Mildy deranged LFTs in the GP setting

A man in his mid 30s was invited to make a routine appointment to discuss his LFTs.

6 months ago Now Reference range
Alanine Transferase  67 132 < 40 IU/L
Aspartate Transferase  Not done Not done < 48 IU/L
Alkaline Phosphatase  85 91 30 – 130 IU/L 
Gamma GT  43 38 < 50 IU/L in men< 35 IU/L in women
Bilirubin  16 18 < 21 µmol/L
Albumin  42 44 35 – 50 g/L

 

He used to drink quite heavily as a student, but was now drinking about a pint of beer every two weeks since he graduated.

He had lived in the Far East for five years, and returned to the UK two years ago. He used to use heroin and amphetamines IV whilst in the Far East. He had never received a blood transfusion.

He had never been jaundiced.

He was overweight, with a BMI of 33. His fasting glucose was 4.5. His total cholesterol was 6.6 mmol/L with HDL 0.7 mmol/L.

There was no family history of liver disease, but his father did have a coronary stent put in at the age of 40.

On examination, there were no signs of chronic liver disease, and his liver was not enlarged nor tender.

He had an US abdomen 6 months ago, which showed a diffusely fatty liver.

Old me: Bloody hell. Treat the patient, not the number. It’s just a slightly abnormal isolated LFT; these things are common.

New me: We’re probably underestimating the extent of liver disease in our general population. Most of the time (90-95%) patients with abnormal LFTs do actually have an underlying liver disease.

Of those who don’t, some have a non-liver sources for their enzymes (commonly muscle/heart for AST and bone for alkaline phosphatase).

And to make things worse, our reference range probably misses some liver disease. Lots of slow burning chronic liver disease can occur without dramatic hepatocyte death, so the intracellular enzymes from the liver that we use as markers of liver injury (AST and ALT) don’t rise so dramatically.  In South Korea, a prospective cohort study (wonderful Wikipedia diagram of how a cohort study works) involving 94 533 people found that having your AST or ALT in the upper end of the normal range was associated with having increased mortality from liver disease. The authors suggested that reducing the reference range to around 30 IU/L would pick up liver disease earlier. Does this apply in the UK? The prevalence of hepatitis B (UK: 0.3%, S. Korea 4%) and C (UK: 0.5%, S.Korea 1.3%) is lower here, but our burden of liver disease is thought to be significantly underestimated.

Old me: OK, so we should probably take it seriously. Full liver screen, see him in two weeks with the results.

New me: In this patient’s case, there is a clear risk factor for viral hepatitis. IVDU in the Far East is a dangerous game. However, if this risk factor were not present, would we still send the panel?

You should first check the patient does not have any evidence of decompensation. This means no ascites, variceal bleeding or encephalopathy. These patients may need admission.

You should also consider any acute problems leading to markedly deranged LFTs. In particular, drug-induced, ischaemia and infection can cause an acute rise in the transaminases > 1000 IU/L.

If there’s nothing too dramatic going in, you could split the possible causes into those initially treatable in GP world and those that need a referral to a Liver God. The main initially treatable ones in GP world ones are drug induced, alcohol and NASH. So if this is the first occasion of an LFT derangement, the patient is asymptomatic and the derangement is not too marked (<2x upper limit of normal), you could repeat the LFTs at 3-6 months having stopped any offending drugs (including over the counter culprits), cut down the alcohol, got the BMI below 25 and reassessed. If the LFTs have not resolved after 6 months, or if the derangement was initially marked (>2x upper limit of normal), you should proceed to a liver screen.

Old me: Drug induced, eh? This means you would stop a statin/not start him on a statin because of his LFTs.

New me: NICE (1.4.33) still recommend a baseline LFT and stopping if LFTs reach more than three times the upper limit of normal at 3 months. This will probably change eventually, and most hepatologists do not consider the transient elevation of transaminases that occurs when starting statins to be linked with liver failure. There is even evidence that NASH improves with statin therapy. This patient would benefit from a statin given his lipid profile and his family history of CV disease.

Old me: And to assess severity, its not about the degree of derangement of the liver enzymes. It’s about the functional state of the liver.

New me: Absolutely. It’s like amylase in acute pancreatitis – you get the initial organ damage and this releases an intracellular enzyme that we use for diagnosis, but not prognosis. You’ll notice that the King’s College criteria for paracetamol induced and non-paracetamol induced liver failure both ignore the transaminases and alkaline phosphatase levels. They care about the functional bits – pH and bilurubin (metabolic function), encephalopathy (detox function) prothrombin time (synthetic function) etc. The prognosis (in terms of mortality) can be estimated using the MELD score or Child Pugh score.

