Abdominal system MRCPCH Flashcards

1
Q

ABDOMINAL EXAMINATION

A

INTRODUCTION

  • Look around for alcohol gel and use it
  • Introduce yourself to parent and child
  • Ask for child’s name and age
  • Confirm who child has with them
  • Thank for coming to the exam
  • Explain that you have been asked to examine the abdomen
  • Ask for permission (from parent only if young child)
  • Ask about any pain, tell child to stop you right away if anything you do hurts
  • Position flat +/- expose as appropriate, ideally underwear only

INSPECT

  • Make a show of taking a step back and inspecting from the end of the bed
  • Growth/nutrition: body habitus, pallor, thin hair
  • Paraphernalia – NGT/PEG, oxygen, IV access, monitors, meds
  • General health/comfort at rest – also look at chest/resp status as may get a CF pt
  • Dysmorphism, Cushing’s
  • Colour (pink, pale, cyanosed, jaundiced)
  • Obvious scars, stomas, distension
  • Legs – erythema nodosum, pyoderma gangrenosum, etc.

HANDS

  • Cannula scars
  • Xanthoma
  • Nails – leukonychia, koilonychias
  • Make a show of looking for clubbing! (IBD, CF, chronic malabsorption, cirrhosis)
  • Turn hands over - palmar erythema, creases

ARMS

  • AV dialysis shunt
  • Have child bend elbows, look for dermatitis herpetiformis
  • Check for hepatic flap (and tacrolimus tremor)

FACE

  • Sclerae - jaundice, blue sclerae (seen in IDA)
  • Eyes - cataract, KF rings
  • Xanthoma - cholestasis
  • Conjunctiva - anaemia (can have child pull down lid and look up)
  • Spider naevi
  • Oral mucosa - pigmentation (Peutz-Jeghers), angular cheilitis, ulcers
  • Tongue - stomatitis, large tongue (BWS, Down)
  • Teeth - dental caries at back in GORD, front in poor diet
  • Cushingoid? - always be alert to signs of steroid toxicity

NECK

  • Scars, lines, ports
  • Supraclavicular lymphadenopathy (Virchow’s node)
  • Ideally check for axillary LN

ABDOMEN

Inspect

  • Distension, asymmetry
  • Scars (loin, groin, laparoscopic, flank)
  • Scratch marks
  • Injections sites! Lipohypertrophy….
  • Abnormal vessels – caput medusa (drain from umbilicus)
  • Herniae/visible lumps

Palpate + percuss

  • Explain, reassure shouldn’t hurt, etc
  • Go down on knees!
  • Superficial
  • Deep
  • Liver - percuss resonant to dull and characterise
  • Spleen - as for liver; consider having child roll towards you
  • Kidneys – ballot
  • Percuss down towards the bladder
  • Percuss from the midline to the flank + shifting dullness as appropriate
  • Flank dullness/ shifting dullness only if distended
  • Suspected hernia: ask to cough; routinely check over incisions
  • Ideally check groins for LN + hernias

Auscultate

  • Bowel sounds
  • Hepatic rub or bruit
  • Renal bruit
  • Listen over suspected hernia
  • Listen over AV fistulae

BACK

With child leaning forward

  • Inspect for scars
  • Feel for cervical lymphadenopathy
  • Consider checking for renal angle tenderness
  • Consider percussing over left 12th rib – if resonant, splenomegaly is unlikely

LEGS

  • ?any skin changes
  • Be alert to hemihypertrophy
  • Check for pitting oedema over ankles

COMPLETION

  • Measure height and weight and plot on a centile chart +/- anthropometry
  • Examine the hernial orifices, external genitalia, perianal area
  • Check for fluid thrill/shifting dullness if not already done
  • Consider BP, urinalysis
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2
Q

