Surgery Flashcards
Pathophysiology of acute pancreatitis
Pancreatic enzymes released and activated-> multi stage process
Oedema + fluid shift + vomiting —> hypovolaemic shock
Enzymes—-> autodigestion
Vessel autodigestion—> retroperitoneal haemorrhage
Inflammation—–> pancreatic necrosis
Implications of pancreatic necrosis
Super-added infection in 50% of patients with necrosis
Epidemiology of acute pancreatitis
1% of surgical admissions
4th and 5th decades
10% mortality
Aetiology of pancreatitis
Idiopathic (?microstones)
Gallstones
Ethanol
Trauma
Steroids
Mumps (+ other infections e.g. Coxsackie B)
Autoimmune: PAN
Scorpion (Trinidadian)
Hyperlipidaemia, Hypercalcaemia, Hypothermia
ERCP
Drugs: thiazides, azathioprine
Severe epigastric pain radiating to the back
May be relieved by sitting forward
Vomiting
?Acute pancreatitis
Raised HR, Raised RR
Fever
Hypovolaemia—> shock
Epigastric tenderness
Jaundice
Ileus (absent bowel sounds)
Ecchymoses
?Acute pancreatitis
Grey turner’s
Flank ecchymoses
Cullen’s
Periumbilical ecchymosis (tracks up falciform)
Grey Turner’s sign
Flank ecchymosis
Acute pancreatitis
Cullens sign
Peri-umbilical ecchymosis
Acute pancreatitis
Ddx for acute pancreatitis
Perforated duodenal ulcer
Mesenteric infarction
MI
Difference between Glasgow and Ranson criteria
Glasgow criteria valid for EtOH and gallstones
whereas Ranson only applicable to Etoh and can only be fully applied after 48 hours
Components of modified glasgow score
PANCREAS
PaO2 <8kPA
Age >55
Neutrophils >15 x 10^9
Ca <2mM
Renal function, U >16mM
Enzymes: LDH >600iu/L, AST >200 iu/L
Albumin <32 g/L
Sugar >10mM
Modified Glasgow criteria cut offs
1= mild
2= moderate
3= severe
Ix in acute pancreatitis and what would be seen
Bloods
Bloods:
FBC- raised WCC
Raised amylase (>1000/3x ULN) and raised lipase
U+Es: dehydration and renal failure
LFTs: cholestatic picture, raised AST, raised LDH
Ca: reduced
Glucose: raised
CRP: monitor progress, >150 after 48 hours= severe
ABG: reduecd O2 suggests ARDS
Ix in acute pancreatitis and what would be seen
Urine
Glucose
Raised conjugated bilirubin
Reduced urobiliongen
Ix in acute pancreatitis and what would be seen
Imaging
CXR: ARDS, exclude perforated DU
AXR: sentinel loop, pancreatic calcification
USS: gallstones and dilated ducts, inflammation
Contrast CT: Balthazar severity score
Cut offs for amylase in acute pancreatitis
>1000/ 3xULN
Difference between lipase and amylase
Lipase is more sensitive and speciic
CRP >150 after 48hrs in acute pancreatitis
Severe
What is used to grade severity of pancreatitis on CT?
Balthazar severity score
Complications of acute pancreatitis
Early: systemic
Respiratory: ARDS, pleural effusion
Shock: hypovolaemic or septic
Renal failure
DIC
Metabolic: hypocalcaemia, raised glucose, metabolic acidosis
Complications of acute pancreatitis
Late (>1w)
Pancreatic necrosis
Pancreatic infection
Pancreatic abscess: may form in pseudocyst or in pancreas, may require open or percutaenous drainage
Bleeding: e.g. from splenic artery, may require embolisation
Thrombosis: splenic artery, GDA or colic branches of SMA, may subsequently lead to bowel necrosis. Portal vein, may subsequently lead to portal HTN
Fistula formation: pancreato-cutaneous due to skin breakdown
Def: pancreatic pseudocyst
Collection of pancreatic fluid in the lesser sac, surrounded by granulation tissue
Occurs in 20% especially in EtOHic pancreatitis
4-w after acute attack
Persisting abdominal pain
Epigastric mass-> early satiety
?Pancreatic pseudocyst
Complications of pancreatic pseudocyst
Infection-> abscess
Obstruction of duodenum or common bile duct
Ix in pancreatic pseudocyst
Persistently raised amylase +/- deranged LFTs
USS/CT
Management of pancreatic pseudocyst
<6cm: spontaneous resolution
>6cm:
Endoscopic cyst-gastrostomy
Percutaenous drainage under US/CT
Causes of chronic pancreatitis
AGITS
Alcohol: 70%
Genetic: CF, HH
Immune: lymphoplasmacytic sclerosing pancreatitis (raised IgG4)
TGs raised
Structural: obstruction by tumour, pancreas divisum
Sentinal loop
Focal dilated proximal jejunal loop in the LUQ
Acute pancreatitis
Pancreatic calcification
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 weight loss
(Polyuria and polydipsia)
(Epigastric mass)
Chronic pancreatitis
(DM)
(pancreatic pseudocyst)
Complications of chronic pancreatitis
Pseudocyst
DM
Pancreatic cancer
Pancreatic swelling-> biliary obstruction
Splenic vein thrombosis
Ix in chronic pancreatitis
Raised glucose
Reduced faecal elastase= indicative of reduced exocrine function
LFTs
USS: pseudocyst
AXR: speckled pancreatic clacifications
CT: pancreatic calcifications
Serum amylase in chronic pancreatitis
serum amylase level is not routinely raised, is not diagnostic in chronic pancreatitis, and testing should therefore not be performed.
Px of chronic pancreatitis
1/3rd die within 10y
Conservative management of chronic pancreatitis
No EToH or smoking
Reduced fat and increased carb diet
Medical management of chronic pancreatitis
Analgesia: NSAIDS/paracetamol first line. ?weak opiate (codeine phospohate) if not effective. May need additional pain relief in primary care e.g. coeliac plexus block.
Enzyme supplementation e.g. Creon
Cobalamin/thiamine supplementation
ADEK vitamins
DM Rx
(Octreotide: somatostatin analgoe that inhibits pancreatic enzyme secretions)
Screening in chronic pancreatitis
DM
Osteoporosis
Indications for Surgical Mx of chronic pancreatitis
Unremitting pain
Weight loss
Duct blockage
Surgical options of management of chronic pancreatitis
Distal pancreatectomy: Whipple’s
Pancreaticojejunostomy: drainage
Endoscopic stenting
Monitoring in management of acute pancreatitis
Manage at appropriate level e.g. ITU if severe
Constant reassessment:
Hourly TPR, UO
Daily FBC, U+Es, Ca, glucose, amylase
Medical management of acute pancreatitis
ABC approach
Aggressive fluid resus: keep UO >30ml/h
Catheter+/- CVP
Pancreatic rest:
NBM
NGT if vomiting
TPN may be required
Analagesia:
pethidine or buprenorphine ± intravenous (IV) benzodiazepines. Morphine is relatively contra-indicated because of possible spastic effect on the sphincter of Oddi.
Antibiotics:
Not routinely given, use if suspected infection or before ERCP
Penems often used, but use to treat specific infections
Mx complications
Mx of the complications of acute pancreatitis
ARDS: O2 therapy or ventilation
Raied glucose: insulin sliding scale
Ca
EToH withdrawal: chlordiazepoxide
ERCP use in acute pancreatitis
Diagnostic
Can be used if pancreatitis with dilated ducts secondary to gallstones. ERCP and sphincterectomy -> reduces complications
Indications for surgical management of acute pancreatitis
Infected pancreatic necrosis
Pseudocyst or abscess
Unsure re dx
Operations used in treatment of acute pancreatitis
Laparotomy + necrosectomy (pancreatic debridement)
Laparotomy + peritoneal lavage
Laparostomy: abdomen left open with sterile packs in ITU
Epidemiology of gallstones
~8% of the population >40 years
Incidence increasing
Slight increased incidence in females
90% of gallstones remain asymptomatic
5Fs of gallstones
Fair
Fat
Female
Forty
Fertile
What is the general composition of gallstones
Phopsholipids: lecithin
Bile pigments (broken down Hb)
Cholesterol
What are the relative proportions of the different types of gall stones?
Mixed stones: 75%
Cholesterol stones: 20%
Pigment stones: 5%
What is the aetiology of gallstones
Lithogenic bile: Admirand’s triangle
Biliary sepsis
GB hypomotility-> stasis: pregnancy, OCP, TPN, fasting
What is admirand’s triangle
A delicate balacnce exists between the levels of bile acids, phospholipids and cholesterol
When this balance is disrupted, especially when there is supersaturation with cholesterol, there is predisoposition to the formation of lithogenic bile and the conseuqent development of cholesterol-type gallstones.
This is because when cholesterol supersaturates it tends to crystallise and in the presence of enucleating factors can be a nidus for stone formation
Large often solitary gallbladder stone
Cholsterol
Formation of cholesterol gallstones
According to Admirand’s triangle:
decreased bile salts
decreased lecithin
increased cholesterol
What are the risk factors for the development of cholesterol stones?
Female
OCP/pregnancy
Increasing age
High fat diet + obesity
Racial e.g. American Indian tribes
Loss of terminal ileum (reduction in bile salt reabsorption)
What is the composition of pigment stones in the gall bladder
Calcium bilirubinate
With what are pigment GB stones associated?
Haemolysis
Small, black gritty, fragile GB stones
Pigment stones
Often multiple GB stones with cholesterol as the major component
Mixed stones
What are the complications of gallstones
In the gallbladder:
Biliary colic
Acute cholecystitis +/- empyema
Chronic cholecystitis
Mucocele
Carcinoma
Mirizzi’s syndrome
In the CBD:
Obstructive jaundice
Pancreatitis
Cholangitis
In the gut:
Gallstone ileus
Mirizzi’s syndrome
Mirizzi’s syndrome is a rare complication in which a gallstone becomes impacted in the cystic duct or neck of the gallbladder causing compression of the common bile duct (CBD) or common hepatic duct, resulting in obstruction and jaundice. The obstructive jaundice can be caused by direct extrinsic compression by the stone or from fibrosis caused by chronic cholecystitis (inflammation). A cholecystocholedochal fistula can occur
Pathogenesis of biliary colic
Gallbladder spasm against a stone impacted in the neck of the gallbladder: Hartmann’s pouch
Less commonly, the stone may be in the CBD
What is Hartmann’s pouch?
a spheroid or conical pouch at the junction of the neck of the gallbladder and the cystic duct.
RUQ pain radiating to back (scapular region)
Associated with sweating, pallor, N+V
Attacks may be precipitated by fatty food and last <6h
O/E tenderness in right hypochondrium
(jaundice)
?Biliary colic
(if stone is in the CBD)
DDx for biliary colic
Cholecystitis/other gallstone disease
Pancreatitis
Bowel perforation
Ix in biliary colic
Urine
Same work up as cholecystitis
Urine:
Bilirubin, urobilinogen, Hb
Ix in biliary colic
Bloods
Bloods: FBC, U+E, amylase, LFTs, G+S, clotting CRP
Ix in biliary colic
Imaging
AXR: 10% of gallstones are radio-opaque
Erect CXR: ?perforation
USS:
stones: acoustic shadow
dilated ducts >6mm
Inflamed GB: wall oedema
Indications for MRCP in biliary colic
bile duct dilated and or liver function tests abnormal and USS has not detected CBD stones
What is the indication for endoscopic USS in biliary colic
If MRCP does not allow diagnosis to be made
Mx of biliary colic
Conservative:
Rehydrate and NBM
Opioid analgesia: morphine 5-10mg/2h max
High recurrence rate therefore surgical management is favoured
NB asymptomatic gallbladder stones do not need treatment
Surgical:
Laparoscopic cholecystectomy:
Urgent (within 1w of diagnosis in those with acute cholecystitis)
Elective at 6-12w
Percutaenous choleystotomy
Indications for percutaenous cholecystotomy
Management of gallbladder empyema when:
surgery is contraindicated at presentation and conservative management is unsuccessful.
Reconsider lap chole for people whho have had percutaenous cholecystotomy once they are well enough for surgery
Mx of CBD stones
Offer bile duct clearance and lap chole to people with symptomatic or asymptomatic CBD stones
Clear the bile duct:
surgically at the time of lap chole
or with ERCP before or at time of surgery
If the bile duct cannot be cleared with ERCP, use bilirary stenting to achieve drainage as a definitive measure until definitive clearance
Pathogenesis of acute cholecystitis
Stone or sludge impaction in Hartmann’s pouch leading to chemical and or bacterial inflammation
5% are acalculous: sepsis, burns, DM
Sequelae of acute cholecystitis
Resolution +/- recurrence
Gangrene and rarely perf
Chronic cholecystitis
Empyema
Servere RUQ pain
Continuous radiating to right scapula and epigastrium
Fever
Vomiting
?Acute cholecystitis
Local peritonism in RUQ, tachycardia with shallow breathing
+/- jaundice
Murphy’s sign
Phlegmon
Boas’s sign
?Acute cholecystitis
What is Murphy’s sign
2 fingers over the GB and ask patient to breath in
Pain and breath catch, must be -ve on the left
What is phlegmon
May be palpable in acute cholecystitis
Mass of adherent omentum and bowel
What is Boas’ sign
Hyperaesthesia below the right scapula
Ix in acute cholecystitis
Urine
Bilirubin, urobilinogen
Ix in acute cholecystitis
Bloods
FBC: raised WCC
U+E: dehydration from vomiting
Amylase, LFTs, G+S, clotting, CRP
Ix in acute cholecystitis
Imaging
AXR: gallstone, porcelain GB
Erect CXR: perforation
USS:
stones, acoustic shadow
Dilated ducts >6mm
Inflamed GB: wall oedema
MRCP if dilated ducts seen on USS
Porcelain gallbladder is an uncommon manifestation of chronic cholecystitis, characterized by intramural calcification of the gallbladder wall [1]. The term “porcelain gallbladder” is used to describe the bluish discoloration and brittle consistency of the gallbladder wall seen in this condition [
Mx of acute cholecystitis
Admit
Conservative:
NBM
Fluid resuscitation
Analgesia: paracetamol, diclofenac, codeine, naproxen, IM pethidine
Abx:
cef and met
80-90% settle over 24-48h
Deterioration may be suggestive of perforation/empyema
Surgical:
May be elective surgery at 6-12w (once inflammation has reduced)
Or if <72h can perform lap chole in acute phase
High fever
RUQ mass
Think ?GB empyema
Percutaenous drainage via cholecystotomy may be indicated
Vague upper abdominal discomfort
Distension, bloating
Nausea
Flatulence, burping
Symptoms exacerbated by fatty foods
Flatulent dyspepsia
?Chronic cholecystitis
Ddx in chronic cholecystitis
PUD
IBS
Hiatus hernia
Chronic pancreatitis
Ix in chronic cholecystitis
AXR: porcelain GB
US: stones, fibrotic, shrunken GB
MRCP
Mx of chronic cholecystitis
Medical: bile salts (not very effective)
Surgical:
Elective cholecystectomy
ERCP first if USS shows dilated ducts and stones
What are the features of gallstone mucocele
Neck of the GB blocked by stone but contents remain sterile
Can be very large-> palpable mass
May become infected–> empyema
Features of GB carcinoma
Rare
Associated with gallstones and gallbladder polyps
May see porcelain GB
Incidental Ca found in 0.5-1% of lap choles
Features of Gallstone ileus
Large stone >2.5cm erodes from GB into duodenum through a cholecysto-duodenal fistula 2o to inflammation
May impact in the distal ileum leading to obstruction
Rigler’s triad
What is Rigler’s triad
Pneumobilia
SBO
Gallstone in RLQ
Rigler triad consists of three findings seen in gallstone ileus:
pneumobilia
small bowel obstruction
gallstone, usually in the right iliac fossa
Rigler triad should not be confused with Rigler sign or the Hoffman-Rigler sign.
What is Bouveret’s syndrome?
Gastric outlet obstruction due to gallstone
Causes of obstructive jaundice
Rule of 30%s…
30% stones
30% Ca head of the pancreas
30% other
What are other causes of obstructive jaundice
LNs @ porta hepatis: TB, Ca
Inflammatory: PBC, PSC
Drugs: OCP, sulfonylureas, fluclox
Neoplastic: cholangiocarcinoma
Mirizzi’s syndrome
Jaundice
Dark urine, pale stools
Itch
Obstructive jaundice
Itch due to bile salts
At what [serum] is obstructive jaundice noticeable and where is it seen first
Noticable at ~50mM
Seen at tongue frenulum first
Ix in obstructive jaundice
Urine
Dark
Raised bilirubin
Reduced urobilinogen
Ix in obstructive jaundice
Bloods
FBC: raised WCC in cholangitis
U+Es: hepatorenal syndrome
LFTs: raised conjugated bilirubin, ++ ALP, +AST/ALT
Clotting: reduced VitK–> Raised INR
G+S: may need ERCP
Immune: AMA, ANCA, ANA
Ix in obstructive jaundice
Imaging
AXR: may visualise stone
Pneumobilia suggests gas forming infection
USS:
DIlated ducts >6mm
Stones (95% accurtate)
Tumour
MRCP or ERCP
PTC: percutaneous transhepatic colangiography
What is PCT
Percutaneous transhepatic cholangiography (PTHC or PTC) or percutaneous hepatic cholangiogram is a radiologic technique used to visualize the anatomy of the biliary tract. A contrast medium is injected into a bile duct in the liver, after which X-rays are taken.
Pneumobilia
May be suggestive of a gas forming infection
Mx of stone causing obstructive jaundice
Conservative:
Monitor LFTs, stone passage may lead to resolution
Vits ADEK
Analgesia
Cholestyramine
Interventional:
If no resolution, worsening LFTs or cholangitis
ERCP with sphincterectomy and stone extraction
Surgical:
Open/lap stone removal with T tube placement
T tube cholangiogram 8d later to confirm stone removal
Delayed cholecystectomy to prevent recurrence
MOA cholestyramine
Cholestyramine is a bile acid sequestrant. It works by helping the body remove bile acids, which can lower cholesterol levels in the blood. The medicine is also used to relieve itching that’s caused by a bile duct blockage
Features of ascending cholangitis
Charcot’s triad
Reynolds pentad
What is Charcot’s triad
Fever/rigors
RUQ pain
Jaundice
What is Reynolds pentad
Charcot’s tirad
Shock
Confusion
Mx of ascending cholangitis
Cef and met
1st ERCP
2nd: open or lap stone removal with T tube drain
Risk factors for pancreatic carcinoma
SINED
Smoking
Inflammation: chronic pancreatitis
Nutrition: high fat diet
EtOH
DM
Pathology of pancreatic carcinoma
90% are ductal adenocarcinomas
Present late, metastasise early
Direct extension to local structures, lymphatics, haematogenously to liver and lungs
Location of pancreatic adenocarcinoma
60% in head
25% in body
15% in tail
(Male) >60y
Painless obstructive jaundice picture
or epigastric pain radiating to back and relieved by sitting forward
Anorexia, weight loss and malabsorption
Acute pancreatitis
Sudden onset DM
?Pancreatic carcinoma
Palpable gallbladder
Jaundice
Epigastric mass
(Trousseau’s sign)
Splenomegaly
Ascites
Pancreatic adenocarcinoma
(Thrombophlebitis migrans)
Splenomegaly due to PV thrombosis leading to portal HTN
What is Courvossier’s law
In the presence of painless obstructive jaundice, a palpable gall bladder is unlikely to be due to stones
Why does Coruvossier’s sign occur
Cause unlikely to be gallstones, gallstones form over an extended period of time resulting in a shrunken, fibrotic gall bladder that does not easily distend, this is less likely to be palpable on examination
In contrast, the gallbladder is more enlarged in pathologies that cause obstruction of the biliary tree over longer periods of time e.g. pancreatic malgiancny leading to passive distension from back pressure
Ix in pancreatic carcinoma
Bloods
Cholestatic LFTs
Ca 19-9
Raised Ca
Ix in pancreatic carcinoma
Imaging
USS: pancreatic mass, dilated ducts, hepatic mets, guide biopsy
EUS: better than CT/MRI for staging
CXR: mets
Laparoscopy: mets, staging
ERCP in pancreatic caricnoma
Shows anatomy
Allows stenting
Biopsy of peri-ampullary lesions
5y survival of pancreatic carcinoma
<2%
Mean survival <6m
Mx of pancreatic carcinoma
Sx:
fit, nomets, tumour <3cm (<10% patients)
Whipple’s pancreaticoduodenectomy
Distal pancreatectomy
Post-op chemo delays progression
Palliation:
Endoscopic/percutaneous stenting of CBD
Paliative bypass surgery: cholecystojejunosostomy, gastrojejunostomy
Pain relief: may need coeliac plexus block
Epidemiology of pancreatic endocrine neoplasia
30-60 y/o
15% associated with MEN1
With which MEN are pancreatic endocrine neoplasias associated?
MEN1
Fasting/exercise induced hypoglycaemia
Confusion, stuipor< LOC
Raised insulin, raised c-peptide, reduced glucose
Insulinoma
Hypergastrinaaemia–> hyperchlorhydia—> PUD and chronic diarrhoea due to inactivation of pancreatic enzymes
Gastrinoma (Zollinger-Ellison)
Raised glucagon
Necrolytic migratory erythema
Glucagonoma
Necrolytic migratory erythema
Characteristic rash of glucagonoma
Watery diarrhoea
Hypokalaemia
Achlorrhydia
Acidosis
VIPoma/ Verner-Morrison/ WDHA syndrome
MOA somatostatin
Inhibits glucagon and insulin release
Inhibits pancreatic enzyme secretion
DM
Steatorrhoea
Gallstones
Usually very malignant tumour with poor prognosis
Somatostatinoma
Favoured sites are stomach and duodenum followed by jejunum and ileum
Usually located in submucosa
Maybe visualised as a sessile mass
May cause pain from localised inflammation or more rarely, mucosal bleeding
2% of tumours arise in this tissue
Ectopic pancreas
Failuire of fusion of dorsal and ventral buds—> bulk of pancreas drains through smaller accessory duct.
Usually asymptomatic
May present with chronic pancreatitis
Pancreas divisum
Fusion of dorsal and ventral buds around duodenum
May present with infantile duodenal obstruction
Annular pancreas
Pancreas divisum
Annular pancreas
What is a Klatskin tumour
Typically occuring cholangiocarcinoma at confluence of right and left hepatic ducts
Features of cholangiocarcinoma
Rare bile duct tumour
Adenocarcinoma
[Klatskin tumour[
Klatskin tumour
Risk factors for cholangiocarcinoma
PSC
UC
Choledocholithiasis
Hep B/C
Choledochal cysts
Lynch 2
Flukes
Progressive painless obstructive jaundice
GB not palpable
Steatorrhoea
Weight loss
?Cholangiocarcinoma
Ix in cholangiocarcinoma
Cholestatic LFTs
CA19-9
Mx of cholangiocarcinoma
Poor Px
Palliative stenting
Pathophysiology of Hydatid cyst
Zoonotic infection by Echinococcus granulosus
Occurs in sheep-rearing communities
Parasite penetrates the portal system and infects the liver—> calcified cyst
Mostly asymptomatic
Pressure effects: non-specific pain, abdominal fullness, obstructive jaundice
Rupture: biliary colic, jaundice, urticaria, anaphylaxis, 2o infection
?Hydatid cyst
Ix in hydatid cyst
Eosinophilia
CT
Rx in hydatid cyst
Rx: albendazole
Sx: cystectomy for large cysts
What are the aims of pre-operative assessment and planning
Informed consent
Assess risk vs benefits
Optimise fitness of patient
Check anaesthesia/analgesia type with anaesthetist
OP CHECS
Operative fitness: cardiorespiratory comorbidities
Pills
Consent
History: MI, asthma, HTN, jaundice, complications of anaesthesia, DVT
Ease of intubation: neck arthritis, dentures, loose teeth
Clexane: DVT prophylaxis
Site: correct and marked
Anticoagulants pre-op
Balance risk of haemorrhage with risk of thrombosis
Avoid epidural, spinal and regional blocks
AED pre-op
Continue as usual
Post-op give IV or via NGT if unable to tolerate orally
OCP/HRT pre-op
Stop 4w before major/leg sx
Restart 2w post-op if mobile
Beta-blockers pre-op
Continue as normal
What are the routine pre-op bloods?
FBC
U+Es
G+S
Clotting
Glucose
What specific bloods are used pre-op
LFTs: liver disease, EtOH, jaundice
TFT: thyroid disease
Electrophoresis if from risk background
Cross-match for gastrectomy
4u
X-match for AAA
6u
How is cardiorespiratory function assessed pre-operatively
CXR: cardiorespiratory disease/symptoms, >65 y/o
Echo: poor LV function,?murmurs
ECG: HTN, Hx of cardiac disease, >55y
Cardiopulmonary exercise testing
PFT: known pulmonary disease or obesity
Why may you do an C spine XR pre-operatively
Flexion and extension views, in RA/AS
What are the different ASA grades
1: Normally healthy
2: Mild systemic disease
3: Severe systemic disease that limits activity
4: Systemic disease which is a constant threat to life
5: Moribund, not expected to survive 24h even with operation
NBM pre-op
>2h for clear fluids
>6h for solids
Bowel prep indications
May be needed in left-sided operations
Not usually needed in right-sided procedures
Necessity is controversial
What are the risks of bowel prep
Liquid bowel contents spilling during Sx
Electrolyte disturbance
Dehydration
Increased rate of post-op anastamotic leak
Indications for prophylactic Abx
Gi Sx
Joint replacement
Elective GI Sx post-op infection rate
20%
When are prophylactic Abx given preoperatively
15-60 mins before Sx
What are some bowel prep options
Picloax: picosulfate and Mg citrate
Klean-prep: macrogol
Abx prophlyaxis for
Biliary sx
Cef 1.5g and met 500mg IV
Abx prophlyaxis for
CR or appendicetomy
Cef and Met TDS
Abx prophlyaxis for
Vascular Sx
Co-amoxiclav 1.2g IV TDS
DVT prophylaxis in surgery
Low risk: early mobilisation
Medium risk: early mobilisation + TEDs + 20mg enoxaparin
High: early mobilisation + TEDS + 40mg enoxaparin and intermittent compression boots perioperatievely
Risk of DM in surgery
Increased risk of post-operative complications
How does DM increase the risk of post-operative complications?
Sx leads to the release of stress hormones which antagonise insulin
Patients are NBM
Increased risk of infection
Coexistant IHD and PVD
What should be done in DM patients pre-operatively?
Urine dipstick: proteinuria
Venous glucose
U+Es: K
What is the practical management of patients with IDDM when having surgery
Put patient first on list and inform surgeon and anaesthetist
Some centres prefer to use GKI infusions (mixture of glucose, insulin and potassium)
Sliding scale is not always necessary for minor ops, if in doubt, liase with diabetes specialist nurse
Management of insuilin pre and peri-operatively
Stop long acting insulin the night before
Omit AM insulin if sx if in the morning
Start sliding scale
Outline sliding scale
5% Dextroes with 20mmol KCl 125ml/hr
Infusion pump with c50u actrapid
Check CPG hourly and adjust insulin rate
What is target glucose when on a sliding scale
7-11mM
Post-op Mx of sliding scale
Continue sliding scale until tolerating food
Switch to SC regimen around meal
Mx of NIDDM and surgery
If glucose control poor (fasting glucose >10mM) treat as IDDM
Omit oral hypoglycaemics on the AM of Sx
Eating post-op: resume oral hypoglycaemics with meal
Not eating post-op: check fasting glucose on AM of surgery, start insulin sliding scale. Consult specialist team about restrting PO Rx
Mx of diet controlled DM in surgery
Usually no problem
Patient may be briefly insulin-dependant post-op
Monitor CPGs
Risks of steroids and surgery
Poor wound healing
Infection
Adrenal crisis
Mx of LT steroids and surgery
Need to increase steroids to cope with stress
Consider cover if high-dose steroids have been received within the past year
Steroid Rx in major surgery
Hydrocortisone 50-100mg IV with pre-med then 6-8 hourly for 3d
Usual pre-operative steroids +25 mg hydrocortisone @ induction +100 mg day-1 for 48 – 72h
Steroid Rx in minor surgery
As for major but only for 24h
Jaundice and surgery
Best to avoid operating
Use ERCP instead
Risks of jaundice and surgery
Patients with obstructive jaundice have increased risk of post-op renal failure, need to maintain a good UO
Coagulopathy
Increased infection risk—> cholangitis
Pre-Op Mx of jaundice
Avoid morphine in pre-med due to possible spastic effect on the sphincter of Oddi
Check clotting and consider pre-op vit K
Give 1L NS pre-op unless CCF-> moderate diuresis
Catheterise to monitor UO
Abx prophlyaxis
Intra-op Mx of jaundice
Hourly UO monitoring
NS titrated to output
Post-op mx of jaundice
Intensive monitoring of fluid status
Consider CVP and frusemide if poor output despite NS
Anticoagulated patients and surgery
Risk of haemorrhage vs risk of thrombosis
Consultant surgeon, anaesthetist and haemotologist
Very minor surgery can be undertaken without stopping warfarin if INR <3.5
Avoid spinal, epidural and regional blocks
In general continue aspirin/clopidogrel unless risk of bleeding is high, in which case stop 7d before surgery
Mx of anticoagulated with low-thromboembolic risk e.g. AF
Stop warfarin 5d pre-op, need INR <1.5
Restart next day
Mx of anticoagulated with high thromboembolic risk e.g. valves, recurrent VTE
Need bridging with LMWH
Stop warfaring 5d pre-op and start LMWH
Stop LMWH 12-18h pre-op
Restart LMWH 6h post-op
Restart warfarin next day
Stop LMWH when INR >2
Mx of anticoagulated patients requiring emergency surgery
Discontinue warfarin
Vit K 5mg slow IV
Request FFP or PCC (prothrombin complext concentrate) to cover surgery
Risks of COPD and surgery
Basal atelectasis
Aspiration
Chest infection
Pre-op Mx of smoking/COPD
CXR
PFTs
Physio
Quit smoking at least 4w prior to surgery
What are the aims of anaesthesia
Hypnosis, analgesia, muscle relaxation
Principles of anaesthesia
Induction
Muscle relaxation
Airway control
Maintenance
End of anaesthesia
Induction agent for anaesthesia
IV propofol
Muscle relaxation for anaesthesia
Depolarising: suxamethonium
Non-depolarising: vecuronium , atracurium
Airway control for anaesthesia
ET tube
LMA
Maintenance for anaesthesia
Usually volatile agent added to NO2/O2 mix e.g. halothan, enflurane
End of anaesthesia
Change inspired gas to 100% O2
Reverse paralysis: neostigmine and atropine (prevents muscarinic side effects)
Pre-medications for anaesthesia
7As
Anxiolytics and Amnesia: temazepam
Analgesics: opioids, NSAIDs, paracetamol
Anti-emetics: ondansteron 4mg/ metoclopramide 10mg
Antacids: lansoprazole
Anti-sialogue: glycopyrolate (reduces secretion)
Antibiotics
Features of regional anaesthesia
May be used for minor procedures or if unsuitable for GA
Nerve or spinal blocks
Use long-acting agents e.g. bupivacaine
What are the contraindications to nerve/spinal blocks
Local infection
Clotting abnormality
Complications of
Propofol induction
Cardiorespiratory depression
Complications of
Intubation
Oro-pharyngeal injury with laryngoscope
Oesophageal intubation
Complications of
Loss of pain sensation
Urinary retention
Pressure necrosis
Nerve palsies
Complications of
Loss of muscle power in anaesthesia
Corneal abrasion
No cough—> atelectasis + pneumonia
Complications of
Malignant hyperpyrexia
Rare complication precipitated by halothane or suxamethonium
AD inheritance
Rapid rise in temperature and masseter spasm
Rx: dantrolene and cooling
Complications of
Anaphylaxis in anaesthetics
Rare
Possible triggers:
antibiotics
colloid
NM blockers
What is the necessity of analgesia in surgery
Pain-> autonomic acitvation–> arteriolar constriction-> reduced wound perfusion–> impaired wound healing
Pain-> decreased mobilisation-> increased VTE and decreased function
Pain-> decreased respiratory excursion and decreased cough–> atelectasis and pneumonia
Humanitarian considerations
General guidance for anaesthesia
Give regular doses at fixed intervals
Consider best route: PO if possible
PCA (patient-controlled) should be considered: morphine, fentanyl
Follow stepwise approach
Liaise with acute pain service
Pre-op analgesia
Epidural e.g. bupivacaine
End-op analgesia
Infiltrate wound edge with LA
Infiltrate major regional nerves with LA
Features of spinal/epidural anaesthesia
Decreased SE as drugs more localised
First line for major bowel resection
Caution: respiratory depression, neurogenic shock (reduced BP)
What is the WHO pain ladder
Non-opiod +/- adjuvants
Weak opiod + non-opioid +/- adjuvants
Strong opiod + non-opioid +/- adjuvants
Non-opioid pain medications
Paracetamol
NSAIDs: ibuprofen, diclofenac
Weak opioid pain medications
Codeine
Dihydrocodeine
Tramadol
Strong opioid analgesia
Morphine
Oxycodone
Fentanyl
What is ERAS
Enhanced recovery after surgery
Commonly employed in colorectal and orthopaedic surgery
Aims of EPAR
Optimisie pre-op preparation for surgery
Avoid iatrogenic problems e.g. ileus
Minimise adverse physiological/immunological responses to surgery: (raised cortisol, reduced insulin) (hypercoagulbility) (immunosuppression)
Increase speed of recover and return to function
Recognise abnormal recovery and allow early intervention
Pre-op approach EPAR
Optimisation:
Aggressive physiological optimisation e.g. Hydration, BP, anaemia, DM, co-morbidities
Smoking cessation >4w before surgery
Admission on day of surgery, avoidance of prolonged fast
Carb loading prior to surgery
Fully informed patient encouraged to participate in recovery
Intra-op approach EPAR
Short-acting anaesthetic agents
Epidural use
Minimally invasive technqiues
Avoid drains and NGTs where possible
Post-op approach to EPAR
Aggressive Rx of pain and nausea
Early mobilisation and PT
Early resumption of oral intake
Early discontinuation of IV fluids
Remove drains and urinary catheters ASAP
How can surgical complications be characterised
Immediate (<24h)
Early (1d-1m)
Late (>1m)
What are the immediate surgical complications
<24h
Intubation leading to oropharyngeal trauma
Surgical trauma to local structures
Primary or reactive haemorrhage
What are the early surgical complications
1d-1m
Secondary haemorrhage
VTE
Urinary retention
Atelectasis and pneumonia
Wound infection and dehiscence
Antibitoic associated colitis
What are the late surgical complications
>1m
Scarring
Neuropathy
Failure or recurrence
How can post-op haemorrhage be classified?
