Category Archives: General paediatrics

Scoring systems

Clinical, General paediatrics

As usual, any system that has reasonable sensitivity has rubbish specificity (negative predictive value).  Retrospective analysis of 9000 UK A&E attendees <15yrs –

  • a modified Yale Observation Scale (YOS) – sensitivity of 54.0% and specificity of 63.7% at a cut-off of 10.
  • Pediatric Advanced Warning Score (PAWS) – sensitivity of 58.0% and specificity of 81.3% if any ‘red’ sign was present.
  • Alert, Voice, Pain, Unresponsive (AVPU) scale;
  • Recognising Acute Illness in Children (RAIC) score; sensitivity of 76.0% and specificity of 6.2% for ruling out serious bacterial infection at a score of 5 or less.
  • Oxford Vital Signs score sensitivity of 80.0% and specificity of 49.3% if any sign was present.
  • 2007 version of NICE CG160 (Fever guideline) traffic light system. 100% sensitivity and specificity on 0.12% if any ‘amber’ or ‘red’ sign was present, and had sensitivity of 62% and specificity of 74.5% if any ‘red’ sign was present  But data available covered only a selection of red and amber features.

[Verbakel, Pediatric Emergency Care 2014; 30: 373–80]

Same author applied rules to different data sets across UK, Netherlands and Belgium, found that all had lower performance than in their original derivation studies, but also wide variation across datasets eg NICE CG160 specificity ranged from 1-28.7%! Hard to understand differences.  [BMC Medicine 2013; 11: 10]

Lacour scoring system (“Laboratory-Score”) based on CRP, PCT and urinalysis. Has sensitivity of 94%, spec of 81%. Would reduce incidence of antibiotic use from 65 to 40% but good enough? [Lacour, PIDJ 2008 PMID 18536624]

 

Malaria

General paediatrics, Infectious disease

Protozoal infection, spread by Anopheles mosquitoes.

A crippling problem in sub-Saharan Africa but also seen in South and South East Asia, Caribbean (Dominican Republic has low risk). The only malaria free zones in the tropics are cities (some) and communities at altitude. Used to be endemic in Europe (even Southern England) and southern states of US.  800 000 deaths per year, mostly young African children.  Hypoendemic areas eg SE Asia do not acquire immunity and whole population is at risk of severe disease.

Resistance continues to be a major problem and a vaccine remains elusive. The prevalence of fake medicines in endemic countries is another major problem.

Malaria has been with human beings for a long time in evolutionary terms, as seen in the numerous genetic mutations that occur for the express benefit of conferring partial immunity eg sickle cell trait, G6PD, hereditary spherocytosis, HLA B53 (confers 40% protection vs severe malaria). At the same time, the parasite has evolved multiple ways of avoiding the immune system, which is why developing a vaccine has proved so difficult.

  • Plasmodium falciparum – causes the most severe disease, predominates in Africa, widespread resistance, but no liver stage
  • Plasmodium vivax/ovale – cause less severe disease, predominates in Asia, resistance rare, liver stage
  • Plasmodium malariae – causes less severe disease, predominates in Asia, resistance rare, but no liver stage
  • Plasmodium knowlesi – rarely severe

The parasite sporozoite form is injected with salivary secretions into the human host. It circulates until it reaches hepatocytes, where it replicates and forms clusters called schizonts. These release trophozoites into the blood stream, where red cells are infected and further replication occurs. Disease only appears once widespread haemolysis has occurred, usually 3 weeks or more after initial infection. A proportion of trophozoites transform into gametocytes. When these are ingested along with human blood by another mosquito, they can then continue the life cycle in the mosquito. In P vivax and ovale, longlasting hypnozoites may persist in the liver, which can be responsible for late reactivation of disease. So suspect for up to a year after exposure (although Falciparum will present within 3 months).

Clinical

Young children, hyposplenic, pregnant at particular risk (even if prev immunity).

