From hypotensive crisis to LM stenting…keeping life in balance
I don’t mind leading life full of challenges and crisis. I don’t pray for it, but take it for fact, life is already complicated as it is. It really depends on how you look at it. It is my choice, sometimes there is good in looking at something as crisis, so you can act on it, the positive result may boost your confidence and bring you closer to your goal.
Anyway, life as interventionist is never an easy one. I always try to keep the balance between aggressiveness and safety, between extravagance and moderation, more importantly balancing between harm and benefit in the long term. Unfortunately many of those aspiring interventionists are driven by passion to acquire certain skills or status who go on performing procedures of questionable indications or of debatable benefit. Most often scenario is revascularisations by means of PCI for patients with stable coronary disease.
Nevertheless even when you try to keep a most balanced attitude there would be many occassions when you would be required to act or else be seen as a loser. Or face a demanding patient who dictates you what to do with his or her coronary lesions…to the extent of telling you which devices and which stents to use (ouch…).
Ok enough of moaning. Lets have a little flashback of the this past 7 days or so in my little intervention world.
When hypotension pays you a visit…
First is how do you face a hypotensive patient on a cathlab table. I had this wonder last week and had to get my mind working fast or else face an embarassing case of a perfectly well patient collapsing during a simple, routine angiogram. The patient is a middle aged man who had a coronary bypass 3 years ago now back with recurrent angina. The operation report indicated that he had a left internal mammary on his LAD and two SVGs, one to RCA-PDA and the other a jump graft to Diagonal and obtuse marginal. I had completed the SVG injection when suddenly noted that patient’s aortic pressure dipping rapidly from 140 to 60mmHg. Patient appeared quite ok though. No significant ECG changes, and I did not think that I had caused any damage to the graft. Since this was an elective case then there isn’t any reason of patient decompensating from an acute closure or the like despite severe native coronary disease.
The access was femoral since it was a graft study. Arterial puncture was straight forward, no haematoma on the site and advancement of catheter did not meet any resistance or anything funny, therefore I would not suspect any peripheral complication like retroperitoneal haematoma or iliac or aortic dissection. What I was left with was the little possibility of anaphylaxis or idiosyncratic reaction from contrast media. I quickly administered hydrocortisone and chlorpheniramine, followed by subcutaneous adrenaline injection. Intravenous plasma fluid was administered and the patient now complained of some funny feeling on his throat and chest. The tongue appeared large and thick. However his breathing not affected and I did not have the previlige of auscultating his lung to detect any ronchi. There were diffuse reddish skin discolouration on his upper trunk.
The BP returned swiftly and the symptoms improved. Now I still had to complete the angiogram by shooting the LIMA. So I changed the contrast media from Iopramide to Omnipaque. However the patient complained of extreme chill and started to shiver, I therefore had to accept suboptimal result by several subselective injection of LIMA to dilineate the distal anastomosis. IV fluid was continued and another injection of steroid repeated later, the patient returned to the ward uneventfully.
I still think its a bid odd to accept anaphylaxis when the patient was ok till that point, rather than having immediate reaction following the first injection of contrast. However the rest of clinical picture very much consistent with anaphylaxis.
Another hypotensive patient…
The above was not an infrequent event and we have a sort of rehearsed protocol to deal with it, dictated by what we think the most likely underlying cause is. However this nightmare of hypotensive patients don’t just happen in the cath lab. More frightening is when it happen in the ward, in the middle of night, managed by your poorly informed MOs (err…most of our MOs are well informed ones).
However, that very same day, while I was doing my daily round in the private ward, Hamat my specialist called me about another patient who was post PCI, having a sudden drop in BP. Reportedly the BP was recorded at 50mmHg SBP on arrival to the ward, from the cath lab! Knowing the patient was post PCI, done by me I was feeling utmost responsibility to salvage him whatever the cost. They told me that there was some ECG changes suspected of acute stent thrombosis, therefore a return to cath lab is being arranged so the freshly implanted stents can be relooked at. Hmm not very convincing I thought. Unless the ECG showed a barn door changes of ST elevation MI, I am not going to buy the idea of stent thrombosis this time. For a patient who just returned from cath lab to develop hypotension, there are lists of things that must be immediately ruled out. Stent thrombosis/reinfarction is just one, another is bleeding of course, especially if femoral route had been employed like in this case. But I am concerned with the third possibility of a tamponade. Well, I was told an echo was done, and the result was negative for pericardial effusion.
