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Selected surgical topicsBy

DR.IBRAHIM .M. AL TMEZEH

&COAGULATION BLOOD PRODUCTS

NORMAL COAGULATION

Three initial responses to vascular injury: vascular vasoconstriction platelet aggregationthrombin generation

Normal half-life - RBCs: 120 days; platelets: 7 days; PMNs: 1-2 days

Factor VIl - shortest half-life Factors V and VllI - labile factors, activity

lost in stored blood, activity not lost FFP

Factor VIll - only factor not synthesized in liver (synthesized in endothelium)

Vitamin K-dependent factors - II, Vll, IX, and X; proteins C and S

Vitamin K - takes 6 hours to take effect FFP - effect is immediate and lasts 6 hours

Cryoprecipitate - contains highest concentration

ofvWF VllI; used in von Willebrand's disease and hemophilia A also contains fibrinogen

FFP - has high levels of all factors (including labile factors V and VlII), protein C, protein S, and AT-III

DDAVP and conjugated estrogens- cause release ofVlll and vWF from endot

COAGULATION MEASUREMENTS

PT - measures ll, V, Vll, and X; fibrinogen; best for liver synthetic function

PTT - measures most factors except VIl and XIll

ACT = activated clotting time ACT 150-200 sec for routine

anticoagulation, 460 sec for cardiopul. bypass

INR >1.5 - relative contraindication to performing surgical procedures

INR >1.3 - relative contraindication to central line placement, percutaneous biopsies, and eye surgery

CONDITIONS CAUSING ABNORMAL BLEEDING Incomplete hemostasis - most common cause of surgical bleeding

von Willebrand's disease

• Most common congenital bleeding disorder • Types I and 11 are autosomal dominant; type III is autosomal recessive • Have long bleeding time (ristocetin test) • Type I is most common (70% of cases) and often has only mild symptoms • Type ill causes the most severe bleeding • Type I and lll - reduced quantity of circulating vWF • Tx: recombinant Vlll:vWF, DDAVP, cryoprecipitate, conjugated estrogens

• Type II - defect in vWF molecule itself, have enough vWF but does not work well • Tx: recombinant VIII:vWF, cryoprecipitate

CONDITIONS CAUSING ABNORMAL BLEEDING

Hemophilia A (VIll deficiency Sex-linked recessive Need levels 100% preoperatively; keep 30% after surgery Prolonged PTT- and normal PT Factor VllI crosses placenta - newborns may not bleed at circumcision

Hemophiliac joint no aspiration Tx: ice, keep joint mobile with range of motion exercises, factor Vlli concentrate or cryoprecipitate Epistaxis, intracerebral hemorrhage, and hematuria may occur Tx: recombinant Vlll:vWF or cryoprecipitate; possibly DDAVP

CONDITIONS CAUSING ABNORMAL BLEEDING

Hemophilia B (IX deficiency) - Christmas diseas

• Sex-linked recessive• Need level 100% preoperatively• Prolonged PTT and normal PT• Tx: recombinant factor IX concentrate or FFP Factor Vll deficiency • - prolonged PT and normal PTT, bleeding tendency. -• Tx: factor Vll concentrate, FFP

Disseminated intravascular coagulation ((DIC Microvascular coagulation due to

inflamation from sipses, trauma….cons.c.fac. coagulapathy

Decreased platelets, prolonged PT, prolonged PTT

Low fibrinogen, high fibrin split products, high D-dimer

Often initiated by tissue factor Need to treat underlying cause

• ASA - stop 7 days before surgery; patients will have prolonged bleeding time Inhibits cyclooxygenase in platelets, ‡TXA2

Coumadin - stop 7 days before surgery, consider starting heparin while Coumadin wears off

Platelets - keep >50,000 before surgery, >20,000 after surgery Prostate surgery - can release urokinase, activates plasminogen ->

thrombolysis Tx: s-Aminocaproic acid (Amicar H and P - best way to predict the bleeding risk Normal circumcision - does not rule out bleeding disorders; can still have

clotting factors from mother Abnormal bleeding with tooth extraction or tonsillectomy - picks up 99%

patients with bleeding disorder Epistaxis - common with vWF deficiency and platelet disorders Menorrhagia - common with bleeding disorders

Heparin

• Heparin –activates antithrombin III• Reversed with protamine• Half-life 60-90 min• Long –term heparin ;

osteoporosis,alopecia ,does not cross-blacental barrier, warfarin does

CONDITIONS CAUSING ABNORMAL HYPERCOAGULABILITY

Leiden factor - 30% of spontaneous venous thromboses

Most common congenital hypercoagulability disorder

Resistance to activated protein C, defect on factor V

Tx: heparin, warfarintobacco (most common factor causing acquired hypercoagulability (

Warfarin-induced skin necrosis occurs when placed on Coumadin without being

heparinized first

Due to short half-life of proteins C and S.

Patients with relative protein C deficiency are especially susceptible

Tx: heparin if it occurs; prevent by placing patient on heparin before starting warfarin

Key elements in the development of venous thromboses Virchow's triad endothelial injury, stasis and hypercoagulability

Key element in the development of arterial thrombosis

- endothelial injur DEEP VENOUS THROMBOSIS stasis, venous injury, and hypercoagulability risk factors- treatment1st warfarin for 6 months2nd warfarin for 1 year 3rd or significant PE — warfarin for lifetime

PULMONARY EMBOLISM PE one of the most common cause of death in

hospitalized pt

90% of deaths occur within 72 hours of the onset of the initial symptoms

PE develops in about 10%-40% of pts with DVT

Most common from the iliofemoral region

Risk factors Surgery & critical illness Pregnant & postpartum women 5x Estrogen therapy 4-7x (dose dependant) Heart disease 3-4x (depends on severity) Obesity 1.5-2x Carcinoma 2-3x Major trauma(spinal cord injury & femoral shaft fracture ) History of PE Varicose veins 2x Older age

SYMPTOMSClassic signs :in only 24%Hemoptysis ,pleural friction rub ,cardiac gallop cyanosis , chest splittingNonspecific findings :Tachycardia (60%) ,tachypnea (85%), dyspnea(85%)bronchospasm ,pleuritic chest pain

TreatmentCardiovascular support includes O2, correction of cardiac

arrhythmia tx of shock Heparin initial 10000-20000IU,heparin continued for at

least 7 days ,followed by long term anticoagulation for 3-6 months

Thrombolytic (in acute life threatening)

Pulmonary embolectomy

long term anticoagulation :oral warfarin for life (INR2-3X)

BLOOD PRODUCTS

• All blood products carry the risk of HIV & hepatitis except of albumin & serum globulins

• Stored blood is low in2,3DPG causes left shift

• Clerical error leading to ABO incompatibility (1st cause of death from transfusion)

Hemolysis reactions

Acute hemolysis ABO incompatility (antibody mediated) oliguria-most common manifes.

Tx :histamine blockers ,HCO3 diuretics &fluid Delayed hemolysis minor antigens (antibody

mediated) Tx observation

Nonimmune hemolysis (squeezed blood) Tx fluid & diuretics

Other reactions Febrile nonhemolytic transfusion reaction: (most

common)

Anaphylaxis :IgG against IgA in IgA-deficientrecipient

Urticaria :against plasma proteins or IgA

Transfusion related acute lung injury (TRALI)

Other transfusion problem

• Cold -poor clotting• Dilutional thrombocytopenia• Hypocalcemia • hyperkalemia• Antiplatelet antibody• Coagulapathy(pRBC,s do not contain clot. Fac.)• Viral hipatitis most common fatal infectious comp.• Most common bacterial contamination is GNRs (E,coli)• Most common BLOOD PRODUCTS source contamination-

platelets(not refrigerated)

. Stored blood is deficient in:(a) factor II(b) factor VII

(c )factor VIII(d )factor IX(e )factor XI

. von Willebrand’s disease:(a )is an autosomal dominant disorder

(b )results in prolonged prothrombin time(c )is associated with normal bleeding time

(d )is due to decreased hepatic synthesis of vonWillebrand’s factor

(e )is typically associated with joint bleeding

. Coumadin-induced skin necrosis is due to:(a )protein S deficiency(b )protein C deficiency

(c )antithrombin III deficiency(d )disseminated intravascular coagulation

. The most common complication of heparin reversal

with protamine is:(a )bradycardia(b )hypotension

(c )thrombotic crisis(d )thrombocytopenia

(e )leukopenia

. The endothelial cells are the source of:(a )factor II(b )factor V(c )factor VII(d )factor VIII

(e )factor X

. The most common complication of blood transfusion

is:(a )hemolytic reaction

(b )human immunodeficiency virus transmission(c )allergic reaction(d )volume overload

(e )coagulopathy

. The most common agent transmitted by blood

transfusion is:(a )human immunodeficiency virus

(b )hepatitis B virus(c )hepatitis C virus(d )Cytomegalovirus

INFECTION

INFECTION Microflora• Stomach: virtually sterile (GPCs,yeast)

• Proximal small bowel 10(5) bacteria mostlyGPCs

• Distal small bowel 10(7) GPCs GPRs GNRs

• Colon 10(11)almost all anerobes

• Bacteroides fragilis — most common anaerobe in the colon

• Escherichia coli — most common aerobic bacteria in the colon

GRAM NEGATIVE SEPSIS E,coli most common

Endotoxin (lipopolysaccharide lipid A) is released

Triggers the release ofTNF-a (from macrophages), complement & coagulation cascade

Early gram-negative sepsis —dec.insulin,inc.glucose (impaired utiliiaiioim)

Late gram-negative sepsis — inc. insulin, inc. glucose secondary to insulin resistance

Hyperglycemia — often occurs just before the patient becomes septic

• Optimal glucose level in a septic patient - 100-120 mg/dI

Clostridium colitis• Dx :fecal leukocytes in stool C,difficile toxin• Tx :oral vancomycin or flagyl • Stop other antibiotics or change them

Abscesses • 90% of abdominal abscesses have anaerobes • 80%have both anaerobic& aerobic bact • Tx drainage • Antibiotics :with diabetes ,cellulitis ,sepsis fever

elevated WBCs or who have bioprosthetic hardware

Wound infection

• Staphylococcus aureus - coagulase-positive Most common organism overall in surgical wound INFECTION

• Staphylococcus epidermidis — c-negatmve

• Malnutrition — most common cause of immune deficiency • E. coli — most common GNR in surgical wound infections

• B. fragilis - most common anaerobe in surgical wound infections

Wound infection - classifications Clean(hernia) 2% Clean contaminated(elective colon resection)

3%-5% Contaminated(gunshot to colon)5%-10% Gross contamination(abscess)30% Risk factors : Long operations,hematoma or seroma

formation, advanced age chronic diseases ,malnutrition ,immunosuppressive drugs

Line infection: S,epidermis, S,auareus, Yeast Femoral lines >subclavian &intrajugular lines Central line cultures >15 colony forming units

=line infection needs new site

Systemic Inflammatory Response SyndromeDefinition of SIRS

T > 38ºC or < 36ºCHR > 90RR > 20 or pCO2 < 32WBC > 12 or < 4

Peritoneal dialysis catheter infections • S. aureus and S. epidermidis most common

• Fungal infections hard to treat

• Tx: intraperitoneal vancomycin and gentamicin; increased dwell time and intraperitoneal heparin may help

• Removal of catheter for peritonitis that lasts for 4—5 days

• Fecal peritonitis requires laparotomy to find perforation

• Some say need removal of peritoneal dialysis catheter for all fungal, tuberculous, and Pseudomonas infections

Causes of post. Op. fever

WIND – lungs are often the 1o source in the first 48 hours

WATER:UTI 3-d day pos. op.

WOUND: wound infection 5- day pos. op.

WALK: DVT.thromb-ts 7-10. day pos. op.

WONDER DRUGS: drug fevers . any tim

Other surgical infection within 48 h.of procedure

• Injury to bowel with leak• C.perfringens• Beta-hemolytic strep.

Wound infection• Most common surgical infection- wound infection

• Most common nonsurgical infection - urinary tract infection (most commonly E. coli)

Biggest risk factor — urinary catheters

• Leading cause of infectious death after surgery nosocomial pneumonia

• Most common organisms in ICU pneumonia #1 S. aureus, #2 Pseudomonas

• GNRs #1 class of organisms in ICU pneumonia

Necrotising soft tissue infections : B-hemolytic strepyococcus (group A),C perfringes &

mixed organism Usually in pts who are immunocomprised or have

poor blood supply Necrotising fascitis : B-hemolytic strepyococcus (group A),can be

polyorganismal The overlying skin is normal in early stages Skin:pale red progress purple with blister or bullae Tx :early debridment ,high dose penicillin

C,perfringens infection : has alpha toxin Necrotic tissue Pain out of proportion to exam May not show the skin signs with deep infection Gram stain : GPRs without WBCs Myonecrosis & gas gangrene- common presentations Can occur with farming injuries Tx :early debridment ,high dose penicillin

Fournier”s gangrene: Sever infection in perineal &scrotal area Risk factors — diabetes mellitus and immunocompromised state Caused by mixed organisms (GPCs, GNRs, anaerobes) Tx: early debridement; try to preserve testicles if possible; antibiotics

Spontaneous (primary) bacterial peritonitis Protein<1gm/dl in peritoneal fluid. — risk factor Monobacterial (50% E. coil, 30% Streptococcus, 10%

Kiebsiela) Secondary to decreased host defenses (intrahepatic

shunting ,impaired bactericidal activity in ascites); not due to transmucosal migration

Fluid culture negative in many cases PMNs>500 cells/cc Tx :3rd generation cephalosporins Fluoroquinolones good for short term prohylaxis Need to rule out intra-abdominal source (diverticular abscess,

perforation) if not getting better on antibiotics or if cultures are polymicrobial

Secondary bacterial peritonitis Intra abdominal sources (transmecosal

migration ,perforated viscus) Polymicrobial B. fragilis, E coil, Enterococcus most

common organisms Tx :need laparotomy to find the source

HIVExposure risk:• Blood transfusion 70%• Infant from +ve mother 30%• Needle stick from +ve pt 0.3%• Mucous membrane exposure 1%• Seroconversion occures in 6-12 weeks• AZT & lamvudine can help dec seroconversion after exposure • Should be given within 1-2 hours of exposure

Opportunistic infection :• Most common cause of laparotomy in HIV pt(CMV)• Neoplastic 2nd cause of laparotomy

Lymphoma in HIV pt Stomach followed by rectum Mostly non-Hodgkins ,70% B cell Tx : chemotherapy

GI bleeds: Lower GI bleeds more common than upper GI bleeds Upper GI bleeds –Kaposi sarcoma ,lymphoma Lowerv GI bleeds –CMV ,HSV

CD4 count 800-1200 normal 300-400 symptomatic ds. 200 apportunistics

HEPATITIS C

• Now rarely transmitted with blood transfusion (0.0001%/unit)

• 1%—2% of population infected

• Fulminant hepatic failure rare

• Chronic infection occurs in 60%

• Cirrhosis in 15% over 20 years

• Hepatocellular carcinoma in i%—5%

• Interferon may help prevent development of cirrhosis

OTHER INFECTIONS

• Brown recluse spider bites — Tx: dapsone initially; may need resection of area and skin graft for large ulcers later

• Acute septic arthritis —, staph, H. influenzae, strep ,gon. Tx: drainage, 3rd-generation cephalosporin and vancomycin until cultures

show organism

• Diabetic foot infections — mixed staph, strep, GNRs, and anaerobes Tx: broad-spectrum antibiotics (Unasyn, Zosyn)

• Eikenella found only in human bites; can cause permanent joint injury• Pasteureila multocida found in cat and dog bites Tx: broad-spectrum antibiotics (Augmentin)

OTHER INFECTIONS

• erysipelas, cellulitis,LYMPHANGITIS(DUCT) ,LYMPHADINITIS(NODE)—strep most common organisms

• Impetigo, -S. aureus - most common organisms

• Furuncle — boil; usually S. epidermidis orS. aureus. Tx: drainage +/— antibiotics

• Carbuncle a multiloculated furuncle

tetanus

• Non—tetanus-prone wounds infec. — give tetanus toxoid only if patient has received <3 doses or tetanus status unknown

• Tetanus-prone wounds infec. (>6 hours old; obvious contamination and devitalized tissue; crush, burn, frostbite, or missile injuries) always give tetanus toxoid unless patient has had 3 doses and it has been <5 years since last booster

• Tetanus immune globulin - give only to patient with tetanus-prone wounds who have not been immunized or if immunization status unknown

ABCESSE

It has fluctuation that differentiate it from cellulitis

4Bs,P. ABCESSES that need drainag without to be fluctuat ;

breast ABCESSE buttok ABCESSE Palm ABCESSE parotid ABCESSE

ANTIBIOTICS • Antiseptic :kills & inhibits organisms on body

• Disinfectant :kills & inhibits organisms on inanimate objects

• Sterlization :all organisms killed

• Common antiseptics in surgery:• Iodophors good for GPCs GNRs ,poor for fungal • Chlorhexidine gluconate good for GPCs GNRs & fungus

• Preoperative antibiotics :• To prevent wound infection • Need to be given within 2 h before incision

Effective for entrococcus : Vancomycin Ampicillin \amoxicillin Gentamicin with ampicillin Effective for pseudomonas ,acintobacter

&serratia :• Ticarcillin\pipercillin• Timentin\zoycin 3rd generation cephalosporin • Aminoglycosides • Meropenem \ imipenem

• Fluoroquinolons

. The most common source of bacteria in wound

infection after groin hernia repair is:(a )the patient’s skin

(b )the patient’s nasopharynx(c )operating room air

(d )surgical instruments(e )operating room staff

. Hand infection caused by a human bite is due to:

(a )Staphylococcus aureus(b )Clostridium difficile

(c )Herpes simplex(d )Eikenella corrodens

(e )Candida species

. Colonic perforation in a patient with acquiredimmunodeficiency syndrome is most likely due to:

(a )Clostridium difficile(b )Cytomegalovirus

(c )Bacteroides(d )Salmonella typhi

(e )Escherichia coli

. Infection caused by dog and cat bites is due to:

(a )Pasteurella species(b )Mycobacterium

(c )Staphylococcus aureus(d )Actinomyces

(e )Candida

. The most common causative agent in nosocomial

sinusitis in the ICU is:(a )Pseudomonas aeruginosa

(b )Staphylococcus aureus(c )Staphylococcus epidermidis(d )Streptococcus pneumoniae

