Monday, 19 November 2018

Erysipelas

Part of a spectrum of infection.

1. Impetigo - see http://adultemergencymedicine.blogspot.com/2018/08/rashes-impetigo.html 

2. Erysipelas is a superficial cellulitis, with similar risk factors. It looks a lot worse than cellulitis with ruptured bullae and vivid bright red erythema. Almost all erysipelas is caused by group A beta haemolytic strep. It can recur due to persistence of risk factors and lymphatic drainage. Complications can include abscesses, gangrene, chronic leg swelling

Signs and symptoms are normally abrupt, affecting predominantly the lower limb and face. It has a sharp raised border, and is bright red and swollen. The swelling may lead to dimpling, blistering, and even necrosis.

3. Cellulitis
Cellulitis is very rarely bilateral. 35-50% of patients will have a leukocytosis, 60-92% will have an elevated ESR, and 75-95% will have an elevated CRP.  Blood cultures are unlikely to be helpful.
Orals are very bioavailable so most of the time are just as good as IVs.

Often caused by strep and staph. Atypicals are common: Cat bites can have pasteurella, sea water Vibrio vulnificus, fresh water Aeromonas hydrophila, fish farms Streptococcus iniae. These atypicals can cause a rapidly progressive cellulitis.

Class I: No signs of systemic toxicity or co-morbidities. Can be managed on POs.
Class II: 2 or more SIRS, but no organ dysfunction, or have a co-morbidity. May need IV outpatient management.
Class III: Sepsis and organ dysfunction, or unstable co-morbidities normally require admission.
Class IV: Severe life threatening infection.

4. Necrotising Fascitis

https://www.dermnetnz.org/topics/erysipelas/
https://journalfeed.org/article-a-day/2018/lrinec-score-physical-exam-or-imaging-for-necrotizing-infection
http://www.emdocs.net/cellulitis-mimics-ed-considerations/
https://first10em.com/cellulitis-antibiotics/
https://www.rcemlearning.co.uk/modules/cellulitis-and-other-skin-infections/
https://journalfeed.org/article-a-day/2018/is-a-blood-culture-needed-in-cellulitis
https://www.rcemlearning.co.uk/references/cellulitis/
http://www.tamingthesru.com/blog/2018/9/3/necrotizing-fasciitis-and-the-spectrum-of-soft-tissue-infections

Tuesday, 13 November 2018

Bleeding in Pregnancy

<23 Weeks - Early Pregnancy 
This has been covered here: https://www.rcemlearning.co.uk/foamed/induction-bleeding-in-early-pregnancy/

Later Pregnancy
https://www.rcemlearning.co.uk/modules/bleeding-in-pregnancy/

Antepartum Haemorrhage
>24 weeks gestation
Placenta praevia - stage depends how much of the os is covered by the placenta. Bright red and painless bleeding.
Placental abruption - complete or partial separation of the placenta. Causes lots of bleeding which may be concealed. Normally associated with continuous abdominal pain.
Vasa praevia - the fetal blood vessels run everywhere, not protected by the placenta. They may run over the cervix. High perinatal mortality - easy to rupture the fetal blood vessels. Can cause painless bleeding.
AntiD may be needed after a potentially sensitising event.

Hopefully all of these will be identified by screening, and hopefully these patients will present to the maternity assessment unit, not the ED!

PostPartum Haemorrhage
Primary PPH - in first 24hours. Secondary PPH - up to six weeks. Again, hopefully these patients will present to MAU not ED.

In pregnancy, problems are the 4Ts
 Tone, trauma, tissue, thrombin.
 Tone: uterine massage, bimanual compression, catheterise, give syntrometrin

Bleeding should slowly stop after a 12 weeks. It's often significantly less after the first few hours, and should change from  bright red to brown (lochia).
The commonest cause is endometritis. There may be retained products - start IVs, get an USS. If there's no RPOC, there could still be endometritis. The uterus in endometritis will remain palpable after 14days after delivery.  Endometritis is a clinical diagnosis.
I think bleeding persistently after delivery needs to see O&G.
Bleeding that stops and starts again is probably "new" bleeding.


https://www.bmj.com/content/358/bmj.j3875?sso=
http://www.emdocs.net/postpartum-endometritis-ed-setting-presentation-evaluation-management/


B12 Anaemia

B12 deficiency, cobalamin deficiency or pernicious anaemia is also knon as Biermer's anaemia, Addison's or Addison-Biermer anaemia. It's one of the megaloblastic anaemias.

