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Paediatrics > Nephrology > Flashcards

Nephrology Flashcards

1
Q

What are the causes of dehydration?

A

Hypotonic dehydration
- Decreased intake: inadequate sodium intake after vomiting/diarrhea
- Increased loss
>> Adrenal failure (e.g. CAH)
>> Adrenalectomy
>> Thiazide diuretics
>> Diarrhea/fistula Isotonic dehydration
- GI losses
>> Vomiting
>> Diarrhea
>> Fistulae
>> GI bleeding
- Skin losses
>> Fever
>> Burns

Hypertonic dehydration
- Decreased water intake
>> Acute illness
>> Breast feeding
>> Eating disorders
- Increased water loss
>> Sweating
>> Urinary loss
:: Osmotic diuresis by DKA/hyperglycemia
:: Diuretics
:: Diabetes insipidus
:: Post-ATB recovery diuresis/polyuric phase of ARF
:: Chronic nephropathy
>> Respiratory loss
:: Hyperventilation
:: Bronchiolitis
:: Pneumonia

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2
Q

How do we grade the severity of dehydration?

A
  • *>2 years of age**
  • Mild: 3%
  • Moderate: 6%
  • Severe: 9%
  • *<2 years of age**
  • Mild: 5%
  • Moderate: 10%
  • Severe: 15%
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3
Q

What are the clinical parameters used to assess the degree of dehydration?

A
  • Eyes: normal or sunken
  • Skin tugor: normal, decreased or tenting
  • Oral mucosa: dry or moist
  • Capillary refill: instantaneous or >3 seconds
  • Anterior fontanelle: normotensive or sunken?
  • Pulse
  • Blood pressure
  • Urine output
  • *C BASE H2O**
  • *C**apillary refill
  • *B**lood pressure
  • *A**nterior fontanelle
  • *S**kin tugor
  • *E**yes sunken
  • *H**eart rate
  • *O**ral mucosa
  • *O**utput of urine

+ Decreased body weight

The first thing to go is URINE OUTPUT

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4
Q

What is nephritic syndrome?

A

Acute or chronic syndrome affecting the kidney,
characterized by glomerular injury and inflammation

HEMATURIA (>5RBCs/>10RBCs per high-powered microscopy field - Canada/UK) with the presence of dysmorphic RBCs and RBC casts on urinalysis

Often accompanied by at least one of the following:

  • Proteinuria (<50mg/kg/day)
  • A: Azotemia
  • R: RBC casts in urine
  • O: Oliguria
  • H: Hypertension
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5
Q

What is the most common cause of acute glomerulonephritis in paediatrics?

A

Post-infectious/post-streptococcal glomerulonephritis

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6
Q

What is the cause of hypertension in nephritic syndrome?

A
  • Fluid retention
  • Increased renin secretion by ischemic kidneys
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7
Q

What is the most common cause of hematuria in children?

A

Urinary tract infection (but rarely as the only symptom)

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8
Q

When is a renal biopsy indicated in hematuria?

A
  • Significant persistent proteinuria
  • Recurrent macroscopic hematuria
  • Renal function is abnormal
  • Complement levels are persistently abnormal
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9
Q

When is a renal biopsy indicated in nephritic syndrome?

A
  • No evidence of streptococcal infection
  • Normal C3/C4 levels
  • Acute renal failure (abnormal renal function)
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10
Q

When is a renal biopsy indicated in nephrotic syndrome?

A
  • *Age of onset**
  • Presentation before first year of life (likely to be congenital nephrotic syndrome)
  • Presentation after 12 years of life (need to rule out more serious renal pathology than minimal change disease)
  • *Clinical features at presentation**
  • Hypertension (increased risk for focal segmental glomerular sclerosis)
  • Gross hematuria
  • Abnormal renal function
  • Low serum C3/C4
  • *Management response**
  • No response to steroids after 4 weeks of therapy
  • Frequent relapses: >2 relapses in 6 months
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11
Q

What is the classical clinical course of post-streptococcal nephritis?

A

Following a streptococcal pharyngitis or skin infection with evidence of a recent streptococcal infection by:

  • Culture of the organism (throat swab)
  • Raised anti-streptolysin O (ASO) titres
  • Anti-DNAse B titres

Also characterized by low complement C3 levels that RETURN TO NORMAL after 3-4 weeks

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12
Q

What are the characteristic clinical features of Henoch-Schonlein purpura?

A
  • Palpable rash over the buttocks and extensor surfaces of the bilateral lower limbs
  • Abdominal pain
  • Arthralgia with periarticular edema
  • Hematuria/glomerulonephritis

>> Usually preceded by an URTI
>> Usually between ages 3-10 years
>> M:F 2:1
>> Gastrointestinal petechiae can cause hematemesis and melena
>> Associated with intussusception

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13
Q

What are the causes of hematuria?

