SURGERY

By Dr.Mohammad Z. abu sheikha@

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 Shock
-Shock - Is a systemic state of low tissue perfusion which is inadequate for normal cellular respiraton. With insufficient delivery
of oxygen and glucose, cells switch from aerobic to anaerobic metabolism. If perfusion is not restored in a timely fashion, cell
death ensues
+Pathophysiology Of Shock :
1) At first there is peripheral vasoconstriction to maintain perfusion to vital organs (brain, heart, liver and kidneys)
2) Vasoconstriction: about 70% of blood is present in the veins so vasoconstriction pushes more blood into the dynamic
circulation, causing tachycardia & helps to maintain COP (except in sepsis)
+Vasoconstriction is mediated by (activation of alpha adrenergic receptors on the arterioles)
3) Respiration: minute ventilation ↑ by 1.5-2 times & the respiratory rate ↑ 2:3 times to maintain oxygenation (except in
cardiogenic shock & pulmonary edema)
4) Hypoxia: results in anaerobic metabolism and accumulation of lactic acid  metabolic acidosis. This will affect Na/K pump
and may lead to cellular edema (Hypoxia at the cellular level decreases ATP production, and this result in changes in
intracellular calcium signaling)
5) There is activation of renin-angiotensin system with production of angiotensin and aldosterone leading to vasoconstriction,
salt & water retention (increased sodium and water reabsorption by the kidney) and ↓ of GFR
+Renal: decreased perfusion pressure in the kidney leads to reduced filtration at the glomerulus and a decreased urine output.
6) Release of ADH causing ↓ of urine volume (water and sodium losses) and ↑ in its concentration (Mesenteric
vasoconstriction is seen as a result of this increased level of ADH)
7) Neuroendocrine response with production of ACTH, GR, corticosteroids and glucagon  result in ↑ blood sugar, Na & water
retention
8) Microcirculatory changes: there is inadequate tissue perfusion, leak of plasma from the capillaries, build-up of lactic acid and
CO2, sludging of blood with red cell aggregation. Later several coagulation factors may be consumed leading to DIC which leads
to tendency to bleed
9) End-stage:
a) cerebral hypoxia: agitation, restlessness, followed by confusion and coma
b) diminished coronary blood flow leading to HF
c) diminished renal blood flow leading to oliguria & finally to acute tubular necrosis
-Classification Of Shock :
.hypovolemic (M.C type)
.septic
.cardiogenic
.neurogenic
.anaphylactic
-Signs & Symptoms :
st
.tachycardia (1 sign)
.hypotension (most dangerous sign) (documented in septic shock and neurogenic shock)
.decreased pulse pressure
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.poor urine output

.decreased mental status (most important sign – best indicators of tissue perfusion)
.pale
.diaphoretic (sweating)
.tachypnea
.poor capillary refill
-Laps :
.ABGs (acidosis associated with inadequate tissue perfusion)
.KFT
.BUN (blood urea nitrogen)
+The initiating event in shock are (driven by tissue hypoperfusion and the developing cellular energy deficit)
+Bleeding in abdomen or chest can cause (shock) – but intracranial bleeding (don't cause shock)
+Neuroendocrine response of shock is hypothermia
+Tumor necrosis factor alpha (TNF-a) – Cytokines is released immediately after major injury
+Base deficit can be used to indirectly estimate the oxygen debt incurred during shock
+Recent data in trauma patients suggest that a systolic blood pressure (SBP) of less than 110mmHg is a clinically relevant
definition of hypotension and hypoperfusion based upon an increasing rate of mortality below this pressure

+Base deficit classified as :

.mild (-3 to -5mmol/L)
.moderate (-6 to -9mmol/L)
.severe (< -10mmol/L)

*Hypovolemic Shock
-Is an emergency condition in which severe blood and fluid loss make the heart unable to pump enough blood to the body. This
type of shock can cause many organs to stop working (reduced circulating volume) (Hypovolemia may be due to hemorrhagic or
non-hemorrhagic causes) or; Is decreased intravascular volume (third space loss, such as hemorrhage, diarrhea, vomiting,
drugs)
-Signs & Symptoms :
.tachycardia (M.C vital sign-change associated with hypovolemic shock)
.thirst and dry mouth
.hypothermia (cold skin), pale skin
.confusion
.decreased or no urine output
.sweating
.tachypnea
.low Bp, low body temperature, rapid pulse (often weak and thready)
-Causes :
th
.hemorrhage (losing about a 5 or more of the normal amount of blood in your body) - crush injury
.non-hemorrhage (poor fluid intake – dehydration, excessive fluid loss due to vomiting, diarrhoe or urinary loss – diabetes,
evaporation, third-spacing – where fluid is lost into the gastrointestinal tract and interstitial spaces, as for example in bowel
obstruction or pancreatitis)
+The amount of circulating blood in your body may drop when you lose too many other body fluids. This can be due то (burns,
diarrhea, excessive perspiration, vomiting)
+spacing occurs when too much fluid moves from the intravascular space (blood vessels) into the interstitial or "third" space -
the non functional area between cells
+Why does decreased pulse pressure occur with early hypovolemic shock ?
.because of vasoconstriction, resulting in an elevated diastolic Bp
-Complications :
.kidney damage (acute liver insufficiency)
.brain damage
.lung (acute respiratory distress syndrome)
.gangrene of arms or legs
.cardiac (cardiovascular failure)
.clotting (coagulopathy)
.death
-Investigations :
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.blood chemistry, CBC

.CT-scan, U/S, X-ray, ECHO
.endoscopy and/or colonoscopy
.Rt. heart (Swan-Ganz) catheterization
.urinary catheterization (tube placed into the bladder to measure urine output)
-Treatment :
.keep the Pt. confortable and warm (to avoid hypothermia)
.IV fluids
.medications (dopamine, dobutamine, epinephrine, norepinephrine) may be needed to increase Bp and the amount of blood
pumped out of the heart (cardiac output)
+Do not give fluids by mouth
+If person is having an allergic reaction, treat the allergic reaction, if you know how
+If the person must be carried, try to keep him or her flat, with the head down and feet lifted. Stabilize the head and neck
before moving a person with a suspected spinal injury
*Septic Shock
-Is a serious medical condition that occurs when sepsis, which is organ injury or damage in response to infection, leads to
dangerously low blood pressure (hypotension) and abnormalities in cellular metabolism
+Septic shock is a subclass of distributive shock, a condition in which abnormal distribution of blood flow in the smallest blood
vessels results in inadequate blood supply to the body's tissues, resulting in ischemia and organ dysfunction. Septic shock refers
specifically to distributive shock due to sepsis as a result of infection
+Is a documented infection and hypotension
+The primary infection is most commonly by bacteria, but can also be by fungi, viruses, or parasites, and can be located in any
part of the body, but most commonly in the lungs, brain, urinary tract, skin, or abdominal organs
+M.C is gram-negative septicemia (E.coli) / Less common is gram-positive septicemia, fungus
-Signs & Symptoms :
+Initial - vasodilation (resulting in warm skin)
.full pulses
.normal urine output
+Delayed - vasoconstriction and poor urine output
.low Bp
.mental status changes
.hypotension
.myocardial dysfunction
+Other
.tachypnea
.tachycardia
.fever or hypothermia
3 3
.low WBC (<4000 cells/mm ) or high WBC (12000 cells/mm )
.positive blood culture (evidence of infection)
.signs of pneumonia on CXR
.signs of end organ dysfunction are present (kidney failure, liver dysfunction, changes in mental status, high lactate)
-Factors increase the susceptibility to septic shock (any mechanism that increases susceptibility to infection) :
.trauma
.corticosteroids
.hematologic disease
.diabetes
.immunosuppression
+Its M.C victims are children, immunocompromised individuals, and the elderly
-Complications :
.multiple organ dysfunction syndrome (known as multiple organ failure)
.DIC
.death
+Septic shock can be regarded as a stage of SIRS (Systemic Inflammatory Response Syndrome), in which sepsis, severe sepsis
and multiple organ dysfunction syndrome (MODS) represent different stages of a pathophysiological process. If an organism
cannot cope with an infection, it may lead to a systemic response - sepsis, which may further progress to severe sepsis, septic
shock, organ failure, and eventually result in death
-Lab Findings :
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.hyperglycemia, glycosuria, respiratory alkalosis (early)

.leukocytosis, acidosis, elevated lactic acid (late)
+Septic shock is diagnosed if there is refractory hypotension (low blood pressure that does not respond to treatment). This
means that intravenous fluid administration alone is not enough to maintain a patient's blood pressure
+Septicemia may be present but septic shock can occur without septicemia
+The precipitating infections which may lead to septic shock if severe enough include, but are not limited to, appendicitis,
pneumonia, bacteremia, diverticulitis, pyelonephritis, meningitis, pancreatitis, necrotizing fasciitis, and mesenteric necrosis
-Treatment :
.fluid resuscitation is an initial treatment to increase blood volume
+Crystalloids such as (normal saline and lactated Ringer's solution) are recommended as the initial fluid of choice
.antibiotics within the first hour following recognition of septic shock
.antimicrobial therapy
+Among the choices for vasopressors, norepinephrine is superior to dopamine in septic shock. Norepinephrine is the preferred
vasopressor, while epinephrine can be added to norepinephrine when needed. Low-dose vasopressin may also be used as an
addition to norepinephrine, but is not recommended as a first-line treatment. Dopamine can cause rapid heart rate and
arrhythmias, and is only recommended in combination with norepinephrine in those with slow heart rate and low risk of
arrhythmia. In the initial treatment of hypotension in septic shock, the goal of vasopressor treatment is a mean arterial
pressure (MAP) of 65 mm Hg
+Causes Of Septic And Vasodilatory Shock :
.systemic response to infection
.noninfectious systemic inflammation (pancreatitis, burns)
.anaphylaxis
.acute adrenal insufficiency
.prolonged, severe hypotension (hemorrhagic shock, cardiogenic shock, cardiopulmonary bypass)
.metabolic (hypoxic lactic acidosis, carbon monoxide poisoning)

*Cardiogenic Shock
-Is a cardiac insufficiency; left ventricular failure (usually), resulting in inadequate tissue perfusion
+Is when the heart has been damaged so much that it is unable to supply enough blood to the organs of the body
-Signs & Symptoms :
.pulsus alternans (increased pulse with greater filling following a weak pulse or absent pulse)
.signs on CXR (pulmonary edema)
-Causes :
.MI (heart attack)
.papillary muscle dysfunction
.massive cardiac contusion
.cardiac tamponade
.tension pneumothorax
.cardiac valve failure
+M.C.Cs are serious heart complications. Many of these occur during or after a heart attack (MI). These complication include :
.rupture of the heart muscle
.heart rhythms (ventriculat tachycardia, centriculat fibrillatio or supraventricular tachycardia)
.pericardial tamponade
.bradycardia or problem with the electrical system of the heart block
-Treatment :
.medicines to increase blood pressure and improve heart function (Dobutamine, Dopamine, Epinephrine, Levosimendan,
Milrinone, Norepinephrine) (These medicines may help in the short-term. They are not often used for a long time)
.Cardiac catheterization with coronary angioplasty and stenting
.Heart monitoring to guide treatment
.Heart surgery (coronary artery bypass surgery, heart valve replacement, left ventricular assist device)
.Intra-aortic balloon counterpulsation (IABP) to help the heart work better
.Pacemaker

*Neurogenic Shock
-Is a inadequate tissue perfusion from loss of sympathetic vasoconstrictor tone
+Is a distributive type of shock resulting in low blood pressure, occasionally with a slowed heart rate, that is attributed to the
disruption of the autonomic pathways within the spinal cord
+The best describes the hemodynamic response to neurogenic shock is (Increased cardiac index, unchanged venous
capacitance)
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+It can occur after damage to the central nervous system such as spinal cord injury
-Signs & Symptoms :
.bradycardia (only in neurogenic shock)
.hypotension
.increased heart rate
.tachypnea
.normal pulse pressure
.decreased diastolic Bp
.warm
.priapism (due to vasodilation)
.neurologic deficit suggesting cord injury (associated findings)
rd
+If the injury is above the 3 cervical vertebra, the patient will go into respiratory arrest immediately following the injury, due
to loss of nervous control of the diaphragm
-Causes :
.spinal cord injury (M.C.C) (complete transection of partial cord injury with spinal shock, spinal anesthesia)
+You MUST rule out in a trauma Pt. who has what you think is spinal shock (Hemorrhagic shock)
+Severe central nervous system damage (brain injury, cervical or high thoracic spinal cord). This causes them to relax
(vasodilation) resulting in a sudden decrease in blood pressure (secondary to a decrease in peripheral vascular resistance)
th
+Neurogenic shock results from damage to the spinal cord above the level of the 6 thoracic vertebra
-Treatment :
.Dopamine (Intropin)
.Vasopressin (antidiuretic hormone ADH)
.Certain vasopressors (ephedrine, norepinephrine). Phenylephrine may be used as a first line treatment, or secondarily in
people who do not respond adequately to dopamine
.Atropine (is administered for slowed heart rate)

*Anaphylactic Shock
-Is a serious allergic reaction that is rapid in onset and may cause death. It typically causes more than one of the following (an
itchy rash, throat or tongue swelling, shortness of breath, vomiting, lightheadedness, and low blood pressure)
+Symptoms typically come on over minutes to hours (with an average onset of 5 to 30 minutes if exposure is intravenous and 2
hours if from eating food)
-Signs & Symptoms :
.skin rash & itchiness
.flushing, or swelling (angioedema) of the afflicted tissues
.swelling of the tongue or throat occurs in up to about 20% of cases
.runny nose and swelling of the conjunctiva
.the skin may also be blue tinged because of lack of oxygen
.respiratory (shortness of breath, wheezes, or stridor)
.cardiovascular (coronary artery spasm may occur with subsequent myocardial infarction, dysrhythmia, or cardiac arrest,
Bezold–Jarisch reflex (hypopnea), slow heart rate, low blood pressure, feeling of lightheadedness or loss of consciousness)
.Gl symptoms (crampy abdominal pain, diarrhea, and vomiting)
.loss of bladder control or pelvic pain similar to that of uterine cramps
.dilation of blood vessels around the brain may cause headaches
.feeling of anxiety or of "impending doom"
+The M.C areas affected include: skin (80–90%), respiratory (70%), gastrointestinal (30–45%), heart and vasculature (10–45%),
and central nervous system (10–15%
-Causes :
.venom from insect bites or stings
.foods (food additives such as monosodium glutamate and food colors)
.medication
.biological agents (semen, latex, hormonal changes)
.six vaccines (MMR, varicella, influenza, hepatitis B, tetanus, meningococcal) are recognized as a cause for anaphylaxis, and HPV
may cause anaphylaxis as well
+The M.C medications are (β-lactam antibiotics - such as penicillin, followed by aspirin and NSAIDs, during anesthesia,
neuromuscular blocking agents, latex, vancomycin, morphine, x-ray contrast)
-Risk Factors :
.people with atopic diseases such as asthma, eczema, or allergic rhinitis are at high risk of anaphylaxis from food, latex, and
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radiocontrast
.mastocytosis or of a higher socioeconomic status
-Treatment :
.Epinephrine (adrenaline) is the primary treatment for anaphylaxis
.Antihistamines (both H1 and H2)
.Nebulized salbutamol (may be effective for bronchospasm that does not resolve with epinephrine)
.Methylene blue (used in those not responsive to other measures due to its presumed effect of relaxing smooth muscle)
+Medications
.benadryl (allerfin)
.aminophylline
.steroids
.epinephrine (adrenaline)

+Obstructive Shock
In obstructive shock rhere is a reduction in preload due to mechanical obstruction of cardiac filling. Common causes of
obstructive shock include (cardiac tamponade, tension pneumothorax, massive pulmonary embolus or air embolus). In each
case, there is reduced filling of the left and/or right sides of the heart leading to reduced preload and fall in cardiac output
+Distributive Shock
Describes the pattern of cardiovascular responses characterising a variety of conditions, including (septic shock, anaphylaxis and
spinal cord injury)
+Endocrine Shock
May present as a combination of hypovolemic, cardiogenic or distributive shock. Causes of endocrine shock include (hypo and
hyperthyroidism and adrenal insufficiency)

Clinical Features Of Shock

Compensated Mild Moderate Severe

Lactic Acidosis + ++ ++ +++
Urine Output Normal Normal Reduced Anuric
Conscious Level Normal Mild anxiety Drowsy Comatose
Respiratory Rate Normal Increased Increased Laboured
Pulse Rate Mild increase Increased Increased Increased
Blood Pressure Normal Normal Mild hypotension Severe hypotension

Cardiovascular and characteristics of Shock

Hypovolemia Cardiogenic Obstructive Distributive

Cardiac output Low Low Low High
Vascular resistance High High High Low
Venous pressure Low High High Low
Mixed venous Low Low Low High
saturation
Base deficit High High High high

Hemodynamic Responses To Different Types Of Shock

Cardiac SVR Venous CVP/PCWP Svo2 Cellular/Metabolic

index Capacitance Effects
Hypovolemic Decreased Increased Decreased Decreased Decreased Effect
Septic Increased+ Decreased Increased Increased/Decreased Increased/Decreased Cause
Cardiogenic Decreased+ Increased+ Dilation Increased Decreased Effect
Neurogenic Increased Decreased Dilation Decreased Decreased Effect

Inflammatory Mediators Of Shock

Proinflammatory Anti-inflammatory
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Interleukin-1a/b Interleukin-4
Interleukin-2 Interleukin-10
Interleukin-6 Interleukin-13
Interleukin-8 Prostaglandin E2
Interferon TGFb
TNF
PAF

+Central Venous Pressure CVP (normal CVP is 2-6 Hg) :

.elevated by (overhdration which increases venous return, heart failure or PA stenosis, MI, positive pressure breathing,
straining)
.decreases with (hypovolomic shock from hemorrhage, spinal cord injury, fluid shift, dehydration, negative pressure breathing)
By Dr.Mohammad Z. abu sheikha@

HEMORRHAGE
Hemorrhage must be recognised and managed aggressively to reduce the severity and duration of shock and avoid death and/
or multiple organ failure. Haemorrhage is treated by arresting the bleeding – not by fluid resuscitation or blood transfusion.
Although necessary as supportive measures to maintain organ perfusion, attempting to resuscitate patients who have ongoing
haemorrhage will lead to physiological exhaustion (coagulopathy, acidosis and hypothermia) and subsequently death
-Pathophysiology :
.hemorrhage leads to a state of hypovolemic shock. The combination of tissue trauma and hypovolemic shock leads to the
debelopment of an endogenous coagulopathy called acute traumatic coagulopathy (ATC)
+Ongoing bleeding with fluid and red blood cell resuscitation leads to a dilution of coagulation factors which worsens the
coagulopathy
+In a patient with ongoing hemorrhage, the risk of death increases 1% every 3 minutes in the ER
+Haemorrhage may be revealed or concealed
.Revealed haemorrhage is obvious external haemorrhage, such as exsanguination from an open arterial wound or from massive
haematemesis from a duodenal ulcer
.Concealed haemorrhage is contained within the body cavity and must be suspected, actively investigated and controlled. In
trauma, haemorrhage may be concealed within the chest, abdomen, pelvis, retroperitoneum or in the limbs with contained
vascular injury or associated with long-bone fractures. Examples of non-traumatic concealed haemorrhage include occult
gastrointestinal bleeding or ruptured aortic aneurysm
+Primary haemorrhage is haemorrhage occurring immediately due to an injury (or surgery)
+Reactionary haemorrhage is delayed haemorrhage (within 24 hours) and is usually due to dislodgement of clot by
resuscitation, normalisation of blood pressure and vasodilatation. Reactionary haemorrhage may also be due to technical
failure, such as slippage of a ligature
+Secondary haemorrhage is due to sloughing of the wall of a vessel. It usually occurs 7–14 days after injury and is precipitated
by factors such as infection, pressure necrosis (such as from a drain) or malignancy

Traditional Classification Of Hemorrhagic Shock

Class 1 Class 2 Class 3 Class 4

Blood volume lost as <15% 15-30% 30-40% >40%
percentage of total

+class 1 (hemorrhage - <15% or 750cc blood loss) (mild anxiety, normal vital signs)
+class 2 (hemorrhage – 15%-30% or 750-1500 cc blood loss) (normal systolic Bp, low pulse pressure, tachycardia, tachypnea,
anxiety)
+class 3 (hemorrhage – 30%-40% or 1500-2000 cc blood loss) (low Bp, low pulse pressure, tachycardia ‘heart rate >120’,
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tachypnea ‘respiratory rate >30’, confusion)

+class 4 (hemorrhage - >40% or >2000cc blood loss) (low Bp, low pulse pressure, tachycardia ‘heart rate >140’, tachypnea
‘respiratory rate >35’, confusion and lethargic, no urine output)

Signs And Symptoms Of Advancing Stages Of Hemorrhagic Shock

Class I Class II Class III Class IV

Blood loss (mL) Up to 750 750-1500 1500-2000 >2000
Blood loss (%) Up to 15% 15-30% 30-40% >40%
Pulse rate <100 >100 >120 >140
Blood pressure Normal Normal Decreased Decreased
Pulse pressure Normal or Increased Decreased Decreased Decreased
(mmHg)
Respiratory rate 14-20 20-30 30-40 >45
 Urine output (mL/h) >30 20-30 5-15 Negligible
CNS/mental status Slightly anxious Midly anxious Anxious and Confused Confused and
Lethargic

By Dr.Mohammad Z. abu sheikha@

BLOOD TRANSFUSION
-Thrombocytopenia (low platelet count <100.000)
-Common Causes Of Thrombocytopenia In The Surgical Pt. :
.sepsis
.H2 blockers, heparin, antibiotics
.massive transfusion
.DIC
.spurious lab value
.Swann-Ganz catheter
-Indications For Blood Transfusion :
.acute blood loss, to replace circulating volume and maintain oxygen delivery
.perioperative anemia, to ensure adequate oxygen delivery during the perioperative phase
.symptomatic chronic anemia, without hemorrhage or impending surgery
-The Symptoms Of A Transfusion Reaction :
.fever (What Component Of The Blood Transfusion Can Cause A Fever ? ans. Is WBC)
.chills
.nausea
.hypotension
.lumbar pain
.chest pain
.abnormal bleeding
-Treatment For Transfusion Hemolysis :
.stop transfusion
.provide fluids
.perform diuresis (lasix) to protect kidneys
.alkalinize urine (bicarbonate)
.give vasopressor as needed
-Each Unit Is Tested For Evidence Of :
.hepatitis B
.hepatitis C
.HIV-1, HIV-2
.syphilis
-Complications From A Single & Massive Transfusion :
A) Complications from a single transfusion include:
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• incompatibility haemolytic transfusion reaction

• febrile transfusion reaction
• allergic reaction
• infection
.bacterial infection (usually due to faulty storage)
.hepatitis
.HIV
.malaria
• air embolism
• thrombophlebitis
• transfusion-related acute lung injury (usually from FFP).
B) Complications from massive transfusion include:
• coagulopathy
• hypocalcaemia
• hyperkalaemia
• hypokalaemia
• hypothermia
+In addition, patients who receive repeated transfusions over long periods of time (e.g. patients with thalassaemia) may
develop iron overload. (Each transfused unit of red blood cells contains approximately 250 mg of elemental iron)
+Donations are leukodepleted as a precaution against variant Creutzfeldt–Jakob disease
+Packed red cells (Packed red blood cells are spun-down and concentrated packs of red blood cells. Each unit is approximately
330 mL and has a haematocrit of 50–70 per cent. Packed cells are stored in a SAG-M solution (saline-adenine-glucose mannitol)
to increase shelf life to 5-6 weeks at 2–6°C. (Older storage regimens included storage in CPD – citrate-phosphate-dextrose
solutions which have a shelf life of 2–3 weeks)
+Fresh-frozen plasma (Fresh-frozen plasma (FFP) is rich in coagulation factors and is removed from fresh blood and stored at
−40 to −50°C with a two-year shelf life. It is the first-line therapy in the treatment of coagulopathic haemorrhage. Rhesus D-
positive FFP may be given to a rhesus D-negative woman although it is possible for seroconversion to occur with large volumes
due to the presence of red cell fragments, and rhesus D immunization should be considered)
+Cryoprecipitate (Cryoprecipitate is a supernatant precipitate of FFP and is rich in factor VIII and fibrinogen. It is stored at −30°C
with a two years shelf life. It is given in low fibrinogen states or factor VIII deficiency)
+Platelets (Platelets are supplied as a pooled platelet concentrate and contain about 250 × 109/L. Platelets are stored on a
special agitator at 20–24°C and have a shelf life of only 5 days. Platelet transfusions are given to patients with
thrombocytopenia or with platelet dysfunction who are bleeding or undergoing surgery. Patients are increasingly presenting on
antiplatelet therapy such as aspirin or clopidogrel for reduction of cardiovascular risk. Aspirin therapy rarely poses a problem
but control of haemorrhage on the more potent platelet inhibitors can be extremely difficult. Patients on clopidogrel who are
actively bleeding and undergoing major surgery may require almost continuous infusion of platelets during the course of the
procedure. Arginine vasopressin or its analogues (DDAVP) have also been used in this patient group, although with limited
success)
+Common medication causes platelets to irreversible malformation (Aspirin)
+Platelet count is associated with spontaneous bleeding is (less than 20.000)
+Before surgery, the platelet count should be (greater than 50.000)
+You should prophylactic platelet transfusions be given when (platelets below 10.000)
+Blood group O is the universal donor type as it contains no antigens to provoke a reaction. Conversely, group AB individuals
are ‘universal recipients’ and can receive any ABO blood type as they have no circulating antibodies
+Acute hemolytic transfusion reaction (AHTR) is a type of transfusion reaction that is associated with hemolysis. It occurs very
soon after the transfusion, and within 24 hrs post-transfusion
+M.C.C of transfusion hemolysis (ABO incompatibility as a result of clerical error)
+The normal life of RBCs (120 days)
+The normal life of platelets (7-10 days)
+Factor is deficient in hemophilia A (factor VIII - 8) / PTT is elevated with hemophilia A)
+Factor is deficient in hemophilia B (factor IX – 9) / PTT is elevated with hemophilia B)
+Hemophilia A and B inherited (sex-linked recessive)
+Von willebrand`s disease vWD (deficiency of von willebrand factor ‘vWF’ and factor 8) / Von willebrand`s disease inherited
(Autosomal dominant) / Bleeding time with Von Willebrand`s disease
+DDAVP or cryoprecipitate is used to correct Von Willebrand`s disease
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By Dr.Mohammad Z. abu sheikha@

 TRAUMA
+Timing Or Death After Severe Trauma :
1) Immediate death (Due to – injury of vital structures, brain-stem, upper spinal cord, heart, great vessels) (Account for 50%)
2) Within few hours (Due to – hypoxia or hypovolemia) (Account for 30% but can be reduced to 9% with good care)
3) Weeks after injury (Due to – multi-organ failure, raised intracranial pressure or pulmonary embolism) (Account for 20%)
+Management At The Scene Of Accident :
.splint the neck (collar or sand bags and tape)
.ensure air-way
.provide oxygen
.start IV line and give ringer lactate and morphin for severe pain (EXCEPT in head injury)
.stop bleeding by pressure bandage and splint fractures use of MAST or PASG

*Primary Survay
-The Five Steps Of The Primary Survey “AcBCDEs” :
A) Airway (cervical spine stabilization – cervical spine control)
+Ensure airway is clear and give O2
.if the Pt. talks freely then the airway is clear
.cervical spine may be already immobilized by paramedics, if not put a semi-rigid collar
.lift the mandible anteriorly; chin lift and jaw thrust (to lift the tongue base away from airway)
.open the mouth, look inside and apply suction if there is blood or gastric contents and remove dentures
.place oropharyngeal or nasopharyngeal airway
.if this is not enough, an endotracheal tube is passed by the anesthetist. On rare occasions a cricothyroidotomy or
minitracheostomy is done

B) Breathing
+Once the airway is secure, checks for tracheal deviation and congested neck veins and examines all areas of the chest by
inspection, palpation, percussion and auscultation
+Look for and treat :
.flail chest (apply strapping and endotracheal tube, then connect it to the ventilator)
th
.open chest wounds (first covered with occlusive dressings and insert a chest tube in the 5 interocostal space in the mid-
axillary line - at anterior axillary line)
th
.massive hemothorax (insert a large chest tube in the 5 IC space in MAL)
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nd th
.tension pneumothorax (put first a wide bore needle in the 2 IC space in mid-clavicular line and put a chest tube in the 5 IC
space in MAL)
.cardiac tamponade (put a wide bore needle into the pericardium from the left side of the xiphoid area and directed upwards
then apply suction)

C) Circulation (hemorrhage control)

.attach pulse oximetry, BP and ECG leads
.assess the Pts. skin color, capillary refill time, pulse rate, BP and arterial O 2 saturation
.if there is apparent source of bleeding – control by direct pressure or pressure bandage
.insert two large-bore cannulae (Gauge 14) in the veins of the forearm
.if difficult insert a central line (jugular or subclavial veins)
.take a blood sample and sent for urgent blood grouping, cross-matching and base-line hemorrhagical and biochemical analysis
.if there is hypovolemia start with litres of ringer lactate solution followed by type specific blood
+Look for :
.internal bleeding into the thorax, abdomen and pelvis
.other causes of shock (cardiogenic, neurogenic, sepsis and anaphylaxis)

D) Disability (neurological impairment) - Goals in assessing disability is determination of neurologic injury (neurologic
disability)
+Assessment Of Disability :
.mental status (Glasgow Coma Scale GCS) (AVPU scale – Alert / Responsive to verbal stimuli / Responding to painful stimuli /
Unresponsive)
.pupils (puplis are examined for size, reaction and inequality) (a blown pupil suggests ipsilateral brain mass (blood) as herniation
of the brain compresses CN3)
.motor / sensory (extremity movement)
+GCS scoring system :
+Eye Opening (E)
.4 (opens spontaneously)
.3 (opens to voice-command)
.2 (opens to painful stimulus)
.1 (does not open eyes)
+Verbal Response (V)
.5 (appropriate and oriented)
.4 (confused)
.3 (inappropriate words)
.2 (incomprehensible sounds)
.1 (no sounds)
+Motor Response (M)
.6 (obeys commands)
.5 (localizes painful stimuli)
.4 (withdraws from pain)
.3 (decorticate-flexion posture)
.2 (decerebrate posture)
.1 (no movement)
+Normal human GCS is (15)
+Score for a dead man is (3)
+Score for a Pt. in a coma is (< 8) and at this score , Pt. need for intubation (indication)

E) Exposure and Environment

.Keep a warm Environment (keep the Pt. warm; a hypotheramic Pt. can become coagulopathic)

+Immediately Life-Threatening Injuries To Be Identified During The Primary Survey :

.Airway (airway obstruction, airway injury)
.Breathing (tension pneumothorax, open pneumothorax, flail chest with underlying pulmonary contusion)
.Circulation (hemorrhagic shock, massive hemothorax, massive hemoperitoneum, mechanically unstable pelvis fracture,
externity losses, cardiogenic shock, cardiac tamponade, neurogenic shock, cervical spine injury)
.Disability (intracranial hemorrhage, mass lesion)
Page12

++NOTES
+The Maneuvers Used To Establish An Airway Is :
st
.1 step is (chin lift, jaw thrust, head tilt)
.if these methods (Airway) are unsuccessful, is the next maneuver used to establish an airways is (endotracheal intubation)
.if all other methods are unsuccessful, the definitive airway is (cricothyroidotomy)
+What is the best and preferred intravenous (IV) access in the trauma Pt. ?
.tow large-bore IVs (14-16 gauge), IV catheters in the upper extremities (peripheral IV access)
+Alternate Sites Of IV Access :
.central access into femoral
.jugular
.subclavian veins
.break-culafic
+For a femoral vein catheter, how can the anatomy of the Rt. groin be remembered ?
.nerve
.lymphatics
.artery
.vein
.empty space
+Remember (venous close to penis)
+Lactated Ringer`s (LR) solution is the trauma resuscitation fluid of choice
+Types Of Decompression Do Trauma Pts. Receive :
.gastric decompression with NG tube
.foley catheter bladder decompression (after normal rectal exam and no indication of urethral injury)
+Contraindications To Placement Of A Foley Catheter :
.signs of urethral injury
.severe pelvic fractures in men
.blood at the urethral meatus (penile opening)
.high-riding ballotable prostate (on rectal exam)
.scrotal / perineal injury / ecchymosis
+Test should be obtained prior to placing a foley catheter if urethral injury is suspected is (Retrograde UrethroGram RUG)
+Remember if there is a life threating problem in (I), you can`t proceed to (II) until the airway is secured, also if there is a life
threating problen in (II), you can`t proceed to (III) unless it is dealt with – is a severely injured Pt. you may never get to (V)

+Flail Chest
-Tow separate fractures in three or more consecutive ribs
-Diagnosis :
.flail segment of chest wall that moves PARADOXICAL (sucks in with inspiration and pushes out with expiration opposite the rest
of the chest wall)
+Major cause of respiratory compromise with flail chest is (underlying pulmonary contusion)
-Treatment :
.intubation
+Massive Hemothorax
-Treatment :
.tube thoracostomy (chest tube)
-Indications For Emergent Thoracotomy For Hemothorax (massive hemothorax) :
.>1500cc of blood on initial placement of chest tube
.persistent >200cc of bleeding via chest tube per hour * 4hrs
+Pneumothorax
-Injury to the lung, resulting in release of air into the pleural space between the normally apposed parietal and visceral pleura
-Diagnosis :
1.tension pneumothorax (clinical diagnosis-dyspnea, jugular venous distension, tachypnea, anxiety, pleuritic chest pain,
unilateral decreased or absent breath sounds, tracheal shift away from the affected side, hyperresonance on the affected side)
2.open pneumothorax (usually obvious, with air movement through a chest wall defect and pneumothorax on CxR)
-Treatment :
1.tension pneumothorax
nd
Page13

.rapid thoracostomy incision or immediate decompression by needle thoracostomy in the 2 intecostal space midclavicular
line
.followed by tube thoracostomy placed in the anterior / midaxillary line in the 4 th intercostal space (level of the nipple in men)
2.open pneumothorax
.occlusive dressing over chest wall defect
.tube thoracostomy
+Sucking chest wound is (open pneumothorax)
+Thoracostomy is (chest tube)
+Pneumothorax look like on CxR (loss of lung marking; a Rt-sided pneumothorax, arrows ponit out edge of lung-air interface;
shift away from pneumothorax)
+Cardiac Tamponade
-Bleeding (fluids) into the pericardial sac, resulting in constriction of heart, decreasing inflow and resulting in decreased cardiac
output (pericardium does not stretch)
-Symptoms :
.tachycardia
.shock
.pulsus paradoxus
.Beck's triad (hypotension, muffled heart sound, JVD)
.Kussmaul`sign (JVD with inspiration)
-Diagnosis :
.echo
-Treatment :
.pericardiocentesis

*Secondary Survey (Once the Pt. is stable start the 2nd survay)
st
.at 1 take an AMPLE history (full medical Hx) (A- allergies / M- medication / P- past medical history / L- last meal / E- events of
the injury)
.give analgesics
.setup pulse oximetry and ECG leads
.monitor conscious level (GCS) and urine output
.send blood sample for investigations
.do the 3 trauma X-ray (AP chest, pelvis, C-spine)
.undress the Pt. but keeping him warm and do detailed head-to-toe examination

+Signs Of Basilar Skull Fracture :

.raccoon eyes (periorbital bleeding)
.battle's sign
.clear otorrhea
.rhinorrhea
.hemotympanum
+Diagnosis in the anterior chamber must not be missed on the eye exam is (Traumatic hyphema = blood in the anterior
chamber of the eye)
+Concomitant injury to the abdomen, must be considered in every penetrating injury of the thorax at or below the level of the
nipple (the diaphragm extends to the level of the nipples in the male on full expiration)
+Indicates PTX-pneumothorax, is the significance of subcutaneous air
+Seatbelt Sign (ecchymosis on lower abdomen from wearing a seatbelt - M.C is small bowel perforation)
+What Must Be Documented From The Rectal Exam ?
.sphincter tone (as an indication of spinal cord function)
.presence of blood (as an indication of colon or rectal injury)
.prostate position (as an indication of urethral injury) (prostate should be ‘normal’ smooth and tethering)
+Complication after prolonged ischemia to the lower extremity is (compartment syndrome), and treated by (fasciotomy-for
compartment below the knee)

*Trauma Studies
+Classic Blunt Trauma ER x-rays :
Page14

.AP (anterior-to-posterior) chest film

.AP pelvis film
+Studies Are Available To Evaluate For Intra-Abdominal Injury :
.U/S (diagnostic test of choice for evaluation of the UNSTABLE Pt. with blunt abdominal trauma)
.CT scan (for STABLE pt.)
.DPL (diagnostic peritoneal lavage) (for UNSTABLE VITAL SIGN as hypotension)
+DPL Performed :
.place a catheter below the umbilicus (in Pts. without pelvic fractures)
.place catheter above the umbilicus (in Pts. with a pelvic fracture)
.grossly positive DPL is ( >10cc blood aspirated)

+The Indicators Of A Positive Peritoneal Lavage In Blunt Trauma :

.RBCs > 100.000/mm3
.WBCs > 500/mm3
.lavage fluid (LR/NS) drained from chest tube, foley, NG tube
.bile present
.bacteria present
.feces present
.vegetable matter present
.elevated amylase level
+Treatment Of Gunshot Wound To The Belly (abdomen) Is :
.exploratory laparotomy
+Indication For Admission To Hospital :
.loss of consciousness for more than 5mins
.confusion or decreased GCS
.skull fracture
.neurological symptoms or signs
.open injuries
.rhinorrhea and otorrhea

*Abdominal Injuries
+Classification Of Abdominal Injuries :
A) Intra-thoracic Abdomen
.it is contained within the lower rib cage (ribs-cut) and contains the diaphragm, liver, spleen and stomach
.injury leads to internal hemorrhage
B) True Abdomen
.it contains small and large intestines, urinary bladder “when distended” and the pregnant uterus
.injury leads to peritonitis
C) Pelvic Abdomen
.it contains the recto-sigmoid colon, urinary bladder, urethra, lower ileum and female genital tract
.it is associated with pelvic fractures and there is internal hemorrhage and peritonitis
D) Retroperitoneal Abdomen
.it contains the kidneys, the pancreas and the 2nd & 3rd parts of duodenum, the aorta and IVC
.the signs at first are minimal. A large retroperitoneal hematoma may form and there is the risk of sudden vascular
decompensation of its intra-abdominal rupture
+Principles Of Management Of Abdominal Injuries :
1) Resuscitate and do 1ry & 2ry survay
2) The Pt. then passes into either a stable or unstable state :
a) Unstable Pt. :
.there are signs of acute abdomen, this Pt. needs urgent laparatomy
.US scan may be done to show hemoperitoneum (sonolucent areas + the crescent moon sign)
b) Stable Pt. :
.US scan is done to confirm hemoperitoneum
.CT scan may be done (it takes 45-60min so the Pt. must be hemodynamically stable / it is useful in children)
.diagnostic laparoscopy by a 5mm laparoscope may be done under IV sedation and local anesthesia. It can reliably exclude
intra-abdominal injury
+Diagnostic Peritoneal Lavage DPL :
.useful when the physical signs are equivocal. It is done under local anesthesia
Page15

.dialysis catheter is inserted into the peritoneum below the umbilicus

.next infuse one litre of ringer lactate and siphon it out after 5-10min
3 3
.the next test is +ve if (RBCs >100.000/m – WBCs >500/mm – Gram stain showing organisms – GIT contents aspirated)

+Specific Intra-abdominal Injuries :

A) Hepatic Injuries
-Types :
.minor injuries (require no surgical treatment, and followed by CT scan)
.moderate sized tears (need liver suture – with evidence of continued blood needs laparotomy and simple suture)
.severe injuries (extensive trauma to one or both lobes – may need resectional debridement)
.major injuries (with bleeding from the hepatic veins or vena cava, bleeding is contolled by packing the Rt. supracolic
compartment of the abdomen with gauze rolls. The pack is removed after 48hr under general anesthesia or the Pt. is sent to a
special hepatobiliary center)
B) Diaphragmatic Injuries
 -More common in the Lt. diaphragm
-Types :
.minor tears (may pass unnoticed and Pt. presents yrs later with incarcerated hernia)
.severe injuries (there is extensive herniation of the stomach, colon, omentum and small bowel and the spleen on the Lt. side
and the liver on the Rt. side – might lead to mediastinal shift, respiratory distress and hypotension)
-Investigation :
.chest X-ray may show air and fluid level
.contrast radiography or CT scan may be needed
-Treatment :
.by surgical repair

C) Splenic Injuries
-Commonest ijured organ in RTA
-Types :
.incomplete tear
.complete laceration
.severe fragmentation with avulsion of hilar vessels
-Investigation :
.U/S
.DPL
.CT scan or mini-laparoscopy
-Management :
a) The rule is splenic preservation whenever possible because of the risk of overwhelming post-splenectomy infection by
encapsulated organisms especially Streptococcus
b) Laparotomy is done
.if stable and injury is mild with no contamination due to bowel injury – suturing is tried first
.if not possible - splenectomy
c) Post-operative measures after splenectomy
.vaccination with pneumovax (pneumococcus), HIV vaccine and meningovax
.long term penicillin prophylaxis is also advisable especially in children till the age of 21yrs and for 2yrs in adults
+Encapsulated Organisms :
.Haemophilus influenza type B (HIB)
.Streptococcus pneumonia (pneumococcus)
.Neisseria meningitides (meningococcus)
.Group B streptococcus (GBS)
.Klebsiella pneumonia
.Salmonella typhi
D) Pancreatico-duodenal Injuries
-Blunt trauma to the pancreas is becoming common and is due to compression against the vertebral clumn
-Types :
.minor injury (contusion with no duct disruption / managed conservatively)
.intermediate injury (distal gland damage with duct disruption / distal - may require resection of the tail)
Page16