Primary
Reactive
Secondary
What is primary haemorrhage
Continuous bleeding starting during surgery
What is reactive bleeding
Bleeding at the end of surgery or early post-op
2o to increased CO and BP
What is secondary bleeding
Bleeding >24h post op
Usually due to infection
What are the causes of post-op urinary retention?
Drugs: opioids, epidural/spinal, anti-AChM
Pain: sympathetic activation leading to sphincter contraction
Psychogenic: hospital environment
What are the risk factors for post-op urinary retention?
Male
Increasing age
Neuropathy e.g. DM, EtOH
BPH
Surgery type: hernia and anorectal
Mx of post-op urinary retention
Conservative:
Privacy, ambulation, void to running taps or in hot bath, analgesia
Catheterise +/- gent 2.5mg/kg IV stat
TWOC: if failed may be sent home with silicone catheter and urology output f/up
Features of pulmonary atelectasis
Occurs after nearly every GA
Mucus plugging + absorption of distal air—> collapse
What are the causes of pulmonary atelectasis
Pre-op smoking
Anaesthetic: increases mucus production, reduced mucociliary clearance
Pain inhibitng respiratory excursion and cough
First 48 hours post-sx
Mild pyrexia
Dyspnoea
Dull bases with reduced air entry
?Pulmonary atelectasis
Mx of pulmonary atelectasis
Analgesia to aid coughing
Chest PT
Features of wound infection
5-7d post-op
S. aureus and coliforms
How can operations be classified
Clean
Clean/cont
Contaminated
Dirty
What is a clean operation
Incision of uninfected skin without opening viscus
What is a clean/cont operation
Intraoperative beach of viscus (not colon)
What is a contaminated operation?
Breach of viscus and spillage or opening of colon
What is a dirty operation
Site already contaminated- faeces, urine, trauma
How can the risk factors for post-op wound infection be classified?
Pre-operative
Operative
Post-operative
What are the pre-op risk factors for wound infection
Increasing age
Comorbidities e.g. DM
Pre-existing infection e.g. appendix perf
Patient colonisation e.g. MRSA
What are the operative risk factors for wound infection?
Op classification and wound infection risk
Duration
Technical: pre-op Abx, asepsis
What are the post-operative risk factors for wound infection
Contamination to wound from staff
Mx of wound infection
Regular wound dressing
Abx
Abscess drainage
Occurs 10d post-op
Preceded by serosanguinous discharge from wound
Wound dehiscence
How can the risk factors for wound dehiscence be classified?
Pre-op
Op
Post-op
What are the pre-op risk factors for wound dehiscence?
Increasing age
Smoking
Obesity, malnutrition, cachexia
Comorbidities e.g. DM, uraemia, chronic cough, Cancer
Drugs: steroids, chemo, RTx
What are the operative risk factors for wound dehiscence?
Length and orientation of incision
Closure technique: follow Jenkin’s rule
Suture material
What is Jenkin’s rule?
It is a rule for closure of the abdominal wound. It states that for a continuous suture, the length of suture used should be at least four times the length of the wound with sutures 1cm apart and with 1cm bites of the wound edge
(More recent research has shown that the optimal ratio may in fact be 6:1)
What are the post-operative risk factors for wound dehiscence?
Increased IAP e.g. prolonged ileus leading to distension
Infection
Haematoma/seroma formation
Mx of wound dehiscence
Replace abdo contents and cover with sterile soaked gauze
IV Abx: cef and met
Opioid analgesia
Call senior and arrange theatre
Repair:
wash bowel, debride wound edge, close with deep non-absorbable sutures e.g. nylon
May require VAC dressing or grafting
What are the Cxs of cholecystectomy
Conversion to open: 5%
CBD injury: 0.3%
Bile leak
Retained stones needing ERCP
Fat intolerance/ loose stools
What are the early complications of inguinal hernia repair?
Haematoma/seroma formation: 10%
Intra-abdominal injury (laparoscopic)
Infection
Urinary retention
What are the late complications of inguinal hernia repair?
Recurrence (<2%)
Ischaemic orchitis (0.5%)
Chronic groin pain/paraesthesia (5%)
What are the complications of appendicectomy
Abscess formation
Fallopian tube trauma
Right hemicolectomy e.g. for carcinoid, caecal necrosis
What are the early complications of colonic surgery?
Ileus
AAC (acute acalculous cholecystitis)
Anastomotic leak
Enterocutaneous fistulae
Abdominal or pelvic abscess
What are the late complications of colonic surgery?
Adhesions leading to obstruction
Incisional hernia
What are the causes of post-op ileus?
Bowel handling
Anaesthesia
Electrolyte imbalance
Post surgery:
Distension
Constipation +/- vomiting
Absent bowel sounds
?post-op ileus
Mx of post-op ileus
IV fluids and NGT
TPN if prolonged
What are the complications of anorectal surgery?
Anal incontinence
Stenosis
Anal fissure
What are the complications of small bowel surgery?
Short gut syndrome (<250cm)
Def: short gut syndrome
Malabsorption disorder caused by the surgical removal of a large portion of the small intestine
Abdominal pain
Diarrhea and steatorrhea (oily or sticky stool, which can be malodorous)
Fluid depletion
Weight loss and malnutrition
Fatigue
?Small gut syndrome
May also have complications caused by malabsorption in vitamin absoprtion e.g. anaemia, hyperkeratosis, easy brusing, muscle spasms, poor blood clotting and bone pain
What are the complications of splenectomy
Gastric dilatation 2o to gastric ileus: prevent with NGT
Thrombocytosis-> VTE
Infection: encapsulated organisms
What are the complications of arterial surgery
Thrombosis and embolisation
Anastomotic leak
Graft infection
What are the complications of aortic surgery?
Gut ischaemia
Renal failure
Aorto-enteric fistula
Anterior spinal syndrome
Emboli: distal ischaemia–> trash foot
Complications of breast surgery
Arm lymphoedema
Skin necrosis
Seroma
What are the complications of urological surgery?
Sepsis
Uroma: extravasation or urine
What are the complications of prostatectomy?
Urinary incontinence
Erectile dysfunction
Retrograde ejaculation
Prostatitis
What are the complications of thyroidectomy?
Wound haematoma–> tracheal obstruction
Recurrent laryngeal nerve trauma-> hoarse voice
- transient in 1.5%
- permanent in 0.5%
Damage to R nerve more common due to it being more medial
Hypoparathyroidism—> hypocalcaemia
Thyroid storm
Hypothyroidism
What are the complications of tracheostomy?
Stenosis
Mediastinitis
Surgical emphysema
What are the complications of # repair?
Mal/non-union
Osteomyelitis
AVN
Compartment syndrome
What are the complications of hip replacement?
Deep infection
VTE
Dislocation
Nerve injury: sciatic, SGN
Leg length discrepancy
What are the complications of cardiothoracic surgery
Pneumo/haemothorax
Infection: mediastinitis, empyema
How can post-op pyrexia be classified?
Early 0-5d
Delayed >5d
What are the early causes of post-op pyrexia
0-5d post-op
Blood transfusion
Physiological: SIRS from trauma, 0-1d
Pulmonary atelectasis: 24-48hr
Infection: UTI, superficial thrombophlebitis, cellulitis
Drug reaction
What are the delayed causes of post-op pyreixa
>5d post-op
Pneumonia
VTE: 5-10d
Wound infection: 5-7d
Anastomotic leak: 7d
Collection: 5-20d
Examination work up in post-op pyrexia
Obs, notes and drug chart
Wound
Abdo + DRE
Legs
Chest
Lines
Urine
Stool
What are the Ix in post-op pyrexia?
Urine: dip, MC+S
Bloods: FBC, CRP, cultures +/- LFTs
Cultures: wound swabs, CVP tip for culture
CXR
Cause of post-op pneumonia
Anaesthesia-> atelectasis
Pain-> reduced cough
Sx-> immunosuppression
Rx of post-op pneumonia
Chest physio: encourage coughing
Good analgesia
Abx
Malaise
Swinging fever, rigors
Localised peritonitis
Shoulder tip pain (if subphrenic)
Post-op
?Collection
What are the locations of collections?
Pelvic: 4-10d post-op
Subphrenic: present 7-21d post-op
Paracolic gutters
Lesser sac
Hepatorenal recess (Morrison’s space)
Small bowel (interloop spaces)
What is Morrison’s space
Hepatorenal recess
Ix in collection
FBC, CRP, cultures
USS, CT
Diagnostic lap
Rx of post-op collection
Abx
Drainage/washout
Def: cellulitis
Acute infection of subcutaneous connective tissue
Cause of cellulitis:
Beta haemolytic strep and staph aureus
Pain, swelling, erythema and warmth
Systemic upset
+/- lymphadenopathy
Cellulitis
Rx of cellulitis
Benpen IV
Pen V and fluclox PO
Def: diverticulum
Out-pouching of tubular structure
True diverticulum
Composed of complete wall e.g. Meckel’s
Def: false diverticulum
Composed of mucosa only (pharyngeal, colonic)
Diverticular disease
Symptomatic diverticulosis
Def: diverticulitis
Inflammation of diverticula
Epidemiology of diverticular disease
30% have diverticulosis by 60 years
F>M
Pathophysiology of diverticular disease
Associated with increased intraluminal pressure: low fibre diet has no osmotic effect to keep stool wet
Mucosa herniates through muscularis propria at points of weakness i.e. where perforating arteries enter
Most commonly located in the sigmoid colon
What is Saint’s triad
Unifying factor?
Hiatus hernia
Cholelithiasis
Diverticular disease
?Obesity
Symptoms of diverticular disease
Altered bowel habit +/- left sided colic, relieved by defecation
Nausea
Flatulance
Altered bowel habit +/- left sided colic, relieved by defecation
Nausea
Flatulance
?Diverticular disease
Rx for diverticular disease
High fibre diet
Mebeverine may help
Elective resection for chronic pain
Pathophysiology of diverticulitis
Inspissated faeces-> obstruction of diverticulum
Think in elderly patient with previous history of constipation
Presentation of diverticulitis
Abdominal pain and tenderness
Typically LIF
Localised peritonitis
Pyrexia
Abdominal pain and tenderness
Typically LIF
Localised peritonitis
Pyrexia
Diverticulitis
Ix in diverticulitis: bloods
FBC
Raised WCC
Raised CRP/ESR
Amylase
G+S/x-match
Ix in diverticulitis: imaging
Erect CXR: ?perforation
AXR: fluid level/air in bowel wall
Contrast CT
Gastrograffin enema
Ix in diverticulitis: endoscopy
Flexi sig
Colonscopy (not used in acute attack)
What can be used to grade diverticulitis perforation
Hinchey grading
Hinchey 1
Localised para-colonic abscess- surgery rarely needed
Hinchey 2
Large abscess extending into pelvis
May resolve without surgery
Hinchey 3
Generalised purulent peritonitis
Surgery needed
Hinchey 4
Generalised faecal peritonitis
Surgery needed
Mx of mild acute diverticulitis
Can be treated at home with bowel rest (fluids only)
and abx- some conflicting evidence about use of abx in uncomplicated diverticular disease.. (augmentin +/- met)
Indications for admission acute diverticulitis
Unwell
Fluids can’t be tolerated
Pain can’t be controlled
Medical Mx of acute diverticulitis
NBM
IV fluids
Analgesia: paracetamol
Antibiotics: cef and met
Most cases settle
NSAIDs and opioid analgesics in diverticulitis
Have been identified as risk factors for perforation
Indications for surgical management of diverticulitis
Perforation
Large haemorrhage
Stricture leading to obstruction
Surgical procedure used in diverticulitis
Harmann’s to resect diseased bowel
Complications of diverticulitis
Perforation
Haemorrhage
Abscess
Fistulae
Strictures
Sudden onset pain
Generalised peritonitis and shock
+/- preceding diverticulitis
?Perforation
Mx of perforation in diverticulitis
CXR: free air under the diaphragm
Rx: Hartmann’s
Suddeen painless, bright red PR bleed
Following diverticulitis
?Haemorrhage
Ix in ?haemorrhage in diverticulitis
Mesenteric angiography or colonoscopy
Mx of haemorrhage in diverticulitis
Usually stops spontaneously
May need transfusion
Colonoscopy +/- diathermy/adrenaline
Embolisation
Resection
Walled off perforation
Swinging fever
Localising signs e.g. boggy rectal mass
Leukocytosis
Hx of diverticulitis
?Abscess
Mx of diverticulitis abscess
Abx + CT/US guided drainage
Types of of fistulae following diverticulitis
Enterocolic
Colovaginal
Colovesicular
Pneumaturia + intractable UTIs
?Colovesciular fistula
What may occur after diverticulitis
Colon may heal with fibrous strictures
Mx of strictures post diverticulitis
Resection (usually with primary anastomosis)
Stenting
How can bowel obstruction be classified
Simple
Closed loop
Strangulated
Simple bowel obstruction
1 obstructing point + no vascular compromise
May be partial or complete
Closed-loop bowel obstruction
Bowel obstructed at two points
Left CRC with competent ileocaecal valve. Volvulus
Gross distension can lead to perforation
Strangulated bowel obstruction
Compromised blood supply
Localised, constant pain + peritonism
Fever and raised WCC
What are the commonest causes of SBO
Adhesions: 60%
Hernia
What are the commonest causes of LBO
Colorectal neoplasia (60%)
Diverticular stricture (20%)
Volvulus 5%
How can bowel obstruction be classified
Non-mechanical
Mechanical
What is non-mechanical bowel obstruction?
Paralytic ileus
Causes of paralytic ileus
Post-op
Peritonitis
Pancreatitis or any localised inflammation
Posions/drugs: anti-AChM
Pseudo-obstruction
Metabolic: hypokalaemia, hyponatraemia, hypomagnesia, uraemia
Mesenteric ischaemia
Intestinal pseudo-obstruction
Intestinal pseudo-obstruction is a clinical syndrome caused by severe impairment in the ability of the intestines to push food through. It is characterized by the signs and symptoms of intestinal obstruction without any lesion in the intestinal lumen.[1] Clinical features can include abdominal pain, nausea, severe distension, vomiting, dysphagia, diarrhea and constipation, depending upon the part of the gastrointestinal tract involved.[2] The condition can begin at any age and it can be a primary condition (idiopathic or inherited) or caused by another disease (secondary).[3]
It can be chronic[4] or acute.[5]
How can mechanical bowel obstruction be classified?
Intraluminal
Intramural
Extramural
What are the intraluminal causes of bowel obstruction
Impacted matter: faeces, worms, bezoars
Intussuception
Gallstones
What are the intramural causes of mechanical obstruction?
Benign stricutre: IBD, Sx, ischaemic colitis, diverticulitis, RTx
Neoplasia
Congenital atresia
What are the extramural causes of bowel obstruction
Hernia
Adhesions
Volvulus (sigmoid, caecal, gastric)
Extrinsic compression: pseudocyst, abscess, haematoma, tumour e.g. ovarian, congenital bands e.g. Ladds
Ladd’s bands
Ladd’s bands, sometimes called bands of Ladd, are fibrous stalks of peritoneal tissue that attach the cecum to the abdominal wall and create an obstruction of the duodenum. This condition is found in malrotation of the intestine.
Presentation of bowel obstruction
Abdominal pain:
Colicky, central but level depends on gut region, constant/localised pain suggest strangulation or impending perforation
Distension:
with lower bowel involvement
Vomiting:
early in high, late or absent in low
Absolute constipation
Abdominal pain:
Colicky, central but level depends on gut region, constant/localised pain suggest strangulation or impending perforation
Distension:
with lower bowel involvement
Vomiting:
early in high, late or absent in low
Absolute constipation
?Bowel obstruction
Absolute constipation
Of flatus and faeces
Examination findings in bowel obstruction
Tachycardia: hypovolaemia, strangulation
Dehydration, hypovolaemia
Fever: suggests inflammatory disease or strangulation
Surgical scars
Hernias
Mass: neoplastic or inflammatory
Bowel sounds: increased in mechanical obstruction, reduced in ileus
PR: empty rectum, rectal mass, hard impacted stool, blood from higher pathology
Bowel obstruction, increased bowel sounds
Mechanical obstruction
Bowel obstruction, reduced bowel sounds
Ileus
Ix in bowel obstruction: bloods
FBC: raised WCC
U+Es: dehydration, electrolyte abnormalities
Amylase: ++ in strangulation/perforation
VBG: raised lactate in strangulation
G+S, clotting: may need Sx
Ix in bowel obstruction: imaging
Erect CXR
AXR +/- erect film for fluid levels
CT: can show transition point
Ix in bowel obstruction: gastrograffin studies
Look for mechanical obstruction: no free flow
Follow through or enema
Follow through may relive mild mechanical obstruction, usually adhesional
Ix in bowel obstruction: colonoscopy
Can be used in some cases
Risk of perforation
May be used to therapeutically stent
AXR findings in ileus
Both small and large bowel may be visible
No clear transition point
SBO AXR findings
Diameter >3
Central
Valvulae coniventes: completely across
LB gas absent
Many loops
Many, short fluid levels
LBO AXR findings
>6cm (caecum >9cm)
Peripheral loccation
Haustra- partially across
LB gas present in rectum
Few loops
Few, long fluid levels
Def: Meckel’s diverticulum
Ileal remnant of vitellointestinal duct
Joins yoke sac to midgut lumen
Features of Meckel’s diverticulum
A true diverticulum
2 inches long
2ft from ileocaecal vavle on antimesenteric border
2% of population
2% symptomatic
Contain ectopic gastric or pancreatic tissue
Symptomatic Meckel’s presentation
Rectal bleeding from gastric mucosa
Diverticulitis mimicking appendicitis
Intussuception
Volvulus
Malignant change: adenocarcinoma
Raspberry tumour: musoca protruding at umbilicius: vitello-intestinal fistula
Littre’s hernia
Rectal bleeding from gastric mucosa
Diverticulitis mimicking appendicitis
Intussuception
Volvulus
Malignant change: adenocarcinoma
Raspberry tumour: musoca protruding at umbilicius: vitello-intestinal fistula
Littre’s hernia
Meckels diverticulum
Littre hernia
Littre hernia is a hernia containing a Meckel’s diverticulum. Also known as a persistent omphalomesenteric duct hernia. It is most frequently encountered in the inguinal region.
Dx of Meckel’s
Tc pertechnecate scan +ve in 70% (detects gastric mucosa)
Rx Meckels
Surgical resection
Def: intussuception
Portion of the intestine (the intussuception) is invaginated into its own lumen (the intussuscipiens)
Causes of intussuception
Hypertrophied Peyer’s patch
Meckel’s
HSP
Petuz-Jeghers
Lymphoma
Presentation of intussuception
6-12mo
Colicky abdo pain: episodic incosolable crying, drawing up legs +/- bilious vomiting
Redcurrent jelly stools
Sausage shaped abdominal mass
6-12mo
Colicky abdo pain: episodic incosolable crying, drawing up legs +/- bilious vomiting
Redcurrent jelly stools
Sausage shaped abdominal mass
Intussuception
NB intussuception in adults
Rarely occurs
If it does, consider neoplasm as a lead point
Mx of intussusception
Resuscitate and X-match, NGT
US + reduction by air enema
Sx if irreducible
Def: mesenteric adenitits
URTI/viral infeciotn-> enlargement of mesenteric LNs= pain tenderness and fever
Differentiating features of mesenteric adenitis
Post URTI
Headache + photophobia
Higher temperature
Tenderness is more generalised
Lymphocytosis
Gross anatomy: External ear
Auricle
External auditory meatus
Gross antomy: middle ear
Tympanic:
malleus, incus and stapes
Gross anatomy: inner ear
Semicircular canals, vestibule, cochlea
Purpose of audiometry
Quantify loss and determine its nature
Features of pure tone audiometry
Headphones deliver tones at different frequencies and strengths
Patient indicates when sound appears and disappears
Mastoid vibrator- bone conduction threshold
Threshold at different frequences are plotted to give an audiogram
Purpose of tympanometry
Measures stiffness of the ear drum
Evaluates middle ear function
Flat tympanogram=
Mid ear fluid or perforation
Shifted tympanogram=
+/- mid ear pressure
Features of evoked response audiometry
Auditory stimulus with measurement of elicited brain response by surface electrode
Used for neonatal screening if otoacoustic emission test negative
Presentation of otitis externa
Watery discharge
Itch
Pain and tragal tenderness
Watery discharge
Itch
Pain and tragal tenderness
?Otitis externa
Causes of otitis externa
Moisture e.g. swimming
Trauma e.g. fingernails
Absence of wax
Hearing aid
Organisms causing otitis externa
Pseudomonas
Staph aureus
OE
OE
Mx of otitis externa
Conservative: remove precipitating factors
Medical:
Analgesia e.g. paracetamol or ibuprofen
Treat inflammation:
Topical acetic acid
For more severe cases consider topical antibitoic +/- corticosteroid
Surgical:
?Cleaning of ear if required
Rx in non-infected eczematous OE
Betamethasone
Combination therapies for OE
Betamethasone with neomycin
Hydrocortisone with gentamicin
Rx for fungal OE
Consider clotrimazole
Consideration for amingoglycoside treatment of OE
If perf can lead to ototoxicity
Severe otalgia which is worse at night
Copious otorrhoea
Granulation tissue in the canal
(90% in DM)
Malignant otitis externa
Implications of malignant OE
Life-threatening infection which can lead to skull osteomyletitis
Look for tenderness of mastoid process
Rx of malignant OE
Admit for IV abx
+/- surgical debridement
Malignant OE
Def: bullous myringitis
Painful haemorrhagic blisters on deep meatal skin and tympanic membrane
Associated with influenza infection
With what is bullous myringitis associated
Influenza infection
Bullous myringitis
What are the symptoms of TMJ dysfunction
Earache (referred pain from auriculo temporal nerve)
Facial pain
Joint-clicking/popping
Teeth-grinding (bruxism)
Stress (associated with depression)
Joint tenderness exacerbated by lateral movements of open jaw
?TMJ dysfunction
Ix of TMJ dysfunction
MRI
Mx of TMJ dysfunction
NSAIDs
stabilising orthodontic occlusal prostheses
How can OM be classified?
Acute
OME
Chronic
Chronic suppurative OM
Acute OM=
Acute phase OM
OME=
Effusion after symptom regression
Chronic OM=
Effusion >3mo if bilateral or >6mo if unilateral
Def: chronic suppurative OM
Ear discharge with hearing loss and evidence of central drum perforation
Presentation of acute OM
Usually children post viral UTI
Rapid onset ear pain, tugging
Irrritability, anorexia, vomiting
Purulent discharge if perforation
Usually children post viral UTI
Rapid onset ear pain, tugging
Irrritability, anorexia, vomiting
Purulent discharge if perforation
Acute OM
Bulging red TM
Fever
Acute OM
Rx in acute OM
Paracetamol
Amoxicillin: may used delayed presecription
How can the cx of OM be classified
Intratemporal
Intracranial
Systemic
Intratemporal complications of OM
OME
Perforation of TM
Mastoidis
Facial N. palsy
Intracranial Cxs of OM
Meningitis/encephalitis
Brain abscess
Sub/epidural abscess
Systemic cxs of OM
Bacteraemia
Septic arthritis
IE
Acute OM
Features of delayed antibiotic prescribing strategies
Should be started if symptoms not improving within 4d of onset of symptoms or signficiant worsening of symptoms
Safety net
Inattention at school
Poor speech development
Hearing impairment
?OME
OME
Retracted, dull TM
Fluid level
Audiometry in OME
Flat tympanogram
Mx of OME
Usually resolves spontaenously
Consider grommets if persistent hearing loss
SE: infections and tympanosclerosis
Painless discharge with hearing loss
Chronic suppurative OM
Chronic suppurative OM
Rx chronic suppurative OM
Aural toilet
Abx/steroid ear drops
Complications of chronic suppurative OM
Cholesteatoma
Def: mastoiditis
Middle-ear inflammation-> destruction of mastoid air cells and abscess formation
Fever
Mastoid tenderness
Protruding auricle
?Mastoiditis
Ix in mastoiditis
CT
Mx in mastoiditis
IV Abx
Myringotomy and mastoidectomy
Def: cholesteatoma
Locally destructive expansion of stratified squamous epithelium within the middle ear
How can cholesteatoma be classified?
Congenital
Acquired: secondary to attic perforation in chronic suppurative OM
Foul smelling white discharge
Headache/pain
CN involvement: vertigo, deafness, facial paralysis
?Cholesteatoma
Cholesteatoma
Pearly white with surrounding inflammation
Cx of cholesteatoma
Deafness (ossicle destruction)
Meningitis
Cerebral abscess
Mx of cholesteatoma
Sx
Def: tinnitus
Sensation of sound without external sound stimulation
How can causes of tinnitus be classified?
Specific
General
Drugs
Specific causes of tinnitus
Meniere’s
Acoustic neuroma
Otosclerosis
Noise-induced
Head injury
Hearing loss e.g. presbyacusis
Presbyacusis
Loss of hearing that gradually occurs in most individuals as they grow older
General causes of tinnitus
Raised BP
Anaemia
Drugs causing tinnitus
Aspirin
Aminoglycosides
Loop diuretics
ETOH
Components of tinnitus history
Character: constant or pulsatile
Unilateral (acoustic neuroma)
FHx: otoscleoris
Alleviating/exacerbating factors e.g. worse at night
Associations:
Vertigo: Meniere’s, acoustic neuroma
Deafness: Meniere’s, acoustic neuroma
Causes e.g. head injury, noise, drugs, Fhx
Def: otosclerosis
Hereditary disorder causing progressive deagness due to bone overgrowth in the inner ear
Examination in tinnitus
Otoscopy
Tuning fork tests
Pulse and BP
Ix in tinnitus
Audiometry and tympanogram
MRI if unilateral to exclude acoustic neuroma
Mx of tinnitus
Treat underlying causes
Psych support: tinnitus retraining therapy
Hypnotics at night may help
Def: vertigo
The illusion of movement
How can the causes of vertigo be classified
Peripheral/vestibular
Central
Drugs
Peripheral causes of vertigo
Meniere’s
BPPV
Labyrinthitis
Central causes of vertigo
Acoustic neuroma
MS
Vertebrobasilar insufficiency
Stroke
Head injury
Inner ear syphillis
Drugs causing vertigo
Gentamicin
Loop diuretics
Metronidazole
Co-trimoxazole
Components of vertigo history
Is it true vertigo or light-headedness: which way are things moving: spinning/whirling when not moving (vertigo), sense of imbalance or staggering when walking (disequilibirium), light headedness (presyncope), dizziness caused by hyperventilation
Timespan
Associated symptoms: n/v, hearing loss, tinnitus, nystagmus
Nystagmus
Condition of involuntary eye movement
can be physiological or pathological
Examinations and tests in vertigo
Hearing
Cranial nerve
Cerebellar and gait
Rombergs +ve= vestibular or proprioception
Hallpike manouvre
Audiometry, calorimetry, LP, MRI
Meniere’s triad
Vertigo
Tinnitus
Hearing loss
Pathology of Meniere’s disease
Dilatation of endolymph spaces of membranous labyrinth (endolymphatic oedema)
Attacks occuring in clusters lasting up to 12h
Progressive SNHL
Vertigo and n+v
Tinnitus
Aural fullness (pressure in the ears)
?Meniere’s
Audiometry showing low frequency SNHL which fluctuates
Meniere’s
Mx: Meniere’s disease
Medical:
Symptomatic reliefe: prochlorperazine (if severe) or betahistine or cyclizine
Surgical:
Gentamicin instillation via grommets
Saccus decompression
Follows febrile illness (e.g. URTI)
Sudden vomiting
Severe vertigo exacerbated by head movemenet
Vestibular neuronitis/viral labyrinthistis
Mx of viral labyrinthitis
Cyclizine
Improvement in days
Pathology of BPV
Displacement of otoliths in semicircular canals
Common after head injury
Sudden rotational vertigo for <30s
Provoked by head turning
Nystagmus
BPV
Features of classic BPPV
Geotropic nystagmus with the problem ear down
Predominantly rotatory fast phase toward undermost ear
Latency (a few seconds)
Limited duration (< 20 s)
Reversal upon return to upright position
Response decline upon repetitive provocation
How can nystagmus be classified
Begins as a slow pursuit movement followed by a fast rapid, resetting phase
Named by direction of the fast phase
Right or left beating (horizontal nystagmus)
Up-beating or down-beating (vertical)
Or direction changing
If the movements are not horizontal or vertical then the nystagmus is rotational (clockwise or counter-clockwsie)
Can also have visual evoked nystagamus (VER)- implies central lesion
Causes of BPV
Idiopathic
Head injury
Otosclerosis
Post-viral
Dx of BPV
Hallpike manoeuvre-> upbeat torsional nystagmus
Rx of BPV
Self-limiting
Epley manoeuvre
Betahistine
Difference between primary and secondary otalgia
Primary there is usually abnormality on examination
Secondary is normal looking ear
Causes of primary otalgia
OE/OM
FB
Barotrauma
Rarely:
OME
Ramsay hunt
Perichorditis
Cellulitis
Relapsing polychondritis etc.
Causes of secondary otalgia
Can be classified on basis of nerve territory
e.g.
