PAEDS gastro, renal, MSK, endocrine, neonates Flashcards
What are the clinical features of IBS?
Abdominal pain, often worse before defecation
Bloating
Explosive, loose or mucousy stools
Feeling of incomplete defecation
Constipaton - often alternating with normal or loose stools
When should H.pylori or duodenal ulcers be suspected? How would you test for this and treat it?
If epiastric pain that keeps them awake at night or history of peptic ulcers in first degree relative
H.pylori causes nodular antral gastritis - identified on antral biopsies
C-labelled urea by mouth and C13 breath test
Treat - amoxicillin + metronidazole/clarithromycin and PPI
What is the commonest cause of gastroenteritis in the developed countries?
Rotavirus
Presents winter to spring in under 2 yrs
What features of gastroenteritis suggest bacterial infection? Give some examples of causative organisms
Blood in stools Campylobacter jejuni Shigella Cholera E.coli
Give the features of gastroenteritis
Sudden watery or loose stools often with vomiting
Contact or recent travel abroad
What assessment must be done in a child with gastroenteritis?
Hydration!
No clinical dehyration (<5%)
Clinical dehydraton 5-10%
shock >10%
How does hyponatraemic dehydration occur?
Sodium and water leave in diarrhoea together so plasma concentration stays the same. But when drink hypotonic solution/water, they retain water but lose sodium causing hyponatraemia.
Causes shift of water into ICF - increased brain volume, convulsions
How does hypernatraemic dehydration occur?
Somtimes water loss exceeds sodium loss - so plasma sodium conc increases
Usually in fever, hot, dry environment or low-sodium diarrhoea
Causes shift from ICF to ECF of water - sunken fontanelle, eyes, reduced tissue elasticity
Cerebral shrinkage - jittery movements, increased muscle tone, hyperreflexia, altered consciousness, seizures, cerebral haemorrhage (small)
Transient hyperglycaemia
What investigations would you do in gastroenteritis?
Usually none needed. Stool culture if child is septic, blood or mucus or immunocompromised
Check electrolytes, urea, creatinine, glucose
Blood culture if going to start antibiotics
How would you manage hypernatraemic dehydration?
Oral rehydration solution
IV fluids slow (<0.5mmol/L per hour) over 48hrs, regular monitoring of sodium (risk of hyponatraemic cerebral oedema)
When would you use antibiotics in gastroenteritis?
Not routinely even if bacterial
Only if sepsis, extra-intestinal spread of infection, salmonella gastroenteritis <6 months, malnourished or immunocompromised children or specific ones
(C. diff, cholera, shigellosis, giardiasis)
How would you support a child nutritionally after gastroenteritis?
Increased nutritional intake
Zinc supplementation
What is post-gastroenteritis syndrome?
Return to normal diet after gastroenteritis can result in watery diarrhoea
Transient lactose intolerance (Clinitest positive - non-absorbed sugar in stools)
Return to oral rehydration solution for 24hrs, then re-introduce normal diet
Other allergies may occur e.g. CMPA, coeliac - may need specialist diet or parenteral nutrition until mucosa recovers
When and how does coeliac disease present?
8-24mnths when introduce wheat foods Failure to thrive Abdominal distension Buttock wasting Abnormal stools General irritability
What are some features of Crohn’s disease?
Failure to thrive, delayed puberty, abdo pain, diarrhoea, weight loss, fever, lethargy, oral or perianal lesions, arthralgia, uveitis, erythema nodosum
Raised ESR, CRP, platelet count
Iron deficiency anaemia, low serum albumin
Transmural, subacute, chronic - mostly affecting distal ileum and proximal colon
Inflammation, then strictures and/or fistulae
How is Crohn’s disease diagnosed?
Upper and lower GI endoscopy biopsies
Non-caseating epithelioid cell granulomata
Imaging - narrowing, fisuring, mucosal irregularities, bowel wall thickening
How would you induce and maintain remission in Crohn’s?
Normal diet replaced by whole protein modular feeds (polymeric diet) for 6-8 wks. Systemic steroids if ineffective
If relapse: Azathioprine, mecaptopurine or methotrexate to maintain remission
Infliximab/adalimumab if these fail
Surgery for complications
How does ulcerative colitis present?