Old me: You do an FBC to look for a low platelet count, which goes with alcohol.

New me: Yes it does go with alcohol, for many reasons. But in terms of liver things, any chronic fibrosis can lead to portal hypertension and hypersplenism. As a result of the hypersplenism you get thromboycytopenia.

Old me: You do a liver screen to look for autoimmune, metabolic and infectious etiologies. If this is negative and the LFTs are still deranged, refer.

New me: There is information in the history and examination that cannot be obtained in the blood tests. Alcohol use is the main feature on the history. The presence of heart failure on history or examination is important too, as this can cause a congestive hepatopathy. If the liver screen is negative despite all this, an ultrasound of the abdomen can help distinguish some biliary problems and provide some information about the structure of the liver. Referral is usually done after US of the abdomen and a liver screen unless there is a clinical urgency.

According to the BSG, the liver screen should consist of:

Hepatitis B surface antigen

Hepatitis C antibody

Anti-mitochondrial antibody

Anti-smooth muscle antibody

Anti-nuclear antibody

Serum immunoglobulins (IgG can be markedly raised in autoimmune hepatitis)

Serum ferritin

Transferrin saturation

Copper and caeruloplasmin (under 40 years)

a1 antitrypsin level

 

 

 

 

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Syncope query cause? Risk stratification is the aim of the game

As an FY1 when I saw syncope I saw my job as taking a nice pre, during and post history of the event and working out what the most likely cause was. This still mostly holds, but I realise the job of the A&E doctor is both less than this and yet beyond this.

I recently saw a man in his 60s present as ? head injury. He had just left the shower and felt like he was about to vomit. He then sat down on the toilet (not using the toilet but just sitting on it) and a few seconds later fainted. He was unconscious for about 20 seconds as witnessed by a family member. There was no incontinence, tongue biting or unusual movements. There was no chest pain or palpitations before the fall, and he felt fine afterwards. He may have banged his head on the radiator on the way down, but was otherwise fine and complained of no injuries.

He was being investigated for obstructive jaundice at the time.

His past medical history included Type II diabetes, a meningioma excised 5 years ago and purportedly hypertension. His medications were metformin, ramipril, simvastatin and loratidine.

Neurologically he was intact apart from a right pupil of 4mm compared to a left pupil of 3mm. There was a scar from a previous resection of a meningioma.

Cardiovascular examination was unremarkable. Postural blood pressures showed a significant drop (133/76 versus 101/74).

An ECG showed sinus bradycardia at 54.

FBC, U&Es and CRP were all unremarkable. LFTs confirmed obstructive jaundice.

Using the four groups of 3 trick, I worked through the list.

Cardiac: Arrythmia, ACS, outflow obstruction (basically aortic stenosis or HOCM)

Neurological: Seizure, stroke/TIA, raised ICP causes (especially bleeds in the acute setting)

Neurologically mediated: Vasovagal, carotid sinus hypersensitivity, cough/micturition syncope

Oddballs: (I think of these as ‘PH, P, H’): Postural Hypotension, PE, Hypoglycemia

I felt that this patient probably had a syncope related to his postural hypotension from ramipril or autonomic failure from diabtes, with an arrhythmia less likely.

The A&E registrar decided that the patient should go under the medics.

When I made the referral, I expected to be quizzed as to my likely cause for the syncope. Instead, I got asked quite simply: “What’s his risk?”

His risk of what? Of each of the causes of syncope?

“Risk…?” I said

“His risk.”

I didn’t realise what she was talking about. Was this specifically for arrhythmia?

“Well he is in sinus at 54. The ECG was otherwise unremarkable.”

“Has he got any cardiac failure?”

Ah, getting warmer. This is the risk for arrhythmia/cardiac causes.

“Not really, though he is a diabetic with hypertension so has a decent ischaemic risk.”

“Fine”  she said in a voice that was anything but fine with it.

I decided to find out what this risk was. It turns out there are scoring systems for predicted the risk of a cardiac cause for the syncope in the ED. You can use the ROSE score  but even this isn’t fully accepted. It places emphasis on the BNP, which is quite expensive and not often measured in the ED.