.major injury (proximal gland damage involving the head with duct disruption / proximal - may require pancreato-
duodenectomy / major – need laparotomy)
-Investigation :
.serum amylase (may and may not be elevated)
.abdominal X-ray (may show associated duodenal injury and free gas)
.CT-scan (will outline the injury)
E) Small Bowel Injuries
-Mechanism :
.crushing of the bowel against the vertebral column
.brusting due to sudden rise of intra-abdominal pressure
.tears at relatively fixed points along the attachment of intestinal mesentery
-Diagnosis :
.confirmed on DPL
-Treatment :
 .small perforation can be repaired by suture
.resection of devitalized segment of the bowel with end-to-end anastomosis
F) Colonic Injuries
-They are rare / The commonest part affected is the transverse colon and then the Rt. colon
-Treated by laparotomy
G) Genito-Urinary Trauma
st
.at 1 examine the external urinary meatus in males for the presence of blood. If found it indicates the presence of urethral
injury
.in this case never pass a catheter but do a retrograde urethrography to diagnose the site of urethral injury
.if there is no blood – pass a catheter and examine the urine for the presence of blood. If +ve do retrograde cystography to
rule out a bladder injury
.if this is ruled out – do IV urography taking film at 0, 5, 10 & 15mins after injection
.this will establish the presence of 2 kidneys, their function and whether injury is present
.CT-scan should be done to delineate better the renal injury

+Chest Trauma
-The overall mortality of chest injuries <10% and <15% require thoracotomy
-Trauma is either blunt or penetrating and there may be associated abdominal injuries
-Classification Of Thoracic Injuries :
A) Injuries encountered during 1ry survey
1) chest wall trauma (fracture ribs, flail chest, fracture of the sternum)
2) pneumothorax (simple and tension pneumothorax)
3) hemothorax
4) cardiac tamponade
B) Injuries encountered during 2ry survey
1) pulmonary contusion
2) aortic disruption
3) diaphragmatic disruption
4) oesophageal disruption
+Primary Survay Chest Injuries :
A) Chest wall trauma
1) fracture ribs
th th
.usually the lower ribs from 5 to 9 ribs
.they may be associated with abdominal injuries
st
.the upper 4 ribs especially 1 are not fractured except by severe trauma
.a simple rib fracture requires no specific treatment except adequate analgesia
2) flail chest
.it occurs with severe trauma
.there are 2 or more consecutive ribs are fractured in 2 or more places
.the flail segment undergoes paradoxical motion on inspiration impending ventilation of the ipsilateral lung
.treatment (adequate analgesia, strapping of the segment, sometimes endotracheal intubation and IPPV is needed)
3) fracture of the sternum
Page17

.usually due to severe impact on a solid structure e.g. a driver hitting the steering wheel
.danger (injury to the mediastinum)
.treatment (monitor the Pt. by ECG and cardiac enzymes
B) Pneumothorax
.cause (either a rib fracture secondary to blunt trauma or penetrating trauma)
-Types :
1) tension pneumothorax
.result when a penetrating injury allows air to enter the pleural cavity but not leave
.the mediastinum shifts to the opposite side, decreased VR and finally cardiac arrest occurs
.clinical picture (dyspnea / trachea displaced to the opposite side / the injured side of the chest fails to expand is hyper-
resonant and breath sound is absent)
2) Simple pneumothorax
.result when there is a defect in the chest wall that allows air to enter and leave
.no deviation of the mediastinum
.clinical picture (there is sucking chest wound with hyper-resonance of the affected side)
C) Hemothorax
.usually due to laceration of lung and is more common in penetrating than in blunt trauma
.it may be small or massive
+Massive Hemothorax
-Def. (when there is rapid accumulation of more than 1 litre of blood)
-Clinical Picture :
.hypovolemic shock
.dull percussion note
.absent breath sounds
.diminished expansion of the side of the chest
-Management :
th
.insertion of a large chest tube (gauge 32) into the 5 in the MAL and connected to underwater seal
.if blood loss <1 litre the management is expectant
.if blood loss >1 litre or continuing loss >200 ml/hr urgent thoracotomy is indicated
D) Cardiac Tamponade
.the pericardial sac is filled with blood which restricts the filling and contraction of the heart and leads to shock
.commonly result of penetrating injury but sometimes may result from severe blunt trauma
.diagnosis by Beck`s triad (increased JVP / decreased BP / muddled heart sound)
.treatment (pericardiocentesis / next formal cardiac surgery is needed)
+Secondary Survay Chest Injuries :
A) Pulmonary Contusion
.it occurs usually in blunt trauma (there is bruising of lung tissue)
.it leads gradually to respiratory distress
.treatment (support the respiratory system by intubation and IPPV)
B) Aortic Disruption
.it occurs especially after very rapid deceleration
.site of disruption is usually at the ligamentum arteriosum
.clinical picture (the Pt. initially is stable then become hypotensive / chest X-ray shows widening of the mediastinum / this
should rise suspicious and CT or angiography should be done to confirm diagnosis / the Pt. should be immediately transferred
to cardio-thoracic centre for emergency operation)
C) Diaphragmatic Injury
.it result from either a penetrating trauma or blunt compressional force
.commonly it is missed early and Pt. may present yrs later as obstructed hernia
.diagnosis is made on chest X-ray by finding elevated diaphragm and stomach with fluid level in the chest. Contrast may be
given to ensure diagnosis
D) Tracheo-Bronchial Disruption
.it is uncommon
.usually the Pt. dies at the scene of the accident
E) Oesophageal Disruption
.trauma is usually penetrating
.sometimes the esophagus may tear due to forceful expulsion of contents from the stomach during huge impacts
.gastric contents and air will leak into the mediastinum resulting in mediastinitis and also surgical emphysema
.also the Pt. may develop pneumothorax on the Lt. more the Rt.
Page18

.diagnosis is confirmed by finding gastric contents drained by the chest tube

*Penetrating Neck Injuries

+What depth of neck injury must be further evaluated ?
.penetrating injury through the platysma (is a superficial muscle that overlaps the sternocleidomastoid)
-Anatomy Of The Neck By Trauma Zones :
.zone 3 (angle of the mandible and up)
.zone 2 (angle of the mandible to the cricoid cartilage)
.zone 1 (below the cricoid cartilage)
+Minimal urine output for an adult trauma Pt. is (50mL/hr)
+Intra-abdominal injury is associated with seatbelt use is (small bowel injuries)
+Bleeding from pelvic fractures is most commonly caused by (venous bleeding 85%)
+M.C intra-abdominal organ inujred with penetrating trauma is (small bowel)
+M.C injured abdominal organ with blunt trauma is (liver)
+Treatment For Human And Dog Bites Is :
.leave wound open
.irrigation
.antibiotics (penicillin)
+Humat bites (streptococcus viridans)

*Raised Intracranial Pressure (ICP)

+Values :
.ICP = 10mmHg (Normal)
.ICP >20mmHg (Abnormal)
.ICP >40mmHg (Death)
+Causes :
.hematoma
.edema secondary to contusion or laceration
.edema secondary to ischemia
.rarely obstruction of CSF
+Effects Of Raised ICP :
.tentorial herniation
.pupillary dilatation as a result of 3rd cranial nerve compression
.motor weakness as a result of cortico-spinal tract compression
.coning (this result in compression of cardio-respiratory centers against the bone as the brain stem is squeezed through the
foremen magnum)
+Clinical Effects Of Rising ICP :
.decreased respiratory rate
.decreased heart rate
.increased systolic BP
.increased pulse pressure
+Death results from respiratory arrest secondary to brain stem infarction
+Direct measurement of ICP is the best method to follow severe injuries. It is usually done invasively by sensors placed
extradurally, subdurally or intraventriculary
+Cerebral blood flow is increased by (increased CO 2 levels, increased extracellular K+ level and decreased PO2)
+General Treatment Plan For Severe Head Injuries :
1) Laparotomy or thoracotomy if needed should be done first
2) Skull fractures
.linear fractures of the vault (do not require treatment)
.compound depressed fractures
.basal fractures (anterior cranial fossa – rhinorrhea, periorbital hematoma and subconjunctival hemorrhage / middle cranial
fossa – otorrhea)

+M.C indication for intubation in a trauma patient is altered mental status

Page19

By Dr.Mohammad Z. abu sheikha@

 Surgical Infection
-Signs & Symptoms of inflammation/infection :
.tumor (mass = swelling/edema)
.calor (heat)
.dolor (pain)
.rubor (redness = erythema)
-Define :
.SIRS (systemic inflammatory response syndrome – fever, tachycardia, tachypnea, leukocytosis)
.Cellulitis (blanching erythema from superficial dermal/epidermal infection, usually streptococcus > staphylococcus)
.Superinfection (a new infection arising while a Pt. is receiving antibiotics for the original infection at a different site)
.Nosocomial infection (infection originating in the hospital)
+M.C nosocomial infection is UTI
+M.C nosocomial infection causing death is RTI-pneumonia

**Urinary Tract Infections (UTIs)

-Diagnostic Tests :
.urinalysis
.culture
.urine microscopy for WBC
+Number of colony-forming units (CFU) confirms the diagnosis of UTI is (100.000 or 10 *5 CFU)
-Common Organisms :
.E.coli
.klebsiella
.proteus (enterococcus, staphylococcus aureus)
Page20

-Treatment :
.antibiotics with gram-negative spectrum (sulfamethoxazole/trimethoprim, gentamicin, ciprofloxacin)
+Treatment Of Bladder Candidiasis :
.remove or change foley catheter
.administer systemic fluconazole or amphotericin bladder washings

**Central Line Infections

-This is a long tube (catheter) that goes into a vein in your chest, arm, or groin and ends at your heart. Your central line will
carry nutrients and medicine into your body. It can also be used to take blood when you need to have blood tests
+Internal jugular vein / Axillary vein / Femoral vein
-Signs & Symptoms :
.redness (erythema) at the site (or red streaks around the site)
.swelling or warmth at the site
.yellow or green drainage (pus)
.pain or discomfort
.fever
.mental status change
.hypotension
.tachycardia (shock)
.unexplained hyperglycemia
-Causes (the M.C.C of catheter-related blood-stream infections) :
.coagulase-negative staphylococcus
.enterococci
.staphylococcus aureus
.gram-negative rods
+Anyone who has a central line can get an infection. Your risk is higher if you :
.are in the intensive care unit (ICU)
.have a weakened immune system or serious illness
.are having a bone marrow transplant or chemotherapy
.have the line for a long time
.have a central line in your neck or groin

+When should you change central lines?

.when they are infected; there is NO advantage to changing them every 7 days
+Hyperal (TPN) – the central line infusion increases the risk of infection
-Treatment :
.remove central line (send for culture)
.+/- IV antibiotics
.place NEW central line in a different site (every 72 to 96hrs you should change peripheral IV short angiocatheters)

**Wound Infection
-These infections arise classically, postoperative days 5-7
-Signs & Symptoms :
.pain at incision site
.erythema (redness)
.drainage (pus)
.induration
.warm skin
.fever
-Treatment :
.remove skin sutures/staples
.pack wound open
.send wound culture
.administer antibiotics
+M.C bacteria found in postoperative wound infections (Staphylococcus aureus, Escherichia coli, Enterococcus)
+Bacteria cause fever and wound infection in the first 24hrs after surgery (Streptococcus, Clostridium ‘bronze-brown weeping
tender wound’)
Page21

-Complications :
.fistula
.sinus tracts
.sepsis
.abscess
.suppressed wound healing
.superinfection (new infection that develops during antibiotics treatment for the original infection)
.hernia
-Indications for antibiotics after drainage of a subcutaneous abscess :
.DM
.surrounding cellulitis
.prosthetic heart valve
.immunocompromised state
*Peritoneal Abscess (abscess within the peritoneal cavity)
-Sites Of Occurrence :
.pelvis
.morison`s puch
.subphrenic
.paracolic gutters
.periappendiceal
.lesser sac
-Diagnosis :
.abdominal CT or ultrasound (after postoperative day 7)
-Treatment :
.percutaneous CT-guided drainage (option for drainage of pelvic abscess is transrectal drainage or transcaginal)
+All abscesses must be drained EXCEPT type (amebiasis)
+Bacteria can be found in the stool (colon) (anaerobic - bacteroides fragilis, aerobic - escherichia coli)
+Bacteria are found in infections from human bites (Streptococcus viridans, S.aureus, Peptococcus, Eikenella)
+M.C ICU pneumonia bacteria (gram-negative organisms)
+Organism causes tetanus (Clostridium tetani)

*Fever
-Postoperative fever (Temperature >38.5C or 101.5F)
-Postoperative Timing For The Following Causes Of Postoperative Fever :
.atelectasis (wind) – first 24 to 48 hrs (M.C.C of fever on postoperative days 1-2 / streptococcus, clostridium-bronze brown
weeping wound)
.UTI (water) – anytime after postoperative day 3
.wound infection (wound) – usually after postoperative day 5 (but it can be anytime)
.DVT / PE / thrombophlebitis (walking) – postoperative days 7 to 10
.drug fever (wonder drugs) – anytime
+Cause Fever At Any Time :
.IV site infection
.central line infection
.drug fever
+Causes Fever Before 24 Postoperative Hours :
.atelectasis
.beta-hemolytic streptococcal or clostridial wound infections
.anastomotic leak
.drug fever
+Causes Fever From Postoperative Days 3-5 :
.UTI
.pneumonia
.IV site infection
.wound infection
.drug fever
Page22

+Causes Fever From Postoperative Days 5-10 :

.wound infection
.pneumonia
.abscess
.infected hematoma
.C.difficile colitis
.anastomotic leak
.DVT
.peritoneal abscess
.drug fever
.pulmonary embolism
.parotitis
+Day 1-2 (M.C.C is atelectasis) / Day 3 (UTI, pneumonia) / Day 5 (abscess)
+Anesthetic drugs can cause intra-operative hyperthermia (called “malignant hyperthermia”), and treated by (Dantrolene)
*Wounds
-Inhibits Wound Healing (Risk Factors For Development Of Surgical Site Infections) :
.infection – chronic inflammatory process
.older age
.obesity
.DM
.cortisone (Vit A – mask the effect of cortisone on wound healing)
.hypoxia, hypothermia
.prolonged procedure
.peripheral vascular disease
.chronic skin disease
.carrier state (chronic staphylococcus carriage)
.ischemia – lical tissue necrosis
.malnutrition
.anemia
.steroids
.cancer
.radiation
+Vit C, Zinc, Selenium (improve wound healing)
-Phases Of Wound Healing :
.inflammation + vasoconstriction
.epithelialization (occur at 24 – 48 hrs / waterproof)
.fibroplasia (fibroblast produce collagen and elastin)
.wound contraction (myofibroblasts)
+How long until a sutured wound epithelialized ?
.24-48 hrs
+What reverses the deleterious effects of steroids on wound healing ?
.antidote (Vit A)

*Tumor Marker
+Colon cancer (CEA)
+Hepatoma (Alpha-fetoprotein)
+M.C cancers in women (lung, breast, colorectal)
+M.C cancer in men (prostate, lung, colorectal)
+M.C cancer causing death in both men and women (lung)
st nd
+Neutrophil (is the predominant cell is 1 -2 day)
nd
+Monocyte (Macrophage) (is the predominant cell after 2 day)
+Wound infection (>100.000 bacteria) and prevent epithelialization
+Maximum wound strength occur 6wks
+M.C site of scars (Sternum) / Hypertrophic scar (within the wound margin) – Keloid scar (beyond the wound margin)
Page23
By Dr.Mohammad Z. abu sheikha@

Fluids And Electrolytes

-Tow Major Body Fluid Compartments (60%) :
+
.intracellular (40%) (major K - potassium)
+
.extracellular (20%) (major Na - sodium) (interstitial fluid 13-15% / intravascular fluid 5-7%)
+Blood (plasma) account for 7% of total body weight (5 liters)
+How many liters of blood are in a 70kg man ? (Percentage of ideal body weight does blood account for in adult 7%)
.0.07*70(BW)=5 liters
-Fluid Requirements Every 24hrs (Daily Need Of) :
+
.potassium K (1-2mEq/Kg)
+
.chloride CL (1.5-2mEq/Kg)
+
.sodium Na (1-2mEq/Kg)
.water (30-35mL/Kg)
-Levels And Sources Of Normal Daily Electrolyte loss :
+
.sodium (Na ) and potassium (K) (100 mEq)
+
.chloride (CL ) (150 mEq)
-Levels And Sources Of Normal Daily Water Loss :
.urine (1200-1500mL) (25-30mL/Kg)
Page24

.feces (100-200mL)
.sweat (200-400mL)
.respiration (500-700mL)

**Third Spacing
-Fluid accumulation in the interstitium of tissues, as in edema, loss of fluid into the interstitium and lumen of a paralytic bowel
rd
following surgery (intravascular and intracellular spaces as the first tow spaces) (Occur around the 3 postoperative day)
(Classic Signs - tachycardia, decreased urine output)
-The Surgical Causes Of The Following Conditions :
+Causes of Metabolic Acidosis (loss of Hco3-)
.loss of bicarbonate (diarrhea, ileus, fistula, high-output ileostomy, carbonic inhibitors)
.increase in acids (lactic-acidosis, keto-acidosis, renal failure, necrotic tissue)
 +
+Causes of Metabolic Alkalosis (loss of H )
.vomiting
.NG suction
.diuretics
.alkali ingestion
.mineralo-corticoid excess
+Causes of Respiratory Acidosis (increased Co2)
.hypoventilation
.drugs
.PTX
.pleural effusion
.lung disease
.acute airway obstruction
+Causes of Respiratory Alkalosis (decreased Co2)
.hyperventilation
+Causes of Hypochloremic Alkalosis
.NGT suction
.loss of gastric HCL through vomiting
+The Quantities Of Daily Secretions :
.saliva (1500 mL/24hrs)
.Bile (1000 mL/24hrs)
.gastric (2000 mL/24hrs)
.pancreatic (600 mL/24hrs)
.small intestine (3000 mL/24hrs)
+Normal daily dietary requirements for adults (Protein 1g/kg/day – calories 30 kcal/kg/day)

**Common IV Replacement Fluids (All values are per liter)

+ +
.Comprises Normal Saline NS (154 mEq/ of CL – 154 mEq/ of Na )
.1/2NS (77-77)
.1/3NS (51/51)
.1/4NS (39/39)
.1/5NS (31/31)
-Comprises Lactated Ringer`s LR
+
.130 mEq Na
+
.109 mEq Cl
.28 mEq lactacte
+
.4 mEq K
+
.3 mEq Ca
+What Comprises D5W (5% dextrose in water) ?
Page25

.5% dextrose (50g) in H2O (1L D5W contain 59gm glucose)

+D5W - is a solution with a sugar (usually glucose, as known as dextrose, with water as the solvent) used for intravenous
therapy
+Common adult maintenance fluid (D5 ½ NS with 20 mEq KCI/L)
+Common pediatric maintenance fluid (D5 ¼ NS with 20 mEq KCI/L)
+Why should sugar (dextrose) be added to maintenance fluid ?
.to inhibit muscle breakdown
+The minimal urine output for an adult on maintenance IV (30 mL/hr - 0.5 cc/Kg/hr) / In children (1cc/Kg/hr)
+The minimal urine output for an adult trauma patient (50 mL/hr – 1 cc/Kg/hr)
+Common cause of electrolyte abnormalities is (Lab error)

**Calculation Of Maintenance Fluids

+What is the 100/50/20 rule ?
.100 mL/Kg for the first 10Kg
.50 mL/Kg for the next 10Kg
.20 mL/Kg for every Kg over 20 (divide by 24 for hourly rate)
+What is the 4/2/1 rule ?
.4 mL/Kg for the first 10Kg
.2 mL/Kg for the next 10Kg
.1 mL/Kg for every Kg over 20
+Example :
-Maintenance For A 70Kg Man Is :
.Using 100/50/20 (100*10Kg = 1000 / 50*10Kg = 500 / 20*50Kg = 1000 (Total 2500 – divided by 24hrs = 104 mL/hr maintenance
rate)
.Using 4/2/1 (4*10Kg = 40 / 2*10Kg = 20 / 1*50Kg = 50 (Total 110 mL/hr maintenance rate)
+M.C trauma resuscitation fluid (LR) (Ringer best for trauma and burn)
+M.C postoperative IV fluid after a laparotomy (LR or D5LR for 24-36hrs)
+LR is used to replace duodenal or pancreatic fluid loss
+ +
+ Major intracellular cation (K ) 40% / Major extracellular cation (Na ) 20%
+For adult we use D5 half saline / For children we use D5 quarter saline

**Total Parenteral Nutrition (TPN)

-Parenteral nutrition (PN) is feeding a person intravenously, bypassing the usual process of eating and digestion (IV nutrition)
.it is used only if enteral feeding is not possible or is contraindicated
.it is usually given through a central line in the internal jugular or subclavian vein
.sometimes, it may be given in a wide peripheral vein and maneuvered into a central vein
.if it is going to be given for a long time, the central line is passed in a subcutaneous tunnel and may have a subcutaneous port
-Indications :
.severe malnutrition
.inability to swallow
.sepsis
.Gl disorders (bowel obstruction, short bowel syndrome (<120cm), gastroschisis, prolonged diarrhea regardless of its cause,
high-output intestinal fistula, very severe CD or UC, and certain pediatric GI disorders including congenital GI anomalies and
necrotizing enterocolitis)
.burns involving upper GIT
.cancer Pts.
+We give (proteins/carbohydrate, lipid/electrolyte, minerals, vitamins + insulin)
.lipid (20-30% of calories)
.protein (1.7g/Kg/day) (10-20% of calories)
.carbohydrate (50-60% of calories)
+TPN is given by central line (jugular vein - subclavian vein)
-Complications Of TPN :
.central line infection-sepsis (M.C bacteria is Staphylococcus epidermidis) (Infection is a common cause of death in these Pts.,
and death usually results from septic shock)
.electrolyte changes (mineral overload / deficiency)
Page26

.refeeding syndrome (hypokalemia, hypoglycemia, hypophosphatemia and hypomagnesemia)

.vitamin deficiency
.pneumothorax from central line insertion
.hemothorax
.cardiac tamponade
.gallstones and cholecystitis
.GI mucosal atrophy (Gut atrophy)
.fatty liver and liver failure
.blood clots (death can result from pulmonary embolism wherein a clot that starts on the IV line but breaks off goes into the
lungs)
+Major Source Of GI Nutrient :
.small bowel (glutamine)
.large bowel (butyrate)
+Mirizzi's Syndrome
.is a rare complication in which a gallstone becomes impacted in the cystic duct or neck of the gallbladder causing compression
of the common bile duct (CBD) or common hepatic duct, resulting in obstruction and jaundice

**(K)
*Hyperkalemia
-Normal range for potassium level (3.5-5 mEq/L)
-Causes :
.blood transfusion
.renal failure
.drugs (diuretics) - iatrogenic overdose
.acidosis
.tissue destruction (injury / hemolysis)
+ECG findings (Peaked T waves)
+Medications That Can Increase Blood Potassium Levels :
.ACE inhibitors (captopril, enalapril)
.non steroidal anti-inflammatory drugs NSAIDs
.angiotensin 2 receptor blockers ARBs
.potassium-sparing diuretics

*Hypokalemia
-Causes :
.drugs (diuretics, steroids, insulin, amphotericin-antifungal drug, certain antibiotics)
.alkalosis
.intestinal fistula
.NG aspiration
.diarrhea, vomiting
+ECG findings (Flattening of T waves, U waves, ST segment depression, atrial fibrillation)
-Treatment :
.(KCI IV) (the maximum amount that can be given through a peripheral IV is 10 mEq/hr)
(the maximum amount that can be given through a central line is 20 mEq/hr)

**(Na)
*Hypernatremia
-The normal range for sodium level is (135-145 mEq/L)
-Causes :
.dehydration
.diabetes insipidus
.diarrhea, vomiting
.diuresis (increased or excessive production of urine)
.diaphoresis (sweating)
.tachypnea
.iatrogenic (TPN)
Page27

*Hyponatremia
-Causes :
.cirrhosis of the liver
.congestive heart failure CHF
.massive edema of any cause
.states of severe pain or nausea
.in the setting of trauma or other damage to the brain
.nephrotic syndrome
.SIADH
.hypothyroidism
.glucocorticoid (steroid) deficiency
.Addison's disease
.congenital adrenal hyperplasia in which the adrenal glands do not produce enough steroid hormones
.adrenal insufficiency
.primary polydipsia
+M.C.C of mild postoperative hyponatremia is (Fluid overload)

**(Ca)
*Hypercalcemia
-The normal blood calcium level is between 8.5 to 10.5 mg/dL (2.12 to 2.62 mmol/L)
-Causes :
.calcium supplementation IV
.hyperparathyroidism (hyperthyroidism)
.immobility / iatrogenic (thiazide diuretics)
.mets / milk alkali syndrome
.paget`s disease (bone)
.addison`s (colon, lung, breast, prostate, multiple myeloma)
.zollinger-ellison syndrome (as part of MEN 1)
.excessive Vit D, Vit A
.sarcoid
+ECG findings (short QT interval, prolonged PR interval)

*Hypocalcemia
-Causes :
.short bowel syndrome
.intestinal bypass
.Vit D deficiency
.sepsis
.acute pancreatitis
.osteoblastic metastases
.aminoglycosides
.diuretics
.renal failure
.hypomagnesemia
.rhabdomyolysis
+ECG findings (prolonged QT, ST interval)
+Best way to check the calcium level in the ICU (check ionized calcium)

**(Mg)
*Hypemagnesemia
-The normal range for magnesium level is (1.5-2.5 mEq/L)
-Causes :
.TPN
.renal failure
.IV over supplementation
Page28

*Hypomagnesemia
-Causes :
.TPN
.renal failure
.hypocalcemia
.gastric suctioning
.aminoglycosides
.diarrhea, vomiting

**Glucose
*Hyperglycemia
-Causes :
.diabetes (poor control)
.infection
.stress
.TPN
.drugs
.lab error
.drawing over IV site
.somatostatinoma (is a malignant tumor of the delta cells of the endocrine pancreas that produces somatostatin)
.glucagonoma (is a rare tumor of the alpha cells of the pancreas that results in the overproduction of the hormone glucagon)
+The goal glucose level in the ICU is (80-110 mg/dL)

*Hypoglycemia
-Causes :
.excess insulin
.decreased caloric intake
.insulinoma
.drugs
.liver failure
.adrenal insufficiency
.gastrojejunostomy

**Phosphate
*Hyperphosphatemia
-The normal range for phosphorus level is (2.5-4.5 mg/dL)
-Causes :
.renal failure
.sepsis
.heart block
.hyperthyroidism

*Hypophosphatemia
-Causes :
.GI losses
.inadequate supplementation
.medications
.sepsis
.alcohol abuse
.renal loss
-Complication :
.respiratory failure

+NOTES
+Causes Coma :
.hyperglycemia
.hypoglycemia
Page29

.hypernatremia
.hyponatremia
*Hypekalemia (NOT)
+The Major Cardiac Electrolytes :
.potassium (dysrhythmias)
.magnesium (dysrhythmias)
.calcium (dysrhythmias/inotrope)
+M.C.C of electrolyte-mediated ileus is (hypokalemia)
+Fluid is used to replace NGT (gastric) aspirate (D5 ½ NS with 20 KCI)
+Electrolyte is associated with succinylcholine (hyperkalemia)
+Suxamethonium chloride, also known as suxamethonium or succinylcholine, is a medication used to induce muscle relaxation
and short-term paralysis, usually to help with tracheal intubation. It is sometimes used in combination with pain medications
and sedatives for euthanasia and immobilization of horses
+Side Effects Of Furosemide :
.hypokalemia
.hyperuricemia
.hyperglycemia
.ototoxicity
+Tetany May Occur In :
.hyperventilation syndrome
.metabolic alkalosis
.hypokalemia
.hypomagnesaemia
+The serum alkaline phosphatase level is characteristically normal in Hemolytic Jaundice
+Causes Of Hyperuricemia :
.high dose aspirin
.chronic renal disease
.alcohol
.leukemia
.carcinoma
.severe psoriasis
+Renin is secreted by Juxtaglomerular apparatus / Renin is produced by Juxtaglomerular cells

By Dr.Mohammad Z. abu sheikha@

Common Surgical Medications

*Antibiotics
-Antibiotics Are Commonly Used For Anaerobic Infections :
.metronidazole
.clindamycin
.cefoxitin
-Antibiotics Are Commonly Used For Gram-Negative Infections :
.gentamicin
Page30

.ciprofloxacin
.third-geenration cephalosporins
.sulfamethoxazole
-Antibiotics Option For Colon/Appendectomy Coverage If The Pt. Is Allergic To Penicillin :
.IV ciprofloxacin (cipro)
.IV clindamycin or IV flagyl
+Antibiotics, if taken with alcohol, will produce a disulfiram-like reaction is metronidazole (flagyl)
+The drug of choice for treating amoebic infections is metronidazole (flagyl)
+Antibiotics is associated with cholestasis is ceftriaxone (rocephin)
+Antibiotics cannot be given to children or pregnant women is ciprofloxacin
+Antibiotics must serum levels be determined are (aminoglycosides, vancomycin)

*Steroids
-Uses :
.immunosuppression (transplant)
.autoimmune disease
.hormone replacement (addison`s disease)
.spinal cord trauma
-Side Effects :
.adrenal suppression
.immunosuppression
.weight gain with central obesity
.acne
.hirsutism
.purple striae
.hyperglycemia
.sodium retention / hypokalemia
.hypertension
.myopathy
.ischemic bone necrosis (avascular necrosis of the hip)
.GI perforations
+‘STRESS DOSE’ (100mg of hydrocortisone IV every 8hrs)
+Vit A - helps counteract the deleterious effects of steroids on wound healing
+Steroids can not be stopped abruptly

*Heparin
-Heparin binds with and activates antithrombin 3
-Uses :
.DVT
.pulmonary embolism
.stroke
.atrial fibrillation
.acute arterial occlusion
.cardiopulmonary bypass
-Side Effects :
.bleeding complications (can cause thrombocytopenia)
+aPTT (activated partial thromboplastin time) – laboratory test should be used to follow effect
+Who is at risk for a protamine anaphylactic reaction (Pts. with type 1 Dm, prostate surgery)
+Half-life of heparin is (90mins / 1-2hrs) / before surgery should it be discontinued from 4-6hrs preoperatively

*Warfarin (COUMADIN)
-Inhibits Vit K-dependent clotting factors 2, 7, 9, 10
-Uses :
.long term anticoagulation (PO)
-Side Effects :
.bleeding complications
.teratogenic in pregnancy
Page31

.skin necrosis
.dermatitis
+PT (prothrombin time) - laboratory test should be used to follow effect
+Half-life of warfarin is (40hrs / it takes about 2 days to observe a change in the PT) / before surgery should it be discontinued
from 3-5 days preoperatively and IV heparin should be begun

++NOTES
+Type of antihypertensive medication is contraindicated in Pts. with renal artery stenosis is (ACE inhibitors)
+Medications are used to stop seizures (benzodiazepine – lorazepam)
+Cimetidine (tagamet) / ranitidine (zofran) - H2 blocker (ulcer/gastritis)
+Ondansetron (zofran) – anti-nausea / antiemetic
+PPI – gastric acid secretion inhibitors (works by inhibiting the K, H –ATPase ‘omeprazole’)

**Types Of Surgery
+Clean Surgery
.no entry to abdomen, pelvis cavity / Example – thyroidectomy
.risk of wound infection 0% / No need to give prophylactic antibiotics
+Clean-Contaminated Surgery
.entry into chest, abdomen, pelvic cavity
.risk of wound infection 3% / You should give prophylactic antibiotics
+Contaminated Surgery
.entry to chest, abdominal, pelvic cavity
.risk of wound infection is 50% / You should give prophylactic antibiotics
+Dirty Surgery
.like intra-abdominal abscess, ruptured appendix, peritonitis or gunshot to abdomen with major spillage of GI contents
.risk of wound infection is 30% / You should give prophylactic antibiotics

+Prophylactic Antibiotics Should Be Given :

.1hr before skin incision
.M.C bacteria that cause wound infection is (Staphylococcus aureus)
.M.C source of Staphylococcus aureus is Pt. skin

By Dr.Mohammad Z. abu sheikha@

Complications
**Atelectasis
-Collapse of alveoli
-Symptoms :
.fever
Page32

.decreased breath sounds with rales

.tachypnea
.tachycardia
.increased density on CXR
.Pt. cannot breath deeply secondary to pain on inspiration
-Risk Factors :
.COPD
.smoking
.abdominal or thoracic surgery
-Prophylactic Measures Can Be Taken :
.preoperative smoking cessation
.incentive spirometry (preoperative treatment)
.good pain control
**Post-operative Respiratory Failure
-Respiratory impairment with increased respiratory rate, shortness of breath, dyspnea
-Treatment :
.supplemental O2
.chest PT (suctioning, intubation and ventilation if necessary)
-Indication For Intubation And Ventilation :
.unconscious (cannot protect airway)
.hypoxemia (Pao2<55)
.acidosis (pH<7.3 / Pco2 >50 / RR >35)
-Possible Causes Of Postoperative Pleural Effusion :
.fluid overload
.pneumonia
.diaphragmatic inflammation
-Treatment Of Postoperative Wheezing :
.albuterol nebulizer
+Why May It Be Dangerous To Give A Pt. With COPD Supplemental Oxygen ?
.this Pt. uses relative hypoxia for respiratory drive, and supplemental O 2 may remove this drive

*Pulmonary Embolism PE
-DVT that symbolizes to the pulmonary arterial system
-DVT (deep venous thrombosis – a clot forming in the pelvic or lower extremity vein)
-DVT is more common in the left iliac vein (Lt. is more common 4:1, because the aortic bifurcation crosses and possibly
compresses the left iliac vein)
-Signs & Symptoms Of DVT :
.lower extremity pain
.swelling
.tenderness
.homan`s sign (calf pain with dorsiflexion of the foot)
.pulmonary embolism PE
+Up to 50% can be asymptomatic
+Test to evaluate for DVT (Duplex ultrasonography)
-Signs & Symptoms Of PE :
.shortness of breath
.tachypnea
.hypotension
.fever
2
.loud pulmonic component of S
.hemoptysis with pulmonary infarct
-Risk Factors for DVT and PE :
.postoperative status
Page33

.multiple trauma
.paralysis
.immobility
.CHF
.cancer
.advanced age
.polycythemia
.MI
.HIT syndrome
.hypercoagulable state (protein C / protein S deficiency)
-Diagnostic Test :
.CT angiogram
-Lab Findings :
.ABG (decreased PO2 and PCO2) - from hyperventilation
-CXR Findings :
.westermark's sign
.opacity with base at pleural edge from pulmonary infarction
-ECG Findings :
.more than 50% are abnormal
.ECG most commonly shows flipped T waves or ST depression

*Aspiration Pneumonia
-Signs & Symptoms :
.respiratory failure
.CP (cerebral palsy)
.increased sputum production
.fever
.cough
.mental status changes
.cyanosis
.infiltrate on CXR
-Risk Factors :
.intubation / extubation
.impaired consciousness
.dysphagia
.nonfunctioning NGT
.trendelenburg position
.emergent intubation with full stomach
.gastric dilation
-Associated CXR findings :
.early (fluffy infiltrate or normal CXR)
.late (pneumonia, ARDS)
-Organisms are commonly involved :
.commonly acquired (gram-positive / mixed)
.hospital / ICU (gram-negative rods)
-Diagnostic tests :
.CXR
.sputum
.gram stain
.sputum culture

**Gastrointestinal Complications
-Possible NGT Complications :
.aspiration-pneumonia / atelectasis
.sinusitis
.minor UGI bleeding
.epistaxis
Page34

.pharyngeal irritation
.gastric irritation

*Post-operative Small Bowel Obstruction (SBO / ileus)

-SBO (adhesions) (Signs – flatus PR, stool PR)
-Ileus (laparotomy, hypokalemia or narcotics intraperitoneal infection)

*Blind Loop Syndrome

-Bacterial overgrowth in the small intestine
-The Surgical Causes Of B12 Deficiency :
.gastrectomy
.excision of the terminal ileum (site of B12 absorption)

*Dumping Syndrome
-That can develop after surgery to remove all or part of your stomach or after surgery to bypass your stomach to help you lose
weight
+Rapid gastric emptying is a condition where ingested foods bypass the stomach very rapidly and enter the small intestine
largely undigested
-Signs & Symptoms :
.abdominal cramps
.diarrhea (10 to 30 minutes after eating)
.nausea, vomiting
.bloating
.dizziness
.fatigue
+"Late" dumping happens one to three hours after eating. Symptoms of late dumping include (weakness, sweating, and
dizziness)
+Many people have both types
+The syndrome is most often associated with gastric bypass (Roux-en-Y) surgery

**Endocrine Complications
*Diabetic Ketoacidosis DKA
-Life-threatening complication in people with diabetes mellitus. It happens predominantly in those with type 1 diabetes, but it
can occur in those with type 2 diabetes under certain circumstances. DKA results from a shortage of insulin; in response the
body switches to burning fatty acids and producing acidic ketone bodies that cause most of the symptoms and complications
+Deficiency of body insulin, resulting in hyperglycemia, formation of keto acids, osmotic diuresis, and metabolic acidosis
-Signs & Symptoms :
.polyuria
.tachypnea
.low Bp
.dehydration
.confusion
.abdominal pain
.abdominal tender
.vomiting
-Lab Findings :
.elevated glucose
.increased anion gap
.hypokalemia
.urine ketones
.acidosis
+Electrolyte must be monitored closely in DKA (potassium and HYPOkalemia)
+You must rule out in a diabetic with DKA (infection)

*Addisonian Crisis
-is a medical emergency and potentially life-threatening situation requiring immediate emergency treatment. It is a
Page35

constellation of symptoms that indicate severe adrenal insufficiency caused by insufficient levels of the hormone cortisol
(ADRENAL DOWN)
-Signs & Symptoms :
.hypovolemic shock
.abdominal pain
.hypotension
.decreased Na+ / increased K+

*SIADH
-Syndrome of inappropriate antidiuretic hormone (ADH) secretion (low sodium)
-Causes :
.CNS trauma
.oat-cell lung cancer (or small cell carcinoma)
.pancreatic cancer
.duodenal cancer
.pneumonia
.lung abscess
.stroke
.general anesthesia
.idiopathic
.postoperative
.morphine

*Diabetes Insipidus DI
-Failure of ADH renal fluid conservation resulting in dilute urine in large amounts (decreased ADH)
+The source of ADH (posterior pituitary)
-Major Types :
.central (neurogenic DI) (decreased production of ADH) (Causes; brain injury, tumor, surgery, infection)
.nephrogenic DI (decreased ADH effect on kidney) (Causes; hypercalcemia, chronic kidney infection, amphotericin B)

**Cardiovascular Complications
-Common Causes Of Dyspnea Following Central Line Placement :
.pneumothorax
.pericardial tamponade
.carotid puncture (which can cause a hematoma that compresses the trachea)
.air embolism

*Myocardial Infarction MI
-The most dangerous period for a postoperative MI following a previous MI is (6 months after an MI)
-How do postoperative MI is present ?
.often without chest pain
.new onset arrhythmia
.hypotension
.tachypnea
.tachycardia
.bradycardia
.nausea / vomiting
.neck pain / arm pain

**Postoperative Renal Failure

-Increase in serum creatinine and decrease in creatinine clearance, usually associated with decreased urine output
+Anuria (<50cc urine output in 24hrs)
+Oliguria (>50cc and <400cc urine output in 24hrs)

**DIC
Page36

-Disseminated intravascular coagulation (DiC) is a serious disorder in which the proteins that control blood clotting become over
active
-Causes :
.tissue necrosis
.shock
.massive large-vessel coagulation
.allergic reaction
.massive blood transfusion reaction
.cardiopulmonary bypass
.cancer
.obstetric complications
.trauma
.burn injury
.liver dysfunction
**Abdominal Compartment Syndrome
-Increased intra-abdominal pressure usually seen after laparotomy or after massive IVF resuscitation (i.n., burn Pts.)
+Normal intra-abdominal pressure (<15mm Hg)
+Intra-abdominal pressure (25mm Hg), are indicates need for treatment
+How to measure intra-abdominal pressure ?
.read intrabladder pressure (foley catheter hooked up to manometry after instillation of 50-1100cc of water)

**Urinary Retention
-Enlarged urinary bladder resulting from medications or spinal anesthesia / Treated by foley catheter

**Wound Hematoma
-Collection of blood (blood clot) in operative wound

**Wound Seroma
-Postoperative collection of lymph and serum in the operative wound

**Pseudomembraneous Colitis
-Antibiotics-associated diarrhea
-Signs & Symptoms :
.diarrhea
.fever
.hypotension
.tachycardia
+Classic antibiotic causes C.difficile - clindamycin (but almost all antibiotics can cause it)
+Pt. should be NPO (nothing by mouth) at least 8 hrs before surgery
+Antihypertensive medication should be given on the day of surgery
+If Pt. on insulin or oral hypoglycemic agent (should be stopped)
+Heart failure is number 1 cause of post-operative cardiac complication
+Myocardial infarction within 6 months is the second cause of post-operative cardiac complication / MI – usually occur in 3rd
post-operative day (usually silent)
+B-blocker (atenolol, metoprolol) – decreased risk of post-operative cardiac events
+Elective surgery should be delayed for at least 6 months post-MI

By Dr.Mohammad Z. abu sheikha@

Page37

General Surgery
**Acute Abdomen And Referred Pain
-Peritoneal Signs :
.extreme tenderness
.percussion tenderness
.rebound tenderness (pain upon releasing the palpating hand pushing on the abdomen)
.voluntary guarding (abdominal muscle contraction with palpation of the abdomen)
.involuntary guarding (rigid abdomen as the muscles)
.motion pain (classic position of a Pt with peritonitis is motionless-with knee flexed)
.rigidity (late)
-Diagnosis By Quadrant :
.RUQ (M.C.C is cholecystitis)
.LUQ (M.C.C is PUD)
.LLQ (M.C.C is diverticulitis)
.RLQ (M.C.C is appendicitis)
+Classic position of a Pt. with peritonitis (motionless)
+Classic position of a kidney stone (cannot stay still, restless, writhing in pain)
+Unique differential diagnosis for the Pt. with AIDS and abdominal pain (M.C is CMV)
+Appendicitis must be considered in every Pt. with an acute abdomen (M.C.C of acute abdominal surgery)
+B-HCG (human chorionic gonadotropin) should every woman of childbearing age with an acute abdomen receive, to rule out
pregnancy / ectopic pregnancy
+Gastroenteritis (viral or bacterial infection of the GI tract, usually with vomiting and diarrhea, pain usually after vomiting, non-
surgical)
+Classic Locations Of Referred Pain :
.cholecystitis (right subscapular pain, also epigastric)
.appendicitis (early – periumbilical / rarely – testicular pain)
.diaphragmatic irritation (from spleen, perforated ulcer, or abscess) (shoulder pain – on the left + kehr`s sign)
.small bowel (periumbilical)
.rectal pain and uterine pain (midline small of back pain)
+Differential Diagnosis Of Epigastric Pain :
.PUD
.MI
.gastritis
.pancreatitis
+Differential Diagnosis Of Thoracic Causes Of Abdominal Pain :
.MI (especially inferior)
.pneumonia
.dissection aorta
.aortic aneurysm
.empyema
.esophageal rupture/tear
.esophageal foreign body
+Differential Diagnosis Of Scrotal Causes Of Lower Abdominal Pain :
.testicular torsion
.epididymitis
.orchitis
.inguinal hernia
.referred pain from appendicitis or nephrolithiasis
+Possible Causes Of Suprapubic Pain :
.cystitis
.colonic pain
.gynecologic causes
.appendicitis
+Endocrine Problems Can Cause Abdominal Pain :
.addisonian crisis
Page38

