ACUTE ABDOMEN

Definition
Any severe abdominal pain, caused by acute disease of or injury to the internal organs, for which emergency surgery must be considered

Aetiologies
Medical causes O&G causes Surgical causes

System
Cardiac

Disease
Myocardial infarction Acute pericarditis

System

Disease
Addisonian crisis

Endocrine Diab ketoacidosis

Pulmonary Pneumonia
PE

Metabolic

Acute porphyria Mediterranean fever

GI

Acute pancreatitis Gastroenteritis Acute hepatitis Pyelonephritis

Musculoskeletal

Rectus muscle hematoma

GU

CNS
Vascular
Aortic dissection

Tabes dorsalis (syph)

Sickle cell crisis

Heme

O & G etiology
Organ Ovary Lesion
Ruptured graafian follicle Torsion of ovary Tubo-ovarian abscess (TOA)

Fallopian tube

Ectopic pregnancy Acute salpingitis Pyosalpinx

Uterine rupture Endometritis

Uterus

Classification of Surgical Causes

Inflammation Inflammation Obstruction Obstruction Ischemia Ischemia Perforation (any of above can end here) Perforation (any of above can end here)

Offended organ becomes distended Offended organ becomes distended Lymphatic/venous obstrux due pressure Lymphatic/venous obstrux dueto to pressure Arterial pressure exceeded ischemia Arterial pressure exceeded ischemia Prolonged ischemia perforation Prolonged ischemia perforation

Inflammation vs Obstruction
Organ Stomach Biliary Tract Lesion
Gastric Ulcer Duodenal Ulcer Acute choly +/choledocholithiasis

Location

Lesion

Adhesions Small Bulges Bowel Obstruction Cancer Crohns disease Gallstone ileus Intussusception Volvulus

Pancreas
Small Intestine Large Intestine

Acute, recurrent, or chronic pancreatitis

Crohns disease Meckels diverticulum Appendicitis Diverticulitis

Malignancy Large Volvulus: cecal or Bowel sigmoid Obstruction

Diverticulitis

Ischemia/Perforation
Acute mesenteric ischemia
Usually acute occlusion of the SMA from thrombus or embolism Typically smoker, vasculopath with severe atherosclerotic vessel disease

Chronic mesenteric ischemia Ischemic colitis

Any inflammation, obstructive, or ischemic process can progress to perforation

Ruptured abdominal aortic aneurysm

 Right lower lobe pneumonia/emb olism

Cholecystitis Biliary colic hepatitis
Renal colic Appendicitis

MI Pancreatitis Gastritis Perforated gastric ulcer

Left lower lobe pneumonia/em bolism

Large bowel obstruction

Small bowel obstruction Crohn`s dz Intestinal ischemia Aortic aneurysm Gastroenteritis

Renal colic Large bowel obstruction

Sigmoid diverticulitis
Left tubo-ovarian pathology

Appendicitis Crohn`s dz Right tuboovarian pathology

Cystitis Urinary retention Dysmenorrhea endometriosis

Diagnostic Approach
History
Pain
Site - Where is the pain? Or the maximal site of the pain. Onset - When did the pain start, and was it sudden or gradual? Include also whether if it is progressive or regressive. Character - What is the pain like? An ache? Stabbing? Radiation - Does the pain radiate anywhere? Associations - Any other signs or symptoms associated with the pain? Time course - Does the pain follow any pattern? Exacerbating/Relieving factors - Does anything change the pain? Severity - How bad is the pain?

 Onset
Sudden
Perforated PU, gallstone colic, aortic dissection, ruptured AAA, SMA embolism, ruptured ectopic pregnancy, ruptured/twisted ovarian cyst

Insidious
Acute appendicitis, acute pancreatitis, intestinal obstruction, acute pyelonephritis, gastritis, gastroenteritis

 Age
Childhood : acute appendicitis, intussusception, viral enteritis Adult: infection-inflammation, female reproductive organs, Middle-to old age: malignancy, degenerative dz

 Nature of pain
Constant : inflammation Colicky: acute obstruction of hollow viscous organs ( biliary tree, small bowel ) Shearing/tearing: aortic dissection, ruptured AAA

 PARTS OF THE

GUT

Stomach to 2ndpart of duodenum, including liver, biliary trees, pancreas, and spleen are derived from FOREGUT 3rd and 4thpart of duodenum, jejunum, ileum, appendix, ascending colon to proximal 2/3 of transverse colon are derived from MIDGUT Distal 1/3 of transverse colon to anal canal above dentate line are derived from HINDGUT

 Visceral pain from organs derived from FOREGUT and MIDGUT is at midline and above or around the umbilicus. Visceral pain from organs derived from HINDGUT is at midline and below the umbilicus.

 Abdominal pain is typically derived from one or more three distinct pain pathways 1. Visceral, 2.Parietal (Somatic ) 3.Referred

Sympathetic and parasympathetic nerve innervations(C fibers) Character -dull or cramping pain -insidious -sensitive to distension, ischemia,squeeze -insensitive to heat, cutting, or electric

Visceral Abdominal Pain is usually caused by distention of hollow organs or capsular stretching of solid organs.

 Somatic nerve innervations (A fibers) Somatic nerve distribution (T7-L2, umbilicus at T12) Character -----sharp and exquisite pain Sensitive to mechanical stimuli (stretching, pinprick, pinch), heat, electrical shock, chemical stimulus, infection-inflammation

Results from ischemia, inflammation , or stretching of the parietal Peritoneum.

The parietal pain , in contrast to visceral pain pain, , often can be localized to the region of the painful stimulus.

