Category Archives: OPD

Migraine

Common, General paediatrics, Neurology, OPD

International Headache Society 2004 Migraine without aura def:

  • A – at least 5 attacks fulfilling B-D
  • B – lasting 1-72hr
  • C – at least 2 of:
    • unilateral, may be bilateral frontotemporal but not occipital;
    • pulsing;
    • moderate or worse pain;
    • aggravation by routine physical activity eg walking, stairs
  • D – during headache at least 1 of: nausea +/or vomiting, photophobia and phonophobia (which may be inferred from behaviour)
  • E – not attributed to other disorder

Aura – Hemianopia or spreading scintillating scotoma. Note that migraine with aura is a contraindication to treatment with combined oral contraceptives.

Some specific types:

  • Hemiplegic – can be familial or sporadic.  Can be confusion.  Rare to not have headache with it (but then diagnosis perhaps not recognised!?).  Triptans were initially thought to be risky, but more recently good evidence of usefulness and no longer contraindicated in BNFc.
  • Ocular/retinal – blindness or flashing lights, may not be headache.  NOT aura, which is prodromal.  Horner’s syndrome seen.
  • Basilar (also called Bickerstaff’s – but better termed migraine with brainstem aura) – transient dysarthria, vertigo, tinnitus, hearing impairment, diplopia, ataxia, confusion, bilateral paresthesia,
  • Confusional

Pathology

Neuronovascular condition – baseline hyperexcitability in cortex.

Double the risk if you had infant colic, which is not true for tension headache!  Sleep disruption as common factor? [JAMA 2013;309:1607-12]

Several genetic links found eg C677T mutation of the methylenetetrahydrofolate reductase gene (MTHFR), EAAT2. [J Headache Pain. Jan 2012; 13(1): 1–9.  doi:  10.1007/s10194-011-0399-0]

Investigations

Beware Occipital epilepsy!

American Academy of Neurology recommendations are that neuroimaging should be considered in:

  • recent onset of severe headache;
  • change in type of headache;
  • or neurological dysfunction;
  • seizures

Factors

  • Biofeedback and relaxation/stress management are as effective as beta blockers. Indian trial of yoga for migraine showed substantial improvement at 3 months [neurology 2020]
  • Sleep disturbance is associated but not necessarily causal – so recommend good sleep hygiene.
  • Exercise is beneficial.
  • Obesity – clusters with diet, exercise, sleep issues of course.
  • Missing breakfast is a common precipitant.
  • Episodic migraine (without aura) can become chronic (ie 15 days per month or more), but in this case you would always want to exclude medication overuse.
  • Caffeine is linked to headache and also sleep/mood disorder which exacerbates. Withdrawal headache can last as long as a week.
  • Wine is well recognised trigger in adults!
  • Often linked to menstrual cycle.
  • Screen time (>2hrs per day) linked to migraine but not non-migraine headache in French and Sri Lankan students.  Doesn’t necessarily mean reducing screen time helps, of course.  But note eye strain, posture relevant too.  And possibly differences between TV/PC use and mobile devices.
  • Some evidence for magnesium and zinc supplementation

[CurrOpPeds Dec 2004]

Diet

Although popular perception is that migraine is caused or at least triggered by dietary factors, there is a wide variation in reporting of dietary triggers. Certainly migraine is associated with obesity, and dietary habits seem to be as important as specific foods, and there is probably a cycle of inconsistent nutrition and poor control of migraine.

My colleagues talk about 4Cs (chocolate, cheese, coffee, citrus) but I have found no evidence for this.  Awareness of possibility of dietary triggers actually has greater influence on perception of personal triggers than personal experience!  See below.

Some evidence for lipid intake esp PUFA (decreased ingestion of lipids was associated with a decrease in the frequency, intensity, and duration of migraines and a decrease in the use of medication) but confounded by obesity, weight reduction, and changes in nutrient intake.  Another study found reduced migraine spells among children subjected to a diet rich in fibre. Not much evidence for cheese at all! [Nutrition Reviews. 70(6):337-56, 2012 Jun.  UI: 22646127]

Trial of cyanocobalamin, folate, and pyridoxine (2 mg of folic acid, 25 mg vitamin B6, and 400 microg of vitamin B12) in patients with MTHFR gene defects found a reduction of homocysteine levels and improvement of migraines. [Pharmacogenetics and Genomics. 22(10):741-749, October 2012]

Medication

Paracetamol, ibuprofen, and nasal-spray sumatriptan are all effective symptomatic treatments for episodes of migraine (peds sys rv 2005). Migraleve is paracetamol, codeine (8mg), buclizine – for 10yr plus. Paramax, with metoclopramide, for 12 yr plus.  Anti-emetic improves pain killer absorption so potential benefit even if no nausea!

