BASIC SURGERY(AFTER MIDTERM)

CHAPTER-6 INTESTINAL DISEASES

1.Short bowel syndrome
a.Essentials of diagnosis
 Extensive small bowel resection
 Diarrhea
 Steatorrhea
 malnutrition
b.Treatment
General measures: treatment of severe small bowel syndrome divided into three stages
Stage 1(intravenous feeding): During this period, which lasts 1-3 months, patients should receive
nothing by mouth
Stage 2(intravenous and oral feeding) oral intake until diarrhea less than 2.5L/d, intravenous
nutrition should continue. An oral rehydration solution used for diarrhea are applicable. Milk may
aggravate diarrhea. Making breakfast the largest meal of the day is advantagable
Stage 3(complete oral intake): After about 6 months, complete dependence on oral intake may
expected in patients with 1-2 meters of remaining small bowel, but full adaptation may require up
to 2 years.
Adjunctive surgical procedure:
Surgical procedures to slow intestinal transit, reduce gastric acidity, or increase the absorptive
surface are not recommended routinely. Cholecystectomy should be avoided.
2.Crohn’s disease
a.Essentials of diagnosis:
 Diarrhea
 Abdominal pain and palpable mass
 Low-grade fever, lassitude, weight loss
 Anemia
 Radiographic findings of thickened, stenotic bowel with ulceration and internal fistulas
b.Clinical findings:Diarrhea;Recurrent abdominal pain;Anorectal lesion;Anemia;Malnutrition ;Acute
onset
c.Treatment
 The initial treatment of Crohn’s disease is nonoperative. Physical rest, relief of emotional
stress, and a confinding patient-doctor relationship has favorable effects. A low- residue,
milk-free, high-protein diet may provide adequate nutrition
 The indication for operation is obstruction in about ½ of cases; perforation, interal fistula,
external fistula, abscess, perianal disease, and growth failure in children are other reasons
for operation
3.Intestinal Obstruction
i.Etiology and classification
a.According to the causes:
1) Mechanical obstruction
 obturation obstruction
 intestine compression
  lesions in the intestinal wall
2) Nonmechanical obstruction: dynamic ileus----->including paralytic ileus and spastic ileus
b.According to the blood circulation to the bowel, no impaired or impaired :
1)simple ileus 2) strangulation ileus
c.According to obstructive level
1)high level:jejunum and proximal ileum 2) low level:colon and distal ileum
d.According to degree
1) incomplete 2)complete
e.According to the duration
1) Acute obstruction 2)Chronic obstruction
f.Specific type:closed-loop
ii.Pathological changes:
 proximal distention,distal empty,interbording is obstruction point
 intestinal wall edema,dark-red
 venous is compression,permeability of microvascular increase,fluid exudation into bowel
and abdomen
 artery blood circulation is obstructed and necrosis of the bowel wall, gangrene and
perforation occur
iii.Local Effects of Obstruction
 peristalsis->hyperperistalsis->abnormal peristalsis
 secretion increase and absorption decrease
 accumulation of fluids and electrolytes
 distension of intestinal lumen
 edema of the bowel wall ->anoxemia->necrosis
iv.Systemic Effects of Obstruction
 water and electrolyte losses
 toxic materials and toxemia
 cardiopulmonary dysfunction
 shock
LOSE OF BODY FLUID：
 digestive fluid: 6-8 L/24h
 Saliva 1200 ml gastric juice 2000ml
 Pancreatic juice 1200ml bile juice 700ml
 duodenal juice 50ml
 intestinal juice 2000ml large bowel juice 60ml
Closed-loop Obstruction
1.It is dangerous form because of the propensity for rapid progression to strangulaton of the blood
supply
2. the secretory pressure in the closed loop quite rapidly reaches a level sufficient to interfere with
venous return from the loop.
4.Colon Obstruction
1.usually not strangulation
2. fluid and electrolyte sequestration progresses more slowly
a.CLINICAL FEATURES:Abdominal pain,Vomiting,Constipation,Distention
b.Diagnosis :
i.continuous rather than intermittent pain .
ii.the presence of shock and rapid pulse, elevated temperature and white blood count.
iii.the presence of peritoneal irritation
iv.a palpable tender abdominal mass.
v. vomitus , gastrointestinal decompression is bloody.
vi.active nonoperative treatment is no use.
vii.X-ray examination show isolated. large intestinal loop.
Common Types of Intestinal Obstruction
5.Volvulus is a twisting or rotation of bowel upon its mesentery , often resulting in intestinal
obstruction. Circulatory impairment may follow , particularly when the twist is more than 180
degree .
DIAGNOSIS
a.Sigmoid volvulus :
 1,common in the elderly with chronic constipation.
 2, cramping abdominal pain is a constant complaint.
 3, nausea and vomiting are inconstant symptoms. And tend to occur late
 4, there is an enormous gas -filled loop of the large intestine.
b. Small bowel volvulus :
 1, common in the young person.
 2, presents following labor activity after eating.
 3, sudden onset of severe abdominal pain ,nausea, vomiting and distention.
 4, shock in the early stage with the necrosis of a large segment or entire small intestine.
 5, not easy differentiated from other types of mechanical intestinal obstruction until
laparotomy.
6.Intussusception:An intussusception is an invagination of part of the intestinal tract into the
lumen of the adjacent intestine.80% of intussusception occur in children under 2 years. In adults ,in
contrast to children, the cause is usually related to intestinal tumors.
7.Pseudo-Obstruction of The Colon
1, Cause : surgical or blunt trauma but may be related to other extracolonic or extraabdominal
disease.
2, Signs: massive dilatation of the cecum and ascending and transverse colon with no vomiting and
no peritoneal signs. No air in distal portion of colon.
3, Treatment: conservative methods. If conservative methods fail ,and cecum is greater than 12cm,
laparotomy is indicated. And if signs of acute abdomen. Usually cecostomy is the choice.
8. Polyps And Polyposis
a.Defination:
 Polyps:the protrude lesion into bowel lumen from the mucosa surface of the bowel
 Polyposis:polyps with specific clinical manifestation and quantity more than 100
b.Pathology:adenomatous polyps
inflammatory polyps
hamartomatic polyps
 metaplastic polyps & mucosa hypertrophy neoplasm
c.Clinical manifestation
 Recurrent abdominal pain
 Intestinal bleeding
 Intestinal obstruction
 Intestinal intussusception
 Malignant change
d.Treatment
 Endoscopy electric coagulation or ligature
 Operation for local resection or segment resection
9.Peutz-Jeghers syndrome
Characteristic:
 mostly young patient
 family history
 harmatomatic,malignant change
 all the alimentary tract，mostly the small intestine. Mouth, lips, hand, foot and pupendum
pigmentation complicated with intususceptionand bleeding
10.Familial adenomatous polyposis
 Characteristic:APC gene mutation
 mostly young,propensity malignant change, large bowel, less frequent invade into small
intestine. operation
11.Gardner Syndrome:Polyposis complicated with multiple osteoma and soft tissue tumor called
as Gardner syndrom
 Characteristic:30~40 years old,hereditary
 malignant change, operation

