Paeds - GI & Renal Flashcards
What is GORD?
- Contents from the stomach reflux through the lower oesophageal sphincter into the oesophagus, throat and mouth.
What are signs of problematic reflux? (6)
-Chronic cough
-Hoarse cry
-Distress, crying or unsettled after feeding
-Reluctance to feed
-aspiration Pneumonia
-Poor weight gain
Management of GORD
Practical
-Small, frequent meals
-Burping regularly to help milk settle
-Not over-feeding
-Keep the baby upright after feeding (i.e. not lying flat)
Medical
-Gaviscon mixed with feeds
-Thickened milk or formula
-Proton pump inhibitors
What is sandifers syndrome
rare condition causing brief episodes of abnormal movements associated with gastro-oesophageal reflux in infants
Two features of sandifer syndrome
Torticollis: forceful contraction of the neck muscles causing twisting of the neck
Dystonia: abnormal muscle contractions causing twisting movements, arching of the back or unusual postures
Differential diagnosis of sandifers syndrome
-Infantile spasms (West syndrome)
-seizures.
What are some secondary causes of constipation in children
Hirschprungs disease
CF
Hypothyroidism
Cerebral palsy
Typical features of constipation
-Less than 3 stools a week
-Hard stools that are difficult to pass
-Rabbit dropping stools
-Straining and painful passages of stools
-Abdominal pain
-Holding an abnormal posture, referred to as -retentive posturing
-Rectal bleeding associated with hard stools
-Faecal impaction causing overflow soiling, with -incontinence of particularly loose smelly stools
-Hard stools may be palpable in abdomen
-Loss of the sensation of the need to open the bowels
What is encopresis
- a sign of chronic constipation where the rectum become stretched and looses sensation
-the large hard stools remain but the loose stool sneak around and leak out
Causes of encopresis
Spina bifida
Hirschprung’s disease
Cerebral palsy
Learning disability
Psychosocial stress
Abuse
Lifestyle factors causing constipation
- not regularly opening the bowels
-low fibre diet
-poor fluid intake and dehydration
-sedentary lifestyle
-abuse
Red flags that are serious when it comes to come constipation
Not passing meconium - may suggest CF or Hirschprungs
Vomiting - may suggest obstruction or Hirschprungs
-ribbon stool - anal stenosis
-neurological Sx - may suggest cerebral palsy or spinal cord lesion
-abnormal lower back - spina bifida
Managment of constipation in children
- recommend high fibre diet and hydration
- laxative - movicols 1st line, senna
-encourage going to the toilets - e.g using schedules and diaries
Faecal impaction tx
Disimpaction regimen with high laxative at first then slowly tapered off
What is the definition of constipation
the infrequent passage of dry, hardened faeces often accompanied by straining or pain
What is hirschprungs disease
Congential condition where nerve cells of the myentetic plexus are absent in the distal bowel and rectum resulting in narrowing of the bowel segment
What syndromes are associated with hirschsprungs
-Downs syndrome
-Neurofibromatosis
-Waardenburg syndrome (a genetic condition causing pale blue eyes, hearing loss and patches of white skin and hair)
-Multiple endocrine neoplasia type II
Presentation of Hirschprungs (5)
-Delay in passing meconium (more than 24 hours)
-Chronic constipation since birth
-Abdominal pain and distention
-Vomiting
-Poor weight gain and failure to thrive
What is Hirschprungs associated enterocolitis
Inflammation and obstruction of the intestine occur in gin 20% of children with hirschprungs
Presentation of HAEC
-fever
-abdominal distension
-diarrhoea ( can be with blood)
What are the complications of HAEC
-perforation of the bowel
-toxic megacolon
-death
Mx of HAEC
-ABX
-fluid resuscitation
-decompression of obstructed bowel
Diagnosis of Hirschprungs
GS
Suction rectal biopsy - to find absence of myenteric ganglion
Barium/ anaorectal manometry - to determine length of a ganglionic segment
MX of Hirschprungs
Colostomy - Removing the aganglionic part of the bowel
What is pyloric stenosis
-Hypertrophy (thickening) and narrowing of the pylorus preventing the food travelling from the stomach to the duodenum
Clinical features of pyloric stenosis (3)
• Vomiting, which increases in frequency and
forcefulness over time, ultimately becoming
projectile
• Hunger after vomiting until dehydration leads to
loss of interest in feeding
• Weight loss if presentation is delayed
How is pyloric stenosis diagnosed
-ultrasound
-test feed performed
may see gastric peristalsis from Left to right
Feel a pyloric mass like an olive
Management of pyloric stenosis
initial priority
-correct fluid and electrolyte balance with IV FLUIDS - potassium and dextrose
Then
-pyloromytomy - reducing the hypertrophic tissue
What metabolic imbalances occur in pyloric stenosis (3)
-hypochloreamic metabolic alkalosis
-hyponatraemia
-hypokalaemia
Presentation of pyloric stenosis
-failure to thrive
-projectile vomiting
What is gastroenteritis
Inflammation from the stomach to the intestines and presents with nausea, vomiting and diarrhoea.
