Health Assessment in Aboriginal and Torres Strait Islander People

Life Style:
Alcohol Consumption - Hazardous ingestion of alcohol is more prevalent among indigenous Australian males and females aged 35–44 years than among the general population.

• Strongly advise pregnant women and those likely to conceive to abstain from alcohol.
• Base assessment of problem drinking follow by brief interventional counselling commencing at a young age (14–15 years). Repeat opportunistically at least annually, but care is needed to avoid jeopardising the client’s ongoing relationship with the health care provider.
• Simple advice about safe drinking
• Referral to specialist service or therapist
  

Smoking - Indigenous Australian adults from age 18 years are approximately twice as likely to be current smokers than non-Indigenous adults.

• Advise smokers at a higher risk of developing smoking related complications and those with smoking related disease about the benefits of quitting.
• Offer smokers support including self help health promotion materials.

Immunisation:
Influenza - Influenza and secondary pneumonia contribute to the much higher rates of hospitalisation for respiratory diseases among Indigenous Australians.

• Offer annual influenza vaccination from age 50 years.
• Offer annual influenza vaccination to clients with chronic illness from age 6 months.

Pneumococcal - The rate of invasive pneumococcal disease in the Aboriginal and Torres Strait Islander population far exceeds that in the non-Indigenous population. Some reported rates have been the highest ever recorded in the world.

• The 7vPCV is recommended for all Aboriginal and Torres Strait Islander children as part of the Australian Standard Childhood Vaccination Schedule.
• Offer 23vPPV with a single repeat vaccination 5 years after the initial dose from age 50 years.
• The 23vPPV is specifically recommended for Aboriginal and Torres Strait Islander clients aged 15–49 years who smoke or who have chronic illnesses (eg. chronic cardiac, renal and pulmonary disease, diabetes and/or alcohol related problems). Re-vaccination is required after 5 years, and again 10 years later or at 50 years, whichever is later.

Screening:
Pap smear - Cervical cancer is the most common cause of death due to cancer among Aboriginal women. There is an overall mortality rate that is more than nine times greater than that of non-Aboriginal women.

• Screen women who have no symptoms or history suggestive of cervical pathology with Pap tests every 2 years.
• Commence Pap tests for all women who have ever been sexually active at 18–20 years or 2 years after their first sexual intercourse, whichever is later.

Mammogram - Aboriginal and Torres Strait Islander women may be less likely than other women to be diagnosed with breast cancer. However, the incidence of breast cancer may be increasing.

• Screen women aged 50–69 years using mammography every 2 years.
• Advise women aged 40–49 years that there may be a small benefit in mammography screening when weighed against factors such as their age (the benefits of screening may increase through the decade), family history, possible risk factors, personal concerns, levels of anxiety, inconvenience, cost, and discomfort.
• Clinical breast examination is not recommended for breast cancer screening alone or in place of mammography.

Eye:
Visual Acuity - The Aboriginal and Torres Strait Islander population has a higher risk of developing cataracts than the general Australian population.

• Screen adults (from age 40 years) for reduced visual acuity at least every 2 years. The need for cataract surgery and/or correction of any refractive errors should be identified.

Active trachoma - Active trachoma is endemic in the Aboriginal populations of northern and
central Australia, and predominantly affects children.

• Perform an opportunistic eye examination as part of any child health assessment where trachoma affects a community.
• Single dose azithromycin is the treatment of choice for active trachoma.

Trichiasis - Trichiasis affects a significant proportion of the elderly Aboriginal population (defined as aged >50 years) in remote areas of northern and central Australia.

• Screen for trichiasis as part of the routine annual examination from age 40 years if the region is or has been endemic for trichiasis.
• Refer for surgery when trichiasis is present.

Vascular Health:
Blood Pressure -

• Measure BP of adults (>18 years) at every visit (ensuring BP has been measured at least annually).
• Screening may commence earlier (from 15 years) in regions known to have a high prevalence of hypertension from this age.
• Screen 6-monthly for those with diabetes or target organ damage.

