Re: Cast study 9 Breaking bad news

Today, I saw a patient who may have a potential diagnosis of lung cancer. As a junior GP, I do not break bad news often. Breaking bad news is similar to other skills, it takes preparation and practice with a set of framework. There are many guidelines and acronyms out there, the acronym I used is called "SPIKE".

SPIKE stands for:

S: Setting up the interview
P: Assessing the patient's perception
I: Obtaining the patient's invitation
K: Giving knowledge and information to the patient
E: Addressing patient's emotions with empathetic response

In my own experience, preparation is the key. Clean up your room, tell the receptionist to hold the calls, check the investigations and look up anything that you are uncertain. Finally, prepare yourself emotionally. Breaking bad news require energy so I tend to take a small break from the last patient so that I can concentrate on the next consultation.

I usually break the bad news in two separate consultations. The first consultation I tell them about the diagnosis and organise a referral for them to see a specialist. Then, I will ask them to return in 1 week. Returning after 1 week serves two purposes. One is to answer any questions that they may have. Two is to make sure that they have an appointment with the specialist. You will be surprised by the number of times that the patients returned after a week and still have not made an appointment.

Finally, look after yourself. Breaking bad news is exhausting. Take breaks before and after breaking bad news. Debrief with other colleagues or your supervisors if you need to.

Re: Case study 8 Patch of numbness

60 yr old man presented with 1 year history of left lateral thigh numbness.

He saw a different GP 1 year ago and was diagnosed with sciatica. The numbness resolved after a few weeks. This episode started again around 2-3 weeks ago.

His main complaint was numbness on the lateral part of his thigh. It tended to get worse with prolonged walking and standing. There was no associated weakness on his lower limb. There was no back pain

On examination, you mapped out the area of sensory change on his left lateral thigh. The lower leg neurological examination was normal. The straight leg raise was negative.

Question 1
What is your diagnosis ?

Question 2
What can you do about it ?

Answer 1

This is lateral cutaneous nerve of thigh entrapment. The nerve gets trapped when it passes through the inguinal ligament. It is a pure sensory nerve so motor function is not affected.

It is more common in obese people and also associated with diabetes.

Answer 2

Nothing. There is really not much you can do. You tell them to lose weight and you warn them about wearing tight pants or belt which may compress on the nerve. Most of the time, the symptom resolves by itself. In some occasions, it persists and anti epileptic may help.

Case 6: Headache

21 year old female presented with 6 months history of intermittent headache associated with transient visual loss.

She presented to the clinic multiple times and saw a different general practitioner with headache for the last 6 months. She is generally well with no past medical problems.

She is currently on the pill and has been on it for the last few years.

She described the headache as throbbing and bilateral. There was no particular trigger. There was no associated vomiting or weakness. The headache usually does not wake her up at night.

She has had extensive investigations in the past , including CT and MRI Brain. MRI reported empty sella. Patient was prescribed a low dose of amitriptyline and had a good response.

She re-presented today because she found that the amitriptyline no longer worked. She has been experience headache almost daily. She also described transient visual field defect in a few occasions for 1-2 minutes. The vision returned to normal after that.

Question 1
What are your differential diagnoses?

Question 2
Is the MRI finding significant?

Question 3
What are the clinical presentations of IIH?

Question 4
What is the diagnostic criteria?

Question 5
What is the treatment?

Answer 1

This is a tricky case as she has had headache for some time and it is getting worse. Imaging results seem to be relatively normal. She now has new neurological symptom.

Using the murtagh model:
Red flags: malignancy, benigh intracranial hypertension, venous thrombosis, malignant hpertension
Common presentations: tension headache, migraine

Answer 2
Empy sella is a relatively common incidental finding, however, it has a well-established association with benign intracranial hypertension.

Given the headache, transient visual loss, patient's age (she is not overweight), gender, and the empty sella sign. She is likely to have benign intracranial hypertension.

Answer 3

Typical presentation of IIH is young, obese woman with headache with papilloedema on examination.