.DKA (diabetic ketoacidosis)

**Hernias
-Is a protrusion of a peritoneal sac through a musculoaponeurotic barrier
-Small defect (hernia) is more dangerous
-Causes :
.abnormal congenital anatomic route (M.C.C)
.increased intra-abdominal pressure
.straining at defecation or urination (colon caner, rectal cancer, prostatic enlargement, constipation)
.obesity
.pregnancy
.ascites
.valsavagenic (coughing)-COPD, e.g
-Complications :
.incarceration
.strangulation
.bowel necrosis
.small bowel obstruction SBO
.pain
+Reducible (ability to return the displaced organ or tissue / hernia to their usual anatomic site)
+Incarcerated (swollen or fixed within the hernia sac and may cause intestinal obstruction)
+Strangulated (incarcerated hernia with resulting ischemia)
+Littre`s hernia (hernia involving a meckel`s diverticulum)
+Obturator hernia (hernia through obturator canal / F > M / M.C in pregnancy)
+Incisional hernia (recurrent hernia;hernia through an incisional site / M.C.C is a wound infection)
+Epigastric hernia (hernia through the linea alba above the umbilicus)
+Umbilical hernia (hernia through the umbilical ring, in adults associated with ascites, pregnancy, abesity, congenital
hypothyroidism in children)
+Femoral hernia (hernia medial to femoral vessels – under inguinal ligament)
+Hesselbach`s hernia (hernia lateral to femoral vessels - under inguinal ligament )
+Indirect hernia (inguinal hernia lateral to hesselbach`s tringle)
+Direct hernia (inguinal hernia within hesselbach`s tringle)
+Hiatal hernia (hernia through esophageal hiatus)

+Boundaries Of Hesselbach`s Hernia :

.inferior epigastric vessels
.inguinal ligament (poupart`s)
.lateral border of the rectus sheath
+Layers Of The Abdominal Wall :
.skin
.subcutaneous fat
.scarpa`s fascia
.external oblique (muscle)
.internal oblique (muscle)
.transversus abdominis (muscle)
.transversalis fascia (metacarpals fascia)
.preperitoneal fat
.peritoneum

*Direct Hernias
-Hernia within the floor of hesselbach's triangle, the hernia sac does not traverse the internal ring
-Cause :
.acquired defect from mechanical breakdown over the years
+Ilioinguinal nerve L1 - runs with the spermatic cord in the inguinal canal

*Indirect Hernia
-Hernia through the internal ring of the inguinal canal, traveling down toward the external ring; it may enter the scrotum upon
exiting the external ring
-Causes :
Page39

.patent processus vaginalis (M.C.C)

+50% of all indirect hernias cases (Rt. side) / 25% (Lt. side) / 25% (Bilateral)
+The Risk Of Strangulation :
st
.Femoral hernias (1 highest risk)
nd
.Indirect hernias (2 )
rd
.Direct hernias (3 )
-Treatment :
.of emergent (herniorrhaphy is indicated if strangulation is suspected or acute incarceration is present)
.otherwise (elective herniorrhaphy is indicated to prevent the chance of incarceration or strangulation) *Femoral Hernias
+Inferior and lateral to the pubic tubercle / Below the inguinal ligament outside the inguinal canal / Medial to femoral vein /
High risk of strangulation / Surgery is indicated
+Hernia traveling beneath (under) the inguinal ligament down the femoral canal medial to the femoral vessels
+Women, pregnany and exertion are associated with femoral hernias (F > M)
+M.C hernia in women is indirect inguinal hernia

*Umbilical And Paraumbilical Hernias

-Umbilical - everted umbilicus, common in infants, and usually not complicated, repaired if remained at 5 yrs
-Paraumbilical - crescent shape umbilicus / Paraumbilical hernia is more common in adult females / High risk of strangulation /
Surgery indicated in symptomatic cases and if the content is bowel

*Epigastric Hernia
-Supra umbilical, normal shape umbilicus / Usually contains extraperitonial fat / Commonly multiple / Surgery indicated for
symptoms

*Incisional Hernia
-Usually after abdominal surgery / May be after penetrating abdominal trauma / Commonly multiple defects / 20 to 30 percent
after surgery / Open and laparoscopic repair

*Esophageal Hiatal Hernias

-Type 1 (sliding)
-Type 2 (paraesophageal)
-Type 3 (combined type 1 + type 2)
-Typer 4 (organ; colon or spleen, e.g)

1.Sliding Esophageal Hiatal Hernia

-Both the stomach and gastroesophageal junction herniate into the thorax via the esophageal hiatus (90% of all hiatal hernias)
-Symptoms :
.asymptomatic, but the condition can cause reflux
-Complications :
.reflux
.esophagitis
.Barrett`s esophagus
.cancer and stricture formation
.aspiration pneumonia
.UGI bleeding from esophageal ulcerations
-Surgical Treatment :
.laparoscopic Nissen Fundoplication (LAP NISSEN)

2.Paraesophageal Hiatal Hernia

-Herniation of all or part of the stomach through the esophageal hiatus into the thorax without displacement of the
gastroesophageal junction (5% of all hiatal hernias)
-Symptoms :
.most cases asymptomatic, but not associated with reflux
.obstruction, dysphagia, stasis gastric ulcer and strangulation
-Complications :
Page40

.hemorrhage
.incarceration
.obstruction
.strangulation

+From internal oblique muscle layer is the cremaster muscle derived

+From external oblique muscle aponeurosis layer is the inguinal ligament derived
+To what does the inguinal (poupart`s) ligament attach ?
.anterior oblique iliac spine to the pubic tubercle
+ilioinguinal nerve travels on the spermatic cord / ilioinguinal nerve is found on top pf the spermatic cord
+Genital branch of the genitofemoral nerve travels within the spermatic cord
+Spermatic Cord Contents :
.cremasteric muscle fibers
.vasa deferens
.testicular artery
.testicular pampiniform venous plexus (testicular vein)
.hernia sac (lymphatics)
.genital branch of the genito-femoral nerve
+M.C nerve injured during repair surgery (inguinal hernia) is (ileo inguinal nerve)
+Hernia sac made of (peritoneum ‘direct’ or patent processus vaginalis ‘indirect’)
+Gubernaculum attaches the testicle to the scrotum
+M.C organ in an inguinal hernia sac in men (M.C content inguinal hernia in men) (small intestine)
+M.C organ in an inguinal hernia sac in women (M.C content inguinal hernia in women) (ovary / fallopian tube)
+Round ligament lies in the inguinal canal in females instead of the VAS
+Testicular appendage is a small outpouching of testiculat tissue off the testicle
+Direct hernia goes through hesselbach`s triangle
+Inguinal anatomy :
.inguinal ligament (poupart's ligament)
.transversus aponeurosis
.conjoint tendon
+In strangulated inguinal hernia during childhood (Immediate operation must be done even the hernia reduced by sedation)
+A 3 months old infant found to have a right inguinal hernia, the best management is Surgical treatment as soon as possible
+The symptoms of epigastric hernia usually resemble Peptic ulcer
+Regarding Indirect Inguinal Hernia In Children :
.right side is M.C than left side
.boys are affected much more than girls
.incarceration occurs more often in small babies
.inguinal truss is nowadays not used in the management
+Concerning Femoral Hernia :
.the hernial sac passes through the femoral ring
.the femoral vein lies lateral to the hernial neck
.when large, it can be missed as an inguinal hernia
.it may not give positive expansive cough impulse
+Spermatic Cord Contains :
.autonomic nerve fibers
.lymphatics
.artery of the vas
.pampiniform plexus
+Rare Abdominal Wall-Hernias :
.spigelian
.lumbar
.parastomal
.obturator
.gluteal
.sciatic

**Laparoscopy
-CO2 (gas is used) because of better solubility in blood and thus, less risk of gas embolism; noncombustible, cheap, available
Page41

-Contraindications :
.absolute (hypovolemic shock, severe cardiac decompensation)
.relative (extensive intraperitoneal adhesions, diaphragmatic hernia, COPD)
-Complications :
.CO2 embolus (M.C complication)
.pneumothorax
.bleeding
.perforation injuries
.infections
.intestinal injuries
.solid organ injury
.major vascular injury
.bladder injury
.hernia at larger trocar sites
.DVT
+Classic Finding With CO2 Gas Embolus :
.hypotension
.decreased end tidal CO2 (low flow to lung)
.mill-wheel murmur
+Advantages Over Laparotomy :
.shorter hospitalization
.less pain and scarring
.lower cost
.decreased ileus
+The safest time for laparoscopy during pregnancy is (second trimester)

**Burns
+Skin Consist Of :
A) Epidermis
.the outermost layer of the skin and formed of (stratified squamous epithelium)
.contains no blood vessels
B) Dermis (divided into 2 areas – papillary region-superficial area / reticular region-deep area)
.the layer beneath the epidermis and formed of (connective tissue)
.it contains the hair follicles, sweat glands, sebaceous glands, lymphatic and blood vessels
C) SC-fat
.not part of the skin and lies below the dermis
.it attaches the skin to underlying bone and muscle and supplying it with blood vessels and nerves
+Causes :
.thermal burns (flame burns / flash burns / hot liquid or steam)
.electrical burns
.chemical burns
.lonizing radiation

+Burn Wound :
-Severity of burn is determined by its size and depth :
A) Size Of Burn
.assessed as % of TBSA
.if TBSA >15% in adults and >10% in children (serious and need hospitalization)
+RULE OF NINES measure is (burn severity determined) :
.each upper limb = 9%
.each lower limb = 18%
.anterior and posterior trunk = 18%
.head and neck = 9%
.whole hand, perineum and genitalia = 1%
Page42

B) Depth Of Burn
1) superficial burn
.involve epidermis
.it blisters and when rupture, the dermis is (pink and moist, blanches on pressure, sensitive-painful)
.heals within 3wks if no infection. There is hypo-pigmentation at first
2) deep partial thickness (deep dermal) burn
.involve superficial dermis
.it blisters but wound surface is (mottled - pink and white, no pain but discomfort, capillary refilling is slow, wound less
sensitive to pin prick)
.heals within 3-4wks if no infection but with considerable scarring
3) deep full thickness burn
.involves epidermis, dermis and may SC-fat and muscles
.the burn (white – red - brown or black, looks leathery – firm and depressed, insensitive, known as burn eschar)
.the eschar separate after 3wks. It can heal only by granulation tissue and epithelization from the edges
 .it causes contractures deformities
-Alkali chemical burns more serious than acid, because the body cannot buffer the alkaline
+Why are electrical burns so dangerous ?
.most of the destruction from electrical burns is internal because the route of least electrical resistance follows nerves, blood
vessels anf fascia; injury is usually worse than external burns at entrance and exit sites would indicate
.cardiac dysrhythmias (M.C)
.myoglobinuria (treated by-HAM; Hydration with IV fluids, Alkalization of urine with IV bicarbonate, Mannitol diuresis)
.acidosis
.renal failure (hyperkalemia)
+Myoglobinuria - is the presence of myoglobin in the urine, usually associated with rhabdomyolysis or muscle destruction.
Myoglobin is present in muscle cells as a reserve of oxygen

*First Degree Burns

.epidermis only
-Symptoms :
.painful
.dry
.red areas
.don`t (without) form blisters
-Treatment :
.pain medications
.keep clean
.neosporin

*Second Degree Burns

.epidermis and varying levels of dermis
-Symptoms :
.painful
.hypersensitive
.swollen
.mottled areas
.with blisters
.open weeping surface
-Treatment :
.pain medications + IV fluide
.remove blisters
.apply antibiotic ointment (silvadene and dressing)
+The burn center referral criteria (>20% TBSA + 10-50 yrs of age)

*Third degree burns

.also known as ‘full thickness’; all layers of the skin including the entire dermis
-Symptoms :
.painless
.insensate
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.swollen
.dry
.mottled white
.charred areas
.dried leather (dry skin)
-Treatment :
.early excision of eschar (within first week postburn) and split thickness skin graft
+The Burn Center Referral Criteria (>5% TBSA)
.2nd degree >10% TBSA in children and the elderly
.any burns involving the face, hands, feet or perineum
.any burns with inhalation injury
.any burn with associated trauma
.any electrical burns
.any chemical burns
.circumference burns

*Fourth degree burns

.burn injury into bone or muscle

nd rd rd nd
+Major clinical difference between 2 and 3 degree burns is (3 degree burns are painless and 2 degree burns are painful)
+Tetanus (prophylaxis should the burn Pt. get in the ER)
-Signs Of Smoke Inhalation :
.smoke and soot in sputum, mouth, nose, nasal, facial hair burns
.carboxyhemoglobin (lab value assessed smoke inhalation-treated with 100% O2 and time)
.mouth, throat erythema
.history of loss of consciousness
.explosion
.fire in small enclosed area
.dyspnea
.low O2 saturation
.confusion
.headache
.coma
+Diagnostic imagine is used for smoke inhalation is (bronchoscopy)
+The air way managed in the burn Pt. with an inhalation injury (intubation)
nd rd
+Parkland formula-for 2 and 3 degree burns - (V volume = TBSA burn % * weight kg * 4) used to estimate the volume of
crystalloid necessary for the initial resuscitation of the burn patient (given in the first 8 hrs, the rest in the next 16 hrs)
+Brooke formula (replace 2cc for the 4cc)
+You can place an IV or central line through burned skin
+Adult urine output goal is (30-50cc) / minimal urine output for burn Pt. is (adults 30cc - children 1-2cc/kg/hr)
+How is volume status monitored in the burn Pt.?
.urine output
+Staphylococcus aureus is the common organism found in burn wound infections
+Complication of circumferential, full-thickness burns to the extremities is (distal neurovascular impairment) and treated by
(escharotomy: full-thickness longitudinal incision through the eschar with scalpel or electrocautery)
+Major infection complication (other than wound infection) in burn Pt. is (pneumonia M.C)
rd
+From 3 degree burns wound is water evaporation highest
+Carbon monoxide inhalation overdose treated by (100% O2 or+ hyperbaric O2)
+
+Na electrolyte must be closely followed acutely after a burn
+Curling`s ulcer is the name of gastric / duodenal ulcer associated with burn injury

+Types +Layers Involved +Appearance/Feel +Sensation +Healing Time

st
.Superficial (1 degree) .Epidermis .Red without blisters (dry) .Painful .5-10 days
Page44

.Superficial partial thickness .Extends into superficial .Redness with clear blister. .Painful (very) .< 2-3wks
nd
(2 degree) (papillary) dermis Blanches with pressue (moist)

.Deep partial thickness .Extends into superficial .Yellow or white. Less blanching. .Pressure and .3-8wks
nd
(2 degree) (reticular) dermis May be blistering (fairly dry) discomfort

.Full thickness .Extends through .Stiff and white/brown. .Painless .Prolonged-months

rd
(3 degree) entire dermis NO blanching (leathery)

th
.(4 degree) .Extends through skin, .Black; charred with eschar .Painless .Require excision
into underlying fat, muscle (dry)
 and bone

+Prognosis
.Heals well; Repeated sunburns increase the risk of skin cancer later in life
.Local infection/cellulitis but no scarring typucally
.Scarring, contractures (may require excision and skin grafting)
.Scarring, contractures, amputation (early excision recommended)
.Amputation, significant functional impairment, and in some cases death
-Complications Of Burns :
.pneumonia
.cellulitis
.urinary tract infections
.respiratory failure
.anemia secondary to full thickness burns of greater than 10% TBSA is common
.electrical burns may lead to compartment syndrome
.rhabdomyolysis due to muscle breakdown
.blood clotting in the veins of the legs
.post-traumatic stress disorder

By Dr.Mohammad Z. abu sheikha@

Page45

Upper GI Bleeding
-Bleeding into the lumen of the proximal GI tract, proximal to the ligament of treitz (is a thin muscle connecting the junction
between the duodenum, jejunum)
-Signs & Symptoms :
.hematemesis
.melena (>50cc of blood)
.syncope
.shock
.fatigue
.coffe-ground emesis
.hematochezia (maroon coloured stool – fresh-blood)
.epigastric discomfort
.epigastric tenderness
.signs of hypovolemia
.guaiac-positive stools
+M.C.C of significant UGI bleeding is (PUD - duodenal and gastric ulcers)
-Causes :
.duodenal ulcer
.gastric causes (acute gastritis, gastric ulcer, gastric cancer, gastric varices, gastric antral vascular ectasia)
.esophageal causes (esophageal varices, esophagitis, esophageal cancer, esophageal ulcers, mallory-weiss tear)
+EGD is the diagnostic of choice with UGI bleeding
.Treatment Options With The Endoscopy During An EGD :
.coagulation
.injection of epinephrine (for vasoconstriction)
.injection of sclerosing agents (varices)
.variceal ligation (banding)
+Selective mesenteric angiography - test may help identify the site of MASSIVE UGI bleeding, when EGD fails to diagnose cause
and blood continues per NGT
-Indications For Surgical Intervention In UGI Bleeding :
.refractory or recurrent bleeding and site known
.>3 PRBCs to stabilize or >6 PRBCs overall
-Risk Factors For Death Following UGI Bleeding :
.age older than 60yrs
.shock
.>5 units of PRBCs transfusion
.concomitant health problems

**Peptic Ulcer Disease PUD

-Is a break in the lining of the stomach, first part of the small intestine, or occasionally the lower esophagus
+An ulcer in the stomach is known as a gastric ulcer
+In the first part of the intestines is known as a duodenal ulcer
-A peptic ulcer is caused by acid-pepsin digestion of mucous membranes
-Occur only when there is a functioning gastric mucosa capable of secretion both acid and pepsin
-Sites (an acid-pepsin secreting mucosa does not digest itself but will do so to adjacent mucous membranes of the following
Page46

sites) :
1) first part of the duodenum (commonest)
2) lesser curvature of the stomah
3) gastric antrum
4) jejunum after a gastrojejunostomy
5) lower esophagus (in reflux esophagitis)
6) small intestine adjacent to a Meckel`s diverticulum contain ectopic gastric mucosa
-Types Of Peptic Ulcers :
1) type I (ulcer along the lesser curve of stomach)
2) type II (tow ulcers present – one gastric, one duodenal)
3) type III (prepyloric ulcer)
4) type IV (proximal gastroesophageal ulcer)
-Signs & Symptoms :
.at night with upper abdominal pain or upper abdominal pain that improves with eating (pain as burning or dull ache)
.belching
.vomiting (copious vomiting), nausea
.hematemesis (vomiting of blood) (this can occur due to bleeding directly from a gastric ulcer, or from damage to the
esophagus from severe/continuing vomiting)
.weight loss, or poor appetite
.bloating and abdominal fullness
.water-brash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus - although this is more associated
with gastroesophageal reflux disease)
.melena (tarry, foul-smelling feces due to presence of oxidized iron from hemoglobin)
.rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute peritonitis, extreme, stabbing pain
+The pain caused by peptic ulcers can be felt anywhere from the navel up to the sternum, it may last from few minutes to
several hours and it may be worse when the stomach is empty
-Causes :
.history of heartburn
.gastroesophageal reflux disease (GERD)
.medicines associated with peptic ulcer include (NSAIDs that inhibit cyclooxygenase) (glucocorticoids - dexamethasone,
prednisolone)
.H.pylori (60% of gastric and up to 50-75% of duodenal ulcers) (M.C.C)
.stress (it does not seem to independently increase risk. Even when coupled with H. pylori infection)
.dietary factors, such as (spice consumption, caffeine and coffee, alcohol, smoking) (it does not seem to independently increase
risk. Even when coupled with H. pylori infection)
.gastrinoma (Zollinger–Ellison syndrome), rare gastrin-secreting tumors, also cause multiple and difficult-to-heal ulcers
-Complications :
.gastrointestinal bleeding (M.C complication) (it occurs when the ulcer erodes one of the blood vessels, such as the
gastroduodenal artery)
.perforation (sign is Valentino's syndrome)
.penetration (is a form of perforation in which the hole leads to and the ulcer continues into adjacent organs such as the liver
and pancreas)
.gastric outlet obstruction (is the narrowing of pyloric canal by scarring and swelling of gastric antrum and duodenum due to
peptic ulcers / Patient often presents with severe vomiting without bile)
.malignant transformation of a gastric ulcer
-Differential Diagnosis :
.gastritis
.stomach cancer
.gastroesophageal reflux disease
.pancreatitis
.hepatic congestion
.cholecystitis
.biliary colic
.inferior myocardial infarction
.referred pain (pleurisy, pericarditis)
.superior mesenteric artery syndrome

**Helicobacter Pylori
Page47

-It is a spirochete, spiral shape, gram negative organism

-Transmitted by feco-oral route or disinfected endoscopies
-Risk due to H.Pylori infection :
.peptic ulcer
.chronic gastritis “type B”
.cancer stomach
.mucosal associated lymphatic tissue “MALTomas”
.increase incidence of GERD
-Investigations :
.biopsy (will show the spirochete)
.rapid urease test “RUT” (done by placing a gastric biopsy into a gel containing urea and pH sensitive color indicator – if H. Pylori
is present : urea will be hydrolyzed and will change color of media / False negative result can occur in taking antibiotic or PPI)
.urea breath test “C14 breath test”
.detection of Abs against H. Pylori in blood
-Treatment :
.PPI + tow antibiotics as metronidazole and amoxicillin
+The Diagnosis Of Helicobacter Pylori Can Be Made By :
.urea breath test (radioactive carbon to detect H. pylori - carbon dioxide)
.direct culture from an EGD biopsy specimen
.direct detection of urease activity in a biopsy specimen by rapid urease test
.measurement of antibody levels in blood (does not require EGD)
.stool antigen test
.histological examination and staining of an EGD biopsy
+Malignancy (gastric cancer) (this is especially true in ulcers of the greater (large) curvature of the stomach; most are also a
consequence of chronic H. pylori infection)
+The M.C presentation of ulcer disease is midepigastric pain / There is no definite way to distinguish between duodenal and
gastric ulcers simply by symptoms
-Treatment :
.younger patients with ulcer-like symptoms are often treated with antacids or H2 antagonists before endoscopy
.people who are taking non steroidal anti-inflammatories (NSAIDs) may also be prescribed a prostaglandin analogue
(misoprostol) in order to help prevent peptic ulcers
.acid reducing medication (ranitidine and famotidine, which are both H2 receptor antagonists, provide relief of peptic ulcers,
heartburn, indigestion. They decrease the amount of acid in the stomach helping with healing of ulcers)
+In the absence of H. pylori, 4 weeks of a PPIs are also often used
.When H. pylori infection is present, the most effective treatments are combinations of 2 antibiotics (e.g. clarithromycin,
amoxicillin, tetracycline, metronidazole) and a proton-pump inhibitor (PPI)
.In complicated, treatment-resistant cases, 3 antibiotics (e.g. amoxicillin + clarithromycin + metronidazole) may be used
together with a PPI and sometimes with bismuth compound
+Surgery (stop bleeding with cautery, injection, or clipping - endoclip)
+Indication For Surgery :
.massive bleeding
.perforation (most emergent that need surgery)
.obstruction
.cancer
.failure of medical treatment (intractable)
+Valentino`s sign is (the name of the sign with RLQ pain / peritonitis as a result of succsus collecting from a perforated peptic
ulcer)

*Duodenal Ulcers (DU)

-Commoner than GU / M > F / The M.C pathophysiologic mechanism of DU is primarily related to (Gastric acid hypersecretion)
+Increased gastric acid secretion / increased gastric emptying / decreased duodenal pH
+Chronic duodenal ulcer usually occurs in the first part of the duodenum (bulb of duodenum) just distal to the junction of lyloric
and duodenal mucosa; 50% are on the anterior wall
-Signs & Symptoms :
.mid-epigastric pain, tenderness typically before meals at night, relieved by eating or drinking milk
.abdominal pain (in case of duodenal ulcers the pain appears about 3hrs after taking a meal, when the stomach begins to
release digested food and acid into the duodenum)
.nausea, vomiting
+Symptoms of duodenal ulcers would initially be relieved by a meal, as the pyloric sphincter closes to concentrate the stomach
Page48

contents, therefore acid is not reaching the duodenum

+Perforation (anterior duodenal ulcer)
+Bleeding (posterior peptic ulcer)
-Risk Factors :
.H.pylori
.drugs (aspirin, NSAIDs, steroids)
.blood group O
.smoking
.cancer of stomach
.zollinger-ellison syndrome (syndrome must you always think of with a duodenal ulcer)
.crohn disease
.head truma
.hyperparathyroidism
.chronic pulmonary insufficiency
-Diagnosis :
.upper GI endoscopy
-Treatment (medical) :
.PPIs (proton pump inhibitors)
.H2 receptor antagonists
+How is a bleeding duodenal ulcer surgically corrected ?
.opening of the duodenum through the pylorus
.oversewing of the bleeding vessel (figure 8 stitch)
+Gastroduodenal artery is involved with bleeding duodenal ulcers
+For duodenal perforation (Graham patch) (duodenal ulcer-can cause Rt. Lower quadrant abdominal pain)
+Kissing ulcer is (tow ulcers ,each on opposite sides of the lumen so that they can ‘kiss’)
+Diagnosis of perforated peptic ulcer (standing CXR - Gas under diaphragm)
+Why may a perforated duodenal ulcer present as LQ abdominal pain ?
.fluid from stomach/bile drains down paracolic gutters to LQ and causes localized irritation
-Surgery Indicated With A Bleeding Duodenal Ulcer :
.>6 PRBCs units transfusions
.>3 PRBCs units needed to stabilize
.rebleed
-Surgery Indicated :
.intractability
.hemorrhage (massive or relentless)
.obstruction
.perforation or penetration

*Gastric Ulcers
-Occur mainly on the elderly / GU may become malignant (DU are not)
-Signs & Symptoms :
.asymptomatic or epigastric pain
+Pain during the meal, as gastric acid production is increased as food enters the stomach
.weight loss
-Risk Factors :
.H.pylori
.smoking
.NSAIDs
.reflux of deudenal-contents
.delayed gastric emptying
.stress
.alcohol
.neurosurgery (cushing`s ulcers)
-Diagnosis :
.upper GI endoscopy
.biopsies from the ulcer`s rim and base
-Drugs (used in the treatment of duodenal ulcer) :
.sucralfate
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.bismuth
.sirazepine
.H2-receptors antagonists
+When and why should biopsy be performed ?
.with all gastric ulcers, to rule out gastric cancer
.if the ulcer does not heal in 6 weeks after medical treatment ,REBIOPSY must be performed (for quadrant biopsy)
-Indication For Surgery - I CHOP :
.intractability
.cancer (rule out)
.hemorrhage (massive or relentless)
.obstruction
.perforation or penetration
+Common option for a poor operative candidate with a perforated gastric ulcer (Graham patch)
+What must be performed in every operation for gastric ulcers ?
.biopsy looking for gastric cancer
+Cushing`s ulcer (PUD/gastritis associated with neurologic trauma/Head trauma or tumor)
+Curling`s ulcer (PUD/gastritis associated with major burn injury)
+Marginal ulcer (Ulcer at the margin of a GI anastomosis)
+Dieulafoy's ulcer (pinpoint gastric mucosal defect bleeding from an underlying vascular malformation)

Duodenal Ulcer Gastric Ulcer

+Age .younger .elder
+M:F .5:1 .2:1
+Pain .2-3hrs after meals .shortly after meals
.nocturnal pan
.hunger pan
+Vomiting .may occur .present with bile
.doesn`t relief the pain .relief the pain
+Appetite .good .afreaid to eat
+Weight .may be over weight .weight loss
+Size .smaller .larger
+Malignancy .not associated .associated

**Perforated Peptic Ulcer

-Symptom :
.acute onset of upper abdominal pain
+Causes pain in LQ is (passage of perforated fluid along colic gutters)
-Signs Of Posterior Duodenal Erosion/Penetration :
.bleeding from gastroduodenal artery-and possibly acute pancreatitis
-Signs Of Anterior Duodenal Perforation :
.free air-anterior perforation is more common than posterior penetration
-Diagnostic Test :
.Chest X-ray (possible to: air free within the peritoneal cavity, results from bowel or stomach perforation)
.best position for detection of free air is (Upright CxR), if you cannot get an upright CxR is the 2 nd best plain X-ray for free air is
(left lateral decubitus)
-Treatment :
.NGT tube
.IVF
.foley catheter
.antibiotics
.PPIs
.surgery
+What is the significance of hemorrhage and perforation with duodenal ulcer ?
.may indicate tow ulcers (kissing); posterior is bleeding and anterior is perforated with free air)
+Type of penetrant ulcer may present just like acute pancreatitis is (posterior duodenal ulcer)
+Classic difference between duodenal and gastric ulcer symptoms as related to food ingestion (duodenal = decreased pain /
gastric = increased pain)
Page50

**Mallory – Weiss Syndrome

-Refers to bleeding from a laceration in the mucosa at the junction of the stomach and esophagus
-This is usually caused by severe vomiting because of alcoholism or bulimia, but can be caused by any conditions which causes
violent vomiting and retching such as food poisoning
-The syndrome presents with painful hematemesis. The laceration is sometimes referred to as a Mallory-Weiss tear
+Is a non transmural tear of the lower esophagus that is related to repeated episodes of retching and vomiting
+The tear involves mucosa and submucosa but not the muscular layer (contrast to Boerhaave syndrome which involves all the
layers)
-Signs & Symptoms :
.painless swallowing (NOT difficulty)
.painless upper GI bleeding
.black stool from melena (if the volume of bleeding is >100mL or with hematemesis)
-Causes :
.alcoholism
.eating disorders
.hiatal hernia
.forceful vomiting
.NSAID abuse
+The mean age is more than 60yrs (M > F)
-Diagnosis :
.upper endoscopy
-Treatment :
.epinephrine
.cauterization

**Esophageal Variceal Bleeding

-Bleeding from formation of esophageal varices from back up of portal pressure via the coronary vein to the submucosal
esophageal venous plexuses secondary to portal hypertension from liver cirrhosis, hepatitis stones, e.g
-Signs & Symptoms :
.liver disease
.portal hypertension
.hematemesis
.caput medusa
.ascites
-Diagnosis :
.EGD
-Treatment :
.medications (lower partial pressure, somatostatin, vasopressin, B-blocker - propranolol)
+In the Pt. with coronary artery disease CAD, you must give in addition to the vasopressin (nitroglycerin)-to prevent coronary
artery vasoconstriction that may result in an MI
.sclerotherapy
.band ligation via endoscope
.TIPS (trans jugular intrahepatic portosystemic shunt - BEST TEST)
.liver transplant
+Sengstaken-Blakemore balloon is (tamponades with an esophageal balloon and a gastric balloon) and it only for bleeding from
esophageal varices – you can`t the Sengstaken-Blakemore balloon be used for treatment of mallory-weiss tear bleeding
+Problems With Shunt (TIPS) :
.decreased portal pressure
.but increased encephalopathy

**Esophageal Perforation
-M.C.C is iatrogenic (post-endoscopy)
-Symptoms :
.chest pain, subcutaneous emphysema
+Valentino Sign (RLQ pain after perforation of duodenum)
Page51

By Dr.Mohammad Z. abu sheikha@

 Stomach
-Surgical Anatomy Of The Stomach :
.the stomach is a pyriform organ lies in upper part of abdomen mainly in Lt. side
-The Parts Of The Stomach :
.cardia (lies immeduately below the end of the esophagus / represents the upper end of the organ, but is not its highest point)
.fundus (the part of the stomach which lies above and to the Lt. of the cardia)
.body (it is the major part and extends from the fundus to the antrum / the junction between the antrum and the body is a line
drawn from the incisura angularis to meet the greater curvature)
.antrum (the distal part of the stomach which ends at the pyloric sphincter)
.incisura angularis
.lesser curvature
.greater curvature
.pylorus (joins duodenum and marked from outside by the vein of Mayo)
-The Blood Supply To The Stomach :
.left gastric artery (celiac artery)
.right gastric artery (gastroduodenal artery, hepatic artery, celiac artery)
.right gastroepiploic artery (gastroduodenal artery, hepatic artery, celiac artery)
.left gastroepiploic artery (splenic artery, celiac artery)
.short gastrics (splenic artery)
-What Space Lies Behind The Stomach ?
.lesser sac; the pancreas lies behind the stomach

**GI hormones and physiology

-Stomach Cells :
.Parietal cells (secrete - HCL, intrinsic factor IF)
.Chief cells (secrete - pepsinogen)
.G-cells (secrete – gastrin) (G-cells are found in the antrum)
.Mucous neck cells (secrete - bicarbonate mucus)
+Pepsin (proteolytic enzyme that hydrolyzes peptide bonds)
+Intrinsic factor (protein secreted by the parietal cells that combines with Vit B12 and enables absorption in the terminal ileum)
-Receptors on the parietal cell that stimulate HCL release :
.histamine (enterochromaffin)
.acetylcholine (vagus nerve)
.gastrin (G-cells)
+Calcium Ca+ - Iron – folic acid – amino acid – glucose (absorbed in duodenum + jejunum)
+Vit B12 – Bile (absorbed in terminal ileum) (Vit B12 does a Pt. need after removal of the terminal ileum or stomach)
+Bile duct and pancreatic duct empty into duodenum (large intestine)
+Reabsorbs water and electrolytes (Liver)
+Hormone primarily controls gallbladder contraction (CCK)
Page52

+Gallstones made of (cholesterol)

+Electrolytes does the colon actively secrete (Na, Cl)
+Electrolytes does the colon actively secrete (HCO3)
+Electrolytes does the colon Passively secrete (K)
-GI Hormones :
.cholecystokinin (responsible for contraction of gallbladder)
.somatostatin (inhibits secretion of other GI hormones) (stimulate pancreatic secretion)
-The Blood Supply To The Liver :
.portal vein (75%)
.hepatic artery (25%)
+Small Intestine (3 meters long)

**Gastritis
A) Acute Erosive Gastritis
 .caused by NSAIDs, aspirin and alcohol
.NSAIDs inhibit cyclo-oxygenase type 1 (COX1)  decreased prostaglandin synthesis  decrease mucosal repair
B) Chronic Gastritis
1) Atrophic Gastritis
-Etiology :
.unknown
-Pathology :
.atrophy of mucosal gastric glands and chronic inflammatory reaction
.intestinal metaplasia may occur
-Types (2 types, both are associated with a higher risk of gastric carcinoma) :
.type A – pernicious anemia (involves the proximal stomach) (associated with parietal cell antibodies in the serum  atrophy
of the parietal cell mass  decrease Vit B12 absorption  lead to pernicious anemia)
.type B – non-erosive or H. Pylori associated gastritis (commoner and starts in the pylorus and spreads proximally) (there are
no parietal cell antibodies, and the acid secretion and Vit B 12 absorption are not affected)
2) Menetrier`s Disease
.a rare disorder characterized by  hypertrophic gastric mucosal folds, excessive secretion of mucus resulting in protein loss,
hypochlorhydria
.premalignant and presented by hypoproteinemia and anemia
.Trt (gastroectomy)
3) Other Types :
.phlegmonous (necrotizing) gastritis (occur in elderly diabetics and commonly caused by Hemolytic Streptococci)
.Granulomatous Gastritis (in tubercilous gastritis and CD)
.AIDS Gastritis (occur 2ry to infection with Cryptosporidiosis)
.Eosinophilic Gastritis (due to allergy and treated by steroids)
.Lymphocytic Gastritis (characterized by infiltration of gastric mucosa by T-cells)
.Refluc Gastritis
.Stress Gastritis

**Gastroeso phageal Reflux Disease GERD

-Is a chronic condition of mucosal damage caused by stomach acid coming up from the stomach into the esophagus (chronic
reflux) / GERD is caused by a failure of the lower esophageal sphincter
-Signs & Symptoms :
.heartburn and regurgitation (M.C symptoms of GERD)
.dyspepsia, odynophagia
.sore throat, hoarseness
.nausea, vomiting (repeated vomiting in infants)
.epigastric pain, chest pain (pain in the substernal area)
.coughing
.respiratory problems (wheezing, bad breath)
.increased salivation (also known as water brash)
.weight loss
.gastritis
Page53

-Risk factors :
.hiatal hernia
.obesity (delayed gastric emptying, increase-gastric volume as after large meal, gastric pressure as obesity)
.smoking, alcohol
.pregnancy, obesity
.surgery in achalasia
.Zollinger-Ellison syndrome
.high blood calcium level
.scleroderma and systemic sclerosis
.the use of medicines (prednisolone, tricyclic)
.visceroptosis or Glénard syndrome
+Factors that have been linked with GERD (but not conclusively) :
.obstructive sleep apnea
.gallstones
-Differential Diagnosis :
.chest pain such as heart disease
.respiratory and laryngeal signs and symptoms, is called laryngopharyngeal reflux (LPR) or "extraesophageal reflux disease"
(EERD). Unlike GERD, LPR rarely produces heartburn, and is sometimes called silent reflux
-Diagnosis :
.pH monitor (gold standard) (may be useful in those who do not improve after PPIs and is not needed in those in whom
Barrett's esophagus is seen)
+Investigation for H. pylori is NOT usually needed
-Treatment :
.PPIs (proton-pump inhibitors)
.omeprazole, esomeprazole, lansoprazole (will all reliably increase the PH of gastric contents)
.H2 blockers (should only be used in Pt. has very mild, intermittent symptoms)
.elevation of head at night and no meals prior to sleeping
.Lap nissen (name of surgery is nissen fundoplication) (360ْ fundoplication – 2cm long) (2cm this length of abdominal
esophagus)

+M.C.C GERD in childrens is faulty feeding habits

+M.C.C GERD in adults is relaxation of the lower tone of esophageal sphincter
+Major concern with barrett's esophagus is (developing cancer)
+Type of cancer develops in barrett's esophagus is (adenocarcinoma)
+M.C cancer of esophagus is squamous cell carcinoma + anus (other organ of GI is adenocarcinoma)
+Coronary artery disease CAD (must be ruled out when the symptoms of GERD are present)

**Achalasia
-Failure of relaxation of the lower oesophageal sphincter LES / Is a failure of smooth muscle fibers to relax, which can cause a
sphincter to remain closed and fail to open when needed
+Achalasia can happen at various points along the gastrointestinal tract; achalasia of the rectum, for instance, in Hirschsprung's
disease
-Characterized by :
.F > M / 40yrs of age
.regurgitation and aspiration pneumonia are common (food and liquid, including saliva, are retained in the esophagus and may
be inhaled into the lungs - aspiration)
.difficulty in swallowing (dysphagia - tends to become progressively worse over time and to involve both fluids and solids)
.regurgitation (of undigested food)
.sometimes chest pain (behind the sternum) (cardiospasm and non-cardiac chest pain can often be mistaken for a heart attack)
.weight loss
.coughing when lying in a horizontal position
+The M.C form is primary achalasia (which has no known underlying cause, it is due to the failure of distal esophageal inhibitory
neurons)
+Secondary achalasia (occurs to other conditions, such as esophageal cancer or Chagas disease (an infectious disease common
in South America)
-Causes :
.lymphoma
.carcinoma
Page54

.shaga`s disease
.neurotropic viruses
.ischemia
.irradiation
.drugs and toxins
.postvagotomy
+The cause of most cases of achalasia is unknown
-Diagnosis :
.esophageal manometry
.barium swallow radiographic studies
.esophagogastroduodenoscopy EGD
-Treatment :
.pneumatic balloon dilation
.pneumatic dilation or surgery (surgical myotomy)
.botulinum toxin
**Esophageal Cancer
-Is cancer arising from the esophagus—the food pipe that runs between the throat and the stomach
+Squamous cancer can arise in any part of the esophagus, and almost all tumors in the upper oesophagus are squamous
cancers
+Adenocarcinomas typically arise in the lower third of the oesophagus from barrett's esophagus or from the cardia of the
stomach
-Types :
.squamous-cell carcinoma
.adenocarcinoma
+Squamous-cell carcinoma (is linked to lifestyle factors such as smoking and alcohol)
+Adenocarcinoma (is linked to effects of long-term acid reflux - history of GERD and Barrett's esophagus)
+Long standing GERD can induce a change of cell type in the lower portion of the esophagus in response to erosion of its
squamous lining
+Tobacco is a risk factor for both types
+Both types are more common in men and in the over-60s
-Signs & Symptoms :
.narrowing of the tube
.difficulty in swallowing (M.C symptom) (with solid foods and later with softer foods and liquids)
.weight loss (is often an initial symptom in cases of squamous-cell carcinoma, though not usually in cases of adenocarcinoma)
.pain behind the breastbone or in the region around the stomach
.heartburn
.husky, raspy, or hoarse-sounding cough
.nausea and vomiting, regurgitation
-Complications :
.increased risk of aspiration pneumonia
.fistulas (that may develop between the esophagus and the trachea)
.coughing on drinking or eating
.vomiting of blood
.upper airway obstruction
.superior vena cava syndrome
.hypercalcemia
.result of the tumor affecting the recurrent laryngeal nerve
-Diagnosis :
.endoscopy (BEST)
.barium swallow
-Treatment :
.esophagectomy is the removal of a segment of the esophagus
.chemotherapy depends on the tumor type (chemotherapy may be given after surgery or if surgery is not possible; in this case,
cisplatin and 5-FU are used)
.radiotherapy is given before, during, or after chemotherapy or surgery, and sometimes on its own to control symptoms
+In patients with localised disease but contraindications to surgery, "radical radiotherapy" may be used with curative intent
Page55

