claudication
distance over time

Surgical Interventions
1- Angioplasty- with our without stenting- not durable and only short segment
obstructions qualify
2- Endarterctomy
3- Bypass graft- preferred
4- Amputation- if intervention fails or the person with critical limb ischemia
does not meet the criteria

Artherosclerosis

67
Defn: A chronic inflammatory process affecting elastic and muscular arteries
- May be a response to repetitive injury to the endothelium from the trauma
of turbulent blood flow and toxins

** As a result there is formation of the artherosclerotic plaque. The plaque

consists of the following:
- Smooth muscle cells
- Connective tissue cells
- Lipid
- Inflammatory cells

** Slow progression of the plaque formation causes chronic obstruction

- Rupture or ulceration of the fibrous cap exposes the thrombogenic lipid
core
- This results in platelet adherence, thrombosis and acute on chronic
obstruction

** Disease in non-diabetics tends to be in the larger vessels above the knee

- EX: infrarenal abdominal aorta, superficial femoral artery, popliteal artery

** Disease in the diabetics tends to predominate below the knee in smaller vessels
- This makes surgical correction difficult in diabetics

Note: 50% of persons with critical ischemia die within 5 years from MI or stroke

Peptic Ulcer Disease- Dr. East

Defn: Refers to gastric and duodenal ulcer disease

** The incidence of PUD reflects the incidence of H. pylori infection

- Therefore marked decrease in developed countries and decreasing in
developing counties
- Admissions for complications of PUD (perforation + pyloric stenosis) has
decreased but bleeding incidence has increased

68
** H. pylori is associated with 90% of duodenal ulcers and 75% of gastric ulcers
- Antral infection is associated with DU
- Corporal infection- associated with GU
- Destroys mucin-producing cells and degrades the quality of mucin, thereby
reducing its barrier effect
- Destroys parietal cells resulting in decreased acid secretion, atrophic
gastritis, gastric ulcer and cancer

** H. pylori is a gram-negative rod

- Penetrates the mucus lining the stomach
- Has urease activity that splits urea and produces ammonia
- This neutralizes the pH of the area surrounding the organism
- Direct damage along with the resultant inflammation, impairs the gastric
mucosal barrier and allows further damage by gastric acid

** The development of a peptic ulcer involves a disturbance in the balance

between the secretion of acid and pepsin by the stomach and the mucosal barrier
- Therefore when mucosal defense is compromised the acid cause mucosal
ulceration

** Usual sites for peptic ulcers are the:

- Esophagus
- Stomach
- First part of the duodenum
- Adjacent to a Meckel’s diverticulum when ectopic parietal cells are present

** NSAID use accounts for most of the ulcers not caused by H. pylori
- Associated with GU more commonly than DU
- NSAIDs block COX-I enzyme and reduces the secretion of cytoprotective
prostaglandin

** Zollinger-Ellison Syndrome- caused by a non-insulin secreting islet cell tumor

of the pancreas that produces a gastrin like hormone
- The result is gastric acid hypersecretion

69
- Severe disease with multiple ulcers that tend to be widespread within the
small bowel
- The gastrinomas may be solitary or multiple
- May be found in the head of the pancreas, duodenal wall or regional lymph
nodes
- Treated by excision of the tumor if possible and proton pump inhibitors

Clinical Symptoms
** 80% of peptic ulcers occur in the duodenum
- Duodenal ulcers have a peak in the 30s-40s and predominantly in males
(80%)
- Gastric ulcers occur mainly in males BUT the sex preponderance is less
marked (3:1)
- Tends to affect an older age group (40s-50s)

** Physical signs in the uncomplicated case are absent or confined to epigastric

tenderness
- The ulcer may be clinically silent before the acute presentation
- The pain is usually epigastric and occurs in attacks that lasts of for days or
weeks
- Pain that radiates to the back and comes constant suggests a posterior
penetrating ulcer
- Usually the pain wakes the patient in the early morning
- May be associated heartburn, nausea and vomiting
- Water Brash- regurgitation of watery acid from the stomach

Note: GU pain is usually epigastric and felt after eating

- DU pain is usually relieved by food

Differential Diagnosis Bleeding DU

- Erosive gastritis
- Esophageal varices
- Lower GI bleed

Bleeding PUD

70
** Gastroduodenoscopy should be performed in all cases of upper GI bleeding
** The stigmata predictive of persistent bleeding or re-bleeding are:
- Spurting artery
- Adherent Clot
- Visible vessel
- Ulcer >1 cm

** The bleeding may be treated by photocoagulation, hot probe, eletrocautery,

clipping, rubber banding or injection of normal saline (tamponade) or epinephrine

Differential Diagnosis: Chronic PUD

- Ischemic heart disease
- GERD
- Biliary colic
- Mesenteric ischemia (mesenteric angina)
- Chronic pancreatitis
- Pancreatic cancer

** Gastroduodenoscopy has 97% sensitivity and is the investigation of choice

- Should be performed on ALL patients with GU to rule out malignancy
- DU biopsy is not necessary

** Barium meal has a sensitivity of 80-90%

- However it cannot rule out malignancy in gastric ulcers

** H. pylori Testing
1- Serology- 90% sensitivity and specificity. Not useful for testing for
eradication because it may takes years to become negative
2- HpSA- H. pylori stool antigen test, useful for both diagnosis and
confirmation of eradication
3- Urea breath test- patient ingests labeled urea. The urea is metabolized to
ammonia and labeled bicarbonate if there is H. pylori infection. The labeled
bicarbonate is excreted as labeled CO2 in breath

Treatment

71
** The treatment of bleeding PUD involves an attempt at endoscopic treatment if
active
- Continue high dose IV or oral PPI
- Start empirical H. pylori treatment

** Surgical treatment is reserved for cases where complications of ulceration

occur. The commonest indications for emergency surgery are bleeding or
perforation

** Indications for surgery include:

i- Spurting artery- at endoscopy which cannot be controlled
ii- Clinical evidence of re-bleed in hospital- fresh blood in NG tube,
recurrence of tachycardia + hypotension

DU:
- Under sewing of ulcer
- Vagotomy + pyroplasty
- Gastrojejunostomy

GU:
- Biopsy + under sewing or excision of ulcer
- Vagotomy + pyloroplasty
- Gastrojejunostomy

Note: Modify risk factors

- Stop smoking
- Stop NSAID use
- Reduce alcohol + coffee

H. pylori Triple Therapy:

- Amoxil 1 gm bd
- Clarithromycin 500 mg bd x 10/7 days
- Omeprazole 20 mg bd x 4/52

72
- Amoxil 1gm bd
- Metronidazole 500 mg bd
- Bismuth subsalicylate 525 qid x 2/52
- Omeprazole 20 mg bd x 4/52

Note: PPI are more effective than H2 antagonists and achieve a similar level of
acid suppression to vagotomy/antrctomy

** The complications of peptic ulceration include:

i- Perforation- into the general peritoneal cavity or into adjacent structures
(liver, pancreas, colon)
ii- Stenosis- pyloric stenosis
iii- Hemorrhage
iv- Chronicity- due to formation of fibrous tissue at the ulcer base
v- Malignant change- may occur in relation to gastric ulcer

Perforated Peptic Ulcer

Differential Diagnosis
- Acute pancreatitis
- MI
- Acute cholecystitis
- Acute mesenteric arterial occlusion
- Ruptured aortic aneurysm
- Other causes of generalized peritonitis

Clinical Features
- Pain is sudden onset and extreme severity
- Subphrenic irritation may be referred to the shoulder
- Pain is aggravated by movement so the patient lies still
- Occasionally there is hematemesis or melena
- Abdomen is rigid and silent
- Liver dullness is diminished in 50% of cases because air has escaped in to
the peritoneal cavity
- Eventually the patient shows signs of generalized peritonitis

73
Treatment
- ABC
- Pass an NG tube to empty the stomach
- Opiate analgesia
- Prophylactic antibiotics
- IV H2 blocker or PPO

Dysphasia + Achalasia- 20-10-09- Dr. Fray

Dysphagia

Defn: Dysphagia is difficulty in swallowing

- The causes of obstruction may be local or general

Local Causes: In the lumen

- Foreign body

In the wall
- Congenital atresia
- Inflammatory stricture secondary to reflux esophagitis
- Caustic stricture
- Achalasia
- Plummer-Vinson syndrome with oesophageal web
- Pharyngeal pouch
- Tumor of esophagus or cardia
- Chatzi- with hiatus hernia seen in scleroderma

Outside the wall

- Pressure of enlarged lymph nodes- mediastinal, retrosternal lymphatics
- Thoracic aortic aneurysm
- Bronchial carcinoma
- Retrosternal goiter
- Aneurysm of the arch- syphilis

74
General Causes
- Myasthenia gravis
- Bulbar palsy
- Bulbar poliomyelitis
- Diphtheria
- Hysteria- globus hystericus- dysphagia in moments of tension
- Post-vagotomy

** Dysphagia for liquid suggests a functional problem

- Dysphagia for solids suggest mechanical obstruction

History
- May be a history of swallowed caustic substance
- Previous history of reflux esophagitis suggests peptic stricture
- Patients with achalasia tend to be young and have a long history without
weight loss
- Malignant stricture has a short history and occurs usually in elderly people
and associated with severe weight loss
- Examination may show evidence of Plummer-Vinson Syndrome (smooth
tongue, anemia, koilonychias)
- Secondary nodes from a carcinoma of the esophagus may be felt in the neck
and supraclavicular fossa

** Other signs of dysphagia include:

- Evidence of weight loss
- Halitosis- because the esophagus is not emptying
- Esophageal cancer may have late features of hepatomegaly and
lymphadenopathy

Investigations
1- Barium Swallow- may demonstrate the appearance of cervical web,
extrinsic compression and the dilated esophagus of achalasia
2- Upper GI Endoscopy-
3- CT Scan of Chest

75
4- Bronchoscope

Note: Upper GI endoscopy in achalasia is not helpful because it is a functional

disability; therefore mucosa is normal in achalasia

Achalasia of the Cardia

Defn: Neuromuscular failure of relaxation at the lower end of the esophagus with
progressive dilatation, torturosity, in coordination of peristalsis and often
hypertrophy of the esophagus above

** Achalasia can occur at any age, but usually in the third decade. The peak is
between age 20’s and 30’s. The ration of females to males is 3:2
- Achalasia resembles Chagas Disease which occurs secondary to
Trypanosma cruzi infection
- The parasite destroys the intermuscular ganglion cells of the esophagus

** The result of achalasia is progressive dysphagia over months to years

- Regurgitation of fluids from the dilated esophageal sac may be followed by
an aspiration pneumonia

** In achalasia there is progressive degeneration of the myenteric plexus leading

to non-relaxation of the lower esophageal sphincter
- Leads to aperistalsis of the body of the esophagus
- Solids are swallowed due to gravity and swallowing liquids are problematic
- Eventually it progresses to both dysphagia for solids and liquids

** Clinical features include chest pain and regurgitation of undigested food into
the mouth and airway
** There are 4 criteria to diagnose achalasia and one need two out of the 4
1- Established aperistalsis of the body of the esophagus
2- Demonstrate failed and incomplete relaxation of the lower esophageal
sphincter
3- Demonstrate an increase in LES pressure
4- Increase in intra-esophageal body pressure

76
Investigations
1- Chest X-ray- may reveal the dilated esophagus as a mediastinal mass, with
an air-fluid level, and pneumonitis from aspiration of esophageal contents
2- Barium Swallow- shows gross dilatation of the esophagus, leading to an
unrelaxing narrowed segment at the lower end (rat-tail sign or bird’s beak)
3- Further GI Endoscopy- because achalasia increases the risk of esophageal
carcinoma
4- Stricture of Lower Esophagus- may appear as achalasia

Note: The gold standard of endoscope every 2 years after surgery because the risk
of increased cancer

Treatment: Medical + Surgical treatment

1- Calcium channel blockers- nifedipine, sindelafil

2- Endoscopic Botulinum Injection- every 3-12 months
3- Pneumatic Dilatation
4- Surgical Myotomy- Heller’s operation is a cardiomyotomy that divides the
stomach of the lower end of the esophagus and the upper stomach down to the
mucosa

** The complications of Heller’s procedure include reflux esophagitis. Therefore

combine the cardiomyotomy with fundoplication procedure
- Wrap fundus of the stomach 180 degrees
- Nissan fundoplication- 360 degree wrap around LES

Esophageal Carcinoma
** 4% of all GI tract lesions are in the esophagus
** Majority are squamous cell carcinomas. A small proportion are due to
adenocarcinoma because of Barrett’s esophagus
- Males more than women and blacks more than whites
- Peak age = 50-60 years
- Smoking and alcohol increase the risk of developing esophageal carcinoma

Upper 1/3 = 20% of cancer

77
Middle 1/3 = 30% of cancer
Lower 1/3 =50% of cancer

** Esophageal cancers tend to present late with fungating growth outside into the
surrounding tissue
- Pericardiac effusion, pneumonia, lung abscesses, bronchitis
- Distant metastases to liver, lungs and adrenals
- Progressive dysphagia, initially to solids because liquids can trickle through
- Weight loss
- Hoarseness if the tumor infiltrates the recurrent laryngeal nerve
- Pain if it grows inward into the plexus
- Anemia

Investigations
- Plain chest x-ray
- Barium Swallow
- Endoscopy- shows the fungating mass
- Bronchoscopy if CT is not available

Treatment
** If found early the treatment is esophagectomy + palliation
** If found late the only option is palliation with the use of self-expandable metal
stent
- The best palliation is allowing the patient to remain eating by mouth

SHOCK
Defn: Shock is due to an abnormality of the circulatory system that results in
inadequate organ perfusion and tissue oxygenation

** Tissue perfusion requires an adequate blood pressure

- BP = CO x SVR
- CO = HR X SV

78
** Shock is inadequate tissue perfusion. May result from factors relate to the
pump (heart) and factors relating to the systemic circulation

Cardiogenic Shock
- A primary failure of cardiac output in which the heart is unable to maintain
adequate stroke volume in spite of satisfactory filling
- Compensation involves an increase in heart rate and systemic vascular
resistance
- Clinical Manifestations: tachycardia, sweating, pallor + coldness (due to
cutaneous vasoconstriction)

** Causes of cardiogenic shock include:

- Massive MI
- Pulmonary embolism
- Acute ventriculoseptal defect
- Mitral + aortic valve rupture
- Acute cardiac tamponade

Fluid Loss
- Reduction in circulating volume results in a reduction in stroke volume
and cardiac output
- Blood pressure is initially maintained with increased sympathetic activity
- This helps to increase the peripheral vascular resistance
- Clinical Picture: cold clammy patient with tachycardia
- As volume losses increase, the blood pressure falls

** Causes of hypovolemic shock include:

i- Hemorrhage
ii- Burns- with massive loss of plasma and electrolytes
iii- Severe diarrhea/vomiting- with fluid and electrolyte loss, especially in
colitis or pyloric stenosis
iv- Bowel obstruction- where large amounts of fluid are sequestered into the
gut
v- Peritonitis- with large fluid losses into the abdomen due to infection or
chemical irritation

79
vi- GI fistulae- with fluid + electrolyte loss
vii- Urinary losses- osmotic diuresis of DKA or polyuria in resolving acute
tubular necrosis

Classes of Hemorrhage
1- Class I- <15% of blood volume
- Minimal tachycardia
- No measurable change in blood pressure, pulse pressure or respiratory rate

2- Class II- 15-30% of blood volume

- Tachycardia, tachypnea,
- Urinary output is only mildly affected (20-30 ml/hr)

3- Class III- 30-40% of blood volume

- Least amount of blood loss to consistently cause fall in systolic pressure
- Tachycardia, tachypnea, altered mental state
- Almost always requires transfusion

4- Class IV- >40% of blood volume

- Immediately life threatening
- Requires rapid transfusion and immediate surgical intervention
- Marked tachycardia, significant hypotension, very narrow pulse pressure
- Negligible urinary output
- Mental status markedly depressed
Reduction in Systemic Vascular Resistance
- Reduction in SVR increases the size of the systemic vascular bed producing
a relative hypovolemia, reduced diastolic filling, reduced stroke volume + fall in
BP
- As a result there is vasodilation
- Therefore the patient appears warm rather than cool and clammy
- The heart compensates by increasing in output