However, on arrival the patient was obviously distressed, complaining of central mediastinal chest pain. His peripheries were ice cold. The systolic BP was around 70mmHg, an inotropic support had been started. First I told them to transduce and connect the femoral line to the monitor, what a relieve when the arterial pressure waveform showed systolic reading above 100mmHg. I looked at the ECG – there were some peaked T waves anteriorly, mild diffuse ST changes at the inferior leads. The story, the patient underwent elective PCI of an occluded RCA. The RCA was previously patent proximally with occluded distal/PDA, however on reangio that day, the proximal vessel was already occluded. Therefore I decided to intervene on the proximal-mid section. Wire was successfully threaded distally, presumably to the PDA, I was able to pass small balloon distally with no resistance, however elected not to dilate the distal tree. Proximal to mid RCA was ballooned and subsequently stented uneventfully. Final angiography was fine.
Looking at the ECG there was a distant possibility of a stent thrombosis or in another word unlikely. However I was wary of the chest pain in case a dissection had taken place, not a very likely thing though since there was no ostial stenting performed and angiography did not suggest such harrowing phenomena. Bleeding, retroperitoneal haematoma…hmm I need to work on this fast. Another is bleeding from other source such as sudden GI bleed (with high dose antiplatelets loaded it is a certain possibility) – they had sent the Hb though it was ok I would not take it as final, as the changes in Hb may be seen a little later. Physical examination did not suggest any bleeding cause. Heart sounds quite ok. No pulsus paradoxus etc. Despite the initial echo failed to show any effusion, I decided another echo would do no harm. Surprisingly this time a large effusion was detected with evidence of RV partial collapse.
We arranged an immediate evacuation via pericardiocentesis. Pure blood was extracted, about 200ml or so. Since it was still under 4 hours post procedure, I ordered half dose protamine sulfate. Following the pericardiocentesis, pigtail was left in situ to drain. Echo repeated at two hours did not show any reaccumulation and the Hb remain stable with SBP remaining around 120mmHg, while patient was symptomatically better.
Diagnosis: wire perforation – it typically produces delayed pericardial effusion, since the fluid (blood) accumulation takes place slowly. In fact effusion could develop as late as 4 to 6 hours.
This reminded me of another similar event years ago. Sorry, sometimes you must not trust MO to do everything (my hardworking, trustworthy MOs excluded…). There was this elderly lady who was post PCI with successful implantation of stents to LAD. She was fine on return to ward but about 4 hours later developed hypotension. The MO who called me was quite casual in his presentation, giving impression that ‘its the usual hypotension, I just put up fluid and inotrop it should settle…’. I quickly ordered him to do Echo, he said yes. Alas, I later forgot about the case completely, only to return the next morning noting that patient’s BP was hovering around 80mmHg. Thankfully she was otherwise ok! I was deeply annoyed on finding out that Echo was never done, despite my order…I quickly did one and a large effusion was present. Again, the BP returned spontaneously following pericardiocentesis. Another case of wire perforation.
Other cases of extravasation as result of subintimal passage of wire/devices, or extension of subinitimal haematoma leading to perforation, usually happen more acutely and dramatically, on a small number of cases we fail to revive these patients despite aggressive measures. So do not take things lightly, timing of hypotensive episodes mean a lot.
And yet…another hypotensive patient!
This was another episode that happened quite a while ago, though simple but let me have it mentioned for the sake of sharing and learning. This was a middle aged man, who had a successful implant of a dual chamber pacing. Returned to ward in a stable form and monitored under routine monitoring. A few hours later I overheard one of the registrars were talking over the phone to an MO in the ward who reported the man has ‘collapsed’ and had low BP. The registrar immediately ordered the ‘routine’ treatment of fluid and inotrope. I shouted, asking what’s the case and was informed that this was the man who we just implanted PPM. Well, I said, get an immediate CXR.