CHAPTER-7 APPENDICITIS
*1.Location:originate from the root of cecum; three colonic bands converge at the base.(imp during
surgery to identify the appendix
*2.Mc Burney’s point : lateral one-third on the way from the right iliac anterior superior spine to
the umbilicus
3.Lenz point:Right and middle 1/3 from right iliac anterior superior spine to the left anterior
superior spine
4.Morris point:Crossing point of two line- the line from right iliac anterior superior spine to the
umbilicus and the Lateral border of rectus abdominus
*5.Common positions of appendix
 anterior ileum appendix ;
 posterior ileum appendix
 pelvic appendix;
 posterior cecum appendix ;
 inferior cecum appendix
6.Blood supply & nerve innervation
Appendiceal mesenterium contains A. V. N. L.
 • appendix artery: a final artery from ileocolic artery (*impaired blood supply results in
gangrene)
• appendix vein: portal vein (*if there is appendix inflammation, it can cause pylephlebitis
and hepatic abcesses)
• sympathetic nerve : celiac plexus and lesser splanchnic nerve *T10,T11(referred pain
around umbilicus and epigastrium)
6.Acute appendicitis is the most common cause of acute abdomen.
A. ETIOLOGY
 *Obstruction:
 anatomy :worm-shaped, narrow, plenty of lymph glands
 mechanical reason: fecalith, food residue, ascarid, tumor, etc.
 *Bacteria invasion: all kinds of G- bacillus and anaerobe.
*B.FOUR TYPES:
 Acute simple appendicitis(early stage;canbe treated with antibiotics or surgery without any
complications)
 Acute purulent appendicitis(inflammation severe, cannot be cured with antibiotics,localized
peritonitis,post operative complications are more-infection of incision,fistula formation)
 Perforation and gangrenous appendicitis
 Periappendiceal abscess(when there is inflammation greater omentum moves towards the
appendix and wraps around it forming a mass)
C.RESULTS
 Inflammation disappear
 Inflammation localized: periappendiceal abscess
 Inflammation diffused: diffused peritonitis, purulent pylephlebitis, infection shock
D.CLINICAL MANIFESTATION
 *Symptoms :
 Abdominal pain :Periumbilical or epigastric pain that migrates to right lower abdomen. Pain
becomes persistent and well localized. It worsens with moving,breathing deeply, coughing,
sneezing, walking, or being touched.
 Gastrointestinal symptoms: anorexia, nausea, and vomiting occur after the onset of pain;
constipation; diarrhea; bladder and rectum stimulus symptoms (tenesmus)
 General symptoms : tired ,headache, fever, rapid pulse, SIRS (systemic inflammatory
response syndrome)
 *Signs :
 Tenderness at the right lower abdomen (Mc Burney’s point)
 Peritoneal irritation sign :
 muscular rigidity
 rebound tenderness (Blumberg sign)
 bowel sounds disappear
 *Rovsing’s sign: pain at the right lower quadrant upon palpation of the left lower quadrant.
 *Psoas sign : pain on active elevation of the right legs
 *Obturator sign: pain at internal and external rotation of the right hip.
 Right lower abdominal mass
  Lab test
 Blood routine: mildly to moderately elevated WBC with nuclear left shift ,
10000-20000/mm3
 Urine routine: a few RBCs or WBCs
 pregnancy test (β-HCG)
 Imaging examination:Ultrasound; X-ray; CT.
*E.DIAGNOSIS: Key points-
 Migrating right lower abdominal pain
 Tenderness at Mc Burney’s point.
 Elevated WBCs
 Ultrasound
F. DIFFERENTIAL DIAGNOSIS
Two types : A:required surgery
B:not required surgery
*A: Required surgery:
 Perforation of gastointestinal tract---- ulcer, tumor, diverticulitis
 Obstetrics and gynecologic disease---- ectopic pregnancy, ovarian torsion
B: Not required surgery
 Pelvic inflammation
 Mesenteric adenitis: enlarged lymph nodes in the mesentery
 Viral & bacterial gastroenteritis
 Pneumonia, pleurisy
G.TREATMENT
** (1)Early operation: surgical removal (appendectomy)
 Acute simple appendicitis: appendectomy
 Acute purulent and gangrenous appendicitis: appendectomy and/or drainage
 Appendiceal abscess:
 if localised at right lower quadrant: antibiotic therapy and general treatment
 if infection diffused: incision and drainage
***Operation
i. Incision : generally at McBurny point----McBurney’s incision(oblique); or transverse skin
incision; 3—6cm long
ii.Process:
 The colonic bands are followed to the base of the appendix
 Mesoappendix is divided between clamps and ligated
 The base of appendix is ligated at 0.5cm from cecum and inverted using a purse-string
iii.Laparoscopy appendectomy
iv.Suspected case: not definite.
 Admit the patient to the hospital for further observation 12-24hrs
 exploration incision: right rectus abdominis incision
* * (2)Antibiotic thearpy:
 Acute simple appendicitis with contraindication of operation
  Appendiceal abscess- Broadspectrum antibiotics: 3rd generation cephalosporin(gram
negative bacillus )＋metronidazole (anaerobe )
H. COMPLICATION
 Complication of acute appendicitis:
• Abdomen abscess
• Inter or extra fistula
• Pylephlebitis
 Complication of appendectomy:
• Incision infection
• Peritonitis and abdomen abscess
• Bleeding
• Stool fistula
• Stump infection
• Adhesive intestinal obstruction

CHAPTER-8 COLONIC RECTAL AND ANAL DISEASES

1.Colon:Colon includes: cecum, ascending colon, transverse colon, descending colon, sigmoid colon.
Length: 120-200cm.
 Three symbols: haustra of colon, band of colon, epiploic appendices.
 Wall of colon: serosa, muscular layer, submucosa, mucosa.
2.Rectum
 Length: 12-15 cm.
 Diameter: Upper part à same of sigmoid (4cm) but lower is dilated (rectal ampulla).
 Beginning: rectosigmoid junction (sacral promontory).
 End: 2.5 cm below and in front of the tip of coccyx.
a.Arterial Supply:
 Superior rectal artery (chief artery)
 Middle rectal artery
 Median Sacral artery
b.Venous Drainage:
 Superior rectal venous plexus
 Inferior rectal venous plexus
c.Lymphatic:
 Upper ½ periaorta or internal iliac L.N.
 Lower ½ inguinal or external iliac L.N.
3.Anal Canal
 Length: 1.5-2 cm
 Extent: from anorectal junction (Dentate Line) to the anus.
 Interior:Upper part:Anal column,Anal valve,Anal sinus,Dentate line
Dentate line: is a line which divides the upper 2/3rds and lower 1/3rd of the anal canal.
Differences between above and below dentate line
 Above the dentate line: Rectum- mucosa S.& I. rectal A. S.rectal V.- Portal V. L.
 Below the dentate line: Anus -skin ,Anal A. ,Anal V.- vena cava L.
4.Perirectal Spaces:these are divided by the levator ani muscles
 Pelvirectal space & Retrorectal space-above
 Ischiorectal space & Perianal space-below
5.Physical Examination
 Inspection:red, swollen, blood, pus, stool, mucus, fistula orifice, ulcer, mass, hemorrhoid
 Rectal digital examination: 70% rectal cancers can be detected
 Methods: R. hand, latex gloves, lubricator-mass, tenderness, fluctuation, stenosis, blood,
mucus et al.
6.Colon Cancer
a.General types:
 Mass:right
 Infiltrating:left
 Ulcerative:volcanic
b. Pathology:
 adenocarcinoma
 mucinous carcinoma
 undifferentiated carcinoma
c.Dukes Staging
 Stage A :only lying in the intestine wall
 A1 mucosa and submucosa
 A2 superficial muscular layer
 A3 deep muscular layer
 Stage B: penetrating intestine wall without lymphatic metastasis
 Stage C: lymphatic metastasis
 C1 metastasis around carcinoma
 C2 metastasis to mesenterium and base
 Stage D:Distant metastasis, wide infiltration,unresectable.
d.Metastasis Pathway
1. lymph metastasis:main way
2. blood metastasis:liver, lung, bone
3. direct infiltration
4. abdominal implantation
e.Clinical Manifestation
1. Changes of bowel evacuation habits and stool characteristics: earliest
2. Abdominal pain
3. Abdominal mass
4. Intestinal obstruction
5. General symptoms
Question: Differences of clinical manifestation between R. colon ca and L. colon ca.
The right colon is spacious, and cancers of the right colon can grow to large sizes before they cause
any abdominal symptoms. Typically, right-sided cancers cause iron deficiency anemia due to the
slow loss of blood over a long period of time. Iron deficiency anemia causes fatigue, weakness, and
shortness of breath.
The left colon is narrower than the right colon. Therefore, cancers of the left colon are more likely
to cause partial or complete bowel obstruction. Cancers causing partial bowel obstruction can
cause symptoms of constipation, narrowed stool, diarrhea, abdominal pains, cramps, and bloating.
Bright red blood in the stool may also indicate a growth near the end of the left colon or rectum .
f.Diagnosis
High risk people
 over 40 years
 first degree relatives have colon/rectal ca history;
 have cancer history or intestinal adenoma/polyp history;
 stool occult blood (+)
 stool with mucus and blood, chronic diarrhea, chronic constipation, chronic appendicitis
history; psychic trauma (two or more of the five)
 Other examination: barium enema, colonoscope, ultrasound, CT
 Evaluation of prognosis and relapse: CEA (carcino-embryonic antigen)
g.Treatment
i.Radical operation :right colectomy, transverse colectomy, left colectomy, radical resection of
sigmoid colon.
ii.Chemotherapy: 5-FU
Operation principle of colon ca with acute intestinal obstruction
Preoperative preparation: intestinal evacuation+ antibiotics p.o.
7.Rectal Cancer
a.General types：
 ulcer :50%, poor differentiation, early metastasis.
 mass:
 infiltrating
b.Histological types:
 Adenocarcinoma:papillary, tubular, mucus, signet-ring
 Adenosquamous ca
 Undifferentiated ca
c.Clinical staging and metastasis are similar to colon cancer.
d.Clinical manifestation: bloody stool, frequent stool, slender stool, mucus stool, anal pain,
tenesmus, and constipation
e.Diagnosis: history, physical examination (digital exam), lab test (occult blood), image,endoscope,
tumor marker, et al.
f.Treatment
• 1. Operation
• 2. Chemotherapy
• 3. Radiotherapy
• 4. Neoadjuvant chemotherapy and radioterapy
8.Perirectal and Perianal Abscess
1. Perianal, Ischiorectal, Intersphincteric, Supralevator location.
2. Caused by infection of mucus-secreting anal glands.
3. Tender mass at anal verge or on rectal digital exam.
 4. Fistula in anus may be present. Re-examine in 2-3 weeks.
5. Incision and drainage may be done under local anesthesia. Limit packing to keep skin edges
open.
6. Antibiotics to G- bacillus.
7. Warm sitting bath.
8. Local physical treatment.
9. Purgatives p.o.
9.Hemorrhoids
 Internal hemorrhoids are dilated blood vessels and the surrounding tissue above the
dentate line. Covered by mucosa.
 External hemorrhoids are below the dentate line and are covered with modified squamous
epithelium and richly innervated with somatic nerves.
 Hemorrhoids tend to enlarge over time and prolapse.
a.Grades of Internal Hemorrhoid:The severity is graded by the degree of prolapse
 Grade 1 -no prolapse and cause painless bleeding.
 Grade 2 - prolapse on defecation, go back spontaneously. Seen on straining.
 Grade 3 - prolapse and have to be pushed back leading to bleeding and aching pain.
 Grade 4 - Can’t be pushed back leading to mucoid discharge, bleeding, pain, necrosis.
b.Treatment of Hemorrhoid
a.Conservative
• Dietary advise
• Bulk laxatives
• Sitz bath
• Treatment will be effective at 6 month
• Rubber band ligation.
--Complication of band separates
– Hemorrhage
– Sepsis
– Pain
b.Hemorrhoidectomy
Complication of hemorrhoidectomy
• Acute urinary retention
• Secondary hemorrhage
• Anal stenosis
c.PPH(procedure for prolaps and hemorrhoids):Tubiform stapler, 2cm above dentate line, anal
cushion move upward.

