General surgery Flashcards
Upper + lower GI
Why does SBO present so acutely?
Large amounts of gastric + pancreatic-biliary secretions prevented from passing
What are the causes of bowel obstruction?
- Within wall: tumours, inflammatory strictures, drug-induced strictures, lymphoma, intussusception (segment of SB telescoped into segment distal to it)
- Within lumen: impacted faeces, gallstones, phytobezoar, trichobezoar
- Outside wall: adhesions (surgery/infection), congenital bands, compressing tumours, strangulated hernias
Small bowel obstruction?
- Main cause is adhesions
- Other causes: hernias, compression by internal/external masses, Crohn’s disease
- Dilatation of SB >3cm in central loops, valvulae conniventes more visible
Large bowel obstruction?
- Most caused by malignancy, others include diverticular strictures, volvulus and hernias.
- Dilatation of LB >6cm (peripheral not loops), haustral lines visible
Bowl obstruction presentation?
- Vomiting-earlier when obstruction more proximal, semi-digested suggests gastric outlet obstruction, bile-stained suggests upper SBO, faeculent suggests more distal obstruction (altered SB contents)
- Pain-upper/middle/lower for foregut/midgut/hindgut, colicky as peristalsis tries to overcome obstruction
- Constipation-absolute
- Incomplete obstruction - less distinct features basically. e.g. intermittent vomiting, erratic bowels, chronic incomplete obstruction e.g. from cancer often visible peristalsis in abdomen
Why is LBO more gradual onset?
Larger capacity
What is the relevance of the ileocaecal valve?
In LBO, if the valve is competent no retrograde flow occurs so the caecum distends until it ruptures, whereas if valve is incompetent then the SB can dissent to reduce chance of perforation
So incompetent valve is better
Incomplete obstruction?
Most common cause is colorectal cancer. Less distinct features e.g. intermittent vomiting, erratic bowel habit, if chronic gradual hypertrophy of bowel wall muscle
Clinical signs of bowel obstruction?
General: abdo distention, anaemia, lymphadenopathy
Groin: look for hernias
Tender when strangulated/perforated, resonant percussion in centre then more dull at periphery (gas rises), high pitched tinkling bowel sounds
Complications of bowel obstruction?
ischaemia, perforation, peritonitis, dehydration, renal impairment
How would you manage a patient with bowel obstruction?
- NBM, NG tube, IV fluids, correct electrolytes
- Urinary catheter + fluid balance
- Analgesia + anti-emetics
- Adhesions treat conservatively unless strangulation/ischaemia, if contrast doesn’t reach colon in 6h need surgery
- Surgery (laparotomy) in: suspected ischaemia, closed loop obstruction , virgin abdomen, strangulated hernia, failure to respond to conservative management in 48h (most LBO need surgery) // or emergency hernia repair. Can sometimes try endoscopic stenting (good for left-sided obstruction)
Causes of bowel strangulation
Partial obstruction: occludes venous return, oedema worsens obstruction, closed loop of bowel dilates with gas as bacteria ferment, inhibits arterial flow, ischaemia, infarction
Commonest cause are strangulated hernias (usually inflamed but femoral often small and non-tender), others include being trapped by adhesions, passing through omental/mesenteric defect, volvulus
Signs of bowel strangulation
Signs of obstruction
Abdominal tenderness
Rising tachycardia + leukocytosis
Manage w fluids + urgent surgery
Causes of peritonitis
Localised - transmural inflammation of bowel (e.g. appendicitis, Crohn’s, diverticulitis) or of viscera (e.g. salpingitis, cholecystitis)
Generalised: chemical peritonitis (bile, stomach contents, exudate from pancreatitis) or bacterial (ruptured abscess, faecal contamination from bowel perforation, surgical spillage, anastomotic leak)
Clinical features of peritonitis
Localised peritonitis-inflammation, pain localises when PP involved, systemic toxicity
Generalised-rapidly v ill, hypovolaemia from exudation of inflammatory fluid into peritoneal cavity, sepsis
Intra-abdominal abscess
Worsening continuous pain, diarrhoea, adynamic bowel (from local irritation), swinging pyrexia, leucocytosis, palpable mass, PR hot tender mass. Pt often quite well (except post-op abscess)
May occur after bowel perforation (momentum + adjacent bowel wall wall off the defect, e.g. appendiceal abscess), or as a complication of bowel surgery (localised faecal contamination or anastomotic leak)
M: may drain spontaneously into rectum (pass pus + blood PR), or Abx + drainage if unwell
What causes abdominal viscus perforation?
