Introduction To Surgery Short Notes

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1.1. History of surgery (simulated: approaching a surgical patient (history taking & P/E)
1.2. Metabolic response to injury
1.3. Shock,
1.4. Electrolytes and fluid management of a surgical patient
1.5. Wound healing and principles of wound care (case related to wound)
1.6. Ulcer
1.7. Burn(case of burn);Depth/%TBSA; calculate rate,quantity of fluid be given; techniques for treating burn.
1.8. Surgical infections and use of antibiotics in surgery
1.9. Trauma (case related to trauma); injury scoring ;repair of laceration (suturing)
1.10. Perioperative management (case related to perioperative mgt); preoperative evaluation.
1.11.Simulated practice: infection control & patient safety (hand washing, use of personal
protective equipment, safe handling of sharps and other equipment, medical waste
management,
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1.1. History of surgery (simulated: approaching a surgical patient (history taking & P/E)

1.2 METABOLIC RESPONSE TO INJURY

1.2 Metabolic response to injury
oBasic concepts
• Homeostasis is the foundation of normal physiology
• ‘Stress-free’ perioperative care helps to preserve homeostasis following
elective surgery
• Resuscitation, surgical intervention and critical care can return the severely
injured patient to a situation in which homeostasis becomes possible once
again.

Neuroendocrine response to injury/critical illness

• The neuroendocrine response to severe injury/critical illness is biphasic:
1. Acute phase: characterised by an actively secreting pituitary and elevated
counter-regulatory hormones (cortisol, glucagon, adrenaline). Changes are
thought to be beneficial for shortterm survival.
2. Chronic phase: associated with hypothalamic suppression and low serum levels of the
respective target organ hormones. Changes contribute to chronic wasting.

Systemic inflammatory response syndrome following major injury

• Is driven initially by proinflammatory cytokines (e.g. IL-1, IL-6 and TNFα)
• Is followed rapidly by increased plasma levels of cytokine antagonists and
soluble receptors (e.g. IL-1Ra, TNF-sR)
• If prolonged or excessive may evolve into a counterinflammatory response
syndrome

Physiological response to injury

o The natural response to injury includes:
1.Immobility/rest
2.Anorexia
3.Catabolism
o The changes are designed to aid survival of moderate injury in the absence of
medical intervention.
o Injuries or infections induce unique neuroendocrine and immunologic responses

that differentiate injury metabolism from that of unstressed fasting.

Purpose of neuroendocrine changes following injury

o The constellation of neuroendocrine changes following injury acts to:
1. Provide essential substrates for survival
2. Postpone anabolism
3. Optimise host defence
o These changes may be helpful in the short term, but may be harmful in the long
term, especially to the severely injured patient who would otherwise not have
survived without medical intervention.

o The magnitude of metabolic expenditure appears to be directly proportional to

the severity of insult, with thermal injuries and severe infections having the
highest energy demands
o The increase in energy expenditure is mediated in part by sympathetic
activation and catecholamine release, which has been replicated by the
administration of catecholamines to healthy human subjects.

Changes in body composition following major surgery/critical illness

o Catabolism leads to a decrease in fat mass and skeletal muscle mass
o Body weight may paradoxically increase because of expansion of extracellular
fluid space

Fig1: Influence of injury severity on resting metabolism (resting energy expenditure, REE). The shaded area indicates
normal REE (schwartzs 11th edition)
 Lipid Metabolism after Injury

 Ketogenesis
 Carbohydrate Metabolism
 Protein and Amino Acid Metabolism

Factors that exacerbate the metabolic response to surgical injury

1.3 SHOCK

1.3 SHOCK
1. Pathophysiology of shock
2. Severity of shock; stage of shock
3. Clinical features of shock
4. Forms of shock / classification of shock

1.3 SHOCK
o Shock is defined as a failure to meet the metabolic demands of cells and tissues
and the consequences that ensue.
o Shock consists of inadequate tissue perfusion marked by decreased delivery of

required metabolic substrates & inadequate removal of cellular waste products.
o This imbalance between cellular supply and demand leads to neuroendocrine

and inflammatory responses, the magnitude of which is usually proportional to
the degree and duration of shock.

1.3 SHOCK
PATHOPHYSIOLOGY OF SHOCK
o Physiologic responses to shock are based on a series of afferent (sensing) signals
and efferent responses that include neuroendocrine, metabolic, and
immune/inflammatory signaling
o Decreased tissue perfusion can result directly from hemorrhage/hypovolemia,
cardiac failure, or neurologic injury.
o Decreased tissue perfusion and cellular injury can then result in immune &
inflammatory responses.
o Alternatively, elaboration of microbial products during infection or release of
endogenous cellular products from tissue injury can result in cellular activation to
subsequently influence tissue perfusion and the development of shock.
1.3 SHOCK
Fig 2: Pathways leading to decreased tissue perfusion and shock.

1.3 SHOCK
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2: Pathways leading to decreased tissue perfusion and
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1.3 SHOCK
SEVERITY OF SHOCK
1.Compensated shock
 The body’s cardiovascular and endocrine compensatory responses reduce flow to non-
essential organs to preserve preload.
 In compensated shock, there is adequate compensation to maintain central blood volume
and preserve flow to the kidneys, lungs and brain.
 Apart from a tachycardia and cool peripheries (vasoconstriction, circulating
catecholamines), there may be no other clinical signs of hypovolaemia.
2. Decompensation
 Progressive renal, respiratory and cardiovascular decompensation.
 In general, loss of around 15% of the circulating blood volume is within normal
compensatory mechanisms.
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1.3 SHOCK
3. Mild shock
 Initially there is tachycardia, tachypnoea, a mild reduction in urine output and
 The patient may exhibit mild anxiety.
 BP is maintained although there is a decrease in pulse pressure.
 The peripheries are cool and sweaty with prolonged capillary refill times (except in
septic distributive shock).
4. Moderate shock
 As shock progresses, renal compensatory mechanisms fail, renal perfusion falls and
 Urine output dips below 0.5 mL/kg per hour.
 There is further tachycardia, and now the blood pressure starts to fall.
 Patients become drowsy and mildly confused.
1.3 SHOCK
5. Severe shock
 In severe shock, there is profound tachycardia and hypotension.
 Urine output falls to zero and
 Patients are unconscious with laboured respiration.

1.3 SHOCK

1.3 SHOCK
CLINICAL FEATURES OF SHOCK

oIn early stage —tachycardia, sweating, cold periphery, hypotension, restlessness,
air hunger, tachypnoea, oliguria, collapsed veins.
oIn late stage —cyanosis, anuria, jaundice, drowsiness

1.3 SHOCK
FORMS OF SHOCK / CLASSIFICATION OF SHOCK

1.3.1 Hypovolemic/Hemorrhagic
1.3.2 Traumatic Shock
1.3.3 Septic Shock (Vasodilatory Shock) /Vasogenic
1.3.4 Cardiogenic Shock
1.3.5 Obstructive Shock
1.3.6 Neurogenic Shock
o
o Hypovolaemic shock is due to a reduced circulating volume.
o It is the most common form of shock
o It also the most common cause of shock in the surgical or trauma patient is loss of circulating
volume from hemorrhage.
 Cause Hypovolemic/Hemorrhagic
1. Haemorrhagic or causes
Acute blood loss
2. Nonhaemorrhagic
Poor fluid intake (dehydration),
Excessive fluid loss due to vomiting, diarrhoea, urinary loss (e.g. Diabetes), evaporation, or
‘thirdspacing’ where fluid is lost into the gastrointestinal tract and interstitial spaces, as for example in
bowel obstruction or pancreatitis.
1.3.1 Hypovolemic/Hemorrhagic …
Table: Classification of hemorrhage

 Diagnosis of Hypovolemic/Hemorrhagic
o The clinical signs of shock may be evidenced by:
1. Agitation,
2. Cool clammy extremities,
3. Tachycardia,
4. Weak or absent peripheral pulses, and
5. Hypotension.
o Such apparent clinical shock results from at least 25% to 30% loss of
the blood volume.

o Loss of up to 15% of the circulating volume = little in terms of obvious symptoms,

o Loss of up to 30% of the circulating volume (1.5 L) = mild tachycardia,
tachypnea, and anxiety.
o Loss > 30% of the blood volume = Hypotension, marked tachycardia (i.e., PR
110–120 bpm), and confusion may not be evident.
o Loss of 40% of circulating volume (2 L) is immediately life threatening and
generally requires operative control of bleeding.

o Recent data in trauma patients suggest that a systolic blood pressure (SBP) of less
than 110 mmHg is a clinically relevant definition of hypotension and
hypoperfusion based on an increasing rate of mortality below this pressure.
o Serum lactate and base deficit are measurements that are helpful to both
estimate and monitor the extent of bleeding and shock.
oThe amount of lactate that is produced by anaerobic respiration is an indirect
marker of tissue hypo perfusion, cellular O2 debt, and the severity of
hemorrhagic shock.

Treatment of hypovolemic/hemorrhagic
oThe management strategy known as damage control resuscitation
oThe appropriate priorities in patients are
1. Secure the airway,
2. Control the source of blood loss, and
3. Intravenous (IV) volume resuscitation.
• Initial resuscitation is limited to keep SBP around 80 to 90 mmhg. This prevents
renewed bleeding from recently clotted vessels.
• Resuscitation and intravascular volume resuscitation are accomplished with
blood products and limited crystalloids.
• Too little volume persistent severe hypotension & hypoperfusion is dangerous,
• Too vigorous of a volume resuscitation may be just as deleterious.
oControl of hemorrhage is achieved in the

• operating room, and
• efforts to warm patients and
• to prevent coagulopathy using multiple blood products and pharmacologic agents
oThe benefit of hypertonic saline solutions may be immunomodulatory.
Pharmacologic effects resulting in:
1. decreased reperfusion-mediated injury with decreased O2 radical formation,
2. less impairment of immune function compared to standard crystalloid solution, and
3. less brain swelling in the multi-injured patient.
oPrevention of hypothermia, acidemia, and coagulopathy is essential in the
management of patients in hemorrhagic shock by ongoing fluid requirements
despite adequate control of hemorrhage,
oCurrent recommendations in stable ICU patients aim for a target hemoglobin of 7

to 9 g/dL
oThe current standard in severely injured patients is termed damage control
resuscitation and consists of transfusion with
1. Red blod cells,
2. Fresh frozen plasma (FFP), and
3. Platelet units given in equal number.
oHypothermia in bleeding trauma patients is an independent risk factor for
bleeding and death. This likely is secondary to impaired platelet function and
impairments in the coagulation cascade.

RATE OF FLUID REPLETION
Initial – At least 1 to 2 liters of isotonic crystalloid are initially given as rapidly as possible in an
attempt to restore tissue perfusion.
Early correction of the volume deficit is essential in hypovolemic shock to prevent the decline in
tissue perfusion from becoming irreversible. Irreversible shock is associated with loss of vascular
tone, a drop in systemic vascular resistance, pooling of blood in the capillaries and tissues, and an
impaired response to vasoactive medications
Maintenance – Fluid repletion should continue at the initial rapid rate as long as the systemic
blood pressure remains low in the setting of hypovolemia.
• Clinical signs, including blood pressure, urine output, mental status, and peripheral perfusion,
are often adequate to guide resuscitation.
• The development of peripheral edema is often due to acute dilutional hypoalbuminemia and
should not be used as a marker for adequate fluid resuscitation or fluid overload
o CHOICE OF REPLACEMENT FLUID — For patients with hypovolemic shock, the
three major classes of replacement fluids are:
1. Crystalloid solutions – includes saline solutions, buffered (chloride-restrictive)

solutions (eg, Ringer's lactate, Hartmann's solution, Plasma-lyte, bicarbonate
buffered 0.45% saline)
2. Colloid-containing solutions – includes albumin solutions, hyperoncotic starch,
dextran, gelatin
3. Blood products or substitutes – includes packed red cells, blood substitutes

oThe systemic response after trauma, combining the effects of soft tissue injury,
long bone fractures, and blood loss, is clearly a different physiologic insult than
simple hemorrhagic shock.
oMultiple organ failure, including ards, develops relatively often in the blunt
trauma patient, but rarely after pure hemorrhagic shock (such as a gi bleed).
oThe hypoperfusion deficit in traumatic shock is magnified by the

proinflammatory activation that occurs following the induction of shock.
oExamples of traumatic shock include:
o Small-volume hemorrhage accompanied by soft tissue injury (femur fracture, crush injury) or
o Any combination of hypovolemic, neurogenic, cardiogenic, and obstructive shock that
precipitates
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oIn laboratory models of traumatic shock, the addition of a soft tissue or long
bone injury to hemorrhage produces lethality with significantly less blood loss
when the animals are stressed by hemorrhage.
oTreatment of traumatic shock is focused on correction of the individual elements

to diminish the cascade of pro-inflammatory activation and includes
Prompt control of hemorrhage,
Adequate volume resuscitation to correct O2 debt,
Débridement of nonviable tissue,
Stabilization of bony injuries, and
Appropriate treatment of soft tissue injuries.
1.3.3 Septic shock: Vasodilatory /Vasogenic Shock
oVasodilatory shock is characterized by peripheral vasodilation with resultant
hypotension and resistance to treatment with vasopressors.
oHypotension results from failure of the vascular smooth muscle to constrict
appropriately.
oIt is the result of dysfunction of the endothelium and vasculature secondary to
circulating inflammatory mediators and cells or as a response to prolonged and
severe hypoperfusion.
oDespite the hypotension, plasma catecholamine levels are elevated, and the
renin-angiotensin system is activated .
oThe most frequently encountered form of vasodilatory shock is septic shock.
oSeptic shock is a by-product of the body’s response to disruption of the host-
microbe
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equilibrium, resulting in invasive or severe localized infection.
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oOther causes of vasodilatory shock include:
 Hypoxic lactic acidosis,
 Carbon monoxide poisoning,
 Decompensated & Irreversible hemorrhagic shock,
 Terminal cardiogenic shock, and
 Postcardiotomy shock.

o When this response is overly exuberant or becomes systemic rather than
localized, manifestations of sepsis may be evident.
o These findings include:
o Enhanced cardiac output, peripheral vasodilation, fever, leukocytosis, hyperglycemia, and
tachycardia.
oIn septic shock, the vasodilatory effects are due, in part, to the upregulation of
the inducible isoform of nitric oxide synthase (iNOS or NOS 2) in the vessel wall.
oiNOS produces large quantities of nitric oxide for sustained periods of time. This
potent vasodilator suppresses vascular tone and renders the vasculature resistant
to the effects of vasoconstricting agents.
Diagnosis.
oCriteria for the diagnosis of sepsis in the hospitalized adult include manifestations
of the host response to infection in addition to identification of an offending
organism.
oMagnitude of infection (systemic inflammatory reaction) is quantified as:
1.Sepsis: patients have evidence of an infection, as well as systemic signs of inflammation
(e.G., Fever, leukocytosis, and tachycardia).
2. Severe sepsis: which shows hypo-perfusion with sign of organ dysfunction (lactic acidosis,
dysfunction of liver, kidney, lungs).
3. Septic shock: with more significant evidence of tissue hypo-perfusion and systemic
hypotension (BP < 90 mmhg in spite adequate fluid therapy), severe organ dysfunction (acute
lung, kidney, liver injury), maldistribution of blood flow, shunting in microcirculation.
oThe clinical manifestations of septic shock will usually become evident and
prompt the initiation of treatment before bacteriologic confirmation of an
organism or the source of an organism is identified.
oIn addition to fever, tachycardia, and tachypnea, signs of hypoperfusion such as
confusion, malaise, oliguria, or hypotension may be present.
oThese should prompt an aggressive search for infection, including a thorough
physical examination, inspection of all wounds, evaluation of intravascular
catheters or other foreign bodies, obtaining appropriate cultures, and adjunctive
imaging studies, as needed.

TREATMENT
oAssessment of the adequacy of their airway and ventilation.
oSeverely obtunded patients and patients whose work of breathing is excessive
require intubation and ventilation to prevent respiratory collapse.
oBecause vasodilation and decrease in total peripheral resistance may produce
hypotension, fluid resuscitation and restoration of circulatory volume with
balanced salt solutions is essential.
oThis resuscitation should be at least 30 mL/kg within the first 4 to6 hours.
oStarch-based colloid solutions should be avoided, as recent evidence suggests
that these fluids may be deleterious in the setting of sepsis.
oEmpiric antibiotics must be chosen carefully
TREATMENT

TREATMENT
o Initial investigations — Quickly obtaining is preferable (within 45 minutes of presentation) but
should not delay the administration of fluids and antibiotics:
CBC with differential, chemistries, liver function tests, and coagulation studies including D-
dimer level. Results: indicate the severity of sepsis, and provide baseline.
Serum lactate – An elevated serum lactate (eg, >2 mmol/L) may indicate the severity of
sepsis and is used to follow the therapeutic response .
Arterial blood gas (ABG) analysis – It may reveal acidosis, hypoxemia, or hypercapnia.
Peripheral blood cultures (aerobic & anaerobic cultures from at least 2 different sites), U/A,
& microbiologic cultures (eg, sputum, urine, intravascular catheter, wound or surgical site,
body fluids) from readily accessible sites – For patients with a vascular catheter, blood
should be obtained both from the catheter and from peripheral sites.
Imaging targeted at the suspected site of infection (eg, CXR, CT of chest & abdomen)
Procalcitonin – Its diagnostic value and value in deescalating antibiotic therapy are
controversial and poorly supported by evidence.
TREATMENT
 IMMEDIATE EVALUATION AND MANAGEMENT —
Securing the airway (if indicated) and correcting hypoxemia, and
Establishing venous access for the early administration of fluids and
Antibiotics are priorities in the management of patients with sepsis and septic
shock
INITIAL RESUSCITATIVE THERAPY — the cornerstone of initial resuscitation;
Aggressive administration of intravenous fluids (IVF), usually crystalloids
(balanced crystalloids or normal saline) given at 30 ml/kg (actual body
weight) within the first three hours following presentation.
Empiric antibiotic therapy is targeted at the suspected organism(s) and site(s)
of infection and preferably administered within the first hour.


oCardiogenic shock is defined clinically as circulatory pump failure leading to

diminished forward flow and subsequent tissue hypoxia, in the setting of
adequate intravascular volume.
oHemodynamic criteria include:
Sustained hypotension (i.e., SBP <90 mmHg for at least 30 minutes),
Reduced cardiac index (<2.2 L/min per square meter), and
Elevated pulmonary artery wedge pressure (>15 mmHg).


oMortality rates for cardiogenic shock are 50% to 80%.

oAcute, extensive MI is the most common cause of cardiogenic shock;
oCardiogenic shock complicates 5% to 10% of acute MIs.
oCardiogenic shock is the most common cause of death in patients hospitalized with
acute MI.
o75% of patients who have cardiogenic shock complicating acute MIs develop
signs of cardiogenic shock within 24 hrs. after onset of infarction (average 7 hrs.).

oRapid assessment,
oAdequate resuscitation, and
oReversal of the MIs are essential in optimizing outcome in patients with acute MI.
oPrevention of infarct extension is a critical component.
oLarge segments of nonfunctional but viable myocardium contribute to the
development of cardiogenic shock after mi.
oInadequate cardiac function can be a direct result of cardiac injury, including;
Profound myocardial contusion, blunt cardiac valvular injury, or direct myocardial damage

Diagnosis:
oIn evaluation of possible cardiogenic shock, other causes of hypotension must be
excluded, including;
Hemorrhage, sepsis, pulmonary embolism, and aortic dissection.
oSigns of circulatory shock include;
 Hypotension, cool &mottled skin, depressed mental status, tachycardia, & diminished pulses.
oCardiac exam may include;
 Dysrhythmia, precordial heave, or distal heart tones.
o Confirmation of a cardiac source for the shock requires;
Electrocardiogram and urgent echocardiography.
oOther useful diagnostic tests include;
o CXR,
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TREATMENT.
oAfter ensuring that an adequate airway is present and ventilation is sufficient,
attention should be focused on support of the circulation.
oIntubation and mechanical ventilation often are required, if only to decrease work
of breathing and facilitate sedation of the patient.
o Treatment of cardiac dysfunction includes; maintenance of adequate oxygenation to ensure
adequate myocardial O2 delivery & judicious fluid administration to avoid fluid overload
&dev’t of cardiogenic pulmonary edema.
o Electrolyte abnormalities, cmnly hypokalemia & hypomagnesemia, should be corrected.
o Pain is treated with IV morphine sulfate or fentanyl.
o Significant dysrhythmias and heart block must be treated with antiarrhythmic drugs, pacing,
or cardioversion, if necessary.
Predictors of mortality:
• Increasing age (odds ratio 1.49 for each 10 year increase)
• Prior MI
• Physical findings at the time of diagnosis (the presence of altered sensorium
and cold, clammy skin)
• Oliguria

o In obstructive shock there is a reduction in preload due to mechanical obstruction
of cardiac filling.
oIn each case, there is reduced filling of the left and/or right sides of the heart
leading to reduced preload and a fall in cardiac output.


oNeurogenic shock refers to diminished tissue perfusion as a result of loss of
vasomotor tone to peripheral arterial beds.
oLoss of vasoconstrictor impulses results in increased vascular capacitance,
decreased venous return, and decreased cardiac output.
oNeurogenic shock is usually secondary to spinal cord injuries from vertebral body
fractures of the cervical or high thoracic region that disrupt sympathetic
regulation of peripheral vascular tone.

oAcute spinal cord injury results in activation of multiple 2ndry injury mechanisms:
(A) vascular compromise to the spinal cord with loss of autoregulation,
vasospasm, and thrombosis;
(B) Loss of cellular membrane integrity and impaired energy metabolism; and
(c) Neurotransmitter accumulation and release of free radicals

 DIAGNOSIS:
oAcute spinal cord injury may result in bradycardia, hypotension, cardiac
dysrhythmias, reduced CO , and decreased peripheral vascular resistance.
oPatients with complete motor injuries are over 5 times more likely to require
vasopressors for neurogenic shock compared to those with incomplete lesions.
oThe classic description of neurogenic shock consists of;
o Decreased BP associated with bradycardia (absence of reflexive tachycardia due to
disrupted sympathetic discharge),
o Warm extremities (loss of peripheral vasoconstriction),
o Motor and sensory deficits indicative of a spinal cord injury, and
o Radiographic evidence of a vertebral column fracture.

TREATMENT.
oAfter the airway is secured and ventilation is adequate,
oFluid resuscitation and restoration of intravascular volume often will improve
perfusion in neurogenic shock.
oMost patients with neurogenic shock will respond to restoration of intravascular
volume alone, with satisfactory improvement in perfusion and resolution of
hypotension.
oDopamine may be used first. A pure αagonist, such as phenylephrine, may be

used primarily or in patients unresponsive to dopamine

1.3 SHOCK

1.4. Electrolytes and fluid management of a
surgical patient

1.4.1. Body Fluids
1. Total Body Water
2. Fluid Compartments
3. Composition of Fluid Compartments
1.4.2. Classification of Body Fluid Changes; Disturbances in Fluid Balance
1. Volume Control
2. Concentration Changes
3. Composition Changes:

1.4.3. Fluid and Electrolyte Therapy
1. Parenteral Solutions
2. Alternative Resuscitative Fluids
3. Correction of Life-Threatening Electrolyte Abnormalities
4. Preoperative Fluid Therapy
5. Intraoperative Fluid Therapy
6. Postoperative Fluid Therapy
7. Special Considerations for the Postoperative Patient
1.4.4. Electrolyte Abnormalities in Specific Surgical Patients
1. Neurologic Patients
2. Malnourished Patients: Refeeding Syndrome
3. Acute Renal Failure Patients
4. Cancer Patients
1.4.1. Body Fluids
1. Total body water (TBW)
oIn an average young adult male, TBW accounts for 60% of total body weight,
whereas adult female, it is 50%.
The lower Percentage of TBW in females correlates with a higher percentage of adipose
tissue and lower percentage of muscle mass
oEstimates of percentage of TBW should be adjusted;
o Downward approximately 10% to 20% for obese individuals and
o Upward by 10% for malnourished individuals.
oNewborns, approximately 80% of their total body weight comprised of water.
oThis decreases 65% by 1 year of age and thereafter remains fairly constant.

1.4.1. Body Fluids …
2. Fluid compartments
oTBW is divided into three functional fluid compartments:
1. Plasma (fluid the vascular system) Extra cellular fluid = 1/3 of TBW
2. Extravascular interstitial fluid
3. Intracellular fluid =2/3 of TBW

3. Composition of fluid compartments

oThe ECF compartment is balanced cations (sodium, Cl) & bicarbonate.
oThe ICF= cations (potassium, magnesium),anion(phosphate,sulfate),& proteins.
oThe concentration gradient between compartments is maintained by ATP –driven
Na/K pumps located with in the cell membranes.
oPlasma & interstitial fluid differs only slightly in ionic composition.

o The slightly higher protein(organic anions) in plasma than interstitial fluid.
o Proteins add to the osmolality of the plasma and contribute to the balance of forces that
determine fluid balance across the capillary endothelium.

3. Composition of fluid compartments …

oWater is distributed evenly throughout all compartments of the body so a given
volume of water increases the volume of any one compartment relatively little.
oSodium, however, is confined to the ECF compartment, and because of its osmotic
and electrical properties, it remains associated with water.
o Therefore, sodium-containing fluids are distributed throughout the ECF and add to the
volume of both the intravascular and interstitial spaces.
o Although the administration of sodium-containing fluids expands the intravascular volume, it
also expands the interstitial space by approximately 3 times as much as the plasma.