** The principal causes are:

i- Anaphylaxis
ii- Sepsis

80
iii- Spinal shock

Septic Shock
- May be produced as the result of severe infection from either gram-positive
or gram-negative organisms
- Infection with gram-negative organisms is seen mainly after colonic, biliary
and urological surgery and with infected severe burns
- The endotoxins cause vasodilation of the peripheral circulation along with
increased capillary permeability
- These effects are also partly due to activation of normal tissue inflammatory
responses such as the complement system and cytokines

Sequelae of Shock
** A continued low blood pressure produces a series of irreversible changes. The
lack of oxygen affects all the vital organs
i- Cerebral hypoperfusion- results in confusion or coma
ii- Renal hypoperfusion- results in reduced glomerular filtration with
oliguria or anuria
iii- Heart failure- due to inadequate perfusion of the coronaries
iv- Pulmonary capillaries- may reflect the changes in the systemic
circulation with transudation of fluid
- The result is pulmonary edema
- Pulmonary edema hinders oxygen transfer and causes further arterial
hypoxemia and tissue hypoxia

v- DIC- precipitated by sepsis may be further aggravated by hypothermia

unless active re-warming is undertaken

Principles in the Management of Shock

Physical examination (resuscitation)
- ABCDE
- Vital signs
- Urinary output

Airway:

81
- Maintain patent airway with definitive intervention
- Immobilize C-spine

Breathing:
- Adequate ventilation
- Supplemental oxygen

Circulation
- Control obvious hemorrhage
- Adequate IV access- 2 large bore IV catheters
- Ensure adequate tissue perfusion

Disability- Neurologic Examination

- GCS
- AVPU

Exposure
- Fully undressed

Fluid Therapy
- Isotonic electrolyte solutions- lactated ringers or normal saline
- Colloid solutions
- Blood products
** Give an initial fluid bolus of 2 liters for adults and 20ml/kig for pediatric patient
- 3ml of crystalloids are required for every 1 ml of blood loss

Note: No benefit to colloid solutions other than blood in initial resuscitation

- Group (10 mins) and cross match (1 hr)
- Therefore in emergency use type specific un cross matched or type O packed
cells
Monitoring
- Oxygen saturation
- Central venous pressure- 4-8 cm water

82
- Pulmonary capillary wedge pressure (Swan-Ganz catheter)- cardiac
pulmonary dysfunction- 6-12 mmHg
- Urinary output- 0.5- 1ml/kg/hr

** If there is a rapid and good response to the bolus it usually indicates there was
less than 20% of blood loss
** If there is a transient response- that is responds to initial bolus BUT
deteriorates when fluids slowed to maintenance
- Indicates 20-40% blood loss

** Minimal or no response to the initial 2L bolus suggests that the patient requires
urgent surgical intervention
- Also needs blood component therapy

Phases of Resuscitation
1- Phase I- From injury to surgery- Control of hemorrhage
- Hypovolemic, vasoconstricted, impaired perfusion, progressive academia
- Therapy- infusion of balanced electrolyte solutions
- Transfusion is essential if loss is greater than 30%

2- Phase II- Fluid Sequestration- Ebb phase

- Completion of hemostasis
- Intracellular and interstitial fluid expansion
- The duration and magnitude is proportional to severity of shock
- Abdominal visceral edema is common

3- Phase III- Diuresis- Flow phase

- Final recovery phase- negative fluid balance
- Begins within 2-4 days of phase I
- Absence of the diuretic phase may indicate complication (sepsis) or pre-
existing heart, kidney disease

Note: Signs of irreversible shock are the lethal triad

- acidosis

83
- hypothermia
- coagulopathy

Cardiac Compressive Shock

Peri-Anal Disorders- Dr. East

Benign
- Hemorrhoids
- Anal fissure
- Abscess
- Fistula-in-ano
- Pilonidal disease
- Condyloma acuminatum
- Other STDs
- Hidradenitis suppurative

Neoplastic
- Bowen’s disease
- Paget’s disease
- Basal cell carcinoma
- Squamous cell carcinoma
- Verrucous carcinoma
- Adenocarcinoma
- Melanoma

Hemorrhoids
** Hemorrhoids are clinical abnormalities of the anal cushions
- NOTE: Hemorrhoids are NOT varicose veins

** The anal cushions are highly vascular tissue lining the anal canal
- Have a rich blood supply from the rectal arteries
- The rectal arteries anastamose with the draining veins

84
** The anal cushions are normal, highly vascularized masses of thick submucosa
containing blood vessels (arteries, veins + AV shunts), smooth muscle and elastic
and connective tissue
- Found in the right anterior, right posterior and left lateral sections of the
anal canal
- Function to preserve continence by closing the anus completely

** Hemorrhoids may be classified according to their relationship to the anal orifice

into:
- Internal- congested vascular cushions with dilated venous components
draining into the superior rectal veins
- External-
- intero-external- internal hemorrhoids that prolapse

** The development of internal hemorrhoids may be due to:

i- Gravity- related to upright position
ii- Straining- constipation, tenesmus
iii- Pelvic Venous Congestion- upright position, straining, pregnancy and
other cause of raised intra-abdominal pressure
- In pregnancy the anal cushions become prominent due to the venous
congestion caused by the large gravid uterus
- Also due to the laxity of supporting tissues due to the influence of
progesterone

iv- Genetics- severe disease often runs in families

v- Age- attenuation of supportive connective tissue

Note: All these factors contribute to failure of the supportive connective tissues in
the anal cushions
- This results in the downward sliding (prolapse) and chronic congestion of
veins and AV shunts

85
Note: The usual arrangement of hemorrhoids is at the 3:00, 7:00 and 11:00
positions

Clinical Features:
1- Bleeding- bright red blood on defecation, wiping or spontaneously. The
blood is not mixed with stool, but may occur at the beginning or end of defecation
2- Protrusion- prolapse
3- Fecal discharge- because of the failure of the cushioning mechanism to
close off the anus completely
4- Mucus discharge- because of exposure of rectal mucosa
5- Tenesmus- sensation of incomplete evacuation- associated with large
internal hemorrhoids
6- Pain- is NEVER associated with uncomplicated hemorrhoids
- Pain is associated with prolapsed, thrombosed internal hemorrhoid or
thrombosed external hemorrhoids

** DRE is done mainly to rule out other conditions; uncomplicated hemorrhoids

cannot usually be felt

Differential Diagnosis:
- Colorectal carcinoma- all patients with bleeding over 25 years should have
sigmoidoscopy and all patients over 35 should have sigmoidoscopy + barium
enema or colonoscopy
- Inflammatory bowel disease- ulcerative colitis or Crohn’s
- Peri-anal disorders- anal fissure
- Full-thickness rectal prolapse

** The treatment of hemorrhoids depends on clinical stage and whether

complicated or not
1- First Degree- bleeding but not prolapsed
2- Second Degree- bleeding + prolapse during defecation BUT reduce
spontaneously
3- Third Degree- bleeding + prolapse during defecation and require manual
reduction
4- Fourth Degree- bleed and irreducible prolapse

86
** For prolapsed thrombosed internal hemorrhoids treat with:
- Analgesic
- Stool softener
- Sitz baths
- Emergency hemorrhoidectomy

** For thrombosed external hemorrhoids:

- Incise and evacuate clot or excise hemorrhoid under LA if painful
- If pain subsiding, analgesic, stool softener, Sitz baths

** To treat uncomplicated internal hemorrhoids:

i- First Degree- treat constipation by increasing fiber in diet.
- Infrared coagulation or injection sclerotherapy if bleeding persists
- Sclerotherapy is a procedure used to treat blood vessels
- Injection into the blood vessels with a sclerosing solution that makes them
shrink
- 2-3 mls of 5% phenol in almond oil is injected as the sclerosing agent

ii- Second Degree- treat constipation, infrared coagulation, injection

sclerotherapy, rubber band ligation
iii- Third Degree- treat constipation, rubber band ligation, procedure for
prolapse and hemorrhoids or hemorrhoidectomy
iv- Fourth Degree- Treat constipation, PPH, hemorrhoidectomy

Anal Fissure
** An anal fissure is a linear ulcer of the anal canal.
- Tear at the anal margin
- Mucosa becomes sliced by hard stool forced over the promontory of the
ano-rectal junction
- The site is usually posterior in the midline
- The posterior position is due to the arrangement of the external anal
sphincter, which has its superficial fibers pass forward to the anal canal from the
coccyx
- These leaves an unsupported V posteriorly

87
- 90% posterior in the midline and <10% anterior

Note: Fissures away from the anterior and posterior midline should raise suspicion
of underlying disease
- Ex: Crohn’s disease

** Other risk factors for anal fissure include:

- Chronic diarrhea and constipation
- Anal sex
- Crohn’s disease
- HIV infection
- Leukemia

Clinical Features:
1- Pain- on defecation, which gradually subsides and begins again at the next
defecation
2- Bleeding- bright red on defecation
3- Purulent discharge
4- Linear ulcer- with sentinel pile at apex on inspection
- The sentinel pile protrudes from the anus and represents the torn tag of anal
epithelium
- The anal sphincter may also be in spasm

** Treatment of an acute fissure is stool lubricant or softener or bulking agents

and Sitz baths

** Chronic fissure- the internal sphincter spasms must be addressed

- Reversible chemical sphincterotomy
- Nitroglycerin ointment- relaxes the anal sphincter and allows the torn
epithelium to heal
- Diltiazem ointment
- Botulinum toxin injections

** Surgical treatment includes anal stretch

88
- Stretch the anal sphincter by insertion of a well lubricated plastic dilator
twice daily
- May be complicated by incontinence

** Other surgical treatments include lateral internal sphincterotomy

- Division of the internal sphincter under general anesthetic
- Surgical sphincterotomy has a risk of incontinence
- All patients have transient incontinence for flatus and liquid stool

Note: Recurrences of fissure-in-ano may be due to anal sex, Crohn’s disease,

leukemia, and HIV disease

Anal Abscess
- Originates in the anal glands
- The infection begins in an anal gland and the clinical presentation depends
on how pus spreads from the intersphincteric anal glands
- If the pus tracks down to the perineum between the sphincters it forms a
peri-anal abscess
- The pus can penetrate the external sphincter to reach the ischiorectal fossa

Note: if the abscess is drained externally, or bursts quickly, the anal gland is
usually destroyed
- BUT if it continues to secrete, a fistula will develop

** Abscesses present with severe, throbbing pain

- Pain makes sitting, moving and defecation difficult
- Patient may have a tender, indurated swelling close to the anus

** The systemic effects of an abscess are:

- Malaise, loss of appetite, sweating and rigors
- Patients with an ischiorectal abscess tend to be more systemically unwell
because there is a larger space to fill up with pus

Treatment: Surgical drainage

89
Anal Fistula
- About 50% of peri-anal abscesses become fistulae
- There is an internal opening at the anal gland site, a track and an external
opening

** The classification depends on the path of the track

Anal Fistula- presents as a non-healing sore beside the anus with recurrent abscess
formation
** The direction of the track can usual be predicted from Goodsall’s Rule
** Goodsall’s rule states that the internal opening of an anterior fistula lies along
a radial line drawn from the external opening to the anus
- The internal opening of a posterior fistula is in the midline posteriorly

Treatment
** Treat inter and trans-sphincteric fistulae with a fistulotomy
** Treat supra + extra-sphincteric fistulae with:
- Seton drain with slow sphincterotomy, rectal mucosal flap, fibrin glue

Pilonidal Disease
** Consists of sinuses and cysts high in the natal cleft
- Associated with hairs- either a foreign body reaction to embedded hair or a
disease of hair follicles

Note: The word pilonidal means a nest of hairs

- These sinuses are usually found in the midline skin covering the sacrum and
coccyx
- Pilonidal sinus is lined by granulation tissue and not skin

** Treated by curretage, diversion of track from midline, wide excision and

rotation flap
- Tends to be resistant to treatment

90
** Pilonidal sinuses are always in the midline of the natal cleft and lie over the
lowest part of the sacrum and coccyx
- The opening of a fistula can be anywhere around the anus
- Note: In an acute episode the inguinal lymph nodes do not enlarge because
the infection is mostly mild and chronic
- This is unlike a perianal abscess/fistulae which are often associated with
enlarged and tender inguinal lymph nodes

Condyloma Acuminatum
- Also known as veneral warts or peri-anal warts
- May spread over the entire perineum, including the labia majora and back of
scrotum
- Caused by HPV and can be transmitted by sexual contact
- Florid infections seen in immunocompromised patients

Treatment:
- Podophyllin
- Dichroloracetic acid
- Aldara- Imiqiomod- immune response modifier
- Intralesional interferon alfa
- Electrocautery- precautions should be taken because the virus can become
aerosolized and inhaled and transmitted

Hidradenitis Suppurativa
- Chronic inflammatory process affecting apocrine sweat glands
characterized by abscesses and sinus formation
- Treatment: Wide, deep excision + rotation or transferred flap

Neoplastic Disorders
Bowen’s Disease
- In-situ squamous cell carcinoma
- Brownish macules
- Treated by wide excision and flap closure

91
Paget’s Disease
- In-situ adenocarcinoma
- Associated with underlying adenocarcinoma in 50-85% of cases
- Eczematoid plaques with whitish-gray ulcerations or papillary lesions

Basal cell carcinoma

- Nodular appearance as elsewhere on skin

Squamous cell carcinoma

- Combination radiation + chemo
- AP resection only for failed chemoradiation

Verrucous Carcinoma
- Squamous cell cancer arising in Condyloma

Adenocarcinoma
- Arising from columnar epithelium in transitional zone or from anal glands or
apocrine cells

Melanoma
- May produce a mass, pain + bleeding

Fluid & Electrolyte Management- 6/10/09- Dr. Fray

** In an average person water is 60% of total body weight
- 40% of body weight is intracellular fluid
- 20% is extracellular fluid

Note: ICF is 2/3 of total body fluid and ECF (interstitial + intravascular) is 1/3 of
total body water
- Fluid may cross from compartment to compartment by osmosis which
depends on a solute gradient

92
- Fluid can also cross based on filtration which is a result of the hydrostatic
pressure gradient

** Intracellular fluid has a low sodium and high potassium concentration

- Extracellular fluid has a high sodium and low potassium concentration
- In the extracellular compartment, interstitial fluid has a low protein
concentration in comparison to intravascular fluid which has a high protein
concentration

** To calculate daily fluid and electrolyte requirements, the daily losses should be
measured or estimated
- 100 ml/kg for the first 10 kg
- 50ml/kg for the next 10 kg
- 20ml/kg for the remainder of the weight

** Therefore the maintenance requirement is defined by weight of the patient

** Normal urinary losses are around 1500-2000ml/day
** Normal fecal losses is about 300 ml/day

Electrolyte Requirements
1- Potassium- 0.5 – 1 mEq/kg/day
2- Sodium- 1-2 mEq/kg/day

** In 1L of normal saline there is 154 mEq of sodium

- In 500ml of Lactated ringers there is 139 mEq of sodium
- In the maintenance regime one L is given as normal saline and the rest is
given as dextrose water

** All NG losses are added to the maintenance as normal saline

- Therefore for every L of NG aspirate, add 1 L of normal saline to the
maintenance regime
- Also for every L of NG aspirate add 10-20 mEq of potassium

Effects of Surgery
** ADH is released in response to surgery; therefore water tends to be conserved

93
- Hypovolemia will cause aldosterone secretion and salt retention by the
kidney
- Potassium is released by the damaged tissues and potassium levels can be
further increased by blood transfusions.
- Therefore if renal perfusion is poor and urine output is decreased, potassium
can build up in the body post-surgery
- Therefore supplementary potassium may not be necessary in the first 48 hrs
following surgery or trauma

Note: The metabolic response to the injury of surgery causes Na+, K+ and water
retention
- Therefore potassium should not be added to the regime until the patient is
passing adequate urine
** Potassium is an irritant to peripheral veins. Therefore administration can cause
thrombosis of the veins
- As a result the drip site should be changed daily
- Potassium should NOT be given as a bolus because it will stop the heart
- Should be added to the fluid bag
- Never give more than 20eQ of potassium in 500 ml

