Surgery Final Notes

MHAM
COLLEGE OF MEDICINE CLASS 2024

Fluid and Electrolyte Management in the Surgical Patient
Dr. Jan Michael Yap | August 25, 2021
SURGERY
Outline B. FLUID COMPARTMENTS

I. Body Fluids • Water is distributed evenly throughout all fluid
A. Total Body Water compartments
B. Fluid Compartments • Sodium is confined to ECF remains associated with
C. Osmotic Pressure water because of its osmotic and electrical properties
II. Body Fluid Changes • Sodium - containing fluids
® Increases volume of ECF
A. Normal Exchange of Fluid and
® Expands the interstitial space 3x as much as the
Electrolytes
plasma
B. Disorders in Fluid Balance • TBW is divided into 3 functional fluid compartments:
C. Disturbances in Fluid Balance ® Plasma
D. Volume Control ® Extravascular Interstitial Fluid
Extracellular Fluid
E. Concentration Changes ® Intracellular Fluid
F. Acid-Base Homeostasis • ECF + Plasma + Interstitial Fluid = 1/3 of Total Body
G. Metabolic Derangement Weight
III. Fluid and Electrolyte Therapy • ICF = 2/3 of Total Body Weight
A. Parenteral Solution
B. Alternative Resuscitative Fluids
C. Preoperative Fluid Therapy
D. Intraoperative Fluid Therapy
E. Postoperative Fluid Therapy
IV. Electrolyte Abnormalities in Specific Surgical
Patients
LEGENDS
Presentations remember lecturer previous
exams
Example: • Extracellular
• Important sentence might come out in exams.
® Cation Na
• Important points that lecturer said but not in book or ® Anion Cl, HCO3
ppt.
• Intracellular
® Cation K
I. BODY FLUIDS ® Anion HPO4, SO4
A. TOTAL BODY WATER • Plasma
• 50-60% TBW - reflects the amount of body fat ® Proteinaceous
® Lean Tissue > Fat
® Males > Females
® Malnourished > Obese
® Younger Age > Older Age
• The relationship between total body weight and
TBW is relatively constant
• Is primarily a reflection of body fat
• In an average young adult male TBW 60%
• In an average young adult female TBW 50%
• Estimates of percentage of TBW should be
adjusted downward
• Approximately 10% to 20% for obese individuals
and upward by 10% for malnourished individuals
• Newborns TBW 80% and decreases to
approximately 65% by 1 year of age
SURGERY TRANS 1.02 | Trans Team: Delos Santos, R., Edillor, Estremos, Guigayoma, Sogunle | Editor: Angus 1 of 10
C. OSMOTIC PRESSURE C. DISTURBANCES IN FLUID BALANCE
• Measure is osmoles or milliosmoles (mOsm) • Causes of volume deficits
® Number of osmotically active particles ® GI fluid loss
• The principal determinants: Sodium, Glucose, and ® Sequestration
BUN ® Soft tissue injuries
® Calculated serum osmolality = 2 sodium + ® Burns
(glucose/ 18) + (BUN/2.8) ® Intra-abdominal process
• 290 and 310 mOsm • Causes of Volume excess
• Change in osmotic pressure in one compartment is ® Iatrogenic
accompanied by a redistribution of water until the ® Secondary
effective osmotic pressure between compartments is ® Renal dysfunction
equal. ® CHF
® Cirrhosis
II. BODY FLUID CHANGES
A. NORMAL EXCHANGE OF ECF Volume Deficit
FLUID AND ELECTROLYTES • Most common fluid disorder in surgical patients
• The healthy person consumes an amount of about
2000 mL of water in a day and approximately 75% of
® Acute deficits
that water is taken from oral intake and the rest is
§ Cardiovascular and CNS signs
extracted from solid food ® Chronic deficits
• Insensible water losses are made up of basically two § Cardiovascular and CNS signs + tissues
routes: signs
® Skin (75%)
® Lungs (25%) ECF Volume Excess
• Insensible water loss can be increased by fever, • Plasma and interstitial fluid are increased
metabolism, and hyperventilation ® CV and pulmonary signs
D. VOLUME CONTROL
B. DISORDERS IN FLUID BALANCE • Basically, the body senses changes in fluid volume
• Volume through:
® Hypovolemia ® Osmoreceptors
® Hypervolemia § Detect mainly osmotic pressure
• Concentration § Specialized sensors that detect even the
® Hyponatremia smallest changes in fluid osmolality. Those
® Hypernatremia changes drive “thirst sensors” and “kidneys”
• Composition through diuresis.
® Acid-Base Imbalance ® Baroreceptors (aortic arch, carotid sinus)
§ Detect mainly blood pressure
® Changes in Calcium levels
• Hypothalamus is stimulated to secrete vasopressin,
® Magnesium
which increases water reabsorption in the kidneys.
® Potassium These mechanisms return the plasma osmolality to
normal.
• Baroreceptors modulate value in response to the • Signs and Symptoms of Hyponatremia
changes in pressure and circulating volume through
specialized sensors located in the aortic arch and
carotid sinuses.
• Baroreceptor responses are both:
® Neural, through sympathetic and
parasympathetic pathways
® Hormonal, through substances including renin-
angiotensin, aldosterone, ANP, and renal
prostaglandins.
• The net result of alterations in the renal sodium
excretion ad free water reabsorption is restoration of
volume to the normal state
E. CONCENTRATION CHANGES
• Changes in serum sodium concentration are inversely
proportional to TBW (total body water)
• Abnormalities in TBW are reflected by abnormalities
in serum sodium levels. • Evaluation of Hyponatremia
→ Systematic review of the causes:
§ Exclude hyperosmolar causes
SODIUM (hyperglycemia or mannitol) and
pseudohyponatremia
Hyponatremia § Depletional vs. Dilutional causes:
• A low serum sodium level occurs when there is an o Depletional - Dehydration extrarenal
excess of extracellular water relative to sodium. - Urine sodium is low (20 mEq/L)
Extracellular volume can either be high, normal or o Dilutional - High effective circulating
low. volume
→ In most cases of hyponatremia, sodium § Normal volume status: Evaluate for SIADH
concentration is decreased as a consequence of o For patients who underwent CNS or
either sodium dilution or depletion. spinal surgeries; the patient is unable
→ Dilutional Hyponatremia to excrete water due to high ADH
§ Frequently results from excess extracellular secretions.
water and therefore is associated with a high • Treated with free water restriction and administration
extracellular water and therefore is of sodium (severe cases)
associated with a high extracellular volume • Symptoms do not occur in serum Na (sodium) level
status. greater than 120 mEq/L
§ Postoperative patients are particularly prone → Symptomatic:
to increased secretion of Antidiuretic § 3% normal saline to increase Na
Hormone (ADH) which increases absorption (sodium) by no more than 1mEq/L
of free water from the kidneys with per hour until serum level reaches
subsequent volume expansion and 130 mEq/L or neurological symptoms
hyponatremia. improved
→ Depletional Hyponatremia → Asymptomatic:
§ Are associated with either decreased intake § Should increase the Na (sodium)
or increased loss of sodium containing fluids level by no more than 0.5mEq/L to a
§ Low ECF volume is most commonly seen maximum increase of 12mEq/L per
§ Most common causes: day.
o Decreased sodium intake, such as • Hyponatremia Correction
consumption of low-sodium diet or use ® Rapid Correction of Hyponatremia leads to:
of enteral feeds § Central Pontine Myelinolysis
o GI losses from vomiting o Manifested by: Seizures,
o Prolonged nasogastric suctioning weakness/paresis, akinetic
o Diarrhea movements, and unresponsiveness
o Renal losses due to diuretic use o Sometimes may lead to permanent
o Renal disease. brain damage and death
§ For every 100mg/dL increment in plasma
glucose above normal, the plasma sodium
Hypernatremia
should decrease by 1.6 mEq/L
§ We typically won’t see hyponatremia until the • Results from a loss of free water or a gain of sodium
sodium level goes below <120mEq/L that is in excess of water.
• Like hyponatremia it can be associated with an POTASSIUM
increased, normal or decreased extracellular volume
• Hypervolemic hypernatremia • Normal level: 3.5-5.50 mEq/L
® Usually is caused either by iatrogenic • The most abundant Intracellular cation
administration of sodium-containing fluids, • Normal values vary from laboratory to laboratory or
including excess sodium bicarbonate, or hospitals to hospitals.
mineralocorticoid as seen in → Potassium levels are maintained by renal
Hyperaldosteronism, Cushing syndrome, and excretion
Congenital adrenal hyperplasia. • 2% is located in ECF
• Normal Hypernatremia/Hypernatremia with → Important for cardiac and neuromuscular
normal ECF volume function
® Causes are basically non-specific. • Symptoms of abnormalities:
§ Skin losses → GI
§ GI losses → Neuromuscular
§ Renal water loss → Cardiac
§ Renal disease
§ Diuretics
§ Diabetes Insipidus
• Hypovolemic Hypernatremia
® Basically, water losses are non-renal water loss.
§ Skin losses
§ GI losses
§ Renal water loss
§ Renal (tubular) disease
§ Osmotic diuretics
§ Diabetes Insipidus
§ Adrenal Failure
• Symptoms of Hypernatremia
• HYPERKALEMIA vs HYPOKALEMIA
• Hypernatremia Correction
→ Treat water deficit
§ Hypovolemic - normal saline
§ Euvolemic - hypotonic fluid (5% dextrose, 5%
dextrose in 1/4 normal saline, Enteral water)
→ Remember that glucose level in the blood
correlates closely with sodium levels.
→ It is important to choose properly the parenteral
fluid to use in correction of sodium.
→ Water deficit is calculated as such: → Most hyperkalemic patients have a history of
• Water deficit (L) = Serum Na - 140 x TBW 140 potassium supplementation
• Estimate TBW as 50% in men; 40% in women → Long lasting BT (Blood Transfusions)
• Rate of correction § In which RBC tend to undergo lysis during
→ No more than 1mEq/h and 12 mEq/d for BT process. For it is in the RBC where most
accurate hypernatremia. potassium is contained.
→ 0.7 mEq/h for chronic hypernatremia → Endogenous load/destruction
• Rapid concentration can lead to CEREBRAL EDEMA § Potassium is an abundant intracellular
AND HERNIATION cation.
§ Any cell destruction will cause a spike in
potassium levels.
§ ECG changes that often lead to cardiac
arrest
→ Cardiac arrest (pulseless electrical activity or
asystole)
• Hypokalemia Correction
→ K repletion (replenish potassium stores)
§ Rate of repletion is determined by the
symptoms:
o Oral repletion: If patient is mild and
asymptomatic
o IV route: Symptomatic or unable to
tolerate oral route
- 10-20 mEq/h (unmonitored
→ Most hypokalemic patients we see that in most setting)
cases there is: - (With ECG monitoring) increase to
§ Inadequate intake 20-40 mEq/h
§ Excessive Potassium Excretion - Special consideration should be
§ GI losses exercised when there is renal
impairment or renal failure
Hyperkalemia
• Goal of Therapy
→ Reduction of the total body K
§ Cation-exchange resin (kayexalate)
§ Chelation can be done
→ Shift K from extracellular to intracellular, this is
done by using either:
§ Glucose and bicarbonate
§ Insulin
§ Albuterol (also Salbutamol)
→ Protect the cells from the effects of increased K
§ By giving the patient Calcium chloride &
§ Calcium carbonate
→ All exogenous sources of K should be
discontinued.
→ DIALYSIS - when conservative measures fail
(severe cases)
• Treatment
→ Potassium removal
§ Kayexalate
§ Oral administration is 15-30g in 50-100mL of
20% sorbitol
§ Rectal administration is 50g in 200mL of
20% sorbitol
§ Dialysis
→ Shift potassium
§ Glucose 1 ampule of D50 and regular insulin
5-10 units IV CALCIUM
§ Bicarbonate 1 ampule IV
→ Counteract cardiac effects • <1% of Ca in the body is in ECF.
§ Calcium gluconate 5-10 mL of 10% solution → It is primarily contained in the BONE.
• Normal Value: 8.5 to 10.5 mEq/L
Hypokalemia → 40% is protein bound
• Symptoms → 10% is complexed
→ Ileus → 50% is ionized (4.2 - 4.8 mg/dL) (iCa)
→ Constipation § Most physicians order iCa levels because
→ Weakness it is the most abundant portion of the
→ Fatigue calcium that can be measured in the body.
→ Diminished tendon reflexes § It correlates with Neuromuscular stability.
→ Paralysis • Since it is protein bound, there is a strong correction
→ ECG changes with Albumin or protein levels.
§ Shows the severe cases • If Albumin is decreased by 1g/dL, Total Ca should
decrease by 0.8mg/dL
• pH affects iCa concentrations → Associated hypokalemia and hypomagnesemia
• Total body calcium balance is under complex should be corrected because hypocalcemia will
hormonal control be refractory if hypomagnesemia is not
corrected.
Calcium Abnormalities
PHOSPHORUS
HYPERCALCEMIA HYPOCALCEMIA
• Hyperparathyroidism • Pancreatitis • This is a primary Intracellular anion
• Bony metastasis • Massive soft tissue infections • Contained in
• PTHrp (PTH • Renal failure → Metabolically active cells
Recombinant Protein • Pancreatic and small bowel → High-energy phosphate product
Therapy) fistulas • It is renally excreted (Renal Excretion)
• Hypoparathyroidism
• TSS (Toxic Shock Syndrome)
Phosphorus Abnormalities
• Mg-abnormalities
• Tumor lysis syndrome • Hyperphosphatemia
• Parathyroidectomy → It is mainly due to decreased urinary excretion
• Malignancy § Impaired renal function
• Massive blood transfusion § Hypoparathyroidism or Hyperthyroidism
→ Increased intake of
• Symptoms of Calcium Abnormalities § IV hyperalimentation solutions
§ Phosphorus containing laxative
INCREASED SERUM DECREASED SERUM → Endogenous mobilization of phosphorus as in
LEVELS OF CALCIUM LEVELS OF CALCIUM
cell destruction
(2.5mg/dL)
→ Patients are mainly asymptomatic
Anorexia, Nausea/vomiting, Hyperactive reflexes, → In Metastatic deposition of soft tissue and
Abdominal pain Paraesthesias, Calcium-Phosphorus complexes they may
Carpopedal spasm, convert to a symptomatic stage
Seizures • Hypophosphatemia
→ It is due to decrease intake in
Weakness, Confusion coma, Heart failure § Malabsorption
Bone pain § Administration of phosphate binders
→ Decreased dietary intake
Hypertension, Arrhythmia,
§ Intracellular shift of phosphorus
Polyuria
§ Respiratory alkalosis
Polydipsia § Insulin therapy
§ Refeeding syndrome
§ Hungry bone syndrome
Hypercalcemia Correction → Increase in excretion
• Treat when symptomatic (> 12mg/dL serum level) → Patients may be asymptomatic until levels fall
→ Initial management: significantly
§ Correct volume deficit, because most of § Cardiac dysfunction or muscle weakness
these cases are volume problems not an
actual calcium problem Phosphorus Correction
§ Induce brisk dialysis with normal saline • Hyperphosphatemia Correction
o Dialysis done is different from that of → Patient will be given phosphate binders
the kidney, here the blood is just (sucralfate)
washed out with more fluid → Calcium acetate tablets, which are useful when
hypocalcemia is also present
Hypocalcemia Correction → Dialysis
• Correction is done based on the type of patient’s • Hypophosphatemia Correction
symptomatology → Patients are managed depending on the level of
→ Asymptomatic: depletion and tolerance to oral
§ Oral or IV calcium supplementation.
→ Acute symptomatic:
§ IV with 10% calcium gluconate
§ CaCO3 suspension 1250mg/5mL Q6 MAGNESIUM
§ Ca gluconate 2gm/IV over 1h
§ These are done to achieve serum levels • It is the 4th most common mineral in the body
7-9 mg/dL • Half of the total body content is in bone
• ⅓ in ECF is bound to albumin
Magnesium Abnormalities F. ACID-BASE HOMEOSTASIS
● Hypermagnesemia ● Normal value of pH of the body is 7.35-7.45
→ Severe renal insufficiency → Any values less than 7.35 is Acidosis
→ Magnesium containing antacids and laxatives → Any value more than 7.45 is Alkalosis
→ TPN- Total Parenteral Nutrition → The narrow range pH (7.35-7.45) is maintained
→ Massive trauma by the ability of the kidneys to generate very
→ Thermal injury large amounts of bicarbonate and also the
→ Severe acidosis normal large acid load produced by the body as
● Hypomagnesemia a by-product of metabolism.
→ Decreased intake ● Important buffers: This indigenous acid load is
■ Starvation, Alcoholism, Prolonged IV fluid efficiently neutralized by buffer systems
therapy, and TPN with inadequate → Intracellular proteins and phosphates
supplementation of magnesium → Extracellular bicarbonate-carbonic acid system
→ Increased renal excretion
■ Alcohol abuse, Diuretic use, Compensation for Acid-Base Derangements
Administration of amphotericin B, and ● We have compensatory mechanisms like the kidneys
Primary aldosteronism. and your lungs. All of these helps maintain a normal
→ Pathologic losses acid homeostasis
■ GI losses ● It is important to note that in the correction of acid-
→ Manifested mainly by neuromuscular and base balance the compensation is basically the
central nervous system hyperactivity, Cardiac counterpart of the buffer
function like Arrhythmias. ● If the problem is mainly metabolic the compensation
→ Magnesium correlates closely with albumin and is respiratory system
calcium so can produce hypocalcemia and lead ● If the problem is mainly respiratory the compensation
to persistent hypokalemia is metabolic (kidneys)
● Symptoms of Magnesium Abnormalities ● Important buffers:
INCREASED SERUM DECREASED SERUM
→ Intracellular proteins and phosphates
LEVELS OF LEVELS OF MAGNESIUM → Extracellular Bicarbonate-Carbonic System
MAGNESIUM ● Compensation for acid-base derangements
→ Respiratory compensation
Nausea / Vomiting - → Metabolic compensation
Weakness, Lethargy, Hyperactive reflexes, G. METABOLIC DERANGEMENT

Decreased reflexes Muscle tremors, Tetany,
Seizures
Hypotension, Arrest Arrhythmia
Hypermagnesemia Correction
→ Withhold exogenous sources of magnesium
■ Correct volume deficit
■ Correct acidosis if present with bicarbonate
→ Calcium chloride (5 to 10 mL) - To antagonize
the cardiovascular effects
→ Dialysis - In severe cases
Hypomagnesemia Correction
● Oral: Mild and asymptomatic patients
● IV: Symptomatic patients
→ Severe deficits (< 1.0 mEq/L) or symptomatic: Metabolic Acidosis
→ 1 to 2g of MgSO4 IV over 15 minutes or over 2 • Increase intake of acids
minutes if with torsade’s de pointes
• Increase generation of acids
■ Can be administered either IV
(Intravenous) or IM (Intramuscular) • Increase loss of carbonate
● Calcium gluconate • Compensatory Response:
→ Will counteract the adverse side effects of a → Produce buffers
rapidly rising magnesium level circulating agent → Increase ventilation
● Correct hypocalcemia which is frequently associated → Increase renal reabsorption and generation of
with hypomagnesemia bicarbonate
→ Increase secretion of Hydrogen ion
Anion Gap (AG) ● Treatment
• Need to be measured in evaluation patients with → Replacement of volume deficit with isotonic
metabolic acidosis and low serum bicarbonate level saline and K once adequate urine output is
• ensured
An index of unmeasured anions
→ AG = [Na] – [Cl + HCO3]
→ Normal AG is 8-12 mmol/L
→ Corrected AG = actual AG – (2.5 [4.5-albumIN])
• Calculating the anion gap is clinically useful, as it
helps in the differential diagnosis of a number of
disease states
• Bicarbonate: Controversial; can lead to
→ Metabolic Alkalosis (Hypoxemia/arrhythmias)
→ Intracellular Acidosis (Carbonic acid)
→ Respiratory Acidosis (Increase PCO2)
• Metabolic acidosis with normal AG
→ Acid administration
→ HCl/NH4 Respiratory Acidosis
→ Loss of bicarbonate ● Most are acute in nature and secondary to alveolar
→ GI losses (diarrhea, fistulas) hyperventilation
→ Ureterosigmoidostomy ● ETIOLOGY
→ Renal loss → Pain or anxiety
• Bicarbonate loss is accompanied by a gain of → Neurologic disorders (Meningitis, Trauma)
chloride; thus, the AG remains unchanged → Drugs (Salicylates)
→ Fever
Metabolic Alkalosis → Gram negative bacteremia
• Develops only when an increase in both bicarbonate → Thyrotoxicosis
generation and impaired renal function occur → Hypoxemia
• Hypochloremic hypokalemic metabolic alkalosis ● Hypocapnia causes uptake of K and PO4 and
increased binding to calcium to albumin
(hypokalemia, hypophosphatemia, and
hypocalcemia)
● Signs/Symptoms
→ Arrhythmias, Paresthesias, Muscle cramps,
Seizures
● Treatment
→ Treatment of underlying cause
→ May also require direct treatment of
hyperventilation
• Concomitant hypokalemia (extracellular K ions

exchange with intracellular H ions to buffer excess
(HCO3)
● Initially, urinary bicarbonate levels are high to
compensate for alkalosis
● H ion reabsorption also ensues with an accompanied
K ion excretion
● Aldosterone- mediated sodium reabsorption is
accompanied by K ion excretion III. FLUID AND ELECTROLYTE THERAPY
● Resulting hypokalemia causes excretion of H+ ions in A. PARENTERAL SOLUTION
the face of alkalosis (a paradoxic ACIDURIA) • The type of fluid administered depends on the
patient’s volume status and the type of concentration
or compositional abnormality present
• Plasma-Lyte, lactated Ringer’s solution, and normal → Acute deficits - Cardiovascular signs
saline are considered isotonic and are useful in predominate accompanied by oliguria and
replacing GI losses and correcting extracellular hemoconcentration.
volume deficits. → Correct volume deficits before surgery as much
as possible.
B. ALTERNATIVE RESUSCITATIVE FLUIDS → Resuscitate with isotonic crystalloid basically
Colloids LACTATED RINGER’S, PLASMA-LYTE or
NORMAL SALINE.
• Confined to Intravascular space (high MW) therefore
→ CV signs: Give bolus 1-2L followed by
more efficient plasma volume expander
continuous infusion.
• Can cause/worsen edema and impair tissue
→ Adequacy of resuscitation is measured by
oxygenation under conditions of severe hemorrhagic
reversal of signs of volume deficit (When there
shock (increased capillary membrane permeability)
is reversal of signs especially when the urine
• 4 major types: output has become adequate but this may take
→ Albumin several hours also).
→ Dextran → Accompanying electrolyte abnormalities should
→ Hetastarch
be corrected first prior to surgical intervention.
→ Gelatins
D. INTRAOPERATIVE FLUID THERAPY
• Induction of anesthesia - Hypotension will develop
if volume deficits are not corrected preoperatively
→ Avoided if volume deficit is corrected
preoperatively
→ Replace ongoing losses
→ Provide adequate maintenance
• Intraoperative volume loss is caused by:
→ Blood loss (from the operation itself)
→ Third-space loss in open abdominal surgeries
(once you open up the abdomen you are freeing
up any fluid that was contained inside of the
abdomen, you are freeing it up for release.)
E. POSTOPERATIVE FLUID THERAPY

