VII.

PATHOPHYSIOLOGY

Episodes of Low fiber Diet

constipation Male

Occlusion of foreign body

to the appendix

↑ Intra luminal Pressure

Vasocongestion

↓ Blood supply in the

appendix

↓ Oxygen supply in the

appendix

Disruption of cell
membrane of appendix

Start of Inflammatory
process

RLQ
Abdominal pain, Inflammation of appendix
Vomiting

Rupture of appendix

Release of fecal materials Hypoactive

↓ Peristalsis
in the abdomical cavity bowel sounds

Abdominal
Secondary Peritonitis
distention

Hyperthermia
↑ Immune response
↑ WBC

Release of chemical
mediators
(macrophages, fibrin, blood cells)

Adhesions

Intestinal obstruction

Ischemia of the bowel wall

Exploratory
Necrosis of the intestine
Lapatoromy

49 | Pathophysiology
 Delayed wound
Hypoalbuminemia
healing

Disruption of
anastamosis

yellowish abdominal
Anastamosis leak
secretion

Tertiary Peritonitis

Bipedal Edema Third space fluid Cardiogenic ↑ Pulse rate

Septic Shock Delayed capillary
Poor skin turgor shift shock refill

Cardiac
Hypovolemic shock Vasodilation
contractility

Decrease venous
return

Low cardiac output

Blood pressure of
Hypotension
70/50 mmhg

Microcirculatory
changes
Poor perfusion of vital
organ

Inability to Major organ

Decrease oxygen
utilize/remove dysfunction
delivery
metabolic waste acidosis

↓ Oxygen Subcellular
and cellular ↓ Urine production
saturation
injury ↑ Urine concentration
Constipation

Release of toxic products

Down regulation of oxygen metabolism
Failure of energy production
acidosis Septicemia

DEATH

50 | Pathophysiology
Interpretation:

The appendix is a small, finger-like appendage attached to the cecum just below

the ileocecal valve. Because it empties into the colon inefficiently and its lumen is small,

it is prone to becoming obstructed and vulnerable to infection.

The factors that increases the risk of the patient of having appendicitis is that he is

a male having episodes of constipation, and consuming a low fiber diet. These factors

might contribute to the occlusion of foreign body to the appendix. Once occlusion

happens, an increase in intra luminal pressure and vasocongestion occurs. This decreases

the blood supply as well as oxygen supply in the appendix which will disrupt the cellular

membrane and functions. Due to the disruption of the cell membrane of appendix,

inflammation of the appendix occurs as manifested by right lower quadrant abdominal

pain and vomiting.

Once rupture, the appendix releases fecal materials in the abdominal cavity,

which causes a decrease in peristaltic movement and secondary peritonitis.

The release of fecal materials in the abdominal cavity causes a decrease in peristaltic

movement due to increase gas and fluid content as evidence by abdominal distention and

hypoactive bowel sounds.

Secondary Peritonitis occurs as an inflammatory response of the peritoneum

secondary to rupture of underlying organs. Because peritoneum is particularly well

adapted for producing an inflammatory response, hyperthermia, and increase white blood

cell count is evident. Release of chemical mediators such as macrophages, fibrin, and

blood cell adheres to structures (adhesions) to seal of the appendix and localized the

51 | Pathophysiology
infection. Localization is enhanced by sympathetic stimulation that limits intestinal

motility and leads to obstruction of the intestines. Intestinal obstruction causes the bowel

wall to be ischemic. Ischemia leads to necrosis of the intestine.

Surgical management such as exploratory laparotomy was done to remove the

ruptured appendix and intestines. Resection and anastomosis of the distal ileus to prevent

further necrosis of the intestine. Due to poor compliance to medication and treatment

course, hypoalbuminea occurs. Albumin is a protein responsible for wound healing; a

decrease will cause a delay in the process of wound healing. Due to hypoalbuminea, a

disruption in the anastomosis and leaking happens as evidence by yellowish abdominal

secretions that lead to tertiary peritonitis.

Tertiary peritonitis is an inflammation of the peritoneum after a surgical

procedure to control secondary peritonitis. It leads to more serious complications because

it affects other bodily functions and patient may die because of generalized septicemia.

Tertiary peritonitis causes fluids to shift to the extravascular space as evidence by

poor skin turgor and edema. It also causes vasodilation and an increase in cardiac

contractility as evidence by increase pulse rate and delayed capillary refill. Decrease

venous return and cardiac contractility and vasodilation results to a low cardiac output.

Hypotension and changes in the microcirculatory functions such as poor perfusion of

vital organ happens. Major organ dysfunction, release of toxic products, down regulation

of oxygen metabolism, failure of energy production and acidosis are subcellular and

cellular injury that may result to septicemia and eventually the death of the patient.

52 | Pathophysiology