Author: Mark Winstanley / Published: 04/10/2019
Dose the administration of the chinese herbal remedy XueBiJing improve outcomes in pneumonia
XueBiJing Injection Versus Placebo for Critically Ill Patients With Severe Community-Acquired Pneumonia: A Randomized Controlled Trial
Song, Critical Care Medicine, June 2019
– this is not new. I found a systematic review of 49 RCTs of this stuff that were almost all positive. At the very least it’s worth looking at the evidence
– in case you don’t know what this is “Carthamus tinctorius, radix paeoniae rubra, ligusticum wallichii, salvia miltiorrhiza, angelica sinensis, etc…” (from Shi et al 2019 AJEM)
– theory is that it’s “blood activating, stasis dissolving, scattering toxins and controlling the exaggerated inflammatory response.” If that all sounds like homeopathic nonsense then fair enough but remember we have a similarly vague and unsatisfactory theory for steroids in sepsis.
– large double blind RCT in China
– had to have severe pneumonia to get in but excluded folk with “severe primary diseases” and don’t elaborate which makes me a bit sceptical
– randomised to 100mls of XueBiJing IV for 5 days versus placebo. Everyone got antibiotics and steroids if needed (there’s actually a reasonable evidence base supporting steroids in pneumonia in sepsis)
– unfortunately powered to look at improvement in pneumonia severity index at 8 days, which is not very patient orientated and not at all what that scale was designed for.
– 700 patients, 60% ventilated
– 60% improvement in the XueBiJing group v 45% in the standard group
– while not the primary outcome mortality was 16% v 25% favouring XueBiJing and the separation didn’t become apparent till at least 2 weeks in.
– everyone, including myself is probably appropriately sceptical about this stuff. We have little idea of how it works and we dismiss it as it comes from the realms of “traditional chinese medicine”. Yet there’s probably more evidence for this than there is for the vitamin C cocktail that’s out there at the minute for sepsis.
– I will not be reaching for this in my next ICU shift but I would love to see a decent RCT of this stuff in a western context to see how it holds up in a practice more similar to our own.
Dr Becky Maxwell @maxirebecca
Dr Chris Connolly @chrisconnolly83
This podcast is based on the latest NICE Guidance on Renal colic published in January 2019.
The Guideline doesn’t give any actual diagnostic criteria, for me it is someone who presents to the ED in SEVERE pain, usually loin to groin… if suspected do a urine dipstick, this can help with the diagnosis if there is micro (or microscopic haematuria), but remember 15% of patients with renal colic will have no blood in the urine! So whilst supportive of the diagnosis cannot use urine dip to rule it out…. the sensitivity is around 85% and the PPV around 70%.
The first part of the guideline mentions that we should arrange the following imaging:
• Offer urgent (within 24 hours of presentation) low-dose non-contrast CT to adults with suspected renal colic. We get these pretty easily (probably too easily in my opinion!) pretty much 24/7, if the patients pain has settled we can discharge them and bring them back the next morning for a reserved CT slot where they go straight to CT then book back into us….
• What about young people? The guideline mentions for children and young patients meaning patients under 16 do an USS first.
• If uncertain about the diagnosis proceed to low dose CT scan without contrast
• Offer a non-steroidal anti-inflammatory drug (NSAID) by any route as first-line treatment for adults, children and young people with suspected renal colic – I tend to go straight for PR diclofenac – works like a dream
• IV paracetamol should be offered if NSIADs contraindicated or not working (I tend to use both of these together to be honest)
• Consider opioids for adults, children and young people with suspected renal colic if both NSAIDs and intravenous paracetamol are contraindicated or are not giving sufficient pain relief
• Do not offer antispasmodics to adults, children and young people with suspected renal colic
We refer all for an OP appointment but discuss the following
• Stones > 6mm
• Hydronephrosis/ hyrdroureter
• WCC >16
• Ongoing high analgesia requirements
All patients get an Xray KUB on their way out of the dept. (we don’t review but urology use it at clinic)
Tamsulosin or not… to be honest I can’t keep up with what urology want as they seem to have changed their position on this a fair bit but this guideline does recommend that you give an alpha blocker to those with stones less than 10 mm
ADVICE ON DISCHARGE:
I’m pretty bad at this on reading the guideline – I usually tell them to drink plenty of water, avoid dehydration particularly if it is warm outside but not much of the rest of the guideline suggests…
• adults to drink 2.5 to 3 litres of water per day, and children and young people (depending on their age) 1 to 2 litres
• adding fresh lemon juice to drinking water a quick Google search by Chris says it can increase citrate levels which reduces stones
• avoiding carbonated drinks – This is due to phosphoric acid in the drinks apparently
• adults to have a daily salt intake of no more than 6 g, and children and young people (depending on their age) 2 to 6 g
• not restricting daily calcium intake, but maintaining a normal calcium intake of 700 to 1,200 mg for adults, and 350 to 1,000 mg per day for children and young people (depending on their age)
Dr Nikki Abela @nikkiabela
Dr Paul Reavley @paulreavleypaul
Dr Nikki Abela @nikkiabela
Dr Anna Dobbie @dobbieanna
– should we be using intralipid in our overdose patients?
– Utilization of lipid emulsion therapy in fatal overdose cases: an observational study
– Smolinske, Sept 2018, Clinical Toxicology
– Intralipid came on the tox scene around 15 years ago as a rescue treatment for local anaesthetic toxicity. They call it “intrvenous lipid emulsion therapy” (ILE) in this paper but that sounds too much like something you can get on a 3 for 2 special in B and Q. If you accidentally gave a bunch of bupivacaine IV and the patient seized and had a cardiac arrest then intralipid might save the day. The drug itself is concentrated triglycerides and is part of the make up of a bag of TPN. There has been a definite degree of “indication creep” over the years and it became compulsory in any talk on tox to include intralipid somewhere, just as it’s compulsory to include ECMO in any talk on anything today. There are a few theories as to how it might work. the first was the lipid sink – the idea that if you flood the vasculature with lipid then the lipid soluble poison might be taken up by it and reduce the toxicity, secondly it was thought that all those triglycerides act as a sort of superfuel for the failing poisoned heart. I have never used it but have always had a list of cases and trigger points in my head as to when i might give it. And this paper made me curb my enthusiasm so to speak
– this is a review of large scale poison centre data from the US. So lots of caveats here – you only get in this study if someone rang the poison centre. That seems to be fairly common practice in the US but seems to be done quite rarely in the UK or Ireland.
– they only included people who got lipid therapy and who died. This was mainly due to the logistics of the data base as they couldn’t track those who got ILE and lived.
– they split the ILE administration into 4 indications (cardiac arrest, last resort, first line and the wonderfully titled “cocktail”
– they had a similar method of tracking the response to ILE
– 460 patients between 2010 and 2015
– clear trend of it becoming more common over time
– 2/3 were for Ca channel blockers or beta blocker poisonings. Of note the guidelines (for what they’re worth) recommend it for LA, buproprion and TCAs only…
– only 20% or so were given it for what they feel were legitimate reasons
– in terms of what happened when it was given: half the time there was on change. another 40% it wasn’t clear if there was a +ve or negative effect.
– 10% had fairly clear adverse events
– this is low level of evidence but that is kind of the point. The authors make the point that all the indication creep was driven by even lower level evidence and hugely affected by publication bias.
– given the potential for serious adverse effects we should be fairly cautious in how we employ it.