Surgery - General Flashcards
What are the most common causes of small and large bowel obstruction?
- Most common small bowel causes = adhesions, hernia
- Most common large bowel causes = malignancy, diverticular disease, volvulus
How does bowel obstruction present?
- Presentation
- Abdo pain (colicky or crampy)
- Vomiting (early in proximal, late in distal)
- Abdo distension
- Absolute constipation (early in distal, late in proximal)
- O/E
- Surgical scars (adhesions etc), hernia, abdo distension
- Assess fluid status
- Tympanic on percussion
- Tinkling bowel sounds on auscultation
- Abdo tenderness (but if there is guarding/rebound tenderness then suspect ischaemia!!! Do vbg for lactate)
How would you investigate and manage bowel obstruction?
- Investigations
- Definitive = ct abdo pelvis with iv contrast
- Differentiates between pseudo-obstruction and mechanical too
-
AXR
- S bowel = dilated >3cm, central, valvulae conniventes (lines totally across bowel)
- L bowel = dilated >6cm or >9cm in caecum, peripheral, haustra visible (incomplete lines across bowel)
- In perforation you can see Riglers sign (both sides of bowel visible) or psoas sign (loss of sharp delineation of psoas muscle border)
- Erect CXR if suspected bowel perf = pneumoperitoneum
- Definitive = ct abdo pelvis with iv contrast
- Management
- Conservative = “drip and suck”
- NBM + NG tube to decompress bowel
- IV fluids and correct electrolytes
- Urinary catheter, fluids
- Analgesia, anti-emetics
- Adhesions = usually conservative unless strangulated/ischaemic
- Do water soluble contrast study if not resolved in 24 hours
- If contrast does not reach colon in 6 hours then take to theatre as it is unlikely to resolve
- Conservative = “drip and suck”
- Surgical = generally a laparotomy, sometimes resection + stoma
- For ischaemia or closed loop bowel obstruction
- Or if patients treated conservatively don’t improve
What two ways does an upper GI bleed present as?
Melena (black tarry offensive smelling stools)
Haematemesis (vomiting blood)
What are some differentials for an upper GI bleed?
-
Peptic ulcer disease
- Most signif bleeding if ulcer erodes through posterior gastric wall into gastroduodenal artery (also common in lesser curve of stomach)
- Suspect in nsaids or steroids, dyspepsia like hx, h pylori positive
-
Variceal bleeds
- Commonly Oesophageal varices due to alcoholic liver disease
- Upper gi malignancy
-
oesophagitis
- inflammation of intraluminal epithelial layer of the oesophagus
- due to GORD (most common), or infections (candida albicans), meds (bisphosphonates), radiotherapy, crohns
-
Mallory Weiss tear
- Recurrent vomiting then haematemesis
- Forceful vomiting causes a tear in the epithelial lining of the oesophagus
- Meckels diverticulum
- Vascular malformations eg. dieulafoy lesion
How would you investigate an upper GI bleed generally?
+ scoring systems
- Investigations
- Oesophagogastroduodenoscopy is definitive
- CT abdo with iv contrast to assess any active bleeding
- Fbc, u&es, lfts, clotting, group and save, abg
- Erect cxr if perforated peptic ulcer suspected
- Glasgow-Blatchford Bleeding score for upper gi bleeds
- Rockall severity score for GI bleeding post endoscopy
- AIMS65 score for risk of in-hospital mortality from upper gi bleed
How would you manage an upper GI bleed generally?
(peptic ulcer and varices too)
- Peptic ulcer
- During OGD, give adrenaline injection** and **cauterise bleeding.
- High dose ppi eg. iv 40mg omeprazole
- Active bleeding can be treated with angio-embolisation
- Oesophageal varices
- Endoscopic banding
- Prophylactic antibiotics
- Somatostatin analogues (eg. octreotide) or vasopressors (eg terlipressin) to reduce splanchnic blood flow
- Sengstaken-Blakemore tube for uncontrollable/severe
- Longterm = repeated banding and long term BB
- Blood products for hb<70g/L
- FFP+/- platelets for impaired liver function
- Reversal agents for anticoagulants
What are some differentials for a lower GI bleed?
