Food Intolerance

Food Intolerance

It involves any reaction to food without involvement of immune system.

Food intolerance is often diagnosed by an elimination diet.

Skin prick tests or specific IgE measurements are not appropriate or helpful for the diagnosis of food intolerance.

The most common food intolerances are: lactose intolerance and monosaccharide intolerance, both of which are characterised by

• Persistently fluid stool.
• Excessive flatus.
• Excoriation of the buttocks.
• Typically, these infants appear well.
  

Lactose intolerance
Following infectious diarrhoea, infants may have temporary lactose intolerance.

Management

• Breast-feeding should continue unless there are persistent symptoms with buttock excoriation and failure to gain adequate weight.
• Formula-fed infants should be placed on a lactose-free formula for 3–4 weeks.

Note: A clinical response after change to soy formula may indicate either post-infectious lactose intolerance or allergy to cow’s milk protein, as soy formulae available in Australia are lactose-free.

Monosaccharide intolerance

Infrequently, infants with severe bowel damage secondary to gastroenteritis may be unable to absorb normal amounts of monosaccharide such as glucose or fructose. Diarrhoea will continue even with a lactose-free formula. Monosaccharide intolerance requires specialist consultation.

Food Allergy

A food allergy is an adverse reaction to a generally harmless substance within a food (usually a protein) that is mediated by the immune system.

Cow’s milk, egg, peanut, tree nuts, fish, shellfish, soy and wheat cause more than 90% of food allergies in children.

There are essentially three main types of food allergy: IgE mediated; IgE and non-IgE mediated; and non-IgE mediated.

IgE-mediated food allergy

The commonest IgE-mediated food allergens are egg, peanuts and milk.

Wheat, soy, fish and tree nuts are the next most common. Many food allergic children will have more than one food allergy.

Diagnosis is made on the history and confirmed by skin-prick testing.

The main principle of management is avoidance of the offending antigen.

• Oral allergy syndrome

Some patients with seasonal allergic rhinitis/conjunctivitis experience itch and irritation of the tongue, mouth and throat after ingestion of some fresh fruits and vegetables.

• Anaphylaxis

Non-IgE and IgE mediated Food Allergy

Atopic dermatitis and food allergy

Many parents perceive that food allergy is the underlying cause of their child’s atopic dermatitis and will try vigilantly to pinpoint the cause. Evidence would suggest that only about 40% of children with moderate to severe atopic dermatitis have a true food allergy.

Eosinophilic oesophagitis

Non-IgE-mediated food allergy

• Cow’s milk protein intolerance / soy intolerance

Infants are irritable and have blood or mucous in their stool typically some hours after the ingestion of these proteins.

Most resolve by 3 years old.

First-line treatment is usually a formula containing cow’s milk protein hydrosylate. Soy-based formulas should not be used in infants under 6 months old as many are also soy protein intolerant.

• Food protein-induced enterocolitis syndrome

In acute presentations, the child ingests the food and typically within 1.5 to two hours vomits profusely and may become shocked. It is frequently misdiagnosed as sepsis or bowel obstruction.

In chronic forms, young infants exposed to these proteins on a daily basis typically manifest symptoms of daily vomiting, diarrhoea, failure to thrive and, occasionally, melaena.

The pathophysiology of FPIES is unclear but skin tests are negative.

Diagnosis is based on history and management involves strict avoidance of the food.

Cow’s milk and soy FPIES usually resolve between the ages of 1 and 2 years and resolution is established by formal supervised food challenge.

Nutrition

If breast milk is not available, either from the breast or as expressed milk, a commercially prepared formula should be chosen.

All formulas are classified based on three parameters: caloric density, carbohydrate source, and protein composition.

• Pre-term & enriched formula
• Term formula
• Specialised term formula

Term formula

These formulas are modeled after breast milk and contain 20 kcal per ounce. Their carbohydrate source is lactose, and they contain cow’s-milk protein.

All infants should receive iron-fortified formula to prevent iron deficiency anemia.

