Abdominal Aortic Aneurysms Tuesday, 4 September 2012 8:46 PM Overview Aneurysm: dilation greater than 1.

han 1.5 x than normal Average diameter 2 cm so anything greater than 3 cm is aneurysmal 95% of AAA are infrarenal (important because the surgical treatment of aneurysms of renal arteries are complicated) Most are fusiform or football shaped as opposed to saccular (true aneurysms: 3 layers) AAA ruptured: 25% survive, 50% will make it hospital but only 50% of those will survive repair Overall survival will be 10% as many ppl who die in their sleep will never to diagnosed

Definition and Pathophysiology Majority are due to genetic predisposition, same risk factors as coronary artery disease Atherosclerotic weaken walls and allow for expansion, as radius increases the wall tension increases by a power of 4, acclerating growth and increasing chance of rupture (balloon analogy: less force required as it grows larger) Aneurysms can also be caused by infections: Syphillis and salmonella and staph aureus (rare in developed world). Infectious = mycotic aneurysms (fresh fungus vegetations). But if treated infectious aneurysms expand at a faster rate and rupture more than the more common degenerative type. Last 5-10%: inflammatory aneurysms, thickened aneurysmal wall, peri-aneurysmal fibrosis, and adherence of the aneurysmal sac to adjacent structures. Patients present differently but treatment is the same Risk factors Modifiable and non-modifiable o Non-modifiable: age, male gender (x5), caucasian race, family hx (brothers), connective tissue disease, marfan's, ehler-danos o Modifiable: same as coronary artery disease: hypertension, diabetes, dyslipidemia, smoking (increases risk and acclerates growth) Presentation 3 main ways Asympatoc and unruptured: either as a palpable mass or incidental finding or screening, palpable mass present in only 30% of patients (it's becoming reduced as it gets captured on imaging), pulsates with the patient's heart beat (pulsatile expansile mass: no point in measuring it out as you need ultrasound or imaging to quantify it: as Vidavich mentioned). Always check careful for AAA in a obese patient Sympomatic and unruptured: 25% will present with symptoms (unruptured), pain is the most common compliant (abdominal radiating to back or flank), pain on palpation: rapidly expanding or Impending rupture, AAA may present with thromboembolic events, emboli may cause painful blue toes or acutely cold painful pulseless leg, thrombose will cause bilateral lower extremeity ischemia but usually it will mural thrombus is stable. Infecitous AAA: fever, inflammatory: triad of abdominal pain, weight loss, and elevated ESR or CRP Symptomatic and ruptured (frightening): class triad: abdo pain, hypotension, pulsatile mass (atypical is typical: only 20% is truly hypotensive, 65% abdo pain, 85% palpable abdo mass), can present as kidney stone: flank pain radiating to groin plus haematuria. Gross hametouria delays diagnosis. Ruptured AAA misdiagnosed as diverticulitis, usually it's a sudden event but can mimic a grumbling presentation of an infection. No silent presentation of ruptured AAA Imaging/Diagnosis Abdominal U/S: good for screening and whenever AAA is in your Dx Abdominal CT: will show aneurysms with greater detail is usually unnecessary for screening and diganosis, so it's better for ruling out ddx: kidney stones and when surgery, Abdo xray: calcified aortic shadow Thick mural thrombus in AAA: may show up with contrast as a normal aorta

Medical/Surgical treatment Smoking cessation slows the growth of AAA but non-surgical intervention does not do anything Hypertension and hyperlipidemia should be controlled: to reduce further CV events Elective surgical repair: 5.5 cm for men, 5.0 for women. Yearly mortality from rupture exceeds surgical repair complications Consider surgery if diameter is increasing by 0.5 cm / year Open repair vs. endovascular. Open: true repair, lifetime failure rate is very low, replacing aneurysm with graft, operation is hard on the patient, full recovery by 3 months. No follow up imaging is needed. Endovascular repair: endograft put through the groin, controls the flow through the aneurysm, however it is a compression fit, it can loosen and move...because of this they are CT'd every year. But since the patients only need 2 groin incisions every year and they only stay in hospital for 2-3 days...this operation is better option for sicker higher risk patients if they are expected to live less than 5 years. If greater years expected: open repair Summary AAA same risk factors as cardiovascular disease: so risk reduction is key to reducing this All males must be screened (greater than 65)

