Wednesday, 22 November 2017

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

Monday, 20 November 2017

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>

Saturday, 4 November 2017

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

Tuesday, 31 October 2017

Adrenal Crisis


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 

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/

Tuesday, 24 October 2017

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

Thursday, 19 October 2017

Tetanus

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

Monday, 9 October 2017

Tumour Lysis Syndrome

https://lifeinthefastlane.com/ccc/tumour-lysis-syndrome/
http://bestpractice.bmj.com/best-practice/monograph/936/diagnosis/step-by-step.html
https://wikem.org/wiki/Tumor_lysis_syndrome
http://www.emdocs.net/9077-2/
http://dontforgetthebubbles.com/acute-lymphoblastic-leukaemia-day4/

Tumour lysis syndrome - probably something we've all seen in the ED, but never quite given a name. Is it important to give it a name - probably as it's a constellation of biochemical abnormalities that often requires intensive care treatment to correct...

What is it:
Cancer cells have got lots of electrolytes inside them. When they burst or lyse, normally due to chemotherapy, but maybe spontaneously, they release all these electrolytes into the circulation. Because in cancer there is a high cell mass turnover, this really causes problems.

Specifically:
- K+ up - rapid expulsion of intracellular K+ into circulation --> ventricular arrhythmias, weakness, paeasthesia, GI upset
- Tumour cells can have up to 4x normal levels of phosphate, so this is released by cell lysis. They need phosphate binders, and maybe dialysis.
The rapid increase in phosphate precipitates the calcium causing muscle cramps etc. Treat this with calcium only if they are symptomatic as there is a risk of precipitation with the phosphate.
- Release of purine nucleic acids into the circulation. Metabolised to uric acid --> renal failure. Allopurinol can help. No evidence for urine alkalisation.

It is more common in children and young adults with haematological malignancies, and normally happens at the beginning of their treatment. As we said, it can happen spontaneously but is normally 12 - 72 hours post chemo, and can be anything between -3 to 7 days before chemoterapy. It is most common in ALl, but can happen in other leukaemias, and poorly differentiated lymphoma like  burkitt lymphoma, high grade non- Hodkin). It can heppen in fast growing solid tumours. So unwell post chemo - might be neutropenic sepsis, but just have a think about the electrolytes.

All these electrolytes around cause renal failure is multifactorial but maybe due to volume depletion, cytokine mediated, precipitation of uric acid, calcium phosphate nephropathy.



Definition:
Cairo-Bishop Definition
Laboratory Tumour Lysis Syndrome:
Laboratory TLS is defined as an abnormality in 2 or more of the following, occurring within 3 days before or 7 days after chemotherapy:
Uric acid >476 micromol/L (8 mg/dL) or 25% increase
Potassium >6.0 mmol/L (6 mg/L) or 25% increase
Phosphate >2.1 mmol/L (6.5 mg/dL) in children or >1.45 mmol/L in adults (4.5 mg/dL) or 25% increase
Calcium <1.75 mmol/L (7 mg/dL) or 25% decrease from baseline.

Clinical
Laboratory syndrome + creatinie >1.5times upper age limit, cardiac dysrhythmia, seizure

Presentation
Presents with GI upset fluid overload, haematuria, symptoms of metabolic derrangements

Look for signs of metabolic derrangement
- arrhythmias, weakness, paraesthesia, tetany, renal failure

Investigate
All the electrolytes
- K+ high, phosphate +, calcium low, urea up, low bicarb, high LDH

Management
Prevention - allopurinol (inhibition of xanthine oxidase can last 18-30hours. Acts slowly so is more prevention), pre chemo hydration
 aggressive hydration, maybe with diuretics. Aim for 3L urine output in 24hours.
 metabolic correction
 support of renal failure

Rasburicase – a medication that converts uric acid to allantoin which is water soluble and excreted in the urine.

Often need ICU care for electrolyte correction

Further Reading
https://lifeinthefastlane.com/oncology-quandary-002/
https://emsimcases.com/2016/09/13/tumour-lysis-syndrome/ for a

Cerebral Venous Thrombosis

In a lot of places I work, headaches either go home for GP review, or get admitted as a ?SAH. And if they're a possible SAHs, they get a normal CT in six hours (maybe) and many go home without an LP. This really worries me, as there's loads of other serious causes of headache I don't think we exclude thoroughly. In the "old" days, a second doctor generally reviewed the ?SAH to do (or get the results of) a lumbar puncture. So one of the diagnoses we could be missing that worries me is a cerebral  venous thrombosis - this is dangerous to miss.


 Is there a difference between cerebral venous thrombosis and cavernous venous sinus thrombosis?
CVT and CVST have common underlying etiologies including thrombosis, and terms are occasionally used synonomously. CVST is specifically thrombosis in the cavernous sinus, normally with infection, so cerebral venous thrombosis is a safer term.

Pathology
If you can't remember your venous sinus anatomy, check out Andy's posts on emergency medicine ireland. I can not think of a better way to learn anatomy.
At a very basic level, what happens is you get a clot in one of the veins in the head, which causes problems. At its worst, this can cause death and coma. Middling effects present as a stroke, especially now anyone slightly lopsided seems to get a stroke call. At the "mild" end, a headache may be the only presenting symptom.