-
Diverticular disease
- Outpouchings of bowel wall consisting of mucosa
- Commonly in descending and sigmoid colon
- Diverticular disease bleeds are painless
- Diverticulitis bleeds are painful
- Ischaemic/infective colitis
-
Haemorrhoids
- Engorged vascular cushions in anal canal
- Blood on surface of stool not mixed
-
Malignancy
- In elderly, always suspect colorectal cancer
- Angiodysplasia
- Crohns
- UC
- Radiation proctitis
How would you investigate and manage a lower GI bleed? and scoring systems
Investigations
- Oakland score (stratifies if pt with lower gi bleed can be managed as outpatient)
- Fbc,u&es, lfts, clotting, group and save, stool cultures
- Urgent ct angiogram for haemodynamically unstable (can embolise during)
-
Flexi sigmoidoscopy
- Full colonoscopy if nothing on flexi sig
- OGD if nothing on colonoscopy
- Capsule endoscopy or mri small bowel can also be done
Management
- A-e resus
- Packed rbc for hb<70, reverse anticoagulation
- Endoscopic haemostasis methods eg. adrenaline injection
- surgical
What are risk factors of GORD?
- male, old age, obesity, alcohol, smoking, caffeine, spicy food
How dose GORD present?
-
Burning retrosternal chest pain (worse after meals, lying down, bending over, straining)
- Relieved by antacids
- Excessive burping
- Odynophagia
- chronic/nocturnal cough
How would you investigate and manage GORD?
Investigations
- Los Angeles classification of reflux oesophagitis
-
OGD to rule out red flags for upper gi malignancy
- Dysphagia
- >55 with weight loss, upper abdo pain, dyspepsia, reflux
- OGD also investigates oesophagitis, structuring, barretts
- Gold standard for GORD = 24 hour pH monitoring
- Oesophageal manometry to rule out oesophageal dysmotility
Management
- Conservative
- Avoid alcohol, coffee, fatty foods
- Weight loss
- Smoking cessation
- PPIs
- Surgical
- Fundoplication (se = bloating, dysphagia, inability to vomit)
What are the two kinds of oesophageal cancer?
How would they present?
Squamous cell = middle and upper 1/3 of oesophagus
- Risk factors = smoking, alcohol, low vit a, chronic achalasia
Adenocarcinoma = lower 1/3 of oesophagus
- Risk factors = barretts (metaplastic epithelium that progresses to dysplasia), GORD, obesity, high fat intake
Presentation
- Progressive dysphagia (solids first)
- Weight loss, cachexia, supraclavicular lymphadenopathy
- Odynophagia
How would you investigate and manage oesophageal cancer?
Investigations
-
Urgent OGD in 2weeks
- Biopsy and send to histology
- CT CAP and PET CT for mets
- Endoscopic US to assess penetration into oesophageal wall (T stage)
- Staging laparoscopy for intraperitoneal mets
- Fine needle aspiration of palpable cervical lymph nodes
- Bronchoscopy for hoarseness or haemoptysis
Management
- Definitive
- SCC = difficult to operate on so usually chemoradiotherapy
- Adenocarcinoma = neoadjuvant chemo or chemoradiotherapy, followed by oesophageal resection
- Most will need a feeding jejunostomy after surgery to aid nutrition
- Surgery risks = anastomotic leak, pneumonia etc
- Palliative
- Oesophageal stent for difficulty swallowing
- Radiotherapy/chemotherapy to reduce tumour size/bleeding
- Nutritional support = thickened fluid and nutritional supplements
- Radiological inserted gastrostomy (RIG) tube insertion for severe dysphagia
Oesophageal tears:
Boerhaave’s Syndrome is full thickness, Mallory Weiss is lacerations of the mucosa.
How does Boerhaave’s present?
- Stomach contents leak into mediastinum and pleural cavity
- Severe inflammatory response and multi organ failure
- Causes = iatrogenic like endoscopy or forceful vomiting
- Presentation
- Severe sudden onset retrosternal chest pain, resp distress, subcutaneous emphysema
- Hx of severe vomiting and retching
- Mackler’s triad = vomiting, chest pain, subcut emph
How would you investigate and manage Boerhaaves?
