Surgery Pre-Operative / Post-Operative Care

RISK ASSESSMENT CARDIAC DISEASE

- Major risk factors unstable coronary syndromes, recent MI, severe valvular disease, ventricular
arrhythmias
- Intermediate risk factors asymptomatic MI, diabetes mellitus, compensated CHF
- Minor risk factors history of stroke, uncontrolled hypertension
- Goldman Criteria for Cardiac Risk
- Laboratory assessment for cardiac diseases resting LV function, ambulatory EKG monitoring, exercise
stress test, and nonexercise stress testing by using either myocardial perfusion imaging or dobutamine
stress echo
o Resting ventricular function can be evaluated with echo or radionuclide angiography
Patients with an EF < 35% are at greatest risk for complications
Patients with poorly controlled CHF should have an objective assessment of LV function
o Ischemia characterized by ST-segment depression can be identified by ambulatory EKG
monitoring
o Patients with peripheral vascular disease cannot attain target heart rates and thus have
nondiagnostic exercise stress test results
- Indications for preoperative coronary angiography patients with suspected left main disease or triplevessel coronary occlusive disease or patients with unstable coronary syndromes
- In summary:
o Patients undergoing high-risk surgical procedures or those at intermediate risk should be
considered for non-invasive testing for further risk stratification
o Patients at high risk should be considered for angiography
o Patients at low risk should receive no further testing
- Preoperative treatment for cardiac diseases:
o Surgical revascularization with CABG or coronary angioplasty is questionable
o Medical therapy for coronary artery disease beta-blockers, CCBs, nitrates to ensure that
myocardial oxygen demand does not exceed supply
Beta-blockers before surgery can decrease rate of MI, especially give in those at
intermediate and high-risk
- With respect to cardiac complications, the length of time with the anesthetic used rather than the route or
type of agent contributes to the perioperative cardiac risk
History of MI
- Patients with documented prior MI have acute MI at a rate of 6.6% as compared with patients with no history
of MI (0.13%)
- Need history of DOE and other issues, as well as dates of MIs (suspected or confirmed)
- Other clues to the existence of coexisting heat disease syncope, palpitations, arrhythmia
Unstable Angina
Valvular Disease
- Patients with a history of rheumatic heart disease require prophylactic antibiotics to prevent endocarditis,
even for minor procedures
Hypertension
Arrhythmias
Heart Failure

RISK ASSESSMENT PULMONARY DISEASE

- Postoperative pulmonary complications are the most common form of postoperative morbidity experienced
by patients who undergo general surgical abdominal procedures and thoracotomy
o Pneumonia, massive lobar collapse due to mucus plugging, pneumonitis, atelectasis, and more
can cause respiratory insufficiency
o Most postoperative pulmonary complications develop as a result of changes in lung volume that
occur in response to dysfunction of muscles of respiration and other changes in chest-wall
mechanics
- Abdominal and thoracic surgical procedures cause large reductions in vital capacity and smaller but crucial
reductions in functional residual capacity (FRC)
o FRC reduces in lower abdominal operations by 10-15%, in upper abdominal operations by 30%,
and after thoracotomy/lung resection by 35%
None in other procedures
o FRC is decreased by the supine position, obesity, sepsis, ascites, and the development of
peritonitis
- The other important factor in the etiology of postoperative pulmonary complications is the closing volume
(CV), which is the volume at which the flow from the dependent portion of the lungs stops during expiration
because of airway closer
o Factors that promote increased CV advanced age, tobacco use, fluid overload, bronchospasm,
and the presence of airway secretions
- Under stable baseline conditions, FRC is about 50%, and CV about 30% of total lung capacity
o When FRC is reduced or CV is increased, portions of the lung are subject to premature airway
closure and atelectasis. This condition results in a ventilation-perfusion mismatch, resulting in
hypoxemia, and promotes trapping of secretions, which promotes pneumonitis and causes
respiratory insufficiency
- Preoperative lab assessment for pulmonary disease:
o All candidates for lung resection should have preoperative PFTs
o Overall debatable
History of Asthma
COPD
- Elective surgery should be deferred in patients who have an acute exacerbation of underlying COPD
o Treat exacerbation as if non-operative
- Lung-expansion maneuvers are the mainstay of postoperative prevention of complications and include
deep-breathing exercise (a component of chest physical therapy), and incentive spirometry

RISK ASSESSMENT METABOLIC DISEASE

- Diabetes, hepatic dysfunction, adrenal insufficiency, and hyperthyroidism may alter the approach to the
surgical patient
History of Diabetes
- Surgical incisions cause increased stress hormone levels and relative insulin deficiency and resistance
- Catecholamines, growth hormone, glucagon, ACTH, and cortisol all increase in the operative period
o Inhalational anesthetics also induce a similar stress hormone release
- All this causes hyperglycemia in the postoperative patient
o Causes decreased wound healing and decreased neutrophil function (and thus more would
infections)
- Try to make them the first case of the day because they will not be eating and it is thus easier to simplify
glucose control
- The general rule is to give one-half of the usual dose of injectable insulin the morning of surgery
(intermediate or long-acting). If they are normally just on oral meds, still only give one-half dose of
intermediate-acting insulin
o Also give a continuous infusion of 5% dextrose to provide 10 grams of glucose per hour
o Intraoperatively, glucose levels should be assessed by fingertip, and postoperatively, every 6 hours
at least. Then give sliding scale insulin based on the q6h glucose
- Goal to keep blood glucose at 150-200 mg/dL
Adrenal Insufficiency
- Prolonged use of steroids for inflammatory disorders (asthma, rheumatoid arthritis, IBD, etc) can cause
suppression of the hypothalamic release of corticotropin-releasing hormone and the pituitary release of
corticotropin, (ACTH). This leads to a decrease in the adrenal production of cortisol, particularly if
exogenous steroids are suddenly removed or reduced before surgery
- Any outpatient dose greater than the equivalent of 30 mg of hydrocortisone or 7.5 mg prednisone exceeds
the bodys daily basal requirements and places the patient at risk for adrenal suppression
- Intranasal, inhalational, and topical steroids reduce but do not eliminate the risk of adrenal suppression
- An IV drip of hydrocortisone at 10 mg/hr or doses of 100 mg q8h provides adequate replacement for those
having major procedures. Taper replacement therapy by 20% each day until operative stress is resolved
RISK ASSESSMENT HEMATOLOGIC DISEASE
- Anemia is very common in the perioperative period
o Determined by hemoglobin. Hemoglobin of 10 g/dL is considered safe
o Hematocrit < 30% is worrisome also
History of Clotting Disorders
Anticoagulant Use
Tobacco Use / Dependence
Substance Abuse
Post-Operative Fever
- Very common in the post-op period
- Early diagnosis is critical
- The classic 5 Ws wind (pneumonia), wound, walking (DVT), water (UTI), and wonder drugs (drug
reaction) should be considered in all patients
o The most common causes of fever in the perioperative period
- Fevers on the first day after surgery are generally attributed to the inflammatory stress of the surgery or
atelectasis
- If fever is high, the wound should be examined to rule out rapidly progressing infection, typically caused by
gram-positive cocci
- C. diff is a common source of fever. Suspect if diarrhea

Wound Infections
- Check wounds for erythema and discharge
- Particularly worrisome murky brown discharge that may represent a dehiscence or necrotizing fasciitis
- Factors that increase the risk for infection malnutrition, advanced age, immunosuppressive drugs,
prolonged hospitalization, recent antibiotics, obesity, catheters, poor tissue perfusion, steroids, radiation
- Preoperative showering with hexachlorophene soap may decrease wound infection. Can also be harmful
- Systemic prophylactic antibiotics are of most value in operations in which significant bacterial contamination
can be anticipated
o Contraindicated if the anticipated degree of contamination is less than 2%
o The duration of contamination must be limited to brief periods
o Give about 30-60 minutes prior to operation
o Continue IV for no more than 48-72 hours
- Remove hair from the operative field
- Systemic manifestations fever, chills, malaise, fatigue, tachycardia, tachypnea, signs and symptoms of
hypovolemia (dry oral mucosa, hypotension, oliguria, concentrated urine)
- Local manifestations erythema, swelling, heat, pain, tenderness
- Leukocytosis
- Gram stain is important
o KOH, silver, or Giemsa stains to identify fungal hyphae or spores
o Mycobacteria can be identified using the Ziehl-Neelson
- Treat more pronounced infections with antibiotics
- If it persists after 48 hours of appropriate antibiotics, suspect abscess formation, and open and drain the
wound
- Class of wounds:
o 1 clean
Breast biopsy, inguinal hernia repair
Usually staph (not as often strep)
First generation cephalosporin
May not need prophylaxis unless there will be a prothesis
o 2 clean contaminated
GI, GU, gyn organs entered, no gross contamination
Cephalosporins
First generation for elective cholecystectomy
Second or third generation for cholecystectomy for acute cholecystitis
Second generation for gastric and proximal small bowel surgery
o 3 contaminated
Perforated appendectomy, colectomy for diverticulitis, perforated ulcer or bowel,
penetrating GI trauma
Second-generation cephalosporin or ampicillin/gentamycin/flagyl
o 4 dirty
Traumatic wounds, burns older than 72 hours, free colon perforation
- Keep the skin open in classes 3 and 4
- Use vancomycin only in penicillin-allergic patients or if MRSA

Necrotizing fasciitis is a life-threatening infection that involves the different facial layers of the body
o Most commonly caused by streptococci
o Occurs in contaminated soft-tissue infections, especially diabetics and peripheral vascular disease
o Fourniers gangrene is a type that originates in the urethral glands and spreads to the perineal
tissue
o Debride tissues
o Antibiotics and hemodynamic support with IV infusion
Broad-spectrum ampicillin/sulbactam + clindamycin + ciprofloxacin
Add vancomycin if concern for MRSA
- Suppurative thrombophlebitis can occur as a complication to IV catheters
Deep Venous Thrombosis
- Thromboembolus involving deep veins of lower extremities (deep saphenous) or pelvis
- Most often occurs in the lower extremities and pelvis 80% deep veins of calf, 20% femoral or iliac vein
- Physical exam not always reliable
- Virchows Triad stasis, vascular injury, hypercoagulable state
- Precipitators prolonged bed rest or immobility (ortho surgery especially total hip replacement), long air
travel, malignancy, nephrotic syndrome, use of oral contraceptives and hormone replacement therapy, and
hypercoagulable syndromes (protein C/S, Factor V Leiden, Antithrombin III, PNH, homocystinuria)\
- Other risk factors advanced age, type A blood, obesity, multiparity, IBD, lupus erythematosus
- 50% asymptomatic
- Classic Symptoms swelling of involved area with hear and redness over the site
- Dull aching pain in calf / leg, worse with ambulation
- Edema in affected limb, palpable cord, low grade temperature, tachycardia
- Homan Sign + ~50% of the time (unreliable)
- Diagnostic Studies:
o Duplex ultrasonography is the preferred study for DVT. Negative results in a patient with high
suspicion for DVT indicate the need for further study
Also Doppler analysis
Both are non-invasive but operator dependent
o Venography is the most accurate method for definitive diagnosis of DVT, but it is associated with
increased risk and rarely is needed
o D-dimer a fibrin degradation product that is elevated in the presence of thrombus
An elevated D-dimer does NOT sufficiently diagnose
BUT an NEGATIVE D-dimer test (< 500 ng/dL) can r/o and omit need for US
o If pulmonary emboli suspected, VQ scan versus spiral CT (Wells criteria)
o Hypercoagulable work up if no identifiable predisposing event (pregnancy, cancer, limb trauma,
surgery, immobility)

Treatment:
o Prevention of DVT in bedridden patients elevation of foot in bed, leg exercises, compression
hose
In high-risk patients, may need anticoagulation
o Prevention of perioperative and travel-associated DVT early or frequent ambulation, leg
exercises, compression hose
o Preferred treatment is anticoagulation with LMWH (longer t than unfractionated heparin)
Heparin followed by warfarin may be used
Need heparin until INR is therapeutic for 48 hours
Warfarin (INR 2.0-2.5)
1st event & idiopathic 6 months warfarin
Non-idiopathic or recurrent event ~ consider indefinite therapy
o Thrombolytic therapy indicated in younger patients with large (ileofemoral) thrombi that are
detected within 2 weeks of onset
o Embolectomy (now can do percutaneously) gaining popularity as have less bleeding risk than lytics
o IVC filter used in cases of contraindication to anticoagulation, failure of anticoagulation, or
prophylactic use against high-risk of PE
o Treatment geared to reduce chance of clot propagation and risk of PE
o Embolectomy (now can do percutaneously) gaining popularity as have less bleeding risk than lytics
- Complications pulmonary embolism, ischemic limb, varicose vein formation, chronic venous insufficiency
- Wells Criteria
o Clinical evidence for DVT 3 points
o PE number one diagnosis 3 points
o Heart rate > 100 bpm 1.5 points
o Immobilization / Surgery in past 4 weeks 1.5 points
o Previous DVT / PE 1.5 points
o Cancer 1 point
o Hemoptysis 1 point
**Score of < 2 makes diagnosis highly unlikely. > 6 means highly likely
- Clinical risk factors for perioperative DVT:
o < 40 years old
o Prolonged immobility/paralysis
o Prior DVT
o Cancer
o Major surgery (pelvic, abdomen)
o Obesity
o Varicose veins
o CHF
o MI
o Stroke
o Fractures of pelvis, leg, hip
o Indwelling femoral vein catheters
o IBD
o Nephrotic syndrome
o Estrogen use
o Hypercoagulable states
- Low-dose unfractionated heparin and LMWH are most effective at reducing perioperative DVT

DVT prophylaxis heparin 5000 units subcutaneously started 2 hours before the operation and continued
every 8-12 hours after surgery until fully ambulatory or discharged
o Or enoxaparin 40 mg qd. Also intermittent pneumatic compression and/or compression stockings
Fluid / Volume Disorders (Volume Overload / Depletion)
- Total body water accounts for 60% or more of body weight
- Water is contained primarily in skeletal muscle. The amount of total body water decreases with obesity,
because mature adipose tissue is nearly water-free
- Intracellular water is total body water and extracellular is the remaining
o Interstitial water is 75% extracellular water or 15% body weight
o Intravascular water is 25% extracellular water or 4-7% body weight
- In the intracellular compartment, potassium is the dominant cation
o Most is located in the skeletal muscle
o Concentration gradient is essential for the function of muscle and nerve. This gradient is
maintained by sodium-potassium ATPase
- Magnesium is the second most plentiful intracellular cation
o 50% found in bone, the rest in skeletal muscle, liver, and other nonmuscular soft tissue
- Phosphate is principally reabsorbed in the jejunum
o 85% of phosphate is found in bone, but this does not contribute to maintenance
o Kidneys are the principal regulator
o PTH and vitamin D3 both decrease renal reabsorption of phosphate, and dietary phosphate
deprivation markedly increases renal phosphate reabsorption
o Phosphate is the principal intracellular anion
- A very low urinary chloride concentration is a good indicatory of ECF contraction from vomiting or
nasogastric losses
- In the interstitial and intravascular compartments, sodium is the dominant cation
- Electrical neutrality is maintained by a balanced amount of chloride and bicarbonate anions
- Sodium determines the volume, osmolarity, and tonicity of the ECF
- Calcium is mostly in bone. Reduced calcium stimulates the release of PTH which increases calcium
reabsorption from bone. PTH enhances calcium reabsorption from the distal convoluted tubule and
stimulates the formation of the active metabolite of vitamin D that increases gut absorption of elemental
calcium and facilitates PTH effect on bone resorption
- Fluid Homeostasis:
o Normally, an adult ingests 2-3 L of water per day. is liquid and is from ingested solids
o Water loss include those in urine (800-1500 mL/day) and feces (250 mL/day)
Also insensible losses of about 10 mL/kg/day
- Chronic volume depletion is manifested by oliguria, loss of skin turgor, orthostatic hypotension, low urine
sodium concentration, and a BUN/creatinine ratio that exceeds 15:1
o Hematocrit will be elevated 5-6% per liter of volume deficit
- Acute volume losses are manifested by hypotension, tachycardia, and tachypnea
o Signs of end-organ hypoperfusion may be present and include oliguria and altered mentation
o In severe volume deficits, skin mottling and acidosis are present
- The assessment of a patient must account for existing deficits, ongoing losses, and maintenance
requirements
- The totally volume fluid deficit is best approximated by the volume required to restore physiologic
parameters to normal. A urinary output greater than 0.5 mL/kg is desirable
o An isotonic solution, such as lactated Ringers, is effective in restoring circulating volume
o Normal saline (0.9% NaCl) is also commonly used
- Blood lost during surgery may require rapid replacement in the immediate postoperative period. Same with
evaporative water losses
-

o
o

During laparotomy, estimated evaporative fluid loss is 10 mL/kg/hr

Peritoneal surface is as much as 50% of body surface area

Dehydration with accompanying salt loss is the most frequent disorder in the preoperative patient
o Conditions that cause this intestinal obstruction, pyloric outlet obstruction, diarrhea, various
enterocutaneous fistulas, sequestration of ECF into injured tissues
o Fluid losses secondary to vomiting and diarrhea are apparent and are reflected as weight losses
o Can also be cause iatrogenically cathartic use, enemas in prep for bowel surgery
Third-space or internal losses are often not appreciated until they reach massive proportions
o Causes fluid sequestration in obstructed bowel loops, underneath burns, in soft tissue
subjected to massive trauma, and by loss of ascitic fluid caused by cirrhosis of the liver or
peritonitis
Volume loss usually becomes clinically significant when it reaches 5% of body weight
o Depressed skin turgor, dry mucous membranes, decreased and hyperconcentrated urine volume
Supplemental fluids and electrolytes must be administered to account for ongoing losses. In surgical
patients, these losses are most commonly due to nasogastric output and to fistula and diarrheal losses.
o In addition, considerable fluid may be sequestered at the operative site (third space)
Third space losses are replaced with isotonic saline
o Record the quantity of losses daily
Under normal ambient conditions, an average-sized adult requires 2500 mL of maintenance fluid per day
o To this is added maintenance amounts of sodium (average 1.0-2.0 mEq/kg/day) and potassium
(average 0.5-1.0 mEq/kg/day)
o Calcium, magnesium, and phosphorus supplements are not required for short-term therapy unless
a patient is critically ill
o If the patient is febrile, maintenance fluid must be increased by 10% for each degree above 37.2C
Never replace all losses in a single 24-hour period!!
If electrolytes are relatively normal in the face of volume depletion, can use Ringers lactate
If chloride losses exceed sodium losses, as occurs with vomiting, isotonic saline or normal saline can be
used
In hypernatremic state, as expected in those with tube feedings, use water alone as 5% dextrose in water
Hyponatremia responds to water restriction, but may need hypertonic saline (careful to prevent fluid
overload, compromised cardiac function, or pulmonary edema)
Usually, administration of isotonic saline is adequate
Potassium losses can also accompany salt and water deficits especially with vomiting and diarrhea
States of overhydration can also be seen in the preoperative patient
o Manage with volume restriction and gentle removal of excess fluid by mild diuretics
o Pure water excess is usually seen in CNS lesions and burns. Usually due to SIADH
Cessation of all water administration coupled with the use of solute diuretics (mannitol) is
the treatment of choice
o Fluid administration in the postop patient can prevent renal failure and optimize cardiac function.
Excess fluid may cause CHF and edema and thus inhibit wound healing
Want to keep urine output > 30 mL/hr

Electrolyte Disorders
- HYPERNATREMIA
o Serum sodium > 150 mEq/l
o Always accompanied by hyperosmolarity
The hyperosmolar state will drive thirst and ADH release
Abnormalities of ADH synthesis (central diabetes insipidus) or activity (nephrogenic
diabetes insipidus) may cause massive free-water losses
o May occur with volume depletion, volume excess, or euvolemia
o May be due to excess salt intake, excessive water loss, reduced salt excretion, or reduced water
intake
o In surgical patients, hypernatremia may result from the administration of loop diuretics, which lead
to free water depletion, and from gastrointestinal losses
o The principal target organ is the CNS
o Symptoms malaise, lethargy, vomiting, generalized seizures, coma
In the acute setting, rapid hypernatremia can cause intracerebral hemorrhage
o Therapy is first directed at restoring circulating volume with isotonic saline solution
Once intravascular volume is restored, hypernatremia is corrected by administration of
free water in the form of D5W
Correction should not progress at a rate >0.5 mEq/L/hr, unless neurologic symptoms are
present
- HYPONATREMIA
o Serum sodium < 135 mEq/L
o May be caused by excessive water intake, impaired renal water excretion, and loss of renal diluting
capacity
o Symptoms are mostly neurologic and are due to cellular swelling induced by ECF hypo-osmolality
o Cerebral swelling causes lethargy, confusion, vomiting, seizures, and coma
Rarely occur unless sodium < 120
o May occur with volume excess, euvolemia, or volume depletion
Hypervolemic usually have edema. Causes include renal failure, CHF, COPD with
hypercarbia, severe liver disease
Normovolemic the most common cause is SIADH (hyponatremia occurs with a large
urinary sodium output). SIADH is seen in patients with CNS pathology such as stroke or
injury and in pulmonary conditions such as tuberculosis and cancer
Hypovolemic renal or extrarenal losses of sodium that exceed water losses.
Urinary sodium > 20 mEq/L indicates renal losses (diuretic use, aldosterone
deficiency, salt-losing nephritis, renal failure, subarachnoid hemorrhage)
Urinary sodium < 10 mEq/L indicates a normal tubular responsiveness to
hyponatremia
Extrarenal losses include those due to vomiting, fistula, or diarrhea

Treatment:
In hypervolemic patients volume restriction and loop diuretics
Patients with SIADH usually respond to fluid restriction
In hypovolemic patients salt and water replacement
If hyponatremia is due to specific endocrine abnormalities, treatment with hormonal
replacement is indicated
In asymptomatic patients, treat slowly
Isotonic saline if you need volume therapy
Fluid restriction, a loop diuretic, and treatment of the underlying condition will suffice in
those with normovolemic or hypervolemic states
Symptomatic hyponatremia that is associated with seizures or coma requires more
aggressive therapy
If sodium concentration is increased too rapidly, further neurologic damage may
ensue. Specifically myelin sheath damage primarily located in the pons (central
pontine myelinolysis)
Current recommendations are to increase serum sodium concentration no faster
than 0.5 mEq/L/hr
o Even slower once you reach 120 (this is considered safe)
In patients with stupor, coma, or other severe neurologic symptoms, hypertonic
saline (3% NaCl) solution is used
HYPERKALEMIA
o Serum potassium > 5.5 mEq/L
o Can result from renal or adrenal insufficiency, metabolic acidosis, or iatrogenic causes
Other extrarenal causes intravascular hemolysis, rhabdomyolysis, seizures, severe GI
bleeding
Iatrogenic causes medications (NSAIDs, ACE inhibitors), excessive administration of
potassium
o The myocardial effects of severe hyperkalemia are the most important
On EKG, myocardial toxicity can be detected when the serum potassium is >6. The
earliest abnormality is the peaked T wave. With further increase, the PR interval prolongs
and RR interval increases. Even further increases cause loss of P waves and widened
QRS complex. Finally, complete heart block, ventricular tachycardia, and cardiac
standstill occur
o Extracardiac symptoms paresthesias, flaccid paralysis, ileus
o Treatment:
10-20 mL of 10% calcium gluconate (calcium antagonizes effects of hyperkalemia)
Concurrent treatment with insulin or sodium bicarbonate moves potassium into the cells
Potassium can only be removed from the body with Kayexalate (takes longer) or sorbitol
The most effective method of removing potassium is hemodialysis
HYPOKALEMIA
o Serum potassium < 3.5 mEq/L
o Common in surgical patients. Caused by GI losses from vomiting, diarrhea, or fistula. Or by the
use of diuretics
o Metabolic alkalosis often coexists. It exacerbates hypokalemia
o Clinical manifestations often mild. Generalized weakness and fatigue
EKG may show T-wave flattening or inversion, diminished QRS voltage, and U waves
In patients taking digoxin, hypokalemia can provoke life-threatening arrhythmias
o Treatment:
o

Oral potassium, unless the hypokalemia is severe (<2.5), the patient is symptomatic, or
the enteral route is contraindicated
Oral supplements (60-80 mEq/day) coupled with normal dietary intake
HYPERCALCEMIA
o Serum calcium > 5.3 mg/dL
o Most frequently associated with hyperparathyroidism in surgical patients. Also commonly
associated with cancer
Both cause excessive bone resorption and overwhelm the renal excretory capacity
Other causes of enhanced bone resorption Pagets disease, pheochromocytoma,
hyperthyroidism, use of thiazide diuretics
o Patients with mild-moderate hypercalcemia tend to be asymptomatic or complain only of malaise
o Those with severe (>6.5) have a variety of neurologic, cardiovascular, renal, and GI symptoms that
may be life threatening
Neurologic begin with lethargy and progress to stupor and coma
Cardiovascular arrhythmias and shortened QT interval
GI anorexia, constipation, pancreatitis, hyperacidity
Renal polyuria
o Treatment:
Severe (>6.5) requires immediate therapy.
If hyperparathyroidism is the cause, the best treatment is surgery
Initial supportive therapy saline diuresis and furosemide to increase calcium excretion
Calcitonin reduces bone resorption and has an immediate effect. Lasts 48 hours. Can be
prolonged with concomitant corticosteroids
Bisphosphonates can inhibit osteoclast activity but have a delayed onset (2-3 days)
HYPOCALCEMIA
o Serum calcium < 4.4 mg/dL
o In the surgical patient, may occur after parathyroid or thyroid surgery
o Also seen in association with severe pancreatitis, magnesium deficiency, and after massive blood
transfusion
o Mild-moderate hypocalcemia is usually asymptomatic
o Severe (<3.2) causes neuromuscular and cardiovascular manifestations
Neuromuscular paresthesia, muscular spasm, seizures, tetany, weakness. Rarely
laryngospasm or bronchospasm
Trousseau or Chvostek sign on exam
o Trousseau a sign of latent tetany. A blood pressure cuff is placed
around the arm and inflated to a pressure greater than SBP and left for
3 minutes to occlude the brachial artery. This causes spasm of the
muscles in the hand and forearm. The MCP joints flex, the DIP and PIP
joints extend, and the fingers adduct
o Chvostek when the facial nerve is tapped at the angle of the jaw
(masseter muscle), the facial muscles on the same side of the face will
contract momentarily (nose or lips twitch). A sign of nerve
hyperexcitability (tetany)
Cardiovascular arrhythmias, heart block, bradycardia, refractory hypotension
EKG may show prolonged QT or T-wave inversion
o Treatment:
Directed at the underlying disorder
No supplements if asymptomatic

If symptomatic or severe, IV calcium therapy

100 mg over a 5-10 minutes period, then calcium infusion of 0.5-2.0 mg/kg/hr
Once corrected, enteral therapy with elemental calcium is begun at 1-4 g/day

HYPERMAGNESEMIA
o Serum magnesium > 2.1 mEq/L
o As GFR < 10-30, renal excretion of magnesium decreases
Must curtail magnesium intake (antacids) in those with renal failure
o Can also occur in those with Addisons disease
o Symptoms usually seen once >4
Neuromuscular sequelae loss of DTRs, somnolence, impaired respiratory drive or
apnea
Cardiac effects bradycardia, heart block. Cardiac arrest with profound elevations
o Treatment:
In symptomatic patients, antagonize the effects of magnesium with calcium infusion (5-10
mEq), followed by immediate dialysis
If renal function is intact, prompt saline diuresis should be initiated
Long-term therapy includes removing all exogenous magnesium intake
HYPOMAGNESEMIA
o Serum magnesium < 1.6 mEq/L
o A common electrolyte disorder in surgical patients and has a variety of causes
A result of GI losses, reduced absorption (short bowel syndrome), and excessive urinary
losses from alcoholism, primary aldosteronism, and use of diuretics or aminoglycosides
o Associated with other electrolyte disorders
Promotes renal potassium wasting (hypokalemia)
Promotes diminished renal tubular phosphate absorption (hypophosphatemia)
Hypocalcemia occurs as a result of a hypomagnesemia-induced reduction in PTH release
(hypoparathyroidism) and diminished renal PTH response
o Symptoms occur when <1
Neuromuscular tremor, ataxia, carpopedal spasm, tetany
Cardiotoxicity prolonged QT interval, can lead to vtach (torsades de pointes)
o Treatment:
Symptomatic is treated with magnesium infusion (8-16 mEq over a 5-10 minute period,
followed by 48 mEq/day)
If treatment is not urgent, give oral supplements
HYPERPHOSPHATEMIA
o Serum phosphate > 4.5 mg/dL
o Most common cause is renal insufficiency. Most severe in those with acute renal failure due to
rhabdomyolysis or tumor cell lysis. May result from rhabdomyolysis due to muscle ischemia or
crush injury
Other causes thyrotoxicosis, malignant hyperthermia, hypoparathyroidism
o Few symptoms mostly discovered by lab testing
o Major complication is hypocalcemia
o If chronic, elevated phosphate may cause metastatic calcifications and even arterial obstruction
(calciphylaxis)
o Treatment:
Treat underlying renal failure
In chronic hyperphosphatemia, phosphate-binding antacids are effective
Dialysis require in acute setting or with end-stage renal disease

HYPOPHOSPHATEMIA
o Serum phosphate < 2.5 mg/dL
o Commonly seen as a consequence of many disease processes
o Attributable to transcellular shifts, excessive urinary losses, decreased dietary intake, or decreased
intestinal absorption. More than one of these mechanisms is usually operative in a given patient
o Mild-moderate may be caused by diuretic use, hyperparathyroidism, malabsorption,
hypomagnesemia, and vitamin D deficiency
o Severe (<1) may be caused by chronic respiratory alkalosis, chronic alcoholism, severe burns, and
treatment of diabetic ketoacidosis
o Rarely causes symptoms unless severe
Earliest signs are myalgias and muscle weakness
If persistent, can result in rhabdomyolysis
Progressive muscular dysfunction may precipitate CHF and respiratory insufficiency
May cause tissue hypoxia
o Treatment:
Oral or parenteral phosphate repletion and correction of underlying disorder
Acid / Base Disorders
- METABOLIC ACIDOSIS
o pH < 7.35
o Plasma bicarbonate < 22 mEq/L
o Increase in hydrogen ion concentration
In spontaneously breathing patients, the increase in hydrogen ion should stimulate a
compensatory increase in ventilatory rate and thus decrease pCO2
o Presence or absence of an anion gap helps to categorize
Anion gap is calculated as the difference between the concentration of the major
extracellular cation sodium and the major anions chloride plus bicarbonate
Normal anion gap = 8-12 mEq/L and corresponds to unmeasured anions, primarily
plasma protein and a small amount of fixed acids
o Anion Gap Metabolic Acidosis
Causes (Dr. Maples) diabetic ketoacidosis, renal failure, methanol, alcohol,
paraldehyde, lactic acidosis, ethylene glycol, salicylates
In surgical patients, the most important causes are lactic acidosis (occurs secondary to
hypoperfusion and blood loss), diabetic ketoacidosis, renal failure, and ethanol ingestion
In trauma patients, assume it is due to blood loss (hypoperfusion, and tissue hypoxia) until
proven otherwise
o Non-Anion Gap Metabolic Acidosis
Characterized by loss of buffer base
Causes GI tract losses (especially biliary and pancreatic losses), renal tubular
acidosis, Addisons disease, TPN, and use of carbonic anhydrase inhibitors
o Metabolic acidosis has detrimental effects on body homeostasis myocardial depression,
hypotension, arrhythmias, hyperkalemia, hyperventilation, insulin resistance, obtundation, coma
o Treatment depends on etiology
In trauma patients, restore blood and fluid
In DKA, manage insulin and restore volume
If acidosis is severe (pH <7.2), or patients have life-threatening ventricular arrhythmias,
hemodynamic instability, inadequate compensatory response, treat with sodium
bicarbonate