. Which of the following distinguishes adrenal insufficiency

from sepsis?(a )hypotension

(b )fever(c )tachycardia

(d )altered mental status(e )hypoglycemia

Wound healing

Wound healing Wound healing phases :

Hemostasis and Inflamation :(days 1-7) Proliferation (4days- 12days) Maturation and Remodeling: (3weeks-1year)

Hemostasis and Inflamation :(days 1-7)

Hemostasis- 1-vascular constriction (10m) 2-platlet plug formation 3-fibrin formation 4-fibrinolysis (-platlet 1-ist in Wound healing )

Inflamation- PMNs 1-ist cell.(24h-48h) , macrophages(48h-96h)essential for Wound healing, epithelization .(24h-48h) 1-2mm/day- Epithelial integrity — most

important factor in healing open wounds (secondary intention) , Lymphocytes(7day)

Proliferation (4days- 12days)

fibroblasts(5day) ,

Neovascularization, production of collagen &granulation tissue

Type Ill collagen — predominant collagen type synthesized for days 1—2

Maturation and Remodeling: (3weeks-1year)

Type III collagen replaced with type 1 Collagen cross linking occur Tensile strength most important factor in healing closed incisions (primary

intention) Type I collagen — predominant collagen type synthesized by days 3—4 Type III replaced by type I collagen by 3 weeks At 6 weeks, wound is 80% of its final strength and 60% of its original strength At

8 weeks, wound reaches maximum tensile strength, which is 80% of its original strength

Maximum collagen accumulation at 2—3 weeks after that —> the amount ofcollagen stays the same but continued cross-linking improves strength

d-Penicillamine — inhibits collagen cross-linking Peripheral nerves regenerate at rate 1mm/day

Order of cell arrival in woundPlt,PMNs ,macrophages ,fibroblasts ,lymphocytes

collagen (18types)

• cøllagen type I • Most common type of collagen:• skin, bone, and tendons • Primary collagen in a healed wound• cøllagen type II• Cartilage• cøllagen type III• Increased in healing wound, also in blood vessels and skin• cøllagen type IV• Basement membranes• cøllagen type V• Widspread, particulary found in the cornea

Impediments to wound healing

• Bacteria> 105/cm2,local infec. (most common )—.Loxygen content, collagen lysis, prolonged inflammation

• Devitalized tissue and foreign bodies — retards granulation tissue formation and wound healing (most common )

• Cytotoxic drugs — 5FU, methotrexate, cyclosporine, FK-506, etc., can impair wound healing

• Diabetes — can contribute to poor wound healing by impeding the early-phase response

• Albumin <3.0 - risk factor for poor wound healing• Jaundice• anemia• Steroids — prevent wound healing by inhibiting macrophages, PMNs, and

collagen synthesis by fibroblasts; - wound tensile strength as well Vitamin A (25,000 IU qd) — counteracts effects of steroids on wound healing

Wound ischemia

• Fibrosis• Pressure (sacral decubitus ulcers)• Poor arterial inflow• Poor venous outflow• Smoking• Radiation• Edema• Vasculitis

Types of wound closure

1 .primary intention.clean2 .secondary intention .infected

3.ter. intention. (delayed primary intention) . contaminated

Diseases associated with abnormal wound healing

• Osteogenesis imperfecta type I collagen defect• Ehlers—Danlos syndrome — 10 types

identified, all collagen disorders• Marfan’s syndrome — fibrillin (collagen) defect• Epidermolysis bullosa — excessive fibroblasts.

Tx: phenytoin• Scurvy• Pyoderma gangrenosum

Essentials for wound healing

• Moist environment (avoid desiccation)• Oxygen delivery - optimal fluids, no smoking,

pain control, arterial reconstruction, supplemental oxygen

Want transcutaneous oxygen measurement (TCOM) > 25 mm Hg

• Avoid edema - leg elevation, compression •Remove necrotic tissue

Hypertrophic scar and Keloids• Keloids — autosomal dominant; dark skinned Collagen goes beyond original scar Tx: XRT, steroids, silicone, pressure garments

• Hypertrophic scar tissue — dark skinned; flexor surfaces of upper torso

• Collagen stays within confines of scar• Often occurs in burns or wounds that take a long time to

heal• Tx: steroids, silicone, pressure garments

. The adverse effects of steroids on wound healing

can be reversed with:(a )vitamin C(b )vitamin A

(c )copper(d )vitamin D(e )vitamin E

. In contrast to adults, fetal wound healing:(a )has a higher content of type III collagen

(b )has a higher level of transforming growthfactor-β

(c )has an exaggerated inflammatory phase(d )has much less hyaluronic acid content

. Which cell type is essential for wound healing?

(a )neutrophil(b )macrophage

(c )fibroblast(d )lymphocyte(e )endothelial

Fluid & electrolytes

Fluid & electrolytes 2/3 Role;• Roughly 2/3 of the total body weight is water

(men); infants have a little more body water, women have a little less

• 2/3 ofwater weight is intracellular (mostly muscle)

• 1/3of water weight is extracellular - 2/3 of extracellular water is interstitial - 1/3of extracellular water is in plasma

Fluid & electrolytes• Proteins — determine plasma/interstitial compartment osmotic pressures

• Na — determines intracellular/extracellular osmotic pressure

• Volume overload - most common cause is iatrogenic; first sign is weight gain

• 0.9% normal saline: Na 154 and Cl 54

• Lactated Ringer’s solution (LR; ionic composition of plasma): Na 130, K 4, Ca 2.7, Cl 109, bicarb 28

• Plasma osmolarity: (2 X Na) + (glucose/18) + (BUN/2.8) Normal: 280-295

ESTIMATES OF VOLUME REPLACEMENT

4cc/kg/h for lst lo kg 2cc/kg/h for 2nd lo kg 1 cc/kg/h for each kg after that

35ml/kg/24 120ml/h

Best indicator of adequate volume replacement is urine output Urine output — should be kept at least 0.5 cc/kg/h; should not be replaced, usually sign of normal postoperative di uresis

During open abdominal operations, fluid loss is 0.5—1.0 L/h unless there are measurable blood losses

Usually do not have to replace blood lost unless it is >500 cc

Insensible fluid losses — 10 cc/kg/day, 75% skin, 25% respiratory, pure water(600ml)

IV replacement after major adult gastrointestinal surgery

During operation and 1st 24 hours, use LR

After 24 hours, switch to D5 1/2 NS with 20 mEq K

5% dextrose will stimulate insulin release, resulting in amino acid uptake and protein synthesis (also prevents protein catabolism)

D5 ½ NS @ 125ml/h provides 150 g glucose per day (525 kcal/day)

GI FLUID SECRETION Stomach 1—2 L/day Biliary system 500—1,000 mL/day Pancreas 500-1,000 mL/day Duodenum 500-1,000 mL/day

Normal K requirement: 0.5—1.0 mEq/kg/day Normal Na requirement: 1-2 mEq/kg/day

GI ELECTROLYTE LOSSES Sweat — hypotonic Saliva — K (highest concentration of K in body) Stomach - H and CL Pancreas - HCO3 Bile-HCO3 Small intestine — HCO3 , K Large intestine — K

Gastric losses — replacement is D5 1/2 NS with 20 mg K Pancreatic/biliary/small intestine losses - replacement is LR with HCO3 Large intestine (diarrhea) losses — replacement is LR with K GI losses — should generally be replaced cc/cc

POTASSIUM (NORMAL 3.5-5.0) Hyperkalemia - peaked T waves initial finding on

EKG Tx; • Calcium gluconate (membrane stabilizer for heart) • Sodium bicarbonate (causes alkalosis, K enters

cell in exchange for H) • 10 U insulin and 1 ampule of 50% dextrose (K

driven into cells along with glucose) • Kayexalate • Dialysis if refractory

Hypokalemia —T waves disappear • May need to replace Mg before you can correct K

SODIUM (NORMAL 135-145) Hypernatremia — restlessness, irritability, ataxia, seizures Tx; • Correct with D5 water slowly to avoid brain swelling • Total free water deficit 0.6 X patient’s weight (kg) X [(Na/140) — 1] • TBW (total body water) = 0.6 X patient’s weight (kg) • Change Na no more than 0.5 mEq/h -1 mEq/h(16 mEq/day for below)

Hyponatremia — headaches, delirium, seizures, nausea, vomiting • Na deficit = 0.6X weight ( kg) X (140 — Na) • Water restriction is the first treatment for hyponatremia, then diuresis,

then replacement • Correct Na slowly to avoid central pontine myelinosis (no more than 1

mEq/h) • Hyperglycemia can cause pseudohyponatremia for each 100

increrement of glucose over normal, add 3 points to the Na value • SIADH results in hyponatremia

CALCIUM (NORMAL 8.5-10.0; NORMAL IONIZED Ca 4.4-5.5)

Hypercalcemia (Ca usually> 13 or ionized > 6—7) causes lethargic state • No lactated Ringer’s (contains Ca) • No thiazide diuretics (these retain Ca) • Tx: NS at 200—300 cc/h, Lasix For malignant disease —mithramycin,

calcitonin, alendronic acid, dialysis

HYPERCALCEMIACAUSES Malignancy:1st cause Hematologic (25%) – lytic bone lesions(U\ cAMP dec.) bone destruction Nonhematologic (75%)-small cell (lung) ,breast met. to bone most

common (U\cAMP inc.) no bone destruction Hyperthyrodisim Hyperparathyrodisim Familial hypercalcemic hypocalciuria Immobilization Granulomatous diseases (sarcoidosis,tb) Excess vit D Milik alkali syndrome Thiazide diuretics

Hypocalcemia (Ca usually < 8 or ionized Ca < 4) o Hyperreflexiao Chvostek’s sign; (tapping on face produces twitching), perioral tingling and numbness, o Trousseau’s sign (carpopedal spasm), prolonged QT

o May need to correct Mg before being able to correct Ca

o Protein adjustment for calcium - for every 1-g decrease in protein, add 0.8 to Ca

MAGNESIUM (NORMAL 2.0-2.7)

Hypermagnesemia — causes lethargic state; burn, trauma, and renal dialysis patients

Tx: calcium

Hypomagnesemia - signs similar to hypocalcemia

METABOLIC ACIDOSIS

Anion gap = Na — (HCO3 + CI) Normal: <10—15

Anion gap acidosis - “MUDPILES” = methanol, uremia, diabetic ketoacidosis, paraldehydes, isoniazid, lactic acidosis, ethylene glycol, salicylates

Normal gap acidosis usually due to loss of Na/HC03 (ileostomies, small bowel fistulas)

Tx: underlying cause; keep pH > 7.20 with bicarbonate; severely dec.pH can affect myocardial contractility

METABOLIC ALKALOSIS

Usually contraction alkalosis Nasogastric suction - results in hypochloremic, hypokalemic, metabolic alkalosis, and paradoxical aciduria Loss of CL and H ion from stomach secondary to nasogastric tube (hypochloremia and alkalosis) Loss of water causes kidney to reabsorb Na in exchange for K (Na/K ATPase), thus losing K

(hypokalemia) Na+/H exchanger activated in an effort to reabsorb water along with K/H exchanger in an effort to

reabsorb K — results in paradoxical aciduria

Acid—Base Balance

pH CO2 HCO3Condition

Respiratory acidosis dec. Inc. Inc. Respiratory alkalosis inc. Dec. Dec.Metabolic acidosis dec. Dec. Dec.Inc. Inc. inc. alkalosis Metabolic

The most effective method of treating hyperkalemia

is:(a )intravenous calcium gluconate

(b )intravenous sodium bicarbonate(c )hemodialysis

(d )cation-exchange resin(e )intravenous glucose-insulin

. The highest potassium concentration is found in:

(a )saliva(b )gastric secretion

(c )bile(d )small intestine

(e )pancreatic secretion

. Normal anion gap acidosis is associated with:

(a )ketoacidosis(b )lactic acidosis

(c )salicylate poisoning(d )severe diarrhea(e )uremic acidosis

. The colon secretes:(a )water

(b )sodium(c )chloride

(d )potassium

. The initial step in management of a hypercalcemic

crisis is intravenous:(a )steroids

(b )calcitonin(c )saline

(d )furosemide(e )mithramycin

. Peaked T-wave on electrocardiogram is a feature of:

(a )hypernatremia(b )hypermagnesemia

(c )hyperkalemia(d )hypocalcemia(e )hyponatremia

. The most common cause of hypercalcemic crisis is:

(a )sarcoidosis(b )primary hyperparathyroidism

(c )secondary hyperparathyroidism(d )malignancy(e )renal failure

LOCAL ANESTHESIA

LOCAL ANESTHETICS• Work by increasing action potential threshold, preventing Na influx• Can use 0.5 cc/kg of l% lidocaine• Infected tissues hard to anesthetize secondary to acidosis• Length of action — bupivacaine > lidocaine > procaine• Epinephrine (1;200000) allows higher doses to be used, stays locally• No epinephrine with arrhythmias, unstable angina, uncontrolled hypertension, poor collaterals (penis and ear), uteroplacental insufficiency• Side effects: tremors, seizures, tinnitus, arrhythmias (CNS symptoms occur

before cardiac)• Amides (all have an “i” in first part of the name) — lidocaine, bupivacaine,

mepivacaine - rarely allergic reactions• Esters — tetracaine, procaine, cocaine; allergic reactions common

for any drug or solution, 1% = 10 mg/mL. For a 50-kg person, the toxic dose of bupivacaine would be

approximately 3 mg/kg, or 3 x 50 = 150 mg.

A 0.5% solution of bupivacaine is 5 mg/mL, so 150 mL/5 mg/mL = 30 mL as the upper limit for infiltration.

For lidocaine in the same patient, the calculation is 50 kg x 5 mg/mL = 250 mg toxic dose. If a 1% solution is used, the allowed amount would be 250 mg/10 mg/mL = 25 mL.

. Which of the following is an aminoester?(a )tetracaine

(b )lidocaine(c )bupivacaine(d )mepivacaine

(e )etidocaine

. The most common complication of epidural analgesia

is:(a )hypotension

(d )nausea(c )respiratory depression(d )deep vein thrombosis

. The most commonly injured nerve under general

anesthesia is:(a )radial nerve(b )ulnar nerve

(c )median nerve(d )brachial plexus

(e )common peroneal nerve

ONCOLOGY

ONCOLOGY

• MC CA in women - breast CA• MC cause of CA-related death in women —

lung CA• MC CA in men - prostate CA• MC cause of CA-related death in men — lung

CA

1#children’s malignancy overall — leukemia1# solid tumor class - CNS tumorso 1# general surgery tumor - neuroblastoma o 1 # in child <2 years —* neuroblastoma1# in child >2 years —* Wilms tumor1# liver tumor in children — hepatoblastoma; 2/3 of

liver tumors in children are malignant1 # lung tumor in children — carcinoid

ONCOLOGY

• Hyperplasia — increased number of cells

• Metaplasia — replacement of one tissue with another (GERD squamous epithelium in esophagus changed to columnar gastric tissue)

• Dysplasia — altered size, shape, and organization (Barrett’s esophagus)

types

• Carcinomas-are malignancies that arise from epithelium

• adenoCarcinomas-are malignancies that arise from epithelium And have glandular compononent

• Sarcomas-are malignancies that arise from mesodermal tissues

TUMOR MARKERS

• CEA-colonCA• AFP — liver CA• CA 19-9 — pancreatic CA• CA 125- ovarian CA• Beta-HCG — testicular CA, choriocarcinoma• PSA — prostate CA (thought to be the tumor marker

with the highest sensitivity)• NSE - small cell lung CA, neuroblastoma• BRCA I and II - breast CA• Half-lives — CEA: 18 days; PSA: 18 days; AEP: 5 days

(RADIATION THERAPY (XRT M phase — most vulnerable stage of cell cycle for XRT Most damage done by formation of oxygen radicals —*

maximal effect with high oxygen levels Main target is DNA Very radiosensitive tumors — seminomas, lymphomas Very radioresistant tumors - epithelial, sarcomas Kidneys, lungs, liver, and lymphocytes have increased sensitivity

to XRT Large tumors less responsive to XRT due to lack of oxygen in the

tumor Brachytherapy — source of radiation in or next to tumor (Au-

198, I-128); delivers high, concentrated doses of radiation

Li—Fraumeni syndrome – defect in p53 gene —* patients get • childhood sarcomas, • breast CA, • brain tumors, • leukemia,• adrenal CA

. The most useful serum marker for cancer screening

is:(a )prostate-specific antigen

(b )CA 19.9(c )α-fetoprotein

(d )carcinoembryonic antigen

. The initial site of distant metastasis in breast cancer is:

(a )lungs(b )liver

(c )bones(d )brain

The most common cause of cancer-related death in

females is:(a )breast cancer

(b )colon cancer(c )ovarian cancer

(d )pancreatic cancer(e )lung cancer

. Li-Fraumeni syndrome shows increased incidence

of:(a )colon cancer

(b )ovarian cancer(c )lung cancer

(d )breast cancer(e )pancreatic cancer

Critical careshock

Critical care

• Hypotension most common cause of postoperative renal failure

• 70% nephrons to be damaged before renal dysfunction occurs

• FeNa = (urine Na/Cr)/(plasma Na/Cr) —*best for azotemia

• Prerenal cause of acute renal failure FeNa <1%, urine Na <20, BUN/Cr ratio>20, urine osmolality> 50O mOsm; otherwise consider renal cause of azotemia, Oliguria

Steroid potency

1 X . cortisone, hydrocortisone

5X . prednisone, prednisolone, methylprednisolone

30X . dexamethasone

shock • Definition ;

• tissue Hypoperfusion• Inadequate oxygen delivery to meet metabolic

demands results in global tissue hypoperfusion and metabolic acidosis

• Shock can occur with a normal blood pressure and hypotension can occur without shock

Epidemiology

Mortality Mortality > 20%

– Septic shock – 35-40% (1 month mortality)– Cardiogenic shock – 60-90%– Hypovolemic shock – variable

Classification of Shock

Hypovolemic Cardiogenic Septic (vasogenic) Neurogenic Traumatic Obstructive anaphylactic

Types of Shock• Hypovolemic shock; – from ↓preload the most common type

– Hemorrhage ;The most common cause– Fluid Loss (Vomiting, Diarrhea, Burns)– initial alteration is incr. diastolic pressure

• Cardiogenic shock – pump failure or ↓SV– MI, arrhythmia, aortic stenosis, mitral regurg– extensive MI is the most common cause– cardiogenic shock is the most common cause of death in patients

hospitalized with acute MI– Extracardiac obstructive causes such as PE, tension

pneumothorax, tamponade• Distributive (vasodilatory) shock - ↓SVR

– Septic, anaphylactic, and neurogenic shock– Pancreatitis, burns, multi-trauma via activation of the

inflammatory response

Classification of Hemorrhage

Class Parameter I II III IV

Blood loss (mL) <750 750–1500 1500–2000 >2000

Blood loss (%) <15 15–30 30–40 >40

Heart rate (bpm) <100 >100 >120 >140

Blood pressure Normal Orthostatic Hypotension Sev. Hypo .

