General surgery Flashcards
CEA is a tumour marker associated with which cancer?
Colorectal
CA125 is associated with…
Ovarian cancer
CA19-9 is associated with…
Pancreatic cancer
CA15-3 is associated with…
Breast cancer
Alpha-feto protein (AFP) is associated with…
Hepatocellular cancer
Teratoma
Gallstones are generally composed of…
Phospholipids
Cholesterol
Bile pigments
Risk factors for gallstones
Female OCP, pregnancy increased age High fat diet and obesity Racial e.g. American Indian tribes Loss of terminal ileum (due to reduced bile salts)
Complications of gallstones
In the gallbladder: Cholecystitis Chronic cholecystitus Biliary colic Mucocele Carcinoma
In the CBD:
Cholangitis
Pancreatitis
Obstructive jaundice
In the gut: gallstone ileus
Presentation of biliary colic
RUQ pain radiating to back N/V Sweating Pallor Precipitated by fatty food and last less than 6 hours Possible jaundice is stone is in the CBD
Presentation of cholecystitis
Severe RUQ. Continuous and radiating to the right scapular and epigastrium Fever Vomiting Possible jaundice Murphy's sign
Presentation of cholecystitis
Severe RUQ. Continuous and radiating to the right scapular and epigastrium Fever Vomiting Possible jaundice Murphy's sign
Thumb printing of the small bowel is seen in
Crohn disease Ulcerative colitis Infection (i.e. pseudomembranous colitis) Ischaemic bowel Diverticulitis Mucosal/submucosal haemorrhage 2 Lymphoma Amyloid
TNM staging of oesophageal tumours
Tumour
T1- the tumour is confined to the submucosa
T2- the tumour has grown into (but not through) the muscularis propria
T3- the tumour has grown into (but not through) the serosa
T4- the tumour has penetrated through the serosa and the peritoneal surface. If extending directly into other nearby structures (such as other parts of the bowel or other organs/body structures) it is classified as T4a. If there is perforation of the bowel, it is classified as T4b.
Nodes
N0- no lymph nodes contain tumour cells
N1- there are tumour cells in up to 3 regional lymph nodes
N2- there are tumour cells in 4 or more regional lymph nodes
Metastases
M0- no metastasis to distant organs
M1- metastasis to distant organs
Management of anal fissure
Management of an acute anal fissure (< 6 weeks)
dietary advice: high-fibre diet with high fluid intake
bulk-forming laxatives are first line - if not tolerated then lactulose should be tried
lubricants such as petroleum jelly may be tried before defecation
topical anaesthetics
-analgesia
topical steroids do not provide significant relief
Management of a chronic anal fissure (> 6 weeks)
the above techniques should be continued
topical glyceryl trinitrate (GTN) is first line treatment for a chronic anal fissure
if topical GTN is not effective after 8 weeks then secondary referral should be considered for surgery or botulinum toxin
Risk factors for pancreatitis
SINED
Smoking Inflammation (e.g. chronic pancreatitis) Nutrition: high fat diet Ethanol Diabetes Mellitus
Causes of acute pancreatitis
I GET SMASHED
Idiopathic Gallstones Ethanol Trauma Steroids Mumps and other infections (e.g. Coxsackie virus) Autoimmune: e.g. PAN Scorpion bite Hyperlipidaemia/hypercalciaemia ERCP Drugs: thiazides, azathioprine
Causes of chronic pancreatitis
AGITS
Alcohol (70%)
Genetic: CF, HH
Immune: lymphoplasmacytic sclerosing pancreatitis
Triglycerides: high levels
Structural: Obstruction by tumour, pancreas divisum
Presentation of chronic cholecystitis
Flatulant dyspepsia. So you get: Bloating and distension Vague upper abdominal discomfort Nausea Flatulence and burping Symptoms exacerbated by fatty foods
Causes of obstructive jaundice
Stones
Cancer of head of the pancreas
Other:
LNs at porta hepatis: TB, Ca
Inflammatory: PBC, PSC
Drugs: OCP, sulfonylureas, flucloxacillin
Neoplastic: Cholangiocarcinoma
Mirizzi’s syndrome: gallstone becomes impacted in the cystic duct or neck of the gallbladder causing compression of the common bile duct (CBD) or common hepatic duct.
