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Chapter25: The Child with an Abdominal Mass 157
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tumour spillage. However, this approach carries the
potential risk of treating a child with an inappropriate
chemotherapy regimen for a non-Wilms renal tumour.
Treatment
As introduced earlier, the timing of Wilms tumour surgery relative to biopsy and/or chemotherapy remains
controversial. This notwithstanding, tumour nephrectomy is an integral component of successful Wilms
tumour management. This is typically undertaken by an
open and transabdominal approach, but select indications for laparoscopic Wilms tumour surgery are being
recognised. Bilateral Wilms tumour presents particular
challenges, and in this uncommon setting, renal-sparing
surgery may need consideration.
Chemotherapy regimens vary from 18 to 34 weeks,
depending upon the tumour stage and the international
protocols, and may utilise two or three chemotherapeutic agents. Radiotherapy is used in patients with spilt
or residual tumour, as well as in metastatic disease.
Prognosis
Wilms tumours, in contrast to neuroblastoma, are associated with excellent rates of survival. Cure rates for
stage I are as high as 95%, and even in those with stage
V disease, the cure rates approach 75%. Late recurrence
is rare, but patients must be followed for the late effects
associated with both chemotherapy and radiotherapy,
including:
1 Cardiotoxicity – occurs in 5% of patients treated with
doxorubicin.
2 Musculoskeletal disorders – increased risk of scoliosis.
3 Reduced fertility – females may experience early pri-
mary ovarian failure, while males may have hypogo-
nadism and azoospermia.
4 Development of secondary tumours – typically associ-
ated with the field of radiation. Most common forms
of malignancy are leukaemia and lymphoma.
5 Renal failure – patients must be followed for up to 20
years to monitor the risk of renal failure in the remain-
ing kidney.
Liver tumours
Hepatoblastoma is the most common malignant tumour
presenting as a right upper quadrant mass in children
less than 1 year of age. Alternative diagnoses include an
haemangioendothelioma (the most common benign
vascular tumour of the liver in infancy, typically presenting before 6 months of age) and mesenchymal hamartoma (a benign tumour that almost exclusively occurs
in children under 2 years of age). The mass in an infant
with hepatoblastoma is typically large, but the infant
may also present with systemic features such as weight
loss, vomiting and anaemia. Elevation of the tumour
marker serum alpha-fetoprotein in a patient with a liver
mass strongly suggests hepatoblastoma.
Accurate preoperative imaging is necessary, including
ultrasonography, CT scan, MRI and angiography. The
staging of liver tumours is according to the Pretreatment
Extent of Disease (PRETEXT) system, which comprises
four levels based upon the degree of liver involvement.
Operative resection of the lesion, either locally or by
lobectomy, remains the main treatment for all primary
liver tumours, but preoperative chemotherapy significantly improves survival. There is almost no chance of
cure in hepatoblastoma patients without complete
resection. Liver transplantation is an option for those
patients whose tumour is limited to the liver but remains
unresectable after neo-adjuvant chemotherapy.
KEY POINTS
• A child with an abdominal mass needs immediate clinical
assessment and investigation to exclude malignancy.
• Abdominal masses in toddlers may be huge before diagnosis.
• Ultrasonography is an effective screening test for malignancy.
• A patient with a presumed abdominal tumour needs
immediate referral to the regional surgical and oncology
centre.
Further Reading
Davidoff AM (2012) Neuroblastoma. Semin Pediatr Surg 21:
2–14.
Hallett A, Traunecker H (2012) A review and update on neuro-
blastoma. Paediatr Child Health 22: 103–107.
Hamilton TE, Shamberger RC (2012) Wilms tumor: recent advances
in clinical care and biology. Semin Pediatr Surg 21: 15–20.
Meyers RL, Czauderna P, Otte J-B (2012) Surgical treatment of
hepatoblastoma. Pediatr Blood Cancer 59: 800–808.
