Paediatric Renal and Urology Flashcards

1
Q

Urinary tract infections

A

The urinary tract includes the urethra, bladder, ureters and kidneys. Urinary tract infections are infections anywhere along this pathway.

Acute pyelonephritis is when the infection affects the tissue of the kidney. It can lead to scarring in the tissue and consequently a reduction in kidney function.

Cystitis means inflammation of the bladder, and can be the result of a bladder infection.

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2
Q

Signs and symptoms of UTIs

A

Fever may be the only symptom of a urinary tract infection, especially in young children. Always consider (and exclude) a urinary tract infection in a child with a temperature, unless there is a clear alternative source of infection.

Babies will present with very non-specific symptoms:

Fever
Lethargy
Irritability
Vomiting
Poor feeding
Urinary frequency
Signs and symptoms in older infants and children are more specific:

Fever
Abdominal pain, particularly suprapubic pain
Vomiting
Dysuria (painful urination)
Urinary frequency
Incontinence

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3
Q

Acute pyelonephritis

A

The diagnosis of acute pyelonephritis is made if either there is:

A temperature greater than 38°C
Loin pain or tenderness
This is a very important point to note, as it affects the way you would investigate the child for recurrent infections.

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4
Q

Urine dipstick

A

The ideal urine sample is a clean catch sample, avoiding contamination. This can be tricky in younger children and babies, particularly girls. This often involves the parent sat with the infant without a nappy and a urine pot held ready to catch the sample if it occurs. A clean catch sample is important to avoid contamination and unreliable microbiology results.

Nitrites – gram negative bacteria (such as E. coli) break down nitrates, a normal waste product in urine, into nitrites. The presence of nitrites suggest bacteria in the urine.

Leukocytes – leukocytes are white blood cells. There are normally a small number of leukocytes in the urine, however a significant rise can be the result of an infection or another cause of inflammation. A urine dipstick tests for leukocyte esterase, a product of leukocytes that give an indication about the number of leukocytes in the urine.

Nitrites are a better indication of infection than leukocytes. If both are present the patient should be treated as a UTI. If only nitrites are present it is worth treating as a UTI. If only leukocytes are present the patient should not be treated as a UTI unless there is clinical evidence they have one.

If nitrites or leukocytes are present, the urine should be sent to the microbiology lab. If neither are present the patient is unlikely to have a UTI.

Send a midstream urine (MSU) sample to the microbiology lab to be cultured and have sensitivity testing.

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5
Q

Managing UTIs

A

All children under 3 months with a fever should start immediate IV antibiotics (e.g. ceftriaxone) and have a full septic screen, including blood cultures, bloods and lactate. A lumbar puncture should also be considered.

Oral antibiotics can be considered in children over 3 months if they are otherwise well. Children with features of sepsis or pyelonephritis will require inpatient treatment with IV antibiotics. Always follow local guidelines. Typical antibiotic choices in urinary tract infections in children are:

Trimethoprim
Nitrofurantoin
Cefalexin
Amoxicillin

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6
Q

Investigating recurrent UTIs

A

Recurrent UTIs should be investigated for an underlying cause and renal damage. This is a summary of the NICE guidelines on urinary tract infections in under 16s. Please read the full guidelines before treating patients.

Ultrasound Scans

All children under 6 months with their first UTI should have an abdominal ultrasound within 6 weeks, or during the illness if there are recurrent UTIs or atypical bacteria
Children with recurrent UTIs should have an abdominal ultrasound within 6 weeks
Children with atypical UTIs should have an abdominal ultrasound during the illness

DMSA (Dimercaptosuccinic Acid) Scan

DMSA scans should be used 4 – 6 months after the illness to assess for damage from recurrent or atypical UTIs. This involves injecting a radioactive material (DMSA) and using a gamma camera to assess how well the material is taken up by the kidneys. Where there are patches of kidney that have not taken up the material, this indicates scarring that may be the result of previous infection.