Pathophysiology
Normally, B12 is absorbed through the ileum with the help of intinsic factor which is secreted by the parietal cells.
Various things can stop this happening - antibiodies to parietal cells, like in atrophic gastritis, antibodies to intrinsic factor like in pernicious anaemia, lack of a terminal ileum, or disease of the ileum - like Crohn's disease, and reduced b12 intake.
It takes a while for the disease to become apparent as there's 3-5 years worth of reserves in the liver.
Lack of B12 means that DNA replication is slow, so cells divide less but grow bigger. This gives you your macrocytic or megaloblastic anaemia.
Lack of B12 means the conversion of homocysteine to methionine is reduced, so there are high levels of homocysteine - causing things like atherosclerosis, thromboembolism and osteoporosis.
More importantly, B12 is a cofactor in the conversion of methylmalonic acid into succinyl CoA. Without this, the dorsal and lateral spinal columns are demyelinated, through an unknown mechanism, so you get neurological symptoms.

Investigation
FBC will show macrocytic anaemia, and maybe neutropaenia and thrombocytopenia.
A blood film will show anisocytosis and poikilocytosis.
Bilirubin may be increased because of haemolysis.
Then you can look for autoantibiodies, and maybe an absorption test like the Schilling test.


Symptoms
Symmetrical, legs > arms
Ataxia
Loss of position sense
Loss of vibration sense

Low grade pyrexia, weight loss, diarrhoea, jaundice due to haemolysis, pallor due to anaemia, premature greying of the hair.

Treatment
If B12 levels are low, then patients need intramuscular B12 and a haematology referal. If there is neurological involvement, 5 - 6 loading doses of 1000mcg, followed by maintainence of 1000mcg every three months.
If B12 levels are borderline, then oral B12 may have a reponse and be diagnostic.
Patients often feel better within 24hours of starting treatment.
If patients are asymptomatic, there is debate about their treatment- monitoring seems preferred.

B12 is naturally found in animal products - fish, meet, eggs, milk. It's not generally present in plant foods, but is in fortified cereals. It's worth mentioning that pabrinex doesn't contain B12!

http://calgaryguide.ucalgary.ca/vitamin-b12-deficiency/
https://www.gpnotebook.co.uk/simplepage.cfm?ID=1288699922&linkID=26150&cook=no

Wednesday, 24 October 2018

Tasers

A Taser Two weighted barbs attached to long insulated wires They fire at 180 feet / second Deliver 50 000 volts of electricity, in pulses Removal Stretch surrounding skin, and tug sharply. If difficult: 1. Anesthetize the area at the site of attachment. Possibly using an insulin syringe. 2. Insert an 18 gauge needle along the side of the barb with the bevel of the needle facing the barb. 3. Advance the needle about half a centimeter. 4. Pull out the needle and the barb together at the same time. If this doesn’t work, use a scalpel. http://epmonthly.com/blog/dont-taze-me-bro/ https://emj.bmj.com/content/21/2/136 http://epmonthly.com/article/they-tased-me-doc/ https://www.ncbi.nlm.nih.gov/pubmed/?term=Vilke+Bozeman+taser