Recently, formulas with long-chain polyunsaturated fatty acids have been heavily marketed to promote eye and brain development. Clinical trials of the effects of AA and DHA on cognitive, social, and motor development have been inconsistent. Although no harm has been demonstrated, most well-conducted randomized trials show no benefit.

Preterm and Enriched Formulas

Preterm infants have higher protein and calorie requirements. It is currently the standard of care to prescribe these formulas for preterm infants.

There are no studies to guide timing for the discontinuation of enriched formula. Although preterm and enriched formulas may improve shortterm growth parameters, they do not appear to affect longer-term growth or development at 18 months of age.

Specialized Term Formulas

SOY FORMULAS - for infants with galactosemia or congenital lactase deficiency.

LACTOSE-FREE FORMULAS - for infants with galactosemia or congenital lactase deficiency. It is an alternative to soy formula in lactose intolerance.

HYPOALLERGENIC AND NONALLERGENIC FORMULAS - for milk protein allergy.

• IgE medicated milk protein allergy can present with any combination of cutaneous, respiratory, and gastrointestinal complaints; blood in the stool is a classic symptom. It is usually diagnosed in the setting of a strong family history of allergies or atopic disease. Referral to an allergist may be helpful because skin prick tests and IgE levels.
• Non-IgE-mediated milk protein allergy can manifest as enteropathy and enterocolitis.

Because most infants with milk-induced enteropathy will be equally sensitive to soy protein, hypoallergenic and nonallergenic formulas are the preferred alternatives.

ANTIREFLUX FORMULAS - Reflux may be considered physiologic and does not require treatment unless it is accompanied by poor weight gain or significant infant discomfort.

Infant Formula and Colic

Soy and lactose-free formulas are heavily marketed for colic without a formal diagnosis of lactose intolerance.

Most colic improves spontaneously between four and six months of age; new formulas tried during this time may be credited with the improvement.

Evidence for soy formula in the treatment of colic is limited and based on poor-quality trials, and so there is no proven role for soy in the management or prevention of colic.

There is no evidence to support lactose-free formula either, but a short trial may be reasonable in infants with colic who also have gastrointestinal symptoms.

Two systematic reviews have found some benefit with hypoallergenic formula; this potential benefit must be weighed against substantially greater cost.

Urticaria

Definition:

Urticaria is characterised by the occurence of pruritic, raised lesions with surrounding erythema that are transient and resolve without scarring.

Angioedema is characterised by swelling involving the lower dermis and subutis. It is also tranisent but generally longer lasting than urticaria. Angioedema occurs in 40 to 50 % of patients with urticaria.

Classification:

It is important to differentiate physical from spontaneous urticaria.

Physical urticaris is provoked by external physical stimuli, usually soon after contact ( except in the case of delayed pressure urticaria ).

• Dermographism - induced by shearing forces on the skin
• Cholinergic urticaria - triggered by changes in core temperatures such as exercise, hot baths and stress.
• Delayed pressure - occurs four to eight hours after exposure to pressure. It typically involves the palm, soles and buttocks.
• Cold urticaria - stimulated by a sudden drop in skin temperature.
• Heat urticaria
• Solar urticaria - due to serum factors acting as IgE dependent photoallergens.

There are usually no serious underlying conditions associated with the physical urticarias, except cold urticaria.

Causes:
For the purpose of classifying aetiology, urticaria is subdivided into acute ( less than 6 weeks ) and chronic.

Acute:
Most acute urticaria has identifiable triggers, but it can be spontaneous which can be:

• IgE mediated

Food allergy
Hymenoptera venom - bee, wasp, ant
Medications

• Complement mediated

Post viral infections

• Direct mast cell degranulation

Radiocontrast media
Opioids
Vancomycin

• Imbalance of arachidonic acid metabolism

NSAIDs
Aspirin

Chronic:
Unlike acute urticaria, chronic urticaria is unlikely to be IgE mediated. An external cause for the conditon cannot be found in at least 80 - 90 % of patients with chronic urticaria.

Conditions associated with chronic urticaria are:
autoimmune thyroid disease
hepatitis B, A

Management:

History taking is the most important tool for identifying the cause for urticaria.