A
  • *Hematological/Vascular causes**
  • Sickle cell anemia
  • Bleeding disorders: e.g. hemophilia, vWF disease
  • Renal vein thrombosis

Lower urinary tract/Nonglomerular
- Urinary tract infections
>> Bacterial
>> Viral
>> TB
>> Schistosomiasis
- Trauma
- Stones/Hypercalciuria
- Tumours

Upper urinary tract/Glomerular
- Nephritic syndrome
>> Acute glomerulonephritis (+/- proteinuria)
>> Chronic glomerulonephritis (+/- proteinuria)
>> IgA nephropathy
>> Familial nephritis (Alport syndrome)
>> Thin basement membrane disease
>> Can also classify by primary/secondary and normal/decreased C3 levels

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14
Q

Name the causes of nephritic syndromes that are associated with decreased C3 levels.

A

Primary

  • Post-streptococal/post-infectious glomerulonephritis
  • Membranoproliferative glomerulonephritis

Secondary

  • SLE (systemic lupus erythematosus)
  • Bacterial endocarditis
  • Abscess/shunt nephritis
  • Cryoglobulinemia
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15
Q

What are the four types of rapidly progressive glomerulonephritis/crescentic glomerulonephritis?

A
  • *Type I: Anti-GBM Mediated**
  • With lung hemorrhage: Goodpasture’s disease
  • Without lung hemorrhage: Anti-GBM disease

Type II: Immune-complex mediated
- C3 normal
>> IgA nephropathy
>> Henoch-Schonlein Purpura
- C3 decreased
>> Membranoproliferative GN
>> Post-infectious GN
>> Systemic lupus erythematosus (SLE)
>> Bacterial endocarditis
>> Cryoglobulinemia

Type III: Non-immune mediated
- c-ANCA (anti-neutrophil cytoplasmic antibody) +
>> Granulomatosis with polyarteriitis
- p-ANCA +
>> Churg-Strauss disease
>> Microscopic polyangiitis

  • *Type IV: Double antibody positive disease**
  • Features of type I and III combined
  • Double antibody positive
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16
Q

What are the causes of nephritic syndrome?

A

Primary
- Decreased C3 levels
>> Post-streptococcal GN
>> Membranoproliferative GN
- Normal C3 levels
>> IgA nephropathy
>> Idiopathic rapidly progressive GN (RPGN)
>> Anti-GBM disease

Secondary
- Decreased C3 levels
>> SLE
>> Bacterial endocarditis
>> Cryoglobulinemia
>> Shunt nephritis/abscess
- Normal C3 levels
>> Goodpasture’s syndrome
>> Henoch-Schonlein Purpura
>> Polyarteritis nodosa
>> Granulomatosus with polyarteriitis

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17
Q

What are the investigations that will be helpful in cases of nephritic syndrome?

A
  • *Urine**
  • Dipstick: hematuria and 0-+2 proteinuria
  • Microscopy: >5 RBCs/HPF, RBC casts and acanthocytes

Bloods
- CBC: mild anemia from hematuria
- RFT
>> Increased Cr and BUN
>> Hyperkalemia
>> Hyperphosphatemia
>> Hypocalcemia
- LFT
>> Hypoalbuminemia from proteinuria
- ABG
>> pH decreased: impaired H excretion in the kidneys
- Bloods to determine etiology:
>> C3/C4 levels
>> ASO titre and anti-DNAse B
>> ANA, ANCA (c-ANCA and p-ANCA), anti-dsDNA Ab
>> Anti-GBM Ab
>> Serum IgA levels
>> Cryoglobulins

  • *Renal biopsy (indicated when:)**
  • Acute renal failure
  • No evidence of streptococcal infection
  • Normal C3/C4 levels Imaging
  • Renal USG to R/O oubstruction

Audiology if Alport’s syndrome is suspected (less in nephritic syndrome)

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18
Q

What are the possible complications of nephrotic syndrome?

A
  • Hypertension
  • Heart failure
  • Pulmonary edema
  • Chronic kidney injury requiring renal transplant
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19
Q

What is the typical age of presentation in children for nephritic syndrome?

A

5-15 years of age

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20
Q

What is the typical age of presentation in children for nephrotic syndrome?

A

2-6 years of age (M>F)

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21
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal change disease (glomerular infiltration absent on renal biopsy) – >90%

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22
Q

What is the management plan for nephritic syndrome?

A
  • Monitoring >> Serial BP >> Daily urinalysis >> Daily body weight >> Accurate I&O chart - Supportive treatment: consider dialysis if severe - Adequate hydration - Fluid and salt restriction with diuretics if edema is present - Consider ACEI/ARBs in hypertension, but avoid in acute cases as these drugs can further decrease GFR
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23
Q

What is nephrotic syndrome?

A

Clinical syndrome affecting the kidney:

P: Proteinuria (>50mg/kg/day)
A: HypoAlbuminemia (<20g/L)
L: HyperLipidemia
E: Edema

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24
Q

What is the earliest sign of nephrotic syndrome in children?