The most common symptoms of idiopathic intracranial hypertension were (1):

• Headache 84-92 percent
• Transcient visual obscuration (68-72%)
• Intracranial noises (52-69 %)
• Photopsia 48-54%
• Back pain 53 %
• Retrobulbar pain 44%
• Diplopia 18-38%
• Sustained visual loss 26-32%

On examination, the most common signs in IIH are:

• Papilledema
• Visual field loss 
• Sixth nerve palsy 

Answer 4 

The modified Dandy criteria:

• Symptoms and signs of increased intracranial pressure
• No other neurological abnormalities or impaired level of consciousness
• Elevated intracranial pressure with normal cerebrospinal fluid composition 
• A neuroimaging to exclude secondary cause
• No other cause of intracranial hypertension apparent

Answer 5 

• Carbonic anhydrase inhibitors: acetazolamide, topiramate
• Loop diuretics: Frusemide 
• Corticosteroids (not recommended on UpToDate)
• Indomethacin 
• intermittent lumbar puncture to relieve pressure

Case 5: Below Knee DVT

35 year old Female presented with ultrasound confirmed diagnosis of right below knee DVT.

She ruptured her ACL 2 weeks ago while playing netball. After the injury, she had a MRI and saw an orthopaedic surgeon. She wanted to have the knee reconstruction ASAP.

Few days ago, she started to feel throbbing pain in her right leg. Incidentally, she had an appointment with another GP at a different clinic for skin cancer check. During the consultation, she mentioned her lower limb swelling and an ultrasound was ordered which confirmed the below knee thrombus.

She was started on clexane and sent back to you.

Question 1
Other than clexane, what are other options?

Question 2
How long will you put her on anti-coagulation for?

Question 3
She is extremely concerned about her ruptured ACL. She wants to have it fixed ASAP. What do you tell her ?

Answer 1

I still remember prescribing clexane and warfarin for people with below knee DVT when I was an intern 5 years ago. With the new oral anticoagulants, there are many more options.

The available treatments (1):

• Subcutaneous low molecular weight heparin such as clexane in this case
• The oral factor Xa inhibitors rivaroxaban or apixaban
• Bridging clexane then warfarin 
• Dabigatran or edoxaban. (requiring 5 to 10 days course of heparin prior to commencement of treatment)

The standard practice now at most hospitals is rivaroxaban (starting with 15 mg for 3 weeks, then increase to 20 mg). Interestingly, therapeutic guideline in Australia is till recommending clexane and warfarin as first line treatment. 

Of course, there is no hard and fast rule in selecting anticoagulants. If in doubt, use clexane for the first few days so that you and the patient can have time to think about the options.

Answer 2

According to therapeutic guideline, a person with provoked DVT, the minimum length of treatment is 3 months. Usually we will re-assess with ultrasound to ensure the resolution of the thrombus prior to ceasing the anti-coagulation.

Answer 3

Many patients have a fixed perception that ruptured ACLs have to be fixed ASAP. They probably get the idea from the media. It often reports Australian footy player receives surgery right away after an ACL rupture, and 2 months later, they are playing on the field again! (They forgot to mention the players are getting paid few hundred thousand dollars per game.)

So far, there is no evidence that early ACL repairs improve outcome. The rehabilitation time after an ACL repair is long, usually 6 - 12 months. It takes motivation and effort to return to pre-injury level activities. I have seen many people with poor outcome from ACL re-constructions.

Many people can continue playing sports without ACLs. In short, there is absolutely no indication for an urgent ACL repair. (Of course, unless you are getting paid 100,000 per game)

I told her that no orthopaedic surgeon will risk her life (the chance of developing a PE from having the surgery) with an ACL reconstruction.

References:

Lip G, Hull R. Overview of the treatment of lower extremity deep vein thrombosis (DVT). In: UpToDate, Post TW(Ed), UpToDate, Waltham, MA. (Accessed on April 26,2017)

Friedberg R. Anterior cruciate ligament injury. In: UpToDate, Post TW(Ed), UpToDate, Waltham, MA. (Accessed on April 26, 2017)

Case 4: A suspicious haematoma

A 75 years old man presented with an enlarging left thigh lump after he fell down from a roof 6 months ago.