**Gastric Cancer (Stomach)

-Most commonly in the antrum or the lesser curvature
-Histopathology :
.adenocarcinoma (90%) (is a malignant epithelial tumor)
.lymphomas (5%) (MALTomas, or MALT lymphoma)
.carcinoid and stromal tumors
-Signs & Symptoms :
.weight loss (M.C symptom)
.emesis
.anorexia
.pain/epigastric discomfort
.obstruction
.nausea
.sweating
+M.C early symptoms is (mild epigastric and indigestion)
.anemia (megaloblastic anemia, anemia of chronic disease)
.melena
.hemoccult (guaiac test)
.epigastric mass (in advanced disease)
.hepatomegaly
.coffe-ground emesis
.blumer`s shelf (solid peritoneal deposit anterior to the rectum, forming a ‘shelf’, palpated on rectal exam)
.virchow`s node (metastatic gastric cancer to the nodes in the LEFT supraclavicular fossa)
.enlarged ovaries
.axillary adenopathy
-Risk Factors :
.diet (smoked meats, high nitrates, low fruits and vegetables/a diet that includes fruits and vegetables rich in Vit C, alcohol,
tobacco)
.environment (raised in high-risk area, poor socioeconomic status)
.atrophic gastritis
.gastric ulcers
.male gender (M > F)
.blood group type A (associated with gastric cancer) (Blood group tpe O is risk factor for peptic ulcer)
.previous partial gastrectomy
.pernicious anemia
.polyps
.H.pylori
+Sister mary joseph's sign is (periumbilical lymph node gastric cancer metastasis; present as periumbilical mass)
+Krukenberg's tumor is (gastric cancer or other adenocarcinoma, that has metastasized to the ovary)
+Irish`s node is (left axillary adenopathy from gastric cancer metastasis)
+Surveillance laboratory findings is (CEA elevated in 30% of cases)
+Histology (adenocarcinoma) / anus – esophagus (squamous cell carcinoma)
-Histologic Types :
.intestinal (glands)
.diffuse (no glands)
-Morphology Types :
.ulcerative (M.C morphologic type of gastric cancer)
.polypoid
.scirrhous
.superficial
.linitis plastica (leather bottle)
+Gastric cancer more common on the lesser curvatures / proximal gastric cancer is more common
-Gastric adenocarcinoma metastasize (spread to other sites in the body by metastasize) :
.hematogenously
.lymphatically
.90% are adenocarcinoma
.5% of gastric malignancies are lymphomas (M.C GI lymphoma)
.M.C site for GI lymphoma is stomach
Page56

.metastasis occurs in 80-90% of individuals with stomach cancer

.M.C site for metastasis is liver
-Diagnosis :
.upper endoscopy + biopsy
-Management :
.chemotherapy and radiation
+Signs of advanced Gastric cancer :
.krukenberg tumor (metastasis to ovary)
.irish nodes (axillary nodes)
.virchow nodes (it supraclavicular lymph nodes)
.sister mary joseph nodes
+Pts. with gastric cancer are NON-operative :
.distant metastasis (liver metastasis, bone metastasis)
.peritoneal implants
+Genetics markers (genetic alteration) :
.gastric cancer (P53)
.pancreatic carcinoma (ca-19-9)
.colon cancer (CEA)
+H.pylori can cause :
.peptic ulcer
.gastric cancer
.maltoma (gastric lymphoma)

**Gist
-Gastrointestinal stromal tumor / previously known as leiomyosarcoma
-Cell of origin is (CAJAL, interstitial cells of cajal)
+CAJAL cells is found in (GI tract –esophagus to rectum, most commonly found in stomach)
-Signs & Symptoms :
.GI bleed
.occult GI bleed
.abdominal pain
.abdominal mass
.nausea
.distension
-Diagnosis :
.CT scan
.EGD
.colonoscopy
+Tumor marker is (C-KIT)(CD117 antigen)
+Prognosis (>5cm size - >5per 50HPE mitotic rate)
+Chemotherapy for metastatic or advanced disease is (imatinib-tyrosine kinase inhibitor)
+H.pylori is causative agent
-Treatment :
.nonsurgical (treat H.pylori by antibiotics
.triple therapy and chemotherapy
.radiotherapy (XRT) in refractory cases

**Bariatric Surgery
-(Weight loss surgery) includes a variety of procedures performed on people who have obesity. Weight loss is achieved by
reducing the size of the stomach with a gastric band or through removal of a portion of the stomach (sleeve gastrectomy or
biliopancreatic diversion with duodenal switch) or by resection and re-routing the small intestine to a small stomach pouch
(gastric bypass surgery
+BMI (body mass index) >40 (>100 pounds above ideal body weight)
+BMI >35 (with a medical problem related to morbid obesity)
Page57

By Dr.Mohammad Z. abu sheikha@

 Small Intestinal
**Small Bowel
-Comprises The Small Bowel :
.duodenum (12 inches)
.jejunum
.ileum
+Treitz is (marks the end of the duodenum and the start of the jejunum)
+Length of the entire small bowel is (6 meters-20 feet)
+Provides blood supply to the small bowel (branches of the superior mesenteric artery)
-The Major Structural Differences Between The Jejunum And The Ileum Is :
.jejunum (long vasa recta, large plicae circulares, thicker wall)
.ileum (shorter vasa recta, smaller plicae circulares, thinner wall)

*Small Bowell Obstruction (SBO)

-Signs & Symptoms :
.abdominal discomfort/distension
.colicky abdominal pain
.cramping
.nausea
.vomiting (green) (early sign in SBO / late sign in LBO)
.constipation
.high-pitched bowel sounds (hyperactive bowel sounds)
.previous abdominal or pelvic surgery
-Causes (M.C.C of adult SBO) :
.adhesions (M.C in adults) (postoperative adhesions)
.bulge (hernias) (M.C in childrens)
.cancer/tumors
+Other causes
.gallstone ileus
.intussusception
.volvulus (sigmoid)
.external compression
.SMA syndrome
.bezoars
.bowel wall hematoma
.abscesses
.diverticulitis
.IBD (CD, UC)
.radiation enteritis
Page58

.annular pancreas
.meckel's diverticulum
.peritoneal adhesions
.stricture
-Classic Electrolyte/Acid-Base Findings With Proximal Obstruction :
.hypovolemic
.hypochloremic
.hypokalemic
.alkalosis
+You must be ruled out on physical exam in Pts. with SBO (incarcerated hernia)
+ incarcerated hernia - if the omentum or a loop of intestine becomes trapped in the weak point in the abdominal wall, it can
obstruct the bowel, leading to severe pain, nausea, vomiting, and the inability to have a bowel movement or pass gas /
triangulation. An incarcerated hernia may cut off blood flow to part of your intestine. This condition is called strangulation, and
it can lead to the death of the affected bowel tissue
+Major AxR Findings Are Associated With SBO (dilated small-bowel loops of small bowel with air-fluid levels on upright film)
-Complication :
.closed loop strangulation of the bowel leading to bowel necrosis
+Test can differentiate partial from complete bowel obstruction (CT scan with oral contrast)
+Superior mesenteric artery (SMA syndrome) :
.seen with weight loss –SMA compression duodenum, causing obstruction (gastro-vascular disorder)
-Treatment of SBO :
.initial management (NPO, NG tube, IV fluid, Foley)
.laparotomy
.lysis of adhesions (LOA)
.tumors or hernia (need surgery)
+M.C indication for abdominal surgery in Pts. with crohn`s disease is (SBO due to strictures)
+The #1 cause of SBO in adults is (postoperative adhesions)
+The #1 cause of SBO around the world is (hernias)
+The #1 cause of SBO in children is (hernias)
+Signs Of Strangulated Bowel With SBO :
.fever
.shock
.peritoneal signs
.acidosis
+Absolute Indication For Operation With Partial SBO :
.peritoneal signs
.free air on CXR
+Tumor classically caused SBO due to ‘mesenteric fibrosis’ is carcinoid tumor
+In small intestine obstruction, the most helpful diagnostic method is CT scan
+On supine abdomen X-Ray for intestinal obstruction, the small bowel is identified by Valvulae conniventes
+Obstruction Of The Lower Intestinal Tract Could Be Caused By :
.Hirschsprung's disease
.Meconium ileus
.Ileal atresia
.Malrotation of the colon
+The M.C.C of colonic obstruction is cancer

*Large Bowel Obstruction (LBO)

-Symptoms :
.abdominal distension (M.C symptom)
.vomiting (late sign)
-Causes :
.neoplasms (colon cancer is the M.C)
.hernias
.IBD (CD, UC)
.colonic volvulus (sigmoid, caecal, transverse colon)
.adhesion
.constipation (fecal impaction)
Page59

*Small Bowel Tumors (SBT)

-SBT account for 1-5% of GI tumors (rare) (SBT is less than colon tumor)
-Signs & Symptoms :
.abdominal pain
.weight loss
.obstruction (SBO)
.perforation
.bleeding
-The Differential Diagnosis Of Benign Tumors Of The Small Intestine Is :
.leiomyoma (M.C benign small bowel tumor)
.lipoma
.lymphangioma
.fibroma
.adenomas
.hemangiomas

-The Differential Diagnosis Of Malignant Tumors Of The Small Intestine Is :

.adenocarcinoma (M.C malignant small bowel tumor) (mostly in duodenum) (GI – adenocarcinoma except esophagus and anus
and M.C site is stomach)
.carcinoid (M.C in appendix)
.lymphoma (arising in ileum)
.sarcomas
-Treatment for malignant small bowel tumor :
.resection and removal of mesenteric draining lymph nodes
+Malignancy is classically associated with metastasis to small bowel is melanoma

*Meckel`s Diverticulum
-A true congenital diverticulum, is a slight bulge in the small intestine present at birth and a vestigial remnant of the
omphalomesenteric duct (also called the vitelline duct or yolk stalk)
-More common in males – most in the first 2yrs of life, but can occur at any age
+Major differential diagnosis (appendicitis)
+M.C congenital GI anomalies / M.C malformation of the GI
+M.C symptoms is painless lower GI bleeding
-Signs & Symptoms :
.SBO (intestinal obstruction is M.C complication in adults)
.the majority of people with a Meckel's diverticulum are asymptomatic (An asymptomatic Meckel's diverticulum is called a
silent Meckel's diverticulum - If symptoms do occur, they typically appear before the age of two years)
.painless rectal bleeding such as melena-like black offensive stools (M.C symptom) (lower GI bleeding)
.intestinal obstruction, volvulus and intussusception
.Meckel's diverticulitis may present with all the features of acute appendicitis (RLQ pain)
.severe pain in the epigastric region is experienced by the patient along with bloating in the epigastric and umbilical regions
.the symptoms are so painful that they may cause sleepless nights with acute pain felt in the foregut region, specifically in the
epigastric and umbilical regions
+In most cases, bleeding occurs without warning and stops spontaneously. The symptoms can be extremely painful, often
mistaken as just stomach pain resulting from not eating or constipation
-Possible Complications :
.intestinal hemorrhage (painless)
.intestinal obstruction (M.C complication in adults)
.inflammation (+perforation)
+M.C ectopic tissue in a Meckel`s diverticulum (gastric mucosa)
-Diagnosis :
.technetium-99m (99mTc) pertechnetate scan, also called Meckel scan (this scan detects gastric mucosa)
-Treatment :
.surgical, potentially with a laparoscopic resection
+In patients with bleeding, strangulation of bowel, bowel perforation or bowel obstruction, treatment involves surgical
resection of both the Meckel's diverticulum itself along with the adjacent bowel segment, and this procedure is called a "small
bowel resection"
Page60

+In patients without any of the aforementioned complications, treatment involves surgical resection of the Meckel's
diverticulum only, and this procedure is called a “simple diverticulectomy”
+Rule Of 2's In Meckel's Diverticulum :
.occur in 2% of the population
.are 2 inches (5cm) long
.are 2 feet (60cm) from the ileocecal valve
.2/3rds have ectopic mucosa
.2 types of ectopic tissue are commonly present (mostly gastric and pancreatic)
.2% become symptomatic
.symptoms start before 2yrs of age
+Hernia associated with incarcerated meckel`s diverticulum is (littre's hernia)
+M.C.C of small bowel bleeding is (small bowel angiodysplasia)
By Dr.Mohammad Z. abu sheikha@

Appendix
-The vermiform appendix is a blind-ending hollow muscular tube that arises from the caecum at the confluence of the taeniae
coli commonly present in the Rt. iliac fossa
+How can the appendix be located if the cecum has been identified ?
.follow the taenia coli down to the appendix; tha taenia converge on the appendix
+Length 7.5- 10cm
+Diameter of appendix is 3-8mm
+Diameter of lumen is 1-3mm
-Anatomical Position Of Appendix :
.retrocaecal appendicitis (74% - M.C site) (abdominal examination reveals minimal tenderness, rigidity or guarding-silent
appendix / pain is felt in the Rt. loin / +ve psoas sign)
nd
.pelvic appendicitis (21% - the 2 common) (doesn`t produce somatic pain but may cause suprapubic discomfort / tenesmus
and early diarrhea from rectal irritation / frequent micturation or dysuria from bladder irritation / abdominal signs are minimal
and tenderness is elicited on pelvic examination / +ve obturator sign)
.paracaecal (2%)
.subcaecal (1.5%) (pain and tenderness are higher than the McBurney`s point / the condition is commonly misdiagnosed as
cholecystitis)
.pre-ileal (1%)
.post-ileal (0.5% - the least common) (pain shifting may not occur / diarrhea is a feature due to irritation of the ileum)
*NB. :
.short ascending colon (the caecum will be subhepatic)
.long ascending colon (the caecum may lie in the pelvis)
.pregnancy change the position (the enlarging uterus progressively displaces the caecum and the appendix up towards the Rt.
hypochondrium
.in some cases with nonexistent mesoappendix (the appendix lies beneath the serosa of the caecum and is called a subserous
appendix)
+McBurney's point is the name given to the point over the right side of the abdomen that is 1/3 of the distance from the
anterior superior iliac spine to the umbilicus (navel). This point roughly corresponds to the most common location of the base
of the appendix where it is attached to the cecum
-Vessel Provides Blood Supply To The Appendix :
.appendiceal artery (branch of the ileocolic artery) – Superior mesenteric artery

**Appendicitis
-Inflammation of the appendix caused by obstruction of the appendiceal lumen, producing a closed loop with resultant
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inflammation that can lead to necrosis and perforation (Obstructive of appendix lumen, cause by fecalith, lymphoid-
hyperplasia)
-Appendicitis is the M.C acute abdominal surgical emergency
-Pathology :
.luminal obstruction with continues mucus secretion and inflammatory exudation, increase intraluminal pressure, obstructing
lymphatic drainage (Lymphedema)
.odema, mucosal ulceration, bacterial translocation to the submucosa
.continues rise in pressure lead to venous obstruction and ischemia of the appendix wall
.ischaemic necrosis of the wall produce gangrene and peritonial contamination
.greater omentum and small bowel loops adhere to localize the inflammation
-Types :
A) Gross Type
1) Obstructive Acute Appendicitis
.occur in about 2/3 of cases
.inflammation is initiated by obstruction of the lumen and caused by (Commonly – faecolith-inspissated stool / swelling of the
 lymphoid tissue in response to viral infection) (Less commonly – kinking by adhesions / intestinal parasites, pin worms-oxyuris
vermicularis / tumors of the appendix or the caecum)
2) Non-obstructive Acute Appendicitis
.occur in 1/3 of cases
.common in Pts. having constipation
.inflammation usually starts in the mucosa and tends to remain there (catarrhal inflammation)
.it may spread but at a slower rate and is less likely to occur
B ) Course (in untreated cases the course of the disease is variable)
1) Acutely inflamed appendix may resolve but recurrence is likely to occur
2) Persistent obstruction (particularly with a faecolith) tends to produce gangrene and perforation –
.it occurs either at the tip where the appendicular vessels are very close to the wall or are even intramural or a the site of
impaction of the faecolith
.perforation is followed by generalized or localized peritonitis, depending on the severity of inflammation and the efficiency of
of the body defense
.the incidence of perforation is high in the very young below 5yrs and in the elderly
.the risk of perforation is 25% after 24hrs from onset of pain and rises to 50%, after 36hrs
3) Perforation of the appendix within an appendicular mass produces ana appendicular abscess
4) Portal Pyaemia (Pylephlebitis)
.rare complication
.results from suppurative thrombophlebitis of the portal venous system
.hallmarks of this grave condition (chills, high fever, low grade jaundice and later hepatic abscesses)
-Special Signs :
.Obturator sign (is pain on internal rotation of the flexed Rt. thigh is caused by irritation of the obturator internus by pelvic
appendicitis and seen in Pts. with pelvic appendicitis)
.Psoas sign (is pain on extension of the Rt. thigh that is caused by psoas spasm as a result of irritation by retrocaecal
appendicitis and seen in retrocecal appendicitis)
.Rovsing`s sign (if palpation of the LLQ of a person's abdomen increases the pain felt in the RLQ)
.Valentino`s sign (is pain presenting in the RLQ of the abdomen caused by a duodenal ulcer with perforation through the
retroperitoneum)
.McBurney's sign
-Clinical Features :
.shifting acute pain (the pain shifts to the Rt. iliac fossa and becomes sharper and more localized)
.peri-umbilical colic
.the pain is aggravated by movement or cough
.anorexia and nausea (always present)
.vomiting (occurs in about ¾ of the Pts. and is not usually repeated) (always is preceded by the pain and if vomiting precedes
the abdominal pain, ou should think of another diagnosis “like gastroenteritis”)
.constipation (is usual)
.temperature and pulse
.rebound tenderness – localized tenderness is present in the Rt. iliac fossa over the McBurney`s point (tenderness may be
absent)
.it also reveals tenderness or a mass in case of pelvic appendicitis
+Restricated abdominal wall movement with respiration indicates peritonitis
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+If the Pt. presents on the 3rd or 4th day of attack, a tender appendicular mass may be felt in the Rt. iliac fossa
+Rigidity indicates perforation
-Causes :
.low fiber diet / High sugar diet
.luminal obstruction (fecalith – is M.C, stricture, lymph node enlargement - lymphoid-hyperplasia, tumor, foreign body,
pinworms)
.bacterial over growth within the lumen (mixed aerobic, anaerobic)
+It is most prevalent in 20-30yrs old, after that the risk decrease with age -
.in the infant (the appendix is wide-mouthed and well drained – very rare)
.in the elderly (the lumen is almost obliterated and the wall contains little lymphoide tissue “senile atrophic appendix”)
.male to female ratio 3:2 - at age of 25yrs thereafter this declines
.life time risk for appendectomy is 8.6% for males and 6.7% for females
+Appendicitis in infants and young children (rare but more serious and below the age of 3yrs, 80% of Pts. will have perforated
appendicitis due to the following) :
.difficulty of examination of an infant or young child
.the greater omentum is not well developed and so localization is difficult
.there is prominent vomiting and the case may wrongly be diagnosed as gastritis or enteritis
+Appendicitis in the elderly :
.produces little tenderness and rigidity, but perforation and gangrene is common
.eliciting the signs of acute appendicitis is more difficult if the Pt. is obese
.the danger of late diagnosis of a perforated appendix is further aggravated by the natural weakness of the immune system

+Appendicitis With Pregnancy :

.usually the site of pain is displaced upwards as pregnancy progresses
.also the localization by the omentum is less efficient and the condition is often misdiagnosed as pyelitis
.if the diagnosis and operation are delayed until perforation (the risk of abortion or premature labour are 50%, while if the Pt. is
operated upon before perforation, premature labour occurs only in 30% of cases)
.appendix may be in RUQ because of the enlarged uterus
-How does appendicitis classically present ?
.start periumbilical pain (intermittent and crampy) (Visceral pain - dull, poorly localized)
.nausea / vomiting-once
.anorexia (M.C sign-early sign)
.pain migrates to RLQ (T10 nerve) (constant and intense pain / usually in 6hrs) (Parital pain - sharp, well localized)
.mild fever
-Physical Exam :
.RLQ-tenderness + Rebound tenderness
.Rovsing sign (LLQ lead to RLQ)
.Psoas sign
.Obturator sign
.Hamburger sign
-Complications Of Acute Appendicitis :
.perforation (with generalized peritonitis) - fever, tachycardia, generalized peritonitis (rare before 12 hr) (treated by I.V
antibiotics + percutaneous drainage + appendectomy after 4-6wks)
.postoperative wound infection - 3%-4.7%.
.intra-abdominal and pelvic abscesses (liver abscess – rare) - u/s or CT guided aspiration
.pylephlebitis - septic portal vein thrombosis, E.coli (It is usually a complication of intra-abdominal sepsis, most often following
diverticulitis, perforated appendicitis, or peritonitis)
.intestinal obstruction - X4 in perforated
.enterocutaneous fistula - leak from the stump
-Risk Factors For Perforation Of The Appendix :
.extremes of age
.immunosuppression
.DM
.fecalith or coprolith obstruction
.pelvic appendix
.previous abdominal surgery
-Tests Should Be Performed :
.CBC (increased WBCs >10.000per/mm3) – a leukocytosis with a predominance of neutophils is usual (however, a normal WBC
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count does not rule out appendicitis)

.urinalysis (may show few RBC) (the presence of a large RBCs or pus cells raises the suspicion of a ureteric calculus or UTI)
+Selective Investigations :
.pregnancy test (if ectopic pregnancy is suspected)
+You can have an abnormal urinalysis with appendicitis (mild hematuria and pyuria are common in appendicitis with pelvic
inflammation, resulting in inflammation of the ureter / A positive urinalysis don`t rule out appendicitis)
+Radiographic Signs Of Appendicitis On AxR :
.scoliosis away from the right because of pain
.mass effect (abscess)
.very rarely a small amount of free air if perforated
-Preoperative Medications / Preparation :
.rehydration with IV fluids (LR)
.preoperative antibiotics with anaerobic coverage (appendix is considered part of the colon) (metronidazole)
+M.C general surgical abdominal emergency in pregnancy is (appendicitis) (appendix may be in RUQ because of the enlarged
uterus)
+M.C postoperative complication is (wound infection)
+You can find the appendix after identifying the cecum (follow the taenia down to where they converge on the appendix)
-Differential Diagnosis (depending on age and sex of the Pt.):
+Children
.gastroenteritis
.mesenteric lymphadenitis (commonest organism is Yersinia)
.intussusception (appendicitis is Uncommon before the age of 2yrs, but the median age of intussusception is 18 months)
.henoch-schonlein purpura (preceded by sore throat or respiratory infection(
.lobar pneumonia and pleurisy
.cyclic vomiting
+Adult female
.mittelschmerz
.PID
.pyelonephritis
.ectopic pregnancy and tubal abortion
.torsion / rupture of ovarian cyst
.endometriosis
.red degeneration in a fibroid
+Adult
.regional enteritis
.ureteric colic
.Rt. pyelonephritis
.perforated peptic ulcer
.torsion of testis (testicular torsion)
.acute pancreatitis
.rectus sheath haematoma
+Elderly
.sigmoid diverticulitis
.intestinal obstruction
.colonic carcinoma (cancer of the caecum)
.torsion appendix epiploica
.mesenteric infarction
.leaking aortic aneurysm
+Other Differential Diagnosis
.prehepatic pain of herpes zoster affecting Rt. 10th, 11th and 12th dorsal nerves
.acute cholecystitis
.iliac adenitis
+Medical Differentials
.DKA
.familial mediterranean fever
+Differential Diagnosis Of An Appendicular Mass :
.carcinoma of the caecum (associated with anemia and weaknes)
.CD
.hyperplastic ileo-caecal
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+Appendectomy is contraindicated in Pts. with CD

*Appendiceal Tumors (Neoplasms The Appendix)

-M.C appendiceal tumor is (carcinoid tumor)
+Carcinoid Tumors (Argentaffinoma)
-Slow growing type of neuroendocrine tumor - Kulchitsky cell or Enterochromaffin cell / Mostly benign and <5% malignant
-Most commonly found in appendix / M.C site for metastasis is liver
-The appendix is also the commonest site in the gut to be affected by carcinoid tumor (65%) while the ileum is affected in (25%)
-About 10% of carcinoids secrete excessive levels of a range of hormones – Secrete Serotonin (5-HT) and this hormone can
cause carcinoid syndrome
-The tumor arises from Kultchitsky cells in the depth of the mucosal pits
-The distinction between benign and malignant tumors depends maily on the biological behavior (tumors <1cm are usually
benign) (tumors >2cm are almost always malignant and metastasize to the liver so may produce the rare carcinoid syndrome
because of their production of serotonin)
+Can occur in any part but commonly found in the distal 1/3
-Clinical Features :
.commonly asymptomatic
.carcinoid tumor is sometimes an accidental histological diagnosis in an appendix that has been removed because of chronic
acute appendicitis
.carcinoid syndrome (rare and produced only by malignant carcinoid tumors that metastasize to the liver) – It includes one or
more of the following (flushing with attacks of cyanosis – Redness / diarrhea with borborygmi – rumbling in the stomach caused
by intestinal gas / wheezing – bronchospasm and pulmonary stenosis / abdominal cramping / cardiac valvular disease with
long-standing cases - Rt. side heart failure)
-Common Sites Of Occurrence :
.Appendix (M.C)
.ileum
.Rectum
.bronchus
-Diagnosis :
.high levels of 5-HIAA (5-hydroxy indole acetic acid) in the urine (high urinary concentrations of the serotonin metabolite 5-
hydroxyindoleacetic acid)
-Treatment :
.surgery
+On apex and <1.5cm (Appendectomy)
+On base or >1.5cm (Open Rt. Hemicolectomy) - (open right colectomy) is a procedure that involves removing the cecum

+Adenocarcinoma
-Very rare
-The tumor behaves as carcinoma of the colon
-Trt (if it is confined to the appendix and the regional lymph nodes – Rt. hemicolectomy)

*Appendectomy
-Indications :
.acute appendicitis is the commonest indication and is an urgent one
.for appendicular mass and abscess, apendicectomy is performed 3-6 months after resolution “interval appendectomy”
.chronic appendicitis
.carcinoid tumor smaller than 2cm and confined to the appendix
-Steps :
.the Pt. should be fasting for a few hrs before the operation
.prophylactic parenteral antibiotics (they are started one hour before the operation and mey be continued after the operation
for a variable time depending on the severity of appendicitis and the presence of peritonitis
a) for uncomplicated cases (one preoperative dose and another given after 6hrs are sufficient; the so called peri-operative
antibiotic prophylaxis)
b) the standard to use a combination of an agents against (Anaerobes – metronidazole or clindamycin) (Gram negative bacilli
– aminoglycoside)
.anaesthesia (under general or spinal anaesthesia with Pt. lies in supine position)
.incisions :
a) gridiron (McBurney`s) incision
Page65

.the best for most Pts.

.located over the area of maximal tenderness wich is usually, but not always, the McBurney`s point
.the gridiron incision is an oblique one 2-3 inches long
b) rutherford morison`s incision
.preferred in some cases if the appendix is para-caecal or retro-caecal
.this is done by cutting through the internal and transversus abdominis muscles
c) exploratory lower Rt. paramedia incision
.done if the diagnosis is doubtful particularly in the presence of intestinal obstruction
.if pus or serous fluid is present in the peritoneal cavity, a sample is taken for culture and sensitivity and the pus is then
evacuated
.exploration of pelvis and terminal ileum is done to exclude gynecologic problems and Meckel`s diverticulitis for Pts. in whom
the appendix is not apparently inflamed
.the caecum is located and the appendix is found at the confluence of the taeniae coli
+Complications Common To All Surgical Procedure :
.bleeding ftom a slipped mesoappendix ligature
.chest infection
.wound infection
.deeo vein thrombosis DVT
.distension due to paralytic ileus or early fibrinous adhesions
.intestinal obstruction
.female infertility
.incisional hernia
+Complications Specific To Appendicectomy :
.peritonitis
.iliac or pelvic abscess
.faecal fistula

**Mesenteric Lymphadenitis
-Is an inflammation of lymph nodes. The lymph nodes that become inflamed are in a membrane that attaches the intestine to
the abdominal wall. These lymph nodes are among the hundreds that help your body fight disease. They trap and destroy
microscopic "invaders" like viruses or bacteria
-Mesenteric lymphadenitis often causes abdominal pain. It is most common in children and teens
-Signs & Symptoms :
.sore throat
.RLQ or center abdomen pain, tenderness
.high fever, feeling ill
.loss of appetite
.raised WBCs
.nausea, vomiting, diarrhea
-Causes :
.infections (M.C.C) (Yersinia enterocolitis) (common infections; Viral - rotavirus, norovirus / Bacterial - salmonella, staphylo.,
strepto., Yersinia entero., HIV)
.cancers (lymphoma, breast cancer, lung cancer, pancreatic cancer, gastrointestinal cancer)
.inflammatory conditions (appendicitis, TB, gastroenteritis, IBD, diverticulitis, pancreatitis)
-Complication :
.septicemia (which can cause death)
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By Dr.Mohammad Z. abu sheikha@

Colon And Rectum

-Parts Of GI Tract Do Not Have A Serosa :
.esophagus
.middle rectum
.distal rectum
-Major Difference Between The Colon An The Small Bowel :
+Colon +Small Bowel
.taenia coli .serosa
.haustra .blecaser colares
.appendices epiploicae .no fat appendages
(fat appendages)
-Blood Supply To The Rectum :
.proximal (superior hemorrhoidal-superior rectal) from inferior mesenteric artery IMA
.middle (middle hemorrhoid or middle rectal) from the hypogastric (internal iliac)
.distal (inferior hemorrhoidal or inferior rectal) from the pudendal artery (a branch of the hypogastric artery)
-Venous Drainage Of The Rectum :
.proximal (via the inferior mesenteric artery IMA, then to the portal vein)
.middle (via the iliac vein to the IVC)
.distal (via the iliac vein to the IVC)

**Colorectal Carcinoma (Colorectal Cancer)

-Adenocarcinoma of the colon or rectum
-Incidence :
.M.C GI cancer
(Female: lung cancer / breast cancer / colon cancer) (9%)
(Male: prostate cancer / lung cancer / colon cancer) (10%)
(M-F: lung cancer / colon cancer)
th
.it is the 4 M.C tumor of all tumor (Broncogenic carcinoma, Breast cancer, Cervical tumor, Colorectal cancer)
.second M.C.C of cancer deaths
.incidence increase with age starting at 49 yrs and peaks at 70-80 yrs
.metachronous  increase the risk of a second tumor in the same organ
+Lynch Syndrome (Hereditary nonPolyposis Colorectal Cancer / autosomal-dominant / inheritance of high risk for development
Page67

of colon cancer / 100% malignant)

-Etiology :
1) genetic (hereditary non polypoid colorectal carcinoma)
2) precancerous lesions (as ulcerative colitis “pseudopolyps”, chronic disease in small intestine and FAB)
3) environmental (low residue diet)
4) failial
5) predisposing factors (smoking, obesity, ureterosigmoidostomy, pelvic irradiation, history of cholesystectomy 20-25yrs)
-Clinical Pathology :
.site (the M.C site to develop cancer is the lower part of the organ, 70% in rectosegmoid and 15% in cecum)
.spread (direct – penetration of the bowel wall and neightboring structures / lymphatic – epicolic, paracolic, intermediate and
central / transcoelmic)
-Signs & Symptoms :
.weight loss (late sign)
.blood in the stool
.constipation
.change in bowel habit (if associated with bleeding)
.rectal bleeding
.anemia (iron-deficiency anemia)
+Right-Sided Lesions
.right side of bowel has a large luminal diameter (large size tumor) – Rt. iliac fossa
.microcytic anemia
.occult / melena more than hematochezia (fresh blood)
.postprandial discomfort
.fatigue
.diarrhea
.M.C in females
+Left-Sided Lesions
.smaller lumen and semi-solid contents
.change in bowel habits (small-caliber stools)
.colicky pain
.sign of obstruction (large bowel obstruction because  narrow lumen and hard content)
.abdominal pain
.heme (+) or gross red blood
.nausea, vomiting, constipation
.M.C in males
+Lt. > Rt.
+Melena more common from (Right-Sided colon cancer) / +Hematochezia more common from (Left-Sided colon cancer)
+Rt. Colon cancer (bleeding) / Lt. Colon cancer (obstruction)
+Cancer on the Rt. Side (ascending colon and cecum) / Lt. Side tend to be circumferential, and can obstruct the bowel
+Tumot marker (carcinoembryonic Antigen)
-Signs & Symptoms Of Rectal Cancer :
.hematochezia (M.C symptom) – bleeding per rectum
.tenesmus
.feeling of incomplete evacuation of stool (because of the mass)
.rectal mass
.spiuris diarrhea (Early morning diarrhea, doesn`t pass stool but mucus)
-Risk Factors :
.dietary (low-fiber, high-fat diets) (alcohol, red meat intake, obesity, smoking)
.genetic (family history is important when taking history, FAP, gardner syndrome, HNPCC or lynch syndrome)
.IBD (UC > CD) (previous colon cancer)
-Complications :
.intestinal obstruction
.bleeding per rectum
.peritonitis
.metastasis
-Diagnostic Test is (colonoscopy / CBC / heme occult)
.via tumor biopsy, typically done during sigmoidoscopy or colonoscopy
+Microcytic anemia signify until proven otherwise in a man or postmenopausal women in colon cancer
+Preoperative workup for colorectal cancer is (CEA)
Page68

-TNM Sages :
.stage 1 (invades submucosa or muscularis propria)
.stage 2 (invades through muscularis propria or surrounding structures but with negative nodes)
.stage 3 (positive nodes, no distant metastasis)
.stage 4 (positive distant metastasis)
-Treatment :
.resection (surgical margins are needed for colon cancer is- >5cm (you should take as minimum 5cm); the minimum safety
margins in colectomy must be at least 2cm)
.chemotherapy (for advanced disease)
.NO radiotherapy in colon cancer
+Types Of Colon Cancer Surgery :
.low anterior resection (LAR)
.abdomino-perineal resection (APR) (if colon cancer is >7cm – from anal canal)
-Follow-up :
.carcinoembryonic antigen (CEA) blood level measurments (if CEA increased after surgery – recurrence / recurrence is more in
first 2-3yrs) (CEA is for FOLLOW-UP NOT for DIAGNOSIS)
+M.C site of distant (hematogenous) metastasis from colorectal cancer is liver
+M.C.C of colonic obstruction in the adult population (colon cancer, diverticular disease, colonic volvulus)
+Colon cancer is M.C.C of Large bowel obstruction
+M.C colon cancer is adenocarcinoma
-Prevention :
.increasing the consumption of whole grains, fruits and vegetables
.reducing the intake of red meat
.aspirin and celecoxib (decrease the risk of colorectal cancer in those at high risk)
.Vit D intake
.adenoctomy
th
.screening for high risk population (>55yrs  occult blood in stool / UC  after 10yrs annual colonoscopy / FAB  at the 10
annual colonoscopy)
-Screening (three main screening tests) :
.fecal occult blood testing
.flexible sigmoidoscopy
.colonoscopy

*Colonic And Rectal Polyps (Colorectal Polyps)

-Tissue growth into bowel lumen, usually consisting of mucosa, submucosa, or both
-Symptoms :
.bleeding per rectum
.mucus
.diarrhea
.hypokalemia
-Anatomically Classified :
.sessile (flat)
.pedunculated (on a stalk)
-Histologically Classified (Types) :
.inflammatory (benign) (pseudopolyp - no malignant)-as an CD or UC (UC > CD)
.hamartomatous (benign) (normal tissue in abnormal configuration - no malignant)
.hyperplastic (benign-normal cells - no malignant)
.neoplastic (adenomatous-adenomas or malignant) (proliferation of undifferential cells - premalignant or malignant cells)
+Subtypes of neoplastic polyps :
.tubular adenomas (M.C type) – 5% risk of cancer
.tubulovillous adenomas – 20% risk of cancer
.villous adenomas – 40% risk of cancer
+Histology and cancer potential of an adenomatous polyp (villous > tubulovillous > tubular)
+Most polyps are found in (rectosigmoid)
+Size Of Polyp :
.<1cm (<1% risk of cancer)
.1cm (10% risk of cancer)
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.2cm (15% risk of cancer)

-Diagnosis :
.Colonoscopy
-Treatment :
.removal of polyp during colonoscopy
.prophylactic (colectomy)

**Polyposis Syndromes
*Fmilial Adenomatous polyposis (FAP)
-Familial adenomatous polyposis FAP / Autosomal dominant / Mutation on chromosome 5 – APC gene - Genetic defect (tumor
marker) is (APC-adenomatous polyposis coli) gene
-Characteristics :
.100% malignant
.hundreds (>100) of adenomatous polyps within the rectum and colon
.developing at puberty (start at young age) / all undiagnosed-untreated Pts. develop cancer by ages 40-50yrs
-Treatment :
.total proctocolectomy and ileostomy
.total colectomy and rectal mucosal removal (mucosal proctectomy) and ileoanal anastomosis
+With FAP, other tumor must be looked for is (duodenal tumors)

*Gardner`s Syndrome
-Autosomal dominant
-Characteristics :
.100% malignant
.neoplastic (adenomatous) polyps of the small bowel and colon
.cancer by age 40 yrs in 100% of undiagnosed Pts., as in FAP
-Other Associated Findings :
.osteomas of skull (seen on x-ray)
.sebaceous cyst
.adrenal and thyroid tumors (Desmoid tumor)
-Treatment :
.total proctocolectomy and ileostomy
.total colectomy and rectal mucosal removal (mucosal proctectomy) and ileoanal anastomosis

*Peutz-Jeghers` Syndrome
-Autosomal dominant / Hemartoma polyp + Hyperpigmentation
-Characteristics :
.hamartomas (not malignant) (jejunum-ileum > colon > stomach)
-Associated cancer risk for women with peutz-jeghers is (Ovarian cancer)
-Other signs :
.melanotic pigmentation (Hyperpigmentation) (black/brown) of buccal mucosa (mouth), lips, digits, palms, feet (soles), nippels
-Treatment :
.removal pf polyps
+Juvenile Polyps is (benign hamartomas in the small bowel and colon; not premalignant)

*Turcot Syndrome (Colonic polyp + CNS tumor) *Juvenile Polyp (Hemartoma / Benign)
*Colonic Volvulus (Twisting of colon on itself about its mesentery, resulting in obstruction and if complete, vascular
compromise with potential necrosis, perforation, or both / Most type of colonic volvulus is - Sigmoid volvulus)
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By Dr.Mohammad Z. abu sheikha@

Lower GI bleeding
-Bleeding distal to the ligament of treitz; vast majority occurs in the colon
-Signs & Symptoms :
.hematochezia (fresh blood)
.with or without abdominal pain
.melena (black stool)
.anorexia
.fatigue
.syncope
.shortness of breath
.shock
+M.C.C of lower GI bleeding is (Diverticulosis) / 2 nd cause is (vascular ectasia)
+You must ruled out in Pts. with lower GI bleeding is (Upper GI bleeding)
-Causes :
.colitis (ischemic, ulcerative, infectious-E.coli, shigella, salmonella, campylobacter jejuni ‘Bloody diarrhea’)
.hemorrhoids
.angiodysplasia
.neoplasm (cancer)
.diverticular disease (diverticulosis - M.C.C of massive painless LGIB, diverticulitis)
.anal fissure
.rectal foreign bodies
.UC, CD
.pseudomembranous colitis (antibiotic associated diarrhea)
.infectious diarrhea
.radiation colitis
.mesenteric ischemia
.colonic polyps
.colon cancer
+Antibiotic kills normal flora (overgrowth of clostridium difficile bacteria) / treated by (metronidazole-flagyl, vancomycin)

**Diverticular Disease Of The Colon

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*Diverticulosis
-Condition in which diverticula can be found within the colon, especially the sigmoid; diverticula are actually false diverticula /
diverticula involve all layers of the bowel wall and RARE in the colon (False Diverticulum)
-M.C site is (Sigmoid) / M.C.C of massive painless lower GI bleeding
-Symptoms :
.constipation
.lower GI bleeding
-Risk Factors :
.low-fiber diet
.old age
.constipation
-Complications :
.bleeding (may be massive)
.diverticulitis
.asymptomatic (80% of all cases)
-Diagnosis :
.colonoscopy or barium enema

*Diverticulitis
-Infection or perforation of a diverticulum
-Pathophysiology is (obstruction of diverticulum by a fecalith)
-Symptoms :
.LLQ pain
.fever
-Diagnosis :
.Best test is (abdominal CT-scan) (colonoscopy + barium enema is contraindicated) / Best test for diverticulosis is (Colonscopy)
-Treatment :
.I.V antibiotics
.surgery (after 2 attacks / abscess or perforation)
-How common is massive lower GI bleeding with diverticulitis ?
.very RARE ! Massive lower GI bleeding is seen with diverticulosis, not diverticulitis
+M.C.C of massive lower GI bleedign in adults is (Diverticulosis / 2 nd cause is vascular ectasia or angiodysplasia)
+M.C.C of massive bleeding lower GI bleeding in children is (meckel's diverticulum)
+M.C.C of bleeding lower GI bleeding in children is (anal fissure)

**Anus
-Anatomy :
.anal columns
.dentate line
.rectum
.external sphincter
.internal sphincter
.levator ani muscle

*Anal Cancer
- M.C carcinoma of the anus is (squamous cell carcinoma) / M.C symptom (rectal bleeding)
-Risk Factors :
.old age
.immunosuppression
.smoking
.homosexual (HPV virus)
-Treatment :
.nigro protocol (chemotherapy + radiotherapy)

*Fistula In Ano
-Anal fistula, from rectum to perianal skin
-Causes :
.anal crypt (cryptitis) / gland infection
Page72

-Signs & Symptoms :

.perianal drainage
.perirectal abscess
.recurrent perirectal abscess
.diaper rash
.itching
.pain
+Disease considered with fistula in ano is (Crohn's disease)
-Diagnosis :
.exam
.proctoscope
+Goodsall's rule :
.anterior to a transverse line through the anus will course straight ahead
.posteriorly have a curved tract
-Management of anorectal fistulas :
.marsupialization of fistula tract (fistulotomy)
.wound care (sitz baths and dressing changes)

*Perirectal Abscess
-Abscess formation around the anus/rectum
-Signs & Symptoms :
.rectal pain
.drainage of pus
.fever
.perianal mass
-Causes :
.crypt abscess in dentate line with spread
-Diagnosis :
.physical
.digital exam
-Treatment :
.drainage
.sitz bath
.anal hygiene
.stool softeners

