Abdomen Flashcards
1
Q
GI history
A
- Opening consultation wash hands, PPE, Intro, confirm patient, explain, consent
- PC – Do not interrupt
- HPC – SOCRATES (Site, onset, character radiation, associated symptoms, time course, exacerbating or relieving factors, severity).
- ICE
- Summarise, signpost
- Systemic enquiry: Fevers, weight change, fatigue, anorexia, weight loss, nausea, fever, pruritis confusion, bowel changes…
- Travel history (if suggestive of infective aetiology) – area, diet, insect bites, contaminated water
- PMH: Medical conditions (eg endoscopy, iron def anaemia, constipation, crohns, coeliac, gallstones…), surgery, procedures, allergies and reaction
- Drug History – prescribed or OTC, dose, type, frequency, route, side effects, contraception and pregnancy. Meds with GI S/E = opiates penicillin, ondansetron.
- FH – of GI disease (liver/bowel problems), if close relatives deceased ask age and how.
- SH – Accomm, living, carer, support, smoking, alcohol, recreational drug use, diet, exercise sexual history.
- Closing – summarise, questions/concerns, thank, dispose PPE, wash hands.
*
2
Q
Upper GI symptoms
A
- Jaundice – hepatitis, liver cirrhosis, biliary obstruction
- Aphthous ulceration – ulcers inside mouth, can be associated with iron, B12+folate def, Crohn’s
- Vomiting – Infections, GORD, pyloric stenosis, vowel obstruction, gastroparesis pharyngeal pouch and oesophageal structure
- Haematemesis – vomiting blood Mallor Weiss tear, oesopehageal variceal rupture) or coffee ground in appearance (eg, gastric or duodenal ulcer)
- GORD – epigastric discomfort burning in nature
- Dysphagia – Difficulty swallowing which may affect solid food, liquids or both depending on its severity
- Odynophagia – pain during swallowing which may be associated with oesophageal obstruction (eg, stricture) or infection.
3
Q
Lower GI symptoms
A
- Abdo paain – localised or generalised
- Abdominal distention – ascites, constipation, bowel obstruction, organomegaly and malignancy
- Constipation – dehydration, reduced bowel motility + medications
- diarrhoea – causes include infection (CDiff), IBS, IBD, Meds (laxatives), constipation (overflow) and malignancy
- Steatorrhoea – Presence of excess fat in faeces so appear pale and difficult to flush. Pancreatitis, pancreatic cancer, biliary obstruction, coeliac disease and medications (Orlistat)
- Malaena – dark, tar luje sticky stools containing digested blood secondary to upper GI bleeding (peptic ulcer)
- Haematochezia – Fresh red blood passed per rectum which may be caused by haemorrhoids, anal fissures and lower GI malignancy
4
Q
Location of pain in relation to pathology
A
- R Iliac fossa = appendicitis, crohn’s disease, ectopic pregnancy
- L iliac fossa = diverticulitis, ectopic pregnancy
- Epigastric pain = oesophagitis and gastritis
- R Upper quadrant = cholecystitis and hepatitis
- Flank pain = renal colic and pyelonephritis
- Suprapubic pain = UTI
5
Q
GI risk factors
A
pre-existing medical conditons (GORD, Crohn’s), FH GI disease, alcohol, smoking, recreational drugs, diet.
6
Q
What is an acute abdomen?
A
Sudden onset of severe abdominal pain over short period. Initial assessment should attempt to determine if the patient has an acute surgical problem that required immediate and prompt surgical intervention or urgent medical therapy.
7
Q
When is Urgent vs less urgent intervention needed for acute abdomen
A
- Bleeding (AAA, ruptured ectopic pregnancy, gastric ulcer, trauma)
- Perforated viscus -> peritonitis. Rigid abdomen, invol guarding, reduced/absent bowel sounds, tachycardia.
- Ischaemic bowel – severe pain out of proportion to clinical signs is this until proven otherwise. Also raised lactate and physiologically compromised. Diffuse and constant pain
Less Acute:
- Colic: Abdominal pain that crescendos to be very severe then goes away. Biliary/ureteric colic and bowel obstruction
- Peritonism – locatsed inflamm
8
Q
Invetsiagtions for Acute abdomen
A
Lab tests:
- Urine dipstick = signs infection or haematuria and prgenancy test
- ARterial blood gas = bleeding or septic patients, lactate for signs tissue hypoperfusion and rapid Hb level
- Routine bloods = FBCS, U&Es, LFTs, CRP, amylase and G&S surgery likely
- Bloo cultures
Imaging:
- Erect CXR (for free abdominal air or lower lobe lung pathology)
- US = kidneys, ureters, bladder, biliary tree, liver
- CT imaging = of abdomen
- If emergency then ECG to exclude cardio pathology as referred pain
9
Q
Core management of an acute abdomen
A
- IV access
- Nil by mouth status
- Analgesia
- Antiemetics
- Intiial imaging
- VTE prophylacis
- Urine dip
- Bloods
- If unwell consider urinary catheter and or nasogastric tube if needed and start IV fluids and monitor flud balance.