3. Composition of fluid compartments …

1.4.2. Classification of Body Fluid Changes
Disorders in fluid balance may be classified into three general Categories
1. Volume Control changes
2. Concentration Changes
3. Composition Changes

Disturbances in Fluid Balance
oExtracellular volume deficit is the most common fluid disorder in surgical patients.
oCan be either acute or chronic.
1. Acute volume deficit is associated with cardiovascular and central nervous system signs,
2. Chronic deficits display tissue signs, such as;
 A decrease in skin turgor and sunken eyes, in addition to CVS & CNS signs.
o Laboratory examination: an elevated blood urea nitrogen level if the deficit is severe
enough to reduce glomerular filtration and hemo-concentration.
oExtracellular volume excess may be:
Iatrogenic or secondary to renal dysfunction, congestive heart failure, or cirrhosis.
o Both plasma and interstitial volumes usually are increased.
o Symptoms are primarily pulmonary and cardiovascular.
Disturbances in Fluid Balance

1. Volume control changes
oVolume changes are sensed by both osmoreceptors and baroreceptors.
1. Osmoreceptors are specialized sensors that detect even small changes in;
Fluid osmolality and drive changes in thirst and diuresis through the kidneys.
Eg.1. When plasma osmolality is increased, thirst is stimulated & water consumption increases, mechanism not
known.
2. Aditionally, the hypothalamus is stimulated to secrete vasopressin, which increases water reabsorption in the
kidneys.
2. Baroreceptors also modulate volume in response to changes in;
 Pressure & circulating volume through specialized pressure sensors located in the aortic
arch and carotid sinuses.
o Are both:
A. Neural; through sympathetic and parasympathetic pathways), and
B. Hormonal; including renin-angiotensin, aldosterone, atrial natriuretic peptide, &renal prostaglandins.
o The net result of alterations in renal sodium excretion and free water reabsorption .
2. Concentration changes
oChanges in serum sodium concentration are inversely proportional to TBW.
1. Hyponatremia.
oCauses:
Excess of extracellular water relative to sodium.
Sodium depletion or dilutional (excess extracellular water) = In most cases;
Excessive oral water intake or iatrogenic IV excess free water administration
Postoperative patients are particularly prone to increased secretion of
antidiuretic hormone (ADH), which increases reabsorption of free water from
the kidneys with subsequent volume expansion and hyponatremia.

2. Concentration changes
oChanges in serum sodium concentration are inversely proportional to TBW.
2. Hypernatremia.
oCauses:
Loss of free water or a gain of sodium in excess of water.
Like hyponatremia, associated with an increased, normal, or decreased EC
volume.
Hypervolemic hypernatremia usually is caused either by;
• Iatrogenic administration of sodium-containing fluids, including sodium bicarbonate, or
• Mineralocorticoid excess as seen in hyperaldosteronism, cushing’s syndrome, and
congenital adrenal hyperplasia.





Cause of Respiratory Alkalosis;hyperventilation

o Are acute & secondary to alveolar
hyperventilation.
o Causes include:
 Pain, anxiety, and neurologic disorders,
including CNS injury and assisted ventilation.
 Drugs such as salicylates,
 Fever,
 Gram-negative bacteremia,
 Thyrotoxicosis, and hypoxemia are other
possibilities.
 Acute hypocapnia .


4. Pre-operative Fluid Therapy
5. Intra-operative Fluid Therapy
6. Post-operative Fluid Therapy
7. Enhanced recovery after surgery (ERAS)

oThe type of fluid administered depends on the patient’s volume status and the
type of concentration or compositional abnormality present.
oPlasma lyte, lactated Ringer’s solution and normal saline are considered isotonic;
 are useful in replacing GI losses and correcting EC volume deficits.
oLactated Ringer’s is slightly hypotonic in that it contains 130 mEq of lactate.
oSodium chloride is mildly hypertonic, 154 mEq of Na &154 mEq of Cl.
oPlasma lyte: is resembles electrolyte composition to human plasma
o Have additional buffers to address acidosis.
o Contains small quantity of K; so used for pts with renal impairment

o1. Parenteral Solutions …

oless concentrated sodium solutions, such as 0.45% NaCl, are useful for;
Replacement of ongoing GI losses as well as for maintenance fluid therapy in the postop.
o It provides sufficient free water for insensible losses and enough sodium to aid the kidneys in
adjustment of serum sodium levels.
oThe addition of 5% dextrose (50 g of dextrose per liter) supplies 200 kcal/L
oDextrose is always added to solutions containing <0.45% NaCl.
To maintain osmolality and thus prevent the lysis of red blood cells that may occur with
rapid infusion of hypotonic fluids.
oThe addition of potassium is useful once adequate renal function and urine output
are established.



oHypertonic saline solutions (3.5% and 5%) are used for;
 correction of severe sodium deficits
oHypertonic saline (7.5%) has been used as;
A treatment modality in patients with closed head injuries.
 It can increase cerebral perfusion and decrease intracranial pressure, thus
decreasing brain edema.
However, there have also been concerns about increased bleeding, because
hypertonic saline is an arteriolar vasodilator



o The formula used to estimate
the amount of water required
to correct hypernatremia is
as follows:


4. Pre - operative Fluid Therapy
oThe following is a frequently used formula for calculating the volume of
maintenance fluids in the absence of pre-existing abnormalities:
oFor example, a 60-kg female would receive a total of 2300 mL of fluid daily:
1000 mL for the first 10 kg of body weight (10 kg ×100 mL/kg per day),
500 mL for the next 20 kg (10 kg ×50 mL/kg per day), and
800 mL for the last 40 kg (40 kg ×20 mL/kg per day).

oAn alternative approach is to replace the calculated daily water losses in urine,
stool, and insensible loss with a hypotonic saline solution rather than water
alone, which allows the kidney some sodium excess to adjust for concentration.
oFor all, an appropriate choice of 5% dextrose in 0.45% sodium chloride at 100

mL/h as initial therapy,
With potassium added for patients with normal renal function.
However, many surgical patients have volume and/or


oVolume deficits should be considered in patients who have;
Obvious GI losses, such as emesis or diarrhea, poor oral intake secondary to their disease.
Less obvious: fluid losses known as third-space or nonfunctional ECF losses that occur with GI
obstruction, peritoneal or bowel inflammation, ascites, crush injuries, burns, and severe soft
tissue infections such as necrotizing fasciitis.
oThe diagnosis of an acute volume deficit is primarily clinical, although the
physical signs may vary with the duration of the deficit.
Cardiovascular signs of tachycardia and orthostasis predominate with acute volume loss,
usually accompanied by oliguria and hemoconcentration.
Acute volume deficits should be corrected as much as possible before the time of operation.

4. Pre - operative fluid therapy

oFluid replacement with an isotonic crystalloid, depending on the measured serum
electrolyte values.
oPatients with cardiovascular signs of volume deficit should receive a bolus of 1 to
2 L of isotonic fluid followed by a continuous infusion.
oResuscitation should be guided by the reversal of the signs of volume defici;
Restoration of acceptable values for vital signs,
Maintenance of adequate urine output (½–1 ml/kg per hour in an adult), and
Correction of base deficit.
oPatients whose volume deficit is not corrected after this initial volume challenge
and those with impaired renal function and the elderly should be consider;
Early invasive monitoring of central venous pressure or cardiac output may be necessary.

oFor correction of severe hypernatremia associated with a volume
deficit, an unsafe rapid fall in extracellular osmolarity from 5%
dextrose infusion is avoided by slowly correcting the hypernatremia;
With 0.45% saline or even lactated Ringer’s solution rather than 5% dextrose alone.
This will safely and slowly correct the hypernatremia while also correcting the associated
volume deficit.

5. Intra-operative Fluid Therapy (IOFT)

oWith the induction of anesthesia, compensatory mechanisms are lost, and
hypotension will develop if volume deficits are not appropriately corrected
before the time of surgery.
oIn addition to measured blood loss, major open abdominal surgeries are
associated with continued extracellular losses in the form of bowel wall edema,
peritoneal fluid, and the wound edema during surgery.

5. Intra-operative Fluid Therapy

oLarge soft tissue wounds, complex fractures with associated soft tissue injury, and
burns are all associated with additional third-space losses that must be
considered in the operating room.
These functional losses have been referred to as parasitic losses, sequestration,or third-
space edema, b/se the lost volume no longer participates in the normal functions of the ECF.
oCurrent concept; saline administration is necessary to restore ECF losses.

oReplacement of ECF during surgery often requires 500 to 1000 mL/h of a
balanced salt solution to support homeostasis.
oAddition of albumin or other colloid containing solutions to IOFT is not necessary.


o Postoperative fluid therapy should be based on the patient’s current estimated
volume status and projected ongoing fluid losses.
oThird-space losses, although difficult to measure, should be included in fluid
replacement strategies.
oIn the initial postoperative period, an isotonic solution should be administered.
oThe adequacy of resuscitation should be guided by the restoration of acceptable
values for vital signs and urine output and, in more complicated cases, by the
correction of base deficit or lactate.
oIf uncertainty


oParticularly in patients with renal or cardiac dysfunction, a central venous catheter
or Swan-Ganz catheter may be inserted to help guide fluid therapy.
oAfter the initial 24 to 48 hours, fluids can be changed to 5% dextrose in 0.45%
saline in patients unable to tolerate enteral nutrition.
oIf normal renal function and adequate urine output are present, potassium may
be added to the IV fluids.
oDaily fluid orders should begin with assessment of the patient’s volume status
and assessment of electrolyte abnormalities.
oAll measured losses, including losses through vomiting, nasogastric suctioning,
drains, and urine output, as well as insensible losses, are replaced with the
appropriate
5/16/2020 parenteral solutions as previously
Gizachew Assefa reviewed. 103
7. Enhanced recovery after surgery (ERAS)

oERAS recommendation allow clear liquids up to 2hr prior to surgery.
oERAS protocol includes the use of carbohydrate and electrolyte rich fluids to
enhance hydration and metabolic response to surgery.
oIn addition to pre operative enteral hydration; it focus on restriction of intra and
post operative Na & IV fluids.
o Fluid over load has been associated with prolonged ileus and coagulation
abnormalities.
oEarly enteral intake is advised with prompt discontinuation of IV fluids.


o Volume excess is a common disorder in the postoperative period.
oThe administration of isotonic fluids in excess of actual needs may result in excess
volume expansion.
This may be due to the overestimation of third-space losses or to ongoing GI losses that
oThe earliest sign of volume overload is weight gain.
oThe average postoperative patient who is not receiving nutritional support should
lose approximately 0.11 to 0.23 kg/d from catabolism.
oPeripheral edema may not necessarily be associated with IV volume overload,
because overexpansion of total ECF may exist in association with a deficit in the
circulating plasma volume.

oVolume deficits also can be encountered in surgical patients if preoperative
losses were not completely corrected.
oThe clinical manifestations: include tachycardia, orthostasis, and oliguria,
hemoconcentration also may be present.
oTreatment will depend on the amount and composition of fluid lost.
oIn most cases of volume depletion, replacement with an isotonic fluid will be
sufficient while alterations in concentration and composition are being evaluated.

4. Cancer Patients

1. Neurologic patients
oSyndrome of inappropriate secretion of antidiuretic hormone (SIADH)occur after:
Head injury or surgery to the central nervous system,
But it also drugs such as morphine, nonsteroidals, and oxytocin, and
Pulmonary and endocrine diseases, including:
Hypothyroidism and glucocorticoid deficiency.
Malignancies; small cell cancer of lung, pancreatic carcinoma, thymoma,& hodgkin’s disease.

oSIADH should be considered in patients who are euvolemic and hyponatremic with
elevated urine sodium levels and urine osmolality.
oADH secretion is considered inappropriate when it is not in response to osmotic or
volume-related conditions.
oIn most cases, restriction of free water will improve the hyponatremia.
oThe goal is to achieve net water balance while avoiding volume depletion that
may compromise renal function.

oRefeeding syndrome is a potentially lethal condition that can occur with rapid
and excessive feeding of patients with severe underlying malnutrition due to
starvation, alcoholism, delayed nutritional support, anorexia nervosa, or massive
weight loss in obese patients.
oWith refeeding, a shift in metabolism from fat to carbohydrate substrate
stimulates insulin release, which results in the cellular uptake of electrolytes,
particularly phosphate, magnesium, potassium, and calcium.
oIt associated with enteral/parenteral refeeding, & symptoms include;
Cardiac arrhythmias, confusion, respiratory failure, and even death.
o To prevent refeeding syndrome; underlying electrolyte & volume deficits should be corrected.
o Additionally, thiamine should be administered before the initiation of feeding.

oA number of fluid and electrolyte abnormalities are specific to patients with acute
renal failure.
oWith the onset of renal failure, an accurate assessment of volume status must be
made.
oIf prerenal azotemia is present, prompt correction of the underlying volume
deficit is mandatory.
oOnce acute tubular necrosis is established, measures should be taken to restrict
daily fluid intake to match urine output and insensible and GI losses.
oOliguric renal failure requires close monitoring of serum potassium levels.

4. Cancer patients
oFluid and electrolyte abnormalities are common in patients with Cancer.
oThe causes may be common to all patient populations or May be specific to
cancer patients and their treatment.
oHyponatremia is frequently hypovolemic due to renal loss of sodium caused by
diuretics or salt-wasting nephropathy as seen with Some chemotherapeutic agents
such as cisplatin.

1.5. Wound healing and principles of wound care
1. Wound
2. Classification of wounds
3. Wound healing
4. Treatment of wounds

1. Wound
oWound: is a break in the integrity of the skin or tissue disruption in
structure and function.
oUlcer: is one type of wound which is a break or disruption in continuity
of any lining; skin or mucus membrane.

2. Classification of wounds
oBased on :
1. Duration
 Acute: < 4 weeks
 Chronic: > 4wks ; cmnly > 3mths
2. Rank &Wakefield Tidy wounds Untidy wounds
 Tidy wounds  Incised  Crushed/ avulsed
 Untidy wounds  Clean  Contaminated
 Health tissue  Devitalized tissue
 Seldom tissue loss  Often tissue loss

2. Surgical wounds: Wound class, representative procedures, and expected infection rates
No. Class of wound Description Example of cases Infection rate
1 (Class I) No infection  Hernia repair 1-2%

Clean : No hallow viscous  Breast biopsy
entered  Surgery of Brain, Joint , Heart, Transplant
2 (Class II) Open hallow  Cholecystectomy 2.1-9.5%

Clean contaminated: viscous (RS, GI)  Elective GI surgery (not colon)
 Appendectomy
 Colorectal surgery 4-14%
3 (Class III) Open accidental  Acute abdomen 3.4-13.2%
Contaminated: wound  Open fresh penetrating wound/ large tissue
 Enterotomy during bowel obstruction
4 (Class IV) -  Perforated diverticulitis 3.2-12.8%

Dirty wounds:  Necrotizing soft tissue infection
 Fecal peritonitis
5/16/2020  Pyocele,
Gizachew Assefa empyema of GB 116
3. Wound healing
ois a complex cellular and biochemical cascade that leads to restitution of
anatomical & functional integrity of disrupted tissue
 Phase of wound healing:
1. Phase I: hemostasis & inflammation phase
2. Phase II: proliferative phase
3. Phase III: remodeling & maturation phase

3. Wound healing…
 Stage of wound healing:
1. Stage I: inflammation
2. Stage I: granulation
3. Stage I: epithelialization
4. Stage I: scar formation
5. Stage I: maturation

3. Wound healing…
 Type of wound healing
1. Primary wound healing – first intention
2. Secondary wound healing – second intention
3. Tertiary wound healing – third intention
1. Primary wound healing
oOccur in clean incised or surgical wound.
oWound edge approximate with sutures.
oHave more epithelial regeneration than fibrosis.
oHeals; rapidly, completely with minimal scar.
oConnective
5/16/2020 tissue repair. Gizachew Assefa 119
3. Wound healing…
 Type of wound healing …
2. Secondary wound healing
oOccurs in extensive soft tissue loss such as; major trauma, burn, & wound in sepsis.
oIncrease inflammation and proliferation.
oHave Contracture and epithelialization.
oHeals slowly; with granulation, fibrosis, wide scar & hypertrophied.
3. Tertiary wound healing (delayed primary closure)
o Occur in contaminated or mixed tissue wounds.
o Contracture, connective tissue repair.
o Rx: initially wound debridement, control local infection &left open.
Next close with suture and skin graft.
3. Wound healing…
o The healing spectrum of acute wounds is broad by examining the acquisition of mechanical
integrity and strength during healing;
1. Normal healing; is characterized by a constant and continual increase that reaches a
plateau at some point post injury.
2. Delayed healing: wounds are characterized by decreased wound-breaking strength in
comparison to wounds that heal at a normal rate; however, they eventually achieve the
same integrity and strength as wounds that heal normally.
 Conditions such as nutritional deficiencies, infections, or severe trauma cause delayed
healing, which reverts to normal with correction of the underlying pathophysiology.
3. Impaired healing: is characterized by a failure to achieve mechanical strength equivalent
to normally healed wounds.
 Patients with compromised immune systems such as those with diabetes, chronic steroid
usage, or tissues damaged by radiotherapy
5/16/2020 Gizachew Assefaare prone to this type of impaired healing.
121
3. Wound healing…
 Normal healing is affected by both systemic and local factors
1. Age: older age and poor wound healing outcomes such as

dehiscence and incisional hernia
2. Metabolic Disorders: Uncontrolled diabetes results in
reduced inflammation, angiogenesis, and collagen
synthesis.
3. Infections. Wound infections affect the outcome of surgical
procedures (surgical site infections), and for their impact
on the length of hospital stay and medical costs.
4. Hypoxia, Anemia, and Hypoperfusion: Low oxygen
tension. Fibroplasia, although stimulated initially by the
hypoxic wound en’t, is significantly impaired by local
hypoxia.
3. Wound healing…
fig : The acquisition of wound mechanical strength over time in normal, delayed, and impaired healing.
3. Wound healing…
 Fetal Wound Healing
o Main characteristic that distinguishes healing of fetal from adult wounds is the lack of scar formation.
o Although early fetal healing is characterized by the absence of scarring and resembles tissue
regeneration, there is a phase of transition during gestational life when a more adult like healing
pattern emerges; called “transition wound” occurs at the beginning of the 3rd trimester.
o Characteristics that may influence the differences between fetal and adult wounds include:
1. Wound environment: The fetus is bathed in a sterile, temperature-stable fluid environment.
2. Inflammatory responses: Reduced fetal inflammation due to the immaturity of immune; lack of
scarring. Fetus is neutropenic, & fetal wounds contain lower numbers of PMNs & macrophages.
3. Growth factor: Fetal absence of TGF-β, which may have a significant role in scarring.
4. Wound matrix: fetal wound is chax. by excessive hyaluronic acid production;
 Hyaluronic acid may aid in the orderly organization of collagen.
 It is used topically to enhance healing and to inhibit postoperative adhesion formation
3. Wound healing…
 Complication of wound Healing
1. Chronic wound ; delayed or non healing:
oChronic wound: are defined as wounds that have failed to proceed through the
orderly process that produces satisfactory anatomic and functional integrity.
oThe majority of wounds that have not healed in 3 months are considered chronic;
or is healing not achieved after 4 week treatment.
oSkin ulcers, which usually occur in traumatized or vascular compromised soft
tissue, are also considered chronic in nature.
oCauses of chronic wound :
 Repeated trauma,
 Poor perfusion or oxygenation, and
 Excessive inflammation
3. Wound healing…
 Complication of wound Healing…
2. Excess healing :
 Tendon: frozen repairs.
 GIT: Stricture or stenosis.
 Solid organ: cirrhosis, pulmonary fibrosis.
 Peritoneal cavity: adhesive disease.
 Skin: mutilating or debilitating scars; burn contracture.
 Dermal healing: keloid or hypertrophic scars (HTs).

3. Wound healing…
 Complication of wound Healing…

3. Wound healing…
3. Wound infection:
 Wound infections more common in:
oDM pts
oImmunosuppressed pts
oMalnourished pts
oPts with cancer

3. Wound healing…
4.Wound dehiscence:
o Wound dehiscence is where a wound fails to heal, often re-opening a few days after surgery
(most common in abdominal surgery).
o Abdominal wound dehiscence (burst abdomen, fascial dehiscence) is a severe postoperative
complication.
o It can be divided into two clinical entities:
1. Superficial/partial dehiscence – the skin wound alone fails, with the rectus sheath
remaining intact & separation of portion of incision.
2. Complete dehiscence - with separation of all layers / entire incision/ and total
disruption. Complete dehiscence of an abdominal wound usually leads to evisceration.
o Fascial dehiscence can be:
o Early – is asurgical emergency
o Late – is incisional hernia
3. Wound healing…
4.Wound dehiscence:
 Risk factors for wound dehiscence:
1. Patient factors (independent)
 Age 2. Technical factors
 Sex: male 1. Incisional factors
 Pulmonary disease (chronic)  Length of incision > 18cm
 Ascites  longitudinal > transverse incision
 Anemia 2. Suture factors
 Emergency surgery  Suture breakage
 Post operative coughing  Knot failure
 Wound infection  Excessive stich interval
 Type of surgery
 Others:malignancy,obesity,poornutrition(hypo
albuminemia), sepsis,chronic costicosteroid use
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Gizachew 130
 1.Local care:
oExamination of the wound should asses the depth and configuration of
the wound, the extent of nonviable tissue, and the presence of foreign
bodies and other contaminants.
oExamination of the wound may also require irrigation and
débridement of the edges of the wound and is facilitated by use of
local anesthesia.
oAntibiotic administration and tetanus prophylaxis may be needed.
 1.Local care …
oAfter completion of the history, examination, and administration of
tetanus prophylaxis,
oThe wound should be meticulously anesthetized. Lidocaine (0.5%–1%) or
bupivacaine (0.25%–0.5%) combined with a 1:100,000 to 1:200,000 dilution of
epinephrine provides satisfactory anesthesia and hemostasis.
oEpinephrine should not be used in wounds of the fingers, toes, ears, nose,
or penis, due to the risk of tissue necrosis secondary to terminal arteriole
vasospasm in these structures.
 1.Local care …
1. Examination
2. Preparation
3. Approximation
4. Follow up

 2. Antibiotics
oAntibiotics should be used only when there is an obvious wound infection.
oSigns of infection to look for include:
 Erythema, Cellulitis, Swelling, and Purulent Discharge.
oAntibiotic treatment of acute wounds must be based on organisms suspected
within the infected wound and the patient’s overall immune status.
oAntibiotics also can be delivered topically as part of irrigations or dressings,
although their efficacy is questionable.

 3. Dressings
o The main purpose of wound dressings is to provide the ideal environment
for wound healing.
oThe dressing should facilitate the major changes taking place during healing
to produce an optimally healed wound.

 3. dressing…
oDressings can be classified as primary or secondary.
1. Primary dressing: is placed directly on the wound and may provide
absorption of fluids and prevent desiccation, infection, and adhesion of a
secondary dressing.
2. Secondary dressing: is one that is placed on the primary dressing for
further protection, absorption, compression, and occlusion.

 3. Type of dressing
 Absorbent Dressings
 Non Absorbent Dressings
 Occlusive and Semiocclusive Dressings
 Hydrophilic and Hydrophobic Dressings.
 Hydrocolloid and Hydrogel Dressings
 Alginates
 Absorbable Materials
 Medicated Dressings
 Mechanical
5/16/2020
Devices Gizachew Assefa 137
 3. Dressings…

 4. Skin Replacements
oAll wounds require coverage in order to prevent evaporative losses and
infection and to provide an environment that promotes healing.
oBoth acute and chronic wounds may demand use of skin replacement.
oConventional Skin Grafts.
oSplit- (partial-) thickness grafts consist of the epidermis plus part of the dermis.
oFull-thickness grafts retain the entire epidermis and dermis.
oAutologous grafts (autografts) are transplants from one site on the body to another;
oAllogeneic grafts (allografts, homografts) are transplants from a living nonidentical
donor or cadaver to the host; and
oXenogeneic grafts (heterografts) are taken from another species (e.g., porcine).
1.6. Ulcer
oAn ulcer is a break in the continuity of the covering epithelium, either skin or
mucous membrane due to molecular death.
 Parts of an Ulcer
1. Margin: It may be regular or irregular.
 It may be rounded or oval.
2. Edge: is the one which connects floor of the ulcer to the margin.
3. Floor: It is the one which is seen.
 Floor may contain discharge, granulation tissue or slough.
4. Base: is the one on which ulcer rests.
 It may be bone or soft tissue

1.6. Ulcer
 Parts of an Ulcer
 Classifications of ulcer
 Examination of an of ulcer

1.6. Ulcer
 Parts of an Ulcer …
oDifferent edge types:
1. Sloping edge: It is seen in a healing ulcer.
 Its inner part is red because of red, healthy granulation tissue.
 Its middle part is blue due to epithelial proliferation.
 Its outer part is white due to scar/fibrous tissue.
2. Undermined edge: is seen in a tuberculous ulcer.
 Disease process advances in deeper plane (subcutaneous tissue) whereas (skin) epidermis proliferates inwards.
3. Punched out edge: is seen in a gummatous (syphilitic) and trophic ulcer.
 It is due to endarteritis.
4. Raised and beaded edge (pearly white): is seen in a rodent ulcer (BCC).
 Beads are due to proliferating active cells.
5. Everted edge (rolled out edge): It is seen in a carcinomatous ulcer.
 Due to spill of the proliferating malignant
5/16/2020 tissues over the normal skin.
Gizachew Assefa 142
1.6. Ulcer
 Induration of an Ulcer
oInduration: is a clinical palpatory sign which means a specific type of hardness in
the diseased tissue.
oIt is obvious in well-differentiated carcinomas.
oInduration is felt at edge, base and surrounding area of an ulcer.
oInduration at surrounding area signifies the extent of disease (tumour).
oOutermost part of the indurated area is taken as the point from where clearance
of wide excision is planned.
oBrawny induration is a feature of an abscess.

1.6. Ulcer
I. Clinical classification
1.Spreading ulcer:
oEdge is inflamed, irregular and oedematous.
oSurrounding area is red and edematous.
oFloor does not contain healthy granulation tissue.
oProfuse purulent discharge and slough;
oIt is an acute painful ulcer;
oRegional (draining) lymph nodes(LNs) are enlarged &tender due to inflammation.
oThere will be associated;
 Fever, pain, impairment of functions with local tissue destruction and with
little evidence of regeneration.
1.6. Ulcer
I.Clinical classification
2. Healing ulcer:
oEdge is sloping with healthy pink/red healthy granulation tissue
oWith scanty/minimal serous discharge in the floor; slough is absent;
oRegional LNs may or not be enlarged but when enlarged always non-tender.
oSurrounding area does not show any signs of inflammation or induration;
oBase is not indurated.
o Three zones are observed in healing ulcer.
1. Innermost red zone of healthy granulation tissue;
2. Middle bluish zone of growing epithelium;
3. Outer whitish zone of fibrosis and scar formation.
1.6. Ulcer
I.Clinical classification
3. Non-healing ulcer:
oIt may be a chronic ulcer depending on the cause of the ulcer;
oEdge will be depending on the cause:
 Punched out (trophic),
 Undermined (tuberculous),
 Rolled out (carcinomatous ulcer),
 Beaded (rodent ulcer);
 Floor contains unhealthy granulation tissue and slough,
 Serosanguineous/purulent/bloody discharge;
 Regional draining lymph nodes may be enlarged but non-tender.
1.6. Ulcer
I. Clinical classification
4. Callous ulcer (stationary):
o It is also a chronic non-healing ulcer;
o Floor contains pale unhealthy, flabby, whitish yellow granulation tissue &thin scanty serous
discharge/often with copious serosanguinous discharge,
o Edge: Indurated non- tender;
o Base is indurated, non-tender and often fixed.
o Ulcer does not show any tendency to heal; it lasts for many months to years.
o Tissue destruction is more with absence of or only minimal regeneration.
o Surrounding area: Induration and pigmentation may be seen.
o There is no/less discharge.
o Regional LNs may be enlarged; are firm/hard and non-tender.
o Callous
5/16/2020
means—insensitive and cruel; and hard skinned.
Gizachew Assefa 147
1.6. Ulcer
II. Classification II (Based on Duration)
1. Acute ulcer—duration is less than 2 weeks.
2. Chronic ulcer—duration is more than 2 weeks (long).