Incubation period 10-21 days, but up to 3 months for falciparum, and note liver stage and late reactivation above.

No typical clinical features! Even fever is not a reliable sign!  Can present with GI symptoms, sore throat, lower respiratory complaints!

Clinical effects due to RBC destruction, cytokines release, micro circulation disturbance.

In endemic areas, intermittent asymptomatic low level parasitaemia is seen commonly, with recurrent, usually self-limiting, episodes of mild disease (plus chronic anaemia). Severe disease on the other hand can present as:

  • cerebral malaria
  • severe haemolysis
  • ARDS
  • acidosis

In non-endemic disease, particularly travellers or people who have lost their immunity by long term lack of exposure after emigration, the infection is more likely to be symptomatic, and the disease is more likely to be severe.

Mild disease

Fever, chills, sweats, myalgia, headache.  Anaemia, splenomegaly. Gastro and resp symptoms (even sore throat) common! Fever periodicity traditionally described as daily (falciparum), Tertian (vivax/ovale), Quartan (malariae) ie spikes every 3 or 4 days.  In practice this is wholly unreliable!

Moderate Risk

Parasitaemia >5% (not very well correlated, and not relevant for non-falciparum)

Sickle cell disease (who have worse outcomes, despite being relatively protected!)

High Risk

  • Pregnancy (high levels in placenta, even if not so obvious in blood).  Use clinda instead of doxy.
  • Asplenic or splenic dysfunction
  • Acidosis (BE >-8)
  • Hyperkalaemia (>5.5mmol/L)
  • Hypoglycaemia
  • Impaired conscious level

Respiratory distress usually due to acidosis rather than cardiac failure. Hence Kussmaul breathing predicts death.

Diagnosis

Do not wait for the results of tests if symptoms/signs suggestive, since falciparum can be rapidly aggressive.  Stop chemoprophylaxis, as can obscure!

Malarial retinopathy (Malawi eye) found in severe malaria: patchy white spots similar to hard exudates, frosted branch appearance of vessels, and ring shaped haemorrhages (not pathognomic though, seen in infarction).

The blood smear is the classic test. Thin smears are best for identifying the particular type of malaria and the percentage parasitaemia (percentage of erythrocytes infected), but thick smears are more sensitive. Repeat testing is important – at 12-24hrs and again at another 24hrs. Best at time of fever spike? Sensitivity is only 70% on a single smear, but rises to over 95% with 3 smears.

Having >20% of periph forms with pigment (mature) reflects high burden of deep circulating parasites cf young ring forms, so a risk factor for poor outcome. >5% neutrophils containing ingested pigment is another risk indicator.

New molecular based antigen tests are expensive but are less reliant on operator experience.

  • HRP2 (histidine rich protein) is specific to falciparum.
  • pLDH versions are available for falciparum and vivax.
  • Aldolase is a pan-specific antigen, but probably not as sensitive as the others.

These are pretty much as good as smears for falciparum and vivax, not quite as good for other species.

Thrombocytopenia common, not significant in isolation.  Check FBC, U&Es, LFTs, Glucose.  If ill, lactate, blood gas, blood cultures (accompanying bacterial sepsis common esp salmonella in endemic areas). Consider LP if impaired consciousness, seizures.

Notifiable! Other family members likely to be infected too?

Differential

Typhoid, hepatitis, dengue, VHF, HIV, avian influenza

Treatment

UK Guidelines 2016. Journal of Infection. 72(6), 635-649 (Lalloo, Shingadia).

Treatment of choice for non-falciparum is 3/7 oral Chloroquine or Co-artemether.  Co-artemether if mixed infection or concern about chloroquine resistant vivax (some areas). Must be followed by Primaquine, the only effective treatment for liver stage – beware G6PD deficiency (test at same time as doing films! Use only under expert supervision!)

For falciparum, treatment of choice for uncomplicated is Riamet (co-artemether) – alternative is Eurartesim.  If not available, use oral quinine or atovaquone-proguanil (Malarone).