Risks of sodium bicarbonate therapy include hypernatremia, hyperosmolarity,

volume overload

METABOLIC ALKALOSIS
o Inability of the kidneys to excrete excess bicarbonate or retain hydrogen ion
o Usually accompanied by respiratory compensation (increase in pCO2)
o Causes are divided by response to chloride
Chloride Responsive nasogastric losses, vomiting, past use of diuretics, volume
contraction, posthypercapnic
Usually have a contracted ECV and chloride deficit (urinary chloride <10 mEq/L)
Chloride Resistant mineralocortical excess, aldosteronism, renal artery stenosis, reninsecreting tumor, Cushings syndrome, Bartters syndrome
Normovolemic or hypervolemia and urinary chloride >10
o Severe metabolic alkalosis (pH > 7.60 and HCO3- > 35 mEq/L is associated with cerebral
hypoperfusion, a leftward shift of the oxyhemoglobin dissociation curve, and hypokalemia
Respiratory symptoms hypoventilation and hypoxemia
o Treatment directed at underlying deficit
Contraction alkalosis is treated with saline
Chloride-unresponsive may require carbonic anhydrase inhibitors (acetazolamide)
RESPIRATORY ACIDOSIS
o pH is low and pCO2 is elevated
o Can be acute or chronic
o Due to ineffective alveolar ventilation
o Causes decompensation of preexisting respiratory disease, asthma, neuromuscular disorders,
CNS depression, airway obstruction
o Plasma bicarbonate concentrations do not increase much in acute. In chronic, renal adaptation is
substantial
o Treatment directed at improving alveolar ventilation
May require intubation and mechanical ventilation
RESPIRATORY ALKALOSIS
o pH is high and pCO2 is low
o May be acute or chronic
o Caused by alveolar hyperventilation
In surgical patients, may be due to hypoxia, CNS lesions, pain, hepatic encephalopathy,
mechanical ventilation
o In acute, renal compensation is minimal. However, in chronic, the kidney responds by decreasing
the excretion of hydrogen ion. Serum bicarbonate also decreases
o Most patients are asymptomatic
Severe may cause carpopedal spasm, circumoral numbness, cramps, and confusion
o Hyperventilation is particularly dangerous is those with subarachnoid hemorrhage because it
exacerbates vasospasm
o Treat the underlying cause

Surgery Cardiovascular
Chest Pain, History of Angina
Syncope
Dyspnea on Exertion
Claudication
Aortic Aneurysm / Dissection
- An ANEURYSM is an abnormal dilation of an artery
o Saccular aneurysms occur when a portion of the artery forms an outpouching, or mushroom
o Fusiform aneurysm occur when the entire arterial diameter grows
- True aneurysms involve all layers of the arterial wall intima, media, adventitia
- An artery is considered aneurysmal if the diameter is >1.5 times its normal size (otherwise an enlarged
artery is considered ectatic)
- A DISSECTION occurs when a defect in the intima allows blood to enter between the layers of the wall.
Blood pressure then causes the layers of the wall to separate from one another.
- AORTIC DISSECTION is a disease process in which the intima of the aorta tears and allows blood entry
into the media of the aorta
o Associated with hypertension, Marfan syndrome, connective tissue disorders, bicuspid aortic valve,
trauma, aortic manipulation, or catheter injury
o More common than thoracic or abdominal aneurysms
o Can cause aortic rupture, peripheral or organ ischemia due to flow occlusion, stroke, aortic valve
insufficiency, and cardiac tamponade
o Dissection is usually initially seen with chest pain or back pain between the shoulder blades
May have aortic regurgitation murmur, widened mediastinum on CXR, ischemia of EKG,
or changes in pulse on exam
The best modalities for imaging are TEE, spiral CT, and MRI/MRA
o Two groups of aortic dissection:
Stanford Type A tear is in the ascending aorta distal to the aortic valve
Stanford Type B patients whose tear is distal to the left subclavian artery in the
descending aorta
o Also the DeBakey classification:
Type 1 ascending and descending aorta
Type 2 only ascending aorta
Type 3 only descending aorta
o Type A is treated surgically with excision of the tear and a portion of the ascending aorta,
replacement with aortic graft, and repair or replacement of the aortic valve
Treated surgically due to the risk of rupture into the pericardium with resulting tamponade,
risk of acute AR with onset of severe CHF, and risk of ischemia
o Type B (uncomplicated) is treated medically with tight control of blood pressure with beta-blockers
and afterload reducers (sodium nitroprusside)
Beta-blockers are primary because they decrease the stress on the aortic wall
Complicated type B may need surgery either by aortic excision and graft replacement
with necessary revascularizations or by refenestration of the false lumen to allow passage
of blood back into the true lumen

ABDOMINAL AORTIC ANEURYSM:

o Localized irreversible arterial dilatation that increases the area of the abdominal aorta by at least
50%. Normal diameter is about 2 cm, so AAA has diameter of 3 cm or more
o More common in whites than blacks
o Branches of the AA include the celiac trunk, SMA, IMA, renal arteries, gonadal arteries
Most AAA (95%) begin distal to the takeoff of the renal arteries
o Most are associated with atherosclerosis.
o Abdominal/flank pain and hypotension are the most common symptoms of rupturing or expanding
(symptomatic) AAA
Most aneurysms (75%) are discovered when still asymptomatic, either as a pulsatile mass
on exam or incidentally on other work-up
When palpable, usually located to the left of the midline, above the umbilicus, in the
epigastric area
The primary physical finding is a laterally expansile pulsating abdominal mass in the
epigastrium. The width, not the intensity, of the pulsation suggests the presence of AAA
o Ultrasound is an accurate and noninvasive method to assess the size of the aneurysm and
presence of clot
o CT or MRI/MRA provides anatomic detail and precise localization of the aneurysm
CT is the best way to monitor growth of AAA
o Treatment:
If asymptomatic, treatment depends on size of the lesion (proportional to its risk of leak or
rupture)
< 4 cm in diameter are unlikely to rupture. Medically manage with beta-blockers
o Re-scan ever 6th months
4-5 cm in diameter can have two options early operation or close follow-up
> 5 cm in diameter has a rupture incidence of >25% at 5 years, and repair is
recommended
Any patient with symptoms should have immediate workup. If diagnosed with rupture or
leak, immediate fluid resuscitation and operative intervention
o Repair of the AAA:
Gold standard surgical placement of a vascular prosthesis within the lumen of the
aneurysm via a midline or left retroperitoneal incision below the 12th rib
Basic principles proximal aortic control above the aneurysm as well as distal control
below the aneurysm.
The proximal anastomosis is done to the neck of the aorta, which is the nonaneurysmal
aorta just above the aneurysm. The graft is then sewn to healthy aorta just below the AAA
If the AAA disease extends to the distal aorta, a bifurcated graft is sewn to both
iliac arteries
Endovascular repair is now widely used endovascular stented graft via open femoral
access. The distal limbs of the grafts are placed in both iliac arteries
o Always have blood available!!!
Arterial Embolism / Thrombosis

Peripheral Arterial Disease

- PAD usually is a result of atherosclerosis and is a significant independent risk factor for cardiovascular
morbidity and mortality
- Lower extremity disease results in ischemia and pain, causing significant limitation of activity or disability
- Acute arterial occlusion may be caused by thrombosis or embolism
- Thrombotic disease also may be a result of trauma, hypovolemia, inflammatory arteritis, polycythemia,
dehydration, repeated arterial punctures, and hypercoagulable states
- Three patterns of disease:
o Type 1 15-20% of patients, limited to the aorta and common iliac artery, most commonly found
in those 40-55 years old who smoke heavily or have hyperlipidemia
o Type 2 25% of patients, involves the aorta, common iliac artery, and external iliac artery
o Type 3 most common (60-70% of patients), multilevel disease affecting the aorta and the iliac,
femoral, popliteal, and tibial arteries
- Patients with type 2 and 3 PAD have typical risk factors for atherosclerotic disease and usually a high
incidence of cerebrovascular and coronary artery disease
- Modifiable risk factors = smoking, diabetes, HTN, lipids, sedentary lifestyle / obesity
o Atherosclerosis is the most common cause of chronic lower limb occlusive disease
- Clinical Findings:
o Intermittent Claudication muscular pain in lower leg induced by exercise and relieved by rest
Usually the first symptom of peripheral disease
Later, pain at rest occurs (frequently nocturnal)
o Femoral and distal pulses will be weak or absent
o An aortic, iliac, or femoral bruit may be present
o Erectile dysfunction occurs with iliac artery disease (Leriches syndrome)
o Severe, chronic disease results in numbness, tingling, and ischemic ulcerations (may lead to tissue
necrosis or gangrene)
o Symptoms of occlusion depend on the artery, the area it supplies, and the collateral circulation
Buttock / Hip = aortoiliac disease
Thigh = common femoral artery
Upper calf = superficial femoral artery
Lower calf = popliteal artery
Foot = tibial / peroneal artery
o Extremity occlusion usually results in pain, pallor, pulselessness, paresthesias, poikilothermia, and
paralysis. The FIVE Ps!!!!!!!!!
Cool skin temperature or abnormal skin color, poor hair growth
- Laboratory Studies:
o Doppler flow studies are used to determine systolic pressures in the posterior tibial and dorsalis
pedis arteries
o Ankle / Brachial Index (ABI)
ABI is a non-invasive test performed to assess asymptomatic PAD or mild-moderate
claudication
They are helpful to predict critical limb ischemia and amputation, propensity for wound
healing, and patient survival
Can be used as a screening tool or to monitor the efficacy of therapeutic interventions
ABI = ratio of SBP ankle / SBP arm
Normal ABIs (inpatients without PAD) ankle systolic pressure is 10-15 mmHg higher
than brachial systolic pressure

An ABI of < 0.9 indicates significant disease

Normal = 1.0+
< 0.9 = diagnosis of peripheral vascular disease
< 0.7 = intermittent claudication
< 0.4 = rest pain
< 0.1 = impending tissue necrosis
o CT or magnetic resonance angiography is used for locating stenotic sites and for accurate
diagnosis of thrombosis or embolism
- Treatment:
o Smoking cessation, progressive exercise, lipid-lowering medications (reduce the risk for new-onset
or worsening claudication)
o Cilostazol (Pletal) is the main drug treatment
o Antiplatelet therapy (aspirin, clopidogrel) should be used routinely in all patients without a
contraindication
o Erectile dysfunction may require revascularization or treatment with a phosphodiesterase, such as
sildenafil
o Lower extremity revascularization must be preceded by a thorough cardiac and carotid evaluation
o Thromboendarterectomy, embolectomy, thrombolytic therapy, and endovascular surgery may be
indicated
o Indications for operation for carotid artery disease 75% stenosis, 70% stenosis and symptoms,
bilateral disease and symptoms, or >50% stenosis and recurring TIAs despite aspirin therapy
Acute Mesenteric Ischemia
- Includes disease of the celiac axis (arterial supply to the liver, spleen, pancreas, stomach), the SMA
(supplies the pancreas, small bowel, and proximal colon), and IMA (supplies the distal colon and rectum)
- Patients with acute mesenteric ischemia present with pain out of proportion to exam and a mechanism for
embolic disease is usually present
o Guaiac-positive stool
o History of atrial fib or CHF
o Sudden onset abdominal pain, diarrhea, vomiting
- Chronic mesenteric ischemia results in weight loss and abdominal pain and is frequently mistaken for
malignant disease
Arterial / Venous Ulcer Disease
Varicose Veins
- Approximately 15% of adults, particularly women who have been pregnant, develop varicosities.
o Other risk factors family history, prolonged sitting or standing, history of phlebitis
- The main mechanisms are superficial venous insufficiency and valvular incompetence. Inherited defects in
vein walls or valves also play a role
o Pathology related to venous valve incompetence and subsequent venous reflux from increased
pressure
- Dilated, tortuous veins develop superficially in the lower extremities, especially in the distribution of the long
saphenous vein (and tributaries)
- Smaller blue-green, flat reticular veins, telangiectasias, and spider veins are further evidence of venous
dysfunction
- Asymptomatic to dull, aching leg with associated fatigue
o Worse after prolonged standing
o Symptom severity is not correlated to number or size of varicosities
o Warmth aggravates, cold relieves

Chronic distal edema, abnormal pigmentation (mild browning thinning of skin above ankles), fibrosis, and
skin ulceration may develop in severe or prolonged disease

Complications:
o Thrombophlebitis rarely occurs; sluggish blood in varicose vein leads to localized thrombosis
presents as subacute to acute localized pain and palpable hardness at the site of the phlebitis
Caused by pregnancy, trauma
The Brodie-Trendelenburg test differentiates saphenofemoral valve incompetence from perforator vein
incompetence
Secondary varicose veins due to chronic venous insufficiency of deep vein, retroperitoneal venous
obstruction, arteriovenous fistula (will hear bruit over it), congenital venous malformation
Laboratory studies are not necessary however, Doppler sonography locates incompetent valves before
surgery and identifies those due to congenital malformation
Treatment:
o Graduated elastic stockings give external support
o Leg elevation and regular exercise for symptomatic relief
o Small venous ulcers heal with leg elevation and compression bandages, but larger ulcers may
require compression boot dressing or skin grafts
o Interventional techniques endovenous radiofrequency or laser ablation, compression
sclerotherapy, surgical stripping of the saphenous tree

Surgery Hematologic System

Easy Bruising / Bleeding
Anemia
Fatigue

Surgery Gastrointestinal
Abdominal Pain / Acute Abdomen
- By definition, acute abdomen implies severe abdominal pain arising rather suddenly and of less than 24
hours duration
o Location is important:
o Foregut structures cause EPIGASTRIC pain stomach, pancreas, duodenum, and biliary tree
o Midgut structures cause PERIUMBILICAL pain small bowel, right and transverse colon
o Hindgut structures cause HYPOGASTRIC pain left colon, sigmoid, rectum
- Nerves to the parietal peritoneum:
o Sensory pathways for visceral pain are present in the lower thoracic and lumbar splanchnic nerves
and in the parasympathetic nerves of the vagus and sacral plexus
- Two types of pain:
o Steady, well-localized pain that usually occurs after ischemia, perforation, inflammation, or
hemorrhage
o Intermittent, colicky, poorly localized pain found with obstruction of the GI tract
- Timing is important:
o Sudden onset of excruciating pain perforation, rupture, or ischemia of a visceral organ
o Pain of gradual onset suggests a subacute process PUD, gastritis, cholecystitis, IBD,
diverticulitis
- Physical exam is important
o Auscultate:
Absence of bowel sounds means ileus
High-pitched sounds with splashes, tinkles, and rushes, especially in the presence of
distention, indicate SBO
o Percuss to determine the amount of distention
o Rebound tenderness suggests peritoneal irritation
o Rectal and pelvic exams may also be important
- Lab tests CBC is the most important
o Increased WBC and left shift indicates an inflammatory process, but the absence of it does not
exclude
o Elevated hematocrit can suggest dehydration
o Anemia can suggest chronic bleeding
o Serum electrolytes may show hypokalemia (during vomiting or diarrhea)
o Serum bicarbonate and anion gap can demonstrate acid-base disturbances
o If suspected biliary disease, check LFTs
o Check amylase and lipase if pancreatic involvement
o Check urinalysis on all patients and pregnancy test on women of child-bearing age
- Imaging:
o Standard series of films supine an upright abdominal, standard CXR
Presence of free air can be determined on CXR
Supine and upright abdominal films can reveal intestinal obstruction and the presence of
air-fluid levels
Can also find fecaliths (appendicitis) and kidney stones
o Ultrasound can detect solid organs, free fluid in abdomen, degree of ascites
Duplex ultrasound can also assess vascular structures such as a ruptured or leaking
aortic aneurysm, AV fistula, venous thrombi

CT can assess all solid organs (intraabdominal and retroperitoneal)

In the diagnosis of hollow organs, such as the small and large intestine, you can evaluate
bowel-wall thickness and the presence of air within the bowel wall as well as the
mesentery
Superior to other radiographic modalities in assessing abnormalities in the kidneys,
pancreas, duodenum, and aorta
Can also detect small amounts of free air in the abdomen, much less than that required in
an upright CXR
o MRI not really used since it is expensive and time consuming. But good for soft-tissue
structures
o Angiography usually used for therapeutic reasons. Can confirm diagnoses
o Barium Studies role has diminished since ultrasound and CT are less invasive
Still useful for colonic carcinoma, volvulus, and determining the extent of mucosal disease
in colitis
o Radionucleotide Scans helpful in localizing the site of a GI bleed
Abdominal scintigraphy with 99mTc (sulfur colloid or labeled RBCs)
Can detect bleeding rates as low as 0.1 mL/min (more sensitive that angiography)
o Endoscopy direct visualization of the GI tract. Diagnostic and therapeutic
Upper endoscopy can visualize bleeding peptic and duodenal ulcers, as well as outlet
obstruction from tumors or strictures
Colonoscopy can reveal inflammation of the colon, neoplasms, intussusception, and
volvulus
Laparoscopy and Laparotomy:
o Laparoscopy is most commonly used for an unclear diagnosis of appendicitis, especially if pelvic
disease is in the DDX
Also for patients with acute cholecystitis as the initial disease approach
o Laparotomy is the final pathway in many with acute abdominal pain
When the patient shows signs of peritonitis or the diagnosis is unclear with a worsening
clinical picture, abdominal exploration via midline laparotomy is the final option
Common Conditions Leading to an Acute Abdomen:
o Peritonitis (GI tract perforation)
Diffuse, severe abdominal tenderness
Guarding and rigidity on physical exam
Absent bowel sounds
Quickly develop systemic sepsis
Upright KUB or CXR will show free intraperitoneal air under the diaphragm
Bring to OR for exploratory laparotomy
o Appendicitis
Mild fever and focal RLQ (McBurneys point) pain with rebound tenderness
Anorexia, nausea, vomiting are common in early disease
Pain may begin periumbilically
Moderate leukocytosis
Mandatory to do pelvic and rectal exams
Fecaliths on plain films
CT has become more widely used instead of ultrasound
o

Acute Pancreatitis
Rapid onset of severe epigastric pain, radiates to back
Anorexia, nausea, vomiting
Rebound tenderness not uncommon
Hypoactive or absent bowel sounds
Order CBC (to determine elevated WBC or decreased hematocrit due to hemorrhage),
amylase, lipase
CT with oral and IV contrast to determine presence of pseudocysts, necrosis, or masses
in the gland
Usually supportive medical care. Surgery if there is infection or severe pancreatic
necrosis
Cholecystitis
Usually in women 40-60 years who are overweight and previous history of pregnancy
Hard to differentiate from biliary colic
RUQ pain accentuated by inspiration (Murphys sign) and accompanied by nausea and
vomiting
Febrile, distended abdomen, guarding
Order CBC, LFTs, amylase, lipase
Ultrasound is test of choice to evaluate gallbladder and biliary tree
Often find gallstones and thickened-wall gallbladder with pericholecystic fluid
Evaluate biliary tree to detect dilated ducts or intraductal stones
HIDA scans (hepatobiliary iminodiacetic acid) can suggest acute cholecystitis if the cystic
duct is occluded and the gallbladder fails to take up the radiolabeled bile
Laparoscopic approach is safe in both acute and chronic settings
Diverticulitis
Usually in the left and sigmoid colon (although diverticulosis can be anywhere)
Sigmoid diverticulitis usually causes LLQ pain with fever and chills
Tenderness to palpation. Occasionally a palpable mass in the case of a phlegmon
CT with oral contrast is diagnostic
Emergency surgery with signs of perforation and significant abscess formation
Small-Bowel Obstruction
Nausea, bilious vomiting, distention
Sharp, colicky abdominal pain
In advanced disease tachycardia, hypotension, fever
Abdominal distention on exam, as well as high-pitched bowel sounds and a tympanitic
abdomen
Labs may show hypochloremic, hypokalemia, metabolic alkalosis
Supine and upright abdominal films useful to show dilated loops of small bowel and airfluid levels
CT or upper GI series can show a lead point for obstruction
Can be initially treated with a nonoperative course such as bowel rest and nasogastric
suction
Large-Bowel Obstruction
Constipation and abdominal distention
Pain is gradual in onset
Most common causes colon carcinoma, acute diverticulitis, volvulus
Abdominal tenderness and distention on physical exam

Plain films of the abdomen and retrograde contrast studies can help localize site of
obstruction
For volvulus, colonoscopy is both diagnostic and therapeutic

Mesenteric Ischemia:
Sudden onset of severe abdominal pain
Nausea, vomiting, diarrhea, GI bleeding
Classic finding pain out of proportion to the amount of tenderness elicited by
abdominal palpation
At risk for sudden development of sepsis (hypotension, tachycardia, hypovolemia)
Plain films are nondiagnostic
CT can reveal thickened loops of affected bowel with air in the bowel wall (pneumatosis)
Once resuscitated, taken to OR for exploratory laparotomy and removal of disease bowel
Ruptured Aortic Abdominal Aneurysm
Abdominal pain accompanied by back or flank pain
Often first seen in shock and are hypovolemic
On exam pulsatile supraumbilical mass is present
Patients with known aneurysm who have abdominal pain, shock, and pulsatile mass are
presumed to have ruptured
Ultrasound, CT, and angiography can confirm the diagnosis but time does not permit
these studies
Surgery is vital
Gynecologic Causes:
The most life-threatening is ruptured ectopic pregnancy
Another common cause is PID (ages 15-35 years)
Crampy lower-quadrant abdominal pain and high fever
Pelvic exam shows hyperemic, extremely tender cervix with vaginal discharge
Positive diagnosis can be made with a cervical smear and culture
Ultrasound is used to diagnosis tuboovarian abscess
Other causes ovarian cysts, endometriosis, ovarian torsion, ruptured uterus
Nonsurgical Causes

Anorexias
- Almost a universal complain in appendicitis
Heartburn / Dyspepsia
Nausea / Vomiting
- Occur commonly after anesthesia and surgery
- Because nausea is one of the symptoms of myocardial ischemia, the possibility of ischemia should always
be considered if nausea and vomiting occur in high-risk cardiac patients
- The most commonly used antiemetics metoclopramide, scopolamine, ondansetron
o Metoclopramide increases the LES tone and promotes gastric emptying
o Ondansetron is a serotonin-receptor antagonist that is highly effective but is much more expensive
o Scopolamine is an anticholinergic agent (like atropine) that is applied preoperatively as a
transdermal patch and left in place postoperatively. Some patients experience annoying CNS side
effects (dysphoria)
- Others prochlorperazine, diphenhydramine, small doses of propofol
- NG tubes inserted intraoperatively may decreased post-op nausea if it is placed on active suction
Jaundice
Hematemesis
Diarrhea / Constipation / Obstipation / Change in Bowel Habits
Melena / Hematochezia

Achalasia
- An idiopathic motor disorder of the esophagus
- Aperistalsis of the esophageal body and impaired relaxation of the LES
- Peaks in the 5th decade
- Dysphagia & regurgitation are predominant symptoms & can lead to weight loss & pulmonary complications
- A 16-fold increased risk of esophageal cancer
- Chagas disease is a related disorder endemic to Central America and parts of South America
o Infection with the parasite Trypanosoma cruzi and, like achalasia, involves degeneration of the
myenteric plexus neurons. The two are typically indistinguishable and have the same treatment
- Dysfunction of the myenteric plexus of the esophagus. Histologically, this plexus is replaced with dense
lymphocytic infiltration and a loss of ganglion cells. A selective loss of inhibitory neurons occurs, with
sparing of the stimulatory cholinergic innervation. This leads to failure of the LES to relax with swallowing
- Most frequent findings dysphagia, regurgitation, weight loss
o When there is a change in position, liquid spills into the mouth or into the lungs
o Regurgitation is usually not sour tasting because it does not contain gastric contents
- First study is a barium swallow characteristic appearance of a dilated esophagus with a birds beak
taper of the distal esophagus
- Aperistalsis on esophageal-motility study
o Most have weak or absent contractions in the esophageal body, but 10% can have high pressure,
simultaneous contractions (vigorous achalasia).
o Most patients have an elevated LES pressure (>25 mmHg), with associated incomplete LES
relaxation (nadir pressure, >10 mmHg)
- EGD is the next step and is essential for ruling out malignancy
o Retroflexed view of the cardia and GE junction
o The endoscope should pass through the LES with an easy pop
o If passage is obstructed, seek a malignant cause
- There is no cure symptom alleviation
- Medical therapy is aimed at decreasing LES pressure to allow the esophagus to empty
o CCBs and nitrates have little success
- Balloon dilation is designed to rupture the fibers of the LES. A postprocedure barium swallow is important to
rule out esophageal perforation
- Botox injections can block release of acetylcholine at the neuromuscular junction and may be injected
directly into the LES with endoscopic guidance. This is good for symptom relief, but you need repeat
injections every 6-9 months
- Surgical treatment involves division of the fibers of the LES. Heller myotomy. May use an abdominal or
thoracic approach. To ensure that sphincter division is complete, it is recommended that the myotomy be 68 cm in length and extend at least 2 cm below the LES onto the anterior surface of the stomach. If
adequate, it should decrease the resting pressure of the LES to less than 10 mmHg
Esophageal Perforation
- May be spontaneous (Boorhaaves syndrome), traumatic, or iatrogenic
o Spontaneous is associated with forceful prolonged retching
o Most commonly is iatrogenic from instrumentation
- Clinical presentation is usually the development of acute systemic toxicity, chest pain, and pleural effusion
after a spell of violent and extended vomiting
- Diagnosis is established by performing a water-soluble contrast radiograph or chest radiograph
o Usually reveals mediastinal or free peritoneal air as the initial radiologic manifestation
o Confirmed by CT scan
o No role for endoscopy
- If perforation is fresh (< 24 hours), thoracotomy and repair of the perforation with chest drainage is
successful. Usually the repair is buttressed with pericardium or pleura

- When the perforation is more than 24 hours old, primary repair usually fails
Esophageal Strictures
- Various substances can cause damage to the esophagus when ingested.
- The alkali, or lye, stricture is usually associated with the ingestion of liquid drain cleaner and may be fatal.
In survivors, a long stricture will develop
o Common in pediatrics and suicide attempts
o Therapy esophageal dilation
Esophageal Cancer
- Esophageal neoplasms are almost always malignant
- Benign tumors (< 1%) are usually leiomyomas or congenital cysts
- Worldwide, most malignant neoplasms are squamous cell, but in the U.S. the most common is
adenocarcinoma
o Most cases of adenocarcinoma arise in the distal third or gastroesophageal junction
- Metastases are usually to the liver, lungs, and bones
o At least 35% of patients with distant metastases at the time of diagnosis
- Poor prognosis overall 5-year survival rate of only 5%
- Mucosal insult is usually the cause chronic ingestion of extremely hot liquids, esophageal burns from
acid or base ingestions, radiation-induced esophagitis, and reflux esophagitis
o Alcohol, smoking, nitrosamines, and malnutrition / vitamin deficiency also play a role
o Barrett esophagus, which occurs when the normal squamous epithelium becomes columnar in
response to injury from acid reflux, is considered a premalignant lesion
10% of these patients will develop adenocarcinoma
Obtain an upper GI contrast radiography
o In patients with achalasia, about 6% will develop squamous cell carcinoma
- At the time of diagnosis, most have advanced disease and are not surgical candidates for curative resection
- The lack of a serosal lining and the rich submucosal lymphatic network of the esophagus allows early
extension of tumor into adjacent mediastinal structures as well as early local lymph node spread
o 75% of patients have mediastinal or extrathoracic lymph node metastases at the time of diagnosis
- The classic presentation of distal esophageal adenocarcinoma older man with a history of GERD
complaining of progressive dysphagia** to solids initially, and then to liquids
o Typically, the patient feels well and has no other symptoms
o Some report mild weight loss, but this is usually due to diminished caloric intake than due to
cachexia from metastatic disease
o Chest pain and odynophagia (pain with swallowing) may also occur
o Invasion of a recurrent laryngeal nerve may cause hoarseness from vocal cord paralysis
- Patients with esophageal squamous cell carcinoma often have a history of heavy alcohol and tobacco use
and present with more pronounced symptoms owing to more advanced disease
- Signs are nonspecific, and patient will appear well unless significant metastatic disease is present

Diagnostics:
o Barium esophagogram (barium swallow) detects malignant lesions in 96% of patients
Findings range from small mucosal defects to apple core lesions to complete obstruction
This is usually the initial study for the evaluation of new onset dysphagia
o Definitive diagnosis of cancer requires confirmation by flexible endoscopy with tissue biopsy
o If Barrett esophagitis alone is noted, the extent of disease can be determined and biopsies
performed to look for dysplasia or carcinoma in situ
o To determine the stage of the primary tumor (T) and regional lymph node status (N), endoscopic
ultrasound is used
Ultrasound is best for evaluating local staging the intramural extent of the tumor as well
as assessing for lymph node enlargement or abnormality
Ultrasound depicts the normal five layers of the esophagus (squamous epithelium that
becomes columnar at the GE junction, submucosa containing the Meissner plexus, inner
circular muscle layer, Auerbach/myenteric plexus, outer longitudinal muscular layer). It
also accurately determines the T status in 85-90% of patients
FNA biopsy of abnormal-appearing lymph nodes under ultrasound guidance may be
performed
o Evaluation of regional and distant disease is best done by CT scan and PET scan
CT should be performed first after initial diagnosis, because lung and liver mets are often
detected
If CT is negative for mets, then EUS is performed
TNM staging system
Treatment:
o Because there is no serosal layer covering the esophagus, disease is often locally advanced or
metastatic on presentation, leading to poor overall survival statistics
o Surgical cure rates are 20-30% at best
o The goals of surgical treatment are removal of the tumor and regional lymph nodes followed by reestablishment of GI tract continuity
o For early-stage disease, esophagectomy provides the possibility of cure
o Preoperatively, induction chemoradiotherapy may be administered, especially to downstage
patients with resectable bulky tumors
o Generally, the most common surgical approaches are transthoracic (thoracotomy) and transhiatal
without thoracotomy. Incisions may be required in the neck, chest, and abdomen
The most common transthoracic esophagectomy is the Ivor Lewis esophagectomy
useful for patients with tumors of the middle and lower esophagus. There is a two-layer
anastomosis in the upper chest
For tumors of the upper esophagus, many surgeons use a modified approach, called the
McKeown modification
The tubularized stomach is used as the esophageal substitute in most cases. other
possible substitutes are the colon and small bowel
Esophagectomy without thoracotomy is called the transhiatal approach. This involves a
cervical anastomosis

Hiatal Hernia
- Involves protrusion of the stomach through the diaphragm via the esophageal hiatus. It can cause GERD.
Acid reduction may suffice, and surgical repair can be used for more serious cases
- Occurs when the upper part of the stomach, which is joined to the esophagus (gullet), moves up into the
chest through the hiatus in the diaphragm.
o Promote GERD by separating the two components of the reflux barrier (LES and the crural
diaphragm) which work in concert to prevent reflux
o Normally, the crural diaphragm contracts during inspiration, helping to close the GE junction when
the pressure gradient across the diaphragm is greatest
o Once stretched by the herniated stomach of a patient with a hiatal hernia, the crural diaphragm
cannot provide adequate pressure to prevent the siphoning of gastric contents into the herniated
stomach
o These gastric contents can trigger frequent transient LES relaxations, releasing a toxic refluxate
into the distal esophagus
o Finally, migration of the GE junction into the chest results in loss of the normally acute
cardioesophageal angle (angle of His). This angle is a necessary component of the flapper-valve
mechanism whereby pressure in the fundus of the stomach leads to pinching of the GE junction
- Probably the most important pathophysiologic factor in severe GERD
- Epidemiology:
o Most common in overweight middle-aged women and elderly people
o It can occur during pregnancy.
- Common
- Often asymptomatic
- Types of hernia:
o Sliding hernia (I) 95% of hernias:
Characterized by widening of the muscular hiatal tunnel and circumferential laxity of the
phrenoesophageal membrane, allowing a portion of the gastric cardia to herniate upward.
The phrenoesophageal membrane remains intact and the hernia is contained within the
posterior mediastinum.
o Paraesophageal:
The less common types of hiatal hernia, account for about 5%.
Recognized complication of surgical dissection of the hiatus as occurs during antireflux
procedures, esophagotomy, or partial gastrectomy.
A type II hernia results from a localized defect in the phrenoesophageal membrane, while
the gastroesophageal junction remains fixed to the preaortic fascia and the median
arcuate ligament. Thus, the gastric fundus serves as the leading point of herniation
Type III hernias have elements of both types I and II. With progressive enlargement of the
hernia through the hiatus, the phrenoesophageal membrane stretches, displacing the
gastroesophageal junction above the diaphragm, thereby adding a sliding element to the
type II hernia.
Type IV hiatus hernia is associated with a large defect in the phrenoesophageal
membrane, allowing other organs, such as the colon, spleen, pancreas, and small
intestine, to enter the hernia sac.