There are lots of theories about what is happening to cause these symptoms. It is thought that venous occlusion leads to the development of collateral veins, which combined with altered arachnoid absorption of CSF causes cerebral oedema - which can cause the headache. They can also cause cerebral venous infarction (in 50% of cases) and even haemorrhage.


Risk Factors
Excess Oestrogen: 
oral contraceptive pill: very common cause in female patients <50 years of age 2
pregnancy, IVF
puerperium - more common then than in the pregnancy

Clotty 
prothrombotic haematological conditions: 35% 2
e.g. prothrombin 20210 (factor II) mutation 7
infection: especially mastoid sinus (dural sinus occlusive disease - DSOD)
systemic illness
dehydration: e.g. gastroenteritis
sepsis
malignancy
connective tissue disorders

Local Factors
skull abnormalities/trauma
compressing mass: e.g. meningioma

steroids
idiopathic: ~12% - this is worrying. If you're going to get a rare disease, being in the rarest bit of rare is unlucky!

Presenting Features
Headache (70-90% of cases)
    There is no particular "type" of headache, but it is normally persistent. Onset may be sudden, like in sub-arachnoid, or gradual. Most patients present with symptoms that have evolved over days or weeks.
Headache is the most frequently (80–90%) occurring symptom in cerebral venous thrombosis and often the first symptom reported by patients. The International Classification of Headache Disorders describes the headache as having no specific characteristics[2] but one study found the headache was usually acute or subacute in onset, localised, continuous and moderate to severe.[23] Cases have been reported where headache is the only neurological symptom or sign but this is very rare.

"Stroke"
  Stroke without any typical risk factors, especially in young people may be due to CVT. Up to 75% of cases have focal deficit and headache.
Diplopia here (CN VI palsy) is a focal sign here, and should stimulate you to look for papiloedema...and really think hard about CVT.

Symptoms are not always classic, but they can be associated with the thrombus location.3,4
– Cortical vein thrombosis presents with motor and sensory deficits, as well as seizure.
– Sagittal sinus thrombosis may present with motor deficits, bilateral deficits, and seizures.
– Patients with thrombus in the lateral sinus may present with intracranial hypertension and headache alone.
– Thrombosis of the left transverse sinus can present as aphasia.
– Thrombosis of the deep venous sinus can cause behavioral symptoms due to lesions in the thalamus.

Cavernous sinus thrombosis is associated with ocular pain, chemosis, proptosis, and oculomotor palsies.3,4


 Seizures
 Seizures occur in 30- 50% of presentations, and they are often followed by a Todd's paresis. Superior sagittal sinus thrombosis (4%) can present with bilateral or alternating neurological deficits.

 Coma or encephalopathy
This isn't common, but you can get a rapidly progressive illness with deepening coma, headache, nausea and pyramidal signs, due to extensive involvement of the deep cerebral veins.
More often other clinical manifestations present at onset or develop during the course of the disease. These include papilloedema, focal deficits, altered consciousness, seizures and cranial nerve signs, in particular diplopia caused by sixth nerve palsy. Psychosis, in conjunction with focal neurological signs, has also been reported.[25] The development of symptoms may occur over hours, days or even weeks.


Examination Features
 Papilloedema
 Altered vision
 Neurological symptoms

Investigations
Examination of the cerebrospinal fluid (CSF) does not necessarily help in establishing the diagnosis as there are no pathognomonic features. Abnormalities are found in up to 84% of cases and include raised CSF pressure, increased protein content, the presence of red blood cells and pleocytosis.
D-dimers probably not useful

Radiology 
CT -             Often normal, but there may be subtle hyperdensity of the affected sinus or vein for the first 7 - 14 days. May have associated venous haemorrhage or infarction. Haemorrhagic infarcts may be multiple, in no particular location.

String Sign
Seen in 25% of patients with a cavernous sinus thrombosis. It looks like elongated hyperdense image relating to the brain parenchyma.

Dense Triangle
This can be seen in the first two weeks in up to 60% of patients. Fresh, coagulated blood causes a superior sagittal sinus opacification. The opposite of this is the empty delta sign, where contrast is administered highlighting an intraluminal filling deficit. It is not a specific sign.


Treatment
Anticoagulation - In the last Confidential Enquiries into Maternal Deaths in the United Kingdom report there were four deaths from CVT compared with eight in 2003–05.[22] The previous report expressed the hope that increasing application of thromboprophylaxis among at-risk women will reduce deaths from both pulmonary embolism and CVT but figures are as yet too small to draw a conclusion.[1]


General measures like proper headboard inclination, adequate oxygenation, and protection of airway due to risk of bronchoaspiration are recommended (although now this has been disproved in stroke, I wonder if its accurate).
Anti-convulsant treatment after even a single seizure is reasonable

Lumbar puncture not recommended by LITFL

Full References 
http://onlinelibrary.wiley.com/doi/10.1111/tog.12101/full
http://onlinelibrary.wiley.com/doi/10.1111/tog.12101/abstract
https://lifeinthefastlane.com/ccc/cerebral-venous-thrombosis/
http://pmj.bmj.com/content/76/891/12
http://www.emdocs.net/cerebral-venous-thrombosis-pearls-and-pitfalls/
http://emedicine.medscape.com/article/1162804-overview#a7
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3858762/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4517419/
http://emergencymedicineireland.com/2012/03/anatomy-for-emergency-medicine-8-cerebral-venous-sinuses/
https://radiopaedia.org/articles/cerebral-venous-thrombosis
https://emin5.com/2017/02/22/approach-to-headaches/
https://stmungos-ed.com/s/N8.pdf

Tuesday, 1 August 2017

Management part 3 - Safety and Risk

Blog post retyped as somehow, it converted itself into Greek (ish).