He saw a general practitioner few weeks after the injury. Two ultrasounds were performed and the diagnosis of a large intramuscular haematoma was made. He was advised to manage the swelling with warm compress and simple analgesic.

He re-presented today because he noticed that the lump was enlarging and it started to affect his walking, however, there was minimal pain. In addition, he reported weight loss of around 10 kg and feeling fatigue over the last few months.

Physical examination revealed a large firm immobile mass in the medial-posterior aspect of the left thigh. There was significant oedema on his left leg. There was no evidence of neuromuscular compromise of the extremity.

An urgent MRI was performed. (Figure 1)

 
Figure 1



1. What does the MRI show?

Case continues: Patient was referred to an orthopaedic surgeon with a special interest in sarcoma. A biopsy confirmed the diagnosis of a myxofibroidsarcoma.

2. Could this lesion be associated with his injury?

3. Can the use of imaging differentiate a soft tissue sarcoma from a benign haematoma ?

4. Is the delay in diagnosis of soft tissue tumour common?

5. How would you manage this patient?


1. The MRI showed a large intra muscular mass with heterogeneous enhancement measuring in the posteromedial thigh. It rose the possible diagnosis of a sarcoma.


2. An association between trauma and soft tissue sarcoma has been suggested for over 200 years.(5) Currently, there is no evidence to say that the relationship is causal. The usual history is of a traumatic incident occurring shortly prior to the awareness of the mass. Because of the relatively short time frame, we think that the trauma merely brings the patient's attention to the mass. (5)(7).

3. Even with the advances in modern technology, we cannot use imaging to safely differentiate a soft tissue sarcoma from a haematoma.  (2,5,7,8). Gomez et al reported three cases similar to our case study. All three patients had history of trauma prior to consulting their family physicians with lumps. They had MRIs and CTs, and were all initially reported as haematomas. This highlights the difficulty in differentiating malignant tumour from a benign haematoma using imaging alone. The imaging results need to be interpreted in the context of clinical history and examination. When there is enough clinical suspicion of a soft tissue sarcoma, patient should be referred to a specialist unit for biopsy. (8)

4. The delay in diagnosis of soft tissue sarcoma is a common problem. Many studies were conducted in an attempt to identify the sources of delay.  (2,3,4) The identified sources of delay include patient delay in presentation, mis-diagnosis, and waiting for investigations such as imaging and biopsy. The average time frame between the onset of symptoms to patient presentation is around 12 months, and the average time frame between patient presentation to referral to a specialist unit is 13.5 months.

Sarcoma is a rare tumour. There are around 800 new cases diagnosed in Australia per year. Most general surgeons or general practitioners will only encounter a soft tissue sarcoma once or twice in their careers. Therefore, it is important to be vigilant and treat any lump greater than 5 cm or deep to the fascia as sarcoma until proven otherwise.

5. Studies have shown that early referral to a specialist unit improves survival rate and treatment outcome.  Imaging and biopsies at non-specialist units are often inadequate and further delay the diagnosis. Poor biopsy techniques can potentially complicate future surgical excisions. Hence, an early referral for biopsy or management is recommended.

Case continue

Further imaging at the specialist unit showed pulmonary metastases. He underwent radiotherapy and definite surgical excision. The surgical excision was of palliative intent due to his pulmonary metastases. At the time of writing, he had returned home and recovered well from his surgery. He will require regular review and ongoing surveillance .

Key points:
- Any lumps greater than 5cm in diameter or deep in fascia should be treated as sarcoma until proven otherwise.
- Imaging results need to interpreted in the context of clinical history and examination. A biopsy is required to exclude soft tissue sarcoma.
- An early referral to a specialist unit provides the best survival rate and treatment outcome.


References:

Cancer Council Australia Sarcoma Guidelines Working Party. Clinical practice guidelines for the management of adult onset sarcoma.

Sydney: Cancer Council Australia. [Version URL: http://wiki.cancer.org.au/australiawiki/index.php?oldid=138276, cited 2017 Apr 11].

