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DR. WONG SEAK KHOON (2 November 2011)Present by: Soediqin Akmal
Abdomen Abdomen is part of trunk that lies between the thorax and pelvis. It is divided into 9 parts by 2 vertical lines, right and left midclavicular lines and also 2 horizontal lines, subcostal and intertubercular lines.
Right Left Hypochondriu Epigastrium Hypochondriu m m Right Lumbar Umbilic Left lumbar alRight iliac fossa Hypogastrium Left iliac fossa
Stomach Spleen Liver Pancreas Tail of pancreas Gallbladder Lt lobe of liver Fundus of stomach Coils of Right kidney Left kidney smallAscending colon Descending instestine colon Caecum Urinary Sigmoi Appendix bladder d colon
StomachGallbladder Duodenum Pancreas Small Kidney intestine Kidney Caecum Caecum Transverse Sigmoi Appendix colon d Bladder colon
Abdominal pain is pain that is felt in the abdomen Acute abdomen refers to a sudden, severe abdominal pain of unclear etiology that is less than a week in duration ◦ eg. acute peritonitis, acute pancreatitis, acute cholecystitis, acute cholangitis, acute appendicitis diabetic ketoacidosis
1. Somatic pain: - due to irritation of parietal peritoneum - parietal peritoneum covers: (a) anterior & posterior abd. wall (b) undersurface of diaphgram (c) pelvic cavity
- Nerve supply: derived from nerve supplying muscles & skin of abdominal wall (T5- L2) *exception: central portion of diaphrgam (phrenic nerve: C3,C4,C5)- Sensitive to: mechanical thermal chemical
- Response to irritation: (i) reflex contraction of corresponding segment of muscle guarding (ii) hyperaesthesia of overlying skin- Nature: sharp, localised, knife-like
2. Visceral pain: - due to irritation of visceral peritoneum - visceral peritoneum covers partially/ completely the intra-abdominal viscera - pain is mediated through sympathetic branches of autonomic system, to thoracic (T6-T12) & lumbar (L1,L2) segment of spinal cord
- Sensitive only to tension- Nature: dull, poorly localised, deep, referred to overlying skin with same embryological origin
Causes ofAbdominal Pain Surgical Non-traumatic Traumatic Medical
1. Mild attack: ◦ Fluid resuscitation and analgesia ◦ NBM meant to rest the pancreas ◦ Treat predisposing factors such as gall stones ◦ Discouraged alcohol abuse ◦ NG tube to aspirate stomach content and prevent vomiting ◦ Prophylactic antibiotic i.e. imipenem and cephalosporin ◦ Daily measurement of plasma amylase – progression of ds ◦ LFT and renal profile
2. Severe attack: ◦ Resuscitate ◦ Defined by Ranson’s or Glasgow criteria ◦ Admit to ICU immediately ◦ Fluid and electrolyte management ◦ Treat hypocalcaemia ◦ Ventilatory support3. Surgery: - Abscess drainage - Cholecystectomy-if stone in gall bladder
The stomach and duodenum. 1.The insulin test: Consist of an injection of insulin which produces hypoglycemia Stimulates the nucleus of vagus in the brain stem Helpful when a patient develops a recurrent ulcer following vagotomy for duodenal ulceration. The blood sugar has to fall below 45mg/100ml Measure before and after insulin in injected by slow i.v infusion 2.Plain x-ray: Patients lying in supine position Suspected peritonitis due to perforation of gastric or duodenal ulcer Gas maybe seen under the diaphragm Usually on the right side
3. Barium meal: Radiographic investigation Patient swallows a suspension of radiopaque barium sulphate Principally use in the diagnosis of gastric and duodenal ulcer and gastric carcinoma. Chronic gastric ulcer: seen as a projection from the wall or as a ronded deposit. Duodenal ulcer:seen a face with a stellate appearance of the mucosal fold. Pyloric stenosis: an increased amount of resting juice present and grossly enlarged stomach .4.Endoscopy and biopsy: Possible to see the whole of the oesophagus,stomach and duodenum Biopsy forceps:to obtain specimens for histological and cytological examination. Can differentiate benign from malignant lesions Rapid diagnosis of upper gastrointestinal bleeding.