Rectal bleeding, diarrhoea, colicky pain
Weight loss, failure to thrive (less than Crohn’s)
Erythema nodosum, arthritis
How would you diagnose ulcerative colitis?
Upper and lower endoscopy - exclude infective causes of colitis, check small bowel for crohns
Histology - mucosal inflammation, crypt damage, ulceration
How is ulcerative colitis managed?
Mild - aminosalicylates (balsalazide, mesalazine)
Possibly topical steroids or systemic if more aggressive
Fulminating disease - IV fluids, steroids
Ciclosporin if this fails to induce remission
Colectomy with ileostomy if severe/toxic megacolon
Regular colonoscopic screening after 10yrs from diagnosis
What is definition of constipation?
Infrequent passage of dry, hardened faeces often accompanied by straining or pain
What conditions should be considered in a child with constipation?
Baby - Hirschsprung disease, anorectal abnormalities, hypothyroidism, hypercalcaemia
Dehydration, toilet training, unpleasant toilets or stress
What does examination show in constipation?
Palpable mass in abdomen, in well-looking child
PR only if pathology suspected by specialist
What can occur in long-standing constipation?
Rectum becomes overdistended, loss of feeling the need to defecate and involuntary soiling due to overflow
How would you manage acute or chronic constipation?
Acute - mild laxatives and extra fluids
Chronic with overflow - Disimpaction regimen - stool softeners with macrogol laxative (e.g. Movicol) with escalating dose over 1-2wks. If not tolerated, osmotic laxative
If unsuccessful - stimulant (senna, sodium picosulphate) as well
Maintenance - macrogol (+stimulant) reduced over months
If severe impaction - enema or manual evacuation under anaesthetic
What is Hirschsprung disease?
Aganglionic section of large bowel - narrow, contracted segment from rectum proximally (distance varies) - mostly rectosigmoid
Causes dilated colon at normal innervation sites
How does Hirschsprung disease present?
Neonatal - failure to pass meconium in first 24hrs
Abdominal distension and bile-stained vomiting
PR - narrowed segment with liquid stool and flatus on withdrawing of finger
Sometimes infants present due to C.diff infection with Hirschsprung enterocolitis
Later childhood - chronic constipation, abdo distension, no soiling, growth failure
How is Hirschsprung disease diagnosed and managed?
Rectal biopsy - absence ganglion cells and large acetylcholinesterase positive nerve trunks
Anorectal manometry or barium studies - length of section
Management - surgery - colostomy, anastamose innervated bowel to anus
What tests may assess renal function in children?
Plasma creatinine concentration
eGFR - better as does not depend upon muscle bulk like creatinine does
inulin or EDTA GFR - more accurate, but repeated blood tests so not used as much in children
Creatinine clearance - requires timed urine collection and blood tests so not used as much
Plasma urea concentration - increased in renal failure before creatinine Also in high protein or catabolic state
Why might congenital kidney disease not be obvious for the first few days of life?
Newborn kidney has low GFR and urine flow so signs of obstruction may not be obvious especially if mild, until urine flow demand increases
How might a UTI present?
Varies - subtle as food aversion and severe as sepsis
Unexplained fever >38
If alternative site of infection, but does not improve when treated for other site of infection
If older - abdominal pain or dysuria
Vomiting common
Which children should ALWAYS get urine microscopy and culture if presenting with fever?
Infants under 3 months!
How might urine samples be obtained in children?
If able to wee on command - MSU
Otherwise “clean catch”
Also collection pads/adhesive plastic bag - less sterile
Catheter or suprapubic aspiration
Always say how urine sample collected on form
What might be done with urine sample to check if UTI?
Look at urine first
Urinalysis - nitrites, leukocytes
MC+S - what organism, what antibiotics
What do urinalysis and MC+ results suggest for treatment?
Positive WCC and growth = UTI, treat Abx
if growth - treat as UTI regardless of WCC
Positive WCC and no growth - treat with antibiotics if symptomatic
What is the bacteriological criterion for UTI?
More than 100 000 (10 to power 5) organisms per ml of urine on CCU/MSU
OR any growth on suprapubic aspiration
What organisms cause UTIs in children?
Commonest = E. coli
Proteus also commoner in boys
if abnormal organism e.g. Pseudomonas - suspect structural abnormality
What 3 groups require admission to hospital for suspected UTI?