1.6. Ulcer
Classifications of ulcer
III. Classification (Pathological)
1. Specific ulcers:
 Tuberculous ulcer.
 Syphilitic ulcer: It is punched out, deep, with “wash-leather” slough in the floor
and with indurated base.
 Actinomycosis.
 Meleney’s ulcer.

1.6. Ulcer
2. Non- Specific ulcers:
 Traumatic ulcer: Mechanical, physical, chemical- cmn.
 Arterial ulcer: Atherosclerosis, TAO
 Venous ulcer: Gravitational ulcer, post-phlebitic ulcer.
 Trophic ulcer/Pressure sore.
 Infective ulcers: Pyogenic ulcer.
 Tropical ulcers: in tropical countries; is callous type of ulcer, e.g. Vincent’s ulcer.
 Ulcers due to chilblains and frostbite (cryopathic ulcer).
 Martorell’s hypertensive ulcer.
 Bazin’s ulcer.
 Diabetic
5/16/2020 ulcer. Gizachew Assefa 150
1.6. Ulcer
3. Malignant ulcers:
 Carcinomatous ulcer
 Rodent ulcer.
 Melanotic ulcer.

1.6. Ulcer
1. Trophic ulcer (pressure sore/decubitus ulcer)
oPressure sore is tissue necrosis and ulceration due to prolonged pressure.
oBlood flow to the skin stops once external pressure becomes more than
30 mmHg (more than capillary occlusive pressure) and
oThis causes tissue hypoxia, necrosis and ulceration.
oIt is more prominent between bony prominence and an external surface.

1.6. Ulcer
1. Trophic ulcer (pressure sore/decubitus ulcer) is due to:
 Impaired nutrition.
 Defective blood supply.
 Neurological deficit.
o Neurological cause
 Diabeticneuropathy Spinal injury
Peripheral neuritis  Paraplegia
 Tabes dorsalis  Peripheral nerve injury
 Spina bifida  Syringomyelia
5/16/2020  Leprosy Gizachew Assefa 153
1.6. Ulcer
1. Trophic ulcer (pressure sore/decubitus ulcer)…
oCommon sites for pressure sore.
 Over the ischial tuberosity (28%).
 Greater trochanter (19%)
 Sacrum (17%).
 Heel (9%).
 Maleolus ( lateral> medial)
 Occiput.
 In relation to heads of metatarsals.
 Buttocks & over the shoulder. Gizachew Assefa
5/16/2020 154
1.6. Ulcer
 Staging of pressure sore/ulcer.
1. Stage 1: Non-blanching erythema; early superficial ulcer
2. Stage 2: Partial thickness skin loss; late superficial ulcer
 Exposed to dermis, blistering.
3. Stage 3: Full thickness skin loss extending into subcutaneous tissue
 but not through fascia; early deep ulcer
4. Stage 4: Full thickness skin loss with fascia & underlying structures like
muscle/tendon/bone, etc.; late deep ulcer
1.6. Ulcer
oClinical Features
 Occurs in 5% of all hospitalised patients.
 Painless ulcer which is punched out.
 Ulcer is non-mobile with base formed by bone

1.6. Ulcer
o INVESTIGATIONS
 Study of discharge,
 Blood sugar,
 Biopsy from the edge,
 X-ray of the part,
 X-ray spine.

1.6. Ulcer
oTREATMENT
 Cause should be treated.
 Nutritional supplementation.
 Rest, antibiotics, slough excision, regular dressings.
 Vacuum-assisted closure (VAC):
 It is the creation of intermittent negative pressure of minus 125 mmHg to
promote formation of healthy granulation tissue.
 Negative pressure: reduces tissue edema, clears interstitial fluid & improves
perfusion, increases the cell proliferation
5/16/2020 Gizachew Assefa and so promotes the healing. 158
1.6. Ulcer
2. DIABETIC ULCER
oCauses
 Increased glucose in the tissue precipitates infection.
 Diabetic microangiopathy which affects microcirculation.
 Increased glycosylated haemoglobin decreases oxygen dissociation.
 Increased glycosylated tissue protein decreases oxygen utilization.
 Diabetic neuropathy involving all sensory, motor & autonomous.
 Associated atherosclerosis.
1.6. Ulcer
2. DIABETIC ULCER
oCommon Sites
o Foot-plantar aspect—is the most common site.
o Leg
o Upper limb, back, scrotum, perineum.
o Diabetic ulcer may be associated with ischaemia.
o Ulcer is usually spreading and deep.

1.6. Ulcer
2. DIABETIC ULCER
oInvestigations
 Blood sugar both random and fasting.
 Urine ketone bodies.
 Discharge for culture and sensitivity.
 X-ray of the part to see osteomyelitis.

1.6. Ulcer
II. Classification II (Based on Duration)
2. DIABETIC ULCER
 Wagner’s Grading/Classification of Ulcer
 Grade 0 – Pre-ulcerative lesion/healed ulcer; high risk foot pts.
 Grade 1 – Superficial ulcer; full skin thickness.
 Grade 2 – deep to subcutaneous tissue exposing soft tissues/muscle.
 Grade 3 – Abscess formation underneath/osteomyelitis; cellulitis.
 Grade 4 – Gangrene of part of the tissues/limb/foot; localized.
 Grade 5 – Gangrene of entire one area/foot; extensive whole foot.
1.6. Ulcer
1. Local Examination of an Ulcer
 Inspection:
 Site of an Ulcer
 Size of an Ulcer
 Shape of an Ulcer
 Number of an Ulcer
 Margin, Edge, Floor, Base and surrounding area of an Ulcer
 Edge; soft =healing ulcer; firm =non-healing ulcer; hard =malignant
 Surrounding skin should be looked for oedema, inflammation, pigmentation, pallor.
 Discharge from Ulcer Bed
1.6. Ulcer
1. Local Examination of an Ulcer…
 Inspection:
 Different discharges in an ulcer(as well as from asinus)
 Serous: in healing ulcer
 Purulent: in infected ulcer
 Bloody: malignant ulcer, healing ulcer from healthy granulation tissue
 Seropurulent
 Serosanguineous: serous and blood
 Serous with sulphur granules: Actinomycosis
 Yellowish: Tuberculous ulcer
 Staphylococci: yellowish and creamy
 Streptococci: bloody and opalescent
 Pseudomonas: greenish colour
1.6. Ulcer
 Palpation
 Tenderness: should be elicited over the edge, base & surrounding area.
 Acute ulcers are tender.
 Chronic ulcer is usually non-tender but can be tender if there is
secondary infection, involvement of deeper structures like periostitis
in venous ulcer.
 Malignant ulcer is non-tender but; It may become tender in later
period when it infiltrates into deeper plane.
1.6. Ulcer
 Palpation
 Temperature:
 Warmness over surrounding area signifies acute inflammation.
 Checking temperature in surrounding area &comparing opposite/normal area
 Induration/Fixity:
 Palpation of Base for Induration/Fixity
 Depth of Ulcer
 Trophic ulcer is deep with bone as its base. Depth
 is measured in mm.
1.6. Ulcer
 Palpation
 Bleeding on Palpation and Touching
 Floor and edge should be palpated.
 Malignant ulcer is vascular and friable hence bleeds on touch.
 Healthy & exuberant granulation tissues in the floor can bleedon
touch.
 Palpation of Deeper Structures :
 Bone and soft tissues should be palpated.
 Bone thickening signifies periostitis/osteomyelitis due to ulcer penetration
1.6. Ulcer
2. Focal examination
 Examination of adjacent joint joints:
 Examined for both active and passive movements.
 Active movements are done by the patient.
 Passive movements are elicited by the clinician

1.6. Ulcer
 Examination of regional lymph nodes:
 Infective conditions: Tender, soft, palpable regional LNs.
 Sepsis: Tender swelling, soft & enlarged, suppurated & may form
abscess
 Tuberculosis: Non-tender, firm, matted often may lead to cold
abscess or collar stud abscess.
 Hunterian chancre: Shotty, firm, discrete LNs.
 Carcinoma: Stony hard, initially discrete and mobile LNs, but later
when advanced fixed to deeper structures.
1.6. Ulcer
 Examination of Arterial Pulse:
 Examination of arterial pulse peripherally in relation to ulcer should be done
 Examination for Varicose Veins:
 Varicose veins are examined in standing position
 Examination of Peripheral Pulses:
 Examination of peripheral pulses should be done to confirm ischaemia.
 Examination of Spine and Neurological System:
 Like sensation and muscle power in the region etc.
 Examination of Gait of the Patient:
 Gait of the patient should be checked to find out the severity of loss of function due to ulcer
1.6. Ulcer
3. Systemic examinations
 Abdominal system examinations
 Respiratory system examinations
 Cardiovascular system examinations should be done properly

1.7. Burn
 Burn definition
 Classification of burns
 Criteria for admission
 Burn injury to the airway and lungs
 Extent of burn injury
 Prognosis
 Care for burn patient
 Primary survey : Resuscitation
 Secondary survey: Nutrition
 Complications in burn care
1.7. Burn
Burn:
 Burns are commonly thought of as injury to the skin caused by excessive
heat (>44 0c).
 Broadly, burns result from traumatic injuries to the skin or other tissues
primarily caused by heat, electrical, friction, chemicals, or radiation.
 Is a type of co-agulative necrosis due to heat.
 Burn affect:
 Skin –commonest site
 Lung
 Other tissues
1.7. Burn
Classification of Burns:
1. Depend on mechanism/ cause of injury
Thermal, electrical, chemical, radiation, cold& friction burns.
2. Depending on the Percentage of Burns (Burn Severity Classification)
Mild (Minor), Moderate, Severe (Major).
3. Depend on burn depth/ Dupuytren classification
1st, 2nd, 3rd, 4th 5th & 6th degree burn.
4. Depend on zone of burn injury/ Jackson classification
Coagulation, stasis, & hyperemia zone.

1.7. Burn
A. Thermal burn injury
 It is primarily association with structural fires & the accompanying
inhalation injury and/or CO poisoning.
 It consists:
 Flame burns: most common cause admission of burns, & highest mortality.
 Scald burns: spillage of hot liquids, or stream.
 Contact burns: contact with hot metals/objects/materials
 Flash burns: due to exposure of natural gas, alcohol, combustible liquids
1.7. Burn
B. Electrical burn injury
 Electrical burns make up only 4% of U.S. Hospital admissions
 Have special concerns including the potential for;
 Cardiac arrhythmias and
 Compartment syndromes with concurrent rhabdomyolysis.
 A baseline ECG is recommended in all pts with an electrical injury;
normal ECG in a low-voltage injury may preclude hospital admission.
 It may be due to (types):
1. Low-voltage electrical injury: Less than 1000 volts.
2. High-voltage electrical injuries: (>1000 V) & Compartment syndrome &
rhabdomyolysis are Common.
1.7. Burn
C. Chemical burn injury
 Are less common which accounts 3%; but potentially severe burns.
 Chemical burns due to acid = result coagulation necrosis.
 Chemical burns due to alkali = liquefactive necrosis.
 Initial therapy are careful removal of the toxic substance from the Pts
& irrigation of affected area with water for a minimum 30 min.
 Formic acid: cause hemolysis and hemoglobinuria, and
 Hydrofluoric acid: causes hypocalcemia.
1.7. Burn
D. Cold burn injury
 It is due to ice exposure for prolonged time.
 It is due to:-
 Industrial accident: eg. Liquid nitrogen.
 Frost bite: damage to your skin by freezing it.

1.7. Burn
E. Radiation burn injury
 Radio frequency energy or ionizing radiation can cause damage to
skin and tissues.
 The most common type of radiation burn is the sunburn.
 Radiation burns are most commonly seen today following therapeutic
radiation therapy and radiation from diagnostic procedures

1.7. Burn
2. Depending on the Percentage of Burns (Burn Severity Classification)
A. Mild (Minor):
 Partial thickness burns <15% in adult or <10% in children.
 Full thickness burns less than 2%.
 Can be treated on outpatient basis.
B. Moderate:
 Second degree of 15–25% burns (10–20% in children).
 Third degree between 2–10% burns.
 Burns which are not involving eyes, ears, face, hand, feet, perineum.
C. Major (severe):
 Second degree burns more than 25% in adults, in children more than 20%.
 All third degree burns of 10% or more.
 Burns involving eyes, ears, feet, hands, perineum.
 All inhalation and electrical burns.
 Burns with fractures or major mechanicalGizachew
5/16/2020
trauma.
Assefa 180
1.7. Burn
3. Depend on burn depth/ Dupuytren classification
Depth of Burn of thickness Appearance Sensation Healing time
burn
1st degree Superficial ; Dry, red; blanches with Painful; no 3-6 days
epidermal pressure blister
2nd degree Superficial: papillary Moist, red, weeping Painful to air, 7-21 days
(Partial
thickness) Deep: reticular dermis Blanches with pressure pressure With scaring
Have blister
3rd degree Full thickness skin Dry, leathery, Painless Rare to heal;
Non-blanching require grafting
4th degree Underling soft tissue Extend to fascia Painless Never
5th degree Muscle to bone _ _
6th degree
5/16/2020 Charring bone _ Gizachew Assefa _ 181
1.7. Burn
3. Depend on burn depth classification …

1.7. Burn
3. Depend on burn depth classification …

1.7. Burn
4. Depend on zone of burn injury/ Jackson classification
 Based on Jackson classification divided in to 3 zone of burn injury.
No. Type of zone Related to burn site Description & example of causes
1 Zone of Center No blood flow; necrotic ,coagulated tissue.
coagulation Most severely burned, irreversible;
Like full thickness burn
Need excision & grafting
2 Zone of stasis Peripheral Decreases perfusion of blood
Vasoconstriction w/c leads to ischemia
Like 2nd degree burn
Need appropriate resuscitation
3 Zone of Outer Minimal & no scarring, vasodilation ; reversible
hyperemia
5/16/2020
Like 1st degree burn
Gizachew Assefa 184
1.7. Burn
 THE CRITERIA FOR ACUTE ADMISSION TO A BURNS UNIT.
 Suspected airway or inhalational injury
 Any burn likely to require fluid resuscitation
 Any burn likely to require surgery
 Patients with burns of any significance to hands, face, feet or perineum
 Patients whose psychiatric or social background .
 Any suspicion of non-accidental injury
 Any burn in a patient at the extremes of age
 Any burn with associated potentially serious sequelae, including;
High-tension electrical burns and concentrated hydrofluoric acid burns
1.7. Burn
 BURN CENTER REFERRAL CRITERIA*
 Partial-thickness burns greater than 10% of TBSA
 Burns that involve the face, hands, feet, genitalia, perineum, or major joints
 Third-degree burns in any age group
 Electrical burns, including lightning injury
 Chemical burns
 Inhalation injury
 Burn injury in patients with preexisting medical disorders
 Any patient with burns and concomitant trauma (such as fractures)
 Burned children in hospitals without qualified personnel/equipment for child care
 Burn injury in pts who will require special social, emotional, or rehabilitative intervention

1.7. Burn
oBURN INJURY TO THE AIRWAY AND LUNGS
1. Physical burn injury to the airway
A. Above the larynx
 Hot gases can physically burn the nose, mouth, tongue, palate and larynx.
 Once burned, linings of these structures will start to swell.
 After a few hours, they may start to interfere with the larynx and may
completely block the airway.
B. Below the larynx
 This is a rare injury, However, steam has a large latent heat of evaporation
& can cause thermal damage to the lower airway.
 In such injuries, the respiratory epithelium rapidly swells and detaches from
the bronchial tree.
 This creates casts, which can block the main upper airway
1.7. Burn
2. Metabolic poisoning
oCarbon monoxide is most common given off fire enclosed spaces.
oThis is the usual cause of a person being found with altered
consciousness at the scene of a fire.
oCO binds to haemoglobin with an affinity 240X > oxygen and
therefore blocks the transport of oxygen.
oLevels of carboxyhaemoglobin in the bloodstream can be measured.
oConc. >10% are dangerous & need treatment with pure O2/>24 hrs.
oDeath occurs with conc. around 60%.
oAnother metabolic toxin produced in house fires is hydrogen cyanide, which
causes a metabolic acidosis by interfering with mitochondrial respiration.
1.7. Burn
3. Inhalational injury
 Inhalational injury is caused by the minute particles within thick smoke,
 Which, b/se of their small size, are not filtered by the upper airway,
but are carried down to the lung parenchyma.
 They stick to the moist lining, causing an intense reaction in the alveoli.
 This chemical pneumonitis causes oedema within the alveolar sacs and
decreasing gaseous exchange over the ensuing 24 hours and
 Often gives rise to a bacterial pneumonia.
1.7. Burn
oWarning signs of burns to the respiratory system
 Burns around the face and neck
 A history of being trapped in a burning room
 Change in voice
 Stridor

1.7. Burn
oDangers of smoke, hot gas or steam inhalation
oInhaled hot gases can cause supraglottic airway burns & laryngeal oedema.
oInhaled steam can cause subglottic burns and loss of respiratory epithelium.
oInhaled smoke particles can cause chemical alveolitis and respiratory failure.
oInhaled poisons, such as carbon monoxide, can cause metabolic poisoning.
oFull-thickness burns to chest can cause mechanical blockage to rib movement.

1.7. Burn
oExtent of burn injury
 Method of estimation of burn size or %TBSA
1. Rule of NINE
2. Lund Browder chart
3. Palm method

1.7. Burn
1. Rule of NINE
1. Head ---------- 9% TBSA

2. Each arm ---- (2X) 9% TBSA
3. Each leg ---- (2X)18% TBSA
4. Anterior trunk - 18% TBSA
5. Posterior trunk - 18% TBSA
6. Genitalia - -------1% TBSA
Figure. The “rule of nines” can be used as a quick reference for estimating a patient’s burn size by dividing the body
into regions to which total body surface area is allocated
5/16/2020 in Assefa
Gizachew multiples of nine. 193
1.7. Burn
2. Lund Browder chart
 is the most accurate for adult & children.
Figure . The Lund and Browder chart

1.7. Burn
o Birth to 1 10 to 14
Area* 1 to 4 years 5 to 9 years Adult
year years
Head 9.5 8.5 6.5 5.5 4.5
Neck 1 1 1 1 1
Trunk 13 13 13 13 13
Upper arm 2 2 2 2 2
Forearm 1.5 1.5 1.5 1.5 1.5
Hand 1.25 1.25 1.25 1.25 1.25
Thigh 2.75 3.25 4 4.25 4.5
Leg 2.5 2.5 2.5 3 3.25
Foot 1.75 1.75 1.75 1.75 1.75
Buttock 2.5 2.5 2.5 2.5 2.5
Genitalia
5/16/2020 1 1 1
Gizachew Assefa 1 1 195
1.7. Burn
3. Palm method
oUsed for small or patchy burns.
 Palm with out finger – 0.5% TBSA
 Palm with finger – 1%TBSA
For both child & adult

1.7. Burn
oPROGNOSIS OF BURN INJURY
 The Baux score (mortality risk = age plus %TBSA); strongest predictors.
 Highest predictive value for burn mortality were;
1. Age: elderly pts; a single variable strongly predicts burn mortality.
:Non-elderly pts, comorbidities such as pre-injury; HIV,
metastatic cancer, and kidney or liver disease
2. %TBSA (burn size),
3. Inhalation injury,
4. Coexistent trauma, and pneumonia.

1.7. Burn
Complications and long-term outcomes of a severe burn
 Major determinants of the outcome of a burn
 Percentage surface area involved
 Depth of burns
 Presence of an inhalational injury
 Complication of severe burn can be:
1. Short term/ immediate complication
2. Long-term outcomes/complication

1.7. Burn
Complications and long-term outcomes of a severe burn
1. Short term/ immediate complication
 Multiple organ dysfunction syndrome
 Is continuum with the systemic inflammatory response syndrome which
affects most patients with a severe burn, with or without an infection.
 Early: due to hypoperfusion and under-resuscitation, or
 Late: due to sepsis
 The risk of MODS increases with burn wounds:
 >20% TBSA, Increasing age, Male, Sepsis, Hypo-perfusion, &
under-resuscitation.

1.7. Burn
Complications and long-term outcomes of a severe burn …
 MODS …
 There is early & late cascade of organ failure following a severe burn
Early clinical sequence is chax. by: Later clinical sequence chax. By:
 Resuscitation failure  Pulmonary failure
 Inhalation injury  Hemodynamic instability
 Acute respiratory distress syndrome  Renal failure
 Hemodynamic failure  Gastrointestinal failure: Mal-
 Renal failure absorption
 Liver failure  Liver failure
 Gastrointestinal failure
 Infection; on burn site
1.7. Burn
2. Long-term outcomes/ complications
A. Metabolic alterations:
 Partial-thickness/ full-thickness burns covering >40% TBSA are associated with
a significant stress response, inflammation, and severe hyper-metabolism,
resulting in hyper-dynamic circulation, augmented body temperature
regulation, proteolysis, glycolysis, lipolysis, and inefficient substrate cycling.
B. Keloid and hypertrophic scarring:
C. Heterotopic ossification:
 It is not simply calcification of tissue, but is the formation of lamellar bone in
an abnormal location (eg, joint) after a prolonged inflammatory state.

1.7. Burn
2. Long-term outcomes/ complications
D. Psychological aspects:
 Psychiatric/psychologic support of the burn patient should be an early and
routine component of management.
 Focused on measures of function, adjustment, sexuality & community integration
 Depression & post-traumatic stress disorder are the most common problems
 Risk factors for:
 Depression: pre-burn depression & female gender with facial disfigurement.
 PTSD: pre-burn depression, baseline depressive symptoms, anxiety related to
pain, & visibility of burn injury.
E. Unable to return work:
 Due to functional limitations of a burn
5/16/2020 and contracture.
Gizachew Assefa 202
1.7. Burn
CARE FOR BURN PATIENT
1. Pre-hospital care
2. Hospital care

1.7. Burn
1. PRE-HOSPITAL CARE
oThe principles of pre-hospital care are:
 Ensure rescuer safety: important in house fires, electrical & chemical
injuries.
 Stop the burning process:
 Cool the burn wound: for a minimum of 10 min and is effective up to 1 hr after
the burn injury; especially scalds for about 15°C.
 Give oxygen: especially if there is an altered consciousness level.
 Elevate: Sitting a pts up with a burned airway life-saving and Elevation
of burned limbs will reduce swelling and discomfort.

1.7. Burn
2. HOSPITAL CARE
1. PRIMARY SURVEY AND TREATMENT:
 Use ATLS; Advanced Trauma Life Support.
 The principles of managing an acute burn injury same as acute trauma.
A. Airway control: asses airway obstruction & difficulty
B. Breathing and ventilation: oxygenation
C. Circulation: check hemorrhagic & non-hemorrhagic shock
D. Disability: – neurological status; GCS
E. Exposure with environmental control: completely undressed & avoid
hypothermia b/c it induces coagulopathy.
F. Fluid resuscitation:
1.7. Burn
1. PRIMARY SURVEY AND TREATMENT …
F: Fluid resuscitation:
1. Approach to resuscitation
 Burn shock during the initial 24 to 48 hours following major burns is
characterized by; myocardial depression and increased capillary
permeability resulting in large fluid shifts and depletion of IV volume.
 Rapid, aggressive fluid resuscitation & maintain end-organ perfusion is
crucial.
 Delays in fluid & inadequate resuscitation are increased mortality.
 Monitor BP; urine output to determine adequacy of fluid resuscitation.

1.7. Burn
1. Approach to resuscitation …
 Any patient with >15 % TBSA non-superficial burns should receive
>60 mmHg
formal fluid resuscitation.

 Patients with major burns should have two large-bore IV lines placed
through unburned skin, if possible, may require central venous access.
 Continuation of fluid volumes should depend on the
 Time since injury,
 Urine output – to >60 mmHg
>30 mL/h.
 Mean arterial pressure (MAP)- to >30 mL/h. >60 mmHg

1.7. Burn
1. Approach to resuscitation …
 Fluid substitutes intra vascular volume and have two considerations.
A. Inadequate resuscitation: checked by UO.
B. Over-resuscitation: age, weight, %TBSA, and intubation on admission were
significant predictors of more fluid delivery during the resuscitation period &
can result
 Acute respiratory distress syndrome,
 Pneumonia, pleural effusions.
 Multi-organ failure,
 Abdominal, Extremity, and orbital compartment syndromes.

1.7. Burn
2. Initial fluid selection
 Initial fluid resuscitation of the patient with moderate or severe burns
consists of IV crystalloid solution, typically lactated Ringer’s solution.
 LR contains physiologic concentrations of major electrolytes, and
 lactate may reduce the incidence of hyper-chloremic acidosis.
 Hartmann’s solution, another isotonic solution that differs slightly from
LR in its concentrations of lactate and electrolytes, is also used.
 Recent American burn association recommened 2ml/kg/% burn of RL.
 Hypertonic solution high risk of hyper-chloremic acidosis.

1.7. Burn
3. Estimating initial fluid requirements
 There is no precise formula method determine burn fluid requirements.
 Factors such as: patient age, severity of burn, associated injury, and
comorbidities can substantially alter the actual fluid requirements.
 Eg, Patients with inhalation injury require greater resuscitation volumes.

1.7. Burn
3. Estimating initial fluid requirements…
1. Parkland or Baxter formula- most commonly used formula;

 3 -4 mL/kg/% burn of lactated Ringer’s, inhalation injury required an
average of 5.76 mL/kg/% burn,
 Which half is given during the first 8 hours after burn and the remaining half
is given over the subsequent 16 hours
2. Modified Brooke formula- alternative to Parkland
 According to which the fluid requirement during the initial 24 hrs of treatment
is 2 mL/kg of body weight for each percent of TBSA burned, given IV.

1.7. Burn
3. Estimating initial fluid requirements …
 Another alternative method in adults with severe burns is the Rule of Tens
1. Estimate burn area (TBSA) to the nearest 10 percent.
2. Multiply the %TBSAx10: gives the initial fluid rate in mL/hour for weighing 40 to 80 kg.
3. For patients >80 kg, increase the rate by 100 mL/hour for every additional 10 kg wt.
 Galveston formula
• Children require maintenance fluid in addition to calculated fluid resuscitation volumes, and
also need dextrose in the resuscitation fluid.
• 5000 mL/m² per %TBSA; Add 2000 mL/m² per day for maintenance requirements.

