GI Flashcards
Causes of bloody diarrhoea
ischaemic colitis campylobacter, shigella, salmonella, E. coli, amoeba, pseudomembranous colitis UC, Crohn’s CRC, polyps
Causes of pus in stools
IBD, diverticulitis, abscess
Management for diarrhoea
Treat cause
Oral or IV rehydration
Codeine phosphate or loperamide after each loose stool
Anti-emetic if assoc. n/v: e.g. prochlorperazine
Abx (e.g. cipro) in infective diarrhoea → systemic illness
What is C.diff
Gm+ve spore-forming anaerobe
Release enterotoxins A and B
Spores are v. robust and can survive for >40d
Risk factors for c.diff infection
Abx: clindamycin, cefs, co-amox, ciprofloxacin
- up to 2m after
↑age
In hospital: ↑ ̄c length of stay, ↑ ̄c C. diff +ve contact
PPIs
Clinical presentation of infection with c.diff
Asymptomatic Mild diarrhoea Colitis Pseudomembranous colitis - fever, dehydration, abdo pain, bloody diarrhoea, mucus PR Fulminant colitis
Investigations for c.diff
Bloods: ↑↑CRP, ↑↑WCC, ↓albumin, dehydration
CDT ELISA -toxin A&B
Stool culture
Complications of c.diff infection
Paralytic ileus
Toxic dilatation → perforation
Multi-organ failure
Management of c.diff
Barrier nursing - put in side room
Stop causative Abx
Avoid antidiarrhoeals and opiates
Enteric precautions
1st line: Metronidazole 2wk 2nd line: Vanc 125mg
Severe: Vanc 1st
Urgent colectomy may be needed if
Toxic megacolon
↑ LDH
Deteriorating condition
Causes of constipation
OPENED IT Obstruction - mechanical (adhesion/hernia/ca) or post op ileus Pain - fissure Endocrine/ electrolytes - ↓T4, ↓Ca, ↓K, uraemia Neuro - MS, Myelopathy, Cauda Equina Elderly Diet/ Dehydration IBS Toxins - opiods
Management of constipation
Drink more
↑ dietary fibre
Bulking: ↑ faecal mass → ↑ peristalsis - fybogel (Ispaghula husk)
CI: obstruction and faecal impaction
Osmotic: retain fluid in the bowel - Lactulose
Stimulant: ↑ intestinal motility and secretion - Senna
CI: obstruction, acute colitis
SE: abdo cramps
Softeners
For painful anal condition - Liquid paraffin
Phosphate enema (osmotic)
Suppositories
Glycerol (stimulant)
Diagnosis of IBS
Abdo discomfort / pain for ≥ 12wks which has 2 of:
Relieved by defecation
Change in stool frequency (D or C)
Change in stool form: pellets, mucus
\+2of: Urgency Incomplete evacuation Abdo bloating / distension Mucous PR Worsening symptoms after food
Exclusion criteria >40yrs Bloody stool Anorexia Wt. loss Diarrhoea at night
Management of IBS
Bloods - incl Coeliac and TSH
+/- colonoscopy
- Exclusion diets can be tried
- Fybogel for constipation and diarrhoea
- Antispasmodics for colic/bloating (e.g. mebeverine)
- Amitriptyline may be helpful
- CBT
Causes of dysphagia
Inflammatory Tonsillitis, pharyngitis Oesophagitis: GORD, candida Oral candidiasis Aphthous ulcers
Mechanical Block - Luminal FB Large food bolus - Mural > Benign stricture Web (e.g. Plummer-Vinson) Oesophagitis Trauma (e.g. OGD) > Malignant stricture- Pharynx, oesophagus, gastric Pharyngeal pouch - Extra-mural Lung Ca Rolling hiatus hernia Mediastinal LNs (e.g. lymphoma) Retrosternal goitre Thoracic aortic aneurysm
Motility Disorders - Local Achalasia Diffuse oesophageal spasm Nutcracker oesophagus Bulbar / pseudobulbar palsy (CVA, MND) - Systemic Systemic sclerosis / CREST MG
Presentation of dysphagia
Dysphagia for liquids and solids at start
- Yes: motility disorder
- No, solids > liquids: stricture
Difficulty making swallowing movement: bulbar palsy
Odonophagia: Ca, oesophageal ulcer, spasm
Intermittent: oesophageal spasm
Constant and worsening: malignant stricture
Neck bulges or gurgles on drinking: pharyngeal pouch
Signs that dysphagia could present with
Cachexia Anaemia Virchow’s node (+ve = Troisier’s sign) Neurology Signs of systemic disease (e.g. scleroderma)
Investigations for dysphagia
URGENT upper GI endoscopy +- biopsy (if >55, with weight loss, abdo pain, dyspepsia)
Bloods: FBC, U+E
Barium swallow ± video fluoroscopy
Oesophageal manometrry
+- USS/EUS/CT thorax
Pathophysiology of achalasia
Degeneration of myenteric plexus (Auerbach’s)
↓ peristalsis
LOS fails to relax
- most commonly idiopathic
Presentation of achalasia
Dysphagia: liquids and solids at same time
Regurgitation
Substernal cramps
Wt. loss
Investigations for achalasia
Ba swallow: dilated tapering oesophagus (Bird’s beak)
Manometry: failure of relaxation + ↓ peristalsis
CXR: may show widended mediastinum
OGD: exclude malignancy
Rx of achalasia
Med: CCBs, nitrates
Int: endoscopic balloon dilatation, botulinum toxin injection
Surg: Heller’s cardiomyotomy (open or endo)
Pharyngeal pouch pathophysiology
Outpouching of oesophagus between upper boarder of cricopharyngeus muscle and lower boarder of inferior constrictor of pharynx
Weak area called Killian’s dehiscence.
Defect usually occurs posteriorly but swelling usually bulges to left side of neck.
Food debris → pouch expansion → oesophageal
compression → dysphagia.
Presentation and rx of a pharyngeal pouch
Pres: regurgitation, halitosis, gurgling sounds
Rx: excision, endoscopic stapling
Diffuse oesophageal spasm presentation
Intermittent chest pain ± dysphagia
Ba swallow shows corkscrew oesophagus
Nutcracker oesophagus presentation
Intermittent dysphagia ± chest pain
↑ contraction pressure ̄c normal peristalsis
Causes of an oesophageal rupture
- Iatrogenic - endoscopy, biopsy, dilatation
- violent emesis (boerhaave’s syndreom)
- carcinoma
- Trauma (surgical emphysema ±pneumothorax)
Features of oesophageal rupture
- Odonophagia
- Mediastinitis (tachypnoea, dyspnoea, fever, shock)
- surgical emphysema
management of oesophageal rupture
PPI, Abx, NGT
Symptoms of dyspepsia
Epigastric pain Bloating Heartburn ALARM Anaemia Loss of wt. Anorexia Recent onset progressive symptoms Melaena or haematemesis Swallowing difficulty
Causes of dyspepsia
Inflammation: GORD, gastritis, PUD
Ca: oesophageal, gastric
Functional: non-ulcer dyspepsia
Management of new onset dyspepsia
OGD if >55 or ALARMS - Try conservative for 4 weeks > stop NSAIDS, CCBS > Lose wt., stop smoking, ↓ EtOH > Avoid hot drinks and spicy food > OTC - Antacids/gaviscon
- Test for H. pylori if no improvement: breath or serology
+ve → eradication therapy
-ve → PPI trial for 4wks
OGD if no improvement
Eradication therapy for H.Pylori
Triple therapy for 1 week
- PPI
- Amoxicillin
- Clarithromycin
Presentation of Duodenal Ulcers v gastric ulcers
DU Epigastric pain: Before meals and at night Relieved by eating or milk GU Epigastric pain: Worse on eating Relieved by antacids Wt. loss
Risk factors for PUD
H. pylori (90%) Drugs: NSAIDs, steroids Smoking EtOH gastric emptying (↑ DU, ↓GU) Blood group O (PU) Stress --> Cushings, burns, sepsis, trauma
Complications of PUD
Haemorrhage
Haematemeis or melaena
Fe deficiency anaemia
Perforation
Peritonitis and distension, vomiting
Gastric Outflow Obstruction
Vomiting, colic, distension, succission splash
Malignancy
↑ risk ̄c H. pylori
Investigations for PUD
Bloods: FBC, urea (↑ in haemorrhage)
C13 breath test
OGD (stop PPIs >2wks before)
Campylobacter-like organism test (CLO) / urease test for H. pylori (urea –> CO2 + ammonia - neutralises stomach acid)
Biopsy ulcer to check for Ca
Gastrin levels if Zollinger-Ellison suspected
Conservative Management of PUD
Lose wt. Stop smoking and ↓ EtOH Avoid hot drinks and spicy food Stop drugs: NSAIDs, steroids OTC antacids
Medical management of PUD
OTC antacids: Gaviscon, Mg trisilicate H. pylori eradication Full-dose acid suppression for 1-2mo PPIs: lansoprazole 30mg OD H2RAs: ranitidine 300mg nocte Low-dose acid suppression PRN
Surgical management of PUD
No acid → no ulcer
Acid secretion
stimulated by gastrin and vagus N.
Vagotomy +/- antrectomy ( distal half of stomach removed)
Subtotal gastrectomy
Complications of gastric surgery
Physical Stump leakage Abdominal fullness Reflux or bilious vomiting (improves ̄c time) Stricture
Metabolic
- Dumping syndrome
Abdo distension, flushing, n/v
Early: osmotic hypovolaemia
Late: reactive hypoglycaemia
- Blind loop syndrome → malabsorption, diarrhoea
Overgrowth of bacteria in duodenal stump
Anaemia: Fe + B12
Osteoporosis
- Wt. loss: malabsorption of ↓ calories intake
Pathophysiology of GORD
LOS dysfunction → reflux of gastric contents → oesophagitis.
