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Example Diagnostic Assessment

Atopic Eczema — DVA claim example

A de-identified example Diagnostic Assessment for Atopic Eczema, written by the Veterans Health Centre to show how a DVA compensation claim is argued. A Diagnostic Assessment is the claim: it is the document a DVA delegate decides on. Read it in full below — the named diagnosis and ICD-10 code, the ADF and occupational history, the clinical timeline, and every Statement of Principles factor argued and met.

Example document — fictitious patient. Every report published here is a sample prepared to show the standard, structure and depth of a VHC report. The veteran described is fictitious: names, dates of birth, service numbers, units, locations and treating clinicians have been invented and all dates changed. It must not be relied upon as a record of any real claim.

Diagnostic Assessment — Atopic Eczema

Example 1 of 1 · fictitious patient (Veteran DM)

Example document — fictitious patient. This report is a sample prepared to show the standard, structure and depth of a VHC report. The veteran described is fictitious and bears no relationship to any real person, living or deceased. Names, dates of birth, contact details, service numbers, units, locations and treating clinicians have been invented and all dates have been changed. It must not be relied upon as a record of any real claim.

Diagnostic Assessment

Atopic Eczema

No Statement of Principles applies to this condition (non-SOP claim).

ADF History

Veteran DM, date of birth 19 May 1985, Australian Army, Armoured Vehicle Crewman (Cavalry), enlisted 07 March 2004, medically discharged 26 June 2017. Operational service: Iraq, 15 April 2006 to 30 November 2006 (warlike); Afghanistan, 10 June 2009 to 20 January 2010 (warlike); Afghanistan, 05 March 2012 to 15 October 2012 (warlike).

Occupational History

As an armoured vehicle crewman the veteran operated, drove and crewed light armoured vehicles, spent long periods in enclosed crew compartments that reached 50 degrees Celsius or more in desert summers, wore body armour, helmets and fire-retardant coveralls for 10 to 14 hours a day, and carried out daily vehicle maintenance involving diesel, hydraulic fluid, lubricants, solvents and degreasers.

Mounted operations in Iraq and Afghanistan involved prolonged heat and sweating under occlusive equipment, very dry dusty air, limited opportunities to wash or change clothing, chlorinated and desalinated water supplies, burn-pit smoke and diesel exhaust, skin infections spread in shared accommodation, and repeated exposure to improvised explosive device strikes and contacts with the enemy.

History

Veteran DM, an armoured vehicle crewman in the Australian Army, developed adult-onset atopic eczema on 22 August 2009 on warlike service in Afghanistan, on a background of allergic rhinitis, posttraumatic stress disorder and smoking, after months of heat and sweating under body armour in a very dry, dusty environment, daily contact with fuels and solvents, burn-pit smoke, chlorinated water and a staphylococcal skin infection, and two weeks after an improvised explosive device strike on his vehicle. The condition worsened severely, with secondary infection, on his next deployment to Afghanistan on 14 July 2012.

