ABDOMINAL HERNIA

1. Hernia: An abnormal sprout of a viscus or part of a viscus through a defect in its

surrounding wall.
2. External Abdominal Hernia: It is an abnormal sprout of intra-abdominal tissue or viscus
through the defect in the abdominal wall. Most occur in the groin.
3. Etiology:
 Intensity of abdominal wall decrease
1) Occur at natural points of weakness, the site that some tissues pass through the
abdominal wall, eg: Spermatic cord, femoral ring.
2) Incision and infection cause nerve damage and muscle weakness.
3) Obesity, older age always results in the abnormal collagen metabolite.
 Intra-abdominal pressure increases, such as: chronic cough, chronic constipation,
urinary outflow obstruction, cry, pregnancy, heavy lifting.
 Decrease and increase: external abdominal hernia.
4. Pathological Anatomy of Hernia:
 Hernia ring.
 Hernia sac: protrusion of peritoneum. Hernia sac – neck (is narrow where the sac
emerges from the abdomen).
 Hernia content: small intestine, major omentum.
 Hernia covering: skin, subcutanous tissue.
5. Four major types of hernia:
 Reducible hernia: The contents of the hernia will return easily to the abdominal cavity. It
can return easier when the patient is supine.
 Irreducible hernia (including slidling hernia): Adherent, Huge sac and excesive content,
Slidling Hernia (Viscus which is adherent to the sac forms a portion of the wall of the
hernia sac, so it can not be easy reduced. It is may be colon or bladder).
 Incarcerated hernia: The hernia contents cannot be returned to the abdomen, with
severe symptoms. It occurs when the inside pressure increase suddenly, and the
content is forced and pushed into the sac. When the pressure disappear, the content is
locked by the hernia ring.
 Strangulated hernia: The contents of the sac become stuck through the hernial ring and
the blood supply is cut off, so the content become ischemic, and later necrosis. Patients
have symptoms of small bowel obstruction.
6. How to distinguish incarcerated and strangulated hernia?
 Incarcerated hernia isn’t with ischemia of tissue; strangulated hernia is with ischemia of
tissue.
 Incarcerated hernia & strangulated hernia are the two stages which belong to one
pathologic process.
7. Special types of incarcerated hernia: (color, movement and pulse).
 Richter’s hernia (intestinal wall hernia): The hernia involves only one sidewall of the
intestine.
 Littre hernia: An incarcerated hernia involves diverticulum (usually Meckel diverticulum).
 Retrograde incarcerated hernia (maydl & “W” hernia): Two adjacent loops of small
intestine are within a hernia sac with a tight neck. The intervening portion of bowel in
the abdomen is deprived of its blood supply and eventually becomes necrotic.
8. Anatomy of inguinal area
 Anatomic layers: total 9 layers.
 Anatomy of inguinal canal.
 Hesselbach’s triangle.
9. Anatomic layers of inguinal hernia:
 Skin, superficial fascia (Camper fascia), profounda fascial (Scarpa fascia). Because most
hernias are repaired through an anterior approach, it is essential to understand the
anatomy from the skin surface to the preperitoneal space.
 External oblique muscle and aponeurosis
1) External ring of inguinal canal: An ovoid opening of the external oblique aponeurosis
that is positioned superior and slightly lateral to the pubic tubercle.
2) Inguinal ligament: The inferior edge of the external oblique aponeurosis and extends
from the anterior superior iliac spine to the pubic tubercle, turning posteriorly to
form a shelving edge.
3) Lacunar ligament: Formed by the insertion of the inguinal ligament to the pubis.
4) Pectineal ligament (Cooper’s ligament): Formed by the periosteum and fascia along
the superior ramus of the pubis.
 Internal oblique and tranversus abdominal muscle：
1) The internal oblique muscle fibers are directed superiorly and laterally in the upper
abdomen; however, they run in a transverse direction in the inguinal region. It also
serves as the superior border of the inguinal canal.
2) Conjoined tendon: Structure formed from the lower part of transversus abdominis
muscle as it inserts into the crest of the pubis. Usually conjoint with the tendon of
the abdominal internal oblique muscle. It forms the roof of the inguinal canal.
 Transversalis fascia:
1) Internal inguinal ring is the point at which the spermatic cord or round ligament
passes through the transversalis fascia to enter the inguinal canal.
2) Surface marking: 2cm superior to the point midway between the anterior superior
iliac spine and the pubic tubercle.
 Extraperitoneal fat and peritoneum: inferior epigastric vessels and spermatic cord.
10. Inguinal Hernia: A protrusion of part of the tissue or vescus through the inguinal region of
the abdominal wall.
 Indirect inguinal hernia: The sac of an indirect inguinal hernia passes from the internal
inguinal ring obliquely toward the external inguinal ring and ultimately into the scrotum.
 Direct inguinal hernia: The sac of a direct inguinal hernia protrudes outward and
forward and is medial to the internal inguinal ring and inferior epigastric vessels.
11. Inguinal region:
 Upper bound: The level from anterior superior iliac spine to the rectus abdominis
muscle.
 Lower bound: Inguinal ligament.
 Inside bound: Lateral border of the rectus abdominis muscle.
12. Anatomy of inguinal canal:
 Deep and superficial inguinal rings.
 Boundaries:
1) Anterior: skin, superficial fascia, and external ablique aponeurosis.
2) Posterior: transversalis fascia and the aponeurosis of transversus abdominis muscle.
3) Superior: conjoined tendon.
4) Inferior: inguinal ligament and lacunar ligament.
 Contents: spermatic cord (Male), round ligament(Female).
13. Hesselbach’s triangle: The margins of the floor of the inguinal canal.
 Bounded by:
1) The inguinal ligament: Serve as the inferior border.
2) The inferior epigastric vessels: Serve as its superolateral border.
3) The lateral edge of rectus muscle: Serve as medial border.
 Direct hernias occur within the Hesselbach triangle, whereas indirect inguinal hernias
arise lateral to the triangle. It is not uncommon, however, for medium and large indirect
inguinal hernias to involve the floor of the inguinal canal as they enlarge.
14. Clinical presentation and Diagnosis of Inguinal Hernia:
 Symptoms: A bulge in the inguinal region remains the main diagnostic finding in most
groin hernias. There may be associated pain or vague discomfort in the region. But the
hernias are usually not extremely painful unless incarceration or strangulation has
occurred.
 Sign: Reducible or irreducible lump.
 Physical examination: The inguinal region should be examined with the patient in both
supine and standing positions. The examiner should visually inspect and palpate the
inguinal region, observing for asymmetry, bulges.
 Ultrasonography also can aid in the diagnosis. There is a high degree of sensitivity and
specificity for ultrasound in the detection of occult direct, indirect, and femoral hernias.
15. Etiology of Inguinal Hernia:
 Weakness of the abdominal wall.
 High intra-abdominal pressure.
 The strength and continuity of this muscle and aponeurosis are important for the
prevention of inguinal hernia.
16. Differences between indirect and direct hernia:
Feature Indirect Direct
Age Children young Aged or old
Pathway of protrusion Pass through external ring, Pass through Hesselbach’s
inguinal canal, can enter the triangle, rarely enter the
scrotum scrotum
Contours of sac Elliptic pear-shaped Hemispheric wide base
Compress the internal ring Controlled Uncontrolled
Relationship with spermatic Posterior to the sac Anterior and lateral to the
cord sac
Relationship with inferior Sac neck is lateral to it Sac neck is medial to it
epigastric artery
Incarcerated incidence High Low
17. Differential diagnosis of Inguinal Hernia:
 Hydrocele testis: It can be diagosis by the translucent test (+). It is common in infants,
swelling or protusion, without discomfort, be transilluminable.
 Communicated hydrocele: It can be diagosis by the translucent test (+).
 Hydrocele of cord: Not reducible. Pull the testis and the lump will move.
 Undescended testis: No testis in the scrotum. Special sense of pain while pressing the
lump, the same lateral testis is vacant.
 Acute intestinal obstruction. Some intestinal obstruction is caused by incarcerated
hernia. So we should inspect groin carefully.
18. Therapy of Inguinal Hernia:
 Nonoperative therapy: Indications: <1 year old; elderly patients or with severe systemic
disease. Always use truss to prevent the hernai heavier.