Stomach and duodenum - PUD Sigmoid colon - diverticular disease, cancer Appendicitis Severe constipation Severe acute cholecystitis
How may perforation present?
Small perforations - local abscess as perforation walled off by omentum/bowel e.g. appendicitis
Large colonic perforation-sudden overwhelming faecal peritonitis
Peptic ulcer: board-like rigidity, initially little systemic upset as fluid mostly sterile
What surgical repair is employed in the common perforations?
Duodenal - plug with omentum
LB - Hartmann’s (end colostomy + rectal stump, temporary colostomy, as an anastomosis won’t heal cos of contamination)
Not suitable for surgery - restrict fluids, NG aspiration, acid suppression, ABx (this is only if can’t have GA)
What is acute bowel ischaemia?
Acute occlusion of SMA - ischaemia of midgut-derived structures (jejunum, ileum, right colon) - infarction of right colon + most of SB - perforation
Caused by embolism (e.g. AF), thrombosis of artery (e.g. low output HF), mesenteric vein thrombosis often patchy inflammation so may be better prognosis
What is the presentation + management of acute bowel ischaemia?
Severe pain, abdo usually soft without guarding, later CV collapse, metabolic acidosis, raised lactate
Urgent laparotomy (if limited resection may work), often necrosis so severe that care should be palliative
Causes of CF of major GI haemorrhage
- Gastric/duodenal erosions - haematemesis/melaena. Common
- Colon cancer/polyps-altered blood PR, common
- Diverticular disease-fresh PR bleeding, common
- Rectal cancer/haemorrhoids-fresh PR bleeding usually small amount
- Ischaemic colitis-abdo pain + fairly fresh PR blood. Quite common
- Colonic angiodysplasias-depends on location within colon, quite common
- Oesophageal varices-haematemesis/melaena
- Mallory Weiss tears-haematemesis/altered blood PR
- Stress gastric ulcers-haematemesis/melaena
- Acute UC-bloody diarrhoea
- Malignant SB tumours or angiodysplasias of SB - altered blood PR
Dieulafoy lesion?
Large tortuous arteriole that bleeds
Anatomy of the appendix
Blind-ending tube from caecum at meeting of three taenia coli, base is in RIF close to McBurney’s point (2/3 way from umbilicus to ASIS) - suspended by mesentery and floats around - inflammation fixes in a point e.g. over pelvic brim, retroperitoneally
Pathophysiology of appendicitis
Faecolith/obstruction - inflamed mucosa - spreads to serosa (VP) - spreads to adjacent structures - gangrene of appendix wall causes perforation. Then there is either a walling off reaction, or not and spreading peritonitis occurs
How is the likelihood of appendicitis graded?
Alvarado score: if 4 or less v unlikely to be appendicitis
1 point each for: migration of pain from centre to RIF, anorexia, N/V, rebound tenderness, temp >37.5, neutrophilia >75%
2 points for tenderness in RIF and leucocytosis (>10)
How does appendicitis present?
Abdo pain <72h
Migrates from centre (visceral P) to RIF (parietal P, somatic pain)
Local peritonitis: guarding, tender, rebound/percussion tenderness (as by palpation v severe pain), tender in RIF, ask to blow out abdo wall and draw in
Fever 37.3-38.5 (temp over this makes viral/UTI more likely)
No evidence of UTI
Anterior tenderness on DRE
Atypical: urinary symptoms if appendix near bladder, if near rectum diarrhoea, if retrocaecal irritation of psoas muscle (pain on extension, involuntary R hip flexion), high retrocaecal (pain below R costal margin), pelvic pain
In kids peritonitis and perforation more common, in elderly often walled off by loops of SB
Differential diagnoses for appendicitis?
UTI - nitrates in dip
Mesenteric adenines - esp in kids after recent sore throat/viral illness, inflammation of LNs, fever higher
Large bowel disorders - constipation, diverticulitis
Gynae issues-mittelschmerz, salpingitis (lower pain, discharge, adnexal tenderness), torsion of cyst, ectopic pregnancy (anaemia, hypotension)
Small bowel: inflamed Meckel’s diverticulum (sam presentation), terminal ileitis from CD
Acute pancreatitis (pain also in epigastric)
Gastroenteritis
What is a Lily-White appendix?
