Patofisiologi

Nyeri ulu hatiObstruksi → distensi lumen yang berlebihan / spasme otot polos dinding appendix → Impuls yang diterima reseptor regang berjalan di dalam serabut syaraf aferen (Slow conducting C fibers) yang mengikuti serabut syaraf simpatis Plexus mesentericus superior dan nervus splanchnicus minor ke medulla spinalis (segmen T10) → Menimbulkan sensasi nyeri yang tidak terlokalisisr dengan baik di daerah periumbilical dan epigastrium → Nyeri ulu hati (KASUS)

Nyeri perut kanan bawah

Nyeri perut kanan bawah pada kasus disebabkan oleh meluasnya proses peradangan pada appendiks vermiformis yang mengenai peritoneum parietal setempat.

Hiperplasia folikel limfoid, fekalit, benda asing, striktur karena perdangan sebelumnya, neoplasma → penyumbatan lumen appendix → mucus terbendung → tekanan intralumen ↑ → menghambat aliran limfe → edema, diapedesis bakteri, dan ulserasi mukosa → appendicitis akut fokal ( nyeri epigastrium) → jika berlanjut → tekanan makin meningkat → obstruksi vena → edema ↑ dan bakteri menembus dinding → peradangan meluas → merangsang peritoneum parietal → nyeri di daerah kanan bawah perut.

Mual dan muntahPeradangan apendiks → peregangan lumen, spasme otot apendiks → stimulasi N. vagus → pusat muntah di medula → Impuls motorik oleh n. kranialis V, VII, IX, X, dan XII pada saluran pencernaan dan melalui saraf spinal ke diafragma dan dinding abdomen → Mual dan Muntah

DemamProses inflamasi pada appendiks → pelepasan sitokin (IL-1, IL-6, TNF α) → sitokin sampai di otak → mengaktivasi jalur asam arakidonat → menghasilkan PGE2 → meningkatkan set point termostat di hipotalamus → demam

Manifestasi KlinisApendisitis memiliki gejala kombinasi yang khas, yang terdiri dari : Mual, muntah dan nyeri yang hebat di perut kanan bagian bawah. Nyeri bisa secara mendadak dimulai di perut sebelah atas atau di sekitar pusar, lalu timbul mual dan muntah. Setelah beberapa jam, rasa mual hilang dan nyeri berpindah ke perut kanan bagian bawah. Jika dokter menekan daerah ini, penderita merasakan nyeri tumpul dan jika penekanan ini dilepaskan, nyeri bisa bertambah tajam. Demam bisa mencapai 37,8-38,8° Celsius.Pada bayi dan anak-anak, nyerinya bersifat menyeluruh, di semua bagian perut. Pada orang tua dan wanita hamil, nyerinya tidak terlalu berat dan di daerah ini nyeri tumpulnya tidak terlalu terasa. Bila usus buntu pecah, nyeri dan demam bisa menjadi berat. Infeksi yang bertambah buruk bisa menyebabkan syok.

ACUTE APPENDICITIS

INCIDENCE AND EPIDEMIOLOGY The peak incidence of acute appendicitis is in the

second and third decades of life; it is relatively rare at the extremes of age. Males and

females are equally affected, except between puberty and age 25, when males predominate in

a 3:2 ratio.

Perforation is more common in infancy and in the aged, during which periods mortality rates

are highest. The mortality rate has decreased steadily in Europe and the United States from

8.1 per 100,000 of the population in 1941 to _1 per 100,000 in 1970 and subsequently. The

absolute incidence of the disease also decreased by about 40% between 1940 and 1960 but

since then has remained unchanged. Although various factors such as changing dietary habits,

altered intestinal flora, and better nutrition and intake of vitamins have been suggested to

explain the reduced incidence, the exact reasons have not been elucidated. The overall

incidence of appendicitis is much lower in underdeveloped countries, especially parts of

Africa, and in lower socioeconomic groups.