Investigations
- Fbc, u&es, lfts, clotting
- Definitive = urgent ct abdo pelvis with iv and oral contrast
- Cxr for pneumomediastinum or intrathoracic air fluid levels
- If high clinical suspicion, just do urgent endoscopy in theatre
Management
- A-e resus
- Surgical
- Endoscopy to determine site of perf
- Thoracotomy to Control leak and wash out chest
- Do a contrast ct at 10 days before starting oral intake as leaking is common
- Insert feeding jejunostomy in surgery for nutrition
- Non operative (iatrogenic perfs usually more suitable as they are more stable)
- Resus and transfer to icu/hdu
- Antibiotics and antifungal cover
- NBM for 1-2 weeks, ng tube insertion on drainage
- Large bore chest drain insertion
- TPN or feeding jejunostomy insertion
How would a Mallory Weiss tear present?
- Typically at gastro-oeosphgeal junction
- Presentation
- Hx of profuse vomiting then short period of haematemesis
- Usually fine unless clotting abnormalities or anti-coag drugs
What is Achalasia? How would it present?
Achalasia = failure of LOS to relax, progressive failure of contraction of proximal oesophageal smooth muscle
- Due to progressive destruction of ganglion cells in the myenteric plexus
Presentation
- Progressive dysphagia with solids and liquids
- Regurgitation
- Coughing especially at night
- Chest pain
- Weight loss
How would you investigate and manage Achalasia?
Investigations
- Barium swallow
-
oesophageal manometry is gold standard for motility disorders
- shows absence of oesophageal peristalsis, failure of relaxation of LOS, high resting LOS tone
- urgent OGD to rule out oesophageal cancer
Management
- Conservative
- Sleeping on pillows
- Eating slowly
- Chewing food thoroughly
- More fluids with meals
- CCB or nitrates (temporary)
- Botox injections in LOS by endoscopy (temporary)
- Surgical
- Endoscopic balloon dilation
- Laparoscopic heller myotomy
What is diffuse oesophageal spasm?
How would it present
Diffuse oesophageal spasm = multi focal high amplitude contractions of the oesophagus
- Due to dysfunction of oesophageal inhibitory nerves
Presentation
- Severe dysphagia to solid and liquids
- Central chest pain exacerbated by food
- Responds to nitrates
How would you investigate and manage diffuse oesophageal spasm?
Investigations
- Manometry shows repetitive, simultaneous and ineffective contractions of the oesophagus
- Barium swallow can show corkscrew appearance
Management
- Nitrates or CCB to relax smooth muscle
- Pneumatic dilation
- Myotomy for severe
What is a hiatus hernia and what are the two types?
Hernia = Protrusion of a whole or part of an organ through the wall of the cavity that contains it into an abnormal position
Hiatus hernia = protrusion of an organ from the abdo cavity into the thorax through the oesophageal hiatus (usually stomach)
- They can be classified into sliding or rolling
- Sliding = Gastro-oesophageal junction + abdo part of oesophagus + cardia of stomach slides up through diaphragmatic hiatus into the thorax
- Rolling = upward moving of gastric fundus so it lies beside a normal GOJ, resulting in a “bubble” of stomach in the thorax
What are some risk factors of a hiatus hernia?
- old age (loss of diaphgragmatic tone), increased abdo pressure (eg. coughing, obesity, pregnancy, ascites)
How would a hiatus hernia present?
- Mainly asymptomatic
- Reflux eg. burning epigastric pain worse on lying flat
- Hiccups or palpitations (large hernias can irritate diaphragm or pericardial sac)
- Swallowing difficulties (oesophageal stricture formation)
- Vomiting and weightloss
- Bleeding/anaemia (oesophageal ulceration)
How would you investigate and manage a hiatus hernia?
Investigations
- OGD is gold standard
Management
- PPI like omeprazole
- Weight loss, smaller meal portions with low fat content, sleeping with head of bed raised
- Smoking cessation, reduce alcohol
- Surgery like cruroplasty or fundoplication
What are some complications of a hiatus hernia?