Monclair T, Brodeur GM, Ambros PF et al. (2009) The International
Neuroblastoma Risk Group (INRG) staging system: an INRG
Task Force Report. J Clin Oncol 27: 298–303.
CHAPTER26
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Spleen, Pancreas and Biliary Tract
CASE 1
A 4-year-old girl presents with a distended epigastrium and
paralytic ileus. On physical examination, there are several old
fractures with callus formation.
Q 1.1 What are the principal causes of pancreatitis?
Q
1.2 How may pancreatitis be diagnosed?
1.3 What is a pancreatic pseudocyst?
Q
The spleen
Elective splenectomy, usually done laparoscopically, is indicated for a variety of conditions in childhood [Box26.1].
Overwhelming post-splenectomy infection
Overwhelming post-splenectomy Post-splenectomy
infection (OPSI) occurs in 1–5% of children following
splenectomy and is typically caused by encapsulated
organisms such as pneumococcus, meningococcus and
Haemophilus. The risk of OPSI is lifelong (though it more
commonly occurs in the first year post-splenectomy)
and has been associated with mortality rates in affected
patients ranging from 10 to 70%. OPSI is more common
when the spleen is removed for haematological conditions and when splenectomy is done in younger children. Preoperative immunisation against encapsulated
organisms is essential, while the role for post-operative
penicillin remains controversial.
Hereditary spherocytosis
Hereditary spherocytosis is an autosomal dominant
condition resulting in variable degrees of haemolytic
anaemia. In spherocytosis, the red cells are abnormally
CASE 2
A 3-week-old neonate develops gastroenteritis from her older
siblings. After resolution of diarrhoea, she is noted to be jaundiced.
Q
2.1 How would you determine whether obstructive jaundice
was present?
Q
2.2 What are the differences in management between a patient
with a bile duct stone and a patient with biliary atresia?
spherical and are destroyed within the spleen. This may
result in:
1 Chronic anaemia
2 Episodic haemolytic jaundice
3 Increased tendency to form pigment gallstones
These complications may be controlled by splenectomy.
However, unless complications are severe, splenectomy
is delayed until at least the age of 7 years of age to minimise the risk of OPSI. Cholecystectomy may be required
at the same time.
Idiopathic thrombocytopenic
purpura
Idiopathic thrombocytopenic purpura is an autoimmune condition of unknown aetiology that causes
destruction of platelets. It presents most commonly in
the acute form, which usually resolves spontaneously.
Administration of gamma globulin is sometimes required
in severe episodes to control the platelet count, and splenectomy is rarely indicated. A small percentage of children will develop a chronic form of the condition in
whom splenectomy may be required if medical therapy
is unsuccessful.
Jones’ Clinical Paediatric Surgery, Seventh Edition. Edited by John M. Hutson, Michael O’Brien, Spencer W. Beasley,
Warwick J. Teague and Sebastian K. King.
© 2015 John Wiley & Sons, Ltd. Published 2015 by John Wiley & Sons, Ltd.
158
Chapter26: Spleen, Pancreas and Biliary Tract 159
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Box 26.1 Indications for splenectomy in childhood
Hereditary spherocytosis
Idiopathic thrombocytopenic purpura
Thalassaemia
Sickle cell anaemia
Metabolic storage diseases
Hypersplenism
Neoplasms
Congenital and acquired cysts
Trauma
Thalassaemia
In thalassaemia major, a homozygous, autosomal recessive
condition, abnormal haemoglobin chains result inchronic
haemolytic anaemia. In the past, chronic anaemia, blood
transfusions and subsequent increasing iron stores have
resulted in the patient developing a secondary hypersplenism with a very large spleen. The enlarged spleen tended to
destroy all cellular elements in the blood.
Transfusions keep children healthy, while regular
parenteral desferrioxamine chelates excess iron liberated from haemolysed red cells and maintains normal
serum iron levels. In thalassaemia, splenectomy is indicated if the splenomegaly causes abdominal symptoms
or difficulties with respiration or if the secondary hypersplenism is difficult to control.