Trrigeminal TMJ problems
Facial: CPA lesions etc
Glossopharyngeal: tumours in PNS/pharynx
Vagus: tumours in pharynx/larynx, GORD
Spinal nerves: arthritis/tumours
Borders of the anterior triangle of the neck
Mandible
Midline
Sternocleidomastoid
Borders of the posterior triangle of the neck
Sternocleidomastoid
Trapezius
Clavicle
Quinsy=
Peritonsillar abscess
Definition of a definitive airway
In the trachea
Cuffed below the vocal cords
Attached to oxygen
Secured
What are the indications for intubation
A: protection and patency
B: respiratory failure, increase FRC, decreased WOB, secretion management, to facilitate bronchoscopy
C: minimise oxygen consumption and optimise O2 delivery
D: unresponsive to pain, prevent brain injury
E: temperature control
Causes of stridor
Children: croup, inhaled FB, tracheitis, abscess (retropharyngeal, peritonsillar), anaphylaxis, epiglottits, laryngomalacia, VC dysfunction, subglottic stenosis, laryngeal web, laryngeal tumours, tracheomalacia, choanal atresia, tracheal stenosis
Adults: anaphylaxis, laryngitis, epiglottits/supraglottitis, FB, abscess, laryngospasm, tumour
Sound of stridor
Insipiratory
NB: stridor can be biphasic if obstruction is at the level of the glottis
Causative organisms in epiglottits
Strep
Staph
HiB
Pseudomonas
Moraxella catarrhalis
TB
Rapid onset
Unwell
Odynophagia
Drooling
Fever
Anterior tenderness over hyoid bone
Lymphadenopathy
Tripod sign
Progressing rapibldy to SOB, resp distress, airway obstruction, stridor
?Epiglottis/supraglottits
Ix in epiglottits
Airway prep
Lateral neck XR
Bloods +/- cultures
Mx of epiglottits
IV antibiotics: usually 3rd gen cephalosporin
Steroids
Intubation +/- cricothyroidotomy c trachy if airway obstructed
Mx of stridor
ABCDE
Appropriate area e.g. A&E resus
Adrenaline (1:1000) nebulised
Steroids: budenoside nebs + IV dex
O2
Intubation if needed
Cricothyroidotomy either needle or surgical
Site of location of cricothyroidotomy?
Through cricothyroid membrane inbetween thyroid cartilage and cricoid
Can be done with large bore cannulae or surgically
Mx of epistaxis
- External compresion: 90% anterior, 10% posterior, lean forward and distal part of nose, spit anything that enters mouth
- Packing:
Anterior: merocel (nasal tampon)/ Rapid rhino
48hrs
After removal cauterise and give naseptin cream (NB contain peanut oil)
Posterior packing: urinary catheter, insert until tip seen at back of mouth, inflate balloon slowly, don’t let go of catheter
- Cautery using silver nitrate
- Theatre
Surgical ligation of the sphenopalantine artery
What is Little’s area?
AKA Kiesselbach’s plexus
Kiesselbach’s plexus, which lies in Kiesselbach’s area, Kiesselbach’s triangle, or Little’s area, is a region in the anteroinferior part of the nasal septum where four arteries anastomose to form a vascular plexus. The arteries are:[1]
Anterior ethmoidal artery and posterior ethmoidal artery (both from the ophthalmic artery)
Sphenopalatine artery (terminal branch of the maxillary artery)
Greater palatine artery (from the maxillary artery)
Septal branch of the superior labial artery (from the facial artery)
90% of nosebleeds occur here due to the drying effect of air
What are the red flags in epistaxis?
Age >50y
Nasal obstruction
Facial pain
Hearing loss
Proptosis/double vision
Lymphadenopathy, weight loss
Middle-aged Chinese people with epistaxis think
?Nasopharyngeal carcinoma as high incidence
Occupational exposure to dust/chemicals with epistaxis
Think nasopharyngeal carcinoma as RF
Epistaxis in child <2
Shouldn’t happen
?NAI
Risk factors for mastoiditis
Young children
Immunocompromised
Cholesteatoma
Organisms causing mastoiditis
Strep pneumonia, pyogenes, staph, pseudomonas, HiB
Unwell
Fever
Painful over mastoid process
Swollen and boggy
Young children: irritable, pinna protrusion +/- discharge
TM perforation
Hx of otitis media
Chronic: recurrent otalgia, headache, fever, OME/suppurative OM
?Mastoiditis
Mastoiditis
O/E
6th or 7th nerve palsy
Conductive deafness
Boggy swelling behind ear
?Mastoiditis
Ix in mastoiditis
FBC, CRP, blood cultures
Ear swab
CT/MRI
Audiogram
Mx of mastoiditis
High dose broad specrutm IV Abx
Analgesia
Emergency mastoidectomy for cholesteatoma and mastoid oteitits or intracranial spread or not improving
Dizziness what other questions should you ask?
N+V
Tinnitus
Hearing loss
Feeling of aural fullness
Headaches
Visual changes
Weakness
Numbness
Usually preceded by paranasal sinusitits
Medical emergency
Also caused by local trauma, insect or animal bites, FB, URTI
Periorbital cellulitis
Ocular pain
Eyelid swelling
Erythema
?Periorbital cellulitis
What differentiates between periorbital cellulitis and orbital cellulitis
Orbital also presents with painful eye movements, proptosis, opthalmoplegia, visual impairment, chemosis
Aetiology of SNHL
Usually idiopathic
Mx of idiopathic SNHL
Short-course high dose steroids (+/- PPI cover)
With repeat audiogram F/U
Def: acoustic neuroma
Benign slow-growing tumour of the vestibular nerve (vestibular schwanomma)
Sudden onset or progressive SNHL, tinnitus, balance issues, vertigo
?Acoustic neuroma
Local effects of acoustic neuroma
5th trigeminal causing facial numbness and tingling
Facial nerve can also be affected
If very large can compress the brainstem or cuse raised ICP
Most common site of acoustic neuroma growth
Cerebellopontine angle
Mx of acoustic neuroma
Watchful waiting with MRI/audiogram
Stereotactic radiotherapy
Cx of acoustic neuroma sx?
Loss of hearing
Damage to other cranial nerves esepcially the 7th
Bell’s palsy
Sudden onset unilateral facial droop
+/- hyperacusis
Loss of sensation in anterior 2/3rds of tongue
Bell’s palsy
What differentiates between LMN and UMN Bell’s palsy
UMN lesions have forehead sparing as frontalis receives innervation from both hemispheres)
For it to be true Bell’s it must not have forehead sparing
Why should Lyme disease serology be done in Bell’s palsy in endemic areas
As LD can lead to facial nerve palsy
Mx of Bell’s palsy
Short term high dose (60-80mg) steroids + eye care (drops with taping at night)
Bell’s palsy px
Incomplete lesions have better prognosis
What is Ludwig’s angina
Submandibular space infection
Aggressive and rapidly spreading cellulits from which patients can become quickly septic with compromised airway
Unwell
Fever
Mouth pain
Drooling
Dysphagia
Ludwig’s angina
Mx of Ludwig’s angina
IV Abx with anaerobe cover
Close monitoring
Airway +++
Def: conductive hearing loss
Impaired conduciton anywhere between auricle and round window
How can the causes of conductive hearing loss be classified?
External canal obstruciton
TM perforation
Ossicle defects
Inadequate eustachian tube ventilation of midddle air
Causes of external canal obstruction Leading to conductive hearing loss
Wax
Pus
FB
Causes of TM perforation Leading to conductive hearing loss
Trauma
Infection
Causes of ossicle defects leading to conductive hearing loss?
Otosclerosis
Infection
Trauma
Def: sensorineural hearing loss
Defects of cochlea, cochlear nerve or brain
Which drugs can cause sensorineural hearing loss?
Aminoglycosides
Vancomycin
Which post-infective syndromes are associated with sensorineural hearing loss?
Meningitis
Measles
Mumps
Herpes
What are some miscellaneous causes of sensorineural hearing loss?
Meniere’s
Trauma
MS
CPA lesions e.g. acoustic neuroma
Low B12
Acoustic neuroma=
Benign slow-growing tumour of superior vestibular nerve
Slow onset, unilat SNHL, tinnitus ± vertigo
Headache (↑ICP)
CN palsies: 5,7 and 8
Cerebellar signs
?Acoustic neuroma
All patients with unilateral tinnitus/deafness should receive
an?
MRI
What syndrome associated with acoustic neuromas?
NF2
What accounts for 80% of CPA tumours?
Acoustic neuromas
Common cause of CPA syndrome?
Acoustic neuromas
Bruns nystagmus
Dancing eyes
Seen in large tumours due to compression of the flocculi in CPA syndrome
Features of CPA syndrome
Tumours within nerve cannaliculi: unilateral SNHL, tinnitus or disequilibirium
Tumours extending into the CPA may present with disequilibrium and ataxia
With brainstem extension, midfacial and corneal hypesthesia, hydrocephalies and other CN palsies become more prevalent
(speech discrimination out of proportion to hearing loss and difficulty talking on the telephone are frequent accompaniements)
DDx slow onset unilateral SNHL
Meningioma
Cerebellar astrocytoma
Mets
Otosclerosis
AD condition characterised by fixation of the stapes at the oval window
F>M 2:1
Begins early in adult life
Bilateral conductive deafness + tinnitus
HL improved in noisy places (Willis’ paracousis)
Worsened by pregnancy/menstruation
Otosclerosis
>65y
Bilateral slow onset hearing loss
+/- tinnitus
Age-related hearing loss i.e. presbyacussis
Congenital causes of conductive hearing loss in children
Anomalies of pinna, external auditory canal, TM or ossicles
Congenital cholesteatoma
Pierre-Robin
Congenital causes of SNHL in children
AD: Waardenburgs: SNHL, heterochromia + telecanthus
AR: Alports (SNHL + haematuria), Jewell-Lange-Nielson
X-Linked: Alports
Infections: CMV, rubella, HSV, toxo, GBS
Ototoxic drugs
Perinatal causes of paediatric hearing loss
Anoxia
CP
Kernicterus
Infeciton: meningitis
Acquired causes of paediatric hearing loss
OM/OME
Infection: meningitis, measles
Head injury
What are some congenital anomalies seen in the ear
1st and 2nd branchial arches form auricle while 1st branchial groove forms external auditory canal
Malfusion leads to accessory tags/auricles and preauricular pits, fistulae or sinuses
Sinuses may get infected
Features of pinna heamatoma
Blunt trauma leading to subperichondrial haematoma
Can lead to ischaemic necrosis of cartilage and subsequent fibrosis to cauliflower ears
Mx of pinna haematoma
Aspiration and firm packing to auricle contour
Def: exostoses
Smooth, symmetrical bony narrowing of external canals
Pathology of exostoses
Bony hypertrophy due to cold exposure e.g. from swimming/surfing
Asymptomatic unless narrowing occludes the canal leading to conductive deafness
Causes of TM perforation
OM
Trauma
Barotrauma
FB
What are the classifications of allergic rhinosinusitis?
Seasonal
Perennial
Pathology of allergic rhunosinusitis?
T1HS Ig-E mediated inflammation from allergen exposure leading to mediator relesase from mast cells
Allergens include pollen, house dust mites
Sneezing
Pruritus
Rinorrhoea
?Allergic rhinosinusitis
Swollen, pale and boggy nasal turbinates
Nasal polyps
?Allergic rhinosinusitis
External nose parameters
Extends from the nasal bones and surrounding parts of the maxilla and frontal bone
Supported by the central septal cartilage and its lateral processes
At the apex there are two major alar cartilages
Near the maxilla there are smaller minor alar cartilages
Internal nose parameters
Comprises two paired nasal cavities which extend and expand supero-posteriorly from the anterior nares
Nasal septum separates left and right
Hard palate makes up the floor of the cavities and separates them from the oral cavity
Posterior nares open posteriorly into the nasopharynx
What are the three regions of the internal nose?
Vestibular: just inside nostrils
Respiratory: ciliated epithelium making up the bulk of the cavity walls
Olfactory: specialised olfactory epithelium on the roofs of the cavities
What are found on the lateral walls of each nasal cavities?
Superior middle and inferior conchae
Which bone do the superior and middle conchae arise from?
Ethmoid
Which bone do the inferior conchae extend from?
The maxilla
What do the conchae form?
Narrow air passages known as the superior, middle and inferior meatus
What is the major route for nerve entry into the nasal cavity?
Sphenopalatine formaen and is found on the postero-lateral wall of the superior meatus
What is the space above the superior concha called?
The spheno-ethmoidal recess
What are the 4 paranasal sinuses?
Ethmoidal
Sphenoidal
Maxillary
Frontal
Features of the ethmoidal sinus
Collection of specialised ethmoidal air cells in the respiratory region of the nose
Openings in the bulla ethmoidalis on the lateral wall of the middle meatus
Cells between medial and lateral plates of the ethmoid labyrinths
Features of the sphenoidal sinuses?
Posterior to the nasal cavity within the sphenoid bone
Openings in the posterior wall of the spheno-ethmoidal recess
Immediately antero-inferior to the pituitary fossa
What is the largest of the nasal sinuses?
Maxillary
Features of the maxillary sinus
Beyond the lateral walls of the nasal cavity within the maxillae
Openings in the hiatus semilunaris floor on the lateral wall of the middle meatus
Drain at the apex- prone to filling with fluids that are hard to drain
Features of the frontal sinus
Superior to the nasal cavities within the frontal bone
Openings in the hiatus semilunaris roof on the lateral wall of the middle meatus
Drains through the frontonasal duct to the ethmoidal infundibulum
What is the course of the nasolacrimal duct?
Carries tears from the corner of the eye opening in the inferior meatus, inerfo-anterior to the hiatus semilunaris
Whence does the blood supply of the nose come?
Internal and external carotid arteries
What are the significant arteries supplying the nose?
Sphenopalantine artery
Greater palantine artery
Anterior and posterior ethmoidal arteries
Features of the sphenopalatine artery?
Terminal branch of the maxillary artery- branch of external carotid
Enters the cavity through the sphenopalatine formaen
Gives lateral branches supplying most of the lateral wall and medial branches to medial wall
Features of the greater palatine artery
Branch of maxillary artery: branch of external carotid
Enters the anterior floor of the nasal cavity through the incisive canal and supplies the anterior septum and floor
Anastomoses with septal branches of the sphenopalatine artery
From which artery do the ethmoidal arteries branch and what carotid does it originate from?
Ophthalmic artery
Internal carotid
How do the ethmoidal arteries enter the nasal cavity?
Through the cribiform plate
Course of the anterior and posterior ethmoidal arteries
Anterior: anastomoses with branches of the sphenopalatine artery and terminates as the external nasal artery
Posterior division supplies the upper lateral and medial walls
Whence comes the general sensory innervation of the nose?
Ophthalmic and maxillary division of V
What innervates the mucous glands in the nose?
Parasympathetic fibres of the facial nerve: arise form the pterygopalatine ganglion and run with V2 fibres
Branches of the facial nerve
To Zanzibar By Motor Car
Temporal
Zygomatic
Buccal
Mandibular
Cervical
Branches of the trigeminal nerve
Ophthalmic
Maxillary
Mandibular
Cranial exits of trigeminal nerve branches
Standing
Room
Only
Superior orbital fissure
Foramen rotundum
Foramen ovale
Features of ophthalmic nervous supply of the nose
Two key branches: ethmoidal nerves
Anterior branch: travels with anterior ethmoidal artery and supplies the anterior medial and lateral walls before terminating as the external nasal nerve
Posterior branch supplies the ethmoidal air cells and does not enter the nasal cavity
Features of maxillary nerve supply of nasal cavity
Lateral branches supply the lateral wall
Nasopalantine nerve supplies the medial wall before terminating in the oral muscoa
Ix in allergic rhinosinusitis
Skin-prick testing to find allergnes
RAST
Mx of allergic rhinitis
Allergen avoidance: regulalry washing bedding, avoid pollen
Rx:
1st Line:
PRN: Oral antihistamine e.g. cetirazine, desloratidine or intranasal e.g. azelastine
Preventative: intranasal corticosteroid e.g. beclometasone (if nasal blockage or polyps) or oral antihistamine
2nd line:
Intranasal steroid + antihistamine (oral)
3rd line:
Zafirlukast (leukotriene antag)
4th line:
Immunotherapy: to induce desensitisation to allergen
Oral corticosteroids can be considered for severe symptoms
What are some adjuvant nasal decongestants?
Pseudoephedrine, otrivine
Pathophysiology of sinusitis
Viruses-> mucosal oedema and decreased mucosal ciliary actions leading to mucus retention and secondary bacterial infection
Causative organisms acute bacterial sinusitis?
Pneumococcus, Haemophilus, Moraxella
Causative organisms chronic bacterial sinusitis
S. aureus, anaerobes
Causes of sinusitis
Majority are bacterial infection 2o to viral
5% due to dental root infections
Diving/swimming in infected water
Anatomical variation may leave individuals susceptile e.g. deviated septum, nasal polyps
Systmic disease e.g. PCD/Kartagener’s
Pain increasing on bending/straining
Discharge from nose-> foul taste
Nasal obstruciton/congestion
Anosmia or cacosmia (bad smell without external source)
Systemic symptoms
?Bacterial sinusitis
Which sinus liklely to be invovled if cheek/teeth pain in sinusitis
Maxillary
Which sinus liklely to be invovled if pain between eyes in sinusitis
Ethomidal
Ix in sinusitis
Nasendoscopy +/- CT
Mx of acute single episode of sinusitis
Bed-rest, decongestants, analgesia
Nasal douching and topical steroids
Abx of uncertain benefit
Mx of chronic/recurrent sinusitis?
Usually a structural or drainage problem
Stop smoking and fluticasone nasal spray
Functional endoscopic sinus sx if medical therapy fails
Complications of sinusits (rare)
Mucoceles-> pyoceles
Orbital cellulitis/abscess
Ostemoyelitis e.g. staph in frontal bone
Intracranial infection e.g. meningitis, encephalitis, abscess, CVST
What are the sites of nasal polyps
Middle turbinates
Middle meatus
Ethmoids
Water, anterior rhinorrhoea
Purulent post-nasal drip
Nasal obstruciton
Sinusitis
Headaches
Snoring
?Nasal polyps
Mobile pale insensitive growths in nasal cavity
?Nasal polyps
What are the associations of nasal polyps?
Allergic/non-allergic rhinitis
CF
Aspirin hypersensitvity
Asthma
Single unilateral nasal polyp
May be a sign of rare but sinister pathology e.g.
Nasopharyngela Ca
Glioma
Lymphoma
Neuroblastoma
Sarcoma
CT + histology
Nasal polyps in children
Rare in <10, must consider neoplastic disease or CF
Mx of nasal polyps
Drugs:
Betamethasone for 2/7
Short course of oral steroids
Endoscopic polypectomy
No direct response but intact conseunsual response to light
Cannot initiate consensual response in contralteral eye
Dilatation on moving light from normal to abnormal eye
What is the defect?
Afferent defect
Cause of afferent pupillary defect?
Total CNII lesion
Marcus-Gunn pupil=
RAPD
Minor constriction to direct light
Dilatation on moving light from normal to abnormal eye
RAPD- Marcus Gunn pupil
Causes of RAPD
Optic neuritis
Optic atrophy
Retinal disease
Dilated pupil does not react to light
Initiates consensual response in contralateral pupil
Ophthalmoplegia and ptosis
Efferent defect
Cause of efferent pupillary defect
3rd nerve palsy
Medical 3rd nerve palsy
Pupil sparing as the visceral constrictive fibres run on the outisde of the nerve so are spared in vascular aetiologies
Complete 3rd nerve palsy=
“surgical third”
Ptosis
Down and out pupil
Dilated pupil
?3rd nerve palsy
Causes of third nerve palsy
DM (75% pupil sparing)
Temporal arteritis
SLE
MS
Cavernous sinus thrombosis
Amyloid
PCA aneurysm
Tumour
Ipsilateral third nerve palsy with contralateral hemiplegia
Weber syndrome= midbrain stroke
Whence does the CNIII arise?
Rostral midbrain
What are the nuclei of CNIII?
Oculomotor nucleus (somatic fibres)- eye movements
Edinger-Westphal nucleus (visceral fibres)- pupillary constriciton
Course of the oculomotor nerve?
Passes between the posterior cerebral and superior cerebellar arteries and then through the cavernous sinus and out through the superior orbital fissure
Branches of CNIII
Superior branch- levator palpebrae
Inferior branch- MR, IR and IO muscles and carries the visceral fibres
3rd nerve palsy
ptosis
‘down and out’ pupil
dilated pupil
DDx of a fixed, dilated pupil
Mydriatics e.g. tropicamide
Iris trauma
Acute glaucoma
CN3 compression: tumour, coning
RAPD
Young woman with sudden blurring of near vision
Initially unilateral and then bilateral pupil dilatation
Dilated pupil has no response to light and sluggish response to accomodation
= a tonic pupil
Holmes-Adie pupil
Iris shows spontaneous wormy movmenets on slit-lamp examination
Iris streaming
Holmes-Adie pupil
Aetiology of Holmes-Adie pupil
Damage to postganglionic parasympathetic fibres
Idiopathic: may have viral aetiology
Homes-Adie pupil
Tonic pupil + absent knee/ankle jerks + reduced BP=
Holmes-Adie syndrome
Johann Horner
Swiss opthalmologist
Features of Horner’s syndrome
PEAS
Ptosis: partial (superior tarsal muscle)
Enophthalmos
Anhydrosis
Small pupil
Horner’s syndrome
How can the causes of Horner’s syndrome be classified?
Central
Pre-ganglionic
Post-ganglionic
What are the central causes of Horner’s
MS
Wallenberg’s Lateral Medullary Syndrome
Small, irregular pupils
Accomodate but don’t react to light
Atrophied and depigmented Iris
Argyll-Robertson
Argyll-Robertson pupil
“prostitutes pupil”
Accomodates but doens’t react
Causes of Argyll Robertson
DM
Quaternary syphillis
Reduced acuity
Reduced colour vision (especially red)
Central scotoma
Pale optic disc
RAPD
?Optic atrophy/opticneuropathy
What are the most common causes of optic atrophy?
MS and glaucoma
How can the causes of optic neuropathy be classified?
CAC VISION
Congenital
Alcohol and other toxins
Compression
Vascular
Inflammatory
Sarcoid
Infection
Oedema
Neoplastic infiltration
What are the congenital causes of optic atrophy?
Leber’s hereditary optic neuropathy
Hereditary motor and sensory neuropathy/ Charcot Marie Tooth
Friedrich’s ataxia
Wolfram (DIDMOAD)
Retinitis pigmentosa
Attacks of acute visual loss, sequential in each eye
+/- ataxia and cardiac defects
FHx
Onset in 20-30s
Leber’s hereditary optic neuropathy
Mitochondrial disease
What are the toxins causing optic neuropathy?
Ethambutol
Pb
B12 deficiency
What are the compressive causes of optic neuropathy
Neoplasia: optic glioma, pituitary adenoma
Glaucoma
Paget’s
What are the vascular causes of optic atrophy
DM, GCA, thromboembolic
What are the inflammatory causes of optic atrophy
MS, Devic’s, DM
Devic’s disease
Neuromyelitis optica (NMO), also known as Devic’s disease or Devic’s syndrome, is a heterogeneous condition consisting of the simultaneous inflammation and demyelination of the optic nerve (optic neuritis) and the spinal cord (myelitis). It can be monophasic or recurrent.
What are the infective causes of optic atrophy?
Herpes zoster, TB, syphillis
oedematous causes of optic atrophy
Papilloedema
Anteroposterior anatomy of the eyeball
Cornea
Anterior chamber (aqueous humours)
Uvea (Iris, ciliary body, choroid plexus)
Posterior chamber
Lens
Vitreous humour
What are the two muscles responsible for eyelid movement
Obicularis oculi- closes the eyelids, innervated by CN7 (Bell’s palsy)
Levator palpebrae- opens the eyelid, innervated by CN3 (Horner’s)
What is the conjunctiva
Mucus membrane covering the eyeball
Semi-transparent hence the white colouring
Starts at the edge of the cornea (imbus) and loops forward to form the inner surface of the eyelid.
Where are the majority of tears produced?
Accessory tear glands located within the eyelid and the conjunctiva
Lacrimal gland itself is primarily responsible for reflexive tearing.
What is a consideration for lid laceration in the nasal quadrant of the lid?
Compromising the canalicular tear-drainage pathway.
What is a consideration re drug administration and nasolacrimal duct
Nasal absorption of drugs can have profound effects.
hence why squeezing the medial canthus during administration of eye drops can help mitigate htis
Features of the sclera
White fibrous outer layer of the eyeball, continuous with the cornea anteriorly and the optic nerve sheath posteriorly
Anterior chamber of the eye=
Between cornea and the iris
Posterior chamber of the eye
Between the iris and the lens
Viterous chamber of the eye
Extends from the lens to the retina
What is PVD in the context of ophthalmology?
Posterior viterous detachment
usually benign but can cause retinal tears
Where in the eye is the aqueous humor produced?
Posterior chamber, flowing through the pupil into the anterior chamber where it drains into the venous circulation via the Canal of schlemm
Features of the cornea
Avascular receiving its nutrition from tears on the outside and aqueous fluid internally with peripheral blood vessels
What are the layers of the cornea
Epithelium
Bowman’s layer (belfry)
Stroma
Descemet’s membrane (deep)
Endothelium
Damage to which layer of the cornea can lead to scar formation?
Corneal stroma
What forms the anterior chamber angle
Angle formed by the inner cornea and the root of the iris
Location of the Schlemms canal
Def: uvea
Iris
Ciliary body (secretes aqueous fluid and controls the shape of the lens)
Choroid plexus
Components of the lens
Capsule
Nucleus
Cortex
How are cataracts described?
Described by where they occur
I.e. nucleur, cortical, subcapsular
What does contraction of the ciliary muscle lead to?
Causes the zonule ligaments holding the lens in place to relax
Allowing the lens to become rounder
Presbyopia
Difficulty focusing on nearby objects
What is the macula
Pigmented area of the retina responsible for central vision
Within the macula lies the fovea (susceptible to injury during retinal detachments)
What are the bones making up the orbital walls?
Frontal
Sphenoid (greater wing)
Ethmoid
Lacrimal
Palatine
Maxillary
Zygomatic
What is the entry point for the nerves and vessels supplying the orbit
Orbital apex
Nerves passing through the orbital fissure
Live Frankly To See Absolutley No Insult
Lacrimal and Frontal divisions of V1
Trochlear nerve
Superior division fo the oculomotor nerve
Abducens
Nasociliary branch of V1
Inferior division of III
What is the thinnest bone in the orbit?
Ethmoid
Mose likely to perforate from an eroiding sinus infection in children
Funciton of LR
Abduction
Function of MR
Adduction
Extraocular muscle lesion, patients report
Diplopia when looking in the affected direction
Featuers of Horner’s syndrome
PAMEL
Ptosis
Anhydrosis
Miosis
Enophthalmos
Loss of ciliospinal reflex
Ciliospinal reflex
The ciliospinal reflex (pupillary-skin reflex) consists of dilation of the ipsilateral pupil in response to pain applied to the neck, face, and upper trunk. If the right side of the neck is subjected to a painful stimulus, the right pupil dilates (increases in size 1-2mm from baseline). This reflex is absent in Horner’s syndrome and lesions involving the cervical sympathetic fibers. The enhanced ciliospinal reflex in asymptomatic patients with cluster headache is due to preganglionic sympathetic mechanisms.
Mydriasis
Excessive dilataion of the pupil
Crossed eye
Nerve palsy
6th nerve palsy
Causes of 6th nerve palsy
Vasculopathic
Tumour
False localising sign i.e. raised ICP
Action of Trochlear nerve
SO
Causes eye depression and intorsion
Looking towards nose: more up down
Looking laterally: more rotational
4th nerve palsy
Nasal upshoot
Nasal upshoot nerve palsy causing?
4th nerve palsy
Causes of 4th nerve palsy
Vasculopathic
Tumour
Congenital
Trauma
Why do pupils blow first in 3rd nerve compression
As the fibres controlling pupillary constriction run on the external surface of the nerve
Pseudotumour cerebri
=Idiopathic intracranial HTN
What are the components of visual history?
Vision
Sensation
Appearance
Discharge
What are some significant symptoms in a red eye history
Vision
Blurred
Distorted
Diplopia
Field defect/scotoma
Floaters/flashes
What are some significant symptoms in a red eye history:
Sensation
Irritation
Pain
Itching
Photophobia
FB
What are some significant symptoms in a red eye history
Appearance
Red: ?distribution
Lump
Puffy lids
What are some significant symptoms in a red eye history
Discharge
Watering
Sticking
Stringy
What are the key questions in the examination of a red eye?
Inspect A-P
Is acuity affected
Is the globe painful
Pupils equal and reactive?
Corena: intact, cloudy? Use fluorescein
What are the signs of serious disease in a red eye history?
Photophobia
Poor vision
Corneal fluorescein staining
Abnromal pupil
Red eye
++++ pain
No photoboia
Reduced acuity
Hazy/cloudy cornea
Large pupil
Raised IOP
?Acute glaucoma
?Acute glaucoma
Eclipse sign
The eclipse sign using an oblique flashlight has been well described as a tool to detect shallow anterior chamber. A beam of light shone from the temporal aspect of the cornea towards the root of nose produces a semicircular shadow of the iris in the nasal area. The width of the semicircular shadow gives an indication of the depth of the anterior chamber. A shallow anterior chamber produces a broader shadow compared to an anterior chamber of normal depth as it is the eclipse of the light.
Red eye
++ pain
++ photophobia
Reduced acuity
Pain on accomodation
Normal cornea
Small pupil
Normal IOP
?Anterior uveitis
Red eye
Abdominal pain
?Acute closed angle glauocma
Red eye
+/- pain
+ photobia
Normal acuity
Normal cornea
Normal pupil
Normal IOP
?Conjunctivitis
How can the ddx of red eye be classified?
Site:
Lids
Conjunctiva
Sclera
Cornea
Anterior chamber
What are the mechanical causes of red eye
Lids:
Ectropion, entropion, FB, trichiasis
Conjunctiva:
Sub cojunctival haemorrhage
Sclera:
Perforation
Cornea:
Foreign body
Abrasion
Anterior chamber;
Acute glaucoma
What are the inflammatory causes of red eye?
Lids:
Blepharitis, Chalazion
Conjunctiva:
Allergic conjunct
Sclera:
Chemical burn, episcleritis, scleritis
Anterior chamber:
Iritis/uveitis
What are the infective causes of red eye?
Lids:
Perioribital cellulitis, orbital cellulitis
Conjunctiva:
Conjunctivitis
Cornea:
Keratitis
Ant chamber:
Endophthalmitis
Anterior uveitis
Scleritis
Aetiology of acute closed angle glaucoma?
Blocked drainage of aqueous from anterior chamber vis the canal of Schlemm
Pupilar dilatation worsens the blockage
IOP rises from 15-20–> 60mmHg
RFs for acute closed angle glaucoma
Hypermetropia
Shallow anterior chamber
Female
FHx
Increased age
Drugs:
anticholinergics
sympathomimetics
TCAs
Anti-histmaines
Prodrome: rainbow haloes around lights at night time
Severe pain with n+v
Reduced acuity and blurred vision
Acute closed angle glaucoma
Cloudy cornea with circumcorneal injection
Fixed dilated, irregular pupil
Raised IOP makes eye feel hard
Acute cloesd angle glaucoma
Ix in acute closed angle glaucoma
Tonometry: raised IOP, usually >40mmHg
Mx of acute closed angle glaucoma
Refer to ophthalmology
Lie the person flat
Pilocarpine eye drops (2% blue, 4% brown) (miosis opens blockage)
Acetazolamide 500mg IV stat: reduces aqueous formation
Analgesia
+/- antiemetic
What are the aims of the treatment of angle closure glauocma
Reduce intraocular pressure
Ease symptoms
Prevent development/further progression of glaucoma
Definitive treatment for angle closure glaucoma
Laser iridotomy to allow aqueous humour to freely flow into posterior chamber.
Pathophysiology of uveitis
Inflammation of uvea (iris, ciliary body and choroid)
If just iris and ciliary body= anterior uveitis
Acute pain and photophobia
Pain on accomodation
Blurred vision
?Acute uveitis
Small pupil initially, irregular later
Circumcorneal injection
Hypopyon (pus in anterior chamber)
Keratic precipitates on back of cornea
Talbots test: pain on convergence
Anterior uveitis
What are the systemic associations of anterior uveitis
Seronegative arthritits: AS, psoriatic, Reiter’s
Stills’/JIA
IBD
Sarcoidosis
Behcet’s
Infections: TB, leprosy, syphilis, HSV, CMV, toxo
Mx of anterior uveitis
Refer to ophthalmology
Prednisolone
Cyclopentolate drops: dilates pupil and prevents adhesions between the iris and lens
Def: episcleritis
Inflammation below conjunctiva in the episclera
Localised reddening that can be moved over sclera
Painless/mild discomfort
Acuity preserved
Episcleritis
Causes of episcleritis
Usually idiopathic
May complicate RA or SLE
Rx in episcleritis
Topical or systemic NSAIDs
What is the most common cause of red eye?