All children <3 months Systemically unwell (fever, loin pain, tenderness) Risk factors (kidney transplant, renal disease)
What treatment is given for children systemically unwell with suspected UTI?
MIN 2 days IV antibiotics (cefotaxime then adjusted), send home on 7-10 days oral
Advise to return if no better at 24-48hrs
What treatment would be given to children with suspected UTI <3 months and systemically well?
2 days IV Abx (cefotaxime then adjusted) and 3 days oral
Advise to return if no better at 24-48hrs
Who requires follow up after UTI to check for structural abnormalities?
Recurrent or atypical UTIs
What defines an atypical UTI?
Septicaemia/requires IV antibiotics Non E.coli UTI Poor urine flow Abdominal mass/bladder mass Raised creatinine Failure to respond to suitable antibiotics within 48hrs
What defines a recurrent UTI?
2 or more UTI episodes with at least one episode of systemic signs/symptoms
3 or more UTI episodes without systemic signs/symptoms
How would you investigate for structural abnormalities in urinary tract?
USS urinary tract - observer dependent, dynamic, allows size of kidneys, bladder and drainage checked
If abnormality present or <3yrs: (wait 3 mnths if poss)
Micturating Cystourethrogram (MCUG) - urinary catheter into bladder, fills it with dye to see if vesicoureteric reflex, gives outline of bladder and urethral valve (<3yrs)
DMSA - renal scarring, relative renal function (IV cannula giving nuclear dye taken up by kidney) - 1-3yrs
Other than antibiotics what supportive measures are done to prevent UTIs?
High fluid intake Regular voiding, double micturition Prevention or treatment constipation Good perineal hygiene Probiotic - lactobacillus acidophilus Antibiotic prophylaxis? - under 2yrs with urinary tract abnormality or severe reflux (trimethoprim at night)
How should children with recurrent UTIs, renal scarring or reflux be followed up?
Urine culture with any non-specific illness
Long-term low dose antibiotic prophylaxis
Circumcision in boys
Anti-reflux surgery - if progresses, but unsure
Blood pressure checked annually, height, weight, test for proteinuria
Regular assessment of renal growth and function
Further symptomatic UTIs - investigate to see if new scars or continuing reflux
What different ways can oedema present?
Facial puffiness Pitting oedema Pulmonary oedema Ascites Pleural effusions
What is the triad of symptoms for nephrotic syndrome?
Heavy proteinuria
Hypoalbuminaemia
Oedema - periorbita, scrotal/vulval, legs/ankles, ascites, breathlessness
What tests on urine sample are indicative of nephrotic syndrome?
Urine looks frothy/foamy
3+ protein or more on dipstick
But best is:
First morning Urine Protein:Creatinine Ratio (normal <20, hypoalbuinaemia>600)
How might you test for hypoalbuminaemia?
Blood test: albumin.
Normal = 35-45, hypoalbuminaemia <25-30
Why are nephrotic patients at increased risk of infection or thrombosis?
Loss of protein through kidneys/urine occurs with antibodies and anti-thrombotic factors too
When might proteinuria occur in children?
Transient proteinuria in febrile illness/after exercise Orthostatic proteinuria Glomerular abnormalities Increased glomerular filtration pressure Hypertension Reduced renal mass Tubular proteinuria Nephrotic syndrome
Give features of steroid-sensitive nephrotic syndrome
Age 1-10 yrs, commoner in Asian children, weak association atopy Normal blood ressure No macroscopic haematuria Normal complement levels Normal renal function Minimal change on biopsy Responds to steroids
How would you treat steroid-sensitive nephrotic syndrome?
4 weeks ORAL PREDNISOLONE 60mg/m2
then
4 weeks at 40mg/m2 on alternate days
Other meds: Water and sodium moderation, diuretics
Penicillin, vaccines for measles, VZV, pneumococcus
What are the features of steroid-resistant nephrotic syndrome?
Raised BP Haematuria Impaired renal function often similar to nephritis Failure to respond to steroids Histology - glomerulopathy - basement membrane abnormality
How is steroid-resistant nephrotic syndrome treated?