This pain is typically sharp, knife- like and constant; coughing and moving are likely likely to aggravate it.

Referred pain
Is defined as pain felt at a distance from the diseased organ . It results from shared central pathways for afferent neurons from different locations .

Associated symptoms
Fever nausea/vomiting Jaundice Bowel habits : diarrhea/constipation, bloody/mucus stool Gynaecologic hx: menstruation, sexual intercourse Concomitant hx: family hx, past med/surg hx, medication

examination
Exposure TYPES OF ABDOMEN: Flat rounded or convex Scaphoid protuberant

 Flat is normal LARGE CONVEX ABDOMEN -- 7 FS

Fat Faeces Fluid (ascites) Foetus Flatus Fatal growth (malignancy) Fibroid tumor

CONCAVE OR SCAPHOID ABDOMEN Decreased fat deposits Malnourished state Flaccid muscle tone

 THE ABDOMEN SHOULD BE SYMMETRICAL BILATERAL Asymmetry indicates

tumor cysts bowel obstruction enlargement of abdominal organs scoliosis

Normally no retractions -- the abdomen rises and falls with each respiration Abnormal due to abdominal disorders
appendicitis with local peritonitis pancreatitis biliary colic or ac. cholecystitis perforated ulcer

 Masses or nodules -- tumors, metastasis or pregnancy Visible Peristalsis -- indicative of obstruction Pulsation -- aortic aneurysm

 Lightly palpate to note Skin temperature Tenderness Large masses

Use both hands -- one on each rectus Check for tensing during expiration When positive it is indicative of peritoneal irritation -- peritonitis

 Palpate the liver margin at the lateral border of the rectus muscle
Have the patient take a deep breath If patient exhibits pain and stops inhaling this is a positive Murphys Sign present in Cholecystitis

Pull up with left hand and push in with right hand on inspiration Will only be able to feel if 3 times normal size Splenomegaly inflammation congestive heart failure cancer cirrhosis

 Assess the width of the aorta by placing your Apply firm pressure for several seconds to the hands on each side of the abdomen with hand at right angles and fingers extended aorta just above the Quickly release the pressure umbilicus Test away from site where pain is initially Abdominal aortic determined aneurysm -- width greater than 4 cm with lateral pulsations

 Normal liver span

6-12 cm in males 10.5 cm in females

Percuss from symphisis pubis (urine filled gives dull sound) - if patient unable to empty it is secondary to: Neurogenic dysfuntion Benign prostatic hypertrophy Post-op case Urethral stricture

 Normal Bowel Sounds are high pitched with Clicks and Gargles , which occur every 5 to 15 seconds intervals

Use diaphragm of stethoscope lightly placed RLQ->RUQ->LUQ->LLQ Bowel sounds4-12/min High-pitched always heard RLQ-ileo-ceacal area

Bowel Sounds are high pitched sounds & are classified into 4 categories 1.Normal 2.Hypoactive 3.Absent 4.Hyperactive

Borborygmi -- stomach growling -- normal, hyperactive, gurgling sound

 Hypoactive bowel sounds -indicates decreased motility Peritonitis Mechanical obstruction Non-mechanical obstruction adhesions, hernias, masses Inflammation Non-mechanical obstruction Gangrene no intestinal contraction (paralytic ileus) -- physiological, Electrolyte imbalances neurogenic, and chemical Intraoperative manipulation of imbalances the bowel
Absent bowel sounds no sound for 4-5minutes-Late intestinal obstruction

 High pitched tinkling hyperactive bowel sounds Caused by powerful peristaltic action indicative of partial obstruction Abdominal cramping

Hyperactive bowel sounds -- increased motility of the bowel Gastroenteritis Diarrhea Laxative use Subsiding ileus

Venous hum A continuous pulsing or fibrillary sound If present in the periumbilical area is secondary to portal vein obstruction Portal hypertension caused by cirrhosis

Friction Rub Using the diaphragm of the stethoscope a sound similar to rubbing sandpaper together Sound increases with inspiration Tumors Inflammation Infarction

Acute appendicitis
The position of the base of the appendix is constant, being found at the confluence of the three taeniae coli of the caecum, which fuse to form the outer longitudinal muscle coat of the appendix. At operation, use can be made of this to find an elusive appendix, as gentle traction on the taeniae coli, particularly the anterior taenia, will lead the operator to the base of the appendix.

The appendiceal orifice opens into the cecum. Its blood supply, the appendiceal artery, is a terminal branch of the ileocolic artery, which traverses the length of the mesoappendix and terminates at the tip of the organ

Appendicitis occurs most frequently in the second and third decades of life.

 The natural history of appendicitis is similar to that of other inflammatory processes involving hollow visceral organs. Initial inflammation of the appendiceal wall is followed by localized ischemia, perforation, and the development of a contained abscess or generalized peritonitis.
Right lower quadrant (right anterior iliac fossa) abdominal pain Anorexia Nausea and vomiting
Indigestion Flatulence Bowel irregularity Diarrhea Generalized malaise

The pain is typically periumbilical in nature with subsequent migration to the right lower quadrant as the inflammation progresses

The symptoms of appendicitis vary depending upon the location of the tip of the appendix an inflamed anterior appendix produces marked, localized pain in the right lower quadrant retrocecal appendix may cause a dull abdominal ache The location of the pain may also be atypical in patients who have the tip of the appendix located in the pelvis, which can cause tenderness below McBurney's point.
Such patients may complain of urinary frequency and dysuria or rectal symptoms, such as tenesmus and diarrhea Patients with a retrocecal appendix may not exhibit marked localized tenderness in the right lower quadrant since the appendix does not come into contact with the anterior parietal peritoneum. The rectal and/or pelvic examination is more likely to elicit positive signs than the abdominal examination.