Another approach to picking out the patients at high risk of cardiac syncope is to use the patient’s age to mentally risk stratify them:

pre test syncope causes

You can see how past the age of 60 non simple causes become a lot more prevalent. In fact, the cardiac causes of syncope have a bimodal distribution; the smaller peak is young people with inherited cardiac conditions and the larger peak is people over 65.

You can then use the ESC guidelines to get an idea of the risk for a cardiac cause. This could then inform the medical team about the likelihood that there is a cardiac cause worthy of further investigation.

risk

It’s a change from how I used to think about things a year ago, where I was focused on making the diagnosis as accurately as possible. Now I realise the job is to work out where the patient is heading next, even if we cannot quite label the condition at the moment.

By Viral Thakerar

Rare presentation of a rare condition (which is a common presentation of a common exam condition)

In some ways, our job consists of making the colourful spectrum of real life medicine fit the black and white confines of the hospital protocol or the textbook definitions. Though the presentation of this next case was as black and white as it gets, the way it was dressed up to the AMU could lead you up the wrong path. As you go down the case you will get more clues; see how early you can figure it out.

A 59 year old man originally from Eastern Europe had felt tired for the past 3 months. He had seen his GP, who discovered a normocytic anaemia (Hb 7.4) with a normal WCC and platelets. (The patient’s haematinics were normal, making a mixed iron/folate/B12 deficiency unlikely. His reticulocyte count and kidney function were also normal.)

The patient reported no source of bleeding, including normal bowel habits. He had no skin or joint symptoms. He felt there was no change to his appetite, but did notice about 5 kg of weight loss over this time. There was no fever, but yes, there were occasional drenching night sweats.

PMH revealed rheumatic fever as a child, which left him with a systolic murmur of some sort that the GP was unable to classify further.

He took no regular medications.

Apart from this he was normally a fit and well builder. He had been unable to go to work in the past month because of the tiredness. He lives with his wife. Social history was otherwise unremarkable.

On examination, his obs were Pulse 105, BP 134/90, RR 16, Sats 99% on air and T 37.8. The clerking FY1 noted this:

Splinter Haemorrhage
Splinter Haemorrhage

On palpation there was splenomegaly.

On auscultation there was a loud pansystolic murmur radiating to the axilla.

Bloods confirmed a normocytic anaemia with a WCC of 10.1 and a CRP of 53. His U&Es, LFTs and Coagulation were all normal.

A urine dipstick showed haematuria (+++).

A transthoracic echo showed a mitral valve oscillating vegetation, with severe mitral regurgitation and normal LVEF.

Three sets of blood cultures returned two days later which all grew strep viridans sensitive to benzylpenicillin.

What is actually going on in IE?

As the under review HPA guidelines on blood cultures states:

“IE is infection of the heart valves and/or other areas of the endocardium. It usually occurs at the site of a predisposing cardiac lesion or congenital defect where there is turbulent blood flow, encouraging endocardial damage and adhesion of platelets. A fibrin clot is deposited on the damaged endocardial surface and becomes colonised with organisms which have entered the bloodstream, so forming infected vegetation. Viable bacteria may be present deep within the vegetation as well as on the surface making antimicrobial treatment difficult.”

Why did this man get IE?

Intact valvular endothelium is normally quite resistant to colonisation. The rheumatic fever caused some degree of valve damage, which makes it easier for any bacteria that happens to be in the blood to make a camp there.

What bugs are most likely in this case?

According to the UK guidelines (2012), the most common causes of NVE in non-intravenous drug users are currently S. aureus (28%), coagulase-negative staphylococci (CoNS; 9%), streptococci (35%) and enterococci (11%); 9% are culture-negative.

The main times staph aureus dominates over streptococci is healthcare associated IE, IVDU associated IE and in the first year following a prosthetic valve placement. Staph aureus is the second most common cause of IE in prosthetic valves in the first year after coagulase negative staphylococci. In fact, the closer it is now to the time of the prosthetic valve placement, the more likely that any IE the patient is currently having on that valve is caused by coagulase negative staphloccoci.

How should cultures be taken?

According to the UK guidelines:

“In patients with a chronic or subacute presentation, three sets of optimally filled blood cultures should be taken from peripheral sites with ≥6 h between them prior to commencing antimicrobial therapy.”

It adds:

“There is no evidence to support the commonly perpetuated view that blood cultures should be taken from different sites. All skin surfaces are colonized by bacteria and adequate skin disinfection is key to reducing contamination. Taking blood cultures at different times is critical to identifying a constant bacteraemia, a hallmark of endocarditis.”