Incident – an untoward or unexpected event including verbal abuse and threats.
Accident – an incident that results in loss or damage like violence.
Clinical Incident – an incident occurring to a patient during or because of treatment.
Clinical Accident – a clinical incident that results in actual harm to the patient
Serious Incidents - where there is potential for learning, or high consequences to patients, families, and staff as so significant that they warrant extra resources to investigate.
Never Event - must be reported. See below.

Should be declared internally as soon as possible. Reports should be completed within 60 days. A root cause analysis should be carried out - there are three levels of this.  
- Concise, comprehensive or independent (which may take 6 months).

 

Negligible
Minor
Moderate
Major
Catastrophic

- Open and transparent
- Preventative
- Objective
- Timely and responsive
- Symptoms based
- Proportionate
- Collaborative

Check patient, and then staff are safe. Obtain and secure all evidence. Offer support to any witnesses. Identify someone to do an initial incident review, and determine level of investigation required. Inform commissioners. Contact family, and support Log on incident management
Serious incidents must be reported to the commissioner within 2 days, sooner if media / public interest.

Retained foreign object post procedure.
Giving strong K+ instead of something else
Parentally administered oral meds OD of insulin due to abbreviations or incorrect device
OD of midazolam due to wrong strength administered
Chest or neck entrapment in bedrails
ABO mismatch transfusion
Misplaced NG or OG tube
Scalding of patients

If it's moderate - severe harm --> report externally to CCG
Never Events must be AId
 - Investigate and always do root cause analysis regardless of harm to patient
 - Reported externally
 - Should be process to stop these happening

https://www.england.nhs.uk/patientsafety/serious-incident/
http://www.npsa.nhs.uk/nrls/improvingpatientsafety/patient-safety-tools-and-guidance/risk-assessment-guides/risk-matrix-for-risk-managers/

Thursday, 6 July 2017

Knee Aspiration

Contraindications
Joint replacement or prosthesis
Sepsis - local skin sepsis, bacteraemia, osteomyelitis
Cellulitis
Abnormal clotting eg haemophilia or anticoagulation
Immunocompromised or poorly controlled diabetes
Patient refusal.

Complications
Pain
Haemorrhage
Infection
Recurrence - of effusion or symptoms

Procedure
- Expose and position the knee in a relaxed semi-flexed position
- Palpate and identify the patella, patella tendon, and tibial tuberosity
- Mark a point approximately 1 cm medial and inferior to the lower pole of the patella, just medial to the patella tendon overlying the medial joint compartment
- Clean the skin
- Attach a 21G or 23G sterile needle to the syringe and insert the needle directly into the knee joint where previously marked
- Remove 10-20ml of fluid

References
http://bestbets.org/bets/bet.php?id=83
https://lifeinthefastlane.com/procedures/joint-aspiration/
http://learning.bmj.com/learning/modules/flow/JIT.html?execution=e2s1&moduleId=10033838&status=LIVE&action=start&_flowId=JIT&sessionTimeoutInMin=90&locale=en_GB&shouldStartAtQuestionSection=false

Ascites

Abdominal drains are part of our syllabus, but in practice they are normally not done in the ED.

Anatomy
The needle should not insert the rectus abdominus muscle, which is either side of the midline. This can cause epigastric bleeding. Aim for about 15cm lateral to the umbilicus.
Use the Z technique - pierce the skin, pull the skin tight, then aspirate.
The needle pierces:
    Skin
    Subcutaneous fat
    Superficial fascia
    External oblique muscle
    Internal oblique muscle
    Transversalis muscle
    Parietal peritoneum.

Contraindications
Patient refusal or distress
Pregnancy
Abdominal obstruction or distended bowel loops
Cellulitis overlying the puncture site
Severe coagulopathy

Complications
Abdominal Haematoma (1 in 100 patients)
Severe bleeding (haemoperitoneum)
Infection (secondary bacterial peritonitis)
Bowel perforation/organ damage
Persistent site leakage
Hypovolaemia or hypotension
Recurrence (highly likely unless followed up with diuretic therapy)

Causes of Ascites
High SAAG (“transudate”)
cirrhosis, hepatic failure, hepatic venous occlusion, constrictive percarditis, kwashiorkor, cardiac failure, alcoholic hepatitis, liver metastasis

Low SSAG (“exudate”)
malignancy, infection (bacterial, fungal, Tb), pancreatitis, nephrotic syndrome, bowel obstruction or infarction, bile leak

References
http://www.healthline.com/health/z-track-injection#what-are-z-track-injections1
https://lifeinthefastlane.com/ccc/ascitic-fluid/
https://lifeinthefastlane.com/procedures/paracentesis/
http://learning.bmj.com/learning/modules/end/JIT.html?moduleId=10033853&resType=&resTypeId=&locale=en_GB&presourceId=0&site=

Wednesday, 5 July 2017

Lumbar Puncture

None of the EDs I have worked in recently require us to perform lumbar punctures, but it is one of our competencies - so we should be able to do it...and could be tested on it! 