Risk factors for GORD
Hiatus hernia Smoking EtOH Obesity Pregnancy Drugs: anti-AChM, nitrates, CCB, TCAs Iatrogenic: Heller’s myotomy
Symptoms of GORD
Oesophageal Heartburn Related to meals Worse lying down / stooping Relieved by antacids Belching Acid brash, water brash Odonophagia Hoarseness
Extra-oesophageal
Nocturnal asthma
Chronic cough
Laryngitis, sinusitis
Anti- reflux mechanisms
- LOS
- Angle of His
- Pressure in abdominal cavity higher than thoracic
- R crus of diaphragm acts as a sling around oesophagus
Complications of GORD
Oesophagitis: heartburn
Ulceration: rarely → haematemesis, melaena, ↓Fe
Benign stricture: dysphagia
Barrett’s oesophagus
- metaplasia of squamous to gastric columnar epithelium and goblet cell
Oesophageal adenocarcinoma
- Metaplasia → dysplasia → adenocarcinoma
Differential diagnosis of GO reflux
Oesophagitis Infection: CMV, candida IBD Caustic substances / burns PUD Oesophageal Ca
Investigations for GORD
Isolated - no Ix Bloods: FBC CXR: hiatus hernia may be seen OGD if: >55yrs Symptoms >4wks Dysphagia Persistent symptoms despite Rx Wt. loss OGD allows grading by Los Angeles (A-D) Classification Ba swallow: hiatus hernia, dysmotility 24h pH testing ± manometry pH <4 for >4hrs (demeester score)
Conservative management of GORD
Lose wt. Raise head of bed Small regular meals ≥ 3h before bed Stop smoking and ↓ EtOH Avoid hot drinks and spicy food Stop drugs: NSAIDs, steroids, CCBs, nitrates
Medical management of GORD
OTC antacids: Gaviscon, Mg trisilicate 1: Full-dose PPI for 1-2mo Lansoprazole 30mg OD 2: No response → double dose PPI BD 3: No response: add an H2RA Ranitidine 300mg nocte Control: low-dose acid suppression PRN
Surgical management, indications and complications of GORD
Nissen Fundoplication - Mobilise gastric fundus and wrap around lower oesophagus - Indications: all 3 of: Severe symptoms Refractory to medical therapy Confirmed reflux (pH monitoring)
Complications - Gas-bloat syn.: inability to belch / vomit - Dysphagia if wrap too tight OTHER Radiofrequency ablation. magnetic beads
Classifications of hiatus hernias
Sliding (80%)
GOJ slides up into chest
assoc.GORD
Rolling (15%)
GOJ remains in abdomen but a bulge of stomach rolls into chest alongside the oesophagus
LOS remains intact so GORD uncommon
Can → strangulation
Mixed (5%)
Gastric volvulus symptoms
Borchardt’s triad
- severe epigastric pain
- retching without vom
- inability to pass NG tube
Ix for hiatus hernia
OGD: assess for oesophagitis and upwards displacement GOJ
CXR: gas bubble and fluid level in chest
24h pH + manometry: exclude dysmotility or achalsia
Ba Swallow
Rx of hiatus hernias
Lose wt.
Rx reflux
Surgery if intractable symptoms despite medical Rx OR rolling
- funoplication/ curoplasty
Risk factors for hiatus hernia
Age (reduced diaphragm tone) raised intra-abdo pressure 0 pregnancy 0 obesity 0 ascites
Differentials of Haematemesis
VINTAGE
Varices Inflammation (PUD/ oesopha/gastr- itis) Neoplasia (oesoph/gastric) Trauma (Mallory-weiss/ Boerhavve) Angiodysplasia/ HHT/ Dieulafoy lesion Generalised bleeding diathesis - warfarin, thrombolytics, CRF Epistaxis
Difference between mallory-weiss and boerhaave’s
Mallory-Weiss - mucosal Tear
Boerhaave’s Syndrome - Full-thickness tear
2cm proximal to LOS
Signs on examination after an Upper GI bleed
Signs of CLD - telangectasia, purpura, jaundice PR:melaena Shock? - Cool, clammy, CRT>2s - ↓BP (<100) or postural hypotension (>20 drop) - ↓ urine output (<30ml/h) - Tachycardia - ↓GCS - ↓ JVP
What is the Rockall score
Prediction of re-bleeding and mortality after Upper GI bleed - Initial score pre-endoscopy Age Shock: BP, pulse Comorbidities - Final score post-endoscopy > Final Dx + evidence of recent haemorrhage Active bleeding Visible vessel Adherent clot
Initial score ≥3 or final >6 are indications for surgery
Pathology of oesophageal varices
Portal HTN → dilated veins @ sites of porto-systemic anastomosis: L. gastric and inferior oesophageal veins
Causes of portal hypertension
Pre-hepatic: portal vein thrombosis
Hepatic: cirrhosis (80% in UK), schisto (commonest
worldwide), sarcoidosis.
Post-hepatic: Budd-Chiari, RHF, constrict pericarditis
Management of oesophageal varices
- bleed prevention
1: β-B, repeat endoscopic banding
2: β-B, repeat banding, TIPSS (Transjugular Intrahepatic Porto-Systemic Shunt) - IR creates artificial channel between hepatic vein and portal vein → ↓ portal pressure.
Management of an Upper GI bleed
- Head-down
- High flow oxygen + protect airway
- 2 x 14G cannulae + IV bolus
- Bloods: FBC, U+E (↑ urea), LFTs, clotting, x-match 6u, ABG, glucose
- if remains shocked - o- blood
- notify surgeons if severe
IF VARICEAL BLEED - Terlipressin IV (splanchnic vasopressor)
Prophylactic Abx: e.g. ciprofloxacin 1g/24h
Urgent endoscopy
- Haemostasis of vessel or ulcer:
Adr injection; Thermal coagulation; Fibrin glue; Endoclips
Variceal bleeding: 2 of: banding, sclerotherapy, adrenaline, coagulation Balloon tamponade ̄c TIPSS
Indications for surgery after Upper GI bleed
Re-bleeding
Bleeding despite transfusing 6u
Uncontrollable bleeding at endoscopy
Initial Rockall score ≥3, or final >6.
Risk factors for oesophageal cancer
- alcohol
- smoking
- achalasia
- GORD
- Fatty diet
- Low vit A/C
Pathophysiology of oesophageal cancer
- 65% adenocarcinoma - lower 3rd
- 35% SCC - upper and middle 3rd
Presentation of oesophageal cancer
- Progressive dysphagia
- weight loss
- retrostrenal chest pain and dyspepsia
- lymphadenopathy
- hoarseness (recurrent laryngeal n invasion)
- cough +/- aspiratino pneumonia
- odonophagia
- mets - jaunice, hepatomegaly, ascites
Ix for oesophageal cancer
OGD + biopsy
- Bloods
- Staging CT
EUS - t stage
Staging used for oesophageal cancer
TMN T1 - submucosa T2 - muscularis propria T3 - adventitia T4 - adjacent structures
Causes of perforation
Inflammatory
- chemical - PUD, Foreign body
- infection - appendicitis, diverticulitis, meckels, cholecystitis,
- ischaemia - mesenteric,, obstructive Ca, Bezoar, faeces
- colitis - fistula, toxic megacolon
Traumatic
- iatrogenic - surgery. endoscopy
- penetrating force
- direct rupture - booerhavve/ mallory weiss
Ix for perforated GIT
- Blood - FBC, Amylase, CRP, clotting, ABG
- urine dipstick
- Erect CXR (erect 15min)
- AXR - (riglers and psoas sign)
- CT scan
Mx of Perforated PU
- A-E
- NBM
- fluid resuscitation
- catheter +/- CVP line
- analgesia
- Abx
- NGT
+/- surgery is systemically unwell - abdominal washout and repair (patch - DU); may require gastrectomy
Ix for gastric outflow obstruction
- ABG - hypercholraemic hypokalaemic met alkalosis
- AXR (dilated gastric air bubble air fluid level, collapsed distal bowel)
- OGD
Rx for gastric outflow obstruction
- correct metabolic abnormalities
- benign –> endscopic ballow dilation/ gastroenterostomy
- malignant - stent/ resection
Risk factors for gastric cancer
- atrophic gastritis - pernicious anaemia, h.pylori)
- diet high nitrates
- smoking and alcohol
- blood group A
- low social class
- familial - E cadherin abnormality
- partial gastrectomy
Pathology of gastric cancer
Mainly adenocarcinomas, located on gastric antrum
Symptoms of gastric cancer
- weight loss + anorexia
- dyspepsia
- dysphagia
- n + v
Signs of gastric cancer
- anaemia
- epigastric mass
- jaundice
- ascites
- hepatomegaly
- virchow’s node
- acanthosis nigricans
Complications of gastric cancer
- perforation
- upper Gi bleed - haematemesis, melaena
- gastric outlet obstruction
Ix for gastric cancer
URGENT OGD + biopsy
- CXR/USS/ CT - mets
Staging - CT CAP
Complications of gastrectomy
- death
- anastomotic leak
- poor QoL
- Vit B12 def
- re-operation
describe the excretion of bilirubin
Hb → unconjugated to BR by splenic macrophages
uBR → cBR by BR-UDP-glucuronyl transferase in liver
Secreted in bile then cBR → urobilinogen (colourless)
Some urobilinogen is reabsorbed, returned to liver and re-excreted into bile.
Some reabsorbed urobilinogen is excreted into the urine
The urobilinogen that remains in the GIT is converted to stercobilin (brown) and excreted.
Causes of pre-hepatic jaundice
Excess BR production
Haemolytic anaemia
Ineffective erythropoiesis
e.g. thalassaemia
Causes of Hepatic jaundice
Unconjugated ↓ BR Uptake Drugs: contrast, RMP CCF ↓ BR Conjugation Hypothyroidism Gilbert’s (AD) Crigler-Najjar (AR) Neonatal jaundice is both ↑ production + ↓ conjug.