Admit falciparum initially – risk of deterioration on  treatment, and check tolerating oral therapy.

Quinine is effective but poorly tolerated in prolonged treatment, and should always be supplemented by additional treatment, typically doxycycline in adults, clindamycin or Fansidar (Pyremethamine-sulfadoxine) in children.  All with falciparum should be admitted for at least 24hrs, given risk of sudden deterioration even with treatment.

IV artesunate should be used for severe disease, or infections with >2% parasitaemia, until well enough to tolerate oral treatment.  IV artesunate works quicker and is more effective in selected situations than IV quinine but is unlicensed, obtain through specialist centre on named patient basis. If not immediately available start IV quinine (and monitor for hypoglycaemia).

Adjunctive

  • Broad spectrum antibiotics in severe cases until bacterial infection excluded.
  • Surprisingly, shock usually responds to just 1 bolus of fluid. Excessive fluid resuscitation is likely to precipitate cardiac failure in severe anaemia, may exacerbate anaemia and raised intracranial pressure. Albumin appears to be superior to crystalloid (esp in coma – less mortality, ?membrane stabilizing).
  • Oxygen for respiratory distress
  • Glucose if hypoglycaemia
  • Poor evidence for exchange transfusion – consider for persistent acidosis or multiorgan failure, sickle cell
  • Seizures: follow standard guidelines. Partial, subtle seizures are common. No evidence to support prophylactic phenobarbitone.  Posturing common, assoc with spike in ICP so ventilation with paralysis may be advantageous. Exclude hypoglycaemia.

Follow up

Haemolysis occurs in 10-15% of patients treated with IV artesunate – check FBC at 14 days.

Vaccine?

A vaccine would be fantastic, but a potential candidate is yet to be found. There are several barriers:

  • Antigens of the different life cycle stages differ
  • Need to generate v high immune response
  • Need to overcome escape mechanisms

First phase III results in 2011 in Africa showed that RTS,S vaccine reduced clinical reports of malaria by 51 per cent.  After 3 years, reduces cases by 36%.  60 000 to be recruited across 7 countries.  Works against circumsporozoite protein (CSP) so blocks liver infection, has HBsAg adjuvant.

 

Nasal flu vaccine

General paediatrics, Immunology, Infectious disease

Live attenuated influenza vaccine (LAIV).  Now available in quadrivalent form, Fluenz Tetra in Europe, Flumist in US.  Transmission to another person has only ever been documented once, and it was asymptomatic!

The extra B hopefully makes it better than 2014/15 where poor coverage.  Live attenuated is more effective and has less systemic effects than injected vaccines.

Current annual programme in Scotland is for all 2-5yr olds to be offered vaccine by public health, whereas all primary and secondary school children will be offered vaccine at school.
Cut off for 2yr olds is age 2 on 1st September.
For infants between 6 months and 2, previous hospital admission for lower respiratory tract infection (which would include all our bronchiolitis babies!) is a clinical risk indicator, along with asthma, chronic heart/kidney/neuroresp disease, or indeed anything else where you thing getting flu is likely to exacerbate the underlying condition.

If you miss your school appointment, up to the family to request another via NHS Lanarkshire vaccine helpline 01698 687456.

Although GPs aren’t much involved anymore in vaccine programme, they should still offer it if a family prefers it, or if a family are keen to get it earlier than they might otherwise as part of the schools programme.

Most kids will be offered nasal live flu vaccine (Fluenz Tetra).  Contraindications to nasal flu vaccine are:

  • under 2yrs of age,
  • wheezing or extra bronchodilator within the previous 72 hours,
  • severe immunodeficiency (esp cellular) or immunosuppression eg leukaemia/lymphoma, high dose oral steroids
  • aspirin use (eg Kawasaki) – theoretical risk of Reyes [reported with wild type influenza and aspirin]

Kids on high dose inhaled steroids no longer require consultant approval to get nasal vaccine.