Common cause of gastroenteritis
Viral
Key concern regarding gastroenteritis
Dehydration
Management of gastroenteritis
rehydration
-clinical dehydration - ORS
-shock - IV 0.9 sodium chloride solution an consult paediatrician
-if sepsis suspected then give abx
How is clinical dehydration managed in children
ORS
-give fluid deficit replacement (50ml/Kg) over 4 hours and maintenance fluids
-if vomiting give NG tube
If still not getting better
-IV therapy for rehydration 100ml/Kg if shocked
-give 0.9% nacl solution
Most common causative organism of gastroenteritis in developed countries
Rotavirus
DDX of gastroenteritis
-Infection (gastroenteritis)
-Inflammatory bowel disease
-Lactose intolerance
-Coeliac disease
-Cystic fibrosis
-Toddler’s diarrhoea
-Irritable bowel syndrome
-Medications (e.g. antibiotics)
Viral causes of gastroenteritis
-rotavirus
-norovirus
-adenovirus (less common)
Why should antibiotics not be given in E.coli gastroenteritis
-increases the risk of haemolytic uraemic syndrome
How does e.coli cause Haemolytic uraemic syndrome
- releases shiga toxin
-destroying blood cells
Which bacteria is most commonly responsible for travellers diarrhoea
Enterogenic e.coli
2nd is campylobacter jejuni
How is c.jejuni spread
Raw or improperly cooked poultry
Untreated water
Unpasteurised milk
Antibiotics used for for c.jejuni infection
-azithromycin/clarithromycin
-cirpofloxacin
How is salmonella spread
-eating raw eggs or poultry, or food contaminated with the infected faeces of small animals
Sx of salmonella
-watery diarrhoae can be with mucus or blood
-abdo pain
-vomiting
How is bacillus cereus spread
-grows well on food not immediately refrigerated after cooking. The typical food is fried rice left out at room temperature.
Bacillus cereus infection symptoms
-abdo cramps
-vomiting
-watery diarrhoea
What is the course of a bacillus cereus infection
-vomiting within first 5 hours
-watery diarrhoea after 8 hours
-all Sx resolve within 24 hours
Post Gastroenteritis Complications (4)
-Lactose intolerance
-Irritable bowel syndrome
-Reactive arthritis
-Guillain–Barré syndrome
How due gardia lamiblia spread
faeco oral transmission
-lives in small intestine of mammals
-cysts released in stools of infected mammals
-which contaminate food or water
Tx of giardiasis infection
Metronidazole
How to diagnose gardiasis
Stool microscopy
Red flag signs of dehydration
-appears unwell
-sunken eyes
-tachycardia
-tachypnoea
-reduced skin turgor
-lethargy
What is appendicitis
Inflammation of the appendix
Peak age of appendicitis
10-20 year olds
Key presenting features of appendicitis (7)
-abdo pain - central moving down to the right iliac fossa and localising there
- loss of appetite
- nausea and vomiting
-rosvings sign - LIF palpation causes RIF pain
-rebound tenderness
-percussion tenderness
-Guarding
How to diagnose appendicitis
- clinical presentation + diagnostic laparoscopy
- inflammatory markers
- CT scan - to confirm
- Ultrasound in females to exclude ectopic pregnancy or other gynae pathology
Differential diagnosis of appendicitis
-ectopic pregnancy
-ovarian cyst/ torsion
-meckels diverticulum
-mesenteric Adenitis
-appendix mass
What do you do to exclude ectopic pregnancy
Serum / urine b HCG (pregnancy test)
What is mesenteric Adenitis
-inflamed abdominal lymph nodes, accompanied by abdo pain
-often associated with tonsillitis or URTI
Mx of appendicitis
-immediate admission under the surgical team
Appendectomy
Complications of appendicectomy
-bleeding and infection
-pain and scars
-damage to the bowel bladder
-removal of a normal appendix
-anaesthetic risk
-VTE (DVT and PE) from surgery
What is biliary atresia
- congential condition where a section of the bile duct is either narrow or absent
-leads to cholestasis where the bile cannot be transported from liver to bowel
-prevents the excretion of conjugated bilirubin
Management of biliary atresia (2)
Kasai portoenterostomy
-attaching a section of small intestine to the liver
Full liver transplant
Presentation of babies with biliary atresia
-mild jaundice
-stools are pale
-urine dark
-hepatomegaly
-Splenomegaly
Diagnostic treatment of biliary atresia
Laparotomy by cholangiography - doesnt show the outline of biliary tree
What are choledochal cysts
-cystic dilatations of the bile ducts
Presentation of choledochal cysts
-abdo pain
-palpable mass
-Jaundice
Diagnosis of choledochal cyst
Ultrasound/ radionuclide scanning
Tx of choledochal cyst
-surgical excision
Complications for choledochal cyst
Cholangitis
Malignancy in biliary tree
What is intussusception
Condition where the bowel invaginates of proximal bowel into the distal part
-most commonly ileum passing into the caecum
What the most common cause of intestinal obstruction in infants
Intussusception
Presentation of intussusception (6)
-sudden, severe, colicky pain
-pallor
-refuse feeds
- vomiting (can be bilestained depending on site
-palpable sausage shaped mass
-redcurrant jelly stool comprising of blood stained mucus
-abdominal distension
Investigations for intussusception
X-ray
-distension of small bowel
-abscence of gas in distal colon
Abdo ultrasound - first line
-TARGET SHAPED MASS
Contrast enema
In boys what should you always consider for acute abdo pain?
- strangulated inguinal hernia
- torsion of testis
Treatment of intussusception (3)
- immediate fluid resuscitation
- reduction by rectal air insufflation
- surgery if above unsuccessful
Complications of intussusception (4)
Venous Obstruction
Gangrenous bowel
Perforation
Death
What is meckels diverticulum
Failure of the obliteration of the vitelline ducts
How to diagnose meckels diverticulum
Technetium scan - shows ectopic gastric mucosa in RIF
Extra intestinal manifestation of Crohn’s disease in children?