1.7. Burn
3. Estimating initial fluid requirements…
Q1. if a 50 years man comes in emergency OPD due to flame burn with
25% TBSA and his weight is 70kg, so what will fluid to be given in the
first 24hr after burn injury.
Answer:
= 3-4ml x 70 x 25/24hr
Use parkland formula = 3 - 4ml/kg/%TSBA/24hr
= 5250 - 7000ml/24hr
Give ½ in the 1st 8 hr =2625 - 3500ml; 328 - 437ml/hr
Give ½ in the 16 hr = 2625 - 3500ml; 164 -218ml/hr

1.7. Burn
4. Monitoring fluid status
 Confirming the adequacy of resuscitation is more important than strict
adherence to any fluid resuscitation formula.
 Monitoring urine output using an indwelling bladder catheter (eg,
Foley catheter) is a means of assessing fluid resuscitation.
 Hourly urine output should be maintained at 0.5 mL/kg/hr in adults.
 Clinical signs of volume status, such as;
• Heart rate, blood pressure, pulse pressure, distal pulses, capillary refill, and color and
turgor of uninjured skin are monitored every hour for the first 24 hours.
• Inadequate fluid resuscitation is the most common cause of diminished distal pulses in the
newly burned patient.
1.7. Burn
4. Monitoring fluid status ….
 Inadequate fluid resuscitation is the most common cause of diminished
distal pulses in the newly burned patient.
 Specific laboratory measurements such as;
• Mixed venous blood gas – decrease
• Serum lactate concentration – increase Suggest inadequate end-organ perfusion

1.7. Burn
5. Blood transfusion
 Blood transfusions have been associated with increased mortality in
patients with severe thermal burns, and we suggest that aggressive
transfusion be avoided.
• Increased numbers of transfusions were associated with increased
infections and higher mortality in burn patients, even when correcting
for burn severity.
• A restrictive transfusion policy in burned children showed that a
hemoglobin threshold of 7 g/dL had no more adverse outcomes vs. a
traditional transfusion trigger of 10 g/dL.
1.7. Burn
2. Secondary survey and management
1. Laboratory studies and monitoring
 Ongoing pulse oximetry and cardiac monitoring are performed for all
patients with significant thermal burns.
 Routine laboratory studies include:
 Complete blood count,
 Electrolytes,
 Blood urea nitrogen,
 Creatinine,
 Glucose,
 Venous blood gas (VBG), and carboxyhemoglobin.
 Arterial blood gas (ABG),
 Chest radiograph, and ECG areGizachew
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217
1.7. Burn
2. Chemoprophylaxis
 Patients with extensive burns are considered to be immunosuppressed; altered
neutrophil activity, T lymphocyte dysfunction, & imbalance production of cytokines.
 The burn also destroys the physical barrier to tissue invasion, which permits
spread of the bacteria to the dermis and through the lymphatics.
1. Tetanus: Tetanus immunization should be updated if necessary for any burns
deeper than superficial-thickness.
 Tetanus immune globulin: should give pts who have not receive complete 10 immunization.
2. Antibiotics: Topical chemoprophylaxis is continued until wound
epithelialization is complete.
 Never administer prophylactic intravenous antibiotics, it increase fungal infection
& resistance organisims.
1.7. Burn
2. Chemoprophylaxis …
 Silver sulfadiazine: has a wide range of antimicrobial activity, primarily as
prophylaxis for burn wound infections rather than treatment of existing infection
 Contraindicated: burns/donor sites in proximity; b/se it can destroys skin grafts.
 It may retard epithelial migration in healing partial-thickness wound.
 Mafenide acetate: cream/solution; is effective even in the presence of eschar and
can be used in both treating and preventing wound infections.
 Use may be limited by pain with application to partial-thickness burns.
 Major side effect: is metabolic acidosis from carbonic anhydrase inhibition.
 Silver nitrate: has broad-spectrum antimicrobial activity as a topical solution.
 The solution used must be dilute berore use
1.7. Burn
2. SECONDARY SURVEY AND MANAGEMENT…
3. Burn wound management
A. Wound dressings
 Wounds should be cleaned & clothing/materials are removed by irrigation.
 Tar/asphalt remove with a mixture of cool water & mineral oil; not debrided.
 Polymyxin-B bacitracin zinc oint for several days; will emulsify residual tar.
 Skin disinfectants (Hibiclens,Betadine), inhibit healing process & discouraged.
 Growing support for washing the wound using only mild soap and water.
 Needle aspiration of blisters never performed, it increases risk of infection.
 Non-adherent, mesh gauze (eg, Telfa) typically is applied.
 Circulatory impairment is minimized by applying this nonadherent dressing in
successive strips rather than wrapping it around the wound.
1.7. Burn
3. Burn wound management …
B. Escharotomy
 With deep dermal and full thickness burns, the dermis can become stiff
and unyielding, and this tissue is referred to as an eschar.
 Escharotomy is incision of an eschar & may be necessary to preserve
respiratory function or prevent ischemia

1.7. Burn
4. Gastrointestinal interventions
 Shock from thermal burn injuries results in mesenteric vasoconstriction
predisposing to gastric distension, ulceration (so-called Curling's ulcer),
and aspiration.
 Therefore, a nasogastric tube should be placed in patients with
moderate or severe burns >20 % TBSA.
 High-risk patients receive medication to reduce gastric acid secretion.

1.7. Burn
5. NUTRITION
 Hyper-metabolic response in burn injury may raise baseline metabolic
rates by as much as 200%.
 This can lead to catabolism of muscle proteins & decreased lean body
mass that may delay functional recovery.
 Early enteral feeding for patients with burns >20% TBSA is safe &
may reduce loss of lean body mass, slow the hyper-metabolic
response and result in more efficient protein metabolism.
 If the enteral feeds are started within the first few hours after
admission, gastric ileus can be avoided.
 Adjuncts such as metoclopramide promote gastrointestinal motility
1.7. Burn
5. Nutrition
 Calculating appropriate caloric needs of burn patient is challenging.
1. Harris-Benedict equation: which calculates caloric needs using factors
such as; Gender, Age, Height, and Weight.
 It commonly used formula in non burned patients
 For burns, the basal energy expenditure is multiplied by two.
 It may be inaccurate in burns of < 40% TBSA
2. Curreri formula: more appropriate in burn pts < 40% TBSA

 It estimates caloric needs to be 25 kcal/kg/d plus 40 kcal/%TBSA/d.
1.7. Burn
6. Pain management
 Burn pain also varies depending upon depth of burn
 Superficial partial-thickness burns result hyperalgesia& mild-to-moderate pain.
 Moderate partial-thickness: marked hyperalgesia & moderate-to-severe pain.
 Deep partial-thickness to full-thickness burns are chax. by absence of pain.
 Drugs:
1. Opioid analgesics: Morphine sulfate.
2. Non-opioid analgesics: Dexmedetomidine, Ketamine, Acetaminophen, &
NSAIDs, provide mild analgesia.
3. Anxiolytics: Benzodiazepine; Lorazepam 1 mg.
4. Antipsychotic medications: Haloperidol, Quetiapine.
5. Anesthesia:
5/16/2020
Bupivacaine Gizachew Assefa 225
1.7. Burn
COMPLICATIONS IN BURN CARE
 Ventilator-associated pneumonia, as in all critically ill patients, is a
significant problem in burned patients.
 Massive resuscitation of burned patients may lead to an abdominal
compartment syndrome characterized by increased airway pressures
with hypoventilation, and decreased urine output and hemodynamic
compromise.
 Decompressive laparotomy is the standard of care for refractory
 Deep vein thrombosis (DVT) has been commonly believed to be a rare
phenomenon in burned patients.
 Unfortunately, the use of both prophylactic and therapeutic heparin
may be associated with heparin-associated thrombocytopenia (HIT).
 Prevention and Treatment of Surgical Infections
 General Principles
 Appropriate Use of Antimicrobial Agents
 Infections of Significance in Surgical Patients
 Surgical Site Infections
 Intra-Abdominal Infections
 Organ-Specific Infections
 Infections of the Skin and Soft Tissue
 Postoperative Nosocomial Infections
 Sepsis
 Blood-Borne Pathogens




1.9. Trauma
 Initial Evaluation and Resuscitation of the Injured Patient
 Primary Survey
 Secondary Survey
 Mechanisms and Patterns of Injury
 Regional Assessment and Special Diagnostic Tests
 General Principles of Management
 Transfusion Practices
 Prophylactic Measures
 Operative Approaches and Exposure
 Damage Control Surgery
 Injury scoring
 Repair of laceration (suturing)
1.9. Trauma
Trauma:
 Trauma, or injury, is defined as cellular disruption caused by an
exchange with environmental energy that is beyond the body’s
resilience which is compounded by cell death due to
ischemia/reperfusion.

1.9. Trauma

1.9. Trauma

1.9. Trauma

1.9. Trauma

1.9. Trauma

1.9. Trauma

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1.10. Perioperative management (case related to perioperative mgt); preoperative evaluation.
1.11. Simulated practice: infection control & patient safety (hand washing, use of
personal protective equipment, safe handling of sharps and other equipment, medical
waste management, instrument processing)

 This page is intentionally blank.

2.1. Trauma of the Head
2.2. Cerebrovascular disease
2.3. Tumors of the Head
2.4. Common surgical conditions of the head & neck (cleft lip and palate,
diseases of salivary glands)
• Case related to the topics in the week (brain tumour/ head & spinal injuries)
• Simulated practice:
• Cardiopulmonary resuscitation ( CPR)
• Communication with a surgical patient with reduced or altered consciousness
• Breaking bad news (communicating diseases with poor prognosis like brain
tumors) to a surgical patient and relatives

 Head injury accounts for 3–4% of emergency department attendances,

with around 1500 cases per 100 000 population per year in the UK.
 Significant traumatic brain injury can be considered a combination of
the primary injury sustained on impact, and secondary injury
developing in the following hours and days.
 Head injuries are one of the common causes of death in road traffic
accidents.
 Young males are commonly affected.

 The frontal areas:
 Are involved in executive function, decision making, and restraint of
emotions.
 The motor strip, or precentral gyrus, is the most posterior component
of the frontal lobes, and is arranged along a homunculus with the
head inferior and lateral to the lower extremities superiorly and
medially.
 The motor speech area (broca’s area) lies in the left posterior
inferior frontal lobe in almost all right-handed people and in up to
90% of left-handed people.
2.1. Trauma of the Head : NEURO-ANATOMY…


 The parietal lobe:
 Lies between the central sulcus anteriorly and the occipital lobe
posteriorly.
 The postcentral gyrus is the sensory strip, also arranged along a
homunculus.
 The rest of the parietal lobe is involved with awareness of one’s
body in space and
 Relative to the immediate environment, body orientation, and spatial
relationships.


 Temporal lobes: lie below the sylvian fissures.
 Hippocampus, amygdala, & lower optic radiations (Meyer’s loops):
involved in memory, emotion, and vision, respectively.
 Receptive speech area (Wernicke’s) typically is found in the area of
the left posterior superior temporal lobe & inferior parietal lobe.
 The basal ganglia include the caudate, putamen, globus pallidus,
subthalamic nucleus, substantia nigra, and nucleus accumbens.
 These structures are involved in the selection, activation and
termination of movement, and facilitate learning of appropriate
context-dependent motor behaviors.


 Occipital lobes: are most posterior.
 The visual cortex is arrayed along the apposing medial surfaces of
the occipital lobes.
 The left occipital lobe receives and integrates data from the left half
of each retina.
 A left occipital lesion would therefore result in an inability to see
objects right of center.








 Patterns of motor responses
associated with various
lesions.
A. Left hemispheric lesion with
right hemiplegia and left
localization.
B. Deep cerebral/thalamic
lesion with bilateral flexor
posturing.
C. Midbrain or pontine lesion
with bilateral extensor
posturing.
D. Medullary lesion with general
flaccidity.


2.1. Trauma of the Head : NEUROLOGIC EXAMINATION
 NEUROLOGIC EXAMINATION
 First, one must assess mental status. A patient may be;
1. Awake,
2. Lethargic (will follow commands and answer questions, but then
returns to sleep),
3. Stuporous (difficult to arouse), or
4. Comatose (no purposeful response to voice or pain).

 NEUROLOGIC EXAMINATION …
 Cranial nerves may be thoroughly tested in the awake patient, but
 Pupil reactivity, eye movement, facial symmetry, and gag are the
most relevant measures when mental status is impaired.
 Motor testing is based on maximal effort of major muscle groups in
those able to follow commands,
 While assessing for amplitude and symmetry of movement to deep
central pain may be all that is possible for stuporous patients.

 Characteristic motor reactions to pain in patients with depressed mental
status.

 Aphasia box:

Trauma to Head may be:

1. Scalp injury:
2. Skull Fracture:
3. Traumatic brain injury:

1. Scalp injury:
 Blunt or penetrating trauma to the head can cause injury to the densely
vascularized scalp, and significant blood loss can result.
 Direct pressure initially controls the bleeding.
 Laceration can be:
 Simple laceration: it should be copiously irrigated and closed primarily.
 Short, a single-layer: percutaneous suture closure will suffice.
 Long or has multiple arms: need debridement & closure in the operating room.
 Careful reapproximation of galea will provide more secure closure & hemostasis.
 Blunt trauma also can cause crush injury with subsequent tissue necrosis.
 require debridement & consideration of advancement flaps to cover a defect.
2. Fracture of skull:
 Skull fractures generally indicate that a significant amount of force was
transmitted to the head & should increase the suspicion for intracranial
injury.
 The fracture may be characterized by skull X-rays or head CT.
 Based on site it classified in to:
1. Skull vault fracture
2. Skull base fracture

 Fracture of skull …
1. Skull vault fracture
A. Closed: is covered by intact skin.
 Do not normally require specific treatment.
B. Open/compound: is associated with disrupted overlying skin.
 Require repair of the scalp and operative debridement
 The fracture lines may be
 Single: linear
 Multiple: and radiating from a point (stellate).
 Comminuted: creating fragment of bone.
 Depressed: inner & outer cortices of the skull are disrupted, and a fragment of
bone is pressed in toward the brain in relation to adjacent intact skull.
 5/16/2020
Non depressed: Gizachew Assefa 263
1. Skull vault fracture ..
 Craniotomy is required to elevate the fracture, repair dural disruption,
and obtain hemostasis.
 Indications for craniotomy
1. Depression greater than the cranial thickness,
2. Intra cranial hematoma and
3. Frontal sinus involvement

 Fracture of skull:
2. Skull base fracture
 Skull base fractures requiring intervention include those with an associated
cranial nerve deficit or CSF leak.
 Fracture of the temporal bone; can damage the facial or vestibulocochlear
nerve, resulting vertigo, ipsilateral deafness, facial paralysis.
 CSF test:
 Halo test: drop the fluid on an absorbent surface such as a facial tissue.
 If blood is mixed with CSF, the drop will form a double ring, with a darker
center spot containing blood components surrounded by a light halo of CSF.
 If this test is indeterminate, the fluid can be sent for beta-2 transferrin testing,
a carbohydrate-free isoform of transferrin exclusively found in the CSF
2. Skull base fracture…
 Rhinorrhea: CSF drainage from the nose.
 Otorrhea: CSF drainage into the pharynx via the eustachian tube /from the ear
 Cranial nerve palsy
 Anosmia: loss of smell; due damage to the olfactory nerve.
 Battle’s sign: bruising over mastoid area; Extravasation of blood results
in ecchymosis behind the ear.
 Raccoon eye sign: bilateral peri-orbital bruising; periorbital ecchymoses.

 Indications for Hospitalization in head injury.
1. Any altered level of consciousness
2. Skull fracture
3. Focal neurological features
4. Persistent headache, vomiting, systolic hypertension, bradycardia
5. Alcohol intoxication
6. Bleeding from ear or nose
7. Associated injuries
3. Traumatic brain injury
 Classification Head injuries
A. Based on GCS
1. Mild head injuries: GCS =13-15
2. Moderate head injuries: GCS = 9-12
3. Severe head injuries: GCS 3- 8
B. Based on fracture skull with meningeal injuries causing CSF leak or not.
1. Open head injuries: more risk of intracranial infection including meningitis
2. Closed head injuries: CSF leak is not present.

3. Traumatic brain injury…

C. Based on type/ Mechanisim of injury
1. Blunt head injuries
2. Penetrating head injuries
 High velocity: >2000ft/s
 Low velocity: <2000ft/s

 Traumatic brain injury …
D. Based on risk for intracranial injury
1. Low risk for intracranial injury
 Asymptomatic, who have only;
 Headache, dizziness, or scalp lacerations, and
 No lose of consciousness,
 Have a low risk for intracranial injury and
 May be discharged home without a head CT scan.

D. Based on risk for intracranial injury…
2. Moderate risk for intracranial injury
 Patients with a history of altered consciousness,
 Amnesia,
 Progressive headache,
 Skull or facial fracture,
 Vomiting, or seizure
 Should undergo a prompt head CT.
D. Based on risk for intracranial injury…
3. High risk for intracranial injury
 Patients with depressed consciousness,
 Focal neurologic deficits,
 Penetrating injury,
 Depressed skull fracture, or
 Changing neurologic examination
 Need immediate head CT and admission for observation or
intervention as needed.
 Closed head injury (CHI)
 is the most common type of TBI and a significant cause of morbidity
and mortality in the United States.
 There are two important factors that affect the outcome of CHI.
1. Primary injury: defined as the immediate injury to neurons from
transmission of the force of impact on:
Brain stem or hemispheric contusion, DAI,& cortical
lesion/laceration.
 Prevention strategies: wearing helmets, is the best means to
decrease disability.
 Closed head injury (CHI) …
2. Secondary injury: is a subsequent neuronal damage due to sequelae of trauma.
 Mechanisms of secondary injury/ cause.
 Hypoxia,
 Hypotension (SBP<90mmHg),
 Hydrocephalus,
 Intracranial hypertension
 Raised ICP ( >20mmHg, Normal 4-14mmHg)
 Decreased cerebral perfusion pressure (CPR = MAP-ICP)
 Thrombosis, and
 Intracranial hemorrhage may all be mechanisms of secondary injury.
 Closed head injury (CHI) …
 Phenytoin prophylaxis has been shown to decrease the incidence of
early posttraumatic seizures.
 Hyperglycemia and hyperthermia are toxic to injured neurons and
contribute to secondary injury.
 Head-injured patients have an increased prevalence of peptic
ulceration and GI bleeding.
 Peptic ulcers occurring in patients with head injury or high ICP are
referred to as Cushing’s ulcers.
 Types of Closed Head Injury
1. Concussion: is defined as temporary neuronal dysfunction following
non-penetrating head trauma.
 CT is normal, and deficits resolve over minutes to hours.
 Transient loss of consciousness (some), any alteration of mental status.
 Memory difficulties, especially amnesia (very common).
 Concussions may be graded (Colorado grading system)
 Grade1: Head trauma patients with confusion only.
 Grade 2: Patients with amnesia, and
 Grade 3: Patients who lose consciousness.
 Types of Closed Head Injury …
2. Contusion: is either croup or contre-coup injury.
 is a bruise of the brain, and occurs when the force from trauma is;
 Cause breakdown small vessels & extravasation of blood into the brain.
 The contused areas appear bright on CT scan.
 The frontal, occipital, and temporal poles are most often involved.
 Edema may develop around a contusion, causing mass effect (frank hematoma
>1cm), in 1st 24hrs.
 Contusions may occur in brain tissue opposite the site of impact; is known as a
contre-coup injury.
3. Diffuse Axonal Injury:
 is caused by damage to axons throughout the brain, due to rotational
acceleration and then deceleration.
 Axons may be completely disrupted & then retract, forming axon balls.
 Small hemorrhages can be seen in more severe cases, esp. on MRI.
 Hemorrhage is classically seen in the corpus callosum & dorsolateral
midbrain.

4. Penetrating Injury: have two main subtypes are:
1. Missile (e.g., due to bullets or fragmentation devices) and
2. Non-missile (e.g., due to knives or ice picks).
 Skull X-rays, CT scans & Cerebral angiography considered.
 High-velocity missile injuries (from high-powered hunting rifles or
military weapons) are especially deadly.
 Projectiles that penetrate both hemispheres or traverse the ventricles
are almost universally fatal.
 Traumatic Intracranial Hematomas.
 Hematomas can expand rapidly and cause brain shift and subsequent
herniation.
 Emergent neurosurgical evaluation and intervention often are
necessary.

 Traumatic Intracranial Hematomas…
1. Epidural Hematoma (EDH):
 Is the accumulation of blood between the skull and the dura.
 It usually due to arterial disruption, especially of the middle meningeal
artery; in some cases it may due to Dural-venous tearing.
 Common sites: temporal bone, pterion which is thinnest part of skull &
place of largest meningeal artery.
 Usually, it is associated with fracture of temporo-parietal region.
 It can be unilateral or bilateral.
1. Epidural Hematoma (EDH)…
 EDH has a classic, 3-stage clinical presentation; seen 20% of cases.
1. The patient is initially unconscious from head trauma.
2. The patient then awakens and has a “lucid interval,”
3. Hematoma: as volume grows, ICP increases, the pts rapidly
becomes lethargic & herniates.
 Patient soon regains consciousness and again after 6–12hr starts
deteriorating (Lucid interval).
 Features of raised ICP: high BP, Bradycardia, Vomiting, convulsions (Occasionally)

1. Epidural Hematoma (EDH) …
 Cushing’s triad of raised ICP: bradycardia; HTN; respiratory irregularities.
 Uncal herniation from an EDH classically causes ipsilateral 3rd nerve
palsy (eg.pupillary dilation) and contralateral hemiparesis.
 Imaging:
 X-ray skull may show fracture of temporal bone.
 Head CT; is diagnostic.
 The blood clot is bright,
 Biconvex in shape (lentiform), and
 Has a well-defined border that usually respects cranial suture lines.
1. Epidural Hematoma (EDH) …
 Management of EDH
1. Conservative management: for self limited which is in some cases.
 For pts with; clot volume <30cm3, maximum thickness <1.5cm & GCS score>8.
2. Open craniectomy for evacuation of the congealed clot and
hemostasis generally is indicated for EDH.
 Prognosis after successful evacuation is better for EDH than subdural hematoma.
 EDHs associated with lower-energy trauma with less resultant primary brain injury.
 Good outcomes may seen in 85%-90% of pts, with rapid CT scan & intervention.

Traumatic Intracranial Hematomas…
2. Subdural Hematoma (SDH):
 SDH is an accumulation of blood between arachnoid membrane & dura.
1. Acute Subdural Hematoma
 Acute SDH usually results from venous bleeding, typically from tearing
of a bridging vein running from the cerebral cortex to the dural sinuses.
 The bridging veins are subject to stretching & tearing during
acceleration/deceleration of the head.
 Elderly & alcoholic patients are at higher risk for acute SDH formation
after head trauma due to brain atrophy.
 Acute Subdural Hematoma…
 INVESTIGATION
 Head CT scan:
 Clot is bright or mixed-density; white /hyper dense/ for 3 days.
 Crescent-shaped (lunate),
 Less distinct border, and
 Does not cross the midline due to the presence of the falx.

 MANAGEMENT
1. Open craniotomy for acute SDH is indicated for any of the following:
1. Thickness >1 cm,
2. Midline shift >5 mm, or
3. GCS drop by >2 points from the time of injury to hospitalization.
2. Non-operatively managed hematomas may stabilize and eventually
reabsorb, or evolve into chronic SDHs.
 This management requires frequent neurologic examinations until the clot
stabilizes based on serial head CT scans.
 The prognosis for functional recovery is significantly worse for acute
SDH than EDH because;
 It is associated with greater primary injury to brain parenchyma from
high-energy impacts.
 Prompt recognition and intervention minimizes secondary injury.
 The elderly patients with low admission GCS, or high postoperative ICP
do poorly, with as few as 5% attaining functional recovery.

2. Chronic Subdural Hematoma
 Chronic SDH is a collection of blood breakdown products that is at least
2 to 3 weeks
 Chronic SDHs often occur in patients without a clear history of head
trauma, as they may arise from minor head injury.
 Alcoholics, the elderly, and patients on anticoagulation are at higher

risk for developing chronic SDH.

2. Chronic Subdural Hematoma…
Clinical presentation:
 Patients may present with headache, seizure, confusion, contralateral
hemiparesis, or coma.

2. Chronic Subdural Hematoma
 Imaging:
 Head CT scan:
<3 days: white (hyperdense)
 >3 days: isodense
After 2 to 3wks: hypodensity
 A true chronic SDH will be nearly as dark as CSF on CT.
 Traces of white are often seen due to small, recurrent hemorrhages into
the collection.
 These small bleeds may expand the collection enough to make it
symptomatic; this phenomenon is referred to as an acute-on-chronic SDH.
MANAGEMENT OF CHRONIC SDH
Surgical drainage if
1. A chronic SDH thickness >1 cm or
2. Any symptomatic SDH.
 A simple burr hole can effectively drain most chronic SDHs.
Unlike acute SDH, which consists of a thick, congealed clot,
Chronic SDH typically consists of a viscous fluid with the texture and
dark brown color reminiscent of motor oil.
 There are various strategies to prevent reaccumulation of blood.
• Subdural or subgaleal drains may be left in place for 1 to 2 days.
• Mild hydration & bed rest with the head of the bed flat may
encourage brain expansion.
• High levels of inspired oxygen may help draw nitrogen out of the
cavity.

Traumatic Intracranial Hematomas…
3. Intraparenchymal Hemorrhage
 Is isolated hematomas within the brain parenchyma.
 Most often associated with:
1. Hypertensive hemorrhage or
2. Arteriovenous malformations (avms).
 Bleeding may occur in a contused area of brain.
 Mass effect from developing hematomas may present as a delayed
neurologic deficit.
 Delayed traumatic intracerebral hemorrhage is most likely to occur
within the first 24 hrs.
3. Intraparenchymal Hemorrhage …
 Imaging:
 Head CT: Patients with contusion on the initial head CT scan should
be reimaged 24 hours after the trauma to document stable
pathology.
 MANAGEMENT
1. Craniotomy: Indications for craniotomy include:
1. Any clot volume >50 cm3 or
2. Clot volume >20 cm3 with referable neurologic deterioration (GCS 6–8) and
3. Associated midline shift >5 mm or basal cistern compression.