- Rolling ones are prone to incarceration and strangulation
-
Gastric volvulus can occur and cause obstruction and tissue necrosis
- Borchardt’s triad of severe epigastric pain, retching without vomiting, inability to pass an NG tube
What is peptic ulcer disease?
- A break in the lining of the GI tract extending through to the muscularis mucosae
- Most commonly in the lesser curvature of the proximal stomach or the first part of the duodenum
- Normal protective mechanisms = hco3- ions and mucous secretion by the gi mucosa
What are some risk factors of peptic ulcer disease?
- Hpylori, Nsaids, corticosteroids, physiological stress, head trauma, Zollinger Ellison syndrome
- Hpylori
- Produces urease to break down urea into co2 and ammonia (neutralises stomach acid to create an alkaline environment)
- Sets off inflammatory response
- Zollinger Ellison syndrome
- Triad of severe peptic ulcer disease + gastric acid hypersecretion + gastrinoma
- Characteristic finding is a fasting gastrin level of >1000pg/ml
- Associated with Multiple Endocrine Neoplasia Type 1 syndrome
How does peptic ulcer disease present?
- Retrosternal or epigastric pain
- Gastric is worse on eating, duodenal is worse 2-4 hours after eating or even alleviated by eating
- Nausea, bloating, post-prandial discomfort, early satiety
How would you investigate and manage peptic ulcer disease?
Investigations
- Nice says to do an urgent ogd for people with…
- New onset dysphagia
- >55 years old with weight loss and upper abdo pain/reflux/dyspepsia
- New dyspepsia not responding to ppi
- Ogd usually for older pts or red flag symptoms.
- Biopsy any peptic ulceration for histology and rapid urease test
- Most young low risk pts just need Non invasive h pylori testing
- Carbon 13 urea breath test
- Serum antibodies to h pylori
- Stool antigen test
Management
- Conservative
- Smoking cessation, weight loss, reduce alcohol
- Stop nsaids
- Start on PPI for 4-8 weeks then reassess
- Triple therapy for hpylori +ve (PPI + oral amoxi + clarithro OR metronidazole for 7 days)
- Surgery for Emergencies like perf or severe relapsing disease = partial gastrectomy or selective vagotomy
How would Gastric cancer present?
And some risk factors
- Typically Adenocarcinomas
- Risk factors = male, hypylori, old age, smoking, alcohol
Typically present really late
- Dyspepsia
- Dysphagia
- Early satiety
- Vomiting
- Melaena
- Epigastric mass, Anorexia, weight loss, anaemia in late stage
- Troisier sign = palpable left supraclavicular node (Virchows)
How would you investigate and manage a gastric cancer?
Investigations
- OGD and biopsy for histology, CLO test and HER2/neu protein expression
- CT CAP and staging laparoscopy
Management
- Nutritional assessment and support
-
Peri-op chemo and surgery (gastrectomy of some sort)
- SE of gastrectomy = anastomotic leak, dumping syndrome, vit b12 deficiency
- Early t1 tumours may have endoscopic mucosal resection
- Palliative for late presentation (chemo, stenting, supportive)
How would Gastroenteritis typically present? What would you do to investigate? (just one test)
Presentation
- Diarrhoea = 3 or more loose stools per day (WHO)
- Acute <14 days, chronic >14 days
- vomiting, night sweats, weight loss
- Dehydration and pyrexia
- crampy abdo pain
- typical hx = affected fam or friends, hx of travel, antibiotics within 4 weeks (c diff)
Investigations
- Stool culture
What are some common viral and bacterial causes of gastroenteritits?
Viral = norovirus, rotavirus (kids), adenovirus (kids)
Bacterial
-
Campylobacter = G-ve bacillus
- Food poisoning from chicken, eggs milk
- Can result in reactive arthritis, GBS, HUS, TTP
-
EColi = G-ve bacillus
- Most common cause of travellers diarrhoea
-
Salmonella = G-ve flagellated bacillus
- Uncooked poultry or raw eggs
- Bloody diarrhoea
-
Shigella = G-ve bacillus
- Contaminated dairy or water
- Bloody diarrhoea
What are some common parasitic causes of gastroenteritis? How would you manage them?