Sickle cell anaemia
In sickle cell disease, the abnormal haemoglobin S causes
abnormally shaped red cells during hypoxia. These sickle
cells tend to impede blood flow through small vessels,
causing ischaemia in the organ involved. Splenic infarcts
may occur. Splenectomy is usually contraindicated as
the resulting higher haemoglobin causes more sickling of
the red cells in other organs.
Trauma
Splenectomy for trauma is now exceptionally rare (see
Chapter38).
The pancreas
Acute pancreatitis
Acute pancreatitis in childhood is an uncommon clinical
entity. The known aetiologies in the paediatric age
group are extensive. Some of the more common causes
of pancreatitis in childhood are listed below [Box26.2].
Box 26.2 Common causes of pancreatitis in childhood
1 Trauma (handlebar injury, motor accident, child
abuse)
2 Drugs (steroids, azathioprine)
3
Viral
4 Biliary tract disorders (choledochal cyst, gallstones)
5 Hereditary
6 Metabolic (hyperlipidaemia)
Traumatic pancreatitis
The pancreas is the fourth most common abdominal
organ injured in childhood trauma. Nearly all cases
result from blunt abdominal trauma, as penetrating
trauma in Australasian children is rare. The most
common cause in most Western countries is a
handlebar injury, but child abuse may present this
way, secondary to a kick or punch to the abdomen.
The morbidity associated with blunt pancreatic trauma
is determined by whether there is disruption of the
pancreatic duct. The best initial investigation is a CT
scan: if this suggests disruption of the pancreatic duct,
then further investigations to confirm this may be
indicated. In this situation, a magnetic resonance
cholangiopancreatogram (MRCP) or endoscopic retrograde cholangiopancreatogram (ERCP) may be useful.
Most cases do not involve a duct injury and are
managed conservatively, while management of duct
disruption remains controversial. Some advocate conservative management, accepting the risk of a pseudocyst (see following text), while others advocate an
early distal pancreatectomy.
Pseudocyst
A pancreatic pseudocyst is a collection of pancreatic
fluid within a non-epithelial-lined cavity that forms at
least 6weeks after the initial pancreatic insult. Although
it may complicate pancreatitis from any cause, it is
most often the result of trauma. Most pancreatic pseudocysts lie in the lesser sac. Treatment is initially nonoperative, as many resolve spontaneously. The progress
of the collection is followed by serial ultrasound scans.
Intervention is indicated if the pseudocyst is enlarging
or causing symptoms. Internal drainage of the pseudocyst into the stomach via an endoscopic cystogastrostomy or open cystogastrostomy is the preferred
technique.
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Hyperinsulinism (causing hypoglycaemia)
Excessive production of insulin may occur in several
situations:
1 In babies of diabetic mothers as a temporary response
to high maternal sugar levels.
2 Beta-cell hyperplasia – an idiopathic condition in
which there is excessive production of insulin, which
usually resolves with drug treatment (diazoxide). Neartotal pancreatectomy is only necessary occasionally.
3 Beckwith–Wiedemann syndrome – a condition of
newborn babies that is characterised by exomphalos,
organomegaly (large tongue and abdominal organs),
hemihypertrophy and transient low blood sugar from
excessive insulin and insulin-like growth factor
production.
4 Islet cell tumours – rare cause of hypoglycaemia.
They may be cured if the tumour (usually benign) is
localised and excised.
The biliary tract
Neonatal jaundice
Jaundice in the neonatal period most commonly results
from a prehepatic or hepatic cause. Posthepatic causes of
jaundice result in conjugated hyperbilirubinaemia and
may require surgical treatment. These causes include:
1 Biliary atresia (represents 80% of cases)
2 Choledochal cyst
3 Inspissated bile syndrome
4 Bile duct stricture
5 Spontaneous biliary perforation
All cases of conjugated hyperbilirubinaemia in the neonatal period should be promptly investigated.
