Gastrointestinal and Liver Flashcards
What is an Anal Fissure?
Split in the skin of distal anal canal
Acute < 6 weeks
Chronic > 6 weeks
RF of Anal Fissures
- constipation
- IBD
- STIs e.g. HIV, syphilis, herpes
- pregnancy
- opiates
H&E of Anal Fissures
- Painful, bright red, rectal bleeding
- Tearing sensation on passing stool
- Fresh blood on stool of paper
- Anal spasm
Investigations for Anal Fissures
- Clinical Diagnosis
- Anal manometry (in patients with resistant fissures)
- Low resting pressure
- Anal ultrasounds (in patients with suspected anal sphincter deficits)
Acute Management of Anal Fissures
- Soften stool
- High fibre diet with high fluid intake
- Bulk-forming laxative
- Petroleum jelly lubricant
- Topical analgesics
- Analgesia
Chronic Management of Anal Fissures
Same as Acute +
- Topical GTN
- If not effective after 8 weeks, refer for sphincterotomy or botulinum toxin
What are haemorrhoids?
Haemorrhoids, also known as piles, are swollen and inflamed veins in the anus and rectum that can cause discomfort, pain, itching, and bleeding
H&E of Haemorrhoids
- Painless bright PR bleeding is most common
- Anal itching or irritation, tenesmus with prolapsing internal haemorrhoids
- May be pain, itching, bleeding or lump in anal area
- DRE may reveal swollen, tender or prolapsed haemorrhoids
Investigations for Haemorrhoids
- Proctoscopy to confirm diagnosis and exclude sinister pathology
- If there is concern, a colonoscopy may be indicated
Management for Haemorrhoids
- Conservative measures include increasing dietary fibre, taking sitz baths, and using topical creams or ointments to relieve symptoms.
- If symptoms persist or are severe, non-surgical interventions such as rubber band ligation, injection sclerotherapy, or infrared coagulation may be considered.
- Phenol injections are usually only used for minor internal haemorrhoids
- Surgery may be indicated for patients with large or persistent haemorrhoids that do not respond to conservative or non-surgical management. Surgical options include haemorrhoidectomy or stapled haemorrhoidopexy.
- Prolapsed haemorroids are best managed surgically if symptomatic
Thrombosed Haemorrhoids
- Typically present with significant pain and tender lump
- Exam reveals purplish, oedematous, tender subcutaneous perianal mass
- If patient present within 72 hours, refer for excision
- Otherwise patients can usually be managed with stool softener, ice packs and analgesia
What is a Hiatus Hernia?
- Prolapse of upper stomach through diaphragmatic oesophageal hiatus
- Sliding - 80% - hernia moves in and out of chest, acid reflux as LOS becomes less competent
- Rolling - 20% - hernia goes through hole in diaphragm next to oesophagus
RF for Hiatus Hernia
Things that increase intra-abdominal pressure, e.g. obesity, weightlifting, pregnancy
H&E for Hiatus Hernia
- Usually asymptomatic
- GORD symptoms that are worse when lying flat
- Palpitations or hiccups indicate pericardial irritation
Investigations for Hiatus Hernia
- Chest X-ray
- Retrocardiac bubble
- Barium swallow
- Consider OGD, CT/MRI, and high-resolution oesophageal manometry and pH monitoring
Management of Hiatus Hernia
- Weight loss
- PPI
- Surgery if symptomatic rolling hernia
What is GORD?
Gastro-oesophageal Reflux Disease
- Inflammation of oesophagus caused by gastric acid +/ bile
- Disruption of mechanisms that prevent reflux
H&E for GORD
- Heartburn : especially after consumption of food and drink
- Acid regurgitation
- Waterbrash (inc. saliva)
- Pain relief by antacids
- Aspiration : nocturnal cough + wheeze
- Dysphagia
PE usually normal, might be epigastric tenderness + wheeze
Investigations for GORD
- Resolution of symptoms after 8-week PPI trial
- OGD (if > 55, longer than a month, dysphagia, relapse or weight-loss)
- Oesophageal manometry if OGD inconclusive
Lifestyle management of GORD
Lifestyle :
- weight-loss
- elevate head
- stop smoking
- reduce fat intake
- avoid large meals in evening
Medical management of GORD
PPI e.g. omeprazole for 4-8 weeks
- Low dose if responsive to manage symptoms if they recur
- If no response but endoscopically positive, double dose
- If no response but endoscopically negative, H2RA or pro kinetic for 1 month
Surgical management of GORD
Increase LOS pressure
Nissen fundoplication
Complications of GORD
- Oesophagitis
- Ulcers
- Anaemia
- Benign strictures
- Barrett’s
- Oesophageal carcinoma
What is Irritable Bowel Syndrome (IBS) and the types?