 Opertive methods: High ligation of the sac, repair the walls of the inguinal canal. And
the repair operations include the conventional repairs and tension-free hernioplasty.
 High ligation of hernia sac always used in infants, and patients with severe local
infection.
19. Repair of walls of the inguinal canal:
 Repair of the anterior wall --- Ferguson repair.
 Repair of the posterior wall:
1) Bassini repair: Lower edge of internal oblique muscle and the conjoined tendon are
approximated to inguinal ligament on the iliopectineal line of the pubis.
2) McVay repair: Lower edge of internal oblique muscle and the conjoined tendon are
approximated to Cooper’s ligament on the iliopectineal line of the pubis.
3) Shouldice repair: The posterior wall of the inguinal canal is repaired by dividing the
transversalis fascia from the pubis to adjacent to the inferior epigastric vessel, then
imbricate sutures.
4) Halsted repair: Like the Bassini repair, but the Spermatic cord is superficial to
external oblique aponeurosis.
 All above methods have a common drawback: the different structures of anatomical
level are forced to be stitched together, which would cause larger tension, and is
unfavorable for healing.
20. Tension-free hernioplasty:
 Great tension in a conventional repair is the principal cause of recurrence (10%).
 Lichtenstein firstly employ a synthetic mesh prosthesis to bridge the defect without
tension.
 Tension-free repair has become the dominant method of inguinal hernia repair
recurrence decrease (1%).
21. Tension-Free Herniorrhaphy including:
 Lichtenstein.
 Mesh plug & patch.
 Stoppa.
 PHS (prolene hernia system).
 Laparoscopic repair.
22. Laparoscopic repair of inguinal hernia: The minimally invasive technique of laparoscopic
surgery can be used to repair the most common types of hernias.
23. Treatment-incarcerated &strangulated hernia:
 Colour, Movement, Pulse.
 Indications for manual reduction:
1) Duration <3-4 hours, no local tenderness, no abdominal tenderness, no rigidity of
abdominal muscle.
2) Elderly patients or with other severe diseases, and the intestinal loop is still alive.
 Usually requires emergency operation if manual reduction is fail.
 Bowels resection is necessary when the incarcerated bowel is gangrene, then do only
high ligation of the sac. (Hernioplasty is not suitable in this case)
24. Femoral hernia: A protrusion of peritoneum through the femoral canal. Usually in women >
40 years. Causes: laxity of groin tissue and elevated intra-abdominal pressure. Below the
inguinal ligament.
25. Anatomy of femoral canal:
 Femoral ring.
 Anterior: inguinal ligament.
 Posterior: pectineal ligament.
 Medial: lacunar ligament.
 Lateral: femoral vein.
26. Clinical presentation and diagnosis of femoral canal:
 Reducible femoral hernia: asymptomatic lump, localized intermittent discomfort.
 Irreducible femoral hernia: constant lump and localized discomfort.
 Strangulated femoral hernia.
27. Differential diagnosis of femoral canal:
 Inguinal hernia.
 Groin lymph nodes.
 Long saphenous varix.
 Iliolumbar tuberculous abscess.
28. Treatment of femoral canal:
 Not be treated conservatively.
 Rule operation: excision or reduction of the hernia sac, and narrowing of the stretched
femoral opening.
29. Methods of femoral canal:
 McVay repair.
 Tension-free hernioplasty.
 Laparoscopic repair of inguinal hernia.
30. Incisional hernia: Occurs in an area of weakness caused by an incompletely-healed surgical
wound, since median incisions in the abdomen are frequent for abdominal exploratory
surgery. The most common Risk factors is Wound infection.
31. Treatment of Incisional hernia: Laparoscopic vs. open repair.
32. Risk factors of Incisional Hernia: Technical, Wound infection, Smoking, Hypoxia/ ischemia,
Tension, Obesity, Malnutrition
ABDOMINAL TRAUMA
1. Classification:
 Blunt abdominal trauma: Most common and Diagnosis is more likely to be delayed or
altogether missed because clinical signs are less obvious.
 Penetrating abdominal trauma (sharp instrument injury): Incised wounds, Stab wounds,
Bullet wounds.
2. Cause:
 Blunt trauma: Crash, Falls, Strike, Beat and kick, Squeezing, Blast.
 Penetrating trauma: Stab/cut, Gunshot, Shrapnel.
3. Mechanism:
 Direct impact.
 Compressive, stretching or shearing forces.
 Acceleration-deceleration forces (abruptly movement of organs).
 Gunshot wounds are higher energy than stab wounds, are usually more damaging than
the latter.
4. Pathophysiology:
 Hemorrhagic shock.
 Hollow organ rupture (Infectious shock): Irritating and infectious contents spill into the
peritoneal cavity—Peritonitis.
5. Clinical manifestations:
 Abdominal pain: Continuous, sharp, extending.
 Ecchymoma (subcutaneous hematoma).
 Shock: Haemorrhagic shock, Infectious shock, Both.
 Peritoneal irritation signs:
1) Tenderness; rebound tenderness; muscular tension.
2) Hollow organ rupture is more serious than solid organ rupture.
 Gastrointestinal symptoms: vomiting, nausea, hematochezia, haematemesis.
6. Treatment:
 Penetrating abdominal trauma and most of closed abdominal trauma need emergency
operations.
 Do operations as early as possible.
 For multiple trauma, pay attention to order of priority:
1) Cardio-pulmonary resuscitation (CPR) is chief task.
2) Treating abdominal trauma is prior besides CPR.
3) Solid viscera injury is prior to hollow viscera.
 Prevention and cure of shock is an important part, intra-abdominal organs injury is
prone to shock.
  About operation:
1) Anesthesia--endotracheal anesthesia.
2) Incision--medial incision: Open abdomen quickly, Easy to extend incision.
3) Control bleeding quickly.
4) Orderly explore every viscus--liver, spleen, diaphragm, gastrointestinal tract, pelvic
cavity, back wall of stomach, pancreas.
7. Diagnosis:
 Determine if there are visceral injuries.
1) The history of traumatic event:
 Place of traumatic event.
 Time of traumatic event.
 Mechanism of injury.
 Type of weapon.
 Height of a fall.
 Emergent treatment outside hospital.
2) Monitor vital signs: signs of shock.
3) Physical examination:
 Degree and extent of Tenderness, rebound tenderness and muscular tension.
 The boundary of liver dullness and shifting dullness.
 Enterocinesia: suppression.
 Digital rectal examination.
 Other injury outside of abdomen.
4) Laboratory examination:
 Falling hematocrit suggest abundant hemorrhage.
 Leukocytosis and neutrophile granulocyte rising:
 Infection caused by viscera ruptured.
 Stress reaction caused by trauma.
 Blood and urine amylase:
 Pancreas injury.
 Perforation of gastrointestinal tract.
 Hematuria: Injury of urinary system.

Any one of the following suggest viscera ruptured：

 Early shock, especially haemorrhagic shock.
 Continual or progressive abdominal sharp pain accompanied with nausea and
vomiting.
 Peritoneal irritation signs.
  Pneumoperitoneum: The boundary of liver dullness reduces.
 Shifting dullness.
 Hematochezia, haematemesis or hematuria.
 Tenderness, fluctuation, bloodstain by digital rectal examination.
 Determine which viscera are hurted: Firstly determine which category of viscera are
hurted, then determine which viscera are hurted:
1) Nausea, vomit, pneumoperitoneum, hematochezia suggest gastrointestinal injury.
2) Dysuria, hematuria and referred pain of perineum suggest injury of urinary system.
3) Referred pains of shoulder suggest injury of epigastric viscera.
4) Inferior rib fracture suggests injury of liver or spleen.
5) Pelvic fracture suggests injury of rectum, bladder or urethra.
 Determine if there are multiple injuries.
1) Multiple ruptures in one viscus.
2) Multiple viscera are injured.
3) Abdominal trauma accompanied with other trauma outside of abdomen.
4) Trauma outside of abdomen involves abdominal viscera.
 How to do when diagnosis is difficult.
1) Other accessory examination.
 X-ray:
 Inferior rib or pelvic fracture suggest injury of corresponding viscera.
 Subdiaphragmatic free air suggest rupture of gastrointestinal tract.
