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Paeds > Kidney & Urinary Tract > Flashcards

Kidney & Urinary Tract Flashcards

1
Q

What are the common causative organisms of a UTI?

A
  • E. coli (90%)
  • Proteus (males)
  • Pseudomonas
  • Klebsiella
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2
Q

What are the RFs of UTI?

A
  • Incomplete bladder emptying > infrequent voiding, hurried micturition, obstruction due to constipation, neuropathic bladder
  • Vesicoureteric reflux > developmental abnormality
  • Poor hygiene
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3
Q

What are the S/S of a UTI?

A

Infants

  • Poor feeding
  • Vomiting
  • Irritability

Young children

  • Abdominal pain
  • Fever
  • Dysuria

Older children

  • Dysuria
  • Frequency
  • Haematuria
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4
Q

What is the difference between an upper and lower UTI?

A

Upper / pyelonephritis

  • Bacteriuria + fever >38
  • Bacteriuria + loin pain/tenderness

Lower / cystitis

  • Dysuria but no systemic sx
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5
Q

What are the features of an atypical UTI?

A
  • Seriously ill / septicaemia
  • Poor urine flow
  • Abdominal or bladder mass
  • Raised creatinine
  • Failure to respond to treatment with suitable antibiotics within 48 hours
  • Infection with non-E. coli organisms.
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6
Q

What is the preferred urine collection method?

A
  • Clean catch preferrable
  • If not possible, urine collection pads
  • If not possible, invasive methods e.g. suprapubic aspiration
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7
Q

What are the investigations for a UTI?

A

Examination and obs:

  • Including for signs of dehydration
  • Check ENT

Bloods:

  • FBC, U&Es, ?culture

Urine analysis:

  • Urine dip > Nitrite stick test (very specific), Leucocyte esterase test (+ve in children with febrile illness without UTI and in balanitis and vulvovaginitis)
  • Urine MC&S (diagnostic)

Acute USS: > to identify structural abnormalities

  • If atypical or recurrent UTI

DMSA: > to identify renal scarring
Within 4-6m of acute infection

  • If <3yrs with atypical or recurrent UTI
  • If >3yrs with recurrent UTI

MCUG: > looks for causes of recurrent UTI

  • If atypical / recurrent UTI
  • If USS abnormality is detected
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8
Q

What is the management of a UTI?

A

<3m:

  • Immediate referral to paeds + admission
  • IV abx e.g. co-amoxiclav
  • Then switched to oral prophylaxis

>3m + upper UTI:

  • Consider admission and IV abx
  • Or oral abx (e.g. cephalosporin or co-amox)

>3m + lower UTI:

  • Oral abx (usually trimeth, nitrofurantoin, cephalosporin or amox)
  • Safety net > bring child back if remain unwell after 24-48hrs

Recurrent UTI:

  • Long-term low-dose abx prophylaxis
  • Anti-VUR surgery

Conservative:

  • High fluid intake
  • Ensure complete bladder emptying
  • Good perianal hygiene
  • Regular voiding
  • Tx/prevention of constipation
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9
Q

What is enuresis?

A

The involuntary passage of urine during sleep after the age when continence is anticipated

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10
Q

When should children have achieved continence?

A

Dry by day = 4yrs
Dry by night = 5yrs (most by 3-4yrs)

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11
Q

What are the types of enuresis?

A

Primary = Never achieved continence

Secondary = Child has been dry for >6m before

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12
Q

What are the causes of enuresis?

A
  • Developmental: immature bladder control, disorder affecting arousal from sleep
  • Environmental: stress, family break-up, maternal separation, moving, birth of younger sibling, hospital attendance
  • Abuse: sexual, physical, emotional
  • Structural: decreased bladder capacity, congenital anomalies
  • Medical: UTI, constipation, epilepsy, occult spina bifida, diabetes, hyperthyroidism, neurogenic bladder
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13
Q

What are the S/S of enuresis?

A
  • Frequency, nocturia, urgency, daytime incontinence, changing of clothes, thirst, polyuria
  • Abuse and family stresses
  • Hard stool in abdomen
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14
Q

What are the investigations for enuresis?

A
  • Urine MC&S
  • Bladder USS (pre-voiding capacity, wall thickness, residual volume)
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15
Q

What is the management of enuresis?

A

1. Treat any causes

2. General advice:

  • Reassurance
  • Bladder training/regular daytime voiding plans
  • Positive reward system

3. Enuresis alarm:

  • First-line for children
  • Have sensor pads that sense wetness
  • High success rate

4. Desmopressin:

  • If short-term control is needed
  • If an enuresis alarm has been ineffective
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16
Q

What is phimosis?