EXAMPLE:
** In a 70-kg patient with normal U/Es and a daily urine output of 1500 ml who
also has NG losses of 2L what should the fluid replacement regime be?
ANS: Total volume to be replaced is 4.5 L (2.5L maintenance + 2L NG
replacement)
- 3L = normal saline and 1.5 L = dextrose water
- 60 mEq of KCl should also be added
Note: For every ml of blood lost, 3 ml of crystalloids should be given as
replacement
- This is because at least 2 ml of the crystalloid will move into the interstitial
compartment and 1 ml will stay in the intravascular compartment
08-10-09- Dr. Fray Chest Injuries

** Dangerous complications of chest injury are:

- Paradoxical respiration

94
- Tension pneumothorax
- Penetration of the lung
- Massive hemothorax
- Cardiac tamponade
- Large vessel damage

Chest Tube Insertion

** A chest tube insertion is a procedure to place a flexible, hollow drainage tube
into the chest to remove an abnormal collection of air or fluid from the pleural
space

** There are 4 common conditions that can require surgical chest tube insertion:
i- Pneumothorax- air leak from the lung into the chest
ii- Hemothorax- bleeding into the chest
iii- Empyema- lung abscess or pus in the chest
iv- Pneumothorax or hemothorax- after surgery of from trauma to the chest

** Lung ventilation depends on the following:

- a patent main airway
- Pulmonary alveoli
- Rigid bony skeleton of the thorax
- Integrity of the nerves that control the movement of the ribs and the
diaphragm

** Complications of chest injury are:

- Paradoxical respiration
- Pneumothorax
- Penetration of the lung
- Hemothorax
- Cardiac tamponade due to laceration of the heart
- Large vessel damage

Fractures of the Ribs

** The commonest injury to the chest is fracture of the ribs by a direct blow
- The most commonly affected ribs are the 7th-9th

95
- The fracture usually occurs in the mid-axillary line

Pneumothorax
** Occurs when the lung is penetrated and air escapes into the pleural cavity
** A tension pneumothorax results if the pleural tear is valvular, and allows air
to be sucked into the pleural cavity at each inspiration
- BUT prevents the air from returning to the bronchi on expiration
- A tension pneumothorax produces rapidly increasing dyspnea
- The trachea and apex beat are displaced away from the side of the
pneumothorax
- On the left side cardiac dullness may be absent
- The chest on the affected side gives a tympanitic percussion note with
bulging of the intercostals spaces

** A tension pneumothorax will present clinically with absent breath sounds and
hyperresonsance
- Treatment is needle decompression by placing a brannula in the 2 nd
intercostals space mid-clavicular line
- Note: on the left side go a bit more lateral to avoid the heart

** A tension pneumothorax kinks the IVC and therefore impairs venous return to
the heart, causing demise

Subcutaneous Emphysema
** Develops when a fractured rib tears the overlying soft tissue and allows air to
enter the subcutaneous tissues.
- The skin over the trunk, neck and sometimes face gives a peculiar crackling
feel to the examining fingers (crepitations)

Note: If subcutaneous emphysema is seen, suspect tracheal injury

Sucking Wound of the Chest

** Traumatic penetration to the chest (knife stab, gunshot wound) may produce a
wound that has a valvular effect

96
- Therefore air is sucked into the chest cavity during each inspiration but
cannot escape on expiration
- As a result a tension pneumothorax forms

Hemothorax
The bleeding may be from an intercostals artery in the lacerated chest wall or
from underlying contused lung
- The hemothorax may also be the result of injury to the heart or great vessels

Treatment
** The priorities in the management of chest injuries are:
i- Airway Control- may involve the passage of an endotracheal tube.
Aspiration of vomit is prevented by passing a NG-Tube to empty the stomach
ii- Breathing- Ensure the patient is breathing and maintaining adequate
oxygenation
- Oxygen saturation below 80% or a PCO2 above 7.3 kPa (55mmHg) are
indications for considering intubation and ventilation

iii- Sucking Wounds- should be closed

iv- Lung Expansion- should be achieved by insertion of an intercostals
drain with underwater drainage

** A traumatic pneumothorax requires insertion of a chest drain

- In contrast to a spontaneous pneumothorax which may resolve without
intervention

** A tension pneumothorax requires urgent emergency treatment by inserting an

intercostals tube drain
** A chest drain (chest tube) is inserted into the pleural cavity via an intercostals
space
- After cutting through the overlying skin the remaining insertion is by blunt
dissection into the pleural cavity
- The tube (drain) is inserted and connected to an underwater seal
- When the pressure in the pleural space is increased on expiration the air
escapes through the water

97
- BUT the air cannot re-enter the chest at inspiration because it is prevented
by the water seal

Note: Continuous bubbling in the chest tube system indicates a leak in the system
- May also indicate a bronchopleuric fistula which is treated with thoracic
suction

Emypema (Pyothorax)
** A pyothroax is a collection of pus in the pleural cavity

Etiology:
- Underlying lung disease- pneumonia, bronchiectasis, lung carcinoma, TB
- Penetrating wounds of the chest wall or infection following trans-thoracic
operation
- Perforation of the esophagus
- Trans diaphragmatic infection from a subphrenic abscess
- Hematogenous spread

Complications
- Rupture into a bronchus forming a bronchopleural fistula
- Discharge through the chest wall (empyema necessitans)
- Cerebral abscess

** The patient usually has a history of the underlying cause

- Patient is febrile, toxic, and may be anemic
- Signs of fluid in the chest on the affected side
- In chronic cases, finger clubbing may be present

Chest Tube Insertion

** The point of insertion in the chest most commonly occurs on the side (lateral
thorax)
- At a line drawn from the anterior axillary line to the lateral side of the
nipple in males

98
- Or 5cm above the sternoxiphoid junction in females

** The skin is sterilized with antiseptic solution covering a wide area

- Local anesthesia is administered to minimize discomfort
- At the rib chosen for insertion, the skin over the rib is anesthetized with
lidocaine
- The tissues, muscles, bone and lining covering the lung are also anesthetized

** Chest tube size is selected depending on the condition:

- 18-20 French catheter- for pneumothorax
- 32-26 F- for hemothorax

** The patient’s arm is placed over the head. The incision is made and the tube
inserted into the pleural space
- A suture is used to keep the tube in place

** The chest tube usually remains securely in place until imaging studies show that
air or fluid has been removed from the plural cavity

** Complications from a chest tube insertion include:

i- Bleeding from an injured intercostals artery
ii- Accidental injury to the heart, arteries, or lung resulting from the chest
tube insertion
iii- Local or generalized infection from the procedure
iv- Persistent or unexplained air leaks in the tube
v- Dislodgement of the tube
vi- Open or tension pneumothorax

Note: Indications for thoracotomy include:

- Signs of shock
- Draining 1L or more of fluid, if the tube is placed in directly after an acute
injury
- Draining 100-200 mls or more of fluid for more than 2hrs

Cardiac Tamponade

99
Defn: Compression of the heart that occurs when blood or fluid builds up in the
space between the myocardium and the pericardium
- Therefore fluid collects in the pericardial sac
- The pericardium can only expand to a certain amount
- As a result of the fluid collection the ventricles are restricted and cannot
expand fully
- Therefore they cannot fill enough or pump blood adequately

** Cardiac tamponade is characterized by a rise in venous pressure and a fall in

arterial pressure
** Clinically diagnosed by the presence of Beck’s Triad:
- Muffled heart sounds
- Distended neck veins
- Hypotension

** Treatment is thorocotomy and repair

** In a patient with a history of syncope or a hypotensive episode with a

precordial injury; suspect cardiac tamponade.
- The patient must be investigated to rule out tamponade. Investigations
include:
- FAST ultrasound (Focused Assessment with Sonography in Trauma)
- Echocardiogram
- Sub-xiphoid pericardial window

Note: Pericardiocentesis is ONLY done as an emergency procedure to

decompress and remove the fluid buildup as a stopgap method to prevent the
patient from decompensating before thoracotomy and repair

Flail Chest
Defn: Two or more ribs broken in two or more places
- On inspiration the flail part of the chest comes indrawn by the negative
intrathoracic pressure
- This is because this part of the chest is no longer in structural continuity with
the bony thoracic cage

100
- On expiration the flail part is pushed out while the rest of the ribs are
indrawn
- This is known as paradoxical movement of the chest

** The patient becomes anoxic because of failure of adequate expansion of the

affected side
- Also due to the shunting of deoxygenated air from the lungs on the side of
the fracture to the opposite side
- Patient develops ARDS due to the severely contused lung beneath the flail
part of the chest

Diaphragmatic Rupture
- More common on the left side
- Treatment: Decompress with chest tube and close the diaphragm surgically

Widened Mediastinum
- Seen on x-ray indicates bleeding in the mediastinum

Esophageal Tear
- Can cause infection of the mediastinum (mediastinitis)
- Can also cause air to build up in the mediastinum

Achalasia
- Rat tail on barium swallow
- Laparoscopic Heller’s operation with dorfundopliation

Featureless Bowel
- Is seen with a double contrast barium enema
- Feature of ulcerative colitis and ischemic colitis
-
Acute Abdomen- AIKEN

101
Defn: Any sudden, spontaneous non-traumatic disorder whose chief
manifestation is in the abdominal area and for which urgent operation may be
necessary

Symptoms:
- Mainly acute abdominal pain
Associated Symptoms:
- Vomiting
- Distention
- Alterations in bowel movement
- Urinary Symptoms
- Gynecologic Symptoms

** The peritoneal cavity is divided into the greater sac and the lesser sac
- Connected by the epiploic foramen

** The greater sac is divided into supramesocolic and inframesocolic (pelvis)

compartments
- The paracolic gutters- connect the supramesocolic spaces with the pelvis
- Right: Hepatorenal space
- Left: connects subphrenic and splenorenal (obstructed by the phrenicocolic
ligament)

Visceral Pain:
- Senses stretching and ischemia only
- Mediated via visceral afferent fibers
- These fibers follow the blood supply
- Visceral pain tends to be diffuse and not mapped 1:1 on the sensory cortex

Tenderness:
- A result of somatic afferent innervation of the parietal peritoneum and the
abdominal wall
- This is precisely related to the sensory cortex

Causes of the Acute Abdomen

102
Gynecologic Pathology:
- Pelvic inflammatory disease
- Ectopic pregnancy
- Ovarian pathology
- Uterine fibroids
- Dysmenorrhea

Abdominal Pathology
i- Inflammatory Bowel disease
ii- Mesenteric adenitis- an inflammatory process that affects the mesenteric
lymph nodes in the right lower quadrant
- The presentation of mesenteric adenitis mimics acute appendicitis
- Therefore it should enter the differential diagnosis for acute appendicitis
- Most frequently caused by viral pathogens
- Other etiologic agents include Yesinia enterocolitica, campylobacter jejuni
and salmonella
- Clinical Presentation: fever, abdominal pain, nausea, sometimes diarrhea
- Pain and tenderness are centered in the right lower quadrant, but may be
more diffuse than appendicitis

iii- Aortic aneurysm

iv- Mesenteric thrombosis/ischemia
v- Hepatitis
vi- Liver abscess
vii- Splenic infarct
viii- Renal colic
ix- Pyelonephritis
x- Intra-abdominal abscess
xi- Primary peritonitis
xii- Volvulus

Management Strategy
** The management strategy involves making a diagnosis of a cause within a
reasonable time (24 hrs)

103
- The stability of the patient and the suspected cause determines the waiting
period for investigation/observation
- Tailored inquiry
- The final inquiry may end up being a Laparotomy/laparoscopy

1- History
- Pain- Location, character, intensity, periodicity, radiation,
aggravating/relieving factors
- Associated Symptoms: vomiting, diarrhea, constipation, distention,
jaundice, fever, weight loss, bleeding per orifice
- PMH
- Menstrual history
- Drug history
- Family history

2- Physical Examination
- General observation
- Systemic signs
- Vital signs
- Fever
- Abdominal Signs- Inspection, palpation, percussion, auscultation
- DRE/Vaginal exam

3- Resuscitation
4- Tailored Investigations
- Urinalysis
- Bhcg
- Blood studies
- Abdominal + chest x-rays
- Abdominal ultrasound
- CT scan
- Others: IVU, contrast studies, endoscopy

5- Diagnosis
6- Treatment +/- Laparotomy

104
Pneumoperitoneum
Defn: The presence of air within the peritoneal cavity
- The most common cause is a perforation of the abdominal viscus
- Ex: perforated ulcer, perforation of any part of he bowel, trauma
- EXCEPTION: A perforated appendix rarely causes a pneumoperitoneum
- A pneumoperitoneum is common after abdominal surgery, however it
usually seals off 3-6 days post surgery

Note: The most common cause of a spontaneous pneumoperitoneum is the

introduction of air through the female genital tract

** Causes of pneumoperitoneum include:

1- Ruptured hollow viscus- perforated peptic ulcer, rupture/perforated
Meckel’s diverticulum, toxic mega colon, IBD
2- Infection of the peritoneal cavity- with gas forming organisms and/or
rupture of adjacent abscess
3- Iatrogenic factors-
4- Bowel obstruction- caused by a neoplasm, imperforate anus

http://emedicine.medscape.com/article/372053-overview

Intestinal Obstruction (Griffiths)- 20-10-09

Defn: A restriction to the normal passage of intestinal contents. Can be divided
into two main groups:
- Paralytic obstruction
- Mechanical obstruction

** Mechanical obstruction is further classified according to:

i- Speed of onset- acute, chronic, acute on chronic
- In acute obstruction the onset is rapid and the symptoms are severe
- Chronic obstruction- the symptoms are insidious and slowly progressive
- Note: A chronic obstruction may develop acute symptoms as the
obstruction suddenly becomes complete

105
- EX: when a narrowed lumen becomes totally occluded by inspissated
bowel contents (acute on chronic obstruction)

ii- Site- high or low

iii- Nature- simple versus strangulating
- Simple obstruction occurs when the bowel is occluded without damage to
its blood supply
- Strangulating obstruction occurs when the blood supply of the involved
segment of intestine is cut off
- Ex: strangulated hernia, volvulus, intussusception
- Intussusception- is the prolapse of one portion of the bowel into an
immediately adjacent segment
- Most commonly occurs at the terminal ileum
- The mesentery of the intussusceptum is compressed and subsequent
swelling of the bowel wall leads to obstruction
- Venous engorgement and ischemia of the intestinal mucosa cause bleeding
and outpouring of mucus
- 90% of cases are idiopathic. Predominate cause of intestinal obstruction in
persons aged 3 months to 6 years
- M > F 3:1
- Clinical Presentation: otherwise healthy infant, sudden onset of colicky
abdominal pain with vomiting and red current jelly stools
- http://emedicine.medscape.com/article/802424-overview

iv- Aetiology- can be classified according to causes:

- Inside the lumen- fecal impaction, gallstone ileus (usually obstructs small
intestine), food bolus, tumor
- Foreign objects- bezoar- a ball of swallowed foreign material, usually hair
or fiber, that collects in the stomach and fails to pass through the bowel

- Outside the lumen- strangulated hernia, volvulus, obstructions due to

adhesions (small bowel more likely), intussusception, enlarged lymph nodes,
- Hypertrophic intestinal tuberculosis- may causes obstruction at the ileocecal
valve
- Uterine fibroids- can compress large bowel

106
Note: Adhesions are NEVER a cause of obstruction in the large bowel
- Adhesive obstruction is the most common cause of small bowel obstruction

- Within the wall- congenital atresia, strictures (due to Crohn’s disease and
diverticular disease)
- Note: Strictures are more commonly due to diverticular disease than
Crohn’s disease
- Jejunal diverticulum

Note: Women over the age of 80 may have femoral hernias that can cause
obstruction of the small bowel

** Different types of intestinal obstruction can occur in various age groups

1- Neonatal-
- Congenital atresia + stenosis
- Imperforate anus
- Volvulus
- Hirschsprung’s disease
- Meconium ileus

