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

Pelvic binders. Do we slide up from knees to GTs, or tilt onto a folded binder? Can't find a consensus! #foamed @JGoulding444 @mattdoc1979

— Charlotte Davies (@OneLongPlait) November 3, 2015

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 

Meningitis

Causes
Viral or aseptic meningitis is the most common form and may be caused by enteroviruses.
Meningococcal disease is the most common (Neisseria meningitides) - infancy and adolescence and over the Winter months.
Pneumococcal - commonest cause in elderly people. Often have a distant focus of pneumococcal infection like pneumonia, otitis media, mastoiditis, sinusitis or endocarditis. Has a 30% mortality rate.
TB meningitis - often develop gradually over days or even weeks and is more  common in the immunocompromised, especially with HIV.
Listeria meningitis remains uncommon. Neonates, the elderly, and immunocompromised people are at greatest risk.


Recurrent lymphocytic meningitis, also known as Mollaret’s meningitis, is a rare disease that is estimated to have a prevalence of 2.7 per 100 000 population. HSV-2 is the most common cause of recurrent lymphocytic meningitis, being responsible for 84% of recurrent meningitis in one study.
A suddenly worsening headache, followed by emerging signs of meningism, is often associated with rupture of the abscess. Rupture of a brain abscess is associated with a high mortality: up to 80%. Emergency surgery is indicated.


Clinical Presentation When a patient recovers from bacterial meningitis, headache, fatigue, and difficulty with coordination, concentration, and memory may persist for several months.


Rash - may be petechial, or in its early stages may be erythematous. The rash occurs in at least 60% of adults.


Triad of fever, headache, and neck stiffness(70% sensitivity) in less than 50% of patients. Changes in mental state are relatively sensitive and tend to occur more often in bacterial than viral meningitis.

Kernig's test is positive if there is pain or resistance in the lower back or posterior thigh when the knee is extended while the hip is flexed to 90°. Kernig's sign can be a useful test if positive, but a negative test does not exclude meningitis.

Brudzinski’s sign is not specific for meningococcal meningitis. You can elicit the sign by passive flexion of the neck, resulting in flexion of the hips and knees if positive.


Encephalitis  has a similar presentation to meningitis, but confusion and drowsiness tend to be more prominent.


Management of Suspected Meningitis in the Emergency Department

1. Recognise
2. Investigate – Take extra two EDTA (purple) tubes for meningococcal or pneumococcal DNA using PCR. Do not wait for the results before commencing treatment. It is difficult to differentiate viral meningitis from bacterial meningitis on clinical grounds alone so we need to do a LP.
3. Treat –
   a. Sepsis 6 with antibiotics as per trust antimicrobial guidelines
   (Ceftriaxone 2g + amoxicillin 2g if >50years or immunocompromised)
   b. Dexamethasone 10mg IV
   c. Aciclovir if features of encephalitis (fluctuating consciousness, motor or sensory deficits, altered behaviour and personality changes, and speech or movement disorders).
   There are currently no treatments with a proven benefit for the common causes of viral meningitis, although acyclovir is often used, despite it being nephrotoxic and lowering seizure threshold. It does reduce the mortality of encephalitis from 70% to less than 30%. Treatment should be supportive.
4. CT would be indicated if there are focal neurological signs, papilloedema, controlled or uncontrolled seizures, GCS <12 or diagnostic uncertainty. The medical team may ask the ED team to arrange the CT, but this should not delay their review of the patient.
5. For continuity of care, it is expected that the medical team will report “acute meningitis” to  Health Protection Team (SLHPT) .
6. Isolate – as per trust policy
   A patient with known or suspected meningococcal meningitis should be isolated in a single room with droplet precautions for 24 hours from the time that effective antibiotic treatment has been started.
   Staff caring for the patient should observe the standard infection control precautions and wear FFP3 masks, gloves and aprons.
   Staff performing procedures that may generate aerosols, for example suctioning, intubation or inserting an airway, should wear properly fitted FFP3 masks and eye protection.
7. Antibiotic Prophylaxis for close contacts should be coordinated by SLHPT. OH Assist will coordinate antibiotic prophylaxis for healthcare workers
   Antibiotic prophylaxis is offered to the following groups of people:
8. Those who have had prolonged close contact with the patient during the seven day incubation period. This includes people who live or sleep in the same household, dormitory or halls of residence.
9. Intimate (kissing) contacts.
10. Those exposed transiently to large droplets from the upper respiratory tract of the patient during their admission to hospital. For example, a healthcare-worker inserting an airway or suctioning the upper respiratory tract without wearing appropriate personal protective equipment may be at risk.