A

Unretractile foreskin
(secondary to either a physiological or pathological process)

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17
Q

What are the causes of phimosis?

A

Physiological:

  • By 1yrs > 50% have non-retractable foreskin
  • By 4yrs > 10%
  • By 17yrs > 1%
  • If persistent to puberty > increased risk of infection and problems with urination / intercourse

Pathological:

  • Secondary to balanitis xerotica obliterans (BXO)
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18
Q

What are the S/S of phimosis?

A

> > Forceful retraction should not be attempted (often the child will self-retract)

Physiological:

  • Hx of spraying / ballooning of urine
  • Distal erythema
  • Should have a spout of mucosa as the foreskin is retracted

Pathological / Balanitis:

  • White fibrotic ring at the distal foreskin
  • Absence of normal mucosal spout
  • Oedema, erythema, tenderness
  • Generation of purulent material from the distal phimotic foreskin
  • Haematuria
  • Painful erections
  • Recurrent UTI
  • Weak stream
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19
Q

What is the management of phimosis?

A

<2yrs:

  • Reassurance
  • Personal hygiene promotion
  • RV in 6m

>2yrs:

  • Circumcision or topical steroid creams (depends on severity)

Balanitis:

  • Gentle saline washes, ensuring to properly wash under the foreskin
  • 1% hydrocortisone used for a short period in severe cases
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20
Q

What is paraphimosis?

A

UROLOGICAL EMERGENCY

  • Foreskin becomes trapped in retracted position proximal to swollen glans
  • Restricts blood flow to head of penis > penis turns dark purple
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21
Q

What is the management of paraphimosis?

A

1. Manipulation with topical analgesia (with ice packs, compression, osmotic agents)

2. Puncture technique - perforating the foreskin at multiple locations to allow exudation of oedematous fluid (if manipulation was unsuccessful)

3. Surgical reduction followed by circumcision

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22
Q

What is hypospadias?

A

Congenital abnormality of the penis
Wrongly positioned meatus (opening of the urethra is on underside of the penis instead of at the tip)

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23
Q

What are the S/S of hypospadias?

A
  • Ventral foramen
  • Foreskin not fused ventrally
  • End-membrane
  • Hooded foreskin
  • Chordee (downward curve of the penis)
  • Abnormal spraying during urination
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24
Q

What is the management of hypospadias?

A
  • Surgery NOT mandatory
  • May be performed on functional or cosmetic grounds (after 3 months)
  • Ultimate functional aim of surgery is to allow boys to pass urine in a straight line whilst standing and to have a straight erection

IMPORTANT: boys with hypospadias should NOT be circumcised before repair, because the skin is important for the repair

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25
Q

What conditions are associated with hypospadias?

A

cryptorchidism and inguinal hernias

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26
Q

What is balanoposthitis?

A

Inflamed / purulent discharge from foreskin
(Single attacks common)

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27
Q

What is the management of balanoposthitis?

A
  • Clean penis daily with lukewarm water and dry gently
  • Advise on sources of written information and support
  • Consider topical hydrocortisone
  • Candidal = imidazole cream
  • Bacterial = fluclox
  • If recurrent (rare) > circumcision
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28
Q

What is testicular torsion?

A

Twist of the spermatic cord resulting in testicular ischaemia and necrosis

MUST be excluded in any boy with acute abdomen

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29
Q

When does testicular torsion occur?

A

Most common 10-30yrs (peak 13-15)

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30
Q

What are the S/S of testicular torsion?

A
  • Severe, sudden onset pain in testes > can be referred to lower abdomen
  • Nausea / vomiting

O/E

  • Swollen, tender testes retracted upwards
  • Skin may be reddened
  • Cremasteric reflex lost
  • Elevation of testes does NOT ease pain (Prehn’s sign)
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31
Q

What are the investigations for testicular torsion?

A

Doppler USS
(cannot delay surgery)

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32
Q

What is the management for testicular torsion?

A

EMERGENCY > urgent urological referral

  • Exploration surgery +/- bilateral orchiopexy +/- fixation of contralateral testes
  • Supportive care > analgesia, sedation, antiemetics
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33
Q

What is nephrotic syndrome?

A

Triad of:

  • Proteinuria
  • Hypoalbuminaemia
  • Oedema
  • +High cholesterol and triglycerides

(protein-losing nephropathy > kidney losing protein in urine)

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34
Q

What are the causes of nephrotic syndrome?