In women, right adnexal area tenderness may be present on pelvic examination, and differentiating between tenderness of pelvic origin versus that of appendicitis may be challenging.

 McBurney's point tenderness is described as maximal tenderness at 1.5 to 2 inches from the anterior superior iliac spine (ASIS) on a straight line from the ASIS to the umbilicus. (Sensitivity 50 to 94 percent; specificity 75 to 86 percent)

Rovsing's sign refers to pain in the right lower quadrant with palpation of the left lower quadrant. This sign is also called indirect tenderness and is indicative of right-sided local peritoneal irritation. (Sensitivity 22 to 68 percent; specificity 58 to 96 percent)
The psoas sign is associated with a retrocecal appendix. This is manifested by right lower quadrant pain with passive right hip extension. The inflamed appendix may lie against the right psoas muscle, causing the patient to shorten the muscle by drawing up the right knee. Passive extension of the iliopsoas muscle with hip extension causes right lower quadrant pain. (Sensitivity 13 to 42 percent; specificity 79 to 97 percent) obturator sign is associated with a pelvic appendix. This test is based on the principle that the inflamed appendix may lay against the right obturator internus muscle. When the clinician flexes the patient's right hip and knee followed by internal rotation of the right hip, this elicits right lower quadrant pain, (Sensitivity 8 percent; specificity 94 percent)

 Acute 14,500 Gangrenous 17,100 Perforated 17,900 Mild elevations in serum bilirubin

Computed tomography findings The following findings suggest acute appendicitis on standard abdominal computed tomography (CT) scanning with contrast including: Enlarged appendiceal diameter >6 mm with an occluded lumen Appendiceal wall thickening (>2 mm) Periappendiceal fat stranding Appendiceal wall enhancement Appendicolith (seen in approximately 25 percent of patients)

Ultrasound findings The most accurate ultrasound finding for acute appendicitis is an appendiceal diameter of >6 mm

The modified Alvarado scale assigns a score to each of the following diagnostic criteria: Migratory right iliac fossa pain (1 point) Anorexia (1 point) Nausea/vomiting (1 point) Tenderness in the right iliac fossa (2 points) Rebound tenderness in the right iliac fossa (1 point) Fever >37.5C (1 point) Leukocytosis (2 points)
A low Alvarado score (<5) has more diagnostic utility to rule out appendicitis than a high score (7) does to rule in the diagnosis.

 A patient with a score of 0 to 3 could be considered to have a low risk of appendicitis and would be discharged with advice to return if there was no improvement in symptoms, subject to social circumstances. A patient with a score of 4 to 6 would be admitted for observation and reexamination. If the score remains the same after 12 hours, operative intervention is recommended. A male patient with a score of 7 to 9 would proceed to appendectomy. A female patient who is not pregnant with a score of 7 to 9 would undergo diagnostic laparoscopy, then appendectomy if indicated by the intraoperative findings..

 Advantages of US compared with CT imaging include:

Results may be obtained more efficiently (institution and practitioner dependent) No radiation exposure No use of intravenous or intestinal contrast agents

Disadvantages of US compared with CT imaging include:

Less diagnostic accuracy Less likely to reveal an accurate alternative diagnosis Accuracy is operator dependent Technical challenges: Patients with a large body habitus and/or a large amount of overlying bowel gas

DDx
Perforated appendix
Once significant inflammation and necrosis occur, the appendix is at risk of perforation, which leads to localized abscess formation or diffuse peritonitis temperature exceeds 103.0F (39.4C), the WBC count is greater than 15,000 cells/microL, and imaging studies reveal a fluid collection in the right lower quadrant.

Cecal diverticulitis
usually occurs in young adults Patients with right-sided diverticulitis tend to be younger than those with leftsided disease and often are misdiagnosed with acute appendicitis. Computed tomographic (CT) scanning of the abdomen with IV and oral contrast is the diagnostic test of choice

 A Meckel's diverticulum is a congenital remnant of the omphalomesenteric duct and is located on the small intestine two feet from the ileocecal valve
If an inflamed appendix is not found on abdominal exploration for acute appendicitis, the surgeon should search for an inflamed Meckel's diverticulum.

Acute yersiniosis
right lower abdominal pain, fever, vomiting, leukocytosis, and understated diarrhea At surgery, findings include visible inflammation around the appendix and terminal ileum and inflammation of the mesenteric lymph nodes; the appendix itself is generally normal.

 Crohn's disease can present with symptoms similar to appendicitis, particularly when localized to the distal ileum.
Fatigue, prolonged diarrhea with abdominal pain, weight loss, and fever, with or without gross bleeding, are the hallmarks of Crohn's disease

A tubo-ovarian abscess (TOA)

These abscesses are found most commonly in reproductive age women and typically result from upper genital tract infection. Tubo-ovarian abscess is usually a complication of pelvic inflammatory disease. The classic presentation includes acute lower abdominal pain, fever, chills, and vaginal discharge The recent onset of pain that worsens during coitus or with jarring movement the onset of pain during or shortly after menses is particularly suggestive Rebound tenderness and decreased bowel sounds are common. On pelvic examination, the finding of a purulent endocervical discharge and/or acute cervical motion and adnexal tenderness with bimanual examination is strongly suggestive of PID

 Rupture of an ovarian cyst

common occurrence in women of reproductive age associated with the sudden onset of unilateral lower abdominal pain. The pain often begins during strenuous physical activity Rupture of a simple cyst usually results in only mild to moderate tenderness on deep palpation.