Referred to paediatric nephrologist
Oedema managed - diuretics, salt restriction, ACE-I, sometimes NSAIDs which reduce proteinuria
What are features of congenital nephrotic syndrome?
presents in first 3 months of life
Most common is recessive
High mortality rate due to hypoalbuminaemia
Unilateral nephrectomy may be required to stop proteinuria, followed by dialysis for renal failure until can get renal transplant
What can cause nephrotic syndrome?
Congenital Many are unknown in cause HSP and other vasculitides SLE Infections Allergens
What is minimal change disease?
Cause of nephrotic syndrome - glomerular disease but no change seen on microscope
Requires electron microscope to see pathology
Symptoms of nephrotic syndrome may occur quicker
How do you determine haematuria?
Urine dipstick - if Hb on dipstick should be done under microscopy
>10 RBC per high power field
How might urine from glomerular haematuria present?
Brown urine - RBC deformed as pass through glomerular membrane and casts
What are the features of glomerulonephritis?
Visible haematuria, some proteinuria
Impaired GFR, raised creatinine, less urine output
Salt and water retention - oedema, HTN
What is the most common cause of glomerulonephritis?
Post-streptococcal nephritis (Group A B haemolytic strep) - body autoimmune response to antigens on kidneys similar to those on bacteria
Nephritis usually 10 days post-infection
How is post-streptococcal glomerulonephritis diagnosed?
Evidence of recent strep infection (culture of organism from throat swab, raised ASO/antiDNAse B titres)
Low complement C3 + C4 levels (normal in 3-4wks)
How is glomerulonephritis managed?
Fluid balance Reduce fluid intake Diuretics, salt restriction Correct other electrolyte imbalances Dialysis may be needed Penicillin - to correct strep infection
What is HSP?
Vasculitis affecting multiple parts of body
Presents with: (often fever)
Skin rash - leg extensors, buttocks, non-blanching purpura raised and palpable
Arthralgia, periarticular oedema - red, swollen
Abdominal pain - petechiae, bleed, intussusception
Glomerulonephritis
Biopsy - shows IgA deposition but diagnosis made off clinical assessment of rash
What may occur in the kidneys as a result of HSP?
Asymptomatic Nephrotic syndrome Glomerulonephritis/acute nephritis Haematuria/proteinuria Renal impairment Hypertension
How is HSP managed?
Analgesia, watch and wait
Corticosteroids if severe colicky abdo pain
FBC, U+Es, CPR, ESR
Urinalysis - for degree of haematuria/proteinuria. If heavy proteinuria - renal biopsy to decide treatment
Prednisolone if nephrotic syndrome occurs
What syndrome is familial nephritis?
Alport syndrome - X-linked recessive
End-stage renal failure in early adult life in males
Sensorineural deafness and ocular defects
Mother may have haematuria
What types of vasculitis other than HSP can cause nephritis?
Polyarteritis nodosa Microscopic polyarteritis Wegener granulomatosis Check for ANCA Treat - steroids, plasma exchange, IV cyclophosphamide
What should always be investigated if there is haematuria?
All regardless: Urine microscopy
Protein and calcium excretion
Kidney and urinary tract USS
Urea, electrolytes, creatinine, calcium, phosphate, albumin
FBC, platelets, clotting screen, sickle cell screen
Glomerular haematuria:
ESR, complement, anti-DNA
Throat swab, antistreptolysinO/anti-DNAse
Hep B and C screen
Renal biopsy if indicated
Test mother’s urine for blood and hearing test (Alport)
What might suggest nephritis due to SLE?
Multiple antibodies - anti-dsDNA, ANA
Low C3 and C4
Other symptoms:
Malaise, arthralgia, malar rash (often photosensitive)
What are some congenital renal malformations?
Multicystic dysplastic kidney Autosomal recessive PCKD, autosomal dominant PCKD Tuberous sclerosis Pelvic kidney or horseshoe kidney Duplex system Bladder extrophy Prune-belly syndrome (absent muscular syndrome) Neuropathic bladder Posterior urethral valves
What is vesicoureteric reflux?
Developmental anomaly of vesicoureteric junctions
Familial or with neuropathic bladder, urethral obstruction, temporarily after UTI
Ureters displaced laterally, at less of an angle and shorter intramural course
Reflux amount varies
Intra-renal reflux increases risk of renal scarring if UTIs occur. Increased risk pyelonephritis, UTI, renal damage due to bladder voiding pressure
What is the triad of haemolytic uraemic syndrome?