Vesico-Ureteric Reflux (VUR)

Vesico-ureteric reflux (VUR) is where urine has a tendency to flow from the bladder back into the ureters. This predisposes patients to developing upper urinary tract infections and subsequent renal scarring. This is diagnosed using a micturating cystourethrogram (MCUG).

Management of vesico-ureteric reflux depends on the severity:

Avoid constipation
Avoid an excessively full bladder
Prophylactic antibiotics
Surgical input from paediatric urology

Micturating Cystourethrogram (MCUG)

Micturating cystourethrogram (MCUG) should be used to investigate atypical or recurrent UTIs in children under 6 months. It is also used where there is a family history of vesico-ureteric reflux, dilatation of the ureter on ultrasound or poor urinary flow. A MCUG is used to diagnose VUR.

It involves catheterising the child, injecting contrast into the bladder and taking a series of xray films to determine whether the contrast is refluxing into the ureters. Children are usually given prophylactic antibiotics for 3 days around the time of the investigation.

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7
Q

Vulvovaginitis

A

Vulvovaginitis refers to inflammation and irritation of the vulva and vagina. It is a common condition often affecting girls between the ages of 3 and 10 years.

This irritation is caused by sensitive and thin skin and mucosa around the vulva and vagina in young girls. The vagina is more prone to colonisation and infection with bacteria spread from faeces. It can be exacerbated by:

Wet nappies
Use of chemicals or soaps in cleaning the area
Tight clothing that traps moisture or sweat in the area
Poor toilet hygiene
Constipation
Threadworms
Pressure on the area, for example horse riding
Heavily chlorinated pools
Vulvovaginitis improves and is much less common after puberty, as oestrogen helps keep the skin and vaginal mucosa healthy and resistant to infection.

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8
Q

Presentation of vulvovaginitis

A

Vulvovaginitis is a common presentation in young girls before puberty. It presents with:

Soreness
Itching
Erythema around the labia
Vaginal discharge
Dysuria (burning or stinging on urination)
Constipation
A urine dipstick may show leukocytes but no nitrites. This will often result in misdiagnosis as a urinary tract infection.

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9
Q

Managing vulvovaginitis

A

Often patients have already been treated for urinary tract infections and thrush, usually with little improvement in symptoms. It is unusual for girls to develop thrush before puberty.

Generally no medical treatment is required and management focuses on simple measures to improve symptoms:

Avoid washing with soap and chemicals
Avoid perfumed or antiseptic products
Good toilet hygiene, wipe from front to back
Keeping the area dry
Emollients, such as sudacrem can sooth the area
Loose cotton clothing
Treating constipation and worms where applicable
Avoiding activities that exacerbate the problem
In severe cases an experienced paediatrician may recommend oestrogen cream to improve symptoms.

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10
Q

Nephrotic syndrome

A

Nephrotic syndrome occurs when the basement membrane in the glomerulus becomes highly permeable to protein, allowing proteins to leak from the blood into the urine. It is most common between the ages of 2 and 5 years. It presents with frothy urine, generalised oedema and pallor.

Nephrotic syndrome features a classic triad of:

Low serum albumin
High urine protein content (>3+ protein on urine dipstick)
Oedema
There are three other features that occur in patients with nephrotic syndrome:

Deranged lipid profile, with high levels of cholesterol, triglycerides and low density lipoproteins
High blood pressure
Hyper-coagulability, with an increased tendency to form blood clots

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11
Q

Causes of nephrotic syndrome

A

The most common cause in children is minimal change disease, causing over 90% of cases in children under 10. In minimal change disease, nephrotic syndrome occurs in isolation, without any clear underlying condition or pathology. There are a number of secondary causes of nephrotic syndrome, where it occurs due to an underlying condition.

It can be secondary to intrinsic kidney disease:

Focal segmental glomerulosclerosis
Membranoproliferative glomerulonephritis
It can also be secondary to an underlying systemic illness:

Henoch schonlein purpura (HSP)
Diabetes
Infection, such as HIV, hepatitis and malaria

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12
Q

Minimal change disease

A

Minimal change disease is the most common cause of nephrotic syndrome in children. It can occur in otherwise healthy children, without any clear risk factors or reason for developing the condition. It is not clear why it occurs in most cases.