Available from: http://wiki.cancer.org.au/australia/Guidelines:Sarcoma

2. Ashwood N, Witt JD, Hallam PJ, Cobb JP. Analysis of the referral pattern to a supraregional bone and soft tissue tumour service. Ann R Coll Surg Engl 2003 Jul;85(4):272-6 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/12855033.
4. Stiller CA, Passmore SJ, Kroll ME, Brownbill PA, Wallis JC, Craft AW. Patterns of care and survival for patients aged under 40 years with bone sarcoma in Britain, 1980-1994. Br J Cancer 2006 Jan 16;94(1):22-9 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/16317433
5. Soft tissue sarcomas of the extremities. Blake A. Morrison. Available at
6. Uptodate pathogenetic factors in soft tissue and bone sarcomas
7. http://www.bcmj.org/article/soft-tissue-sarcomas-extremities-how-stay-out-trouble
8. High grade sarcomas mimicking traumatic intramuscular hematoms: a report of three cases. Pablo Gomez and jose Morcuende Available at:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1888428/pdf/1555-1377v024p106.pdf
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Case 3: Lung function test

68 yr old male came for regular check up.

He had a lung function test last year.

He used to be a heavy smoker, quit last year. His exercise tolerance is limited to around 50m.

What is your diagnosis ?

With a long smoking history and shortness of breath, this lung function indicates Chronic Obstructive Pulmonary Disease (COPD) . COPD is confirmed by the presence of persistent airflow limitation. FEV1/FVC < 0.7.

The problem we are having now is that we over diagnose people with COPD. Around 20-30% of patients who have a diagnosis of COPD has never had spirometry. Remember, COPD is a spirometry diagnosis.

What are your differential diagnoses?

COPD has many causes including asthma, smoking, occupation exposures, and anti tripsin 1 deficiency.

Is this severe disease ?

The current classification from lung foundation Australia classify this patient with severe disease.

How would you manage this patient?

This patient requires multi-disciplinary approach. 

1. GP management plan and TCA
2. Prevention of exacerbation: flu vaccination and pneumococcal vaccination
3. Stop smoking 
4. Optimise medications: use COPD stepwise treatment flowchart (link)
5. COPD action plan 
6. Refer to lung rehabilitation or physiotherapist or exercise physiologist to improve lung function 
7. Regular review and assess inhaler techniques 

According to the latest COPD guideline, severe COPD with more than 2 exacerbations per year should be managed by LABA + Inhale corticosteroid. 

Reference:

1. COPD-X concise guideline

Jaundice

68 yr old woman presented with jaundice. (Really jaundice, sort of like simpson kind of yellow)

It started 2 weeks ago. There is intermittent abdominal discomfort but mostly pain free. She noted that her stool is getting pale and hard to flush. The urine is getting darker and darker.

She is otherwise well. Not any medication. Denies ETOH abuse or any new medications.

This is the first time you see her.

Examination is essentially normal other than jaundice. She is haemodynamically stable, afebrile. Abdomen is soft, non tender, no ascites and no hepatomegaly.

What are your differentials at this stage ? How would you manage this patient ?

A structured approach will break down jaundice into pre, intra and post hepatic cause.

 In my mind, I thought this is going to be carcinoma of head of the pancreas. (Painless jaundice).

I was putting all my money on post hepatic jaundice.

The differentials listed in Murtagh

• Intrahepatic 
• Alcoholic hepatitis/cirrhosis 
• Drugs
• Primary biliary cirrhosis 
• Viral hepatitis 
• Extrahepatic 
• Cancer of bile ducts
• Cancer of pancreas
• Other cancer: primary or secondary spread
• Cholangitis
• Pimary sclerosing cholangitis 
• Common bile duct gallstones
• Pancreatitis
• Post-surgical biliary stricture or oedema 

I spoke to my supervisor because I thought about sending this patient to the hospital. 

The final decision was that we started the initial work up first. 

What investigations would you order? Any bedside test?