Surgery: Presenting your case Wednesday, 5 September 2012 1:29 PM Introduction It's intimidating presenting to consultant, so take a minute to prepare. Internal medicine might want more detail than a surgical. Summarise the key features of the case in 1-2 minutes (short attention span) Guide: positive findings and relevant negative (so not all negative findings) Quickly get to the point, show you understand the features, investigations and treatment plan Hone your presentation skills Case presentation ED: admitted with abdo pain, med student has seen her first Shannon: recorder part mastered...work out what's the most important information Consultant: important part of history and exam, and the 2nd part is presenting it succintly. Key features of presentation: age of patient, how long has she been sick for, main complaint, what's the pain like: SOCRATES Key features on exam: 2 sentences summarised: Mrs. M, 58 year old lady, presents with a 3 day history of worsening pain in the right upper abdomen, precipitated by eating, and associated with nausea and vomiting. There is no surgical history of note, and on the exam she is pyrexic and flushed, with tenderness in the right upper quadrant and a positive murphy's sign. Consultant can then ask further questions: so you still have to ask all the questions What's the most likely diagnosis in this patient? Cholecystitis, why do you think that? DDx: pancreatitis, gastroenteritis, hepatitis (most ppl are jaundiced though) What tests would you like to organise? Labs: WCC (elevated: Chole), lipase (pancreatitis), LFT's (rule out heptatitis), electrolytes and creatinine Imaging: ultrasound of abdomen (to look at gallbladder) What would the treatment plan? Diet: NPO, nothing to eat or drink until U/S Activity: as tolerated by patient Vital signs: take her vitals every 4 hours IV fluids: put her on it Ins and outs: nurses will look out for this Investigations: carry on with this, see what happens with the U/S Drugs : pain and nausea drugs

Go back to the start: give the 2 sentences Mrs. M, 58 year old lady, presents with a 3 day history of worsening pain in the right upper abdomen, precipitated by eating, and associated with nausea and vomiting. There is no surgical history of note, and on the exam she is pyrexic and flushed, with tenderness in the right upper quadrant and a positive murphy's sign. I think the most likely diagnosis is cholecystitis but I would include pancreatitis, gastroenteritis and hepatitis in the DDX. I would like to arrange labs including a FBC and lipase and a U/S scan of the abdomen. I think we should admit her to the surgical ward, keep her NPO and AET with vitals Q4, get some IV fluids running and prescribe some analgesia and anti-emetics. Pending the results of the U/S scan, she may need some antibiotics as well and possibly a cholecystectomy. DON'T OVERSIMPLIFY THE PATIENTS WITH COMPLICATED HISTORIES

Reading a Abdominal X-ray by a General Surgeon Wednesday, 5 September 2012 3:22 PM 3 views Upright chest x-ray Supine abdo xray Upright abdo xray If patient unable to sit upright for abdo: then left lateral decubitus is done Indications Performed for abdo obstruction Perforated viscus Foreign body Contraindications: Right upper quadrant and epigastric pain: gallstone related disease (U/S instead: gallbladder ) Right lower quadrant pain: appendicitis (clinical exam or U/S or abdo CT) Trauma patients For Trauma patients: AP CXR AP pelvis Lateral C-spine Fast U/S CT (if abdo xray is inconclusive) Simple system to interpret any abdo x-ray 1. Assessing gas pattern and bowel dilation: best assessed on supine abdo xray, a. description of gas pattern: central (small bowel), peripheral (colonic gas), non-specific gas patterns (not diagnositic of small or large). Description of bowel can be assessed on supine abdo, stomach has a gastric bubble, small bowel has a plica circularis (folds cross the length of the entire length), large bowel has haustra which the colonic markings don't cross the entire length of the large bowel. Stool has a spiculated appearance on a supine abdo x-ray. b. Bowel dilation: easily performed by a computer caliper. In general: SB Diameter greater than 3 cm is pathological, caecal diameter of greater than 12 cm is concerning for a impending perforation of caecum, transverse colon diameter greater than 10 cm or descending colon diameter greater than 8 cm is concerning for excessive colonic dilation. 2. Assessing for presence or absence of gallstones: 10-15% gallstones are radioopaque and can appear in routine abdo x-rays, in contrast this is different from kidney stones where 85-90% of them are radioopaque and can appear on abdo films. 3. Air in the biliary tree: quite simple, involves air in the right upper quadrant near the liver, there are only several entities that can lead to air in the biliary tree: previous surgical interventions like ERCP, biliary anteric-anastomosis, gallstone ileus rare but can cause air in the biliary tree and synchronous small bowel obstruction due to gallstone in the bowel.