10
Q
AReas of the abdomen pain and pathology
A
11
Q
Patho of Acute appendicitis
A
Typically due to direct luminal obstruction, usually secondary to faecolith or lymphoid hyperplasia, impacted stool or rarely an appendiceal or caecal tumor. When obstructed, commensal bacteria in the appendix can multiply resulting in acute inflammation. Reduced venous drainage and localized inflammation can result in increased pressure within the appendix and can result in ischemia.
If untreated, ischameia within appendiceal wall can lead to necrosis and appendix can perforate.
12
Q
Risk factors of acute appendicitis
A
FH, Ethnicity (Caucasians more common but if minorities get it then more risk perforation), environmental (summer).
13
Q
Investigations for appendicitis
A
Investigations: clinical diagnosis but ultrasound or CT often requested to help.
Risk stratification scores: Men (appendicitis inflammatory response score), women (adult appendicitis score), children (shera score).
14
Q
Describe and elicit from a given patient the classical presentation of acute appendicitis
A
- Abdominal pain: Initially peri-umbilical, classically dull and poorly localised (from visceral peritoneum inflammation) but later migrates to right iliac fossa to be localised and sharp (from parietal peritoneum inflammation).
- Vomiting (typically after pain), anorexia, nausea, diarrhoea or constipation
- Rebound tenderness and percussion pain over McBurney’s point (2/3 away between umbilical and ASIS) and guarding (especially if perforated appendix)
- If severe – sepsis, tachycardic, hypotensive
- Appendiceal abscess may also present with RIF mass
- Rovsing’s sign: RIF fossa pain on palpation of LIF.
- Psoas sign: RIF pain with extension of the right hip. Specifically suggests inflamed appendix abutting psoas major muscle in retrocaecal position.
15
Q
Typical clinical presentation acuet appendicits in children
A
Mostly present atypical like diarrhoea, urinary symptoms or even left sided pain. Therefore, exam cardiorespiratory and urinary as well as GI. In all boys do genital exam to exclude testicular torsion or epididymitis.
In a child under 6 who has had symptoms for over 48hours is significantly more likely to be suffering from perforated appendix so period of active obs is needed.
16
Q
Main differential diagnosis of appendicitis
A
- Gynaecological – pvarian yst rupture, ectopic pregnancy, pelvic inflammatory disease
- Renal – ureteric stones, UTI, pyelonephritis
- GI – IBD, Meckel’s diverticulum, diverticular disease
- Urological – testicular torsion, epididymo-orchitis
17
Q
right iliac fossa pain differentials
A
GI causes:
- Appendicitis
- Crohn’s disease
- Mesenteric adenitis – by viral or bacteria infection. May have high temp and other evidence of viral infection. If laparotomy then enlarged mesenteric lymph nodes
- Diverticulitis – Diverticula and inflammation and/or abscesses may occur in ascending colon and perforation
- Meckel’s diverticulitis – Meckels diverticulum is congenital in 2%
- Perforated peptic ulcer – usually upper quadrant pain but may be lower.
- Right inguinal hernia/femoral hernia – may also be tenderness and irreducible swelling over hernial orifice and symptoms of bowel obstruction.
- Malignancy – carcinoma of caecum or AC can present with bowel perforation
Gynaecological causes:
- Pelvic inflammatory disease/salpingitis/ pelvic abscess with typically vaginal discharge
- Ectopic pregnancy in right fallopian tube
- Ovarian torsion – usually when ovary enlarged by cucts. Adnexal tenderness
- Threatened or complete miscarriage – esp if history bleeding
- Mittelschmerz (ovulation pain), Fibroid degeneration, Pelvic tumour
Urological: Ureteric colic (shooting, intermittent pain), UTI, testicular torsion or epididymo-orchitits
Other: Infections (TB, typhoid, Yersinia spp, herpes zoster), AAA, situs inversus
Chronic – IBS, Carcinoma, Crohns, pelvic tumours, endometriosis, right hip pathology, familial Mediterranean fever.
