30 COMMON CHILDHOOD COMPLAINTS 1. The small child Fahad (received) 2. The obese child Fahad (received) 3. Child who is failing to thrive Peter 4. The child with cough/wheeze Muneera (received) 5. The child with stridor Dema (received) 6. The child with URI Muneera Ali 7. Child with recurrent headaches Muneera Ali (received) 8. The drowsy child Selverus 9. The child who has had a funny turn (Fits, faints and funny turns) Hassan (received) 10. The child who is slow to walk Omar M 11. The child who is slow to talk Hassan (received) 12. The child with a limp Selverus (received) 13. Child with an unsteady gait Imran 14. Child with a waddling gait Dorra (received) 15. The child with a swollen/painful joint Dema (received) 16. The child with chronic diarrhea Omar S received) 17. The child with chronic constipation Aysha (received) 18. The child with recurrent abdominal pain Sara (received) 19. The child with acute abdominal pain with/without vomiting Sara (received) 20. The child who is vomiting Mohammed (received) 21. Child with a heart murmur Dorra (received) 22. The cyanosed/dusky child Aysha 23. The child with an itchy rash Reem AW (received) 24. The child with a non-itchy rash Ahmed 25. The child who bruises easily Nusiebeh (received) 26. The pale child Mohammed (received) 27. The child who is bed-wetting Reem AW (received) 28. The child with an emotional/ behavior disorder (Irrelevant) 29. The child with neck swelling Nusiebeh (received) 30. The child with a squint Muneera (received)

1. THE SMALL CHILD ! less than the 0.4th centile. Important to measure the rate of growth as well. Causes of Short Stature: - Familial o To measure the mid parental height in males: (Height of father + 12.5 + Height of mother)/2 o To measure the mid parental height in females: (Height of father – 12.5 + Height of mother)/2 - Intrauterine Growth Restriction and Extreme Prematurity o Ask about birth (Size and weight) - Constitutional Delay o Usually occurs in the parent of the same sex o Has anyone else had a problem with height in the family? Were they short for a long time and then suddenly grew? - Endocrine o The child is usually short and fat • Ask about /assess the weight! o Hypothyroidism • : • Cardiac o Bradycardia • Neurological o Learning difficulties o Slow relaxing reflexes • Metabolic o Cold intolerance o Constipation o Weight gain despite decreased appetite • Thin, dry, hair o Cushing’s • Are they taking any medication? (Corticosteroids) o deficiency • Either isolated or secondary to panhypopituitarism • Panhypopituitarism • Can be caused by carniopharyngioma o Problems with vision (Bitemporal hemianopia) • Laron Syndrome ! growth hormone resistance - Nutritional/Chronic renal disease o What are their eating habits? o Any chronic illnesses? • Crohn’s, Coeliac, chronic renal disease o Assess nutrition on examination - Psychosocial Deprivation - Chromosomal Disorders o Downs o Turner’s o Russel silver o Prader Willi - Idiopathic short stature - Disproportionate Short Stature: Ex. storage disorder, scoliosis or achondroplasia. Focused Questions: - Compared to his siblings, have you noticed that he is significantly shorter? (Familial or not) - Is this problem common in the family? And does it tend to resolve? (Constitutional delay. You might have a father who says that all the men in the family tend to be short for the first few years then they suddenly grow) - Was he small from birth - How is his eating habits? Is he able to put on weight normally? (Nutritional) - Is he obese? (Obese and short tends to be metabolic) - Ask about hypothyroidism symptoms - Any known medical illnesses? Is he on any medication? o Nephrotic syndrome, asthma or anything that requires corticosteroids) o Crohn’s and Coeliac - Developmental milestones o Chromosomal abnormality - Consanguinity ! Chromosome Important to plot the child and see if there is any fall in the centile lines. If the child has a steady growth but is just short, this is probably normal. If he has is falling in the centile lines, you would be worried. Quick recap: History • Familial • General Health • Constitutional delay • Positive history if same condition is present in the same sex parent • Can be normal and all you need to do is reassure the parents. • Signs of hypothyroidism • Iatrogenic steroids • Psychological • IUGR • Chromosomal syndromes • Prader Willi o Hypotonic o Obesity o Learning difficulty • Russel Silver o Triangular face o Very short o Asymmetry of limbs • Laron syndrome o GH resistance o Midfacial hypoplasia o Increased growth hormone and low IGF-1 o Does not respond to GH • Turner’s Syndrome o 45 X, O o Wide spaced nipples in adults o Short stature o Congenital cardiovascular defects (Especially coarctation of the oarta) o Webbed neck o Infertility o Lymphodemia of the hands and feet o Wide carrying angle o Investigations • FBC ! Anemia • Coeliac, crohn’s, hypothyroidism o Coeliac and crohn’s can also cause short stature • Thyroid function test • X ray to check bone age • You ask for an X ray of the left hand • Creatinine + Electrolytes (rule out chronic renal failure) • Karyotyping (For females to check for turner’s) • Hormones • IGF1, GH o If IGF-1 is low and there is delayed bone age, you go for growth hormone stimulation test. • Using either glucagon, insulin, clonidine or arginine • If GH is more than 20 units/L this is normal • If it is below that, you do an MRI to check the pituitary gland • To check for panhypopituitirism: TSH, LH, FH, ACTH (By checking cortisol), Prolactin, ADH, Oxytocin o Treatment of GH deficiency ! Once daily subcutaneous GH o Other indications for subcutaneous growth hormone: • GH deficiency • Turner’s • Chronic renal failure • Idiopathic short stature

2. THE OBESE CHILD Obesity ! 98th centile and above on BMI chart in young children. Children who are 12 years and older, a BMI that is equal to or greater than 30 is considered obese. If a child is obese and short, you would consider an endocrine or chromosomal cause. The biggest problem that is brought to the clinic is obesity If they’re tall and fat ! Too many calories If they’re short and fat ! consider another problem, such as endocrine. DDx: - Diet and reduced exercise (Most common and increasing in prevalence) - Endocrine (Rare) o Hypothyroidism o Cushing’s - Chromosomal o Prader Willi Focused questions: - How is his eating habits? - Does he get the chance to move around and exercise? - Signs and symptoms of Hypothyroidism o Constipation o Decreased appetite and increased weight o Excessive tiredness o Cold intolerance o Dry skin and brittle hair - Any known medical illnesses? - Does he take any medication? o Corticosteroids - Developmental assessment o Prader Willi ! Delayed development Management depends on the cause.

4. THE CHILD WITH COUGH/ WHEEZE Nature of the cough Wet cough typically results from excessive mucus production, mostly due to infection or inflammation (eg, bronchiectasis, cystic fibrosis, primary ciliary dyskinesia, asthma, and chronic aspiration). In contrast, pure bronchoconstriction or structural causes for airway narrowing (eg, asthma, airway malacia or compression, foreign body, vascular ring) are usually associated with a dry cough.