PATHOGENESIS

Luminal obstruction has long been considered the pathogenetic hallmark. However,

obstruction can be identified in only 30 to 40% of cases; ulceration of the mucosa is the

initial event in the majority. The cause of the ulceration is unknown, although a viral etiology

has been postulated. Infection with Yersinia organisms may cause the disease, since high

complement fixation antibody titers have been found in up to 30% of cases of proven

appendicitis. Whether the inflammatory reaction seen with ulceration is sufficient to obstruct

the tiny appendiceal lumen even transiently is not clear. Obstruction, when present, is most

commonly caused by a fecalith, which results from accumulation and inspissation of fecal

matter around vegetable fibers. Enlarged lymphoid follicles associated with viral infections

(e.g., measles), inspissated barium, worms (e.g., pinworms, Ascaris, and Taenia), and tumors

(e.g., carcinoid or carcinoma) may also obstruct the lumen. Secretion of mucus distends the

organ, which has a capacity of only 0.1 to 0.2 mL, and luminal pressures rise as high as 60

cmH2O. Luminal bacteria multiply and invade the appendiceal wall as venous engorgement

and subsequent arterial compromise result from the high intraluminal pressures. Finally,

gangrene and perforation occur. If the process evolves slowly, adjacent organs such as the

terminal ileum, cecum, and omentum may wall off the appendiceal area so that a localized

abscess will develop, whereas rapid progression of vascular impairment may cause

perforation with free access to the peritoneal cavity. Subsequent rupture of primary

appendiceal abscesses may produce fistulas between the appendix and bladder, small

intestine, sigmoid, or cecum. Occasionally, acute appendicitis may be the first manifestation

of Crohn’s disease.

While chronic infection of the appendix with tuberculosis, amebiasis, and actinomycosis may

occur, a useful clinical aphorism states that chronic appendiceal inflammation is not usually

the cause of prolonged abdominal pain of weeks’ or months’ duration. In contrast, recurrent

acute appendicitis does occur, often with complete resolution of inflammation and symptoms

between attacks. Recurrent acute appendicitis may become more frequent as antibiotics are

dispensed more freely and if a long appendiceal stump is left after laparoscopic

appendectomy.

CLINICAL MANIFESTATIONS The history and sequence of symptoms are important

diagnostic features of appendicitis. The initial symptom is almost invariably abdominal pain

of the visceral type, resulting from appendiceal contractions or distention of the lumen. It is

usually poorly localized in the periumbilical or epigastric region with an accompanying urge

to defecate or pass flatus, neither of which relieves the distress. This visceral pain is mild,

often cramping, and rarely catastrophic in nature, usually lasting 4 to 6 h, but it may not be

noted by stoic individuals or by some patients during sleep. As inflammation spreads to the

parietal peritoneal surfaces, the pain becomes somatic, steady, and more severe, aggravated

by motion or cough, and usually located in the right lower quadrant. Anorexia is very

common; a hungry patient does not have acute appendicitis. Nausea and vomitin occur in 50

to 60% of cases, but vomiting is usually self-limited. The development of nausea and

vomiting before the onset of pain is extremely rare. Change in bowel habit is of little

diagnostic value, since any or no alteration may be observed, although the presence of

diarrhea caused by an inflamed appendix in juxtaposition to the sigmoid may cause serious

diagnostic difficulties. Urinary frequency and dysuria occur if the appendix lies adjacent to

the bladder. The typical sequence of symptoms (poorly localized periumbilical pain followed

by nausea and vomiting with subsequent shift of pain to the right lower quadrant)

occurs in only 50 to 60% of patients.

Physical findings vary with time after onset of the illness and according to the location of the

appendix, which may be situated deep in the pelvic cul-de-sac; in the right lower quadrant in

any relation to the peritoneum, cecum, and small intestine; in the right upper quadrant

(especially during pregnancy); or even in the left lower quadrant. The diagnosis cannot be

established unless tenderness can be elicited. While tenderness is sometimes absent in the

early visceral stage of the disease, it ultimately always develops and is found in any location

corresponding to the position of the appendix. Abdominal tenderness may be completely

absent if a retrocecal or pelvic appendix is present, in which case the sole physical finding

may be tenderness in the flank or on rectal or pelvic examination. Percussion, rebound

tenderness, and referred rebound tenderness are often, but not invariably, present; they are

most likely to be absent early in the illness. Flexion of theright hip and guarded movement by

the patient are due to parietal peritoneal involvement. Hyperesthesia of the skin of the right

lower quadrant and a positive psoas or obturator sign are often late findings and are rarely of

diagnostic value. When the inflamed appendix is in close proximity to the anterior parietal

peritoneum, muscular rigidity is present yet is often minimal early.

