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Flashcards in Surgery (non-ortho) Deck (270)
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1

A 29 year old man has had a sore throat for the past 5 days. Over the past 24 hours he has notices increasing and severe throbbing pain in the region of his right tonsil. He is pyrexial and on examination he is noted to have a swelling of this area. What is the most likely cause?

Tonsillar cancer
Lymphoma
Quinsy
Glandular fever
Common cold

Unilateral swelling and fever is usually indicative of quinsy. Surgical drainage usually produces prompt resolution of symptoms.

Acute tonsillitis
Characterised by pharyngitis, fever, malaise and lymphadenopathy.
Over half of all cases are bacterial with Streptococcus pyogenes the most common organism
The tonsils are typically oedematous and yellow or white pustules may be present
Infectious mononucleosis may mimic the condition.
Treatment with penicillin type antibiotics is indicated for bacterial tonsillitis.
Bacterial tonsillitis may result in local abscess formation (quinsy)

2

A 76 year old man presents with a painful right arm (he is right handed). On examination, he has a cool right forearm and absent radial and brachial pulses. A duplex scan shows thrombus occluding the brachial artery. What is the most appropriate course of action?

Administration of therapeutic low molecular weight heparin
Brachial embolectomy without fasciotomy
Intra arterial thrombolysis
Systemic thrombolysis
Brachial embolectomy with fasciotomy

Brachial embolectomy without fasciotomy

Options to treat upper limb embolic events include either anticoagulation or surgery. Background arterial lesions are very rarely present in the upper limb so embolectomy is usually successful. Anticoagulation with intravenous unfractionated heparin is a reasonable alternative. However, note that low molecular weight heparin is not used in this setting as its difficult to control perioperatively.

Acute limb ischaemia
Thrombosis of a pre-existing site of atherosclerosis if the commonest cause of acute limb ischaemia
Acute thrombosis of popliteal aneurysms poses the greatest threat to the limb
Sudden occlusion of a large proximal vessel results in the typical appearances of acute limb ischaemia

Clinical appearances
Less than 6 hours = White leg
At 6 -12 hours = Mottled limb with blanching on pressure
More than 12-24 hours = Fixed mottling

Management of acutely ischaemic leg
- White leg with sensorimotor deficit Surgery and embolectomy
- Dusky leg, mild anaesthesia Angiography
- Fixed mottling Primary amputation

Role of thrombolysis
Intra arterial thrombolysis is better than peripheral thrombolysis
Mainly indicated in acute on chronic thrombosis
Avoid if within 2 months of CVA or 2 weeks of surgery
Aspiration of clot may improve success rate if the thrombosis is large

Surgery
Both groins should be prepared
Transverse arteriotomy is easier to close
Poor inflow should be managed with iliac trawl- if this fails to improve then consider a femoro-femoral cross over or axillo-femoral cross over.
A check angiogram should be performed on table and prior to closure
Systemic heparinisation should follow surgery
Fasciotomy should be considered if the time between onset and surgery exceeds 6 hours

3

A 14 year old boy presents with enlarged tonsils that meet in the midline. Oropharyngeal examination confirms this finding and you also notice peticheal haemorrhages affecting the oropharynx. On systemic examination he is noted to have splenomegaly. What is the most likely cause?

Oral candidiasis
Infection with Streptococcus pyogenes
Infection with Rickettsia rickettsii
Infection with Epstein Barr virus
Infection with Staphylococcus aureus

EBV - A combination of pharyngitis and tonsillitis is often seen in glandular fever. Antibiotics containing penicillin may produce a rash when given in this situation, leading to a mistaken label of allergy. Infection with candidiasis can occur in individuals with systemic illness of which splenomegaly may be a feature. However, its unlikely to only affect the tonsils.

Acute tonsillitis
Characterised by pharyngitis, fever, malaise and lymphadenopathy.
Over half of all cases are bacterial with Streptococcus pyogenes the most common organism
The tonsils are typically oedematous and yellow or white pustules may be present
Infectious mononucleosis may mimic the condition.
Treatment with penicillin type antibiotics is indicated for bacterial tonsillitis.
Bacterial tonsillitis may result in local abscess formation (quinsy)

4

An 8 year old boy presents with abdominal pain,a twelve hour history of vomiting, a fever of 38.3 0C and four day history of diarrhoea. His abdominal pain has been present for the past week. What is the most likely cause?

Coeliac disease
Appendix abscess
Irritable bowel syndrome
Mesenteric adenitis
Diverticulitis

Appendix Abscess

The high fever and diarrhoea together with vomiting all point to a pelvic abscess. The presence of pelvic pus is highly irritant to the rectum, and many patients in this situation will complain of diarrhoea. Mesenteric adenitis is less likely to run such a protracted course. IBS does not typically produce such marked systemic symptoms. Diverticulitis is almost unheard of in children.

Appendicitis
Pain radiating to right iliac fossa
Anorexia (very common)
Short history
Diarrhoea and profuse vomiting rare

Crohn's disease
Often long history
Signs of malnutrition
Change in bowel habit, especially diarrhoea

Mesenteric adenitis
Mainly affects children
Causes include Adenoviruses, Epstein Barr Virus, beta-haemolytic Streptococcus, Staphylococcus spp., Escherichia coli, Streptococcus viridans and Yersinia spp.
Patients have a higher temperature than those with appendicitis
If laparotomy is performed, enlarged mesenteric lymph nodes will be present

Diverticulitis
Both left and right sided disease may present with right iliac fossa pain
Clinical history may be similar, although some change in bowel habit is usual
When suspected, a CT scan may help in refining the diagnosis

Meckel's diverticulitis
A Meckel's diverticulum is a congenital abnormality that is present in about 2% of the population
Typically 2 feet proximal to the ileocaecal valve
May be lined by ectopic gastric mucosal tissue and produce bleeding

Perforated peptic ulcer
This usually produces upper quadrant pain but pain may be lower
Perforations typically have a sharp sudden onset of pain in the history
Incarcerated right inguinal or femoral hernia
Usually only right iliac fossa pain if right sided or bowel obstruction.
Bowel perforation secondary to caecal or colon carcinoma
Seldom localised to right iliac fossa, although complete large bowel obstruction with caecal distension may cause pain prior to perforation.

Gynaecological causes
Pelvic inflammatory disease/salpingitis/pelvic abscess/Ectopic pregnancy/Ovarian torsion/Threatened or complete abortion/Mittelschmerz

Urological causes
Ureteric colic/UTI/Testicular torsion
Other causes
TB/Typhoid/Herpes Zoster/AAA/Situs inversus

5

A 74 year old man presents with a painful right leg. The pain developed suddenly the preceeding evening. However, he wondered if it might resolve overnight, instead, it has got worse. On examination, his right leg is cold and white with diminished distal sensation. A CT angiogram shows a thrombus occluding the external iliac artery with no atheromatous disease. What is the most appropriate course of action?

Femoral embolectomy and below knee fasciotomy
Femoral embolectomy alone
Femoral popliteal bypass graft without fasciotomy
Femoral embolectomy with above and below knee fasciotomy
Femoro-femoro cross over graft with above and below knee fasciotomy

Femoral embolectomy and below knee fasciotomy

Delayed limb re-perfusion = Risk of compartment syndrome

Delayed surgery for limb ischaemic carries a risk of re-perfusion injury and compartment syndrome. Where surgery is delayed beyond 6 hours, most surgeons would perform a fasciotomy at the same time as the embolectomy. However, whilst the compartments below the knee are vulnerable, its very rare for this to occur in the thigh and so, as a rule, the thigh is not treated in this manner.

Acute limb ischaemia
Thrombosis of a pre-existing site of atherosclerosis if the commonest cause of acute limb ischaemia
Acute thrombosis of popliteal aneurysms poses the greatest threat to the limb
Sudden occlusion of a large proximal vessel results in the typical appearances of acute limb ischaemia

Clinical appearances
Less than 6 hours = White leg
At 6 -12 hours = Mottled limb with blanching on pressure
More than 12-24 hours = Fixed mottling

Management of acutely ischaemic leg
- White leg with sensorimotor deficit Surgery and embolectomy
- Dusky leg, mild anaesthesia Angiography
- Fixed mottling Primary amputation

Role of thrombolysis
Intra arterial thrombolysis is better than peripheral thrombolysis
Mainly indicated in acute on chronic thrombosis
Avoid if within 2 months of CVA or 2 weeks of surgery
Aspiration of clot may improve success rate if the thrombosis is large

Surgery
Both groins should be prepared
Transverse arteriotomy is easier to close
Poor inflow should be managed with iliac trawl- if this fails to improve then consider a femoro-femoral cross over or axillo-femoral cross over.
A check angiogram should be performed on table and prior to closure
Systemic heparinisation should follow surgery
Fasciotomy should be considered if the time between onset and surgery exceeds 6 hours

6

A 22 year old man is investigated for weight loss. A duodenal biopsy taken as part of his investigations shows total villous atrophy and lymphocytic infiltrate. He has a skin lesion that has small itchy papules.


A. Pyoderma gangrenosum
B. Erythroderma
C. Dermatitis herpetiformis
D. Acanthosis nigricans
E. Multiple lipomata
F. Multiple neurofibromata
G. Multiple telangectasia
H. None of the above

Dermatitis herpetiformis

The patient has coeliac disease and this is associated with dermatitis herpetiformis.

Skin lesions may be referred for surgical assessment, but more commonly will come via a dermatologist for definitive surgical management.


Basal Cell Carcinoma
Most common form of skin cancer.
Commonly occur on sun exposed sites apart from the ear.
Sub types include nodular, morphoeic, superficial and pigmented.
Typically slow growing with low metastatic potential.
Standard surgical excision, topical chemotherapy and radiotherapy are all successful.
As a minimum a diagnostic punch biopsy should be taken if treatment other than standard surgical excision is planned.

Squamous Cell Carcinoma
Again related to sun exposure.
May arise in pre - existing solar keratoses.
May metastasize if left.
Immunosupression (e.g. following transplant), increases risk.
Wide local excision is the treatment of choice and where a diagnostic excision biopsy has demonstrated SCC, repeat surgery to gain adequate margins may be required.