Kids previously in PICU for asthma, or who require regular oral steroids for asthma, require consultant approval to get nasal vaccine. Otherwise they should get injectable.

If you can’t have nasal, then should get injectable (inactivated) vaccine.  Can be given from age 6 months.

A second dose is needed after 4 weeks minimum if you are in a clinical risk group, and under 9yrs, and this is the first time you are getting flu vaccine.  This applies whether you get nasal or injectable flu vaccine.

For egg allergy, advice, as before, is that children with egg allergy – including those with previous anaphylaxis to egg – can be safely vaccinated with nasal vaccine in any setting (including primary care and schools). The only exception is for children who have required admission to intensive care for previous severe anaphylaxis to egg, who should be offered nasal flu vaccine in hospital [lack of data, not definite risk!].

If a kid with egg allergy has a contraindication to nasal flu vaccine (eg immunosuppressed) and needs injectable vaccine, then it should be either an egg free (cell based) injectable vaccine (the one from Seqirus is licensed from age 2) or low egg content (“split virion inactivated vaccine”), viz less than 0.12mcg/ml (equivalent to 0.06 µg for 0.5 ml dose).

NSAID hypersensitivity

Allergy, General paediatrics, Immunology

Ibuprofen etc are a common cause of reactions, but mostly non immune mediated, via COX -1 inhibition. Previously called pseudo-allergy or intolerance, best called hypersensitivity, then subdivided into allergic or non-allergic. Often occurs in patients with underlying problem eg asthma, chronic urticaria, rhinosinusitis – exacerbates underlying condition. Hypersensitivity can be to a single drug, or cross-reactive, ie to unrelated drugs from different families (salicylates ie aspirin, propionic derivatives eg ibuprofen, acetic acid derivatives eg diclofenac, etc). Cross reactivity suggests a non-immune mechanism. Without history to support single drug (or family) hypersensitivity, you would have to advise the patient to avoid all NSAIDs.

Testing

  • Skin testing with culprit drug is appropriate if you have an acute urticarial or angioedema reaction in a single drug/family.
  • Oral challenge is appropriate to confirm all types of hypersensitivity, esp in equivocal histories. At the same time, challenge with aspirin to check cross-reactivity, and with next best alternative NSAID. Start 1/10 dose, increase every 2 hours.
  • For nasal/bronchial symptoms, inhaled lysine aspirin is safer and faster, but only 77-90% sensitive cf 90% for oral. Intranasal is equivalent if inhaled/oral not possible.
  • If patient is on long term steroids, or else has been well controlled for a long time, sensitivity seems less!
  • Consider proceeding to challenge with COX2 (coxib) if challenge positive.

Aspirin desensitization works for NSAID exacerbated respiratory disease, and NSAID induced (cross reactive) skin disease, controversial for chronic urticaria and no data for single drug skin disease or anaphylaxis. But needs maintenance dosing so only really useful for chronic conditions eg needing antiplatelet therapy.

Allergy 2013:68;1219

UTI Treatment

Clinical, Common, General paediatrics

See NICE CG224 (refers then to CG111 (pyelonephritis) and CG109 (lower tract UTI)): Under 3 months get IV treatment. Else 3 days oral treatment if lower tract, 7-10 days oral for upper tract. IV for vomiting, unable to take oral or severe illness (but also says underlying known anomalies should influence choice) 2-4 days IV then oral for total of 10 days (!). No preference between cefuroxime, ceftriaxone and gentamicin. Upper tract defined as fever else loin pain/tenderness

Cochrane review concluded that 2-4 day course of oral antibiotic is as effective as a 7-14 day course in the treatment of lower-tract UTIs in children. PMID 12535494 The majority of febrile infants with UTI have nuclear scan evidence of pyelonephritis, suggesting that infants should not receive short course treatment.

