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ABDOMINAL PAINDR. WONG SEAK KHOON
(2 November 2011)
Present by: Soediqin Akmal
Introduction 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.
9 regions of abdomen
EpigastriumRight
Hypochondrium
Left Hypochondri
um
Umbilical
Right Lumbar Left lumbar
Right iliac fossa
Hypogastrium
Left iliac fossa
9 regions of abdomen
StomachPancreasLt lobe of
liver
LiverGallbladder
SpleenTail of pancreasFundus of stomachCoils of
small instesti
ne
Right kidneyAscending colon
Left kidneyDescending colon
CaecumAppendix
Urinarybladder
Sigmoid
colon
9 regions of abdomen
StomachDuodenumGallbladder Pancreas
Small intestin
eCaecum
Kidney Kidney
CaecumAppendix
Transverse colon
Bladder
Sigmoid
colon
Definition 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
Pathophysiology of abdominal pain:
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
Medical
Non-traumatic
Traumatic
Cause of Abdominal Pain
Principal Causes of Abdominal Pain
Hemorrhage
Infarction/ Strangulation Obstruction
Perforation
Inflammation/Infection
Non- traumaticAbdominal Pain
Pathology Disease
Inflammation •Diverticulitis•Salphingitis•Acute Pancreatitis
•Acute appendicitis•Acute cholecystitis
Obstruction •Ureteric obstruction•Urinary retention
•Intestinal obstruction•Biliary obstruction
Ischaemia •Strangulated hernia•volvulus
•Torsion of ovarian cyst
Perforation •Perforated peptic ulcer•Perforated cancer
•Biliary peritonitis
Rupture •Ruptured ectopic pregnancy
•Ruptured aneurysm
Example of Non-traumatic causes
The causes of generalized abdominal pain :• Irritable bowel syndrome
• Recurrent adhesive obstruction• Mesenterric carcinoma
• Carcinomatosis• Chronic constipation
• Radiation damage• Reptriperitonial tumours
• Endomettriosis• Pelvic-uriteric junction obstruction
• Lumbar spine pain• Retroperitonial fibrosis
• psychosomatic•
General abdominal pain
Management:
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 support
3. Surgery: - Abscess drainage - Cholecystectomy-if stone in gall bladder
Complications:1. Pancreatic necrosis & pseudocyst formation2. Abscess formation3. Haemorrhage4. Thrombosis5. Fistulae6. Recurrent edematous pancreatitis
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
Differentials diagnosis
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 abcess
3. 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 duodenography
3. 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 oesophagus
4.Radiation: -Right scapula: gallbladder -Shoulder-tip: diaphragmatic irritation -Mid-back: pancreas.
HISTORY TAKING
5.Associated symptoms, e.g vomiting, diarrhoea, painful micturition etc
6.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 cycle
7.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 Crohn's 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.
PAIN...
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
Acute appendicitis:
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
Anatomy of appendix:
Base of appendix: McBurney’s point
Pathogenesis of acute appendicitis:Initiation of inflammation
Acute inflammation of mucosa
Extension 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 wall
Attempt to wall off perforation by: omentum, adjacent bowel
Intense & extensive walling-off rxn Inadequate
containment
Appendiceal mass
Generalised peritonitis
Appendiceal abscess
Clinical features:1. Pain: -vague - begin at central abdomen/ retrosternal - poorly localised - colicky - assoc. with Nausea & Vomiting - duration: few hours/ days - pain then shifted to Rt iliac fossa
2. Localising symptoms depends on anatomical relations of inflammed appendix
e.g. inflammed retrocecal appendix: - irritates psoas muscle>> involuntary Rt hip flexion, pain on extension
Examination:
1. General appearance: - Facial flush - Low-grade pyrexia - Tachycardia
2. Abdomen: (i) Inspection: - Mild abdominal distension - Reduced abd. movement at Rt iliac fossa
(ii) Palpation: Rt iliac fossa: - Guarding (indicator of tenderness severity) - Tenderness, Rebound tenderness
- +ve Rovsing’s sign(iii) Percussion: pain at Rt iliac fossa(iv) Auscultaion: Bowel sound present Bowel sound absent when perforation & generalised peritonitis cause paralytic ileus
Cardinal features of acute appendicitis:
1. abdominal pain <72 hours2. Vomiting 1-3 times3. Facial flush4. Tenderness at Rt iliac fossa5. Low-grade pyrexia6. no evidence of UTI
Investigation:
No need if it can be diagnosed through history and physical examination
AXR for confusing findings, may detect free gas from perforated appendix.