2- Infants-
- Intussusception
- Hirschsprung’s disease
- Obstructions due to Meckel’s diverticulum

3- Young adults + middle age- Strangulated hernia

- Adhesions + bands
- Crohn’s disease

4- Elderly- strangulated hernia, bowel carcinoma, colonic diverticulitis,

impacted feces

Fitz-Hugh-Curtis Syndrome- is a rare complication of PID

- Usually caused by gonorrhea or Chlamydia bacteria

107
- The bacteria causes a thinning of the cervical mucosa and bacteria from the
vagina into the uterus and oviducts
- This causes infection and inflammation
- In the syndrome the inflammation causes scar tissue to form on Glisson’s
capsule, which is a thin layer of connective tissue surrounding the liver.
- Therefore the result is adhesions of the liver to the anterior abdominal wall
- Symptoms: Acute onset, upper-right quadrant abdominal pain + tenderness
aggravated by breathing coughing or movement
- Treatment: Removal of adhesions laparoscpically
-

Pathology
** When the bowel is obstructed by a simple occlusion, the intestine distal to the
obstruction rapidly empties and becomes collapsed
- The bowel above the obstruction becomes dilated
- Partly with gas which is mostly swallowed air
- Partly with fluid poured out by the intestinal wall together with gastric,
biliary + pancreatic secretions
- There is increased peristalsis in an attempt to overcome the obstruction
- The increased peristalsis results in intestinal colic

** As the bowel distends, the blood supply to the intestinal wall becomes
impaired
- If the distention continues there can be mucosal ulceration and eventually
perforation\
- Perforation is due to the production of the local ischemia necrosis

** In strangulating obstruction, the integrity of the mucosal barrier is lost as

ischemia progresses
- Therefore bacteria and their toxins can no longer be contained within the
lumen
- Transduction of organisms into the peritoneal cavity occurs
- Followed by secondary peritonitis
- If the strangulation is unrelieved it can lead to gangrene of the ischemic
bowel with perforation

108
** The deleterious effects of intestinal obstruction result from fluid + electrolyte
loss due to the vomiting and loss into the bowel lumen
- Protein loss into the gut
- Toxemia due to migration of toxins and intestinal bacteria into the peritoneal
cavity

Clinical Features
** The four cardinal symptoms of intestinal obstruction are:
1- Colicky abdominal pain- usually the first symptom of intestinal obstruction
- Small Bowel- pain is periumbilical
- Distal colonic obstruction- may be more suprapubic in location

2- Distension- is usually marked in chronic large bowel obstruction and

sigmoid volvulus
- There is swelling and dilation of the proximal bowel because fluid becomes
trapped

3- Absolute constipation- is the failure to pass either flatus or feces

- Usual feature of acute obstruction
- Partial or chronic obstruction may be accompanied by the passage of small
amounts of flatus
- Note: Absolute constipation is an early feature of large bowel obstruction
BUT it is a late feature of small bowel obstruction
- This is because even if the obstruction is complete, the patient may pass one
or two normal stools as the lower bowel empties after the onset of obstruction

4- Vomiting- more common in early small bowel obstruction

- Often a late sign or absent in chronic or large bowel obstruction
- In the late stages of intestinal obstruction the vomiting becomes feculent
- Feculent vomiting is due to the bacterial decomposition of the stagnant
contents of the obstructed small intestine

Clinical Examination
Inspection:

109
- Patient may be obviously dehydrated (mucus membranes, skin turgor)
- Patient may be in painful distress (colicky pain)
- Pulse is usually elevated But the temperature is usually normal
- A raised temperature and tachycardia suggest strangulation
- Abdomen is distended and visible peristalsis may be present

Note: Important to look for the presence of hernias because these may be
strangulated
- Also the presence of abdominal scars suggestive of previous surgery and
adhesive bowel disease

Palpation
- Generalized abdominal tenderness
- Mass may be present

Auscultation
- Bowel sounds are usually accentuated
- Rectal examination may reveal an obstruction mass in the pouch of Douglas,
apex of an intussusception, fecal impaction
- Rectal examination may also demonstrate the presence of Blumer’s Shelves
(rectal shelves)
- Rectal Shelves- a shelf palpable by rectal examination due to metastatic
tumor cells stemming from an abdominal cancer and growing into the rectovesical
or rectouterine pouch

Special Investigations
1- Erect Chest x-ray- to look for free air under the diaphragm
2- Abdominal x rays erect + supine. Loop(s) of distended bowel are usually
seen along with air-fluid levels on an erect film
- Small bowel obstruction- is suggested by a ladder pattern of dilated loops
- Also centrally placed and presence of striations that pass completely across
the width of the distended loop produced by the circular mucosal folds (plicae
circulare)
- Distended large bowel- tends to lie peripherally and to show haustrations
of the tenia coli, which do not extend across the whole width of the bowel

110
3- Barium Follow-through- small bowel obstruction
4- Water-soluble contrast enema- Emergency contrast enema is useful in the
demonstration of a suspected large bowel obstruction due to carcinoma or
diverticular disease
- Barium enema may also be useful in determining if the cause of large bowel
obstruction is non-mechanical

5- CT scan- useful to detect obstructing lesions and colonic tumors and

unusual hernias (obturator hernia)

Treatment
** Treatment can either be surgical or conservative (non-surgical) management
- Chronic large bowel obstruction is slowly progressive and incomplete and
can be further investigated
- Via sigmoidoscopy, colonoscopy, barium enema))
- Acute obstruction of a sudden onset that is complete and has a risk of
strangulation usually requires emergency surgical intervention

Pre-Operative preparation in Acute Obstruction

1- Gastric Aspiration- via nasogastric suction. Helps to decompress the
bowel and to remove the risk of inhalation of gastric contents during anesthesia
induction
2- Intravenous Fluid Replacement- required due to the fluid loss of copious
vomiting as well as third space losses
- Also because the large amount of fluid being sequestered in the gut

3- Antibiotic Therapy- began if there is evidence of intestinal strangulation or

perforation

Conservative Treatment (Drip + Suck)

** Conservative treatment of obstruction by means of IV fluid and NG aspiration
is indicated in the following conditions:
- If distinction from post-operative paralytic ileus is uncertain

111
- Obstruction is a part of repeated episodes due to massive intra-abdominal
adhesions which would make surgery hazardous
- If during the time of drip and suck there is an increase in distention,
aggravation of pain, increase in abdominal tenderness or tachycardia, there are
indications to explore the abdomen surgically

** Conservative therapy provides bowel rest and helps to avoid the need of going
to OT
- Conventional surgery teaching was that drip and suck should only be
performed for a maximum of 24 hrs and that if the patient has not settled by that
time, they should be taken to OT
- However the new practice is that you can drip and suck for 48-72 hrs in a
patient who has had previous abdominal surgery and you suspect the cause of
obstruction are adhesions
- Extending the period of conservative management helps to prevent the
development of further adhesions
- And these patients should only be operated on if they become emergent

Volvulus
Defn: A twisting of a loop of bowel around its mesenteric axis that results in
obstruction along with occlusion of the main vessels at the base of the involved
mesentery
- Most commonly affects the sigmoid colon, cecum and small intestine

Aetiology:
- Abnormally mobile loop of intestine
- Abnormally loaded loop- chronic constipation
- Loop fixed at its apex by adhesions around which it rotates
- Loop of bowel with narrow mesenteric attachment

** occurs usually in elderly, constipated patients

- 4x more common in men than in women
- Often seen in countries where high-fiber diets are common (Africa, India)

112
** Plain X-ray of the abdomen shows an enormously dilated oval gas shadow on
the left side
- Characteristic omega sign
- If left untreated the strangulated bowel undergoes gangrene and results in
death from peritonitis

Treatment
- Initial decompression with a flatus tube passed through a sigmoidoscope
- If the volvulus fails to untwist it can be done at Laparotomy

Note: Cecal volvulus is usually associated with a congenital malrotation

- Acute onset of RIF with rapid abdominal distension

Surgical Nutrition + IV Therapy (Powerpoints)

** Malnutrition predisposes a patient to immunological incompetence
- As well as altered wound or anastomotic healing

** A nutritional assessment is based on:

- History and physical examination
- Determination of protein (visceral + somatic) and fat reserves

- 24 hr nitrogen balance determination

- Nitrogen Balance = N (intake) – N (output)
- Nitrogen Intake- nitrogen from enteral and parenteral feeding
- Nitrogen Output- nitrogen excreted in urine, fistula, diarrhea

- Assessments of GI function- can the patient tolerate an enteral diet?

- Calculation of daily caloric and protein requirements

Dietary History: involves an estimate of intake

- calories
- protein
- vitamins

113
- trace metals

** History of recent weight loss

- Underlying diseases may suggest certain deficiencies
- Ex: liver disease may result in protein deficiencies

** The physical examination can provide information about the extent of the
malnutrition
1- Caloric Intake- subcutaneous tissue on extremities, buttocks, buccal fat
pads
2- Protein Status- bulk and strength of extremity muscles and temporal muscle
wasting
3- Vitamin Malnutrition- changes in the texture of skin, glossitis, hair
changes
4- Trace Metals- like vitamin deficiencies plus mental status changes

Protein & Fat Reserves

** Visceral and protein reserves are estimated from:
i- Serum total protein
ii- Albumin- has a long half life (18-21 days)
iii- Transferrin levels
iv- Total lymphocyte count
v- Antigen skin test

** Because albumin has a long half-life, it is possible to have a normal albumin

level and be in the early stages of malnutrition
** Other proteins are more sensitive indices of acute changes in nutritional status
- transferrin
- prealbumin
- retinol-binding protein
- ceruloplasmin

** Somatic protein reserve- can be measured midarm muscle circumference

** Fat reserves measured using triceps skin fold

114
Caloric and Protein Requirements
Weight Maintenance: 30-35 kcal/kg/day
Weight Gain- 35-40 kcal/kg/day

** Calories can come from glucose or fats

- 1 g glucose = 3.4 kcal
- 1 g fat = 9.2 kcal
Protein Requirements- 1 g – 1.5 g/kg/day
- 6.25 gm protein = 1 gm nitrogen

Note: To minimize protein catabolism a sufficient amount of non-protein calories

(fat, carbohydrates) must be given
- A calories-nitrogen ratio of 100-150 : 1 is required

Electrolyte + Minerals
- Na, Cl, K+, PO4, Mg, Ca

Trace Metals + Vitamins

- Manganese, copper, zinc, chromium

Indications for Nutritional Support

1- NPO for 7-10 days
2- Unable to maintain nutrition through usual enteral route

Enteral Nutrition
** Indicated in patients unable to maintain adequate oral intake AND has a
functioning GI tract
1- Nasogastric
2- Gastrostomy
3- Jejunostomy
4- Nasoduodenal

** With gastric feeding, feeding can be done via bolus doses because the stomach
can hold a large volume and is a storage organ

115
** With small bowel feeding- feeding has to be intermittent and controlled by a
pump

** Complications of enteral feeding include:

1- Gastrointestinal Causes- cramping, distention, vomiting, diarrhea
2- Aspiration-
3- Mechanical Causes- tube displacement, perforation, intestinal obstruction
4- Electrolyte Imbalance- hyperglycemia, hypernatremia, hyperosmolar non-
ketotic coma
5- Dehydration

Parenteral Nutrition
Peripheral Vein Nutrition
- Use isotonic solutions containing: amino acids, 5-10% dextrose, fat
emulsions
- Indicated for short-term therapy to supplement poor nutritional intake
- Peripheral veins are at risk of phlebitis when the osmolality exceeds 600
mOsm (10% glucose)

Central Vein Nutrition

- Requires the insertion of a catheter into a central vein

** Complications of TPN:
1- Catheter- Placement, sepsis, thrombosis
2- Metabolic- essential fatty acid deficiency, zinc deficiency, hypo or
hyperglycemia, abnormal serum electrolytes, hyperchloremic acidosis, elevated
LFT’s

** Monitoring of TPN is necessary to reduce metabolic complications and monitor

progress
- Nitrogen balance
- Electrolytes + LFTs
- Daily weight- input/output recordings

Pancreatitis- VALENTINE

116
** The pancreas develops as a dorsal and a ventral bud from the duodenum
- The ventral bus rotates posteriorly and encloses the superior mesenteric
vessels
- Ventral bud forms the major part of the head of the pancreas and its duct
becomes the main duct of Wirsung
- The main duct has a shared opening with the common bile duct in the
ampulla of Vater
- The larger dorsal bud becomes the body and tail and its duct becomes the
accessory duct of Santorini

** Annular Pancreas- a developmental anomaly that occurs when the two

developmental buds may envelop the second part of the duodenum
- Produces a rare form of duodenal extrinsic obstruction

** Heterotopic Pancreas- Produced by an accessory budding from the primitive

foregut
** The pancreas has both exocrine and endocrine functions
- Produces pancreatic enzymes for digestion
- Also produces bicarbonate

Acute Pancreatitis
Defn: Acute inflammation of the pancreas

Aetiology
** The most common causes of acute pancreatitis are alcohol and gallstones
Note: Both alcohol and gallstones are cause of both acute and chronic
pancreatitis

1- Gallstones- causes pancreatitis by both obstruction of the pancreatic duct at

the ampulla of Vater and passage of the stone through the duodenum. This is
because as the stone passes, due to the proximity of the pancreas there is reflux of
biliary contents into the pancreas (common channel theory)
2- Alcohol- the breakdown products of alcohol are directly toxic to the
pancreas

117
3- Tumor- pancreatic cancer
4- Infection- mumps, CMV, coxsackie
5- Drugs- corticosteroids, sodium valproate, bactrim, thiazide diuretics,
sulfasalazine
6- Hyperlipidemia
7- Autoimmune- SLE
8- Hypercalcemia
9- Scorpion Toxin
10- ERCP

** In acute pancreatitis there is auto digestion of the pancreas that results from the
liberation of digestive enzymes
- The pancreas is normally protected from auto digestion by storing its
enzymes in zymogen granules before secreting them as pro-enzymes

** Duodenopancreatic reflux is an important factor in the initiation of

autodigestion. May occur as a result of a number of the etiological factors:
i- Injury to the papilla following endoscopic cannulation or trauma
ii- Damage to the sphincter due to the recent passage of a stone

** As a result duodenal fluid containing enterokinase refluxes into the duct, and
activates the pancreatic proenzymes
- As the inflammation proceeds, local infarction may occur as arterioles
thrombose
- This causes more proenzymes to leak from the necrotic cells
- The inflammation and autodigestion progresses, liquefying necrotic material
- Inflammatory exudate collects in the lesser sac
- This fluid is walled off by the stomach in front and the necrotic pancreas
behind (pseudocyst)

Clinical Features
** Pain is of rapid onset, is severe and constant
- Usually epigastric pain that radiates into the back
- The epigastric pain usually progresses to generalized abdominal pain
- The patient often sits forward and repeated retching is common

118
- The patient is often doubled over in pain
- Vomiting is early and profuse
- Patient may be shocked with a rapid pulse, cyanosis and raised temperature,
tachypnic
- Fever is because it is an inflammatory process
- The shock is due to the severe fluid shifts that occur in pancreatitis
- Patient may also have signs of dehydration
- Mucus membranes may also be pale due to retroperitoneal hemorrhage
- Note: Patient may also give a history of previous gallstones or heavy alcohol
use
- The abdomen has generalized tenderness and guarding
- 30% of cases are slightly jaundice because of the edema of the pancreatic
head obstructing the CBD
- Therefore the jaundice is a result of compression of the CBD due to the
inflammation of the pancreas
- May have abdominal distention as a result of the fluid shifts
- Shifting dullness may be present due to the ascites
- There may be a palpable epigastric mass that develops because the small
bowel has migrated to the site of inflammation
- Decreased bowel sounds due to the ileus

** There may be decreased chest expansion due to splinting

- Signs of pleural effusion due to irritation of the diaphragm

Note: Both Cullen’s Sign and Grey Turner’s Sign may be present
- Cullen’s sign is discoloration around the umbilicus that is indicative of
retroperitoneal hemorrhage. The blood may track along the falciform ligament
to the umbilicus
- Grey Turner’s Sign- may occur a few days a severe attack. The patient
develops a bluish discoloration in the loins from extravascation of bloodstained
pancreatic juice into the retroperitoneal tissues

