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