Hepatocellular Dysfunction Congen: HH, Wilson’s, α1ATD Infection: Hep A/B/C, CMV, EBV Toxin: EtOH, drugs AIH Neoplasia: HCC, mets Vasc: Budd-Chiari1
Causes of post-hepatic jaundice
Obstruction Stones Ca pancreas Drugs - OCP, sulfonylureas PBC PSC Biliary atresia Choledochal cyst Cholangio Ca Inflammatory LN at porta hepatis - TB/ Ca Mirizzi's syndrome
Ix for Jaundice
- Urine
pre - No BR (acholuric); ↑ urobilinogen; ↑Hb if intravascular haemolysis
hepatic - ↑BR; ↑ urobilinogen
post- ↑↑BR; No urobilinogen - LFTs
pre - ↑uBR; ↑AST; ↑LDH
hepatic - ↑ cBR (usually); ↑AST:↑ALT; >2=EtOH/ <1=Viral; ↑ GGT (EtOH, obstruction); ↑ALP; Function: ↓ albumin, ↑ PT
post- ↑↑cBR; ↑AST,↑ALT; ↑↑ALP; ↑GGT - Other
pre - FBC and film, Coombs, Hb electrophoresis
hepatic - FBC, Ab, a1AT, Liver biopsy
post - Abdo US (dilated ducts >6mm), ERCP/MRCP; Ab
Causes of liver failure
- cirrhosis
- acute
Infection: Hep A/B, CMV, EBV, leptospirosis
Toxin: EtOH, paracetamol, isoniazid, halothane
Vasc: Budd-Chiari
Other: Wilson’s, AIH
Obs: eclampsia, acute fatty liver of pregnancy
Signs of liver failure
Jaundice Oedema + ascites Bruising Encephalopathy Aterixis Constructional apraxia (5-pointed star) Fetor hepaticus Signs of cirrhosis / chronic liver disease
Ix for liver failure
Blood FBC: infection, GI bleed, ↓ MCV (EtOH) U+E - ↓U, ↑Cr: hepatorenal syndrome. Urea synth in liver -->poor test of renal function LFT - AST:ALT > 2 = EtOH - AST:ALT < 1 = Viral - Albumin: ↓ in chronic liver failure - PT: ↑ in acute liver failure Clotting: ↑INR Glucose ABG: metabolic acidosis Cause: Ferritin, α1AT, caeruloplasmin, Abs, paracetamol levels
Microbiology
Hep, CMV, EBV serology
Blood and urine culture
Ascites MCS + SAAG
Radiology
CXR
Abdo US + portal vein duplex
Pathophysiology and classification of hepatorenal syndrome
Cirrhosis → splanchnic arterial vasodilatation → effective circulatory volume → RAS activation → renal arterial vasoconstriction.
Persistent underfilling of renal circulation → failure
Type 1: rapidly progressive deterioration (survival
<2wks)
Type 2: steady deterioration (survival ~6mo)
Rx of hepatorenal syndrome
IV albumin + splanchnic vasoconstrictors (terlipressin)
Haemodialysis as supportive Rx
Liver Tx is Rx of choice
Mx of liver failure
Manage in ITU
Rx underlying cause: e.g. NAC in paracetamol OD
Good nutrition: e.g. via NGT ̄c high carbs
Thiamine supplements
Prophylactic PPIs vs. stress ulcers
Monitor - fluids, bloods, glucose
Complications of liver failure
Bleeding: Vit K, platelets, FFP, blood
Sepsis: tazocin (avoid gent: nephrotoxicity)
Ascites: fluid and salt restrict, spiro, fruse, tap, daily wt
Hypoglycaemia: regular BMs, IV glucose if <2mM
Encephalopathy: avoid sedatives, lactulose ± enemas,
rifaximin
Seizures: lorazepam
Cerebral oedema: mannitol
Drugs to avoid prescribing in liver failure
opiates, oral hypoglycaemics, Na-containing IVI
- Warfarin effects ↑
- Hepatotoxic drugs: paracetamol, methotrexate,
isoniazid, salicylates, tetracycline
Poor prognostic factors in liver failure
Grade 3/4 hepatic encephalopathy Age >40yrs Albumin <30g/L ↑INR Drug-induced liver failure
Criteria for liver transplant
Kings college
Paracetamol-induced pH< 7.3 24h after ingestion Or all of: PT > 100s Cr > 300uM Grade 3/4 encephalopathy
Non-paracetamol PT > 100s Or 3 out of 5 of: Drug-induced Age <10 or >40 >1wk from jaundice to encephalopathy PT > 50s BR ≥ 300uM
Pathophysiology of cirrhosis
Irreversible loss of hepatic architecture with bridging fibrosis and nodular regeneration
Signs of cirrhosis
Hands Clubbing (± periostitis) Leuconychia (↓ albumin) Terry’s nails (white proximally, red distally) Palmer erythema Dupuytron’s contracture
Face
Pallor: ACD
Xanthelasma: PBC
Parotid enlargement (esp. ̄c EtOH due to dehydration increasing salvia production)
Trunk
Spider naevi (>5, fill from centre)
Gynaecomastia
Loss of 2O sexual hair
Abdo
Striae
Hepatomegaly (may be small in late disease)
Splenomegaly
Dilated superficial veins (Caput medusa)
Testicular atrophy
Hyperdynamic circualtion
Complications of cirrhosis
- Decompensation –> heptatic failure (jaundice, encephalopathy, ↓Albumin, bruising (↑INR), hypoglycaemia)
- Spontaneous bacterial peritonitis
- Portal hypertension Splenomegaly Ascites Varices - oeosphgeal, caput medusa, piles Encephalopathy
- ↑ risk of HCC
Ix to find cause of cirrhosis
EtOH: ↑MCV, ↑GGT NASH: hyperlipidaemia, ↑ glucose Infection: Hep, CMV, EBV serology Genetic: Ferritin, α1AT, caeruloplasmin (↓ in Wilson’s) Abs Ca: α-fetoprotein
Abdo US + PV Duplex Small / large liver Focal lesions Reversed portal vein flow Ascites - Ascitic Tap + MCS - PMN >250mm3 indicates SBP
Liver biopsy
Different Ab in cirrhosis
AIH: SMA, SLA, LKM, ANA
PBC: AMA
PSC: ANCA, ANA
Ig: ↑IgG – AIH, ↑IgM – PBC
Mx of cirrhosis
Good nutrition EtOH abstinence Colestyramine for pruritus Screening HCC: US & AFP every 3-6 m Oesophageal varices: endoscopy +/- banding
Specific
HCV: Interferon-α
PBC: Ursodeoxycholic acid
Wilson’s: Penicillamine
Decompensation
Ascites: fluid and salt restrict, spiro, fruse, tap, daily wt
Coagulopathy: Vit K, platelets, FFP, blood
Encephalopathy: avoid sedatives, lactulose ± enemas,
rifaximin
Sepsis / SBP: tazocin (avoid gent: nephrotoxicity)
Hepatorenal syndrome: IV albumin + terlipressin
What is the Child-Pugh Grading score
Grades Cirrhosis
Predicts risk of bleeding, mortality and need for Tx
Graded A-C using severity of 5 factors Albumin Bilirubin Clotting Distension: Ascites Encephalopathy
Score >8 = significant risk of variceal bleeding
Where are the portosystemic anastomoses
Oesophageal varices
- Left and short gastric veins
and Inf. oesophageal veins
Caput medusae
Peri-umbilical veins and Superficial abdo wall veins
Haemorrhoids
Sup. rectal veins and Inf. and mid. Rectal veins
Pathophysiology of Encephalopathy
↓Hepatic metabolic function
Diversion of toxins from liver directly into systemic
system.
Ammonia accumulates and pass to brain where
astrocytes clear it causing glutamate → glutamine
↑ glutamine → osmotic imbalance → cerebral oedema
Classification of Encephalopathy
1: Confused – irritable, mild confusion, sleep inversion
2: Drowsy – ↑ disorientated, slurred speech, asterixis
3: Stupor – rousable, incoherence
4: Coma – unrousable, ± extensor plantars
Presentation of encephalopathy
Asterixis, ataxia Confusion Dysarthria Constructional apraxia Seizures
Precipitants of encephalopathy
HEPATICS Haemorrhage: e.g. varices Electrolytes: ↓K, ↓Na Poisons: diuretics, sedatives, anaesthetics Alcohol Tumour: HCC Infection: SBP , pneumonia, UTI, HDV Constipation (commonest cause) Sugar (glucose) ↓: e.g. low calorie diet
Management of encephalopathy
20 degrees head up
- Correct any precipitants
Avoid sedatives
Lactulose ± PO4 enemas to ↓ nitrogen-forming bowel
bacteria → 2-4 soft stools/d
Consider rifaximin PO to kill intestinal microflora
Pathophysiology of ascites
Back-pressure → fluid exudation
↓ effective circulating volume → RAS activation
(In cirrhosis: ↓ albumin → ↓ plasma oncotic pressure
and aldosterone metabolism impaired)
Symptoms of ascites
Distension → abdominal discomfort and anorexia
Dyspnoea
↓ venous return
Ix for ascites
Bloods: FBC, U+E, LFTs, INR, chronic hepatitis screen
US: confirm ascites, liver echogenicity, PV duplex
Ascitic tap MCS and AFB Cytology Chemistry: albumin, LDH, glucose, protein SAAG = serum albumin – ascites albumin
Liver biopsy
Management of ascites
Daily wt. aiming for ≤0.5kg/d reduction
Fluid restrict <1.5L/d and low Na diet
Spironolactone + frusemide (if response poor)
Therapeutic paracentesis ̄c albumin infusion (100ml
20% albumin /L drained)
- Respiratory compromise
- Pain / discomfort
- Renal impairment
Refractory: TIPSS
Spontaneous bacterial peritonitis
- causative organisms
- Ix
- management
- ascites and peritonitic abdomen
E. coli, Klebsiella, Streps
Complicated by hepatorenal syn. in 30%
Ix: ascitic PMN > 250mm3 + MC+S
Rx: Tazocin or cefotaxime until sensitivities known
Prophylaxis: high recurrence - cipro long-term
Presentation of an alcoholic
Fatty liver → hepatitits → cirrhosis
AST:ALT >2, ↑ GGT
GIT Gastritis, erosions PUD Varices Pancreatitis Carcinoma
CNS
Poor memory / cognition
Peripheral polyneuropathy (mainly sensory)
Wernicke’s encephalopathy
- Confusion; Ophthalmoplegia (nystagmus, LR palsy); Ataxia
Korsakoff’s: amnesia → confabulation
Fits, falls
Heart
Arrhythmias: e.g. AF
Dilated cardiomyopathy
↑BP
Blood
↑MCV
Folate deficiency →anaemia
Screening tool for alcoholics
CAGE Cut down? Annoyed by people’s criticisms Guilty about drinking Eye opener?
