ACUTE ABDOMENBy :

1.Baraka Kadiva2. Poh Yi

3.Rowan Jetly4.‘Aisyah Amir

Definition

• Sudden & severe onset of abdominal pain of less than 24 hours, of unclear etiology, which requires an urgent and specific diagnosis, hospitalization and surgical intervention to treat and prevent it from becoming catastrophic.

• Acute appendicitis

• Acute peptic ulcer

• Acute cholecystitis

• Acute pancreatitis • Acute diverticulitis

• Acute peritonitis

Acute peptic ulcer • Peptic ulcer is a break in the lining of the stomach or duodenum, or

occasionally the lower esophagus, which caused by a local inflammation, hyperacidity and decreased mucosal resistance.

• An ulcer in the stomach is known as a gastric ulcer ass. With decreased mucosal resistance( presented mostly at the lesser curvature) while that present in the first part of the duodenum is also known as a duodenal ulcer( associted with hyperacidity).

• They also may occur on the stoma following gastric surgery, in the lower oesophagus and even in a Meckel’s diverticulum, which contains ectopic gastric epithelium.

• Ulcers in the stomach or duodenum may be acute or chronic and both can penetrate the muscularis mucosae but the acute ulcer shows no evidence of fibrosis and erosions, do not penetrate the muscularis mucosae.

Causes

• Helicobacter pylori (most common)• NSAIDS ingestion• Cigarette smoking• Diet • Stress• Gastrinoma (Zollinger Ellison Syndrome)

H.pylori

• H. pylori is Gram-negative and spiral, and has multiple flagella at one end, which make it motile, allowing it to burrow and live beneath the mucus layer adherent to the epithelial surface.

• It uses an adhesin molecule to adhere on the epithelial cells.

• Any acidity in the stomach is buffered by the organism’s production of the enzyme urease. This produces ammonia from urea and raises the pH around the bacterium, therefore providing a conducive environment for it to colonise. H. pylori exclusively colonises the gastric-type epithelium.

• Also H. pylori causes depletion of somatostatin (from D cells) and increased gastrin release from G cells.

Clinical features

• Abdominal pain which is epigastric in location, often described as gnawing in nature, intermittent, radiating to the back and associated with food. Pain associated with duodenal ulcer occurs 3 hrs after taking a meal.

• One of the classic features of untreated peptic ulceration is periodicity. Symptoms may disappear for 2-6 months to return again. This periodicity may be related to the spontaneous healing of the ulcer.

• Vomiting( cofee ground colour vomit: GU , acidic vomiting: DU)

• Weight loss or, sometimes, weight gain may occur. Patients with gastric ulceration are often underweight but this may precede the occurrence of the ulcer. DU patients mostly maintain their weight.

• Acute presentation with haematemesis (which can occur directly from the bleeding of the gastric ulcer) and melaena.

Physical Examination

• GE-pallor, cyanosis, jaundice.• Vital signs (BP,RR,HR,T)• Nutrition status: (Lean patients-GU, Fairly nourished-DU.• Abdomen examination: epigatric tenderness• Rule out gastric outlet obstruction(signs)

Investigation

• Gastroduodenoscopy

• This is the highly accurate investigation of choice in the management of suspected peptic ulceration done in the hands of a well-trained operator. In the stomach, any abnormal lesion should be biopsied in the case of a suspected benign gastric ulcer, numerous biopsies must be taken to exclude, as far as possible, the presence of a malignancy.

• Barium contrast X-rays.

• Rapid Urease test for the H.pylori

(results received after 3 hours)

• FBC (WBC,HB)

• BGL

Benign incisural gastric ulcer shown at gastroscopy

Benign gastric ulcer shown by barium meal.

Duodenal ulcer at gastroduodenoscopy

Duodenal ulcer shown by barium meal

Treatment

• Medical treatment- H. pylori eradication

• All patients with proven ulcers who are H. pylori-positive

• should be offered eradication therapy as primary therapy. Treatment which is based upon a PPI (Omeprazole) taken simultaneously with two antibiotics (from amoxicillin, clarithromycin and metronidazole) for 7 days.

