Professional Documents
Culture Documents
Victoria Pemicu 4 Blok GIT
Victoria Pemicu 4 Blok GIT
Victoria (405080027)
Acute abdomen
Neonate Colic Dietary protein allergy Volvulus Necrotizing enterocolitis Testicular torsion Adhesions
2 months-2 years Gastroenteritis Viral illness Trauma (including inflicted injury) Incarcerated hernia Intussusception Urinary tract infection Foreign body ingestion Sickle cell syndrome vasoocclusive crisis Dietary protein allergy Tumor
2-5 years Gastroenteritis Viral illness Trauma (including inflicted injury) Appendicitis Pharyngitis Constipation Urinary tract infection Pneumonia Intussusception Foreign body ingestion
>5 year s Gastroenteritis Viral illness Appendicitis Trauma Constipation Pharyngitis Pneumonia Urinary tract infection Diabetic ketoacidosis Sickle cell syndrome vasoocclusive crisis Henoch Schnlein purpura
Neonate
2 months-2 years Hirschsprung disease Adhesions Hemolytic uremic syndrome Toxin Meckel's diverticulum Hepatitis
2-5 years Sickle cell syndrome vasoocclusive crisis Henoch Schnlein purpura Ovarian torsion Intraabdominal abscess Tumor Adhesions Hemolytic uremic syndrome Hepatitis Meckel's diverticulum Toxin Primary bacterial peritonitis
>5 year s Ovarian torsion Testicular torsion Inflammatory bowel disease Intraabdominal abscess Ruptured ovarian cyst Cholecystitis Pancreatitis Urolithiasis Hepatitis Meckel's diverticulum Perforated ulcer Adhesions Hemolytic uremic syndrome Myocarditis, pericarditis Primary bacterial peritonitis
life-threatening causes
Trauma Appendicitis Intussusception Malrotation with midgut volvulus Incarcerated inguinal hernia Adhesions Necrotizing enterocolitis Peptic ulcer disease Ruptured ovarian cyst Ectopic pregnancy Pelvic inflammatory disease Foreign body ingestion
Hemolytic uremic syndrome (HUS) typically develops after an infection with Shiga toxin-producing enterohemorrhagic E. coli (EHEC) or Shigella .HUS has also been associated with pneumococcal infection, HIV, and genetic factors. Clinical features of HUS include hemolytic anemia, thrombocytopenia, and acute renal injury. Primary bacterial peritonitis, usually caused by Streptococcus pneumoniae or E. coli, is a life-threatening infectious complication of nephrotic syndrome. Myocarditis may cause abdominal pain as the result of passive hepatic congestion from heart failure. Pericarditis may cause referred abdominal pain.
Common cause
Constipation Gastrointestinal infection Other infections
Urinary tract infections Streptococcal pharyngitis Pneumonia Viral illnesses Colic
Pathophysiology
Visceral pain Somatic pain Referred pain Peritonitis
Pathophysiology
Visceral pain comes from the abdominal viscera, which are innervated by autonomic nerve fibers and respond mainly to the sensations of distention and muscular contractionnot to cutting, tearing, or local irritation. Visceral pain is typically vague, dull, and nauseating. It is poorly localized and tends to be referred to areas corresponding to the embryonic origin of the affected structure. Foregut structures (stomach, duodenum, liver, and pancreas) cause upper abdominal pain. Midgut structures (small bowel, proximal colon, and appendix) cause periumbilical pain. Hindgut structures (distal colon and GU tract) cause lower abdominal pain.
Pathophysiology
Somatic pain comes from the parietal peritoneum, which is innervated by somatic nerves, which respond to irritation from infectious, chemical, or other inflammatory processes. Somatic pain is sharp and well localized.
Referred pain is pain perceived distant from its source and results from convergence of nerve fibers at the spinal cord. Common examples of referred pain are scapular pain due to biliary colic, groin pain due to renal colic, and shoulder pain due to blood or infection irritating the diaphragm.
Pathophysiology
Peritonitis: Peritonitis is inflammation of the peritoneal cavity. The most serious cause is perforation of the GI tract, which produces immediate chemical inflammation followed shortly by infection from intestinal organisms. Peritonitis can also result from any abdominal condition that produces marked inflammation (eg, appendicitis, diverticulitis, strangulating intestinal obstruction, pancreatitis, pelvic inflammatory disease, mesenteric ischemia). Intraperitoneal blood from any source (eg, ruptured aneurysm, trauma, surgery, ectopic pregnancy) is irritating and results in peritonitis. Barium causes severe peritonitis and should never be given to a patient with suspected GI tract perforation.
Pathophysiology
Peritonitis: Peritoneo-systemic shunts, drains, and dialysis catheters in the peritoneal cavity predispose a patient to infectious peritonitis, as does ascitic fluid. Rarely, spontaneous bacterial peritonitis occurs, in which the peritoneal cavity is infected by blood-borne bacteria. Peritonitis causes fluid shift into the peritoneal cavity and bowel, leading to severe dehydration and electrolyte disturbances. Adult respiratory distress syndrome can develop rapidly. Kidney failure, liver failure, and disseminated intravascular coagulation follow. The patient's face becomes drawn into the masklike appearance typical of hippocratic facies. Death occurs within days.