Features of alcohol withdrawal
0-72h after last drink
Consider in new ward pt (≤3d) ̄c acute confusion
signs
- Confusion, fits, hallucinations: esp formication (DTs)
- ↑HR, ↓BP, tremor
Management of alcohol withdrawal
Tapering regimen of chlordiazepoxide PO / lorazepam IM
Thiamine
Management of alcholism
Group therapy or self-help (e.g. AA)
Baclofen: ↓ cravings
Acamprosate: ↓ cravings
Disulfiram: aversion therapy
Presentation of alcoholic hepatitis
Anorexia D/V Tender hepatomegaly Ascites Severe: Jaundice, bleeding, encephalopathy
Ix findings in alcoholic hepatitis
Bloods: ↑MCV, ↑GGT, AST:ALT>2
Ascitic tap
Abdo US + PV duplex
Management of alcoholic hepatitis
Stop EtOH Rx withdrawal High dose B vitamins: Pabrinex Optimise nutrition Daily wt., LFT, U+E, INR Mx complications of failure
Score that predicts mortality in alcoholic hepatitis
Maddrey score predicts mortality
Mild: 0-5% 30d mortality
Severe: 50% 30d mortality
1yr after admission: 40% mortality
Describe the different HBV Ab
HBsAg +ve = current infection
(>6mo = chronic disease)
HBeAg +ve = high infectivity
Anti-HBc IgM = recent infection
Anti-HBc IgG = past infection
Anti-HBs = cleared infection or vaccinated
Presentation of hepatitis B
Prodromal phase
Fever, malaise, arthralgia, nausea, anorexia
Distaste for cigarettes
Icteric phase
Jaundice, HSM, lymphadenopathy, cholestasis
Extra-hepatic features due to immune complexes Urticaria or vasculitic rash Cryoglobulinaemia PAN GN Arthritis
Types of viral hepatitis, causes and how they are spread
A- FO Seafood, especially abroad B- IV Blood, body fluids, babies (vertical) C- IV Mainly blood. Less vertical cf. HCV D- IV Dependent on prior HBV infection E- FO Developing world
Management of viral hepatitis
A & E - supportive, avoid alcohol, +/- IFN α (fulminant hepatitis)
B - supportive, avoid alcohol, +/- PEGinterferon α2b (chronic disease)
C - PEGinterferon α2b + ribavirin
Risk factors for non-alcoholic fatty liver disease
Obesity
HTN
T2DM
Hyperlipidaemia
Presentation of NAFLD
Mostly asymptomatic
Hepatomegaly and RUQ discomfort may be present.
Ix and Mx for NAFLD
BMI
Glucose, fasting lipids
↑ transaminases: AST:ALT <1 Liver biopsy
Mx -
Lose wt.
Control HTN, DM and lipids
Pathophysiology of NAFLD
↑ Fat diet and ↓ exercise ↓ hepatic steatosis ↓ ↓ FAA ox and ↑ lipogenesis and ↑ lipid export ↕ Insulin resistance
What is Budd-Chiari syndrome and causes
Hepatic vein obstruction → ischaemia and hepatocyte damage → liver failure or insidious cirrhosis.
- hypercoagulable - myeloproliferative, OCP, Anti-PL
- Local tumour - HCC
Presentation of Budd-Chiari syndrome
RUQ pain: stretching of Glisson’s capsule
Hepatomegaly
Ascites: SAAG ≥1.1g/dL
Jaundice (and other features of liver failure)
Rx of Budd-Chiari syndrome
Anticoagulate unless there are varices
Ascites: fluid and salt restrict, spiro, fruse, tap, daily wt
Other options: thrombolysis, angioplasty, TIPSS
Transplant if fulminant hepatic failure or cirrhosis
Rx underlying cause
Presentation of AI hepatitis
Cushingoid: hirsute, acne, striae HSM Fever/ malaise Amenorrhoea Polyarthritis Pulmonary infiltration Pleurisy
Presentation of PBC
Pruritus and fatigue Pigmentation of face Bones: osteoporosis, osteomalacia (↓ vit D) Big organs: HSM Cirrhosis and coagulopathy (↓ vit K) Cholesterol ↑: xanthelasma, xanthomata Steatorrhoea
Jaundice often occurs late
Pathology of PBC
Intrahepatic bile duct destruction by chronic
granulomatous inflammation → cirrhosis
Rx of PBC
Symptomatic
Pruritus: colestyramine, naltrexone
Diarrhoea: codeine phosphate
Osteoporosis: bisphosphonates
Specific
ADEK vitamins
Ursodeoxcholic acid: ↓LFTs but no effect on mortality or need for transplant
Liver transplant
End-stage disease or intractable pruritus
Recurrence occurs in ~20% but doesn’t usually
→ graft failure.
Pathophysiology of PSC
Inflammation, fibrosis and strictures and intra- and
extra-hepatic ducts.
Chronic biliary obstruction → secondary biliary cirrhosis → liver failure
Presentation of PSC
Symptoms
Jaundice
Pruritus and fatigue
Abdo pain
Signs
Jaundice: dark urine, pale stools
HSM
Complications and associations of PSC
Bacterial cholangitis
↑ Cholangiocarcinoma
↑ CRC
ASSOCIATED UC
- pANCA +ve
Rx of PSC
NEED TRANSPLANT
Pruritus: colestyramine, naltrexone
Diarrhoea: codeine phosphate
ADEK vitamins
Ursodeoxycholic acid improves cholestasis only
Abx for cholangitis
Endoscopic stenting for dominant strictures
Screening - Cholangiocarcinoma: US + Ca19-9 and CRC: colonoscopy
Signs and Symptoms of liver tumours
Symptoms
Benign tumours are usually asymptomatic
Systemic: fever, malaise, wt. loss, anorexia
RUQ pain: stretching of Glisson’s capsule
Jaundice is often late, except in cholangiocarcinoma
May rupture → intraperitoneal haemorrhage
Signs Hepatomegaly: smooth or hard and irregular Signs of chronic liver disease Abdominal mass Hepatic bruit (HCC)
Pathology of liver tumours
90% of liver tumours are 2O metastases
stomach, lung, colon, breast, uterus
90% of primary tumours are HCC.