CNS symptoms Normal Anxious Confused Obtunded

Obstructive shock;Physical obstruction resulting in dec. cardiac

output is the hallmark

Traumatic causes of cardiogenic shock-• Cardiac tamponade• Crdiac contiosion• Tension pneumothorax• Pulmonary embolism

shock • neurogenic shock

Causes-Spinal cord trauma

-Spinal cord neoplasm -Spinal/epidural anesthetic

loss of sympathetic tone Usually have dec. HR,dec.BP, warm skin

Tx: give volume 1st, then phenylephrine after resuscitation; give steroids for blunt spinal trauma with deficit

Cardiac tamponade

Causes decreased diastolic ventricular filling and hypotension

Beck’s triad — hypotension, jugular venous distention, and muffled heart sounds

Echocardiogram shows impaired diastolic filling of right atrium initially (1st sign 0f cardiac tamponade)

Pericardiocentesis blood does not form clot

Tx: fluid resuscitation initially; need pericardial window or pericardiocentesis

Early sepsis triad

• hyperventilation, • confusion, • respiratory alkalosis

adrenaI insufficiency

• Acute — cardiovascular collapse; characteristically unresponsive to fluids and pressors

• Chronic - hyperpigmentation, weakness, weight loss, GI symptoms, inc. K, dec.Na, fever, hypotension

. Which of the following distinguishes adrenal insufficiency

from sepsis?(a )hypotension

(b )fever(c )tachycardia

(d )altered mental status(e )hypoglycemia

. The best indicator of adequate resuscitation in

shock is:(a )normal blood pressure

(b )normal pulse(c )adequate urine output(e )improved mental status

(f )decreased lactate level

. Distinction between prerenal and renal azotemia is

best made by:(a )urine sodium level(b )serum sodium level

(c )urine creatinine level(d )serum creatinine level

(e )urine microscopy

Burn

Burn Classifications 1st epidermis Sunburn erythema 2nd a- Superficial dermis .Painful to touch; blebs and blisters; hair follicles intact; blanches (papillary) b - Deep dermis Decreased sensation; loss of hair follicles (need skin grafts) (reticu lar) 3rd Leathery feeling (charred parchment); down to subcutaneous fat 4th Down to bone, into adjacent adipose or muscle tissue

Burn Deaths highest in children and elderly (trouble getting away)

Scald burns — most common

Flame burns — more likely to come to hospital and be admitted

Assessing percentage of body surface burned (rule of 9s) Head = 9, arms = 18, chest = 18, back = 18, legs = 36, perineum = 1

Can also use patient’s palm to estimate injury (palm = 1%)

ADMISSION CRITERIA

2nd- and 3rd-degree burns >10% BSA in patients aged <10 or >50 years

2nd- and 3rd-degree burns >20% BSA in all other patients 2nd- and 3rd-degree burns to significant portions of hands,

face, feet, genitalia, perineum, or skin overlying major joints 3rd-degree burns >5% in any age group Electrical , chemical burns , inhalational injury preexisting medical conditions ,mechanical traumas Injuries in patients with special social, emotional, or long-

term rehabilitation needs Suspected child abuse or neglect

Parkland formula

For burns 20% — give 4 cc/kg X % burn in first 24 hours; give 1/2 in first 8 hours

Use lactated Ringer’s solution (LR) in first 24 hours

Urine output best measure of resuscitation (0.5—1 .0 cc/kg/h in adults, 2—4 cc/kg/h in children < 6 months)

Colloid (albumin) in 1st 24 hours can cause pulmonary/respiratory complications — can use colloid after 24 hours

BURN WOUND INFECTIONS

Pseudomonas is most common organism in burn wound infection, followed by

Staphylococcus E. coIl, and Enterobacter - More common in burns > 30% BSA

HSV most common viral infection in burn wounds

<I05 organisms - not a burn wound infection

-Pneumonia most common infection in burn wound patients -Also most common cause of death after inhalation injury

Topical agents

Silfadine (silver sulfadiazine) — can cause neutropenia and thrombocytopenia

Silver nitrate can cause electrolyte imbalances — hyponatremia and hypochloremia, hypocalcemia

and hypokalemia

Sulfamylon (mafenide sodium) - painful application

can cause METABOLIC acidosis Good eschar penetration

Marjolins ulcer highly malignant squamous cell CA that arises in chronic nonhealing burn wounds or unstable scars

Hypertrophic scar -Usually occurs 3-4 months after injury secondary to

neovascularity - heal by contraction and epithilial spread, or heal across

flexor surfaces - Wait 1-2 years before scar modification • Tx: grafiirig, sieroids, silicone, compression

Curling’s ulcer gastric ulcer that occurs with burns

. Metabolic acidosis is a complication of topical application

of:(a )sodium mafenide

(b )silver nitrate(c )silver sulfadiazine

(d )Betadine(e )bacitracin

. Hyponatremia is a complication of topical application

of:(a )bacitracin

(b )povidone-iodine(c )silver sulfadiazine

(d )Sulfamylon(e )silver nitrate

. The most common fatal infection in burn victims is:

(a )pneumonia(b )venous line–related sepsis

(c )burn wounds sepsis(d )urinary tract infection

. A 70-kg male with 50% body surface area seconddegreeburn requires:

(a )7,000 mL of lactated Ringer’s solution over thefirst 6 hours

(b )7,000 mL of lactated Ringer’s solution over thefirst 8 hours

(c )8,000 mL of lactated Ringer’s solution over thefirst 8 hours

(d )10,000 mL of lactated Ringer’s solution over thefirst 8 hours

nutrition

Calori

• Caloric Need - approximately 25 kcal/kg/day• 1 g protein/kg/day is needed, of which 20%

should be essential amino acids• 30% fat calories — important for essential

fatty acids• Rest of calories should be as carbohydrates

CaloriTrauma, surgery, or sepsis, stress can increase kcal

requirement 20%—40%Pregnancy increases kcal requirement 300 kcal/dayLactation increases kcal requirement 500 kcal/dayBurns Calories: 25 kcal/kg/day + (30 kcal/day X % burn) Protein:

1—1.5 g/kg/day + (3 g X % burn)Much of the energy expenditure is used for heat

production Basal metabolic rate increases 10% for each degree above

38.0°C

Calori

fat 9 kcal/g protein 4 kcal/g carbohydrates 4 kcal/g dextrose 3.4 kcal/g

TPN

Central line TPN - glucose based; maximum glucose administration - 3 g/kg/h

Peripheral line parenteral nutrition (PPN) - fat based

Short-chain fatty acids - fuel for colonocytes -Glutamine - fuel for small bowel enterocytes - Most common amino acid in bloodstream

and tissuePrimary fuel for neoplastic cell — glutamine Ideal body weight (IBW) • Men = 106 lb + 6 lb for each inch over5ft • Women = 100 lb + 5 Ib for each inch over5 ft

Preoperative signs of poor nutritional status• Acute weight loss >10% in 6 months• Weight <85% of IBW• Albumin <3.0• Low albumin (<3.0)- strong risk factor for

morbidity and mortality after surgery

POST OPERATIVE PHASES• Diuresis phase — postoperative days 2—5• Catabolic phase - postoperative days 0- 3

(negative nitrogen balance)• Anabolic phase - postoperative days 3-6

(positive nitrogen balance)6.25g of protein contains 1g of nitrogenTotal protein synthesis for a healthy,70kg

male is250g/day

• Late starvation — gluconeogenesis occurs in kidny

• Fat (ketones) is the main source of energy in trauma and starvation

• Most patients can tolerate a 15% weight loss without major complications

• Patients can tolerate about 7 days without eating; if longer than that, place a Dobbhoff tube or start TPN

• Brain — utilizes ketones with progressive starvation (normally uses glucose)

• Elemental formula — all protein given in the form of amino acids (given IV, expensive)

• PEG — consider when regular feeding not possible (e.g., CVA) or predicted to not occur for >4 weeks

NONHEALING FISTULA

“FRIENDS”+H — mnemonic for causes of nonhealing fistula: Foreign body, Radiation, Inflammatory bowel disease, Epithelialization, Neoplasm, Distal obstruction, Infection/sepsis

High-output

High-output fistulas ; are more likely with proximal bowel (duodenum or proximal portion ofjejunum) and are less likely to close with conservative management

Colonic fistulas ; are more likely to close than those in small bowel

Patients with persistent fever— need to check for abscesses (fistulogram, abdominal CT, upper GI with small bowel follow-through series)

Most fistulas iatrogenic and treated conservatively 1st —* TPN, skin protection, NG tube, stoma appliance, octreotide

40% close spontaneously

Surgical options: resect bowel segment containing fistula and perform primary anastomosis

Potassium is absorbed by passive diffusion in the jejuni Sodium is actively transported, and once a gradient is established,

chloride follo passively. absorption in jejuni Calcium is actively transported in the jejunum (enhanced by vitamin D

and parathyro hormone). Iron is absorbed as the ferrous (reduced) ion Fe2. active transport in

the duodeni. and jejunum, and 1O%—26% (maximally) of dietary iron is absorbed.

Fat absorption occurs mainly in the jejunum..). The fat-soluble vitamins A, D, E, and K are absorbed from micelles by

the mucosa. B12 is complexed with intrinsic factor and absorbed in the distal ileum. Vitamin C, thiam and folic acid are actively transported. The remaining

water-soluble vitamins are absor by passive diffusion.

Refeeding syndrome Occurs when feeding after prolonged

starvation/malnutrition Results in .dec. K, Mg, and P04 causes cardiac

dysfunction and fluid shifts Prevent this by starting at a low rate (10—15 kcal/kg/day)

Cachexia- anorexia, weight loss, wasting Thought to be mediated byTNF-a. Glycogen breakdown, lipolysis, protein catabolism

FAT DIGESTION Triacylglycerides (TAGs), cholesterol, lipids Broken down by pancreatic lipase, cholesterol

esterase, and phospholipase to micelles and free fatty acids

Protein DIGESTIONBegin with stomach pepsinogen,then

trypsin,chymotrypsin,carboxypeptidase. The process is completed at the brush border,

yielding tripeptidc ,dipeptides, and amino acids All are absorbed by active transport

CARBOHYDRATE DIGESTION Begins with salivary amylase, then pancreatic

amylase and disaccharidases

Glucose and galactose — absorbed by secondary active transport; released into portal vein

Fructose — facilitated diffusion; released into portal vein

Sucrose -fructose + glucose Lactose- galactose + glucose Maltose- glucose + glucose

. Dry, scaly, pruritic rash on the trunk and extremitiesof a patient receiving total parenteral nutrition iscaused by:

(a )zinc deficiency(b )vitamin A deficiency(c )vitamin C deficiency

(d )free fatty acid deficiency

. Enterocytes’ energy requirements are provided by:

(a )arginine(b )alanine

(c )glutamine(d )glycine

. In critical illness, immune function can be enhanced by:

(a )arginine(b )glutamine

(c )alanine(d )glycine

. During prolonged starvation, the brain’s main fuel is:

(a )glucose(b )amino acids

(c )ketones(d )short-chain fatty acids

. The layer responsible for the strength of an intestinal anastomosis is the ;

(a )mucosa(b )submucosa

(c )muscularis propria(d )serosa

. The most abundant amino acid in the body is:

(a )alanine(b )valine(c )leucine

(d )glutamine(e )arginine

. Spontaneous closure is least likely in fistulae originating from:

(a )colon(b )esophagus

(c )pancreas(d )stomach

(e )small intestine

. The most common cause of spontaneous intestinal fistula is:

(a )radiation injury(b )malignancy

(c )Crohn’s disease(d )ulcerative colitis

(e )diverticular disease

. Refeeding syndrome is most commonly related to:

(a )hyponatremia(b )hypocalcemia

(c )hypophosphatemia(d )hypokalemia

. Biliary-enteric fistula most commonly connects:

(a )gallbladder and ileum(b )gallbladder and duodenum

(c )common bile duct and jejunum(d )gallbladder and jejunum

(e )common bile duct and ileum

. The main fuel for most cancer cells is:

(a )butyrate(b )glutamine(c )L-arginine

(d )glucose(e )ketones

. The main source of fuel in sepsis is:

(a )glucose(b )fatty acids

(c )ketones(d )amino acids

. Mucosal defense is provided by immunoglobulin:

(a )A(b )G(c )M(d )D(e )E

. Optimum calorie/nitrogen ratio for protein synthesis Is;

(a )25–50 : 1(b )50–75 : 1(c )75–100 :1

(d )100–150: 1

. The most reliable means of preoperative nutritional assessment is:

(a )clinical history of weight loss(b )serum albumin level

(c )impaired cell-mediated immunity(d )triceps skinfold measurement

. The gastroduodenal artery is a branch of the:

(a )celiac axis(b )right gastric artery

(c )common hepatic artery(d )right hepatic artery

(e )left hepatic artery

trauma

1st peak for trauma deaths (0—30 minutes) — deaths due to lacerations of heart, aorta, brain, brainstem, spinal cord. Cannot really save these patients; death is too quick

2nd peak for trauma deaths (30 minutes—4 hours) —

deaths due to head injury (#1) and hemorrhage (#2). These are the patients you can save with rapid assessment (golden hour)

3rd peak for trauma deaths (days to weeks) — deaths

due to multisystem organ failure and sepsis

• Blunt injury — 80% of all trauma;liver most commonly injured (some texts say spleen)

• Falls — age and body orientation biggest predictors of survival. • Penetrating injury -small bowel most commonly injured (some

texts say liver)• Hemorrhage — most common cause of death in 1st hour• Blood pressure is usually OK until 30% of total blood volume is

lost• Head injury — most common cause of death after reaching the

ER alive• Infection- most common cause of death in the long term• Tongue — most common cause of upper airway obstruction —+

perform jaw thrust• Seat belts — small bowel perforations, lumbar spine fractures,

sternal fractures

Diagnostic peritoneal lavage (DPL)• Used in hypotensive patients with blunt

trauma• Positive if>10 cc blood, >100,000 RBCs/cc,

food particles, bile, bacteria,>500 WBC/cc• Need laparotomy if DPL is positive• DPL needs to be supraumbilical if pelvic

fracture present• DPL misses — retroperitoneal bleeds,

contained hematomas

FAST scan (focused abdominal sonography for trauma)

• Ultrasound scan used in lieu of DPL• Checks for blood in perihepatic fossa, perisplenic

fossa, pelvis, and pericardium• Examiner dependent• Obesity can obstruct view• May not detect free fluid < 50—80 mL• Need laparotomy if FAST scan is positive• FAST scan misses — retroperitoneal bleeding,

hollow viscous injury

Need a CT scan following blunt trauma in patients

with abdominal pain,need for general anesthesia, closed head injury,

intoxicants on board, paraplegia. distracting injury ,hematuria

Patients requiring DPL that turned out negative will need an abdominal CT scan

CT scan misses - hollow viscous injury, diaphragm injury

pituitary Hypothalamus - releases TRH, CRH, GnRH, GHRH, and dopamine.