Presentation scheme for abdominal examination

A
  • To complete my examination I would like to
    • plot growth on a centile chart,
      • examine the hernial orifices, external genitalia and perianal area and
      • measure the blood pressure.
      • And as appropriate: urinalysis, check for fluid thrill/shifting dullness. Would you like me to do any of these now?
  • I have examined the abdomen of x-month/year-old Y.
  • Y appears (comment on growth), and I would like to plot his/her growth on an appropriate centile chart.
  • Comfort at rest and dysmorphism
  • Paraphernalia: NGT, PEG, IV access, meds, stomas etc.
  • Other readily apparent findings on general inspection:
    • Colour – pallor, jaundice
    • Obvious scars, distension, leg rashes
  • Clubbing (and other obvious hand signs if present)
  • Arm signs if present: fistulas, dermatitis herpetiformis, tremor/flap
  • Face signs if obvious
  • Neck signs if obvious: scars, lymph nodes – comment on lymphadenopathy here regardless
  • Chest signs if relevant: chest wall deformities, ports
  • On closer inspection of the abdomen…distension +/- and….
  • On palpation:
    • Comment on general softness and tenderness
    • Describe palpable masses in terms of location, firmness, tenderness, ability to get above it, movement with respiration, percussion note, size, ballotable, auscultation.
    • If hernia: reducibility, bowel sounds and response to coughing
  • Percussion: e.g. rest of abdomen resonant …shifting dullness
  • Auscultation: bowel sounds, bruits, AV fistulae, etc
  • Legs: pitting oedema, skin changes

In summary, ….include comment on growth/nutrition.
Differential diagnoses that I would consider…..commenting on features for/against
Complications that I would be alert to include…
Baseline investigations that I would consider include….

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3
Q

What is OEIS complex?

A

OEIS complex (omphalocele-exstrophy-imperforate anus-spinal defects)

  • Cloacal exstrophy is a rare and complicated condition that affects the lower abdominal wall structures of infants.
  • Occurs in 1 out of 200,000 pregnancies and 1 in 400,000 live births.
  • Often diagnosed on antenatal USS.
  • Development of the lower abdominal wall (ventral) is interrupted during its normal embryonic migration and folding leaving many of the inner-abdominal structures exposed. These structures include the bladder, intestines and reproductive organs.
  • The pattern of inheritance for cloacal exstrophy is unknown due to the small number of patients.
  • Four features of Cloacal exstrophy are frequently found together, and referred to as an OEIS Complex
    • Omphalocele: protrusion of variable proportion of abdominal contents outside abdominal cavity; can include spleen, liver and intestine.
    • Exstrophy of the bladder and rectum: development of the bladder in utero is separated into two halves and open. The colon and rectum are also open with a segment of the rectum situated between the halves of the bladder and located on the surface of the abdomen.
    • Imperforate anus: The colon may connect to the urethra, bladder or vagina through a fistula.
    • Spinal defects: Infants with cloacal exstrophy often are born with further spinal complications including spina bifida.
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4
Q

Example abdo case for MRCPCH (OEIS syndrome with other congential abnormalities)

A

4-year-old girl with cloacal extrophy (OEIS syndrome)

  • Rappel: Ex 35+2 week identical twin (sister entirely normal) born with OEIS complex. Also orthopaedic issues: left-sided talipes and malformed lower right limb with only a tibia – has had an above-knee amputation and mobilises by crawling + wheelchair. Surgical repairs to date: myelomeningocoele and spina bifida repair, malrotation repair, ileostomy, gastrostomy (GJ tube), Nissen fundoplication, neo-urethra (no control over constant leakage of urine), vaginoplasty. Previous line and drain scars in neck, groin, abdomen. Involved professionals: Under GOS urology, endocrinology (premature adrenarche without premature puberty), gastroenterology, orthopaedics, neurosurgery, general paeds. Local dietician and physiotherapist + community paediatric nurses. Attends mainstream nursery and has normal/precocious cognitive, speech, social, fine motor development. Current meds: loperamide, ciprofloxacin prophylaxis for recurrent UTIs, alimemazine tartrate (trimeprazine tartrate), the latter being a in the antihistamine class. Attended CAU with 3 days of fever, cough, coryza. Subltle creps (audible and palpable/tactile fremitus) in right upper zone ?atelectasis secondary to scoliosis, ? viral r/o bacterial super-infection. Systemically very well. Mum was using granules to thicken stoma contents. You did okay with this consult until wrapping up – frame decision to parent, clarify reasoning, safety net, and say you will run your decision/assessment by your senior.