Causes and Mx of HCC
Viral hepatitis
Cirrhosis: EtOH, HH, PBC
Aflatoxins (produced by Aspergillus)
- resection
- chemo, percutaneous ablation and embolization
Causes of Cholangiocarcinoma
Flukes (Clonorchis)
PSC
Congenital biliary cysts
UC
Presentation and Mx of Cholangiocarcinoma
Fever, malaise
Abdominal pain, ascites, jaundice
↑BR, ↑↑ALP
Mx - resect; pallative stent
Indications for liver transplant in CLD
Advanced cirrhosis
HCC
Contra- indications for liver transplant in CLD
Extra-hepatic malignancy Severe cardiorespiratory disease Systemic sepsis HIV infection Non-compliance ̄c drug therapy
Complications of liver transplant
Acute rejection (T-cell mediated) 50% @ 5-10 days Pyrexia, tender hepatomegaly ↑ or change immunosuppressants Sepsis Hepatic artery thrombosis CMV infection Chronic rejection (6-9mo): shrinking bile ducts Disease recurrence (e.g. HBV)
Epidemiology of UC v CD
UC - 30s
Smoking protective TH2-mediated
CD - 20s
Smoking ↑ risk TH1/TH17-mediated
Macroscopic features of UC v CD
> UC
Rectum + colon ± backwash ileitis
Contiguous
No Strictures
> CD
Mouth to anus esp. terminal ileum
Skip lesions
Strictures
Microscopic features of UC v CD
> CD Transmural Inflammation Ulcers - Deep, thin, serpiginous → cobblestone mucosa Marked Fibrosis Granulomas Fistulae
> UC
Mucosal Inflammation and Crypt Abscesses
Ulcers - Shallow, broad
Pseudoplyps
Presentation of UC v CD
Fatigue, anorexia, malaise
+/- fever
Abdominal tenderness
UC Diarrhoea Blood ± mucus PR Abdominal discomfort Tenesmus, faecal urgency
CD Diarrhoea (not usually bloody) Abdominal pain Wt. loss RIF mass, Perianal abscess, fistulae, tag anal/rectal stricture
Extra-intestinal features of IBD
Apthous ulcers Pyoderma gangrenosum Iritis Erythema nodosum Sacroilitis Arthralgia/AS Clubbing, Ca - Cholang, gall/renal stones
Complications of UC
Toxic megacolon - Diameter >6cm - Risk of perforation Bleeding Malignancy - CRC and Cholangiocarcinoma Strictures → obstruction Venous thrombosis
Complications of CD
Fistulae
- Entero-enteric/colonic → diarrhoea
- Enterovesical → frequency, UTI
- “pepperpot” anus
Strictures → obstruction
Abscesses
Abdominal
Anorectal
Malabsorption Fat → Steatorrhoea, gallstones B12 → megaloblastic anaemia Vit D → osteomalacia Protein → oedema
Toxic megacolon and Ca may occur (< cf. UC)
Ix findings in UC
FBC: ↓Hb, ↑WCC
LFT: ↓albumin
↑CRP/ESR
Blood cultures
Stool
MCS: exclude Campy, Shigella, Salmonella, C.diff
Imaging AXR: megacolon (>6cm), wall thickening CXR: perforation CT Ba / gastrograffin enema - Lead-pipe: no haustra - Thumbprinting: mucosal thickening - Pseudopolyps: regenerating mucosal island
Ileocolonoscopy + regional biopsy (at least 2 from 5 sites)
Classification of UC severity
Mild
Fewer than 4 motions/ day; small amount of blood
Moderate
4-6 motions/ day; mild-severe blood
Severe 6 + motions a day. Visible blood \+ 1 of: Pyrexia HR >90 Anaemia Erythrocyte sedimentation rate (mm/hour) > 30
Management of acute severe UC
Resus: Admit, IV hydration, NBM Hydrocortisone: IV 100mg QDS + PR; switch to oral when improve then taper (IV ciclosporin if CI) Transfuse if required Thromboprophylaxis: LMWH Monitoring - Bloods: FBC, ESR, CRP, U+E - Vitals + stool chart - Twice daily examination - ± AXR
Medical management of UC
Inducing Remission - 5- ASAs (Mesalasine - Prednisolone \+/- suppositories/enemas - Infliximab if steroid sparing
Maintaining remission
1) Sulfasalazine/mesalasine (PO/ Topical)
2) Azathioprine/ Mercaptopiurine PO
3) Inflixmab
Indications for emergency and elective surgery in UC/CD
Toxic megacolon
Perforation
Massive haemorrhage
Failure to respond to medical Rx
Elective - Chronic symptoms despite medical therapy
- Carcinoma or high-grade dysplasia
Surgical management of UC
- emergency
- elective
Total / subtotal colectomy –> end ileostomy ± mucus fistula
After ~3mo
Completion proctectomy + Ileal-pouch anal anastomosis (IPAA) or end ileostomy
Ileorectal anastomosis (IRA)
Elective
Panproctocolectomy –> end ileostomy or IPAA
Total colectomy –> IRA
Complications after UC surgery
Abdominal SBO Anastomotic stricture Pelvic abscess Stoma: retraction, stenosis, prolapse, dermatitis Pouch Pouchitis (50%) (abdo pain, bloody diarrhoea, nausea) metronidazole + cipro ↓ female fertility Faecal leakage
Ix for CD
Bloods FBC: ↓Hb, ↑WCC LFT: ↓albumin ↑CRP/ESR Haematinics: Fe, B12, Folate Blood cultures
Stool
MCS: exclude Campy, Shigella, Salmonella, C.diff
Imaging
AXR: obstruction, sacroileitis
CXR: perforation
MRI - severity, pelvic disease and fistula
Small bowel follow-through or enteroclysis
- Skip lesions
- Cobblestoning: ulceration + mural oedema
- String sign of Kantor: narrow terminal ileum
Endoscopy
Ileocolonoscopy + regional biopsy
Management of a severe CD attack
↑temp, ↑HR, ↑ESR, ↑CRP, ↑WCC, ↓albumin
Resus: Admit, NBM, IV hydration Hydrocortisone: IV + PR if rectal disease (switch oral when can) Abx: metronidazole PO or IV Thromboprophylaxis: LMWH Dietician Review - Elemental diet; Consider parenteral nutrition Monitoring - Vitals + stool chart - Daily examination
No improvement –> methotrexate +/- infliximab
Medical management of CD
Inducing remission
1) Sulfasalazine
2) prednisolone
3) methotrxate
4) infliximab
Maintaining remission
1) azathioprine or mercaptopurine
2) methotrexate
3) Infliximab / adalimumab
Indications for surgery in CD
Emergency
Failure to respond to medical Rx
Intestinal obstruction or perforation
Massive haemorrhage
Elective
Abscess or fistula
Perianal disease
Chronic ill health Carcinoma
Surgical management of CD
and its complications
Limited resection: e.g. ileocaecal
Stricturoplasty
Defunction distal disease ̄c temporary loop ileostomy
Complications Stoma complications Enterocutaneous fistulae Anastomotic leak or stricture Short gut syndrome (Steatorrhoea ; ADEK and B12 malabsorption; Bile acid depletion → gallstones; Hyperoxaluria → renal stones)
Presentation of coeliac disease
GLIAD
GI malabsorption - fatigue and weakness
- n/v/d, abdo distension, colic, flatus, weight loss, steatorrhoea, vit def
Lymphoma and carcinoma
Immune associations - T1DM, IgA def
Anaemia
Dermatitis herpetiformis and apthous ulcers
Ix findings in coeliac disease
- Anaemia, ↓alb, vitamin def
- Anti-endomysial IgA Ab and anti-TTG IgG, Anti-gliadin
Definition of true and false diverticulum
Diverticulum is an outpouching of tubular structure
- true - composed of complete wall
- false - composed of only mucosa
Pathophysiology of diverticular disease
- Associated with raised intraluminal pressure (low fibre diet, no osmotic effect keeping stool wet)
- mucosa herniates through muscularis propria at points of weakness where perforating arteries enter
- most often sigmoid
Symptoms of diverticular disease
- altered bowel habit +/- left sided colic (relieved by defecation)
- nausea
- flatulence
Presentation of diverticulitis
- abdominal pain and tenderness (often LIF, localised peritonitis)
- pyrexia
Pathophysiology of diverticulitis
- inspissated faeces –> obstruction of diverticulum
Complications of diverticulitis
- perforation (sudden onset chest pain, peritonitis and shock - air under diaphragm)
- haemorrhage (PR bleed)
- abscess (swinging fever, leukocytosis)
- fistulae
- strictures
Management of acute diverticulitis
- mild - bowel rest (fluids only) + co-amox
- admit if unwell, cant tolerate fluids and uncontrolled pain
medical
- NBM
- IV fluids
- Analgesia
- Abx - cefuroxime and metronidazole
Surgery - if perforation haemorrhage, stricture/ obstruction
- hartmanns / resection
Hinchley grading of perforation due to diverticulitis
1) small confined pericolic abscess
2) large abscess extending into pelvis
2) generalised purulent peritonitis
3) generalised faecal peritonitis
Symptoms of B3 (niacin) deficiency
Diarrhoea, Dermatitis, Dementia
Different types of gallstones
Cholesterol Stones: 20% Large Often solitary Formation ↑ according to Admirand’s Trangle - ↓ bile salts - ↓ lecithin - ↑ cholesterol
Pigment Stones: 5%
Small, black, gritty, fragile
Calcium bilirubinate
Associated c¯ haemolysis
Mixed Stones: 75%
Often multiple
Cholesterol is the major component
Risk factors for gallstones
Female OCP, pregnancy ↑ age High fat diet and obesity Racial: e.g. American Indian tribes Loss of terminal ileum (↓ bile salts)
Complications of gallstones
In the Gallbladder
- Biliary Colic
- Acute cholecystitis ± empyema
- Chronic cholecytsitis
- Mucocele
- Carcinoma
- Mirizzi’s syndrome
In the CBD
- Obstructive jaundice
- Pancreatitis
- Cholangitis
In the Gut
1. Gallstone ileus
Pathogenesis and presentation of biliary colic
Gallbladder spasm against a stone impacted in the neck of the gallbladder – Hartmann’s Pouch.
RUQ pain radiating → back (scapular region)
Assoc. c¯ sweating, pallor, n/v
Attacks may be ppted. by fatty food and last <6h
o/e may be tenderness in right hypochondrium
± jaundice if stones passes in to CB
Differentials of biliary colic
Pancreatitis
Cholecystitis
Bowel Perforation
Ix for gallstone disease
Urine: bilirubin, urobilinogen, Hb
Bloods: FBC, U+E, amylase, LFTs, G+S, clotting, CRP
Imaging AXR: 10% of gallstones are radio-opaque - pneumobilia - gas froming infection eCXR: look for perforation US: - Stones: acoustic shadow - Dilated ducts: >6mm - Inflamed GB: wall oedema
If Dx uncertain after US - HIDA cholescintigraphy: shows failure of GB filling
(requires functioning liver)
If dilated ducts seen on US → MRCP
Management of biliary colic
Conservative
Rehydrate and NBM
Opioid analgesia: morphine 5-10mg/2h max
High recurrence rate - surgical Rx favoured
Surgical
As for conservative + either:
Urgent lap chole (same admission)
Elective lap chole @ 6-12wks
Differences between biliary colic, acute cholecystitis and Ascending cholangitis
All - RUQ
Fever - Acute cholecystitis and ascending cholangitis
Jaundice - Ascending cholangitis
Pathogenesis of acute cholecystitis
Stone or sludge impaction in Hartmann’s pouch
→ chemical and / or bacterial inflammation
Complications of acute cholecystitis
- recurrence
- Gangrene and rarely perforation
- Chronic cholecystitis
- Empyema
Symptoms and signs of Acute Cholecystitis
Symptoms Severe RUQ pain - Continuous - Radiates to right scapula and epigastrium Fever Vomiting Signs Local peritonism in RUQ Tachycardia c¯ shallow breathing ± jaundice Murphy’s sign - 2 fingers over the GB and ask pt. to breath in → pain and breath catch. Must be –ve on the L
Management of acute cholecystitis
Conservative NBM Fluid resuscitation Analgesia: paracetamol, diclofenac, codeine Abx: cefuroxime and metronidazole 80-90% settle over 24-48h Deterioration: perforation, empyema
Surgical
May be elective surgery @ 6-12wks (↓ inflam)
If <72h, may perform lap chole in acute phase
Empyema
High fever
RUQ mass
Percutaneous drainage: cholecystostomy
Symptoms of chronic cholecystitis
Flatulent Dyspepsia Vague upper abdominal discomfort Distension, bloating Nausea Flatulence, burping Symptoms exacerbated by fatty foods - CCK release stimulates gallbladder
Differentials of chronic cholecystitis
PUD
IBS
Hiatus hernia
Chronic pancreatitis
Ix findings from chronic cholecystitis
AXR: porcelain gallbladder
US: stones, fibrotic, shrunken gallbladder
Mx of chronic cholecystitis
Medical - Bile salts (not very effective)
Surgical
- Elective cholecystectomy
- ERCP first if US shows dilated ducts and stones
What is a mucocele
Neck of gallbladder blocked by stone but contents
remains sterile
Can be very large → palpable mass
May become infected → empyema
What is Mirizzi’s syndrome
Large stone in GB presses on the common hepatic duct
→ obstructive jaundice.