18
Q
Treatment options for acute appendicits
A
Current definitive is laparoscopic appendicectomy. Some debate about conservative antibiotic therapy in uncomplicated appendicitis. If cases of appendiceal mass, antibiotic therapy is favoured, with interval appendectomy then 6-8weeks later.
Surgical Intervention: Gold standard for laparoscopic appendectomy as low morbidity and in females better visualisation of uterus and ovaries. Appendix should be routinely sent to histopathology to look for malignancy and entirety of abdomen inspected for other pathology like Meckel’s diverticulum.
19
Q
Explain possible complications of acute appendicits
A
Mortality associated with appendicitis in developed health systems is low (0.1-0.24%).
- Perforation – and can cause peritoneal contamination (children may have delayed presentation)
- Surgical site infection – depends on simple or complicated appendicitis
- Appendix mass- where omentum and small bowel adhere to appendix
- Pelvic abscess – presents as fever with palpable RIF mass, can be confirmed CT scan for confirmation, management usually with antibiotics and percutaneous drainage of abscess,
20
Q
Acute pancreatitis - what is it
A
- inflammation of the pancreas. Can be distinguished form chronic by it limited damage to the secretory function of the gland with no structural damage developing. Repeated acute episodes can eventually lead to chronic.
21
Q
Patho of acute pancreatitis
A
- All causes trigger premature and exaggerated activation of digestive enzymes within pancreas and hence pancreatic inflammatory response which leads to increased vascular permeability and fluid shifts.
- Enzymes are released from the pancreas into systemic ciruclation, causing autodigestion of fats an blood vessels
- Fat necrosis can cause the release of FFA which react with serum calcium to form chalky deposits in fatty tissue resulting in hypocalcaemia
- Severe or end stage pancreatitis will eventually result in partial or complete necrosis of pancreas
22
Q
DDx of pancreatitis
A
(Pain that radiates to the back)
- AAA
- Renal calculi
- Chronic pancreatitis
- Aortic dissection
- Peptic ulcer disease
23
Q
Investigations for pancreatitis
A
- Lab tests: serum amylase (3x normal), LFTs, serum lipase
- IMaging: abdominal US if cause unknown (can show sentinel loop sign), contrast enhanced CT
24
Q
Explain the causes of pancreatitis
A
Majority can occur secondary to gallstone disease or excess alcohol consumtpion but causes are wide ranging ‘GET SMASHED’
- Gallstones
- Ethanol (alcohol)
- Trauma
- Steroids
- Mumps
- Autoimmune disease like SLE
- Scorpion venom
- Hypercalcaemi
- Endoscopic retrograde cholangio-pancreatography (ERCP)
- Drugs like azathioprine, NSAIDs or diuretics
25
Possible presentations of patients with acute pancreatitis
* Sudden onset severr epigastric pain which can radiate through to the back with nausea and vomiting
* Often epigastric tenderness with or without guarding
* In severe cases - may be haemodynamically instable
* Less common:
* Cullens sign -bruising around umbilicus
* Grye turners sign - bruising in flanks
* Representing retroperitoneal hameorrhage. Tetany may occur from hypocalcaemia an dgallstone aetiology may also cause concurrent obstructive jaundice
26
describe commonly used scoring system for grading severity of acute pancreatitis
Modified Glasgow criteria used to assess severity within first 48hours of admission.
Anyone above \>/3 positive factors within 48hrs should be considered severe pancreatitis and high dependency care referral.
PANCREAS: p02\<8kPa, Age\>55m Neutrophils/WCC \>15x10^9/L, Calcium\<2mmol/L, Renal function (urea)\>16mmol/L, Enzymes LDH\>600U/L or AST\>200U/L, Albumin\<32/L, Sugar (blood glucose)\>10mmol/L
Other scores: APACHEII score, Ranson Criteria, Balthazar score (CT scoring system)
27
Explain intiial management acte pancreatitis and concepts of later management of acute pancreatitis
No curative management so supportive measures. Treat the underlying cause
**Supportive treatment**s:
* IV fluid resuscitation and 02 therapy (use balanced crystalloid)
* Nasogastric tube if vomiting profusely
* Catheterisation to acutely monitor urine output and start fluid nalance chart
* Opioid analgesia
HDU or ITU if severe acute pancreatitis. Broad spectrum antibiotic such as imipenem should be ocnsidered for prophylaxis against infection in cases of confirmed pancreatic necrosis.