Small intestine.1.Barium meal follow through X-rays: Studied by thaking filmx of abdomen at intervals after a barium meal. Abnormalities in the transit time to the colon and in small bowel pattern such as dilatation,narrowing, fistula and mucosal abnormalities.2. Biopsy: Small intestine biopsy importance in diagnosis of the malabsorption syndrome where a flat mucosa is seen. Colon ,rectum and anus.1.Protoscopy: Can see piles as reddish/blue swelling which bulge into the lumen Can see internal opening of an anal fistula,an anal or low rectal polyp and chronic anal fissure
2. Sigmoidoscopy: Necessary to examine the rectum and colon Proctitis,polyps and carcinomas may be seen. Particulary useful in the differential diagnosis of diarrhoea of colonic region.3. Barium enema: Can see the obstruction of the colon,tumours,diverticular disease,fistulae and other abnormalities can be recognize.4.Colonoscopy: Inspect the whole colonis mucosa round to the caecum. Polyps and diverticulitis can be seen.
The liver.1.Ultrasound scan: Diagnosis of fluid-filled lesions such as cysts and abcesses Detecting intrahepatic bile ducts.2.Needle biopsy of liver: Diagnosis for liver abcess3. Liver function test: To see the albumin,globulin,AST and ALT level.
Gallbladder and bile ducts:1.Percutaneous transhepatic cholangiography: Useful investigation in patients with jaundice due to obstruction of the main bile ducts. Investigations the site of the obstruction due to tumours of the head of the pancreas,iatrogenic and alignant bile ducts strictures –can be accurately localized and diffrentiated.2.ERCP(endoscopic retrograde cholangiopancreatography) Useful in the rapid diagnosis and localization of the different causes of jaundice due to obstruction of the main bile ducts.
The pancreas.1.Lundh test; Assessment of tryptic activity in pancreatic juice collected following duodenal intubation Indirect stimulation of the pancreas by prior ingestion of a meal. Tryptic activity is less than 6 iu/litre.2. Triple test. Exocrine function. Cytology Hypotonic duodenography3. ERCP
Pain1.Site-9 region2.Onset: acute or recurrent or gradual3.Character : -colicky- comes and goes in waves and indicates obstruction of a hollow, muscular- walled organ (intestine, gallbladder, bile duct, ureter). -burning-an acid cause and is related to the stomach, duodenum or lower end of the oesophagus4.Radiation: -Right scapula: gallbladder -Shoulder-tip: diaphragmatic irritation -Mid-back: pancreas.
5.Associated symptoms, e.g vomiting, diarrhoea, painful micturition etc6.Timing: since onset Episodic or continuous. If episodic, duration and frequency of attacks; If continuous, any changes in the severity Variation by day or night, during the week or month, e.g. relating to the menstrual cycle7.exacerbation & relieving factor8.Severity
Past medical history Ask especially about: Previous surgical procedures including peri- and postoperative complications and anaesthetic complications. Chronic bowel diseases (e.g. IBD including recent flare-ups and treatment to date). Possible associated conditions (e.g. diabetes with haemachromatosis).
Drug history Think about drugs that can precipitate abdominal diseases and remember to ask about over-the-counter drugs. For example: Hepatitis: halothane, phenytoin, chlorothiazides, pyrazinamide, isoniazid, methyl dopa, HMG CoA reductase inhibitors (statins, sodium valproate, amiodarone, antibiotics, NSAIDs. Cholestasis: chlorpromazine, sulphonamides, sulphonylureas, rifampicin, nitrofurantoin, anabolic steroids, oral contraceptive pill. Fatty liver: tetracycline, sodium valproate, amiodarone. Acute liver necrosis: paracetamol. Ask also about previous blood transfusions
Smoking Smokers are at risk of peptic ulceration, oesophageal cancer, colorectal cancer. Smoking may also have a detrimental outcome on the natural history of Crohns disease. Alcohol a detailed history is required.If dependence is suspected
Urethral pain: variable in presentation ranging from a tickling discomfort to a severe sharp pain felt at the end of the urethra (tip of the penis in males) and exacerbated by micturition. Can be so severe that patients attempt to hold on to urine causing yet more problems! Small bowel obstruction: colicky central pain associated with vomiting, abdominal distension & constipation. Colonic pain: as above under small bowel but sometimes temporarily relieved by defaecation or passing flatus.