Asthma History Features:

●Intermittent episodes of wheezing that usually are the result of a common trigger (ie, upper respiratory infections, weather changes, exercise, or allergens) ●Seasonal variation ●Family history of asthma and/ or atopy ●Good response to asthma medications

Features that suggest a diagnosis other than asthma include the following

●Poor response to asthma medications ●A history of neonatal or perinatal respiratory problems and wheezing since birth suggests a congenital abnormality. ●Wheezing associated with feeding or vomiting can result from gastroesophageal reflux or impaired swallowing complicated by aspiration. ●A history of choking, especially with associated coughing or shortness of breath, suggests foreign body aspiration, even if it does not immediately precede onset of wheezing symptoms. ●Poor weight gain and recurrent ear or sinus infections suggest cystic fibrosis, immunodeficiency, or ciliary dysfunction. ●History of progressive dyspnea, tachypnea, exercise intolerance, and suggest interstitial lung disease. Differential: Asthma( see table!) Transient Early Wheezing Non-topic Wheezing(Following RSV LRTI) Atopic Asthma Broncholitis: 1-9months. Pneumonia Cardiac Failure Inhaled Foreign Body Aspiration Feeds(NM disorder) Focused History Questions: Age Is important to reach the appropriate diagnosis. Describe the sound that you hear when your child is breathing? (whistling sound) WHEN did you start hearing it? determine if acute or chronic. DURATION constantly heard? Is it associated with Cough? Nature of cough? (wet versus dry). Frequency What brings the cough/ makes it worse? What relieves it? Is it constant throughout the day or increased in the morning or night? Associated Symptoms: Laboured breathing? Fever? Lethargy? PMH Is this the first time he/she have these symptoms? PMH Any known medical illness PMH Previous admissions PMH drugs(if uses inhaler, establish severity) + allergies BIRTH HISTORY Complications/stay in NICU NUTRITION Poor feeding? Vomiting? FMH of Asthma FMH of Eczema or allergy SOCIAL Missing school if it’s a young child! establish impact of life. SOCIAL Recent sick contact Physical Examination: 1. Plot weight on Growth chart, vital signs including oxygen saturation. 2. General Inspection 3. Respiratory distress (calculate RR)+ listen for Audible sounds upon breathing, color, hydration, nutrition, dysmorphic fx, paraphernalia. 4. Hands: a. presence of cyanosis or clubbing. b. Pulse

5. Face: Central cyanosis, nasal flaring, 6. Inspect Chest: a. Skin: Scars, eczema( atopic patients) b. Bone: deformities c. Muscle Recession d. Lung: symmetrical breathing, pattern of breathing( abdomino-thoracic in young/ thoracico-abdominal in older. e. Shape of the lung(barrel shaped) 7. Palpate: a. Trachea b. chest expansion. c. Liver: displaced in bronchiolitis. 8. Percussion: Any differences in resonance among lung regions? 9. Auscultation: a. characteristics and location of wheezing, as well as variations in air entry among different lung regions b. Crackles can be present in conjunction with wheezing in asthma, pneumonia, bronchiolitis, cystic fibrosis c. Heart Sounds: Heart Murmur-> cardiac failure. Response to treatment : For patients with diffuse wheezing, a trial of inhaled bronchodilators can be used to confirm the presence of reversible airway disease. Decreased wheezing after bronchodilator therapy is suggestive of asthma. Laboratory investigations: In most cases, the probable diagnosis is suspected on the basis of the clinical history and physical examination. The role of laboratory tests, when indicated, is either to confirm the diagnosis or to rule out other less likely diagnoses [Complete blood counts are important in patients with chronic or systemic symptoms and may reveal anemia, leukocytosis, or leukopenia. Eosinophilia in this setting supports an underlying allergic process or possible parasitic infection. Sputum stain and cultures may be useful in a setting suggestive of bacterial infections, Sweat chloride test — The sweat chloride test allows clinicians to assess physiologic changes associated with cystic fibrosis and is indicated in children with chronic lung problems, including wheezing. Immunoglobulin levels can be used to screen for immunodeficiency. Elevated IgE can be indicative of an allergic process.

Treatment: 1. Bronchiolitis: a. Humidified oxygen via nasal cannula

b. Nebulised bronchodilators (salbutamol and ipratropium bromide)

c. Mechanical ventilation in extremely severe cases (2%) 2. Pneumonia: Amoxicillin with Co-amoxiclav in those unresponsive.

3. Asthma:

Differential Findings Diagnosis Asthma

5. THE CHILD WITH A STRIDOR: upper airway obstruction History: When did the stridor start? - Age of onset: If it was since birth, then this is suggestive of laryngomalacia or a congenital airway abnormality) Is the stridor getting worse with time? Is it worse in the morning or at night? What makes it worse? (E.g. feeding, crying) Do you have difficulty breathing or swallowing? Does it affect your speech? How severe is it? Does the baby change colour? (Cyanosis) Does the child have other symptoms such as fever, sore throat, drooling, and cough? Perinatal history Has the child been vaccinated? Physical examination: Inspection: - Patient will look ill, with a fever. Check the oxygen saturation - See if the patient is in respiratory distress. You can hear the stridor - Color: cyanosis – observe for signs of hypoxia - Mouth open with drooling saliva (suggestive of epiglottitis) - Comment on shape of chest - Tachycardia - Describe the cough (barking) - Chest recession (subcostal or intercostal) NEVER examine the throat Palpation: - Deviation of trachea Auscultate: - Nose, neck and chest (to help locate the stridor) Possible causes: - Croup (most common) - Epiglottitis - Bacterial tracheitis - Inhaled foreign body Laryngomalacia

7. CHILD WITH RECURRENT HEADACHES Clinical Approach to a child with recurrent headache 1. History from the parent and child Site Onset Character Radiation Association Timing exacerbating and relieving factors severity - Family history in first degree relative in migraine 2. Red flags (wakes from sleep, in the morning, vomiting, neuro signs, change in behaviour) 3. Measure head circumference and BP 4. Look for skin markers (café au lait spots) NF1 more prone for brain tumours 5. Examine ear, teeth, and sinuses 6. Examine eye (pupil, fields, visual) Migraine - Recurrent headache separated by symptom free intervals and 3 of the following: • Unilateral headache • Throbbing quality • Aura (visual, auditory, sensory) • Abdominal pain + N/V • Relieved after sleep • Family history - Two main types: • Common migraine: most common (80%), not associated with aura • Classic migraine: less common, usually associated with aura (flashy lights) - Migraine syndromes • Periodic syndrome: occurs in young children, presents with severe episodes of vomiting and weakness, becomes dehydrated and requires IV hydration. Often misdiagnosed to having abdominal pathology • Opthalmoplegic migraine: can occur in adults, complains of double vision • Hemiplegic migraine, acute confusion migraine, and footballer’s migraine - Management • Acute attack: Paracetamol, Sleep • Prevention (must identify triggering factors by headache diary): • Decrease stress and adequate sleep • Good calorie intake • Avoid: Chocolate, caffeine, nuts, Citrus fruits, dairy products and bananas • Anti-migraine drugs: pizotifen (weight gain and sleepiness), clonidine, propranolol. These drugs are used as prophylactic, however, they are not highly recommended. Tension headaches - Usually more than 10 years of age

- Worsens as day ends, relieved by relaxation

- Symmetrical band-like pressure

Psychogenic headaches - Diffuse headaches

- Persistent, not incapacitating

- Difficult to describe by patient

Raised intracranial pressure headaches - Diffused or localized

- No symptom free intervals, just change in severity

- Usually there is a change in frequency, quality, and pattern over time

- Increase when laying down and in the morning

- Usually associated with morning vomiting (causing relief)

- Change in personality & school preformance

- Could be associated with neurological signs:

• Visual field deficits

• CN abnormalities (squint and diplopia)

• Ataxia

• Tilting of the head

• Papilloedema

• Growth failure (eg.craniopharyngioma)

- Could be associated with brain tumours, if in doubt CT and MRI must be performed (50% of those with brain tumour will have neurological signs 2-3months after the onset of headache)