1.  Palpate the iliac crests and draw an imaginary line between the two. Mark this space (L3/L4) or the one below (L4/5) with a gentle indentation. Ask the patient if it feels like this is in the dead centre. 
Remember the spinal cord ends at L1/2 in adults. 

2. Surgically scrub. 

3. Clean the skin with antiseptic. If you're using a gallipot, remove the chlorhexidine after washing so there is no chance of accidentally injecting it. We should be using 0.5% chlorhexidine - it is better at preventing infection than iodine, and is less neurotoxic than 2%. 

4. Infiltrate local anaesthesia into the space

5. Insert a 20 or 22 gauge spinal needle into the space, with the stylet. 
You will pierce the skin, supraspinous ligament, the interspinous ligament, and then feel a slight resistance as you go through the ligamentum flavum. The needle then goes through the dura with a pop, and through the arachnoid into the sub arachoid space. 

6. Angle the needle slightly caudally, with the bevel parallel to the flanks so it pushes, rather than tears the dura. 

7. Check opening pressure if needed.

8. Collect CSF - get the patient to extend legs to speed up flow if needed. 

9. Replace the stylet before removing the needle to reduce pressure. 

10. Encourage ambulation. 

Complications
Post-LP headache
Infection
Bleeding
Cerebral herniation
Minor neurologic symptoms such as radicular pain or numbness
Late onset of epidermoid tumors of the thecal sac
Back pain

Contraindications
Possible raised intracranial pressure (headache, blurred vision, reduced GCS, vomiting, papilloedema)
Thrombocytopenia or other bleeding diathesis (including ongoing anticoagulant therapy)
Suspected spinal epidural abscess, cellulitis overlying the area

References

Monday, 26 June 2017

Vision Loss


Retinal Haemorrhage
This presents with sudden onset of floaters. Signs are reduced red reflex, with visible clots of blood. They must be seen by ophthalmology as retinal detachment presents very similarly, and can cause haemorrhage, and ophthalmoscopy can be normal.

There are lots of things that cause retinal haemorrhage, including:
diabetes mellitus                                      hypertension
raised intracranial pressure                      trauma and retinal detachment
retinal vein thrombosis                            subarachnoid haemorrhage
arteritis (giant cell arteritis, PAN etc.)     severe anaemia, especially pernicious anaemia
bleeding diathesis - defects in platelets (particularly leukaemia), coagulation factors, vessels.

Retinal Artery Occlusion
Sudden, painless visual loss. Central vision may be preserved if a cilioretinal artery is present. If suspected, patients should have ocular massage, and IV acetazolamide (500mg) to help. Make sure you exclude a temporal arteritis.

Central Retinal Vein Occlusion
Pizza pie on fundoscopy - flame haemorrhages with cotton wool spots. The artery has a cherry red spot with a pale macula.  Treat the cause (HT, DM,chronic glaucoma, hyperviscosity) and give antiplatelet.


Glaucoma
IV acetazolamide 500mg IV followed by 500mg PO (1g max in 24hours), topical antihypertensives (such as timolol drops) and miotics such as pilocarpine (1 drop in the affected eye), will reduce corneal oedema and lower intraocular pressure.

Subacute attacks
Subacute attacks with blurred vision, headache and pain around the eye, nausea and vomiting, and halos seen around lights, most commonly in the evening. They resolve spontaneously.

Non-traumatic Subconjunctival Haemorrhage
Exclude systemic causes - check BP, and coag if on anticoagulants.
Reassure patients - takes 2-3 weeks to heal

Episcleritis
You get localised conjunctival injection. It is normally benign, but may be associated with rheumatological diseases like RA, sarcoidosis, and IBD. Patients complain of irritation. It is self-limiting, but normally gets ophthalmology review to ensure it is not uveitis. The redness disappears 5 minutes after phenylephrine instillation.

Scleritis is also an inflammatory condition, frequently associated with an underlying rheumatological disorder. Patients complain of a deep dull aching pain in the eye, that is often worse at night, and ocular movement. The engorgement persists even after phenylephrine drop instillation.

Uveitis
The majority of cases have the HLA B27 serotype (so associated with sarcoidosis, ankylosing spondylitis, and IBD) but can also occur with herpetic keratitis, and after surgery.

Patients present with a deep, boring pain worse on accommodation. There is perilimbal injecition, and the pupil may be irregular.

Acute ischaemic optic neuropathy
Acute ischaemic optic neuropathy is most commonly caused by giant cell arteritis. Vascular wall inflammation leads to eventual occlusion, causing infarction of the optic nerve. This should be recognised, and oral prednisolone started. 1mg/kg/day for four weeks seems pragmatic. As giant cell arteritis is the most common cause, temporal artery biopsies should be performed.

A non ischaemic neuropathy usually affects young women. Pain is worse on eye movement, and visual acuity is normally reduced. There may be a central scotoma. Make sure you exclude a space occupying lesion, and refer urgently to ophthalmology.

Corneal Abrasion
Eye pads do not speed up recovery, and may worsen things.
Dilating drops are no long recommended.
Topical corticosteroids have been shown to slow corneal epithelial and stromal healing, increase the risk of infection, and cause serious scarring and visual loss if a dendritic ulcer has been missed.