References
http://www.journalofinfection.com/article/S0163-4453(16)00024-4/abstract http://www.journalofinfection.com/cms/attachment/2048213088/2058279234/mmc1.pdf
https://www.uptodate.com/contents/viral-encephalitis-in-adults?source=search_result&search=meningitis%20aciclovir&selectedTitle=3~150 http://lgnet/download.cfm?ver=10662
https://www.rcemlearning.co.uk/modules/intracranial-infections/
http://learning.bmj.com/learning/modules/flow/ICH.html?execution=e1s1&moduleId=5003335&status=LIVE&action=start&_flowId=ICH&sessionTimeoutInMin=90&locale=en_GB&shouldStartAtQuestionSection=false
http://learning.bmj.com/learning/modules/flow/ICH.html?execution=e2s1&moduleId=10041919&status=LIVE&action=start&_flowId=ICH&sessionTimeoutInMin=90&locale=en_GB&shouldStartAtQuestionSection=false

Phenytoin Toxicity

An 80 year old attends your emergency department "not right". He is known epileptic, but you are unable to get a collateral history to know what form his seizures normally take. He is on phenytoin, and as far as you know is compliant. He looks well, but has a strange rhythmic movement of his mouth, and upper limbs. You wonder what is causing this...luckily the medics take a phenytoin level...

Phenytoin 
Phenytoin is a sodium channel blocker with slow and erratic oral absorption.
Peak levels are delayed by 24 – 48 hours
It is 90% protein bound, so dialysis is ineffective.
It is metabolised in the liver, importantly this metabolism is saturable and plasma levels can rise dramatically with only a slight increase in daily dosing.
Elimination half-lives in a poisoned patient can vary between 24 to 230 hours.

Problems
Acute overdose has cardiovascular side effects as the biggest problem. Because of the poor oral absorption, these are only really likely with IV - bradycardia, hypotension, vf, asystole, wide QRS.

Neurological signs are the most common with nystagmus (initially on forced lateral gaze only, later becomes spontaneous), ataxia, decreased consciousness.

Can also cause Nausea and vomiting

"Purple glove syndrome" and Stevens Johnson can also occur

Anticonvulsant hypersensitivity syndrome


Toxicity symptoms by phenytoin level^
Level Sypmtoms
>10 Usually no symptoms
10-20 Occasional mild nystagmus
20-30 Nystagmus
30-40 Ataxia, slurred speech, Nausea/vomiting
40-50 Lethargy, confusion
>50 Coma, seizure (rare)
Correct the phenytoin level for albumin = Observed phenytoin (mg/L) (O.2 x albumin [g/dL]) + 0.1. If possible, take a trough level (ie just before next dose), but if you suspect toxicity or need to treat status, just take a level - treat the patient not the numbers.