Malignant Melanoma
The main diagnostic features (major criteria):
Change in size
Change in shape
Change in colour
Secondary features (minor criteria)
Diameter >6mm
Inflammation
Oozing or bleeding
Altered sensation

Treatment
Suspicious lesions should undergo excision biopsy. The lesion should be removed in completely as incision biopsy can make subsequent histopathological assessment difficult.
Once the diagnosis is confirmed the pathology report should be reviewed to determine whether further re-excision of margins is required (see below):

Margins of excision-Related to Breslow thickness
Lesions 0-1mm thick 1cm
Lesions 1-2mm thick 1- 2cm (Depending upon site and pathological features)
Lesions 2-4mm thick 2-3 cm (Depending upon site and pathological features)
Lesions >4 mm thick 3cm


Further treatments such as sentinel lymph node mapping, isolated limb perfusion and block dissection of regional lymph node groups should be selectively applied.

Kaposi Sarcoma
Tumour of vascular and lymphatic endothelium.
Purple cutaneous nodules.
Associated with immuno supression.
Classical form affects elderly males and is slow growing.
Immunosupression form is much more aggressive and tends to affect those with HIV related disease.

Non malignant skin disease:

Dermatitis Herpetiformis
Chronic itchy clusters of blisters.
Linked to underlying gluten enteropathy (coeliac disease).

Dermatofibroma
Benign lesion.
Firm elevated nodules.
Usually history of trauma.
Lesion consists of histiocytes, blood vessels and fibrotic changes.

Pyogenic granuloma
Overgrowth of blood vessels.
Red nodules.
Usually follow trauma.
May mimic amelanotic melanoma.

Acanthosis nigricans
Brown to black, poorly defined, velvety hyperpigmentation of the skin.
Usually found in body folds such as the posterior and lateral folds of the neck, the axilla, groin, umbilicus, forehead, and other areas.
The most common cause of acanthosis nigricans is insulin resistance, which leads to increased circulating insulin levels. Insulin spillover into the skin results in its abnormal increase in growth (hyperplasia of the skin).
In the context of a malignant disease, acanthosis nigricans is a paraneoplastic syndrome and is then commonly referred to as acanthosis nigricans maligna. Involvement of mucous membranes is rare and suggests a coexisting malignant condition.

7

A 72 year old man is investigated for weight loss. On examination he is deeply jaundiced and cachectic. He also has a dark velvety lesion coating his tongue.


A. Pyoderma gangrenosum
B. Erythroderma
C. Dermatitis herpetiformis
D. Acanthosis nigricans
E. Multiple lipomata
F. Multiple neurofibromata
G. Multiple telangectasia
H. None of the above

Acanthosis nigricans

Acanthosis nigricans may be associated with GI malignancies such as gastric and pancreatic cancer.

Skin lesions may be referred for surgical assessment, but more commonly will come via a dermatologist for definitive surgical management.


Basal Cell Carcinoma
Most common form of skin cancer.
Commonly occur on sun exposed sites apart from the ear.
Sub types include nodular, morphoeic, superficial and pigmented.
Typically slow growing with low metastatic potential.
Standard surgical excision, topical chemotherapy and radiotherapy are all successful.
As a minimum a diagnostic punch biopsy should be taken if treatment other than standard surgical excision is planned.

Squamous Cell Carcinoma
Again related to sun exposure.
May arise in pre - existing solar keratoses.
May metastasize if left.
Immunosupression (e.g. following transplant), increases risk.
Wide local excision is the treatment of choice and where a diagnostic excision biopsy has demonstrated SCC, repeat surgery to gain adequate margins may be required.

Malignant Melanoma
The main diagnostic features (major criteria):
Change in size
Change in shape
Change in colour
Secondary features (minor criteria)
Diameter >6mm
Inflammation
Oozing or bleeding
Altered sensation

Treatment
Suspicious lesions should undergo excision biopsy. The lesion should be removed in completely as incision biopsy can make subsequent histopathological assessment difficult.
Once the diagnosis is confirmed the pathology report should be reviewed to determine whether further re-excision of margins is required (see below):

Margins of excision-Related to Breslow thickness
Lesions 0-1mm thick 1cm
Lesions 1-2mm thick 1- 2cm (Depending upon site and pathological features)
Lesions 2-4mm thick 2-3 cm (Depending upon site and pathological features)
Lesions >4 mm thick 3cm


Further treatments such as sentinel lymph node mapping, isolated limb perfusion and block dissection of regional lymph node groups should be selectively applied.

Kaposi Sarcoma
Tumour of vascular and lymphatic endothelium.
Purple cutaneous nodules.
Associated with immuno supression.
Classical form affects elderly males and is slow growing.
Immunosupression form is much more aggressive and tends to affect those with HIV related disease.

Non malignant skin disease:

Dermatitis Herpetiformis
Chronic itchy clusters of blisters.
Linked to underlying gluten enteropathy (coeliac disease).

Dermatofibroma
Benign lesion.
Firm elevated nodules.
Usually history of trauma.
Lesion consists of histiocytes, blood vessels and fibrotic changes.

Pyogenic granuloma
Overgrowth of blood vessels.
Red nodules.
Usually follow trauma.
May mimic amelanotic melanoma.

Acanthosis nigricans
Brown to black, poorly defined, velvety hyperpigmentation of the skin.
Usually found in body folds such as the posterior and lateral folds of the neck, the axilla, groin, umbilicus, forehead, and other areas.
The most common cause of acanthosis nigricans is insulin resistance, which leads to increased circulating insulin levels. Insulin spillover into the skin results in its abnormal increase in growth (hyperplasia of the skin).
In the context of a malignant disease, acanthosis nigricans is a paraneoplastic syndrome and is then commonly referred to as acanthosis nigricans maligna. Involvement of mucous membranes is rare and suggests a coexisting malignant condition.

8

A lesion that may occur in a 32 year old man with long standing Crohns disease.


A. Pyoderma gangrenosum
B. Erythroderma
C. Dermatitis herpetiformis
D. Acanthosis nigricans
E. Multiple lipomata
F. Multiple neurofibromata
G. Multiple telangectasia
H. None of the above


Pyoderma gangrenosum

Pyoderma gangrenosum may occur in Crohns disease.

Skin lesions may be referred for surgical assessment, but more commonly will come via a dermatologist for definitive surgical management.


Basal Cell Carcinoma
Most common form of skin cancer.
Commonly occur on sun exposed sites apart from the ear.
Sub types include nodular, morphoeic, superficial and pigmented.
Typically slow growing with low metastatic potential.
Standard surgical excision, topical chemotherapy and radiotherapy are all successful.
As a minimum a diagnostic punch biopsy should be taken if treatment other than standard surgical excision is planned.

Squamous Cell Carcinoma
Again related to sun exposure.
May arise in pre - existing solar keratoses.
May metastasize if left.
Immunosupression (e.g. following transplant), increases risk.
Wide local excision is the treatment of choice and where a diagnostic excision biopsy has demonstrated SCC, repeat surgery to gain adequate margins may be required.

Malignant Melanoma
The main diagnostic features (major criteria):
Change in size
Change in shape
Change in colour
Secondary features (minor criteria)
Diameter >6mm
Inflammation
Oozing or bleeding
Altered sensation

Treatment
Suspicious lesions should undergo excision biopsy. The lesion should be removed in completely as incision biopsy can make subsequent histopathological assessment difficult.
Once the diagnosis is confirmed the pathology report should be reviewed to determine whether further re-excision of margins is required (see below):

Margins of excision-Related to Breslow thickness
Lesions 0-1mm thick 1cm
Lesions 1-2mm thick 1- 2cm (Depending upon site and pathological features)
Lesions 2-4mm thick 2-3 cm (Depending upon site and pathological features)
Lesions >4 mm thick 3cm


Further treatments such as sentinel lymph node mapping, isolated limb perfusion and block dissection of regional lymph node groups should be selectively applied.

Kaposi Sarcoma
Tumour of vascular and lymphatic endothelium.
Purple cutaneous nodules.
Associated with immuno supression.
Classical form affects elderly males and is slow growing.
Immunosupression form is much more aggressive and tends to affect those with HIV related disease.

Non malignant skin disease:

Dermatitis Herpetiformis
Chronic itchy clusters of blisters.
Linked to underlying gluten enteropathy (coeliac disease).

Dermatofibroma
Benign lesion.
Firm elevated nodules.
Usually history of trauma.
Lesion consists of histiocytes, blood vessels and fibrotic changes.

Pyogenic granuloma
Overgrowth of blood vessels.
Red nodules.
Usually follow trauma.
May mimic amelanotic melanoma.

Acanthosis nigricans
Brown to black, poorly defined, velvety hyperpigmentation of the skin.
Usually found in body folds such as the posterior and lateral folds of the neck, the axilla, groin, umbilicus, forehead, and other areas.
The most common cause of acanthosis nigricans is insulin resistance, which leads to increased circulating insulin levels. Insulin spillover into the skin results in its abnormal increase in growth (hyperplasia of the skin).
In the context of a malignant disease, acanthosis nigricans is a paraneoplastic syndrome and is then commonly referred to as acanthosis nigricans maligna. Involvement of mucous membranes is rare and suggests a coexisting malignant condition.

9

A 67 year old male is diagnosed as having a 7cm infra renal abdominal aortic aneurysm. What is the likely risk of rupture over the next 5 years?

<10%
20%
25%
75%
35%

Risks of abdominal aortic aneurysm rupture (over 5 years):
5-5.9cm = 25%
6-6.9cm= 35%
7cm and over = 75%

Aneuryms greater than 5cm in diameter on USS should be formally assessed using CT scanning with arterial phases to delineate anatomy and facilitate surgical planning.