Physical activity -

• Recommend moderate intensity physical activity (such as brisk walking) of 30 minutes or more on most, if not all, days of the week. The total 30 minutes may be accumulated in shorter bouts, such as three 10-minute walks.

Cholesterol and lipids -

• Commence lipid screening at age 18 years and continue annually thereafter.
• Those whose cholesterol levels are raised but who are at low to moderate absolute risk of CVD should be given dietary and other lifestyle advice and monitored more closely over the next year.

Limping Child

A limp is an abnormal gait pattern, as a result of pain, weakness or deformity of the musculoskeletal system.

It is useful to assess the child by considering common presenting conditions at each age group.

• Toddler (1 - 4 years)
• Child (4 - 10 years)
• Adolescent (10 - 16 years)
  

At all ages the following MUST be considered

• TRAUMA
• TUMOUR
• INFECTION

Type of Limp:

The gait has two phases - stance phase and swing phase.

• Antalgic gait - the stance phase is shortened and the patient hurries off the painful side.
• Trendelenburg gait - is due to weakness of the hip abductor muscles and the body tends to lurch to the affected side. The lurching gait may be unilateral or bilateral. If the condition is bilateral, waddling is seen, with the trunk swaying from side to side. The causes may involve an abnormal hip joint such as in developmental dysplasia of the hip, congenital coxa vara or Perthes’ disease. It may also be caused by muscle weakness such as in polio, cerebral palsy or spina bifida.
• Stiff knee gait - is characterised by loss of knee motion resulting in circumduction and pelvic elevation on the affected side during the swing phase. This may be caused by knee disorders to minimise the motion of a painful knee.
• Short-leg gait - the head and pelvis fall as the body weight is taken on the short leg. This may be difficult to detect if the discrepancy is less than 2 cm. The gait may be disguised by tilting of the pelvis and by holding the ankle of the short leg in a plantar flexed position. To compensate for difference in leg lengths, circumduction of the leg on the long side may occur instead. A heel raise corrects the gait.

Common Causes of Limping in Children:
Toddler (1 - 4 years)

• Developmental - Developmental dysplasia of the hip,Perthes disease
• Infection - Osteomyelitis, Septic arthritis
• Inflammatory - Irritable hip (transient synovitis)
• Trauma - Accidental or non-accidental
• Tumour - Ewing's sarcoma, Secondaries
• Neurological - Cerebral palsy

Child (4 - 10 years)

• Developmental - Perthes disease
• Infection - Osteomyelitis, Septic arthritis
• Inflammatory - Juvenile rheumatoid arthritis, Irritable hip (transient synovitis)
• Trauma - Accidental or non-accidental
• Tumour - Ewing's sarcoma, Secondaries

Adolescent (10 - 16 years)

• Developmental - Residual effects from childhood and toddler conditions, Tarsal coalition, Slipped upper femoral epiphysis (SUFE)
• Infection - Osteomyelitis, Septic arthritis
• Inflammatory - Juvenile rheumatoid arthritis, Irritable hip (transient synovitis)
• Trauma - Accidental ( sport related )
  
• Tumour - Osteosarcoma

Clinical Assessment:
History including antenatal, perinatal and postnatal history, developemental history, trauma and features of infection
Examination:

• Gait
• Walk on toes and heel
• Trendelenburg test
• Spine examination
• An assessment of leg lengths can be determined by palpating the anterior superior iliac spines or the posterior superior iliac spines. If there is any significant tilting of the pelvis, level the pelvis by placing an appropriate height block under the foot on the short side.
• The hip, knee and ankle joints are examined and a neurological assessment is undertaken.

Checking for Non-adherence

Definitions:
Compliance/Adherence/Concordance - the extent to which a patient acts in accordance with the prescribed interval and dose of a dosing regimen.
Persistence - the duration of time from initiation to discontinuation of therapy.
Adherence: may also be defined as the combination of both compliance and persistence.

The validated Morisky questionnaires can help you identify non-adherence in patients, and gives an insight into the nature of any non-adherence.