The temperature is usually normal or slightly elevated [37.2 to 38_C (99 to 100.5_F)], but a

temperature _38.3_C (101_F) should suggest perforation. Tachycardia is commensurate with

the elevation of the temperature. Rigidity and tenderness become more marked as the disease

progresses to perforation and localized or diffuse peritonitis. Distention is rare unless severe

diffuse peritonitis has developed. The disappearance of pain and tenderness just before

perforation is extremely unusual. A mass may develop if localized perforation has occurred

but will not usually be detectable before 3 days after onset.

Earlier presence of a mass suggests carcinoma of the cecum or Crohn’s disease. Perforation is

rare before 24 h after onset of symptoms, but the rate may be as high as 80% after 48 h.

Diagnosis is based primarily on clinical grounds. Although moderate leukocytosis of 10,000

to 18,000 cells/_L is frequent (with a concomitant left shift), the absence of leukocytosis does

not rule out acute appendicitis. Leukocytosis of _20,000 cells/_L suggests probable

perforation. Anemia and blood in the stool suggest a primary diagnosis of carcinoma of the

cecum, especially in elderly individuals. The urine may contain a few white or red blood cells

without bacteria if the appendix lies close to the right ureter or bladder. Urinalysis is most

useful in excluding genitourinary conditions that may mimic acute appendicitis.

Radiographs are rarely of value except when an opaque fecalith (5% of patients) is observed

in the right lower quadrant (especially in children). Consequently, abdominal films are not

routinely obtained unless other conditions such as intestinal obstruction or ureteral calculus

may be present. In some patients with recurrent or prolonged symptoms, computed

tomography (CT) may reveal an extrinsic defect on the medial wall of the cecum or a

calcified fecalith. The predictive value of CT scan in acute appendicitis is being evaluated.

The diagnosis may also be established by the ultrasonic demonstration of an enlarged and

thick-walled appendix. Ultrasound is most useful to exclude ovarian cysts, ectopic pregnancy,

or tuboovarian abscess. While the typical historic sequence and physical findings are present

in 50 to 60% of cases, a wide variety of atypical patterns of disease are encountered,

especially at the age extremes and during pregnancy. Infants under 2 years of age have a 70

to 80% incidence of perforation and generalized peritonitis. Any infant or child with diarrhea,

vomiting, and abdominal pain is highly suspect. Fever is much more common in this age

group, and abdominal distention is

often the only physical finding. In the elderly, pain and tenderness are

often blunted, and thus the diagnosis is frequently delayed and leads

to a 30% incidence of perforation in patients over 70. Elderly patients

often present initially with a slightly painful mass (a primary appendiceal

abscess) or with adhesive intestinal obstruction 5 or 6 days after

a previously undetected perforated appendix.

Appendicitis occurs about once in every 1000 pregnancies and is

the most common extrauterine condition requiring abdominal operation.

The diagnosis may be missed or delayed because of the frequent

occurrence of mild abdominal discomfort and nausea and vomiting

during pregnancy. During the last trimester, when the mortality rate

from appendicitis is highest, uterine displacement of the appendix to

the right upper quadrant and laterally leads to confusion in diagnosis

because pain and tenderness are similarly displaced.

DIFFERENTIAL DIAGNOSIS Appendicitis can be confused with any condition

that causes abdominal pain. Diagnostic accuracy is about 75 to

80% for experienced clinicians based solely on the clinical criteria

outlined. It is probably better to err slightly in the direction of overdiagnosis,

since delay is associated with perforation and increased

morbidity and mortality. In unperforated appendicitis, the mortality

rate is 0.1%, little more than that associated with general anesthesia;

for perforated appendicitis, overall mortality is 3% (15% in the elderly).

In doubtful cases, 4 to 6 h of observation is always more beneficial

than harmful. The most common conditions discovered at operation

when acute appendicitis is erroneously diagnosed are, in order

of frequency, mesenteric lymphadenitis, no organic disease, acute pelvic

inflammatory disease, ruptured graafian follicle or corpus luteum

281 Acute Appendicitis and Peritonitis 1807

TABLE 281-1 Conditions Leading to Secondary Bacterial Peritonitis

Perforations of bowel

Trauma, blunt or penetrating

Inflammation

Appendicitis

Diverticulitis

Peptic ulcer disease

Inflammatory bowel disease

Iatrogenic

Endoscopic perforation

Anastomotic leaks

Catheter perforation

Vascular

Embolus

Ischemia

Obstructions

Adhesions

Strangulated hernias

Volvulus

Intussusception

Neoplasms

Ingested foreign body,

toothpick, fish bone

Perforations or leaking of other

organs

Pancreas—pancreatitis

Gall bladder—cholecystitis

Urinary bladder—trauma, rupture

Liver—bile leak after biopsy

Fallopian tubes—salpingitis

Bleeding into the peritoneal cavity

Disruption of integrity of peritoneal

cavity

Trauma

Continuous ambulatory peritoneal

dialysis (indwelling catheter)

Intraperitoneal chemotherapy

Perinephric abscess

Iatrogenic—postoperative,

foreign body

cyst, and acute gastroenteritis. In addition, acute cholecystitis, perforated

ulcer, acute pancreatitis, acute diverticulitis, strangulating intestinal

obstruction, ureteral calculus, and pyelonephritis may present diagnostic

difficulties.