Mittelschmerz
midcycle pain in an ovulatory woman caused by normal follicular enlargement

Renal colic
waxes and wanes in severity Paroxysms of severe pain usually last 20 to 60 minutes.

Intestinal obstruction
Bowel obstruction occurs when the normal flow of intraluminal contents is interrupted. The cause of the obstruction may be external to the bowel (extrinsic), within the wall of the bowel (intrinsic), or due to a luminal defect that prevents the passage of gastrointestinal contents. Obstruction of the small intestine can be partial or complete. A type of complete obstruction, a closed-loop obstruction, occurs when the intestine is obstructed at two locations, creating a segment with no proximal or distal outlet. Closed-loop obstruction can rapidly progress to bowel strangulation

Pathophysiology Obstruction leads to progressive dilation of the intestine proximal to the blockage, while distal to the blockage the bowel will decompress as luminal contents pass. Swallowed air, and gas from bacterial fermentation, can accumulate, adding to bowel distention. As the process continues, the bowel wall becomes edematous, normal absorptive function is lost, and fluid is sequestered into the bowel lumen There may also be transudative loss of fluid from the intestinal lumen into the peritoneal cavity. With proximal bowel obstruction, ongoing emesis leads to additional loss of fluid containing Na, K, H, and Cl, and metabolic alkalosis. These fluid losses can result in hypovolemia.

Bacterial overgrowth can also occur in the proximal small bowel, which is normally nearly sterile, and emesis can become feculent.

 If bowel dilation is excessive, the intramural vessels of the small intestine become compromised and perfusion to the wall of the intestine is reduced If perfusion to a segment of intestine is inadequate to meet the metabolic needs of the tissue, ischemia will occur, which will eventually lead to necrosis and perforation

The most common causes of mechanical small bowel obstruction are postoperative adhesions and hernias. Other etiologies of small bowel obstruction include disease intrinsic to the wall of the small intestine (eg, tumors, stricture, intramural hematoma) and processes that cause intraluminal obstruction (eg, intussusception, gallstones, foreign bodies).

Small bowel obstruction

The most important risk factors include:
Abdominal wall or groin hernia Intestinal inflammation History of, or increased risk for neoplasm Prior irradiation History of foreign body ingestion

Features of obstruction
In high small bowel obstruction, vomiting occurs early and is profuse with rapid dehydration. Distension is minimal with little evidence of fluid levels on abdominal radiography In low small bowel obstruction, pain is predominant with central distension. Vomiting is delayed. Multiple central fluid levels are seen on radiography In large bowel obstruction, distension is early and pronounced. Pain is mild and vomiting and dehydration are late. The proximal colon and caecum are distended on abdominal radiography

The nature of the presentation will also be influenced by whether the obstruction is: acute; chronic; acute on chronic; subacute.
Acute obstruction usually occurs in small bowel obstruction, with sudden onset of severe colicky central abdominal pain, distension and early vomiting and constipation Chronic obstruction is usually seen in large bowel obstruction, with lower abdominal colic and absolute constipation followed by distension. In acute on chronic obstruction , there is a short history of distension and vomiting against a background of pain and constipation. Subacute obstruction implies an incomplete obstruction.

Distension In the small bowel the degree of distension is dependent on the site of the obstruction and is greater the more distal the lesion. Visible peristalsis may be present.
Constipation This may be classified as absolute (i.e. neither faeces nor flatus is passed) or relative (where only flatus is passed) Absolute constipation is a cardinal feature of complete intestinal obstruction. The rule that constipation is present in intestinal obstruction does not apply in: Richters hernia; obstruction associated with pelvic abscess; partial obstruction (faecal impaction/colonic neoplasm) in which diarrhoea may often occur.

Dehydration Dehydration is seen most commonly in small bowel obstruction because of repeated vomiting and fluid sequestration. It results in dry skin and tongue, poor venous filling and sunken eyes with oliguria. The blood urea level and haematocrit rise, giving a secondary polycythaemia. Pyrexia in the presence of obstruction may indicate:
the onset of ischaemia; intestinal perforation; inflammation associated with the obstructing disease

 Abdominal pain associated with small bowel obstruction is

frequently described as periumbilical and cramping with paroxysms of pain occurring every four or five minutes A progression from cramping to more focal and constant pain may indicate peritoneal irritation related to complications (ischemia, bowel necrosis). A sudden onset of severe pain may suggest acute intestinal perforation With proximal small bowel obstruction (duodenum, proximal jejunum), nausea and vomiting can be relatively severe, and patients with proximal small bowel obstruction typically cease taking in food or liquids orally.

Clinical features of strangulation

Constant pain Tenderness with rigidity Shock

 Abdominal inspection should also look for any surgical scars and evidence for abdominal wall hernia (including incisional hernia) or groin hernias Acute mechanical bowel obstruction is characterized by high-pitched tinkling sounds associated with the pain. With significant bowel distention, bowel sounds may become muffled, and as the bowel progressively distends, bowel sounds can become hypoactive Distention of the bowel results in hyperresonance or tympany to percussion throughout the abdomen. However, fluid-filled loops will result in dullness. If percussion over the liver is tympanitic rather than dull, it may be indicative of free intraabdominal air. Tenderness to light percussion suggests peritonitis. Digital rectal examination should be performed to identify fecal impaction or rectal mass as the source of obstruction. Gross or occult blood may be related to intestinal tumor, ischemia, inflammatory mucosal injury, or intussusception

Lab studies Plain radiography demonstrate findings that indicate the immediate need for urgent decompression (eg, sigmoid volvulus) or surgical intervention (eg, pneumoperitoneum, cecal or midgut volvulus)
Dilated loops of bowel with air-fluid levels In the supine position, the air-fluid interface is parallel to the x-ray plate, and the entire width of air and fluid-filled loops of bowel will be visible. This allows an estimation of the amount of distention. In an upright position, the air-fluid interface is perpendicular to the film and is evident as an air-fluid level. Multiple air-fluid levels with distended loops of small bowel are seen in small bowel obstruction.