Peptic Ulcer Disease

- Any ulcer of the upper digestive system (e.g., gastric ulcer, duodenal ulcer)
- Caused by any discreet break in mucosa injury, NSAIDs, stress, alcohol, or other irritants
o H. pylori is the most common cause of PUD. When this is the cause, the ulcer disease can be
eradicated with treatment
- Lifetime risk 5-10%. M=F. Duodenal ulcers typically occur at a younger age than gastric ulcers
- Both gastric ulcers and HP are highly associated with gastric malignancy. Although most patients with HP or
a gastric ulcer will not get gastric cancer, almost all patients with gastric cancer have had HP or a gastric
ulcer
- Abdominal pain or discomfort is the primary clinical feature
o The pain may be described as burning or gnawing and often radiates to the back
o The pain of a duodenal ulcer often improves with food, whereas the pain of a gastric ulcer typically
worsens, which leads to anorexia and associated weight loss
o Pain for duodenal ulcer is typically in the upper and midepigastric region and is described as sharp,
bright, and intense
o Pain for gastric ulcer is described as a constant, unrelenting pain in the epigastrium, which is
burning or dull. May be localized somewhat to the left of the midline
- Dyspepsia (belching, bloating, distention, heartburn) or nausea is also reported
- Complications bleeding, perforation, penetration
o Bleeding manifests as melena
o PUD is the most common cause of nonhemorrhagic GI bleeds
- Laboratory Studies:
o Endoscopy is best for detecting small or healing ulcers. It differentiates gastritis from ulcer disease
and allows immediate biopsy of gastric or suspicious ulcers to rule out malignancy
Duodenal ulcers are usually encountered in the bulb, which is that portion just beyond the
pylorus
The endoscopic appearance of a duodenal ulcer is characterized by a whitish, granular
base with surrounding erythema and heaped-up mucosa. The ulcer is often sharply
demarcated and looks as if it were punched out of the mucosa
Gastric ulcers are usually in the lesser curve of the stomach near the incisura
The endoscopic appearance of a gastric ulcer is a 1 cm or larger defect on the lesser
curve with a white, fibrinous base and heaped-up edges with erythema
o Barium radiography was once widely used and cheaper, but it is less sensitive, with a 30% falsenegative rate. Endoscopy is more sensitive and definitive
o Urea breath test may be helpful for detecting HP, as will stool or blood antibody tests
Breath testing confirms infection
PPIs, bismuth, and antibiotics can interfere with the test

Treatment:
o Avoid irritating factors (smoking, NSAIDs, alcohol). Dietary modifications do NOT play a big role
o Combination therapy for HP regimen should be taken for 14 days. Options:
PPI + clarithromycin + amoxicillin (sometimes add metronidazole)
Bismuth salicylate + tetracycline + metronidazole + PPI
o Prophylactic treatment with misoprostol or a PPI should be considered in patients with a history of
ulcer who require daily NSAID use, a history of complications such as bleed, a need for chronic
steroids or anticoagulants, or significant other comorbidities
o A small percentage of patients (15-20%) will have refractory disease and require surgical
management
Classic indications for duodenal ulcer operation intractability, perforation, hemorrhage,
and obstruction
Four procedures used for duodenal ulcers:
Truncal Vagotomy and Gastroenterostomy used much more in the past.
Transect the vagus nerve and make an anastomosis between the jejunum and
greater curve of the stomach, thus bypassing the ulcer disease in the duodenum.
SELDOM PERFORMED, only if severe obstructive disease
Truncal Vagotomy and Pyloroplasty transect the vagus nerve, drainage
procedure (Heineke-Mikulicz pyloroplasty). Rarely the procedure of choice
Vagotomy and Antrectomy GOLD STANDARD. Transect the vagus nerve,
remove the lower third of the stomach (including the antrum and thus completely
removing the gastrin G cells). This operation eliminates acetylcholine and
gastrin input to acid production, so results in a 90% decrease in acid production.
Then, after antrectomy, do an anastomosis either gastroduodenostomy or
gastrojejunostomy
Proximal Gastric Vagotomy resect only those nerves innervating the acidsecreting portion of the stomach in the fundus and corpus. The branch to the
liver is left intact, as are the branches supplying the antropyloric pump. Less
complications but higher recurrence rates
For gastric ulcers, vagotomy is not required. The operation of choice is a subtotal
gastrectomy with elimination of the ulcer. Reconstruction is usually with a
gastrojejunostomy anastomosis
Postgastrectomy complications diarrhea, bloating, dumping (tachycardia, diaphoresis,
dizziness, light-headedness, and weakness after eating within 30 minutes), tachycardia,
diaphoresis, malaise. Symptoms usually disappear within 3-6 months. May also get an
iron-deficiency anemia
Symptoms of dumping syndrome are worse when liquid or sugar-rich foods are
consumed during the meal
- Zollinger-Ellison Syndrome is a disease in which a gastrin-secreting tumor (gastrinoma) causes
hypergastrinemia, which results in refractory PUD
o Initial tests are fasting serum gastrin*, acid output to confirm the presence of gastric acid
hypersecretion, and serum infusion test
Gastric Cancer
- Fewer than 10% of patients with stomach cancer survive 5 years
- Endemic in Japan
- Environmental and diet factors influence the development of gastric cancer
o Smoked fish and meats contain benzopyrene, a probable carcinogen to gastric mucosa
o Nitrosamines are known carcinogens that are formed by the conversion of dietary nitrogen to
nitrosamines in the GI tract by bacterial metabolism

Atrophic gastritis, seen in patients with hypogammaglobulinemia and pernicious anemia, is

considered to be a premalignant condition for developing gastric cancer, because high pH
encourages bacterial growth
Chronic atrophic gastritis results in achlorhydria, and 75% of patients with gastric cancer
are achlorhydric
o Gastric polyps also are associated with the development of gastric cancer hyperplastic polyps
and adenomatous polyps. Hyperplastic are more common but are rarely malignant
Most tumors are adenocarcinomas, and spread is via lymphatics, venous drainage, and direct extension
o Diffuse or intestinal adenocarcinomas
Diffuse has a genetic association and is associated with blood group A. Younger patients,
body or cardia of stomach, poorly differentiated cells and poo prognosis
Intestinal is in older patients and usually the distal stomach, cells are better differentiated,
better prognosis
Most tumors are located in the antral prepyloric region
Gastric tumors can be typed according to gross appearance
o Polyploid fungating nodular tumors are usually well differentiated and carry relatively good
prognosis after surgery
o Ulcerating or penetrating tumors are the most common and are often mistaken for benign peptic
ulcers because of their sessile nature
o Superficial spreading lesions (infiltrative) diffusely infiltrate through mucosa and submucosa and
have a poor prognosis because most are metastatic at the time of diagnosis. Usually involve the
entire stomach giving it a leathery, hard appearance. This condition is known as linitis plastica and
is thought to be surgically incurable
The pathologic staging of gastric cancer is based on depth of tumor invasion and lymph node status
Patients usually have a history of vague and nonspecific symptoms
o Upper abdominal discomfort, dyspepsia, early satiety, belching, weight loss, anorexia, nausea,
vomiting, hematemesis, or melena is common
o Definite symptoms do not occur until tumor growth causes luminal obstruction, tumor infiltration
results in gastric dysmotility, or erosion causes bleeding
By the time of diagnosis, tumors are usually unresectable
Later symptoms indicative of metastatic disease are abdominal distention owing to ascites, resulting from
hepatic or peritoneal metastases, and dyspnea and pleural effusions, resulting from pulmonary metastases
Few findings on physical exam except in advanced disease
o A firm, nontender, mobile epigastric mass can be palpated, and hepatomegaly with ascites may be
present
o Other distant signs of metastatic disease include Virchow supraclavicular sentinel node, Sister
Joseph umbilical node, and Blumer shelf on rectal exam (nodes in the pouch of Douglas)
o

Diagnostics:
o Anemia is often found on routine blood studies. Usually hypochromic and microcytic secondary to
iron-deficiency
o Stool is often positive for occult blood
o Upper endoscopy has replaced barium-contrast upper GI study as the imaging modality of choice
Allows direct visualization and biopsy of the tumor
At least 4 biopsies should be made of the lesion
o Once diagnosis is made, CT is performed to evaluate local extension and to look for evidence of
ascites or metastatic disease
- TNM staging
- Treatment :
o The theory behind curative resection involves en bloc primary tumor resection with wide diseasefree margin and disease-free lymph nodes
o Tumors are located either in the proximal, middle, or distal stomach and the type of operation
depends on the location
Distal lesions located in the antral or prepyloric area are treated with subtotal gastrectomy
and gastrojejunostomy anastomosis (Billroth II) or Roux-en-Y anastomosis
Midgastric and proximal lesions are treated with total gastrectomy, with extensive lymph
node dissection.
The lesser and greater omentum are removed, along with the spleen. If the body
or tail of the pancreas is involved, distal pancreatectomy can be performed
Reconstruction with Roux-en-Y anastomosis (gastrojejunostomy)
Proximal lesions carry a poor prognosis, and surgical intervention is usually palliative
If there is extension into the distal esophagus, it is resected, along with the cardia and
lesser curvature. The remaining stomach tube is closed, and the proximal aspect is
anastomosed to the midesophagus through a right thoracotomy
If extensive esophageal involvement is discovered, radical near-total gastrectomy and a
near-complete esophagectomy are performed, with continuity restores using a distal
transverse colon and proximal left colon interposition
o Chemo and radiation are not very useful
- Other types of stomach cancer lymphoma, gastrointestinal stromal tumors (GIST)
Pyloric Stenosis
- A common cause of nonbilious vomiting in early infancy characterized by gastric outlet obstruction due to
hypertrophy and hyperplasia of the circular muscle of the pylorus
- Infants appear well during the first 1-2 weeks of life
- Regurgitation of food and nonbilious vomiting usually begin during weeks 3-5 of life often prompting one or
more formula changes
o Over the next few days, the disease progresses and the vomiting becomes more forceful and
eventually projectile
- The infant remains hungry after vomiting and otherwise appears well
- If no intervention, the infant becomes dehydrated and lethargic
- Physical exam dry mucous membranes, visible gastric peristaltic waves in the LUQ, and a palpable
pylorus or olive
o Examination of the abdomen may be facilitated by elevating the lower extremities (to relax the
abdominal musculature) and giving the infant a pacifier or a small amount of 5% dextrose in water
o Gently palpate the epigastrium from right to left, beginning just beneath the liver edge
- Other causes of nonbilious vomiting poor feeding technique, gastroenteritis, malrotation, duodenal or
antral web, or an enteric duplication cyst of the pyloric channel

Ultrasound criteria:
o Muscle thickness of 4 mm and a channel length of at least 16 mm
- If ultrasound is not available or if the pylorus is obscured by gas in the overlying bowel, a barium upper GI
study should be performed
o Positive findings narrow, elongated pyloric channel (string sign) and indentation of the gastric
antrum by the hypertrophied pyloric muscle
o Evacuate any remaining barium with an NG tube to prevent perioperative aspiration
- Recurrent vomiting causes loss of chloride and hydrogen ions, leading to metabolic alkalosis and
hypochloremia
o Continued vomiting depletes the intravascular volume, causing a hypokalemia. This leads to
aciduria
- Severely dehydrated infants should be resuscitated with normal saline (20 mL/kg), after which 5% dextrose
in normal saline (D5NS at 175-185 mL/kg/day) should be given until urine output is established. Then,
potassium may be added to the maintenance fluid at 10 mEq/500 mL.
- Infants who are not severely dehydrated should be managed with 5% dextrose in half-normal saline
(D50.45NS with KCl 10 mEq/500 mL
- Resuscitation sufficient to proceed to the operating room is characterized by a urine output of 1-2 mL/kg/hr,
normal sodium and potassium levels, and a bicarbonate level of less than 30
- Treatment:
o The standard operation is Ramstedts pyloromyotomy
Transverse RUQ incision, circumumbilical, or laparoscopically
o The most common complication is wound infection. Other complications include wound
dehiscence, incisional hernia, inadequate myotomy, and perforation
Acute Cholecystitis
- In the vast majority of cases (>90%), obstruction of the cystic duct by a stone is the initiating event
- Typically it is distinguished from an attack of biliary colic by persistent (as opposed to intermittent) RUQ
pain, fever, elevated WBCs, and alteration of liver chemistries
- After obstruction of the cystic duct, the gallbladder distends, causing subserosal edema, venous and
lymphatic obstruction, cellular infiltration, and localized areas of ischemia
- Associated with a variety of bacterial pathogens in 50-75% of cases
o E. coli, Klebsiella, Streptococcus fecalis, Clostridium spp., Enterobacter spp., Proteus spp.
o Tailor antibiotic regimens to cover these pathogens
- If left untreated, severe, gangrenous cholecystitis (usually seen in diabetics) may develop, leading to
increased morbidity and mortality from perforation of the gallbladder or overwhelming sepsis
o Another potential complication of untreated cholecystitis is perforation of the gallbladder into the
wall of adjacent hollow viscera (duodenum, jejunum, or colon), causing a cholecystenteric fistula
o If a stone subsequently passes into the hollow viscera, bowel obstruction may result. This is called
GALLSTONE ILEUS

Diagnosis:
o Abdominal symptoms referable to the biliary tree
o Persistent RUQ pain with peritoneal irritation (rebound tenderness or Murphys sign) is the most
characteristic symptom and sign
o Pain can be in RUQ and/or midepigastrium and can radiate to the back and/or right shoulder
o In contrast to biliary colic (pain lasting minutes to hours), pain from acute cholecystitis may last for
several days
o Nausea, vomiting, and anorexia are common
o Physical exam reveals an ill-appearing patient with a fever
Can frequently palpate inflamed gallbladder in the RUQ as a tender, distended mass (but
not always present)
Diabetics in particular may have severe cholecystitis with minimal exam findings
Murphys sign sudden pain from deep palpation in the RUQ during inspiration, as the
inflamed gallbladder descends to meet the examining hand. Patients often stop their
inspiratory effort during mid-breath
o Lab findings elevated WBC with associated bandemia.
Elevated LFTs (particularly AST, ALT, alkaline phosphatase)
Total bilirubin is usually moderately elevated (1-2), although significant elevation (>2)
should raise suspicion of concomitant common bile duct obstruction
o Two most common radiologic studies used are abdominal ultrasound and HIDA scan
Plain radiographs are of limited utility because only 15% of gallstones are radio-opaque
On ultrasound gallstones present? Gallbladder distended? Thickening of gallbladder
wall and/or pericholecystic fluid found? Is dilatation of the intrahepatic or extrahepatic bile
ducts present?
Gallbladder-wall thickening is often used as a criterion for diagnosis
The most reliable ultrasound signs are documentation of stones, a distended gallbladder,
and presence or absence of ultrasonic Murphys sign
Must always evaluate the diameter of the extrahepatic bile ducts to exclude the possibility
of choledocholithiasis
If the diagnosis is questionable, use a HIDA scan
If there is obstruction of the cystic duct, the gallbladder will not be visualized
Test is not very useful for NPO
- Treatment:
o Admit, NPO, start IV fluids
o If the diagnosis is confirmed, start IV antibiotics
o Unless contraindications exist (MI, pancreatitis, cholangitis), cholecystectomy should be performed
in the first 24-36 hours of admission
If patients do not present until day 4 or 5 of the illness, may want to manage with
antibiotics and defer surgery, because the inflammatory process is the most severe
between 72 hours and 1 week
Chronic Cholecystitis

Cholelithiasis / Choledocholithiasis
- CHOLELITHIASIS is the presence of gallstones within the gallbladder
- CHOLEDOCHOLITHIASIS refers to stones in the common bile duct
- Biliary colic is pain produced when the gallbladder contracts against a transiently obstructing stone in the
neck of the gallbladder. There is no inflammatory or infectious process
- Composed of cholesterol, calcium bilirubinate (pigment), or a mixture of both
o Cholesterol stones make up about 75% in Western countries
- Stone formation occurs when bile becomes supersaturated with cholesterol. Cholesterol crystals then
precipitate out of solution and agglomerate to form stones
- A high-cholesterol diet causes increased concentrations of cholesterol and may have a role in the
pathogenesis of cholesterol stones.
- Pigment stones are composed of calcium bilirubinate and are either black or brown
o Black pigment stones are usually found in the gallbladder and are associated with cirrhosis and
hemolytic processes, such as sickle cell anemia, thalassemia, and spherocytosis
o Brown stones are associated with chronic biliary tract infection and are often found in the bile ducts
Patients with indwelling biliary stents or with intraluminal nonabsorbable sutures in the
ducts from prior surgery are prone to developing brown stones
- More common in women
- Risk factors obesity, multiparity, chronic TPN use, high-dose estrogen oral contraceptives, rapid weight
loss, diabetes, and increasing age. High prevalence in American Indians. Spinal cord injuries predispose to
cholesterol stones
o The Five Fs female, forties, fertile, fair complexion, fat
- Most people are asymptomatic
- Biliary colic pain in the RUQ and/or epigastrium that radiates to the right flank or back, also to right
shoulder
o Usually postprandial
o Can be precipitated by fatty food intake
o Lasts several hours before resolving spontaneously
o Associated nausea and vomiting
- Choledocholithiasis can result in transient or complete blockage of the common bile duct. Patients may
relate episodes of passing dark urine or light-colored stools caused by the inability of bile pigments to reach
the GI tract and from subsequent renal clearance
o Can also leading to ascending cholangitis (RUQ pain, fever, chills)
- Physical exam in simple biliary colic reveals RUQ tenderness but no fever
o Choledocholithiasis may be also be associated with jaundice
o A palpable, nontender, distended gallbladder in the clinical setting of jaundice indicated malignant
biliary obstruction Courvoisier law
- Diagnostics:
o Labs are usually unremarkable with biliary colic
o Choledocholithiasis is classically associated with increased serum bilirubin and alkaline
phosphatase
o Ultrasound is the best modality for imaging the gallbladder and bile ducts (98% sensitivity and
specificity for detecting gallstones)
Gallstones appear as opacities, with echoless shadows posteriorly
Moving the patient during ultrasound often demonstrates migration of the stones to the
dependent portion of the gallbladder
o Choledocholithiasis can be diagnosed by intraoperative cholangiography at the time of surgery or
preoperatively or postoperatively by ERCP
Visualizes the ampulla of Vater where the pancreatic and bile ducts enter the duodenum

Complications:
o Most gallstones are quiescent
o Cholecystitis can develop
o Gallstone pancreatitis can develop
o Chronic perforation may result in a bilioenteric fistula usually in older patients when a large
gallstone erodes through the gallbladder wall and causes a fistula to form between the gallbladder
and bowel (usually duodenum, rarely colon). The large stone can then pass out of the gallbladder,
through the fistula and into the bowel, resulting in distal bowel obstruction (gallstone ileus)
Stone obstruction of the small bowel is typically at the terminal ileum, whereas large bowel
obstruction is usually at the sigmoid colon
Pneumobilia and a smooth obstructing mass on imaging studies are classic findings
- Treatment:
o No need for cholecystectomy if asymptomatic
o If biliary colic, can do laparoscopic cholecystectomy usually elective
o The procedure of choice for gallstones is laparoscopic cholecystectomy
In the setting of acute inflammation and infection, the procedure is more difficult and
causes more complications higher conversion rate to open procedure
o If preoperative workup suggests presence of common duct stones ERCP or intraoperative
cholangiography
Eventual cholecystectomy
Gallstone Pancreatitis
- About 40% of all cases of acute pancreatitis in the U.S. are caused by the passage of gallstones through the
common bile duct and temporary obstruction of the pancreatic duct at the ampulla of Vater
- Patients usually have epigastric pain, often with radiation to the back. Also nausea and vomiting
- Elevated serum amylase and lipase are typical early in the course of disease
- If mild to moderate disease, usually observe initially. If the patients signs and symptoms improve during the
first 48 hours and gallstones are considered the source, then cholecystectomy is performed during that
hospital admission
- If jaundice accompanies the pancreatitis, preoperative ERCP is indicated to rule out retained common bile
duct stones
- If a patient deteriorates in the first 48 hours, ERCP may be indicated to determine if a stone is impacted at
the ampulla of Vater
- Be careful ERCP may make pancreatitis worse!
- Once obstruction is relieved, the pancreatitis becomes the focus of management
- When pancreatitis resolves and patients are discharged, schedule cholecystectomy for months later to
prevent future attacks

Cholangitis
- An infection of the common bile duct
- Usually caused by choledocholithiasis
- Gram-negative organisms are the most common cause
- Classically marked by fever, RUQ pain, jaundice Charcot Triad
- Progression of cholangitis to sepsis defines Reynolds Pentad Charcot + hypotension + mental status
changes
- Causes elevated serum bilirubin and transaminase levels, as well as leukocytosis
- Requires rapid diagnosis and treatment
- Prompt treatment with IV antibiotics, fluid resuscitation, and urgent biliary decompression and drainage are
indicated
- ERCP with sphincterotomy is the primary intervention
- If the obstructing stone is unable to be extracted, an indwelling biliary stent can be passed proximal to the
stone to allow decompression and drainage of infected bile into the duodenum
o Other methods of decompression percutaneous transhepatic drainage or open surgical
drainage with common bile duct exploration and T-tube placement
- Overall mortality is about 15%
Hepatic Carcinoma
- Liver cancers are hepatomas, also known as hepatocellular carcinoma, or metastases from other primaries
- 95% of liver tumors are malignant
- Cholangiocarcinoma (bile duct carcinoma) also occurs in the liver
- Cirrhosis is a predisposing factor, and thus, hepatitis B (the leading cause of cirrhosis) and alcoholism are
associated with hepatoma development
o Chronic viral hepatitis is the most common cause of HCC
- Fungal-derived aflatoxins have been implicated as causes of hepatoma, as have hemochromatosis,
smoking, vinyl chloride, and oral contraceptives
- Patients may complain of weight loss, RUQ or shoulder pain, and weakness
- Hepatomegaly may be appreciable, and signs of portal hypertension, including splenomegaly and ascites,
may be present. Jaundice occurs in about half of patients
- Labs may show abnormal LFTs
- -Fetoprotein is a specific marker for hepatoma but can also be elevated in embryonic tumors
- Radiographic studies differentiate benign and malignant lesions
- Ultrasonography** can distinguish cystic from solid lesions
o Ultrasound and AFP can be used to screen for hepatocellular carcinoma
o Routinely ordered at 6-month intervals in conjunction with AFP in high-risk people
- Contrast CT or MRI can reveal multiple lesions and clarify anatomic relationships
o Also demonstrate the nodularity of the liver, hypersplenism, and portal hypertension, indicative of
underlying liver disease
- Hepatic arteriography can diagnose a hemangioma
- Because most cancers occur in the setting of liver disease and cirrhosis, it is important to perform viral
studies for hepatitis

Treatment:
o Before considering resection, the underlying health of the liver should be assessed using the ChildTurcotte-Pugh system
Clinical variables encephalopathy, ascites, bilirubin, bilirubin in PBC or PBS (primary
biliary cirrhosis or primary sclerosing cholangitis), albumin, and prothrombin time (seconds
prolonged or INR)
Scores 1-3 points for each variable
Class A = 5-6 points. Class B = 7-9 points. Class C = 10-15 points
Patients with Child class C disease will generally not tolerate a resection. Patients with
Child class B disease may tolerate a limited resection
Extrahepatic metastatic disease, multifocality within the liver (not encompassable with
standard resection), or advanced cirrhosis renders patients unresectable
o If the patient is a surgical candidate, treatment involves resection of the tumor
o Survival without treatment averages 3 months. Resection can extend survival to 3 years, with a 5year survival rate of 11-46%
o When possible, wedge resection should be performed, because formal hepatic lobectomy does not
provide any additional survival benefit
Liver resection that removes more than 70% of the original liver volume is associated with
severe cholestasis, progressive liver failure, sepsis, and death
o Patients with small tumors who are not candidates for resection because of tumor location or
concomitant cirrhosis should be considered for liver transplantation
o Patients who meet Milan criteria (tumor < 5 cm or no more than three tumors, the largest of which
is < 3 cm) will receive extra points on the liver transplant list
- Metastatic disease occurs in decreasing frequency from lung, colon, pancreas, breast, and stomach
- When colon cancer metastasizes to the liver, resection of up to three lesions has been shown to improve
survival
- In general, liver metastases from other tumors should not be resected
Acute / Chronic Pancreatitis
- ACUTE:
o The most common causes are cholelithiasis or alcohol abuse, but hyperlipidemia, trauma, drugs,
hypercalcemia, and penetrating PUD also may cause pancreatitis
o Also associated with medications, especially many of the antiretroviral medications used to treat
HIV
o The range of presentation is wide ranges from mild episodes of deep epigastric pain with nausea
and vomiting to the sudden onset of severe pain with shock
o The classic presentation is epigastric pain radiating to the back. The pain typically lessens when
the patient leans forward or lies in a fetal position
o Nausea and vomiting are common
o Fever, leukocytosis, and sterile peritonitis may occur
o Severe hypovolemia, adult respiratory distress syndrome, and tachycardia of greater than 130 bpm
indicated a grave prognosis

Laboratory Studies:
Elevation of serum amylase occurs but may be transient and can return to normal about
48-72 hours
Serum lipase is more sensitive and specific than amylase for acute pancreatitis, but only
with elevated of threefold or greater
WBC count generally is elevated, and hemoconcentration may occur with third spacing of
fluid
Liver enzymes may increase as a result
of biliary obstruction
Mild hyperbilirubinemia and bilirubinuria,
hyperglycemia, and hypocalcemia may
occur
Poor prognosis is indicated by Ransons
criteria, and risk of mortality rises with
each additional factor
On admission age > 55 years, WBC > 16,000, glucose > 200, LDH > 350,
AST > 250
Requires 48 hours of hospitalization for determination. If hematocrit drops
>10%, serum calcium < 8, base deficit > 4, BUN increase > 5, arterial pO2 <
60mmHg, or fluid sequestration >6L
Ultrasound to detect biliary disease
CT is the study of choice for acute pancreatitis
Parenchymal or peripancreatic edema and inflammation. Also pancreatic
necrosis and pseudocyst formation
Add IV contrast to determine severity of pancreatic necrosis
o Nonenhancement of 50% of more of the pancreas is strongly
suggestive of infectious complications
Treatment:
Oral intake must be stopped to prevent continued secretion of pancreatic juices
NPO and NG suction
Fluid volume must be restored and maintained. Parenteral hyperalimentation should be
started early to prevent nutritional depletion
Pain is managed with meperidine. Antibiotics should be considered
The patient must be monitored closely for complications, including pancreatic pseudocyst,
renal failure, pleural effusion, hypocalcemia, and pancreatic abscess
Surgery is directed at complications
Complications:
Pancreatic necrosis. May eventually liquefy and may become infected if they are unable
to reabsorb and heal. Infected collections require surgical debridement and drainage to
avoid fatal septic complications
Pancreatic pseudocysts drain if >6 cm in diameter and persist for >6 weeks. Standard
therapy is internal drainage into the stomach, duodenum, or small intestine
Abscess formation may occur in the later stage of disease
Ischemic parenchyma necrosis bacterial seeding abscess formation
Antibiotics are not sufficient. Must drain and debride

CHRONIC:
o Almost 90% of cases are caused by alcohol abuse. Other causes cholelithiasis, PUD,
hyperparathyroidism, and hyperlipidemia
o Some chronic cases can resolve if alcohol consumption is decreased
o The classic triad of pancreatic calcification, steatorrhea, and diabetes mellitus occurs in only 20%
of patients
o Clinical features are the same as acute
Also fat malabsorption and steatorrhea late in the disease. Fecal fat will be elevated if
malabsorption is present
o Laboratory Studies:
The amylase level may be elevated early but will decrease with each episode of
pancreatitis and cease to be a useful marker
Abdominal plain-film radiography reveals calcification in 20-30% of patients
o Treatment:
Same as acute. Recommend a low-fat diet at discharge
Surgical removal of part of the pancreas can control pain
The only definitive treatment for chronic pancreatitis is to address the underlying cause,
which most commonly is alcohol
o For a patient with a chain of lakes appearing pancreatic duct, caused by sequential ductal
scarring and dilatation, a longitudinal pancreaticojejunostomy (Puestow procedure) is indicated to
achieve drainage
Gallstone Pancreatitis
- About 40% of all cases of acute pancreatitis in the U.S. are caused by the passage of gallstones through the
common bile duct and temporary obstruction of the pancreatic duct at the ampulla of Vater
- Patients usually have epigastric pain, often with radiation to the back. Also nausea and vomiting
- Elevated serum amylase and lipase are typical early in the course of disease
- If mild to moderate disease, usually observe initially. If the patients signs and symptoms improve during the
first 48 hours and gallstones are considered the source, then cholecystectomy is performed during that
hospital admission
- If jaundice accompanies the pancreatitis, preoperative ERCP is indicated to rule out retained common bile
duct stones
- If a patient deteriorates in the first 48 hours, ERCP may be indicated to determine if a stone is impacted at
the ampulla of Vater
- Be careful ERCP may make pancreatitis worse!
- Once obstruction is relieved, the pancreatitis becomes the focus of management
- When pancreatitis resolves and patients are discharged, schedule cholecystectomy for months later to
prevent future attacks
Pancreatic Pseudocyst
- Walled-off collections of fluid and debris resulting from disruption of the pancreatic duct. Most commonly
associated with acute and chronic pancreatitis
- Develop in up to 10% of patients after an episode of acute alcoholic pancreatitis. They may also occur after
trauma or in association with neoplasm
- The wall is vascularized inflammatory tissue without an epithelial lining and may contain pancreatic
parenchyma
- Can occur in any region of the gland
- Fluid collections occurring within 3 weeks of an acute episode of pancreatitis are considered acute fluid
collections, and 30-40% of these will resolve spontaneously
- The most common presentation is abdominal pain (present in about 90% of patients)
- Physical exam often reveals a tender abdominal fullness or mass
- Nonspecific complaints of nausea, vomiting, early satiety, and weight loss are common