28
Describe systemic complications of acute pancreatitis and how to identify them
Usually within days of initial onset
* Disseminated Intravascular coagulation (DIC)
* Acute Respiratory Distress Syndrome (ARDS)
* Hypocalcaemia – Fat necrosis from released lipases results in release FFA which react with serum calcium to form chalky deposits in fatty tissue.
* Hyperglycaemia – Secondary to destruction of islets of Langerhans and subsequent disturbances to insulin metabolism.
29
Describe the local complications of acute pancreatitis and how to identify them in patients
**Pancreatic Necrosis** – Suspect in patients with evidence of persistent systemic infection for more than 7-10days after onset. If suspected then confirm by CTand treatment will often warrant pancreatic necrosectomy. This is prone to infection and suspect if clinical deterioration associated with raised infection markers this can also be confirmed by fine needle aspiration of necrosis.
**Pancreatic Pseudocysts** – Collection of fluid containing pancreatic enzymes, blood, necrotic tissue which can be anywhere in or near pancreas but most likely in lesser sac. Typically formed weeks after initial acute pancreatitis episode and lack epithelial lining so have vascular and fibrotic wall surrounding collection. May be found incidentally on imaging or can present with symptoms of mass effect like biliary obstruction or gastric outlet obstruction and prone to haemorrhage or rupture and can get infected. 50% ish will spontaneously resolve so conservative management usually initial treatment. If cysts longer than 6weeks then surgical debridement or endoscopic drainage as unlikely to resolve spontaneously.
30
Risk factors for gallstones
* Fat, female, fertile, family hsitory, forty
* Also pregnancy, oral contraceptives, haemolytic anaemia (Pugment stones) and malabsroption.
31
DDx gallstones
* GORD
* Peptic ulcer disease
* Acute pancreatitis
* IBD
32
Investigations for gallstone related problems
* **Lab tests:** FBC, crp, lft (raised ALP but alt + bilirubin normal), amylase (or lipase). Urinanalysis for pregnancy test
* **Imaging**: Trans-abdominal US. often visualise present gallstones or sludge, gallbladder wall thickeness, bile duct dilation. If inconclusive then gold tsandard is Magnetic resonance cholangiopancreatography (MRCP) and can show potential defects in biliary tree caused by gallstone disease.
33
Anatomy of Biliary system
**Biliary tre**e = GI ducts allowing newly synthesised bile from the liver to be concentrated and stored in the
gallbladder (prior to release into duodenum).
Bile = Hepatocytes -\> canaliculi -\> Interlobar ducts -\> collecting ducts -\> L/R hepatic ducts -\> common hepatic duct.
Hepatopancreatic ampulla pf Vater empties into duodenum via major duodenal papilla which is regulated by muscular valve (sphincter of Oddi).
* Celiac plexus carries sympathetic and sensory fibres and vagus nerve is parasympathetic. Parasympathetic stimulation produces contraction of the gallbladder and the secretion of bile into the cystic duct due to relaxation of the sphincter of Oddi. Majority is mediated by cholecystokinin as part of gustatory response.
* Lymph from gallbladder drains into cystic lymph nodes and these go into hepatic lymph nodes the coeliac lymph nodes.
*
34
Different types of gallstones
Gallstones (or choleliths) are solid masses formed from bile precipiates which may occur in gallbladder or biliary tract.
* Cholesterol stones- yellow-green and primary made of hardened cholesterol. Predominately in women and obese people and associated with bile supersaturated with cholesterol. Account for 80% gallstones and more commonly involved in obstruction and inflammatory.
* Pigment stones – May be black or brown.
* Black pigment stones = pure calcium bilirubinate or complexes of calcium, copper and mucin glycoproteins. Typically form in conditions of stasis (eg, parenteral nutrition) or excess unconjugated bilirubin (hemolysis or cirrhosis). More likely to remain in gallbladder.
* Brown pigment stones – calcium salts of unconjugated bilirubin with small amounts of cholesterol and protein. Often in bile ducts causing obstruction and usually found in conditions where infected bile. Prevalent in Asian countries an rarely in those in US
* Mixed stones – cholesterol and bile pigments
35
Explain the different conditions caused by gallstones and how they present clinically
* Gallstones (Cholelithiasis) may be associated with pain, jaundice and systemic upset.
* Cholelithiasis = uncomplicated gallstones
* Biliary colic = typically right upper quadrant pain following fatty ,e as gallstones obstruct the cystic duct during contraction of the gallbladder. Not associated with systemic upset. Associated with nausea and vomiting.