A renal biopsy and standard microscopy in minimal change disease is usually not able to detect any abnormality. Urinalysis (analysis of the urine) will show small molecular weight proteins and hyaline casts.

Management of minimal change disease is with corticosteroids (i.e. prednisolone). The prognosis is good and most children make a full recovery, however it may reoccur.

TOM TIP: Minimal change disease comes up fairly frequently in exams as the most common cause of nephrotic syndrome in children. If you spot a 2 – 5 year old child with oedema, proteinuria and low albumin, you may be asked about the underling cause. The answer is likely to be nephrotic syndrome.

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13
Q

Managing nephrotic syndrome

A

Nephrotic syndrome should be managed by experienced paediatricians with input from renal specialists. General management is with:

High dose steroids (i.e. prednisolone)
Low salt diet
Diuretics may be used to treat oedema
Albumin infusions may be required in severe hypoalbuminaemia
Antibiotic prophylaxis may be given in severe cases
High dose steroids are given for 4 weeks and then gradually weaned over the next 8 weeks:

80% of children will respond to steroids, and are referred to as steroid sensitive
80% of steroid sensitive patients will relapse at some point and need further steroids
Patients that struggle to wean steroids due to relapses are referred to as steroid dependant
Patients that do not respond to steroids are referred to as steroid resistant
In steroid resistant children, ACE inhibitors and immunosuppressants such as cyclosporine, tacrolimus or rituximab may be used.

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14
Q

Complications of nephrotic syndrome

A

Hypovolaemia occurs as fluid leaks from the intravascular space into the interstitial space causing oedema and low blood pressure.
Thrombosis can occur because proteins that normally prevent blood clotting are lost in the kidneys, and because the liver responds to the low albumin by producing pro-thrombotic proteins.
Infection occurs as the kidneys leak immunoglobulins, weakening the capacity of the immune system to respond. This is exacerbated by treatment with medications that suppress the immune system, such as steroids.
Acute or chronic renal failure
Relapse

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15
Q

Nephritis

A

Nephritis refers to inflammation within the nephrons of the kidneys. It causes:

Reduction in kidney function
Haematuria: invisible or visible amounts of blood in the urine
Proteinuria: although less than in nephrotic syndrome
The two most common causes of nephritis in children are post-streptococcal glomerulonephritis and IgA nephropathy (Berger’s disease).

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16
Q

Post-Streptococcal Glomerulonephritis

A

Post-streptococcal glomerulonephritis occurs 1 – 3 weeks after a β-haemolytic streptococcus infection, such as tonsillitis caused by Streptococcus pyogenes. Immune complexes made up of streptococcal antigens, antibodies and complement proteins get stuck in the glomeruli of the kidney and cause inflammation. This inflammation leads to an acute deterioration in renal function, causing an acute kidney injury.

Consider a diagnosis of post-streptococcal glomerulonephritis where there is evidence of recent tonsillitis caused by streptococcus. This could be a history of tonsillitis, positive throat swab results and anti-streptolysin antibody titres found on a blood test.

Management is supportive and around 80% of patients will make a full recovery. In some cases patients can develop a progressive worsening of their renal function. They may need treatment with antihypertensive medications and diuretics if they develop complications such as hypertension and oedema.

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17
Q

IgA nephropathy

A

IgA nephropathy is also known as Berger’s disease. This condition is related to Henoch-Schonlein Purpura, which is an IgA vasculitis. IgA deposits in the nephrons of the kidney causes inflammation (nephritis). When a renal biopsy is taken the histology will show “IgA deposits and glomerular mesangial proliferation”.

It usually presents in teenagers or young adults.

Management involves supportive treatment of the renal failure and immunosuppressant medications such as steroids and cyclophosphamide to slow the progression of the disease.