Biliary atresia
Biliary atresia is a condition of progressive obliteration
of the extrahepatic ducts as a result of an, as yet, undiagnosed inflammatory condition. This process may
involve part of or the entire extrahepatic biliary tree.
The ducts may shrivel and disappear or, more commonly, persist as a fibrous cord.
The incidence of biliary atresia is about 1 per 15,000
live births. The aetiology remains unknown, although
there is a wide range of hypotheses based on infective,
embryological, metabolic and vascular studies. In up to
20% of cases, biliary atresia is associated with a distinct
syndrome known as the biliary atresia splenic malformation syndrome (BASM). Associated anomalies in
thissyndrome include splenic abnormalities (asplenia or
polysplenia), situs inversus, intestinal malrotation,
cardiac anomalies and a preduodenal portal vein.
Biliary atresia presents as prolonged jaundice after
transient neonatal physiological jaundice should have
resolved. Progressive obstructive jaundice occurs in the
first 6 weeks of life with pale stools and dark urine.
Typically, these infants are thriving at the time of
presentation.
Diagnosis
Prompt diagnosis is essential in biliary atresia as the
long-term results of surgery are correlated with the timing of operation. Ultrasonography is the most important
initial investigation and will exclude other surgical
causes of jaundice (see preceding text). In biliary atresia,
a fasting ultrasound scan will usually show a small and
contracted gall bladder. A presumptive diagnosis is best
made by liver biopsy (typically percutaneous), which in
experienced hands will yield a positive diagnosis in up
to 95% of cases. The definitive diagnosis is made at laparotomy by confirming non-patency of the extrahepatic
biliary tree. HIDA scans are of limited value as their
interpretation in neonates is difficult.
Treatment
Biliary atresia is treated by portoenterostomy (Kasai
procedure). This operation involves dissecting out the
obliterated extrahepatic ducts up to the portal plate and
shaving off the inflammatory tissue at the portal plate
flush with the liver surface. A Roux-en-Y loop of the
jejunum is then anastomosed to the edges of the portal
plate. The operation relies on bile draining into the Roux
loop from microscopic bile ductules in the portal plate.
Drainage rates of up to 60% may be achieved in experienced centres. There is a dramatic decrease in drainage
rates if the operation is performed after 100 days of life. It
is not possible to determine at the time of operation
whether the operation will be successful in the long term.
Liver transplantation is required if the operation fails.
Choledochal cysts
Choledochal cyst is a congenital dilatation of the extrahepatic biliary tree. There are various forms, but in the
most common variant, there is dilatation of the gall
bladder, cystic duct, common hepatic duct and common
Chapter26: Spleen, Pancreas and Biliary Tract 161
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unite outside the duodenal wall and the ampulla of Vater
in the third part of the duodenum and the resultant
abnormal common channel is not surrounded by the
normal sphincter mechanism. This situation encourages
reflux of pancreatic juice into the common bile duct,
which is thought to result in progressive damage of the
biliary tree.
The most common presenting features of a choledochal cyst are obstructive jaundice and recurrent
abdominal pain. Pancreatitis is not uncommonly the
presenting complaint. Rarely, a choledochal cyst may
present as an abdominal mass. The majority of choledochal cysts present before the age of 10 years and
increasingly are being detected antenatally. Antenatal
diagnosis may be made as early as 15 weeks’ gestation.
In some situations, differentiation from other congenital
cysts in the upper abdomen such as duplication cysts,
(a)
ovarian cyst and the rare cystic form of biliary atresia
may be difficult.
Diagnosis
The diagnosis is easily made on ultrasonography. More
detailed information of the nature of the dilatation is
now obtained using an MRCP.
(b)
Figure 26.1 Contrast x-ray (a) and ultrasonography (b) of the
biliary tract showing the massive tubular dilatation of a
choledochal cyst.
bile duct. The dilatation is usually cystic, but fusiform
variants are well described [Fig.26.1].