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Assessment of free air: best assessed in upright chest, upright abdo, or left lateral decubitus. Air under diaphragm (right or left). The two most pathological entities of perforated viscus and free air in abdominal xray are: perforated duodenal ulcer, perforated sigmoid diverticulitis. Caution when performing abdo xrays in the first 5 post op days after laparatomy or laparaoscopy as it can show free air under diaphragm. Look for foreign bodies: surgical staples, surgical clips, NG tube, swallowed foreign body, rectal foreign body, artificial bones joints or rods, ECG leads Air-fluid levels: upright or left lateral decubitus abdo, up to 6 air-fluid levels may be normal (non-specific finding) but multiple air-fluid levels are suggestive of bowel obstruction Air in rectum: best assessed in a supine abdo x-ray: air in lower portion of the pelvis in the setting of the bowel obstruction may represent partial or incomplete as it is present in the distal portion of bowel Thumb printing and bowel wall thickening: assessed by supine or upright abdo xrays: thickening of the bowel wall: edema or obstruction. Thumb priting pattern: bowel ischemia, small bowel enteritis, toxic colitis.

Abdo xrays useful for diagnosing SB obstruction or LB obstruction. It's important to differentiate: Common findings: Small bowel obstruction: dilated loops of smal lbowel greater than 3 cm, visualisation of plicae circularis and absence of colonic haustra + gas pattern in central location and there are multiple air fluid levels DDx: 1. Adhesions 2. Hernias 3. Caecal carcinoma 4. Small bowel neoplasm 5. Crohn's disease 6. Gallstone ileus 7. Mecke's diverticulum 8. Intussception 9. Small bowel foreign body Large bowel obstruction: dilated loops of large bowel, peripheral gas pattern involving haustra, usually absence of plicae ciruclaris, large amount of obstructed stool or air seen by spiculated appearance, large amount of obstructed air or stool, potential mulitple air fluid levels. Common causes of obstruction are: colorectal carcinoma, diverticulitis, sigmoid or caecal volvulus, adynamic paralytic ileus (has a bowel gas pattern: dilated central and peripheral gas pattern: large and small bowel obstruction)

Another way to assess the abdominal radiograph General points Name, sex, and age Radiographic densities Air: black Fat: dark grey Water: soft tissue mainly water and is light grey Bone: calcium is white Metal: intense white Air Fat

Stomach: supine: gas in antrum and body Small bowel: supine: central, valvulae conniventes more frequent in the proximal small bowel and decreases in frequency along its length Large bowel: located peripherally, caecum can be mottled in appearance due to faeces and gas

Intra-abdominal fat outlines the liver, spleen, kidneys, psoas muscle, and bladder Obliteration of fat planes may indicate inflammatory change, haemorrhage, or tumour in that area Eg: obliteration of the right psoas margin may indicate inflammation of the fat surrounding the appendix

Soft tissues Kidneys: left higher than right Liver: large soft tissue density in right upper quadrant Spleen: soft tissue mass in left upper quadrant (not often visible in abdo xray) Urinary bladder: soft tissue density in pelvis Causes of abdominal calcifications Most renal stones calcified 20% of gallstones calcified and radio-opaque Phleboliths (calcification within a vein) Calcified mesenteric lymph nodes Appendicolith (calcified deposit in the appendix) Vascular calcification (an abdominal aortic aneurysm may be visible due to calcification of the wall) Calcification in chronic pancreatitis Metal Metallic objects may be present on an abdo radiograph and should be examined closely Surgical staples (central midline) Metallic stents Sterilisation clips in pelvis Systemic review of abdo x-ray Abnormal gas? Bowel (position, diameter) Bowel wall thickness Assess for pneumoperitoneum (if indicated in clinical history) Soft tissues (liver, renal, spleen). Organomegaly or displacement? Psoas muscle clearly defined? Abnormal calcification? (abdominal aorta, splenic artery calcification, renal calculi, appendicolith) Bones (pelvis, spine, sacroiliac joints, proximal femora, ribs). Any degenerative changes, evidence of malignancy? Lung bases (do not miss cancer at lung base)

