PRE-EXAM SURGICAL

NOTES
NB: THESE NOTES ARE COMPLEMENTARY TO THE
CLINICAL HISTORY AND EXAMINATION SHEET

Shock, Electrolyte and Fluid Therapy

Definition: Shock is a physiologic state characterized by systemic reduction in

tissue perfusion, resulting in decreased tissue oxygen delivery
Compensatory mechanisms in shock:
It is a trial to maintain adequate blood flow to vital organs as brain, heart and lung
These mechanisms include:
1. Sympathetic nervous system:
Release of norepinephrine, epinephrine, dopamine, and
cortisol vasoconstriction, increase in HR, and increase of
cardiac output
2. Renin-angiotensin axis:
Water and sodium conservation and vasoconstriction
Decreases urine output to increase blood volume and blood
pressure
3. Vasoconstriction of skin, splanchnic, musculoskeletal, and
renal blood flow to maintain cerebral and cardiac perfusion

4. Cellular responses to decreased systemic oxygen delivery

- ATP depletion ion pump dysfunction
- Cellular edema
- Hydrolysis of cellular membranes and cellular death
Decreased perfusion will lead to hypoxia anaerobic metabolism
systemic metabolic lactic acidosis that overcomes the bodys
compensatory mechanisms if fail organ dysfunction irreversible
shock death

Stages of Shock
Preshock:- Compensated (class I hemorrhage)
Body is able to compensate for perfusion.
Less than 15% reduction in blood volume.
Tachycardia to cardiac output & perfusion.
Shock:- Classes ll - lV of blood loss
> 15 -< 40% reduction in blood volume
Compensatory mechanisms overwhelmed.
End-organ dysfunction:- Leading to irreversible organ damage &
death.

Hypovolemic (oligemic) shock

Decreased circulatory blood volume due to:
1. Blood loss (hemorrhagic shock)
2. Plasma loss; as in burns, peritonitis and pancreatitis
3. Water and electrolyte loss: as in repeated vomiting ( as in intestinal
obstruction) and diarrhoea

NB: Hemorrhage may be:

External: as bleeding wound, hematemesis, hematuria, vaginal
bleeding, etc
Internal: as hemoperitoneum, hemothorax, hemopericardium,
intracranial hemorrhage, etc
Also it may be: according to the onset
Primary: at the time of surgery or trauma
Reactionary: within 24 hours of surgery (due to post operative rise in
blood pressure opening of small vessels or slipped ligature of larger
vessels
Secondary: after1-2 weeks due to infection and erosion of blood vessels

Classes of Blood Volume Loss (or Hemorrhage)

It is a clinical tool to determine the amount of fluid (or blood) loss
So, we can determine the type and amount of fluid required to replace the
loss and restore blood volume
CLASS I
Loss of up to 15% of the circulating volume (700 to 750 mL) for a 70-kg
patient may produce little in terms of obvious symptoms
Cardiovascular: mild tachycardia (pulse around 100) with normal
blood pressure
Respiratory: Rate normal
anxious

- Neurologic: Slightly

- Skin: Warm and pink & Capillary Refill <2 seconds

 - Renal: Normal urine output

Adults: >0.5 ml/kg/hour (>30 cc/hour)
Children: >1 ml/kg/hour

Class l is compensated and no need for IV fluids

CLASS II
loss of up to> 15 - < 30% of the circulating volume (750 1500 ml)
Cardiovascular
Tachycardia: 100 -120/m and pulse is week
Blood Pressure normal in recumbent but may be orthostatic
hypotension
Normal pH
Respiratory: Mild Tachypnea :16 -20/m
Neurologic: Irritable, Confused, and Combative (patient must be
sedated)
Skin: Cold extremities, pale, & Delayed Capillary Refill (>2 seconds)
- Renal: urine volume < 30 - >20 ml/m

This patient must be initially replaced by 2 liters of lactated

Ringers solution and blood is given if hematocrit < 30
CLASS III
More than 30 - < 40% of the blood volume has been lost (Adults: 2000
ml blood loss)
Cardiovascular:
Pulse 120 -< 140/m, Hypotension
Metabolic Acidosis
- Respiratory: Tachypnea, 20 - < 30/m
- Neurologic: Irritable, Lethargic, Diminished pain response

- Skin: Cold extremities, severe pallor or mottling, & Prolonged

Capillary Refill
- Renal: Oliguria (< 20 - > 10 ml/m)
Blood Urea Nitrogen (BUN) increased

Treatment must included volume to volume colloid replacement

( blood if hemorrhage, plasma in burn, peritonitis, and
pancreatitis
In all cases till blood or plasma are ready give 2 liters of
Lactated Ringers
CLASS IV
Loss of 40% of circulating volume (2 L)
- Cardiovascular: weak thready pulse (>140/m)
Significant Hypotension & Significant acidosis
- Respiratory: tachypnea > 30/m
- Neurologic: Lethargic and finally Coma
- Skin: Cold extremities and may be Cyanosis
- Renal: Anuria (urine < 10 ml/m)

Treatment must included volume to volume colloid replacement

( blood if hemorrhage, plasma in burn, peritonitis, and
pancreatitis
In all cases till blood or plasma are ready give 2 liters of
Lactated Ringers
Class LV is a life threatening, and generally requires urgent
operative control of bleeding

Other Types of Shock

Cardiogenic shock:
may be cardiac: as in myocardial infarction
Extracardiac (obstuctive): as in massive pulmonary embolism, cardiac
tamponade, and tension pneumothorax
Distributive shock :- Vasodilatory, as in
A.Septic: severe infection with release of bacterial or fungal endotoxin
B. Anaphylactic: following injection of certain drugs as penicillins or
intake of some food (most commonly shell fish)
C.Neurogenic shocks:
Spinal shock (loss of sympathetic tone after spinal anesthesia or
spinal injury)
Severe pain: Vasovagal attack with marked bradycardia decrease
cardiac out put
Fear : release of big amount of adrenaline vasodilatation in the
muscles pooling of blood in the muscles on expense of other sites

Common Features of Shock

Hypotension (not an absolute requirement)
SBP < 90mm Hg, not seen in preshock, class I
Cold, clammy skin
Vasoconstrictive mechanisms to redirect blood from periphery to vital
organs
Exception is warm skin in early distributive shock, specially septic
shock
Oliguria

(kidney perfusion)

 Altered mental status

(brain perfusion).

Metabolic acidosis.
Tachycardia but bradycardia in spinal shock and vasovagal attacks

Initial Assesment ABC

Airway: Does pt have mental status to protect airway?
GCS less than eight means intubate
Airway is compromised in anaphylaxis
Breathing: If pt is conversing with you, A & B are fine
Place patient on oxygen: 40% in class I & II and 100% in class III &
IV
If apnea ventilate the patient
Circulation:
Stop bleeding by compression or tourniquet if bleeding wound
otherwise resuscitate the patient first
2 large bore (#16g) IV, start fluids by 2 liters of Ringers lactate
(careful if cardiogenic shock)
Prepare blood if hematocrit < 30 and in class lll & lV
Continuous monitor : best monitor of shock is urine out put (so
catheter is mandatory) as central venous pressure may be high in
cardiogenic shock
In a trauma, perform ABCDE, not just ABC
Deficit or Disability
Assess for obvious neurologic deficit.
Moving all four extremities & Pupils.
Glascow Coma Scale (M6, V5, E4).

Glasgow Coma Scale

Eye

Verb
al

Does not
open eyes

Opens eyes in
response to
painful stimuli

Opens eyes in
response to
voice

Opens eyes
spontaneousl
y

N/A

N/A

Incomprehensible
sounds

Utters
inappropriate
words

Confused,
disoriented

Oriented
,
converse
s
normally

N/A

Extension to
painful stimuli
(decerebrate
response)

Abnormal
flexion to
painful stimuli
(decorticate
response)

Flexion /
Withdrawal
to painful
stimuli

Localizes
painful
stimuli

Obeys
comman
ds

Makes no
sounds

Makes no
Moto
movemen
r
ts

Exposure: and full examination from head to toes

Adjuncts F & G: Foleys catheter and gastric tube (why?)

Acidosis in surgery
Causes:
Metabolic
Shock
Long ischemic part of intestine or limb
Diabetic ketoacidosis
Cardiac arrest (combined respiratory and metabolic)
Renal failure

 Respiratory: chest injury, chronic chest diseases, marked chest deformity

TTT: treatment of the cause first
Ringers lactate can be given in mild cases and in advanced cases use sodium
bicarbonate (dose: measure deficit in bicarbonate X 40% X body weight)

Hypokalemia in surgery
Causes:
Repeated vomiting (pyloric obstruction, postoperative vomiting, intestinal
obstruction)
Prolonged nasogastric suction
Use of diuretics, excessive fluid intake with polyuria
Presentation: weakness, hypotonia, distension, and even paralytic ileus
Treatment: in mild cases use RL but in advanced cases use potassium
chloride IV, slowly after correction of urine out put by normal saline first

IV Fluid Therapy

Shock

Nutrient solutions
!It contain some form of carbohydrate and
water.
!Water is supplied for fluid requirements and
carbohydrate for calories and energy.
!They are useful in preventing dehydration
and ketosis but do not provide sufficient
calories to promote wound healing, weight
gain, or normal growth of children.
!Common nutrient solution :D5W.

$
Shock

Electrolyte solutions
(Crystalloid)

!fluids that consist of water and dissolved crystals,

such as salts and sugar.
!Used as maintenance fluids to correct body fluids
and electrolyte deficit .
!Commonly used solutions are:
-Normal saline
(0.9% sodium chloride solution).
-Ringers solutions
(contain sodium, chloride, potassium, and
calcium).
-Lactated Ringers solutions
(contain sodium, chloride, potassium ,calcium and
lactate) .

Shock

Volume expanders (Colloid)

Are used to increase the blood volume
following severe loss of blood
(haemorrhage) or loss of plasma (burns
and pancreatitis).
Expanders present in:dextran, plasma, and albumin, other
preparations as hemogel.

$
Shock

Parenteral Nutrition (PN)

Parenteral nutrition is a form of nutritional support that

supplies protein, carbohydrate, fat, electrolytes ,
vitamins, minerals, and fluids via the IV route to meet the
metabolic functioning of the body.
Indications:
Patient cannot tolerate internal nutrition as in case of
paralytic ileus, intestinal obstruction, persistent vomiting.
Patient with hyper metabolic status as in case of burns
and cancer.
Patient at risk of malnutrition because of recent weight
loss of > 10%, NPO for > 5 days.
Side effects: lactic acidosis, must be applied through
central line with risk of infection, if prolonged use gall
stones will be formed

!
Maintenance daily Requirements for adult (70 kg unless you are given
another weight
1st 10kg x 100ml

= 1000ml

2nd 10kg x 50ml

Next 50kg x 20ml

= 1000ml

TOTAL

= 2500 ml /day

500ml

Replacement of ongoing loss

As in:
NG
drains
fistulae
third space losses
Concentration is similar to plasma ! Replace volume per volume with
crystalloid solutions

3rd space losses !!!

Shock

1st Spacing: Normal distribution within ECF and ICF.

2nd spacing: accumulation within the interstitial compartments, oedema

formation but available for physiological exchange between compartments

3rd spacing: Accumulation in parts of the body where its not available for
exchange between the different compartments: Ascitis, tissue inflammation,
oedema from burns/surgery, pancreatitis.

Replacing Third Space Losses

Superficial surgical trauma: 1-2 ml/kg/hr
Minimal surgical trauma : 3-4 ml/kg/hr
- head and neck, hernia, knee surgery
Moderate surgical trauma : 5-6 ml/kg/hr
- hysterectomy, chest surgery
Severe surgical trauma: 8-10 ml/kg/hr (or more)
- AAA repair, nehprectomy

Blood transfusion
Blood transfusion is a common procedure that usually goes without complications. But
there are some risks. Some transfusion reactions happen during the transfusion, while
others may take several weeks to develop or become noticeable.
1. Allergic reaction and hives

May occur even with matched blood

Signs and symptoms are usually limited to hives and itching. These types of
transfusion reactions are usually treated with antihistamines and are seldom serious.
Rarely, a more serious allergic reaction may occur and signs and symptoms may
include difficulty breathing, low blood pressure, anxiety, rapid heartbeat and nausea.
2. Fever

fever and rigors may develop quickly during the transfusion or soon after (febrile
reaction). Fever usually isn't serious. But because fevers can be a sign of a serious
reaction, so you have to stop the transfusion to do further tests before deciding
whether to continue.
3. Acute immune hemolytic reaction

This is a very rare but serious transfusion reaction in which the body attacks the
transfused red blood cells because the donor blood type is not a proper match.
Released hemoglobin will be precipitated in renal tubules as acid hematin ending in
renal failure unless treated. Signs and symptoms include fever, nausea, chills, lower
back or chest pain, and dark urine.

TTT: stopping blood and giving matched blood with forced alkaline diuresis using
manitol and Na bicarbonate
4. Lung injury

Transfusion-related acute lung injury (TRALI) characterized by the acute onset of noncardiogenic pulmonary edema following transfusion of blood products specially plasma and
platelets but may occur with packed RBCs. TRALI is thought to be immune mediated. Usually,
TRALI occurs within one to six hours of the transfusion. People usually recover, when
treated by respiratory support
5. Bloodborne infections

Blood banks screen donors for risk factors and test donated blood to reduce the risk of
transfusion-related infections, but they occasionally still occur. It can take weeks or
months after a blood transfusion.
Estimated risks of contracting these diseases after a blood transfusion:

HIV 1 in 2.3 million transfusions.

Human T-lymphotropic virus 1 of every 2 million transfusions.
Hepatitis B 1 in 350,000 transfusions.
Hepatitis C affects 1 in 2 million transfusions.
West Nile virus 1 of every 350,000 units of blood in the United States.
Sepsis (bacterial infection of the blood) 1 in 1 million transfusions.
6. Delayed hemolytic reaction

This is similar to acute immune hemolytic reaction, but it occurs much more slowly.
often one to four weeks >decrease in red blood cell levels.
7. Iron overload

Multiple blood transfusions may lead to iron deposition (hemochromatosis) in the

liver and heart.
TTT: iron chelation therapy.
8. Graft-versus-host disease

The white blood cells in the donor blood attack the cells of the recipient. This disease
is often fatal. It's also a very rare condition affecting mainly immunocompromized
patients Signs and symptoms include fever, rash, diarrhea and abnormal liver function
test results.

Thyroid
GOITER = THYROID ENLARGEMENT
Simple (non toxic) goiter: diffuse (parenchymatous, usually physiological or
colloid) OR nodular (solitary or multi)
Toxic: Diffuse (Graves'): commonest cause of thyrotoxicosis in young females
or nodular: solitary autonomous or multinodular, commonest cause of
thyrotoxicosis in middle age
Thyroiditis: Infective is extremely rare, commonest is autoimmune
(Hashimoto) then subacute and Riedle's thyroiditis = woody or hard thyroid
which have to be differentiated from malignancy
Neoplastic:
Follicular adenoma (5 microscopical variants)
Carcinoma: 1ry is commoner than 2ry
Primary: according to incidence [papillary (60-70%), follicular (about
15-20%), anaplastic (about 5-10%), lymphoma, and medullary (each about
5%)

For clinical picture please read carefully the thyroid case

sheet

INVESTIGATIONS:
SUMMARY:

Start investigation by: CBC (Anemia?), TSH, and if abnormal do

FT4 (functional) and US (anatomical)! the proceed to other
investigations according to the findings of the previous work up, see
below

The best pathological investigation is FNAC though it is not

sensitive in follicular tumors

If you are in doubt about Hashimoto (very common, middle age

female with thyroid swelling starting toxic the becomes
hypothyroid) ! do Antibodies (anti TPO)

The most important preoperative investigation is indirect

laryngoscopy (medico legal)
DETAILED

condition

normal

hyperthyroidis
m

Hypothyroidis
m
primary

Hypothyroidism
secondary

TSH

normal

low

high

low

T4

normal

High
Except in T3
toxicosis

low

low

T4 and T3 circulate almost entirely bound to transport proteins, and the

change in levels of these proteins could change the total T4 and T3 levels (as
in pregnancy, use of contraceptive pills, nephrotic syndrome, liver diseases
etc), so the measurement of the free hormone level will be more accurate.

TSH Tests
The best way to initially test thyroid function is to measure the
TSH level.
High TSH level indicates hypothyroidism and low TSH level
indicates hyperthyroidism.

Exceptions
Secondary hypothyroidism (due to pituitary dysfunction) has
low TSH levels.
The rare form of hyperthyroidism due to TSH secreting pituitary
adenoma has high TSH levels.

T4 Tests
When TSH is abnormal, we measure the free T4 (FT4).
In hypothyroidism, low values will be found.
In hyperthyroidism, high values will be found.
Exception
T3 toxicosis, a type of toxic goiter (usually nodular) secretes only T3
(T4 is usually normal or low) and the patient commonly present by
cardiac manifestations only (thyrocardiac).
T3 Tests
Helpful to diagnose T3 toxicosis and to determine the severity of
the hyperthyroidism.
T3 testing is rarely helpful in the hypothyroid patient, since it is the
last test to become abnormal.
Patients can be severely hypothyroid with a high TSH and low FT4, but
have a normal T3.
Thyroid Antibody Tests
Thyroid is a sequestrated antigen (isolated from the immune system) and
autoimmune conditions as Graves' disease and Hashimoto thyroiditis will
be associated with formation of antithyroid antibodies.
Two common antibodies are directed against thyroid cell proteins:
thyroid peroxidase (TPO) and thyroglobulin.
Positive anti-thyroid peroxidase and/or anti-thyroglobulin
antibodies in a patient with goiter will diagnose Hashimotos
thyroiditis.
TSH receptor antibodies are increased in Graves' disease (its
measure is rarely required to follow up medical treatment).
Thyroglobulin

 Is used as a tumor marker for follow up of differentiated thyroid

malignancy (as papillary).
Calcitonin
Is the tumor marker of medullary thyroid carcinoma (for follow
up and for screening (the only diagnostic tumor marker) of the
relatives of the patient).
Other biochemical investigations:
Increase cholesterol level in myxedema.
Alimentary glucosuria in thyrotoxicosis.
Increase calcium level in thyrotoxicosis.

Imaging:
U/S: to confirm; anatomical diagnosis, nodularity and to determine if it is solitary
or multiple, cystic or solid.
Plain X-rays: may be helpful in retrosternal goiter.
CT: for local tumor infiltration and to detect retrosternal goiter.
Technetium scan: Done if you suspect retrosternal goiter, ectopic thyroid and to
detect bony metastases.
Histopathological diagnosis: FNAC needle is valuable, however it cannot
differentiate follicular adenoma from carcinoma (cannot detect vascular and
capsular invasion) in such condition we can do:
Tru cut needle is painful and may cause hematoma.
Open biopsy: removing the whole thyroid lobe (hemithyroidectomy)
and examine it by paraffin section.
Indirect laryngoscope: most important investigation before surgery to determine
if there is vocal cord injury (silent recurrent laryngeal nerve injury) for medico
legal purpose.
Treatment

- Physiological goiter: L-thyroxin (levo-thyroxin) to suppress TSH

and for prophylaxis we use iodinized salt).
- Simple multinodular goiter: Subtotal thyroidectomy in case of
pressure symptoms, cosmetic, and suspicious malignancy,
(removes the excess of the gland and leave as normal size = 2x5 cm
of the gland in each side in the posterior medial aspect to preserve the
RLN and the parathyroids).
Postoperative: Give L-thyroxin as replacement and to decrease
recurrence.
- Graves' disease: in young; anti thyroid drugs and if failed ! total
thyroidectomy (best as it is auto immune disease, to get rid of the
source of antigen) or subtotal thyroidectomy ( leaving half of the
normal lobe 1x5cm on each side).
Postoperative: L-thyroxin as before.
But if more than 45y: radioactive iodine is better (unless there is indication of
surgery as usual = pressure or cosmetic).
MALIGNANCY WITH THYROTOXICOSIS IS EXTREMELY RARE
-Toxic nodular goiter: if toxic nodule do hemithyroidectomy and if multiple
do total or subtotal thyroidectomy.
Postoperative: L-thyroxin.
TTT of malignancy: (sometimes the Qs start by asking you to enumerate the
types of thyroid malignancy, which is mentioned below)
- Papillary: total thyroidectomy with central lymphadenoctomy .
- Follicular: if less than 1cm; hemi thyroidectomy, but if more than
1.5cm; total thyroidectomy with radioactive iodine after surgery.
NB: L-thyroxin: is usually given for all patient after surgery
In malignancy L-thyroxin is given to:
In Papillary: the tumor is TSH dependent so L-thyroxin will
decrease TSH and for replacement.
In Follicular: only for replacement.

Other tumors:
- Anaplastic carcinoma: the tumor is inoperable so do isthmectomy +
tracheostomy + radiotherapy
- Medullary CA: total thyroidectomy + radical neck dissection and
screen other family member.
- Lymphoma: thyroidectomy + chemo and radio therapy.
Thyroiditis
Hashimoto: In early toxic stage give anti thyroid drugs and in
hypothyroid stage give L-thyroxin.
If pressure manifestation: do thyroidectomy.
Sub acute thyroiditis: there is good response to prednisolone.

CASE PRESENTED WITH

SOLITARY THYROID NODULE
What is your DD?
Simple (non-toxic) nodule.
Autonomous thyroid nodule (toxic).
Adenoma: Follicular adenoma (with variable subtypes).
Follicular carcinoma, less common Papillary (more common to
be multinodular) and medullary CA.
Simple cyst
Incidence of malignancy in true solitary nodule (solid) from 12-30 %,

Highest risk in young male

How can you manage this patient?

1. Exclude toxicity:
Toxic symptoms: Most important, weight loss despite of
polyphagia , intolerance to weather & palpitation.

in addition to other symptoms as neurological, cardiac and

genitourinary manifestations.
Toxicity signs: Mainly;
Pulse (tachycardia & arrhythmias).
Eye sign (Lid retraction, starring Gaze, lid lag, inability to
maintain convergence exopthalmos, occurs in AI
conditions (not with autonomous nodule.
Enlarged hypervascular gland.
In addition to being underweight, flushing, warm sweaty
hands, tremors, hair changes, nail changes,and pretibial
myxedema in AI conditions (not with autonomous
nodule).
2. Neck sonography: to confirm being, cystic or solid or presence of
other nodules.
NB: True solitary nodule= palpable one nodule without enlargement of the rest
of the gland, confirmed by sonography (if the rest of gland is enlarged it will be
multinodular goitre with Dominant nodule)
3. Thyroid profile: TSH first, then if abnormal ! measure free T4
and T3
4. FNAC( fine needle aspiration cytology): trustable in all thyroid
pathology and it is the most important diagnostic test in solitary
thyroid nodule
But If follicular neoplasm it cannot differentiate adenoma from
carcinoma, so we do hemi-thyroidectomy, paraffin section to see
capsular and vascular invasion in follicular carcinoma.
NB: No use of radioactive scan: Only to detect metastasis and
ectopic thyroid tissues.

CLINICAL PICTURE SUGGESTIVE OF MALIGNANCY IN THYROID

SWELLING
Rapid enlargement indicates malignant change.