I contemplated whether to send this woman to hospital to work up in the community. Because she was well so I decided to order some blood tests and review her in a few days time. 

The blood tests I ordered at that time: FBE, LFT, Ca-125, ESR, CRP, UEC, Hepatitis B, Hepatitis A and hepatitis C serology, urinalysis

Hepatitis screen is normal.

The following is the LFT.   What does it tell you and What would you do now ?

This LFT picture is worrying. The bilirubin is 20 times over the normal limit. Combining this with the derrange ALP and GGT. This lady requires an urgent decompression. I ordered an urgent CT chest, abdo and pelvis. The following is the report. 

 It shows gross intrahepatic biliary dilatation likely secondary to cholangiocarcinoma. I contacted one of the local surgeons and he said this patient needs urgent decompression. 

She was transferred to a tertiary hospital for urgent decompression. An ERCP was performed and a stent was inserted. The surgery was complicated by post-op haematoma and re-obstruction. The obstruction subsequently resolve by itself and patient was discharged with out patient upper GI follow up for curable surgery. 

Lessons learned from this case:

- Get advice from other people when you are not sure

- Needs a structured approach to jaundice 

- Clinical appearance can be deceiving
- Urinalysis can be helpful in determining the cause of jaundice. The presence of bilirubin in urine  and the absence of urobilinogen indicates post hepatic obstruction.

Dermatofibrosarcoma protuberans (DFSP)

What is dermatofibrosarcoma protuberans?

• Rare tumour 
• most likely to be of fibroblastic lineage

How does it present?

• it has smooth appearance resembling a keloidal scar
• its site on the trunk in young to middle-aged patients

What is the management

• excision with wide surgical margins 

Reference:

• Primary certificate of dermatology RACGP 

Benign lymphocytic infiltrates

What is benign lymphocytic infiltrates?

• The are benign infiltrates of lymphocytes occurring in the dermis
• They are categorised into B cell and T cell proliferations. 
• Lymphocytoma cutis is the name used for B cell infiltrates
• Jessner's lymphocytic infiltrate is an example of a T-cell pseudo lymphoma 

How does it present?

• Rare
• The presentation is often in the third or fourth decade of life, but may occur at any age 
• They present as smooth red apple,es, plaques or nodules, which may be multiple and coalesce
• The face is most commonly involved, including the ear lobes

What the skin biopsy shows?

• moderately dense infiltrate lymphocytes within the dermis 
• distinction from lymphoma is sometimes difficult

What is the management?

• typical treatment includes
• potent topical steroids 
• intralesional steroids 
• phototherapy 
• hydroxychloroquine 
• spontaneous resolution sometimes occur 
• recurrence is common 
• small number may progress to lymphoma 

Reference:

• Primary certificate of dermatology RACGP 

Cutaneous B-cell lymphoma (CBCL)

What is cutaneous B-cell lymphoma (CBCL)?

• It can be either primary disease of the skin or secondary from nodal (non-Hodgkin's) lymphoma
• It is rare and less common than mycosis fungicides
• Men are more commonly affected, most cases present in the sixth or seventh decade of life

How does it present?

• solitary or multiple nodules localised to one area of the body
• Usually pink or violaceous in colour, smooth, firm, non tender 
• favour neck and head region
• lymph nodes in other area may be involved 

What does it look like on skin biopsy?

• dense infiltrate of lymphocytes throughout the mid and lower dermis 
• B lymphocytes do not localise to the epidermis, hence, no scale

What is the treatment ? 

• Referral to a dermatologist or oncologist is recommended for staging and treatment 
• Treatment options 
• radiotherapy 
• surgery for localised lesion s
• chemotherapy 
• rituximab 

What is the prognosis?

• In general good prognosis > 90 % 5 year survival rate for the follicle centre and marginal zone b cell lymphoma 
• less so for the variant occurring on the legs 
• Secondary CBCL is associated with a poor prognosis 

Reference:

1. primary certificate of dermatology RACGP 

Tennis Elbow

Tennis elbow is quite a common presentation at general practice. The diagnosis is usually quite straight forward, occasionally, it is complicated by referred neck pain. Most of the time, the patient will be able to tell you the diagnosis is Tennis Elbow.


