About this blog: information for everyone else

Hi there! I’m a GP and this blog consists of the notes I take on journal articles, as part of my continuing professional development. It is intended purely for my own use in recording and remembering the things I learn so that I can refer back to them in the medical setting. While anyone is welcome to read it, please do not take it as any kind of substitute for seeing your own doctor for any medical-related queries or problems.

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About this blog: information for appraisers

This blog consists of notes made on any learning points I come across in the course of CPD and want to remember/look up later. The two main sources for this are on-line learning modules, and articles which I identify in the course of journal reading as meeting a learning need. Credits for the former are obviously counted elsewhere, so I’ve grouped the latter in a separate category in order to estimate the learning credits I’ve obtained from structured reading. You can find all posts in that category for the 2013 – 14 appraisal year here.

Posted in About this blog, Credits 2016 | 2 Comments

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)

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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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Parkinson’s disease

Features of Parkinson’s disease:

  • Bradykinesia
  • Hypokinesia (paucity of movement)
  • Resting tremor
  • Rigidity
  • Postural instability (usually the last of the cardinal signs)

Those are the cardinal signs.Tremor is typically made worse by stress, tiredness, or the feeling that other people are noticing.

Speech pattern can also be affected:

  • Hypernasal speech (soft palate can’t block the back of the nose)
  • Poor fluency of speech – ‘stuttering’ speech, frequent pauses, repetition of words/syllables
  • ‘Flattening’ of speech – loss of ability to change pitch and volume, leading to a loss of natural rhythm.

Other symptoms/signs:

  • Difficulty turning (they tend to turn ‘en bloc’) either while standing/walking or in bed.
  • Depression occurs in one in three Parkinson’s patients (over the course of their lifetime) and anxiety is also common and can predate the diagnosis.
  • Excess sleepiness/daytime dozing occur in approximately half of Parkinson’s patients and can predate the diagnosis.
  • Bladder dysfunction occurs in around 40% – nocturia is the most common symptom, but frequency, urgency and urge incontinence can also occur.
  • Constipation occurs in around 50%.
  • Sexual difficulties; ED in men and lack of arousal, difficulty in climaxing, dyspareunia and vaginismus in women.
  • Orthostatic hypotension – in almost half
  • Excessive salivation/drooling
  • Excessive sweating
  • Pain – in up to half- can be sensory-type pain or pain due to muscle rigidity.

Note that these symptoms are typically more of a problem than the cardinal Parkinson’s symptoms.

 

Things you wouldn’t expect to see in Parkinson’s disease:

  • Frequent falls at an early stage
  • Rapid progression/early loss of mobility
  • Symmetrical symptoms initially
  • Dementia as a prominent early feature
  • Cerebellar signs
  • Pyramidal signs
  • Abnormalities of eye movements, or double vision
  • Lack of tremor
  • Lack of response to L-dopa

Any of these features would call the diagnosis into question; as would medications such as metoclopramide which could account for a Parkinsonian picture. If a patient with a diagnosis of Parkinson’s develops any of these, refer back to neurology (or, in our case, the geriatrician with a special interest in Parkinson’s who sees our patients with it) for a review of the diagnosis.

 

Arteriosclerotic pseudoparkinsonism

This is caused by a series of small strokes affecting the basal ganglia and creating a Parkinson’s-like picture. It typically presents with a shuffling gait and frequent falls in a patient with arteriopathic risk factors; it typically does not cause tremor.

 

Management of Parkinson’s

NICE guidelines advise referring to a specialist rather than starting treatment yourself. (This is what I would do anyway, so it’s good to know I’m right there.)

(BMJ Learning module)

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Pelvic congestion syndrome

I distantly remembered reading something about this many years ago; when a patient’s ultrasound showed pelvic varices, I realised I’d need to refresh my memory.

Presentation

Dull aching or throbbing pain, typically on one side of the pelvis although can be on both, worse at the end of the day or after prolonged sitting/standing. May be associated with vulval varices, varicose veins (typically worse on left), and/or haemorrhoids. Pressure from the dilated veins can cause worsening of stress incontinence or of IBS symptoms. Patients may get dragging sensations in the pelvis or fullness of the legs.

Diagnosis

In this case we got lucky and saw the varices on scan; in others, it may need a pelvic venogram.

Treatment

  • NSAIDs
  • Medroxyprogesterone (only article I found that gave the dose in the abstract advised 30 mg daily for six months)
  • Goserelin
  • Pelvic embolisation

 

Options for pelvic congestion syndrome – Clinical Advisor

Pelvic venous congestion syndrome – British Society for Interventional Radiology

Pelvic venous congestion syndrome – diagnosis and treatment (NCBI article)

RCT abstract – MPA & goserelin

RCT abstract – MPA & psychotherapy

Posted in Credits 2017, Gynaecology | Leave a comment

BRONJ (bisphosphonate-related osteonecrosis of the jaw)

The latest BJGP carries an article about this. Recommended management from the GP point of view:

Asymptomatic BRONJ (exposed bone with no pain or evidence of local infection):

  • Routine max-facs referral
  • Antimicrobial mouth rinse, such as chlorhexidine 0.12%

Pain/evidence of soft tissue inflammation or infection:

  • Also prescribe co-amoxiclav or similar

The following require immediate discussion with on-call max-facs:

  • Acute infection with facial or neck swelling
  • Cutaneous sinus formation
  • Possible pathological fracture

Suspected malignancy, of course, is referred on 2ww pathway as usual.

Dental extractions increase the risk; the article advised that they should be avoided where possible in patients on IV BPs, and that patients on oral BPs should have their extractions done in a specialist setting with a prophylactic antimicrobial mouth rinse. They also advised that patients who have been on oral BPs for >3 yrs should take a ‘drug holiday’ (discontinue the BP) for three months before and after invasive dental procedures.

In terms of prevention, they advise a thorough dental assessment for all patients about to start BP therapy. This struck me as being quite a lot to implement; I asked on Doctors.net.uk what doctors there thought and one GP posted the British Dental Association guidelines, which in fact advise that this is not necessary for patients going on BPs for osteoporosis due to the low risk. (It’s a different matter for patients undergoing treatment for malignancy.)

They also advise encouraging patients to improve their risk factors – stop smoking, reduce alcohol intake, and practice good oral hygiene. That sounds like good advice.

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