* Cholecystitis = inflammation of the gallbladder. Pain is often associated with nausea, vomiting or fever. Tender in RUQ and positive murphys sign. Check for guarding and signs of sepsis.
* Murphy’s sign = Whilst applying pressure in RUQ, ask them to inspire. It is positive when halt in inspiration due to pain, indicating inflamed gallbladder.
* Choledocholithiasis = gallstone within common bile duct. Often causes deranged liver function tests
* Cholangitis = Infection of the common bile duct often secondary to choledocholithiasis. Typically presents with right upper quadrant pain, fever and jaundice (Charcot’s triad).
36
Management of Biliary Colic
* Analgesia
* Advised about lifestyle factors to help like low fat diet, weight loss and increasing exercise
* Following first presentation wit this there’s high chance symptom recurrence or complications so elective laparoscopic cholecystectomy warranted and should be offered within 6weeks of 1st presentation.
37
Acute cholecystitis management
* Appropriate IV antibiotics and concurrent analgesia and antiemetics
* Laparoscopic cholecystectomy indicated within 1 week but ideally within 72hours.
* If not fit for surgery or not responding to antibiotics then percutaneous cholecystostomy can be performed to drain infection.
* Any patient readmitted with RUQ pain post-cholecystectomy, it is important to exclude retained CBD stone post-op. US abdomen may be useful but then maybe MRCP.
38
Complications of gallstones
* Mirizzi Syndrome: Stone in Hartmanns pich or Cystic duct can cause compression on adjacent common hepatic duct leading to obstructive jaundice. Confirm with MRCP then usually laparoscopic cholecystectomy
* Gallbladder Empyema: Gallbladder becomes filled with pus. Patients become unwell, often septic, presenting with similar clinical picture to acute cholecystitis. Associated with signficiant morbidity and mortality. Diagnosed by US scan or CT, treatment being laparoscopic cholecystectomy or percutaneous cholecystostomy.
* Chronic Cholecystitis: Typical history of recurrent or untreated cholecystitis which has lead to persistent inflammation of the gallbladder wall. Patients present with ongoing RUQ or epigastric pain with associated nausea and vomiting. Diagnosed by CT and management being elective cholecystectomy. Main complications are gallbladder carcinoma and biliary enteric fistula.
* Bouverets Syndrome and Gallstone Ileus: Inflammation causes fistula between gallbladder wall and small bowel (cholecystoduodenal fistula) allowing gallstones to pass directly into small bowl and can get bowel obstruction:
* Bouveret’s syndrome = stone impacts in proximal duodenum, causing gastric outlet obstruction.
* Gallstone ileus = stone impact at terminal ileum
39
Diverticular disease
Diverticulum = outpouching of the bowel wall most commonly found in the sigmoid colon, but can be present throughout.
4 manifestations:
* Diverticulosis = presence of diverticula (asymptomatic, incidental on imaging)
* Diverticular disease = symptoms arising from diverticula
* Diverticulitis = inflammation of the diverticula
* Diverticula bleed = where diverticulum erodes into a vessel and causes a large volume painless bleed.
* Diverticulosis is present in around 50% of \>50 and 70% \>80 but only 25% become symptomatic.
40
Pathology of divertiuar disease
Aging bowels become weak and the movement of stool will cause increase in luminal pressure so you get a outpouching of the mucosa through the weaker areas of bowel wall. Bacterial can overgrow leading to inflammation of the diverticulum (diverticulitis) which can perforate and lead to diffuse peritonitis sepsis and death. Fistulas can also form in chronic cases. Complicated diverticulitis is where abscesses (needed IV antitiobits and radiological drainage as possibility) or free preforation
41
RFS for diverticula
Age, low dietary fibre intake, obesity, smoking, family history, NSAID use.
42
DDx
IBD or bowel cancer. Also other causes of abdominal pain like mesenteric ischemia, gynecological causes or renal stones.
43
Invetsigations for Diverticular disease
**Lab tests:** routine bloods (FBC, U&Es, CRP), consider fecal calprotectin if less clear diagnosis. Those with suspected diverticulitis should also have Group and Save and venous blood gas and urine distick may rule out urological
**Imaging:** CT abdomen-pelvis scan where for diverticulitis you may see thickening of colonic wall, pericolonic fat stranding, abscesses, localized air bubble or free air. For uncomplicated diverticular suspected then may start with flexible sigmoidoscopy.
44
Explain the acute presentation of patients with diverticular disease and be able to recognise thisclinically
Mostly asymptomatic and only found incidentally with no clinical significance.