Courvoiser’s law
In the presence of a painless obstructive jaundice, a palpable gallbladder is unlikely to be due to stones
Presentation of pancreatic Ca
Male of 60
Painless obstructive jaundice
Epigastric pain radiating to back relieved by sitting forward
Weight loss, reduced appetite, malabsoprtion
Acute pancreatitis
Sudden onset DM in the elderly
Usual pathology of pancreatic cancers
Ductal adenocarcinomas (in head of the pancreas)
Definition of a hernia
Protrusion of a viscus or part of a viscus through the walls of its containing cavity into an abnormal position
Cause of bowel obstruction
Non-mechanical (paralytic ileus) Post op Inflammation e.g. peritonitis, pancratitis Drugs: Anti-MAch Mesenteric ischaemia Metabolic: low K, Na, Mg or uraemia
Mechanical Intra luminal:
Impacted matter e.g. faeces, worms
Intussusception
Gallstones
Mechanical intramural:
Benign stricture e.g. due to IBD, surgery, ischaemic colitis, diverticulitis, radiotherapy
Neoplasia
Congenital atresia
Mechanical extramural : Hernia Adhesions Volvulus (usually sigmoid) Extrinsic compression e.g. tumour, pseudocyst, abscess, haematoma
Definition of a diverticulum
Outpouching of tubular structure
Dukes staging of colorectal cancer
A: Confined to the bowel wall
B: Through the bowel wall but no LNs
C: Regional LNs
D: Distant lymph nodes
TNM staging of colorectal cancer
Tis: carcinoma in situ
T1: Tumour has invaded the submucosa
T2: tumour has invaded the muscularis propria
T3: Tumour has invaded the subserosa
T4: Tumour has invaded through the serosa to the adjacent organs
N1: 1-3 nodes
N2: 4 or more nodes
M0
M1
What is a Hartman’s procedure
A proctosigmoidectomy or Hartmann’s procedure is the surgical resection of the rectosigmoid colon with closure of the anorectal stump and formation of an end colostomy.
Features of familial adenomatous polyposis
Autosomal dominant inheritance
APC gene on 5q21
Affected individuals have 100-1000s of adenomas by age 16
100% develop CRC by age 40
May also have hypertrophy of the retinal pigment epithelium
Features of Peutz-Jegher’s syndrome
Autosomal dominant inheritance
STK11 mutation
Present at 10-15 years
Mucocutaneous hyperpigmentation appearing as macules on palms and buccal mucosa
Multiple GI harmartomatous polyps. Can cause intussusception and haemorrhage
Increased cancer risk: CRC, pancreas, breast, lung, ovarian, uterus
Management of familial adenomatous polyposis
Prophylactic colectomy by age 20:
Colectomy with ileorectal anastamosis: requires life long stump surveillance.
Proctocolectomy plus ileal pouch anal anastamosis: still requires surveillance for gastric and duodenal Ca (endoscopy)
Features of hereditary non-polyposis colorectal cancer
Autosomal dominant
Most common inherited CRC
Mutation of mismatch repair gene
Presentation of mesenteric ischaemia
Nearly always small bowel Triad of: Acute severe abdominal pain with/wo PR bleed Rapid hypovolaemia leading to shock No abdominal signs
Possible AF
Degree of illness is greater than the clinical signs
Gasless abdomen on AXR
Thumprinting on AXR
Raised Hb, amylase, WCC and lactate
Management of mesenteric ischaemia
Fluids Abx: Cef and met NBM LMWH Laparotomy to resect necrotic bowel
Boundaries of the inguinal ligament
The anterior wall is formed by the aponeurosis of the external oblique, and reinforced by the internal oblique muscle laterally.
The posterior wall is formed by the transversalis fascia.
The roof is formed by the transversalis fascia, internal oblique and transversus abdominis.
The floor is formed by the inguinal ligament (a ‘rolled up’ portion of the external oblique aponeurosis) and thickened medially by the lacunar ligament.
Difference between indirect and direct inguinal hernia
Indirect: The peritoneal sac enters the inguinal canal via the deep inguinal ring. Degree to which it herniates depends on the amount of processus vaginalis still present. Sac will have the same 3 coverings as the canal. It enters the canal lateral to the epigastric vessels. Patients usually younger.
Direct: Due to weakening of the abdominal muscles. The periotoneal sac bulges into the canal via the posterior wall (formed by the transversalis fascia) through Hesselbach’s triangle. The sac enters the inguinal canal medial to epigastric vessels.
Boundaries of Hesselbach’s triangle
Medial border: Lateral margin of the rectus sheath, also called linea semilunaris
Superolateral border: Inferior epigastric vessels
Inferior border: Inguinal ligament, sometimes referred to as Poupart’s ligament
Mnemonic RIP (Rectus sheath (lateral border), Inferior epigastric artery, Poupart’s ligament (inguinal ligament)).
Complications of inguinal hernias
Early: Haematoma formation Intraabdominal injury Infection Urinary retention
Late
Recurrence
Ischaemic orchitis
Chronic groin pain
Presentation of femoral hernia
Painless groin lump inferior and lateral to the pubic tubercle
Cough impulse
Often irreducible due to tight borders
Commonly present with obstruction/strangulation:
Tender, red, hot
Abdo pain, distension, vomiting, constipation
50% strangulate within 1 month (urgent surgery)
Diverticulae are most commonly found in which part of the bowel
Sigmoid colon
Important complications following thyroid surgery
Anatomical such as recurrent laryngeal nerve damage.
Bleeding. Owing to the confined space haematoma’s may rapidly lead to respiratory compromise owing to laryngeal oedema.
Damage to the parathyroid glands resulting in hypocalcaemia.
Signs of a basal skull fracture
Battle’s sign – bruising of the mastoid process of the temporal bone.
Raccoon eyes – bruising around the eyes, i.e. “black eyes”
Cerebrospinal fluid rhinorrhea.
Cranial nerve palsy.
Bleeding (sometimes profuse) from the nose and ears.
Hemotympanum.