If you were to present this patient:

I have performed a general examination of 4-year-old Ella. On looking around her bed, I note a wheelchair. On general inspection, Ella appears well at rest and is demonstrating good fine motor skills playing a game on her ipad. Ella does not have any dysmorphic facial features and appears slight for her age, though I would like to assess her growth formally. There are multiple notable findings on general inspection, including an above knee amputation of the right lower limb, talipes affecting the left lower limb, ileostomy bag and gastrostomy tube. There were no findings of note in her hands or arms. Her pulse rate was 115 beats per minute and of normal volume and character. Her respiratory rate was 20/min, and she showed no increased work of breathing in room air, and is not cyanosed. She has multiple scars consistent with previous central access in her neck, but no lymphadenopathy nor tracheal deviation. She is not jaundiced and her oral cavity was normal. Her apex beat was not displaced and she had no heaves nor thrills. Her heart sounds were normal with no murmurs. Examination of her respiratory system was remarkable for scoliosis, a wet cough, and fine inspiratory crepitations in the right upper zone with tactile vocal fremitus over the same area. Air entry and expansion were normal. On ear, nose and throat examination she had normal tonsils but a dull left tympanic membrane that was not bulging. On examination of her abdomen, she had a healthy ileostomy with formed yellow stool in her stoma. Her gastrostomy site was healthy. On closer inspection, she has laparoscopic scars consistent with Nissen fundoplication. She had scars in both groins. On inspection of the perineum, she has evidence of a vaginoplasty with premature adrenarche apparent. There was a urethral opening but no anal opening. Her abdomen was soft and nontender with no organomegaly nor masses and normal bowel sounds. There is a scar over her lumbar spine. She is moving all four limbs. Ella was very cooperative with examination and showed evidence of excellent comprehension of instructions and fine motor skills.

In summary, Ella is a delightful four year-old girl who is systemically well today, though she evidence of having undergone multiple complex surgical procedures for congenital anomalies…..She has…..Underlying conditions that I would consider include complex cloacal anomalies as well as spina bifida. Such anomalies could be part of a unifying association or syndrome such as OEIS complex.

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5
Q

Example abdo case 8-year-old girl with multiple stomas and scars

A

Scenario: Please examine this girl’s abdomen. (So you will sometimes need to ask age at the start.)

To complete my examination I would like to examine the hernial orifices, external genitalia and perianal area, measure the blood pressure and perform a urine dipstick test. In this instance I would also like to examine the neurology of the lower limbs. Would you like me to do any of these before moving on?

I have examined the abdomen of 8-year-old Lauren. Lauren appears reasonably well-grown for her age, although I would like to plot her on a centile chart. She appeared comfortable at rest and has no dysmorphic features. Obvious findings on general inspection are a mucocutaneous fistula in the midline below the umbilicus and a mitrofanoff stoma button in the right lower quadrant. She was not clubbed. There was no lymphadenopathy palpable. On closer inspection of the abdomen there was also a transverse lower abdominal incision. On palpation the abdomen was soft and non-tender with no masses nor organomegaly. There did not appear to be any incisional or parastomal hernia. The stoma appeared healthy. There was no evidence of urinary leakage around the metrofanoff. Bowel sounds were unremarkable. On examination of the back there was a vertical scar over the lower back. There was no ankle or sacral oedema. In summary, Susan is a well-appearing 8-year-old girl with a metrofanoff stoma, healthy mucocutaneous fistula, transverse scar over the lower abdomen and vertical scar over the lumbar vertebrae. Underlying diagnoses that I would consider that might make sense of these findings include spina bifida or a complex lower urinary tract anomaly such as a cloacal anomaly. The defect on Susan’s back was not typical of spina bifida, and although spina bifida may be associated with a neuropathic bowel, it is unusually for this to lead to a colonic stoma. However, I am aware that cloacal anomalies and spina bifida can co-occur, for example in OEIS complex, so both remain possibilities.