Conjunctivitis
Def: scleritis
Vasculitis of the sclera
Severe pain worse on eye movement
Vessels won’t move over sclera
Conjunctival oedema (chemosis)
Scleritis
Causes of scleritis
Wegener’s
RA
SLE
Vasculitis
Scleritis, what should you do?
RFTs as may be first presentation of Wegner’s
Cx of scleritis
Scleromalacia leading to globe perforation
Mx of scleritis?
Refer to specialist
Most need corticosteroids or immunosuppressants
Often bilateral with purulent discharge
Bacterial: sticky (staph, strep, haemophilus)
viral: watery
Discomfort
Vessels may be moved over slcera
Acuity unaffected
Conjunctivitis
What are the classes of conjunctivitis?
Viral
Bacterial
Allergic
Rx bacterial conjunctivitis
Chloramphenicol 0.5% ointment
Rx allergic conjunctivitis
Anti-histamine drops e.g. emedastine
What are the divisions of the pharynx
Nasopharynx
Oropharynx
Laryngopharynx
Extent of the nasopharynx
From the posterior nares to the soft palate
Extent of the oropharynx
From the soft palate to the superior margin of the epiglottis
Extent of the laryngopharynx
From the superior margin of the epiglottis to the oesophagus
How are the layers of the neck arranged
In various fascial layers: superficial fascia which surrounds the anterior neck and is innervated by CNVII
Deep fascia: surrounds rest of the neck, several different layers
What are the layers of the deep fascia in the neck?
Investing layer: surrounds all structures within the neck
Carotid sheaths: laterally surrounds the neurovascular components
Pre-treacheal layer: ventrally, surrounds the viscera
Pre-vertebral layer: dorsally: surrounds the vertebrae and associated muscles
What are the four longitudinal compartments in the neck
2 vascular compartments: bilaterally, covered by the carotid sheath
Visceral compartment: ventrally: covered by the pre-tracheal fascia
Vertebral compartment: dorsally: covered by the pre-vertebral fascia
What are the contents of the vascular compartment of the neck?
Internal jugular vein
Common carotid
Vagus nerve
What are the contents of the visceral compartment of the neck?
Contains the pharynx, larynx, trachea, oesophagus and thyroid gland
What are the contents of the vertebral compartment of the neck?
Contains the vertebral column and associated deep muscles
What are the branches of the external carotid artery?
Some Anatomists Like Fucking, Others prefer S and M
Superior thyroid: supplies thyroid gland
Ascending pharygneal: small posterior branch supplying around the pharynx
Lingual: anterior branch to the tongue
Facial: supplies the front of the face, soft palate and submandibular glands
Occipital: supplies the posterior scalp
Posterior auricular: ssupplies the ear
Terminates at the parotid gland, bifurcating into two terminal branches:
Superficial temporal: supplies the parotid gland, lateral face and temple region
Maxillary: supplies numerous structures around the maxilla and mandible
Where does the common carotid bifurcate?
At the superior margin of the thyroid cartilage
How can the muscles of the neck be divided?
Supra and infrahyoid (strap)
What are the suprahyoid muscles?
Digastric: both insert on the medial hyoid: anterior belly (innervated by nerve to mylohyoid (of V3), posterior belly (arises from mastoid process and innervated by CNVII
Stylohyoid: arses from the base of the sytloid process and inserts on the lateral hyoid (CNVII)
What is the innervation of the infra-hyoid strap muscles?
C1-C3
What are the infra-hyoid muscles?
Omohyoid
Sternohyoid
Thyrohyoid
Sternothyroid
Action of the suprahyoid muscles
Depress the mandible or raise the hyoid
Actions of the infrahyoid
Depress the hyoid or fix the hyoid so that the suprahyoid muscles can act
What are the constricter muscles of the pharynx?
Superior: from the pterygomandibular raphe to the pharyngeal tubercle
Middle: from the hyoid bone
Inferior: from the thyroid cartilage
All overlap to make up the pharyngeal walls
What innervates the constrictor muscles of the pharynxx?
Vagus nerve
What are the three longitudinal muscles of the pharynx?
Stylopharyngeus
Salpingopharyngeus
Palatopharyngeus
All innervated by vagus except stylopharyngeus which is innervated by the glossopharyngeal
Which muscle of the pharynx is innervated by glossopharyngeal nerve rather than vagus?
Stylopharyngeus
def: corneal abrasion
Epithelial breach w/o keratitis
Cause: trauma
Pain
Photophobia
Blurred vision
Following trauma
?Corneal abrasion
Ix in corneal abrasion
Slit lamp: fluorescein stains defect green
Rx in corneal abrasion
Chloramphenicol ointment for infection prohpylaxis
Causes of corneal ulcer + keratitis
Bacterial, herpetic, fungal, protozoa, vasculitic (RA)
Corneal ulcer
Dendritic ulcer=
Herpes simplex keratitis
Dendritic ulcer
Herpes simplex keratitis
Acanthomoeba
Protozoal infection affecting contact lens wearers in swimming pools
Acanthomoeba
Pain, photophobia
Conjuncitval hyperaemia
Reduced acuity
White corneal opacity
?Corneal ulcer
RF for corneal ulcer?
Contact lens wearers
Ix in corneal ulcer
Fluorescein on slit lamp
Rx in corneal ulcer
Refer to specialist who will
Take smears and cultures
Abx drops, oral/topical aciclovir
Cyclopegics/mydriatics to ease photophobia
NB steroids may worsen symptoms
Complications of corneal ulcer
Scarring and visual loss
Def: ophthalmic shingles
VZV of CNV1
20% of all shingles
Pain in CNV1 dermatome preceding blistering rash
keratitis, iritis
Hutchinson’s sign
Ophthalmic involvement: keratitis + corneal ulceration
?Opthalmic shingles
Hutchinson’s sign
Nose-tip zoster due to involvement of nasociliary branch
Increased risk of globe involvement as nasociliary involvement also supplies globe
Ophthalmic shingles
Hutchinson’s sign
Nose tip zoster due to involvement of nasociliary branch
Increased risk of globe involvement as nasociliary branch also supplies globe
Key questions in sudden loss of vision
HELLP
Headache associated? GCA
Eye movements hurt? Optic neuritis
Lights/flashes preceding visual loss? Retinal detachment
Like curtain descending? TIA/GCA
Poorly controlled DM? Vitreous bleed from new vessels
Anterior ischaemic optic neuropathy
Optic nerve damage due to occlusion of posterior ciliary arteries, etiher by inflammation or atheroma
Pale/swollen optic disc
Causes of anterior ischaemic optic neuropathy?
Arteritic: GCA
Non-arteritic: HTN, DM, raised lipids, smoking
Unilateral loss of acuity over hours-days
Reduced colour discrimination (dyschromatopsia)
Eye movements may hurt
Reduced acuity
Reduced colour vision
Enlarged scotoma
Optic disc may be: swollen, normal, blurred
Afferent defect
?Optic neuritis
Causes of optic neuritis?
MS (45-80% >15y)
DM
Drugs: ethambutol, chloramphenicol
Vitamin deficiency
Infection: Zoster, Lyme disease
Rx Optic neuritis
High dose IV methyl predniosolone for 72h
Then oral pred for 11/7
What are the sources of vitreous haemorrhage
New vessles: DM
Retinal tears/detachment/trauma
Optic neuritis
Small black dots/ring floaters
Obscured vision
?Viterous haemrorrhage
Viterous haemorrhage
What can happen in large vitreous bleeds
Can obscure vision-> no red reflex
Difficulty visualising retina
Mx of vitreous haemorrhage
Vitrectomy may be performed in dense VH
Usually undergoes spontaneous absorption
Dramatic unilateral visual loss in seconds
Afferent pupil defect may precede retinal changes
Pale retina with cherry-red macula
Central retinal artery occlusion
Causes of central retinal artery occlusion
GCA
Thromboembolism: clot, infective, tumour
Rx in retinal artery occlusion
If seen <6h aim is to increas retinal blood flow by reducing IOP:
Ocular massage, surgical removal of aqueous, local and systemic antihypertensives
What is more common retinal vein or artery occlusion
Retinal vein occlusion
Retinal artery occlusion
Pale retina with cherry red macula
Causes of central retinal vein occlusion?
Arteriosclerosis, raised BP, DM, polycythaemia
Sudden unilateral visual loss with RAPD
?Central Retinal vein occlusion
Fundus:
Stormy sunset apperaance
Torutous dilated vessels
Haemorrhages
Cotton wool spots
?Central Retinal vein occlusion
Stormy sunset apperaance
Torutous dilated vessels
Haemorrhages
Cotton wool spots
Central retinal vein occlusion
Cx of central retinal vein occlusion?
Glaucoma
Neovascularisation
Px for central retinal vein occlusion
Possibel improvement for 6mo-1 year
Unilateral visual loss
Segemental fundal changes
?Retinal vein branch occlusion
Blood supply of the retina
Central retinal artery branches off the ophthalmic artery
What supplies blood to the fovea?
The choroid
Of which cartoid is the ophhthalmic artery a branch?
Internal
What is the aetiology of cherry red sport in central retinal artery occlusion
Retina supplied by retinal artery
Fovea supplied by the vascular choroid that surrounds the eye
Thus in retinal artery occlusion the retinal blood supply is compromised and becomes pale and swollen, while the central fovea appears reddish as the choroid colour shows throguh
Complications of branch artery occlusion?
Retinal ischaemia-> VEGF release and neovascularisation
Treated with anti-VEGFR monoclonal
Def: retinal detachment
Holes/tears in retina which allow fluid to separate sensory retina from retinal pigmented epithelium.
May be secondary to cataract surgery, trauma, DM
4Fs
Floaters: numerous, acute onset, spiders web
Flashes
Field loss
Fall in acuity
Painless
?Retinal detachment
Grey, opalescent retina ballooning forwards
?Retinal detachment
Rx in retinal detachment
Urgent surgery
Vitrectomy and gas tamponade with laser coagulation to secure the retina
What are the causes of transient visual loss?
Vascular: TIA, migraine
MS
Subacute glaucoma
Papilloedema
What are common causes of gradual visual loss?
Diabetic retinopathy
ARMD
Cataracts
Open-angle glaucoma
What are rarer causes of gradual visual loss?
Genetic retinal disease: retinitis pigmentosa
HTN
Optic atrophy
What is the commonest cause of blindness >60y?
ARMD
What are the risk factors for ARMD?
Smoking
Increasing age
Genetic factors
Elderly patient
Central visual loss
ARMD
What are the two types of ARMD
Dry: geographic atrophy and Wet: subretinal neovascularisation
Drusen: fluffy white spots around macula
Macula degeneration
Slow visual decline over 1-2y
Dry ARMD
Aberrant vessels growing into retina from choroid with haemorrhage
Rapid visual decline (sudden/days/weeks) with distortion
Fundoscopy shows macular haemorrhage + scarring
Wet ARMD
What can be used to detect wet ARMD
Amsler grid
What is OCT?
Optic coherence tomography
Used to give high resolution images of the retina
Rx for Wet AMRD
Intravitreal inhibitors
e.g. Bevacizumab
Ranibizumab
Antioxidant vitamines (C,E) and zinc may help ARMD
What are Bevacizumab and ranibizumab?
Intravitreal VEGF inhibitors
Optic atrophy
Loss of red/green discrimination
Scotoma
Due to toxic effects of cyanide radicals when combined with thiamine deficiency
Tobacco-alcohol amyblopia
Rx in tobacco-aclohol ambylopia
Vitamins may help
Pathogenesis of chronic simple (open-angle) glaucoma
Depends on susceptibility of patients retina and optic nerve to raised IOP damage
IOP >21mmHg: reduced blood flow and damage to optic nerve leading to optic disc atrophy + cupping
Optic disc atrophy and cupping
Chronic simple glaucoma
Peripheral visual field defect: superior nasal first
Central field is intact with acuity maintained until late
Presentation is thus delayed until optic nerve damage is irreversible
Chronic Simple Glaucoma
Def: glaucoma
Optic neuropathy +/- pressure (pressure is not part of definition)
What population are at high risk of glaucoma?
>35y
Afro-carribean
FHx
Drugs: steroids
Comorbidities: DM, HTN, migraines
Myopia
Screening
Tonometry: IOP >21mmHg
Cupping of optic disc
Visual field loss: peripheral in arcuate pattern
Chronic simple glaucoma
What are the commonest causes of blindness worldwide?
Trachoma
Cataracts
Glaucoma
Keratomalacia: vitamin A deficiency
Onchoceriasis
Diabetic retinopathy
Mx of open angle glaucoma
Life long F/U
Set target pressure related to degree of damage
Medical therapy first line
1st line:
Prostaglandin analogue
Latanoprost, travoprost
2nd line:
Beta blockers:
timolol, betaxalol
muscarinic alpha agonsts e.g. brominidine, apraclonidine
Carbonic anyhdrase inhibitors: dorzolamide, drops, acetazolmide PO
Miotics
Non-medical options include laser trabeculoplasty, generally if drugs fail
Action in treatment of chronic glaucoma:
Prostaglandin analogues
Increase aqueous outflow via the uveoscleral route
Action in treatment of chronic glaucoma:
Beta blockers
Reduce aqueous secretion by inhibiting beta=adrenoreceptors on the ciliary body
Action in treatment of chronic glaucoma:
Carbonic anhydrase inhibitors
Reduce aqueous secretion by ciliary body
Action in treatment of chronic glaucoma:
Sympathomimetics
Reduce aqueous secretion and increase outflow through trabecular meshwork
Action in treatment of chronic glaucoma:
Miotics
Open up the drainage channels in the trabecular meshwork by ciliary muscle contraction
Issue with beta blockers in treating glaucoma
Caution in asthma/heart failure
Side-effects of prostaglandin analogues in chronic glaucoma
Change in eye colour and lash lengthening
Issue with DM and the eye
Leading cause of blindness up to 60y
30% have ocular probelms at presentation
Good BP and sugar control reduces diabetic retinopathy
Pathophysiology of diabetic eye disease
Cataract:
DM accelerates cataract formation, lens absorbs glucose which is converted to sorbitol by aldose reducatse
Retinopathy:
Microangiopathy-> occlusion
Occlusion-> ischaemia and new vessel formation in retina: bleed-> viterous haemorrhage, carry fibrous tissue with them-> retinal detachment
Occlusion also leads to cotton wool spots (ischaemia
Vascular leakage-> oedema and lipid exudates
Rupture of micro-aneurysms-> blot haemorrhage
Screening of DM in context of eye disease
All diabetics should be screened annually
Fundus photogrophay
Refer those with maculopathy, NPDR and pDR to opathlmologist
Conversion rate of NPDR to DPR?
30% in 1y
Ix in DM eye disease
Fluorescein angiography
Mx of diabetic eye disease
Good BP and glycaemic control
Rx concurrent disease: HTN, dyslipidaemia, renal disease, smoking, anaemia
Laser photocoagulation: maculopathy: focal or grid, proliferative disease: pan-retinal
What EOM palsies occur in DM?
CNII and VI
In diabetic CNIII the pupil may be spared as its nerve fibres run peripherally and receive blood from plial vessels
DM eye grading
Background retinopathy: leakage
Pre-proliferative retinopathy: ischaemia
Proliferative retinoapthy
Maculopathy
Dots and blots with hard exudates
Background DM retinopathy
Dots in DM retinopathy
Microaneurysms
Blots in DM retinopathy
Haemorrhages
Hard exudates in DM retinopathy
Yellow lipid patches
Cotton wool spots
Venous beading
Dark haemorrhages
Intra-retinal microvascular abnormalities
Pre-proliferative retinopathy (ischaemia)
New vessels
Pre-retinal or vitreous haemorrhage
Retinal detachment
Proliferative Retinopathy
Macular oedema
Reduced acuity
Hard exudates within one disc width of macula
Maculopathy
Diabetic maculopathy
Anatomy relevant to nose #
Upper 3rd of nose has bony support
Lower 2/3rd and septum are cartilaginous
Aspects of #nose hx
Time of injury
LOC
CSF rhinorrhoea
Epistaxis
Previous nose injury
Obstruction
Consider facial# check for teech malocclusion, diplopia (orbital floor#)
Ix in nose #
Cartilaginous injury won’t show and radiographs don’t alter management
Mx of nose #
Exclude septal haematoma
Re-examine after 1w once swelling reduced
Reduction under GA with post-op splinting best within 2w
Features of septal haematoma
Septal necrosis and nasal collapse if untreated as cartilage blood supply comes from the mucosa
Boggy swelling and nasal obstruction
Needs evacuation under GA with packing and suturing
Septal haematoma
Causes of epistaxis
80% unknown
Trauma: nose picking/fractures
Local infection: URTI
Pyogenic granuloma: overgrowth of tissues on Little’s area due to irritation or hormonal factors
Osler-Weber-Rendu/HHT
Coagulopathy: Warfarin, NSAIDs, haemophilia, thrombocytopenia, vWD, EToH
Neoplasm
Initial mx of epistaxis
Wear PPE
Assess for shock and manage accordingly
If bleeding not controlled, remove clots with suction or by blowing and try to visualise bleeding through rhinoscopy
Post epistaxis advice
Don’t pick nose
Sit upright, out of sun
Avoid bending, lifting or straining
Sneeze through mouth
No hot food or drink
Avoid EtOH and tobacco
Inheritance of OWR/HHT
Autosomal dominant with 5 genetic subtypes
Telangectasias in mucosae: recurrent spontaneous epistaxis, painless GI bleeds
Internal telangectasias and AVMs in lungs, liver, brain
Pulmonary HTN
Colonic polyps-> CRC
Osler-Weber-Rendu/HHT
Osler-Weber-Rendu/HHT
Sore throat, fever, malaise
Lymphadenopathy esp. jugulodigastric node
Inflamed tonsils and oropharynx
Exudates
Tonsillitis
Most common cause of tonsilitis
Viruses (consider EBV)
Organisms causing tonsillitis
Viruses (EBV)
GAS: pyogenes
Staph
Moraxella
Mx of tonsiltis
Swabbing superficial bacteria is irrelevant and can lead to overdiagnosis
Analgesia: ibuprofen/paracetamol +/- diffiam gargle
Consider Abx only if ill, use Centor criteria:
Pen V 250mg QDS (125mg TDS in children) or erythromycin for 5/7
Why is amoxicillin not used in tonsilitis
EBV-> maculopapular rash
Centor criteria
Fever >38 by history
Tender anterior cervical adenopathy
Tonsilar exudates
Absence of cough
Cut offs for Centor criteria
0-1: no Abx (risk of strep infection <10%)
2: consider rapid Ag test + Rx if +ve
3: Abx
Indications for tonsillectomy
Recurrent tonsilitis if all of the below criteria are met:
Caused by tonsilitis
5+ epsidoes/y
Symptoms >1y
Episodes are disabling and prevent normal functioning
Quinsy
Suspicion of carcinoma: unilateral enlargement or ulceration
Methods of tonsillectomy
Cold steel
Cautery
Cx of tonsillectomy
Reactive haemorrhage
Tonsillar gag may damage teeth, TMJ or posterior pharyngeal wall
Mortality is 1/30000
EBV tonsillitis
Strep tonsillitis
Trismus, odonophagia, halitosis
Tonsillitis, unilateral tonsilar enlargement, contralateral uvula displacement, cervical lymphadenopathy
Typically occuring in adults
?Quinsy
Quinsy
Mx of Quinsy abscess
Admit
IV Abx
I&D under LA or tonsillectomy under GA
Unwell child with stiff extended neck who refuses to eat and drink
Fails to improve with IV Abx
Unilateral swelling of tonsil and neck
?Retropharyngeal absceess
Ix in retropharyngeal abscess
Lateral neck XR show soft tissue swelling
CT skull and thorax
Rx in Retropharyngeal abscess
IV Abx
I&D
Throbophlebitis of the internal jugular vein occuring as a complication of bacterial sore throat infection
Most commonly affect lungs
Lemierre’s syndrome
Which bacteria is associated with Lemierre’s syndrome?
Fusobacterium necrophorum
Rx in Lemierre’s syndrome
IV Abx: pen G, clindamycin, metronidazole
Sandpaper like rash on chest, axillae or behind ears 12-48h after pharyngotonsillits
Circumoral pallor
Strawberry tongue
Scarlet fever
Rx in Scarlet fever
Start Pen V/G and notify HPA
Rheumatic fever
CASES
Carditis
Arthritis
Subcutaenous nodules
Erythema marginatum
Sydenham’s chorea
Malaise and smoky urine occuring 1-2w after pharyngitis
?Post-streptococcal GN
What are the functions of the larynx?
Phonation
Positive thoracic pressure including auto-PEEP
Respiration
Prevention of aspiriation
Features of Laryngitis
Usually viral and self-limiting
2o bacterial infection may develop
Pain, hoarseness and fever
Redness and swelling of the vocal cords
?Laryngitis
Rx in laryngitis
Supportive, Pen V if necessary
Pedunculated vocal cord swellings caused by HPV
Present with hoarsness
Usually occur in children
Rx laser removal
Laryngeal papilloma
Hoarseness
Breathy voice with bovine cough
Repeated coughing from aspiration due to reduced supraglottic sensation
Exertional dyspnoea due to narrow glottis
Recurrent laryngeal nerve palsy
Action of the recurrent laryngeal nerve
Supplies all of the intrinsic muscles of the larynx except cricothyroideus
Exterior branch of superior laryngeal nerve
Responsible for ab and adduction of the vocal folds
Causes of laryngeal nerve palsy
30% are cancers: larynx, thyroid, oesophagus, hypopharynx, bronchus
25% iatrogenic: para-/thyroidectomy, carotid endarterectomy
Other: aortic aneurysm, bulbar/pseudobulbar palsy
Associations of laryngeal SCC
Smoking, EtoH
Male smoker
Progressive hoarseness-> stridor
Dys/odono-phagia
Weight loss
?Laryngeal SCC
Trismus
spasm of the jaw muscles, causing the mouth to remain tightly closed, typically as a symptom of tetanus.
Origin
Ix in laryngeal SCC
Laryngoscopy + biopsy
MRI staging
Mx of laryngeal SCC
Based on stage
RTx
Laryngectomy
Post total laryngectomy
Patients have a permanent tracheostomy
- speech valve
- electrolarynx
- oesophageal speech
Regular f/u for recurrence
Immature and floppy aryepiglottic folds and glottis leading to laryngeal collapse on inspiration
Stridor
Seen in neonates
Laryngomalacia
What is the commonest cause of stridor in children?
Laryngomalacia
Stridor
Presenting within first weeks of life
Noticeable at certain times: lying on back, feeding, excited/ upset
Problems can occur with concurrent laryngeal infections
Conservative management
Laryngomalacia
Sudden onset
Continuous stridor
Drooling
Toxic
?Epiglottits
Pathogens causing epiglottitis
Haemophilus
GAS
Rx in epiglottitis
Don’t examine
Consult anaesthetist and ENT
O2 + nebulised adrenaline
IV dexamethasone
Cefotaxime
Take to theatre for airway securing
Sudden onset stridor in a previously normal child
?FB
Mx of foreign body in throat
Encourage cough
Back slaps
Needle cricothyrotomy if necessary
FB in bronchus can only be excluded through bronchoscopy
Stridor
FTT
?Subglottic stenosis
Causes of subglottic stenosis
Prolonged intubation
Congential abnormalities
Def: Bell’s palsy
Inflammatory oedema from entrapment of CNVII in narrow facial canal
Probably of viral origin
75% of facial palsy
Sudden onset (e.g. overnight)
Complete, unilateral facial weakness
Failure of eye closure-> dryness and conjunctivitis
Drooling/speech difficulty
Numbness or pain around the ear
Reduced taste
Hyperacusis
Bell’s palsy
Ix in Bell’s palsy
Serology: borrelia or VZV Abs
MRI: SOL, stroke, MS
LP
Mx of Bell’s palsy
Protect eye: dark glasses, artifical tears, tape closed at night
Give high dose prednisolone within 72h: 60mg/d PO for 5/7 followed by tapering
Valaciclovir if ?zoster, otherwise antivirals don’t help
Plastic surgery if no recovery
Complications of Bell’s palsy
Aberrant neural connections:
Synkinesis e.g. blinking causes up-turning of mouth
Crocodile tears: eating stimulates unilateral lacrimation rather than salivation
Px of Bell’s palsy
Incomplete paralysis usually recovers completely within weeks
With complete lesions, 80% get full recovery but the remainder may have delayed or permanent neurological/cosmetic abnormalities
Hx of Ramsay Hunt syndrome
American neurologist James Ramsay Hunt in 1907
Def: Ramsay Hunt Syndrome
Reactivation of VZV in geniculate ganglion of CNVII
Preceding ear pain or stiff neck
Vesciular rash in auditory canal +/- TM, pinna, tongue, hard palate
Ipsilateral facial weakness
May also affect CNVIII-> vertigo, tinnitus, deafness
Ramsay Hunt Syndrome
What is Ramsay Hunt syndrome without the rash known as?
Zoster sine herpete
Mx of Ramsay Hunt Syndrome
Valaciclovir and prednisolone within first 72h
Px of Ramsay Hunt?
Rxed within 72h: 75% recovery
Otherwise: 1/3 full, 1/3 partial, 1/3 poor
What features may suggest an alternative cause of facial palsy?
Bilateral symptoms (Lyme, GBS, leukaemia, sarcoid)
UMN signs: sparing of frontalis and obicularis oculi
Other CN palsies (also seen in 8% of Bell’s)
Limb weakness
Rahses
Ramsay Hunt Snydrome
How can the causes of facial nerve palsy be classified?
Intracranial
Intratemporal
Infratemporal
Systemic
What are the intracranial lesions causing facial nerve palsy?
Vascular, MS, SOL: motor cortex= UMN signs. Brainstem nuclei= LMN signs
Cerebellopontine angle lesion: may be accompanied by 5th, 6th and 8th CN palsy
What are the intratemporal lesions causing facial nerve palsy?
Otitis media
Cholesteatoma
Ramsay Hunt
What are the infratemporal lesions causing Facial nerve palsy
Parotid tumours
Trauma
What are the potential systemic causes of facial nerve palsy?
Peripheral neuropathy e.g. GBS (demyelinating) or DM, Lyme, HIB, Sarcoid (axonal)
Pseudopalsy e.g. MG, botulism
What are the components of CNVII function
Motor: innervates the muscles of facial expression, the posterior belly of digastric, the stylohyoid and stapedius muscles
Sensory: nil
Special sensory: taste sensation to anterior 2/3rds of the tongue
PNS: supplies the submandibular, sublingual, nasal, palatine, lacrimal and pharyngeal glands
What provides taste sensation to anterior 2/3rds of tongue?
Facial nerve
Intracranial course of the facial nerve
Arises in the pons, begins as two roots a large motor and small sensory root (intermediate nerve is the part of the facial nerve that arises from the sensory root)
The two roots travel through the internal acoustic meatus, a 1cm opening in the petrous part of the temporal bone
Leaves the internal acoustic meatus and enters the facial canal where:
The two roots fuse to form the facial nerve.
The nerve forms the geniculate ganglion
The nerve gives rise to the greater petrosal nerve, the nerve to staepdius and the chorda tympani
Exits via the facial canal, posterior to the styloid process of the temporal bone
Greater petrosal nerve
Branch of facial nerve, PNS fibres to glands
Nerve to stapedius
Facial nerve branch
Motor fibres to stapedius muscle
Chorda tympani
Branch of the facial nerve, special sensory fibres to the anterior 2/3rds of the tongue
What innervates the parotid gland
Sensory and autonomic innervation
Sensory innervation is supplied by the auriculotemporal nerve (V3)
Parasympathetic innervation begins with CNIX which then synapses with the otic ganglion. The auriculotemporal nerve then carries fibres from the otic ganglion to the parotid
Sympathetic innervation originates from the superior cervical ganglion.
Extracranial course of the facial nerve
First branch is the posterior aruicular nerve- provides motor innervation to some of the muscles around the ear, immediately dital to this it sends branches to the posterior belly of digastric and the stylohyoid muscle
Main trunk, now termed the motor root continuse anteriorly and inferiorly to the parotid (which it does not innervate)
Within the parotid gland, the nerve splits into its 5 terminal branches
TZBMC
Posterior auricular nerve
Branch of the facial nerve
Ascends in front of the mastoid process and innervates the intrinsic and extrinsic muscles of the outer ear
What is innervated by (of facial nerve)
Temporal
Innervates the frontalis, obicularis oculi and corrugator supercili
What is innervated by (of facial nerve)
Zygomatic
Innervates obicularis ori
What is innervated by (of facial nerve)
Buccal
Innervates the obicularis oris, buccinator and zygomaticus
What is innervated by (of facial nerve)
Marignal mandibular branch
Innervates the mentalis muscle
What is innervated by (of facial nerve)
Cervical branch
Innervates the platysma
Increasing myopia
Blurred vision-> gradual visual loss
Dazzling in sunshine/bright lights
Monocular diplopia
?Cataracts
Causes of cataracts?
Age: >75% of >65
DM
Steroids
Congenital:
Idiopathic
Infeciton: rubella
Metabolic: Wilson’s, galactosaemia
Myotonic dystrohpy
Ix in cataracts
Visual acuity
DIlated fundoscopy
Tonometry
Blood glucose to exclude DM
Mx of cataracts
Conservative: glasses
Medical: mydriatic drops and sunglasses may give some relief
Sx:
Consider if symptoms affect lifestyle or driving
Day case surgery
Pacoemulsion and lens implant
Cx of cataracts sx
1% risk of serious complication
Anterior uveitis/iritis
VH
Retinal detachment
Secondary glaucoma
Endophthalmitis (blindness in 0.1%)
Post op capsule thickening is common and treated with laser capsulotomy
Post-op eye irritation is common and requires drops
Def: The retina
Outer pigmented layer in contact with the choroid
Inner sensory layer in contact with vitreous
At the centre is the fovea
Colour of the optic disc
Pale pink
Pale optic disc
?Optic atrophy
Blurred margins of optic disk
?Papilloedema and optic neuritis
What are the features of the optic disk
Colour
Contour
Cup: physiological- 1/3rd. Cup widening and deepening seen in glaucoma
Normal retina
Optic atrophy
What is the most prevalent inherited degeneration of the macula?
Retinitis pigmentosa
Various modes of inheritance
Mostly AR, AD has best prognosis
X-linked has worst prognosis
Affects 1/2000
Night blindness
Reduced visual fields-> tunnel vision
Most registered blind by mid 30s
?Retinitis pigmentosa
Pale optic disc
Peripheral retinal pigmentation
?Retinitis pigmentosa
Classic Retinitis pigmentosa, with mid-peripheral bony spicules, baring of RPE, vessel attenuation, and sparing of central macula
DM retinopathy post laser treatment
What conditions are associated with retinitis pigmentosa?
Friedrich’s ataxia
Refsum’s disease
Kearns-Sayre syndrome
Usher’s syndrome
Inheritance of retinoblastoma
Herediatry type differs from non-hereditary type
AD mutations of RB gene
Patients typically have on mutant allele in every retinal cell, if the other alleles mutates-> retinoblastoma
2 HIT hypothesis
With what conditions are retinoblastomas associated?