**Diverticular disease** = intermittent lower abdominal pain, typically colicky in nature and relieved by defecation. Altered bowel habit, associated nausea and flatulence. There will be no systemic features present.
**Acute diverticulitis** = Acute abdominal pain, typically sharp and normally localised to LIF worsened by movement. On examination there will be localised tenderness, features of systemic upset like decreased appetite, pyrexia or nausea. A perforated diverticulum will present with signs of localised peritonism or generalised peritonitis and they are often extremely unwell and can be fatal.
45
Explain the possible complications of diverticular disease
Recurrence of diverticulitis after first episode is about 10-35%. Elective segmental resection may be performed in those with recurrent disease. Complications of develop in severe, recurrent or chronic cases most commonly are structure formation or fistula formation.
* **Diverticular stricture:** Following repeated episodes of acute inflammation as the bowel becomes scarred and fibrotic so benign stricture. This can result in large bowel obstruction and may require sigmoid colectomy (elective or urgent) depending on presentation. Colonic stenting is temporary.
* **Fistula Formation**: Due to repeated inflammation, they can form secondary to diverticulitis which nearly all require surgical intervention. Most commonly:
* Colovesical fistula between bowel and bladder. Most commonly present with recurrent UTIs, pneumoturia (gas bubble in urine) or passing faecal matter in to urine
* Colovaginal fistula between bowel and vagina. Generally present with copious vaginal discharge or recurrent vaginal infections.
46
Explain the posible complicatiosn of dicerticular disease
* **Diverticular disease**: Uncomplicated then outpatient with simple analgesia and oral fluid intake but do colonoscopy outpatient to check no malignancies masked. With diverticular bleeds then manage conservatively. If fail to respond conservatively then may get embolization or surgical resection.
* **Acute diverticulitis:**
Most can be conservatively with antibiotics, IV fluids, analgesia. Young + uncomplicated can be considered for ambulatory management.
Symptoms tend to improve 2-3days and clinical deterioration or lakc of improvement should prompt repeat imaging to check for disease progression or complication and oral intake encouraged where possible.
Surgical management: For those with perforation with faecal peritonitis or overwhelming sepsis. This is a major procedure and usually involves a Hartmanns procedure (sigmoid colectomy with formation of an end colostomy), an anastomosis with reversal of colostomy may be possible at a later date.
47
Bowel obstruction - what is it and the clinical features
* Mechanical blcokage of the bowel whereby a electrolyte rich fluid into the bowel.
* Urgent fluid resuscitatio and careful fluid balance required.
**Clinical Features:**
* Abdominal pain - colicky or cramping in nature
* Vomiting - occuring early in roximal obstructions and late in distal obstructions
* Abdominal distention
* Absoloute constipaion - occuring early in distal obstruction and late in proximal obstruction.
O/E - patients may show evidence of the underlying caise or baodminal distension and chekc their fluid status. Palpate for focal tenderness (guarding and rebound tenderness). Percussion may reveal a tympanic sound and auscultation may reveal tinkling bowel sounds.
48
DDx of bowel obstruction
* Pesudo-obstruction, paralytic ileus, toxic megacolon, constipation
49
investigations for bowel obstruction
* Lab tests – routine urgent bloods (FBC, CRP, U&Es, LFTs, G&S) and monitor electrolyte changes and third space losses (Movement fluid from blood vessels into interstitial spaces). Venous blood gas to evaluate signs of ischemia (high lactate) for immediate assessment of any metabolic derangement.
* Imaging – CT scan with IV contrast of abdomen + pelvis. Better than AXR as more sensitive, can differentiate between mechanical + pseudo-obstruction (resembles blockage but no blockage), can demonstrate site and cause and presence of metastases.
* AXR still sometimes used:
* Small bowel obstruction dilated bowel \>3cm, central abdominal location, valvulae conniventes visible.
* Large bowel obstruction: Dilated bowel (\>6cm, or \>9cm if at caecum), peripheral location, haustral lines visible.
* May also use erect chest XR to assess free air under diaphragm if clinical features suggest bowel perforation.
* Water soluble contrast study can be useful in small bowel obstruction caused by adhesions from previous surgery.
50
The different types of bowel obstruction
* Closed loop obstruction where there’s a second obstruction proximally (sch as in a volvulus or in large bowel obstruction with competent ileocaecal valve) which is emergency. As bowel will continue to distend till ischemic or perforation.
