Would you have spotted how to save two hours of investigations? | Podcast

A girl with factor V leiden presented with two episodes of loss of consciousness.

The losses of consciousness occurred while she was in bed at around 8am, and neither episode was witnessed. There were no warning signs. There was no chest pain, palpitations, shortness of breath or sweats. The first episode probably lasted three to five minutes according to the patient (using clocks in the room) and she felt very tired afterwards. The second collapse happened about 20 minutes later and was similar in nature. There was nothing suggestive of seizure activity.

A pregnancy test was positive. She thinks she may have miscarried a few days before based on copious PV bleeding, but was not sure.

After appropriate investigations, no cardiac or neurological pointers were found.

The post-take ward round planned to send her home after PE was ruled out.

Going back to my post on the 12 causes of syncope, PE was the only serious cause left to rule out.

At this point, we actually had enough information to discharge her with full medical justification, but we did not realise this at the time and carried on the work up for PE. Can you see what we had overlooked?

The fact that she may have been pregnant made investigations a bit tricky. CTPAs are avoided in pregnancy as much as possible, and half dose V/Q scans are considered a necessary evil in selected cases. A miscarriage seemed likely, but it was difficult to be sure what her current pregnancy status was. Her Well’s score was 0, but then again the Well’s score does not take into account thrombophilias. Is this a high risk or low risk pretest probability? In any case if she were pregnant, the d-dimer would be raised. Was a d-dimer justified in this scenario?

Interestingly, Factor V Leiden poses a paradox, as it causes an increased risk of DVT but not pulmonary embolism. Go figure.

An early pregnancy assessment unit ultrasound was done. The endometrium of the uterus was thin and no foetus was visible, which all but ruled out a normal pregnancy.

The patient’s consultant had long since gone home, so I spoke to the on call consultant.

This consultant said something which has stuck with me.

“Surely if it were a massive PE leading to a collapse, she would be periarrest?”

“Oh yes.”

There are four severities of PE:

1. Cardiac arrest
2. Massive PE (BP<90mmHg or drop of 40mmHg for 15 minutes)
3. Submassive PE (signs of right ventricle strain/failure)
4. Non massive PE (everything else)

To have a loss of cerebral perfusion secondary to a PE, you would have to be at least a massive PE. There is no way the patient would be walking and talking.

Had anyone thought of this at the start, the patient may have been discharged during the day.

This episode inspired me to make a podcast on PE management with a friend, in line with the BTS guidance.

[Edit: 1/10/2012: I have added video bits to the podcast]


The best kept cannulation secrets | Follow up of stroke thrombolysis case

Our belief that we are good or bad at something tends to become self-fulfilling.

“I can’t cannulate” –> Avoiding cannulation wherever possible (Ever caught yourself asking yourself “I wonder if this patient could manage with PO amoxicillin?” on a patient who is clearly septic) –> De-skilling/never skilling –> “I can’t cannulate”

I found cannulation pretty difficult at the start. I owe a massive debt to all the patients who I have poked in my journey from total crap to where I am now, culminating today in getting a pink cannula in a patient with an Hb of 5.4 needing an urgent transfusion that the critical care outreach team could not cannulate on 3 attempts. There is still a long way to go, but at least I no longer feel like I am using patients as pinboards to practice on. It feels like I am providing patients with a service. This changes my whole approach, and I can feel a difference in how patients respond.

In the interests of reducing the international patient poke count (IPPC), I will share a few pearls I have learnt. I am really keen to hear your top tips.

1. Take your time.

The bloods/cannulas I have failed have almost inevitably been when patients were anxious, or told me they were sick of being poked. This made me anxious, and made me avoid hunting around too long as I could feel their lack of patience/loss of faith in me as I cycled between the same three areas over and over, feeling obliged to poke one of the sites pretty soon.

I now engage the patient in conversation very early on in the process, and ask how they are getting on. I try to talk about non medical things as much as possible. I keep the conversation away from cannulation and “which veins normally works?” unless I really need this information.

2. The antecubital fossa really is king.

I used to give up quickly on the ACF when doing bloods or cannulas, feeling more pro if I headed down to the hand/forearm like the seniors often do. A cannula lower down the forearm is preferable for comfort if possible, but this post is about the difficult veins, and beggars can’t be choosers. A phlebotomist once taught me that every patient must have a vein somewhere in the ACF. If she is completely stuck, she goes deep into the ACF over anything that feels springy, and it often works. Bottom line: There must be a vein somewhere there.

(Just make sure you are not going near the brachial artery.)