• Fluid therapy should consider:
→ Current volume status
C. PREOPERATIVE FLUID THERAPY → Projected ongoing losses
• Maintenance Fluids → Preoperative losses
→ First 0-10 kg: 100 mL/kg per day → Intraoperative losses
→ Next 10-20 kg: Additional 50 mL /kg per day → Third space losses
→ For weight >20kg: additional 20 mL/kg per day • Adequacy of resuscitation should be guided by
→ Example: restoration of vital signs, urine output, base deficit or
§ A 60 kg female would receive a total of lactate
2300 mL of fluid daily:
• CVP line may be inserted to guide fluid therapy
§ 1000 mL for the first 10 kg of the body
weight (10 kg x 100 mL/kg per day)
§ 500 mL for the next 20 kg (10 kg x 50
Fluid Management in ERAS (Enhanced Recovery
mL/kg per day), and After Surgery) Pathway
§ 800 mL for the last 40 kg (40 kg x 20 • It is a joined approach by anesthesiology and the
mL/kg per day) surgical field.
• Volume deficits should be considered in: • Basically, led by anesthesiologist and they have
→ Emesis established guidelines in treatment of patients who
→ Diarrhea are undergoing the ERAS PATHWAY.
→ Poor oral intake • 2011 European Society of Anesthesiology
→ GI obstruction Guidelines
→ Peritoneal /bowel inflammation → Clear liquids up to 2 hours prior to surgery
→ Ascites → Carbohydrate and electrolyte-rich fluids
→ Crush injuries → Restriction of intra- and postoperative sodium
→ Burns and intravenous fluids
→ Severe soft tissue infections → Postoperatively early enteral intake
• Diagnosis basically here of volume deficits is primarily Special Considerations for the Postoperative
clinical and based on the history of the patient. Patients
• Patient may have cases where there are VOLUME § Cellular uptake of electrolytes
EXCESS this is basically caused by: (Phosphate, Magnesium, Potassium, and
→ Overestimation of third-space losses Calcium)
→ GI losses that are difficult to quantitate § Severe hyperglycemia may result from
→ Weight gain- earliest sign of volume overload blunted basal insulin secretion
→ ¼ to ½ pound/day: Average weight loss of → Prevention: Correct underlying electrolyte and
postoperative patients not receiving nutritional volume deficits.
support, but an increase in weight in a patient § Thiamine
who is post op should be a red flag to the doctor § Caloric repletion should be instituted
→ Peripheral edema slowly and should gradually increase
• Patients may have also VOLUME DEFICIT which is over the first week.
caused by:
→ Preoperative losses not completely corrected Cancer Patients
→ Intraoperative losses underestimated • Fluid and electrolyte abnormalities are very common.
→ Postoperative losses greater than appreciated • Tumor Lysis Syndrome
→ Tachycardia, Orthostasis, Oliguria, → Rapid release of uric acid, K, and phosphorus
Hemoconcentration → Hyperuricemia, Hyperkalemia,
• Management Hyperphosphatemia, Hypocalcemia, and Acute
→ Depend on the amount and composition of fluid renal failure
loss; Isotonic solution → Lymphomas, Leukemias, a number of solid
tumors
V. ELECTROLYTE ABNORMALITIES IN § Develops following chemotherapy,
SPECIFIC SURGICAL PATIENTS radiotherapy
Neurologic Patients → Management:
• Syndrome of Inappropriate Secretion of § Volume expansion
Antidiuretic Hormone (SIADH) § Correct electrolyte
→ Head injury
→ Surgery to CNS
→ Drugs (Morphine, Nonsteroidal and Oxytocin)
→ Pulmonary disease (Pneumonia, Abscess,
Tuberculosis)
→ Endocrine disease (Hypothyroidism and
Glucocorticoid deficiency)
→ Malignancies (Small-cell cancer of the lungs,
Pancreatic CA, Thymoma, Hodgkin’s disease)
• Laboratories:
→ Euvolemic and Hyponatremic with elevated
urine Na (usually greater than 20 mEq/L) and
urine osmolality
→ ADH stimulation is considered inappropriate in
that it is not caused by osmotic or volume-
related condition
• Management: Correction of underlying problem
• GOAL: Achieve water balance but to avoid volume
depletion the compromises’ renal function
→ Restriction of free water
→ Furosemide
→ Isotonic or hypertonic fluids
• Neurologic Patients Chronic SIADH
→ Long-term fluid restriction is difficult to maintain
or Demeclocycline and Lithium can be used.
Malnourished Patients
• Refeeding Syndrome
→ Rapid and excessive feeding of patients with
severe underlying malnutrition
→ Shift in metabolism from fat to carbohydrate
substrate
§ Stimulates insulin release
MHAM
Shock
Dr. Cedric Lester Amodia | September 8 & 15, 2021
SURGERY
Outline
I. Learning Objectives
II. Definition of Terms
III. Pathophysiology of Shock
IV. Ischemia-Reperfusion Injury
V. Classifications of Shock
A. Hypovolemic Shock
B. Cardiogenic Shock
C. Vasodilatory Shock
D. Septic Shock
E. Neurogenic Shock
F. Obstructive Shock
G. Traumatic Shock
→ The most common pattern is Septic Shock which
VI. Core Principles in Management is due to infection. The trigger to initiate the
A. Assessment of Endpoints process leading to shock are the bacterial
B. Controversies on Fluid Resuscitation products (Lipopolysaccharides). They will
C. Blood Transfusion activate pattern recognition receptors (TLRs,
D. Hypotensive Resuscitation RAGE) causing cellular activation. Eventually
VII. Shock Review leading to shock.
→ Trauma causes tissue injury, which will release
LEGENDS DAMPs (HMGB1, Heparan Sulfate) that will
Presentations remember lecturer previous activate pattern recognition receptor activation.
exams Eventually this process will lead to shock.
→ The most common is the septic shock and the
trauma shock.
I. LEARNING OBJECTIVES → But basing on the diagram, they termed it as
hemorrhagic shock/loss of blood.
General Objective
→ The Hemorrhagic shock, Acute Heart Failure and
• To understand the pathophysiology and diagnosis of
Neurogenic shock do not undergo inflammatory
shock as well as the priorities for their management.
reactions, it immediately proceeds to decreased
tissue perfusion because their effect is directly
Specific Objectives in the intravascular volume. Due to decrease
• To understand the pathophysiology of shock and blood flow, leading to cellular hypoxia or ischemia
Ischemia-Reperfusion Injury and eventual shock.
• To know the different patterns of shock and the
principles and priorities of resuscitation III. PATHOPHYSIOLOGY
• To know the appropriate monitoring and endpoints of ATP + H2O → ADP + Pi + H+ + Energy
resuscitation → The formula shown above is for the release of energy
from the ATP.
II. DEFINITION OF TERMS → When there is patient injury, there will be a decrease
• Shock: “A momentary pause in the act of death. “ in the energy substrate. Then there will be increase
– John Collins Warren, 1800S utilization of ATP. Once ATP is consumed, it will be
→ Shock is not a disease, It is a state of the body divided into ADP and Phosphate, and its biproduct is
→ Inadequate organ perfusion to meet the tissue’s Hydrogen Ion.
oxygenation demand → When there is decrease energy, the formula goes
→ Inadequate removal of cellular waste products forward to produce more energy, and at the same
• Summary of the different patterns of shock: time more hydrogen ion.
→ When there is increase in hydrogen ion, there will be
decrease in pH. A decrease in pH is acidosis. The
body becomes more acidotic. Therefore, patients with
shocks presents metabolic acidosis.
→ Acidosis results from the accumulation of acid when
during anaerobic metabolism the creation of ATP
from ADP is slowed.
→ Hydrogen shifts extracellularly and metabolic
acidosis.
SURGERY TRANS 1.04 | Aniñon, Cullantes, Delos Santos, R., Edillor, Estremos, Guigayoma, Pelayo, Sogunle, Ursal, Ymbong | Editor: Angus, Tiu 1 of 9
IV. ISCHEMIA-REPERFUSION SYNDROME Stages or Spectrum of Shock
→ Direct effects of tissue hypoxia and local activation of • Preshock aka compensated/warm shock
inflammation → Up to 10% reduction in blood volume
→ Acid and potassium load lead to direct myocardial → Tachycardia- initial compensatory mechanism
depression, vascular dilatation and further regardless of the etiology
hypotension. • Shock
→ Cellular and humoral elements flushed back into the → Compensatory mechanisms overwhelmed
circulation cause further endothelial injury. → 20-25% reduction in blood volume
→ Attenuated by reducing the extent and duration of the • End-organ dysfunction – end phase
tissue hypoperfusion. → Leads to irreversible organ damage/death
→ In summary (for the ischemia part of the syndrome),
when there is tissue hypoxia, there is local activation
of inflammation.
→ When there is local activation of inflammation, there
will be a release of cellular and humoral elements
which are the inflammatory mediators. This is the first
part of the syndrome; the Ischemia.
→ The second part of the syndrome is Reperfusion.
When the tissue, which is initially ischemic or hypoxic,
becomes reperfused, oxygen will be introduced which
will now interact with the cellular and humoral
elements producing superoxide, O2-, H2O2, and
Vicious Cycle of Shock
oxygen radicals. The molecules produced are very
toxic to the healthy tissues • 4 Major injuries that may cause to the patient
• Ischemia, cellular and humoral elements are → Decreased Venous Return- seen in Hypovolemic
produced. Shock
• Reperfusion, there is introduction of oxygen which is → Metabolic Acidosis + Intracellular Fluid loss =
exposed to these elements producing harmful oxygen Cellular hypoxia- seen in Septic Shock
molecules and radicals which is then flushed back → Decreased Coronary Perfusion- seen in
into the circulation leading to endothelial injury. Cardiogenic Shock
Reperfusion of hypoxic tissue doesn’t mean you • All of which will cause decreased cardiac output. The
doing the patient a favor, rather you are causing more decreased in cardiac output will directly lead to
injury to the patient. decreased tissue perfusion leading to parenchymal
injury à Endothelial Activation and damage still
V. CLASSIFICATIONS OF SHOCK progressing back to à Decreased Tissue perfusion
• Blalock Classification of Shock (not the latest à feeding the initial injury (refer to 4 Major Injuries
classification) that may cause to the patient)
→ Basic Hypovolemic Shock- it is loss of
circulating blood volume (i.e., it is intravascular) The Triad of Death
→ Vasogenic Shock- it is decrease in resistance
within capacitance vessels (capillaries and
veins)
→ Neurogenic Shock- it is acute loss of
sympathetic vascular tone. The vascular tone
are the arterioles.
→ Cardiogenic Shock- failure of the heart as a
pump
• Clinical Classification
→ Hypovolemic shock- loss of circulating blood
volume
→ Distributive (Vasodilatory) Shock
§ Septic
§ Neurogenic → When your patient is going to shock, they will
§ Anaphylactic present acidosis (the increase in your hydrogen
§ Adrenergic ion concentration). A patient in acidosis will lead
→ Cardiogenic Shock to defect in coagulation cascade (lead to loss of
§ Intrinsic permeability in endothelial lining, so there will be
§ Compressive loss in volume) which leads to hypothermia à
→ Obstructive Shock leads to malfunction of enzymes and causes
→ Traumatic Shock further acidosis.
→ Patient will spiral towards an organ deficiency Natural History of Shock
and organ shock and eventual irreversible and
organ damage and death.
→ Once patient is in acidosis eventually, they will
have:
§ Coagulopathies- which will lead to
hypothermia and after will lead to end organ
dysfunction.
Clinical Features
*Memorize the entire table
• Treatment
→ Secure the airway
→ Control the source of blood loss
→ Intravenous volume resuscitation
→ Acidosis
§ H+ ions cannot be measured directly on the B. CARDIOGENIC SHOCK
tissue so they try to measure it using the • Pump Failure (Heart)
SERUM LACTATE that is why it is called • Mechanical complications
LACTIC ACIDOSIS. → Acute Mitral regulations form Papillary Muscle
→ Patients already in severe shock they will be Rupture
presenting with end organ damage. → Ventricular Septal Defect
→ ANURIA (represents the renal function) → Free-wall Rupture
→ COMATOSE (represents the neurologic → Pericardial Tamponade (Obstructive shock)
function) → Right Ventricular Infarction
• Signs that the patient is proceeding to end organ • Other causes
dysfunction: → End-stage Cardiomyopathy
→ Anuric → Myocarditis
→ Loss of consciousness → Severe Myocardial Contusion
→ Labored breathing or being intubated → Prolonged Cardiopulmonary Bypass
→ Severe hypotension. → Septic Shock with Severe Myocardial Depression
→ Left Ventricular Outflow Obstruction
A. HYPOVOLEMIC SHOCK → Obstruction to Left Ventricular Filling
• With total body depletion → Acute Aortic Insufficiency
→ Hemorrhage • Circulatory pump failure
→ GI Tract losses → Diminished forward flow and subsequent hypoxia
→ Renal losses • Hemodynamic criteria
§ Central DI or Diabetes Insipidus which → Sustained hypotension
causes urine output of about 3,000-4,000 → Reduced cardiac index
§ Patients who are taking furosemide, they → Elevated pulmonary artery wedge pressure
have increase renal output • 60-80% mortality
→ Skin losses • Myocardial Infarction
→ Open wound losses → Most common cause, always consider that they
→ Burns might go into cardiogenic shock
• Without total body fluid depletion → Myocardial Ischemia à Myocardial dysfunction
→ Redistribution of the intravascular fluid to the à Myocardial ischemia
interstitial or intracellular space • Signs
→ Decreased preload due to increased → Hypotension
intravascular capacity (Distributive Shock) → Cool and mottled skin
• Acute blood loss à Decreased baroreceptor → Depressed mental status
stimulation à Decreased inhibition of vasoconstrictor → Tachycardia
centers; Diminished output (Atrial Stretch Receptors) → Diminished pulses
à Increase vasoconstriction & Peripheral arterial • Diagnostics
resistance → ECG (Acute MI: ST elevation/NSTEMI)
• HYPOVOLEMIA à SYMPATHETIC STIMULATION → Echocardiography/2D echo
→ CXR
→ ABG D. SEPTIC SHOCK
→ Electrolytes • Sepsis: Evidence of an infection & systemic signs of
→ CBC inflammation
→ Cardiac Enzymes (CK-MB / Trop I) If infection & local signs, it’s cellulitis not sepsis
→ Invasive cardiac monitoring • Severe sepsis
§ Excludes Right Ventricular Infarction, → Hypoperfusion with signs of organ dysfunction
Hypovolemia, and possible mechanical • Septic shock
complications → Severe sepsis with more significant evidence of
Tachycardia is always the initial compensatory tissue hypoperfusion and systemic hypotension.
mechanism → Other presentation like anuria, lethargy, and
• Treatment labored breathing
→ Maintenance of adequate O2 • Treatment
→ Fluid administration → Fluid resuscitation and restoration of circulatory
§ Before proceeding to further treatment, check volume
for any electrolyte imbalance → Antibiotics- the initial treatment should be broad
→ Pain management (Morphine) spectrum antibiotics
→ Anti-arrhythmic drugs, pacing or cardioversion → Vasopressors- more preferred vasopressor is
→ Inotropic support (Dobutamine/Dopamine) Norepinephrine/Epinephrine for anaphylactic
§ Improves cardiac contractility and cardiac reaction
output → Intensive insulin therapy- because of Insulin
• Surgical treatment of choice resistance
→ Percutaneous Transluminal Coronary → Activated Protein C
Angiography (PTCA) → Corticosteroids
C. VASODILATORY SHOCK (DISTRIBUTIVE) E. NEUROGENIC SHOCK

→ Patients with VS are usually secondary to → Diminished tissue perfusion from loss of
systemic response to infection (Septic shock) vasomotor tone to peripheral arterial beds
• Non-infectious systemic inflammation • Etiology
→ Pancreatitis → Spinal cord injuries
→ Burns → Spinal cord neoplasms
• Anaphylaxis → Spinal epidural/anesthetics
® Vasodilation secondary to an exogenous trigger. → Iatrogenic injury- the most common cause
Trigger maybe toxin secondary to insect bite or • Classic Description
exposure to food. → Decreased blood pressure
• Acute adrenal insufficiency → Warm extremities
® Addison’s disease → Motor & Sensory deficits
• Metabolic → Radiographic evidence of vertebral column
® Hypoxic lactic acidosis fracture
® Carbon monoxide poisoning • Management
• Prolonged severe hypotension secondary to → BP Control
® Hemorrhagic shock → Oxygenation
® Cardiogenic shock → Hemodynamics
® Cardiopulmonary bypass → Preferred medication is phenylepinephrine
• Failure of the vascular smooth muscle to constrict
® Capacitance vessels or veins and capillaries F. OBSTRUCTIVE SHOCK
• Characterized by: • Results in mechanical obstruction of venous return
® Peripheral vasodilation with resultant hypotension (lack of venous return à shock)
® Resistance to treatment with vasopressors • Causes
• Final common pathway for profound and prolonged ® Pericardial tamponade
shock ® Pulmonary embolus
• 30-50% mortality ® Tension pneumothorax
• Findings: ® IVC obstruction can be caused by:
® Enhanced Cardiac Output § Deep venous thrombosis
® Peripheral Vasodilation § Gravid uterus on IVC
§ Neoplasms
® Fever- Inflammatory response
® Increased intrathoracic pressure
® Leukocytosis- Inflammatory response
® Excess positive end-expiratory pressure
® Hyperglycemia- Insulin resistance (hallmark of
sepsis)
Tension Pneumothorax
iNOS à vasodilatory effects
® Most common in trauma patients
® Reduced filling of the right side of the heart from § Best performed in the OR under GA
increased intrapleural pressure secondary to § Approaches:
air accumulation o Subxiphoid incision
® Decreased cardiac output with increased venous o Transdiaphragmatic
pressure o Upon relief of tamponade,
• Diagnosis and Treatment hemodynamics improves dramatically
® Classic findings in Tension pneumothorax are: o Exposure of the heart can be achieved
§ Respiratory distress by extending the incision to a median
§ Diminished breath sounds sternotomy, performing a left anterior
§ Hyperresonance thoracotomy, or performing bilateral
anterior thoracotomies (‘clamshell’)
Cardiac Tamponade § Access the pericardium and to get a
• Beck’s Triad: specimen sample for biopsy
→ Hallmark symptoms of Cardiac tamponade: § Fluid from the pericardium can be drained
§ Hypotension through the window
§ Muffled heart sounds § The fluid will drain towards the thorax
§ Neck vein distension (preferably the left hemothorax), and insert
→ Present only in 30% of cases a tube at the left hemothorax to drain the
pericardial fluid
® Occurs when sufficient fluid has accumulated in
§ In essence, what you’re performing is
the pericardial sac to obstruct blood flow to the
simple decompression. You decompress
ventricles
the thorax and pericardium. And that’s how
® Caused by pericardial effusion; An increased
you treat your obstructive shock.
intrapericardial pressure
® Heart cannot fully expand; Results in limited
G. TRAUMATIC SHOCK
ventricular filling of the right side of the heart
• Non-infectious and pro-inflammatory.
® The major determinant of the degree of
• Systemic response after trauma (soft tissue injury,
hypotension is pericardial pressure
long bone fractures, and blood loss will release
• Invasive hemodynamic monitoring may support the
DAMPs that triggers the response).
diagnosis of cardiac tamponade if the ff are present:
→ Elevated central venous pressure
Trauma à DAMPs à TLRs à RAGE à↓Tissue
→ Pulsus paradoxus
perfusion à SHOCK
→ Increased right atrial and right ventricular
pressure
• Treatment:
• Patients who present with circulatory arrest from
→ Control of hemorrhage
cardiac tamponade require emergency pericardial
→ Adequate volume resuscitation
decompression, usually through a left thoracotomy
→ Debridement of necrotic tissues
• Treatments: → Stabilization of bony injuries
® Pleural / Pericardial Decompression → With emergent orthopedic procedures
® Immediate Tube Thoracostomy → Appropriate treatment of soft tissue injuries
§ For Tension Pneumothorax (during
emergencies: “Needle Thoracostomy”) VI. CORE PRINCIPLES IN MANAGEMENT
§ Should be inserted rapidly, but carefully,
• Secure airway
and should be large enough to evacuate
• Prompt control of active hemorrhage
any blood that may be present in the pleural
space. • Volume resuscitation
§ Most recommended level:
o Fourth intercostal space (Nipple Goal of Treatment
level) at the anterior axillary line. • Restoration of adequate organ perfusion & tissue
® Echocardiography oxygenation.
§ The preferred test for diagnosis of cardiac
tamponade A. ASSESSMENT OF ENDPOINTS
® Pericardiocentesis • Managing patients in shock you need to have
§ For Pericardial Tamponade endpoints and know how to measure.
§ Used to diagnose pericardial blood and • In systemic measure, you have to understand that in
potentially relieve tamponade managing trauma, you have to replace your oxygen
§ Safer and reliable with ultrasound (2D debt, because your trauma is decreasing oxygen
Echo) guidance supply (hypoxia). Oxygen is the molecules needed to
® Diagnostic Pericardial Window bring your patient out of acidosis.
§ Represents the most direct method to • Oxygen Transport
determine the presence of blood within the → Supranormal O2 transport variables
pericardium § O2 delivery >600mL/min per sq. meter
§ Cardiac index >4.5L/min per sq. meter • Right Ventricular End-Diastolic Volume Index
§ O2 consumption index >170mL/min per sq. (RVEDVI)
meter → Correlate with preload-related increases in
→ Inability to repay O2 debt- predictor of mortality & cardiac output
organ failure → LVP > 320 mmHg L/min per sq. meter
§ If you are unable to replace O2 debt, most → invasive and rarely used
likely the patient will go into severe shock
and becomes irreversible injured B. CONTROVERSIES ON
→ O2 debt correlates with serum lactate and base FLUID RESUSCITATION
deficit
• Crystalloid / Colloid solutions
→ Very difficult to measure the actual tissue oxygen
→ No difference in overall mortality, length of stay,
concentration
or incidence of pulmonary edema
• Classifications of Measure: → Marginal benefit with the infusion of hypertonic
→ Systemic/Global saline (7.5% Sodium Chloride)
§ Lactate → Immunomodulatory
§ Base deficit
§ Cardiac output
C. BLOOD TRANSFUSION
§ Oxygen delivery and consumption
→ Tissue specific • Used to avoid Hemodilution
§ Gastric tonometry • Inherent risks:
§ Tissue pH, oxygen, carbon dioxide levels → Transfusion reactions
§ Near infrared spectroscopy → Infection
→ Cellular → Immunosuppression
§ Membrane potential • When to transfuse?
§ Adenosine triphosphate (ATP) → Hgb (7.0-9.0g/dL) & Hct levels (>30%)
§ For acute/Sudden blood loss, transfuse if
Systemic/Global Hgb is at 9 or 10 g/dL
§ For chronic, transfuse if 7 g/dL
• Lactate § Appropriate in the treatment of critically-ill
→ Conversion of pyruvate (lactate patients
dehydrogenase) in the setting of insufficient
oxygen (anaerobic environment)
D. HYPOTENSIVE RESUSCITATION
→ Metabolized by the liver (50%) and kidneys
(30%) • Conclusion:
→ Indirect measure of oxygen debt → Any delay in surgery for control of hemorrhage
→ If there is still O2 debt there is still serum lactate increases mortality
→ With uncontrolled hemorrhage attempting to
(↑ O2 debt = ↑ Serum Lactate)
achieve normal BP may increase mortality
• Base Deficit
§ SBP goals:
→ (ABG) amount of base in millimoles that is
o Penetrating injury: 80-90 mmHg
required to titrate 1L of whole blood to a pH of
o Blunt injury: 110 mmHg
7.40 with the sample fully saturated with O2 at
→ Profound hemodilution should be avoided by
37°C and PaCO2 of 40mmHg
early transfusion of RBC in a ratio 1:1:1
§ Mild (3-5 mmols)
§ Moderate (6-14 mmols)
§ Severe (>15 mmols) VII. SHOCK REVIEW
Serum Lactate and Base Deficit are the most commonly 1. Which of the following hormones is not under
used measures in assessing endpoints in patients in direct Anterior Pituitary regulation?
shock.
a. ACTH
b. Cortisol
Tissue Specific
c. Growth Hormone-Releasing Hormone
• Gastric Tonometry
→ Used to assess perfusion of GIT d. Thyroid Stimulating Hormone
→ pHi ≥ 7.3 indicates decrease in O2 delivery e. Insulin-like Growth Hormone
§ Good prognosis indicator
• Near infrared spectroscopy Answer: C
→ Measure tissue oxygenation & redox state of
Rationale: Growth Hormone-Releasing Hormone is
cytochrome α, α3
→ Direct; the amount of the oxygen is measured posterior while the rest are anterior pituitary regulation
directly from the tissue; rarely used
• Tissue pH, O2, & CO2 Concentrations
→ Tissue probes with optical sensors
2. Which of the following statements about Tumor 6. A 25-year-old man is involved in a car crash while
Necrosis Factor (TNF) is not true? travelling in excess of 70mph. He sustains an
intrabdominal injury and a fracture of the femur. The
a. It is not one of the earliest mediators of host blood pressure is 60/40 mmHg, and the haematocrit
responses to injury or infection is 16%. There is likely to be a proportionately greater
b. It is a potent mediator of host response due to its increase in blood to which of the following organs?
prolonged half-life in the body
c. During stress, It shunts the available amino acids a. Liver
to the hepatic circulation as fuel substrates b. Kidneys
d. Kupffer cells represent the single largest c. Heart
concentration of cells that synthesize TNF d. Skin
e. The primary sources of TNF synthesis include e. Thyroid gland
monocytes/macrophages and T cells
Answer: C
Answer: B Rationale: Heart and Brain
Rationale: Not prolonged, it has short half-life 7. A 57-year-old man is involved in a moving vehicle
3. Which of the following is not related to accident. He suffered significant blunt trauma in the
catecholamine release during severe injury? sternum during the accident. He has a systolic BP of
95, CVP of 15 and normal Chest Xray. Which of the
a. Ketolysis following is the likely cause of the hypotension?
b. Gluconeogenesis
a. Cardiac contusion
c. Inhibits aldosterone release
b. Spinal cord injury
d. Glycogenolisis
c. Myocardial infarction
e. Lipolysis
d. Intraabdominal hemorrhage
Answer: A e. Cardiac tamponade
Rationale: Found in patients with prolonged starvation; Answer: C

the rest are injury patients.
Rationale: Rule out cardiac contusion because you have
4. The initiating event in shock is normal chest x-ray. No Spinal cord injury because the
injury is in the sternum. Intraabdominal haemorrhage will
a. Hypotension present with decrease CVP and cardiac tamponage will
b. Decreased Cardiac output present with elevated CVP and enlarge cardiac shadow.
c. Electrolyte Imbalance
d. Cellular energy deficit 8. Shock following severe carbon monoxide
e. Decreased Oxygen delivery poisoning is most commonly
a. Hypovolemic shock
Answer: D
b. Obstructive shock
Rationale: Hypotension (severe), Decreased Cardiac c. Cardiogenic shock
output (pre-shock), Electrolyte Imbalance (not related), d. Vasodilatory shock
Decreased Oxygen delivery (pre-shock), Cellular energy e. Neurogenic shock
deficit (shock phase)
Answer: D
5. Which of the following can be used to indirectly
estimate the oxygen debt? Rationale:
a. Arterial pH
b. Arteriolar-alveolar o2 Gradient
c. Pulmonary capillary wedge pressure
d. Base deficit
e. Serum bicarbonate
Answer: D
Rationale: Should be base deficit and lactate

Source: Brunicardi, F. Schwartz’s Principles of Surgery
concentrate. The rest of the choices are direct.
11th Ed. Page 146
9. A 35 year old man is admitted with systolic BP of When feasible, percutaneous transluminal coronary
60mmHg and a heart rate of 150bpm following a angioplasty (generally with stent placement) is the
gunshot to the liver. What is the effect on the treatment of choice.
kidneys?
Coronary artery bypass grafting seems to be more
a. They undergo further ischemia if hypothermia is appropriate for patients with multiple vessel disease or left
present main coronary artery disease.
b. They are affected and cause an increased
Source: Schwartz 9th ed., p. 106.
creatinine clearance
c. They tolerate satisfactorily ischemia of 3-4hrs 12. A 70-year old woman has low cardiac output with
duration increased PCWP and increased systemic vascular
d. They can become damaged, even though urine resistance. What should be the drug of choice?
output exceeds 1500cc/day
a. Dopamine
e. They are prevented from further damage by
b. Norepinephrine
vasopressors
c. Dobutamine
Answer: D. d. Epinephrine
e. Phenylphrine
10. A patient arrives at the ER following a motor
vehicular accident with multiple injuries. Hypotension Answer: C
in this patient is defined as systolic BP less than:
Rationale: Dobutamine is the drug of choice for
a. 110 mmHg improving cardiac function. It is a β1-receptor agonist and
b. 100 mmHg increases myocardial contractibility and also reduces
c. 90 mmHg afterload by β2 effect. Dopamine at low doses (1–3
d. 80 mmHg mg/kg/min) stimulates dopaminergic receptors and
e. 70 mmHg increases renal blood flow. At moderate doses (3–10
mg/kg/min), it stimulates β-receptors, resulting in a
Answer: A positive inotropic and chronotropic effect. Systolic and
mean BP are increased; whereas, diastolic BP is usually
Rationale: Recent data in trauma patients suggest that a unchanged. At higher doses (10–20 mg/kg/min),
systolic blood pressure of less than 110 mmHg is a stimulation of α-receptors occurs and it significantly
clinically relevant definition of hypotension. increases systemic vascular
resistance. Norepinephrine, epinephrine, and
Source: Schwartz 11th Edition Chapter 5 page 142
phenylephrine are powerful vasoconstrictors.
11. A 73 year-old woman suffered an acute MI and 12
Source:
hours later is in Cardiogenic shock. Which of the
https://accesssurgery.mhmedical.com/content.aspx?boo
following is the best treatment for this patient?
kid=585&sectionid=44023639#6398006
a. Inotropic support until stabilized then PTCA
13. A 20-year-old man involved in a car crash
(Percutaneous Transluminal Coronary
sustained severe injuries to the chest, abdomen, and
Angiography)
lower extremities. He is intubated and requires
b. Immediate PTCA to define anatomy followed by increasing concentration of Oxygen to main his pO2.
coronary artery bypass graph The pathologic changes do which of the following?
c. Immediate PTCA with stenting if needed
d. None of the above a. They cause the alveolar capillary membrane to
become more impermeable
Answer: C b. They most frequently occur after severe injuries
c. They show characteristic localized pattern on x-
Rationale: Current guidelines of the American Heart
ray
Association recommend percutaneous transluminal
coronary angiography for patients with cardiogenic shock, d. They are associated with low compliance
ST elevation, left bundle-branch block, and age less than e. They involve a decrease in dead space
75 years. ventilation
Early definition of coronary anatomy and Answer: C

revascularization is the pivotal step in treatment of
patients with cardiogenic shock from acute MI. Rationale: Increased airway resistance (stiff lung) may
be noted early in shock lung. The alveolar capillary
membrane becomes more permeable. There is a leak of
a high-protein fluid from the capillary to the interstitial
tissues and then into the alveoli. This is commonly called
ARDS. Sepsis syndrome is the most frequent cause of
ARDS (39%), followed by aspiration, multiple transfusion,
massive soft-tissue injury, multiple traumas, near
drowning, fat embolism, DIC, and pancreatitis. ARDS is
associated with ventilation–perfusion imbalance. In some
areas of lung, there is ventilation with no perfusion,
whereas, in other areas, nonventilated alveoli are being
perfused. The net result is decrease in functional residual
capacity, shunting, and increased dead space ventilation.
Chest x-ray reveals diffuse alveolar infiltration, and
findings are normal in the initial stage.
Source:
https://accesssurgery.mhmedical.com/content.aspx?boo
kid=585&sectionid=44023639#6398006
14. In septic shock, which of the following is true?
a. The mortality rate is between 10 to 20%

b. Gram negative organisms are involved
exclusively
c. Two or more organisms are responsible in most
cases
d. The majority of patients are elderly
e. The most common source of infection is the
alimentary tract
Answer: D
Rationale: A. Mortality is 30-50%, B. Gram negative

organisms are not exclusive. C. Commonly mono-
infection. E. Most common: UTI vs Implants.
15. Recommended first line vasopressor in cases of

septic shock that is non responsive to fluid challenge.
a. Dopamine
b. Dobutamine
c. Epinephrine
d. Amiodarone
e. Lidocaine
Answer: C
Rationale: A. Dopamine and B. Dobutamine: Inotropic