 Image of psoas major muscle disappear suggest retroperitoneal hematoma.
 The normal profile of liver disappear and right diaphragm rising suggest
rupture of liver.
 Ultrasound:
 Free intraperitoneal fluid: Peri-hepatic, peri-spleen, pelvic.
 Evaluate the liver and the spleen.
 It can be done expeditiously and repeatedly.
 Useful in the resuscitation room or emergency department.
 Gas interfere cause false-negatives for retroperitoneal and hollow viscus
injuries.
 Lower sensitivity for free fluid <500 mL.
 Angiography (interventional therapy):
 Evaluate renal artery thrombosis.
 Manage pelvic hemorrhage with embolization.
 Manage bleeding from minor hepatic and splenic injuries.
  Diagnostic abdominocentesis and diagnostic peritoneal lavage:
 Procedure:
a. Local anesthesia.
b. The position of puncture: one third of the distance from the iliac spine to
the umbilicus.
c. A catheter is inserted towards the pelvis and aspiration of fluid using a
syringe.
d. If no blood is aspirated, 1 litre of warm 0.9% saline is infused and after a
few (usually 5) minutes this is drained and sent for analysis.
 Standard criteria for a positive results:
a. Aspiration of blood or enteric contents (stool, food).
b. A bloody lavage effluent.
c. Red blood cell count > 100,000/mm3.
d. White blood cell count > 500/mm3.
e. Amylase value > 175 IU/dL.
f. The detection of bile, bacteria, urine.
 The disadvantage:
a. Some contraindications: Serious flatulence, Middle and later period of
pregnancy, Move restlessly, Previous abdominal operations.
b. Some significant injuries may be missed: Retroperitoneal injury
(duodenum, pancreas), Diaphragmatic tears, Minor intestinal injuries.
 CT:
 The most frequent method to evaluate the stable patient with closed
abdominal trauma.
 The best method to evaluate retroperitoneal trauma.
 Contrast medium applied make lesions clearer.
 False-positive is less.
 It is not reliable for diagnose of hollow viscus injuries.
 Diagnostic laparoscopy:
 Invasive and expensive method.
 Does not seem to be superior to other methods.
2) Closely monitor:
 Measure vital signs every 15~30 min.
 Do abdominal physical signs every 30 min.
 Detect RBC count, hemoglobin every 30~60min.
 Do abdominocentesis and peritoneal lavage once again in necessity.
 Don’t give analgesic and foods.
 Fluid infusion, gastro-intestinal decompression, antibiotic administration.
 3) Exploratory laparotomy - The indications：
 Abdominal pain and peritoneal irritation signs aggravate progressively.
 Bowelsound fade away or obvious abdominal distension.
 Systemic situation deteriorate-thirst, irritable, Tachycardia, fever or leukocytosis.
 Progressively falling hematocrit.
 Stable blood pressure becomes unstable or falling.
 Hematochezia or haematemesis.
 Positive measures of anti-shock don’t work or deteriorate.

Open trauma is easy to be diagnosed, but the following should be notable.

 Penetrating trauma or non-penetrating trauma should be differentiated firstly.
 The entrance or exit of penetrating trauma may be not at abdomen but at chest,
shoulder, waist or perineum.
 The path of penetrating trauma may be curved.
 May be accompanied with blunt visceral injury.
 The size of wound is not in proportion to the severity of trauma，especially gunshot
injury.

Closed trauma is difficult to be diagnosed:

 Determine if there are visceral injuries.
 Determine which viscera are hurted.
 Determine if there are multiple injuries.
 Accessory examination when diagnosis is difficult.
8. Common visceral injuries:
 Solid organs: Splenic rupture, liver rupture, pancreatic injury.
 Hollow organs: Gastric injury, duodenal injury, small intestine rupture, colon rupture,
rectal injury.
9. Splenic rupture:
 Most common in blunt or closed abdominal trauma.
 Clinical Findings:
1) Commonly, 9-10th ribs on the left are fractured.
2) Left upper quadrant tenderness and tachycardia present.
3) Pain in the left shoulder (referred pain).
4) Local irritation of the peritoneum--rebound sensitivity and guarding.
  Diagnosis:
1) Left upper quadrant tenderness.
2) Tachycardia or hypotension.
3) Ultrasound finds free intraperitoneal fluid.
4) CT scanning in those who are stable.
5) Abdominocentesis or peritoneal lavage.
6) Exploratory laparotomy.
 Treatment:
1) Small lacerations can be observed without repair.
2) Larger lacerations may be treated with oversewing, or by splenectomy.
10. Liver rupture:
 The liver is the second most commonly involved solid organ in the abdomen after the
spleen. However liver injury is the most common cause of death.
 Liver laceration may be caused by either blunt or penetrating trauma.
 Biliary tract injury is unusual, and harder to diagnose.
 Clinical manifestations:
1) Fractures of the 7-10th ribs overlying the liver are common.
2) Right upper quadrant tenderness.
3) Peritoneal irritation — Rebound sensitivity and guarding.
4) Pain in the right shoulder.
 Diagnosis:
1) Penetrating trauma involves the right lower chest or right upper abdomen.
2) Right upper quadrant tenderness in blunt trauma.
3) Ultrasound or CT scan.
4) Abdominocentesis or peritoneal lavage.
5) Exploratory laparotomy.
 Treatment:
1) Small lacerations can be followed conservatively.
2) Large lacerations require repair.
 Control bleeding temporarily, find out injury as soon as possible.
 Merely suture the ruptures.
 Ligation of hepatic artery.
 Packing hemostasis with gauze.
 Hepatectomy.
11. Pancreatic injury:
 Usually injured in penetrating trauma
 Blunt trauma is usually in crush injuries (hitting by handlebars or steering wheel)
 Duodenal or biliary duct injuries are often present as well.
 Clinical manifestations:
1) Vague upper and mid-abdominal pain that radiates into the back.
2) Tenderness at upper and mid-abdomen.
3) Peritoneal irritation signs.
4) Shock.
 Pancreatic injury is notoriously difficult to diagnose.
 Most cases are discovered only at surgical exploration.
 Diagnosis:
1) Localized blow to the mid-abdomen.
2) Clinical manifestations.
3) Serum amylase determinations sometimes no helpful in the acute setting.
4) A CT scan establishes the diagnosis.
 Treatment: May be surgical or conservative, depending on the degree of injury, and on
the presence of associated injuries.
 Prognosis:
1) Pancreas injury has a high mortality.
2) Delayed complications include fistula, abscess, sepsis.
3) Hemorrhage may lead to significant mortality.
4) Early diagnosis is crucial for better prognosis.
12. Gastric injury:
 Often result from penetrating trauma. rarely from blunt trauma.
 Any penetrating abdominal injury, particularly in the upper abdomen, should be
suspected of gastric injury.
 A nasogastric tube should be inserted and if the aspirate is positive for blood, an gastric
injury to should be suspected.
 Careful examination of the anterior and the posterior gastric wall during operation.
13. Colon rupture:
 Morbidity is lower than small intestine rupture.
 Peritonitis is later but more serious because bacteria is much and irritative fluid is few.
 Enterostomy or intestinal exteriorization is applied to the majority of patients.
 Enterectomy is only suitable for patients with small rupture, fewer pollution and good
systemic condition.
14. Small intestine rupture:
 Small intestine takes up a large part of the abdomen and is likely to be damaged in
penetrating injury.
 It is not difficult to diagnose small intestine rupture because of early occurrence of
peritonitis.
 Pneumoperitoneum isn’t common manifestations in this disease.
 May be associated with complications such as infection, abscess, bowel obstruction,
and the formation of a fistula.
 Operations is necessary: Close perforation by suture or excise damaged intestine and
anastomosis.
15. Duodenal injury:
 Mostly caused by penetrating trauma, rarely by blunt trauma.
 Mostly accompanied by other abdominal injuries.
 A motor vehicle accident causing a steering wheel blow to the epigastrium is the most
common mechanism of blunt duodenal injuries.
 Injury of intra-abdominal duodenum is easy to diagnosis.
 Early diagnosis is difficult for injury of retroperitoneal duodenum (second and third
portions).
 Hyperamylasemia raise suspicion the duodenal injury.