Commonly travellers diarrhoea
- Cryptosporidium
- Entamoeba hystolytica = metronidazole
- Giardia intestinalis = metronidazole
- Schistosomas = praziquantel
How does hospital acquired C.Difficile gastroenteritis occur?
Hospital acquired = C. difficile (G+ve)
- Following broad spec antibiotics that disrupt normal microbiota in bowel
- C diff overgrow and produce excess exotoxin A and B
- Results in inflammatory response in colonic mucosa = severe bloody diarrhoea
- Complications = toxic megacolon if untreated
Investigate with stool culture + Cdiff toxin testing
Manage with IV fluids and oral metronidazole
What is an inguinal hernia? What are the two different types
- When abdo cavity contents enter the inguinal canal
- Most common hernia
Direct (20%) = bowel enters inguinal canal through Hesselbach’s triangle
- Typically in older patients due to increased intra abdo pressure or abdo wall laxity
- Medial to inferior epigastric vessels
Indirect (80%) = bowel enters inguinal canal via deep inguinal ring
- Typically due to incomplete closure of processes vaginalis
- Lateral to inferior epigastric vessels
How would an inguinal hernia present?
- Lump in the groin that disappears when lying down
- Incarcerated hernia = painful, tender, erythematous
- Signs of bowel obstruction if bowel lumen is blocked
- Features of strangulation if blood supply is compromised
- Strangulation = irreducible, tender, tense, pain out of proportion to signs
- Inguinal hernias are superomedial to the pubic tubercle, femoral is inferolateral
How would you investigate and manage an inguinal hernia?
Investigations
- Ultrasound first line
- Obstruction or strangulation = ct imaging
Management
- Symptomatic is offered surgical intervention
- Strangulation = urgent surgical exploration
- Primary inguinal hernias = open mesh repairs (Lichenstein technique)
- Bilateral or recurrent inguinal hernias, or younger active patients with PIH = laparoscopic approach
- Mesh repair has a risk of chronic pain
- Non symptomatic = conservative
What are some complications of hernias? (3)
Incarceration = contents cannot return to original cavity
Obstruction = lumen of bowel is obstructed
Strangulation = compression of hernia has compromised its blood supply leading to ischaemia
What is a femoral hernia? What are some risk factors?
- Less common but really high rate of strangulation!!
- Rigid borders of femoral ring eg. lacunar ligament
- More common in women due to wider bony pelvis
- abdominal visceral pass through femoral ring into potential space of femoral canal
- Risks = female, pregnant, high intra abdo pressure, old age
How does a femoral hernia present?
What are some differentials?
- Small lump in groin (inferolateral to pubic tubercle, medial to femoral pulse)
- Usually not reducible due to tight borders of femoral ring
- Differentials = inguinal hernia, saphena varix, femoral artery aneurysm
- Saphena varix will disappear when lying flat, palpable thrill when coughing, varicose veins
How would you investigate and manage a femoral hernia?
Investigations
- Ultrasound Or CT abdo pelvis (high strangulation risk)
- Surgical exploration
Management
- All are managed surgically within 2 weeks of presentation due to risk of strangulation
- Reduce hernia and narrow femoral ring
What are some other types of abodminal wall hernias? (5)
Epigastric hernias
- Occurs in upper midline through fibres of linea alba
- Due to chronic raised intra abdo pressure
Paraumbilical hernia
- Through linea alba around umbilical region
- Due to chronic raised intra abdo pressure
Spigelian hernia
- At semilunar line around level of arcuate line
Obturator hernia
- Hernia of pelvic floor through the obturator foramen into obturator canal
- Mass in upper medial thigh and features of small bowel obstruction
- compression of obturator nerve causes +ve howship-romberg sign
Richters hernia
- Partial herniation of bowel where anti-mesenteric border becomes strangulated
- Tender irreducible mass + obstruction
What is angiodysplasia?
How would it present?
- Arteriovenous malformations between previously healthy blood vessels
- Commonly in caecum and ascending colon
- Can be acquired or congenital
Presentation
- 10% asymptomatic = diagnosed on colonoscopy
- majority are Painless occult PR bleeding
- 10-15% is acute haemorrhage
How would you investigate and manage angiodysplasia?