Abdominal aortic aneurysms are a common problem in vascular surgery.
They may occur as either true or false aneurysm. With the former all 3 layers of the arterial wall are involved, in the latter only a single layer of fibrous tissue forms the aneurysm wall.
True abdominal aortic aneurysms have an approximate incidence of 0.06 per 1000 people. They are commonest in elderly men and for this reason the UK is now introducing the aneurysm screening program with the aim of performing an abdominal aortic ultrasound measurement in all men aged 65 years.

Causes
Several different groups of patients suffer from aneurysmal disease.
The commonest group is those who suffer from standard arterial disease, i.e. Those who are hypertensive and have been or are smokers.
Other patients such as those suffering from connective tissue diseases such as Marfan's may also develop aneurysms. In patients with abdominal aortic aneurysms the extracellular matrix becomes disrupted with a change in the balance of collagen and elastic fibres.

Management
Most abdominal aortic aneurysms are an incidental finding.
Symptoms most often relate to rupture or impending rupture.
20% rupture anteriorly into the peritoneal cavity. Very poor prognosis.
80% rupture posteriorly into the retroperitoneal space
The risk of rupture is related to aneurysm size, only 2% of aneurysms measuring less than 4cm in diameter will rupture over a 5 year period. This contrasts with 75% of aneurysms measuring over 7cm in diameter.
This is well explained by Laplaces' law which relates size to transmural pressure.
For this reason most vascular surgeons will subject patients with an aneurysm size of 5cm or greater to CT scanning of the chest, abdomen and pelvis with the aim of delineating anatomy and planning treatment. Depending upon co-morbidities, surgery is generally offered once the aneurysm is between 5.5cm and 6cm.

Indications for surgery
Symptomatic aneurysms (80% annual mortality if untreated)
Increasing size above 5.5cm if asymptomatic
Rupture (100% mortality without surgery)

Surgical procedures
Abdominal aortic aneurysm repair

Procedure:

GA
Invasive monitoring (A-line, CVP, catheter)
Incision: Midline or transverse
Bowel and distal duodenum mobilised to access aorta.
Aneurysm neck and base dissected out and prepared for cross clamp
Systemic heparinisation
Cross clamp (proximal first)
Longitudinal aortotomy
Atherectomy
Deal with back bleeding from lumbar vessels and inferior mesenteric artery
Insert graft either tube or bifurcated depending upon anatomy
Suture using Prolene (3/0 for proximal , distal anastomosis suture varies according to site)
Clamps off: End tidal CO2 will rise owing to effects of reperfusion, at this point major risk of myocardial events.
Haemostasis
Closure of aneurysm sac to minimise risk of aorto-enteric fistula
Closure: Loop 1 PDS or Prolene to abdominal wall
Skin- surgeons preference

Post operatively:

ITU (Almost all)
Greatest risk of complications following emergency repair
Complications: Embolic- gut and foot infarcts
Cardiac - owing to premorbid states, re-perfusion injury and effects of cross clamp
Wound problems
Later risks related to graft- infection and aorto-enteric fistula

Special groups

Supra renal AAA
These patients will require a supra renal clamp and this carries a far higher risk of complications and risk of renal failure.

Ruptured AAA
Pre-operatively the management depends upon haemodynamic instability. In patients with symptoms of rupture (typical pain, haemodynamic compromise and risk factors) then ideally prompt laparotomy. In those with vague symptoms and haemodynamic stability the ideal test is CT scan to determine whether rupture has occurred or not. Most common rupture site is retroperitoneal 80%. These patients will tend to develop retroperitoneal haematoma. This can be disrupted if Bp is allowed to rise too high so aim for Bp 100mmHg.
Operative details are similar to elective repair although surgery should be swift, blind rushing often makes the situation worse. Plunging vascular clamps blindly into a pool of blood at the aneurysm neck carries the risk of injury the vena cava that these patients do not withstand. Occasionally a supracoeliac clamp is needed to effect temporary control, although leaving this applied for more than 20 minutes tends to carry a dismal outcome.

EVAR
Increasingly patients are now being offered endovascular aortic aneurysm repair. This is undertaken by surgeons and radiologists working jointly. The morphology of the aneurysm is important and not all are suitable. Here is a typical list of those features favoring a suitable aneurysm:
Long neck
Straight iliac vessels
Healthy groin vessels

Clearly few AAA patients possess the above and compromise has to be made. The use of fenestrated grafts can allow supra renal AAA to be treated.

Procedure:

GA
Radiology or theatre
Bilateral groin incisions
Common femoral artery dissected out
Heparinisation
Arteriotomy and insertion of guide wire
Dilation of arteriotomy
Insertion of EVAR Device
Once in satisfactory position it is released
Arteriotomy closed once check angiogram shows good position and no endoleak

Complications:
Endoleaks depending upon site are either Type I or 2. These may necessitate re-intervention and all EVAR patients require follow up . Details are not needed for MRCS.

10

A 48 hour old neonate develops increasing abdominal distension. He had a normal delivery but has yet to pass any meconium. Following digital rectal examination liquid stool is released.

A. Meckel diverticulum
B. Pyloric stenosis
C. Acute appendicitis
D. Mesenteric adenitis
E. Intussusception
F. Malrotation
G. Hirschsprung disease

Hirschsprung disease

Hirschsprungs may present either with features of bowel obstruction in the neonatal period or more insidiously during childhood. After the PR there may be an improvement in symptoms. Diagnosis is by full thickness rectal biopsy.

Paediatric Gastrointestinal disorders
Pyloric stenosis
M>F
5-10% Family history in parents
Projectile non bile stained vomiting at 4-6 weeks of life
Diagnosis is made by test feed or USS
Treatment: Ramstedt pyloromyotomy (open or laparoscopic)
Acute appendicitis
Uncommon under 3 years
When occurs may present atypically
Mesenteric adenitis
Central abdominal pain and URTI
Conservative management
Intussusception
Telescoping bowel
Proximal to or at the level of, ileocaecal valve
6-9 months age
Colicky pain, diarrhoea and vomiting, sausage shaped mass, red jelly stool.
Treatment: reduction with air insufflation
Malrotation
High caecum at the midline
Feature in exomphalos, congenital diaphragmatic hernia, intrinsic duodenal atresia
May be complicated by development of volvulus, infant with volvulus may have bile stained vomiting
Diagnosis is made by upper GI contrast study and USS
Treatment is by laparotomy, if volvulus is present (or at high risk of occurring then a ladds procedure is performed
Hirschsprung's disease
Absence of ganglion cells from myenteric and submucosal plexuses
Occurs in 1/5000 births
Full thickness rectal biopsy for diagnosis
Delayed passage of meconium and abdominal distension
Treatment is with rectal washouts initially, thereafter an anorectal pull through procedure
Oesophageal atresia
Associated with tracheo-oesophageal fistula and polyhydramnios
May present with choking and cyanotic spells following aspiration
VACTERL associations
Meconium ileus
Usually delayed passage of meconium and abdominal distension
Majority have cystic fibrosis
X-Rays may not show a fluid level as the meconium is viscid (depends upon feeding), PR contrast studies may dislodge meconium plugs and be therapeutic
Infants who do not respond to PR contrast and NG N-acetyl cysteine will require surgery to remove the plugs
Biliary atresia
Jaundice > 14 days
Increased conjugated bilirubin
Urgent Kasai procedure
Necrotising enterocolitis
Prematurity is the main risk factor
Early features include abdominal distension and passage of bloody stools
X-Rays may show pneumatosis intestinalis and evidence of free air
Increased risk when empirical antibiotics are given to infants beyond 5 days
Treatment is with total gut rest and TPN, babies with perforations will require laparotomy

11

A 7 month old girl presents with vomiting and diarrhoea. She is crying and drawing her legs up. There is a a sausage shaped mass in the abdomen.

A. Meckel diverticulum
B. Pyloric stenosis
C. Acute appendicitis
D. Mesenteric adenitis
E. Intussusception
F. Malrotation
G. Hirschsprung disease

Intussusception

Sausage shaped mass (colon shaped) is common in intussusception. The other common sign is red jelly stool.

Paediatric Gastrointestinal disorders
Pyloric stenosis
M>F
5-10% Family history in parents
Projectile non bile stained vomiting at 4-6 weeks of life
Diagnosis is made by test feed or USS
Treatment: Ramstedt pyloromyotomy (open or laparoscopic)
Acute appendicitis
Uncommon under 3 years
When occurs may present atypically
Mesenteric adenitis
Central abdominal pain and URTI
Conservative management
Intussusception
Telescoping bowel
Proximal to or at the level of, ileocaecal valve
6-9 months age
Colicky pain, diarrhoea and vomiting, sausage shaped mass, red jelly stool.
Treatment: reduction with air insufflation
Malrotation
High caecum at the midline
Feature in exomphalos, congenital diaphragmatic hernia, intrinsic duodenal atresia
May be complicated by development of volvulus, infant with volvulus may have bile stained vomiting
Diagnosis is made by upper GI contrast study and USS
Treatment is by laparotomy, if volvulus is present (or at high risk of occurring then a ladds procedure is performed
Hirschsprung's disease
Absence of ganglion cells from myenteric and submucosal plexuses
Occurs in 1/5000 births
Full thickness rectal biopsy for diagnosis
Delayed passage of meconium and abdominal distension
Treatment is with rectal washouts initially, thereafter an anorectal pull through procedure
Oesophageal atresia
Associated with tracheo-oesophageal fistula and polyhydramnios
May present with choking and cyanotic spells following aspiration
VACTERL associations
Meconium ileus
Usually delayed passage of meconium and abdominal distension
Majority have cystic fibrosis
X-Rays may not show a fluid level as the meconium is viscid (depends upon feeding), PR contrast studies may dislodge meconium plugs and be therapeutic
Infants who do not respond to PR contrast and NG N-acetyl cysteine will require surgery to remove the plugs
Biliary atresia
Jaundice > 14 days
Increased conjugated bilirubin
Urgent Kasai procedure
Necrotising enterocolitis
Prematurity is the main risk factor
Early features include abdominal distension and passage of bloody stools
X-Rays may show pneumatosis intestinalis and evidence of free air
Increased risk when empirical antibiotics are given to infants beyond 5 days
Treatment is with total gut rest and TPN, babies with perforations will require laparotomy

12

A 1 month old baby girl presents with bile stained vomiting. She has an exomphalos and a congenital diaphragmatic hernia.