Also concluded that for pyelonephritis oral antibiotics are as effective as the combination of parenteral followed by oral antibiotics. Based on:

  • Hoberman’s RCT children under 2 with fever and UTI (n=300) – oral cefixime for 2 weeks as good as IV: no difference in defervescence, reinfection, scarring at 6 months (and much cheaper!). Severely ill excluded (eg CRT>3sec) – only 3! Funny group though, mean age of 8 months, 90% female, and a low scarring rate (15%). Pediatrics 99 Vol. 104: 79, Hoberman A.
  • Montini Multicentre RCT non-inferiority (n=502, 1/12 to 7yrs). Oral co-amoxiclav for 10 days equivalent to ceftriaxone for three days followed by oral in terms of DMSA scars, time to defervescence. BMJ 2007; 335:386-8

Crucial that oral antibiotics are not vomited, of course.

Gauthier et al treated infants and toddlers with febrile UTIs as outpatients using a single daily dose of intravenous gentamicin until the children were afebrile for at least 24 hours, after which oral amoxicillin (!) was given until the urinary culture report was available. Successful in three quarters. Current Opinion in Pediatrics. 18(2):134-8, 2006

1/3 of UTI E coli resistant to trimethoprim, 2/3 if underlying renal abnormality. 61% of women with UTIs and resistant organisms do not reconsult! So should we use community surveillance to guide prescribing rather than individual culture and sensitivity?

UTI prophylaxis did not reduce recurrent infection (n=611). But lower rate (12%) reported than might be expected. Higher resistance rates are seen in recurrent infections, which could be anticipated (JAMA 2007;298;179)

UTI Follow up investigations – GGC guideline 2020

Clinical, Common, General paediatrics

Same definitions of upper, lower and atypical. UTI definitions

  • Under 6/12, USS for all, within 6 weeks. Urgent if recurrent or atypical features (other than funny bugs).

UTI imaging under 6 months

  • Provided things settle within 48 hours of treatment, no further investigations are required unless atypical or recurrent, in which case everyone gets DMSA (6 months after infection) and MCUG.
  • 6/12 to 3yrs: USS only if doesn’t settle within 48 hours of treatment. If atypical or recurrent then USS and DMSA (USS urgent if atypical features, other than funny bugs), else within 6 weeks.

UTI imaging 6/12-3yrs

  • Consider MCUG if dilatation on US, or family history of VUR, or atypical bugs, or poor flow. (MAG3 if continent)
  • Over 3yrs: same, except no DMSA even if atypical features, and no mention of MCUG at all.

UTI imaging 3yrs+

If USS abnormal, refer for consideration of further imaging.

But:

  • USS – not much evidence for benefit, esp if normal antenatal scan, rarely changes management even if something minor found, but harmless. If dilatation seen, do MCUG urgently.
  • MCUG – like GORD, maybe you see reflux, maybe you don’t, so can you rely on it? NB Cost, radiation, discomfort…
  • DMSA – acutely, diagnoses pyelonephritis. Then remain positive for up to 6 months after an infection. Late scan diagnoses scars. But if negative during first UTI episode, rarely (NPV 88%) have VUR and never high-grade VUR. [J Pediatrics Volume 150, 1 , January 2007, 96-99]
  • Antibiotic prophylaxis – not routinely.  If considered on the basis of risk/benefit discussion, then use trimethoprim.  If trimethoprim resistance, consider strategy of early empirical treatment rather than use a broad spectrum antibiotic such as co-amoxiclav or cefalexin (else risk of highly resistant bugs). [Hoberman A, NEJM 2003] Review every 3-6 months.
  • Cycling of antibiotic for prophylaxis may be more rational eg every 2-4 weeks

Studies do not address whether placebo or nothing is worse than prophylaxis (Cochrane: suggests about 36% reduction in infection, but all 3 studies biased, and most other work has prophylaxis vs surgery). Eg Sweden, only screen if additional risk factor, and v low prevalence of scars. Garin study (Paeds 2006) non placebo controlled, found no protection from recurrent infection with antibiotic prophylaxis (the rate for those with reflux was close to significance but seemed to be cystitis rather than pyelo) – plus the bugs were resistant. The rate of scarring was actually higher in the prophylaxis group…