• We can also stop the NSAIDS.

• We also encourage the patient to change his/her lifestyle and avoid cigarette smoking.

• Surgical Treatment: Billroth II gastrectomy

• Truncal vagotomy with gastrojejunostomy (drainage procedure)

Picture showing a Truncal vagotomy

complications

• Perforations• Gastric outlet obstruction• Gastric Cancer

Acute Cholecystitis

• Is the inflammation of the gall bladder. • 90 % are due to obstructions by *gall stones – Acute calculous cholecystitis• 10% occur in the absence of gallstone – acute acalculous cholecystitis.

• *Risk factors of patients with gall stones: include female, increasing age, pregnancy, oral contraceptives, obesity, diabetes mellitus, ethnicity , rapid weight loss.

HEPATOBILIARY TREE

Pathophysiology Acute calculous cholecystitis

due to gallstones, obstruction of the bile duct

gallbladder distension

edema & ischemia of the cells lining the gallbladder

Resulting release of inflammatory mediators (prostaglandins)

aggravates the inflammation

lining wall of the gallbladder undergo necrosis and gangrene

Swelling and Inflammation of gall bladder

•Most patients with gallstones do not have symptoms. But When a gallstone becomes intermittently lodged in the cystic duct, they suffer from biliary colic pain.• Biliary colic is the abdominal pain in the right upper quadrant or epigastrium that is usually episodic, occurs after eating greasy or fatty foods, and leads to nausea and/or vomiting.

•. Pain might radiate to the right shoulder and the tip of the scapula( Boas sign).

• Fever, anorexia, nausea and vomiting is common and vomiting occurs in 75% of people with cholecystitis.

• On physical examination, guarding and focal tenderness in the RUQ•Pain with deep inspiration leading to termination of the breath while pressing on the right upper quadrant of the abdomen usually causes pain (Murphy's sign). Murphy's sign is sensitive, but not specific for cholecystitis.

•Mild Jaundice may occur and if severe, suggests another cause of symptoms such as choledocholithiasis. Elderly patients, diabetes mellitus, chronic illness, or who are immunocompromised may have vague symptoms.

Clinical Features

http://nclexies.files.wordpress.com/2011/01/cholecystitis.jpg

Investigations •Right upper quadrant abdominal ultrasound is most commonly used to diagnose cholecystitis. Ultrasound findings suggestive of acute cholecystitis include gallstones, fluid surrounding the gallbladder, gallbladder wall thickening, dilation of the bile duct, and sonographic Murphy's sign.

Acute cholecysitis as seen on ultrasound. Closed arrow points to gall bladder wall thickening. Open arrow points to stones in the Gall bladder.

Continued…..Blood tests

complete blood count (Leukocytosis) C-reactive protein( elevated) bilirubin levels in order to assess for bile duct blockage. (elevated (1–4 mg/dL)) If bilirubin levels are more significantly elevated, alternate or additional diagnoses should be considered such as gallstone blocking the common bile duct (choledocholethiasis).

Less commonly, blood aminotransferases are elevated.

Serum amylases( to rule out pancreatitis).

The degree of elevation of these laboratory values may depend on the degree of inflammation of the gallbladder.

Treatment laparoscopic cholecystectomy (immediate, emergency, delayed) has become the

treatment of choice for acute cholecystitis because

1. compared to open cholecystectomy, Patient undergoing laparoscopic surgery report less incisional pain postoperatively

2. as well as having fewer long term complications and less disability following the surgery.

3. Additionally, laparoscopic surgery is associated with a lower rate of surgical site infection.

Supportive measures Analgesics: Morphine or Miperidine These measures include fluid resuscitation and antibiotics (such as gentamicin, ciprofloxacin, ceftriaxone) targeting enteric organisms, such as E coli

X-Ray during laparoscopic cholecystectomy

Operative image of a laparoscopic cholecystectomy.Forceps (arrowed) are dissecting the cystic duct.