A. Meckel diverticulum
B. Pyloric stenosis
C. Acute appendicitis
D. Mesenteric adenitis
E. Intussusception
F. Malrotation
G. Hirschsprung disease

Malrotation

Exomphalos and diaphragmatic herniae are commonly associated with malrotation.

Paediatric Gastrointestinal disorders

Pyloric stenosis
M>F
5-10% Family history in parents
Projectile non bile stained vomiting at 4-6 weeks of life
Diagnosis is made by test feed or USS
Treatment: Ramstedt pyloromyotomy (open or laparoscopic)

Acute appendicitis
Uncommon under 3 years
When occurs may present atypically
Mesenteric adenitis
Central abdominal pain and URTI
Conservative management

Intussusception
Telescoping bowel
Proximal to or at the level of, ileocaecal valve
6-9 months age
Colicky pain, diarrhoea and vomiting, sausage shaped mass, red jelly stool.
Treatment: reduction with air insufflation

Malrotation
High caecum at the midline
Feature in exomphalos, congenital diaphragmatic hernia, intrinsic duodenal atresia
May be complicated by development of volvulus, infant with volvulus may have bile stained vomiting
Diagnosis is made by upper GI contrast study and USS
Treatment is by laparotomy, if volvulus is present (or at high risk of occurring then a ladds procedure is performed

Hirschsprung's disease
Absence of ganglion cells from myenteric and submucosal plexuses
Occurs in 1/5000 births
Full thickness rectal biopsy for diagnosis
Delayed passage of meconium and abdominal distension
Treatment is with rectal washouts initially, thereafter an anorectal pull through procedure

Oesophageal atresia
Associated with tracheo-oesophageal fistula and polyhydramnios
May present with choking and cyanotic spells following aspiration
VACTERL associations

Meconium ileus
Usually delayed passage of meconium and abdominal distension
Majority have cystic fibrosis
X-Rays may not show a fluid level as the meconium is viscid (depends upon feeding), PR contrast studies may dislodge meconium plugs and be therapeutic
Infants who do not respond to PR contrast and NG N-acetyl cysteine will require surgery to remove the plugs

Biliary atresia
Jaundice > 14 days
Increased conjugated bilirubin
Urgent Kasai procedure

Necrotising enterocolitis
Prematurity is the main risk factor
Early features include abdominal distension and passage of bloody stools
X-Rays may show pneumatosis intestinalis and evidence of free air
Increased risk when empirical antibiotics are given to infants beyond 5 days
Treatment is with total gut rest and TPN, babies with perforations will require laparotomy

13

A 6 year old child develops ballooning of the foreskin on micturition and is brought to the clinic by his anxious mother. One examination the foreskin is non retractile but otherwise normal. By which age are 95% of all foreskins retractile

2 years
16 years
8 years
5 years
10 years

By 16 years of age almost all foreskins should be retractile and if they are not circumcision should be considered at around this time.

Paediatric urology- foreskin disorders
Disorders of the foreskin
At birth and in the neonatal period the normal foreskin is non retractile due to the presence of adhesions between the foreskin and glans. In most cases these will separate spontaneously. By the end of puberty 95% of foreskins can be retracted. In some children the non-retractile foreskin may balloon during micturition. This is a normal variant and requires no specific treatment.

Balanitis This is inflammation of the glans penis. It may occur in both circumcised and non-circumcised individuals.
Posthitis This is inflammation of the foreskin. It may occur as a result of infections such as gonorrhoea and other STD's. It may also complicate diabetes. Posthitis may progress to phimosis and as this may make cleaning of the glans difficult and allow progression to balanoposthitis.
Paraphimosis Prolonged retraction of the foreskin proximal to the glans may allow oedema to occur. This may then make foreskin manipulation difficult. It can usually be managed by compression to reduce the oedema and replacement of the foreskin. Where this fails a dorsal slit may be required and this followed by delayed circumcision.
Phimosis This is inability to retract the foreskin and may be partial or complete. It may occur secondary to balanoposthitis or balanitis xerotica obliterans. Depending upon the severity and symptoms treatment with circumcision may be required.
Balanitis xerotica obliterans This is a dermatological condition in which scarring of the foreskin occurs leading to phimosis. It is rare below the age of 5 years. Treatment is usually with circumcision.

14

A neonate is noted to have colonic obstruction, what is the most likely cause?

Imperforate anus
Meconium plugs
Colonic atresia
Anal atresia
Sigmoid volvulus

Cystic fibrosis is the most common cause of meconium plugs and such cases can be treated with intestinal lavage, this should be followed by formal testing for CF.

Paediatric Gastrointestinal disorders
Pyloric stenosis
M>F
5-10% Family history in parents
Projectile non bile stained vomiting at 4-6 weeks of life
Diagnosis is made by test feed or USS
Treatment: Ramstedt pyloromyotomy (open or laparoscopic)

Acute appendicitis
Uncommon under 3 years
When occurs may present atypically

Mesenteric adenitis
Central abdominal pain and URTI
Conservative management

Intussusception
Telescoping bowel
Proximal to or at the level of, ileocaecal valve
6-9 months age
Colicky pain, diarrhoea and vomiting, sausage shaped mass, red jelly stool.
Treatment: reduction with air insufflation

Malrotation
High caecum at the midline
Feature in exomphalos, congenital diaphragmatic hernia, intrinsic duodenal atresia
May be complicated by development of volvulus, infant with volvulus may have bile stained vomiting
Diagnosis is made by upper GI contrast study and USS
Treatment is by laparotomy, if volvulus is present (or at high risk of occurring then a ladds procedure is performed

Hirschsprung's disease
Absence of ganglion cells from myenteric and submucosal plexuses
Occurs in 1/5000 births
Full thickness rectal biopsy for diagnosis
Delayed passage of meconium and abdominal distension
Treatment is with rectal washouts initially, thereafter an anorectal pull through procedure

Oesophageal atresia
Associated with tracheo-oesophageal fistula and polyhydramnios
May present with choking and cyanotic spells following aspiration
VACTERL associations

Meconium ileus
Usually delayed passage of meconium and abdominal distension
Majority have cystic fibrosis
X-Rays may not show a fluid level as the meconium is viscid (depends upon feeding), PR contrast studies may dislodge meconium plugs and be therapeutic
Infants who do not respond to PR contrast and NG N-acetyl cysteine will require surgery to remove the plugs

Biliary atresia
Jaundice > 14 days
Increased conjugated bilirubin
Urgent Kasai procedure

Necrotising enterocolitis
Prematurity is the main risk factor
Early features include abdominal distension and passage of bloody stools
X-Rays may show pneumatosis intestinalis and evidence of free air
Increased risk when empirical antibiotics are given to infants beyond 5 days
Treatment is with total gut rest and TPN, babies with perforations will require laparotomy

15

A 42 year old teacher presents with an ulcer associated with varicose veins in the long saphenous vein territory. Apart from a DVT 1 year ago, she has no other past medical history.

A. No further management needed
B. Injection sclerotherapy using 0.5% Sodium tetradecyl sulphate
C. Injection sclerotherapy using 5% phenol
D. Long saphenous vein ligation
E. Long saphenous vein stripped to the ankle
F. Long saphenous vein stripped to the knee
G. Doppler scan
H. Duplex scan
I. Endothermal ablation

Duplex scan

This patient needs a duplex scan to assess the patency of her deep venous system before surgery can be undertaken. Other indications for duplex scan include recurrent varicose veins or complications.


Chronic venous insufficiency and varicose veins
Wide spectrum of disease ranging from minor cosmetic problem through to ulceration and disability. It is commoner in women than men and is worse during pregnancy. Varicose veins are best considered as being a saccular dilation of veins (WHO). Chronic venous insufficiency is a series of tissue changes which occur in relation to pooling of blood in the extremities with associated venous hypertension occurring as a result of incompetent deep vein valves.

The veins of the lower limb consist of an interconnected network of superficial and deep venous systems. Varices occur because of localised weakness in the vein wall resulting in dilatation and reflux of blood due to non union of valve cusps. Histologically the typical changes include fibrous scar tissue dividing smooth muscle within media in the vessel wall.

Tissue damage in chronic venous insufficiency occurs because of perivascular cytokine leakage resulting in localised tissue damage coupled with impaired lymphatic flow.

Diagnosis
Typical symptoms of varicose veins include:
Cosmetic appearance
Aching
Ankle swelling that worsens as the day progresses
Episodic thrombophlebitis
Bleeding
Itching

Symptoms of chronic venous insufficiency include:
Dependant leg pain
Prominent leg swelling
Oedema extending beyond the ankle
Venous stasis ulcers

The typical venous stasis ulcer is:
Located above the medial malleolus
Indolent appearance with basal granulation tissue
Variable degree of scarring
Non ischaemic edges
Haemosiderin deposition in the gaiter area (and also lipodermatosclerosis).

Differential diagnosis
Lower limb arterial disease
Marjolins ulcer
Claudication
Spinal stenosis
Swelling due to medical causes e.g. CCF.

Exclusion of these differentials is by means of physical examination and ankle brachial pressure index measurement.

Examination
Assess for dilated short saphenous vein (popliteal fossa) and palpate for saphena varix medial to the femoral artery
Brodie-Trendelenburg test: to assess level of incompetence
Perthes' walking test: assess if deep venous system competent

Investigation
Doppler exam: if incompetent a biphasic signal due to retrograde flow is detected
Duplex scanning: to ensure patent deep venous system (do if DVT or trauma)

All patients should have a Doppler assessment to assess for venous reflux and should be classified as having uncomplicated varicose veins or varicose veins with associated chronic venous insufficiency. In the history establishing a previous thrombotic event (DVT/ lower limb fracture) is important and patients with such a history and all who have evidence of chronic venous insufficiency should have a duplex scan performed.

