Surgery Flashcards
(258 cards)
Define acute cholecystitis
Acute inflammation of the gall bladder, most commonly caused by gall stones
epidemiology of acute cholecystitis
- Develops in 10% of people with symptomatic gall stones
- Gall stones are common - 10% of people over the age of 50y have gall stones
- Females > Males (3:1) before the age of 50 years
- Can occur at any age but most commonly occurs in overweight, middle-aged women
Aetiology of acute cholecystitis
• Calculous Cholecystitis (Gall bladder stones) - 90-95%
⁃ Stone Types:
1. Pure cholesterol stones - 10%
⁃ Often solitary, large and round
⁃ Most common stone in Asia
⁃ Radiolucent
- Pure pigment (bile salts) stones - 10%
⁃ Occasionally associated with haemolytic anaemia due to increased formation of bile
pigment from Hb
⁃ Radiolucent - Mixed stones - 80%
⁃ Combination of calcium salts, cholesterol and pigment stones
⁃ Usually multiple stones
⁃ 10% are radioopaque
• Acalculous Cholecystitis (Others):
⁃ Severe trauma
⁃ Sepsis
⁃ Helminthic infection - common in Asia
⁃ Salmonella associated Typhoid fever –> 2° cholecystitis
⁃ CMV associated with AIDs-related cholecystitis
⁃ Longterm TPN
Risk factor for acute cholecystitis
5Fs of gallbladder disease - fair, forty, female, fat, fertile
- Increasing age
⁃ Female (pregnancy and use of the OCP)
⁃ Obesity or rapid weight loss
⁃ Chronic haemolytic disorders (pigment stones)
⁃ Longterm TPN (alters bile constituents)
⁃ Previous Sx or inflammation (Crohnʼs) affecting the terminal ileum (alters bile constituents as most of
the bile salts are reabsorbed here)
Pathophysiology of acute cholecystitis
Calculous cholecystitis:
1. Obstruction of the GB neck or cystic duct causing a closed-loop obstruction
⁃ Usually by impacted gall stones –> acute inflammation of the GB wall
⁃ Choledocholilithiasis
2. Distention of the GB
⁃ Due to continuing mucus secretion from the cells located at the neck of the GB
⁃ Bacterial multiplication
3. Blood flow and lymphatic drainage compromised
⁃ Due to increased pressure of the closed-loop obstruction
4. Arterial blood flow compromised
⁃ Pressure increases above arterial pressure –> ischaemia, necrosis and perforation
Acalculous cholecystitis:
• Exact mechanism unknown
clinical features of acute cholecystitis
• Hx:
⁃ Severe continuous RUQ abdominal pain lasting >30min
⁃ May begin in the epigastrium and migrate to the RUQ
⁃ Associated nausea, vomiting and anorexia
⁃ Right shoulder tip or scapular pain:
Due to peritoneal irritation involving the diaphragm (phrenic nerve)
⁃ Previous Hx of biliary colic:
Intermittent severe epigastric and RUQ pain that resolves after a few hours
GB tenderness during episodes
• Examination:
⁃ Fever (common)
⁃ Murphyʼs Sign
⁃ Pain on inspiration when two fingers are placed over the RUQ
⁃ RUQ mass - GB may be palpated in 30-40% of cases
⁃ Jaundice (uncommon) - due to obstruction of the common bile duct
investigations for acute cholecystitis
- Bloods:
⁃ FBC - Elevated WBCs (unlike in biliary colic)
⁃ CRP - Elevated (unlike biliary colic)
⁃ LFTs - Elevated GGT, ALP and bilirubin
⁃ Serum amylase - to exclude acute pancreatitis
⁃ Trop T - ECG - rule out MI
- RUQ U/S:
⁃ Distended GB
⁃ Thickened GB wall
⁃ +/- Gall stones
⁃ Positive Murphyʼs Sign
⁃ Pericholecystic fluid (collection of fluid seen around the GB during)
DDx of acute cholecystitis
• Appendicitis - highly situated appendix
• Right basal pneumonia
• Perforated peptic ulcer
• Pancreatitis
• MI
• Biliary colic
• Acute cholangitis - Charcotʼs triad of fever,
jaundice and RUQ pain
Management of acute cholecystitis