More dramatic presentations may result from free intraperitoneal rupture, intracyst hemorrhage or infection,
gastric variceal bleeding resulting from splenic or portal vein thrombosis, or intraperitoneal hemorrhage from
adjacent pseudoaneurysm rupture
- Lab findings are nonspecific, although amylase elevation is common
- Imaging with CT is preferred, but ultrasound can be used for follow-up to determine interval changes in size
- Sampling of a post-pancreatitis fluid collection is rarely indicated, however, if a preceding episode of
pancreatitis has not occurred, fluid cytology and chemistry can help differentiate a pseudocyst from a more
likely mucinous or serous cystic neoplasm
- The natural history of asymptomatic pseudocysts reveals that nearly half remain stable, decrease in size, or
completely resolve at 1-year follow-up, irrespective of size
o However, pseudocysts larger than 6 cm are more likely to require operation
- Pseudocysts present for more than 12 weeks almost never resolve spontaneously and have a high rate of
complications
- Current management of pancreatic pseudocysts takes into account the presence or absence of symptoms,
the age and size of the pseudocyst, and the presence or absence of complications
- Post-pancreatitis fluid collections that are asymptomatic in a stable patient can be followed up with monthly
imaging to evaluate resolution, stability, or enlargement
o Failure to resolve or evidence of enlargement is an indication for intervention
- If the pseudocyst is symptomatic, early intervention should be considered
- Generally, a period of 6 weeks is desired before surgical intervention to assure adequate maturation of the
cyst wall
- The preferred operative management of a pseudocyst is internal drainage into the GI tract. This can be
accomplished by anastomosis of the opened cyst wall to the stomach (cystogastrostomy), duodenum
(cystoduodenostomy), or a Roux-en-Y limb of jejunum (cystojejunostomy) depends on the location of the
pseudocyst
- Multiple pseudocysts can be addressed simultaneously by connecting pseudocysts and draining as one, or
separately draining each cyst into a Roux-en-Y jejunal limb or a combination of these internal drainage
procedures
- A lateral pancreatic jejunostomy also should be added when the pancreatic duct is dilated
- A biopsy of the cyst wall should be obtained on all occasions cystic neoplasms of the pancreas can mimic
a pseudocyst
- Infected pseudocysts are generally treated as pancreatic abscesses
- Simple aspiration of pseudocyst will fail to resolve the fluid collection in as many as 80% of patients
o Prolonged catheter drainage has better results but may take months
Pancreatic Carcinoma
- ADENOCARCINOMA
o Ductal carcinoma accounts for 80% of the cancer types and is usually found in the head of the
gland
o Local spread to contiguous structures occurs early ,and mets to regional lymph nodes and liver
follow
o Etiology is largely unknown, but genetic and environmental factors have been implicated
Strong association with cigarette smoking and exposure to some chemical carcinogens
Less convincing diets high in fat and red meet, coffee consumption, diabetes,
cholelithiasis, and after partial gastrectomy
o Poor prognosis. Only 20% of patients with resectable tumor
o First present with vague abdominal pain and weight loss
Obstructive jaundice is frequent with lesions in the head of the gland
A painless, dilated, palpable gallbladder (Courvoisiers sign) may accompany distal
common bile duct obstruction
Anorexia, weakness, altered bowel habits, and pruritus also may be present

Back pain is frequent often ominous

o Physical is often unremarkable with the exception of a palpable mass
o CT and ERCP are the modalities of choice
CT reveals the location of the mass, the extent of tumor invasion or metastasis, and the
degree of ductal dilatation
ERCP defines the ductal anatomy and the extent of ductal obstruction and provides
biopsy specimens for tissue diagnosis
o Dont use drainage stents can cause infection!
o Imaging suggesting unresectability local tumor extension, contiguous organ invasion, superior
mesenteric vein or portal vein invasion, ascites, and distant metastases
o Tumor markers may be helpful to differentiate benign and malignant pancreatic disease
Carbohydrate antigen (CA) 19-9. Elevated in 78% of patients with pancreatic cancer.
Levels greater than 1000 units/mL are associated with unresectable disease
May also be elevated in carcinoma of the gallbladder, bile duct, colon and
rectum, stomach, liver, lung, and ovary. Also in hepatitis and cirrhosis
o The operation for resectable tumors in the head of the pancreas is pancreaticoduodenectomy
(Whipple procedure) entails the en bloc resection of the antrum, duodenum, proximal jejunum,
head of pancreas, gallbladder, and distal common bile duct
Body and tail lesions should be treated with a distal pancreatectomy and splenectomy
o Most patients die within 1 year of diagnosis. 3% 5-year survival rate, increases to 15-20% with
Whipple procedure
o No real evidence for chemotherapy or radiation
CYSTIC NEOPLASMS
o About 20% of all pancreatic cysts are NOT pseudocysts. Up to 10% are cystadenomas
o Often multilobulated and heterogenous in appearance compared with pseudocysts
o Predilection for middle-aged women
o Vague abdominal symptoms. Obstructive jaundice is rare
o Serous cystadenomas are almost always benign, whereas the mucinous type has a greater
malignancy potential
o Resect all impossible to differentiate benign from malignant
SOLID & CYSTIC PAPILLARY NEOPLASMS
o Usually in females aged 10-40 years
o Heterogenous histologic appearance consisting of microcystic, papillary, and solid components,
and contain frequent areas of cystic degeneration and hemorrhage
o Grow large before detection and arise predominantly from the body and tail
o Complete resection is recommended and curative
INTRADUCTAL PAPILLARY MUCINOUS TUMORS
o Also known as mucinous ductal ectasia
o Distinguished from other cystic lesions of the pancreas in that the pancreatic duct is enlarged
because of mucin deposition
o Unlike other cystic pancreatic neoplasms, IPMT is usually symptomatic in the form of chronic
pancreatitis-like symptoms or recurrent bouts of acute pancreatitis. However, patients are usually
20-30 years older than those with chronic pancreatitis and have no identifiable risk factors for
pancreatitis
o ERCP demonstrates mucin in the duct
o These lesions have malignant potential and require resection, but have excellent long-term
prognosis
LYMPHOMA

o
o

Primary pancreatic non-Hodgkins lymphoma is unusual

Combination chemotherapy appears to be the preferred treatment

INSULINOMA
o The most common endocrine tumor of the pancreas
o Characterized by Whipples triad fasting hypoglycemia that induces symptoms (palpitations,
tachycardia, shaking), blood glucose levels less than 50 mg/dL, and relief of symptoms after
glucose administration
o Hypoglycemic symptoms result from the autonomous secretion of insulin from the tumor
o Most are benign. Usually small (< 2 cm), solitary, and evenly distributed throughout the pancreas
o Suspect MEN-1, especially if lesions are multiple
o Patients will have an immunoreactive insulin-to-glucose ratio of greater than 0.3 and elevated
proinsulin and C-peptide levels
o Many of these tumors are too small to be seen on CT
o Should be resected
GASTRINOMA
o A rare neuroendocrine tumor of the pancreas
o Defined by gastrin hypersecretion, causing the severe PUD of Zollinger-Ellison syndrome
o 80% of cases are sporadic, 20% associated with MEN-1
o Usually in the pancreas, but can also occur in the duodenum or other areas
Nearly 90% are found in the gastrinoma triangle junction of the cystic duct and
common bile duct cephalad, the second and third portions of the duodenum inferiorly, and
the neck and body of the pancreas medially
o Symptoms acid hypersecretion, ulcers, secretory diarrhea
o Patients will have elevated gastrin levels greater than 1000 pg/mL is virtually diagnostic
o Also will have elevated basal acid output (> 15 mEq/hr or > 5 mEq/hr if previous acid-reducing
operations have been performed)
o The test of choice is secretin stimulation(infusion) test an absolute increase in serum gastrin of
200 pg/mL over the baseline gastrin level is diagnostic
o Somatostatin scintigraphy to localize the tumor
o Initial treatment consists of control of gastric hypersecretion PPIs (substituted benzimidazoles)
o Resection is all cases if metastases has been excluded
VIPOMA
o Vasoactive intestinal polypeptide is the most likely islet cell tumor product responsible for the
watery diarrhea, hypokalemia, hypochlorhydria (WDHH or Verner-Morrison) syndrome.
o Oversecretion of VIP results in profuse secretory diarrhea (> 3 L/day) and subsequent potassium
loss and dehydration
o More than 50% are malignant
o Correct electrolyte deficits and replace fluids first
o Surgical resection if a solitary lesion is identified
o For metastatic disease, use octreotide. Also streptozotocin and 5-FU
OTHERS glucagonoma, somatostatinoma, nonfunctional islet cell tumors

Appendicitis
- Occurs when obstruction of the appendix leads to inflammation and infection
- The base of the appendix is located at the junction of the three tenia
- The appendiceal artery lies posterior to the cecum or terminal ileum
- The most common cause is a fecalith
o Less common causes infection (CMV, adenovirus, histoplasma, other), collagen vascular
disease, and IBD
- Patients usually between 10-30 years old. Affects 10% of U.S. population the most common abdominal
surgical emergency
- Perforation and peritonitis occur in about 20% of patients with appendicitis, causing high-grade fever,
generalized abdominal pain and increased leukocytosis
- Initial symptom is intermittent periumbilical or epigastric pain
- In about 12 hours, pain typically localized to the RLQ (McBurneys point), becomes constant, and is
worsened by movement, leading to rebound tenderness on examination
- Nausea and anorexia are common. Vomiting may occur, but generally is isolated and begins subsequent to
the onset of pain. Diarrhea may occur but is not common. A low-grade fever is common (but a high-grade
fever is unlikely)
- Psoas sign (patient is supine and attempts to raise the leg against resistance) and obturator sign (patient is
supine and attempts to flex and internally rotate the right hip with the knee bent) generally are positive,
indicating inflammation adjacent to those muscles
- Variability in anatomy can cause unusual presentations of appendicitis, with symptoms reflecting location of
the appendix
- Laboratory Findings:
o Leukocytosis (usually 10,000-20,000 cells/mL) is characteristic. Higher levels suggest perforation
and peritonitis
o Some microscopic hematuria and pyuria may be seen
o Abdominal CT may be used in some cases to confirm the diagnosis and to locate an abnormally
placed appendix
- Treatment is appendectomy.
o If there is any reason to suspect perforation, broad spectrum antibiotics are administered before
and after surgery
o Operative approaches include oblique (McBurney) incision, transverse (Rocky-Davis) incision,
midline laparotomy, and laparoscopy
- Many patients can be progressed to a diet and discharged within 24-48 hours of surgery
o In more advanced cases, postoperative ileus is not uncommon.
o When perforation is encountered, a longer course of antibiotics, wound care, and hospitalization is
the norm
- Septic complications are by far the most frequently seen problem after appendectomy
o Other complications formation of intraabdominal abscess, pylephlebitis, etc.

Inflammatory Bowel Disease

- CROHNS DISEASE (refractory enteritis)
o An IBD for which there is some genetic predisposition, although the cause is unknown
o May involve both the small and large bowels as well as the mouth, esophagus, and stomach. Most
commonly the terminal ileum and right colon are involved, but the rectum frequently is spared.
Skip areas are characteristic
o Unlike UC where the disease is confined to the mucosa, CD has segmental transmural
inflammation
o Complications include fistulas, abscesses, aphthous ulcers, renal stones, and predisposition to
colonic cancer
Perianal fistulas, palpable abdominal mass, strictures and obstruction, and perforations
are more common than in UC
o The success or failure of treatment is variable. The disease usually waxes and wanes throughout
life
o Abdominal cramps and diarrhea in a patient younger than 40 years are the most common
presenting complaints
o Low-grade fever, polyarthralgia, anemia, and fatigue frequently are encountered
o Blood is often present in stool
o Colonoscopy is the most valuable tool for establishing the diagnosis, determining the extent and
severity of disease, and guiding the treatment
o Contrast studies and endoscopic procedures should be avoided in patients with fulminant disease
because of the possibility of inducing toxic megacolon or perforation
o Biopsy will reveal involvement of the entire bowel wall in Crohns disease. Granulomas are
frequent (non-caseating granulomas)
o Blood tests may include increased sedimentation rate, anemia, and nutritional and electrolyte
imbalances during exacerbations
o For acute attacks, oral corticosteroids (prednisone) are used with or without aminosalicylates
(sulfasalazine). Metronidazole or ciprofloxacin is added in perianal disease, fissures, or fistulae.
Infliximab may be used in refractory cases
o Elemental diet is nearly as effective as corticosteroids, but relapse is more likely
o Mesalamine is generally the best option for maintenance therapy
o For patients with malabsorption, supplementation may be needed especially for vitamin B12, folic
acid, and vitamin D
o Smoking cessation is critical for reducing the frequency and severity of attacks
o Surgery is not curative in Crohns disease and is reserved for treatment of complications.
Segmental resection is the approach of choice
The primary indication for surgery of the small intestine is obstruction due to fibrosis and
stricture
Subtotal colectomy with ileostomy and Hartmann closure of the rectum is the operation of
choice in an emergency

ULCERATIVE COLITIS
o The disease generally starts distally, at the rectum, and progresses proximally. Disease is
continuous, and skip areas are NOT seen
o Disease is confined to the colorectal mucosa
o Onset generally is gradual but also can be abrupt
o Tenesmus and bloody, pus-filled diarrhea are the most common symptoms
Bloody diarrhea is a clinical hallmark
o Pain is less common but may occur, typically in the LLQ
o Weight loss, malaise, and fever may occur in more severe disease
o Toxic megacolon and malignancy are more likely in UC than in Crohns disease
o Other complications scleritis and episcleritis, arthritides, sclerosing cholangitis, and skin
manifestations (erythema nodosum and pyoderma gangrenosum)
o As opposed to Crohns disease, where smoking increases disease, ironically smoking seems
protective in UC. Smokers who have recently quit will often have a disease flare
o Anemia, increased sedimentation rate, and decreased serum albumin are common
o Abdominal plain-film radiography may show colonic dilatation. Sigmoidoscopy or colonoscopy is
the best method of establishing the diagnosis
Endoscopy demonstrates thickened, friable mucosa
o Colonoscopy and barium enema should be avoided in acute disease because of the risks of
perforation and toxic megacolon
o Topical or oral aminosalicylates and corticosteroids are the mainstays of medical treatment.
Immunomodulators are indicated for refractory disease
Sulfasalazine or 5-ASA
Steroids for more advanced disease
o Also treat symptoms antidiarrheals, antispasmodics. May need antibiotics
o Surgery can be curative in UC. Segmental resection is possible, but total proctocolectomy is the
most common surgical cure
Subtotal colectomy with ileostomy is the procedure of choice in the emergency setting or if
you cannot differentiate between UC and Crohns
Colectomy, mucosal proctectomy, and endorectal ileal pouch-anal anastomosis (IPAA)
has become the operation of choice for patients with refractory UC
Pouch dysfunction is the most common late complication (bowel obstruction
early)
o Indications for surgery colonic obstruction, massive blood loss, failure of medical therapy, toxic
megacolon, cancer

Small Bowel Carcinoma

- The most common benign neoplasms occurring in the small intestine are adenomas, leiomyomas, and
lipomas
- The most common malignant neoplasms are adenocarcinomas, carcinoid tumors, lymphomas, and
gastrointestinal stromal tumors (GIST)
o All are rare
Probably due to a lower concentration of bacteria in the small bowel, rapid transit of
chyme through the small intestine, mucosal protection by secretory IgA, and more
effective apoptosis (programmed cell death)
- Tend to be asymptomatic until they become large
- Symptoms are the result of bleeding into or partial obstructions of the intestinal lumen
- Because of the lack os specific symptoms, most are not diagnosed until they become large, or until
advanced-stage disease ensues
- A contrast examination of the small intestine is the test of choice
o Enteroclysis is more sensitive than the upper GI with small-bowel follow through, especially for
tumors in the distal small intestine
o CT good for staging
o Endoscopy to visualize and take biopsies in extreme proximal or distal intestine, but usually the
small intestine is beyond the reach of a standard endoscope
- Adenocarcinomas are most often found in the duodenum
o Tumors in the periampullary region are treated with pancreaticoduodenectomy
5-year survival rates after resection are 50-60%
o Adenocarcinoma in the remainder of the small intestine have a poorer prognosis and are rarely
amenable to curative resection
For localized disease, segmental resection of the involve intestine and lymph nodebearing mesentery are performed, but 5-year survival is only 5-30%. Usually resection is
done for palliation. Chemotherapy of no benefit
- GISTs are treated with wide local resection of the involved intestine
o In advanced disease, palliative resection to relieve obstruction or stop bleeding
o For resected lesions, tumor size and mitotic index are the most important prognostic factors
o 5-year survival after resection is 35-60%
o Standard chemo is ineffective, but imatinib (a tyrosine kinase inhibitor) can help
- Carcinoids are usually found in the appendix, where they are associated with benign prognoses. However,
in the small intestine, they are more aggressive and are usually first seen with metastatic disease
o If localized, treat with wide local resection. Prognosis is excellent
o Moderately responsive to chemotherapy
o Manifestations of carcinoid syndrome diarrhea, flushing, hypotension, tachycardia, fibrosis of
the endocardium and valves of the right hear
Treat with octreotide
- Lymphomas predominate in the ileum (this is where the greatest concentration of lymphoid tissue is)
o Usually non-Hodgkins B-cell lymphomas
o Localized disease is treated with segmental intestinal resection
o Diffuse disease is treated with chemotherapy rather than surgery
o Overall 5-year survival rates from 20-40%
With localized disease amenable to surgery, 5-year survival rate is 60%

Toxic Megacolon
- A complication of undiagnosed Hirschsprungs disease (aka Hirschsprungs enterocolitis)
o Hirschsprungs is a motility disorder that is characterized by the absence of ganglion cells in the
rectum or more proximal bowel. A cardinal sign is delayed passage of meconium in the first 48
hours of life. Neonates present with bilious emesis, abdominal distention, and delayed or
diminished stool frequency
- Etiology is related to stasis, but lots of patients have C. difficile in the stools
- May develop at any age and usually appears with increasing abdominal distention, borborygmus (rumbling,
growling noise in stomach), and foul-smelling diarrhea
- May progress to fever, vomiting, abdominal pain, and explosive watery diarrhea
- Dehydration follows compounded by mucosal slough and a massive loss of protein-rich fluid into the
dilated bowel
- Can progress to vascular collapse and an early septic death if the patient is not aggressively fluid
resuscitated
- Hirschsprungs is diagnosed with contrast enema aganglionic segment as a transition between dilated
proximal colon and a segment of narrow distal colon or rectum
o In toxic megacolon, a contrast enema may show mucosal spiculation in the affected region,
submucosal dissection of contrast material, or perforation
- Diagnosis of Hirschsprungs is confirmed with rectal biopsy hypertrophied nerve trunks and absence of
ganglion cells in Auerbachs inter-myenteric plexus and Meissners submucosal plexus
- Treatment for Hirschsprungs can be either the Swenson, Duhamel, or Soave endorectal pull-through.
o Diverting colostomy performed at the most distal portion of the colon where normal ganglion cells
are seen. Eventually taken down (usually after 6-12 months)
Colorectal Carcinoma
- The third leading cause of cancer death in the United States after lung cancer and skin cancers. ~90%
occur in those older than 50 years old
- UC, Crohns, and Gardner syndrome all predispose
- Hereditary Nonpolyposis Colorectal Cancer also leads to an extremely high risk of colon cancer, and those
with familial polyposis have a virtually 100% risk of developing the disease
- Gene mutations ras (50%) and p53 (75%)
- Prognosis is good in early disease
- Adenomatous polyps are either tubular or villous (some have both features). The higher the villous
component, the higher the risk of malignancy. As the lesion grows in size, the likelihood of malignant
transformation increases significantly
- 90% of colon cancers are adenocarcinomas (types include ulcerative*, polypoid, annular, diffusely
infiltrating)
o 20% of these are mucinous (worst prognosis)
o Other types squamous, adenosquamous, lymphoma, sarcoma, and carcinoid
- When the cancer involves only the mucosa (Dukes A), the 5-year survival rate is greater than 90%.
Penetration through the wall or involvement of regional lymph nodes (Dukes B) has a 5-year survival rate of
70-80%. When there is metastasis (Dukes C = lymph node positive, Dukes D = distant metastases), the 5year survival rate drops to 5%

Colorectal cancer is slow growing, and symptoms often appear late in the disease
o Clinical presentation usually depends on the site of the lesion
o Abdominal pain, change in bowel habits, occult bleeding, and intestinal obstruction are common
presentations
Right-sided (ascending) neoplasms are often asymptomatic or only present with occult
blood in the stool and weight loss
Left-sided lesions typically present with more obstructive symptoms (change in stool,
tenesmus, constipation)
In general, this is due to fecal matter entering the right colon in liquid form and easily
transiting a large cecal lesion, whereas desiccated stool in the left colon tends to obstruct
when confronted with malignant luminal narrowing
o Any adult patient who lacks a history of prior abdominal surgery or recent colonoscopy who
presents with large bowel obstruction must be considered to have obstructing colon cancer until
proven otherwise
o Fatigue and weakness may occur if chronic blood loss has led to anemia
o Changes in stool size and shape may be noted, as may frank blood in the stool
Liver is the most common site for metastases
Watershed areas of the colon (poor blood supply) splenic flexure (Griffiths point), rectosigmoid junction
(Sudecks point)
The strongest layer of the bowel wall is the submucosa
Laboratory Findings:
o Occult blood in the stool can be an early marker and is used for screening adults older than 40
years. Flexible colonoscopy is recommended in those older than 40-50 years. Overall screening
recommendation is after age 50 (every 5-10 years, depending on the method)
o Carcinoembryonic antigen (CEA) may be used to monitor, but not to detect, colorectal cancer
o Sigmoidoscopy, colonoscopy, or barium enema may all be used to visualize suspected colonic
masses, whereas chest radiography and CT are used to detect metastases
Treatment:
o Surgical resection of the malignant lesion and associated lymph nodes
Bowel prep the night before
A good oncologic resection of a colon cancer involves proximal ligation of the named
vessel(s) supplying the length of the bowel being removed. A good oncologic resection of
a rectal cancer involves total mesorectal excision (for mid and distal rectal tumors) and a
proximal ligation of the inferior mesenteric vessels, just distal to the left colic
The proximity of the lesion to the anal sphincter is what defines whether the patient will
need a permanent colostomy
Within 2 cm of it usually requires one
Requirements of a good anastomosis good blood supply, tension free, air
tight
For cancers of the cecum and ascending colon, right hemicolectomy is indicated
Avoid the duodenum and right ureter
Tumors of the transverse colon require transverse colectomy, with removal of hepatic and
splenic flexures
Descending colon tumors require left colectomy
Sigmoid tumors are treated with sigmoidectomy

Most rectal tumors are treated with low anterior resection, whereas very low rectal
cancers near the anus occasionally require abdominoperineal resection, which entails
resection of the anus with closure of the perianal skin and creation of a permanent end
colostomy, because anastomosis may not be technically feasible
Resection of the distal sigmoid or rectum, where anastomosis is possible, is
referred to as low anterior resection
Reconstruction of the bowel continuity is performed with anastomosis (hand-sewn or
stapled). For low colon or rectal anastomosis, use of an end-to-end anastomosis stapler
placed through the anus is preferred technique
Careful to avoid the ureter!!!
Other complications bleeding, abdominal abscess, anastomotic leak, splenic injury,
ureteral injury, small-bowel injury, wound infection, incisional hernia, DVT, MI, stroke,
death
o Add chemo in patients stage III (Dukes C) or higher. Sometimes in stage II (Dukes B)
Postoperative chemo
o Radiation may be used for rectal tumors preoperatively
Diverticular Disease
- DIVERTICULOSIS can be described as large outpouchings of the mucosa in the colon
- DIVERTICULITIS is defined as inflammation of the diverticula caused by obstructing matter
- In patients with diverticulosis, diverticulitis and its complications can be prevented with a high-fiber diet and
avoidance of obstructing or constipating foods
- Diverticulosis is the most common cause of lower GI bleeding (usually from the right colon)
- Diverticulitis
o Generally presents with sudden-onset abdominal pain, usually in the LLQ or suprapubic region,
with or without fever
o Symptoms may range from mild disease to severe infection with peritonitis
o Most commonly occurs in the sigmoid and is rare in the right colon
o Altered bowel movement as well as nausea and vomiting are common
- Diverticular bleeding generally presents as sudden-onset, large-volume hematochezia. It resolves
spontaneously, although continuous or recurrent bleeding are indications for surgery
- Occult blood in the stool and mild to moderate leukocytosis may occur with diverticulitis
- Plain-film radiography should be done to rule out free air seen under the diaphragm with perforations
- CT is warranted if patients do not respond to therapy
o Pericolic fat stranding, bowel wall thickening, or abscess may be seen
- Barium enema should be avoided during an acute episode, because it may lead to perforation and
peritonitis
- Low-residue diet and broad-spectrum antibiotics are appropriate for patients with mild diverticulitis
o Metronidazole + cipro
- Hospitalization for IV administration of antibiotics, bowel rest, and analgesics often is required. A
nasogastric tube is inserted if ileus develops

Surgical management may be necessary in severe cases including peritonitis, large abscesses, fistulae, or
obstruction
o In the event of free perforation or failure of medical management, surgical exploration with
resection and colostomy is usually required (Hartmann procedure)
Usually after 3 or more episodes
The distal point of resection of sigmoid is the coalescence of teniae coli (the anatomic
starting point of the rectum)
Ideally, surgery is elective with resection and primary anastomosis (avoid colostomy). Not
always possible in emergent situations
Mobilization of the splenic flexure is usually required to create a tension-free
anastomosis
o Abscess can be treated with percutaneous drainage about 75% of the time
- Patients with diverticulosis should maintain a high-fiber diet to prevent diverticulitis. Recent studies have
negated the need to recommend avoidance of nuts, seeds, and popcorn
Celiac Disease (Celiac Sprue)
- Amongst the most common genetic conditions in Europe and the United States (multifactorial inheritance)
- Characterized by inflammation of the small bowel, with the inflammation of the small bowel, with the
ingestion of gluten-containing foods such as wheat, rye, and barley leading to malabsorption
- Clinical presentation is highly variable, often leading to a delay in diagnosis in milder cases
- Diarrhea, steatorrhea, flatulence, weight loss, weakness, and abdominal distension are common
- Infants and children may present with failure to thrive
- Older patients may present with iron deficiency, coagulopathy, and hypocalcemia
- IgA antiendomysial and antitissue transglutaminase antibodies are the serologic screening tests
- Small bowel biopsy is needed to confirm the diagnosis
- Treatment involves a gluten-free diet. Refer to nutritionist. A lactose-free diet may also be needed initially
until the intestinal inflammation resolves
- Supplementation may be needed to correct nutritional deficiencies in iron, B12 and folic acid, calcium and
vitamin D
- Prednisone may be required in refractory cases
Rectal Prolapse
- A medical condition where a section of the wall of the rectum falls down from the normal anatomical position
with associated pelvic floor dysfunction. May occur while straining to defecate, or during rest
- May have mucous discharge, rectal bleeding, degrees of fecal incontinence, and obstructed defecation
symptoms
- Proctoscopy / sigmoidoscopy / colonoscopy may reveal congestion and edema (swelling) of the distal rectal
mucosa. May have a solitary rectal ulcer on the anterior rectal wall
- External prolapse can be treated successfully with surgery. Internal prolapse is harder to treat

Small Bowel Obstruction

- Mechanical SBO is the most frequently encountered surgical disorder of the small intestine
- Obstruction of the small bowel lumen causes progressive proximal accumulation of intraluminal fluids and
gas. Peristalsis continues to transport swallowed air and secreted intestinal fluid through the bowel proximal
to the obstruction, resulting in small bowel dilation and eventual abdominal distention
o As the bowel distends, intraluminal and intramural pressures increase, and the intestinal epithelium
exhibits net fluid secretion, rather than net absorption
o If the intramural pressure becomes high enough, microvascular perfusion to the intestinal wall is
impaired, ultimately leading to strangulation, with intestinal ischemia and necrosis resulting
- Partial SBO includes only a portion of the intestinal lumen that is occluded, allowing passage of some gas
and fluid. Progression to strangulation is more slowly that with complete SBO
- Progression to strangulation occurs rapidly with closed-loop obstruction, in which a segment of intestine is
obstructed both proximally and distally (e.g., volvulus)
- The obstructing lesions is classified by its anatomic relation to the bowel as intraluminal (e.g., foreign
bodies, gallstones, or meconium), intramural (e.g., tumors, inflammatory strictures, or hematomas) or
extrinsic (e.g., adhesions, hernias, or carcinomatosis)
- Hard to distinguish from ileus, which is intestinal obstruction caused by impaired peristalsis rather than
mechanical obstruction
- Depending on the location of the obstruction, vomiting occurs early in proximal obstruction and later in more
distal blockage
- Crampy abdominal pain initially occurs as active proximal peristalsis exacerbates bowel dilation
- With progressive bowel wall edema and luminal dilation, however, peristaltic activity decreases and
abdominal pain lessens.
- At presentation, patients exhibit abdominal distention and complain of mild diffuse abdominal pain
- The most common causes of SBO are adhesions (1) and hernia (2).
o Other causes are neoplasms, obturation/strictures, diverticular disease, Crohns disease, gallstone,
bezoar, intussusception, Meckels diverticulum, volvulus, SMA syndrome, intramural hematoma
o Most adhesions are caused by postoperative internal scar formation
o The mechanisms of obstruction is important because it relates to the possibility of vascular
compromise and bowel ischemia
o Volvulus can cause closed-loop obstruction and is at high risk for vascular compromise
o Another mechanism causing bowel ischemia is incarceration in a fixed space. Incarceration and
subsequent strangulation impedes venous return, causing edema and eventual bowel infarction
- Patients present with complaints of intermittent crampy abdominal pain, abdominal distention, obstipation,
nausea, and vomiting
o Vomiting of feculent material usually occurs later in the course of obstruction
o Constant localized pain or pain out of proportion to physical findings may indicate ischemic bowel
and is a clear indication for surgical exploration
- Variable manifestations depend on level of blockage
o High frequent vomiting, no distention, intermittent pain by not classic crescendo type
o Middle moderate vomiting, moderate distention, intermittent pain (crescendo, colicky) with
frequent intervals
o Low vomiting late, feculent vomiting, marked distention, variable pain, may not be classic
crescendo type