Sumatriptan was previously contraindicated for hemiplegic migraine, but this was probably a theoretical concern, and there is evidence that it works. No caution or contraindication mentioned in BNF now.

Mefenamic acid for menstrual, esp with dysmenorrhea.

CGRP receptor antagonists – olcegepant, telcagepant [not in BNF].  Now erenumab [monthly subcut injections, BNF says specialist use only, minimum 4 migraines per month – SMC approved with restrictions], eptinezumab etc vs same calcitonin gene-related peptide receptor.  Significant improvement in headaches in 40%, about 3 less headache days per month.

For prophylaxis, Pizotifen does not work (grade I evidence, plus makes you fat), flunarizine (CCB) is the most effective (not in BNF), also amitriptyline (dangerous in overdose), propanolol (dizziness, sleep disturbance, depression etc, also dangerous in overdose). Encouraging data (grade IV) for anti-epileptic mediations topiramate, valproate, levetiracetam, zonisamide. Cyproheptadine? Candesartan (anti-hypertensive, in BNF for migraine prevention)?

Always increase preventer dose to maximum before giving up, note that often symptoms worsen after initial benefit.

Current evidence on the efficacy of percutaneous closure of patent foramen ovale (PFO) for recurrent migraine is inadequate in quality and quantity. The evidence on safety shows a small incidence of well-recognised but sometimes serious adverse events, including device embolisation and device prolapse (each reported in less than 1% of patients). Therefore this procedure should only be used with special arrangements for clinical governance, consent and audit or research. [NICE]

Contraception

Combined oral contraceptives are contraindicated in migraine with aura.  But may be useful if menstrual pattern to headaches if no aura.

Prognosis

50% migraine in childhood remits at puberty. Onset in adolescence associated with persistence.

Support

Patient support at Migraine Trust.

Sleep

Common, Community, General paediatrics, OPD

Poor sleep associated with hyperactivity, obesity, poor school performance, depression.  And affects parents, of course!  Caffeine and Propranolol (as used for migraine prophylaxis) affect sleep!

Normal sleep

REM (rapid eye movement) phase is light sleep. Usually in later part of night after deep sleep.  Slow wave (deep) sleep is associated with increased anabolic hormone release, mitotic repair. Higher proportion of sleep in adolescence is slow wave.  60% of newborn sleep is REM.

Recommended sleep duration: [National Sleep Foundation]

  • Newborn 0-3 months: 14-17 hours
  • Infants 4-12 months: 12-15 hours
  • 1-2yrs: 11-14 hours
  • Preschool 3-5yrs: 10-13 hours
  • School age 6-13yrs: 9-11 hours
  • Teenagers 14+: 8-10 hours

Some sources suggest adolescents have increased sleep requirements.

Late insomnia (early morning waking) in depression. Cf early – mood disorders, anxiety (cortisol vs melatonin).

30 mins high intensity exercise is as good as melatonin. But ideally 3hrs before bed time!?

Sleep latency 19 min under 2yrs, 17-19 mins thereafter.

Night wakenings are normal! But parental response varies!

Excessive sweating seen in 11% of children, so considered normal. But beware weight loss, lethargy!  Can also be associated with obstructive sleep apnoea.

Sleep problems

For infants not going to sleep, options are extinction vs gradual retreat. Not appropriate for under 6/12 of age as may affect bonding. No adverse effects otherwise.

Melatonin does not increase total sleep time! Helps prepare brain for sleep – does not induce sleep, as such.  Earlier waking as well!

Nocturnal seizures – stereotyped, multiple in one night, sudden stop and start, mostly after first third of sleep.  Seen in BECTS.

Restless legs associated with iron deficiency!

Benign nocturnal leg pain common in children.

Teenagers generally do have different body clock, but not helped by major changes in bed/wake times at the weekend. Blue light from screens suppresses natural melatonin production besides distraction.

For autism – Hope for autism do not need diagnosis, others do. Waiting times? National Autistic Society page. Arch, Reach websites.