 Proximal bowel dilation with distal bowel collapse Small bowel obstruction can be diagnosed if the more proximal small bowel is dilated more than 2.5 cm (outer wall to outer wall) and the more distal small bowel is not dilated the presence of air-fluid levels differing more than 5 mm from each other within the same loop of small bowel on upright films supports a diagnosis of mechanical small bowel obstruction A gasless abdomen may be due to complete filling of loops of bowel with sequestered fluid

Abdominal CT
more useful than plain radiographs for identifying the specific site (ie, transition point) and severity of obstruction (partial versus complete) ; determining the etiology by identifying hernias, masses , or inflammatory changes; and for identifying complications (ischemia, necrosis, perforation) Bowel wall thickening >3 mm (nonspecific)

Submucosal edema/hemorrhage Mesenteric edema Ascites Target sign alternating hypo/hyperdense layers, indicative of intussusception Whirl sign rotation of small bowel mesentery, suggesting a twist or a volvulus Venous Cut-off Sign venous flow to a loop of small bowel that is cut off suggests thrombosis

 On imaging studies, a closed-loop obstruction often appears as a distended, fluid-filled, sometimes C-shaped or U-shaped bowel segment. A diagnosis of perforation relies on the finding of extraluminal air in diagnostic imaging studies and may be detected as:
Free air under the diaphragm on upright chest or upright abdominal radiograph Free air over the spleen or liver on lateral abdominal film or abdominal CT Free air as a football sign on supine abdominal film or abdominal CT

Ddx
Adynamic (paralytic) ileus Paralytic ileus occurs to some degree after almost all open abdominal operations and can also be caused by peritonitis, trauma, intestinal ischemia, and medications (eg, opiates, anticholinergics). It is exacerbated by electrolyte disorders, particularly hypokalemia. As the intestine becomes distended, the patient experiences many of the same symptoms as mechanical obstruction. However, on radiologic examination, there is no demonstrable mechanical obstruction

In differentiating early postoperative ileus from postoperative adhesive disease,

it is useful to note that nearly all patients with early postoperative bowel obstruction have an initial of return of bowel function and oral intake, which is then followed by nausea, vomiting, abdominal pain, and distention,

whereas patients with adynamic ileus do not experience return of bowel function

 Pseudo-obstruction
Intestinal pseudoobstruction is a chronic condition characterized by symptoms of recurrent abdominal distention that may be associated with nausea, vomiting, and diarrhea. The colon is generally affected more than the small intestine. No mechanical cause can be demonstrated

Ogilvie syndrome is the acute pseudo-obstruction and dilation of the colon in the absence of any mechanical obstruction in severely ill patients
Colonic pseudo-obstruction is characterized by massive dilatation of the cecum (diameter > 10 cm) and right colon on abdominal X-ray. especially following coronary artery bypass surgery and total joint replacement

 Large bowel obstruction tumour, adhesion, volvulus Volvulus

Caecal volvulus This may occur as part of volvulus neonatorum or de novo and is usually a clockwise twist. It is more common in females and usually presents acutely with the classic features of obstruction. At first the obstruction may be partial, with the passage of flatus and faeces.

 Sigmoid volvulus
The symptoms are of large bowel obstruction, which may initially be intermittent followed by the passage of large quantities of flatus and faeces. Presentation varies in severity and acuteness, with younger patients appearing to develop the more acute form. Abdominal distension is an early and progressive sign, which may be associated with hiccough and retching; vomiting occurs late. Constipation is absolute. In the elderly, a more chronic form may be seen.

abdominal CT scan
of a grossly dilated cecum or sigmoid colon quickly distinguish volvulus from small bowel obstruction and indicate the need for treatment, which is surgical (right colectomy) for cecal volvulus, and, for sigmoid volvulus, involves endoscopic decompression and derotation, followed by surgery in selected patients.

adenocarcinoma of the colon and rectum

predominant malignancy causing obstruction. Colonic obstruction complicates 10 to 20 percent of colon cancers. Because tumors are slow growing and often located more distally in the colon, symptoms are chronic and progressive, and rarely confused with acute small bowel obstruction.

 Intussusception
rare in adults, accounting for 1 to 5 percent of mechanical bowel obstructions a/w lymphoid hyperplasia, Kaposi's sarcoma, and non-Hodgkin's lymphoma

Initially, the passage of stool may be normal, whereas, later, blood and mucus are evacuated the redcurrant jelly stool.

treatment

Acute pancreatitis
Pathophysiology
The precise mechanism by which obstruction of the sphincter of Oddi by a gallstone or microlithiasis (sludge) causes pancreatitis is unclear, although it probably involves increased ductal pressure. The underlying mechanism of injury in pancreatitis is thought to be premature activation of pancreatic enzymes within the pancreas, leading to a process of autodigestion.

Anything that injures the acinar cell and impairs the secretion of zymogen granules, or damages the duct epithelium and thus delays enzymatic secretion, can trigger acute pancreatitis.
Once cellular injury has been initiated, the inflammatory process can lead to pancreatic oedema, haemorrhage and, eventually, necrosis.

