Anatomy of intestines, appendix, greater omentum, peritoneum and

abdominal wall.
Physiology of vomiting
Vomiting is the forceful ejection of stomach and intestinal content from the
mouth.
Can be caused by cerebral cause, visceral cause or altering in body chemistry.
1. Irritation of mucosal of upper GIT
2. Afferent nuclei from vestibular nuclei mediate nausea and vomiting of motion
sickness
3. Psychological sensory stimuli produce emetic response in vomiting centre
4. Chemoreceptor trigger zone in medulla detect changes in body pH.
5. Serotonin from enterochromaffin cells in small intestine trigger vomiting.
Before vomiting, nausea is felt. Stomach musculature is relaxed. Deep inspiration
takes place with closing of glottis and rising of soft palate. Sudden increase in
abdominal pressure brought by contraction of abdominal muscle. Violent
contraction of diaphragm and abdominal muscle compressing the stomach. This
forces gastric contents through relaxed stomach and oesophagus into mouth.
Physiology of peristalsis of intestine
Intestinal motility is controlled by peristalsis contraction, segmentation
contraction and tonic contraction. Peristalsis propels the chyme towards large
intestine. Segmentation contraction move the chyme to and fro, also increase its
exposure to the mucosal surface to facilitate digestion and absorption.
Ileum is linked to caecum by ileocaecal valve that restricts the reflux of colonic
content. Each time peristaltic wave reaches it, it open briefly, permitting some
chyme to squeeze into the caecum. When food leaves the stomach, the caecum
relaxes and passage of chyme across the ileocaecal valve increases, which is
known as gastroileal reflex.
Pathogenesis of appendicitis
Stages of appendicitis
1. Early stage- Obstruction of appendiceal lumen can be caused by lymphoid
hyperplasia, faecalith, foreign bodies, parasitic worm infection or inflammatory
stricture. Obstruction of appendix will cause fluid and mucus accumulation,
causing increased intraluminal pressure. This leads to bacterial growth within the
trapped mucous (as it is a good cultural environment) and appendiceal
distention. Acute inflammatory response occurs as the bacteria can produce
toxin and stimulate the aggregation of inflammatory cytokines. Inflammatory
response will cause oedema. Visceral nerve fibres are stimulated which patient
perceives as periumbilical pain, as the nerve that innervates the appendix and
umbilical dermatome is the same (T10).

3. and could be even worsened by motion sickness due to the road condition. It is a protective mechanism to propel the obstructed material inside intestine.Increasing intraluminal pressure and oedema will exceed the capillary perfusion pressure. which is continuous and more severe than early pain. The inflammatory response causing swelling of lymph nodes which will further obstruct the lumen of appendix. causing inflammation on the overlying parietal peritoneum.When the arterial blood flow become fully compromised by the inflammation and oedema. This results in more inflammatory fluid invasion and bacterial growth. The second pain is felt only when the inflammation has gone transmural and eventually penetrates through the serosal surface. Pain at periumbilical region is because of inflammation of appendix. Suppurative appendicitis.The perforated appendix can be walled off by adjacent greater omentum.2. could be also indicating the inflammation has been spread to peritoneum layer causing peritonitis. The second pain that shifted to the right iliac fossa is due to the inflammation of the underlying parietal peritoneum beneath the skin. this will lead to tissue ischemia and gangrenous appendicitis. Tenderness (increased pain sensitivity) over right iliac fossa is due to swelling of appendix pushes the parietal layer of peritoneum to abdominal wall. Pathophysiology of appendicitis Nausea and vomiting is caused by intestinal obstruction and increased luminal pressure. 4. This helps in development of peritoneal irritation. When the inflamed serosa of appendix comes in contact with the parietal peritoneum. The peritoneum has its own somatic innervation so the well localised pain is felt. resulting in perforation with release of faecal and suppurative content into peritoneal cavity. Persisting tissue ischaemia in appendiceal infarction will cause full thickness necrosis of appendiceal wall. Oedema and venous congestion will cause the inflammatory response goes transmural. Abscess formation and peritonitis. as ischaemic condition starts to occur in the entire appendix. which its autonomic nerve is derived from the supply of T10. thus increase its somatic pain sensitivity upon palpation. perforation is free is peritoneal cavity and generalised peritonitis can occur. Gangrenous and perforated appendicitis. . Could be also caused by increased abdominal pressure due to swollen appendix pressing the intestine. patient will experience classic shift of pain from periumbilicus to the right lower abdominal quadrant. A localised walled-off abscess occurs. If the pathological condition rapidly advanced. The condition worsen when the patient takes 5 hours journey to the hospital because the inflammation has developed to the serious stage. The pain is referred because the periumbilical region is innervated by the same T10 level somatic sensory nerve.