Chronic condition characterised by recurrent abdominal pain associated with bowel dysfunction.
- IBS-D : with diarrhoea
- IBS-C : with constipation
- IBS-M : mixed type
What are the RF for IBS?
History of abuse
PTSD
Bacterial Gastroenteritis
FHx
F > M
H&E for IBS
- Cramping in lower / mid abdomen
- Alteration of stool consistency
- Defecation relieves abdominal pain / discomfort
- NORMAL ON EXAMINATION
Diagnosis for IBS
+ve diagnosis if patient has these symptoms for 6+ months :
A - Abdominal pain +/
B - Bloating +/
C - Change in bowel habit
+ve diagnosis if patient has abdominal pain relieved by defecation or altered bowel frequency stool form + 2 of the 4 :
- altered stool passage (straining, urgency, incomplete
- bloating, distension, tension or hardness
- symptoms worse when eating
- passage of mucus
Also lethargy, N, backache and bladder symptoms may support diagnosis
Investigations for IBS
Diagnosis of exclusion :
- Exclude coeliac with anti-tTG
- Exclude IBD with calprotectin, lactoferrin, CRP, colonoscopy
- Exclude colorectal cancer with FBC, FOB and FIT test
Lifestyle Management for IBS
Increase fibre intake
Avoid caffeine, lactose, fructose
Stress management
Avoid sorbitol if diarrhoea
Medical management for IBS
First line according to predominant symptoms:
- pain : antispasmodic agents
- constipation : laxatives but avoid lactulose (for 12+ months consider linaclotide)
- diarrhoea : loperamide
Second line :
- low dose TCAs
Other :
- psychological intervention (CBT, hypno/psycho therapy)
What is Crohn’s disease?
Crohn’s disease (CD) is a chronic inflammatory bowel disease
- Characterised by transmural inflammation and skip lesions
- Can affect any part of the gastrointestinal (GI) tract from the mouth to the anus
- The aetiology remains unknown, but it is believed to involve a complex interplay of genetic predisposition, environmental factors, and dysregulated immune responses
- Clinical presentation varies but may include abdominal pain, diarrhoea, weight loss, and fatigue, with potential extraintestinal manifestations such as arthritis, uveitis, and erythema nodosum
RF for Crohn’s
- FH, smoking, Oral contraceptive pills, high refined sugars
- Affects Ashkenazi Jews, and biomodal peak (15-40 and 60-80)
H&E for Crohn’s
- Crampy or constant abdominal pain
- Right lower quadrant and peri umbilical (terminal ileum)
- Diarrhoea
- Mucus, blood, pus
- Can be nocturnal
- Perianal lesions
- Skin tags, fistulae, abscesses
- Fatigue, weight loss, mouth ulcers, malnourishment
Extra-intestinal manifestations of Crohn’s
- Arthropathy (joint pain)
- Skin lesions
- Erythema nodosum
- Pyoderma gangrenosum
- Uveitis and episcleritis
On Exam - abdominal tenderness/lower right mass, apthous ulcers, perianal lesions
Investigations for Crohn’s
Bloods
- FBC, iron studies, vitamin/folate, ESR, albumin, B12 + folate
- Anti-saccharomyces cerevisiae antibodies (ASCA) and perinuclear anti-neutrophil cytoplasmic antibodies to differentiate between CD and UC
- CRP correlates well with disease activity
Stool Tests
- Cultures, calprotectin to help differentiate between IBD and infectious or non-inflammatory causes
Colonoscopy
- deep ulcers, skip lesions
- cobblestone appearance
Histology
- inflammation is all layers from mucosa to serosa
- goblet cells
- non-caseating granulomas
Small bowel enema (X-ray)
- high sensitivity and specificity for exam of terminal ileum
- strictures (Kantor’s string sign)
- proximal bowel dilation
- ‘rose thorn’ ulcers
- fistulae
Management of Crohn’s
Stop smoking as this can cause relapse, but smoking may help UC
Steroids (oral or IV +/- topical) to induce remission
- predisolone, budesonide
Immunomodulators to reduce and maintain remission
- Azathioprine, mercaptopurine, methotrexate (2nd)
Biological therapy (IV)
- Adalimumab, infliximab, vedolizumab
Surgery
- For severe remissions/presentation, refractory disease and obstruction, fistulas and abscesses
What is done when remission of Crohn’s is achieved?