Case notes:

In a cloacal anomaly the rectum, vagina and urethra fail to develop separately and typically drain via a single channel onto the perineum. It is an uncommon anomaly, occurring in 1 in 20-50,000 live births.
The bladder is usually affected by cloacal anomaly and is often neuropathic. Detrusor hyper-reflexia is commonly seen. Anticholinergics such as oxybutynin, tolterodine and solefenicin are first line agents to treat this, with consideration being given to intravesical botulinum toxin in the worst cases.

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6
Q

Example abdo case 3 wk old wiht stoma

A

I have examined the abdomen of 3-week-old Alice. She appears somewhat small for her age and I would like to plot her growth on a centile chart. She was not in apparent distress at rest and had no obvious dysmorphic features. The main feature on general inspection is a stoma bag overlying a double mucocutaenous fistula. There were no other peripheral findings apart from a degree of pallor and evidence of recent cannulas in the hands. On closer inspection of the abdomen it was soft and non-tender with a clean healing incision just visible to the edge of the stoma. The stoma contained liquid brown green stool. There were no palpable masses nor organomegaly. Normal bowel sounds were present. The hernial orifices, external genitalia and anus appeared normal, as did the lower back. The extremities were well perfused with no pitting oedema. In summary, Alice is a 3-week-old girl who appears generally well at present though small. She has two mucocutaneous fistulas covered by a stoma. Her stoma is clearly functioning and her scar is healing nicely. Underlying differential diagnoses that I would consider include intestinal obstruction caused by, for example, malrotation and volvulus, bowel atresia, intussusception and meconium ileus.

Case Notes:

  • Meconium ileus is one of the commonest causes of neonatal intestinal obstruction. It accounts for around a third of cases of neonatal IO and is strongly associated with cystic fibrosis. Other causes of neonatal IO include malrotation, volvulus, intussusception, and intestinal atresias.
  • About 90% of babies with meconium ileus have cystic fibrosis. Between 7-10% of cystic fibrosis patients get meconium ileus.

Meconium ileus occurs in both simple and complicated forms. The simple form occurs when the thickened meconium forms in utero and obstructs the mid-ileum typically causing proximal dilatation, bowel wall thickening and obstruction. In the complicated form the above leads to volvulus, atresia or pseudocyst formation.

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7
Q

What percentage of neonates with meconium ileus have CF? What percentage of children with CF present with meconium ileus?

A

About 90% of babies with meconium ileus have cystic fibrosis. Between 7-10% of cystic fibrosis patients get meconium ileus

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8
Q

Give 5 causes of neonatal IO. What is the commonest cuase of neonatal IO?

A

Meconium ileus is one of the commonest causes of neonatal intestinal obstruction. It accounts for around a third of cases of neonatal IO and is strongly associated with cystic fibrosis. Other causes of neonatal IO include malrotation, volvulus, intussusception, and intestinal atresias.

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9
Q

What distinguishes simple/uncomplicated meconium ileus from complicated meconium ileus?

A

Meconium ileus occurs in both simple and complicated forms. The simple form occurs when the thickened meconium forms in utero and obstructs the mid-ileum typically causing proximal dilatation, bowel wall thickening and obstruction. In the complicated form the above leads to volvulus, atresia or pseudocyst formation.

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10
Q

Give four differential diagnoses for ascites.

A

CCNP:

Cirrhosis

Congestive cardiac failure

Nephrotic syndrome

Protein-losing enteropathy

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11
Q

Differential for hepatomegaly

Differential for a massive liver?