-oral lesions like apthous ulcers
-perianal skin tags
-uveitis
-arthralgia
-erythema nodosum
Classic presentation of Crohn’s disease in child
-abdo pain
-diarrhoea
-weight loss
-fever
-lethargy
-growth failure
-delayed puberty
What is Crohn’s disease
A form of IBD
Characterised by transmural inflammation, skip lesions most commonly affecting terminal ileum due to T cell immune mediated response
Where does Crohn’s disease most commonly affects
-Where GI tract
-most commonly proximal colon/ terminal ileum
How to diagnose Crohn’s disease
-Biopsy + endoscopy
-raised faecal calcprotectin (in all IBD)
-ANCA -ve unlike UC
-CRP, ESR, platelet count raised
-iron deficiency present
What are the finding of biopsy and endoscopy in crohns diseases
Biopsy
-transmural inflammation (all 4 layers of gut)
-non caseating granuloma
Endoscopy
-skip lesions
-cobblestoning
Micro and macro features of Crohn’s disease
Macro
-skip lesions
-cobblestone appearance due to fissures and ulcers
-thickened and narrow
Micro
-transmural
-non caseating granulomas
-increased goblet cells
Pathology of Crohn’s disease
-Faulty GI epithelium allows pathogen to enter wall
-leading exaggerated inflammatory response
-formation of granulomas and destruction of GI tissue
-leading to transmural ulcers and skip lesion and cobblestone appearance
-as the wall heals adhesions and fistulae form
Treatment for Crohn’s disease
Initially
-polymeric diet (liquid) 6-8 weeks works in 75% of cases
Steroids (oral prednisolone/ IV hydrocortisone)
Relapse then add
1st - azathioprine
2nd - Methotrexate
3rd - infliximab/ adalinumab (anti TNF)
When is surgery used in crohns
to treat complications such as:
Fistulae
Obstruction
Abscess formation
When disease is localised
What is ulcerative colitis
A form of IBD
That is a recurrent, inflammatory and ulcerating disease involving the mucosa of the colon
Inflammation goes from rectum upwards but never going past ileoceacal valve
What genes are associated with UC
HLAb27
What antibody is associated with UC
Positive pANCA
Symptoms of UC
-Pain in LLQ
-tenesmus
-bloody, mucus and watery diarrhoea
-weight loss and growth failure - more common in crohns
Extra intestinal features in UC
-arthritis
-erythema nodosum
-PSC
-clubbing
-episcleritis
-aphthous ulcers
How is UC diagnosed
Endoscopy (upper and ileocolonscopy)
Biopsy - crypt abscesses
Barium enema
Bloods - raised CRP and ESR
- faecal calprotectin
-iron deficiency aneamia
-positive pANCA
Stool sample - rule out infective colitis
Abdo x-ray - check for toxic megacolon
Macro and micro features of UC
macro
-continuous inflammation
-ulcers
-pseudo polyps
Micro
-Mucosal inflammation
-no granulomata
-depleted goblet cells
-increased crypt abscesses
What’s the inflammation like in UC
-continuous inflammation of LARGE bowel
-only affecting mucosa and sub mucosa
-can lead to crypt abscesses
How does UC differ in adults compared to children§
-the colitis is not confined to the distal colon and instead 90% of children have PANCOLITIS (all large bowel)
Treatment for UC
Mild UC
1st line -aminosalicylates (mesalazine/ balsalazide)
2nd line -topical steroids
Severe UC
1st line - IV corticosteroids (hydrocortisone) + azathioprine
2nd line - IV ciclosporin
GOLD - Colectomy with ileostomy
1st line TX for maintaining remission of UC
Aminosalicylate
-mesalazine
-azathioprine
-mercaptopurine
Complications of crohns
-peri anal abscess
-anal fissure
-anal fistula
-obstruction
-strictures (narrowing)
-anaemia
-malabsorption
-osteoporosis
Complications of UC
-toxic megacolon
-perforation
-colonic adenocarcinoma
-obstruction
-strictures
Score for UC
Truelove and WITTS score
What is coeliac disease
utoimmune condition where exposure to gluten causes an immune reaction that creates inflammation in the small intestine usually developing in childhood
Pathophysiology of coeliac
-autoantibodies are created in response to exposure to gluten.
-These autoantibodies target the epithelial cells of the intestine and lead to inflammation.
Two antibodies involved in coeliac
anti-tissue transglutaminase (anti-TTG)
anti-endomysial (anti-EMA)
How does coeliac lead to malabsorption
-inflammation affects the jejunum particularly
-constant inflammation causes atrophy of the villi
-causes decreased Surface area of gut wall causes decreased nutrient uptake
Presentation of coeliac
-OFTEN ASX
-Failure to thrive in young children
-Diarrhoea
-Fatigue
-Weight loss
-Mouth ulcers
-Anaemia secondary to iron, B12 or folate deficiency
-**Dermatitis hepetiformis ** - is an itchy blistering skin rash that typically appears on the abdomen
What condition is linked and always tested for alongside coeliac
Type 1 diabetes
Genetic association with coeliac (2)
- HLA-DQ2 gene (in 90%)
- HLA DQ8 gene
Why do you test for total IgA levels in coeliac
-because Anti-TTG and Anti-EMA are IgA
-so some patients have IgA deficiency
-so will be false negative even if they have coeliac
**so then you test for IgG version of anti-TTG/EMA
Dx of coeliac (3)
-MUST BE DONE WHILE STILL ON GLUTEN DIET
-Check total immunoglobulin A levels to exclude IgA deficiency before checking for coeliac disease specific antibodies:
Raised anti-TTG antibodies (first choice)
Raised anti-endomysial antibodies
-Endoscopy and intestinal biopsy show:
Crypt hypertrophy
Villous atrophy
Coeliac disease associations (6)
-type 1 diabetes
-thyroid disease
-autoimmune hepatitis
-PBC
-PSC
-Down’s syndrome
Tx of coeliac
Lifelong gluten free diet
Complications of coeliac
-Vitamin deficiency
-Anaemia
-Osteoporosis
-Ulcerative jejunitis
-Enteropathy-associated T-cell lymphoma (EATL) of the intestine
-Non-Hodgkin lymphoma (NHL)
-Small bowel adenocarcinoma (rare)
What is intestinal obstruction
-physical obstruction prevents the flow of faeces through the intestines.