Maintain immunomodulators +/- biologics
Can also give anti-spasmotics (cramp relief) and anti-diarrhoeals
What is Ulcerative Colitis (UC)?
- Diffuse inflammation of colonic mucosa (one layer)
- Only affects the rectum and colon
- Starts from rectum and extends proximally
- Affects variable lengths of colon
- Continuous inflammation
- No known cause
- Environmental + immune dysfunction + genetic predisposition (HLA-27)
RF for UC
- Family history, HLA-B27
- Smoking is protective against UC
- Affects males more than females
- Bimodal peak (20-40 and 60)
H&E for UC
- Bloody diarrhoea
- Rectal bleeding and mucus
- Abdominal pain and cramps
- Tenesmus
- Weight loss
Extra-intestinal manifestations of UC
- Joints - peripheral arthritis and ankylosing spondylitis (HLA-B27)
- Skin - erythema nodosum and pyoderma gangrenosum
- Ocular - episcleritis
On exam, anaemic pallor, blood on DRE, abdominal tenderness
Investigations for UC and findings
- Colonoscopy + biopsy
- colonoscopy contraindicated in severe colitis due to risk of perforation, flexible sigmoidoscopy preferred
- Double contrast barium enema
- loss of haustrations
- superficial ulceration, ‘pseudopolyps’
- long standing disease : colon is narrow and short ‘drainpipe colon’
- Abdominal X-ray
- Dilated bowel
- Thumbprinting
- Bloods
- FBC for anaemia
- LFTs for primary sclerosing cholangitis
- Stool sample
- Increased faecal calprotectin indicates inflammation
- Positive pANCA in most cases
Typical findings during colonoscopy for UC
Typical findings:
- red, raw mucosa, bleeds easily
- no inflammation beyond. submucosa (unless fulminant disease)
- crypt abscess
- widespread ulceration with preservation of adjacent mucosa which has the appearance of polyps (‘pseudopolyps’)
- inflammatory cell infiltrate in lamina propria
- depletion of goblet cells and mucin from gland
- granuloma is infrequent
How is UC severity classified?
Mild : <4 stools/day, small amount of blood
Moderate : 4-6 stools/day, varying amounts of blood, no systemic upset
Severe : >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)
Management of UC
Mild-moderate :
- Mesalazine (topical/rectal then oral)
- Steroids if remission not achieved
- Oral beclamethasone
Severe :
- IV steroids (hydrocortisone)
- IV ciclosporin if remission not achieved
Maintain remission :
- Aminosalicylate (mesalazine) if mild-moderate
- Oral azathioprine or mercaptopurine if severe relapse or >= 2 exacerbations in the past year
If nothing working, recuse therapy with infliximab
What happens in severe pan-colitis?
In severe pan-colitis, where the ileocaecal valve is damaged and fixed open, you may get “backwash ileitis” where the inflammatory exudate from the colonic mucosa has caused minor inflammation in the very last section of ileum.
What is acute cholangitis?
Infection of biliary tree caused by choledocholithiasis and benign and malignant strictures
H&E for Acute Cholangitis
Key diagnostics :
- Charcot’s triad
- RUQ pain
- Fever
- Jaundice
- RUQ Tenderness
Other diagnostics :
- Pale stools (lack of bile secretion)
- Pruritis
- Hypotension and confusion (Reynold’s pentad)
RF for Acute Cholangitis
- > 50 years old
- History of cholelithiasis, primary or secondary sclerosing cholangitis, stricture of the biliary tree (benign or malignant), post-procedure injury of bile ducts, radiological intervention with resulting inadequate biliary drainage
Investigations of Acute Cholangitis
First investigations to order :
- Abdominal US
- FBC, CRP, LFTs
- Serum urea, creatinine, potassium, magnesium
Other to consider :
- Abdominal CT with contrast - US negative
- MRCP - US and CT negative
- Blood cultures and ABG if suspecting sepsis
Management of Acute Cholangitis
- IV antibiotics
- ECRP after 24-48h - can be used for diagnosis and biliary stone extraction (immediately in severe cases)
- Biliary decompression if deteriorating
- Consider lithotripsy
What is Cholecystitis?