Note: The patient with acute pancreatitis may present with signs of localized or
generalized peritonitis

119
Differential Diagnosis
- Acute cholecystitis
- Perforated peptic ulcer
- Coronary thrombosis
- Small bowel obstruction

Investigations
1- CBC- WCC count may be increased. Hb can be increased or decreased due
to hemoconcentration
2- U&E- to check for electrolyte abnormalities and BUN may be elevated
3- Serum amylase- amylase is released into the circulation by the damaged
pancreas
- Exceeds the kidney’s ability to excrete it, therefore the serum concentration
rises
- Usually significantly raise (5x) in the acute phase BUT returns to normal in
2-3 days
- Note: Because amylase rapidly falls within 24-48 hrs a patient that is
presenting after a few days of illness may have a normal serum amylase

4- Lipase- is a better indicator of pancreatitis because it remains elevated for 7

days
5- Serum Calcium- may be lowered due to fat saponification
- Calcium becomes bound to fat in the circulation

6- Serum bilirubin- is often raised

7- Blood glucose- may be elevated
8- Abdominal X-ray- useful in excluding other causes of abdominal pain eg.
Perforation, obstruction etc
- In some cases there may be a solitary, dilated loop of proximal jejunum
(sentinel loop sign)

9- CT Scan- provides good view of the pancreas and can confirm pancreatitis
if the amylase is normal
- CT is both diagnostic and prognostic
- At later stages, necrotic pancreas, abscess or pseudocyst may be visualized

120
- CT abdomen can demonstrate: necrosis of the pancreas, fluid collection,
areas of inflammation

10- Ultrasound- can demonstrate associated gallstone and dilation of the CBD

Scoring Systems
Ranson Criteria- is a clinical prediction rule for predicting the severity of acute
pancreatitis
Parameters used:
At Admission: - GA LAW
1- Age in years > 55years
2- WCC > 16
3- Blood glucose > 11 mmol
4- Serum LDH > 350 IU/L
5- Serum AST > 250 IU/L

At 48 hrs- C-HOBBS
1- Calcium < 2.0 mmol/L
2- PO2 < 60 mmHg
3- Fluid sequestration > 6L
4- Base excesses > 4 mEq/L
5- BUN increased by 1.8 or more m/mol after IV fluid hydration

** For each positive feature on the lists assign a 1

- Mild < 3
- Severe >3
- A score of 7-8 has a mortality of 90%
- A score of 304 has a 15% mortality

APACHE II- Acute Physiology and Chronic Health Evaluation

- Designed to measure the severity of disease for adult patients admitted to
ICU

Management

121
1- IV Fluid Therapy- IV crystalloids and monitor rehydration
- Therapy to treat shock and establish a diuresis

2- Resting the Pancreas- by passing an NG tube and removing stimuli for

secretion. Keep NPO
3- Antibiotics- in severe cases and if the pancreatitis is associated with
gallstones
- Must use agents like the carbapenems or quinolones
- Because normal antibiotics do not penetrate
- Prone to infection by GI bacteria due to translocation of organisms
- Note: Patients with mild pancreatitis do not benefit from prophylactic
antibiotics
-
4- Analgesics- opioid analgesics are indicated
- Use pethidine rather than morphine because morphine causes spasms of the
Sphincter of Oddi

5- Early ERCP- may be helpful in severe gallstone pancreatitis

- Endoscopic sphincterotomy performed early may be useful in gallstone
pancreatitis

6- Surgery- in the case of gallstone pancreatitis, cholecystectomy should be

done as soon as the patient recovers from the acute attack
- Surgery may be necessary later in the disease for operative debridement of a
necrotic pancreas
- Drainage of a pseudocyst

Complications of Pancreatitis
1- Abscess Formation- with pancreatic necrosis, characterized by pyrexia +
persistent leukocytosis

2- Pancreatic Pseudocyst- characterized by persistently raised serum amylase

and pain into the second week, as well as an epigastric mass
- Pseudocyst formation is due to an acute fluid collection

122
3- GI Bleeding- from acute gastric erosions or peptic ulceration

4- Renal Failure- associated with shock and pancreatic necrosis

5- Pulmonary Insufficiency- leading to acute lung injury and ARDS
6- Relapsing Pancreatitis
7- Diabetes Mellitus- as a result of a severe attack with pancreatic necrosis
8- Aneurysm of the splenic artery
9- Rupture into a pseudocyst
10- Colonic stricture- spasm of the transverse colon in acute pancreatitis
- Seen on x-ray as the colon-cut off sign
11- Retroperitoneal hemorrhage from the splenic artery-
12- Pancreatic ascites- the pancreatic duct opens into the peritoneal cavity.
Therefore the ascitic fluid is actually pancreatic fluid that is accumulating and
contains inactive enzymes
- Can be treated by ERCP + papillotomy
- Remove the sphincter and encourages the flow of the fluid into the area of
least resistance

KPH NOTES: 02-11-09- FRANCIS- Gallstones + Pancreas

** 10-15% of persons have gallstones
- 10% of these persons will have symptomatic gallstones
- 10% of this 10% will develop complications of the gallstones
- F > M 4:1

** Bile is made up of:

- cholesterol
- Lecithin
- Bile salts
- Bilirubin- bound to albumin and transported in blood. Indirect bilirubin
measures unconjugated bilirubin and direct bilirubin measures conjugated bilirubin
- Electrolytes
- Alkaline phosphatase

Note: 95% of bile salts are absorbed in the terminal ileum

123
** In the pathogenesis of cholesterol stones there are several factors, which
contribute:
1- Secretion of Lithogenic Bile- bile becomes lithogenic due to changes in the
bile
- Increase in cholesterol in the bile- the hormones of pregnancy (estrogen)
result in increased cholesterol
- Decrease in bile salts- seen in cirrhotic patients and terminal ileum
disease
- Smalls Triangle: Cholesterol, phospholipids and bile salts
- Note: Most stones in the bile duct are secondary to formation of stones in
the gallbladder
- Therefore the formation of primary common bile duct stones are RARE

2- Stasis- In pregnancy, there are high levels of progesterone, which result in

decreased activity of smooth muscle. Leading to atonicity of the gallbladder
3- Role of Infection- bacteria may act as a nidus for stone formation

** The consequences of gallstones follow a progression:

1- Biliary Colic- peristalsis of the hollow viscus in an attempt to pass the stone
resulting in colicky pain
2- Acute Cholecystitis- inflammation of the gallbladder resulting in epigastric
+ RUQ pain and vomiting
- May be complicated or uncomplicated
- May be become infected and form an empyema
- Perforation leading to generalized or localized peritonitis

3- Chronic Cholecystitis- thickening of the gallbladder wall due to repeated

attacks

Differential Diagnosis:
- Perforated peptic ulcer- perform an erect chest x-ray and look for air beneath
the right hemidiaphragm

124
- Pancreatitis- if serum amylase is elevated about 1000IU it is suggestive of
pancreatitis
- Both lipase and urinary amylase can be done if serum amylase is
inconclusive
- Acute cholecystitis- ultrasound should show:
- Pericholic cystic fluid
- Thickening of the gallbladder wall
- Sonographic Murphy’s sign

Treatment
- Pass an NG tube and keep NPO
- IV fluid therapy
- Analgesia
- Only give antibiotics if there is evidence of pyrexia and increased WCC
- Admit and review abdominal exam, the majority settle with conservative
therapy
- Note: The gold standard in the treatment of cholecystitis is same-admission
laparoscopic cholecystectomy
- In Jamaica only cholecystitis in diabetics is treated aggressively all others
are scheduled for a re-admit cholecystectomy
- Abnormal LFT’s- suggests choledocholithiasis

Complications of Choledocholithiasis
1- Obstructive Jaundice- Dark urine, pale stools, pruritis and yellowed sclera
2- Acute pancreatitis
3- Ascending cholangitis- bacterial infection superimposed on an obstruction
of the biliary tree
- Most commonly due to choledocholithiasis but may also be associated with
neoplasm or stricture
- The biliary obstruction decreases host antibacterial defenses and increases
small bowel bacterial colonization
- As a result the infection ascends into the hepatic ducts causing serious
infection
- Increased biliary pressure pushes the infection into the biliary canaliculi,
hepatic veins and perihepatic lymphatics

125
- Leading to bacteremia
- Male to female ratio is roughly equal in cholangitis although gallstones are
more common in women

** Ascending cholangitis is characterized by Charcot’s Triad:

i- Right upper quadrant pain
ii- Fever
iii- Jaundice

Reynold’s Pentad (Charcot’s Triad + 2 more)

- Altered mental status
- Hypotension

Treatment (Choledocholithiasis)
1- ERCP + removal of stone. ERCP can be both therapeutic and diagnosis
2- Cholecystectomy & CBD exploration- done as an open procedure
- Leave a T-tube in place for cholangiogram done 7-10 days afterward
- Wait 7-10 days before doing the cholangiogram to ensure the fibrous tract is
in place
- This tract seals off the peritoneum and prevents leakage of contrast
material into the peritoneal cavity

3- Transduodenal Sphincteroplasty

Note: If the duct is >1,5 cm a choledochoduodenostomy can be done which allows

the stone to pass directly into the small bowel and become passed out in the stool

Obstructive Jaundice
** Normal serum bilirubin is below 17 mmol/L
- Excess bilirubin becomes clinically detectable when the serum level rises to
over 35 mmol/L∫
- Gives a yellow tinge to the sclera and skin

Bilirubin Metabolism
** Red cells are destroyed in the reticulo-endothelial system

126
- The iron is released and used for further hemoglobin synthesis
- The bilirubin-globin reaches the liver as a lipid-soluble, water-insoluble
substance
- In the liver, the bilirubin is conjugated with glucoronic acid in the
hepatocytes and excreted in the bile as the water-soluble bilirubin glucoronide

** In the bowel lumen, bilirubin is reduced by bacterial action to the colorless

urobilinogen
- Most of the urobilinogen is excreted in the feces
- In the feces it is broken down into urobilin which is pigmented and gives
the stool its normal color
- A small amount of urobilinogen is reabsorbed from the intestine tin to the
portal venous system and passes to the liver
- Some reaches the systemic circulation and is excreted in the kidney

Classification of Jaundice
1- Pre-Hepatic Jaundice- Increased production of unconjugated bilirubin by
the RE system exceeds the ability of the liver to conjugate
- Usually caused by hemoglobinopathies
- Also known as achloric jaundice because of the unconjugated bilirubin the
urine remains pale

2- Hepatic Jaundice- In the presence of hepatocellular damage the liver is

unable to conjugate bilirubin efficiently
- As a result less is excreted into the canaliculi
- Therefore BOTH unconjugated and conjugated bilirubin accumulate in the
blood
- Occurs in cirrhosis and hepatitis

3- Post-Hepatic (Obstructive) Jaundice- The pruritis is due to the

accumulation of bile salts under the skin
- 90% of obstruction is due to cancer of the head of the pancreas and
gallstones
- Intraluminal causes- gallstones, liver flukes

127
- Intramural Causes- Iatrogenic strictures due to ligation of the CBD post-
cholecystectomy
- Bile duct strictures- cholangiocarcinoma
- Sclerosing cholangitis
- Biliary atresia
- Choledocal cysts
- Extra luminal Causes:
- Malignant nodes- especially due to gastric cancer
- Carcinoma at head of the pancreas

** Obstruction of the intrahepatic or extra hepatic bile ducts prevents excretion

of conjugated bilirubin
- Without pigment, the stools become pale
- The conjugated bilirubin builds up in the blood and is excreted in the urine,
turning it dark brown

Courvoisier’s Law- states that in the presence of a palpable gall bladder, painless
jaundice is unlikely to be caused by gallstones
- Because gallstones are formed over a longer period of time this results in a
shrunken, fibrotic gallbladder which does not distend easily
- Therefore the gall bladder is more often enlarged in pathologies that cause
obstruction of the biliary tree over a shorter period of time such as pancreatic
malignancy

Note: If direct bilirubin is more than 2/3rds elevated than the indirect bilirubin,
obstructive jaundice can be diagnosed
- After blood investigations, do ultrasound
- Ultrasound may show dilated CBD, stones or a mass, dilated bile ducts in
the liver
- CT scan- if there is evidence of head of the panaceas cancer
- Percutaneous trans-hepatic cholangiogram
- ERCP cholangiogram

Pancreatic Cancer
** Fourth most common gastric cancer after: colon, esophagus, stomach

128
- The majority are adenocarcinoma arising from the exocrine pancreas
- 60%-75% are situated in the head of the pancreas
- 25% in the body
- 15% in the tail- usually associated with backache rather than constitutional
symptoms

** Tumors of the head of the pancreas are divided into:

i- Head Proper- 75%
ii- Peri-ampullary- 25%- have a better prognosis because they present
earlier

** Pancreatic tumors have a less than 5% 5 year survival

** Pancreatic carcinoma tends to spread via direct invasion into:

i- Common bile duct- causing obstructive jaundice
ii- Duodenum- occult or overt intestinal bleeding
iii- Portal Vein- portal vein thrombosis, portal hypertension +ascites
iv- Inferior vena cava- bilateral leg edema

** Also spreads via lymphatics to adjacent lymph nodes and nodes in the porta
hepatis
- Spread via blood stream to the liver and then to the lungs

Note: Tends to spread hematogenous and by direct spread to the vasculature

** Palliation for obstructive jaundice includes:

i- Stenting
ii- Cholecystojejunostomy- or double bypass with gastrojejunostomy\

Clinical Features
** Carcinoma of the pancreas may present in a variety of ways
1- Painless progressive jaundice- most often found in the peri-ampullary type
of tumor. This is because the bile duct is compressed at an early stage before
extensive, painful invasion of surrounding tissues

129
2- Pain- at least 50% present with epigastric pain of a dull, continuous aching
nature that radiates into the upper lumbar region
3- Intermittent Jaundice- may temporarily remit as necrosis of the tumor
occurs and allows transient escape of bile into the duodenum
4- Diabetes- glycosuria of recent onset
5- Thromboplebitis migrans (Trouseau’s sign)
6- General features of malignant disease- anorexia, weight loss

** On examination the patient is frequently jaundice and half have a palpable

gallbladder
- In larger tumors there may be a palpable epigastric mass
- The liver is usually enlarged due to the back pressure of biliary obstruction
or due to secondary deposits

** Treatment is mainly palliative. Attempting curative surgical resection is rare

because only certain types can be resected
- Only possible if the disease is confined to the peri-ampullary region
- Whipple’s pancreaticoduodenectomy involves removal of the duodenal C
along with the pancreatic head and CBD
- Accompanied by a gastroenterostomy and biliary drainage using a loop of
jejunum

Note: Most pancreatic carcinomas are inoperable because of their diagnosis in the
late stage after metastasis has occurred
- Also because there is often involvement of large vessels (SMA + portal vein)

Medical Diseases in the Surgical Patient- 21-10-09- VALENTINE + LEAKE

PPT

- Endocrine Disease- diabetes + thyroid

- Cardiovascular
- Pulmonary
- Renal
- Hematological

130
- Pregnancy
- Elderly

Diabetes Mellitus

1- Hyperglycemia- leads to poor wound healing and increased peri-operative

infection rate
- Due to stress (increased catecholamine + cortisol levels) and inactivity

2- Hypoglycemia

** The aim of the pre-surgery work up in the diabetic patient is to assess the
patient’s risk:
- Thorough history + examination
- Cardiac risk- ECG
- Pulmonary risk- chest x-ray
- Renal risk- electrolytes + urinalysis

Note: Weight the risk versus the benefit depending on the nature of the surgery

** With Type II diabetics controlled on diet or on oral hypoglycemics it is

important to avoid hypoglycemia
- Therefore discontinue long-acting drugs one day before surgery
- Convert to soluble insulin the day before the surgery
- Patients on metformin should stop taking the drug 48-72 hrs prior to
surgery
- Because metformin tends to cause metabolic acidosis under anesthesia
- Note: Because surgery is a stress, patients may also need to have insulin
added to them in theater