Conductive or perceptive deafness, nystagmus, vomitus.
Describe the modified Glasgow score (pancreatitis severity)
The Modified Glasgow Score is calculated to predict the severity of pancreatitis. Three or more of the following factors identified within 48 hours of onset indicates severe pancreatitis.
Pa02 <8kPa Age >55 years Neutrophilia WBC >15x10^9 Calcium <2mmol/L Renal function Urea >16mmol/L Enzymes LDH >600 ; AST >200 Albumin <32g/L Sugar Blood glucose >10mmol/L
What is Rovsing’s sign?
Rovsing’s sign is positive if palpation of the left lower quadrant of the abdomen increases the pain felt in the right lower quadrant.
This may be an indicator of appendicitis, although it is not positive in all cases.
Colorectal cancer:
Who should undergo foecal occult blood testing
NHS now has a national screening programme offering screening every 2 years to all men and women aged 60 to 74 years. Patients aged over 74 years may request screening.
In addition FOBT should be offered to:
patients >= 50 years with unexplained abdominal pain OR weight loss
patients < 60 years with changes in their bowel habit OR iron deficiency anaemia
patients >= 60 years who have anaemia even in the absence of iron deficiency
Grading system for internal haemorrhoids
Grade I Do not prolapse out of the anal canal
Grade II Prolapse on defecation but reduce spontaneously
Grade III Can be manually reduced
Grade IV Cannot be reduced
What is the pectinate line
The pectinate line (dentate line) is a line which divides the upper two thirds and lower third of the anal canal. Developmentally, this line represents the hindgut-proctodeum junction.
Haemorrhoids above are internal, below are external.
Lymph drainage: above is internal iliac lymph nodes, below is superficial inguinal lymph nodes.
Arteries: above is superior rectal artery, below is middle and inferior rectal arteries
Borders of the anterior triangle of the neck
Superior: inferior border of the mandible
Lateral: Sternocleidomastoid
Medial: Imaginary sagittal line down midline of the body
Causes of lumps in the anterior triangle of the neck
Pulsatile
Carotid artery aneurism
Tortuous carotid artery
Carotid body tumour
Non-pulsatile Goitre Branchial cysts Laryngocele Parotid tumour (lump in postero-superior area)
Borders of the carotid triangle of the neck
Superior: posterior belly of the digastric muscle
Lateral: Medial border of the sternocleidomastoid muscle
Inferior: Superior belly of the omohyoid muscle
Main contents of the carotid triangle of the neck
Common carotid artery (and its bifurcation)
Internal jugular vein
Hypoglossal nerve
Vagus nerve
Borders of the submandibular triangle
Superiorly: Body of the mandible.
Anteriorly: Anterior belly of the digastric muscle.
Posteriorly: Posterior belly of the digastric muscle.
Contents of the submandibular triangle
Salivary gland
Lymph nodes
Facial artery
Facial vein
Causes of lumps in the submandibular triangle
Salivary stone
Sialadenitis
Salivary tumour
Borders of the posterior triangle of the neck
Anterior: Posterior border of the sternocleidomastoid
Posterior: Anterior border of the trapezius muscle.
Inferior: Middle 1/3 of the clavicle.
Contents of the posterior triangle of the neck
External jugular vein (within the posterior triangle it empties into the subclavian vein.
The distal part of the subclavian artery
Accessory nerve
The cervical plexus forms within the muscles of the floor of the posterior triangle (it forms the phrenic nerve)
The trunks of the brachial plexus cross the floor of the posterior triangle
Causes of lumps in the posterior triangle
Cervical ribs LNs Pharyngeal pouch Cystic hygromas Pancoast's tumour
Causes of midline lumps
<20yrs
Thyroglossal cyst
Dermoid cyst
> 20yrs
Thyroid isthmus mass
Ectopic thyroid tissue
A cystic hygroma is…
Usually congenital Multiloculated lesion Contains lymph Benign but disfiguring Usually occurs in left posterior triangle of neck and armpits
Presentation of branchial cysts
Usually present before 20yrs
Lump along the anterior border of the sternocleidomastoid (junction of middle and upper third)
Can become infected and form an abscess
May be associated with a branchial fistula (may discharge mucus)
Lining and content of a branchial cyst
Squamous epithelium
Granular and keratinaceous cellular debris. Cholesterol crystals may be found in the fluid extracted from a branchial cyst.
Presentation of carotid body tumour
Located at carotid body bifurcation
Just anterior to upper 3rd if sternocleidomastoid
Pulsatile
Moves laterally but not vetically
Pressure may cause dizziness and syncope
Most are benign
Doppler or angiogram will show splaying of the carotid artery bifurcation
Treatment of carotid body tumour
Complete surgical removal
What is a laryngocele
Lump in the anterior triangle of the neck
Cystic dilation of the laryngeal saccule
Cogenital usually but can be acquired e.g. glassblowers
Exacerbated by blowing
Presentation of a laryngocele
Lump in the anterior triangle of the neck
Symptoms vary accordingly to the size and extension of the lesion, and may include: sore throat, dysphagia, stridor, neck lump, and/or airway obstruction.