Bowel Obstruction Thursday, 6 September 2012 11:45 PM What is meant by a bowel obstruction Anything that compromises passage of contents through the lumen, complete or incomplete, mechanical or functional obstruction. Anywhere from duodenum to anus. Small or large bowel obstruction. Functional bowel obstruction: ileus, motility is compromised. The different causes of bowel obstruction Small bowel obstruction is the most common type of mechanical obstruction, in adults: adhesions, hernias, tumours. Adhesions are the scars that are created inside peritoneum following surgery or inflammatory process. The highly mobile small bowel can become tethered to the abdominal wall or another piece of bowel by an adhesion. By chance the bowel may kink or twist at the point of the adhesion resulting in the compromise of the bowel lumen. In any patient with a history of abdo surgery (most importantly appendectomy and hysterectomy) this is by far the most common cause of small bowel obstruction. Hernias are the next most common cause. This includes any time of hernia through the abdominal wall including inguinal, femoral, umbilical, ventral, incisional. The mechanism includes a small segment of

the small bowel contained in the hernia sac becoming incarcerated leading to compromise of the bowel lumen Tumours: most often metastatic or extending from another organ rather than a primary small bowel cancer like a Adenoma. Examples of met cancer include: melanoma, colon cancer, and ovarian cancer. Primary small bowel cancers include: adenocarcinoma, carcinoid tumours, and GI stromal tumours. REMEMBER IF THE PATIENT HAS AN OBSTRUCTION BUT NO SCARS OR hernias EVIDENCE OF SURGERY THEN THEY HAVE A CANCER UNTIL PROVEN OTHERWISE Sometimes a patient with Crohn's can present with bowel obstruction secondary to inflammed and swollen segment of Crohn's affected small bowel Miscellaneous cause of obstruction: abscesses, haemotomas, endometriosis, foreign bodies (all in adults)

Rare cause of obstruction: Gallstone ileus Results from a gallstone passing from the biliary tract into the small intestine and eventually getting lodged at some point and causing a obstruction Point of obstruction is most commonly the ileo-caecal valve The way in which the stone enters the bowel is via colo-cystic enteric fistula, straight from the gallbladder to bowel, as a result on x-ray a radioopaque object in the lower quadrant of the abdomen and gas in the biliary tree in the right upper quadrant against the backdrop of findings of a small bowel obstruction Large bowel obstruction In adults: most commonly caused by colon cancer , often a history of an insidious onset , more and more constipation and bloating along with weight loss Diverticular disease is another potential cause, either due to an abscess or chronic scarring and narrowing of the bowel Fecal impaction is another cause Elderly patients with compromised mental states are on medications that affect bowel motility, this functional compromise can lead to mechanical obstruction as faeces become impacted and it solidifies, it can be so severe that you need surgery to relieve it or treat its complications such as megacolon or perforation. Adhesions: far less common cause Volvulus: important and dramatic cause, refers to the twisting of the bowel around its axis of mesentery which leads to a complete obstruction compromising its blood supply to the volvuli segment of the colon, it can occur anywhere there is a mobility of mesentery: sigmoid and caecum. Volvulus of the transverse colon and splenic flexure is possible but not common. This is an emergency because of the compromise of the blood supply. Pediatric Bowel Obstruction Mid-gut volvulus: malrotation of the bowel, did not undergo 270 degree rotation anticlockwise during development, the result is that the small bowel doesn't have a wide based mesentery instead it has a narrow mesentery. The entire midgut can twist on this mesentery and cause obstruction and compromise of the circulation to entire small bowel. Untreated: Fatal. Vomiting of baby: mid-gut volvulus until proven otherwise. Other causes: web's atresia or stenosis of small bowel or even imperforate anus. Neonates: meconium ileus (especially if they have CF) Children that don't pass meconium in the first 24 hours have: Hirschsprung's disease, functional obstruction caused by congenital absence of the parasympathetic ganglion cells in the rectum. Intussception: telescoping of the bowels over itself usually over the lead points: mesenteric adenitis or meckel's diverticulum. It's common to find hernias in children as well: bowel obstruction.

Functional obstruction or ileus (generalised ileus) is also encountered which is common after surgery several days (lapratomy: resolves spontaneously), hypokalaemia (a metabolic disorder) or hypomagnesaemia, peritonitis, trauma, drug effects (narcotics and anticholinergics) Focal ileus: anything inflammatory process that affects the adjacent bowel