Bowel ischaemia: dull, severe, constant, right upper quadrant/central abdominal pain exacerbated by eating. Biliary pain: severe, constant, right upper quadrant/epigastric pain that can last hours and is often worse after eating fatty foods. Pancreatic pain: epigastric, radiating to the back and partly relieved by sitting up and leaning forward. Peptic ulcer pain: dull, burning pain in the epigastrium. Typically episodic at night, waking the patient from sleep. Exacerbated by eating and sometimes relieved by consuming
1. Commenest abdominal emergency (Lifetime incidence 6%)2. Causes: (a) Obstruction by faecolith or lesion in caecum (b) Recurrent inflammation (c) Enlargement of lymphoid follicles
Base of appendix: McBurney’s point
Initiation of inflammation Acute inflammation of mucosaExtension of inflammation across appendiceal wall Involvement of serosa by inflammation Visceral peritonitis (referred pain) Peritonitis spread to adjacent structure (localised pain)
Necrotic glandular mucosa sloughs into lumen Lumen distended with pus End-artery (appendiceal artery) thrombosed Appendix infarction Gangrenous appendix Perforation of appendix wallAttempt to wall off perforation by: omentum, adjacentbowel
Medical ◦ Antibiotics Surgical ◦ Appendicectomy Abdominal wall incision ( Lanz/ Classic Gridiron incision) Dividing the blood supply Removing the appendix Closure
1. Perforation2. Appendiceal mass (usually resolve in the next 2-6 weeks) - pyrexia - LOA - malaise - dull on percussion3. Appendiceal abscess (formed from appendiceal mass that fails to resolve) - swinging pyrexia - tachycardia
Obstuction of pancreatic duct Duodenopancreatic reflux Enterokinase reflux Activate pancreatic proenzymes Inflammation, arterioles thrombose, local infarctionMore proenzymes leak out of necrotic cells to be activated Widespread autodigestion
(iv) Auscultation: - Bowel sound present in first 24 hrs - Bowel sound absent when paralytic ileus develops
1. FBC (WBC ,RBC )2. Plasma amylase (>1200 IU/mL), (rises within 12 hrs, return to normal in next 48- 72 hrs)3. Plasma lipase (elevated level persists for 7-10 days), usefull in late-presenting cases4. LFT (bilirubin usually )5. ABG (hypoxia occurs in severe attack)
6. Plain CXR (free gas under diaphragm)7. Plain AXR (no psoas shadow >>retroperitoneal fluid)8. Ultrasound9. CT scan to confirm pancreatitis if amylase level normal10. ERCP (to find the cause)
1.Scoring system by Ranson2.Glasgow Criteria by Imrie
A. At admission or B. During initial 48 hrs diagnosis1. Age >55 years (70yrs in 1. Hematocrit fall >10 percent gall stone disease)2. Leukocytosis >16,000 3 2. Fluid sequestration >6L /mm3. Hyperglycemia >10 3. Hypocalcemia <2mmol/L mmol/L 4. Hypoxemia (PO2 <604. Serum LDH >400 IU/L mmHg) 5. BUN rise >10mmol/L after5. Serum AST >250 IU/L IV fluids 6. Hypoalbuminemia <3.2 g/dL
A - Age > 55 P - PO2 < 8 kPa (60mmHg) n=10.6 N - Neutrophil count ( > 16 x 109 /L ) C - Calcium < 2.0 mmol/L R - Raised Urea > 10 mmol/L E - Enzyme (LDH > 350 IU/L) A – Albumin (plasma) < 32 g/L S - Sugar (plasma glucose) >10mmol/L in the absence of history of diabetes)* (3 or > factors indicates severe pancreatitis)
clinical assessment, relief of pain and resuscitation come before imaging tests Hematology biochemistr imaging y
Blood tests1.Haemoglobin ◦ -may be normal immediately after an acute bleed ◦ -low haemoglobin concentration may represent chronic anaemia due to occult blood loss2.White blood count -leucocytosis is non-specific and rarely of much diagnostic value unless greater than about 14 × 103/L3.Pcv—degree of hydration(vomit,diarhoea)4.Blood culture-only in patients with rigors or shock without obvious blood loss5.Blood group and ordering of blood for transfusion- for severely anaemic patients, in major haemorrhage or when major surgery is contemplated
1.C-reactive protein ◦ -non-specific indicator of inflammatory activation ◦ -confirms organic illness if substantially elevated2.Plasma amylase-whenever pancreatitis cannot be excluded3.Urea and electrolytes-indicated in vomiting and diarrhoea, dehydration, poor urine output, diuretic therapy, urinary tract disease, known or suspected renal failure, pancreatitis and sepsis
4.Glucose-for diabetics or those with glycosuria (beware of hyperglycaemia due to acute stress or steroid therapy)5.Liver function tests and calcium estimation-for pancreatitis and acute biliary disease6.Clotting studies-for acute pancreatitis and septicaemia (DIC), severe bleeding (consumption coagulopathy) or those with a history of bleeding disorders