Posterior pituitary (neurohypophysis) accumulate ; • ADH — supraoptic nuclei, in hypothalamus • Oxytocin — paraventricular nuclei in hypothalamus • Neurohypophysis does not contain cell bodies

Anterior pituitary (80% of gland, adenohypophysis) • ACTH, TSH, GH, [ FSH, and prolactin • Does not have its own direct blood supply; passes through

neurohypophysis 1st

The total volume of the CSF 150 ml (at rate of 0.35ml/min. 150 three times/day

80%of the CSF is produced by the choroid plexus

The upper limit of normal ICP 15 mm Hg

The skull a rigid box with volume 1900 ml (85% brain ,7% blood , 7% CSF)

HEAD TRAUMA

Glasgow Coma Scale (GCS) • Motor• 6-follows commands• 5 — localizes pain• 4-withdraws from pain• 3 — flexion with pain (decorticate)• 2 — extension with pain (decerebrate)• • 1 — no response • Verbal• 5 — oriented• 4—confused• 3 - inappropriate words• 2 — incomprehensible sounds• 1 — no response • Eye opening• 4 spontaneous opening• 3 - opens to command• 2-opens to pain• • 1 — no response GCS score — 14: head CT; 10: intubation; 8: ICP monitor

Epidural hematoma most commonly due to arterial bleeding from the middle meningeal artery Head CT — shows lenticular (lens-shaped) deformity Patients initially have loss of consciousness (LOC) —* then lucid

interval —> then sudden deterioration (vomiting, restlessness, LOC) Operate for significant neurologic degeneration or significant mass

effect (shift> 5 mm)

Subdural hematoma most commonly from tearing of venous plexus (bridging veins) between dura and arachnoid Head CT — shows crescent-shaped deformity Operate for significant mass effect Chronic subdural hematomas — usually in elderly after minor fall

Need drainage if>1 cm or causing significant symptoms

indications for thoracotomyin Hemothorax

• >l500cc after initial insertion, >250 cc/h for 3 hours, 2500 cc/24 h, or bleeding with instability — all relative indications for thoracotomy in OR

• Need to drain all of the blood (in <48 hours) to prevent fibrothorax, pulmonary entrapment, infected hemothorax

• Unresolved hemothorax after 2 well-placed chest tubes — thoracoscopic or open drainage

Flail chest;- >2 or= consecutive ribs broken at>2or= sites result in paradoxical motion

Underlying pulmonary contusion –biggest pulmonary impairment

Recurrence risk of spon. pneumothorax

• After 1st pneumothorax 30%• After 2nd pneumothorax 60% • After 3rd pneumothorax 80%

Indecaition for surgery in pneumothorax

• Recurrence• Larg blebs in CT• Air leak >7days• Nonreexpansion

LIVER TRAUMA

• Lobectomy rarely necessary• Common hepatic artery - can be ligated with collaterals through

gastroduodenal artery• Hepatic lobar arteries can be ligated without complication unless the

patient is hypotensive, which could lead to liver ischemia• Pringle maneuver (clamping portal triad) does not stop bleeding from

hepatic veins • Pringle maneuver . If possible, clamp times should be limited(15-

20)minute intervals.• Perihepatic packing — can pack severe penetrating liver Injuries if

patient becomes unstable in the OR. Go to the ICU and get the patient resuscitated and stabilized. Live to fight another day

• Portal triad hematomas - need to be explored

Common bile duct injury

• <50% of circumference — repair over stent• >50% or complex injury— go with choledochojejunostomy• May need intraoperative cholangiogram to define injury• 10% of duct anastomoses leak• Portal vein injury - need to repair• May need to transect through the pancreas to get to the injury

in the portal vein• Will need to perform distal pancreatectomy with that maneuver• Ligation of portal vein associated with 50% mortality• Omental graft - can be placed in liver laceration to help with

bleeding and prevent bile leaks• Leave drains with liver injuries

Conservative management of blunt liver injuries

• Has failed if patient becomes unstable despite aggressive resuscitation, including 4 units of PRBCs (HR> 120 or SBP < 90) or requires >4 units of PRBCs to keep Hct> 25. Go to OR

• Active blush on abdominal CT or pseudoaneurysm also indication for OR

If postrior, may be better off going to angiogram (when in doubt —* OR)

If anterior go to OR

• With conservative management, need bed rest for 5 days

SPLENIC TRAUMA

• Fully healed after 6 weeks• Postsplenectomy sepsis most common in 1st 5 years of life; greatest risk

within 2 years of splenectomy• Splenic salvage is associated with increased transfusions

Conservative management of blunt splenic injuries

• Has failed if patient becomes unstable despite aggressive resuscitation, including 2 units of PRBCs (HR> 120 or SBP<or=90) or requires >2 units of PRBCs to keep Hct> 25. Go to OR

• Active blush on abdominal CT or pseudoaneurysm also indication for OR• With conservative management, need bed rest for 5 days• Threshold for splenectomy in children is much higher; hardly any

children undergo splenectomy

RENAL TRAUMA

• Hematuria is best indicator of renal trauma• All patients with hematuria need CT scan• Left renal vein — can be ligated near IVC; has adrenal and

gonadal vein collaterals. Right does not• Anterior — posterior renal hilum structures — vein, artery, pelvis• 95% of injuries are treated nonoperatively• Not all urine extravasation injuries require operation• Indications for operation • Acutely — ongoing hemorrhage with instability • After acute phase — major collecting system disruption,

unresolving urine extravasation, severe hematuria• Penetrating renal injury with hematoma — open unless preop

CT/IVP shows good function without significant urine extravasationn

BLADDER TRAUMA

Hematuria best indicator of bladder trauma

>95 % associated with pelvic fractures

Signs and symptoms - meatal blood, sacral or scrotal hematoma

Dx: cystogram

Tx: • Extraperitoneal bladder rupture - Foley 7-14 days• Intraperitoneal bladder rupture — operation and repair of defect,

followed by Foley drainage

URETERAL TRAUMA Hematuria unreliable —* IVP and retrograde urethrogram (RUG) best tests

If large ureteral segment is missing (>2 cm) and cannot perform reanastomosis:

o Upper 1/3 injuries and middle 1/3 injuries with percutaneous nephrostomy (tie off both ends of the ureter) if patient unstable.

•Can go with ileal interposition or trans-ureteroureterostomy later• stable, most urologists would perform trans-ureteroureterostomy

o Lower 1/3 injuries — reimplant in the bladder; may need bladder hitch procedure

If small ureteral segment is missing (<2 cm), perform primary repair over stent in the upper or mid 1/3ureter.

reimplant in the lower 1 /3ureter

Leave drains for all ureteral injuries

URETHRAL TRAUMA Hematuria or blood at meatus best sign; free-floating

prostate gland; usually associated with pelvic fractures

No Foley if this injury is suspected

Urethrogram best test Significant tears — Tx: suprapubic cystostomy and repair in 2

—3 months (safest method) • High stricture and impotence rate if repaired early

Small, partial tears — Tx: may get away with bridging urethral catheter across tear area and repair in 2—3 months

• upper EXTREMITY• Anterior shoulder dislocation-- Axillary nerve• posterior shoulder dislocation-- Axillary artery• proximal humerus-- Axillary nerve• midshaft humerus (or spiral humerus fracture)-- Radial nerve• distal (supracondylar) humerus-- Brachial artery• elbow dislocation-- Brachial artery• distal radius-- Median nerve• Lower EXTREMITY• anterior hip dislocation-- Femoral artery• posterior hip dislocation-- Sciatic nerve• distal (supracondylar) femur-- Popliteal artery• posterior knee dislocation-- Popliteal artery• fibuIa neck-- Common peroneal nerve

. A trauma patient has a Glasgow Coma Scale of 13, blood pressure 80/40,widened mediastinum

on chest x-ray, and bloody peritoneal tap. The next step in management is:

(a )obtain head computed tomography scan(b )perform thoracotomy

(c )perform arch angiography(d )monitor intracranial pressure

(e )perform laparotomy

. Spontaneous pneumothorax:

(a )is more common in young females(b )is typically postexertional

(c )is recurrent in at least 30% of cases(d )often requires thoracotomy in the first

episode(e )is often associated with severe persistent

pain

. For penetrating chest injury, thoracotomy is indicated if:

(a )initial chest tube output is 500 cc(b )initial chest tube output is 1,000 cc(c )initial chest tube output is 1,500 cc(d )initial chest tube output is 2,000 cc

(e )persistent chest tube output of 100 cc/hr

. After reduction of posterior knee dislocation, patient should undergo the :

(a )observation(b )discharge

(c )splinting(d )angiogram

(e )internal fixation

. The most common cause of esophageal perforation is:

(a )penetrating neck injury(b )iatrogenic

(c )spontaneous(d )foreign body

(e )malignancy

. Volkmann’s contracture is a complication of:

(a )humeral head fracture(b )femoral neck fracture

(c )posterior dislocation of the knee(d )supracondylar humeral fracture

(e )Colles’ fracture

. The most commonly injured organ in a patient with seatbelt sign is:

(a )the liver(b )the spleen

(c )the colon(d )the pancreas

(e )the small intestine

. A patient with head injury opens his eyes and withdraws his arm to pain. He is making incomprehensible sounds. His Glasgow Coma Scale score is:

(a )12(b )10

(c )8(d )6

. The most appropriate method to diagnose small bowel injury in a conscious trauma patient with seatbelt injury is:

(a )diagnostic peritoneal lavage(b )ultrasound

(c )computed tomography scan(d )serial abdominal examination

(e )plain abdominal film

. The initial fluid bolus for an injured child is:

(a )10 mL/kg of lactated Ringer’s solution(b )20 mL/kg of lactated Ringer’s solution(c )30 mL/kg of lactated Ringer’s solution(d )40 mL/kg of lactated Ringer’s solution

. Risk of irreversible tissue damage in pressure sores is highest with:

(a )constant pressure of 50 mm Hg for 2 hours(b )constant pressure of 70 mm Hg for 2 hours

(c )constant pressure of 100 mm Hg for 30 minutes(d )constant pressure of 150 mm Hg for 20 minutes

. The fluid of chylothorax is composed of:

(a )pure fat(b )fat and neutrophils(c )fat and lymphocytes(d )fat and macrophages

. A 28-year-old male has a closed head injury, pulmonary contusion, grade III splenic injury, and closed femoral shaft fracture. The ideal management of his fracture is:

(a )external fixation(b )skeletal traction

(c )intramedullary nailing within 24 hours of injury(d )intramedullary nailing 1 week after the injury

(e )use of metal plates and screw

. Trauma cesarean section is indicated if the fetus is viable and:

(a )the mother is unstable and cardiac arrest is anticipated(b )5 minutes of cardiopulmonary resuscitation were

successful(c )5 minutes of cardiopulmonary resuscitation were

unsuccessful(d )cardiopulmonary resuscitation has just been

initiated

neck

Landmarks

1. Hyoid bone2. Thyroid cartilage3. Cricoid cartilage4. Trachea5. Sternocleidomastoid

muscles

Anatomy of the neck

The sternocleidomastoid muscle divides each side of the neck into 2 major triangles:

Anterior triangle Borders:1. Laterally: anterior border of the SCM2. Medially: midline3. Superiorly: lower border of the mandible4. contains the carotid sheath

Posterior triangleBorders: • Anteriorly: posterior border of the SCM• Inferiorly: clavicle• Posteriorly: anterior border of trapezius muscle• contains the spinal accessory nerve and the brachial plexus

Anatomy of the neck

1. Anterior triangle (digastric & sup. Belly of omohyoid)– Submandibular triangle– Submental triangle– Carotid triangle– Muscular triangle

2. Posterior triangle (inf. Belly of omohyoid)– Occiptal triangle– Supraclavicular triangle

Anatomy of the neck

• Parotid glands — secrete mostly serous fluid• Sublingual glands - secrete mostly mucin• Submandibular glands - 50/50• In larynx, the false vocal cords are superior to

the true vocal cords• Trachea has U-shaped cartilage and a

posterior portion that is membranous

Anatomy of the neck

• Vagus nerve — runs between lJ and carotid arteries

• Phrenic nerve — runs on top of the anterior scalene muscle

• Trigeminal nerve - ophthalmic, maxillary, mandibular branches

- Gives sensation to most of face - Mandibular branch — taste to anterior 2\3 of

tongue, floor of mouth, and gingiva

Anatomy of the neck

• Facial nerve — temporal, zygomatic, buccal, marginal mandibular, and cervical branches

- Motor function to face

• Glossopharyngeal nerve - sensory to posterior tongue

- Motor to stylopharyngeus - Injury affects swallowing

Anatomy of the neck

• Hypoglossal nerve — motor to all of tongue except palatoglossus . Tongue deviates to side of injury

• Recurrent laryngeal nerve — innervates all of larynx except cricothyroid muscle

• Superior laryngeal nerve — innervates the cricothyroid muscle

Anatomy of the neck

• Thyrocervical trunk — “STAT”: suprascapular artery, transverse cervical artery, ascending cervical artery, inferior thyroid artery

• External carotid artery— 1st. branch is superior thyroid artery

Anatomy of the neck

• Radical neck dissection (RND) — takes accessory nerve (CN XII), sternocleidomastoid, internal jugular, omohyoid, submandibular gland, sensory nerves C2—C5, cervical branch of facial nerve, and ipsilateral thyroid

- Most morbidity occurs from accessory nerve resection

• Modified radical neck dissection (MRND) — takes omohyoid, submandibular gland, sensory nerves C2—C5, cervical branch of facial nerve, ipsilateral thyroid

- No mortality difference compared with RND

neck mass The most common neck mass is a reactive node

Most neck masses in children are benign.

In adults, neck masses are more likely to be malignant.

The “rule of sevens” is a useful guide: A mass that has been present for 7 days is inflammatory. One present for 7 months is malignant. One present for 7 years is congenital

Dx of mass in the neck depend on:

Age of the pt.

Clinical course.

Solid or cystic swelling.

Site.

• Mid lin swelling:1. Solid swelling: a- submental L.N. enlargment b- nodule in the isthmus of the thyroid gland.2. Cystic swelling: a- thyroglosal cyst. (most common) b- dermoid cyst. c- subhyoid bursitis d- laryngocoele. e- cyst in the thyroid gland. f- cold abscess.

thyroglosal cyst

• Swelling in the submandibuler triangle: 1- enlarged submandibular L.N. 2- enlarged submandibular salivery gland.• Swelling in the carotid triangle: 1- solid swelling: a- enlarged upper deep cervical L.N. b- carotid body tumour. c- upper part of enlarged latral lobe of thyroid 2- Cystic swelling: a- cold abscess. b- branchial cyst.

Carotid body tumor

compressible mass that refills rapidly on the release of pressure.

Slowly growing tumour thate Originate from small chemoreceptive and baroreceptive organs

Located at the adventitia of the common carotid artery bifurcation. (paragangliomas)

c\p: present at middle age,slowly growing, usully smoth but may be lobular,

The swelling moves from side to side but not vertically,it exhibits transmeted pulsation from underlying C.A

• Dx:• angiography can prove the dx.• Ttt:• Tumour excision with preservation of the

internal carotid artery or if not possible the artery should be replaced by graft even before excision to avoid blood flow inerruption to the brain.

branchial cyst

Develops under the skin between SCM & pharynx.due to grow the 2nd arch over the 3rd and 4th arch then it fuse with neck.

• Swelling in poster triangel:• 1- solid swelling:• a- enlarge lymph node.• b- neurofibroma arising from brachial plexus.• c- cervical rib.• 2- cystic swelling: a- cystic hygroma. b- pharyngeal pouch. c- cold abscess. d- pneumatocele.

• Cystic hygromas– Large, soft, painless, and compressible

masses,increas size with coughing and crying.– Usually present at birth or by the age of 3. – Most commonly present in the lower part of

posterior triangle.

• Other swelling that may arise anywhere: 1- lipoma. 2- sebaceous cysts. 3- haemangioma.

PLUNGING RANULA•Mucus retention cyst or a mucus extravasation

pseudocyst arising from an obstructed sublingual gland.

•Simple ranula is confined to the oral cavity- cystic unilateral mass of the floor of the mouth.

•Plunging ranula may pierce the mylohyoid and present as a paramedian or lateral neck mass with or without an obvious oral cavity ranula.

• Work up– Cyst aspiration - fluid with high levels of

protein and salivary amylase.

– CT or MRI -.

• Surgical treatment - excision in continuity with the sublingual gland of origin.

PLUNGING RANULA

Ranula

• Cystic swelling floor of mouth

• Mucous extravasation from sublingual salivary gland

• Plunging Ranula, extend through FOM muscles into neck

SALIVARY GLAND

Parotid, submandibular, sublingual, and minor salivary glands

• Submandibular or sublingual tumors — can present as a neck mass or swelling in the floor of the mouth

• Mass in large salivary gland — more likely mass is benign

• Mass in minor salivary gland —* more likely mass is malignant, although the parotid gland is the most frequent site for malignant tumor

Malignant tumors

Mucoepidermoid CA - #1 malignant tumor of the salivary glands

- Wide range of aggressiveness

Adenoid cystic CA — #2 malignant tumor of the salivary glands; #1 malignant salivary tumor of the minor salivary glands

Often present as a painful mass but can also present with facial nerve paralysis or lymphadenopathy

General Principles for Surgical Treatment

• Malignant tumors of the parotid gland total parotidectomy.

• The facial nerve should be sacrificed only for direct tumor invasion or for preexisting facial paralyses.

• Patients with high-grade tumors should undergo elective neck dissection if there is no clinical neck disease or a modified neck dissection for palpable adenopathy.

• Postoperative radiotherapy is indicated for all high- grade tumors; close margins; recurrent disease; skin, bone, nerve, or extraparotid involvement; positive nodes; or unresectable diseas

Benign tumors Pleomorphic adenoma (mixed tumor) — #1 benign tumor of the salivary glands Malignant degeneration in 5% Tx: superficial parotidectomy If malignant degeneration, need total parotidectomy; if

high grade also need M RN D Warthin’s tumor— #2 benign tumor of the salivary Often present as a painless mass glands Males, bilateral in 10% • Tx: superficial parotidectomy

SALIVARY GLAND

. Most common injured nerve with parotid surgery greater auricular nerve (numbness over lower

portion of auricle)

. For submandibular gland resection — need to find mandibular branch of facial nerve .

lingual nerve, hvpoglossal nerve

.Most common salivary gland tumor in children - hemangiomas

THYROID CANCER

Most common endocrine malignancy in the United States

Follicular cells on FNA — 5%—10% chance of malignancy (unable to differentiate between follicular cell adenoma, follicular cell hyperplasia, normal thyroid tissue, and follicular cell CA on FNA)

Worrisome for malignancy — solid, solitary, cold 20%, slow growing, hard; male, age> 50, previous neck XRT, MEN Ila or llb

THYROID CANCER Sudden growth could be hemorrhage into previously

undetected nodule or malignancy

Patients can also present with voice changes and dysphagia

Thyroid adenomas — need to be differentiated from carcinomas — require lobectomy

Follicular adenomas — colloid, embryonal, fetal • no increase in cancer risk • Still need lobectomy to prove it is adenoma

THYROID CANCER

Papillary thyroid carcinoma

Follicular thyroid carcinoma

Medullary thyroid carcinoma

Hürthle cell carcinoma

Anaplastic thyroid cancer

Papillary thyroid carcinoma

Most common (80%-90%) thyroid CA Least aggressive,slow growing,has the best prognosis Young adults, women, children most common tumor following neck XRT Older age (>40—50 years) predicts a worse prognosis Lymphatic spread 1st but is not prognostic Prognosis based on local invasion Rare metastases - lung most common Pathology — psammoma bodies (calcium) and Orphan

Annie nuclei 95% 5-year survival rate; death secondary to local

disease

Follicular thyroid carcinoma

• Hematogenous spread (bone most common) 50% have metastatic disease at the time of presentation

• More aggressive than thyroid papillary CA

• Older adults (50—60), women

• FNA shows just foliccular cells — 10% chance of malignancy; need thyroidectomy

•70% 5-year survival rate

•prognosis based on stage

Medullary thyroid carcinoma

• Tumor arises from parafollicular C cells (which secrete calcitonin)

• Can be associated with MEN IIa or lIb, Need to screen for hyperparathyroidism and pheochromocytoma

• Pathology - shows amyloid deposition

• lymphatic spread and Hematogenous spread , Early metastases to lung, liver, and bone

• 50% 5-year survival rate;

• prognosis based on presence of regional and distant metastases

Hürthle cell carcinoma

• Most are benign (Hurthle cell adenoma); presents in older patients

• Early nodal spread if malignant

• Metastases go to bone and lung

• Tx: total thyroidectomy; MRND for clinically positive nodes

Anaplastic thyroid cancer

• Elderly patients with long-standing goiters

• Most aggressive thyroid CA

• Rapidly lethal (0% 5-year survival rate); usually beyond surgical management by diagnosis

• Tx: total thyroidectomy for the rare lesion that can be resected

• Can perform palliative thyroidectomy for compressive symptoms or give palliative chemotherapy or XRT

. The most important diagnostic test for a thyroid nodule is:

(a )ultrasound(b )radioactive isotope scan

(c )thyroid function test(d )fine-needle aspiration

(e )computed tomography scan

. Follicular thyroid carcinoma:

(a )is the most common thyroid cancer(b )is readily diagnosed with fine-needle

aspiration(c )spreads via hematogenous route

(d )is commonly multifocal

. Pleomorphic parotid adenoma:

(a )requires core biopsy before resection(b )is adequately treated with enucleation

(c )commonly undergoes malignant transformation

(d )commonly results in facial palsy(e )is the most common parotid neoplasm

. Which of the following is preserved in radical neck dissection?