CHAPTER-9 LIVER DISEASE

1.Liver Abscess
a.Causes & route: Bacteria- Biliary tree, Portal vein, Hepatic artery, Direct extension of a nearby
focus of infection, Trauma
 Most common bacteria: Escherichia coli andKlebsiella pneumoniae(gas-forming)
The main infection pathway for bacterial hepatic abscess-bileduct
b.Clinical Features :Secondary to some infectious diseases, acute onset
 Chill
 High fever 39~40℃ remittent fever
 Pain in hepatic area(Right upper quadrant pain,tenderness)
 Hepatomegaly
 Jaundice
c. Laboratory findings & special examinations
 Blood route WBC↑
 X-ray :right diaphragm elevate ;reactive pleurisy or pleural effusion
 B-ultrasound: The main diagnostic method;positive diagnostic rate≥96%
 CT
d.Differential diagnosis
i. Amebic liver abscess
ii.Right subphrenic abscess
iii.Liver cancer
iv.Biliary infection
e.Treatment
i.General supporting therapy
ii. Antibiotic therapy
iii.Percutanous transhepatic paracentesis & drainage-indication : single and big abscess,liquefaction
iv.Surgical drainage
v.Chinese medicine therapy
2.Neoplasms of liver
 Malignant :Primary hepatic cancer & Secondary/metastatic
 Benign :cavernous hemangioma;FNH(Focal nodular hyperplasia);LCA(Liver cell adenoma)
PRIMARY HEPATIC CELLULAR CARCINOMA
i.The most common primary malignancy of the liver, and one of the most common malignancies
worldwide
ii.Etiology :Hepatic Viral Infections, Environmental Exposures, Alcohol Use, Smoking, Genetic
Metabolic Diseases, Cirrhosis
Most common cause of primary liver cancer in china-HBV infection
iii.Pathobiology
a.Gross classification :
 Massive
 Nodular(>80%)
 Diffuse( small >2cm,£5cm; minute HCC£2cm large HCC>5cm, £10cm; huge HCC>10cm )
b.Microscopic classification :
 Hepatocellular carcinoma,HCC
 Cholangiocellular carcinoma
 Combined hepatocellular and cholangiocarcinoma）
iv.Metastasis pathways
a.Portal vein b.Direct invasion c.Lymph d.Peritoneal disseminate
v.Clinical findings
 Early: Symptomless
 Mid-late: pain
 Site: Right Upper Quadrant Or Epigastric
 Character: Dull, Aching Pain
 Ruptured & Bleeding → Dramatic Increase Or Sudden Onset Of Pain
 Systematic and digestive symptoms:Fatigue, Weight Loss , Fever (37.5-38℃)Anorexia
Nausea ,Vomiting, Diarrhea
 Hepatomegaly :Non-tender and hard
 Metastatic symptoms
vi.Complications: Alimentary Tract Hemorrhage, Tumor Rupture , Infection , Hepatic
Encephalopathy
vii.Diagnosis
Most important in diagnosis of primary liver cancer:A-fetoprotein,AFP
Pathway of HCC early diagnosis:Monitor the high risk population
1. Age>35ys
2. Hbsag (+)
3. Cirrhosis (+)
4. Active hepatitis>5 years
5. Family history of liver cancer
 Monitoring includes-A-fetoprotein,AFP & B-US
 Theoretically, screning by examining AFP & ultrasound every 4-6months, all ≤3cm liver cancers
can be tested out in general check-up.
 Ultrasound:Test out the lesion ³2cm;Non-invasive ,Sensitivity 84%
 Colour-us: 1-2cm
 CT: Test out lesions³1cm; Positive rate 90%
 MRI:Differentiate hemangioma
 Selective arteriography: Best Location Diagnosis Method for the lesions£2cm ;sensitivity
90%
 Diagnostic criteria of radio-immune method
1. AFP ≥400ug/L lastingly
2. exclude pregnancy ,active liver diseases,embryonic tumors
viii.Diagnostic Procedures
 AFP(+) Image(+) ® HCC (+)
 AFP(–) Image(+) ® Test AFP heteroplasmon
 AFP heteroplasmon(+)® HCC(+)
 AFP heteroplasmon(–)® Differential diagnosis
 AFP(+) Image(–) ® liver cancer(±) ® Close Follow-up
ix.Treatment:Surgical resection is the best choice for primary liver cancer
Surgical resection Indications :
 Good general condition
 Localized tumor(≤ half liver)
 No severe cirrhosis
  Good compensatory function
 No invasion of 1st, 2nd hilum and inferior vana cava
 No severe injuries of other organs.
NOTE : In hepatectomy, 30% good liver tissue or 50% cirrhotic liver tissue must be remained
at least.
Other surgery treatment for special cases
 Ligation of hepatic artery
 Embolism of hepatic artery
 Microwave treatment Crymotherapy
 Re-resection for recurrence
Most common hepatic malignant tumor-Hepatic cellular carcinoma
Most important in the Dx of primary liver cancer-AFP
No of hepatic segments according to counoid segmentation-8(eight)
Pyloric obstruction is not a complication of liver cancer