Other laboratory testing
LFTs, hepatic dysfunction increases risk of phenytoin toxicity
CBC, frequently show eosinophilia or marked leukocytosis
Total CK
ECG, may see arrhythmias, AV block, or sinus arrest with junctional or ventricular escape
POC glucose, rule out hypoglycemia as cause of AMS
Acetaminophen and salicylate levels, rule out common coingestion
Urine pregnancy test


Management
Supportive care
avoid lidocaine (same antidysrhythmic properties as phenytoin)
Activated charcoal PO
Falls risk

References
https://www.rcemlearning.co.uk/references/dystonia/
https://wikem.org/wiki/Phenytoin_toxicity
http://www.emdocs.net/em3am-phenytoin-toxicity/
https://lifeinthefastlane.com/tox-library/toxicant/anticonvulsants/phenytoin/
http://journals.sagepub.com/doi/pdf/10.1177/201010581302200307


<blockquote class="twitter-tweet" data-lang="en"><p lang="en" dir="ltr">Phenytoin effects at therapeutic and toxic levels<a href="https://twitter.com/hashtag/InsidersGuideITE?src=hash&amp;ref_src=twsrc%5Etfw">#InsidersGuideITE</a> <a href="https://twitter.com/hashtag/FOAMed?src=hash&amp;ref_src=twsrc%5Etfw">#FOAMed</a> <a href="https://twitter.com/hashtag/EMBoardReview?src=hash&amp;ref_src=twsrc%5Etfw">#EMBoardReview</a> <a href="https://twitter.com/hashtag/MedEd?src=hash&amp;ref_src=twsrc%5Etfw">#MedEd</a> <a href="https://t.co/4AVsCWXmlF">pic.twitter.com/4AVsCWXmlF</a></p>&mdash; Adam Rosh (@RoshReview) <a href="https://twitter.com/RoshReview/status/671166731914711040?ref_src=twsrc%5Etfw">November 30, 2015</a></blockquote>
<script async src="https://platform.twitter.com/widgets.js" charset="utf-8"></script>

<blockquote class="twitter-tweet" data-lang="en"><p lang="en" dir="ltr"><a href="https://twitter.com/RCollEM?ref_src=twsrc%5Etfw">@RCollEM</a> be careful when drawing up phenytoin and always administer with cardiac monitoring <a href="https://twitter.com/hashtag/FOAMed?src=hash&amp;ref_src=twsrc%5Etfw">#FOAMed</a> <a href="https://twitter.com/hashtag/FOAMcc?src=hash&amp;ref_src=twsrc%5Etfw">#FOAMcc</a> <a href="https://twitter.com/hashtag/FOAMped?src=hash&amp;ref_src=twsrc%5Etfw">#FOAMped</a> <a href="https://t.co/LLatwq4hJA">pic.twitter.com/LLatwq4hJA</a></p>&mdash; Hasan Qayyum (@hasqay) <a href="https://twitter.com/hasqay/status/796446929693605888?ref_src=twsrc%5Etfw">November 9, 2016</a></blockquote>

<script async src="https://platform.twitter.com/widgets.js" charset="utf-8"></script>

Adult C-Spine Immobilisation

I think the RCEM guidelines say everything we need to know about adult c-spine immobilisation. 

They're summarised beautifully by ALIEM here together with a good discussion on distracting injuries. 

Adrenal Crisis

Addison's Disease

Anterior pituitary - ACTH, GH, FSH, LH, TSH, PRL

Posterior pituitary- ADH, oxytocin

Presentation

History of recent physical stress like stress, major injury, myocardial infarction 

Nausea and vomiting, muscle pains, confusion, coma, fatigue
Low BP or postural hypotension, tachycardia

Risk if ≥5 mg prednisolone equivalent for more than 4 weeks

Investigations

Hypoglycaemia
Low sodium

High potassium 

A patient with hypothyroidism feels worse on thyroxine

T1 DM with unexplained hypoglycaemia

Hyperuraemia
Hypercalcaemia
Metabolic acidosis
Random 9am cortisol  or short synacthen test - helps differentiate between primary and secondary adrenal insufficiency. 