 Complications of Head Injuries
1. Early
 Brainstem injury—due to coning.
 Compression over cerebellum and medulla.
 CSF rhinorrhoea: due to communication between intracranial cavity & nose.
 Meningitis—common.
 Pituitary damage and endocrine failure—requires high dose of hydrocortisone
200 mg, 6th hourly.
 Aerocoele.
 CSF otorrhoea.
 Dural venous sinuses injury : due to depressed fractures.
 Complications of Head Injuries …
2. Late
 Chronic subdural haematoma.
 Early post-traumatic epilepsy—they need anti-convulsants for 3 years.
 Late post-traumatic epilepsy is due to scarring and gliosis of cerebrum.
 Post-traumatic amnesia.
 Post-traumatic hydrocephalus.
 Post-traumatic headache

2.2. CEREBROVASCULAR DISEASE
 Cerebrovascular disease is the most frequent cause of new, rapid-onset,
nontraumatic neurologic deficit.
 Vascular structures are subject to a variety of chronic pathologic
processes that compromise vessel wall integrity; such risk factors are:
 Diabetes,
 High cholesterol,
 High blood pressure, and
 Smoking
 Type of cerebrovascular disease are:
1. Ischemic diseases
 Thrombotic
 Embolic disease
2. Hemorrhagic diseases

HARRISON;20th edition:
 Medical management of stroke and TIA.
 Rounded boxes are diagnoses;
 Rectangles are interventions.
 Numbers are %ages of stroke overall.
 ABCs, airway, breathing, circulation;
 BP, blood pressure;
 CEA, carotid end arterectomy;
 ICH, intra cerebral hemorrhage;
 SAH, subarachnoid hemorrhage;
5/16/2020 Gizachew Assefa  TIA, transient ischemic attack. 300
1. ISCHEMIC DISEASES
 Ischemic stroke accounts for approximately 85% of acute
cerebrovascular events.
 The circle of willis provides extensive collateral circulation, as it
connects the right & left carotid arteries to each other and each to the
vertebra-basilar system.
 Patients with complete occlusion of the carotid artery:
 Proximal to the circle of willis may be asymptomatic; due to
contralateral carotid and the basilar artery.
 Distal to the circle of willis generally results in a stroke in the
territory supplied by that particular artery.
1. ISCHEMIC DISEASES…
 Neurologic deficit from occlusive disease may be temporary or
permanent.
 A patient with permanent deficit has had a completed stroke.
 A patient with sudden-onset focal neurologic deficit that resolves within
24 hours has had a transient ischemic attack.
 Cause of ischemic stroke:
A. Thrombotic disease
B. Embolic disease
A. Thrombotic Disease
 The most common area of neurologically significant vessel thrombosis
is the carotid artery in the neck; occurs at the carotid bifurcation.
 Thrombosis of a carotid artery chronically narrowed by atheroma can
lead to acute carotid occlusion; this can be asymptomatic.
 The more common concern is thrombo-embolus.
 Intracranial arterial occlusion by local thrombus formation may occur,
but it is rare compared to embolic occlusion.

A. Thrombotic Disease …
 MANAGEMENT:
 Complete occlusion of the carotid artery without referable neurologic
deficit requires no treatment.
 A patient with new neurologic deficit and an angiographically
confirmed complete carotid occlusion contralateral to the symptoms
should be considered for emergent carotid endarterectomy; within 2
hours of symptom onset.

B. Embolic Disease
 Emboli causing strokes may originate from a No. of sources, including:
 left atrium in atrial fibrillation,
 Hypokinetic left ventricular wall segment,
 Valvular vegetations,
 Atheromatous aortic arch,
 Stenotic/atheromatous carotid bifurcations, or
 Systemic venous system in right to left shunt, such as a patent foramen ovale.
The majority of emboli enter the anterior (carotid) circulation rather
than the posterior (vertebrobasilar) circulation.
B. Embolic Disease…
 MANAGEMENT:
 Ischemic stroke management has two goals:
1. Reopen occluded vessel &
2. Maintain blood flow to ischemic “penumbra” tissues bordering the
vascular territory; with recombinant tPA.
 tPA within 3hrs of the onset of neurologic deficit improves outcome in 3 mths.
 Contraindications to tPA therapy:
 Intracranial hemorrhage,
 Major surgery within the previous 2 weeks,
 GI or genitourinary hemorrhage in the previous 3 weeks,
 Platelet count less than 100,000/μL, and
 Systolic
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B. Embolic Disease…
 MANAGEMENT…
 Systolic blood pressure >180 mmHg may require treatment, but the
optimal mean arterial pressure goal is between 100 to 140 mmHg.
 Give normal saline solution without glucose (which could injure neurons in the
penumbra), and aim for normovolemia.
 Significant swelling from an MCA or cerebellar strokes may cause
herniation and brain stem injury.
 A decompressive hemicraniectomy or suboccipital craniectomy can be a
life-saving intervention for these select stroke patients.
2. HEMORRHAGIC DISEASES
 Intracranial/intraparenchymal hemorrhage from abnormal or diseased
vascular structures accounts for approximately 15% of acute
cerebrovascular events.
 Causes for intra-parenchymal hemorrhage :
1. Hypertension – common
2. Amyloid angiopathy - common
3. AVMs, aneurysms, venous thrombosis, tumors, hemorrhagic conversion of
ischemic infarct, and fungal infections also may be the cause.

2. HEMORRHAGIC DISEASES …
 Intracranial hemorrhage causes local neuronal injury and dysfunction
and also may cause global dysfunction due to mass effect.
 AVM/aneurysm rupture SAH immediate concussive-like neuronal dysfunction.
 Hemorrhagic stroke typically occurs within the basal ganglia or cerebellum.
 The patient is usually hypertensive on admission and has a history of
poorly controlled hypertension.
 Such patients are more likely to present with lethargy or obtundation,
compared to those who suffer an ischemic stroke.

 Depressed mental status results from brain shift and herniation
secondary to mass effect from the hematoma in deep structures.
 Ischemic stroke does not cause mass effect acutely; and therefore,
patients are more likely to present with normal consciousness and a
focal neurologic deficit.
 Hemorrhagic strokes tend to present with a relatively gradual decline in
neurologic function as the hematoma expands, rather than the
immediately maximal symptoms caused by ischemic stroke.
A. Hypertension:
 It increases the relative risk of intracranial hemorrhage by
approximately 4X, likely due to chronic degenerative vasculopathy.
 Hypertensive hemorrhages often present in the basal ganglia, thalamus,
or pons, and result from breakage of small perforating arteries.
 Most hypertensive hemorrhages should be medically managed.
 Medical management includes:
 Moderate BP control, normalizing platelet &clotting function, phenytoin, & electrolyte mgnt.
 Intubate patients who cannot clearly follow commands to prevent aspiration & hypercarbia.
B. Amyloid Angiopathy.
 The presence of pathologic amyloid deposition in the media of small cortical
vessels compromises vessel integrity &tends to cause more superficial (lobar)
hemorrhages than hypertensive intracranial hemorrhage.
 Amyloid laden vessels may hemorrhage multiple times.
 The superficial location of amyloid hemorrhages may make surgical
evacuation less morbid compared to typical deep hypertensive
hemorrhages.
 Nonetheless, medical management and family counseling should be
approached similarly to patients with hypertensive hemorrhages




2.3. TUMORS OF THE CENTRAL NERVOUS SYSTEM
 TUMORS OF THE CENTRAL NERVOUS SYSTEM
 A wide variety of tumors affect the brain and spine.
1. Primary benign and malignant tumors arise from the various
elements of the CNS, including Neurons, Glia, and Meninges .
2. Tumors metastasize to the CNS from many primary sources.
 Presentation varies widely depending on relevant neuroanatomy.
 Prognosis depends on histology and anatomy.

2.3. TUMORS OF THE CENTRAL NERVOUS SYSTEM…
1. Intracranial tumors can cause brain injury from;
 Mass effect,
 Dysfunction or destruction of adjacent neural structures,
 Swelling, or
 Abnormal electrical activity (seizures).

1. Intracranial tumors …
 Supra-tentorial tumors commonly present with focal neurologic deficit,
such as:
 Contralateral limb weakness,
 Visual field deficit,
 Headache, or seizure.
 Infra-tentorial tumors often cause increased ICP due to:
 Hydrocephalus from compression of the fourth ventricle,
 Leading to headache, nausea, vomiting, or diplopia.
 Infratentorial tumors rarely cause seizures.
 Cerebellar hemisphere or brain stem dysfunction can result in ataxia,
nystagmus, or cranial nerve palsies.
 All patients with symptoms concerning for brain tumor should undergo
MRI with and without gadolinium.
 Initial management of a patient with a symptomatic brain tumor
generally includes:
 Dexamethasone for reduction of vasogenic edema and
 Phenytoin if the patient has seized.
 Patients with significant weakness, lethargy, or hydrocephalus should be
admitted for observation until definitive care is administered.
1. Primary Brain Tumours …
1. Gliomas (43%).
A. Astrocytomas: are the commonest type.
 They are usually malignant.
 Peak incidence is in 4th decade.
 Grades based on the quantity of adult and primitive cells.
 Grade I: Cystic , Grade II: Diffuse , Grade III: Anaplastic& Grade IV: Glioblastoma
multiforme; It is aggressive type of astrocytoma
B. Oligo-dendro-gliomas: are slow growing tumour; commonly arising from frontal
lobes, lasts for years; shows calcification.
C. Spongioblastoma polare:
D. Medulloblastoma: is highly malignant embryonal tumour, is PNETs.
E. Ependymomas:
1. Primary Brain Tumours …
2. Meningiomas (18%):
 They are usually globular, arising from the arachnoids.
 Meningiomas are classified as:
 Fibroblastic, endothelial and angioblastic.
 Sites
 Para-sagittal
 Fronto-basal
 Posterior fossa
 Choroid plexus
1. Primary brain tumours …
3. Schwannoma (8%): common in auditory nerve, also called as acoustic
neuroma.
• Occurs in the internal auditory meatus which projects into the cerebello-
pontine angle (c- pangle), compressing 5, 6, 7, 8th nerves.
• It presents with compressive features like unilateral deafness, trigeminal
neuralgia, squint, cerebellar compression syndrome.
4. Pituitary tumours (12%):
5. Craniopharyngiomas (5%):
6. Blood vessel tumours (2%):
2. Metastatic Tumors
 The sources of most cerebral metastases are (in decreasing frequency):
 lung, breast, kidney, GI tract, and melanoma.
 Lung and breast cancers account for >1/2 of cerebral metastases.
 Metastatic cells usually travel to the brain hematogenously and
frequently seed the gray-white junction.
 Other common locations are the cerebellum and the meninges.
 Meningeal involvement may result in carcinomatous meningitis, also
known as leptomeningeal carcinomatosis.

2. Metastatic Tumors …
 Management largely depends upon:
 The primary tumor, overall tumor burden, patient’s medical condition, and
location and number of metastases.
 Craniotomy plus whole-brain radiation therapy (WBRT) or stereotactic
radiosurgery (SRS) to the tumor bed has been shown to benefit;
 Patients with a single surgically accessible metastatic lesion, compared to
radiation therapy alone.

-
-
• Common surgical conditions of the head & neck (cleft lip and palate, diseases
of salivary glands)
• Case related to the topics in the week (brain tumour/ head and spinal
injuries)
• Simulated practice:
• Cardiopulmonary resuscitation
• Communication with a surgical patient with reduced or altered
consciousness
• Breaking bad news (communicating diseases with poor prognosis like
brain tumors) to a surgical patient and relatives

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Surgical diseases of the thyroid & parathyroid glands
 Steps involved in the synthesis of thyroid hormones
 Evaluation of Patients with Thyroid Disease
 Thyroid malignancies
 Benign Thyroid Disorders
 Malignant Thyroid Disease
 Case related to thyroid
 Simulated practice: Assessing a patient with neck mass (history
and physical examination)
STEPS INVOLVED IN THE SYNTHESIS OF THYROID HORMONES
1. Iodide trapping: from the blood into the thyrocyte is the first step in
the formation of T3 and T4.
 Thiocyanates and perchlorates block this step.
2. Oxidation: of iodide to inorganic iodine; catalyzed by thyroid
peroxidase (TPO)
 Blocked by: Thioamides; sulfonamide, para-amino-salicylic acid, carbimazole
& PTU.
3. Organification/Iodination of tyrosine residues on Tg; catalyzed by TPO.
 Iodine + Tyrosine = MIT (monoiodotyrosine) and diiodotyrosine (DIT)
 This step is inhibited by thiourea group of drugs, i.e. carbimazole.
Steps involved in the synthesis of thyroid hormones…
4. Coupling reactions
 Coupling of two molecules of DIT results T4 and
 Coupling one molecule of DIT with one molecule MIT results T3.
 This stage is blocked by carbimazole.
5. Hydrolysis:
 The hormones combine with globulin to form a colloid thyroglobulin (Tg).
 Tg are stored in the thyroid gland & released by process of hydrolysis.
 Tg is hydrolyzed to release free iodothyronines (T3 and T4); mono & di-
iodotyrosines.
6. Deiodination: mono- and di iodotyrosines are deiodinated to yield iodide, which
is reused in the thyrocyte.
Evaluation of Patients with Thyroid Disease
1. Thyroid Function Test: Lab investigation/studies
2. Thyroid gland imaging
3. Thyroid gland pathology
4. Thyroid gland examination

1. Thyroid Function Test: Lab investigation
1.1. Serum Thyroid-Stimulating Hormone (TSH)
1.2. Total T4
1.3. Total T3
1.4. Free T4
1.5. Free T3

1. Thyroid Function Test: Lab investigation
1.1. Serum Thyroid-Stimulating Hormone (TSH): Normal: 0.5–5 μU/mL
 TSH is secreted from anterior pituitary; its secretion is inversely related
to circulating thyroid hormones.
 It reflect the ability of the anterior pituitary to detect free T4 levels.
 Inverse relationship free T4 level & logarithm of the TSH conc.
 Small changes in free T4 lead to a large shift in TSH levels.
 TSH is the only test necessary in most patients with thyroid nodules that
clinically appear to be euthyroid.
Evaluation of Patients with Thyroid Disease …
1.1. TSH …
 The ultrasensitive TSH assay has become the most sensitive and specific
test for:
 Diagnosis of hyper- and hypothyroidism and
 Optimizing T4 therapy.

1.2. Total T4 (Reference Range 55–150 nmol/L)
 Total T4 levels are measured by radioimmunoassay and measure both
the free and bound components of the hormones.
 Total T4 levels reflect the output from the thyroid gland,
 Total T4 levels are increased not only in hyperthyroid patients,
 but also in those with elevated Tg levels secondary to?
 pregnancy, estrogen/progesterone use, or congenital diseases.

1.2. Total T4 …
 Total T4 levels decrease in hypothyroidism and in patients with
decreased Tg levels due to:
 Anabolic steroid use and protein-losing disorders like nephrotic syndrome.
 Individuals with these latter disorders may be euthyroid if their free T4
levels are normal.

1.3. Total T3 (Reference Range 1.5–3.5 nmol/L).
 Total T3 levels are measured by radioimmunoassay and measure both
the free and bound components of the hormones.
 Total T3 levels reflects in the non-stimulated thyroid gland are more
indicative of peripheral thyroid hormone metabolism, and are,
therefore, not generally suitable as a general screening test.
 80% of T3 is from deiodination of T4 at periphery in liver, muscle,
kidney and pituitary.
1.3. Total T3…
 T3 is 3- 4 times more potent than T4.
 The half-life of T3 is approximately 24 hours, whereas half-life of T4
is about 7 days
 Measurement of total T3 levels is important in clinically hyperthyroid
patients with normal T4 levels, who may have T3 thyrotoxicosis.
 Total T3 levels often are increased in early hypothyroidism.

1.4. Free T4 (Reference Range 12–28 pmol/L)
 These radioimmunoassay-based tests are a sensitive and accurate
measurement of biologically active thyroid hormone.
 Free T4 estimates are not performed as a routine screening tool in
thyroid disease.
 Use of this test is confined to cases of early hyperthyroidism in which
total T4 levels may be normal but free T4 levels are raised.
 In patients with end-organ resistance to T4 (Refetoff’s syndrome), T4
levels are increased, but TSH levels usually are normal.
1.4. Free T4 …
 Free T4 levels may also be measured indirectly using the T3-resin
uptake test.
 If free T4 levels are increased, fewer hormone binding sites are
available for binding radiolabeled T3 that has been added to the
patient’s serum.
 Therefore, more T3 binds with an ion-exchange resin, and the T3-resin
uptake is increased
1.5. Free T3 (3–9 pmol/L)
 Free T3 is most useful in confirming the diagnosis of early
hyperthyroidism, in which levels of free T4 and free T3 rise before total
T4 and T3.
 It is the best single test in assessing hyperthyroidism.

Thyrotropin-Releasing Hormone:
 This test is useful to evaluate pituitary TSH secretory function.
 is performed by administering 500μg of TRH intravenously and
measuring TSH levels after 30 and 60 minutes.
 In a normal individual, TSH levels should increase at least 6 μIU/mL from
the baseline.
 This test also was previously used to assess patients with borderline
hyperthyroidism but has largely been replaced by sensitive TSH assays.
Thyroid Antibodies:
 Thyroid antibodies include:
 Anti-Tg,
 Anti-microsomal, or
 Anti-TPO and
 Thyroid-stimulating immunoglobulin (TSI).
 Anti-Tg & anti-TPO antibody levels don’t determine thyroid function, but
rather indicate the underlying disorder, usually an autoimmune thyroiditis
 80% of pts with Hashimoto’s thyroiditis have elevated thyroid antibody
levels
 However, levels may also be increased in patients with Graves’ disease,
multinodular goiter, and occasionally, thyroid neoplasms.
Serum Thyroglobulin (Tg): Normal value is 0.5–50 µg/L
 Tg is only made by normal or abnormal thyroid tissue.
 It normally is not released into the circulation in large amounts but
increases dramatically in destructive processes of the thyroid gland, such
as:
 Thyroiditis, or
 Overactive states such as Graves’ disease and
 Toxic-multinodular goiter.
Serum Thyroglobulin (Tg)…
 The most important use for serum Tg levels is in monitoring patients with
differentiated thyroid cancer for recurrence, particularly after total
thyroidectomy and RAI ablation.
 Elevated anti-Tg antibodies can interfere with the accuracy of serum Tg
levels and should always be measured when interpreting Tg levels.

Serum Calcitonin (0–4 pg/mL Basal)
 This 32-amino-acid polypeptide is secreted by the C cells and
 Functions to lower serum calcium levels, although in humans, it has only
minimal physiologic effects.
 It is also a sensitive marker of MTC.

2. Thyroid Imaging
2.1. Radio-nuclide imaging:
 Both iodine123 & iodine131are used to image thyroid gland.
 Iodine123 (123I):
Emits low dose radiation; 30 mrad; (γ-rays are used)
Has a half-life of 12 to 14 hours, and
Is used to (Dx.); image lingual thyroids or goiters (retrostemal).
 Iodine131( 131I) :
Leads to higher-dose radiation exposure; 500 mrad; (β-rays are used).
Has a half-life of 8 to 10 days
Is used to screen and treat patients with differentiated thyroid cancers for
metastatic
5/16/2020 disease (bony metastasis).
Gizachew Assefa 345
2.1. Radionuclide imaging …
 The images obtained by these studies provide information:
1. The size and shape of the gland, and
2. The distribution of functional activity of the gland.

 Based on radioactivity/ radioisotope study of glands:
1. Cold: is non-functioning nodule;
 Nodule will not take up isotope (under-active) than the surrounding gland.
 It is 80% common; of which risk of malignancy is 20% in cold lesions.
2. Warm: is normally functioning nodule.
 Nodule and surrounding normal thyroid will take up the isotope (active).
 It is 10% common of which 5% can be malignant.
3. Hot: Means autonomous toxic nodule; Nodule is overactive.
 Normal surrounding thyroid tissue is inactive and so will not take up isotope.
 It is 5% common of which only 5% can be risk malignant.
 Technetium Tc 99m pertechnetate:
 Advantage: having a shorter half-life and minimizes radiation exposure.
 It is particularly sensitive for nodal metastases.
 Positron emission tomography (PET) combined with computed tomography (CT):
 Used to screen for metastases in patients with thyroid cancer for other imaging
studies are negative.
 PET scans: are not routinely used; however, they may show clinically
occult thyroid lesions.
2.2. Ultrasound:
 It is an excellent noninvasive & portable imaging study of the thyroid;
 Advantage of no radiation exposure.
 It is helpful in the evaluation of thyroid nodules,
 Distinguishing solid from cystic ones, and
 Providing information about size and multicentricity.
 Best for un-palpable lateral nodules.
 Ultrasound is also especially helpful for assessing cervical
lymphadenopathy and to guide FNAB (USG-FNAC).
2.2. Ultrasound …
 In addition, characteristics such as:
 Echo-texture,
 Shape,
 Borders and Can provide useful information
 Presence of calcifications, and regarding risk of malignancy.
 Vascularity
Hyper echoic imaging Hypo echoic imaging
 Benign  Malignant
 Well defined border  Poorly defined border
 Cystic  Heterogenic
 Halo around nodule  Micro calcifications
5/16/2020 Gizachew Assefa
 High vascularity 350
2.3. Computed Tomography/Magnetic Resonance Imaging
 Scan CT and MRI studies provide excellent imaging of the thyroid gland
and adjacent nodes and
 Are particularly useful in evaluating:
 The extent of large, fixed, or substernal goiters (which cannot be
evaluated by ultrasound) and
 Their relationship to the airway and vascular structures.

 Best for to check metastasis.
2.3. Computed Tomography/Magnetic Resonance Imaging…
 Non-contrast CT scans should be obtained for patients who are likely to
require subsequent RAI therapy.
 If contrast is necessary, therapy needs to be delayed by several months.
 Combined PET-CT scans are increasingly being used for Tg-positive, RAI-
negative tumors.

2.4. Radiography /X-ray
 Chest and thoracic X-ray.
 Look:
 Retro-sternal goiter.
 Tracheal deviation and compression.
 Pulmonary metastasis.

3.Thyroid gland pathology
A. FNAC: is the investigation of choice in discrete thyroid swellings.
 Reliable:
 Non reliable:
1. Papillary carcinoma
1. Follicular adenoma and Follicular carcinoma
2. Medullary carcinoma
2. Hurthle cell carcinoma: B/c vascular & capsular invasion.
3. Anaplastic carcinoma
3. Hashimotos thyroiditis VS thyroid lymphoma.
B. Biopsy:
 Core needle biopsy: does not tell benign VS malignancy.
 Incisional biopsy: for advanced biopsy.
 Excisional biopsy: for treatment.
 Fine-needle aspiration biopsies are now classified into six groups
based on the risk of malignancy (Bethesda criteria).
1. Thy1: Non-diagnostic
2. Thy1c: Non-diagnostic cystic
3. Thy2: Non-neoplastic
4. Thy3: Follicular
5. Thy4: Suspicious of malignancy
6. Thy5: Malignant

4. Thyroid gland examination
COMPLAINTS - HISTORY TAKING
1. Swelling:
 Long duration of thyroid swelling indicates:
 Benign condition, e.g. Multinodular goitre (MNG), colloid goitre.
 Short duration with rapid growth indicates:
 Malignancy such as: anaplastic carcinoma.
 Majority of thyroid swellings do not produce pain.

COMPLAINTS-HISTORY TAKING …
2. Rate of growth:
 Usually slow-growing in benign disease.
 If it is a rapid growth, it can be 'de novo' malignancy or malignancy
developing in a benign lesion, e.g. follicular carcinoma in MNG.
 Sudden increase in the size of swelling with pain indicates haemorrhage
in the MNG (multinodular goitre).

3. Dyspnoea:
 Difficulty in breathing in a patient with goiter can be due to:
 Small goitre, rapid growth - anaplastic carcinoma infiltrating the trachea.
 When lower border is not seen, is called retrostemal goitre.
 Hyperthyroidism causing arrhythmias leading to congestive cardiac
failure can cause dyspnoea and orthopnoea.
 Long-standing MNG compresses on the tracheal cartilages and
produces pressure atrophy of tracheal cartilages.
 This is called trachea-malacia.
4. Dysphagia:
 is relatively uncommon because oesophagus is a posterior structure.
5. Hoarseness of voice indicates malignancy.

 It always occurs in carcinoma thyroid infiltrating the recurrent
laryngeal nerve (never in benign diseases of thyroid).

6. Toxic features suggestive of hyperthyroidism:
A. CNS symptoms are predominantly seen in Graves‘ disease.
 Tremors of the hand
 Sweating
 Intolerance to heat
 Preference to cold
 Excitability
 Irritability
 Prominent eyes are observed by other persons.
 Double vision, oedema of the conjunctiva can be the presenting
complaints in late cases.
6. Toxic features suggestive of hyperthyroidism …
B. Cardiovascular symptoms are predominantly seen in 2ndry thyrotoxicosis.
 Even though both forms of thyrotoxicosis produce palpitations,
 It is a significant complaint in multinodular goitre with thyrotoxicosis (2ndry)
 Late manifestations of secondary thyrotoxicosis:
 Precordial chest pain and
 Dyspnoea on exertion.
Summary of history taking

EXAMINATION ON THYROID GLAND
1. Inspection
 S: Site/location/ of the swelling: in front of the neck, or lateral.
 Extending from one sternomastoid to the other sternomastoid
 Vertically from supra-stemal notch to the thyroid cartilage.
 S: Size of goiter/thyroid ; eg.10x 5cm
 S: Shape of goiter/thyroid; Butterfly
 S: Surface:
A. Smooth: Adenoma, Puberty goitre, Graves' disease
B. Irregular: Carcinoma of the thyroid
C. Nodular: Multinodular thyroid
 S: skin color change, scar, or opening.
1. Inspection…
 Borders: are usually round.
 Pulsation: Visible or not with eye.
 Protrusion: Movement on protrusion of the tongue suggests thyroglossal cyst.
 This test should be done when there is a nodule or a cyst in the region of
isthmus of the thyroid gland.
 This test has no relevance in cases of MNG or other thyroid swellings.

1. Inspection…
 Deglutition test: Swelling moves up with deglutition due to:
 Thyroid is enclosed by pretracheal fascia which is condensed to form
a ligament posteromedially called ligament of Berry.