A

Periorbital edema particular on waking

>> Edema is gravity-dependent: periorbital edema decreases with pretibial edema increases over the day

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25
Q

What are the clinical signs of nephrotic syndrome?

A
  • Periorbital edema upon waking
  • Scrotal/vulval, leg and ankle edema
  • Breathlessness from pleural effusions and abdominal distention (ascites)
  • Foamy urine as a possible sign of proteinuria
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26
Q

What are the features suggestive of steroid-sensitive nephrotic syndrome?

A
  • Age: 1-10 years
  • No macroscopic hematuria
  • Normal blood pressure
  • Normal renal function
  • Normal complement levels

>> Often precipitated by respiratory infections (similar to HSP and ITP!!!)

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27
Q

What are the physiological causes of proteinuria?

A

Transient proteinuria

  • Febrile illnesses
  • After exercise
  • Does not require investigations

Orthostatic proteinuria

  • Only found when the child is upright/during the day
  • Dx: early morning urine protein/creatinine ratio in series
  • Prognosis is excellent
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28
Q

What are the causes of proteinuria in children?

A
  • *Physiological**
  • Orthostatic proteinuria
  • Transient proteinuria from febrile illnesses/exercise

Pathological
- Overflow
>> Multiple myeloma
>> Amyloidosis
>> Waldenstrom’s macroglobulinemia
- Tubular: Fanconi’s syndrome
- Glomerular
>> Primary
:: Minimal change disease
:: Focal segmental glomerular sclerosis
:: Membranoproliferative glomerulonephritis
:: IgA nephropathy
>> Secondary
:: Infections: HIV, HBV, HCV, post-strep, bacterial endocarditis
:: Inflammatory/Autoimmune: SLE, JIA, RA, DM, vasculitis (HSP, GPA)
:: Malignancies: lymphoma, leukemia
:: Genetic: Alport syndrome, sickle cell disease, polycystic kidney disease
:: Medications: captopril, NSAIDs, anticonvulsants

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29
Q

What are the presenting features of nephrotic syndrome?

A
  • *Nonspecific signs**
  • General malaise
  • Weakness
  • Anorexia
  • Nausea and vomiting
  • Diarrhea
  • Irritability
  • Dull lumbar pain
  • *Edema**
  • Periorbital and pretibial edema
  • Scrotal/labial edema
  • Breathlessness from pleural effusions and ascites
  • *Glomerular leakage**
  • Hematuria
  • Proteinuria (foamy urine)

Glomerular blockage
- Edema (refer to above)
- Hypertension
>> Encephalopathy
>> Congestive heart failure

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30
Q

What is the definition of acute glomerulonephritis?

A

Acute inflammatory process of presumed immunological origin affecting predominantly or exclusively the glomerulus - nephritic syndrome is only one of the clinical manifestations

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31
Q

What is the prognosis of post-streptococcal glomerulonephritis?

A
  • 90% complete recovery
  • Mortality 0.5-2% in acute stage
    >> Uremia
    >> Heart failure
    >> Encephalopathy
  • Morbidity: <10% develop chronic renal failure
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32
Q

What are the C3/C4 levels in post-streptoccocal glomerulonephritis?

A

C3 levels are typically decreased with subsequent recovery in 4-6/6-8 weeks

C4 levels are typically normal.
If depressed, one must rule out the following:
- SLE
- MPGN
- Bacterial endocarditis with renal involvement

>> Failure to recover is a poor prognostic sign indicating chronic glomerulonephritis

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33
Q

What is the specific management for post-streptococcal glomerulonephritis?

A
  • Oral penicillin x 10 days
  • Salt and fluid restriction with I.V. frusemide
  • IM hydralazine for moderate hypertension
  • Aggressive treatment for hypertensive encephalopathy
  • Dialysis when indicated
  • NOT STEROIDS NECESSARY

Follow-up
- 4-6 weeks clinic visits for 6 months
>> Urinalysis
>> BP measurement
- Hypertensive control

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34
Q

What are the indications for renal biopsy in post-streptococcal glomerulonephritis?

A
  • Rapidly deteriorating renal function
  • Atypical presentation
    >> Anuria
    >> Nephrotic syndrome
    >> Severe azotemia
    >> Lack of evidence of streptococal etiology
    >> Family or personal history of renal disease
    >> Systemic evidence for SLE etc.
  • Delay in resolution
    >> Oliguria and/or azotemia persisting beyond 2 weeks
    >> Hypertension/gross hematuria persisting beyond 3 weeks
    >> Low C3 beyond 6 weeks
    >> Persistent proteinuria with or without hematuria beyond 6 months
    >> Persistent hematuria beyond 12 months
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35
Q

What is the most accurate predictor for eventual renal failure in Henoch-Schonlein Purpura?

A

Persistence of nephrotic-range proteinuria (>50mg/kg/day; >40mg/m2/hour)

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36
Q

How do we quantify response to treatment in nephrotic syndrome?

