Diagnosing Achilles tendon rupture

Another one from the archives; this one from the BJGP of December 2015.

Acute Achilles tendon rupture is easily missed, since a patient may demonstrate all of the following on examination:

  • Lack of a palpable gap in the tendon – due to swelling/oedema
  • Ability to walk – due to other tendons in the calf muscle complex
  • Ability to plantarflex – ditto
  • Ability to stand on tiptoes with both feet together (though not on the injured foot alone) – ditto

So, what’s a poor GP to do? Fortunately, there is a simple answer; check Simmonds’ calf squeeze test. (Patient kneels on couch facing away from you or lies prone; squeeze each calf muscle in turn and look at passive plantarflexion. Same thing as I’ve already been doing, but I didn’t realise it was as crucial as it is in diagnosis.)

If Simmonds’ test is positive, refer to orthopaedics. Don’t mess around with scans, BTW – they can be misleading and tend to show up as ‘partial tear’ when the Achilles tendon rupture is actually complete.

So, bottom line: Check a Simmonds’ calf squeeze test in all patients with ankle or calf injuries. Lack of passive plantarflexion with Simmonds’ test = prompt referral to fracture clinic. And there you have it.

(By the way, apparently nobody has yet resolved just what the orthos are meant to do with these patients – i.e. surgery or not – when they get there. But that’s their problem.)

Three other points to note:

  1. A positive test is one where movement is not seen (i.e., one where the results are commensurate with rupture). For clarity, however, document what was actually found (e.g. symmetrical movement/no movement) rather than writing ‘positive’ or ‘negative’.
  2. False negatives are rare, but may occur in the following cases:
  • History of joint fusion surgery to that hindfoot
  • Very stiff ankle from arthritis or trauma
  • Severe calf muscle wasting from neurological causes
  • Prior surgery such as Achilles tendon lengthening (e.g. with club foot treatment)

This has me confused as logically I would have thought those would produce false positives. I think I might write to doctors.net.uk. No, wait, better idea – the article gives a contact e-mail address for the main author, so I’ll e-mail him.

3. Chronic¬†Achilles tendon rupture is a different matter as far as diagnosis is concerned; in those cases, Simmonds’ can’t be relied upon to the same extent. The best test to use there is the hyperdorsiflexion test; the ankle with chronic rupture will show a greater range of passive dorsiflexion than the normal ankle, as the tendon that’s healed untreated will be longer than the good one.

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Posted in Credits 2017, Orthopaedics, Tendons | Leave a comment

Food allergy

(From Pulse Learning module)

IgE-mediated food allergies will normally have skin and/or gastrointestinal symptoms. If neither of these are present, respiratory symptoms are unlikely to be due to an allergy.

Symptoms come on within minutes and include:

  • Urticaria (may be localised or generalised
  • Pruritus
  • Angioedema – typically of face/mouth and/or around the eyes
  • Nausea/vomiting
  • Colicky abdominal pain
  • Diarrhoea
  • Wheeze/cough/chest tightness/SOB
  • Rhinorrhoea/blocked nose/nasal itching/sneezing

If IgE allergy is suspected in primary care, it can be tested for by either of the following:

  • Blood test for specific IgE antibodies
  • Skin prick testing, if available.

Patch testing and oral food challenges for suspected IgE-mediated allergy should not be undertaken in primary care.

Non-IgE allergy symptoms I listed in this post. Remember that non-IgE food allergy should be considered if any of the following are not responding to treatment:

  • Atopic eczema
  • GORD
  • Chronic gastrointestinal conditions, including constipation.

Investigation is via elimination diet (2 – 6 weeks) followed by reintroduction. If milk is the food being excluded, arrange dietician consultation.

According to NICE guidelines, confirmed IgE-mediated allergy does not need automatic referral to an allergy clinic unless the child also has asthma (as high risk of anaphylaxis). Strong clinical suspicions of allergy with negative tests should be referred. Other referral criteria include:

  • Symptoms do not respond to a single allergen elimination diet.
  • Faltering growth with at least one gastrointestinal symptom
  • More than one acute systemic reaction such as anaphylaxis, or severe delayed reactions. (Wait a minute. One episode of anaphylaxis isn’t considered enough for referral? Not something I’d be comfortable with in primary care…
  • Significant atopic eczema where multiple or cross-reactive food allergies are suspected.
  • Possible multiple food allergies.
  • Persisting parental suspicion of food allergy even when history not backing it up.