Timeline

  • 14 Feb 2005 — While posted to a cavalry regiment in northern Australia the veteran presented with persistent sneezing, nasal blockage and itchy eyes. Skin prick testing showed strong reactions to house dust mite and grass pollens and his total IgE was 410 kU/L. The medical officer diagnosed allergic rhinitis and commenced an intranasal corticosteroid. His skin was recorded as normal. "allergic rhinitis, IgE 410"
  • 03 Jun 2008 — A psychiatrist diagnosed posttraumatic stress disorder arising from an improvised explosive device strike on his vehicle convoy in Iraq on 10 October 2006, in which a soldier in the vehicle ahead was seriously injured. He reported nightmares, hypervigilance and sleeping four to five hours a night. He was smoking 15 cigarettes a day. Sertraline and psychological therapy were commenced. "PTSD, smoking 15 per day"
  • 05 Aug 2009 — On warlike service in Afghanistan the veteran's light armoured vehicle struck an improvised explosive device. He was concussed briefly and helped extract an injured crew member under fire. He returned to mounted patrols three days later, wearing body armour and fire-retardant coveralls for 12 hours a day in crew compartment temperatures recorded at 48 to 55 degrees Celsius. "IED strike, crew extracted"
  • 25 Aug 2009 — The veteran presented to the role 1 facility with three days of intensely itchy, red, weeping patches in the elbow and knee flexures, on the neck under the body armour collar and on the backs of the hands, beginning on 22 August 2009. Crusted lesions on the forearms were swabbed and grew Staphylococcus aureus, following a folliculitis outbreak in his platoon in July 2009. Flucloxacillin, a moderate-potency topical corticosteroid and emollient were prescribed. "itchy flexural rash, Staph aureus"
  • 18 Mar 2010 — After his return, a dermatologist diagnosed atopic eczema, meeting the Hanifin and Rajka criteria, with an Eczema Area and Severity Index (EASI) of 18 and a Dermatology Life Quality Index of 14. Total IgE was 1,240 kU/L and skin biopsy showed spongiotic dermatitis. The rash had persisted continuously since August 2009 and worsened with heat and sweating. "atopic eczema, EASI 18"
  • 14 Jul 2012 — On warlike service in Afghanistan, in peak summer heat under body armour, the eczema flared to involve 60 per cent of his body surface, with weeping, crusting and fissuring. Swabs grew methicillin-sensitive Staphylococcus aureus. EASI was 38. He was treated in theatre with oral prednisolone and flucloxacillin and remained on duty because no dermatology review was available. "severe flare, EASI 38"
  • 10 Apr 2013 — A dermatologist recorded persistent severe atopic eczema since the 2012 deployment, with an EASI of 32, a Dermatology Life Quality Index of 22, lichenification of the flexures and hands, and sleep disturbance from itch. Ciclosporin was commenced. He was downgraded from mounted duties because he could not tolerate body armour or vehicle heat. "severe AE, ciclosporin started"
  • 14 Nov 2016 — Ciclosporin had been stopped because of hypertension and changed to methotrexate. The dermatologist recorded continuing moderate to severe disease, an EASI of 24, recurrent skin infections and an inability to wear protective equipment. He was medically discharged on 26 June 2017. "methotrexate, EASI 24"

Symptoms

At onset the veteran had intense itch, worse with heat, sweating and at night, with red, weeping, crusted patches in the elbow and knee flexures, on the neck where his body armour collar rubbed, and on the backs of the hands. Scratching caused bleeding and infection, and the itch disturbed his sleep.

After the 2012 worsening the eczema was widespread, with fissuring of the hands, thickened lichenified skin, recurrent infections and constant itch. He now reports daily itch, broken sleep, painful cracked hands that limit gripping tools, flares with heat, sweat and stress, embarrassment about visible skin disease, and the need for systemic treatment and daily emollients.

Imaging

No imaging is required to establish this diagnosis.

Onset Date

The most likely date of onset of this condition is 22 Aug 2009.

At that date the veteran was on warlike service in Afghanistan as a crewman on light armoured vehicles, conducting mounted patrols in peak summer heat. He had worn body armour and fire-retardant coveralls for 12 hours a day in crew compartments of 48 to 55 degrees Celsius since June 2009, and his vehicle had struck an improvised explosive device on 05 August 2009. The itchy flexural rash began on 22 August 2009.

This date is appropriate because his pre-deployment medical examination of 02 May 2009 recorded normal skin, and he presented to the role 1 facility on 25 August 2009 with a three-day history of the rash. The diagnosis was confirmed by a dermatologist on 18 March 2010, after the rash had persisted continuously. It falls within warlike service.

For the heat, occlusive clothing, low humidity, irritant and water causes, the 1 month before onset runs from 22 Jul 2009 to 22 Aug 2009, and each of those exposures continued daily from 10 June 2009 throughout it. For the particulate air pollution cause, the 1 year before onset runs from 22 Aug 2008 to 22 Aug 2009, during which he was exposed to burn-pit smoke and diesel exhaust from 10 June 2009. For the Staphylococcus aureus cause, the 3 months before onset run from 22 May 2009 to 22 Aug 2009, covering the folliculitis outbreak of July 2009. For the psychological cause, the 6 months before onset run from 22 Feb 2009 to 22 Aug 2009, during which he had posttraumatic stress disorder, and the strike of 05 Aug 2009 fell 17 days before onset. For smoking, the 1 year before onset runs from 22 Aug 2008 to 22 Aug 2009, during which he smoked 15 cigarettes a day. Allergic rhinitis was established in February 2005 and present at onset.

For the worsening factors, the documented worsening is 14 Jul 2012, on warlike service in Afghanistan, when the EASI rose from 18 to 38. The 1 month before it runs from 14 Jun 2012 to 14 Jul 2012, during which he again worked daily under body armour in extreme heat. The 6 months before it run from 14 Jan 2012 to 14 Jul 2012, during which his posttraumatic stress disorder relapsed. The secondary staphylococcal infection was present at the worsening.

1. What is the formal diagnosis of the condition claimed above?

The formal diagnosis is atopic eczema (atopic dermatitis) of adult onset (ICD-10 L20.8). No Statement of Principles has been determined for this condition.