A
  • Minimal Change Disease (MCD) > most common cause
  • Focal segmental glomerulosclerosis (FSGS)
  • Membranous nephropathy (MN)

Also - diabetes, lupus, amyloidosis, drugs, infections (HIV, HBV, HCV, malaria)

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35
Q

Describe MCD

A
  • Patient is young (2-4yrs)
  • Disease is mild (selective proteinuria)
  • Prognosis is excellent (great response to steroids)
  • Normal renal function / BP
  • Glomeruli look normal on light microscopy, but electron microscopy shows loss of foot processes
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36
Q

What are the causes of MCD?

A

Primary = Idiopathic
Secondary = Hodgkin’s Lymphoma, infections, medications

37
Q

Describe FSGS

A

> Segmental or focal scarring of glomeruli and foot process fusion

  • The patient is older
  • The disease is more severe (non-selective proteinuria)
  • Proteinuria, high BP, kidney failure
  • The prognosis is worse (poor response to steroids, 50% > CKD)
38
Q

What are the causes of FSGS?

A

Primary = Idiopathic
Secondary = HIV, heroin, ParvoB19

39
Q

Describe Membranous Nephropathy

A

> Widespread thickening of membranes in the glomeruli, granular deposits of Ig and complement

  • Patient is older (20-60)
  • Non-selective proteinuria
  • Poor response to steroids
  • PLA2R antibodies
  • Microscopic haematuria
40
Q

What are the causes of membranous nephropathy?

A

Primary = Idiopathic
Secondary = Syphilis, malaria, cancer, HBV/HBC, Hodgkin’s, SLE

41
Q

What are the S/S of nephrotic syndrome?

A
  • 1st = Peri-orbital oedema (e.g. bilateral puffy eyes)
  • 2nd = Peripheral oedema (leg / face / scrotum swelling, ascites, plural effusion, pulmonary oedema)
  • Oliguria
  • Lethargy
  • Diarrhoea / abdo pain
  • Poor feeding
42
Q

What are the investigations for nephrotic syndrome?

A

Urine:

  • Dip (proteinuria, microscopic haematuria)
  • MC&S
  • PCR (high)

Bloods:

  • FBC, ESR/CRP
  • Renal function
  • U&Es
  • LFTs (hypoalbuminaemia)
  • Lipid profile (hyperlipidaemia)

Renal USS:

  • Check for other causes of proteinuria e.g. PKD
  • Mandatory to assess kidney size to ensure it is safe to proceed with renal biopsy

Renal biopsy:

  • In children, almost all cases due to MCD - therefore treat empirically and only perform renal biopsy if patient is unresponsive to treatment

Also: (to differentiate cause)

  • HIV, HBV, HCV, malaria screen
43
Q

What is the management of nephrotic syndrome?

A
  • 1st = oral prednisolone 4-6w (reduce dose from 4w)
  • 2nd (unresponsive / atypical) = specialised renal biopsy
  • Sx tx = low-sodium diet and diuretics
44
Q

What are the complications of nephrotic syndrome?

A
  • Thrombosis (loss of protein = less anticoagulant proteins, also dehydration, immobility, diuretics, steroids)
  • Infection (loss of protein = weakened immune system)
  • Hypercholesterolaemia
  • High BP
  • AKI / CKD
45
Q

What are the S/S of renal failure?

A
  • Oliguria or anuria
  • Oedema > feet, legs, abdomen
  • Weight gain
  • Discoloured urine > brown
  • Fatigue, lethargy
  • N/V
46
Q

What are the investigations for renal failure?

A

Urine:

  • Dip, MC&S, PCR

Bloods:

  • FBC, ESR/CRP
  • Renal function
  • U&Es
  • LFTs
  • Lipid profile

Renal USS / CT:

  • Identify obstruction
  • CKD = small kidneys
  • AKI = large, bright kidneys with loss of cortical medullary differentiation

Renal biopsy:

  • Help diagnose underlying cause
47
Q

What is the diagnostic criteria for an AKI?

A
  1. Increase in serum creatinine of >=0.3mg/dL in 48hrs
  2. Increase in serum creatinine to 1.5x the baseline within 7 days
  3. Urine output <0.5mL/kg/h for >=6 hours
48
Q

What are the causes of pre-renal AKI?