(a )internal jugular vein(b )sternomastoid muscle(c )spinal accessory nerve

(d )submandibular salivary gland(e )posterior belly of the digastric muscle

. The inferior parathyroid gland originates from the:

(a )first pharyngeal pouch(b )second pharyngeal pouch

(c )third pharyngeal pouch(d )fourth pharyngeal pouch

. The hallmark of multiple endocrine neoplasia type 2 syndromes is:

(a )hyperparathyroidism(b )pheochromocytoma

(c )medullary thyroid carcinoma(d )pituitary adenoma(e )neural gangliomas

. Recurrence of thyroid carcinoma after definitive treatment is best detected by:

(a )ultrasound of the neck(b )thyroid-stimulating hormone level measurement

(c )thyroglobin serum measurement(d )computed tomography scan of the neck

(e )triiodothyronine/thyroxine measurement

Anatomy/Physiology• Muscular tube 25 cm long• From C6 – T11• Majority in mediastinum, post/lat to trachea• Outer longitudinal & inner circular muscles• Upper 1/3 striated muscle, lower half all smooth

muscle• Upper 2/3 squamous lower 1/3 columnar epithelium• Two sphincters; UES cricopharyngeus muscle, LES

lower 1-2 cm of esophagus• No serosal covering• Esophageal peristaltic pressures range from 30 to

120 mm Hg.

Anatomy/Physiology

• Three anatomic constrictions:– Cricopharyneus– Aortic arch/left mainstem bronchus– Gastroesophageal junction

Anatomy

Arterial supply to the esophagus.

Three specialized areas of the

esophagus:•Upper esophageal sphincter•The Body•Lower esophageal or

gastroesophageal sphincter.

Congenital:AtresiaTraumatic:FBCaustic ingestionPerforationNeoplastic:Benign (rare)MalignantFunctional:GERDNeuro-muscular:Achalasia

Congenital:AtresiaTraumatic:FBCaustic ingestionPerforationNeoplastic:Benign (rare)MalignantFunctional:GERDNeuro-muscular:Achalasia

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Cricopharyngeal dysfunction and Zenker's diverticulum (Pathophysiology)

• Cricopharyngeal dysfunction is caused by a failure of the upper esophageal sphincter to relax properly.

• The problem may be an incoordination between relaxation in the upper esophageal sphincter and simultaneous contraction of the pharynx, which results in a pharyngoesophageal (Zenker's) diverticulum. This is a false diverticulum that consists only of mucosa that herniate posteriorly between the fibers of the cricopharyngeal muscle. Usually seen after age 50

• Cricopharyngeal dysfunction and Zenker's diverticulum is often associated with hiatal hernia and gastroesophageal reflux

Symptoms of Zenker's diverticulum

• dysphagia,• halitosis, • regurgitation of undigested food,• nocturnal aspiration, • recurrent aspiration pneumonia• Feeling of a neck mass ( left side )

Midesophageal Diverticula

• Traction diverticulum

• Is a true diverticulum usually lateral

• Due to inflammation,granulomatous disease,tumor

• Usually in the Midesophagus

Midesophageal Diverticula

Symptoms and Diagnosis

• Most patients with a midesophageal diverticulum are asymptomatic

• Dysphagia• Regurgitation• Hemoptysis

Treatment

• Determining the etiology for midesophageal diverticula is critical to guiding treatment

• In tuberculosis or histoplasmosis, medical treatment with antituberculin or antifungal agents is indicated

• Excision and primary closure• May need palliative therapy (i.e,XRT)

Epiphrenic Diverticula

• Rare,associated with esophageal motility disorders

• Epiphrenic diverticula are found adjacent to the diaphragm in the distal third of the esophagus(distal 10 cm )

• Most are asymptomatic; can have Dysphagia, Regurgitation

• DX:esophagogram and Esophageal manometry

Barium swallow showing mid- and distal esophageal diverticula

Treatment

• In documented motor abnormality, diverticlectomy and long esophagomyotomy is indicated on the side opposite diverticlectomy

Achalasia • Achalasia is an esophageal disease of unknown etiology, although

it may be secondary to ganglionic dysfunction, which causes:– High resting LES pressure– Failure of the LES to relax during swallowing– Absence of coordinated peristalsis in the body of the esophagus

• The body of the esophagus becomes dilated, and the muscle hypertrophies in an attempt to force material through the dysfunctional LES. A similar symptom complex can be caused by Chagas disease, which is caused by the organism Trypanosoma cruzi.

• Carcinoma of the esophagus is 10 times more common in patients with achalasia than in the general population.

Achalasia of the cardia

Incidence;commonly middle agedneurotic female

Etiology:Degeneration of ganglion cells ofAuerbach’s plexus (parasympathetic)in the wall of the esophagus Failureof relaxation of the cardiac sphincterduring swallowing marked dilatation

of the lower two thirds of the esophagus

Failure of relaxation ofCardiac sphincter

Marked Dilatation of the lower two thirds esophagus above the cardia

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Symptoms

• classic triad: dysphagia, followed by regurgitation, weight loss

• Frequently, • respiratory symptoms caused by aspiration are

present

Symptoms:Dysphagia: more to fluids Why?Regurgitation of undigested acid free food

Signs:Excessive food stagnation

Marked dilatation …….InvestigationsBarium swallowManometric study: increase pressureof the lower segment

Swalowing of fluids needs highly co-ordinated act of swallowingSolids can descend by gravity

Marked dilatation of the lower 2/3 of the esophagus (segmoid

esophagus)Tapering of the lower end

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Diagnosis • Radiographic studies reveal a dilated esophagus with

a bird's beaklike extension into the lower narrowed segment at the LES.

• Esophageal manometry reveals the high resting LES pressure, failure of relaxation during swallowing, higher than normal resting pressure in the body of the esophagus, and absence of peristalsis.

• Esophagoscopy is required to rule out neoplasia and to document the extent of esophagitis

Barium swallow

Treatment:- Conservative:Muscle relaxant as Amyl nitite before

meals to relax the cardiac sphincter-Repeated dilatation of the sphincter

- Surgical:Cardiomyotomy operation ( Hiller’s operation)

Division of the muscle fiber without injury of the mucosa

Interventional

• Dilation; Nonsurgical treatment consists of forced pneumatic dilatation of the spastic lower esophageal sphincter, which is just above the gastroesophageal junction

• Injections of Botulinum toxin

Surgical treatment• is esophagomyotomy by the modified Heller procedure, via

laparotomy/laparoscopy, or occasionally left thoracotomy. Care is taken not to disturb the vagus nerve attachments to the esophagus to prevent reflux. The myotomy is confined to the lower portion of the esophagus, usually 6–8 cm in length.

• Surgical results with the Heller procedure are generally better than with pneumatic dilatation for relief of dysphagia.

• Esophagomyotomy can be combined with an antireflux procedure if indicated

• Esophagectomy is considered in any symptomatic patient with tortuous esophagus (megaesophagus)

Heller MyotomyTechnique

Diffuse esophageal spasm Pathophysiology

• Diffuse esophageal spasm is a disorder of esophageal

motility that consists of strong nonperistaltic contractions.

• Unlike achalasia, this condition has normal sphincteric relaxation and may be associated with gastroesophageal reflux.

• Symptoms consist of chest pain, which can radiate to the back, neck, ears, jaw, or arms and may be confused with typical angina pectoris. The pain usually occurs spontaneously, and many patients are considered to have a psychoneurosis

Diagnosis

• Manometry reveals high-amplitude repetitive contractions with a normal sphincteric response to swallowing.

• Radiographs are normal in one half of the cases but may reveal diverticula, segmental spasm, and a corkscrew appearance of the esophagus.

Barium esophagram of diffuse esophageal spasm

Treatment

Medical treatment ; Calcium channel blockers smooth muscle relaxants, such as nitrates,

may ameliorate symptoms

Treatment • Surgery is moderately effective with good results obtained in

over two thirds of the patients. The best results are obtained in emotionally stable patients with severe disease and without associated lower gastrointestinal problems.

• Surgery consists of a long esophagomyotomy that extends from the arch of the aorta to just above the LES.

• Care is taken to preserve LES function, which is usually normal in these patients.

• If significant gastroesophageal reflux is present, an antireflux procedure is performed.

GERD - Definition

Retrograde flow of gastric contents tothe esophagus, pharynx and larynxdue to frequent spontaneous relaxationof the cardiac sphincter

GERD

• Esophageal reflux is a common condition that may affect up to 80% of the population in varying degrees. Gastroesophageal reflux disease remains a multifactorial disease.

• Loss of LES pressure results in gastric reflux.

• Esophageal motility, in the normal esophagus, causes refluxed secretions to be cleared by esophageal peristalsis.

• Gastric secretions, gastric acid, pepsin, and bile reflux have been shown to produce severe esophagitis.

GERD

• 25% of adults• Weak or transient relaxing of LES is primary cause• Other causes - high fat diet, -nicotine, ETOH, caffeine, pregnancy,

- meds(nitrates, Ca channel blockers, estrogen, - decreased endogenous gastrin production,

- operation on or near esophageal hiatus, - scleroderma,

- a sliding-type hiatal hernia• Heartburn is classic symptom

Gastro-esophageal Reflux Disease GERD

Definition:Incidence:Etiology:- Deceases pressure of cardiac sphincter e.g in hiatus hernia- Gastric hypersecretion: stress, smoking alcohol, caffiene, spicy foods, citrus frits

Complications:- esophagitis ulcer stricture- Chronic pharyngitis & Laryngitis- Cancer esophagus & Larynx

Retrograde flow of gastric contents tothe esophagus, pharynx and larynx

due to frequent spontaneous relaxationof the cardiac sphincter

Infants Above 40

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Esophageal reflux Symptoms

• substernal pain, • heartburn, • regurgitation, • all of which may increase with bending and

lying down

Symptoms:Esophageal;Retrosternal burning sensation (frequently absent)

Pharyngeal:Throat irritation hmemming & Hawking to clear the throat

Laryngeal:Chronic irritative cough, hoarsness of voice,In infants , nocturnal laryngeal irritation laryngismus stridulus

Signs:-esophagitis-ulcerMay be strictureInvestigations:24 hours double probe(esophageal &pharyngeal) ph monitoringMeasure the time the Ph is less than 4It is diagnostic if the time is more than 5%

Symptoms:Esophageal;Retrosternal burning sensation (frequently absent)

Pharyngeal:Throat irritation hmemming & Hawking to clear the throat

Laryngeal:Chronic irritative cough, hoarsness of voice,In infants , nocturnal laryngeal irritation laryngismus stridulus

Signs:-esophagitis-ulcerMay be strictureInvestigations:24 hours double probe(esophageal &pharyngeal) ph monitoringMeasure the time the Ph is less than 4It is diagnostic if the time is more than 5%

GERD - Symptoms

Atypical Symptoms

AsthmaCough

HoarsenessChest Pain

Typical Symptoms

Heartburn

Regurgitation

Trouble Swallowing

Diagnosis

• Manometry, which reveals decreased LES pressure

• Esophagoscopy, which reveals varying degrees of esophagitis

• Twenty-four hour pH measurements in the lower esophageal area, which demonstrate increased acidity

Esophageal reflux Medical treatment

• Proton pump inhibitors and H2-receptor antagonists to reduce acidity

• Cisapride and metoclopramide, which increase both LES pressure and gastric motility, thus increasing the rate of gastric emptying

• Antacids• Weight reduction• Abstinence from smoking and alcohol• Elevation of the head of the bed at night

Esophageal refluxSurgical treatment

Indications for surgery include:

• Symptoms refractory to medical treatment

• Additional problems, such as esophageal webs or severe esophagitis, stricture formation, or Barrett's esophagus with severe dysplasia (i.e., replacement of the normal epithelial lining with columnar epithelium in the lower esophagus secondary to esophagitis


• are designed to increase LES tone.

• All of the operations involve wrapping the lower esophagus with gastric fundus and restoring the distal esophagus to its original intra-abdominal position with the gastroesophageal junction below the diaphragm.


• The Nissen fundoplication, which is a 360-degree wrap of the stomach around the esophagus performed through the abdomen. The procedure may now be successfully performed laparoscopically with minimal pain and a shorter recovery time.

• Belsey Mark IV operation, which is a 270-degree wrap performed through a left thoracotomy

• The Hill repair, or posterior gastropexy, which uses the arcuate ligament to re-establish the intra-abdominal position of the distal esophagus

Barrett's Esophagus

• columnar epithelium replaces the stratified squamous epithelium that normally lines the distal esophagus.

• Chronic gastroesophageal reflux is the factor that injures the squamous epithelium

• Affects 10% of patients with severe GER

• 40-fold increase in risk for developing esophageal cancer

• Patients require endoscopic surveillance

• Esophagectomy for severe dysplasia/cancer

Barrett’s EsophagusDevelopment of Cancer Based on Grade

• No dysplasia 3%

• Low-grade dysplasia 18%

• High-grade dysplasia 28%

Hiatal Hernias Epidemiology

• Herniation of the stomach through the esophageal hiatus

• Para-esophageal type - 5% – Occurs in elderly patients (~ 65 years)

– Frequent co-morbid conditions

• Classification depends on location of GEJ– Type I- “sliding” hiatal hernia

– Type II- true paraesophageal hernia

– Type III- “mixed” hernia- sliding hernia and true

paraesophageal hernia

– Type IV- intra-abdominal organ involvement

ClassificationHiatal Hernias

Congenital Anomalies

The most common; Atresia with Tracheo-esophageal fistula Regurgitation of food aspiration, chocking and cyanosis

A catheter fail to enter the stomach

Atresia with Tracheo-esophageal fistula

The commonestcongenital anomaly of theEsophagus

The upper segment endsas a blind pouch

The lower segment isconnected to the trachea

Clinical PictureImmediately after birth:Marked regurgitation andDrollingOral Catheter fails to enter the

stomach

Investigations;Lipidol swallow

Treatment:Immediate surgical repair

1- Foreign body2- Caustic ingestion- Corrosive esophagitis- Stricture of the esophagus3-Esophageal perforation

Children : the commonest. It is accidental

Adult : suicidal

Type of patientType of foreign body

In children: the commonest is coin & disc battery

In adult: fish & meat boneIn elderly : dentures and meat

limpIn suicisal cases: razor or pins

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At the upper end: below the cricopharyngealsphincter. The commonest site At normal constrictionsAnywhere with sharp FB• Type of patient

• Type of foreign body• Site of impaction• Sequlae:

Mechanical obstruction dysphagia &regurgitation

Disc batteries liquifactive necrosis and even perforation

Sharp FB mucosal tears &even perforation



Type of patient Type of foreign body Site of impaction Sequlae: Symptoms Signs Investigations Complications: perforation

Treatment :Removal by esophagoscope

HistoryDysphagia

It may be severe with drolling of saliva

Regurgitation of undigested food

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Etiology- Strong Alkalies (common) liquid

cleaners &disc batteries progessive liquifactive necrosis and even perforation

- Strong Acids: (rare) self limited coagulative necrosis act as a barrier protect the mucosa

Symptoms:History: Severe mouth and throat painDysphagia: so severe , the patient cann’t

swallow his saliva drolling Stridor and hoarsness: due to laryngeal

edema

بطاريات ءما

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اFist Aid :Combat shock ; IV fluids and

analgesics Buffering solution:-Vinegar or diluted lemon to

neutralize alkalies- Anti-acid for strong acids Emoluent solution;Egg white and milk to protect the

mucosa

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TreatmentAnalgesic AntibioticsCorticosteroidsNasogastric tubeEndotracheal intubation ortracheostomy if indicatedi.e if there is signs of

respiratory obstruction

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Complications:Local:PerforationHealing by fibrosis strictureSystemic:- Dehydration &electrolyte

disturbance- Scock:- Neurogenic due to pain- Hypovolaemic

stricture

Etiology: healing of corrosive esophagitis by

fibrosisSymptoms Signs: flexible esophagoscopyInvestigations: Barium swallow

Treatment:- Permeable strictures Repeated dilatation through an

esophagoscope- Impermeble strictures- colon bypass operation

• After a latent period of a few weeks- progressive dysphagia to solids then to fluids also- Regurgitation of undigested acid free

food



Diagnosis

• The diagnosis may be made by the history of caustic ingestion and the presenting symptoms, which may be mild or very severe. Shock may ensue from severe burning or perforation of the esophagus. It is important to identify airway compromise early.

• Endoscopy is indicated within 24 hours to determine the extent of damage.

Treatment

• Broad-spectrum antibiotics are administered.• Corticosteroids are no longer indicated.• Radiographs of the esophagus are performed at 10–

14 days to determine if strictures are developing.– Strictures occur in 5%–10% of patients who have ingested

lye.– If strictures have formed, a program of dilatation, using

esophageal dilators, is begun 3–4 weeks after ingestion.

• Esophageal replacement with stomach or colon may be necessary.

Strictures secondary to esophagitis and reflux

• Pathophysiology:These strictures are caused by a recurrent alternating pattern of mucosal destruction secondary to gastric acid reflux and subsequent healing.

• The strictures most often occur at the gastroesophageal junction.

• In severe cases, a long stricture may result.

Diagnosis

• A history of reflux symptoms and dysphagia is suggestive of strictures.