 Diagnosis:
1) Requires plain films or CT.
2) Diagnostic peritoneal lavage is unreliable in detecting retroperitoneal injuries.
3) Intraoperative evaluation requires an adequate exposure of the second, the third
and fourth portions.
16. Rectal injury:
 Upper rectal injury (above peritoneal reflection) is familiar to colon rupture.
 Lower rectal injury (under peritoneal reflection) can’t cause peritonitis but severe
peripheral rectal infection.
 Sigmoid Colostomy.
 After 2-3 months, when rectal injuries heal, reduce the sigmoid.
17. During the evaluation of a trauma patient, an upright CXR showed gastric bubble shifted
to the right. No free air is present. What is the main concern? Splenic injury
18. Small bowel injury is the most common injury resulting from blunt abdominal trauma.
19. The Classification of abdominal trauma: Blunt and penetrating abdominal trauma.
20. Which organ is the most common in blunt or closed abdominal trauma splenic rupture.
21. Peritoneal irritation signs: Tenderness, rebound tenderness, muscular tension.
22. The major findings with injury of the solid abdominal organs are those of hemorrhagic
shock. Signs with solid organ injury include all of the following EXCEPT:
 Abdominal pain and tenderness.
 Early bacterial peritonitis.
 Development of rebound, guarding and rigidity.
 Hypotension and tachycardia.
 Palpable mass and radiographic mass effect (may result from confined hemorrhage).

ACUTE APPENDICITIES
1. Anatomy and physiology:
 The appendix is a slender, worm-shaped pouch, average 5-10cm in length, that
protrudes from the top of the colon in the lower right abdomen. It is 0.5-0.7 cm in
diameter.
 Appendix is at the base of cecum, the meeting of three colic bands. It’s located in right
iliac fossa (right lower quadrant).
 The inner lining of the appendix produces a small amount of mucus that flows through
the open center of the appendix and into the cecum.
 The wall of the appendix contains lymphatic tissue that is part of the immune system for
making antibodies.
 Like the colon, the wall of the appendix also contains a layer of muscle, but the muscle is
poorly developed.
 Its projection on body surface is Mcburney’s point, which is a point one-third of the
distance between the right anterior superior iliac spine and the umbilicus.
 Neighboring organs are: Ovary (female), right ureter, cecum, ascending colon, the end
of the ileum.
2. The blood supply of appendix:
 Appendiceal artery is a terminal artery, no branch, when blood obstacles, appendix is
easy to necrotic.
 Appendicular vein finally enter portal vein. When appendix gets inflamed, the bacteria
embolus can cause the pylephlebitis and bacterial liver.
3. The nerve supply of appendix: Sympathetic nerve: Celiac plexus and lesser splanchnic
nerve-T10, T11.
4. Anatomic Position: Preileal, Pelvic, Retrocecal, Subcecal, Lateral cecal, Retroileal.
5. Malrotation or maldescent of the cecum is associated with abnormal location of the
appendix, which may be found in anywhere between the right iliac fossa and the left
subsplenic area, such as: subhepatic area, the left lower quadrant, the pelvis.
6. Epidemiology:
 The commonest cause.
 Approximately 7% of people in Western countries have appendicitis.
 Appendicitis is most common between the ages of 10 and 20 years but can occur at any
age.
 The incidence is falling.
 A normal appendix is removed at 10-20% appendicectomies.
7. Etiology: (blockage and bacterium invasion)
 Obstruction of the appendiceal lumen, by lymphoid hyperplasia, occasionally by a
fecalith, foreign body, or worms.
 The obstruction leads to distention, bacterial overgrowth, ischemia, and inflammation,
necrosis, gangrene, and perforation.
 If the perforation is contained by the omentum, peripheral appendiceal abscess results.
 Hyperplasia of submucous lymphoid follicles followed by infection (60%).
 The presence of fecal stasis and fecalith (35%).
 The presence of no specific inciting cause, parasites, foreign bodies, tumors (5%).
8. Four stages of appendicitis:
 Acute simple appendicitis: Mucus accumulating, bacteria multiply, WBC accumulating,
Edema of the appendix.
 Acute purulent appendicitis: A further rise in intraluminal pressure, Venous obstruction,
Further edema and ischemia in the appendix, Bacterial invasion through the wall of
appendix, The formation of pus.
 Perforation and gangrenous: Venous and arterial thrombosis, The area with poorest
blood supply infracted, Perforation, Spilling accumulating pus, Localized Peritonitis,
Generalized Peritonitis.
 Appendiceal abscess / periappendical abscess: Generalized peritonitis, Localized
peritonitis, Healing.
9. Clinical diagnosis: Rest on (patient history and clinical symptom, physical examination,
laboratory findings).
10. Essentials diagnosis:
 Abdominal pain (shifting pain).
 Gastrointestinal symptoms (Anorexia, nausea and vomiting).
 Localized abdominal tenderness in RLQ (most important).
 Lower fever.
 Leukocytosis.
11. History and symptoms:
 Abdominal pain
1) Patient feels vague abdominal discomfort followed by slight nausea, anorexia. The
pain is persistent and continuous.
2) Within several hours, the pain shifts to the right lower quadrant, becoming rather
sharply localized and causing discomfort on moving, walking or coughing.
3) Symptoms of appendicitis may take 4-48 hours to develop.
4) Typical pain (shifting pain)(70-80%):
 Initial diffuse visceral pain in the epigastrium or periumbilical area.
 Localized somatic pain in the right lower quadrant.
5) Atypical Pain: At the onset of the appendicitis it never become localized and may
remain diffuse, more found in old patient or child.
6) Visceral Pain: Because the appendix and the small bowel have the same visceral
nerve supply, the obstruction of appendix and the accumulation of fluid and mucus
then pus lead to higher intraluminal pressure which cause the pain, so the patient
feel pain in the epigastrium or periumbilical area.
7) Somatic Pain: Inflammation stimulates the peritonium, leading to localized
peritonitis, because the peritoneum has somatic nerve supply, so the painful area
can be exactly pointed (McBurney point).
 Gastrointestinal symptoms: Anorexia, Nausea, Vomiting, Diarrhea or constipation,
Bladder and rectum stimulus symptoms.
 Low fever after the other symptoms.
Temperature and pulse are normal at first. Low grade fever then develops. A rising pulse
rate may be an indication of peritonitis. Chill fever: Appendicular perforation. High fever
jaundice: pylephlebitis.
12. Physical examination:
 Localized tenderness in RLQ.
 Rebound tenderness, muscular guarding.
 A tenderness mass in RLQ .
 Rovsing sign (Pain felt in the right lower quadrant with palpation of the left lower
quadrant), obturator sign (flex the right thigh and internally rotate the hip - pelvic
appendix), psoas sign (extend the hip and abduct the thigh with patient on left side-
retro-caecal appendix).
 Peritoneal irritation sign (Acute suppurative appendicitis, Acute gangrenous appendicitis,
Acute perforating appendicitis): Localized tenderness, Rebound tenderness, Muscular
tension.
 Rectal examination: localized tenderness and may be the only sign of an inflamed retro-
caecal or pelvic appendix.
13. Laboratory tests:
 White Blood Cell Count:
1) It can be normal in early stage, always has an elevation of the white blood cell count.
90% of patients have counts over 10,000/L.
2) In three-fourths of patients, the differential white count shows more than 80~90%
neutrophils.
 Urinalysis:
1) The urine is usually normal, but a few leukocytes and erythrocytes may be noted,
particularly in retrocecal or pelvic appendicitis.
2) It excludes problems such as urinary infections or kidney stones, which at times can
be confused with appendicitis.
 Abdominal X-Ray: It may detect a fecalith.
 Ultrasound:
1) If the appendix is enlarged, the diagnosis is strongly suggested.
2) It excludes painful conditions involving the ovaries, fallopian tubes and uterus.
 CT.
 Laparoscopy: The appendix can be directly visualized.
14. Differential diagnosis: The essential differential diagnosis is to eliminate those illness that
do not need operative therapy and to decided suitable operation for those that need
operative therapy.
 Inflammatory diseases of the right upper abdomen such fluids may come from a
perforated duodenal ulcer, gallbladder disease, or inflammatory diseases of the liver (a
liver abscess).