*Anal Fissure
-Tear or fistula in the anal epithelium
-M.C site is posterior midline 90% (6 o'clock) / anterior 10% / lateral (crohns or TB)
-Signs & Symptoms :
.severe anal pain on defecation
.painful bowel movement
.rectal bleeding
.blood on toilet tissue after bowel movement (or with stool)
.constipation
.sentinel tag
.tear in the anal skin
.extremely painful rectal exam
.sentinel pile (thickened mucosa / skin at the DISTAL end of ana anal fissure that is often confused with a small hemorrhoid)
.hypertrophic papillae
-Causes :
.hard stool passage (anal sphincter muscle spasm with constipation)
.homosexual (anal sex)
.hyperactive sphincter
.disease process (crohn`s disease)
-Anal fissure triad for a chronic fissure :
.fissure
.sentinel pile (distally)
.hypertrophied anal papilla (proximally)
Page73

-Treatment :
.sitz baths
.stool softeners
.high fiber diet
.excellent anal hygiene
.stool softeners (laxative)
.topical nifedipine
.botox
+Best surgical option (the surgical procedure of choice for anal fissures) :
.lateral internal sphincterotomy (LIS) – cut internal sphincter to release it from spasm
+Diseases processes must be considered with a chronic anal fissure :
.crohn`s disease
.anal cancer
.sexually transmitted disease
.UC
.AIDS
+PR (per rectal examination) is contraindicated in anal fissure

*Parianal Warts
-Warts around the anus / perineum
-Causes is (condyloma acuminatum) (human papilloma virus) (M.C sexual trans.)
-Major risk is (squamous cell carcinoma)
-Treatment if warts are small is (topical podophyllin,imiquimod)
-Treatment if warts are large is (surgical resection or laser ablation)

*Hemorrhoids
-Engorgement of the venous plexuses of the rectum, anus, or both; with protrusion of the mucosa, anal margin, or both
-Internal hemorrhoid is (M.C) (hemorrhoid above the ‘proximal’ dentate line / not painful / may bleed) (M.C.C of LGIB in young
adults)
-External hemorrhoid is (hemorrhoid below the dentate or pectinate line / painful / prone to thrombosis)
-Signs & Symptoms :
.anal mass / prolapse
.bleeding-per rectum (M.C symptom of internal hemorrhoids is bright red blood)
.itching
.pain (external hemorrhoids are painful)
-Causes :
.constipation / straining
.portal hypertension
.pregnancy
-Hemorrhoid Quadrants :
.left lateral (3 o'clock)
.right posterior (7 o'clock)
.right anterior (11 o'clock)
.circumferential (3-7-11 o'clock)
-Classification By Degree (for internal hemorrhoids) :
.1st degree hemorrhoid (NO prolapse)
.2nd degree hemorrhoid (prolapses with defecation, but spontaneously reduce)
.3rd degree hemorrhoid (prolapses with defecation and must be manually reduced)
.4th degree hemorrhoid (prolapsed hemorrhoid that cannot be reduced + pain)
-Treatment :
.conservative treatment typically consists of increasing dietary fiber, sitz baths, laxatives
.grade 3-4 needs surgery (Hemorrhoidectomy)
+Contraindication for hemorrhoidectomy (crohn`s disease)
+You must be ruled out with lower GI bleeding believed to be caused by hemorrhoid (Colon cancer-colonoscopy) if Pt. >50yrs
+Hemorroidectomy is the M.C.C of anal stricture (anal stenosis)
Page74
By Dr.Mohammad Z. abu sheikha@

Inflammatory Bowel Disease IBD

(Crohn`s Disease and Ulcerative Colitis)

-Is a group of inflammatory conditions of the colon and small intestine

+Cause of IBD is (no one knows, but probably an autoimmune process with environmental factors contributing)
-Extraintestinal Manifestations Seen In Both Types Of IBD :
.ankylosing spondylitis (HLA-B27)
.aphthous (oral) ulcers
.iritis
.pyoderma gangrenosum
.erythema nodosum (painful rash on leg)
.clubbing of fingers
.sclerosing
.cholangitis
.arthritis
.kidney disease (nephrotic syndrome-amyloid deposits)

*Crohn`s Disease
-CD can affect any part of the gastrointestinal tract, from mouth to anus (skip lesions - not continuous) / F > M
-The majority of the cases start in the – M.C site (terminal ileum)
-Signs & Symptoms :
.abdominal cramps and pain (M.C site to be affected by CD is ileocecal valve-differential diagnosis, appendix)
.diarrhea (bloody)
.severe urgency to have a bowel movement
.fever
.weight loss (loss appetite – anorexia)
.anal disease
.anemia (due to blood loss)
+Anatomic distribution (mouth to anus)
+Route of Spread (small bowel, colon or both with skip areas of normal bowel, regional enteritis)
+Bowel Wall involvement (full thickness-transmural involvement)
+Anal involvement (Common – fistula, abscesses, fissures, ulcers, hemorrhoids)
+Rectal involvement (Rare)
Page75

-Mucosal Findings :
.apthoid ulcers
.granulomas
.linear ulcers
.transverse fissure
.swollen mucosa
.full-thickness wall involvement
.fat creeping
-Complications (intestinal complications of IBD) :
.abscess
.perianal disease and fistula - enterovaginal fistula, colovesical fistula (M.C fistula) (More in crohn's)
.perforation (rupture) of the bowel (More in crohn's)
.toxic megacolon (acute nonobstructive dilation of the colon) (More in UC)
.hemorrhage (profuse bleeding from the ulcers)
.strictures and obstruction (More in crohn's)
.malignancy (More in UC)
-Diagnostic :
.colonoscopy
-Treatment :
.metronidazole – flagyl / ciprofloxacin – cipro
+Appendectomy is contraindicated in CD
+M.C indication for surgery in CD is obstruction
+Lateral anal fissure seen in CD

*Ulcerative Colitis
-M > F
-Signs & Symptoms :
.bloody diarrhea
.fever
.weight loss
+Anatomic distribution (Colon only)
+Route of spread (almost always involves the rectum and spreads proximally always in a continuous route without skip areas)
+Bowel Wall involvement (mucosa / submucosa only)
+Anal involvement (Uncommon)
+Rectal involvement (100%)
-Mucosal Findings :
.granular, flat mucosa
.ulcers
.crypt abscess
.dilated mucosal vessels
.pseudopolyps
.hyposplenism
.lead pipe appearance
-Diagnostic :
.colonscopy
-Complications :
.cancer (cancer risk in UC > CD) (risk developing colon cancer at 10yrs)
.toxic megacolon (UC > CD)
.colonic perforation
.hemorrhage
.strictures
.obstruction
.complications of surgery
+No fistula
-Treatment :
.mesalazine-steroids
+antibiotics not used in UC (only in CD)
+Treatment of IBD (sulfasalazine – steroids)
+Cobblestoning more often on endoscopic exam in CD
Page76

+UC has pseudopolyps on colonoscopic exam

+CD has lead pipe appearance
+Rectal bleeding / bloody diarrhea is hallmark of UC
+M.C indication for surgery in Pts. with crohn`s disease is small bowel obstruction SBO
+Fat creeping are the intraoperative findings of CD and (cushing`s disease)
+Why do you see fistulas and abscesses with CD and NOT UC ?
.CD is transmural
+Pancolitis (when the entire colon is involved)

+CD
.affect all GI from mouth to anus
.mainly affect terminal ileum
(rarely affect rectum)
.transmural (affect entir thickness)
+UC
.affect colon only (large bowel)
.affect mainly rectum (100%)
.superficial (mucosa + submucosa)
.skip lesions - NO continuous .continuous – NO skip lesion
.more risk for (fistula, perforation, obstruction) .more risk for (Cancer, toxic megacolon)
.increased by smokin .relieved by smoking

**Fistula
-Abnormal communication between tow hollow organs or a hollow organ and the skin (tow epithelial cell layers)
-Predisposing factors and conditions that maintain patency of a fistula (Causes fistula NOT to close) :
.High output fistula – small bowel (>500cc/day)
.Low output fistula – large bowel + another organ (<500cc/day)
.Short segment fistula (<2.5cm) (long fistula close faster than short fistula)
.Intestinal destruction (>50%)
.Foreign body
.Radiation
.Infection
.Epithelization (colostomy)
.Neoplasm
.Distal obstruction
-Types :
.vesicoenteric (due to sigmoid diverticulitis)
.vesicovaginal (M.C.C is iatrogenic – after gynecological surgery and lead to urine incontinence) (most are secondary to
gynecologic procedures)
-Treatment :
.NPO + IV fluid
.somatostatin (octreotide)

*Colonic Fistulas
-Include :
.colovesical fistula (M.C type) - is the presence of a communication between the lumen of the colon and that of the bladder
.colocutaneous fistula
.colovaginal fistula
.coloenteric fistula
+M.C.C of colovesical fistula is (Diverticulitis) / 2nd M.C.C of colovesical fistula is (IBD)
-Symptoms :
.feces in urine
.pneumaturia
+cholecystoenteric fistula (M.C site is duodenum)
Page77
By Dr.Mohammad Z. abu sheikha@

Liver
+Name of the liver capsule is (Glisson`s Capsule)
+Cantlie`s line is (line drawn from the gallbladder to a point just to the left to the inferior vena cava, which transects the liver
into the right and left lobes
+Falciform ligament is (ligament goes from the anterior abdominal wall to the liver)
+Coronary ligament is (peritoneal reflection on top of the liver that crowns – the liver and attaches it too the diaphragm
+The origin of the hepatic arterial supply is from the proper hepatic artery off of the celiac artery (celiac trunk to common
hepatic artery to proper hepatic artery)
-Arterial Branches Of The Celiac Trunk :
.celiac trunk
.splenic artery
.left gastric artery
.common hepatic artery (gastroduodenal artery – proper hepatic artery)
.proper hepatic artery (left hepatic artery – right hepatic artery)
+Venous supply is (portal vein – formed from splenic vein and the superior mesenteric vein)
-What Sources Provide Oxygen To The Liver ?
.portal vein blood
.hepatic artery blood
-What Sources Does The Liver Receive Blood ?
.portal system
.hepatic artery system
+Maximum amount of liver that can be resected while retaining adequate liver function is >80% - the original mass can be
regenerated
+liver enzymes are made by hepatocytes is (ALT-AST)
-Signs & Symptoms :
.hepatomegaly
.splenomegaly
.icterus (jaundice)
.pruritus (from bile salts in skin)
.blanching spider telangiectasia
.gynecomastia
Page78

.testicular atrophy
.caput medusae
.dark urine
.clay-colored stools
.bradycardia
.edema
.ascites
.fever
.fetor hepaticus (sweet musty smell)
.hemorrhoids
.variceal bleeding
.anemia
.body hair loss
.liver tenderness
.palmar erythema
+Portal Systemic Shunt :
.hepatomegaly
.splenomegaly
.caput medusae
.ascites
.hemorrhoids
.variceal bleeding
.inferior hypogastric venous distortion
+Causes Of Pruritus :
.liver failure
.renal failure
.pregnancy
.DM
.some drugs
.eczema
.allergic
.hodgkin lymphoma
.obstructive jaundice

**Tumors Of The Liver

+M.C liver cancer is (Metastatic disease – primary site is usually the GI tract)
+M.C primary malignant liver tumor is (hepatocellular carcinoma – hepatoma) (Hepatoblastoma is M.C in infants and children)
+M.C primary benign liver tumor is (hemangioma)
+Lobectomy is (removal Rt. or Lt. lobe of the liver)

*Hepatocellular Carcinoma (Hepatoma)

-Associated Risk Factors (Hepatoma - a cancer of the cells of the liver) :
.hepatitis B virus (HBV)
.cirrhosis
.aflatoxin (from aspergillus)
.alpha-3-antitrypsin deficiency
.hemochromatosis
.steroids
.clonorchis sinensis
.polyvinyl chloride (PVC)
-Signs & Symptoms :
.RUQ pain (painful hepatomegaly)
.weight loss
.ascites
.fever
.anemia
.splenomegaly
.polycythemia
Page79

-Diagnosis :
.needle biopsy
-Treatment :
.surgical resection
.liver transplant
.if not fit for surgery (intra-arterial chemotherapy / ethanol injection)
+Fibrolamellar hepatoma is the best prognosis / usually affect after young adult
+M.C site of metastasis is lung
+Tumor marker (hepatoma) is (elevated α-fetoprotein) (AFP, α-fetoprotein, α -1-fetoprotein, α-feto globulin)
+M.C location of abscess in the liver is (Rt. lobe > Lt. lobe)
+M.C type world wide is (amebic)

*Hepatocellular Adenoma
-Benign liver tumor / F > M (9:1) / Age 30-35yrs
-Histology (hepatocyte without bile duct)
-Associated with use of OCP
-M.C complications (rupture, bleeding)
-Treatment (small – stop OCP / large >5cm – surgical resection)

*Focal Nodular Hyperplasia FNH

-Benign liver tumor / F > M
-Histology (hepatocyte with bile duct)
-Treatment (observation)

*Hepatic Hemangioma
-M.C benign liver tumor
-Complications :
.pain
.heart failure
.obstructive jaundice
.kasabach-merritt syndrome (thrombocytopenia-coagulopathy)
-Diagnosis :
.CT-scan with contrast
+Biopsy is contraindicated (risk of bleeding)

*Amebic Liver Abscess

-Entamoeba histolytica (typically reaches liver via portal vein from intestinal amebiasis)
-Bacterial - M.C is Gram(-), E.coli / Treated by (aspiration + IV antibiotics) / Most commonly involved is (Rt. lobe of the liver)
-Viral – Treated by (metronidazole)
-Spread (fecal – oral transmission)

*Hydatid Liver Cysts

-Hydatid disease is a parasitic infestation by a tapeworm of the genus
+Usually a Rt. lobe cyst filled with (Echinococcus granulosus)
+Echinococcosis can involve any organ. The liver is the M.C organ involved, followed by the lungs
-Signs & Symptoms :
.most symptomatic cysts are larger than 5cm in diameter
.RUQ pain
.obstructive jaundice
.abdominal pain
.involvement of the lungs produces chronic cough, dyspnea, pleuritic chest pain and hemoptysis
-Risk Factors :
.travel
.sheep, pigs, camels, cattle, goats, horses, dogs and other animals are the host
-Diagnosis :
.serology (Echinococcus titer – antibody)
.CT-scan (cyst with calcification)
Page80

.Casoni test
.Indirect hemagglutination antibody test (don`t stool test with E.g)
+Findings on AxR is (Possible calcified outline of cyst)
+Risk of surgical removal of echinococcal (hydatid) cyst is (Rupture or leakage of cyst contents into the abdomen may cause a
fatal anaphylactic shock)
-Treatment :
.mebendazole-albendazole, followed by surgical resection
+Toxic irrigations are used (Hypertonic saline, ethanol or cetrimide)
By Dr.Mohammad Z. abu sheikha@

Portal Hypertension
-The Anatomy Of The Portal Venous System :
.portal vein
.splenic vein
.SMV (superior mesenteric vein)
+Pathophysiology of portal hypertension is (elevated portal pressure resulting from resistance to portal flow)
+Normal level of portal pressure is (<10mm Hg) / Intra-abdominal pressure (15-20mm Hg)
+M.C.C of portal hypertension is (Cirrhosis) / M.C.C of cirrhosis is (Alcoholism)
+With most Pts. with cirrhosis develop esophageal varices
-Associated CLINICAL Findings In Portal Hypertension :
.esophageal varices
.splenomegaly (M.C physical findings in Pts. with portal hypertension)
.caput medusae (engorgement of peritumbilival veins)
.hemorrhoids
.hepatomegaly
.inferior hypogastric venous distortion
.ascites
-Other Findings Associated With Cirrhosis And Portal Hypertension :
.spider angiomas
.palmar erythema
.encephalopathy
.asterixis (liver flap)
.gynecomastia
.jaundice
+Budd-Chiari syndrome is (Thrombosis of the hepatic veins)
+Most feared complication of portal hypertension is (Bleeding from esophageal varices)
-Signs & Symptoms :
.hematemesis
.melena
.hematochezia
Page81

-Initial Treatment Of Variceal Bleeding :

.IV fluid
.foley catheter
.type and cross blood, send labs
.correct coagulopathy (vitamin K, fresh frozen plasma)
.intubation to protect from aspiration
+M.C.C of upper GI bleeding in cases of liver failure is (duodenal ulcer)
-Diagnosis :
.EGD – upper GI endoscopy
-If esophageal varices cause bleeding, what are the EGD treatment options ?
.emergent endoscopic sclerotherapy
.endoscopic band ligation
+Pharmacologic Options :
.somatostatin
.IV vasopressin (with nitroglycerin, to avoid MI)
.if bleeding continues, consider balloon (sengstaken blakemore tube) tamponade of the varices
.beta-blocker
-Options if sclerotherapy and conservative methods fail to stop the variceal bleeding or bleeding recurs :
.repeat sclerotherapy / banding
.TIPS (transjugular intrahepatic portosystemic shunt)
.surgical shunt (THE BEST)
+TIPS (between the hepatic vein and a branch of the portal vein via percutaneous jugular vein route)
+Lap value roughly correlates with degree of encephalopathy (serum ammonia level)
By Dr.Mohammad Z. abu sheikha@

Biliary Tract
-Ducts of Luschka is (The small ducts that drain bile directly into the gallbladder from the liver)
-Spiral valves of heister is (Name of the valves of the gallbladder)
-Bile (cholesterol, lecithin-phospholipid, bile acids and bilirubin)
-Enterohepatic circulation (circulation of bile acids from liver to gut and back to the liver)
-Bile acids absorbed in (the terminal ileum)
-Cholecystokinin (Stimulates gallbladder emptying) (source – duodenal mucosal cells)
-Level of serum total bilirubin does one start to get jaundiced is ( >2.5 = 25)
-Under the tongue, the anatomic location where one first finds evidence of jaundice
-Signs & Symptoms Of Obstructive Jaundice :
.jaundice
.dark urine
.clay-colored stools
.pruritus (itching) (causes of itching in obstructive jaundice is bile salts in the dermis-NOT bilirubin)
.loss of appetite
.nausea
+Cholethiasis (Gallstones in gallbladder)
+Choledocholithiasis (Gallstones in common bile duct)
+Cholecystitis (Inflammation of gallbladder - >6hrs)
+Cholanitis (Infection of biliary tract)
+Cholangiocarcinoma (Adenocarcinoma of bile duct)
+Biliary Colic (pain from gallstones <6hrs)
-Diagnosis :
.U/S
.ERCP (endoscopic retrograde cholangioPanceatography)
.PTC
.IOC
.HIDA/PRIDA scan (Non-opacification of the gallbladder from obstruction of the cystic duct)
+Lap Chole (laparoscopic Cholecystectomy)
+Sphincterotomy or Papillotomy (cut through sphincter of Oddi to allow passage of gallstones from the common bile duct; most
Page82

often done at ERCP)

+Lap results are associated with obstructive jaundice (elevated alkaline phosphatase)

**Gallstone
-Presence of stones in the gallbladder is referred to as cholelithiasis
-Characteristics and Composition :
nd
.cholesterol stones (2 M.C)
+2
.pigment stones (Ca bilirubinate) (is seen in hemolytic disease)
.mixed stones (M.C type)
-Signs & Symptoms :
.may be asymptomatic (do not require treatment)
.pain in the upper Rt. Side of the abdomen (RUQ pain) radiating to Rt. shoulder or scapula
.nausea, vomiting
.a Pt. may also experience referred pain between the shoulder blades or below the Rt. Shoulder
.positive Murphys sign (on physical findings) (seen too in cholecystitis)
-Causes :
.female, fat, fertile (multiparity), fair, forty (40yrs of age)
.low-fiber and high-cholesterol diets
.rapid weight loss
.hemolytic anemias (such as sickle-cell disease and hereditary spherocytosis)
.cirrhosis and biliary tract infections
-Diagnosis :
.ultrasound
-Treatment :
.surgical (cholecystectomy – gallbladder removal) (surgery is only indicated in symptomatic Pts.)
+M.C artery injured during cholecystectomy is Rt. Hepatic artery
-Complications Of Gallbladder Stones :
.choledocholithiasis
.ascending cholangitis (fever, jaundice, obstructive intestinal)
.pancreatitis (M.C.C of acute pancreatitis is Gallstone)
.gallstone ileus
.gallbladder cancer
+Pigment stones (Brown – infected / Black – non-infected)
+Brown stones (associated with biliary tract infection)
+Black stones (contain calcium bilirubinate) (causes-hemolysis, cirrhosis)

*Choledocholithiasis
-Is the presence of gallstones in the common bile duct. This condition causes jaundice
-Signs & Symptoms :
.positive murphys sign (is common finding on physical examination)
.jaundice (obstructive jaundice – cholestatic jaundice)
.clay-colored stool
.dark urine (cola-tea colored)
+If there is fever the diagnosis is ascending cholangitis
-Diagnosis :
.abdominal ultrasound
.MRCP (Magnetic resonance cholangiopancreatography)
-Treatment :
.removing the stone using ERCP the gallbladder is then removed (cholecystectomy)
+M.C complication post-ERCP is acute pancreatitis

*Cholelithiasis
-Formation of gallstones
-Risk Factors Big Fs :
.female
.fat
Page83

.forty
.fertile (multiparity)
.fair
-Less common risk factors :
.oral contraceptives
.bile stasis
.chronic hemolysis (pigment stones)
.cirrhosis
.infection
.rapid weight loss/gastric bypass
.IBD (CD)
.terminal ileal resection
.hyperlipidemia
.somatostatin therapy
-Types Of Stones :
.cholesterol stones (M.C) (pour / mixed) (mixed > cholesterol)
.pigment stones (black stones / brown stones)
+Black stones (contain calcium bilirubinate) (causes-hemolysis, cirrhosis)
+Brown stones (associated with biliary tract infection)
+Pathogenesis of cholesterol stones is (secretion of bile supersaturated with cholesterol)
+Hypercholesterolemia is NOT risk factor for gallstone formation, but hyperlipidemia is
-Signs & Symptoms :
.biliary colic
.cholangitis
.choledocholithiasis
.gallstone
.pancreatitis
+Boa's sign is (Referred right subscapular pain of biliary colic)
-Five Major Complications Of Gallstones :
.acute cholecystitis
.choledocholithiasis
.gallstone pancreatitis
.gallstone ileus
.cholangitis
+Asymptomatic or complicated cases of choleithiasis treated by (Cholecystectomy)
-Complications of a Lap-Chole :
.common bile duct injury
.Rt. hepatic duct / artery injury
.cystic duct leak
.biloma (collection of bile)
-Indications for cholecystectomy in the asymptomatic Pt. :
.sickle-cell disease
.calcified gallbladder (porcelain gallbladder)
.Pt. is a child
-Management of choledocholithiasis :
.ERCP with papillotomy and basket ballon retrieval of stones
.laparoscopic
.open common bile duct exploration
+Major feared complication of ERCP is (Pancreatitis)

*Acute Cholecystitis
-Obstruction of cystic duct leads to inflammation of the gallbladder
+Risk factor is (Gallstones)
-Signs & Symptoms :
.unrelenting RUQ pain or tenderness
.fever
.nausea, vomiting
.painful palpable gallbladder
.positive Murphy`s sign (acute pain and inspiratory arrest elicited by palpation of the RUQ during inspiration) (negative – stones
Page84

and cholangitis)
.right subscapular pain (referred)
.epigastric discomfort (referred)
-Complications :
.abscess
.perforation
.choledocholithiasis
.cholecystoenteric fistula formation
.gallstones ileus
-Lap results :
.increased WBS
.elevation in alkaline phosphatase
.LFTs
.elevation in amylase
-Signs of acute cholecystitis on U/S :
.thickened gallbladder (>3mm)
.distended gallbladder
.pericholecystic fluid
.gallstones present / cystic duct stones
.sonographic Murphy`s sign
-Treatment :
.IV fluid
.antibiotics
.cholecystectomy

*Acute Acalculous Cholecystitis

-Acute cholecystitis without evidence of stones

*Cholangitis
-Bacterial infection of the biliary tract from obstruction
-Signs & Symptoms :
.charcot`s triad (fever/chils, RUQ pain and jaundice)
.reynold`s Pentad (Charcot`s traid plus altered mental status and shock)
-Common Causes :
.choledocholithiasis
.ERCP
+M.C.C of cholangitis is (gallstones in common bile duct) (E.coli)
-Organisms (isolated with cholangitis is) :
.gram (-) organism (E.coli, klebsiella)
.anaerobes are less common
-Treatment :
.IV fluid
.antibiotics
.Lap Chole

*Gallstone Ileus
-Small bowel obstruction from a large gallstone ( >2.5cm)
-Classic site of obstruction (ileocecal valve)
-Classic Findings Of Gallstone Ileus :
.air in the hepatic bile ducts
.SBO with air fluid levels
.gallstone in ileocecal valve
-Diagnostic Tests :
.abdominal x-ray (show air in the biliary tract)
.abdominal CT (reveals air in biliary tract, gallstone in intestine)
-Treatment :
Page85

.surgery (cholecystectomy)

*Cholangio Carcinoma
-Primary bile duct cancer
-Almost all are adenocarcinoma

+Porcelain Gallbladder (Calcified gallbladder)

+Courvoisier's Gallbladder (Palpable, non tender gallbladder ‘unlike gallstone disease’ associated with cancer of the head of
the pancreas)
+Mirizzi Syndrome (Common hepatic duct obstruction as a result of extrinsic compression from a gallstone impacted in the
cystic duct)
+Gallstones in an infant or child are most frequently associated with Sickle cell anemia

*Jaundice
+Direct
-Obstructive (cholestasis) :
.common duct stone
.cholangitis
.cholangiocarcinoma
.biliary stricture
.pancreatic head trauma
-Non-obstructive :
.hepatitis cirrhosis
+Indirect
.hemolysis
.gilbert's syndrome
.crigler najjar syndrome
+Characteristics Of Obstructive Jaundice :
.steatorrhea
.pale stool (clay-colored)
.bad smell stool
.dark urine (cola-tea colored)
.itching (pruritus)
st
+1 site for jaundice (under the tongue)
+Increased direct bilirubin (increased bilirubin in urine / NO urobilinogen in urine)
+Increased indirect bilirubin (NO bilirubin in urine / increased urobilinogen in urine)
Page86

By Dr.Mohammad Z. abu sheikha@

 Pancreas
+Regions Of The Pancreas :
.head
.neck (in front of the SMV)
.body
.tail
+Structure is the tail of the pancreas said to ‘tickle’ (Spleen)
+Pancreatic ducts :
.wirsung duct (The major duct)
.santorini duct
+Why must the duodenum be removed if the head of the pancreas is removed ?
.they share the same blood supply (gastroduodenal artery)
+Endocrine function of the pancreas :
.islets of langerhans (alpha-glucagon / beta-cells or insulin)
+The exocrine function of the pancreas :
.digestive enzymes (amylase, lipase, trypsin, chymotrypsin, carboxypeptidase)

**Pancreatitis
-Inflammation of the pancreas (can be acute or chronic)
-Acute pancreatitis is inflammation of the pancreas that occurs suddenly and usually resolves in a few days with treatment
-Signs & Symptoms :
.usually begins with gradual or sudden pain in the upper abdomen that sometimes extends through the back
.swollen and tender abdomen
.fever
.rapid pulse (tachycardia)
.epigastric pain (radiates to back)
.nausea/vomiting
.epigastric tenderness
Page87

.decreased bowel sounds (adynamic ileus) (M.C.C of ileus is hypokalemia)

.dehydration/shock (hypovolemic)
.cyanosis, dyspnea
.low-grade fever, Leukocytosis
.hypotension, tachycardia (rapid pulse)
.jaundice
.abnormal lung sounds - Crackles
.discoloration of abdominal wall – Turner’s or Cullen’s sign / fox sign
+Epigastric pain that radiates to back and relieved by leaning forward – aggravated by lying supine
-Causes :
.gallstones (M.C of acute pancreatitis)
.idiopathic
.gallstones
.ethanol (alcohol abuse)
.trauma
.scorpion bite (the least common cause)
.mumps virus (coxsackievirus)
.autoimmune
.steroids
.hyperlipidemia/hypercalcemia
.ERCP
.diuretics (thiazide)
.azathioprine (immunosuppressive drug) - used in organ transplantation and autoimmune diseases
-Diagnostic (lap tests) :
.CBC (high WBC)
.LFT
.elevated amylase and lipase
.CT-scan / abdomen ultrasound
.ABG
.calcium
.chemistry
.coags
.serum lipids
.RBS
.KFT
.LDH
-Complications :
.pseudocyst – resolve spontaneously by 6wks (M.C complication) (M.C indication for surgery in acute pancreatitis)
.infection and sepsis (M.C.C if death in acute pancreatitis)
.infection / sepsis (M.C.C of death in pancreatitis)
.pancreatic necrosis / abscess
.pancreatic hemorrhage
.splenic / mesenteric / portal vessel rupture or thrombosis
.pancreatic ascites / pancreatic pleural effusion (left)
.DM (type 1)
.ARDS / sepsis / MOF (multiple organ failure)
.coagulopathy
.encephalopathy (NH3) (treated by lactulose)
.severe hypocalcemia
.acidosis
.shock
+Prognosis (Based On Ranson`s Criteria)
-Ranson`s criteria :
+At admission
.age >55
.WBC >16000 cells/mm3
.blood glucose Glc >200mg/dL
.AST >250IU/L
Page88

.LDH >350IU/L
+During The Initial 48hrs
.base deficit >4 mEq/L (bicarbonate)
.BUN increase >5mg/dL / I.V fluid hydration
.sequestration of fluids >6L
.serum calcium Ca <8.0mg/dL
.Hematocrit (fall) decrease >10%
.Oxygen (PO2 (ABG) <60mm Hg) - (type 1 respiratory failure)
+Amylase + lipase - protein (enzyme) value is NOT one of Ranson`s criteria
+Mortality per positive criteria = (0-2) <5% / (3-4) 15% / (5-6) 40% / (7-8) 100%
-Treatment :
.NPO (non per oral)
.IV fluids
.antibiotics
.analgesia
.if the cause is gallstone (cholecystectomy should be done once patient stabilized)
+Indication for surgery :
.>6cm
.>6wks
.obstruction (stomach)
.pain

*Chronic Pancreatitis
-Is a long-standing inflammation of the pancreas that alters the organ's normal structure and functions. It can present as
episodes of acute inflammation in a previously injured pancreas, or as chronic damage with persistent pain or malabsorption
-Signs & Symptoms :
.epigastric pain
.malabsorption (steatorrhea), diarrhea
.DM
.skin pigmentation (over the abdomen and back-flank)
.jaundice (obstructive)
+Chronic pancreatitis (Risk for pancreatic cancer)
+Pain may be relieved by leaning forwards or by drinking alcohol
-Causes :
.alcohol abuse (M.C.C)
.idiopathic
-Possible complications of chronic pancreatitis :
.insulin dependent diabetes mellitus
.steatorrhea (cystic fibrosis/celiac disease)
.biliary obstruction
.malnutrition
.splenic vein thrombosis
.gastric varices
.pancreatic pseudocyst (M.C) / abscess (pseudocyst and pancreatic ascites – in both types of pancreatitis)
.cancer
.narcotic addiction
.duodenal stenosis
.peptic ulcer
.pancreatic ascites/pleura; effusion
.splenic artery aneurysm
+Complications is associated with splenic vein thrombosis is (Gastric varices-treatment with splenectomy)
-Diagnosis :
.CT-scan (Best)
-Treatment :
.analgesia
.pancreatic enzyme (lipase, protease)
.insulin
+M.C indication for surgery is pain
Page89

+In chronic cases (may be normal amylase + lipase)

**Hemorrhagic Pancreatitis
-Cullen`s Sign (Bluish discoloration of the periumbilical area from retroperitoneal hemorrhage)
-Grey Turner`s Sign (Ecchymosis or discoloration of the flank in Pts. with retroperitoneal hemorrhage from dissecting blood
from the retroperitoneum)
-Fox's Sign (Ecchymosis of the inguinal ligament from blood tracking from the retroperitoneum and collecting at the inguinal
ligament)

**Pancreatic Pseudocyst
-Encapsulated collection of pancreatic fluid
-Wall is formed by inflammatory fibrosis, Not epithelial lining
-Associated Risk Factors :
.chronic pancreatitis > acute pancreatitis
.pancreatitis from alcohol
+Chronic pancreatitis (alcohol) / Acute pancreatitis (gallstone)
+M.C.C of pancreatic pseudocyst is (Chronic alcoholic pancreatitis)
-Treatment :
.drainage of the cyst or observation
+M.C.C of death due to pancreatic pseudocyst is (Massive hemorrhage into the pseudocyst)

**Pncreatic Carcinoma
-Adenocarcinoma of the pancreas arising from duct cells
-Percentage arise in the pancreatic head is (66% in the head / 33% arise in the body and tail)
-Signs & Symptoms :
.painless jaundice
.pruritus
.courvoisier`s sign (Palpable, nontender, distended gallbladder)
.back pain
+Metastatic lymph nodes described classically for gastric cancer can be found with metastatic pancreatic cancer (virchow`s
node - lift side) , sister mary joseph`s nodule - per umbilicus)
+Tumor markers (pancreatic cancer) is (CA-19-9)
-Treatment (based on location) :
.head of the pancreas (Whipple procedure / pancreaticoduodenectomy)
.body or tail (Distal resection)
+WADHA syndrome (Pancreatic VIPoma-Vasoactive Intestinal Polypeptide tumor or Verner-Morrison Syndrome)
+Tumor secretes VIP, which causes :
.watery
.diarrhea
.hypokalemia
.achlorhydria (inhibit gastric acid secretion)
+M.C islet cell tumor is (Insulinoma)
+Regarding anular pancreas usually present with duodenal obstruction
Page90

By Dr.Mohammad Z. abu sheikha@

 Breast Cancer
+Anatomy :
.skin (nipple and areola)
.fat (in which the mammary gland is embedded)
+Blood Supply
.mammary branches of lateral thoracic artery
nd rd th
.perforating branches of to the internal mammary artery 2 , 3 and 4
nd rd th
.lateral branches of 2 , 3 and 4 intercostal arteries
+Special Investigations Of Breast Disease :
A) Radiological Investigations
1) U/S
.done in young Pt. <35yrs
.it can early diagnose for (cystic masses, benign solid masses, breast cancer)
2) Mammography
.only done in females >35yrs
.mammography is used in mass screening for early detection of breast cancer and done for all females aged 50-70yrs every
3-5yrs
3) MR mammography
.done for females <35yrs with suspicious U/S image
.also for females with implants
.it is useful to distinguish scar from recurrence in females who had previous breast conservative therapy for cancer
B) Breast Biopsy
1) Fine needle aspiration cytology (FNAC)
.done in outpatient, using 4cm long 22 gauge needle attached to 10ml syringes
Page91

2) Core needle biopsy

.performed using a 14 gauge needle “true cut needle” and using a local anesthesia and a small punctured wound
.2 or more biopsies may be taken
*NB. : FNAC and core biopsy can differentiate between benign and malignant masses and detect receptor status, but FNAC
can`t differentiate between invasive and in-situ carcinoma while core biopsy can
3) Biopsy of non-palpable breast lesion
.localization is made by mammography
.then the tip of a thin wire hook is positioned close to the lesion
.next, the Pt. is taken to the operation theatre
.a cast of normal tissue 1cm in diameter around wire removed with an area of breast around the hook
.before leaving th operating room, an X-ray is done to confirm complete excision of the suspicious lesion
+Triple Assessment :
.done to all females presenting with a breast lump
.consist of clinical, radiological and pathological assessment
A) Clinical Assessment
1) History
.Pt`s. age
.age at menarche and menopause
.family Hx of breast cancer and other cancers
.No of children, age at child birth “pregnancy and delivery after 30, increase incidence”
.drug Hx (OCT and HRT)
.duration and progressive of the lump
2) Examination
.inspection (both breast at the same time, notice skin tethering or dimpling)
.palpation (each quadrant palpated to look for lump, next both axilla and supra-claviculat fossae)
B) Radiological Assessment
.if >35yrs (U/S is done. If there is suspicion - MR mammography)
.if >35yrs (mammography and U/S are done)
C) Pathological Assessment
st
.FNAC is done 1 , if there is a cyst it will be cured, but if the fluid withdrawn is bloody or a lump is persist, it has to be removed
.if the cytology`s is inadequate or unhelpful, the next step is Core biopsy
+Diagnosis Of Breast Cancer Is Made On Finding :
.a solid mass with satellite margin
.clustered Micro-calcification “carcinoma in-situ”
.a systemic thickening of breast tissue
*NB. : The test sensitivity increases with age as the breast become less dense

**Breast Pain
A) Referred Pain (start somewhere else and referred to the breast – angina, pneumonia, pleurisy, intercostal neuralgia,
esophagitis, osteochondritis)
B) Mastalagia
1) Cyclical mastalagia
.most females complain of Pre-menstrual mastalagia for 3-5 days
.reassurance (not associated with increased risk of cancer)
.if it is severe or prolonged it needs for treatment (primrose oil 100mg daily for 3months / tamoxifen 20mg daily for 8months /
st
danazol – given on the 1 day of the cycle / bromocriptine – synthetic dopamine agonists “Anti-prolactin” 2.5mg twice/day)
2) Non-cyclical mastalagia
.less common and more dificult to treat
.may benefit from combination of evening primrose oil, NSAIDS and massage of NSAIDS cream into the area of tenderness

**Acute Inflammation Of Female Breast

*Acute Mastitis Of Lactation
-Superficial infection of the breast
-Occurs usually during the 1st month of lactation
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-Predisposed by milk engorgement because milk provides a good media for bacteria
-Causative organism (Staphylococcus aureus or Strep.) – Route of infection :
.Staph. (enters through the lactiferous duct, secrets coagulase enzyme – clotting milk and helps to localize the inflammation)
.Strep. (enters through cracks or fissure in the nipple, secrets fibrinolysin enzyme which helps inflammation to spread)
-Signs & Symptoms :
.severe pain the breast
.swollen, tender, indurated and skin may be red
.axillary (enlarged and tender)
.fever and malaise
-Prophylaxis :
.during the last 2 months of prefnancy (massage the nipple if not protruding and keep them clean and paint them with glycerin)
.after delivery (the nipples should be cleaned after each suckling / if the breast is engorged – evacuate it with a pump or by
manual expression)
-Treatment :
.empty the breast (with a pump or by manual expression)
.anitibiotics (combination of ampicillin and flucloxacillin)
.firm support to the breast and analgesics to relieve the pain
.if she isn`t going to lactate her child (stop lactation by anti-prolactin tablets)
+Stop breast-feeding and use a breast pump instead / apply heat / administer antibiotics)

*Acute Inflammatory Abscess (Breast Abscess)

-In the past, the 1st sign of pus formation (the presence superficial pitting edema) / Later (pus may be obtained from the nipple
on squeezing of breast) / Finally (fluctuation becomes apparent and indicated that abscess cavity has become very large and
multi-locular
-In neglected cases (skin becomes red and stretched and finally bit sloughs and the abscess burts leaving a sinus)
-Causes :
.mammary ductal ectasia (stenosis of breast duct)
.mastitis
-Most Common Bacteria :
.nursing – infection of the breast during breastfeeding (Staphylococcus aureus)
.non lactating (mixed infection)
+Must be ruled out with a breast abscess in a non lactating women (Breast cancer)
+In breast abscess the commonest causative bacteria are Staphylococcus
*Chronic Inflammatory Abscess
-Follows inadequate drainage or injudicious antibiotic treatment
-Leading to pus, becoming encapsulated within a thick wall of fibrous tissue and simulate carcinoma and biopsy will be needed
to exclude carcinoma

*Duct Ectasia (Peri-ductal mastitis)

-Dilatation of the breast ducts associated with peri-ductal inflammation / Dilatation of one or more of main lactiferous duct
which fill with stagnant brown or green secretion which may discharge
-Treatment :
.antibiotics therapy (flucloxacillin and metronidazole)

*Fibro-adenoma
-Benign tumor of the breast (but it`s better considered as ANDI)
-Ranges from small fibroadenoma seen in teenage
-Clinical Presentation Of A Fibroadenoma :
.solid
.mobile
.well-circumscribed round breast mass
.usually <40yrs of age

A) Juvenile fibro-adenoma
.arises from breast lobule
.age 15-20yrs old
.it is smooth firm, not tender and moves easily within breast (breast mouse)
.sometimes multiple
Page93

B) Giant fibro-adenoma
.>5cm in diameter
.may be seen during puberty, but usually in women >30yrs
.grows rapidly
.can be enucleated through a sub-mammary incision
C) Phylloides tumors
.previously known as cyst sarcoma of Brodie
.occurs in women >40yrs sometimes in younger women
.presented as large, sometimes massive tumor with nodular surface
.occasionally, the overlying skin may undergo pressure necrosis with ulceration, microscopic picture is variable
.sometimes it looks benign like fibro-adenoma
.sometimes there is a high miotic index and in this xase it may recur after enucleation
.massive tumors recunent and those of the malignant type require mastectomy
**Abnormal Discharge From The Nipple
A) Clear Serous
.this may be physiological parous
.sometimes it may occur with duct papilloma
B) Blood Stained
.fibro-adenoma (fibrocystic disease)
.duct ectasia
.duct papilloma
.duct carcinoma
+M.C.C of bloody nipple discharge in a young woman is (Intraductal papilloma)
*NB. : Unilateral blood-stained discharge is usually due to intra-ductal papilloma and sometimes to intra-ductal carcinoma
C) Black or Green Discharge
.duct ectasia
D) Pus
.in acute inflammation and abscess
E) Milky Discharge
.if from a single duct (it may physiological – lactation)
.if bilateral and from many ducts (it may be due to increases serum prolactin level – hypothyroidism, pituitary tumors)
F) From The Skin
.paget`s disease
.skin disease (eczema, psoriasis)
.rare causes (chancre)
+These Pts. must have triple assessment with U/S of the retro-areolar area
+Investigations :
.dipstik test to confirm the presence of blood
.ducto-graphy may be helpful in showing a space occupying lesion in the duct
+Paget’s Disease Of The Breast :
.is a malignant condition that outwardly may have the appearance of eczema, with skin changes involving the nipple of the
breast – Superficial manifestation of an underlying breast carcinoma
.the condition is an uncommon disease accounting for 1 to 4.3% of all breast cancers
.it is a sort of chronic eczema of the nipple – It presents as eczema like lesion of nipple and areola which persists despite locat
treatment
.it is usually bilateral
.associated with nipple retraction in early stages
.biopsy from nipple (show large ovoid cells with clear cytoplasm in the epidermis)
.needs long treatment with steroid ointment
+Paget's disease of the breast is (Scaling rash / dermatitis of the nipple caused by invasion of skin by cells from a ductal
carcinoma)
+The Pt. may present as inflammatory swell in inflammatory carcinoma, bleeding per nipple in due carcinoma or erosion of the
nipple
+Unilateral Retraction Of The Nipple May Occur In :
.Duct ectasia
.Intraductal carcinoma
Page94