Acute renal failure
Microangiopathic haemolytic anaemmia
Thrombocytopenia
What is HUS often secondary to? Give pathophysiology of HUS
Gastrointestinal infection e.g. E.coli O157:H7 (animal contact or meat) or Shigella
Prodrome of bloody diarrhoea
Toxin enters GI mucosa and localises to kidney endothelium - causes intravascular thrombogenesis and activation of coagulation cascade - normal clotting
Platelets consumed by this and damage to RBC in microcirculation which is occluded
Brain, pancreas and heart may also be affected
How is HUS managed?
Supportive therapy, including dialysis (good prognosis)
Follow-up to check for persistent proteinuria, hypertension, renal decline in function
Intracerebral involvement - plasma exchange or plasma infusions
What is atypical HUS?
No diarrhoeal prodrome
May be familial and frequent relapses
High risk of HTN and mortality
Also may need plasma exchange or plasma infusions
What are the commonest causes of acute renal failure in children?
Pre-renal - hypovolaemia, circulatory failure
Renal - HUS or multi-system failure
Post-renal - urinary tract obstruction
Manage - treat underlying cause, metabolic abnormalities, dialysis if necessary
What are features of nocturnal enuresis?
Bed wetting at night, boys:girls is 2:1
Genetically determined delay in acquiring sphincter competence - 2/3 first degree relative
Interference in learning to become dry - stress or lack of parental approval
Organic cause: UTI, faecal retention pressing on bladder, osmotic diuresis (diabetes, chronic renal failure)
What investigation should be done in nocturnal enuresis?
Urinalysis - glucose, protein, check for infection
How is nocturnal enuresis managed?
Treatment rarely taken until after 6yrs old
Instead, explain that is common, beyond conscious control and stop any punishments
Star chart - reward for dry bed
Enuresis alarm - sensor on bed or child’s pants and sounds when bed wet, wakes child to go and pass urine
Desmopressin - short term relief for bed wetting e.g. holidays, sleepovers
Self-help groups
When are fractures more common in children?
More common in boys
More common when bone growth rate at its fastest
Very common in mobile children >1yr. Be wary if non-mobile and fracture - NAI?
Give WHO definition of osteoporosis
Low bone mass and microarchitectural deterioration of bone tissue leading to enhanced bone fragility and consequent increased risk of fracture
What may suggest osteoporisis in children?
1 or more vertebral crush fractures
2 or more long bone fractures by age 10
3 or more long bone fractures by age 19
Bone density scan - < - 2SD
What are the possible causes of acquired osteoporosis?
Drug-induced (especially steroids) Endocrinopathies - e.g. raised corticosteroids Malabsorption Immobilisation Inflammation
What are the inherited causes of osteoporosis?
Commonest = osteogenesis imperfecta Others = galactosemia, haematological disorders, idiopathic
What is the commonest inheritance pattern and genetic pathology behind osteogenesis imperfecta?
Mostly autosomal DOMINANT
Defect in gene coding for type 1 collagen
Causes bones to be FRAGILE and BRITTLE
What are some presenting features of osteogenesis imperfecta?
Fractures, Deformities due to fractures or bowing deformities (type 1), Bone pain
Impaired mobility, Poor growth
Blue appearance to sclerae
Deafness
Hernias
Valvular prolapse
The more severe, the more growth is affected
What are the different types of OI?
1 = mild 2 = lethal 3 = progressively deforming, severe 4 = moderate
What occurs in type 2 OI?
Many infants are stillborn or born with multiple fractures
Lethal - no air in lungs and major deformities
How is OI managed?
MDT - physician, surgeon, dietitian, physio, nurse
BISPHOSPHONATES
Surgery - may have rods to repair deformities etc.
How is osteoporosis managed?
Dietary supplements - calcium, vit D
Regular weight-bearing exercise
Minimise corticosteroids
Sometimes Bisphosphonates
What is rickets?
Decreased mineralisation of bone
often due to vitamin D or calcium deficiency
What features may be present in history of a child with rickets?
Poor sunlight exposure Low vitamin D dietary intake Darker skin Swollen costo-chondral joints Limb deformity, bow legs, metaphyseal swellings Weakness Misery, bone pain Respiratory distress
What is the role of vitamin D/calcitriol?