Topical antibiotics may reduce the risk of infective complications in patients with a corneal abrasion. In contact lens wearers an anti-pseudomonal antibiotic must be used.

Infective Conjunctivitis 
Role of antibiotics is controversial.
Always prescribe topical antibiotics:
  Purulent / mucopurulent secretion and patient discomfort and ocular redness
  Patients and staff in nursing homes, neonatal units, critical care units etc
  Children going to nursery
  Contact lens wearers

Ultraviolet Burns

Topical and oral analgesics may be used
A mydriatic (cyclopentolate) may be helpful for photophobia due to ciliary muscle spasm

CS Spray
Dispersed as a fine dust. Irrigation can worsen the symptoms as it's highly soluble in water. Place the patient in a room, and blow a fan across, making sure no cross contamination occurs.

History and Working out what happens
- Rapid is generally vascular or retinal detachment. Slower may be a space occupying lesion.
- Partial loss of vision must be differentiated between;
    a loss of part of the visual field e.g. quadrantopia, hemianopia or central scotoma
    a curtain coming down across the vision a typical description of a retinal detachment
    flashes usually due to retinal ischaemia
    floaters due to opacities in the vitreous after retinal detachment

Examination
Local anaesthetic may be needed. Cyclopentolate takes 15-30min to work, Tropicamide - takes 15-30min to work, Tetracaine = really stings

Distance from patient to the chart / lowest line patient can be seen
Finger counting, then hand motion, then light perception

Look for aniscoria (unequal pupils) - normal in 19%. Pathologically, may occur due to release of prostaglandins on the sphincter pupillae. No reaction to light may be due to an occulomotor nerve palsy. Asides from trauma and eye drops, causes are:
Oculomotor nerve palsy (dilated pupil)
Holmes-Adie syndrome (dilated pupil)
Horners syndrome (constricted pupil)
Argyll Robertson pupil (constricted pupil)

To do fundoscopy you  may need dilating drops. Tropicamide is good - very tiny risk of precipitating acute glaucoma.

Ongoing Referral
Post op Patients:-
Less than 2 weeks post op
         Moderate or severe pain / visual loss IMMEDIATE
         Mild pain, no visual loss WITHIN 24 HOURS, in clinic if possible
More than 2 weeks post op
         Moderate or severe pain/visual loss WITHIN 24 HOURS
         Mild pain, no visual loss NEXT AVAILABLE CONSULTANT CLINIC

Flashing lights/floaters:-
Less than 6 weeks history
         Loss of vision/ field defect IMMEDIATE
         No loss of vision WITHIN 24 HOURS
More than 6 weeks history
         Loss of vision/field defect WITHIN 24 HOURS
         No loss of vision/field defect CONSULTANT CLINIC

Trauma:-(including foreign body/abrasion,chemical)
WASH OUT ALL CHEMICAL INJURIES IMMEDIATELY
Severe pain/risk of penetrating injury IMMEDIATE
Mild pain, including suspected foreign body WITHIN 24 HOURS

Sight loss or distortion
Sudden, less than 24 hours IMMEDIATE
              More than 24hours WITHIN 24 HOURS
Gradual, less than 2 weeks WITHIN 24 HOURS
              More than 2 weeks CONSULTANT CLINIC

Pain/photophobia
Assess if FB or abrasion first, if so assess for trauma
If associated visual loss use to increase priority if indicated
Severe or moderate IMMEDIATE
Associated general malaise/jaw claudication IMMEDIATE
Mild, less than 2 weeks WITHIN 24 HOURS
More than 2 weeks CONSULTANT CLINIC

Redness or swelling
Assess any associated symptoms eg pain ,photophobia, sight loss first to increase priority if necessary. Associated general malaise or pyrexia IMMEDIATE
Less than 2 weeks WITHIN 24 HOURS
More than 2 weeks CONSULTANT CLINIC

Double vision:-ALWAYS REFER TO ORTHOPTIST FIRST
Onset less than 2 weeks, pain and/or ptosis IMMEDIATE
                                        No pain/ptosis WITHIN 24 HOURS
Onset more than 2 weeks, ptosis and pain IMMEDIATE
                                          Ptosis/no pain WITHIN 24 HOURS

                                          No pain or ptosis CONSULTANT CLINIC




https://www.rcemlearning.co.uk/modules/sudden-visual-loss/
https://first10em.com/2015/06/16/ebmlecturehandout2topicalanaestheticsfocornealabrasions
https://www.rcemlearning.co.uk/references/eye-initial-assessment/
https://www.rcemlearning.co.uk/references/corneal-injuries/
https://www.rcemlearning.co.uk/references/atraumatic-red-eye/
https://www.rcemlearning.co.uk/modules/more-than-meets-the-eye/
https://www.rcemlearning.co.uk/references/eye-infections/
https://www.rcemlearning.co.uk/modules/the-blind-side/
https://www.rcemlearning.co.uk/curriculum/hst-acute/hap32/
https://www.rcemlearning.co.uk/foamed/ophthalmology-clinical-2/
https://www.rcemlearning.co.uk/modules/more-than-meets-the-eye/
http://learning.bmj.com/learning/module-intro/qt-red-eye.html?moduleId=10051483&searchTerm=%E2%80%9Ceyes%E2%80%9D&page=1&locale=en_GB