4 points questionaire:

• Do you ever forget to take your medication?
• Are you careless at times about taking your medication?
• When you feel better, do you sometimes stop taking your medication?
• Sometimes, if you feel worse when you take your medication, do you stop taking it?

Premenstrual Syndrome

Premenstrual syndromeis a cyclical disorder of young and middle-aged women, which is characterized by emotional and physical symptoms that consistently occur during the luteal phase of the menstrual cycle.

• Affective Symptoms: Depression, Sadness, Irritability, Anger, Anxiety, Tension, Appetite Change and Food Cravings, Change in sexual interest
• Cognitive Symptoms: Impaired concentration, confusion, forgetfulness, temper outburst
  
• Fluid Retention: Breast tenderness or swelling, weight gain, abdominal bloating or swelling, swelling of extremities
  
• General Somatic Symptoms: Fatigue, Dizziness, vertigo, nausea and insomnia
  

Women with more severe affective symptoms are classified as having premenstrual dysphoric disorder.

Aetiology:

• The role of ovarian hormones is unclear, but symptoms often improve when ovulation is suppressed.
• Some evidence suggests that the disorder is related to enhanced sensitivity to progesterone in women with underlying serotonin deficiency.

Management:

Premenstrual syndrome and premenstrual dysphoric disorder are diagnoses of exclusion; therefore, alternative explanations for symptoms must be considered before either diagnosis is made.

PMS also must be distinguished from simple premenstrual symptoms (e.g., bloating, breast tenderness) that do not interfere with daily functioning and are characteristic of normal ovulatory cycles.

When PMS or PMDD is suspected, patients should be instructed to keep a premenstrual daily symptom diary for several consecutive months.

Non-pharmacological Therapies: should be offered to all patients and includes education, supportive therapy, rest, exercise, dietary modifications such as low fat, high fibre diet with reduced salt, sugar and caffeine.

Pharmacologic Therapies:

• Selective Serotonin Reuptake Inhibitor - Administration only during the luteal phase decreases drug cost, minimizes drug exposure and side effects, and may be more acceptable to some women. For intermittent therapy, fluoxetine or sertraline can be given during the 14 days before the menstrual period, or treatment can be initiated just before the expected onset of symptoms.

• Diuretics - Spironolactone is the only diuretic that has been shown to effectively relieve PMS symptoms such as breast tenderness and fluid retention.

• Non-steroidal Anti-inflammatory Drugs - mefanamic acid and naproxen sodium have been the most studied.

Dysmenorrhoea

Dysmenorrhoea is painful menstruation and may be

• primary in the absence of detectable pelvic pathology
  
• secondary to organic pelvic disease.

Primary Dysmenorrhoea

Dysmenorrhea is thought to be caused by the release of prostaglandins in the menstrual fluid, which causes uterine contractions and pain. Vasopressin also may play a role by increasing uterine contractility and causing ischemic pain as a result of vasoconstriction.

Risk Factors:
* Age < 20 years
* Attempts to lose weight
* Depression/anxiety
* Disruption of social networks
* Heavy menses
* Nulliparity
* Smoking

Clinical Features:
* Age - 6 - 12 months after the onset of menarche
* Onset - 24 hrs before menstruation and rarely persists for more than 48 - 72 hours.
* Pain - in the lower abdomen which may radiate to the inner surface of the thigh and lower back.
* Nausea and vomiting may be prominent, due to a prostaglandin effect or as a result of severe pain.

Treatment:

Nonsteroidal anti-inf lammatory drugs (NSAIDs): are the best-established initial therapy for dysmenorrhea. They have a direct analgesic effect through inhibition of prostaglandin synthesis, and they decrease the volume of menstrual f low.

Hormonal therapies:
# Oral Contraceptive Pills - it acts by reducing prostaglandin release during menstruation.
# Other - Depo-medroxyprogesterone acetate injection and levonorgestrel intrauterine device (Mirena).

Complementary and Alternative Medicines:
# Thiamine at a dosage of 100 mg daily was found to be effective in treating dysmenorrhea in a double-blind RCT of more than 500 East Indian women aged 12 to 21 years with moderate to severe symptoms.
# The Japanese herbal remedy toki-shakuyakusan (TSS) has been shown in an RCT to be better than placebo in the treatment of women with dysmenorrhea.