Stone may erode through into the ducts
Pathogenesis, symptoms and mx of gallstone ileus
Large stone (>2.5cm) erodes from GB → duodenum through a cholecysto-duodenal fistula secondary to chonic inflam. May impact in distal ileum → obstruction
Symptoms Rigler’s Triad: Pneumobiliia Small bowel obstruction Gallstone in RLQ
Mx - stone removal via enterotomy
management of gallstones
Conservative Monitor LFTs: passage of stone may → resolution Vitamins ADEK Analgesia Cholestyramine
Interventional
If: no resolution, worsening LFTs or cholangitis
ERCP c¯ sphincterotomy and stone extraction
Surgical
Open / lap stone removal c¯ T tube placement
T tube cholangiogram 8d later to confirm
stone removal.
Delayed cholecystectomy to prevent recurrence
Features of ascending cholangitis
Charcot’s triad: fever/rigors, RUQ pain, jaundice
Reynolds pentad: Charcot’s triad + shock + confusion
Management of ascending cholangitis
Cef and met
1st: ERCP
2nd: Open or lap stone removal c¯ T tube drain
Risk factors for pancreatic carcinoma
Smoking Inflammation: chronic pancreatitis Nutrition: ↑fat diet EtOH DM
Pathology of pancreatic carcinoma
90% ductal adenocarcinomas Present late, metastasise early - Direct extension to local structures - Lymphatics - Blood → liver and lungs 60% located in head, 25% body, 15% tail
Presentation of pancreatic carcinoma
Typically male >60yrs
Painless obstructive jaundice: dark urine, pale stools
Epigastric pain: radiates to back, relieved sitting
forward
Anorexia, wt. loss and malabsorption
Acute pancreatitis
Sudden onset DM in the elderly
Signs of pancreatic carcinoma
Palpable gallbladder
Jaundice
Epigastric mass
Thrombophlebitis migrans (Trousseau Sign)
Splenomegaly: PV thrombosis → portal HTN
Ascites
Courvoisier’s Law
In the presence of painless obstructive jaundice, a
palpable gallbladder is unlikely to be due to stones.
Ix for pancreatic carcinoma
Bloods: cholestatic LFTs, ↑Ca19-9 (90% sens), ↑Ca
Imaging US: pancreatic mass, dilated ducts, hepatic mets, guide biopsy EUS: better than CT/MRI for staging CXR: mets Laparoscopy: mets, staging
ERCP
Shows anatomy
Allows stenting
Biopsy of peri-ampullary lesions
Rx of pancreatic carcinoma
Surgery Fit, no mets, tumour ≤3cm (≤10% of pts) Whipple’s pancreaticoduodenectomy Distal pancreatectomy Post-op chemo delays progression 5ys = 5-14%
Palliation
Endoscopic / percutaneous stenting of CBD
Palliative bypass surgery:
– cholecystojejunostomy + gastrojejunostomy
Pain relief – may need coeliac plexus block
Pathophysiology of acute pancreatitis
Pancreatic enzymes released and activated in vicious
circle → multi-stage process.
- Oedema + fluid shift + vomiting → hypovolaemic
shock while enzymes → autodigestion and fat necrosis - Vessel autodigestion → retroperitoneal haemorrhage
- Inflammation → pancreatic necrosis
- Super-added infection: 50% of pts. c¯ necrosis
Causes of acute pancreatitis
Aetiology
Gallstones (45%)
Ethanol (25%)
Trauma
Steroids Mumps + Coxsackie B Autoimmune: e.g. PAN Scorpion (Trinidadian) Hyperlipidaemia (I and V), ↑Ca, Hypothermia ERCP: 5% risk Drugs: e.g. thiazides, azathioprine
Idiopathic (20%): ?microstones
Symptoms and signs of acute pancreatitis
Symptoms Severe epigastric pain → back - May be relieved by sitting forward Vomiting Signs ↑HR, ↑RR Fever Hypovolaemia → shock Epigastric tenderness Jaundice Ileus → absent bowel sounds Grey Turners: flank Cullens: periumbilical (tracks up Falciform)
Criteria used for acute pancreatitis
Glasgow (IMRIE)
- assess severity and predict mortality
1 = mild; 2 = mod; 3 = severe
PaO2 <8kPa Age >55yrs Neutrophils >15 x109/L Ca2+ <2mM Renal function U>16mM Enzymes LDH>600iu/L AST>200 iu/L Albumin <32g/L Sugar >10mM
Criteria for diagnosis of acute pancreatitis
- 2/3
1) CT
2) Amylase x 3
3) epigastric pain radiatating to back
Ix findings in acute pancreatitis
Bloods FBC: ↑WCC ↑amylase (>1000 / 3x ULN) and ↑lipase - ↑ in 80% - Returns to normal by 5-7d U+E: dehydration and renal failure LFTs: cholestatic picture, ↑AST, ↑LDH Ca2+: ↓ Glucose: ↑ CRP: monitor progress, >150 after 48hrs = sev ABG: ↓O2 suggests ARDS
Urine: glucose, ↑cBR, ↓urobilinogen
Imaging
CXR: ARDS, exclude perfed DU
AXR: sentinel loop, pancreatic calcification
US: Gallstones and dilated ducts, inflammation
Contrast CT: Balthazar Severity Score
Conservative Mx of acute pancreatitis
Manage @ appropriate level: e.g. ITU if severe
Constant reassessment is key
Hrly TPR, UO
Daily FBC, U+E, Ca2+, glucose, amylase ABG
Fluid Resuscitation
- Aggressive fluid resus: keep UO >30ml/h
- Catheter ± CVP
Pancreatic Rest
NBM
NGT if vomiting
TPN may be required if severe to prevent catabolism
Analgesia
- Pethidine via PCA
- Or morphine 5-10mg/2h max
Antibiotics
Not routinely given if mild
Used if suspicion of infection or before ERCP
Penems often used: e.g. meropenem, imipenem
OTHER
- ARDS: O2 therapy or ventilation
- EtOH withdrawal: chlordiazepoxide
Interventional and surgical management for pancreatitis
ERCP + spincheterotomy –> If pancreatitis c¯ dilated ducts 2O to gallstones
Surgery
Laparotomy + necrosectomy (pancreatic debridement)
Laparotomy + peritoneal lavage
Laparostomy: abdomen left open c¯ sterile packs in ITU
Indications for surgery in acute pancreatitis
Infected pancreatic necrosis
Pseudocyst or abscess
Unsure Dx
Early complications of acute pancreatitis
Systemic Respiratory: ARDS, pleural effusion Shock: hypovolaemic or septic Renal failure DIC Metabolic ↓ Ca2+ ↑ glucose Metabolic acidosis
Late complications of acute pancreatitis
> 1wk: Local
Pancreatic necrosis
Pancreatic infection
Pancreatic abscess
- May form in pseudocyst or in pancreas –> Open or percutaneous drainage
Bleeding: e.g. from splenic artery –> May require embolisation
Thrombosis –> Splenic A., GDA or colic branches of SMA
= May → bowel necrosis
- Portal vein → portal HTN
Fistula formation –> Pancreato-cutaneous → skin breakdown
What is a pancreatic pseudocysts and how is it managed
Collection of pancreatic fluid in the lesser sac surrounded by granulation tissue
4-6wks after acute attack
Persisting abdominal pain
Epigastric mass → early satiety
Complications Infection → abscess Obstruction of duodenum or CBD Ix --> Persistently ↑ amylase ± LFTs DO US / CT
Rx
<6cm: spontaneous resolution
>6cm - Endoscopic cyst-gastrostomy OR Percutaneous drainage under US/CT
Causes of Chronic Pancreatitis
AGITS Alcohol (70%) Genetic - CF Immune - Lymphoplasmacytic sclerosing pancreatitis (↑IgG4) Triglycerides ↑ Structural - Obstruction by tumour
Presentation of Chronic Pancreatitis
Epigastric pain
Bores through to back
Relieved by sitting back or hot water bottle → erythema ab igne
Exacerbated by fatty food or EtOH
Steatorrhoea and wt. loss
DM: polyuria, polydipsia
Epigastric mass: pseudocyst
Ix for chronic pancreatitis
↑ glucose
↓ faecal elastase: ↓ exocrine function
US: pseudocyst
AXR: speckled pancreatic calcifications
CT: pancreatic calcifications
Management of acute pancreatitis
Diet No EtOH ↓ fat, ↑ carb Drugs Analgesia: may need coeliac plexus block Enzyme supplements: pancreatin (Creon) ADEK vitamins DM Rx Surgery - Indications Unremitting pain Wt. loss Duct blockage --> Whipple’s/ endoscopic stenting
Complications of chronic pancreatitis
Pseudocyst DM Pancreatic Ca Pancreatic swelling → biliary obstruction Splenic vein thrombosis → splenomegaly
Differentials of upper abdominal pain
- cholecystitis (R)
- pyelonephritis
- uteric colic
- hepatitis (R)
- pneumonia
- gastric ulcer (L)
Differentials of RIF pain
appendicitis Cholecystitis Diverticulitis Meckel’s diverticulitis Cyst accident: torsion, rupture, haemorrhage testicular torsion Salpingitis / PID Ruptured ectopic Mesenteric adenitis UTI Crohn’s Inguinal hernia
Causes of LLQ pain
- ureteric colic
- inguinal hernia