http://learning.bmj.com/learning/module-intro/glaucoma-diagnosis-and-management-in-primary-care.html?moduleId=10056345&searchTerm=%E2%80%9Ceyes%E2%80%9D&page=1&locale=en_GB

https://www.wikijournalclub.org/wiki/Optic_Neuritis_Treatment_Trial

http://learning.bmj.com/learning/module-intro/sticky-eye-diagnostic-picture-tests.html?moduleId=6056483&searchTerm=%E2%80%9Ceyes%E2%80%9D&page=1&locale=en_GB

http://learning.bmj.com/learning/module-intro/sticky-eye-diagnostic-picture-tests.html?moduleId=10007412&searchTerm=%E2%80%9Ceyes%E2%80%9D&page=1&locale=en_GB

http://learning.bmj.com/learning/module-intro/.html?moduleId=10053762&searchTerm=%E2%80%9Ceyes%E2%80%9D&page=1&locale=en_GB

http://emj.bmj.com/content/17/5/324

http://learning.bmj.com/learning/module-intro/red-eye-diagnostic-picture-tests.html?moduleId=5004450&searchTerm=%E2%80%9Ceyes%E2%80%9D&page=1&locale=en_GB

https://www.rcem.ac.uk/docs/Local%20Guidelines_Audit%20Guidelines%20Protocols/12ri.%20Red%20Eye%20Algorithm.pdf
https://www.rcemlearning.co.uk/modules/in-your-face/

https://lifeinthefastlane.com/resources/retinal-haemorrhage-ddx/

Wednesday, 21 June 2017

Genital Ulcers

Genital Ulcers are specifically mentioned on our syllabus. They are more likely to be non sexually tramsitted than sexually transmitted (surprisingly!).

Herpes
HSV1 is now the most common cause of genital herpes. HSV2 is more likely to result in recurrent episodes. The majority of infections are subclinical and symptomatic viral shedding, or symptomatic lesions can occur.

Get painful ulceration, dysuria, urethral or vaginal discharge. May get fever and myalgia. On examination, you get blistering and ulceration with painful lymphadenopathy.

Treat with a full sexual health screen, and oral aciclovir. Condoms won't reliably prevent transmission - abstain for a week after symptoms resolve.

Syphillis
Syphillis should be treated in specialist GUM clinics. It is more common in MSM. It normally presents with a painless ulcer, with a clean base. Secondary infection has multisystem involvement.


Bechets
A systemic vasculitis of unknown aetiology (not considered to be auto-immune), that typically starts in young adults. You get recurrent oral and genital ulceration, uveitis, skin changes, arthritis, neuro involvement and tendency to thrombosis. It is prevalent in Japan, the middle East, and some Mediterranean countries. Treatment depends on which organ is involved.
Genital ulcers are less common than oral ulcers.

Reactive
EBV, CMV and parathyphoid can cause post infective or reactive genital ulcers (lipschutz ulcers). They can be very painful, and associated with lymphadenopathy. They normally resolve within a few weeks. The ulcers normally have a yellowish centre, that may become black due to tissue necrosis, with a surrounding red rim. They may be associated with swelling.
Take viral and bacterial swabs. Look for underlying illness, and test for EBV. Treat according to the cause.

Crohn's
Cancer
Pemphigus
Pemphigoid
Steven-Johnson syndrome
Erythema multiforme

References 
http://www.dermnetnz.org/topics/non-sexually-acquired-genital-ulceration/
http://www.aafp.org/afp/2012/0201/p254.html
http://www.gpnotebook.co.uk/simplepage.cfm?ID=-1167392705
http://pmj.bmj.com/content/76/900/629
http://learning.bmj.com/learning/module-intro/genital-ulceration-diagnosis-management.html?moduleId=10058483&searchTerm=%E2%80%9Culcers%E2%80%9D&page=1&locale=en_GB

Tuesday, 20 June 2017

Penile Problems

Most penile problems are better evaluated if you have a nerve block in place.

Dorsal Penile Nerve Block
The two dorsal nerves are at 10 and 2 o'clock positions at the root of the penis.
Ramifications of these nerves usually commence 1 cm distal to the penile root, and a nerve block should be just proximal to those.
The depth of the needle need not be more than 0.25 to 0.5 cm.
Aim to hit the pubic symphysis, and then go below.

Phimosis
Check for diabetic control
Palpate the glans - and if there is a lump, refer urgently to urology
Consider a steroid cream - like betnovate

Paraphimosis
Remove a catheter or any piercings first
Start with analgesia - a nerve block might be helpful!

Manual Reduction - put pressure or a compression bandage on the distal penis
Ice 
Sugar on glans and penis
Puncture oedematous band
After reduction, urology follow up as is likely to happen again!

Fracture of the Penis
Differential is rupture of the deep dorsal vein of the penis
- You don't hear a crack or popping sound
- Detumescence doesn't occur
- Needs to be surgically explored
- Can get urethral injury

Priapism
Most of the time, this is primary (idiopathic) 40%

Secondary causes:
  Haematological   (sickle cell, leukaemia, myeloma)
  Neurologic    (spinal cord injury - leave these alone, time heals)
  Traumatic   (genital, perineal) 10%
  Neoplastic   (bladder, prostate)
  Medication   (antipsychotic like chlorpromazine and haloperidol   antidepressants like fluxetine, anticoagulation, recreational drugs like cocaine, intracavernosal injections)

  - analgesia
  - hydration
  - exercise (run up and down the stairs)
  - cold bath, or maybe a warm bath
  - therapeutic masturbation can help
  - involve urology team for drainage. This needs written consent - there is a high risk of associated impotence. It involves consent, cleaning, inserting a needing into the side of the penis to a depth of 1cm, take blood gas, then aspirate up to 100ml thick dark blood.