Raised thyroid stimulating hormone (TSH)

Pathophysiology

Primary - disease affecting the adrenal gland  Addison's 

  Autoimmune 

  Infective (including TB, HIV and fungal) 

  Iatrogenic

  Haemorrhage or infarction (Waterhouse- Friedrichsen- meningococcemia)

  Malignant infiltration (metastasis, lymphoma) 

  Non malignant infiltration (sarcoidosis, haemochromatosis, amyloidosis)

  Genetic 

Secondary/Tertiary adrenal insufficiency (twice as common as addisons)

Panhypopituitarism

Pituitary apoplexy – infarction or hemorrhage of tumor

Chronic steroid therapy (suppresses HPA axis)

Tumors, granulomas

Treatment

1L/hour to maintain their BP

Hydrocortisone 100 mg with subsequent doses of 100 to 200 mg over 24 hours divided into three or four doses.

Look for and treat trigger 

Adrenal crisis. Do a random cortisol. Give steroids! ↓Na less likely unless SIADH, ↑K+ unlikely. #foamedhttps://t.co/K6h3shBZRJ pic.twitter.com/tTcoPehG3N

— South London EM FOAM (@slemfoam) June 15, 2017

Sick Day Rules
Double hydrocortisone if fever > 37.5 C or for infection or sepsis requiring an antibiotic

For severe nausea (often with a headache), 20 mg of hydrocortisone orally and sip rehydration or electrolyte fluids (such as dioralyte)

On vomiting, they should use their emergency injection if they have one (eg 100 mg of hydrocortisone) immediately. Then they should call a doctor, saying ‘Addison’s emergency’

They should take 20 mg of hydrocortisone orally immediately after a major injury to avoid shock

If patients have persistent vomiting or diarrhoea that is likely to interfere with absorption of medication or fluid balance, you should admit them to hospital for intravenous hydrocortisone

Some authors recommend that the dose of hydrocortisone should be increased (by 5 mg to 10 mg) before strenuous exercise.

Pituitary Apoplexy

Acute haemorrhagic or non-haemorrhagic necrosis of the pituitary gland. An existing pituitary macroadenoma is usually present (60-90%) but it can occur with healthy glands in few isolated cases. It is also more likely with medical treatment of a prolactinoma, pregnancy (Sheehan) and cerebral angiography, trauma and sudden changes in ICP.  

As the gland suddenly enlarges it may cause compression of structures adjacent to the sella leading to: 

  sudden headache

  loss of visual acuity with a chiasmal field defect

  oculomotor palsies (CN III) 

  Decreased level of consciousness, hypopituitanism, Addisonian crisis and subarachnoid irritation. 

Investigation

CT -  routine CT is insensitive to the diagnosis unless frank intracranial haemorrhage is present. The pituitary mass may be evident and be hyperdense. Fluid debris levels may also be evident. Useful to do to exclude a sub-arachnoid. 

MRI - typically demonstrates a pituitary region mass. Confirms the diagnosis in over 90% of patients. A pituitary CT is indicated if MRI is contraindicated or not possible.

Endocrine evaluation with blood samples for random serum cortisol, TSH, free T4, prolactin, IGF1, LH, FSH, testosterone (men), oestradiol (women) for later analysis

Hyponatraemia in 40% of cases 

Treatment

Hydrocortisone 100 mg i.m. bolus followed by 50–100 mg six hourly by intramuscular injection or 100–200 mg as an intravenous bolus followed by 2–4 mg per hour by continuous i.v. infusion can be used

Neurosurgical intervention should be considered in patients with:

   Severely reduced visual acuity

   Severe and persistent visual field defects

   Deteriorating level of consciousness

References 
https://lifeinthefastlane.com/ccc/adrenal-insufficency/

https://wikem.org/wiki/Adrenal_crisis

http://www.emdocs.net/em3am-acute-adrenal-insufficiency/

https://lifeinthefastlane.com/pediatric-perplexity-012/

http://sinaiem.org/tag/adrenal-crisis/

https://radiopaedia.org/articles/adrenal-insufficiency-1

http://www.emdocs.net/core-em-adrenal-crisis/

https://emsimcases.com/2017/02/14/adrenal-crisis/

http://www.endocrineconnections.com/content/5/5/G12

https://emedicine.medscape.com/article/765753-overview

http://learning.bmj.com/learning/module-intro/-diagnose-manage-adults-addison%27s-disease.html?moduleId=10013263&searchTerm=%E2%80%9Cadrenal%E2%80%9D&page=1&locale=en_GB