Complications

Complications may occur from cholecystitis if not detected early or properly treated. Signs of complications include high fever, shock and jaundice. Complications include the following:

1. Gangrene2. Gallbladder rupture3. Empyema4. Fistula formation and gallstone ileus5. Rokitansky-Aschoff sinuses

Acute AppendicitisKhoo Poh Yi

BMS12081076Group 3

Anatomy

Appendix

• Narrow, hollow, blind-ended tube

• Connected to cecum• 3 teania coli on the asc. colon

and cecum converge to from the base of the appendix

• Separated from ileum by mesoappendix

• Mesoappendix contains appendicular artery

• No direct local nerve supply• McBurney’s point

Location of McBurney's point (1), located two thirds the distance from the umbilicus (2) to the right anterior superior iliac spine (3).

Superior Mesenteric Artery >

Illeocolic Artery >

Appendicular Artery

Clinical Significant:•End artery•Acute infection of the appendix may result in thrombosis of the appendicular artery with rapid development of gangrene and subsequent perforation.

Nerve supply:•Sympathetic nerves: T9 and T10 spinal segments through the celiac plexus•Parasympathetic nerves: Vagus

Clinical•Both the appendix and the umbilicus are innervated by segment T10 of the spinal cord and hence the pain caused by appendicitis is first felt in the region of umbilicus (referred pain). •With increasing inflammation pain is felt in the right iliac fossa due to involvement of the parietal peritoneum of the region which is sensitive to pain in contrast to pain insensitive visceral peritoneum.

History TakingBullet questions

• Abdominal pain. Typically, symptoms begin as periumbilical or epigastric pain migrating to the right lower quadrant (RLQ) of the abdomen. This pain migration is the most discriminating feature of the patient's history, with a sensitivity and specificity of approximately 80%.

• Patients usually lie down, flex their hips, and draw their knees up to reduce movements and to avoid worsening their pain.

• Nausea & vomiting: it nearly always follows the onset of pain. (Vomiting that precedes pain is suggestive of intestinal obstruction, and the diagnosis of appendicitis should be reconsidered).

• Anorexia • Diarrhoea or constipation.

Physical Examination

• Tenderness on palpation in the RLQ• Rigidity, and guarding• Rebound tenderness over the McBurney point is the most important sign

in these patients.• RLQ tenderness is present in 96% of patients;

Rarely, left lower quadrant (LLQ) tenderness has been the major manifestation in patients with situs inversus or in patients with a lengthy appendix that extends into the LLQ.

• Rovsing sign suggests peritoneal irritation in the RLQ precipitated by palpation at a remote location.

• Obturator sign (RLQ pain with internal and external rotation of the flexed right hip) suggests that 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.

AlvaradoDiagnostic Scoring

(MANTRELS)

Characteristic ScoreM = Migration of pain to the RLQ 1A = Anorexia 1N = Nausea and vomiting 1T = Tenderness in RLQ 2R = Rebound pain 1E = Elevated temperature 1L = Leukocytosis 2S = Shift of WBCs to the left 1Total 10Source: Alvarado.[19]

RLQ = right lower quadrant; WBCs = white blood cells

Score of 5 or 6 is compatible with the diagnosis of acute appendicitis.Score of 7 or 8 indicates a probable appendicitisScore of 9 or 10 indicates a very probable acute appendicitis.

Investigation

Full Blood Count

• Low Hb – chronic bleeding• Increase in white cell count with neutrophil leukocytosis may indicate

(inflammatory or infective process )

U & E

• Fluid loss – renal impairment (dehydrated)• Vomiting – electrolyte abnormalities

Ultrasound

• Ascites, cholecystitis/ biliary colic, Renal colic, bladder stone (TRO)• Appendiceal mass

Appendicitis can be diagnosed when the outer diameter of the appendix measures greater than 6mm.

Longitudinal graded compression ultrasound image demonstrates a mildly dilated appendix (black arrows) with preservation of the expected multilayered appearance of bowel. Note blind end of the appendix (white arrow). There is no evidence of an appendicolith or adjacent fluid.

