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