Physical Exam distended abdomen with diffuse midabdominal tenderness to palpation

o Also hyperactive bowel sounds
Hypoactive or absent with bowel strangulation
o Typically, no signs of peritonitis
o If constant localized tenderness is apparent, indicating localized peritonitis, then ischemia and
gangrene must be suspected
o An essential aspect of the physical exam is to check for abdominal wall hernias, especially in
postsurgical patients
o No fever in uncomplicated cases
o Tachycardia may be present from hypovolemia secondary to persistent vomiting or from toxemia
caused by intestinal gangrene
o Check stool for gross or occult blood, which would suggest strangulation
Diagnostics:
o Upright radiographs classically demonstrate distended loops of small bowel with multiple air-fluid
interfaces
The findings specific for SBO are the triad of dilated small-bowel loops (> 3 cm in
diameter), air/fluid levels seen on upright films, and a paucity of air in the colon
Occasionally show the etiology and site of obstruction and whether it is partial or complete
Dilated small bowel in the presence of a dilated colon suggests the diagnosis of paralytic
ileus, not SBO
o A small bowel contrast study may be necessary to demonstrate transit of contrast into the colon,
thereby ruling out SBO. This study can differentiated mechanical obstruction vs. ileus
o Free air indicates perforation of the intra-abdominal GI tract, whereas biliary gas and an opacity
near the ileocecal valve indicate gallstone ileus
o Abdominal CT can demonstrate the transition point where the dilated bowel proximal to the
point of obstruction transitions to the decompressed bowel more distally. This is seen with
mechanical obstruction, but not ileus
Also, in cases where the bowel has twisted on its mesentery, a swirl sign can be seen as
the mesenteric vasculature twists on itself, creating a distinctive swirling radiographic
pattern
o Labs often reveal a hypokalemia alkalosis owing to dehydration from repeated emesis
WBC count and amylase may be mildly elevated
Lactic acidosis is cause for concern and may indicate intestinal necrosis
Treatment:
o Most patients can be safely managed medically in the absence of peritonitis or other worrisome
clinical findings
NG decompression to relieve proximal GI distention and associated nausea and vomiting
Fluid resuscitation and supportive hydration
o The decision to operate is based on the nature of the obstruction and the patients clinical condition
On initial presentation, if ischemia or perforation is suspected, immediate operation is
needed
Surgery depends on the etiology lyse adhesions, reduce and repair hernias, resect
tumors
Regardless of etiology, always resect nonviable bowel
Criteria for viability normal color, peristalsis, and marginal arterial pulsations

Large Bowel Obstruction

- Patients with LBO have constipation and abdominal distention, and pain is often gradual in onset
- Most common causes carcinoma of the colon, acute diverticulitis, and volvulus
- Physical exam reveals abdominal tenderness and distention
- Radiographic tests plain film of abdomen, retrograde contrast studies that help localize the site of
obstruction
- Any older patient who lacks a history of prior abdominal surgery or recent colonoscopy who presents with a
LBO must be considered to have obstructing colon cancer until proven otherwise
Volvulus
- Occurs when a portion of the colon rotates on the axis of its mesentery, compromising blood flow and
creating a closed-loop obstruction.
- The sigmoid colon (75%) and cecum (25%) are the most commonly involved
- The relative redundancy of the sigmoid loops causes torsion around the mesenteric axis, whereas poor
fixation of the cecum in the right iliac fossa leads to either axial torsion (cecal volvulus) or anteromedial
folding (cecal bascule)
- Risk factors age (most patients older than 65), chronic constipation, previous abdominal surgery,
neuropsychiatric disorders
- Acute onset of crampy abdominal pain and distention
- On physical exam, the abdomen is tender and distended, and peritoneal signs of rebound tenderness and
involuntary guarding may be present
o Tympanitic to percussion with positive bowel sounds
- Frank peritonitis and shock may follow
- Abdominal radiographs may reveal a massively distended colon with a corkscrew or birds beak at the
point of torsion. The distended colonic loop has the appearance of a bent tire or large coffee bean
- If contrast flows freely to the cecum, a volvulus is not present
- Treatment:
o Sigmoid volvulus may be reduced by enemas or endoscopy. Can also use flexible sigmoidoscope
Try this first if no signs of peritonitis and hemodynamically stable
o Rectal tubes are sometimes used to prevent acute recurrence and aid decompression
o High rate of recurrence operative repair recommended
o In the acute setting fixation of the untwisted loop to the respective fossa may suffice for cases of
viable bowel.
Otherwise, resection is performed with either primary anastomosis or end colostomy
(Hartmann procedure) in cases of sepsis or gangrene
o Treatment of cecal volvulus is usually operative at outset
Anal Disease (Fissures, Abscess, Fistula)
- ANAL FISSURES
o Small tears in the anoderm typically in the posterior midline, although sometimes seen anteriorly
o Any fissure off the midline should raise suspicion for Crohns disease
o Most commonly caused by the passage of a large or hard stool, however diarrhea can sometimes
cause it
o Often heal on their own but sometimes require medical or surgical management
Failure to heal has been ascribed to persistent trauma from hard stools, poor blood
supply, spasm of the internal sphincter, or a combination
o Chronic fissures (>3 weeks) often have a sentinel skin tag at the distal aspect caused by
inflammation
o Pain initiated with each bowel movement that can last several hours
o The expectant pain with defecation can compound the problem by causing increasing constipation
and harder stools

Blood is usually on the toilet paper, but bleeding should not be profuse
Differential patients with anal pain usually have a fissure, an abscess, or a thrombosed external
hemorrhoid
o Commonly, the onset of symptoms can be pinpointed to a day, and often to the passage of a hard
stool
o Pain often subsides between bowel movements
o Examination generally shows a small, radial tear in the anoderm, with or without a sentinel skin tag,
and internal sphincter muscle fibers can sometimes be identified at the base of the tear
o The best form of initial treatment is correcting the constipation with a high-fiber diet, increased
liquid intake, and the addition of a bulking agent and a stool softener
o Sitz baths and lidocaine jelly
o Chronic fissures (>3 weeks) and recurrent fissures do not respond well
o Can also try topical nitroglycerin (side effect is severe headache) or topical diltiazem
o Fissures that fail conservative management are best treated with surgery lateral internal
sphincterotomy. This is extremely effective
The biggest risk of sphincterotomy is incontinence to gas or liquid. Usually is temporary
and resolves within a few weeks. Occurs in up to 30%
Also bleeding and infection, but these are rare
ANAL ABSCESS / FISTULA-IN-ANO
o Most anorectal abscesses are believed to be cryptoglandular in origin
o An abscess starts from an infected anal gland, which begins at the dentate line and terminates
within the intersphincteric space. The infection can remain within this space or extend by fistulizing
into the ischiorectal, supralevator, or perianal space. Most commonly, it extends into the
ischiorectal space, and the patient has a swollen, red, tender area on the buttock
o Drainage of the abscess then creates a fistulous connection between the anal canal and the skin
o This fistula will spontaneously obliterate in 50-70% of patients. When it does not, it must be
opened surgically to prevent recurrent infections
Fistula tracks follow Goodsalls rule, if they are not caused by Crohns disease. This rule
states that the external opening of the fistula situated behind the transverse anal line will
open into the anal canal in the midline posteriorly
o Patients with Crohns have a much higher incidence of anorectal abscesses. They can sometimes
be the initial presenting symptom of the disease. Evaluate patients with multiple or recurrent
abscesses for Crohns
o Most anorectal abscesses are first seen with a painful, red, swollen area on the perianal skin
o Symptoms usually develop over 1 or many days
o Occasionally, the abscess will drain spontaneously, and the patient will have a fistula
o The fistula will produce persistent tenderness with a mucus discharge
o A small opening near the anus is usually seen
o Recurrent abscesses are almost always due to the presence of a fistula
o An intersphincteric abscess will often cause rectal pain, but no abnormalities will be seen
o A digital exam will be extremely painful, but a mass will not always be palpable, because they can
be small
o Pain for weeks to months or the presence of bleeding would make one think more of a thrombosed
hemorrhoid or anal fissure
o The extension of swelling and erythema onto the scrotum or crepitus is a sign of perineal
necrotizing fasciitis (Fourniers gangrene), which requires immediate surgical debridement and
which is life threatening
o Usually dont need labs or CT scan. If needed, CT is helpful for a supralevator abscess
o
o

o
o

An abscess will often erupt through the perianal skin if a patient seeks no treatment
On presentation to a physician, an undrained abscess should be opened

o
o

Antibiotics alone have no role, but may help for abscesses that have adequately drained on their
own
Perianal cellulitis may develop in neutropenic patients, but they are unable to form pus.
Because no abscess is present to drain, antibiotics will usually resolve this condition
Can often be drained under local anesthesia, but more complex lesions may need general
anesthesia (i.e., Crohns)
A cruciate incision is made over the most fluctuant area. A packing is placed initially to provide
hemostasis and should be removed within 12-24 hours, and then warm soaks for 20 minutes three
times per day are begun to aid healing
Repacking is painful and unnecessary
Patient should be seen within 10 days to ensure a fistula is not present
Usually dont need antibiotics unless diabetic or cellulitis/induration
A fistula-in-ano requires probing under spinal or general anesthesia. Can be done in one stage if
superficial, or two stages if it encircles the sphincter muscle
A probe is used to identify the tract, and if no external anal sphincter muscle is
incorporated, the tissue is divided down to the probe, and the tract curetted. If muscle is
involved, a cutting seton is placed to allow fibrosis of the tract, so that division at a
second stage will decrease the chance of incontinence

Hemorrhoids
- Varices of the hemorrhoidal plexus
- Pregnancy predisposes
- External hemorrhoids are visible perianally. Usually are painful. Found below the dentate line and are
covered with anoderm
- Internal hemorrhoids are found above the dentate line where little to no sensation is present, and are
covered with mucosa. Most often present in the left lateral, right posterior, and right anterior portions of the
anal canal. The blood inside the hemorrhoids is arterial
o Stage I internal hemorrhoids are confined to the anal canal and may bleed with defecation.
Bleeding without prolapse
o Stage II internal hemorrhoids protrude from the anal opening but reduce spontaneously. Bleeding
and mucoid discharge may occur. Prolapse outside the anal canal with spontaneous reduction
o Stage III internal hemorrhoids require manual reduction after bowel movement. Patients may
develop pain and discomfort.
o Stage IV internal hemorrhoids are chronically protruding and risk strangulation. Prolapse that will
not reduce (incarcerated) outside the anal canal
- Internal hemorrhoids usually enlarge from constipation and straining. They are NOT painful unless a
thrombosed external hemorrhoid component is present. Bleeding is common
- External hemorrhoids are very painful the worst in the first 48-72 hours. Bleeding is uncommon unless the
clot has eroded through the skin from pressure necrosis
- Other causes of rectal bleeding diverticulosis, AVM, IBD, ischemia, anal fissures
- Always consider carcinoma until proven otherwise! Suspect if recent weight loss, change is stools, or family
history of colon cancer
- External hemorrhoids can be seen on physical exam no need for digital exam
- Internal hemorrhoids, if not prolapsed, are best diagnosed by anoscopy

Treatment:
o External hemorrhoids will almost always resolve on their own if one can ignore the pain
o Internal hemorrhoids usually only resolve completely after pregnancy. Otherwise they wax and
wane and get worse
o Thrombosed external hemorrhoids should be treated with warm soaks, stool softeners, and pain
medicine. In general, if patients are seen within 4 days of onset, excision is indicated
If patients are seen later than 4 days, Sitz baths and reassurance are treatment of choice
o Internal hemorrhoids can often improve by avoiding constipation and straining a high-fiber diet,
increased liquid intake, bulking agents, and stool softeners are very effective
o Painful thrombosed external hemorrhoids that are not improving or worsening should be excised
Excise the clot, vein, and part of the overlying skin in an elliptical fashion under local
anesthesia (can be done in the office). Removing just the clot is incomplete and can lead
to persistent bleeding or rethrombosis
o Stage I and II disease can be managed with a high-fiber diet and increased fluids. Bulk laxatives
are helpful
o Higher-stage hemorrhoidal disease may benefit from suppositories with anesthetic and astringent
properties
o Surgical treatment is indicated for those unresponsive to conservative treatment and all stage IV
hemorrhoids. Choices include injection, rubber band ligation, or sclerotherapy
Stage I banding (done with an anoscope, place the band on the mucosa above the
dentate line where no sensation exists, the banded tissue sloughs in 4-8 days, can place
up to 2 bands at one time) or surgical excision if banding fails
Surgical excision is best for large or prolapsed hemorrhoids or those that fail banding.
Patient is in the prone, jackknife position and the buttocks are separated. Give epi before
to aid in hemostasis. Remove the entire column down to the internal sphincter. Typically
all 3 columns are removed to prevent recurrence. Avoid excessive tissue excision
because it can lead to anal stenosis
Complications are uncommon bleeding, infection, recurrence
With banding, the biggest risk (although rare) is sepsis. Also bleeding, severe
pain, thrombosis, and urinary retention
Surgical excision carries the same risks as well as incontinence and anal
stenosis
Hernias (Inguinal, Femoral, Incisional)
- INGUINAL HERNIA
o The innermost layer of the abdominal wall is the transversalis fascia, then the transversus
abdominis, the internal oblique, then the external oblique
o The inguinal canal boundaries:
Anterior external oblique aponeurosis
Posterior transversalis fascia and transversus abdominis aponeurosis
Inferior the inguinal and lacunar ligaments
Superior the internal oblique and transversus abdominis muscle and aponeurosis
o The spermatic cord in males and the round ligament in females enter the inguinal canal through the
transversus abdominis fascia at the internal inguinal ring. The cord then travels the length of the
canal and exits through the external oblique aponeurosis at the external inguinal ring
o Indirect come through the internal inguinal ring and enter the inguinal canal. With time, they
may extend along the canal and exit though the external ring into the scrotum
Usually caused by a lack of obliteration of the processus vaginalis during development
and are congenital
The most common

Direct come through the posterior wall of the inguinal canal and are a defect in the transversalis
fascia. This area is medial to the epigastric vessels and is called Hesselbach triangle defined as
the edge of the rectus sheath medially, the inguinal ligament inferiorly, and the inferior epigastric
vessels laterally. They infrequently extend along the canal and enter the scrotum.
The main etiologic factor in the direct hernias is any maneuver that increases
intraabdominal pressure, such as frequent heavy lifting. Cigarette smoking, advanced
age, and chronic illness are also risk factors
History and physical are very important
Most patients are asymptomatic or complain of a bulge in the groin that is more prominent
with coughing, standing for long periods, or increasing intraabdominal pressure by lifting.
The bulge can usually be reduced manually or simply by lying down
Exam with the patient standing. Palpate groin with and without coughing. Lateral aspect
of the scrotal skin is evaginated with the index finger until the external inguinal ring is
palpated
Incarcerated hernias cannot be reduced
Strangulated hernias are tender as a result of peritoneal inflammation. Abdominal
distention is often encountered as a result of bowel obstructions
Treatment is surgical due to the risk of incarceration and strangulation
Anterior (Inguinal Canal) Approach:
Incision at the midpoint between the pubic tubercle and ASIS. Dissect down to
the external oblique aponeurosis. Incise external oblique aponeurosis so it
connects with the external inguinal ring. Take care to mobilize the nerves.
Expose the transversalis fascia of the posterior inguinal wall. Free the spermatic
cord from all attachments. (if indirect, also need to divide the cremaster muscle
and expose the underlying cord structures).
Then, identify and open the hernia sac. Do not need to excise it!!
Then, repair:
o Bassini Repair suture the conjoined tendon of the transversus
abdominis/internal oblique to the inguinal ligament, iliopubic tract, or
preferably both
o Coopers Ligament (McVay) Repair indicated for direct, large
indirect, and recurrent inguinal hernias. Suture the conjoined tendon of
Coopers ligament from the pubic tubercle to the femoral canal.
Continue anteriorly by suturing the conjoined tendon to the inguinal
ligament until the internal inguinal ring is adequately reconstructed
o Prosthetic Repair mandatory only when a suture repair would be
under undue tension. Use either polypropylene or
polytetrafluoroethylene (PTFE) mesh. Suture the prosthesis to
Coopers ligament, the iliopubic tract, and/or the inguinal ligament
inferiorly and the conjoined tendon or internal oblique aponeurosis
superiorly. The lateral edge of the material is slit to let the spermatic
cord pass, and then they are sutured together, incorporating the inguinal
ligament and the transversus abdominis muscle

Posterior (Preperitoneal) Approach:

Ideal for recurrent hernias, incarcerated or strangulated hernias, and complicated
hernias
Laparoscopic Repair:
TAPP (transabdominal preperitoneal) or TEPA (total extraperitoneal approach)
Prosthetic material is usually used for the repair and is sutured to Coopers
ligament inferiorly, the posterior rectus fascia superiorly and medially, and
laterally to the transversus abdominis aponeurotic arch
o Complications wound infection, hematomas occur in 1-2%
o Direct hernias recur at a rate of 5-10%, indirect at a rate of 1-5%
FEMORAL HERNIA
o More common in women
o The boundaries of the femoral canal:
Anterior the iliopubic tract and inguinal ligament
Posterior Coopers ligament
Medial the lacunar ligament
Lateral the femoral vein
o The sac is below the inguinal ligament in the groin or upper thigh area
o The bulge from a femoral hernia protrudes beneath the inguinal ligament medial to the femoral
vessels and is palpable in the thigh just below the groin crease
o Femoral hernias usually have a narrow neck, so they can be difficult to reduce
o They feel like a small mass and have no impulse on coughing
o Confused with inguinal LAD or a lipoma. Can also be misdiagnosed as inguinal hernias
o Similar exam as inguinal hernias. Initially, groin pain may be the only finding
o The only acceptable treatment is operative
Same approaches as inguinal hernia
In the anterior approach, the Coopers ligament repair is used
The open, preperitoneal approach is preferred by many surgeons because it is easy to
reduce incarcerated hernias
INCISIONAL HERNIA
o Occur through a previous surgical excision
o Usually due to a wound infection, inadequate healing of the surgical wound, malnutrition, ascites,
pregnancy, chemotherapy, steroids, or other conditions causing strain on the wound
o The fascial edges separate, and a hernia protrudes through the defect
o The diagnosis is usually obvious
o When the patient performs a Valsalva maneuver, a bulge is seen that usually reduces
spontaneously when the patient exhales
o The edges of the fascial defect are usually palpable
VENTRAL HERNIA
o Occur in the midline along the linea alba, usually between the xiphoid and umbilicus. There is a
weakness and herniation through the linea alba
o The vast majority occur at the site of a previous abdominal incision
OTHERS parastomal (at an ostomy opening), Spigelian (at the lateral edge of the rectus muscle and the
semilunar line, usually below the semicircular line of Douglas), obturator (through the obturator canal in the
pelvis), lumbar (dorsal), sciatic (in the greater sciatic foramen), perineal (through the pelvic diaphragm)

Portal Hypertension
- Caused by processes that impede hepatic blood flow, either at the presinusoidal, sinusoidal, or
postsinusoidal levels
o Presinusoidal causes schistosomiasis and portal vein thrombosis
o Sinusoidal cirrhosis (from alcohol and hepatitis B and C)
o Postsinusoidal Budd-Chiari syndrome (hepatic vein occlusion), pericarditis, right-sided heart
failure
- Bleeding varices are a life-threatening complication
o When portal pressures increase, flow through the hemorrhoidal, umbilical, or coronary veins
becomes the low-resistance route for blood flow. The coronary vein empties into the plexus of
veins draining the stomach and esophagus. Engorgement of these veins places the patient at risk
of bleeding into the esophagus or stomach
- Physical exam ascites, jaundice, cherubic face, spider angioma, testicular atrophy, gynecomastia, and
palmar erythema
- Labs increased liver enzymes, abnormal clotting times and serum albumin
- Treatment:
o Beta-blockers decreases risk of bleeding
o Endoscopic surveillance and banding to prevent bleeding episodes
o For patients with upper GI bleeds, large-bore IV lines and volume resuscitation immediately
NG tube to confirm diagnosis
If the patient cannot be lavaged clear, suggesting active bleeding, emergency endoscopy
If this fails, balloon tamponade and vasopressin infusion
Transjugular intrahepatic portosystemic shunting (TIPS) has a high rate of success in
controlling acute bleeding
o Patients with bleeding varices and cirrhosis will be considered for liver transplant
o If no cirrhosis, or if there is good residual liver function, surgical shunts have better long-term
patency than TIPS
- Altered mental status in patients with cirrhosis and portal hypertension (encephalopathy) is a warning sign of
poor hepatic reserve and would generally contraindicate shunting until resolved
o Hepatic encephalopathy should be treated with parenteral nutrition. Malnutrition can be quite
severe and these patients are prone to vitamin and mineral deficiencies
Bariatric Surgery
- Weight loss surgery. Limits the amount of food the stomach can hold by reducing the stomachs capacity to
a few ounces.
- In addition to reducing food intake, some weight loss surgeries also alter the digestive process, which curbs
the amount of calories and nutrients absorbed
- Bariatric surgery is the most effective method to achieve long-term weight loss
- Indications patient between the age of 21-55 years with either a BMI of 40 or a BMI greater than 35 with
life-threatening comorbidities, and for whom supervised weight-reducing programs have failed
- Surgical procedures can be classified as either being restrictive, malabsorptive, or a combination
o Restrictive adjustable gastric banding (AGB), sleeve gastrectomy, and vertical banded
gastroplasty
o Malabsorptive jejunal-ileal bypass or biliopancreatic diversion
Falling out of favor due to issues with malnutrition and organ failure
- The two most common are the AGB and Roux-en-Y gastric bypass (RYGB)
o RYGB is the most popular in the United States and is both restrictive and malabsorptive
o Can both be performed either openly or laparoscopically

RYGB creation of a proximal gastric pouch of approximately 30 mL capacity. Intestinal continuity is

restored by attaching a limb of proximal jejunum to this gastric pouch with biliopancreatic continuity
established via a jejunojejunostomy
o Postoperatively, patients may experience dumping syndrome after RYGB, especially with
consumption of highly concentrated sweet
Dumping Syndrome abdominal cramps, nausea, vomiting, flushing
Can cause a negative association with sweets
Other risks of the procedure leaks from intestinal anastomoses, ulcers, strictures,
internal hernias
o All patients that are obese are at a higher risk for DVT, diabetes, HTN, OSA, heart disease
o Associated with 75-80% excess weight loss
Excess weight = preoperative weigh ideal body weight
o Also associated with resolution of diabetes, HTN, OSA
AGB placing a silicone band around the upper portion of the stomach. A catheter connects the band to
an injection chamber, which is implanted subcutaneously. In the postoperative period, this chamber is used
to inflate the band gradually to progressively narrow the gastric inlet and limit caloric intake by controlling
portion sizes
o Because no intestines are bypasses, dumping syndrome does not occur
o Complications slippage of the stomach around the band, erosion of the band into the lumen of
the stomach, infection, leakage, migration of the band and injection chamber
o 30-40% excess weight loss within a year. Long-term weight loss is about 50-55% at 5-10 years
post-op
o Also diabetes improvements
o Good weight loss results are particularly dependent on healthy diet habits (no dumping syndrome)
Patients who continue to overeat and disregard restrictions on portion size run the risk of dilating the gastric
pouch in either RYGB or AGB
Important nutritional complications anemia (iron and B12 based), calcium deficiency, electrolyte
deficiencies, dehydration, protein malnutrition

Surgery Pulmonary
Shortness of Breath
Hemoptysis
Weight Loss, Fatigue
Pulmonary Embolus
- Arises from thrombi in the systemic venous circulation or the right side of the heart
- More than 90% of PEs originate as clots in the deep veins of the lower extremities. Others include air
emboli from central lines, amniotic fluid from active labor, and far from long bone (femur) fracture
- Risk factors revolve around Virchows triad hypercoagulable state, venous stasis, vascular intimal
inflammation or injury
o Specific risks surgical procedures (orthopedic, pelvic, abdominal), cancer, oral contraceptives,
and pregnancy
- 50-60% of patients with DVT will experience a PE. Half of these will be asymptomatic
- Symptoms pleuritic chest pain, dyspnea, apprehension, cough, hemoptysis, and diaphoresis
- Signs tachycardia, tachypnea, crackles, accentuation of the pulmonary component of the second heart
sound, low-grade fever.
o Homans sign lacks sensitivity and specificity
- ABG measurements show acute respiratory alkalosis secondary to hyperventilation
- EKG shows tachycardia and nonspecific ST-T wave changes.
- CXR may show nonspecific abnormalities such as basilar atelectasis. The main purpose of obtaining CXR
is to rule out other abnormalities and aid in interpreting V-Q scan
- V-Q scan shows perfusion defects with normal ventilation. A normal scan rules out clinically significant
thromboembolism
- Pulmonary angiography remains the definitive test for diagnosis but is reserved for cases in which the
diagnosis is uncertain after noninvasive testing
- Measuring plasma D-dimer may be useful, especially to rule out PE if clinical suspicion is low and D-dimer is
negative
- Spiral CT has now replaced V-Q scans as the initial method of identifying PE
- Anticoagulation should be initiated. Heparin is the anticoagulant of choice. Warfarin is continued after the
acute phase. INR should be in the range of 2.5-3.0
o Duration of therapy depends on the clinical situation. Minimum of 3 months
- Vena cava interruption (filter) is helpful in patients at high risk of recurrence who are unable to tolerate
anticoagulants
- Prevention is key. For high-risk patients, consider early ambulation, intermittent compression stockings,
low-dose heparin and LMWH

Lung Carcinoma
- Epidemiology:
o Most common cause of cancer death in US
o Incidence nearing equality between men and women (increasing)
o Primarily caused by cigarette smoking. If a person quits smoking, risk declines, and by 10 years
the lung cancer risk is only slightly above that of someone who had never smoked.
- Etiology:
o Cigarette smoking
Benzo-pyrene identified as major carcinogen
Relative risk 10-30x non-smokers
Clear dose-response relationship i.e. 40 pk yr hx 60-70x relative risk
Occupational exposures asbestos, benzene, nickle, radiation
Environmental exposures asbestos, radon
Genetics:
Oncogenes and suppressor genes
o Ex. P16 cell cycle regulator (can be detected in sputum, if gene is
present they have a 50/50 chance of developing cancer in the future)
EGFR increases risk of lung cancer (Asian women, common mutation)
Multi-hit theory of pathogenesis: mutations can accumulate, making more susceptible
- Paraneoplastic syndromes common to all pathologic types anemia, DIC, eosinophilia, thrombocytosis,
acanthosis nigricans
- Pathology:
o Small cell carcinoma (25-35%) 100% are associated with smoking
Oat cell
More likely to spread early and rarely is amenable to surgery (mean survival 6-18 weeks)
Associated with paraneoplastic syndromes, often these are the presenting signs of cancer
SIADH
Cushing syndrome
Myopathy / Neuropathy (Eaton-Lambert)
CNS dysfunction
Generally hilar / mediastinal origin. Tends to originate in the central bronchi
Very early metastasis to regional lymph nodes and distant sites
Defined as either limited disease or extensive disease
Most chemo sensitive cell type surgery is not beneficial, generally only to relieve
symptoms
o Non-small cell carcinoma
Grows more slowly and is more amenable to surgery
Includes SCC, adenocarcinoma, large cell
Arise as discrete masses within the lung parenchyma that can spread to regional lymph
nodes and then metastasize to distant sites.
These tumors are not very responsive to chemotherapy

Squamous (25-35%)
Most common cell type in males
95% patients are smokers
Usually hilar / endobronchial in origin
Centrally located mass
Cavitation common
More likely to present with hemoptysis, thus more likely to be diagnosed via
sputum cytology
May be associated with hypercalcemia (paraneoplastic syndrome)
Resectable if caught early
Radiosensitive, chemo resistant
Histology Keratin Pearl
Adenocarcinoma (35-40%)
Most common cell type in females
Weakest associated with tobacco
o Bronchoalveolar sub-type may not be associated with smoking at all.
Generally peripheral in origin
o Bronchoalveolar subtype may resemble pneumonia
Resectable if caught early
Typically metastatic to distant organs
Arises from mucus glands, usually appears in the periphery of the lung, and is
not amenable to early detection through sputum examination
May be associated with thrombophlebitis (paraneoplastic syndrome
Histology Glandular Formation
o Series of cells try to form a lumen of a gland
o Large nuclei, heterogenous
o Large amount of cytoplasm
Large cell (10%)
A heterogenous group of undifferentiated types that do not fit elsewhere
Rapidly growing
Usually peripheral in origin
Resectable if caught early
Resistant and recurrent
Metastasis is early
May occur with gynecomastia (paraneoplastic syndrome)
May be central or peripheral masses
Poorer prognosis than others.
Histology:
o Hard cytoplasm, darker
o Large cells

Metastatic:
o Breast, GI, melanoma, sarcoma most commonly
o Generally unresectable
Sarcoma, renal cell possible exceptions (metastasectomy)
o Peripheral nodule most common presentation
Breast, colon, renal cell occasionally endobronchial
o Very poor prognosis.
o Cancers like to go to the lung because of the large capillary bed (lots of circulation).
Other rare types of lung neoplasms:
o Carcinoid
o Primary pulmonary lymphomas
o Bronchoalveolar cancers
o Mesotheliomas
Symptomsprimary tumor:
o Central / Endobronchial Symptoms:
Cough
SOB
Hemoptysis
Wheezing / stridor
Post-obstructive pneumonia
o Peripheral Symptoms:
Chest wall pain or sensation of chest tightness
Cough
Symptomsregional spread:
o Nodal spread:
Tracheal / esophageal obstruction (mediastinal mass)
Hoarseness (compressed recurrent laryngeal nerve)
Paralyzed hemidiaphragm (compressed phrenic nerve)
SVC syndrome (obstruct superior vena cava face swelling, plethora, headache, mental
status changes)
o Local spread:
Chest wall pain
Pleural effusion (very common presentation, exudative)
Pancoasts Tumor (tumor of the lung apex, causes Horners syndrome and shoulder pain,
affects brachial plexus and cervical sympathetic nerve)
Horners syndrome (ptosis, miosis, unilateral facial anhidrosis = invades the spine)
Brachial plexopathy (C8, T1, T2)
Endocrine (carcinoid syndrome flushing, diarrhea, telangiectasias)
Symptomsextrathoracic:
o Brain mets:
Seizure
Headache
Aphasia, paresis
Confusion
o Bony mets:
Pathologic fracture
Spinal cord compression

Bone marrow invasion

Adrenal mets:
Addisons unusual

Clinical ManifestationsParaneoplastic:
o Systemic weight loss, anorexia, fatigue, fever
o Endocrine:
Hypercalcemia PTH hormone, squamous cell
Hyponatremia SIADH, small cell
Cushing Syndrome ACTH like, small cell
o Neurologic:
Eaton-Lambert small cell
Neuropathy all types
o Skeletal / connective tissue
Presentation:
o 10% incidental, routine CXR or CT
o 55% due to local / regional symptoms
o 35% due to distant/paraneoplastic symptoms
Diagnostic Approaches:
o Step 1 CXR screening does not lower mortality rates
o Step 2 CT may be better for screening
o Step 3 Bronchoscopy
With bronchial washings, brushings, and/or biopsy
The location of a lesion determines accessibility.
Sensitivity is pretty good for large masses
o Trans-thoracic Needle Aspiration (TTNA)
Peripheral masses can be sampled with CT guided TTNA
Rarely indicated for hilar mass
Pneumothorax occurs in 1/3 of patients undergoing the procedure
o Step 4 Surgery (rarely indicated)
Mediastinoscopy often preferred. Incision is made in the suprasternal notch and a biopsy
is taken via a mediastinoscope
Treatment:
o Non-small cell surgery is treatment of choice
Stage I & II:
Resection
Chemotherapy for Stage IB and Stage II
5 year survival about 50%
Stage IIIA
Resection if possible
Neoadjuvant chemo often used
30% IIIA patients technically resectable
5 year survival about 30% for those resected
Stage IIIB:
High does radiotherapy for those with disease confined to chest
Chemo often given in conjunction
Median survival ~12 months
5% five year survival in those with disease confined to chest
Stage IV:
Radiation to symptomatic sites chemo
Median survival <6 months vs. 8-12 with chemo