CAMHS won’t prescribe melatonin but do prescribe methylphenidate!?

Bio melatonin 3x the price, not approved by SMC. Modified release melatonin may be useful with or without standard if early waking in night.

Parasomnias

In early part of night, likely to be non REM, cf later in night.

Classic non REM =

  • Confusional arousal – can appear fully awake but don’t make much sense, no recollection in morning.
  • Sleep walking – quite complex behaviours possible (riding a motorcycle!)
  • Sleep terror – worse for partner/parents, as rarely remembered

REM related =

  • REM sleep behaviour disorder – typically violent, dream can often be remembered, can escalate. Can be sexual.
  • Sleep paralysis – up to several minutes, usually terrifying (“like being dead”), often with hallucinations.

Sleep hygiene, then consider melatonin and CBT (stress often provokes non-REM). Benzodiazepines can help non REM but can worsen REM.

Beware Narcolepsy – poor sleep quality at night, then daytime somnolence, plus hypnagogic/hypnapompic hallucinations, sleep paralysis, cataplexy (laughing causes collapse). Genetic, treatable with stimulants.

Support

Growth Charts

General paediatrics, Nutrition, OPD

Current charts are UK-WHO, which is to say a combination of UK growth cohorts with world wide cohorts.  This is to correct for the low prevalence of breast feeding and high prevalence of obesity in the UK, and assumes that there is little genetic differences in growth.

Downloads and online growth tool at RCPCH.

Usage Tips

Between 37 and 42 get plotted as term.  No centiles for first 2 weeks as dip expected.  One in 5 still below birth weight at 2 weeks, only one in 50 will be 10% below or more.  Still mainly well, but suggests feeding problem worthy of further assessment, and in a few there will be an otherwise occult pathological condition eg cardiac or metabolic disorder.

Preterms get plotted on both Preterm section of chart AND day 0!  Because assessing early growth works best on day 0 centile, whereas later growth more likely to be related to preterm centile.  Plot after birth on preterm section until you hit the end (42 weeks) then continue on to main 0-1yr chart, plotting a point for calendar age but adding arrow indicating gestational age.   Otherwise unclear whether corrected or not.

Children up to age 2 get weighed without clothes or nappy.  From 2, minimal clothing and no shoes.  Height is hard! Only act on several measurements that appear consistent!

Growth Faltering and Failure to Thrive

General paediatrics, Nutrition, OPD, Sociology

Infants are at high risk of undernutrition – high requirements for growth, frequent infections affecting appetite and increasing requirements, inefficient metabolism, dependence on adults for food!

Faltering on growth chart

See Growth charts for details on different centile charts available.

There are various ways of defining or looking for undernutrition:

  • Wasting – ie low BMI or weight for height.  Pushed by WHO as way of identifying most vulnerable, but in affluent societies seems to mostly identify tall children
  • Stunting – low height for age, indicating chronic poor growth.  But in affluent societies, more likely to be constitutional or organic disease?  Social gradients in height in UK persisted until 1990s, but socially deprived short children had shorter parents and were smaller at birth, so not all nutritional.
  • Low weight centile – usually just selects out low birth weight babies.
  • Falling through weight centiles (“growth faltering”) selects for relatively large infants regressing to mean.

“Failure to thrive” has gone out of fashion.  “Thrive” seems to suggest something more than growth, but really we are just talking weight and height.  “Failure” suggests not only that there is a definite problem, but also that it’s somebody’s fault! Variability in definition and use.

The main issue here is poor sensitivity and specificity for a genuine problem.  27% of Danish cohort infants met one or more of 7 different growth criteria in at least one of the two age groups (2–6 and 6–11 months of life). The concurrence among the criteria was generally poor, with most children identified by only one criterion. Positive predictive values of different criteria ranged from 1% to 58%. Most single criteria identified either less than half the cases of significant undernutrition (found in 3%) or included far too many, thus having a low positive predictive value. [Olsen, Arch Dis Child 2007;92:109-114 doi:10.1136/adc.2005.080333 ]

Things get even less consistent in older kids, where you can have low fat but apparently normal growth except at the extreme end of range.