- IBD
- UTI
- Gynaecological
- testicular torsion
- diverticulitis
Causes of epigastic pain
- PUD
- Cholecystitis
- Pancreatitis
- MI
Causes of Peri-umbilical pain
- SI obstruction
- LI obstruction
- Appendicitis
- AAA
Features of carcinoid syndrome
FIVE HT
Flushing: paroxysmal, upper body ± wheals
Intestinal: diarrhoea
Valve fibrosis: tricuspid regurg and pulmonary stenosis
whEEze: bronchoconstriction
Hepatic involvement: bypassed 1st pass metabolism
Tryptophan deficiency → pellagra (3Ds)
Pathogenesis of acute appendicitis
Obstruction of the appendix Faecolith most commonly Lymphoid hyperplasia post-infection Tumour (e.g. caecal Ca, carcinoid) Worms (e.g. Ascaris lumbicoides, Schisto)
Gut organisms → infection behind obstruction → oedema → ischaemia → necrosis → perforation
Peritonitis
Abscess
Appendix mass
symptoms of acute appendicitis
Colicky abdo pain
Central (visceral irritation)→ localised in RIF ) parietal irritation)
Worse on movement
Anorexia
Nausea (vomiting is rarely prominent)
Constipation / diarrhoea
Signs of appendicitis
Low-grade pyrexia: 37.5 – 38.5 ↑HR, shallow breathing Foetor oris Guarding and tenderness: @ McBurney’s point - +ve cough / percussion tenderness Appendix mass may be palpable in RIF Pain PR suggests pelvic appendix. Rovsing’s Sign Pressure in LIF → more pain in RIF Psoas Sign Pain on extending the hip: retrocaecal appendix
Management of acute appendicitis
- Urine dip - Pregnancy test and exclude UTI
- US - exclude gynae and visialise appendix
- fluids
- abx - cef + met
- analgesia
If uncertain - observe
If certain - appendicetomy
Complications of acute appendicitis
> Appendix Mass - Abx + NBM
Resolution of mass → interval appendicectomy
Exclude a colonic tumour: colonoscopy
> Appendix Abscess
Mass enlarges, pt. deteriorates - Abx + NBM
CT-guided percutaneous drainage
If no resolution, surgery may involve right hemicolectomy.
> Perforation - peritonitis
Commonest causes of Small and Large bowel obstruction
- + a non-mechanical cause
SBO Adhesions: 60% Hernia Neoplasm - mets/ lymphoma LBO Colorectal Neoplasia: 60% Diverticular stricture: 20% Volvulus: 5%
- paralytic ileus
Causes of paralytic ileus
Post-op - bowel handling/ anesthesia Peritonitis Pancreatitis/ localised inflammation TCAs Pseudo-obstruction Metabolic: ↓K, ↓Na, ↓Mg, uraemia Mesenteric ischaemia
Presentation of SB v LB obstruction
SBO
Early - Vom and mild distension.
Late - Absolute constipation
Colicky pain every 2-3 minutes
LBO
Early - Abdo pain and distension with absolute constipation
Late - Vomiting and can be faeculant
Colicky Pain every 10-15 minutes
- constant pain –> strangulation
Signs of bowel obstruction
↑HR: hypovolaemia, strangulation Dehydration, hypovolaemia Fever- inflam disease or strangulation Surgical scars Hernias Mass: neoplastic or inflammatory Bowel sounds - ↑: mechanical obstruction - ↓: ileus PR - Empty rectum; Rectal mass; Hard impacted stool; Blood from higher pathology
Ix for bowel obstruction
Bloods
FBC: ↑WCC
U+E: dehydration, electrolyte abnormalities
Amylase: ↑↑ if strangulation/ perforation
VBG: ↑ lactate - strangulation
G+S, clotting: ?surgery
Imaging
Erect CXR
AXR: ± erect film for fluid levels
CT: can show transition point
Gastrograffin studies
Look for mechanical obstruction: no free flow
Follow through or enema
Follow through may relieve mild mechanical
obstruction: usually adhesional
Colonoscopy
Can be used in some cases
Risk of perforation
May be used therapeutically to stent
Findings on AXR of SBO v LBO
SBO
≥3cm; central; Valvulae coniventes; many loops, and many, short fluid levels; LB Gas Absent
LBO
≥6cm (caecum ≥9- emergency if ileocaecal valve working); Peripheral;
Haustra; LB Gas Present; few loops; Few, long fluid levels
medical management of bowel obstruction
NBM
IV fluids: aggressive as pt. may be v. dehydrated
NGT: decompress upper GIT, stops vomiting, prevents
aspiration
Catheterise: monitor UO
Analgesia: may require strong opioid
Antibiotics: cef+met if strangulation or perforation
Gastrograffin study: oral or via NGT
Consider need for parenteral nutrition
Regular clinical examination is necessary to ensure that
the pt. is not deteriorating.
- ↑ distension/ pain/ tenderness/ ↑ HR/ ↑RR
Repeat imaging and bloods
Indications for surgery in bowel obstruction
Closed loop obstruction
Obstructing neoplasm
Strangulation / perforation → sepsis, peritonitis
Failure of conservative Mx (up to 72h)
Surgical management of. bowel obstruction
SBO: adhesiolysis
LBO
Hartmann’s (proctosigmoidectomy)
Colectomy + 1° anastomosis + on table lavage
Palliative bypass procedure
Transverse loop colostomy or loop ileostomy
Caecostomy
Types of stoma
Colostomy - flush to skin; LIF
- loop –> entire loop of colon exteriorised and both proximal and distal end open into common stoma opening and are not transected
- end –> created from proximal end of colon, distal end stapled/ sewn shut and remains as blind pouch
Ileostomy; RIF; spout as enzymes toxic to skin
- loop - Loop SI brought out, colon ann rectum removed
- end - colon and rectum removed, and of ileum brought out
Pathophysiology of a sigmoid volvulus and sign on AXR
Long mesentery c¯ narrow base predisposes to torsion
Usually due to sigmoid elongation 2° to chronic
constipation
↑ risk in neuropsych pts.: MS, PD, psychiatric
Disease or Rx interferes c¯ intestinal motility
→ closed loop obstruction
- coffee bean sign on AXR
Mx of sigmoid volvulus
Sigmoidoscopy and flatus tube
insertion
2) Sigmoid colectomy if Failed endoscopic decompression/ Bowel necrosis
Presentation and Prevention of paralytic ileus
Presentation
Distension
Constipation ± vomiting
Absent bowel sounds
Prevention ↓ bowel handling Laparoscopic approach Peritoneal lavage after peritonitis Unstarched gloves
Mx of paralytic ileus
NBM
IV fluids: aggressive as pt. may be v. dehydrated
NGT: decompress upper GIT, stops vomiting, prevents
aspiration
Catheterise: monitor UO
Correct any underlying causes
Drugs
Metabolic abnormalities
+/- parenteral nutrition
What is obstruction and mx
Clinical signs of mechanical obstruction but no
obstructing lesion found
Usually distension only: no colic
- assoc elderly, CR disorders, hip arthroplasty and trauma
Mx - neostigmine and colonoscopic decompressino
Pathology and. Presentation of L v R colorectal carcinoma
ADENOCARCINOMA
Left Altered bowel habit PR mass (60%) Obstruction (25%) Bleeding / mucus PR Tenesmus Right Anaemia Wt. loss Abdominal pain
Either Abdominal mass Perforation Haemorrhage Fistula
Ix for colorectal carcinoma
Bloods
FBC: Hb - anaemia
LFTs: mets
Tumour Marker: CEA (carcinoembryonic Ag) (to monotor disease progression)
Imaging CXR: lung mets US liver: mets CT and MRI (rectal and liver)- staging Endoanal US: staging rectal tumours
Endoscopy + Biopsy
Flexi sig: 65% of tumours accessible
Colonoscopy
Staging and grading of colorectal carcinomas
Dukes A Confined to bowel wall B Through bowel wall but no LNs C Regional LNs D Distant mets
TNM TIS: carcinoma in situ T1: submucosa T2: muscularis propria T3: subserosa T4: through the serosa to adjacent organs N1: 1-3 nodes N2: >4 nodes
Grade - low - high based on Dysplasia, mitotic index, hyperchromatism
Surgical management of colorectal carcinomas
o R Hemicolectomy
o Left Hemicolectomy
o Sigmoidcolectomy (Sigmoid colon tumours)
o Anterior Resection (High rectal tumours >5cm from the anus)
o Abdominoperineal (AP) Resection (Low rectal tumours <5cm from the anus)
Screening for colorectal carcinoma
FOB Testing
60-75yrs - Home FOB testing every 2yrs: ~1/50 have +ve FOB
Colonoscopy if +ve: ~1/10 have Ca
Flexi Sig
55-60yrs
Once only flexi Sig
Risk factors for CRC
- FAP
- age (>60yrs)
- Fhx
- IBD
- ↓ fibre diet; ↑processed meat intake
- smoking
- ↑ alcohol intake.