Management of headaches 1. Psychosocial support and relaxation techniques

2. Analgesics (Paracetamol and NSAIDs) as early as possible if the severity is increasing

3. Antiemetic (if vomiting): metoclopramide

4. Serotonin agonist: nasal preparation for children above 12 years 5. Prophylactic: pizotifen and propranolol

9. THE CHILD WHO HAS HAD A FUNNY TURN Each has a distinctive identification character, trigger or symp. To be extractd from history May mimic or be mimicked by seizures/ epilepsy. “Reflex anoxic seizures mainly triggered by pain/ DDx discomfort” • Seizures “Could involve tonic clonic • Epilepsy episode induced by • Meningitis hypoxia” • Breath holding attacks ! upset, tempered, cyanosed, loss of consciousness, recovers fully • Reflex anoxic seizures ! pain/ discomfort trigger, breath holding, cyanosis, tonic-clonic seizure, Family Hx • Syncope ! long standing time, hot weather, fear • Migraine ! GI disturbances & light-headedness • Benign paroxysmal vertigo ! recurrent, Nystagmus, falling. • Cardiac arrhythmia !related to exercise • Fabricated ! observatory skills dependent Hx Qs • Any Family history? V. Common • First episode? Similar triggers/ conditions to a previous episode if any? • Loss of consciousness? • Trauma? ! Reflex anoxic seizure • Was the child Upset/afraid previous to episode? Y! breath holding attacks/ reflex anoxic seizures/ Syncope • Was the child cyanosed? breath holding attacks/ reflex anoxic seizure (tonic clonic component) • Loss of consciousness during? breath holding attacks/ reflex anoxic seizure • Symmetrical or asymmetrical tonic clonic? Asymmetric is not a funny turn (focal seizure! red flag) • Cold food? ! Reflex anoxic seizure • Incontinence ! reflex anoxic seizure • Nystagmus! benign paroxysmal vertigo • Fall (unsteadiness) ! benign paroxysmal vertigo/ Syncope PEx +ves: Mainly a history diagnosis, if physical examination is remarkable along with an indicating history • EEG Investigations: a history diagnosis, no investigations implicated Treatment: no treatment for any of the funny turns, none of them is an actual limiting pathology 11. THE CHILD WHO IS SLOW TO TALK Key in such history: must determine is cause if Delay or Disorder. The whole approach and subjects of suspicion while progressing through your history depends on the age of the child. DDx • Delay o Hearing loss o Global Dev Delay o Difficulty in speech production- Anatomical anomaly (Cleft palate and lip) o Environmental deprivation/ lack of social contact to learn the skill o Normal variant of speech development in the family • Disorder in o Comprehension of speech o Language expression: knows what must be said just cant/ difficult o Disordered phonation (stammering/ dysarthria) o Pragmatics (the sentence meaning is different amongst the speaker and listener) o Abnormal social/communication skills (autistic behave) Hx Important Questions: • Any previous admissions? What for? (Also dig deep to preg and delivery history) • Determine which component of the speech production process is dysfunctional (initiation, production or execution) by evaluating the communication and responsiveness of the case. • Any other related abnormality that can accompany a disorder will further re-direct you to the correct system. • The severity of the disability can determine if it’s a mild deviation from the norm or a potentially more global dilemma. • Any previous testing done? Result? • Emotional/ psychological distress associated? (Cause/ result of) Physical +ves • Notice and dimorphic features or and detectable abnormality • The nature of any +ves on the Neurological Examination would further guide you towards a more probable cause (motor/ sensory/ Cognitive/ severity/ systems involved) Investigations: • Assess global and cognitive development • “the symbolic toy test” ! for v. early lang dev • “the reynell test” ! determine id receptive or expressive dysfunction is cause Treatment • Fix anatomical deformity and restore velopharyngeal patency if indicated • Speech and language therapy • Cochlear implant • Psychological support (essential as it could be caused/ worsened by psychological influence) • Refer to an audiologist • Special schooling

12. THE CHILD WITH A LIMP History key points -AGE (some diseases only in a certain ages eg SCFE-> adolescence) - ONSET (must determine acute vs chronic limp) - PAIN ! hip pain ? knee pain ? if yes pain only on moving or even at rest ? - recent cough/cold/flu ? (more likely to be transient synovitis) - fever ? how high ? (really high could be septic arthritis/osteomyelitis) -any trauma ? falls ? - focused systemic qs : rashes ?(HSP) joint swelling ? ? (tumours) blood transfusions ? (sickle) Weight ? (scfe if obese) DDX for limp pneumonic : STARTSS HOT Septic arthritis HSP Trauma (VERY COMMON) Osteomyelitis AVN (perthes) Tumours (bone tumours/leukemia) RA (JIA) Transient synovitis SCFE Sickle NB. MUST DIFFERENTIATE BETWEEN TRANSIENT SYNOVITIS AND SEPTIC ARTHRITIS ! coz both present with acute limp. Transient synovitis Septic arthritis ACUTE ONSET, NON WEIGHT BEARING No/mild fever Moderate/high fever Child looks well Child looks ill Hip pain on movement Hip pain AT REST ESR normal ESR raised

Some points about each differential: In the really young (1-3 years) suspect DDH that wasn’t caught on the normal screening and so now presented with a limp. (no pain). Specially in females. Transient synovitis • Commonest age : 2-12 • Acute hip pain (on movement only !) • Usually follows a viral infection • Treatment ? Bed rest SCFE Look for the OBESE ADOLESCENT. Physical : No way they’d get. Coz most are painful and they wont have 19 students inflicting pain on a child. Just a normal ortho exam, and ask about tenderness anywhere before touching. And comment on posture of child before anything. (septic arthritis posture would have hip flexed and abducted + would look really ill.) 14. CHILD WITH A WADDLING GAIT Myopathic Gait (Waddling Gait) Hip girdle muscles are responsible for keeping the pelvis level when walking. If you have weakness on one side, this will lead to a drop in the pelvis on the contralateral side of the pelvis while walking (Trendelenburg sign). With bilateral weakness, you will have dropping of the pelvis on both sides during walking leading to waddling. This gait is seen in patient with myopathies, such as muscular dystrophy.

Differential: SMA DMD-onset of waddling gat begins from 3-5 years old Muscular dystrophies more frequent in boys, delayed walking (>18 months), family hx (carrier status) proximal muscle weakness (Gower sign), Trendelenberg gait, inability to jump, prominent but weak "pseudohypertrophied" calf muscles (symmetric), cardiomyopathy, scoliosis, nonambulant by teenage years Congenital hip dysplasia Development hip dysplasia peak age 12 to 24 months; first-born females; breech birth; family history; oligohydramnios; may present with delayed walking neonates: clicky hips, positive Barlow maneuver, positive Ortolani maneuver; older child/toddler: leg length discrepancy (short ipsilateral side), asymmetric skin creases (posterior thigh), positive and bilateral Trendelenberg gait (rolling- waddling gait)

History • What are the parent's concerns? • Take a detailed medical history including pregnancy, birth and development. Perinatal events and motor development may reveal a diagnosis of cerebral palsy. • Duration of complaint and progression. History should clarify if the problem began at birth, or before or after walking. How has the problem changed during the past few months? • Family history; there is frequently a familial tendency. • Is there really concern about the gait or is it appearance? A toddler's gait and legs are different from those of an adult. Parental concern often stems from a lack of understanding regarding the maturation of the gait. • Signs and symptoms; ask about pain, limping, tripping and falling (Toe walking and falling frequent in history of DMD case) • Sitting habits; internal tibial torsion is commonly associated with sitting on the feet, while increased femoral anteversion is associated with sitting in a 'W' position. • Aggravating factors; torsional deformities become more apparent with fatigue. • Delayed achievement of motor milestones • Impact on life/school/daily activities Diagnosis of DMD: • A positive Gowers' sign reflects the more severe impairment of the lower extremities muscles. The child helps himself to get up with upper extremities: first by rising to stand on his arms and knees, and then "walking" his hands up his legs to stand upright. • Affected children usually tire more easily and have less overall strength than their peers. Creatine kinase (CPK-MM) levels in the bloodstream are extremely high. • An electromyography (EMG) shows that weakness is caused by destruction of muscle tissue rather than by damage to nerves. Genetic testing can reveal genetic errors in the Xp21 gene. • A muscle biopsy (immunohistochemistry or immunoblotting) or genetic test (blood test) confirms the absence of dystrophin, although improvements in genetic testing often make this unnecessary.