- increases calcium absorption from gut and calcium resorption from bone, increase renal calcium reabsorption from PCT
- immune function
- maternal vit D influences bone size and mass in childhood
What occurs in large vitamin D deficiencies in babies who are exclusively breastfed?
Life-threatening cardiomyopathy Hypocalcaemia Convulsions Rickets Bowed legs when start walking Often have gross motor delay
What other organ dysfunction may be leading to vitamin D deficiency?
Kidney disease - produces active vitamin D
Liver disease - produces precursor to vit D
Also biliary disease - lack of bile prevents absorption of fab-soluble vitamin D e.g. cholestasis, biliary atresia
How is rickets treated?
Treat calcium deficiency as hypocalcaemia can be dangerous
Vitamin D: <2yrs 3000 units/day, 2-10yrs 6000 units/day, >10 yrs is 10 000 units/day
Stoss therapy if complicance issue - high dose vit D stat
What are the commoner causes of limp in children aged less than 3 years?
Trauma, Infection (cellulitis, osteomyelitis), developmental dysplasia of the hip
What are the commoner causes of limp in children aged 3-10yrs?
Trauma Transient synovitis Osteomyelitis Septic arthritis Perthe's disease
What are the commoner causes of limp in chidlren over 10yrs old?
Trauma, OA, septic cellulitis
Slipped upper femoral epiphysis
Anterior knee pain (chondromalacia)
Perthe’s
Where is pain commonly referred to in children with limp?
Hip pain often referred to knee!
If child complains of knee pain, always check hip
What other area outside of limbs and spine is important to examine for other causes?
Abdomen - appendicits and constipation can cause limp. Testicles may also cause limp
What is Toddler’s fracture?
undisplaced spiral fracture of tibia in pre-school children
Usually only small fall or twisting injury
Tenderness over tibial shaft, may not see fracture on XR
Immobilise for management
What is transient synovitis/irritable hip?
Inflammation of synovium - commonest cause of hip pain in children aged 2-12 yrs
Often follows or accompanied by resp viral infection
affects boys more, usually unilateral
Sudden onset pain in hip or knee, limp, refuse to walk
No pain at rest or passive movement
Decreased ROM
How would you investigate transient synovitis?
XR - may be normal
USS - may show effusion
FBC and ESR slightly elevated or normal
How would you manage transient synovitis?
Bed rest
Symptomatic + pain relief - ibuprofen
What is the most common form of arthritis in childhood?
Reactive arthritis
- transient joint swelling <6 wks often ankles/knees
- Usually follows gastroenteritis, STIs, Lyme disease, rheumatic fever, post-streptococcal
Low grade fever, mildly elevated CRP, WCC
XR normal
No treatment, NSAIDs pain relief
Give features of septic arthritis
Usually <2 yrs but any age possible
Unwell, non-specific early signs, fever
Pain at rest, resist attempt at movement, reluctant to weight bear, ROM reduced and painful
Red, hot, swollen joint acutely. Raised WCC, CRP
XR - may be normal or effusion (if later)
USS - effusion
Can cause permanent damage to peri-articular bone
How is septic arthritis managed?
FBC, CRP, ESR
Blood cultures
USS of deep joints, XR to exclude trauma/others
MRI - to exclude adjacent osteomyelitis?
Immediately joint aspiration under US - culture
Then give antibiotics - prolonged IV (ceftriaxone)
Initially immobilised then mobilised
May require surgical drainage
What is Knocher’s criteria?
Criteria used to determine likelihood of being septic arthritis using fever, weight bear, ESR in first hour, WBC more than 12
Fever and CRP are most important
What is Perthe’s disease?
Avascular necrosis of the capital femoral epiphysis
Followed by revascularisation and reossification over 18-36 months
Mainly affects boys aged 5-10yrs
How does Perthe’s disease present?
Insidious, onset of limp or hip or knee pain, mostly unilateral but can be bilateral
Similar in presentation to transient synovitis
Movement of hip painful especially on internal rotation
No history of trauma
What might be shown on XR for Perthe’s disease?
Might do bilateral if suspect
May be no signs or sclerosis, fragmentation and irregular femoral head
Bone scan or MRI may be helpful if no changes seen on XR to make diagnosis