Presentation of dermoid cyst
Common <20yrs
Found at junctions of embryological fusion e.g. neck midline and under tongue
Contains ectodermal elements e.g. hair follicles and sebaceous glands
Contents of dermoid cyst
Contains ectodermal elements e.g. hair follicles and sebaceous glands
What is a dermoid cyst
A developmental inclusion of epidermis along lines of skin fusion
What is a thyroglossal cyst
Cyst formed from persistant thyroglossal duct
Presentation of thyroglossal cyst
Located anywhere from foramen caecum and the thyroid.
Usually found just inferior to the hyoid or just above the hyoid
Fluctuant lump (sign it contains fluid)
Moves up and down with tongue protrusion
Usually asymptomatic but can cause dysphagia or pain.
Can become infected and form a fistula
Treatment of thyroglossal cyst
Surgical excision of the cyst and the thyroglossal duct.,
Presentation of cervical ribs
Mostly asymptomatic
Hard swelling
Reduced radial pulse on abduction and external rotation of arm
Vascular symptoms: Compress subclavian artery causing:
Raynaud’s
Venous outflow obstruction leading to oedema
Neuro symptoms: compress lower trunk of brachial plexus, or T1 nerve root causing:
Wasting of intrinsic hand muscles
Parasthesia along medial border of the arm
Presentation of pharygeal pouch
Swelling of left side of the neck Regurgitation and aspiration Halitosis Gargling sounds Food debris causes pouch expansion which causes oesophageal compression which in turn causes dysphagia
Birds beak appearance on barium swallow
Treatment of pharyngeal pouch
Excision and cricopharyngeal myotomy
Endoscopic stapling
Presentation of cystic hygroma
Infants
Lower part of posterior triangle but may extend to axilla
Increases in size when the child coughs or cries
Transilluminates brilliantly
Key features to mention when describing cervical lymphadenopathy
Consistency Number Fixation Symmetry Tenderness
Features to assess in a neck lumo
Size – width / height / depth
Location – can help narrow the differential – anterior triangle / posterior triangle / mid-line
Shape – well defined?
Consistency – smooth / rubbery / hard / nodular / irregular
Fluctuance – if fluctuant, this suggests it is a fluid filled lesion – cyst
Trans-illumination – suggests mass is fluid filled – e.g. cystic hygroma
Pulsatility – suggests vascular origin – e.g. carotid body tumour / aneurysm
Temperature – increased warmth may suggest inflammatory / infective cause
Overlying skin changes – erythema / ulceration / punctum
Relation to underlying / overlying tissue – tethering / mobility (ask to turn head)
Auscultation – to assess for bruits – e.g. carotid aneurysm
Causes of cervical lymphadenopathy
LIST
Lymphoma and leukaemia
Infection
Sarcoidosis
Tumours
Infective causes of cervical lymphadenopathy
Bacterial:
TB
Tonsillitis, dental abscess
Bartonella henselae (cat scratch disease)
Viral:
EBV
HIV
Protazoal:
Toxoplasmosis (HIV related)
Causes of thyroid goitre (separate diffuse, multinodular and solitary nodule)
Diffuse:
Simple colloid goitre: endemic (iodine deficiency)
Simple colloid goitre: Sporadic: autoimmune, hereditary, goitrogens (e.g. sulphonylureas, lithium)
Graves
Thyroiditis: Hashimoto’s, De Quervain’s Subacute lymphocytic (e.g. post-partum)
Multinodular with nodules too small to feel
Multinodular
Multinodular colloid goitre (commonest)
Multiple cysts
Multiple adenomas
Solitary Nodule: Dominant nodule in multinodular goitre Adenoma (hot or cold) Cyst Malignancy
Common cause of De Quervain’s thyroiditis
Coxsackie virus
Most common thyroid malignancy type
Papillary
Thyroid malignancy associated with MEN2
Medullary
Tumour cell origin in medullary thyroid cancer
Parafollicular C cells
Role of parafollicular C cells
Secrete calcitonin
Risk factors for malignancy in thyroid nodules
Solitary Solid Young Male Cold Radiation exposure
Complications of thyroid surgery
Early:
Reactionary haemorrhage causing haematoma (can cause airway obstruction)
Laryngeal oedema: due to damage during intubation or surgical manipulation. Can also cause airway obstruction
Recurrent laryngeal nerve palsy
Hypocalcaemia
Thyroid storm
Late:
Hypothyroidism
Recurrent hyperthyroidism
Keloid scar
Causes of salivary gland enlargement (whole and localised)
Whole gland: Parotitis Sjogren's Sarcoid Amyloid ALL Chronic liver disease Anorexia or bulimia
Localised:
Tumours
Stones
Causes of acute parotitis
Viral: mumps, coxsackie A, HIV
Bacterial: S. Aureus (associated with calculi and poor oral hygeine)
Complications of mumps
Inflammation of the testicles (orchitis) in males who have reached puberty; rarely does this lead to fertility problems
Encephalitis
Meningitis
Oophoritis, mastitis
Deafness
Presentation of salivary gland calculi
Recurrent unilateral swelling and pain
Worse on eating
Red, tender swollen gland
80% are submandibular
Treatment of salivary gland calculus
Gland exision
Investigations in suspected salivary gland calculus
Plain X-ray
Saliography (contrast injected into salivary gland)
Components of Reynolds pentad
Fever RUQ pain Jaundice Shock Altered mental status
Lead pipe colon on abdo X ray is caused by…
Ulcerative colitis
Phyllodes tumour
Stromal tumour
Breast
Large non-tender mobile lump
50% of breast cancers are in which quadrant?