 Pain indicates extra capsular invasion and pain is referred to

ear through vagus nerve (Arnold branch) which supplies the
back and the lobule of the ear.
What other symptoms and signs which may help diagnosis?
Symptoms: Dyspnea, stridor, dysphagia, hoarseness, metastatic
(skull, femur) and lung.
Signs:
Hard nodule, irregular nodule, fixed nodule.
If papillary multinodular and lymph nodes
Weak or absent carotid pulsation(Berrys sign)
May be hypervascular gland with pulsation, thrill and bruit.
What are the investigations which establish diagnosis?
-FNAC.
-Tumor marker: Thyroglobulin for papillary and follicular CA, and
calcitonin for medullary CA.
-Before operation direct laryngoscope (for medico legal issues to detect
silent RLN injury)
-CXR , lung and liver CT.
NB: Radioactive scan to detect metastases is done after thyroidectomy to
avoid uptake of radio iodine to metastases.

4.

How can you manage this case?

-Total thyroidectomy.
-Remove enlarged lymph nodes or do central block dissection.
Metastasis:
-Radioactive I131.
POSTOPERATIVE COMPLICATIONS OF THYROIDECTOMY
1. Respiratory distress which if not treated urgenly !
suffocation
Describe priorities in management of this patient

Ensure patent airway

Open wound in the bed
Evacuate any hematoma
If no immediate improvement; do laryngostomy or at least insert
wide bore canula in the trachea to be followed by tracheostomy.

Mention the causes of post-thyroidectomy respiratory distress

i. Hematoma :reactionary hemorrhage (bleeding within
24hr)
ii. Laryngeal edema
iii. Bilateral partial recurrent laryngeal nerve injury
NB;TO REMEMBER
RLN injury
PR: P (Partial injury) affects R (Respiration)
Partial unilateral Dyspnea
Partial bilateral Suffocation
CV: C (Complete injury) affects V (voice)
Complete unilateral Hoarseness
Complete bilateral Aphonia
iv. Acute tetany (laryngismus stradulus)
2. Other complications of thyroid surgery?
Endocrine:
- HypoparatyroidismTetany
- Hypothyroidism
- Recurrent Toxic Goiter
External laryngeal nerve injury: shocking
Tracheal and esophageal injury
Keloid

LIPOMA
Commonest sites: U &LL & trunk specially back but may occur in any site
(universal tumor) except (areas don't contain fat); intracranial (but may occur
extradural in V Column), eye lids, glans penis and clitoris
May be subcutaneous, subfascial, intermuscular, subsynovial (around knee),
subperiosteal and sub-mucous (dangerous in larynx as it may cause
suffocation and in intestine as it causes intussusception)
C/O:
Painless slowly growing tumor
May be painful if infected, under tension as subperiosteal type, if pressing
nerve, adiposa delerosa (see below)
Very rarely to change to liposarcoma (doubtful, and liposarcoma is malignant
from the start)
O/E:
SC lipoma: Soft lobulated tumor with slippery edge and attached to skin by
multiple dimples
Fibrolipoma is firm
Angiolipoma is bluish
Intermuscular or subfascial lipoma have no dimples and become less prominent
with contraction of the related muscles

Dimpling and slippery edge

Complications (very rare): infection, calcification, malignancy?, suffocation
and intussusception (see before)
Multiple lipomas may be seen and may be painful (adiposa delerosa)
NB: adiposa means lipoma and delerosa means painful
TTT: excision if large or causing discomfort of patient as complications are rare

DERMOID CYSTS
Cysts lined by squamous epithelium
Types:
A. Teratomatous dermoids:
Are found in the ovary, testis, retroperitoneum , superior mediastinum,
and the presacral area.
Teratomas (variable degrees of malignancy), arise from totipotent
cells, from all three embryonic layers: ectoderm, endoderm,
mesoderm .so, it contains hair, teeth, muscle, gland tissue.

B. Sequestration dermoids:
Formed by the inclusion of epithelial nests beneath the skin at sites of
embryonal fusion (midline of oral cavity and neck, external angular
process, root of nose, around ear and may be in internal organs)
Usually present as painless slowly growing swelling which is cystic
(Paget's test) and not attached to skin and deeper structures
Treatment by excision (if in the head wait till the sutures close)

$
C. Implantation dermoids:
Follow puncture wounds, commonly of the fingers, when living
epithelial cells are implanted beneath the surface
More; in hair dresser, gardeners and tailors
Present as painless slowly growing swelling in hand or over scar
TTT: Excision
NB: no sequestration dermoids in limbs as it develop by budding with any embryonal fusion
D. Tubulo-dermoids: as thyroglossal and branchial cysts (cystic changes in
embryonic remnants)
E. SEBACEOUS CYST (Retention Dermoids):
Due to obstruction (usually start by inflammation) of the sebaceous gland duct
(of the hair follicle)
Not found in palm and sole (no hair follicles)
This is a cyst contains keratin, sebum, and is surrounded by an epithelial wall.
Occurs at any age but rare in childhood
C/O:
Painless slowly growing swelling commonly in face, scalp, neck, trunk, or limbs
Becomes painful and increases in size if infected
O/E:
Hemispherical swelling (may be multiple), attached (tethered) to skin by single
point (punctum or the black point), cystic (Paget's) and mobile
If inflamed become hot, red, and tender
Complications:
1- Infection
2- Ulceration
3- Sebaceous horn

TTT:
Excision with skin ellipse to remove the punctum if not infected
If infected, drain it first by incision with antibiotic and excise it after resolution
of infection

SWELLINGS OF THE LYMPH NODES

There are approximately 800 lymph nodes in the body, 300 of them lie in the
neck.
Usually multiple swellings.
May be part of generalized lymphadenopathy, as:
1. Viral (HIV, infectious mononucleosis)
2. Bacterial as in septicemia (non specific) or specific as TB and syphilis
3. Parasitic as toxoplasmosis, lishmaniasis
4. Neoplastic: as lymphoma, leukemia, and rarely generalized carcinomatosis
(usually localized enlargement)
5. Autoimmune, sarcoidosis, etc
Localized lymphadenopathy:
1. Infection or malignant deposits may come from any part of head and
neck, as, the oral and nasal cavities, the ear, the scalp, the oropharynx
and face.
2. In lower deep cervical nodes (supraclavicular), the source may be breast,
lung, liver in right side or advanced visceral malignancy on left side
(Virchow's LNs)
3. Most of lymphoma start in lower deep cervical LNs

Cervical LNs, Group I submental above hyoid, II submandibular and

upper part of upper deep LNs, III ant triangle from thyroid crtllage to
cricoid, IV ant triangle fom cricoid to clavicle, V LNs in post triangle
including supra clavicular, VI anterior group (pre-laryngeal and
pretracheal LNs)

TUBERCULOUS CERVICAL LYMPHADENITIS

May be:

 Blood borne:
Usually secondary to pulmonary TB
The lymph nodes are enlarged, firm and arranged in chains (like rosary)
It must be differentiated from lymphoma by lymph node biopsy

Lymphatic borne:
1. If the infection starts in upper deep cervical lymph nodes:
The tonsils act as portal (gate) only and no TB lesion is found in it
The organism is bovine type which is transmitted through
contaminated milk
2. If the infection starts in lower deep cervical lymph nodes:
Infection comes from active pulmonary TB
The organism is human type
NB: if start of infection in any group it may spread the other i.e. upper lower

Pathological changes of lymphatic borne TB: The inflammation starts an

the capsule and around it (peri-adenitis)! MATTED lymph nodes !
tuberculous reaction inside the nodes Caseation with breaking of the septa
!Cold Abscess ! penetrates fascia then skin to open by multiple sinuses
with undermined edges

Clinically:
Painless or slightly painful neck swelling
Loss of weight and loss of appetite
Night fever and night sweating
Manifestation of pulmonary TB if lower deep cervical lymphadenitis
If upper deep cervical TB lymphadenitis ! the tonsils appear free
Enlarged nodes: first firm with matting ! cystic cold abscess ! multiple
sinuses with undermined edges

Investigations: Most important lymph node biopsy but start by

1. CBC will show anemia and lymphocytosis, leukemia
2. CXR! pulmonary TB only if the infection starts in lower deep
cervical LNs
3. Tuberculin is good negative test but not in Immunocompromized
patients
Treatment: Anti-tuberculous drugs, drainage of cold abscess, dressing of
the sinuses with anti-tuberculous drugs

LYMPHOMA
Hodgkin lymphoma: Curable tumor
Age: peak around 15 and another around 45 years
Commonly to start in lower deep cervical lymph nodes but may start
in upper or any other group
Usually start as uni-centric enlarged node ! lymphatic spread to
other lymph nodes in the same group (first like satellite ! discrete
lymph nodes)
It is rubbery in consistency

$
Hodgkin lymphoma discrete lymph nodes

Clinically:
Painless enlargement of lymph nodes, may become painful after
intake of Alcohol or late after infiltration of nerves
May be manifestation of Mediastinal syndrome (dyspnea, dysphagia,
hoarseness and hic-cough due to phrenic N irritation)
Abdominal swelling (spleen or para-aortic LNs)
Systemic manifestation:
1. Fever, may be typical Pel-Ebstien
2. Itching; may be the first presentation
3. Significant loss of weight

4. Anemia
STAGES:
1. Stage I: one group is affected
2. Stage II: more than one group on one side of the diaphragm (above
or below)
3. Stage III: more than one group on both sides of the diaphragm
4. Stage IV: extra- lymphatic spread as bone, peritoneum, CNS
S: means involved spleen
E means involved extra-nodal disease as gastric, intestinal or thyroid
A: no systemic manifestations
B: presence of systemic manifestations

Investigations:
Mainly depends on biopsy, but we start by
CBC may show anemia and esinophilia
CT chest for Mediastinal syndrome, and for abdomen for any
abdominal lesion

Treatment:
Stages I, II IIIA! Radiotherapy
Stages IIIB and IV! chemotherapy

Non Hodgkin's lymphoma

More common
May be related to infection as HP (gastric), EB virus, HCV, HIV
infection

 Multicentric
Spread by blood
Symptoms as Hodgkin's but wit rapidly progressive course
Lymph nodes are first firm or hard the consistency becomes variable
due to necrosis
Rapid fusion of lymph nodes which form irregular fixed mass
Staging, investigations and ttt as Hodgkin disease but with less
favorable prognosis

DIFFERENTIAL DIAGNOSIS OF NECK SWELLING

A.
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.

Middle Swellings:
Ludwig Angina
Enlarged submental lymph node
Sublingual dermoid
Lipoma in submental region
Thyroglossal cyst
Subhyoid bursitis
Extrinsic carcinoma of the larynx (late)
Goiter (thyroid isthmus / pyramidal lobe/ Retrosternal goiter
Enlarged suprasternal lymph node
Dermoid cyst ( can occur anywhere in the midline )

B. In the side of the neck:

Parotid swelling: in the gap between mastoid and angle of mandible below the
external auditory canal
IN THE SUBMANDIBULAR TRIANGLE
1. Enlarged lymph nodes
2. Submandibular salivary gland
3. Deep or plunging ranula
4. Extension of growth from the jaw
IN THE CAROTID TRIANGLE
1. Aneurysm of the carotid arteries
2. Carotid body tumor
3. Branchial cyst
IN ANTERIOR TRIANGLE
1. Goiter
2. LNs

3.

1.
2.
3.
4.
5.
6.
7.

Sternomastoid tumor
IN THE POSTERIOR TRIANGLE
Supraclavicular lymph nodes
Cervical rib
Cystic hygroma
Lipoma
Pharyngeal pouch
Subclavian aneurysm
Aberrant thyroid

1. SWELLINGS OF THE SUBMANDIBULAR SALIVARY

GLAND:
Commonly infection and rarely neoplasms
Infection is usually associated with submandibular salivary stone.
In stage of stone alone: a history of enlargement of the swelling (with
salivary duct colic) at the time of meals which subsides after meals
May be followed by acute suppuration and abscess formation (FAHMR)
In stage of chronic sialoadinitis, there is a slightly painful swelling which can
be palpated bimanually where the deep part of the salivary gland can be felt
Further, pressure on the swelling may result in the flow of pus through the
orifice of the Wharton's duct.
NB: submandibular gland swelling; is single, fixed to mandible with no groove with it, and
better to be palpated bimanually
NB: submandibular LN swelling; multiple, has a groove between it and the mandible, can be
rolled over the mandible (mobile), and can be palpated from outside only
2. Ludwig angina:
Ludwig angina: Is a form of cellulitis that starts in the submandibular region and
spread to the floor of the mouth.
It produces a diffuse swelling beneath the jaw and inside the mouth with fixing
the tongue.
Usually polymicrobial
It might have dangerous complication:
A. Edema of glottis may obstruct the airways, necessitating tracheotomy
B. Mediastinitis
C. Fatal septicemia

Ludwig Angina
3.

Branchial cyst:
From the vestigial remnants of the second branchial cleft
Branchial cyst though congenital, it usually appears in adolescent and adults.
Oval cystic swelling deep to the upper third of the sternomastoid muscle
The diagnosis is confirmed by finding cholesterol crystals in aspiration
It passes between bifurcation of carotid vessels, which may cause difficulty in
excision ! recurs or causes fistula

$
Branchial Cyst
4. CERVICAL RIB:
Extra rib arising from the 7th cervical vertebra in less than 1% of population
Clinical types:
Lump in the lower part of the neck which may be visible (collection of fat
similar to lipoma over the rib)
Cervical rib with vascular symptoms (if complete); as Reynaud's syndrome
Cervical rib with nerve-pressure symptoms (C8 & T1)
Diagnosed by x-rays & treated by excision
5. Thyroglossal cyst:
May be present in any part of the thyroglossal tract, from foramen cecum to
pyramidal lobe of the thyroid isthmus
The common site in order of frequency, are beneath the hyoid, in the region of
the thyroid cartilage, and above the hyoid bone.
The swelling moves upwards on protrusion of the tongue as well as on
swallowing.
The wall contains nodules of lymphatic tissue, so it is liable to inflammation.
An infected cyst is often mistaken for an abscess and incised, a thyroglossal
fistula arises which is never congenital , it follows infection or inadequate
removal of a thyroglossal cyst
Do Technetium scan and if it is the only thyroid tissue leave it but if the
patients wants to remove it implant it to abdominal muscles or give the patient
L thyroxin

 The operation is sis-trunk operation removing the cyst or ectopic thyroid with
the whole thyroglossal duct from tongue to thyroid, including the middle part of
hyoid bone to avoid recurrence or fistula formation (same ttt of the fistula)
6. ECTOPIC THYROID:
Residual thyroid tissue along the course of the thyroglossal tract
May be lingual (if enlarged ! respiratory obstruction), cervical or intra-thoracic
Median ectopic thyroid:
Swelling in the upper part of the neck and is usually mistaken for a thyroglossal
cyst but solid
Lateral aberrant thyroid:
May be a metastasis in a cervical lymph node from an occult thyroid carcinoma.
Manage median type as thyroglossal cyst
NB: Lingual thyroid is liable to hemorrhage ! suffocation and it is the most liable
thyroid tissues for malignant change, so it must be excised.
7. Carotid body tumor: Chemodectoma or potato tumor:
Common in high altitude area and may be bilateral
This potentially malignant growth is located at the bifurcation of the
common carotid artery, i.e. at the level of the upper border of the thyroid
cartilage.
It gives rise to a hard ovoid lobulated swelling under the upper third of the
sternomastoid (site of branchial cyst, but not cystic)
Movable laterally but not vertically, as it is attached to the carotid.
Pulsation of the carotid arteries can be felt in front, but the swelling itself is
not pulsating.
Pressure over the swelling has to be avoided as it may cause slowing of the
pulse-rate and a feeling of faintness ( carotid body syndrome )
Investigations: Carotid angiography and CT
TTT: excision
8. Aneurysm of the carotid or subclavian A:
Thromboembolic complications in arm with digital acute ischemia
(90%).
Punctate cynotic lesion in hand.
Brachial plexus compression ! pain
A Pulsatile palpable mass in supraclavicular fossa or carotid triangle
Palpable thrill and Auscultate loud bruit
Radial/ ulnar pulse may be lost.
Duplex and angiogram are diagnostic
9. Sternomastoid tumor:
Is not a tumor
It is the result of birth injury to the sternomastoid muscle, causing thrombosis
and subsequent fibrosis.
It gives rise to a circumscribed firm mass within muscle, this usually subsides
spontaneously but may, later on, lead to torticollis

10.

Cystic Hygroma:
Dilated afferent lymphatics (not true lymphangioma)
Arising under the deep fascia and extending deeply between the muscles.
Usually located at the root of the neck and may spread to the mediastinum and
pectoral region.
Mediastinum extension is suspected if it gets tense on straining
It is usually multilocular but may be unilocular & translucent (hydrocele of the
neck)
TTT: excision best before school age

Surgical Disease of the Adrenal Gland

Blood supply
Arterial
3 arterial sources of flow:
1. Inferior phrenic artery
2. Aorta
3. Renal artery
Venous
single main vein most important surgical structure
- right IVC (long)
- left renal vein (short, may be injure during
operation)
The Incidental Adrenal Tumor
(Incidentaloma)
0.5 5% of abdominal CTs show abnormal adrenal glands
85% of adrenal masses are nonfunctional and BENIGN
Def. of incidental mass:
Mass >1cm, discovered on exam for non-adrenal cause - absence of signs or
symptoms of adrenal disorder
It may be:
Nonfunctioning adenoma 82%
- Functioning:
Cushings
5%
Pheochromocytoma
5%
Aldosteronoma (Conns)
1%
- Malignancy:
Metastasis
3%
Adreno cortical carcinoma (ACC)
4%
NB: If mass >6cm ACC will be 65%
Hormonal assessment
Serum potassium (if HTN) Conns
Plasma metanephrines: most sensitive test for pheochromocytoma

24-hr urine cortisol (Cushings)

Treatment: Hormonally active surgical removal
Non active:
> 3 cm removal
< 3 cm observe
Pheochromocytoma
functioning tumor of the adrenal medulla
Rules of 10
Bilateral
Familial (non-sporadic, may be a part of MEN II)
Pediatric
Malignant
Normotensive
Extra-adrenal (paraganglioma)
Multiple
NB: Childhood presentation breaks the rules- 25% bilateral, multiple, extraadrenal
Symptoms: are due release of epi/norepinephrine - - Hypertension present 90%
cases
- Orthostatic hypotension may occur due to low plasma volume
Triad: headache, tachycardia, diaphoresis
Other symptoms: Pallor, flushing, palpitations, abd/chest pain, weakness, psychosis
NB: Small tumors more likely symptomatic
Diagnosis:
Plasma free metanephrines- most sensitive test
-seen 99% of patients
24 hours urinary catecholamines or its metabolites as VMA (2x normal is diagnostic)
Localization by CT or MRI
MIBG for suspected metastases
Treatment: adrenalectomy
Preoperative preparation:
Early alpha blockade
Goal to control hypertension, use phenoxybenzamine
Do NOT use b-blocker before alpha blocker as it will lead to unopposed alpha agonism
severe hypertension
IV hydration
Cushing Syndrome
Is a group of signs and symptoms caused by prolonged excessive amounts of circulating
cortisol.
Iatrogenic: exogenous cortisol
Adrenocortical adenoma or rarely CA

Cushing disease: pituitary adenoma secreting ACTH leading to bilateral adrenal

hyperplasia
Clinically
Obesity :Typically the distribution of fat involves the trunk, particularly the
cervicodorsal region (buffalo hump), supraclavicular area, and abdomen. The face is
round and plethoric (moon face). The extremities are thin in relation to the rest of the
body.
The skin of patients with Cushing's syndrome is thin and fragile, ecchymoses and
hematomas results from a combination of thin skin and capillary fragility.
In the Cushing disease there dark skin due to excess ACTH
Striae rubra: when present, are usually located on the abdomen, breast, and axillae.
Occasionally, they may be found on the back and on the extremities. They are pink or
purplish in color and wider than 1 cm
Hypertension
Proximal muscular weakness affecting predominantly the muscles of the pelvic girdle
Acne, hirsutism, and menstrual irregularities
Osteoporosis, compression fractures and persistent back pain
Peripheral edema
psychiatric manifestations, including anxiety, depression, and even frank psychosis
Diagnosis:
1. Glucose intolerance, glucosuria is often seen, but ketoacidosis or the chronic
complications of hyperglycemia are very uncommon
2. The level of cortisol in plasma and 24 hours urinary cortisol and ACTH
3. Dexamethasone suppression test
4. Radiologic diagnosis includes X-ray examination for a pituitary tumor, and computed
tomography which is the most popular procedure for visualizing the adrenals in patients
with Cushing's syndrome
Treatment:
Pituitary ablation in the disease (surgical or irradiation)
Adrenalectomy in adrenal tumors
Conns syndrome
Hyperaldosteronism leading to surgically correctable hypertension with hypokalemia
(adrenalectomy)
Parathyroid gland
Anatomy:
Superior glands usually dorsal to the RLN at level of cricoid cartilage
Inferior glands located ventral to nerve
Usually derive most of blood supply from branches of inferior thyroid artery, although
branches from superior thyroid supply at least 20% of upper glands.

 Glands drain ipsillaterally by superior, middle, and inferior thyroid veins.

Calcium metabolism:
The parathyroid cells regulate PTH secretion by sensing extracellular calcium levels
PTH secretion also is stimulated by low levels of 1,25-dihydroxy vitamin D and
hypomagnesemia.
PTH functions to regulate calcium levels via its actions on three target organs, the bone,
kidney, and gut.
Increased PTH secretion leads to an increase in serum calcium levels by increasing bone
resorption and enhancing renal calcium reabsorption.
PTH also stimulates renal 1-a Hydroxylase activity, leading to an increase in 1,25dihydroxy vitamin D, which also exerts a negative feedback on PTH secretion
At the kidney, PTH acts to limit calcium excretion at the distal convoluted tubule via an
active transport mechanism.
PTH also inhibits phosphate reabsorption (at the Proximal convoluted tubule) and
bicarbonate reabsorption.
PTH and hypophosphatemia also enhance 1-hydroxylation of 25-Hydroxyvitamin D,
which is responsible for its indirect effect of increasing intestinal calcium absorption.
HYPERPARATHYROIDISM
Primary hyperparathyroidism occurs in 0.1 to 0.3% of the general population and is
more common in women than in men (4: 1).
Primary hyperparathyroidism is characterized by increased parathyroid cell proliferation
and PTH secretion which is independent of calcium levels.
Etiology unknown, but radiation exposure, and lithium implicated, associated with
MEN1, and MEN 2A
Parathyroid adenoma in approximately 80% of cases, multiple adenomas or
hyperplasia in 15 to 20% of patients and parathyroid carcinoma in 1% of patients.
Clinically:
Kidney stones, painful bones, abdominal groans, psychic moans, and fatigue overtones
Kidney stones calcium phosphate and oxalate
Osteopenia, osteoporosis, and osteitis fibrosa cystica, is found in approximately 15% of
patients with PHPT. Increased bone turnover can usually be determined by documenting
an elevated blood alkaline phosphatase level.
Peptic ulcer disease, pancreatitis
Psychiatric manifestations such as florid psychosis, obtubdation, coma, depression,
anxiety, fatigue
Investigations:
Hypercalcemia can be from other sources. Intact PTH measurement and elevated PTH
level very sensitive for hyperparathyroidism
Pre-operative localization

The predictive value of ultrasonography, magnetic resonance imaging, or thalliumtechnetium dual isotope scintigraphy ranges from 40 to 80 percent
Most sensitive is Tc sistamibi scan due to delayed washout
Surgery:
Bilateral neck exploration is gold standard
With pre-operative imaging techniques can have minimally invasive focused surgery
towards adenoma
If hyperplasia excise 3.5 glands and implant the other half in the deltoid to avoid neck
exploration if recurrence occurs
Intraoperatively, cancer is suggested by the presence of a large parathyroid tumor that is
invasive into surrounding tissues
bilateral neck exploration, with en bloc excision of the tumor and the ipsilateral thyroid
lobe.
Modified radical neck dissection is recommended in the presence of lymph node
metastases
Secondary in prolonged hypocalcemia in renal failure will increase PTH and if it
persists the gland will act autonomously and problems like primary will occur

BREAST CASES
The breast is developed from the milk line (from axilla to groin),
each line can produce more than one breast or nipple.
Polymazia: means presence of more than 2 breasts
The extra one must be excised as it is very liable for malignant changes
Polythelia: more than 2 nipples, it may be excised for cosmetic
purposes.
Lactating mastitis
predisposed by lack of hygiene ,fissures , cracks and retracted
nipple.
Milk engorgement is a stage of the disease rather than a
predisposing factor.
Organisms:
o Staphylococcus aureus localized to abscess (90%) and
Streptococcus species (diffuse infection).

o Stages:
1-Milk engorgement:
.Sector of the breast

. Dull aching pain.