* Mechanical blockage = structural pathology physically block the passage of intestinal contents. Around 15% of acute abdomen cases are found to have bowel obstruction. Once the bowel segment has become occluded, gross dilation of the proximal limb of bowel occurs so increased peristalsis of the bowel and you get large volumes
* Functional obstruction or paralytic ileus where it’s not mechanically blocks but doesn’t work properly eg from inflammation or electrolyte derangement.
51
Identify the causes of smal bowel obstructions
Most commonly from scar tissue, hernia or cancer
52
Identify causes of large bowel obstruction
Large bowel – malignancy, diverticular disease, volulvulus
53
Causes of bowel obstructions
* Intraluminal = gallstone ileus, ingested foreign body, faecal impaction
* Mural = cancer, inflammatory strictures, intusseption, diverticular strictures, Mecke’ls diverticulum, lymphoma
* Extramural = Hernias, adhesions, peritoneal metasisis, volvulus.
54
Early non-surgical management of small bowel obstruction
Urgent fluid resuscitation and urinary catheter. Urgent surgery if closed loop bowel obstruction or evidence ischaemia.
* Nil-by-mouth (NBM) and insert nasogastric tube to decompress bowel
* Start IV fluids and correct any electrolyte disturbances (drip)
* Urinary catheter and fluid balance
* Analgesia with suitable anti-emetics.
Adhesional small bowel obstruction from previous surgery is treated conservatively in first instance with success rate of around 80%). Water soluble contrast study should be performed in cases that do not resolve within 24hours conservative management and if contrast doesn’t reach colon by 6hours then unlikely to resolve so take to theatre.
(Large or small obstructions with no previous surgery rarely settles without surgery)
55
Porvide broad overview of surgical options for managing patient with small bowel osbtruction
Small bowel resection – diseased or blocked part is surgically removed. Can be laparscopic or open and if two pieces healthy bowel left then ends stitched together and oleostomy with ostomy bag.
Can do strictureplasty for those with corCrohn’sns which mostly affects small bowel. The narrowed section of bowel is cut and sewn horizontally to widen the intestine
56
Provide a broad overview of the surgical options for managing a patient with large bowel obstruction
Large bowel resection – blocked or diseased part of your colon or large bowel may be removed surgically if you have a total blockage. This can be laparoscopically or open surgery in emergency. If two pieces of bowel are left healthy then ends will be stitched together and may be given colostomy and wear ostomy bag.
57
What is Peritonitis
= Redness and swelling (Inflammation) of the tissue that lines your belly or badomen.
58
Explaint he cause of peritonitis
Peritonitis is caused by infection. Bacteria can enter the lining of your bely from a hole in your GI tract. This can happen if you have a hole in your colon or burst appendix.
Other causes:
* Hole in stomach, intestine, gallbladder, uterus or bladder
* An infection durign treatment for end stage kidney disease
* Infection of fluid in belly from end stage liver disease (cirrhosis)
* Pelvic inflammatory disease in women
* Surgery (If abcteria enters belly n surgery)/
59
CLinical presentations of patients with peritonitis
* Severe belly pain that gets worse with any motion
* Nausea and vomiting
* Fever
* Sore or swollen belly
* Fluid in the belly
* Not being able to have bowel movement or pass gas
* Less urine than normal
* Thirst
* Trouble breathing
* Low BP and shock
60
Describe the broad principles of early management of patient presentign with peritonitis.
* Antibiotics – depends on severity and type of peritonitis. Start with broad spectrum m the narrow.
* Surgery – often to remove infected tissue, treat the underlying cause of infection and prevent infection from spreading.
* Other treatments – pain medications, IV fluids, oxygen, and sometimes a blood transfusion.
61
Explain the investigation of patient presenting with peritonitis
* Medical history and physical exam
* Blood tests - WBC count and blood culture
* Imagign tests - XRay to check for hole or perforations in GIT. US may also be used and possibly CT instread of XRay
62
Explain the principles of management of patients with peritonitis
* Might take 10-14 days to recover
* IV antibiotics (or if from kidney dialysis then Abs straight into stomach lining)
* Ay have feeding tube or liquid nutrients as you may struggle to digest food
* Surgery – may need this is part of your stomach lining has been seriously damaged by infection. Sometimes abscesses develop in the lining and need to be drained with a needle under local anaesthetic. Might also need operation to deal with the cause of peritonitis eg, remove a burst appendix.
63
AbdominalXray
* Limited role
* CT not available – Evaluation of bowel gas, evaluation of pneumoperitoneum.