What is the management?

• There are many treatments available. Why ? Because none is effective. 
• Treatments include:
• physiotherapy: ultrasound, manual therapy
• NSAIDs: oral, topical. Some mild benefit with topical NSAID gel. 
• ESWT: no benefit. Cochrane recommended against it. 
• Surgery: no evidence. Final Resort. 
• Platelets rich plasma : no definite conclusion can be drawn. No benefit has been shown so far. 
• orthotic device : no definite conclusion can be drawn. 
• GTN patch: not mentioned in cochrane. Usually used in combination with an exercise program. 

I looked at cochrane review, there is no evidence for any particular treatment.

The following is a succinct summary from reference 1. 

Essentially, in acute stage, watch and wait. 

Subacute stage, refer to physiotherapy or structured exercise program. 

Chronic stage, can try cortisone injection. Refer for specialist opinion. 

• 

Patient handout: https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/elbow-pain
(I read quite a few handouts online and I found the one from the victoria state government to be the most accurate and up to date)

References:

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3781883/

2. http://www.cochrane.org/CD001821/MUSKEL_orthotic-devices-for-the-treatment-of-tennis-elbow

Acute sinusitis

I came across this article on Australian prescriber. It looks like all common management strategies that we use have little or no evidence.

Including: systemic steroid, sinus wash. There is small benefit using intranasal steroid in mild disease.

References:
https://www.nps.org.au/australian-prescriber/articles/acute-sinusitis

Actinic keratosis

Key points:

• estimated around 10% of them becomes Squamous cell carcinoma 
• thought to be an intraepidermal lesion 
• multiple treatment modalities, the most common one is cryotherapy
• biopsy lesion if it does not respond to treatment

What is actinic keratosis?

• They are keratotic lesions with malignant potential 
• They are considered intraepidermal, pre-cursor or early lesions of squamous cell carcinoma 
• lesions are most commonly found in the sun-exposed areas of elderly patients with fair skin types who have had significant sun exposure in their lifetime

What are the histological changes?

• epidermal cell dysplasia 
• dilated upper dermal blood vessels 
• degeneration of collagen and elastin in the dermis (solar elastosis)

Who's at risk?

• Celtic descents 
• Skin types 1 and 2 
• immunosuppressant therapy
• elderly

What are the differential diagnoses?

• BCCs
• lupus erythematous
• actinic porokeratosis
• SCCs

How does it present?

• usually in caucasians > 40 in sun exposed area
• actinic keratoses initially present as a poorly defined area of redness or telangiectasia
• over time, the lesion becomes more defined and develops a thin, adherent, yellowish or transparent scale
• with time, the adherent scale becomes progressively thicker and yellow in colour 

How is it diagnosed?

• most of the time by clinical examination 
• advance lesions may require biopsies to differentiate from squamous cell carcinoma
• the histologic hallmark is a disordered epidermis with intraepidermal keratinocyte atypia 

What is the prognosis?

• small number of actinic keratoses will progress to SCC, and the trouble is we don't know which one is going to progress and which one is not 
• We think the thicker ones are more worrisome 
• SCC that develop on the ear, the scalp, or at the vermilion border are more likely to metastasise, so actinic keratoses in the above areas need to be treated aggressively

What treatment is available ?

• cryotherapy
• imiquimod
• Efudix 
• photodynamic therapy
• emollients containing keratolytics e.g. 2-4% salicylic acid in sorbolene cream
• Tretinoin 
• Laser

Why are there so many treatments available?

• None work 100 % 

Why do lesions recur after treatment?

1. The lesion may have been treated inadequately
2. Wrong diagnosis: could be BCCs, SCCs, Bowen's lupus erythematous or psoriasis. Therefore, failed treatment usually means biopsy

Reference:

• Habif: skin disease diagnosis and treatment third edition

Autistic spectrum disorder

I have absolutely no interest in dealing with behavioural problems in kids, unfortunately, it is part of the job as a GP. There is a strong push from parents and schools to label these children with a diagnosis. Once they have a diagnosis, they can receive extra fundings and extra help at school. Having said that, it is also important to diagnose children with ASD early so that there is a better chance for them to function independently in the future.