Upper outer
TNM classification of breast cancer
Tis means ductal carcinoma in situ (DCIS)
T1 means that the tumour is 2 centimetres (cm) across or less.
T2: 2-5cm with skin fixation
T3: 5-10cm with ulceration and pectoral fixation
T4: >10cm chest wall extension, skin involved
N1 mobile nodes
N2 Fixed nodes
Clinical staging of breast cancer
1: Confined to breast, mobile, no LNs
2: Stage 1 plus nodes in ipsilateral axilla
3: Stage 2 plus fixation to muscle (not chest wall). LNs matted and fixed, large skin involvement
4: Complete fixation to chest wall
Management of stage 2 breast cancer
WLE and radiotherapy
1st line treatment of mastalgia
Evening primrose oil
Side effects of tamoxifen
Menopausal symptoms
Endometrial Ca (as it is a SERM that acts as an agonist in the uterus)
Venous thromboembolism
Side effects of anastrazole
Menopausal symptoms
Key features of acute mastitis
Usually lactating woman
Painful red breast
May lead to abscess (lump near nipple)
Treatment of acute mastitis
Flucloxacillin
Add incision and drainage if fluctuant abscess present
Key features of fat necrosis breast lump
Associated with previous trauma Painless Palpable Non-mobile May calcify simulating Ca
Treatment of fat necrosis breast lump
Analgesia
Features of duct ectasia
Age 50-60 (post menopausal) Slit like nipple Often bilateral Peri-areolar mass MAY be present Thick white/green discharge May be calcified on mammography Usually painless
Ducts shorten and widen with age. Discharge produced which can get trapped and irritate the ducts.
Minimum age for mammography
35 years
Treatment of duct ectasia
Distinguish from Ca
Surgical excision of the duct if mass is present or discharge is troublesome
Features of periductal mastitis
Painful erythematous sub-areaolar mass
Associated with purulent discharge and inverted nipple
May lead to abscess or discharging fistula
Features of fibroadenosis
Pre-menstrual breast nodularity and pain
Often in upper outer quadrant
Tender “lumpy bumpy” breasts
Treatment of fibroadenosis
Triple assessment
Reassurance
Good bra
Can also recommend evening primrose oil
Features of cyclical mastalgia
Under 35 years
Premenstrual pain
Relieved by menstruation
Commonly in upper outer quadrants bilaterally
Features of non-cyclical mastalgia
Over 45 years
Severe lancing breast pain (often left)
May be associated with back pain
Management of mastalgia
Reassurance and good bra (works for most)
1st line medication is evening primrose oil
OCP
Topical NSAIDs
Bromocriptine
Danazol
Tamoxifen
Treatment of stage 3-4 breast cancer
Tamoxifen if ER positive
Chemo for relapse
Her2+ve may respond to trastuzumab
Supportive:
Bone pain: dexamethasone , bisphosphonates, analgesia
Brain: occasional surgery, dexamethasone, steroids, antiepileptic drugs.
Lymphoedema: decongestion, compression
Breast surgery: muscles used for flaps in reconstruction
Latissimus dorsi
Tranverse rectus abdominus muscle (gold standard). No implant necessary and combined tummy tuck.
Types of breast cancer
DCIS/LCIS
Invasive ductal carcinoma: commonest (feels hard)
Medullary: younger pts, feels soft
Colloid/mucinous: occur in elderly
Inflammatory: pain, erythema, swelling, peau d’orange
Papillary
Features of fibroadenoma
Commonest benign tumour Under 35 years Rare post menopause Increased rate in blacks PAINLESS rubbery mobile mass Often multiple and bilateral Popcorn calcification
Features of DCIS of the breast
Microcalcifications on mammogram
Rarely associated with symptoms
Increased cancer risk in ipsilateral breast
Ca rate 1%/year
Features of Paget’s disease of the breast
Unilateral Scaly Erythematous Itchy Possible palpable mass Usually caused by underlying invasive or DCIS breast cancer
Features of LCIS
Incidental biopsy finding (no calcifations)
Often bilateral (20-40%)
Young women
Increased cancer risk in both breasts
Signs/symptoms of critical limb ischaemia
Rest pain:
Especially at night
Usually felt in the foot
Pt hangs foot out of bed: due to reduced cardiac output and loss of gravity help
Ulceration
Gangrene
Features of Leriche’s syndrome
Caused by atherosclerotic occlusion of abdominal aorta and iliacs
Triad of:
Buttock claudication and wasting
Erectile dysfunction
Absent femoral pulses
Signs of chronic limb ischaemia
Pulses: reduced pulses and increased cap refill time Ulcers: painful, punched out, on pressure points Nail dystrophy/ oncholysis Skin: pale, cold, absent hair, atrophy Venous guttering Muscle atrophy Buerger's angle \+ve Buerger's sign
Normal Buerger’s angle
Greater than or equal to 90 degrees
Note: <20 indicates severe ischaemia
What is venous guttering?