Initial management/Supportive care:
⁃ Nill by mouth (NBM)
⁃ IV hydration, correction of electrolyte abnormalities, Analgesia
⁃ Antibiotics (gram negative cover) - 2nd gen cephalosporin + metronidazole
Rx is usually initially conservative unless complicated (e.g. perforation)
⁃ As above
⁃ +/- Cholecystectomy performed after 48 hours (“hot lap chole”)
⁃ or Allow inflammation to settle and GB removal in 2-3 months
Complicated –> Sx
Poor surgical candidates receive a percutaneous cholecystostomy tube
complications and prognosis of acute cholecystitis
Complications:
• Perforation - 10%
⁃ Due to failed conservative management and delayed presentation due to transient symptom relief
from GB decompression
⁃ Leads to generalised biliary peritonitis
⁃ 30% mortality rate with free perforation
• Suppurative cholecystitis
⁃ Thickened GB wall infiltrated with WBCs, intra-wall abscess and necrosis
⁃ May result in perforation
• Gangrenous cholecystitis - 2-30%
⁃ Occurs most commonly at the fundus of the GB due to vascular compromise
Prognosis:
• Gall bladder perforation carries a 30% mortality rate
• Untreated acute acalculous cholecystitis is life-threatening - up to 50% mortality rate
epidemiology and risk factors of gall stones
Epidemiology
⁃ Common - 10% of age>50 years
RF:
⁃ Females, overweight, multiparity, increases with age
clinical features of gall stones
⁃ Often asymptomatic until they obstruct
⁃ “Colicky pain” - Pain that comes and goes in the RUQ due to impaction of the stones into the neck of the GB
⁃ Obstructive jaundice if stones involve the common bile duct
sequelae of gall stones
- Non-obstructive gall stones –> asymptomatic
⁃ Transient obstruction of the cystic duct –> biliary colic
⁃ Recurrent obstruction –> chronic cholecystitis
⁃ Permanent obstruction of the cystic duct –> acute cholecystitis
⁃ Obstructed common bile duct –> obstructive jaundice
⁃ Obstructed ampula –> acute pancreatitis
Ix of gall stones
-LFTs - Obstructive picture
⁃ Increased PTT due to vit K deficiency
⁃ U/S - presence of gall stones
⁃ ERCP - can also be interventional in removing stones near the ampula
⁃ MRCP (magnetic resonance cholangiopancreatography) - visualise the biliary tree but no therapeutic use
⁃ Haemolysis screen if pigmented stones suspected or found
define colorectal cancer
any malignancy arising from the colon or rectum
epidemiology of CRC
- 3rd most common cancer in men and women in the developed world
- Rare before 50 years
- Mortality rates are similar in men and women but increase in men over 50 year
AETIOLOGY of CRC
Risk factors:
Family Hx
Western Diet
Low fibre and high fats –> prolongs colonic transit time
Processed and red meats –> toxic nitrogenous waste fermented in the gut
Risk demonstrated in migrating populations to western countries and adopting western diet
Excess alcohol
T2DM
Ulcerative colitis - Risk increases by 1% per year after 10 years of active disease Smoking
Inherited genetic causes:
FAP (Familial Adenomatous Polyposis)
⁃ Autosomal dominant mutation in the APC gene –> >100 polyps forming by teenage years
⁃ Inevitably 100% will develop colorectal cancer if untreated
HNPCC (Hereditary Non-Polyposis Colorectal Cancer) or Lynch Syndrome
⁃ Defects in mismatch repair genes –> 70% lifetime risk of developing CRC
⁃ Increase risk of other cancers such as endometrial, ovarian, urothelial, small bowel and brain
⁃ Exhibits “incomplete penetration” (not everyone with the defect will develop the disease)
Peutz Jaghers Syndrome
⁃ Causes hamartomatous polyps throughout the GIT