Acute gastroduodenal ulcer perforation:
1) An ulcer history.
2) The most painful area is at epigastrium.
3) Tenderness and guarding more severe.
4) Air under diaphragm is detected by x-ray.
Meckel's diverticulitis: A small outpouching of the small intestine which usually is
located in the right lower abdomen near the appendix. The diverticulum may become
inflamed or even perforate (break open or rupture). If inflamed and/or perforated, it
usually is removed surgically.
 Ureteral stone: Suddenly sharp extreme pain, Less tenderness and guarding, The pain
may spreads to the groin, RBCs were detected in the urine, B-ultrasound show dilation
of ureter.
  Gynecologic diseases:
1) Pelvic inflammatory disease (PID): (acute salpingitis , endometritis).
2) Relationship to the last menstrual period.
3) No nausea and vomiting.
4) More often with bilateral tenderness.
5) Culdocentesis yield pus.
Ruptured Ectopic Pregnancy: Menolipsis, Symptoms relate to blood loss, a palpable
tubal mass on pelvic examination, Culdocentesis yield noncoltting blood.
Intermenstrual pain or mittelschmerz: Onset in midmenstrual cycle, Symptom
spontaneously subsides in few hours.
 Acute mesenteric adenitis: It often happened in children or young patient, have
respiratory infection history, abdominal tenderness is not localized.
 Others: Gastroenteritis, Diverticulitis, Acute cholecystitis, Perforating cecal carcinoma,
Torsion of An Ovarian Cyst.
15. Treatment:
 Early operation because treatment delay increases mortality: Surgical removal
(appendectomy).
 Acute simple appendicitis: appendectomy.
 Acute purulent and gangrenous appendicitis: appendectomy and/or drainage.
 Appendiceal abscess:
1) If local in right low quadrant: antibiotic therapy and general treatment.
2) If infection diffusion: incision and drainage.
 Operation: Appendectomy.
Incision: incision over the point of maximal tenderness, generally at McBurney point,
the McBurney’s incision: 3—6cm.
 New method: Laparoscopy appendectomy.
16. Complications:
 Acute appendicitis: Abdomen abscess, Inter or extra fistula, Phylephlebitis.
 Operation: Incision infection, Peritonitis and abdomen abscess, Bleeding, Stool fistula,
Stump infection, Adhesive intestinal obstruction.
17. Special types of appendicitis:
Children and the elderly often have fewer symptoms, which makes their diagnosis less
obvious and the incidence of complications more frequent.
 Appendicitis in pregnancy:
1) Appendix displaced superiorly: Tenderness site upper shift.
2) Elevation of abdominal wall: Inconspicuous of tenderness, rebound tenderness,
muscular rigidity.
3) Without adherent blanket of omentum: Peritonitis diffusion.
  Appendicitis in neonate:
1) Seldom.
2) Non-specific clinical manifestation: Anorexia, nausea, and vomiting diarrhea,
dehydration.
3) Difficult in early diagnosis.
4) High rate of perforation.
5) High mortality.
6) Carefully physical exam.
7) Early operation.
 Appendictis in the elderly:
1) Less well-defined symptoms and signs.
2) Severe pathologic type.
3) Error diagnosis easily.
4) High rate of perforation.
5) Pay attention to tumor.
 Appendicitis in child:
1) Quick onset and severe.
2) High fever and vomiting present early.
3) Non-typical tenderness at right low quadrant.
4) High rate of perforation.
5) High mortality.
6) More complication.
7) Early operation.
8) Transfusion and correct dehydration, Broadspectrum antibiotics.
18. Treatment:
 Operation: appendectomy, early operation.
 To early and late pregnancy: abortion, premature birth.
 Superior Incision.
 Broad spectrum antibiotics.

STOMACH AND DUODENUM DISEASES

1. Anatomy:
 Left gastric A.: (celiac trunk)
 Right gastric A.: (proper hepatic A)
 Right gastroepiploic A.: (gastroduodenal A.)
 Left gastoepiploic A.: (splenic A.)
 Short gastric A.: (splenic A.)
2. Peptic ulcer: Any gastrointestinal ulcer caused by contact with acid-pepsin secretions.
3. Three main types of peptic ulcer:
 Duodenal ulcer diathesis (duodenal,pyloric channel,and synchronous gastric and
duodenal ulcer).
 Chronic gastric ulcer.
 Acute gastric mucosal ulcerations.
4. Duodenal ulcer: Men are more frequently affected than women. Psychological factors
(chronic psychic stress) are accepted as the most common link in the genesis of duodenal
ulcers. Coffee drinking and excess alcohol intake might increase the incidence of duodenal
ulcer.
5. Signs: The only common sign is mild tenderness in the right upper abdomen.
6. Symptoms:
 Pain, in most patients, is usually located in the epigastrium. It is variably described as
aching, burning, or gnawing.
 The character is that pain appears at the hungry time or during the midnight. Food, milk,
or antacid preparations give temporary relief.
7. Laboratory examination:
 Endoscopy: Gastro duodenoscopy will confirm the diagnosis in problem cases.
 Radiographic Studies: Barium X-ray studies of the stomach and duodenum will usually
show duodenal deformities and an ulcer crater in the proximal portion of the duodenum
(duodenal bulb). The ulcer itself may be seen either in profile or, more commonly,
enface.
 Gastric analysis: BAO and MAO.
1) Measurement of acid production by the unstimulated stomach under basal fasting
conditions; the result is expressed as H+ secretion in meq/h and is termed the basal
acid output (BAO).
2) Measurement of acid production during stimulation by histamine or pentagastrin
given in a dose maximal for this effect. The result is expressed as H+ secretion in
meq/h and is termed the maximal acid output (MAO).
 Serum gastrin :
1) Normal basal gastric levels average 50 – 100 pg/mL, and levels over 200 pg/mL can
almost always be considered high.
2) The high gastrin level is responsible for the increased acid and resulting peptic
ulceration. The best-defined clinical condition in this category is Zollinger-Ellison
syndrome (gastrinoma).
8. Treatment:
Acute duodenal ulcer can be controlled by suppressing acid secretion in most patients, but
the long-term course of the disease (ie, frequency of relapses and of complications) is
unaffected unless H. pylori infection is eradicated.
  Medical treatment:
1) The principal drugs consist of H2 receptor antagonism (eg, cimetidine, ranitidine)
and proton pump blockers (e g, omeprazole).
2) At present, the optimal daily regimen consists of the following combination of drugs:
 An H2 receptor antagonist (cimetidine,-ranitidine), or proton pump blockers
( omeprazole);
 A bismuth compound (De-Nol);
 Antibiotics: tetracycline,and metronidazole.
3) The H2 receptor antagonist is given until the ulcer has healed or for 16 weeks; the
last three drugs are given for 3 weeks.
 Surgical treatment:
1) Recommended principally for the treatment of complications: bleeding, perforation,
or obstruction.
2) If medical treatment has been optimal, a persistent ulcer may be judged intractable,
and surgical treatment is indicated. This is now uncommon.
3) The surgical procedures that can cure peptic ulcer are aimed at reduction of gastric
acid secretion. Excision of the ulcer itself is not sufficient for either duodenal or
gastric ulcer; recurrence is nearly inevitable with such procedures.
4) Methods of treating duodenal ulcer are:
 Subtotal gastrectomy.
 Vagotomy:
 Truncal vagotomy with a drainage procedure (pyloroplasty).
 Parietal cell vagotomy (proximal gastric vagotomy,highly selective vagotomy)
without a drainage procedure.
 Antrectomy and vagotomy.
 Subtotal gastrectomy.
9. Surgical complications:
 Early Complications: Duodenal stump leakage, gastric retention, and hemorrhage may
develop in the immediate postoperative period.
 Late Complications:
1) Recurrent ulcer (marginal ulcer, stomal ulcer, anastomotic ulcer).
2) Gastrojejunocolic and gastrocolic fistula.
3) Dumping syndrome.
4) Alkaline gastritis.
5) Anemia.
6) Postvagotomy diarrhea.
10. Essential diagnosis:
 Epigastric pain at hungry time or during midnight (relieved by food or antacids).
 Epigastric tenderness.
 Normal or increased gastric acid secretion.
 Ulcer on endoscopy, or Signs of ulcer disease on upper gastrointestinal X-rays.