What is Autism?

• Lifelong neurodevelopment disability that affects how an individual communicates and interacts with people and their environment. There are difficulties in 2 primary areas. 
• social interaction 
• repetitie behaviours and interests

How common is autism ?

• Australia 1/160 - 1/100
• USA & Europe 6-7/1000

What cause autistic spectrum disorder?

• exact cause is unknown 
• multifactorial is the keyword in exam 
• some genetic factors in play
• monozygotic twins 60%
• dizygotic 3 %
• More common in males than females 4:1
• More common in certain chromosomal disorders e.g. Fragile X syndrome 
• Increased in neurogenetic disorders e.g. tuberous sclerosis 

• NOT CAUSED BY VACCINATION

How do children with Autistic spectrum disorder present?

• Parents usually aware before 18 months 
• Most common parental concerns include delayed speech and behaviour problems

What is the Role of GP?

• Identify problem early and refer 
• Need to conduct a full history and physical exam
• Appropriate referrals e.g. hearing/vision, intervention services+/-therapy, paediatrician
• ongoing multidisciplinary management and review

What are some absolute indications for immediate refer?

• No Babbling, pointing or other gestures by 12 months
• No sharing of interests in objects with another person
• No single words by 16 months
• No 2 word spontaneous phrases by 24 months
• Any loss of language or social skills at any age

Any screening tools available ?

• M-Chat (16-30 months) Free to download online. Just type M-Chat on google.

What are some key elements in intervention?

• The earlier the better, the more the better
• early intervention between 15-25 hours a week
• Multidisciplinary supportive individualized
• In collaboration with family 
• Strategies to be able to generalise skills
• Develop functional, spontaneous communication 
• Reduction of maladaptive behaviours
• Teach functional adaptive skills
• Opportunity for neurotypical peer interaction 
• Clear Goal setting, predictability and routine 
• Continual review 

Does medication help?

• In general, medication does not help. 
• It is mainly used to treat other co-morbidities e.g. ADHD, insomnia, anxiety etc

What is the prognosis?

• 10 % adults with ASD live independently 

References: 

• Austism spectrum disorder by Dr. Gillian Brooks from diploma of child health webcast 2016

Attention Deficit Hyperactivity Disorder (ADHD)

What is ADHD?

• It is a development problem which results in poor concentration and control of impulses. 
• It can affect children's learning and social skills, and also family functioning
• About 3-5 of every 100 children in Australia have ADHD

What are the symptoms and diagnosis ?

• Inattention 
• Difficult concentrating, forgetting instructions, moving from one task to another without completing anything 
• Impulsivity
• Talking over the top of others, losing control of emotions easily, being accident prone
• Overactivity 
• Constant fidgeting and restlessness

What are the treatments?

• Stimulatns 
• Behaviour strategies 

References:

• RCH: ADHD 

Non-Alcoholic fatty liver disease (NAFLD)

• What is Non-Alcoholic fatty liver disease?

• It is a clinical histopathological entity with evidence of hepatic steatosis, either by imaging or by histology and, by definition, occurs in patient with little or no history of alcohol consumption. The disease ranges from fat accumulation in liver cells to a necro-inflammatory component, known as non-alcoholic steatoheaptitis (NASH).