Owing to litigation patients with saphenopopliteal incompetence should have a duplex scan performed and the site marked by scan on the day of surgery.

Treatment
Indications for surgery:
Cosmetic: majority
Lipodermatosclerosis causing venous ulceration
Recurrent superficial thrombophlebitis
Bleeding from ruptured varix

Condition Therapy
Minor varicose veins - no complications Reassure/ cosmetic therapy
Symptomatic uncomplicated varicose veins In those without deep venous insufficiency options include; endothermal ablation, foam sclerotherapy, saphenofemoral / popliteal disconnection, stripping and avulsions, compression stockings
Varicose veins with skin changes Therapy as above (if compression minimum is formal class I stockings)
Chronic venous insufficiency or ulcers Class 2-3 compression stockings (ensure no arterial disease).

Application of formal compression stockings (usually class II/III). In patients who have suffered ulceration, compression stockings should be worn long term. Where ulceration is present and established saphenofemoral reflux exists this should be addressed surgically for durable relief of symptoms, either at the outset or following ulcer healing.
Injection sclerotherapy (5% Ethanolamine oleate), foam is increasingly popular, though transient blindness has been reported. Endo venous laser therapy is another minimally invasive option
Sapheno-femoral or sapheno-popliteal ligation, in the case of the LSV; stripping and multiple phlebectomies

Current best practice guidance
In the United Kingdom the National Institute of Clinical Excellence guidance on varicose veins suggests that for patients with symptomatic varicose veins the first line procedure of choice should be endothermal ablation (see reference for more information). Where this is unavailable or unsuitable then foam sclerotherapy should be the second line option. Surgery is currently the third line treatment option.

Trendelenburg procedure (sapheno-femoral junction ligation)
Head tilt 15 degrees and legs abducted
Oblique incision 1cm medial from artery
Tributaries ligated (Superficial circumflex iliac vein, Superficial inferior epigastric vein, Superficial and deep external pudendal vein)
SF junction double ligated
Saphenous vein stripped to level of knee/upper calf. NB increased risk of saphenous neuralgia if stripped more distally

16

A 42 year old accountant presents with thrombophlebitis of a long standing varicosity of the inner thigh. His past medical history is unremarkable apart from a conservatively managed tibial fracture of the ipsilateral limb 10 years ago. Doppler and clinical assessment demonstrate saphenofemoral junction incompetence.

A. No further management needed
B. Injection sclerotherapy using 0.5% Sodium tetradecyl sulphate
C. Injection sclerotherapy using 5% phenol
D. Long saphenous vein ligation
E. Long saphenous vein stripped to the ankle
F. Long saphenous vein stripped to the knee
G. Doppler scan
H. Duplex scan
I. Endothermal ablation

Duplex scan

Tibial fractures are a well recognised risk factor for occult lower limb deep venous thrombosis and most surgeons would perform a duplex scan to exclude deep venous insufficiency prior to surgery.

Chronic venous insufficiency and varicose veins
Wide spectrum of disease ranging from minor cosmetic problem through to ulceration and disability. It is commoner in women than men and is worse during pregnancy. Varicose veins are best considered as being a saccular dilation of veins (WHO). Chronic venous insufficiency is a series of tissue changes which occur in relation to pooling of blood in the extremities with associated venous hypertension occurring as a result of incompetent deep vein valves.

The veins of the lower limb consist of an interconnected network of superficial and deep venous systems. Varices occur because of localised weakness in the vein wall resulting in dilatation and reflux of blood due to non union of valve cusps. Histologically the typical changes include fibrous scar tissue dividing smooth muscle within media in the vessel wall.

Tissue damage in chronic venous insufficiency occurs because of perivascular cytokine leakage resulting in localised tissue damage coupled with impaired lymphatic flow.

Diagnosis
Typical symptoms of varicose veins include:
Cosmetic appearance
Aching
Ankle swelling that worsens as the day progresses
Episodic thrombophlebitis
Bleeding
Itching

Symptoms of chronic venous insufficiency include:
Dependant leg pain
Prominent leg swelling
Oedema extending beyond the ankle
Venous stasis ulcers

The typical venous stasis ulcer is:
Located above the medial malleolus
Indolent appearance with basal granulation tissue
Variable degree of scarring
Non ischaemic edges
Haemosiderin deposition in the gaiter area (and also lipodermatosclerosis).

Differential diagnosis
Lower limb arterial disease
Marjolins ulcer
Claudication
Spinal stenosis
Swelling due to medical causes e.g. CCF.

Exclusion of these differentials is by means of physical examination and ankle brachial pressure index measurement.

Examination
Assess for dilated short saphenous vein (popliteal fossa) and palpate for saphena varix medial to the femoral artery
Brodie-Trendelenburg test: to assess level of incompetence
Perthes' walking test: assess if deep venous system competent

Investigation
Doppler exam: if incompetent a biphasic signal due to retrograde flow is detected
Duplex scanning: to ensure patent deep venous system (do if DVT or trauma)

All patients should have a Doppler assessment to assess for venous reflux and should be classified as having uncomplicated varicose veins or varicose veins with associated chronic venous insufficiency. In the history establishing a previous thrombotic event (DVT/ lower limb fracture) is important and patients with such a history and all who have evidence of chronic venous insufficiency should have a duplex scan performed.

Owing to litigation patients with saphenopopliteal incompetence should have a duplex scan performed and the site marked by scan on the day of surgery.

Treatment
Indications for surgery:
Cosmetic: majority
Lipodermatosclerosis causing venous ulceration
Recurrent superficial thrombophlebitis
Bleeding from ruptured varix

Condition Therapy
Minor varicose veins - no complications Reassure/ cosmetic therapy
Symptomatic uncomplicated varicose veins In those without deep venous insufficiency options include; endothermal ablation, foam sclerotherapy, saphenofemoral / popliteal disconnection, stripping and avulsions, compression stockings
Varicose veins with skin changes Therapy as above (if compression minimum is formal class I stockings)
Chronic venous insufficiency or ulcers Class 2-3 compression stockings (ensure no arterial disease).

Application of formal compression stockings (usually class II/III). In patients who have suffered ulceration, compression stockings should be worn long term. Where ulceration is present and established saphenofemoral reflux exists this should be addressed surgically for durable relief of symptoms, either at the outset or following ulcer healing.
Injection sclerotherapy (5% Ethanolamine oleate), foam is increasingly popular, though transient blindness has been reported. Endo venous laser therapy is another minimally invasive option
Sapheno-femoral or sapheno-popliteal ligation, in the case of the LSV; stripping and multiple phlebectomies

Current best practice guidance
In the United Kingdom the National Institute of Clinical Excellence guidance on varicose veins suggests that for patients with symptomatic varicose veins the first line procedure of choice should be endothermal ablation (see reference for more information). Where this is unavailable or unsuitable then foam sclerotherapy should be the second line option. Surgery is currently the third line treatment option.

Trendelenburg procedure (sapheno-femoral junction ligation)
Head tilt 15 degrees and legs abducted
Oblique incision 1cm medial from artery
Tributaries ligated (Superficial circumflex iliac vein, Superficial inferior epigastric vein, Superficial and deep external pudendal vein)
SF junction double ligated
Saphenous vein stripped to level of knee/upper calf. NB increased risk of saphenous neuralgia if stripped more distally

17

A 43 year old lady presents with a thigh varicosity in the territory of the long saphenous vein. She underwent endovenous laser therapy 5 years previously. On duplex assessment she has a patent deep venous system and sapheno-femoral junction incompetence.

A. No further management needed
B. Injection sclerotherapy using 0.5% Sodium tetradecyl sulphate
C. Injection sclerotherapy using 5% phenol
D. Long saphenous vein ligation
E. Long saphenous vein stripped to the ankle
F. Long saphenous vein stripped to the knee
G. Doppler scan
H. Duplex scan
I. Endothermal ablation

Long saphenous vein stripped to the knee

In the UK, NICE, suggest the use non operative measures such as endothermal ablation for first time varicose veins. Recurrences respond far less favourably and are best managed with surgery.

Chronic venous insufficiency and varicose veins
Wide spectrum of disease ranging from minor cosmetic problem through to ulceration and disability. It is commoner in women than men and is worse during pregnancy. Varicose veins are best considered as being a saccular dilation of veins (WHO). Chronic venous insufficiency is a series of tissue changes which occur in relation to pooling of blood in the extremities with associated venous hypertension occurring as a result of incompetent deep vein valves.

The veins of the lower limb consist of an interconnected network of superficial and deep venous systems. Varices occur because of localised weakness in the vein wall resulting in dilatation and reflux of blood due to non union of valve cusps. Histologically the typical changes include fibrous scar tissue dividing smooth muscle within media in the vessel wall.

Tissue damage in chronic venous insufficiency occurs because of perivascular cytokine leakage resulting in localised tissue damage coupled with impaired lymphatic flow.

Diagnosis
Typical symptoms of varicose veins include:
Cosmetic appearance
Aching
Ankle swelling that worsens as the day progresses
Episodic thrombophlebitis
Bleeding
Itching

Symptoms of chronic venous insufficiency include:
Dependant leg pain
Prominent leg swelling
Oedema extending beyond the ankle
Venous stasis ulcers

The typical venous stasis ulcer is:
Located above the medial malleolus
Indolent appearance with basal granulation tissue
Variable degree of scarring
Non ischaemic edges
Haemosiderin deposition in the gaiter area (and also lipodermatosclerosis).

Differential diagnosis
Lower limb arterial disease
Marjolins ulcer
Claudication
Spinal stenosis
Swelling due to medical causes e.g. CCF.

Exclusion of these differentials is by means of physical examination and ankle brachial pressure index measurement.