In practice, this means it would be 12 hours from your first suspicion of IE to giving your first set of IV antibiotics in a patient with a chronic or subacute presentation.

But the sepsis six! Each hour’s delay results in a 7.8% increase in mortality! What should I do if the patient is septic with IE?

According to the same guidelines:

“In patients with suspected IE and severe sepsis or septic shock at the time of presentation, two sets of optimally filled blood cultures should be taken at different times within 1 h prior to commencement of empirical therapy, to avoid undue delay in commencing empirical antimicrobial therapy.”

If you spoke to a sepsis champion, they would feel very uncomfortable about knowingly delaying giving antibiotics in any patient with severe sepsis or septic shock. In fact, the guidance from the sepsis world is to give fluids, oxygen and antibiotics ASAP and only take cultures before giving antibiotics if this would not delay giving antibiotics.

I’ll have to cross check what to do in this situation with a sepsis don.

What is the most common extracardiac manifestation of IE? 

Though this man had a splinter haemorrhage, this could be related to his occupation as a builder. The patient was unsure if this line in his nail was new or old. Splinter haemorrhages are a pretty rare feature of IE in the developed world, where the presentation is usually fairly early. Janeway lesions, Osler nodes and clubbing are all subacute signs, and are also quite rare in the developed world.

Cerebral complications are the most severe extracardiac complications of infective endocarditis, as well as the most frequent (occurring in 15 to 20% of patients). A haemorrhagic or ischaemic stroke may result. In other words, if a patient has an unexplained stroke, we may question whether or not there is underlying IE (after dealing with the stroke).

To TOE or not to TOE?

Same guidelines:

Role of TOE in IE
Role of TOE in IE

What should the first line antibiotics be whilst awaiting culture results in this case?

According to the same guidelines:

Empirical antibiotics in IE
Empirical antibiotics in IE

Note amoxicillin rather than the benzylpenicillin. Although you should follow your hospital policy, it seems that amoxicillin has better activity against enterococci, which cause 11% of native value IE. The newest versions of the BNF support this.  Fully sensitive streptococci might still be managed with benzylpenicillin.

Early warning, late realisation

Early warning scores are in use throughout NHS hospitals to spot patients who are deteriorating. So where did they come from, and what are their limitations?

At Barts in 1997, it was noted that patients admitted to ITU from the wards had a high mortality.   During the summer and autumn of 1997, a new ‘patient at risk’ team (PART) was set up at Barts in Whitechapel. Their role was to assess ward based patients with a view to fixing things before they got worse, and thinking early about potential ITU/ceiling of care decisions.

Patients were selected for review by the PART based on a scoring system, where more deranged physiology led to a higher score. A certain score would trigger the nurse to call the ward doctor or the PART directly.

Noble stuff. Did it help? Of the 97 patients admitted to ITU over this six month period, 28 were seen by the PART within the preceding 48h. The incidence of CPR among this group pre-ITU admission was 3.6% compared to 30.4% among those patients not assessed by the PART (p<0.005). Mortality once at ITU was 25% for the PART group vs 44.9% for the non PART group, although this did not quite reach statistical signficiance (p=0.07).

Over time, various warning scores were developed, ranging from single parameters to aggregated scores. There is now a drive by the RCP to encourage NEWS, which is a nationalized early warning score.

What are the limitations? The National Patient Safety Agency published a report in 2007 which in part assessed how the early warning scores were working. 16 clinicians were interviewed, including 5 junior doctors. It’s worth reading this – key problems were communication, observations being seen as low priority and trigger fatigue (too many bleeps for “Just thought I’d let you know Mr Peters is scoring a 5…”)

From my own experience, there are three things I wish I understood better at the start of FY1 about using early warning scores.

1.    Communication

Personally, I sometimes spent more time trying to write a comprehensive and totally unambiguous management plan than actually with the sick patient. I was often confused when I then got bleeped asking what the plan was.

This was because I assumed that nurses will read the medical notes. It only dawned on me that nursing notes and medical notes are kept in separate folders about two months into my first placement. Lesson learnt: spending 30 seconds explaining the plan to the nurses saves you twenty minutes from having to revisit the patient when your plan wasn’t followed.

2.    Not all unwell patients score

There are some sick patients who don’t always score very highly on early warning scores. This includes patients with meningitis, patients with raised ICP, stroke, sepsis (especially neutropenic sepsis) and overdoses. It is worth mentioning that the elderly have a lower baseline temperature than the young, and that not only is the febrile response is blunted in 20-30% of elderly patients with acute infection, but a blunted response is associated with a poorer prognosis.