 

Note that cows’ milk protein allergy usually resolves within the first few years of life. Retesting for tolerance CMP allergy i.e. should be considered after six months of a dairy-free diet, which for babies will normally be within 9 and 12 months of age. If there has never been an immediate reaction to CMP and the child does not currently have eczema, reintroduction can be tried at home. If there is current eczema, try skin prick test or specific IgE testing first, but if those are negative and there is no history of immediate reaction then reintroduction can be tried at home (using the milk ladder, which starts with well-cooked milk such as biscuits). Otherwise, discuss with allergy clinic as the challenge may need to be in a secondary care setting.

Interesting point (to me): 0.5% of purely breastfed infants can get cows’ milk protein allergy (BMJ 2009;389:b2275).

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Normal lower limb variants in children

Another very useful one from the archives; a BMJ article from 2015 about which issues with children’s legs don’t have to be referred to orthopaedics. Always good to know.

Possible normal lower limb variants

  • Rotational: intoeing and outtoeing
  • Angular: genu valgum and genu varum
  • Flexible flat feet (I think this is meant to be part of the outtoeing section – article’s a little unclear at some point)

Intoeing

  • Metatarsus adductus
  • Internal tibial torsion
  • Femoral anteversion

Metatarsus adductus:

Metatarsus adductus is an internal angulation of the forefoot on a neutral or flexible hindfoot (what’s meant by ‘neutral or flexible’ isn’t clarified, but I guess it means no other deformities such as club foot?) In the normal foot, the lateral border should be straight and the heel bisector line should pass between the 2nd and 3rd toes. In metatarsus adductus, the lateral border is curved and the heel bisector falls lateral to the normal line.

Incidence is 1:1000, making it the most common congenital foot deformity.

Almost 90% will resolve spontaneously; if the foot is flexible, wait and see. Serial casting may help in cases where the foot is rigid or the adductus does not resolve by 6 – 9 months.

Internal tibial torsion:

Most common cause of intoeing overall. Feet are internally rotated while patella is in neutral position.

Check the angular difference between the transmalleolar axis of the ankle and the bicondylar axis of the knee.

Can show up as clumsiness/frequent tripping. Can be unilateral (1/3 affected children) and can be associated with metatarsus adductus (also 1/3 affected children). Usually most apparent when child begins to walk.

Resolves naturally. Occasionally needs rotational osteotomy if still present >10 years and causing significant problems with trips/falls at that point.

Femoral anteversion:

The angular difference between the axis of the femoral neck and the transcondylar axis of the knee (there will normally be at least some difference; an average of 16 deg in adulthood, though the average at birth is 40 deg).

Most pronounced between the ages of 4 and 6. Shows up with:

  • Sitting in W position (a kind of splayed-out-sideways kneel)
  • Intoeing while walking
  • Tripping due to feet crossing
  • Squinting patella – patellas point inwards
  • Eggbeater running pattern – inward rotation of the thighs, outward rotation of the legs and feet

Spontaneously resolves in >80% by late childhood. Rarely needs treatment. Rotational osteotomy of the femur is possible, but has a high rate of complications and is rarely necessary. (Orthotics have never been shown to help.)

Outtoeing

In infancy:

Normal, and usually resolves by 18 – 24 months of age. However, can also be caused by:

  • Calcaneovalgus (generally responds to passive plantarflexion stretching exercises)
  • Congenital vertical talus (typically needs serial casting or surgical correction)

Those two conditions can usually be differentiated by a lateral radiograph of the plantarflexed foot. Unfortunately, the article didn’t clarify how to differentiate either from normal physiological outtoeing, apart from mentioning rocker-bottom feet.

In older children:

Usually external tibial torsion and occasionally femoral retroversion. However, can also be caused by more severe conditions such as Perthes and SUFE, so these should always be considered, especially in unilateral outtoeing.