(cardiac contractility), C. Epinephrine: Vasoconstrictor –
In septic shock, a vasodilatory shock is experienced and
a vasoconstrictor is given to counteract the shock. D.
Amiodarone and E. Lidocaine are antiarrhythmics.
*Questions from Dr. Amodia’s lecture
MHAM
Trauma
Dr. Jayson B. Sia | October 7, 2021
SURGERY
Outline
I. Trauma
II. Primary Survey
A. Airway
B. Breathing
C. Circulation
D. Disability
E. Exposure
III. Concurrent Resuscitation
IV. Secondary Survey
V. Diagnostic Evaluation
VI. Definitive Care
VII. Classes of Blood Loss
VIII. Fluid Resuscitation
IX. Common Radiographic and Laboratory Tests
X. Examination of the Head
A. Neck
XI. Examination of the Chest
XII. Examination of the Abdomen
XIII. Trauma A. AIRWAY
• Ensuring a patent airway is the first priority in the
LEGENDS primary survey.
Presentations remember lecturer previous • All patients with blunt trauma require cervical spine
exams immobilization (hard collar or placing sandbags in
both sides of the head with the patient’s forehead
taped across bags to the backboard) until injury is
I. TRAUMA excluded.
• Most common cause of death for all individuals → In trauma patients, until proven otherwise, you
between the ages of 1 and 44 years. should expect that there is a possibility of cervical
• Third most common cause of death regardless of injury.
age. • Patients who are conscious, do not show
• Most common cause of years or productive life lost. tachypnea, and have a normal voice do not require
• Initial management of seriously injured patients early attention to the airway EXCEPT the following:
according to the Advanced Trauma Life Support → Patients with penetrating injuries to the neck
(ATLS) consists of the following: with an expanding hematoma.
→ Primary survey → Evidence of chemical or thermal injury to the
→ Concurrent resuscitation mouth, nares, or hypopharynx.
→ Secondary survey → Extensive subcutaneous air in the neck.
→ Diagnostic evaluation → Complex maxillofacial trauma.
→ Definitive care → Airway bleeding
• Goal is to identify and treat conditions that constitute
an immediate threat to life.
I. PRIMARY SURVEY
• Assessment of the “ABCDE”
→ Airway with cervical spine protection
→ Breathing
→ Circulation
→ Disability • Indications for establishing a definitive airway:
→ Exposure → Patients with apnea
→ Inability to protect the airway due to altered
mental status (low GCS)
§ Ex. Patient is sleepy or cannot be roused
→ Impending airway compromise due to
inhalation injury, hematoma, facial bleeding, soft
tissue swelling, or aspiration.
→ Inability to maintain oxygenation.
SURGERY TRANS 1.06 | Trans Team: Aniñon, Cullantes, Delos Santos, R., Edillor, Estremos, Guigayoma, Pelayo, Sogunle, Ursal, Ymbong | Editor: Angus, Tiu 1 of 11
Types of Airway Management
• Nasotracheal Approach
® Only done in patients, who are breathing
spontaneously, requiring emergent airway
support in whom chemical paralysis cannot be
used.
• Orotracheal
® Most common technique to establish a
definitive airway.
→ When doing tracheostomy, it is usually inserted

at the second or third tracheal rim.
B. BREATHING
• Once a secure airway is obtained, adequate
oxygenation and ventilation must be assured
• All injured patients should receive supplemental
oxygen and be monitored by pulse oximetry
• Surgical (Cricothyroidotomy) • The following conditions constitute an immediate
® Done in patients whom attempts at intubation threat to life due to inadequate ventilation:
have failed or who are precluded from intubation ® Tension Pneumothorax
due to extensive facial injuries. ® Open Pneumothorax
® In patients under the age of 11, ® Flail Chest with Underlying Pulmonary
cricothyroidotomy is relatively contraindicated Contusion
due to the risk of subglottic stenosis, and
tracheostomy should be performed.
Tension Pneumothorax
• Lung on the right:

® Collapsed
® Filled with air
• Presence of tracheal deviation going to the left.
• Diagnosis
→ Diagnosis is implied by respiratory distress and
hypotension in combination with any of the
following physical signs in patients with chest
• Surgical (Emergent Tracheostomy)
trauma:
® Indicated in patients with laryngotracheal
§ The tracheal deviation away from the
separation or laryngeal fractures in whom
affected side
cricothyroidotomy may cause further damage or
§ Lack of or decreased breath sounds on the
result in complete loss of airway.
affected side. When the right lung (refer to
the figure above) is auscultated, there will be
decreased breath sounds
§ This picture shows a subcutaneous
emphysema.
• Treatment
→ Needle thoracostomy decompression in the
2nd ICS in the MCL may be indicated in the acute
setting
→ Closed tube thoracostomy should be
performed immediately before a chest radiograph
is obtained → Then put a cover, seal the incision site
→ The purpose of needling is to decompress the → Then the hemothorax and pneumothorax is
trapped air in a particular lung. Then followed by monitored regularly, because these are the
the closed tube thoracostomy. parameters to know when to remove the CTT.
• According to the latest ATLS, needling should be

done at the 4th to 5th ICS in the mid-clavicular line
Open Pneumothorax
(MCL), instead of the 2nd ICS in the MCL in adult
patients. (This is the latest recommendation when • Occurs with full thickness loss of the chest wall,
doing needling). permitting free communication between the
pleural space and the atmosphere
• Complete occlusion of the chest wall defect
WITHOUT a tube thoracostomy may convert an open
pneumothorax to a tension pneumothorax
• The defect is temporarily managed with and occlusive
dressing that is taped on three sides, which allows
accumulated air to escape from the pleural space
thus prevent tension pneumothorax.
Figure: Site for needling
• Closed Tube Thoracostomy

→ You have to identify which part of the rib to insert,
usually in the 4th or 5th rib, mid to anterior axillary
line
→ Then you violate the pleura; insert fingers to know
that you are in the pleural space
→ Then insert the tube
→ When this occurs, you tape the wound area, 3

sides, to convert it into a one-way valve
→ Meaning air can go out but cannot go in; chest is C. CIRCULATION
a negative pressure • Initial approximation of the patient's cardiovascular
→ Then insert a CTT away from the open status can be obtained by palpating peripheral
pneumothorax pulses
→ Do not use the open pneumothorax site for the → Carotid pulse: 60 mmHg systolic BP
site of CTT → Femoral pulse: 70 mmHg
• Treatment → Radial pulse: 80 mmHg
→ Definitive treatment is closure of the chest wall • Any hypotensive episode (SBP <90 mmHg) is
defect and closed tube thoracostomy remote assumed to be caused by hemorrhage until proven
from the wound otherwise in a trauma patient
• IV access for fluid resuscitation is obtained with 2
Flail Chest with Pulmonary Contusion peripheral catheters, 16 gauge or larger in adults
• Flail Chest, the fracture is two-point in one rib and • In patients under 6 years old, an intraosseous
continuous is at least three or four successive ribs. needle (indicated for patients in whom one or two
• Occurs when 3 or more contiguous ribs are fractured attempts at IV access have failed) - can be placed in
in at least 2 locations the proximal tibia (preferred) or distal femur of an
unfractured extremity
• A rule of thumb to consider for secondary access is

placement of femoral access for thoracic trauma
and jugular or subclavian access for abdominal
trauma
• Internal jugular or subclavian catheters provide a
more reliable measurement of Central Venous
Pressure (CVP)
• When you inhale, the air goes into your lungs • Saphenous vein cut down are excellent sites for fluid
• However, due to the flail chest, the particular area resuscitation access
where there is multiple refracture, it will depress in
that area causing atelectasis
• When you exhale the air goes out of the lungs, the
particular place is dilated or goes the other way,
causing paradoxical breathing
• Associated pulmonary contusion is typically the
source of post injury pulmonary dysfunction
(decreased compliance and increased shunt fraction)
• Treatment
→ May require presumptive intubation and
mechanical ventilation
• External control of any visible hemorrhage should be
achieved promptly while circulating volume is
Massive Air Leak restored
• Occurs from major tracheobronchial injuries • Manual compression of open wounds with ongoing
→ Type I injuries are those occurring within 2 cm bleeding should be done with a single 4 × 4 gauze
of the carina; not associated with a and a gloved hand
pneumothorax due to the envelopment in the → Never put a tourniquet on the extremity where
mediastinal pleura there is bleeding because it will cause necrosis
→ Type II injuries are more distal injuries within if you put a tourniquet for a long period of time.
the tracheobronchial tree and manifest with
pneumothorax
• Bronchoscopy confirms diagnosis and directs
management.
• Early in the course of tamponade, blood pressure and
cardiac output will transiently improve with fluid
administration
• Treatment
→ Pericardiocentesis is successful in
decompressing tamponade in approximately
80% of cases. Landmark is the Xiphoid Process
→ If a weapon is still in place, it should be removed and estimate a 45 degrees angle and insert a
in the operating room because it could be large board needle in the pericardial area.
tamponading a lacerated blood vessel.
Four life-threatening injuries must be identified

promptly
• Massive hemothorax
• Cardiac tamponade
• Massive hemoperitoneum
• Mechanically unstable pelvic fractures with bleeding
Three critical tools used to differentiate these in Emergency Department Thoracotomy

the multisystem trauma patient • Patients with a SBP <70
mmHg warrant emergency
• Chest Radiograph department thoracotomy
• Pelvis Radiograph (EDT) with opening of the
• Focused Abdominal Sonography for Trauma (FAST) pericardium to address the
injury.
Massive hemothorax • EDT is best accomplished
• Defined as >1,500 mL of blood or, in the pediatrics, using a left anterolateral
1/3 of Patient’s blood volume in the pleural space thoracotomy, with the
• After a blunt trauma, hemothorax is usually due to incision started to the right
multiple rib fractures with severed intercostal of the sternum
arteries, but occasionally bleeding is from lacerated
lung parenchyma
• After a penetrating trauma, a systemic or
pulmonary hilar vessel injury should be presumed
• Treatment: Operative intervention
Cardiac Tamponade
• Occurs most commonly after penetrating thoracic
injuries, although occasionally blunt rupture of the
heart, particularly the atrial appendage, is seen
• <100 mL of pericardial blood may cause pericardial
tamponade (in an acute setting)
• Beck’s Triad (Dilated neck veins, Muffled heart
tones, Decline in arterial pressure) is NOT often
observed. You need to correlate the history and the
physical examination you have
• Diagnosis is best achieved by ultrasound of the
pericardium (FAST)
*Memorize this table
*Memorize clinical signs and symptoms
• Left anterolateral thoracotomy (You open the left side

of the chest, then do also chest compression during
that said procedure. If your patient is rested during the E.g A 45 year patient who presented with a multiple stab
said procedure, you can open the pericardium space
wound in the chest and abdomen, arrived in the
if there is cardiac tamponade)
emergency room with a pulse rate of <120, hypotensive,
• Left anterior lateral thoracotomy is a good access in
a patient with trauma. respiratory rate of <30 to 40, urine output of >50. What
class is that? Answer: Class III
Glasgow Coma Scale (GCS) Score *Very important to know this, so you will know what
• Should be determined for all injured patients amount/volume blood is lost the patient, based on the
• Scores of 13 to 15 indicate mild head injury, 9 to 12 parameters in the table. (PE)
moderate injury, <9 severe injury
• Abnormal mental status should prompt an immediate VII. CLASSES OF BLOOD LOSS
re-evaluation of the ABCs and consideration of • CLASS I
central nervous system injury ® <1L of blood loss
• CLASS II
® 750-1000mL of blood loss
• CLASS III
® 1-2L
• CLASS IV
® >2L of blood loss
Trauma patient with blood loss the Goal is to:
• Re-establish tissue perfusion

• Monitor the Urine Output
® Is a quantitative, reliable indicator of organ
perfusion
Quantity of acute blood loss correlates with physiologic
abnormalities ® Know the normal urine output
• Adult
• Tachycardia ® 0.5 to 1mL/kg/hr
® Earliest sign of on-going blood loss • Child
® Watch out for relative tachycardia (HR ® 2mL/kg/hr
<90 in patients with a resting pulse rate • Infant
in the 50s) ® <1 year of age
• Bradycardia
® An ominous sign, occurs with severe VIII. FLUID RESUSCITATION
blood loss, often heralding impending • Begins with a 2L[1L fluid + 1L blood products] (adult)
cardiovascular collapse or 20ml/kg (child) IV bolus of isotonic crystalloid
• Hypotension ® Typically Ringer’s Lactate
® NOT a reliable early sign of hypovolemia • Persistent Hypotension
® Because blood volume must decrease by ® Repeated once for Adults
>30% before hypotension occurs
® Repeated twice in a Child → Vaginal examination with speculum also should
o Before RBCs are administered be done in women with pelvic fractures to exclude
• Monitor as well the vital signs an open fracture (OB-GYN may help with the
® To check the response of your resuscitation examination)
→ Nasogastric tube (NGT) should be inserted in
ALL intubated patients - contraindicated in
During Resuscitation patients with mid-facial fractures
Based on the initial response to fluid resuscitation, → Foley catheter should be inserted in patient
hypovolemic injured patients can be separated into three unable to void to:
broad categories:
• Decompress the bladder
• Responders
• Obtain a urine specimen
® Know if the patient is responding to the
• Monitor urine output
resuscitation
® Individuals who are stable or have a good Contraindications of foley catheter, until the patient with
response to the initial fluid therapy as signs of urethral injury has undergone urologic
evidenced by normalization of vital signs, evaluation:
mental status, and urine output → Blood at the meatus
• Transient responders → Perineal or scrotal hematomas
® Even though you’re pushing fluids or blood, → A high-riding prostate
and patient is still not responding; idea to
bring the patient in the operating room Presence of these prohibits catheter insertion
® Volume loading by an increase in blood
IX. COMMON RADIOGRAPHIC & LAB TESTS
pressure only to then hemodynamically
Severe blunt trauma patients:
deteriorate once more
• Non-responders → Lateral cervical spine radiograph (neck x-ray)
® These patients have persistent hypotension → Chest radiograph
despite aggressive → Pelvic radiograph
Once the immediate threats to life have been All these 3 should be obtained. (The Big 3)
addressed:
Truncal gunshot wound patients:
• Thorough history – is obtained
• Anteroposterior and lateral radiographs of both
® Patient is examined in a systematic fashion
chest and abdomen - in order to identify the
trajectory of the gunshot
*Remember the mnemonics: “AMPLE”
Allergies, Medications, Past illnesses or Pregnancy (for Critically Injured Patients

penile patients), Last meal, and Events related to the LABORATORY:
Injury • Routine trauma panel
→ Type and cross-match
*Primary survey the “E” is exposure
→ CBC
*Secondary survey the “E” is Events → Blood chemistry
→ Coagulation studies
→ Physical exam should be head to toe with special → Lactate level
attention to patient’s back, axilla and perineum, → Arterial blood gas analysis (ABG)
because injuries here are easily overlooked CBC and blood typing are the most important if immediate
→ All potentially serious injured patients should operation should be done
undergo digital rectal examination to check for
sphincter tone (atony may signify injury in the Less Severely Injured Patients
spinal cord), presence of blood, rectal LABORATORY:
perforation, or a high-riding prostate (non-
palpable prostate because the prostate is already • CBC
floating with blood around it) • Urinalysis
→ DRE (Digital Rectal Examination) is particularly
critical in patients with suspected spinal cord → All injured patients undergoing operation should
injury, pelvic fracture, or trans pelvic gunshot receive preoperative antibiotics
→ Extended postoperative antibiotic therapy is X. EXAMINATION OF THE HEAD
given ONLY FOR OPEN FRACTURE or • Scalp
SIGNIFICANT INTRA-ABDOMINAL • Eyes
CONTAMINATION • Ears
→ Tetanus prophylaxis is given to all patients • Nose
→ Give DVT prophylaxis particularly in trauma • Mouth
patients who are: • Facial bones
o With multiple fractures of pelvis and lower • Intracranial sutures
extremities
o In coma or with spinal cord injury
→ Important to perform eye examination early because
o Requiring ligation of large veins in the orbit swelling may impede later examination
abdomen and lower extremities → Tympanic membrane is examined to identify
hemotympanum, otorrhea, or rupture which may
These patients are at risk of venous thromboembolism
signify an underlying disease
and its associated complication → All patients with a significant closed head injury (GCS
score <14) should undergo CT scanning of the head
• Lower Molecular Weight Heparin (LMWH) → Elderly patients or those patients on antiplatelet
→ Initiated as soon as bleeding has controlled agents or anticoagulant should be imaged despite a
and there is no intracranial pathology GCS of 15
→ High-risk patients, removal of inferior → Pain skull films may be helpful in penetrating head
vena caval filters should be considered if injuries
there are contraindications to
administration of LMWH A. NECK
• Pulsatile compression stockings or sequential If you have a neck injury, it is very important as well to
compression device identify the locations of the injuries.
→ Used, unless there are fractures
• Divided into three distinct zones that is important in
the management of neck injuries
→ Zone 1: Below Clavicle
→ Zone 2: Between Clavicle and mandible
→ Zone 3: Above angle of mandible
• Thermal protection
→ Maintains a comfortable ambient
temperature, covering stabilized patients
with warm blankets, and administering
warmed IV fluids and blood products
→ Temperature is very important in a trauma
patient because it affects the outcome
• Imaging option include CT scan or five plain
(done by thermoregulation)
radiograph views of the cervical spine:
→ Ex. A hypothermic and hypotensive patient may → Lateral view with visualization of C7-T1
be at risk → Anteroposterior view
• PRBC should be given if: → Transoral odontoid views
Ø Hgb level: <7 /dl → Bilateral oblique views
Ø 10g/dL : Endpoint of acute phase • Identification of penetrating injuries to the neck with
resuscitation exsanguination, expanding hematomas and airway
• Fresh Frozen Plasma (FFP) is transfused to keep obstruction is apriority during the primary survey.
INR 1.5 and PTT <45 sec
• 100,000/L is the target platelet count with massive
transfusion
• RATIO IN ADMINISTRATION- 1:1:1
→ 1 UNIT OF PRBC, 1 UNIT OF FPP, 1 UNIT OF
PLATELET
Memorize and understand the figure below. Memorize the table below:
• Algorithm for the management of penetrating neck • Penetrating thoracic injuries

injuries. CTA = computed tomographic angiography; → Proper imaging
GSW = gunshot wound. → Pericardial ultrasound
→ CVP measurements
Example: You have a penetrating neck injury in a • Persistent air leaks or mediastinal air
hemodynamically stable patient Zone 2, with a stable vital → Bronchoscopy- Diagnostic and therapeutic
sign you should do CT angiography, if its positive you do
surgical exploration. Or if you can’t do angiogram, you XII. EXAMINATION OF THE ABDOMEN
may do esophagram or bronchoscopy • Diagnostic approach differs for penetrating trauma
(gunshot/stab wound) and blunt abdominal trauma
Note: Know the difference of Hard and Soft signs • As a rule, minimal evaluation is required before
laparotomy for abdominal gunshot or shotgun
XI. EXAMINATION OF THE CHEST wounds because over 90% of patients have
• Most of the chest injuries can be evaluated by significant internal injuries except those isolated in
physical examination and chest radiography with the liver by CT scan
supplemental CT scanning based on initial findings • Abdominal stab wounds are less likely to injure
• Any patient who undergoes an intervention in the ED intraabdominal organs and thus, diagnostic
– endotracheal intubation, central line placement, evaluation can be afforded
tube thoracostomy- needs a repeat chest • Anterior Abdominal Stab Wounds (AASW) should be
radiograph to document the adequacy of the explored under local anesthesia in the ED to
procedure. determine if the fascia has been violated.
→ We only do this if it is a solitary stab wound but
if it is multiple we don’t do local wound
exploration.
• Injuries that do not penetrate the peritoneal cavity do
not require further evaluation, and the patient is
discharged from the ED.
→ If it doesn’t penetrate the peritoneal cavity and
the patient is stable and does not present with
• The x-ray image shows the pneumothorax (A), an acute abdomen (soft abdomen) we put the
meaning there is free air in the right chest area. As patient at the Emergency room. However, if
you can see in B, a close tube thoracostomy is done there is facial penetration further evaluation
in order to expand the lung because as you can see should be done because chances are there are
in A there’s no vascular markings, it’s all black 50% chance of requiring laparotomy. Usually we
• The image on the right side shows a patient with admit this patient and observed.
tracheostomy. It’s very important to do an x-ray after • Patients with facial penetration must be further
doing tracheostomy evaluated for intraabdominal injury, because,
because there is up to a 50% chance of requiring
laparotomy
• This diagram below should be memorized and
understand because this will help to decide what to do
in a patient with penetrating abdominal trauma.
• For example, hemodynamically unstable patient
(hypotensive, direct rebound tenderness in the
abdomen, massive bleeding) operating room right
away. On the other hand, if the patient is stable you • The fluid from the DPL will be sent to the laboratory
have to identify first if it is stab wound or gunshot and they will examine the RBC, WBC, Amylase,
wound, where is the gunshot wound located? Is it Alkaline Phosphatase and Bilirubin level. If fluid
anterior? Right Upper Quadrant (RUQ)? Or particle is seen it means that there is already food
tangential? leakage, there is bowel penetration. For example
• If it is RUQ or tangential you have to do a CT scan and you have an abdominal injury patient and the WBC
later on the patient progresses or having an abdominal is more than 100,000/mL it is a positive DPL.
pain proceed to operation room Correlate the physical examination of the patient
• For Left-sided thoracoabdominal injury, you need to do and the vital sign and BRING THE PATIENT TO
your laparoscopy if the findings are positive bring the THE OPERATING ROOM.
patient to the operating room.
Focused Assessment with Sonography for

Trauma
• Blunt abdominal trauma usually evaluated by FAST
Diagnostic Peritoneal Lavage (PDL) (focused assessment with sonography for trauma)
• We make a small incision 2cm below the umbilicus exam in major trauma centers
• Penetrate or open the linea alba • FAST is not 100% sensitive so diagnostic peritoneal
• Put the tube and 1 liter of fluid and siphoned it out and aspiration is still advocated in hemodynamically
have it examined to the laboratory unstable patients without a defined source of blood
• However, after you insert the tube and you have 10 loss to rule out abdominal hemorrhage
mL gross blood coming out from the tube which • Procedure:
atomically a positive DPL → The probe is placed in an epigastric area to
check for pericardial fluid
→ Right Upper Quadrant (RUQ) check if there’s a
fluid in Hepatorenal recess.
→ Left Upper Quadrant (LUQ) check if there’s a ® Presence of Hard Signs requires operation
fluid in splenorenal area mandatory
→ Pelvic area ® Presence of Soft Signs requires further
• Those are the dependent areas of the abdominal evaluation
cavity in a supine patient. It was mentioned it
Schwartz’s that about 350-450 mL of fluid is positive • Estimated Blood Loss
for FAST ® Each Rib Fracture: 100-200 mL
® Tibial Fracture: 300-500 mL
® Femur Fracture: 800-1000 mL
® Pelvic Fractures: >2000 mL
• Elderly trauma patients (>65 years of age) are
hospitalized twice as often as those in any other age
group, and this population accounts for one quarter of
all trauma admissions.
• No chronologic age is associated with a higher
mortality or morbidity but the patient’s comorbidities
do impact the individuals post injury course and
outcome
• 50% of patients >65 years old sustained rib fractures
• In a blunt abdominal trauma with PERITONITIS, from a fall of <6ft
OPERATE RIGHT AWAY. If the patient is • Pulmonary contusion is noted to 35% of patients
hemodynamically stable, do the FAST exam if and pneumonia complicates the injuries in 10% to
positive then EXPLORE. If EQUIVOCAL you need to 30% of patients with rib fractures
do Diagnostic Peritoneal Lavage (DPL). • Patients who sustain >6 rib fractures have
pulmonary morbidity rates of >50% and overall
mortality rate of >20%
• Falls are the most common cause of injury in infants
and toddlers
• Bicycle use in children is the most common cause of
severe injury
• Motor vehicular related injury predominates in
adolescents
• Unintentional injuries are the most common type of
injuries in childhood
• Initial evaluation is based on the Trauma ABCs
identification
XIII. Trauma • In cases of head trauma, CT scan should be
• Blunt injury to the pelvis may produce complex performed to determine intracranial pathology
fractures with major hemorrhage followed by skull radiograph to diagnose skull
• CT cystography is performed if the urinalysis findings fractures
are positive for RBCs • For evaluation for abdominal trauma in the pediatric
• Urethral injuries are suspected if examination reveals patient is similar to that in the adult
blood at the meatus, scrotal or perineal hematomas, • Careful evaluation in child sustaining a blow to the
or a high-riding prostate on rectal examination epigastrium should be evaluated for
• Urethrograms should be obtained for stable patients ® Duodenal Hematoma or Pancreatic Resection
before placing a Foley catheter to avoid false passage
• In MVC passenger restraint injuries “Seatbelt
and subsequent stricture
Syndrome” can cause:
• Used to identify for possible urethral injury or
® Abdominal wall contusion
extravasation of fluid
® Small bowel perforation
® Flexion distraction injury of the lumbar spine
® Diaphragmatic hernia
® Abdominal aortic dissection
MHAM
Wound Healing
Dr. Lisa Marie C. Jayme | October 27, 2021
SURGERY
mediators and PDGF → Activation of
Outline coagulation (activated by the PDGF)
I. Phases of Wound Healing • Inflammation
A. Hemostasis and Inflammation → Peak: 24-48 hours (Predominant cells:
B. Proliferation Neutrophils)
C. Maturation and Remodeling § Phagocytosis (bacteria & tissue debris)
II. Heritable Diseases of Connective Tissue § Delay epithelial closure
A. Ehlers-Danlos syndrome § Wound will become at its maximum edema
with surrounding erythema and tenderness
B. Marfan’s Syndrome
(pain upon palpation)
C. Osteogenesis Imperfecta → 48-96 hours: Macrophages
D. Epidermolysis Bullosa § Phagocytosis
E. Acrodermatitis Enteropathica § Microbial stasis
III. Healing in Specific Tissues § Activation & recruitment of other cells
A. Gastrointestinal Tract § Regulate cell proliferation, matrix synthesis
B. Bone & angiogenesis
C. Cartilage → 1 week: T-lymphocytes
D. Tendon § Modulate the wound environment
E. Nerve § Downregulate collagen synthesis
F. Fetal Wound Healing
B. PROLIFERATION
IV. Classification of Wounds
• Days 4-12
V. Factors Affecting Wound Healing
• Tissue continuity reestablished
VI. Chronic Wounds
• Predominant cells:
VII. Excess Healing → Fibroblasts
VIII. Tissue Management § Chemotactic factor: PDGF (Platelet-
A. T.I.M.E Derived Growth Factor)
IX. Dressing § Matrix synthesis (collagen)
§ Regulator: Lactate
LEGENDS → Endothelial cells
Presentations remember lecturer previous § Angiogenesis
exams § Influenced by TNF-α, TGF-β, VEGF
Matrix Synthesis
I. PHASES OF WOUND HEALING • Collagen (Types I & III)
• Wounding → Functional integrity of wound
→ Disruption of tissue integrity (e.g. trauma, tumor → Mostly found in the dermal layer of the skin
extirpation) that’s most important for skin approximation. It
→ Division of blood vessels holds most the collagen so it holds the most
→ Exposure of extracellular matrix (subendothelial tensile strength property of the skin.
collagen) → Vitamin C
§ Electron donor in the hydroxylation and
cross-linking of procollagen
→ Synthesis depends on: Nutrients, cofactors,
local wound environment
• Proteoglycan
® Made up of glycosaminoglycan - Serves as “a
ground substance” of granulation tissue and
protein
A. HEMOSTASIS AND INFLAMMATION ® Serves as a lattice for collagen assembly
• Hemostasis
→ Immediately after injury C. MATURATION AND REMODELING
→ At the area of vessel cut, circulating platelets • Longest and least understood phase
would be attracted to this area of exposed • Reorganization of collagen (broken by MMP’s
endothelial protein. That process is called (metalloproteinases) in a more linear fashion. The
“Platelet Aggregation” fibers are nor finer and stronger.
→ Platelet aggregation →Degranulation • Balance between collagenolysis and collagen
(release of cytokines, proinflammatory synthesis
• A slightly erythematous scar would flatten out and The producing cells will produce the hormone
§
resemble the quality closely to the surrounding that will take effect in the surrounding cells or
normal skin tissues
• Fibril formation and cross-linking leading to decrease ® Endocrine
solubility, increase strength and resistance § When the producing cells will take its effect
• Up to 6-12 months post injury on the distant sites
• In this phase, it starts from day 21 and would last up § The hormone has to undergo in the
to 6-12 months post injury. circulatory system and be transported to
distant sites where it can take its effect
There are 2 processes wherein tissue continuity is
restored. It is brought about by epithelialization and Wound Contraction
wound contraction. These 2 processes begin to occur • Decrease in area of the wound
by the end of the proliferative phase. Approximately at the • This is brought about by Myofibroblast’s contractile
second week post wounding. capability (contains alpha-smooth muscle actin in
thick bundles called stress fibers)
Epithelialization ® Appears at day 6 to 21 (overlaps between the
• Final step in establishing tissue integrity proliferative and remodeling phases. Going
• Characterized by proliferation and migration of towards the end of the proliferative phase and
epithelial cells adjacent to the wound the beginning of the remodeling phase)
• Complete in <48 hours in approximated incisions ® After 4 weeks, these myofibroblasts undergo
natural cell death or apoptosis
II. HERITABLE DISEASES OF