.Developmental occurring at the time of puberty

.Chronic breast abscess

*Galactocele
-Is a retention cyst (rare) containing milk or a milky substance that is usually located in the mammary glands
-It is seen in lactating women on cessation of lactation. It presents as a large, soft, fluctuating lump in the lower part of breast
and it is not usually painful – Presents as a solitary sub-areolar cyst contains milk dating from lactation
-Treated by excision
+Galactocele may be associated with oral contraceptive use

**Breast Cancer
-Commonest cancer in females and commonest cause of death in middle aged females
-More common in the western countries
-Rare occur <35yrs, then the incidence doubles every 5yrs until 50yrs and then countinues increase slightly
-Signs & Symptoms :
.no symptoms
.mass in the breast
.pain (most are painless)
.nipple discharge
.local edema
.nipple retraction
.dimple
.nipple rash
+Commonest Presentation :
.swelling “usually in upper lateral quadrant with tethering of overlying skin”
.nipple may be indurated and elevated
.axillary LNs may be palpable
+In Advanced Cases There May Be :
.swelling become large in size >5cm and fixed to the pectoral fascia or chest wall
.Peaud`Orange (due to cutaneous lymphatic edema, the infiltrated skin is tethered by the sweat ducts and so can`t swell at
these points
.lymphedema of UL eith recurrent attack of lymphangitis
.cancer-en-cuirasse (due to direct infiltration of skin of breast and chest wall which becomes hard, leathery and pigmented
.ulceration and fungation of tumor
.signs of metastasis
*NB. : Peaud`Orange means “orang skin” (used to describe something with the look orange color and texture of an orange peel
– dimpled appearance)
+M.C site of breast cancer is (In the upper outer quadrants)
-Etiology :
A) Genetic Factor
.accounts for 5-8% of cases
.carrier of BRCA1 and BRCA2 gene located in chromosome 17 have life time risk of developing breast and ovarian cancer
.mutation in P53 geen on chromosome 17 lead to breast cancer in very young age
B) Hormonal Factors
st
.predispose factors (prolonged exposure of breast to estrogen – early menarche, late menopause, nulliparity, late 1 birth /
>30yrs doubles the risk to those <20yrs, hormonal replacement therapy HRT, oral contraceptive therapy OCT / use of OCT
below 20yrs may increased risk / high estrogen pills increased risk / low estrogen and progesterone pills are safe)
.protective factor (multiparity and breast feeding)
C) Socio-economic Factor
.common in high classes but in lower classes tend to present with late stages
D) Radiation
.increased risk by 4 folds
E) Familial Factor
.increased risk if one of the 1st degree relatives has breast cancer or ovarian cancer
F) Atypical Epithelial Hyperplasia
.its presence – increased risk
+Smoking and Fibrocystic disease are NOT risk factors for breast cancer
Page95

-Different Types Of Invasive Breast Cancer :

.infiltrating ductal carcinoma (M.C) (in women and men)
.medullary carcinoma
.infiltrating lobular carcinoma
.lobular carcinoma
.mucinous carcinoma
.inflammatory breast cancer (appearance of the edema of the dermis is peau d`orange-orange peel)
+Screening Recommendations For Breast Cancer :
.self-exam of breasts monthly (1 week after menstrual period)
.age 20-40 yrs - >4o yrs (breast exam every 2 or 3 yrs)
.mammogram (every year or every other year after age 40) (More useful diagnostic tool in older women than is younger-breast
tissue undergoes fatty replacement with age; making masses more visible)
.breast ultrasound (is the best initial test to evaluate a breast mass in a women younger than 30 yrs)
+Classic picture of breast cancer on mammogram is (Spiculated mass)
+The Methods For Obtaining Tissue For Pathologic Examination Is :
.fine needle aspiration FNA
.core biopsy (larger needle core sample)
.mammotome stereotactic biopsy
.open biopsy
.excisional
+Spread Of Breasr Cancer :
1) Local Spread
.tumor increased in size and tend to involve skin and to penetrate pectoral Ms and even chest wall
2) Lymphatic Spread
nd rd
.1ry occurs to the axillary LNs and to lesser extent the internal mammary LNs in the 2 and 3 intercostal spaces
3) Blood Spread
.bone (lumbar vertebrae, femur, thoracic vertebrae, ribs and skull “deposits usually osteolytic”
.liver, lungs, brain
.adrenal glands and ovaries
+The initial site of distant metastasis in breast cancer (Bone)
+Clinical Staging Of breast Cancer :
A) TNM Classification :
1) T
.Tx (tumor can`t be assessed)
.T0 (no evidence of 1ry tumor)
.Tis (DCIS, LCIS, Paget`s disease with no tumor)
.T1 (<2cm)
.T2 (2-5cm)
.T3 (>5cm)
.T4 (tumor of any size with – extension of chest wall, Peaud`Orange, ulceration of skin, seattle skin nodules, inflammatory
carcinoma)
2) N
.N0 (no LN metastasis)
.N1 (metastasis to mobile ipsilateral LNs)
.N2 (metastasis to fixed ipsilateral LNs)
.N3 (metastasis to ipsilateral internal mammary LNs)
3) M
.M0 (no distant metastasis)
.M1 (presence of distant metastasis, palpable ipsilateral supra-clavicular LNs)
B) Manchester Classification :
1) Stage I (Tis or T1-2, N0, M0)
Page96

.no palpable LNs

.no distant metastasis
2) Stage II (T1-2, N1, M0)
.mobile LNs in the axilla
.no distant metastasis
3) Stage III (T2-4, N2, M0)
.fixed LNs in the axilla
.no distant metastasis
4) Stage IV (T1-4, N1-3, M1)
.presence of distant metastasis in liver, lungs – bones or palpable supra-claviculat or contra-lateral axillary LNs
+Prognosis Of Breast Cancer (it depends on many factors at the same time) :
.age of the Pt. (if <35yrs – poor prognosis)
.tumor size (the larger the tumor – poor prognosis)
.axillary LN metastasis (if there aren`t metastasis – good prognosis) (presence of metastasis increaset to 3 LNs survival is less)
(>10 LNs – poor prognosis)
.tumor grade (good in grade I, not good in grade II, poor in grade III)
.receptor status (ER and PR status – if +ve, prognosis is good and if –ve, prognosis is poor)
+Types Of TTT :
1) Surgical
2) Radiotherapy
3) Systemic
a) hormonal
b) chemotherapy

A) Surgical
1) Breast conservative surgery
.done for carcinoma in situ & in invasive carcinoma when it is <4cm in diameter
.there are 3 forms :
a) Lumpectomy : Excision of the tumor with 1 cm margin clearance
b) Segmentectomy : Excision of the tumor with 1cm macroscopic margin clearance but with excision of tissue from the nipple
to periphery of the breast
c) Quadrantectomy : Removal of the entire ¼ of the breast containing the 1ry carcinoma with 2-3 macroscopic margin
clearance. Part of the pectoral fascia may be removed as well
+Contraindication:
.multifocal disease in the same ¼
.multicentric disease in separate ¼
.extensive in-situ component >25%
.pregnancy as radiotherapy is contraindicated except in the 3rd trimester when irradiation can be given after delivery
.Hx of previous irradiation to breast “can’t repeat the irradiation”
.large sized tumor in small breast
.presence of scleroderma or collagen disease
.centrally placed tumors
2) Modified radical mastectomy
.incision is usually elliptical & transverse containing nipple, areola & skin over tumor
.the whole breast & the underling pectoral fascia are removed together with fat in axilla & all axillary LNs in one block
.injury of nerve to Serratus ant. should be avoided - will lead to winging of scapula
.a suction drain is left at the end
3) Simple mastectomy (Total)
.it is indicated in DCIS
.removal of all breast tissue & the nipple-areola complex preserving pectoral muscle & axillary LNs
4) Sentinel LN biopsy
5) Breast reconstruction after mastectomy

B) Radiotherapy
Page97

-Always done after conservative surgery to decrease risk of local recurrence

-After mastectomy, it is only done in the following conditions :
1) grade III tumor
2) extensive LN involvement (≥ 4 LN)
3) extensive lymphovascular invasion
-Done only to the chest “not the axilla - severe lymphedema” and usually given after chemotherapy

Tumor Grade Age LN ER & PR

+Low Risk <1cm I >35yrs -ve +ve
+Intermediate Risk 1-2cm II +ve
+High Risk >2cm III <35yrs -ve

*Inflammatory Breast Carcinoma

.characterized by skin change of brawny induration, erythema with raised edge and edema (Peau d'orange)
.may associated with a breast mass
.it can be easily mistaken for bacterial infection of breast
.there are palpable hard axillary LNs and there may be distant metastases
.it used to be fatal
.nowadays neo-adjuvant chemotherapy with Adriamycin-containing regimen may affect dramatic regression in 75% of cases
.may be followed by modified radical mastectomy and radiotherapy to chest wall and supra-clavicular fossa

*Breast Cancer During Pregnancy

.U/S & needle biopsy are used for diagnosis
st nd
.modified radical mastectomy is the surgical procedure of choice during 1 & 2 trimester of pregnancy
rd
.during the 3 trimester - Lumpectomy and axillary LN dissection is considered if adjuvant radiation therapy is deferred until
after delivery and Lactation is suppressed
st
.chemotherapy administrated during the 1 trimester carries a risk of spontaneous abortion a d birth defects

*Male Breast Cancer

.<1% of breast cancer
.present as a firm non-tender mass in ♂ breast and become fixed to the pectoral fascia
.usually ♂ do worse because of the advanced stage at time of diagnosis (stage III or IV)
.treatment is surgical usually modified radical mastectomy followed by adjuvant radiotherapy
.80% are hormone receptor +ve and Tamoxifen is given
.systemic chemotherapy is given for ♂, hormone receptor -ve cancers and for ♂ whose cancers relapse after Tamoxifen therapy
-Risk Factors :
.increased estrogen
.radiation
.gynecomastia from increased estrogen (is not risk factor for male breast cancer)
.estrogen therapy
.klinefelter`s syndrome (XXY)
.BRCA2 carriers

*Breast Cancer In Old Pt. Unfit For Surgery

.tamoxifen (main line of TTT) if hormone receptor +ve
.chemotherapy if hormone receptor -ve
.radiotherapy may also help local control

+Tamoxifen
-Mech. :
.they are anti-estrogen - blocking estrogen receptors
-Dose :
.20 mg/day for 5 yrs, it is given to pre & post-menopausal ♀
-Advantage :
.it ↓ recurrence by 25%, ↓ death by 17% & ↓ risk of contra-lateral breast carcinoma by 50%
.gives protection against osteoporosis & ↓ blood cholesterol
Page98

.in surgically unfit elders & in cases of inoperable cancer who are ER +ve - Tamoxifen is given as neo-adjuvant therapy to render
the tumor operable (Response 75%)
*NB. :Tamoxifen (it binds estrogen receptors) (Side effects of tamoxifen is Endometrial cancer)
+Adjuvant therapy (the treatment given after the primary treatment to decrease recurrence)
+Neoadjuvant therapy (the treatment given before the primary one in advanced cases to make them operable)
+Mammogram is obtained first (mammogram / biopsy)
+Hormone receptors must be checked for in the biopsy specimen (estrogen and progesterone receptors)
+M.C.C breast tumor in Pts. younger than 30 yrs os (Fibroadenoma)
+Number of the breast lobes and in turn the number of the duct orifices at the nipple is (15-20)
+Fibroadenoma may be associated with Fibrocystic disease of breast
+Prolactin (hormone is mainly responsible for breast milk production)
+Benign Breast Disease :
.duct ectasia
.ductal papilloma
.breast abscess
.fibroadenoma
.fibroadenosis (are NOT)

*Benign Breast Disease

-M.C.C of green, straw-colored, or brown nipple discharge is (Fibrocystic disease)
-M.C.C of breast mass after breast trauma is (Fat necrosis)

*Male Gynecomastia
-Enlargement of the male breast
-Causes :
.medications
.illicit drugs (marijuana)
.liver failure
.increased estrogen
.decreased testosterone
+Major differential diagnosis in the older patient (male breast cancer)
+Type of breast cancer do men develop is (Ductal carcinoma)

By Dr.Mohammad Z. abu sheikha@

Spleen And Splenectomy

-Anatomy :
.Spleen is an intra-peritoneal structure with a notched anterior border
.Weight: 80-300 gm
-Surfaces :
A) Convex parietal surface
th th th
.in contact with the diaphragm deep to the 9 , 10 , 11 ribs
th
.its long axis follows the 10 rib down to the midaxillary line
.through the diaphragm the spleen is related to the pleural recess and to the thin inferior border of left lung
B) Visceral surface
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.related to the stomach, left kidney and colon

.hilum of the spleen is related to the tail of pancreas
-Splenic Ligaments :
.spleen is completely covered with peritoneum
.the spleen is suspended at its hilum by 2 peritoneal folds :
a) the lieno-renal ligament: short and transmits the blood vessels to the spleen, the tail of the pancreas lies in this ligament
b) the gastrosplenic ligament: contains short gastric arteries
.the phrenicocolic ligament: attaches colonic splenic flexure to diaphragm. The lower pole of the spleen is in contact with this
ligament which is thought to be one of its main supports
-Blood Supply :
A) Splenic artery
.usually arise from celiac artery but it may arise from aorta or SMA
.it passes along the upper border of the pancreas & at its tail it passes to the front of it and divides into - superior & inferior
terminal branches that enter the splenic hilum
B) Splenic Vein :
 .runs along the posterior pancreatic surface below level of splenic artery
.join SMV at a right angle behind the neck of pancreas to form portal vein
+Arteries Supply The Spleen :
.the splenic artery
.celiac trunk
.short gastric arteries
+33% of the total body platelets are stored in the spleen
-Physiology :
+Functions Of The Spleen :
1) Foetal Erythropoiesis
th th
.during 5 - 8 month of foetal life the spleen shares in the production of both RBCs & WBCs and this function does not
continue in the normal adult
.if the bone marrow production of RBCs becomes defective after birth, splenic erythropoiesis will continue, e.g., in
myelofibrosis
2) Sequestration Of Old Blood Cells
.old & abnormal erythrocytes, abnormal granulocytes, normal and abnormal platelets and cellular debris will be cleared by the
spleen, which is capable of discrimination between these & normal cellular components
.the platelets, under normal conditions, survive about 10 days in circulation & ⅓ normal platelet is normally sequestered in
spleen while in splenomegaly up to 80% of platelets are sequestered & this may lead to thrombocytopenia
3) Defensive Functions
a) reticulo-endothelial macrophages of spleen phagocytise foreign substances which include bacteria, fungi, protozoa and
particulate matter
*NB.: phagocytosis of abnormal lipoid is the cause of splenomegaly in lipoid dystrophies
b) helps in proliferation and maturation of T & B Iymphocytes
c) helps in the production of various antibodies, including :
.IgM
.tuftsin (stimulates phagocytosis by neutrophils)
.opsonins (react with bacteria & fungi to make them more susceptible to phagocytosis)
.properdin (fixes complement to bacterial & fungal surface prior to phagocytosis)
.interferon (an antiviral antibody)
+Functions Of The Human Spleen :
.filters abnormal RBCs
.stores platelets
.produces tuftsin and properdin (opsin)
.produces antibodies (IGM)
.site of phagocytosis

**Splenectomy
-Indications For Splenectomy :
.traumatic injury of the spleen
.malignant diseases (hodgin`s, splenic tumors, hypersplenism caused by other leukemias and non hodgkin's lymphoma)
.hematological causes (hereditary spherocytosis - M.C indication, immune thrombocytopenic purpura ITP, thrombotic
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thrombocytopenic purpura TTP, hairy-cell leukemia, autoimmune hemolytic anemia, thalassemia Major – who require frequent
blood transfusions)
.variceal bleeding with splenic vein thrombosis
.gaucher`s disease
.splenic abscess, cysts, tumors
.felty`s syndrome
.hypersplenism
.esophageal varices
.during radical surgery for the stomach, esophagus or pancreas
+G6PD deficiency / thalassemia Minor (NOT indication for splenectomy)
+Diseases That Cause Autosplenectomy :
.sickle cell anemia
.Pneumococcal septicemia
-Possible Post-Splenectomy Complications :
.reactionary haemorrhage
.atelectasis and pneumonia
.DVT
.wound infection (increased risk of infection by encapsulated bacteria), burst abdomen, incisional hernia (uncommon)
.thrombocytosis (platelet count may rise) – portal vein thrombosis (because splenectomy if frequent followed by rise in WBCs
and platelets)
.increase in blood leukocytes (leukocytosis – WBC increased)
.subphrenic abscess
.atelectasis
.pancreatic fistula may follow damage to the tail of the pancreas
.acute gastric dilation
.gastric fistula due to injury of the wall of the stomach
.subphrenic haematoma or abscess
+Overwhelming Post-Splenectomy Sepsis (OPSS) (Causes - Streptococcus pneumoniae ‘M.C’, Neisseria meningitis, H.influenzae)
(Pt. should receive the pneumococcal conjugate vaccine (prevnar), Hib vaccine and the meningococcal vaccine)
+Post-splenectomy bacterial infections :
.because the spleen phagocytoses bacteria specially the encapsulated type
.Pts. with splenectomy are susceptible to infections produced by Streptococcus pneumonia, Neisseria meningitides and
Haemophilus influenzae
.the risk is higher if done in childhood. A serious form is overwhelming post-splenectomy sepsis (OPSI) which is fatal
.therefore, splenectomized children should receive anti-pneumococcal vaccine (pneumovax) cover until the age of 18

*Congenital Anomalies
A) Agenesis (asplenia)
.absence of the spleen “very rare”
B) Accessory spleens
.occurs in 10-35% of individuals. The majority of accessory spleens occur at the hilum, in the greater omentum or along the
splenic vessels and pancreas. If the spleen is removed for haemolytic anaemia, a careful search must be made for accessory
spleens which can cause recurrent symptoms if not removed
C) Polysplenia
.normal spleen is deeply lobulated or divided into 2 or more parts
D) Splenic cysts of embryonal rests include dermoid and mesenchymal inclusion cysts
E) Wandering spleen (Splenic ectopia)
.caused by laxity of gastrosplenic & splenophrenic ligaments, or defects in their development. Torsion of the pedicle is the
most frequent complication

*Rupture Of The Spleen

-This term is applied to splenic injuries in which there is disruption of the organ's parenchyma, capsule or blood supply
-Etiology :
a) predisposing factors
.splenic enlargement which makes it more liable to trauma
.diseases of the spleen like malaria which make it soft and more friable
-Types Of Trauma :
1) non penetrating trauma: as in blunt abdominal trauma or trauma to lower thoracic cage. This is due to road traffic accidents
and falling from a height
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2) penetrating trauma: due to gunshots or stabbing

3) operative trauma: occurs during an operation on adjacent viscera, e.g. during gastric or colonic surgery. Injuries usually
result from retractors placed against the organ in order to obtain good exposure
4) spontaneous rupture (rare)
-Types Of Splenic Injury :
1) subcapsular haematoma
2) small superficial tears single or multiple
3) deep tear, single or multiple and reaching the hilum
4) avulsion of a pole of the spleen
5) complete pulping of the spleen
6) injury of the vascular pedicle, i.e. avulsion or thrombosis of the vessel
-Signs & Symptoms of ruptured/injured spleen :
.hemoperitoneum
.kehr`s sign (left shoulder pain seen with splenic ruptured)
.LUQ
.abdominal pain
.ballance`s sign (LUQ dullness to percussion)
-Complications :
1) internal haemorrhage (blood may accumulate in the peritoneal cavity, retroperitoneal space, or in the pleura if the injury
involves the diaphragm)
2) associated other abdominal or thoracic injuries
3) splenic cyst may follow a peri-splenic haematoma
-Clinical Picture (3 clinical types of rupture of the spleen) :
A) Fatal Type
.tear is deep or the pedicle is ruptured and haemorrhage is so massive that the patient is severely shocked with rapid death
occurring before any surgical intervention
B) Classical Rupture (commonest)
.general manifestations of internal haemorrhage with increasing pallor, weak and rapid pulse, low blood pressure & air hunger
.bdominal examination :
1) tenderness & rigidity in the left hypochondrium which spreads into abdomen
2) vidence of shifting dullness
3) distension is present due to intestinal paresis
+Special Signs (may be present but they are not essential for the diagnosis) :
1) Balance's Sign
.shifting dullness on the right side and fixed dullness on the left side
.this is due to free fluid blood in the peritoneal cavity in the right flank, but on the left side the fixed dullness is due to blood
clots in the peritoneal cavity, and also due to retroperitoneal haematoma
2) Kehr's Sign
.pain in left shoulder, this is referred pain due to irritation of diaphragm
.this pain occurs especially if the patient is put in Trendlenburg position
.also provoked by pressure on the left hypochondrium
3) Cullen's Sign
.brownish or bluish discoloration around the umbilicus may occur in about 20% of people who have thin linea alba around the
umbilicus through which blood can shine

C) Delayed Rupture
.initial shock is followed by a long lucid interval, which may be few days or weeks
.about 2 weeks after the accident, which may be forgotten, the patient presents with the picture of internal haemorrhage
.this delay of clinical presentation may be due to:
1) the formation of subcapsular haematoma which may rupture later
2) the greater omentum seals the region of the spleen from the peritoneal cavity, and then retracts releasing blood.
3) a clot may form and stop bleeding but later on dislodged when the blood pressure rises or digested by enzymes from
injured pancreas
-Investigations :
1) blood picture
.decreased haemoglobin & haematocrit values
2) abdominal U/S or CT scan
.spleen is visualized with a surrounding haematoma. Serial examinations will diagnose an enlarging haematoma. Free blood in
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the peritoneal cavity is detected

3) abdominal plain x-ray - raises suspicion of rupture of the spleen by the following radiological signs :
.obliteration of psoas shadow
.indentation of left side of gastric air bubble
.fracture of one or more of lower ribs
.elevation of left side of diaphragm
.obliteration of splenic outline
4) peritoneal lavage
.reveals blood
+How is a spleen injury diagnosed ?
.abdominal CT (if the patient is stable)
.DPL or FAST exam (if the patient is unstable)
-Treatment :
.if the patient is severely shocked, there is no need for investigations. The surgeon depends on clinical findings & proceeds for
immediate laparotomy to stop bleeding
.the standard treatment of splenic injury is urgent splenectomy :
1) Rapid correction of hypovolaemic shock by crystalloid and blood transfusions
2) Analgesic for pain
3) Laparotomy - Rapid exploration through a midline incision is performed. In the majority of cases, splenectomy will be the
procedure of choice. Any associated injury is dealt with
4) After conservative surgery meticulous observation is necessary in the post-operative period as the patient may rebleed
5) In children especially < 15 years old every attempt should be made to preserve the spleen due to the vital role it plays in the
immune mechanism in this age group. Several techniques are available including (Suture of a small laceration, Partial
splenectomy, Compression of a lacerated spleen in a polygalactin mesh)
6) If splenectomy is necessary in a young child it is recommended to administer anti-pneumococcal vaccine (pneumovax) every
5 years until the age of 18

*Infarction Of The Spleen

-Etiology :
.may be spontaneous in patients with splenomegaly
.vascular occlusion produced by sickle cell disease
.embolism from infected heart valve or bacterial endocarditis
-Clinical Features :
.may be asymptomatic
.it is commonly accompanied with left upper quadrant abdominal pain
.overlying guarding. A friction rub may be heard over splenic area
-Treatment :
.by rest and analgesics
.sometimes septic infarcts cause an abscess which needs splenectomy

*Infections Of The Spleen

1) Acute Abscess (rare condition)
-Causes :
a) as a sequel of specific fever, e.g. typhoid fever
b) blood borne from a distant septic lesion or during systemic pyaemia
-Treatment :
.splenectomy, but if there are dense adhesions, drainage of the abscess is only performed
2) Chronic Abscess
.also rare and can result from a neglected acute abscess or an infected cyst & the treatment is splenectomy
3) Tuberculosis
.usually a manifestation of generalized miliary TB and rarely a primary affection. Multiple areas of caseation occur
4) Syphilis
.congenital lesion causes enlargement of the spleen
.treatment: anti-syphilitic drugs and not surgery
5) Parasitic Infection
.occurs in schistosomiasis and hydatid cysts
6) Protozoal Infection
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.occurs in malaria and kala azar

+Hydatid Disease (it may lead to the formation of single or multiple cysts of the spleen. Treatment is splenectomy)
+Malarial Spleen (is common in endemic areas of malaria. The spleen may reach a huge size and is soft. It acts as a reservoir for
malaria parasites and every now and then it causes an attack of malaria. Malarial spleen is very liable to rupture as it is soft.
Splenectomy is more difficult because the organ is friable)
+Kala Azar (is characterized by hepatosplenomegaly with progressive emaciation. Blood examination reveals Leishmania
Donovan)

*Cysts Of The Spleen (Rare)

-They may be :
1) Multiple as cystic disease of the spleen is usually associated with cystic disease of liver, kidney lung and pancreas
2) Single as hydatid cyst, lymphatic cyst, blood cyst or cystic degeneration of tumours
-Treatment :
.splenectomy
*Tumours Of The Spleen (Rare)
-They may be :
1) Part of generalized reticulo-endothelial affection as in malignant lymphomas and leukaemias
2) A tumour that is confined to the spleen
• Benign tumours as lymphangioma and cavernous haemangioma
• Primary malignant tumours as localized forms of lymphoma and fibrosarcoma
• Secondary tumours :
.these are very rare as it is supposed that the reticulo-endothelial cells can destroy the secondary malignant cells when they
reach the spleen
.the spleen may be infiltrated by direct extension from carcinoma of the stomach or pancreas

**Splenomegaly
-Normal spleen cannot be palpated clinically
-If the spleen is palpable under the costal margin, it is at least 3 times the normal size
-Enlargement of the spleen varies from being just palpable to a huge size which may reach below the level of the umbilicus or
down to the right iliac fossa
+Moderate splenomegaly, if the largest dimension is between 11-20cm
+Severe splenomegaly, if the largest dimension is greater than 20cm
-Causes Of Splenomegaly :
A) Infections :
1) bacterial (Typhoid, paratyphoid, tuberculosis, typhus, anthrax, abscess, syphilis)
2) viral (Infective mononucleosis, psittacosis)
3) parasitic (Schistosomiasis, hydatid cyst)
4) protozoal (Kala azar, malaria)
B) Blood Diseases :
1) haemolytic anaemias
2) leukaemias
3) thrombocytopenia
4) myelofibrosis
5) polycythaemia vera

C) Metabolic Causes :
1) gaucher's Disease
2) porphyria
3) rickets
D) Collagen Diseases :
1) felty's syndrome
2) still's disease
E) Others :
1) portal hypertension
2) cysts of the spleen
3) tumours of the spleen
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+Causes Of Massive Splenomegaly (>1000g) :

.thalassemia
.visceral leishmaniasis (kala-azar)
+Black fever, and Dumdum fever, is the most severe form of leishmaniasis. Leishmaniasis is a disease caused by protozoan
parasites of the Leishmania genus. This disease is the second-largest parasitic killer in the world (after malaria)
.schistosomiasis
.chronic myelogenous leukemia
.chronic lymphocytic leukemia
.lymphomas
.hairy cell leukemia
.myelofibrosis
.polycythemia vera
.Gaucher's disease
.Niemann-Pick disease
.sarcoidosis
.autoimmune hemolytic anemia
.malaria
-Differential Diagnosis Of A Huge Splenic Enlargement :
1) Thalassaemia
2) Myelofibrosis
3) Portal hypertension
4) Gaucher's disease
5) Malaria
+Clinical Characters Of Splenic Enlargement :
1) An intra-abdominal swelling in left hypochondrium that may descend downwards and medially towards iliac fossa
2) Moves up and down with respiration
3) Has a sharp medial border with a notch
4) Consistency varies from soft (typhoid, malaria) to firm (bilharziasis) to hard (lymphomas and leukaemia)
5) Surface is smooth or nodular spleen may be seen in some cases of lymphomas
6) The fingers cannot be insinuated between the spleen and costal margin
7) The splenic swelling does not fill the loin and does not ballot
8) Percussion reveals dullness anteriorly and resonance posteriorly (the lung passes down behind the spleen)

*Haemolytic Anemias
-Classification :
A) Congenital Anemias - due to an intrinsic abnormality of RBCs
1) cell membrane defect (hereditary spherocytosis, elliptocytosis)
2) Hb defect (thalassaemia, sickle cell anemia)
3) enzyme defect (G6PD deficiency, pyruvate kinase deficiency)
B) Acquired Anemias - due to extracorpuscular factors acting on normal RBCs
1) autoimmune haemolytic anemia
2) Rh incompatibility
3) haemolytic transfusion reaction
4) paroxysmal nocturnal haemoglobinuria
+Haemolytic Anemias That Are Treated By Splenectomy :
1) Heriditary spherocytosis
2) Some cases of thalassaemia
3) Rarely sickle cell anemia or autoimmune types
*NB.: Sickle cell anaemia patients develop acute attacks if exposed to hypoxia so if they require surgery, ensure that adequate
oxygenation all through the operation

**Hyposplenism
-Absent or reduced splenic function, usually due to surgical removal, congenital aplasia, tumor replacement, or splenic vascular
accident. Red blood cell abnormalities, including the presence of inclusions, nucleated red blood cells, and target cells, are
commonly present. Patients with hyposplenism are at increased risk of bacterial sepsis, especially due to infection by
Pneumococcus
-Hyposplenism is not a rare condition and can complicate a remarkable number of illnesses. The two most time-honored
diseases associated with the development of hyposplenism are sickle cell anemia and celiac disease
Page105

-Which Pts. Develop Hyposplenism ?

.Pts. with ulcerative colitis
+Hypersplenism (hyperfunctioning spleen, documented loss of blood elements, large spleen, hyperactive bone marrow)
+The M.C physical findings of portal hypertension (splenomegaly)
By Dr.Mohammad Z. abu sheikha@

Skin Lesions
+The M.C Skin Cancers :
.basal cell carcinoma (75%)
.squamous cell carcinoma (20%)
.malignant melanoma (4%) (M.C skin cancer that causes death) (all melanomas are considered malignant)

**Basal Cell Carcinoma

-M.C skin cancer
Page106

-Presentation :
.slowly growing
.present on sun-exposed areas of the skin (especially the face, rarely metastasize)
.treated with surgery or radiation

**Squamous Cell Carcinoma

nd
-2 M.C skin cancer
-Presentation :
.carcinoma arising from epidermal cells
.firm hard nodules (rapidly growing)
.most in lower lip
.metastasis to lymph nodes but not blood
-M.C Sites :
.head
.neck
.hands
-Risk Factors :
.sun exposure
.pale skin
.chronic inflammatory process
.immunosuppression
+Marjolin's Ulcer (squamous cell carcinoma that arises in an area of chronic inflammation)

**Melanoma
-Neoplastic disorder produced by malignant transformation of the melanocyte; melanocytes are derived from neural crest cells
-Presentation :
.most melanomas are brown to black looking lesions
.M.C type is superficial spreading
.metastasis by blood
.more aggressive
-Risk Factors :
.white Pts. with blonde/red hair, fair skin, blue/green eyes, M > F
.ultraviolet radiation from sun exposure (primary cause skin cancer)
.ionizing radiation
.immunosuppressive medication (M.C cancer from immunosuppression is skin cancer)
.chronic non-healing wound (Marjolin's Ulcer)
-The M.C Sites :
.skin
.eyes
.anus
-‘A, B, C, D`s’ Of Melanoma :
.asymmetry
.border irregularity
.color variation
.diameter >6mm and dark lesion
+M.C site of melanoma in men (back) / +M.C site of melanoma in women (legs) / +M.C type of melanoma (superficial spreading
>70%)

Pediatric Surgery
Section 3 (Subspecialty Surgery)

**Pediatric IV Fluids And Nutrition

-The estimated blood volume of infants and children (about 8% of body weight =80cc/Kg)
-The maintenance I.V fluid for children (D5 ¼ NS + 20 mEq KCI)
-The minimal urine output for children (from 1 to 2 mL/Kg/hr)
Page107

-The Caloric Requirements By Age For The Following Pts. :

.premature infants (80 Kcal/Kg/day)
.children younger than 1yr (100 Kcal/Kg/day)
.children aged 1 to 7 (85 Kcal/Kg/day)
.children aged 7 to 12 (70 Kcal/Kg/day)
.children aged 12 to 18 (40 Kcal/Kg/day)
+20 Kcal/Kg/day are in breast milk

**Pediatric Blood Volumes

-Blood Volume Per/Kg :
.newborn infant (85cc)
.infant 1-3 months of age (75cc)
.child (70cc)
**Aspirated Foreign Body FB
-Which bronchus do FBs go into more commonly (left or right) ?
.younger than age 4 (50/50)
.age 4yrs and older (most go into right bronchus because it develops into a straight shot)
+Most commonly aspirated object (peanut)

**Esophageal atresia (EA)

-Congenital esophageal atresia represents a failure of the esophagus to develop as a continuous passage instead, it ends as a
blind pouch
-M > F / More common in 1st born males
-Signs & Symptoms :
.excessive salivation
.choking
.coughing and sneezing
.cyanosis
.abdomen is flat or scaphoid
.regurgitation
-Associations :
.with other defects (anomalies) – VACTERL :
(Anal atresia, Cardiac defects, Tracheoesophageal fistula and/or Esophageal atresia, Renal & Radial anomalies and Limb defects
association polyhydramnios)
-Diagnosis :
.antenatal ultrasound
-Complications :
.aspiration pneumonia

**Abdomen
-Differential Diagnosis Of Neonatal Bowel Obstruction :
.malrotation with volvulus
.intestinal atresia
.duodenal web
.annular pancreas
.meckel`s diverticulum
.meconium ileus
.maternal hypermagnesemia (ileus)
.sepsis (ileus)
-Differential Diagnosis Of Infant Constipation :
.hirschsprung`s disease
.cystic fibrosis
.polyps

**Infantile Hypertrophic Pyloric Stenosis

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-Is narrowing (stenosis) of the opening from the stomach to the first part of the small intestine duodenum, due to enlargement
(hypertrophy) of the muscle surrounding this opening (the pylorus) / Hypertrophy of smooth muscle of pylorus
-Signs & Symptoms :
.first 2-4wks to months of life / Family history
.nonbilious projectile vomiting (recurrent vomiting can cause – hypokalemic, hypochloremic, metabolic alkalosis)
.weight loss
.dehydration
.constipation
.on exam palpation of the abdomen may reveal a mass in the epigastrium (olive sign)
.peristaltic waves (from Lt. to Rt.)
-Diagnosis :
.ultrasound
-Treatment :
.surgical pyloromyotomy
**Duodenal Atresia
-Is the congenital absence or complete closure of a portion of the lumen of the duodenum / Complete obstruction or stenosis
of duodenum caused by an ischemic insult during development of failure of recanalization
-It causes increased levels of amniotic fluid during pregnancy (polyhydramnios) and intestinal obstruction in newborn babies
-During pregnancy, duodenal atresia is associated with increased amniotic fluid in the uterus, which is called polyhydramnios.
This increase in amniotic fluid is caused by the inability of the fetus to swallow the amniotic fluid and absorb it in their digestive
tract
-Anatomic Location :
.85% are distal to the ampulla of vater
.15% are proximal to the ampulla of cater (these present with nonbilious vomiting)
-Signs & Symptoms :
.bilious vomiting (green vomit) – at 1st day (if distal to the ampulla)
.epigastric distention
.plain abdominal film revealing ‘double bubble’
-Complications :
.serious congenital anomalies.
+Late complications may occur in about 12% of patients with duodenal atresia, and the mortality rate for these complications is
6%
-20-40% of all infants with duodenal atresia have Down syndrome (trisomy 21) / 8% all infants with Down syndrome have
duodenal atresia
-Diagnosis :
.X-ray of the abdomen (double bubble sign)
-Treatment :
.suctioning out any fluid that is trapped in the stomach, providing fluids intravenously
.surgical repair of the intestinal closure

**Meckel`s Diverticulum
-A true congenital diverticulum, is a slight bulge in the small intestine present at birth and a vestigial remnant of the
omphalomesenteric duct (also called the vitelline duct or yolk stalk)
-More common in males – most in the first 2yrs of life, but can occur at any age
+Major differential diagnosis (appendicitis)
+M.C congenital GI anomalies / M.C malformation of the GI
+M.C symptoms is painless lower GI bleeding
-Signs & Symptoms :
.the majority of people with a Meckel's diverticulum are asymptomatic (An asymptomatic Meckel's diverticulum is called a
silent Meckel's diverticulum - If symptoms do occur, they typically appear before the age of two years)
.painless rectal bleeding such as melaena-like black offensive stools (M.C symptom)
.intestinal obstruction, volvulus and intussusception
.Meckel's diverticulitis may present with all the features of acute appendicitis (RLQ pain)
.severe pain in the epigastric region is experienced by the patient along with bloating in the epigastric and umbilical regions
.the symptoms are so painful that they may cause sleepless nights with acute pain felt in the foregut region, specifically in the
epigastric and umbilical regions
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+In most cases, bleeding occurs without warning and stops spontaneously. The symptoms can be extremely painful, often
mistaken as just stomach pain resulting from not eating or constipation
-Possible Complications :
.intestinal hemorrhage (painless)
.intestinal obstruction (M.C complication in adults)
.inflammation (perforation)
+M.C ectopic tissue in a Meckel`s diverticulum (gastric mucosa)
-Diagnosis :
.technetium-99m (99mTc) pertechnetate scan, also called Meckel scan (this scan detects gastric mucosa)
-Treatment :
.surgical, potentially with a laparoscopic resection
+In patients with bleeding, strangulation of bowel, bowel perforation or bowel obstruction, treatment involves surgical
resection of both the Meckel's diverticulum itself along with the adjacent bowel segment, and this procedure is called a "small
bowel resection"
+In patients without any of the aforementioned complications, treatment involves surgical resection of the Meckel's
diverticulum only, and this procedure is called a “simple diverticulectomy”
+Rule of 2's in Meckel's diverticulum :
.occur in 2% of the population
.are 2 inches (5cm) long
.are 2 feet (60cm) from the ileocecal valve
.2/3rds have ectopic mucosa
.2 types of ectopic tissue are commonly present (mostly gastric and pancreatic)
.2% become symptomatic
.symptoms start before 2 yrs of age

**Congenital Diaphragmatic Hernia (CDH)

-A congenital malformation (birth defect) of the diaphragm / More at Lt. side
-Types :
.Bochdalek hernia (M.C type) – Postero-lateral diaphragmatic hernia 90%
.Morgagni hernia – Anterior defect of the diaphragm 10%
.diaphragm eventration
.central tendon defects
-Presentation :
.malformation of the diaphragm allows the abdominal organs to push into the chest cavity (abdomen is scaphoid), and lead to
respiratory distress at birth
.infants born with diaphragmatic hernia experience respiratory failure due to both pulmonary hypertension and pulmonary
hypoplasia.
.pulmonary hypoplasia or decreased lung volume is directly related to the abdominal organs presence in the chest cavity which
causes the lungs to be severely undersized, especially on the side of the hernia
.work has been done to correlate survival rates to ultrasound measurements of the lung volume as compared to the baby's
head circumference. This figure known as the lung to head ratio (LHR)
-Treatment :
.orogastric tube placement
.intubation
.surgery

**Inguinal Hernia
-The M.C inguinal hernia in children (indirect) / The Rt. side is affected more commonly (about 60%) / M > F
-Indirect inguinal hernia (hernia lateral to Hesselbach`s triangle into the internal inguinal ring and down the inguinal canal)
-Hesselbach`s Triangle (a triangle formed by) :
.epigastric vessels
.ingunial ligament
.lateral border of the rectus sheath

**Umbilical Hernia
-Most umbilical hernias close spontaneously within the first 3yrs of life
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-Small-diameter umbilical hernias close earlier than large-diameter umbilical hernias

-Claims that strapping helps cure umbilical hernia are not supported by available data
-Risk Factors :
.black or african american infant
.premature infant
-Indications For Surgical Repair :
.>1.5cm defect
.bowel incarceration
.>4yrs of age

**Undescended Testis (Cryptorchidism)

-Is the absence of one or both testes from the scrotum. In unique cases, cryptorchidism can develop later in life, often as late as
young adulthood. About 3% of full-term and 30% of premature infant boys are born with at least one undescended testis, about
80% of cryptorchid testes descend by the first year of life (the majority within three months)
+It is the M.C birth defect of the male genitalia / In prematurity 30% risk after 1 st yr
+Must Be Distinguished :
.Undescended testes (cryptorchidism) are testes that remain in the abdomen instead of descending into the scrotum just
before birth
.Retractile testes have descended into the scrotum but can move back (retract) into the inguinal canal easily as a reflex
response to stimulation
-A testis absent from the normal scrotal position can be found :
1.the "path of descent" from high in the posterior (retroperitoneal) abdomen, just below the kidney, to the inguinal ring
2.in the inguinal canal - superficial ring (M.C position) (In 90% of cases an undescended testis can be felt in the inguinal canal)
3."wandered" from that path, usually outside the inguinal canal and sometimes even under the skin of the thigh, the perineum,
the opposite scrotum, or the femoral canal
4.undeveloped (hypoplastic) or severely abnormal (dysgenetic)
5.to have vanished (also see anorchia)
+The testis or testes are in the abdomen (Very rare)
-Complication :
.failure of the testicle to produce viable sperm (reduced fertility)
.malignant degeneration of the testicle (increased risk of testicular tumors)
.torsion and traumatic injuries
.there is likely to be an associated inguinal hernia (indirect)
-Treatment :
.surgery – Orchiopexy or orchidopexy (is performed 1-2yrs of age)
+Orchiopexy doesn't reduce the risk of malignancy
+Orchiectomy or Orchidectomy (Orchi) (is a surgical procedure in which one or both testicles are removed)
+Bilateral orchiectomy (The removal of both testicles is the surgical form of castration)
+Sex reassignment surgery (SRS) (for transgender women, or as palliative treatment for advanced cases of prostate cancer)
+Inguinal orchiectomy and also called radical orchiectomy (is performed when an onset of testicular cancer is suspected, in
order to prevent a possible spread of cancer from the spermatic cord into the lymph nodes near the kidneys)