[(Roberts, Kenneth) PIDJ 23(12); 2004:1163-1164 ]

UTI Follow up investigations – NICE CG54

Clinical, Common, General paediatrics
  • Under 6/12, OPD USS sufficient if good response to treatment within 48 hours.
  • Under 6/12 and atypical (see below) or recurrent (see below), then urgent USS to look for obstruction or severe reflux, or if simply non-E.coli then within 6 weeks.  PLUS later OPD DMSA (ie 4-6 months post infection), MCUG.
  • 6/12 to 3 yrs: nothing if good response to treatment within 48 hours. If atypical or recurrent, as above but no MCUG unless:
    • family history,
    • poor flow,
    • dilated tract on US,
    • non-E coli.
  • Over 3yrs: nothing if good response to treatment within 48 hours. If atypical, only needs urgent USS (OPD USS within 6 weeks if simply non-E.coli). If recurrent, do OPD USS and later DMSA.

Atypical defined as seriously ill, poor urine flow, abdominal/bladder mass, raised creatinine, septicaemia, failure to respond to appropriate antibiotics within 48 hrs, non-E. coli infection

Recurrent defined as 3 lower tract UTIs, else 1 upper tract plus any other

If another UTI occurs before the DMSA is done, don’t defer DMSA in case scarring already established.

Prophylactic antibiotics for MCUG (1 day before to 1 day after).

UTI diagnosis

Clinical, Common, General paediatrics, Infectious disease

See NICE 224 (2022).

Classic symptoms – dysuria, frequency, new wetting, dark or cloudy or smelly urine.  Frank haematuria, loin pain.  Fever, shivering (rigors), history of UTI. 

Clean catch ideally, pad (commercial, not cotton wool balls or gauze) if clean catch unsuccessful. Else catheter.  Suprapubic aspiration is an option but needs ultrasound to confirm bladder full.

See Sofia method of urine collection.

 

Testing

Under 3 months – send for culture and microscopy. Urgent?

Microscopy interpretation is simply on basis of pyuria pos/neg, bacteria pos/neg.

Over 3/12, dipstick is standard. A positive dipstick urinalysis for BOTH leucocyte esterase (LE) and nitrite is specific, negative both is a good negative predictor. If dipstick positive for just one, not reliable either way. Metanalysis, Huicho Luis, PIDJ 2002;21:1-11. Previous metanalysis by Gorelick and Shaw (Peds 1999) concluded nitrite/LE tests superior to microscopy!

If nitrites and leucocytes positive, assume infection. Culture only if high risk for serious infection or recurrent UTI.

Nitrites only positive, treat but send culture.

Leucocytes only positive, send culture, treat if classic UTI symptoms or under 3yrs, else await result before treating.

Culture if high risk of serious illness, upper tract signs, poor response to treatment, recurrent UTI.

Most studies show that clean catch is equivalent to suprapubic aspiration (SPA); limited data on pad, nappy or bag specimens.

Uricol (Euron, Newcastle) urine pads. Check at 10 min intervals (discard after 30mins). Cost 18p each. Agrees with clean catch for gluc/ket/blood/nitrite (within 1 block ) but in study only 2 cases with leucocytes so ?reliable.

Health Technology Assessment (Winchester, England). 10(36):iii-iv, xi-xiii, 1-154, 2006 Oct.

Urinary Tract Infection

Common, General paediatrics, Renal

See also:

A common, potentially serious, infection in children.  More common in girls over the age of 3 months, more common in boys below that.

Generally occurs by ascending infection from urethra.  Most common organisms are E coli, Klebsiella, Enterococcus faecalis, Proteus.  Infection appears to develop clinically when bacteria in the urine manage to adhere, hence depends on presence of fimbriae on bacterium, and ability of urothelium to resist adhesion (genetic factors).