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18
Q

Haemolytic uraemic syndrome

A

Haemolytic uraemic syndrome (HUS) involves thrombosis in small blood vessels throughout the body, usually triggered by Shiga toxins from either E. coli O157 or Shigella.

It most often affects children following an episode of gastroenteritis. Antibiotics and anti-motility medication (e.g., loperamide) used to treat gastroenteritis caused by E. coli O157 or Shigella increase the risk of HUS.

HUS leads to the classic triad of:

Microangiopathic haemolytic anaemia
Acute kidney injury
Thrombocytopenia (low platelets)

The formation of blood clots consumes platelets, leading to thrombocytopenia. The blood flow through the kidney is affected by thrombi and damaged red blood cells, leading to acute kidney injury.

Microangiopathic haemolytic anaemia (MAHA) involves the destruction of red blood cells (haemolysis) due to pathology in the small vessels (microangiopathy). Tiny blood clots (thrombi) partially obstruct the small blood vessels and churn the red blood cells as they pass through, causing them to rupture.

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19
Q

Presentation of haemolytic uraemic syndrome

A

E. coli O157 and Shigella cause gastroenteritis. Diarrhoea is the first symptom, which turns bloody within 3 days. Around a week after the onset of diarrhoea, the features of HUS develop:

Fever
Abdominal pain
Lethargy
Pallor
Reduced urine output (oliguria)
Haematuria
Hypertension
Bruising
Jaundice (due to haemolysis)
Confusion

20
Q

Managing haemolytic uraemic syndrome

A

Stool culture is used to establish the causative organism.

HUS is a medical emergency and requires hospital admission and supportive management with treatment of:

Hypovolaemia (e.g., IV fluids)
Hypertension
Severe anaemia (e.g., blood transfusions)
Severe renal failure (e.g., haemodialysis)

It is self-limiting, and most patients fully recover with good supportive care.

21
Q

Enuresis

A

The term enuresis is used to describe involuntary urination. Bed wetting is called nocturnal enuresis. Inability to control bladder function during the day is called diurnal enuresis. Most children get control of daytime urination by 2 years and nighttime urination by 3 – 4 years.

22
Q

Primary Nocturnal Enuresis

A

Primary nocturnal enuresis is where the child has never managed to be consistently dry at night.

The most common cause of primary nocturnal enuresis is a variation on normal development, particularly if the child is younger than 5 years. Often patients will have a family history of delayed dry nights. In this situation reassurance is important, and there is no need to jump to further investigations or management.

Other causes of primary nocturnal enuresis include:

Overactive bladder. Frequent small volume urination prevents the development of bladder capacity.
Fluid intake prior to bedtime, particularly fizzy drinks, juice and caffeine, which can have a diuretic effect
Failure to wake due to particularly deep sleep and underdeveloped bladder signals
Psychological distress, for example low self esteem, too much pressure or stress at home or school
Secondary causes such as chronic constipation, urinary tract infection, learning disability or cerebral palsy
The initial step in management of primary nocturnal enuresis is to establish the underlying cause. It can be helpful to keep a 2 week diary of toileting, fluid intake and bedwetting episodes. This helps establish any patterns and identifies areas that may be changed, such as fluid intake before bed. It is important to take a history and examination to exclude underlying physical or psychological causes.

Management of primary nocturnal enuresis involves:

Reassure parents of children under 5 years that it is likely to resolve without any treatment
Lifestyle changes: reduced fluid intake in the evenings, pass urine before bed and ensure easy access to a toilet
Encouragement and positive reinforcement. Avoid blame or shame. Punishment should very much be avoided.
Treat any underlying causes or exacerbating factors, such as constipation
Enuresis alarms
Pharmacological treatment

23
Q

Secondary Nocturnal Enuresis

A

Secondary nocturnal enuresis is where a child begins wetting the bed when they have previously been dry for at least 6 months. This is more indicative of an underlying illness than primary enuresis. Causes of secondary nocturnal enuresis include:

Urinary tract infection
Constipation
Type 1 diabetes
New psychosocial problems (e.g. stress in family or school life)
Maltreatment
Always think about abuse and safeguarding, particularly with deliberate bedwetting, punishment for bedwetting (despite parental education) or unexplained secondary nocturnal enuresis.