-This blockage will lead to a back-pressure through the gastrointestinal system, causing vomiting and absolute constipation
Cause of intestinal obstruction
-meconium ileus
-hirschsprungs
-oesophageal atresia
-duodenal atresia
-intussusception
-malrotations with volvulus
-strangulated hernia
-imperforate anus
Presentation of intestinal obstruction
-Persistent vomiting - may be bilious
-abdo pain
-distension
-failure to pass stools
-tinkling bowel sounds/ absent bowel sounds
Dx of obstruction
abdo X-ray
-dilated loops of bowel before the obstruction (proximal)
-collapsed loops past the obstruction (distal)
-absence of air in the rectum
Management of obstruction
-nil by mouth
-insert nasogastric tube
-IV fluids to prevent and correct dehydration
-antiemetics and analgesia
-surgery last resort
Presentation of marasmus
-wasted wizened appearance
-skinfold thickness and mid arm circumference reduced markedly
-withdrawn personality
-head appears large for body
-dry brittle skin and hair
-lethargy and weakness
What is marasmus
Severe caloric and Protein energy malnutrition
-child has heigh and weight 3 standard deviations below the average
Tx for marasmus
1- rehydration and fix electrolyte imbalance
2- nutritional rehabiliton - use liquid formulas and tube feeding balances fats, carbs and protein
3- prevention
Presentation of Kwashiokor (9)
-generalised oedema
-severe wasting
-flaky paint skin rash and skin thickening
-angular stomatitis
-sparse hair
-diarrhoea
-hypothermia
-bradycardia
-hypotension
What problems can need to be treated with malnutrition (6)
-hypoglycaemia
-Hypothermia - wrap up the child
-dehydration - IV fluids
-electrolyte imbalance - correct deficiencies
-infection - give ABX
-initiate feeding - small volumes frequently
Reasons for malnutrition in less economically developed countries
- war
-social disruption
-famine
-natural disasters
Reasons for malnutrition in developed countries
-poverty
-parental neglect
-poor education
-Restrictive diets
-feeding disorders
-chronic illness
-anorexia
What is the WHO definition of malnutrition (3)
- weight for height - 3 SDs below the median
- mid upper arm circumference - less than 115mm
-height for age - shows growth stunting and an indication of chronic malnutrition
What is kwashiorkor
A manifestation of severe protein energy malnutrition particularly affecting children in the tropics
What does failure to thrive mean
- Sub optimal weight gain in infants and toddlers when plotted on a centile chart
-is present if the infant weight falls across two centile lines
Give 6 Causes of failure to thrive
Not extensive list
-feeding problems E.g insufficient breast milk
-lack of regular feeding times
-low socioeconomic status
-infant resists feed
-maternal depression
-lack of maternal education
-neglect
-cleft palate
-Crohn’s disease
-CF
-vomiting and GORD
-coeliac
-Down’s syndrome
-malignancy
-CHD
How are inguinal hernia normally caused
Patent Processus vaginalis
how does an inguinal hernia normally present
-an irreducible lump in the groin or scrotum
-irritability
-vomiting
-pain on straining or coughing
Biggest risk in inguinal hernias
Strangulation of the hernia (blood supply compromised to area)
Treatment for inguinal hernias
- opioid analgesia and sustained gentle compression
-surgery urgently to avoid strangulation
Assessment for failure to thrive includes? (7)
-pregnancy, birth, development and social history
-feeding or eating history
-observe feeding
-mums physical and mental health
-parent and child interaction
-HEIGHT,WIEGHT AND BMI and plot on growth chart
-mid parental height
What is the mid parental height
Calculate mean of parental heights
-add 7cm for male infants
-subtract 7cm for female infant s
What is includes in a feeding history
Ask about:
-breast/ bottle fed
-feeding times, volume and frequency
-difficulty with feeding
-food choices
-meal time routines
-appetite of child
-food aversion
how to calculate BMI
Weight Kg/height m2
Outcomes that suggest inadequate nutrition/ growth disorder
-Height more than 2 centile spaces BELOW the mid-parental height centile
-BMI below the 2nd centile
Initial investigations with faltering growth
-urine dipstick for UTI
-coeliac screen (anti TTG/ Anti EMA)
How to manage failure to thrive if inadequate nutrition is the cause
-nutritional supplemental drinks
-dietician review
-energy dense foods to boost calories
-reduce milk consumption to improve appetite for other food
-encourage regular mealtimes
What is cows milk protein allergy
A hypersensitivity reaction to the protein in cows milk can be IgE mediated or non IgE mediated
Difference between IgE mediated and non IgE mediated cows milk protein allergy
IgE mediated - rapid reaction to cows milk occurring within 2 hours
Non IgE mediated -slowly over several days
In who are cows milk protein allergy more common
- formula fed babies
- family history of atopic conditions
Presentation of cows milk protein allergy
GI symptoms
-bloating and wind
-abdo pain
-diarrhoea
-vomiting
Allergic symptoms
-urticarial rash
-angio oedema
-cough or wheeze
-watery eyes
-Eczema
Severe - anaphylaxis
Mx of cow milk protein allergy
Avoid cows milk
-breast feeding mothers avoid dairy products
-replace formula with hydrolysed formula designed for cows milk protein allergy
-normally children outgrow the allergy at 3 years old
Ix for cows milk protein allergy
-full history and examination
-Skin prick testing
How does hydrolysed formulas help cows milk protein allergy
-Hydrolysed formulas contain cow’s milk
-however the proteins have been broken down so that they no longer trigger an immune response.