1. Inspection…
 Deglutition test: Swelling may not moves up with deglutition :
 Restriction of movement, can be due to:
1. Malignancy with fixity to the trachea
2. Retro-stemal goiter Swelling may not moves up with deglutition:
3. Large goitre because of the size 1. Anaplastic carcinoma of thyroid
4. Previous surgery 2. Thyroid cancer with local infiltration
3. Retro-sternal extension with
infiltration
4. Riedel’s thyroiditis
5. Massive thyroid
5/16/2020 6. Lipoma
Gizachew Assefa 366
1. Inspection…
 Pemberton’s sign:
 Patient is asked to raise both the arms above the shoulder so as to touch the
ears and asked to keep like that for 1- 3 minutes.
 Patient will develop dilated veins and cyanosis in the neck & upper chest wall,
puffiness in face, respiratory distress and rarely dysphagia.
 It means sign is positive signifying retrosternal extension of goiter.
 Pizzillo’s method of inspection:
 Is done in obese short necked individuals by pushing the head backwards
against clasped hands placed over the occiput with head extended.
 Thyroid gland becomes more prominent.
2. Palpation
 Is done from behind with the patient sitting and flexing the neck.
 Both thumbs of the examiner are placed over the back of the neck and
fingers of each hand are placed on the respective lateral lobes.
 S: Size:
 S: Shape:
 S: Surface:
A. Smooth
B. Nodular
 Very large nodular surface is described as bosselated surface.
2. Palpation ...
 B: Border:
A. Regular
B. Irregular
 C: Consistency:
 Soft: Graves' disease, colloid goitre.
 Firm: Adenoma, multinodular goitre.
 Hard: Carcinoma, Calcification in the MNG.
?Paradox:
1. Adenoma of thyroid: Soft
2. Cyst of thyroid : Firm
2. Palpation ...
 T: Thrill/bruit: on upper lobe of the gland; 10 toxic goiter.
 T: Temprature: Local rise of temperature is a feature of toxic goitres.
 T: Tenderness:
 D: Deglutition test:
 Confirm the movement with deglutition by holding the thyroid gland.
 M: Mobility of the gland :
 Intrinsic mobility of the gland is very much restricted in carcinoma
because of infiltration into the trachea.
2. Palpation ...
 T: Position of trachea:
 Central: in cases of multinodular goitres, trachea need not be
deviated because of symmetrical enlargement of both lobes.
 Deviated: In cases of solitary nodule confined to one lobe, trachea is
deviated to the opposite side
 LN: Palpation of lymph nodes in the neck.
 If lymph nodes are significant, it indicates papillary carcinoma of the
thyroid.
2. Palpation ...
 CCA: Palpation of common carotid artery:
 Draw a line from mastoid process to sterno-clavicular joint.
 Then draw a horizontal line from upper border of thyroid cartilage.
 The point where these two lines meet is the site of bifurcation of
common carotid artery.
 This artery should be palpated just below this point

2. Palpation ...
 CCA: Palpation of common carotid artery…
 Large multinodular goitres, the artery may be pushed laterally.
 Hence, pulsations are felt in the posterior triangle.
 Carcinoma of the thyroid engulfs the carotid sheath.
 Consequently, pulsations may be absent.
 Absent carotid artery pulsation is called Berry sign positive.

2. Palpation ...
 SMCT: Sterno-mastoid contraction test:
 Is done when only one lobe is enlarged.
In this situation the examiner keeps the hand on the side of the chin,
opposite the side of the lesion and
 asks the patient to push his hand against resistance.
 If the gland becomes less prominent; is indicates the swelling is deep to
the sterno-mastoid muscle.
2. Palpation ...
 CT: Chin test (neck fixation/flextion test):
 Is classically done in multi-nodular goitre, where in both lobes are
enlarged.
The patient is asked to bend the chin downwards against resistance.
This produces contraction of both sterno-mastoids and strap muscles
and the gland becomes less prominent.

2. Palpation ...
 Special tests or methods of examination of thyroid gland: CLPK
1. Crile's method:
 is indicated when there is a doubtful nodule.
Keep the thumb over the suspected area of the nodule and ask the
patient to swallow.
The nodularity is appreciated better with this test.

2. Palpation ...
2. Lahey's method :
 Can be done from front as well as behind.
In order to palpate the right lobe, push the gland to the right side and
feel the nodules in the postero-medial aspect of the gland.
The lobe becomes more prominent & thus nodules are appreciated better.

2. Palpation ...
3. Pizzillo's method:
 Is indicated in obese patients especially short necked individuals.
The patient is asked to clasp her hands and press against her/his occiput
with head extended.
Thyroid gland becomes more prominent and thus, palpation becomes better.

2. Palpation ...
4. Kocher's test:
If gentle compression on lateral lobes produces stridor, it is described as
Kocher's test positive.
 This is due to scabbard trachea.
 Long-standing multinodular goitres causing tracheomalacia and
 Carcinoma with infiltration into trachea
May give rise to stridor.
3. Percussion:
 Percussion over the sternum gives a resonant note in normal cases.
 In retrosternal goitres, it gives a dull note.
4. Auscultation:
 It should be done in the upper pole due to:
 Superior thyroid artery is a direct branch of external carotid artery.
 It is more superficial than inferior thyroid artery.
 Presence of thrill and bruit are the features of toxic goiter.
 After thyroid examination look for by Systemic examination:
1. Sign of thyrotoxicosis Do Systemic examination
2. Sign of hypothyroidism 1. CNS and eye signs: in Graves' disease,
Deep tendon reflexes : a slow relaxation
3. Sign of Myxoedema
phase in hypothyroidism..
4. Sign of Retro-sternal extension 2. Skeletal system: to rule out metastasis as in
5. Sign of Metastasis carcinoma of the thyroid.
3. Cardiovascular system: in cases of toxic goitre.

1. Sign of thyrotoxicosis

GOITER
 Goiter is enlargement of thyroid gland.
 WHO grading of goiter:
1. Grade 0: No visible or no palpable goiter.
2. Grade1: Palpable thyroid/goiter but not visible in normal positioned neck.
 1A: Palpable only.
 1B: Palpable and visible in extended neck.
 Grade 2: Goiter which is visible in normal positioned neck.
 Grade 3: Large goiter.

CLASSIFICATION OF GOITER
I. Simple non toxic goiter
1. Diffuse hyperplastic:
A. Physiological
1. Puberty.
2. Pregnancy.
B. Primary iodine deficiency (Endemic; dietary iodine intake < 100 µg/day).
C. Secondary iodine deficiency:
1. Goitrogens: Cabbage (contains thiocyanates), soya bean, cassava.
2. Excess dietary fluoride.
3. Drugs: PAS & sulfonamides, cause goiter by preventing oxidation of iodide
to iodine. lithium, anti-thyroid drugs, radioactive iodine, amiodarone.
4. Dys-hormone-genetic goiter: inborn errors of metabolism
2. Colloid goiter:
3. Multi-nodular goiter
CLASSIFICATION OF GOITER…
II. Toxic goiter:
1. Diffuse (Primary):- Graves’ disease.
2. Multi-nodular (Secondary thyrotoxicosis):- Plummer’s disease.
3. Toxic nodule (solitary) (Tertiary thyrotoxicosis).

III. Neoplastic goiter:
1. Benign:
 Adenomas: follicular, Hurthle cell.
2. Malignant:
 Carcinomas:
1. Papillary
2. Follicular
3. Medullary
4. Anaplastic
 Lymphomas:
III. Neoplastic goiter…
Benign Follicular
adenoma
Malignant Primary Follicular epithelium – Well differentiated Follicular & Papillary Ca.
Follicular epithelium – Poorly differentiated Anaplastic Ca.
Arising from Para-follicular cells Medullary Ca.
Arising from Lymphoid cells Non-Hodgkin's
Lymphoma.
Secondary Metastatic: from other site due to blood  Malignant melanoma,
spread  Renal cell carcinoma,
 Breast carcinoma
 Lung cell carcinoma
Local infiltration
CLASSIFICATION OF GOITER …
IV. Inflammatory
1. Autoimmune thyroiditis:
 Chronic lymphocytic thyroiditis
 Hashimoto’s disease
2. Granulomatous thyroiditis: De Quervian’s thyroiditis
3. Fibrosing: Riedel's thyroiditis.
4. Infective:
 Acute thyroiditis : Bacterial thyroiditis, Viral thyroiditis,
 Sub-acute thyroiditis
 Chronic thyroiditis: Tuberculous, Syphilitic
V. Other: Amyloid goitres
1. SIMPLE NON -TOXIC GOITER
 Diffuse hyperplastic goiter: Initial persistent increase in TSH level causes
diffuse active lobules.
 Colloid goiter: In late stages of diffuse hyperplasia, TSH stimulation

decreases and Many follicles become inactive, get filled with colloid & is
called colloid goiter.
 is a goiter due to long-standing iodine deficiency with localized
accumulation of significant colloid in the gland.
1. SIMPLE NON -TOXIC GOITER …
MULTINODULAR GOITRE (MNG)
 MNG is discordant growth with functionally and structurally altered
thyroid follicles presenting as multiple nodules in thyroid.
 It may be due to mainly fluctuation in TSH level; other causes may be
iodine deficiency, goitrogens, hereditary, dyshormonogenesis.
 Stages of multi-nodular goiter formation
1. Stage of hyperplasia and hypertrophy
2. Stage of fluctuation in TSH
3. 5/16/2020
Stage of formation of nodules (inactive);
Gizachew Assefa (inter-nodular tissues are active)
390
 Clinical Features of multi-nodular goiter/MNG.
 More common in middle aged females (M:F;10:1).
 It is a slowly progressive disease with many years of history.
 Multiple nodules of different sizes are formed, which is smooth,
usually firm, nodular, non-tender/pain less, moves with deglutition.
 Recent increase in size signifies malignant transformation/haemorrhage.
 Positive Kocher’s test is due to long-standing MNG.
 Nodule when calcified becomes harder; necrosis softens the nodule.
 Complications of MNG
 10-30%, Secondary thyrotoxicosis with CVS involvement; Toxic multi-
nodular goitre is also called Plummer's disease
Tachycardia can be graded as follows-Crile's grading
1. Grade I < 90/min: mild
2. Grade II 90 to 10O/min: moderate
3. Grade Ill > 110/min: severe
 Follicular carcinoma of thyroid (8-10%)

 Hemorrhage in a nodule
 Tracheal obstruction, calcification
 Cosmetic problem
II. Toxic goiter:
 Hyperthyroidism:
 The clinical manifestations are due to an excess circulating thyroid hormone.
 It is important to distinguish disorders such as Graves’ disease and toxic nodular
goiters that result from increased production of thyroid hormone.
 Increase in RAI uptake (RAIU) and
 From those disorders that lead to a release of stored hormone from injury to the
thyroid gland (thyroiditis) or from other non-thyroid gland–related conditions.
 Low in RAI uptake (RAIU)
 These are most relevant to the surgeon:
1. Diffuse (Primary thyrotoxicosis):- Graves’ disease.
2. Multi-nodular (Secondary thyrotoxicosis):- Plummer’s disease.
3. Toxic nodule (solitary) (Tertiary thyrotoxicosis).
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II. Toxic goiter…

1. Diffuse Toxic Goiter (Graves’ Disease):
 Graves’ disease, a diffuse vascular goiter appearing at the same time
as hyperthyroidism,
 Usually occurs in younger women & frequently associated with eye signs.
 Symptoms, signs and swelling appear simultaneously.
 The whole of the functioning thyroid tissue is involved, and the
hypertrophy and hyperplasia are due to:
 Abnormal TSH-RAb that bind to TSH receptor sites and produce a
disproportionate and prolonged effect.

1. Graves’ Disease…
 It is the most common cause of hyperthyroidism in North America, 60-80% of cases.
 The syndrome is primary thyrotoxicosis; 50% of patients have a family history of
autoimmune endocrine diseases.
 Female preponderance (5:1), & peak incidence between the ages of 40 & 60 yrs.
 Graves’ disease is characterized by:
 Thyrotoxicosis,
 Diffuse goiter, and
 Extra-thyroidal conditions include: Ophthalmo-pathy, Dermo-pathy(pretibial myxedema)
 Thyroid acropachy,
 Gynecomastia, and other manifestations
 Etiology, Pathogenesis, & Pathology.
 The exact etiology of initiation to autoimmune process is not known.
 Conditions which have been suggested as a possible triggers are:
1. Postpartum state,
2. Iodine excess,
3. Lithium therapy, and
4. Bacterial and viral infections
5. Genetic factors also play a role, associated with certain human leukocyte antigen.

 Etiology, Pathogenesis, & Pathology…
 Thyroid stimulating antibodies stimulate thyrocytes to grow & synthesize
excess thyroid hormone, which is a hallmark of Graves’disease
 It also associated with other autoimmune conditions such as:
 Type 1 DM, Addison’s disease, pernicious anemia, and myasthenia gravis.
 Macroscopically: diffusely & smoothly enlarged, increase vascularity.
 Microscopically: is hyperplastic & epithelium is columnar with minimal colloid

 FEATURES OF GRAVES' DISEASE
 F: Female with strong family predisposition
 E: Extra-thyroidal manifestations
 M: Middle or young age (20 to 40 years)
 A: Autoimmune mechanism
 L: Leukocyte antigen human (HLA) and T-lymphocyte antigen may contribute.
 E: Enlargement of gland is diffuse
Remember as FEMALE

 Clinical Features:
 Can be divided into related to hyperthyroidism & specific to Graves’disease.
 Hyperthyroid symptoms:  Se adrenergic stimulation symptoms

Heat intolerance, Palpitations,
Nervousness,
Increased sweating and thirst,
Fatigue,
Weight loss despite adequate
Emotional lability,
caloric intake.
Hyperkinesis, and tremors.

 Clinical Features…
 The most common GI symptoms include:
 Increased frequency of bowel movements and diarrhea.
 Female patients: often develop: Amenorrhea, decreased fertility, and
an increased incidence of miscarriages.
Children: experience rapid growth with early bone maturation, whereas
 Older pts: may present with CVS complications such as AF & CHF.

 Signs of primary thyrotoxicosis
1. Signs of thyroid gland in Graves' disease.
2. Central nervous system (CNS) signs.
3. Cardiovascular system (CVS) signs.
4. Eye signs.
5. Thyro-toxic myo-pathy.
6. Thyro-toxic dermo-pathy.

1. Signs of thyroid gland in Graves' disease:
 Uniform, Diffusely and symmetrically enlarged, pyramidal lobe.
 Smooth surface- no nodules (treated cases may have nodularity)
 Gland is soft or firm in consistency
 It is warm - highly vascular.
 Auscultation: a bruit is usually heard.
 There may be an overlying bruit or thrill over the thyroid gland and
 A loud venous hum in the supra-clavicular space.
2. Central nervous system (CNS) signs:
 Fine tremor: Tremors of the tongue when the tongue is within the oral
cavity and tremors of the outstretched hands are characteristics.
 A piece of paper may be placed on the fingers in doubtful cases for
demonstrating the tremors of the hand.
 Extensor surface of the hand is used because extensors are weak when
compared to flexors.
 Hyperkinetic movements.
 Always a moist, warm hand (shake hands)

3. Cardiovascular system (CVS) signs:
 Tachycardia or atrial fibrillation/AF/ is present, with:
 Cutaneous vasodilation leading to a widening of the pulse pressure and
 A rapid falloff in the transmitted pulse wave (collapsing pulse).
 Palpitation & extra-systoles can also be found in primary thyrotoxicosis.
 Fibrillation and cardiac failure are rare.

4. Eye signs:
 50% pts of graves’disease develop clinically evident ophthalmo-pathy.
 The etiology of Graves’ ophthalmo-pathy is not completely known;
 However, orbital fibroblasts &muscles are thought to share a common antigen,TSH-R.
 Prominent eyeballs & retraction of eyelid result in thyro-toxic
exophthalmos; This is due to:
 Retro-bulbar deposition of inflammatory cells & round cells;
 With venous congestion resulting in oedema
 Levator palpebrae superioris muscle is innervated by oculo-motor nerve;
 Contraction of this muscle produces lid spasm.
 4. Eye signs: physical assessment
 True infiltrative eye disease results:
 Peri-orbital edema,
 Conjunctival swelling and congestion (chemosis),
 Proptosis,
 Limitation of upward and lateral gaze (from involvement of the
inferior and medial rectus muscles, respectively),
 Keratitis, and
 Even blindness due to optic nerve involvement.
4. Eye signs: physical assessment
1. von Graefe's sign (Lid lag sign):
 When the patient is asked to look up and down, upper eyelid
cannot cope up with the speed of movement of the finger because of
the lid spasm. Hence, the lid lags behind.
2. Dalrymple's sign (Lid retraction sign):
 Upper sclera is seen above the limbus (upper margin of the cornea
and conjunctiva).
4. Eye signs: physical assessment…
3. Naffziger's method:
 Stand behind the patient and look at the supra-ciliary arch, by tilting
the patient's head backwards.
 In normal cases, eyeball is not seen but in cases of exophthalmos,
eyeball is protruded outside & hence it is seen.
4. Joffroy's sign:
 Absence of wrinkling of the forehead when the patient is asked to
look upwards to ceiling.
 This occurs due to increase in the field of vision due to exophthalmos.
5. Moebius' sign:
 Loss convergence of eyeball occurs due to muscle paresis as a part of
thyro-toxic ophthalmo-plegia.
 Diplopia is due to weakness of extra-ocular muscles (inferior of
oblique elevators).
6. Stellwag's sign:
 Infrequent blinking and widening of palpebral fissure is due to spasm
of sympathetic fibers in the levator palpebrae superioris.

GRADING OF THYROID EYE DISEASES Eye signs only
 Resistance to retro-displacement of eye
Grade 0: No signs or symptoms  Oedema of conjunctiva and caruncle
 Lacrimal gland enlargement
Grade 1: Only signs, no symptoms  Injection of conjunctiva
 Oedema and fullness of lids
Grade 2: Both signs and symptoms /Soft tissue involvement

Grade 3: Proptosis/ more than 22 mm
Grade 4: Extra-ocular muscle involvement
Grade 5: Corneal involvement
Grade 6: Loss of vision with optic nerve atrophy
 6 Ps of graves‘ ophthalmo-pathy
1. Prominent eyes
2. Periorbital oedema
3. Papilloedema
4. Proptosis
5. Palpebral fissure widening
6. Progression to blindness
5. Thyro-toxic myo-pathy:
 Muscle wasting, and Proximal muscle group weakness with hyperactive
tendon reflexes often are present.
 Patient may admit difficulty in climbing steps.
 Weight loss and facial flushing may be evident.
 Mild weakness of ocular and frontal is muscles is not uncommon.
 Weakness of extra-ocular muscles results in double vision (diplopia).
 Features suggestive of myaesthenia gravis, periodic paralysis may found
 Gynecomastia is common in young men.
6. Thyro-toxic dermo-pathy:
 1% to 2% of patients develop dermo-pathy
 It is characterized by deposition of glycos-amino-glycans, leading to thickened
skin in the pretibial region and dorsum of the foot (Pretibial myxedema)
 Pretibial myxoedema (misnomer) is non-pitting in nature and may be
associated with;
 Clubbing of fingers and toes called thyroid acropachy.
 The skin is warm , moist; & african american pts. often darkening of skin.
 Responds to topical steroids and thyroid disorder treatment.
6. Thyro-toxic dermo-pathy…
EXTRATHYROIDAL MANIFESTATIONS PRETIBIAL MYXOEDEMA:
OF GRAVES' DISEASE A: Acropachy: Clubbing of fingers and toes
 Pretibial myxoedema C: Coarse hair
 Proximal myopathy R: Red shiny skin
 Pachy (acropachy) O: Obliteration of initial lymphatics by
 Progressive ophthalmoplegia mucin, oedema non-pitting.
P: Pretibial region, foot and ankle
SKIN CHANGES A: After a few years of toxicosis,it develops
 Pretibial myxoedema C: Cyanotic when cold
 Pruritis H: aluronic acid deposition
 Palmar erythema Y: in dermis-bilateral and symmetrical
 Thinning of hair  Remember as ACROPACHY
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Dupuytren's contracture Gizachew Assefa 415
 Diagnostic Tests:
 Suppressed TSH with or without an elevated free T4 or T3 level.
 Eye signs are present, other tests are generally not needed.
 RAI; 123I uptake and scan: In the absence of eye findings & an
elevated uptake, with a diffusely enlarged gland;
 Confirms the diagnosis of Graves’ disease and
 Helps to differentiate it from other causes of hyperthyroidism.
 Technetium scinti-graphy:
 While technetium scans results in low range of normal uptake and high
background activity.
 Diagnostic Tests…
 Free T4&T3: often elevated in early Graves’or toxic nodules/T3
toxicosis/
 Anti-(Tg&TPO) antibodies: elevated up to 75% of pts. but aren’t
specific
 Elevated TSH-R or thyroid-stimulating antibodies (TSAb) are
diagnostic of Graves’ disease &are increased about 90% of patients
 MRI scans of the orbits: useful in evaluating Graves’ ophthalmo-pathy.
 TREATMENT:
 Graves’ disease may be treated by any of three treatment modalities:
1. Anti-thyroid drugs: Propyl-thio-uracil (PTU) & Methimazole.
2. Thyroid ablation with radioactive 131I: RAI 131I.
3. Thyroidectomy:

 TREATMENT…
1. Anti-thyroid drugs:
 Administered in preparation for RAI ablation or surgery.
 Commonly used drugs are:
1. Propylthiouracil (PTU, 100 to 300 mg three times daily) and
2. Methimazole (10 to 30 mg three times daily, then once daily).
 Methimazole also has been associated with congenital aplasia;
therefore, PTU is preferred in pregnant and breastfeeding women.
 Side effects of treatment include:
 Reversible granulocytopenia, skin rashes, fever, peripheral neuritis, polyarteritis,
vasculitis, hepatitis, and, rarely, agranulocytosis and aplastic anemia.
 TREATMENT…
2. Radioactive Iodine Therapy (131I):
 RAI forms the mainstay of Graves’ disease treatment in North America.
 The major advantages of this treatment are the avoidance of a surgical
procedure and its concomitant risks.

 TREATMENT…
3. Surgical treatment:
 Surgery is recommended when RAI is contraindicated as in patients who:
1. Have confirmed cancer or suspicious thyroid nodules,
2. Young pts.,
3. Desire to conceive soon (<6 months) after treatment,
4. Have had severe reactions to anti-thyroid medications,
5. Have large goiters (>80 g) causing compressive symptoms, and
6. Reluctant to undergo RAI therapy.
 TREATMENT…
3. Surgical treatment…
 Relative indications for thyroidectomy include patients, particularly:
 Smokers, with moderate to severe graves’ ophthalmo-pathy,
 Who desiring rapid control of hyperthyroidism with chance of being euthyroid,
 Those demonstrating poor compliance to anti-thyroid medications.
 Pregnancy is also a relative contraindication, and
 Surgery should be used only when rapid control is needed and antithyroid
medications cannot be used.
 Surgery is best performed in the second trimester.
 Differences between primary and secondary thyrotoxicosis:

2.Toxic Multi-nodular Goiter /TMG/: secondary thyrotoxicosis:
 Toxic multi-nodular goiters usually occur in older individuals,
 Who often have a prior history of a nontoxic multi-nodular goiter.
 Some patients have T3 toxicosis, whereas others may present only with
atrial fibrillation or congestive heart failure.
 Hyperthyroidism also can be precipitated by iodide-containing drugs
such as contrast media and the antiarrhythmic agent amiodarone.
 Symptoms and signs of hyperthyroidism are similar to Graves’ disease,
but extrath-yroidal manifestations are absent.
2.TMG…
 Diagnostic Studies:
 Blood tests are similar to Graves’ disease with a suppressed TSH level
and elevated free T4 or T3 levels.
 RAI uptake also is increased;
 Showing multiple nodules with increased uptake and suppression of the
remaining gland.

2.TMG…
 TREATMENT:
1. RAI therapy: is reserved for elderly patients who represent very poor
operative risks;
 Provided if no airway compression and thyroid cancer is not a concern.
 Because uptake is less than in Graves’ disease, larger doses of RAI often are
needed to treat the hyperthyroidism.
 RAI-induced thyroiditis has the potential to cause swelling & acute airway
compromise; leaves the goiter intact, with possibility of recurrent hyperthyroidism.
2. Surgery: near-total or total thyroidectomy is recommended to avoid
recurrence and the consequent increased complication rates with
repeat surgery.

3.Toxic Adenoma
 Toxic Adenoma:
 Hyperthyroidism from a single hyper-functioning nodule typically occurs
in younger patients;
 Who note recent growth of a long-standing nodule along with the
symptoms of hyperthyroidism.
 Toxic adenomas are characterized by somatic mutations in TSH-R gene,
 although G-protein–stimulating gene (gsp) mutations may occur also.

3.Toxic Adenoma …
 Most hyper-functioning or autonomous thyroid nodules have attained a
size of at least 3 cm before hyperthyroidism occurs.
 Physical examination usually reveals a solitary thyroid nodule without
palpable thyroid tissue on the contralateral side.
 These nodules are rarely malignant.

3.Toxic Adenoma …
 Diagnostic Studies:
 RAI scanning shows a “hot” nodule with suppression of the rest of the
thyroid gland.

3.Toxic Adenoma …
 TREATMENT:
1. Anti-thyroid medications: for smaller nodules.
2. RAI: for smaller nodules also for larger nodules can require higher
doses, which can lead to hypothyroidism.
3. Surgery: lobectomy and isthmus-ectomy is preferred to treat young
patients and those with larger nodules.
4. Percutaneous ethanol injection: has been reported to have reasonable
success rates but has not been directly compared with surgery.
Thyroid storm
 Thyroid storm is a condition of hyperthyroidism accompanied by:
1. Fever,
2. Central nervous system agitation or depression,
3. Cardiovascular and
4. GI dysfunction, including hepatic failure.
 The condition may be precipitated by:
1. Abrupt cessation of anti-thyroid medications,
2. Infection,
3. Thyroid or non-thyroid surgery, and
4. Trauma in patients with untreated thyrotoxicosis.
Thyroid storm…
 Occasionally, thyroid storm may result from:
1. Amiodarone administration or
2. Exposure to iodinated contrast agents or
3. Following RAI therapy.

Thyroid storm…
 TREATMENT:
1. β-Blockers: are given;
 To reduce peripheral T4 to T3 conversion and
 Decrease the hyperthyroid symptoms.
2. Oxygen: supplementation and hemodynamic support.
3. Non-aspirin compounds: can be used to treat pyrexia.
4. Lugol’s iodine or sodium ipodate (IV) should be administered;
 To decrease iodine uptake and thyroid hormone secretion.
Thyroid storm…
 TREATMENT…
5. PTU therapy:
 Blocks the formation of new thyroid hormone and
 Reduces peripheral conversion of T4 to T3.
6. Corticosteroids often are helpful;
 To prevent adrenal exhaustion and
 To block hepatic thyroid hormone conversion.