1.Plain radiography 1.Erect chest X-ray ◦ -cardiovascular disease or abnormality, e.g. cardiomegaly, thoracic aneurysm, aortic dissection, cardiac failure ◦ -respiratory disease ◦ -suspected visceral perforation (gas under diaphragm)
2.Supine abdominal X-ray (erect or decubitus if necessary)◦ -bowel (gas pattern and dilatation, fluid levels, gas in the wall, faeces and faecoliths)◦ -urinary tract (KUB = kidneys, ureters and bladder) shows kidney size and position, calculi◦ -biliary tract (gallstones, gas in biliary tree in gallstone ileus)◦ -aortic calcification (aneurysm)◦ -psoas shadows (obscured by retroperitoneal inflammation or haemorrhage
2.Ultrasound Gallstones Pelvic abnormalities in obstetric and gynaecological practice Chronic enlargement of the spleen Abdominal aortic aneurysm (AAA) Free abdominal fluid and gas indicating perforated bowel Other stones Dilated ducts; air in biliary tree Hydatid, teratomas and other cysts Intra-abdominal abscesses and masses3.Contrast radiology Instant barium enema in colonic obstruction or acute colitis Emergency intravenous urography in ureteric colic
4. CT scanning rapid, cost-effective evaluation of acute abdominal pain Assessment of abdominal trauma-severity and grading of solid organ injury, free intra-abdominal fluid and gas; retroperitoneal injuries including pancreatic and duodenal rupture and vascular injury Often first choice for ureteric colic, suspected aortic aneurysm or aortic dissection Useful where diagnosis remains in doubt, e.g. suspected bowel perforation (detects small amount of free gas), acute diverticulitis Investigation of postoperative complications-abscesses, fluid collections Severe acute pancreatitis, especially if necrosis suspected
Duodenal ulcer:• Surgery (ulcer is sutured or plugged using an omentum patch)• Supportive treatment with nasogastric suction Gastric ulcer:• ~15% of perforated gastric ulcer prove to be malignant. Therefore, definitive surgery is preferred• Simple closure with biopsy @ local excision (in poor-risk patients)
Acute cholecystitis 1st line treatment (medical) : Fasting, intravenous fluid, analgesic Start IV antibiotics (if pt has systemic signs or if no improvement after 12-24 hours) Surgery: Emergency vs elective Open vs laparoscopic
Laparoscopic Cholecystectomy Optimal managementcontraindications advantages disadvantages(i) Uncorrectable (i) Lower mortality (i) Higher incidence Coagulopathy (ii) Less pain of injury to the(ii) Unable to tolerate (iii) Shorter hosp stay common hepatic GA and bile ducts (iv) Recovery rate(iii) Known GB ca faster (ii) Inj tend to be more extensive
Pain after cholecystectomy (I) retained or recurrent stone (ii) iatrogenic biliary leak (iii) stricture of CBD (iv) papillary stenosis/dysfunction of Sphincter of Oddi (v) incorrect pre-op dx (eg irritable bowel syndrome, PUD, GOR
Other treatment modalities : (I) Oral bile acid treatment - monotherapy or combine therapy (6-12 months) - ursodeoxycholic acid and chenodeoxycholic acid (ii) Contact dissolution therapy - chemical litholysis of cholesterol stones (MTBE) (iii) ESWL - used when GB is functioning ; technically difficult when it is subcoastal - long term recurrence rate high (between 28-61%) (iv) percutaneous cholecystectomy
Criteria for non surgical treatment of gallstones: Cholesterol stones (<20mm in diameter) Fewer than 4 stones Functioning gallbladder Patent cystic duct Mild symptoms
MILD ATTACK Hourly pulse, BP, urine output Fluid resuscitation to replace fluid loss from profuse vomiting Analgesics for pain relief – pethidine, morphine Withhold oral intake Treat predisposing factors Remove stone endoscopically, stopped taking alcohol, laparoscopic cholecyctectomy with operative cholangiography before discharge. Nasogastric tube to aspirate gastric content & relief discomfort. Prophylactic parenteral antibiotic (cephalosporin) given. Daily measurement of serum amylase, ABG, BUSE, LFT and serum calcium & phosphate to monitor progress
SEVERE ATTACK Admit to ICU for close monitoring and early Rx of complications Evaluated every 48 hours. May die early b’coz of systemic toxaemia and multiple organ dysfunction. If PaO2 deteriorating- urgent ventilation support before ARDS Massive fluid & electrolytes loss esp protein-rich fluid into peritoneal cavity and 3rd space lead to shock Rx- fluid resuscitation with large amount of colloid & crystalloid Monitor urine output & central venous pressure. Peritoneal lavage – reduce systemic absorption of enzymes & toxins. Intravenous nutrition given in paralytic ileus patient
Medical ◦ Antibiotics Surgical ◦ Appendicectomy Gridiron / Lanz skin incision Abdominal wall incision Dividing the blood supply Removing the appendix Closure