History and Physical exam Bowel obstruction: nausea and biliary or faeculous vomiting combined with obstipation (severe or complete constipation, failure to pass stool and flatus) Abdo pain: crampy in nature initially, excruciating and constant: strangulated bowel is a possibility. Past history : abdominal surgery, hernias, and diverticular disease Family history: bowel cancer and IBD Social history: drugs, weight loss Physical exam Vital signs Dehyration (due to bowel obstruction) Tachycardia or hypotension Fever: unusual but consider infectious causes or possibility of strangulated bowel Abdo exam: look at degree of obstruction, generally the more distal the obstruction the more marked the distension, look for surgical scars AND DON'T FORGET TO LOOK FOR HERNIAS If hernias present: take note of incarceration and signs of strangulation If hernia is soft, reducible and non tender (on incidental finding of another cause of obstruction) chances are it's not the cause of obstruction Palpation of abdomen: take note of any masses , localised tenderness or generalised peritonitis DRE: essential, take note of any masses including impacted stool, check for FOB (if present tumour or compromised bowel)

Labs and diagnostic imaging CBC, electrolytes (magnesium, creatinine, urea) Mild leukocytosis is usual in bowel obstruction but extreme elevations in WCC raises concerns about dead or dying bowel (ischemia) or inflammatory or infectious cause for the obstruction Microcytic anemia: raises the possibility of malignancy Electrolyte imbalances are common: usually hypokalaemia and hypomagnesimia Prolonged vomiting of proximal obstruction: results in hypokalaemic, hypocholraemic metabolic alkalossis Creatinine and urea are increased secondary to dehydration Key is to order: plain abdo xyra: dilated loops of bowel, air-fluid levels proximal to the side of obstruction with little fluid or no gas distal to it. SB obstructions have a classic step ladder appearance where there are stacks of dilated small bowel seen each with a air-fluid level, no gas is seen in the colon or rectum. Colonic obstruction not caused by a volvulus looks different depending up whether the patient has a competent ileo-caecal valve. If the valve is competent there is little or no gas present in the small bowel and marked dilatation of the colon proximal to the side of the obstruction. If the valve is not competent then the obstruction causes the gas to back up into the small bowel. The resulting picture on x-ray is a dilated large AND small bowel. Generalised ileus: appears as air filled large and small bowel extending all the way to the rectum Colonic volvulus: distinctive appearance on xray Sigmoid volvulus: resembles a bent inner tube or a U-shape, with a massively dilated loop of colon seen with its limbs pointing downwards towards the pelvis. Caecal volvulus: appears as a massively dilated segment of bowel with its axis running from right lower quadrant to the epigastrium The approach to management Multiple causes but one management: SUCK AND DRIP Patient is kept NPO, and a NG tube is put in and intermittent suction is done to decompress the bowel, along with this the patient is aggressively rehydrated with IV crystalloid. Foley catheter is put in to monitor urine output and to guide resuscitation The gut is sucked out through NG tube and drip put in Electrolyte abnormalities should be corrected

Other things should be fixed: ppl with peritonitis, tumours or hernias should be taken to OR Sigmoid volvulus can be fixed with sigmoidoscopy Caecal volvulus needs laparatomy to reduce Paralytic ileus: correct the electrolyte abnormality and stop the offending drugs For adhesions: usually suck and drip method alone with fairly high success rate, very often the obstruction resolves within 24-48 hours,

Bowel Obstruction: Medical student Friday, 7 September 2012 8:56 PM Large or small bowel obstruction: what are their signs and symptoms? Small bowel: looking for nausea and vomiting which might be biliuos, colicky abdominal pain, looking for partial or complete obstruction (partial: constipation and flatulence, complete: obstipation). Increase in bowel sounds. Large bowel: nausea and vomiting but it will present later, colicky abdo pain again and there will be abdominal distension. Determine whether it's open or closed loop obstruction, the reason why it's because the outcome and the time you have to intervene is different. With a open loop obstruction, this presents with about 10-20 % of patients, open loop because the ileocaecal valve is incompetent and thus the gas can regurgitate back into the small bowel, this is the safer bowel obstruction Closed loop: 80-90% of patients, unsafe, ileo-caecal valve is competent, no gas is refluxing back into small bowel, and thus there is no relief of pressure. You will see mass colonic distension, in physical exam if you elicit tenderness over the caecum with palpation this indicates impending perforation Why does small bowel obstruction and large bowel obstruction present like this? First: obsruction occurs, this leads to destruction of the ability to pass intestinal contents, this leads to dilation proximally and decompression distally --> abdominal distension, leading to nausea and vomiting and colicky abdo pain. Can you still pass stool or gas after the obstruction is present? Yes because decompression can be delayed up to 24 hours There is an obstruction, or is there? Diagnosis of bowel obstruction, consider pseudoobstruction (acute or chronic) Acute pseudoobstruction: 1. Toxic megacolon due to ulcerative or infectious colitis 2. Post-op sedentary patient who has intraabdominal abscess, or drugs, electorlyte disturbance: paralytic ileus 3. Retroperitoneal haemorrhage 4. Colonic distension: bedridden Chronic pseudo-obstruction: 1. Scleroderma 2. Neurlogical diseases: enteric NS, CNS and PNS Top 3 causes of Small bowel: adhesions, hernia, crohn's and cancer. Other causes: strictures, CF, gallstones, intuss, abscesses, annular pancreas, diverticulitis, mecke'l's diverticulum, foreign bodies Large bowel causes: colo-rectal cancer, diverticulitis, volvulus. Other causes: IBD, benigh tumours, stool impaction, foreign body, endometriosis What do you want to order and what are you looking for? Blood work: CBC and electrolytes (normal in early disease) Dehydration status:BUN, haematocrit, creatinine (B-hcg to exclude pregnancy) Type and screen: just in case for OR Persistent vomiting: hypokalaemic, hypocholraemic metabolic acidosis (vomiting up acidic contents) Imaging x-ray: erect chest, supine and erect abdo (if chest shows: free air under diaphragm, straight away to OR)