• Radiograph of the esophagus confirms the diagnosis.

• Esophagoscopy is important to determine the extent of the disease and to rule out malignancy

Treatment

• Dilatation of the esophagus is attempted first, then an antireflux operation is performed.

• If dilatation and an antireflux operation do not relieve the esophageal obstruction, a reconstructive procedure, using either the stomach or colon for esophageal replacement, may be necessary to restore adequate swallowing function.

Perforation of the Esophagus Etiology

• Perforations of the esophagus have three basic causes:

1. Iatrogenic causes instrumentation (e.g., esophagoscopy or dilatation) account for 50% of all esophageal perforations.

2. Trauma, blunt or penetrating, 20%

3. Boerhaave's syndrome (postemetic rupture of the esophagus), 15%

• Rupture of the esophagus results in acute mediastinitis, which if not corrected is almost always fatal

Etiology:-Accidental: sharp FB or

corrosives- Iatrogenic : unskilled

esophgoscopy

CORROSIVE

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Diagnosis

• History. Patients give a recent history of instrumentation of the esophagus or severe vomiting. All patients complain of severe chest pain, which is usually most prominent in the area of the rupture.

• Physical examination – Crepitation in the neck results from mediastinal air.– Occasionally, a crunching sound can be heard over the

heart (Hamman's sign), which is caused by air in the mediastinum behind the heart.

– Septic shock can also occur.

Diagnosis• Chest radiograph reveals air in the mediastinum and,

possibly, a widened mediastinum.

-If the perforation is in the lower esophagus, air may be present under the diaphragm within the abdomen.

-If the pleura has been violated, a hydropneumothorax may be present.

• A barium swallow should be performed if perforation is suspected. This study is preferred over esophagoscopy for identifying a perforation.

• CT scan is also a very useful diagnostic modality.

Sequlae:ClinicallyInvestigations:Plain X ray: air in the neck, pleura,

mediastinumGastrografin swallow to detect thesite and size of perforation

Air in the neck surgical emphysemaAir n the pleura pneumothoraxAir in the mediastinum pneumo-mediastinum

The patient is feverish and toxicDysphagiaHematemesisRetrosternal chest paindyspnea



Treatment

• Treatment is to perform primary repair with tissue buttress reinforcement, combined with wide mediastinal and pleural drainage.

• If mediastinal inflammation is severe and tissue integrity markedly is compromised, then esophageal resection with cervical esophagostomy and placement of a gastrostomy tube are performed. Esophageal reconstruction is performed at a later date when the patient has sufficiently recovered

Treatment: In ICUConservative:- Nothing by mouth- Massive antibiotic therapy- Nasogastric tube in small perforation- Gastrostomy in large perforation

Surgical- Repair and, cervical or trans-

thoracic drainage-


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Mallory-Weiss Syndrome Pathophysiology

• This condition presents as acute upper gastrointestinal hemorrhage.

• The bleeding occurs in the lower esophagus, usually near the gastroesophageal junction,

• is secondary to a partial-thickness tear in the lower esophagus,

• follows a prolonged period of severe vomiting and retching.

• The tear usually extends into the stomach and may involve the greater curvature of the cardia.

Mallory-Weiss Syndrome

• Diagnosis is made by endoscopy, which is performed to locate the tear and to rule out other causes of bleeding.

• Treatment is by supportive measures, such as

blood volume replacement, antacids, and gastric lavage

• In most cases, the bleeding subsides spontaneously

Surgical treatment

• Exploratory laparotomy : is performed with gastrotomy and suture of the tear from within the stomach if the bleeding persists

• Tear are closed using continuous nonabsorbable suture

• A recurrence is rare

Esophageal Webs Plummer-Vinson syndrome

• Upper esophageal webs are part of the Plummer-Vinson syndrome,

• presents in middle-age, edentulous women with atrophic oral mucosa, anemia, and dysphagia.

• The web occurs just below the esophageal introitus.

• Treatment is usually by esophageal dilatation.

Esophageal Webs Schatzki's rings

• Lower esophageal webs, or Schatzki's rings, commonly occur in patients with reflux.

• Schatzki ring: most common cause of intermittent dysphagia with solids

• Patients have dysphagia.

• Treatment consists of esophageal dilatation and an antireflux procedure.

Esophageal Cancer

• Most esophageal tumors are malignant, fewer than 1% are benign

• 13,000 new patients in the United States each year, and almost matching that figure is the expected death rate of 12,000 patients

• 5% of all GI tumor, 1% of all new tumor• Men have esophageal cancer 3-5 times more

often than women• The mean age at diagnosis is 60 years

Esophageal Cancer

• Most North American patients still present with locally advanced (stage T 3 and/or N 1 ) disease

• Within North America and Europe, the incidence of adenocarcinoma rose 100% in the 1990s, and it had a strong correlation with reflux, Barrett's metaplasia, and dietary factors (e.g., fat).

Esophageal Cancer

• Squamous cell still persists in patients with the usual risk factors for other aerodigestive tract carcinomas, specifically smoking (5-fold) and alcohol (5-fold) abuse.

• Heavy smoking and heavy drinking combine to increase the risk 25- to 100-fold.

• Sarcomas and carcinosarcomas are rare neoplasms, accounting for approximately 0.1 to 1.5% of all esophageal tumors

Risk Factors

• CONSUMPTION OF:Tobacco, Alcohol

• UNDER-CONSUMPTION OF: Fruits, Fresh meat, Riboflavin. Beta-carotene, Vitamin C, Magnesium, Vegetables, Fresh fish,

Niacin, Vitamin A, Vitamin B complex, Zinc• Plummer-Vinson syndrome

Risk Factors

• PREDISPOSING CONDITIONS:Caustic injury, Esophageal webs, Achalasia, Barrett's

esophagus, Esophageal diverticula

• OTHER EXPOSURE:Asbestos, Ionizing radiation, Exceptionally hot

beverages (tea), Location: Middle East, South Africa, northern China, southern Russia, India

Pathology

• Type

– Squamous cell carcinoma is the most common form.– Adenocarcinoma, the next commonest, is the type that occurs in

patients with Barrett's esophagus– Rare tumors of the esophagus include mucoepidermoid carcinoma

and adenoid cystic carcinoma.

• Tumor spread. Esophageal malignancies metastasize through both the lymphatic system and the bloodstream, with metastases occurring in liver, bone, and brain

Epidemiology of Esophageal Cancer in the United States

Adeno Squamous

New cases per year 6000 6000Male-to-female ratio 3:1 7:1Black-to-white ratio 6:1 1:4Most common locations middle distalMajor risk factors smoking Barrett’s

alcohol esophagus

Squamous Cell Carcinoma

• 95% of esophageal cancer worldwide

• Commonly 7th decade of life, 1.5-3 times more common in men

• Thought to occur from prolonged exposure of esophageal mucosa to noxious stimuli in persons with a genetic predisposition to the disease.

Squamous Cell Carcinoma

• Histologically, characterized by invasive sheets of cells that run together and are polygonal, oval, or spindle-shaped with a distinct or ragged stromal-epithelial interface.

• Located mainly in the thoracic esophagus, approximately 60% of these tumors are found in the middle third and about 30% in the distal third.

Adenocarcinoma

• Most common cell type of esophageal cancer in the United States.

• now accounts for over 50% of esophageal cancer in most Western countries

• Adenocarcinoma arises from the superficial and deep glands of the esophagus, mainly in the lower third of the esophagus, especially near the gastroesophageal junction.

Adenocarcinoma

• Whites are at four times greater risk than blacks

• Men have an eightfold higher risk than women.

• In the US and Europe, frequency of this tumor is increasing faster than any other cancer.

Clinical Findings

• Dysphagia in more than 90% of patients with esophageal cancer

• Nonspecific retrosternal discomfort• Indigestion• Weight loss• Pain• Regurgitation, resp symptoms, hoarseness

Clinical Findings

Symptom Percent• Dysphagia 87-95• Weight loss 42-71• Vomiting or regurgitation 29-45• Pain 20-46• Cough or hoarseness 7-26• Dyspnea 5

Diagnosis • A history of dysphagia and weight loss is almost always

present.• Contrast study of the esophagus demonstrates the location

and extent of the tumor.• Computed tomography (CT) scan of the chest and abdomen

is done to evaluate local lymphatic spread, and a thorough search is made for distant metastases.

• Esophagoscopy is essential for tissue diagnosis and determination of the extent of the tumor.

• EUS is done to assess the depth of the invasion and staging.• Bronchoscopy is performed in patients with proximal

esophageal lesions to assess the possibility of invasion of the tracheobronchial tree

5 Year Survival

• Stage I 50-55%• Stage IIA 15-35%• Stage IIB 15-27%• Stage III 4-15%• Stage IV 0-2%

Surgical Treatment

• Transhiatal esophagectomy through a laparotomy and cervical incisions. A complete thoracic esophagectomy is performed bluntly with reconstruction of gastrointestinal continuity with the stomach or, rarely, the colon.

• Ivor Lewis esophagectomy through a right thoracotomy and laparotomy. Reconstruction is also accomplished with the stomach or, rarely, the colon.

• 3-hole esophagectomy ;abdomenal , thoracic , and cervical incisions (need pyloromyotomy(

introduction

• Two major types of IBD• Crohn’s disease

– Incidence - 5 per 100,000 persons– Prevalence - 90 per 100,000 persons

• Ulcerative colitis– Incidence - 10 per 100,000 persons– Prevalence - 200 per 100,000 persons

Definitions• Crown's disease; • - (regional enteritis; granulomatous ileitis) • - is a chronic, transmural granulomatous inflammatory disease that

. can involve any area of the GI tract from mouth to anus

• - Its cause is unknown • Ulcerative colitis ; • - Mucosal inflammation • - (as opposed to transmural inflammation)

- strictly affects the colon

• Equal distribution among Male :Female• Peak incidence between 10-30 yrs & then a second peak between 6th/7th

decade

ETIOLOGY

• Unknown• Genetics- approximately 10-15% have a family history eg:

Ashkanazi jews• autoimmune mechanisms • environmental• Smoking- CD -Yes, Aggrevates UC- Protective• infectious• Developed countries- extreme Hygiene may predispose

(insufficient exposure and challenge of Gut immune system that makes them susceptible)

• Both diseases can occur at any age, but they tend to be diseases of young adults

Distribution

- CD;

-The small bowel alone is involved in 30%

-both the small and the large bowel in 50%, -colon alone in almost 25% -The distal ileum (the most common site) is involved in 70% of all cases,

which accounts for the older name, terminal ileitis.

- UC; -typically involves rectum and extends proximally

CROHNS DISEASE

Lab Findings

p-ANCA Antiglycan antibodies

Crohn’s Disease

Positive in 15% Positive in 75%

Ulcerative Colitis

Positive in 85% Positive in 5%

Extraintestinal manifestations• Peripheral arthritis

• Ankylosing spondylitis and sacroileitis

• Erythema nodosum and pyodermaGangrenosum

• Aphthous stomatitis

• Iritis and episcleriti

• Sclerosing cholangitis (less common than UC)

Crohn’s Disease• Clinical presentation

– Diarrhea (with diffuse colonic disease) is common.

– Cramping abdominal pain and right lower quadrant tenderness (with ileocolic disease) are common.

– Malaise, fever, weight loss, and leukocytosis are common.

– Abdominal abscess (usually right lower quadrant) may occur.

– Fistulas may occur between the involved bowel and the bladder, vagina, skin, or other segments of intestine.

– Anal abscess or fistula is a presenting symptom in 5% of cases.

Crohn’s Disease evaluation

As with UC, evaluation depends on the severity of the disease;

– Abdominal examination is important to evaluate areas of tenderness or mass.

– Anorectal examination should detect abscesses, fissures, or fistulas.

– Proctoscopy is important. If rectal mucosa is not involved, UC is essentially excluded as a diagnostic possibility.

– Serologic markers for IBD, mainly ASCA

Medical treatment

– Steroids are helpful for acute disease. – Immunosuppressive agents appear to provide clinical

improvement, steroid sparing, and fistula healing in patients with active CD:

• 6-Mercaptopurine• Azathioprine• Methotrexate• Intravenous cyclosporine

Medical treatment

– Infliximab therapy,; – -monoclonal antibodies to the proinflammatory

cytokine tumor necrosis factor (TNF), -is indicated for reducing signs and symptoms and inducing

and maintaining clinical remission in patients with moderately to severely active CD (50%)

-reducing the number of draining enterocutaneous and

rectovaginal fistulas and maintaining fistula closure in patients with fistulizing CD.

Medical treatment

– TPN permits bowel rest and induces remission in some patients with significant CD. This remission rate is much higher than the rate for patients with severe UC treated by TPN.

– Broad-spectrum antibiotics are beneficial to decrease luminal bacterial concentrations, tissue invasion and cellulitis, and bacterial translocation.

– Metronidazole and ciprofloxacin appear to be beneficial for treatment of anal disease.

Surgical treatment

– Indications • Intestinal obstruction

• Anorectal abscesses or fistulas that require special considerations (pus should be drained, but large incisions are avoided to prevent sphincter injury)

• Abdominal abscesses, which are preferably drained percutaneously with CT guidance

• Fistulas between the intestine and bladder, skin, bowel, or vagina (there have been reports of such fistulas closing after treatment by immunosuppressive agents)

• Debilitating disease that is not refractory to medical treatment

• Fulminant colitis

• Hemorrhage (rare)

• Cancer (much less common than with UC)

• failure to thrive in childrin

Ulcerative colitis• Clinical presentation;

- Bloody diarrhea is the most common symptom. Rarely, bleeding may be massive and life threatening.

- Mucus and pus may accompany the passage of loose stools.

- Cramping abdominal pain often occurs.

- Malaise, fever, (COMMON)

- weight loss, anemia (COMMON)

Ulcerative colitis• Clinical presentation;

-Severity of disease ranges from occasional episodes of diarrhea to fulminant colitis with toxic megacolon, which is characterized by:

• Dilatation of the transverse colon

• Abdominal pain, tenderness, and distention

• Fever, leukocytosis, and hypoalbuminemia

• Significant risk of colonic perforation

Risk for colon cancer

• The risk is minimal until after 10 years of onset, and then it increases by approximately 2% each year thereafter.

• The risk is minimal in patients with disease limited to the rectum and is highest in patients with pancolitis.

• Dysplasia of the mucosa is associated with an increased risk of cancer.

• Patients who have had UC for longer than 10 years should have an annual surveillance colonoscopy with multiple mucosal biopsies to search for dysplasia.

• Cancers in patients with UC are flat, invasive lesions and are not readily identified by barium enema

Risk for colon cancer

-UC higher risk than CD for malignancy

-In ulcerative pancolitis, - the risk of carcinoma is ; . 2% after 10 years . 8% after 20 years,

. 18% after 30 years

Ulcerative colitis evaluation

– Proctoscopy is the most valuable test to establish the diagnosis.

• Mucosal inflammation beginning at the level of the dentate line is highly suggestive of UC.

• In the presence of fulminant colitis, colonoscopy and barium enema should be avoided because these tests may worsen the condition and lead to toxic megacolon.

• Mucosal biopsies should be taken to confirm the diagnosis. Such biopsies are also helpful in distinguishing UC from Crohn's colitis and infectious colitis

Ulcerative colitis evaluation

– Abdominal radiographs should be obtained if abdominal tenderness is present and symptoms are severe to rule out colonic dilatation.

– Stool samples should be cultured for pathogens and examined for ova and parasites.

– Serologic markers for IBD, mainly pANCA

– If symptoms are mild, the entire colon should be evaluated by colonoscopy and barium enema.

– Small bowel contrast studies should be obtained to rule out small bowel involvement, which would indicate CD.

Medical treatment– Immunosuppressive agents include:

• 6-Mercaptopurine• Azathioprine• Methotrexate• Intravenous cyclosporine

– Broad-spectrum antibiotics are indicated for patients with fulminant colitis and toxic megacolon.

– TPN may be required for patients with severe debilitating disease, usually to prepare the patient for surgery.

Surgical treatment

– Indications

• Hemorrhage

• Fulminant colitis or toxic megacolon that is not responsive to intensive medical treatment

• Debilitating disease that is not refractory to medical treatment

• Colonic stricture (at least 30% incidence of cancer)

• Dysplasia or cancer

Surgical treatment• Most common Extraintestinal manifestationS requiring total colectomy -

failure to thrive in childrin

• Does not get better with colectomy - primary sclerosing cholangitis,ankylosing spondylitis

• get better with colectomy - most ocular problem,artritis,anemia

• 50%get better - pyoderma gangrenosum

• HLA B27 - sacrolitis & ankylosing spondylitis

• pyoderma gangrenosum - Tx: steroids

Summary Clinical findings Ulcerative Colitis Crohn’s

– Perianal Disease Rare Common (1/3 pts)– Fistulas Rare Common (up to 40%)– Abscess Rare 20%– Stricture Rare Common

Colonoscopy findings– Rectal involvement Always Usually spared– Pattern Continuous from rectum Skip lesions

Radiologic findings– Ileal involvement Rare, backwash ileitis 75%

Histologic findings– Depth of inflammation Mucosa to submucosa Transmural– Granulomas Uncommon 20% of biopsies

Polyps

Polyps - defined as any projection from the surface of the intestinal mucosa.

Gross appearance 1. Pedunculated polyps.are attached to the bowel

wall by a stalk. 2. Sessile polyps. are flat growths with no stalk.

Polyps Histologic types

3.Juvenile polyps are hamartomas that occur most frequently in children and may cause

gastrointestinal bleeding or intussusception .

4.Inflammatory polyps- are growths resulting from tissue reaction to inflammation, such as pseudopolyps in ulcerative colitis (UC) or benign lymphoid polyps. They have no neoplastic potential

5 .Neoplastic polyps are by definition benign, but they have the potential to develop into cancer .

These polyps are classified by histology into three types:

a.Tubular adenomas (75% of adenomas) have a smooth, firm surface and are often on a stalk.

b.Villous adenomas (10% of adenomas) are soft, sessile lesions with frondlike projections. Large

villous adenomas may cause watery diarrhea and potassium loss.

c. Tubulovillous adenomas (15% of adenomas) have elements of both tubular and villous

adenomas .