Acute urticaria is self limiting and does not require laboratory investigation.

• Laboratory tests should be tailored individually and requested based on clues in the history.
• Many experts recommend routine FBC, ESR and CRP. Screening for thyroid hormones, thyroid autoantibodies and antinuclear antibodies can be requested if the history is suggestive in chronic urticaria.

Treatment:
Step 1: H1 receptor antagonist
Step 2: If there is no improvement, add an H2 receptor antagonist.
Step 3: If there is no improvement and/or sleep disturbance, consider adding doxepin to the regimen.
Step 4: Referral to immunologist, if there is no response to above or suspected of urticarial vasculitis or chronic angioedema without urticaria.

Juvenile Idiopathic Arthritis

Definition:
It is defined as a persistent arthritis of unknown aetiology that begins before 16 years of age and persists for a least six weeks.

Aetiology:
Its cause is unknown but it is assumed that environmental factors especially viral aetiology act as a trigger in a genetically susceptible individuals.
However, it is unusual for more than one child in a family to have arthritis.

Differential diagnosis:

• Septic arthritis
• Truamatic
• Post-infectious or reactive arthritis
• Rheumatic fever
• Acute lymphoblastic leukaemia/ Bone tumour
• Osteomyelitis

Classification:
Juvenile idiopathic arthritis can be classified into seven subtypes:
• Oligoarticular - four or fewer joints and is the most common subtype.
• Polyarticular - five or more joints are involoved.
rheumatoid factor positive
rheumatoid factor negative
• Systemic - associated with high spiking fever, erythematous rash, lymphadenopathy and hepatosplenomegaly.
• Enthesitis related arthritis - associated with enthesitis or with lower axial skeletal involvement. Human leukocyte antigen (HLA) B27 is present or there is a family history of a first-degree relative with a HLA B27-related disease. A significant
proportion of patients will develop sacroiliitis as adults, but back and sacroiliac joint involvement is uncommon during childhood.
• Psoriatic - assoicated with asymmetrical involvement of small and large joints, and either the development of psoriasis or other evidence of a psoriatic diathesis.
• Undifferentiated

Management:

Diagnosis

Arthritis is defined as the presence of a joint effusion with reduced range of motion, pain on movement and/or warmth of the joint.
Arthritis can be inflammatory or traumatic. A consistent and important clinical feature is the timing of symptoms during the day. As a general guide:

• early morning stiffness and/or stiffness after rest or sleep suggests an inflammatory cause
• postactivity pain suggests a mechanical cause.

Investigations

The diagnosis of JIA is essentially a clinical one. The laboratory investigations are only used to confirm the diagnosis and to aid the classification of JIA.

RACGP guidelines recommend

• FBC, CRP and ESR should be performed if the symptoms are present for more than four weeks.
• Rheumatoid factor (RF) should be performed in patients with polyarthritis as its presence has prognostic significance.
• ANA should be performed in all patients as it can confer the risk of asymptomatic uveitis especially in oligoarticular arthritis.
• Anticyclic citrullinated peptide (anti-CC P) antibodies
  are not routinely tested in JIA, but may indicate severe disease.
• Human leukocytic antigen (HL A) B27 should be tested in children who present with signs and symptoms consistent with enthesitis related arthritis and can indicate susceptibility to the development of axial arthritis.
• If there is concern that arthritis is part of an underlying connective tissue disease or vasculitis then dsDNA, extractable nuclear antigens (EN A), C3, C4 and immunoglobulin testing is useful.
• Imaging ( X ray +/_ USS is recommended if there is symptoms more than 4 weeks.
  

Treatment

Early referral to paediatric rheumatologist and multidisciplinary care are important.
Three mainstays of treatment.

• Non-steroidal anti-inflammatory drugs
• Disease Modifying Anti-rheumatic Drugs ( Methotrexate and biologic agents )
• Intra-articular corticosteroid injection

Course of JIA

Approximately 50% of children will have active disease
as adults.

Vertigo

Vertigo

Vertigo is the illusion of motion

The first step in the management of vetigo is to distinguish peripheral and central vertigo.