3. Do everything you can to maximise the vein

Does fist pumping work? Does slapping the vein work? I don’t know. I just do everything that I have been taught, as there is no harm to the patient. This includes fist pumping, rubbing the vein, tapping the vein, tourniquet about 5cm above the site. I make sure the tourniquet is as tight as the patient will tolerate. I used to neglect gravity, but now I make sure that I get the vein as low as possible. Sometimes giving it a little time with the tourniquet on helps, but anything greater than 2 minutes can invalidate certain blood results e.g. calcium and potassium.

4. Triple palpation

Try this right now. Feel your ACF. Feel it lightly, with your fingertips applying virtually no pressure to the surface, but rather rolling over the skin surface. Now feel it going about 2-3mm deep, rolling your fingers to feel the veins beneath. Finally, sink your fingers in about 5mm or more. On each palpation, you build up different tactile maps of the area. You will notice that the veins have a certain depth at which they are most palpable. That elusive vein in that tricky patient has often been hiding in just one of these depths, and I would have often missed it had I palpated at the same depth throughout.

5. See it in 3D

Once you think you have found a vessel, imagine you have x-ray vision. Use your sense of touch to build a 3D image of the vessel that becomes clearer and clearer the more you palpate it. Once I am confident in where exactly the vessel is, and how mobile it is, I like to keep my gaze fixed on my “xray” vision of the vessel as I clean the area, wait for it to dry and advance the needle.

What have you discovered works?

As for the thrombolysis patient in my 24th September post, the CT reported a clearly developing infarct, with more edema than previously. No haemorrhage was identified.

Lesson learnt: An ischaemic stroke can still progress despite thrombolysis. That is so unlucky.

Difficult patient to bleed? 7 ways your lab could help

I visited the path lab today to find out what is the minimum amount of blood you need in each bottle, and why. 7 useful facts about blood sample processing at your hospital lab:

1. The U&E tubes are centrifuged on arrival, and the gel at the bottom mixes with the plasma. This is why they need to be at least one third full to get U&Es, as below this there isn’t enough plasma that hasn’t been claimed by the gel, and it is only the plasma that can be used for U&Es.

2. FBC in the EDTA tubes can be done with only 0.2ml in theory, but this would require the lab doing it by hand rather than machine. This takes them time, so you will have to ask very nicely.

3. The coagulation tube must be fully filled to ensure the citrate in the tube is adequately diluted, or the INR will be spuriously high. Some labs offer smaller tubes with less citrate.

4. However, the d-dimer test works by binding the d-dimer products to a special antibody. This forms a solid mass. The amount of light transmitted through a certain volume of the blood sample when mixed with the d-dimer antibody is inversely proportional to the concentration of d-dimers. This means they can actually do the test with less than fully filled bottles.

5. Troponin needs a tiny amount of blood. Send whatever you can get for troponin; it will probably work.

6. TFTs need half a U&E bottle.

7. If the patient is difficult to bleed, use a paediatric tube, or ask the lab for their smaller bottles. They have reduced levels of all the EDTA/gel, so need less blood to get decent results.


The patient who was forced to play God

Please consent this patient for thrombolysis following his ischaemic stroke.

He is a previously well man in his early 30s accompanied by his wife. He has suddenly lost all movement down the left of his body. He has now got global aphasia.

This happened about 1 hour ago. Please explain to him in his current state all the risks and benefits. Explain this to a man who for the first time since the age of 11 months cannot say a word.

Overall, of every 100 patients treated, 32 will have a better and 3 will have a worse final global disability outcome as a result of therapy. Please explain this to his wife, who has not stopped crying since being at the hospital.

Please also explain that the longer they wait, the less likely it is to be successful.

On the weekend, I saw this patient thrombolysed for stroke. His power on the right at admission was 0/5, and after thrombolysis climbed to 4/5.

1 hour later it was back to 0/5, and he was becoming confused and vomiting.

An urgent CT head was requested and I will report the results tomorrow. I have some reservations about getting too academic about what must have been amongst the hardest decisions a patient will ever take in this age of medicine. It is literally a life or death decision, with immense time pressure.

However, it is this emotional detachment that allows us to make rational plans, and present the options to the patient as clearly and objectively as possible. Were it one of our loved ones, the fear of causing their death would probably cloud any attempt to really weigh up the options.

I really like the way this information is presented here:

Patient information presented brilliantly. Give information in the format you would like to receive it in.

In many ways, this patient was the ideal candidate for thrombolysis. You want someone who has potentially much to gain from thrombolysis, without any cautions or contradictions. NICE recommends alteplase for thrombolysis for stroke provided that the following three criteria are met:

  1. Haemorrhagic stroke has been excluded.
  2. The patient presents within three hours of having the event.
  3. Access to specialised services is available.

Excluding hemorrhagic stroke is a job for experienced radiologists, who must be on call 24 hours a day if the hospital is a stroke centre. CT head will do, though MRI can be used (and is better for more chronic bleeds).