The incidence in Western countries is between 1 in
10,000 and 1 in 15,000 live births, but a higher frequency is seen in Asia. The cause remains unclear, but in
China and Japan, most patients with a choledochal cyst
have an anomalous junction between the terminal
common bile duct and the pancreatic duct. The ducts
Treatment
Treatment is excision of the cyst and drainage of the
proximal common hepatic duct by a Roux-en-Y loop of
the jejunum. Choledochal cysts that have been diagnosed antenatally and remain asymptomatic are electively excised from 6 months of age.
Inspissated bile syndrome
Inspissated bile syndrome is a condition causing obstructive jaundice in neonates resulting from inspissation of
bile in the lower third of the common bile duct. This
condition most commonly occurs in premature neonates requiring prolonged total parenteral nutrition
(TPN). It is also associated with extravascular haemolysis and may occur in otherwise normal neonates after
gastroenteritis and dehydration.
The diagnosis is made on ultrasonography, which
reveals a dilated proximal biliary tree in association with
biliary sludge or stones.
Most cases resolve spontaneously. Resistant cases may
be cleared by percutaneous transhepatic irrigation of the
bile ducts or retrograde irrigation by ERCP. Operative
intervention is only rarely required.
162 Part IV: Abdomen
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Bile duct strictures
Bile duct strictures are a rare but well-known cause of
obstructive jaundice in neonates. Most strictures are
idiopathic, and the most common site of obstruction is
the distal common bile duct. A small proportion occur
in association with a long common channel (see preceding text), where the presumed aetiology is reflux
of pancreatic juice into the common bile duct.
Diagnosis is made using percutaneous transhepatic
cholangiography or ERCP. The obstruction may be
relieved by balloon dilatation using the same modalities. If this is unsuccessful, then operative biliary
diversion is required.
Spontaneous biliary perforation
Spontaneous biliary perforation is a rare condition
resulting in progressive obstructive jaundice and ascites
in neonates. Most cases present between 1 week and 2
months of age. The site of the perforation is almost
always at the junction of the cystic and common hepatic
duct. The aetiology is unknown and the presentation is
usually insidious. Ascites results from a localised biliary
peritonitis, and the jaundice occurs as a result of both
proximal biliary obstruction secondary to oedema and
reabsorption of bile through the peritoneum. The diagnosis is made on ultrasonography, which demonstrates
a loculated collection in the portal region. Operative
intervention with drainage is required.
Cholelithiasis in children
In children, the cause of gallstone formation may be
divided into the following groups:
1 Haemolytic disorders. Conditions such as sickle cell
anaemia, thalassaemia and hereditary spherocytosis
cause pigment stones due to increased red cell
breakdown.
2 TPN. The association of TPN and biliary sludge and
cholelithiasis is well recognised. The exact cause is
unknown, but biliary stasis due to impairment of
the enterohepatic circulation of bile is probably
important.
3 Ileal resection. This is a well-known risk factor for cho-
lelithiasis. In children, the most common reason for
ileal resection is necrotising enterocolitis in premature neonates. The traditional explanation for gallstones in this setting is that normal reabsorption of
bile salts in the terminal ileum is impaired, leading to
depletion of bile salts in the enterohepatic circulation.
Box 26.3 Presentation of the child with gallstones
1 Biliary colic: pain from a stone in the neck of the gall
bladder or common bile duct
2 Cholecystitis: chemical or bacterial inflammation of the
gall bladder, usually associated with cystic duct obstruction
3
Obstructive jaundice: dark urine and pale stools due to
a stone obstructing the common bile duct
4 Pancreatitis
This promotes lithogenic bile. The neonates affected
by necrotising enterocolitis will have also required a
period of TPN during their recovery.
4 Mechanical causes. Any condition that leads to biliary
stasis is associated with the formation of gallstones,
such as bile duct strictures, choledochal cysts and
congenital gall bladder abnormalities.