A patient’s change in their observations from their baseline is a better measure than the early warning score of how they are doing. A patient who is normally hypertensive with a BP drop from 175/100 to 100/65 in two hours doesn’t score on most systems, but this could lead to end organ hypoperfusion in this patient.

3.    Some not so unwell patients score

Lots of hospital inpatients will have a raised pulse from simply pain and anxiety. Many patients with well controlled COPD on home oxygen may score highly for oxygen and low sats on admission to hospital despite being at their baseline for these criteria.

Again, a patient’s change in their observations from their baseline is a better measure than the early warning score of how they are doing. A stable COPD patient whose sats have been between 88% and 92% for the past 2 days may move from 90% to 89% and suddenly score enough to trigger a colour change to amber, but this doesn’t mean there is a new acute problem.

What does this mean for the junior doctor on call?

Early warning scores are most effective at selecting a select group of patients that the nurses should generally seek a doctor’s opinion on. It may be end up being nothing serious; this is not a reason to get angry with the nurse. Your clinical assessment supersedes the score as the measure of the severity of the problem. For all subsequent dealings with this patient, you should use your knowledge of the situation together with the trend in observations to manage accordingly; you should not be using the early warning score alone to decide if the patient is improving or deteriorating.

Talking directly to the nurses after you have seen the patient will save you time in the long term. Unwell patients and the early warning score are far from perfectly correlated. Whilst it is true that for the whole group of hospital patients there is a correlation between early warning scores and general unwellness, there are specific disease processes that are not well matched to the early warning scores, and an individual’s variation from baseline supercedes the early warning score as a measure of how that individual patient is.

The early warning score is undoubtedly useful, but we need to remember it is a screening tool, nothing more.

Complete run through of the MRCP Part I – Day 2 of 40

Wow. This is a long syllabus. It’s taken me three hours to put this next section together, which leaves me with little time for pretty pictures/mnemonics. Let’s crack page 83.

 

Occupational asthma

This accounts for one sixth of all cases of asthma. Forget asbestosis, silicosis or smelly mould fancier’s lung – occupational asthma is the most common occupational lung disease.

Common allergens include flour, grain, wood dust, animal bits and isocyanates.

The history is more useful for excluding occupational asthma rather than confirming it i.e. if you have symptoms which are worse at home then at work, you don’t have occupational asthma. However, if your symptoms are worse at work, you may or may not have occupational asthma.

To be sure, you need to do confirm a relationship between asthma and work exposure by performing Serial measurements of PEFR at home and at work. Measurements should be made every two hours from waking to sleeping for four weeks, keeping treatment constant and documenting times at work.

Rhinitis and asthma often co-exist, including when occupational.

Once the relationship is confirmed, the patient must not work in that environment. At all.

 

Other common allergies

1. Latex allergy

Affects medical workers, people with spina bifida and rubber workers. The allergen is either natural or synthetic rubber

Remember the fruit latex syndrome in 30-50% of those with latex allergy. This involves allergy to avocado, banana, chestnut, kiwi, peach, tomato, potato and bell pepper.

2. Insect strings 

Usually bee and wasp stings

3. Drug allergy

I had no idea there was guidance specifically for drug allergy – see http://www.bsaci.org/guidelines/drug-allergy

MRCPwise, it’s probably worth going through the table of Type I – IV hypersensitivities on page 45. The guidance tells you about risk factors for developing allergies as well as how to test for allergy semi-safely.

I also learnt from this guidance that intradermal tests are more sensitive but less specific than skin patch tests, and have a higher risk of causing anaphylaxis.

4. Food allergy

The Medical Masterclass focuses on nut allergies, which are the commonest food allergies. Peanuts account for >50% of all food allergies.

In children, failure to thrive, vomiting and eczema can all be explained by food allergy.

Distinguishing between intolerance and allergy can be tricky. Allergy happens within seconds of ingestion, and only minute quantities are needed. In contrast, intolerances take hours to develop, and a small quantity poses no problem.

Intolerance e.g. lactose intolerance produces bloating and diarrhoea. Allergies may provoke eczema, reflux, GORD as well as anaphylaxis.

A food diary, combined with skin prick testing/appropriate IgE tests can be helpful.