Inflammation of the gallbladder
Develops secondary to gallstones in 90% of patients (acute calculous cholecystitis) - impacted in gallbladder neck or cystic duct
H&E of Cholecystitis
- RUQ pain + tenderness
- Signs of inflammation (fever)
- Palpable mass
- Murphy’s sign - inspiratory arrest on palpation of RUQ
Other diagnostic features
- N+V
- Anorexia
RF for Cholecystitis
- Gallstones
- Severe illness
- Total parenteral nutrition (TPN) - causes gallbladder stasis, biliary sludge and gallstones due to decreased emptying
- Diabetes
First order investigations for Cholecystitis
- Abdominal ultrasound to identify presence of gallstones
- If diagnosis unclear : cholescintigraphy scan
- Bloods - FBC, CRP, bilirubin, LFT, serum lipase/amylase
What are other investigations to consider for cholecystitis?
- Contrast-enhanced CT or MRI if sepsis suspected to diagnose gangrenous cholecystitis or gallbladder perforation
- Blood cultures if septic
- MRCP if US hasn’t detected common bile duct stones but bile duct is dilated and/or LFTs are abnormals
- Endoscopic US if MRCP doesn’t lead to diagnosis
Management of Cholecystitis
- Analgesia, fluid resus and IV antibiotics (Ceftriaxone and metronidazole)
- Laparoscopic cholecystostomy within 1 week of diagnosis
- Percutaneous cholecystectomy if unfit for surgery but not improving after analgesia and antibiotics
- Postop management
What is a Gastrointestinal perforation?
Medical emergency - hole or tear develops in the wall of the GI tract
What are the causes of a Gastrointestinal perforation?
- Peptic ulcer disease
- Diverticulitis
- GI cancer
- IBD
- Trauma
- Foreign body ingestion
History of Gastrointestinal perforation
- Sudden onset of severe abdominal pain - can be diffuse or localised
- N+V
- Fever
- Signs of shock - tachycardia, hypotension + tachypnoea
Examination of Gastrointestinal perforation
- Abdominal distension
- Tenderness
- Guarding
- Rebound tenderness
- In severe cases - signs of peritonitis - rigidity, board-like abdomen + absent bowel sounds
Investigations of Gastrointestinal perforation
- Abdominal X-ray, which may show free air under diaphragm or within abdominal cavity
- Erect CXR if acute upper abdominal pain
- CT or US can be used to confirm diagnosis + location + extent
- FBC, U&E + cultures to assess for sepsis + complications
Management of Gastrointestinal perforation
- Suspected or confirmed - admission to hospital
- Resuscitation w/ IV fluids, broad spectrum antibiotics + analgesics
- Surgical intervention : exploratory laparotomy / laparoscopy to repair perforation / remove necrotic tissue
- In some cases (small perforations or poor surgical candidates), conservative management such a s bowel rest + antibiotics may work
What is Boerhaave’s syndrome?
- Spontaneous rupture of oesophagus as a result of repeated vomiting - distally sited and on left side
How does Boerhaave’s syndrome present?
Mackler Triad:
Triad of vomiting or retching, severe retrosternal chest pain, typically radiating to the back + subcutaneous emphysema
How is Boerhaave’s syndrome diagnosed?
CT contrast swallow
Management of Boerhaave’s syndrome
Thoracotomy + lavage
- If less than 12 hours after onset then primary repair is usually feasible
- If delayed beyond 12 hours is best managed by insertion of a T tube to create a controlled fistula between oesophagus and skin
- Delays >24 hours are associated with very high mortality
What is the biggest complication of Boerhaave’s syndrome?
Severe sepsis occurring secondary to mediastinitis
What is Constipation?