 Evidence of Helicobacter pylori infection.
11. Gastric ulcer: 3 to 4 times less common than duodenal ulcer. Occurs more frequently in
middle aged and elderly persons and about equally in men and women. Evidence points to a
defective mucosal barrier and back-diffusion of acid as the immediate cause. About 80% of
gastric ulcers appear in stomachs that secrete normal or smaller amounts of acid. Other 20%
of gastric ulcer usually occur just inside the pylorus or are associated with duodenal ulcer,
arising in a hyperacidic environment, belong in the duodenal ulcer group.
12. Clinical findings of gastric ulcer:
 Compared with duodenal ulcer, the pain in gastric ulcer tends to appear earlier after
eating, often within 30 minutes.
 Vomiting, anorexia, and aggravation of pain by eating.
13. Differential diagnosis:
 The characteristic symptoms of gastric ulcer are often clouded by numerous nonspecific
complaints.
 Uncomplicated atrophic gastritis, chronic cholecystitis, irritable colon syndrome, and
undifferentiated functional problems are distinguishable forms peptic ulcer only after
appropriate radiologic studies and sometimes not even then.
 Gastroscopy and biopsy of the ulcer should be performed to rule out malignant gastric
ulcer.
14. Treatment:
 Medical Treatment: Medical management of gastric ulcer is the same as for duodenal
ulcer.
 Surgical Treatment:
1) Failure to heal.
2) Suspicion of malignancy.
3) Recurrence.
4) Complications (persistent bleeding, perforation, and obstruction).
5) The most effective surgical treatment was distal hemigastrectomy (including the
ulcer), and a Billroth-I reconstruction is preferred.
15. Comparison of Duodenal and Gastric Ulcer.
Duodenal ulcer Gastric ulcer
Cause Inc. acid secretion, inc. Defective mucosal barrier
gastrin, defect in acid disposal and back-diffusion of acid
Age Younger (20 to45 years) Somewhat older (40-60)
Sex Male:female,7:1 Male:female,1:1
Symptoms Much the same. Pain appears Much the same. Pain
at the hungry time or during appears earlier after eating
the midnight
Malignancy Rare 5%
Free HCL 12 hour night 60 mEq (average), Normal or 12 mEq (average), lower
secretion Higher Than the normal
Medical treatment Excellent (successful in over Poor (successful in 50%)
90%)
Surgical treatment Vagotomy and antrectomy or Removal of the ulcer with
pyloroplasty,parietal cell limited partial gastrectomy
vagotomy,subgastrectomy
16. Essential diagnosis of gastric ulcer:
 Epigastric pain (appears earlier after eating).
 Epigastric tenderness.
 Decreased gastric acid secretion.
 Ulcer on endoscopy, or Signs of ulcer disease on upper gastrointestinal X-rays.
 Evidence of Helicobacter pylori infection.
17. Hemorrhage from Peptic Ulcer: Peptic ulcer is the most common cause of massive upper
gastrointestinal hemorrhage, amounting for over half of all cases. “Blind subgastrectomy”.
Bleeding occurs in 10% to 15% of patients with duodenal or gastric ulcer. The diagnosis is
unreliable when based on clinical findings, so endoscopy and endoscopic therapy should be
performed early (i.e, within 24 hours) in most cases.
18. Endoscopic therapy:
 May stop active bleeding or recent rebleeding.
 Effective methods include injection into the ulcer of epinephrine, epinephrine plus1%
polidocanol (a sclerosing gent), or ethanol; or cautery using the eater probe, monopolar
or multipolar electrocautery, or the YAG laser.
 Decreases transfusion requirements (by about half) and the rate of rebleeding (by about
three-quarters) compared with sham-treated controls.
 The indications: Active bleeding at the time of endoscopy and the presence of a visible
vessel in the base of the ulcer.
19. Medical treatment:
 Most patients (75%) with bleeding peptic ulcer can be successfully managed by medical
means alone. Initial therapeutic efforts usually halt the bleeding.
 H2 receptor antagonist (cimetidine) decreases the risk of rebleeding, and proton pump
blockers (omeprazole) can also decrease the risk of rebleeding but have no effect on
active bleeding.
20. Emergency surgery:
 Depends on such factors as the patient’s age, general health, length of ulcer symptoms,
and presence or history of other ulcer complications.
 About 10% of patients require emergency surgery. Selection of those most likely to
survive with surgical compared with medical treatment rests on the rate of blood loss
and the other factors associated with a poor prognosis.
 The mortality for a single bleeding episode is 5% to 10%. It significantly less after
vagotomy and pyloroplasty than after gastretomy for bleeding ulcer, and rebleeding
occurs with about equal frequency after either procedure.
21. Clinical findings of Pyloric Obstruction due to Peptic Ulcer:
 Most patients with obstruction have a long history of symptomatic peptic ulcer, and as
may as 30% have been treated for perforation or obstruction in the past.
 The patient often notes gradually increasing ulcer pains over weeks or months, with the
eventual development of anorexia, vomiting, and failure to gain relief from antacids.
 Weight loss may be marked if the patient has delayed seeking medical care.
 Dehydration and malnutrition may be obvious on physical examination but are not
always present.
 Peristalsis of the distended stomach may be visible of gross inspection of the abdomen,
but this sign is relatively rare. Most patients have upper abdominal tenderness.
 Tetany may appear with advanced alkalosis.
22. Laboratory findings:
 Anemia is found in about 25% of patients.
 Prolonged vomiting leads to a unique from of metabolic alkalosis with dehydration.
 Measurement of serum electrolytes shows hypochloremia, hypokalemia, hyponatremia,
and increased bicarbonate.
 Saline load tests: This is a simple means of assessing the degree of pyloric obstruction
and is useful in following the patient’s progress during the first few days of nasogastric
suction.
  Imaging studies:
1) Plain abdominal x-rays may show a large gastric fluid level.
2) An upper gastrointestinal series should not be performed until the stomach has
been emptied, because dilution of the barium in the retained secretions makes a
worthwhile.
 Endoscopy: Gastroscopy is usually indicated to rule out the presence of an obstructing
neoplasm.
23. Treatment:
 Medical Treatment:
1) A large (32F) tube should be passed and the stomach emptied of its contents and
lavaged until clean.
2) After the stomach has been completely decompressed, a smaller tube should be
inserted and placed on suction for several days to allow pyloric edema and spasm to
subside and to permit the gastric musculature to regain its tone.
3) A saline load test may be performed at this point to provide a baseline for later
comparison.
 Surgical Treatment:
1) If 5-7 days of gastric aspiration do not result in relief of the obstruction, the patient
should be treated surgically. Persistence of nonoperative effort beyond this point in
the absence of progress rarely achieves the result hoped for.
2) Failure of the obstruction to resolve completely (e.g, if the patient can take only
liquids) and recurrent obstruction of any degree are indications for surgery.
3) Surgery treatment may consist of a truncal or parietal cell vagotomy and drainage
procedure, Truncal vagotomy and gastrjejunostomy is the easiest to perform
laparoscopically.
24. Clinical findings of Perforated Peptic Ulcer:
 Symptoms and Signs:
1) The perforation usually elicits a sudden, severe upper, abdominal pain whose onset
can be recalled precisely.
2) The patient appears severely distressed, lying quietly with the knees drawn up and
breathing shallowly to minimize abdominal motion. Abdominal distention and
diffuse tympany may result if delay.
3) There are abdominal muscles rigid (owing to severe involuntary spasm), Epigastric
tenderness and rebound tenderness, which may not be as marked as expected in
elder patients.
4) Escaped air from the stomach may enter the space between the liver and abdominal
wall, and upon percussion the normal dullness over the liver will be tympanitic.
 5) A small duodenal perforation may slowly leak fluid that runs down the lateral
peritoneal gutter, producing pain and muscular rigidity in the right lower quadrant
and thus raising a problem of confusion with acute appendicitis.
 Laboratory Findings:
1) A mild leukocytosis in the range of 12,000/uL is common in the early stages. After
12-24 hours, this may rise to 20,000/uL or more if treatment has been inadequate.
2) The mild rise in the serum amylase value that occurs in many patients is probable
caused by absorption of the enzyme from duodenal secretions within the peritoneal
cavity. Direct measurement of fluid obtained by paracentesis may show very high
levels of amylase.