 

Angioedema and urticaria

I found the patient information to the British Association of Dermatologists helpful:

The weals of urticaria may be flesh-coloured, pink or red. They can be of different shapes and sizes, but usually look like nettle stings. An important feature of urticaria is that although the rash may persist for weeks, individual lesions usually disappear within a day, and often last only a matter of hours. However, they sometimes leave bruising especially in children. New weals may then appear in other areas. In ordinary urticaria, the weals can occur anywhere on the body, at any time.

The deeper swellings of angioedema occur most frequently on the eyelids, lips and sometimes in the mouth, but they may occur anywhere. They are not usually itchy, and tend to settle within a few days. If the hands and feet are affected, they may feel tight and painful.

Angioedema occurs beneath the dermis and affects the skin and mucosa, whereas urticarial occurs above the dermis and only affects the skin. Angioedema is painful and tense; urticarial is itchy.

Almost any medicine can cause ‘acute’ urticaria, but painkillers (especially aspirin and medicines like ibuprofen), antibiotics (especially penicillins) and vaccinations are most likely to be responsible. Angioedema, in particular, can be caused by a type of drug (ACE inhibitors) used to treat high blood pressure.

Where does C1 esterase deficiency come into it?

Hereditary angioedema causes provoked or unprovoked attacks lasting 2-5 days of laryngeal odema, subcutaneous swelling and abdominal pain. The tests you want initially is C4 level and if this is low, then C1 INH function and level of protein.

What about ACE inhibitors?

Any individual can get angioedema from ACE inhibitors, though it is more common in Afro-Carribeans. It can occur years after uneventful ACE inhibitor use, and is poorly responsive to antihistamines, corticosteroids or adrenaline. The episodes may persist for some months after stopping the ACE inhibitor. Switching to ARBs is usually successful.

What is the management of angioedema?

See http://www.patient.co.uk/doctor/angio-oedema. In general, the acute attack usually needs nothing, although if there is airway compromise then manage as anaphylaxis. Chronic angioedema should be started with an antihistamine, although antihistamines don’t always work in angioedema.

And urticaria? 

First line is a non sedatating H1 antihistamine e.g. cetirizine plus three days of 50mg prednisolone.

 

Allergen sensitisation…

Step 1: Choose an allergen

Step 2: Get a B-cell to get excited by this allergen

Step 3: Invite this B-cell to mature into a plasma cell and secrete IgE specific to this antigen

Step 4: Stick the IgEs onto mast cells

You have now sensitized the patient!

Primary prevention of allergy prevents this sensitization from happening. This means allergen avoidance.

Secondary avoidance means preventing further sensitization once the process has started. This means leaving the job which triggers occupational asthma.

…and immunotherapy

Indications:

  1. Hay fever that cannot be controlled with the usual management (unless asthmatic)
    To manage hay fever needs allergen avoidance, education and meds. Avoidance needs knowledge of the allergen, which can be found by skin prick tests
    Topical antihistamines for nasal symptoms are great, but only tackle nasal symptoms. Topical intranasal steroids are safe long term and more effective, but risk dryness, crusting and bleeding.
    Oral antihistamines are the mainstay, and work on neutrally mediated itch, sneezing and rhinorrhea. They don’t cover the blocked nose as well as intranasal steroids however.
    There are also nasal decongestants, and eye drops eg sodium cromoglicate

  2. Hypersensitivity to wasp and bee venom

What happens?

Administer gradually increasing quantities of specific allergens to patients with IgE-mediated conditions until a dose is reached that is effective in reducing disease severity from natural exposure.

How does it work?

Eventually, the allergen stimulates IgG rather than IgE production.

Contraindications?

ACE inhibitors – they may trigger an anaphlyactoid reaction (anaphylactoid is basically anaphylaxis that is not IgE mediated)

Beta blockers – reduce the efficacy of adrenaline, which may be needed

 

Allergen avoidance

The main allergens are house dust mite, mould, pollen, pets and dust. Advice on avoidance is given at http://www.allergyuk.org/the-management-of-allergy/allergen-avoidance

 

Natural history of allergic diseases

Asthma stops in about 55% of children by the time they reach adulthood. This is more likely the earlier the asthma started.

Eczema stops in around a third of children when they reach adulthood.

Rhinitis tends to persist into adulthood.

