Tasty Morsels of EM 123 – #FRCEM Pneumonia

I’m entering a few months prep for the UK and Ireland exit exam in Emergency Medicine: the FRCEM. I’ll be adding lots of little notes on pearls I’ve learned along the way. A lot of my revision is based around the Handbook of EM as a curriculum guide and review of contemporary, mainly UK guidelines. I also focus on the areas that I’m a bit sketchy on. With that in mind I hope they’re useful.

You can find more things on the FRCEM on this site here.

(Featured image: James Heilman MD on Wikimedia Commons, CC License)

Hopefully a brief one from the NICE 2014 guidance. I don’t find it the most helpful guidance but worth knowing.

What tests should we do?

  • the guidelines do allow for the clinical diagnosis in primary care without a CXR
  • for moderate/severe
    • take blood and sputum cultures (though we know esp blood cultures are rarely helpful)
    • ‘consider’ urine legionella and pneumococcus
  • the say ‘consider’ CRP for monitoring

[collapse]
How do we assess severity?

  • they suggest CURB-65
  • (I have lots of issues with the CURB65 but it’s in the guideline)
  • 2 or more for hospital treatment but they allow clinical judgement to guide this

[collapse]
How do we treat it?

  • for low severity use single antibiotic for 5 days
  • systems should be in place for diagnosis and antibiotics within 4 hours
  • for moderate and severe
    • ‘consider’ 7-10 days dual antibiotic
      • amoxicillin/macrolide for moderate
      • ‘beta lactamase stable’ (things like co amoxiclav and common cephalosporins) antibiotic/macrolide for severe

[collapse]
What should we tell patients to expect?

(this is practice changing for me…)

  • 1 week: fever should have resolved
  • 4 weeks: chest pain and sputum production should have substantially reduced
  • 6 weeks: cough and breathlessness should have substantially reduced
  • 3 months: most symptoms should have resolved but fatigue may still be present
  • 6 months: most people will feel back to normal.

[collapse]

Tasty Morsels of EM 122 – #FRCEM DKA and diabetic emergencies

I’m entering a few months prep for the UK and Ireland exit exam in Emergency Medicine: the FRCEM. I’ll be adding lots of little notes on pearls I’ve learned along the way. A lot of my revision is based around the Handbook of EM as a curriculum guide and review of contemporary, mainly UK guidelines. I also focus on the areas that I’m a bit sketchy on. With that in mind I hope they’re useful.

You can find more things on the FRCEM on this site here.

When should we diagnose DKA in adults?

  • Ketnoaemia:
    • urine ++ ketones
    • >3mmol/l
  • Glucose
    • >11
    • known diabetes
  • Bicarbonate < 15 or venous pH <7.3

[collapse]
How should we manage DKA in adults?

this is of course a superficial summary of the bits that have changed in recent years and that I’m likely to forget…

  • venous gases rather than arterial
  • can also be used for electrolytes with intermittent lab confirmation
  • bedside blood ketone and glucose monitoring encouraged
  • use fixed rate insulin infusions (0.1unit/kg/hr) (note no bolus)
  • aim for
    • reduce ketones 0.5/hr
    • reduce glucose 3/hr
    • keep K between 4 and 5.5
  • add 10% glucose infusion when glucose <14 (continue the saline too)
  • continue the patients normal long acting insulin
  • they suggest systolic of 90 as the trigger for fluid boluses otherwise it’s a bit slower (1000 in first hour, 1000 over the following 2 hours etc…)
  • don’t forget the euglycaemic DKA with the new meds

[collapse]
What is HHS and how should we treat it?

(2012 Guideline)

  • Features
    • hypovolaemia
    • glucose >30 without significant ketonaemia or acidosis
    • osmoloality >320
  • Fluid losses 10-20 litres!
  • give 0.9% saline and expect a small rise in sodium initially
  • don’t reduce the sodium more than 10 in 24 hrs
  • aim +ve fluid balance of 3-6 littres at 12 hours
  • aim to reduce sugar no more than 5/hr
  • only introduce insulin IV if the sugar stops falling with fluids (and even then at 0.05units/kg, half that of DKA)
  • most patients should have VTE prophylaxis
  • they highlight the frequency of foot ulceration in these folk

[collapse]
What about DKA in kids?

BSPED 2015

  • Diagnosis
    • pH<7.3, Bicarb <18
    • Ketonaemia >3
    • usually glucose >11
  • pH<7.1 = severe DKA
  • Management
    • do not give fluid bolus unless shocked, even if pH<7.1
    • if giving it in a shocked DKA kid give a single 10ml/kg bolus
    • Fluid requirement = deficit + maintenance
      • they acknowledge that estimating deficit is witchcraft inaccurate so give this guide
        • 5% deficit if pH.7.1
        • 10% deficit if pH<7.1
        • replace this over 48 hrs
      • Maintenance is lower than normal (and not the usual APLS)
        • <10kg = 2ml/kg/hr
        • 10-40kg = 1ml/kg/hr
        • >40kg = fixed 40ml/hr
      • they note that all fluids should contain potassium (0.9% saline 500mls with 20mmol KCL)
    • Insulin
      • give 1-2 hrs after fluid starts
      • use 0.05-0.1 unit/kg
    • Once glucose under 14 then need to add glucose. The concentration depends a bit on the ketone level. See the guideline
  • Signs of cerebral oedema
    • headache
    • irritability
    • slowing pulse
    • increasing pulse pressure
    • reducing GCS
  • If suspected give mannitol (20% 0.5-1 g/kg over 10-15 minutes)