**Acute Scrotum
-Testicular or scrotal pain occurs when part or all of either one or both testicles hurt. Pain in the scrotum is also often included
-Causes :
.post vasectomy (post-vasectomy pain syndrome PVPS)
.infections such as epididymitis, prostatitis and orchitis (caused by gonorrhea or chlamydia)
.varicocele, hydrocele, spermatocele, polyarteritis nodosa, testicular torsion, hematocele, cancer
.previous surgery and trauma
.fournier's gangrene (spreading infection of the perineum)
.idiopathic scrotal edema

**Intussusception
-Is a medical condition in which a part of the intestine invaginates (folds into) into another section of intestine, similar to the
way the parts of a collapsible telescope retract into one another. This can often result in an obstruction. The part that prolapses
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into the other is called the intussusceptum, and the part that receives it is called the intussuscepiens
-Telescoping of bowel inside each other / M > F
-Obstruction caused by bowel telesoping into the lumen of adjacent distal bowel
+M.C.C of small bowel obstruction in toddlers <2yrs old (Intussusceptoin)
-The Usual Age At Presentation :
.4-12 months of age (60%)
.by 2yrs of age (80%)
-M.C Site :
.terminal ileum involving ileocecal valve (M.C site is ileocecal)
.extending into ascending colon
-Signs & Symptoms :
.abdominal pain (intermittent moderate to severe cramping abdominal pain)
.nausea, vomiting (sometimes green in color from bile)
.pulling legs to the chest area / cry, draw their knees up to their chest
.Later signs include rectal bleeding, often with "red currant jelly" stool (stool mixed with blood and mucus), and lethargy
.physical examination may reveal a "sausage-shaped" mass (RLQ mass), felt upon palpating the abdomen / empty RLQ on
palpation (dance`s sign)
.dyspnea (difficult or painful breathing) with paroxysms of pain
.Fever is not a symptom of intussusception (intussusception can cause a loop of bowel to become necrotic, secondary to
ischemia due to compression to arterial blood supply. This leads to perforation and sepsis, which causes fever)
+Complication of Henoch-Schönlein purpura (HSP), an immune-mediated vasculitis disease in children
-Causes :
.hyperplasia of Peyer's patches (many Pts. have prior viral illness)
.infections (rotavirus, adenovirus) (M.C.C)
.anatomical factors
.altered motility, duplication
.Meckel's diverticulum
.polyp
.appendix
.idiopathic
+The causes of intussusception in older Pts. (Meckel's diverticulum, polyps, tumors)
-Differential Diagnosis :
.acute gastroenteritis (Abdominal pain, vomiting, and stool with mucus and blood are present in acute gastroenteritis, but
diarrhea is the leading symptom)
.rectal prolapse (Rectal prolapse can be differentiated by projecting mucosa that can be felt in continuity with the perianal skin,
whereas in intussusception the finger may pass indefinitely into the depth of sulcus)
-Diagnosis :
.ultrasound
.barium enema
-Treatment :
.hydrostatic pressure
.surgery

**Meconium Ileus
-Meconium is the first stool (bowel movement) that a newborn has. This stool is very thick and sticky. Meconium ileus is a
bowel obstruction that occurs when the meconium in your child's intestine is even thicker and stickier than normal meconium,
creating a blockage in a part of the small intestine called the ileum / Intestinal obstruction from solid meconium concretions
+Most infants with meconium ileus have a cystic fibrosis / X-ray
-Signs & Symptoms :
.bilious vomiting (green)
.abdominal distension (a swollen belly)
.failure to pass meconium (no passage of meconium)
.Neuhauser`sign (refers to a soap bubble appearance seen in the distal ileum in cases of meconium ileus, related to the air
mixed with meconium. It may be seen with barium enema if contrast passes beyond the ileocaecal valve or with small-bowel)
.peritoneal calcifications
**Hirschsprung's disease (HD)
-Also called congenital megacolon or congenital aganglionic megacolon, is a form of megacolon that occurs when part or all of
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the large intestine or antecedent parts of the gastrointestinal tract have no ganglion cells and therefore cannot function
-M > F and 10% of cases are familial / M.C site is Rectum
-Hirschsprung's disease is diagnosed shortly after birth, although it may develop well into adulthood, because of the presence
of megacolon, or because the baby fails to pass the first stool (meconium) within 48 hours of delivery / Some cases are
diagnosed later, into childhood, but usually before age 10
-Signs & Symptoms :
.green or brown vomit
.explosive stools after a doctor inserts a finger into the rectum
.swelling of the abdomen (meconium ileus)
.lots of gas and bloody diarrhea
.fecal retention, constipation or abdominal distention
+M.C.C of death in children with HD is (enterocolitis) / Complication (enterocolitis)
-Diagnosis :
.rectal biopsy (Best)
-Treatment :
.surgical removal (resection) of the abnormal section of the colon, followed by reanastomosis

**Omphalocele
-Is a rare abdominal wall defect in which the intestines, liver, and occasionally other organs remain outside of the abdomen in a
sac because of a defect in the development of the muscles of the abdominal wall (exomphalos), and is associated with a high
rate of mortality (25%) and severe malformations, such as cardiac anomalies (50%) and neural tube defect (40%),
Approximately 15% of live-born infants with omphalocele have chromosomal abnormalities
-An omphalocele is often detected through AFP screening or a detailed fetal ultrasound. Genetic counseling and genetic testing
such as amniocentesis are usually offered during the pregnancy
-Causes :
.genetic disorder, such as - Edward's syndrome (Trisomy 18) or Patau Syndrome (Trisomy 13)
.Beckwith-Wiedemann syndrome (BWS) (is an overgrowth disorder usually present at birth, characterized by an increased risk
of childhood cancer and certain congenital features)
.Pentalogy of Cantrell
.OEIS complex (omphalocele, exstrophy of the cloaca, imperforate anus, spinal defects)

**Gastroschisis
-Represents a congenital defect characterised by a defect in the anterior abdominal wall through which the abdominal contents
freely protrude. There is no overlying sac or peritoneum, and the size of the defect is usually less than 4cm. The abdominal wall
defect is located at the junction of the umbilicus and normal skin, and is almost always to the right of the umbilicus. The defect
occurs 5-8wks after conception, most likely due to a disruption of the blood supply to the developing abdominal wall
-Genetic counseling and further genetic testing, such as amniocentesis, may be offered during the pregnancy
-Causes :
.disruption of the blood supply to the developing abdominal wall from the omphalomesenteric duct artery by the 8 th wk of
gestation
.aspirin
.a change in paternity (childbearing with different fathers)
.immune system of the mother (It is most commonly seen in young mothers)
.newborns are often smaller for gestational age
.gastroschisis has clustered in families and exhibits autosomal recessive or dominant inheritance

+Omphalocele
.involves the umbilical cord itself
(opening in umbilicus)
.covered by membrane
.associated with other congenital
anomalies
.mortality rate higher
+Gastroschisis
.the umbilical cord is not involved
(lateral to umbilicus)
.NOT covered by membrene
.rarely associated with congenital
anomalies
.mortality rate lower

**Appendicitis
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-Obstruction of the appendiceal lumen

+Most common surgical disease requiring emergency surgery in children / Very rare before 3yrs of age (affected age)
-Signs & Symptoms :
.peritoneal irritation may be present
.guarding, muscle spasm
.rebound tenderness
.obturator, psoas signs, hamburger sign
.low-grade fever rising to high grade if perforation occurs
-Differential diagnosis :
.intussusception
.volvulus
.Meckel`s diverticulum
.CD
.ovarian torsion
.cyst
.tumor
.perforated ulcer
.pancreatitis
.PID
.ruptured ectopic pregnancy
+The common bacterial cause of mesenteric lymphadenitis (Yersinia enterocolitica)
-The Associated Findings :
.increased WBS (>10.000 with a left shift in most)
.evaluate for possible pyelonephritis or renal calculus, but mild hematuria and pyuria are common in appendicitis
-How long should antibiotics be administered if nonperforated ?
.24hrs
-How long if perforated ?
.usually 5-7 days or until WBCs are normal

**Pediatric Trauma
-The leading cause of death in pediatric Pts. (trauma)
-How do you estimate normal systolic blood pressure (SBP) in a child ?
.80 plus 2 multiplied by age (a 5yr old child should have an SBP of about 90)
-CT scan Findings Suggest Small Bowel Injury :
.free fluid with NO evidence of liver or spleen injury
.free air
.contrast leak
.bowel thickening
.mesentery streaking
+Treatment of choice for duodenal hematoma (observation with NGT and TPN)

**Hydrocele
-Denotes a pathological accumulation of serous fluid in a body cavity / Localized to the scrotum / Fluctuation of the scrotal size
during the day
-Types :
.communicating
.non communicating hydrocele
-Treatment :
.observation for 1-2 yrs of age, before recommending repair

**Neck Masses
+Congenital
.Branchial Clefts
.Pre-Auricular Cysts
.Thyroglossal Ducts
.Dermoid & Epidermoid Cysts
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.Ranula
.Torticollis
+Inflammatory
.Supurrative adenitis
.Chronic adenitis
.Mycobacterial lymphadenitis
.Cat-Scratch disease

**Cleft Lip And Palate

-Cleft Lip (treated within the first 2-3 months after birth)
-Cleft Palate (usually performed between 6-12 months)
-Failure Of Fusion Of Maxillary Bone :
.nasal speech
.difficulty in feeding
.aspiration pneumonia
.middle ear infection (OM)

**Other Pediatric Surgery Questions

-The common pediatric sedative (chloral hydrate)
+When should an umbilical hernia be repaired ?
.after 4yrs of age
-The Indications For Operation In Hemangiomas :
.severe thrombocytopenia
.congestive heart failure
.functional impairment (vision, breathing)
-Treatment Options For Hemangiomas :
.steroids
.radiation
.surgical resection
.angiographic embolization
+The M.C benign liver tumor in children (hemangioma)
-The M.C Cancers In Children :
.leukemia
.CNS tumors
.lymphoma
+The M.C solid neoplasm in infants (neuroblastoma)
+The M.C solid tumor in children (CNS tumors)
+What syndrome must you consider in the Pt. with abdominal pain, hematuria, history of joint pain, and a purpuric rash ?
.Henoch-Schonlein syndrome
+The M.C.C of small bowel obstruction in children (hernias)
+What is the ‘Dubble-Bubble’ sign on AXR ?
.gastric dubble and duodenal bubble on AXR
+The M.C.C of rectal bleeding in infants (anal fissure)
+What chromosomal abnormality is associated with duodenal web/atresia/stenosis ?
.trisomy 21
+What is the usual age at presentation of the following conditions ?
.pyloric stenosis (from 2 weeks to 2 months of age)
.intussusception (from 4 months to 2yrs of age)
.wilms` tumor (between 1 and 4yrs of age)
.malrotation (birth to 1yer of age)
.neuroblastoma (50% present by 2yrs of age, and more than 80% present by 8yrs of age)
.hepatoblastoma (younger than 3yrs of age)
.appendicitis (older than 3yrs of age, but must be considered at any age)

By Dr.Mohammad Z. abu sheikha@

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Thoracic Surgery
**Thoracic Outlet Syndrome TOS
-Compression of the (subclavian artery, subclavian vein or brachial plexus at the superior outlet of the thorax)
-Causes :
.various congenital anomalies (cervical rib or abnormal fascial bands to the first rib)
.trauma (fracture of clavicle or first tib dislocation of humeral head crush injuries)
.repetitive motor injuries
+M.C problem seen with TOS (neurological symptoms)
+Which nerve is most often involved ?
.ulnar nerve

**Chest Wall Tumors

-The M.C Types :
.fibrous rib dysplasia
.chondroma
.osteochondroma

**Malignant Tumors
-The M.C Types :
.fibrosarcoma
.chondrosarcoma
.osteogenic sarcoma
.rhabdomyosarcoma
.myeloma
.ewing`s sarcoma

**Pleural Effusion
-Is excess fluid that accumulates in the pleural cavity, the fluid-filled space that surrounds the lungs. This excess can impair
breathing by limiting the expansion of the lungs
+A pneumothorax is the accumulation of air in the pleural space and is commonly called a "collapsed lung"
-Types :
.hydrothorax (serous fluid)
.hemothorax (blood)
.urinothorax (urine)
.chylothorax (chyle) (most commonly caused by trauma)
.pyothorax or empyema (pus) / Empyema (Infected pleural effusion)
-By Pathophysiology :
.transudative pleural effusion (specific gravity <1.016, protein content <3g/dL, few cells, fluid protein/serum protein <0.5,
serum albumin/effusion albumin SAAG >1.2g/dL, fluid LDH/LDH effusion-serum ratio <0.6, cholesterol cont. <45)
.exudative pleural effusion (specific gravity >1.016, protein content >3g/dL, many cells, fluid protein/serum protein >0.5, serum
albumin/effusion protein SAAG <1.2, fluid LDH/LDH effusion >0.6, cholesterol content >45 )
-Signs & Symptoms :
+Once accumulated fluid is more than 300 mL
.decreased movement of the chest on the affected side
.dullness to percussion over the fluid
.dyspnea
.diminished breath sounds on the affected side
.decreased vocal resonance and fremitus (though this is an inconsistent and unreliable sign)
.pleural friction rub (pleuritic chest pain)
+Causes Of Transudative :
.heart failure (CHF) and cirrhosis (M.C.C)
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.nephrotic syndrome (leading to the loss of large amounts of albumin in urine and resultant low albumin levels in the blood and
reduced colloid osmotic pressure is another, less common, cause)
.Severe hypoalbuminemia
.parapneumonic effusion due to pneumonia
.acute atelectasis
.myxedema
.peritoneal dialysis
.meigs' syndrome
.obstructive uropathy
.end-stage kidney disease
+Causes Of Exudative :
.M.C.C of exudative pleural effusions are bacterial pneumonia, cancer (with lung cancer, breast cancer, and lymphoma causing
approximately 75% of all malignant pleural effusions), viral infection, and pulmonary embolism
.red blood cell counts are elevated in cases of bloody effusions (for example after heart surgery or hemothorax from incomplete
evacuation of blood)
.amylase levels are elevated in cases of esophageal rupture, pancreatic pleural effusion, or cancer
.glucose is decreased with cancer, bacterial infections, or rheumatoid pleuritis
.pH is low in empyema (<7.2) and may be low in cancer
.if cancer is suspected, the pleural fluid is sent for cytology. If cytology is negative, and cancer is still suspected, either a
thoracoscopy, or needle biopsy of the pleura may be performed
.if tuberculosis is possible, examination for Mycobacterium tuberculosis (either a Ziehl–Neelsen or Kinyoun stain, and
mycobacterial cultures) should be done. A polymerase chain reaction for tuberculous DNA may be done, or adenosine
deaminase or interferon gamma levels may also be checked
.after heart surgery (from incomplete evacuation of blood)
.malignancy (either lung cancer or metastases to the pleura from elsewhere)
.infection (emypema due to bacterial pneumonia)
.trauma
.pulmonary infarction
.pulmonary embolism
.autoimmune disorders
.pancreatitis
.ruptured esophagus (Boerhaave's syndrome)
.rheumatoid pleurisy
.drug-induced lupus
-Diagnosis :
.CXR
.thoracentesis (needle drainage)
.studies including (cytology)

**Lung Abscess
-Is a type of liquefactive necrosis of the lung tissue and formation of cavities (> 2 cm) containing necrotic debris or fluid caused
by microbial infection
-This pus-filled cavity is often caused by aspiration (staphylococcal or gram-negative bacillary pneumonias), which may occur
during altered consciousness
+Alcoholism is the most common condition predisposing to lung abscesses
-Lung Abscess Is Considered :
.primary (60%) when it results from existing lung parenchymal process
.secondary when it complicates another process e.g. vascular emboli or follows rupture of extrapulmonary abscess into lung
-Signs & Symptoms :
.cough (cough can be productive of foul smelling purulent mucus or less frequently with blood in one third cases)
.fever with shivering, and night sweats
.shortness of breath, lethargy
.finger clubbing
.dental decay is common especially in alcoholics and children
.on examination (dullness on percussion and bronchial breath sounds)
-Causes :
.aspiration of oropharyngeal or gastric secretion
.septic emboli
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.necrotizing pneumonia
.vasculitis (granulomatosis with polyangiitis)
.necrotizing tumors (higher in older people; primary squamous carcinoma of the lung is the most common)

-Diagnosis :
.CXR (Lung abscesses are often on one side and single involving posterior segments of the upper lobes and the apical segments
of the lower lobes. Presence of air-fluid levels implies rupture into the bronchial tree or rarely growth of gas forming organism)
.lab studies (Raised inflammatory markers (high ESR, CRP) are common but nonspecific. Examination of the coughed up mucus
is important in any lung infection and often reveals mixed bacterial flora)
.bronchoscopy (transtracheal or transbronchial aspiration)
-Complications :
.spread of infection to other lung segments
.bronchiectasis
.empyema
.bacteremia with metastatic infection such as brain abscess
-The Surgical Option :
.lobectomy of lobe with abscess
.tube drainage

**Hemoptysis
-Bleeding into the bronchial tree / is the act of coughing up blood or blood-stained mucus from the bronchi, larynx, trachea, or
lungs
+Hemoptysis is considered massive if there is more than 300mL/24hrs. In such cases, the primary danger comes from choking,
rather than blood loss
+Blood-laced mucus from the sinus or nose area can sometimes be misidentified as symptomatic of hemoptysis (such
secretions can be a sign of nasal or sinus cancer, but also a sinus infection)
+Extensive non-respiratory injury can also cause one to cough up blood
+Cardiac causes like congestive heart failure and mitral stenosis should be ruled out
+The origin of blood can be identified by observing its color (bright-red, foamy blood comes from the respiratory tract) (dark-
red, coffee-colored blood comes from the gastrointestinal tract) Sometimes hemoptysis may be rust-colored
-Causes :
.lung cancer (tumor mass 20%)
.infections such as (tuberculosis, bronchitis (M.C.C), or pneumonia) (50%)
.certain cardiovascular conditions
.lung cancer, including both (non-small cell lung carcinoma and small cell lung)
.carcinoma
.sarcoidosis
.aspergilloma
.tuberculosis
.histoplasmosis
.pneumonia
.pulmonary edema
.pulmonary embolism
.foreign body aspiration and aspiration pneumonia
.goodpasture's syndrome
.granulomatosis with polyangiitis
.eosinophilic granulomatosis with polyangitis (Churg-Strauss syndrome)
.bronchitis
.bronchiectasis
.pulmonary embolism
.anticoagulant use
.trauma
.lung abscess
.mitral stenosis
.tropical eosinophilia
.bleeding disorders
.cystic fibrosis
.hughes-Stovin Syndrome and other variants of Behçet's disease
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-Diagnosis :
.past history, history of present illness, family history
.imaging examination (CXR, CT-scan)
.lab tests (blood test-WBC, sputum)
.bronchial fiber endoscopy
-Treatment :
.iced saline
.topical vasoconstrictors such as adrenalin or vasopressin
.bronchial intubation (can be used to collapse the lung that is bleeding)
.laser photocoagulation (can be used to stop bleeding during bronchoscopy)
.angiography of bronchial arteries (can be performed to located bleeding)
.surgical option is usually the last resort (can involve, removal of a lung lobe or removal of the entire lung)
+Non–small-cell lung cancer can also be treated with erlotinib or gefitinib
+Cough suppressants can increase the risk of choking
**Spontaneous Pneumothorax
-Spontaneous pneumothorax is a collection of air or gas in the space between the lungs and the chest that "collapses" the lung
and prevents it from inflating completely / Spontaneous means there is no traumatic injury to the chest or lung
-Types Of Spontaneous Pneumothorax :
.primary spontaneous pneumothorax
.secondary spontaneous pneumothorax
+Primary spontaneous pneumothorax occurs in people without lung disease. It occurs most often in tall, thin, young people.
Sometimes people have a family history of this problem. People who have had one spontaneous pneumothorax are at higher
risk of the same thing (on the same side or the other side) occurring again (M.C.C of primary SP idiopathic)
+Secondary spontaneous pneumothorax occurs in people who have underlying lung disease. The M.C lung disease that causes
spontaneous pneumothorax is chronic obstructive pulmonary disease (COPD)
-Other lung diseases associated with spontaneous pneumothorax include:
.asthma
.cystic fibrosis
.interstitial lung disease
.lung cancer
.pneumonia
.tuberculosis
.bleb disease-emphysema
-Symptoms (symptoms often begin suddenly, and may occur during rest or sleep) :
.abnormal breathing movement
.cough
.rapid respiratory rate
.shortness of breath
.sudden chest pain or chest tightness (breathing or coughing makes pain worse / chest pain may be dull, sharp, or stabbing)
-Diagnosis :
.CXR
.ABGs
-Treatment :
.chest tube

**Bronchogenic Carcinoma
-Is a malignant lung tumor characterized by uncontrolled cell growth in tissues of the lung. If left untreated, this growth can
spread beyond the lung by process of metastasis into nearby tissue or other parts of the body
-Most cancers that start in the lung, known as primary lung cancers, are carcinomas that derive from epithelial cells. The main
primary types are small-cell lung carcinoma (SCLC) and non-small-cell lung carcinoma (NSCLC)
+Cancer arises more often in which lung (Rt. > Lt. / upper lobes > lower lobes) / M > F
-Types :
.squamous cell carcinoma (central)
.small cell lung cancer (central)
.adenocarcinoma (peripheral)
.large cell carcinoma (peripheral)
-Signs & Symptoms :
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.respiratory symptoms (coughing, coughing up blood, wheezing, or shortness of breath)

.systemic symptoms (weight loss, weakness, fever, or clubbing of the fingernails)
.symptoms due to the cancer mass pressing on adjacent structures (chest pain, bone pain, superior vena cava obstruction, or
difficulty swallowing)
.hypercalcemia, syndrome of inappropriate antidiuretic hormone (SIADH, abnormally concentrated urine and diluted blood)
(paraneopalstic syndrome)
.Lambert–Eaton myasthenic syndrome (muscle weakness due to autoantibodies)
+Common sites of spread include the brain, bone, adrenal glands, opposite lung, liver, pericardium, and kidney
+Primary lung cancers themselves most commonly metastasize to the brain, bones, liver and adrenal glands
+The lung is a common place for the spread of tumors from other parts of the body
+About 10% of people with lung cancer do not have symptoms at diagnosis (these cancers are incidentally found on routine
chest radiography)
+Horner Syndrome (can result from apical lung cancer / compression of sympathetic system / enophthalmos, ptosis, miosis,
anhidrosis)
+Superior Vena Cava Syndrome (SVC syndome) (result from compression of superior vena cava / symptoms – facial edema, arm
swelling, dilated chest veins)
-Causes :
.smoking (Most important risk factor)
.radon gas
.asbestos
.air pollution
.genetics (lung cancer is due to inherited factors. This is likely due to a combination of genes. Polymorphisms on chromosomes
5, 6 and 15 are known to affect the risk of lung cancer)
.ionizing radiation
.silica dust
+Cancer develops following genetic damage to DNA and epigenetic changes (these changes affect the normal functions of the
cell, including cell proliferation, programmed cell death (apoptosis) and DNA repair)
+The types of lung cancer arise in non smoker (adenocarcinoma) (Most in female)
-Treatment :
.surgery
.chemotherapy, and radiation therapy (small cell lung carcinoma-chemotherapy) (Non-small cell lung carcinoma-surgery)
+CT scan and positron emission tomography are used for this determination
+Mediastinoscopy may be used to sample the nodes and assist staging
+Blood tests and pulmonary function testing are used to assess whether a person is well enough for surgery
+M.C cancer benign lung tumor (Hematoma)

**Diseases Of The Esophagus

*Diffuse Esophageal Spasm (DES)
-Is a condition characterized by uncoordinated contractions of the esophagus, which may cause difficulty swallowing
(dysphagia) or regurgitation. In some cases. The cause of DES remains unknown; sphincter function is usually normal
-Symptoms :
.dysphagia (for solid foods and liquids)
.it may causes symptoms such as chest pain, similar to heart disease (angina pectoris)
.spontaneous chest pain that radiation to the back, ears, neck, jaw or arms
-Diagnostic :
.Esophageal manometry / Barium swallow x-ray
+Abnormalities on x-ray imaging are commonly observed in DES, such as a "corkscrew" or "rosary bead esophagus”
-Treatment :
.proton pump inhibitors
.nitroglycerin
.calcium channel blockers
.hydralazine
+People with DES have higher incidences of gastroesophageal reflux disease (GERD) and anxiety

*Gastroesophageal Reflux Disease (GERD)

-Is a chronic condition of mucosal damage caused by stomach acid coming up from the stomach into the esophagus (chronic
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reflux). Occasional reflux causes heartburn, but chronic reflux leads to reflux esophagitis, GERD, and sometimes Barrett
esophagus / Failure of the lower esophageal sphincter
-Reflux of gastric contents into the lower esophagus resulting from the decreased function of the LES
+Changes in the junction between the stomach and the esophagus, including (abnormal relaxation of the lower esophageal
sphincter, impaired expulsion of gastric reflux from the esophagus, or a hiatal hernia)
+These changes may be permanent or temporary
-Signs & Symptoms :
.substernal pain
.symptoms are worse when Pt. is supine and after meals
.vomiting (in infants and childrens)
.heartburn
.regurgitation
+Less-common symptoms include (pain with swallowing/sore throat, increased salivation (also known as water brash), nausea,
chest pain, and coughing)
-Causes :
.decreased LES tone
.decreased esophageal motility
.gastric outlet obstruction
.NGT
.tobacco and alcohol
.hiatal hernia
.obesity (increasing body mass index)
.Zollinger-Ellison syndrome (can be present with increased gastric acidity due to gastrin production)
.high blood calcium level (can increase gastrin production, leading to increased acidity)
.scleroderma and systemic sclerosis (can feature esophageal dysmotility)
.the use of medicines such as (prednisolone)
.visceroptosis or Glénard syndrome
.obstructive sleep apnea
.gallstones (can impede the flow of bile into the duodenum, which can affect the ability to neutralize gastric acid)
-Complications (GERD sometimes causes injury of the esophagus) :
.reflux esophagitis (necrosis of esophageal epithelium causing ulcers near the junction of the stomach and esophagus)
.esophageal strictures (the persistence narrowing of the esophagus caused by reflux-induced inflammation)
.Barrett's esophagus (intestinal metaplasia – ‘changes of the epithelial cells from squamous to intestinal columnar epithelium’
of the distal esophagus)
.esophageal adenocarcinoma
.sinusitis, recurrent ear infections, and idiopathic pulmonary fibrosis
-Diagnosis :
.esophageal pH monitoring (the current gold standard for diagnosis of GERD)
+Barium swallow X-rays should not be used for diagnosis
+Esophageal manometry is not recommended for use in diagnosis being recommended only prior to surgery
+pH monitoring may be useful in those who do not improve after PPIs and is not needed in those in whom Barrett's esophagus
is seen
+Investigation for H. pylori is not usually needed
-Treatment :
.Proton-pump inhibitors (PPIs), such as omeprazole, are the most effective
.H2 receptor blockers, such as ranitidine
.Nissen fundoplication (the standard surgical treatment for severe GERD)
-Complications Require Surgery :
.failure of medical therapy
.esophageal strictures
.progressive pulmonary insufficiency
.barrett`s esophagus (replacement of the lower esophageal squamous epithelium with columnar epithelium secondary to
reflux)

*Esophageal Carcinoma
-Is cancer arising from the esophagus (the food pipe that runs between the throat and the stomach)
-Types :
.esophageal squamous-cell carcinomas (ESCC) - similar to head and neck cancer (M.C histology) (Causes; smoking and alcohol)
.esophageal adenocarcinomas (EAC) - at the GE junction (long-term acid reflux (history of GERD), obesity, Barrett's esophagus)
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+Both types are more common in men (M > F) and in the over-60s / Tobacco is a risk factor for both types
-Signs & Symptoms :
.chest-back pain
.difficulty in swallowing-dysphagia (M.C symptom)
.weight loss
.pain when swallowing
.hoarse voice (hoarseness)
.enlarged lymph nodes (glands) around the collarbone
.dry cough
.vomiting blood
.heartburn
.increased risk of aspiration pneumonia
.the abnormal connections (fistulas) that may develop between the esophagus and the trachea (windpipe)
+If the cancer has spread elsewhere, symptoms related to metastatic disease may appear. Common sites of spread include
nearby lymph nodes, the liver, lungs and bone
-Association Conditions :
.head and neck cancer is associated with second primary tumors in the region, including esophageal squamous-cell carcinomas
.history of radiation therapy for other conditions in the chest is a risk factor for esophageal adenocarcinoma
.corrosive injury to the esophagus by accidentally or intentionally swallowing caustic substances is a risk factor for squamous
cell carcinoma
.tylosis with esophageal cancer is a rare familial disease that has been linked to a mutation in the RHBDF2 gene: it involves
thickening of the skin of the palms and soles and a high lifetime risk of squamous cell carcinoma
.achalasia appears to be a risk factor for both main types of esophageal cancer
.Plummer–Vinson syndrome (a rare disease that involves esophageal webs) is also a risk factor
.human papillomavirus (HPV) and esophageal squamous-cell carcinoma
.celiac disease and esophageal cancer
-Treatment :
.Esophagectomy (the removal of a segment of the esophagus)
.Chemotherapy ( fluorouracil 5-FU) and radiotherapy
+Rare histologic types of esophageal cancer non-epithelial tumors, such as (leiomyosarcoma, malignant melanoma,
rhabdomyosarcoma, lymphoma)

By Dr.Mohammad Z. abu sheikha@

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Orthopaedic Surgery
**Fractures & Dislocations General Principles
-Fracture (loss in the normal continuity of a bone)
-Dislocation (disruption of normal articulation between 2 bones with loss of opposition)
-Subluxation (partioal disruption of the joint and the articular surfaces are still opposed)
-Etiology :
1) Traumatic Fractures (mechanism differs according to type of bone) 
a) direct injury
.the fracture occurs at the point of impact
.fracture of the ulna due to trauma to it
.if both bones of the leg or forearm are involved, they are usually fractured at the same level
b) indirect violence
.the fracture occurs at a distance from the point of impact
.fracture of the ulna due to fall on the outstretched hand
.if both bones of the leg or forearm are involved, they are usually fractured at different levels
2) Pathological Fractures (due to abnormal fragility of the bones which break by a minor trauma. They are 2ry to) 
a) local bone disease (osteomyelitis, cysts, primary tumors or secondaries)
b) generalized bone disease (osteogenesis imperfecta, osteoporosis, hyperparathyroidism, paget`s disease and multiple
myelomatosis)
3) Stress Fractures (fatigue fractures)
a) they occur 2ry to repeated traumas
nd rd
b) march fractures which occur in the 2 & 3 metatarsals due to prolonged walking
-Clinical Diagnosis :
1) history of trauma (except in stress fractures and some cases of pathological fractures)
2) symptoms (pain, loss of function or deformity)
3) signs
.swelling and ecchymosis (due to effusion of blood from the broken bone ends and torn soft tissues)
.deformity (due to displacement of the fragments by either  the trauma, the weight of the limb and the gravity, the action of
muscles)
.tenderness
.loss of function (which varies from minimal to complete)
.crepitus (felt as a sensation of grating when the bone ends are moved against each other)
.abnormal mobility (except in incomplete and impacted fractures)
.examination of the motor and sensory innervation of the limb and peripheral circulation
-Fracture Description :
1) Site Of The Fracture
.intra-articular
.epiphyseal
.metaphyseal or diaphyseal
2) Extent Of The Fracture
a) complete fractures
.the bone is broken into 2 or more fragments which tend to become displaced “2 cortices are involved”
b) incomplete fractures
.the bone is incompletely broken so that displacement cannot occur “one cortex is involved”
.fissures, greenstick fractures and subperiosteal cracks of children
3) Fracture Line
a) transverse  angle <30 “direct trauma”
b) oblique or spiral  angle >30 “indirect trauma”
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c) comminuted (>2 bone fragments)

d) avulsion (separation of a bony process with its attached muscles)
e) epiphyseal Separation In Children (occurs on the metaphyseal side of the epiphyseal cartilage so that the separated
epiphysis always includes the epiphyseal cartilage with a triangular fragment from the meyaphysis)
4) Displacement
.def.  the deformity presents after a fracture or dislocation
.discribes  the position of distal component in relation to proximal one
.causes  affect of the trauma / gravity / power of the surrounding muscles / movement of the Pt. during transport
-Types :
1) Lateral Displacement (the distal fragment deviates to one side with loss of opposition)
*NB. : (Varus – dispalcement to the midline / Valgus – displacement away from midline)
2) Angulation (loss of the normal longitudinal axis of the shaft and it may be anterior, posterior, medial and lateral)
3) Over-riding (the distal fragment overlaps the proximal fragment with shortening of the limb)
4) Rotation (the distal fragment is rotated along its long axis)
5) Distraction (the fragments are separated either by  excessive traction during treatment – common / excessive muscle pull
at the time of injury – rare)
6) Impaction (the distal fragment is forcibly driven into the proximal fragment so than abnormal mobility and crepitus can`t be
elicited)
7) Depression (a fragment of bone is displaced, e.g. a skull fracture)
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5) Stability
.def.  a stable fracture in which there is no displacement after reduction
.factors controlling stability are  (oblique, spiral, comminuted fractures are unstable / muscle pull / integrity of the supportig
 Ligaments)
6) Soft Tissue Damage
a) simple (closed) fractures (in which the skin surface is intact)
b) compound (open) fractures (in which the skin wound communicates with the fracture haematoma) – types 
.compound from within (wound caused by a fracture fragment penetrating the skin from its deep surface)
.compound from without (wound caused by direct injury to the skin)
+Closed Fracture (intact skin over fracture/hematoma)
+Open Fracture (wound overlying fracture, through which fracture fragments are in continuity with outside environment; high
risk of infection)
+Simple Fracture (one fracture line, tow bone fragments)
+Transverse Fracture (fracture line perpendicular to long axis of bone)
+Comminuted Fracture (results in more than tow bone fragments; also known as fragmentation)
+Oblique Fracture (fracture line creates an oblique angle with long axis of bone)
+Spiral Fracture (severe oblique fracture in which fracture plane rotates along the long axis of bone; caused by a twisting injury)
+Longitudinal Fracture (fracture line parallel to long axis of bone)
+Impacted Fracture (fracture resulting from compressive force; end of bone is driven into contiguous metaphyseal region
without displacement)
+Pathologic Fracture (fracture through abnormal bone)
+Stress Fracture (fracture in normal bone from cyclic loading on bone)
+Greenstick Fracture (incomplete fracture in which cortex on only one side is disrupted; seen in children)
+Torus Fracture (impaction injury in children in which cortex is buckled but not disrupted – A.K.A buckle fracture)
+Avulsion Fracture (fracture in which tendon is pulled from bone, carrying with it a bone chip)
+Periarticular Fracture (fracture close to but not involving the joint)
+Intra-articular fracture (fracture through the articular surface of a bone)
+Boxer`s Fracture (fracture of the metacarpal neck, calssically of the small finger)
+Night Stick Fracture (ulnar fracture)
+Clay Shoveler`s Avulsion Fracture (fracture of spinous process of C6-C7)
+Hangman`a Fracture (fracture of the pedicles of C2)
+Transcervical Fracture (fracture through the neck of the femur)
+Pilon Fracture (distal tibial fracture)
+Pott`s Disease (tuberculosis of spine)
-Complications Of Fractures :
+General Complications
.shock (neurogenic or hypovolaemic shock may accompany major fractures as fracture spine, pelvis or femur)
.fat embolism (occurs when immobilization and reduction of long bones are delayed) (C/P  dyspnea, chest pain and
drowsiness)
.DVT
.respiratory complications (occurs due to prolonged recumbency particularly in elderly including aspiration pneumonitis or
pulmonry embolism)
.urinary calculi (prolonged immobilization leads to demineralization of the skeleton with the formation of calcium phosphhate
calculi) (avoided by  high fluid intake and early mobilization)
.Bed Sores (occur due to prolonged recumbency particularly in elderly) (avoided by  frequent change of the Pt. position in
bed, massage, assurance of dry bed sheets and the use of an air-mattress)
.tetanus (tetanus organisms grow only in dead tissues. It produces an exotoxin which passes to CNS via the blood from the
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infected region, e.g. in compound fractures) (avoided by  tetanus toxoid)

+Local Complications
.skin injury (by the fractured bone ends from inside – compund from within)
.vascular injuries (trt  open reduction and internal fixation then vascular injuries are repaired)
.nerve injuries (E.g.  radial nerve injury in fracture shaft humerus)
.tendon or muscle injury
.infection (this may complicate compound fractures. It leads to delayed healing, non-union or osteomyelitis)
.avascular necrosis of bone (due to damage of the blood supply to some areas of bones) (E.g.  intracapsular fracture of the
neck of the femur which may lead to avascular necrosis of the head of the femur)
.visceral injury (a fracture of the pelviss may be complicated by injury to the bladder or urethra)
+Delayed Local Complications
.malunion (union but with deformity “angulation or rotation” leading to cosmetic or functional disability) (due to lack of perfect
reduction or failure of stabilization) (Avoided by  open reduction and internal fixation)
.delayed union and non-union (delayed union  fractures fails to heal in usual time but will heal if the cause of the delayed
healing is corrected) (dealyed non-union  failure of fracture fragments to unit and healing process has stopped)
.sudek`s atrophy (seen after colles fracture) (C/P  osteoporosis, swelling of the soft tissue, vascular stasis, pain and joint
stiffness complicating fracture)
.myossitis ossificans (seen after dislocation of the elbow, shoulder or hip)
.joint stiffness and osteoarthrosis (joint stiffness occurs after prolonged immobilization and after intra-articular fractures and
affect certain joints as the elbow, shoulder and hip) (osteoarthrosis occur after damage to articular cartilage or avascular
necrosis of bone following an intra-articular fracture)
.growth disturbance (may occur if the fracture affects the epiphyseal growth plate in children)
.osteoporosis (due to prolonged immobilization)
-Injuries Of Joints :
.ligament Injuries
.traumatic Effusion
.haemarthrosis (a severe injury may lead to bleeding inside the joint)
.internal derangement of a joint (this refers to the various injuries which impair movements and stability of the joint)

**Orthopaedic Trauma
-The main risk when dealing with an open fracture (Infection)
+Which fracture has the highest mortality ?
.pelvic fracture (up to 50% with open pelvic fractures)
+The M.C.C of a ‘pathologic’ fracture in adults (Osteoporosis)
+The M.C site of compartment syndrome (Calf)

**Dislocations
*Shoulder
-Types :
.anterior (M.C – 90%) (M.C nerve injured is axillary nerve loss sensation over deltoid muscle)
.posterior (Rare) (electrical shock – seizure)
-Treatment :
.manual reduction

*Elbow
-The M.C type (Posterior)
+Which structures are at risk ?
.brachial artery
.ulnar nerve
.medium nerve

*Hip
-The M.C type (Posterior)
-The M.C.C if a hip dislocation (The velocity trauma)
+Which Structures Are At Risk ?
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.sciatic nerve (blood supply to femoral head-avascular necrosis AVN)

*Knee
-The M.C type (Anterior or Posterior)
+Which Structures Are At Risk ?
.popliteal artery and vein, peroneal nerve

**Orthopaedic Infections (Bone Infections)

-Types Of Bone Infections :
A) Acute Bone Infections
1) acute haematogenous osteomyelitis
2) acute osteomyelitis secondary to open fractures
3) acute osteomyelitis in association with orthopedic implants, e.g., after internal fixation of fractures or joint replacement
B) Chronic Bone Infections
+Chronic Non Specific Osteomyelitis
1) chronic osteomyelitis as a sequel to acute osteomyelitis
2) brodie`s abscess (affects adolescents and adults with high resistance resulting in localization of infection)
3) chronic sclerosing osteomyelitis (Garre`s type) (affecting shafts of long bones)
+Chronic Specific Osteomyelitis
1) TB
2) spirochaetal infection (syphilis) is rare
3) mycotic infection is rare

*Osteomyelitis
-Inflammation / infection of bone marrow and adjacent bone
-Signs & Symptoms :
.severe limb pain, malaise and fever
.severe localized tenderness (earliest sign)
.edema and the skin is red
.any movement of the limb is painful
-The Most Likely Causative Organisms :
.neonates (Staphylococcus aureus  M.C , gram-negative streptococcus)
.children (S.aureus, haemophilus influenzae, streptococci)
.adults (S.aureus)
.immunocompromised/drug addicts (S.aureus, gram-negative)
.sickle cell (salmonella)
-Site :
.occur in the metaphysis of long bones; often at lower and upper and of femur and upper end of tibia
-Complications :
.metastatic infection (pyaemic abscesses)
.chronic osteomyelitis
.suppurative arthritis (occurs only in joints where part of the metaphysis is intracapsular – shoulder joint)
.pathological fracture
.acute exacerbation
.toxemia and amyloidosis
-Differential Diagnosis :
.cellulitis
.acute suppurative arthritis
.rheumatic arthritis
.haemarthrosis
.ewing`s sacroma

*Septic Arthritis
-Inflammation of a joint beginning as synovitis and ending with destruction of articular cartilage if left untreated (joint warm to
touch)
-Signs & Symptoms :
.manifestations of toxemia with severe throbbing pain and swelling of the affected koint
.deformity, redness, tenderness and limitation of joint movements
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.muscle spasm
.high leukocytosis and elevated ESR
-The Causative Agents :
.same as in osteomyelitis (except that gonococcus is a common agent in the adult population) (Staphylococcus aureus)
(Haemophilus influenza in children <3yrs of age)
-Routes Of Infection :
.following joint punctures
.direct extension from a nearby infection such as osteomyelitis
.by haematogenous spread from a distant site
-Site :
.commonly in the knee and the hip joint (yet any joint may be infected)
-Complications :
.chronicity
.pathological dislocation
.secondary osteoarthrosis
.pyaemia