Elevating the legs empties the foot veins which later re-fill when the legs are dependent. In an ischaemic limb, the response to the postural change is delayed, and for a time, the veins remain collapsed. The time necessary for the “gutter” to fill up is an indication of the severity of the arterial insufficiency.
Fontaine classification of chronic limb ischaemia
1: asymptomatic (subclinical)
2a: Intermittent claudication >200m
2b: Intermittent claudication <200m
3: Ischaemic rest pain
4: Ulceration/gangrene
Rutherford classification of chronic limb ischaemia
Stage 0 - Asymptomatic
Stage 1 - Mild intermittent claudication
Stage 2 - Moderate intermittent claudication
Stage 3 - Severe intermittent claudication
Stage 4 - Ischaemic rest pain
Stage 5 - Ischemic ulceration not exceeding ulcer of the digits of the foot
Stage 6 - Severe ulceration or frank gangrene
Doppler wave forms in chronic limb ischaemia
Normal: Triphasic
Mild stenosis: Biphasic
Severe stenosis: Monophasic
Interpretation of ankle brachial pressure index
> 1.2 Abnormally hard vessel (e.g. calcified) – this can often be a false negative as there is likely significant peripheral vascular disease but the hardened vessels give a higher ABPI reading, so correlation with clinical findings is advised.
1.0-1.2 Normal
0.8-0.9 Mild arterial disease: mild claudication
0.5-0.79 Moderate arterial disease: severe claudication
<0.5 Severe arterial disease: rest pain, ulceration and gangrene (critical ischaemia)
Cause of falsely high ABPI measurement
Vessel calcification due to DM or CRF
Management of chronic limb ischaemia
Conservative: Stop smoking Exercise and exercise programs Weight loss Foot care
Medical: Manage risk factors e.g. BP, lipids, DM Antiplatelets: aspirin/clopidogrel Analgesia: opitates may be needed Parenteral prostanoids if unfit for surgery
Surgical:
Percutaneous transluminal angio and stent
Bypass: fem-pop, fem-distal, aortobifemoral
Endarterectomy
Amputation
Presentation of acute limb ischaemia
6Ps
Pallor Pain Perishingly cold Pulseless Parasthaesia Paralysis
Most cases of acute limb ischaemia are caused by…
Thrombosis in situ. Previously stenosed vessel with olaque rupture
If acute limb ischaemia is caused by an embolus the clot most likely originated in…
The LA due to AF
Typically lodge at femoral bifurcation.
Note: Often complete ischaemia
Acute limb ischaemia: differences between thrombus and embolus
Onset: Thrombus is days/hours. Embolus is sudden
Severity: Embolus is more severe, often complete ischaemia. Thrombus will have collaterals to reduce severity.
Claudication history present in thrombosis. Absent if embolus.
Diagnosis of embolus will be clinic, thrombus will be angio
Treatment: Embolus requires embolectomy and warfarin. Thrombus requires thrombolysis and bypass surgery.
Management of acute limb ischaemia
Contact senior
NBM
Rehydrate: IV fluids
Analgesia: morphine and metoclopramide
Antibiotics: if signs of infection.(co-amoxiclav is an option)
Unfractionated heparin IV infusion: to prevent extension
If complete occlusion: urgent surgery
If incomplete: angiogram and observe for deterioration
Complications post embolectomy
Reperfusion injury:
Local swelling causing compartment syndrome
Acidosis and arrhythmia secondary to high K
ARDS
GI oedema causign endotoxic shock
Chronic pain
Management of carotid artery disease
Conservative
Aspirin or clopidogrel
Control risk factors
Surgical: Carotid endarterectomy if
Symptomatic and stenosis>70%
Symptomatic and stenosis>50% and low risk (typically <75yrs)
Asymptomatic and stenosis >60% and low risk (benefit if low risk)
Stenting: biggest benefit over CEA is in younger pts
shorter IP stay, reduced infection risk, reduced CN injury risk. No sig diff in mortality. Increased stroke risk especially in older patients.
Complications of carotid endarterectomy
Stroke Death HTN Haematoma MI Nerve injury: hypoglossal, great auricular (numb ear lobe), recurrent laryngeal
Definition of an aneurysm
Abnormal dilatation of a blood vessel >50% of its diameter.