https://radiopaedia.org/articles/pituitary-apoplexy

http://www.endocrineconnections.com/content/5/5/G12.full

https://link.springer.com/article/10.1007/BF02112028

http://www.bmj.com/content/342/bmj.d1270

Hyperemesis Gravidarum

We all know that nausea and vomiting in pregnancy is common affecting 50–75% of pregnant women any time from the 4th week of pregnancy, most common in the 9th and 12 week, and we probably misdiagnose some of these people with hyperemesis gravidarum which affects less than 1%. To me, I'm not sure that the precise difference matters, as I think I'd struggle to send home a ketotic pregnant lady with at least some of the hyperemesis protocol...

Hyperemesis Gravidarum
Persistent, intractable nausea and vomiting beginning in the first trimester
Associated with a weight loss of >5% of pre-pregnancy weight
Dehydration, electrolyte imbalance and ketosis

Cause
Likely multifactorial - typically higher levels of human chorionic gonadotrophin
H. pylori may have a part to play
Make sure you exclude other causes - molar pregnancy is the most serious. These patients are unlikely to improve enough to be able to go home.

Treatment
Antiemetics:
Ginger - evidence base says ginger tablets improve symptoms in four days

Other:
Small meals (6 times a day). Eat as soon as you feel hungry. Avoid likely triggers - like fatty food.
Fluids- cold, clear, and carbonated like ginger ales and lemonades as well as smoothies or slushies.

Thiamine - thiamine requirements increase in pregnancy, so give if "prolonged" vomiting. Some say if no meal in a weak, others say vomiting for more than three weeks.
Oral thiamine 100mg / day, or IV thiamine (pabrinex is OK, but does have other B vitamins). Toxbase suggests overdose of thiamine is low risk.

Antiacids- treat non ulcer dyspepsia if there are signs of it. PPIs are thought to be safe. There is some evidence that H. pylori increases vomiting, so if the patient has prolonged vomiting, consider

Corticosteroids - can be used as a third line. I'd like O&G do that bit.

Patient Advice 
No proven effects on the fetus, except fetal growth restriction, pre-term delivery. The pregnancy may be complicated by triploidy, trisomy 21 and hydrops fetalis. It may be due to a molar pregnancy.
Mum can get problems from electrolyte derangement - wernickes, central pontine myelinolysis due to hyponatraemia, ATN, splenic avulsion and increased VTE risk. Peripheral neuropathies are rare. One case report of epistaxis due to vitamin K deficiency!

Results
Ketones in the urine
Hypochloremic alkalosis
Slightly elevated liver enzymes - amniotransferases elevations are 2-3 times normal, but can be 15-20 times normal. They should resolve
Electrolyte abnormalities, typically hypokalaemia
Transient hyperthyroidism


1st Line - Cyclizine
Antihistamines (Cyclizine) and phenothiazines should be prescribed.

2nd Line - Metoclopramide
Safe and effective but there is a risk of extrapyramidal side effects.

3rd Line - Ondansetron
Some mostly unproven link with ondansetron and septal defects.

Fluids
RCOG says no evidence any fluid is better than another.
Nausea apparently resolves faster with dextrose containing fluid, but you need to check the sodium and consider thiamime replacement first - with the dogma that otherwise you can precipitate Wernickes.