Atopic eczema is a chronic, relapsing inflammatory skin disease characterised by intense itch, dry skin and eczematous lesions with a typical distribution in the skin flexures, neck and hands in adults. It results from a defective skin barrier, with increased water loss and penetration of irritants and allergens, together with a type 2 immune response, and is commonly associated with other atopic conditions such as allergic rhinitis and asthma and with raised IgE. Although it most often begins in childhood, adult onset is well recognised, triggered by environmental factors that damage the skin barrier or activate the immune system, including heat and sweating, low humidity, irritants, infection with Staphylococcus aureus, pollution and psychological stress.

In this veteran the condition began on warlike service in Afghanistan on 22 August 2009, in the presence of multiple service exposures. It was confirmed on 18 March 2010 and worsened severely on warlike service in Afghanistan on 14 July 2012.

2. For each diagnosis identified, please also provide the following dates:

When did the veteran first experience symptoms attributable to this condition?

22 August 2009.

When did the veteran first present to a health / medical provider for this condition?

25 August 2009.

When was the condition confirmed / formally diagnosed?

18 March 2010.

When did the veteran first present to you (or your practice) for this condition?

15 October 2025.

3. How was this diagnosis confirmed? i.e. what were the key symptoms and signs, investigation results, specialist opinions?

The diagnosis was made by a dermatologist on 18 March 2010. The veteran met the Hanifin and Rajka criteria: an itchy skin condition with typical flexural lichenified and eczematous lesions, a chronic relapsing course, a personal history of atopy with allergic rhinitis, and minor features including xerosis, hand dermatitis, raised IgE of 1,240 kU/L, susceptibility to cutaneous Staphylococcus aureus infection and itch with sweating. He also met the UK Working Party criteria. Skin biopsy showed spongiotic dermatitis, and patch testing on 30 April 2010 excluded allergic contact dermatitis as the primary diagnosis. Disease severity was moderate, with an EASI of 18.

The worsening was confirmed on 14 July 2012 by extension of the eczema to 60 per cent of the body surface, an increase in the EASI from 18 to 38, positive swabs for Staphylococcus aureus and the need for systemic corticosteroid, followed by persisting severe disease with an EASI of 32 requiring ciclosporin on 10 April 2013.

4. What do you consider to be the cause(s) of the condition in this veteran? Give consideration to constitutional and common risk factors, pre-existing injuries or diseases, and occupational or lifestyle risks, as well as direct causative mechanisms.

No Statement of Principles has been determined by the Repatriation Medical Authority for atopic eczema. The claim is therefore decided on the sound medical-scientific evidence of what causes and worsens the condition, without the limits a Statement of Principles would impose. The recognised causes below are drawn from the dermatological and occupational medicine literature, and each is addressed against the veteran's service and clinical history.

Legislation: the clinical onset of this condition was on 22 August 2009, after 1 July 2004, during warlike service in Afghanistan. This is a Military Rehabilitation and Compensation Act 2004 (MRCA) claim. Where a Statement of Principles exists, the Reasonable Hypothesis instrument applies to operational service and the Balance of Probabilities instrument to peacetime service; here the condition arose and worsened on warlike service in Afghanistan, and the posttraumatic stress disorder that contributed arose on warlike service in Iraq. Each cause must be related to the person's service. Under the beneficial approach required by the legislation, the absence of documentation does not mean that an event or exposure did not occur: lack of evidence is not evidence of lack.

Recognised causes on the medical-scientific evidence (no Statement of Principles)

Causative factors

Cause 1: being exposed to high ambient temperatures with prolonged sweating on most days for at least the 1 month before the clinical onset of atopic eczema; — MET

- From 10 June 2009, on warlike service in Afghanistan, the veteran crewed light armoured vehicles in which compartment temperatures were recorded at 48 to 55 degrees Celsius, for 10 to 14 hours a day, sweating heavily throughout. This continued daily for the 1 month before onset, from 22 July 2009 to 22 August 2009. Sweat retained on the skin is a potent irritant and itch trigger, and heat and sweating are among the most consistent provoking factors for atopic eczema.

Cause 2: wearing occlusive protective clothing or equipment in contact with the skin for at least 8 hours a day on most days for at least the 1 month before the clinical onset of atopic eczema; — MET

- On warlike service from 10 June 2009 the veteran wore body armour, a helmet and fire-retardant coveralls for 10 to 14 hours a day, with limited opportunities to wash or change clothing. The rash began exactly where friction and occlusion were greatest, on the neck under the armour collar and in the elbow and knee flexures. Occlusion and friction disrupt the skin barrier and trap sweat against the skin.