Examination
Assess for dilated short saphenous vein (popliteal fossa) and palpate for saphena varix medial to the femoral artery
Brodie-Trendelenburg test: to assess level of incompetence
Perthes' walking test: assess if deep venous system competent

Investigation
Doppler exam: if incompetent a biphasic signal due to retrograde flow is detected
Duplex scanning: to ensure patent deep venous system (do if DVT or trauma)

All patients should have a Doppler assessment to assess for venous reflux and should be classified as having uncomplicated varicose veins or varicose veins with associated chronic venous insufficiency. In the history establishing a previous thrombotic event (DVT/ lower limb fracture) is important and patients with such a history and all who have evidence of chronic venous insufficiency should have a duplex scan performed.

Owing to litigation patients with saphenopopliteal incompetence should have a duplex scan performed and the site marked by scan on the day of surgery.

Treatment
Indications for surgery:
Cosmetic: majority
Lipodermatosclerosis causing venous ulceration
Recurrent superficial thrombophlebitis
Bleeding from ruptured varix

Condition Therapy
Minor varicose veins - no complications Reassure/ cosmetic therapy
Symptomatic uncomplicated varicose veins In those without deep venous insufficiency options include; endothermal ablation, foam sclerotherapy, saphenofemoral / popliteal disconnection, stripping and avulsions, compression stockings
Varicose veins with skin changes Therapy as above (if compression minimum is formal class I stockings)
Chronic venous insufficiency or ulcers Class 2-3 compression stockings (ensure no arterial disease).

Application of formal compression stockings (usually class II/III). In patients who have suffered ulceration, compression stockings should be worn long term. Where ulceration is present and established saphenofemoral reflux exists this should be addressed surgically for durable relief of symptoms, either at the outset or following ulcer healing.
Injection sclerotherapy (5% Ethanolamine oleate), foam is increasingly popular, though transient blindness has been reported. Endo venous laser therapy is another minimally invasive option
Sapheno-femoral or sapheno-popliteal ligation, in the case of the LSV; stripping and multiple phlebectomies

Current best practice guidance
In the United Kingdom the National Institute of Clinical Excellence guidance on varicose veins suggests that for patients with symptomatic varicose veins the first line procedure of choice should be endothermal ablation (see reference for more information). Where this is unavailable or unsuitable then foam sclerotherapy should be the second line option. Surgery is currently the third line treatment option.

Trendelenburg procedure (sapheno-femoral junction ligation)
Head tilt 15 degrees and legs abducted
Oblique incision 1cm medial from artery
Tributaries ligated (Superficial circumflex iliac vein, Superficial inferior epigastric vein, Superficial and deep external pudendal vein)
SF junction double ligated
Saphenous vein stripped to level of knee/upper calf. NB increased risk of saphenous neuralgia if stripped more distally

18

An elderly diabetic male presents with a severe deep seated otalgia and a facial nerve palsy, he has completed a course of amoxycillin with no benefit. What is the most likely diagnosis?

Malignant otitis externa
Otosclerosis
Acoustic neuroma
Meniers disease
Viral illness

A combination of severe otalgia and facial nerve palsy in a diabetic should raise suspicion of malignant otitis externa. This is a condition caused by pseudomonas. It commences as otitis externa and then progresses to involve the temporal bone. Spread of the disease outside the external auditory canal occurs through the fissures of Santorini and the osseocartilaginous junction.

Acute otitis externa Boil in external auditory meatus Acute pain on moving the pinna
Conductive hearing loss if lesion is large
When rupture occurs pus will flow from ear Ear packs may be used
Topical antibiotics
Operative debridement may be needed in severe cases

Chronic otitis externa Chronic combined infection in the external auditory meatus usually combined staphylococcal and fungal infection Chronic discharge from affected ear, hearing loss and severe pain rare Cleansing of the external ear and treatment with antifungal and antibacterial ear drops

Acute suppurative otitis media Viral induced middle ear effusions secondary to eustacian tube dysfunction Most common in children and rare in adults
May present with symptoms elsewhere (e.g. vomiting) in children
Severe pain and sometimes fever
May present with discharge is tympanic rupture occurs Antibiotics (usually amoxycillin)

Chronic suppurative otitis media May occur with or without cholesteatoma
Those without cholesteatoma have a perforation of the pars tensa
Those with cholesteatoma have a perforation of the pars flaccida Those without cholesteatoma may complain of intermittent discharge (non offensive)
Those with cholesteatoma have impaired hearing and foul smelling discharge Simple pars tensa perforations may be managed non operatively or a myringoplasty considered if symptoms troublesome.
Pars flaccida perforations will usually require a radical mastoidectomy

Otosclerosis
Progressive conductive deafness
Secondary to fixation of the stapes in the oval window
Treatment is with stapedectomy and insertion of a prosthesis

Acoustic neuroma
Symptoms of gradually progressive unilateral perceptive deafness and tinnitus
Involvement of the vestibular nerve may cause vertigo
Extension to involve the facial nerve may cause weakness and then paralysis.

Pre auricular sinus
Common congenital condition in which an epithelial defect forms around the external ear
Small sinuses require no treatment
Deeper sinuses may become blocked and develop episodes of infection, they may be closely related to the facial nerve and are challenging to excise

19

An 18 month old boy is brought to the emergency room by his parents. He was found in bed with a nappy filled with dark red blood. He is haemodynamically unstable and requires a blood transfusion. Prior to this episode he was well with no prior medical history. What is the most likely cause?

Necrotising enterocolitis
Anal fissure
Oesophageal varices
Meckels diverticulum
Crohns disease

Meckels diverticulum is the number one cause of painless massive GI bleeding requiring a transfusion in children between the ages of 1 and 2 years.

Meckel's diverticulum
Congenital abnormality resulting in incomplete obliteration of the vitello-intestinal duct
Normally, in the foetus, there is an attachment between the vitello-intestinal duct and the yolk sac.This disappears at 6 weeks gestation.
The tip is free in majority of cases.
Associated with enterocystomas, umbilical sinuses, and omphaloileal fistulas.
Arterial supply: omphalomesenteric artery.
2% of population, 2 inches long, 2 feet from the ileocaecal valve.
Typically lined by ileal mucosa but ectopic gastric mucosa can occur, with the risk of peptic ulceration. Pancreatic and jejunal mucosa can also occur.

Clinical
Normally asymptomatic and an incidental finding.
Complications are the result of obstruction, ectopic tissue, or inflammation.
Removal if narrow neck or symptomatic. Options are between wedge excision or formal small bowel resection and anastomosis.

20

Which of the following statements relating to sebaceous cysts is false?

When infected are also known as Cocks peculiar tumour
Typically contain pus
Are usually associated with a central punctum
Most commonly occur on the scalp
They will typically have a cyst wall


Sebaceous cysts usually contain sebum, pus is only present in infected sebaceous cysts which should then be treated by surgical incision and drainage.

Sebaceous cysts
Originate from sebaceous glands and contain sebum.
Location: anywhere but most common scalp, ears, back, face, and upper arm (not palms of the hands and soles of the feet).
They will typically contain a punctum.
Excision of the cyst wall needs to be complete to prevent recurrence.
A Cock's 'Peculiar' Tumour is a suppurating and ulcerated sebaceous cyst. It may resemble a squamous cell carcinoma- hence its name.

21

A 42 year old lady who has systemic lupus erythematosus presents to the clinic with a 5 day history of a painful purple lesion on her index finger. On examination she has a tender red lesion on the index finger.

A. Malignant fibrous histiocytoma
B. Oslers nodes
C. Heberdens nodes
D. Bouchards nodes
E. Carpal tunnel syndrome
F. Complex regional pain syndrome
G. Osteoclastoma
H. Osteosarcoma
I. Ganglion

Oslers nodes

Osler nodes are normally described as tender, purple/red raised lesions with a pale centre. These lesions occur as a result of immune complex deposition. These occur most often in association with endocarditis. However, other causes include SLE, gonorrhoea, typhoid and haemolytic anaemia.

Dupuytrens contracture
Fixed flexion contracture of the hand where the fingers bend towards the palm and cannot be fully extended.
Caused by underlying contractures of the palmar aponeurosis . The ring finger and little finger are the fingers most commonly affected. The middle finger may be affected in advanced cases, but the index finger and the thumb are nearly always spared.
Progresses slowly and is usually painless. In patients with this condition, the tissues under the skin on the palm of the hand thicken and shorten so that the tendons connected to the fingers cannot move freely. The palmar aponeurosis becomes hyperplastic and undergoes contracture.
Commonest in males over 40 years of age.
Association with liver cirrhosis and alcoholism. However, many cases are idiopathic.
Treatment is surgical and involves fasciectomy. However, the condition may recur and many surgical therapies are associated with risk of neurovascular damage to the digital nerves and arteries.

Carpel tunnel syndrome
Idiopathic median neuropathy at the carpal tunnel.
Characterised by altered sensation of the lateral 3 fingers.
The condition is commoner in females and is associated with other connective tissue disorders such as rheumatoid disease. It may also occur following trauma to the distal radius.
Symptoms occur mainly at night in early stages of the condition.
Examination may demonstrate wasting of the muscles of the thenar eminence and symptoms may be reproduced by Tinels test (compression of the contents of the carpal tunnel).
Formal diagnosis is usually made by electrophysiological studies.
Treatment is by surgical decompression of the carpal tunnel, a procedure achieved by division of the flexor retinaculum. Non - surgical options include splinting and bracing.

Osler's nodes Osler's nodes are painful, red, raised lesions found on the hands and feet. They are the result of the deposition of immune complexes.

Bouchards nodes Hard, bony outgrowths or gelatinous cysts on the proximal interphalangeal joints (the middle joints of fingers or toes.) They are a sign of osteoarthritis, and are caused by formation of calcific spurs of the articular cartilage.

Heberdens nodes Typically develop in middle age, beginning either with a chronic swelling of the affected joints or the sudden painful onset of redness, numbness, and loss of manual dexterity. This initial inflammation and pain eventually subsides, and the patient is left with a permanent bony outgrowth that often skews the fingertip sideways. It typically affects the DIP joint.

Ganglion Swelling in association with a tendon sheath commonly near a joint. They are common lesions in the wrist and hand. Usually they are asymptomatic and cause little in the way of functional compromise. They are fluid filled although the fluid is similar to synovial fluid it is slightly more viscous. When the cysts are troublesome they may be excised.