Combination of weight faltering and low BMI is perhaps best.  These kids subsequently have growth and body composition patterns suggestive of previous undernutrition.  Overall, about 2/3 of kids with either weight faltering or low BMI probably adequate nutrition but variant growth pattern.  Weight faltering kids are relatively short at follow up, but not more so than parents, so probably “catching down”. [Proceedings of the Nutrition Society. 71(4):545-55, 2012 Nov. PMID: 22954067]

Causes

Deprivation

Undernutrition is NOT associated with deprivation in UK, presumably as welfare focuses on families with young children. In the Gateshead Millennium Baby Study, both the highest and the lowest levels of deprivation were associated with weight faltering; this was independent of the type of milk feeding. No relation was found with maternal educational status.

Thrive index by deprivation quintile, under 6 weeks and up to 1 yr

Abuse and neglect are a factor in only a minority of cases.

Some evidence of differences in maternal feeding behaviour and appetite, eating behaviour. In Gateshead study maternal eating restraint (“I need to control how much I eat”) was unrelated to weight gain.  Response to food refusal seems important.

In Gateshead study, infants of mothers with high depression symptom scores (EPDS >12) had significantly slower weight gain and increased rates of weight faltering up to 4 months (relative risk 2.5), especially if they came from deprived families, but by 12 months they were no different from the remainder of the cohort. [Arch Dis Child 2006;91:312-317 doi:10.1136/adc.2005.077750]

Either low appetite or actually not undernourished in strict sense!

Fussy eating

Being faddy was only weakly associated with poor growth, and simply eating a limited variety was unrelated to growth [cf high eating restriction scores]. High milk consumption was associated with lower appetite but not with poor growth.[ Pediatrics. 120(4):e1069-75, 2007 Oct. UI: 17908727]

See Fussy eating

Outcome

In Newcastle, There was a significant positive relationship between weight gain in infancy and picture vocabulary at age 10, adjusted for economic deprivation, gestational age and birthweight, but not with any of the other outcomes. There was a statistically significant association between birthweight and all four outcomes, where best outcome is at or just above average birthweight. In this population, the association between early growth and cognitive outcomes is stronger for growth before birth, postnatal weight gain having a relatively minor impact.[ Paediatr Perinat Epidemiol. 2007 Jan;21(1):57-64.]

Management

Being able to see what happens in the house at mealtimes is the most useful thing! Interventions that include home visits work best.  So Health Visitor is key.

Speech and Language, Dietician advice may be appropriate in some cases.

Identifying children with underlying medical problem important, even if these are a minority.  Similarly those with social concerns. But proportionate response to symptoms and signs important, rather than long lists of investigations.

Although tempting, high energy oral supplements eg Pedisure suppress appetite for normal food.  In series of 48 kids referred to a tertiary feeding clinic who were taking predominantly supplements (half neurodevelopmentally abnormal), most were successfully weaned off and had improved feeding behaviour a year later.  Average weight Z score unchanged, 17% had significant catch up growth. [Archives of Disease in Childhood. 100(11):1024-7, 2015 Nov. UI: 25809349]

 

Episodic autonomic symptoms

Clinical, General paediatrics, Neurology, OPD

Renal investigations

Common, General paediatrics, OPD, Renal

Ultrasound

Renal uss image anotated

Incomplete bladder emptying cannot be diagnosed on a single post-void residual urine on ultrasound, due to significant intra-individual variability. Two post-void residual urine tests are recommended; larger volumes are seen if the bladder has been over distended (eg initial volume greater than 115% of expected), and in younger children. Greater than 20 ml is more specific than 10% bladder capacity. [J urology 2009 (182):1933]

Bladder capacity is = (Age +1) x 30 (ml) max 390ml.

 

Hair loss

Dermatology, General paediatrics, OPD
  • Tinea capitis – “ringworm”, actually fungal.  Scalp abnormal.
  • Telogen effluvium – lots of hair shed all at the same time following some sort of trigger esp birth (both baby and mother can be affected!), infection.  Trigger usually 2-3 months preceding.  Clumps or general thinning, underlying scalp healthy.
  • Alopecia areata
  • Trichotillomania

On Examination

Exclamation mark hairs (thin proximally, at scalp, normal distally) suggest alopecia areata, but may be seen in trichotillomania, so not very predictive.

Pull test – gentle traction on about 20 (some people say 60) hairs in 3 different locations.  Positive if more than 3-5 hairs extracted – confirms active hair loss but not very specific. Usually telogen effluvium but can be early alopecia areata. 