• Why do we worry about NAFLD?
• It can become Non alcoholic steatohepatitis (NASH)
• NASH is histologically indistinguishable from alcoholic steatoheaptitis, and may progress to cirrhosis in up to 20 % of patients
• NAFLD does not increase short morbidity or mortality but if it progresses to NASH, it increases chance of cirrhosis and may require liver transplant

• Who gets NAFLD?
• Anyone can get it but criteria require the person to be diagnosed to have no history of ETOH abuse 
• Other risk factors 
• central obesity 
• type 2 diabetes mellitus 
• dyslipidaemia 
• metabolic syndrome 

• What causes it?
• Unknown 

• How do you diagnose it?
• Demonstration of hepatic steatosis by imaging or biopsy 
• Exclusion of significant alcohol consumption 
• Exclusion of other causes of hepatic steatosis 
• No coexisting causes for chronic liver disease
• Other investigations to exclude other causes
• anti hepatitis C virus antibody 
• hepatitis A IgG
• Hepatitis B surface antigen 
• Plasma iron, ferritin, and total iron binding capacity 
• Serum gamma-globulin level, antinuclear antibody, anti-smooth muscle antibody, and anti-liver/kidney microsomal antibody - 1

• What is the treatment?
• Weight lose 
• lifestyle changes

Gastroenterology index page

• Giardiasis
• Gastroenterology examination video 
• Non alcohol fatty liver disease (NAFLD)
• 
  

Giardiasis

• What is giardia? 
• Giardia duodenalis is a parasite
• It is the most common gastrointestinal protozoan that causes chronic diarrhoea 

• How dose it spread?
• It is transmitted by the ingestion of food or water contaminated by faeces, by exposure to faecally contaminated surfaces and through person-to-person contact. 

• What are the signs and symptoms?
• stomach cramps
• excessive gas or bloating 
• diarrhoea, which may be water, usually last 1 to several weeks
• frequent loose or pale, greasy faeces which may float in the toilet bowl 
• fatigue
• weight loss
• lactose intolerance may occur in 20 to 40% cases and last several weeks
• fever and bloody diarrhoea are uncommon 
• symptoms usually appear 1-2 weeks following infection and resolver within 2-4 weeks

** many infected have no symptoms**

• How do you diagnose it ?
• Diagnosis is made by stool MCS or multiplex

• How do you treat it ?
• Tinidazole 2 g orally 
• metronidazole 2g orally daily for 3 days or 400 mg orally 8 hourly for 5-7 days 

Reference

• http://www.sahealth.sa.gov.au/wps/wcm/connect/Public+Content/SA+Health+Internet/Health+topics/Health+conditions+prevention+and+treatment/Infectious+diseases/Giardia+infection/

Iron deficiency

What is iron deficiency?

• Royal College of pathologists of Australasia definition of iron deficiency is serum ferritin level of < 30 for an adult 

Who gets iron deficiency?

• Basically everyone 
• Pre-menopausal and pregnant women are at higher risk
• Vegetarian with a balanced diet should not have iron deficiency

What causes iron deficiency?

• 2 major categories
• Not taking in enough iron such as coeliac disease, poor diet etc
• Loosing iron such as blood loss

What are the clinical features of iron deficiency?

• No clinical features in many cases and found out from routine blood test
• Clinical features include: fatigue

How is it diagnosed?

• It is diagnosed via iron studies, not as straight forward as it sounds 
• Ferritin is the most reliable indicator of iron level but it elevates with acute inflammation so a CRP is recommended to order with ferritin together 
• Transferrin saturation levels reflecting transport iron, if it is less than 20% indicate an iron supply that is insufficient to support normal erythropoiesis
• Total iron binding capacity increases in iron deficiency in an attempt to increase iron uptake 

What is the treatment for iron deficency?

• Dietary modification is inadequate to treat iron deficiency, only enough to prevent 
• treatment is around 100 - 200 mg elemental iron daily in divided doses 
• Over the counter product only contains very small amount of iron content
• If iron replenish is required urgently (prior to operation or pre-obstetric delivery), IV iron can be used. (Usually ferronjet 1000 mg can be given over 15 minutes)
• There are quite many iron oral formulas available: Here

What is the outcome?

• Variable depends on the cause
• takes 3 to 4 weeks to have a clinical significant impact
• Hb level should increase by approximately 20 g/L every 3 weeks

References:

• RACGP check program 2016 Blood disorder 
• South Australia health. Blood safe iron deficiency anaemia resources

Respiratory history

System review questions:

• chest pain
• shortness of breath
• wheeze
• cough
• sputum
• haemoptysis 
• exercise tolerance
• smoking history