Cause 3: living and working in an environment with a relative humidity below 30 per cent for at least the 1 month before the clinical onset of atopic eczema; — MET

- Meteorological records for his base in southern Afghanistan show a mean daytime relative humidity of 12 to 18 per cent in July and August 2009, throughout the 1 month before onset. Very low humidity increases transepidermal water loss, dries the skin and impairs barrier function, and is associated with the onset and flaring of atopic eczema.

Cause 4: having skin contact with irritant chemicals, such as fuels, solvents, degreasers or detergents, on most days for at least the 1 month before the clinical onset of atopic eczema; — MET

- As a vehicle crewman the veteran carried out daily maintenance with diesel, hydraulic fluid, lubricants and solvent degreasers, without adequate gloves, and cleaned weapons with solvents, on most days from 10 June 2009 to onset. The dermatitis began on the backs of the hands as well as the flexures. Repeated irritant contact strips skin lipids and damages the barrier, and is a recognised trigger of adult-onset atopic eczema.

Cause 5: bathing in hard or heavily chlorinated water on most days for at least the 1 month before the clinical onset of atopic eczema; — MET

- Water at his base in Afghanistan was supplied by reverse osmosis and bore treatment with heavy chlorination, and testing in 2009 recorded hardness above 300 mg/L as calcium carbonate and free chlorine of 2 to 4 mg/L. He showered in it daily throughout the 1 month before onset. Hard water and chlorine increase skin irritation and barrier damage and are associated with atopic eczema.

Cause 6: being exposed to air pollution with fine particulate matter, such as burn-pit smoke or diesel exhaust, for at least 500 hours within the 1 year before the clinical onset of atopic eczema; — MET

- From 10 June 2009 the veteran lived within a kilometre of an open burn pit whose smoke regularly covered the base, and worked daily in and around running diesel engines and vehicle exhaust. In the ten weeks to onset this amounted to more than 700 hours of exposure, within the 1 year before onset, on warlike service. Particulate pollution causes oxidative damage to the skin barrier and is associated with the development and flaring of atopic eczema.

Cause 7: having a skin infection with Staphylococcus aureus within the 3 months before the clinical onset of atopic eczema; — MET

- In July 2009 a folliculitis and impetigo outbreak affected the veteran's platoon in shared accommodation, and he was treated for folliculitis of the forearms. Swabs of crusted lesions on 25 August 2009 grew Staphylococcus aureus. The infection was within the 3 months before onset. Staphylococcus aureus toxins act as superantigens that drive skin inflammation and are closely linked to the onset and severity of atopic eczema.

Cause 8: having a clinically significant psychiatric disorder, including posttraumatic stress disorder, for at least the 6 months before the clinical onset of atopic eczema, or experiencing a severe traumatic event within the 1 month before the clinical onset of atopic eczema; — MET

- Posttraumatic stress disorder was diagnosed on 03 June 2008 after an improvised explosive device strike on warlike service in Iraq on 10 October 2006, and it was active throughout the 6 months before onset, from 22 February 2009 to 22 August 2009. On 05 August 2009, 17 days before onset, his own vehicle struck an improvised explosive device and he extracted an injured crew member under fire. Psychological stress acts on the skin through neuroimmune pathways and is a recognised trigger of atopic eczema.

Cause 9: smoking an average of at least 10 cigarettes per day for at least the 1 year before the clinical onset of atopic eczema; — MET

- The veteran took up smoking in initial training in 2004 and smoked about 15 cigarettes a day, recorded on 03 June 2008 and at his pre-deployment medical, throughout the 1 year before onset, from 22 August 2008 to 22 August 2009, increasing on deployment. Active smoking is associated with an increased risk of adult-onset atopic eczema.

Cause 10: having allergic rhinitis or asthma at the time of the clinical onset of atopic eczema; — MET

- Allergic rhinitis was diagnosed on 14 February 2005, while the veteran was serving in northern Australia, with positive skin prick tests to house dust mite and grass pollens and a raised IgE, and it was active and treated at onset on 22 August 2009, aggravated by dust in Afghanistan. Coexisting atopic disease reflects the type 2 immune predisposition underlying atopic eczema.

Worsening factors

Worsening 1: being exposed to high ambient temperatures with prolonged sweating under occlusive clothing on most days for at least the 1 month before the clinical worsening of atopic eczema; — MET

- On warlike service in Afghanistan from 05 March 2012 the veteran again crewed armoured vehicles in summer heat, wearing body armour and coveralls for 10 to 14 hours a day, throughout the 1 month before the worsening, from 14 June 2012 to 14 July 2012. The EASI rose from 18 to 38 on 14 July 2012.