CONNECTIVE TISSUE
• Generalized, genetically determined, primary
disorder of one of the elements of connective tissue:
collagen, elastin, or mucopolysaccharide.
• 5 Major Types:
® Ehlers-Danlos syndrome
® Marfan’s Syndrome
® Osteogenesis Imperfecta
® Epidermolysis Bullosa
® Acrodermatitis Enteropathica
A. EHLERS-DANLOS SYNDROME
• Group of 10 disorders present as a defect in collagen
formation
• Quantitatively/structurally defective collagen type V
• “Classic” EDS:
® Thin, friable skin
® Prominent veins
® Easy bruising
® Poor wound healing
• Proliferation comes from the periphery of the wound ® Atrophic scar
with migrating epithelial cells, and also mainly from ® Recurrent hernias
the lining cells of the pile of sebaceous units ® Hyperextensible joint
• For surgical incision wounds, epithelialization is • Considered in every child with recurrent hernias and
already being completed in less than 48 hours coagulopathy.
• We expect a surgical wound to be closed primarily in
clean and clean contaminated cases. (Usually in Types of EDS
elective cases)
• Most of the inheritance in EDS are autosomal
dominant
Role of Growth Factors in Normal Healing
• Stimulates cellular migration, proliferation and Clinical, genetic, and biochemical aspects of Ehlers-
Danlos subtypes
function
® Autocrine CLINICAL BIOCHEMICAL
§ When the cell producing the hormone itself TYPE INHERITANCE
FEATURES DEFECT
will take into effect
® Paracrine
Skin: soft, Hypermobile Absence of
hyperextensible, TNX joints, skin AR tenascin X
easy bruising, fragility protein
fragile, atrophic
I scars; AD Not known AD = Autosomal Dominant;
hypermobile AR= Autosomal Recessive;
joints; varicose XLR = X-linked Recessive.
veins premature
births
Similar to type I,
II except less AD Not known
severe
Skin: soft, not

hyperextensible,
normal scars;
III AD Not known
small and large
joint
hypermobility
Skin: thin,
translucent,
visible veins,
normal scarring,
no
IV hyperextensibility; AD
Type II Clinical Presentation of EDS
collagen defect
no joint • Severe forms present with
hypermobility; → Hyperextensible skin
arterial, bowel,
and uterine
→ Hyperextensible joints
rupture → Hyperextended knee
→ Easy bruising in lower extremities
V Similar to type II XLR Not known → Prominent pains
• Less severe forms present with
Skin: → Hyperextensible joints
hyperextensible,
fragile, easy Lysyl
VI bruising; AR hydroxylase Clinical Significance
hypermobile deficiency
joints; hypotonia;
• Inguinal hernias in children
kyphoscoliosis → It is brought about by the pathophysiology of a
patent processus vaginalis (PPV)
Skin: soft, mild → Children with normal wound healing, without
hyperextensible, collagen defect, the gold standard of the
no increased
VII fragility; AD
Type I collagen treatment of PPV is just plain herniotomy or
gene defect ligation of the PPV
extremely lax
joints with → Children with EDS these hernias are best
dislocations managed with mesh or felt repair. Normally,
mesh or felt repair is only done for inguinal
Skin: soft,
hyperextensible, hernias of adults, where the defect or
easy bruising, pathophysiology is brought about by a
abnormal scars weakened inguinal floor, but with children with
with purple EDS management is by mesh and felt repair
VIII AD Not known
discoloration;
hypermobile because of their poor wound healing brought
joints; about by the structural defect in collagen
generalized • Wound repair:
periodontitis
→ Closed in 2 layers,
Skin: soft, lax;
→ Done under tension,
bladder → Stitches left twice as long,
diverticula and Lysyl oxidase → External fixation with adhesive tape
rupture; limited defect with
IX XLR
pronation and abnormal
supination; broad copper use
clavicle; occipital
horns
Similar to type II
Fibronectin
X with abnormal AR
defect
clotting studies
B. MARFAN’S SYNDROME • Slightest trauma causes fracture
• There is defective fibrillin • Blue sclera
→ Increase in TGF- β • Dealignment of the spine
signaling, particularly in
the aortic wall D. EPIDERMOLYSIS BULLOSA
• Classic phenotype • Defective type 7 collagen
→ Tall structure → Responsible for connecting the epidermis to the
→ Arachnodactyly dermis
→ Lax ligaments • 4 major subtypes:
→ Myopia → EB simplex
→ Scoliosis → Junctional EB
→ Pectus excavatum → Dystrophic EB
→ Aneurysm of the → Kindler’s Syndrome
ascending aorta • Impaired tissue adhesion within epidermis, basement
• Prone to hernias membrane or dermis therefore there is tissue
• Skin may be hyperextensible but shows no delay in separation & blistering with minimal trauma.
wound healing • Oral erosions & esophageal obstruction which
compromise nutrition
C. OSTEOGENESIS IMPERFECTA • Cutaneous manifestation:
• Mutation of type I collagen → Like partial thickness burns, and there will be
• Presentation: bullae formation and the epidermal layer will
→ Brittle bones separate from the dermis
→ Osteopenia • Surgical interventions:
→ Low muscle mass → Esophageal dilatation
→ Hernias → Gastrostomy tube placement (because the oral
→ Ligament and joint laxity erosions and esophageal obstruction will
→ Dermal thinning and increased bruisability compromise nutrition)
• Scarring is normal → Dermal incisions meticulously placed (to avoid
• Skin is not hyperextensible further skin trauma)
• Main feature: Bones fracture easily under minimal → Skin requires non-adhesive pads covered by a
stress à surgery can be successful but difficult “bulky” dressing
• Cutaneous manifestation of epidermolysis bullosa on
OSTEOGENESIS IMPERFECTA: the face of the child
CLINICAL AND GENETIC FEATURES • Looks more like a
TYPE CLINICAL FEATURES INHERITANCE
burn
Mild bone fragility,
I
blue sclera
Dominant • What is important
Prenatal lethal: crumpled here?
II long bones, thin ribs, Dominant • Wound care
dark blue sclera
management, like
Progressively deforming;
III Multiple fractures; early Dominant / recessive burns
loss of ambulation • Nonadherent
Mild to moderate bone materials and
fragility; Stenting
IV Dominant
Normal or gray sclera;
mild short statue • Anatomic structures
such as the external
nasal airway or the nares of the nose, wherein the use
of nasal conformers to avoid stricture of the external
nares. So that the external airway will not be
contracted or compromised
Classic Presentation
• Usually, babies
• Present with lower extremities deformities brought
about by multiple fracture sites
• Mesothelial (serosal) and mucosal healing can
occur without scarring, Ex. Facial fractures from
motor vehicular crashes
Technical Consideration
• For an anastomosis to heal without complications
it must be:
→ Tension free
→ Have an adequate blood supply
→ Adequate nutrition
→ Free of sepsis
• Overzealous fluid administration will lead to fluid third
spacing, tissue edema and increased intraabdominal
pressure.
→ Distal blood flow to the edges of the bowel
segments being anastomosed and repaired will
be compromised therefore there will be
interference of the GI healing
→ If left unrecognized, it will lead to dehiscence
E. ACRODERMATITIS ENTEROPATHICA and anastomotic leak and etc
• Inability to absorb sufficient zinc from breast milk/food
leading to inhibition of cell proliferation and impaired
granulation tissue formation
• Diagnostic: Blood zinc level <100 mg/dL
• Impaired wound healing and erythematous pustular
dermatitis (extremities and orifices)
• Treatment: Zinc sulfate 100-400 mg/day, orally-
curative for impaired healing
III. HEALING IN SPECIFIC TISSUES B. BONE

A. GASTROINTESTINAL TRACT • Phases of healing resemble those observed in dermal
• Full thickness injury: Repair by surgical or healing
mechanical reapposition (sutures and staples). In • Fracture site hematoma → Liquefaction and
ileocolic anastomoses, staplers have lower incidence degradation (inflammatory symptoms) →
of anastomotic leak. Revascularization
• Submucosa layer: Greatest tensile strength and • 3-4 days: Soft callus stage (cessation of pain)
suture-holding capacity. Layer that one should be • 2-3 months: Hard callus stage
able to get in its bites during suture to afford a seal off • Remodeling
of the defect
• Failure of healing: Dehiscence of the repair, C. CARTILAGE
therefore there will be anastomotic leaks, which leads • Avascular (depends on diffusion for nutrients)
to spillage of intestinal contents into the abdominal • Superficial injury:
cavity sometimes leading to formation of fistulas ® Healing power often inadequate → Regeneration
• Excessive healing: Lumen stricture & stenosis is incomplete → Slow healing with persistent
eventually making a form of obstruction structural defect
• Deeper injury:
® Exposure of vascular channels of underlying
bone/soft tissue → Hemorrhage → Inflammation
→ activation of cellular repair
® Example:
§ Cauliflower ear deformity in boxers that
usually gets traumatized cartilaginous
portions of the ear, so they will end up with
disfigurement of the ears.
D. TENDON
• Healing progresses in similar fashion as in other
areas of the body
• Hypovascular tendons: Heal with less motion and
more scar formation
Different Way On How Wound Would Heal
E. NERVE
• Primary Intention – Through process of
• 3 types of nerve injuries
® Neuropraxia: Focal demyelination Epithelialization and Connective Tissue Repair
® Axonotmesis: Interruption of axonal continuity ® Edges of the wounds are opposed edge to edge
but preservation of Schwann cell basal lamina § Surgically – Either by a suture or a skin
® Neurotmesis: Complete transection stapler, fibrin glues or skin adhesives
• Heal in 3 Crucial steps: • Secondary Intention – Picture in the middle, left row;
® Survival of axonal cell bodies you can see defect of the tissue injury
® Regeneration of axons ® No surgical intervention is being done and tissue
§ To reach the distal stump
will still restore its continuity by the process of
® Migration and connection of the regenerating
nerve ends to the appropriate nerve ends/organ Contraction and Epithelialization
targets ® Fibroblasts will lay down collagen and ground
substance in the area of the defect
F. FETAL WOUND HEALING § Eventually will form a scar tissue
• “IDEAL WOUND HEALING” ® Continuity is restored by scar tissue formation
• Early gestation • Tertiary Intention – Combination of primary and
® Lack of scar formation
secondary intention
® Resembles tissue regeneration
® Processes of Contraction and Connective
• Third trimester: “transition wound”
® Scarless healing Tissue Repair
® Loss of skin appendage regeneration ® Applicable to dirty contaminated wounds
• Eventually follows adult pattern but faster wherein you cannot oppose primarily for the
• Wound environment (Amniotic fluid) great risk of surgical side infection
→ Bathed in a sterile, temperature-stable fluid
environment Types Of Wounds
• Inflammation • Opt to leave it open for a certain period of time usually
→ Reduced due to immaturity of fetal immune four to five days or sometimes even longer; if the
system infection present is still not resolved
→ Lesser inflammation, lesser scar formation
• Growth factors • Time period wherein the wound is left open will help
→ Absence of TGF-β (significant role in scarring) to prepare the wound bed for the definitive closure
• Wound Matrix • Wound bed is clean and free from infection and ready
→ Excessive and extended hyaluronic acid for definitive closure; Do surgical repair
production ® Edge to Edge
→ Collagen pattern is reticular in nature → ® Re-approximation
resembles surrounding tissue
® Skin grafting
IV. CLASSIFICATION OF WOUNDS ® Flat closure
• Acute • Regular wound: Maximal wound strength reached
® Heal in a predictable manner and time frame after 6weeks of healing (75%-80% of a normal tissue)
• Chronic • Conditions that delay healing:
® Healing not achieved after 4 weeks of treatment ® Nutritional deficiencies
® Infections
® Severe Trauma Breast cancer patient who undergoes
§
® Immunocompromised Host mastectomy or modified radical
mastectomy (MRM)
V. FACTORS AFFECTING WOUND HEALING § Advanced stages wherein; do adjuvant
• Subdivided into: chemotherapy, wait for at least 2 weeks
→ Systemic and Local Factors before initiate adjuvant chemotherapy
• Systemic Factors
• Metabolic Disorders
® Age
® Diabetes Mellitus
® Nutrition § Have optimal glycemic control ideally 120
® Trauma mg per dl levels
® Metabolic diseases § To achieve optimal wound healing
® Immunosuppression ® Uremia: Tissue deposition of calcium phosphate
® Connective tissue disorders ® Mobidity: uremic gangrene syndrome
® Smoking (Calciphylaxis)
• Local Factors • Nutrition
® Mechanical injury ® Check BMI
® Infection ® To know whether a patient can heal normally or
® Edema not
® Ischemia/necrotic tissue ® Levels of albumin
® Topical agents ® Albumin globulin ratio
® Ionizing radiation • Infection
® Low oxygen tension → Important factor that may affect the wound
® Foreign bodies healing process
→ Difference between infection and contamination
should be identified
→ Organism >10/gm of tissue is threat to the
wound healing
→ Most common:
§ Staph sp.
§ Coagulase (-) Strep
§ Enterococci
§ E. Coli
→ Develops in 5-10% of post-op patients
→ Depending on the type of wound. (clean, clean-
• Age contaminated, or dirty wound)
® Elderly: Delayed healing Surgical Site Infection Classification
§ Dehiscence • Superficial Incisional
§ Incisional hernia – “Eventual hernia”; Hernias → Skin and subcutaneous only
occur post laparotomy incision → 75% of cases
• Hypoxia, Anemia, and Hypoperfusion • Deep Incisional
® Anemia with 15% less hematocrit (Threat to → Immediately adjacent to the fascia
normal wound healing) → Most dangerous: Necrotizing fasciitis
• Steroids and Chemotherapeutic Drugs • Organ/space wound infection
® Inhibit inflammatory phase → Involves deeper structures
→ Involves the fascia, muscle, or the abdominal
§ Cannot readily proceed to the next phase
cavity
which is the proliferative phase
→ May progress into sepsis or septic shock
§ It will tend to minimize the signs and symptoms
of inflammation; however it will also prolong VI. CHRONIC WOUNDS
that certain phase wound healing process • Wounds that do not heal in 3 months or do not heal in
cannot proceed succeeding phase 4 weeks despite treatment
® Inhibit epithelialization and contraction • Skin ulcers in traumatized or vascular compromised
® Delay steroid use after 3-4 days post-op; soft tissue are example of this
supplement Vitamin A • Other causative mechanisms
→ Unresponsive to normal regulatory signals
® Delay chemo use after 2 weeks
→ Fibroblasts have decreased proliferative potential • Physical Exam
→ Malignant transformation, example in extensive → Ulcer that fails to re-epithelialize despite the
burns leading to marjolin’s ulcer presence of adequate granulation tissue
→ A form of skin cancer → Skin color changes (pigmented)
→ Painless
Ischemic Arterial Ulcer → Most common site:
§ Above the medial malleolus (cockett’s
• Lack of blood supply
perforator)
• Typically extremely painful
• Management
• Usually associated with other peripheral vascular → Compression therapy
disease (PVD) § Most common: Zinc oxide – Impregnated,
• Mostly affect distal portions of the extremities non-elastic bandage)
§ To regulate the constant amount pressure
needed to bring back the venous outflow
→ Wound care (Hydrocolloids)
Diabetic Wound
• 25% of diabetic patients

• Major contributors:
→ Neuropathy (60-70%)
→ Foot deformity
→ Ischemia
• Treatment
→ Glycemic control
→ Debridement of necrotic tissue
• Physical Exam
→ Upon palpation: Diminished/ absent pulses → Infection control (adequate antimicrobial therapy)
(decrease ABI)
→ Poor granulation tissue formation
→ Wound: shallow, smooth margins, pale base
→ Signs of ischemia
§ Dry skin, hair loss, scaling, pallor
• Management
→ Treat the underlying cause
§ Revascularization
→ Wound care
§ Wound care will not be efficient if the
underlying cause is not treated
Venous Stasis Ulcer
• Pathophysiology:
Venous stasis +
Increased venous
pressure
• What happens
when there is
increase in Decubitus or Pressure Ulcers
pressure?
→ Fibrinogen leaks from the capillaries > • Localized area of tissue necrosis when soft tissue is
Perivascular cuffing > Impedance of oxygen compressed between a bony prominence and an
blood flow external surface
→ Capillary endothelial plugging (because of stasis • Common in:
and increased pressure) > diminished blood flow → Paraplegic patients
• Capillary damage > Extravasation of Hemoglobin > → Post-traumatic injury with spinal injury
Lipodermatosclerosis > Brownish pigment of skin → Post cerebrovascular accident
combined with the loss of subcutaneous fat) → Stroke patients
• Stages:
→ Stage 1: No blanching erythema of intact skin
→ Stage 2: Partial-thickness skin loss involving
epidermis/dermis or both
→ Stage 3: Full-thickness skin loss, but not through
the fascia
→ Stage 4: Full-thickness skin loss + muscle & bone
• Treatment
→ Multidisciplinary wound care team, (physicians,
nurses, dietitians, physical therapists, and
nutritionists)
VII. EXCESS HEALING

• Problematic scarring
→ Part of wound healing • Below are the locally available treatment that we
• When there is an imbalance between collagen
have, except for burn scars
formation and lysis and there would be excessive scar
formation that is also an abnormal response to injuries → A topical silicone gel may be used for 1 to 2
• Two types of excessive scarring: months example Dermatix Ultra
→ Keloid → The silicon sheet for example CICA-CARE is
→ Hypertrophic Scar maintained over the elevated scar for 28-30 days.
Meaning 1 sheet can be used approximately for
about 1 month. The maximum period of therapy
is 2 months. More than 2 months of usage of
silicon will no longer give you a significant
outcome in flattening of the scar. If there’s still
elevation of the scar after 2 months of therapy,
then you might need: Compression garment
therapy as well as intralesional steroids
injection or sometimes laser therapy
*Found in Schwartz, please familiarize
• Clinical example: Keloid formations in midline • Below is an example of Hypertrophic Scarring from a
stereotomy incisions in open heart surgeries
high-voltage Electrical Burns
• Classic example: Keloid or elevated scarring in the
deltoids- Injection site during childhood immunization
• Diagram of an overview of a problematic scar
management whether it is a keloid or a hypertrophic
scar. Just except if it is brought about by burns, they
have similar management that is through silicon scar
or therapy
meticulous alignment for us to be able to get
• With so much elevated scarring of the entire face a fine line scar outcome. Use nonabsorbable
causing contracture deformity: Closing the nares of suture in the skin. Why? To have lesser
the nose, and pulling up the right lateral commissure inflammatory reactions examples: nylon,
of the mouth, exposed calvarial bone of the scalp staples, monofilament sutures, and dermal
• Management glues.
→ Refer to a nutritionist to build for adequate or • Follow-up
optimal wound healing. → We have to determine if there is cellulitis or
§ Tissue debridement by removing the drainage?
devitalized bone of the calvarium using an → If there is none, suture removal is done. 4 to 5
outer table craniectomy and allowing days for the face other than that 7 to 10 days
granulation tissue formation by the used of other skin.
hydrocolloid dressing to maintain the optimal
amount of moisture
§ Burn scars are usually resistant to silicon
therapy and so the patient is on intralesional
steroids injection. After 6 months, flattening of
scar is observed. Areas containing hair
follicles for example beard and mustache
areas are hard to treat. Those areas are in
contact with the external environment and so
when treated with steroid opportunistic might
thrive and cause an infection for example
folliculitis
• Treatment of Wounds VIII. TISSUE MANAGEMENT
→ It will depend whether you are dealing with A. T.I.M.E.
chronic or acute wound. So you have to • T: Tissue Non-Viable
determine what kind of wound you are facing for ® Debridement
you to be able to treat it § Necessary to remove defective tissues,
• Algorithm of treating acute wound slough, exudate and debris that are known to
delay healing and cause infection build-up
→ First, examine the wound, this involves
§ If patient is not a good candidate for
determining the depth of the injury. Are there debridement, alternative:
underlying structures that are involved? o Chemical debridement
Configuration and the absence and presence of o Maggot therapy (least amount of
nonviable tissue? If nonviable tissue it will lead to bleeding)
the removal of the tissue in a process called • I: Infection & Inflammation
debridement ® Remove or Reduce Bacterial Load
→ Second, preparation this involves § Consider biofilms in chronic wounds where
protective layers of built-up become resistant
§ With an infiltration of an anesthetics, usually
to the action antimicrobials, including
using short-acting lidocaine with or w/o antibiotics
epinephrine. The purpose of adding § Further investigate the cause of infection
epinephrine is it gives us the additional effect § Would bed culture and sensitivity post
of peripheral constriction to minimize blood debridement for antimicrobial therapy
loss and to have a better view of the operative • M: Moisture Balance
field and also increase the therapeutic dose ® Restore Moisture Balance
§ Essential for wound healing to be achieved
of lidocaine.
§ Risk of wet wounds: Maceration (Heavy
§ Exploration, to further determine the depths exudate)
of injury. § Risk of dry wounds: Desiccations (dry
§ Cleansing, by pulsed irrigation using saline. wound bed)
→ Third, approximation § Achieving right amounts of moisture is
§ Deep layers. If the fascia is involved you have controlled by the appropriate type of
to repair the fascia independently. Use dressing
• E: Edge of Wound
absorbable suture as much as possible.
® Address T/I/M issues
§ Superficial layers. Should consider
§ If the wound edges failed to contract and • Skin Grafting
reduce in size, the edge of wound will not
epithelialize unless the wound bed is well
prepared
• Right picture:
® Granulation tissue – Red color, Free from
exudates, no malodor
® Clinically free from infection
• Left picture:
IX. DRESSINGS ® Skin graft at 100% successful
• Seven Classes: ® Skin graft incorporated to the previous raw
wound bed
® Films, Composites, Hydrogels,
Hydrocolloids, Alginates, Foams, Absorptive ® Donor site at the lateral thigh
Dressings ® Dressing was maintained using a Hydrocolloid
• The amount and type of exudate in the wound will every 4-5 days and after 2 weeks it has
determine type of dressing that will be used spontaneously re-epithelialized.
• Less Exudates
® Hydrogels (Solosite)
® Films
® Composite
§ For minimally exudative or dry wounds
• Moderate Exudates
® Hydrocolloids (DuoDerm)
§ Examples of moderately exudative wounds
o Venous stasis ulcers
o Arterial ischemic ulcers
o Donor sites of partial thickness skin
grafting
§ Last for 4-5 days
§ At donor sites of split thickness skin grafting,
it will spontaneously re-epithelialize due to
less frequency of change of dressing
• Heavy Exudates
® Alginates (Kaltostat)
§ May come in antibiotic impregnated form:
(Alginate + Silver)
§ If silver impregnated, may do dressing once a
day
® Foams (Allevyn Adhesive)
§ Capable of absorbing large amounts of
exudates
§ Can be used for up 4-5 days
® NPWT (Negative Pressure Wound Therapy)
§ VAC – Vacuum Assisted Closure
§ Utilizes suctioning mechanism
§ Continuous drainage of exudates
§ Significantly decreases the proinflammatory
cytokines in the affected area
§ Suctioning force promotes granulation tissue
formation enhancing wound bed preparation
decreasing the length of time of wound bed
preparation prior to closure via skin graft or
flap closure.
MHAM
Burns
Dr. Oliver L. Belarma | October 21, 2021
→ Occurs during the first few years of life and
SURGERY
Outline between 20 and 59 years of age