** Schedule diabetic patients for early surgery

- Administer glucose +/- insulin
- Check blood glucose every 3-4 hours
- AIM: glucose levels of 5-11 mmol/L

131
** If they become hypoglycemic give IV 50% dextrose or glucose load
- Hyperosmolar coma- results in dehydration from osmotic diuresis.
Therefore fluid management is key

** Type I Diabetics require insulin

- Convert from long-acting insulin to short-acting
- Subcutaneous- has a risk of delayed absorption
- Intravenous- is more predictable absorption and control. Therefore less risk
of hypo or hyperglycemia
- Monitor glucose levels every 2 hours and adjust insulin infusion

** Post-operative return to normal insulin or oral hypoglycemics once the patient

is re-established on diet
- Continue monitoring the blood glucose levels
- Note: if the glucose is hard to control post-op consider occult infection

Thyroid Disease: Hyperthyroidism

** Risk of thyroid storm- hypertension, severe dysrhythmias, congestive heart
failure
- Can occur in any operation but mainly in thyroidectomy

** Ensure the patient is euthyroid by checking thyroid function tests

- Place on drugs if necessary- propylthiouracil, neomercazole
- In emergencies potassium iodide block the uptake of iodine given along with
beta blocker + propylthiouracil

Hypothyroidism
- Risk of hypotension, shock, hypothermia during surgery
- Myxodema coma- failure to breathe and they end up retaining CO2
- Ensure the patient is euthyroid- treat with levothyroxine if necessary
- Emergencies- IV or oral levothyroxine in large doses

Adrenal Insufficiency
- Patients on steroids with suppressed adrenal glands

132
- These patients are at risk of Addisonian crisis- salt wastage, hypotension,
shock, death
- Surgery is a stressor therefore these patients need adrenal support or
corticosteroid support
- Administer stress doses of steroids peri-operatively

Heart Disease
- The stress of surgery causes the release of catecholamines
- Anesthetic agents are also a source of cardiac stress
- Changes in heart rate, myocardial demand, contractility
- Risk of myocardial ischemia
- Risk is greatest in the first 72 hours post-operatively due to fluid shifts and
fluctuations in HR/BP
- Therefore it is important to identify pre-existing heart disease

** In an emergency setting optimize the patient with beta-blockers and nitrates

and then proceed to surgery
** In the elective setting coronary artery assessment may be requirement and
revascularization may be needed before the elective procedure can be done

** High-risk patients for surgery include:

1- Recent MI- 30% at 3 months; 10-15% at 4-6 months
- Delay elective surgery for 3-6 months

2- Unstable angina- indicates an underlying coronary artery disease

3- Decompensate Heart Failure- risk for peri-operative death
4- Severe hypertension- especially >180/110 mmHg
5- Valvular stenosis

Note: Patients on diuretic should have their diuretics stopped on the morning of
surgery
- BUT continue other anti-hypertensives up to surgery
- Operate on hypertensive patients earlier in the morning

Intra-Operative Monitoring

133
- Central venous pressure monitoring
- Pulmonary wedge pressure (Swan Ganz Catheter)
- Trans-esophageal echocardiography- visualize the left ventricle with
contractility

Respiratory Diseases
** Respiratory disease is the main source of peri-operative complications
(atelectasis pneumonia)
- Depends on the site of surgery (chest + upper abdominal are more
susceptible) and pre-existing lung disease
- Risks are reduced with laparoscopic surgery
- Smaller incisions
- Reduced surgical trauma
- Less post-op pain
- Improved breathing

** The risk factors for pulmonary complications include:

1- Upper Respiratory Infection- due to compromised respiratory defense
2- Lower Respiratory Infection- absolute contraindication to elective surgery
but in an emergent setting must optimize the patient
3- COPD- optimize pre-operatively with bronchodilators, physiotherapy,
cessation of smoking
4- Asthma- increases the risk of pulmonary complications, optimize similar to
COPD

** For patients at risk of pulmonary complications:

- History/examination- site of surgery, dyspnea, exercise tolerance, smoking,
cough
- Pulmonary function tests

Renal Disease
** Patients with pre-existing renal disease have a risk of:
- Fluid overload
- Risk of worsening renal failure- due to fluid shifts with hypotension, use of
contrast

134
** Renal complications perioperatively:
- Acute renal failure- may be pre-renal, renal, post-renal
- Mainly due to fluid depletion, severe heart failure

** For patients in renal failure schedule dialysis before surgery

- May also need to be dialyzed after surgery to help clear the anesthetics in
their systemic circulation

** Patients that go into acute renal failure may progress to chronic renal failure.
Risk of hyperkalemia (cardiac arrhythmias and death)

Note: Prevention is key

- Therefore appropriate fluid management
- Avoid toxic substances- contrast, drugs that require renal excretion
- Note: Dose adjustments for drugs for patients with renal disease

Hematological Disease
Anemia
- Risk of decompensation/heart failure if severe
- More significant for patients with cardiac disease (risk of myocardial
ischemia)
- No absolute value for pre-op transfusion
- Aim for >10g/dl for cardiac patients
- Anticipate type of operation, amount of blood loss, co-existing disease

Sickle Cell Disease

- Both anoxia and acidosis induce sickling
- Peri-operative risk of bony crisis, sequestration and acute chest syndrome
- In these patients pre-operative hydration and post-op hydration is very
important
- Admit sicklers pre-op even for minor procedures
- High risk of pulmonary infarcts, atelaectasis
- Therefore physiotherapy is important
- Reduce their sickle Hb to < 30%

135
Anti-coagulation Patients
- Have a risk of bleeding BUT risk of clotting is also high if their medication
is discontinued
- For minor procedures continue anticoagulation and ensure the INR is about
2
- Major procedures- must discontinue their anticoagulation
- Convert them to IV heparin which has a short half life and discontinue 4-6
hrs before the surgery

Note: If the patient ends up being over-anticoagulate use an antidote

- Heparin = protamine sulphate or FFP
- Warfarin = Vitamin K or FFP

Platelet Dysfunction
- Surgery can be performed with counts as low as 50 x 10 9 if there are no
signs of bleeding
- If there are lower counts or evidence of hemorrhage treat the underlying
disorder
- EX: steroids for autoimmune disorders, +/- platelet transfusion
- Discontinue aspirin because it causes qualitative platelet dysfunction
- Renal failure is associated with platelet dysfunction

Coagulation Disorders
** Hemophilias A, B, C
- Must have factor transfusion before surgery
- Minor surgery- 50-75% target factor level
- Major surgery- 100%

Liver Disease
- Liver synthesizes factors II, V, VII, VIII, IX, X, XI, XIII and fibrinogen
- Liver failure results in bleeding risk and prolonged PT/PTT
- Thrombocytopenia is related to hypersplenism

136
Pregnancy
- There may be changes to the anatomy and physiology

** IN acute appendicitis there is a change in location of tenderness based on

gestation
- Peritoneal signs may be less pronounced
- Higher than normal WBC expected in pregnancy
- Increased risk of perforation due to delays

Hernias in Pregnancy
- Increased intra-abdominal pressure
- Symptomatic exacerbations
- Repair after delivery unless they become complicated

Elderly
** The elderly have changes in their reserves:
1- Pulmonary- decreased function, risk of post-op hypoxia, atelectasis,
pneumonia
2- Cardiovascular- associated myocardial dysfunction, CAD arrhythmias
3- Renal- risk of post-op renal failure due to reduced renal blood flow
4- Liver- diminished function

Note: For emergency surgeries in patients with multiple co-morbidities one must
weigh the risk of delaying surgery
- Attempt to decrease cardiac risk by optimizing the patient
- Obtain some measure of BP control before going to theater
- Use IV agents to come as close to normotensive as possible
- Add beta-blockers, nitrates to encourage vasodilation

Wound Healing- (powerpoint)

Defn: Wound healing is the restoration of normal structure and function after
injury
- Barrier is reformed to fluid loss and infection

137
- Re-establishment of normal blood and lymphatic flow patterns
- Restoration of mechanical integrity

Regeneration- is the perfect restoration in the absence of scar formation

- EX: Embryonic development, bone + liver

Repair- perfect reorganization is sacrificed for more rapid return of function

** Wound healing can be divided into 3 distinct phases:

i- Inflammatory phase
ii- Proliferative phase
iii- Remodeling phase

Types of Repair
1- Primary Repair- suture and skin graft and flap closure
- Also known as healing by first intention

2- Secondary Repair-:
- Contaminated wounds
- Closure by re-epithelialization/contraction
- If the wound edges are not re-approximated immediately delayed primary
healing or secondary repair occurs
- This may be desired in the case of contaminated wounds
- By Day 4 phagocytosis of contaminated tissue is under way
- The processes of epithelialization, collagen deposition and maturation are
occurring
- Foreign materials are walled off by macrophages that may transform into
epithelioid cells
3- d

Grand Rounds KPH 27-10-09- Case of acalculous cholecystitis

** To determine the age-appropriate size of the common bile duct

- Add 4 mm for each decade above 40 and add 1 mm

138
- The size of the CBD should be about 1/10th of a persons age in numbers

** Biliary enteric fistula is most common between the fundus of the gallbladder
and the duodenum
- Can lead to a gallstone ileus
- The stone usually lodges in the terminal ileum

** Mertizy Syndrome (check spelling) - is compression of the CBD leading to

fistula between the CBD and biliary system

Ward Rounds 27-10-09

** The complications of the bedridden patient include:
1- DVT- because of the stasis and pooling in the venous system of the legs.
DVT can lead to PE and potentially death
2- Disuse atrophy- of muscles which can be treated with
electromyostimulation and physiotherapy. Can lead to reduced function after
recovery from the illness
3- Osteoporosis
4- Pneumonia- due to stasis of secretions (orthostatic pneumonia) that acts as a
nidus for infection. Pneumonia can lead to sepsis and death
5- Bladder Calculi- due to the stasis of urine in the bladder
6- UTI- due to the indwelling catheter
7- Depression
8- Constipation- due to the increased tonicity of the bowel

** Right Hemi-colectomy
- Cecum
- Ascending colon
- Hepatic flexure

** Extended Right Hemi-colectomy-

- Cecum
- Ascending colon
- Hepatic flexure
- Transverse colon

139
** SUMP drain
- A drain consisting of a smaller tube within a larger tube through which
fluid passes as a result of suction
- This is a open active drain
- Used to draw out fluids from a cavity through one tube, while allowing air
to enter the cavity to replace the fluids
- The outer chamber utilizes passive drainage according to atmospheric
pressure
- The inner chamber is where the active suction is applied

** Neuropathic ulcers- demonstrate full thickness necrosis

- Usually are punched out ulcers with clean margins

Ward Rounds 28-10-09

Gas Gangrene- is a bacterial infection that produces gas within tissues in
gangrene
- Can cause myonecrosis, gas production and sepsis
- Caused by exotoxin producing Clostridial species
- The toxins destroy tissue and generate gas at the same time
- Other organisms such as Klebsiella pneumoniae can cause gas gangrene
- Streptococcus A may also cause gas gangrene, as well as staph aureus

** Clostridium perfringens, C. septicum + C. novi cause most of the cases

- The hallmarks of the disease are rapid onset of myonecrosis with muscle
swelling, severe pain, gas production and sepsis

** Clostridium species are gram-positive, spore forming, anerobis rods

- Normally found in the soil and GI tract of humans
- Traumatic gas gangrene is usually occurs through direct inoculation of a
wound
- With a compromised blood supply, the wound has an anaerobic
environment that is ideal for multiplication of C. perfringens

140
** Spontaneous gas gangrene is usually due to hematogenous spread of C.
septicu from the GI tract in patients with colon cancer

** Treatment is usually debridment and excision with amputation being

necessary in most cases
- Antibiotics alone are not effective because they cannot penetrate the
ischemic muscle

Symptoms:
- Subcutaneous emphysema- felt as crepiations around the wound and can be
seen on plain x-ray
- Drainage from the tissues, foul smelling
- Tachycardia
- Moderate to high fever
- Moderate to severe pain around a skin injury
- Progressive swelling around a skin injury

Hyperglycemia Treatment
** The sequelae of hyperglycemia includes:
- Dehydration
- Acidosis
- Hypokalemia
- Hypercalcemia

** In a diabetic emergency management begin with addressing the ABC’s

- Hydrate the patient immediately
- To calculate a bolus dose use 20-30ml/kg of fluid = 2 L in a 70 kg patient

Dr. Francis KPH Clinical #1- Scrotal + Inguinal Swellings

Scrotal Swellings
History: How long as the swelling been present

141
- Dos the hernia disappear at night or when lying down
- Associated pain. Pain suggests infection, recurrent torsion, recurrent
incarceration, varicocele
- If reducible, is there any straining on defecation or micturition or any
chronic cough

Examination
- Start the examination ideally with the patient standing up
- Palpation: Does it feel cystic or solid or like a bag of worms. Can the testis
be felt
- Can you get above the swelling, therefore can you feel the cord structures
above the swelling

** If you can get above it, it is a scrotal mass and it is unlikely to be hernia
- Ultrasound can be used for definitive diagnosis

** The differential diagnosis for scrotal masses include:

i- Vaginal Hydrocele- cystic and gices straw colored fluid
ii- Epididymal Cyst (Spermatocele)- Cystic and contains watery or white
fluid
iii- Varicocele- feels like a bag of worms
iv- Testicular tumor- hard
v- Chronic Orchitis- firm to soft

** Vaginal Hydrocele can be congenital as a result of a patent processus

vaginalis.
- Primary hydrocoele occurs in 90% of cases

** Vaginal hydrocoele secondary to:

- Orchitis, testicular tumor
- Trauma
- Epididymitis

Note: In women hydroceles are known as hydrocoele of the Cord of Nook

142
Hydrocele Treatment
1- Surgical- Hydrocelectomy
2- Non-surgical- sclerotherapy

Note: Aspiration alone is not an acceptable treatment for idiopathic hydrocoele.

