pre exam surgical notes 2

8/18/2019 Pre Exam Surgical Notes 2

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PRE-EXAM SURGICAL

NOTESNB: THESE NOTES ARE COMPLEMENTARY TO THE

CLINICAL HISTORY AND EXAMINATION SHEET

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

tissue perfusion, resulting in decreased tissue oxygen delivery

Compensatory mechanisms in shock:

It is a trial to maintain adequate blood flow to vital organs as brain, heart and lung

These mechanisms include:

1. Sympathetic nervous system:

• Release of norepinephrine, epinephrine, dopamine, and

cortisol à vasoconstriction, increase in HR, and increase ofcardiac output

2. Renin-angiotensin axis:

• Water and sodium conservation and vasoconstriction

• Decreases urine output to increase blood volume and blood

pressure

3. Vasoconstriction of skin, splanchnic, musculoskeletal, andrenal blood flow àto maintain cerebral and cardiac perfusion

Shock, Electrolyte and Fluid Therapy


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4. Cellular responses to decreased systemic oxygen delivery

- ATP depletion ! ion pump dysfunction

- Cellular edema

- Hydrolysis of cellular membranes and cellular death

Decreased perfusion will lead to hypoxia à anaerobic metabolism à

systemic metabolic lactic acidosis that overcomes the body’s

compensatory mechanisms àif fail à organ dysfunction à irreversible

shock à death

Stages of Shock

• Preshock :- Compensated (class I hemorrhage)

– Body is able to compensate for " perfusion.

– Less than 15% reduction in blood volume.

– Tachycardia to #cardiac output & perfusion.

• Shock :- Classes ll - lV of blood loss

– > 15 -< 40% reduction in blood volume

– Compensatory mechanisms overwhelmed.

• End-organ dysfunction:- Leading to irreversible organ damage &

death.

Hypovolemic (oligemic) shock

Decreased circulatory blood volume due to:

1. Blood loss (hemorrhagic shock)

2. Plasma loss; as in burns, peritonitis and pancreatitis

3. Water and electrolyte loss: as in repeated vomiting ( as in intestinal

obstruction) and diarrhoea


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Classes of Blood Volume Loss (or Hemorrhage)

• It is a clinical tool to determine the amount of fluid (or blood) loss

• So, we can determine the type and amount of fluid required to replace the

loss and restore blood volume

CLASS I

• Loss of up to 15% of the circulating volume (700 to 750 mL) for a 70-kg

patient may produce little in terms of obvious symptoms

– Cardiovascular: mild tachycardia (pulse around 100) with normal

blood pressure

– Respiratory: Rate normal - Neurologic: Slightly

anxious

– - Skin: Warm and pink & Capillary Refill


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– - Renal: Normal urine output

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

• Children: >1 ml/kg/hour

Class l is compensated and no need for IV fluids

CLASS II

loss of up to> 15 - < 30% of the circulating volume (750 – 1500 ml)

– Cardiovascular

• Tachycardia: 100 -120/m and pulse is week

• Blood Pressure normal in recumbent but may be orthostatichypotension

• Normal pH

– Respiratory: Mild Tachypnea :16 -20/m

– Neurologic: Irritable, Confused, and Combative (patient must be

sedated)

– Skin: Cold extremities, pale, & Delayed Capillary Refill (>2 seconds)

– - Renal: urine volume < 30 - >20 ml/m

This patient must be initially replaced by 2 liters of lactated

Ringers solution and blood is given if hematocrit < 30

CLASS III

More than 30 - < 40% of the blood volume has been lost (Adults: 2000

ml blood loss)

Cardiovascular:

Pulse 120 -< 140/m, Hypotension

Metabolic Acidosis

- Respiratory: Tachypnea, 20 - < 30/m

- Neurologic: Irritable, Lethargic, Diminished pain response


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

Capillary Refill

- Renal: Oliguria (< 20 - > 10 ml/m)

Blood Urea Nitrogen (BUN) increased

Treatment must included volume to volume colloid replacement

( blood if hemorrhage, plasma in burn, peritonitis, and

pancreatitis

In all cases till blood or plasma are ready give 2 liters of

Lactated Ringers

CLASS IV

Loss of 40% of circulating volume (2 L)

- Cardiovascular: weak thready pulse (>140/m)

Significant Hypotension & Significant acidosis

- Respiratory: tachypnea > 30/m

- Neurologic: Lethargic and finally Coma

- Skin: Cold extremities and may be Cyanosis

- Renal: Anuria (urine < 10 ml/m)

Treatment must included volume to volume colloid replacement

( blood if hemorrhage, plasma in burn, peritonitis, and

pancreatitis

In all cases till blood or plasma are ready give 2 liters of

Lactated Ringers

Class LV is a life threatening, and generally requires urgent

operative control of bleeding


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Other Types of ShockCardiogenic shock:

! may be cardiac: as in myocardial infarction

! Extracardiac (obstuctive): as in massive pulmonary embolism, cardiac

tamponade, and tension pneumothorax

Distributive shock :- Vasodilatory, as in

A.Septic: severe infection with release of bacterial or fungal endotoxin

B. Anaphylactic: following injection of certain drugs as penicillins or

intake of some food (most commonly shell fish)

C.Neurogenic shocks:

• Spinal shock (loss of sympathetic tone after spinal anesthesia or

spinal injury)

• Severe pain: Vasovagal attack with marked bradycardia à decrease

cardiac out put

• Fear : release of big amount of adrenaline à vasodilatation in the

muscles à pooling of blood in the muscles on expense of other sites

Common Features of Shock

• Hypotension (not an absolute requirement)

– SBP < 90mm Hg, not seen in “preshock, class I”

• Cold, clammy skin

– Vasoconstrictive mechanisms to redirect blood from periphery to vital

organs

– Exception is warm skin in early distributive shock, specially septic

shock

• Oliguria ("kidney perfusion)


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• Altered mental status (" brain perfusion).

• Metabolic acidosis.

• Tachycardia but bradycardia in spinal shock and vasovagal attacks

Initial Assesment – ABC

• Airway: Does pt have mental status to protect airway?

– GCS less than “eight” means “intubate”

– Airway is compromised in anaphylaxis

• Breathing: If pt is conversing with you, A & B are fine

– Place patient on oxygen: 40% in class I & II and 100% in class III &

IV

– If apnea à ventilate the patient

• Circulation:

– Stop bleeding by compression or tourniquet if bleeding wound

otherwise resuscitate the patient first

– 2 large bore (#16g) IV, start fluids by 2 liters of Ringers lactate

(careful if cardiogenic shock)

– Prepare blood if hematocrit < 30 and in class lll & lV

– Continuous monitor : best monitor of shock is urine out put (so

catheter is mandatory) as central venous pressure may be high in

cardiogenic shock

• In a trauma, perform ABCDE, not just ABC

• Deficit or Disability

– Assess for obvious neurologic deficit.

– Moving all four extremities & Pupils.

– Glascow Coma Scale (M6, V5, E4).


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• Exposure: and full examination from head to toes

Adjuncts F & G: Foley’s catheter and gastric tube (why?)

Acidosis in surgery

Causes:

Metabolic

• Shock

• Long ischemic part of intestine or limb

• Diabetic ketoacidosis

• Cardiac arrest (combined respiratory and metabolic)

• Renal failure

Glasgow Coma Scale

1 2 3 4 5 6

EyeDoes not

open eyes

Opens eyes in

response topainful stimuli

Opens eyes in

response tovoice

Opens eyes

spontaneously

N/A N/A

Verb

al

Makes no

sounds

Incomprehensible

sounds

Utters

inappropriatewords

Confused,

disoriented

Oriented,

converse

snormally

N/A

Moto

r

Makes nomovemen

ts

Extension topainful stimuli

(decerebrate

response)

Abnormalflexion to

painful stimuli(decorticate

response)

Flexion /Withdrawal

to painful

stimuli

Localizespainful

stimuli

Obeyscomman

ds

http://en.wikipedia.org/wiki/Abnormal_posturing#Decorticatehttp://en.wikipedia.org/wiki/Abnormal_posturing#Decerebratehttp://en.wikipedia.org/wiki/Pain_stimulus


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

TTT: treatment of the cause first

Ringer’s lactate can be given in mild cases and in advanced cases use sodium

bicarbonate (dose: measure deficit in bicarbonate X 40% X body weight)

Hypokalemia in surgery

Causes:

• Repeated vomiting (pyloric obstruction, postoperative vomiting, intestinal

obstruction)

• Prolonged nasogastric suction• Use of diuretics, excessive fluid intake with polyuria

Presentation: weakness, hypotonia, distension, and even paralytic ileus

Treatment: in mild cases use RL but in advanced cases use potassium

chloride IV, slowly after correction of urine out put by normal saline first

IV Fluid Therapy


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Shock

Nutrient solutions

!It contain some form of carbohydrate andwater.

!Water is supplied for fluid requirements andcarbohydrate for calories and energy.

!They are useful in preventing dehydrationand ketosis but do not provide sufficientcalories to promote wound healing, weightgain, or normal growth of children.

!Common nutrient solution :-D5W.

Shock

Electrolyte solutions

(Crystalloid)

!fluids that consist of water and dissolved crystals,such as salts and sugar.

!Used as maintenance fluids to correct body fluidsand electrolyte deficit .

!Commonly used solutions are:-Normal saline

(0.9% sodium chloride solution).-Ringer’s solutions

(contain sodium, chloride, potassium, andcalcium).