I. Learning Objectives • The major causes of severe burn injury in younger
II. Background patients are liquid scalds, and flame burns are more
III. Types of Burns common in adult patients
A. Thermal • Most burn deaths are caused by flame burns, while
B. Chemical liquid scald burns account for the second largest
C. Electrical number of deaths
IV. Burn Depth
A. Superficial Thickness Philippine Statistics
B. Partial or Intermediate Thickness • From 2010 to 2012, a total of 883 fires were reported
C. Full Thickness • Fires occurred most often between 12:00 AM to 3AM
• The median length of time of a fire was 1 hour and 5
D. Fourth Degree
minutes
V. Zones of Injury
• 26.7% of all fires had reported casualties, for a total
VI. Phases of Wound Healing of 824 casualties from 2010 to 2012
A. Hemostasis • Of these casualties, 33.5% were deaths and 65.9%
B. Inflammation were injuries (5 casualties were unclassified)
C. Proliferation • The cause of majority of fires were undetermined
D. Remodeling (87.7%), faulty electrical wiring (2.9%) and neglected
VII. First Aid open flames were (2.4%)
A. Initial Evaluation
B. Primary Survey III. TYPES OF BURNS
VIII. Circulation
IX. Disability
X. 2 Compartments of the Arm
XI. 4 Compartments of the Leg
XII. Determining the Severity of the Burn Injury
XIII. Secondary Survey
XIV. Nutrition
XV. Tetanus Prophylaxis
XVI. Initial Management of the Burn Wound
XVII. Surgical Management of Burn Wound
XVIII. Wound Coverage
XIX. Control of Infection
XX. Petroleum-Based Anti-microbial Ointments
A. Polymyxin B, Neomicin. Bacitracin
XXI. Chemical Burns A. THERMAL
XXII. Exercise • The depth of the burn injury is related to
→ Contact temperature
→ Duration of contract of the external heat source
LEGENDS
Presentations remember lecturer previous → The thickness of the skin
exams • Flame: A burn injury by fire
→ House fires, smoking related fires, improper use
of flammable liquids, automobile accidents, fall
I. LEARNING OBJECTIVES into open fire
• To recognize and diagnose burn injuries • Scald: A burn injury by moist heat/steam
→ Scalds from hot water are most common cause of
• To discuss the initial evaluation of burn patients
burn
• To identify the complications of burn injuries
→ Most frequent home injuries; hot water, liquids,
• To discuss the initial management of burns and foods are most common cases
→ Above 65°C cell death
II. BACKGROUND • Flash: Explosion of natural gas, gasoline & other
• 1.25 million people burned annually in the US, where flammable liquids cause intense heat for a brief time
30,000 patients require admissions to burn centers • Contact: Direct conduction of heat from a hot surface
every year and about 3,400 die to the body
• Highest incidence of burn injury
B. CHEMICAL • Painful
• Corrosive Substances • Does not blister
→ Strong Acid • Does not scar
§ Coagulative Necrosis
→ Strong Base B. PARTIAL OR INTERMEDIATE THICKNESS
§ Liquefactive Necrosis • Second degree
• Influenced by the Duration, Concentration and • Superficial partial thickness burns do not require
Volume surgery, but may scar and be more painful
C. ELECTRICAL
• Divided into:
® Low voltage
§ Usually at our homes
§ Below 500 volts
® High voltage → Moist
§ Above 500 volts → Painfully hypersensitive
§ High tension wires → Potentially blistered
§ Most patients that report to have high → Homogenously pink, and blanch to touch
voltage injury usually works on roofs, or line • Deep partial thickness burns require surgery and
man’s working on an electric company form more scars and are less painful
§ Patients have:
o Deep muscle necrosis
o Vessel thrombosis and nerve injury
• Management:
® With any significant electrical injury, vigorous
intravenous resuscitation should be given with
attention to myoglobinuria from muscle damage → Dry
® Urine Output should be maintained at greater → Less painful
then 1mL/kg/h with fluid administration and → Potentially blistered
mannitol to increase renal tubular flow if needed → Red or mottled in appearance
® Mannitol will be given if urine output is → Do not blanch to touch
insufficient. • Blisters and weeps
§ Complication for Electrical Injury: • With increasing depth, increased risk of infection and
Rhabdomyolysis scarring
o Take/monitor the creatinine kinase not
the hgb. C. FULL THICKNESS
• Third degree
IV. BURN DEPTH • Full thickness burns
→ Leathery
→ Translucent or waxy
white
→ Surface is painless
(because the nerve
endings are destroyed)
→ Underlying dermis red
initially
• Dry
• Insensate to light touch and
pin prick
• Small areas will heal with substantial scar or
contracture
A. SUPERFICIAL THICKNESS • Large areas require skin grafting
• Less painful compared to second degree burn
• First degree because of the extent of injury that led down to the
→ Superficial dermis, causing damage to the nerves
§ Erythema • High risk of infection
§ Pain
§ Non-life C. FOURTH DEGREE
threatening • Involves anything beyond the subcutaneous
§ Epidermis intact adipose tissue
• Involves the epidermis
• Leads to loss of the burned part • Zone with the most damage
• Involvement of underlying tissue excluding the • Maximum damage from the heat
muscle • Proteins becomes denatured
• Cell death is imminent due to the destruction of blood
Appearance: vessels resulting into ischemia in the area
1st Degree
• Involvement: Epidermis • The injury in the area is irreversible
• Signs & Symptoms: Pain • The damaged area will be undergoing coagulative
++ necrosis
• Healing: 3-5 days, • Necrotic, much like a third-or-fourth degree burn
spontaneous
• No Scarring • Need excision and grafting
2nd Degree Partial Thickness

Appearance: Zone of Ischemia/ Zone of Stasis
• Involvement: Epidermis + • Surrounds the zone of coagulation
Dermis
• Moderate insult with decrease tissue perfusion
• Signs & Symptoms: Pain
++ • With variable degrees of vasoconstriction and
• Healing: 2 weeks, minimal resultant ischemia, much like a second-degree burn
scarring, minimal • Can survive or progress to coagulative necrosis
discoloration
depending on the wound environment
2nd Degree Deep Burns Appearance: • Appropriate resuscitation and wound care may
• Involvement: Epidermis +
Dermis
prevent conversion to a deeper wound, but infection
• Signs & Symptoms: or suboptimal perfusion may result in an increase in
Painful-less severe burn depth. This is clinically relevant because many
• Healing: 2-6 weeks superficial partial-thickness burns will heal with
Hypertrophic nonoperative management, and majority of deep
scarring/formation of
contractures partial-thickness burns benefit from excision and skin
Appearance: grafting. (Schwartz, Principles of Surgery 11E pg253)
3rd Degree
• Involvement: Epidermis +
Dermis + Subcutaneous
Zone of Hyperemia
• Signs & Symptoms: • Outermost region of the wound
Painless, Insensitive, • Characterized by increase inflammatory vasodilation
Severe Edema
• Healing: No spontaneous
• Results of vasodilation from inflammation
healing surrounding the burn wound
• Clearly viable tissue
Appearance:
th
4 Degree • Much like a superficial or first-degree burn
• Involvement: Epidermis + • Will heal with minimal or no scarring and is most like
Dermis + Subcutaneous + superficial partial thickness burn or first-degree burn
Muscles, tendons, & Bones
(Schwartz, Principles of Surgery 11E pg253)
• Signs & Symptoms: No
Edema
• Healing: No spontaneous
healing
V. ZONES OF INJURY
• Jackson’s model for wound healing
• Because after injury, the wound is divided into 3
zones:
The degree of cellular injury varies depending on

the zone of injuries.
The 3 zones are clinically important because it will

aid the physician to know the adequacy of the
resuscitation.
Zone of Coagulation
• Center damage/Center of the wound
• Most severely burned portion
localized vasodilation and initiate the inflammation
phase.
B. INFLAMMATION
• After 24hrs the inflammatory
response begins, from a period
of hemostasis and then a
period of inflammation occurs.
Usually, they last for weeks
and as long as months
depending on the severity of
Basing on the picture above, from the zone of the injury. So, neutrophils and
statis, with adequate resuscitation, it will preserve or will macrophages release
decrease the zone of hyperemia, and it will heal over time. cytokines and chemokines into
the IL-1, IL-8, and tumor
If there is inadequate resuscitation, there will be necrosis factor (TNF) and
deterioration, and increases the zone of coagulation. Growth factors (TGFβ, EGF,
Leading to the development of coagulative necrosis and IGF) and vascular endothelial
gangrene over time. growth factor (VEGF) which remove debris and
pathogens from the injury site.
VI. PHASES OF WOUND HEALING
C. PROLIFERATION
• It involves the
recruitment and
activation of
fibroblasts and
keratinocytes
into the wound
site. During this
proliferation, it is
characterized by
the replacement
of the
provisional
matrix with a connective tissue matrix. Granulation
(new connective tissue and microscopic vessels),
angiogenesis, and epithelization occurs.
• Keratinocyte assists in both epithelization (wound
surface closure) and angiogenesis (restoration of
blood flow), which are vital to wound healing.
A. HEMOSTASIS • Endothelial cells are activated by growth factors
• For wound healing, (VEGF, fibroblast growth factors (FGF) and
there are 4 phases hepatocyte growth factors (HGF)) to initiate
of the natural angiogenesis. Resident fibroblasts are transformed
wound healing that into myofibroblast, which are involved in the
occurs immediately extracellular matrix (ECM) deposition.
after injury.
Homeostasis D. REMODELLING
occurs and involves • The final phase,
the granulation tissue
vasoconstriction. matures and ECM is
• Platelet activation remodeled under
and aggregation the influence of
and release in growth factors (TGF,
clotting factors. PDGF, FGF2),
Such as the platelet derived growth factor, epidermal Matrix
growth factor by platelets, keratinocytes, fibroblast Metalloproteinases (MMPs) and Tissue Inhibitors of
and macrophages resulting in your fibrin clot Metalloproteinases (TIMPs), which leads to increased
deposition at the injury site. Monocytes and tensile strength. The length of healing depends on
Neutrophils are recruited in the injury site, owing the multiple factors including the injury severity,
inflammatory cascade activation, nutrition and
activation of interferons (IFN). muscle mass, decrease in weight) and due to the
whole body catabolism organ dysfunction occurs and
the patient is highly susceptible to infection, when the
patient is infected they will easily go into sepsis and
eventually death.
• After initial injury, after 72 – 96hrs, patient is initially in

the ebb phase or there is presence of hypometabolic
response, which is potentially caused by intracellular
process, such as increased endoplasmic reticulum
stress and mitochondrial dysfunction and • In addition to the hypovolemic state and
characterized by decreased metabolic rate and hypermetabolic responses, burn injury has a
intravascular volume, poor tissue perfusion and low profound effect on the immune system from the
cardiac output. damage associated molecular patterns (DAMPs),
• After which, a hypermetabolic state is typically meaning any trauma or damage will increase in this
observed after injury in patients with severe burns DAMPs which will lead to hypovolemic shock and
(flow phase). The hypermetabolic state after burn vascular leak. So, immune cells including the
injury persists for up to 3years or 36 months after the monocytes, macrophages and neutrophils are
initial injury. It is caused by the stress hormones such activated in response to burn injury within a few
as catecholamines, glucocorticoids (produced by the hours, recognize endogenous factors such as DAMPs
adrenal glands) and glucagon (produced by the or alarmins that are generated as a result of burn-
pancreas), which increases blood pressure, mediated tissue damage. DAMPs and their
peripheral insulin resistance and breaks down exogenous counterparts, pathogen-associated
glycogen, proteins and lipids. It results in an molecular pattern molecules (PAMPs) which are
increased resting energy expenditure, increased triggered from infection or any bacterial pathogens,
body temperature, total body protein loss, muscle are recognized via pattern recognition receptors,
wasting and increased stimulated synthesis of acute namely Toll-like receptors (TLRs) and Nod-like
phase proteins (such as insulin-like growth factor 1 receptors (NLRs). The ligation of TLRs and NLRs by
(IGF-1)) which has an anabolic effect, ultimately their specific ligands results in the activation of
resulting in organ catabolism associated with organ downstream inflammatory pathways, leading to the
dysfunction and death. This is the reason why release of multiple inflammatory mediators (such as
nutritional therapy is done in burned patients. IL-1, IL-6, IL-8, IL-18 and TNF). As you can see
• Due to the burned injuries, the CNS response will there’s tissue oedema, tissue injury, risk of bacterial
increase in sympathetic nervous system and infection, elevated IL-6, IL-10, TNF, and PGE,
decrease in the cholinergic activity. Thereby decrease in Class II MHC expression and antigen
increasing the cardiac output, cardiac index, oxygen presentation, which will lead to immunosuppression
consumption, heart rate, and also increase in because IL-10 is significant, preventing or decreasing
glucocorticoids, cytokines, catecholamines, glucagon the inflammatory response.
and insulin. Due to the CNS response, there is gut • Once there is immunosuppression and increase in IL-
wall atrophy leading to increase in ammonia levels, 4, IL-10, and decrease in IL-2 and in proliferation, and
glutamine and bacterial translocation. the function of macrophages and neutrophils
• All of these will cause derangement in the kidney, decreases (decrease in phagocytosis and bacterial
leading to increase in ammonia and nitrogen wasting, activity), there will be bacterial multiplication leading
and the adipose tissues begin to breakdown which to SIRS and/or sepsis, and multiple organ failure
leads to an increase in fatty acids, lipolysis and because the patient is in a hypermetabolic state
triglycerides, which eventually causes a stain in the without adequate nutrition the patient would rapidly go
liver, such as a patient may develop fatty liver from into shock and death eventually.
increased level of lactate, lipid complexes,
gluconeogenesis and glycogenolysis, all these will VII. FIRST AID
eventually lead to muscle catabolism (decrease in • Extinguish the fire
• Remove burning textile or jewelry Breathing
• Thermoregulate (to prevent hypothermia) • Breathing concerns arise from 3 general causes:
• Chemical Burns (flushing with cool water) → Hypoxia
• Avoid home remedies → Carbon monoxide poisoning
→ Smoke Inhalation Injury
A. INITIAL EVALUATION • Management: Administer supplemental oxygen with
• 4 Crucial Assessment or without intubation
→ Airway Management • Inhalational injury can be divided into three types:
→ Evaluation of other Injuries → Systemic Toxicity due to products of combustion
→ Estimation of burn size (Carbon monoxide, and Cyanide poisoning)
→ Diagnosis of Carbon Monoxide and Cyanide → Upper Airway thermal injury
Poisoning → Lower Bronchi and distal airway chemical injury
• Inhalational Injury
B. PRIMARY SURVEY → Products of combustion, including carbon
A - Airway Maintenance with Restrictions of cervical spine particles, and toxic fumes
motion → Smoke particles settles into the distal
B - Breathing and Ventilation bronchioles, leading to damage and death of the
C - Circulation with hemorrhage control mucosal cells
D - Disability (Neurologic Evaluation) → Damage to the airways then leads to an increased
E - Exposure and Environmental Control inflammatory response, which in turn leads to an
increase capillary leakage, resulting in increased
Airway fluid requirements and an oxygen diffusion defect
• Priority: Identify any airway obstruction. → Diminished clearance of the airway produces
• One hundred percent is administered, and O2 sat is plugging, which results in an increased risk for
administered pneumonia
• Application of cervical collar if cervical spine injury is • Carbon Monoxide Poisoning
suspected → High affinity to hemoglobin
• The Airway can be obstructed → Always assume carbon monoxide (CO) exposure
→ Direct Injury in patients who were burned in enclosed areas
→ Massive edema resulting from the burn injury → The diagnosis is made primarily from a history of
exposure and direct measurement of
• Ask for history of fall, confinement in a burning
carboxyhemoglobin (HbCO).
environment.
→ Presentation:
• When in doubt, examine the patient’s oropharynx, for
§ Headache and Nausea (20%-30%)
signs of inflammation, mucosal injury soot in the
§ Confusion (30%-40%)
pharynx, and edema, taking care not to injure the area
§ Coma (40%-60%)
further
§ Death (>60%)
• Perioral burns and singed nasal hairs are signs that → Pulse Oximetry & Arterial Blood Gas Monitoring
the oral cavity and pharynx should be further are not reliable in ruling out CO poisoning
evaluated for mucosal or inhalational injury: → Management: 100% oxygen for 4 to 6 hours
Bronchoscopy → This will decrease the half-life of CO from 4-6
• Signs of impending respiratory compromise hours at room air to 40-80 minutes with 100% O2.
→ Hoarse voice • Patients with smoke inhalation often present with a
→ Wheezing history of exposure to smoke in a closed space
→ Stridor stridor, hoarseness, wheezing, carbonaceous
→ Dyspnea sputum, facial burns, and singed nasal vibrissae
• Indications for Early Intubation • Bronchoscopy can reveal early inflammatory changes
→ Signs of airway obstruction such as erythema. Edema, ulceration, sloughing of
→ Extent of the burn (total body surface area burn mucosa, and prominent vasculature in addition to
<40%-50%) infraglottic soot.
→ Extensive and deep facial burns
• Mechanical Ventilation may be needed to maintain
→ Burns inside the mouth
gas exchange, and repeated bronchoscopies may
→ Significant Edema or Risk for Edema
reveal continued ulceration of the airways with the
→ Difficulty for swallowing
formation of granulation tissue and exudate,
→ Signs for respiratory compromise:
inspissation of secretions, and edema.
§ Inability to clear secretions
• Management of an inhalation injury is directed at
§ Respiratory fatigue
maintaining open airways, clearing secretions, and
§ Poor oxygenation or ventilation
maximizing gas exchange while the lungs heal.
→ <GCS 9
→ Anticipated patient transfer of large burn with • Mechanical ventilation should be used to provide gas
airway issue without qualified personnel to exchange with as little barotrauma as possible
intubate enroute.
VIII. CIRCULATION colloid for these patients or colloids for plasma
• Replace the ongoing losses from capillary leak due to volume expansion
inflammation. • 8 L or 8000 mL for the first 24 hours
• Goal: Provide burn resuscitation fluids for deep partial • Half we will give the first eight (8) hours
and full-thickness burns larger than 20% TBSA, ® If the patient arrives four (4) hours post injury
taking care not to over resuscitate. instead of 4000 divided by 8; you divide it by 4,
• Establish intravenous access with two larger-caliber for your initial treatment so the initial treatment
(at least 18-gauge) intravenous lines in a peripheral is eight (8) hours
vein. ® He arrives four hours after injury, divide it by 4
• INITIAL FLUID RATE as a STARTING POINT: ® Normal circumstance when the patient arrives
→ 5 years old and younger: 125ml LR per hour immediately after; divide by 8; 4000/8 = 500 mL
→ 6-13 years old: 250ml LR per hour for the first 8 hours
→ 14 years and older: 500ml LR per hour ® Most of the time patient arrives three to four
hours post injury
• Remember: “For the first 8 hours 500 cc/hr; for
Parkland Formula the next 16 hours 4000/16 = 250 cc/hr”
• Why updated ringer solution? Why not NSS?
® Because according to studies, effectively treats
both Hypovolemia and Extracellular Sodium
Deficits; caused by the burn injury without
causing any issues of yourselves
® It is Isotonic and it is also inexpensive readily
available and easily stored
® There’s a risk of developing hypochloric
metabolic acidosis from pain d&c light solution
4 mL x % body surface area (which can determine once

we go into the exposure) x weight (kg) (or the estimated
weight of the patient)
• Once computed; the total requirement divides it

into two:
® The first half, will be given on the first eight (8) • Part of the circulation:
hours from the time of injury; NOT from the ® Check the pulses of the individuals
time of arrival at the institution § Especially in full thickness burns with the
® The next sixteen (16) hours we’ll give the other rigid eschar usually form tourniquet effect;
half; e.g. causes edema leading to compromised
§ 50 kg patient was involved in a burn incident venous outflow and eventually arterial
where you estimated around 40% TBSA inflow problems causing ischemia
§ 500 cc your Initial dose; while you’re doing § Some will do eschalotomy or fasciotomy
the primary survey if you have signs of compartment syndrome
• To compute: • During resuscitation
§ 4 (which is the standard or the factor use in ® Urine Output
parkland formula) x 40% x 50 kg = 8000 mL § 0.5 cc/kh/hr Adults
§ 8000/2 = 4000 mL § 1 cc/kg/hr Children (with a thermal burst)
4000/8 = 500 mL § If they come due to electrical burns;
4000/16 = 250 mL maintain 1 cc/kg/hr
§ First eight (8) hours (from time of injury) ® Heart Rate
4000 cc of 500 cc/hr § Goal is to decrease the HR but in all burn
§ Next sixteen (16) hours 4000 cc at 250 cc/hr patients they have an elevated HR because
• “Why four (4)? Not two 2? of the increased cytokine levels; 100, 110
® Different institutions, different countries have to 120 HR
different interpretation or ways in giving the fluids § In the young just maintain and adequate
® For the sake of the discussion we will be using urine output
the traditional parkland formula; purely giving ® Blood Pressure (Mean Arterial Pressure > 65)
lactated ringer solutions 4 mL x % BSA x weight § Usually goal in resuscitating burn patients or
® Using the parkland formula will result into higher any pre-operative septic patients
incidence of congestion but the motivated a
modified parkland formula where they use 2 cc
instead of 4 cc; vigorously monitor Urine output,
heart rate or any size of dehydration, giving
IX. DISABILITY • 2 incisions are made to decompress the posterior
• Determine the Neurologic and anterior compartment
status
• Identify Limb injuries XI. 4 COMPARTMENTS OF THE LEG
® Fractures
® Wounds
® Compartment
syndrome
• Compartment syndrome
® Results from the
combination of decreased skin elasticity and
increased edema in the soft tissue
® Pressure of > 30 mmHg with the compartment can
lead to muscle necrosis
X. 2 COMPARTMENTS OF THE ARM
• Compartments of the leg can be easily accessed thru

incision of the lateral leg (both sides)
• Anterior
→ Biceps, brachialis
→ Musculocutaneous nerve
→ Brachial artery
• PosterIor
→ Triceps
→ Radial nerve
§ Escharotomy and fasciotomy are usually
done in these areas.
• Any patients developing compartment syndrome, we
make incision on the volar and dorsal aspects of the
arm
• Incisions are usually made from joint to joint to

release the fascia
• Patients with signs of compartment syndrome are
sent to OR for this procedure to release the fascia
XII. DETERMINING THE SEVERITY

OF THE BURN INJURY
• Extent of burn injury
→ Decisions regarding care of burn patients are
based on “estimates” of extent of the burn injury
→ Should be recorded as accurately as possible
using a body diagram “RULE OF NINES”
→ Inaccurate estimation may lead to an inadequate
fluid resuscitation or over-resuscitation
→ Superficial areas are not counted in estimation,
only partial or full thickness burn
→ Patient’s open hand including the digits Berkow
§ Approx. 1%
The Rule of Nines
• Berkow or Lund and Browder are used to estimate

burn size in children
• More preferred than the rule of nines because of
accuracy in giving the percentage of burn injury
XIII. SECONDARY SURVEY

• A- Allergies
• M- Medications
• P- Past medical history
• L- Last meal
• E- Events surrounding the injury
• Just add the number depending on which part is → Nature of incidence
affected. Ex. If only the anterior chest is affected, use → Place of incidence
9. If both are affected (anterior and posterior), use → Date of incidence
18%. → Time of incidence
• Always follow the AMPLE format in presenting the
patient. Then do a complete physical examination
→ Burn patients are affected by hypothermia
→ Easier to prevent than treat
→ Increased metabolic oxygen demands
→ Proportional to degree of injury
→ Tissue ischemia
• Hypothermia
→ May lead to acidosis and coagulopathy
→ Causes peripheral vasoconstriction and impairs
oxygen to tissues
→ Metabolic changes to anaerobic
§ Increased lactate
§ Decreased serum Ph
→ Common condition upon patient arrival
§ Upon arrival, always make sure to cover them
up, remove anything, any metals, shirts
because these may increase the tissue
damage
§ Thermoregulate the patient to avoid
hypothermia
• Pain management
→ Main issue in burns is inconsistent and
inadequate pain management
→ Opioids- long acting analgesics
→ Ketamine- used for extensive burn dressing
changes and procedure like escharotomies
→ Anxiolytics are also used
• Drugs used
→ Tramadol
→ Fentanyl → Overfeeding may happen
→ Oxycodone → Increased blood sugar level may decrease
→ Morphine wound healing capabilities
§ Start up with a lower dose → Make sure to monitor blood sugar to avoid
• Benzodiazepines (BZDZ) - Anxiolytics overfeeding
→ Alprazolam
→ Midazolam XV. TETANUS PROPHYLAXIS
→ Lorazepam
→ Diazepam
• Anxiolytics are given when patients are anxious upon
arrival
• May cause hypotension and decreased
respiratory effort to the patient
• Administer only PRN (if needed). If patient is really
agitated, you may give midazolam (dormicum)
XIV. NUTRITION
• Indirect calorimetry
→ Non-invasive, reliable and valuable tool in
assessing energy expenditure and fuel utilization • Patients who have no documented history of a
by the body complete primary vaccination course (3 doses) with a
→ Clinicians have used this to optimize the tetanus-containing vaccine should receive all missing
nutritional support in metabolic disorders and to doses and must receive tetanus Ig for tetanus prone
quantify the energy requirement of the patients wounds.
→ If indirect calorimetry is unavailable, we can use
Toronto formula XVI. INITIAL MANAGEMENT
OF THE BURN WOUND
Toronto Formula • After the initial patient assessment and institution of
measures to life threatening problems, attention is
turned to local care of the wounds
• Loose, devitalized tissue is generally trimmed away
• Pain and bleeding are kept to a minimum
• Blisters of a medium size are preferable left intact and
allowing underlying wounds to heal spontaneously
• Arguments, based on several studies, advocate
puncturing the blister at one end with a needle and
evacuating the fluid but leaving the blister over the
• Measuring the total energy expenditure using the wound as a protective biologic covering
Harris Benedict Formula to determine the nutritional • The wound is gently irrigated or washed with warm
needs of the patient water and a mild bland soap. Chlorhexidine soap is
• Curreri’s formula may also be used desirable for its antimicrobial activity
• After cleansing, a topical antibiotic cream is applied
Curreri’s Formula and wound is covered with absorbent gauze dressing
held in place by elastic bandage
• In wounds that will heal spontaneously without skin
grafts, topical antimicrobial cream or silver-based
dressings limit wound contamination and provide a
moist environment for healing.
• The choice of dressing should be individualized based
on the characteristics of burn
® First-degree burns
Aare minor with minimal loss of barrier
function
§ These wounds require no dressing and are
treated with lotion to keep the skin moist
® Second-degree burns
• Much easier way of determining the nutritional § Can be treated by an antibiotic cream or
requirement of the ptatient ointment such as silver sulfadiazine and
• However, according to the studies done on this covered with gauze under elastic wraps.
formula, this tends to over-estimate the metabolic
requirement for the patients
• Once the initial resuscitation is complete and the
patient is hemodynamically stable, attention should
be turned to excising the burn wound
• Burn excision and wound coverage should ideally
start within the first several days, and in larger burns,
serial excisions can be performed as patient condition
allows
• Tangential excision is performed with repeated
tangential slices of burned tissue using a Watson or
Goulian blade until a viable tissue plane is reached
→ Do this until you find bleeding
→ Done early (5-7 days) after burn injury (this is the
old adage)
→ the latest study showed that this can be done as
early as 48 to 72 hours as long as the patient is
stable or there was no need to do a massive
• For deep parcel thickness burns, it can be covered by resuscitation
biologic or synthetic covering to close the wound.
® These coverings eventually slough as the wound XVIII. WOUND COVERAGE
re-epithelializes underneath • Take from a patient’s healthy skin from the back and
® These types of dressings provide stable inner thighs and use to cover the areas involved
coverage with decreased pain and a barrier to • Usually, skin is meshed to cover large wound
evaporative loss • Wounds less than 20% can usually be closed in one
® They may also have added benefit of not operation with autograft skin taken from the patient’s
inhibiting epithelialization, a feature of most available normal skin (donor site)
topical antimicrobial agents (see table below)
• These should be applied within 24 hours of the burn