22

A 62 year old lady presents with an non tender lump overlying the distal interphalangeal joint of the index finger. On examination she has a hard, non tender lump overlying the joint and deviation of the tip of the finger.

A. Malignant fibrous histiocytoma
B. Oslers nodes
C. Heberdens nodes
D. Bouchards nodes
E. Carpal tunnel syndrome
F. Complex regional pain syndrome
G. Osteoclastoma
H. Osteosarcoma
I. Ganglion

Heberdens nodes

Heberdens nodes may produce swelling of the distal interphalangeal joint with deviation of the finger tip.

Dupuytrens contracture
Fixed flexion contracture of the hand where the fingers bend towards the palm and cannot be fully extended.
Caused by underlying contractures of the palmar aponeurosis . The ring finger and little finger are the fingers most commonly affected. The middle finger may be affected in advanced cases, but the index finger and the thumb are nearly always spared.
Progresses slowly and is usually painless. In patients with this condition, the tissues under the skin on the palm of the hand thicken and shorten so that the tendons connected to the fingers cannot move freely. The palmar aponeurosis becomes hyperplastic and undergoes contracture.
Commonest in males over 40 years of age.
Association with liver cirrhosis and alcoholism. However, many cases are idiopathic.
Treatment is surgical and involves fasciectomy. However, the condition may recur and many surgical therapies are associated with risk of neurovascular damage to the digital nerves and arteries.

Carpel tunnel syndrome
Idiopathic median neuropathy at the carpal tunnel.
Characterised by altered sensation of the lateral 3 fingers.
The condition is commoner in females and is associated with other connective tissue disorders such as rheumatoid disease. It may also occur following trauma to the distal radius.
Symptoms occur mainly at night in early stages of the condition.
Examination may demonstrate wasting of the muscles of the thenar eminence and symptoms may be reproduced by Tinels test (compression of the contents of the carpal tunnel).
Formal diagnosis is usually made by electrophysiological studies.
Treatment is by surgical decompression of the carpal tunnel, a procedure achieved by division of the flexor retinaculum. Non - surgical options include splinting and bracing.

Osler's nodes Osler's nodes are painful, red, raised lesions found on the hands and feet. They are the result of the deposition of immune complexes.

Bouchards nodes Hard, bony outgrowths or gelatinous cysts on the proximal interphalangeal joints (the middle joints of fingers or toes.) They are a sign of osteoarthritis, and are caused by formation of calcific spurs of the articular cartilage.

Heberdens nodes Typically develop in middle age, beginning either with a chronic swelling of the affected joints or the sudden painful onset of redness, numbness, and loss of manual dexterity. This initial inflammation and pain eventually subsides, and the patient is left with a permanent bony outgrowth that often skews the fingertip sideways. It typically affects the DIP joint.

Ganglion Swelling in association with a tendon sheath commonly near a joint. They are common lesions in the wrist and hand. Usually they are asymptomatic and cause little in the way of functional compromise. They are fluid filled although the fluid is similar to synovial fluid it is slightly more viscous. When the cysts are troublesome they may be excised.

23

A 17 year old boy is brought to the clinic by his mother who is concerned about a lesion that has developed on the dorsal surface of his left hand. On examination he has a soft fluctuant swelling on the dorsal aspect of the hand, it is most obvious on making a fist.

A. Malignant fibrous histiocytoma
B. Oslers nodes
C. Heberdens nodes
D. Bouchards nodes
E. Carpal tunnel syndrome
F. Complex regional pain syndrome
G. Osteoclastoma
H. Osteosarcoma
I. Ganglion

Ganglion

Ganglions commonly occur in the hand and are usually associated with tendons. They are typically soft and fluctuant. They do not require removal unless they are atypical or causing symptoms.

Dupuytrens contracture
Fixed flexion contracture of the hand where the fingers bend towards the palm and cannot be fully extended.
Caused by underlying contractures of the palmar aponeurosis . The ring finger and little finger are the fingers most commonly affected. The middle finger may be affected in advanced cases, but the index finger and the thumb are nearly always spared.
Progresses slowly and is usually painless. In patients with this condition, the tissues under the skin on the palm of the hand thicken and shorten so that the tendons connected to the fingers cannot move freely. The palmar aponeurosis becomes hyperplastic and undergoes contracture.
Commonest in males over 40 years of age.
Association with liver cirrhosis and alcoholism. However, many cases are idiopathic.
Treatment is surgical and involves fasciectomy. However, the condition may recur and many surgical therapies are associated with risk of neurovascular damage to the digital nerves and arteries.

Carpel tunnel syndrome
Idiopathic median neuropathy at the carpal tunnel.
Characterised by altered sensation of the lateral 3 fingers.
The condition is commoner in females and is associated with other connective tissue disorders such as rheumatoid disease. It may also occur following trauma to the distal radius.
Symptoms occur mainly at night in early stages of the condition.
Examination may demonstrate wasting of the muscles of the thenar eminence and symptoms may be reproduced by Tinels test (compression of the contents of the carpal tunnel).
Formal diagnosis is usually made by electrophysiological studies.
Treatment is by surgical decompression of the carpal tunnel, a procedure achieved by division of the flexor retinaculum. Non - surgical options include splinting and bracing.

Osler's nodes Osler's nodes are painful, red, raised lesions found on the hands and feet. They are the result of the deposition of immune complexes.

Bouchards nodes Hard, bony outgrowths or gelatinous cysts on the proximal interphalangeal joints (the middle joints of fingers or toes.) They are a sign of osteoarthritis, and are caused by formation of calcific spurs of the articular cartilage.

Heberdens nodes Typically develop in middle age, beginning either with a chronic swelling of the affected joints or the sudden painful onset of redness, numbness, and loss of manual dexterity. This initial inflammation and pain eventually subsides, and the patient is left with a permanent bony outgrowth that often skews the fingertip sideways. It typically affects the DIP joint.

Ganglion Swelling in association with a tendon sheath commonly near a joint. They are common lesions in the wrist and hand. Usually they are asymptomatic and cause little in the way of functional compromise. They are fluid filled although the fluid is similar to synovial fluid it is slightly more viscous. When the cysts are troublesome they may be excised.

24

Which of the following statements relating to Keloid scars is untrue?

They have a predilection for sternal , mandibular and deltiod area wounds
They are confined to the margins of the original injury
They often recur following excision
May occur even after superficial injury
They may be treated by injection of triamcinolone

Hypertrophic scars remain confined to the wound edges.

Keloids (by definition) will tend to extend beyond the margins of the wound and in wounds of any depth.

Wound healing
Surgical wounds are either incisional or excisional and either clean, clean contaminated or dirty. Although the stages of wound healing are broadly similar their contributions will vary according to the wound type.

The main stages of wound healing include:

Haemostasis
Minutes to hours following injury
Vasospasm in adjacent vessels, platelet plug formation and generation of fibrin rich clot.

Inflammation
Typically days 1-5
Neutrophils migrate into wound (function impaired in diabetes).
Growth factors released, including basic fibroblast growth factor and vascular endothelial growth factor.
Fibroblasts replicate within the adjacent matrix and migrate into wound.
Macrophages and fibroblasts couple matrix regeneration and clot substitution.

Regeneration
Typically days 7 to 56
Platelet derived growth factor and transformation growth factors stimulate fibroblasts and epithelial cells.
Fibroblasts produce a collagen network.
Angiogenesis occurs and wound resembles granulation tissue.

Remodeling
From 6 weeks to 1 year
Longest phase of the healing process and may last up to one year (or longer).
During this phase fibroblasts become differentiated (myofibroblasts) and these facilitate wound contraction.
Collagen fibres are remodeled.
Microvessels regress leaving a pale scar.

The above description represents an idealised scenario. A number of diseases may distort this process. Neovascularisation is an important early process. Endothelial cells may proliferate in the wound bed and recanalise to form a vessel. Vascular disease, shock and sepsis can all compromise microvascular flow and impair healing.

Conditions such as jaundice will impair fibroblast synthetic function and immunity with a detrimental effect in most parts of the healing process.

Problems with scars:

Hypertrophic scars
Excessive amounts of collagen within a scar. Nodules may be present histologically containing randomly arranged fibrils within and parallel fibres on the surface. The tissue itself is confined to the extent of the wound itself and is usually the result of a full thickness dermal injury. They may go on to develop contractures.

Keloid scars
Excessive amounts of collagen within a scar. Typically a keloid scar will pass beyond the boundaries of the original injury. They do not contain nodules and may occur following even trivial injury. They do not regress over time and may recur following removal.

Drugs which impair wound healing:
Non steroidal anti inflammatory drugs
Steroids
Immunosupressive agents
Anti neoplastic drugs

Closure
Delayed primary closure is the anatomically precise closure that is delayed for a few days but before granulation tissue becomes macroscopically evident.

Secondary closure refers to either spontaneous closure or to surgical closure after granulation tissue has formed.

25

What is the investigation of choice to look for renal scarring in a child with vesicoureteric reflux?

Abdominal x-ray
Ultrasound
DMSA
CT KUB
Micturating cystourethrogram

DMSA

Vesicoureteric reflux (VUR) is the abnormal backflow of urine from the bladder into the ureter and kidney. It is relatively common abnormality of the urinary tract in children and predisposes to urinary tract infection (UTI), being found in around 30% of children who present with a UTI. As around 35% of children develop renal scarring it is important to investigate for VUR in children following a UTI

Pathophysiology of VUR
ureters are displaced laterally, entering the bladder in a more perpendicular fashion than at an angle
therefore shortened intramural course of ureter
vesicoureteric junction cannot therefore function adequately

The table below summarises the grading of VUR

{Grade}
I Reflux into the ureter only, no dilatation
II Reflux into the renal pelvis on micturition, no dilatation
III Mild/moderate dilatation of the ureter, renal pelvis and calyces
IV Dilation of the renal pelvis and calyces with moderate ureteral tortuosity
V Gross dilatation of the ureter, pelvis and calyces with ureteral tortuosity

Investigation
VUR is normally diagnosed following a micturating cystourethrogram
a DMSA scan may also be performed to look for renal scarring

26

A 24-year-old female is referred to the acute surgical team as she is noted to have an absent left radial pulse. Apart from some dizziness and lethargy, the patient does not have any features suggestive of an acute ischaemic limb. Blood tests are as follows:

Na+ 136 mmol/l
K+ 4.1 mmol/l
Urea 2.3 mmol/l
Creatinine 77 µmol/l

ESR 66 mm/hr

What is the most likely diagnosis?