A

Due to decreased blood flow into kidneys:

  • Haemorrhage
  • Dehydration (D/V)
  • Severe burns
  • Heart failure
  • Low blood pressure (sepsis, anaphylaxis)
  • Renal vein stenosis / embolus

> Should be urgently addressed with fluid replacement and circulatory support

49
Q

What are the causes of intrinsic AKI?

A

Damage to the kidney itself

  • HUS
  • Acute Tubular Necrosis
  • Glomerulonephritis
  • Interstitial nephritis, vasculitis, pyelonephritis

> High calorie, normal protein feed will decrease catabolism, uraemia, and hyperkalaemia

50
Q

What are the complications of intrinsic AKI?

A
  • Hyperkalaemia
  • Metabolic acidosis
  • Fluid overload
51
Q

What are the causes of post-renal AKI?

A

Obstruction to outflow of urine:

  • Intra-abdominal tumours
  • BPH
  • Kidney stones

> Requires assessment of the site of obstruction

> Relief can be achieved by nephrostomy or bladder catheterisation

52
Q

What is the management of an AKI?

A
  • Treat underlying cause (e.g. stop nephrotic medication, treat infection)
  • Supportive therapy: Electrolyte balance, fluid balance, nutritional support, BP management
  • Close monitoring
53
Q

What is the management of renal failure?

A
  • Lifestyle changes: Healthy diet, exercise, quit smoking
  • Diuretics PRN (i.e. to tx fluid overload or oedema whilst awaiting dialysis)
  • ACEi’s to lower BP and reduce proteinuria
  • Dialysis for end-stage renal disease
  • Kidney transplant
54
Q

What are the indications for dialysis?

A
  • Failure of conservative mx
  • Multisystem failure
  • Refractory hyperkalaemia
  • Refractory fluid overload
  • Metabolic acidosis
  • Uraemic sx (encephalopathy/confusion, N/V, pruritis, malaise, pericarditis)
  • CKD stage 5
55
Q

What is HUS?

A

When small vessels in kidney become damaged and inflamed
> Commonest cause of AKI in children

Presents with a triad of:

  • Renal failure (AKI)
  • Thrombocytopaenia (small petechia)
  • Haemolytic anaemia (microangiopathic)
56
Q

What are the causes of HUS?

A

Most common = E. coli
(undercooked meat, unpasteurised milk, water, veg)

Also = pneumococcus, salmonella, shigella, campylobacter

57
Q

What are the S/S of HUS?

A
  • May be asx
  • Abdominal pain
  • Bloody diarrhoea
  • Decreased UO
  • May have superficial bleeding (petechiae, purpura)
  • Pallor, fatigue, weakness
58
Q

What are the investigations for HUS?

A

Bloods:

  • FBC: Platelets low, RBC low, Hb low, Hct low, MCV normal
  • Coagulation screen: BT high, PT normal, APTT normal
  • Renal function: GFR low

Blood smear:

  • Schistocytes

Coombs test:

  • Negative

Stool culture

59
Q

What is the management for HUS?

A

> Consult nephrology & haematology specialists
>Children with typical presentation should be ADMITTED

> > SELF-LIMITING < <

Supportive:

  • Ensure fluid / electrolyte balance
  • Maintain BP - treat with CCBs if elevated (ACEi’s can reduce renal perfusion)

> 50% will require dialysis in the acute phase

Avoid:

  • Antibiotics
  • Anti-diarrhoeals
  • Narcotic opioids
  • NSAIDs
  • Plt transfusion (unless life-threatening bleeding)

Long-term follow-up:

  • May be persistent proteinuria and development of HTN / progressive CKD
60
Q

Describe atypical HUS

A

Not caused by E. Coli, caused by genetic mutation

  • More common in adults
  • NO diarrhoeal prodrome
  • May be familial and frequently relapses
  • High risk of HTN and progressive CKD with a high mortality
61
Q

What is acute glomerulonephritis?

A

Bilateral inflammation of renal glomeruli with proliferation of cellular elements secondary to an immunological mechanism

62
Q

What are the causes of acute glomerulonephritis?

A
  • Infections e.g. GAS, Hep B/C, HIV
  • Systemic inflammatory conditions e.g. HUS, SLE, HSP
  • Drugs e.g. NSAIDs, heroin
  • Malignancy e.g. Hodgkin’s lymphoma
63
Q

What are the types of acute glomerulonephritis?