5 Specific conditions. Certain conditions such as cystic
fibrosis, Crohn disease and diabetes are associated
with an increased incidence of cholelithiasis.
6 Adult causes. Adolescents with typical adult-type risk
factors, including obesity, oral contraceptive pill and
family history, have the same tendency to develop
gallstones.
The ways in which a child with gallstones may present
are summarised in Box26.3.
Treatment
Treatment involves laparoscopic cholecystectomy with
removal of stones in the common bile duct, if present.
KEY POINTS
• Splenectomy is avoided in small children because of the risk
of overwhelming post-splenectomy infection (1–5%).
• Ruptured spleen rarely requires a splenectomy, as bleeding
stops.
• Pancreatitis may occur with trauma.
• Prolonged jaundice in neonates needs investigation to
exclude biliary atresia.
• Gallstones are increasingly common in children.
Further reading
Adzick NS (2012) The pancreas. In: Coran AG, Adzick NS,
Krummel TM, Laberge T-M, Shamberger RC, Caldamone
AA (eds) Pediatric Surgery, 7th Edn. Elsevier Saunders,
Philadelphia, pp. 1371–1384.
Chapter26: Spleen, Pancreas and Biliary Tract 163
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Barsness KA, Reynolds M (2012) The spleen. In: Coran AG,
Adzick NS, Krummel TM, Laberge T-M, Shamberger RC,
Caldamone AA (eds) Pediatric Surgery, 7th Edn. Elsevier
Saunders, Philadelphia, pp. 1385–1394.
Cowles RA (2012) The jaundiced infant: biliary atresia. In: Coran
AG, Adzick NS, Krummel TM, Laberge T-M, Shamberger RC,
Caldamone AA (eds) Pediatric Surgery, 7th Edn. Elsevier
Saunders, Philadelphia, pp. 1321–1330.
Davenport M, Betalli P, D’Antiga L, Cheeseman P, Mieli-Vergani
G, Howard ER (2003) The spectrum of surgical jaundice in
infancy. J Pediatr Surg 38: 1471–1479.
Di Sabatino A, Carsetti R, Corazza GR (2011) Post-splenectomy
and hyposplenic states. Lancet 378: 86–97.
Gonzales KD, Lee H (2012) Choledochal cyst. In: Coran AG,
Adzick NS, Krummel TM, Laberge T-M, Shamberger RC,
Caldamone AA (eds) Pediatric Surgery, 7th Edn. Elsevier
Saunders, Philadelphia, pp. 1331–1340.
Holcomb GW III, Andrews WS (2012) Gallbladder disease and
hepatic infections. In: Coran AG, Adzick NS, Krummel TM,
Laberge T-M, Shamberger RC, Caldamone AA (eds) Pediatric
7th Edn. Elsevier Saunders, Philadelphia, pp. 1341–1354.
Morgan TL, Tomich EB (2012) Overwhelming post-splenectomy
infection (OPSI): a case report and review of the literature.
JEmerg Med 43(4): 758–763.
Srinath AI, Lowe ME (2013) Pediatric pancreatitis. Pediatr Rev
34: 79–90.
Sur gery,
CHAPTER27
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Anus, Perineum and Female Genitalia
CASE 1
A 3-month-old boy presents with a tender, red, indurated area
× 2 cm) adjacent to the anal verge. Twice in recent weeks, antibiotics
(2
were prescribed for a similar problem that resolved. On palpation and
compression of the mass, a drop of pus appears at the anus.
Q 1.1 What is the diagnosis, and how would it best be managed?
Anorectal problems occur commonly in children, with
abscesses, fistulae and fissures affecting infants, while
pilonidal disease, haemorrhoids and polyps tend to
affect older children.
Anal fissures
These are confined mostly to infants and toddlers in
whom the passage of a hard stool splits the anal mucosa.
There is a sharp pain on defecation and a few drops of
bright blood on the surface of the stool (see Chapter23).