before bacterial colonization of the wound occurs.
• Closed wound dressings on burns are used to
serve three main purposes: • Split-thickness sheet autografts harvested with a
® Provide protection and isolation of wound from dermatome make the most durable wound coverings
the environment and have a decent cosmetic appearance
® Absorb drainage • In large burns, meshed autografted skin provides a
® Decrease wound pain larger area of wound coverage
• This also allows drainage of blood and serous fluid to
XVII. SURGICAL MANAGEMENT prevent accumulation under the skin graft with
OF THE BURN WOUND subsequent graft loss
• Deep partial-thickness burns may not heal and full- • Portions of the wound that cannot be covered with
thickness burns will not heal in a timely fashion without widely meshed autograft skin due to scarcity of
autografting available autograft skin are temporarily covered with
• Also, burned tissues serve as a nidus for infection and allograft skin in preparation for auto grafting when
inflammation donor sites are healed and available
• Early excision and skin grafting of these wounds is • Ideally, areas with less cosmetic importance are
now practiced by most burn surgeons in response to covered with the widely meshed skin to close most of
literature showing benefit over serial debridement in the wound prior to using nonmeshed grafts for the
terms of survival, blood loss, and length of cosmetically important areas such as the hands, face,
hospitalization and neck
• Early excision is now the standard of care or improved • Autologous skin grafts are still the gold standard for the
survival of this patients meaning 24 to 48 hours after treatment of full-thickness burns.
the patient is stable, surgeons usually bring the
patients to the operating room for debridement XIX. CONTROL OF INFECTION
• Early excision and skin grafting of wounds • Invasive infections in burn wounds can be reduced by
early excision and closure and the timely and effective
use of antimicrobials. • Commonly used for the treatment of facial burns, graft
• Antimicrobials that are used can be divided into those sites, healing donor sites, and small partial thickness
given topically and to those given systemically burns
® It is not recommended to give systemic (Oral or • Mupirocin
IV) antibiotic in acute burns. ® Is an ointment that has improved activity against
§ Promote bacterial resistance to antibiotics gram-positive bacteria, particularly Methicillin-
§ Kills patient’s normal flora thus promoting Resistant Staphylococcus aureus
fungal infection • The usual burn wound will have Staphylococcus
® Topically applied antimicrobials will provide aureus as the predominant flora
higher concentration of the agent on the wound • Subsequently, gram negative opportunistic species
surface where microbial numbers are usually appear
highest ® These include Proteus, Klebsiella and coliform
§ Topical agents penetrate eschar to a species as well as Pseudomonas
variable extent, which should be considered ® Anaerobes are infrequently isolated
in the selection of the topical antimicrobial • The goal of topical antimicrobial therapy is to initially
to be used delay and minimize wound microbial colonization
• Some of the topical antibiotic salves include:
® 8.5% mafenide acetate XXI. CHEMICAL BURNS
® 1% silver sulfadiazine- commonly used • Careful removal of the toxic substance from the
® Polymyxin B patient and irrigation of the affected are with water for
® Neomycin Both used in a minimum of 30 minutes
® Bacitracin patients with • Generally:
® Mupirocin positive growth ® Acids cause coagulative necrosis and are
in the wound confined to the skin
• No single agent is completely effective, and each has ® Base solutions cause liquefactive necrosis and
advantages and disadvantages. extend further into the tissues
• 8.5% Mafenide acetate • After the chemical injury has been controlled, the
→ It is a water-soluble cream which has excellent remaining burn is treated in the same way as thermal
antibacterial activity against most gram positive injuries
and gram negative organisms particularly for • Assessment of burn depth is often difficult, but is
Pseudomonas and Enterococcus species typically deeper than it appears
→ Advantage: Good eschar penetrance • Hydrofluoric acid is a highly dangerous substance,
→ Disadvantages include: Pain on the application, yet it is used widely in industrial setting
an allergic skin rash, and inhibition of carbonic ® Causes hypocalcemia
anhydrase activity that can result in metabolic ® Causes severe burns and systemic effects
acidosis when applied over large surfaces ® When it is exposed to biological tissues, the
→ For these reasons, mafenide acetate is typically fluoride ion precipitates calcium and may cause
reserved for small full-thickness burns and ear systemic hypocalcemia
burns to prevent chondritis ® Exposed skin should be treated with 2.5%
• 1% Silver sulfadiazine calcium gluconate gel to provide pain relief and
→ The white cream is relatively painless to apply limit the spread of the fluoride ion
and does not stain bed linens. ® Patients should be monitored closely for
→ It has in vitro activity against a wide range of prolongation of QT interval, torsade de pointes,
organisms including: S.aureus, E. coli,
or ventricular fibrillation
Pseudomonas, Proteus, Enterobacter, and
® Changes in QT interval should be treated with
Candida.
20ml of 10% Calcium Gluconate repeated as
→ The drug penetrates the eschar poorly but
needed to maintain normal serum calcium levels.
softens it. Its toxic effect is a transient leucopenia
2-4 days following its discontinued use which is
reversed on discontinuation of the cream. XXII. EXERCISE
→ When the leucopenia resolves, silver sulfadiazine
may be reapplied without recurrence.
XX. PETROLEUM-BASED
ANTIMICROBIAL OINTMENTS
A. Polymyxin B, Neomycin, Bacitracin
• Clear on application and allow for observation of the
wound
• Painless and provides a moist environment
• TBSA
® Entire right upper extremity – 9%
® Anterior chest – 9%
® Entire anterior aspect of thigh and leg – 18%
• Degree of Burn
® Second to Third Degree
® Arrange the Diagnosis based on:
§ Classification, Depth, TBSA
® Example:
§ Thermal Burn, Second to Third Degree,
36% TBSA
§ Add subtype (if any) to the Classification
§ EX: Direct Thermal Burn Second to Third
Degree, 36% TBSA
• Resuscitation
® Parkland Formula
® Volume of Ringer’s Lactate = 4xWeightxTBSA
§ Case: 4x80kgx36% = 11520cc
§ 11520 / 2 = 5760cc
§ 5760cc / 8hrs = For the first 8hrs, 5760cc at
720cc/hr.
§ 5760cc / 16hrs = For the next 16hrs, 5760cc
at 360cc/hr.
® Currie Formula
® Adult (25kcal x Kg) + (40 x %BSA Burn)
® Children (60kcl x Kg) + (35 x %BSA Burn)
§ Case: (25kcal x 80kg) + (40 x 36% BSA)
§ 3440kcal/kg/day
MHAM
Surgical Oncology
Dr. Ma Dulce L. Consuegra | November 10, 2021
SURGERY
Outline I. OBJECTIVES
I. Objectives • List the ten most common cancers in the world and in
II. Epidemiology the Philippines
III. Cancer Biology • Describe cancer biology and realize its importance to
A. Changes in Physiology Resulting to implement personalized cancer therapy
Malignancy • Recognize that modern cancer therapy is
B. The Cell Cycle multidisciplinary
IV. Etiology • State the use of tumor markers for the management
A. Bad Genes of cancer patients
B. Hereditary Cancer Syndromes • Explain the role of chemotherapy, hormonal therapy,
C. Etiology targeted therapy, immunotherapy, gene therapy and
radiotherapy as treatment of cancer
V. Risk Assessment
• Describe the surgical principles in handling tumor
A. Cancer Risk Assessment intraoperatively
B. Gail Model
VI. Screening What is Oncology
VII. Diagnosis • Onco + Logos
A. FNAB → Onco – Greek word ὄγκος (ongkos) meaning,
B. CNB “burden, volume, mass” and “barb”
C. Excisional Biopsy → Logos – Greek word λόγος (logos) meaning
D. Incisional Biopsy “study”
E. Other Biopsy Techniques • Surgical Oncologist
VIII. Tumor Markers → “A surgical oncologist is a well-qualified surgeon
A. Serum Markers who has obtained additional training and
IX. Staging experience in the multidisciplinary approach to
A. Clinical Stage the prevention, diagnosis, treatment, and
rehabilitation of cancer patients and devotes a
B. Surgical Stage
major portion of his or her professional practice to
C. Pathologic Stage these activities and cancer research” – Surgical
D. Staging Modalities Oncology Society of the Philippines (2016)
E. Staging Work-Up Approach
X. Treatment Definition of Terms
XI. Therapeutic Modalities • Neoplasm
XII. Therapeutic Intent → Altered cell population characterized by an
XIII. Surgery: Other Therapeutic Roles excessive non-useful proliferation of cells that are
XIV. Chemotherapy unresponsive to normal control mechanisms and
XV. Radiotherapy to organizing influences of adjacent tissue
A. Curative Radiotherapy → Two types:
B. Palliative Radiotherapy § Malignant- Cancer cells that exhibit
C. Pre-operative Radiotherapy uncontrolled proliferation and impairment in
the function of the normal organs by local
D. Post-therapy Radiotherapy
tissue invasion and metastatic spread to
E. Intra-operative Radiotherapy distant anatomic sites
F. Radiotherapy Complications § Benign- Composed of normal appearing
XVI. Newest Trends in Cancer Therapy cells that do not invade locally and
XVII. Cancer Prevention metastasize to other sites
• Primary Definitive Surgical Therapy
LEGENDS → Surgical treatment done on a patient as the
Presentations remember lecturer previous main treatment, per se, of the cancer
exams • Adjuvant Therapy
→ Treatment modalities that are given in the post-
operative period
• Neo-adjuvant therapy
→ Treatment modalities that are given pre-
operatively
II. EPIDEMIOLOGY III. CANCER BIOLOGY
A. CHANGES IN PHYSIOLOGY
RESULTING TO MALIGNANCY
• Self-sufficiency of growth signals
• Insensitivity to growth-inhibitory signals
• Evasion of Apoptosis (Programmed cell death)
• Potential for limitless replication
• Angiogenesis (Formation of new vessels within the
tumor)
• Invasion and metastasis (Chance to spread to other
organs)
• Reprogramming of energy metabolisms
• Evading immune destruction
• Other changes:
→ Loss of contact inhibition
→ Altered appearance and poor adherence to
other cells or the substratum with loss of
anchorage for growth
→ Immortalization
→ Gain of tumorgenicity (The ability to give rise to
tumors when injected into an appropriate host)
• Inner circle: Tells you the different physiologic

mechanisms that happen within the cell during
malignancies and those
• Outer portion: Normal processes/Normal inhibitors
that have these abnormal cellular changes within the
cancer cell
→ Most of the time, the action of these inhibitors is
Surgeon’s Role in Oncology mimicked by Anti-cancer drugs (e.g., Genome
• “Surgery makes its contribution to cancer treatment in instability & mutation is inhibited by OARP
concert with other modalities. Advances in the inhibitors, and there are certain drugs that are
treatment of cancer will derive from improved develop that have the action of these inhibitors in
orchestration with the other modalities rather than order to stop genomic instability & mutation)
from improved operative technique alone.” – Bernard
Fischer (1977)
• Prevention – Educate the lay people in terms of the
early signs and symptoms of cancer in order to catch
the disease at an early stage
• Screening – Recommend screening modalities that
are useful for a certain group of population
• Diagnosis
• Treatment
• Rehabilitation
• Follow-up care
• Palliative care
• Terminal care
B. THE CELL CYCLE B. HEREDITARY CANCER SYNDROMES
• Describes a sequence of steps through which both Retinoblastoma Gene rb1
normal and neoplastic cells grow and replicate ® It is the rb protein that controls the cell cycle
differentiation and apoptosis in a normal
development
® First suppressor gene to be cloned in the
laboratory
® Any problem in the retinoblastoma gene would
lead to the formation of the retinoblastoma
® Retinoblastoma- A type of cancer that is found
among pediatric patients involving the retina
P53 and Li-Fraumeni Syndrome

• Bone or soft tissue sarcoma <45 years
• The cell cycle is divided into two phases: • 1st degree relative with cancer before age 45 years
→ Proliferating and Non-proliferating • Another 1st or 2nd degree relative with either a
• Cell cycle starts from G0 phase sarcoma diagnosed at an early age or any cancer
→ “Gap phase” or “Resting phase” diagnosed before age 45 years
→ Stage where the group of cells are not involved • Li-Fraumeni Syndrome is characterized by early
in actual proliferation onset of breast cancer, associated with the formation
• G1 phase of soft tissue cancers, brain tumors, adrenocortical
→ Cells undergo biochemical changes in tumors and leukemia
preparation of entry to S phase • P53 gene derangement was first defined on the
• S phase basis of observed clustering of malignancy. It is the
→ Period of time that involves the synthesis of most commonly mutated gene within the cancer cells
DNA because it tends to regulate cell cycle progression as
→ Time where the cell generates a complete copy well as apoptosis
of its genetic material prior to the entry to the Positive BRCA gene indicates that patient is at high risk
next phase which is G2 phase of developing breast cancer and ovarian cancer.
• G2 phase Approximately as high as 87% risk for breast cancer and
→ Second gap/Second growth period that involves 50% risk for ovarian cancer.
the synthesis of the RNA and the protein as the
cell prepares itself for the M phase APC gene and Familial Adenomatous Polyposis
• M phase (Mitosis) (FAP)
→ Where the production of mitotic spindles • In FAP disease there is formation of hundreds to
happens thousands of polyps along the colon or rectum
→ Stage where actual cell division occurs (cell • Commonly seen among adolescent patients
divides into two daughter cells) • Associated with congenital hypertrophy of the retinal
• After cell division, the cell will either directly re-enter pigment epithelium, epidermoid cysts or osteomas
the cell cycle at G1 to undergo further maturation, • Because of the multiple polys within the GIT, there will
replication, or await activation by resting at the G0 be a tendency to develop upper GI neoplasms as well
phase as hepatobiliary pancreatic tumors, thyroid cancer,
• Mitosis is divided into phases (PMAT) desmoid, and medulloblastomas
→ Prophase
→ Metaphase Lynch Syndrome
→ Anaphase • Predisposed to develop colorectal cancer without
→ Telophase polyposis and other types of cancer like endometrial,
transitional cell carcinoma of the bladder, gastric
IV. ETIOLOGY carcinoma, small intestine, ovarian and pancreatic
A. “BAD” GENES type of cancer
• The majority of the studies done on cancer etiology
had found out that cancer is typically a genetic Cowden Disease
disease
• Presence of multiple hamartoma syndrome
• Somatic vs. Germline mutation
® Increased risk of breast and thyroid carcinoma
→ Cancer is somatic in nature
§ Somatic- acquired
MEN 2A & MEN 2B
§ Germline mutation- Inherited from one
generation to another • Multiple Endocrine Neoplasia
• Studies have shown that there are approximately 70 • A syndrome associated with pituitary tumors,
genes associated with hereditary cancer pheochromocytoma and parathyroid tumors
Factors that Suggest the Presence of a § Substances commonly used – Cigarette,
Hereditary Cancer Alcohol, Processed meat and Solar
• Tumor development at a much YOUNGER age than exposure
usual → Group 2A
§ Probably carcinogenic to human
• Presence of bilateral disease
→ Group 2B
• Presence of multiple primary malignancies
§ Possibly carcinogenic to humans
(Sometimes both ovarian and breast cancer can
→ Group 3
happen at the same time)
§ Carcinogenicity not classifiable
• Presentation of a cancer in the less affected sex (Ex. → Group 4
Male breast cancer)
§ Probably not carcinogenic
• Clustering of the same cancer type in relatives
• Occurrence of cancer in association with another
conditions (Ex. Mental retardation (MR) or
pathognomonic skin lesions)
C. ETIOLOGY
• There are other etiologies that are usually
encountered in the environment of an individual, and
most of these are what we call Carcinogens
• Carcinogen- Any agent that contributes to the
formation of cancer. They are divided to chemical
carcinogen, physical carcinogen and viruses.
→ Chemical carcinogens
§ Genotoxins, Cocarcinogens, Tumor
promoters
→ Physical carcinogen
§ Chronic non-healing wounds
o Predisposing factor for the formation of
Squamous cell carcinoma
§ H. pylori
o Commonly seen within the GI tract
o Increases the predisposition of a person
to develop Esophageal and Gastric
carcinoma)
§ Asbestos fibers
o Patients who are exposed to asbestos
has a higher chance of developing
Mesothelioma
§ Radiation
o Exposure to radiation is associated with
the formation of Lymphoma
→ Viruses
§ Hepatitis B & C
o Infection of these can lead to the
formation of Hepatocellular or
Hepatobiliary carcinoma
§ HIV
o Has an increased propensity for the
development of Kaposi’s sarcoma
§ HPV
o Particularly HPV16 & 18 have a higher
infection of these types of viruses
o Increases the chance of a person to
develop Cervical carcinoma
International Agency for Research on Cancer V. RISK ASSESMENT

(IARC) Carcinogen Classification A. CANCER RISK ASSESSMENT
• It is an important part of any initial evaluation of the
• They are divided into 4 groups patient
→ Group 1
§ Carcinogenic to human
• Risk is an important determinant of cancer screening § For example: Tumor in the breast, it is just
recommendations and may change how aggressive confined to the affected breast
the findings will be pursued for diagnosis. → Regional disease
• It is important that as we see the patient initially, we § Involves already the lymphatic drainage, with
get the proper history and physical examination a large lymph node, of the nearest lymphatic
drainage of the organ
B. GAIL MODEL (BREAST CANCER RISK § For example: For the breast, the common
ASSESSMENT TOOL) area for lymphatic involvement will be the
axillar, so any enlarge lymph nodes of the
axillary area at the time of cancer diagnosis
will indicate a possible regional disease
spread
→ Distant disease
§ Patients who come in very late, there is
already evidence of metastatic spread to
other organs such as the lungs, the liver, the
bone as well as the brain at cases where
there is presence of neurologic symptoms
Diagnosis
• This is an example of how we assess the risk of a • Thorough history and PE
patient in terms of her propensity to have breast • Biopsy techniques:
cancer in the later part of her life → FNAB
• The Gail model is based upon several questions, and → CNB
each question there is a point system for each answer → Excisional Biopsy
• This determines the 5 year risk of a patient to develop → Incisional Biopsy
the disease overtime
• A patient can be categorized as an average risk for A. FINE NEEDLE ASPIRATION BIOPSY (FNAB)
developing the cancer or a high risk for developing the • Fine needle and syringe are used to withdraw a fluid
cancer sample for laboratory testing
• It is calculated through this assessment tool
VI. SCREENING
• What is the purpose of screening?
→ Screening pertains to performing laboratory
imaging or physical examination among patients
who don’t manifest the disease or don’t present
the symptoms
• For large lesions, we can do it immediately in the
• Who are the population we subject for screening? clinics through palpation guidance, however for deep
→ The target population are usually those that are
seated lesions and smaller lesions there might be
not affected with the disease a need to utilize imagining modalities to visualize the
• Does screening achieve its purpose? tumor such as CT scan and an ultrasound
→ The purpose of screening is to be able to detect • Least invasive using a G-22 needle
lesions earlier, in order to prevent cancer
• Direct palpation
formation
• Deeper lesions – CT/UTZ guided
• Rapid, minimally traumatic and accurate
VII. DIAGNOSIS
• Most useful for solid epithelial neoplasms (Breast &
• It is important to diagnose cancer as early as
Thyroid)
possible, either through
→ Public education • Cytology only / No grading
→ Physician education • (-) FNAB should not be a basis to rule out
→ Screening malignancy
→ Early detection
• And as precise as possible B. CORE NEEDLE BIOPSY (CNB)
• Specially designed G-14 needle
Spectrum of Clinical Presentation • Usually used needle: G-14 or G-16
• Local anesthesia
• Patients who come in to the hospital will present
with either of the three types of disease:
→ Localized disease
§ Confined within the area of concern
C. EXCISIONAL BIOPSY
• Complete excision of the suspected tumor
• Small lesions (<4 cm)
• Done if FNAB or CNB result is uncertain
• Curative for benign lesions
• Ideal for lymphoma
• Histologic diagnosis: Although less invasive

procedure, it can give histologic diagnosis because a
tissue sample is taken out from the lesion itself
• May result to bleeding, hematoma, or perforation of
the viscera or thorax
• Ideal for soft tissue sarcoma D. INCISIONAL BIOPSY
• Next step for tumors in which FNAB is non-diagnostic • Useful for larger tumors (> 4 cm)
or unsatisfactory • Done for soft tissue sarcoma if CNB is not available
Short Video of How a Core Needle Biopsy is

Done
• A video of an ultrasound guided core needle
breast biopsy
E. OTHER BIOPSY TECHNIQUES

Fresh/Frozen Section Biopsy
• The lesion is localized using ultrasound • Pathologist will freeze the tissue, slicing a very thin
portion for microscopic examination
• Pathologist will the inform the surgeon of the findings
→ Useful in determination of adequate clear surgical
margins intra-operatively
→ Presence of malignant cells in the harvested
specimen (ex. Sentinel Node Biopsies)
• Should not be relied on to provide the pathologist
diagnosis
• Local anesthesia is injected in the biopsy side • Can result to unnecessary preop staging metastatic
work-up if it turns out to be a benign lesion
• If malignant, it deprives the patient and his relatives
the opportunity to discuss and fully understand the
true nature of the disease
• To avoid unnecessary trauma to the skin, a small

skin incision is made with a scalpel blade prior to
the biopsy.
A. SERUM MARKERS
Prostate Specific Antigen
• Normally present in low concentration in adult males
• Elevated in BPH, Prostatitis, Prostate CA
• Useful in evaluating effectiveness of treatment and
recurrence
Biopsy Considerations
• Seeding of Malignant cells Carcinoembryonic Antigen
→ Plan the biopsy site to be included during the • Found in the Embryonic Endothermal Epithelium
definitive treatment • May be used as prognosticating factor
• Adequate Hemostasis • Also elevated among smokers, pancreatitis,
→ Hematomas with potential malignant cells may cirrhosis, COPD, etc.
contaminate surrounding tissue planes
• Pathologic diagnosis maybe unnecessary in some Alpha Fetoprotein
instances when the biopsy result will not change the • Commonly seen patients with Hepatocellular
surgical management option (ex. Pancreatic head carcinoma or Germ cell tumor
tumor) • Produced by developing fetus
• Increased levels suggest HCC or germ cell tumor
Breast Carcinoma T4N1M0 (Stage III-B) (Ovary and Testes)
CA 19- 9
• Pancreatic Cancer
CA 15- 3
• Metastatic Breast Cancer
VIII. TUMOR MARKERS IX. STAGING

• Prognostic vs Predictive Tissue Marker • A prerequisite for an individualized therapy
• Prognostic Marker- Molecular markers that predict • Determining the extent of tumor spread is critical
disease-free survival, specific survival and the overall because it is the most important predictor of the
survival of a patient patient’s diagnosis
→ Ex: 21 gene assay (Breast Oncotype Diagnosis) • Will decide on the best treatment plan
§ Used to predict the recurrence of a person
with no negative estrogen receptor positive Local Disease
breasts cancer who are treated Anti- • Tumor is confined to the tissue of origin
estrogen drug known as Tamoxifen • Relationship with the adjacent vital organs
→ MamaPrint 70 gene assay • Imaging studies are helpful in widely infiltrative and
§ Also used to predict the recurrence rate for deep tumors
patients with early Breast Carcinoma
• Predictive Tissue Marker- Used to in the context of Regional Disease
predicting response to certain therapies
→ Ex: Commonly requested Breast Panel • Tumor that has spread beyond the tissue of origin into
§ includes ER (Estrogen Receptor), PR the draining lymph nodes
(Progesterone Receptor determination • Cellular basement membrane has been invaded
status), positivity to these receptors indicates
a patient’s response to treatment or Distant or Metastatic Disease
chemotherapy • Malignant cells were disseminated from the primary
site and established in distant sites favorable for
tumor growth
How do we stage a cancer patient? E. STAGING WORK-UP APPROACH
• AMERICAN COMMITTEE ON CANCER (AJCC) • Symptom-directed Metastatic Work-up
T- PRIMARY TUMOR → Use of any diagnostic test to investigate the
N- REGIONAL LYMPH NODE presence of distant metastasis to specific organ
M- DISTANT METASTASIS is dictated by the patient’s associated
symptoms at the same time of cancer diagnosis
→ Minimize the costs of diagnosis since majority
are negative if asymptomatic
• Routine or Intensive Metastatic Work-up
→ Tests are done even in the absence of
symptoms referable to that organ
→ Dictated by the primary tumor biology and
natural history
X. TREATMENT
• Study The Table
A. CLINICAL STAGE
• cTNM
• From all available clinical information including results
of invasive and non-invasive test
• Used as guide to the selection of primary therapy • Studies have shown that a wide array of available
options (as mentioned above) can also lead to better
B. SURGICAL STAGE outcomes; In addition to the main removal of the
• sTNM tumor which is done by the surgical part
• From the findings of surgical exploration that
precedes the actual surgical resection XI. THERAPEUTIC MODALITIES
• Finally assess any evidence referable to local • Surgery
resectability and distant metastasis that could have • Chemotherapy
been missed from the clinical staging • Radiotherapy
• Ultimate guide on the extent and intent of surgical • Combined modality
treatment (curative vs palliative)
XII. THERAPEUTIC INTENT
C. PATHOLOGIC STAGE Curative Treatment
• pTNM • CURE: Ultimate goal that is long disease-free survival
• Uses the histopathologic exam result of the surgically • Requires the eradication of every neoplastic cell
removed specimen ® Metastasis in the lymph node can still do curative
• Used as a guide to the need for adjuvant and final treatment
estimation of patient’s prognosis ® Systemic disease; Stage 4 disease chance for
curative intent is difficult
D. STAGING MODALITIES § Cannot eradicate every neoplastic cell that
• History and PE has been affected
• Non-invasive diagnostic work-up § Especially if there are already multiple
→ CXR metastases found in the body
→ UTZ
→ CT Scan Palliative Treatment
→ MRI
• For locally advanced malignancy or with evidence of
→ Bone Scan
widespread disease and no hope for cure by any
→ PET Scan
option of therapy
• Invasive staging diagnostic work-up
® Improve on their functional status
→ Biopsy
® Improve on their current symptoms such as pain
→ Laparoscopy
and bleeding
→ Endoscopic UTZ
→ Staging laparotomy (may be done in lymphoma) • Goals of Palliative Treatment
® Relief of symptoms
® Improvement of the quality of life
• Prolongation of survival XIII. SURGERY
® Questionable because there are times or there • Most important aspect of treatment
are data that would say the removal of tumor • In many instances surgical resection alone is curative
burden might improve or increase the survival for • Palliative surgery for too advanced or metastatic
about a few months disease
® No significant change in the prolongation of the • Radical surgery is the treatment of choice for readily
survival accessible tumors when it can be achieved with undue
mutilation
• Less radical surgery can still be curative when
combined with other modalities
PRIMARY TUMOR: The Need for Radical Surgery