 Imaging Studies:
1) Plain x-rays of the abdomen reveal free subdiaphragmatic air in 85% of patients.
Films should be taken with the patient both supine and upright.
2) If the findings are questionable, 400mL of air can be insufflated into the stomach
through a nasogastric tube and the films repeated. Free air in the abdomen in a
patient with sudden upper abdominal pain should clinch the diagnosis.
25. Differential diagnosis:
 Includes acute pancreatitis and acute cholecystitis. The former does not have as
explosive an onset as perforated ulcer and is usually accompanied by a high serum
amylase level. Acute cholecystitis with perforated gallbladder could mimic perforated
ulcer closely but free air would not be present with ruptured gallbladder.
 Intestinal obstruction has a more gradual onset and is characterized by less severe pain
that is crampy and accompanied by vomiting.
 Free perforation of colonic diverticulitis and acute appendicitis are other rare causes.
26. Treatment:
 The diagnosis is often suspended before the patient is sent for confirmatory x-rays.
 Whenever a perforated ulcer is considered, the first step should be to pass a nasogastric
tube and empty the stomach to reduce further contamination of the peritoneal cavity.
 Blood should be drawn for laboratory studies, and intravenous antibiotic (eg, cefazolin,
cefoxitin) should be started.
 If the patient’s overall conditions precarious owing to delay in treatment, fluid
resuscitation should precede diagnostic measures. X-rays should be obtained as soon as
the clinical status will permit.
27. Nonoperative treatment: This kind of treatment for perforated ulcer consists of continuous
gastric suction and the administration of antibiotics in high doses. Although this has been
shown to be effective therapy, with a low death rate, a peritoneal and subphrenic abscess
occasionally accompanies it, and side effects are greater than with laparoscopic closure.
28. Surgical treatment:
 The simplest surgical treatment, laparoscopy (or laparotomy) and suture closure of the
perforation solves the immediate problem.
 More aggressive treatment involves a definitive ulcer operation for most patient with
acute perforation, eg subgastrectomy, parietal cell vagotomy plus closure of the
perforation or truncal vagotomy and pyloroplasty. Now that eradicating H pylori can
cure ulcer disease, the value of anything more than simple closure will have to be
reexamined.
 Concomitant hemorrhage and perforation are most often due to two ulcers, an anterior
perforated one and a posterior one that is bleeding. Perforated ulcers that also obstruct
obvious cannot be treated by suture closure of the perforation alone. Pyloro-plasty
should be performed.
 Perforated anastomotic ulcers require a vagotomy or gastrectomy, since in the long
times, closure alone is nearly always inadequate.
29. Gastric carcinoma: Gastric cancer is one of the commonest malignant tumors. It often be
found in 40 to 60 years people. The ratio of male/female is 3/1.
30. Pathology:
 Early gastric cancer: Tumor is limited in the mucosa or submucosa,whether there is
lymphatic metastasis or not.
 Advanced gastric cancer:
1) Borrmann I: Polypoid carcinoma.
2) Borrmann II: Ulcerating carcinoma.
3) Borrmann III: Invasived ulcerating carcinoma.
4) Borrmann IV: Linitis plastic.
5) Borrmann V: (mixed).
31. Clinical findings:
 Symptoms: The earliest symptom is usually vague postprandial abdominal heaviness
that the patient does not identify as a pain. Anorexia, Weight loss, Vomiting, Dysphagia.
 Signs :
1) An epigastric mass, Hepatomegaly, The stool will be positive for occult blood in half
of patients, and melena is seen in a few.
2) Metastases to the neck along the thoracic duct may produce a Virchow node. Rectal
examination may reveal a Blumer shelf, a solid peritoneal deposit anterior to the
rectum .Enlarged ovaries (Krukenberg tumors) may be caused by intraperitoneal
metastases; further dissemination may involve the liver, lungs, or bone.
 Laboratory Findings: Anemia is present in 40% of patients. Carcinoembryonic antigen
(CEA) levels are elevated in 65%, usually indicating extensive spread of the tumor.
  Imaging studies: An upper gastrointestinal series is diagnostic for many tumors, but the
overall false-negative rate is about 20%. Major diagnostic problems are posed by
ulcerating tumors. All patients with a newly discovered gastric ulcer should undergo
gastroscopy and gastric biopsy.
 Gastroscopy and Biopsy: Large gastric carcinomas can usually be identified as such by
their gross appearance at endoscopy. All gastric lesions, whether polypoid or ulcerating,
should be examined by taking multiple biopsy and brush cytology specimens during
endoscopy. False results are seen occasionally as a result of sampling error, and a
minimum of six biopsies is necessary for greatest accuracy.
32. Surgical treatment:
 Surgical resection is the only curative treatment. About 85% of patients are operable,
and in 50% the lesions are amenable to resection; of the respectable lesions, half are
potentially curable (ie, no signs of spread beyond the limits of resection).
 The surgical objective should be to remove the tumors, and adjacent uninvolved margin
of stomach and duodenum, the regional lymph nodes, and, if necessary, portions of
involved adjacent organs. The proximal margin should be a minimum of 6 cm from the
gross tumor.
 Palliative resection is usually indicated if the stomach is still movable and life expectancy
is estimated to be more than 1-2 months.
33. Chemotherapy: Adjuvant chemotherapy after curative surgery for advanced disease,
doxorubicin or 5-fluorouracil alone, each of which results in a 20% response rate, is as good
as a combination of chemotherapeutic agents. Now, more new chemotherapic medicine are
discovered.

INTESTINAL OBSTRUCTION
1. Intestinal obstruction: An interference in the normal movement of the bowel contents
through the intestinal tract. The small bowel is about 20 feet long, and the large bowel is 5
feet long. This 4 to 1 ratio parallels the ratio of mechanical obstruction that occur in the
small and large bowels; 80% occurs in the small bowel, and only 20% involve the large
bowel.
2. Two main types of obstruction occur:
 Mechanical obstruction,which arises from structural lesions (adhesive bands, tumors,
hernias, etc.) that block the bowel lumen.
 Paralytic ileus, which arises from a failure of neuromuscular propulsive action of the
bowel wall.
 Besides, intestinal obstruction may be caused by vascular occlusion, which occurs when
an impedance to the arterial flow or venous return sets to the stage for bowel infarction.
3. According to the blood supply two types are divided:
 Simple obstruction.
 Strangulation obstruction.
Simple obstruction,in contrast to strangulation obstruction,occurs when the blood supply to
the obstructed bowel is adequate.
4. Intestinal obstruction may be divided in another types, such as:
 Acute obstruction,in contrast to chronic obstruction.
 Upper obstruction, in contrast to lower obstruction.
 Partial obstruction, in contrast to complete obstruction.
5. Mechanical obstruction:
 The “big three” causes of adult mechanical obstruction are hernias (incarcerated or
strangulated), adhesions, and tumors. Hernias and adhesions together account for
about 70%. Tumors cause about 15% of all bowel obstruction, but they are the most
common cause of large bowel obstruction.
1) Adhesions: Adhesions are by farther most common cause of mechanical small bowel
obstruction.
2) Hernia: Incarceration of an external hernia (including incisions) is the second most
common cause of intestinal obstruction. Inguinal, femoral, or umbilical hernias may
have been present for years.
3) Neoplasms: Neoplasms of the small bowel are rare cause of obstruction. In contrast,
neoplasms cause most obstructions of the colon. Left colon lesions may cause
tremendous dilation of the proximal colon when the ileocecal valve is competent.
4) Intussusception: It’s more often seen in children; an organic lesion is not required,
and the syndrome of colicky pain, passage of blood per rectum, and a palpable mass
is characteristic.
5) Volvulus: Twisting of a portion of gastrointestinal tract. Sigmoid vovulus is the most
common; cecal vovulus occurs when the cecal mesentery is long; vovulus of the
stomach is rare.
6) Obturation: Results when materials within the gut occlude the lumen. Such as: fecal
impaction, gallstone, bezoar, ingested foreign bodies, ascaris lumbricoides.
7) Inflammatory bowel disease: Disease often causes obstruction when the lumen is
narrowed by inflammation or fibrosis of the wall. Such as: tuberculosis, regional
eneritis,ulcerative colitis and amebiasis.