A

Reduction in rate of urinary excretion of protein to <4mg/m2/hr (albustix 0-trace) for 3 consecutive days

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37
Q

How do we quantify a relapse of nephrotic syndrome?

A

Reappearance of proteinuria >=3+ on albustix or >=4mg/m2/hr for 3 consecutive days

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38
Q

What is the definition of frequent relapse in nephrotic syndrome?

A
  • 2 relapses within 6 months of the initial response
  • 4 or more relapses within any 12-month period
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39
Q

How do we define steroid dependency in nephrotic syndrome?

A
  • Relapse within 14 days after the end of a course of therapy
  • Relapse during the tapering regimen
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40
Q

What are the investigations to help diagnose the nephrotic syndrome and its cause?

A
  • *Urine**
  • Dipstick: proteinuria and microscopic hematurita
  • Microscopy: hyaline casts
  • First morning urine protein/creatinine ratio >0.2g/mmol

Blood
- RFT
>> Hyponatremia
>> Hyperkalemia
>> Hypocalcemia
>> Increased creatinine and BUN
- LFT
>> Hypoalbuminemia
- Lipid profile
>> Hypercholesterolemia (TC >5mmol/L)
>> Hyperlipidemia
- To rule out secondary causes
>> CBC and smear
>> C3/C4 levels
>> ANA and other autoimmune markers
>> ASOT, HBV/HCV titres, HIV serology etc.

Renal biopsy when indicated

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41
Q

What are the diagnostic investigation results for nephrotic syndrome?

A
  • Hypoalbuminemia (5mmol/L TC)
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42
Q

What is the treatment regimen for minimal change disease?

A

Oral prednisone 60mg/m2/day in 3 divided doses for 6 weeks + 40mg/m2 single morning dose in alternate days for 6 weeks

Relapse: oral prednisone 60mg/m2/day until protein free for 5 out of 7 days + 35mg/m2 single morning dose in alternate days for 4 weeks

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43
Q

What is the management plan for frequent relapsers of minimal change disease?

A

Oral prednisone 60mg/m2/day until protein-free urine for 5 out of 7 days + 35mg/m2 single morning dose in alternate days for 4 weeks

(same as for relapse)

Alternative treatment
- Cyclophosphamide x 8-12 weeks (+ prednisone)
- Cyclosporin x 6 months
>> Need renal monitoring
>> Indicated in steroid dependence with toxicity after 1 course of cyclophosphamide
>> Indicated in steroid dependence in pre-pubertal boys
- Levamisole alternate days for 6m-1y
>> Usually used as an adjunct
>> S/E: Leucopaemic, rash

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44
Q

What is the management plan for nephrotic syndrome?

A
  • Treatment of underlying disease (e.g. oral prednisone)
  • Symptomatic treatment
    >> Edema: salt and water restriction; furosemide + albumin if severe
    >> Hyperlipidemia: usually resolves with remission
    >> Hypoalbuminemia: usually resolves with remission
    >> BP changes: control and monitor
    >> Secondary infections (peritonitis)
    :: Parenteral penicillins for gram positives
    :: Parenteral aminoglycosides for gram negatives
    >> Watch out for hypercoagulability (rare in Chinese)
  • Diet: supplement with Ca and vit D if on steroids
    - Monitoring
    >> Daily weight
    >> Blood pressure
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45
Q

What are the complications of nephrotic syndrome?

A
  • *Increased risk of infections**
  • Spontaneous peritonitis
  • Cellulitis
  • Sepsis
  • *Hypercoagulability**: decreased intravascular volume and antithrombin III depletion
  • Pulmonary embolism
  • Renal vein thrombosis
  • *Others**
  • Intravascular depletion >> shock
  • Renal failure
  • Drug side effects (Cushing’s syndrome)
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46
Q

What is the rate of relapse in minimal change disease?

A

80%

>> Usually sustained remission with normal kidney function by adolescence

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47
Q

What is the definition of acute kidney injury (AKI)?

A
  • Reversible increase in Cr and BUN/nitrogenous waste
  • Inability to regulate fluid and electrolyte homeostasis
48
Q

How do we classify acute kidney injury?

A

pRIFLE classification

R: Risk ———– U/O <0.5mg/kg/hour x 8 hours
I: Injury ———– U/O <0.5mg/kg/hour x 16 hours
F: Failure ——– U/O <0.5mg/kg/hour x 24 hours; Anuric x 12 hours
L: Loss ———– Persistent failure x 4 weeks
E: End-stage — Persistent failure x 3 months

49
Q

What is the definition of oliguria?

A

Newborn: <0.5mL/kg/hr
Infants: <1.0m/kg/hr
Children: <200mL/m2/day
Adolescents or adults: <400mL/1.73m2/day

50
Q

What is the blood volume of term newborns?

A

80mL/kg >> Easily over-hydrated

51
Q

What are the risk factors for acute kidney injury in children?