True= all layers. Saccular (Berry aneurism) and fusiform (AAA),
False= Collection of blood around a vessel wall that communicates with the vessel lumen
False aneurisms are usually caused by
Iatrogenic. e.g. puncture, cannulation
Presentation of popliteal aneurism
Easily palpable popliteal pulse
50% bilateral
Rupture is rare
Main complications are thrombosis and distal ischaemia causing acute limb ischaemia
Management of stable popliteal aneurism
Elective grafting or tie off vessel
Management of acute (unstable) popliteal aneurism
Embolectomy or fem-distal bypass
Definition of a AAA
Dilation of the aorta of at least 3cm
90% infrarenal
30% involve iliacs
Presentation of AAA
Incidental finding Rupture Back pain or umbilical pain radiating to groin Acute limb ischaemia Blue toe: due to distal embolisation
Expansile mass just above umbilicus
Bruits
Tenderness and shock if rupture
Gold standard investigation for AAA
CT/MRI
Indications for surgery in AAA
Symptoms e.g. back pain
Diameter above 5.5cm
Rapidly expanding: >1cm/yr
Complications e.g. emboli
How often to image (CT/US) a AAA
Yearly if <4cm
6-monthly if 4-5.5cm
Advantage of EVAR over open AAA repair
Reduced perioperative mortality
AAA screening in UK
One off US at age 65yrs. MEN ONLY
Risk factors for AAA rupture
Size. >6cm=25% mortality/yr High BP Smoker Female Strong family history
Management of ruptured AAA
High flow O2
2 large bore canulae in each ACF: give fluid but keep SBP under 100mmHg
O neg blood if desperate
Bloods: FBC. U+E, Clotting, amylase, Xmatch 10 units
Major haemorrhage protocol
Call vascular surgeon, anaesthetist and warn theatre
Analgesia
Abx prophylaxis; cef and met
Urinary catheter
CVP line
US or CT if stable and diagnosis uncertain
Take to theatre: clamp neck and insert dacron graft
What is a Type A aortic dissection
Involves ascending and descending aorta
Note: higher mortality likely due to cardiac involvement.
Usually require surgery
Makes up 70% of thoracic aorta dissection
What is a type B aortic disection
Involves only descending aorta distal to left subclavian artery (so below the aortic arch).
Management of gas gangrene
Hyperbaric O2
Debridement
Ben Pen and metronidazole
Presentation of gas gangrene
Toxaemia Haemolytic jaundice Oedema Crepitus from surgical emphysema Bubbly brown pus
Causes of varicose veins
Primary: Prolonged standing OCP Pregnancy Obesity FH
Secondary: Valve destruction causing reflux e.g. DVT Obstruction: DVT, foetus, pelvic mass Constipation AVM Overactive pumps e.g. cyclists
3 mains sites of varicose veins
SPJ: popliteal fossa
SFJ: 3cms below and 3cm lateral to pubic tubercle
Perforators draining the GSV: 3 medial calf and 1 medial thigh
Presentation of varicose veins
Signs: Bleeding Cosmetic defect Ulcers (medial malleolus/gaiter area) Oedema Thrombophlebitis Swelling Skin changes
Symptoms:
Pain, cramping, heaviness
Tingling
Swelling
Skin changes caused by varicose veins
Venous stars Haemosiderin deposition Venous eczema Lipodermatosclerosis Atrophie blanche
Investigations in varicose veins
Duplex ultrasound to see:
Anatomy
Presence of incompetence
Caused by obstruction or reflux
Indications for varicose vein surgery
SFJ incompetence
Major perforator incompetence
Symptoms e.g. ulcers, skin changes, pain
Complications post varicose vein surgery
Haematoma (esp groin) Wound sepsis Damage to cutaneous nerve (esp long saphenous which passes down gaiter region) Superficial thrombophlebitis DVT Recurrence
Varicose vein surgery post op management
Bandage tightly
Elevate for 24h
Discharge with compression stockings
Encourage daily walks
Features of venous leg ulcers
Painless, sloping shallow ulcers
Ragged edges
Gaiter region/ medial malleolus
Surrounding skin changes: haemosiderin deposition and lipodermatosclerosis.
Risk factors for venous leg ulcers
Venous insufficiency
Varicosities
DVT
Obesity
Features of arterial leg ulcers
Painful
Deep
Punched out lesions
Reduced pulses and other signs of chronic leg ischaemia
Occur at pressure points e.g. heel, tips of and between toes, metatarsal heads
Features of neuropathic ulcers
Painless
Insensate surroundign skin
Warm foot with good pulses
Most common type of leg ulcer
Venous
Marjolin’s ulcer is a form of which cancer type?