Management of DMD: DMD is not curable, however treatment is available. Predisone 0.75mg/kg/day to increase strength and function Treatment goals: maintain function, prevent contractures and provide support to child and family. Treatment is generally aimed at controlling the onset of symptoms to maximize the quality of life, and include the following: Corticosteroids such as prednisolone and deflazacort increase energy and strength and defer severity of some symptoms. • Randomised control trials have shown that beta2-agonists increase muscle strength but do not modify disease progression. Follow-up time for most RCTs on beta2-agonists is only around 12 months and hence results cannot be extrapolated beyond that time frame. • Mild, non-jarring physical activity such as swimming is encouraged. Inactivity (such as bed rest) can worsen the muscle disease. • Physical therapy is helpful to maintain muscle strength, flexibility, and function. • Orthopedic appliances (such as braces and wheelchairs) may improve mobility and the ability for self-care. Form-fitting removable leg braces that hold the ankle in place during sleep can defer the onset of contractures. • Appropriate respiratory support as the disease progresses is important.

15. THE CHILD WITH A SWOLLEN/PAINFUL JOINT: HISTORY: Pain: - Location: where is the pain? - Radiation: does it go anywhere? - Characteristic: can you describe the pain? - Onset: when did the pain start - Periodicity: how often do you get the pain? - Duration: how long have you had the pain? - Severity: on a scale of 1-10 how bad is the pain? - Aggravating factors: what makes the pain worse? - Relieving factors: what makes the pain go away? - Associated symptoms: rash, fever Is it worse in the morning? Does it limit your everyday activity? Does it limit sport activities? Joint swelling: - Has there been much swelling? - Was there any previous trauma? - Which joints are affected? - How long has it been swollen for? (acute vs chronic) Stiffness: - Is the patient stiff in the morning or evening Systemic review: - Any previous similar symptoms? - Other joints affected? - Have you noticed any rashes? Or any colour changes in skin? - Have you had any problems with your eyes? - Do you feel cold or warm? Family history: - Any musculoskeletal disorders running in the family? Social history: - If they live in a house one floor or more - Do you use walking aids EXAMINATION: Inspection: - Any rash - Erythema - Scars Specific to joint: - Erythema - Swelling - Deformity Around the area: - Muscle wasting (E.g. knee check for quadriceps wasting) Palpation: look for signs of discomfort on patients face while palpating - Warmth - Tenderness - Swelling: joint effusion – fluid can be shifted within the joint Movement: - Passive movement: check for limitation of movement, crepitus and joint stability - Active movement Special knee tests: - Patellar tap Back examination: - Check for scoliosis by 1. Comparing the two shoulder lengths 2. asking the patient to bend and look for any deformity - Palpate the vertebrae - Shober test - Winging of the scapula Differentiation between juvenile idiopathic arthritis, septic arthritis and osteomyelitis: Septic arthritis: - The kid looks generally ill (fatigue) with fever - Usually one joint is affected only – swollen, tender and red - The affected joint cannot be moved as it will cause pain - If the hip is affected, the kid can present with a limp Investigations: - CBC (WBC, CRP, ESR) - Blood culture (because hematogenous spread) JIA: - Prolonged joint swelling more than 6 weeks - Could be more than one joint affected - Fever and rash - Morning stiffness is common - Complain of pain after long hours of immobility of joint Osteomyelitis: - Remember it is an infection of the metaphysis and not the joint! However it can go on to affect the neighboring joint - It can be a multi-focal loci – so make sure to ask if other places have been affected - Painful immobile LIMB (not joint) in a child with fever (moving the limb causes severe pain) - Over the affected limb there could be swelling, tenderness and it is red

16. THE CHILD WITH CHRONIC DIARRHEA Diarrhea is increased stool volume, usually with looser consistency and increased frequency than normal. Frequency may not change however. These qualitative attributes are relative to the person’s normal bowel pattern. Acute viral gastroenteritis, one of the most common causes, usually resolves in 2-5 days. Chronic diarrhea is defined as diarrhea lasting more than 2 weeks. With chronic diarrhea there is often a cycle of infection, malabsorption and which propagates the diarrhea. Osmotic diarrhea usually will cease once the offending agent is stopped such as juice (Toddler’s diarrhea) or dairy products (Lactose intolerance). It has a low stool electrolyte content. Weight loss and failure to thrive may be seen. Secretory diarrhea will continue even when taking nothing by mouth. It has a high stool electrolyte content. Infectious diarrhea often is accompanied by fever, nausea, emesis, prior antibiotic use and possibly bloody stools. More commonly it is an acute problem. Inflammatory diarrhea is generally chronic with other signs of disease such as failure to thrive, arthritis, perianal lesions, and/or rash. Diarrhea prevention includes high standards of hygiene include water, food and personal hygiene. Vaccination against Rotavirus is available in many countries. Treatment for acute diarrhea includes oral rehydration solutions, intravenous isotonic fluids, and early refeeding. Antimicrobials for identified microorganisms depends on the organism and presenting problems. Treatment for chronic diarrhea includes removal of the offending agent (e.g. cow’s milk, laxative, juice, etc.), and appropriate evaluation to identify the disease process and its treatment. Learning Point Common causes of diarrhea include: Acute • Allergic enteritis – cow’s milk allergy, soy allergy • Brush border deficiency – Fructose, Isomaltose, Lactose, Sucrose • Infectious • Bacteria – common organisms include Aeromonas, Campylobacter, Clostridium, E. coli, Klebsiella, Plesiomonas, Salmonella, Shigella, Vibrio cholera, Yersinia • Parasite – common organisms include Amoeba, Cryptosporidium, Giardia, Strongyloides • Viral – common organisms include Adenovirus, Astrovirus, Calcivirus, Norovirus, Rotavirus • Medications – laxative use or abuse, Magnesium-containing antacids, opioid withdrawal, medication colorants and flavorings such as sorbitol • Methylxanthines – caffeine, theophylline • Surgical problems – Ascites, Appendicitis, Intussception, Malrotation, Necrotizing enterocolitis, Peritonitis Chronic • Allergic enteritis – cow’s milk allergy, soy allergy, eosinophilic enteritis • Bile salt malabsorption • Brush border deficiency – Fructose, Isomaltose, Lactose, Sucrose • Celiac disease • Endocrine – Addison’s disease, diabetes, hypoparathyroidism, pancreatic insufficiency (Cystic fibrosis, Schwachman-Diamond syndrome), thyrotoxicosis • Fecal impaction – including Hirshsprung disease • Infectious • Parasites – common organisms include Cryptosporidium, Giardia,Tuberculosis • Viruses – common organisms include HIV • Inflammatory bowel syndrome • Irritable bowel syndrome • Malnutrition – failure to thrive, acrodermatitis entropathica • Medications – alcohol, laxative use or abuse, medication colorants and flavorings such as sorbitol, NSAID enteritis • Psychological – secondary to stress • Surgical problems – short gut syndrome, feeding tube problems • Toddler’s diarrhea – excessive intake of clear, sweet liquids • Tropical sprue • • Deficiency – Folate, Niacin • Toxicity – Niacin

Stool colors Red/Pink Stool • Blood • Diazepam syrup • Ampicillin • Viprynium • Phenophthalein • Red Jell-O • Dioralyteoral rehydration solution • Yellow Stool • Normal in formula-fed babies • Green/Greenish Gold Stool • Normally in fully breastfed babies • Stomach infection Black Stool • Blood • Iron • Pepto-Bismol • Black licorice • Blueberries • Green-leafy vegetables • Lead • Charcoal • Coal • Dirt White/Clay Colored Stools • Malabsorption • Biliary system blockage • Barium • Aluminum Hydroxide

Questions to Ask A good history is crucial to gain a clinical picture of the patient’s problem. Generally, the history should be directed to: (1) ensure that the child is, in fact, experiencing an episode of diarrhea, (2) determine the timing and severity, and (3) lead you to a differential diagnosis. The following questions may be helpful. • When did the current problem start?

• How many bowel movements per day?

• What is the normal pattern for this child?

• Are the loose movements interspersed by normal ones?

• Has the child ever experienced this before?

• What is the child’s dietary history (rule out overfeeding)?

• What is the consistency of the stool?

• What is the volume of stool that the child is passing?