A
  • Sepsis and toxemia
  • Hypotension and hypovolemia
  • Hypoxia and acidosis
  • Anesthesia
  • Surgery and/or trauma
  • Chronic disease states
  • Nephrotoxic agents
52
Q

What is the management plan for AKI?

A

1. Assess the volume status
2. Optimize:
>> Circulation
>> Blood pressure
>> Hematocrit
>> Oxygen delivery
3. Restore renal:systemic vascular resistance ratio
>> Ionotropic agents: dopamine
>> Furosemide: synergistic with dopamine (do NOT use in volume depletion)
>> Calcium channel blocker

53
Q

What are the indications for dialysis in AKI?

A

Due to complications of AKI itself
- Fluid overload unresponsive to conservative management
>> Congestive heart failure
>> Pulmonary edema
>> Severe hypertension +/- encephalopathy
- Life-threatening/uncontrollable metabolic disturbances
>> Hyperkalemia
>> Intractable metabolic acidosis
>> Hyperuricemia
>> Hyperphosphatemia
- Symptomatic azotemia leading to lethargy or seizures
- Prolonged oliguria with problematic nutritional support

  • *Due to underlying etiology**
  • Poisoning due to dialyzable compounds
  • *- Tumour-lysis syndrome**
  • *- Hyperammonemia**
  • Organic acidemia
54
Q

Why are antibiotics contraindicated in hemolytic uremic syndrome?

A

Death of bacteria leads to increased toxin release and worsens clinical outcome

55
Q

What are the presenting features of hemolytic uremic syndrome?

A
  • Non-immune microangiopathic hemolytic anemia
  • Thrombocytopenia
  • Acute renal failure
56
Q

What are the types of HUS (hemolytic uremic syndrome)?

A

Diarrhea-positive: 90% (E. coli O157:H7 shiga-like toxin)

Diarrhea-negative
>> No prodrome of diarrhea
>> Other bacteria, viruses, familial causes and drugs

If presents with fever and seizure: thrombocytopenic purpura (TTP)

57
Q

What is the pathophysiology of hemolytic uremic syndrome (HUS)?

A

Toxin invades and destroys colonic epithelial cells >> bloody diarrhea

Toxin enters systemic circulation >> injures endothelial cells,
especially in the kidney >> renal failure

Toxin causes platelet/fibrin thrombi in multiple organ systems >>
thrombocytopenia and microangiopathic hemolytic anemia

58
Q

What are the investigations useful for diagnosing HUS?

A
  • *Bloods**
  • CBC: anemia and thrombocytopenia
  • Blood smear: schistocytosis
  • RFT: renal failure (Cr/BUN increased)
  • *Urine**
  • Urinalysis: microscopic hematuria
  • *Stool**
  • Culture and stain
  • Verotoxin/shigella toxin assay
59
Q

What is the management for HUS?

A

MAINLY SUPPORTIVE

  • Nutrition/Hydration
  • Ventilation
  • Blood transfusion
  • Monitoring
  • Dialysis if indicated

RMB:
>> Steroids are NOT helpful
>> Antibiotics are CONTRAINDICATED as the death of bacteria leads to increased toxin release and worse clinical course

60
Q

What is the prognosis of HUS?

A

>95% survive the acute phase

~10-30% have renal damage

61
Q

What are the differential diagnoses for antenatal hydronephrosis?

A
  • Urethrovesicular junction obstruction
  • Posterior urethral valve in boys
  • Vesicoureteric reflex
  • Duplication anomalies
  • Ureterocele
  • Ectopic ureter
  • Multi-cystic dysplastic kidney
62
Q

What is the most common congenital obstructive urethral lesion in males?

A

Posterior urethral valve

63
Q

What is the presentation of posterior urethral valve?

A

Age-dependent

  1. Antenatal
    • Bilateral hydronephrosis
    • Distended bladder
    • Oligohydramnios
  2. Neonatal, recognized at birth
    • Palpable abdominal mass
    • Ascites from transudation of retroperitoneal urine
    • Respiratory distress from pulmonary hypoplasia due to oligohydramnios
    • Weak urinary stream
  3. Neonatal, not recognized at birth
    • Urosepsis
    • Dehydration
    • Electrolyte abnormalities
    • Failure to thrive
  4. Toddlers
    • Recurrent urinary tract infections
    • Voiding difficulties
  5. School-aged boys
    • Voiding difficulties >> urinary incontinence
64
Q

What are the investigations for posterior urethral valve?

A
  • Prenatal USG: keyhole sign from dilated posterior urethra
  • Voiding/Micturating cystourethrogram
    >> Dilated and elongated posterior urethra
    >> Trabeculated bladder
    >> Vesicoureteral reflux
65
Q

What is the pathophysiology of posterior urethral valve?

A

Abnormal mucosal folds at the distal prostatic urethra in males causing varying degrees of obstruction

66
Q

What is the management of posterior urethral valve?

A
  • Immediate catheterization to relieve obstruction
  • Cystoscopic resection of PUV when stable
  • Cystectomy if PUV resection is not possible
67
Q

What is the most common congenital defect of the ureter?