Yes suggests recurrent problems such as ulcer disease, gallstone colic, diverticulitis, or mittelschmerz Sudden: like a light switching on (perforated ulcer, renal stone, ruptured ectopic pregnancy, torsion of ovary or testis, some ruptured aneurysms) Less sudden: most other causes
Severe pain (perforated viscus, kidney stone, peritonitis, pancreatitis) Pain out of proportion to physical findings (mesenteric ischemia)
Right scapula (gallbladder pain) Left shoulder region (ruptured spleen, pancreatitis) Pubis or vagina (renal pain) Back (ruptured aortic aneurysm)
Vomiting precedes pain and is followed by diarrhea (gastroenteritis) Delayed vomiting, absent bowel movement and flatus (acute intestinal obstruction; the delay increases with a lower site of obstruction) Severe vomiting precedes intense epigastric, left chest, or shoulder pain (emetic perforation of the intraabdominal esophagus)
Red Flags
Severe pain Signs of shock (eg, tachycardia, hypotension, diaphoresis, confusion) Signs of peritonitis Abdominal distention
Interpretation
Distention, especially when surgical scars, tympany to percussion, and high-pitched peristalsis or borborygmi in rushes are present, strongly suggests bowel obstruction. Severe pain in a patient with a silent abdomen who is lying as still as possible suggests peritonitis; location of tenderness suggests etiology (eg, right upper quadrant suggests cholecystitis, right lower quadrant suggests appendicitis) but may not be diagnostic
Back pain with shock suggests ruptured abdominal aortic aneurysm (AAA), particularly if there is a tender, pulsatile mass. Mild to moderate pain in the presence of active peristalsis of normal pitch suggests a nonsurgical disease (eg, gastroenteritis) but may also be the early manifestations of a more serious disorder
Ileus
hypomotility of the gastrointestinal tract in the absence of mechanical bowel obstruction
Epidemiology
20% of admissions due to acute abdominal pain are due to intestinal obstruction. Of these, approximately 80% have small intestinal obstruction 16% of colorectal malignancies present with obstruction
Etiology
Sepsis Drugs (eg, opioids, antacids, warfarin, amitriptyline, chlorpromazine) Metabolic (eg, low potassium, magnesium, or sodium levels; anemia; hyposmolality) Myocardial infarction Pneumonia Trauma (eg, fractured ribs, fractured spine) Biliary colic and renal colic Head injury and neurosurgical procedures Intra-abdominal inflammation and peritonitis Retroperitoneal hematomas
Macam ileus
Nyeri Usus
Distensi
Muntah borborigmi
Bising usus
Ketegangan abdomen
++ (kolik)
+++
Meningkat
+++ (Kolik)
+++
+ Lambat, fekal
Meningkat
Obstruksi strangulasi
++
+++
+ +++++
++++ +++
+ +++
Menurun Menurun
Mechanical ileus
Is mechanical or organic obstruction of the small intestine or colon and maybe complete or partial (subacute obstruction) Its commonly caused by fibrous bands and adhesion, hernias, malignant disease, impacted faeces or inflammatory bowel disease In the short duration of obstruction some gas may be seen in loops of intestine distal to the site In the long duration of obstruction no gas in the distal obstruction
Distention of the intestine is caused by the accumulation of gas and fluid proximal to and within the obstructed segment. Between 70 and 80% of intestinal gas consists of swallowed air, and because this is composed mainly of nitrogen, which is poorly absorbed from the intestinal lumen, removal of air by continuous gastric suction is a useful adjunct in the treatment of intestinal distention. The accumulation of fluid proximal to the obstructing mechanism results not only from ingested fluid, swallowed saliva, gastric juice, and biliary and pancreatic secretions but also from interference with normal sodium and water transport. During the first 1224 h of obstruction, a marked depression of flux from lumen to blood occurs of sodium and consequently water in the distended proximal intestine. After 24 h, sodium and water move into the lumen, contributing further to the distention and fluid losses. Intraluminal pressure rises from a normal of 24 cmH2O to 810 cmH2O. The loss of fluids and electrolytes may be extreme, and unless replacement is prompt, hypovolemia, renal insufficiency, and shock may result. Vomiting, accumulation of fluids within the lumen, and the sequestration of fluid into the edematous intestinal wall and peritoneal cavity as a result of impairment of venous return from the intestine all contribute to massive loss of fluid and electrolytes.