• Principal Oncologic Considerations:
® Adequate margins of clearance
§ How much margins of normal tissue to be
included in the primary tumor is arbitrary
§ Both gross and microscopically negative
margins will give an assurance that no tumor
was left
® 48 year old male patient; mass located in the § Squamous Cell Carcinoma Antigen (SCCA)
fundus of the stomach; multiple liver lesions skin = 1 cm
• Qualities of Acceptable Palliation § Melanoma < 1 mm thickness = 1 cm
® Low associated morbidity and mortality o 1-4 mm thickness = 2 cm
® Effective relief of symptoms § Soft tissue sarcoma = 2 cm
® Reasonable quality of life § Rectal Adenocarcinoma (Distal) = 2 cm
® Possible increased survival time § Breast = 1 cm
• Modalities of Treatment • Avoidance of tumor violation
® Locoregional ® Avoid potential for tumor spillage and wound
§ Surgery implantation
§ Radiotherapy ® As much as possible, dissection is done
® Systemic carefully to avoid any perforation and violation of
§ Cytotoxic chemotherapy the capsule
§ Hormonal therapy ® For cysts, try to avoid violation the cysts to
§ Immunotherapy prevent potential tumor spillage and wound
® Supportive implantation
§ Psychosocial • En-bloc resection for structures adherent or
§ Nutritional fixed to the primary tumor
o Plant-based diet less of saturated fats ® Adherent structures should be assumed that the
o Several supplements attachment is malignant in nature and not just
§ Rehabilitation simply inflammatory
• Cancer pain relief § There is possibility of infiltration of the tumor
from the main site to the adjacent structures
® The involved tissue should be removed along
with the neoplasm
® Ex. in breast cancer, if the tumor has adhered to
the pectoralis ms, during the mastectomy, you
should involve the portion of the muscle in which
the tumor has adhered to.
® Do not try to separate the tumor from the pecs
because it might still leave some tumors in the
® Patient with a huge mass in the neck; Thyroid pecs which still may proliferate
Carcinoma
® Underwent total thyroidectomy with removal of REGIONAL LYMPH NODE: The Need for
lateral group of lymph nodes on both sides by Lymphadenectomy
doing a modified radical neck dissection • Evidenced by clinically enlarged lymph node, there
® Entire thyroid gland was removed as well as the is need for lymphadenectomy
lymph nodes • The need to eradicate the likelihood of nodal
® During surgery it is important that you have to do metastasis for tumors with propensity for lymphatic
the procedure well to make sure all the traces of spread through extension of surgical resection to
tumor that you can see should be removed include areas of regional spread
• Provides surgical control of the regional diseases as
well as rationale for further systemic therapy
• Considerations
® When doing lymphadenectomy, it is important to
consider en-bloc resection (Removal of tumor
together with the involved tissue, in order to void
cutting across lymphatic channel or node which
may contain metastatic foci)
® Should provide information that will change any
further plan of treatment or outcome based on the
node status. If the histopathology comes out • Elective Node Dissection
positive, you may plan further tx., either chemo or ® En-bloc removal of LN bearing tissue in patients
radiation therapy with clinically negative nodes bit with primary
® Benefit should outweigh its potential tumors that have increased probability of occult
complications nodal metastasis
§ Ex. Squamous cell CA because they have
higher chance for being aggressive in terms
Goals Of Lymphadenectomy
of LN spread even if the patient does not
• Staging Lymph Node Dissection: present with a palpable LN
® Determination of the status of the initial echelon § Elective node dissection is recommended
group of lymph nodes wherein the presence of
occult nodal metastasis indicates further Palliative Surgery
treatment either locally or systematically • Relieve symptoms in order to improve quality of life
§ Remember, in the body, there are group of
• Surgery- longer duration of palliation
lymph nodes wherein particular organs drain
• Locally or regionally confined tumors are not
into. (Ex, breast drains into the axillary LN)
surgically resectable because of invasion to adjacent
® Supraomohyoid Dissection
vital structures or organs
§ There are 7 groups of lymphatic chains within
• Locally resectable tumors with evidence for distant
the neck
metastasis
§ Supraomohyoid LN is a common chain for
• Considerations
drainage (Ex. from the oral cavity, thyroid,
parotid glands) ® Only for symptomatic patients
§ For neck lesions, especially involving these ® Surgeon must be thoroughly familiar with
groups of LNs, specimens are drawn and symptoms to be palliated
sent out for biopsy. If positive, a formal neck § Inform the patient that palliative surgery is
dissection should be done intra-operatively in just to alleviate the symptoms and does not
order to clear out other groups of LNs in the have survival benefits
neck. • Less invasive procedures should be considered such
® Axillary Lymph Node Dissection as endoscopic stent placement, percutaneous nerve
® En-bloc Mesocolon Dissection block or even radiotherapy depending on the
§ For colon surgeries, you have to include the symptoms to be palliated
mesocolon in dissection because it is the
location of the lymph nodes found within GIT, XIII. SURGERY: OTHER THERAPEUTIC ROLES
particularly the colon Tumor Debulking
§ Resection is based on the blood supply. For • Debulk- Take out as much as we can to reduce the
right hemicolectomy, we cut off the ileocecal tumor burden inside the patient’s body
artery and the right colonic artery. • CYTOREDUCTIVE SURGERY + HIPEC
§ For left side, we ligate the left colic artery as (Hyperthermic intraperitoneal chemotherapy)
well the left portion of the middle colic artery ® Useful when dealing with widespread disease in
• Therapeutic Lymph Node Dissection the abdomen and already involving the
® Goal is to cure the disease together with doing peritoneum
the primary surgery ® Patients with very big abdomens secondary to the
® En-bloc removal of clinically detectable lymph tumor sitting inside
node metastasis ® Patients with malignant ascites caused by the
® Provide regional control and improvement in tumor that is forming excess fluid within the
over-all survival peritoneal cavity
® Ex. Modified Radical Neck Dissection (MRND) for • Not an oncologic curative treatment
oral ca with palpable LN • Violates the tumor
® Tumors other than the breast (melanoma, SCCA • Does not increase patient’s survival
of the skin) axillary dissection should include level • In some instances (ovarian CA), debulking with
I, II, and III. intensive chemotherapy may improve pt outcome
• Example of a patient with a very huge breast mass.
Main problem is the ulceration because it causes
bleeding and multiple blood transfusion for this
patient. During work up, the patient has already
evidence of liver metastasis but still the doctors
decided to undergo with the procedure, operating the
patient because they want to palliate the bleeding and
improve the quality of life
• Last image on the right shows the post-operative site,
as you notice they can’t close the skin primarily due
to the huge tumor so they close the skin with multiple
application of skin grafts
XIV. CHEMOTHERAPY
• Image is an example of how HIPEC is done The Cell Cycle
• 60-year-old patient who came in with a history of
mucinous adenocarcinoma. She had a previous
ovarian surgery for mucinous cyst adenoma which had
a degeneration form of cancer which is called the
pseudomyxoma peritonei that involves greatly the
peritoneum of the abdomen. What happened here is
that the doctor tried to remove all visible evidence of
the disease including the peritoneum that was involved
and after clearing the tumor, they apply HIPEC to the
abdomen
Metastasectomy
• Done usually on stage 4 patients
• Remove a focus of metastasis as evidence by clinical
• Describes a sequence of steps through which both
and physical examination as well as imaging
normal and neoplastic cells grow and replicate
• No curative benefit for most patients
• The use of anti-cancer drugs usually interferes with
• In some, results to long term survival the normal process of the cell cycle
→ Colorectal carcinoma with liver metastasis
• Either these drugs will inhibit nucleic acid
§ Removal of liver mets can show 25-40%, 5
biosynthesis or there would be alteration of the
year survival rate
nucleic acid structure or inhibition of protein synthesis
→ Soft tissue sarcoma with pulmonary metastasis
• At times, the drugs focused into the process of mitosis
§ Complete resection of lung mets can show
wherein they produce mitotic arrest or alteration of the
30%, 5 year survival
hormonal environment thereby holding or causing a
• General Selection Criteria
stop into the proliferation or cell division of the tumor
→ Primary cancer must be amenable for curative
cells
resection
→ Metastasis to only one distant site
Curative Chemotherapy
→ Complete metastatic tumor removal while leaving
enough functional normal parenchyma to be • Induction Chemotherapy
compatible with life → Primary treatment for patients who present with
→ No evidence of locoregional recurrence advanced cancer for which no alternative
→ Patient must be physically fit to tolerate the treatment exists (E.g Leukemia; advanced
operation lymphoma)
• Adjuvant Chemotherapy
→ After the completion of initial local treatment
either by surgery or RT
→ Eliminate possible disseminated occult micro
metastatic disease
• Neoadjuvant (Primary Chemo)
→ Chemotherapy as the initial treatment for
patients who present with localized cancer for
which there is an alternative but less than
completely effective local treatment
→ Permits in-vivo chemosensitivity testing
→ Can downstage locally advanced disease and
render it resectable
→ May allow breast-conservation surgery (in breast there a decrease in the size of the tumor and the
cancer) to be performed ulcerated area has already dried up. In the 3rd cycle
there’s a significant decrease in size of the tumor as
Palliative Chemotherapy well as in the 4th cycle. Usually after the 2nd cycle of
• Patients with incurable local recurrence or distant chemotherapy it is already expected for the tumor to
metastases in an attempt to relieve symptoms and to decrease in size. If there is no response, we usually
prolong an enjoyable life assess after the 2nd cycle, then there might be a need
• Depends on patients’ performance status to change the regimen.
® Because if the patient is pale, in undergoing
chemotherapy you have to admit that there are
side effects that you have to consider. So, if the
patient status is not good there might be a
difficulty to initiate palliative chemotherapy
• Single Agent Chemotherapy
® One drug is used
® Unsuccessful in achieving long term remissions
® Produced cell lines resistant to further drug
therapy
® Produced severe lethal toxicities when given in
doses adequate to eradicate the tumor
• Combination Chemotherapy • Image below is an example of head and neck lesion.
® SEVERAL DRUGS are involved This patient underwent neoadjuvant chemo before
® CURRENT TREND in cancer chemotherapy undergoing surgery. The good thing about
® Drugs with synergistic MOA neoadjuvant is that it helps decreasing the tumor size
§ More effective tumor cell kill and eventually led us to surgical procedure that would
§ Decreased tumor cell drug resistance allow us to remove all of the tumor within the mandible
§ Cumulatively lower toxicity by means of
decreased dosage of all agents
® Drugs should have different mechanisms and
sites of action within the cell cycle. For example,
one drug would act on the G1 phase while the
other drug would act on mitotic phase.
® Should have different toxic side effects
® Drugs should be individually active against the
tumor
• How to know if the patient has responded to the XV. RADIOTHERAPY
initiation of the chemotherapy? We usually follow 2
guidelines: The RECIST AND WHO
® RECIST stands for Response evaluation criteria
in solid tumors. Below is a table for the scoring
system for both guidelines.
Teletherapy
• Source of radiation is away from the target tissue (80-
100cm)
• Cobalt-60
® Old method
® Disadvantages
§ Low dose rate
§ Limited penetration to tissues
• The image below is an example of a patient who came § Large penumbra around the beam edges
to us for neoadjuvant chemotherapy for a locally § Co-60 decays spontaneously and should be
advanced disease of the breast. The first picture is replace every 6 years
prior to the administration of the 1st cycle. After the 2nd ® Advantages
cycle of chemotherapy was given, you noticed that § Less expensive
§ Available in many centers D. POST-OPERATIVE RADIOTHERAPY
• Linear Accelerator • Advantages
® Uses electricity to emit x-rays ® Better tailoring of treatment
® Advantages ® Accurate histopathology staging
§ High dose rate ® Normal healing of tissues
§ Small penumbra ® Higher dose maybe delivered
§ Reliable since radiation source does not • Disadvantages
decay ® Tumor maybe less radiosensitive due to
disturbed vasculature
Brachytherapy ® Surgical complication may be delayed in
• Radiation source is in contact with the tumor radiotherapy
• Modes of delivery ® Scarry may trap normally mobile structure in the
® Intracavitary radiation field
§ E.g., Transvaginal placement for cervical or
endometrial cancer E. INTRA-OPERATIVE RADIOTHERAPY
® Interstitial • Radiation can be done intraoperatively
§ Placement of applicator directly into the • Intraoperative Brachytherapy can minimize
target tissue complications by surgically displacing normal tissues
• Advantages away from the path of radiation beam
® Delivers high dose rate
® Limits irradiation to surrounding normal tissue F. RADIOTHERAPY COMPLICATIONS
• Disadvantage • Acute Reactions
® Difficult to deliver homogenous dose in the tumor ® Can occur during or after radiotherapy
bed ® Tissues with high mitotic activity (skin, GIT)
® Dermatitis, Mucositis, Enteritis
A. CURATIVE RADIOTHERAPY ® Self-limited; Resolves in 2-4 weeks after RT
• Improve local recurrence and overall survival • Late Complications
• Only form of treatment that can be given if the patient ® Damage of more slowly dividing parenchymal
cannot undergo surgery or chemotherapy cells and stromal tissues
• Definitive/Single modality ® Increasing fibrosis
® Nasopharyngeal Carcinoma (NPCA) ® Occurs 6 months to 1 hear or anytime thereafter
® Squamous Cell Carcinoma (SCCA) ® Not self-limited, may progress with time
§ Skin lesions <2cm ® Pericarditis, Pulmonary Fibrosis, Hepatitis,
® Laryngeal Carcinoma (Stage I, II) Ulcer, Perforation of GIT, Stricture, Infarct
• Adjuvant Modality (Brain), Renal Failure
B. PALLIATIVE RADIOTHERAPY XVI. NEWEST TRENDS IN CANCER THERAPY

• Can be done for pain relief • Immunotherapy
• Controls bleeding ® Use of immunomodulators found in the genetic
• Relieves bronchial obstruction makeup of the patient
• Palliates symptoms of brain metastasis ® Monoclonal Antibodies can target components of
the immune system agonize co-stimulatory
C. PRE-OPERATIVE RADIOTHERAPY molecules, such as CD137, OX40, and CD40
• Advantages ® Inhibit immune checkpoints, such as cytotoxic T-
® Undisturbed tissue vasculature, tumor is more lymphocyte-associated antigen 4 (CTLA-4),
responsive programmed cell death-1 (PD-1) and its
® Less radical surgery may be required corresponding ligand PD-L1
® Unresectable tumor may become resectable • Gene therapy
® Tumor dissemination during surgery may be ® Gene makeup study and certain genes are
decreased corrected
® Tumor cells are rendered non-viable before
surgically dislodged XVII. CANCER PREVENTION
• Disadvantages • 10 Commandments of Cancer Prevention
® Definitive surgery is delayed ® Avoid tobacco
® Post-op recovery may be prolonged ® Eat properly
® Increased post-op morbidity ® Exercise regularly
® Apparent reduction in histopathology stage ® Stay lean
® Technical difficulty during dissection of tissue ® If you choose to drink, limit yourself to an
brought about by tissue fibrosis caused by average of one drink a day
radiotherapy preoperatively ® Avoid unnecessary exposure to radiation
® Avoid exposure to industrial and environmental
toxins
® Avoid infections that contribute to cancer
® Make quality sleep a priority
® Get enough Vitamin D
§ Around 800-1000 IU decreases the risk for
the formation of cancer
MHAM
The Skin and Subcutaneous Tissue
Dr. Carlito Astillero II | March 18, 2022
SURGERY
OUTLINE • The epidermis and its appendages are of

I. The Skin ectodermal origin, whereas the dermis and
A. Epidermis hypodermis are of mesodermal origin
B. Dermis
C. Hypodermis (Subcutaneous Fat, Panniculus A. EPIDERMIS
Adiposus) • The epidermis consists of stratified epithelium that
undergoes continuous regeneration
II. Inflammatory Conditions
• 90-95% of these epithelial cells are ectodermally
A. Hidradenitis Suppurativa derived keratinocytes
B. Pyoderma Gangrenosum • Transit time (keratinization) is approximately 30 days
C. Toxic Epidermal Necrolysis (TENS) and • Epidermal thickness differs between skin regions,
Stevens-Johnson Syndrome (SJS) ranging from 50 μm on the eyelids to 1 mm on the
III. Injuries soles
A. Radiation-Induced Injuries
B. Trauma-Induced Injuries Epidermal Components
IV. Bacterial Infections of the Skin and
Subcutaneous Tissue
A. Uncomplicated Skin Infections
B. Complicated Skin Infections
C. Actinomycosis
V. Viral Infections with Surgical Implications
A. Human Papilloma Virus
VI. Benign Tumors
A. Hemangioma
B. Nevi (Mole)
C. Cystic Lesions
VII. Malignant Tumors
A. Basal Cell Carcinoma
B. Squamous Cell Carcinoma
C. Melanoma
D. Merkel Cell Carcinoma
E. Kaposi Sarcoma Keratinocytes
F. Dermatofibrosarcoma Protuberans • Basal layer keratinocytes
G. Angiosarcoma ® Are columnar or cuboidal cells with a basophilic
cytoplasm and large nucleus, and they are
LEGENDS aligned with an underlying basement membrane
Presentations Remember Lecturer Book and anchored by hemidesmosomes
• Granular layer keratinocytes
→ Are flattened cells lying parallel to the skin
I. THE SKIN surface, with a diameter of 25 μm; they contain
• The skin is a complex organ encompassing the keratohyalin granules and keratin and lamellar
body’s surface and continues with the mucous bodies
membranes • Corneum layer keratinocytes
• Accounting for approximately 15% of total body ® Are highly flattened, hexagonal, eosinophilic
weight, it is the largest organ in the human body cells, containing mainly keratin matrix, that are
• Enabled by an array of tissue and cell types, intact eventually shed from the skin surface and
skin protects the body from external insults contribute to the skin’s barrier function
• However, the skin is also the source of a myriad of
pathologies that include inflammatory disorders, Langerhans Cells
mechanical and thermal injuries, infectious diseases, • These are mobile, dendritic, antigen-presenting cells
and benign and malignant tumors present in all stratified epithelia that originate from
• Components of epithelial, connective, vascular, bone marrow precursors
muscular, and nervous tissue are organized into 3
histologic layers (Epidermis, Dermis, and
Hypodermis), which vary in consistency between
various body parts
Pilosebaceous Follicles
• These structures are derived from the epithelial germ
layer and lie obliquely in the dermis, with their
deepest part reaching the hypodermis
• They are present throughout the integument,
excluding the glabrous skin (palms, soles) and
portions of the genitalia
• Their growth is cyclic and proceeds through three
distinct phases of uneven duration (anagen, catagen,
and telogen) during which their histology varies
considerably
Nails
• The nails overlie the dorsal aspect of the distal
phalanges of the fingers and toes
Melanocytes • They consist of three parts:
→ Root, covered by the proximal nail fold,
• Originating from the neural crest, these cells migrate
continuous with the lateral nail folds
into the epidermis where they produce melanin, the
→ Nail plate, comprised of hard keratin
main natural pigment of the skin
→ Free edge, overlying the hyponychium, a
• They are distributed regularly among basal thickened epidermis
keratinocytes, at a ratio of 1 melanocyte for every 4
to 10 keratinocytes
B. DERMIS
• Their density reaches 500 to 2000 cells per mm2 of
cutaneous surface, with regional variations (Maximal
Dermal Fibers
density on genital skin) • The majority (>90%) of dermal fibers are collagen,
• Melanin is produced through the enzymatic activity of predominantly types I and III, which are responsible
tyrosinase on the substrate tyrosine and is then for the mechanical resistance of the skin
stored in the melanosomes • Collagen
• These are transported along the dendritic processed ® Is important in the density and structure of your
of melanocytes and are eventually transferred to skin
adjacent keratinocytes where they form an umbrella- • Elastic fibers
like cap over the nucleus, protecting it from the ® Are responsible for the retractile properties of
effects of ultraviolet (UV) light the skin due to their ability to stretch to twice
their resisting length and return to their baseline
Sweat Glands shape after the deforming force is relieved
• Are tubular exocrine glands, consisting of a secretory
coil and an excretory duct Cells
• Eccrine sweat glands • Fibroblasts
® Are the main sweat glands in human, playing a ® Are the fundamental cells of the dermis and all
vital role in the process of thermoregulation connective tissues that synthesize all types of
→ They are present almost everywhere on the skin fibers and the ground substance
(except mucous membranes), with a maximal • Myofibroblasts
density over the palms, soles, axillae, and ® Are cells derived from fibroblasts, namely during
forehead the process of wound healing
• Apocrine sweat glands → When cleansing a wound, use a NSS (Normal
® Are less abundant in humans and are derived Saline Solution)
embryologically from the germ cells that • Dermal dendrocytes
produce the pilosebaceous follicle and are, ® Complement the immunologically functional cells
therefore, structurally associated with it of the epidermis
→ These glands are found in the axillary, • Mast cells
anogenital, and nipple regions ® Are mononuclear cells of the bone marrow
• Apoeccrine glands origin, sparsely distributed in the perivascular
® A third type of sweat gland more recently and periadnexal dermis
described in the axillary region
→ Are atrichial glands, opening directly to the skin Cutaneous Vasculature
surface, but their secretory coil is similar to that • The skin possesses a rich vascular network that
of apocrine glands and they present during largely exceeds the skin metabolic requirements
puberty → Especially in the neck area
• This network plays a role in thermoregulation (e.g.
sweating), wound healing, immune reactions, and
blood pressure control
→ That is why when there is laceration in the head
or neck area, it bleeds profusely but it can heal
faster than the different parts of the body
→ When there are sutures in the head and neck,
sutures must be removed after 3-4 days after
suturing
Cutaneous Innervation Seen in the picture are atrophic and hypertrophic scars. There are
• Afferent limb interconnecting sinuses.
® Is responsible for the perception of eternal
stimuli (touch, pressure, vibration, pain • Axilla, inguinal, perineal, mammary, and
temperature, itch) via a network of sensory inframammary areas corresponding to a “milk-line”
myelinated and nonmyelinated fibers, free distribution
terminal nerve endings, and tactile corpuscles • Pathophysiologic mechanism is that there is follicular
• Efferent limb occlusion
® Is supported by nonmyelinated fibers of the • Poor hygiene, smoking, alcohol consumption, and
sympathetic system that regulate vasomotricity, bacterial involvement are thought to exacerbate
sweat secretion and piloerection rather than initiate the disease process
• Respond to topical or systemic antibiotics
(Clindamycin is first-line therapy)
• Refractory cases respond best to wide surgical
debridement of the affected sites
• Recurrence rates tend to be higher in the
inframammary and inguino-perineal regions, reaching
up to 50%
B. PYODERMA GANGRENOSUM
• A relatively uncommon noninfectious neutrophilic
dermatosis
• Commonly associated with inflammatory bowel
Dermal layer – the thick layer. Which consists most of the structures of disease, rheumatoid arthritis, hematologic
our skin. malignancies, and monoclonal gammopathies
• Characterized by the presence of sterile pustules,
C. HYPODERMIS (SUBCUTANEOUS FAT, which progress and ulcerate to variable depth and
PANNICULUS ADIPOSUS) dimensions
• The deepest part of the skin, separating it from the
underlying muscle fascia or the periosteum
• The main cells of the hypodermis are the adipocytes-
large, rounded cells with a lipid-laden cytoplasm
(triglycerides, fatty acids) compressing the nucleus
against the cell membrane
II. INFLAMMATORY CONDITIONS • Lesion borders are purplish in color with

