Paeds - Fever without a focus Flashcards

1
Q

What is the difference between sepsis and septicaemia?

A

Septicaemia = when bacteria enter bloodstream, and cause blood poisoning which triggers sepsis

Sepsis = life-threatening physiological response to infection that causes systemic inflammation, organ failure and death

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2
Q

In which (adults or children) should symptoms of a UTI prompt an investigation for underlying causes / kidney damage?

A

Children

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3
Q

What are the common causative organisms of a UTI in children?

A

E. Coli ( ~ 80% of cases)

  • Proteus
  • Pseudomonas
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4
Q

What factors predispose children to developing a UTI?

A
  1. incomplete emptying
  2. infrequent voiding - resulting in bladder enlargement
  3. hurried micturition
  4. obstruction by full rectum due to constipation
  5. neuropathic bladder
  6. vesicoureteric reflux - abnormal backflow of urine from bladder into ureter / kidney (present in ~30% of children who present with UTI)
  7. poor hygiene - not wiping front to back in girls
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5
Q

Up till 3 months of age, UTIs are more common in which gender?

A

Males (due to more congenital abnormalities)

then it becomes substantially higher in girls past 3-months

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6
Q

How does a UTI present for the following age groups:

  • Infants
  • Children
A

Infants:

  • Fever
  • Poor feeding
  • Vomiting
  • Irritability
  • Jaundice
  • Offensive urine smell
  • Febrile convulsions ( > 6-months old)

Children:

  • Fever
  • Dysuria
  • Urinary frequency
  • Abdo pain or loin tenderness
  • Haematuria
  • Vomiting
  • Diarrhoea
  • Constipation
  • Lethargy
  • Recurrence of enuresis
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7
Q

Dysuria without other symptoms is often due to

what in each of boys / girls?

A

Boys = balanitis (in uncircumcised boys)

Girls = vulvitis

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8
Q

In Infants what ways can be used to collect a urine sample?

A
  1. ‘Clean-catch’ (preferred) - sample into a waiting clean pot when nappy is removed
  2. Urine collection pads - can be used if a clean-catch sample is not possible
    • Never use cotton wool balls or gauze to obtain a sample
  3. Urethral catheter - if sample is urgent + no urine is being passed
  4. Suprapubic aspiration (SPA) /w ultrasound to confirm urine present in bladder - only to be used if non-invasive methods aren’t possible
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9
Q

How are UTI’s in children managed?

A
  • < 3-months old –> immediate referral to hospital (require IV Abx e.g. cefotaxime)
  • > 3-months old + upper UTI –> consider admission to hospital
    • if not admitted –> oral Abx for 7-10 days e.g. cephalosporin or co-amoxiclav
  • > 3-months old + lower UTI –> oral Abx for 3 days e.g. trimethoprim, nitrofurantoin, cephalosporin or amoxicillin
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10
Q

Which 2 features on a Urine dipstick can be used to indicate whether a pt likely has a UTI?

A

Leucocyte esterase (+ve)

&

Nitrite (+ve)

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11
Q

For each of the following 4 urine dipstick results in a child what action do you take?

  1. Leucocyte +ve & Nitrite +ve
  2. Leucocyte -ve & Nitrite +ve
  3. Leucocyte +ve & Nitrite -ve
  4. Leucocyte -ve & Nitrite -ve
A

If the conclusion of a urine dipstick is that a UTI is likely then:

  1. Send a clean-catch sample (or other suitable sample) for M,C&S
  2. Start antibiotics whilst awaiting urine culture
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12
Q

What features are measured on a urine dipstick?

A
  • Leucocyte esterase
  • Nitrates
  • Glucose
  • Blood
  • Protein
  • Ketones
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13
Q

For each of the following aspects of a urine dipstick, if the result is abnormal what subsequent test might you suggest?

  • Glucose
  • Blood
  • Protein
  • Ketones
A

Glucose:

  • Indicative of: Diabetes
  • Action: Check blood glucose / HbA1C

Blood:

  • Indicative of: Tumour, trauma or infection
  • Action: if no indication or infection then USS urgent

Protein:

  • Indicative of: Tubular or glomerular disease
  • Action: Recheck, check Protein:Creatinine ratio

Ketones:

  • Indicative of: Fat metabolism e.g. fasting as compensation of DKA
  • Action: monitor or consider checking blood glucose
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14
Q

What are the hallmarks of nephrotic syndrome?