.No fever
The affected sector is tender and indurated.
No enlarged axillary nodes
2-Diffus mastitis:
.Burning pain

.Fever.

.Hot ,red ,tender,and indurated sector.

.Axillary nodes :enlarged and soft.
3.Stage of localization:
.Throbbing pain

. Hectic fever

. The affected sector as in diffuse mastitis but with bulge and

edema
.Axillary nodes enlarged and soft
NB: Never we wait till the abscess becomes fluctuant (very late)
4.Complicated cases:
.pus from nipple

.sinus formation

.Antibioma(fibrous wall and sterile pus)

DD: Diffuse mastitis must be differentiated from inflammatory CA
(more than one third of breast, no fever ,more edema,LNs are hard and
non tender ,no leukocytosis and no response to antibiotics).
Treatment:
- Good hygiene .
- Treatment of fissures and cracks.
- Hot foments .
- Antibiotics against resistant staph .
- Drainage of formed abscess

 Incision: at most dependent and most pointing if dont meet, do

incision and counter incision
Lactation: use safe antibiotic for the fetus and lactate from the normal
side and evacuate the other side by suction pump.
Mammary Duct Ectasia

Dilatation of large ducts

Stasis
Periductal (plasma cell)mastitis
Abscess

Chronic mass colored discharge

Fibrosis (DD: CA)

Fistula
Treatment:
- Infection :antibiotics to anaerobes
- Abscess : drainage
- Fistula : excision
- Mass : triple assessment
- Discharge :see latter
Fibrocystic changes
(Fibroadenosis, Mammary dysplasia)
The changes consist of 4 features:
Adenosis (increase no of glands)
Epitheliosis with or without papillomatosis,
Fibrosis sometimes-extensive forming hard mass (sclerosing adenosis)
simulating cancer.
Cyst formation.
The changes may be proliferative (premalignant)

or non proliferative
Clinically:
Age:Around 30s.
Symptoms:
Cyclical mastalgia (exaggerated premenstrual mastalgia).
Discharge : thick green or straw yellow.
Localized mass: usually aggregated or large cyst or sclerosing adenosis
Signs:
The disease is usually bilateral but may be unilateral.
The lesion is usually diffuse but may be localized.
May be solid or cystic.
Cysts are granular ,nodular or large.
NB fibrocystic changes are commonly known as painful nodular condition of
the breast.
Axillary nodes may be enlarged and small (like gun shots)
Investigations:
Diffuse bilateral lesions:
with dischrge:measure prolactin level to exclude pituitary microadenoma
with hyperprolactinemia (simulate the disease).
Localized lesion:
Triple assessment to exclude carcinoma.
Discharge: see below
Microwave radiometry can differentiate proliferative (more heat production)
from non proliferative lesions.
Treatment:
Reassurance
Firm bra to decrease mobility of breast.
Avoid excess fat &caffine (tea , choclate ,coca , coffee)
Vitamin E, thiamine, magnesium, and evening primrose oil may be of help.

 Simple analgesic for pain.

Bromocryptin in intractable pain but causes severe nausea.
Cases proved to be proliferative need regular screening for breast cancer.
Duct papiloma
Pathology Situated in one of the major ducts near its orifice usually single
but may be multiple and peripheral (Multiple Papillomatosis)
Clinical Picture young adult female (30-45) presenting with blood
discharge from the nipple.
on examination a fresh drop of blood is seen on pressure at a certain point
or a palpable small fusiform retroareolar mass is felt (retention cyst due to
obstruction of the duct by clotted blood) pressure on it produces the
discharge.
Investigations guiac test discharge is +ve for blood.
Galactography using lipiodol shows regular filling defect
Treatment microdochectomy & if multiple do excision of major ducts.
Fibroadenoma
Age: 15-35.
Size: 2-3 cm.
Diagnosis: by triple assessment
Symptoms: discrete lump.
Signs: normal skin, not tender, not hot, 2-3cm, hemispherical,
smooth, well defined, firm to rubbery, freely mobile.
NB if presentation is delayed to above 35 ys it will be soft .
Giant fibroadenoma is rapidly growing variant in adolescent
Phylloid tumor: huge fibroadenoma in middle age (needs mastectomy).
TTT TRIPPLE ASSESSMENT FOLLOWED BY EXCISION BIOPSY

Differential Diagnosis
DD: Of Painless lump
1. Fibroadenoma ( breast mouse)
2. Breast cancer
3. Cyst
4. Fibrosed hematoma or chronic fat necrosis
DD of breast pain
A. Painful lump
1. Fibrocystic changes (common)
2. Mastitis and absecess
(Usually postpartum or lactational or duct ectasia)
3. Acute hematoma or acute fat necrosis
4. Infected cyst
5. Rarely carcinoma (inflammatory).
6. Localized milk engorgement
B. Pain without lump:
1. Cyclical breast pain (cyclical mastalgia) is associated with fibrocystic
breast changes and it is usually with lump and rarely without. Mild degrees
of cyclical breast pain and tenderness are normal in premenstrual syndrome
(PMS).
2. Noncyclical breast pain: as hormonal changes in puberty (both in girls
and boys), in menopause and during pregnancy and post partum due to
fissures and cracks of the nipple, and may be due to alcohol or drugs.
3. Tietze syndrome is a benign inflammation of one or more of the costal
cartilages.and leads r to pain (increase with respiration) and tender costal
cartilages which may be mistaken with breast pain
1. What is the differential diagnosis of colored discharge from
nipple?
Bloody ! duct papilloma is the commonest but may be in duct
carcinoma or duct ectasia.
Creamy ! duct ectasia (commonest breast discharge and it
can take any color).
Milky ! hyperprolactinemia due to pituitary microadenoma

NB. Galactocele is a retention cyst contains milk and follows

lactation and milk appears by squeezing I, we treat it by
squeeze or aspiration if any doubt!excision biopsy.
NB .If in lactation; it is normal secretion.
Brownish, green, yellow, watery etc in carcinoma or
fibrocystic changes.
Pus in neglected abscess.

2. How can you manage this case?

Take full clinical history with concentration on:
Discharge: if found, ask about;
Left, right or both?
Color: see before
Amount.
Odor
Recent history of breast feeding?
With nipple retraction?
If associated lump or not?
If associated pain?
If any systemic manifestations?
Examination of breast as usual with zonal squeeze of all parts of the breast to
see the discharge colour and if it comes from one or more ducts
NB. Search for presence of lump; clinically and by mammographysonography examination
If there is a lump manage by triple assessment and treat according
to the findings (see the table in the summary at the end).

 If no lump with bilateral milky discharge!measure prolactin

level! if high!give the patient bromocryptin (parlodel which
causes severe nausea).
If no lump and coming from one duct! microdochectomy
(remove the affected duct only and send for histopathology).
If no lump and coming from multiple ducts!search for blood by
Guiac or benzidine test:
!If negative for blood: follow up if lump appears! triple
assessment
!If positive for blood! Pt < 45 years! follow up
! Pt > 45 years! excision of the major
ducts
NB. Ductography is expensive and not in common use
NB. Cytological examination of the discharge may be requested
if doubtful intraductal tumors
CARCINOMA OF THE FEMALE BREAST
Etiology:
I-Genetic Factors:
Mutation of the following Suppressor genes:
1-Breast carcinoma gene
BRCA I on chromosome 17
BRCA II on chromosome 13
2-Positive family history in mother or sister (marked increase in
incidence if both are affected, especially if occurs premenopausally)
NB: Genetic factors are responsible for 5-10% of all breast cancer and
it is usually bilateral and multifocal.
II-Endocrinal factors:
Prolonged exposure to estrogen as in:
1-Early menarche below 12 years and late menopause after 50 years
2-Delayed onset of 1-st pregnancy and lactation:
-Nullipara: First pregnancy after 30 years.

-Sterility and females who never lactate.

-High estrogen contents of contraceptive pills.
-Post menopausal hormone (estrogen) replacement therapy (HRT).
III-Obesity:
Due to conversion of the suprarenal androgen to estradiol in fatty
tissues.
NB: diet as junk food, plays a rule through induction of obesity or
presence of carcinogenics
Some forms of diet decrease risk if reach in vitamin D and leukopines
(in tomato and red grapes) with other antioxidants
IV-Previous affection of one breast:
Bilatrality in general about 15-20%
increases over 25-50% if invasive lobular carcinoma
V-Precancerous Lesions: Benign lesion ! turns malignant
-Duct papilloma specially if multiple.
-proliferative forms of fibrocystic changes.
-In situ tumors will become invasive.
Types: Ductal, lobular, Paget, and inflammatory
I. Ductal Carcinoma: 80%
A-Non-Invasive Duct Carcinoma (Duct carcinoma in situ or DCIS)
Usually multifocal
B- Invasive duct carcinoma: it may be
1. Adenocarcinoma with productive fibrosis (scirrhous, simplex, NST),
80%
Eighty percent of invasive breast cancers are described as invasive
ductal carcinoma of no special type (NST).
These cancers generally have a worse prognosis than special-type
cancers.
Usually associated with dimpling and retracted nipple
2. Medullary carcinoma 4% (Encephaloid): soft brain like tumor,
Better prognosis than NST
Usually attains large size at discovery with ulcers or fungation.
II. Lobular CA: 15%
A-Non invasive Lobular Carcinoma (lobular carcinoma in situ, LCIS)
Usually multifocal.

It is not a rule to turn to invasive lobular CA but it is a mark

that an invasive cancer will be developed.
Invasive Lobular Carcinoma
It is bilateral in 25-50% and the bilaterality is usually mirror
image
III. Pagets Disease: 1%
It starts intraductal then becomes invasive
-It arises from main ducts near the nipple.
-The disease starts by: Erosion of nipple, then areola and
after 2 years a mass of infiltrating duct carcinoma will
appear.
IV. Mastitis Carcinomatosa (Inflammatory carcinoma)
Occurs mostly during pregnancy and lactation (due to high hormonal
level) if such; it will be known as acute lactating carcinoma, but may occur
at any age unassociated with these events.
Diffuse infiltration of the whole breast with no localized mass, peau
dorange, retracted nipple, with enlarged hard non tender lymph nodes
DD: Condition may resemble acute bacterial mastitis (but in the latter;
less than one third is affected in addition to fever, enlarged soft tender
lymph nodes and Leukocytosis.
Spread of carcinoma of the Breast:
I-Direct (Local) spread:1st within the breast tissue itself, then to the skin,
pectoral muscles and fascia, serratus anterior muscle and chest wall.
II-Lymphatic spread: By both embolization and permeation.
A-Embolization: - To lymph nodes.
-75% to axillary lymph nodes (Especially from tumors of lateral part
of breast)
-Internal mammary lymph node (especially from medial half)
-Posterior intercostal lymph nodes
N.B: Tumors in lower medial quadrant may invade rectus sheath lymph
vessels umbilicus malignant umbilical nodule inguinal lymph node
Or to lymphatics of Falciform ligament Porta hepatis and liver.
B- Permeation: Retrograde growth in lymphatics to form either: Separate
skin nodules or multiple nearby nodules known as cancer en cuirasses
III-Blood Spread: First to bone (vertebral column) then liver , lung,
brain
IV-Trans-coelomic spread:

A-Ovaries Krukenburg tumor (bilateral) may by retrograde lymphatic

permeation.
B-Nodules in Douglas pouch (Blummer shelf nodules)

Staging:
TNM Classification
T = Tumour
Tx unknown primary
T0 or Tis Carcinoma in situ
T1 Less than 2cm
T2 Tumor diameter 2-5cm
T3 Larger than 5cm or pectoralis invasion
T4 Any size invading skin or chest wall
N = Nodes
N0 Nonpalpable axillary LN
N1 Ipsilateral mobile LN
N2 Ipsilateral fixed LN
N3 Supraclav. Int mammary contralateral axillary LN
M = Metastases
M0 No metastases
M1 Distant metastases
Manchester Classification
Stage I Mass confined to the breast, skin involvement over and smaller
Than tumor size
Stage II Same + palpable mobile one group LNs in Ipsilateral axilla
Stage III breast mass + one of the following:
1- Skin invasion larger than size of the mass
2- Mobile more than one group of Ax. LNs
3- Mass fixed to underlying muscles & fascia
Stage IV any of the above + one of the following:
1-Marked skin affection nodules, ulcer
2-Fixed Ipsilateral axillary LNs

3- Ipsilateral supraclavicular LNs

4- Mass fixed to chest wall or serratus.
5- Distant deposits, other breast, contralateral axilla
Symptomsrelated to the primary lesion
A painless breast lump noticed incidentally that is increasing in size.
Distortion in the shape of the breast (ulceration, skin changes,
pigmentation).
Alteration in the nipple (inversion, destruction, deviation, bloody
discharge).
Breast discharge which may bloody, thick greenish or straw yellow
Symptoms related to secondary deposits
Axillary lump(s)
Swelling of the arm.
Backache, limb pain, fracture.
Dyspnea, chest pain.
Jaundice.
Mental status changes, fits.
Generalized malaise and loss of weight are rare in breast carcinoma.
See clinical sheet for clinical history and examination
NB: if you are asked in the exam what are the investigations? You have to
start as usual by lab investigations as: CBC, Organ profile, Tumor marker
Triple assessment
Clinical history and exam, see the sheets.
Imaging (mammography / sonography)
In malignancy there will be microcalcification or star shaped
(irregular mass) and to detect bilateral or multifocal lesions
MAMMOGRAM REPORTS BI-RADS
By the American College of Radiology (ACR): In this system, the results are
sorted into categories numbered 0 through 6. This system is called the : Breast
Imaging Reporting And Data System(BI-RADS)
1.

Category 0: X-ray assessment is incomplete.

Additional imaging evaluation and/or comparison to

prior mammograms is needed. X-ray assessment is

complete
2.

Category 1: Negative\negative means nothing bad

was found.

3.

Category 2: Benign (non-cancerous)

findingDescribe a finding known to be benign, such
as benign calcifications, lymph nodes in the breast,
or calcified fibroadenomas.

4.

Category 3: Probably benign finding Follow-up in

a short time frame is suggested in 6 months for 2
years

5.

Category 4: Suspicious abnormality Biopsy should

be considered. Findings do not definitely look like
cancer but could be cancer.

6.

Category 5: Highly suggestive of malignancy

Appropriate action should be taken. The findings
look like cancer and have a high chance (at least
95%) of being cancer. Biopsy is very strongly
recommended.

7.

Category 6: Known biopsy-proven malignancy

Appropriate action should be taken. Mammograms
may be used in this way to detect multifocality.

MRI
Suitable for:
Detection of multifocality
Doubtful axilla
Recurrence after excision to differentiate it from post operative
scarring

Biopsy:
Start by FNAC and confirm during operation by
Frozen section biopsy
Open biopsy if FNAC is not conclusive:
- Excision biopsy (remove all mass with
safety margin).
- Incisional biopsy (remove part of the mass).

If the lesion is proved to be malignant we examine the specimen for ER, PR,
and search for metastases (liver US, bone scan and chest X-rays) and for follow
up CA15.3 (tumor marker).

I. Treatment:

Stage
1. Inflammat
ion of the
breast

Commones Treatment
t
Presentatio
n

i. Milk
Dull aching Hot formants
engorgem pain
Massage
ent
ii. Diffuse
mastitis.

Sever
burning
pain

Hot foments +
Antibiotic.
Suction from the
effected and feeding
from other

iii. Abscess.

Throbbing Drainage by Incision,

pain, hectic counter incision and
fever
antibiotic

2. Duct
ectasia

3. Duct
papilloma

4. Fibroaden
osis =
Fibrocysti
c changes.

5. Fibroaden
oma

Creamy
Metronidazole or/and
discharge + amoxicillin-clavulonic
inflammato acid.
ry mass
and drainage of any
formed abscess.
Blood per
nipple from
single or
multiple
ducts.

guaiac or benzidine test

to confirm blood.
a.Microdochectomy if
from one duct.
b.Excision of major
ducts if multiple.

Brown or
greenish
discharge

Reassurance
Stop caffeine, chocolate
and cola.
Wearing firm brassiere
Oil primorse
Simple analgesics
Severe non responding
cases !bromocriptine
(causes nausea)
Excisional biopsy

1) early
Stage
1+2
6. carcinoma

Lumpectomy if
mass 4cm with
Axillary
clearance
Post
operative
radiotherapy
Chemothera
py and
hormonal
therapy
Modified radical
mastectomy: if
large mass
or small
breast.
central mass
as in Paget
multifocal
mass
if irradiation
is
contraindica
ted.
With post operative
chemo and hormonal
therapy as in advanced
stages (but adjuvant).

2) Advanc
ed
Stage
3+4

Palliative surgery:
Mastectomy
Palliative
radiation:
Palliative
chemotherapy:
TAC
Hormonal:
Postmenopausal
use tamoxifen or
anstrazole.
LHRH analogues
in premenopausal.
NB: Neoadjuvant
chemotherapy if locally
advanced tumor we give
preoperative
chemotherapy to
downstage the tumor to
become operable.

Pediatric Surgery
Esophageal atresia

$
The commonest is blind upper pouch and lower one is communicating with stomach
Clinically:
Continuous pouring of saliva from mouth since birth
Shocking with each feed

Diagnosis by gastrographin to see the atresia or and fistula

Treatment: thoracotomy, excise the fistula and repair

Congenital hypertrophic pyloric stenosis

The baby is usually first borne male

He is borne with failure of relaxation of pylorus! muscles of pylorus hypertrophies to
overcome resistance!obstructs pylorus
It will lead to projectile vomiting (without nausea) !dehydration and hypokalemia
Examination reveals visible peristalsis and palpable epigastric mass like olive
Diagnosis by US
Treatment rehydration and pyloromyotomy

Hirschsbrung disease

Rectum and sigmoid

are
aganglionic ! fails to relax

Clinically: if long segment ! neonatal intestinal obstruction

If shorter it will lead to progressive constipation with distended colon and failure to thrive
P/R: there is grasping of the rectum over the examining finger and on withdrawal ! gush of
fluid feces
Biopsy must be taken to exclude acquired megacolon due to fissure
Operation at 10 months (10 KG) !. Excise the aganglionic segment and do coloanal
anastmosis

Intussusception

See intestinal obstruction

Anorectal anomalies

$
It presents by neonatal intestinal obstruction
It may be high with anorectal agenesis fistula with vagina or urinary bladder
Or low: imperforate anus, ectopic anus or anal stenosis
It requires colostomy (immediate) if to be followed by anorectoplasty (10 months 10 KG)
Low anomaly can be incised or dilated

ABDOMINAL CASES
DD OF SWELLINGS OR PAIN ARE VERY IMPORTANT AND
ESSENTIAL TO PASS THE EXAM
Differential diagnosis of abdominal swellings:
The following must be considered for DD of any regional (localized) or diffuse
abdominal swelling or pain:
1. Anatomical background of the abdominal region involved
2. Different causes and pathological disorders affecting this region
3. The most common swellings related to this region

!
Dont forget swellings arising from skin as sebaceous cyst, subcutaneous lipoma,
Hernias, Muscle lesions as firbrosarcoma, nerves as neurofibroma and bony
lesions as primary or secondary tumors
DIFFERENTIAL DIAGNOSIS OF REGIONAL ABDOMINAL
SWELLINGS
Diffuse abdominal swellings (distension): remember the 6 Fs +
L;
1. Fat (obesity)
2 & 3. Flatus or/and Faeces (simple distension, constipation, megacolon
intestinal obstruction)
4. Foetus (pregnancy)
5. Fluid: free (ascites) or encysted
6. Fibroid
Large tumors or organomegaly
As
Large ovarian cyst
Retroperitoneal sarcomata
Hepatosplenomegally or polycystic kidney
Commonest swellings in right lower quadrant (Rt iliac fossa)
1. Appendicular mass

or

2. Appendicular abscess
3. Carcinoma of the cecum
4. Gynaecological as ovarian cyst, ectopic pregnancy, salpingitis,
fibroid
5. Terminal ileitis (Crohns disease)
6. Mesenteric lymphadenitis
7. Other lesions; as tuberculosis, ectopic kidney, lymphadenopathy,
aneurism, etc as mentioned before anatomically and pathologically
NB: Undesended testis is not palpable intra-abdominally unless
malignant change occurs
In left LQ: As right side but the GIT masses are different including;
diverticulitis, carcinoma of the sigmoid or descending colon
NB: the tumors of the left side of the colon are rarely palpable and
forming a stricture and the palpable mass is commonly fecal mass
(can be indented with pressure).
Masse from LUQ: Most commonly to be
1. Enlarged spleen
2. Enlarged kidney
3. Carcinoma of splenic flexure
4. Suprarenal tumor
5. Tumor from the tail of pancreas.
6. In addition to other swellings from the related anatomical
structures (sebaceous cyst, lipoma, muscle tumor, etc)

Causes of splenomegaly:
1. Infection: tender and soft, as in typhoid, malaria, Kala-azar
2. Congestive: portal hypertension due to bilharziasis , cirrhosis, and portal or
splenic vein thrombosis
3. Congestive heart failure
4. Cellular proliferation: Neoplastic or Hyperplastic
Myeloid and lymphatic leukaemia
Polycythemia rubra Vera
Thrombocytopenic purpura
Myelofibrosis
Spherocytosis and thalathaemia