Management of secondary nocturnal enuresis is based on treating the underlying cause. The most common and easily treatable secondary causes are urinary tract infections and constipation. Other problems may require referral to secondary care for further management.

24
Q

Diurnal Enuresis

A

Diurnal enuresis is daytime incontinence. This occurs when the person has become dry at night but still has episodes of urinary incontinence during the day. This occurs more frequently in girls. Incontinence comes in two main types:

Urge incontinence is an overactive bladder that gives little warning before emptying
Stress incontinence describes leakage of urine during physical exertion, coughing or laughing.
Other causes of diurnal enuresis include

Recurrent urinary tract infections
Psychosocial problems
Constipation

25
Q

Pharmacological treatment of enuresis

A

Medication for nocturnal enuresis is usually initiated by a specialist.

Desmopressin is an analogue of vasopressin (also known as anti-diuretic hormone). It reduces the volume of urine produced by the kidneys. It is taken at bedtime with the intention of reducing nocturnal enuresis.

Oxybutinin is an anticholinergic medication that reduces the contractility of the bladder. It can be helpful where there is an overactive bladder causing urge incontinence.

Imipramine is a tricyclic antidepressant. It is not clear how it works, but it may relax the bladder and lighten sleep.

26
Q

Polycystic kidney disease

A

There are two types of polycystic kidney disease (PKD). This section focuses on autosomal recessive polycystic kidney disease (ARPKD). Autosomal dominant, known as ADPKD, presents later in life, usually in adults.

Autosomal recessive polycystic kidney disease (ARPKD) presents in neonates and is usually picked up on antenatal ultrasound scans. It is the result of a mutation in the polycystic kidney and hepatic disease 1 (PKHD1) gene on chromosome 6. This gene codes for the fibrocystin/polyductin protein complex (FPC), which is responsible for the creation of tubules and the maintenance of healthy epithelial tissue in the kidneys, liver and pancreas.

27
Q

Features of autosomal recessive polycystic kidney disease

A

The underlying pathology causes:

Cystic enlargement of the renal collecting ducts
Oligohydramnios, pulmonary hypoplasia and Potter syndrome
Congenital liver fibrosis

ARPKD usually presents in the antenatal period with oligohydramnios and polycystic kidneys seen on antenatal scans. Oligohydramnios is a lack of amniotic fluid caused by reduced urine production by the fetus. A lack of amniotic fluid leads to Potter syndrome, which is characterised by dysmorphic features such as underdeveloped ear cartilage, low set ears, a flat nasal bridge and abnormalities of the skeleton. The oligohydramnios leads to underdeveloped fetal lungs (pulmonary hypoplasia), resulting in respiratory failure shortly after birth. Additionally, large cystic kidneys can take up so much space in the abdomen it becomes hard for the neonate to breath adequately. Patients may require renal dialysis within the first few days of life. Most patients develop end stage renal failure before reaching adulthood.

Patients with polycystic kidney disease have a number of ongoing problems throughout life:

Liver failure due to liver fibrosis
Portal hypertension leading to oesophageal varices
Progressive renal failure
Hypertension due to renal failure
Chronic lung disease

The prognosis is poor. Survival depends on very extensive interventions from a number of different specialties both in the neonatal period and throughout life. Around 1/3 will die in the neonatal period. Around 1/3 will survive to adulthood.

28
Q

Multicystic Dysplastic Kidney

A

Multicystic dysplastic kidney (MCDK) is a separate condition to PKD, where one of the baby’s kidneys is made up of many cysts while the other kidney is normal. In rare cases it can be bilateral, which inevitably leads to death in infancy. MCDK is normally diagnosed on antenatal ultrasound scans.