Graded compression ultrasound of the right lower quadrant reveals a non-compressible, enlarged appendix (arrows). Definition of the bowel wall layers, particularly the echogenic submucosa, is lost, suggesting perforation.

Management

• Appendix mass is a complication of acute appendicitis, it is an inflammatory mass composed of edematous omentum, small bowel loops, cecum and sometimes sigmoid colon, all walling off an inflamed appendix. It is one of the earliest complications of acute appendicitis and it can be management without immediate operative intervention.

• Ochsner-Sherren regimen is the expectant management giving to a patient with an appendix mass. It is expectant because it is expected that the symptoms and signs the patient presented with will improve during the course of the management and the patient may later be scheduled for elective/interval appendicectomy.

• The aim of the Ochsner Sherren regimen is to treat infection, relieve pain and supplement the fluids and electrolyte over a period of 48-72 hours during which the clinician will expect the condition to have improved

The specific treatment given to the patient is as follows1.Admit2.Administer maintenance fluids, and potassium in fluid3.Give vitamin C and B co in the fluids4.Give antibiotics (against enterobactereocea and anerobes – ciprofloxin andmetronidazole)5.Give analgesics ( paracetamol and pentazocine)6.Pass nasogastric tube to decompress the stomach and rest the bowel7.Monitor the urine output as measure of adequacy of the hydration8.Monitor pulse hourly or two hourly other vital signs 4hourly9.Measure the mass the diameter of the abdominal mass every 12 hours10.Check for presence of new symptoms and signs and resolution of the old symptoms and signs ( these include tenderness, distension, skin changes – edema, desquamation of the anterior abdominal wall, this will include a vomit chart to record the quantity and quality of the vomitus)

Open Appendectomy•Conventional method and the standard treatment for appendicitis. The surgeon makes an incision in the lower right abdomen, pulls the appendix through the incision, ties it off at its base, and removes it. Care is taken to avoid spilling purulent material (pus) from the appendix while it is being removed. The incision is then sutured.•If the appendix has perforated (ruptured), the surgeon cleans the pus out of the abdomen with a warm saline solution to reduce the risk for infection. A drain may be inserted through the incision to allow the pus to drain from the abdomen. In this case, the skin is not sutured, but left open and packed with sterile gauze. The gauze and drain remain in place until the pus is completely drained and there is no sign of infection.•If the abdomen is so inflamed that the surgeon cannot see the appendix, the infection is drained and treated with antibiotics, and then the appendix is removed.

Laparoscopic Appendectomy•Standard of care for appendicitis. The procedure has several advantages, including lower risk for postoperative infection, faster recovery time, a smaller scar, and a shorter hospital stay.•The surgeon makes a very small incision right below the navel and inserts an instrument called a laparoscope. The laparoscope is a long tube with a lens at one end and a miniature video camera at the other. The laparoscope enables the doctor to see the appendix. Several more tiny incisions are made to allow for the passage of instruments, which are used to cut and clamp off the appendix.•The laparoscope is also used as a diagnostic tool. The doctor is able to see if the appendix is inflamed and, if the appendix is not the cause of the patient's symptoms, other organs can be seen in order to identify the source of the symptoms

Case 1

• Mohammad Tohid, 67 yo healthy Malay, gentlemen with one day hx of acute severe abdominal pain. Pain was pulsatile and dull in right lower abd with no radiation. He was farming at that time. Aggravated by movement and relieved by rest. No fever or cough. Appetite reduced but no weight loss

• PMHx: Hypertensive and hypercholesterolemia• PSurgHx: negative• Meds: Atenolol and Simvastatin• Allergy: None• Social hx: smoker, one pack per day, 52 years, no alcohol• Family hx: Father HT, Mother DM

• Physical exam:• T: 37.0, HR: 95, BP 130/76, R: 18, O2 sat: 100% room air• Uncomfortable appearing, slightly pale• Abdomen: soft, non-distended, tender to palpation in RIF with mild

guarding, Rovsing’s sign positive, Murphy’s sign negative

Acute Pancreatitis

ROWAN RAJ JETLY

Pancreatitis

Acute : It is a sudden disorder of the exocrine pancreas, associated with inflammation and cell injury caused by release of inflammatory mediators and pancreatic enzymes (lipases, trypsin)*generally reversible

Chronic : Irreversible damage to the pancreas that clinically presents with recurrent abdominal pain, malabsorption and associated with recurrent inflammation, fibrosis and injury to both exocrine and endocrine tissues.