Small Cell combined chemo is treatment of choice

Limited disease:
Combination chemo / XRT
Prophylactic brain irradiation
5 year survival 15-25%
50% patients with complete remission
Extensive stage:
Combination chemo
Radiation for brain if mets present
30% complete remission
5 year survival <5%

Pleural Effusion
- Most common cause is CHF
o Bilateral or right-sided
o Due to increase in interstitial edema
o Most often associated with LV dysfunction
o Typically transudative, small to moderate in size, and free flowing (left lateral decubitus view may
be helpful)
- The most common cause of malignant pleural effusions is carcinoma of the lung in men and carcinoma of
the breast in women
o Others lymphomas, ovarian carcinoma, kidney cancer, colon cancer, prostate cancer
- Thoracentesis will result in immediate resolution of the dyspnea but reaccumulation of fluid commonly
occurs
- Thoracostomy and chemical pleurodesis provide the most definitive therapy for malignant pleural effusions
o A chest tube is inserted through the sixth or seventh intercostal space in the midaxillary line and
the effusion is completely drained
- Chemical pleurodesis will be effective only if the drainage is less than 150 mL/day
o Iodized talc is the most effective sclerosing agent and is successful in more than 80% of patients
o Talc may be given as a slurry through the chest tube or insufflated under direct-visualization by
thoracoscopy
o Most common side effects pain and fever
Talc microemboli, pneumonitis, and adult respiratory distress syndrome can occur
o Talc results in a dense fibrothorax, and therapy is not recommended for benign disease or in young
patients that may need thoracic procedures in the future
- When chemical pleurodesis is unsuccessful, pleurectomy and the insertion of a pleuroperitoneal shunt also
may be considered
o However, occlusion of the shunt occurs frequently, and pleurectomy is associated with increased
morbidity and mortality in these debilitated patients

Pneumothorax
- The accumulation of air in the pleural space
- The cause may be spontaneous (primary pneumothorax), traumatic, or iatrogenic
o Ruptured bleb, trauma, injured bronchus or esophagus
- Pleural rupture results in entry but not exit of air in the pleural space
o Inspiration results in a greater negative intrapleural pressure, thus further increasing the amount of
air within the pleural space
o During expiration, this results in a tension pneumothorax, which causes a shift of the mediastinum,,
which decreases venous return and results in results in a decreased cardiac output, cardiovascular
collapse, hypoxemia, and cyanosis
- Tall, thin males between 10-30 years old are at greatest risk
- Tension pneumothorax is secondary to a sucking chest wound or a pulmonary laceration that allows air to
enter the chest with inspiration but does not allow it to leave on expiration
- Characterized by acute onset of ipsilateral chest pain and dyspnea
- Physical findings depend on the size of the pneumothorax and may include unilateral chest expansion,
decreased tactile fremitus, hyperresonance, and diminished breath sounds on the involved side
o May be cyanotic
o May have a crunching sound (Hammans sign) with mediastinal emphysema
- Tension pneumothorax is associated with a mediastinal shift to the contralateral side and impaired
ventilation, leading to cardiovascular compromise
o Neck-vein distention, and the trachea and cardiac apex are deviated toward the uninvolved side
- Most pneumothoraces can be seen on a PA CXR taken on inspiration. Air is seen as a hyperlucent spaced
devoid of pulmonary markings in the periphery of the hemithorax.
o If no pneumothorax is seen on inspiratory and patient is still suspicious, get expiratory (expiration
reduces lung volume and increases the radiographic density of the lung, thereby increasing the
contrast between the lung and the air in the pleural space)
- Expiratory CXR reveals the presence of pleural air. A visceral pleural line may be the only evidence of a
small pneumothorax
- ABG analysis, if done, reveals hypoxemia
- Small pneumothorax resolve spontaneously
- For severely symptomatic or large pneumothorax, chest tube placement is performed
- Tension pneumothorax is a medical emergency. If it is suspected, a large-bore needle should be inserted to
allow air to move out of the chest. Placement of chest tube follows the decompression
- Patients should be followed with serial CXR every 24 hours until resolved
- SPONTANEOUS PNEUMOTHORAX:
o Primary:
Result of a ruptured bleb, most commonly at the apices of the upper lobes
Patients tend to be young adults (85% are < 40 years)
Higher incidence among smokers
20-50% recurrence rate
o Secondary:
Most common etiology is COPD
Patients tend to be older (45-65 years) and have a higher morbidity and mortality
Other causes malignant neoplasms, tuberculosis

Treatment:
Small ones can be observed. Monitor and repeat CXR in 48 hours
Approximately 1.25% of all intrapleural air is absorbed daily from the pleural
cavity, so it will take weeks for the lungs to fully expand
If the pneumothorax grows or symptoms develop, admit for thoracostomy (chest)
tube
Needle or small-catheter aspiration of risky difficult to reexpand the lung fully, cannot
use with an active leak, unsuccessful in 70% of patients
Most successful therapy thoracostomy tube
4th or 5th intercostal space in the anterior axillary fold or the 2nd or 3rd interspace in
the midclavicular line
It results in complete re-expansion of the lung, resulting in adherence between
the visceral and parietal pleurae
Also results in an inflammatory reaction, which obliterates the pleural space
In healthy and compliant patients, after complete re-expansion of the lung, a
Heimlich valve can be attached to the tube, and then the tube can be removed in
3-4 days
o Patients with severe underlying pulmonary disease, incomplete reexpansion of the lung, and a continuous air leak, cannot be treated with
this technique
Surgical indications persistent air leak for more than 72 hours, a second recurrence,
hemothorax, empyema, a previous contralateral pneumothorax, and bilateral
simultaneous pneumothoraces
Patients with high-risk occupations, such as airline pilots and scuba divers, and
those that live in remote areas, should have surgery after the first episode
Surgical technique stapling the bleb tissue and performing a manual pleural abrasion
to ensure adherence of the lung to the chest wall
Pneumonia (Post-Operative)
- The most common infectious complication in surgical patients
- Decrease in tidal volume due to anesthesia, analgesia, or pain induced by thoracotomy or laparotomy
predisposes a patient to pulmonary atelectasis, disruption of pulmonary defense mechanisms, and growth of
bacteria, leading to pneumonia
- Fever (>102F) in the immediate post-op period is usually due to atelectasis
- Decreased breath sounds (usually in the base of the lung fields) in a patient who is taking shallow breaths is
consistent with atelectasis
- CXR to confirm
- Egophony
- Examine sputum thick green or brown should prompt investigation for pneumonia
- Empiric antibiotics until sputum culture is ready
o S. pneumo and H. flu are common in post-op
o Sometimes Pseudomonas (especially if long hospital stay)
- Patients on a respirator are at high risk
- The triad of fever, infiltrate on CXR, and purulent sputum are accepted as clinical proof of pneumonia
o

Surgery Neurology (Neurosurgery)

Change in Vision
Change in Speech
Motor and/or Sensory Loss
Cerebral Vascular Accident
- Stroke is the 3rd most common cause of death in the United States and the most disabling neurologic
disorder
- Incidence increases with age. Higher in men, higher in blacks
- Major risk factors hypertension, hypercholesterolemia, diabetes, oral contraceptives, cigarette smoking,
heavy alcohol use, AIDS, and elevated blood homocysteine levels
- A previous stroke increases the susceptibility to additional strokes
- Ischemic strokes account for 80% of all strokes. of ischemic strokes are thrombotic and embolic.
Emboli commonly arise from the heart, aortic arch, or large cerebral arteries
- Hemorrhagic strokes, which usually are secondary to hypertension, account for 20% of strokes
- Clinical Features:
o Signs and symptoms begin abruptly and, by definition, last longer than 24 hours. They correlate
with the area of the brain that is supplied by the affected vessel, especially with ischemic events
o In most cases, hemiparesis or hemisensory deficit is revealed on history and physical examination.
One can localize the lesion to one side, contralateral to these deficits
o Strokes involving the anterior circulation (anterior choroidal, anterior cerebral, middle cerebral
arteries), which supplies the cortex, subcortical white matter, basal ganglia, and the internal
capsule, commonly are associated with hemisphere signs and symptoms (aphasia, apraxia,
hemiparesis, hemisensory losses, visual field defects)
o Strokes involving the posterior circulation (vertebral and basilar arteries), which supples the brain
stem, cerebellum, thalamus, and portions of the temporal and occipital lobes, commonly are
associated with evidence of brain stem dysfunction (coma, drop attacks, vertigo, nausea, vomiting,
ataxia)
o Thrombotic strokes evolve in a stepwise fashion and often are preceded by TIAs. Embolic strokes
occur abruptly and without warning. Hemorrhagic strokes are less predictable because of
complications of blood dispersion, cerebral edema, and increased intracranial pressure
- Laboratory Studies:
o Routine blood tests include CBC, ESR, platelet count, PT, PTT, cholesterol and lipids, and blood
glucose level
o Additional blood tests VDRL test for syphilis, antinuclear antibodies, and antiphospholipid
antibodies depending on the patients risk factors. Blood cultures should be considered if
endocarditis is suspected
o CT is recommended during the acute phase and is the best modality for differentiating ischemic vs.
hemorrhagic stroke
o Additional imaging tests to evaluate stroke patients MRI, carotid ultrasonography, echo,
angiography
o EKG may reveal arrhythmia or a recent MI as the possible source of embolus
o Lumbar puncture and angiography should be reserved for patients with suspected hemorrhage or
vascular malformations

Treatment:
o Acute treatment is aimed at reversing the ischemia and salvaging tissue in the core and
surrounding penumbra
o Thrombolytic therapy (recombinant tissue plasminogen activator) is given to reduce the extent of
deficit. It is most effective within 3 hours of symptoms but can be attempted up to 12 hours
The major complication is bleeding
Contraindications evidence or suspicion of intracranial bleed, recent intracranial
surgery, serious head trauma or previous stroke, history of intracranial bleed or known
bleeding diathesis, uncontrolled hypertension (> 185/ >110), seizure at stroke onset,
active internal bleeding, intracranial neoplasm, AVM or aneurysm, heparin use within 48
hours, or platelet count < 1000,000/mm3
o Antiplatelet therapy is initiated for ischemic stroke and TIA, whereas anticoagulant therapy is
indicated in the setting of cardiac embolus
o Endarterectomy may be indicated if 70-99% stenosis of the common or internal carotid artery is
present
o Hemorrhagic stroke is treated with conservative and supportive measures, including management
of hypertension and antiedema therapy (mannitol or corticosteroids). Endovascular repair and
surgical clipping or coil embolization are options available for some patients with specific anatomic
foci.
o Supportive therapy, follow-up physical therapy, and social supports are important
Vascular Disorders (Carotid Disease)
- Carotid Artery Disease
- Symptoms are the result of atherosclerosis
o Morbidity due to plaque rupture, ulceration, hemorrhage, thrombosis, low flow states
- A major cause of stroke
o Other risk factors HTN, DM, smoking, hypercholesterolemia
- Carotid artery dissection is treated with anticoagulation for 3-6 months
- Previous neurologic events, including focal motor deficits, weakness, clumsiness, and expressive or
cognitive aphasia are usually reported
o Can be TIAs, reversible ischemic neurologic deficit, or fixed neurologic deficits
- One characteristic presentation for carotid disease is amaurosis fugax, or transient monocular blindness,
usually described as a shade being pulled down in front of a patients eye
o Due to occlusion of a branch of the ophthalmic artery
- Hollenhorst plaques on retinal examination are evidence of previous emboli
- Carotid bruit is evidence of turbulence in carotid flow, but is not necessarily significant. An absence does
not rule out disease
- Carotid duplex scanning and MRA (best for degree of stenosis)
- Treatment depends on history, degree of stenosis, and characteristics of the plaque
- Antiplatelet therapy with aspirin to prevent neurologic events
- If not hemorrhagic (determined by CT), consider heparin
- Indications for endarterectomy >75% stenosis, >70% stenosis and symptoms, bilateral disease and
symptoms, and >50% stenosis with recurrent TIAs despite aspirin therapy
- Give IV first-generation cephalosporin before the procedure
- The most devastating complication is cerebral infarction
- Cranial nerve injury after endarterectomy is uncommon. 2-8%. Vagus, hypoglossal, and glossopharyngeal
nerves
- Major cause of death after the procedure is MI

Subarachnoid Hemorrhage
- Develop when intracranial aneurysms rupture and bleed
o Intracranial aneurysms are saccular, berry-shaped aneurysms found at the arterial branch points
within the circle of Willis
- Sudden onset of severe headache worst headache of my life
- ICP transiently increases with each cardiac contraction, causing a pulsatile headache
- Progressive neurologic deficits may develop as a result of blood clot mass effects, vasospasm with
infarction, or hydrocephalus
o Coma and death may occur
- Use the five-point Hunt-Hess system to gram severity
o Grade 1 mild headache and slight nuchal rigidity
o Grade 2 CN palsy, severe headache, nuchal rigidity
o Grade 3 mild focal deficit, lethargy, or confusion
o Grade 4 stupor, hemiparesis, early decerebrate rigidity
o Grade 5 deep coma, decerebrate rigidity, moribund appearance
- CT
o If negative but SAH still suspected, do a lumbar puncture to look for RBC or xanthochromia
o If SAH is present, four-vessel cerebral angiography is performed to define the aneurysm neck and
relationship with surrounding vessels
- Initial medical treatment control hypertension with IV medications
o Phenytoin for prophylactic treatment of seizures
o Mannitol to control edema
o Nimodipine to reduce risk of developing delayed neurologic deficits from vasospasm
- Hyponatremia is a common problem with SAH, so monitor serum sodium
- Emergency external ventricular drainage may be indicated to decrease ICP
- In rare cases with progressive neurologic deterioration, emergency craniotomy and evacuation of a blood
clot are required to prevent herniation
- Definitive treatment is obliteration by microsurgical clipping or endovascular coiling of the aneurysm
Subdural Hematoma
- In contrast to epidural hematomas, subdural hematomas are usually low-pressure bleeds secondary to
venous hemorrhage. Both spontaneous and traumatic subdural bleeds occur
- Source of hemorrhage is from ruptured bridging veins that drain blood from the brain into the superior
sagittal sinus
- Usually a result of trauma
- Older patients, those with brain atrophy, and patients treated with anticoagulants are at particularly
increased risk
- Less common causes rupture of a cerebral aneurysm, AVM, metastatic tumors
- Headache, drowsiness, unilateral neurologic symptoms are the presenting symptoms
o Seizure and papilledema are uncommon
- Prompt imaging!!! Head CT shows a quarter moon shaped abnormality
o Consider MRI. More sensitive
o If no history of trauma, may use angiography to identify the root cause
- Treatment
o Nonoperative management is limited to patients with small lesions and no evidence of herniation
o Patients with significant neurologic deficits secondary to mass effect may need urgent burr-hole
decompression or craniotomy
o Other indications for surgical management lesion >10mm, >5mm of midline shift, or declining
GCS
o Important to identify and ligate the bleeding vessel

Epidural Hematoma
- Usually seen in patients with head trauma who have sustained a skull fracture across the course of the
middle meningeal artery, causing an arterial laceration and an expanding hematoma
o Usually due to high-energy deceleration injury
o Classically, a lateral blow to the temporal bone
- The increasing pressure of the arterial-based hematoma strips dura mater from the inner table of the skull,
producing a lens-shaped mass capable of causing brain compression and herniation
- Commonly presents as a head injury followed by an initial loss of consciousness, recovery (the honeymoon
period), and then progressive deterioration.
- Use the GCS. 7 is considered severe, 8-12 is moderate, and >12 is mild
o <8 require immediate endotracheal intubation for airway protection and rapid neurosurgical
evaluation
- CT is crucial for diagnosis. Biconvex hyperdensity
- For patients presenting with a depressed skull fracture and a neurologic exam indicating a deteriorating
level of consciousness, airway control and emergency cranial decompression must be performed
o Burr holes made over the area of the hematoma seen on CT, a flap is quickly turned, and the clot is
decompressed, with resultant decrease of the ICP
o Control bleeding of the middle meningeal artery
o Fix the dura to the bone to prevent reaccumulation

Surgery Genitourinary
Edema
Orthostatic Hypotension
Urinary Retention
Dysuria
Testicular Carcinoma
- The most common malignancy in young men
- Risk factors history of cryptorchidism or a previous history of testicular cancer
- More than 90% present with a painless, solid, testicular swelling. Patients may also complain of heaviness
in the testicle. Occasionally, patients with painful testicular masses are erroneously diagnosed as having
epididymitis or orchitis
- Pan-aortic lymph node involvement can present as ureteral obstruction
- Patients may also present with abdominal complaints from an abdominal mass or with pulmonary symptoms
from multiple nodules
- Scrotal ultrasonography may reveal a suspicious intratesticular echogenic focus
- Radiologic studies for staging include radiography of the chest and CT of the chest, abdomen, and pelvis.
- Tumors are classified pathologically as seminomatous (35%) or nonseminomatous (65%). Subtypes of
nonseminomatous include embryonal carcinoma (20%), teratoma (5%), mixed cell type (40%), and
choriocarcinoma (<1%)
- Elevated blood levels of -fetoprotein or -human chorionic gonadotropin are diagnostic for
nonseminomatous germ cell tumors. The majority of patients with seminoma have normal levels
- Treatment depends on pathology and stage. Staging is based on degree of lymph node spread
o Radical inguinal orchiectomy is performed for diagnostic and therapeutic reasons
o Seminomatous tumors are radiosensitive. Nonseminomatous tumors are radioresistant
- Nonseminomatous tumors:
o Stage I disease limited to the testis can be treated with nerve-sparing retroperitoneal lymph node
dissection or rigorous surveillance without surgery or chemotherapy
o Stage II tumors can be treated with surgery or chemotherapy
o Stage III disease should be treated with surgery and chemotherapy
- Seminomatous tumors:
o The mainstay of therapy for stage I disease isolated to the testis is radiation therapy to the paraaortic and ipsilateral iliac nodal areas
o Therapy for stage IIa and IIb adds increased radiation to the affected nodes
o Therapy for stages IIc and III is chemotherapy
Wilms Tumor
- Nephroblastoma
- Usually a pediatric tumor. The most common malignant renal tumor of childhood
o Usually ages 3-4 years
- Most common presenting sign is an asymptomatic abdominal mass
- Hypertension may be present because of the production of renin by tumor cells
- Hematuria is usually microscopic but may become gross after an episode of trauma
- Associated with several congenital anomalies, especially ocular and genitourinary malformations (e.g.,
hypospadias and cryptorchidism)
- CBC to check for presence or absence of polycythemia, which may result from excessive secretion or
erythropoietin by the tumor
- Urinalysis obtained
- Obtain blood chemistries, LFTs, coagulation studies
- Check tumor markers AFP, HCG, urinary excretion of VMA and HVA, because intrarenal neuroblastomas
and teratomas are well described

Abdominal CT scan
o Check bilateral kidneys because in 5% of Wilm tumors, both are affected
- Chest CT to evaluation of lung metastases
- Duplex imaging or magnetic resonance venography of the IVC to evaluate for presence of intracaval tumor
extension via a renal vein
- Treatment:
o Operative therapy begins with exploration of the abdomen (evaluate liver, hilar and perirenal lymph
nodes, and kidneys)
o Palpate renal veins and IVC to exclude intravascular tumor extension
o If the tumor is confined to one kidney radial nephroureterectomy
o Biopsy alone is performed if the tumor is deemed unresectable or a second tumor is found in the
contralateral kidney
o Unresectable tumors are pretreated with chemotherapy to reduce tumor bulk before definitive
rumor resection
Sometimes add radiation if bilateral disease
- Prognosis:
o Overall survival rate of children with unilateral, favorable-histology Wilms tumor is >90% at 4 years
o Risk factors for local recurrence anaplastic (unfavorable) histology, positive para-aortic nodes,
tumor rupture, liver metastases (as opposed to lung metastases), and early relapse (< 15 months
from diagnosis)
Bladder Carcinoma
- 5th most common malignancy in the United States
- Males > females (3:1)
- Cigarette smoking increases risk 4x
- Also industrial exposures aniline dyes from the textile industry, acrolein (by-product of
cyclophosphamide)
o Can take 20-30 years to express themselves
- Also can be infective (usually squamous cell and in Egypu) parasite Schistosoma haemotobium
- Nearly 90% of bladder cancers arise from the transitional epithelium that lines the urinary system
o Of these urothelial carcinomas, 70% are papillary, 10% are sessile, and 20% are mixed
- TNM staging
o Low grade, stage Ta lesions are at low risk for disease progression and have a high survival rate
- Superficial carcinomas have a high relapse rate (50-70%)
o 15-20% of superficial carcinomas will progress to muscle-invasive disease. Bad prognosis dead
in 2 years
- Carcinoma in-situ arises from the lining of the bladder. Commonly is multifocal and found with invasive
disease
- Adenocarcinoma is less than 2% of bladder cancers, and may arise from a urachal remnant. Often
associated with cystitis glandularis or bladder exstrophy. Poor prognosis
- Squamous cell carcinomas account for about 6% of bladder cancers in the United States (75% in Egypt).
Frequently associated with chronic bladder inflammation from foreign objects such as Foley catheter or a
bladder stone
- Total, painless, gross hematuria is the most common presenting symptoms
o Higher-stage disease may cause flank pain from obstruction of a ureter, or lower extremity edema
from bulky pelvic LAD
o Urinary frequency, urgency, or dysuria (irritative symptoms) may be found with CIS or invasive
tumors
- Physical exam to search for disease spread
o Lymph node palpation

Bimanual exam to assess mobility of the bladder fixed bladder suggests locally advanced
disease
Cystoscopy with biopsy confirms the diagnosis
All patients require a transurethral resection or biopsy for tissue diagnosis
o A sample of underlying bladder muscle as well as the tumor itself is required to evaluate the tumor
stage fully
o Also send random biopsies of apparently normal-appearing urothelium, because CIS can have a
wide array of presentations
Urine is sent for cytologic evaluation lots of high-grade tumors and most cases of CIS will shed malignant
cells
Evaluate those with muscle-invasive tumors or recurrent high-grade disease for metastases
Elevated alkaline phosphatase rases suspicion for bone mets, abnormal LFTs for liver mets
Imaging CXR and CT of abdomen and pelvis
Intravenous pyelogram (IVP) or even a retrograde pyelogram is necessary to evaluate the renal pelvis and
ureters and clear them of disease
May need radionuclide bone scan or plain films t0 search for bony spread
Treatment depends on tumor stage and grade
o Nearly all superficial tumors can be completely resected transurethrally
o All patients with previously resected disease should undergo surveillance with quarterly cystoscopy
for the first year, with lengthening intervals thereafter
o Also perform periodic IVP
o Recurrent superficial disease, T1 lesions, high-grade superficial tumors, or CIS are excellent
candidates for intravesical therapy. The most commonly used drug is bacille Calmette-Guerin
(BCG), an attenutated strain of Mycobacterium bovis. When placed in the bladder, BCG incites an
intense immune response and has been proven to reduce time to disease recurrence and
progression in both papillary tumors and CIS. Typically given one per week for 6 weeks
Can induce irritative symptoms or low grade fevers
Systemic sepsis can occur an emergency!
o Various chemotherapeutic agents also have been used intravesically but results are not as good as
with BCG
Mitomycin C, thiotepa, doxorubicin (Adriamycin)
o Muscle-invasive cancers (T2 and higher) and aggressively recurrent superficial tumors are
candidates for radical cystectomy
Removal of the bladder, prostate, perivesical fat, and pelvic lymph nodes
In women, the anterior vaginal wall and uterus and ovaries are typically removed
On removal of bladder, must perform a urinary diversion create a conduit to the skin
from a loop of ileum or colon. A stoma is created, and the patient wears a collection bad
o Radiation therapy alone is not effective
Neoadjuvant XRT followed by salvage cystectomy is frequently associated with increased
rates of higher complications
o Chemotherapy is offered to patients at high risk for failure (pathologic stage T3b, T4, and N1/2
disease) in the adjuvant setting or for those patients first seen with advanced disease
Standard regimen methotrexate, vinblastine, doxorubicin (Adriamycin), and cisplatin
(MVAC)
Prognosis:
o 5-year survival rates are 60-80% after cystectomy for T2 bladder cancers
o

Renal Cell Carcinoma

- Arises from the proximal convoluted tubules
- The most consistent chromosomal changes are deletions and translocations of the short arm of
chromosome 3 (3p)
- Usually clear cell
- No clear environmental factors, but a weak association with cigarette smoking
- The most common malignancy arising from the renal parenchyma
o However, the most frequently encountered renal mass less is the simple renal cyst
- First complaints are nonspecific back pain, weakness, weight loss, fever
- Hematuria (usually microscopic) is the single most common sign
- Classic triad only 10% of the time hematuria, flank pain, palpable abdominal mass
- Often discovered incidentally
- May be associated with paraneoplastic syndromes
- CBC and electrolytes
- Baseline renal function is important
- Liver enzymes and alkaline phosphatase to search for metastatic disease. Also a CXR
- CT with and without contrast is the standard tool to evaluate renal masses
o Exhibit at least a 20-Hounsfield unit enhancement with IV contrast
o MRI can confirm tumor extension into the renal vein or IVC
Choice for diagnosis if contrast is contraindicated (due to renal insufficiency or allergy)
- Most frequently metastasizes to the lungs, bone, brain
- Treatment is radical nephrectomy resection of kidney, peripheric fat, and Gerotas fascia
- Does not respond well to radiation, although painful bony mets may respond to palliative treatment
- Very resistant to chemotherapy
Chronic Renal Failure (Shunts/Access)
Renal Vascular Disease
- The two disorders that may be improved by renal revascularization are hypertension and chronic renal
failure
- Renal artery stenosis causes HTN by activation of the renin-angiotensin system
o Accounts for 7% of all hypertension
o May have a bruit in the epigastrium
- Diagnostic evaluation should include a captopril radionucleotide renal scan, and if this is positive, then an
MRA, which may identify a renal arterial stenosis
- Chronic renal failure is usually caused from a primary intrarenal disorder, however some patients also have
an extrarenal contributing factor (a renal arterial stenosis)
- Generally, all patients with creatinine > 2 mg should have an MRA to evaluate possibility of renal artery
stenosis
- Treatment is with primary angioplasty/stenting
o surgical revascularization by direct endarterectomy of the renal artery or bypass from the aorta to
the distal renal artery is usually reserved for patients who have failed angioplasty

Nephrolithiasis
- Renal calculi. Occur throughout the urinary tract and are common causes of pain, infection, and obstruction
- Stones are caused by increased saturation (supersaturation) of urine with stone-forming salts (calcium,
oxalate and other solutes) or a possible lack of inhibitors (citrate) in the urine to prevent crystal formation. If
either situation happens, then precipitation occurs and crystalluria develops
o Typically formed in the proximal tract and pass distally. Lodge at the ureteropelvic junction (kidney
stones), the ureterovesicular junction (bladder stones), or the ureter at the level of the iliac vessels
- Nephrolithiasis commonly occurs during the 3rd-4th decade of life. The disease is 2-3x more common in
males than females
- Four major types of stones:
o Calcium 75-85% of stones are formations of calcium crystals. Radiopaque
o Uric Acid 5-8% of stones are formed by precipitation of uric acid. Radiolucent. Form in
individuals with persistently acid urine with or without hyperuricemia
o Cystine less than 1% of stones are caused by an impairment of cystine transport. These stones
are radiolucent. They occur only in autosomal recessive cystinuria
o Struvite 10-15% of stones are formed by the combination of calcium, ammonium, and
magnesium. They are radiopaque. Formation is increased by urinary tract infections with ureaseproducing bacterium; therefore, this type is common in patients with abnormal urinary tract
anatomy and urinary diversions and in those who require frequent catheterization
- Patients usually have complete return to health, but recurrence can occur. Frequency of recurrence has
been up to 30-50% in 5 years
- Clinical Features:
o Nephrolithiasis generally is asymptomatic until inflammation or complete or partial ureteral
obstruction develops
o Clinical features of nephrolithiasis include unilateral back pain and renal colic that waxes and
wanes
o Symptoms include hematuria, dysuria, urinary frequency, fever, chills, nausea, and vomiting
o Location can determine direction of pain and its radiation
A stone in the upper ureter the pain tends to radiate to the anterior abdomen
A stone in the lower part of the ureter the pain tends to radiate to the ipsilateral groin,
testicle in men, or labia in women
A stone lodged in the UVJ urinary frequency and urgency are noted as well as lower
pelvic pain
As the stone passes through the ureter it may mimic other acute conditions, for example,
acute cholecystitis, acute appendicitis, acute cystitis, and diverticulitis
- Laboratory Findings:
o Serum chemistries are usually normal, however there may be a leukocytosis from infection or
stress
Urinalysis usually reveals microscopic or gross hematuria and may show leukocytes
and/or crystals
Urine culture should be performed to rule out infection
o Imaging modality of choice is the helical (spiral) CT. this does not require the use of radiocontrast
and can detect stones as small as 1 mm
o Plain-film radiography of the abdomen can identify radiopaque stones; unfortunately it may miss a
small stone even if radiopaque
o Renal ultrasonography can only identify stones in the kidney, proximal ureter, or the UVJ
o An intravenous pyelogram (IVP) is a rarely indicated in the treatment and evaluation of a patient
with nephrolithiasis. If an IVP is considered, remember to make sure that the patient has normal
renal function

Treatment all stones should undergo chemical analysis, as the type of stone may dictate additional
treatment
o Stones measuring less than 5 mm
Many are likely to pass spontaneously and, in an otherwise healthy individual, may be
managed on an outpatient basis
Drink lots of fluids, use analgesics
Strain urine to catch the stone and save it for analysis
An alpha blocker or calcium channel blocker may facilitate passage
Follow-up weekly or biweekly to monitor progress. Most stones that pass do so within 2-4
weeks of onset of symptoms
o Stones measuring 5-10 mm
Less likely to pass spontaneously. Consider early elective intervention if no other
complicating factors (e.g., infection, high-grade obstruction, solitary kidney, anatomic
abnormality preventing passage, intractable pain)
Increased fluids and analgesics
Elective lithotripsy (ESWL) or ureteroscopy with stone basket extraction may be used
o Extracorporeal shock wave lithotripsy is contraindicated in the face of active infection,
coagulopathy, uncontrolled hypertension, and pregnancy
o Percutaneous kidney stone surgery (PCNL) is usually reserved for stones larger than 2 cm
o Stones measuring greater than 10 mm
Not likely to pass spontaneously. Patients are more likely to have complications
The patient should be treated on an inpatient basis if he or she is unable to maintain
adequate oral intake
Vigorous hydration
Ureteral stent or percutaneous nephrostomy (gold standard) should be used if renal
function is jeopardized
Urgent treatment with extracorporeal shock wave lithotripsy can be used for renal stones
of less than 2 cm or for ureteral stones of less than 1 cm. Ureteroscopic fragmentation
also may be used. Percutaneous nephrolithotomy can be used for stones of greater than
2 cm
o Analgesics should be administered, including morphine, meperidine, or ketorolac. Depending on
stone makeup antibiotics if signs of infection are present. HCTZ to decrease urine calcium
excretion. Allopurinol to decrease urine uric acid excretion. Alkali to increase urine citrate
excretion