As inflammatory mediators are released into the circulation, systemic complications can arise, such as haemodynamic instability, bacteraemia (due to translocation of gut flora), acute respiratory distress syndrome and pleural effusions, gastrointestinal haemorrhage, renal failure and disseminated intravascular coagulation (DIC).

 CLASSIFICATION
Mild acute pancreatitis, which is characterized by the absence of organ failure and local or systemic complications Moderately severe acute pancreatitis, which is characterized by transient organ failure (resolves within 48 hours) and/or local or systemic complications without persistent organ failure (>48 hours) Severe acute pancreatitis, which is characterized by persistent organ failure that may involve one or multiple organs

aetiology
I GET SMASHED

Idiopathic: Hypertensive sphincter or microlithiasis Gallstones (45%) Ethanol (35%) Tumours: Pancreas. Ampulla. Choledochocele Scorpion stings Microbiological
Bacteria: Mycoplasma. Campylobacter. TB. M. avium intracellular. Legionella. Leptospirosis Viral: Mumps. Rubella. Varicella. Viral hepatitis. CMV. EBV. HIV. Coxsackie virus. Echovirus. Adenovirus Parasites: Ascariasis. Clonorchiasis. Echinococcosis

Autoimmune: SLE. Polyarteritis nodosa. Crohns Surgery or trauma

Manipulated sphincter of Oddi (ERCP). Post cardiac surgery. Blunt trauma to abdomen. Penetrating peptic ulcer

Hyperlipidemia
(TG >11.3 mmol/L; >1000mg/dL). Hypercalcemia. Hypothermia

Emboli or ischemia Drugs or toxins

Azathioprine. Mercaptopurine. Furosemide. Estrogen. Methyldopa. H2blockers. Valproic acid. Antibiotics. Acetaminophen. Salicylates. Methanol. Organophosphates. Steroids

 cardinal symptom: epigastric pain. Constant ache. The pain may radiate to the back, chest, flanks, and lower abdomen. Patients are usually restless and bend forward (the knee-chest position) in an effort to relieve the pain.

Nausea and vomiting are often present along with accompanying anorexia. Persistent in nature.

Physical examination
The majority of patients exhibit jaundice- obstructive jaundice because of the choledocolithiasis or Mirizzi syndrome Abdominal tenderness, muscular guarding, and distension are observed in most patients. Bowel sounds are often hypoactive due to gastric and transverse colonic ileus. Guarding tends to be more pronounced in the upper abdomen. Ileus is explained by the inflammation extension to the mesentery and mesocolon and by chemical peritonitis. Abdominal distension sometimes can appear due to pancreatic ascites, pseudocyst

 Some patients experience dyspnea, which may be caused by irritation of the diaphragm (resulting from inflammation), pleural effusion, or a more serious condition, such as acute respiratory distress syndrome (ARDS). patients with severe acute pancreatitis are often pale, diaphoretic, and listless
physical findings associated with severe necrotizing pancreatitis:
The Cullen sign is a bluish discoloration around the umbilicus resulting from hemoperitoneum. The Grey-Turner sign is a reddish-brown discoloration along the flanks resulting from retroperitoneal blood dissecting along tissue planes. Erythematous skin nodules may result from focal subcutaneous fat necrosis. These are usually not more than 1 cm in size and are typically located on extensor skin surfaces. In addition, polyarthritis is occasionally seen. Purtscher retinopathy, this ischemic injury to the retina appears to be caused by activation of complement and agglutination of blood cells within retinal vessels. It may cause temporary or permanent blindness

Lab tests Amylase/lipase/urine diatase

diagnosis of acute pancreatitis requires two of the following three features: 1) abdominal pain characteristic of acute pancreatitis, 2) serum lipase 3 times the upper limit of normal, and 3) characteristic findings of acute pancreatitis on CT scan.
(hypocalcemia resulting from saponification of fats in the retroperitoneum). Serum electrolytes, BUN, creatinine, and glucose: measure these to look for electrolyte imbalances, renal insufficiency, and pancreatic endocrine dysfunction. LFT

FBC
C-reactive protein (CRP) value can be obtained 24-48 hours after presentation as an indicator of prognosis. A CRP value > 150mg/dL strongly indicates severe pancreatitis.

Arterial blood gases: we have to measure them if a patient is dyspneic for determining whether tachypnea is due to acute respiratory distress syndrome or diaphragmatic irritation.

investigations
AXR : detect free air in the abdomen for differential diagnosis with perforated ulcer. The inflammatory process may damage peripancreatic structures, resulting a sentinel loop, or an ileus.
CXR: PE

Ultrasound is valuable in detecting free peritoneal fluid, gallstones and dilatation of the bile ducts.
Abdominal CT scanning is not indicated for all patients, being reserved for unclear cases, severe forms and complication. interstitial and necrotizing pancreatitis can be made much more readily when a contrast-enhanced CT scan. Endoscopic ultrasonography (EUS): evaluating the cause of severe pancreatitis, particularly microlithiasis and biliary sludge.

ERCP is indicated for clearance of bile duct stones in patients with severe pancreatitis, in those with cholangitis, in those who are poor candidates for cholecystectomy, in those who are postcholecystectomy, and in those with strong evidence of persistent biliary obstruction.

Balthazar score

ddx
mesenteric ischemia or infarction; - Perforated gastric or duodenal ulcer; - Biliary or renal colic; - Dissecting aortic aneurysm; - Intestinal obstruction; - Inferior wall myocardial infarction.