8) Paralytic ileus:
 Direct peritoneal irritation from any source: Acute cholecystitis, pancreatitis,
appendicitis, perforation of a hollow viscus, or any abdominal operation.
 Extraperitoneal irritation: hemorrhage, trauma to retroperitoneal nerve,
pneumonitis, etc.
  Systemic imbalances: Infections, electrolyte imbalance, shock, uremia,
myxedema.
 Neurogenic disorders: Severe strokes, central nervous system trauma ,or spinal
cord lesion.
9) Vascular obstruction is the reverse, pathologically, of stragulation obstruction;
primary blood vessel blockage precedes and causes bowel obstruction. Occlusion of
the superior mesenteric vessels produces vascular compromise of that segment of
small intestine distal to the point of occlusion. The causes are embolism or
thrombosis. Embolism originate within the left side of heart,generally associated
with auricular fibrillation. Thrombosis may be caused by increased venous pressure
(abdominal tumor, cirrhosis, congestive heart failure), hypercoagulability
(polycythemia, some cancers), or vascular diseases (collagen diseases, vasospastic
diseases, prolonged infections, or trauma).
 In the child, intestinal obstruction limited primarily to congenital defects and
intussusception.
6. Pathophysiology:
 The bowel proximal to a point of obstruction distends with gas and fluid.
 Enormous quantities of fluid from the extracellular space are lost into the gut and from
the serosa into the peritoneal cavity.
 Hypovolemia leads to multi-organ system failure and is the cause of death in patients
with nonstrangulating obstruction.
 The vomitus becomes feculent, particularly with distal obstruction, as the illness
progressed.
 Abdominal distention elevates the diaphragm and impairs respiration, so that
pulmonary complications are frequent.
7. Symptoms:
 Abdominal pain.
Pain is typically cramping and intermittent. Each episode of cramps has a crescendo-
decrescendo pattern, lasts for a few seconds to a few minutes, and recurs every few
minutes. Continuous pain usually signifies strangulation or perforation. Vomiting
temporarily relieves the pain from upper gastrointestinal obstruction.
 Vomiting: In high obstruction vomiting occurs as an early symptom. In low obstruction
feculent vomiting results from stagnation and bacterial putrefaction.
 Abdominal distention: In high (proximal small bowel) obstruction, distention is minimal.
In low obstruction, distention is massive because of the greater amount of bowel that is
filled with gas and liquid.
  Obstipation: Because intestinal obstruction may be only partial or intermittent.
However, complete obstruction usually produces eventual failure to pass either gas or
feces.
8. Signs:
 General signs:
1) Vital signs may be normal in the early stages, but dehydration is noted with
continued loss of fluid and electrolytes.
2) Temperature is normal or mildly elevated. When strangulation supervenes in simple
obstruction, high fever may develop.
3) Shock that appears early in the course of obstruction suggests a strangulated closed
loop.
 Abdominal signs:
1) Inspection:
 Abdominal distention is minimal to absent in proximal obstruction but is
pronounced in more distal obstruction.
 Peristalsis in dilated loops of small bowel may be visible beneath the abdominal
wall in thin patients.
 Incarcerated hernias should be sought.
2) Palpation: Mild tenderness may be elicited. When strangulation supervenes in
simple obstruction, abdominal tenderness and rigidity may appear.
3) Percussion: Later, there may be percussion dullness, moved with position, when
there is fluid in the peritonum.
4) Auscultation: Peristaltic rushes, gurgles, and high-pitched tinkles are audible in
coordination with attacks of cramping pain in distal obstruction.
9. Laboratory findings:
 X-ray findings:
1) Supine and upright plain abdominal films reveal a ladder-like pattern of dilated small
bowel loops with air–fluid levels. These features may be minimal or absent in early
obstruction, proximal obstruction, or closed loop obstruction or in some cases when
fluid-filled loops contain little gas.
2) Plain films of the abdomen may also show free air in the peritoneal cavity,calculi in
the biliary or renal areas,fecaliths,tumors,or radiopaque foreign bodies.
3) Barium enemas help to localize the area of colon obstruction.
4) In suspected cases of obstruction, radiologists use oral barium cautiously because of
the inspissation of the barium above the obstruction.
  Laboratory examinations:
1) Blood studies: In the early stages, laboratory examinations may be normal; with
progression of disease, there are hemoconcetration, leukocytosis,and electrolyte
abnormalities. Serum amylase may be slightly elevated.
2) Urinalysis: Glycosuria or proteinuria should indicate the paralytic ileus caused by
diabetic acidosis or primary renal disease.
10. Diagnosis:
 Is there intestinal obstruction or not? According to symptoms (abdominal pain, vomiting,
abdominal distention, obstipation), signs and X-ray, Intestinal obstruction can be
diagnosed in most patients.
 Is it mechanical obstruction or paralytic ileus?
Paralytic ileus Mechanical Obstruction
Cause Peritoneal irritation. Hernia, Adhesions, Tumors.
Site Entire bowel is dilated. Dilatation proximal to
obstruction.
Clinical findings Distension,vomiting,obstip- Cramping pain, Distension,
ation;silent abdomen; vomiting, obstipation;
abdomen may or may not hyperactive bowel sounds
be tender. at first; later silent
abdomen.
X-ray findings Gas throughout Gas and fluid proximal to
obstruction. No gas distal to
obstruction.
Treatment Conservative with Operative release or bypass
treatment of the cause of of the obstruction.
the ileus.
 Is it simple or strangulated intestinal obstruction? Since stragulation obstruction
requires immediate operative treatment,the physician must constantly look for these
five diagnostic features: when intermittent, coliky pain becomes steady and unrelenting;
when abdominal tenderness (and rebound) become evident; when a mass becomes
palpable; when the temperature and pulse increase; and when laboratory studies
suggest acute inflammation.
 Is it partial or complete intestinal obstruction? For partial intestinal obstruction,
obstipation is not absolute. However,complete obstruction usually produces eventual
failure to pass either gas or feces.
  Is it upper or lower intestinal obstruction?
1) Differentiating colon from small bowel obstruction depends on radiographic
evidence, either plain abdominal films or barium enema demonstration of an
obstructing lesion of the colon.
2) Obstruction in an older patient with no hernia or previous abdominal operations and
with distension and no vomit, usually indicates carcinoma of the large bowel.
3) Sharp frequent abdominal cramps, severe vomiting, and early fluid and electrolyte
imbalance are suggestive of small bowel obstruction.
 What causes the intestinal obstruction? Adhesions, Hernias, Neoplasm, Others.
11. Treatment:
 Partial intestinal obstruction can be treated expectantly as long as there is continued
passage of stool and flatus. Plain abdominal x-rays show gas in the colon, and small
bowel contrast x-ray proves the diagnosis. Decom-pression with a nasogastric or long
intestinal tube (ileus tube) is successful in 90% of such patients. Operation is required if
obstruction persists for several days even though it is incomplete.
 Complete intestinal obstruction is treated by operation after a short period of careful
[Link] compelling reason for operation is that strangulation cannot be
excluded with certainty, and strangulation is associated with high rates of complications
and death.
 There are exceptions to the general rules that operation must be performed promptly:
Incomplete obstruction, postoperative obstruction, a history of numerous previous
operations for obstruction, radiation therapy, inflammatory bowel disease and
abdominal carcinomatosis are situations demanding mature judgment, and judicious
nonoperative management may be in the patient’s best interests.
12. General treatment:
 Nasogastric suction: Nasogastric tube should be inserted immediately upon admission
to the emergency ward in order to relieve vomiting, avoid aspiration, and reduce the
contribution of further swallowed air to the abdominal distention.
 Fluid and electrolyte resuscitation: Depending upon the level and duration of
obstruction, fluid and electrolyte deficits are mild to severe. Losses of gastrointestinal
fluid also entail acid-base deficits.
 Antibiotics treatment: Antibiotics should be given if strangulation is even remotely
suspected.
13. Operation: Operation may commence when the patient has been rehydrated and vital
organs are functioning satisfactorily. Occasionally, the toxic effects of strangulation may
force operation at an earlier time. Details of the operative procedure vary according to the
cause of obstruction.