There is a concept called the ‘allergic march’ – see http://www.worldallergy.org/professional/allergic_diseases_center/allergic_march/

 

The tests

The skin prick test needs resuscitation facilities to hand, but is most useful for food allergy and rhinitis (include tree pollen, grass and weed)

Not great if: dark skin, dermatitis, dermatographism, unable to stop antihistamines for 48 hours before

Allergens introduced to skin through pricking. If positive, a wheal of at least 2/3mm develops. Negative predictive value is 95%, but positive predictive value is only 50%, which means a good history makes a big difference.

A skin test for A. fumigatus is done for ABPA, as well as total IgE.

RAST and ELISA are blood tests looking for specific IgEs. They are expensive, but are not affected by antihistamines or the condition of the skin.

Oral food challenge is the definitive but risky test for food allergy.

Patch testing – read at 48-72 hours, and is used for contact dermatitis and Type IV stuff in general.

Lactose intolerance is tested by the Lactose hydrogen breath test:

The patient ingests a standardised amount of lactose (2 g/kg, maximum 25 g) after an overnight fast with measurement of exhaled hydrogen over a 2- to 3-hour period. A positive test is an increase of >20 ppm of exhaled hydrogen after approximately 60 minutes. (BMJ Learning)

Why we should never ask if your saddle-region is numb

I guess the ideal doctor would have experienced first hand every condition that can affect a human. He or she would then be able to pattern recognise what the patient is describing, and tease out the relevant information during history taking to diagnose the problem.

The ideal doctor is not possible, so we instead rely on reading textbooks, reviews and listening to clinical pearls from experienced colleagues. We also gain experience over time.

The common theme to all of these sources is that ultimately the information comes from patients. Patients are our ultimate clinical tutor for history taking.

This is what makes this podcast on back pain especially brilliant. You have the uniquely useful situation where the patient is the doctor, describing his own case.

I listened to this podcast during my car journeys, and one point stuck with me. When the doctor-patient was asked “Do you have numbness around your buttocks?” he would always answer no. When instead he was asked “Does it feel different when you sit down?” he would answer yes. He found it difficult to explain exactly how it was different, but it just felt funny.

He ended up having cauda equina.

So, with this in mind here’s the case. A 65-year-old man had a background of chronic back pain. Whilst bending over to do some gardening, he had a sudden onset of pain in his lumbar back.

The pain was central and 10/10 severity. It worsened with sudden movements, coughing and weight bearing. It was relieved by lying flat. The pain stopped him sleeping, and was progressively worsening. There was radiation to the right leg only. There was some tingling in the left leg. He was finding it harder to walk, and he was normally an independently mobile man.

A red flag review revealed:

Fracture risk:

No known osteoporosis
Osteoporosis risk factors: maternal hip fracture
No major or minor trauma

Malignancy risk:

PMH of melanomas, surgically excised 5 years ago
No weight loss
Some night sweats for the past week with fever for the past two days
No thoracic pain
No point tenderness
Age > 50

Infection risk:

No immunosuppression
Fevers and night sweats as noted
Age > 50

Neurological involvement, including CE:

“Does it feel different when you sit down?”
“Yes”
“How so?”
“It feels like I’m always sitting on a pillow.”

“Any changes to your bowel habits?”
“I haven’t gone in the past two days.”
“And does it feel different in any way when you wipe yourself?”
“Yes – it’s numb.”

No bladder symptoms
No weakness
Some new paraesthesia in the left foot

On examination

There was diffuse erythema and warmth around the L3/L4 area. No point tenderness, but tender to palpation diffusely from L1-L5 ish. The pain was worst centrally, and there was no paraspinal tenderness or obvious muscle spasm.

Straight leg raise caused pain at 5 degrees elevation, with pain spreading all the way down the leg into the feet as well as pain in the back. This was bilateral. Ankle dorsiflexion worsened the pain, again bilaterally.

Neurologically, power was intact. All lower limb reflexes were normal, with downgoing plantar reflexes. Sensation was abnormal perianally. The patient described it as lots of layers of cloth between the skin and the stimulus.

I organised an urgent MRI and referred to orthopaedics. I’ll post tomorrow what the outcome of all this was.

The case bore striking resemblance to the podcast’s story, of ‘different’ but not numb perianal sensation. On a BMJ article on cauda equina, it gives a patient’s perspective which reinforces this further:

“…I remember wiping myself with the toilet paper and it feeling decidedly odd—not completely numb but distant. It was my refusal to admit to numbness that fooled my general practitioner. He asked if I could feel him touching me, not whether his touch felt normal…”

I guess the lesson from this post is: don’t just ask for the presence or absence of sensation. Ask the patient to describe if the sensation is different in any way. This goes not just for cauda equina, but history taking and examination for sensation in general.