Difference between cows milk intolerance and cows milk allergy
-with allergy children will not be able to tolerate it at all, in tolerance will just suffer GI symptoms
-they both have GI symptoms but allergy will have rash, angio oedema, sneezing and coughing
Differential diagnosis of toddlers diarrhoea
-lactose intolerance
-fructose/sucrose intolerance
-infective causes - rotavirus, norovirus, gastroenteritis
-IBD
How can diarrhoea be helped
4F’s
-low fat diet
-6-8 cups of fluid
-regulate the amount of fruit due to fructose not being as easily absorbed at a young age
-fibre intake - 12/18g per day
What is toddlers diarrhoea
-benign diarrheal disorder that presents with 6-8 watery stools per day for more than 3 weeks without evidence of systemic illness
What is a UTI
An infection of anywhere along the urinary tract including the urethra, bladder, ureters and kidneys
What is cystitis
Imflammation of the bladder
What is pyelonephritis
Infection of the kidneys can lead to scarring and reduced kidney function
Symtoms of UTI in babies
Babies:
FEVER
Lethargy
Irritability
Vomiting
Poor feeding
Increase frequency
Symptoms of UTI in older children
FEVER
Abdo pain - particularly suprapubic
Vomiting
dysuria - pain on urination
Urinary frequency + urgency
Incontinence
Diagnostic criteria for acute pyelonephritis (2)
-temp greater than 38
-loin pain/ tenderness
Methods to get urine from a child (5)
-clean catch sample into a waiting clean pot when nappy is removed - GS
-adhesive plastic bag applied to perineum that has been washed
-urethral catheter if urgency needed
-suprapubic aspiration - fine needle inserted directly into the bladder
-older children - can use midstream sample
When should a urine sample always be collected and tested
-patient has temperature of 38 or above
Bacterial and host factors that predispose to UTI (4)
-the infecting organism (hygiene) - E.coli comes from bowel flora
-constipation
-Immunosuppression
-antenatal diagnosed renal or urinary tract abnormality
-incomplete bladder emptying
-vesicouteric reflux - backflow of urine into renal pelvis
What do nitrites and leukocytes suggest in a urine dipstick
Nitrites - gram negative bacteria break down nitrates to nitrites - so suggest bacteria in the urine
Leukocytes - raised number can suggest an infection or inflammation - urine dipstick test for leukocyte esterase
Management of UTI in children
All children under 3 months with a fever
- start immediate IV Abx e.g cefotaxime
- AND full septic screen and refer
Over three months - pyelonephritis/ UUTI
- oral antibiotics usually cefalexin or co amoxiclav 7-10 days unless sepsis suspected then IV Abx
Over three months cystitis/ LRTI
- oral antibiotics for 3 days 1st line trimethoprim 2nd line amoxicillin/ nitrofurantoin
Typical antibiotics of choice for UTI in child (4)
Trimethoprim
Nitrofurantoin
Cefalexin
Amoxicillin
What is a DMSA scan
- injecting a radioactive material (DMSA)
- using a gamma camera to assess how well the material is taken up by the kidneys.
-where some parts of the kidney have not taken the material indicates scarring from previous infection
What is a micturating cysturethrogram (MCUG)
-catheterise the child
-inject contrast into the bladder
-take x-rays to determine wether the contrast is releasing into the ureters - checking for reflux
How is vesico uteric reflux diagnosed
Micturating cystourethrogram (MCUG)
Management of vesico uteric reflux
-Avoid constipation
-Avoid an excessively full bladder
-Prophylactic antibiotics
-Surgical input from paediatric urology
When should children have abdo ultrasound scans for UTIs (3)
- all children under 6 months with their first UTI within 6 weeks
- children who have recurrent UTIs within 6 weeks
- children with atypical UTIs during illness
What is nephrotic syndrome
When the basement membrane in the glomerulus become highly permeable to protein, allowing leakage of proteins from blood to urine
Clinical signs of nephrotic syndrome (4)
-periorbital oedema - especially on waking
-scrotal or vulval, leg and ankle oedema
-ascites
-breathlessness - due to pleural effusion and abdo distension
-foamy urine - due to excess protein
Pyelonephritis triad of symptoms
- loin pain
-fever
-nausea and vomiting
Investigations for pyelonephritis
-urine dipstick And MC+S
-if recurrent then abdo ultrasound
Medical advice to prevent UTIs (3)
- high fluid intake
- regular voiding
- ensure complete bladder emptying
Classic triad of nephrotic syndrome
Hypoalbuminaemia < 3.4 g/dL
High urine protein content >3 on urine dipstick (frothy urine)
Oedema
Other than the classic triad what are three other features that occur in patients with nephrotic syndrome
Deranged lipid profile, with high levels of cholesterol, triglycerides and LDLs
High blood pressure
Hyper-coagulability, with an increased tendency to form blood clots
Most common cause of nephrotic syndrome in children
Minimal change disease (90%) in under 10s
What are some causes of nephrotic syndrome (6)
Isolated
- minimal change
Secondary to intrinsic kidney disease
- focal segmental glomerulosclerosis
- membranoproliferative glomerulonephritis
Secondary to systemic illness
- henoch schonlein purpura
- diabetes
- infection
What infections can cause nephrotic syndrome
HIV
Malaria
Hepatitis
What is minimal change disease
Most common cause of nephrotic syndrome in children That can occur in otherwise healthy children without any clear reason
Investigations in minimal change disease
Urinalysis - small molecular proteins and hyaline casts
Renal biopsy - no abnormality
Management of minimal change disease
Corticosteroids (prednisolone)
Management of nephrotic syndrome
- high dose steroids for 4 weeks and then weaned over 8 weeks (prednisolone) + PPI
- low salt diets
- diuretics for oedema
- albumin infusions for hypoalbuminaemia
- antibiotic prophylaxis in severe cases
What is steroid sensitive nephrotic syndrome
Children that shows the proteinuria resolves with corticosteroid therapy
Management for steroid resistant nephrotic syndrome
- cyclosporine
-tacrolimus
-referred to paediatric nephrologist
-given diuretics for oedema
-salt restriction
-ACE inhibitors
-sometime NSAIDS
Complications of nephrotic syndrome
-hypovolaemia
-thrombosis
-infection
-hypercholesteroleamia
-acute renal failure
Why can hypovolaemia occur in nephrotic syndrome
fluid leaks from the intravascular space into the interstitial space causing oedema and low blood pressure.