Investigations
- Group and save or crossmatch and other routine tests
- Haematinics as some have iron def anaemia
- Exclude malignancy with an OGD or colonoscopy
- Wireless capsule endoscopy to identify small bowel bleeds
- Mesenteric angiography to find location of bleed
Management
- Minimal bleeding = bed rest, IV fluids, tranexamic acid
- Severe bleeding where site is identified
- 1st line = argon plasma coagulation + endoscopy
- Mesenteric angiography for small bowel lesions that cannot be treated endoscopically
- Last resort is surgical (only for severe life threatening bleeds with multiple lesions etc)
Pathophysiology of appendicitis?
- Inflammation of the appendix
- Luminal obstruction (secondary to faecolith, stool, caecal tumour)
- Commensal bacteria multiply and cause acute inflammation
- Obstruction causes reduced venous drainage and localised inflammation, resulting in increased pressure in the appendix
- This can result in ischaemia and necrosis = perforation
How does appendicitis present?
- Initially dull poorly localised periumbilical pain (visceral peritoneum inflammation)
- Becomes well localised sharp RIF pain (parietal peritoneum inflammation)
- Vomiting that comes on after the pain
- Anorexia, nausea, diarrhoea or constipation
- Rebound tenderness and percussion pain over McBurney’s point
- Guarding (esp in perforation)
- Severe = sepsis (hypotensive, tachy)
- On examination =
- Rovsings (RIF pain on LIF palpation)
- Psoas (RIF pain on right hip ext)
- Remember presentation can be atypical in kids and with boys check for testicular torsion or epididymitis too. Also rule out intussusception and acute mesenteric adenitis
How would you investigate and manage appendicitis?
Investigations
- Urinalysis to rule out renal/urological causes (uti, pyelo, stones, TT etc)
- Pregnancy test for women +serum bhcg
- Routine bloods (fbc, u&es, lfts, crp, esr, clotting)
- Ultrasound or CT not very conclusive, typically clinical diagnosis
- Risk stratification scores
- Men = Appendicitis inflammatory response score
- Women = adult appendicitis score
- Children = Shera score
Manage
-
Laparoscopic appendectomy is gold standard
- Send to histopathology for malignancy
- Appendiceal mass (appendiceal abscess?) = antibiotics then interval appendectomy 6 weeks later
What are the different stages of diverticular disease?
Diverticulum = outpouching of bowel wall commonly in sigmoid colon
Diverticulosis = presence of diverticula
Diverticular disease = symptomatic diverticula
Diverticulitis = inflammation of diverticula
Diverticular bleed = diverticulum erodes into a vessel and causes large vol painless bleeding
What is the pathophysiology of diverticular disease?
- Aging bowel walls becomes weak and stool moving through the lumen increases luminal pressure
- Therefore outpouchings of mucosa will form through weaker areas of bowel (typically where blood vessels penetrate or at junctions of muscle sheets)
- Bacteria can overgrow in the outpouchings = diverticulitis
- This can then cause perforation = peritonitis, sepsis, death
How does diverticulosis, diverticular disease and diverticulitis present?
Diverticulosis = Typically asymptomatic and incidentally found on routine colonoscopy
Diverticular disease
- Intermittent colicky lower abdo pain, relieved by defecation
- Altered bowel habit, nausea, flatulence
- No systemic features
Diverticulitis
- Acute sharp abdo pain localised to LIF, worsened by movement
- Localised tenderness
- Systemic features eg. decreased appetite, pyrexia, nausea
- Perforation = localised peritonism or generalised peritonitis
- People on corticosteroids or immunosuppressants may have atypical symptoms
- Diverticular abscess can form as a complication (IV antibiotics +/- radiological drainage for big ones)
How would you investigate and manage diverticular disease?