Life Style Modification:
# Low-fat vegetarian diet decreases duration and intensity of dysmenorrhea.
# Some studies have reported a benefit with exercise.

Secondary Dysmenorrhoea

It is uncommon before the age of 25 years.

The precise clinical picture is determined by the underlying cause.

A history that is inconsistent and/or physical findings of a pelvic mass, abnormal vaginal discharge, or pelvic tenderness that is not limited to the time of the menstrual period suggest a diagnosis of secondary dysmenorrhea.

Glaucoma

Glaucoma and IOP elevation are not synonymous.

Glaucoma is characterized by damage to the optic nerve that results in visual field loss regardless of the IOP level.

Many patients with elevated IOP show no evidence of optic nerve damage or visual field loss. This condition is known as "ocular hypertension." Much debate exists as to when glaucoma therapy should be initiated in patients with mild ocular hypertension alone.

Glaucoma may manifest as

• Optic disc changes – cupping resulting from reduced width of the neuroretinal rim or notch-like nerve-head deficit with associated nerve fibre layer irregularities – detectable loss and thinning
• Visual field losses
• Usually both of the above, but the disc changes often precede the field loss.

There are two main types of glaucoma:

• Open angle – most commonly primary open-angle glaucoma
• Closed angle.

Management:

Screening: RACGP does not recommend routine screening of glaucoma with tonometer or visual field testing. However, high risk patients should be referred for further assessment every 12 months.

• a family history of glaucoma
• age ≥60 years
• high myopia >8 diopters
• diabetes
  
• history of long term steroid use

The aim of treatment of open-angle glaucoma is to normalise IOP and thus stabilise disease. Clinical trials indicate that the lower the IOP, the greater the likelihood of achieving stable disease.

Pharmacological Method -

When a topical medication is chosen as first-line therapy in a patient with primary open-angle glaucoma, a stepped approach is used. Thus, a single topical agent is given up to its maximum dosage, as tolerated, before another agent is added or a different agent is tried.

A prostaglandin derivative, or ß-blocker are most commonly chosen, and should be used at the lowest possible concentration, and as infrequently as possible while achieving the desired outcome.

ß-blockers

Non-selective ß-blocker - timolol 0.25% or 0.5% lowers IOP by reducing aqueous secretion.

Selective ß₁-adrenegic-blocking agent betaxolol is nearly as effective as timolol, but has the advantage of having little effect on the cardiopulmonary system.

Combining a topical and systemic ß-blocker can increase the risk of ß-blocker-related side effects. For patients taking an antihypertensive medication the possibility of low nocturnal blood pressure should be considered. Nocturnal hypotension has been linked to progression of glaucoma.

Prostaglandin derivatives

The synthetic prostaglandins – latanoprost, travoprost, bimatoprost – lower IOP by increasing aqueous outflow through the uveo-scleral pathway.

They commonly cause hyperaemia and can increase the length of eyelashes and can increase periorbital skin pigmentation.

α ₂-adrenergic agents

These agents – aproclonidine, brimonidine – stimulate α 2-receptors in the ciliary epithelium to reduce the formation of aqueous humour, and enhancing uveoscleral outflow. In long term treatment aproclonidine tends to diminish in efficacy over time and both agents have a relatively high incidence of local allergy.

Carbonic anhydrase inhibitors

Both topical – dorzolamide, brinzolamide and oral – acetezolamide – carbonic anhydrase inhibitors are used in the treatment of glaucoma, where they decrease the formation of aqueous humour, presumably by slowing the formation of bicarbonate ions resulting in reductions in sodium and fluid transport.

Miotics

Miotics – pilocarpine, carbachol – were the traditional agents used to treat glaucoma. They act by stimulating cholinergic receptors, reducing IOP by contraction of the ciliary muscle causing pressure on the trabecular meshwork and a consequent increase in the outflow.