5% occur with pineal or other tumour
Increased risk of osteosarcoma and rhabdomyosarcoma
Strabismus
Leukocoria
?Retinoblastoma
Leucokoria
?Retinoblastoma
An abscess/infection in a lash follicle which points outwards
Rx with local Abx e.g. fusidic acid
Stye or horeolum externum
Hordeolum externum (stye)
Abscess of the Melbomian glands which point inwards onto the conjunctiva
Chalazion or hoedolum internum
Hordeolum internum/ Chalazion
Def: Blepharitis
Chronic inflammation of the eyelid
Red eyes
Gritty/itchy sensation
Scales on lashes
Rosacea
?Blepharitis
Causes of Blepharitis
Seborrhoic dermatitis
Staphs
Rx in Blepharitis
Clean crusts of lashes with warm soaks
May need fusidic acid drops
Blepharitis
Entropion
Lid inversion-> corneal irritation
Degeneration of the lower lid fascia
Ectropion
Low lid eversion-> watering and exposure keratitis
Associated with ageing and facial N. palsy
Def: true ptosis
Intrinisc LPS weakness
Causes of bilateral ptosis
Congenital
Senile
MG
Myotonic dystrophy
Causes of unilateral ptosis
3rd Nerve palsy
Horner’s (partial)
Mechanical: xanthelasma, trauma
Def: lagophthalmos
Difficulty in lid closure over the globe which may lead to exposure keratitis
Causes of lagophthalmos
Exophthalmos
Facial palsy
Injury
Rx of lagophthalmos
Lubricate eyes
Temporary tarsorrhaphy may be needed if corneal ulcers develop
Pinguecula
Yellow vascular nodules either side of the cornea
Pinguecula
Pterygium
Similar to pinguecula but grows over the cornea-> reduced vision
Benign growth of conjunctiva
Associated with dusty, wind-blown life styles, sun exposure
Pterygium
Pathophysiology of orbital cellulitis
Infection spreading locally e.g from paranasal sinuses, eyelid or external eye
Staphs, pneumococcus, GAS
Inflammation of the orbit and lid swelling
Pain and reduced range of eye movement
Exopthalmos
Systemic signs e.g. fever
Tenderness over the sinuses
Orbital cellulitis
Orbital cellulitis
Rx in orbital cellulitis
IV Abx: Cefuroxime (20mg/kg/8h IV)
Cx of orbital cellulitis
Local extension-> meningitis and cavernous sinus thrombosis
Blindness due to optic nerve pressure
Features of carotico-cavernous fistula
May fallow carotid aneurysm rupture with reflex of blood into cavernous sinus
Spontaneous/trauma
Engorgement of eye vessels
Lid and conjunctival oedema
Pulsatile exophthalmos
Eye bruit
Carotico-cavernous fistula
Carotid-cavernous fistula
Exophthalmos/proptosis
Protrusion of one or both eyes
Common causes of proptosis
Graves: 25-50%, increased in smoker’s, anti-TSH Abs-> retro-orbital inflammation and lymphocyte infiltration leading to swelling
Orbital cellulitis
Trauma
Other causes of proptosis
Idiopathic orbital inflammatory disease
Vasculitis- Wegener’s
Neoplasm: lymhpoma, optic glioma, capillary haemangioma, metastatic
Carotico-cavernous fistula
What is used to classify hypertensive retinopathy?
Keith-Wagener Classification
Keith-Wagener classification of hypertensive retinopathy
- Tortuosity and silver wiring
- AV nipping
- Flame haemorrhages and soft/cotton wool spots
- Papilloedema
Grades 3 and 4= malignant HTN
A. Earliest sign of hypertension showing only generalized narrowing of the arterioles with no change in the vessel wall thickness or reflex. B. Grade II hypertension showing generalized narrowing plus focal constriction and grade I arteriolar sclerosis with widening of the reflex stripe. C. Grade III hypertension showing generalized narrowing, focal constriction, hemorrhages, and exudate, and grade I arteriolar sclerosis with widening of the light reflex. D. Grade IV hypertension showing generalized narrowing, focal constriction, hemorrhages, and exudates and edema of the disc with grade I arteriolar sclerosis
What are the granulomatous disorders causing uveitis and choroidoretinitis
TB, sarcoid, toxoplasmosis, leprosy, brucella
What inflammatory diseases are associated with:
Conjunctivitis
SLE, reactive arthritis, IBD
What inflammatory diseases are associated with:
Scleritis/episcleritis
RA, vasculitis, SLE, IBD
What inflammatory diseases are associated with:
Iritis
Ank spond
IBD
Sarcoid
What inflammatory diseases are associated with:
Retinopathy
Dermatomyositis
Reduced tear production
Dry eyes and ry mouth
1o
or 2o: SLE< RA, sarcoid
Keratoconjuncitivities SIcca/ Sjogren’s
Roth spots associated with?
Infective endocarditis
As a consequence of microemboli
Boat shaped haemorrhage with pale centre
Roth spot
Infective endocarditis
Kayser-Fleischer Rings
Wilson’s
Exophthalmos
Grave’s disease
Corneal calcification
Hyperparathyroidism
CMV retinitis
Pizza-pie fundus + flames
HIV retinopathy
Cotton wool spots
What are the mydriatics?
Anti-muscarinics
Sympathomimetics
Indications for mydriatics
Eye examination
Prevention of snechiae in anterior uveitis/iritis
Caution with mydriatics?
May lead to acute glaucoma if shallow anterior chamber
Class of drug:
Tropicamide, cyclopentolate
Anti-muscarinic
Tropicamide -3h
Cyclopentolate- 24h
Effects of anit-muscarinics on eye
Pupil dilatation and loss of light reflex
Cyclopegia-> blurred vision
What class of drug is pilocarpine?
Muscarinic agonist
Use of pilocarpine
Acute closed-angle galucoma
What is tetracaine
Anaesthetic used to permit examination of a painful eye
What are emedastine and antazoline
Topical anti-histamines used in ophthalmology
What is hypomellose and carbomer
Eye lubricants
Whence do refractive errors arise?
Disorders of the size and shape of the eye
Myopia=
Short-sightedness
Problem in myopia
Eye is too long, distant objects are focussed too far forward
Genetic or excessive close work in early decades
Solution to myopia
Concave lenses
Problem in astigmatism
Cornea or lens doesn’t have the same degree of curvature in horizontal and vertical planes
Image of object is distorted longitudinally or vertically
Hypermetropia=
Long-sightedness
Problem in hypermetropia
Eye is too short
When the eye is relaxed and not accomodating, objects are focussed behind the retina
Contraction of ciliary muscles to focus image-> tiredness of gage and psosible a convergent squint in children
Solution to hypermetropia
Convex lenses
Presbyopia
With age, the lens becomes stiff and less easy to deform
Start at about 40y and are complete by 60y
Use convex lenses to correct
Esotropia=
Convergent squint
May be idiopathic or due to hypermetropia
Esotropia
Exotropia
Divergent squint
common in older children, often divergent
Exotropia
Diagnosis of non-paralytic squint
Corneal reflection: should fall centrally and symmetrically on each cornea
Cover test: movement of uncovered eye to take up fixation demonstrates manifest squint
Mx of non-paralytic squint
3Os
Optical: correct refractive errors
Orthoptic: patching good eye encourages use of squinting eye
Operation: e.g. resection and recession of rectus muscles
Diplopia most on looking in direction of pull of paralysed muscle
Eye won’t fixate on covering
Paralytic squint
How to determine which eye is malfunctioning in paralytic squint
Cover each eye in turn, whichever eye sees the outer image is malfunctioning
In paralytic squint, how can you determine which muscle is affect
Diplopia most on looking in direction of pull of paralysed muscle
Ptosis
Fixed dilated pupil
Down and out
CNIII lesion
Causes of CNIII palsy
Medical: DM, MS, infarction
Surgical: raised ICP, cavernous sinus thrombosis, posterior communicating artery aneurysm
Diplopia, espsecially on going down stairs
Head tilt
?CNVI palsy
Causes of CNIV palsy
Peripheral: DM (30%), trauma (30%)- nerve exits posterior of brainstem, compression
Central: MS, vascular, SOL
Eye is medially deviated and cannot abduct
Diplopia in the horizontal plane
?CNVI palsy
Causes of CNVI palsy
Peripheral: DM, compression, trauma
Central: MS, vascular, SOL
Mx of eye trauma
Record acuity of both eyes
Take detailed Hx of event
If unable to open injured eye, instill LA e.g. tetracaine
Ix in ?FB in orbit
XR orbit if metal suspected
Fluorescein may show corneal abrasions
Mx of eye trauma
Chloramphenicol drops 0.5% to prevent infection, usually with coag negative staph
Eye patch
Cycloplegic drops may reduce pain e.g. tropicamide, cyclopentolate
Features of intra-ocular haemorrhage
Blood in anterior chamber- hyphaema
Small amounts clear spontaneously but some may need evacuation
Complicated by corneal staining and glaucoma
Keep IOP down and monitor
Features of orbital blowout #
Blunt injury-> sudden increase in orbital pressure with herniation of orbital contents into maxillary sinus
Opthalmoplegia and diplopia (tethering of IR and IO)
Loss of sensation to lower lid skin (infraorbital nerve injury)
Ipsilateral epistaxis (damage to anterior ethmoidal artery)
Reduced acuity
Irregular pupil that reacts slowly to light
?Orbital blowout fracture
Mx of chemical injury to the eye
Alkaline solutions are particulary damaging due to saponification
Mx with copious irrigation and specialist referral
Small dark spots in the visual field
Floaters
Sudden showers of floaters in one eye may be due to?
Blood or retinal detachment
Causes of floaters
Retinal detachment
VH
Diabetic retinopathy/ HTN
Old retinal branch vein occlusion
Syneresis (degenerative opacities in the vitreous)
Flashes in vision=
Photopsia
Causes of flashes
Either from intraocular or intracerebral pathology
Headached, NV: migraine
Flashes and floater= retinal detachment
What can cause haloes
May be caused by hazy ocular media- cataract, corneal oedema, acute glaucoma
Haloes + eye pain=
Acute glaucoma
Jagged haloes which change shape are usually
Migrainous
Rx in seasonal allergical conjuncitivitis
Antazoline: antihistamine drops
Cromoglycate: inhibits mast cell degranulation
Small papillae on tarsal conjuncitvae
?Seasonal allergic/ perenial allergic conjuncitivites
Rx of perennial conjuncitivis
Olopatadine (anti-histamine and mast cell stabiliser)
Causes of giant papillary conjuncitvitis
Mx
Iatrogenic FBs: contact lenses, prostheses, sutures
Removal of FB, mast cell stabilisers
Giant papillary conjunctivitis
Mx of allergic eye disorders
Remove the allergen responsible where possible
General measures: cold compress, artificial tears, oral antihistamine (loratadine 10mg/pd PO)
Eye drops:
Antihistamines: antazoline, azelastine
Mast cell stabilisers: cromoglycate, lodoxamide
Steroids: dexamethasone (NB of inducing glaucoma)
NSAIDs: Diclofenac
Pathophysiology of trachoma
Caused by Chlamydia trachomatis (A, B, C)
Spread by flies
Inflammatory reaction under the lids-> scarring-> entropion-> eyelashes scratching cornea-> ulceration-> blindness
Rx Trachoma
Tetracycline 1% +/- PO
Pathophysiology of onchoceriasis
Caused by microfilariae or nematode Onchocerca volvulus
Spread by flies
Fly bites-> microfilariae infeciton-> invade the eye-> inflammation-> fibrosis-> corneal opacities and synechiae
Rx in onchoceriasis
Ivermectin
Xerophthalmia and keratomalacia are manifestations of?
Vitamin A deficiency
Night blindness and dry conjunctivae
Corneal ulceration and perforation
?Vitamin A deficiency
Rx in Vitamin A related Xerophthalmia?
Vitamin A/palmitate reverses early corneal changes
Which two cranial nerves originate from the cerebrum?
Olfactory and optic
What is the origin of the trochlear nerve?
The midbrain, comes from the posterior side of the midbrain and has the longest intracranial length
What is the origin of the oculomotor nerve?
Midbrain-pontine junction
What is the origin of the trigeminal?
Pons
What is the origin of the abducens, facial and vestibulocochlear nerves?
Pontine medulla junction
What is the origin of glossopharyngeal, vagus, accessory nerve?
Posterior to the olive in the medulla oblongata
What is the origin of the hypoglossal?
Anterior to the olive in the medulla oblongata
What cranial nerve exits through the cribiform plate?
Olfactory
What cranial nerve exits through the optic canal?
III
What CNs exit through the superior orbital fissure?
III
IV
V1
VI
What cranial nerve exits through the foramen rotundum
V2
What CN exits through the formaen ovale?
V3
What cranial nerve exits through the internal acoustic meatus?
VII
VIII
What cranial nerves exit through the jugular foramen?
IX
X
XI
What CN exits through the hypoglossal canal?
XII
What modality is carried by:
CNI
Special visceral sensory: smell
What modality is carried by:
CNII
Special somatic sensory (Vision)
What modality is carried by:
III
General somatic motor: skeletal muscles
General visceral motor: pupillary sphincter (autonomic)
What modality is carried by:
IV
General sensory motor: SO
What modality is carried by:
V1
General somatic sensory: scalp, forehead and nose
What modality is carried by:
V2
General somatic sensory: cheeks, lower eye lid, nasal mucosa, upper lip, upper teeth, palate
What modality is carried by:
V3
General somatic sensory: anterior 2/3rd tongue, skin over mandible and lower teeth
Special visceral motor: Muscles of mastication
What modality is carried by:
VI
General somatic motor: LR
What modality is carried by:
VII
General somatic sensory: sensation to part of external ear
Special visceral sensory: taste from anterior 2/3rds of tongue and soft palate
General somatic motor: muscles of facial expression
General visceral motor: lacrimal, submandibular, sublingual glands and mucous glands of mouth and nose
What modality is carried by:
VIII
Special somatic sensory: hearing and balance
What modality is carried by:
IX
General somatic sensory: posterior 1/3rd of the tongue, external ear and middle ear cavity
General visceral sensory: carotid body and sinus
Special visceral sensory: taste from posterior 1/3rd of tonuge
General visceral motor: parotid gland
Special visceral motor: stylopharyngeus
What modality is carried by:
X
General somatic sensory: external ear, larynx, pharynx
General visceral motor: larynx, pharynx and thoracic and abdominal viscera
Special visceral sensory: taste from epiglottis region of tongue
General visceral motor: smooth muscles of the pharynx larynx and most of the GIT
Special visceral motor: most muscles of the pharynx and larynx
What modality is carried by:
Accessory nerve?
General somatic motor: trapezius and sternocleidomastoid
Special visceral motor: few fibres run with CNX to visceral
What modality is carried by:
XII
Intrinsic and extrinsic tongue muscles (except palatoglossus)
What innervates palatoglossus?
CNX
Only muscle of the tongue not innervated by XII
What is the composition of the olfactory nerve?
Peripheral olfactory processes (in the olfactory mucosa)
Central processes that return the information to the brain
Course of the olfactory nerve
Enters the cranial cavity through the cribiform plate of the ethmoid bone
Once in the cranial cavity the fibres enter the olfacory bulb which lies in the olfactory groove in the anterior cranial fossa.
Pass posteriorly to the olfactory tract
As the tract reaches the anterior perforated substance it divides into lateral and medial stria
Lateral stria carries axons to the primary olfactory cortex
Medial stria carry axons to the olfactory bulb on the other side
How does the optic nerve enter the cranial cavity
Through the optic canal, a passage in the sphenoid bone running along the middle cranial fossa in close proximity to the pituitary gland
Intracranial course of the optic nerve
Within the middle cranial fossa the optic nerves from each eye unite to form the optic chiasm
At the optic chiasm the nerves cross over and form the optic tracts
Each tract travels to its corresponding cerebral hemisphere to reach the lateral geniculate nucleus, a relay system in the thalamus where the fibres synpase
Axons from the LGN carry information via optic radiation
The upper optic radiation carries fibres from the superior retinal quadrants (corresponding to the inferior visual field quadrants), travelling through the parietal lobe to reach the visual cortex
The lower optic radiation carries fibres from the inferior retinal quadrants (superior visual field quadrants) and travels through the temporal lobe via Meyer’s loop.
Course of the oculomotor nerve
Originates from the anterior branch of the midbrain, moving anteriorly
Passes below the posterior cerebral artery and above the superior cerebellar artery
Pierces the dura mater and enters the cavernous sinus
Within the cavernous sinus it receives sympathetic branches from the internal carotid plexus, that travel within its sheath
Leaves the cranial cavity via the superior orbital fissure, where it divides into the superior and inferior branches
What does the superior branch of oculomotor innervate?
SR and LPS
Sympathetic fibres run with the superior branch to innervate the superior tarsal muscle
What does the inferior branch of III innervate?
IR, MR IO
PNS fibres run to the ciliary ganglion which ultimately innervates the sphincter pupillae and ciliary muscles
Which SO do the IV neurones innervate?
. As the fibres from the trochlear nucleus cross in the midbrain before they exit, the trochlear neurones innervate the contralateral superior oblique.
What is unique about the trochlear nerve?
The trochlear nucleus is unique in that its axons run dorsally and cross the midline before emerging from the brainstem posteriorly. Thus a lesion of the trochlear nucleus affects the contralateral eye. Lesions of all other cranial nuclei affect the ipsilateral side.
Also the only CN to emerge from the posterior of the brainstem
Action of SO
Depress and intort the eyeball- down and in
What is innervated by the motor component of trigeminal
Only the mandibular branch of CN V has motor fibres. It innervates the muscles of mastication: medial pterygoid, lateral pterygoid, masseter and temporalis. The mandibular nerve also supplies other 1st pharyngeal arch derivatives: anterior belly of digastric, tensor veli palatini and tensor tympani.
Parasympathetic supply and the trigeminal
The post-ganglionic neruones of the PNS ganglia travel with branches of the trigeminal but the trigeminal nerve is not part of the cranial outflow of PNS supply
Anatomical course of V
Originates from three sensory nuclei (mesencephalic, principal sensory, spinal nuceli) and one motor nucleus extending from the midbrain to the medulla
At the level of the pons, the sensory nuclei merge to form a sensory root
The motor nucleus continues to form a motor root
In the middle cranial fossa the sensory root expands into the trigeminal ganglion which is located lateral to the cavernous sinus. In a depression of the temporal bone- the trigeminal cave
Trigeminal gives rise to V1, V2, V3. Motor root passes inferiorly to the sensory root and its fibres are only carried in V3
Function of the ophthalmic nerve
Gives rise to 3 terminal branches, frontal, lacrimal and nasociliary which innervate the skin and mucous membrane of derivatives of the frontonasal prominence
Also provides PNS supply to the lacrimal gland from the pterygopalatine ganglion (facial nerve derivative) travel with V2 then join the lacrimal branch of V1 providing PNS innervation to the lacrimal gland
Corneal reflex arms
Afferent: V1
Efferent: facial nerve
V2 function
Sensory
PNS: initially carries post ganglionic fibres from the pterygopalatine ganglion (VII derivative) and travel with the zygomatic branch of V2 then join the lacrimal branch of V1
Nasal glands: PNS fibres are also carried to the mucous glands of the nasal mucosa travelling with branches of V2
What is the motor funciton of V
Carried by V3
Muscles of mastication: medial and lateral pterygoids, massester, temporalis
Anterior belly of digastric and mylohyoid muscles
Tensor veli palatini
Tensory tympani
PNS: post ganglionic fibres from the submandibular ganglion travel with the lingual nerve to innervate submandibular and sublingual glands
Parotid gland: post ganglionic fibres from the otic ganglion (derived from CN IX) travel with the auriculotemporal branch of V3 to innervate the parotid gland
Anatomical course of the VIII
Vestibular and cochlear portions of the VIII are functionally discrete so orignate from different nuclei in the brain
Vestibular: vesitublar nuclei complex in the pon and medulla
Cochlear: from the ventral and dorsal cochlear nuclei in the inferior cerebellar peduncle.
Combine in the pons, nerve emerges from the brain at the CPA and exits the cranium via the internal acoustic meatus of the temporal bone. Splits distal to the internal acoustic meatus.
Clinical relevance of basilar skull # to VIII
Basilar skull fracture can cause damage to VIII in the internal acoustic meatus producing symptoms of vestibular and cochlear nerve damage.
Course of CN IX
Arises from the medulla oblongata
Leaves the cranium via the jugular foramen at which point the tympanic nerve arises.
Immediately outside the jugular foramen lie two ganglia known as the superior and inferior (or petrous) ganglia that contain the cell bodies of the sensory fibres in the glossopharyngeal nerve.
Descends to give innervation to stylopharyngeus and the carotid sinus nerve which provides sensation to the carotid sinus and body.
What are the components of the gag reflex?
Afferent= CNIX
Efferent= CNX
Course of the vagus nerve in the head
Originates from the medulla and exits via the jugular foramen
Within the cranium the auricular branch arises which supplies sensation to the posterior part of the external auditory canal and external ear
Anatomical course of the vagus nerve in the neck
Passes into carotid sheath, travelling inferiorly with the internal jugular vein and common carotid.
Right vagus passes anterior to the subclavian artery and posterior to the sternoclavicular joint, entering the thorax
Left vagus passes inferiorly between the left common carotid and the left subclavian arteries, posterior to the sternoclavicular joint.
Branches of the vagus nerve in the neck?
Pharyngeal branches: motor innervation to the muscles of the pharynx and soft palate
Superior laryngelal nerve: internal and external branches, external innervate the cricothyroid muscle, the internal providing sensory innervation to the laryngopharynx and superior part of the larynx
Recurrent laryngeal nerve (on the right only) hooks underneath the subclavian artery and ascends to the larynx, innervating the majority of the intrinsic muscles of the larynx
Course of the vagus nerve in the thorax
Right vagus forms the posterior vagal trunk
The left forms the anterior vagal trunk
Branches from these trunks contribute to the oesophageal plexus
Two other branches arise: the left recurrent laryngeal nerve (hooks under the arch of the aorta)
Cardiac branches
Vagal trunks enter the abdomen via the oesophageal hiatus
Lesion to one recurrent laryngeal nerve causes?
Both?
Dysphonia
Aphonia
Anatomical course of the accessory nerve (spinal)
Spinal portion arises from neurones of the upper SC (C1-C5/C6) of the spinal nerve roots.
Coalesce to form the spinal part of the accessory nerve which then runs superiorly to enter the cranium via the foramen magnum
It travels to the posterior cranial fossa to reach the jugular foramen where it meets the cranial portion of the accessory nerve before exiting the skull.
Descends along the internal carotid to reach sternocleidomastoid which it innervates.
Extracranial course is relatively superficial leaving it vulnerable to damage.
Cranial course of the accessory nerve
Much smaller and arises from the lateral aspect of the medulla.
Leaves the cranium via the jugular foramen where it briefly contacts the spinal part of the accessory nerve.
Immediately after leaving the skull, the cranial portion combines with the vagus at the inferior ganglion of the vagus.
The fibres are then distributed through the vagus nerve.
What is the most common cause of accessory nerve damage?
Iatrogenic e.g. cervical LN biopsy or cannulation of the IJV.
Clinical features include muscle wasting and partial paralysis of the sternocleidomastoid, resulting in the inability to rotate the head or weakness in shrugging the shoulders. Damage to the muscles may also result in an asymmetrical neckline.
Accessory nerve palsy
Asymmetrical neck line
What muscles are innervated by the hypoglossal nerve?
All muscles of the tongue except palatoglossus (innervated by the vagus nerve)
What are the extrinsic muscles of the tongue?
Genioglossus
Hypoglossus
Styloglossus
[Palatoglossus- vagus nerve]
What are the intrinsic muscles of the tongue?
Superior longitudinal
Inferior longitudinal
Transverse
Vertical
Classification of hypoglossal nerve palsy
Can be supranuclear (UMN), nuclear, or infranuclear (LMN)
UMN: tongue will deviate away from injured side. Only seen during the initial days after the injury, after which it will not deviate.
Infranuclear lesions lead to parlaysis of the hpyoglossal nerve leading to atrophy of muscles of the tonuge, tongue will be deviated TOWARDS lesion. Due to weaker geniglossal muscle.
What may be seen in supranuclear damage to the left and right tracts of CNXII
Damage to facial and trigemnial nerve dysfunction as a consequence of damage to the brainstem following arteriosclerosis of the vertebrobasilar artery
CN palsy + pain
?Cartoid dissection
What is the only muscle of the tongue not innervated by hypoglossal?
Extrinsic, palatoglossus (Vagus)
Right subclavian arises from the brachiocephalic trunk
Left subclavian directly from the arota
When do the subclavian arteries become the axillary arteries?
When they cross the lateral edge of the first 1 rib and enter the axilla
Course of the axillary artery
Passes through the axilla underneath pectoralis minor enclosed in the axillary sheath
At the humeral surgical neck the posterior and anterior circumflex humeral arteries arise
Circle posteriorly around the humerus to supply the shoulder region
The subscapsular artery also arises here (largest brach of the axillary artery)
At the level of the teres major the axillary artery becomes the brachial artery
Where does the axillary artery become the brachial
At the lower margin of teres major
What in the axilla can compress the brachial plexus producing neurological symptoms and can be treated surgically
Axillary artery aneurysm
Course of the brachial artery
Immediately distal to teres major gives the profunda brachii- deep artery of the arm
which travels along the posterior surface of the humerus in the radial groove, supplying the posterior aspect of the arm
Brachial artery descends down the arm immediately posterior to the median nerve, as it crosses the cubital fossa underneath brachialis it terminates by bifurcating into the radial and ulnar arteries
Course of the arteries in the forearm
Radial- posterior aspect of the forearm
Ulnar- anterior
Areteries anastomose by forming the superficial palmar arch and the deep palmar arch
What are the major superifical veins of the upper limb
The cephalic and basilic veins
Course of the superficial veins of the upper limb
Basilic vein originates from the dorsal venous network of the hand ascending the medial aspect of the upper limb. At the border of teres major the vein moves deep into the arm where it combines with brachial veins to form the axillary vein
The cephalic vein arises from the dorsal venous network of the ascending ascending on the anterolateral aspect of the upper limb, passing anteriorly at the elbow.
At the shoulder the cephalic vein travels between the delotid and pec major muscles in the deltopectoral groove and enters the axilla via the clavipectoral triangle.
It terminates here by joining the axillray vein.
At the elbow the cephalic and basilic veins are connected by the median cubital vein
What is the course of the deep veins of the upper limb
Paired veins that accompany and lie either side of an artery
Brachial veins are the largest in size and are situated either side of the brachial artery
These are vena comitantes
Perforating veins run between the deep and superficail veins of the upper limb, connecting the two systems
What are at risk of damage in axillary LN dissection?
Long thoracic nerve (winged scapula)
Or the thoracodorsal nerve
Describe the course of the femoral artery
Continuation of the EIA which becomes the femoral artery when it crosses under the inguinal ligament and enters the femoral triangle
In the femoral triangle the profunda femoris artery arises from the posterolateral aspect. It travels posteriorly giving off three main branches:
Lateral femoral circumflex: wraps around the anterior, lateral side of the femur supplying muscles in the lateral side of the thigh
Medial circumflex artery: wraps around the posterior side of the femur supplying the head and neck (avascular necorsis in intracapsular #)
Perforating branches: 3/4 arteries that perforate the adductor magnus
After exiting the femoral triangle the femoral artery continues down the anterior surface of the thigh via the adductor canal.
The adductor canal ends at the adductor hiatus at which point the femoral artery enters the posterior compartment of the thigh proximal to the knee
Borders of the femoral triangle
Superior border: inguinal ligament
Lateral border: sartorius
Medial border: medial border of adductor longus
Anteriorly the roof of the femoral triangle is the fascia lata
Posteriorly the base is formed by pectineus, ilopsoas and adductor longus muscles.
Contents of the femoral triangle
NAVEL
Femoral nerve: innervates the anterior compartment of the thigh
Femoral artery
Femoral vein
Empty space
Lymph canal
Contained in the femoral sheath
Location of the femoral pulse
Midway between the pubic symphysis and ASIS
Describe the course of the other arteries supplying the thigh
Obturator artery arises from the IIA in the pelvic region, descends via the obturator canal to enter the medial thigh bifurcating into the canal.
Gluteal region is largely supplied by the superior and inferior gluteal arteries which exit the pelvis via the GSF.
The IGA also contirbutes to the vasculature of the posterior thigh
What differentiates between the SGA and the IGA
Both exit the GSF
SGA superior to piriformis
IGA inferior to piriformis
Describe the arterial supply of the leg
Popliteal artery descends down the posterior thigh giving off genicular branches that supply the knee joint.
Moves through the popliteal fossa between gastrocnemius and popliteus.
At the lower border of popliteus it terminates by dividing into anterior and posterior tibial artery.
Posterior tibial continues inferiorly along the surface of the deep muscles accompanying the tibial nerve entering the sole of the foot via the tarsal tunnel.
During the descent of the posterior tibial the fibular artery arises which moves laterally penetrating the lateral compartment of the leg.
The anterior tibial artery passes anteriorly between the tibia and fibular through a gap in the interoesseous membrane. Moving inferiorly down the leg and into the foot where it becomes dorsalis pedis.
What is the clinical revelance of the fact that the popliteal fascia is tough and non-extensable
Aneurysm of the popliteal artery has consequences for other contents of the popliteal fossa.
The tibial nerve is particularly susceptible to compression from the popliteal artery
Major features are absent/weakened plantar fleixion, paraesthesia of the foot and posterolateral leg.
Can be detected through obvious expansile pulsatile mass and an arterial bruit
Describe the arterial supply of the foot
Dorsalis pedis- continuation of the anterior tibial artery
Posterior tibial enters through the sole of the foot through the tarsal tunnel and supplies the lateral and medial plantar surfaces
Where can the femoral pulse be palpated?
be palpated as it enters the femoral triangle, midway between the anterior superior iliac spine of the pelvis, and the pubis synthesis (the mid-inguinal point).
Where can the dorsalis pedis be palpated?
Dorsum of the foot in the fist intermetatarsal space, lateral to the tendon of the great toe
Where can the posterior tibial pulse be palpated
Behind and below the medial malleolus
Where can the popliteal pulse be palpated
In the midline in the popliteal fossa with gentle knee flexion
Describe the course of the deep venous drainage of the lower limb
Dorsal arch drains mainly into the superficial veins, some penetrate deep into the leg forming the anterior tibial vein.
On the plantar aspect of the foot the medial and lateral plantar veins arise and combine to form the posterior tibial and fibular vein.
The posterior tibial vein accompanies the posterior tibial artery, entering the leg posteriorly to the medial malleolus.
On the posterior surface of the knee the anterior tibial, posterior tibial and fibular veins unite to form the popliteal vein which enters the thigh through the adductor canal
Course of the deep venous drainage of the thigh
The popliteal vein becomes the femoral vein once it enters the thigh and is situated anteriorly.
The profunda femoris vein is the other main venous structure. Empties into the distal section of the femoral vein.
The femoral vein leaves the thigh to become the EIV
Outline the superficial venous drainage of the leg
Two major veins, the great and small saphenous
Great saphenous is formed by the dorsal venous arch of the foot. Ascends on the medial side of the leg, passing anteriorly to the medial malleolus and posterior to the medial condyle at the knee.
As the vein moves up the leg it receives tributaries from other small superficial veins, and terminates by draining into the femoral vein immediately inferior to the inguinal ligament.