Appendix actually fine when do surgery but remove it as otherwise in future people may assume its been removed thus miss appendicitis
Complications of appendicectomy
Early: appendix stump blow out, generalised peritonitis, abscess, retained faecolith, haematoma, wound infection, dehiscence
Late: obstruction from adhesions, infertility from tubal occlusion if pelvic infection, incisional hernia
Acute abdomen causes
Upper GI: acute cholecystitis, acute pancreatitis, PUD, gastroenteritis, GI haemorrhage, hepatitis
Lower GI: acute appendicitis, Meckel’s diverticulitis, diverticulitis, intestinal obstruction, acute intestinal ischaemia, GI haemorrhage, mesenteric adenitis, terminal ileitis from CD, strangulated hernia
AAA, vasculitis
Gynae: ectopic pregnancy, PID, tubo-ovarian abscess, salpingitis
Renal: renal colic, acute urinary retention, testicular torsion, pyelonephritis
Non-surgical: pneumonia, MI, pericarditis, sickle cell crisis, DKA, opiate withdrawal, acute intermittent porphyria
Common surgical scars
Kocher - inferior + parallel to R costal marching. For open GB surgery
Mercedes Benz modification - cevron + break through xiphisternum.
Chevron (rooftop): gastrectomy, b/l adrenalectomy, liver transplant
Loin: renal surgery
Midline laparotomy
Paramedian (sides of umbilicus) : spleen, kidney, adrenal
Lanz: Mcburney’s point for appendicectomy (open, not used now), Rutherford-Morrison is extension of this for kidney transplant
Pfannenstiel-along pubic hairline, for C section, pelvic bladder prostate surgeries
Oesophageal carcinoma
Adenocarcinoma most (RF-Barrett’s oesophagus squamous to columnar metaplasia, survey every 2y, red mucosa w ulceration at GOJ) squamous cell carcinoma (upper 2/3, RF smoking alcohol)
CF: dysphagia solids then liquids, odynophagia, RLN invasion, oesophago-tracheal fistula, wasting, hepatomegaly from mets, L Virchow’s node
M: surgery to relieve obstruction + allow swallowing, chemoradiotherpay, palliative
Hiatus hernia
Proximal part of stomach goes through diaphragmatic hiatus into stomach
Sliding HH: GOJ drawn up into chest, bit of stomach constricted at hiatus, hernia slides up with each peristaltic contraction, can become v big, often defective LOS - reflux
Para-oesophagela/rolling HH: GOJ remains below, bulge of stomach herniates through hiatus next to oesophagus, usually pain/dysphagia, sphincter is fine
CF: oesophagitis, pain, regurgitation, worse at night – most asymptomatic
Comps: persistent inflammation from reflux causing fibrosis + strictures, Barrett’s oesophagus
M: weight loss, change diet (e.g. alcohol + smoking relax sphincter so reduce), alginates (foam coats surface to protect), pro kinetic dopamine antagonists (e.g. metoclopramide) to increase S emptying, PPI to reduce acid, dilatation of strictures, surgery (dissect GOJ at hiatus, tightens crura, wrap funds around oesophagus to recreate flutter valve - Nissen operation
Achalasia
Neuro issue in parasympathetic plexus - disrupts peristalsis - uncoordinated contraction + inadequate relaxation of LoS (so proximal oesophagus dilates w food)
CF: dysphagia, recurrent chest infection, halitosis, WL, reflux, spluttering dysphagia + coughing (fluids spill over into trachea), vomiting, retrosternal CP
Predisposes to SCC of oesophagus (after 15yish)
CXR-widened mediastinal shadow, fluid level behind heart, barium-tapering constrictor at lower end
M - Heller’s cardiomyotomy incision to widen, botulinum toxin injections
Diffuse oesophageal spasm
Contractions due to dysfunction of inhibitory nerves. Severe dysphagia, central CP which may respond to nitrates.