Causes of Vertigo:

Peripheral – 93 percent are due to acute vestibular neuronitis, Benign paroxysmal positional vertigo and Meniere’s disease.

Other includes: acute labyrinthitis and drugs

Central – CVA, intracranial neoplasms and migraine.

How to differentiate:

Feature	Peripheal	Central
Nystagmus	Combined horizontal and torsional; inhibited by fixation of eyes onto object; fades after a few days; does not change direction with gaze to either side	Purely vertical, horizontal, or torsional; not inhibited by fixation of eyes onto object; may last weeks to months; may change direction with gaze towards fast phase of nystagmus
Imbalance	Mild to Moderate; able to walk	Severe; unable to stand still or walk
Nausea, vomiting	May be severe	Varies
Hearing loss, tinnitus	Common	Rare
Nonauditory neurologic symptoms	Rare	Common
Latency following provocative diagnostic maneuver	Longer (up to 20 seconds)	Shorter ( up to 5 seconds )
Head Thrust Test	Positive	Negative

Peripheral Vertigo:

History and Physical examination help to distinguish the different causes of peripheral vertigo.

Upper respiratory tract infection suggests acute vestibular neuronitis

Immunosuppression suggest herpes zoster oticus

Head trauma suggest possibility of perilymphatic fistula

Provoking factors with changes in head position suggest acute labyrinthitis, benign paroxysmal positional vertigo, cerebellopontine angle tumour, perilymphatic fistula and multiple sclerosis.

A positive Hallpike test has the following characteristics and suggests a diagnosis of BPPV:

• brief latency – in BPPV, there is usually a brief latency of several seconds before the onset of nystagmus and it usually lasts 10–20 seconds

• nystagmus – usually torsional (rotational around the anteroposterior axis of the eye globe) but may be horizontal. In BPPV, on performing the Hallpike manoeuvre, there is usually upbeating, torsional nystagmus arising from otolithic debris in the ipsilateral posterior semicircular canal. Horizontal nystagmus on positioning suggests that the lateral canal is affected. Downbeating, torsional nystagmus which occurs on positioning indicates that the ipsilateral anterior semicircular canal is affected

• reversal – upon sitting after a positive manoeuvre, the direction of nystagmus is reversed for a brief period of time

• fatigability – repetition of the test will result in less nystagmus each time.

Treatment of Peripheral Vertigo:

General Principles:

Medications are most useful for treating acute vertigo that lasts a few hours to several days. They have limited benefit in patients with benign paroxysmal positional vertigo, because the vertiginous episodes usually last less than one minute.

Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter in the vestibular system. Benzodiazepine enhance the action of GABA in the central nervous system (CNS) and are effective in relieving vertigo and anxiety.

Vestibular rehabilitation exercises commonly are included in the treatment of vertigo.

Thumb-tracking: Hold your thumb out 1 to 2 feet in front of your face. As you look at your thumb, turn your head from right to left, then left to right, then up and down. Increase speed gradually. Do the exercise for 90 seconds. Repeat the exercise four times a day.

Target-change: Pick two objects (targets) that you have to turn your head from left to right to look at. Look at one object, blink your eyes, and then turn your head quickly to look at the other object. Go back and forth quickly between the objects. Repeat several times per session, at least two sessions per day.

Lying-to-standing: Move from a lying-down position on a sofa or bed to a standing position as quickly as possible without falling. Get up toward both right and left sides quickly. Do the exercise five times on each side per session, at least two sessions per day.

Tightrope: Walk heel to toe as if you are walking on a tightrope or a line. Do the exercise in a hallway with available support, such as a wall or railing. For 30 minutes per day, practice walking 10 steps at a time without using a support.

Walking turns: Walk toward an eye-level target on a wall (such as a picture). As you get near the wall, turn your body to one side but keep your eyes and head locked on the target. When your body cannot move any farther, close your eyes and quickly turn your head to face forward. Repeat the exercise five times for each side, turning your eyes and head to the right and left sides. Slowly increase your speed for at least 30 minutes per day.