CHAPTER-10 ACUTE ABDOMEN

Acute abdomen refers to any conditions involving the inflammation of the abdominal viscera.
Characterizing the pain is the key in diagnosing acute abdomen-Onset, duration, location, character
1.CHARACTER
– Visceral pain → dull & poorly localized i.e. distension, inflammation or ischemia
– Parietal pain → sharper, better localized ;Sharp “RUQ pain”(chol’y), “LLQ pain”(divertic)
– Kidney / ureter → flank pain
2.LOCATION
– Upper abdomen → PUD, chol’y, pancreatitis
– Lower abdomen → Divertic, ovary cyst, TOA
– Mid abdomen → early app’y, SBO
3.MIGRATORY PATTERN
– Epigastric → Peri-umbil → RLQ = Acute app’y
– Localized pain → Diffuse = Diffuse peritonitis
4.“REFERRED PAIN”
– Biliary disease → R shoulder or back
– Sub-left diaphragm abscess → L shoulder
– Above diaphragm(lungs) → Neck/shoulder
Acute onset & unrelenting pain is bad where as Pain which resolves ususally not surgical
5.LOCATION OF PAIN BY ORGAN
 RUQ:Gallbladder
 Epigastrum:Stomach,Pancreas
 Mid abdomen:Small intestine
 Lower abdomen:Colon, GYN pathology
6.Abdominal Pain Secondary to Inflammatory Lesions of the Gastrointestinal Subsystem
 Stomach:Gastric ulcer &Duodenal ulcer
 Biliary tract:Acute cholecystitis with or without choledocholithiasis
 Pancreas:Acute, recurrent, or chronic pancreatitis
  Small intestine:Crohn’s disease & Meckel’s diverticulum
 Large intestine:Appendicitis &Diverticulitis
 Jejunum & Ileum:Malignancy,Volvulus,Adhesions,Intussusception
 Colon:Malignancy,Volvulus: cecal or sigmoid,Diverticulitis
7.GYN Etiologies
 Ovary: Ruptured graafian follicle,Torsion of ovary,Tubo-ovarian abscess (TOA)
 Fallopian tube:Ectopic pregnancy,Acute salpingitis ,Pyosalpinx
 Uterus:Uterine rupture,Endometritis
8.CATEGORIES FOR DDX:Inflammation,Obstruction,Ischemia,Perforation
– Offended organ becomes distended
– Lymphatic/venous obstrux due to ↑pressure
– Arterial pressure exceeded → ischemia
– Prolonged ischemia → perforation
– Inflammation versus Obstruction
Ischemia / Perforation
 Acute mesenteric ischemia:Usually acute occlusion of the SMA from thrombus or embolism
 Chronic mesenteric ischemia:Typically smoker, vasculopath with severe atherosclerotic
vessel disease
 Ischemic colitis:Any inflammation, obstructive, or ischemic process can progress to
perforation
 Ruptured abdominal aortic aneurysm
9.TREATMENT
Non-Surgical management
 Fluid Resuscitation
 Antibiotics
 Blood & colloid replacement
 Nutrition support
If the patient turns to be UNSTABLE,DON’T BE HESITATE TO HAVE A SURGERY
Indications for surgery:
 Peritonitis:Tenderness w/ rebound, involuntary guarding
 Severe / unrelenting pain
 “Unstable” (hemodynamically, or septic):Tachycardic, hypotensive, white count
 Intestinal ischemia, including strangulation
 Pneumoperitoneum
 Complete or “high grade” obstruction
Special Circumstances
 Situations making diagnosis difficult:Stroke or spinal cord injury;Influence of drugs or
alcohol
 Severity of disease can be masked by:Steroids;Immunosuppression (i.e. AIDS);Threshold to
operate must be even lower
In general consider the following in case of acute abdomen
Perforated DU,Appendicitis (+/- perforation);Diverticulitis(+/- perforation);Bowel
obstruction;Cholecystitis;Ischemia or perforated bowel;ruptured aneurysm;Acute pancreatitis
 CHAPTER-11 ACUTE GASTROINTESTINAL HEMORRHAGE
1.Manifestations:
i.Hematemesis: bright red blood vs. coffee grounds
ii.Hematochezia: bright red blood vs. melena
iii.Vomiting prior to bleed: Mallory-Weiss tear
iv.Abdominal pain:
 Epigastric: peptic ulcer disease
 Central or lower abdominal pain (colicky): passage of large amounts of blood through the
small and/or large intestine
 Heartburn/Dysphagia: Gastroesophageal reflux or esophagitis
2.Upper Gastrointestinal Hemorrhage:Defined as any bleed proximal to the ligament of treitz
i.Causes include:
 Peptic ulcer disease
 Esophageal varices
 Mallory-Weiss tear
 Dieulafoy lesion
 Aortoenteric fistulae
A.Peptic Ulcer Disease:Most common cause of acute hemorrhage of the upper gastrointestinal
tract
Causes:NSAID use;ASA use;Helicobacter pylori;Stress ulcer;Hypersecretory states
 NSAIDs may cause both duodenal or gastric ulcers
 NSAIDs inhibit prostaglandin production and cause breakdown of the protective barrier of
the gastric mucosa
 Complications of NSAID therapy usually occur within the first month
 NSAIDs not only induce ulcers but may increase the chance of bleeding in patients who have
underlying ulcer disease
 ASA(Aalicylates, Acetylsalicylic acid) -Ulcer risk is dependent on dose
 Helicobacter Pylori:H. pylori is the most common cause of peptic ulcer disease
 Stress Ulcers:Pathogenesis is due to disruption of gastric mucosal integrity
Recent study reported two major risk factors:
 Mechanical ventilation >48 hours
 Patients with underlying coagulopathy
ii.Treatment:Endoscopy,Medications,Surgery
 Endoscopy is the standard of care for all patients that present with UGIB
 Endoscopy serves both as a diagnostic and therapeutic tool
 The success rate of endoscopy to control bleeding in one recent study was 91.3% 1
 Endoscopy has Risk of Rebleeding
Surgery for Peptic Ulcer Disease:
a.Indications for surgery include-
 Age >60
 > 6 units of blood transfusion
 Failure of endoscopy after a second attempt
b.Types of Surgical Procedures
  Over sewing of vessel
 Vagotomy and Antrectomy (<1%)
 Vagotomy and pyloroplasty (10%)
 Partial gastrectomy (2%)
 Total gastrectomy (0%)
B.Esophageal Varices
 Esophageal varices are damaged veins due to portal hypertension
 Bleeding varices are the most serious complication of portal hypertension
 Causes of Portal Hypertension
 The PV drains blood from the intestine and spleen & Carries toxins to be cleared by liver
 Portal hypertension can be due to:
a.Intrahepatic diseases
i. Pre-sinusoidal(Periportal fibrosis,Schistosomiasis)
ii.Post-sinusoidal(Cirrhosis,Hemachromatosis ,Wilson’s disease,Congenital hep fib)
b.Extrahepatic diseases
i.Inflow obstruction(Portal vein thrombosis,compression,Congenital PV obstruction)
ii.Outflow obstruction(Hepatic vein thrombosis ( Budd- Chiari ),RHF/Tricuspid regurg)
iii.No obstruction:Arterio-portal venous fistulae
 Portal Circulation:Communications between the central venous circulation and peripheral
venous circulation
 Caput medusa
 Esophageal varices
 Gastric varices
 Internal hemorrhoids
Medical Management of Bleeding Esophageal Varices
i. Endocopy
 Variceal band ligation(first line therapy)
 Sclerotherapy
ii.Direct tamponade with Sangstoken-Blakemore tube or Minnesota tube
iii.Initiation of drug therapy:Pitressin ,Somatostatin,B-Blockers
iv.Transjugular Intrahepatic Porto-systemic Shunt
Surgical Procedures for Esophageal Varices
 Types of procedures available:
 Porto-caval shunt
 Spleno-renal shunt
 Meso-caval shunt
 Spleno-renal causes least increase in encephalopathy
C.Mallory-Weiss tear
 Longitudinal tear at gastro-esophageal junction
 Bleeding starts after severe retching
 Management consists of NPO and proton pump inhibitors
D.Dieulafoy lesion
 Aberrant submucosal vessel not associated with an ulcer
  Amenable to endoscopy treatment or surgical ligation
E.Erosive gastritis
 Diffuse gastritis or ulcerations
 Managed with proton pump inhibitors but sometimes requires surgery
F.Aorto-enteric fistula:
 Must be excluded in any patient with history of AAA repair with UGIB
 Surgical emergency
3.Lower Gastrointestinal Bleeding:Any bleeding distal to the Ligament of Treitz(Accounts for 10-
20% of all cases of GI bleeding)
Most common causes of acute bleeding are:
 Arteriovenous malformations
 Diverticulosis
Occult bleeds usually due to carcinoma
A.Arteriovenous Malformations(Also known as vascular ectasias, or angiodysplasia)
 Most commonly occur in cecum and ascending colon
 May be associated with:Aortic stenosis,Osler-Weber- Rendo,Chronic renal failure
B.Diverticulosis
 May occur in 50% of patients in the ninth decade of life
 Small out-pouchings of colon that consist of mucosa and muscularis mucosa
 Small vessels within diverticulum stretch and bleed
 May occur anywhere in colon
 Most commonly bleed from the ascending colon
 A druken man has severe vomiting prior to hematemisis.What is the most possible diagnosistic-
Mallory-Weiss tear
 A 30 yr old man with hematemisis presents with orthostatic hypotension---blood loss is 20-
40%