NB: in sickle cell anaemia repeated splenic infarctions may lead to autosplenectomy but if splenic vein thrombosis occurs huge splenomegaly may occur
5. sarcoidosis
6. Storage diseases
RENAL SWELLINGS
NB: Commonest cause of renal swelling is hydronephrosis, other causes are;
polycystic kidney, pyonephrosis, tumors, and renal cyst
NB: Commonest cause of unilateral hydronephrosis is stone and commonest
cause of bilateral hydronephrosis is senile enlarged prostate
NB: Renal cysts are very common but rare are large enough to be palpated or
cause symptoms
NB: Renal cell CA (hypernephroma) is the commonest tumor in adults and
nephroblastoma (Wilms tumor) is the commonest in children
DD of a mass in right upper quadrant mass in right hypochondrium
1. Hepatomegaly
2. Gall bladder swellings
3. Enlarged kidney
4. Carcinoma of the hepatic flexure of the colon
5. Suprarenal mass
6. Other swellings related to different anatomical structures
ENLARGED LIVER WITHOUT JAUNDICE
1. Congestive heart failure (smooth)
2. Early stages of cirrhosis (smooth)
3. Established cirrhosis (sharp border and granular)
4. Hepatocellular carcinoma (usually cirrhotic with localized mass)
5. Liver secondaries (enlarged with knobbly surface)
6. Other causes as, lymphoma, storage diseases, liver cysts etc
ENLARGED LIVER WITH JAUNDICE
1. Infective hepatitis (smooth and tender)
2. Obstructive jaundice as in gallstones or CA of head of the pancreas (smooth
and non tender).
3. Cholangitis (smooth and tender, with Charcot s triad)
4. Portal pyemia (smooth and tender)
5. Decompensated cirrhosis

6. Liver abscess; commonly amoebic and it follows the attack of amoebic

colitis but may be pathogenic e.g infected hydatid cyst
7. Hydatid cyst
CAUSES OF ENLARGED GALL BLADDER
1. Obstruction of the cystic duct, commonly by gallstone and rarely by CA
The patient is usually jaundiced
It may contain bile and mucus (mucocele)
It contains pus (empyema)
2. Obstruction of the common bile duct; by gallstone or CA of head of the
pancreas
Courvoisiers law: in patient with obstructive jaundice palpable and distended
gall bladder is usually indicative that the cause is not gall stone
This is due to that gallstones are associated with chronic inflammation with thick
fibrotic wall (non distensible)
Exception includes; empyema and mucocele and others which will be discussed
in jaundice.
Courvoisier's sign: palpable gall bladder in obstructive jaundice (commonly
malignant OJ or due to obstruction by primary stone
3. Carcinoma of gallbladder; rarely large to be palpated and usually diagnosed
first as gallstone disease
4. Gall bladder mass as appendix mass (acutely inflamed gall bladder with
adherent omentum)
It is palpated as diffuse tender swelling which does not move with respiration

EPIGASTRIC MASS
Gastric tumors (advanced Ca or lymphoma)
Enlarged left lobe of the liver
Pseudopancreatic cyst
True pancreatic cyst
Aortic aneurism
Mesenteric cyst
Dont forget; epigastric hernia and divarication of the recti

ABDOMINAL PAIN
DIFFERENTIAL DIAGNOSIS OF REGIONAL ABDOMINAL PAIN

Right upper quadrant: Left upper quadrant pain as the right but replace
hepatobiliary by splenic causes (as perisplenitis, splenic abscess and splenic
infarction)
1. Hepatobiliary: Biliary colic, acute cholecystitis & hepatitis
2. Urological: renal stone or UTI
3. Referred from the chest
-Lobar pneumonia (basal).
-Pleurisy.
Epigastric pain:
1. GERD.
2. PUD
3. Acute pancreatitis.
4. Acutely perforated peptic ulcer starts epigastric then becomes generalized.
5. Leaking or dissecting aortic aneurism.
6. Reference from chest: Inferior wall MI.
Central abdominal pain:
1. Intestinal obstruction.
2. Peritonitis: starts first at site of perforation then becomes
generalized as; if perforated appendicitis starts at RLQ, perforated
PU starts epigastric, perforated GB starts in RUQ, perforated
diverticulitis starts in LLQ
3. Mesenteric vascular occlusion.
4. Leaking or dissecting aortic aneurism.
5. Gastroenteritis
6. General causes:
Diabetic ketoacidosis.
Withdrawal symptoms in opiate addicts.
Pain in right lower quadrant: The pain in left LQ as right but replace GI causes
by diverticulitis of the colon
Intraperitoneal:
7. Acute appendicitis.
8. Meckels diverticulitis.
9. Crohn's disease
10.Tonsillitis (tonsillar tummy) and mesenteric adenitis.
Retroperitoneal:
11.Pyelonephritis.
12.Ureteric or renal stones.

Gynaecological causes:
Mittel Schmerz pain.
Disturbed ectopic pregnancy.
Rupture ovarian cyst.
Salpingitis.
Cystitis.
Urinary bladder stone
Referred from chest
Lobar pneumonia (basal).
Pleurisy.
NB: Visceral pain will be referred to the original dermatome, from which
this visceral structure was developed, as:
Heart (inferior wall myocardial infarction)Epigastric pain.
Foregut (PU, Biliary colic) Epigastric pain.
Midgut (appendicitis & enteritis)periumbilical pain.
Hindgut (diverticulosis and colitis)suprapubic pain.
Somatic Pain: It is will localized form of pain.
Examples of somatic pain from the start:
Esophagus (GERD)retrosternal and epigastric burning pain.
Pancreatitis epigastric pain radiating to back.
Pyelonephritis loin stabbing pain radiates along course of ureter and
genetalia.
Examples of pain starting visceral somatic
DU early epigastric pain then points to right.
Acute cholecystitis early epigastric pain then shift to right upper quadrant
after irritation to parietal peritoneum.
Acute appendicitis early periumbilical pain then shift to lower right
quadrant.
Diverticulitis early suprapubic pain then shift to left lower quadrant.
APPENDICITIS
Age : Max 15-30 years and in extreme of ages it is rare but
dangerous as omentum is defective
It may be obstructive or non obstructive
The pathology is mainly due to hypertrophy of lymphoid tissues
in the submucosa which usually starts non obstructive then turn to
obstructive due to more lymphoid hypertrophy

 It may start obstructive from the start by fecolith, parasite, or fruit

seed (less common)
Organism: yersinia, E coli and bacteroids
Complications:
1. Appendicular mass, abscess, localized and diffuse peritonitis (see
appendicular mass
2. Portal pyemia in immune compromised patients especially with post
ileal type (near ileocecal vein ! portal vein)
3. Fecal fistula: Iatrogenic
postoperative passage of fecal matter from the wound and if
drainage if not good it may cause fecal peritonitis
cecum is injured usually due to trial to remove the appendix in
presence of marked inflammation and adhesions ( mass, abscess,
Crohn's)

Mnemonic for the diagnostic score (Alfredo Alvarado, MD

Plantation, Florida) of acute appendicitis:
MANTRELS
Symptoms
Migration of pain
Anorexia-acetone
Nausea-vomiting
Signs
Tenderness in right lower quadrant
Rebound tenderness
Elevation of temperature
Laboratory
Leukocytosis
Shift to the left

1
1
1

2
1
1

2
1

Total score
10
A score of 5-6 is usually diagnostic; however, overlap may occur
with other diseases

History
DON'T FORGET THE GENERAL RULES AS; STANDING ON RIGHT
SIDE OF PATIENT, INTRODUCE YOURSELF, CONSENT, PRIVACY, AND
NURSE
1) The patient is commonly admitted from ER
2) Personal history: Sex, age, name
3) Chief complain: RLQ pain for ..(duration )
4) HPI:
Analysis of C/O:
Site of pain: usually starts paraumbilical then shifts to right
lower quadrant (Most important symptom is the shifting pain)
NB: pain may not be shifted in ileal & pelvic type
Aggravating and relieving factor
Radiation

Associated symptom (anorexia it is very important, nausea,

vomiting, constipation)
NB: Diarrhea in pelvic (due to rectal irritation) & ileal due to ileal
irritation
NB: In ileal type there is no shifting of the central abdominal pain,
nausea, vomiting, and diarrhea so may be diagnosed as
gastroenteritis (missed appendix)
Ask about other GI symptoms
Ask about urological symptoms (color of urine, dysuria, burning
micturition, any other urinary problem)
If female ask about gynecological symptoms as; missed period,
LMP for the mid cycle pain, and ay gynecological problem
Ask about any abdominal swelling
Ask about hospital course: as operation, its complications or
the operation is postponed due to discovery of mass by
examination under anesthesia
5. Systemic review, specially sore throat, chest infection and pleurisy, and
other systems in brief
6. past history: As usual
7. Family history: As usual
8. Social history: residence, occupation, marriage, children, smoking,
methods of contraception in females, etc
Examination:
General: Fever, toxic look
Hand: Pulse,
Pallor
Local examination: do not forget to expose the patient from the
nipple to mid of the thigh (till the doctor that)

Inspection:
Inspect abdomen completely and in appendicitis you may find
Decreased abdominal movement with respiration
Flexion of the hip (psoas spasm)

Palpation:
1. Superficial palpation: for temperature, superficial swellings,
tenderness and rigidity
2. Deep palpation: of whole abdomen and last area is the right
lower quadrant for tenderness, rebound tenderness, guarding or
rigidit
Special tests as
+ve psoas if retrocecal
+ve obturator if pelvic
+ve Rovsing
And do not forget to examine hernial orifices and ask for PR or
PV
NB: PR or PV may be the only way to diagnose pelvic appendicitis
DD: See pain and swellings in RLQ
III) Investigations:
CBC: WBC (Leukocytosis; neutrophilia , shift to left)
Urine analysis: to exclude UTI
Pregnancy test to exclude ectopic pregnancy, US if
unmarried
Plain X-ray (stone ureter and fecolith)
U.S: to exclude gynecological problems and if there is any
mass or abscess
If there a doubtful mass do CT
IF YOU ARE IN DOUBT DO DIAGNOSTIC AND
THERAPEUTIC LAPAROSCOPE (for females to decrease
adhesion and exclude DD)
IV) Treatment: appendectomy for uncomplicated cases
Female: laparoscopic appendectomy is preferred (but open
method can be used) to diagnose any problem + decrease
adhesions.
Male: appendectomy by grid iron incision at Mc Burney's
point and sometimes we do laparoscope
Before any operation u have to do examination under
anesthesia to palpate any mass or abscess (no pain, no
rigidity)

 If there is mass postpone the operation and start

conservative treatment:
- NPO (Nil per Os)
- IV antibiotic and fluid.
- Hot foments.
- Mark around the mass
- Monitor: Pulse, Pain, Fever, and size of the mass
If improved (decreases of the size of mass, no pain or fever,
decrease the pulse): Discharge ! by interval appendectomy
(after 1 1/2-3 month)
If Not improved (increase in temperature and becomes
hectic, size of mass increases , tachycardia , throbbing pain):
Abscess is formed !drainage by muscle cutting extraperoteneal
drainage
Appendectomy after 6 months

C) If the fever disappears and mass remains:

We have to do barium meal follow through+ endoscopy + CT
Because it may be cancer Cecum or Crohn's disease

Indication of exploration (midline incision):

If diffuse peritonitis occurred: to do peritoneal toilet,
Appendectomy, and Drainage
Indication of immediate surgical intervention:
Children: because of short omentum, so they are at high
risk of generalized peritonitis
Old age: atrophied omentum
Pregnancy: 1st trimester (to minimize risk of abortion)
3rd trimester (as omentum shifted by uterus)
NB: Most common tumor in appendix is carcinoid tumor
And most common site of carcinoid tumor is appendix
APPENDICULAR MASS

 Appendicular mass (inflammatory mass following none treated acute

appendicitis, where omentum tries to localize infection by adhesion to
appendix, cecum, loops of intestine).
Appendicular abscess if the appendix perforates after the mass is
formed; the mass will enlarge with throbbing pain and hectic fever.
NB: If perforation occurs early due to defect in omentum (child, elderly or
pregnancy in third trimester) perforation will end in generalized peritonitis
with diffuse distension

(picture like appendicitis but operation

was postponed after anesthesia or US)
Same Qs as appendicitis and during
examination you will find the mass
marked

!
DD: See DD of mass in right lower quadrant; ovarian cyst, salpingitis &
ectopic pregnancy (so pregnancy test must be done to all young females).
In males and females: appendicular abscess (see treatment of appendicitis to
differentiate), CA of cecum, & Crohn's disease
In children: mesenteric adenitis starts by tonsillitis and enlargement of
mesenteric LNS!picture like appendicitis! mass with shifting tenderness.
Management: see before.

PERITONITIS
USUALLY A POSTOPERATIVE CASE
APPLY THE ABDOMINAL CASE SHEET
THE HOSPITAL COURSE IS VERY IMPORTANT
Peritonitis: may be localized or generalized, and may infectious or noninfectious.
I.

Infected peritonitis:

Perforated hollow viscus as: appendicitis, PU, acute cholecystitis, colon, small
intestine

1. Perforated acute appendicitis: Predisposed by defect in omentum (see

before), decrease immunity, and obstructive appendicitis with rapid
perforation before mass is formed
2. Perforated PUD: more in anterior ulcers specially DU (posterior ulcer near
the gastro duodenal artery or its branches and usually bleeds).
3. Acute cholecystitis especially in gangrenous non calcular in diabetic
patients or perforated empyema in the calcular type.
4. Perforated colon which may follow diverticulitis.
5. Perforated small intestine or/and colon in neglected (> 6 hours) intestinal
strangulation as strangulated hernia, volvulus, intussusception, and late
stages of mesenteric vascular occlusion.
6. Perforated Meckel's diverticulitis.
7. Postoperative specially after performing anastomosis (especially in colon
due to lack of blood supply and contamination) ! anastomotic leakage.
8. Trauma: Penetrating abdominal wounds and gun shots ! perforation of
any viscus (Blunt Trauma may lead to tear at DJ junction and terminal
ileum).
9. Primary peritonitis (blood borne) and may complicate portal hypertension.
10.TB: Blood borne or transmission from tuberculous mesenteric LNs (tabes
mesenterica)
NB: Infection may be transmitted from the infected viscus even without
perforation ! localized peritonitis !if neglected ! generalized peritonitis
II. Non-infected peritonitis:
1. Early stages of perforated PU (chemical stage) which soon
becomes infected.
2. Pancreatitis: which occurs first due to leak of enzymes the may be
infected.
DIAGNOSIS
CLINICAL PICTURE OF THE ORIGINAL DISEASE
FOLLOWED BY GENERALIZED ABDOMINAL PAIN,
MARKED TOXEMIA, ILEUS WITH DISTENSION, NAUSEA
AND VOMITING
Example; perforated PU: In 50% of cases there is a history of PU
and in the other 50% history may be absent or not clear. Perforation

is usually precipitated by heavy meal, stressful condition, or

corticosteroids intake.
C/O: The history starts by attack of vomiting perforation !
chemical peritonitis
With severe epigastric pain becomes generalized all over the
abdomen shock
O/E: shocked patient with tachycardia and hypotension
Abdomen is tender with board like rigidity, maximum at epigastrium
Percussion shows diminished hepatic dullness (gas under
diaphragm)
Lucid interval: within few hours the patient shows improvement
due to neutralization of acid by exudate (plasma), but tachycardia,
rigidity and diminished hepatic dullness persist
Lucid interval lasts for about 6 hours in average (dependent of the
site, size of ulcer and patient resistance
Stage of septic peritonitis: generalized abdominal pain returns, with
fever, distension (ileus), tenderness, rebound, rigidity
IF THE PATIENT IS NOT TREATED HE WILL DIE FROM
SEPTIC SHOCK
NB: In other conditions as appendicitis, cholecystitis, diverticulitis
the patient already has infective disease so he will has the picture of
the original disease + picture of stage of septic peritonitis
INVESTIGATIONS
1. Laboratory:
CBC: marked Leukocytosis with shift to left
Organ profiles will be disturbed late if septic shock and important
in pancreatitis for scoring index, and liver function tests are
essential in GB diseases

Disturbance in electrolyte and acid base balance: dehydration,

hypokalemia, and acidosis
Amylase and lipase if you suspect pancreatitis
2. Imaging:
Plain X-Rays: Will show gas under diaphragm if perforated gut
(but not in appendicitis, cholecystitis and pancreatitis)
US: Very important to diagnose fluid collection (localized or
generalized) in addition to the original disease as picture of
appendicitis, acute cholecystitis, and pancreatitis.
CT: Important in pancreatitis (CT severity index) and when US is
not conclusive for other diseases
3. Endoscopy: Upper GI in PUD and lower GI if perforated
colon as diverticulitis
4. Special tests if traumaonly: As FAST, and DPL
TREATMENT
Admission
NG tube
IV fluids
Antibiotics
Open or laparoscopic peritoneal lavage
Definitive treatment:
1. Perforated PU !closure of the defect with omentum patch
(Grahams method) or fibrin glue seal
2. Appendicitis: appendectomy (but not done if localized
abscess for presence of adhesions)
3. Cholecystitis: Cholecystectomy

4. Gangrenous intestine: must be resected with primary

anastomosis in small intestine and after right
hemicolectomy, or colostomy if left colon
AFTER OPERATION OF THE PERITONITIS YOU HAVE TO
PUT DRAINS; ONE AT SITE OF PERFORATION, ONE IN
PELVIS
NB: In perforated diverticulitis or gangrenous sigmoid we resect
the sigmoid colon with end colostomy and closure of the rectal
stump (Hartman's operation)
NB: Acute pancreatitis there is no surgery but conservative ICU
ERCP

CASE OF PATIENT WITH STOMA

Types of stoma: Oral question
Tracheostomy: will be discussed separately with the
airways
Esophagostomy: Tube (usually large caliber Foley's
catheter) in left side of the neck, to drain saliva in
advanced cases of congenital atresia
Gastrostomy : Tube (usually large caliber Foley's catheter)
in epigastric and to left, for feeding
Jejunostomy: Tube (usually large caliber Foley's catheter)
in left hypochondrium, better than gastrostomy for feeding
Ileostomy: after total colectomy or to help healing after
colonic anastomosis, see below
Colostomy: to relieve obstruction or after colectomy in
emergency non prepared patient, see below
Cholecystostomy: in difficult cholecystectomy (tube,
usually large caliber Foley's catheter) inserted in Rt
hypochondrium
Nephrostomy: In pyonephrosis (usually large caliber
Foley's catheter) inserted in lumbar region
Ureterostomy: after cystectomy (the ureters are
anastomosed to skin)

Cystostomy: in retention of urine if difficult urethral

catheterization, we use suprapubic catheter

COLOSTOMY OR ILEOSTOMY
o
o
o
o

Clinical Case
Apply the abdominal case sheet to diagnose the presenting
disease
Hospital course is very important and the operation is
usually done as emergency
Add to examination: The examination of the site of stoma
(ileostomy, transverse colostomy, or sigmoid colostomy)
Remove the stoma bag and comment on the stoma: the
normal is pink and the abnormal may be: edematous,
congested, prolapsed, retracted or surrounded by infection
Do Per Stoma (PS) examination to detect abnormality as
Stenosis

!
A

B
C
Ileostomy: Found in the Rt side (A), stoma bag (B), and the
spout (like nipple to fit for the stoma bag and to facilitate
collection of fluid fecal matter

Permanent colostomy after abdominoperineal resection (APR)

of rectum and anal canal (A), Hartman's procedure (B)

$
A
B
Loop transverse (sub hepatic) colostomy in RUQ (A) and different
types of colostomy (B)
NB: The colostomy or ileostomy will be permanent if the distal part is
resected as after APR or total colectomy also in locally advanced malignancy
when reconstruction is impossible
NB: If no permanent cause reconstruction is done after 3 months

CASE OF INTESTINAL OBSTRUCTION

 The abdominal case sheet must be applied and never to forget the
hospital course (most of patients are postoperative cases)

NB: postoperative obstruction if after few days it is ileus and very

rarely fibrinous adhesions, few weeks and more it will be adhesive but if
it is associated with irreducible swelling at the incision scar it is
strangulated incisional hernia

OVERVIEW OF ETIOLOGY
1. Simple obstruction:
A.Dynamic;
Cause in the lumen as FB, ascaris worms, and gall stone ileus
Cause in the wall as Ca of the colon or the intestine or benign stricture
(Crohn's, TB, etc)
Pressure from outside as postoperative adhesions (commonest in
developed countries, and if pressure is marked it may cause
strangulation). Tumors of other abdominal structures may cause
pressure on intestine
B.Adynamic:
Ileus: absent peristalsis which may be postoperative (physiologically
it may persist for 48-72 hours otherwise it is considered pathological),
other causes of ileus include; peritonitis, pancreatitis, trauma (rupture
organs, spine, pelvis, femur), hypokalemia and drugs
2. Strangulation:
A.Dynamic:
Strangulated hernia (commonest in developing countries)
Intussusception which may be primary in child following G
Enteritis due to increase motility and hypertrophy of Pyre's
patches! imagination of the proximal ileum in the cecum
Secondary if there is a tumor or polyp in the wall acting as an apex
of the invaginated loop
Volvulus of the sigmoid colon (in middle aged patient with prolonged
constipation and congenital long colon) or small intestinal loop which
usually associates adhesion where the adhesive band acts as axis around
which the loop rotates
B.Adynamic

 Defective propulsive peristalsis in mesenteric vascular occlusion

CARDINAL SYMPTOMS AND SIGNS OF INTESTINAL OBSTRUCTION
1. Pain: colicky in nature which is more frequent than simple obstruction
and in between the attacks; no complete relief as strangulation adds
element of ischemic pain.
NB. If perforation occurs (after established gangrene which takes at least 6
hours to occur); colic disappears and pain becomes continuous due to
development of peritonitis
NB. In ileus, which is Adynamic form of intestinal obstruction; there is no
colic in all cases and it is quite painless in postoperative type, however, in
other conditions the pain of the cause may be found as peritonitis,
pancreatitis or internal hemorrhage
2. Vomiting:
If the strangulated part is jejunum (high small bowel obstruction); the
vomiting will be early and repeated
If the strangulated part is ileum (low small bowel obstruction); vomiting
will be delayed 12-24 hours after onset allowing bacteria to act ! brown
offensive vomitus (feculent vomiting which is similar to feces but not true
feces)
NB. True fecal vomiting occurs if fistula between colon and stomach
develops, usually after gastric operations.
If the strangulated part is large bowel (colonic), vomiting will be
delayed for 2 days
3. Constipation: Absolute constipation (the patient, has the desire but
unable to pass stool or flatus)
NB: In partial (incomplete obstruction the patient may pass some stool
NB. Early in intestinal obstruction the patient may pass some stool
which is retained distal to the site of obstruction.
NB. In some cases of strangulation as intussusception and mesenteric
vascular occlusion the patient may pass bloody diarrhea instead of
constipation.
4. Distension:
Upper abdominal in high small intestinal obstruction

 Central abdominal in lower intestinal obstruction and the distended

loops of the intestine may be seen like the Ladder steps
Peripheral abdominal, in colonic obstruction
5. Shock: more in;
High small intestinal obstruction due to early and repeated
vomiting! hypovolemic shock due to water and electrolyte loss
Strangulation due to congestion of the strangulated loops (veins are
low pressure so it will be obstructed first leading to marked congestion
and extravasation of blood)! hypovolemic shock due to blood loss
Established gangrene ! perforation ! peritonitis !loss of plasma
(exudate) ! hypovolemic shock
Peritonitis also will lead to Septic Shock

In addition to the previous cardinal symptoms and signs of intestinal

obstruction, the clinical picture of the cause may be found as;
1.History suggestive of strangulated hernia: the patient had a history of
painless reducible swelling which recently became painful, irreducible
with increase in size and examination reveals swelling which does not give
impulse on cough, which is tense and tender
NB. Femoral and paraumbilical hernias are the most liable hernias to strangulate
but the oblique inguinal hernia is more common in incidence so it is the most
common hernia seen strangulated

2. Postoperative obstruction if after few days it is ileus and very rarely

fibrinous adhesions, few weeks and more it will be adhesive but if it is
associated with irreducible swelling at the incision scar it is strangulated
incisional hernia

3.Progressive constipation with change in bowel habits, sometimes with

bleeding per rectum followed by obstruction is suggestive of
rectosigmoid carcinoma
May be palpable fecal mass (tumor is usually stricture form) in LLQ if CA
of sigmoid
PR may reveal palpable mass in carcinoma of the lower rectum
Obstructed CA of cecum presents by acute IO with mass in LRQ

4.Prolonged history of constipation with

sudden onset of obstruction during defecation followed by pain,
abdominal distension, and tympanitic abdomen! volvulus of sigmoid

5. Severe abdominal pain with minimal abdominal signs in elderly

followed by bloody diarrhea !mesenteric vascular occlusion

6. Child aged 6-24 months with vomiting, colic, distension and passage of
mucus and blood (like red currant jelly) !intussusception (the disease
usually follows attack of gastroenteritis

Expected complications if treatment is delayed

Shock, see before
Gangrene with perforation!peritonitis
Electrolyte disturbance and renal impairment
Death secondary to multiorgan dysfunction
Radiological evidences of intestinal obstruction?
1. Plain X-rays in 2 position will show:
Erect: multiple air and fluid levels (> 3)
Supine: will show the obstructed loop
See the images in the lecture of abdominal swellings
2. CT scan is of value if suspected tumor
3. Investigations which help to establish diagnosis and to detect
complications?
In addition to radiology we can do:
CBC: Leukocytosis if perforation and anemia if extravasation
Electrolytes and blood gases including pH study
Organ profile; will show impairment in the end stage with organ
dysfunction
MANAGEMENT OF INTESTINAL OBSTRUCTION
1. Hospitalization
2. Nasogastric suction to decrease vomiting, prevent aspiration, decrease
distention and to make a fluid chart
3. NB. Nasogastric suction will relieve pain in simple obstruction but not in
strangulation
4. IV fluids, start by Lactated Ringers as it replaces Na, K, and prevents
acidosis
5. Give blood if hematocrit < 30
6. Antibiotics to cover gram negative, gram positive and anaerobic
bacteria; as metronidazole (mainly for anaerobes), 3rd generation
cephalosporines (cover most of the organisms) aminoglycosides (for
difficult gram ve infection).