A
  1. Proteinuria ( > 3.5g / 24hrs, ++++ Protein dipstick, frothy urine)
  2. Hypoalbuminaemia (< 30g/L)
    • albumin lost in urine due to gaps in podocytes of glomerulus
  3. Oedema
    • albumin lost in urine –> ↓ intravascular oncotic pressure –> fluid moves into into surrounding tissues
  4. Hyperlipidemia
    • liver compensates for hypoalbuminaemia by ↑ production, but side effect is ↑ lipid production

Also you will see:

  • Lipiduria
  • Loss of immunoglobulins –> increased risk of infection
  • Loss of antithrombin-III, proteins C and S (endogenous anticoagulants) –> increase thrombosis risk
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15
Q

Proteinuria can occur transiently for physiological reasons (non pathological),

name some instances where this can occur?

A
  1. Post-exercise (transient but can by up to 10g/day)
  2. Post-prandial (transient & thought to be due to insulins actions on podocytes)
  3. Febrile illness
  4. Orthostatic proteinuria (only when upright and not during early morning)
  5. Pregnancy
  6. High BP
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16
Q

What are the 4 main features of Nephritic Syndrome?

A
  1. Haematuria (+++ Blood dipstick - microscopic or macroscopic)
    • Possible ‘red cell casts’ = microscopic cylindrical structure, present in urine, produced in nephrons in diseased states
    • Haematuria occurs due to gaps in podocytes of glomerulus
  2. Proteinuria (++ Protein dipstick = small amount)
  3. Hypertension (usually mild)
  4. Low Urine Volume (i.e. oliguria, < 300 ml/day) - due to ↓ renal function
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17
Q

Which has greater sensitivity for low levels of proteinuria;

Protein:creatinine ratio

OR

Albumin:creatine ratio

A

Albumin : Creatinine Ratio

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18
Q

Which method of monitoring proteinuria is recommended for diabetics;

Protein:creatinine ratio

OR

Albumin:creatine ratio

A

Albumin : Creatine ratio

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19
Q

What are normal values for:

  1. Adult PCR (Protein : Creatinine ratio)
  2. Child PCR (Protein : Creatinine ratio)
  3. ACR (Albumin : Creatinine ratio)
A

Adult PCR < 15 mg/mmol

Child PCR < 20 mg/mmol

ACR < 3 mg/mmol

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20
Q

Reminder: what is the classic triad of nephrotic syndrome?

How are the values for this triad different in children?

A

Nephrotic syndrome Triad:

  1. Proteinuria > 1 g/m2/24hrs (as opposed to > 3.5g/24hrs)
  2. Hypoalbuminaemia < 25 g/L (as opposed to < 30 g/L)
  3. Oedema
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21
Q

At what ages is nephrotic syndrome most common in children?

A

2 -5 years old

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22
Q

What are ~80% of Nephrotic Syndrome cases in children

due to?

A

Minimal Change Glomerulonephritis

~80% of childhood nephrotic syndrome

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23
Q

For the following, at what threshold do we diagnose Proteinuria?

  1. Protein : Creatinine ratio
  2. Albumin : Creatinine ratio
A
  1. Adult - PCR > 15 mg/mmol = proteinuria
  2. Child - PCR > 20 mg/mmol = proteinuria
    1. PCR > 200 mg/mmol = nephrotic range
  3. ACR > 30 mg/mmol
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24
Q

Which protein is secreted by renal tubules up to 150 mg/day

and forms the boundary for the normal level of protein in urine

(<150 mg/day)?

A

Tamm-Horsfall Glycoprotein (THP) also called Uromodulin

  • > 150 mg/day = proteinuria –> suggests ↑ glomerular permeability
  • This protein is not tested for by urine dipstick (which usually tests for albumin)
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25
Q

What is the commonest cause of nephrotic syndrome in adults?

A

Membranous Nephropathy / Membranous Glomerulonephritis

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26
Q

What can cause Minimal Change Glomerulonephritis (MCG)?

A

Most cases = Idiopathic!!

10-20% of cases due to:

  • Drugs: NSAIDs, rifampicin
  • Hodgkin’s lymphoma or thymoma
  • Infectious mononucleosis (glandular fever)
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27
Q

What are the features of MCG?