CHAPTER-12 PORTAL HYPERTENSION

1.Portal pressure gradient 12 mmHg(>25cmH2O, Average hydrostatic pressure18cmH2O,Range
13~24cmH2O) or more
2.The main cause of portal hypertension is post hepatic cirrhosis
3.Variceal hemorrhage is the most common complication
4.The most important collateral in portal venous hypertension-Esophageal and gastro venous
plexus
5.Normal pressure of portal hypertension:13-24cm of H2O
6.The features of massive hemorrhage in portal hypertension-Happen quickly and in large
amounts
7.Esophageal and gastro venous plexus bleeding is an indication in portal hypertension to
perform a shunt operation
8.Types of shunts
i.Total Portosystemic shunts
 shunt larger than 10mm between portal vein and IVC
  decreases the portal pressure quickly but high risk(40-5-%) for hepatic encephalopathy
after the procedure
ii.Partial portal systemic shunts reduce the size to 8mm in diameter.
 Use an interposition graft between portal vein and IVC.
 90% control of bleeding, decreased incidence of encephalopathy and liver failure.
iii.Warren distal splenorenal shunt
 the most commonly used for patients with refractory bleeding and good liver function
 Lower incidence of encephalopathy (15%), preserves some liver function. It does produce
ascites
9.Signs of portosystemic collateral formation.
 Dilated veins in abdominal wall
 Caput medusa
 Rectal hemmorhoids
 Ascites
 Umbilical hernia
10.Signs of Liver Disease: Ascites,Jaundice,Palmar erythema,Asterixis,Testicular atrophy,
gynecomastia,Muscle wasting, Dupuytren contracture,Splenomegaly,Caput Medusa
11.TIPS Indications
 Active bleeding despite endoscopic or pharmacologic treatment
 Recurrent variceal bleeding despite adequate endoscopic treatment.
 Potential indications include bleeding gastric fundic varices, refractory ascites
12.Complications of TIPS
 Hematoma, cardiac arrythmias, bacteremia
 Perihepatic hematoma, rupture of liver capsule
 Extrahepatic punture of portal vein
 Arterioportal fistula, portobiliary fistula
 Encephalopathy (30%)
 Liver failure
13.Collateral pathways in portal venous hypertension
 Esophageal and gastrovenous plexus
 Umbilical vein from the left portal vein to epigastric venous system
 Retoperitoneal collateral vessels
 Hemorroidal venous plexus