Endoscopy often normal, may have dysfunction of LoS, barium may show corkscrew appearance
M: relaxation of oesophageal smooth muscle with nitrates/CCBs, myotomy for severe
Pharyngeal pouch
Rare cause of dysphagia. Lack of coordination between inferior constrictor muscle + cricopharyngeus - Killian’s dehiscence (area of weakness) - mucosal out pouching
Easily perforated in endoscopy
Oesophageal web
Dysphagia due to circumferential mucosal folds, predispose to cancer
Dysphagia + anaemia + atrophic glossitis = Plummer-Vinson syndrome
Gastro-oesophageal varices
Portal venous hypertension - abnormal connections between portal + systemic venous circulation - shunting - large submucosal veins at lower end of oesophagus + gastric fundus - when pressure rises can cause massive haemorrhage
Not normally treated until bleeds
M: resuscitation (avoid excess Na and water due to ascites, give FFP), endoscopy to source bleeding (may be varices or ulcer or Mallory Weiss), try to band or inject with sclerosant, infusion of vasopressin or octreotide, try tamponade, if continues TIPS (trans jugular intrahepatic portal-systemic shunting-catheter in intrahepatic IJV with a stent to connect portal system to vena cava). There’s also emergency surgery but high mortality e.g. trans gastric oesophageal stapling
Oesophageal tears
Perforation: Boerhaave’s syndrome (transmural perforation, often ass w vomiting or iatrogenic), causes severe inflammatory response
CF: sudden onset retrosternal CP, resp distress, subcutaneous emphysema, pneumomediastinum, intra-thoracic air-fluid levels.
M: resuscitate, ABs, control leak. Mortality 50-80%
Mallory-Weiss tears: non transmural superficial mucosal tears, most common at GOJ, usually after profuse vomiting (short period of haematemesis), usually self-limiting unless on anticoagulants/clotting abnormal. Mostly conservative management
Causes of portal venous hypertension?
Cirrhosis from ALD
Portal vein thrombosis
Hepatic vein thrombosis - Budd-Chiari syndrome
Schistosomiasis
Causes of peptic ulcer disease
H pylori - colonises mucosa over a long time, stimulates acid + compromises natural defence
Acid-pepsin production by parietal cells. In duodenal main issue is excess acid, in gastric main issue reduced defence
Mucosal resistance reduced by NSAIDs-block prostaglandins so less mucus
Direct AI of mucosa by NSAIDs, alcohol, cigarettes
Zollinger-Ellison syndrome: gastrin-secreting tumour of pancreas
How does PUD present?
Epigastric pain
- Dyspepsia - retrosternal pain, bitter regurgitation, N/V, anorexia, abdo bloating, relationship to food (G ass w eating, D relieved by food, this is tenuous tbh)
- Oesophageal disorders: reflux, often HH, transient/reflux oesophagitis, persistent inflammation (sometimes can cause strictures, UGIB etc)
- Stomach disorders: most in antrum and along lesser curve e.g. gastritis (mild inflammation but can bleed), stress ulcers (develop rapidly in v ill people, may perforate or bleed), chronic ulceration (usually worse with food esp acidic/spicy, may have WL + chronic anaemia, sx fluctuate, rarely may perforate into transverse colon causing gastro-colic fistula + faeculent vomiting)
*Duodenal disorders: duodenitis, ulcer, complete pyloric obstruction by scarring
Perforation + peritonitis
H pylori eradication?
PPI + 2 antibiotics (clarithromycin + amoxicillin / metronidazole) for 1w
Management of PUD
- Control factors like avoid dietary triggers, avoid NSAIDs/add gastroprotection, stop smoking
- H pylori eradication (PPI + 2 Abx for 1w)
- Reduce irritation: antacids (aluminium containing cause constipation and magnesium containing cause diarrhoea)
- Mucosal protection e.g. sucralfate - used in ICU to prevent stress ulcers
- Reduce acid secretion: PPIs first like as more potent, H2RA
- Correct secondary issues e.g. strictures, pyloric stenosis
Peptic ulcer perforation
Sudden epigastric pain, brownish/blood fluid, not toxic until later secondary infection as first is chemical peritonitis, board-like rigidity
Free gas + fluid in abdomen
Need resuscitation + laparotomy - peritoneal toilet, close perforation in duodenum or excise it in gastric
Pyloric stenosis