A
  • Nephrotic syndrome
    • Hyperproteinuria is selective i.e. only intermediate-sized proteins such as albumin & transferrin leak through the glomerulus
  • Normal BP (HTN is rare)
  • Renal biopsy:
    • Normal glomeruli on light microscopy
    • Electron microscopy shows fusion of podocytes + flattening of foot processes
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28
Q

How is minimal change glomerulonephritis managed?

A
  1. Corticosteroids - majority of cases (80%) are steroid-responsive
  2. Fluid restriction + low-salt diet - to manage oedema
  3. Penicillin prophylaxis - nephrotic oedema can cause ascites –> increased risk of spontaneous peritonitis
  4. Cyclophosphamide - if steroid-resistant (alternatives = ciclosporin / tacrolimus)
    • Cytotoxic (alkylating agent) –> forms cross-linking of DNA
    • SE: haemorrhagic cystitis, myelosuppression, transitional cell carcinoma
29
Q

What is the prognosis of minimal change glomerulonephritis?

A

Rule of 1/3rds

  • 1/3 have just one episode
  • 1/3 have infrequent relapses
  • 1/3 have frequent relapses which stop before adulthood
30
Q

What are the complications of minimal change glomerulonephrtiis in childhood?

A
  • Streptococci infection - can be sudden & severe
    • A pneumococcal infection is caused by Streptococcus pneumoniae
  • Spontaneous peritonitis
    • nephrotic oedema often causes ascites which predisposes those with minimal change disease to spontaneous peritonitis
    • Penicillin prophylaxis = common
  • Recurrent minimal change disease
    • 1/3rd infrequent relapse, 1/3rd frequent relapse & stopping before adulthood
31
Q

When in gestation do the kidneys begin to form?

A

5-weeks gestation

(glomeruli still forming until 34-weeks(

32
Q

What is the commonest congenital renal anomaly?

A

Renal Hypoplasia

33
Q

What is renal dysplasia?

A

Renal dysplasia:

A congential kidney malformation which results in a undifferentiated kidney, sometimes with cysts

(worse kidney function than renal hypoplasia)

34
Q

What is renal hypoplasia?

A

A congenital kidney malformation, which results in fewer nephrons than normal

35
Q

What are the features of an inguinal hernia?

A
  • Account for 75% of abdominal wall hernias
  • Male - ~ 95% of inguinal hernias are in men
  • Groin lump - disappears on pressure or when the patient lies down
  • Discomfort & ache - worse with activity, severe pain is uncommon
  • Stragulation = rare
36
Q

How are inguinal hernias managed?

A

Despite anatomical differences between; indirect (hernia through the inguinal canal) and direct hernias (through the posterior wall of the inguinal canal) –> they are managed the same!

  • Laproscopic mesh repair - even is asymptomatic
    • risk of strangulation is higher in children

Complications of surgery:

  • Early: bruising, wound infection
  • Late: chronic pain, recurrence
37
Q

What is Hypospadias?

A

Hypospadias is a congenital abnormality of the penis (3 in 1000 infants) in which the opening of the urethra is on the underside of the penis

Is 2nd most common birth abnormality of male reproductive system

Characterised by:

  1. Ventral urethral meatus (underside) - can also be more proximal than normal
  2. Hooded glans of penis - due to underdevelopment of foreskin on underside of penis
  3. Chordee (ventral curvature of the penis) - severe forms
38
Q

How is Hypospadias managed?

A

Corrective surgery before 2-years old

ESSENTIAL that child is NOT circumcised prior as foreskin may be used in corrective procedure!

Very distal disease = no treatment

39
Q

Name some risk factors for UTI and serious underlying pathology in children (< 16yrs) - NICE list

A
  • recurrent fever of uncertain origin
  • poor growth
  • high BP
  • constipation
  • poor urine flow
  • Hx of previous UTI
  • Fhx of vesicoureteric reflux (VUR) or renal disease
  • dysfunctional voiding
  • enlarged bladder
  • abdominal mass
  • spinal lesion
  • antenatally-diagnosed renal abnormality
40
Q

What are the NICE definitions of recurrent UTI for < 16 yrs?