Surgical Therapy:

• Laser therapies
• Selective laser trabeculoplasty
• Peripheral laser iridotomy
• Filtration surgery

It is essential for the best outcomes that all patients be followed-up on a regular basis. After initiation of therapy patients should be seen at 2–4 week intervals until control of IOP is achieved.

Once IOP has been controlled patients should be reviewed every 3–6 months.

Early Detection Of Prostate Cancer

Men who are between the ages of 50 - 75 years and men older than 40 years with family history of prostate cancer are most likely to benefit from the early detection of prostate cancer.

For early detection digital rectal examination and prostate specific antigen are required.

Chance of prostate cancer given positive PSA test is one in three and chance of cancer given both abnormal PSA and DRE test is one in two.

Prostate cancer can still be present with normal PSA.

• Interpretation of PSA testing:

Age 50th centile 95th centile
40 - 49 .....0.65..............2.0
50 - 59......0.85............. 3.0
60 - 69......1.39..............4.0
70 - 79.......1.64..............5.5

Men whose PSA above 50th centile but below the 95th centile have been shown to be at higer long term risk of prostate cancer compared with those below the median.

PSA velocity which is calculated by meansuring PSA over 12 - 18 months can suggest the higer risk if it is over 0.75 ng/ml/yr.

Precentage of free PSA: Prostate cancer is likely if FTP is below 10% and a low risk if FTP is over 25%.

Perinatal Mental Health

Perinatal refers to the period from conception until 12 month postpartum.

• Baby Blues

Up to 85% of women may become tearful, irritable or hypersensitive in their interactions with others and their mood may be very labile. This is commonly known as the ‘baby blues’.

In most cases, baby blues occur within the first week after childbirth and resolve within seven - 10 days.

Most women will not require specific treatment apart from sensitive support and will recover in a few days.

• Perinatal Depression

Postnatal depression is best described as a depressive disorder with an onset in the first 12 months following childbirth.

Women with genetic vulnerability may be particularly at risk. Antenatal depression and past or family history of depression or anxiety disorders are the best predictors of future episodes of depression.

Other risk factors include: unplanned pregnancy, first pregnancy, indigenous background, poverty, stressful life events and lack of support.

According to DSM - IV criteria, at least five of the following symptoms are required for the diagnosis of major depression

• Depressed mood/irritability.
• Diminished interest in activities.
• Significant weight or appetite change.
• Sleeping problems e.g. insomnia or hypersomnia.
• Fatigue.
• Feelings of worthlessness/guilt.
• Inability to think clearly or concentrate.
• Recurrent thoughts of death and/or suicide.
• Psychomotor agitation and/or retardation.

Effects on Infant:
Infants are very sensitive to the quality of care they receive early in life.

Securely attached infants are more socially competent and can express a wide range of emotions, confident of a sensitive response from their mother.

Insecurely attached infants may avoid closeness or may be highly anxious, lacking confidence that their mother will be there for them.

Increasingly, research is finding a clear association between
severe maternal antenatal stress/anxiety, as well as depression,
on both foetal and later child development.

Prostatitis

Prostatitis is the third most significant prostate pathology after prostate cancer and benign prostatic hyperplasia.

With the development of a new prostatitis classification system in 1995 at the National Institutes of Health (NIH) conference, promising ongoing research may change the way men with prostatitis are managed.

NIH category Name
I Acute bacterial prostatitis
II Chronic bacterial prostatitis
III Chronic prostatitis/chronic pelvic pain syndrome ( Inflammatory or non-inflammatory )
IV Asymptomatic inflammatory prostatitis

• Category I ( Acute bacterial prostatitis )
  

It is characterized by local symptoms of dysuria, urgency and urinary frequency which can be associated with suprapubic or perianal pain and urinary retention.

These symptoms can be preceded by systemic symptoms such as fever and rigors.

Per rectal digital examination will show an exquisitely
tender, warm, boggy prostate.

Urine cultures, blood cultures and routine blood tests (including full blood count and electrolytes, urea and creatinine measurements) should be performed.