Surgery Endocrinology
Tremors
Fatigue
Palpitations
Heat / Cold Intolerance
Adrenal Insufficiency
- Due to disease of the adrenal glands (primary) or disorders of the pituitary gland (secondary) can be acute
or progressive
- ACUTE Adrenal Insufficiency aka Adrenal Crisis:
o Can occur in the patient with poor adrenal reserve who is exposed to surgery, infection, injury,
stress, lymphoma, metastatic cancer, amyloidosis, scleroderma, hemochromatosis, or cessation of
corticosteroid medication. These patients may complain of nausea and abdominal pain, and appear
ill.
o Overt Shock
- PRIMARY Adrenal Insufficiency aka Addisons disease
o Deficiencies of all 3 zones of adrenal cortex
Cortisol, aldosterone and adrenal androgens
o Usually related to an autoimmune etiology
o The most common cause is autoimmune destruction of the adrenal cortex (80% of cases)
o Can occur alone or as part of a polyglandular autoimmune (PGA) syndrome or genetic disorders
such as adrenoleukodystrophy
o Tuberculosis can be a leading cause in areas of prevalence
- SECONDARY
o Deficiencies only in cortisol
Exogenous glucocorticoids = most common (discontinuation of long term therapy)
o Commonly see in patients on therapeutic doses of glucocorticoids.
o Usually caused by pituitary failure
- Also occurs in sepsis, AIDS, trauma, surgery, autoimmune disease, adrenal hemorrhage
- Clinical Manifestations aldosterone AND cortisol problem
o Addisons disease begins insidiously with nonspecific problems fatigue, weakness, weight loss,
nausea, anorexia, abdominal pain, irritability/anxiety
o Most patients have myalgias and arthralgias
o Many have GI symptoms
o Amenorrhea is common in females
o Many patients develop hypersensitivities
o Hyperpigmentation** (due to elevated ACTH, ONLY in primary disease) often seen in the skin folds,
pressure areas, and nipple areas
o Vitiligo and pallor (white patches)
o Orthostatic hypotension**. Common. Systolic BP less than 110 mmHg found in 90% of patients
o Delayed DTRs
o Salt craving
o Small heart, hyperplasia of lymphoid tissues, scant axillary and pubic hair, hypogonadism
o Addisonian crisis hypotension, acute pain (abdomen, low back), vomiting, diarrhea,
dehydration, altered mental status. If untreated, can be fatal

Laboratory Findings:
o Hyponatremia primary and secondary
o Hyperkalemia primary only
o Hypoglycemia
o Mild hypercalcemia
o Low BUN
o Neutropenia, mild anemia (normochromic, normocytic), relative lymphocytosis, and eosinophilia
may occur
o Mild acidosis
Diagnosis:
o AM Cortisol (8:00 am):
Normal reference 6-24 ug/dL
18 is a normal result rules out AI
3 g/dL is a positive result rules in AI
Accompanied by elevated of plasma ACTH (> 200 pg/mL)
o Cosyntropin Stimulation Test (ACTH)
Diagnosis is confirmed with a suboptimal one hour cortisol response to cosyntropin. A
serum cortisol rise of < 20 g/dL after administration of cosyntropin is suspicious
o To distinguish between primary adrenal insufficiency from secondary, measure 8am Cortisol and
ACTH level. ACTH >100 = primary (adrenal gland failure)
Low levels of ACTH indicate secondary disease
o Antiadrenal antibodies will be present in 50% of patients. Antithyroid antibodies are found in 45%
of patients
o Serum dehydroepiandrosterone (DHEA) levels are < 1,000 ng/mL. A level higher than this
excludes Addisons disease
o Order adrenal CT or pituitary MRI
o CXR and abdominal CT scanning may be indicated for suspected secondary disease
Treatment:
o Primary disease is treated with oral hydrocortisone or prednisone. Many patients also require
fludrocortisone acetate for its sodium-retaining effects (mineralocorticoid replacement)
Maintenance therapy hydrocortisone 15-25 mg daily in divided doses.
o Require stress-dose steroids at times of surgery or severe illness. 50-100mg IV hydrocortisone
o DHEA may be given to women who have adrenal insufficiency
o Patient should wear a medic-alert bracelet
o Addisonian Crisis requires aggressive IV saline, glucose, and glucocorticoids as well as treatment
of underlying cause
o ADRENAL CRISIS:
DO NOT WAIT FOR PENDING LAB RESULTS BEFORE BEGINNING EMPIRIC TX
Treat HYPOTENSION with volume 2 to 3 L of NS or D5NS
Give IV DEXAMETHASONE 4mg or IV HYDROCORTISONE 100mg
If less ill, can give oral hydrocortisone (20mg/kg)

Primary Aldosteronism
- Also called Conns syndrome
- Caused by the renin-independent overproduction of aldosterone.
- Characterized by the presence of hypertension, hypokalemia, and metabolic alkalosis
- The finding of an aldosterone/renin ratio that exceeds 20:1 suggests the diagnosis
o Confirm the diagnosis with a salt-loading test to demonstrate that plasma or urine aldosterone
levels are insuppressible
In this test, aldosterone levels are measured after the patient is given 2L of intravenous
saline solution over a 4-hour period
A plasma aldosterone concentration exceeding 10 ng/dL or a 24-hour urinary
tetrahydroaldosterone level exceeding 65 g is consistent with insuppressible aldosterone
secretion
- After biochemical confirmation, CT or MRI can look for an adrenal abnormality
o A unilateral aldosterone-producing adenoma (APA) is the most common type of primary
aldosteronism and is treated with surgical removal
- Adrenal venous sampling is considered to be the gold standard for differentiating APA from primary adrenal
hyperplasia (PAH)
- Patients with idiopathic hyperaldosteronism should be treated medically spironolactone (aldosterone
antagonist) is first-line
- In patients with unilateral APA, PAH, or aldosterone-producing carcinoma, a unilateral complete
adrenalectomy is the treatment of choice
o Usually dont need intraoperative stress steroids
o Hypokalemia resolves rapidly by resolution of hypertension may take longer (1-3 months)
Cushings Disease and Syndrome (Hypercortisolism)
- CUSHINGS SYNDROME may be exogenous or endogenous. The exogenous form is caused by chronic
excess glucocorticoid, most commonly from corticosteroid drugs used to treated other diseases
o Overproduction of cortisol can be either ACTH-dependent or ACTH-independent
- CUSHINGS DISEASE is caused by excess secretion of ACTH by the pituitary, often resulting from a small,
benign pituitary adenoma
o The major cause of endogenous Cushings Syndrome. Most common in premenopausal women
o Normal regulation of cortisol is controlled by corticotropin-releasing hormone (CRH), which is
produced by the hypothalamus
o CRH stimulates ACTH, which stimulates cortisol secretion from zona fasciculata of adrenal cortex.
o Cortisol induces catabolism of fats and proteins and also has antiinflammatory effects.
- Adrenocortical tumors and nonpituitary ACTH-producing tumors (most often small cell lung carcinoma) may
also cause Cushings syndrome
- Hypercortisolism may present as obesity, HTN, and thirst and polyuria with or without glycosuria
o Obesity is centripetal, and extremities appear wasted
- Fat deposition also causes the characteristic buffalo hump, moon facies, and supraclavicular peak
- The most specific signs are proximal muscle weakness and pigmented striae more than 1 cm wide. Striae
are purple. Located on lateral abdomen, axillae, internal thighs
Patients may present with backache and headache
- Oligomenorrhea or amenorrhea and erectile dysfunction are common
- Disorders of calcium metabolism may cause osteoporosis, vertebral fractures, hypercalciuria, and kidney
stones. Avascular necrosis may occur
- Impaired wound healing, acne, easy bruisability, and superficial skin infections occur
o If ACTH dependent hyperpigmentation
- Psychiatric symptoms range from emotional lability to psychosis

Laboratory Studies:
o Excretion of free cortisol in the urine of greater than 125 mg/dL in 24 hours is diagnostic, as is
greater than 95 mcg of cortisol per gram of creatinine
o Salivary cortisol assays are now available
o In Cushings disease, the overnight dexamethasone suppression test will result in a plasma cortisol
of greater than 10 g/dL (< 5g/dL is normal)
o The cortisol excretion test and plasma cortisol test should be confirmed with a low-dose
dexamethasone suppression test. False positives are caused by rifampin, phenytoin, primidone,
phenobarbital, carbamazepine, fenofibrate, estrogens, and pregnancy
o Plasma ACTH of less than 20 pg/mL suggests adrenal tumor. Higher levels suggest pituitary or
ectopic production (making ACTH)
o MRI is preferred to identify pituitary tumors (especially in Cushings disease). CT may show
adrenocortical or other tumors. Somatostatin receptor scintigraphy is useful to detect occult tumors
o Hyperglycemia, impaired glucose tolerance, and hypokalemia (without hypernatremia) are not
unusual
- Treatment:
o Treatment of Cushings disease is transsphenoidal resection of the pituitary adenoma and
hydrocortisol replacement. An alternative is gamma knife radiosurgery
o Surgical removal of tumors is the treatment of choice for Cushings syndrome
o In patients who fail surgery, bilateral adrenalectomy will eliminate Cushings. However, then
patients need lifelong glucocorticoid and mineralocorticoid replacement
Nelsons Syndrome continued enlargement of the adenoma due to lack of feedback
o Radiation and chemotherapy may be used for nonresectable tumors
o Adrenal inhibitors also can be used
Metyrapone and/or ketoconazole may suppress hypercortisolism
Parenteral octreotide suppresses ACTH in of cases
Hyperparathyroidism
- Parathyroid glands are endocrine organs regulating calcium and phosphate metabolism
- PTH works on bone and kidney tubules to increase blood calcium
- PRIMARY HYPERPARATHYROIDISM (HPT) results from excess PTH, which causes mobilization of
calcium deposits from bone, inhibition of renal phosphate reabsorption, and stimulation of renal tubular
absorption of calcium. Overall, both total body calcium and phosphate wasting occur, leading to
osteoporosis and bony mineral loss
- SECONDARY HYPERPARATHYROIDISM is from hyperplasia of the parathyroid glands, occurring in those
with chronic hypocalcemia, as is usually seen in patients with renal disease. The hyperphosphatemia
suppresses calcium levels, leading to excess PTH production
- TERTIARY HYPERPARATHYROIDISM is a consequence of secondary HPT becoming autonomous
- HPT is the most common cause of hypercalcemia, followed by malignant disease
o The majority of HPT cases occur sporadically or in a nonfamilial form, often from a single
hyperfunctioning gland or adenoma
- Patients with MEN 1 (parathyroid, pituitary, pancreas) and MEN 2A (HPT, pheo, medullary cancer of thyroid)
have HPT involving multigland hyperplasia of the parathyroids
- Solitary parathyroid adenoma accounts for 80% of primary HPT
o 15% due to hyperplasia, where up to all 4 glands are involved
- Patients present with long-term complications related to stones, bones, groans, moans
o Renal stones / nephrocalcinosis
o Bone aches and arthralgias
o Abdominal pain from constipation, pancreatitis, or PUD
o Mood swings, fatigue, anxiety, memory loss

Guidelines for surgery:

o Serum calcium > 1.0 mg/mL above upper limit of normal or >12 mg/dL
o >400 mg/d hypercalciuria
o Sequelae of hypercalcemia resulting from primary HPT, such as nephrolithiasis, osteitis fibrosis
cystica, classic neuromuscular disease, severe psychoneurologic disorder
o Cortical bone density reduction with T score < 2.5 of lumbar spine, hip, or wrist
o <30% reduction in renal function in the absence of other cause
o Age < 50 year
o Inability to have appropriate follow-up
- Rarely findings on physical. A palpable neck mass is suspicious for parathyroid carcinoma (rare, <2%)
- A combination of elevated calcium and PTH levels is highly suggestive of primary HPT. Rule out benign
familial hypocalciuric hypercalcemia by the presence of low urinary calcium
- A surgical disease only parathyroidectomy can successfully treat the disease
o Must stabilize hypercalcemic crisis before surgery vigorous IVhydration and forced diuresis with
furosemide
o Preoperative localization of the suspecting glands may be performed usually done with
technetium (Tc)-sestamibi scanning
Can also use ultrasound or CT
o To maximize success of surgery, preoperative TC-sestamibi scanning and intraoperative rapid PTH
assay are recommended
- Once the tumor is removed, PTH levels should decrease to <50% of the baseline values in as short as 10
minutes
- Sometimes can get hypocalcemia symptoms after procedure
- A rare complication is recurrent laryngeal nerve damage can cause hoarseness and a reduction in voice
volume
Hyperthyroidism
- The most common causes are Graves disease and toxic nodular goiter
o TNG is also referred to as Plummers disease. The mechanism of action is through autoproduction
of thyroid hormones regardless of TSH control
o Graves disease is an autoimmune process in which the bodys own autoantibodies stimulate the
TSH receptor, causing excess T4 and T3 in addition to gland growth
- Both diseases can lead to similar signs and symptoms anxiety, heat sensitivity, excessive sweating,
nervousness, weight loss, fatigue, palpitations, tachycardia, palpable goiter, hyperdefecation, irritability,
bounding pulse, elevated SBP, fine and silky hair, fine tremor of hands and tongue, hyperreflexia, etc.
o Findings unique to Graves disease eye proptosis or exophthalmos(irreversible) and pretibial
myxedema (raised, thickened, hyperpigmented areas that look like an orange peel)
Usually associated with goiter, ophthalmopathy, and dermopathy
Women in the 3rd 4th decade of life
The gland is typically diffusely enlarged and may vary in consistency from soft to first
A bruit or thrill indicative of hypervascularity may be apparent over the gland
- Laboratory tests TSH and free T4
o TSH is suppressed near zero
o Elevated T4
- Radioactive iodine uptake testing will differentiate thyroiditis from Graves disease but it is not necessary for
the confirmation if the clinical picture is consistent with Graves disease
o In TNG, diffuse areas of uptake will be seen
- Treatment can be medical radioactive iodine (RAI)
- For Graves disease, you can use drugs that inhibit synthesis of thyroid hormones, such as methimazole
and propylthiouracil. Can also use beta blockers for symptoms

For TNG, RAI or surgery

Surgery is the best option when patients are symptomatic from their goiters (e.g., dysphagia or pressure-like
sensations in the neck), when malignancy cannot be excluded in the enlarged thyroid, and when radioactive
iodine is not a suitable option (children, pregnant women, resistant cases, etc.)
- Specifically, bilateral subtotal thyroidectomy is performed to minimize risk of hyperthyroidism recurrence
- However, surgery also puts the patient at risk for long-term hypothyroidism, particularly in Graves disease,
where a euthyroid state is rarely achieved after surgery alone
- All patients preoperatively must be made euthyroid using methimazole or propylthiouracil. Also betablockers to control adrenergic signs and symptoms.
o Iodide preparations are avoided preoperatively as they may worsen the patients condition,
whereas iodides are often used preoperatively in Graves disease to minimize vascularity of the
thyroid
For 7-10 days before surgery, oral potassium iodide should be given
- Patients who require an emergency thyroidectomy and are thyrotoxic should be treated preoperatively for 5
days with dexamethasone, iopanoic acid, propranolol, and propylthiouracil
- Surgical Technique:
o Most can be done through a low transverse collar incision (Kocher incision)
o The most frequent procedure is the bilateral subtotal thyroidectomy
However, an alternative treatment is a total lobectomy on one side and a subtotal
resection on the opposite side (Dunhill procedure), leaving a slightly greater and more
easily manageable remnant of tissue
- Complications nerve injury, hypoparathyroidism (be careful not to injure parathyroid glands!),
hematomas, airway obstruction (from subglottic or supraglottic edema)
o For transient hypoparathyroidism, give vitamin D and supplemental calcium
Thyroid Nodules
- Women more than men
- Almost 90% are benign
- A nontoxic or diffuse multinodular goiter (simple goiter) is defined as thyroid enlargement that is not caused
by autoimmune thyroid disease, thyroiditis, or neoplasia and is not associated with clinical or biochemical
evidence of thyroid dysfunction
o May evolve secondary to iodine deficiency or exposure to naturally occurring goitrogens. Can also
occur in familial patterns or sporadically
o The rate of malignancy in multinodular goiters is 25-60% that of a solitary nodule
o Can transition to TNG
- Risk factors for malignancy history of head/neck radiation, family history of thyroid cancer (familial
medullary thyroid carcinoma, multiple endocrine neoplasia syndrome), male sex (females usually have
benign nodules), very young age (< 20 years old), old age (> 60 years old), rapid enlargement of the nodule,
voice changes, and presence of thyroid disease
- Signs and symptoms hypo/hyperthyroidism symptoms, dysphagia, sudden onset hoarseness
o On exam, a fixed hard mass, cervical LAD, and symptoms of airway obstruction are strongly
suggestive of thyroid cancer
- A nodule in the setting of hypothyroidism likely represents a component of Hashimotos disease, whereas
one occurring in the setting of hyperthyroidism may represent a benign toxic adenoma
- Check TSH level and do an ultrasound
o If TSH is abnormal, do further workup and treatment. If normal, so FNA biopsy
o May also want to check T3, T4, and antithyroid antibodies
o Ultrasound can characterize the nodule by echogenicity borders, vascularity, and calcifications.
Can also evaluate LAD
- Nodules 1-1.5 cm are considered biologically significant and should undergo FNA

A palpable nodule on examination or incidental nodules on radiologic studies can be definitively tested with
FNA (gold standard)
o Repeat FNA is recommended if you get an inadequate specimen
o Presence of follicular or Hrthle cells without malignancy is an indication for surgical intervention,
because cytological examination alone is insufficient for determining presence of malignancy
o Presence of capsular invasion or angioinvasion can only be seen on histological examination
where the thyroid architecture is intact
- The initial FNA biopsy results dictate the next step in patient management
o In patients with a follicular neoplasm, especially if serum TSH is low, a radionuclide scan is
indicated
If the scan shows a hyperfunctioning (hot) nodule, the patient is monitored clinically and
evaluated for hyperthyroidism
If the scan shows a hypofunctioning (cold) or eufunctioning nodule, the patient is treated
surgically or medically (levothyroxine)
- For a benign solitary thyroid nodule, clinical observation or treatment with levothyroxine is indicated
Thyroid Carcinoma
- Rare. Greater in women
- Favorable mortality compared with other cancers
- Multiple types distinguished by cell origin.
o Most common = follicular cell neoplasms, which include papillary and its variants, follicular and
Hrthle cell, poorly differentiated, and anaplastic
o Other cancers include medullary cancer derived from C cells and lymphoma
o Papillary and follicular cancers are considered differentiated and tend to have a more favorable
prognosis than medullary and anaplastic variants
- Staging according to TNM. All anaplastic are considered stage 4
- PAPILLARY THYROID CARCINOMA:
o The most common form (80% of differentiated thyroid carcinoma)
o Peaks in 3rd-4th decade of life
o Arises from follicular epithelial cells, grows slowly, and is associated with a favorable prognosis
o More common in iodine-rich areas and ionizing radiation
o A thyroid nodule discovered incidentally on routine physical examination is often the initial clue to
the diagnosis of PTC. Occasionally, enlarged cervical lymph nodes are the presenting feature of
the disease
o Perform TSH FNA treat
o Typically non-encapsulated, well-demarcated lesions. They may be cystic. Microscopically
characterized by papilliform axial fibrovascular stroma arranged in a branching or treelike pattern.
Large overlapping nuclei with loose chromatin, cytoplasmic inclusions (Orphan Annie nuclei),
longitudinal nuclear grooves, and clefts are all classic feature of PTC. About 50% contain
psammoma bodies or laminated calcifications thought to represent remnants of infarcted papillae
o MACI system for prognostic scoring metastases, age, completeness of surgery, invasiveness of
the tumor, size of the tumor
o Surgery is the mainstay of treatment. Can range from lobectomy and isthmectomy to total
thyroidectomy
Usually lobectomy and isthmusectomy are sufficient if it is small (1-1.5cm) and welldifferentiated
TSH is suppressed postoperatively with thyroidal hormone replacement, and RAI may be
used to ablate any residual thyroidal tissue

Measurement of serum thyroglobulin, which is a tumor marker for well-differentiated

thyroid cancer, can be performed after total thyroidectomy and at follow-up to monitor
signs of recurrence
o Can be multicentric and spread into nearby lymph nodes
FOLLICULAR THYROID CARCINOMA:
o About 10% of all thyroid cancers. Decreased incidence with the institution of iodination, but
continues to be prevalent in geographic regions of endemic goiter
o Like PTC, FTC arises from follicular epithelial cells, occurs predominantly in women, grows slowly,
and has a favorable prognosis. Usually patients with FTC are older than those with PTC (about 50
years old)
o Unlike PTC, FTC is not commonly associated with regional lymph node and contralateral
involvement. FTC metastasizes via the bloodstream to the lungs, bone, and liver (occasionally to
the brain)
o The tumor cells are osteolytic, so mets may not be detected with conventional bone scans
o Like PTC, patients often have a painless, solitary thyroid nodule. In contrast to PTC, patients with
FTC usually do not have cervical LAD
o Hoarseness, dysphagia, cough, and dyspnea suggest advanced disease
o Cytologic evaluation of aspirate from the FNA biopsy is unable to differentiate a malignant follicular
neoplasm from a benign follicular adenoma. Demonstration of capsule invasion or angioinvasion is
needed for definitive diagnosis can be gleaned only by surgical removal of the nodule and
subsequent detailed pathologic analysis
o FTCs have a follicular differentiation pattern, but they lack the characteristic features of PTCs
(ground-glass nuclei, well-formed papillae, and psammoma bodies.
They are usually encapsulated, and invasion of the capsule and blood vessels is the
major feature that differentiates them from follicular adenomas
o Three risk factors for prediction of aggressiveness age older than 50 years, marked
angioinvasion, metastatic disease at diagnosis
o Treatment of choice is usually total thyroidectomy, but lobectomy may be sufficient in low-risk
patients
HRTHLE CELL CARCINOMA:
o Fewer than 5% of all thyroid cancers. W>M. Peaks 5th and 6th decade. Usually a history of
radiation exposure
o A variant of follicular carcinoma
o Hrthle cells are large, polygonal thyroid follicular cells with abundant granular cytoplasm and
numerous mitochondria
o Hrthle cell carcinoma is defined as an encapsulated group of follicular cells made up of at least
75% Hrthle cells
o The carcinomas demonstrate capsular invasion, vascular invasion, or invasion of the surrounding
adjacent tissues and therefore the diagnosis cannot be made by cytologic examination alone
o Total or near-total thyroidectomy is usually indicated
o Generally, RAI is not indicated because these carcinomas do not concentrate 131I
However, it may be indicated in some since they have been reported to produce
thyroglobulin
MEDULLARY THYROID CARCINOMA:
o 5-10% of thyroid cancers. May be sporadic* or familial. 5th to 6th decade (if sporadic). Most
commonly presents as a solitary nodule in the upper portion of the thyroid lobe
o MEN type IIa, MEN type IIb, and familial medullary thyroid carcinoma (FMTC)
Patients with MEN type IIa have MTC, pheochromocytoma, and parathyroid hyperplasia

Patients with MEN type IIb have MTC, pheochromocytoma, and mucosa neuromas
(especially around the lips and mouth). Often have a marfanoid habitus, occasionally
have intestinal ganglioneuromas, and lack parathyroid hyperplasia
Patients with FMTC have MTC but lack other features of the MEN syndromes.
Various mutations in the RET proto-oncogene are responsible

MTC develops from the parafollicular cells (C cells) of the thyroid. These cells are located in the
upper third of the lobe and synthesize and secrete calcitonin. The C cells are derived from neural
crest cells and thus MTC may have histologic features of other neuroendocrine tumors (such as
carcinoid, islet cell tumors)
o MTC is multicentric in many patients and is often bilateral in FMTC
o Frequently metastasizes to regional lymphatics of the neck and mediastinum (may also
metastasize to lung, liver, bone, brain)
o Diagnose with FNA biopsy
o Cytologic evaluation typically demonstrates sheets of spindle-shaped pleomorphic cells without
follicular development. May initially be misdiagnosed as anaplastic carcinoma
Occasionally, red cytoplasmic granules are visualized, and the stroma often stains positive
for amyloid
Immunocytologic stains are positive for calcitonin
o Must determine if sporadic or familial! Need to treat pheo ASAP
Collect 24-hour urine sample to test for catecholamines, metanephrines, and
vanillylmandelic acid
Also screen for RET mutations
o Staining of FNA for calcitonin and absence of thyroglobulin is diagnostic
o If the patient demonstrates a germline mutation, then total thyroidectomy should be scheduled and
first-degree relatives should be screened (and if positive, have total thyroidectomy at age 5 years
or older)
o Regardless of whether it is sporadic or familial, total thyroidectomy is performed
o Consider lateral neck node sampling with MEN type IIb or lesions >2 cm
o Postoperatively, monitor for recurrent disease with basal or stimulated serum calcitonin. Also CEA
can be a marker
ANAPLASTIC CARCINOMA:
o Fewer than 5% of all thyroid cancers. Incidence highest in regions of endemic goiter. Mean age is
65 years
o The most aggressive type. Usually develops in the background of well-differentiated thyroid
cancers or benign thyroid tumors
o Mets are present at initial visit about 90% of the time
o Commonly first seen with SOB, dysphagia, hoarseness, pain, cough, hemoptysis
o Unlike patients with differentiated forms of thyroid cancer, these patients also have constitutional
symptoms (weight loss, fever)
o Exam shows a fixed, hard, asymmetrical thyroid gland with cervical LAD
o May invade the jugular veins, carotid arteries, and larynx
o CT or MRI may be indicated.
o FNA biopsy
o Cytologic exam demonstrates pleomorphic cells that are medium to large in size, have prominent
nuclei, and show evidence of mitosis. Multinucleated giant cells containing abnormal mitotic
figures are frequently encountered, as are malignant-appearing spindle cells. Sarcomatous
changes also may be present
o Rarely treated surgically presents with a rapid enlarging neck mass and is considered lethal with
short survival time (months). Airway management
o

MALIGNANT LYMPHOMA OF THE THYROID:

o Fewer than 5% of all thyroid cancers. W>M. Peaks in the 7th decade
o Most patients have a long-standing history of Hashimotos thyroiditis
o Characterized by a rapidly enlarging, painless goiter or mass that is occasionally associated with
hoarseness, dysphagia, and dyspnea. On palpation, the mass is firm and may be fixed to
surrounding structures
About 50% of patients have cervical lymph node involvement
o Cytologic findings derived from B cells (usually Non-Hodgkin), and the majority are of the
diffuse large cell type or follicular cell origin.
FNA biopsy typically demonstrates an abundant infiltration of lymphoid cells
o The prognosis is more favorable for follicular tumors than for diffuse large cell or immunoblastic
lymphomas. Prognosis for malignant lymphoma overall is better than anaplastic carcinoma
o Surgery is rarely indicated yet this is controversial.
If disease is localized to the neck (stage I or II, may resect with subsequent local radiation
and chemo).
Stage III or IV is treated with external radiation and chemo
Adrenal Carcinoma
- Rare, aggressive cancer
- Hyperfunctioning in 50-70% and nonfunctioning in the remainder
o Hyperfunctioning can be seen in association with isolated Cushings, concomitant Cushings and
virilization, isolated virilization, feminization, and hypertension
- Median age is 40
o Hyperfunctioning is usually in females and nonfunctioning is usually in males
- Key is early detection
- Usually silent until advanced malignancy, large mass, or hormonal excess
- Hyperfunctioning do not produce early symptoms, because malignant cells are highly inefficient in
synthesizing steroids, and a large mass is required to elevate steroid levels
- Usually 9 months before symptoms reported
- In nonfunctioning pain, palpable abdominal mass, metastases
o Also fatigue, weight loss, fever
- Hyperfunctioning manifestations vary. Include those associated with virilization, feminization, Cushings
- Lab values most commonly include elevated testosterone and DHEAS in serum, as well as elevated free
cortisol and 17-ketosteroids in urine
- CT is the best study
- Complete surgical excision is the only effective and potentially curative treatment
o Adjuvant radiation is not helpful
o Sometimes can use mitotane after surgery
Pheochromocytoma
- Catecholamine-secreting rumors that are derived from chromaffin cells
- Most occur within the adrenal glands
o Extra-adrenal pheochromocytomas are also called paragangliomas
- The term means dusky-colored tumor and refers to the appearance of tumor cells when they are stained
with chromium salts
- Affect the right adrenal gland more than the left
- Females > males. 3rd 5th decade of life. 10% of tumors are malignant
- Found in 0.1% of hypertensive patients
- Rare, but diagnosis is important because they may precipitate life-threatening HTN or cardiac arrhythmias if
not discovered

Rule of 10s 10% extra-adrenal, 10% malignant, 10% bilateral, 10% incidental, 10% in children, 10%
recur
Occur in association with several familial disorders 50% of MEN type IIa, 50% of MEN type IIb, 1% of
neurofibromatosis type I, 20% of von Hippel-Lindau disease
Clinical manifestations due to excessive catecholamine secretion by the tumor
o Stimulation of 1-adrenergic receptors causes elevated blood pressure, increased cardiac
contractility, glycogenolysis, gluconeogenesis, and intestinal relaxation. Causes an increased heart
rate and contractility
Factors that precipitate catecholamine discharge from a pheochromocytoma childbirth, anesthesia
induction, use of radiographic contrast media, opiates, dopamine antagonists, catecholamine reuptake
inhibitors (TCAs, cocaine), cold medications
o Can also be precipitated by physical exertion, tyramine-containing foods, nicotine, succinylcholine,
and propranolol
Secretions of the normal adrenal medulla contain about 85% epinephrine. Most pheochromocytomas
secrete predominantly norepinephrine, but familial ones secrete lots of epinephrine
History and Physical:
o Spells of palpitations, headaches, diaphoresis classic triad
In association with hypertension
o Other symptoms nausea, weakness, anxiety, flushing, epigastric pain, flank pain, constipation,
weight loss, postural hypotension, retinopathy, fever, pallor, tremor, arrhythmias, ileus, caf au lait
spots, neurofibromas
o The five Ps palpitations, pain, pallor, perspiration, pressure
24-hour urine sample to measure levels of total catecholamines, metanephrines, and vanillylmandelic acid
(VMA)
o Elevated metanephrine levels are the most sensitive and specific
o Elevated VMA are the least specific
o Optimally, collect urine during a crisis
Blood tests may reveal hyperglycemia, hypercalcemia, and erythrocytosis
Tests for plasma levels of chromogranin A
Only image after biochemical studies confirm the diagnosis
o MRI is preferable to CT
Surgical resection is the treatment of choice
Preoperative preparation:
o -blockers and beta-blockers are required to control blood pressure and prevent an intraoperative
hypertensive crisis
From 7-10 days before surgery, blockade with phenoxybenzamine should be started
o Liberal salt intake
o Only start beta-blockers after you ensure blockade is working
If started too early, unopposed stimulation could precipitate a hypertensive crisis
Isolated beta blockade in the setting of catecholamine surge can produce shock, as
cardiac function is prevented from increasing while systemic vascular resistance
increases
o Give the last doses of -blockers and beta-blockers the morning of surgery
o Place an arterial line and Swan-Ganz catheter
o Cardiac monitoring
o If bilateral resection is planned, stress steroids (hydrocortisone) should be administered to
compensate for the fact that cortisol output will be suppressed
Laparoscopic adrenalectomy is the procedure of choice for adenomas < 8 cm
Complications hypotension (treat with 0.9% IV saline or colloid solution)

At 2 weeks and then yearly for 5 years after the surgery, check 24-hour urine sample again

