Discussing TEP/ceiling of care plans

An article on how to discuss ceiling of care (including resuscitation); this is something I do with every new patient at the care home I cover (or with their family, if the resident isn’t able to have that discussion) so I read this with interest. Suggestions:

  • Start with a discussion of the person’s understanding of his or her condition and correction of any unrealistic expectations
  • Explain the different views people have on the types of treatment that they would want in the case of sudden illness (this is pretty much what I do already).
  • Explore what’s important to the patient for the future; what things do they like doing and want to be able to continue, or to start doing again? What could help them with this?
  • What aims of treatment are important to them, particularly in terms of comfort vs. sustaining life and how these things balance out?

And then discuss specifics of CPR and admission.

One other helpful suggestion was that, in cases of disagreement, a second opinion should be offered and arranged.

Posted in Ceiling of care, Credits 2017 | Leave a comment

Easy bruising

I normally just use a full blood count to investigate easy bruising; I’ve ummed and ahhhed about getting a clotting screen as well, but it seems like overkill to me. However, the authors of an article in the latest BMJ advise that not only should I also be doing a clotting screen, including INR (I thought that was automatically included, but they list it separately), but I should also add a blood film (for platelet abnormalities) and renal and liver function tests (renal impairment can cause acquired platelet dysfunction, and liver failure can also lead to platelet dysfunction as well as, of course, reduced clotting factor production).

Also, a point worth remembering; easy bruising or bleeding can be caused by nutritional deficiency, as a result of gastrointestinal problems or of poverty. (Vitamin C leads to collagen defects and hence to defects in blood vessels; Vitamin K deficiency means decreased clotting factor synthesis.)

Posted in Haematology, Investigations | Leave a comment

MRI for nerve root compression/sciatica?

Latest guidelines from our local hospital have some useful pointers for when to refer for MRI and when not to:

Radicular thoracic pain should be referred for MRI. Sciatica, however, probably not – if <6/52 then wait and see, and if >6/52 refer to pain clinic or orthopaedic services.

Posted in Credits 2017, Musculoskeletal, Radiology | Leave a comment

Neutropenia

An old article; unearthed an old BMJ I’d saved but never got round to making notes on. BMJ 2014;349:g5340.

Neutropenia is defined as a neutrophil count <1.5 x 10^9. It’s classified in increments of 0.5 (1 – 1.5 is mild, 0.5 – 0.9 is moderate, and <0.5 is severe). It may be normal in some ethnic groups; benign ethnic neutropenia affects 25 – 50% of people of African/Afro-Caribbean origin, plus some of Arabic/Middle Eastern origin, and has no clinical significance. This article therefore recommends using a cutoff of 1.0 rather than 1.5 for investigating people of Afro-Caribbean ancestry.

Causes:

  • Drug-related (cytotoxic drugs or idiosyncratic effect)
  • Acute infection – usually viral (infectious mononucleosis, CMV, toxoplasmosis) – usually resolves in 3 – 4 weeks
  • Chronic viral infection – HIV, Hep B, Hep C
  • Auto-immune diseases – e.g. SLE, Sjogren’s, RA (may be due to the drug treatment or the underlying disease – normally only shows up in cases that are otherwise symptomatic)
  • Haematological malignancy*
  • Marrow infiltration (eg mets)*
  • Haematinic deficiency*
  • Copper deficiency or deficiency of other trace elements*
  • Starvation (eg anorexia) – partly due to haematinic deficiencies, partly due to serous atrophy of the marrow
  • Primary immune neutropenia – normally shows up in early childhood and remits spontaneously, rare in adults
  • Chronic idiopathic neutropenia – diagnosis of exclusion, may be immune-related

(*Normally affects other cell lines as well)

 

Possible investigations:

  • Blood film if moderate or severe
  • Haematinics – rare for deficiency to cause isolated neutropenia, but authors recommend as is straightforwardly treatable cause (I’m more wary – we’ve had a lot of problems with borderline B12s getting picked up and overtreated and the lab is now warning us against overtesting).
  • Monospot and/or acute virology – may be useful if clinical features (fever, sore throat, general malaise) or if blood film shows reactive T-cells
  • Viral serology for HIV/Hep B & C for persistent unexplained neutropenia

It is not normally worth bothering with checking for autoimmune diseases in the absence of other symptoms, as unlikely to show up as first symptom and a positive ANA/RF in an otherwise asymptomatic patient is only going to lead to confusion/overtreatment.

Refer if:

  • Other features suggest serious underlying disease
  • Neutrophils persistently < 1.0
  • Persistent downward trend

 

Drug-related neutropenia

Depending on severity and on need for the drug in question, may have to weigh up the risks of continuing vs. stopping.

 

 

Posted in Credits 2017, Haematology | Leave a comment

Squints in childhood

My son has a squint, so I’m familiar with treatment of childhood squints. However, I wasn’t previously aware of red flags to look for when children present with a squint:

  • Abnormal red reflex
  • Limited abduction
  • Diplopia
  • Headaches (the article just says this? Since this is in the context of possible intracranial pathology, I would have thought we’d be assessing the headaches themselves for red flag symptoms)
  • Nystagmus
  • Face turned to the side
  • Other neurological features

These are because strabismus can be a feature of neurological disease such as cerebral palsy and can also be a sign of intracranial lesions and of ocular pathology such as retinoblastoma.