Investigations
- Routine bloods
- Faecal calprotectin to rule out differentials
- Diverticulitis = group and save, VBG, urine dipstick
-
CT abdo pelvis for diverticulitis = thickened colonic wall, pericolonic fat stranding, abscesses, localised air bubbles, free air
- Hinchey classification to stage acute diverticulitis (Based on CT findings)
-
Flexible sigmoidoscopy for diverticular disease
- Do not do this in diverticulitis as can risk perf
Management
- Diverticular disease
- Outpatient management = simple analgesia and oral fluids
- Outpatient colonoscopy to exclude malignancies
- Diverticular bleeds can also be managed conservatively or else with embolization and surgical resection
- Acute diverticulitis
- Conservative = antibiotics, iv fluids, analgesia
- Surgical = for perf with faecal peritonitis or overwhelming sepsis
- Typically Hartmann’s procedure
What are some complications of diverticular disease?
- Recurrence
- Diverticular stricture due to repeated inflammation
- can cause large bowel obstruction (needs sigmoid colectomy)
-
Fistula due to repeated inflammation
- Colovesical between bowel and bladder (recurrent utis, faeces in urine, pneumoturia)
- Colovaginal between bowel and vagina (copious vag discharge, recurrent vag infections)
Crohns and UC in GI MEDICINE Notes (compare)
What is pseudo-obstruction or Ogilvie syndrome?
- Dilation of the colon due to an adynamic bowel in the absence of mechanical obstruction
- Due to interruption of autonomic nervous supply to colon resulting in absence of smooth muscle action
Presentation = abdo pain, distension, constipation, vomiting is a late sign
What are some causes of ogilvie syndrome?
- Electrolyte imbalance eg. hypercalcaemia, hypothyroid, hypomagnesium
- Meds eg. opioids, CCB, antidepressants
- Recent surgery, illness, trauma
- Neuro eg. parkinsons, ms, hirschsprungs
How would you investigate and manage ogilvie syndrome?
Investigations
- Routine bloods, u&es, ca2+, mg2+, tfts
- AXR for bowel distension (but will show similar to mechanical)
- CT abdo pelvis with iv contrast will show dilation and exclude mechanical obstruction and assess for complications like perf
Management
- Conservative
- Treat underlying cause
- NBM and iv fluids, ng if vomiting
-
Endoscopic decompression if not resolved in 48 hours
- Involves insertion of flatus tube
- If limited resolution, use iv neostigmine
- Nutritional support and review
- Surgery is sometimes required for non responding cases, perf or ischaemia
Describe the blood supply to the gut?
Foregut (stomach, duodenum, biliary, liver, pancreas, spleen) = coeliac artery
Midgut (distal duodenum, 1st half of transverse colon) = superior mesenteric artery
Hindgut (2nd half of the transverse colon to rectum) = inferior mesenteric artery
What is chronic mesenteric ischaemia?
How would it present?
Mesenteric ischaemia is the lack of bloodflow through the mesenteric vessels supplying the intestines = ischaemia.
Pathophysiology:
- Narrowing of the mesenteric vessels due to atherosclerosis
- Presentation is essentially like angina but with your abdo ie pain when the blood supply can’t keep up with demand
Presentation:
- Central colicky abdo pain starting 30mins after eating
- Weight loss due to food avoidance
- Abdominal bruit on auscultation
How would you diagnose and manage chronic mesenteric ischaemia?
Diagnosis = CT angiography
Management:
- Reduce risk factors eg smoking, diabetes, htn, cholesterol
- Secondary prevention eg statins, antiplatelets
- Revascularisation
- 1st line is endovascular like percutaneous mesenteric artery stenting
- 2nd line is open surgery like endarterectomy
How does acute mesenteric ischaemia occur?
How would that present?
- Rapid blockage in blood flow through superior mesenteric artery due to a thrombus in the artery (either a thrombus or an embolus)
- Risk factors eg. AF
Presentation:
- Acute, non specific abdo pain
- Pain is disproportionate to exam findings
- Can go into shock, peritonitis, sepsis
- Eventually ischaemia –> necrosis of bowel tissue –> perf
How would you investigate and manage acute mesenteric ischaemia?
Investigations:
- Contrast CT
- Metabolic Acidosis
- Raised Lactate
Management:
- Remove necrotic bowel
- Remove or bypass thrombus (open surgery or endovascular)
What is a volvulus?
- Twisting of intestine around its mesenteric attachment resulting in a closed loop bowel obstruction
- Can compromise bowel supply and cause ischaemia, necrosis, perf
- Typically in sigmoid colon due to long mesentery (increases with age).