Anal fissures are superficial and may heal so rapidly
that the fissure is already healed by the time it is brought
to medical attention and examined. If not healed, it is
usually visible anteriorly or posteriorly. A chronic fissure may be associated with a sentinel skin tag. Multiple
fissures and those that are not in the midline may be
due to other pathological processes such as inflammatory
bowel disease, infection or trauma.
Treatment
An acute anal fissure is of no consequence in itself, and
treatment is directed to the underlying constipation (see
Chapter22), which is commonly associated with food
allergy. Cow milk protein is usually the trigger food.
Chronic and/or prominently symptomatic anal fissures
may warrant specific treatment, with both operative and
CASE 2
A worried mother rushes her 8-month-old daughter to the emergency
department after noticing that no vaginal opening is visible. She is
frightened something serious is wrong with the child’s genitalia.
Q 2.1 What is the diagnosis?
2.2 How is it treated and recurrence prevented?
Q
non-operative options available. Many of these therapies
target relief of the internal sphincter spasm commonly
associated with anal fissures. This spasm is thought to
result in a degree of local ischaemia and contribute to
the accompanying anal pain.
Historically (and more so in adults), various surgical
strategies have been proposed to treat chronic anal
fissures. These range from simple anal dilatation to
open or closed internal sphincterotomy and even skin
flap coverage of the fissure. Operative management
achieves cure in 90% but at the expense of incontinence (usually to flatus) in 10%. Interestingly, anal
stretch has higher reported rates of incontinence than
limited lateral sphincterotomy and so should be used
cautiously in children.
The risk of postoperative incontinence drove development of non-operative therapies, particularly topical
agents to provide anal analgesia and/or internal sphincter
relaxation. A wide variety of agents have been investigated
including lignocaine, hydrocortisone, calcium channel
blockers such as nifedipine, nitroglycerin ointment (GTN),
and more recently botulinum toxin (Botox). Trials
show GTN, nifedipine and Botox to be only marginally
betterthan placebo, with chronic fissure healing in 55%
versus 35% for placebo. Unfortunately, topical GTN causes
headaches in up to 40% of patients, which may be severe
enough to lead to treatment cessation. Late recurrence following medical therapy occurs in 50% of patients.
Jones’ Clinical Paediatric Surgery, Seventh Edition. Edited by John M. Hutson, Michael O’Brien, Spencer W. Beasley,
Warwick J. Teague and Sebastian K. King.
© 2015 John Wiley & Sons, Ltd. Published 2015 by John Wiley & Sons, Ltd.
164
In summary, most anal fissures can be managed by
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treating the underlying constipation if the fissure does
not heal spontaneously, and other modalities can be
reserved for the problematic or persistent symptomatic
fissure. Persistence of a fissure may cause the child to
experience pain and distress during defecation and even
inappropriately hold on to stools because of their
association of pain with defecation. The emotional
tension built up around the act is more difficult to treat
than the fissure itself and may be the forerunner of the
whole vicious circle of constipation (Chapter22).
Perianal abscess
This is fairly common in infants and arises from infection in the anal glands, which open into the crypts of
the anal valves. Although the abscess almost always
presents superficially, the fistulous tract passes through
the most superficial of the internal sphincter fibres to
open inside an anal valve.
Treatment involves identifying and laying open the
fistula and draining the abscess [Fig. 27.1]. Failure to
deal with the fistula may result in recurrent infection.
Sometimes, young children may develop a superficial
subcutaneous abscess in the buttock or near the anus,
which is often secondary to a nappy rash and infection
with skin organisms. In these cases unrelated to anal gland
infection, simple drainage and antibiotics are curative.
Chapter27: Anus, Perineum and Female Genitalia 165
Figure 27.1 In perianal abscess, there is a fistula running from
the abscess to the anus inside an anal valve. The tract is
displayed by a lacrimal probe.