NB. Adhesive intestinal obstruction is treated mainly conservatively and

surgery is indicated if no improvement after 48 hours or presence of signs
of strangulation as increase pain with tenderness and rebound tenderness
The operation is adhesiolysis which can be done by open method or by
laparoscope
Surgery in other forms of IO: Relieve obstruction and remove the cause
surgically as soon as the patient is resuscitated
In surgery if a gangrenous loop is found it must be resected
Primary anastomosis in small intestine (good blood supply and less
contaminated)
If right colon is gangrenous we do right hemicolectomy with primary
ileocolic anastomosis (as small intestine)
See types of colectomy after lower GI bleeding
In left colon we resect the gangrenous part but primary anastomosis is not
done (poor blood supply and marked contamination) instead we do colostomy
(see types of colostomy in the clinical surgery sent for the students before)
NB: Ileus is treated by NG tube, IV fluids, antibiotics, and treatment of the cause
as, correction of hypokalemia, drainage of peritonitis etc

CASE OF LOWER GI BLEEDING

Bleeding distal to the ligament of Treitz
INCLUDING REVISION OF ANAL, RECTAL AND COLONIC
DISORDERS
Apply the abdominal case sheet and don't forget the hospital course
specially blood transfusion, endoscopy surgery
With any case of GI bleeding you have to ask about manifestations of
bleeding tendency as; bleeding gums, menorrhagia, echymoses etc
In drug history never to forget Aspirin, NSAIDs, anticoagulants, and
antiplatelets

NB: Massive upper GI bleeding may lead to passage of fresh blood per rectum
instead of melena, so it should be excluded by history, examination and
insertion of NG tube to see if there is blood in stomach or not.
DIFFERENTIAL DIAGNOSIS OF BLEEDING PER RECTUM
DD:
1.In 30% of cases upper GI is the cause as; bleeding PU, gastric erosions,
or esophageal varices
2.Diverticular disease (massive)
3.Angiodysplasia (massive)
4.Hemorrhoids (piles), usually mild to moderate.
5.In acute fissure & chronic fissure (mild)
6.CA of rectum: most important for any adult patient
7.Inflammatory bowel diseases
8.Meckel's diverticulum: with ectopic gastric tissues
9.Hamartomatous polyps: In children and other polyps as FAP in young
adults
10.General causes: liver diseases (hypoprothrombinemia
),
anticoagulant therapy as in DVT, leukemia, purpura, hypersplenism, and
congenital bleeding disorders as hemophilia
IN ANY CASE OF BLEEDING PER RECTUM, EVEN WITH PRESENCE OF
BENIGN LESION AS PILES OR FISSURE, CA OF THE RECTUM MUST
BE EXCLUDED BY PR AND PROCTOSCOPE.

AN OVER VIEW OF DISEASES CAUSING BLEEDING PER RECTUM

1.Massive bleeding/rectum: is usually due to diverticular disease (in the
left colon), and is usually associated with angiodysplasia (in the right
colon, discovered during colonoscopy or angiography).
C/O:
- Massive bleeding in elderly male.
- With long history of constipation, colicky pain, passage of fecal
pellets, and if diverticulitis it presents like acute appendicitis but on
left side.
- General examination may reveal shock anemic manifestations
(usually corrected in the hospital)
- Local examination is usually unremarkable

2.Painless mild to moderate bleeding: commonest cause is hemorrhoids

C/O:
- Bright red blood at the beginning or the end of defecation with
protruding lump during defecation
- Bleeding is usually mild causing anemia and more in 1st or 2nd degree
while in 3rd and 4th the patient is mainly complaining of the protruding
lump, pruritus, and discharge.
- Piles will be painful if complicated by thrombosis, infection, or fissure
formation.
O/E:
- Mother piles: may appear at 3, 7, and 11 o'clock daughter and
granddaughter piles.
- 1st degree! if no lump protrudes on straining.
- 2nd degree ! lump protrudes and returns spontaneously.
- 3rd degree ! lump protrudes and returns manually.
- 4th degree! permanently prolapsed piles.
3.Painful fresh blood: commonest cause is perianal fissure
C/O:
- Bleeding occur at beginning or end of defecation
- In acute fissure there is a history of constipation followed by recent
onset of severe pain during defecation which persists for about 20-30
minutes after defecation.
- In chronic fissure there is a long history of less severe pain
O/E:
- In acute fissure the anus is spastic and PR is not allowed by the patient.
- Posterior superficial tear can be seen (in females; the fissure may be
formed anteriorly as complication of obstructed or prolonged labor)
- In chronic fissure PR reveals:
Sentinel tag
Button hole like fissure which is fixed and indurated
4.Passage of blood superficial to stool: Expect CA of rectum
- The disease is more common in middle age but no age is immune

- It is usually associated with sensation of incomplete defecation (it is a

type of tenesmus = spurious diarrhea) due to the presence of the
tumor in the rectum
- PR: Rectal mass or ulcer can be palpated and seen by proctoscope
5.Passage of blood mixed with stool: commonest is CA of left colon
- Middle age, males > females
- Most important associated symptom is change in bowel habits with
progressive constipation which may end in partial or complete
intestinal obstruction
- General examination may reveal anemia
- Abdominal exam: may reveal mass in LLQ (fecal matter as the tumor
is usually stricture form)
- PR: Usually unremarkable
6.Passage of blood and mucus (bloody diarrhea): Is suggestive of
inflammatory bowel diseases
A.It may be infective: Non surgical, but must be excluded
- Bacillary dysentery there is marked toxemia (FAHMR) and the stool
is fluid and mixed with blood and mucus
- Amoebic dysentery , the stool is more or less bulky and toxemia is
less
B.Non infective:
Ulcerative colitis:
- Young adult with chronic intermittent bloody diarrhea (remissions
and relapse)
- Systemic manifestations, as anemia (iron def), uvieitis, arthritis, etc
- Rectal examination may show 2ry piles due to congestion and
proctoscope will show congested mucosa with ulceration
Crohn's disease:
- May presents by bleeding per rectum
- There is a long history of abdominal colic, chronic diarrhea, picture
like acute appendicitis, intestinal obstruction or mass in Rt iliac
fossa
- PR: multiple perianal fistulas are characteristic.
NB. Anemia of Crohn's disease is megaloblastic as it affects terminal
ileum interfering with absorption of folic acid
Ischemic colitis Ischemic colitis:

- Ischemic colitis results from a sudden and often temporary reduction

in mesenteric blood flow, typically caused by hypoperfusion,
vasospasm, or occlusion.
- The usual areas affected are the splenic flexure and the rectosigmoid
junction.
- Clinically, elderly patient presenting with abdominal pain, usually
accompanied within 24 hours by bloody diarrhoea.
- Patients usually have significant atherosclerosis or cardiac disease.
7. Neonatal bleeding/rectum commonly associate bleeding Meckel's
diverticulum (if expected diagnose it by HIDA and technetium scan)
8. Bleeding/rectum in children is usually due to hamartomatous polypi
which can be easily seen by rectal examination

MANAGEMENT
1. Hospitalize
2. Resuscitate: 2liters RL on admission and give blood if HCT < 30%
3. Sedation and avoid morphia and benzodiazepines in hepatic patients
to avoid encephalopathy
4. NG tube to exclude upper GI causes and if found wash with cold
saline + adrenaline to decrease bleeding and prepare for upper GI
endoscope
5. Rapid history and examination: Abdominal case sheet and stress on
- Color of blood
- Amount of blood
- Relation to stool (separated, superficial, mixed, bloody diarrhea)
- Associated collapse
- Protruding lump (pile) with defecation
- Pain with defecation (fissure)
- Tenesmus like symptoms and morning diarrhea +/- change bowel
habits (colorectal CA)
- Change in bowel habits with partial or complete intestinal obstruction
- Picture of diverticulosis (see before)
- Bloody diarrhea with remissions and relapses (UC)
- Repeated attacks of abdominal colic with diarrhoea
- Ask about other GI symptoms with special concern on hematemesis
- Symptoms suggestive of UGIB ( PUD, NSAIDs, cirrhosis)

- Don't forget the rest of the other GI, urinary, swelling and
gynecological symptoms
- Don't forget the hospital course specially blood transfusion,
endoscopy surgery
- With any case of GI bleeding you have to ask about manifestations of
bleeding tendency as; bleeding gums, menorrhagia, echymoses etc
- In drug history never to forget Aspirin, NSAIDs, anticoagulants, and
antiplatelets + all other items of past history
- FH, social history
Examination:
General: As usual with special stress on
-Signs of shock and class of hemorrhage (usually corrected0
-Anemia
-Stigmata of liver cell failure if varices
Local: with stress on
-Hepatosplenomegally & PU (tender epigstrium to left or right)
- PR ask for it to detect CA of rectum and piles or tender button hole like
(Anal fissure)
Investigations:
- CBC, bleeding profile (PT, PTT), blood grouping and cross
matching to be ready for blood transfusion
- After resuscitation do organ profile specially for liver
- Proctoscopy: to exclude rectal lesions as: Polyps, CA, ulceration
with mucosal congestion and edema in UC
- Lower GI endoscopy:
Stool must be washed first
You may see the cause as: Ostea of diverticulae, flat hyperemic
lesions with central arteriole in angiodysplasia (in cecum and
ascending colon), colonic CA, and picture of UC or Crohn's (coble
stone lesion)
- Biopsy if doubtful lesions
Try to stop bleeding:
- Diverticular bleeding and angiodysplasia are treated with
coagulation, hemoclip application, or injection of epinephrine.
Failure indicates colectomy: total if both are found but if
diverticulosis only Hartman's operation is done

- Crohn's and UC are treated first conservatively and failure

indicates proctocolectomy
- CA of rectum:
Bleeding is not severe
Patient can be resuscitated and prepare the colon for
definitive surgery
Elective APR for tumors of lower part of rectum
Anterior resection of rectum and sigmoid for tumors of upper
2/3 and rectosigmoid followed by colo-anal anastomosis
If obstructed patient: do transverse colostomy first and
definitive surgery after 1-2 weeks
- Sigmoid CA:
Bleeding is not severe
Sigmoid colectomy with colorectal anastomosis if the patient
stops bleeding and prepared
Sigmoid colectomy if not prepared with Hartman's operation
- Descending colon:
Bleeding is not severe
Left hemicolectomy if patient is prepared
Obstructed do transverse colostomy first
NB: FOR TYPES OF COLECTOMY SEE BELOW
- Piles; after stopping bleeding do sclerotherapy, band ligation, or
LASER photocoagulation in 1st and second degrees and
hemorrhoidectomy for 3rd and 4th degrees
- Fissure: if acute conserve (bulky laxative, local anaesthetics, local
nitrates) and if chronic do lateral sphincterotomy
IF THE SOURCE OF BLEEDING IS OCCULT
Angiography
- Diagnostic
- Therapeutic: Inject intra-arterial vasopressin or do Embolization
Tagged red blood cell (TRBC) scan
Only diagnostic
More sensitive than angiography
Can detect bleeding rate of 0.1-0.5 mL/min
TYPES OF COLECTOMIES AND RECONSTRUCTION OF EACH

A
C

Right
hemicolectomy with anastomosis
of
ileum to transverse colon(A), left hemicolectomy with colo-sigmoid anastomosis(B), sigmoid
colectomy with colo-rectal anastomosis(C), transverse colectomy with colo-colic
anastomosis(D), and abdominoperineal resection of rectum and anal canal with end colostomy
(E)

$
D

Hartman's procedure done in emergency sigmoid

colectomy
As in obstructive tumors, non controlled diverticular bleeding and gangrenous sigmoid
volvulus

UPPER GI BLEEDING
ABDOMINAL CASE SHEET AS IN LOWER GI BLEEDING
Upper GI Bleeding = proximal to ligament of Treitz
Hematemesis: vomiting of altered blood which is coffee ground, however if
it is severe it will fresh red blood
This is diagnostic of upper GI bleeding
Melena = passage of soft tarry offensive stool
Hematochezia = Bright red blood per rectum
How to manage?

 Hospitalization
Resuscitation and restoration of the blood volume
Diagnosis
Stop bleeding
Prevent complicaions
First aid: ABC
Consider elective intubation prior to Esophago-GastroDuodenoscopy (EGD) if:
1. Active bleeding
2. Altered respiration
3. Altered mental status
2 large bore IV lines, start infusion by Ringers Lactate
Send blood sample for grouping and cross matching, CBC & Coagulation
profiles
Give blood once it is ready according to the class of hemorrhage
Place patient on O2 & continuous monitor
Sedation: is essential in hemorrhagic shock as the patient is anxious or
even combative.
In hepatic patients, sedatives may precipitate encephalopathy, so, use safe drug as
paraldehyde
Insert NGT and lavage with cold saline which help in:
To confirm if the bleeding source is upper GI
Decrease bleeding by causing vasoconstriction
Differential Diagnosis
Most common causes:
1. Bleeding peptic Ulcer Disease (PUD) >50% cases
Commonly from posteriorly situated DU (near the gastroduodenal artery) while
the anterior ulcer usually perforates causing peritonitis
2. Erosive gastritis / hemorrhagic duodenitis (15-30%)
Usually following NSAID use, specially COX1
3. Bleeding varices (esophageal & fundic) from portal hypertension (10-20%)
4. Mallory-Weiss tears at GE junction (5%)
5. Esophagitis (GERD) (3-5%)
Other less common causes
Malignancy
Dieulafoys lesion (1-3%) is a medical condition characterized by a large
tortuous arteriole in the stomach wall that erodes and bleeds. It can cause
gastric hemorrhag.

 Nasopharyngeal bleed swallowed blood

History & Physical Examination
History of prior ulcers, NSAID use, stress
History of Helicobacter pylori infection & treatment
History of viral hepatitis or bilharziasis portal hypertension
Alcohol abuse:
Repeated vomiting -> Mallory Weiss tear
Alcoholic cirrhosis -> portal hypertension and varices
On examination:
Assess the shock status and the class of hemorrhage
Look for stigmata of cirrhosis & portal HTN..
Laboratory investigations as in lower GI bleeding
Perform Upper GI endoscopy (EGD)
For ulcers or erosions: Stop bleeding by clipping, injection of adrenaline in
saline, or LASER photocoagulation.
This will be followed by IV PPI and if PUD triple therapy is given
Failure of conservative treatment surgery to ligate, coagulate, or
suture the bleeder
If multiple non controllable bleeding erosions gastrectomy
For bleeding esophageal varices : Endoscopic injection sclerotherapy or
endoscopic band ligation.
If bleeding is controlled give IV somatostatin (octeriotide).
Failure or Rebleeding: we can do
surgical ligation
stapling of esophagus
or even emergency selective shunt operation (preserving the portal
circulation to liver while the venous drainage of the lower esophagus,
stomach and spleen is shunted to the renal vein (distal splenorenal
shunt, see figure below) and spleen
TIPSS: Trans jugular porto-systemic shunt lowers portal pressure but
disturb the anatomy so, it should not be done if liver transplantation
is decided
After stopping bleeding: repeated enema, gastric lavage, and
lacteolose to prevent development of encephalopathy

CASE OF PATIENT WITH STOMA

Types of stoma: Oral question

Tracheostomy: will be discussed separately with the

airways
Esophagostomy: Tube (usually large caliber Foley's
catheter) in left side of the neck, to drain saliva in
advanced cases of congenital atresia
Gastrostomy : Tube (usually large caliber Foley's catheter)
in epigastric and to left, for feeding
Jejunostomy: Tube (usually large caliber Foley's catheter)
in left hypochondrium, better than gastrostomy for feeding
Ileostomy: after total colectomy or to help healing after
colonic anastomosis, see below
Colostomy: to relieve obstruction or after colectomy in
emergency non prepared patient, see below
Cholecystostomy: in difficult cholecystectomy (tube,
usually large caliber Foley's catheter) inserted in Rt
hypochondrium
Nephrostomy: In pyonephrosis (usually large caliber
Foley's catheter) inserted in lumbar region
Ureterostomy: after cystectomy (the ureters are
anastomosed to skin)
Cystostomy: in retention of urine if difficult urethral
catheterization, we use suprapubic catheter

COLOSTOMY OR ILEOSTOMY
o
o
o
o

Clinical Case
Apply the abdominal case sheet to diagnose the presenting
disease
Hospital course is very important and the operation is
usually done as emergency
Add to examination: The examination of the site of stoma
(ileostomy, transverse colostomy, or sigmoid colostomy)
Remove the stoma bag and comment on the stoma: the
normal is pink and the abnormal may be: edematous,
congested, prolapsed, retracted or surrounded by infection
Do Per Stoma (PS) examination to detect abnormality as
Stenosis

!
A

B
C
Ileostomy: Found in the Rt side (A), stoma bag (B), and the
spout (like nipple to fit for the stoma bag and to facilitate
collection of fluid fecal matter

$
A

Permanent colostomy after abdominoperineal resection (APR)

of rectum and anal canal (A), Hartman's procedure (B)

$
A

B
Loop transverse (sub hepatic) colostomy in RUQ (A) and different
types of colostomy (B)
NB: The colostomy or ileostomy will be permanent if the distal part is
resected as after APR or total colectomy also in locally advanced malignancy
when reconstruction is impossible
NB: If no permanent cause reconstruction is done after 3 months

!
Distal splenorenal shunt
HEPATO-PANCREATICO-BILIARY CASES
Abdominal sheet will be used and start by the hepatobiliary
symptoms (asking about all complications of gall stones, as,
described below)
You will be asked about DD of pain and swellings in ULQ and other
abdominal quadrants (see before)
Types of gallstones
1. Cholesterol stones (Often solitary)
2. Mixed stones (multiple, often faceted) [90% of gallstones]
3. Pigment stones: occur in children with congenital hemolytic anemias as
Spherocytosis or Sicklers at age 8-10 years (calcium bilirubinate)
Non symptomatic: About 50% of gallstones are and
discovered incidentally by abdominal US

The disease is common in Female (but males are also affected),

Fatty, Fertile (multipara), Forty or Fifty (however any age can
be affected and in young and children suspect pigment stones
due to hemolysis as in sicklers)
Symptomatic gallstones: are usually due to its complications
which can be summarized by the mnemonic acronym MIMO
(Migration, Infection, Malignant transformation, and
Obstruction)
M. MIGRATION: leading to biliary colic (colicky, referred
mainly to right shoulder and may be back (radiation to back
only! suspect pancreatitis), lasts for less than 6 hours with
no fever
I. INFECTION: Acute, Chronic Cholecystitis, and
Cholangitis
1.Acute cholecystitis:
- Sudden onset of pain like biliary colic which lasts for
more than 6 hours with no fever
- Nausea, vomiting, constipation
- Jaundice with yellow skin and sclera with dark urine
NB: jaundice in acute cholecystitis is due to edema of
CBD, pressure by impacted stone in
Hartman's pouch on CHD (degree of
Mirizzi's syndrome), and transmitted
infection to liver
- O/E: Jaundice, fever, positive Murphy's sign
And may be palpable tender empyema or
mucocele (difficult to palpate due to rigidity)

2.Chronic calcular cholecystitis:

- Biliary dyspepsia: Chronic right hypochondrial chronic pain
and discomfort which increases by fatty meals
- May be positive Murphy's sign
3. Cholangitis:
- The patient has obstructive Jaundice with
- Charcot's triad and enlarged tender liver
- Reynaud's pentate if septic shock occurs

M. Malignant transformation:
- CA of gall bladder: to cholangio CA and if metaplasia occurs
to SCC
- Cholangiocarcinoma of hepatobiliary tree
O. Obstruction:
- Choledocholithiasis with obstructive jaundice, cholangitis, or
pancreatitis (will be discussed separately)
- Gall stone ileus: due to migration of large gall stone through a
fistula between GB and duodenum to be impacted in terminal ileum
causing obstruction
The patient present by history of repeated attacks of cholecystitis and
the last attack is followed by picture of intestinal obstruction

INVESTIGATIONS OF GALL STONES

Laboratory:
1. CBC: For hemolytic anemia and Leukocytosis if infection
2. LFT:
- AST and ALT rise in VH and if high do viral markers
- ALP and Direct bilirubin increase in obstructive jaundice
ALP is not specific as it increases in other diseases as
bone diseases, so you can measure also -GT

- PT and INR (International Normalized Ratio of PT) are

prolonged in obstructive jaundice with decreased
absorption of vitamin K or cirrhosis due to decrease
synthesis
- Albumin: decreases in cirrhosis
3. RFT: May be impaired if hepatorenal failure
4. Tumor markers: If you suspect malignancy as CA 19.9 in
pancreatic tumors
Imaging:
1. Plain X-rays:
-85-90 of gallstones are radiolucent
- Radiopaque stones appear as Signet rings
- You can see porcelain GB which is
premalignant condition
2. Abdominal US:
US can detect:
- Gallstones: Acoustic shadow
- Cholecystitis: Distended or shrunken
gall bladder, Thickened wall (> 3mm) Pericholecystic
fluid and positive sonographic Murphy's sign (more
accurate than clinical one)
- Choledocholithiasis: Dilated CBD (> 6mm) or Stone in
CBD.
According to the findings of LFT and US: The management proceeds as follow
- If both are normal except for GB stones do lap chole if
symptomatic gallstones
NB: Some surgeons perform Lap Chole for non symptomatic gall stones if the
patient has risks of complications as diabetics, large stones >2 cm, typhoid
carriers, and hemolytic anemias
- If US shows dilatation or stone in CBD abnormal LFT
! ERCP (diagnostic & therapeutic ! sphincterotomy &
stone extraction) to be followed by Lap Chole
ERCP: Endoscopic Retrograde Cholangio
Pancreatography
- If LFT are abnormal ( in ALP or direct bilirubin) but
CBD is normal by US do MRCP stone ERCP +
Lap Chole
MRCP: Magnetic Resonance Cholangio Pancreatography


- If MRCP confirms normal CBD: do Lap Chole
NB: In acute cholecystitis:
- If the patient presents in 1st 48 hours do cholecystectomy
but if delayed ! medical ttt 1st
- Do surgery if no response to medical ttt or patient develops
complications,
- Operation will be difficult and if such do partial
cholecystectomy or even cholecystostomy (put draining
tube in gall bladder) and cholecystectomy will be done
after adhesions resolve.