Note that external tibial torsion is associated with increased prevalence of patellofemoral instability and/or pain, so isn’t entirely harmless.

Flexible pes planus (flat feet)

Normal in infancy/toddlerhood due to fat pad. Normally resolves between 4 and 8 years.

In older children, differentiate between flexible and rigid flat feet – do this by seeing whether the arch reconstitutes when the child is on tiptoe or the foot is dependent. If so, and if the child has no symptoms, then there is now a consensus that no action is necessary and that they can be treated symptomatically. However, flexible flat feet aren’t always asymptomatic; they can sometimes be painful, though it isn’t clear how best such feet are managed. They can also be a sign of underlying disorders:

  • Neurological – e.g. cerebral palsy
  • Muscular – e.g. muscular dystrophy
  • Connective tissue – e.g. Marfan’s, Ehler’s-Danlos

So do examine the child for underlying problems.

Rigid flat foot, which is much less common, is usually painful and can be due to:

  • Tarsal coalitions
  • Congenital vertical talus
  • Inflammatory disorders (pes planus is a common feature of juvenile idiopathic arthritis)

Angular variants

Obscure interesting fact learned from a follow-up letter to the article: The names for these (varum and valgum) are the wrong way round. ‘Valgus’ was actually the Latin for ‘bow-legged’ and ‘Varus’ is the name of a famous Roman general who was in fact knock-kneed. I guess that mistake is beyond redemption at this point, as the confusion that would result from changing them over would be past bearing, but it’s good to know. Thank you, Basil Moss of Nottingham.

Genu varum:

Intercondylar distance >6 cm when medial malleoli in contact. (I think. Article a bit fuzzy at that point.)

Physiological in growing children. (Internal tibial torsion can also make it look worse.) Pathological causes include:

  • Blount’s disease
  • Metabolic (rickets, renal osteodystrophy)
  • Post-trauma
  • Post-infection
  • Skeletal dysplasia such as achondroplasia
  • Tumours

Causes for concern:

  • Unilateral or asymmetric
  • Severe
  • Progressive (I assume this means after age 6 months, which is when it’s typically maximal according to a study the article cited).
  • Associated with short stature (I assume this is if achondroplasia is suspected)
  • Seen in a child > 3 years.

Otherwise, reassure and observe – but consider possibility of Vitamin D deficiency and also role of obesity.

Genu valgum

Intermalleolar distance >8 cm with knees in contact. Normal in young children (maximal at 4 years, typically diminishes by 11 years). Can also be idiopathic. Pathological causes include:

  • Congenital (fibrous dysplasia)
  • Obesity
  • Neuromuscular
  • Metabolic (as for genu varum)
  • Post-trauma
  • Post-infection
  • Skeletal dysplasia such as pseudoachondroplasia
  • Tumours

Causes for concern:

  • Unilateral or asymmetrical
  • Severe
  • Progressive
  • Accompanied by short stature
  • Seen in a child <2 years

Otherwise, as for genu varum above. (Note that rickets is more typically associated with bow legs, but can cause knock knees.)

 

Musculoskeletal examination in children

Height and weight

Rotational profile:

  • Observe gait and foot progression angle (angle the child’s foot makes with the direction in which he/she is walking)
  • Observe standing – squinting patella? Flat foot?
  • Observe sitting – W position?
  • Observe running – will accentuate any problems
  • Observe lying down
  • Check shape of foot – lateral edge (should be straight) + heel bisector line (should be between 2nd & 3rd toes)
  • Tibial rotation – prone position, knees flexed to 90 deg, measure angle foot makes with thigh
  • Femoral rotation – still in above position – check hip rotation symmetrical in internal and external rotation
  • Check for hypermobility (involves something called the Beighton score, which I take it is beyond the scope of the article as wasn’t otherwise discussed).

Angular profile:

  • Distance between knees while standing and lying with ankles together (should be <6 cm)
  • Distance between ankles while standing and lying with the knees together (should be <8 cm)

 

BMJ 2015:351;h3394

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Diabetes in pregnancy

Affects approximately 5% of pregnant women, of whom over 80% have gestational diabetes and the rest had pre-existing DM of either type.