 

An n=1 trial into how a patient’s drawings reveal his underlying mood and maybe treat his depression

A man with vascular dementia was admitted following a suicide attempt. The Crisis consultant felt it was high risk, and recommended him to be admitted.

There’s “oh, dementia” and “oh…dementia”. This patient belonged in the first category. He looked after his house alone, and kept it in immaculate condition. He self-cared better than most students.  He had the air of an aged rock star, looking back over his life with pride and no regrets yet probably quite looking forward to living in a gentler gear.  The only time his dementia surfaced in our conversation was when he would freeze mid sentence, suddenly unaware of what he was talking about and as much embarrassed as frustrated by this.

I noticed how he used tricks to work around his memory problems which were quite similar to the memory tricks I use for learning medicine.  If he could not remember the name of someone, he would find a picture to remind him of them, and flood the picture with as many details as he could which would trigger off his memory.

When I can’t remember the features of a medical problem, I try and create an image to link them all together. I think that the reason this works so well is not so much the image, but that the very process of creating them forces you to engage with the material that much more.  Have a look at this totally not peer reviewed summary.

It seems this man was self-administering cognitive rehabilitation. Cognitive rehabilitation is defined as “any intervention strategy or technique which intends to enable clients or patients, and their families, to live with, manage, by-pass, reduce or come to terms with deficits precipitated by injury to the brain.” Examples of cognitive rehabilitation strategies include:

  • Build on the memory skills the patient already has using prompts to achieve whatever you need. Then fade the prompts. This video on errorless learning demonstrates it really well.
  • Use alternative skills to compensate e.g. pictures of clothes to remind you what the washing machine is used for.

This patient enjoyed drawing throughout his life. It seems he was using his presumably well developed visual neural circuitry to compensate for his short term declarative memory problems.

He wanted to show me his sketches. The first one was of Elvis Presley. It was quite impressive, especially given he did it at 3am.

Done at 3am. Quite impressive for an inpatient on a dementia ward.
Done at 3am. Quite impressive for an inpatient on a dementia ward.

Then he asked me something which caught me off guard:

“Can you see the anger?”

I looked at the drawing with my anger-filter switched on to maximum.

“His expression?” I suggested initially pointing to the face, and then further outwards looking optimistically for any signs of agreement.

“You’re nearly there. It’s all these lines.”

He pointed to the strokes towards the edge of the drawing.

“You see these lines? They are much darker. When someone makes me angry, or I’m getting frustrated, I don’t draw delicate lines. Can you see the anger in those lines?”

The angry bits are highlighted in red. Note how the lines are darker.
The angry bits are highlighted in red. Note how the lines are darker.

I could. It’s how I feel with Adobe Illustrator and the Image Trace function has been butchering my sketches. Sometimes I just give up and make the whole thing MS Paint-y. That’s a sign I got angry.

“Every time I’m angry, I remember it in my drawings. I remember what made me make those lines darker. It’s usually a loud noise, or someone disturbing me.”

I then realised his drawings might be one of the best ways of assessing his mood. This patient was giving us something that most advanced brain scan could never pick up. It was actually a pretty good functional assessment of his mood, recorded as is and without any attempt to pigeon hole his thoughts and feelings into any questionnaire criteria.

I looked at his old sketches with him. He could tell me exactly what he was feeling at the time, where he was and what he was thinking when he drew them. You could argue we do not know that he was not confabulating for the old sketches. However, the events he described surrounding the recent sketches done whilst an inpatient had actions associated with them that were verifiable with other members of staff e.g. a patient walking into him one evening. This is a man who was normally unable to recall events of the day before. It seems his drawings allow him to access memories of the recent past by coding emotionally significant events into their very structure.

Could this skill be used for his benefit? One of his greatest frustrations was not knowing what happened in the ‘in between time’. This was the time between the last few hours and the olden days, such as one week ago. Not knowing what happened depresses him. I could see why, given how well his other cognitive functions were and his high level of insight.

I wanted to see if we could help him help himself. I suggested keeping a drawing diary, and that when significant events happen that he wants to remember, perhaps he could sketch whatever he feels would capture it best. Although this would not capture all the details such as what he had for breakfast three days ago, it would capture the most significant memories. If we could capture those memories, I felt he would be less depressed.

He has decided to give it a go. He is also on mirtazapine 30mg NOCTE.

14/5/13: He has improved considerably, and his newer drawings reflect this.