Lower Back Pain
Lower back pain presentation to A+E is a classic, its one that that we see a lot of and often there isn’t a dangerous underlying pathology.
I find it’s a great example to demonstrate the EM classic thought process of what is the worse case and what’s the most likely condition. In thinking this way we can clinically and through our investigations make sure the patient is appropriately and safely managed – remember that safety netting is a management tool in our armoury.
It’s a worthy exercise to think through the problems that can present with lower back pain and then think of the suggestive features and investigations required to finalise the diagnosis. Lets start by casting a really wide net and think about anything that might present with lower back pain – it is probably worth using a Structured approach to help make sure we don’t miss anything (see the 2 examples, neither of these lists are exhaustive but cover most hopefully).
As an aside, we can also do the same for upper back pain (as a thought experiment, rather than a tangent)
So in the session at this point we will build a structured assessment for back pain that is easily and quickly repeatable.
Use the differential list to determine what we are going to assess and how. Hopefully we will generate a red flags list as we go.
Red flags and reasons:
Now just the list of red flags is almost useless in real life practice without the understanding of what we are looking out for in behind them. Now we have an understanding of what we are looking for we can start build out an assessment. Its easy to use a blunderbuss approach to our assessment and history taking but as we progress we want to become more refined in what we are doing. To refer to some of the other work we have been doing our “illness script” needs to be precise enough to allow us to work through our differential rapidly (see the clinical reasoning section). We should all be able to take a history and examine a patient thoroughly so what is going to help refine our differential appropriately is understanding the potential conditions we may have as part of our differential. Let’s start with the big one that causes us the most problems in ED but also has potential significant problems for the patient.
Cauda Equina Syndrome (CES)
Here I will cover CES as a problem and will refer to both the RCEM recommendations and the recent national guidance released by NHS England (GRIFT) in conjunction with neuro/spinal surgery and radiology (note not Emergency medicine or General Practice).
The problem with CES is that it is a time critical condition with a very low sensitivity of clinical findings and so MRI is the gold standard for diagnosing. Whilst any peripheral neuropathy and back pain is most likely to be a lumbar disc prolapse and the most common cause for CES is central disc prolapse, the actual incidence of CES in patients presenting to ED is 1.0/100000.
Given the diagnostic challenges and the potential for significant harm if left untreated everyone is agreement that prompt MRI should be strived for, however, the realty is that this isn’t achievable in most large centre emergency departments, let alone DGS. If you want to read RCEMs take on this you can here.
So now we’ve looked at some of the politics, what is CES?
Firstly it is worth remembering that CES does not have a set of symptoms, a clinical pattern and cannot be ruled out with physical testing if subjective symptoms are present.
Patients presenting with the any of the following in the last 14 days in addition to back or leg pain warrant urgent MRI:
- Difficulty initiating micturition or impaired sensation of urinary flow
- Altered perianal, perineal or genital sensation(S2-5), this can be objectively tested or subjectively reported
- Severe or progressive neurological deficit of both lower limbs
- Loss of sensation of rectal fullness
- Sexual dysfunction, the ability to achieve erection or ejaculate or loss of genital sensation
Sudden onset bilateral radicular leg pain or unilateral radicular pain that has progressed to bilateral leg (sciatica) pain maybe a warning symptom for CES
(Radicular: pain associated with compression of a nerve causing pain radiating along the dermatome of the nerve)
- These patients require a 2WW to an MSK triage service as long as they don’t have any of the other CES features
Bladder Scans
- Useful as an adjunct to an assessment but should not be used as a discriminator in deciding to request MRI or undertake emergency surgery (60% of emergency decompression surgeries had a residual, post void bladder volume of <200ml)
- We should be catheterizing anyone with a residual volume of >600ml in the context of CES to avoid bladder distention injury
- If they retain >200ml then CES is 20x more likely
MRI
- The current aim from both the surgical teams and from RCEM is to scan any suspected CES within 4 hours. However, there are recognized limitations for this in terms of service capability.