Dyspraxia, or Developmental Coordination Disorder (DCD)

Community, General paediatrics, Neurology, OPD

Developmental Co- ordination Disorder (DCD), as outlined in DSM IV (American Psychiatric Association 1994):

  • Performance in daily living activities that required motor co-ordination is substantially below that expected given the person’s chronological age and measured intelligence. This may be manifested in delays in achieving motor milestones (i.e. walking, crawling, sitting) dropping things, ‘clumsiness’.  Significantly interferes with academic achievement or activities of daily living.
  • The disturbance is not due to a general medical condition (e.g. Cerebral Palsy, Hemiplegia or Muscular Dystrophy), and does not meet the criteria for a pervasive Developmental disorder.
  • If Global Learning Difficulties are present the motor difficulties are in excess of those associated with it.

It is essential that early referral is made in order that children do not develop behavioural difficulties due to their frustration at not being able to carry out the same tasks as their peers.

Clues are:

  • Does the child’s motor skill appear to be behind their cognitive skills?
  • Dose the child appear to move generally in an uncoordinated way i.e. walking, running, manoeuvring around objects?
  • Does the child fall over constantly, bump into things, and /or knock thing over?
  • Has the child developed a dominant hand i.e. does he/she prefer to use one hand for more tasks?
  • Does the child have difficulties with dressing especially organising themselves? Do they find laces, small fastening and cutlery difficult?
  • What is their attention span like? Are they always fidgeting or squirming?
  • Are they having significant difficulties in the classroom in relation to their peer e.g. poor behaviour, avoidance of tasks, poor handwriting, dislikes gym?

N.B  Most children in their early school years will demonstrate one (or more) of these areas of difficulty but this does not mean they all have DCD!  Children with DCD will present with many of the difficulties above for a prolonged period.

Tic Disorders and Tourette Syndrome

General paediatrics, Neurology, OPD

Tics are recurrent, sudden, non-rhythmic twitches. Can be in 1 muscle or muscle group, but can also be a more complex semi-purposeful movement, or even present as a bizarre gait. Typically affect face (eg blinking, grimacing), neck, shoulder.  Can be more complex sequences of movements. Characteristics are:

  • Tend to be situational, with stress making them worse.
  • Initially they are suppressible, although depending on the situation this suppression can be virtually effortless! Usually though, suppression leads to rising anxiety and then a rebound in frequency.
  • There is often a premonitory feeling.
  • They can be suggestible.

Differential includes stereotypy, spasms, chorea.

Although tics can wax and wane over time, there is a general tendency to improve, and they are very unusual in adulthood.

Tics occur most commonly in boys. Usually they are transient, lasting for between 4 weeks and 1 year. A chronic tic disorder does exist distinct from Tourettes.

Vocal tics (clearing throat, yelps, coughs, sniffs, grunts) can occur in isolation, but a combination of vocal and motor tics suggests Tourette’s syndrome.

Tourette’s syndrome

Thought to affect 1% of children, so probably a lot subclinical! An inherited neuropsychiatric condition, it starts at a mean age of 7 but can be as young as 2yrs. Motor tics come first, about a year before vocal tics. Complex vocal tics may be seen but contrary to public understanding, most kids do not swear (coprolalia)!

Definition requires that motor and vocal/phonic tics are present (at some point) for at least a year, on a daily basis, with onset prior to 18yrs, in absence of substance misuse, medical condition or medication.  The characteristic features of Tourette’s are:

  • Echolalia – repeating phrases
  • Palilalia – repeating other people’s words
  • Coprolalia – swearing or abusive language. Involuntary, and causes distress to the patient, who will often try to conceal the outburst by coughing, etc.
  • Copropraxia – making obscene gestures
  • Palipraxia – imitating other people’s gestures

Tics wax and wane, evolve over months.  Can be self harming eg scratching, rubbing, head banging, punching, poking, stabbing oneself (see also obsessive compulsive co-morbidity below).

In some patients, there is a non-obscene compulsion to shout socially inappropriate things (NOSI).  Often worsens around puberty. 50% abate after puberty, but mostly just better self-management?

Differential is basal ganglia or cerebellar abnormality eg post-encephalitis, Huntingtons.  Investigations only necessary where unusual deterioration or progression of symptoms.