Why can thrombosis occur in nephrotic syndrome
- proteins that normally prevent blood clotting are lost in the kidneys (antithrombin)
-liver responds to the low albumin by producing pro-thrombotic proteins.
- lead to PE and DVT
Why can infection be a complication in nephrotic syndrome
-kidneys leak immunoglobulins, weakening the capacity of the immune system to respond.
-This is exacerbated by treatment with medications that suppress the immune system, such as steroids.
-most common infection is pneumococcus and seasonal influenza
What would be seen on light and electron microscopy for minimal change, FSGS, membranous nephropathy
Minimal change:
Light microscope - no change
Electron microscope - podocyte effacement and fusion
Focal segmental glomerulosclerosis
Light microscope - segmental sclerosis less than 50%
Electron microscopy - podocyte effacement
Membranous nephropathy
Light microscope - thickened GBM
Electron microscope - sub podocyte immune complex deposition
What inheritance pattern of congenital nephrotic syndrome
Autosomal Recessive
Which groups are more likely to get congenital nephrotic syndrome
-Finnish people
-consanguineous families
Tx for congenital nephrotic syndrome
- unilateral nephectomy to control albuminuria
-then dialysis for renal failure
-until old and fit enough for kidney transplant
Causes of acute nephritis
-Post-infectious (including streptococcus)
-Vasculitis Henoch–Schönlein purpura, SLE, Wegener granulomatosis, microscopic poly-
arteritis, polyarteritis nodosa)
-IgA nephropathy and mesangiocapillary
glomerulonephritis
-Goodpasture syndrome – very rare.
What is nephritis
Inflammation within the nephrons of the kidneys causing
-reduction in kidney function leading to hypertension
-haematuria
-proteinuria (less than in nephrotic)
How does post strep glomerulonephritis occur
- 1- 3 weeks after a beta haemolytic strep infection such as tonsillitis (strep pyogenes)
-immune complex made up of strep antigens, antibodies and complement proteins get stuck in the glomeruli
-leading to inflammation and deterioration of kidney function
Management of post strep glomerulonephritis
-antihypertensive for HTN
-diuretics for oedema
What is IgA nephropathy
-IgA deposits in the nephrons of the kidney causing inflammation
-closely related to henoch schonlein purpura
Mx of IgA nephropathy
antihypertensives
-ACE inhibitors
-ARBs
immunosuppressants
-Steroids
-Cyclophosphamide
How does henoch schonlein purpura lead to nephritis
-causes increased circulating IgA antibodies and disrupt IgG antibodies
-causes production of complexes that activate complement and are deposits Ed in organs like the kidney
-leading to inflammatory response
What is Alport syndrome
-an X-linked dominant/recessive disorder due to mutation of COL4A5 that progresses to end-stage renal failure by early adult life in males
-associated with nerve deafness and ocular defects and kidney disease
Management of alport syndrome
Slow the progression
- ACE inhibitors - BP
- ARBs - BP
- diuretics - oedema
Kidney Transplant IS CURE
Hearing aid for hearing loss
Treatment for vasculitis related nephritis (3)
- Steroids
- plasma exchange
- IV cyclophosphamide
Symptoms of vasculitis
- fever
- Malaise
- weight loss
- skin rash
- arthropathy
Findings of post strep GN under:
Light microscope
Electron microscope
Immunofluorescence
Light microscope - hyper cellular glomeruli
Electron microscope - subendothelial immune complex deposition
Immunofluorescence - starry sky appearance of IgG, IgM and C3 deposits along GBM
How to diagnose lupus
Anti DsDNA antibodies
ANA +ve
Management of SLE related nephritis (3)
- Steroids
- Hydroxychlorquine
- Cyclophosphamide
Difference in findings between HSP and IgA nephropathy
IgA nephropathy - will only see IgA deposition in the kidneys
HSP - will see it all over organs such s kidney, liver, skin
What type of hypersensitivity reactions are most causes of nephritic syndrome
Type 3 (except goodpastures)
Classic triad of haemolytic Uraemic syndrome
- Microangiopathic haemolytic anaemia
- Acute kidney injury
- Thrombocytopenia (low platelets)
What is microangiopathic haemolytic aneamia
-destruction of red blood cells due to pathology in small vessels
-Tiny blood clots partially obstruct the small vessels and cause rupturing of RBC
What is haemolytic uraemic syndrome
- involves thrombosis in small blood vessels throughout the body
-often affects children following an episode of gastroenteritis
Which bacteria often lead to HUS
Shiga toxins released from
- E.coli 0157
- shigella
What medications can increase the risk of developing HUS (2)
Antibiotics e.g quinines
Anti motility meds (loperamide)
Presentation of HUS
First Sx - Diarrhoea that turns bloody after 3 days
Then:
Fever
Abdominal pain
Lethargy
Pallor
Reduced urine output (oliguria)
Haematuria
Hypertension
Bruising
Jaundice (due to haemolysis)
Confusion
How to treat HUS (5)
Usually self limiting with supportive care
- Stool culture to establish causative organ and give Appropraite Abx
Hospital admission to treat:
Hypovolaemia (e.g., IV fluids)
Hypertension
Severe anaemia (e.g., blood transfusions)
Severe renal failure (e.g., haemodialysis)
What is a hypospadia
-a congenital condition where the opening of the urethra is abnormally displaced to the bottom side of the penis toward the scrotum
Management of hypospadias
- Mild cases may not require any treatment
-Surgery performed after 3 – 4 months of age,
aims to correct the position of the meatus and straighten the penis
Complications of hypospadias (3)
Difficulty directing urination
Cosmetic and psychological concerns
Sexual dysfunction
Bleeding
Ulceration
Why are parents of children with hypospadias warned to not get their children circumsized?