Differentiation of pelvic inflammatory disease from acute appendicitis

on clinical grounds may be virtually impossible. Gram-negative

intracellular diplococci on cervical smear are not pathognomonic unless

Neisseria gonorrhoeae can be cultured. Pain on movement of the

cervix is not specific and may occur in appendicitis if perforation has

occurred or if the appendix lies adjacent to the uterus or adnexa. Rupture

of a graafian follicle (mittelschmerz) occurs at midcycle and will

spill off blood and fluid to produce pain and tenderness more diffuse

and usually of a less severe degree than in appendicitis. Fever and

leukocytosis are usually absent. Rupture of a corpus luteum cyst is

identical clinically to rupture of a graafian follicle but develops about

the time of menstruation. The presence of an adnexal mass, evidence

of blood loss, and a positive pregnancy test help differentiate ruptured

tubal pregnancy, but a negative pregnancy test is present when tubal

abortion has occurred. Twisted ovarian cyst and endometriosis are occasionally

difficult to distinguish from appendicitis. In all these female

conditions, ultrasonography, laparoscopy, and occasionally CT may

be of great value.

Acute mesenteric lymphadenitis is the diagnosis usually given

when enlarged, slightly reddened lymph nodes at the root of the mesentery

and a normal appendix are encountered at operation in a patient

who usually has right lower quadrant tenderness. Whether this is a

single, discrete entity is unclear, since the causative factor is not

known. Some of these patients have infection with Y. pseudotuberculosis

or Y. enterocolytica, in which case the diagnosis can be established

by culture of the mesenteric nodes or by serologic titers (Chap.

143). The diagnosis is essentially impossible clinically, although retrospectively

these patients may have a higher temperature and more

diffuse pain and tenderness. Children seem to be affected more frequently

than adults. Acute gastroenteritis usually causes profuse watery

diarrhea, often with nausea and vomiting, but without localized

findings. Between cramps, the abdomen is completely relaxed. In Salmonella

gastroenteritis, the abdominal findings are similar, although

the pain may be more severe and more localized, and fever and chills

are common. The occurrence of similar symptoms among other members

of the family may be helpful. When the diagnosis of acute pelvic

appendicitis with perforation has been missed, gastroenteritis is the

most common previous working diagnosis. Persistent abdominal or

rectal tenderness should eliminate the diagnosis of gastroenteritis. Regional

enteritis (Crohn’s disease) is usually associated with a more

prolonged history, often with previous exacerbations regarded as episodes

of gastroenteritis unless the diagnosis has been established previously.

Meckel’s diverticulitis usually cannot be distinguished from

acute appendicitis but is very rare.

TREATMENT

Cathartics and enemas should be avoided if appendicitis is under consideration,

and antibiotics should not be administered when the diagnosis

is in question, since they will only mask the perforation. The

treatment is early operation and appendectomy as soon as the patient

can be prepared. Appendectomy is increasingly accomplished laparoscopically

and may have some benefits over the open technique.

Preparation for operation rarely takes more than 1 to 2 h in early

appendicitis but may require 6 to 8 h in cases of severe sepsis and

dehydration associated with late perforation. The only circumstance in

which operation is not indicated is the presence of a palpable mass 3

to 5 days after the onset of symptoms. Should operation be undertaken

at that time, a phlegmon rather than a definitive abscess will be found,

and complications from its dissection are frequent. Such patients

treated with broad-spectrum antibiotics, parenteral fluids, and rest usually

show resolution of the mass and symptoms within 1 week. Interval

appendectomy should be done safely 3 months later. Should the mass

enlarge or the patient become more toxic, drainage of the abscess is

necessary. The complications of subphrenic, pelvic, or other intraabdominal

abscesses usually follow perforation with generalized peritonitis

and can be avoided by early diagnosis of the disease.