A

Ureteropelvic Junction (UPJ) Obstruction

68
Q

What is the common presenting complaints in ureteropelvic junction obstruction?

A

Infants: abdominal mass, urinary infection
Children: pain, vomiting, failure to thrive
Adolescents: triggered by episodes of increased diuresis, e.g. after alcohol

69
Q

What is vesicoureteral reflux?

A

Retrograde passage of urine from the bladder through the ureterovesicular junction (UVJ) into the ureter

70
Q

What is the grading for vesicoureteral reflux (VUR)?

A

Grade 1: only ureters
Grade 2: ureters and pelvis
Grade 3: ureters and pelvis with some dilation
Grade 4: ureters, pelvis and calyces with significant dilation
Grade 5: ureters, pelvic and calyces with major dilation and tortuosity

71
Q

What are the causes of vesicoureteral reflux (VUR?)

A

Primary: incompetent or inadequate closure of UVJ

Secondary: abnormally high intravesical pressure

  • Anatomic bladder obstruction: posterior urethral valve
  • Functional bladder obstruction: neurogenic bladder
72
Q

What are the investigations necessary for VUR?

A
  • *History: symptoms of voiding dysfunction**
  • Frequency
  • Urgency
  • Diurnal enuresis
  • Constipation
  • Encopresis
  • *Infection/Renal failure screening**
  • UTI, pyelonephritis and urosepsis
  • RFT: uremia
  • BP: hypertension
  • *Evaluation of other complications due to renal scarring:**
  • Height and weight
  • Blood pressure
  • Creatinine
  • Urinalysis and urine stain C/ST
  • Renal ultrasound
  • Dimercaprosuccinic acid scan (DMSA)
73
Q

What are the risk factors for vesicoureteral reflux?

A
  • Caucasians
  • Female
  • <2 years of age
  • Genetic predisposition
74
Q

What is the management for VUR?

A

TO PREVENT INFECTION OR RENAL DAMAGE

Medical treatment
- Long-term ABx prophylaxis at half of treatment dose for half of treatment time
>> Trimethroprim-sulfamethoxazole
>> Trimethroprim
>> Nitrofurantoin
>> Cephalexin (1st generation cephalosporin)

  • *Surgical treatment**
  • Ureteral reimplantation +/- ureteroplasty
  • Subureteral injection with debulking agents (e.g. Deflux)
75
Q

What are the indications for surgical therapy in VUR?

A
  • Persistent high-grade VUR
    >> Frequency
    >> Severity
  • Failure of medical treatment (Non-compliance)
    **- Breakthrough urinary tract infections
  • Presence and severity of renal scarring**
76
Q

What is hypospadias?

A

When the urethral meatus opens on the ventral side of the penis, proximal to the normal location in the glans penis

77
Q

What is hypospadias associated with?

A
  • Ventral penile curvature
  • Disorders of sexual differentiation
  • Undescended testicles
  • Inguinal hernia
78
Q

What is an absolute contraindication to circumcision?

A

Hypospadias

  • Or epispadias, penile curvature and other genitalial problems
  • The foreskin may be utilized in surgical correction for these conditions
79
Q

What is the average age of incidence for Wilm’s tumour/nephroblastoma?

A

3 years

80
Q

What is the chance that Wilm’s tumour is bilateral?

A

5%

81
Q

What is the common clinical presentation of Wilm’s tumour?

A
  • Large, firm and unilateral abdominal mass
  • Hypertension in 25%
  • Flank tenderness
  • Microscopic hematuria
  • Nausea/vomiting
82
Q

What is the management plan for Wilm’s tumour?

A
  • Check for contralateral involvement
  • Unilateral: radical nephrectomy +/- RT +/- chemo
  • Bilateral: neoadjuvant chemo + nephron-sparing OT
83
Q

What are the complications of cryptorchidism?

A
  • Reduction in fertility
  • Increased malignancy risk
  • Increased risk of testicular torsion
84
Q

What are the types of disorders of sexual differentiation?

A
  1. 46XY
    • Defect in testicular synthesis of androgens
    • Androgen resistance in target tissues
    • Palpable gonad
  2. 46XX
    • Congenital adrenal hyperplasia
  3. Ovotesticular DSD
  4. Mixed gonadal dysgensis
    • 46XY
    • 45XO
85
Q

When should reconstruction of external genitalia take place in patients with disorders of sexual differentiation?

A

6-12 months

86
Q

What is circumcision?

A

Removal of some or all of foreskin from the penis

87
Q

What are the medical indications for circumcision?

A
  • Phimosis and recurrent phimosis
  • Recurrent UTIs
  • Balantitis xerotica obliterans or other inflammatory conditions
88
Q

What are the contraindications for circumcision?

A
  • Unstable/sick infants
  • Congenital genital abnormalities: hypospadias
  • Family history of bleeding disorders
89
Q

What are the possible complications of circumcision?