• Is there blood or pus contained within the stool? • Is it extremely foul-smelling or contain oil droplets (malabsorption)?

• Bloody diarrhea may suggest specific infectious agents, inflammatory bowel disease, bowel ischemia (or necrotizing enterocolitis) or cow’s milk protein allergy.

• Does the child have a fever?

• Has the child also been vomiting (very common and can exasperate dehydration)? What is the child’s current urine output (oliguria or anuria suggests a large volume deficit)? Has the child been able to take in any fluids?

• Do we have records of the child’s weight (useful to compare these to the current to assess the degree of dehydration)?

• Is the child immunocompromised (if yes, think unusual infections)?

• Has the child been exposed to anyone else with a similar illness?

• Has the child been institutionalized?

• Has there been any travel or has the child newly immigrated?

• Has there been any recent use of antibiotics?

• Are there any other concurrent problems or pertinent past medical history?

17. CHILD WITH CHRONIC CONSTIPATION CONSTIPATION: infrequent passage of dry, hardened faeces often accompanied by straining or pain. There may be abdominal pain which waxes and wanes. It really depends on the age of the patient. Causes of constipation • Dietary • Dehydration • Anal fissure/stenosis • Hirschsprung’s disease • Intestinal obstruction e.g. stricture post-necrotizing enterocolitis • Spinal cord lesion (abnormality below the lesion) • Cystic fibrosis (meconium ileus equivalent) • Cow’s milk intolerance • Drugs, e.g. opiates, vincristine, lead poisoning • Hypothyroidism • Sexual abuse • Anorexa Nervosa

HISTORY (important to know the AGE) 1. Duration a. If acute- ask about any previous febrile illness b. 2. What do you mean by constipation? a. Hardness of stool b. Painful defecation (maybe perianal fistula, fissure ! Crohn’s?) c. Decreased frequency of defecation d. 3. If decreased frequency ! Ask about the difference between now and before? 4. 5. Is this the first time? 6. 7. What was given to him at home/ health centre? 8. 9. Any abdominal pain? a. Maybe abdominal pain which waxes and wanes with passage of stool b. Overflow soiling????!! c. 10.Vomiting 11. 12.Changes in weight 13. 14.Ask about the diet 15. 16.Any back pain 17. 18.Birth History… trying to R/O Hx of Hirschsprung, NEC 19. 20.Any previous hospital admissions? Surgeries? 21. 22.Does the child have any medical condition? 23. 24.Any family history of a. IBD b. Cystic fibrosis c. Thyroid problem d.

Differential diagnosis of Constipation BABIES- Hirschsprung disease Anorectal abnormalities Hypothyroidisim Hypercalcaemia Coeliac disease (FTT) CHILDREN- Psychological Problem with toilet training Stress

Examination- palpable abdominal mass in a well-looking child. DRE done when pathological cause is suspected. WHAT ARE THE RED FLAG SYMPTOMS OR SIGNS IN THE CHILD WITH CONSTIPATION pg.237 Acute constipation (following febrile illness) Resolve spontaneously Dietary change, increase fluid intake Use mild laxatives +extra fluid Chronic constipation (rectum would be over-distended with subsequent loss of feeling the need to defecate) - Involuntary soiling (contractions of the full rectum will inhibit the internal sphincter leading to overflow) AIM: to evacuate overloaded rectum completely Disimpaction regimen of stool softener 1. Macrogol laxative eg. Polyethylene glycol + electrolytes for 1-2 weeks until impaction resolves 2. IF NOT TOLERATED ! give osmotic laxatives (lactulose) 3. NOT SUCCESSFUL ! stimulant laxative eg. Senna or sodium picosulphate 4. Dietary interventions and sufficient fluid intakes (balanced diet with adequate fibre) 5. Encouragement a. Sit in toilet following meals to utilise the physiological gastrocolic reflex. b.

HIRSCHSPRUNG DISEASE: Loss of the ganglion cell from the myenteric and submucosal plexuses of part of the large bowel results in a narrow, contracted segment. The abnormal bowel extends from the rectum for a variable distance proximally, attached to a normally innervated dilated bowel. CLINICAL SYMPTOMS/ SIGNS OF HIRSCHSPRUNG Neonatal- - Failure to pass meconium within 24 h of life - Abdominal distension - Later- bile stained vomiting EXAMINATION- narrow segment and withdrawal of the examining finger ! releases a gush of liquid stool and flatus. Causes delay in diagnosis because of temporary improvement. Infants (few weeks of life) - Present with severe life-threatening Hirschsprung enterocolitis due to infection with Cl.difficile. - Children - Profound Chronic constipation - Abdominal distension - Growth failure -

DIAGNOSIS Suction rectal biopsy- demonstrating the absence of ganglion cells together with the presence of large acetyl cholinesterase positive nerve trunk Anorectal manometry or barium studies – useful for the surgeon to give an idea of the length of the aganglionic segment TREATMENT OF HIRSCHSPRUNG DISEASE SURGICAL - Initial colostomy - Anastomosing normally innervated bowel to the anus -

18. CHILD WITH RECURRENT ABDOMINAL PAIN. DDX: IBD, Abdominal migraine, PUD, UTI, gastritis, CRAP! (chronic recurrent abdominal pain). HX: Pain aggravated or relieved by food? loss of weight? Fever? Bowel habit? Vomiting? Affects Quality of Life? Misses school because of this pain? Mouth ulcers or peri-anal ulcers? (Crohn’s) Hx of headaches? Family hx of migraines or IBD 19. CHILD WITH ACUTE ABDOMINAL PAIN WITH OR WITHOUT VOMITING. DDX: acute abdomen Surgical Medical Extra-abdominal Acute appendicitis Gastroenteritis URTI Intussusception (obstruction) IBD (more of chronic..) Lower lobe pneumonia Inguinal hernia DKA Torsion of the tests Inflamed Meckel’s diverticulum Hepatitis Hip and spine Peritonitis UTI and pyelonephritis

Vomit Bile stained Intestinal obstruction Hematemesis Peptic ulcer Projectile vomiting Pyloric stenosis GIT Abdominal distension Intestinal obstruction Blood in stool Intussusception Others Severe dehydration Gastroenteritis, DKA Failure to thrive GORD, celiac disease

• Key questions to ask in History:- When did the pain start? Where is it? Radiation? Severity? Fever? Vomiting? (blood or bile?) Change in bowel habit? What is the stool like? Urine (burning sensation, color)? SOB? Cough?

20. THE CHILD WHO VOMITS Causes: 1.GI (i.e., obstruction, pyloric stenosis, reflux, appendicitis, gatroenteritis, hEpatitis A) 2. CNS disease (tumours, migraine headaces, meninigtis) 3. pulmonary problems (astma-Children will cough up a fleck of sputum that initiates a gag response, tumours again, inflammatory- eg pneumonia) 4. renal disease (kidney stone, peylonephritis, UTI, renal failure) 5. endocrine/metabolic disorders (DKA common) 6. drugs (either as side effects or in overdosages) 7. psychiatric disorders or stress. Commonest causes: • Gastroenteritis:

• Food allergies and irritations: Although any food can provoke a reaction, several in particular tend to cause most food allergies, including eggs, milk, peanuts, shellfish, soy, tree nuts, wheat, and fish. Nausea, vomiting, and abdominal pain can occur within minutes or hours after ingesting the offending food.

• Anxiety and stress: Worries about the new school year. all kinds of emotional upsets can lead to nausea and vomiting, though this tends to happen more often with adults or older children.

• flu and other illness: A few other common reasons kids might have nausea or vomiting include ear infections, seasonal flu, swine flu, acid reflux, and reactions to medication, metabolic disorders.

• Eating too much

• Food poisoning

History:

-PC -when did it start

-how many times did the child vomit

-projectile or non-projectile

-colour

-blood or mucous

-after introducing food or drugs or not necessarily

-associated wit diahrrea or fever.