-Lactated Ringer’s solutions(contain sodium, chloride, potassium ,calcium andlactate) .


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Shock

Volume expanders (Colloid)

• Are used to increase the blood volume

following severe loss of blood

(haemorrhage) or loss of plasma (burns

and pancreatitis).

• Expanders present in:-

dextran, plasma, and albumin, other

preparations as hemogel.

Shock

Parenteral Nutrition (PN)Parenteral nutrition is a form of nutritional support that

supplies protein, carbohydrate, fat, electrolytes ,

vitamins, minerals, and fluids via the IV route to meet themetabolic functioning of the body.

Indications:

• Patient cannot tolerate internal nutrition as in case of

paralytic ileus, intestinal obstruction, persistent vomiting.

• Patient with hyper metabolic status as in case of burns

and cancer.

• Patient at risk of malnutrition because of recent weight

loss of > 10%, NPO for > 5 days.

• Side effects: lactic acidosis, must be applied through

central line with risk of infection, if prolonged use gall

stones will be formed


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Maintenance daily Requirements for adult (70 kg unless you are given

another weight

1st 10kg x 100ml = 1000ml

2nd 10kg x 50ml = 500ml

Next 50kg x 20ml = 1000ml

TOTAL = 2500 ml /day

Replacement of ongoing loss

As in:

• NG

• drains

• fistulae

• third space losses

Concentration is similar to plasma! Replace volume per volume with

crystalloid solutions


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Blood transfusion

Blood transfusion is a common procedure that usually goes without complications. Butthere are some risks. Some transfusion reactions happen during the transfusion, while

others may take several weeks to develop or become noticeable.

1. Allergic reaction and hives

May occur even with matched blood

Signs and symptoms are usually limited to hives and itching. These types of

transfusion reactions are usually treated with antihistamines and are seldom serious.

Rarely, a more serious allergic reaction may occur and signs and symptoms may

include difficulty breathing, low blood pressure, anxiety, rapid heartbeat and nausea.

2. Fever

fever and rigors may develop quickly during the transfusion or soon after (febrile

reaction). Fever usually isn't serious. But because fevers can be a sign of a serious

reaction, so you have to stop the transfusion to do further tests before deciding

whether to continue.

3. Acute immune hemolytic reaction

This is a very rare but serious transfusion reaction in which the body attacks the

transfused red blood cells because the donor blood type is not a proper match.

Released hemoglobin will be precipitated in renal tubules as acid hematin ending in

renal failure unless treated. Signs and symptoms include fever, nausea, chills, lower

back or chest pain, and dark urine.

Shock

3rd space losses !!! • 1st Spacing: Normal distribution within ECF and ICF.

• 2nd spacing: accumulation within the interstitial compartments, oedema

formation but available for physiological exchange between compartments

• 3rd spacing: Accumulation in parts of the body where it’s not available for

exchange between the different compartments: Ascitis, tissue inflammation,

oedema from burns/surgery, pancreatitis.

Replacing Third Space Losses

• Superficial surgical trauma: 1-2 ml/kg/hr

• Minimal surgical trauma : 3-4 ml/kg/hr

- head and neck, hernia, knee surgery

• Moderate surgical trauma : 5-6 ml/kg/hr

- hysterectomy, chest surgery

• Severe surgical trauma: 8-10 ml/kg/hr (or more)

- AAA repair, nehprectomy


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TTT: stopping blood and giving matched blood with forced alkaline diuresis using

manitol and Na bicarbonate

4. Lung injury

Transfusion-related acute lung injury (TRALI) characterized by the acute onset of non-

cardiogenic pulmonary edema following transfusion of blood products specially plasma and platelets but may occur with packed RBCs. TRALI is thought to be immune mediated. Usually,

TRALI occurs within one to six hours of the transfusion. People usually recover, when

treated by respiratory support

5. Bloodborne infections

Blood banks screen donors for risk factors and test donated blood to reduce the risk of

transfusion-related infections, but they occasionally still occur. It can take weeks or

months after a blood transfusion.

Estimated risks of contracting these diseases after a blood transfusion:• HIV — 1 in 2.3 million transfusions.

• Human T-lymphotropic virus — 1 of every 2 million transfusions.

• Hepatitis B — 1 in 350,000 transfusions.

• Hepatitis C affects — 1 in 2 million transfusions.

• West Nile virus — 1 of every 350,000 units of blood in the United States.

• Sepsis (bacterial infection of the blood) — 1 in 1 million transfusions.

6. Delayed hemolytic reaction

This is similar to acute immune hemolytic reaction, but it occurs much more slowly.

often one to four weeks —>decrease in red blood cell levels.

7. Iron overload

Multiple blood transfusions may lead to iron deposition (hemochromatosis) in theliver and heart.

TTT: iron chelation therapy.

8. Graft-versus-host disease

The white blood cells in the donor blood attack the cells of the recipient. This disease

is often fatal. It's also a very rare condition affecting mainly immunocompromized

patients Signs and symptoms include fever, rash, diarrhea and abnormal liver function

test results.

http://en.wikipedia.org/wiki/Immune_systemhttp://en.wikipedia.org/wiki/Pulmonary_edema


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

FT4 (functional) and US (anatomical)! the proceed to other

investigations according to the findings of the previous work up, see

below

• The best pathological investigation is FNAC though it is not

sensitive in follicular tumors

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

female with thyroid swelling starting toxic the becomes

hypothyroid)! do Antibodies (anti TPO)

• The most important preoperative investigation is indirect

laryngoscopy (medico legal)

DETAILED

TSH Tests• The best way to initially test thyroid function is to measure the

TSH level.• High TSH level indicates hypothyroidism and low TSH level

indicates hyperthyroidism.

condition normal hyperthyroidis

m

Hypothyroidis

m

primary

Hypothyroidism

secondary

TSH normal low high low

T4 normal High Except in T3

toxicosis

low low

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

change in levels of these proteins could change the total T4 and T3 levels (as

in pregnancy, use of contraceptive pills, nephrotic syndrome, liver diseases

etc), so the measurement of the free hormone level will be more accurate.


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T4 Tests

When TSH is abnormal, we measure the free T4 (FT4).• In hypothyroidism, low values will be found.• In hyperthyroidism, high values will be found.

T3 Tests• Helpful to diagnose T3 toxicosis and to determine the severity of

the hyperthyroidism. • T3 testing is rarely helpful in the hypothyroid patient, since it is the

last test to become abnormal. Patients can be severely hypothyroid with a high TSH and low FT4, but

have a normal T3.

Thyroid Antibody Tests

• Two common antibodies are directed against thyroid cell proteins:thyroid peroxidase (TPO) and thyroglobulin.

• Positive anti-thyroid peroxidase and/or anti-thyroglobulinantibodies in a patient with goiter will diagnose Hashimoto’sthyroiditis.

• TSH receptor antibodies are increased in Graves' disease (its

measure is rarely required to follow up medical treatment).

Thyroglobulin

Exceptions

• Secondary hypothyroidism (due to pituitary dysfunction) has

low TSH levels.•

The rare form of hyperthyroidism due to TSH secreting pituitaryadenoma has high TSH levels.

Exception

T3 toxicosis , a type of toxic goiter (usually nodular) secretes only T3

(T4 is usually normal or low) and the patient commonly present by

cardiac manifestations only ( thyrocardiac ).

Thyroid is a sequestrated antigen (isolated from the immune system) and

autoimmune conditions as Graves' disease and Hashimoto thyroiditis will

be associated with formation of antithyroid antibodies.


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

malignancy (as papillary).

Calcitonin

•

Is the tumor marker of medullary thyroid carcinoma (for followup and for screening (the only diagnostic tumor marker) of the

relatives of the patient).

Other biochemical investigations:

• Increase cholesterol level in myxedema.

• Alimentary glucosuria in thyrotoxicosis.

•

Increase calcium level in thyrotoxicosis.

Imaging:

U/S: to confirm; anatomical diagnosis, nodularity and to determine if it is solitary

or multiple, cystic or solid.

Plain X-rays: may be helpful in retrosternal goiter.

CT: for local tumor infiltration and to detect retrosternal goiter.

Technetium scan: Done if you suspect retrosternal goiter, ectopic thyroid and to

detect bony metastases.

Histopathological diagnosis: FNAC needle is valuable, however it cannot

differentiate follicular adenoma from carcinoma (cannot detect vascular and

capsular invasion) in such condition we can do:

• Tru cut needle is painful and may cause hematoma.

• Open biopsy: removing the whole thyroid lobe (hemithyroidectomy)

and examine it by paraffin section.

Indirect laryngoscope: most important investigation before surgery to determine

if there is vocal cord injury (silent recurrent laryngeal nerve injury) for medico

legal purpose.

Treatment


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

and for prophylaxis we use iodinized salt).

- Simple multinodular goiter: Subtotal thyroidectomy in case of

pressure symptoms, cosmetic, and suspicious malignancy,(removes the excess of the gland and leave as normal size = 2x5 cm

of the gland in each side in the posterior medial aspect to preserve the

RLN and the parathyroids).

Postoperative: Give L-thyroxin as replacement and to decrease

recurrence.

- Graves' disease: in young; anti thyroid drugs and if failed! total

thyroidectomy (best as it is auto immune disease, to get rid of thesource of antigen) or subtotal thyroidectomy ( leaving half of the

normal lobe 1x5cm on each side).