Because it is often needed for the reconstructive surgery
What is a Chordee
Ventral curvature of the shaft of the penis (downwards) particularly seen during erection
What is phimosis
The inability to retract the foreskin which at first is physiological, but can then be pathological
which disease causes pathological phimosis
Local skin disease called Balanitis xerotica obliterans (BXO) AKA: lichen sclerosis
Management of phimosis
Circumcision - to reduce risk of UTI
How to diagnose alport sydrome (2)
-Genetic testing
-Biopsy
Skin
Kidney - review of Glomerular basement membrane
Alport syndrome clinical features (5)
- microscopic haematuria in childhood
- proteinuria
- hypertension due to renal impairment
- sensorineural hearing loss
- ocular pathology
What are the ocular effects that Alport syndrome can cause
Anterior lenticonus: protrusion of the lens due to weakness of the lens capsule.
Retinal granulations: white / yellow granulations seen on the retina.
Cornea: recurrent corneal erosions.
Symptoms of nephritic syndrome (7)
Lethargy
Recent infection: fever, sore throat, coryzal symptoms. Typical of poststreptococcal glomerulonephritis and IgA nephropathy
Haematuria
Oliguria: reduce urine output
Oedema: peripheral or periorbital
Shortness of breath: due to fluid overload
Haemoptysis: due to pulmonary haemorrhage (e.g. Anti-GBM, ANCA-vasculitis)
Pathophysiology of lupus nephritis
-Immune complexes form due to anti-double-stranded DNA and deposit within the renal glomeruli.
-compliment proteins also activated
-leading to immune reaction
What are ANCA associated vasculitis
Microscopic polyangiitis (MPA)
Wegener’s granulomatosis
Eosinophilic granulomatosis with polyangiitis (EGPA)
How do ANCA associated vasculitis lead to glomerulonephritis
-the positive ANCAs which are antibodies target small blood vessels
-causes inflammation of small blood vessels and affects the glomeruli leading to poor filtration
Treatment of ANCA glomerulonephritis
-corticosteroids
-cyclophosphamide
Causes of AKI
Pre renal the most common cause in children: Hypovolaemia caused by infections such as gastroenteritis, burns, sepsis, haemorrhage and nephrotic syndrome
Renal: HUS, vasculitis, renal vein thrombosis, acute tubular necrosis, glomerulonephritis, pyelonephritis
Post renal: obstructions such as posterior urethral valves, blocker catheters, stones
What is enuresis
Involuntary bed wetting
What is primary nocturnal enuresis
Child has never managed to be consistently dry at night.
Causes of primary nocturnal enuresis
-family history of delayed dry nights
-overactive bladder
-fluid intake prior to bedtime e.g caffeine as is a diuretic
-failure to wake
-psychological distress - school stress and low self esteem
-secondary causes - constipation, UTI, cerebral palsy
Initial step of management primary nocturnal enuresis
2 week diary of:
-toileting
-fluid intake
-bed wetting episodes
Management of primary nocturnal enuresis
-reassurance to parents and children under 5 years is normal
-lifestyle changes - less fluid before bed/ pass urine before bed
-positive reinforcement and encouragement and avoid punishment
-treat underlying factors such as constipation
-enuresis alarms
-pharmacological treatment
What is secondary nocturnal enuresis
where a child begins wetting the bed when they have previously been dry for at least 6 months
-more indicative of underlying illness
causes of secondary nocturnal enuresis (5)
-Urinary tract infection
-Constipation
-Type 1 diabetes
-New psychosocial problems (e.g. stress in family or school life)
-Maltreatment - always think abuse
What is diurnal enuresis
Daytime incontinence, dry at night but still has episode of urinary incontinence during the day
-more frequent in girls
Two main types of diurnal incontinence
Urge incontinence - is an overactive bladder that gives little warning before emptying
Stress incontinence - describes leakage of urine during physical exertion, coughing or laughing
Pharmacological treatment for nocturnal enuresis
Nocturnal enuresis
Desmopressin - analogue vasopressin (ADH)
Urge incontinence
Oxybutinin - anticholinergic reducing the contractility of the bladder
Imipramine is a TCA - relax the bladder and lighten sleep
What is the definition of malrotation
-condition where bowel twists abnormally in utero
What is volvulus
Twisting of the bowel loops which leads to intestinal obstruction
Presentation of volvulus or malrotation
-abdo pain
-bilious vomiting
-abdo distension
-tachycardia with HTN due to severe abdo pain
Ix for malrotation/ volvulus
Barium enema
Abdo x- ray with contrast
Treatment for malrotation
Period of monitoring
Ladds procedure via laparoscopy
IV fluids and antibiotics
Treatment for volvulus
Ladds procedure
-intestine is straightened out and divided where small intestine moved to right and colon to the left
What is necrotising entercolitis
Acute inflammatory disease affecting preterm neonates leading to bowel necrosis and multisystem organ failure
Risk factors for necrotising enterocoltiis
-low birth weight
-most common surgical emergency in neonates
-prematurity
-Abx Therapy for longer than 10 days
Clinical presentation of necrotising entercolitis
-feeding intolerance
-vomiting (can be bilious)
-fresh blood in stools
-abdo distension
-reduced bowel sounds
Ix for necrotising entercolitis
Bloods - thrombocytopenia, neutropenia
Blood gas - acidotic
X ray - riglers sign- both sides of bowel are visible due to gas in the cavity
Mx for necrotising entercolitis
-nil by mouth
-bowel decompression by NG tube
-IV cefotaxime
-surgery to remove necrotic bowel
What is neonatal physiological jaundice
-Breakdown of in utero heamaglobin by the baby
-the immature liver cannot process high concentrations of bilirubin
-starts at 2-3 days of life
What is pathological neonatal jaundice
-when it comes on less than 24 hours after birth
-indicates G6PD deficiency, spherocytosis, rhesus diseases, blood group incompatibility
What is Prolonged neonatal jaundice
What are some causes of
Jaundice for longer than 14 days in term infants
Causes:
-biliary atresia
-hypothyroidism
-breast milk jaundice
-UTI
Investigations for neonatal jaundice (3)
-TCB - transcutaneous bilirubinometry non invasive test to determine the need for serum bilirubin
-Coombs test - detects antibodies
-infection screen
-FBC
-TFT
-blood and urine cultures
-G6PD levels
Mx for neonatal jaundice
-use of treatment threshold graphs specific for gestational age
-phototherapy if above threshold and repeat serum bilirubins every 4-6 hours
-if levels reach second threshold then exchange transfusion
(See TCBM measurement)
What is oesophageal atresia?