Polyps

Histologic types

Malignant potential

Probably more than 95% of colorectal cancers arise from neoplastic polyps. At least three characteristics of polyps are associated with malignancy:

1.Size Polyps <1 cm: 1% malignant

Polyps 1–2 cm in size: 10% malignant Polyps >2 cm in size: 50% malignant

2.Histologic type Tubular: 5% malignant

Tubulovillous: 20% malignant Villous: 40% malignant

3.Grade of atypia Mild: 5% malignant

Moderate: 20% malignant Severe: 35% malignant

Treatment of polypsNeoplastic polyps should be removed because of their

malignant potential. 1 .Endoscopic polypectomy (excision with a colonoscope or sigmoidoscope ) is ideal for

pedunculated polyps. Small, superficial, sessile polyps are often amenable to piecemeal removal by this technique .

2 .Transanal polypectomy. Rectal polyps may be removed surgically through the

anus.

Treatment of polyps

3 .Segmental colectomy is required both for sessile polyps that cannot be excised

with an endoscope and for most polyps that are

malignant. Removal of the polyp through a colotomy, or a surgically made opening in the colon, is a

historical procedure that has no place in

treatment of polyp disease

Peutz-Jeghers syndrome

.autosomal dominant disorder

.hyperpigmented spots on the lips, buccal mucosa ,face, and digits

.hamartomas throughout the gastrointestinal tract.

.Complications. The polyps may cause gastrointestinal bleeding and intussusception.

.Cancer risk. There is an increased risk of malignancy of the intestine and other organ systems.

.Treatment. Symptomatic polyps should be removed, with a goal of preservation of intestine.

Cowden's syndrome

.autosomal dominant disorder

.hamartomas throughout the GIT

.mucocutaneous abnormalities (e.g., facial and oral papules, keratotic growths on the hands and feet); and breast, thyroid, or uterine

cancer. .Treatment is not usually required for the polyps but is directed toward the extraintestinal malignancies.

Cronkhite-Canada syndrome

.noninherited syndrome

.generalized intestinal hamartomas association with alopecia , cutaneous pigmentation, and atrophy of the fingernails and

toenails.

.Symptoms include vomiting, diarrhea, malabsorption, and protein-losing enteropathy .

. no malignant potential

.The cause is unclear .

.Mortality is usual; most patients die within a short time after diagnosis, but there have been reports of spontaneous remission.

.Treatment is reserved for complications such as intestinal obstruction.

Diffuse juvenile polyposis

.autosomal dominant disease

.a heterogeneous population of polyps ,

.both hamartomas and adenomas.

.Complications. Intussusception, diarrhea, and protein loss may occur.

.Cancer risk. There is at least a 10% risk of developing colon cancer.

.Treatment is most commonly subtotal colectomy and ileorectal anastomosis.

.Proctoscopy of the remaining rectum should be done every 6 months, and any new rectal polyps should be excised .

.diffuse rectal polyps, total prctocolectomy with either an ileostomy or preferably an ileal pouch-anal anastomosis is indicated

FAP

.is characterized by more than 100 adenomatous polyps throughout the

colon and rectum .

.If untreated, almost 100% of patients develop colon cancer by the fifth decade of life.

FAPGenetic transmission;

.autosomal dominant syndrome with high penetrance .

.Fifty percent of offspring of affected patients develop the disease .

.Almost all cases caused by germline mutations of (APC) gene located on 5chromosome.

.One third of patients with FAP have no family history of the disease: They represent spontaneous mutations

FAP

Clinical presentation;

.the disease is inherited ,

.polyps are not present at birth ,

.rarely appear before puberty .

.Fifty percent of FAP patients develop adenomas by age 15 and 95% by age 35.

.Complications. The polyps may cause bleeding or, rarely, intussusception.

FAP

Extraintestinal expressions are common and include:

.Epidermoid cysts.Osteomas

.Cutaneous fibromas.Desmoid tumors of the abdomen and mesentery

.Gastrointestinal polyps.Retinal pigmentation

.Periampullary carcinoma most, (common cause ofdeath)

.Thyroid carcinoma

FAP

Screening;

.First-degree relatives of FAP patients should undergo screening for FAP at age 10–12 years.

.Screening test of choice is testing for mutation of the APC gene.

.If genetic testing cannot be done, patients are advised to pursue yearly endoscopy beginning at age 12.

FAP

Diagnosis;

is made by confirming the numerous polyps by endoscopy and obtaining a biopsy to ensure the adenomatous nature of the polyps.

FAP

Treatment: If untreated, virtually all patients will develop

colon cancer with the average age of onset between 34 and 43 years. Treatment is aimed at colectomy and includes:

FAPTreatment:

.Total proctocolectomy with ileostomy.

.Total proctocolectomy and continent ileostomy.

.Colectomy with ileorectal anastomosis. Patients must be examined by .proctoscopy every

6/12 .Celecoxib, a selective cyclooxygenase-2 inhibitor, This feature may be advantageous for patients treated by

this operation .

.Total protocolectomy with ileal pouch–anal anastomosis

FAP association

.Gardner's syndrome; is FAP with osteomatosis, epidermoid cysts, and skin fibromas.

.Turcot's syndrome; is FAP associated with central nervous system

malignancies (e.g.medulloblastoma of the spinal cord, glioblastoma of the cerebrum).

HNPCC Lynch I

HNPCC, unlike FAP, cancer arises from a single colorectal lesion in the absence of polyposis.Characteristics include:

1.Accounts for 3%–5% of all colorectal cancers2.Autosomal dominant inheritance

3.Predominance of proximal colon cancers4.Increased synchronous colon cancers

5.Early age of onset (average age is 44 years)6.Increased risk of metachronous cancers

7.Increased incidence of mucinous or poorly differentiated carcinomas

8.Improved survival stage for stage compared with those who have sporadic tumors

HNPCC Lynch syndrome II

.Same as Lynch I but additional risk for

extracolonic adenocarcinomas of the uterus,ovary, cervix, breast , stomach, hematopoietic,small bowel, and skin

HNPCC causes

.HNPCC is caused by a single mutation of a DNA mismatch repair gene .

.include: hMSH2, hMLH1, hPMS1, hPMS2, hMSH6.

Diagnosis of HNPCC

is based on Amsterdam criteria, which includes the following:

1 .Three or more relatives with histologically verified colorectal cancer, one of whom is a first-

degree relative of the other two .

2 .Colorectal cancer involving at least two generations .

3 .One or more colorectal cancer cases diagnosed before the age of 50.

screening in HNPCC

–Recommendations:

.In the absence of genetic testing, first-degree relatives of affected individuals should undergo

colonoscopy every 1–2 years beginning at age 20 and yearly past the age of 40 .

.In known germline mutation individuals, it is recommended that colonoscopy begins either at age 25 or when the age is 5

years younger than the first diagnosed family member , whichever comes first, and should continue annually

INCIDENCE.the most common malignancy of the GIT

.third most common cause of cancer deaths overall

.130,000 new cases and 55,000 deaths each year .

.Incidence increases with increasing age starting at age 40 rapid

.increase at 50y and peaks at 60–79 years of age .

.75% sporadic

.At presentation 37% localized, 37% regional, 20% metastatic

.1 and 5y survival is 80% and 61% overall

Risk factors

.A family history of colorectal cancer. People who have two or more close relatives with

colorectal cancer make up about 20% of all people with colorectal cancer .

.FAP and HNPCC, accounts for 5%–10% of patients with colorectal cancer .

.Ethnic background. Jews of Eastern European descent (Ashkenazi Jews) are thought to have a higher rate of colorectal cancer

Risk factors

.A personal history of colorectal polyps

.A personal history of chronic inflammatory bowel disease

including UC and Crohn's disease (CD) ;-UC higher risk than CD for malignancy

-In ulcerative pancolitis, the risk of carcinoma is approximately 2% after 10 years ,

8% after 20 years, and

18% after 30 years

Risk factors

.Age. Chances of developing colorectal cancer increase markedly after age 50. Greater than

90% of people found to have colorectal cancer are older than 50.

.Diet high fat, Diets

low Fiber Diets low Calcium Diets

low Fruits and vegetables

Risk factors

.Activity. Physically inactive individuals are at increased risk of developing colorectal cancer.

.Obesity. Risk of dying of colorectal cancer is increased in overweight people .

.Diabetes increases the chance of developing colorectal cancer by 30%–40%. Diabetics also tend to have a higher death

rate after diagnosis.

.Smoking. Smokers are 30%–40% more likely than nonsmokers to die from colorectal cancer. Smoking may be responsible

for causing about 12% of fatal colorectal cancers.

.Alcohol intake. Colorectal cancer has been linked to the heavy use of alcohol.

Risk factors

.adenoma-carcinoma sequence. Cumulative evidence suggests a progression from benign neoplasia to

malignancy in colorectal polyps. Supporting observations include:

1.Patients with colorectal cancer often have synchronous adenomatous polyps

2.Histopathologic studies have shown a transition from adenoma to carcinoma in polyps. The peak incidence for discovery of colon polyps is 50 years

of age; the peak incidence for development of cancer is 60 years of age .This fact suggests a 10-year span for adenomas to transform to cancer

Risk factors adenoma-carcinoma sequence

3.Patients with familial adenomatous polyposis (FAP) develop colon cancer if not treated .

4.Polypectomy has been shown to reduce the risk of colorectal cancer.

5.Molecular genetic studies ;four main genetic alterations in colorectal adenomas and

carcinomas (ras mutations and deletions from chromosomes 5, 17, and 18 .)

GENES

Genes involved in development CA include; 1.APC (INITIAL MUTATION) 2.P53 3.DCC

4.K-ras

Spread and metastases-Spreads to lymphatic nods first

-nodal status most important prognostic factor

-liver #1 site of metastases via portal vein

-lung #2 site of metastases via iliac vein

-colon CA does not go to bone

-5% get drop metastases to ovaries

rectal CA can met. to spine via batsons plexus -

Clinical presentationdepends on the location, size, and extent of the tumor.

.Right-sided cancer- Melanotic stools

- Iron deficiency anemia - Right-sided abdominal mass

.Left-sided cancer- Change in bowel habits

- Passage of red blood via rectum

- Cramping abdominal pain (caused by partial obstruction ) Both: Weight loss, anorexia

STAGING

Dukes System (old system)A: Limited to wallB: Through wall of bowel but not to lymph nodesC: Metastatic to regional lymph nodesD: Distant metsTNM System (more current system)T1: Invasion of submucosaT2: Invasion of muscularis propriaT3: Invasion of subserosa, or nonperitonealized pericolic or perirectaltissuesT4: Invasion of visceral peritoneum/direct invasion of other organsN0: No nodal diseaseN1: 1–3 pericolic or perirectal lymph nodes

N2: 4 or more lymph nodes N3;any node along the vascular trunkM0: No evidence of distant metsM1: Distant mets

evaluation

1.Abdominal examination2.Rectal examination

a.Digital examination is useful to assess the location, size, and extent of invasion of a tumor

in the distal rectum .B.Rigid proctosigmoidoscopy is useful to

determine the exact location of a rectal tumor in relation to the anal verge. C.Endorectal ultrasound provides information concerning the depth of invasion into the

bowel wall by a rectal tumor and involvement of lymph nodes

evaluation

3.Colonoscopy with biopsy of the lesion and inspection of the remaining colon is necessary to exclude synchronous

lesions. 4.barium enema is often not required if the

colonoscopic examination is satisfactory. If the colonoscope does not reach the

cecum, a barium enema should be obtained to evaluate the entire colon.

5.Chest radiograph

evaluation

6.Laboratory studies include; carcinoembryonic antigen (CEA); liver enzymes; and hemoglobin, hematocrit, or

both .7.CT scan is used to evaluate the liver and

abdomen for metastases and both kidneys

Treatment

.Surgical resection is the preferred treatment for most cases of colorectal cancer. Important

aspects of surgery include: -Proper preparation of the patient, including bowel

preparation- Thorough exploration of the abdomen to search

for metastases and other intra-abdominal disease

- Removal of the segment of colon containing the tumor and the lymphovascular pedicle, which

contains the lymph nodes that drain the cancer

Treatment

-Anastomosis without tension between segments of bowel with satisfactory blood supply

-Operations for rectal cancer require special considerations ;

1.Upper-third lesions (10–15 cm above the anus) can be treated by resection through the abdomen with

anastomosis between the left colon and the remaining rectum (low anterior resection).

Treatment2.Middle-third lesions (5–10 cm above the anus)

are usually amenable to low anterior resection, using circular stapling instruments to fashion the anastomosis .

3.Lower-third lesions. Several options may be considered. Resection of the rectum, anus, and anal sphincters by a

combined abdominal and perineal approach requires construction of a colostomy (abdominoperineal

resection, also called Miles procedure) .

- pull-through operations. In almost all patients, a temporary colostomy is fashioned to allow the anastomosis to heal without the danger of anastomotic leak and sepsis. The colostomy may be closed 10–12 weeks after the initial operation. -most Rt. Sided colon CA can be Tx; with primary anastomosis

Treatment -Rectal pain with rectal CA –need APR need 2cm margins -low rectal T1 can be excised transanally if ;

. < 4cm . has (-)margin 1cm . well diff. . no N.or V. invasion . otherwise APR or LAR

- low rectal T2 or higher – APR or LAR

no APR unless cancer is present -

Treatment -Polypectomy shows T1 lesion - adequate if

-margins clear(2mm) -is well differentiated -no vascular/lymphatic invasion -otherwise need formal colon resection

-pathology shows T2 lesion - patient need APR orLAR

O

A to C, ileocecectomy; + A + B to D, ascending colectomy; + A + B to F, right hemicolectomy; +A + B to G, extended right hemicolectomy; + E + F to G + H, transverse colectomy; G to I,

left hemicolectomy; F to I , extended left hemicolectomy; J + K, sigmoid colectomy; + A + B toJ, subtototal colectomy; + A + B to K, total colectomy; + A + B to L, total proctocolectomy.

Treatment-Local excision, fulguration, and contact radiotherapy may be

used for select, very favorable rectal cancers in which the chance of metastases is small, for example :

1.Superficial lesions, freely moveable by digital examination 2.Those that are not poorly differentiated histologically

3.Those that are confined to the rectal wall, as detected by endorectal ultrasound

4.Those in which there are no palpable retrorectal lymph nodes

5.Nonulcerated, exophytic lesions

Treatment

-Adjuvant therapy

.Chemotherapy, as combinations of 5-fluorouracil (5-FU), leucovorin, and more recently oxaliplatin are currently recommended for patients with positive lymph nodes or

metastatic disease .

.Radiation therapy given preoperatively to patients with advanced rectal cancer has been shown to shrink the cancer and

reduce local recurrence .

.Combinations of adjuvant radiation therapy and

chemotherapy for advanced rectal cancers are also being employed

Treatment

-Neoadjuvant therapy . Rectal cancer:

Preop radiation using 5-FU as a radiosensitizer (this sequence is called “

neoadjuvant” therapy because it occurs prior to the definitive surgical treatment .

Treatment

-Neoadjuvant therapy .Rectal cancer:

Preop radiation using 5-FU as a radiosensitizer

(this sequence is called “ neoadjuvant” therap

because it occurs prior the definitive surgical treatment .

Treatment-Isolated hepatic metastases may be resected with a

25% 5-year survival .-Solitary pulmonary metastases may be resected with

a 20% 5-year survival .

-to local recurrence. Total mesorectal excision (TME) reduces the rates of local recurrence

-Chemotherapy and radiation therapy are palliative for recurrent nonresectable colorectal cancer.

recurrence

-50% have recurrence within 6 months

- 100% have recurrence by 3 years

- 5% have another primary.main reason for surveillance colonoscopy

PrognosisCure Rate

M Level N Level

T Level

Dukes Classification

Stage

100% M0 N0 Tis — 0

90% M0 N0 T1 or T2

A I

80% M0 N0 T3 or T4

B II

60% M0 N1, N2, or N3

Any T C III

5% M1 Any N Any T D IV

Follow-up

-Physical examination seldom reveals early tumor recurrences .

-Colonoscopy should be performed 1 year after surgery to detect any new polyps.

If polyps are found and removed, the colonoscopy should be repeated annually until there are no polyps.

After a negative colonoscopy, the examination should be repeated every 3–5 years to detect any new polyps.

Follow-upFollow-up after resection of colorectal carcinoma (CRC)

- Perioperative colonoscopy to remove any synchronous cancer

- Colonoscopy 1 year postop and yearly thereafter to look for metachronous lesions

- Colonoscopy 3 years after one negative test - Colonoscopy every 5 years once a 3-year test is

negative

Follow-up

-CEA .is the most sensitive indicator of recurrent colorectal

cancer ..CEA is a glycoprotein that is secreted by colorectal tumors. .measuring

the CEA level is a nonspecific test .. Most surgeons recommend obtaining CEA levels:

-Every 3 months during the first two

postoperative years - Every 6 months during the third, fourth, and fifth

postoperative years -A rising CEA level is an indication for a chest

radiograph and an abdominal CT scan.

Screening Recommendations

.Fecal occult blood test (FOBT) Every year after 50

.Flexible sigmoidoscopy Every 5 years after 50, with FOBT

.Colonoscopy Every 10 years

. Persons at high risk for colon

cancer (FAP, HNPCC, UC, highrisk adenomatous polyps) Regular endoscopic

screening by a specialist

Carcinoid tumors

-arise from neuroectodermal cells [APUD] tumors)

- The gastrointestinal tract is the most common site ,

(-in decreasing order of frequency ) carcinoids arise in the , , appendix ileum

, , r ectum stomach and colon .

-The tumors are usually small, submucosal nodules.

Carcinoid tumorsColon carcinoids;

- account for less than 2% of gastrointestinal carcinoids ;- they may be multicentric ,

- they may cause the carcinoid syndrome from liver metastases.Rectal carcinoids;

-account for 15% of gastrointestinal carcinoids .- They are usually solitary ,

-they do not cause the carcinoid syndrome.Treatment is related to size of the tumor;

- Tumors smaller than 2 cm seldom metastasize and can be locally excised.- Tumors larger than 2 cm are usually malignant and should be treated by

radical resection .