Always recurs and requires repeated aspiration

Acute Scrotal Swellings

Testicular Torsion
- Acute, severe pain that often comes on during sleep
- May untwist spontaneously and present as recurrent testicular pain
- Associated with shortening of cord and bloody vaginalis fluid
- Ultrasound diagnostic
- Requires urgent surgery and fixation of both testes

Inguinoscrotal Swelling
** Inguino scrotal hernias are always indirect, direct hernia never descend into the
scrotum
1- Attempt to reduce it and ask the patient to cough
2- Try to control the hernia by putting one finer over the deep ring. It is
controlled it is an indirect hernia

143
Note: The repair of a hernia is the same, regardless of whether it is indirect or
direct
** Indirect hernias are more likely to incarcerate than direct hernias

Complications of Hernia Repair

1- Hematoma, infection
2- Chronic groin pain- from nerve entrapment at surgery or as the fibrous
capsule contracts

** If a mesh repair becomes infected:

- Open the wound, expose the mesh, dressings and antibiotics
- If the infection persists, the mesh needs to be removed and replaced

Definitions

1- Incarceration Hernia- The contents are fixed in the sac because of their
size and adhesions. The hernia is irreducible but the bowel is not strangulated or
obstructed
2- 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
- Strangulated hernias are painful, tender and irreducible
- Richter’s Hernia- occurs when the sac is small and a small piece of bowel
is caught in the sac and strangulated without causing intestinal obstruction

3- Sliding Hernia- If bowel that is normally extraperitoneal forms one side of

the sac. Therefore one of the walls of the sac is formed by a viscus
- Ex: cecum and bladder or sigmoid and bladder

Central Venous Line Insertion

** The central venous pressure (CVP) is the pressure of the blood in the thoracic
vena cava, near the right atrium of the heart
- CVP reflects the amount of blood returning to the heart and the ability of the
heart to pump the blood into the arterial system

144
- Therefore CVP is a good approximation of right atrial pressure
- Because the CSVC communicates with the right atrium, CVP is also known
as right atrial pressure

** Normal CVP is measured from two points of reference:

- Sternum- 0-5 cm water
- Mid-axillary line: 5-10 cm water

Normal values are 2-8mmHg

** Factors, which increase CVP, include:

- Hypervolemia
- Forced exhalation
- Tension pneumothorax
- Heart failure
- Pleural effusion
- Decreased cardiac output
- Cardiac tamponade

** Factors, which decrease CVP, include:

- Hypovolemia
- Deep inhalation
- Distributive shock

** Indications for the insertion of a CVP line include:

1- Hemodynamic pressure monitoring-
- Right heart filling pressures
- Pulmonary capillary wedge pressure monitoring
2- Large bore intravenous access- for rapid fluid resuscitation and rapid
administration of blood replacement
3- Infusion of therapeutic drugs- Vasoactive substances
- Chemotherapy
- Hyper alimentation
- Other substances that are too hyperosmolar to be given peripherally
4- Plasmapheresis

145
5- Renal dialysis
6- Aspiration of air embolism

Absolute Contraindications
- Patient refusal
- Infection at the insertion site
- Anatomical variance at the insertion site
- SVC syndrome

Relative Contraindications
- Coagulopathy
- Systemic infection
- Right-sided ventricular assist device
- Presence of indwelling catheters at the insertion site

**Central venous line placement is usually performed at four sites in the body:
i- Right or left internal jugular vein- follows a line from the inferior aspect
of the external acoustic meatus to the medial aspect of the clavicle
- Passes deep to sternocleidomastoid and joins the subclavian vein to form
brachiocephalic, posterior to the clavicle

ii- Right or left subclavian vein- is a continuation of the axillary vein

- Begins at the lateral border of the first rib and ends at the thoracic inlet
where it meets IJV
- The SCV passes over the first rib and apical pleura and runs along the
underside of the clavicle parallel with subclavian artery
- Separated from the artery by the anterior scalene muscle

iii- External jugular

iv- Femoral veins

Note: CV catherization via internal jugular has a lower incidence of

pneumothorax, compared to the SCV

146
- SCV catheterization is more comfortable for awake patients and less prone
to contamination from respiratory secretions, especially in patients with
tracheotomies

Procedure- Infraclavicular Approach

- Use universal precautions and sterile technique
- Place the patient in a Trendelenberg position (15-30 degrees head down) to
reduce the chance of an air embolism
- Turn the patient’s head to the side contralateral to the site chosen
- Place a rolled towel/sheet between the shoulder blades to make the clavicles
more prominent
- Place the arms to the sides of the patient

- Locate landmarks:
i- The SCV is a continuation of the axillary vein
ii- SCV is deep to the middle third of the clavicle and runs parallel to it
iii- The SCV has a diameter of about 1-2 cm
iv- The SC artery is superior and posterior to the vein and separated by
anterior scalene muscle

v- The costoclavicular ligament connects the first rib to the clavicle. Found
at the junction of the medial third and middle third of the clavicle
vi- The SCV follows an imaginary line connecting two points established by
placing the thumb on the ligament and the index finger in the supra-sternal notch

vii- Right SCV is preferred because the dome of pleura of the right lung is
usually lower than the left lung
viii- Mark the point and prep and dress the area

ix- Use a needle to inject lidocaine and anesthetize the structures deep to the
spot marked
x- Use the 22 gauge (seeker needle) on a 3 cc syringe to locate the vein,
aspirating until a flash of blood returns
xi- Remove the seeker needle and use an 18 gauge needle on a 5 cc syringe
to follow the path of the vein

147
xii- Remove the syringe and thread the guide wire into the needle
xiii- Remove the needle from the guide wire and make a small cut in the skin
adjacent to the entry site of the wire using a scalpel

xiv- Thread the dilator over the wire and advance the dilator fully into the
chest
xv- Remove the dilator while leaving the wire in place and remove the hub
from the long central catheter
xvi- Thread the long central catheter over the wire into the vein
xvii- Remove the J wire and attach the IV tubing to the catheter
xviii- Discontinue trendelendberg and secure the catheter in place using sutures
and ties
xix- Perform a post-procedure chest x-ray

http://apps.med.buffalo.edu/procedures/centralvenous.asp?p=6

Seldinger Technique- is a medical procedure to obtain safe access to blood

vessels and other hollow organs
- The desired vessel is punctured with a sharp hollow needle (trocar)
- A round tipped guide wire is inserted into the trocar and the trocar is
withdrawn
- Seldinger technique is used for angiography, insertion of chest drains and
central venous catheters, insertion of PEG tubes

Tracheotomy & Tracheostomy

Tracheotomy- refers to the procedure of cutting into the trachea and is done as an
emergency procedure
Tracheosotmy- refers to the making of a permanent or semi-permanent opening in
the trachea

Benign Prostatic Hyperplasia- Dr. Harrison- 11-11-09

148
Pathological BPH- is hyperplasia that is discovered incidentally at autopsy, and
therefore the patient never complained of related symptoms
- Therefore it is hyperplasia found at autopsy BUT did not manifest itself
clinically
- 50% for 51-60 years
- >90% for 80 years and older

Clinical BPH- a patient who presents with clinical symptoms and signs of BPH
- 25% at age 55 years
- 50% at age 75

Aetiology
- Multifactorial and endocrine controlled
- Increased estrogen levels with age; resulting in increased androgen
receptors and increased BPH
- Men have a period of andropause where the levels of testosterone decrease
BUT the prostate becomes increasingly sensitive to dihydrotestosterone

Pathology
** The prostate consists of stromal and epithelial components
- BPH develops in the transitional zone
- Prostate cancer develops in the peripheral zone

Note: The lateral and medial lobes are known as the pathological lobe because
they develop as the prostate enlarges

** The bladder undergoes compensatory changes to overcome the resistance

created by the enlarging prostate
1- Compensatory Phase- hypertrophy with trabeculations, cellules, saccules
and diverticula
2- Decompensatory Phase- distended bladder, overflow incontinence

Note: In BPH there is a poor correlation between size and symptoms

149
- There is both a static component and a dynamic component to the
obstruction of flow
- Dependent on what parts of the prostate undergo hyperplasia
- If there is predominantly smooth muscle that has undergone hyperplasia,
there is a greater dynamic element at play. Therefore the increased smooth muscle
will contract and cause more retention than if the glandular elements underwent
hyperplasia

** Prostates that have more smooth muscle hyperplasia tend to be smaller than
prostates with more glandular hyperplasia
- However these smaller prostates may give more symptoms because there is a
greater dynamic element to the prostate

Clinical

Irritative (Storage Symptoms)

- Frequency
- Nocturia- Normal passage of urine is 3-4x daily and maybe 0-1x nightly
- Urgency, urge incontinence
- Burning @ micturition (dysuria)
- Hematuria

Obstructive (Voiding)
- Hesitancy- occurs because it takes time for the bladder to contract to build
up enough pressure to overcome the obstruction
- Strain- to overcome the obstruction must use abdominal muscles
- Stream
- Incomplete bladder emptying
- Double void
- Dribbling

Note: The irritative symptoms tend to be the symptoms that develop first
HOWEVER the obstructive symptoms are the ones that the patients first present
with

150
- This is because the irritative symptoms are often ignored by the patients
because they do not affect daily life so much

Note: Keyhole incontinence is NOT pathological

Examination
** General Exam
** Specific- abdomen + DRE
DRE- note size, shape, consistency, median + lateral grooves
- In BPH the median groove becomes more pronounced BUT prostate cancer
obliterates the median groove

Note: When the bladder contains 150 mls it is percussable

- When the bladder contains 250 mls of urine you are able to palpate the bladder

Differential Diagnoses
i- Acute Urinary Retention- tender abdomen, painful distress, patient is
restless, mass in the pelvic area. Treat with catherization or suprapubic tap
ii- Chronic urinary retention- is painless. Associated with a risk of renal
impairment
- Ureters are dilated, deranged U/E’s
- May have overflow incontinence
- Should be admitted due to the risk of post-obstructive diuresis
- After being in retention for an extended period of time, once catherized these
patients can lose 5-8L in one night
- Therefore they are at high risk of shock, especially if their CVS is not
compliant
- They should be admitted and replace ½ to 2/3rds of the volume they have
lost
- Note: Acute on chronic retention- has features of pain and large bladder plus
deranged U/E’s

iii- Urethral stricture

iv- Prostate cancer
v- Carcinoma in-situ of the bladder

151
vi- Neurogenic bladder
vii- Stones

Laboratory
Urine Analysis
- Dipstick and microscopy
- RBC, WBC and bacteria
- Note: Red blood cells, hemoglobin and myoglobin all give positive dipstick
results for the presence of blood
- Therefore microscopy can be done to differentiate

Ultrasound
Creatinine, urea, electrolytes
PSA
Uroflowmetry, cystometrogram + urodynamics

Treatment
Watchful waiting
Medical
- Alpha-blockers- tamsulosin, alfuzosin, terazosin
- 5-alpha-reductase inhibitors- finasteride, dutasteride

Note: Tamulosin is more specific for alpha-receptors on the bladder

- Alpha blockers help treat the dynamic element which is more problematic
in smaller prostates
- The 5-alpha reductase inhibitors tend to help the glandular component of
BPH

Surgical-
- Endoscopic
- Open prostatectomy- can be done transvesical or retropubic

** The gold standard is transurethral resection of prostate (TURP)

- TUNA- transurethral needle ablation

152
- TUIP- transurethral incision of bladder neck
- TUMT- microwave therapy
- TUEVP- electroevaporistaion
- TULIP- laser induced prostatectomy
- Intraurethral stent
- Balloon dilatation

Prostate Cancer- 13-11-09- KPH Urology Lecture II

Epidemiology
- Second leading cause of death in the US
- Incidence increases with age
- Dietary Factors- associated with increased intake of saturated fat.
Therefore obsesity increases the risk
- Vitamin D + calcium also increase the risk
- 1/6 chance of getting prostate cancer BUT a 1/30 chance of dying from
prostate cancer

Pathology
** The majority (95%) are adenocarcinomas
- However the proximal end of the ducts that open into the urethra are lined
by transitional cell epithelium therefore some prostate carcinomas are
transitional cell carcinoma
- Small amount are neuroendocrine carcinoma or sarcomas

60-70%- arise in the peripheral zone

10-20%- transitional zone
5-10%- central zone

High Grade Prostatic Intraepithelial Neoplasm (PIN)- identified as a pre-invasive

stage of adenocarcinoma
- The presence of PIN has a high predictive value as a marker for
adenocarcinoma

153
- Once identified, a repeat biopsy should be performed for concurrent or
subsequent invasive carcinoma
- PIN does not significantly elevate serum PSA therefore the only means of
detection is biopsy
- PIN has most of the changes of cancer without invasion of the basement
membrane
- DEFN: the abnormal proliferation within prostatic ducts, ductules and large
acini of pre-malignant foci of cellular dysplasia and carcinoma in situ without
stromal invasion

http://www.nature.com/modpathol/journal/v17/n3/full/3800053a.html

Atypical Small Acinar Proliferation (ASAP)- is a change that is suspicious for

malignancy
- Highly predictive of subsequent adenocarcinoma
- Repeat biopsy should be obtained
- The atypical small acinar proliferations are usually found most often in the
peripheral zone and rarely in the transition zone
- http://emedicine.medscape.com/article/1611859-overview

Note: Therefore both PIN and ASAP are precursors to prostatic adenocarcinoma
and a repeat biopsy is recommended
- 50% will have carcinoma on repeat biopsy

Gleason Score (Grading System)

- Gleason score 1-5
- Gleason sum- primary + secondary score
- 2-4 well differentiated
- 5-6 moderately differentiated
- 8-10 poorly differentiated
- 7- is a gray area because it can be 4+3 or 3+4
- 4+3 is associated with a worst prognosis because the higher grade is the
dominant pattern
- The Gleason score looks at the glandular pattern on microscopy

154
TNM
- T1- non-palpable tumor that is diagnosed based on PSA or after surgery for
benign disease
- T2- Palpable
- T3- extends through capsule
- T4- adjacent structures in pelvis involved
- N1- regional nodes
- M- metastases

Note: Prostate cancer has a propensity to metastasize to bone, especially the

vertebral column

Screening for Prostate Cancer

- No effective treatment for advanced disease
- Increased detection of organ confined disease
- Ca may be cured if detected early
- However although PSA is sensitive it lacks specificity
- Because a PSA may be elevated for multiple reasons other than cancer
- EX: prostatitis, post-urinary retention, BPH, post-DRE

** Begin screening at age 50

- Can begin at age 40 and those with a family history
- 1-2 yearly follow-up

** Blacks have the highest risk of manifestation of the disease during their
lifetime BUT at autopsy studies have shown that every race has the same risk of
prostate cancer based on pathological prostate cancer diagnosis

DRE
- Overall detection rate of 40%
- 25% of men with prostate cancer have a PSA <4ng/ml. Therefore a DRE
should be done with the PSA
- Therefore a DRE is needed because it allows the size of the prostate to be
assessed along with consistency and mobility

155
PSA- Prostate Specific Antigen
- PSA is produced by the prostatic epithelium
- Glycoprotein that liquefies semen and is increased in most cases of prostate
cancer
- Although PSA rises progressively with age and prostatic volume
- Detects cancer 3-5 years in advance

Note: As prostate cancer develops, the PSA is elevated because at first it resembles
prostatic epithelium and there is a greater amount of the epithelium. However as
the tumor grows and becomes more anaplastic, the epithelium no longer resembles
normal prostatic epithelium
- Therefore the PSA levels will decrease
- Therefore an elevated PSA that is on the low end may indicate a more
aggressive carcinoma

Total PSA
Normal PSA- 0-4 ng/ml
4-10 ng/ml- 25% chance of cancer
> 10 ng/ml- >50% chance of cancer

Note: The free-total ratio of PSA can help to determine whether to biopsy or not
- Benign disease tends to produce more free PSA than total PSA
- Cancer produces more total PSA than free PSA
- Therefore the relationship is an inverse relation between F-T ratio and the
PSA
- BUT there is a direct relationship between cancer and PSA

PSA velocity- tracks how fast the PSA is increasing over time?
- A PSA velocity of >0.75 ng/ml/year is suggestive of malignancy
- Used to monitor a patient when biopsy is negative
- Used before biopsy when suspicion for malignancy is low or the patient is
reluctant to have a biopsy

156
 DRE abnormal DRE abnormal
PSA < 4ng/ml PSA > 4 ng/ml
15%
56% chance

DRE normal DRE normal

PSA < 4 ng/ml PSA > 4 ng/ml
6% 25%

Clinical Presentation
- May be asymptomatic
- Symptoms: lower urinary tract symptoms, bone pain, paraplegia, pedal
edema
- Abnormal DRE

Prostatic Biopsy
- Done under antibiotic coverage
- T3, T4 (advanced cancers) a single finger guided biopsy may be adequate.
Therefore use digital guided biopsy rather than transrectal guidance
- Small and/or impalpable tumors require multiple biopsies
- Transperineal route- has less risk of sepsis but is more difficult
- Transrectal ultrasound guided prostate biopsy

TRUS biopsy is done under antibiotic coverage

- 12 or more core taken
- Taken of the peripheral and transition zones
- Rebiopsy- if there is evidence of PIN or atypical glands
- If the re-biopsy is negative, monitor PSA and PSA velocity

** Diagnosis can be made without biopsy if there is evidence of the following:

- Grossly elevated PSA
- Malignant feeling prostate

157
- Positive bone scan or osteosclerotic lesions seen on X-rays
- Poor physical condition

Note: Prostatic mets tend to appear as sclerotic lesions on x-rays BUT the mets of
other cancers tend to be lytic lesions

Sclerotic Bone Lesions- is the result of a slow-growing process. In which the bone
increase its density around the metastases in order to wall it off from the rest of the
bone

Lytic Lesion- is due to the breakdown of bone

Note: 5 densities can be seen on x-ray

- Metal
- Bone
- Liquid
- Soft tissues
- Air

Investigations
- Anemia, azotemia, alkaline phosphatase, serum acid phosphatase
- PSA
- TRUS
- CT scan
- MRI
- Prostacint (antibody to pSMA)

Treatment
** Watchful waiting and active surveillance is the postponement of treatment
until required
- Asymptomatic patients
- Older patients who may need palliative care
- Younger patients