A congenital condition where the oesophagus and trachea don’t separate normally meaning the food doesn’t pass from mouth to stomach as upper and lower oesophagus dont connect
What condition is also normally present with oesophageal atresia?
tracheal fistula
Risk factors for oesophageal atresia
Maternal use of alcohol
Smoking
Uncontrolled diabetes
Increased maternal age
VACTERL syndrome
Trisomy’s - Down syndrome (21), patau (13), edwards(18)
What is a tracheal fistula
Where the trachea fuses with either the upper/lower/both parts of the oesophagus in oesophageal atresia
Complications of oesophageal atresia with tracheal fistula (6)
-Preoperative
-Postoperative
Preoperative due to aspiration
Bronchiectasis
Lung abcess
Aspiration pneumonia
Posteroperative
-strictures
-recurrence of fistula
-leaking at the site of joining
Why does oesophageal atresia cause polyhydramnios prenatally
Fetus doesn’t swallow amniotic fluid normally so it builds up
Signs of oesophageal atresia (3C’s) (9)
-coughing
-cyanosis
-choking
-Frothy Salivation from mouth and nose
-excess drooling
-inability swallowing feeds
-abdo distension
-vomiting
-resp distress - aspiration pneumonia
Ix of oesophageal atresia
-examination - nasogastric/ orogastric tube cant pass all the way
-Abdo x rays - may see gastric bubbles of air (if lower oesophagus connects to trachea)
Chest x-ray with contrast - diagnostic
Tx of oesophageal atresia
Surgery
What is gastroschisis
when a baby is born with the intestines sticking out through a hole in the belly wall near the belly button
Difference between omphalocele and gastroschisis
Omphalocele is where the abdominal contents protrude into the umbilical cord meaning they are SEALED by a peritoneal layer of the cord
Risk factors for gastroshcisis
Increased Maternal age
Alcohol + Tobacco during pregnancy
Diagnosis of gastroschisis before birth
Ultrasound
Blood test raised alpha feta protein is associated with abdo wall defects
Treatment of gastroschisis (3)
Surgery - where the intestines are placed back in the body and closure of the defect
IV nutrients
ABx for potential infection
What is kernicterus
brain damage caused by excessive bilirubin levels as bilirubin can cross the blood brain barrier
What is the presentation of kernicterus
-non responsive baby
-floppy
-drowsy
-poor feeding
What is the complications of kernicterus (3)
Cerebral palsy
Learning disability
Deafness
What are treatment threshold charts for neonatal jaundice
Charts that measure total bilirubin levels based on their gestational age neonatal jaundice
If it passes the first threshold then give phototherapy
If it passes the second threshold then give exchange transfusion
How does phototherapy work for jaundice
Converted unconjugated bilirbin into isomers that can be excreted without undergoing conjugation inj the liver
-blue light is best + protect the eyes with an eye patch
-monitor bilirubin levels for further 18 hours to make sure it doesn’t spike again
Investigations for UTIs in children
URINE DIP NOT VIABLE IN UNDER 3 MONTHS
Urine culture
Blood culture
LP- for meningitis for any child under 1 with fever
Kidney ultrasound -look for renal malformation
If resistant strain of bacteria for UTI which Abx do you move to
Meropenem
Posterior urethral valve presentation
Difficulty urinating
Weak urinary stream
Chronic urinary retention
Palpable bladder
Recurrent urinary tract infections
Impaired kidney function
Bilateral hydrnephrosis
Oligohydramnios
Underdeveloped fetal lungs
Posterior urethral valve Ix
Abdominal ultrasound - enlarged, thickened bladder and bilateral hydronephrosis
MCUG -location of the extra urethral tissue and reflux of urine back into the bladder
Cystoscopy involves a camera inserted into the urethra to get a detailed view of the extra tissue. Cystoscopy can be used to ablate or remove the extra tissue.
Posterior urethral valve mx
Mild cases - observed and monitored. temporary urinary catheter inserted to bypass the valve whilst awaiting definitive management.
Definitive management- ablation or removal of the extra urethral tissue, usually during cystoscopy.
What is posterior urethral valve
where there is tissue at the proximal end of the urethra (closest to the bladder) that causes obstruction of urine output
What is DMSA used to assess
Kidney scarring and function comparatively to each kidney
Sx of alports syndrome
-sensorineural hearing loss - bilateral
-vision problems - lenticonus
-pregoressive renal failure
-microscopic haematuria
Treatment for c.diff infection
1st line- oral vancomycin
2nd line - oral fidaxomicin
3rd line/ life threatening - Oral Vancomycin + IV metronidazole
Risk factors for c.diff infection
PPI use
Cephalosporins