The most feared complication of acute intestinal obstruction is the presence of a "closed loop." Closed-loop obstruction of the small intestine results when the lumen is occluded at two points by a single mechanism such as a fascial hernia or adhesive band, thus producing a closed loop whose blood supply is often occluded by the hernia or band as well. During peristalsis, when a "closed loop" is present, pressures reach 3060 cmH2O. Strangulation of the closed loop is common in association with marked distention proximal to the involved loop. A form of closed-loop obstruction is encountered when complete obstruction of the colon exists in the presence of a competent ileocecal valve (85% of individuals). Although the blood supply of the colon is not entrapped within the obstructing mechanism, distention of the cecum is extreme because of its greater diameter (Laplace's law), and impairment of the intramural blood supply is considerable, with consequent gangrene of the cecal wall. Once impairment of blood supply to the gastrointestinal tract occurs, bacterial invasion supervenes, and peritonitis develops. The systemic effects of extreme distention include elevation of the diaphragm with restricted ventilation and subsequent atelectasis. Venous return via the inferior vena cava may also be impaired.
Presentation
History Diffuse, central abdominal pain of a colicky nature. Pain is less or absent in paralytic ileus but there may be a history to suggest causes. Vomiting tends to be early in high level obstruction. Faeculent vomiting is extremely unpleasant and is limited to low obstruction Abdominal distension: the lower the level of obstruction Absolute constipation is early in low obstruction and late in high-level obstruction. In paralytic ileus there is no bowel movement and no flatus. In sigmoid volvulus the picture is rather like large bowel obstruction with pain, constipation, late vomiting and a very marked degree of abdominal distension. Half of such patients will have had a previous episode. Severe pain and tenderness suggests ischaemia or perforation.
Examination
Look for signs of dehydration such as poor peripheral perfusion, tachycardia and hypotension. Abdominal distension will be apparent. Massive peristalsis may even by visible. Distended bowel is very resonant on percussion If strangulation or perforation occurs there will be features of an acute abdomen with peritonism. Check hernial orifices Bowel sounds
In obstruction very active and tinkling In ileus silent or nearly so
The patient may be generally toxic and unwell because ischaemia of the bowel allows bacteria and toxins to enter the circulation.
Workup
Fluid charts
are required to monitor intake and output, especially as an intravenous infusion is almost certainly required, a nasogastric tube may be passed and oliguria is an important sign of early dehydration
Blood should be taken for full blood count, urea, electrolytes and creatinine. Glucose may be slightly elevated by stress but very high levels are a cause for concern. Water-soluble contrast may also be helpful in small bowel obstruction due to adhesions. CT scanning
To predict the need for surgery in small bowel obstruction Patients with peritoneal fluid evident on CT scan are three times more likely to require surgical intervention than those who do not have this sign Partial obstruction may not be detected on CT and suspicion should remain high if the clinical picture suggests obstruction despite a normal scan
MRI and ultrasound have been found useful in the diagnosis of small bowel obstruction
A thin barium upper gastrointestinal series may help to differentiate partial from complete obstruction. However, thick barium given by mouth should be avoided when the obstruction is considered to be high grade or complete since retained barium sulfate may become inspissated. CT is the most commonly used modality to evaluate postoperative patients for intestinal obstruction because of its ability in differentiating adynamic ileus, partial obstruction, and complete obstruction (Fig. 293-1). However, the sensitivity and specificity of CT for strangulating obstruction are low (50 and 80%, respectively
Treatment
NGT IV fluids Treatment involves continuous nasogastric suction, npo status, IV fluids and electrolytes, a minimal amount of sedatives, and avoidance of opioids and anticholinergic drugs. Maintaining an adequate serum K level (> 4 mEq/L [> 4 mmol/L]) is especially important. Ileus persisting > 1 wk probably has a mechanical obstructive cause, and laparotomy should be considered. Sometimes colonic ileus can be relieved by colonoscopic decompression; rarely, cecostomy is required. Colonoscopic decompression is helpful in treating pseudo-obstruction (Ogilvie's syndrome), which consists of apparent obstruction at the splenic flexure, although no cause can be found by contrast enema or colonoscopy for the failure of gas and feces to pass this poin
Treatment
Paralytic ileus Is usually self-limiting and is initially treated conservatively Recovery may be expedited with intravenous fluid replacement and gastric aspiration Mechanical ileus Is treated similarly but surgery should be carried out as soon as the patients condition allows Strangulation or infarction surgery Peritonitis antibacterial drugs Nasogastric decompression abdominal distention associated with pain or to relieve recurrent vomiting Ileus after abdominal surgical procedures usually results in return of normal intestinal motility within 24-72 hr. Prokinetic agents may stimulate the return of normal bowel motility and be of assistance to children with prolonged ileus. metoclopramide erythromycin
DD Ileus
Ileus
Pseudo-obstruction
Symptoms
Plain Radiographs
Differential diagnosis
Ischaemia of the gut Acute pancreatitis Perforation of the gut Intussusception Tuberculosis Non-gastrointestinal conditions
Complication
Strangulation or infarction Leading to gangrene Perforation peritonitis
Prognosis
In patients with small bowel obstruction, the mortality is 25% if surgery is delayed beyond 36 hours; under 36 hours this drops to 8% 50% of sigmoid volvulus will recur in the next 2 years 60% of stomas are never reversed Older patients, patients with hypoalbuminaemia and those in whom the primary tumour is not gastrointestinal in origin are less able to withstand the rigours of major surgery