* Assessment of radio-obaque objects
* Assessment of oral contrast flow
* Assessment of lines/tubes
* Kub XRAY (kidney, ureter, bladder)
**Structured approach:**
Bowel (and other organs)
Bones
Calcification (eg, renal stones, gallstones, aorta)
64
Views on an Abdominal xray
* AP (anterior-posterior) view
* Erect view
* Lateral decubitus
* Chest Xray
65
Normal Xrays of the abdomen
66
67
Sigmoid volvulus
68
Bowel obstruction
69
Pneumoperitoneum
70
Kidney sotne on KUB Xray
71
Gastrogaffin study
72
what is this
stent in ureter
73
CT abdomen - planes
74
Contrast studies on CT
* Oral
* Rectal
* IV contrast
75
What you can assess on ct of the abdomen
GIT, Biliary, Urinary, Solid organs, Vessels, Bones, Muscles/Abdominal Wall
76
Limitations/Side effects of CT
Missed lesions/pathologies, contrast induced nephropathy (RFs, eGFR, ways to mitigate it) and contrast allergy.
77
Small vs large bowel on XRAY
* SB mucosal folds (Valvulae conniventes) – visible across full width of bowel
* Large bowel wall features haustra – thicker than valvulae conniventes and typically does not appear to transverse the width of the bowel).
* Faeces- mottled appearance in large bowel, due to air trapping in solid faeces
* Bowel diameter: Upper limits = Small bowel 3cm, colon 6cm, caecum 9cm.
78
Small bowel obstruction on XRay
Small bowel obstruction – dilation of small bowel \>3c,. prominent valvulae conniventes. Caused by adhesions mostly then abdominal hernias and intrinsic/extrinsic compression. String of pearl sign.
79
Whats circled
faeces
80
Whats circled
81
Large bowel obstruciton XRAY
Large bowel obstruction: Colorectal cancer, diverticular structure, hernia, volvulus.
82
Whats this
83
84
IBD on AXR
* **Thumbprinting** – mucosal thickening of the hausta due to inflammation and oedema causing them to appear like thumbprints projecting into the lumen.
* **Lead-pipe** **(featureless) colon** – loss of normal haustral markings secondary to chronic colitis.
* **Toxic megacolon** – Colonic dilation without obatructin associated with colitis.
85
Thumb printing in UC
86
Lead piping in Ulcerative colitis
87
Looking at other organs on AXR
* **Lungs:** inspect the lung bases for pathology (e.g. consolidation) as abdominal pain can, in some cases, be caused by basal pneumonia.
* **Liver:** a large right upper quadrant structure.
* **Gallbladder:** rarely visible on an abdominal X-ray, however, you should quickly inspect for calcified gallstones and cholecystectomy clips.
* **Stomach:** visible between the left upper quadrant and midline, containing a variable amount of air.
* **Psoas muscles:** the lateral edge is marked by a relatively straight line either side of the lumbar vertebrae and sacrum.
* **Kidneys:** both are often visible, the right kidney is lower than the left due to the presence of the liver on the right.
* **Spleen:** located in the left upper quadrant, superior to the left kidney.
* **Bladder**: has a variable appearance depending on the fullness of the bladder.
88
Bony Mets from metastatic prostate cancer
89
Calcifiction and artefact on AXR
* Various high density (white) areas of calcification or artefact may be noted on abdominal X-ray including:
* Calcified gallstones in the right upper quadrant
* Renal stones/staghorn calculi
* Pancreatic calcification
* Vascular calcification
* Costochondral calcification
* Contrast (e.g. following a barium meal)
* Surgical clips
* Jewellery
90
Presentign AXR
Having a structured approach to summarising your findings is key to ensuring you communicate the salient points.
“This is a supine AP abdominal radiograph of Sydney Dixon , date of birth 7th June 1933.. The film is of good quality with adequate exposure. No prior imaging is available for comparison. Both the small and large bowel appear within normal limits. Other abdominal viscera appear normal within the limits of this projection. No obvious bony pathology is identified. No abnormal calcification is visible. In summary, this is a normal plain radiograph of the abdomen.” …
Evidence of dilated small bowel probably secondary to adhesions
91
Investigations – Biliary Disease:
Ultrasound
MRCP – Magnetic resonance cholangiopancreatographic scan
ERCP- Endoscopic retrograde Cholangiopancreatography
92
Management acute cholangitis
Acute Cholangitis:
* IV antibiotics and treat sepsis
* ERCP – endoscopic removal of gallstones and may also caryr out sphincterotomy and insert stent.
* Laparaoscopic cholecystectomy