Causes / Etiology

EtOH35%

Idiopathic10%

Other10% Gallstones

45%

Less common causes

• Idiopathic• Hyperlipidemia• Hypercalcemia (hyperparathyroid , multiple myeloma)• Direct damage / Trauma • Post surgery• Drugs -

failed protectivemechanisms

acinar cellinjury

prematureenzyme activation

Acute PancreatitisPathogenesis

autodigestion of pancreatic tissue

release ofenzymes intothe circulation

activationof whiteblood cells

localcomplications

localvascularinsufficiency

premature enzyme activation

distantorgan failure

Acute PancreatitisPathogenesis

Pathophysiology of Gallstone Pancreatitis

- Triggered by passage of gallstones down the common bile duct.

- Biliary and pancreatic ducts join to share a common channel before ending in the ampulla

- Obstruction of this passage leads to reflux of bile and / or activation of pancreatic enzymes into the duct, causing pancreatitis.

Acute Pancreatitis Pathogenesis

• STAGE 1: Pancreatic Injury• Edema• Inflammation

• STAGE 2: Local Effects• Retroperitoneal edema• Ileus

• STAGE 3: Systemic Complications• Hypotension/shock• Metabolic disturbances• Sepsis/organ failure

SEVERITYSEVERITYMildMild

SevereSevere

Clinical Features

• Pain –Upper abdominal (epigastrium) Sudden Radiating to the back and girdle. (50%) // sometimes can be completely

localized.Associated with nausea and vomiting. Intensity escalates , peaking within 10 to 20 minutes and can persist for

hours.Aggravating factor breathing with chest expansionRelieving factor sitting or leaning forwards*patient may present with shock

Physical Examination

• Extremes either looking well or gravely ill with shock, confusion.• Tachypnea, tachycardia, hypotension• May present with increase of body temperature (fever)• Gall stone pancreatitis Mild jaundice due to biliary obstruction• Grey Turner’s & Cullen’s sign Bleeding into fascial planes causing

bluish discolouration of the flanks (GTS) & umbilicus(CS)• Abdominal distention due to ileus or rarely, shifting dullness. • Guarding in upper abdomen.

Grading Severity

Severe >3 factors present

Investigations

• FBC for infection ; White cell count increased.

• Serum Amylase (increase 4x ; more than 1000IU/mL) normally peaks within 24 hours of symptomsD/d of increase Serum Amylase : Renal failure, cirrhosis, peritonitis, rupture of ectopic pregnancy,

parotitis.

Investigations

• Serum Lipase• The preferred test for diagnosis• Begins to increase 4-8H after onset of symptoms and peaks at 24H• Remains elevated for days• Sensitivity 86-100% and Specificity 60-99%• >3X normal

Other important investigations• Transabdominal ultrasound evaluate changes in pancreas• BUSE determine level of dehydration• Serum calcium suggest saponification• Serum glucose to assess damage to beta cells which interferes

with insulin production leading to hyperglycaemia• Abdominal radiographs (CT)

CT seen normally for gallstones, edema & swollen pancreas , dilated common bile duct

ERCP (Endoscopic Retrograde Cholangio-Pancreatography) is involved in identification and removal of stones in common bile duct in gall stone pancreatitis.

