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Child health > Nephrology and genitourinary 3 (important) > Flashcards

Nephrology and genitourinary 3 (important) Flashcards

1
Q

What is the treatment of pyelonephritis in <3 months old infants

A

Infant < 3 months:
Refer to paediatric specialist.
PO antibiotics 7-10 days (eg. cephalosporin or co-amoxiclav have low resistance patterns)

If IV has to be used, then cefotaxime or ceftriaxone for 2-4 days followed by oral until 10 days of abx

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2
Q

What is the treatment of pyelonephritis in >3 months old infants and children

A

Oral antibiotics for 3 days. Trimethoprim, nitrofurantoin, cephalosporin or amoxicillin

Advise parent to bring back child if still unwell after 24-48 hours

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3
Q

Features of AKI in children

A

Renal failure is most severe: oliguria (<0.5ml/kg/h)

AKI is a sudden reduction in glomerular filtration rate, resulting in increased blood concentration of urea and creatinine nad disturbed fluid and electrolyte homeostasis

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4
Q

Classify AKI

A

Pre-renal: commonest cause in children

Renal: salt and water retention; blood and protein in urine, symptoms of specific disease? (eg. HUS)

Postrenal - urinary obstruction (eg. posterior urethral valves or blocked urinary catheter)

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5
Q

Prerenal causes of AKI

A 
Hypovolaemia:
D+V
Burns
Sepsis
Haemorrhage
Nephrotic syndrome

Circulatory failure

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6
Q

Renal causes of AKI

A

Vascular:
HUS
Vasculitis
Embolus

Tubular:
Acute tubular necrosis
Ischaemic
Toxic

Glomerulonephritis

Interstitial nephritis
Pyelonephritis

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7
Q

Management of prerenal AKI

A

Usually there is hypovolaemia (with sodium depletion):

fluid replacement and circulatory support to avoid tubular necrosis

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8
Q

Management of renal AKI

A

If there is circulatory overload: may restrict fluid and challenge with a diuretic

High-calorie, normal protein feed to decrease catabolism, uraemia and hyperkalaemia

Emergency management of metabolic acidosis, hyperkalaemia and hyperphosphataemia

Renal biopsy if the cause of renal failure not obvious (can identify rapidly progressing glomerulonephritis (needs immediate immunosuppression))

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9
Q

What are the commonest renal causes of acute renal failure in children in the UK

A

HUS

Acute tubular necrosis (usually in multisystem failure)

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10
Q

Management of post-renal renal failure

A

assess site of obstruction

relieve by nephrostomy or bladder catheterisation

Surgery, once fluid volume and electrolyte abnormalities corrected

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11
Q

The triad of abnormalities which define HUS

A

Acute renal failure
Haemolytic anaemia
Thrombocytopenia

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12
Q

Commonest organisms causing diarrhoea associated HUS in childhood

A

Typically secondary to gastrointestinal infection with verocytotoxin-producing E.coli (acquired through contact with farm animals or eating uncooked beef..

Less often Shigella

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13
Q

Features of verocytotoxin-producing E.coli causing diarrhoea leading to HUS (pathophysiology)

A

Prodrome of bloody diarrhoea

Toxin localises to enothelial cells of kidney - causes intravascular thrombocytogenesis

Coagulation cascade is activated and platelets become consumed. Microangiopathic haemolytic anaemia results from damage to RBCs as they circulate through the microcirculation (occluded)

Brain, pancreas and heart may also be involved

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14
Q

Prognosis of diarrhoea associated HUS

A

With early supportive therapy, including dialysis - good prognosis

Folow-up for persistent proteinuria/HTN/declining renal function in following years

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15
Q

Prognosis of non-diarrhoea associated HUS (atypical)

A

Familial?
Frequent relapse

High risk of HTN and chronic renal failure in later life

High mortality

Children with intracerebraö involvement or atypical HUS may be treated with plasma exchange, but efficacy is unproven

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16
Q

What is chronic renal failure (stages)

A

GFR < 15ml/min per 1.73m^2
Quite rare in children. Usually congenital (structural, glomerulonpehritis, hereditary nephropathies, systemic disease).

1: normal GFR>90ml/min1.73m^2 and persistent albuminuria
2: GFR 60-89 and persistent albuminuria
3: GFR 30-59
4: GFR 15-30
5: GFR < 15 or end-stage renal disease

17
Q

Clinical features of chronic kidney disease

A

Anorexia
Lethargy
Polydypsia
Polyuria

FTT
Bone deformities
HTN
Acute-on-chronic renal failure
Proteinuria
Normochronic, normocytic anaemia

Symptoms rarely develop before GFR <30.
Most picked up antenatally on US

18
Q

Which aspects of chronic renal failure need to be managed? (think MDT)

A 
Diet
Prevent renal osteodystrophy
Control of salt and water balance
Control acidosis
Anaemia
Hormonal abnormalities
Dialysis and transplantation
19
Q

Dietary management pf CKD

A

Calorie supplements and NG or gastrostomy feeding often necessary to optimise growth

(anorexia and vomiting common)

Protein intake sufficient for growth and albumin, but low enough to prevent accumulation of toxic metabolic products

20
Q

Prevention of renal osteodystrophy in CKD

A

Decreased activation of Vit D leads to Phosphate retention and hypocalcaemia.