Postoperative: L-thyroxin as before.

But if more than 45y: radioactive iodine is better (unless there is indication of

surgery as usual = pressure or cosmetic).

MALIGNANCY WITH THYROTOXICOSIS IS EXTREMELY RARE

-Toxic nodular goiter: if toxic nodule do hemithyroidectomy and if multiple

do total or subtotal thyroidectomy.

Postoperative: L-thyroxin.

TTT of malignancy: (sometimes the Qs start by asking you to enumerate the

types of thyroid malignancy, which is mentioned below)

- Papillary: total thyroidectomy with central lymphadenoctomy .

- Follicular: if less than 1cm; hemi thyroidectomy, but if more than

1.5cm; total thyroidectomy with radioactive iodine after surgery.

NB: L-thyroxin: is usually given for all patient after surgery

In malignancy L-thyroxin is given to:

• In Papillary: the tumor is TSH dependent so L-thyroxin will

decrease TSH and for replacement.

• In Follicular: only for replacement.


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Other tumors:

- Anaplastic carcinoma: the tumor is inoperable so do isthmectomy +

tracheostomy + radiotherapy

- Medullary CA: total thyroidectomy + radical neck dissection and

screen other family member.

- Lymphoma: thyroidectomy + chemo and radio therapy.

Thyroiditis

• Hashimoto: In early toxic stage give anti thyroid drugs and in

hypothyroid stage give L-thyroxin.

If pressure manifestation: do thyroidectomy.

• Sub acute thyroiditis: there is good response to prednisolone.

CASE PRESENTED WITH

SOLITARY THYROID NODULE

What is your DD?

• Simple (non-toxic) nodule.• Autonomous thyroid nodule (toxic).• Adenoma: Follicular adenoma (with variable subtypes).• Follicular carcinoma, less common Papillary (more common to

be multinodular) and medullary CA.• Simple cyst

Incidence of malignancy in true solitary nodule (solid) from 12-30 %,

Highest risk in young male

How can you manage this patient?

1. Exclude toxicity:• Toxic symptoms: Most important, weight loss despite of

polyphagia , intolerance to weather & palpitation.


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in addition to other symptoms as neurological, cardiac and

genitourinary manifestations.

Toxicity signs: Mainly;

Pulse (tachycardia & arrhythmias).

Eye sign (Lid retraction, starring Gaze, lid lag, inability to

maintain convergence exopthalmos, occurs in AI

conditions (not with autonomous nodule.

Enlarged hypervascular gland .

In addition to being underweight, flushing, warm sweaty

hands, tremors, hair changes, nail changes,and pretibialmyxedema in AI conditions (not with autonomous

nodule).

2. Neck sonography: to confirm being, cystic or solid or presence of

other nodules.NB: True solitary nodule= palpable one nodule without enlargement of the rest

of the gland, confirmed by sonography (if the rest of gland is enlarged it will be

multinodular goitre with Dominant nodule)

3. Thyroid profile: TSH first, then if abnormal ! measure free T4and T3

4. FNAC( fine needle aspiration cytology): trustable in all thyroid pathology and it is the most important diagnostic test in solitarythyroid nodule But If follicular neoplasm it cannot differentiate adenoma from

carcinoma, so we do hemi-thyroidectomy, paraffin section to see

capsular and vascular invasion in follicular carcinoma.

NB: No use of radioactive scan: Only to detect metastasis and

ectopic thyroid tissues.

CLINICAL PICTURE SUGGESTIVE OF MALIGNANCY IN THYROID

SWELLING

• Rapid enlargement indicates malignant change.


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• Pain indicates extra capsular invasion and pain is referred toear through vagus nerve (Arnold branch) which supplies the

back and the lobule of the ear. What other symptoms and signs which may help diagnosis?

• Symptoms: Dyspnea, stridor, dysphagia, hoarseness, metastatic

(skull, femur) and lung.• Signs:

Hard nodule, irregular nodule, fixed nodule.If papillary multinodular and lymph nodesWeak or absent carotid pulsation(Berry’s sign)May be hypervascular gland with pulsation, thrill and bruit.

What are the investigations which establish diagnosis?

-FNAC.

-Tumor marker: Thyroglobulin for papillary and follicular CA, and

calcitonin for medullary CA.

-Before operation direct laryngoscope (for medico legal issues to detect

silent RLN injury)

-CXR , lung and liver CT.

NB: Radioactive scan to detect metastases is done after thyroidectomy to

avoid uptake of radio iodine to metastases.

4. How can you manage this case?

-Total thyroidectomy.

-Remove enlarged lymph nodes or do central block dissection.

Metastasis:

-Radioactive I131.

POSTOPERATIVE COMPLICATIONS OF THYROIDECTOMY

1. Respiratory distress which if not treated urgenly! suffocation

Describe priorities in management of this patient


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Ensure patent airwayOpen wound in the bedEvacuate any hematomaIf no immediate improvement; do laryngostomy or at least insert

wide bore canula in the trachea to be followed by tracheostomy.

Mention the causes of post-thyroidectomy respiratory distress

i. Hematoma :reactionary hemorrhage (bleeding within

24hr)

ii. Laryngeal edemaiii. Bilateral partial recurrent laryngeal nerve injury

iv. Acute tetany (laryngismus stradulus)

2. Other complications of thyroid surgery?

•Endocrine:

- Hypoparatyroidism!Tetany

- Hypothyroidism

- Recurrent Toxic Goiter

• External laryngeal nerve injury: shocking• Tracheal and esophageal injury• Keloid

NB;TO REMEMBER

RLN injury

PR: P (Partial injury) affects R (Respiration)

Partial unilateral !DyspneaPartial bilateral! SuffocationCV: C (Complete injury) affects V (voice)

Complete unilateral! HoarsenessComplete bilateral! Aphonia


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LIPOMA

! Commonest sites: U &LL & trunk specially back but may occur in any site(universal tumor) except (areas don't contain fat); intracranial (but may occur

extradural in V Column), eye lids, glans penis and clitoris

! May be subcutaneous, subfascial, intermuscular, subsynovial (around knee),subperiosteal and sub-mucous (dangerous in larynx as it may cause

suffocation and in intestine as it causes intussusception)

C/O:

! Painless slowly growing tumor

! May be painful if infected, under tension as subperiosteal type, if pressing

nerve, adiposa delerosa (see below)

! Very rarely to change to liposarcoma (doubtful, and liposarcoma is malignantfrom the start)

O/E:

! SC lipoma: Soft lobulated tumor with slippery edge and attached to skin by

multiple dimples

! Fibrolipoma is firm

! Angiolipoma is bluish

! Intermuscular or subfascial lipoma have no dimples and become less prominent

with contraction of the related muscles

Dimpling and slippery edge

! Complications (very rare): infection, calcification, malignancy?, suffocationand intussusception (see before)

! Multiple lipomas may be seen and may be painful (adiposa delerosa)

! NB: adiposa means lipoma and delerosa means painful

! TTT: excision if large or causing discomfort of patient as complications are rare

DERMOID CYSTS ! Cysts lined by squamous epithelium

! Types:A. Teratomatous dermoids:

! Are found in the ovary, testis, retroperitoneum , superior mediastinum,

and the presacral area.

! Teratomas (variable degrees of malignancy), arise from ‘ totipotent ’

cells, from all three embryonic layers: ectoderm, endoderm,mesoderm .so, it contains hair, teeth, muscle, gland tissue.


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B. Sequestration dermoids:

! Formed by the inclusion of epithelial ‘nests’ beneath the skin at sites ofembryonal fusion (midline of oral cavity and neck, external angular

process, root of nose, around ear and may be in internal organs)

! Usually present as painless slowly growing swelling which is cystic(Paget's test) and not attached to skin and deeper structures

! Treatment by excision (if in the head wait till the sutures close)

C. Implantation dermoids:

! Follow puncture wounds, commonly of the fingers, when livingepithelial cells are implanted beneath the surface

! More; in hair dresser, gardeners and tailors

! Present as painless slowly growing swelling in hand or over scar

! TTT: Excision

NB: no sequestration dermoids in limbs as it develop by budding with any embryonal fusion

D. Tubulo-dermoids: as thyroglossal and branchial cysts (cystic changes in

embryonic remnants)

E. SEBACEOUS CYST (Retention Dermoids):

! Due to obstruction (usually start by inflammation) of the sebaceous gland duct(of the hair follicle)

! Not found in palm and sole (no hair follicles)

! This is a cyst contains keratin, sebum, and is surrounded by an epithelial wall.

! Occurs at any age but rare in childhood

C/O:

! Painless slowly growing swelling commonly in face, scalp, neck, trunk, or limbs

! Becomes painful and increases in size if infected

O/E:

! Hemispherical swelling (may be multiple), attached (tethered) to skin by single

point (punctum or the black point), cystic (Paget's) and mobile

! If inflamed become hot, red, and tender

Complications:

1- Infection

2- Ulceration3- Sebaceous horn


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TTT:

! Excision with skin ellipse to remove the punctum if not infected

! If infected, drain it first by incision with antibiotic and excise it after resolution

of infection


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SWELLINGS OF THE LYMPH NODES ! There are approximately 800 lymph nodes in the body, 300 of them lie in the

neck. ! Usually multiple swellings.