Classic symptoms are of cystitis:

  • Urinary urgency and frequency (although amounts may be very small)
  • Dysuria
  • Haematuria
  • Suprapubic pain

There may be systemic features, eg fever, nausea/vomiting, lethargy.  However these are more common if the infection progresses to pyelonephritis:

  • unilateral loin pain
  • features of sepsis

Besides the inconvenience, particularly or recurrent cystitis, there is also the risk of long term kidney damage (chronic pyelonephritis, with renal scarring).

Risk factors

  • Constipation
  • Poor fluid intake
  • Withholding of urine for prolonged periods
  • Indwelling catheter

Immunodeficiencies rarely increase risk of UTI, neutrophil disorders are perhaps the exception.

Complications

Besides septicaemia, the major complication of concern is renal scarring, with potential for long term chronic pyelonephritis and premature renal failure.

Risk factors are: (n=1280)

  • temperature >=39degC,
  • a bug other than Escherichia coli,
  • abnormal ultrasound
  • neutrophil count >60%, CRP>40 mg/L,
  • Vesico-ureteric Reflux (VUR)

Having 2 or more of the first 3 puts you in a high risk group with double the overall risk of scarring (30 vs 15% in this study).  Covers 21% of the total sample.  Sensitivity is so-so: catches 44.9% of all scarring.

Adding in bloods and/or a micturating cystourethrogram (MCUG) only increases the predictive value by 3-5%. [JAMA Pediatrics. 168(10):893-900, 2014 Oct.  PMID: 25089634]

There are many studies showing that scars can develop without reflux, and that many children with reflux (but without infections) do not develop scars. Scars are associated also with delayed treatment.  Cochrane review did not come out strongly in favour of identifying VUR – nine reimplantations would be required to prevent just one febrile UTI, with no reduction at all in the number of children developing any UTI or renal damage. Archives, 2003

What is the risk of long term damage? Low, given that UTI is common, the occurrence of CRF is rare, and acute pyelonephritis with severe long term complications is also rare. The only large population-based study (n= 1221) found a low risk of hypertension after 16-26 years: only 9% of children with scarred kidneys became hypertensive cf 6% for unscarred. Glomerular filtration rate in later life was normal in both those with and without scarring. Archives of Disease in Childhood 2007;92:357-361

Follow up investigations

Apart from addressing risk factors, you need to consider looking for underlying VUR or else evidence of renal scarring.  See NICE CG54 guidelines.  For Scotland, see SPRUN guidelines.

Testes

General paediatrics, Surgical

Bilateral impalpable testes at birth are associated with complex endocrine disorders and prune belly syndrome, so should be investigated within 2 weeks.

Warm hands and room will help find a testis, of course. Can the testis be manipulated into the scrotum? In that case retractile, not undescended.

A testis can be undescended but palpable eg in the inguinal canal. If retractile, then needs no intervention.

For suspected unilateral undescended testis, re-examine at 6–8 weeks, and again at 4–5 months of age, if needed. If the testis remains undescended, refer to paediatric surgery to consider surgery.

Rarely non retractile testis found later in childhood – “ascending testis” – ?cord shortening.  Usually age 8-10, not so urgent as initial development already complete. Seems to be more likely if retractile in the first place – family should keep an eye on them!

If not palpable then may be intraabdominal, absent, small (dysplastic, but in the right place) or else ectopic. Imaging is not sensitive so often diagnostic laparascopy is required. Ectopic testes are found in the perineum or femoral triangle, they are usually normal and orchidopexy is straightforward.

An undescended testis is seen in 5% of term infants but less than 2% of 1yr olds. It is theorized that part of the reason for poor descent is that they are fundamentally abnormal. If left for more than 4yrs then histological abnormalities often seen so generally repaired/removed between 1 and 4 yrs of age. Commonly associated with inguinal hernia, in which case fixed earlier with the hernia.

After surgery, advise self examination as increased risk of testicular cancer.

[NICE CKS]