Other neoplasms

may arise from normal colorectal tissues but are rare, including :

-Lymphoid tissue (lymphoma and lymphosarcoma)

-Adipose tissue (lipoma and liposarcoma) -Muscle tissue (leiomyoma and

leiomyosarcoma

Pediatric surgery

• Foregut — lungs, esophagus, stomach, pancrea’ liver, gallbladder, bile duct, and duode num proximal to ampulla

• Midgut duodenum distal to ampulla, small bowel, and large bowel to distal 1/3 of transverse colon

• Hindgut — distal ‘/3 of transverse colon to anal canal

• Midgut rotates 270 degrees counterclockwise normally

• Immunity at birth — IgA from mother’s milk; 1gM synthesized in child

• #1 cause of childhood death - trauma• Trauma bolus — 20 cc/kg X 2, then give blood

10 cc/kg• Tachycardia — best indicator of shock (neonate

>150; <1 year >120; rc’a >100)• Urine output 2—4 cc/kg/hr• High alkaline phosphatase in children

compared with adults —± bone growth• Umbilical vessels — 2 arteries and 1 vein

MEDIASTINAL MASSES IN CHILDREN

Neurogenic tumors - most common mediastinal tumor in children; usually located posteriorly

• Anterior - T cell lymphoma, teratoma and other germ cell tumors (most common type of anterior mediastinal mass in children), thymoma, thyroid CA

• * Middle — T cell Iyrnphoma, teratorra, and cyst (cardiogenic or bronchiogenic)

• * Posterior - T cell lymphoma, neuroblastoma, and neurogenic tumor

• BRANCHIAL CLEFT CYST

• 2nd branchial deft cyst (most common) - on anterior border of SCM ,Goes through carotid bifurcation into tonsillar pillar

• DIAPHRAGMATIC HERNIAS

• Bochdalek’s hernia most common, located posteriorly

• Morgagni’s hernia rare, located anteriorly• Eventration - failure of diaphragm to fuse

• #1 children’s malignancy overall — leukemia (ALL)• #1 solid tumor class- CNS tumors• #1 general surgery tumor — neuroblastoma #1 in

child <2 years —+ neuroblastoma• #1 in child >2 years —* Wuims tumor• #1 cause of duodenal obstruction in newborns

(<1 week) - duodenal atresia• #1 cause of duodenal obstruction after newborn

period (>1 week) and overall - matrotation• #1 cause of colon obstruction — Hirschsprung’s

disease; some say constipation #1

• liver tumor in children — hepatoblastoma; 2/3 of liver tumors in children are

• malignant• #1 lung tumor in children — carcinoid• Painful lower GI bleeding — #1 benign

anorectal lesions (fissures, etc.)• Pain less lower GI bleeding - #1 Meckel’s

diverticulum• Upper Gl bleeding - 0-1 year —* gastritis,

esophagitis; 1 year to adult —÷ esophageal varices, esophagitis

INTUSSUSCEPTION

• Usually 3 months to 3 years• Currant jelly stools (from vascular congestion, an indication for resection),

sausage mass, abdominal distention, RUQ pain, and vomiting• Invagination of one loop of intestine into another• Lead points in children - enlarged Peyer’s patches (#1), lymphoma, and

Meckel’s diverticulum• 15% recurrence after reduction• Tx: reduce with air-contrast enema —÷ 80% successful; no surgery required

if reduced• Max pressure with air-contrast enema 120 mm Hg• Max column height with barium enema - 1 meter (3 feet)• Need to go to OR with peritonitis or free air, or if unable to reduce• Usually do not require resection unless associated with lead point (Meckel’s,

etc.)

DUODENAL ATRESIA

• #1 cause of duodenal obstruction in newborns (<1 week)• Usually distal to ampulla of Vater and causes bilious vomiting,

feeding intolerance• Associated with polyhydramnios in mother• Associated with cardiac, renal, and other Gl anomalies• 20% of these patients have Down’s syndrome (check

chromosomal studies)• Abdominal x-ray shows double-bubble sign

TRACHEOESOPHAG (TE) FISTU

• Type C - most common type (80%-90%)• • Proximal esophageal atresia (blind pouch) and distal TE fistula

IMPERFORATE ANUS

• More common in males• Need to check for associated anomalies such as renal, cardiac,

and vertebral (VACTERL) = vertebral, anorectal (imperforate anus), cardiac, TE uistula, radius/renal, and limb anomalies

• High (above levators) — meconium in urine or vagina (fistula to bladder/vaginal prostatic urethra)

• • Tx: colostomy, later anal reconstruction with posterior sagittal anoplasty

• Low (below levators) — perform posterior sagittal anoplasty no colostomy needed

• Need postop anal dilatation to avoid stricture; these patients are prone to constipation

Gastroschisis

• Intrauterine rupture of umbilical vein; does have a peritoneal sac * congenital anomalies (only 10%) except mairotation To the right of midline, no peritoneal sac, stiff bowel from exposure to amniotic fluid • Ix: initially place saline-soaked gauzes and resuscitate the patient; can lose a lot of fluid from the exposed bowel; TPN, NPO • Repair when patient is stable • At operation, try to place bowel back in abdomen, may need Vicryl mesh silo • Primary closure at a later date if mesh used UMPHALOCELE

a Failure of embryonal development; midline defect • congenital anomalies (50%); has peritoneal sac with cord attached • ‘ can contain intra-abdominal structures other than bowel (liver, spleen, etc.) Cantrell pentalogy

• Cardiac defects • Pericardium defects (usually at diaphragmatic pericardium) • Sternal cleft or absence of lower sternum • Diaphragmatic septum transversum absence • Omphalocele

THYROGLOSSAL DUCT CYST• From the descent of the thyroid gland from the foramen cecum• May be only thyroid tissue patient has• Presents as a midline cervical mass• Goes through the hyoid• Tx: excision of cyst, tract, and hyoid bone

HEMANGIOMA• Appears at birth or shortly after• Rapid growth during first 6—12 months of life, then begins to

involute• Tx: observation - most resolve by age 7-8• If lesion has uncontrollable growth, impairs function (eyelid or

ear canal), or is persistent after age 8 —* can treat with steroids —3 laser or resection if steroids are not successful

PYLORIC STENOSIS 3—12 weeks, firstborn males Projectile vomiting Can feel olive mass in stomach Get hypochloremic. hypokalemic metabolic alkalosis Ultrasound - pylorus 4 mm thick, 14 mm long For severe dehydration, resuscitate with normal saline boluses until

making urine, then switch to D5 normal saline with 10 mEq K maintenance Avoid fluid resuscitation with K containing fluids in children with severe

dehydration as hyperkalemia can quickly develop Avoid nonsalt-containing solutions in infants as hyponatremia can quickly

develop Infants should always have a maintenance fluid with glucose because of

their limited reserves for gluconeogenesis and vulnerability for hypoglycemia

Tx: pyloromyotomy (RUQ incision; proximal extent should be the circular muscles of stomach)

• L ARYNGOMALACIA • most common cause of airway obstruction in infants

PAPILLOMATOSIS • Most, common tumor of the pediatric larynx

HYDROCELE * Most disappear by 1 year; noncommunicating will resolve; should transilluminate • Tx: surgery at 1 year if not resolved or if thought to be communicating (waxing and waning size); resect hydrocele and

ligate processus vaginalis

AMBILICAL HERNIA • Failure of closure of linea alba; most close by age 3 increased in African-Americans and premature infants Tx: surgery if not closed by age 5 or incarceration or if patient has a VP shunt

INGUINAL HERNIA Due to persistent processus vaginalis; 3% of infants, M > F • Right in 60%, left in 30%, bilateral in 10% * Extension of the hernia into the internal ring differentiates hernia from hydrocele * Tx: emergent operation if not able to reduce; otherwise elective repair with high ligation * Explore the contralateral side if left sided, female, or child <1 year Need operation within next 2—3 days after reduction

DUPLICATION • Most common in ileum; often on mesenteric border Tx: resect cyst

HIRSCHSPRUNG’S DISEASE

1’ cause of colonic obstruction in infants; more common in males Most common sign — infants fail to pass meconium in 1st 24 hours Can also present in older age groups as chronic constipation (age2-3) Barium enema can be normal, although often shows a spastic distal segment

and dilated proximal segment Rectal biopsy diagnostic (absence of ganglion cells in myenteric plexus) k due to failure of the neural crest cells (ganglion cells) to progress in

craniocaudal direction Need to resect colon until proximal to where ganglion cells appear Tx: may need to bring up a colostomy initially, eventually connect the colon to

the (Soave or Duhamel procedure); need colon resection to the point where cells appear Hirschsprung’S colitis — may be rapidly progressive; manifested by abdominal

distention and foul smelling diarrhea Lethargy and signs of sepsis may be present Tx: rectal irrigation; may need emergency colectomy

UNDESCENDED TESTICLES

• Wait until 1 years old to treat• Higher risk of testicular CA in these children• Cancer risk stays the same even if testicles brought into scrotum• Get seminoma• If undescended bilaterally, get chromosomal studies• Ifyou cannot feel the testis in the inguinal canal, you need to get an

MRI to confirm their presence• Tx: orchiopexy through inguinal incision; if not able to get testicles

down —* close and wait 6 months and try again; if will not come down, perform division ofspermatic vessels

• Prune belly syndrome (rare) — hypoplasia of the abdominal wall, urinary tract abnormalities with dilated urinary system, and bilateral cryptorchidism

MECKEL’S DIVERTJCLJLUM

• Found on antimesenteric border of small bowel• Embryology - persistent vitelline duct• Rule of 2s —2 feet from ileocecal valve, 2% population, 2%

symptomatic, 2 tissue types (pancreatic- most common; gastric - most likely to be symptomatic), and 2 presentations (diverticulitis and bleeding)

• #1 cause of painless lower GI bleeding in children• Can get Meckel’s diverticulum scan with pertechnetate if

suspicious of Meckel’s diverticulum and having trouble locating• Tx: resection with symptoms, suspicion of gastric mucosa, or

narrow neck• Diverticulitis involving the base or if the base is >1/3 the size of

the bowel, need to perform segmental resection

• Osteoblasts — synthesize nonmineralized bone cortex• Osteoclasts — reabsorb bone• Stages of bone healing — inflammation, soft callus

formation, mineralization ofthe callus, and removal of the callus

• Cartilage receives nutrients from synovial fluid• Salter-Harris fractures Ill, IV, and V — cross the

epiphyseal plate and can affect the growth plate of the bone; need open reduction and internal fixation (ORIF)

• Salter-Harris types I and I - closed reduction• Type I Type II

• Fractures associated with AVN — scaphoid, femoral neck, and talus

• Fractures associated with nonunion — clavicle. 5th metatarsal fracture (jones’ fracture

• Fractures associated with compartment syndrome— supracondylar humerus and tibia

• Biggest risk factor for nonunion — smoking• a Osteomyelitis — can occur in metaphysis of

long bones in children; most commonly staph

Carpal Tunnel Syndrome The most common location of upper

extremity nerve compression is the median nerve at the carpal tunnel

Cubital Tunnel Syndrome The second most common location of upper

extremity nerve compression is the ulnar nerve where it passes behind the elbow at the cubital tunnel

• Fractures of the Proximal Ulna with Radial Head Dislocation-- (Monteggia Fracture)

• Fractures of the Shaft of the Radius with Radial Ulnar Dislocation-- (Galeazzi Fracture or Piedmont Fracture)

• Fractures of distal radial bone with pos. displasment— colles Fracture

• Fractures of distal radial bone with anterior. Displasment— smeth Fracture

Volkmanns contracture-

• supracondylar H.fracture---occluded anterior interosseous artery –--closd reduction of hemerus-artery opens up-reperfusion injury,edema,and forearm comp. syndrome(flexor comp.)

• p-t have pain in forearm with passive extension weakness,tense forearm and hyperesthesia.

• median nerve affected by swelling

• Tx; fasciotomy

• Felon A felon is a closed-space, purulent infection of the fingertip pulp

Idiopathic adolescent scoliosis — prepubertal females, right thoracic curve most common, usually asymptomatic

Osgood—Schlatter disease — tibial tubercle apophysitis; caused by traction injuryfrom the quadriceps in adolescents aged 13—15; most commonly have purr mmof the knee• X-ray: irregular shape or fragmenting ofthe tibia) tubercle• Tx: mild symptoms — activity limitation; severe symptoms — cast 6 weeks followed by activity limitation

Legg—Calvé—Perthes disease — AVN of the femoral head; (hilmIrlim 2 ymu. oil lifer• Can result from a hypercoagulable state; bilateral in 10%• Symptoms: painful gait limp• X-ray: flattening of the femoral head• Tx: maintain range oi mnom on with limited exeri se; fen head will rr,,todel without sequelae• Surgery if femoral head is not covered by the acetabulum

* Slipped capital femoral epiphysis• Males aged 10—13; iinc. risk AVN of the femoral hid• X-ray: widening and irrcgularity of the epmphyseal plate.• Tx: surgical pinning• Congenital dislocation of the hip More common in females

Clubfoot - Tx: serial casting

Shoulder dislocation • Most common dislocation• anterior dislocation Most common

Hip dislocation• Posterior (85%—95%) — patients have

internal rotation and adduction of leg; risk of sciatic nerve injury. Tx: closed reduction

COMPARFMENT SYNDROME Most likely to occur in the anterior

compartment of leg (get footdrop) after vascular compromise

Can also occur from crush injuries Distal pulses can be present with

compartment syndrome —+ last thing to go Pain with passive motion Pressure >20—30 mm Hg abnormal consider

fasciotomies; leave open 5-10 days

TUMORS Most common is metastatic disease (1.breast,

2.prostate)Multiple myeloma — most common primary

malignant tumor of bone Osteogenic sarcoma — most common

primary bone sarcoma, usually around the kneemost common benign tumor- Osteoid

osteoma

• ANATOMY AND PHYSIOLOGY• Gerota’s fascia — around kidney• Anterior to posterior— renal vein, renal artery, and

renal pelvis• Right renal artery crosses posterior to the IVC

Ureters cross over iliac vessels• Left renal vein — can be ligated from IVC secondary

to increased collaterals (left adrenal vein, left gonadal vein, and left ascending lumbar vein)

• Epididymis — connects to vas deferens• Hypotension — most common cause of acute renal

insufficiency following surgery

KiDNEY STONES• Symptoms: severe colicky pain, restlessness• Urinalysis - blood or stones• Abdominal CT — can demonstrate stones and associated hydronephrosis• Calcium oxalate (phosphate) stones - most common (75%); radiopaque• Mg ammonium phosphate (struvite) stones - 15%; radiopaque• Uric acid stones — 7%; radiolucent• Cysteine stones — 2%; radiolucent to radiopaque• Calcium oxalate stones — 1 in patients with terminal ileum resection due to t oxalate

absorption in colon• Struvite stones — occur with infections (Proteus mirabilis) that are e producing• Can cause staghorn calculi (fill the renal pelvis)• Uric acid stones — 1 in patients with ileostomies, gout, and myeloproliferative disorders U

Cysteine stones — associated with congenital disorders in the reabsorption of cysteine• 90% of kidney stones opaque; >6 mm not likely to pass

Surgery for kidney stones• Intractable pain or infection• Progressive obstruction• Progressive renal damage

• •Solitary kidney

• TESTICULAR TORSION• Peaks in 15-year-olds• Involved testis almost never viable• Usually has intravaginal torsion of the

spermatic cord if viable• Torsion is usually toward the midline• Tx: bilateral orchiopexy• If not, resection and orchiopexy of

contralateral testis

TESTICULAR CANCER #1 cancer killer in men 25—35 Symptom: painless hard mass Most testicular masses are malignant Ultrasound can help with diagnosis Chest x-ray — to check for pulmonary metastases Chest and abdominal CT — to check for retroperitoneal and mediastinal burden LDH correlates with tumor bulk Needs a B-HCG and AFP level 90% of tumors are germ cells — seminoma or nonseminorna Undescended testicles (cryptorchidism) —1’ risk of testicular CA Most likely to get seminoma

Seminoma• #1 testicular tumor• 10% ofseminomatous tumors have beta-HCG elevation• Should not have AFP elevation (if clevared, need to treat like nonseminomatous)• Spreads to retroperitoncum• Seminoma is extremely sensitive to XRT• Tx: all stages get orchiectomy and retroperitoneal XRT - some patients have occult retroperitoneal mctastaIf the paraaortic nuder, in thi abdomen art iilireed, need to extend XRT to themediastinum

Nonseminomatous testicular CA• Types — ernbryonal, teratoma, choriocarcinonii, and yolk sac• Alpha fetoprotein and beta-HCG - 90% havc t liua markers• Spreads hematogenously to lungs• Also spreads to retroperitoneum• Classically, tumors with 1 teratoma componcnt art inure likely to metastasize to the retroperitoneum• Surgical Tx

PROSTATE CANCER• Posterior lobe — most common site• Bone — most common site of metastases• Normal PSA <4 in a patient who has a prostate gland RENAL CELL CARCINOMA (HYPERNEPHROMA)• #1 primary tumor of kidney (15% calcified)• Risk factor: smoking• Abdominal pain, mass, and hematuria• 1/3 have metastatic disease at the time of diagnosis — can perform wedge

resection of isolated lung and colon metastases• Lung - most common location for RCC metastases• Most common tumor in kidney - metastasis from the breast ADDER CANCER• Usually transitional cell CA• Painless hematuria• Males; prognosis based on stage and grade• Risk factors: smoking, aniline dyes, and cyclophosphamide• Dx: cystoscopy, IVP

CARDIAC SURGERY

Ventricular septal defect (VSD) Most common congenital heart defect• Timing of repair CHF resulting in failure to thrive - most common

reason for repair Before school age if does not close spontaneously PVR> 4—6 Woods units also indication for repair PVR> 10—2 Woods units contraindication for repair

— use vasodilators to see if it is reversible; if so, can repair

CARDIAC SURGERY

Ventricular septal defect (VSD) Most common congenital heart defect

Atrial septal defect (ASD)• L—R shunt• Ostium secundum - most common; centrally located,

Tetralogy of Fallot• VSD, pulmonic stenosis, overriding aorta, right ventricular (RV)

hypertrophy• R-L shunt• Most common congenital heart defect that results in cyanosis

OTHER CARDIAC CONDITIONS

• Most common benign tumor- myxoma; 75% in LA, mitral valve stenosis-type symptoms

• Most common malignant tumor – angiosarcoma

• Most common metastatic tumor to the heart - lung CA

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