Presentation of mesenteric ischaemia
Triad
Acute severe abdominal pain ± PR bleed
Rapid hypovolaemia → shock
No abdominal signs
Causes of mesenteric ischaemia
Arterial: thrombotic (35%), embolic (35%)
Non-occlusive (20%)
Splanchnic vasoconstriction: e.g. 2O to shock
Venous thrombosis (5%)
Other: trauma, vasculitis, strangulation
Management of mesenteric ischaemia
- Fluids
- Abx
- LMWH
- Laparotomy to resect necrotic bowel
Presentation of Chronic Small Bowel Ischaemia
Severe, colicky post-prandial abdo pain “gut claudication” PR bleeding Malabsorption Wt. loss
Mx –> angioplasty
Causes of Lower GI bleed
Rectal: haemorrhoids, fissure
Diverticulitis
Neoplasm
Other
Inflammation: IBD
Infection: shigella, campylobacter, C. diff
Polyps
Large upper GI bleed (15% of lower GI bleeds)
Angio: dysplasia, ischaemic colitis, HHT
Mx of Lower GI bleed
Resuscitate
Urinary catheter
Abx: if evidence of sepsis or perf
PPI: if upper GI bleed possible
Keep bed bound: need to pass stool may be large bleed
→ collapse
Stool chart
Diet: keep on clear fluids (allows colonoscopy)
Surgery: only if unremitting, massive bleed
Pathophysiology of Haemorrhoids
Anal cushion: mass of spongy vascular tissue - Positioned @ 3, 7 and 11 O’clock
Where the 3 major arteries that feed the vascular plexuses enter the anal canal
Gravity, straining (+pregnancy, portal HTN) → engorgement and enlargement of
anal cushions
Hard stool disrupts CT around cushions.
Cushions protrude and can be damaged by hard stool → bright red (capillary) bleeding.
Classification of haemorrhoids
1st degree: never prolapse
2nd: prolapse on defecation but spontaneously reduce
3rd: prolapse on defecation but require digital reduction
4th: remain permanently prolapsed
Symptoms of haemorrhoids
Fresh painless PR bleeding - Bright red Pruritis ani Lump in perianal area Severe pain = thrombosis
Mx of haemorrhoids
↑ fibre and fluid intake
Stop straining @ stool
Medical
Anusol: hydrocortisone
Topical analgesics
Laxatives: lactulose, Fybogel
Interventional
Injection c¯ sclerosant - above dentate line - SE: impotence, prostatitis
Barron’s banding → thrombosis and separation - SE: bleeding, infection
Cryotherapy - SE: watery discharge post-procedure
Infra-red coagulation
Surgical: Haemorrhoidectomy Excision of piles + ligation of vascular pedicles Lactulose + metronidazole 1wk pre-op Discharge c¯ laxatives post-op - SE: bleeding, stenosis
Definition and causes of anal fissures
Tear of squamous epithelial lining in lower anal canal
Mostly trauma 2 ° to the passage of hard stool
- Assoc. c¯ constipation
- Spasm of internal anal sphincter contributes to
pain and → ischaemia + poor healing
Crohn’s
Herpes
Anal Ca
Presentation of anal fissures
Intense anal pain - Especially on defecation - May prevent pt. from passing stools - PR impossible Fresh rectal bleeding
Mx of anal fissures
Soaks in warm bath
Toileting advice
Dietary advice: ↑ fibre and fluids
Medical Laxatives: lactulose + fybogel Topical → resolution in 75% Lignocaine/ GTN/ Diltiazem Botulinum injection
Surgical: Lateral partial sphincterotomy
Division of internal anal sphincter @ 3 O’clock
- Complications
Minor faecal/flatus incontinence (= GTN)/ Perianal abscess
Pathogenesis of Fistula in Ano
Abnormal connection between ano-rectal canal and the
skin.
- Usually occur 2° to perinanal sepsis
- Blockage of intramuscular glands → abscess → discharges to form a fistula
Associations
CD, Diverticular disease, Rectal Ca, Immunosuppression
Goodsall’s rule for Fistula’s in Ano
Fistula anterior to anus track in a straight line (radial)
Fistula posterior to anus always have internal opening
at the 6 o’clock position → curved track
Presentation, Rx and Mx of Fistula in Ano
Persistent anal discharge
Perianal pain or discomfort
- Endoanal USS/ MRI
Mx - Low - Fistulotomy and excision –> Laid open to heal by 2° intention
- High - a seton – passed through fistula and gradually
tightened over months
Pathogenesis of peri-anal abscess
Anal gland blockage → infection → abscess
E.g. coli, bacteroides
May develop from skin infections
E.g. sebaceous gland or hair follicle OR Staphs
Presentation of peri-anal abscess
Throbbing perianal pain - Worse on sitting
Occasionally a purulent anal discharge
Fluctuant mass on PR
Septic signs: fever, tachycardia
Rx of peri-anal abscess
Abx may suffice if Rx instigated v. early in course
Most cases require EUA - I&D
Wound packed
Heals by 2O intention
Daily dressing for 7-10d
Pathophysiology and risk factors of pilonidal sinus
Hair works its way beneath skin → foreign body
reaction → formation of abscess
Usually occur in the natal cleft.
Risk Factors
M>F=4:1
Geo: Mediterranean, Middle east, Asians
Often overweight c¯ poor personal hygiene (sweaty)
Occupations c¯ lots of sitting: e.g. truck drivers
Presentation and Rx of pilonidal sinus
Persistent discharge of purulent or clear fluid
Recurrent pain
Abscesses
Rx Hygiene advice Shave / remove hair from affected area Incision and drainage of abscesses Elective sinus excision
Pathology and Presentation of anal carcinoma
80% SCCs
Spread
Above dentate line → internal iliac nodes
Below dentate line → inguinal nodes
Associated HPV
Presentation
Perianal pain and bleeding
Pruritis ani
Faecal incontinence
Ix and Rx of anal carcinoma
Ix ↓ Hb (ACD) Endoanal US Rectal EUA + biopsy CT / MRI: assess pelvic spread
Rx
Chemoradiotherapy: most pts
Surgery: reserved for
Tumours that fail to respond to radiotherapy
GI obstruction
Small anal margin tumours w/o sphincter involvement
Rectal prolapse classification
Protrusion of rectal tissue through the anal canal.
Type 1: Mucosal Prolapse
Partial prolapse of redundant mucosa
Type 2: Full Thickness Prolapse ( elderly)
Presentation of rectal prolapse
Mass extrudes from rectum on defecation
May reduce spontaneously or require manual reduction
May become oedematous and ulcerated → pain and bleeding
Faecal soiling
Assoc. c¯ vaginal prolapse and urinary incontinence
↓ sphincter tone on PR
Rx of rectal prolapse
Partial Prolapse Phenol injection Rubber band ligation Surgery: Delorme’s Procedure Complete Prolapse Pelvic floor exercises/ Stool softeners Rectopexy or Delorme’s Procedure
Define a hernia
Protrusion of a viscus or part of a viscus through the walls of its containing cavity into an abnormal position
Classification of Inguinal hernias
Indirect 80%: commoner in young Congenital patent processus vaginalis Emerge through deep ring Same 3 coverings as cord and descend into the scrotum Can strangulate
Direct
20%: commoner in elderly
Acquired ( ↑IAPe.g. Chronic cough/ constipation/ obesity)
Emerge through Hesselbach’s triangle
Can acquire internal and external spermatic fascia
Rarely descend into scrotum
Rarely strangulate
Clinical features of Inguinal hernias
Children
Lump in groin which may descend into scrotum
Exacerbated by crying
Commonly obstruct
Adults
Lump in groin, exacerbated by straining/cough
May be clear ppting event: e.g. heavy lifting
Dragging pain radiating to groin
May present c¯ obstruction/strangulation
Mx of Inguinal hernia
Non-surgical
Rx RFs: cough, constipation
Lose weight
Truss
Surgical
Tension-free mesh and suture repair
Complications of inguinal hernias
Early Haematoma / seroma formation: 10% Intra-abdominal injury (lap) Infection: 1% Urinary retention
Late
Recurrence (<2%)
Ischaemic orchitis: 0.5%
Chronic groin pain / paraesthesia: 5%
Femoral hernia pathology
Protrusion of viscus through femoral canal (bounded by femoral vein and lacunar ligament) into femoral triangle (inguinal ligament, adductus longus and sartorius)
- more common in females due to shape of pelvis
- acquires - increased intra-abdominal pressure
Clinical features of a femoral hernia
Painless groin lump
inferior (and lateral) to the pubic tubercle.
Cough impulse.
Often irreducible (tight boarders)
Commonly present - obstruction or strangulation
Tender, red and hot
Abdo pain, distension, vomiting, constipation
Mx of femoral hernia
High risk of strangulation
Rx - herniotomy and heniorrhaphy
Differntials of femoral hernia
- low inguinal hernia
- femoral canal lipoma
- femoral LN
- saphena varix ( compressible, disappears when flat)
Definition and risk factors for incisional hernia
Hernia arises through a previously acquired defect
- non- pulsatile, reducible soft and non-tender swelling near site of previous wound
Pre-operative ↑ age Obesity or malnutrition Comorbidities: DM, renal failure, malignancy Drugs: steroids, chemo, radio
Intra-operative Surgical technique/skill (major factor) -Too small suture bites - Inappropriate suture material Incision type (e.g. midline) Placing drains through wounds
Post-operative
↑ IAP: chronic cough, straining, post-op ileus
Infection
Haematoma
Mx of incisional hernia
Conservative
Manage RFs: e.g. constipation, cough
Weight loss
Elasticated corset or truss
Surgical Pre-Op - Optimise cardiorespiratory function - Encourage wt. loss Nylon mesh repair: open or lap