A

Based on the pattern of injury, can be:

  • Diffuse (all glomeruli)
  • Focal (some glomeruli)
  • Segmental (only parts of affected glomerulus)

Causes:

  • Minimal change disease (focal)
  • IgA nephropathy (focal or segmental)
  • FSGS (segmental)
  • Membranous nephropathy (diffuse)
  • Membranoproliferative glomerulonephritis (diffuse)
  • Rapidly progressive glomerulonephritis (diffuse)
64
Q

What are the S/S of acute glomerulonephritis?

A
  • Haematuria
  • Hypertension
  • Oedema (face, ankles, ascites)
  • Impaired renal function > flank pain, decreased UO
  • Seizures
65
Q

What are the investigations for acute glomerulonephritis?

A

Urinalysis + microscopy:

  • Haematuria, proteinuria, dysmorphic RBCs, leukocytes, red cell casts

Bloods

  • FBC (anaemia)
  • U&Es (increased urea)
  • Renal function (high creatinine)
  • LFTs (deranged, hypoalbuminaemia)
  • Increased ESR/CRP
  • VBG (metabolic acidosis)

Imaging

  • Renal USS (small kidneys or normal)

Renal biopsy:

  • Urgently performed if glomerulonephritis is suspected

Specific

  • Increase Antistreptolysin titre (recent strep infection)
66
Q

What is the management of acute glomerulonephritis?

A
  • Treat underlying cause: e.g. if infection or AI disorder
  • Supportive treatment: fluid/electrolyte balance e.g. intake of salt and water may need to be restricted
  • Close monitoring
  • Consider abx if infectious cause (phenoxymethylpenicllin)
  • Consider ACEi or ARBs (decrease proteinuria and control BP)
  • Consider furosemide if HTN
  • Consider steroids (if nephrotic syndrome)
67
Q

What is Henoch-Schonlein Purpura?

A

IgA mediated small vessel vasculitis

RASH, ABDO PAIN, ARTHRITIS/ARTHRALGIA, GLOMERULONEPHRITIS

68
Q

What are the features of Henoch-Schonlein Purpura?

A

Most common vasculitis in childhood (usually before 5yrs)
Usually seen following an infection (URTI)
Degree of overlap with IgA nephropathy (Berger’s disease)

69
Q

What are the S/S of Henoch-Schonlein Purpura?

A

Purpuric rash (100%)

  • Extensor surface of legs, arms, buttocks, ankles (spares trunk)
  • Palpable, maculopapular, urticarial

Arthralgia (60-80%)

  • Periarticular oedema
  • Large joints
  • Joint pain and swelling of knees and ankles

Abdominal pain (60%)

  • Colicky
  • Haematemesis, melena, intussusception

Glomerulonephritis (20-60% > 97% within 3m of onset)

  • Microscopic or macroscopic haematuria
  • Nephrotic syndrome (rare)
70
Q

What are the investigations for Henoch-Schonlein Purpura?

A

Blood Pressure:

  • Normal or elevated (kidney involvement)

Urine dipstick:

  • Early morning urinalysis to assess for renal involvement
  • RBCs, proteinuria, casts

Bloods:

  • Renal function (GFR)
  • Serum creatinine (elevated = renal failure),
  • FBC, clotting screen, U&Es, ESR/CRP

Skin biopsy:

  • Microscopy can be used to confirm diagnosis
71
Q

What is the management of Henoch-Schonlein Purpura?

A

Most cases resolve spontaneously within 4wks, so provide sx treatment

Sx management:

  • Joint pain > NSAIDs
  • Abdo pain > paracetamol
  • Scrotal involvement or severe oedema or severe abdo pain > oral pred

Renal involvement: (impaired GFR / proteinuria)

  • Oral > IV corticosteroids
  • Consider immunosuppressants
  • Consider ACEi or ARB
  • Renal transplant considered in end-stage renal disease

Lifestyle advice:

  • Healthy diet, regular exercise, avoid alcohol / smoking
72
Q

What are the complications of Henoch-Schonlein Purpura?

A
  • Intussusception
  • Acute renal impairment
  • Arthritis involving ankles and knees commonly
  • Pancreatitis (rare)
73
Q

What is nephroblastoma (Wilm’s Tumour) ?

A

Most common kidney cancer in children.

74
Q

When does nephroblastoma present?

A

<5yrs (usually 3)

75
Q

What is nephroblastoma associated with?

A
  • Beckwith-Wiedemann syndrome (specific body parts overgrow)
  • WAGR syndrome (Wilm’s tumour, Aniridia, Genitourinary malformations, mental retardation)
  • Hemihypertrophy
  • 33% loss of function mutation in WT1 gene on chr11
76
Q

What are the S/S of nephroblastoma?