Ranson score
At admission: 1.Age in years > 70 years 2.White blood cell count > 18000 cells/mm3 3.Blood glucose > 12.2 mmol/L (> 220 mg/dL) 4.Serum AST > 250 IU/L 5.Serum LDH > 400 IU/L Within 48 hours: 1.Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL) 2.Hematocrit fall > 10% 3.Oxygen (hypoxemia PO2 < 60 mmHg) 4.BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration 5.Base deficit (negative base excess) > 5 mEq/L 6.Sequestration of fluids > 4 L

acute pancreatitis

Gallstone pancreatitis

 Imrie score

Age >55 years = 1 point Serum albumin <32 g/L (3.2 g/dL) = 1 point Arterial PO2 on room air <8 kPa (60 mmHg) = 1 point Serum calcium <2 mmols/L (8 mg/dL) = 1 point Blood glucose >10.0 mmols/L (180 mg/dL) = 1 point Serum LDH >600 units/L = 1 point Serum urea nitrogen >16.1 mmols/L (45 mg/dL) = 1 point WBC count >15 x 10^9/L (15 x 10^3/microlitre) = 1 point. The addition of the parameter points yields the Glasgow prognostic criteria. The score can range from 0 to 8. If the score is >2, the likelihood of severe pancreatitis is high. If the score is <3, severe pancreatitis is unlikely.

SEVERITY ASSESMENT

Risk factors of severity at admission: - Older age (>55); - obesity (BMI >30); - Organ failure at admission; - Pleural effusion and/or infiltrates. Risk factors of severity at 48 h: - Clinical impresion of severity; - Ranson score >3; - APACHE score > 8; - CRP > 150 UI/ml; - Organ failure. Risk factors of severity at 72 h: - Clinical impression of severity; - Ranson score > 3; - APACHE score > 8; - Maintaining organ failure or MSOF; - CRP > 150 UI/ml. Atlanta Severity Criteria: - Ranson score > 3; - APACHE score >8; - Oorgan failure; - Local complications: necrosis, abscess, pseudo-cyst. Patients with these characteristics may require treatment in a highly supervised area, such as a step-down unit or an intensive care unit

 Resuscitation Transudation of fluid from the intravascular space to the peritoneum is the principle cause of hypovolemia in AP. Balanced electrolyte solutions (9% saline or Ringers lactate) should be given promptly and the rate titrated to frequent assessment of the patients volume status determined by heart rate, blood pressure, urine output and jugular venous pressure insulin administration blood transfusion is indicated if the patients hematocrit is less than 25%; values ranging from 30 to 35% are considered optimal for pancreatic parenchymal perfusion Oxygen saturation should be measured continuously and supplemental oxygen to maintain an arterial saturation greater than 95%

 relieve abdominal pain with a parenterally administered narcotic medication Nutritional support is an integral part of patient care and is started early in the course of disease. Whenever possible, enteral feeding rather than total parenteral nutrition (TPN) is suggested for patients who require nutritional support In mild pancreatitis, oral intake is usually restored within 3-7 days of hospitalization, and nutritional support is not required In severe pancreatitis, nutritional support should be initiated when it becomes clear that the patient will not be able to consume nourishment by mouth for several weeks. This assessment can usually be made within the first 3-4 days of illness.

 antibiotics in necrotizing pancreatitis

 Local complications of pancreatic necrosis, such as pseudocyst and pancreatic abscess, often require surgical or endoscopic intervention.
endoscopic stent placement in a long disrupted pancreatic duct or directly placing the stent into the pseudocyst through the wall of the stomach or duodenum. open or laparoscopic surgery with the formation of an anastomosis between the pseudocyst and part of the gastrointestinal system (stomach, duodenum or Roux loop of jejunum).

Perforated gastric ulcer

Ulcer perforation may be suspected in patients with a history consistent with peptic ulcer disease who develop the sudden onset of severe, diffuse abdominal pain Per abdomen, reveals peritonism. Generalised tenderness with boardlike rigidity. Fever and leukocytosis Pallor, tachycardic Past h/o of melena/hematemasis CXR erect: air under diaphragm. Once a diagnosis of perforation is established, surgical intervention is indicated

 When choosing between these options, the surgeon must consider: The characteristics of the ulcer (location, chronicity, presence of complications) The features of any obstruction (anatomic level, inflammation, pyloric scarring) The patient (age, nutrition, comorbid illness, condition on presentation) The operation (mortality rate, complications, long-term sequelae) Their personal experience

 Ulcer bed management Ulcer bed management may include ligation of bleeding vessels or the placement and fixation of omentum within the ulcer bed to cover the defect and promote healing (ie, Graham patch) Vagotomy Vagotomy is a procedure that transects or removes a portion of the vagus nerves, or branches of the vagus nerves to decrease gastric acid secretion. Vagotomy eliminates direct cholinergic stimulation of acid secretion and renders the acid-producing parietal cells less responsive to histamine and gastrin. Vagotomy also abolishes the vagal stimulus for release of antral gastrin.
sectioning the vagal trunks (ie, truncal vagotomy), sectioning distal nerve fibers (referred to as highly selective vagotomy, parietal cell vagotomy, or proximal gastric vagotomy), or a combination of techniques (eg, Taylor procedure, Hill-Barker procedure).