Ball toss: While standing or sitting, toss a tennis ball at least 3 feet above your head and catch it. Practice for five to 10 minutes per day. When you can do the exercise easily, try it while walking.

Specific Treatments:

BENIGN PAROXYSMAL POSITIONAL VERTIGO

Benign paroxysmal positional vertigo is caused by calcium debris in the semicircular canals (canalithiasis), usually the posterior canal. Medications generally are not recommended for the treatment of this condition.

The vertigo improves with head rotation maneuvers that displace free-moving calcium deposits back to the vestibule. Maneuvers include the canalith repositioning procedure or Epley maneuver and the modified Epley maneuver.

VESTIBULAR NEURONITIS AND LABYRINTHITIS

Treatment focuses on symptom relief using vestibular suppressant medications, followed by vestibular exercises.

MÉNIÈRE’S DISEASE

Treatment lowers endolymphatic pressure. Although a low-salt diet (less than 1 to 2 g of salt per day) and diuretics (most commonly the combination of hydrochlorothiazide and triamterene [Dyazide]) often reduce the vertigo, these measures are less effective in treating hearing loss and tinnitus.

Acute Otitis Media

Treatment of AOM involves the following.

Adequate analgesia

Usually with an oral agent such as paracetamol. Topical anaesthetic drops such as amethocaine, benzocaine or lidocaine have some efficacy at 30 minutes after administration, but not more than paracetamol once they have been absorbed.⁸ Topical anaesthetic drops should not be administered when there is a perforation as they may enter the inner ear and cause vertigo.

Antibiotic therapy

The current recommendations are that children older than 2 years who are not very ill (ie. no systemic features such as significant fever or vomiting) can be treated with observation only; the parents can be given a prescription to be filled if the child is still in pain after 48 hours.⁹ However, there are groups of children who should be treated. These include:
• children 2 years of age or younger, because:
• – they are not able to describe their symptoms
• – they are more likely to have suppurative complications such as meningitis and mastoiditis
• – they are less likely to improve spontaneously
• children with severe illness with pain, or a tympanic membrane perforation (these imply a more virulent organism)
• a child with known immunodeficiency
• indigenous children, including Aboriginal, Torres Strait Islander and Maori and other Pacific Islander children
• children with a cochlear implant.

The usual antibiotic recommended is amoxycillin, 15 mg/kg up to 500 mg three times per day for 5 days. If the child has an allergy to penicillin (excluding immediate hypersensitivity), the alternative medication is cefuroxime in a dose of 10 mg/kg up to 500 mg twice per day for 5 days, or ceflacor in a dose of 10 mg/kg up to 250 mg three times per day for 5 days.¹⁰ The efficacy of ceflacor is thought to be similar to that of amoxycillin but it may be less as it penetrates middle ear mucosa less efficiently.⁶

With a perforation of the eardrum, topical antibiotic drops are useful both to treat the middle ear and also to treat secondary otitis externa if present. The recommended antibiotics are quinolones such as ciprofloxacin with or without steroid, which are not ototoxic when there is a tympanic membrane perforation.⁶ If the tympanic membrane is intact there is no advantage in treating with topical antibiotics.

Follow Up:

Patient should be reviewed in 2 days if he is no better. At that stage, if the AOM has not resolved, institute change to an antibiotic such as amoxycillin/clavulanate.

Patient should also be reviewed at the 2 week mark to ensure that the perforation of the tympanic membrane has healed. Note that at 2 weeks following an episode of AOM, 70% of children will still have a middle ear effusion but most perforations will have healed.



Prevention:
• reduce contact with people with upper respiratory infections, especially large group childcare centres
• avoid tobacco smoke both during and after pregnancy. Children exposed to passive smoking are more likely to have recurrent otitis media and have middle ear effusions that persist for longer
• breastfeed for at least 6 months, preferably 12 months. If bottle fed, prop the baby up as milk can reflux into the ear if lying flat, causing inflammation
• avoid pacifiers/dummies – this possibly increases the risk of AOM by inadvertent sharing in childcare centres
• vaccination with the polyvalent pneumococcal vaccine reduces the incidence of AOM by 8%