Abdomen Flashcards
GI history
- 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.
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Upper GI symptoms
- 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.
Lower GI symptoms
- 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
Location of pain in relation to pathology
- 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
GI risk factors
pre-existing medical conditons (GORD, Crohn’s), FH GI disease, alcohol, smoking, recreational drugs, diet.
What is an acute abdomen?
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.
When is Urgent vs less urgent intervention needed for acute abdomen
- 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
Invetsiagtions for Acute abdomen
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
Core management of an acute abdomen
- 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.
AReas of the abdomen pain and pathology
Patho of Acute appendicitis
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.
Risk factors of acute appendicitis
FH, Ethnicity (Caucasians more common but if minorities get it then more risk perforation), environmental (summer).
Investigations for appendicitis
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).
Describe and elicit from a given patient the classical presentation of acute appendicitis
- 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.
Typical clinical presentation acuet appendicits in children
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.
Main differential diagnosis of appendicitis
- 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
right iliac fossa pain differentials
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.
Treatment options for acute appendicits
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.
Explain possible complications of acute appendicits
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,
Acute pancreatitis - what is it
- 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.
Patho of acute pancreatitis
- 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
DDx of pancreatitis
(Pain that radiates to the back)
- AAA
- Renal calculi
- Chronic pancreatitis
- Aortic dissection
- Peptic ulcer disease
Investigations for pancreatitis
- Lab tests: serum amylase (3x normal), LFTs, serum lipase
- IMaging: abdominal US if cause unknown (can show sentinel loop sign), contrast enhanced CT
Explain the causes of pancreatitis
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
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
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)
Explain intiial management acte pancreatitis and concepts of later management of acute pancreatitis
No curative management so supportive measures. Treat the underlying cause
Supportive treatments:
- 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.
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.
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.
Risk factors for gallstones
- Fat, female, fertile, family hsitory, forty
- Also pregnancy, oral contraceptives, haemolytic anaemia (Pugment stones) and malabsroption.
DDx gallstones
- GORD
- Peptic ulcer disease
- Acute pancreatitis
- IBD
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.
Anatomy of Biliary system
Biliary tree = 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.
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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
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).
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.
Views on an Abdominal xray
- AP (anterior-posterior) view
- Erect view
- Lateral decubitus
- Chest Xray
Normal Xrays of the abdomen
Sigmoid volvulus
Bowel obstruction
Pneumoperitoneum
Kidney sotne on KUB Xray
Gastrogaffin study
what is this
stent in ureter
CT abdomen - planes
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.
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.
Whats circled
faeces
Whats circled
Large bowel obstruciton XRAY
Large bowel obstruction: Colorectal cancer, diverticular structure, hernia, volvulus.
Whats this
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.
Thumb printing in UC
Lead piping in Ulcerative colitis
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.
Bony Mets from metastatic prostate cancer
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