! May be part of generalized lymphadenopathy, as:

1. Viral (HIV, infectious mononucleosis)

2. Bacterial as in septicemia (non specific) or specific as TB and syphilis

3. Parasitic as toxoplasmosis, lishmaniasis

4. Neoplastic: as lymphoma, leukemia, and rarely generalized carcinomatosis

(usually localized enlargement)

5. Autoimmune, sarcoidosis, etc

! Localized lymphadenopathy:

1. Infection or malignant deposits may come from any part of head and

neck, as, the oral and nasal cavities, the ear, the scalp, the oropharynx

and face.

2. In lower deep cervical nodes (supraclavicular), the source may be breast,

lung, liver in right side or advanced visceral malignancy on left side

(Virchow's LNs)

3. Most of lymphoma start in lower deep cervical LNs

"#$ %&'Cervical LNs, Group I submental above hyoid, II submandibular and

upper part of upper deep LNs, III ant triangle from thyroid crtllage to

cricoid, IV ant triangle fom cricoid to clavicle, V LNs in post triangle

including supra clavicular, VI anterior group (pre-laryngeal and

pretracheal LNs)

TUBERCULOUS CERVICAL LYMPHADENITIS

May be:


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• Blood borne:

Usually secondary to pulmonary TB

The lymph nodes are enlarged, firm and arranged in chains (like rosary)

It must be differentiated from lymphoma by lymph node biopsy

• Lymphatic borne:

1. If the infection starts in upper deep cervical lymph nodes:

The tonsils act as portal (gate) only and no TB lesion is found in it

The organism is bovine type which is transmitted throughcontaminated milk

2. If the infection starts in lower deep cervical lymph nodes:

Infection comes from active pulmonary TB

The organism is human type

NB: if start of infection in any group it may spread the other i.e. upper % lower

Pathological changes of lymphatic borne TB: The inflammation starts an

the capsule and around it (peri-adenitis)! MATTED lymph nodes!

tuberculous reaction inside the nodes –Caseation with breaking of the septa

!Cold Abscess! penetrates fascia then skin to open by multiple sinuses

with undermined edges


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Clinically:

• Painless or slightly painful neck swelling

• Loss of weight and loss of appetite

• Night fever and night sweating

• Manifestation of pulmonary TB if lower deep cervical lymphadenitis

• If upper deep cervical TB lymphadenitis! the tonsils appear free

• Enlarged nodes: first firm with matting! cystic cold abscess! multiple

sinuses with undermined edges

Investigations: Most important lymph node biopsy but start by

1. CBC will show anemia and lymphocytosis, leukemia

2. CXR ! pulmonary TB only if the infection starts in lower deep

cervical LNs

3. Tuberculin is good negative test but not in Immunocompromized

patients

Treatment: Anti-tuberculous drugs, drainage of cold abscess, dressing of

the sinuses with anti-tuberculous drugs

LYMPHOMA

Hodgkin lymphoma: Curable tumor

! Age: peak around 15 and another around 45 years

! Commonly to start in lower deep cervical lymph nodes but may start

in upper or any other group

! Usually start as uni-centric enlarged node! lymphatic spread to

other lymph nodes in the same group (first like satellite! discrete

lymph nodes)

! It is rubbery in consistency


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Hodgkin lymphoma discrete lymph nodes

Clinically:

• Painless enlargement of lymph nodes, may become painful after

intake of Alcohol or late after infiltration of nerves

• May be manifestation of Mediastinal syndrome (dyspnea, dysphagia,

hoarseness and hic-cough due to phrenic N irritation)

• Abdominal swelling (spleen or para-aortic LNs)

• Systemic manifestation:

1. Fever, may be typical Pel-Ebstien

2. Itching; may be the first presentation

3. Significant loss of weight


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4. Anemia

STAGES:

1. Stage I: one group is affected

2. Stage II: more than one group on one side of the diaphragm (above

or below)

3. Stage III: more than one group on both sides of the diaphragm

4. Stage IV: extra- lymphatic spread as bone, peritoneum, CNS

! S: means involved spleen

! E means involved extra-nodal disease as gastric, intestinal or thyroid

! A: no systemic manifestations

! B: presence of systemic manifestations

Investigations:

! Mainly depends on biopsy, but we start by

! CBC may show anemia and esinophilia

! CT chest for Mediastinal syndrome, and for abdomen for any

abdominal lesion

Treatment:

Stages I, II IIIA! Radiotherapy

Stages IIIB and IV! chemotherapy

Non Hodgkin's lymphoma

• More common

•May be related to infection as HP (gastric), EB virus, HCV, HIVinfection


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• Multicentric

• Spread by blood

• Symptoms as Hodgkin's but wit rapidly progressive course

• Lymph nodes are first firm or hard the consistency becomes variable

due to necrosis

• Rapid fusion of lymph nodes which form irregular fixed mass

• Staging, investigations and ttt as Hodgkin disease but with less

favorable prognosis

DIFFERENTIAL DIAGNOSIS OF NECK SWELLING

A. Middle Swellings:

1. Ludwig Angina

2. Enlarged submental lymph node

3. Sublingual dermoid

4. Lipoma in submental region

5. Thyroglossal cyst

6. Subhyoid bursitis7. Extrinsic carcinoma of the larynx (late)

8. Goiter (thyroid isthmus / pyramidal lobe/ Retrosternal goiter

9. Enlarged suprasternal lymph node

10. Dermoid cyst ( can occur anywhere in the midline )

B. In the side of the neck:

! Parotid swelling: in the gap between mastoid and angle of mandible below the

external auditory canal

! IN THE SUBMANDIBULAR TRIANGLE1. Enlarged lymph nodes

2. Submandibular salivary gland

3. Deep or plunging ranula

4. Extension of growth from the jaw

! IN THE CAROTID TRIANGLE

1. Aneurysm of the carotid arteries

2. Carotid body tumor

3. Branchial cyst

! IN ANTERIOR TRIANGLE

1. Goiter2. LNs


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3. Sternomastoid tumor

! IN THE POSTERIOR TRIANGLE

1. Supraclavicular lymph nodes

2. Cervical rib

3. Cystic hygroma

4. Lipoma

5. Pharyngeal pouch

6. Subclavian aneurysm

7. Aberrant thyroid

1. SWELLINGS OF THE SUBMANDIBULAR SALIVARY

GLAND:

! Commonly infection and rarely neoplasms

! Infection is usually associated with submandibular salivary stone.

!In stage of stone alone: a history of enlargement of the swelling (withsalivary duct colic) at the time of meals which subsides after meals

! May be followed by acute suppuration and abscess formation (FAHMR)

! In stage of chronic sialoadinitis, there is a slightly painful swelling which can

be palpated bimanually where the deep part of the salivary gland can be felt

! Further, pressure on the swelling may result in the flow of pus through the

orifice of the Wharton's duct.

NB: submandibular gland swelling; is single, fixed to mandible with no groove with it, and

better to be palpated bimanually

NB: submandibular LN swelling; multiple, has a groove between it and the mandible, can be

rolled over the mandible (mobile), and can be palpated from outside only2. Ludwig angina:

! Ludwig angina: Is a form of cellulitis that starts in the submandibular region and

spread to the floor of the mouth.

! It produces a diffuse swelling beneath the jaw and inside the mouth with fixingthe tongue.

! Usually polymicrobial

! It might have dangerous complication:A. Edema of glottis may obstruct the airways, necessitating tracheotomy

B. Mediastinitis

C. Fatal septicemia


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Ludwig Angina

3. Branchial cyst:

! From the vestigial remnants of the second branchial cleft

! Branchial cyst though congenital, it usually appears in adolescent and adults.

! Oval cystic swelling deep to the upper third of the sternomastoid muscle

! The diagnosis is confirmed by finding cholesterol crystals in aspiration

! It passes between bifurcation of carotid vessels, which may cause difficulty inexcision ! recurs or causes fistula

Branchial Cyst

4. CERVICAL RIB:

! Extra rib arising from the 7th cervical vertebra in less than 1% of population

Clinical types:

! Lump in the lower part of the neck which may be visible (collection of fatsimilar to lipoma over the rib)

! Cervical rib with vascular symptoms (if complete); as Reynaud's syndrome

! Cervical rib with nerve-pressure symptoms (C8 & T1)

! Diagnosed by x-rays & treated by excision

5. Thyroglossal cyst:

! May be present in any part of the thyroglossal tract, from foramen cecum to pyramidal lobe of the thyroid isthmus

! The common site in order of frequency, are beneath the hyoid, in the region of

the thyroid cartilage, and above the hyoid bone.

! The swelling moves upwards on protrusion of the tongue as well as on

swallowing.

! The wall contains nodules of lymphatic tissue, so it is liable to inflammation.

! An infected cyst is often mistaken for an abscess and incised, a thyroglossal

fistula arises which is never congenital , it follows infection or inadequate

removal of a thyroglossal cyst

! Do Technetium scan and if it is the only thyroid tissue leave it but if thepatients wants to remove it implant it to abdominal muscles or give the patient

L thyroxin


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! The operation is sis-trunk operation removing the cyst or ectopic thyroid with

the whole thyroglossal duct from tongue to thyroid, including the middle part of

hyoid bone to avoid recurrence or fistula formation (same ttt of the fistula)

6. ECTOPIC THYROID:

! Residual thyroid tissue along the course of the thyroglossal tract

! May be lingual (if enlarged! respiratory obstruction), cervical or intra-thoracic

Median ectopic thyroid:

! Swelling in the upper part of the neck and is usually mistaken for a thyroglossalcyst but solid

Lateral aberrant thyroid:

! May be a metastasis in a cervical lymph node from an occult thyroid carcinoma.