References 
http://bestpractice.bmj.com/best-practice/monograph/765/treatment/step-by-step.html
https://wikem.org/wiki/Priapism 
http://www.foamem.com/2015/04/17/priapism/
http://pedemmorsels.com/phimosis/
http://learning.bmj.com/learning/module-intro/.html?moduleId=10057996&searchTerm=%E2%80%9Cphimosis%E2%80%9D&page=1&locale=en_GB 

Saturday, 17 June 2017

Myocardial Infarction

Definition
ST Elevation 1mm in limb leads
ST elevation 2mm in chest leads
New LBBB
Posterior MI - Tall R waves in V1-V3 ST depression +/- T wave inversion
 plus CP within 10 hours

Features
Diaphoresis is the strongest predictor of AMI, as is nausea and vomiting, and radiating to both shoulders.
Severity of pain is not associated with the likelihood of MI.

ECG Diagnosis

 II, III, aVF = inferior leads
   V1-V2 = septal leads (not V3, V4 as seen in some texts (see Zipes et al, 2004))
   V1-V6 = anterior leads

   I, aVL, V6 = lateral leads


Treatment
Aspirin - inhibits platelet aggregation by inhibiting cyclo-oxygenase, and thus formation of thromboxane A2.

Clopidogrel - promotes formation of platelet c-AMP, lowering platelet calcium, and reducing platelet aggregation.

Ticagrelor - anti-platelet agent that is a useful alternative to clopidogrel.


Fondaparinux - factor Xa inhibitor that has less associated bleeding complications.

Right Ventricular Infarction
In 50% of patients with inferior myocardial infarction, the clinical triad of high central venous pressure, clear lung fields, and hypotension combined with right sided ECG changes is strongly suggestive of right ventricular infarction. Look for this carefully using a V4R which may confirm ST elevation, and do an echo.
This is treated by maintaining right ventricular preload, so drugs that reduce preload (nitrates and opiates) should be avoided. Fluid challenge is important, with careful monitoring.

Troponin
A protein, involved in muscle contraction. Very cardiospecific, with little crossover into skeletal muscle. In renal failure, troponin just isn't cleared as quickly, so can be falsely high. With a roche or abbot high sensitivity troponin - normal at arrival and three hours = rule out ischaemia.
Troponin peaks within 12 - 24 hours, and remains elevated for about two weeks.

Remember troponin is normal in unstable angina

Cocaine Associated
Cocaine causes a sympathomimetic response, with increase in heart rate and blood pressure. It can cause acute thrombosis of the coronary artery - this is probably due to more than an increase in platelet count and activation.
Make sure you rule out aortic dissection as well, and “crack lung,” -  hypoxemia, hemoptysis,
respiratory failure, and diffuse pulmonary infiltrates. Also, think about MI if patient presents with dyspnoea or diaphoresis.

Troponin is still very useful, and about two thirds of MI events occurred within 3 hours of cocaine ingestion. ECGs are abnormal in 56 - 84% of patients, although this may be early repolarisation mis-interpreted.

Treat as per normal ACS, but make sure you give early benzodiazepines. GTN might still help. Beta blockers are probably safe.



References
http://circ.ahajournals.org/content/117/14/1897
http://calgaryguide.ucalgary.ca/wp-content/uploads/image.php?img=2015/04/MI-Findings-on-Investigations.jpg
https://www.rcemlearning.co.uk/modules/chest-pain-syndromes/
https://www.aliem.com/2013/03/chest-pain-value-of-good-history/
https://www.rcemlearning.co.uk/modules/management-of-stemi-and-its-complications/ 
https://www.rcemlearning.co.uk/modules/unstable-angina-and-non-stemi-risk-assessment-and-management/ 
https://www.aliem.com/2010/11/paucis-verbis-sgarbossas-criteria-with-lbbb/
https://www.aliem.com/2013/05/pv-card-early-repolarization-vs-stemi-on-ekg/

Wednesday, 24 May 2017

Prostatitis

There are four main types of prostatitis and each of these is managed differently. In the emergency department, we are most likely to see acute bacterial prostatitis,but might also see chronic infection and pain.



Acute Bacterial Prostatitis
Acute prostatitis is a common disease amongst men over 50 years of age, especially those who are immunocompromised, like in diabetes or HIV/AIDs.  CKD causes immunocompromise - but I couldn't find any obvious links to CKD and prostatitis!

It often presents with frequency, urgency and dysuria. In women, we might attribute these symptoms to a UTI, but UTI is rare in men without anatomical abnormalities, until the prostate starts to get bigger, increasing the frequency again. We should consider doing a scrotal, genital and rectal examination in any man diagnosed with a UTI, to check there isn't something else.

There might be obstructive voiding symptoms in >80% of patients. 38% of people get perineal discomfort which may present as back or rectal pain.
Some people get systemic features. Can get fever in 60% - 86%, maybe with rigors, malaise and myalgias.