A CASE OF ACUTE BILIARY PANCREATITIS

Abdominal case sheet is applied and don't forget
The patient presents to ER with sudden moderate to severe epigastric
pain radiating to back more on lying flat and may decrease on leaning
forward, so, DD of acute abdominal pain, specially epigastric which
would be asked (see before)
Systemic review must be taken carefully to detect complications
which may affect more than one organ, see below
Don't forget hospital course: specially for US, CT, ERCP, ICU which
might be done for the patient
ACUTE PANCREATITIS
Etiology:
Gallstones (30-60% up to 80% in KSA)
Idiopathic, mostly due to undiagnosed microlithiasis (10%)
Ethanol (30%, less in Islamic countaries)
Trauma/Tumor
Drugs : As Diuretics, anti-diabetics, and Steroids
Mumps
Autoimmune: as SLE
Scorpion Bites
Hypertriglycideremia, Hypercalcemia, Hyperparathyroid
Others:
- Pancreatic Divisum
- Sphincter of Oddi Dysfunction
- Congenital Anomalies

- Hypothermia
- Vasculitis
Clinical picture:
Symptoms:
1. Epigastric pain
Moderate to severe, the pain is usually rises in crescendo (Kr-shnd; a
steady increase in intensity or force).
Radiate to the back (retroperitoneal location of the pancreas) but it may
radiate to the flanks, chest, shoulder & lower abdomen.
Steady & boring (not colicky).
2. Nausea and vomiting: repeated and usually with distension and
constipation if ileus develops
3. Fever:
- In 1st week due to acute inflammation, mediated by inflammatory
cytokines.
- 2nd or 3rd week in patients with acute necrotizing pancreatitis is
usually due to infection (gm-ve E-coli, enterobacter) of the necrotic
tissue, more significant.
4. History may reveal the cause, commonly gall stones, alcohol, etc
Examination:
Generally:
Jaundice: due to hemolysis by pancreatic enzymes, liver cellular
.1
damage, and obstructive as inflamed pancreas presses CBD
Hypoxemia (25%) Cyanosis: due to diminished respiratory
.2
movement, pleural effusion, ARDS, and met-hemoglobinemia.
Tachycardia, Hypotension: hypovolemia or initial systemic
.3
inflammatory response syndrome (SIRS)
Left basilar rales (Pleural Effusion)
.4
Abdominal Exam
Abdominal tenderness and rigidity max at epigastrium
Distension: due to ileus
Bowel sounds decreased (ileus)
Palpable upper abdominal mass: Acute fluid collections or
pseudocyst
Cullen's Sign (periumbilical discoloration) after 48 hours in
hemorrhagic type

 Gray-Turner's Sign (flank discoloration) blue-gray discoloration of

abdominal flanks due to exudation of blood-stained fluid into the
subcutaneous tissue.
Complications of acute pancreatitis:
Systemic complications:
Fluid imbalance
Electrolyte imbalance
Cardiac impairment
Renal impairment
Respiratory impairment
Liver failure
Local complications:
Ileus
Duodenal obstruction
Biliary obstruction
Pseudocyst formation
Infected necrosis
Colon necrosis
Investigations:
Complete Blood Count (CBC): Leukocytosis and may be
hemolysis
Serum Amylase:
- Nonspecific: as it may increase in other diseases including
those causing acute abdominal pain
- Starts to increase at (2-12hrs) after the onset of symptoms,
peaks at (12-72hrs) & return to normal within 1 wk.
- DD of hyperamylesemia:

3. Serum Lipase :
- Specific for pancreatic disease.
- Starts to increase at (4-8hrs), peaks at (24hrs) & the leve
decrease within 8-14 days.
- Sensitivity (86-100%) & specificity (50-99%)
4. Serum Electrolytes : Hypercalcemia (cause) -orhypocalcaemia, decreased base deficit, decreased Po2
(complication)
5. Lipids profile: Hypertriglyceridemia (cause or complication
due to lipase effect)
Liver Function Tests: may be impaired (earliest is AST)
6. Other investigations mentioned in the scoring indices
Imaging:
1. Plain x-rays of the abdomen may show dilated sentinel
intestinal loop
2. Abdominal US: to diagnose gallstones, repeat it if negative
before diagnosis of idiopathic pancreatitis, also diagnose fluid
collection and pseudocyst
3. CT scan essential to diagnose, associated lesions, pancreatic
necrosis (CT Severity Index)
4. MRI: may be used but not suitable for patients requiring
respiratory assessment
ERCP: essential in biliary pancreatitis, see below for indications
TO exclude other causes of acute abdomen:
- ECG for inferior wall MI
- Plain X-Rays of the chest (gas under diaphragm in
perforated PU,there may be pericardial or pleural
effusion)
SEVERITY ASSESSMENT
Atlanta classification
Mild pancreatitis (edematous or interstitial): parenchymal inflammation with no
local complications or systemic involvement. It is usually self-limiting with
uneventful recovery
Severe pancreatitis (necrotizing): pancreatic parenchymal inflammation with
local or systemic complications that has a protracted clinical course and has a
higher mortality rate. Defined by >3 Ranson criteria or an APACHE II score >8.
Mostly associated with necrosis

PROGNOSTIC INDICES
Ranson criteria for biliary pancreatitis (gallstone-associated)
Criteria on admission:
1. age >70 years
2. glucose >12.2 mmols/L (220 mg/dL)
3. WBC count >18 x 10^9/L (18 x 10^3/ microlitre);
4. serum AST (SGOT) >250 units/L
5. and serum LDH >400 units/L.
Criteria after 48 hours of admission:
1. Hct fall >10%
2. Estimated fluid sequestration >4 L
3. Base deficit >5 mEq/L;
4. BUN rises >0.7 mmols/L (2 mg/dL)
5. Serum calcium <2 mmols/L (8 mg/dL)
RANSON CRITERIA (NON-GALLSTONE PANCREATITIS)
Used for prediction of severe acute pancreatitis - not diagnosis.
Criteria on admission:
Age >55 years
.1
Glucose > 200 mg/dl
.2
WBC count >16 000/microlitre
.3
Serum AST (SGOT) >250 units
.4
Serum LDH >350 units/L.
.5
Criteria after 48 hours of admission:
1. HCT fall >10%
2. Estimated fluid sequestration >6 L
3. Base deficit >4 mEq/L
4. BUN rises >1.8 mmols/L (5 mg/dl)
5. Serum calcium <2 mmols/L (8 mg/dL)
6. PO2 <8 kPa (60 mmHg)
Number of criteria and approximate mortality (%):
0 to 2 = 0% 3 to 4 = 15% 5 to 6 = 50% >6 = 100%
Modified Glasgow criteria:
1. PaO2 < 60 mmHg
2. Albumin < 32 g/L
3. Ca < 2.0 mmol/L
4. WBC > 15 10 /L
5. AST/ALT > 200 U/L

6. LDH > 600 U/L

7. Glucose > 10 mmol/L( in the absence of diabetes)
8. Urea > 16 mmol/L (not responding to therapy).
Need 48 hrs for full evaluation
APACHE II: Acute Physiology And Chronic Health Evaluation, 12 points
Treatment:
If it is mild:
1.Hospitalization.
2.NPO.
3.Nasogastric tube.
4.Octreotide.
5.Fluid replacement + CVP.
6.I.V antibiotics to prevent secondary infection, but may increase
possibility of fungal infection.
Monitor shock: through urine output and CVP.
If it is severe: as above plus
1.ICU.
2.Feeding nasojejunal tube or feeding Jejunostomy better than TPN
3.In biliary pancreatitis ERCP must be done to extract stone in the first 48
hours in
- Jaundiced patient
- Suspicion of cholangitis
- Severe pancreatitis
Surgery: If biliary pancreatitis, do cholecystectomy within 4 w to avoid
recurrence

CASE OF OBSTRUCTIVE JAUNDICE

Apply the abdominal case sheet
The patient complaint may be yellow discoloration of skin or sclera
but mostly he presents by pain as biliary colic or epigastric pain and
during asking about the hepatobiliary symptoms he may mention that
he has dark urine, pale stool, itching etc
Hospital course is essential as the patient may be not jaundiced if he
extracted the stone by ERCP or if a stent was inserted
ETIOLOGY OF OBSTRUCTIVE JAUNDICE
Extra hepatic obstruction of the biliary tree
1. Common bile duct stones (Choledocholithiasis): commonest cause
2. Malignant obstructive jaundice

3. Postoperative jaundice: retained stones in CBD & strictures

4. Other benign strictures
5. Parasites
6. In infants and young children:
Extrahepatic biliary atresia
Choledochal cysts
Intrahepatic (mostly non surgical)
1.
2.
3.
4.
5.
6.

Intrahepatic biliary hypoplasia or atresia

Drugs or chemical toxins
Estrogens, Pregnancy, Anabolic steroids, Augmentin.
Hepatitis: viral, chemical
Infiltrative tumors
Primary biliary cirrhosis (PBC).

CHOLEDOCHOLITHIASIS
Stone disease is the most common cause of obstructive jaundice.
Gallstones may pass through the cystic duct to CBD and cause
obstruction and symptoms of biliary colic and cholecystitis
Larger stones may be primarily formed in the in the CBD and cause
complete or intermittent obstruction, with increased intraductal
pressure throughout the biliary tree
Mirizzi's syndrome is the presence of a stone impacted in the cystic
duct or the gallbladder neck, causing inflammation with edema and
external compression of the common hepatic duct biliary
obstruction.

Mirizzi's syndrome
MALIGNANT OBSTRUCTIVE JAUNDICE

1. Mainly due to carcinoma of the head of the pancreas

- 2/3 CA of the head proper which is adenocarcinoma compressing
the CBD
- 1/3 Periampullary CA which may cholangiocarcinoma of lower
part of CBD, adenocarcinoma from duodenal papilla or end of
pancreatic duct
2. Cholangiocarcinoma of upper part of CBD or hepatic ducts
3. Carcinoma of the gall bladder
4. Malignant lymph nodes in Porta hepatis (2ries from GIT, breast, or
Lymphoma)
Benign biliary strictures:
95% are due to surgical trauma.
Stone disease is the most common cause of biliary strictures in patients who have not
undergone an operation.
Primary sclerosing cholangitis (PSC): Is commonly associated with inflammatory bowel
disease (IBD), most commonly in patients with pancolitis. PSC is characterized by diffuse
inflammation of the biliary tract, causing fibrosis and stricture of the biliary system. It
generally manifests as a progressive obstructive jaundice and is diagnosed by endoscopic
retrograde cholangiopancreatography (ERCP).
Parasitic causes:
Ascaris lumbricoides can migrate from the intestine up through the bile ducts
Eggs of certain liver flukes (eg, Clonorchis sinensis, Fasciola hepatica) can obstruct the
smaller bile ducts within the liver, resulting in intraductal cholestasis. This is more
common in Asian countries.
Hydatid cysts pressing the biliary tree.

CHOLEDOCHOLITHIASIS VS MALIGNANT OBSTRUCTION

Personal history:
Age & sex: any age or sex but choledocholithiasis is commoner in middle
aged females (F group), in children (over 8 years) if hemolytic anemia
Malignant OJ is commoner in elderly males
Symptoms: if the patient present by jaundice or during history he told you that he
suffered from any symptom suggestive of jaundice ask about the following;
1. Onset:
Sudden in stone disease
Gradual in malignant OJ
2. Course:
Intermittent in stone disease, Periampullary CA, and
cholangiocarcinoma due to central sloughing of the tumor

Progressive in CA of the head proper and rarely due to impacted

large stone in CBD
3. Duration: May be long in stone disease with intermittent or partial
obstruction, but short if malignant obstruction.
4. Pain:
Colicky: in biliary stones due to migration of stones through cystic
duct causing biliary colic (contraction of the gall bladder) or acute
cholecystitis or passage of the stone through the sphincter of Oddi
NB. Non migrating stone in CBD is painless as the duct contains no muscle
fibers.
NB. Colicky pain may be found also in Periampullary CA.
In CA of the head proper the disease is early painless but late after
infiltration, epigastric pain, boring, radiates to back will appear and
increases in severity especially on lying flat and decreases on leaning
forward
5. Fever and rigors: in Choledocholithiasis if cholangitis develops.
NB. Charcots triad: intermittent jaundice, colicky pain, with fever and rigors
in choledocholithiasis if ascending cholangitis develops.
Reynaud's pentate: if septic shock follows cholangitis where hypotension
and mental confusion are added to the triad.
NB. Stones are commonly associated with infection so cholangitis is
commoner than in malignancy.
6. Itching: Specially in limbs, it may be the presenting symptoms, It is
due to the central effect of increased bile salts
7. Bleeding tendency: due to decreased bile salts in the intestine
decreased absorption of Vitamin K hypoprothrombinemia.
8. Urine: Dark (CB) and frothy (Bile salts act like soap) in all types of
obstructive jaundice.
9. Stool: Pale, greasy, and offensive due to increased fat.
NB. In ulcerating Periampullary carcinoma there is melena and its black color
becomes pale due to excess fat (gray, aluminum, or silvery stool)
10.Loss of weight: more marked in malignancy.
11.Ask about; other GI manifestations, Urological, Gynecological,
Swelling, Hospital Course, Systemic Review, PH, FH, and Social
History
Signs:
General:

- Consciousness: may be disturbed in cholangitis and if hepato-renal

failure is developed.
- Jaundice:
Best to be seen in the sclera at the fornices in day light.
It can be seen in skin and mucous membranes (palate & anus).
It is orange yellow in choledocholithiasis and early peri- ampullary CA and
olive green in malignant OJ.
Xanthomata: are associated with primary biliary cirrhosis (PBC).
- Body built: Loss of weight and even cachexia in malignancy especially
in CA of the head of pancreas
Loss of weight is not marked in stone disease as the patient is usually
Fatty.
- Enlarged supraclavicular lymph nodes:
The right drains the dome of the liver (enlarged in infection and
malignancy).
The left in advanced malignancy (Virchows LNs)
- Vital signs:
Bradycardia and hypotension due to depression of sino-atrial node
and myocardium by bile salts.
In infection as acute cholecystitis and cholangitis there will be fever
and tachycardia.
- Itching marks especially at the limbs.
- Echymoses due to bleeding tendency can be easily seen at the sites of
injection and venous lines.
- Stigmata of cirrhosis as: fetor hepaticus, spider nevi,
gynecomastia, palmar erythema, and flapping tremors
Abdominal Examination
1.Ascites: in advanced malignancy and cirrhosis.
2.Malignant umbilical nodule (Sister Joseph) in advanced breast and
visceral malignancy.
3.Liver:
- Enlarged, smooth, and non tender due to hydrohepatosis (liver is
distended with bile) in all types of jaundice.
- In stone disease if cholangitis occurs it will be tender.
- In metastatic CA of pancreas or other malignancy it will be nodular
and tender.
4.Gall bladder:

- Palpable and non tender in malignant obstruction below the cystic

duct (Courvoisier sign)
- Shrunken and non palpable in stone disease
- Positive Murphy sign in cholecystitis.
Exceptions of Courvoisiers law:
Malignant OJ with non palpable gall bladder:
- Obstruction above cystic duct.
- Previous cholecystectomy.
Stone disease with palpable GB:
- Primary stone (no infection).
- Empyema or mucocele.
5.Spleen may be enlarged if the cause of jaundice is lymphoma or
cirrhosis.
6. PR and PV for malignant peritoneal nodules.
7.Urine sample: dark and frothy urine.
Differential Diagnosis: hepatitis is the commonest cause of jaundice
Post hepatic causes: Differentiate stone disease from malignant OJ (see
before).
Hepatic:
Hepatitis; mainly viral (but may be caused by drugs or toxins)
.A
In hepatitis;
The patient presents by jaundice with fever (if infective), upper right
quadrant pain and picture similar to OJ
Enlarged tender liver with no Murphy or Courvoisier' signs
LFT: but in hepatitis there is marked rise in transaminases, normal
or mild rise in ALP, bilirubin is usually biphasic (direct and
indirect) and viral markers are positive
US there is no stone, no tumor and biliary tree is not dilated.
B. Cirrhosis:
History of VH or alcohol consumption
Manifestations of LCF and portal hypertension granular firm liver
Confirm by LFTs (mainly low albumin), US, and biopsy if PT is
normal
C. Pancreatitis: There is obstruction, hemolysis and liver impairment
The most common cause is biliary pancreatitis, the patient
present with history of gallstones, sudden severe epigastric pain
radiating to the back, repeated vomiting, constipation,
distension, shock in severe cases, jaundice, cyanosis in severe

cases, abdominal tenderness, rebound tenderness, and rigidity

which is maximal in epigastrium and in late cases Cullen's and
Gray Turner signs
Establish diagnosis by increase amylase and lipase, US, and ERCP if
impacted stone in ampulla.
Preheatic (Hemolytic jaundice):
- Either congenital or acquired hemolysis
- Patient is anemic
- Repeated attacks of hemolytic crises with fever and rigors
- Lemon yellow jaundice with pallor
- Enlarged spleen in familial forms as Spherocytosis or thalathaemia
(in sicklers may be autosplenectomy due to repeated infarction)
- Acholuric urine, dark stool
- Increase unconjugated bilirubin in blood
INVESTIGATIONS
LABORATORY:
CBC: Anemia and reticulocytosis in hemolysis, Leukocytosis if
infection
Liver function tests (LFTs):
1. Bilirubin increases: Normal 3-17mmol (< 1.2 mg)/L
Mainly the direct bilirubin increases in OJ but the indirect may
be mildly increased in
2. Alkaline phosphatase ALP: more sensitive than bilirubin
But not specific as it may increase in bone diseases (add GT)
In intrahepatic obstruction it increases < 3 times the upper limit of
the normal reference.
Extrahepatic obstruction: ALP > 3 times the upper limit of the
normal reference
NB. In stone disease it increases >3-5 times the upper limit of the
normal reference.
NB. In malignant OJ > 5 times and may reach >10 times (if
complete obstruction)
3. Serum transaminases: ALT & AST
Mildly increased in OJ
Marked increase if there is cholangiohepatitis or viral hepatitis (can be
differentiated by serological viral markers).
4. Albumin: decreases in cirrhosis.
5. Prothrombin time & INR: increases (VIT K absorption)

Renal function tests: may be impaired due to bile pigment

nephropathy and lack of bile salts flourishing of bacterial flora in the
intestine release of bacterial endotoxins vasoconstriction of renal
BVs.
Exclude pancreatitis by amylase and lipase
.6
.7
Imaging
Plain radiographs: Are of limited utility to help detect abnormalities
in the biliary system.
Ultrasonography : US is the procedure of choice for the initial
evaluation of cholestasis, the least expensive, safest, and most
sensitive technique for visualizing the biliary system, particularly the
gallbladder. Current accuracy is close to 95%.
In stone disease, US will show:
GB Stone : Acoustic shadow
If cholecystitis:
- Distended or shrunken gall bladder
- Thickened wall (>3mm)
- Pericholecystic fluid
- Positive sonographic Murphy' sign if cholecystitis
If choledocholithiasis: dilated CBD (>6mm) or stone in CBD.
. Malignant OJ:
- Shows dilatation of CBD distended GB
- It may show also focal metastatic lesions in liver
- It is not sensitive for pancreas
If suspected CA of pancreas do CT to diagnose size, extent and
operability of the tumor
Indications of Magnetic Resonance Cholangio Pancreatography
(MRCP): Abnormality in LFTs but the CBD in US is normal
Indications of Endoscopic Retrograde Cholangio Pancreatography
(ERCP):
Abnormality in CBD by US abnormality in LFT
Abnormality in MRCP
Treatment
Preoperative preparation: IV dextrose 5% (D5), IV VIT K, I.V
antibiotics, Mannitol infusion to decrease bile pigment nephropathy.
Choledocholithiasis:

ERCP for diagnosis, sphincterectomy and stone extraction followed lap

chole.
CA of pancreas including periampullary CA:
If operable: do Whipple operation; Removing GB, lower part of
CBD, head of pancreas and distal stomach and anastomosis of the
CHD, body and tail of the pancreas, and the gastric remnant to the
jejunum.
If inoperable: by pass or stenting.
Cholangio CA and other strictures: the stricture is resected and
hepatico-Jejunostomy is done using Roux en Y technique

$
A
B
Whipple operation: The resected part is colored black (A)
Reconstruction (B)

$
Hepatico-Jejunostomy Roux en Y

A CASE OF LIVER MASS

SEE DD OF SWELLING AND PAIN IN RUQ
APPLY ABDOMINAL CASE SHEET
FOR DETAILED DATA PLEASE REFER TO THE LECTURE
NOTES (BENIGN AND MALIGNANT LIVER MASSES, HOW TO
MANAGE AND NEVER TO FORGET CHILD AND PUGH
SCORE
Case of amoebic liver abscess: Neglected amoebic colitis may be followed by
amoebic liver abscess (right hypochondrial pain, fever with enlarged tender liver
jaundice)
This condition is diagnosed by:
Presence of amoeba in stool
Sonography or ct to see the abscess cavity with irregular wall
ELISA to detect antiamoebic antibodies
Treated by metronidazole and drainage may be required

Skin tumors
Apply clinical sheet of ulcer or swellings
BENIGN TUMORS:
1. Papilloma and warts: not true tumors but viral lesions.
TTT : excision and cautery of base.
2. Xeroderma pigmentosa: hyperkeratotic pigmented skin lesions, autosomal dominant,
liable to change to epithelioma and malignant melanoma.
3. Keratoacanthoma: not a tumor but hyperplastic lesions of sebaceous gland epithelium.