! Manage median type as thyroglossal cyst

NB: Lingual thyroid is liable to hemorrhage ! suffocation and it is the most liable

thyroid tissues for malignant change, so it must be excised.

7. Carotid body tumor: Chemodectoma or ‘potato’ tumor:

! Common in high altitude area and may be bilateral

! This potentially malignant growth is located at the bifurcation of the

common carotid artery, i.e. at the level of the upper border of the thyroid

cartilage.

! It gives rise to a hard ovoid lobulated swelling under the upper third of thesternomastoid (site of branchial cyst, but not cystic)

! Movable laterally but not vertically, as it is attached to the carotid.

!Pulsation of the carotid arteries can be felt in front, but the swelling itself isnot pulsating.

! Pressure over the swelling has to be avoided as it may cause slowing of the

pulse-rate and a feeling of faintness ( carotid body syndrome )

! Investigations: Carotid angiography and CT

! TTT: excision

8. Aneurysm of the carotid or subclavian A:

! Thromboembolic complications in arm with digital acute ischemia

(90%).

!Punctate cynotic lesion in hand.

! Brachial plexus compression! pain

! A Pulsatile palpable mass in supraclavicular fossa or carotid triangle

! Palpable thrill and Auscultate loud bruit

! Radial/ ulnar pulse may be lost.

! Duplex and angiogram are diagnostic

9. Sternomastoid tumor:

! Is not a tumor

! It is the result of birth injury to the sternomastoid muscle, causing thrombosis

and subsequent fibrosis.

! It gives rise to a circumscribed firm mass within muscle, this usually subsidesspontaneously but may, later on, lead to torticollis


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10. Cystic Hygroma:

! Dilated afferent lymphatics (not true lymphangioma)

! Arising under the deep fascia and extending deeply between the muscles.

! Usually located at the root of the neck and may spread to the mediastinum and pectoral region.

! Mediastinum extension is suspected if it gets tense on straining

! It is usually multilocular but may be unilocular & translucent (hydrocele of theneck)

! TTT: excision best before school age

Surgical Disease of the Adrenal Gland

• Blood supply

Arterial

• 3 arterial sources of flow: 1. Inferior phrenic artery

2. Aorta 3. Renal artery

Venous

single main vein most important surgical structure

- right ! IVC (long) - left ! renal vein (short, may be injure during

operation)

The Incidental Adrenal Tumor

(Incidentaloma)

• 0.5 – 5% of abdominal CTs show abnormal adrenal glands

• 85% of adrenal masses are nonfunctional and BENIGN

• Def. of incidental mass:

Mass >1cm, discovered on exam for non-adrenal cause - absence of signs or

symptoms of adrenal disorder

It may be:

• Nonfunctioning adenoma 82%

• - Functioning:Cushing’s 5%

Pheochromocytoma 5%

Aldosteronoma (Conn’s) 1%

- Malignancy:

Metastasis 3%

Adreno cortical carcinoma (ACC) 4%

NB: If mass >6cm à ACC will be 65%

Hormonal assessment

• Serum potassium (if HTN) ! Conn’s

• Plasma metanephrines: most sensitive test for pheochromocytoma


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• 24-hr urine cortisol (Cushing’s)

Treatment: Hormonally active ! surgical removal

Non active:

• > 3 cm ! removal

• < 3 cm observePheochromocytoma

functioning tumor of the adrenal medulla

Rule’s of 10

• Bilateral

• Familial (non-sporadic, may be a part of MEN II)

• Pediatric

• Malignant

• Normotensive

• Extra-adrenal (paraganglioma)

• Multiple

NB: Childhood presentation breaks the rules- 25% bilateral, multiple, extra-

adrenal

Symptoms: are due release of epi/norepinephrine - - Hypertension present 90%

cases

- Orthostatic hypotension may occur due to low plasma volume

• Triad: headache, tachycardia, diaphoresis

•Other symptoms: Pallor, flushing, palpitations, abd/chest pain, weakness, psychosis NB: Small tumors more likely symptomatic

Diagnosis:

• Plasma free metanephrines- most sensitive test -seen 99% of patients

• 24 hours urinary catecholamines or its metabolites as VMA (2x normal is diagnostic)

• Localization by CT or MRI

MIBG for suspected metastases

Treatment: adrenalectomy

Preoperative preparation:

• Early alpha blockade• Goal to control hypertension, use phenoxybenzamine

• Do NOT use b-blocker before alpha blocker as it will lead to unopposed alpha agonism

à severe hypertension

• IV hydration

Cushing’ Syndrome

Is a group of signs and symptoms caused by prolonged excessive amounts of circulating

cortisol.

• Iatrogenic: exogenous cortisol

• Adrenocortical adenoma or rarely CA


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Cushing disease: pituitary adenoma secreting ACTH leading to bilateral adrenal

hyperplasia

Clinically

• Obesity :Typically the distribution of fat involves the trunk, particularly the

cervicodorsal region (buffalo hump), supraclavicular area, and abdomen. The face isround and plethoric (moon face). The extremities are thin in relation to the rest of the

body.

• The skin of patients with Cushing's syndrome is thin and fragile, ecchymoses and

hematomas results from a combination of thin skin and capillary fragility.

• In the Cushing disease there dark skin due to excess ACTH

• Striae rubra: when present, are usually located on the abdomen, breast, and axillae.

Occasionally, they may be found on the back and on the extremities. They are pink or

purplish in color and wider than 1 cm

• Hypertension

• Proximal muscular weakness affecting predominantly the muscles of the pelvic girdle

• Acne, hirsutism, and menstrual irregularities

• Osteoporosis, compression fractures and persistent back pain

• Peripheral edema

• psychiatric manifestations, including anxiety, depression, and even frank psychosis

Diagnosis:

1. Glucose intolerance, glucosuria is often seen, but ketoacidosis or the chronic

complications of hyperglycemia are very uncommon2. The level of cortisol in plasma and 24 hours urinary cortisol and ACTH

3. Dexamethasone suppression test

4. Radiologic diagnosis includes X-ray examination for a pituitary tumor, and computed

tomography which is the most popular procedure for visualizing the adrenals in patients

with Cushing's syndrome

Treatment:

• Pituitary ablation in the disease (surgical or irradiation)

• Adrenalectomy in adrenal tumors

Conn’s syndromeHyperaldosteronism leading to surgically correctable hypertension with hypokalemia

(adrenalectomy)

Parathyroid gland

Anatomy:

• Superior glands usually dorsal to the RLN at level of cricoid cartilage

• Inferior glands located ventral to nerve

• Usually derive most of blood supply from branches of inferior thyroid artery, although

branches from superior thyroid supply at least 20% of upper glands.


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

Calcium metabolism:

• The parathyroid cells regulate PTH secretion by sensing extracellular calcium levels

• PTH secretion also is stimulated by low levels of 1,25-dihydroxy vitamin D and

hypomagnesemia.• PTH functions to regulate calcium levels via its actions on three target organs, the bone,

kidney, and gut.

• Increased PTH secretion leads to an increase in serum calcium levels by increasing bone

resorption and enhancing renal calcium reabsorption.

• PTH also stimulates renal 1-a Hydroxylase activity, leading to an increase in 1,25-

dihydroxy vitamin D, which also exerts a negative feedback on PTH secretion

• At the kidney, PTH acts to limit calcium excretion at the distal convoluted tubule via an

active transport mechanism.

• PTH also inhibits phosphate reabsorption (at the Proximal convoluted tubule) and

bicarbonate reabsorption.

• PTH and hypophosphatemia also enhance 1-hydroxylation of 25-Hydroxyvitamin D,

which is responsible for its indirect effect of increasing intestinal calcium absorption.

HYPERPARATHYROIDISM

• Primary hyperparathyroidism occurs in 0.1 to 0.3% of the general population and is

more common in women than in men (4: 1).

• Primary hyperparathyroidism is characterized by increased parathyroid cell proliferation

and PTH secretion which is independent of calcium levels.• Etiology unknown, but radiation exposure, and lithium implicated, associated with

MEN1, and MEN 2A

• Parathyroid adenoma in approximately 80% of cases, multiple adenomas or

hyperplasia in 15 to 20% of patients and parathyroid carcinoma in 1% of patients.

Clinically:

• Kidney stones, painful bones, abdominal groans, psychic moans, and fatigue overtones

• Kidney stones calcium phosphate and oxalate

• Osteopenia, osteoporosis, and osteitis fibrosa cystica, is found in approximately 15% of

patients with PHPT. Increased bone turnover can usually be determined by documentingan elevated blood alkaline phosphatase level.

• Peptic ulcer disease, pancreatitis

• Psychiatric manifestations such as florid psychosis, obtubdation, coma, depression,

anxiety, fatigue

Investigations:

• Hypercalcemia can be from other sources. Intact PTH measurement and elevated PTH

level very sensitive for hyperparathyroidism

Pre-operative localization


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• The predictive value of ultrasonography, magnetic resonance imaging, or thallium-

technetium dual isotope scintigraphy ranges from 40 to 80 percent

Most sensitive is Tc sistamibi scan due to delayed washout

Surgery:

• Bilateral neck exploration is “gold standard”• With pre-operative imaging techniques can have minimally invasive focused surgery

towards adenoma

• If hyperplasia excise 3.5 glands and implant the other half in the deltoid to avoid neck

exploration if recurrence occurs

• Intraoperatively, cancer is suggested by the presence of a large parathyroid tumor that is

invasive into surrounding tissues

• bilateral neck exploration, with en bloc excision of the tumor and the ipsilateral thyroid

lobe.