A

I3SOM

  • Infection:
    • Hepatitis A
    • Hepatitis B
    • EBV
  • Infiltration
    • Primary liver tumours
    • Secondary tumour (eg lymphoma, leukaemia, neuroblastoma)
  • Idiopathic
  • Storage disorders
    • Fat
      • CF
      • Obesity
      • Malnutrition or TPN
    • Lipid
      • Gaucher’s disease
    • Sphingomyelin-cholesterol
      • Niemann-Pick disease
    • Glycogen storage diseases
  • Obstructive
    • Hepatic vein thrombosis
    • Congestive cardiac failure
  • Miscellaneous
    • Wilson’s disease
    • Alpha 1 antitrypsin deficiency
    • Congenital hepatic fibrosis

Massive liver:

  • Storage disorder
  • Reticuloendothelial disease, eg leukaemia
  • Malignancy
  • Gross fatty change
  • Congestive cardiac failure
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12
Q

Splenomegaly differential

A

INAHDIE

Infection

  • Septicaemia
  • Infectious mononucleosis
  • Malaria

Neoplastic

  • Acute leukaemia
  • Hodgkin disease

Autoimmune

  • JIA
  • SLE

Haemolytic disorders

  • Hereditary spherocytosis
  • Sickle cell anaemia (early)

Disordered splenic flow

  • Portal hypertension
  • Cirrhosis
  • Cardiac failure

Infiltration

  • Gaucher’s disease

Extramedullary haematopoiesis

  • Thalassaemia
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13
Q

Portal HTN differential. How would you classify your differential?

A
  1. Pre-hepatic
    • Portal vein thrombosis
  2. Intra-hepatic
    • Pre-sinusoidal
      • Neoplasia
      • Schistosomiasis
      • Hepatic cyst
    • Sinusoidal
      • Congenital hepatic fibrosis
      • Cirrhosis
      • Biliary atresia
      • Neonatal hepatitis
      • Alpha 1 antitrypsin deficiency
    • Post-sinusoidal
      • Veno-occlusive disease
  3. Post-hepatic
  • Budd-Chiari syndrome
  • Right ventricular failure
  • Constrictive pericarditis
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14
Q

Cirrhosis differential.

A

BIGDAN

Biliary tract disorders

  • Biliary atresia
  • Choledochal cyst
  • Congenital hepatic fibrosis
  • Cystic fibrosis
  • Sclerosing cholangitis

Infection

  • Hepatitis B and C
  • CMV

Genetic and metabolic causes

  • Alpha 1 antitrypsin deficiency
  • Wilson’s disease
  • Glycogen storage disease

Drugs and toxins eg alcohol

Autoimmune

Nutrition eg TPN

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16
Q

Healthy eating for children - Infants

A

Infants • Breast milk is the ideal feed for almost all infants. • Solids are not recommended until age 6mths (↓ food allergies). • Initial solids should be based on baby rice, fruit, and vegetables. • Gluten is acceptable from age 6mths. • Following introduction of solids, infants should experience and progress through a wide variety of tastes and appropriate textures. • Finger foods should be introduced from age 7mths. • Continue complementary breast or formula feeds until age 1yr. Normal full fat cow’s milk can then be introduced as the main drink. • Avoid addition of salt and sugar to food. • Low fat products are not suitable for infants. • Supplemental vitamins A, C, and D are recommended until age 5yrs.

17
Q

Healthy eating aged 1-5 years

A

A well balanced diet in early childhood is important to establish a lifetime pattern of healthy eating. The key recommendations for healthy eating to be achieved by age 5yrs are the following:

• Decrease fat to 35% energy intake by avoiding excess high fat foods and changing milk to semi-skimmed at age 2yrs, and skimmed at age 5yrs. • Include whole grain cereals and 5 portions per day of fruits and vegetables to increase fibre intake. • Monitor for (accelerating weight velocity) and avoid obesity. • Moderate salt intake, e.g. not adding salt to cooking or at the table. • Avoid iron deficiency anaemia by restricting milk intake to 1 pint per day and including foods rich in iron (red meat, cereals, beans, pulses, egg yolk, dark green vegetables, and dried fruit). Add vitamin C as fruit juice at a meal to increase iron absorption. Drinking tea with meals decreases iron absorption. • Excessive consumption of fruit juices or squashes can contribute to chronic non-specific diarrhoea of childhood (toddler diarrhoea) and contribute to feeding problems.