Treatment initially includes intravenous penicillin with aminoglycosides, followed by oral fluoroquinolone antibiotics (e.g. ciprofloxacin) for four to six weeks.

• Category II ( Chronic Bacterial Prostatitis )

It tends to occur in older men.

It classically present with recurrent, symptomatic urinary tract infections, usually caused by the same organism.

In addition to symptoms related to urinary tract infection, they may also experience perineal, lower back or testicular pain, or painful ejaculation.

• Category III (Chronic prostatitis/chronic pelvic pain syndrome)

The hallmark is ‘pelvic’ pain or discomfort which lasts for at least three months. It is a diagnosis of exclusion after careful evaluation of all other causes of pain in the area.

In general practice, evaluation should at least include a detailed history, physical examination including DRE, urinalysis and urine culture.

A renal tract ultrasound with postvoid urine measurement is
reasonable to determine bladder emptying and screen for any obvious bladder pathology, including tumours or bladder stones.

Treatment of CP/CPPS

A multimodality approach to treatment should be adopted for men with CP/CPPS.

Medical treatment has traditionally been based around the three As – antibiotics, alpha blockers and anti-inflammatories.

Antibiotics:
Even though there is no evidence of infective aetiology, there is enough support to use 4 - 6 weeks course of antibiotic therapy initially. However, repeated course of antibiotics therapy is not justified.

Fluoroquinolones such as ciprofloxacin are the antibiotics of choice due to excellent penetration into the prostrate. Norfloxacin can be used but it does not concentrate as effectively in the prostatic fluid as ciprofloxacin.

Trimethoprim is the second line agent.

Alpha blockers: should be used for a minimum duration of three months, and some symptoms may be relieved in about 50 to 60% of patients.

Anti-inflammatories: Ibuprofen and naproxen are generally well tolerated and readily available examples of these drugs.

Hormone therapy: Finasteride is a 5alpha-reductase inhibitor for which there is some evidence of benefit in terms of voiding symptoms and pain in patients with CP/CPPS. In men with concurrent lower urinary tract symptoms and enlarged prostates, this may provide a dual benefit.

Referral to a urologist should be considered for:

• significant pelvic pain
• a history of pelvic pain with bothersome lower urinary tract symptoms
• recurrent urinary tract infections
• microscopic or macroscopic haematuria with pelvic pain, or lower urinary tract symptoms
• a tender prostate or an abnormal DRE
• an abnormal serum prostate specific antigen measurement

Benign Prostatic Hyperplasia

Aetiology:

Dihydrotestosterone is responsible for the developement of BPH and it is produced through the conversion of testosterone by the enzyme 5 alpha-reductase type 2 in the stromal cells of the prostate.

Even though testosterone level declines with age, dihydrostestosterone level remains constant thoroughout the life.

Symptoms:

Compression of prostatic urethra causes lower urinary tract symptoms which includes -
Storage symptoms: Frequency, urgency, nocturia and urge incontinence.
Voiding symptoms: hesitency, poor flow, intermittency, straining, dysuria, incomplete emptying.

Symptoms Score: The International Prostate Symptom Score (IPSS) questionnaire is recommended.

Physical Examination:

Digital rectal examination (DRE) is important and can access the prostrate size:
Small - size of walnut, no protrusion into rectum
Medium - size of egg, Back of prostrate is protruding 1 - 2 cm into the rectum
Large - size of tangerine, more protrusion into the rectum
Extra-large - size of an orange, difficult to feel the entire posterior of the prostrate

Basic neurological examination
Perianal sensation and sphincter tone
Bladder palpation
Caliber of the urethral meatus

Investigations:

Urine analysis: midstream urine: microscopy, culture and
sensitivity (MC&S)

Prostate specific antigen (PSA) levels: can be used to differentiate with prostrate cancer

Renal function

USS - prostrate size, post void residual volume

Treatment:

Choices include - watchful waiting, medical therapy and surgery.

Watchful waiting: it includes education, life style modification ( reduction in alcohol, caffeine intake and fluid intake ) and behaviour training such as double voiding.

It is useful for patients with mild symptoms of LUTS secondary to BPH (IPSS score less than 8).