Squamous cell
Complications of leg ulcers
Osteomyelitis
Development of squamous cell carcinoma in the ulcer (Marjolin’s ulcer)
Management of venous leg ulcer
Refer to community leg ulcer clinic
Analgesia
Bed rest and elevate leg
Graduated compression bandage
Venous surgery
Optimise risk factors e.g. smoking, nutrition, weight
Oral pentoxyfylline (unlicensed indication)
Other:
Desloughing e.g. larval therapy
Topical antiseptics
Features of duct papilloma (breast)
Usually present with nipple discharge
Large papillomas may present with a mass
The discharge usually originates from a single duct
No increase risk of malignancy
Causes of urethral stricture
Trauma e.g. instrumentation/pelvic fracture
Infection: e.g. gonorrhoea
Chemotherapy
Balanitis xerotica obliterans
Presentation of urethral stricture
Hesitancy
Terminal dribbling
Poor stream
Strangury: frequent, small, urgent, incomplete (perception) urination
Pis en duex: urge to urinate soon after voiding
Management of urethral stricture
Dilatation
Stent
Internal urethroplasty
Causes of urinary retention
Obstrutive mechanical: BPH Stricture Clots Stone Constipation
Obstructive dynamic: Increased smooth muscle tone (a-adrenergic)
Post operative pain
Drugs: Phenylephrine, midodrine, metaraminol (short half life)
Neurological: Interruption of sensory or motor innervation Pelvic surgery MS Diabetes mellitus Spinal injury/compression
Myogenic: Over-distension of the bladder
Post anaesthesia
High alcohol intake
Presentation of acute urinary retention
Suprapubic tenderness
Palpable bladder: dull to percussion, can’t get beneath it
Large prostate on PR (need to check anal tone and sacral sensation)
Less than 1L drained on catheterisation
Management of acute urine retention
Conservative: Analgesia Privacy Running water or hot bath Walking
Catheterisation:
Cover with STAT gent
Tamsulosin reduces risk of recatheterisation after retention
TWOC after 24-72hrs
Surgical: TURP if BPH is the cause
If failed TWOC, low RF
Elective procedure
Classification of chronic urinary retention
High pressure: High detrusor pressure at end of micturition
Low pressure: Low detrusor pressure at end of micturition
Causes of high pressure chronic urinary retention
Usually a bladder outflow obstruction
Presentation of chronic urinary retention
Painless Insidious as bladder capacity grows to above 1.5L Overflow incontinence Nocturnal enureses Hydrnephrosis/RF if high pressure Lower abdominal mass UTI
Management of high pressure chronic urinary retention
Catheterise if renal impairment, pain or infection
Hourly urine output and replace: risk of post obstruction diuresis (lose Na and HCO3)
Consider TURP before TWOC
Management of low pressure chronic urinary retention
Avoid catheterisation if possible as risk of introducing infection
Early TURP:
Often do poorly because of poor detrusor function
May need permanent catheter or self-catheterisation
Causes of false haematuria
Rifampicin
Beetroot
PV bleed
Porphyria
Gold standard test for kidney stone
Spiral non-contrast CT-KUB
Kidney stones usually made of…
Calcium oxalate
Imaging used in suspected kidney stone
Spiral CT-KUB without contrast (gold standard, 99% of stones visible)
IVU: dense nephrogram, clubbing of calyces, Failure of flow to the bladder, Standing column of contrast
USS: hydronephrosis
KUB XR
Foods that increase kidney stone risk
High oxalate foods:
Chocolate
Tea
Strawberries
Indications for active kidney stone removal
Low likelihood of spontaneous passage e.g. stone over 10mm
Persistent obstruction
Renal insufficiency
Infection
Initial management of kidney stone
Analgesia: diclofenac 75mg PO/IM or 100mg PR
Opioids if NSAIDS CI
Fluids: IV if unable to tolerate PO
Abx if infection e.g. cefuroxime
Conservative management of kidney stones likely to be successful if…
Stone is <5mm and in lower 1/3 of ureter (or lower)
Presentation of kidney stones
Ureteric colic:
Severe loin pain radiating to the groin
Associated with N&V
Pt cannot lie still
Bladder or urethral obstruction:
Bladder irritability: freq, dysuria, haematuria
Strangury
Suprapubic pain radiating to tip of penis or in labia
Pain and haematuria worse at end of micturition
O/e: haematuria, usually no loin tenderness
Presentation of renal cell carcinoma
50% are incidental
Tirad of: Haematuria, loin pain, loin mass
Systemic: anorexia, malaise, fatigue, weight loss, PUO
Clot retention
Invasion of L renal vein causes varicocele
Cannonball mets causing SOB
Paraneoplastic features
Hormones produced by renal cell cancers
EPO
PTHrP
Renin
ACTH
Also can cause Amyloidosis
Presentation of transitional cell carcinoma (renal)
Painless haematuria
Frequency, urgency dysuria
Urinary tract obstruction
Risk factors for renal cell cancer
Obesity Smoking HTN Dialysis Genetics
Risk factors for renal transitional cell cancer
Smoking
Amine exposure (rubber industry)
Cyclophosphamide
Presentation of bladder cancer
Painless haematuria
Voiding irritability, frequency, urgency
Recurrent UTIs
Retention and obstructive renal failure
Palpable bladder mass, palpable liver and anaemia on examination
All mouth ulcers persisting for greater than….should be sent to oral surgery as a 2 week wait referral.
3 weeks
A cholesteatoma is…
A cholesteatoma consists of squamous epithelium that is ‘trapped’ within the skull base causing local destruction. It is most common in patients aged 10-20 years.
Main features
foul smelling discharge
hearing loss
Other features are determined by local invasion:
vertigo
facial nerve palsy
cerebellopontine angle syndrome
Otoscopy
‘attic crust’ - seen in the uppermost part of the ear drum
Management
patients are referred to ENT for consideration of surgical removal
Features of otosclerosis
Otosclerosis describes the replacement of normal bone by vascular spongy bone. It causes a progressive conductive deafness due to fixation of the stapes at the oval window. Otosclerosis is autosomal dominant and typically affects young adults
Onset is usually at 20-40 years - features include: conductive deafness tinnitus normal tympanic membrane* positive family history