Tasker, Robert C.; McClure, Robert; Acerini, Carlo L. (2013-01-31). Oxford Handbook of Paediatrics (Oxford Medical Handbooks) (Kindle Locations 8956-8964). Oxford University Press. Kindle Edition.

18
Q

Key presentations: Vomiting

3 common clinical scenarios?

Investigations to consider?

Causes?

Mgmt/treatment?

Complications?

A

Vomiting

Three clinical scenarios are recognized:

  1. Acute: discrete episode of moderate to high intensity. Most common and usually associated with an acute illness.
  2. Chronic: low-grade daily pattern, frequently with mild illness.
  3. Cyclic: severe, discrete episodes associated with pallor, lethargy +/ − abdominal pain. The child is well in between episodes. Often there is a family history of migraine or vomiting.

INVESTIGATIONS

Acute (if severe) • FBC • U& E • Creatinine • Stool for culture and virology • AXR • Surgical opinion if obstruction or acute abdomen possible • Exclude systemic disease

Chronic • FBC • ESR/ CRP • U& E • LFT • Helicobacter pylori serology • Urinalysis • Abdominal US • Small bowel enema • Sinus X-rays • Test feed or abdominal ultrasound for pyloric stenosis • Brain imaging (CNS tumour) • Consider urine pregnancy testing in teenage girls • Upper GI endoscopy

Cyclic As for chronic vomiting, plus the following: • Serum amylase • Serum lipase • Blood glucose • Serum ammonia

CAUSES

Acute: GI infection; non-GI infection (e.g. urinary tract infection); GI obstruction (congenital or acquired e.g. pyloric stenosis); adverse food reaction; poisoning; raised intracranial pressure; endocrine/ metabolic disease (e.g. diabetic ketoacidosis).

Chronic (usually GI): peptic ulcer disease; gastro-oesophageal reflux; chronic infection; gastritis; gastroparesis; food allergy; psychogenic (see Psychogenic vomiting); bulimia; pregnancy.

Cyclic (usually non-GI cause): idiopathic; CNS disease; abdominal migraine; endocrine (e.g. Addison’s disease); metabolic (e.g. acute intermittent porphyria); intermittent GI obstruction; fabricated illness.

MANAGEMENTFull history: e.g. early morning vomiting with CNS tumour, or family members with similar illness. • Full examination: including ENT and growth (HC!). Assess for dehydration.

TREATMENTSupportive treatment as needed: e.g. oral or IV fluids. • Treat cause: e.g. pyloromyotomy for hypertrophic pyloric stenosis. • Pharmacological: antihistamines; phenothiazines (side-effects: extrapyramidal reactions); prokinetic drugs, e.g. domperidone. 5-HT 3 antagonists, e.g. ondansetron, are increasingly being used for treating post-operative or chemotherapy induced vomiting. 5-HT 1D agonists, e.g. pizotifen, are useful as prophylaxis and treatment for cyclic vomiting syndrome.

COMPLICATIONS Dehydration, plasma electrolyte disturbance (e.g. ↓ K +, ↓ Cl −, alkalosis with pyloric stenosis), acute or chronic GI bleeding (e.g. Mallory– Weiss tear), oesophageal stricture, Barrett’s metaplasia, broncho-pulmonary aspiration, faltering growth , iron deficiency anaemia.

PSYCHOGENIC VOMITINGCauses: anxiety; manipulative behaviour; disordered family dynamics. A family history of vomiting is common. • Management: exclude organic disease. Refer to child psychologist.