The small saphenous vein moves up the posterior side of the leg, passing posterior to the lateral malleolus along the border of the calcaneal tendon. It moves between the two heads of gastrocnemius and empties into the popliteal vein in the popliteal fossa
What is the location of the saphenofemoral junction
2.5cm below and 2.5cm lateral to the pubic tubercle
Incidence of chronic limb ischaemia
5% of males >50 years have intermittent claudication
Def: chronic limb ischaemia
Ankle artery pressure <50mmHg (toe <30)
And either:
persistent rest pain requiring analgesia for >2w
or
Ulceration or gangrene
Cause of chronic limb ischaemia
Atherosclerosis: typically asymptomatic until 50% stenosis
Vasculitis and fibromuscular dysplasia are v rare causes
Summary of atherosclerosis
Endothelial injury: haemodynamic, HTN, raised lipids
Chronic inflammation: lipid-laden foam cells produce GFs, cytokines, ROS and MMPs-> lymphocyte and SMC recruitment
SM proliferation: conversion of fatty streak to atherosclerotic plaque
Difference betweeen arteriosclerosis and atherosclerosis
Arteriosclerosis= general arterial hardening
Atherosclerosis= arterial hardening specifically due to atheroma
Atheroma pathology
Fibrous cap: SM cells, lymphocytes, collagen
Necrotic centre: cell debris, cholesterol, Ca, foam cells
Modifiable risk factors for chronic limb ischaemia
Smoking
BP
DM
Hyperlipiademia
Reduced exercise
Non modifiable RFs for chronic limb ischaemia
FH and PMHx
Male
Increased age
Genetic
What is the association of vascular disease with chronic limb ischaemia
IHD: 90%
Carotid stenosis; 15%
AAA
Renovascular disease
DM microvascular disease
cramping pain after walking a fixed distance
Pain rapidly relieved by rest
Either calf or buttock
Intermittent claudication
Calf pain in intermittent claudication
Superifical femoral disease (commonest)
Buttock pain in context of intermittent claudication
Iliac disease (internal or common)
Def: critical limb ischaemia
Fontaine 3 or 4
Rest pain
Especially at night, usually felt in the foot
Patient hangs foot out of bad
Due to reduced CO and loss of gravity
Ulceration
Gangrene
Rest pain
Especially at night, usually felt in the foot
Patient hangs foot out of bad
Due to reduced CO and loss of gravity
Ulceration
Gangrene
?Critical limb ischaemia
Leriche’s syndrome
Aortoiliac occlusive disease
Atherosclerotic occlusion of abdominal aorta and iliacs
Triad in Leriche’s syndrome
Buttock claudication and wasting
Erectile dysfunction
Absent femoral pulses
Buerger’s disease=
Thromboangitis obliterans
Young, male, heavy smoker
Acute inflammation and thrombosis of arteries and veins in hands and feet-> ulceration and gangrene
Buerger’s disease
Buerger’s Disease
Thrombangitis obliterans
Weak pulses and CRT >2
Ulcers: painful, punched out on pressure points
Nail dystrophy/ onchylosis
Skin: cold, white, atrophy, absent hair
Venous guttering
Muscle atrophy
?Chornic limb ischaemia
What is Buerger’s test?
The vascular angle, which is also called Buerger’s angle, is the angle to which the leg has to be raised before it becomes pale, whilst in supine decubitus. In a limb with a normal circulation the toes and sole of the foot, stay pink, even when the limb is raised by 90 degrees.
Reduced Buerger’s angle seen in?
Chronic limb iscahemia
Buerger’s angle cut offs?
>90= normal
20-30= ischaemia
<20= severe ischaemia
What is positive Buerger’s sign?
Pale-> reactive hyperaemia due to accumulation of deoxygenated blood in dilated capillaries
How can chronic limb ischaemia be classified?
Fontaine
or
Rutherford
Fontaine classification of chronic limb ischaemia
- Asymptomatic
- Intermittent claudication
a >200m
b <200m
- Iscahemic rest pain
- Ulceration/ gangrene
Rutherford classification of chronic limb iscahemia
- Mild claudication
- Moderate claudication
- Severe claudication
- Ischaemic rest pain
- Minor tissue loss
- Major tissue loss
Ix in Chronic limb iscahemia
ABPI
Doppler
Walk test
Bloods
Imaging
Other: ECG
Doppler waveforms in Chronic limb ischaemia
Normal: triphasic
Mild stenosis: biphasic
Severe stenosis: monophasic
ABPI >1.4
Calcification: CRF, DM
ABPI >1
Normal
ABNPI 0.8-0.9
Asymptomatic
Fontaine 1
ABPI 0.6-08
Fontaine 2
Claudication
ABPI 0.3-0.6
Fontaine 3
Rest pain
ABPI <0.3
Ulceration and gangrene
Fontaine 4
Why might false ABPI results be obtained in DM/CRF?
Due to calcification of vessels: mediasclerosis
Use toe pressure with small cuff, <30mmHg is the cut off
What is the walk test in chronic limb ischaemia Ix
Walk on treadmill @ certain speed and incline to establish maximum claudication distance
ABPI measured before and after, 20% reduction is signifcant
Role of bloods in chronic limb ischaemia Ix
FBC + U+Es: anaemia, renovascular disease
Lipids and glucose
ESR: arteritis
G+S: possible procedure
Role of imaging in chronic limb iscahemia Ix
Assess site, extent and distal run-off
Colour duplex US
CT/MR angiogram with gadolinium contrast
Digital subtraction angiography: invasive, not commonly used for Dx only but used when performing therapeutic angioplasty or stenting
Why perform an ECG in chronic limb ischaemia?
Look for evidence of coronary artery pathology
Mx of chronic limb ischaemia: Conservative
Most patients with claudication can be managed conservatively
Increase exercise and employ exercise programs
Stop smoking
Weight loss
Foot care
Prognosis with conservative management of chronic limb iscahemia
1/3 improve
1/3 stay the same
1/3 deteriorate
Mx of chronic limb iscahemia: Medical
Modification of cardiovascular risk fators: BP, lipis, DM
Beta blockers don’t worsen intermittent caludication but use with caution
Parenteral prostanoids reduces pain in patients unfit for surgery
Antiplatelet drugs: clopidogrel/aspirin
Peripheral vasodilators: naftidrofuryl oxalate
NB re: ACEI intermittent claudication
BP medication may initially worsen pain of claudication but improve LT CV risk
However, 25% of patients with PAD also have RAS so ACEI should be used with caution
Management of chronic limb ischaemia: endovascular
Percutaneous transluminal angioplasty
Good for short stenosis in big vessels e.g. iliacs, SFA
Lower risk for patient as performed under LA
Improved inflow can reduce pain but restoration of foot pulses is required for Rx of ulceration/gangrene
Indications for surgical reconstruction in chronic limb ischaemia
V. short claudication distance e.g. <100m
Symptoms greatly affecting patients QoL
Development of rest pain
NB pre-op assessment as patient likely to have cardiorespiratory co-morbidities
Practicalities of surgery for chronic limb ischaemia
Need good proximal supply and distal run-off
Saphenous vein grafts are preferred below the IL
More distal grafts have increased rates of thrombosis
Classification of surgeries for chronic limb iscahemia
Anatomical: fem-pop, fem-distal, aortobifemoral
Extra-anatomical: axillo-femoral, bifemoral, fem-fem crossover
Other surgical options for chronic limb ischaemia
Endarterectomy
Sympathectomy: chemical or surgical
Amputation
Px 1yr after critical limb ischaemia
50% alive w/o amputation
25% will have had major amputation
25% dead (usually MI or stroke)
Px following amputation in CLI
1/3 complete autonomy
1/3 partial autonomy
1/3 dead
Def: acute limb iscahemia
Ischaemia <14d
Def: acute on chronic limb iscahemia
Worsening symptoms and signs <14d
Def: chronic limb iscahemia
Ischaemia stable for >14d
Incomplete acute limb iscahemia
Limb not threatened
Complete acute limb ischaemia
Limb threatened, loss of limb unless intervention within 6hrs
Irreversible acute limb ischaemia
Requires amputation
Causes of acute limb ischaemia
Thrombosis in situ: 60%
Embolism: 30%
Graft/stent occlusion
Trauma
Aortic dissection
Thrombosis in situ, acute limb iscahemia
A previously stenosed vessel with plaque rupture, usually incomplete iscahemia
Embolism in acute limb ischaemia
80% from LA in AF
Valvular disease
Can be iatrogenic/surgery
Cholesterol in long bone #
Paradoxical via PFO
Typically lodge at femoral bifurcation causing complete limb ischaemia
6Ps of acute limb ischaemia
Pale
Pulseless
Perishingly cold
Painful
Paraesthesia
Paralysis
Acute limb ischaemia:
Onset in hours to days
Less severe collaterals
Claudication history present
Contralateral pulses absent
Diagnosed with angiography
Rx with thrombolysis/bypass surgery
Thrombotic cause
Acute limb ischaemia:
Sudden onset
Profound ischaemia
AF
Absent claudication history
Present contralateral pulses
Clinical diangosis
Rx with embolectomy + warfarin
Embolic acute limb iscahemia
Ix in acute limb ischaemia
Bloods: FBC, U+E, INR, G+S, CK
ECG
Imaging: CXR, Duplex doppler
General management of acute limb ischaemia
SENIOR
NBM
Rehydration: IV fluids
Analgesia: morphine + metoclopramide
Abx if signs of infection
Unfractionated heparin IV: prevent extension
If occlusion is complete: urgent surgery
If incomplete: angiogram + observe for deterioriation
Angiography in acute limb iscahemia
Not performed if there is complete occlusion as it introduces delay
If occlusion is incomplete, pre-op angio will guide any distal bypass
Mx of embolic acute limb iscahemia
- Embolectomy
- Thrombolysis
- Other options
Embolectomy in acute limb ischaemia
Under LA or GA
Wire fed through embolus
Fogarty catheter fed over the top
Balloon inflated and catheter withdrawn removing the embolism
Send embolism for histology to exclude atrial myxoma
Adequacy can be confirmed by on-table angiography
Thrombolysis in acute limb ischaemia
Consider if embolectomy unsuccessful
E.g. local injection of TPA
Other options in acute management of embolic acute limb ischaemia
Emergency reconstruction
Amputation
Mx of acute limb post embolectomy
Anticoagulate: IV heparin-> warfarin
ID embolic source: ECG, echo, US aorta, femoral and pop
Complications
Complications post embolectomy in acute limb ischaemia
Reperfusion injury:
Local swelling-> compartment syndrome
Acidosis and arrhythmia 2o to raised K
ARDS
GI oedema-> endotoxic shock
Chronic pain syndromes
Mx of thrombotic acute limb ischaemia
Emergency reconstruction if complete occlusion
Angiography and angioplasty
Thrombolysis
Amputation
Pathogenesis of carotid artery diesease
Turbulent flow-> reduced shear stress at carotid bifurcation promoting atherosclerosis and plaque formation
Plaque rupture-> complete occlusion or distal emboli
Causes 15-25% of CVA/TIA
CVA/TIA
Bruit
?Carotid artery disease
Ix in carotid artery disease?
Duplex carotid Doppler
MRA
Mx of carotid artery disease
Aspirin or clopidogrel
Control RFs
Surgical: endarterectomy
Symptomatic >70% benefit (5% stroke risk per year)
>50% benefit if low risk
Performed within 2w of presentation
Asymptomatic:
>60% benefit if low risk
What studies have been used to look at the impact of endarterectomy in symptomatic caroit dartery disease?
ECST vs optimal medical therapy
NASCET
Cx of endarterectomy
Stroke or death: 3%
HTN: 60%
Haematoma
MI
Nerve injury
What nerves can be damaged in carotid endarterectomy
Hypoglossal: ipsilateral tongue deviation
Great auricular: numb ear lobe
Recurrent larygneal: hoarse voice, bovine cough
Stenting vs carotid endarterectomy
Less invasive: reduced hospital stay, reduced infection, reduced CN injury
Concern over increased stroke risk, esp. in pts >70y
Meta-analysis shows no sig difference in mortality vs CEA
Def: Aneurysm
Abnormal dilatation of a blood vessel >50% of its normal diameter
Def: true aneurysm
Dilatation of a blood vessel involving all layers of the wall and that is >50% of its normal diameter
Two different morphologies:
Fusiform e.g. AAA
Saccular: e.g. Berry aneurysm
Difference between fusiform and saccular aneurysm
The shape of an aneurysm is described as being fusiform or saccular, which helps to identify a true aneurysm. The more common fusiform-shaped aneurysm bulges or balloons out on all sides of the blood vessel. A saccular-shaped aneurysm bulges or balloons out only on one side.
Def: false aneurysm
Collection of blood around a vessel wall that communicates with the vessel lumen
Usually iatrogenic e.g. puncture, cannulation
Def: dissection
Vessel dilatation caused by blood splaying apart the media to form a channel within the vessel wallt
Layers of a blood vessel
Lumen
Intima
Media
Advenititia
Congenital causes of aneurysms
ADPKD-> Berry aneurysms
Marfan’s, Ehlers Danlos
Acquired causes of aneurysms
Atherosclerosis
Trauma e.g. penetrating trauma
Inflammatory: Takayasu’s, HSP, Kawasaki
Infection:
Mycotic- SBE
Tertiary syphillis (esp. thoracic)
Complications of aneurysms
Rupture
Thrombosis
Distal embolisation
Pressure: DVT, oesophagus, nutcracker syndrome
Fistula (IVC, intestine)
Nutcracker syndrome
Nutcracker syndrome is a vascular compression disorder, and refers to the compression of the left renal vein between the superior mesenteric artery (SMA) and aorta. This can lead to renal venous hypertension, resulting in rupture of thin-walled veins into the collecting system with resultant haematuria.
Relationship between popliteal aneurysms and AAA
50% of patients with popliteal aneurysm also have AAA
AAA is more common than popliteal aneurysm
Very easily palpable popliteal pulse
50% bilateral
Expansile and pulsatile mass
Popliteal aneurysm
Main complication of popliteal aneurysm
Thrombosis and distal embolism-> acute limb ischaemia
Acute Mx of popliteal aneurysm
Embolectomy or fem-distal bypass
Mx of stable popliteal aneurysm
Elective grafting + tie off vessel
Epidemiology of AAA
Prevalence: 5% >50y
Mortality: 10,000 deaths/yr
M>F 3:1
Def: AAA
Dilatation of abdominal aorta >3cm
90% infrarenal
30% involving iliac arteries
Usually asymptomatic: discovered incidentally
May-> back pain or umbilical pain radiating to groin
Acute limb ischaemia
Blue toe syndrome: distal embolisation
Acute rupture
?AAA
Expansile mass just above the umbilicus
Bruits heard
Tenderness and shock suggests?
AAA
Rupture
Ix in AAA
Bloods:
FBC, clotting screen, renal function and liver function
Cross match if sx
ESR and or CRP if an inflammatory cause suspected
AXR: calcification may be seen
Abdo US: screening and monitoring
CT/MRI: gold standard
Angiography: won’t show true extent of aneurysm due to endoluminal thrombus but useful to delineate relationship of renal arteries
AAA
Calcified
Conservative Mx of AAA
Manage CV RFs esp BP
UK small aneurysm trial suggested that AAA <5.5cm in maximum diameter can be monitored by US
<4cm: yearly monitoring
4.5-5cm: 6 monthly monitoring
Surgical Mx of nonacute AAA
Aim to treat aneurysm before it ruptures
Elective mortality: 5%, emergency mortality: 50%
Indications for surgical intervention in AAA
Symptomatic: back pain= imminent rupture
Diameter >5.5cm
Expanding >1cm per year
Causing complications e.g. emboli
Open vs EVAR in AAA repair
EVAR has reduced perioperative mortality
No reduction in mortality by 5 years due to fatal endograft failures
EVAR not better than medical Rx in unfit patients
EVAR requires that the aneurysm should have an adequate 1.2cm neck below the renal arteries for stent fixation, currently 65% with AAA are suitable for endovascular repair.
AAA screening in UK
MASS trial revealed 50% reduction in aneurysm-related mortality in males aged 65-74 screened with US.
UK- one time screen at 65y
Rupture rates of AAA:
<5.5cm
1%/year
Rupture rates of AAA:
>6cm
25%/year
Increased risk of AAA rupture if?
Raised BP
Smoker
Female
Strong FHx
Sudden onset severe abdominal pain
Intermittent or continuous, radiating to back or flanks
Collapse-> shock
Expansile abdominal mass
?AAA rupture
Mx of AAA rupture
ABC
High flow O2
2x large bore cannulae:
Give fluid if shocked but keep SBP<100mHg (permissive hypotension)
Instigate major haemorrhage protocol
Call vascular surgeon, anaesthetist and warn theatre
Abx prophylaxis: cef+met
Analgesia
Urinary catheter + CVP line
If stable + Dx uncertain: US or CT may be feasible
Take to theatre, clamp neck, insert dacron graft
Mortality in AAA rupture
100% without surgery
50% with surgery
Def: thoracic aortic dissection
Blood splays apart the laminar planes of the media to form a channel within the aortic wall
Aetiology of thoracic aortic dissection
Atherosclerosis and HTN cause 90%
Minority caused by underlying CTD e.g. Marfan’s, Ehlers Danlos
Vit CD
Sudden onset, tearing chest pain
Radiating through to back
Tachycardia and hypertension (1o and sympathetic)
?Aortic dissection
Propagation in thoracic aortic dissection
Distal: sequential occlusion of branches
Left hemiplegia
Unequal arm pulses and BP
Paraplegia
Anuria
Proximal propagation: AR, tamponade
Rupture into pericardial, pleural or peritoneal cavities commonest cause of death
What is the classification system for aortic dissection
Stanford
Outline Stanford classification
Type A: proximal
70%
involves ascending aorta +/- descending
Higher mortality due to probable cardiac involvement
Usually require Sx
Type B: distal
30%
Involves descending only, distal to left subclavian artery
Usually managed conservatively
Ix in thoracic aortic dissection
ECG: exclude MI
TTE/TOE can be used in haemodynamically unstable pts
CT/MRI not suitable for unstable paitents
Mx of thoracic aortic dissection
ABC
Bloods:
X-match 10u, FBC, U+E, clotting, amylase
ECG: 20% show ischaemia due to involvement of the coronary ostia
Ix:
CXR, CT/MRI, TOE if haemodynamically unstable
Treat:
Analgesia
Reduce SBP (labetalol or esmolol) 100-110mmHg
Type A: open repair, acute mortality <25%
Type B: conservative, sx if persistent pain or complications, consider TEVAR if uncomplicated
Def: gangrene
Death of tissue from poor vascular supply
Classification of gangrene
Wet: tissue death + infection
Dry: tissue death only
Pregangrene: tissue on brink of gangrene
Black tissues +/- slough
May be suppuration +/- sepsis
?Gangrene
Wet gangrene
Dry gangrene
Pregangrene
Cause of gas gangrene
Clostridium perfringes myositis
RFs for gas gangrene
DM
Trauma
Malignancy
Toxaemia
Haemolytic jaundice
Oedema
Creptius from surgical emphysema
Bubbly brown pus
Gas gangrene
Rx of gas gangrene
Debridement: may need amputation
Benzylpenicllin and metronidazole
Hyperbaric O2
What is synergistic gangrene?
Involves aerobes and anaerobes
Can progress rapidly to nec fasc and myositis
Meleney Gangrene
Synergistic gangrene
Chronic undermining burrowing ulcer (also known as Meleney gangrene, or Meleney’s ulcer) is a cutaneous condition that is a postoperative, progressive bacterial gangrene.[1]:269 It is seen in immunocompromised individuals, mostly after post abdominal surgery and rapidly spreads to involve a large area.[citation needed]
Fournier’s gangrene
Synergistic gangrene
Fournier gangrene is a type of necrotizing fasciitis or gangreneaffecting the perineum.
Mx of gangrene
Take cultures
Debridement
Benzlpenicllin +/- clindamycin
Def: varicose veins
Tortuous dilated veins of the superficial venous system
Pathophysiology of varicose veins
One-way flow from superifical-> deep venous system maintained by valves
Valve failure-> increased pressure in superficial veins-> varicosity
What are the 3 main sites of valve incompetence in varicose veins
SFJ: 3cm below and 3cm lateral to pubic tubercle
SPJ: popliteal fossa
Perforators: draining GSV
What are the 3 medial calf perforators?
Cockett’s
What is the 1 medial thigh perforator called?
Hunter’s
Primary causes of varicose veins
Idiopathic: congenitally weak valves
Prolonged standing, pregnancy, obesity, OCP, FHx
Congenital valve absence (v. rare)
Secondary causes of varicose veins
Valve destruction-> reflux: DVT, thrombophlebitis
Obstruction: DVT, foetus, pelvic mass
Constipation
AVM
Overactive pumps e.g. cyclists
Klippel-Trenaunay: PWS, varicose veins, limb hypertrophy
Trendelenberg test
Torniquet
Start 3cm below and 3cm lateral to pubic tubercle
Lift patient’s leg as high as comfortable and milk leg to empty veins.
Once varicosities are empty place thumb or torniquet over SFJ
Ask patient to stand while pressure is maintained
If varicosities rapidly fill, suggests the incompetent perforator veins lie below the SFJ
Now repeat moving down 3cm each time, when varicosities do not refill, the incompetent perforator is above the torniquet but below the previous one.
Cosmetic defect
Pain, cramping, heaviness in the legs
Tingling
Bleeding; may be severe
Swelling
Varicose veins
Venous stars
Haemosiderin deposition
Venous eczma
Lipodermatosclerosis
Atrophie blanche
Ulcer in medial malleolus/gaiter area
Oedema
Thrombophlebitis
Varicose veins
Venous stars
Haemosiderin deposition
Varicose veins
Venous eczema
Varicose veins
Lipodermatosclerosis
Varicose veins
Atrophie blanche
Venous eczema
Venous ulcer
Ix in varicose veins
Duplex ultrasonography: anatomy, presence of incompetence, caused by obstruction or reflux
Sx: FBC, U&E, clotting, G+S, CXR, ECG
Referral criteria for varicose veins
Bleeding
Pain
Ulceration
Superficial thrombophlebitis
Severe impact on QoL
Classification of varicose veins is with?
CEAP classification
CEAP classification
Chronic venous disease can be classified according to
Clinical signs (1-6 + Symptomatic or Asymptomatic) i.e. 1S or 4A
Etiology
Anatomy
Pathophysiology
Conservative Mx of varicose veins
Treat any contributing factors: lose weight, relieve constipation
Education: avoid prolonged standing, regular walks
Class II Graduated compression stockings: symptomatic relief and slows progression
Skin care: maintain hydration with emollients and treat ulcers rapidly
Indications for minimally invasive therapies in varicose veins treatment
Small below knee varicosities not involving GSV or SSV
Techniques of minimally invasive varicose vein therapy
Local or GA
Injection scleropathy: 1% Na tetradecyl sulphate
Endovenous laser or radiofrequency ablation
Post-operatively:
Compression bandage for 24h
Compression stockings for 1m
Indications for sx management of varicose veins
SFJ incompetence
Major perforator incompetence
Symptomatic: ulceration, skin changes, pain
Procedures for varicose veins
Trendelenberg: SFJ ligation
SSV ligation: popliteal fossa
LSV stripping: no longer performed due to risk of saphenous nerve damage
Multiple avulsions
Perforator ligation: Cockett’s operation
Subfascial endoscopic perforator surgery
Post-op care for varicose vein patients
Bandage tightly
Elevate for 24h
Discharge with compression stockings and instruct to walk daily
Cx of varicose vein surgery
Haematoma (esp. groin)
Wound sepsis
Damage to cutaneous nerve e.g. long saphenous
Superficial thrombophlebitis
DVT
Recurrence: may approach 50%
Def: ulcer
Interruption in the continuity of an epithelial surface
What is the commonest cause of leg ulcer?
Venous
What are the different forms of leg ulcers?
Venous
Arterial
Neuropathic
Traumatic
Systemic disease
Neoplastic
Painless, sloping, shallow ulcer
Usually on gaiter area
Associated with lipodermatosclerosis
RFs: venous insufficiency, varicosities, DVT, obesity
?Venous ulcer
Proportion of leg ulcers that are venous
75%
Proportion of leg ulcers that are arterial
2%
Hx of vasculopathy and risk factors
Painful, deep, punched-out lesions
Occur at pressure points: heel, tips of and between toes, metatarsal heads (esp. 5th)
Other signs of chronic leg ischaemia
Arterial ulcer
Arterial ulcer
Painless ulcer with insensate surrounding skin
Warm foot with good pulses
Neuropathic ulcer
Neuropathic ulcer
Cx of ulcers
Osteomyelitis
Development of SCC in ulcer (Marjolin’s)
Marjolin’s ulcer=
Development of SCC in ulcer
Ix in venous ulcers?
ABPI if possible
Duplex ultrasonography
Biopsy may be necessary to look for malignant change
Mx of venous ulcers
Refer to leg ulcer community clinic
Focus on prevention: graduated compression stockings, venous uclers
Optimise risk factors: nutrition, smoking
Specific Rx for venous ulcers
Analgesia
Bed Rest and Elevate leg
4 layer graded compression bandage if ABPI >0.8
Pentoxyfylline PO: increases microcirculatory blood flow, improves healing rates
DDx fo bilateral leg swelling
Increased venous pressure:
RHF
Venous insufficiency
Drugs e.g. nifedipine
Reduced oncotic pressure:
Nephrotic syndrome
Hepatic failure
Protein losing enteropathy
Lymphoedema
Myxoedema: hyper/hypothyroidism
DDx of unilateral leg swelling
Venous insufficiency
DVT
Infection or inflammation
Lymphoedema
Def: Lymphoedema
Collection of interstitial fluid due to blockage or absence of lymphatics
Primary lymphoedema
Congenital absence of lymphatics
May or may not be familial
Different types of lymphoedema and presentations
Congenital: evident from birth
Praecox: after birth but <35
Tarda: >35
Milroy’s syndrome
Familial AD subtype of congenital lymphoedema: F>M
Secondary causes of lymphoedema
FIIT
Fibrosis; e.g. post RTx
Infiltration:
Ca: prostate, lymphoma
Filariasis
Infection: TB
Trauma: block dissection of lymphatics
Ix in lymphoedema
Doppler US
Lymphoscintigraphy
CT/MRI
Mx of lymphoedema
Conservative:
Skin care, compression stockings, physio, treat or prevent comorbid infections
Surgical: debulking
Epidemiology of DVT post surgically
DVTs occur in 25-50% of surgical patients
Risk factors for DVT post-Sx
Virchow’s triad
Blood:
Surgery-> increased plt and fibrinogen
Dehydration
Malignancy
Increased age
Blood flow:
Sx
Immobility
Obesity
Vessel wall:
damage to veins: esp. pelvic veins
Previous VTE
Peak incidence @5-10d
65% below knee are asymptomatic
Calf warmth, tenderness, erythema, swelling
Low grade pyrexia
Pitting oedema
?DVT
DVT
DDx for DVT
Cellulitis
Ruptured Baker’s cyst
Ix in DVT
D-dimers: sensitive but not specific
Compression US: clot will be incompressible
Thrombophilia screen if no precipitating factors, recurrent DVT or family Hx
Dx of DVT
Assess probability using Well’s Score
Low probability: perform D-dimers
-ve= excludes DVT
+ve= compression US
Medium/high probability: compression USS
What score is used to assess likelihood of DVT?
Well’s score
Well’s criteria
Active cancer
Paralysis, paresis or recent plaster immobilisation of legs
Recently bedridden for >3d or major sx within last 12w
Localised tenderness along the distribution of the deep venous system
Entire leg is swollen
Calf swelling by more than 3cm compared with asymptomatic leg (10cm below the tibial tuberosity)
Piiting oedema (greater than on the asymptomatic leg)
Pitting oedema
Collateral superficial veins
Perviously documented DVT
Subtract two points if an alternative cause is considered more likely than DVT
>2= likely, <2 unlikely
Rx of DVT
Antiocagulate:
Therapeutic LMWH: enoxaparin 1.5mg/kg/24h SC
Start warfrain
Stop LMWH when INR 2.5
Duration depends on cause
Below knee DVT duration of anticoag
6-12w
Above knee DVT duration of anticoag
3-6m
Initiation of warfarin treatment (rapid anticoagulation)
5mg OD for 2 days, measure INR on day 3
subsequent doses depend on INR
What is important about timing of Warfarin dose
Should be taken at the same time each day
What should be considered for patients post-DVT?
Graduated compression stockings to prevent post-phlebitic syndrome
Pre-op prevention of DVT
Pre-op VTE risk assessment
TED stockings
Aggressive optimisation esp. hydration
Stop OCP 4w pre-op
Intra-operative prevention of DVT
Minimise length of sx
Use minimal access surgery where possible
Intermittent pneumatic compression boots
Post-op prevention of DVT
LMWH
Early mobilisation
Good analgesia
Physio
Adequate hydration
Causes of post-operative dyspnoea
Previous lung disease
Atelectasis, aspiration, pneumonia
LVF
PE
Pneumothorax (e.g. due to CVP line insertion)
Pain-> hypoventilation
Ix in post-op dyspnoea
FBC, ABG
CXR
ECG
Rx in post-op dyspnoea
Sit up, give O2, monitor SpO2
Rx cause
Causes of reduced UO post-op
Post renal:
Most common cause- blocked/malsited catheter, acute urinary retention
Pre-renal:
Hypovolaemia
Renal:
NSAIDs, gentamicin
Anuria post-op usually
Blocked or malsited catheter
Oliguria post op usually
Inadequate fluid replacement
Mx of reduced UO post-operatively
Information:
Operation history, obs chart: UO
Drugs chart: nephrotoxins
Examination:
Assess fluid status
Examine for palpable bladder
Inspect drips, drains, stomas, CVP
Action
Flush with 50ml NS and aspirate back
Fluid challenge
Causes of post-op N+V
Obstruction
Ileus
Emetic drugs e.g. opioids
Mx of post-op N+V
Consider NGT, AXR and ondansetron 4mg IV TDS
Post op hyponatraemia
What was the pre-op level
Common causes: SIADH: pain, nausea, opioids, stress
Overadministration of IV fluids
Immediate mx of hypotension post-sx
Tilt bed head down give O2
Assess fluid status
Causes of post-operative hypotension
CHOD
Cardiogenic: MI, fluid overload
Hypovolaemia: inadequate replacement of fluids losses, haemorrhage
Obstructive: PE
Distributive: sepsis, neurogenic shock
Mx of hypovolaemic hypotension
Fluid challenge
250-500ml fluid challenge STAT
Mx of haemorrhagic hypotension post-op
Return to theatre
Mx of septic hypotension post-op
Fluid challenge, start Abx
Mx of neurogenic hypotension post-op
Nadr infusion
HTN and sx
Continue anti-hypertensives during peri-operative period
Causes of post-operative HTN
Pain
Urinary retention
Previous HTN
Rx of post-operative HTN
Rx cause
May use labetalol 50mg IV every 5 mins (200mg max)
Def: dermatome
An area of skin that is mainly supplied by a single spinal nerve
Which dermatome is the thumb?
C6
What dermatome at level of the nipples?
T4
T4 at teat pore
What dermatome at level of xihpoid process?
T7 at bottom of sternum
What dermatome at level of umbilicus?
T10 at belly butTEN
What dermatome at level of the inguinal ligament?
L1 for IL
What dermatome at patella/medial malleolus?
L4 to the floor
What are the KLM sounds?
Series of sounds used to examine cranial nerve function
Each tests a specific muscle and nerve pair
Kuh-kuh-kuh
Muscle tested
Nerve tested
Levator palatini: responsible for palatal elevation
Nerve required: CNX
La-La-La
Muscle required
Nerve required
Glossus muscles
CNXII
Mi-mi-mi
Muscle required
Nerve required
Perioral muscles
CNVII
What are the most common causes of sudden painless loss of vision?
ischaemic optic neuropathy (e.g. temporal arteritis or atherosclerosis)
occlusion of central retinal vein
occlusion of central retinal artery
vitreous haemorrhage
retinal detachment
Flashes of light (photopsia) - in the peripheral field of vision
Floaters, often on the temporal side of the central vision
Posterior vitreous detachment
Dense shadow that starts peripherally progresses towards the central vision
A veil or curtain over the field of vision
Straight lines appear curved
Central visual loss
Retinal detachment
Large bleeds cause sudden visual loss
Moderate bleeds may be described as numerous dark spots
Small bleeds may cause floaters
Vitreous haemorrhage
Red eye
Severe pain (ocular or headache)
Reduced acuity + haloes
Semi-dilated pupil
Hazy cornea
Acute angle closure glaucoma
Red eye
Acute onset
Pain
Blurred vision and photophobia
Small, fixed, oval pupil, ciliary flush
Anterior uveitis
Red eye
Severe pain and tenderness
May be underlying autoimmune disease e.g. RA
Scleritis
Red eye
Purulent discharge (bacterial)
Clear discharge (viral)
Conjunctivitis
Red eye
History of trauma of coughing bouts
Subconjunctival haemorrhage
Mx of herpes zoster ophthalmicus
Oral antiviral treatment for 7-0 days, ideally started within 72h
Oral corticosteroids may reduce duration of pain
Ophthalmology review
Red eye
Serous discharge
Recent URTI
Preauricular lymph nodes
Viral conjunctivitis
Red eye
Bilateral symptoms
Itch is prominent
May be history of atopy
May be seasonal (due to pollen) or perennial (due to dust mite, washing powder or other allergens)
Allergic conjunctivitis
Drusen=
Dry macular degeneration
Characterised by choroidal neovascularisation. Leakage of serous fluid and blood can subsequently result in a rapid loss of vision. Carries worst prognosis
Wet macular degeneration
characterised by drusen - yellow round spots in Bruch’s membrane
Dry macular degneration
intravitreal ranibizumab
Used to treat wet macular degeneration
Anti-VEGF
What are the ocular manifestations of RA?
keratoconjunctivitis sicca (most common)
episcleritis (erythema)
scleritis (erythema and pain)
corneal ulceration
keratitis
Iatrogenic
steroid-induced cataracts
chloroquine retinopathy
Which one of the following is not a risk factor for primary open-angle glaucoma?