Medical therapy:

Alpha Blocker: include - doxazosin, terazosin, alfuzosin and tamsulosin.

It is effective at reducing lower urinary tract symptoms.

However, these medications do not shrink prostate volume or have any effect on PSA levels.

Tamsulosin and alfuzosin are more selective in relaxing prostatic smooth muscle and have no effect on blood pressure. For this reason tamsulosin and alfuzosin do not need to be titrated and can be started directly at therapeutic dosage.

5-Alpha Reductase Inhibitors: includes Dutasteride and Finasteride.

It has been shown to decrease prostate volume resulting in a decrease in the need for BPH surgery by 48% and acute urinary retention by 57% compared to placebo.

It also lead to a significant reduction in PSA levels. If a patient is experiencing an increase in PSA levels after the treatment nadir at 6-12 months after initiation of therapy of 5-alpha reductase inhibitor, adherence should be verified and if this has been confirmed they should be referred to an urologist to rule out prostate cancer.

Combination therapy: α-blocker with 5α-reductase-inhibitor
has been shown to be more beneficial and durable than the
monotherapy of either substance.

Some guidelines advise clinicians to give patients on combination therapy the option to discontinue the alpha blocker after 6-12 months. If symptoms recur, the alpha blocker should be restarted.

However, lifelong use of 5-alpha reductase inhibitors should be considered to prevent BPH progression.

Anticholinergic Agents ( tolterodine ):
Combination therapy with an alpha receptor antagonist and anticholinergic can be helpful for selected patients with bladder outlet obstruction due to BPH and concomitant detrusor overactivity.

Prior to initiation of anticholinergic therapy, baseline PVR urine should be assessed. Anticholinergics should be used with caution in patients with a post-void residual greater than 250 to 300 mL.

Surgery:
Transurethral resection of the prostate (TURP) for prostates 30–80ml
Transurethral incision of the prostate (TUIP) for prostates <30ml
and without middle lobe
Open prostatectomy or TURP for those >80ml
Laser ablation or resection of BPH available in specific surgical
centres.

Specialist referral:

The patient’s symptoms become more serious: their symptom
score moves into the ‘severely symptomatic’ category
The patient’s symptoms significantly interfere with their quality
of life – score of 5 ‘unhappy’ or 6 ‘terrible’ on the IPSS
After an episode of urinary retention, urinary infection, haematuria
No response to treatment
A risk of prostate cancer exists
Post void residual urine on ultrasound assessment more than 100ml

Follow up and Shared-Care:

It is recommended to do follow up every 12 - 18 months but when initiating or changing BPH therapy, consider evaluating the patient at least every 6 months.

Sexually Transmitted Infections

How to get started with an STI discussion?

• Bringing the subject up opportunistically

“ We are offering Chlamydia testing to all sexually active people under the age of 25, would you like to have a test while you’re here or find out more about Chlamydia?”

• Using a ‘hook’

“ Have you heard about HBV or HPV vaccination? They protect against infections that can be sexually transmitted, perhaps we could discuss these while you’re here?”

• As part of a reproductive health consultation

“ Since you’re here today for a pap smear/to discuss about contraception could we also talk about some other
aspects of sexual health, such as an STI check up?”

• Because the patient requests a “checkup” for STIs

“ I’d like to ask you some questions about your sexual activity so that we can decide what tests to do, is that OK?

How to do brief sexual history?

• Are you currently in a relationship?
• In the last 3 months, how many sexual partners have you had? How many partners have you had in the past 12 months?
• Were these casual or regular partners?
• Were your sexual partners male, female or both?
• When was the last time you had vaginal sex/oral sex/anal sex without a condom?
• In the past year were you ever paid for sex?
• Have you previously been diagnosed with an STI?
• Is there anything else that is concerning you?

It is important to find out other risk behaviours

• Have you had any tattoos? If yes, was that here in Australia or overseas?
• Have you ever injected drugs?
• Have you ever shared needles or injecting equipment?
• Have you ever been in gaol?

Which test choices are suitable?