Rare. Chronic ulceration - fibrosis - strictures - partial gastric outlet obstruction - acute exacerbation of ulcer causes mucosal swelling + sphincter spasm - complete obstruction
CF: projectile vomiting with semi-digested food, dehydration, hypochloraemic alkalosis
M: resus, acid suppression + eradicate H pylori (this often underlying cause), gastro-jejunostomy
Gastric carcinoma
Adenocarcinoma
Intestinal type similar to intestinal epithelium, diffuse type cells have signet ring appearance with single file cells + marked stromal reaction (worse prognosis)
4th commonest cancer worldwide, rare pre 50, M>F, East Asia highest
Causes: atrophic gastritis - dysplasia - neoplasia, H pylori (intestinal type), excess salt
CF: inlet/outlet obstruction symptoms like vomiting and dysphagia, pain, N&V, early satiety, anaemia, LN, faecal vomiting from gastro-colic fistula (with TC), Virchow’s node, palpable mass (Troisier’s sign), spread to liver/lung/brain/bone
Gastric polyps
Mostly benign hyper plastic nodules of mucosa
Genuine adenomatous polyps rare
Gastrointestinal stromal tumours
Rare anywhere in GIT but mostly in stomach, originate from interstitial cells of Cajal (pacemakers of gut activity). Most small, prone to haemorrhage from ulceration, if in SB present with SBO
Gastric and SB lymphomas
H pylori an initiator. In stomach most are B cell NHL, in SB occasionally cause intussusception
M: CHOP chemotherapy regimen, excision, subtotal gastrectomy if bleeding,
Carcinoid tumours
Arise from APUD cells of GI endocrine system in any tissue derived from GIT (inc pancreas, biliary)
Most common in appendix, others in SB mostly
Secrete catecholamines + serotonin - carcinoid tumour usually when get liver mets - transient hot flushes, hypotension, asthma, diarrhoea. Measure 5-HIAA in urine as a marker (serotonin metabolite)
Symptom control with octreotide and somatostatin analogue, excise primary lesion + Los, metastases is slow but not curable by radio/chemo
Pathological consequences of pancreatitis?
Disturbed membrane stability - inappropriate activation of zymogens esp trypsin - interstitial oedema - peritoneal exudation - fat necrosis in mesentery/omentum, calcium sequestration (so hypocalcaemia), enzymes cause local damage + activate complement/cytokines - SIRS and organ failure - pancreatic necrosis from ischaemia + reperfusion injury, which dark bloody inflammatory exudate containing lipid in the peritoneum
Causes of pancreatitis?
I GET SMASHED
Commonest are alcohol, gallstones, ERCP and idiopathic
Idiopathic
Gallstones - blockage of PD by large stones/smaller stones transiently obstructing as pass through ampulla
Ethanol - longstanding high intake, or binge
Trauma - ERCP, cardiopulmonary bypass
Steroids
Mumps
Autoimmune
Scorpion/snake venom
Hypercalcaemia/hyperlipidaemia/hypothermia
ERCP
Drugs – SAND. Steroids/sulfonamides, azathioprine, NSAIDs, diuretics (also AB like metronidazole and H2RA)
Clinical features of acute pancreatitis
Pain-sudden, continuous, epigastrium, to back, pancreatic position is better, movement makes worse Vomiting Systemic illness Jaundice Reduced or absent bowel sounds
Presentation of chronic pancreatitis
Persistent severe upper pain, without the other features, amylase may not be raised/only slightly raised, may see fibrosis on ERCP
What investigation results suggest pancreatitis?
Amylase - usually >1000, though often lower in alcoholics. >300 is high, but usually pancreatitis is very high and other causes for moderately raised include pancreatic pseudocyst, mesenteric infarcts, cholecystitis, DKA, perforation
LFTs: ALT high in gallstone
USS of biliary tree 48-72h after onset, ERCP for gallstones
What is severe pancreatitis (Glasgow Ranson criteria)?
3 features out of: P - PaO2 <8kPa A - age >55 N - neutrophils >15 C - calcium <2 R - raised plasma urea >16 E - enzyme, plasma LDH >600 A - albumin <32g/L S - sugar, glucose >10 mmol/L
Meaning high risk of major complications
Management of acute pancreatitis
Mild - fluids, analgesia, treat cause
Severe - supportive (oxygen, fluids, NG tube), TPN may be necessary, manage electrolytes, analgesia
Complications of pancreatitis?