- Therefore this segment of bowel is more prone to twisting on its mesenteric base
- Risk factors = old age, neuropsych disorders, nursing home resident, chronic constipation or laxative use, male, prev abdo operations
How does a volvulus present?
- Bowel obstruction= colicky pain, abdo distension, absolute constipation. Vomiting late
- Onset is pretty rapid (over hours)
- Abdo is tympanic to percussion
How would you imvestigate and manage a volvulus?
Investigations
- Routine bloods (incl ones to exclude pseudo-obstruction)
- Ct abdo pelvis with contrast = whirl sign
- AXR = coffee bean sign in LIF
Management
- Conservative
- decompression with sigmoidoscope and flatus tube insertion
- monitor for ischaemia
- fluid resus
- Surgical = laparotomy for hartmanns
- Indications = ischaemia or perf, repeated failed decompression, necrotic bowel on endoscopy
What is a haemorrhoid and what are the different degrees?
- Abnormal swellings or enlargements of the anal vascular cushions
- There are 3 Anal vascular cushions that help maintain continence (3, 7, 11oclock positions)
Classification
- 1st degree remain in rectum
- 2nd degree = prolapse through anus on defecation but spontaneously reduces
- 3rd degree = prolapse through anus on defecation but requires digital reduction
- 4th degree = remains persistently prolapsed
How do haemorrhoids present?
And some risk factors?
Risk factors = excessive straining (chronic constipation), old age, raised intra abdo pressure, portal hypertension
Presentation
- Painless bright red rectal bleeding after defecation on paper or surface of stool
- Pruritus, rectal fullness or anal lump, soiling
- Large prolapsed haemorrhoids can thrombose = painful, purple/blue oedematous tense tender perianal mass
How would you investigate and manage haemrrhoids?
Investigations
- Proctoscopy
- Routine bloods
- Flexi sigmoidoscopy or colonoscopy to rule out malignancy
Management
- Conservative
- Increased fibre and fluid
- laxatives if necessary
- Topical analgesia (lignocaine gel)
- Rubber band ligation for symptomatic 1st and 2nd degree haemorrhoids
- Surgical
- Haemorrhoidal artery ligation for 2nd or 3rd degree haemorrhoids
- Haemorrhoidectomy for 3rd or 4th degree or symptomatic and not responding to conservative therapies
What is an anorectal abscess? What are the different classifications?
- Collection of pus in anal/rectal region due to plugging of anal ducts, resulting in fluid stasis and infection
- Commonly ecoli, bacteriodes spp, enterococcus spp
- Classified as perianal, ischiorectal, intersphincteric or supralevator
How would an anorectal abscess present?
- Pain in perianal region exacerbated by sitting
- Localised swelling, itching, discharge
- Severe abscess = systemic like fever, rigors, malaise, sepsis
- O/E = erythematous fluctuant tender perianal mass
How would you investigate and manage an anorectal abscess?
Investigations
- DRE
- Examination under anaesthesia
- Some need ct or mri
Management
- Antibiotic therapy and analgesia
-
Incision and drainage of abscess under GA
- Heal by secondary intention
-
Proctoscopy afterwards to check for fistula-in-ano
- Insert a seton if fistula is identified
What is an anal fissure and some risk factors?
- Tear in the mucosal lining of the anal canal typically due to trauma from hard stool defecation
- Acute is <6 weeks, chronic is >6 weeks
- Risk factors = constipation, dehydration, IBD, chronic diarrhoea
How would an anal fissure present?
- Intense pain post defecation
- Bleeding (bright red on wiping) or itching post defecation
- O/E fissures are visible and palpable on dre
- Most fissures are on the posterior midline
- Often DRE is too painful so do examination under anaesthesia
- Fissures within anal canal can be seen with proctoscopy
How would you manage an anal fissure?
- Reduce risk factors = fluids, fibre, stool softening laxatives like Movicol or lactulose
- Topical analgesia like lidocaine or hot baths
- 2nd line is gtn cream or diltiazem cream
Surgery for chronic fissures where med has not worked
- Botox injections into internal anal sphincter
- Or lateral sphincterotomy