Usually the single healthy kidney is sufficient to lead a normal life. Often the cystic kidney will atrophy and disappear before 5 years of age. Having a single kidney can put the person at risk of urinary tract infections, hypertension and chronic kidney disease later in life.

No treatment is required for MCDK. Followup renal ultrasound scans can be used to monitor the abnormal kidney. Prophylactic antibiotics are occasionally used to prevent urinary infections that may affect the working kidney.

29
Q

Wilms’ tumour

A

Wilms’ tumour is a specific type of tumour affecting the kidney in children, typically under the age of 5 years.

Presentation

Consider a Wilms tumour in a child under the age of 5 years presenting with a mass in the abdomen. The parents may have noticed the mass, or they may present with signs and symptoms of:

Abdominal pain
Haematuria
Lethargy
Fever
Hypertension
Weight loss

Diagnosis

The initial investigation is an ultrasound of the abdomen to visualise the kidneys. A CT or MRI scan can be used to stage the tumour. Biopsy to identify the histology is required to make a definitive diagnosis.

Management

Treatment involves surgical excision of the tumour along with the affected kidney (nephrectomy).

Adjuvant treatment refers to treatment that is given after the initial management with surgery. This depends on the stage of the disease, the histology and whether it has spread. The main options are:

Adjuvant chemotherapy
Adjuvant radiotherapy

Prognosis

Early stage tumours with favourable histology hold a good chance of cure (up to 90%). Metastatic disease has a poorer prognosis.

30
Q

Posterior urethral valve

A

A posterior urethral valve is where there is tissue at the proximal end of the urethra (closest to the bladder) that causes obstruction of urine output. It occurs in newborn boys. The obstruction to the outflow of urine creates a back pressure into the bladder, ureters and up to the kidneys, causing hydronephrosis. A restriction in the outflow of urine prevents the bladder from fully emptying, leading to a reservoir of urine that increases the risk of urinary tract infections.

31
Q

Presentation of posterior urethral valve

A

It can vary in severity. Mild cases may be asymptomatic or present with:

Difficulty urinating
Weak urinary stream
Chronic urinary retention
Palpable bladder
Recurrent urinary tract infections
Impaired kidney function
Severe cases can cause obstruction to urine outflow in the developing fetus resulting in bilateral hydronephrosis and oligohydramnios (low amniotic fluid volume). The oligohydramnios leads to underdeveloped fetal lungs (pulmonary hypoplasia) with respiratory failure shortly after birth.

32
Q

Investigating posterior urethral valve

A

Severe cases may be picked up on antenatal scans as oligohydramnios and hydronephrosis.

To investigate cases presenting after birth, for example young boys presenting with urinary tract infections:

Abdominal ultrasound may show an enlarged, thickened bladder and bilateral hydronephrosis
Micturating cystourethrogram (MCUG) shows the location of the extra urethral tissue and reflux of urine back into the bladder
Cystoscopy involves a camera inserted into the urethra to get a detailed view of the extra tissue. Cystoscopy can be used to ablate or remove the extra tissue.

33
Q

Managing posterior urethral valve

A

Mild cases may simply be observed and monitored. If required a temporary urinary catheter can be inserted to bypass the valve whilst awaiting definitive management. Definitive management is by ablation or removal of the extra urethral tissue, usually during cystoscopy.

34
Q

Undescended testes

A

The testes develop in the abdomen and then gradually migrate down, through the inguinal canal and into the scrotum. They have normally reached the scrotum prior to birth.

In about 5% of boys the testes have not made it out of the abdomen by birth. At this point they are called undescended testes. This can also be referred to as cryptorchidism. They might be palpable in the inguinal canal (in the inguinal region), which is not technically classed as undescended testes, although they have not fully descended at that point.

The longer the testes take to descend, the less likely it is this will happen spontaneously. Undescended testes in older children or after puberty hold a higher risk of testicular torsion, infertility and testicular cancer.