A
  • 2 or more upper UTI
  • 1 upper + 1 lower UTI
  • 3 or more lower UTI
41
Q

Seperate the following features as to whether they make a child’s presentation more likely to be due to Upper or Lower urinary tract infection:

  • Bacteriuria + fever of 38 or higher +/- loin tenderness
  • Age > 3 months, no systemic features
  • Bacteriuria but no systemic features
  • Bacteriuria, loin pain/tenderness + fever < 38C
  • Age < 3 months
A

Upper UTI:

  • Bacteriuria + fever of 38 or higher +/- loin tenderness
  • Bacteriuria, loin pain/tenderness + fever < 38C
  • Age < 3 months

Lower UTI:

  • Bacteriuria but no systemic features
  • Age > 3 months, no systemic features
42
Q

For an infant < 6-months old, what imaging investigations need to be arranged for the following scenarios:

  • Pt responds well to treatment within 48hrs
  • Atypical UTI
  • Recurrent UTI
A
43
Q

What is a DMSA scan?

A

A radionucleotide scan that uses dimercaptosuccinic acid (DMSA) to assess renal morphology, structure and function

  • Radioactive technetium-99m is combined with DMSA and injected into a patient
  • Then gamma camera imaging done 2-3 hrs later
  • Unhealthy or scarred renal tissue doesn’t take up the isotope –> appears as filling defect on DMSA
  • Test is VERY sensitive so needs to be done 4-6 months AFTER acute infection so as to avoid diagnosing ‘false’ scars
44
Q

What is a MCUG?

A

A micturating cystourethrogram (MCUG) is a scan that shows how well a child’s bladder works (sometimes valled voiding cystourethrogram)

  • Patient is catheterised & bladder filled with radiocontrast
  • Under fluroscopy (real-time x-rays) a radiologist watches to see if the contract moves into the ureters / kidneys –> diagnosis = vesicoureteral reflux (VUR)
  • Also used to diagnose:
    • bladder abnormalities
    • posterior urethral valves
45
Q

What is the NICE definition of an Atypical UTI?

A

Atypical UTI includes any of the following:

  • Seriously ill
  • Poor urine flow
  • Abdominal or bladder mass
  • Raised creatinine
  • Septicaemia
  • Failure to respond within 48 hours
  • Non E coli organism infection
46
Q

For an child > 6-months old but < 3-years, what imaging investigations need to be arranged for the following scenarios:

  • Pt responds well to treatment within 48hrs
  • Atypical UTI
  • Recurrent UTI
A
47
Q

For an child > 3-years, what imaging investigations need to be arranged for the following scenarios:

  • Pt responds well to treatment within 48hrs
  • Atypical UTI
  • Recurrent UTI
A
48
Q

Why is screening done in various UTI scenarios in children?

A

Because early detection and treatment of UTI’s and associated urinary tract abnormalities is hoped to reduce the likelihood of end stage renal disease in later life

49
Q

What advise might you give to parents to safety net for future instances of UTIs?

A

If child has fever without an obvious cause –> bring them in for:

  1. urine sample
  2. M,C&S
  3. Abx (pending result of urine culture)

This practice should this should minimise any potential kidney scarring

50
Q

What is Nocturnal Enuresis?

A

Nocturnal enuresis is intermittent involuntary voiding during sleep in the absence of physical disease in a child aged > 5-yrs

51
Q

What are the diagnostic criteria for nocturnal enuresis?

A

Minimum of 1 episode per month for at least 3-months

52
Q

What is the difference between primary and secondary nocturnal enuresis?

A
  • Primary = child has never achieved continence
    • Consider - detrusor instability (sudden, urge to void due to contractions), neuropathic bladder (bladder enlarged, fails to empty properly, irregular thick wall, associated with neuro conditions), constipation, ectopic ureter
  • Secondary = child has been dry for at least 6-months before
    • Consider - Diabetes, emotional upset, UTI
53
Q

What features is nocturnal enuresis associated with?

A
  • Daytime urinary incontinence
  • Nocturnal polyuria
  • Reduced bladder capacity
  • Lack of inhibition of bladder emptying during sleep
  • Bowel problems
  • Developmental or psychological problems
  • Defective sleep arousal & disturbed sleep/wake cycle
  • Sleep disorder breathing
54
Q

How is Nocturnal Enuresis managed?

A
  1. Drink 6-8 cups of water during the day and not near bedtime
  2. Avoid tea, coffee, hot chocolate and fizzy drinks
  3. Wee just before going to bed (empty bladder)
  4. Diet involving enough fruit and veg to aid bowel movements (constipation can put pressure on bladder)
  5. Enuresis alarm - have sensors to detect when child starts urinating and wakes them up
  6. Desmopressin (synthetic vasopressin) - upregulates aquaporin-2 in collecting duct –> increases reabsorption of water by kidneys (less urine)
55
Q

What genetic pattern does Adult Polycystic Kidney Disease (APKD) follow?