Death - ARDS, RF, multiple organ dysfunction (e.g. CV collapse, renal insufficiency, DIC)
Pancreatic/peripancreatic necrosis
Fluid collections
Pancreatic pseudocysts (fluid with enzymes + necrotic debris lasting for >6w, pseudo as no epithelial cells)
Pancreatic abscess (swinging fever)
Portal vein thrombosis
Bowel ischaemia esp transverse colon due to position of middle colic artery
Pseudoaneurysms
Diabetes mellitus
Intestinal malabsorption
Pancreatic exocrine cancer
Most ductal adenocarcinoma, a few acinar, most in head, 1/5 in body/tail, often well-diff but met to LN, peritoneum + liver (HPV) so at presentation few are resectable
RF: >50y, smoking, chronic pancreatitis, hereditary, obesity/T2DM
CF: weight loss, abdo pain (in more advanced, deep and knawing, nocturnal, hard to control, better leaning forwards, often from retroperitoneal nerve invasion), obstructive jaundice (in 50%, initially painless, CBD compression in pancreatic head - proximal BD dilates - GB may become palpable (Classically Courvoisier’s law of palpable gallbladder + painless jaundice is pancreatic cancer not gallstones as in gallstones GB wall is thick so not painful; and in GS jaundice is fluctuating, but this is not always the case), dyspeptic symptoms and N&V, ascites, abdo masses, acute pancreatitis, DM (preceding/following diagnosis), gastric outlet obstruction, thrombophlebitis migrans
Ix: CT CAP can show tumour extent + liver + vascular invasion (SMA/V, coeliac artery - these lessen surgical feasibility).
M:
- ERCP may be done to relieve jaundice with stenting
- Whipple’s: pancreatico-duodenectomy. High morbidity + mortality. Post-op chemo with 5-FU or gemcitabine
- Poor prognosis
- Palliation: good analgesia e.g. permanent coeliac ganglion blockade, biliary stent via ERCP for jaundice, surgical bypass to help relieve duodenal obstruction
Pancreatic endocrine tumours
*Neuroendocrine tumours in islets of Langerhans
Insulinomas: beta cells, most benign, cause hypoglycaemia
*Glucagonomas: alpha cells, v rare, DM and migratory necrolytic erythema rash
*Gastrinomas: secrete gastrin, from islets/ectopic cells in duodenum, ass w MEN 1. Zollinger-Ellison when cause peptic ulcers + diarrhoea. Most malignant but slowish to grow
*Multiple endocrine neoplasia syndromes - tumours, autosomal dominant inheritance
MEN 1, 2a and 2b?
1 - islet cell tumours, pituitary adenoma, parathyroid hyperplasia
2a - medullary thyroid carcinoma, pheochromocytoma, parathyroid adenoma/hyperplasia
2b - medullary thyroid carcinoma, pheochromocytoma, neurofibromas, Marfanoid habitus
Pancreatic cyst types
Fluids within pancreas, non-inflammatory (cf pseudocysts)
High risks: mucinous cysts like indraductal papillary neoplasm (ass w PD cancer), mucinous cystic neoplasm (cancer/pre cancer), solid pseudo papillary neoplasm (rare), cystic pancreatic neuroendocrine tumour (MEN1)
Low risk: serous cysts e.g. serous cystic adenoma (honeycomb appearance), simple cyst (always benign), mucinous non-neoplastic, lymphoepithelial
Most asymptomatic, may cause abdo or back pain from compression, post-obstructive jaundice + vomiting, may become infected
Discussed at MDT for resection vs surveillance
Biliary tumours
Cholangiocarcinoma - adenocarcinoma of biliary epithelium (in or out liver), ass w PSC, most extra-hepatic + compress bile drainage causing jaundice, LN + vascular often involved so hard to operate
Periampullary carcinoma - adenocarcinoma of AoV, enters duodenum, friable
Gallbladder carcinoma - old age, most from CI of GI
Gallstone composition?
Mixed with most cholesterol - abnormal bile e.g. removal of terminal ileum so less bile salts reabsorbed, biliary stasis. Multiple
Cholesterol stones
Pigment stones - excess bilirubin excretion due to haemolytic disorders like infection, malaria, leukaemia
Calcium carbonate stones - excess calcium in bile
Mucocele?
GB distended with mucus due to obstruction
Biliary colic
Intermittent CD obstruction by stone
Severe pain rises to a plateau then continues unrelentingly (not true colic), afebrile, often V, some local tenderness
Manage with injection of opiate, USS to find location, cholecystectomy definitive, ?low fat diet beforehand as less stimulus to GB.
Acute cholecystitis
Physical/chemical/bacterial irritation
Pain RUQ, pain that arrests on inspiration (Murphy’s sign), systemically unwell with fever + tachycardia
USS - GS, thickened GB wall
Most dont need ABs as inflammation usually but need cholecystectomy soonish (if done acutely GB may be obstructed + tense etc)