⁃ Typically have freckles around the mouth and on the hands, feet and genitalia
⁃ 50% die by age 50 due to polyp-related complications such as intessusception or cancer
pathophysiology of CRC
• “Adenoma-carcinoma sequence”
• Lesion Characteristics:
⁃ Most lesions are exophytic (protrude into the lumen)
⁃ Later they progressively ulcerate and invade the muscular bowel wall
⁃ Invasion of the serosa and surrounding tissue –> stromal or annular fibrosis –> narrowing & obstruction
metastases of CRC
Direct:
⁃ Tumour directly invades neighbouring tissue and can cause fistulas between adjacent structures such as the stomach, small bowel, bladder,
• Lymphatic:
⁃ Mesenteric LN –> Para-aortic LN
*LN = lymph node
• Haematogenous:
⁃ Liver
⁃ Lungs and brain (uncommon)
Presentation of CRC
• Asymptomatic - in early stages of disease
• Iron-deficiency Anaemia
⁃ Occult bleeding from the tumour surface over time causes iron-deficiency anaemia
⁃ Iron-deficiency anaemia in a patient >50 years is CRC until proven otherwise
⁃ Can be the only presentation of a right-sided CRC
• Rectal bleeding
⁃ Carcinomas distal to the splenic flexure causes visible PR bleeding
⁃ Blood can be mixed into the stool which is a sign of a cancer more proximal
• Change in bowel habit
⁃ Loose stools (in particular) are caused by secretions of blood or mucus into the bowel lumen
⁃ Mucus is secreted by adenomatous lesions and can also cause hypokalaemia if severe
• Bowel Obstruction
⁃ The more distal the tumour, the more likely it is to cause obstruction due to the narrower diameter of the left colon and the formation of harder stools
• Tenesmus
⁃ “The feeling of incomplete evacuation”
⁃ Caused by a tumour in the lower 2/3rds of the rectum causing a sudden urge to defecate
• Bowel Perforation
⁃ Caused by cancer invading completely through the bowel wall –> Acute abdomen with peritonitis
⁃ E.g. Left iliac fossa pain caused by pericolic abscess (collection formed due to perforation)
examination and investigation for CRC
• General: (signs of late disease)
⁃ Cachexia, weight loss, malaise and supraclavicular node enlargement
• Abdo Exam:
⁃ Usually normal
⁃ Mass
⁃ Hepatomegaly (due to liver mets)
• Rectal Exam:
⁃ MUST be performed if CRC is suspected - Most cancers are located in the distal 12cm of the colon
⁃ Assess Pouch of Douglas (through the anterior wall of the rectum)
⁃ Inspect/sample stool/blood/mucus
Ix:
• Bloods
- Anaemia
- Altered liver enzymes - liver mets
• Colonoscopy is gold standard
• Fixed or flexible sigmoidascope can be performed at the time of presentation without bowel prep
- Fixed can reach 50% of CRCs and flexible (75%)
• CXR and CT for analysis of mets
STAGING OF CRC
• Dukes Classification:
⁃ A - Limited to the mucosa
⁃ B - Invaded through the mucosa +/- adjacent tissue but no nodes
⁃ C - Nodal involvement
⁃ D - Distant mets
• TNM:
⁃ Tumour:
⁃ T1 = Tumour invasion of submucosa
⁃ T2 = Muscularis propria
⁃ T3 = Serosa
⁃ T4 = Other adjacent organs
• Nodes:
⁃ Nx - Nodes not assessed
⁃ N0 = No nodal involvement
⁃ N1= Metastasis to 1-3 nodes
⁃ N2 = > 3 nodes
• Metastasis
⁃ N0 = No distant metastasis
⁃ M1 = Metastasis present
management of CRC
• Surgical Resection + Resection of draining lymph nodes
⁃ Depends on the location of lesion
• Radio and chemotherapy play some role in reducing recurrence rates in Duke C tumours
what is VTE
- Venous Thromboembolism (VTE) manifests as DVTs and PEs
- Preventable cause of death in hospital patients
- Many at-risk patients do not receive adequate DVT/PE prophylaxis
- Hospital-acquired DVT/PE usually clinically silent