[collapse]

Tasty Morsels of EM 121 – #FRCEM Sickle cell & other haematological curiosities

I’m entering a few months prep for the UK and Ireland exit exam in Emergency Medicine: the FRCEM. I’ll be adding lots of little notes on pearls I’ve learned along the way. A lot of my revision is based around the Handbook of EM as a curriculum guide and review of contemporary, mainly UK guidelines. I also focus on the areas that I’m a bit sketchy on. With that in mind I hope they’re useful.

You can find more things on the FRCEM on this site here.

(Featured image from NIH Online via Flickr CC License)

This is a big weakness of mine. Hence the review.

Some relevant Guidance:

What is sickle cell disease?

  • genetic mutations of one of the chains of the Hb molecule
  • sickle cell trait involves some of your Hb being HbS
  • in homozygotes the vast majority is HbS
  • HbS polymerises in deoxygenated or acidotic conditions (hence the precipitants). This causes the sickling and deformation of the red cells which then get mopped up by the spleen as abnormal and unwelcome

[collapse]
What are some complications?

  • Long term prone to serious chronic morbidity and functional asplenia (and susceptibility to the encapsulated organisms associated)
  • bone infarctions
  • aplastic anaemia
    • famously with B19, slapped cheek
    • drop in Hb with insufficient reticulocytes to replace what’s lost
  • priapism
  • acute chest syndrome
  • splenic sequestration (mainly kids)
    • can present as hypovolaemic shock

[collapse]
How should we manage acute painful episodes?

From NICE

  • for severe pain (>6/10) bolus of strong opiate is recommended first line or for moderate pain when the usual fails.
  • specifically recommends against pethidine
  • consider PCA if repeated boluses needed

[collapse]
How should we manage acute chest syndrome?

defined as an acute illness characterized by fever and/or respiratory symptoms, accompanied by a new pulmonary infiltrate on chest X-ray. Severe hypoxia is a useful predictor of severity and outcome
  • analgesia as per NICE
  • they recommend ABG if sats <94
  • incentive spirometry for rib pain
  • give fluids but not too much. Like every other guideline then…
  • antibiotics should be given (note chlamidiya pneumonia and mycoplasma are the two commonest bugs here)
  • there’s a lot of other “consider” recommendations and some complex ones around transfusion in sickle cell that I’m not getting into here. In real life get some advice from a specialist.

[collapse]
What is G6PD deficiency?

  • this is a common inherited condition that results in haemolysis in response to certain meds and foods.
  • famously gives some degree of protection against malaria
  • most people remain asymptomatic throughout their life
  • the main complication we will see is the acute haemolytic crisis
    • this is rare but can be provoked by a variety of foods and drugs
    • jaundice, pallor, dark urine
    • can be abdo or back pain associated
    • whole thing lasts about a week
  • can also be a cause of neonatal jaundice
  • Drugs associated
    • classic for the books was primaquin and dapsone
    • fava beans are the classically implicated food

[collapse]
What are the main different haemophilias?

I found this post by Salim really helpful. While no doubt no as detailed and comprehensive as the haematologists might like it it really helped me

I couldn’t find any particularly relevant UK guidelines (most are above are decision point). This recent one on joint bleeds is worth a look if you’re keen.

  • Primary Haemostasis
    • vasc injury > VWF > platelet plug (immediate)
    • deficiency causes superficial bleeding mainly (purpura, petechiae)
  • Secondary Haemostasis
    • clotting factors promote haemostasis
    • deficiency causes deep bleeds (joints, haematomas)
  • ‘The Plug’
    • Fibrin holds it all together
  • On labs look for
    • prolonged APTT (intrinsic pathway) and normal PT (extrinsic, factor 7 which warfarin blocks) and platelets
    • both haemophillia A (Factor 8) and B (Factor 9)
  • Clinically are main emergencies are
    • haemarthroses
      • pain may occur before clinical effusion
    • haematomas
    • ICH (rare but deadly)
  • Treatment
    • analgesia
    • give them their factor (they will usually know it and bring it) If not ring someone. But it’s really important not to delay giving it if the patient knows what it is and you have it available.
    • there are slightly different dosing depending on how deficient they are and the nature of the bleed (ie you give more factor for an ICH than a joint bleed)
    • Of note the haemarthrosis guideline above specifically comments on aspiration and recommends against routine use but occasionally it might be used  with asepsis and factor replacement cover
    • remember DDAVP as an adjunct, can increase factor 8 levels but generally only used in mild bleeds

[collapse]