Small bowel: less than 3 cm, distal colon: less than 6cm, proximal colon: less than 9 cm, caecum (less than 12 cm). If any of the dimensions are greater, this implies greater severity of disease and impending perforation Small bowel: upright: air-fluid levels, levels that differ from each other in the same loop by more than 5mm and levels with the width of 2.5 cm or more. Paucity of gas in the colon. Large bowel obstruction: classic picture frame appaerance, proximal dilation and distal decompression, check for air in the small bowel (ileo-caecal valve is competent or not and thus determine the severity of intervention) Ordering more tests b-HCG (not pregnant, go to CT) Small bowel: CT: helps to determine severity, location, and cause of Small bowel obstruction Obtain upper GI series or small bowel follow through (if there is no apparent cause, also helps determine partial or complete obstruction) Large bowel: Rectal or water soluble enema (instead of barium enema which can lead to complete obstruction) If patient is pregnant: try ultrasound instead What is the difference between Upper GI series and small bowel follow-through? Upper gi series: double contrast study with barium to coat the mucosa and gas pills to distend the stomach. Thoracic oesophagus, stomach and duodenum can be visualised Small bowel follow-through: single contrast study where images are obtained following the upper Gi series which will assess the entire small bowel rather than just the duodenum. There is an obstruction, you need to fix it ABC's, Vitals, oxygen, IV access, fluid resus (for both small bowel and large bowel obstruction) and electrolyte re-balancing. For both types of obstruction: use NG to decompress the bowel and put the patient in NPO (to let the bowel rest) Put foley catheter to monitor fluid balance With small bowel obstruction, if the patient has history of surgery, you can move onto conservative management, close observation, if no improvement in 48-72 hours or if there's complications , you have to proceed to laparatomy for lysis of lesions If patient has Crohn's disease, recurrence small bowel obstruction or carcinomatosis then have a trial with medical management If there is complete or strangulating obstruction: urgent surgery after patient is stabilised For a large bowel obstruction: surgical management includes resection with a temporary diverting colostomy. If volvulus in sigmoid then sigmoidoscopy or endoscopy can decompress it followed by surgical reduction. If reduction is successful, consider sigmoid resection before the patient is discharged home What are the complications? Strangulating obstruction (10% of all bowel obstructions --> surgical emergency). Cramping pain becomes continuous, fever, peritoneal signs or even shock Bloods: leucocytosis with a left shift, lactic acidosis, LDH increase Abdo xray: look for free air, pneumotosis or gas in the bowel wall, thickened bowel wall, air in the portal veins, thickened haustra, dilated small and large bowel, there will eventually become featureless and hose like with ischemia CT: thickened bowel wall due sub-mucosal edema would be apparent and you might even see haemorrhage in the mesentery. If you see thickeend bowel wall --> target sign Treatment :urgent laparatomy after patient is stablised
Other complications: perforation, septicaemia, 3rd space losses: hypovolaemia, caecal perforation and faeculent peritonitis (large bowel especially) Small bowel: non-strangulating death less than 1%, for strangulating it's 8%, and obstruction for greater than 36 hrs will lead to mortality of 25%. If ischemia is present, mortality rises to 50%. Large bowel obstruction: overall mortality is about 10%, if you have caecal perforation and faeculent peritonitis the mortality doubles to 20%.