Hypothyroidism
 Deficiency in circulating levels of thyroid hormone leads to
hypothyroidism and,
 In neonates, to cretinism, which is characterized by:
 Neurologic impairment and
 Mental retardation.
 Hypothyroidism also may occur in Pendred’s syndrome (associated with
sensory neural hearing loss
deafness) and Turner’s syndrome.

Hypothyroidism…

Hypothyroidism
 Clinical Features:
 Failure of thyroid gland development or function in utero leads to
cretinism and
 Characteristic facies similar to those of children with Down syndrome
and dwarfism.
 Failure to thrive and severe mental retardation often are present.
 Immediate testing and treatment with thyroid hormone at birth can
lessen the neurologic and intellectual deficits.
Hypothyroidism…
 C/F…
 Childhood or adolescence in hypothyroidism results in;
 Delayed development and
 May also lead to abdominal distention, umbilical hernia & rectal prolapse.
 Adults patients: symptoms in general are nonspecific, including:
 Tiredness, weight gain, cold intolerance, constipation, and menorrhagia.
 Patients with severe hypothyroidism or myxedema develop characteristic
facial features due to:
 Deposition of glycos-amino-glycans in the subcutaneous tissues; and
 Leading
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to facial and peri-orbitalGizachew
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Assefa 439
Hypothyroidism…
 C/F…
 Skin: becomes rough and dry and often develops a yellowish hue from
reduced conversion of carotene to vitamin A.
 Hair: becomes dry and brittle, and severe hair loss may occur.
 There is also a characteristic loss of the outer two thirds of the eyebrows.
 Tongue: enlarged tongue may impair speech, which is already slowed.
 Abdominal: Non-specific abdominal pain accompanied by;
 Distention and Constipation.
 Libido and fertility are impaired in both sexes.
Hypothyroidism…
 C/F…
 Cardiovascular changes include:
 Bradycardia,
 Cardiomegaly,
 Pericardial effusion,
 Reduced cardiac output, and
 Pulmonary effusions.
 When hypothyroidism occurs as a result of pituitary failure, other
features of hypopituitarism, such as:
 Pale, waxy skin;
 loss of body hair; and
 Atrophic genitalia, may be present.
Hypothyroidism…
 Laboratory Findings:
 T4 and T3 levels: Low circulating levels of T4 and T3.
 TSH Levels:
 Primary thyroid failure; raised TSH levels
 Secondary hypothyroidism; low TSH levels that do not increase
following TRH stimulation.

Hypothyroidism…
 Laboratory Findings…
 Thyroid autoantibodies are highest in patients with;
 Autoimmune disease (Hashimoto’s thyroiditis, Graves’ disease) and
 May also be elevated in patients with nodular goiter and thyroid
neoplasms.
 Electro-cardio-gram/ECG/ demonstrates:
 Decreased voltage with flattening or inversion of T waves.

Hypothyroidism…
 TREATMENT:
 T4 is the treatment of choice and is administered in dosages varying
from 50 to 200 μg/day, depending on the patient’s size and condition.
 The dose can be slowly increased wks to mths to attain euthyroid state.
 A baseline electrocardiogram should always be obtained in patients
with severe hypothyroidism before treatment.
 T4 dosage is titrated against clinical response and TSH levels, which
should return to normal.
Hypothyroidism…
 TREATMENT…
 The management of patients with sub-clinical hypothyroidism (normal T4,
slightly raised TSH) is controversial.
 Some evidence suggests that patients with subclinical hypothyroidism
and increased anti-thyroid antibody levels should be treated,
 Because they will subsequently develop hypothyroidism.
 Patients who present with myxedema coma may require initial
precipitates by:
- MI, STROKE, INFARCTION AND INFECTIONS
emergency treatment with large doses of IV T4(300 to 400 μg),

 With careful monitoring in an intensive care unit setting.
THYROID NEOPLASMS
1. Benign tumours:
 Follicular adenomas present as clinically solitary nodules and
 The distinction between a follicular carcinoma and F.adenoma can only
be made by histological examination;
 In the adenoma there is no invasion of the capsule or of pericapsular
blood vessels.
 For this reason, FNA, which provides cytologic detail but not tissue
architecture, cannot differentiate between benign and malignant
follicular lesions.
 Diagnosis and treatment is therefore, by wide excision, i.e. total
lobectomy.
THYROID NEOPLASMS…
1. Benign tumours…
 Follicular adenoma can be:
A. Colloid (do not have potential for micro-invasion; commonest type);
B. Fetal (micro-follicular – has potential for micro-invasion);
C. Embryonal (atypical – has potential for micro-invasion);
D. Hurthle cell/oxyphil or oncocytic (has potential for micro-invasion);
E. Hyalinising trabecular-adenoma.

THYROID NEOPLASMS…
2. Malignant (Dunhill classification)
A. Differentiated:
1. Papillary carcinoma (80%).
2. Follicular carcinoma (10%).
3. Papillo-follicular carcinoma behaves like papillary carcinoma
4. Hurthle cell carcinoma behaves like follicular carcinoma: 3%
B. Undifferentiated:
1. Anaplastic carcinoma: 1%
C. Medullary carcinoma: 5%
D. Malignant lymphoma: <1%
E. Secondaries in thyroid(rare): from kidney, breast, lung, melanoma.
1. Papillary Carcinoma:
 Papillary carcinoma accounts for 80% of all thyroid malignancies in
iodine-sufficient areas.
 Female-to-male ratio (2:1).
 Mean age at presentation is 30 to 40 years.
 Predominant in children and individuals exposed to external radiation.

1. Papillary Carcinoma…
 Ethiology :
1. Irradiation to the neck during childhood:
2. It can be a complication of Hashimoto's thyroiditis.
3. Papillary cancer of thyroid occurs more often in patients with
Cowden's syndrome, Gardner's syndrome or Camey'ssyndrome.
4. Associated mutations: Chromosomal translocation involving; RET
proto-oncogene (tyrosine kinase) chromosome 10q11.

 Clinical presentation:
 Most patients are euthyroid and
 Present with a slow-growing painless mass in the neck.
 Dysphagia, dyspnea, and dysphonia usually are associated with
locally advanced invasive disease.
 Lymph node metastases are common, especially in children and
young adults, and may be the presenting complaint.
 Very often, the LN in the lower deep cervical region are involved.
 Suspicion of thyroid cancer often originates through physical
examination of patients and a review of their history.
 Diagnosis is established by FNAB of the thyroid mass or lymph node.
 Once thyroid cancer is diagnosed on FNAB, a complete neck ultrasound
is strongly recommended to evaluate:
 Contralateral lobe and lymph node metastases in the central & lateral neck compartments.
 Distant metastases are uncommon at initial presentation, but may
develop up to 20% patients.
 The most common sites are lungs, followed by bone, liver, and brain.
 Prognostic Indicators.
 Patients with PTC have an excellent prognosis with >95% 10-year
survival rate.
 AMES scoring  Age (men <40 years, women <50 years old),
 Metastases,
 Extra-thyroidal spread, and
A: Age less than
Age less than 40 years- better prognosis
Sizeyears-
40 of tumors (< orprognosis
better >5 cm). *Schwartz;11
M: Distant metastasis- poor prognosis
E: Extent of tumour extra-capsular spread- poor prognosis
S: Size less than 4 cm - good prognosis
 Prognostic Indicators…
 AGES scoring USE: Age, histologic Grade, Extrathyroidal invasion, & metastases
& tumor Size to predict the risk of dying from papillary cancer.
A: Age less than 40 years - better prognosis
G: Grade of the tumour- high grade- poor prognosis
E: Extra-capsular spread- poor prognosis
S: Size less than 4 cm, good prognosis
 Low-risk patients are: High-risk patients are:
Young, Older,
With well-differentiated tumors, With poorly differentiated tumors
No metastases, and Local invasion, Distant metastases,
Small
5/16/2020 primary lesions, Gizachew Assefa Large primary lesions. 454
 Prognostic Indicators…
 The MACIS scale is a postoperative system modified from AGES scale.
 MACIS scoring
 M: distant Metastases
 A: Age at presentation (<40 or >40 years old),
 C: Completeness of original surgical resection
 I: extra-thyroidal Invasion
 S: Size of original lesion (in centimeters)
 Prognostic Indicators.
 A simplified system by DeGroot and associates uses four groups:
1. Class I (intra-thyroidal),
2. Class II (cervical nodal metastases),
3. Class III (extrat-hyroidal invasion), and
4. Class IV (distant metastases)—to determine prognosis.


 Key definitions:
 Primary tumor (T)
TX: Primary tumor cannot be assessed
T0: No evidence of primary tumor
T1: Tumor ≤2cm in diameter, in greatest dimension limited to thyroid
T2: Tumor 2-4cm in diameter, greatest dimension limited to thyroid
T3: Tumor >4cm, limited to thyroid or gross extra-thyroidal extension invade only strap muscles
T4: includes gross extra-thyroidal extension invade beyond strap muscles.
Regional LN:  Distant metastasis (M)

NX: Regional lymph nodes cannot be assessed M0: No distant metastases
N0: No evidence loco regional LN metastasis M1: distant metastasis
N1:5/16/2020
Metastasis to regional lymph node.
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 Management:
 Surgery: Based on the above, current guidelines for the evidence based
management of thyroid cancers recommend:
1. Near-total or total thyroidectomy for primary cancers >1 cm unless there are
contraindications to the surgery
2. Thyroid lobectomy alone is considered sufficient treatment for small (<1 cm),
incidentally discovered, low-risk, unifocal, intrathyroidal papillary carcinomas
in the absence of prior head and neck irradiation or radiologically or
clinically involved cervical nodal metastases.

2. Follicular Carcinoma
 Follicular carcinomas account for 10% of thyroid cancers and occur more
commonly in iodine-deficient areas.
 Female-to-male ratio of 3:1, and
 Mean age at presentation of 50 years old.
 Follicular cancers usually present as solitary thyroid nodules,
 Occasionally with a history of rapid size increase &long-standing goiter.
 Pain is uncommon, unless hemorrhage into the nodule has occurred.

2. Follicular Carcinoma …
 Unlike papillary cancers, cervical lymphadenopathy is uncommon at
initial presentation (5%), although distant metastases may be present.
 In <1% of cases, follicular cancers may be hyper-functioning, leading
patients to present with signs and symptoms of thyrotoxicosis.
 FNAB is unable to distinguish benign follicular lesions from follicular
carcinomas.
 Therefore, preoperative clinical diagnosis of cancer is difficult unless
distant metastases are present.
 Large follicular tumors (>4cm) in older men are more likely to be
malignant.

2. Follicular Carcinoma
 Surgical Treatment and Prognosis.
1. lobectomy: Patients diagnosed by FNAB as having a follicular lesion
should undergo thyroid lobectomy;
 because at least 80% of these patients will have benign adenomas.
2. Total thyroidectomy is recommended by some surgeons
 Older patients with follicular lesions >4 cm because of the higher risk
of cancer in this setting (50%) and
 Certainly should be performed in patients with atypia on FNA,
 A family history of thyroid cancer, or a history of radiation exposure.
 Surgical Treatment and Prognosis..
 The cumulative mortality from follicular thyroid cancer is approximately
15% at 10 years and 30% at 20 years.
 Poor long-term prognosis is predicted by
 A: Age over 50 years old at presentation,
 S: Tumor size >4 cm,
 G: Higher tumor grade,
 V: Marked vascular invasion,
 E: Extra-thyroidal invasion, and
 M: Distant metastases at the time of diagnosis

3. Hürthle Cell Carcinoma:
2.1
 Hürthle cell carcinomas account for 3% of all thyroid malignancies and,

 WHO classification, considered to be a subtype of follicular thyroid
cancer.
 Hürthle cell cancers also are characterized by;
 Vascular or capsular invasion and, therefore, cannot be diagnosed by FNAB.
 Hürthle cell tumors differ from follicular carcinomas in that they are more
 Often multifocal and bilateral (about 30%),
 Usually do not take up RAI (about 5%),
 Are more likely to metastasize to local nodes (25%) and distant sites,
 Are associated with a higher mortality rate (about 20% at 10 years).
2.1. Hürthle Cell Carcinoma…
 Management: is similar to that of follicular neoplasms;
1. lobectomy & isthmus-ectomy: are being sufficient surgical treatment for
unilateral Hürthle cell adenomas.
2. Total thyroidectomy: When Hürthle cell neoplasms are found to be
invasive on definitive paraffin section histology.
3. RAI: Although RAI scanning & ablation usually are ineffective, they
probably should be considered;
 To ablate any residual normal thyroid tissue and
 Occasionally ablate tumors because there is no other good therapy

Postoperative Management of Differentiated Thyroid Cancer
1. Radioiodine Therapy
2. External-Beam Radiotherapy and Chemotherapy
3. Novel Therapies: These therapies are directed at the pathways known
to be involved in various thyroid cancers; Oncogenic kinase inhibitors.
4. Thyroid Hormone: T4 is necessary as replacement therapy in patients
after total or near-total thyroidectomy.

Postoperative Management of Differentiated Thyroid Cancer

Follow-Up of Patients with Differentiated Thyroid Cancer
1. Thyroglobulin Measurement: Tg and anti-Tg antibody levels should be
measured initially at 6-month intervals.
 In low-risk patients, who have low suppressed Tg levels in the first
year, serum Tg should be measured after T4 withdrawal or
recombinant TSH stimulation approximately 12 months after ablation
2. Imaging: After the first post treatment scan, low-risk patients with
negative TSH-stimulated Tg and cervical ultrasound do not require
routine diagnostic whole-body radioiodine scans.
 However, diagnostic whole-body scans 6 to 12 months after remnant
ablation may be of value in the follow-up of patients with high or
intermediate risk of persistent disease
3. Medullary Carcinoma
 MTC accounts for about 5% of thyroid malignancies and arises from the
para-follicular or C cells of the thyroid.
 These cells are concentrated supero-laterally in the thyroid lobes, and
this is where MTC usually develops.
 All these variants are known to result secondary to germline mutations in
the RET proto-oncogene.
 The female-to-male ratio is (1.5:1).
 Most patients present between 50 and 60 years old, although patients
with familial disease present at a younger age.
3. Medullary Carcinoma …
 Neck mass: Patients often present with a neck mass that may be
associated with;
 Palpable cervical lymphadenopathy (15% to 20%).
 Pain or aching is more common in patients with these tumors, and
 Dysphagia, dyspnea, dysphonia: due to local invasion may produce
these symptoms.
 Distant blood-borne metastases to the liver, bone (frequently osteo-
blastic), and lung occur later in the disease.
 Medullary thyroid tumors secrete not only calcitonin and carcino-
embryonic antigen (CEA), but also other peptides such as:
 Calcitonin gene–related peptide, histaminadases, prostaglandins
E2 and F2α, and serotonin.
 Diarrhea: Patients with extensive metastatic disease frequently
develop diarrhea, which may result from;
 Increased intestinal motility & impaired intestinal water and electrolyte flux.
 Cushing’s syndrome: About 2% to 4% of patients develop Cushing’s
syndrome due to ectopic production of adrenocorticotropic hormone.
Pathology:
 MTCs typically are unilateral (80%) in patients with sporadic disease and
 Multi-centric in familial cases, with bilateral tumors occurring in up to
90% of familial patients.
 Familial cases also are associated with C-cell hyperplasia, which is
considered a premalignant lesion.
 Microscopically, tumors are composed of sheets of infiltrating neoplastic
cells separated by collagen and amyloid.
Diagnosis:
 The diagnosis of MTC is established by:
 History, physical examination, raised serum calcitonin, or CEA levels, and FNAB
cytology of the thyroid mass.
 Attention to family history is important because about 25% of patients
with MTC have familial disease.
 Calcitonin and CEA are used to identify patients with persistent or
recurrent MTC.
 Calcitonin is a more sensitive tumor marker, but
 CEA is a better predictor of prognosis.
 Diagnosis…
 A neck ultrasound is recommended to evaluate the central and lateral
neck compartments and the superior mediastinum.
 Serum calcitonin, CEA, and calcium levels should also be measured, and
RET proto-oncogene mutation testing should be performed

Treatment:
1. Drugs directed against the RET kinase
 Multikinase inhibitors: Sorafenib, sunitinib, lenvatinib (E7080), and cabozantinib
(XL-184) are some such
 Inhibitors for vascular endothelial growth factor receptor(VEGFR): axitinib and
pazopanib.
 Vandetanib inhibits both targets and is also an epidermal growth factor
receptor (EGFR) inhibitor.
2. An anti-CEA monoclonal antibody:
 Labetuzumab also has shown antitumor response in a small group of patients.
3. Prophylactic total thyroidectomy: is indicated in RET mutation carriers
once the mutation is confirmed
Postoperative Follow-Up and Prognosis.
 Patients are followed by annual measurements of calcitonin and CEA
levels, in addition to history and physical examination.
 Other modalities used to localize recurrent disease include:
 Ultrasound, CT, MRI, and more recently, FDG-PET/CT scans.
 Prognosis is related to disease stage.
 The 10-year survival rate is approximately 80% but decreases to 45%
in patients with lymph node involvement.

4. Anaplastic Carcinoma
 Anaplastic carcinoma accounts for approximately 1% of all thyroid
malignancies in the United States.
 Women are more commonly affected.
 The majority of tumors present in the seventh and eighth decade of life.

4. Anaplastic Carcinoma
 The typical patient has:
 A long-standing neck mass, which
 Rapidly enlarges and
 May be painful.
 Associated symptoms such as;
 Dysphonia, Dysphagia, and Dyspnea are common.
 The tumor is large and may be fixed to surrounding structures or may be
ulcerated with areas of necrosis.
 Lymph nodes usually are palpable at presentation.
 Evidence of metastatic spread also may be present.
4. Anaplastic Carcinoma…
 Diagnosis:
 Confirmed by FNAB revealing characteristic giant &multi-nucleated cells
 Differential diagnoses on FNA can include;
 Lymphomas, Medullary carcinomas, direct extension from a laryngeal
carcinoma, or other metastatic carcinomas or melanoma.
 When spindle cell elements are present, primary and metastatic
sarcomas need to be considered as well.
 Immuno-histochemical markers can aid with excluding other diagnoses.
 Core or incisional biopsy occasionally is needed to confirm the
diagnosis, especially when there is necrotic material on the FNA.
 Pathology.
 On gross inspection, anaplastict umors are firm and whitish in
appearance.
 Microscopically, sheets of cells with marked heterogeneity are seen.
 The three main histologic growth patterns are:
 Spindle cell, Squamoid, and Pleomorphic giant cell.
 Tumors may show a predominance of one pattern or a mixture of
various patterns.
 Foci of more differentiated thyroid tumors, either follicular or papillary,
may be seen, suggesting that;
 Anaplastic tumors arise from more well-differentiated tumors.
Treatment and Prognosis:
 It is one of the most aggressive, with few pts surviving 6mths beyond diagnosis
1. A total or near-total thyroidectomy with therapeutic lymph node dissection is
recommended for patients with an intra-thyroidal mass.
2. Although lobectomy may also be appropriate, particularly if there is concern for
vocal cord paralysis).
3. Adjuvant radiation with should be offered to patients with a good performance
status and no metastatic disease who desire aggressive management.
4. Cytotoxic chemotherapy: with some combination of a taxane, anthracycline,
platinum is typically given concurrently & has been associated with prolonged
survival.
Tracheostomy should be avoided as long as possible unless there is impending
airway loss.

 Lymphoma
 Lymphomas account for <1% of thyroid malignancies, and
 most are of the non-Hodgkin’s B-cell type.
 Although the disease can arise as part of a generalized lymphomatous
condition, most thyroid lymphomas develop in patients with chronic
lymphocytic thyroiditis.
 Chronic antigenic lymphocyte stimulation has been suggested to result in
lymphocyte transformation.

 Lymphoma…
 Clinical presntetion:
 Patients usually present with symptoms similar to those of patients
with anaplastic carcinoma,
 Although the rapidly enlarging neck mass often is painless.
 Patients may present with acute respiratory distress.

 Lymphoma…
 Diagnosis:
 Ultrasound can be useful for early diagnosis, and lymphoma appears as
a well-defined hypoechoic mass.
 The diagnosis usually is suggested by FNAB, but FNAB can be non-
diagnostic, particularly in the setting of low-grade lymphomas.
 Therefore, needle core or open biopsy may be necessary for definitive
diagnosis.
 Staging studies should be obtained expeditiously to assess the extent of
extra-thyroidal spread.
 Lymphoma…
 Treatment and Prognosis Patients with thyroid lymphoma:
1. Respond rapidly to chemotherapy (CHOP—cyclophosphamide, doxorubicin,
vincristine, and prednisone), which also has been associated with improved
survival.
2. Combined treatment with radiotherapy and chemotherapy often is
recommended.
3. Thyroidectomy and nodal resection are used to alleviate symptoms of airway
obstruction in patients who do not respond quickly to the above regimens or who
have completed the regimen before diagnosis.
 Prognosis depends on the histologic grade of the tumor and whether the
lymphoma is confined to the thyroid gland or is disseminated.
 The overall 5-year survival rate is about 50%; patients with extrathyroidal
disease have markedly lower survival rates.
IV. Inflammatory thyroiditis
1. Autoimmune thyroiditis:
 Chronic lymphocytic thyroiditis
 Hashimoto’s disease
2. Granulomatous thyroiditis: De Quervian’s thyroiditis
3. Fibrosing: Riedel's thyroiditis.
4. Infective:
 Acute thyroiditis : Bacterial thyroiditis, Viral thyroiditis,
 Sub-acute thyroiditis
 Chronic thyroiditis: Tuberculous, Syphilitic

IV. Inflammatory thyroiditis …
Thyroiditis:
 Thyroiditis usually is classified into:
1. Acute,
2. Sub-acute, and
3. Chronic forms, each associated with a distinct clinical presentation
and histology

1. Acute (suppurative) thyroiditis:
 The thyroid gland is inherently resistant to infection due to:
1. Its extensive blood and lymphatic supply,
2. Iodide content, and
3. Fibrous capsule.
 However, infectious agents can seed it

A. Via the hematogenous or lymphatic route,
B. Via direct spread from persistent pyriform sinus fistulae or
thyroglossal duct cysts,
C. As a result of penetrating trauma to the thyroid gland, or
D. Due to immune-suppression.
1. Acute (suppurative) thyroiditis…
 Etiology:
 Streptococcus and anaerobes account for about 70% of cases;
 However, other species also have been cultured.
 Acute suppurative thyroiditis is more common in children and
 Often preceded by an upper respiratory tract infection/otitis media.

1. Acute (suppurative) thyroiditis…
 Clinical feature:
 It is characterized by severe neck pain radiating to the jaws or ear,
 Fever, chills,
 Odynophagia, and
 Dysphonia.

1. Acute (Suppurative) thyroiditis…
 Complications such as:
 Systemic sepsis,
 Tracheal or esophageal rupture,
 Jugular vein thrombosis,
 Laryngeal chondritis, and perichondritis or
 Sympathetic trunk paralysis may also occur.

 The diagnosis is established by:
1. leukocytosis on blood tests
2. FNAB for Gram’s stain, culture, and cytology.
3. CT scans:- to delineate the extent of infection & identify abscesses.
 The sensitivity of identification of fistulae in the acute setting:
 Is lowest for barium esophagography (50%) and
 Best for direct endoscopy (100%),
 CT scans being intermediate (80%).
 Treatment:
 Parenteral antibiotics and
 Drainage of abscesses.
 Thyroidectomy may be needed for persistent abscesses or failure of
open drainage.
 Patients with pyriform sinus fistulae require complete resection of the
sinus tract, including the area of the thyroid where the tract
terminates, to prevent recurrence.

2. Sub acute thyroiditis
 Subacute thyroiditis can occur in the painful or painless forms.

2. Sub acute thyroiditis
A. Painful thyroiditis ...
 Although the exact etiology is not known,
 Painful thyroiditis is thought to be:
 Viral in origin or result from a post-viral inflammatory response.
 Genetic predisposition may also play a role, as manifested by its strong
association with the hla-b35 haplotype.
 Painful thyroiditis most commonly occurs in 30-40year-old women and

 Is characterized by the sudden or gradual onset of neck pain,
 Which may radiate toward the mandible or ear.
 History of a preceding upper respiratory tract infection often can be
elicited.
2. Sub acute thyroiditis …
 The gland is enlarged, exquisitely tender, and firm.
 The disorder classically progresses through four stages/phases.
1. Hyperthyroid phase, due to release of thyroid hormone,
2. Euthyroid phase,
3. Hypothyroidism phase, occurs in about 20% to 30% of patients
4. Resolution and return to the euthyroid state in >90% of patients.
 A few patients develop recurrent disease.

 In the early stages of the disease,
 TSH is decreased, and
 Tg, T4, and T3 levels are elevated; due to;
 Release of preformed thyroid hormone from destroyed follicles.
 The erythrocyte sedimentation rate is typically >100 mm/h.
 RAIU also is decreased (<2% at 24 hours), even in euthyroid
patients, due to;
 Release of thyroid hormones from destruction of the thyroid parenchyma.
 TREATMENT: Painful thyroiditis is self-limited, and therefore,
 Is primarily symptomatic.
 Aspirin and other non-steroidal anti-inflammatory drugs are used for
pain relief, but
 Steroids may be indicated in more severe cases.
 Short-term thyroid replacement may be needed and may shorten the
duration of symptoms.
 Thyroidectomy is reserved for the rare patient who has a prolonged
course not responsive to medical measures or for recurrent disease.

B. Painless thyroiditis .
 Is considered to be autoimmune in origin & may occur sporadically or
 In the postpartum period; about 6 weeks after delivery in women
with high TPO antibody titers in early pregnancy.
 This timing is thought to coincide with;
 A decrease in the normal immune tolerance of pregnancy and
 Consequent rebound elevation of antibody titers.

B. Painless thyroiditis ...
 Is more common in women and between 30 and 60 years of age.
 P/E:
 A normal sized or minimally enlarged,
 Slightly firm,
 Non-tender gland.
 Laboratory tests and RAIU are similar to those in painful thyroiditis,
 Except for a normal erythrocyte sedimentation rate.
 The clinical course also parallels painful thyroiditis.
B. Painless thyroiditis .
 TREATMENT:
 Patients with symptoms may require;
 Β-blockers and
 Thyroid hormone replacement.
 Thyroidectomy or rai ablation is only indicated for the rare patient with;
 Recurrent, disabling episodes of thyroiditis.

3. Chronic Thyroiditis: Lymphocytic (Hashimoto’s) Thyroiditis.
 Lymphocytic thyroiditis was first described by Hashimoto in 1912 as
struma lymphomatosa.
 Is a transformation of thyroid tissue to lymphoid tissue.
 It is the most common inflammatory disorder of the thyroid and the
leading cause of hypothyroidism.