Differential Diagnosis:
1. UTI2. Mesenteric adenitis3. Constipation4. Gynaecological disorder (ectopic pregnancy)5. Acute pancreatitis6. Diverticulitis7. Perforated ulcer
Management:
Medical◦Antibiotics
Surgical◦Appendicectomy Abdominal wall incision ( Lanz/ Classic Gridiron incision)
Dividing the blood supply Removing the appendix Closure
Complications:
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
Acute pancreatitis:
Aetiology :
- Gallstones (38%-60%) - Ethanol (35%) - Trauma (1.5%) - Mumps - Autoimmune (PAN) - Scorpion venom - Hyperlipidemia, hypercalcemia, hyperthyroidism - ERCP (5%) & emboli - Drugs * 10%-20% idiopathic
Pathogenesis:
Duodenopancreatic reflux
Enterokinase reflux
Activate pancreatic proenzymes
Inflammation, arterioles thrombose, local infarction
More proenzymes leak out of necrotic cells to be activated
Widespread autodigestion
Obstuction of pancreatic duct
1. Mild attack: - Acute interstitial pancreatitis2. Severe attack: - Acute haemorrhagic pancreatitis - Acute necrotising pancreatitis
Clinical features:1. epigastric pain: - sudden onset - radiate to back - no relieving factor - aggrevated by movement - assoc. with - Nausea & Vomiting
Examination:1. General appearance: - in pain - pale - sweating - dyspneic & cyanosed (respiratory distress in severe attack) - jaundice - tachycardic - signs of hypovoolemic shock
2. Abdomen:
(i) Inspection: - mild abdominal distension - Grey Turner’s sign only in Acute
Haemorrhagic - Cullen’s sign Pancreatitis
- fullness in epigastrium (abscess, pseudocyst)(ii) Palpation:
- Tender - Guarding - Rebound tenderness (iii) Percussion: - Pain >> peritonitis - Dullness >> pseudocyst
(iv) Auscultation: - Bowel sound present in first 24 hrs - Bowel sound absent when paralytic ileus develops
Investigation:
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 cases
4. 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
1.Ranson’s criteria:A. At admission or
diagnosis B. During initial 48 hrs
1. Age >55 years (70yrs in gall stone disease) 1. Hematocrit fall >10 percent
2. Leukocytosis >16,000 /mm3 2. Fluid sequestration >6L
3. Hyperglycemia >10 mmol/L 3. Hypocalcemia <2mmol/L
4. Serum LDH >400 IU/L 4. Hypoxemia (PO2 <60 mmHg)
5. Serum AST >250 IU/L 5. BUN rise >10mmol/L after IV fluids
6. Hypoalbuminemia <3.2 g/dL
2. Glasgow scoring system:
A - Age > 55P - PO2 < 8 kPa (60mmHg) n=10.6N - Neutrophil count ( > 16 x 109 /L ) C - Calcium < 2.0 mmol/LR - Raised Urea > 10 mmol/L E - Enzyme (LDH > 350 IU/L) A – Albumin (plasma) < 32 g/LS - 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
Investigation
Hematology
biochemistry
imaging
Blood tests1.Haemoglobin
◦ -may be normal immediately after an acute bleed ◦ -low haemoglobin concentration may represent chronic anaemia
due to occult blood loss
2.White blood count -leucocytosis is non-specific and rarely of much diagnostic value unless greater than about 14 × 103/L
3.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
Haematology
1.C-reactive protein ◦ -non-specific indicator of inflammatory activation ◦ -confirms organic illness if substantially elevated
2.Plasma amylase-whenever pancreatitis cannot be excluded 3.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
Biochemistry
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 disease
6.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)
Imaging
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 masses 3.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)
Management:
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 management
Management of gallstone disease
contraindications
advantages disadvantages
(i) Uncorrectable Coagulopathy
(ii) Unable to tolerate GA
(iii) Known GB ca
(i) Lower mortality
(ii) Less pain(iii) Shorter hosp
stay(iv) Recovery
rate faster
(i) Higher incidence of injury to the common hepatic and bile ducts
(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
Management of gallstone disease
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
ACUTE PANCREATITIS
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
Acute appendicitis
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