-recent take-away or undercooked food

- recent travel

-if no certain cause, then ask if stressed or not and how well they do in scool

-family –diabetes, sickle cell… -Immunizations - hepatitis maybe.

-nutrition- wt loss, appetite, what they eat or drink.

-stress

Physical:

-look for general status of patient (alert or not)

-signs of dehydration (mucous membranes, skin turgor, capillary refill, sunken eyes and fontanelles)

Treatment:

• ABC

• Check vitals , cbc (metabolic alkalosis), growth,

• Correct dehydration. Mild vs moderate vs severe

• Mild- prevent dehydration, continue breast feeds, encourage fluid intake and don’t give carbonated drinks. ORS if needed

• Moderate- ORS. give fluid deficit replacement+mainatinance fluid. Fluid deficit is 50 ml/k over 4 hours. Maintainance is first 10/100, second 10/50, 1/20.

• Severe- IV therapy. Saline solution 0.9% NaCl. If shocked, fluid deficit given is 100 ml/k, 50 ml/ k if not. And maintain fluid with nacl and 5% glucose. Also give KCl.

• Treat underlying cause.

21. CHILD WITH A HEART MURMUR

Heart murmurs are due to abnormalities of flow within the heart and great vessels. Innocent murmurs are very common but it is essential to assess whether the murmur is haemodynamically significant and whether appropriate antibiotic prophylaxis to prevent endocarditis is required.

History taking: 1. Ask about pre-natal and perinatal history, specifically focusing on infections, teratogenic exposure and presence of gestational diabetes (all of these are risk factors that may have lead to congenital defects) 2. Neonatal history including FTT, poor feedings, cyanosis 3. Age of onset-cardiac failure as a neonate 4. Past surgeries-corrections done after birth 5. In older children; ask about exercise intolerance, chest pain upon exertion, syncope or recurrent URTIs. 6. Medical history to ask about diseases related with cardiac abnormalities. 7. Family history to rule out sudden death in family members, siblings/family members with similar conditions or any genetic disorders such as Marfan,Noonan or Turner syndrome. 8. Impact on life- does the child miss school days, etc. Presentation Murmurs are described by location, intensity (grade 1-6 with grade 1 being virtually undetectable), timing in the cardiac cycle, and radiation.

The absence of symptoms does not exclude important pathology. Certain features indicate that a murmur is more likely to be pathological: • History: lethargy, tiredness, failure to thrive. • Inspection: cyanosis, clubbing, abnormal breathing (tachypnoea, intercostal recession). • Palpation: parasternal or apical impulse; abnormal pulses - diminished, absent or delayed femoral pulses. • Abnormal heart sounds; second heart sound is accentuated and not variably split. • Systolic murmur which is pansystolic or is grade 3 or above. • Murmur which is purely diastolic. • Radiation of murmur to the back. • Presence of an early or midsystolic click. • Presence of cardiac failure or arrhythmia. Innocent murmurs • Innocent murmurs are common in children and tend to become audible or louder when the heart beats faster, such as with a raised temperature or excitement. • Still's murmur (or Fiddle string murmur) is the most common innocent murmur heard in children aged 2 to 8 years old. It is a short, midsystolic murmur with a very characteristic low-frequency buzzing or musical quality.It is localised to the lower left mid-sternal border and radiates to the apex. The murmur is of short duration, low intensity and is loudest when the child is supine, often varying markedly with posture. It is also provoked by fever and anaemia. It can be made to disappear on hyperextension of the back and neck (Scott's manoeuvre). However, it is not always possible to distinguish it from a small ventricular septal defect. Still's murmur usually disappears at puberty. Pathological systolic murmurs • Ejection systolic murmurs: reach a peak midway between 1st and 2nd heart sounds and don't run into the 2nd heart sound. Usually maximal at the upper sternal borders, and possible causes include: • Aortic stenosis. • Pulmonary stenosis. Coarctation of the aorta: murmur is heard over the back, particularly in the interscapular region. • Hypertrophic obstructive cardiomyopathy. • Pansystolic murmurs have uniform intensity between 1st and 2nd heart sounds and merge with the 2nd heart sound, which is therefore not distinguishable. Those at the lower sternal border are more likely to be of regurgitant type due to: • Ventricular septal defect. Atrial septal defect. • Mitral or tricuspid regurgitation. Diastolic murmurs • Diastolic murmurs should always be regarded as pathological. • Early diastolic murmurs: occur just after the 2nd heart sound. They are high-pitched and easily missed. Causes include aortic valve regurgitation (eg bicuspid aortic valve, Marfan's syndrome) and pulmonary valve regurgitation (eg following surgery for Fallot's tetralogy or pulmonary stenosis), or with pulmonary hypertension. • Mid or late diastolic murmurs: are low-pitched and occur at the lower sternal borders in mitral stenosis or tricuspid stenosis. Continuous murmurs These cross the 2nd heart sound and are a feature of: • Venous hum (otherwise they are always pathological). Persistent ductus arteriosus. • Arteriovenous malformation. Investigations • CXR, ECG and echocardiogram are often performed but add little or no information in a child clinically assessed to have an innocent murmur. • Neonatologists and paediatric cardiologists are equally effective in diagnosing cardiac pathology. • An echocardiogram is the gold standard for the diagnosis of a structural heart disease but is not routinely required. Older toddlers who are asymptomatic when referred for echocardiogram, are rarely found to have serious pathology. • Cardiac catheterisation is occasionally necessary.

23. THE CHILD WITH AN ITCHY RASH Differentials: -Acute: • Chicken pox: red vesicular rash over body caused by varicella zoster virus. Treatment: no treatment necessary, fades away on its own. • Urticaria: flesh colored weals resulting from exposure to allergen or viral infection. Treatment: no treatment necessary. Anti-histamines in some occasions. • Scabies: infestation with sarcoptes scabiei mite which burrows in epidermis. Papules and vesicles occur between digits, axilla, buttocks, and in infants includes palms, soles, and trunk. Treatment: permethrin cream. Must check all family members for infestation. • Impetigo (bullous): blistering form of impetigo due to staph aureus infection. Treatment: systemic antibiotics. • Pityriasis rosea: viral origin, beginning with single oval scaly macule on trunk, upper arm, neck, or thigh. Numerous small pink macules develop later. Treatment: no treatment required. -Chronic: • Eczema: due to genetic deficiency of skin barrier function. Usually presents in 1st year of life and uncommon in 1st two months. Rashes are itchy (key clinical feature) and excoriated areas become weeping and crusted. Appear on face and trunk in infants, >2 months and on flexor and friction surfaces in older children. Management: avoiding irritants, emollients, topical corticosteroids, and immunomodulators. • Urticaria: chronic if persisting > 6 weeks, non-allergenic, due to local increase in permeability of capillaries and venules. Investigations: no investigations usually needed as diagnosis is clinical. Rash terminology: Macule: nonpalpable, circumscribed, flat lesion (<1 cm in diameter Papule: palpable , elevated lesion (<1 cm in diameter) Maculopapular: combination of macular and papular lesions Vesicle: fluid-filled, elevated skin lesion (<1 cm in diameter) Questions to ask: When did the rash start? Where did the rash start? Where has the rash spread to? Has there been any change in the rash (appearance, sensation, etc.) What has been used to treat the rash?