 Advocate for a truncal vagotomy combined with a drainage procedure, and against highly selective vagotomy, which was associated with higher long-term recurrence rates Truncal vagotomy is performed by identifying and isolating the anterior and posterior vagus nerves at the level of the distal esophagus, ligating the vagus nerves proximally and distally, and removing the intervening nerve segments Gastric drainage Gastric drainage procedures divide or bypass the pyloric sphincter mechanism to facilitate gastric emptying

 Gastrectomy and reconstruction Partial gastrectomy (eg, antrectomy, subtotal gastrectomy) removes the portion of the stomach containing the ulcer, the gastrin producing cells that stimulate acid secretion, and most of the acid-producing parietal cells To remove all of the gastrin-producing antral tissue, it is necessary to resect at least 35 percent of the distal stomach. The line of resection should be taken high onto the lesser curve, as antral tissue extends to within 2 cm of the gastroesophageal junction. Reconstruction of the stomach is necessary following partial gastrectomy to re-establish gastrointestinal continuity. The Billroth I, Billroth II, and Roux-en-Y reconstruction techniques are the most common

Acute cholecystitis
Acute cholecystitis Acute cholecystitis refers to a syndrome of right upper quadrant pain, fever, and leukocytosis associated with gallbladder inflammation that is usually related to gallstone disease Acalculous cholecystitis Acalculous cholecystitis is clinically identical to acute cholecystitis but is not associated with gallstones and usually occurs in critically ill patients. It accounts for approximately 10 percent of cases of acute cholecystitis and is associated with high morbidity and mortality rates Chronic cholecystitis Chronic cholecystitis is the term used to describe chronic inflammatory cell infiltration of the gallbladder seen on histopathology. It is almost invariably associated with the presence of gallstones and is thought to be the result of mechanical irritation or recurrent attacks of acute cholecystitis leading to fibrosis and thickening of the gallbladder

 History

right upper quadrant or epigastrium. The pain may radiate to the right shoulder or back. Characteristically, acute cholecystitis pain is steady and severe. Associated complaints may include fever, nausea, vomiting, and anorexia. There is often a history of fatty food ingestion one hour or more before the initial onset of pain. The episode of pain is typically prolonged (greater than four to six hours)

ill appearing, febrile, and tachycardic, and lie still on the examining table voluntary and involuntary guarding. Patients frequently will have a positive Murphy's sign Patients with complications may have signs of sepsis (gangrene), generalized peritonitis (perforation), abdominal crepitus (emphysematous cholecystitis), or bowel obstruction (gallstone ileus)

 Patients typically have a leukocytosis with an increased number of band forms (ie, a left shift). Elevation in the serum total bilirubin and alkaline phosphatase concentrations are not common in uncomplicated acute cholecystitis since biliary obstruction is limited to the gallbladder; if present, they should raise concerns about complicating conditions such as cholangitis, choledocholithiasis, or Mirizzi syndrome

U/S findings
Gallbladder wall thickening (greater than 4 to 5 mm) or edema (double wall sign) A "sonographic Murphy's sign" is similar to the Murphy's sign elicited during abdominal palpation, except that the positive response is observed during palpation with the ultrasound transducer. This is more accurate than hand palpation because it can confirm that it is indeed the gallbladder that is being pressed by the imaging transducer when the patient catches his or her breath.

Cholescintigraphy (HIDA scan) Morphine cholescintigraphy Mrcp Ct

Ddx
Biliary colic Pancreatitis Hepatitis Pud Acute appendicitis

 Left untreated, symptoms of cholecystitis may abate within 7 to 10 days. However, complications are common, so patients with suspected acute cholecystitis require definitive treatment (eg, cholecystectomy).

AAA
Patients at greatest risk for AAA are men who are older than 65 years and have peripheral atherosclerotic vascular disease. A true aneurysm is defined as a segmental, full-thickness dilation of a blood vessel that is 50 percent greater than the normal aortic diameter In most adults, an aortic diameter >3.0 cm is generally considered aneurysmal Small aneurysms have a diameter <4.0 cm Medium aneurysms have a diameter between 4.0 and 5.5 cm Large aneurysms have a diameter >5.5 cm Very large aneurysms have a diameter 6.0 cm

Protective factor Risk factors

Smoking (current or past) Male gender Advancing age Caucasian race Atherosclerosis Hypertension Family history of AAA Other large artery aneurysms (eg, iliac, femoral, popliteal

Female gender Non-Caucasian race Diabetes

 Asymptomatic Symptomatic but not ruptured

The development of symptoms may be a sign that AAA configuration is rapidly expanding, has become large enough to compress surrounding structures, or is an inflammatory or infectious aneurysm. Patients with symptomatic AAA most commonly present with abdominal, back, or flank pain, which may or may not be associated with AAA rupture. AAA can also present with other clinical manifestations, such as limb ischemia (acute or chronic), or other systemic manifestations (fever, malaise)

Symptomatic and ruptured

The classic presentation of severe pain, hypotension, and a pulsatile abdominal mass occurs in about 50 percent of patients

 A diagnosis of AAA is established with imaging studies that demonstrate the aneurysm in the patient suspected of having AAA on the basis of risk factors or on physical examination. Physical examination may reliably diagnose a large AAA (>5.5 cm) For nonruptured AAA, the imaging test of choice is abdominal ultrasonography, which has sensitivity and specificity approaching 100 percent for an aortic diameter >3.0 cm Computed tomography is the imaging test of choice for the diagnosis of ruptured AAA.

 The hemodynamically unstable patient with known AAA who presents with classic symptoms/signs of rupture (hypotension, flank/back pain, pulsatile mass) should be taken emergently to the operating room for immediate control of hemorrhage, resuscitation, and repair of the aneurysm. For patients with suspected ruptured AAA who are hemodynamically stable, abdominal imaging is performed urgently to confirm the rupture prior to repair Both open and endovascular techniques can be successfully employed in the treatment of ruptured AAA.

 QUESTION & ANSWER