The specialized services include nursing staff experienced with stroke and thrombolysis, and in particular what the warning signs are post thrombolysis. There must also be immediate access to further neuroimaging services.

As for what happens to aspirin after thrombolysis, it is held off for 24 hours, but then given at 300mg for the remainder of the 14 days after the stroke started.

SIGN guidelines require the documentation of the NIHSS scale pre and post thrombolysis. The greater the NIHSS score, the worse the stroke has been. It follows that those with minor strokes (NIHSS<4) or those with improving symptoms have not got much to gain from thrombolysis, but potentially much to lose. They are usually excluded from thrombolysis even if they meet the 3 NICE criteria.

You can get certified as competent in using the NIHSS scale for free here.

There are of course many contraindications to thrombolysis. In particular, I had never thought of acute pericarditis as a contraindication. I know now that the risk of haemorrhagic tamponade is the concern.

Fingers crossed for our man.

Has anyone ever lured the on-call surgeon out of the mess?

Apologies for the delay. A mixture of on-calls, time off and working on other medical education projects got in the way. Also, I couldn’t find the ? ST Elevation patient’s notes until this week as he had left, and I had to track his hospital number and discharge summary to see what happened.

Drum roll.

Coronary Angiogram (normal angiogram from a different patient)

The angiogram showed a near complete occlusion of the anterior descending coronary artery. I assumed this meant it really was a STEMI, but it turns out this angio result does not prove much beyond the fact he has ischaemic heart disease. I learnt from the interventional cardiologist that the level of occlusion does not in itself actually prove as much as you would think, unless it is a total occlusion or you have a past angiogram to compare it to. Just like in peripheral vascular disease, collaterals develop in chronic ischaemic heart disease.

The clinical outcome of the two revascularisation methods depends on:

1. The total number of diseased vessels revascularized (more vessels–> CABG > PCI)

2. The presence or absence of diabetes. Not only is atherosclerosis more common in diabetes, but it is also more aggressive. This is probably why completely replacing the furred up artery rather than propping it for a little while longer before it re-occludes makes sense.  Some schools of thought feel that CABG should be preferred in all patient deemed to have rapidly progressing coronary artery disease.

3. Left main disease (if present –> CABG > PCI)

4. Left ventricular dysfunction (if present –> CABG > PCI)

In light of the clinical history, the type and level of occlusion (single vessel, not left main stem), the lack of diabetes, decent left ventricular function and the patient’s fitness for intervention, PCI was preferred over CABG and performed there and then. Boom.

A few days later, my consultant gave me the task of referring this patient with extensive venous ulcers to the vascular surgeons.

Beautiful venous ulcer. Did not interest the surgeons.

Normally, this would be pretty straightforward. However, at my hospital there is an excommunicated on-call surgical registrar who has to decide whether or not to refer the patient to the real surgeons 30 minutes drive away. Making a referral to him is greeted with all the enthusiasm you would expect Tim Cook to have for the Galaxy S3 launch party.

The fact that the patient had these ulcers for 8 weeks did not convince the surgeon to come.

The fact it was deeply troubling the patient, who could not leave the house as he could not wear socks, did not convince the surgeon to come.

“Have you taken a swab?”

“No – there are no clinical signs of infection.”

SIGN guidance on signs of infection: cellulitis, pyrexia, increased pain, rapid extension of area of ulceration, malodour, increased exudate. Swabbing wounds without signs of infection is pointless, as all wounds will be colonised. Colonisation does not impair healing.

“Is there any slough?”

My surgery pathology abandoned me. I could not remember the definition of slough.

“I’ll check”

A google search later, and armed with my textbook definition of white-yellow fibrin that is adherent to the surface of a wound that does not wash off with simple irrigation, I confirmed that there was no slough.

“Fine. What are the obs?”

“Stable, apyrexial.”

“So why do you need me now?”

“It looks really bad.”

His unimpressed silence wouldn’t end.

Much as I hate to admit it, looking back, he was probably right. According to NICE, “necrotic material or slough within a wound margin which acts as a medium for bacterial proliferation and therefore should be removed by debridement”. The size of the ulcer in itself is not an indication for anything urgent.

The patient could be managed as an outpatient, despite the extensiveness of the ulcer. Provided there was no concern regarding a different diagnosis (e.g. neuropathic ulcer, arterial ulcer, rheumatoid ulcer or Marjolin’s ulcer) and no features of an acute need for debridement (signs of infection including odour, necrosis or slough), then there is no need for any urgent action. The patient could have an ABPI done, and provided that was >0.8 a non adherent compression multicomponent bandaging could be used. The SIGN guidelines also suggested that:

“Use of pentoxifylline (400 mg three times daily for up to six months) to improve healing should be considered in patients with venous leg ulcers.”