25. EASY BRUISING AND BLEEDING ETIOLOGY Summary: 1. Thrombocytopenia (reduced platelet count) a. Disorders of platelet adhesion b. Impaired platelet production c. Platelet dysfunction d. Destruction/Consumption of platelets 2. Non-Thrombocytopenia (normal platelet count) 3. Acquired disorders of coagulation DIFFERENTIAL OF THROMBOCYTOPENIA 1. Disorders of platelet adhesion a. Von Willebrand disease (vWD) b. Bernard-Soulier syndrome (absence or dysfunction of GpIb/IX) 2. Impaired platelet production a. Fanconi anemia b. Wiskott-Aldrich syndrome 3. Platelet dysfunction a. Glanzmann thromboasthenia (rare; (absence or dysfunction of GpIIb/IIIa)) 4. Increased platelet destruction or consumption a. Immune i. Idiopathic thrombocytopenic purpura ii. SLE b. Non-immune i. Hemolytic uraemic syndrome (HUS) ii. Thrombotic thrombocytopenia purpura (TTP) iii. DIC iv. Congenital heart disease v. Hypersplenism c. Acquired i. Aplastic anemia ii. Leukemia (malaise, infection, pallor, splenomegaly, lymphoadenopathy) iii. Drugs Thrombocytopenia (Mnemonic: HELP ME IT’S DIC) H Haemolytic uraemic syndrome/Thrombotic thrombocytopaenic purpura E Eclampsia/HEELP/Acute fatty liver L Liver disease/portal hypertension P Prosthetic heart valve M Malignancy/Marrow failure E Error (laboratory artifact) I Idiopathic thrombocytopaenic purpura T Transfusion S Storage diseases/hypersplenism D Drugs (heparin, antibiotics) I Infection/sepsis C Collagen vascular disease (especially lupus)

DIFFERENTIAL NON-THROMBOCYTOPENIC BRUISING (Platelet count is NORMAL) Vascular disorders • Congenital: Connective tissue disorders o Marfan syndrome, Ehlers-Danlos, hereditary hemorrhagic telangiectasia • Acquired o Meningococcal septicemia o Vasculitis (i.e. Henoch-Schonlein Purpura (HSP), SLE, ) o Trauma (accidental or non-accidental) ACQUIRED COAGULATION DISORDERS • (mainly neonates or early infancy) o Inadequate intake o Malabsorption (celiac disease, cystic fibrosis, obstructive jaundice) o Vitamin agonist (warfarin) • Liver disease • Idiopathic (ITP) immune thrombocytopenia • Disseminated intravascular coagulation (DIC) ESSENTIAL QUESTIONS IN HISTORY TAKING: 1. Age of onset a. 2-10 years: ITP b. Adolescent: von Willebrand disease may present with menorrhagia 2. Duration between trauma and the signs of bleeding a. Platelet disorder: bleeding comes on immediately after trauma b. Coagulation disorder: bleeding occurs hours to days after injury c. Meningiococemia: acute episode 3. Family hx a. Autosomal dominant (Platelet defect) b. Autosomal recessive (Coagulation defect) c. X-linked recessive = all boys (Coagulation defect i.e. hemophilia) 4. Bleeding history a. Previous surgical procedures; including dental extractions b. After recent viral infection (ITP) 5. Pattern of bleeding a. Mucous membrane bleeding (i.e. von Willebrand disease, thrombocytopenia) i. Bleeding after brushing teeth ii. Epistaxis b. Skin hemorrhage (i.e. von Willebrand disease) c. Distribution of petechiae or purpura i. Lesion confined to buttocks, extensor surfaces of arms and legs (HSP) ii. Wide spread: ITP d. Bleeding into muscles or into joints (hemophilia) e. Hematuria? (HSP) 6. Scarring and delayed hemorrhage (connective tissue disorders) 7. Blanching or non-blanching (meningococcal septicemia) 8. History of recent trauma 9. Concurrent disease 10.Diet: Does your child eat a lot of leafy greens i.e. spinach? 11. Drug history i.e. anticoagulants 12.Unusual pattern or inconsistent history ! Non-accidental injury = Abuse a. Bruising to cheeks, orbits, hidden/healed fractures b. Shape: whiplash, bite, pinch EXAMINATION: • Skin lesion o Purpura o Petechiae o Ecchymoses • Hepatosplenomegaly • Lymphadenopathy • Pallor • Distribution of purpura • Palpable or non-palpable lesions • Swollen tender joints INVESTIGATIONS: 1. Full blood count a. Evaluate for anemia, neutropenia 2. Blood film 3. Bleeding time a. Prothrombin Time (PT) measures factors II, V, VII, X b. Activated partial thromboplastin time (aPTT) measures II, V, VIII, X, XI, XII 4. Thrombin time: deficiency/dysfunction of fibrinogen 5. D-dimers: fibrin degradation products 6. Coagulation Screen 7. Platelet count 8. Liver Function test 9. Renal Function test 10.Bone marrow biopsy (Leukemia or if child is to be treated with steroids) 11. SLE screening Disorder PT aPTT Platelet Count Bleeding Time Haemophilia A N ↑ N N vWD N ↑ N ↑

DIC ↑ ↑ ↓ Or N N

ITP N N ↓ N

TTP N N ↓ N

Qualitative Defects N N N ↑

Liver Disease ↑ ↑ N N

Coag Pathophysiology Differential Diagnosis

1. Prolonged Prothrombin Time The PT evaluates the extrinsic pathway of coagulation (II, V, VII and X and fibrinogen). Liver disease 2. Vitamin K deficiency 3. Warfarin 4. Factor VII deficiency

1. Prolonged aPTT (activated partial thromboplastin time) The aPTT evaluates the intrinsic coagulation pathway (VIII, IX, XI and XII) Heparin administration (this is the most common caused - blood drawn from a line flushed with heparin) 2. von Willebrand's disease 3. Lupus anticoagulant 4. Acquired factor inhibitors 5. Factor deficiencies: a. Factor VIII (Haemophilia A) b. Factor IX (Haemophilia B) c. Factor XI d. Factor XII e.

TREATMENT Summary: • Usually supportive with colloid/blood transfusion if significantly anemia or hypovolemic. • Correct known coagulation or platelet abnormalities • Life-threating bleed! treat with blood (Fresh Frozen plasma) • Avoid IM injections, arterial puncture and NSAIDs • Seek hematologist and contact blood bank 1. Von Willebrand Disease 1. DDAVP 2. Plasma-derived F VIII concentrate (severe cases) 2. ITP 1. Acute i. Oral prednisolone ii. Intravenous anti-D iii. Intravenous immunoglobulin iv. Platelet transfusions (life-threatening hemorrhage) 2. Chronic = i. Monoclonal antibodies i.e. rituximab ii. Thrombopoietic growth factors iii. Splenectomy (patients will require lifelong prophylactic antibiotics) 3. DIC 1. Treat underlying cause 2. Fresh frozen plasma 3. Cryoprecipitate 4. Platelets 5. Anti-thrombin and protein C concentrates 26. THE PALE CHILD Pale child is a child whos skin colour is light. It is usually evident in te face/lips/hands. It is caused by reduction in RBCs or decreased blood flow. Causes/DDX of pale child: • Anemia (blood loss, poor nutrition or underlying condition eg sickle- most common) • Leukemia • • Illness (common cold, hypoglycemia,hypothyroid, etc.) How to approach a child who is pale? History: • age, sex, race, ethnic background • Duration of pallor • if child was sick, abdominal pain, wt loss, lethary,joint pain, bleeding.. • nutrition (important)- type of milk if bottle-fed, duration of breastfeeding; timing of solids introduction and whether an iron-fortified cereal was included after six months of age, cow's milk can cause . • birth - preterm, child received supplements • Family history - should include any history of anaemia, jaundice, early onset of gallstones or splenectomy (which may indicate hereditary spherocytosis). The mother's dietary history is also important as a vegetarian mother deficient in B12 may have a B12-deficient child. Physical: - Look for palmar crease pallor and conjuctival pallor. - Pallor and presence of jaundice can be assessed by an examination of the skin, conjunctiva and creases of the palm. The presence of cafe-au-lait spots may indicate Fanconi's anaemia - Bruising or petechiae may belie a low platelet count and suggests the possibility of leukaemia. - Abdominal examination may reveal liver or spleen enlargement - Heart rate, respiratory rate, temperature and BP. - A cardiac flow murmur may be present if the child is anaemic. - The child should also be examined for the presence of lymphadenopathy. Treatment: ABCs, assess severity of paleness and whether or not they require ventilation (o2 saturation). Then check weight and height and plot on chart. Check vitals. Check if any dehydration present and give IV fluids. If cause is anaemia then treat anemia (if iron def supplement iron, vit d def… ) basically treat underlying cause of paleness. 27. THE CHILD WHO IS BED WETTING Also known as nocturnal enuresis, due to genetically determined delay in acquiring sphincter competence. More common in males than females, usually with a first degree relative affected. Organic causes: • Urinary tract infection • Polyuria from osmotic diuresis (e.g. DM) • Severe fecal retention causing a reduction in bladder volume and causing bladder neck dysfunction On examination: child is usually normal both physically and psychologically. Differentials: UTI, constipation, DM Investigations: Urinalysis is not recommended unless bedwetting is of recent origin, there are daytime symptoms, or symptoms suggesting infection or DM. Investigate (and treat) daytime symptoms before addressing enuresis, eg symptoms suggestive of diabetes, UTIs or constipation. Treatment/management: Considered usually after child is > 6 years old 1. Enuresis alarm: sensor placed in childs pants, sounds an alarm when it becomes wet to wake child up to go to bathroom. Usually effective but requires time/patience. 2. Desmopressin: for short term relief from bed-wetting, the analogue of antidiuretic hormone is given as tablets or sublingually. Questions to ask: 1. Whether the bedwetting started in the last few days or weeks. If so, consider whether this is a presentation of a systemic illness (DM) 2. How many nights a week does bedwetting occur? 3. How many times a night does bedwetting occur? 4. Does there seem to be a large amount of urine? 5. The presence of daytime symptoms in a child with bedwetting, including: • daytime frequency (more than 7 times a day) • daytime urgency • daytime wetting • passing urine infrequently (fewer than four times a day) • abdominal straining or poor urinary stream • pain passing urine.