Diabetes mellitus
Family history
Hypertension
Afro-Caribbean ethnicity
Hypermetropia
Acute angle closure glaucoma is associated with hypermetropia, where as primary open-angle glaucoma is associated with myopia
What differentiates between central, preganglionic and post-ganglionic lesions in Horners?
Anhydrosis of the face, arm and trunk= central
Anhydrosis of the face= preganglionic
No anhydrosis= post-ganglionic
Central causes of horner’s
S
Stroke
Syringomelia
MS
Tumour
Encephalitis
Pre-ganglionic causes of Horner’s
Pancoast
Thyroidectomy
Trauma
Cervical rib
Post-ganglionic causes of horners
Carotid artery dissection
Carotid aneurysm
CVST
Cluster headache
What is the most likely diagnosis?
Ciliary body rupture with lens dislocation
Vitreous haemorrhage
Ischaemic optic neuropathy
Central retinal artery
Retinal detachment
Retinal detachment
Causes of papilloedema
Causes of papilloedema
space-occupying lesion: neoplastic, vascular
malignant hypertension
idiopathic intracranial hypertension
hydrocephalus
hypercapnia
Rare causes include
hypoparathyroidism and hypocalcaemia
vitamin A toxicity
venous engorgement: usually the first sign
loss of venous pulsation: although many normal patients do not have normal pulsation
blurring of the optic disc margin
elevation of optic disc
loss of the optic cup
Paton’s lines: concentric/radial retinal lines cascading from the optic disc
Papilloedema
Theme: Visual field defects
A.Left homonymous hemianopia
B.Unilateral peripheral visual field loss
C.Bitemporal hemianopia, upper quadrant defect
D.Unilateral central visual field loss
E.Left homonymous hemianopia with macula sparing
F.Right homonymous hemianopia
G.Bitemporal hemianopia, lower quadrant defect
For each one of the following please select the associated visual field defect:
Pituitary gland tumour
Primary open angle glaucoma in right eye
Patient who has had an extensive stroke with right-sided hemiplegia
Pit- upper, cranipharyngioma- lower
Bitemporal hemianopia, upper quadrant defect
Unilateral peripheral visual field loss
Right homonymous hemianopia
Remember: the homonymous hemianopia is always on the same side as the paresis.
Upper quadrant vs lower quadrant bitemporal hemianopia
upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour
lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma
A 35-year-old man presents with visual problems. He has had very poor vision in the dark for a long time but is now worried as he is developing ‘tunnel vision’. He states his grandfather had a similar problem and was registered blind in his 50’s. What is the most likely diagnosis?
Leber’s congenital amaurosis
Vitelliform macular dystrophy
Central serous retinopathy
Primary open angle glaucoma
Retinitis pigmentosa
Retinitis pigmentosa primarily affects the peripheral retina resulting in tunnel vision
Features
night blindness is often the initial sign
tunnel vision due to loss of the peripheral retina (occasionally referred to as funnel vision)
fundoscopy: black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium
Associated diseases
Refsum disease: cerebellar ataxia, peripheral neuropathy, deafness, ichthyosis
Usher syndrome
abetalipoproteinemia
Lawrence-Moon-Biedl syndrome
Kearns-Sayre syndrome
Alport’s syndrome
A 35-year-old female who has recently being diagnosed with Grave’s disease presents for review 3 months after starting a ‘block and replace’ regime with carbimazole and thyroxine. She is concerned about developing thyroid eye disease. What is the best way that her risk of developing thyroid eye disease can be reduced?
Reduce alcohol intake
A diet rich in omega-3 fatty acids
Regular exercise
Stop smoking
Lose weight
Smoking is the most important modifiable risk factor for the development of thyroid eye disease
What are the indications for urgent opthalmology r/v in thyroid eye disease?
unexplained deterioration in vision
awareness of change in intensity or quality of colour vision in one or both eyes
history of eye suddenly ‘popping out’ (globe subluxation)
obvious corneal opacity
cornea still visible when the eyelids are closed
disc swelling
A 34-year-old man with a history of ankylosing spondylitis presents with a painful right eye associated with mild photophobia:
Cycloplegic drops have recently been given. What is the most likely diagnosis?
Scleritis
Acute angle closure glaucoma
Anterior uveitis
Conjunctivitis
Episcleritis
Ankylosing spondylitis is associated with anterior uveitis. The history of pain and photophobia combined with the examination findings of a red eye confirm the diagnosis
Note that the pupil in this image is dilated - this is not a typical finding at diagnosis but may reflect the fact that cycloplegic drops are commonly given to patients for pain relief
What is the normal range for intraocular pressure?
10-21 mmHg
A 64-year-old woman presents with bilateral sore eyelids. She also complains of her eyes being dry all the time. On examination her eyelid margins are erythematous at the margins but are not swollen. Of the given options, what is the most appropriate initial management?
Topical chloramphenicol + mechanical removal of lid debris
Hot compresses + topical steroids
Topical chloramphenicol + topical steroids
Hot compresses + mechanical removal of lid debris
Topical chloramphenicol + hot compresses
Hot compresses + mechanical removal of lid debris
symptoms are usually bilateral
grittiness and discomfort, particularly around the eyelid margins
eyes may be sticky in the morning
eyelid margins may be red. Swollen eyelids may be seen in staphylococcal blepharitis
styes and chalazions are more common in patients with blepharitis
secondary conjunctivitis may occur
Blepharitis
What eye condition is more common in patients with rosacea?
Blepharitis
Mx of blepharitis
softening of the lid margin using hot compresses twice a day
mechanical removal of the debris from lid margins - cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo is often used*
artificial tears may be given for symptom relief in people with dry eyes or an abnormal tear film
A 67-year-old man presents as he has developed a painful blistering rash around his right eye. On examination a vesicular rash covering the right trigeminal nerve dermatome is seen. Currently he has no eye symptoms or signs. Which one of the following is most likely to predict future eye involvement?
Presence of the rash on the tip of his nose
Smoking history
Increasing age
Previous courses of corticosteroids
Presence of the rash in the ear canal
This is Hutchinson’s sign which is strongly predictive for ocular involvement.
A 60-year-old woman who has recently started treatment for polymyalgia rheumatica presents with a five day history of headaches and reduced vision on the right side since this morning There is no eye pain but the there is a ‘large, dark shadow’ covering the superior visual field on the right side. On examination she has a tender, palpable right temporal artery. What is the most likely explanation for the reduced vision?
Anterior ischemic optic neuropathy
Central retinal vein occlusion
Optic neuritis
Acute angle closure glaucoma
Central retinal artery occlusion
Anterior ischemic optic neuropathy
What causes the visual disturbances in temporal arteritis?
Anterior ischaemic optic neuropathy
A 54-year-old woman presents with a persistent watery left eye for the past 4 days. On examination there is erythema and swelling of the inner canthus of the left eye. What is the most likely diagnosis?
Blepharitis
Acute angle closure glaucoma
Meibomian cyst
Dacryocystitis
Pinguecula
Dacryocystitis is infection of the lacrimal sac
Features
watering eye (epiphora)
swelling and erythema at the inner canthus of the eye
Management is with systemic antibiotics. Intravenous antibiotics are indicated if there is associated periorbital cellulitis
At what age would the average child be expected to have visual acuity similar to that of an adult?
3 months
6 months
9 months
12 months
2 years
2 years
A newborn’s visual acuity is only about 6/200. This improves to 6/60 at 3 months but does no reach adult levels until about 2 years of age.
The table below summarises the vision tests which may be performed when assessing children:
AgeTest
BirthRed reflex
6 weeksFix and follow to 90 degrees (e.g. Red ball 90cm away)
3 monthsFix and follow to 180 degrees
No squint
12 monthsCan pick up ‘hundreds and thousands’ with pincer grip
> 3 yearsLetter matching test
> 4 yearsSnellen charts
Ishihara plates for colour vision
A 24-year-old man presents to the emergency department complaining of left eye pain. He has not been able to wear his contact lenses for the past 24 hours due to the pain. He describes the pain as severe and wonders whether he has ‘got something stuck in his eye’. On examination there is diffuse hyperaemia of the left eye. The left cornea appears hazy and pupillary reaction is normal. Visual acuity is reduced on the left side and a degree of photophobia is noted. A hypopyon is also seen. What is the most likely diagnosis?
Acute angle closure glaucoma
Viral conjunctivitis
Keratitis
Episcleritis
Anterior uveitis
Whilst a hypopyon can of course be seen in anterior uveitis the combination of a normal pupillary reaction and contact lens use make a diagnosis of keratitis more likely.
A 70-year-old man presented with a watering and sore left eye:
What is the diagnosis?
Left-sided ectropion
Left-sided pinguecula
Stroke
Bell’s palsy
Left-sided entropion
Left sided ectropion
What is the most common cause of blindness in adults 35-65 years old?
Diabetic retinopathy
A 54-year-old man is noted to have papilloedema on examination. Which one of the following may be responsible?
Vitamin D toxicity
Hypercapnia
Hyperkalaemia
Hypercalcaemia
Hypoglycaemia
Hyperventilation to induce hypocapnia may be used in the emergency setting to reduce intracranial pressure
A 23-year-old female presents with recurrent headaches. Examination of her cranial nerves reveals the right pupil is 3 mm whilst the left pupil is 5 mm. The right pupil constricts to light but the left pupil is sluggish. Peripheral neurological examination is unremarkable apart from difficult to elicit knee and ankle reflexes. What is the most likely diagnosis?
Acute angle closure glaucoma
Migraine
Multiple sclerosis
Holmes-Adie syndrome
Argyll-Roberson syndrome
olmes-Adie pupil is a benign condition most commonly seen in women. It is one of the differentials of a dilated pupil.
Overview
unilateral in 80% of cases
dilated pupil
once the pupil has constricted it remains small for an abnormally long time
slowly reactive to accommodation but very poorly (if at all) to light
Holmes-Adie syndrome
association of Holmes-Adie pupil with absent ankle/knee reflexes
A 65-year-old man with a history of primary open-angle glaucoma presents with sudden painless loss of vision in his right eye. On examination of the right eye the optic disc is swollen with multiple flame-shaped and blot haemorrhages. What is the most likely diagnosis?
Diabetic retinopathy
Vitreous haemorrhage
Ischaemic optic neuropathy
Occlusion of the central retinal vein
Occlusion of the central retinal artery
Central retinal vein occlusion - sudden painless loss of vision, severe retinal haemorrhages on fundoscopy
heme: Primary open-angle glaucoma: management
A.Timolol
B.Pilocarpine
C.Brimonidine
D.Dorzolamide
E.Acetylcysteine
F.Ranibizumab
G.Atropine
H.Latanoprost
I.Cyclopentolate
J.Tropicamide
For each one of the following questions please select the correct answer:
Adverse effects include brown pigmentation of the iris
Should be avoided in patients taking MAOI drugs
Causes pupillary constriction, blurred vision and headaches
Latanoprost
Brimonidine
Pilocarpine
A man is recovering after having an operation to remove a meningioma in his left temporal lobe. What sort of visual field defect is he at risk of having following the procedure?
Right inferior homonymous quadrantanopia
Right superior homonymous quadrantanopia
Left inferior homonymous quadrantanopia
Right homonymous hemianopia with macula sparing
Left superior homonymous quadrantanopia
homonymous quadrantanopias: PITS (Parietal-Inferior, Temporal-Superior)
A 70-year-old man is investigated for blurred vision. Fundoscopy reveals drusen, retinal epithelial and macular neovascularisation. A diagnosis of age related macular degeneration is suspected. What is the most appopriate next investigation?
Vitreous fluid sampling
MRI orbits
Ocular tonometry
Fluorescein angiography
Kinetic perimetry
optical coherence tomography: provide cross-sectional views of the macula
if neovascularisation is present fluorescein angiography is performed
73-year-old man complains of a sore right eye:
What is the diagnosis?
Dacryocystitis
Chalazion
Entropion
Blepharitis
Ectropion
If left untreated this patient may develop a corneal ulcer. The definitive management of entropion is surgical although eye lubricants and tape (to pull the eyelid outwards) may be used whilst awaiting surgery.
Theme: Visual defects
A.Right homonymous hemianopia
B.Left homonymous hemianopia
C.Right superior quadranopia
D.Left superior quadranopia
E.Right inferior quadranopia
F.Left inferior quadranopia
G.Upper bitemporal hemianopia
H.Lower bitemporal hemianopia
A 42-year-old woman is admitted to the vascular ward for an endarterectomy. Her CT report confirms a left temporal lobe infarct.
A 22-year-old man is referred to urology with possible urinary retention. He is passing huge amounts of urine. Post void bladder ultrasound is normal.
A 53-year-old man is admitted to the vascular ward for a carotid endarterectomy. His CT head report confirms a left parietal lobe infarct.
Right superior quadranopia
Lower bitemporal hemianopia
Right inferior quadranopia
Conditions associated with anterior uveitits?
ankylosing spondylitis
reactive arthritis
ulcerative colitis, Crohn’s disease
Behcet’s disease
Each one of the following is a cause of a mydriatic pupil, except:
Third nerve palsy
Atropine
Holmes-Adie pupil
Argyll-Robertson pupil
Traumatic iridoplegia
Argyll-Robertson pupil is one of the classic pupillary syndrome. It is sometimes seen in neurosyphilis and is often said to be the prostitute’s pupil - accommodates but doesn’t react. Another mnemonic used for the Argyll-Robertson Pupil (ARP) is Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)
Features
small, irregular pupils
no response to light but there is a response to accommodate
Causes
diabetes mellitus
syphilis
This man presents with unilateral visual loss. On examination he has a relative afferent pupillary defect. Fundoscopy shows the following:
What is the most likely diagnosis?
Central retinal vein occlusion
Subhyaloid haemorrhage
Solar retinopathy
Central retinal artery occlusion
Optic neuritis
Central retinal artery occlusion
The pale retina is the most obvious sign in this slide.
Which one of the following best describes the action of latanoprost in the management of primary open-angle glaucoma?
Carbonic anhydrase inhibitor
Reduces aqueous production + increases outflow
Opens up drainage pores
Increases uveoscleral outflow
Reduces aqueous production
Increases uveoscleral outflow
What are the acquired causes of optic atrophy?
MS
Longstanding papilloedema
Raised IOP
Retinal damage e.g. choroiditis, retinitis pigmentosa
Ischaemia
Toxins: tobacco ambylopia, quinine, methanol, arsenic, lead
Nutritional: vitamin B1, B2, B6 and B12 deficiency
What are the congenital causes of optic atrophy?
Friedrich’s ataxia
Mitochondrial disorders
DIDMOAD (cranial DI, DM, OA, deafness- Wolfram’s)
Which one of the following statements regarding the Holmes-Adie pupil is incorrect?
May be associated with absent ankle/knee reflexes
Bilateral in 80% of cases
It is a benign condition
Slowly reactive to accommodation but very poorly (if at all) to light
Causes a dilated pupil
The Holmes-Adie pupil is unilateral, rather than bilateral, in 80% of patients
Theme: Primary open-angle glaucoma: management
A.Timolol
B.Pilocarpine
C.Brimonidine
D.Dorzolamide
E.Acetylcysteine
F.Ranibizumab
G.Atropine
H.Latanoprost
I.Cyclopentolate
J.Tropicamide
Both reduces aqueous production and increases outflow
First-line treatment in a patient with a history of heart block
Systemic absorption may cause sulphonamide-like reactions
Brimonidine
Latanoprost
Dorzolamide
Causes of tunnel vision
papilloedema
glaucoma
retinitis pigmentosa
choroidoretinitis
optic atrophy secondary to tabes dorsalis
hysteria
A 71-year-old man who has recently been diagnosed with macular degeneration asks for advice regarding antioxidant dietary supplements. Which one of the following may contraindicate the prescription of such supplements?
Current smoker
Pernicious anaemia
Treated hypertension
History of depression
Previous episodes of tendonitis
Beta-carotene has been found to increase the risk of lung cancer and hence antioxidant dietary supplements are not recommended for smokers.
Theme: Visual field defects
A.Optic nerve
B.Optic chiasm
C.Retina
D.Occipital cortex
E.Optic tract
For each one of the following please select where the lesion is likely to be:
A 72-year-old man develops visual problems. He is noted to have a left homonymous hemianopia with some macula sparing.
A 54-year-old man complains of sweating, headaches and ‘tunnel vision’.
A 30-year-old man with a family history of early blindness is concerned that he is developing ‘tunnel vision’.
Occipital cortex
The macula sparing suggests the lesion is most likely to be in the occipital cortex rather than the optic tract.
Optic chiasm
This patient has a pituitary tumour causing compression of the optic chiasm and bitemporal hemianopia. The sweating and headaches are consistent with acromegaly.
Retina
This is a common presentation of retinitis pigmentosa. Extensive pigmentation would normally be noted on fundoscopy.
Each one of the following predisposes to cataract formation, except:
Down’s syndrome
Hypercalcaemia
Diabetes mellitus
Long-term steroid use
Congenital rubella infection
Hypocalcaemia, rather than hypercalcaemia, predisposes to cataract formation.
Causes of cataracts
Majority
Systemic
Ocular
Majority
age related
UV light
Systemic
diabetes mellitus
steroids
infection (congenital rubella)
metabolic (hypocalcaemia, galactosaemia)
myotonic dystrophy, Down’s syndrome
Ocular
trauma
uveitis
high myopia
topical steroids
Causes of lens dislocation?
Marfan’s: upwards
Homocystinuria: downwards
Ehlers-Danlos
Trauma
Uveal tumours
Autosomal recessive ectopia lentis
A 47-year-old female with a history of rheumatoid arthritis presents with a painful and red left eye. Visual acuity is normal. What is the most likely diagnosis?
Scleritis
Episcleritis
Glaucoma
Anterior uveitis
Keratoconjunctivitis sicca
A key way to discriminate between scleritis and episcleritis is the presence of pain. Keratoconjunctivitis sicca is usually bilateral and associated more with dryness, burning and itch
A 62-year-old woman presents with sudden loss of vision in her left eye. Fundoscopy reveals the following:
What is the diagnosis?
Retinal detachment
Ischaemic optic neuropathy
Vitreous haemorrhage
Central retinal vein occlusion
Central retinal artery occlusion
Central retinal vein occlusion - sudden painless loss of vision, severe retinal haemorrhages on fundoscopy
This appearance is sometimes compared to a cheese and tomato pizza.
Composition of bone matrix?
Organic= osteoid (40%)
Collagent Type 1
Resists tension, twisting and bending
Inroganice (60%)
Calcium hydroxapatite
Resits compressive forces
How can bone be classified?
Woven bone: disorganised bone that forms the embryonic skeleton and fracture callus
Lamellar bone:
mature bone that can be of two types:
Cortical/compact= dense outer layer
Cancellous/trabecular: porous central layer
Process of intramembranous ossification
Direct ossification of mesenchymal bone models formed during embryonic development
Skull bones, mandible and clavicle
Process of endochondral ossification
Mesenchyme-> cartilage-> bone
Most bones ossify this way
What are the phases of fracture healing?
Reactive phase
Reparative phase
Remodelling phase
Features of reactive phase of bone healing
Injury-48h
Bleeding into #site-> haematoma
Inflammation-> cytokine, GF and vasoactive mediator release-> recruitment of leukocytes and fibroblasts-> granulation tissue
Features of the reparative phase of bone healing
2d-2w
Proliferation of osteoblasts and fibroblasts-> cartilage and woven bone production-> callus formation
Consolidation-> endochondral ossificaiton of woven bone-> lamellar bone
Features of the remodelling phase of bone healing
1w-7y
Remodelling of lamellar bone to cope with mechanical forces applied to it
Follows Wolff’s law
What is Wolff’s Law
Form follows function
Wolff’s law, developed by the German anatomist and surgeon Julius Wolff (1836–1902) in the 19th century, states that bone in a healthy person or animal will adapt to the loads under which it is placed.[1] If loading on a particular bone increases, the bone will remodel itself over time to become stronger to resist that sort of loading.[2][3] The internal architecture of the trabeculae undergoes adaptive changes, followed by secondary changes to the external cortical portion of the bone,[4] perhaps becoming thicker as a result. The inverse is true as well: if the loading on a bone decreases, the bone will become less dense and weaker due to the lack of the stimulus required for continued remodeling.[5] This reduction in bone density (osteopenia) is known as stress shielding and can occur as a result of a hip replacement (or other prosthesis).[6] The normal stress on a bone is shielded from that bone by being placed on a prosthetic implant.
Healing time for a closed, paediatric, metaphyseal, upper limb #
3w
What are the complicating factors for #s and what do they do?
Double healing time
Adult
LL
Diaphyseal
Open
Anatomy of a long bone proximal to distal
Diaphysis= shaft
Metaphysis: growth plate region
(physis- growth plate)
Epiphysis
Atrciular cartilage over joint surfaces
Anatomy of a long bone
Deep to superficial
Medullary cavity
Endosteum
Cortical bone
Periosteum
How can fractures be classified?
Traumatic
Stress
Pathological
E.g. of traumatic #
Direct e.g. assualt with metal bar
Indirect e.g. FOOSH-> #clavicle
Avulsion
Features of stress#
Bone fatigue due to repetitive strain
E.g. foot #s in marathon runners
E.g. of pathological #s
Normal forces but disease bone
Local- tumours
General: osteoporosis, Cushing’s Pagets
XR of #s
Radiographs must be orthogonal request AP and lat films
Need images of joint above and below #
Structure for describing fracture
PAID
Demographics
Pattern
Anatomical
Intra/extra-articular
Deformity
Soft tissues
Specific #classification/type
Components of pattern when describing #
Transverse
Oblique
Spiral
Multifragmentary
Crush
Greenstick
Avulsion
Deformity when describing XR #
Translation
Angulation or tilt
Rotation
Impaction (shortening)
Describe distal relative to proximal
Features of soft tissue when describing XR#
Open or closed
Neurovascular status
Compartment syndrome
What are the 4Rs of fracture management
Resuscitation
Reduction
Restriction
Rehabilitation
What are the principles of resuscitation in # management
Follow ATLS guidelines
Trauma series in 1o survey: C-spine, chest and pelvis
usually assessed in 2o survey
Assess neurovascular status and look for dislocations
Consider reduction and splinting before imaging when: reduced pain, reduced bleeding, risk of neurovascular imaging
XR once stable
When should #reduction be considered before imaging?
To reduce pain
To reduce bleeding
To reduce risk of neurovascular injury
What are the 6As of open #
Analgesia
Assess: NV status, soft tissues, photograph
Antisepsis: wound swab, copious irrigation, cover with betadine-soaked dressign
Alignment: align # and splint
Anti-tetanus: check status
Abx: fluxclox 500mg IV/IM and benpen 600mg IV/IM
Or augmentin 1.2g IV
Mx of open #
Debridement and fixation in theatre
What is the most dangerous complication of open# and why?
Clostridium perfrigens
Wound infections and gas gangrene +/- shock and renal failure
Rx in c. perfringens infection of open#?
Debride, benpen, clindamycin
What can be used to classify open #s?
Gustillo
Components of Gustillo classification of open #s
- Wound <1cm in length
- Wound >1cm with minimal soft tissue damage
- Extensive soft tissue damage
What are the principles for redcution of #s?
Displaced #s should be reduced unless no effect on outcome e.g. ribs
Aim for anatomical reduction, especially if articular surfaces involved
Alignment is more important than opposition
What are the methods of # reduction?
Manipulation/closed reduction
Traction
Open reduction and internal fixation
Features of manipulation/closed reduction
Under local, regional or general anaesthetic
Traction to disimpact
Manipulation to align
Features of traction for # reduction
Not typically used now
Employed to overcome contraction of large muscles e.g. femoral #s
Skeletal traction vs skin traction
Features of open reduction and internal fixation
Accurate reduction weighed up vs risks of surgery
Intra-articular #s
Open #s
2 #s on 1 limb
Failure in conservative mx
Bilateral identical fractures
What are the principles of restriction in # management
Interfragmentary strain hypothesis dictates that tissue is formed at site dependent on strain it experiences
Fixation reduces strain -> bone formation
Fixation also reduces pain, increases stability and ability to function
What are the methods of restriction in # mx
Non-rigid
Plaster
Functional bracing
Continuous traction
Ex-fix
Internal fixation
What are some examples of non-rigid fixation?
Slings
Elastic supports
What are some methods for plaster restriction of #s
What is an important consideration?
POP
In first 24-48h use back-slab or split cast due to risk of compartment syndrome
What is functional bracing of #
Joints free to move but bone shafts supported in cast segments
What is an example of continuous traction
Collar and cuff sling
Features of external fixation
Fragments held in position by pins/wires which are then connected to an external frame
Intervention is away from field of injury
Useful in open #s, burns, tissue loss to allow wound access and reduce infection risk
However there is a risk of pin-site infections
Features of internal fixation
Pins, plates, screws, IM nails
Usually perfect anatomical alignement
Increased stability
Aid early mobilisation
What are the principles in # rehabilitation
Immobility-> reduced muscle and bone mass, joint stiffness
Need to maximise return to function to reduce later morbidity
What are some methods of # rehabilitation
PT: exercises to improve mobility
OT: splints, mobility aids, home modification
Social services: meals on wheels, home help
What are the general complications of fractures?
Tissue damage:
Haemorrhage and shock
Infection
Muscle damage-> rhabdomyolysis
Anaesthesia:
Anaphylaxis
Damage to teeth
Aspiration
Prolonged bed rest:
Chest infection, UTI
Pressure sores and muscle wasing
DVT, PE
Decreased bone mineral density
What are the immediate complications of fractures?
Neurovascular damage
Visceral damage
What are the early complications of fractures?
Compartment syndrome
Infection (worse if associated with metalwork)
Fat embolism-> ARDS
What are the late complications of fractures?
Problems with union
AVN
Growth disturbance
Post-traumatic osteoarthritis
Complex regional pain syndromes
Myositis ossificans
What is myositis ossificans
far most common type, nonhereditary myositis ossificans (commonly referred to simply as “myositis ossificans”, as in the remainder of this article), calcifications occur at the site of injured muscle, most commonly in the arms or in the quadriceps of the thighs.
The term myositis ossificans traumatica is sometimes used when the condition is due to trauma.[1][2] Also Myositis ossificans circumscripta is another synonym of myositis ossificans traumatica refers to the new extraosseous bone that appears after traum
What is the second, rarer type of myositis ossificans?
The second condition, myositis ossificans progressiva (also referred to as fibrodysplasia ossificans progressiva) is an inherited affliction, autosomal dominant pattern, in which the ossification can occur without injury, and typically grows in a predictable pattern. Although this disorder can be passed to offspring by those afflicted with FOP, it is also classified as nonhereditary, as it is most often attributed to a spontaneous genetic mutation upon conception.
Myositis ossificans
What are the features of neurological complications following #
Severance is rare, stretching over bone edge commoner
Seddon classification describes three types of injury
What are the components of the Seddon Classification
Descrbie neurological damage post #
Neuropraxia
Axonotmesis
Neurotmesis
What is Neuropraxia
Temprorary interruption of conduction without loss of axonal continuity
What is axonotmesis?
Disruption of nerve axon-> distal Wallerian degeneration
Connective tissue framework of nerve is preserved
Regeneration occurs and recovery is possible
Wallerian degeneration
Wallerian degeneration is a process that results when a nerve fiber is cut or crushed, in which the part of the axon separated from the neuron’s cell body degenerates distal to the injury. This is also known as anterograde or orthograde degeneration.
What is neurotmesis?
Disruption of the entire nerve fibre
Surgery is required and recovery is not usually complete
Ant. shoulder dislocation
Humeral surgical neck
Nerve damage
Result?
Axillary nerve
Numb chevron
Weak abduction
humeral shaft
Nerve affected
Clinical manifestation
Radial nerve
Waiter’s tip
Elbow dislocation
Nerve affected
Clinical manifestation
Ulnar nerve
Claw hand
Hip dislocation
Nerve affected
Clinical manifestation
Sciatic nerve
Foot drop
neck of fibula
Knee dislocation
Nerve affected
Clinical manifestation
Fibular nerve
Foot drop
Features of compartment syndrome
Osteofascial membranes divide limbs into separate comparments of muscles
Oedema following # can lead to an increase in compartment pressure, this reduces venous drainage increasing compartment pressure further
If compartment pressure > capillary pressure-> ischaemia
Muscle infarction->
Rhabdomyolsis and ATN
Fibrosis-> Volkman’s ischaemic contractrue
Pain > clinical findings
Pain on passive muscle stretching
Warm erythematous, swollen limb
Prolonged CRT and weak/absent peripheral pulses
?Compartment syndrome
Rx of compartment syndrome
Elevate limb
Remove all bandages and split/remove cast
Fasciotomy
Def: delayed union
Union takes longer than expected
Non-union of fracture is when
fails to unite
What are the causative factors for problems with bone union?
5Is
Ischaemia: poor blood supply or AVN
Infection
Increased interfragmentary strain
Interposition of tissue between fragments
Intercurrent disease: e.g. malignancy or malnutrition
How can non-union be classified?
Hypertrophic: bone end is rounded, dense and sclerotic
Atrophic: bone looks osteopenic
Management of non-union
Optimise biology: infection, blood supply, bone graft, BMPs
Optimise mechanics: ORIF
Def: malunion
healed in an imperfect position
poor position and or function
e.g. gunstock deformity
Gunstock deformity
Cubitus varus (varus means a deformity of a limb in which part of it is deviated towards the midline of the body) is a common deformity in which the extended forearm is deviated towards midline of the body.
Cubitus varus is often referred to as “Gunstock deformity”, due to the crooked nature of the healing.
A common cause is the supracondylar fracture of humerus.
What is Pelllegrini-Stieda disease
Form of myositis ossificans
Calcification of the superior attachment of MCL at the knee following traumatic injury
Pellegrini-Stieda disease
form of MO
Calcification of the superior attachment of MCL @
the knee following traumatic injury.
Def: Complex Regional Pain Syndrome Type 1
=Reflex Sympathetic Dystrophy, Sudek’s atrophy
Complex disorder of pain, sensory abnormalities, abnormal blood flow, sweating and trophic changes in superficial or deep tissues
No evidence of nerve injury
Causes of Complex Regional Pain Syndrome Type 1
Injury: #s, carpal tunnel release, ops for Dupuytren’s
Zoster, MI, Idiopathic
Weeks-Months after injury
Not traumatised area that is affected, affects a neighbouring area
Lancing pain, hyperalgesia or allodynia
Vasomotor: hot and sweaty or cold and cyanosed
Skin: swollen or atrophic and shiny
NM: weakness, hyper-reflexia, dystonia, contractures
Complex Regional Pain Syndrome Type 1
(Reflex Sympathetic Dystrophy, Sudek’’s atrophy)
Allodynia
Pain caused by something that wouldn’t normally cause pain
Rx of CRPS Type I
Usually self-limiting
Refer to pain team
Amitryptilline, gabapentin
Sympathetic nerve blocks can be tried
What is CRPS type II?
Persistent pain following an injury caused by nerve lesions
What can happen in children with fractures
Damage to the physis can result in abnormal bone growth
Salter-Harris classification categorises growth plate injuries
What is the Salter-Harris Classification
SALT C
Used to classify growth plate injuries
- Straight across
- Above
- Lower
- Through
- Crush
Px of SH1
e.g. SUFE
Normal growth with good reduction
Px of SH4
Union across physis may interfere with bone growth
Px of SH5
Crush-> physis injury-> growth arrest
What is the most common point of # clavicle
And mechanism?
Junction of the medial 2/3 and lateral 1/3
After the # the lateral end of the clavicle is displaced inferiorly be the weight of the arm and medially by pectoralis major
Medial end is pulled superiorly by sternocleidomastoid
FOOSH
Winging of the scapula caused by?