Tuesday, 16 October 2018

Possible PE in pregnancy

Possible PE in pregnancy is a nightmare to investigate and to manage. There are several flowcharts...but lets look at the evidence. 1. Is this a PE? Has someone just done a random d-dimer? If they have...think back to the symptoms. We know shortness of breath in pregnancy could have many causes, but we only worry about PE. Take a good history. Anecdotal evidence suggests PEs should be tachycardic. 2. Do a CXR A whole load of investigating is prevented if they've got a pneumothorax or pneumonia. 3. Risk stratify If they're high risk, they need imaging. If they're low risk...continue. 4. In a low risk patient, a negative d-dimer is considered able to rule out VTE. Chances of it being negative are slim. The DiPep study recommends not using d-dimers, as does the RCOG greentop guideline. 5. Consider trimester adjusted d-dimers. We know the d-dimer rises in pregnancy. These values will depend on your d-dimer assay. 1st 750 ng/dL, 2nd 1000 ng/dL, and 3rd 1250 ng/dL D-dimer test with the new threshold for: the first of 286, the second of 457 and the third trimester of 644 ng/mL can be useful in diagnosis of pregnancy related VTE. I can't find any strong evidence these are strongly evidence based - but Jeff Kline is amazingly knowledgable, so I'm sure he's right! 6. Imaging Bilateral leg dopplers - if they're positive for DVT...start treatment VQ scan - probably causes more radiation to the fetus Other Summaries https://emcrit.org/wp-content/uploads/2011/07/PE-DX-by-Jeff-Kline.pdf https://www.aci.health.nsw.gov.au/networks/eci/clinical/clinical-resources/clinical-tools/respiratory/pe/pe-pregnant

Thursday, 30 August 2018

Rashes - impetigo

Impetigo is a superficial infection of the epidermis caused by Staphylococcus aureus, group A beta-haemolytic streptococci or maybe even MRSA. Children should stay away from school until lesions are crusted and healed, or 48 hours after commencing antibiotic treatment. Several clinical forms of impetigo exist. 1. Non-bullous impetigo is the usual form. Red macules form initially, then golden crusts. It is itchy but not painful. Regional lymphadenopathy is common. 2. Bullous impetigo. Here there is sloughing of the epidermis due to toxin production. Vesicles/bullae may be on face, buttocks, nappy area or trunk. Inpatient care is required for infants with bullous impetigo and patients with widespread impetigenised dermatitis who may develop sepsis or dehydration.
Treatment: 1. use mupirocin nasal ointment to eradicate nasal carriage when treating impetigo on the face 2. Remove the scab, and then apply local treatment - fucidin and bactroban 3. Systemic if that fails 4. Remember not to go to school 5. Excellent hygiene References https://wikem.org/wiki/Impetigo https://www.rcemlearning.co.uk/references/cellulitis/ http://www.publichealth.hscni.net/sites/default/files/Guidance_on_infection_control_in%20schools_poster.pdf https://www.summitmedicalgroup.com/library/pediatric_health/hhg_impetigo/ http://www.bad.org.uk/for-the-public/patient-information-leaflets/impetigo/?showmore=1&returnlink=http%3A%2F%2Fwww.bad.org.uk%2Ffor-the-public%2Fpatient-information-leaflets#.W4g8xehKjIU

Monday, 9 July 2018

Pelvic Binders

Most of our patients come in with their binders already on, but sometimes we do have to apply them.

Why
- tamponade blood
 (yet pelvis has space for a baby and a beer filled bladder)
- oppose bone ends and stop bleeding

Why not
There is no evidence that pelvic binders are harmful when applied to patients with proximal femur or acetabular fracture.
They can cause pressure necrosis
Depending on the mechanism, they may make the injury worse.

How
Strip patient - should be to skin
Analgesia
Roll patient to 15 degrees
Put folded binder underneath buttocks

Apply over the greater trochanter or symphysis pubis
Minimise patient movement - ideally they should be scooped on.

SAM Splint:
  Feed black strap through the buckle
  Pull black and orange in opposite directions
  Tighten
  Fasten

Pregnancy - should be OK if applied correctly

Good Resources
https://phemcast.co.uk/2015/11/05/podcast-episode-2-the-pelvic-binder/
https://www.rcemlearning.co.uk/references/abdominal-trauma/ 
https://www.rcemlearning.co.uk/foamed/pelvic-fractures-a-guide-to-treatment-within-a-trauma-unit/ 
https://www.rcemlearning.co.uk/foamed/june-2017/#1496133043616-a1f3a145-a4a3 
https://www.rcemlearning.co.uk/modules/blunt-trauma-to-the-abdomen-don’t-forget-the-kidneys/
http://emergencymedicineireland.com/2013/04/anatomy-for-emergency-medicine-027-basic-anatomy-of-abdomen-and-pelvic-trauma/ 
https://www.resus.com.au/2015/07/31/unstable-pelvic-fractures/ 
https://emj.bmj.com/content/30/12/1070