Co-morbidity

Pure tic disorder is unusual in Tourettes. 85% have comorbidity, most commonly:

  • Obsessive Compulsive Disorder/Behaviour – less to do with cleanliness, more sexual/religious/violent themes, orderliness, symmetry, checking, counting, forced touching.
  • Self-injurious behaviour is well described (see above)
  • ADHD
  • Conduct disorder, affective disorders more rarely.

The comorbidities are often more significant on school performance than the tics.  Comorbidities are common in relatives, even if tics are not.

Treatment

Counselling is useful for self-esteem, anger management, and social functioning. Habit Reversal Training is effective but not widely available – officially 12 weekly hour sessions, need to recognize premonitory urges and then replace tic with controlled movement, or position self to prevent tic (eg chin on chest to prevent shouting).

Drug treatment may be considered eg self harming, but not much evidence for effectiveness.  Traditional or atypical neuroleptics, or clonidine (esp where behaviour or sleep problems) used.

Deep brain stimulation being researched.

Prognosis

Tic frequency and severity decline with age in a large proportion of patients (59–85%).

Predictors of NOT improving include higher childhood tic severity, smaller caudate volumes and poorer fine motor control.

The presence of untreated comorbid psychopathology, such as ADHD and OCD, can adversely affect the long-term outcome of patients with TS.[Funct Neurol. 2012 Jan-Mar; 27(1): 23–27. ]

Tourettes Action parent support group.

[Stern, Curr Peds 2006:16:459]

Haematuria

Common, General paediatrics, OPD, Renal

In a study of 342 kids with asymptomatic microscopic haematuria, no cause was found in the large majority of patients. The most common cause discovered was hypercalciuria (16% of patients) followed by post–streptococcal glomerulonephritis (1%). No evidence for value of early detection of hypercalciuria (may be at long-term risk for nephrolithiasis and bone demineralization).  The children with asymptomatic post–streptococcal glomerulonephritis all improved spontaneously and without complication.  None had evidence of urinary tract infection! Clinically insignificant abnormalities in the upper urinary tracts of 5 children and grade 3 reflux in 1  [Arch Pediatr Adolesc Med. 2005;159(4):353-355. doi:10.1001/archpedi.159.4.353]

Asympt recurrent can be monitored for 5yr!

Beware:

  • frank blood,
  • protein,
  • hypertension,
  • other features (joints, rash, wt loss)

Haematuria defined as persistent dipstick positive on at least 3 occasions for at least 3 months. Else as >2rbc per HPF (not same as flow cytometry). Then consider:

  • Red cells or not?
    • myoglobinuria = haemolysis
    • beetroot!
    • Porphyrins, other unusual pigments
  • Proteinuria or not?

If spot urine abnormal, repeat on early morning urine and then proceed to 12-14hr collection. Urine calcium/creatinine has age specific normals, high at birth (up to 1.5 in toddlers) falling to adult max of 0.7 at age 7. High levels especially significant in the presence of a normal plasma calcium

Investigations – only do bloods if macroscopic or nephritis suspected:

  • Do urine culture and microscopy.
  • Do PCR if proteinuria.
  • If macroscopic, do FBC, U&Es, LFTs, Coag.
  • Renal USS
  • Screen family members with urinalysis
  • Spot urine calcium/creatinine
  • If acute nephritis, do C3/4, ASOT, immunoglobulins, ANCA, anti GBM as below.
  • If stones suspected, do 2 sets of spot urine Ca/creat, Oxalate/creat, Urate, amino & organic acids, pH, KUB.

Differential is:

  • Tumour – bladder (colour changes during voiding, dysuria with sterile culture) or kidney
  • IgA nephropathy – persistent, progressive in 30%, diagnosis on biopsy
  • Alports – usually X dominant, deafness in minority, cataracts in 10%
  • Sickle cell – 1% macroscopic, 16% microscopic. Papillary necrosis, usually painless, episodic. May progress to sickle nephropathy.
  • Venous thrombosis – esp neonates, nephrotics.
  • Vascular – AVM, Nutcracker syndrome (compression of the left renal vein between the abdominal aorta and SMA)
  • Nail-patella syndrome (BM disorder, like Alports)
  • Polycystic Kidney Disease

Biopsy if persistent high grade microscopic, or microscopic with proteinuria (>150 mg/24 hr)/hypertension/impaired renal function, or 2 episodes of gross haematuria. Cystoscopy for bladder problem.