Treatment & Management

• Supplemental oxygen via nasal prongs (as pt. might have risk of ARDS, hypoxemia due to pain)

• Nil by mouth• Aggressive fluid replacement 5 to 10 ml/kg/hr normal saline • Antibiotics Imipenem or Ampicillin or 3rd generation Cephalosporins ; ie

Ceftriaxone ---- to clear out any extrapancreatic infections, sepsis.• Analgesics Acetaminophen, Tramadol• Octreotide Decrease pancreatic secretion• Solve underlying cause (ERCP) when in indicated• Surgery infected pancreatic necrosis , gallstones, cholidocholithiasis• Lifestyle change

Complications• Systemic (common in first week)- CVSshock, arrhythmias- RSP ARDS- Renal failure- Haematological DIC- GI Ileus- NVS confusion, visual

disturbances

Local (after first week)

-Acute fluid collection-Sterile & infected pancreatic necrosis-Pseudocyst Collection of amylase rich fluid enclosed in a wall of fibrous granulation tissue

UROLITHIASIS

Urolithiasis (from Greek oûron-urine and lithos-stone) is the condition where urinary stones are formed or located anywhere in the urinary system.

Urolithiasis

Kidney stones Ureteral stones Bladder stones

Urolithiasis

Four main chemical types:Calcium oxalate stones

Struvite (magnesium ammonium phosphate) stones

Uric acid stones

Cystine stones

Xanthine stones

Calcium oxalate stones account for 75% of Urolithiasis.

Radio-opaque Multiple factors and etiologies Mostly incidental ; irregular sharp

projections

Stones

Account for 15% of renal calculi Infectous stones Gram-negative rods capable of splitting urea

into ammonium, which combines with phosphate and magnesium

More common in females Urine pH is typically greater than 7 Slow growing, painless (non obstructive)

Struvite (magnesium ammonium phosphate) stones

Account for 6% of renal calculi Urine pH less than 5.5

High purine intake eg. organ meats legumes

malignancy

25% of patients have gout

Uric acid stones

Uric Acid Stones

2% of renal calculi Autosomal recessive trait Intrinsic metabolic defect resulting in

failure of renal tubular reabsorption of: Cystine Ornithine Lysine Arginine

Urine becomes supersaturated with cystine, with resultant crystal deposition

*radiofaint appearance

Cystine stones

HistoryKidney stone 30 – 50 yr predominance, silent calculus (incidental) , pain

in posterior renal angle , worst on movement , presents with haematuria ; stone that lodges into ureter >> ureteric colic

Ureter Colic ; loin to groin pain ; 5 sites of narrowing : uteropelvic junction, crossing of iliac artery, juxtaposition of vas def / broad ligament, entrance of bladder, ureteric orifice ; worsens by exercise, relieves by rest.

Bladder suprapubic pain, dysuria, frequency, hesitancy, nocturia, urinary retention. Gross haematuria, sharp/dull pain on terminal voiding of urine at the tip if penis, scrotum, perineum, aggravated by movement. *urinary tract infection is a common symptom

The passage of stones into the ureter is associated with classic renal colic because of:

subsequent acute obstruction proximal urinary tract dilation ureteral spasm

Acute renal colic is probably the most excruciatingly painful event a person can endure

Obstructive ureteral stone

Acute onset of severe flank pain radiating to the groin Gross or microscopic hematuria Nausea, and vomiting not associated with an acute abdomen in

50%

Pain distribution review

Dramatic costovertebral angle tenderness unremarkable abdominal evaluation painful testicles but normal-appearing constant body positional movements (eg,

writhing, pacing) Tachycardia Hypertension Microscopic hematuria

*rule out acute appendicitis & acute cholecystitis

Physical exam

Radiography

A) Kidney-Ureter-Bladder (KUB) film diagnose 90% of stones

Differentials on KUB : calcified lymph nodes, phleboliths.

B) Intravenous Urography (IVU) can diagnose stone presence of radiolucent stones. Important to rule out hydronephrosis & pyenophrosis as the anatomy of urinary system can be seen well.

C) Abdominal Ultrasound

D) CT abdomen investigation of choice for diagnosing uric acid stone

E) Cystoscopy (bladder) visualize stones, assess number, size and position.

Investigations

Urine dipstick, culture & sensitivity microhaematuria, urine pH & crystals.