A

Autosomal dominant

  • Males and females are equally represented
  • There are affected individuals present in each generation after a condition has arisen
  • Spontaneous mutation are common in autosomal dominant conditions in general
  • Autosomal dominant conditions in general, variable penetrance (variable gene expression) is common
56
Q

What condition can posterior urethral valves cause?

A

Bilateral hydronephrosis

57
Q

Which investigation is best for identifying renal scars in children?

A

DMSA

58
Q

AKI in children is defined as what?

A

Acute, reversible, increase in serum creatinine + nitrogenous waste products coupled with the inability of the kidneys to appropriately regulate fluids and electrolytes

59
Q

What are the features of AKI in children?

A
  1. Increased serum creatinine or urea
  2. Reduced urine output (oliguria) < 0.5 ml/kg/hr for 8hrs
  3. eGFR < 0.55 mg/dL (1-13 years old)
  4. Oedema e.g. pulmonary or peripheral
  5. Uraemia symptoms - very diverse (late stage) e.g. nausea & vomiting, leg cramps, pericarditis or encephalopathy
60
Q

Which is the most common cause of AKI in children;

  • Pre-Renal (fluid depletion / poor renal perfusion)
  • Renal (intra-renal pathology)
  • Post-Renal (obstructive)
A

Pre-renal

61
Q

What is a normal eGFR in term infants?

A

15-20 ml/min per 1.73 m2

  • This value rises to the adult vales of 80-120 ml/min per 1.73 m2 at ~ 1-2 years of age
62
Q

Renal agenesis (absence of both kidneys) can be detected on antenatal ultrasound scan - what does this cause?

A

Since amniotic fluid is mainly derived from fetal urine, renal agenesis results in –> severe oligohydramnios (reduced amniotic fluid for gestational age)

Severe oligohydramnios –> causes Potter Syndrome (fatal)

Potter Syndrome Features:

  • Potter face (due to intrauterine compression) - low-set ears, beaked nose, epicanthic folds
  • Pulmonary hypoplasia –> resp failure
  • Limb deformities
63
Q

What 2 congenital renal disorders are associated with Potter’s Syndrome?

A
  1. Renal agenesis
  2. Multicystic dysplastic kidney (MCDK) - if bilateral
    • Affected kidney is non-functioning /w large fluid filled cysts & no connect to bladder
    • Shown in image
64
Q

Where can obstruction occur in the urogenital tract to cause unilateral hydronephrosis?

A
  1. Pelviureteric junction obstruction
  2. Vesicoureteric junction obstruction
65
Q

Where can obstruction occur in the urogenital tract to cause bilateral hydronephrosis?

A
  1. Bladder neck (e.g. dueto disruption of the nerve supply i.e. neuropathic bladder)
  2. Posterior urethra in a boy i.e. mucosal folds / membranes known as posterior urethral valves
66
Q

What is Vesicoureteric reflux (VUR)?

A

A developmental anomoly of the vesicoureteric junctions - resulting in abnormal backflow of urine from the bladder into the ureter / kidney

  • Ureters are displaced laterally + enter bladder directly (as opposed to at an angle) –> resulting in a shortened or absent intramural course –> vesicoureteric junction can’t function normally
  • Found in ~30% of children who present with a UTI
  • Severe cases –> renal dysplasia
  • Familial - 30-50% of occuring in 1st-degree relatives
  • Varying severity e.g.
    • Mild = reflux into distal end of an undilated ureter during micturition
    • Severe = reflux during bladder filling / voiding with a distended ureter, renal pelvis and clubbed calyces - so called intrarenal reflux (IRR)
  • Can occur with bladder pathology e.g. neuropathic bladder, urethral obstruction, or temporarilly post-UTI
67
Q

What complications are associated with VUR?

A
  • Infection (e.g. pyelonephritis) due to Incomplete bladder emptying e.g. urine flowing from dilated ureters into the bladder post-micturition
  • Reflex nephropathy - scarred / shrunken segment of kidney
68
Q

How is vesicoureteric reflux diagnosed?

A

micturating cystourethrogram (MCUG)