29. A CHILD WITH NECK SWELLING DIFFERENTIALS: 1. Infection a. Bacterial (erythematous, warm, tender; most common cause) i. Streptococcus, group A beta-hemolytic ii. Staphylococcus aureus iii. Toxoplasmosis (generalized lymphadenopathy) iv. Cat Scratch disease (Bartonella henselae) v. Haemophilus influenzae vi. Peritonsillar abscess vii.Tonsillitis b. Viral (tender, non-erythematous/warm) i. HIV ii. CMV c. Fungal i. Actinomycosis ii. Histoplasmosis d. Tuberculosis i. Mycobacterium tuberculi (cold, non-tender; systemic symptoms) ii. Atypical Mycobacterium 2. Non-infectious inflammatory mass a. Sarcoidosis b. Sialadenitis 3. Tumor a. Benign i. Teratoma ii. Desmoid tumor iii. Lipoma b. Malignant i. Lymphoma (firm, non-tender cervical lymphadenopathy adherent to overlying skin or underlying structures; systemic symptoms) ii. Leukemia iii. Rhabdomyosarcoma iv. Neuroblastoma 4. Non-lymphadenomatous neck swellings a. Sternocleidomastoid swelling b. Thyroid gland enlargement c. Thyroglossal cyst d. Dermoid cyst e. Branchial cyst (MC congenital neck mass) f. Thymic cyst g. Mumps 5. Vascular lesions a. Hemangiomas b. Cystic hygroma 6. Other a. Head lice b. Kawasaki Disease

IMPORTANT QUESTIONS FOR HISTORY TAKING: • Acute or Chronic Swelling • Symptoms: o Painful or non painful? o Fever? o Night sweats? o Weight loss? o Does your child have difficulty breathing? (lesion causing compression) • Was the child immunized with BCG vaccine? MMR? • Family history of TB • History of contact with TB? • Recent upper respiratory tract infection? • Recent earache or toothache? • Recent head lice infestation or contact with already infested person? o Tickling feeling of something moving in the hair o Itchy scalp or sores on the head? • Travel in the last 6 months? EXAMINATION: • Characteristics of the swelling o Location • Midline: thyroglossal duct cyst, dermoid and epidermoid cyst, cervical clefts or teratomas • Lateral neck: branchial cleft anomalies, lymphatic or vascular malformations • Supraclavicular: lymphoma o Shape – oval, hemispherical, irregular o Size – width, length and height • Cervical and axillary lymph nodes enlargement > 1 cm in diameter • Inguinal nodes enlargement > 1.5 in diameter • Supraclavicular enlargement (needs further investigation) o Temperature – warm vs. cold o Surface – smooth vs. irregular o Consistency – soft, firm, hard o Translucency o Fluctuation o Color -erythema o Tenderness o Mobile • Moves with swallowing ! thyroglossal duct cyst o Fluctuation (indicative of pus formation/abscess) o Attached to the skin o Pulsatility o Compressibility o Bruits • Torticollis? • Must check all lymph nodes • Systemic review: o ENT o Abdomen: Hepatosplenomegaly? INVESTIGATIONS: • Full blood count and film • Coagulation study • Acute Phase reactants o C-reactive protein o ESR • Blood culture • Anti-streptolysin O titre • Paul-Bunnell test: tests for glandular fever (infectious mononucleosis) • Chest X-ray • Mantoux test • Viral serology o HIV o CMV o Epstein-Barr virus (Infectious mononucleosis) • Fine Needle aspiration (gram stain, culture, acid fast stain, immunocytochemistry, cytogenetics) • Biopsy of mass • Imaging o Neck ultrasound (cystic vs. non-cystic) o CT o MRI • Thyroid function test o TSH o T3 and T4 • Thyroid antibodies o Thyroglobulin antibodies o Thyroid peroxidase antibodies TREATMENT: • Analgesia • Streptococcal/Staphylococcal infection: 10 day course of antibiotics i.e. co-amoxiclav • Complete surgical excision (i.e. branchial cleft cyst, thyroglossal duct cyst, dermoid cysts) • Pus/Abscess: surgical incision and drainage • TB treatment o 6-9 months: • Isoniazid • Rifampin • Ethambutol • Pyrazinamide o 2 months following above: • Isoniazid • Rifampin • Malignancy o Chemotherapy o Radiation o Excision

30. The child with a squint (starbismus) Background: Common Condition, were there is misalignment of the visual axes. May be associated with positive family history. Newborn babies have transient misalignment up to 3 months of age. Etiology: Is caused by either failure to develop binocular vision due to refractive errors,(most common cause), cataracts, and retinoblastoma. Types: 1. Non paralytic: common: due to refractive error in both eyes, which is corrected with glasses. Common in children with neurodevelopmental dely. 2. Paralytic: varies with gaze direction, and is due to paralysis of motor nerves.(may indicated underlying space occupying lesion. Focused History Questions: • WHEN? When is the deviation present? (eg, constantly? With fatigue? Only in certain positions of gaze?) • DURATION AND SEVERITY What is the duration and severity of the deviation? • PMH as the deviation been present since early infancy? • PMH Is there any history of trauma? • PMH Is there any history of any other medical problems (eg, headaches)? • PMH Is there a history of exposure to toxins or medications? • PMH What is the developmental/birth history? • FMH Is there a family history of strabismus? Physical Examination: assessment of general health and neurologic status, including an assessment of development. The presence of a consistent head tilt or turn should be noted 4 main steps to look for squint: 1. LOOK 3x 2. Corneal light reflex test: Choose an accommodative target (eg, a small toy) is held several feet in front of the child's face, and a penlight is held next to the toy = Check if eye reflection is symmetrical at same point in each eye.(refer to supplementary diagram) The corneal light reflex test 3. Do the Eye movement: The H. involves shining a light onto the child's eyes from a 4. Cover test: the good eye is covered with a piece of paper, distance and observing the this will result in fixation of the squinting eye. reflection of the light on the cornea with respect to the Treatment: pupil. The location of the 1. Glasses. reflection from both eyes should appear symmetric 2. Eye patch on good eye, so the squint fixes and generally slightly nasal 3. Surgery: mainly to prevent amblyopia(blindness) to the center of the pupil. A) Normal corneal reflex. B) Corneal light reflex in