Serratus anterior muscle originates from ribs 2-8 and attaches to the costal face of the scapula pulling it against the ribcage
This is innervated by the LTN
If the LTN becomes damaged the scapula protrudes out of the back when pushing with the arm.
What rotator cuff muscles attach to the greater tubercle?
Greater tubercle is located laterally on the humerus
Serves as attachment site for 3 of the rotator cuff muscles, supraspinatus, infraspinatus, teres minor.
What rotator cuff muscle is attached to the lesser tubercle of the humerus
Subscapularis
Action of supraspinatus
Initiator of abduction up to first 25
What is the action of infraspinatus and teres minor
External rotators of the shoulder
Infraspinatus acting when the arm is in neutral and teres minor when the arm is in 90% of abduction
What is the action of subscapularis
Main internal rotator of the shoulder
Largest and strongest cuff muslce
Actions of rotator cuff muscles
SITS
Supraspinatus: abduction
Infraspinatus: external rotation
Teres minor: external rotation (when arm is abducted to 90 deg)
Subscapularis: internal rotation
Articulation of the distal humerus with ulna and radius
Trochlea articulates with ulnar: located medially and extends onto the posterior of the bone
Capitulum articulates with the radius
Monteggia’s fracture
Usually caused by a force from behind the ulna
Proximal shaft of the ulna is fractured and the head of the radius dislocates anteriorly at the elbow
Monteggia fracture
The Monteggia fracture is a fracture of the proximal third of the ulna with dislocation of the head of the radius. It is named after Giovanni Battista Monteggia.[1][2]
Fall on an outstretched hand with the forearm in excessive pronation (hyper-pronation injury). The Ulna fractures in the proximal one-third of the shaft due to extreme dislocation. Depending on the impact and forces applied in each direction, degree of energy absorption determines pattern, involvement of the radial head and whether or not open soft tissue occurs.
Direct blow on back of upper forearm would be a very uncommon cause. In this context, isolated ulnar shaft fractures are most commonly seen in defence against blunt trauma (e.g. nightstick injury). Such an isolated ulnar shaft fracture is not a Monteggia fracture.[citation needed] It is called a ‘nightstick fracture’.
Galeazzi’s Fracture – A fracture to the distal radius, with the ulna head dislocating at the distal radio-ulnar joint.
Colle’s fracture
Most common types of radial fracture
Fall onto an outstretched hand causing a fracture of the distal radius.
Structures distal to the fracture (wrist and hand are displaced posteriorly to produce the dinner fork deformity)
Most common type of radial fracture
FOOSH causing a fracture of the distal radius.
Structures distal to the fracture (wrist and hand are displaced posteriorly to produce the dinner fork deformity)
Smith’s fracture
Smith’s Fracture – A fracture caused by falling onto the back of the hand. It is the opposite of a Colles’ fracture, as the distal fragment is now placed anteriorly.
Smith’s Fracture – A fracture caused by falling onto the back of the hand. It is the opposite of a Colles’ fracture, as the distal fragment is now placed anteriorly.
What are the carpal bones
SLTP
TTCH
Scaphoid
Lunate
Triquetrum
Pisiform
Trapezium
Trapezoid
Capitate
Hamate
Which carpal bones are most commonly fractured?
Scaphoid and lunate
FOOSH
Features of scaphoid fracture
Classical clinical features is pain and tenderness in the anatomical snuffbox
Fracture needs to be reduced quickly as the blood supply to the proximal part of the bone can be cut off leading to an avascular necrosis
Features of a lunate fracture
Occurs when there is hyperextension at the wrist
Associated with damage to the median nerve
What is Boxer’s fracture
A fracture of the 5th metacarpal neck
Usually caused by a clenched fist striking a hard object
The distal part of the fracture is displaced posteriorly producing shortening of the affected finger
Boxer’s fracture
Bennet’s fracture
Fracture of the 1st metacarpal base extending into the carpometacarpal joint
It is caused by hyperabduction of the thumb
Bennet’s fracture
Innervation of the rotator cuff muscles
Supraspinatus and infraspinatus both innervated by suprascapular
Teres minor innervated by axillary nerve
Subscapularis upper and lower subscapular nerve
Abduction of the upper limb
Abduction (upper limb away from midline in coronal plane)
The first 0-15 degrees of abduction is produced by the supraspinatus. The middle fibres of the deltoid are responsible for the next 15-90 degrees. Past 90 degrees, the scapula needs to be rotated to achieve abduction – that is carried out by the trapezius and serratus anterior.
Acromioclavicular joint dislocation
What is the difference between tennis elbow and golfer’s elbow?
Most of the flexor and extensor muscles in the forearm have a common tendinous origin. The flexor muscles originate from the medial epicondyle, and the extensor muscles from the lateral. Sportspersons can develop an overuse strain of the common tendon – which results in pain and inflammation around the area of the affected epicondyle.
Typically, tennis players experience pain in the lateral epicondyle from the common extensor origin. Golfers experience pain in the medial epicondyle from the common flexor origin.
Which carpal bones articulate with the radius and ulna?
Scaphoid, lunate, triqeutrum
Epidemiology of hip fracture
80/100,000
50% >80 y
F>M 3:1
Pathophysiology of hip #
Old= osteoporosis with minor trauma e.g. fall
Young= major trauma
What are the risk factors for osteoporosis?
Age
+
Shattered
Age
Steroids
Hyper para/thyroidism
Alcohol and cigarettes
Thin (BMI <22)
Testosterone low
Early menopause
Renal/ liver failure
Ersoive/inflammatory bone disease e.g. RA, myeloma
Dietary Ca low/malabsorption DM
Key questions in hip#?
Mechanism
RFs for osteoporosis/pathological #
Premorbid mobility
Premorbid independence
Comorbidities
MMSE
Hip # O/E
Shortened and externally rotated
Initial management of hip #
Resuscitate: dehydration, hypothermia
Analgesia: M + M
Assess neurovascular status of limb
Imaging: AP and lateral films
Prep for theatre
Orthopaedic prep for theatre
ABCDEFG
Anaesthetist and book theatre
Bloods: FBC, U+Es, clotting, X-match (2u)
CXR
DVT prophylaxis: TEDS, LMWH
ECG
Films: orthogonal XR
Get consent
Imaging in hip XR
Ask for AP and lateral film
Look at Shenton’s lines
Intra or extracapsular
Displaced or non-displaced
Osteopenic?
What is Shenton’s line?
Shenton’s line is formed by the medial edge of the femoral neck and the inferior edge of the superior pubic ramus
Loss of contour of Shenton’s line is a sign of a fractured neck of femur
IMPORTANT NOTE: Fractures of the femoral neck do not always cause loss of Shenton’s line
What is the extent of the joint capsule of the hip?
Capsule envelopes the femoral head and neck
Subcapital, transcervical and basicervical fractures are intracapsular hip fractures
Intertrochanteric and subtrochanteric fractures do not involve the neck of the femur
What is the blood supply of the femoral head
Most of the bloody suppply to the femoral head ariseses from the lateral femoral circumflex artery which gives rise to the retinacular vessels. These run posteriorly until they reach the cartilaginous border of the femoral head.
The obturator artery gives rise to the vessels within the ligemantum teres (artery of ligamentum teres)
An ascending branch of the medial femoral circumflex artery supplies the greater trochanter and anastomoses with the lateral femoral circumflex artery
Key anatomy of the hip joint
Capsular attaches proximally to the acetabular margin and distally to the intertrochanteric line
If retinacular vessels are damaged theres is a risk of AVN of the femoral head -> pain, stiffness and OA
How can hip fractures be classified
Intracapsular:
Subcapital, transcervical, basicervical
Extracapsular:
Intertrochanteric, subtrochanteric
What can be used to classify intracapsular hip #s?
Garden Classification
Components of the Garden Classification of Intracapsular fractures?
- Incomplete # undisplaced
- Complete fracture, undisplaced
- Complete fracture, partially dispalced
- Complete fracture, completely dispalced
Surgical management of intracapsular hip #
Depends on Garden classification
1,2. ORIF with cancellous screws
3,4.
<55: ORIF with screws, FU in OPD and do arthroplasty if AVN develops (30%)
55-75: THR
>75: hemiarthroplasty
Mobilises: cemented Thompson’s
Non-mobiliser: uncemented Austin Moore
Surgical management of extracapsular hip fracture
ORIF with DHS
Discharge of patients with hip #
Involve OT and physios
Discharge when mobilisation and social circumstances permit
What are the specific complications of hip #
AVN of femoral head in displaced #s (30%)
Non/malunion
Infection
OA
Px of hip #
30% mortality at 1y
50% never regain pre-morbid functioning
>10% unable to return to premorbid residence
Majority will have some residual pain or disability
Features of Colles fracture
FOOSH
Most common elderly females with osteoporosis
Dinner fork deformity
Extra-articular # of distal radius within 1.5” of joint
Dorsal displacement of distal fragment
Dorsal angulation of distal fragment (normally 11 degrees volar tilt)
Reduced radial height (norm= 11m)
Reduced radial inclination (norm= 22 deg)
+/- avulsion of ulna styloid. +/- impaction
Colles fracture
Management of Colles
Examine for neurovascular injury as median nerve and radial artery lie close
If there is much displacement: reduction
Under haematoma block, IV regional anaesthesia or GA
Disimpact and correct angulation
Position: ulnar deviation + some wrist flexion
Apply dorsal backslab: provide 3- point pressure
Re-XR: satisfactory position
No: ortho review and consider MUA +/- K wires
Yes: home with clinic follow up witihin 48h for completion of POP
6w in POP + physio
If comminuted: intra-articular or redisplaces: surgical fixation with ex-fix, Kirschner-wries or ORIF and plates
What are the specific complications of Colles fractures?
Median nerve injury
Frozen shoulder/adhesive capsulitis
Tendon rupture especially EPL
Carpal tunnel syndrome
Mal/nonunion
Sudek’s atrophy/CRPS
Fall onto back of flexed wrist
Fracture of distal radius with volar (palmar) displacement and angulation of distal fragment
Reduce to restore anatomy and POP for 6w
Smith’s/Reverse Colle’s
Oblique intra-articular fracture involving the dorsal aspect of the distal radius and dislocation of the radiocarpal joint
Barton’s fracture
Barton fractures are fractures of the distal radius. It is also sometimes termed the dorsal type Barton fracture to distinguish it from the volar type or reverse Barton fracture.
Barton fractures extend through the dorsal aspect to the articular surface but not to the volar aspect. Therefore, it is similar to a Colles fracture. There is usually associated dorsal subluxation/dislocation of the radiocarpal joint.
FOOSH
Pain in anatomical snuffbox
Pain on telescoping the thumb
Scaphoid fracture
Specific management of scaphoid fracture
Request scaphoid XR view
If clinical hx and exam suggest a scaphoid fracture it should be initially treated even if the XR is normal as # may take 10d to become apparent
Place wrist in scaphoid blaster (beer glass position)
If initial XR is negative F/U in clinic in 10d for repeat XR
Fracture visible-> plaster for 6 w
No visible fracture but clinically tender-> 2w
No visible fracture not tender, no plaster
Fracture of proximal 3rd of ulna shaft
Anterior dislocation of radial head at the capitulum
May lead to palsy of deep branch of radial nerve- weak finger extension but no senosry loss
Monteggia
Fractutre of radial shaft between mid and distal 3rds
Dislocation of distal radio-ulna joint
Galleazi fracture
Management of radial and ulna shaft fractures
Unstable: adults: ORIF, children: MUA and above elbow plaster
Fractures of forearm should be plastered in most stable position
Proximal: supination
Distal: pronation
Mid-shaft: neutral
How can shoulder dislocation be classified?
Anterior
Posterior
Features of anterior shoulder dislocation
95% of shoulder dislocations
Direct trauma or falling on hand
Humeral head dislocates antero-inferiorly
Features of posterior shoulder dislocation
Caused by direct trauma or muscle contraction (electrocution, epileptics)
Anterior shoulder dislocation
Posterior dislocation
Lightbulb sign: internally rotated humeral head takes on a rounded appearance
What are the lesions associated with shoulder dislocation?
Bankart lesion
Hill-Sachs lesion
What is a Bankart lesion
Damage to anteroinferior glenoid labrum
What is Hill-Sachs lesion
Cortical depression in the posteriolateral part of the humeral head following impaction against the glenoid rim during anterior dislocaiton
Occurs in 35-40% of anterior dislocaiton
Hill Sachs
Bankart Lesion
Shoulder contour loss: appears square
Bulge in infraclavicular fossa
Arm spported in opposite hand
Severe pain
?Shoulder dislocation
Specific management of shoulder dislocation
Assess for neurovascular deficit: especially axillary nerve- sensation over chevron area before and after reduction
Occurs in 5%
XR: AP and transcapular view
Reduction under sedation
Rest arm in a sling for 3-4w
Physio
What are the methods for reduciton of shoulder dislocation?
Hippocratic
Kocher’s
Features of hippocratic shoulder reduction
Longitudinal traction with arm in 30 degree abduction and counter traction at the axilla
Features of Kocher’s reduction of dislocation
External rotation of adducted arm, anterior movement, internal rotation
Complications of shoulder dislocation
Recurrent dislocation
90% of patietns <20y with traumatic dislocation
Axillary nerve injury
TUBS Recurrent shoulder instability
Traumatic Unilateral dislocations with a Bankart lesion often require Surgery
Mostly young patients: 15-30y
Surgery involves a Bankart repair
AMBRI Recurrent shoulder instability
Atraumatic Multidirectional Bilateral shoulder dislocation is treated with Rehabilitation but may require Inferior capsular shift
Pathology of impingement syndrome/painful arc
Entrapment of supraspinatus tendon and subacromial bursa between acromion and greater tuberosity of humerus
-> subacromial bursitis and or supraspinatus tendonitis
Painful arc: 60-120 degrees
Weakness and reduced ROM
+ve Hawkins test
Impingement syndrome/ painful arc
Hawkins test
The patient is examined while sitting with their shoulder flexed to 90° and their elbow flexed to 90°. The examiner grasps and supports proximal to the wrist and elbow to ensure maximal relaxation, the examiner and the patient then quickly rotate the arm internally.[4][5] Pain located below the acromioclavicular joint with internal rotation is considered a positive test result
Ix in impingement sydnrome
Plain radiographs may see bony spurs
US
MRI arthrogram
Rx of impingement syndrome
Conservative: rest, PT
Medical: NSAIDs, subacromial bursa steroid +/- LA injeciton
Surgical: arthoroscopic acromioplasty
DDx of painful arc
Impingement
Supraspinatus tear or partial tear
AC joint OA
Progressive reduction in active and passive ROM
EXTERNAL ROTATION<30 deg
Abduction <90
Shoulder pain especially at night (can’t lie on affected side)
Frozen shoulder: adhesive capsulitis
Stages of frozen shoulder
Freezing
Frozen
Unfreezing
With what is frozen shoulder associated?
DM
Mx of frozen shoulder
Conservative: rest, PT
Medical: NSAIDs, subacromial bursa steroid +/- LA injection
Features of partial rotator cuff tear
Painful arc
Supracondylar fracture (extension type)
Supracondylar fracture flexion type
A 27-year-old woman complains of recurrent ear discharge. Otoscopy is as follows:
What is the most likely diagnosis?
Otitis externa
Chronic suppurative otitis media
Mastoiditis
Cholesteatoma
Acute otitis media
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
A 35-year-old man presents to his GP surgery as he is having some difficulties with his hearing. He now struggles to follow conversation and often has the TV volume turned up high. Otoscopy is normal. An audiogram is requested:
What does the audiogram show?
Bilateral mixed hearing loss
Right conductive hearing loss
Normal hearing
Bilateral conductive hearing loss
Bilateral sensorineural hearing loss
Audiograms are usually the first-line investigation that is performed when a patient complains of hearing difficulties. They are relatively easy to interpret as long as some simple rules are followed:
anything above the 20dB line is essentially normal (marked in red on the blank audiogram below)
in sensorineural hearing loss both air and bone conduction are impaired
in conductive hearing loss only air conduction is impaired
in mixed hearing loss both air and bone conduction are impaired, with air conduction often being ‘worse’ than bone
A patient presents due to a ‘brown coating’ on his tongue. He is 34-years-old and has no significant medical history. The coating has been present for the past few weeks. He is asymptomatic other than a slight ‘tickling’ sensation on his tongue.
What is the most likely diagnosis?
Lichen Planus
Oral Candida
Iron-deficiency anaemia
Hairy leukoplakia
Black hairy tongue
Black hairy tongue is relatively common condition which results from defective desquamation of the filiform papillae. Despite the name the tongue may be brown, green, pink or another colour.
Predisposing factors
poor oral hygiene
antibiotics
head and neck radiation
HIV
intravenous drug use
The tongue should be swabbed to exclude Candida
Management
tongue scraping
topical antifungals if Candida
This 21-year-old woman has a history of recurrent epistaxis:
© Image used on license from DermNet NZ
What is the most likely underlying diagnosis?
Idiopathic thrombocytopenic purpura
Peutz-Jeghers syndrome
Anorexia nervosa
Combined oral contraceptive pill use
Hereditary haemorrhagic telangiectasia
Osler Weber Rendu
HHT
The chest x-ray shows multiple pulmonary nodules representing arteriovenous malformations, the largest in the right mid-zone. The CT scan shows multiple hepatic arteriovenous malformations
A 7-year-old boy is taken to the Emergency Department after falling during football. He complains of pain in his left wrist.
The x-ray is shown below:
© Image used on license from Radiopaedia
What which one of the following best describes this injury?
Greenstick fracture
Buckle fracture
Salter-Harris type 1 fracture
Salter-Harris type 2 fracture
Salter-Harris type 3 fracture
A typical buckle fracture is shown in this radiograph. This is a common fracture pattern in children due to the pliable nature of the bone.
Buckle, or torus, fractures are incomplete fractures of the shaft of a long bone that is characterised by bulging of the cortex. They typically occur in children aged 5-10 years.
As they are typically self-limiting they do not usually require operative intervention and can sometimes be managed with splinting and immobilisation rather than a cast.
A 10-year-old girl is brought to the Emergency Department after falling from a tree swing. She is complaining of pain in the left forearm. An x-ray is requested:
© Image used on license from Radiopaedia
What type of fracture is seen?
Buckle fracture
Greenstick fracture
Salter-Harris type I
Salter-Harris type II
Salter-Harris type IV
The radiograph shows a fracture involving the palmar surface of the distal radius, with minimal dorsal angulation and no disruption of the dorsal cortex. The growth plate appears normal.
Trough sign
Luxatio erecta (inferior shoulder disloccation)
A 48-year-old woman presents with progressively worsening pain in the right shoulder over the past few weeks. She is generally fit and well but smokes 20 cigarettes/day.
On examination there is diffuse mild tenderness over the lateral aspect of the right shoulder. The pain is recreated when abducting the shoulder to around 70-80 degrees.
A shoulder x-ray is requested:
© Image used on license from Radiopaedia
What is the most likely diagnosis?
Pancoast tumour
Supraspinatus tendonitis
Adhesive capsulitis
Humeral head fracture
Avascular necrosis
The x-ray shows calcification of the supraspinatus tendon consistent with prolonged inflammation. On examination the patient exhibits the classical ‘painful arc’ associated with this condition.
Describe Schatzker Classification
Type 1:
Vertical split of lateral condyle
Fracture through dense bone, usually in the young, may be undisplaced or condylar fragment may be pushed in feriorly
Type 2:
Vertical split of the lateral condyle combined with an adjacent load bearing part of the condyle
The wedge fragment (which may be of variable size), is displaced laterally; the joint is widened. Untreated, a valgus deformity may develop
Type 3:
Depression of the articular surface with intact condylar rim
The split does not extend to the edge of the plateau. Depressed fragments may be firmly embedded in subchondral bone, the joint is stable
Type 4
Fragment of the medial tibial condyle
Two injuries are seen in this category; (1) a depressed fracture of osteoporotic bone in the elderly. (2) a high energy fracture resulting in a condylar split that runs from the intercondylar eminence to the medial cortex. Associated ligamentous injury may be severe
Type 5
Fracture of both condyles
Both condyles fractured but the column of the metaphysis remains in continuity with the tibial shaft
Type 6
Combined condylar and subcondylar fractures
High energy fracture with marked comminution
What is this classificaiton system?
Weber Classification
Relation of fibula # to joint line
A: below joint line
B: at joint line
C: above joint line
Weber’s B and C represent possible injury to the
syndesmotic ligaments between tib and fib → instability
Spondylolisthesis
Scheueurmann’s disease
Autosomal dominant
Vertebral tenderness and kyphosis
XR: wedge-shaped thoracic vertebra
Kohler’s disease
Kienboch’s disease
Lunate bone
Adults
Pain over lunate, esp. on active movement
Impaired grip
Friedberg’s disease
2nd/3rd metatarsal heads
Around puberty
Forefoot pain worse with pressure
Panner’s disease
Capitulum of humerus
Legg-Calve-Perthes Disease of right hip
Osgood-Shlatters
Sinding Larsen’s disease
Tranction tendinopathy with calcification of proximal
attachment of patellar tendon
Children 8-10yrs
Fibrous dysplasia
Ground glass appearance
Simple bone cyst
Well-defined lytic lesion
Fibrous cortical defect
Osteochondroma
Enchondroma
Chondroblastoma
Ollier disease
Marfucci syndrome
Chondrosarcoma
Osteoma
Gardner syndrome
Osteoid osteoma
Osteoclastoma (Giant cell tumour)
Osteosarcoma (Codman triangle)
Ewing’s Sarcoma
A 50-year-old man is admitted to hospital with a 5 day history of worsening abdominal pain. Over the past 24 hours the pain has become very severe. On examination his pulse is 110/min, blood pressure 110/62 mmHg and temperature 37.7ºC. Bloods show the following:
Hb10.5 g/l
Platelets452 * 109/l
WBC16.3 * 109/l
CRP263 mg/l
The abdominal film is shown below:
What is the most likely underlying disorder?
Perforated diverticulum
Sigmoid volvulus
Ulcerative colitis
Spontaneous bacterial peritonitis
Crohn’s disease
This patient had toxic megacolon secondary to underlying ulcerative colitis - note the dilated transverse colon. The abdomen demonstrates a markedly dilated transverse colon (9 cm) with impression of slight dilatation of the descending colon with some ‘thumb printing’ in the wall. No free subphrenic gas is seen.
They went on to have a subtotal colectomy
A 59-year-old woman is admitted to hospital after developing an infection of a non-functioning left kidney, Intravenous antibiotics are given and a nephrostomy tube is inserted. During her recovery she starts to develop a distended abdomen and complains of nausea and abdominal pain.
An abdominal film is requested:
© Image used on license from Radiopaedia
What is the cause of the abdominal distension?
Bowel perforation
Intussusception
Bacterial peritonitis
Caecal volvulus
Subcutaneous emphysema
Small bowel obstruction is clearly visible on this film (note the valvulae conniventes, mucosal folds, that cross the full width of the bowel) secondary to caecal volvulus. Note the left nephrostomy tube in-situ.
What is Frimann Dahl’s sign?
three dense lines converging towards the site of obstruction (Frimann Dahl’s sign) in keeping with sigmoid volvulus.
You are asked to review a 65-year-old woman who has become breathless on the surgical ward. Earlier in the day she had a laparoscopic cholecystectomy for gallstone disease. A chest x-ray has already been obtained:
© Image used on license from Radiopaedia
What complication has developed?
Pneumothorax
Intestinal perforation resulting in pneumoperitneum
Subcutaneous emphysema
Pulmonary embolism
Acute respiratory distress syndrome
This radiograph demonstrates subcutaneous (surgical) emphysema which is a known complication of laparoscopic surgery. If the anterior chest wall is affected air can outline the pectoralis major muscle, giving rise to the ‘ginkgo leaf’ sign.
Characteristic fundus findings of Purtscher retinopathy. Multiple cotton-wool spots surround the optic nerve after blunt thoracic trauma.
Dupuytren’s conracture
Ganglion
Baker’s cyst
Hallux valgus
A 5-year-old boy is seen in the Minor Injury Unit after falling in the playground. His mother observed the fall and describes him falling on an outstretched hand.
The x-ray is shown below
© Image used on license from Radiopaedia
What which one of the following best describes this injury?
Colles’ fracture
Salter-Harris type 1 fracture
Salter-Harris type 2 fracture
Buckle fracture
Greenstick fracture
Buckle, or torus, fractures are incomplete fractures of the shaft of a long bone that is characterised by bulging of the cortex. They typically occur in children aged 5-10 years.
As they are typically self-limiting they do not usually require operative intervention and can sometimes be managed with splinting and immobilisation rather than a cast.
PEG tube
jejunostomy feeding
Pott’s (trimalleolar fracture)
C-spine assessment- systematic: lateral
C-spine systematic approach - Normal Lateral 1
Coverage - All vertebrae are visible from the skull base to the top of T2 (T1 is considered adequate)
- If T1 is not visible then a repeat image with the patient’s shoulders lowered or a ‘swimmer’s’ view may be necessary
Alignment - Check the Anterior line (the line of the anterior longitudinal ligament), the Posterior line (the line of the posterior longitudinal ligament), and the Spinolaminar line (the line formed by the anterior edge of the spinous processes - extends from inner edge of skull)
- GREEN = Anterior line
- ORANGE = Posterior line
- RED = Spinolaminar line
Bone - Trace the cortical outline of all the bones to check for fractures
Note: The spinal cord (not visible) lies between the posterior and spinolaminar lines
-spine systematic approach - Normal Lateral 2
Disc spaces - The vertebral bodies are spaced apart by the intervertebral discs - not directly visible with X-rays. These spaces should be approximately equal in height
Pre-vertebral soft tissue - Some fractures cause widening of the pre-vertebral soft tissue due to pre-vertebral haematoma
- Normal pre-vertebral soft tissue (asterisks) - narrow down to C4 and wider below
- Above C4 ≤ 1/3rd vertebral body width
- Below C4 ≤ 100% vertebral body width
Note: Not all C-spine fractures are accompanied by pre-vertebral haematoma - lack of pre-vertebral soft tissue thickening should NOT be taken as reassuring
Edge of image - Check other visible structures
C spine systmatic assessment AP
C-spine systematic approach - Normal AP
Coverage - The AP view should cover the whole C-spine and the upper thoracic spine
Alignment - The lateral edges of the C-spine are aligned (red lines )
Bone - Fractures are often less clearly visible on this view than on the lateral
Spacing - The spinous processes (orange) are in a straight line and spaced approximately evenly
Soft tissues - Check for surgical emphysema
Edges of image - Check for injury to the upper ribs and the lung apices for pneumothorax
C-spine assessment odontoid peg
C-spine normal anatomy - Open mouth view
This view is considered adequate if it shows the alignment of the lateral processes of C1 and C2 (red circles)
The distance between the peg and the lateral masses of C1 (asterisks) should be equal on each side
Note: In this image the odontoid peg is fully visible which is not often achievable in the context of trauma due to difficulty in patient positioning
C2 odontoid peg fracture - Lateral view
The C2 bone ‘ring’ is incomplete due to a fracture
The odontoid peg is displaced posteriorly
C2 ‘hangman’ fracture - Lateral view
Loss of alignment at C2/C3 with anterior displacement of C2 (large arrow)
Following the cortical outline of C2 (white line) reveals discontinuity due to a fracture
Bilateral perched facets - Lateral view
(Same patient as image below)
Loss of alignment of all three lines at C5/C6 with ‘perching’ of the C5 facet on the C6 facet (ring)
No fracture is visible
The pre-vertebral soft tissue is widened due to a haematoma
Bilateral perched facets - AP view
(Same patient as image above)
There is widening of space between the C5 and C6 spinous processes (SP) with loss of normal alignment
Again no fracture is demonstrated
Note
The spinal canal lies between the posterior (Orange) and spinolaminar (Red) lines
Derangement of the spinal canal due to this injury results in a high incidence of spinal cord injury
Massive haemothorax
Flail chest
Massive pericardial effusion
Massive pericardial effusion produces a triad of…
Low voltage
Tachycardia
Electrical alternans
Electrical alternans is…
when consecutive, normally-conducted QRS complexes alternate in height.
produced by the heart swinging backwards and forwards within a large fluid-filled pericardium.
Patients with this ECG pattern need to be immediately assessed for clinical and echocardiographic evidence of tamponade.
Contained aortic dissection
Pneumomediastinum
Oesophageal achalasia
Bird’s beak
DOS
Pathology
Aetiology is unknown but may be related to loss of inhibitory neurones in the distal oesophagus.
Radiographic features
Fluoroscopy
only 60% of barium swallows will be abnormal
<5% will show “corkscrew oesophagus” or “rosary bead oesophagus” where normal peristalsis is interrupted by many tertiary (non-propulsive) contractions occurring in the distal oesophagus
nonperistaltic contractions, pushing contrast in two directions, can be seen (sometimes the only feature) 5
sacculations and pseudodivertucula may be seen 5
Apple core appearance
Oesophageal carcinoma
Ivor Lewis Oesophagectomy
2 stage approach
In the Ivor Lewis esphagectomy, the esophageal tumor is removed through an abdominal incision and a right thoracotomy (a surgical incision of the chest wall). The esophagogastric anastomosis (reconnection between the stomach and remaining esophagus) is located in the upper chest.
McKeown Oesophagectomy
Three stage
Abdominal + R thoractomoy
and left neck incision
Used for lesions higher in the oesophagus
Cervical anastomosis
Hiatus hernia
retrocardiac opacity with air-fluid level
Hiatus hernia
Chest X-ray showing obvious Chilaiditi’s sign, or presence of gas in the right colic angle between the liver and right hemidiaphragm.
Subdiaphragmatic air
Sister Mary Joseph Nodule
Maydl’s hernia
Emergency femoral hernia repair
High approach in inguinal region to allow inspection and resection of non-viable bowel
Then herniotomy and herniorrhaphy
Vertical incision
Anal fissure with sentinal skin pile
Ba
Lead pipe colon
UC
Dilated transverse colon noted. The abdomen demonstrates markedly dilated transverse colon (9 cm) with impression of slight dilatation of the descending colon with some” thumb printing” in the wall (consistent with mucosal inflammation in the clinical circumstances). No free subphrenic gas is seen.
UC
String sign of Kantor
Sigmoid volvulus
Coffee bean sign
Caecal volvulus
Despite the varying positions of the distended cecum, the plain radiographic features of a caecal volvulus are characteristic, and the caput caecum can typically be identified. The colonic haustral pattern is generally maintained in contradistinction to a sigmoid volvulus although some effacement may be present if ischemia develops.
A 65-year-old woman presents to the Emergency Department with lower abdominal pain and vomiting. On further questioning she has not opened her bowels for the past 2 days and feels bloated.
A CT of her abdomen is requested:
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What is the most likely diagnosis?
Diverticulitis
Small bowel obstruction secondary to a strangulated inguinal hernia
Linitis plastica of the stomach
Large bowel obstruction secondary to volvulus
Ovarian cancer with associated ovarian torsion
The CT shows multiple dilated loops of small bowel. CT is more sensitive than radiographs and will also demonstrate the cause in around 80% of cases. There are variable criteria for maximal small bowel obstruction, but 3.5 cm is a conservative estimate of dilated bowel.
Note the protrusion of small bowel through the inguinal ring
Apple-core sign
CRC
Peutz Jehgers
Soft
Subcutaneous
Imprecise margin
Fluctuant
Madelung’s disease
Central punctum
Firm
Smooth
Intradermal
Sebaceous cyst
Cock’s peculiar tumour
Ganglion
Seborrheic keratosis
Pyogenic granuloma
Dermoid cyst
Dermatofibroma
Superficial spreading melanoma
Lentigo Maligna melanoma
Acral lentigionous melanoma
Nodular Melanoma
Amelanotic melanoma
Xeroderma pigmentosa
Increased risk of SCC skin
SCC
Actinic keratoses
Bowen’s disease
BCC
Branchial cyst
Infected thyroglossal cyst
Cervical rib
Cystic hygroma
Hypertrophic scar
Keloid scar
Inflammatory breast cancer with peau d’orange
WLE + LN biopsy
Mastectomy
?Axillary clearance
Lat dorsi myocutaneous flap
Usually used with implant
Transverse rectus abdominis myocutaneous flap
Bennet’s Fracture
Describe the levles of foot amputaiton