Turner's syndrome
Takayasu's arteritis
Kawasaki disease
Coarctation of the aorta
Breast carcinoma with local spread

Takayasu's arteritis

Inflammatory, obliterative arteritis affecting aorta and branches
Females> Males
Symptoms may include upper limb claudication
Clinical findings include diminished or absent pulses
ESR often affected during the acute phase

Takayasu's arteritis is a large vessel vasculitis. It typically causes occlusion of the aorta and questions commonly refer to an absent limb pulse. It is more common in females and Asian people

Associations
renal artery stenosis

Management
steroids

27

A 28 year old man is playing tennis when he suddenly collapses and has a GCS of 4 when examined.

A. Acute sub dural haematoma
B. Chronic sub dural haematoma
C. Acute extradural haematoma
D. Chronic extradural haematoma
E. Intraventricular haemorrhage
F. Sub arachnoid haemorrhage

Sub arachnoid haemorrhage

A sudden collapse and loss of consciousness is most likely to be due to a sub arachnoid haemorrhage. The other potential causes in the list usually occur as a sequel to a traumatic event, which has not occurred here.

Extradural haematoma Bleeding into the space between the dura mater and the skull. Often results from acceleration-deceleration trauma or a blow to the side of the head. The majority of extradural haematomas occur in the temporal region where skull fractures cause a rupture of the middle meningeal artery.

Features
Raised intracranial pressure
Some patients may exhibit a lucid interval
Subdural haematoma Bleeding into the outermost meningeal layer. Most commonly occur around the frontal and parietal lobes. May be either acute or chronic.

Risk factors include old age and alcoholism.

Slower onset of symptoms than a extradural haematoma.
Intracerebral haematoma Usually hyperdense lesions on CT scanning. Arise in areas of traumatic contusion with fuse to become a haematoma. Areas of clot and fresh blood may co-exist on the same CT scan (Swirl sign). Large haematomas and those associated with mass effect should be evacuated.
Subarachnoid haemorrhage Usually occurs spontaneously in the context of a ruptured cerebral aneurysm but may be seen in association with other injuries when a patient has sustained a traumatic brain injury
Intraventricular haemorrhage Haemorrhage that occurs into the ventricular system of the brain. It is relatively rare in adult surgical practice and when it does occur, it is typically associated with severe head injuries. In premature neonates it may occur spontaneously. The blood may clot and occlude CSF flow, hydrocephalus may result.
In neonatal practice the vast majority of IVH occur in the first 72 hours after birth, the aetiology is not well understood and it is suggested to occur as a result of birth trauma combined with cellular hypoxia, together with the delicate neonatal CNS.

28

A 2 day old premature neonate is born by emergency cesarean section for maternal illness. The baby is noted to become floppy and unresponsive.

A. Acute sub dural haematoma
B. Chronic sub dural haematoma
C. Acute extradural haematoma
D. Chronic extradural haematoma
E. Intraventricular haemorrhage
F. Sub arachnoid haemorrhage

Intraventricular haemorrhage

Neonatal deterioration in premature babies is not infrequently due to intra ventricular haemorrhage. In extreme prematurity the prognosis can be very poor.

Extradural haematoma Bleeding into the space between the dura mater and the skull. Often results from acceleration-deceleration trauma or a blow to the side of the head. The majority of extradural haematomas occur in the temporal region where skull fractures cause a rupture of the middle meningeal artery.

Features
Raised intracranial pressure
Some patients may exhibit a lucid interval
Subdural haematoma Bleeding into the outermost meningeal layer. Most commonly occur around the frontal and parietal lobes. May be either acute or chronic.

Risk factors include old age and alcoholism.

Slower onset of symptoms than a extradural haematoma.
Intracerebral haematoma Usually hyperdense lesions on CT scanning. Arise in areas of traumatic contusion with fuse to become a haematoma. Areas of clot and fresh blood may co-exist on the same CT scan (Swirl sign). Large haematomas and those associated with mass effect should be evacuated.
Subarachnoid haemorrhage Usually occurs spontaneously in the context of a ruptured cerebral aneurysm but may be seen in association with other injuries when a patient has sustained a traumatic brain injury
Intraventricular haemorrhage Haemorrhage that occurs into the ventricular system of the brain. It is relatively rare in adult surgical practice and when it does occur, it is typically associated with severe head injuries. In premature neonates it may occur spontaneously. The blood may clot and occlude CSF flow, hydrocephalus may result.
In neonatal practice the vast majority of IVH occur in the first 72 hours after birth, the aetiology is not well understood and it is suggested to occur as a result of birth trauma combined with cellular hypoxia, together with the delicate neonatal CNS.

29

A 78 year old man is brought to the emergency department by the police. He is found wandering around the town centre and is confused. His family report that he is usually well apart from a simple mechanical fall 3 weeks previously from which he sustained no obvious injuries.

A. Acute sub dural haematoma
B. Chronic sub dural haematoma
C. Acute extradural haematoma
D. Chronic extradural haematoma
E. Intraventricular haemorrhage
F. Sub arachnoid haemorrhage

Chronic sub dural haematoma

The injuries that are responsible for chronic sub dural haematomas are usually fairly trivial and forgotten by the patient and their families. The onset of symptoms can be insidious with vague symptomatology and confusion predominating.

Extradural haematoma Bleeding into the space between the dura mater and the skull. Often results from acceleration-deceleration trauma or a blow to the side of the head. The majority of extradural haematomas occur in the temporal region where skull fractures cause a rupture of the middle meningeal artery.

Features
Raised intracranial pressure
Some patients may exhibit a lucid interval
Subdural haematoma Bleeding into the outermost meningeal layer. Most commonly occur around the frontal and parietal lobes. May be either acute or chronic.

Risk factors include old age and alcoholism.

Slower onset of symptoms than a extradural haematoma.
Intracerebral haematoma Usually hyperdense lesions on CT scanning. Arise in areas of traumatic contusion with fuse to become a haematoma. Areas of clot and fresh blood may co-exist on the same CT scan (Swirl sign). Large haematomas and those associated with mass effect should be evacuated.
Subarachnoid haemorrhage Usually occurs spontaneously in the context of a ruptured cerebral aneurysm but may be seen in association with other injuries when a patient has sustained a traumatic brain injury
Intraventricular haemorrhage Haemorrhage that occurs into the ventricular system of the brain. It is relatively rare in adult surgical practice and when it does occur, it is typically associated with severe head injuries. In premature neonates it may occur spontaneously. The blood may clot and occlude CSF flow, hydrocephalus may result.
In neonatal practice the vast majority of IVH occur in the first 72 hours after birth, the aetiology is not well understood and it is suggested to occur as a result of birth trauma combined with cellular hypoxia, together with the delicate neonatal CNS.

30

Which of the following statements relating to necrotising enterocolitis is false?

It has a mortality of 30%
Most frequently presents in premature neonates less than 32 weeks gestation.
Should be managed by early laparotomy and segmental resections in most cases.
Pneumostosis intestinalis may be visible on plain abdominal x-ray.
May be minimised by use of breast milk over formula feeds.

Most cases will settle with conservative management with NG decompression and appropriate support. Laparotomy should be undertaken in patients who progress despite conservative management or in whom compelling indications for surgery exist (eg free air).

Pyloric stenosis
M>F
5-10% Family history in parents
Projectile non bile stained vomiting at 4-6 weeks of life
Diagnosis is made by test feed or USS
Treatment: Ramstedt pyloromyotomy (open or laparoscopic)

Acute appendicitis
Uncommon under 3 years
When occurs may present atypically

Mesenteric adenitis
Central abdominal pain and URTI
Conservative management

Intussusception
Telescoping bowel
Proximal to or at the level of, ileocaecal valve
6-9 months age
Colicky pain, diarrhoea and vomiting, sausage shaped mass, red jelly stool.
Treatment: reduction with air insufflation

Malrotation
High caecum at the midline
Feature in exomphalos, congenital diaphragmatic hernia, intrinsic duodenal atresia
May be complicated by development of volvulus, infant with volvulus may have bile stained vomiting
Diagnosis is made by upper GI contrast study and USS
Treatment is by laparotomy, if volvulus is present (or at high risk of occurring then a ladds procedure is performed

Hirschsprung's disease
Absence of ganglion cells from myenteric and submucosal plexuses
Occurs in 1/5000 births
Full thickness rectal biopsy for diagnosis
Delayed passage of meconium and abdominal distension
Treatment is with rectal washouts initially, thereafter an anorectal pull through procedure

Oesophageal atresia
Associated with tracheo-oesophageal fistula and polyhydramnios
May present with choking and cyanotic spells following aspiration
VACTERL associations

Meconium ileus
Usually delayed passage of meconium and abdominal distension
Majority have cystic fibrosis
X-Rays may not show a fluid level as the meconium is viscid (depends upon feeding), PR contrast studies may dislodge meconium plugs and be therapeutic
Infants who do not respond to PR contrast and NG N-acetyl cysteine will require surgery to remove the plugs

Biliary atresia
Jaundice > 14 days
Increased conjugated bilirubin
Urgent Kasai procedure

Necrotising enterocolitis
Prematurity is the main risk factor
Early features include abdominal distension and passage of bloody stools
X-Rays may show pneumatosis intestinalis and evidence of free air
Increased risk when empirical antibiotics are given to infants beyond 5 days
Treatment is with total gut rest and TPN, babies with perforations will require laparotomy