Surgery Womens Health

Pain
Skin Changes
Nipple Discharge
Adenopathy
Benign Breast Disease (Fibroadenomas, Fibrocystic Breast Disease)
- FIBROCYSTIC DISEASE
o Symptomatic with pain, especially in the second half of the menstrual cycle
o Clinically, multiple nodular densities are palpable
o Cold compresses, reduced caffeine intake, properly fitted bras, anti-inflammatory agents can help
alleviate symptoms
- FIBROADENOMAS
o Discrete round or ovoid solid rubbery lesions that grown under the influence of estrogen.
o The most common solid lesion in women younger than 40
o Long-term follow up or excision to ensure no malignancy
- CYSTS
o Discrete lesions that, when distended, especially before the menstrual period, may suddenly feel
quite hard
o Ultrasound can confirm diagnosis
o Aspirate for therapeutic management
- DUCTAL ECTASIA
o Presence of ducts ending in the areolar tissue rather than in the nipple
o Often associated with a discharge of thick yellow/green secretions
o Good hygiene is important to prevent secondary infection
o Surgery is not indicated
- PAPILLOMAS
o May occur in any duct in the breast
o Pathologic evaluation is important to look for areas of atypical ductal hyperplasia, dysplasia, or CIS
o When they occur in the major ducts close to the nipple, a spontaneous bloody nipple discharge is
often the presenting sign
o Surgical excision is recommended
- PHYLLOIDES TUMORS
o Clinically resemble fibroadenomas
o Pathologically, they are distinguished by cellular proliferative activity of stroma and epithelium and
compression of surrounding normal tissue
o Complete surgical excision, including the surrounding compressed tissue with 1 cm margins, is
recommended

Breast Carcinoma
- Breast cancer is the most common female malignancy and the second leading cause of death from cancer
in women. Lifetime risk of 1 in 8 (12%)
- Most women with breast cancer have no identifiable risk factors other than female sex and increasing age
(mean age at diagnosis 60-61 years); BRCA1 and BRCA2 genes are associated with 5-10% of cases of
breast cancer but appear in only 1% of the population
- Associated factors include nulliparity, early menarche, late menopause, long-term estrogen or radiation
exposure, and delayed childbearing
- Women with first-degree relatives with breast cancer are at increased risk, especially if the cancer was
premenopausal or bilateral or found in two of these relatives
- Breast cancer increases the risk of endometrial cancer and vice versa
- Ductal carcinomas account for 80-85% of breast cancers; the remainder are lobular carcinomas. Lobular
CIS and atypical ductal hyperplasia predispose to cancer
- Pagets disease is a ductal carcinoma presenting as an eczematous lesion of the nipple
- All invasive lobular carcinomas and of ductal carcinomas are estrogen-receptor positive
- Breast cancer most often presents as a single, nontender, firm, immobile mass. 45% occur in the upper
outer quadrant and 25% under the nipple and areola
- Early carcinoma may also appear with mammographic changes and no palpable masses
- Most women report finding a breast lump while showering or with BSE
- Breast pain is usually associated with benign lesions, but may occasionally be present with malignant
lesions
- Lumps that increase before menses and decrease after menses are usually benign simple cysts or
fibrocystic changes
o Malignant lesions do not vary in size with the menstrual cycle
- Spontaneous or bloody nipple discharge is associated with intraductal papillomas (benign)
- Rarer presentations include nipple discharge or retraction, dimpling, breast enlargement or shrinkage, skin
thickening or peau dorange skin, eczematous changes, breast pain, fixed mass, axillary node enlargement,
ulcerations, arm edema, and palpable supraclavicular nodes
- Patients with advanced stages may have weight loss, odor from ulcerating or fungating lesions, pain from
bone mets (back, chest, or extremities), nausea, or abdominal pain from liver metastasis, or headaches
from brain mets
- On exam, look for skin changes, asymmetry (visible bulge or dimpling of skin), nipple retraction, palpable
masses, and LAD in the axilla and supraclavicular fossa
o Well-circumscribed, mobile, nontender lumps in you ng women are usually fibroadenomas or
phyllodes tumors
o Breast tenderness is associated with fibrocystic changes or simple cysts
o Vague masses or firm lumps with indistinct borders are suggestive of malignancy
o With advanced stages, there may be skin changes such as dimpling, peau dorange (edema of the
skin, making it look like an orange peel), ulceration, erythema, or fixation to the skin or chest wall
o Enlarged or matted lymph nodes may indicate metastasis
o Paget disease usually presents with nipple or areolar rash or excoriation
o Inflammatory breast cancer may have erythema, peau dorange, or skin thickening

Diagnostic Studies:
o A combination of physical examination, mammography (the best screening tool), and fine-needle or
stereotactic core-needle biopsy is highly accurate in establishing diagnosis. Open biopsy may be
required
Mammograms miss 15% of palpable breast cancers
Mammographic signs that suggest malignancy a density with indistinct margines,
spiculated mass, and clusters of or linear/branching microcalcifications
Lesions not seen on prior mammograms need further work up
Also, if the patient reports a palpable lump, then a diagnostic mammogram (additional
views to magnify and/or compress the breast are obtained) and breast ultrasound are
performed
o Ultrasonography and excisional biopsy may be indicated. Biopsy specimen should undergo
estrogen and progesterone receptor analysis as well as histologic analysis
Ultrasound can differentiate between solid and cystic masses. It is not optimal for
screening because it rarely detects microcalcifications and is extremely dependent on the
experience of the person performing the exam
o Breast MRI is increasing in popularity. Current indications include identifying occult primary cancer
with axillary metastasis in women with no clinical breast mass and normal mammogram, screening
high risk women, developing extent of breast cancer to help with surgical planning
o Lesions suggestive of malignancy on diagnostic examination are biopsied with image guidance
mammographic, ultrasonographic, or MRI guided core needle biopsy
o Palpable masses not seen with imaging can be biopsied with FNA, core needle biopsy, excisional
open biopsy, or incisional biopsy
o Malignant lesions require surgical consultation
o If the pathology report shows atypia or LCIS or is discordant with radiologic or clinical findings, then
an open biopsy should be performed. This may require wire localization by the radiologist
o If the patient presents with skin changes over the breast mass, an incisional biopsy should be
considered, taking an ellipse of the skin with the mass to check for cancer involvement of the
dermal lymphatics
o If DCIS or invasive breast cancer is diagnosed pathologically, additional pathologic tests are
performed. The tumor is checked for hormone receptors, HER-2/neu receptor, and, occasionally,
various other biologic markers
o Tumors with better prognostic indicators are well differentiated (low-grade cancer), have
overexpression of estrogen receptors or progesterone receptors, and do not overexpress HER2/neu receptor
o The Oncogene DX test helps determine whether a woman will benefit from chemotherapy in
borderline situations

Treatment:
o Staging should occur before treatment begins
o Breast conservation therapy (lumpectomy), modified radical mastectomy, and partial mastectomy
have equivalent survival rates when surgery is followed by radiation therapy
Mastectomy = from clavicle to rectus muscle and sternum to latissimus dorsi, taking
pectoralis fascia with the breast tissue
Do mastectomy if multicentric cancers (in more than 1 quadrant), extensive high-grade
DCIS, large tumor size relative to size of breast, when clear margins have not been
obtained
o Also check lymph nodes for mets and staging. SLN biopsy (CALND if SLN shows mets)
o Radiation is most commonly performed with external beam irradiation to the breast and may
include the axillary and supraclavicular nodal regions. Whole-breast radiation usually involves daily
treatments over 4-6 weeks
Can also use the Mammosite balloon similar to brachytherapy. Balloon inserted in
lumpectomy cavity and radioactive beads are implanted into the balloon. This gives high
doses of radiation over 4-5 days, then balloon is removed
o Adjuvant chemotherapy and/or hormonal manipulation benefit some women
o Tamoxifen is used to treat women with estrogen receptor-positive disease and postmenopausal
women
Aromatase inhibitors now recommended for postmenopausal women (Tamoxifen for
premenopausal with receptor-positive disease)
This is due to a lower risk of endometrial cancer and thromboembolic events
(however, there is a higher incidence of osteoporosis and fractures
Anastrozole, letrozole, exemestane
o Surgery and radiation are for local control of breast cancer. Chemotherapy and hormonal therapy
are initiated for systemic control
Stage 0, 1, 2 treated with surgery first and then the pathology guides adjuvant therapy
(chemo, hormonal, radiation, or a combo)
Stages 3 and 4 are treated with neoadjuvant chemo (and sometimes hormonal and/or
radiation) followed by surgery and radiation

Surgery Dermatology
Rash
Redness / Erythema
Discharge
Drug Eruptions (Post-Operative)
Urticaria (Post-Operative)
Cellulitis
- An acute, spreading inflammation of the dermis and subcutaneous tissue
- Borders are often indistinct
- Involved area is swollen, red, hot, tender. Pinkish and indurated skin
- Patient may have LAD, fever, chills, malaise
- Etiologic agents GAS (most common), S. aureus, others in special settings
o Usually best to begin treatment that will cover H. flu, Streptococcus sp., Staphylococcus sp.
o GAS cellulitis is common in patients with lymphedema, chronic stasis, or venous grafts
- Mild or early infections may be treated with oral penicillinase-resistant penicillin (dicloxacillin) or a
cephalosporin erythromycin for penicillin-allergic patients
- In severe infections, first-generation cephalosporins are given IV can switch to oral therapy when fever,
chills, malaise subsides
- Mark the margins of involvement before treatment to follow progression or regression of the area
- If there is poor response to antimicrobial therapy or a necrotizing soft-tissue infection is suspected, surgical
intervention is necessary
Burns
**Scald burns are the most common type of burn
Zones of Burn Injury
- The classic description of the burn wound and surrounding tissues is a system of several circumferential
zones radiating from primarily burned tissues, as follows:
o Zone of Coagulation a nonviable area of tissue at the epicenter of the burn
o Zone of Ischemia or Stasis surrounding tissues (both deep and peripheral) to the coagulated
areas, which are not devitalized initially but, due to microvascular insult, can progress irreversibly to
necrosis over several days if not resuscitated properly
o Zone of Hyperemia peripheral tissues that undergo vasodilatory changes due to neighboring
inflammatory mediator release but are not injured thermally and remain viable
Burn Depth Classification
- 1st degree Superficial burns
o Epidermal only
o Caused by sun or minor flash
o No blisters / edema
o Skin is pink or red and is dry
o Hypersensitivity
o Rapid healing, 3-6 days

2nd degree Partial Thickness

o Involves dermis
o Superficial or deep
o Appearance and healing time vary on severity of burn
o Heals in 2-3 weeks
o Superficial Partial Thickness
Caused by flame, scalding, and chemicals
Minimal damage to skin appendages
Edema / blister formation fluid filled
Skin is pink or red
Appears moist
Blanche with pressure
Hypersensitivity Painful
Healing 10-21 days
Blister = 2nd degree / 3rd degree
o Deep Partial Thickness
Deeper dermis involved some skin appendages
Caused by grease, flame, or chemical
Moderate edema, mixed with pallor
Skin pale and dry
Thicker-walled blisters, many of which are ruptured
Decreased sensation, decreased circulation,
Healing takes greater than 21 days
rd
- 3 degree Full Thickness
Destruction of both epidermal and dermal layers
Prolonged exposure to heat
Extensive edema
Skin often dry, leathery or charred can have a pearly white or charred appearance
Painless no sensation, circulation
Will not heal spontaneously
Requires skin grafting
No blister formation
Not all third degree burns are pain less. Do not assume that 3rd degree burns are painless.
They will still have a lot of pain. How would you tell? We call it the poking or the rubbing
test. The way to tell the degree is to poke in the wound bed. If he kicks you it is superficial
partial thickness. If he says What are you doing doc? Then it is deep partial or 3rd degree
burn
th
- 4 degree burn reaching the muscle layer or bone
o Controversial classification
o Significant charring and exposure of muscle or bone
o Extensive damage to nerves results in little to no sensation of pain
Pre-Hospital Management First Aid
- Stop the burning process
o Remove clothing, irrigation of chemicals, etc.
- Cool the burn surface how?
- Cover / protect burn wound
o Prevent heat loss, keep clean
-

Do not put ice or cold water especially on larger burns as it carries a risk of hypothermia. Instead wrap in
clean sheet of dry cloth or blanket before transferring to the ED.

Emergency Management
- Initial care is focused on the patient, not the burn wound
o A = Airway
Assess airway patency
Assess for smoke inhalation injury and carbonaceous deposition
Constantly re-assess upper airway edema develops as fluid resuscitation progresses
o B = Breathing and Ventilation
Assess for spontaneous respiration
Assess for bilateral airflow
Consider bronchoscopy for suspected inhalation injury
o C = Circulation
Assess circulatory status peripheral pulses
Establish IV access
o D = Disability
Quick assessment of disability
Evaluate neurologic function
o E = Exposure / Environmental Control
Remove all clothing
Keep room warm, protect patient against heat loss with blanket
o F = Fluid Resuscitation / Pain Control
Physiologic salt solution (LR, NS) according to formulas
Analgesics IV morphine, titrate as needed, reassess often
Do not attempt to give a pill or write a prescription for a burn patient.
- Secondary Survey full examination
o Nasogastric decompression
o Urinary catheter to monitor resuscitation efforts
o Debride all burns
o Calculate extent and depth of burn
- Baseline labs ABG, CBC, hematocrit, BUN, creatinine, electrolytes, glucose, urinalysis, carbon monoxide
level, CXR, EKG, carboxyhemoglobin (can depend on extent of burn)
- Tetanus booster or immunoglobulin and immunization
- Nutritional requirements for burn patients may exceed twice normal. Whenever possible, use enteral
nutrition 30-35 nonprotein kcal/day; 1.5-2.0 grams protein/kg/day. Fat should not exceed 35% of diet
- To stop the burning process sterile water is usually sufficient. First look for powders if dealing with a
chemical substance pouring water on a chemical can activate it
Calculation of Burn Area
- Rule of Nines
- % of 2nd and 3rd degree burns
- Head is 9%, each arm is 9%, front of each leg is 9%, back of each leg is 9%, front of torso is 18%, back of
torso is 18%, groin is 1%

- Patients hand is approximately 1% TBSA

- Modify for children
- LundBrowder charts, more accurate based on age and body part
- First degree burns are not considered in surface area calculations.
Extent of Burn
- Patients palmar surface (hand + fingers) ~ 1% TBSA

ABA Burn Center Referral Criteria

- 2nd degree burns > 10% TBSA
- Burns to face, hands, feet, genitalia, perineum, major joints
- 3rd degree burns (Any body part anywhere)
- Electric injury (lightning included)
- Chemical burns
- Inhalation injuries
- Burns accompanied by trauma
- People with significant comorbidities (e.g., diabetes)
Fluid Resuscitation
- SIRS
- Edema
- Decreased CO (cardiac output)
- Increased PVR
- Burn Shock
- Acute Renal Failure
- Baxter / Parkland formula
o Guideline for total volume of the first 24 hours of resuscitation (with Ringer lactate [RL] solution) at
approximately 4 mL/kg body weight per percentage burn TBSA. With this formula, half the volume
is given in the first 8 hours postburn, with the remaining volume delivered over 16 hours.
- Why do you need fluid resuscitation?
o Edema maximum in 2nd 24 hours post burn decreased intravascular fluid decreased CO
increased PVR BURN SHOCK (distributive and hypovolemic) , hypoperfusion of tissues leading
to Acute Renal failure and possible brain damage
Adequate resuscitation ameliorates burn shock
Which IV Fluid to Use?

Parkland Formula
- 2-4 cc of LR x weight in kg x % BSA burned = total volume for 1st 24 hours
o in 1st 8 hours
o in 2nd 8 hours
o in 3rd 8 hours
- e.g. 100 kg patient with 30% BSA burn:
o 4 x 100 x 30 =12,000 cc: 6000 cc LR in first 8 hours post burn, then 6000 cc over next 16 hours
o Monitor urine output (0.5ml/kg/hr in adults and 1ml/kg/hr in children <30kg)
o Monitor pulmonary status
o Monitor BP and pulse
- Ringers Lactate solution is recommended
- Colloids can be introduced during the second 24 hours. However, use is controversial because thermal
injury of capillaries may make them particularly prone to leakage. Administration of colloids with leaky
capillaries may cause fluid loss from, rather than retention within, the intravascular space
- Although the Parkland formula serves as a guideline for resuscitation throughout the initial 24 hour postburn,
it is important to remember that the goal of resuscitation is to maintain adequate tissue perfusion while
avoiding complications of over or under resuscitation. The volume of resuscitation fluid infused should
maintain a urine output of 30 to 50 ml per hour in adults and 1 ml/kg/hr in children. It is often necessary to
modify the resuscitation formula and thus the infusion rate based on the patient's response to therapy.
Burn Wound Management
- Cleanse and debride
o Debride blisters > 2cm
o Daily cleaning and debridement, often use tub bath or whirlpool
- Apply topical antibiotics
o Silver sulfadiazine
o Mafenide acetate
- Vaseline gauze dressing after exudative phase
Antibiotics
- All burn wounds will become colonized
- Difference between colonization and spreading infection
o S. Aureus and Pseudomonas are most common pathogens
- Topical antibiotics prevent invasion
- Usually apply twice per day
Topical Antibiotics
- Silver nitrate
o Applied as an occlusive dressing
o No eschar penetration
- Silver Sulfadiazine (Silvadene, SSD) the most commonly used topical burn ointment
o Limited eschar penetration
- Mafenide Acetate (Sulfamylon)
o Good Gram-positive and negative coverage
o Penetrates eschar
o Extremely painful
o Take care when using in large amounts it can block the action of carbonic anhydrase and lead to
severe metabolic alkalosis
- Silver Products Antimicrobial properties
o Kills microbes on contact by poisoning microbe cellular respiration
o Speed of action directly correlated with the silver ion dose in contact with microbes
o Silver resistance is not seen

Safe and non-allergenic

Silver ion is known to have the following biochemical effects on a wound:

o Histologically decreases wound surface inflammation
o Decreases wound surface excess metalloproteinase activity likely by decreasing zinc, essential for
metalloproteinase (MMP) activity
o Oxidizes and binds to sulfur bonds, unlike Zinc and Copper which bind to oxygen. Sulfur bonds are
necessary for MMP activity
o Increase in wound calcium (a pro epithelialization effect)
Antibiotics
- Routine systemic antibiotics not indicated
- Indicated if:
o Suspected wound invasion
Discoloration of the wound
Erythema and induration at wound margin
Fever > 101.5 F
o Positive blood cultures
o Positive wound biopsy / culture
- SIRS = normal response to burns
Surgical Management
- Indications for surgery any burn that does not demonstrate eschar separation and epidermal budding
within 14 days of injury
- Burn wound excision to viable tissue
o Tangential Excision and Split thickness Skin grafting
For third degree burns and deep second degree
Often done in stages uses dermatomes to remove thin layers of eschar until viable
tissue, characterized by punctate capillary bleeding, is encountered
Usually limited to 15-20% TBSA
Accelerates hospital course and rehabilitation
o Fascial excisions with Split thickness Skin grafting for some deep 3rd degree burns
Scalpel or cautery to remove the entire skin and subcutaneous fat down to the level of
underlying fascia, which will support skin grafting
Disfiguring. Can result in joint stiffness and poor mobility
o Once excised, burn wounds are covered with split-thickness grafts obtained from unburned areas
of the body. These grafts are harvested by using the same dermatomes that are used for
tangential excision, set to a thickness of 0.005-0.015 inches
Infiltration of the subcutaneous tissue beneath the graft (or donor) site with balanced salt
solution is used to increase skin turgor, which facilitates harvesting. The addition of
epinephrine to this fluid reduces bleeding significantly
Skin grafts can be applied as intact sheets or expanded by cutting numerous small slits in
the skin, a technique called meshing. Meshed grafts are more durable and take readily,
although their cosmetic result is inferior to that of sheet grafts
- Deep dermal burns and full-thickness burns are typically excised on or about day 3
o Coverage is attained by numerous methods
o Autograph is the best method, but allographing of the skin is acceptable
o Other methods epidermal cell culture, artificial skin, and porcine xenograph

Complications
- Common complications of severe burns inhalation injury, hypovolemic shock, neurogenic shock
secondary to pain, renal failure, multiorgan system dysfunction, and gastric or duodenal ulcerations (termed
Curlings ulcers)
- The most common complications associated with all burns is infection of the burn wound, which has the
potential for hematogenous spread
- Chronic healing burn wounds can undergo malignant transformation into a squamous cell carcinoma
(Marjolins ulcer)
Escharotomy / Fasciotomy
- Address the need for escharotomy in circumferential burns of extremities or the anterior trunk, as they can
cause a compartment syndrome and make ventilation difficult
- Escharotomy a surgical incision into necrotic skin resulting from a severe burn; inelastic leathery dead
skin causing a tourniquet like effect. Rarely indicated prior to transfer
- Fasciotomy a surgical excision of fascia to relieve tension or pressure in muscle compartment
o Indicated for compartment syndrome
o Indicated in electrical burns with muscle injury
- Indications for escharotomy / fasciotomy (5 Ps)
o Pallor cyanosis of distal unburned skin on limb
o Pain unrelenting deep tissue pain
o Paraesthesia progressive numbness
o Paralysis usually late finding
o Pulselessness progressive decrease or absence of pulse
- Chest Escharotomy
o Indicated to relieve respiratory distress due to restricted chest wall excursion
o Location
Anterior axillary line bilaterally
Extend to adjacent abdominal wall as needed
Connecting costal margin transverse incision
- Extremity Escharotomy
o Circumferential full-thickness burns may impair circulation due to increase in edema
o Procedure
Avoid major vessels, nerves, all tendons
Mid-medial or mid-lateral aspect
Extend down through eschar, to subcutaneous fat
Extremity Compartment Syndrome
- Edema within (beneath) deep investing muscle fascia
- Results from
o High-voltage electric injury
o Massive IV fluid infusion
o Crush injury
o Delayed escharotomy (ischemic-perfusion injury)
- Patients with circumferential burns have the highest risk of developing a compartment syndrome and
demand the closest observation. If pulses are lost in an extremity, several issues must be addressed. First,
consider whether the lost pulses are a reflection of underresuscitation in a patient who needs more volume.
Second, consider whether the patient has associated trauma with a potential vascular injury. Lastly, consider
if a compartment syndrome has developed.
- Sustained compartment pressures in the range of approximately 30 mm Hg are considered high and are
suggestive of a compartment syndrome. Compartment pressures documented in the 40s necessitate an
escharotomy or fasciotomy for urgent release.

Pressure Ulcers
- Aka Decubitus ulcers
- Linked to pressure and shear forces over bony
prominences that exceeds local capillary perfusion
pressure. The normal capillary perfusion pressure is
about 30 mmHg, whereas the pressure over the
trochanter in a recumbent patient reaches 65 mHg. The
resulting lack of perfusion, if constant, may lead to tissue
necrosis in as little as 20-30 minutes
- Most patients who develop this complication have an inability to change position and, thus, sustain long
periods of uninterrupted pressure, with subsequent tissue ischemia
- Patients with spinal cord injury are at the greatest risk
- Quantitative wound culture is essential to differentiate between colonization and true infection
- Treatment should encompass a multimodal approach that includes removal of the pressure source,
supplemental nutritional support, and surgical intervention
- Reconstructive procedures are performed only after tissue cultures show that there is no evidence of
infection
- Treatment can include skin grafts or rotational flaps. Antibiotics should be reserved for those patients who
manifest clinical signs of septicemia
o Adequate absorption and removal of the exudate to keep bacteria counts low is very important
o Several dressing products are available the goals are to keep the wound moist and absorb
exudate
Infrequent dressing changes is key. Also protect the surrounding skin from maceration
and minimize skin injury from adhesive
The simplest occlusive dressing is a polyurethane film that facilitates moist healing and
has no absorptive capacity. It is useful for superficial wounds that have essentially no
exudate, such as skin-graft donor sites
The most widely used dressings for open wounds are of the hydrocolloid class. They
consist of hydrophilic materials combined with a special adhesive. Good for chronic
wounds
o Surgical excision of necrotic tissue is the fastest and most effective way to achieve a wound with a
healthy wound bed. Enzymatic debriding agents (collagenases and other proteases derived from
bacteria) can accomplish the same objective without surgery over a longer period. Only use if
wound sepsis is not a concern. A semiocclusive dressing left in place for several days can speed
up the patients own autolytic processes, leading to natural debridement. This option is relatively
inefficient and slow
o Artificial skin equivalents
o Physical devices for use in treating open wounds whirlpool treatments, hyperbaric oxygen
o Electrical stimulation
- Diabetics are at increased risk for atherosclerosis and ulcers due to arterial insufficiency. They are also
more prone to infection and have higher bacterial counts in wounds.
o Most chronic wounds in diabetics are on pressure points on the feet, such as the heel, metatarsal
joint surfaces, and the toes

Basal Cell Carcinoma

- The most common skin cancer. The most common cancer in humans.
- Malignancy of keratinocytes that arise within the epidermal layer of the skin
- Usually slow growing and locally destructive lesions. Metastasis virtually never occurs.
- Most common on the face, scalp, ears, and neck.
- Risk factors include cumulative sun exposure, white-skinned patients with poor tanning, albinos, sunburns
prior to age 14, arsenic ingestion, and prior XRT.
- Usually > 40 years old and M > F
- Several subtypes exist. They all vary in their appearance, aggressiveness, and treatment recommendations.
- NODULAR BCC:
o Most common variant of BCC
o Begins as pearly white or pink, translucent, dome-shaped papule with overlying random
telangiectasias
o As the papule gradually enlarges, the center flattens or ulcerates, the borders become raised or
rolled, and they frequently bleed and develop crust and/or scale
o Treatment includes ED&C, excision, and MMS for recurrent or high risk lesions
- SUPERFICIAL BCC:
o The least aggressive variant
o Seen more commonly on the trunk and extremities
o Usually erythematous and scaly papules or plaques, but may or may not have the rolled border
o May resemble psoriasis, eczema, seborrheic keratosis, Bowens Disease, or tinea corporis
o Treatment includes ED&C and excision
- PIGMENTED BCC:
o These lesions may resemble melanoma. They contain melanin, hence the pigmentation
o Thick, hard area of variegated pigmentation
o Treatment includes ED&C, excision, and MMS for recurrent or high risk lesions
- MORPHEAFORM BCC:
o Least common variant and also the most subtle
o White to yellow patch with poorly-defined borders
o With indistinct margins, the tumor cell may extend far beyond the borders from the clinical lesion
o MMS is the treatment of choice
- ULCERATING BCC:
o Ulcer with a rolled border, often covered with a crust
- SCLEROSING:
o Infiltrating carcinoma, white sclerotic patch with ill-defined border
Squamous Cell Carcinoma
- Potentially invasive, primary cutaneous malignancy of keratinocytes in the skin or mucous membranes
- Most common on the face, scalp, neck, and hands of older patients
- Most cause by ultraviolet radiation, chemicals (arsenic and hydrocarbons), tobacco, chronic infection,
chronic inflammation, burns, and human papillomavirus infection
- SCC accounts for approximately 20% of all skin cancers
- May appear as flesh-colored, pink, yellowish, or red-colored, indurated papules, plaques, or nodules with
scale. May be ulcerated or eroded
- Typically appear at sharply demarcated, scaling, or hyperkeratotic macule, papule, or plaque
o Erythema, scaling, erosions, and crusts may occur. May have a cutaneous horn a wartlike
structure in which the carcinoma is often present at the base of the horn
- Palpate regional lymph nodes for mets, especially for lesions on the ear, scalp, lips, and temples
o Most commonly goes first to the regional adjoining lymph nodes, followed by metastasis of the lung
- Treatment includes ED&C, excision, and MMS for recurrent or high-risk lesions

Radiation therapy is best reserved for three circumstances large lesions that cannot be surgically
resected, for use in patients who cannot undergo surgery, and as an adjunct to surgical care
Bowens Disease
- SCC in situ
- Usually presents as a slow-growing, slightly raised, red plaque with scale.
- Erythroplasia of Queyrat is squamous cell carcinoma in situ of the penis.
- Treatment includes 5-FU, cryotherapy, ED&C, excision, and MMS depending on location, patient, and size
Kaposis Sarcoma
- Indolent sarcoma due to herpesvirus-8.
- Among HIV-infected MSM, the frequency of Kaposi sarcoma fell from 40% to 15%.
- Painless, pigmented nodules, usually on LEs, diffuse pulmonary infiltrates, lymphedema.
- Treatment:
o In many instances, lesions resolve after institution of effective ART. Systemic chemotherapy can
cause remission in many patients with symptomatic visceral disease.
o Interferon, radiation, chemo
Melanoma
- Malignancy of melanocytes.
- Can be flat, raised, nodular, or ulcerated. Color is variable.
- Usually black or dark brown but can be flesh colored. Sometimes have blue, pink, or red components
- Irregular border with outward spreading of pigment. Keep an eye out for new or changing lesions
- This should be in your ddx for any new mole presenting in adulthood or any mole changing in size, shape,
or color.
- Use the ABCD criteria.
- When in doubt, a punch biopsy or incisional biopsy should be performed to ensure a full thickness specimen
for the pathologist
- Breslow level is the depth of the lesion measure in mm from the top of the clinical lesion to the bottom of the
lesion in the tissue specimen
- The Breslow depth is the most important prognostic indicator
- Clark level refers to the level of anatomic invasion and is important, especially in areas with thinner skin like
the eyelids, ears, and genitals
- MM is the 8th most common malignancy in the US
- The incidence of MM is rising faster than the rate of any other human cancer and the mortality rate is
increasing at a rate second only to lung cancer.
- It is the most common cancer in females 25-29 y/o & the second most common cancer in women 30-35 y/o
- Most commonly develop as a new growth, but 30% arise within a preexisting mole
- Risk factors include PMH or FMH of melanoma or atypical nevus, fair skin, blue eyes, blonde or red hair, UV
exposure from both sun and tanning beds, many moles, and history of blistering sunburns
- May appear anywhere on the body and exam should include LN palpation for mets
- Several subtypes exist
- Most common site of metastasis is the skin, but any organ may be involved. CNS mets is the most common
cause of death.
o Frequently metastasize widely to regional lymph nodes, skin, liver, lungs, brain
- Types:
o Lentigo Maligna Melanoma
o Superficial Spreading Malignant Melanoma (most common)
o Nodular Malignant Melanoma
o Acral Lentiginous Melanomas (palms, soles, nail beds)
- Excisional biopsy with 1-2 mm margins is the ideal specimen for diagnosis
o Ideally, the long axis of the excisional biopsy should be parallel to lymphatic drainage. This will
simplify therapeutic resection if the lesion is in fact a melanoma
-

SNL can aid in prognosis, but has no survival benefit.

o Use it for patients with tumors between 1-4 mm in thickness
o Biopsy of the sentinel node with radioactive technetium colloid to help map the draining nodes
o If the sentinel node is cancerous, will need further lymph node dissection
CXR and LDH measurement is sufficient for patients with tumors of intermediate risk
Chemotherapy has shown very modest survival benefit.
Therefore, the best treatment is early detection.
For in situ tumors (Clark level I), surgical resection with a 5 mm margin of healthy tissue down to
subcutaneous fat is sufficient
Tumors that invade up to 2 mm depth should be resected with 1 cm margins of healthy tissue down to but
not including the underlying muscular fascia
Tumors greater than 2 mm in depth should be resected with a 2 cm margin of healthy surrounding tissue
down to the underlying muscular fascia
On Nails:
o Dark brown or black pigmentation at the proximal nail fold (Hutchinsons Sign) is a sign of
melanoma
o Pigmented nail streaks are longitudinal pigmented bands (longitudinal melanonychia). Common
and normal in African Americans, but may be a sign of melanoma in Caucasians