A
  • Bleeding
  • Infection
  • Penile entrapment
  • Glans injury
  • Penile sensation defects
90
Q

What are the features suggestive of pyelonephritis?

A
  • High-grade fever
  • Flank or high abdominal pain
  • Costo-vertebral angle tenderness on palpation
91
Q

What are the possible causative organisms of urinary tract infections in children?

A
  • Gram-negative bacteria
    >> E. COLI
    >> Klebsiella
    >> Proteus
    >> Enterobacter
    >> Pseudomonas
  • Gram-positive bacteria
    >> Staph. saprophyticus
    >> Enterococcus
  • Viral
    >> Adenovirus
  • Fungal
    >> Candida albicans

E. coli causes ~70% of all urinary tract infections

92
Q

How does constipation increase the risk of urinary tract infections?

A

Compression of the bladder and the bladder neck increases bladder storage pressure and post-voiding residual urine volume.

A distended colon also provides a reservoir for pathogens.

93
Q

What are the risk factors for urinary tract infections?

A
  • *Non-modifiable**
  • Female gender
  • Caucasian
  • Previous UTIs
  • Family history

Modifiable
- Urinary tract abnormalities
>> Posterior urethral valve
>> Obstructive uropathy
>> Neurogenic bladder
>> Vesicoureteral reflux
- Dysfunctional voiding
- Repeated bladder catheterizations
- Uncircumcised males
- Labial adhesions
- Sexually active
- Constipation

94
Q

How can we diagnose UTI?

A
  • Gold standard by culture of urine specimen
    >> Clean-catch midstream urine sample
    >> Suprapubic aspiration
    >> Urinary catheterization
  • Urine dipstick
    >> Nitrite
    >> Leukocyte esterase
  • Urine microscopy
    >> For WBC
    >> Examine urine specimen within 2 hours of voiding
95
Q

Why is nitrite elevated in UTI?

A

Gram-negative bacteria in the urine reduces dietary nitrate to nitrite, and thus nitrite will be elevated in UTI dipstick.

>> Sensitivity 37%
>> Specificity 100%
>> PPV 90%, NPV 100%

96
Q

What are other causes of presence of leukocyte/+ve leukocyte esterase in urine dipstick other than UTI?

A
  • Vaginal secretions
  • Dehydration
  • Glomerulonephritis
  • Interstitial nephritis
  • Tuberculosis
97
Q

What are the complications of urinary tract infection?

A
  • Renal scarring
  • Hypertension
  • Proteinuria
  • End-stage renal disease
98
Q

What are the criteria for atypical UTI?

A
  • Severely ill
  • Septicaemia
  • Poor urine flow/output
  • Abdominal or bladder mass
  • Increased creatinine
  • Infection of non E.coli organisms
  • Lack of response to antibiotic treatments after 48 hours
99
Q

What are the criteria for recurrent UTI?

A

Any one of the following within 1 year:

  • 2 or more episodes of upper urinary tract infection/acute pyelonephritis
  • 1 episode of upper urinary tract infection/acute pyelonephritis and 1 or more episodes of lower urinary tract infection/cystitis
  • 3 or more episodes of lower urinary tract infection/cystitis
100
Q

What are the indications for hospital admission of UTI?

A
  • <3 months of age
  • Immunocompromised
  • Persistent vomiting
  • Inability to tolerate oral medication
  • Moderate-severe dehydration
  • Urosepsis
  • Complex urologic pathology
  • Inadequate follow-up
  • Failure to respond to outpatient therapy
101
Q

What is the management of acute UTI?

A
  • *Supportive management**
  • Hydration
  • Pain control

Antibiotics treatment
- According to urine dipstick
>> WBC +, nitrite +: start and send urine for culture
>> WBC -, nitrite +: start and send urine for culture
>> WBC +, nitrite -: hold and send urine for culture
>> WBC -, nitrite -: ABx not necessary
- Neonates: admit for IV ampicillin and gentamicin
- >3 months with upper tract infection
>> Oral antibiotics (cephalexin/Augmentin) x 7-10 days
>> IV antibiotics (ceftriaxone) x 2-4 days
+ oral ABx (cephalexin/Augmentin) for the remaining days until 10 days
- >3 months with lower tract infection
>> Oral antibiotics x 3 days
(TMP-SMX, nitrofurantoin, cephalosporins, amoxicillin)
>> Reassess if still unwell after 48 hours

Imaging
- <6 months old
>> Recurrent UTI
:: USG kidneys during acute illness
:: DMSA 4-6 months after acute illness
:: MCUG
>> Atypical UTI
:: USG kidneys during acute illness
:: DMSA 4-6 months after acute illness
:: MCUG
>> UTI resolving within 48hours of ABx initiation
:: USG kidneys within 6 weeks of acute illness
:: Consider MCUG if USG is abnormal only
- >6 months of age
>> Recurrent UTI
:: USG kidney within 6 weeks of acute illness
:: DMSA 4-6 months after acute illness
>> Atypical UTI
:: USG kidney during acute illness
:: DMSA 4-6 months after acute illness
>> UTI resolving within 48 hours of ABx initiation
:: No imaging necessary
- >3 years of age
>> Recurrent UTI
:: USG kidney within 6 weeks of acute illness
:: DMSA 4-6 months after acute illness
>> Atypical UTI
:: USG kidneys during acute illness only
>> UTI resolving within 48 hours of ABx initiation
:: No imaging necessary

102
Q

What are we looking for in an USG kidney?