Abdominal pain . But after some time. metronidazole and cefuroxime Ampicillin has activity against gram-positive. Cefuroxime is second generation cephalosporin.Migration of pain from abdominal wall to right lower quadrant of abdomen . It is an indication of peritonitis. It is an involuntary response to prevent pain caused by the pressure on abdomen. Cloxacillin has similar target bacterial and similar function. Signs and symptoms of appendicitis . Metronidazole is an antibiotic for anaerobes and antiprotozoal medication. act against aerobic gram positive and gram negative cocci and bacilli.Sensitive to gentle touch on abdominal wall. It can interfere the bacterial cell wall synthesis during active replication. impairing gastric emptying process to reduce peristaltic activity of small bowel. the greater omentum will adhere to the perforated appendix to minimise the spread of inflammation to peritoneum. gram-negative and anaerobic bacteria. swelling of peritoneum pushes it towards the abdomen wall causing pain). It inhibits nuclei acid synthesis by disrupting the DNA of microbial cells. Rigidity on abdomen upon arrival to hospital indicates that the peritonitis has generalised over the lower part of abdomen. cloxacillin.Rebound tenderness is due to releasing of stretched parietal layer of peritoneum. This function only happens when metronidazole is partially reduced and this reduction can only happen in anaerobic cells.Vomiting . Cefuroxime interfere bacterial cell wall synthesis and is bactericidal. pain felt upon application of pressure . indicating generalised peritonitis. Fibrinous material seen around the ileo-caecal region and right paracolic gutter is due to inflammation triggering fibrosis.Fever . causing tenderness and rebound tenderness at right iliac fossa at first. rigidity of abdomen is felt because the inflammation has diffusedly spread around the lower abdomen (when inflammation. but less susceptible to beta-lactamase. Pharmacology of ampicillin.Nausea . Lack of bowel sound is due to triggering of ileo-gastric reflex. This is to stop the movement of chyme towards the small intestine to prevent further blockage. *Initially after the appendix rupture. causing pain when the parietal peritoneum hit back on abdominal wall.

Food bolus). forming faecaliths. These infections can further causing swelling and inflammation of lymph vessels (lymphangitis) and lymph nodes (lymphadenitis). Swelling of lymph node can further worsen the obstruction of appendix.- Rebound tenderness on abdominal wall. Obstruction in GI tract particularly appendix can cause bacterial growth and infection. When obstruction occurs. pain felt upon removal of pressure Loss of appetite Diarrhea or constipation Some patients might have accessory signs such as  Rovsing sign (RLQ pain with palpation of the LLQ): Suggests peritoneal irritation  Obturator sign (RLQ pain with internal and external rotation of the flexed right hip): Suggests the inflamed appendix is located deep in the right hemipelvis  Psoas sign (RLQ pain with extension of the right hip or with flexion of the right hip against resistance): Suggests that an inflamed appendix is located along the course of the right psoas muscle  Dunphy sign (sharp pain in the RLQ elicited by a voluntary cough): Suggests localized peritonitis  RLQ pain in response to percussion of a remote quadrant of the abdomen or to firm percussion of the patient's heel: Suggests peritoneal inflammation  Markle sign (pain elicited in a certain area of the abdomen when the standing patient drops from standing on toes to the heels with a jarring landing): Has a sensitivity of 74% Causes Caused by primary obstruction of lumen of appendix. intestinal worms. This creates a good environment for bacterial growth. The causative agents of obstruction including bezoar (a mass trapped in GI tract eg. lymphadenitis and calcified faecal deposits (faecaliths). Swelling and oedema of appendix will cause thrombosis and occlusion of small vessels and stasis of lymphatic flow. Bacteria will leak out from dying walls. foreign bodies. This will result in appendiceal rupture causing peritonitis. Continued production of mucous and inflammation leads to increased pressure within the lumen and walls of appendix. Calcium salts and faecal debris will form layered material around appendix. trauma. appendix filled with mucous and swells. forming pus around and within the appendix. When there is occlusion of blood vessels. appendix will progress to ischaemic condition and necrosis occurs. Diagnosis . Colonisation of bacteria causes inflammation. Obstruction in appendix is thought to be contributed by faecal retention in colon and prolonged transit time.

Complete blood count.Bowel obstruction . Treatment and management .Appendectomy is the only curative treatment of appendicitis.Sepsis .C-reactive protein count. But CRP count is not specific and does not distinguish between infection and inflammation. For visualisation of appendicoliths in patient associated with appendicitis. Risk factors Refer to cause Preventions It is not possible to prevent appendicitis. But delayed diagnosis and treatment can cause mortality and morbidity associated with appendicitis.Antibiotics prophylaxis should be administered before appendectomy to prevent septicaemia. Overall mortality rate is around 0. Used for confirmation of appendicitis. Epidemiology Many people sakit perut. Absent or incomplete filling of appendix coupled with pressure effect (due to obstruction) suggests appendicitis. Neutrophilia and leucocytosis is seen most patient of appendicitis.Complicated peritonitis Prognosis Good prognosis.Urinalysis.CT scan. Some patients might have blood or pus in the urine. . .. Its measurement could be an early marker of appendicitis. . Some patients may have dysuria or right flank pain. . Perforation and gangrenous appendicitis can cause higher morbidity rate. High CRP especially in patient progressing to gangrene stage of appendicitis.Abdominal or pelvic abscess .Preoperative antibiotics have efficacy in decreasing postoperative wound infection rates.Barium enema study. MRI and ultrasound. . . .Urinary 5-HIAA.Kidneys-ureters-bladder radiographs. this could increase the obstruction. Patients with suspected appendicitis should not be given anything by mouth. CT scan not recommended for children because of its radiation exposure.2 to 0. . Can be used to differentiating appendicitis from UTI.8% attributable complications of disease rather than surgery. .Broad-spectrum antibiotics for aerobic and anaerobic microorganism coverage. . Complications . But the blood test is not specific.Wound infection or dehiscence after surgery .