- Unsatisfactory defecation characterised by infrequent stools and difficult stool passage
- Risk factors include low fibre and water intake, sedentary lifestyle, opiates, CCBs, IBD/IBS, cancer, psychological
- Affects mainly >65
H&E of Constipation
- Infrequent stools (<3 week)
- Difficulty defecating
- Tenesmus
- Excessive straining
On examination:
- Abdominal mass in LLQ
- Anal fissures
- Haemorrhoids
- Hard stool on DRE
Management of Constipation
Lifestyle :
- Increase fibre, water intake, exercise
- Avoid triggering factors like medications
Laxatives :
- Osmotic laxatives - Macrogel, lactulose
- Stimulant laxatives - Senna, bisacodyl
Deal with primary cause if constipation is secondary
Complications of Constipation
- Overflow diarrhoea
- Acute urinary retention
- Haemorrhoids and anal fissures
What is Alcoholic Hepatitis?
- Second stage of alcoholic liver disease (after steatosis, before cirrhosis)
- Inflammation and necrosis
- Reversible
H&E of Alcoholic Hepatitis
- RUQ pain
- Hepatomegaly
- Malnutrition and wasting
- Low-grade fever
- Jaundice (if severe)
RF for Alcoholic Hepatitis
- Prolonged and heavy alcohol consumption
- Hepatitis C
- Female sex
- Smoking
- Obesity
Primary Investigations for Alcoholic Hepatitis
FBC for anaemia
LFTs
- AST + ALT elevated to >30 units/L for men and >19 units/L for women
- AST/ALT ratio >2 (>3 is acute episode)
- Elevated ALP may indicate cholestasis
- Elevated bilirubin
- Elevated gamma-GT
US
Secondary investigations for Alcoholic Hepatitis
- Viral hepatitis serology
- Serum iron, ferritin and transferrin to rule out haemochromatosis
Management of Alcoholic Hepatitis
- Alcohol abstinence +/- alcohol withdrawal management
- Weight reduction and smoking cessation
- Nutritional supplementation
- Immunisation
- Maddrey’s discriminant score for acute episodes
What is Maddrey’s discriminant score for Alcoholic Hepatitis?
Maddrey’s discriminant score is used to guide whether prednisolone should be given in acute episodes of alcoholic hepatitis. A score > 32 is associated with a poor prognosis and prednisolone treatment is indicated in these cases
- it is calculated by a formula usingprothrombin time and bilirubinconcentration
What is Peptic Ulcer Disease?
- Ulceration of GI tract caused by exposure to gastric pain and pepsin
- Usually found in gastric and duodenal
- Imbalance between damaging acid and pepsin and mucosal protective mechanisms
Causes of Peptic Ulcer Disease
- H.pylori
- NSAIDs
- Alcohol
- Bisphosphonates
- Smoking
- Zollinger-Ellison syndrome
What is Gastritis?
Whole stomach lining is inflamed
H&E of Peptic Ulcer Disease and Gastritis
- Epigastric pain which can be pointed to
- Relieved by antacids
- Gastric - pain directly after meals, weight loss
- Duodenal - relieved by eating, pain couple hours after meals, weight gain
- N+V
Complications of Peptic Ulcer Disease and Gastritis
- Haematemesis
- Melaena
Investigations for Peptic Ulcer Disease
- Urea-13 breath test, stool antigen test for H.pylori
- Erect CXR if suspected perforation
- Upper GI endoscopy and biopsy
- Blood antigen test : IgG antibody against H.pylori
- Campylobacter-lie organism test
- Fasting serum gastrin test
Investigations for Gastritis
- Mainly H.pylori tests
Management of Peptic Ulcer Disease and Gastritis
Lifestyle:
- Stop NSAIDs, reduce smoking and alcohol
If H.pylori +
- Triple therapy of PPI and 2 Abx (normally amoxicillin or clarithromycin)
If H.pylori -
- Stop NSAIDs or causative drugs
- 4-8 week PPI therapy
If perforated ulcer:
- Blatchford risk score
- Transfuse
- Therapeutic endoscopy
Mechanism, examples, use and side effects of Aminosalicylates
Free radical scavengers, can reduce leukotriene production and can inhibit the cellular release of interleukin-1
Sulphasalazine or mesalazine
Used to reduce inflammation in bowel such as in UC or Crohn’s
Can cause agranulocytosis - presents in sudden onset rigors, fever and sore throat
In this situation, FBC is most important investigation
Mechanism, examples, use and side effects of NSAIDs
- Anti-inflammatory, COX inhibitor
- Used for pain management
- ibuprofen and naproxen
- Can cause stomach ulcers
Mechanism, examples, use and side effects of PPIs
- Proton pump inhibitors (PPI) cause irreversible blockade of H+/K+ ATPase of the gastric parietal cell
- Omeprazole, lansoprazole
Can cause
- Hyponatraemia, hypomagnasaemia
- Osteoporosis - increase risk of fractures
- Microscopic colitis
- Increased risk of C.diff infections
What is Ascites?