• A sexually active young person under 25 years

PCR for chlamydia - First pass urine OR Self-collected vaginal swab OR Endocervical swab
Consider vaccination for HBV & HPV

• A sexually active Aboriginal young person under 25 years

PCR for chlamydia & gonorrhoea - First pass urine OR Self-collected vaginal swab OR Endocervical swab
Blood test for HBV infection
Consider vaccination for HBV & HPV

• An (asymptomatic) person of any age requesting “a STI checkup”

PCR for chlamydia - First pass urine OR Self-collected vaginal swab OR Endocervical swab
Blood test for HBV , HIV and syphilis infection
Consider vaccination for HBV & HPV

• A man who has sex with men (MSM)

Chlamydia PCR - First pass urine & anal swab
Gonorrhoea PCR - Throat swab & Anal swab
Blood test - HIV, Syphilis, HAV & HBV
Vaccinate for HAV & HBV

• A sex worker

Chlamydia & Gonorrhoea PCR - First pass urine OR Self-collected vaginal swab OR Endocervical swab
Blood test - HIV, Syphilis & HBV
Vaccinate for HBV

• A person who injects drugs

Chlamydia & Gonorrhoea PCR - First pass urine OR Self-collected vaginal swab OR Endocervical swab
Blood test - HIV, Syphilis, HBV & HCV
Vaccinate for HBV

How to do contact tracing?

• Introduce the reasons for contact tracing.

‘It’s really important your partner(s) gets treated so you don’t get the infection again’.
‘Most people with an STI don’t know they have it because they have no symptoms, but still could have complications
or pass it onto a partner’.

• Help identify which partner(s) need to be informed

Use a non-judgemental approach; some people have more than one sexual partner and all can be treated.
‘Try thinking back to when and where you have had sex recently or any special events’.

• Explain the methods and offer choice.

Different methods (in person, phone, SMS, email or letter) might be needed for each partner.
Patient Initiated Referral: Your patient chooses to notify their own contacts; you discuss with them the information they
will provide to their contacts.
Provider Initiated Referral: You, your delegate or another health agency informs the patient’s contacts; get the consent
of your patient; it can be anonymous or not depending on the wishes of your patient. It is indicated in the followings:

• HIV, syphilis and gonorrhoea due to higher morbidity.
• Repeat infections as a partner may not have been tested and treated.
• Within Aboriginal & Torres Strait Islanders communities due to
• stigma and issues around confidentiality.
• Incarcerated or detained partners may be more difficult to contact.
• Casual or ex-partners who are less likely to be notified.
• If the patient requests.

• Support Patient Initiated Referral

– Provide specific STI information – written or web links.
– Discuss how a partner might react and problem solve with the patient.
– Remind them partners could be contacted by telephone, in person, SMS, email or letter. All can be anonymous or not.
– www.letthemknow.com.au
– www.thedramadownunder.info for MSM*
– Your practice staff may be able to assist your patient to send an SMS or email before they leave your clinic.
It is a quick and easy option.
– Provide treatment letter(s) to be given to contacts; see www.gpnsw.com.au for downloadable templates.
– Schedule a follow up visit or phone call to determine if the patient was able to inform their partners. If not notified, offer
further assistance.

• Document discussions in patient notes.

How Far Back in Time to Trace

Contact tracing is not recommended in warts and herpes as there is little proven benefit
Chlamydia - 6 months
Gonorrhoea - 2 months
Syphilis

• Primary syphilis – 3 months plus duration of symptoms
• Secondary syphilis – 6 months plus duration of symptoms
• Early latent syphilis – 12 months

HIV - Start with recent sexual or needle-sharing partners; outer limit is onset of risk behaviour or last known negative result
Hepatitis B -

• 6 months prior to onset of acute symptoms
• For newly acquired cases contact your local public health unit (PHU) &/or specialist physician

Hepatitis C

• 6 months prior to onset of acute symptom; if asymptomatic, according to risk history
• For newly acquired cases contact your local PHU &/or specialist physician

Note - rarely sexually transmitted, usually only in HIV co-infection

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.