CHAPTER-13 PERIPHERAL VASCULAR DISEASES

I.PERIPHERAL ARTERIAL OCCLUSIVE DISEASE
 Arterial occlusive diseases are highly prevalent in Western societies.Adverse events are due
to the effects of impaired circulation on critical end organs or extremities
1.Risk Factors for Atherosclerosis
 Firmly Established :Hypercholesterolemia,Cigarette smoking,Hypertension,DM
 Relative Factors :Advanced age,Male gender,Hypertriglyceridemia,Hyperhomocysteinemia
Sedentary lifestyle,Family history
 2.Guidelines for Risk Factor Modification
FACTOR GOAL APPROACH
Lipid Management Primary-serum LDL <100 mg/dL; Diet <30% fat, <7% saturated fat, <200
secondary-HDL >35mg/dL, TG <200 mg/dL mg/day cholesterol; specific drug therapy
targeted to lipid profile
Weight Reduction <120% of ideal body weight Physical activity, diet as outlined
Smoking Complete cessation Behavior modification, counseling, nicotine
analogues
Blood Pressure <140/90 Weight control, physical activity, sodium
restriction, antihypertensive drugs
Physical Activity At least 30 min of moderate exercise 3 to 4 Walking, cycling, jogging, lifestyle and work
times/wk activities
3.Clinical manifestation
 Early stage: intermittent claudication, Impaired distal pulses, changes of nutritional
dysfunction, the limb is perfused via collateral pathways
 Late stage: rest pain
 Loss of pedal pulses is characteristic of disease of the distal popliteal artery or its
trifurcation.
 The dorsalis pedis pulse, the posterior tibial pulse
4.Differentiation of Arteriosclerosis obliterans and thromboangiitis Obliterans
Arteriosclerosis obliterans thromboangiitis Obliterans
Age >45 <45
Superficial thrombophlebitis No Common
Hypertension,CHD Common Uncommon
Involving vessels Large and medium sized arteries Small and medium sized arteries &
veins
Change of other arteries Common No
Calcification of involving Can be found No
arteries
Arteriography Extensive irregular stenosis and Segmental occlusion,others are
segmental occlusion normal
5.Treatment: A key principle in the treatment of peripheral atherosclerosis is the hemodynamic
assessment of circulatory impairment
Medical Management
 Target: reduce progression, induce regression, and prevent morbid endpoints of lesion
formation.
 Risk factor management is the primary approach
 Lipid-lowering therapy: niacin, bile acid-binding resins, HMG-CoA , clofibrate , and
gemfibrozil.
 Antiplatelet therapy: Aspirin
6.Contraindications to Thrombolytic Therapy
 Absolute:Recent major bleeding;Recent stroke;Recent major surgery or trauma;Irreversible
ischemia of end organ;Intracranial pathology;Recent ophthalmologic procedure
 Relative:History of gastrointestinal bleeding or active peptic ulcer disease;Underlying
coagulation abnormalities;Uncontrolled hypertension;Pregnancy;Hemorrhagic retinopathy
II.THROMBOANGIITIS OBLITERANS(BUERGER DISEASE):It is a nonatherosclerotic, segmental,
inflammatory, vasoocclusive disease that affects the small and medium-sized arteries and veins of
the upper and lower extremities, cyclic upset.It is more common in males, aged 20-45 years.
1. Etiology
 External factors: tobacco, cold or humid weather, chronic trauma, infection
 Internal factors: immunologic dysfunction
 Exposure to tobacco is essential for both initiation and progression of the disease.
2.Pathology
 begin with artery, then vein, from distal to proximal.
 segmental disease
 in active stage, nonsuppurtive inflammation
 in end stage, intraluminal thrombosis progressively organizes, new capillary formation,
vascular fibrosis
 ischemic change
3.Clinical findings
 The hands and feet are usually cool.
 skin is pale, or cyanosis.
 Paresthesias.
 pain in limbs, intermittent claudication
 changes of nutritional dysfunction
 impaired distal pulses in the presence of normal proximal pulses.
 migratory superficial thrombophlebitis.
 painful ulcerations and/or frank gangrene of the digits.
4.Clinical stage
 First stage: local ischemic stage
 Second stage:nutritional ischemic stage
 Third stage:necrotic stage
5.Diagnosis
 Age younger than 45 years, current (or recent) history of tobacco use
 Presence of distal-extremity ischemia
 History of migratory superficial thrombophlebitis
 Impaired distal pulses.
 Exclusion of autoimmune diseases, hypercoagulable states, and diabetes mellitus by
laboratory tests
6.Examination:Arteriography- formation of distinctive small-vessel collaterals around areas of
occlusion known as "corkscrew collaterals"
7.Differential diagnosis:Atherosclerosis obliterans;Takayasu’s arteritis;Diabetes mellitus
8.Treatment
i.General treatment
 Absolute discontinuation of tobacco use is the only strategy proven to prevent the
progression of Buerger disease.
 prevent trauma and thermal or chemical injury, avoidance of cold environments, drugs that
lead to vasoconstriction
  Buerger exercise
ii.Medication
 Chinese traditional treatment
 vasodilators, antiplatelet drugs, and anticoagulants
 antibiotics to treat infected ulcers
iii.Hypertension oxygen treatment
iv.Surgical treatment to improve distal arterial flow
 lumber sympathectomy
 vascular reconstructive procedures: bypass transfer, thrombosis
 Others: Omental transfer & Arteriovenous transfer
v.Distal limb amputation for nonhealing ulcers, gangrene
III. ARTERIAL EMBOLISM
 Brain suffers infarction after only 4 to 8 minutes of ischemia
 Myocardium infarcts after 17 to 20 minutes
 Lower extremity may be salvaged after up to 5 to 6 hours of profound ischemia
1.Clinical Manifestation(5P’s)
 Pain
 Paresthesias
 Paralysis
 Pulselessness
 Pallor, coolness
2.Treatment:The usual immediate management of acute arterial occlusion is immediate heparin
anticoagulation and rapid surgical thromboembolectomy.
i. nonoperative treatment
ii. surgical therapy: direct thromboembolectomy, Fogarty cancal thromboembolectomy
3.Complications:The possibility of reperfusion complications such as compartment syndrome or
myopathic-metabolic-nephrotic syndrome
VENOUS DISEASES
i.Superficial veins, include the lesser and greater saphenous veins and their tributaries. These
include the lateral and medial femoral cutaneous branches, the external circumflex iliac vein, the
superficial epigastric vein, and the internal pudendal vein
ii.Deep veins, include the anterior tibial, posterior tibial, peroneal, popliteal, deep femoral,
superficial femoral, and iliac veins.
iii.Muscular vein
iv.Perforating or communicating veins
Dynamics of blood flow: Muscular pump,Negative pressure in thoracic cavity,Valve function
Pathophysiology:Most varicose disease is caused by elevated superficial venous pressures, but
some people have an inborn weakness of vein walls
IV.SIMPLE LOWER EXTREMITY VARICOSE VEINS
Normal veins dilate under the influence of increased venous pressure,allow venous blood to escape
from its normal flow path and flow in a retrograde direction down into an already congested leg.
1.Etiology and pathophysiology
  Prolonged standing leads to increased hydrostatic pressures that can cause chronic venous
distention and secondary valvular incompetence anywhere within the superficial venous
system.
 If proximal junctional valves become incompetent, high pressure passes from the deep
veins into the superficial veins and the condition rapidly progresses to become irreversible.
2.Clinical manifestation
 Symptoms: uncomfortable, annoying, or cosmetically disfiguring, pain, soreness, burning,
aching, throbbing, cramping, muscle fatigue
 Signs: dilated vessels, mild swelling. inflammatory dermatitis, recurrent or chronic cellulitis,
cutaneous infarction, ulceration, and even malignant degeneration.
3.Diagnosis:Trendelenburg test; Perthes test;Pratt test;others: Doppler, angiography
4.Differentiated diagnosis primary lower extremity deep vein valve insufficiency;sequela of deep
vein thrombosis; arteriovenous fistula
5.Treatment:Treatment is indicated whenever venous reflux produces secondary skin or
subcutaneous tissue changes, symptomatic varicose veins
 Nonoperative treatment: compression stockings, keeping the legs elevated
 Injection sclerotherapy
 Operation: Vein ligation, stab evulsion technique, communicating veins ligation
6.Complications:Superficial thrombophlebitis; ulceration ;Varicose veins bleeding
V.DEEP VENOUS THROMBOSIS :The thrombotic process initiating in a venous segment
canpropagate to involve more proximal segments of the deep venous system, thus resulting in
edema, pain, and immobility.
formation of thrombi, ---chronic venous insufficiency
1.Etiology : The triad of stasis, hypercoagulable state, and vessel injury all exist in most surgical
patients. It is also clear that increasing age places a patient at a greater risk, with those older than
65 years of age representing a higher risk population
Virchow triad (venous stasis, hypercoagulability, endothelial trauma)
2.Clinical types
 upper extremity deep venous thrombosis
 inferior vena cava or superior vena cava thrombosis
 lower extremity deep venous thrombosis
3.Prophylaxis
 “minidose” heparin:every-8-hour dosing 5000unit
 low-molecular-weight heparin (LMWH)
4.Treatment:Thrombolysis & Vena Caval Filter
Indications for a Vena Cava Filter
 Recurrent thromboembolism despite “adequate” anticoagulation
 Deep venous thrombosis in a patient with contraindications to anticoagulation
 Chronic pulmonary embolism and resultant pulmonary hypertension
 Complications of anticoagulation
 Propagating iliofemoral venous thrombus in anticoagulation