• Modified radical neck dissection is recommended in the presence of lymph node

metastases

Secondary in prolonged hypocalcemia in renal failure will increase PTH and if it

persists the gland will act autonomously and problems like primary will occur

BREAST CASES• The breast is developed from the milk line (from axilla to groin),

each line can produce more than one breast or nipple.

• Polymazia: means presence of more than 2 breasts

The extra one must be excised as it is very liable for malignant changes

• Polythelia: more than 2 nipples, it may be excised for cosmetic

purposes.

Lactating mastitis

• predisposed by lack of hygiene ,fissures , cracks and retracted

nipple.

Milk engorgement is a stage of the disease rather than a

predisposing factor.

Organisms:

o Staphylococcus aureusà localized to abscess (90%) andStreptococcus species (diffuse infection).


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o Stages:

1-Milk engorgement:

.Sector of the breast . Dull aching pain.

.No fever

The affected sector is tender and indurated.

No enlarged axillary nodes

2-Diffus mastitis:

.Burning pain .Fever.

.Hot ,red ,tender,and indurated sector.

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

.Throbbing pain . Hectic fever

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

edema

.Axillary nodes enlarged and soft

NB: Never we wait till the abscess becomes fluctuant (very late)

4.Complicated cases:

.pus from nipple .sinus formation

.Antibioma(fibrous wall and sterile pus)

• DD: Diffuse mastitis must be differentiated from inflammatory CA

(more than one third of breast, no fever ,more edema,LNs are hard and

non tender ,no leukocytosis and no response to antibiotics).

• Treatment:

- Good hygiene .

- Treatment of fissures and cracks.

- Hot foments .

- Antibiotics against resistant staph .

- Drainage of formed abscess


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• Incision: at most dependent and most pointing if don’t meet, do

incision and counter incision

• Lactation: use safe antibiotic for the fetus and lactate from the normal

side and evacuate the other side by suction pump.

Mammary Duct Ectasia

Treatment:

- Infection :antibiotics to anaerobes

- Abscess : drainage

- Fistula : excision

- Mass : triple assessment

- Discharge :see latter

Fibrocystic changes

(Fibroadenosis, Mammary dysplasia)

The changes consist of 4 features:

• Adenosis (increase no of glands)

• Epitheliosis with or without papillomatosis,

• Fibrosis sometimes-extensive forming hard mass ( sclerosing adenosis)

simulating cancer.

• Cyst formation.

The changes may be proliferative (premalignant)

Dilatation of large ducts

Stasis

Periductal (plasma cell)mastitis

Chronic mass ± colored discharge

Fibrosis (DD: CA)

Abscess

Fistula


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or non proliferative

Clinically:

Age:Around 30s.

Symptoms:

• Cyclical mastalgia (exaggerated premenstrual mastalgia).

• Discharge : thick green or straw yellow.

• Localized mass: usually aggregated or large cyst or sclerosing adenosis

Signs:

• The disease is usually bilateral but may be unilateral.

• The lesion is usually diffuse but may be localized.• May be solid or cystic.

• Cysts are granular ,nodular or large.

NB fibrocystic changes are commonly known as painful nodular condition of

the breast.

• Axillary nodes may be enlarged and small (like gun shots)

Investigations:

Diffuse bilateral lesions:

• with dischrge:measure prolactin level to exclude pituitary microadenoma

with hyperprolactinemia (simulate the disease).

Localized lesion:

• Triple assessment to exclude carcinoma.

Discharge: see below

Microwave radiometry can differentiate proliferative (more heat production)

from non proliferative lesions.

Treatment:

• Reassurance

• Firm bra to decrease mobility of breast.

• Avoid excess fat &caffine (tea , choclate ,coca , coffee)

• Vitamin E, thiamine, magnesium, and evening primrose oil may be of help.


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• Simple analgesic for pain.

• Bromocryptin in intractable pain but causes severe nausea.

• Cases proved to be proliferative need regular screening for breast cancer.

Duct papiloma

• Pathology Situated in one of the major ducts near its orifice usually single

but may be multiple and peripheral (Multiple Papillomatosis)

• Clinical Picture young adult female (30-45) presenting with blood

discharge from the nipple.

• on examination a fresh drop of blood is seen on pressure at a certain pointor a palpable small fusiform retroareolar mass is felt (retention cyst due to

obstruction of the duct by clotted blood) pressure on it produces the

discharge.

• Investigations guiac test discharge is +ve for blood.

• Galactography using lipiodol shows regular filling defect

• Treatment microdochectomy & if multiple do excision of major ducts.

Fibroadenoma

• Age: 15-35.

• Size: 2-3 cm.

• Diagnosis: by triple assessment

• Symptoms: discrete lump.

• Signs: normal skin, not tender, not hot, 2-3cm, hemispherical,

smooth, well defined, firm to rubbery, freely mobile.

NB if presentation is delayed to above 35 ys it will be soft .

Giant fibroadenoma is rapidly growing variant in adolescent

Phylloid tumor: huge fibroadenoma in middle age (needs mastectomy).

TTT TRIPPLE ASSESSMENT FOLLOWED BY EXCISION BIOPSY


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Differential Diagnosis

DD: Of Painless lump

1. Fibroadenoma ( breast mouse)2. Breast cancer

3. Cyst4. Fibrosed hematoma or chronic fat necrosis

DD of breast pain

A. Painful lump

1. Fibrocystic changes (common)2. Mastitis and absecess

(Usually postpartum or lactational or duct ectasia)

3. Acute hematoma or acute fat necrosis

4. Infected cyst5. Rarely carcinoma (inflammatory).6. Localized milk engorgement

B. Pain without lump:

1. Cyclical breast pain (cyclical mastalgia) is associated with fibrocystic

breast changes and it is usually with lump and rarely without. Mild degreesof cyclical breast pain and tenderness are normal in premenstrual syndrome(PMS).

2. Noncyclical breast pain: as hormonal changes in puberty (both in girlsand boys), in menopause and during pregnancy and post partum due to

fissures and cracks of the nipple, and may be due to alcohol or drugs.

3. Tietze syndrome is a benign inflammation of one or more of the costalcartilages.and leads r to pain (increase with respiration) and tender costal

cartilages which may be mistaken with breast pain

1. What is the differential diagnosis of colored discharge from

nipple?

• Bloody ! duct papilloma is the commonest but may be in duct

carcinoma or duct ectasia.

• Creamy ! duct ectasia (commonest breast discharge and it

can take any color).

• Milky ! hyperprolactinemia due to pituitary microadenoma

http://en.wikipedia.org/wiki/Costal_cartilagehttp://en.wikipedia.org/wiki/Inflammationhttp://en.wikipedia.org/wiki/Pregnancyhttp://en.wikipedia.org/wiki/Menopausehttp://en.wikipedia.org/wiki/Pubertyhttp://en.wikipedia.org/wiki/Premenstrual_syndromehttp://en.wikipedia.org/wiki/Fibrocystic_breast_changes


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NB. Galactocele is a retention cyst contains milk and follows

lactation and milk appears by squeezing I, we treat it by

squeeze or aspiration if any doubt!excision biopsy.

NB .If in lactation; it is normal secretion.

• Brownish, green, yellow, watery etc in carcinoma or

fibrocystic changes.

• Pus in neglected abscess.

2. How can you manage this case?

Take full clinical history with concentration on:

Discharge: if found, ask about;

" Left, right or both?

" Color: see before

" Amount.

" Odor

" Recent history of breast feeding?

" With nipple retraction?

" If associated lump or not?

" If associated pain?

" If any systemic manifestations?

Examination of breast as usual with zonal squeeze of all parts of the breast to

see the discharge colour and if it comes from one or more ducts

NB. Search for presence of lump; clinically and by mammography-

sonography examination

• If there is a lump manage by triple assessment and treat according

to the findings (see the table in the summary at the end).


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• If no lump with bilateral milky discharge!measure prolactin

level! if high!give the patient bromocryptin (parlodel which

causes severe nausea).

•If no lump and coming from one duct! microdochectomy (remove the affected duct only and send for histopathology).

• If no lump and coming from multiple ducts!search for blood by

Guiac or benzidine test:

!If negative for blood: follow up if lump appears! triple

assessment

!If positive for blood! Pt < 45 years! follow up

! Pt > 45 years! excision of the major

ducts

NB. Ductography is expensive and not in common use

NB. Cytological examination of the discharge may be requested

if doubtful intraductal tumors

CARCINOMA OF THE FEMALE BREAST

Etiology:

I-Genetic Factors:

Mutation of the following Suppressor genes:

1-Breast carcinoma gene

BRCA I on chromosome 17

BRCA II on chromosome 13

2-Positive family history in mother or sister (marked increase in

incidence if both are affected, especially if occurs premenopausally)

NB: Genetic factors are responsible for 5-10% of all breast cancer and

it is usually bilateral and multifocal.

II-Endocrinal factors:

Prolonged exposure to estrogen as in:

1-Early menarche below 12 years and late menopause after 50 years

2-Delayed onset of 1-st pregnancy and lactation:-Nullipara: First pregnancy after 30 years.


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-Sterility and females who never lactate.