A

Common:

  • Asx unilateral upper abdominal/flank mass
  • Painless haematuria

Uncommon:

  • Abdominal pain
  • Anaemia (haemorrhage into mass)
  • Anorexia
  • HTN
77
Q

What are the investigations for nephroblastoma?

A

Avoid biopsy as may worsen condition

  • USS and/or CT/MRI > intrinsic renal mass distorting normal structure
  • Bloods - FBC, renal function, LFTs, serum total protein/albumin, coagulation studies, serum Ca
  • Urinalysis
78
Q

What is the staging of nephroblastoma?

A

1 = limited to kidney, completely excisable
2 = not limited to kidney, completely excisable
3 = not limited to kidney, not completely excisable
4 = spread beyond abdomen, haematogenous metastasis
5 = bilateral (each tumour graded separately)

79
Q

What is the management of nephroblastoma?

A
  1. Initial chemotherapy (vincristine, dactinomycin) followed by delayed nephrectomy
  2. Tumour staged subsequently and tx planned according to surgical and pathological findings
  3. Radiotherapy restricted to those with more advanced disease

> 80% cure rate

80
Q

What are the complications of nephroblastoma?

A

Often metastasise early (usually to lung)

81
Q

What is the management of urinary tract calculi?

A

Conservative management:

  • IV fluids, analgesia (morphine) and anti-emetics (ondansetron)
  • High fluid intake is recommended in all affected children

Bacterial Infection:

  • Antibiotic treatment with co-trimoxazole or nitrofurantoin, or surgical decompression

Small stones = medical expulsive therapy

  • Tamsulosin OR alfuzosin OR silodosin

Larger stones / do not pass spontaneously = surgical removal

  • 1st line: Extracorporeal shock wave lithotripsy (ESWL) or ureteroscopy
82
Q

What is hydrocele?

A

Collection of serous fluid between the layers of the membrane (tunica vaginalis) that surround the testes or along the spermatic cord

  • Common in male infants and newborns and typically resolve on their own
  • Main symptom is a painless, swollen scrotum on 1 or both sides, which feels like a water-filled balloon
83
Q

What is the management of hydrocele?

A

< 2 years:

  • Most resolve spontaneously before 2yrs so observation is appropriate provided there is no evidence of underlying pathology

2-11 years:

  • Surgery

11-18 years:

1. Idiopathic hydrocoele

  • Observation is appropriate
  • Surgery may be considered if large or uncomfortable

2. Hydrocoele after varicocelectomy

  • Observation +/- aspiration
  • Surgery considered in cases that don’t resolve

3. Filarial-related hydrocoele

  • Surgery
84
Q

What is the management of epididymo-orchitis?

A

Symptomatic Relief:

  • Bed rest
  • Scrotal elevation
  • Simple elevation
  • If systemically unwell with a high-grade fever, IV antibiotics and fluids are required

Eradication of Infection:

  • Empirical antibiotics
  • Gonococcal or chlamydia – ceftriaxone + doxycycline
  • Enteric organisms – quinolone (e.g. ofloxacin, levofloxacin)
  • Mumps – supportive

Possible complications: abscess formation, infertility, chronic pain

85
Q

What is Vesicoureteric reflux?

A

The abnormal backflow of urine from the bladder into the ureter and kidney

  • Relatively common abnormality of the urinary tract in children
  • Predisposes to UTI
86
Q

What are the S/S of Vesicoureteric reflux?

A
  • Antenatal period: hydronephrosis on USS
  • Recurrent childhood UTIs
  • Reflux nephropathy (chronic pyelonephritis secondary to VUR - renal scar may produce increased quantities of renin causing hypertension)
87
Q

What are the investigations for Vesicoureteric reflux?

A
  • Normally diagnosed following a micturating cystourethrogram (MCUG)
  • A DMSA scan may also be performed to look for renal scarring
88
Q

What are the complications of undescended testes?

A
  • Infertility
  • Torsion
  • Testicular cancer
  • Psychological
89
Q

What is the management of undescended testes?

A

Unilateral undescended testis:

  • Referral should be considered from around 3m, with the baby ideally seeing a urological surgeon before 6m
  • Orchidopexy: Surgical practices vary although the majority of procedures are performed at around 1yr

Bilateral undescended testes:

  • Should be reviewed by a senior paediatrician within 24hours as the child may need urgent endocrine or genetic investigation

Paeds (18 decks)

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