4. Neurofibroma: from endings of cutaneous nerves

2 types affects the skin multiple neurofibromata and pachydermatocele, both are
associated with coffee au lait patches.
5. Angioma: diffuse lymphangiomata , capillary hemangiomata, and glomus tumors.
6. Moles (naevi).
MALIGNANT SKIN TUMORS
Primary tumors:
1. Basal cell carcinoma.
2. Squamous cell carcinoma.
3. Malignant melanoma.
4. Sarcoma: Kaposi sarcoma
Secondary tumors: Locally fungating tumors (eg breast) or metastatic as renal
tumors lymphoma etc.
BASAL CELL CARCINOMA (RODENT ULCER)
The commonest skin tumor
It is locally malignant tumor
Aetiology: most important is prolonged exposure to sunlight(commonest in
Australia).
Microscopically: clusters of malignant cell surrounded by tall columnar
epithelium arranged like a palisade.
Spread: only local
Rodent ulcer: the commonest type, other types are known, as,
pigmented, nodular, and superficial spreading type

Sites: exposed parts of head and neck specially, above line joining
angle of mouth with tragus (commonest site is near medial canthus of
eye).

Starts as a nodule that centrally ulcerates

Painless unless infected.

Rate of growth: slow.

Edge: rolled in and beaded(seems to be eaten by rodent).

Margin: crossed by dilated veins, early soft then becomes
infiltrated.

Floor: pale granulations, covered by crust.

Base: early normal and mobile late infiltrated and fixed.

LNs: not infiltrated but may be enlarged d.t infection.

May turn to SCC (edge becomes everted, rapid growth and

metastases).

DD from other skin tumors.

Confirm diagnosis by biopsy

TTT: Excision with safety1-2cm safety margin with skin graft. Radiotherapy is
very effective.
SQUAMOUS CELL CARCINOMA (EPITHELIOMA)
Predisposing factors:
Prolonged exposure to sunlight.
Basal cell carcinoma.
Smoking (lips).
Microscopically: groups of malignant cells with cell nest formation
(well differentiated moderate or undifferentiated according to degree of
cell nest formation).
Spread: Local, regional LNs and late by blood.
Sites: Face is the most common site specially lower lip (smokers).
Painless early but becomes painful with infection an d infilteration.
Starts as a nodule which rapidly grows then ulcerates.
Edge: everted.
Margin: early normal then infiltrated.
Floor: flakes of pus, necrotics and blood.
Base: early mobile and late infiltrated and fixed.

 Regional LNs: Enlarged d.t infection or spread.

Metastases: late.
Confirm diagnosis by biopsy.
TTT as BCC +radical removal of infiltrated LNs.
MALIGNANT MELANOMA
The most malignant body tumor
Aetiology:
1. Chronic irritation of pre-existing nevus.
2. Exposure to UVR of fair skin people.
Sites: more in upper half of bodies in males and reverse in females.
Microscopically: melanin containing cells arranged in groups or separately.
Grossly: may be nodular, ulcerating, the lesion may be amelanotic (needs
histochemical proof).
1. Local spread: of all layers down to bone.
2. Lymphatic: embolization to regional LNs or permeation forming satellite nodules
around the primary.
3. Blood spread: with high affinity to liver + lung, bone and brain.
Clinically: the lesion may start de novo (nodule,ulcer,acral etc.) or on top of nevus
(grows rapidly, becomes painful, ulcerates, bleeds, satellite or LNs).
Confirm diagnosis by histopathology, histochemistry and staging
TTT: local wide excision with skin graft + radical removal of infiltrated LNs +
chemotherapy. The tumor is radio-resistant.

BURNS
Apply Trauma Sheet
Definition: coagulative destruction of tissues d.t heat, chemicals, electricity,
irradiation etc.
Causes:

Physical (flame, hot water and steam).

Chemical (acids and alkalies).

Electrical usually the

deep effect is more than

externally seen
Irradiation
Priorities of management
1. First aid.
2. Hospitalisation.
3. Assess surface area and degrees.
4. Calculate and start fluid therapy.
5. Local ttt: before and after control of shock.
6. Treatment of late complications.

FIRST AID: ABCDE of primary survey

7. Remove tight clothing & ensure airway.
8. Immerse burnt areas by cold water but avoid hypothermia
(specially in extensive burn or child).
9. Transfer to hospital.
10. Hospitalization for:
Major Burn (>20% 2nd degree and >2% 3rd degree).
Burns of face, neck (laryngeal edema), visceral burns and burns of
creases.
Others will be treated as outpatients.
AT HOSPITAL
11. Escharotomy (see complicatins): of circumfrential burns around
limbs or chest and tracheostomy if required.
12. Oxygen (100% in severe cases).
13. Two venous lines, with CVP and start Ringers lactate infusion till
we calculate requirements.
14. IV strong analgesia (narcotic).
15. IV antibiotics.
16. Catheterisation: to do fluid chart, avoids soiling or retention (NB:
Urine output is the best monitor for shock).
17. NG (Nasogastric Tube) for suction, to avoid ileus, use it in feeding
and early diagnosis of bleeding stress ulcers (Curling Ulcers) .
18. Assess surface area.
19. Assess depth as described below.

Assessment of degree of burn:

To determine if the patient will be hospitalized or

treated as out patient
First degree:

The part affected is painful and hyperemic.

Second degree: can be divided into suprficial and deep

Severe pain up to neurogenic shock.

The affected part is red with vesicles, if superficial partial skin loss.

Moist, pale in deep partial skin loss.

Pin prick test: Causes pain and bleeding.

Third degree:

Absent pain if nerves are destroyed.

Affected part is greyish waxy or black and may be Carbonization which
may reach bones.
No pain or bleeding by pin prick test.

Assessment of surface area: Essential to

calculate fluid therapy

Use Rule of Nines (9% for head and neck, 36% for the trunk -9 for
front of abdomen, 9 for front of chest, 18 for whole back- 9 for upper limb, 18
for lower limb, and 1 for genetalia and perineum.
o The limbs can be divided equally into arm and forearm, thigh and leg and
each into anterior and posterior
Example: burn involves front of chest (9%), front of abdomen (9%), front of
thigh (4.5%) and left forearm (4.5%) --> the Burnt Surface Area will be 27%
o Burnt hand alone is about 1%
In children special tables as head is larger
Use Parkland formula to calculate the fluid requirements
- The daily requirement according to Parkland formula : Surface
Area X 4 X body Wt in Ml /Day.
It is daily used till shock is improved
NB Max % of surface area used is 50% to avoid circulatory
overload.
Half dose is given in 1st 8 hours (max loss) and the other half in the
2nd 16 hours
What fluid we use?
First day give Crystalloid (Ringers Lactate).
Second day give Colloid, plasma & blood (if hematocrit <30%).
Monitor patien: By CVP (central venous pressure) and Urine Output (best).

Complications
General:
1. Respiratory: Asphyxia, pneumonia and atelectasis.
2. Shock:
Early Neurogenic d.t severe pain.
Oligemic with Plasma loss and evaporation from burnt areas.
Septic shock after sepsis.
3. Renal impairment: from shock and burn toxins.
4. Anemia: Hemolytic mainly.
5. GIT: Gastric dilatation, ileus and bleeding (Curling s ulcer).
6. Systemic Inflammatory Response Syndrome (SIRS): due to release of
the cytokines from injured tissues starting non septic then sepsis occurs and
ends with DIC and MODS if proper management is not done.

1. Constricting Eschars: due to tissue coagulation compressing deeper

structure e.g blood vessels or respiratory movement It must be divided early
by Escharotomy.
2. Colonisation with bacteria: with infection and septic shock (most
important is pseudomonas).
3. Development of scars: with disfigurement, keloid, contracture, itching ,and
may change to SCC.
4. Loss of sweating in burnt sites and compensatory hyperhydrosis in rest of
body.
Local treatment:
22. Till shock is controlled use antiseptic cream (best is Silver
preparations as it debride Eschars & kill Pseudomonas).
NB: Medicated Honey gives excellent results.
2. Bandage for limbs and Exposure For Face And Lower Back.
3. After control of shock:
Best ttt is Escharectomy and skin graft for major burns.
Dressings if minor burn, but not so frequent to avoid removal of healing
epithelium.
Treatment of late complications e.g to correct disfigurement

BED OR PRESSURE SORES

The ulcer and general case sheet are applied
If the ulcer in foot or leg apply the case sheet of ischemia (Limb examination
sheet)
Patient is bed ridden and may be comatosed or paraplegic
History will be taken from the patient or his relatives
If the patient in the ICU you will be asked about all devices and lines connected
to the patient which must be mentioned in general exam

THE SITES

$
Site: over right ischium
Irregular shape
10 cm
Punched out edge
Clean floor
Hyperemic margin
Site:
over
sacrum, 15 cm, punched and sloping edge and
necrotic infected & hyperemic margin

Punched out ulcers on lateral side of the heels and

left leg with clear floor which is red and granular = healthy granulations

$
1. STAGE ONE: How to recognize: Skin is not broken (pressure
against bone first obstruct veins with extravasation) but is
indurated & dark red or bluish

Management: Keep pressure off the sore! As in prevention + protect

skin by Opsite or Tincture benzoin.
2. STAGE TWO: The epidermis or topmost layer of the skin is
broken, creating a shallow ulcer reaching S.C fat
Protect the healthy skin as above
Debride any dead tissues either chemical (glycerin
manezia, or honey) or enzymatic (Iruxol) or by surgical
excision.
3. Stage 3: reaches muscles or fascia, ttt as before.
4. STAGE FOUR: reaches bone, treatment as before
NB: the patient improves do skin flap to cover the defect

VARICOSE VEINS AND DVT

Definition: varicose veins are tortuous, dilated, prominent, superficial veins
in the lower limb.
Veins are thin-walled vessels that are easily distended by the chronic
pooling of blood in the lower extremities.
Chronic distention of veins can reduce effectiveness of one-way venous
valves and lead to valvular incompetence.

Primary
Usually due to congenital abnormality with week walls.
Heredity: if both parents affected ! 90%, if one parent was affected !
25 % for men & 62 % for women
The most common cause is absence of valves or the collagen
content is less than normal veins.
This may account for the decreased elasticity.
Secondary
Chronic increase in the intra-abdominal pressure or the pressure in
superficial/deep venous system
As in:
DVT
Pregnancy: due to pressure by gravid uterus, increase venous flow, and
progesterone(relaxing hormone)
If persists after pregnancy it will be considered 1ry and pregnancy just
precipitated it
Pelvic obstruction: Abdominal/pelvic mass.
Obesity
Precipitating factors

 Chronic straining (constipation)

Prolonged standing
Symptoms and Signs of Varicose Veins
See clinical case sheet, for symptoms, signs, and complications
NB: Abnormal veins
1.Telangiectasia (spider): are confluences of dilated Intradermal
venules less than one millimeter in diameter.
2.Reticular veins: are dilated bluish sub dermal veins, one to three
millimeters in diameter. Usually tortuous
3.Varicose veins: subcutaneous dilated veins three millimeters or
greater in size. They may involve the saphenous veins, saphenous
tributaries, or non-saphenous superficial leg veins
- Non-saphenous varicose veins.
- Saphenous varicose veins.
CEAP CLASSIFICATION
Clinical severity.
Etiology or cause.
Anatomy.
Pathophysiology.
C 0: No evidence of venous disease.
C 1: Superficial spider veins (reticular veins) only.
C 2: Simple varicose veins only.
C 3: Ankle oedema of venous origin (not foot edema)
C 4: Skin pigmentation in the gaiter area (lipodermatosclerosis)
C 5: A healed venous ulcer.
C 6: An open venous ulcer.
INVESTIGATIONS
Non-invasive
o Hand-held Doppler
o Duplex ultrasound
Vast majority have superficial incompetence only.
Sensitivity 95 % for identifying the competence of the saphenofemoral and
saphenopopliteal junctions.
Less sensitive for identifying incompetent perforators (40 to 60 %)
Indications of treatment:
1. Cosmetic.
2. Symptomatic

3. Proximal reflux and venous hypertension.

Treatment options:
1. Conservative :
- Leg elevation.
- Exercise.
- Compression stockings.
- Treatment of other underlying conditions.
2. Vein ablation: Classified by method of vein destruction
A.Chemical (injection sclerotherapy); suitable for minor varicosities
B.Thermal
Endovenous laser EVLA (excellent results).
Radiofrequency ablation RFA
C.Mechanical (surgical excision or stripping)
Surgery: traditional surgical approaches
High ligation (of the saphenofemoral junction0 & stripping
of the vein.
Stab avulsion: direct attack and removal of the incompetent
perforators
3. Treatment of venous ulcer: dressings using non irritant
antiseptics or medicated honey and above all bandage and
compression.

DVT
DVT is the formation of a blood clot (thrombus) in one or more of the deep
veins.
It is commonly affects the leg veins
Up to 25% of all hospitalized patients may have some form of DVT which
often remains clinically unapparent.
Majority of lower extremity DVT arise from calf veins and 205 of it will
propagate proximally.
20% begin in proximal veins.
Pathophysiology
Virchow's triad: mechanism of thrombosis
i. Decrease blood flow rate.
ii. Damage to the blood vessel wall.
iii.Increase in the blood viscosity (hypercoagulability)

Risk factors
A.Surgery and trauma:
1. High risk:
Surgery in patients over 40 years with recent DVT.
Extensive abdominal or pelvic surgery for malignancy.
Major orthopedic lower limb surgery.
2. Moderate risk:
a. General surgery in patients over 40 lasting 30 min. or more.
b. General surgery in patient below 40 0n contraceptive pills.
3. Low risk:
a. Uncomplicated surgery in a patient less than 40.
b. Minor surgery in a patient more than 40 without additional risk
factor.
B.Nonsurgical conditions and factors:
o History of DVT.
o Prolonged recumbency: As in
Stroke with paralysis
Acute infection with immobilisation
Acute inflammatory disease with immobilisation
o Central venous catheter
o Acute heart failure.
o Sepsis.
Thrombophilia (as deficiency in protein C & antithrombin III).
Active malignancy.
Varicose veins.
Other risk factors
Pregnancy
Age >60 years
Obesity (BMI >30)
Oestrogen therapy
Clinically:
1.Asymptomatic: DVT may occur without any noticeable
symptoms, and the first presentation may be by PE or
even postphlebitic leg
2.Symptomatic: which can include:
A.Pain (often starts in the calf )
B. Swollen leg

C.Redness and warm leg

D.Fever
E.Complications as: PE, propagation (plegmasia alba and cerulean dolens
or even venous gangrene, see below)
Examination:
Limb swelling
Limb redness
Tenderness
Calf tenderness:
Homans sign: Dorsiflexion of foot elicits pain in posterior calf.
Pratts sign: Squeezing of posterior calf elicits pain.
Unreliable for diagnostic decisions because Up to 50% have none of these
findings & these tests may cause embolization
Phlegmasia alba dolens : white (pallor) painful swollen (edema)
leg, the leg is pale and cold leg due to diminished arterial pulse
caused by spasm as a result of acute occlusion of the iliac and
femoral veins with DVT.
Phlegmasia cerulea dolens: blue (cyanosis) painful swollen leg,
due to acute and nearly total venous occlusion of the entire
extremity outflow including the iliac and femoral veins (more
severe than alba).
Venous gangrene may supervene.
Laboratory tests
1. Complete blood count.
2. Coagulation profiles: PT, APTT,INR.
3. Electrolytes.
4. Renal function.
5. Liver enzyme
6. D-dimer: Soluble fibrin degradation product. An indication that
thrombosis is occurring and the clot is being dissolved by plasmin.
Sensitive for ongoing fibrinolysis also present in bleeding, trauma,
surgery, pregnancy, AAA, malignancy
But not specific for thrombosis
Ultrasound
Sensitivity (85-90%)
Specificity (86-100%)
Spiral CT or MRI scans may be done
Intravenous venography is the gold standard

Prevention:
DVT prophylaxis: in high risk before surgery
Anti embolic compression stockings.
Intermittent pneumatic compression devices.
Low-dose unfractionated heparin.
Low Molecular Weight Heparin.
Warfarin.
Active treatment:
1. Anticoagulation: Initiatally by parentral heparin (to keep PTT 2-3
the normal) .Then Warfarin for 3- to 6-months (monitor by PT and
INR, keeping it 2-3 normal value).
2. Compression stockings: should be routinely applied beginning
within 1 month of diagnosis of proximal DVT and continuing for a minimum
12 months
3. Thrombolysis: is reserved for extensive proximal (iliofemoral
thrombosis).
4. Thrombectomy : Thrombus can be removed with a mechanical
thrombectomy device
5. Inferior vena cava filter:
Indications
Contraindication to anticoagulation
Anticoagulation failure
Complications of the filter:
2 fold increased risk for lower extremity DVTs within 2 years of
placement
5% filter dislodgement
16% filter thrombosis
POSTPHLEBITIC LEG
Post-phlebitic syndrome: Chronic sequel of acute DVT occurring in 30 % of
patients within 10 years
Clinically:
Chronic Leg pain
Leg Swelling
Skin discoloration
10% ulcer complications
Treatment: Compression stockings (30-40 mm Hg)
PULMONARY EMBOLISM

 50% of proven DVT also have PE

70% of proven PE also have DVT
May be small and passes un-noticed if the lung is healthy,
medium sized! symptomatic PE, massive causing acute heart
failure or fatal if blocks the pulmonary circulation completely.
- Clinical picture of the medium sized emboli or small emboli (in
unhealthy lung)
Symptoms:
The classic triad
1. Acute Dyspnea
2. Hemoptysis
3. Pleural Chest Pain
anxiety or nervousness Fear of dying
Collapse
Signs:
Tachycardia
Cyanosis (subclinical)
May be manifestations of DVT

PE Evaluation and Pretest Probability

1. Clinical symptoms of DVT 3 pts (points)
2. Alternate explanation less likely than PE 3 pts
3. Heart Rate > 100 1.5 pts
4. Immobilization or surgery within 4 weeks 1.5
5. Prior VTE 1.5 pts
6. Hemoptysis 1 pt
7. Malignancy 1 pt
>6High probability
2-6 Moderate
<2 Low.
Diagnostic modalities:
1. Chest X-ray
2. Peripheral wedge opacity
3. ECG : T wave inversion
4. ABG.
5. D-Dimer

4. Spiral CT and multislice CT have very good diagnostic

accuracy
5. Ventilation perfusion scan
6. Pulmonary angiography
1. US to diagnose DVT
Treatment:
Medical:
Supportive measures in ICU
Anticoagulation
Thrombolytic therapy
Surgery : Pulmonary embolectomy

Ischemia and Diabetic foot

Diabetic foot ulcer is a major complication of diabetes mellitus. It occurs in 15%
of all patients with diabetes and precedes 84% of all lower leg amputations. It is
due to the development of macro and micro vascular complications, including
failure of the wound healing process. Risk factors include diabetic neuropathy,
peripheral vascular disease, cigarette smoking, poor glycemic control, previous
foot ulcerations or amputations, diabetic nephropathy and retinopathy.
Wagner Grading System for Diabetic Foot Infections
0 - Intact Skin
1 - Superficial ulcer of skin or subcutaneous tissue
2 - Ulcers extend into tendon, bone, or capsule
3 - Deep ulcer with osteomyelitis, or abscess
4 - Gangrene of toes or forefoot
5 - Midfoot or hindfoot gangrene

characteristics

Diabetic foot (Neuropathic)

Ischemic foot

Skin temp.

Warm ( hot ) , hyperemic

Cold , pale

Pain.

Painless

Painful

Skin color.

No change

Dependent rubor (red)

Callous.

Thick at pressure points

May or may not present

Ulcer site

Plantar ulceration at pressure

At tips of toes/over pressure

points (sole) $
areas $
$

$
Peripheral pulse Preserved

Absent

Mixed (with ischemia and neuropathy infected ulcer is commonly present

The Ulcer:
- Site: very important to determine the cause of the ulcer, for example;
neuropathic ulcer in the sole and ischemic at tips of the toes and maleoli.
- Size, Shape
Above all examine
Edge: Usualy sloping or/and punched out
Margin: hyperemic, swollen, and black gangrenous patches or
hyperkeratotic areas may be found
Floor: infected granulations with necrotics
Base: felt only usually indurated and fixed to bone

- Discharge, granulation or necrotic tissues, surrounding tissues.

Neuropathic ulcer:
Site: the planter surfaces of the metatarsal heads and toes.
Ischemic ulcer: at the tips of toes and over pressure areas.
NB: Sometimes the ulcer becomes severely infected and extensive and it
is usually mixed (infective with ischemia and neuropathy).

Investigations
1) CBC: Anemia will increase symptoms due to deficient oxygenation.
2) Blood sugar: best is hemoglobin A1 C which reflects the control of diabetes in
last 3 months + Random& fasting blood sugar (RBS/FBS).
3) Lipid profile
4) Plasma fibrinogen & D-dimer.
5) ECG.
6) X-Rays of the foot to see evidence of osteomyelitis which is a common
complication.
7) Doppler to detect blood flow and measure blood pressure in the ankles and
perform ankle brachial pressure index (ABPI).
8) Exercise test:
Helps to establish the diagnosis of PAD.
A decreased in ABI of 15-20% after exercise
would be diagnostic of PAD if the resting ABI is
normal.
9) Toe-Brachial Index Measurement
- Calculated by dividing the toe pressure by the higher
of the two brachial pressures.
- Accurate when ABI values are not possible due to non-compressible
pedal pulses.
- TBI values 0.7 are usually considered diagnostic for lower extremity
PAD.

$
10)Segmental pressure measurement

$
11)Duplex can determine blood flow, changes in diameter of vessels
and gives a color coded curves of direction and velocity of blood
flow.
Predicting the location and severity of arterial disease in the lower
extremities
Distinguish between stenoses and occlusions.
Predicting access sites for intervention
Detect iatrogenic arterial injury after intervention.

$
12)Arteriography: invasive, only done if we are passing to do direct
arterial surgery as bypass to see the condition of vessels distal to
obstruction (distal run off).