3. Chronic Thyroiditis: Lymphocytic (Hashimoto’s) Thyroiditis…
 Etiology, Pathogenesis, and Pathology.
 Hashimoto’s thyroiditis is an autoimmune process;
 that is thought to be initiated by the activation of CD4+ T (helper) lymphocytes
with specificity for thyroid antigens.
 Hypothyroidism results not only from:
1. The destruction of thyrocytes by cytotoxic T cells;
2. by autoantibodies

 Etiology, Pathogenesis, and Pathology…
 Antibodies are directed against three main antigens;
1. Tg (60%),
2. TPO (95%),and
3. TSH-R (60%)—and,
 less commonly, the sodium/iodine symporter (25%).
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 Etiology, Pathogenesis, and Pathology…
 Apoptosis (programmed cell death) also has been implicated in the
pathogenesis of Hashimoto’s thyroiditis.
 Chronic thyroiditis also has been associated with;
 Increased intake of iodine and
 Administration of medications such as interferon-α, lithium, and amiodarone.
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 On gross examination, the thyroid gland is usually
 Mildly enlarged throughout and
 has a pale, gray-tan cut surface that is
 granular, nodular, and firm.
 On microscopic examination, the gland is;

 diffusely infiltrated by small lymphocytes and Plasma cells and
 occasionally shows well-developed germinal centers.

Clinical Presentation.
 Hashimoto’s thyroiditis is also more common in women.
 Male : female ratio 1:10 to 20) between the ages of 30 and 50 years old.
 The most common presentation is;
 Minimally/moderately enlarged firm granular gland discovered on routine P/E.
 The awareness of a painless anterior neck mass,
 Although 20% of patients present with hypothyroidism, & 5% hyperthyroidism
(Hashi-toxicosis).
 In classic goitrous Hashimoto’s thyroiditis, physical examination reveals a
diffusely enlarged, firm gland, which also is lobulated.
 An enlarged pyramidal lobe often is palpable.

 Diagnostic Studies.
 an elevated TSH and the presence of thyroid autoantibodies usually
confirm the diagnosis.
 FNAB with ultrasound guidance is indicated in patients who present with
a solitary suspicious nodule or a rapidly enlarging goiter.

 Diagnostic Studies.
 Thyroid lymphoma is a rare but well-recognized, ominous complication
of chronic autoimmune thyroiditis and has a prevalence 80 times higher
than expected frequency in this population than in a control population
without thyroiditis.
 Recent studies of clonal similarity indicate that lymphoma may, in fact,
evolve from Hashimoto’s thyroiditis.

 TREATMENT:
 Thyroid hormone replacement therapy is indicated in overtly
hypothyroid patients, with a goal of maintaining normal TSH levels.
 The management of patients with subclinical hypothyroidism (normal T4
and elevated TSH) is controversial.
 Levothyroxine is recommended for all patients with;
 TSH levels >10 μIU/mL and
 Patients with levels of 5 to 10 μIU/mL in the presence of a goiter or anti-TPO
antibodies.

 TREATMENT:
 Treatment is also advised especially for middle-aged patients with
cardiovascular risk factors such as:
 Hyperlipidemia or hypertension and in pregnant patients.
 Surgery may occasionally be indicated for suspicion of malignancy or

for goiters causing compressive symptoms or cosmetic deformity.

Riedel’s Thyroiditis
 Riedel’s thyroiditis is a rare variant of thyroiditis also known as Riedel’s
struma or invasive fibrous thyroiditis.
 is characterized by the replacement of all or part of the thyroid
parenchyma by fibrous tissue,which also invades into adjacent tissues.

Riedel’s Thyroiditis…
 Etiology:
 The etiology of this disorder is controversial,
 it has been reported to occur in patients with other autoimmune diseases
 This association, coupled with the presence of lymphoid infiltration and response
to steroid therapy, suggests a primary autoimmune etiology.
 Riedel’s thyroiditis also is associated with other focal sclerosing

syndromes including:
 Mediastinal, retroperitoneal, per-iorbital, and retro-orbital fibrosis &sclerosing
cholangitis, suggesting that it may, in fact, be a primary fibrotic disorder.

 It occurs predominantly in women between the ages of 30-60 years old.
 It typically presents as:
 Painless,
 Hard anterior neck mass,
 Progresses over weeks to years to produce symptoms of compression,
 Including dysphagia, dyspnea, choking, and hoarseness.
 Patients may present with symptoms of hypothyroidism and hypo-

parathyroidism as the gland is replaced by fibrous tissue.

 Physical examination reveals:
 a hard, “woody” thyroid gland with fixation to surrounding tissues.

 The diagnosis needs to be confirmed by;
 open thyroid biopsy, because the firm and fibrous nature of the
gland renders FNAB inadequate.

 TREATMENT:
 Surgery is the mainstay of the treatment.
 The chief goal of operation is;
 To decompress the trachea by wedge excision of the thyroid isthmus and
 To make a tissue diagnosis.
 Hypothyroid patients are treated with thyroid hormone replacement.
 Some pts who remain symptomatic have been reported to experience
dramatic improvement after treatment with corticosteroids & tamoxifen.
 More recently myco-phenolate mofetil has been used to;
 Attenuate the inflammatory process and
 Led to dramatic symptom improvements.

Complication of thyroid surgery:  Metastasis of thyroid cancers:
Hemorrhage 1. LN
Airway obstruction
Wound infection
2. Skull
Thyroid storm 3. Liver
Hypothyroidism 4. Lung
Hypoparathyroidism 5. Bone
Superior thyroid nerve injury
Keloid
Stich granuloma

No Type of goiter RAI FSH T3 T4
1 Simple goiter Decreased N N N, (free)
2 Graves disease Increased Suppressed May/not May/not
elevated(free) elevated (free)
3 TMNG Increased Suppressed Elevated Elevated
(free) (free)
4 Toxic adenoma Hot nodule
5 Acute thyroiditis Decreased Elevated Elevated
6 Sub acute thyroiditis Decreased Decreased Elevated Elevated
7 Chronic thyroiditis/ - Increased - thyroautoanti

Hashimotos/ bodies
4.1. Surgical diseases of the breast (benign and malignant tumors, breast anomalies)
4.2. Case related to breast lump
4.3. Simulated practice: Assessing a patient with breast lump

Lymphatic system of breast:
Lymphatic system of breast: divides in to two.
1. Axillary LNs which accounts 85% and has 6 groups by surgeons.
2. Internal mammary LNs which accounts 15%
G-I Lateral o Are axillary vein group and

o It contains 4-6 LNs
G-II Anterior/ pectoral o Are external mammary groups and
o consists 5-6 LNs
G-III Posterior/subscapular o Are scapular groups.
o Consists 5-7 LNs
G-IV Central o Receive from GI, GII & GIII LNs groups and breast directly.
o Consists 3-4 LNs
G-V Apical o Are sub-clavicular
o Receive from all axillary LN groups.
o Consists 6-12 LNs
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o Consists 1-4 LNs
Lymphatic system of breast…
Axillary LNs based on anatomic relation ship b/n pectorals minor muscle.
It divides in to 3 levels.
Lvel I o It presents lateral and below lower border of pectoralis minor muscle.
o It includes:
1. Axillary vein LNs
2. External mammary LNs
3. Scapular LNs
Lvel II o Superficial or deep to pectoralis minor.
o It includes:
1. Central LNs
2. Interpectoral LNs
Level III o Medial or above upper border of pectoralis minor.
o It includes:
1. Sub-clavicular / apical LNs
Lymphatic system of breast…

Differential diagnosis for breast disease
If lump is affected. If nipple/areola is affected.
1. Breast cyst 1. Duct ectasia.
2. Fibro adenoma 2. Eczema
3. Breast carcinoma 3. Paget disease
4. Phylloides tumor 4. Intra-ductal papilloma
5. Periductal mastitis / ductal ectasia 5. DCIS
6. Breast abscess 6. Fat necrosis
7. Paget disease
8. Pregnancy
9. Fibrocyst adenosis
10. Fibro adenosis
Examination of breast disease
Inspection:
 Methods to inspect breast:
1. Hands on side, /parallel to standing/.
2. Raising Hands above the head/auchincloss method/
3. Patient lean for ward.
4. Hands on hip.
Compare nipple right & left.

Examination of breast disease …
1. Inspection:
 Visible lump/buldge on breast.
 Discharge:
 Bright red: carcinoma or duct papilloma.
 Dark red: duct papilloma with obstructed duct.
 Clear watery or greenish: Fibro-adenosis.
 Milky white discharge: lactation, galactocelle, gallactorrhoea
(spontaneous milk discharge), mammary duct ectasia.
 Purulent discharge: acute mastitis/chronic abscess with duct ectasia.
 Eczema (unilateral) and destruction: Paget disease.
 Eczema (bilateral) and itching: Allergic eczema.
 Dilated vein: Sarcoma , not carcinoma.
1. Inspection:
:

1. Palpation:
 Temperature and tenderness.
 Size of lump:
 Shape:
 Surface: Smooth , irregular/nodular/.
 Edge: wel-defined or irregular.
 Consistency: soft, firm or hard.
 Fixity : To skin, breast tissue, pectoral fascia & muscle, and chest wall.
 If cystic: fluctuation and trans illumination.

Examination of breast disease…
Systemic examination:
1. Abdomen.
2. Per- vaginal and PR.
3. Chest for effusion /Consolidation/.
4. Bony swelling and tenderness.
 Melanoma /mestasisis to breast/ vs paget disease to breast cancer:

 By tissue biopsy to confirmed Dx.

DIAGNOSIS OF BREAST CANCER
 In~30% of cases, the woman discovers
a lump in her breast.
 Other less frequent presenting signs and

symptoms of breast
cancer include:
1. Breast enlargement or asymmetry;
2. Nipple changes, retraction, or
discharge;
3. Ulceration or erythema of the
skin of the breast;
4. An axillary mass; and
5. Musculoskeletal discomfort.

Eczema Vs Paget’s disease.
Eczema: Paget’s disease:

 Bi-lateral .  Uni-lateral .
 Common in lactation.  Common in meno-pause.
 Has itches.  No itches.
 Has vesicles.  No vesicles.
 May have intact nipple.  Nipple may be destroyed.
 No lumps.  May have lumps.

Discussion on Differential diagnosis for breast disease
1. Acute bacterial mastitis.
2. Breast abscess.
3. Fat necrosis.
4. Breast cyst.
5. Fibro-adenoma.
6. Fibro-adenosis.
7. Phyllodes tumor.
8. ANDI.
9. Duct ectasia/ periductal mastitis.
10. Duct papilloma.
11. Galactocelle.
12. Breast cancer.
1. Acute bacterial mastitis
 It is common in lactation period.
 Presents with swelling and pain.
 RFs:
 Cracks/ fissures of nipple.
 Retracted nipple.
 Oral cavity infection of child.

2. Breast abscess
 It is presented > 48hrs of acute infection.
 CF:
 High grade fever, chills & rigors.
 Soft cyclic fluctuant swelling.
 Necrosis of skin , ulceration & discharge.
 Throbbing type pain.
 Common cause: S.aureus.

3. Fat necrosis

4. Breast cyst
 Is a straw, green or opaque fluid in cavity of breast.
 Commonly present > 35yr to menopause.
 Varies in size with menstruation due to estrogen change.
 It can be multiple, bilateral, recurrent.
 Has less risk to be breast cancer.
 Clinically: smooth , soft, fluctuant , trans illuminating well localized
swelling.
 Common cause: HRT/ Hormonal replacement therapy.

5. Fibro adenoma
 Benign breast tumor & it is ANDI of single lobule.
 Types:
 Peri- canalicular:-fibrosis more: small, hard.
 Intra- canalicular:-fibrosis less: large, soft.
 Giant fibro adenoma if it > 5cm.
 CF:
 Common in 15-25yrs .
 Painless lump.
 Smooth , round bordered, firm to hard.
 Freely movable with in breast (AKA breast mouse).

5. Fibro adenoma…

 Fibro adenoma:  Fibro-adenosis:
 Less common.  More common.
 Benign tumor of one  ADNI in breast.
lobule.  Has pain.
 No pain.  Usually bilateral.
 Unilateral.  Irregular, tender lump.
 Well-defined capsule.  No capsule.
 No discharge.  Serous, green discharge.
 Rare sarcoma.  Carcinoma.
 Rx: Excision  Rx: Excision or drugs.

6. Fibro-adenosis / Fibrocystic breast changes

7. Phyllodes tumor- cystosarcoma phyllodes
 Is fast growing mass that from the periductal stromal cells of the breast.
 It can be benign , border line or malignant.
 If it is benign: massive size.
 CF:
 Rapid growth.
 Stretched or shiny size.
 Red, dilated vein, warm to touch.
 Bosselated surface/ big nodule. Complications:
 Differ from cancer: 1. Necrosis of skin
1. No-fixity to skin or pectoralis. 2. Turn in to carcinoma or sarcoma.
2. No LN involvement.
3. No nipple retraction.
8. ANDI:
 The breast is a dynamic structure that undergoes changes
throughout a woman’s reproductive life and, superimposed
upon this, cyclical changes throughout the menstrual cycle.
 Pathogenesis of ANDI involves disturbances in the breast physiology
extending from a perturbation of normality to well-defned disease
processes.

8. ANDI:


9. Duct ectasia
 Is dilatation of breast duct/lactiferous duct.
 Common in middle age women.
 Cause: infection
 Smoking increase risk.
 Present: Intense inflammation with lymphocytes & plasma cells.
 Fibrosis cause nipple retraction.
 CF:
 Paste like discharge per nipple.
 Lump confused to carcinoma after a time.
 Bilateral slit like retraction.
 Complication:
 Recurrent abscess.
 Fistula
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10. Duct Papilloma:
 It is a benign , single/ rarely multiple, unilateral.
 Common in Middle aged .
 Small swelling.
 Bloody discharge.
 Is a pre-malignant condition.
 Mostly presented with in 5cm of nipple.
 Rx: Micro-dochectomy/a surgical removal of lactiferous duct.

11. Galactocele
 Is AKA lacteal cyst or milk cyst.
 Is a solitary ,sub areolar retraction of cyst filled with milk.
 Is due to inadequate drainage of milk.
 Can occur during or shortly after lactation.

12. Galactorrhea /rhoea
 Is a spontaneous flow of milk from the breast unassociated with breast
feed.
 Cause:
1. Physical: sexual stimulation & extreme reproductive age.
2. Drugs: OCP, Mthyl-Dopa, Atenolol, Cklonidine, CPZ, ranitidine& Haloperidol.

13. Breast cancer
 Breast cancer is the most common site-specific cancer in women and
 is the leading cause of death from cancer for women aged 20-59 years
 It accounts for 29% of all newly diagnosed cancers in females and
 is responsible for 14% of the cancer-related deaths in women.
Primary Breast Cancer.
 More than 80% of breast cancers show productive fibrosis that involves
the epithelial and stromal tissues.
 With growth of the cancer and invasion of the surrounding breast tissues,
the accompanying desmoplastic response entraps and shortens Cooper’s
suspensory ligaments to produce a characteristic skin retraction.

Risk factors for breast cancers
Risk factors: Can be Hormonal or Non Hormonal or others.
1. Hormonal
3. Genetics
 Early menarche < 12yr.
 Familial breast cancer.
 Late meno-pause> 55yr.
 History of Breast, ovarian,
 Nulliparity.
endometrial, colonic cancer.
 Never breast feed.
 First pregenacy > 30 yr.
4. Others
 Exogenous hormone.
 Age> 65yr.
 Obesity.
 Sex: Female: 99%
2. Non Hormonal  BRCA Mutation.
 Radition
 Alcohol
Risk factors for breast cancers…
Risk assessment model:
There are several risk assessment models to predict the risk of breast cancer.
From the Breast Cancer Detection Demonstration Project, a
mammography screening program conducted in the 1970s,
1. Gail et al developed the model most frequently used in the United
States, which incorporates;
 Age,
 Age at menarche
 Age at first live birth.
 No of breast biopsy.
 Hx. Of atypical hyperplasia.
 Family hx. Of breast cancer (1st degree relatives)
 Life time risk: 12%

 At 50yr: 11%.
 At 70yr: 7%.
Risk assessment model …
2. Claus et al, using data from the Cancer and Steroid Hormone Study, a
case-control study of breast cancer, developed the other frequently used
risk assessment model, which is based on assumptions about the
prevalence of high-penetrance breast cancer susceptibility genes.
 Compared with the Gail model, the Claus model incorporates more
information about family history but excludes other risk factors.
 The Claus model provides individual estimates of breast cancer risk
according to decade of life based on presence of first- and second-
degree relatives with breast cancer and their age at diagnosis.

Risk reduction of breast cancer
1. Chemo-prevention: Tamoxifen for age> 60yrs and have DCIS AND LCIS
2. Surgical -prevention : for BRCA.

 Mastectomy
 Salpingo- oophorectomy
3. Intensive surveillance for breast, ovarian Ca.

Cancer Prevention for BRCA Mutation Carriers.
 Risk management strategies for BRCA1 and BRCA2 mutation carriers
1. Risk-reducing mastectomy and reconstruction
2. Risk-reducing salpingo-oophorectomy
3. Intensive surveillance for breast and ovarian cancer
4. Chemoprevention

13. Breast cancer
 Histo-pathology of breast cancer:
1. Insitu breast cancer: not invade/ BM/basement membrane.
2. Invasive breast cancer: it invades BM.

13. Breast cancer…



 Invasive carcinoma:
 Invasive breast cancers have been described as lobular or ductal in
origin.
 Current histologic classifications recognize:
1. Invasive Ductal carcinoma (80%): no special type (NST).
 These cancers generally have a worse prognosis than special-type cancers
2. Special types of breast cancers (10% of total cases),
 Which are defined by specific histologic features.
 To qualify as a special-type cancer, at least 90% of the cancer must contain
the defining histologic features.

 Foote and Stewart classification for invasive breast cancer:
1. Paget’s disease of the nipple
2. Invasive ductal carcinoma: Adenocarcinoma with productive fibrosis
(scirrhous, simplex, NST), 80%.
3. Medullary carcinoma, 4%.
4. Mucinous (colloid) carcinoma, 2%.
5. Papillary carcinoma, 2%.
6. Tubular carcinoma, 2%.
7. Invasive lobular carcinoma, 10%
8. Rare cancers (adenoid cystic, squamous cell, apocrine)

 Prognostic & predictive biomarkers and biologic targets for breast cancer include:
(a) the steroid hormone receptor pathway;
(b) growth factors and growth factor receptors such as: human epidermal growth factor receptor 2
(HER-2)/neu, epidermal growth factor receptor (EGFR), transforming growth factor, platelet-
derived growth factor, and the insulin-like growth factor family;
(c) indices of proliferation such as proliferating cell nuclear antigen (PCNA)&Ki-67;
(d) indices of angiogenesis such as vascular endothelial growth factor (VEGF)& the angiogenesis
index;
(e) the mammalian target of rapamycin (mTOR) signaling pathway;
(f) tumor-suppressor genes such as p53;
(g) the cell cycle, cyclins, and cyclin-dependent kinases;
(h) the proteasome;
(i) the COX-2 enzyme;
(j) the peroxisome proliferator-activated receptors (PPARs); and
(k) indices of apoptosis and apoptosis modulators such as bcl-2 and the bax:bcl-2 ratio
Breast cancer screening:
 Mammography:
 Soft tissue radiographs are taken by placing the breast in direct contact
with ultrasensitive film & exposing it to low-voltage, high-amperage x-
rays.
 The dose of radiation is approximately 0.1 cGy and, therefore,
mammography is a very safe investigation.
 The sensitivity of this investigation increases with age as the breast
becomes less dense.
 In total, 5% of breast cancers are missed mammographic screening.
 A normal mammogram does not exclude the presence of carcinoma.
 Digital mammography is being introduced, which allows manipulation of
the images and computer-aided diagnosis.
Breast cancer screening…
 Mammography…
 Tomo-mammography is also being assessed as a more sensitive
diagnostic modality.
 NCCN: suggest a normal risk women:
1. > 20yrs every 3 year breast examination
2. > 40yrs every year breast examination and yearly mammography.
For age > 50yr: routine and it decreases mortality by 25%.
For age < 50yr: controversial because;
1. Decrease sensitivity due to high density breast.
2. Decrease specificity due to increase False positive result.
3. Low incidence of breast cancer.
 Mammography…
 Six grades by mammography on breast cancer screening.
Grade I: Negative
Grade II: Benign
Grade III: Probable benign
Grade IV: Suspicious malignant
Grade V: High Suspicious cancerous
Grade VI: Known carcinoma
Features that suggest breast ca. by mammography finding.
1. Solid mass with or with out stellate feature.
2. Asymmetric thickening of breast tissue.
3. Clustered micro calcification.
Ultrasound
Ultrasound is particularly useful:
In young women with dense breasts in whom mammograms are
difficult to interpret, and
in distinguishing cysts from solid lesions and
It can also be used to localise impalpable areas of breast pathology.
It is not useful as a screening tool and remains operator dependent.
Increasingly, ultrasound of the axilla is performed when a cancer is
diagnosed,
with guided percutaneous biopsy of any suspicious glands
Suggests: cystic mass:
Well-defined border , smooth margin
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Magnetic resonance imaging
 Useful in a number of settings:
1. To distinguish scar from recurrence in women who have had previous
breast conservation therapy for cancer
(although it is less accurate within 9 months of radiotherapy because of abnormal enhancement);
2. To assess multifocality and multicentricity in lobular cancer and to
assess the extent of high-grade ductal carcinoma in situ (DCIS).
(It is less useful in low-grade DCIS;)
3. It is the best imaging modality for the breasts of women with
implants;
4. As a screening tool in high-risk women (because of family history).
Spread of breast cancer
1. Local: Skin, pectoral muscle, chest wall.
2. LN: Axillary, internal mammary LNs.
3. Blood stream: Bone (lumbar, Femur, vertebra, ribs, skull), Liver, lung,
brain, adrenal ovaries.

Staging of breast cancer: TNM
T: Tumor size N: Lymph node involvement
Tx: Not assessed Clinical:
To: No tumor Nx:
T1: < 2cm No:
T2: 2-5 cm N1: Metastasis movable ipsilateral Level- I & II LNs.
T3: > 5cm N2: Metastasis fixed/matted ipsilateral Level I&II LNs.
T4: Any size N3: Metastasis to Level III LNs.
extend to chest Pathological:
wall, or skin N1: 1-3 LNs & negative intramammary LNs.
N2: 4-9 LNs positive intramammary LNs
N3: > 10LNs, axillary.
M: Metastasis:
Investigation for breast disease:
1. Triple assessment: For patients suspicious to cancer; ppv: 99.9%.
1. Clinical assessment:
2. Imaging : radiological:
3. Sample specimen taking:

Investigation for breast disease…
 Imaging:
1. Mammography:
2. US: not ideal to <1cm.
 Cyst:
 Well-circumscribed wall
 Smooth margin.
 Echo free center.
 Benign:  Cancer:
 Well-defined margin.
Irregular wall.
 Round/oval shape.
Acoustic enhancement.
 Smooth surface. May be smooth.
3. Ductography: Primary for blood nipple discharge; intraductal papilloma.
4. MRI: For Dx. Of Cancer
Investigation for breast disease…
 Pathology:
1. FNAC: it can’t differentiate invasive from insitu cancer of breast.
2. Core biopsy: it can differentiate invasive from insitu cancer of breast.
 Routine workup:
 CBC
 Metastatic work up:
 ALP
 CXR
 Abdominal US
 Bone scan

5.1. Surgical diseases of chest, lungs and heart (injuries, hemoptysis, lung infections,
diseases of the pleura and pericardium, mediastintis)
5.2. Case related to surgical diseases of the thorax

5.3. Surgical diseases of the esophagus (injuries, esophagitis, achalasia)
5.4. Case related to Case related to surgical diseases of the esophagus
5.5. Simulated practice: History and chest examination including interpretation
of radiologic imaging of different chest abnormalities

6.1. Acute abdomen (Case related to acute abdomen)
6.2. Intestinal obstruction (GOO,SBO, LBO); (Case related to intestinal obstruction)
6.3. Surgical diseases of the stomach, small intestine, spleen, pancreas
6.4. Surgical diseases of the liver, biliary tract and gall bladder
6.5. Surgical diseases of the colon, rectum and anal canal
6.6. Simulated practice: History taking and abdominal examination including
interpretation of imaging studies of different abnormalities
6.7. Simulated practice: NG tube insertion
7.1. Surgical disorders of the genito-urinary system (presenting symptoms, injury,
obstruction, urinary retention)
7.2. Abdominal wall and hernias

7.3. Case related to urinary obstruction
7.4. Case related to Hernia
7.5. Simulated practice: Assessing surgical patients with urinary symptoms
7.6. Simulated practice: Catheterization

REFERENCES
1. Schwartz’s Principles of Surgery tenth and eleventh Edition
2. Bailey and Love,s SHORT PRACTICE of SURGERY 27th edition.
3. (SRB’ S) Sriram Bhat M Manual of surgery 5th edition
4. Uptodate 2018

Introduction To Surgery Short Notes

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Introduction To Surgery Short Notes

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Neuroendocrine response to injury/critical illness

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Systemic inflammatory response syndrome following major injury

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Physiological response to injury

o Injuries or infections induce unique neuroendocrine and immunologic responses

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Purpose of neuroendocrine changes following injury

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o The magnitude of metabolic expenditure appears to be directly proportional to

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Changes in body composition following major surgery/critical illness

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 Lipid Metabolism after Injury

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o Shock consists of inadequate tissue perfusion marked by decreased delivery of

o This imbalance between cellular supply and demand leads to neuroendocrine

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Fig 2: Pathways leading to decreased tissue perfusion and shock.

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CLINICAL FEATURES OF SHOCK

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FORMS OF SHOCK / CLASSIFICATION OF SHOCK

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o Loss of up to 15% of the circulating volume = little in terms of obvious symptoms,

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oControl of hemorrhage is achieved in the

oCurrent recommendations in stable ICU patients aim for a target hemoglobin of 7

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1. Crystalloid solutions – includes saline solutions, buffered (chloride-restrictive)

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oThe hypo- perfusion deficit in traumatic shock is magnified by the

oTreatment of traumatic shock is focused on correction of the individual elements

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oCardiogenic shock is defined clinically as circulatory pump failure leading to

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oMortality rates for cardiogenic shock are 50% to 80%.

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oDopamine may be used first. A pure αagonist, such as phenylephrine, may be

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