-High estrogen contents of contraceptive pills.

-Post menopausal hormone (estrogen) replacement therapy (HRT).

III-Obesity:Due to conversion of the suprarenal androgen to estradiol in fatty

tissues.

NB: diet as junk food, plays a rule through induction of obesity or

presence of carcinogenics

Some forms of diet decrease risk if reach in vitamin D and leukopines

(in tomato and red grapes) with other antioxidants

IV-Previous affection of one breast:

■Bilatrality in general about 15-20%■ increases over 25-50% if invasive lobular carcinoma

V-Precancerous Lesions: Benign lesion! turns malignant

-Duct papilloma specially if multiple.

-proliferative forms of fibrocystic changes.

-In situ tumors will become invasive.

Types: Ductal, lobular, Paget, and inflammatory

I. Ductal Carcinoma: 80%A-Non-Invasive Duct Carcinoma (Duct carcinoma in situ or DCIS)

Usually multifocal

B- Invasive duct carcinoma: it may be

1. Adenocarcinoma with productive fibrosis (scirrhous, simplex, NST),

80%

Eighty percent of invasive breast cancers are described as invasive

ductal carcinoma of no special type (NST).

These cancers generally have a worse prognosis than special-typecancers.

Usually associated with dimpling and retracted nipple

2. Medullary carcinoma 4% (Encephaloid): soft brain like tumor,

Better prognosis than NST

Usually attains large size at discovery with ulcers or fungation.

II. Lobular CA: 15%

A-Non invasive Lobular Carcinoma (lobular carcinoma in situ, LCIS)

Usually multifocal.


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

that an invasive cancer will be developed.

Invasive Lobular Carcinoma

It is bilateral in 25-50% and the bilaterality is usually mirror

image

III. Paget’s Disease: 1%

It starts intraductal then becomes invasive

-It arises from main ducts near the nipple.

-The disease starts by: Erosion of nipple, then areola and

after 2 years a mass of infiltrating duct carcinoma will

appear.

IV. Mastitis Carcinomatosa (Inflammatory carcinoma)Occurs mostly during pregnancy and lactation (due to high hormonal

level) if such; it will be known as acute lactating carcinoma, but may occur

at any age unassociated with these events.

Diffuse infiltration of the whole breast with no localized mass, peau

d’orange, retracted nipple, with enlarged hard non tender lymph nodes

DD: Condition may resemble acute bacterial mastitis (but in the latter;

less than one third is affected in addition to fever, enlarged soft tender

lymph nodes and Leukocytosis.

Spread of carcinoma of the Breast:

I-Direct (Local) spread:1st within the breast tissue itself, then to the skin,

pectoral muscles and fascia, serratus anterior muscle and chest wall.

II-Lymphatic spread: By both embolization and permeation.

A-Embolization: - To lymph nodes.

-75% to axillary lymph nodes (Especially from tumors of lateral part

of breast)

-Internal mammary lymph node (especially from medial half)-Posterior intercostal lymph nodes

N.B: Tumors in lower medial quadrant may invade rectus sheath lymph

vessels àumbilicus à malignant umbilical nodule à inguinal lymph node

Or to lymphatics of Falciform ligament à Porta hepatis and liver.

B- Permeation: Retrograde growth in lymphatics to form either: Separate

skin nodules or multiple nearby nodules known as cancer en cuirasses

III-Blood Spread: First to bone (vertebral column) then liver , lung,

brainIV-Trans-coelomic spread:


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

permeation.

B-Nodules in Douglas pouch (Blummer shelf nodules)

Staging:

TNM Classification

T = Tumour

Tx unknown primary

T0 or Tis Carcinoma in situ

T1 Less than 2cm

T2 Tumor diameter 2-5cm

T3 Larger than 5cm or pectoralis invasion

T4 Any size invading skin or chest wall

N = Nodes

N0 Nonpalpable axillary LN

N1 Ipsilateral mobile LN

N2 Ipsilateral fixed LN

N3 Supraclav. Int mammary contralateral axillary LN

M = Metastases

M0 No metastases

M1 Distant metastases

Manchester Classification

Stage I Mass confined to the breast, skin involvement over and smaller

Than tumor size

Stage II Same + palpable mobile one group LNs in Ipsilateral axilla

Stage III breast mass + one of the following:

1- Skin invasion larger than size of the mass

2- Mobile more than one group of Ax. LNs

3- Mass fixed to underlying muscles & fascia

Stage IV any of the above + one of the following:

1-Marked skin affection nodules, ulcer…

2-Fixed Ipsilateral axillary LNs


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3- Ipsilateral supraclavicular LNs

4- Mass fixed to chest wall or serratus.

5- Distant deposits, other breast, contralateral axilla

Symptomsrelated to the primary lesion■A painless breast lump noticed incidentally that is increasing in size.

■Distortion in the shape of the breast (ulceration, skin changes,

pigmentation).

■Alteration in the nipple (inversion, destruction, deviation, bloody

discharge).

■Breast discharge which may bloody, thick greenish or straw yellow

Symptoms related to secondary deposits

■Axillary lump(s)

■Swelling of the arm.

■Backache, limb pain, fracture.

■Dyspnea, chest pain.

■Jaundice.

■Mental status changes, fits.

■Generalized malaise and loss of weight are rare in breast carcinoma.

See clinical sheet for clinical history and examination

NB: if you are asked in the exam what are the investigations? You have to

start as usual by lab investigations as: CBC, Organ profile, Tumor marker

Triple assessment

➢Clinical history and exam, see the sheets.

➢ Imaging (mammography / sonography)

In malignancy there will be microcalcification or star shaped

(irregular mass) and to detect bilateral or multifocal lesions

%&'MAMMOGRAM REPORTS – BI-RADS

By the American College of Radiology (ACR): In this system, the results are

sorted into categories numbered 0 through 6. This system is called the : Breast

Imaging Reporting And Data System(BI-RADS)

1. Category 0: X-ray assessment is incomplete. Additional imaging evaluation and/or comparison to


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prior mammograms is needed. X-ray assessment is

complete

2. Category 1: Negative\negative means nothing bad

was found.

3. Category 2: Benign (non-cancerous)

findingDescribe a finding known to be benign, such

as benign calcifications, lymph nodes in the breast,

or calcified fibroadenomas.

4. Category 3: Probably benign finding – Follow-up in

a short time frame is suggested in 6 months for 2

years

5. Category 4: Suspicious abnormality – Biopsy should

be considered. Findings do not definitely look like

cancer but could be cancer.

6. Category 5: Highly suggestive of malignancy –

Appropriate action should be taken. The findings

look like cancer and have a high chance (at least

95%) of being cancer. Biopsy is very stronglyrecommended.

7. Category 6: Known biopsy-proven malignancy –

Appropriate action should be taken. Mammograms

may be used in this way to detect multifocality.

MRI

Suitable for:

■ Detection of multifocality

■ Doubtful axilla

■ Recurrence after excision to differentiate it from post operative

scarring


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➢ Biopsy:

• Start by FNAC and confirm during operation by

Frozen section biopsy

• Open biopsy if FNAC is not conclusive:

- Excision biopsy (remove all mass with

safety margin).

- Incisional biopsy (remove part of the mass).

If the lesion is proved to be malignant we examine the specimen for ER, PR,

and search for metastases (liver US, bone scan and chest X-rays) and for follow

up CA15.3 (tumor marker).

I. Treatment:

1. Inflammat

ion of the

breast

Stage Commones

tPresentatio

n

Treatment

i. Milkengorgement

Dull aching pain

Hot formantsMassage

ii. Diffuse

mastitis.

Sever

burning pain

Hot foments +

Antibiotic.Suction from theeffected and feeding

from other

iii. Abscess. Throbbing pain, hectic

fever

Drainage by Incision,counter incision and

antibiotic


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2. Duct

ectasia

Creamydischarge +

inflammatory mass

Metronidazole or/andamoxicillin-clavulonic

acid.and drainage of any

formed abscess.

3. Duct

papilloma

Blood per

nipple fromsingle ormultiple

ducts.

guaiac or benzidine test

to confirm blood.a.Microdochectomy iffrom one duct.

b.Excision of majorducts if multiple.

4. Fibroaden

osis =

Fibrocysti

c changes.

Brown or

greenishdischarge

Reassurance

Stop caffeine, chocolateand cola.Wearing firm brassiereOil primorseSimple analgesics

Severe non respondingcases! bromocriptine(causes nausea)

5. Fibroaden

oma

Excisional biopsy


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6. carcinoma

1) earlyStage

1 + 2

• Lumpectomy if

mass ( 4cm withAxillary

clearance

Postoperative

radiotherapy

Chemothera py and

hormonaltherapy

• Modified radical

mastectomy: if

large massor small breast.

central massas in Paget

multifocalmass

if irradiationiscontraindicated.

With post operativechemo and hormonaltherapy as in advanced

stages (but adjuvant).


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Pediatric Surgery

Esophageal atresia

The commonest is blind upper pouch and lower one is communicating with stomach

Clinically:

Continuous pouring of saliva from mouth since birth

Shocking with each feed

2) Advanced

Stage3 + 4

Palliative surgery:Mastectomy

Palliativeradiation:

Palliativechemotherapy:

TACHormonal:• Postmenopausal

use tamoxifen oranstrazole.

• LHRH analoguesin premenopausal.

NB: Neoadjuvant

chemotherapy if locally

advanced tumor we give

preoperative

chemotherapy to

downstage the tumor to

become operable.