- Each trust and region should have its own agreed policy to manage this situation in as a timely manner as possible.
- The suggested way of working around this includes:
o MRI should be an SDM decision from the assessing team, not the surgical team, in an attempt to avoid delays
o If we are doing an emergency scan the patient should be NBM to reflect the potential need for urgent surgery when the scan is performed
o Surgical teams should be happy to review the imaging prior to radiology report
o Patient with absolute MRI contraindications should be reviewed by the surgical team to determine the appropriate path forward ie CT or CT myelogram
Abdominal Aortic Aneurysm
This is one of those presentations that, much like aortic dissection in chest pain, we never want to miss in patients with back pain.
The horror story is always in elderly patients presenting with what seems like a new renal colic – in terms of practice, old people, new renal colic it never is until AAA rupture has been ruled out.
Most AAAs are symptomatic until they rupture. When they present with back and abdominal pains, they may have a palpable abdominal mass and they are likely to have hypotension and potentially signs of lower limb ischaemia.
Normal infrarenal aorta size is 1.7cm in men and 1.5cm in women – if bigger than 1.5cm (or 3cm) then this is pathological.
There is potential for atypical presentations which is one of the reasons we have to discuss all our >75 abdo pains with an SDM and why we do AAA screening in the A+E department.
It is worth noting that our US screening shouldn’t be used as a replacement for CTA to assess the true size and calibre of the aorta. When we see a AAA rupture on US it looks like this, its referred to as a the donut sign:
Our initial management is all about assessing the suitability of the patient for a major abdominal surgery in conjunction with the vascular team, whether they are on site or at a tertiary service. The discussion should be had even for patients who have previously been turned down for elective surgery of their AAA.
These conversations should include the patient and the family where possible as this is likely to be terminal or significantly life changing event even with intervention. Without intervention mortality is 100% after 3 days. With rapid intervention mortality can be as low as 20% (note this is still very high for an operation and condition and in some centres it’s still is 40%, its just much much better than 100%). The longer the delay to treatment the worse the outcome is – progressive volume loss into the abdomen/retroperitoneal space leads to progressive hypotension, compromising everything but there is also potential vessel occlusion from the AAA its self, causing gut or renal ischaemia.
To reinforce the time critical nature of the presentation, patients that have been intubated, arrested or started on vasopressors prior to transfer to a vascular centre are unlikely to survive transfer let alone the necessary procedures, and so need serious consideration and discussion about whether to transfer them.
In terms of management, there are no specific EM interventions after rapid diagnosis and referral that make a significant difference. It is time that matters most. However, maintaining normal physiology and avoiding hypertension through resuscitation with blood products, correction of coagulopathy and establishing appropriate investigations to facilitate an emergent operation is well within the remit of an EM team. This boils down to large bore IV access (ideally 2), FBC, U+Es, Coag, LFTs, amylase, VBG, CT/US to confirm and then resuscitation with fluids + bloods products when available if not delaying transfer. Urinary and central venous catheterisation will be helpful down the line but should not delay transfer.
Symptomatic treatment of acute musculoskeletal lower back pain
Now this is almost a diagnosis of exclusion for patients when they arrive in the emergency department, but unlike some other diagnosis of exclusion the other potential pathology maybe exclude very quickly in a brief assessment.
Back Spasm itself is a very common A+E presentation and is a quick and easy diagnosis to make – they have a locked up, painful back. Often they have had a preceding injury in the last few weeks but there is not always a incident the patient can recall.
There is little evidence for managing acute lower MSK back pain beyond analgesia and movement. I find that the use of paracetamol, NSAID, codeine and diazepam (if there is spasms) is often sufficient to get them moving and then the movement its self allows for a continuation of their rehab and therefore their pain management.
A good explanation for how to manage MSK back pain is that the movement helps the pain settle, the analgesics/muscle relaxant allows for that movement and breaks the cycle of the back pain causing spasm limiting movement and the lack of movement exacerbates the pain and precipitates further spasm.