A
  • Congenital renal and urinary tract anomalies
    >> Hydronephrosis
    >> Ectopic kidney
    >> Duplex collecting system
    >> UPJ obstruction
    >> Uretocele
  • Renal abscess
  • Acute focal bacterial nephritis
103
Q

What is the voiding/micturating cystourethrogram (VCUG/MCUG) for?

A

Gold standard for diagnosing VUR (vesico-ureteric reflux)

>> Should be performed after completion of antibiotics

104
Q

What is the DMSA (dimercaptosuccinic acid) for?

A

Diagnosing renal scarring
>> More sensitive than USG or CT scan

Also sensitive in diagnosing acute pyelonephritis, but does not change clinical management

105
Q

Does primary vesicoureteric reflux resolve spontaneously?

A

YES!

Over 5 years:
Grade I: 82%
Grade II: 80%
Grade III: 40%
Grade IV: 30%
Grade V: 13%

>> Resolution of VUR is particularly true of mid-to-moderate grades of VUR, caused by the lengthening of the submucosal segment of the ureter

106
Q

What are the complications of VUR?

A
  • Recurrent urinary infections
  • Hypertension (20%)
  • Proteinuria
    >> Microalbuminuria
    >> Persistent proteinuria
    >> Nephrotic range of proteinuria
  • End-stage renal disease
107
Q

What are the 4 most common causes of end-stage renal failure in children?

A
  • Obstructive uropathy
  • Renal hypolasia/aplasia
  • Focal segmental glomerular sclerosis (FSGS)
  • Vesicoureteric reflux
108
Q

What is enuresis?

A

Voluntary or involuntary repeated discharge of urine into clothes or bed after a developmental age when bladder control should have been established

109
Q

How can we classify enuresis?

A
  • *Primary noctural enuresis**
  • Lifelong bed-wetting (~90%)
  • Persistent bed-wetting since early childhood until >= 7 years of age
  • A form of personal-social developmental delay
  • *Secondary nocturnal enuresis**
  • Acquired enuresis after being dry for a minimum of 6 months
110
Q

When are children usually toilet-trained?

A

Most children of normal intelligence & health are dry by day before the 5th birthday
>> Dry by NIGHT at a later age

111
Q

What are the risk factors for primary nocturnal enuresis?

A
  • Familial nocturnal enuresis
  • Environmental causes
    >> Later initiation of toilet training
    >> Stressful life events
    >> Lower socioeconomic groups
    >> Overcrowded conditions
  • Personal health causes
    >> Urinary tract infection
    >> Constipation
  • Maternal causes
    >> Maternal smoking
    >> Teenage pregnancy
112
Q

What are the possible causes of secondary nocturnal enuresis?

A
  • *Inorganic causes**
  • Stress
  • Anxiety

Organic causes
- Urinary tract infections
- Polyuric states
>> Diabetes mellitus
>> Diabetes insipidus
- Neurological causes
>> Neurogenic bladder
>> Cerebral palsy
>> Seizures
- Systemic diseases
>> Sickle cell disease

113
Q

What is the management for primary nocturnal enuresis?

A
  1. Time and reassurance (~20% spontaneous resolution each year)
  2. Lifestyle modifications
    >> Avoid fluid intake 2 hours before bedtime
    >> Voiding before sleep
  3. Reward system with star chart - involve child
  4. Enuresis alarm
    >> Works by conditioning
    >> Requires highly-motivated parents and child
    >> Success rate 60-80% in 4 months
  5. Drugs
    >> DDAVP/desmopressin: short-term use; associated with quick relapse
    >> Oxybutynin: anticholinergic effect (detrusor tone)
    >> Imipramine: anticholinergic; not recommended due to narrow therapeutic window and lethal side effects
114
Q

What are the possible complications of imipramine overdose?

A
  • Ventricular tachycardia
  • Seizures
  • Coma
115
Q

What are the side effects of desmopressin?

A
  • Hyponatremia
  • Abdominal discomfort
  • Headache
116
Q

What is diurnal enuresis?

A

Daytime wetting (60-80% also associated with nocturnal enuresis)

117
Q

What are the possible causes of diurnal enuresis?

A
  • Micturition deferral due to psychosocial stress
  • Structural abnormalities
    >> Ectopic urethra
    >> Neurogenic bladder
  • Urinary tract infection
  • Constipation
  • CNS disorders
    >> CP
    >> Seizures

Paediatrics (16 decks)

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