Disadvantage of Arteriography:
Iodine allergy
Nephrotoxic
Exposure to irradiation
Arterial injury
No need to do culture from infected ulcers as the infection is
usually poly microbial, however, if infection is resistant do it
Treatment:
Control diabetes: by parentral insulin, starting by IV route.
Control HTN and hyperlipidemia.
Stop smoking
Antibiotic: Ciprofloxacin (quinolone) & Metronidazole (flagyl) or
third generation cephalosporines.
Debridement: Remove necrotic tissues, gangrenous sloughs and
hyperkeratotic parts.
Amputate the gangrenous parts.
Abscess incision & drainage.
Dressing: Use hygroscopic material (absorb water and helps
debridement) as honey or glycerin.
Off loading by special protective shoes.
Improve circulation: by anticoagulants, drugs increasing blood
flow and balloon intervention or even surgery.
Management of ischemia

Preclaudication: Patient presents with cardiac ischemia or severe ischemia in

one limb and we discover that the other limb is mildly ischemic
Conservative: Modification of atherosclerotic risk factors
1. Smoking cessation
smoking cessation is associated with improved walking distance in
some patients.
2. Weight reduction
Patients who are
overweight (BMI 25-30)
or obese (BMI >30)
should receive counseling for weight reduction by inducing carbohydrate
restriction and increased exercise.
3. Hyperlipidemia is Independent risk factors
for PAD which include elevated levels of
Total cholesterol
Total low-density lipoprotein (LDL)
Total triglycerides
Factors that are protective for the development of PAD are
elevated high-density lipoprotein (HDL)
4. Hypertention associated with a 2-3 fold
increased risk for PAD.
5. Diabetes increases the risk of PAD
approximately 3-4 fold.
Supervised exercise program.
Supervised walking on treadmill for 60 minutes or more
At least three times a week for three months.
Antiplatelet therapies
To decrease the risk of cardiovascular events and improve
survival.
Aspirin
Clopidogrel (Plavix)
Protect the foot by avoiding trauma and infection.
Claudication
If claudication is not disabling (the patient does not in need
prolonged walking) !conservative ttt as above.
Failure of conservative measures or disabling claudication (the
pattern of life of the patient requires prolonged walking) ! Limb

Revascularization !balloon dilatation and stenting, LASER or

Freezing.
Critical limb ischemia (CLI, Pregangrene) ( rest pain , ankle brachial index <
0.4, claudication distance < 50 meters)
The primary goals of the treatment are to
Relieve ischemic pain.
Heal ischemic ulcers
Prevent limb loss
Improve patient function and quality of life.
Prolong survival.
In order to achieve these goals, most patients will ultimately need a
revascularization procedure.
Treated by direct arterial surgery: as bypass, thrombo-endarterectomy or
angioplasty

Gangrene and Ulcer

Ulcer: in non diabetic do sympathectomy as vasodilatation will improve the skin
blood supply.
NB: in diabetic patients the patient does not need sympathectomy due to PN
and treatment of diabetic foot is described before.
Gangrene..
13)It is the end point of Neuro-Ischemic foot due to Macroangiopathy.

14)Mainly the big toe is involved.

15)Manifested as black discoloration and deeper tissue necrosis.
If only the artery is blocked:
1) Dry gangrene (dark, dry, hard, shrunken with clear
line of demarcation) wait for auto- amputation
then revise the line of amputation and reconstruct.
If both artery and vein are blocked, the blood will remain in the
vessels:
2) Wet gangrene (soft, swollen, infected, malodorous
without clear line of demarcation) amputation (2
times the initial amputation to avoid complications
of septic).
st
1 one just amputate the dead part ! wait the infection
complete disappear.
2nd stage: wait until the infection resolve and revise the line
of
amputation according to investigations.

SURGICAL INFECTION

Apply general sheet and if in the limbs (upper or
lower) apply ischemia (limb examination sheet)
1. ABSCESS

It is a localized collection of pus in a cavity;

This cavity may be:

1.

Formed by the proteolytic effect of the suppurative organism or

2.

Infected dead space after surgery (as after removal of tumor)

3.

Infected body cavity (intraperitoneal, intrathoracic, pelvic etc)

Organism:

Subcutaneous abscess, usually caused by staph aureus

NB Streptococcal infection usually causes diffuse inflammation (cellulitis).

Intra-abdominal infection is usually polymicrobial (aerobes &

anaerobes).

History

Pain early burning then throbbing, fever early continuous then hectic
and other constitutional symptoms as anorexia, headache, malaise and
rigors.

O/E

If the abscess is superficial: early diffuse stage (cellulitis stage) will be

hot red, tender and edematous.

After localization a swelling appear and it will be fluctuant (if small +ve
Paget test)

In the following sites dont depend on fluctuation as it will late and diagnose
abscess formation by throbbing pain, hectic fever, failure to respond to
antibiotics for 2 days (1 day in parotid & hand):
1. Hand and parotid (tight fascia severe pain and injury of vital structures)
2. Excess fat as fluctuation will be in advanced stage (breast & gluteal region)
3. Deep seated structures as subphrenic, pelvic, perinephric abscess (in such,
condition we depend mainly on US or even CT)
4. Peri-anal as delayed drainage will lead to fistula
Investigations: For any infection start by CBC, Blood sugar, culture and
sensitivity of aspirated or swapped pus, and if in the limbs investigate like
ischemia
Treatment

Surgical incision or US guided percutaneous drainage.

NB. Antibiotics are used before drainage and at least 2 days after disappearance
of fever

In small abscess we use topical or regional anesthesia and if large, deep,

peri-anal, most of hand infection we use general anesthesia

Incision must be in the most pointing and the most dependent area if are
not coincides we do 2 incisions (incision and counter incision as in breast
abscess)

Direction of incision must be with body creases (Langer lines to decrease

scarring)

If no creases as in limbs we do incision with direction of muscles

In axilla we do longitudinal incision to prevent closure when the arm is

adducted

After incision we have to divide all loculi to open any abscess spaces by
finger but in areas containing vital structures as parotid, hand, neck,
axilla, and groin we use artery or sinus forceps and we open it inside the
abscess cavity in 2 perpendicular directions (Hilton method)

In parotid abscess we open the forceps transversely only to avoid injury

of facial nerve

NB the drain must be put in the most dependent area or put more than one drain
In subcutaneous abscess we use gauze for: drainage, compression to avoid
bleeding and prevention of the incision from closure before complete cure
and usually removed after 48 hours
Intraperitoneal we use tube drain to be removed after 5-7 days
2.

Furuncle (boil):

Abscess in sweat gland/hair follicle. staph

3.

Carbuncle:

It is a type of infective gangrene (Skin necrosis of infectious origin, can occur

in kidney also).
Occurs in diabetics and patients with renal failure
Common site is the nape.
Caused by virulent staph aureus
Multiple furuncles are formed with suppurative extension to adjacent
subcutaneous tissue with thrombosis of blood vessels.
There are multiple small cavities containing pus and gangrenous tissues
Treatment by debridement and antibiotics against resistant staph with control of
diabetes by insulin
4.

Hand infection: for terminology see the following picture and

for CP, investigations, and treatment; see abscess

!
5.

Cellulitis:
Non suppurative inflammation of the subcutaneous tissues.
Caused mainly by streptococcus hemolyticus as it produces
hyalurinidase enzyme

May occur with staphylococcus infection (in diffuse stage of abscess but
soon localization occurs as staph secretes coagulase enzyme).
May be caused by gram negative bacilli in diabetics.
Clinically: burning pain, continuous fever and on examination the affected part is
red, hot, tender, with diffuse ill defined edge.
Treatment: antibiotics (see antibiotics) and hot foments
6.

Lymphangitis:

Usually associates other infections

Inflammation of the lymphatic channels

Streptococcal.

Red streaks +/- tender lymph nodes

7.

Erysipelas

Infection to the subcutaneous lymphatics plexus.

Predisposed by lymphatic obstruction.

Streptococcal.

The patient has marked toxemia and the affected part is bright red, hot,
tender, raised well defined edges.

Usually leads to lymphedema if recurrent

Treatment as cellulitis
8.

Pseudomembranous colitis

Inflammation of the large bowel due to antibiotic administration

Organism: clostridium difficle.
Clinically:

Watery non bloody diarrhea.

Abdominal pain.

Fever.

History of antibiotic intake: any type, any dose. Clindamycin is common

(used mainly in dental infection).

Diagnosis:

Stool analysis: bacteria, necrotics & WBC.

Sigmoidoscopy: white yellow pseudomembranes.

Treatment:

Stop the offending drug.

Metronidazol.

In resistant cases use vancomycin but cardiotoxic

9.

Wound infection

Superficial (75%):

Involves skin and subcutaneous tissue only

Deep:

Involves fascia, muscle, or into the abdominal cavity

Picture of infection appear starting from the 5th postoperative day with fever

Local signs of infection

Early diffuse as cellulites

Late pus is formed with swelling and pus may come between suture

Treatment by antibiotics and drainage (open sutures)

Classification of Surgical Wounds
Based on degree of contamination
1.

Clean

2.

Clean contaminated

3.

Contaminated

4.

Dirty

Class I (clean):

An uninfected surgical wound in which no inflammation is encountered

The respiratory, alimentary, genital or urinary tract is not entered.

Clean wounds are primarily closed

Hernia repair or thyroid surgery are examples.

1-5 % infection rate

Class II (clean/contaminated):

A surgical wound in which the respiratory, alimentary, genital, or urinary

tracts are entered under controlled conditions and without unusual
contamination

Elective colon resection with bowel prep

3-11% infection rate

Class III (contaminated):

Traumatic wounds, major break in sterile techniques, gross spillage of GI

contents, acute non-purulent inflammation.

Appendectomy, repair of gunshot wound to colon.

10-17% infection rate.

Class IV (dirty):

Old trauma wounds; devitalized tissue; existing clinical infection,

perforated viscera.

The organisms causing postoperative infection were present in the

surgical field before the surgery.

Hartmanns operation for diverticular perforation, abscess, peritonitis.

40% infection.

ANTIBIOTICS
Antibiotics are used on basis of culture and sensitivity test
Till the results of the test use empirical antibiotics against the
expected organism
For resistant staph use:
cloxacillin, flucloxacillin, methicillin
You may add clavulonic acid to amoxycillin (Amoxyclav as
Augmentin) or add salbectam to ampicillin (unacin)
However we can use also
Cephalosporines, quinolones, erythromycin or aminoglycosides
Streptococal infection
penicillins, amoxycillin, ampicillins and macrolides ( erythromycin,
xithromycin etc)
Anaerobes: met with peritonitis, oropharyngeal, if the source is colon
metronidazole, clindamycin or third generation cephalosporines
Gram negative organisms: usually mixed with anaerobes if the source is GIT
third generation cephalosporines, aminoglycosides, or quinolones
Biliary infection
aminoglycosides or third generation cephalosporines
Dental and oral infection
Abs against anaerobes
Tonsillitis
Abs against strept
Diabetic infection
polymicrobial infection so no value of culture we use ciprofloxacin
(flourinated Quinolone) and metronidazole
Severe infection: as in polytrauma, SIRS or peritonitis
use combination of: Metronidazole, third generation
cephalosporines and we can add aminoglycosides.
MRSA: Methicillin-Resistant Staphylococcus aureus
Most frequent a nosocomial pathogen
Usually resistant to several other antibiotics

 Treated by vancomycin (CARDIOTOXIC) or rifampicin (hepatotoxic)

CHEST DISEASES AND TRACHEOSTOMY

Never to take history or do examination of the chest diseases, without asking
about and examining the heart
Apply chest sheet and if the disease is due to trauma use the trauma sheet in
addition
In tension pneumothorax and cardiac tamponade, both may complicate
chest injury, the patient is shocked but neck veins are engorged, but in
tension pneumothorax the trachea is shifted and in cardiac tamponade is not
+ heart sound are muffled.
Diagnosis: dependent of CP+ Investigations
Investigations:
Blood gases; Po2, Pco2, O2 saturation, hemoglobin per cent as
anemia worsens the condition.
CBC: for anemia and Leukocytosis (if infection)
Chest x-ray to diagnose fracture ribs, pneumo or/and
hemothorax, effusion(TB, CA. infra diaphragmatic surgery or
pancreatitis), or empyema
Other diagnostic tools as CT, bronchoscopy, sputum examination
and culture
Thoracocentesis to know the nature of aspirate (blood, pus,
exudates, or transudate)
Remember that ultrasound can be a useful tool to diagnose a pneumothorax,
especially in a patient that must remain supine.

PNEUMOTHORAX

A tension pneumothorax should be diagnosed and treated based on your

history and physical exam, without waiting for radiographic imaging by
inserting wide pore canula in the second or 3rd IC space in mid clavicular
line to decrease tension the formal IC tube and under water seal..
A spontaneous pneumothorax
May be primary or secondary & caused by a ruptured emphysematous bleb

(bolus).
$
A schematic drawing of a bulla and a bleb, two lung abnormalities that may
rupture and lead to pneumothorax.

A primary spontaneous pneumothorax occurs in patients that have

no underlying pulmonary disease. It is most common in thin, young
males with a history of tobacco use.
A secondary spontaneous pneumothorax occurs in patients with an
underlying medical disease, such as COPD, cystic fibrosis, lung
cancer and Marfan's disease.
Presentation of both: sudden onset of sharp chest pain, often unilateral,
occasionally the pain is more prominent in the back and shoulder.
Dyspnea, which increases over time as the pneumothorax increases
in size.
Cough, which is usually dry.
Vital signs: tachycardia, tachypnea and, depending on the severity,
hypoxia and hypotension.
Iatrogenic (commonest type) and traumatic pneumothorax:

Present in a clinically similar manner, but after trauma or interventional

procedure.
Traumatic pneumothorax in both penetrating and blunt trauma
( with fracture ribs).
Iatrogenic the most common procedures to cause a pneumothorax
include a central line, thoracentesis, pacemaker, tracheostomy or
biopsy. Other causes include CPR and positive-pressure ventilation.
A tension pneumothorax is is due to valvular external wound or lung tear
allowing air to enter pleural cavity without escape.
The classic presentation will be a patient in distress with tachycardia,
tachypnea, hypotension (shock with engorged neck veins and tracheal shift)
and hypoxia.
A traumatic tension pneumothorax develops quickly, but other causes, such
as positive pressure ventilation, occur gradually.
Definitive ttt: Intercostal tube in 5th ICS mid axillary line.
EMPYEMA THORACIS
May be acute or chronic
Causes:
With Bronchopneumonia= synpneumonic or
After lobar pneumonia= met pneumonic
Suppurative lung diseases as abscess, bronchiectasis,
Infected hemothorax,
Subphrenic abscess or post operative
Symptoms: of pleural empyema may vary in severity. Typical symptoms include:
cough, fever, chest pain, sweating and shortness of breath.[2]
Clubbing may be present in cases of a chronic nature. There is a dull percussion
note and reduced breath sounds on the affected side of the chest. Other diagnostic

tools include a blood white cell count, chest x-ray, CT scan, and ultrasonography
and thoracocentesis.
Treatment
Drainage of the pus iserting A chest tube may be inserted, often using ultrasound
guidance. Intravenous antibiotics are given.
If this is insufficient, surgical debridement of the pleural space may be required.
using video-assisted thoracoscopic techniques but if the disease is chronic,
thoracotomy to fully drain the pus and remove the fibrinopurulent exudate from
the lung and from the chest wall.
Hemothorax
Cause and presentation
Its cause is usually traumatic, from a blunt (with fracture ribs) or penetrating
injury but it may be pathological (usually malignant hemorrhagic effusion).
Source of bleeding: Intercostal arteries, lung injury (low pressure Vs) or major
vessels or heart (fatal).
thorax can hold 3040% of a person's blood volume. Even minor injury to the
chest wall can lead to significant hemothorax
Signs and symptoms: history of trauma with
Tachypnea
Dyspnea
Cyanosis
Decreased or absent breath sounds on affected side
Tracheal deviation to unaffected side if massive
Dull resonance on percussion
Unequal chest movement
Shock according to degree of blood loss.
Management:
Small amount, aspiration and follow up by x-rays.
Moderate amount: IC tube with under water seal, persistent bleeding or
massive bleeding from the start indicates thorcotomy, secure bleeders, + IC tube
and underwater seal.

Clotted blood if early inject thrombolytic and if fibrosed decortications of

pleura.

AIRWAYS IN RESPIRATORY OBSTRUCTION

1. Endotracheal tube
2. Oropharyngeal tube
3. Cricothyrotomy
4. Tracheostomy surgical or percutaneous (using sequential dilators)
5. Wide bore cannulation if there is no other facility

Tracheostomy
(Tracheotomy)
Apply general case sheet and you will be asked about the connections to the
patient
Mostly no history if the patient can't speak (you may ask his relatives)
Tracheotomy

Completed tracheotomy:
1 - Vocal folds
2 - Thyroid cartilage
3 - Cricoid cartilage
4 - Tracheal rings
5 - Balloon cuff

Indications:
Obstruction of the larynx or upper trachea by
1. Tumor
2. Impacted FB
3. Laryngeal edema (allergic, postoperative
4. Burn or trauma to head and neck specially with maxillofacial
nerve injury)
5. Thyroid surgery: bilateral RLNs injury or hematoma after
thyroidectomy, in such you can start by Cricothyrotomy (a tube
or even wide bore canula, inserted through a surgical opening
in the cricothyroid membrane through small incision just
above the cricoid cartilage).
6. Comatosed patient with GCS<8
7. Ventilated patient to decrease dead space and for easier care
than endotracheal tube.
Surgical instruments

$
Tracheostomy tube (The bottom item is a guide to help aid insertion)
Longitudinal incision in skin about inch above suprasternal notch, open
platysma, pretracheal muscles are separated and retracted laterally, thyroid
isthmus is divided between clamps, inverted U shaped incision is done in

tracheal rings 2-5 the flap is raised up and the 1st tube is applied and its wings are
sutured to skin. The other tube is then applied.
Care of tracheostomy:
Use humidified O2 to avoid dryness of secretions
Frequent removal of the inner tube and wash it
Aspirate any secretions: most important
Apply local mucolytics to avoid formation of mucus plugs
Dressing of its wound
Complications:
1. Bleeding from superficial veins (minor) or Ima artery (passing to
isthmus)
2. Obstruction: see care of tracheostomy
3. Infection of wound or respiratory tract
4. Tracheal Stenosis
5. Pressure necrosis with trachea-esophageal, pleural (lead to
pneumothorax)
6. Granuloma, a growth of inflammatory tissue, which is caused by the
irritation of the airway by the tracheostomy tube
CRICOTHYROTOMY
A cricothyrotomy (also called thyrocricotomy, cricothyroidotomy, inferior
laryngotomy, intercricothyrotomy, coniotomy or emergency airway
puncture) is an incision made through the skin and cricothyroid membrane to
establish a patent airway during certain life-threatening situations, such as airway
obstruction by a foreign body, angioedema, or massive facial trauma.
Cricothyrotomy is nearly always performed as a last resort in cases where
orotracheal and nasotracheal intubation are impossible or contraindicated.
Cricothyrotomy is easier and quicker to perform than tracheotomy, does not
require manipulation of the cervical spine, and is associated with fewer
complications.[1] However, while cricothyrotomy may be life-saving in extreme
circumstances, this technique is only intended to be a temporizing measure until a
definitive airway can be established
Procedure

$
$
In cricothyrotomy, the incision or puncture is made through the cricothyroid
membrane in between the thyroid cartilage and the cricoid cartilage.
Technique

$
$
Cricothyrotomy kit
Surgical procedure
In a typical cricothyrotomy procedure, a scalpel is used to create a 1 cm vertical
incision through the skin and the cricothyroid membrane, and the resulting hole is
opened by either inserting the scalpel handle into the wound and rotating 90
degrees or by using a clamp. A tracheostomy tube or endotracheal tube with a 6 or
7 mm internal diameter is then inserted, the cuff is inflated, and the tube is
secured.

BLUNT TRAUMA TO LEFT HYPOCHONDRIUM

IN RIGHT SIDE THE LIVER IS INJURED INSTEAD OF SPLEEN
What are the priorities of management of this patient?
A: Airway
B: Breathing (exclude tension pneumothorax)

Tension pneumothorax is diagnosed without investigations if there are:

Respiratory Distress
Mediastinal Shift
Engorged neck veins and hyper resonant chest

Immediate Decompression Is Life Saving By Insertion Of Wide Bore Needle To The

Second Or Third Intercostal Space Just Above The Rib In Mid-Clavicular Line).

$
C: Circulation

Note that this patient is hypotensive in recumbent position (Class III

hemorrhage)
Apply 2 venous lines (canulas) and start crystalloid infusion (RL)
Take blood sample for cross matching for blood transfusion in hospital.
D: Disability
Examine for associated neurological or musculoskeletal injuries (if fracture
splint)

$
E: Exposure and Environment: Examine patient from head to toe to detect
associated injuries.
Adjuncts of primary survey
F: Foleys catheter, contraindicated if bloodcomes from penis or perineal
hematom: To collect urine for
Monitoring shock (normal urine flow 1/2 -1.5 ml/minute)
Keeping patient dry and
Detect Hematuria.
G: Nasogastric tube (contraindicated in mid facial injury) for:

Suction;
prophylactic against ileus
detect stress ulceration
prevent vomiting and aspiration
Feeding;
Transfer the patient to the hospital
And perform 2ry survey

2. What are the structures expected to be injured from this trauma?

Spleen !internal haemorrhage
Extra peritoneal rupture of left kidney!Hematuria and
retroperitoneal hematoma
Colon, peritonitis will develop within hours
Fracture lower ribs with hemo or/and pneumothorax.
In this case picture of shock and peritoneal irritation is
suggestive of rupture spleen or liver
Hematuria is suggestive of rupture kidney
And respiratory manifestations are suggestive of fracture
lower ribs with hemo/pneumothorax
ADJUNCTS TO SECONDARY SURVEY

Investigations must be performed with simultaneous resuscitation

1. CBC: Leukocytosis and low hematocrit may be found (Lowered
hematocrit can imply significant hemorrhage)
2. CXR: to detect fracture ribs and hemo/pneumothorax.
3. FAST; Focused Assessment with Sonography for Trauma: Is a rapid
bedside ultrasound examination performed as a screening test for blood
around the heart or abdominal organs after trauma.
NB: The four classic areas that are examined for free fluid are the perihepatic
space (Morison's pouch or the hepatorenal recess), peri splenic space,
pericardium, and the pelvis. The extended FAST (eFAST) allows for the
examination of both lungs by adding bilateral anterior thoracic sonography to the
FAST exam which the detection of pneumothorax with good sensitivity
4. CT scanning: if FAST is not conclusive
5. Angiography or Tc scanning if undetermined source of bleeding.

6. Technetium (Tc) scan (blood pool labeling).

7. DPL; diagnostic peritoneal lavage: if you are in doubt about the
nature of peritoneal collection.
8. IVU, only done if operation is indicated to see the function of other
kidney if the possibility of nephrectomy of the injured kidney is
found

The definitive management of this patient

Chest: Intercostal tube (at fifth intercostal space mid-axillary line )
connected to underwater seal.
Abdominal injury: Conserve if s even suspected rupture kidney, liver
or spleen as long as the patient is hemodynamically stable with blood
transfusion.
Exploration is indicated if there is hemodynamic instability and
during operation we have to preserve spleen to avoid post
splenectomy sepsis by compression of superficial tears, suturing deep
tears, do partial splenectomy or wrap the spleen by mesh if
fragmented and rarely we need splenectomy.
Control of bleeding from the liver is better than spleen however
unstability indicates surgery with repair of tears, or Pringle maneuver
(compress free margin of lesser omentum which contains CBD ,PV,
and HA between thumb and index to control bleeding and facilitate
repair , partial resection if fragmented part, the last resort is backing
Failure of conservative treatment in rupture kidney indicates
exploration (anterior approach) and retro peritoneal hematoma is only
opened if expanding or pulsating.
The kidney must be preserved as in spleen and nephrectomy is the
last resort if uncontrollable hemorrhage.

Colonic injury requires colostomy to be followed by repair

Small intestine repair or resect and anastomosis