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Diagnosis by gastrographin to see the atresia or and fistula

Treatment: thoracotomy, excise the fistula and repair

Congenital hypertrophic pyloric stenosis

The baby is usually first borne male

He is borne with failure of relaxation of pylorus! muscles of pylorus hypertrophies to

overcome resistance!obstructs pylorus

It will lead to projectile vomiting (without nausea)!dehydration and hypokalemia

Examination reveals visible peristalsis and palpable epigastric mass like olive

Diagnosis by US

Treatment rehydration and pyloromyotomy

Hirschsbrung disease


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Rectum and sigmoid are

aganglionic! fails to relax

Clinically: if long segment! neonatal intestinal obstruction

If shorter it will lead to progressive constipation with distended colon and failure to thrive

P/R: there is grasping of the rectum over the examining finger and on withdrawal! gush of

fluid feces

Biopsy must be taken to exclude acquired megacolon due to fissure

Operation at 10 months (10 KG)!. Excise the aganglionic segment and do coloanal

anastmosis

Intussusception

See intestinal obstruction

Anorectal anomalies


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It presents by neonatal intestinal obstruction

It may be high with anorectal agenesis ±fistula with vagina or urinary bladder

Or low: imperforate anus, ectopic anus or anal stenosis

It requires colostomy (immediate) if to be followed by anorectoplasty (10 months 10 KG)

Low anomaly can be incised or dilated

ABDOMINAL CASES

DD OF SWELLINGS OR PAIN ARE VERY IMPORTANT AND

ESSENTIAL TO PASS THE EXAM

Differential diagnosis of abdominal swellings:

The following must be considered for DD of any regional (localized) or diffuse

abdominal swelling or pain:

1. Anatomical background of the abdominal region involved

2. Different causes and pathological disorders affecting this region

3. The most common swellings related to this region


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Don’t forget swellings arising from skin as sebaceous cyst, subcutaneous lipoma,

Hernias, Muscle lesions as firbrosarcoma, nerves as neurofibroma and bony

lesions as primary or secondary tumors

DIFFERENTIAL DIAGNOSIS OF REGIONAL ABDOMINAL

SWELLINGS

■ Diffuse abdominal swellings (distension): remember the 6 Fs +

L ;

1. Fat (obesity)

2 & 3. Flatus or/and Faeces (simple distension, constipation, megacolon or

intestinal obstruction)

4. Foetus (pregnancy)

5. Fluid: free (ascites) or encysted6. Fibroid

Large tumors or organomegaly

As

Large ovarian cyst

Retroperitoneal sarcomata

Hepatosplenomegally or polycystic kidney

Commonest swellings in right lower quadrant (Rt iliac fossa)1. Appendicular mass


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2. Appendicular abscess

3. Carcinoma of the cecum

4. Gynaecological as ovarian cyst, ectopic pregnancy, salpingitis,

fibroid

5. Terminal ileitis (Crohn’s disease)

6. Mesenteric lymphadenitis

7. Other lesions; as tuberculosis, ectopic kidney, lymphadenopathy,

aneurism, etc as mentioned before anatomically and pathologically

NB: Undesended testis is not palpable intra-abdominally unless

malignant change occurs

• In left LQ: As right side but the GIT masses are different including;

diverticulitis, carcinoma of the sigmoid or descending colon NB: the tumors of the left side of the colon are rarely palpable and

forming a stricture and the palpable mass is commonly fecal mass

(can be indented with pressure)."#$ %&'

• Masse from LUQ: Most commonly to be

1. Enlarged spleen

2. Enlarged kidney

3. Carcinoma of splenic flexure4. Suprarenal tumor

5. Tumor from the tail of pancreas.

6. In addition to other swellings from the related anatomical

structures (sebaceous cyst, lipoma, muscle tumor, etc)

Causes of splenomegaly:

1. Infection: tender and soft, as in typhoid, malaria, Kala-azar2. Congestive: portal hypertension due to bilharziasis , cirrhosis, and portal or

splenic vein thrombosis

3. Congestive heart failure

4. Cellular proliferation: Neoplastic or Hyperplastic

Myeloid and lymphatic leukaemia

Polycythemia rubra Vera

Thrombocytopenic purpura

MyelofibrosisSpherocytosis and thalathaemia


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NB: in sickle cell anaemia repeated splenic infarctions may lead to auto-

splenectomy but if splenic vein thrombosis occurs huge splenomegaly may occur

5. sarcoidosis

6. Storage diseases

RENAL SWELLINGS

NB: Commonest cause of renal swelling is hydronephrosis, other causes are;

polycystic kidney, pyonephrosis, tumors, and renal cyst

NB: Commonest cause of unilateral hydronephrosis is stone and commonest

cause of bilateral hydronephrosis is senile enlarged prostate

NB: Renal cysts are very common but rare are large enough to be palpated or

cause symptoms

NB: Renal cell CA (hypernephroma) is the commonest tumor in adults and

nephroblastoma (Wilm’s tumor) is the commonest in children

DD of a mass in right upper quadrant mass in right hypochondrium

1. Hepatomegaly

2. Gall bladder swellings

3. Enlarged kidney

4. Carcinoma of the hepatic flexure of the colon

5. Suprarenal mass

6. Other swellings related to different anatomical structures

ENLARGED LIVER WITHOUT JAUNDICE

1. Congestive heart failure (smooth)

2. Early stages of cirrhosis (smooth)

3. Established cirrhosis (sharp border and granular)

4. Hepatocellular carcinoma (usually cirrhotic with localized mass)

5. Liver secondaries (enlarged with knobbly surface)

6. Other causes as, lymphoma, storage diseases, liver cysts etc

ENLARGED LIVER WITH JAUNDICE

1. Infective hepatitis (smooth and tender)

2. Obstructive jaundice as in gallstones or CA of head of the pancreas (smooth

and non tender).

3. Cholangitis (smooth and tender, with Charcot’ s triad)

4. Portal pyemia (smooth and tender)

5. Decompensated cirrhosis


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

colitis but may be pathogenic e.g infected hydatid cyst

7. Hydatid cyst

CAUSES OF ENLARGED GALL BLADDER

1. Obstruction of the cystic duct, commonly by gallstone and rarely by CA

■ The patient is usually jaundiced

■ It may contain bile and mucus (mucocele)

■ It contains pus (empyema)

2. Obstruction of the common bile duct; by gallstone or CA of head of the

pancreas

Courvoisier’s law: in patient with obstructive jaundice palpable and distended

gall bladder is usually indicative that the cause is not gall stoneThis is due to that gallstones are associated with chronic inflammation with thick

fibrotic wall (non distensible)

Exception includes; empyema and mucocele and others which will be discussed

in jaundice.

Courvoisier's sign: palpable gall bladder in obstructive jaundice (commonly

malignant OJ or due to obstruction by primary stone

3. Carcinoma of gallbladder; rarely large to be palpated and usually diagnosed

first as gallstone disease4. Gall bladder mass as appendix mass (acutely inflamed gall bladder with

adherent omentum)

It is palpated as diffuse tender swelling which does not move with respiration

EPIGASTRIC MASS

• Gastric tumors (advanced Ca or lymphoma)

• Enlarged left lobe of the liver

• Pseudopancreatic cyst• True pancreatic cyst

• Aortic aneurism

• Mesenteric cyst

• Don’t forget; epigastric hernia and divarication of the recti

ABDOMINAL PAIN

DIFFERENTIAL DIAGNOSIS OF REGIONAL ABDOMINAL PAIN


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Right upper quadrant: Left upper quadrant pain as the right but replace

hepatobiliary by splenic causes (as perisplenitis, splenic abscess and splenic

infarction)

1. Hepatobiliary: Biliary colic, acute cholecystitis & hepatitis

2. Urological: renal stone or UTI

3. Referred from the chest

-Lobar pneumonia (basal).

-Pleurisy.

Epigastric pain:

1. GERD.

2. PUD

3. Acute pancreatitis.

4. Acutely perforated peptic ulcer starts epigastric then becomes generalized.5. Leaking or dissecting aortic aneurism.

6. Reference from chest: Inferior wall MI.

Central abdominal pain:

1. Intestinal obstruction.

2. Peritonitis: starts first at site of perforation then becomes

generalized as; if perforated appendicitis starts at RLQ, perforated

PU starts epigastric, perforated GB starts in RUQ, perforated

diverticulitis starts in LLQ3. Mesenteric vascular occlusion.

4. Leaking or dissecting aortic aneurism.

5. Gastroenteritis

6. General causes:

Diabetic ketoacidosis.

Withdrawal symptoms in opiate addicts.

Pain in right lower quadrant: The pain in left LQ as right but replace GI causes by diverticulitis of the colon

Intraperitoneal:

7. Acute appendicitis.

8. Meckel’s diverticulitis.

9. Crohn's disease

10.Tonsillitis (tonsillar tummy) and mesenteric adenitis.

Retroperitoneal:

11.Pyelonephritis.12.Ureteric or renal stones.


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Gynaecological causes:

Mittel Schmerz pain.

Disturbed ectopic pregnancy.

Rupture ovarian cyst.

Salpingitis.

Cystitis.

Urinary bladder stone

Referred from chest

Lobar pneumonia (basal).

Pleurisy.

NB: Visceral pain will be referred to the original dermatome, from which

this visceral structure was de

pre exam surgical notes 2

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