CHAPTER-14 BREAST DISEASES

1.Lymphatic Drainage Of Breast
1) Axillary lymph nodes:according to their relationship with the minor pectoral muscle:
level 1: below the muscle
level 2: behind it
level 3: in the apex of axilla above the muscle
Rotter’s lymph node: Lymph nodes in the space between the pectoralis major and minor muscles
are known as the interpectoral group, or Rotter nodes
2) Internal mammary nodes in the 1st 2nd and 3rd intercostal space
3) Direct lymphatic communications between the breasts
4) Drains down the rectus sheath and hepatic sickle-form ligament to liver
2.Examination of breast:Inspection;symmetry;skin;vein;nipple;Palpation-Breast mass: 3
dimensions(Generalized lumpiness)
3.Special examination
1) X-ray: mammography, radiography with molybdenum target tube
2)Other imaging examination
3)Ultrasound technology:Cystic or solid;Blood supply;Benign or maliganant
4)CT.MRI
5)Biopsy
 fine needle aspiration biopsy (FNAB)
 cytology of nipple discharge
 biopsy during operation
4.Ploythelia: accessory nipple
5.Ploymastia: accessory mammary gland-Functional or not
6.Acute mastitis
A. ETIOLOGY
i.Milk stasis
ii.Bacteria invasion:staphylococus aureus( lymph vessels)
B.CLINICAL MANIFESTATION
 local signs: redness, tenderness, induration, fluctuance (abscess formation)
 systemic signs: fever, chill
C.TREATMENT
Rule:elimination of infection, empty breast
1)early stage:antibiotics
2)abscess formation:drainage
3)continue breast feeding:empty affect breast
7.Fibrocystic disease of the breast(mastopathy)
A.ETIOLOGY:endocrine dysfunction
 Disorder of female hormone: relative hyperoestrogenism
 Receptor abnormality
 ANDI: aberrations of normal development and involution
B.CLINICAL FEATURES
1) Breast pain (mastalgia), increase during premenstrual phase
2) Breast mass, size increases during premenstrual phase
3) Middle age, sometimes nipple discharge
C.DIAGNOSIS -differential diagnosis: cancer
D.TREATMENT
1) No treatment
2) Tradition medicine
3) surgery: can not rule out cancer, dysplasia
8.Breast Neoplasm
 Benign tumors: fibroadenoma (3/4); intraductal papilloma (1/5)
 Malignant tumors: breast adenocarcinoma; scarcoma
 Male breast cancer
9.Fibroadenoma
A. ETIOLOGY:Hypersensitivity to estrogen within a lobule
B.CLINICAL FEATURES
 Most common age: 18-25years
 Breast mass, smooth, elastic hardness, mobile
C.TREATMENT: operation
10.Intraductal papilloma
 arises from a single major collecting duct
 women between 40 and 50 years of age
 nipple discharge: bloody, spontaneous
 mass: rare
 localization: ductogram and ultrasound
 treatment: local excision
 may develop to cancer (6%-8%)
11.Breast Sarcomas
 Angiosarcoma, stromal sarcoma, fibrosarcoma, lymphosarcoma,Phyllodes tumor: phyllodes
fibroadenoma, cystosarcoma phyllodes
 Clinical findings: women >50 years;painless, mobile mass;average size 4-6 cm
 Treatment: mastectomy
12.Breast Cancer :7-10%, the 1st or the 2nd most frequent cancer in women
A.ETIOLOGY:Unclear, estradiol and estrone have direct relation
B.RISK FACTORS:
 Early age at menarche;
 Late age at menopause;
 Late age at first full term pregnancy;
 no lactation;
 Fat; enviroment; family history
C.PATHOLOGICAL TYPES
a.noninvasive carcinoma:intraductal carcinoma, lobular carcinoma in situ, Paget disease
b.early invasive carcinoma: ductal; lobular
c.special types of invasive carcinoma
d.non- special types of invasive carcinoma: ductal; lobular
e.others
D.METASTASES PATHWAYS
a.direct extension
b.lymph metastases
 axillary lymph nodes
 internal mammary nodes
c.blood metastases( lung, bone, liver)
E.CLINICAL MANIFESTATION
i.Breast mass:Painless, solitary, hardness, surface is not smooth, unclear borderline, degree of
mobility is small or fixed, enlarge quickly
ii.Changes of skin
 skin dimple ( involvement of Cooper ligament)
 orange peel ( involvement of subcutaneous lymph vessels )
 nipple retraction
 Bloody nipple discharge
iii.Special signs
 Inflammatory breast cancer: develop quickly, bad prognosis, inflammatory sign of local skin
 Paget’s carcinoma of breast:eczematous changes of the nipple, ulcer
F.DIAGNOSIS:Clinical findings, imaging, histology, cytology
G.DIFFERENTIAL DIAGNOSIS:
1.fibroadenoma
2.mastopathy
3.plasma cell mastitis
4.acute mastitis
5.breast tuberculosis
F.TREATMENT
 Indication for operation: stage of 0, I, II, part of III
 Contraindication:distant metastasis, elderly patients or with severe systemic diseases
1. surgical treatment
1) radical mastectomy
2) extensive radical mastectomy
3) modified radical mastectomy
4) total mastectomy
5) lumpectomy and axillary dissection
2.Chemotherapy:For invasive cancer;CMF, CAF;Preoperative chemotherapy
3.Endocrinotherapy:ER (+), PgR (+);Tamoxifen: antiestrogen, binds to ER;Endometrial cancer
4.Radiotherapy
5.Reconstruction of breast