Cause - 
Prostate biopsy - happens in 2% of cases - http://www.ncbi.nlm.nih.gov/pubmed/20577611
Resistance to prophylaxis - http://www.ncbi.nlm.nih.gov/pubmed/21782225
E-coli being the most common pathogen.
Can spread by incomplete voiding.

Sneezing whilst voiding - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4556327/
Sexually transmitted

What examination--> 

Examination - Look for signs of urinary retention. If in retention, go for an SPA
Classically described as ecquisitely painful and boggy, actually you only get a  painful prostate in 68%. Pain or symptom reproducability is probably the most important symptom.    http://www.ncbi.nlm.nih.gov/pubmed/15822390.


Investigations - 
Urinalysis - send sample off for culture.
               Leucocytes and nitrites have a great positive predictive value, but not a great negative predictive value. http://cid.oxfordjournals.org/content/46/6/951.long


 Do NOT do prostatic massage to get a sample - may make things worse!
 Blood cultures - positive in 8 - 21% of cases http://www.ncbi.nlm.nih.gov/pubmed/20237098  http://www.ncbi.nlm.nih.gov/pubmed/17969797
 CRP raised in most cases
If there's microhaematuria on the dip, make sure it gets repeated as it might be a sign of cancer.
 PSA - not clear role, but has a high negative predictive value - http://bestbets.org/bets/bet.php?id=1585
PR without prostatic massage makes minimal difference to the serum PSA value and generally does not cause a clinically significant increase in PSA levels. However, some studies have found that there may be a minority of men in whom the procedure raises PSA. [ 6 ] For this reason some experts recommend that blood for PSA testing should be taken before DRE.

Urethral catheters are allowed in "experienced" hands but pre-treatment with appropriate antibiotics is mandatory. If the catheter is difficult to pass, a suprapubic is indicated.

So how do you tell if someone has prostatitis, or just a UTI? And like many things, there's no real answer. If they've got a painful or boggy mass on examination, then the answer is easy! If they haven't...could it still be prostatitis? Generally, yes it could be. The patients are normally significantly unwell - the risk of bacteraemia is increased in severe UTIs like pyelonephritis and prostatitis. I think it's reasonable if you have a really really sick ?urinary sepsis, to assume prostatitis until proven otherwise.
Review after 7 days 

Treatment - antibiotics
- Broad spectrum (cephalosporin) plus gentamycin if patient is systemically unwell.
- If oral antibiotics are appropriate, use
o Ciprofloxacin 500mg BD for 28 days or
o Ofloxacin 200mg BD for 28 days
- If patient is allergic to quinolones, consider trimethoprim (200mg BD for 28days) as an alternative. It needs to be for a long time because the prostate has quite a poor blood supply.


Laxatives - if defacation uncomfortable
Rest
NSAIDs
It is possible to add on an alpha blocker such as tamsulosin which has been proven as an beneficial adjunct for symptom relief.
Hydration

A referral to the Urology Team should be made upon discharge.

If fails to respond, arrange trans-rectal USS or CT of the prostate to R/U prostate abscess. Prostatic abscesses are relatively uncommon due to clinical practice due antibiotic therapy. Like prostatitis, common presenting features are dysuria, fever, suprapubic pain +/- urinary retention. Urine examination usually reveals pus cells.  The organisms usually involved include:
Escherichia coli
Staphylococcus spp
Gonococcus spp: rare


You should delay PSA testing for six weeks after treatment for a urinary tract infection.
Ciprofloxacin is the antibiotic which the Prostatitis Expert Reference Group (PERG) recommends as first line treatment for chronic bacterial prostatitis and chronic prostatitis/chronic pelvic pain syndrome. It has excellent penetration into the prostate, good bioavailability and good activity against typical and atypical pathogens. Treatment should be guided by bacterial cultures and sensitivities once these are known. You should continue treatment for at least four weeks. Options for second line antibiotics include trimethoprim or a tetracycline such as doxycycline.



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The chronic forms of prostatitis are common and debilitating and between 35 to 50% of men report symptoms suggestive of prostatitis at some time in their life.
Prostatitis is a common urological diagnosis in men under 50 years old and is most prevalent in men aged 36 to 50 years.


Four main domains of symptoms of chronic prostatitis/chronic pelvic pain syndrome [ 1 ]
Pain
Lower urinary tract symptoms
Psychological issues
Sexual dysfunction
and these are beyond the remit of this podcast.



http://emedicine.medscape.com/article/2002872-treatment#d10
https://cks.nice.org.uk/prostatitis-acute#!diagnosissub
http://www.racgp.org.au/download/Documents/AFP/2013/April/201304dickson.pdf
http://www.primarycareurologysociety.org/downloads/2015presentations/Jon%20Rees%20Prostatitis.pdf
https://uroweb.org/wp-content/uploads/19-Urological-infections_LR.pdf
http://www.rcemlearning.co.uk/modules/acute-urinary-retention/
http://radiopaedia.org/articles/prostatitis
http://radiopaedia.org/cases/acute-bacterial-prostatitis-and-abscess
http://wikem.org/wiki/Prostatitis

http://learning.bmj.com/learning/modules/flow/ICH.html?execution=e1s1&moduleId=10051979&status=LIVE&action=start&_flowId=ICH&sessionTimeoutInMin=90&locale=en_GB&shouldStartAtQuestionSection=false