Screening

NICE recommends screening the following high-risk groups:

  • BMI >30
  • Previous baby 4.5 kg or over
  • Previous gestational diabetes
  • 1st-degree relative with diabetes
  • Ethnic minorities with increased risk diabetes

Screening should be done with an oral GTT between 24 and 28 weeks. The exception is with women with previous gestational DM, who need more careful checking; they should be offered an oral GTT as soon as possible after booking, with a second between 24 and 28 weeks if the first is normal. As an alternative, they can be offered the option of self-checking their blood glucose from booking onwards (no details given on this).

Diagnostic thresholds for diabetes on the 2015 NICE guidelines are fasting glucose of 5.6 or greater, and/or 2-hour post-GTT of 7.8 or greater. (Which can be handily remembered as 5678, I suppose.) Note that these are different from both the 2008 guidelines and the WHO guidelines.

Women with gestational diabetes should be referred urgently to a specialist clinic and seen within 1 week. Women with fasting glucoses of 7.0 or greater should be started on insulin directly (plus or minus metformin).

Glycosuria can appear transiently in pregnancy in the absence of diabetes (due to changes in renal absorption), but women who have glycosuria of 2+, or of 1+ on more than one occasion, should be formally tested for gestational diabetes.

 

Management

Some women can manage their glucose levels successfully with diet and exercise, but up to two-thirds require treatment with medication (metformin and/or insulin).

Women needing medication have to self-monitor at least four times daily – at least seven times if on hypoglycaemics. Aim to keep glucose levels above 4. Women will be at high risk of hypoglycaemia due to both the strict glucose control required and the metabolic changes of pregnancy. They should have quick-acting glucose available (not milk or chocolate – the fat slows down absorption) as well as glucagon, which partners should be trained to give in an emergency.

Insulin requirements may double; don’t be surprised if women in the latter half of pregnancy require much more frequent prescriptions (though this may plateau at around week 36). These will drop back to usual after birth, or possibly lower than usual in breastfeeding women.

HbA1c, despite its limitations in pregnancy, is of some use in estimating risk of complications, and should be checked at least once each trimester.

Women with Type 1 DM are at increased risk of ketosis, as pregnancy physiologically mimics a state of starvation. Ketone levels should be checked in any pregnant woman with Type 1 DM who becomes unwell, and if the results indicate ketoacidosis she should be admitted immediately to critical care. Ketosis can develop at normal blood glucose levels in pregnancy.

 

Preconceptual planning

Women with pre-existing diabetes who are planning a pregnancy should ideally, where possible,

  • be referred to a specialist clinic for advice
  • aim for an HbA1c <48 mmol/l (often not possible; any progress towards this is nevertheless going to reduce risk). Their target BMs during the day should be the same as for anyone with Type 1 DM.
  • take 5 mg folic acid daily
  • stop any medications contraindicated in pregnancy

Obviously this ideal state of affairs often doesn’t happen. When a woman with diabetes presents already pregnant, refer urgently, start the folic acid, stop meds where needed, and request a urinary ACR.

 

After birth

Women with gestational DM should have a fasting glucose 6 – 13 weeks after birth and then annual HbA1c thereafter. Diabetes prevention measures (diet, exercise, weight loss), should be strongly advised.

 

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Lab tests in chronic liver disease

ALT/ALP tend not to be very good markers; they reflect acute hepatocellular damage rather than cirrhosis. Normally what you see is:

  • Low albumin
  • Prolonged clotting times
  • Low platelets (platelet sequestration in portal hypertension)
Posted in Investigations, Lab results, Liver | Leave a comment

Haemolysis markers

  • Reticulocyte count up
  • Reduced haptoglobin
  • Raised LDH

(BMJ Learning module on jaundice)

Posted in Haematology, Investigations, Lab results | Leave a comment

Nausea and vomiting in palliative care

I get involved with a lot of palliative care, so this BMJ review article on management of this very common problem was well worth the read.

Good news, first off; as problems go, this is one that’s very amenable to treatment. One study of hospice patients with N&V showed that symptoms were controlled in four-fifths of cases, within an average of two days; another showed that almost all the patients studied had at least some improvement. So this is a problem in which you stand a high chance of making a difference.