Fluid build up in the abdomen
Causes grouped by serum-ascites albumin gradient (SAAG)
Causes of Ascites
SAAG > 11g/L (indicates portal hypertension) :
Liver
- cirrhosis/ alcoholic liver disease
- acute liver failure
- liver mets
Cardiac
- RHF
- constrictive pericarditis
Other
- Budd-Chiari
- portal vein thrombosis
- veno-occlusive disease
- myxoedema
SAAG < 11g/L :
Hypoalbuminaemia
- nephrotic syndrome
- severe malnutrition
Malignancy
- peritoneal carcinomatosis infections
- tuberculous peritonitis
Other
- pancreatitis
- bowel obstruction
- biliary ascites
- post-op lymphatic leakage
- serositis in CT disease
H&E of Ascites
KEY
- abdo distension
- fluid detected in shifting dullness
Investigations of Ascites
1st
- Adbo US
Other
- CT
- MRI
Management of Ascites
- Reducing dietary sodium
- Fluid restriction of sodium < 125mmol/L
- Aldosterone antagonists
- Drainage if tense ascites - therapeutic abdominal paracentesis
- Requires IV albumin to avoid paracentesis-induced circulatory dysfunction (PICD)
- Prophylactic oral ciprofloxacin or norfloxacin to reduce risk of peritonitis
- Consider transjugular intrahepatic portosystemic shunt
What is Peritonitis?
Peritonitis is inflammation of the peritoneum usually caused by infection
Causes of Peritonitis
Primary Infections
- Spontaneous bacterial peritonitis
- Medical equipment
Secondary Infections
- Appendicitis
- Perforation
- Rupture
- Trauma
- Surgery
H&E of Peritonitis
- Abdominal pain and tenderness
- Distension
- Dehydration
- Paralytic ileus
- Fever
- N+V
- Tachycardia
- Dyspnoea
- MCI, oedema and thrombocytopenia if ascites
- Rigidity and rebound tenderness
Investigations for Peritonitis
Bloods
- High WCC
- Cultures
Paracentesis
- SAAG
- can relieve pressure from ascites as well
Management of Peritonitis
IV fluids and broad-spectrum Abx
Specific Abx after culture results
What is Spontaneous Bacterial Peritonitis?
Form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis
H&E of Spontaneous Bacterial Peritonitis
- ascites
- abdo pain
- fever
Investigations for Spontaneous Bacterial Peritonitis
- paracentesis : neutrophil count > 250 cells/ul
- most common is E.coli
Management of Spontaneous Bacterial Peritonitis
IV cefotaxime usually given
Abx prophylaxis given to patients with ascites if:
- patient had an episode of SBP
- fluid protein <15 g/L and either Child-Pugh score of at least 9 or hepatorenal syndrome
- NICE recommend: ‘Offer prophylacticoral ciprofloxacin or norfloxacinfor people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved’
Alcoholic liver disease is a marker of poor prognosis in SBP.
What is a Hernia?
Protrusion of an organ or the fascia of an organ through the wall of the cavity that normally contains it
RF of Hernia
- Obesity
- Ascites
- Increasing age
- Surgical wounds
Features of Hernia
- Palpable lump
- Cough impulse
- Pain
- Obstruction : MC in femoral hernia
- Strangulation : may compromise the bowel blood supply leading to infarction
Features of Inguinal Hernia
- Account for 75% of abdominal wall hernias, 95% of patients are male
- Men have 25% lifetime risk of developing hernia
- Groin lump
- Superior and medial to pubic tubercle
- Direct passes medial to inferior epigastric artery, indirect passes lateral to it
- Disappears on pressure or when patient lies down
- If it still protrudes after putting pressure eon deep inguinal ring, indicates direct hernia
- Discomfort and ache, worse on activity, severe pain is uncommon
- Strangulation is rare
Management of Hernia
- Mesh repair
- Open approach for unilateral
- Laparoscopic for bilateral/recurrent
- Hernia truss if unfit for surgery
What is a Femoral Hernia?