The surgeon was right this time. Next time, I’ll arm myself with the guidelines.

[Poll 2] STEMI or not? You make the call.


ECG at admission

ECG at 12 hours

My answer to the poll. And an apology.

Sorry for the delay. Let’s start by going through the simple intervention that brought down the patient’s EWS from the last post, and then in the next post I’ll talk through how I attempted to apply the NICE guidelines to an MI that I was left pretty much alone to sort out.

The patient from the previous post met the criteria for SIRS, as her respiratory rate was 23 and her temperature was 39. I realised that I didn’t give enough information to allow you to call this sepsis, as I did not mention that she was being treated for a presumed UTI (nitrites positive, leukocytes positive.) Sepsis is defined as SIRS plus a source of infection. The Venn diagram and resources at emedicine are incredibly helpful for clarifying the difference between simple bacterial infections, SIRS, sepsis, septic shock and severe sepsis.

I only recently appreciated that severe sepsis has a mortality rate of 35%, whereas acute coronary syndrome has a mortality of 5%. You won’t find a doctor hanging around when someone presents with ACS, and severe sepsis should prompt the same degree of urgency.

Just a quick aside about nitrites and leukocytes on the dipstick. A positive test for leukocyte esterase is 57-96% sensitive and 94-98% specific for identifying pyuria. Pyuria means more than 10 white cells per mm^3. Pyuria is found in most cases of UTI, but can also be seen in other infections such as STIs and TB (especially for for MCQs). It can also be found in sepsis even when the urinary tract was not the original source of the infection. Stones, urinary tract cancers and papillary necrosis are amongst the commoner non infectious causes.

Leukocyte esterase is 48%-86% sensitive and 17 %-93% specific for identifying UTIs, which reflects the fact that most but not all UTIs cause pyuria (which makes it a bit less sensitive for UTIs) and that there are many cause of pyuria that are not UTIs (which makes it lot less specific for UTIs).

Nitrites are produced by the breakdown of nitrates to nitrites by bacteria, usually gram negative urea splitting bugs like Proteus and E Coli. It is less sensitive than leukocyte esterase (45 %-60% in most situations) with higher levels of specificity (85 %-98%).

Anyway, the patient had a positive dipstick for nitrites and leukocyte esterase.

The management of an unwell patient does of course start with ABC, but there are specific treatments on the way that we should give to optimise the ABCs. For example, we are taught all about airway manoeuvres and all sorts of exciting tubes under airway. However, in an anaphylactic patient the treatment that most non-anesthetists can do that makes the biggest difference to the airway is adrenaline. This tackles the underlying root cause of the airway compromise. You should of course do the manoeuvres and use adjuncts as needed, but without the specific treatment the patient will deteriorate in front of you, just at a slower rate thanks to your interventions. (And the earlier you call the anaesthetist the better, as intubation becomes harder the more tissue swelling develops.)

In a similar way, although we are rightly taught about the importance of fluids under C, in the case of sepsis (or any distributive shock like anaphylactic or neurogenic), you have to also treat the cause of the distributive problem. This means following the Survive Sepsis guidelines. Even though this patient has a likely fluid deficit, treating just with fluids in a septic patient is not sufficient. Septic shock is more severe than severe sepsis, and is defined as systolic blood pressure less than 90 mHg despite adequate fluid resuscitation. This implies that treatment beyond fluids and more fluids is required to fix the low blood pressure. On the ward, immediate IV antibiotics are the first step.   The patient may need pressors in ITU if they go into septic shock.

Now to be a hypocrite. All we did initially was give 500ml of Normal Saline, stat. We started another 500ml over 1 hour whilst we reassessed the patient. We made sure the rest of the Survive Sepsis plan was done whilst reassessing. 2 days later the patient was discharged.

Is there a right answer to the poll? Is this not just a mash up of the most popular two answer? Probably. The point of the poll was to get us thinking about what we prioritise, even if what we do in reality is a mash of a few options. If the situation arose again, I think my priority would be an initial 500ml stat bag of pretty much any fluid other than 5% glucose whilst working through the Sepsis Six. The importance of early antibiotics must be stressed, as there is plenty of evidence that the delay in starting antibiotics in sepsis is associated with increased mortality. The target is 3 hours from A&E presentation to the first dose of antibiotics. How much more seriously do we take an ACS target of 90 minutes ‘door to needle’, the thrombolysis in stroke of 3 hours or even ‘4 hours till they breach’ in A&E despite the mortality of septic shock being 50%.

The difference in how the patient looked subjectively and objectively with just 500ml of fluid is something I will not forget. But the fact that giving the fluid and seeing such a dramatic response does not mean job done is something I must make sure I remember.