It’s worth thinking about the cause of the nausea and vomiting. There are six main causes to be aware of:

  • Chemical
  • Impaired gastric emptying
  • Visceral or serosal
  • Cranial
  • Vestibular
  • Cortical (in response to anxiety, pain, physical distress)

Note that vomiting may well be multifactorial.

Chemical

Drug-induced or metabolic. Causes of metabolic chemogenic vomiting include:

  • Renal failure
  • Liver failure
  • Hypercalcaemia
  • Hyponatraemia
  • Ketoacidosis
  • Tumour products
  • Infection
  • Toxin release from ischaemic bowel (in which case, I’d think visceral causes from bowel obstruction would also be an issue)

May be associated with delirium. Note that hypercalcaemia/hyperglycaemia both cause polydipsia and polyuria.

Check urinalysis, BM, and bloods if appropriate. Review meds list for iatrogenic causes.

Medical treatments:

  1. Haloperidol – 0.5 – 1.5 mg tds, oral or subcut, or 1.5 to 5 mg in syringe driver
  2. Levomepromazine – 3.125 mg to 6.25 mg tds oral or subcut, or 6.25 to 25 mg in SD
  3. 5-HT antagonists (e.g.ondansetron.)

 

Impaired gastric emptying

Can be caused mechanically by tumour infiltration, ascites or hepatomegaly, but also by medications – opioids (obviously), anticholinergics/TCAs, phenothiazines.

Symptoms include early satiety, reflux, and hiccups.

If patient well enough, consider abdominal ultrasound or CT.

Medical treatments:

  1. Domperidone 10 mg qds, before meals
  2. Metoclopramide 10 mg tds or qds (or 30 mg in SD)

 

Visceral or serosal

Can be due to bowel obstruction/mets or severe constipation/impaction. Can also be caused by liver capsule stretch, ureteric distension, difficult expectoration or pharyngeal stimulation.

Gastric outlet obstruction may present with vomiting undigested food hours after ingestion. Intestinal obstruction can present with abdominal pain, change in bowel habit, and progression of vomiting from stomach contents to bile to faeculent material.

Abdominal X-ray and/or CT can be helpful if obstruction suspected; normally manage with admission, if that’s still appropriate (I manage end-of-life cases out of hospital where appropriate).

Medical treatments:

  1. Cyclizine 50 mg oral or SC tds or 150 mg in SD
  2. Levomepromazine (dose as above for treatment of chemical nausea)
  3. Hyoscine butylbromide, or possibly octreotide (hyoscine butylbromide is better for colic)

Metoclopramide can also be used in partial obstruction, but not if complete obstruction or colic present. Haloperidol may be an option for adding to cyclizine. Dexamethasone 4 – 16 mg SC or IV daily may also be used in malignant bowel obstruction, although it’s now looking as though it doesn’t actually help.

If none of this is working, it may help to pass a wide bore NG tube and, if that helps, to consider venting gastrostomy insertion.

 

Cranial

Can be due to RICP from mets, meningeal infiltration, or radiotherapy.

CT or MRI head if feasible (MRI is better if meningeal infiltration suspected). Discuss with oncologist or palliative care specialist.

Medical treatments:

  1. Cyclizine at above dose, plus dexamethasone 8 – 16 mg oral or SC once daily if RICP suspected
  2. Haloperidol – above dose
  3. Levomepromazine – above dose

 

Vestibular

Motion sickness, but can also be secondary to opioids, or caused by a base of skull tumour. Presents with movement-related symptoms (note that this isn’t pathognomonic – it can also occur with gastric stasis). Discuss with oncologist or palliative care specialist. CT/MRI if base of skull tumour suspected.

Medical treatments:

  1. Cyclizine
  2. Levomepromazine
  3. Hyoscine hydrobromide 1 mg/72 hrs (article says topical, but assume they mean transdermal, I’m not applying anything directly to anyone’s inner ear thankyouverymuch) or oral prochlorperazine 5 – 10 mg tds.

 

Cortical

Arrange full psychosocial assessment. Medical treatments:

  1. Lorazepam, 0.5 – 1 mg SC prn qds
  2. Levomepromazine as above

 

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