158
Note: Watchful waiting can be done because prostate cancer tends to be slow
growing

Radical Prostatectomy
- Radical retropubic prostatectomy or perineal prostatectomy
- Incontinence < 10%
- Erectile dysfunction- 40-82%- the degree of erectile dysfunction depends on
if the patient had previous ED before the surgery

Radiation
- External beam radiotherapy
- Brachytherapy- implant multiple “seeds” of radiation into the prostate

** The complications of radiation include:

- Irritative bladder symptoms
- Radiation cystitis
- Secondary bladder tumors
- Erectile dysfunction
- Diarrhea, PR bleeding
- Tenesmus
- Proctitis

Note: For locally advanced tumors use combined radiotherapy with neo-adjuvant
and adjuvant hormonal therapy

Metastatic Disease- Treatment

** Metastasis is defined as discontinuous spread of a malignancy to distant
organs
- Therefore metastasis cannot be spread via direct invasion

1- Androgen Deprivation Therapy (ADT)- Men who are castrated, their cancer
will regress but not disappear
- Can be done surgically by removing the testicles bilaterally
- Medical castration via LHRH analogues

159
- The LHRH analogues eventually block the release of LHRH and androgens
because they create an initial surge. This constant stimulation of the axis
eventually leads to negative feedback and a decrease in testosterone
- Other medical treatments include: ketoconazole, corticosteroids, estrogens

2- Chemotherapy- docetaxel

Note: Radical prostatectomy is NOT offered to men who have life expectancy of
less than 10 years

Prognosis
- Localized cancer- 70-85% at 10 years
- Metastatic cancer- 10-20% dead at 1 year
- 50% dead at 3 years
- 75% dead at 5 years
- 90% dead at 10 years

Urology Lecture III: Renal Stones

Etiology
- 20-40’s M > F 3:1
- Related to water intake and water hardness
- Occupation and diet may also be contributing factors

Stone Pathogenesis
** Epitaxy is the method of depositing a film on a substrate
- In stone pathogenesis there are polycrystalline aggregates that are
composed of varying amounts of crystalloid and organic matrix
- If there is supersaturated urine the pH, ionic strength, solute concentration
and complexation favor the creation of stones

** Nucleating factors are factors that precipitate the formation of stones

- Foreign bodies
- Disorders of tissue sloughing- Vitamin A deficiencies
- Bacteria
- Increased sodium in the diet

160
** Anti-nucleating factors- are factors in the urine that prevent stone formation
- Citrate
- Pyrophosphates
- Sulphates
- Magnesium
- Uropontin

** Oxalates are a by-product of the metabolism, especially liver metabolism

- 15% of oxalate in the body comes from the diet

** Saponification of fats occurs in any condition that decreases fat absorption

- Inflammatory bowel disease, extensive bowel resection, chronic diarrhea
- Therefore as a result of the decreased absorptive surface, less oxalate that is
produced is absorbed
- The excess oxalate combines with calcium to form calcium oxalate stones
- Note: Primary hyperoxaluria is the result of a liver enzyme defect

** Therefore since there are increased fats available, more calcium binds to the fats
and therefore more oxalate is available for absorption across the GI tract
- As a result the oxalate precipitates in the kidneys and form stones

** Phosphates are found in meat, vegetables, and dairy products

- Phosphate stones are the main stone found in hyperparathyroidism
(Calcium phosphate stone)

** Uric acid stones- uric acid is a byproduct of purine metabolism

- There are dietary and endogenous sources of uric acid
- A deficiency of xanthine oxidase causes a build up of uric acid
- Seen in gout, myeloproliferative disease, cytotoxic therapy

** Stone varieties include:

- Calcium- 80-90% of ALL stones are radio opaque because 80-95% of all
stones are calcium stones
- Triple phosphate- can be seen on plain x-ray

161
- Uric acid- stones are radiolucent and therefore NOT seen on x-ray BUT
they can be seen on CT
- Cysteine- can be seen on x-ray but they are not as dense as calcium stones
- Xanthine
- Triamterene
- Silicate
- Indinavir- is an anti-retroviral. Appear radiolucent on plain x-ray and CT
therefore need an ultrasound for diagnosis

Calcium Stones
1- Increased absorption of calcium from the GI tract
2- Increased resorption of calcium from the bone- as in hyperparathyroidism
- Hypercalcemia + hypercalciuria
- There is hypercalcemia despite the hypercaliuric urine because the increased
serum calcium overwhelms the renal ability to reabsorb calcium
- Therefore increased calcium is excreted in the urine

3- Renal induced calciuria- calcium leaks from the renal tubes, therefore the
pathology is at the level of kidneys

Uric Acid Stones

- Accounts for 5% of all stones
- Urine tends to be acidic, therefore uric acid stones tend to form in an acidic
environment
- Therefore alkalinize the urine with sodium, potassium or citrate
- Citrate has the added benefit of being an anti-nucleating factor
- Treat the patient by restricting dietary intake, encourage an increase in fluid
intake and using allopurinol

Triple Phosphate Stones

- Made up of calcium phosphate + magnesium phosphate + ammonium
phosphate
- Although stones on the whole are more common in males than females,
triple phosphate stones are more common in women than men

162
- This is because they are associated with infection and women tend to have
UTI’s more frequently then men
- Triple phosphate stones form due to the actions of urea-splitting organisms
(proteus, pseudomonas, providencia, Klebsiella, staph)
- Note: E. coli is NOT a urea splitting organism
- These organisms produce the enzyme urease which splits urea

Note: Stag horn calculi are named because they describe how the stone fills the
collecting system
- Associated with triple phosphate stones, however they can be uric acid or
cysteine stones as well

Cysteine Stones
- Due to an inborn error of metabolism
- Leads to abnormal absorption of dibasic amino acids in the GI tract and the
renal tubules (cysteine, ornithine, lysine, arginine)
- Cysteine is insoluble in urine

Signs + Symptoms
- Pain, hematuria, infection
- 85% of patients with stones have microscopic hematuria
- Loin to groin pain, scrotal, testes, bladder, Vulval pain
- Urgency, frequency, burning
- Pain may be colicky or non-colicky
- Associated with nausea and vomiting- renal-intestinal reflex

Examination
** Patients with renal colic are often restless and thrashing in pain
- Tachycardia, nausea, sweating, fever
- Renal angle tenderness
- Renal mass- may suggest hydronephrosis

** To elicit renal angle tenderness, use the heel of your closed fist to strike the
patient over the costovertebral angles

163
Investigations
** Urinalysis- blood, bacteria, crystals, pH
Note: A 24-hour urine collection test is only indicated in patients with:
- Family history of stones
- Multiple or recurrent stones
- The 24 hr collection is done for pH, volume, sodium, calcium phosphate,
uric acid, citrate + oxalates

- CT scan, spiral CT

- IVU
- KUB film + ultrasound- will only pick up ureteric stones if the ureter is
massively dilated. Also cannot give information about renal function

Treatment
- Observation
- Medical therapy

< 4mm stones- have 70-80% chance of passing spontaneously.

 6 mm stones- 25% chance of passing spontaneously
 4-6 mm stones- 50% chance of passing spontaneously

Note: Encourage fluid intake per oral. Give medications like alpha-blockers to
relax the ureter

** Shockwave therapy can be used to break up larger stones

- ESWL
- PCNL- non-invasive

** Open stone surgery- pyelo/nephrolithotmoy

** Recurrence preventative treatment involves:

- Increased fluid intake- 3L daily
- Reduce sodium intake
- Reduce oxalate intake

164
- Thiazide diuretics
- Reduce protein intake
- Allopurinol if they are predisposed to uric acid stones
- Alkalinize the urine with sodium or potassium citrate

Note: All patients with renal stones have a 50% risk of recurrence in the first 5
years

Thyroid + Parathyroid- Dr. Francis- KPH- 9-11-09

Physiology
** The thyroid gland synthesizes the following hormones:
- Tetra-iodothyronine- T4
- Tri-iodothyronine- T3
- T3 is the active hormone and T4 is converted to T3 in the periphery
- The thyroid gland secretes calcitonin from the parafollicular C cells
- Calcitonin reduces the level of serum calcium and is antagonistic to
parathormone

** Iodine in the diet is absorbed into the blood as iodide

- Iodide is converted into iodine in the follicle
- Then bound to tyrosine of thyroglobulin to produce the precursors of the
thyroid hormones
- The colloid in the vesicles is made up of thyroglobulin and T3 and T4
- The hormones are cleaved from thyroglobulin after being released into the
circulation

** The production of thyroid hormones can be inhibited by the thiouracils and

carbimazole
- Bock the binding of iodine but do not interfere wit the uptake of iodine by
the gland

** A goiter is an enlargement of the thyroid gland. There are several causes of

swelling of the thyroid gland

165
i- Simple goiter-
- Multinodular goiter- due to iodine deficiency, dyshormongenesis (Pendread
syndrome), ingestion of goitrogens
- Hyperplastic goiter
ii- Toxic goiter
iii- Neoplastic goiter
iv- Thyroiditis- Hashimoto’s, De Quervains, Rydel
v- Miscellaneous- acute thyroiditis, secondary to melanoma

Nodular Goitre: Pathology

** The thyroid gland undergoes periods of activity and regression. There is
excessive thyroid activity at puberty and during pregnancy (produces a
physiological goiter) and a fall in activity after menopause
- In a nodular goiter there is excessive activity and regression resulting in
varied appearance of the gland
- Some follicles are lined with hyperactive epithelium and others with
flattened atrophic cells

Complications:
- Tracheal displacement or compression
- Hemorrhage into a cyst, producing pain and increased swelling
- Toxic change
- Malignant change

** The enlargement begins as a smooth swelling. Then due to the cyclical effect of
growth, the swelling becomes nodular
- This is a non-toxic nodular goiter
- The swelling moves on swallowing

Note: The two indications for thyroid surgery in a non-toxic nodular goiter are:
i- Cosmesis
ii- Pressure symptoms

** The surgery done is a sub-total thyroidectomy. A cuff of thyroid tissue is left

back to help ensure that the parathyroids are still in situ

166
Toxic Goiters
1- Grave’s Disease- the thyroid is uniformly enlarged and there is
hyperactivity of the acinar cells with reduplication and infolding of the epithelium
- The gland is vascular
- Lymphocyte infiltration is a feature
- T4 potentiates the action of adrenaline and therefore many of the features of
hyperthyroidism represent increased activity of the sympathetic nervous system
-
2- Plummer’s Disease- characterized by a multi-nodular goiter in which one of
the nodules becomes autonomous and starts over-secreting thyroid hormone
3- Toxic adenoma- functional tumor of the thyroid gland that produces
excessive thyroid hormone and leads to symptoms of hyperthyroidism

Clinical Features of Hyperthyroidism

** Patient is irritable + nervous and cannot keep still
- Appetite is increased BUT no weight loss
- Diarrhea is occasionally a feature
- Patient prefers cold environments to warm ones
- Palpitations due to tachycardia
- The thyroid is usually smoothly enlarged

Eye Signs:
- Exopthalmos- due to edema and infiltration by mononuclear cells of the
orbital fat + extrinsic muscles of the eye
- Lid retraction- innervation of levator palpebrae superioris is partly under
sympathetic control. Therefore it is over-active and the lid is over-retracted giving
the appearance of staring
- Lid lag- the upper lid does not immediately drop as the patient follows the
finger
- Dilated pupils- due to increased sympathetic pupil dilator tone
- Double vision- following the examiner’s finger to the upper outer quadrant.
Due to infiltration of the extrinsic muscles of the ye

Hands:

167
- Sweating
- Tachycardia
- Fine tremor
- Finger clubbing- thyroid acropachy

** Other signs include pre-tibial myxodema, which is the thickening of the

subcutaneous tissues in front of the tibia

** Patients with hyperthyroidism fall into two groups:

i- Primary Hyperthyroidism- Grave’s disease. Due to the action of
autoantibodies, which bind to and stimulate TSH receptors.
ii- Secondary Hyperthyroidism- over activity in an already hyperplastic
gland. Usually occurs in patients with pre-existing non-toxic goiter

Hypothyroidism
1- Congenital- cretinism
2- Adult hypothyroidism (myxodema)- usually affects women
- Overweight
- Slow, deep voice
- Dry coarse sin + thin hair
- Brady cardia
- Usually constipated

Investigations
1- Serum free T4 + free T3-
2- TSH level- raised in myxodema and suppressed in hyperthyroidism
3- Thyroid Scan- to look for hot and cold nodules. Cold nodule is one that is
not producing T$ and therefore does not take up the radioiodine
4- Thyroid antibodies- acaings thyroglobulin may indicate autoimmune
pathology
5- Thyroid ultrasound- can determine if the mass is cystic or solid, also if it is
multinodular or a single nodule
6- FNAC +biopsy
7- Serum Cholesterol- may be raised in myxoedema
8- ECG

168
** The initial treatment is to make the patient euthyroid
- Use medical management: carbimazole, propylthiuracil (use has decreased
because it has an increased incidence of agranulocytosis)
- Combine with a beta blocker to address the adrenergic effects of T4
- Radioiodine ablation- avoid doing in young females
- Surgery- and leave 1/8th of the normal gland

Neoplastic Goiters
** Neoplastic goiters can be benign or malignant

Benign:
- Follicular adenoma- which are well encapsulated, this is what differentiates
thmen from a malignant follicular carcinoma

Malignant:
1- Follicular Carcinoma- demonstrates capsular + vascular invasion
- Second most common
- Found in F > M
- Presents in an older age group, 3rd-4th decade of life
- Presents as a solitary enlarged nodule similar to follicular adenoma
- BUT demonstrates vascular and capsular invation
- Tends to spread hematogenously mainly to bone and lungs
2- Papillary Carcinoma- is the commonest type
- Arises in the 2nd and 3rd decades of life
- Tends to spread lymphatically
- Multi-focal and TSH dependent

3- Medullary Carcinoma- arises from parafollicular cells

- Has an amyloid stroma
- Arises from the parafollicular cells, therefore calcitonin increase and serum
Ca decreases
- Test for tetany- using Chovstek’s sign or Trousseau’s sign
- Part of MEN II syndrome- phaeochromocytoma, parathyroid, medullar ca

169
4- Anaplastic- has the worst prognosis

** Because both papillary and follicular carcinoma present as a solitary nodule in

the thyroid, the investigations are similar:
1- Thyroid function tests
2- Ultrasound- can differentiate between solitary and multinodular goiters.
About 50% of suspected solitary goiters turn out to be multinodular goiters on
ultrasound
3- Thyroid scan
4- FNAC
5- Biopsy- do a lobectomy if the FNAC is indeterminate
- If the report says papillary Ca, a completion thyroidectomy should be done
because it tends to be multi-focal
- If the report says follicular, completion thyroidectomy should ALSO be
done because the spread is hematogenous
- In addition the treatment is with radioiodine. Therefore if a normal lobe
remains it will take up the iodine preferentially instead of the possible metastases
etc

Parathyroid
- Superior parathyroids arise from the fourth branchial pouch
- Inferior glands arise from the third pouch in association with the thymus

** Parathyroids produce PTH which affects calcium and phosphate metabolism

1- Increases the excretion of phosphate from the kidneys by inhibiting its
tubular re-absorption
2- Stimulates osteoclastic activity in the bones which leads to librarion of
calcium and phosphorous in the blood

Causes of Hyperparathyroidism
- Parathyroid adenoma
- Parathyroid hyperplasia
- Parathyroid carcinoma- 1%

170
** Can do a Sestamibi scan (technicium)- radionuclide scan that uses labeled
technicium to find the glands
** Frozen Section- to find out if the glands are hyperplastic or there is an adenoma
- If hyperplastic remove 3.5 glands

** The clinical features of hypercalcemia are:

- BONES- pathological fractures
- STONES- kidney stones
- GROANS- increased PUD, pancreatitis, constipation
- PSYCHIC OVERTONES- depression, fatigue

** Hypoparathyroidism- results in a low serum calcium

- Hyperirritability of the skeptlat muscle with carpopedal spasm
- The syndrome is known as tetany
- Tetany occurs if serum calcium falls below 1.5 mmol/L

171