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VII.

PATHOPHYSIOLOGY
Episodes of
constipation

Low fiber Diet


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,
Vomiting

Inflammation of appendix

Rupture of appendix

Hyperthermia
WBC

Release of fecal materials


in the abdomical cavity

Peristalsis

Secondary Peritonitis

Abdominal
distention

Hypoactive
bowel sounds

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

Adhesions
Intestinal obstruction
Ischemia of the bowel wall

Necrosis of the intestine

Exploratory
Lapatoromy

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Hypoalbuminemia

Delayed wound
healing
Disruption of
anastamosis
Anastamosis leak

yellowish abdominal
secretion

Tertiary Peritonitis
Bipedal Edema
Poor skin turgor

Third space fluid


shift

Septic Shock

Cardiogenic
shock

Hypovolemic shock

Vasodilation

Cardiac
contractility

Pulse rate
Delayed capillary
refill

Decrease venous
return
Low cardiac output

Hypotension

Blood pressure of
70/50 mmhg

Microcirculatory
changes
Poor perfusion of vital
organ

Inability to
utilize/remove
metabolic waste

Decrease oxygen
delivery
Oxygen
saturation

Subcellular
and cellular
injury
Release of toxic products
Down regulation of oxygen metabolism
Failure of energy production
acidosis

Major organ
dysfunction
acidosis
Urine production
Urine concentration
Constipation

Septicemia
DEATH

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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