1. Calcium stones- Alkaline urine 2. Struvite stones- Alkaline urine 3. Uric acid stones- Acidic urine 4. Cystine stones- Acidic urine

Renal Function test

BUSE

Serum calcium, phospharem oxalate, uric acid

Additional Lab Tests

Management (Acute)

• Hydration• Pain management NSAIDS, Acetaminophen• Antispasmodics , alpha blockers • Antibiotics if there is an infection broad spectrum

(G - & G+)• Potassium citrate for alkalinazation of urine (for uric

acid stone)

Surgical Management

Kidney stone Percutaneous Nephrolithomy-Surgeon makes a small incision to the back & places a hollow tube , where a probe follows inside the hollow tube. Stones are grasped and extracted. Larger stones – a laser is used and fragment pieces of the stones are removed.Complication --- haemorrhage from renal parenchyma, perforation of kidney or bowel.

Ureter small stones , conservative treatment ; ie drink more waterLarger stones --- endoscopic removal or open urolithotomy

Bladder Cystoscopy to visualize stone ; laser is used to fragment the stone ; fragments are removed by a lithrotite where fluid is introduced into the bladder , the bulb is compressed and permitted to expand , and the returning solution carries out the fragments of the stone

Complications

• Hydrocalyx• Hydronephrosis • Impaired renal function• Renal Failure• Ureter ureter colic, hydroureter• Bladder Chronic bladder dysfunction

Diverticulitis‘Aisyah Amir

• Diverticula : acquired out-pouching of colon caused by chronic pressure on abdominal wall, common at sigmoidal colon

Diverticulitis

• Inflammation of one or more diverticula• 50 – 70 yrs , women• Rf : genetics, obesity, low fibre diet

Pathophysiology

Clinical Features

• Pain at lower abdomen, shifts to LIF

• Fever• Nausea• LoA• Constipation/ diarrhea• ± urinary symptoms

• Tachycardia• Abdominal distension• Tenderness & guarding @ LIF• Rovsing’s sign• Rebound tenderness• Mass @ LIF, dull• ± bowel sound changes

Management

• Ix : • FBC leukocytosis, anemia • BUSE abnormalities in pts with diarrhea/vomiting• LFT, serum lipase exclude other causes• UPT in females• CT assess severity and presence of complications. Typical finding : pericolic

inflammatory change• Colonoscopy if suspect coexistent malignancy

• Oral antibiotics (ciprofloxacin/cotrimoxazole)• Clear liquid diet• Hospitalize if severe/ evidence of peritonitis• Surgical Mx Resection

Complications

• Pericolic/paracolic Abscess• Perforation peritonitis• Fistula formation• Strictures

Peritonitis

• Inflammation of the peritoneum• Localised / generalised• Bacterial /non-bacterial (sterile)

Causes

• Primary Infection of ascitic fluid (cirrhosis, heart failure) • Secondary Organ perforation (perforated appendicitis, peptic

ulcer, diverticulitis, trauma)• Irritant bile, blood• Ischemia• Traumatic, allergic

Pathogenesis

Stages of peritonitis

• Early• severe pain at site of lesion

• Late• Rigidity• Distension• Absent bowel sounds• Shock, hippocratic facies

Clinical features- begins with CF of underlying condition

• Fever + chills• Abdominal pain (worsens with

movement)• Diarrhea, anorexia, vomiting,

nausea

• Tachycardia• Hypotension• Abdominal tenderness +

Rebound tenderness• Rigidity, guarding• Reduced/absent bowel sounds

Investigations• Ix :

• Urine dipstick• FBC leukocytosis, Hb• BUSE• Serum amylase acute pancreatitis• CT scan locate pathology• GXM prospective surgery• CXR subdiaphragmatic gas

Management

• Resuscitate• Supportive therapy correct electrolyte imbalances, hemodynamic

abnormalities• Antibiotics, analgesics• Control of cause (surgical/non-surgical)

• Surgical removal of source• Non-surgical percutaneous drainage

• Explore peritoneal cavity, remove exudate

Complications

• Paralytic ileus• Abscess• Bowel obstruction (adhesions)• Septic shock• MODS• Death