Worsening 2: having a clinically significant psychiatric disorder, including posttraumatic stress disorder, for at least the 6 months before the clinical worsening of atopic eczema; — MET

- The veteran's posttraumatic stress disorder relapsed on his 2012 deployment, with nightmares and hypervigilance after repeated contacts, recorded by the deployed psychologist in May 2012, and it was active throughout the 6 months before the worsening, from 14 January 2012 to 14 July 2012.

Worsening 3: having a skin infection with Staphylococcus aureus at the time of the clinical worsening of atopic eczema; — MET

- Swabs taken on 14 July 2012 from weeping, crusted eczema grew methicillin-sensitive Staphylococcus aureus, and he required oral flucloxacillin. The infection, acquired in shared field accommodation on warlike service, was present at the worsening and drove the extension of the eczema.

Worsening 4: having skin contact with irritant chemicals, such as fuels, solvents, degreasers or detergents, on most days for at least the 1 month before the clinical worsening of atopic eczema; — MET

- On his 2012 deployment the veteran resumed daily vehicle maintenance with diesel, lubricants and solvent degreasers, throughout the 1 month before the worsening, and the hand dermatitis became fissured.

Worsening 5: inability to obtain appropriate clinical management for atopic eczema. — MET

- When the eczema flared on warlike service in July 2012 no dermatologist or phototherapy was available in theatre. He was kept on mounted duties under body armour with oral prednisolone and antibiotics, and he could not avoid the heat, sweat and irritants that drove the flare. Systemic treatment was not started until 10 April 2013. Under Brew v Repatriation Commission (1999) this is an inability to obtain appropriate clinical management.

The % contribution of the causes is 100% and significant.

Sequelae

Met. The atopic eczema has caused recurrent secondary staphylococcal skin infections, chronic hand dermatitis with fissuring, lichenification, chronic sleep disturbance from itch, and hypertension from ciclosporin treatment. Each should be considered as a sequela of the accepted condition. The rebound flare after oral prednisolone in 2012 also contributed to the persistence of severe disease.

Unintended Consequence

Met. Oral prednisolone given in theatre in July 2012 caused a rebound flare when it was stopped, and ciclosporin prescribed from 10 April 2013 caused hypertension, both unintended consequences of treatment provided by the Commonwealth while the veteran was serving (section 6A of the DRCA and the equivalent provisions of the MRCA).

Inability to Attain Appropriate Medical Management

MET. On warlike service in Afghanistan in 2012 the veteran had severe, infected eczema involving 60 per cent of his body surface, but there was no dermatologist, phototherapy or systemic immunosuppressive treatment in theatre, and he was kept on mounted duties under body armour in extreme heat. Specialist systemic treatment did not begin until 10 April 2013, nine months after the worsening. Applying the objective and subjective tests in Brew v Repatriation Commission (Full Federal Court, 10 September 1999, Merkel J), the absence of specialist care and the inability to remove himself from the provoking conditions in the operational setting amount to an inability to obtain appropriate clinical management. The seven-month delay between onset in August 2009 and dermatology review in March 2010 is also indicative of barriers to care.

5. Please provide a Health Summary and a medication / prescribing history.

See attached report.

References

  1. 14 Feb 2005, Skin prick test and outpatient health record, Medical Officer, Garrison health centre
  2. 03 Jun 2008, Psychiatric assessment, Consultant psychiatrist
  3. 02 May 2009, Pre-deployment medical examination, Medical Officer
  4. 05 Aug 2009, Deployed health record, Medical Officer, Role 1 facility, Afghanistan
  5. 25 Aug 2009, Deployed health record and wound swab, Medical Officer, Role 1 facility, Afghanistan
  6. 18 Mar 2010, Dermatology consultation, skin biopsy and pathology, Dermatologist
  7. 30 Apr 2010, Patch test report, Dermatologist
  8. 14 Jul 2012, Deployed health record and skin swab, Medical Officer, Afghanistan
  9. 10 Apr 2013, Dermatology consultation, Dermatologist
  10. 14 Nov 2016, Dermatology review, Dermatologist

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Dr Thomas Perkins, Veterans Health Centre

Reviewed by Dr Thomas Perkins

Founding doctor, Veterans Health Centre · former RAAF aviation medical officer · 13 years working exclusively with ADF members and veterans. Full profile →