Occur when section of bowel or any other part of abdominal viscera pass into femoral canal via femoral ring
Much less common than inguinal hernias (5%)
More common in women (1:3)
Features of Femoral Hernia
- Lump within the groin, that is usually middle painful
- Inferolateral to the pubic tubercle
- Typically non-reducible
- Given the small size of the femoral ring, a cough impulse is often absent
Diagnosis of Femoral Hernia
Diagnosis is usually clinical although US is an option
Differential to exclude:
- Lymphadenopathy
- Abscess
- Femoral artery aneurysm
- Lipoma
- Inguinal hernia
Complications of Femoral Hernia
- Incarceration, where the herniated tissue cannot be reduced
- Strangulation - emergency
- Bowel obstruction - emergency
- Bowel ischaemia and resection
Features of strangulated hernia
Can follow from incarceration and is a surgical emergency
These hernias will be tender and likely non-reducible and may also present with a systemically unwell patient
Much higher risk with femoral hernias
Management of Femoral Hernia
- Surgical repair is a necessity, given risk of strangulation - can be laparoscopically or via a laparotomy
- Hernia support belts/trusses should not be used for femoral hernias, again due to the risk of strangulation
- In emergency, laparoscopy may be only option
What is a Umbilical and Paraumbilical Hernia?
Umbilical - symmetrical bulge under umbilicus
Paraumbilical - Asymmetrical bulge directly above or below umbilicus
What is an Epigastric Hernia?
- Lump in midline between umbilicus and xiphersternum
- RF include physical training or coughing
What is an Obturator Hernia?
- Passes through obturator foramen
- Typically presents with bowel obstruction
Symptoms of Strangulated Hernia
- Pain
- Fever
- Increase in size of hernia or erythema of underlying skin
- Peritonitic features
- Bowel obstruction
- Bowel ischaemia
Diagnosis of Strangulated Hernia
- Abdominal XR or CT
- Suspected perforation - CXR
- FBC and ABG for leukocytosis and raised lactate
What is Acute Pancreatitis?
Inflammation of the pancreas caused by auto digestion of pancreatic tissue by the pancreatic enzymes, leading to necrosis
Causes of Acute Pancreatitis
GET SMASHED
- Gallstones (MC)
- Ethanol
- Trauma
- Steroids
- Mumps (other viruses e.g. Coxsackie B)
- Autoimmune, Ascaris Infection
- Scorpion Venom
- Hypertriglyercidaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia
- ERCP
- Drugs (thiazide, loop diuretics, steroids, valproate, UC+Crohn’s drugs)
H&E for Acute Pancreatitis
- Upper abdominal pain that radiates to back
- N+V
- Signs of hypovolaemia e.g. hypotension, dry membranes, decreased skin turgor and sweating
- Signs of pleural effusion
- Anorexia
- Periumbilical discolouration (Cullen’s sign) and flank discolouration (Grey-Turner’s sign)
- Organ dysfunction (e.g. exocrine - steatorrhea and diarrhoea)
- Dyspnoea
- Jaundice
Investigations for Acute Pancreatitis
- Serum Lipase (or Amylase) = >3x upper limit
- Trans-abdominal US
- FBC - leukocytosis + elevated Hct indicates poor prognosis
- Contrast CT
- Elevated CRP
- Hypoxaemia
- LFTs
- CXR
Common factors indicating severe Acute Pancreatitis
- Age > 55
- Hypocalcaemia
- Hyperglycaemia
- Hypoxia
- Neutrophilia
- Elevated LDH and AST
Management of Acute Pancreatitis
- Fluid rests with crystalloids
- Analgesia with IV opioids
- Nutritional support
- Consider supplemental O2 and antiemetic
- IV antibiotics if infection
Surgery:
- Early cholecystectomy if due to gallstones
- If obstructed biliary system do early ERCP
- Debridement may be required if necrosis and worsening organ dysfunction
- Infected necrosis do radiological drainage or surgical necrosectomy
Complications of Acute Pancreatitis
Local:
- Peripancreatic fluid collections 25%
- Pseudocysts
- Pancreatic necrosis
- Pancreatic abscess
- Haemorrhage
Systemic:
- ARDS - high mortality rate of 20%