I also didn’t know that strabismus can show up after birth even in innocent cases; normally it’s within the first three years. They can also be intermittent (in which case check whether dependent on direction of gaze).

Discuss vision; developmental history; family history; frequency and direction of the squint, and which eye, and for how long; and whether diplopia is present. Check eye ROM, red reflexes, and cover test.

Posted in Credits 2017, Ophthalmology, Paediatrics | Leave a comment

Lactose intolerance and cow’s milk allergy

I’ve been going through some old journals. The August ’16 BGJP had a useful article on lactose intolerance and cow’s milk protein allergy.

Lactose intolerance

A digestive problem caused by reduced ability to digest lactose (as distinct from cow’s milk protein allergy which is an immune-mediated reaction).

Primary lactose intolerance – caused by natural reduction in lactase levels after about the age of 3.

Secondary lactose intolerance -caused by mucosal or epithelial damage – severe gastroenteritis, coeliac disease, cow’s milk allergy.

(Congenital lactose intolerance – very rare occurrence in some isolated populations.)

Symptoms are bowel-related only – abdominal pain, bloating, flatus, diarrhoea. It does not cause rectal bleeding. It also doesn’t cause any non-bowel symptoms; when these are triggered by milk, it’s likely to be due to cow’s milk protein allergy.

Symptoms will normally clear up within 48 hours on a low lactose diet. (Breastfeeding is supposed to be continued; I’m not sure of the evidence base or how that works out.) Secondary lactose intolerance typically resolves within about six weeks on a lactose-free diet.

Cow’s milk allergy

May be IgE-mediated or non-IgE-mediated (which still involve the immune system). IgE-mediated reactions typically develop immediately and non-IgE-mediated after up to 48 hours delay. Non-IgE-mediated reactions can be confused with lactose intolerance (or with milk protein intolerance; they are actually allergies rather than intolerances).

Abdominal pain, diarrhoea, and pruritus and erythema of the skin can be caused by either. Other than that, they have separate sets of possible symptoms (as well as developing symptoms on different timescales):

IgE-mediated:

  • Urticaria (localised or generalised)
  • Angioedema
  • Oral pruritus
  • Nausea
  • Vomiting
  • Respiratory tract symptoms, both upper and lower (including conjunctivitis, cough, nasal congestion, and symptoms of hay fever/rhinitis)
  • Anaphylaxis

Non-IgE-mediated:

  • Atopic eczema
  • GORD
  • Blood/mucus in the stools
  • Infantile colic
  • Food refusal/aversion
  • Constipation
  • Perianal redness
  • Pallor
  • Tiredness
  • Faltering growth associated with at least one gastrointestinal symptom

Skin prick or blood tests should be done for suspected IgE-mediated milk allergy but isn’t necessary for suspected non-IgE-mediated milk allergy.

Treatment for a breast-fed baby is for the mother to go on a dairy-free diet with calcium supplementation. For a formula-fed baby (or a breast-fed baby whose mother would prefer to wean), the first-line treatment is extensively hydrolysed formula, except in cases of severe symptoms where the first line of treatment should be an amino acid formula. Amino acid formulas should also be used for formula-fed babies who continue to have symptoms on extensively hydrolysed formula, and for breast-fed babies with cow’s milk allergy who require top-up feeds.

Do not use:

  • Goat’s milk – too much cross-reactivity
  • Soya milk – also cross-reactive (up to 14% in IgE-mediated allergy and up to 60% of those with non-IgE-mediated allergy), but also weak oestrogenic effect of isoflavones
  • Rice milk – too high an arsenic content to be used in children <4.5 yrs.

Retrial of cow’s milk protein can be considered after six months on a CMP-free diet. Tolerance to extensively baked milk products is likely to occur before tolerance to less well-cooked products.

Posted in Allergies, Credits 2017, Food allergy, Food intolerances | Leave a comment

First, second, third and fourth diseases?

This is of no educational value whatsoever, but I couldn’t resist adding it.

In the onrush of facts to be memorised to get through medical school, I spared very little time for wondering why slapped cheek is known as ‘fifth disease’. However, it is a good question, and a doctor writing in the BMJ has now answered it. Apparently, first disease is measles; second disease is scarlet fever; third disease is rubella; and fourth disease seems to have been a medical misclassification and has never been definitely clarified. Also, sixth disease is roseola, and there may or may not be a seventh with the non-snappy name of acute febrile infantile mucocutaneous lymph node syndrome, or MCLS for shorter.

What I’m not yet totally clear on is what the criteria actually are for making the ordinal list, given that plenty of other diseases have been diagnosed during the thousand-odd years in which this list was being compiled (measles was apparently first scientifically described in the tenth century). Infectious disease with a generalised rash, I’m deducing, but it would be interesting to know more about that.

Posted in Infectious Diseases, Uncategorized | Leave a comment