-Differential Diagnosis :
.acute osteomyelitis
.rheumatic fever
.haemarthrosis
.TB arthritis

**Osteoporosis
-Is a disease where decreased bone strength increases the risk of a broken bone. It is the most common reason for a broken
bone among the elderly / F > M
-Characterized by decrease in the amount of bone substance in the skeleton
-Signs & Symptoms :
.increased risk of bone fractures (Collies` fracture, fracture of the vertebral bodies and fracture of the femoral neck) (repeated
minor fractures of the spine cause chronic back pain and kypho-scoliosis)
.no metabolic abnormalities detected
.usually asymptomatic or there is loss of height
+Fractures occur in situations where healthy people would not normally break a bone
+The M.C osteoporotic fractures are of the wrist, spine, shoulder and hip
-Risk Factors :
.advanced age (in both men and women)
.estrogen deficiency following menopause or surgical removal of the ovaries (in female)
.family history of fracture or osteoporosis are at an increased risk
.those who have already had a fracture are at least twice as likely to have another fracture compared to someone of the same
age and sex
.early menopause/hysterectomy
.alcohol intake / smoking
.Vit D deficiency (vit D insufficiency is associated with increased parathyroid hormone (PTH) production)
.lack of exercise
.malnutrition
+Low dietary calcium and/or phosphorus, magnesium, zinc, boron, iron, fluoride, copper, vitamins A, K, E and C (and D where
skin exposure to sunlight provides an inadequate supply)
.excess sodium is a risk factor
.high dietary protein from animal sources
.higher cadmium and lead exposure results in osteomalacia (softening of the bone)
.hypogonadal states can cause secondary osteoporosis. These include Turner syndrome, Klinefelter syndrome, Kallmann
syndrome, anorexia nervosa, andropause, hypothalamic amenorrhea or hyperprolactinemia
.endocrine disorders that can induce bone loss include Cushing's syndrome, hyperparathyroidism, hyperthyroidism,
hypothyroidism, diabetes mellitus type 1 and 2, acromegaly, and adrenal insufficiency. In pregnancy and lactation can cause
reversible bone loss
.gastrointestinal disorders that can predispose to osteoporosis include undiagnosed and untreated coeliac disease (both
symptomatic and asymptomatic people), Crohn's disease, ulcerative colitis, cystic fibrosis, surgery (after gastrectomy, intestinal
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bypass surgery or bowel resection) and severe liver disease (especially primary biliary cirrhosis). People with lactose intolerance
or milk allergy may develop osteoporosis due to restrictions of calcium-containing foods, bulimia, vitamin K - D or vitamin B12
deficiency
.rheumatologic disorders such as rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus and polyarticular
juvenile idiopathic arthritis
.systemic diseases such as amyloidosis and sarcoidosis
.renal insufficiency can lead to renal osteodystrophy
.hematologic disorders linked to osteoporosis are multiple myeloma and other monoclonal gammopathies, lymphoma and
leukemia, mastocytosis, hemophilia, sickle-cell disease and thalassemia
.several inherited disorders have been linked to osteoporosis. These include osteogenesis imperfecta, Marfan syndrome,
hemochromatosis, hypophosphatasia (for which it is often misdiagnosed), glycogen storage diseases, homocystinuria, Ehlers–
Danlos syndrome, porphyria, Menkes' syndrome, epidermolysis bullosa and Gaucher's disease
.people with Parkinson's disease and chronic obstructive pulmonary disease (calcium metabolism and iron metabolism causing
a stiffening of the skeleton and kyphosis)
+The incidence of osteoporosis is lower in overweight people
+Estrogen deficiency. It can appear as early menopause (<45 years) or from prolonged premenopausal amenorrhea (>1 year).
Bilateral oophorectomy (surgical removal of the ovaries) and premature ovarian failure cause deficient estrogen production. In
males, testosterone deficiency is the cause (for example, andropause or after surgical removal of the testes)
+Medications have been associated with an increase in osteoporosis risk : (only steroids and anticonvulsants are classically
associated, but evidence is emerging with regard to other drugs)
.Glucocorticoid
.Antiepileptics (barbiturates, phenytoin)
.L-Thyroxine/Levothyroxine (thyroid hormones)
.Several drugs induce hypogonadism, for example aromatase inhibitors used in breast cancer, methotrexate and other
antimetabolite drugs, depot progesterone and gonadotropin-releasing hormone agonists
.Anticoagulants (heparin, warfarin)
.Proton pump inhibitors (PPIs)
.Thiazolidinediones (used for diabetes) (rosiglitazone, pioglitazone)
.Chronic lithium therapy
+Primary (idiopathic) Osteoporosis (Risk Factors)
.old age
.female
.fair skin
.tobacco and alcohol excess
.menopause before age 45yrs
.sedentary lifestyle
+Secondary Osteopotosis (Risk Factors)
.cushing`s syndrome
.hyperparathyroidism
.calcium, Vit D or C deficiency
.hyperthyroidism
.long-term steroid therapy
-Investigations :
.Dual-energy X-ray absorptiometry (DEXA)
.plain X-ray (not sensitive)
-Treatment :
+Primary Osteoporosis
.calcium 1500 mg/day
.Vit D 400 mg/day
.flouride
.calcitonin and biphosphonates  decreased bone resorption by reducing osteoclastic activity
.hormone replacement therapy for menopausal women
+Secondary Osteoporosis
.trt of the cause
-Prevention :
.Estrogen
.Exercise
.Calcium
.Vit D
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.avoidance of alcohol and smoking

**Osteoarthrosis (Osteoarthritis)
-Is a type of joint disease that results from breakdown of joint cartilage and underlying bone
-Etiology :
1) Primary Osteoarthritis (idiopathic)  with old age
2) Secondary Osteoarthritis – due to 
.demonstrable abnormality (trauma, deformity, avascular necrosis, pethes` disease)
.previous joint disease (septic arthritis, TB arthritis)
-Signs & Symptoms :
.pain and stiffness (pain is worse on movement and by change of weather) (stiffness is most marked in the morning and
decrease by evening)
.Pts. usually present after middle age
.symptoms typically follow an intermittent course, with periods of remission
.affects the weight-bearing joints such as the hip and knee
.joint swelling due to effusion and thickened synovial membrane
.tender joint line
.restricted range of movement
.deformity
.coarse crepitus during movement
-Investigations :
.plain X-ray shows the characteristic changes  (narrowing of the joint space, sub-articular sclerosis, bone cysts, marginal
osteophytes)
-Surgical Treatment :
.total joint replacement

**Orthopaedic Tumors
+The M.C type in adults (Metastatic)
+The common sources (Breast, lung, prostate, kidney, thyroid and multiple myeloma)
+The usual presentation (Bone pain or as a pathologic fracture)
nd
+The M.C primary malignant bone tumor (multiple myeloma 45%) / 2 M.C primary malignant bone tumor (Osteosarcoma)
-The Benign Bone Tumors :
.osteochondroma
.enchondroma
.unicameral/aneurysmal bone cysts
.chondroblastoma
.fibroxanthoma
.fibrous dysplasia (specific radiographic findings are bubbly lytic lesion ‘ground glass’)
.nonossifying fibroma
-The Malignant Bone Tumors :
.multiple myeloma
.osteosarcoma (specific radiographic findings are Sunburst pattern)
.chondrosarcoma
.ewing's sarcoma (specific radiographic findings are onion skinning) (around the knee)
.giant cell tumor (locally tumor)
.malignant melanoma
.metastatic
+Most pediatric bone tumors are benign (Most commonly osteochondroma)
+Most adult bone tumors are malignant (Most commonly metastatic)
+Osteosarcoma
.the usual age at presentation (between 10 – 20yrs) (M > F) (highly malignant)
.the most locations (Two-thirds in the distal femur, proximal tibia)
+M.C site of metastasis (Lung) / Metastatic bone tumors are more common than 1ry bone tumors

**Pediatric Orthopaedics
*Congenital Hip Dislocation
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-Epidemiology :
.F > M
.firstborn children
.breech
-Diagnosis :
.barlow's maneuver
.ortolani's sign (clunk)
 Cell Type Benign Malignant
Bone Ivory osteoma Osteo-sarcoma
Osteoid osteoma
Osteo-blastoma
Cartilage Chondroma Chondro-sarcoma
Osteo-chondroma
Chondroma-blastoma
Chondro-myxoid fibroma
Marrow Eosinophilic granuloma Ewing`s sarcoma
Myeloma
Reticular cell sarcoma
Fibrous Tissue Non-ossifying fibroma (fibrous cortical Fibro-sarcoma
defect)
Vascular Hemangioma Angio-sarcoma
Uncertain Giant cell tumor Malignant giant cell tumor

*Classification Of 1ry Bone Tumors By Cell Type

Vertebral Lesions Flat Bones Long Bones

Osteoid osteoma 2ry +Epiphysis:
Osteo-blastoma Myeloma Giant cell tumor
Hemangioma Chondro-sarcoma Chondro-sarcoma
Myeloma +Metaphysis
2ry Osteo-sarcoma
+Diaphysis
2ry
Ewing`s sarcoma

*Classification Of Bone Tumors According To Site

-C/P :
A) Age
.young age (benign tumors, ewing tumor, osteosarcoma)
.middle age after closure of epiphysis (giant cell tumor)
.17-18yrs old (osteoid osteoma)
.40-60yrs old (chondrosarcoma & fibrosarcoma)
.>60yrs old (myeloma)
.>70yrs old (2ry)
B ) Symptoms
.pain (benign  not painful except osteoid osteoma – compress in a nerve or artery)
(malignant  painful)
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.swelling (wither smooth, lobulated, tender, pulsating, to see the attached skin, fluid and dilated vessels)
.neurological symptoms (as wrist or foot drop)
.pathological fractures
-DD :
.soft tissue hematoma
.myositis ossificans
.osteomyelitis
.callus from unnoticed stress fracture
.tendon avulsion injuries (osgood-schlatter disease)
.bone infection
.gout
.fibrous dysplasia
.brown tumor of hyperparathyroidism
By Dr.Mohammad Z. abu sheikha@

Neurosurgery
**Head Trauma
-The percentage of trauma deaths result from head trauma is 50%
-GCS (the GCS is an objective assessment of the level of conciousness after trauma) / Indicates coma by GCS score is <8
-The Four Signs Of Basilar Skull Fracture :
.raccoon eyes (periorbital ecchymosis)
.battle's sign (postauricular ecchymosis)
.hemotympanum
.CSF (rhinorrhea/otorrhea)
-The Initial Radiographic Imaging In Trauma :
.head CT (if GCS <15)
.C-spine CT
.T/L spine AP and lateral
+Should the trauma head CT be with or without IV contrast ?
.without
+Normal ICP intracranial pressure (between 5 and 15mm H 2O) (worrisome more than 20mm H2O)
+Cushing`s reflex  physiologic response to increased ICP (hypertension, bradycardia, decreased RR)
+The general indications to monitor ICP after trauma :
.GCS <9
.altered level of consciousness or unconsciousness with multiple system trauma
.decreased consciousness with focal neurologic examination abnormality
+Non-operative techniques are used to decrease ICP :
.elevate head of bed (HOB) 30o (if spine cleared)
.diuresis-mannitol (osmotic diuretic), lasix, limit fluids
.intubation (PCO2 control)
.pharmacologic paralysis
.ventriculostomy (CSF drainage)
+Prolonged hyperventilation is so dengerous because it may result in severe vasoconstriction and ischemic brain necrosis (use
only for very brief periods)
+Acute treatment of seizures after head trauma is (Benzodiazepines – Ativan) / For seizure prophylaxis after severe head
trauma give phenytoin for 7 days
+The significance of hyponatremia (low sodium level) after head injury is SIADH (must be ruled out)

**Epidural Hematoma
-Is collection of blood between the skull and dura
-Causes :
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.usually occurs in association with a skull fracture as bone fragments lacerate meningeal arteries (Artery is associated with
epidural hematomas  Middle meningeal artery)
+M.C sign of an epidural hematoma (ipsilateral blown pupil)
+Classic CT findings with an epidural hematoma  lenticular-shaped hematoma
+The surgical treatment for an epidural hematoma is surgical evacuation
+The indications for surgery with an epidural hematoma  any symptomatic epidural hematoma; any epidural hematoma
>1cm

**Subdural Hematoma
-Is collection under the dura
-Causes :
.tearing of “bridging” veins that pass through the space between the cortical surface and the dural venous sinuses or injury to
the brain surface with resultant bleeding from cortical vessels
-Types Of Subdurals :
.acute (symptoms within 48hrs of injury)
.subacute (symptoms within 3 to 14 days)
.chronic (symptoms after 2wks or longer)
+The treatment of epidural and subdural hematomas  the mass effect (pressure) must be reduced. Craniotomy with clot
evacuation is usually required
+Classic CT findings with an epidural hematoma  curved, crescent-shaped hematoma

**Skull Fracture
-A fracture in which one or more fragments of the skull are forced below the inner table of the skull
-The indications for surgery :
.contaminated wound requiring cleaning and debridement
.severe deformity
.impingement on cortex
.open fracture
.CSF leak
-Treatment (for open skull fractures) :
.antibiotics
.seizure prophylaxis (phenytoin)
.surgical therapy

**Spinal Cord Trauma

-Types :
.comlete (no motor/sensory function below the level of injury)
.incomplete (residual function below the level of injury)
+Spinal Shock  loss of all reflexes and motor function, hypotension, bradycardia
+Sacral Sparing  sparing of sacral nerve level (anal sphincter intact, toe flexion, perianal sensation)
-Initial Studies/Intervention Are Important :
.ABCs
.maintain BP
.NG tube (prevents aspiration)
.foley
.high-dose steroids
.complete cervical X-rays and those of lower levels as indicated by examination
+The diagnostic studies (CT, MRI, pain films)
-The Indications For Emergent Surgery With Spinal Cord Injury :
.unstable vertebral fracture
.incomplete injury with extrinsic compression
.spinal epidural or subdural hematoma

**Tumors
-The Usual Location Of Primary Tumors In Adults/Children :
.2/3 of tumors are supratentorial
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.1/3 are infratentorial (in adults)

-The M.C Intracranial Tumors In Adults :
.metastatic neoplasms (gliomas #1 / meningiomas #2)
+Gliomas
.a general name for several tumors of neurological origin (astrocytes, ependymal, oligodendrocytes)
.M.C primary tumor in adults  Glioblastoma multiforme (GBM)
.occur in the white matter of the cerebral hemispheres
.the average age of onset is 5th decade
.the treatment is surgical debulking followed by radiation therapy
+Meningiomas
.the layer of orgination  arachnoid cap cells
.the risk factors  radiation exposure / neurofibromatosis 2 / female sex
.the peak age of occurrence is between 40 and 50yrs / F:M = 2:1
-The M.C Intracranial Tumors In Children :
.medulloblastomas (33%)
.astrocytomas (33%)
.ependymomas (10%)
+Cerebellar Astrocytomas
.the peak age of occurrence is between 5 and 9yrs
.usual location  usually in the cerebellar hemispheres; less frequently in the vermis
+Medulloblastoma
st
.the peak age of occurrence is 1 decade (3 to 7yrs)
.the cell of origin  external granular cells of cerebellum
.M.C location  cerebellar vermis in children; cerebellar hemispheres of adolescents and adults
.signs and symptoms  headache, vomiting and other signs of increased ICP; also usually truncal ataxia
+Pituitary Tumors
.the M.C pituitary tumor is (prolactinoma)
.the M.C presentation of a prolactinoma (bitemporal hemianopsia/lateral visual field blind)
.the blood prolactin levels with a prolactinoma (greater than 300 mg/L is diagnostic for prolactinoma) (>100 mg/L is abnormal)
.medical treatment of a prolactinoma is Bromocriptine
.surgical treatment of a prolactinoma is Transsphenoidal resection of the pituitary tumor
.treatment of a recurrent prolactinoma after surgical resection is radiation therapy
-The Effects Of Tumors On The Brain :
.increased ICP
.mass effect on cranial nerves
.invasion of brain parenchyma, disrupting nuclei/tracts
.seizure foci
.hemorrhage into/around tumor mass
-The Signs/Symptoms Of Brain Tumors :
.neurologic deficit (65%)
.headache (50%)
.seizures (25%)
.vomiting (in the morning)
+The standard diagnostic study is CT or MRI
-The Surgical Indications :
.establishing a tissue diagnosis
.relief of increased ICP
.relief of neurologic dysfunction caused by tissue compression
.attempt to cure in the setting of localized tumor

*Subarachnoid Hemorrhage (SAH)

-Is bleeding into the subarachnoid space—the area between the arachnoid membrane and the pia mater surrounding the brain.
this may occur spontaneously, usually from a ruptured cerebral aneurysm (berry aneurysm), or may result from head injury
-Causes :
.truama
.ruptured berry aneurysm (saccular outpouching of vessels in the circle of Willis, usually at bifurcations)
+The usual location of a berry aneurysm (anterior communicating artery 30%, followed by posterior communicating artery and
middle cerebral artery) / trt  surgical trt by placing a metal clip on the aneurysm – ballon occlusion or coil embolization
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+Medical disease increases the risk of berry aneurysm (polycycstic kidney disease and connective tissue disorders – Marfan`s
Syndrome)
+AVM  a congenital abnormality of the vasculature with connections between the arterial and venous circulations without
interposed capillary network / Occur in supratentorial / trt  radiosurgery (gamma knife) if less than 3cm
-Signs & Symptoms :
.the worst headache of my life “Classic symptom”
.meningismus (is documented by neck pain and positive Kernig`s and Brudzinski`s signs)
.vomiting, nausea, photophobia
-Complications Of SAH :
.brain edema leading to increased ICP
.rebleeding (M.C in the first 24 to 48hrs posthemorrhage)
.vasospasm (M.C.C of morbidity and mortality) (trt for vasospasm  Nimodipine – calcium channel blocker)

*Intracerebral Hemorrhage
-Bleeding into the brain parenchyma / Occur  in the basal ganglia; putamen is the structure most commonly affected
-Causes :
.HTN
.atherosclerotic disease (giving rise to Charcot-Bouchard aneurysms)
.coagulopathies
.AVMs
.amyloid angiopathy
.bleeding into a tumor
.trauma
+Diagnostic study  CT
-Surgical Indications :
.CN III palsy
.progrossive alteration of consciousness

**Nerve Injury
1.Radial nerve injury
.after humerus fracture, cause wrist drop
2.Ulnar nerve injury
.causes claw hand (atrophy of all small muscle of hand)
3.Median nerve injury
.carpal tunnel syndrome (paresthesia in lateral 3 digits + thenar atrophy)
4.Axillary nerve injury
.after anterior shoulder dislocation (causes loss of sensation over deltoid muscle)
5.Common peroneal nerve injury
.causes foot drop (after typical fracture – L4, L5 disk prolapse)
6.Long thoracic nerve
.causes winging of scapula

**Spine
*Lumbar Disc Herniation
-The M.C sites :
.L5-S1 (45%)  signs (decreased ankle jerk reflex, weakness of plantar flexor in foot, pain in back, midgluteal region to posterior
valf to lateral foot, ipsilateral radiculopathy on straight leg raise)
.L4-L5(40%)  signs (decreased biceps femoris reflex, weak extensors of foot)
+Middle-aged and older indiciduals who are affected
+The usual cause (loss of elasticity of the posterior longitudinal ligaments and annulus fibrosis as a result of aging)
+The usual presenting symptom is low back pain
+Indications for emergent surgery (cauda equina syndrome, progressive motor deficits)
+Cauda Equine Syndrome  herniated disc comressing multiple S1, S2, S3, S4 nerve roots, resulting in bowel/bladder
incontinence, “saddle anethsia” over buttocks/perineum, low back pain, sciatica-radicular or nerve root pain

*Cervical Disc Disease

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-The M.C sites :

.C6-C7 (70%)
.C5-C6 (20%)
.C7-T1 (10%)
+Signs C7  decreased triceps reflex, strength, weakness of forearm extension, pain from neck and middle finger
+Signs C6  decreased biceps and branchioradialis reflex, weakness in forearm flexion, pain in neck, radial forearm and thumb
+Signs C8  weakness in intinsic hand muscles, pain in fourth/fifth finger
+Trt  anterior or posterior discectomy with fusion PRN

*Spinal Epidural Abscess

-Signs & Symptoms :
.fever
.severe pain over affected area and with flexion/extension of spine
.weakness
.ultimately leading to paraplegia
.back furuncle
+MRI is test of choice
+LP test is contraindicated because of the risk of seedign CSF with bacteria, causing meningitis
-Causes :
.hematogenous spread from skin infections (M.C)
.distant abscesses/infections
.UTIs
.postoperative infections
.spine surgery
.epidural anesthsia
+M.C organism  Staphylococcus Aureus
+The commonly associated medical condition  Diabetes Mellitus
-The M.C sites :
.thoracic
.lumbar
.cervical
+Trt  surgical drainage and antibiotic coverage

**Pediatric Surgery
*Hydrocephalus
-Abnormal condition consisting of an increased volume of CSF along with distension of CSF spaces
-General Causes :
.increased production of CSF
.decreased absorption of CSF
.obstruction of normal flow of CSF
-The specific causes of hydrocephalus :
.congenital malformation, aqueductal stenosis, myelomeningocele
.tumors obstructing CSF flow, subarachnoid hemorrhage, meningitis
+The normal daily CSF production (approximately 500mL)
+The normal volume of CSF (approximately 159mL in the average adult)

*Miscellaneous
-The M.C bacteria causing postneurosurgery meningitis (Staphylocccus aureuss ‘skin flora’)
-The M.C location of a hypertensive intracerebral hemorrhage (Putamen)

+Cranial Nerves
.I (Olfactory nerve – smell)
.II (Optic nerve – vision)
.III (Oculomotor nerve – upper eye movement, medial eye movement, meiosis in pubic, upper eyelid)
(if injured – ptosis, mydriasis)
.IV (Trochlear nerve – downward, eye movement – down Gaze)
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.V (Trigeminal nerve – face sensation, masticatory muscle)

.VI (Abducens nerve, lateral eye movement) – M.C nerve affected by increased intracranial pressure
.VII (Facial nerve – facial expression, taste sensation, salivary gland ‘except parotid’, lacrimal gland)
.VIII (Vestibulocochlear nerve (hearing and balance)
.IX (Glossopharyngeal nerve – taste for posterior tongue, parotid gland)
.X (Vagus nerve)
.XI (Spinal Accessory nerve – supply sternocleidomastoid muscle + trapezius muscle)
.XII (Hypoglossal nerve – tongue movement)
By Dr.Mohammad Z. abu sheikha@

Urology
-Dysuria (painful urination)
-Frequency (urination more times than usual)
-Polyuria (urination in larger amounts than usul)
-Nocturia (awakening to urinate)
-Hematuria (RBCs in urine)
-Enuresis (involuntary urination while asleep)
-BPH (benign prostatic hyperplasia)
-Impotence (inability to achieve an erection)
-The Causes Of Hematuria :
.bladder cancer
.trauma
.UTI
.cystitis from chemotherapy or radiation
.stones
.kidney lesion
.BPH
-The M.C.C of severe gross hematuria without trauma or chemotherapy/radiation (Bladder cancer)
-The Differential Diagnosis For Kidney Tumor :
.renal cell carcinoma
.sarcoma
.adenoma
.angiomyolipoma
.hemangiopericytoma
.oncocytoma

**Renal Cell Carcinoma RCC

-M.C solid renal tumor (90%) (M > F) (40-60yrs of age)
-Symptoms :
.flank pain
.hematuria
.palpable mass
-Risk Factors :
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.male sex
.tobacco
.von Hippel-Lindau Syndrome
.polycystic kidney
+What gland is removed with a radical nephrectomy ?
.adrenal gland
-Diagnosis :
.IVP
.abdominal CT-scan with contrast
+The unique route of spread (tumor thrombus into IVC lumen)
+The sites of metastases (lung, liver, brain, bone)
+Syndrome of RCC and liver disease (Stauffer`s Syndrome)

**Bladder Cancer
 nd
-2 M.C urologic malignancy (M > F) (White Pts. are more commonly affected than are african american Pts.) (painless
hematuria)
-Is any of several types of cancer arising from the epithelial lining (i.e., the urothelium) of the urinary bladder. Rarely the
bladder is involved by non-epithelial cancers, such as lymphoma or sarcoma. It is a disease in which abnormal cells multiply
without control in the bladder
-Types :
.transitional cell carcinoma (TCC) - urothelial cell carcinoma (M.C histology)
.squamous cell carcinoma
.adenocarcinoma
.others (sarcoma, small cell carcinoma, secondary deposits from cancers elsewhere in the body, carcinoma in situ CIS)
-Signs & Symptoms :
.hematuria (M.C symptom) (painless gross hematuria)
.pain during urination, frequent urination, or feeling the need to urinate without being able to do so
.prostate infections, over-active bladder and cystitis
.Pts. with advanced disease refer pelvic or bony pain, lower-extremity edema, or flank pain
.rarely a palpable mass can be detected on physical examination
+Blood (redness) in the urine. This blood in the urine may be visible to the naked eye (gross/macroscopic hematuria) or
detectable only by microscope (microscopic hematuria)
+There are many other causes of hematuria, such as bladder or ureteric stones, infection, kidney disease, kidney cancers and
vascular malformations
-Risk Factors :
.schistosomiasis (for squamous cell carcinoma)
.chronic bladder irritation (bladder stone, chronic foleys)
.tobacco smoking is the main known contributor to urinary bladder cancer
.cyclophosphamide (side effect – Hemorrhagic cystitis)
.exposure in the workplace to carcinogens such as benzidine. 2-Naphthylamine, which is found in cigarette smoke
.bus drivers, rubber workers, motor mechanics, leather (including shoe) workers, blacksmiths, machine setters, petroleum
workers and mechanics
.hairdressers are thought to be at risk as well because of their frequent exposure to permanent hair dyes
+It has been suggested that mutations at HRAS, KRAS2, RB1, and FGFR3 may be associated in some cases
-Diagnosis :
.biopsy obtained during cystoscopy (the gold standard for diagnosing bladder cancer)
-Staging :
.T1 (mucosa) / treated by – transurethral resection (TUR) (if the cancer is in an early stage (superficial) and growing slowly (low
grade), it may be removed using cystoscopy)
.T2 (muscle) / treated by – radical cystectomy
.T3 (serosa) / treated by – radical cystectomy
.T4 (adjacent organ) / treated by – radical cystectomy
+Painless gross hematuria is bladder cancer, untile proven otherwise

**Testicular Cancer
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-Is cancer that develops in the testicles, a part of the male reproductive system / M.C solid tumor of young adult men (20-40yrs)
+Not all lumps on the testicles are tumors, and not all tumors are malignant (cancerous)
-Tumor Markers :
.β-hCG
.alpha-fetoprotein (AFP)
.LDH
-Types :
.seminoma (M.C) (radiosensitive)
.choriocarcinoma (radioresistant)
.embryonal carcinoma (radioresistant)
.teratoma (radioresistant)
-Signs & Symptoms :
.lump or swelling in the testes (painless testicular mass)
.harp pain or a dull ache in the lower abdomen or scrotum
.feeling often described as "heaviness" in the scrotum
.breast enlargement (gynecomastia) from hormonal effects of β-hCG
.low back pain (lumbago) due to the cancer spreading to the lymph nodes along the back
+It is not very common for testicular cancer to spread to other organs, apart from the lungs. If it has, however, the following
symptoms may be present :
.shortness of breath (dyspnea), cough or coughing up blood (hemoptysis) from metastatic spread to the lungs
.lump in the neck due to metastases to the lymph nodes
+Other conditions may also have symptoms similar to testicular cancer :
.Epididymitis or epididymo orchitis
.Hematocele
.Varicocele
-Diagnosis :
.scrotal ultrasound
+Metastasis to para-aortic lymph node
-Treatment :
.radical inguinal orchiectomy
+Biopsy (FNA) is contraindicated

**Testicular Torsion
-Occurs when the spermatic cord (from which the testicle is suspended) twists, cutting off the testicle's blood supply, a
condition called ischemia / It is most common just after birth and during puberty (10-20yrs)
-Signs & Symptoms :
.sudden, severe, testicular pain (in groin & lower abdomen)
.tenderness
.nausea and vomiting
.the testis may be higher than its normal position
.mild pyrexia and redness of overlying area may be found
.some of the symptoms are similar to epididymitis though epididymitis may be characterized by discoloration and swelling of
the testis, often with fever
.absent or decreased cremasteric reflex
-Causes :
.M.C underlying cause is a congenital malformation known as a "processus vaginalis or bell-clapper deformity" wherein the
testis is inadequately affixed to the scrotum allowing it to move freely on its axis and susceptible to induced twisting of the cord
and its vessels (tunica vaginalis)
-Diagnosis :
.doppler ultrasound
.Prehn's sign (to help determine whether the presenting testicular pain is caused by acute epididymitis or from testicular
torsion)
-Treatment :
.Orchiopexy (or orchidopexy) (is a surgery to move an undescended (cryptorchid) testicle into the scrotum and permanently fix
it there. Orchiopexy typically also describes the surgery used to resolve testicular torsion)
+Epididymo-orchitis (Is differential diagnosis)
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+Testicular Torsion +Epididymo-Orchitis

.sudden pain .gradual
.young (10-20yrs) .old age (sexually active)
.pain NOT relieved by elevation .pain relieved by elevation
.NO cremasteric reflex .present cremasteric reflex
.testis horizontal and high in scrotum .dysuria + UTI + fever
.treated by (surgery) .treated by (antibiotics)

**Prostate Cancer
-Is the development of cancer in the prostate, a gland in the male reproductive system.Most prostate cancers are slow growing;
however, some grow relatively quickly / Most common GU cancer - adenocarcinoma
+The cancer cells may spread from the prostate to other parts of the body, particularly the bones and lymph nodes
-Signs & Symptoms :
.urination
.nocturia (increased urination at night)
.difficulty starting and maintaining a steady stream of urine
.hematuria (blood in the urine)
.dysuria (painful urination)
.problems with sexual function and performance, such as difficulty achieving erection or painful ejaculation
.prostate cancer in the spine can also compress the spinal cord, causing tingling, leg weakness and urinary and fecal
incontinence
+Advanced prostate cancer can spread to other parts of the body, possibly causing additional symptoms. The most common
symptom is bone pain, often in the vertebrae (bones of the spine), pelvis, or ribs. Spread of cancer into other bones such as the
femur is usually to the proximal or nearby part of the bone

-Causes :
.obesity
.elevated blood levels of testosterone
.vasectomy
.starting sexual activity early in life substantially increases the risk of prostate cancer
.age and family history
.genetic (Mutations in BRCA1 and BRCA2, important risk factors for ovarian cancer and breast cancer in women, have also been
implicated in prostate cancer / Hereditary Prostate cancer gene 1 (HPC1), the androgen receptor, and the vitamin D receptor)
.dietary (Red meat consumption / Lower blood levels of vitamin D may increase the risk of developing prostate cancer / Folic
acid supplements have no effect on the risk of developing prostate cancer)
.medication exposure (Use of the cholesterol-lowering drugs known as the statins decrease prostate cancer risk)
.infectious disease (Infection or inflammation of the prostate (prostatitis) may increase the chance for prostate cancer /
infection with the sexually transmitted infections chlamydia, gonorrhea, or syphilis seems to increase risk /
+Prostate cancer is very uncommon in men younger than 45, but becomes more common with advancing age. The average age
at the time of diagnosis is 70
+Found that prostate basal cells were the most common site of origin for prostate cancers
-The Steps In Early Detection And Surveillance :
.prostate-specific antigen (PSA) – most sensitive and specific marker (all men should get a PSA-level check >50yrs old / >40yrs
old if first-degree family history or black patient)
.acid phosphatase (often elevated in metastatic prostate cancer; used mostly to detect recurrences)
.digital rectal examination DRE
-Daignosis :
.gleason Score
.transrectal biopsy
-Indications For Transrectal Biopsy With Normal Rectal Examination :
.PSA >10
.abnormal transrectal ultrasound
+In which area of the prostate does prostate cancer arise ?
.periphery

**Benign Prostatic Hyperplasia BPH

-Disease of elderly men (60-65yrs); prostate gradually enlarges / BPH occur in the periphery of the gland
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+The size of a normal prostate (between 20 and 25gm)

+M.C.C of acute urinary retention in males (BPH)
-Signs & Symptoms :
.poor stream
.intermittency
.hesitancy
.post void dribbling
.urinary outflow obstruction
-Treatment :
.alpha-blocker (tamsulosin) / 5-alpha-reductase inhibitor
.surgical (TURP or open surgery)
+Indications for surgery :
.recurrent acute urinary retension
.failure of medical treatment
.renal failure
.recurrent urinary tract infection
.recurrent hematuria
.bladder stones
+In which area of the prostate does BPH arise ?
.periurethral
-The differential diagnosis :
.prostate cancer
.neurogenic bladder
.acute prostatitis
.urethral stricture
.stone
.UTI

**Calculus Disease (Kidney stone)

-The Types Of Stones :
.calcium oxalate/calcium PO4 (seen with IBD, bowel hypass)
.struvite (MgAmPH) magnesium, ammonium, phosphate – infection stones; seen in UTI (associated with UTI)
.uric acid – stones are radiolucent (are not seen in on AXR)
.cystine – genetic predisposition
-Symptoms :
.loin - flank pain
.hematuria
.infection (pyelonephritis) (M.C.C is E.coli)
-Risk Fctors :
.poor fluid intake
.IBD
.hypercalcemia
.renal tubular
.acidosis
.small bowel bypass
-Diagnosis :
.CT-scan without contrast (BEST)
+2
.kidney ureters bladder X-ray (KUB) (radiopaque - Ca oxalate) (radiolucent - uric acid)
-Treatment :
.if <4mm (Pass spontaneously)
.if >4mm (Extracorporeal shock wave lithotripsy – ESWL or ureteroscopy)
+The Three Common Sites Of Obstruction :
.ureteropelvic junction (UPJ)
.ureterovesicular junction (UVJ)
.intersection of the ureter and the iliac vessels
+The Common Organisms (UTI) :
.E.coli (90%)
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.proteus
.klebsiella, pseudomonas
+The M.C solid tumor of childhood (Wilms` tumor)
+The M.C obstructive urethral lesion in infants (posterior urethral valves)

**Acute Flank Pain (Ureteric or Renal Colic)

-The commonest urologic emergency / One of the commonest causes of the “Acute Abdomen” / Sudden onset of severe pain in
the flank / Most often due to the passage of a stone formed in the kidney, down through the ureter
-The Pain Is Characteristically :
.very sudden onset
.colicky in nature
.radiates to the groin as the stone passes into the lower ureter.
.may change in location, from the flank to the groin, (the location of the pain does not provide a good indication of the position
of the stone)
.the patient cannot get comfortable, and may roll around in agony
.associated with nausea / Vomiting
-Differential Diagnoses :
.leaking abdominal aortic aneurysms
.pneumonia
.myocardial infarction
.ovarian pathology (e.g., twisted ovarian cyst)
.acute appendicitis
.testicular torsion
.inflammatory bowel disease (Crohn’s, ulcerative colitis)
.diverticulitis
.ectopic pregnancy
.burst peptic ulcer
.bowel obstruction

**Urinary Retention
-Also known as ischuria, is an inability to completely empty the bladder. It is a common complication of benign prostatic
hyperplasia (BPH)
-Signs & Symptoms :
.poor urinary stream with intermittent flow
.straining, a sense of incomplete voiding
.hesitancy (a delay between trying to urinate and the flow actually beginning)
.incontinence
.nocturia (need to urinate at night), and high frequency
.anuria, is a medical emergency, as the bladder can stretch to an enormous size, and possibly tear if not dealt with quickly (if
the bladder distends enough, it becomes painful. In such a case, there may be suprapubic constant, dull, pain)
+The increase in bladder pressure can also prevent urine from entering the ureters or even cause urine to pass back up the
ureters and get into the kidneys, causing hydronephrosis, and possibly pyonephrosis, kidney failure, and sepsis
-Causes :
+In the bladder
.detrusor sphincter dyssynergia
.neurogenic bladder (commonly pelvic splanchic nerve damage, cauda equina syndrome, descending cortical fibers lesion,
pontine micturation or storage center lesions, demyelinating diseases or Parkinson's disease)
.iatrogenic (caused by medical treatment/procedure) scarring of the bladder neck (commonly from removal of indwelling
catheters or cystoscopy operations)
.damage to the bladder
+In the prostate
.benign prostatic hyperplasia (BPH)
.prostate cancer and other pelvic malignancies
.prostatitis
+Men
.prostatic enlargement due to BPH
.carcinoma of the prostate
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.urethral stricture
.prostatic abscess
+Women
.pelvic prolapse (cystocoele, rectocoele, uterine)
.urethral stricture
.urethral diverticulum
.post surgery for ‘stress’ incontinence
.pelvic masses (e.g., ovarian masses)
+Both Sex
.haematuria leading to clot retention
.drugs
.pain
.sacral nerve compression or damage (cauda equina compression)
.radical pelvic surgery
.pelvic fracture rupturing the urethra
.neurotropic viruses involving the sensory dorsal root ganglia of S2–S4 (herpes simplex or zoster)
.multiple sclerosis
.transverse myelitis
.diabetic cystopathy
.damage to dorsal columns of spinal cord causing
-Complications :
.bladder damage and chronic kidney failure
.bladder stones
.atrophy of the detrusor muscle (atonic bladder is an extreme form)
.hydronephrosis (congestion of the kidneys)
.hypertrophy of the detrusor muscle (the muscle that squeezes the bladder to empty it during urination)
.diverticula (formation of pouches) in the bladder wall (which can lead to stones and infection)

-Treatment :
.urinary catheterization
.BPH may respond to alpha blocker and 5-alpha-reductase inhibitor therapy, or surgically with prostatectomy or transurethral
resection of the prostate (TURP)
.BPH are treated with medications. These include tamsulosin to relax smooth muscle in the bladder neck, or finasteride or
dutasteride to decrease prostate enlargement
+Acute urinary retention (AUR) (painfull/nor.renal function/nor. Bladder capacity/rapid/foleys)
+Chronic urinary retention (CUR) (painless/renal failure/large capacity/nor rapid/postobstructive dialysis)

**Varicocele
-Is an abnormal enlargement of the pampiniform venous plexus in the scrotum (dilated testicular vein - pampiniform plexus)
+The pampiniform plexus is a network of many small veins found in the human male spermatic cord. It is formed by the union
of multiple spermatic veins from the back of the testis and tributaries from the epididymis
+Varicocele is M.C.C of male infertility / Most Pt. who has varicocele are fertile
-Signs & Symptoms :
.visible or palpable (able to be felt) enlarged vein
.dragging-like or aching pain within scrotum
.feeling of heaviness in the testicle(s)
.atrophy (shrinking) of the testicle(s)
.alteration of testosterone levels
.benign prostatic hyperplasia (BPH) and related urinary problems
-Causes :
.idiopathic
+A majority of idiopathic varicoceles occur on the left side, because the left testicular vein travels superiorly and connects to the
left renal vein (at a 90-degree angle), while the right testicular vein drains directly into the inferior vena cava. Isolated right
sided varicoceles are rare (Lt. > Rt.)
.pelvic or abdominal malignancy
."Nutcracker syndrome" (non-malignant condition in which the superior mesenteric artery compresses the left renal vein,
causing increased pressures there to be transmitted retrograde into the left pampiniform plexus)
.lifestyle factors such as (activity type, bowel health, testicular temperature)
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-Complications :
.affect spermatogenesis
.testicular atrophy
-Indication for surgery :
.pain
.infertility
.testicular atrophy
+Seminal fluid analysis (SFA)
.count (15000.000)
.motility (>40-50%)
.morphology (4%) ?
.pH (7.2-7.8) *alkaline
.liquefaction (<30mins)
.volume (2-5ml)
By Dr.Mohammad Z. abu sheikha@

+Is DVT more common in the Rt. or Lt. iliac vein ?

.Lt. is more common
+Test is used to evaluate for DVT is (Duplex Ultrasonography)
+Associated lab findings (ABG-decreased PO2-PCO2 from hyperventilation)
+Which organisms are commonly involved (Aspiration Pneumonia) ?
.community acquired (gram positive mixed)
.hospital/ICU (gram negative rods)
+Hemorrhage occurring 7-10 days after surgery is called Secondary hemorrhage
+Manifestations of internal hemorrhage :
.Progressive pallor
.Progressive hypotension
.Rapidrespiration
.Cold extremities
+The most common complication post abdominal Surgery is Atelectasis
+Indications for splenectomy :
.congenital spherocytosis
.splenic abscess
.splenic hydatid cyst
.traumatic massive laceration
.massive tear of the spleen
.traumatic rupture
.idiopathic thrombocytopenic purpura
+Grossly enlarged spleen occurs in Chronic myeloid leukemia
+The most common organ injured in blunt abdominal trauma is Spleen
+Causes hepatocellular carcinoma :
.hepatitis B
.hepatitis C
.alcoholic cirrhosis
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.fatty liver
+The length of the esophagus in adults is 25cm
+Carcinoma of the esophagus :
.it occurs usually in elderly ages
.progressive dysphagia is a common symptom
.common sites are in the middle and lower third
.squamous cell carcinoma is the commonest type
.it occurs in males more than in females
.it is squamous cell carcinoma except its lower few centimeters where it is adenocarcinoma
.dysphagia is an important leading symptom
.esophagoscopy is usually diagnostic
+The best radiological examination to diagnose perforated peptic ulcer is Chest X-ray standing
+The most common complication of Meckel's diverticulum is obstriction
+The most common presentation of Meckel's diverticulum in children is Frank rectal bleeding
+Pelvic abscess developed after appendectomy for a perforated appendix (Bacteroides)
+The most common site of carcinoma of the colon is (Recto sigmoid)
+The most useful screening for colon cancer is Test for occult blood in stool
+Concerning carcinoma of the colon :
.although most patients are above 60 years of age, younger ages are not immune
.usually it is either well or moderately differentiated adenocarcinoma
.left colon is affected more than Right
.recent changes of bowel habit and rectal bleeding are early manifestations
.barium enema or colonoscopy must be done in all cases
+Duke's classification used in Colorectal carcinoma

By Dr.Mohammad Z. abu sheikha@

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