Leads to secondary hyperparathyroidism - causes osteitis fibrosis and osteomalacia

Thus, phosphate restriction (few milk products)
Calcium carbonate (bind phosphate)
Activated vit D supplements
21
Q

Control of salt and water balance and acidosis in CKD

A

Many children with CKD caused by congenital malformationss and renal dysplasia have obligatory loss of salt and water.

Salt supplements and free access to water.

Bicarbonate supplements to prevenet acidosis

22
Q

Managing anaemia in CKD

A

Due to reduced EPO production of circulation of metabolites that are toxic to bone marrow..

Administer recombinant human EPO

23
Q

Manage hormonal abnormalities in CKD

A

GH resistance with high GH levels but poor growth

recombinant human GH can improve growth for up to 5 years of treatment.. But whether it improves final height is unknown

Many children with CKD have delayed puberty and subnormal pubertal growth spurt

24
Q

Role of dialysis and transplant in CKD

A

All children can enter renal replacement programme when in end-stage renal failure

> 10kg is necessary though, to avoid renal vein thrombosis

Best chance with kidney from related (living) donor

There are graft losses even with living donor. (acute rejection)

Immunosuppression with combo of prednisolone, tacrolimus and azathrioprine

Ideally transplant should occur before dialysis is needed. Otherwise, dialysis can be started.
Peritoneal dialysis: cycling overnight woth a machine (continuous cycling peritoneal dialysis)
or
manual exchanges over 24 h (continuous ambulatory peritoneal dialysis) which can be done by the parents at home and is therefore less disruptive

Haemodialysis can be done in hospitals (3-4 per week)

25
Q

General trend in BP throughout childhood? How is it compared? What is HTN

A

increases with age and height

Reading should be plotted on a centile chart. (SBP vs age or height)

HTN is BP >95th percentile for height, age and sex

26
Q

What are the commonest causes of HTN in children

A

Renal, cardiac or endocrine

Renal:
Parenchymal disease
Renal artery stenosis
Polycystic kidney disease
Renal tumours

Coarctation of the aorta

Endocrine:
CAH
Cushing syndrome or corticosteroid therapy
Hyperthyroidism

Catecholamine excess:
phaeochromocytoma
neuroblastoma

Essential HTN is a diagnosis of exclusion

27
Q

Presentation of HTN in children

A 
Vomiting
Headaches
Facial palsy
HTN
Retinopathy
Convulsion
proteinuria

FTT and cardiac failure in infants (paroxysmal palpitations/sweating with phaeochromocytoma)

28
Q

Investigations in children with HTN and their importance

A

Some causes are correctable:

Nephrectomy for unilateral scarring (DMSA)
Angioplasty for renal artery stenosis
Surgical repair of coarctation of the aorta
Resection of phaeochromocytoma

In most cases, however antihypertensives have to be taken

HTN can cause serious damage to organs and bleeds
-cause needs to be found and managed.

Early detection of HTN is very important - any child with renal abnormality should have yearly checks.

Children with a FH of essential HTN should be encouraged to restrict salt intake, avoid obesity and regularly check BP

29
Q

What are the presenting features of urinary tract abnormalities

A

Most identified on US scan (1 in every 200-400)

Abnormal renal development or function
Postnatal infection
Can involve urinary obstruction which needs surgery

30
Q

Which anomalies can present on antenatal ultrasound

A

Absence of both kidneys (renal agenesis) - severe oligohydramnios which results in Potter syndrome

Multicystic dysplastic kidney - non-functioning structure with large fluid-filled cysts and no renal tissue or connection to bladder

Autosomal dominant or recessive polycystic kidney disease: some renal function is maintained, but both kidney affected

Pelvic or horseshoe shaped kidney - predispose to infection or obstructs drainage

Posterior urethral valves (leads to urinary outflow obstruction)

Hydronephrosis

31
Q

Which investigations are used for diagnosing antenatal urinary tract abnormalities?

A

GFR is low in a newborn, especially in a premature infant! (15-20ml/min)
Rises to normal adult rate by 2 years

Ultrasound - anatomical assessment
DMSA scan - functional defects
MCUG/VCUG - visualise bladder and urethral anatomy and can detect both reflux and obstruction

MAG3 isotope scan - isotopes excreted from the blood into the urine

Plain abdo X ray - spinal abnormalities and potentially renal stones

32
Q

Managing bilateral hydronephrosis in a male infant?

A

Usually picked up on antenatal scan

Start prophylactic antibiotics at birth

Ultrasound shortly after birth (within 48h)! To exclude posterior urethral valves which ALWAYS require urological intervention (eg. cystoscopic ablation)

If negative, then stop antibiotics and repeat US after 2-3 months

33
Q

Protocol for antenatally found unilateral hydronephrosis or any anomaly in a female?

A

Start prophylactic antibiotics at birth

Do an ultrasound at 4-6 weeks. If normal, stop abx.

Otherwise do more investigations (eg. micturating cystourethrogram (MCUG))

Child health (51 decks)

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