Rectal prolapse
Rectal prolapse is not uncommon in toddlers and is an
alarming experience for the parents [Fig.27.2]. However,
in most cases, it disappears spontaneously after a few
weeks or months without residual damage.
Aetiology
The two common predisposing factors are:
1 Straining at stool by a child with constipation. Less
frequently, straining may occur paradoxically with
diarrhoea, for example, as part of a malabsorption
syndrome such as cystic fibrosis or coeliac disease.
2 Explosive or reluctant defaecation. A healthy child
occasionally develops a rectal prolapse following an
explosive defaecation in which there is little time for
moulding of the stool by the muscles of the pelvic floor.
Figure 27.2 Rectal prolapse. The mucosa is congested and
oedematous and may bleed.
Reluctant defecation describes prolonged attempts to
defaecate with excessive straining in the absence of con-
stipation, often as a result of parents’ ill advice during
toilet training.
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Rare organic causes include:
1 Paralysis of anal sphincters (spina bifida, sacrococcy-
geal teratoma)
2 Hypotonia or starvation
3 Ectopia vesicae (bladder exstrophy with abnormal
pelvic girdle)
4 Complication of surgery for an anorectal malforma-
tion or Hirschsprung disease
Clinical features
Most children with rectal prolapse have normal pelvic
anatomy. The prolapse rolls out painlessly only during
defaecation and usually returns spontaneously; manual
replacement is required infrequently. The mucosa
may become abraded while it is prolapsed and cause
minor bleeding. A digital photograph taken by the
parents may help the surgeon sort out the differential
diagnosis.
Differential diagnosis
1 Rectal polyp: Polyps may prolapse per rectum (see
following text) and may be positively identified by
observation, digital palpation or proctoscopy.
2 Intussusception: Rarely, the apex of an intussus-
ception appears at the anus, albeit usually accompanied by its own and distinctive clinical features
(Chapter19).
3 External haemorrhoids: These are rare in childhood,
but congestion of the submucosal venous plexus during straining at stool sometimes produces a bluish sessile bulge, the parents’ description of which may be
mistaken for rectal prolapse.
Rarely, rectal prolapse proves refractory to conservative medical management, and operative treatment
is required. Various unpalatable and invasive surgical
techniques are described in adult patients, but have
highly selective, if any, application in children. More
commonly, sclerotherapy is performed by injection of a
sclerosant into the submucosal plane of the rectum to
cause fibrosis and contraction of the rectal wall, for
example, 0.5 ml of 5% phenol in almond oil injected
into the submucosa at three equally spaced points, 2
above the anal valves.
cm
Rectal polyps
Juvenile rectal polyps are isolated benign hamartomas
and are a relatively common cause of rectal bleeding.
Bright bleeding is produced painlessly at the end of defecation and is typically intermittent over long periods.
The polyp is almost always within reach of an examining
finger, and occasionally prolapses through the anus
[Fig.27.3].
Treatment
On those uncommon occasions, the polyp protrudes
through the anus; the base may be ligated without
anaesthesia. Otherwise, under general anaesthesia, the
polyp may be located through the proctoscope and
withdrawn to demonstrate its stalk, which is transfixed
with a suture ligature or transected with diathermy.
Higher lesions may be similarly removed at colonoscopy. Recurrence is rare and malignancy unknown.
Treatment
Constipation is the most common cause, and treatment
to ensure no straining at stool is required for at least several weeks (Chapter22). In the absence of constipation,
the possibility of a malabsorption syndrome should be
investigated.
Any errors in the child’s sitting posture at defecation
will need to be addressed, for example, squatting over a
potty on the floor to defaecate, which stretches the
pelvic floor and anal sphincters to maximum disadvantage. A potty chair or an insert for an adult toilet seat
enables the child to sit with support for the pelvic floor.
Also, a reasonable time limit for defecation should be set
to discourage straining.
Figure 27.3 Prolapse of a benign rectal polyp through the anus.
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