35
Q

Risk factors for undescended testes

A

Family history of undescended testes
Low birth weight
Small for gestational age
Prematurity
Maternal smoking during pregnancy

36
Q

Managing undescended testes

A

Watching and waiting is appropriate in newborns. In most cases the testes will descend in the first 3 – 6 months. If they have not descended by 6 months they should be seen by a paediatric urologist. Orchidopexy (surgical correction of undescended testes) should be carried out between 6 and 12 months of age.

37
Q

Retractile Testicles

A

It is normal in boys that have not reached puberty for the testes to move out of the scrotum and into the inguinal canal when it is cold or the cremasteric reflex is activated. This is described as retractile testicles and is considered a normal variant. This usually resolves as they go through puberty and the testes settle in the scrotum. Occasionally they may fully retract or fail to descend and require surgical correction with orchidopexy.

38
Q

Hypospadias

A

Hypospadias is a condition affecting males, where the urethral meatus (the opening of the urethra) is abnormally displaced to the ventral side (underside) of the penis, towards the scrotum. This might be further towards the bottom of the glans (in 90% of cases), halfway down the shaft or even at the base of the shaft. Epispadias is where the meatus is displaced to the dorsal side (top side) of the penis. Usually, the foreskin is abnormally formed to match the position of the meatus. There can also be an associated condition called chordee, where the head of the penis bends downwards.

Hypospadias is a congenital condition affecting babies from birth and is usually diagnosed on the examination of the newborn.

39
Q

Managing hypospadias

A

Hypospadias requires referral to a paediatric specialist urologist for ongoing management. It is important to warn parents not to circumcise the infant until a urologist indicates this is ok.

Mild cases may not require any treatment
Surgery is usually performed after 3 – 4 months of age
Surgery aims to correct the position of the meatus and straighten the penis

40
Q

Complications of hypospadias

A

Difficulty directing urination
Cosmetic and psychological concerns
Sexual dysfunction

41
Q

Hydrocele

A

A hydrocele is a collection of fluid within the tunica vaginalis that surrounds the testes. The tunica vaginalis is a sealed pouch of membrane that surrounds the testes. Originally the tunica vaginalis is part of the peritoneal membrane, but during development of the fetus it becomes separated from the peritoneal membrane and remains in the scrotum, partially covering each testicle.

42
Q

Simple Hydrocele

A

Simple hydroceles are common in newborn males. They occurs where fluid is trapped in the tunica vaginalis. Usually this fluid gets reabsorbed over time and the hydrocele disappears.

43
Q

Communicating Hydrocele

A

Communicating hydroceles occur where the tunica vaginalis around the testicle is connected with the peritoneal cavity via a pathway called the processus vaginalis. This allows fluid to travel from the peritoneal cavity into the hydrocele, allowing the hydrocele to fluctuate in size.

44
Q

Examining hydrocele

A

Hydroceles cause a soft, smooth, non-tender swelling around one of the testes. The swelling will be in front of and below the testicle. Simple hydroceles remain one size, whereas communicating hydroceles can fluctuate in size depending on the volume of fluid from the peritoneal cavity.

The key features to remember when examining a hydrocele is that they transilluminate with light. To transilluminate the hydrocele, hold a pen torch flat against the skin and watch as the whole thing lights up like a bulb.

45
Q

Differentials of a scrotal or inguinal swelling in a neonate

A

The key differential diagnoses of a scrotal or inguinal swelling in a neonate are:

Hydrocele
Partially descended testes
Inguinal hernia
Testicular torsion
Haematoma
Tumours (rare)

46
Q

Managing hydrocele

A

Ultrasound is a useful investigation for confirming the diagnosis and excluding other causes.

Simple hydroceles will usually resolve within 2 years without having any lasting negative effects. Parents can be reassured and followed up routinely. They may require surgery if they are associated with other problems, such as a hernia.

Communicating hydroceles can be treated with a surgical operation to remove or ligate the connection between the peritoneal cavity and the hydrocele (the processus vaginalis).