CHAPTER-15 DISEASES OF PANCREAS

1.Acute pancreatitis
a.Causes:Although there are many causes for acute pancreatitis- the most common cause includes-
gall stones and alcohol
b.Pathology
 acute edematous pancreatitis
 acute hemorrhagic necrotizing pancreatitis(acute hemorrhagic pancreatitis, acute
necrotizing pancreatitis)
c.Clinical finding
 Abdominal pain and Abdominal distention
 Nausea and vomiting
 Respiratory failure, confusion, or coma.
 Low-grade to moderate fever
 Tachycardia and hypotension
 Mild jaundice,
 Pleural effusion.
 Shock
 Peritoneal irritation sign (Abdominal tenderness, rebound tenderness and rigidity)
 Shifting dullness
 Decreased bowel sounds
 Cullen’ sign: discoloration of periumbilical area
 Grey Turner’ sign:discoloration of flanks
d.Laboratory finding
i.Amylase and lipase (elevations of amylase are more sensitive but less specific than lipase in the
diagnosis of acute pancreatitis )
ii.Others include :Serum calcium ,Serum glucose ,Blood gas analysis,CRP(C-reactive
protein),Imunolipase, trypsinogen ,and immuno elastase,ALT and AST (gallstone pancreatitis )
e.Imaging finding
i.X-ray
 Dilated loop of small bowel (sentinel loop)
 Abrupt cessation of gas in the distal transverse colon (colon cutoff sign)
 Radioopaque densities (biliary calculi)
 Left-sided pleural effusion
ii.B-US: pancreatic edema, ascites----
iii.CT: CT is the best diagnostic test for the diagnosis of acute pancreatitis.
iv.Contrast-enhanced CT is excellent for diagnosis of pancreatic necrosis
e.Diagnosis and differential Diagnosis
i.Acute edematous pancreatitis and acute hemorrhagic necrotizing pancreatitis
ii.Other diseases
 Acute appendtitis
 Ileus
 Perforated gastroduodenal ulcer
 Biliary disease
 Ruptured hepatoma
The differential diagnosis also depends on the Clinical findings,Amylase,CT ,Abdominal
paracentesis
f.Treatment
i.Acute edematous pancreatitis—internal medicine (Emergency surgery is not indicated in mild
acute pancreatitis)
ii.Acute hemorrhagic necrotizing pancreatitis
 Supportive care
 Replacement of fluid and electrolytes
 Correction of metabolic abnormalities
 Nutritional support
 Other measures :nasogastric suction and antibiotics
 Agents to inhibit pancreatic secretion(Have not been found to be useful in altering the
course in acute pancreatitis)-Somatostatin(sandostatin stilamin),Glucagon,Protease
inhibitors (trasylol)
g.Surgical Therapy Criteria/Indications:
 Inefficiency by internal medicine (deteroration of clinical status)
 Complication (pancreatic or/and peripancreatic Infection and abscess)(Treatment of
secondary pancreatic infection)
 Combined with biliary diseases(Gallstone ASP) ( Correction of associated biliary disease)
 Diagnosis unclear (Uncertainty of clinical diagnosis)
h.Endoscopic therapy indications:
 acute gallstone pancreatitis
 recurrent pancreatitis due to pancreatic sphincter dysfunction,
 recurrent pancreatitis due to pancreas divisum.
The rationale for endoscopic therapy in each area is the relief of obstruction to flow of pancreatic
juice
2.Chronic pancreatitis
a.Causes :Alcohol,Pancreatic diverticulum ,Tropical pancreatitis,Hyperparathyroidism
Trauma,Obstructive pancreatitis,Idiopathic chronic pancreatitis,Cystic fibrosis,Hereditary chronic
pancreatitis
b.Classification
 Obstructive chronic pancreatitis
 Calcified chronic pancreatitis
 Inflammatory chronic pancreatitis
c.Pathology: pancreatic fibrosis
d.Clinical finding and diagnosis
Abdominal pain , distention,Diarrhage,Dyspepsia,Malnutrtion,Diabetes,Narcotic addiction,Jaundice
e.Biochemical measurements
 Isoamylase,lipase trypsin,and elastase
 Quantitative measurement of fecal fat
 glucose tolerance test
 Secretin stimulation test
 Plasma cholecystokinin (CCK)( may be elevated )
  Bentiromide test
f.Treatment
i.Medical therapy
 Alcohol and cigarette avoidance
 Analgesics
 Enzyme therapy
 Treatment of malnutrition
ii.Surgical therapy:Biliary Obstruction, pancreatic pseudocysts, combined with biliary diseases,
intractable pain,
iii.Celiac nerve block
iv.Therapeutic endoscopy
3.Tumors of Pancreas
I.Pancreatic carcinoma
 Arise from acinar or duct cells
 Early diagnosis is very difficulty , prognosis is poor
 Obstructive jaundice(permanent):main symptom
 Abdominal pain
 Diabetes
 Weakness, emaciation
 Stools: acholic
 Gallbladder:Distended
 Abdominal mass
a.Treatment of pancreatic carcinoma
 Radical operation
 Pancreatoduodenectomy ---- tumor in pancreatic head
 Resection of pancreatic body and tail---tumor in pancreatic body or tail
 Palliative operation: to relieve jaundice
 Biotherapy
II.Pancreatic endocrine neoplasm(PEN):Insulinoma
 Arise from B cell
 Symptoms: whipple’s triad
 Spontaneous hypoglycemia accompanied by central nervous system, psychiatric,or
vasomotor symptoms
 Repeated blood sugar levels below 2.8mmol/L(50mg%)
 Relief of symptoms by oral or intravenous administration of glucose
 Diagnosis: symptom and IRI/G>0.3,B-us,CT,MRI, Endo-US,Angiography,PTPC,ASVS
 Treatment:operation(resection)
III.Carcinoma of periampulla
 Arise from:Papilla of duodenum;Vater ampulla ;Distal CBD
 Symptom: obstructive jaundice
 Treatment :similar to pancreatic carcinoma
 CHAPTER-16 ABDOMINAL TRAUMA
 The primary management of abdominal trauma is to determinate if abdominal injury EXISTS
and operative intervention is required
1.Types of the abdominal trauma
 Blunt abdominal trauma
 Penetrating abdominal trauma
 The recognition of the mechanism of the injury whether is penetrating or non-penetrating
trauma is important for treatment and diagnosis and workup therapy.
 The liver, spleen and kidneys commonly involved in the blunt abdominal injuries
2.Anatomical regions of the abdomen
 Peritoneum
 Intrathoracic abdomen
 True abdomen
 Retroperitoneum abdomen
 Pelvic abdomen
3.Hospital Care and Diagnosis (Evaluation of patient with Blunt / Penetrating Trauma)
a.Initial Management
The resuscitation & Management priorities of patient with major abdominal trauma are the
(ABCDE) of EMERGENCY resuscitations airway, breathing and circulation with hemorrhage control
should be initiated.
b.Folly's Catheter
c.HISTORY: (a) Blunt abdominal trauma (b) Penetrating abdominal trauma.
d.PHYSICAL EXAMINATION:(a) General physical Examination (b)Examination of the abdomen.
ž Inspection ž Palpation ž Percussion ž Auscultation ž Rectal & Vaginal Examination
e. DIAGNOSTIC PROCEDURES
 Blood
 Radiological Studies
 Peritoneal lavage (DPL)
 USS abdomen
 CT abdomen
 Peritoneoscopy (Diagnostic laparoscopy
INDICATIONS FOR SURGERY
 Signs of peritoneal injury
 Unexplained shock
 Positive diagnostic Determination of finding during routine follow up
Common:Liver;Spleen ;Pancreas;stomach and duodenum;Small intestine and colon
4.LIVER TRAUMA
Liver is the largest organ in the abdominal cavity and continues to be the most commonly injured
organs in all patients with abdominal Trauma (Blunt/Penetrating)
i.Mechanism:Hepatic injury result from direct blows, compression between the lower ribs on right
side and the spine or shearing at fixed points secondary to deceleration. Any penetrating gunshot,
stab or shotgun wound below the right nipple on right upper quadrant of the abdomen is also likely
to cause a hepatic injury
ii.Clinical manifestations
Diagnosis of hepatic injury is often made at laparotomy in patients presenting with penetrating
injuries requiring immediate Surgery Or those sustaining blunt Trauma who remain in shock or
present with abdominal rigidity
iii.Investigations
(a) Diagnostic peritoneal lavage (DPL) has been extremely reliable 98% in determining the
presence of blood in the peritoneal cavity once (positive) patient should be taken to the Operating
Room without delay
b) CT Scan abdomen used for diagnosing intra-peritoneal injuries in stable patients after blunt
trauma
Patients sustaining significant Right lower thoracic, Right upper quadrant and epigastric blunt
trauma, should be suspected of having suffered a hepatic injury, clinical assessment and abdominal
paracentesis & DPL are most important factor in determining operative intervention. CT Scanning
may be useful adjuvant method in the hemo-dynamically stable blunt trauma patient
iv.Treatment
When patient arrived to ER the initial management of the patient should be uniform regardless of
organs system injuries. Resuscitation is performed (ABCDE) in the standard fashion
A.NON OPERATIVE APPROACH:
Criteria for nonoperative management include the following
Ü Simple hepatic laceration Or intrahepatic hematoma
Ü No evidence of active bleeding
Ü Intra peritoneal blood loss <250 ml
Ü Absence of other Intra-peritoneal injuries requiring surgery
B.OPERATIVE APPROACH
 Persistent hypotension, despite adequate volume replacement, suggests ongoing blood loss and
mandates immediate operative intervention.
 Injury classification:
 Grade I: Simple injuries – non bleeding
 Grade II:Simple injuries managed by superficial suture alone
 Grade III: Major intra-parenchymal injury with active bleeding but not requiring inflow
occlusion (Pringle maneuver) to control hemorrhage
 Grade IV: Extensive intra-parenchymal injury with major active bleeding requiring
inflow occlusion for hemostatic control
 Grade V: Hepatic venous injury (injury to retrohepatic cava or main hepatic veins)
 Simple techniques includes drainage only of non-bleeding injuries, application of fibrin glue,
and sutures hepatorrhaphy and , Application of Surgery (I & II).
 Advanced Techniques of Repair (III & IV) all performed with Pringle Maneuver in place
v.Complications
a.Recurrent bleeding e. Intra-hepatic Hematoma
b.Hematobilia f.Pulmonary Complications
c.Peri-hepatic abscess g.Coagulopathy
d.Biliary Fistula h. Hypoglycemia
5.SPLEEN TRAUMA
The spleen remains the most commonly injured organ in patients who have suffered blunt
abdominal trauma and is involved frequently in penetrating wounds of the left lower chest and
upper abdomen.The spleen is commonly injured in patients with blunt abdominal trauma because
of its mobility
i.Classification
 Grade I: Subcapsular hematoma
 Grade II: Sub segmental parenchymal injury
 Grade III: Segmental devitalization
 Grade IV: Polar disruption
 Grade V: Shattered organ
ii.Diagnosis
 Patient History
 Physical Examination
 Radiological Evaluation(abdominal X-Ray,Ultrasonography ,CT Scan ,Angiography)
iii.Treatment
 Initial Management (Resuscitation)
 Non operative approach:
CRITERIA FOR NONOPERATIVE APPROACH
 Hemodynamically stable children / adult
 Those patient without peritoneal
 Those who did not require greater than two unit of blood
Contra indication for splenic salvage
 The patient has protracted hypotension
 The patient has other severe injury
 Operative approach: Decision to perform splenctomy or splenorraphy is usually made after
assessment & grading the splenic injury
iv.Postsplectomy and splenorraphy complications
 Early :R Bleeding R Acute gastric distention
R Gastric necrosis R Recurrent splenic bed bleeding
R Pancreatits R Subphrenic abscess
 Late Complications: R Thrombocytosis R OPSS (1 – 6 Week) R DVT
6.PANCREATIC TRAUMA
i.Diagnosis of injury
 Clinical history
 Serum amylase often elevated
 No correlation amylase : severity injury
 CT scan - free fluid around pancreas
- in lesser sac
- oedema / changes in periP fat
ii.Injury classification
 Grade 1 – capsular injury with contusion
 Grade 2 – major duct injury body/tail
 Grade 3 – major duct injury head +/- CBD
 Commonest site of injury = neck
 Asssociated injury = duodenal
iii.Treatment-Initial treatment
 Integrity of main duct is key to management
 Delayed diagnosis associated with poor outcome
 CT reasonable – identifying pancreatic injury
 Poor : assessing duct integrity
 ERCP / MRCP needed
iv.Head Of Pancreas injury
 Drainage only – risk pancreatic fistula
 Alternative : drain into roux loop
 Duodenal injury : 1°repair;Drain into roux loop
 Treatment is tailored to individual injury
v.Complications
 Pancreatic abscess – drain (USS guided)
 Fistula – greater with drainage vs. resection
 Octreotide, NBM, TPN
 Pseudocysts – as acute pancreatitis
 Options : - Percutaneous drainage
- Drainage into GI tract
- Pancreatic stents ineffective
7.Gastric trauma:Seldom;perforation-do operation
8.Duodenal trauma:Do operation once happened
9.Colon and rectum trauma:Do operation once happened
10.Retroperitoneal Trauma:Seldom needs operation