References and Links
http://bestbets.org/bets/bet.php?id=2923
http://pmj.bmj.com/content/postgradmedj/72/853/688.full.pdf
https://www.rcog.org.uk/globalassets/documents/guidelines/green-top-guidelines/gtg69-hyperemesis.pdf
https://wikem.org/wiki/Hyperemesis_gravidarum
http://pmj.bmj.com/content/78/916/76
http://bestpractice.bmj.com/best-practice/evidence/intervention/1405/0/sr-1405-i8.html

Tetanus

Wound Management 

In any patient with a wound, first do a risk assessment of the wound, and then their tetanus status:

Tetanus Prone Wound:  >6 hours old and needs surgical treatment
                                      Open compound fracture
                                      Contaminated puncture wound
                                      Clinical evidence of sepsis

High risk tetanus prone wound?   Yes - give immunoglobulin
                                    Heavy contamination with material likely to contain tetanus eg. manure
                                    Extensive devitalized tissue
                                    >24 hours since injury
                                    >10% burns

Tetanus Status Assessment 
Full immunisation - give immunoglobulin if very high risk
Partial immunization - give DTP if next dose due soon, if high risk give immunoglobulin
Not up to date  -give DTP.  Immunoglobulin
Uncertain - give DTP

Immunoglobulin
Give 500iu if it's a high risk tetanus wound
Give 250iu if it's a tetanus prone wound
Need a second dose of Ig if they can't have DTP, or if they have reduced capacity for antibody formation - radiotherapy, hypogammaglobulinaemia

Give both injections in different arms
If have a bleeding disorder, give SC. There is a higher risk of reaction when these are given SC rather than IM.

Tetanus
Tetanus is caused by C. tetani, a gram positive, anaerobic that is commonly found in soil and manure. It produces tetanospasmin, the neurotoxin that causes tetanus. Incubation 10 days. The infection is a  clinical diagnosis, defined as trismus with one or more of the following:
Spasticity
Dysphagia
Respiratory distress
Muscle spasms
Autonomic dysfunction

Treatment
Metronidazole - stop bacterial replication
Diazepam or midazolam - to control muscle spasms
Intravenous tetanus immunoglobulin -5,000 units < 50kg, 10,000 >  50kg. This is the same as the "treatment".
Intubation - may be needed. Sux is safe but there is a very high risk of autonomic instability
Wound cleansing and debridement

SAQ:
A forty eight year old patient attends the emergency department feeling unwell. They have an infected injection site in their anticubital fossa. They have severe trismus, and are writhing around with severe muscle spasms. Sister thinks security needs to escort them out. You suspect that they have a serious and rare infection from their injection site.

a) How would you manage the muscle spasms?
Supportive care with diazepam or midazolam.
b) How would you treat their infection?
You suspect tetanus - or you should because of the spasms. The patient needs supportive care, with monitoring and consideration of early intubation. Give metronidazole to prevent bacterial relocation. Give IM tetanus immunoglobulin 150 units/ kg. IV is no longer available. Monitor their renal function.
Wound debridement.
Watch for autonomic instability, and cardiac collapse. Sedation, and morphine to help reduce the amount of free catecholamine can be helpful.
c) How would you confirm infection?
Tetanus is a a clinical diagnosis.
You can look for serum levels, but these take so long for results to come back - don't delay treatment for serological confirmation.
- Tetanus IgG - If the antibody level is >0.1 IU/ml before IgG, this excludes current tetanus infection. - Detection of toxin in serum is a bio-assay and is only performed if the antibody level is below the protective threshold.
- Absence of toxin does not exclude tetanus.
- Detection of C. tetani in wound material or from a pure isolate

References
http://pedemmorsels.com/tetanus-prevention/
http://stemlynsblog.org/tetanus-in-the-ed/
https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/441356/IMW166.02_Tetanus_information_for_health_professionals_v1.4__2_.pdf
https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/441355/IMW165.02_Tetanus_Immunoglobulin_Handbook_v1.4.pdf
https://www.gov.uk/government/publications/tetanus-the-green-book-chapter-30
https://www.rcemlearning.co.uk/modules/tetanus/
https://www.rcemlearning.co.uk/foamed/september-2017/#1504201252016-ac52229b-9e50