A. HIDRADENITIS SUPPURATIVA erythematous edges
• A chronic inflammatory disease presenting as painful • Five clinical types are identified:
subcutaneous nodules → Ulcerative
→ Pustular
• It is characterized by multiple abscesses,
→ Bullous
interconnecting sinus tracts, foul-smelling exudate
→ Vegetative
from draining sinuses, inflammation in the dermis,
→ Peristomal
both atrophic and hypertrophic scars, ulceration, and
infection, which may extend deep into the fascia • Treatment of PG combines systemic, topical and
surgical modalities
C. TOXIC EPIDERMAL NECROLYSIS (TENS) 10 to 14 days of exposure, provided other
AND STEVENS-JOHNSON SYNDROME (SJS) parameters are optimized (nutrition, infection, etc.)
• These inflammatory diseases represent a spectrum • Chronic radiation skin injury includes delayed
of an autoimmune reaction to stimuli such as drugs ulcers, fibrosis, and telangiectasias that present
that result in structural defects in the epidermal- weeks to years after exposure
dermal junction • Treatment of minor radiation skin injury consists
• The cutaneous manifestations of Toxic Epidermal primarily of maintaining the integrity of remaining skin
Necrolysis Syndrome (TENS) follow a prodromal with moisturizers until recovery of skin adnexa
period reminiscent of an upper respiratory tract • Management of severe radiation includes surgical
infection excision of damaged tissues as well as control of the
• Typically, a Nikolsky sign develops in which lateral typically opiate-resistant pain
pressure causes the epidermis to detach from the • Environmental-Induced Injuries are from UV
basal layer radiation and solar-induced skin toxicity and are the
most common forms of radiation exposure skin
injuries
• Short-term solar radiation effects include erythema
and pigmentation
• UVB is more effective than UVA in causing a dermal
inflammatory response resulting in erythema in a
delayed phenomenon, peaking at 6 to 24 hours
• Pigmentation occurs as result of photooxidation of
melanin by UVA
• The mildest form of the disease is SJS, which • An acute erythemogenic dose of UVB is necessary
clinically presents as second-degree burns appearing to induce delayed pigmentation; UVA is less effective
as erythema and blisters/bullae of the oropharynx, in tanning and in radiation protection
anoderm and torso • UVB pigmentation results in a homogenous tan and
• It affects the mouth, esophagus, small bowel, and UVA protection
colon, resulting in sloughing of mucosa that may • However, melanization produced by cumulative
present as gastrointestinal bleeding and intestinal UUVA exposures appears to be longer lasting than
malabsorption that acquired with UVB exposures.
• It also affects the eyes, genitalia, and other mucosal • Long-term effects of UV pigmentation can lead to
surfaces irregular pigmentation and hyperpigmented areas,
• The drugs most commonly associated with melasma, post inflammatory pigmentation, and
TENS-SJS include: actinic lentigines (sun spots)
→ Aromatic anticonvulsants • There is also a loss of collagen and a change in
→ Sulfonamides collagen composition (increase in collagen III to
→ Allopurinol collagen I ratio)
→ Oxicams (nonsteroidal anti-inflammatory drugs) • This structural disarrangement manifests as a loss of
→ Nevirapine firmness and resilience of skin, leading to an older
• The two principles of TENS management include appearance to the skin
early withdrawal of the offending drug and supportive
care (e.g. pain control, intravenous fluid repletion, B. TRAUMA-INDUCED INJURIES
prevention of skin infections, enteral feeds, and Mechanical Injury
possible respiratory support) in a burn unit
• Clean lacerations may be closed primarily after
irrigation, debridement, and exploration
III. INJURIES • Many surgeons will primarily close clean wounds if
A. RADIATION-INDUCED INJURIES the injury is treated within 6 hours of the inciting
• Radiation-induced injuries can be the result of event
environmental exposure, industrial/occupational • Contaminated or infected wounds should be allowed
applications, and medical etiologies to heal by secondary intention or delayed primary
• The replicating basal keratinocytes, hair follicle stem closure
cells, and melanocytes are the most radiosensitive • Tangential abrasions should be approached similarly
components of the skin to burns injuries
• Highly dividing cells affected by radiation injuries • Superficial partial-thickness wounds may be left to
• Acute skin changes are the result of injury to the heal spontaneously while providing topical
basal epithelium in the radiated region antimicrobial prophylaxis or sterile biologic dressings
• Within weeks, this manifests as erythema, edema • Deeper wounds may require split-thickness skin
and alopecia grafting
• Re-epithelialization from unaffected wound edges
and from recuperating dermal adnexa begins within
• Degloved skin may be used to provide coverage
similar to a skin graft, or as a temporary dressing, • Injuries related to basic fluids result from liquefactive
provided the wound bed has been cleaned necrosis
• Starting with fat saponification and result in longer
more sustained injuries causing a deeper patter of
injury
• Common examples are sodium hydroxide (drain
decloggers, paint remover) and calcium hydroxide
(cement)
• This permits further penetration of the unattached
molecules, causing further tissue destruction
• Treatment for both type of injuries is based on
neutralization of the inciting solution and starts with
running distilled water or saline over the affected skin
for at least 30 minutes for acidic solutions and 2
hours for alkaline injuries
• Many cases are successfully managed
Bite Wounds conservatively with topical emollients and oral
analgesics
• Bite bacteriology is influenced by normal mouth flora,
as well as the content of the offending animal’s food • If signs of deep second-degree burns develop,
local wound care may include:
• Early presentation bite wounds yield polymicrobial
cultures → Debridement
→ Silvadene
• Bacterial load in dog bites is heavily dependent on
→ Protective petroleum gauze
the content and timing of the last meal and can range
• In severe cases, injury to underlying vessels, bones,
between 10,000 with a dry meal (biscuits) to
muscle, and tendon may occur, and these cases may
100,000,000 within 8 hours of a wet meat meal
be managed within 24 hours by liposuction through a
• The bacterial spectrum found in cat bites is very
small catheter and then saline injection
similar to that of dog bites with higher prevalence of
• Surgery is indicated for tissue necrosis, uncontrolled
Pasteurella species
pain, or deep tissue damage
• Antibiotic coverage must cover gram-positive and
• Antibiotics should not be administered unless signs
anaerobic organisms
of infection are present
• A first-generation cephalosporin in combination with
→ Just like the burns, systemic antibiotic does not
penicillin or ampicillin in combination with clavulanic
absorb the burn area because it can cause scar
acid provides adequate coverage
formation
• To significantly reduce bacterial load and eliminate
• Hydrofluoride is found in air conditioning cleaners
particulate debris in the wound, pressure irrigation
and petroleum refineries
should be performed
→ Treatment of the hydrofluoride burns should
• Preferably with sterile saline solution
include topical or locally injected calcium
• Bite wounds may be closed primarily, particularly in gluconate to bind fluorine ions
areas of aesthetic significance such as the face,
• Intra-arterial calcium gluconate can provide pain
where secondary intention healing will result in relief and preserves arteries from necrosis, whereas
unsightly scarring
intravenous (IV) calcium repletes reabsorbed calcium
• Anti-rabies stores
• IV fluid extravasation results in yet another type of
Caustic Injury chemical injury and occurs in 0.1% to 0.7% of all
• Damage from chemical burns is related to the cytotoxic drug administrations
concentration, duration, and quantity of acidic or • Doxorubicin is often the offending agent, and its
alkaline solution effects are attributable to direct toxicity resulting in
• Acidic injuries typically cause a more superficial burn cellular death, perpetuated by release of doxorubicin
pattern due to eschar formation as a result of from cell lysis and failed wound healing
coagulation necrosis of the skin • Treatment varies from conservative management
• These limits subsequent tissue penetration with limb elevation to saline infiltration (for dilution)
and aspiration with liposuction cannula
• Cold or warm compresses should be avoided
because they may add a thermal injury component to
an area in which thermoregulatory mechanism are
impeded due to vasoconstriction, pressure, and
inflammation
• Surgical intervention includes debridement of • Hypothermic skin injury (Frostbite)
devitalized tissue and reconstruction with appropriate ® Can result from direct cellular damage or the
technique secondary effects of microvascular thrombosis
and subsequent ischemia
® With rewarming, the ice melts and damaged
cells take up water; affected capillaries leak
fluid into the interstitium
® Edema and concomitant inflammatory process
result in epidermal blistering and micro
vasoconstriction, propagating further tissue
injury
Thermal Injury
® Treatment
§ Rapid rewarming to 40 to 42 °C
§ Analgesia
§ Debridement of blisters
§ Hydrotherapy
§ Elevation
§ Topical antimicrobials
§ Topical antithromboxanes (Aloe vera)
§ Systemic antiprostaglandins (Aspirin)
Pressure Injury
• Tissue pressures that exceed the pressure of the
microcirculation (30 mmHg) result in tissue ischemia
• Areas of bony prominence are particularly prone to
ischemia
• The epicenter of the injury undergoes a varying ® The most common areas being ischial
extent of necrosis otherwise referred to as the zone tuberosity (28%), trochanter (19%), sacrum
of coagulation, which is surrounded by the zone of (17%), and heel (9%)
stasis, which has marginal perfusion and • Tissue pressures can measure up to 300 mmHg in
questionable viability the ischial region during sitting and 150 mmHg over
• The outermost area of the skin shows characteristics the sacrum while lying supine
similar to other inflamed tissues and has been • Muscle is more susceptible than skin to ischemic
designated the zone of hyperemia insult due to its relatively high metabolic demand
• Wounds are staged as follows:
→ Stage 1: Nonbalancing erythema over intact skin
→ Stage 2: Partial-thickness injury (epidermis or
dermis) – Blister or Crater
→ Stage 3: Full thickness injury extending down to,
but not including fascia and without undermining
of adjacent tissue
→ Stage 4: Full thickness skin injury with
destruction or necrosis of muscle, bone, tendon,
or joint capsule
• Management principles for pressures sores • Minor primary infections, or a secondarily infected
should include lesion, should be treated
® Pressure relief (air mattresses and gel cushions ® Topical ointments such as 2% mupirocin
for redistribution of pressure) § To provide coverage for methicillin-resistant
® Systemic optimization (particularly nutritional Staphylococcus aureus (MRSA).
support)
• For an uncomplicated furuncle or carbuncle
® Wound care
• Stage 2 and 3 ulcers may be left to heal secondarily (simple abscess), incision and drainage are
after debridement sufficient, and antibiotics are not warranted
® If adequate drainage is noted
• For non-purulent, uncomplicated cellulitis β-
haemolytic streptococci coverage is recommended
(β-lactam such as cephalexin)
® MRSA coverage to be added if no response is
seen within 48 to 72 hours
® Or in the presence of chills, fevers, expanding
• Subatmospheric pressure wound therapy devices erythema or uncontrolled pain
(Vacuum-assisted closure) play a role in wound • Purulent cellulitis that does not meet criteria for a
management by removing excess interstitial fluid, complicated infection requires MRSA coverage
promoting capillary circulation, decreasing bacterial
® Clindamycin, Trimethoprim-Sulfamethoxazole,
colonization, increasing vascularity and granulation
tissue formation, and contributing to wound size Linezolid, and Tetracyclines are options
reduction • The infections can be managed on an outpatient
basis in the vast majority of cases
B. COMPLICATED SKIN INFECTIONS

• Deep-tissue infections (below the dermis) extensive
cellulitis, necrotizing fasciitis, and myonecrosis are
considered complicated skin infection
• Crepitus (gas-forming organism), fluctuance
(abscess), purpura (sepsis in streptococcal
infections), bullae (streptococci, Vibrio vulnificus),
lymphangitis, and signs of a systemic inflammatory
response
• Aspirated fluid from suspected infected collection
should be cultured
• Swabs and aspirates in cellulitis have a low yield
(10%), whereas tissue cultures may have a higher
IV. BACTERIAL INFECTIONS OF THE SKIN
rate of organism recovery (20%-30%)
AND SUBCUTAENOUS TISSUE
A. UNCOMPLICATED SKIN INFECTIONS • Treatment of non-purulent, complicated cellulitis
• Disease processes included in this category are ® Can begin with a β-lactam
limited to the epidermis or its appendages and ® With MRSA coverage added if no response is
involve a surface area that is less than 75 cm2 observed
Impetigo, cellulitis, erysipelas, folliculitis, furuncles, • Empiric MRSA coverage is warranted in all other
and simple abscesses are included in this category complicated skin and subcutaneous infections
• Folliculitis is an infection of a hair follicle that may
progress to a furuncle or a carbuncle (abscess with • Vancomycin is the mainstay of therapy, although it is
multiple draining sinuses) inferior to β-lactams for Methicillin-Sensitive
• Folliculitis and furuncles resolve with adequate Staphylococcus Aureus (MSSA)
hygiene and warm soaks • Clindamycin is also approved for S. aureus;
however, resistance may develop, and diarrhea can
occur in up to 20% (Clostridium difficile related)
• Necrotizing infections
® Can manifest with bullae, skin necrosis, pain
beyond the margins of erythema, crepitus, gas
on imaging, hypotension, or other signs of
systemic inflammatory response syndrome • In the Fournier’s gangrene one should aim to
(SIRS) preserve
• Common sites of origin ® The anal sphincter as well as the testicles
® The genitalia, perineum (Fournier’s gangrene) § Blood supply is independent of the
and abdominal wall overlying tissue
• Involvement of the deep fascia (necrotizing § Usually not infected
fasciitis-deep to the adipose tissue, overlying the • Revision surgery should be planned
muscle) ® “Second look”
® Results in a rapidly progressing infection with ® With 24 to 48 hours
bacteria spreading along low-resistance tissue
planes C. ACTINOMYCOSIS
• Should be considered in differential diagnosis of
any acute, subacute or chronic cutaneous swelling
of head and neck
• Can spread beyond boundaries of tissue planes
and may also mimic chronic osteomyelitis
• Treatment: Combination of penicillin therapy and
surgical debridement
• Three types of necrotizing infections can be

distinguish based on the organism involved
® Type 1 the most common, with a polymicrobial
source including gram-positive cocci, gram-
negative rods and anaerobes (Bacteroides
species, Clostridium perfringens and septicum),
occurring immunocompromised host
® Type 2 is less common. Nonmicrobial infection V. VIRAL INFECTIONS WITH
with β-haemolytic streptococci or staphylococci
SURGICAL IMPLICATIONS
(MRSA rising in frequency to 40%). It can be
A. HUMAN PAPILLOMA VIRUS
• Small DNA viruses if papovavirus family
associated with toxic shock and occur in a
• HPV-1, 2 and 4
previously healthy host, typically on the trunk or ® Cutaneous types
extremities, with a history of trauma commonly ® Cause common warts (verruca vulgaris)
elicited • HPV-5 and 8
® Type 3 is a rare but fulminant subset resulting ® Associated with epidermodysplasia verruciformis
from a V. vulnificus infection of traumatized skin § Extremely rare autosomal recessive
in sea divers disorder of the skin that entails a higher risk
of malignant transformation
• Operative exploration and debridement should not be
• HPV-6 and 11
delayed
® Mucosal type
• Broad-spectrum IV antibiotics should be started as ® Have low malignant potential
soon as possible, with Vancomycin (for MRSA) • HPV-16 and 18
® In addition to Clindamycin or Linezolid (to inhibit ® Higher malignancy potential
toxin synthesis) • Plantar warts occur on soles of feet, and is caused by
® Gram-negative rod coverage (in the form of a HPV-1 and 4, commonly pressure points,
third-generation Cephalosporin or a Quinolone) characterized by keratotic plug surrounded by a
hyperkeratotic ring, with black dotes (thrombosed
• Surgery is the definitive treatment
capillaries) on the surface
• Characteristic “murky dishwater” – like fluid may be
encountered at the affected sites
• Borders for debridement are where tissue planes
cease to readily separate
• 1ST line therapy for single or multiple warts
® Topical salicylic acid
® Silver nitrate
® Glutaraldehyde
® If fails, cryotherapy may be considered
• Treatment of recalcitrant lesions includes variety of
therapeutic options aimed at physically destroying the
lesions by electrodessication, cryoablation, and
pulsed dye laser therapy
VI. BENIGN TUMORS

A. HEMANGIOMA
• Plane warts occur on face, dorsum of hands, and • Results from benign proliferation of endothelial cells
shins that surround blood-filled cavities
• Caused by HPV-3 and 10 and tend to be multiple, • Natural history most commonly presentation soon
flat-topped lesions with smooth lesions with a smooth after birth, rapid growth during the 1st year of life, an
surface and light brown color gradual involution in more than 90% of cases
• They regress spontaneously
• Condyloma acuminatum manifests as multiple
exophytic papillomatous lesions of the anogenital
area
• Sexually transmitted HPV-6 and 11 are responsible
for 90% of genital warts
• Systemic prednisone and interferon-alpha can

impede tumor progression
• If persist into adolescence leaving cosmetically
undesirable telangiectasia, surgical resection may be
considered
• Giant condyloma acuminatum of BuschkeLowenstein • When surgical resection debulking is considered,
is a large exophytic, cauliflower-like tumor is now upfront selective embolization can help with planned
thought to be variant of verrucous carcinoma resection
B. NEVI (MOLE)
• Overgrowth of melanocyte nevus cells may be found
in the epidermis (junctional), partially in the dermis
(compound), or completely within the dermis (dermal)
• Congenital nevi are found in less than 1% of
neonates and when characterized as giant congenital
nevi, they have up to a 5% chance of developing into
a malignant melanoma
• Treatment of choice: Total excision and at times the
large wound defect require serial excisions and local
• Epidermodysplasia verruciformis is a form of
tissue expanders
primary genetic immunodeficiency, rendering patients
susceptible to
infections with HPV- C. CYSTIC LESIONS
5 and 8 • There are 3 types:
• It presents clinically ® Epidermal cysts
as multiple flat warts § The most common
resembling cutaneous cyst
seborrheic keratosis § Histologically
• 30%-50% risk of characterized by
squamous cell mature epidermis
carcinoma complete with granular layer
® Trichilemmal cysts • This variant tends to develop in sun-exposed areas of
§ Second most individuals over the age of 60
common lesion • Superficial BCC accounts for 15% of BCC, is
§ Tend to form on the
diagnosed at a mean age of 57 years, and typically
scalp of females
§ Have a distinct odor appears on the trunk as a pink or erythematous
after rupture plaque with a thin pearly border
§ Histologically lack a granular layer and have • The infiltrative form appears on the head and neck in
an outer layer resembling the root sheath of the late 60s with similar clinical appearance to the
a hair follicle. nodular variant
® Dermoid cysts
• An important variant to keep in mind is the
® Congenital
pigmented variant of nodular BCC because this
® Found in between the
forehead to nose tip may be difficult to differentiate from nodular
® Contain squamous melanoma
epithelium, eccrine • Treatment options include Moh’s microsurgery,
glands and pilosebaceous units, occasionally excisional surgery, and cautery and destruction
developing bone, tooth or nerve tissue • Moh’s microsurgery provides histologic confirmation
® The eyebrow is the most frequent site of of excision and maximal conservation of tissue, which
presentation
is important to keep in mind in cosmetically sensitive
® These cysts are commonly asymptomatic but
can become inflamed and infected, thus areas such as facial lesions
necessitating incision and drainage • Alternative treatment is excisional surgery with 4-mm
® After the acute phase subsides, the entire cyst margins with extension into subcutaneous tissue,
should be removed to prevent recurrence which provides definitive treatment of
nonmorpheaform lesions
VII. MALIGNANT TUMORS • Radiation also may be used in cases of questionable
A. BASAL CELL CARCINOMA resection margins or microscopic positive margins
• Arises from the basal layer of non-keratinocytes and
after surgery
represents the most common tumor diagnosed in the
United States • 6 to 12 weeks of imiquimod, an FDA-approved drug
• The primary risk factor for disease development is and immune modifier, is an option for small-diameter
sun exposure (UVB rays more than UVA rays) <2cm
particularly during adolescence • Topical Fluorouracil is another FDA-approved
• Other factors include immune suppression (i.e organ treatment for superficial BCC
transplant recipients, HIV), chemical exposure, and
• Topical photodynamic therapy has shown some
ionizing radiation exposure
benefit in treatment as well
• The natural behavior of BCC is one of local invasion
rather than distant metastasis • It is critical for each patient to have routine annual
follow up that includes full-body skin examinations
• Untreated BCC can result in significant morbidity
• 60% percent of recurrences develop within 3 years,
• Thirty percent of cases are found on the nose, and
and with a few exceptions occurring decades after
bleeding, ulceration, and itching are often part of the
initial treatment, the remaining recur within 5 years of
clinical presentation
initial treatment
B. SQUAMOUS CELL CARCINOMA

• SCC is the second
most common skin
cancer, generally
afflicting individuals of
lighter skin color
• The primary risk factor
and driving force for
• The most common form of BCC (60%) is the the development of
nodular variant, characterized by raised, pearly pink this common cancer is
papules and occasionally a depressed tumor center UV exposure;
with raised borders giving the classic- rodent ulcer however, other risks include environmental factors
appearance such as chemical agents, physical agents (ionizing
radiation), psoralen and UVA (PUVA), HPV-16 and C. MELANOMA
HPV-18 infections (immunosuppression), and • Melanoma growth most commonly starts as a
smoking localized, radial growth phase followed by a vertical
• Chronic nonhealing wounds, burn scars, and chronic growth phase that determines metastatic risk
dermatosis are other risk factors, and many darker • The subtypes of melanoma include lentigo
maligna, superficial spreading, acral lentiginous,
skin individuals who develop SCC often have a mucosal, nodular, polypoid, desmoplastic,
history of one these risk factors amelanotic, and soft tissue
• Lesions associated with chronic inflammation • The most common subtype is superficial
and located at mucocutaneous junctions may spreading, accounting for 70% of cases
metastasize in 10%-30% of cases, whereas lesions • Nodular melanoma accounts for 15% to 30% of
arising in sun-exposed areas without adverse risk melanomas, and this variant is unique in that it
factors are less likely to spread and have a better begins with a vertical growth phase that partly
accounts for its worse prognosis
prognosis
• Lentigo maligna is typically found in older
• Perineural involvement increases the incidence of individuals and primarily located in the head and
local recurrence and lymph node metastasis and has neck region
a poorer survival • The acral lentiginous variant accounts for 29% to
• Other histologic features indicative of aggressive 72% of melanomas in dark-skinned individuals, is
disease include poor differentiation, thickness greater occasionally seen in Caucasians, and is found on
palmar, plantar, and subungual surfaces
than 4 mm, and adenoid, adenosquamous, and
• Melanoma most commonly manifests as cutaneous
desmoplastic subtypes disease, and clinical characteristics include an
• Treatment modalities for SCC include cautery and Asymmetric outline, changing irregular Borders,
ablation, cryotherapy, drug therapy including Color variations, Diameter greater than 6 mm,
imiquimod, surgical excision, Moh’s microsurgery, and Elevation (ABCDE)
and radiation therapy • Other key clinical characteristics include a
• For lesions less than 2 cm in diameter, wide pigmented lesion that has enlarged, ulcerated, or
bled
excision with a 4 mm margin for low-grade lesions
and a 6 mm margin for high-grade lesions is sufficient
• Factors rendering tumors high risk are size >2 cm
in diameter and involvement of subcutaneous tissue
• When patients are poor surgical candidates,
radiation therapy can play a role in primary modality
treatment
• It may also act as an adjunct to surgical treatment in
cases of lip carcinoma with 30%-50% involvement, Diagnosis And Staging
microscopic positive margins, perineural histology, • History and physical exam
underlying tissue invasion, and multiple recurrences • Entire skin should be checked for synchronous
• The role of lymph node dissection in the setting of primaries, satellite lesions, and in-transit
SCC is evolving metastases, and all nodal basins should be
examined for lymphadenopathy
• Regional palpable nodes should be removed along
• Suspicious lesions should undergo excisional biopsy
with susceptible regional lymph node basins in with 1 to 2mm margins
patients with SCC in the setting of chronic wounds • Tumors that are large or in a cosmetically or
anatomically challenging area can be approached by
incisional biopsy, including punch biopsy
• Suspicious lymph nodes should undergo Fine
Needle Aspiration (FNA)
• Melanoma is characterized according to the
American Joint Committee on Cancer (AJCC) as
localized disease (Stage I and II), regional disease
(Stage III), or distant metastatic disease (Stage IV)
• Overall tumor thickness, ulceration, and mitotic
rate are the most important prognostic indicators of
survival
• If a sentinel node contains metastatic melanoma
with >1mm in size, a sentinel lymph node biopsy
should be done; the number of positive nodes, • If positive, a metastatic staging workup should
thickness, mitotic rate, ulceration of the primary follow, and if negative, treatment of the primary and
tumor, and patient age determine prognosis nodal basin as managed for sentinel lymph node–
• Patients with clinically palpable regional lymph positive disease should be considered
nodes are at high risk for distant metastases and • Important surgical principles for excision of the
should receive additional imaging that includes CT of primary lesion are to excise with wide margins
the chest, abdomen, and pelvis; whole-body PET- down to fascia and complete circumferential and
CT; or brain MRI peripheral deep-margin assessment
• Sentinel Lymph Node Biopsy (SLNB) is a • Recommended management for margins is 1 to 3
standard staging procedure to evaluate the regional cm margins
nodes for patients with clinically node-negative
malignant melanoma
• This technique identifies the first draining lymph
node from the primary and has shown excellent
accuracy and significantly less morbidity compared
to complete resection of nodal basins
Surgical Management Of The Primary Tumor And

Lymph Nodes
• Surgical margins of 0.5 to 1.0 cm are sufficient
• 1.0-cm margins should be obtained in anatomically
feasible areas
• SLNBs are recommended for melanomas 1 to 4 mm

thick
• SLNB may be considered for thin melanoma with
adverse features (i.e., >0.75 mm, >1 mitosis per
mm, ulcerated) E. KAPOSI SARCOMA
• For tumors that are >4 mm, the incidence of • Kaposi’s sarcoma is characterized by the
regional lymph node positivity is 35% to 40% and proliferation and inflammation of endothelial derived
SLNB may provide prognostic information for these spindle cell lesions
thick melanomas • There are five major forms of this
• For patients with clinically evident local regional angioproliferative disorder:
lymphadenopathy, FNA biopsies can confirm ® Classic (Mediterranean)
metastatic disease ® African endemic
• Individuals with face, anterior scalp, and ear ® HIV-negative men having sex with men (MSM)–
primaries who have a positive SLNB should undergo associated
a superficial parotidectomy in addition to a ® AIDS-associated
modified radical neck dissection ® Immunosuppression-associated; they are all
driven by the Human Herpes Virus (HHV-8)
D. MERKEL CELL CARCINOMA • Kaposi’s sarcoma appears as multifocal, rubbery
• This is a rare and aggressive neuroendocrine tumor blue nodules
of the skin most commonly found in white men and • Treatment of AIDS-associated Kaposi’s sarcoma is
diagnosed at a mean age of 70 years with antiviral therapy, and many patients experience
• A rapidly growing, flesh-colored papule or plaque a dramatic treatment response
characterizes the disease. Regional lymph nodes • The benefit of surgery is limited and generally should
are involved in 30% of patients, and 50% will not be pursued except for palliation
develop systemic disease (skin, lymph nodes, liver,
lung, bone, brain) F. DERMATOFIBROSARCOMA PROTUBERANS
• Patients without clinical nodal disease should • This rare, low-grade sarcoma of fibroblast origin
undergo an SLNB preceding a wide local excision commonly afflicts individuals during their third
• In patients with sentinel lymph nodes with decade of life
metastatic disease, completion lymphadenectomy • Presentation is characteristically a slow growing,
and/or radiation therapy may follow asymptomatic, violaceous plaque involving the trunk,
• Patients with clinically positive nodes should head, neck, or extremities
have an FNA to confirm disease
• Treatment is wide local excision with 3-cm margins
down to deep underlying fascia or Moh’s
microsurgery in cosmetically sensitive areas where
maximum tissue preservation will benefit
G. ANGIOSARCOMA
• Angiosarcoma is an uncommon, aggressive cancer
that arises from vascular endothelial cells and
occurs in four variants, all of which have a poor
prognosis
• The head and neck variant presents in individuals
older than 40 years as an ill-defined red patch on the
face or scalp, often with satellite lesions and distant
metastasis, and has a median survival of 18 to 28
months
• Lymphedema-associated Angiosarcoma
(Stewart-Treves) develops on an extremity
ipsilateral to an axillary lymphadenectomy
• It appears on the upper, medial arm as a violaceous
plaque in an individual with nonpitting edema and
has a poor survival
• Radiation-induced Angiosarcoma occurs 4 to 25
years after radiation therapy for benign (acne) and
malignant (i.e., breast cancer) conditions
• The Epithelioid variant of Angiosarcoma involves

the lower extremities and also has a poor prognosis
• Surgical excision with wide margins is the
treatment of choice for localized disease, but the
rate of recurrence is high
• Adjuvant radiation therapy can be considered in a
multidisciplinary fashion

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MHAM

COLLEGE OF MEDICINE CLASS 2024

Outline B. FLUID COMPARTMENTS

Weakness, Lethargy, Hyperactive reflexes, G. METABOLIC DERANGEMENT

Hypotension, Arrest Arrhythmia

• Concomitant hypokalemia (extracellular K ions

E. POSTOPERATIVE FLUID THERAPY

*Memorize the entire table

C. VASODILATORY SHOCK (DISTRIBUTIVE) E. NEUROGENIC SHOCK

Rationale: Found in patients with prolonged starvation; Answer: C

Rationale: Should be base deficit and lactate

Early definition of coronary anatomy and Answer: C

14. In septic shock, which of the following is true?

a. The mortality rate is between 10 to 20%

Rationale: A. Mortality is 30-50%, B. Gram negative

15. Recommended first line vasopressor in cases of

Rationale: A. Dopamine and B. Dobutamine: Inotropic

*Questions from Dr. Amodia’s lecture

→ When doing tracheostomy, it is usually inserted

• Lung on the right:

• According to the latest ATLS, needling should be

Figure: Site for needling

• Closed Tube Thoracostomy

→ When this occurs, you tape the wound area, 3

• A rule of thumb to consider for secondary access is

Four life-threatening injuries must be identified

Three critical tools used to differentiate these in Emergency Department Thoracotomy

• Left anterolateral thoracotomy (You open the left side

Trauma patient with blood loss the Goal is to:

• Re-establish tissue perfusion

Allergies, Medications, Past illnesses or Pregnancy (for Critically Injured Patients

• Algorithm for the management of penetrating neck • Penetrating thoracic injuries

Focused Assessment with Sonography for

II. HERITABLE DISEASES OF

Skin: soft, not

III. HEALING IN SPECIFIC TISSUES B. BONE

• 25% of diabetic patients

Venous Stasis Ulcer

VII. EXCESS HEALING

*Found in Schwartz, please familiarize

Outline between 20 and 59 years of age

2nd Degree Partial Thickness

The degree of cellular injury varies depending on

The 3 zones are clinically important because it will

• After initial injury, after 72 – 96hrs, patient is initially in

4 mL x % body surface area (which can determine once

• Once computed; the total requirement divides it

X. 2 COMPARTMENTS OF THE ARM

• Compartments of the leg can be easily accessed thru

• Incisions are usually made from joint to joint to

XII. DETERMINING THE SEVERITY

The Rule of Nines

• Berkow or Lund and Browder are used to estimate

XIII. SECONDARY SURVEY

• These should be applied within 24 hours of the burn

• Inner circle: Tells you the different physiologic

P53 and Li-Fraumeni Syndrome

International Agency for Research on Cancer V. RISK ASSESMENT

• Histologic diagnosis: Although less invasive

Short Video of How a Core Needle Biopsy is