Again, somehow it was a very hectic day that I completely forgotten the case. Apparently CXR was only done sometimes after midnight, a large pneumothorax was diagnosed and a chest drain was performed at 6am in the morning! On knowing the case I was utterly dismayed at the mediocre management of this case. Some people never learned the difference between a routine and urgent or even emergency…
In a patient who is post-PPM implant, becoming SOB or hypotensive, think of pneumothorax. Other cause such as bleeding from the puncture or subclavian/SVC perforation from wire or lead; or RV wall perforation is a rare thing.
Work better when under pressure? Then, take the challenge…
Today is a Thursday. I am yet facing another busy Thursday. By default Thursday is a long cath lab day. However today I had to finish by around 1pm, go home and get ready to drive to the North – Kuala Kangsar where my wife is having a school meeting. Suddenly I recalled that there is a private coronary angiography case coming. And yet, another last minute addition, of a complex left main stenting. I checked the list, there were already 6 cases (including one PCI), not including the two additional cases. How I am going to finish them by midday? No way. As the only in-house Interventional Consultant, I need to be there till the end of the cath lab day. At this 11th. hour I texted David, apologetically begging him to come to my rescue…furthermore, David, I need an experienced colleague presence for that complext LMS case…thankfully David responded favourably, stating that he should turn up in the lab by around midday, which was perfect for me.
As I arrived at cath lab in the morning, the staf informed me that the PCI case did not turn up, another cancellation so we were left with 4, plus the two additional cases of mine. Hmm not a bad start for the day. We started with two angiogram with provisional PCI – both did not proceed. Then I started the private angiogram cases, which turned out to be much longer than expected – well, its a 73 year old man with hypertension and query recent MI. The radial artery was tortuous first of all, which took a while to negotiate, then the brachial/innominate vessels were supertortuous, even to get the catheter down was a challenge, manipulating was out of question. This set me back for almost 40 minutes. Now it’s 1130 time to start the LMS PCI.
This was a man in his 70’s who previously attended a highly reputed centre for his IHD, diagnosed with severe 3 vessels disease and a tight distal LMS, refused surgery. Knowing the centre, I would have expected they offer him PCI option, there was no mention of same, which could mean that the anatomy was complex enough. Yes, it must, with (on report) CTO of the RCA and LCX, and tight proximal LAD in addition of the distal LMS. If this was not bad enough, the man had an impaired LV with EF of 35%, and a stage 2 CKD. He was admitted to the private ward for an urgent cranial surgery for a rapidly enlarging cerebral tumour. Of course the Surgeon and anaesthetic would not proceed with the tight LMS.
I was thinking of options, well there arent much options are there? I could do a dobutamine stress test…if he passed then just keep him on a betablocker and proceed. But knowing the tight LM and LAD, he’s basically left with nothing, DSE itself could be dangerous, apart from the likelihood of yielding result that you already know. Or, let him go as a high risk case, full betablockade, no way, patient would be ultraworried, and the surgeon and anaesthetist would never take the risk, further they would think that I am such a loser for not doing anything….
A last minute decision to perform a LM stenting…? And I just got under 1 hour to do it…
So, I am left with a high risk LM stenting…I thought I will first delineate the anatomy, then possibly intervene with the highest risk lesions alone ie the LM and LAD, thats it. Do I need an AIBP, this has to be kept in mind. So, I fasted the man early morning, ordered an echo – which confirmed the impaired LV function though on new estimate not as bad, EF estimated at 46%, therefore this has taken him away from the higher risk category. Access via femoral, I started with a 6Fr. Coronary angiography showed a tight LMS and proximal LAD which was rather large, occluded proximal LCX and severe ostial RCA lesion with proximal stenosis as well, followed by CTO from mid segment.
Took a deep breath…we loaded the patient with Ticagrelor 180mg, I kept the 6Fr sheath since the LM stenting is not likely going to involve kissing balloon inflation. First I targeted the RCA in order to allow some decent circulation as a backup during the LM stenting. I managed to cross a Pilot 50 wire distally to PDA. However repeated attempt to cross balloons, including a 1mm balloon failed. Finally I settled with POBA of the ostial/prox RCA which now appeared better up to the point of occlusion.
The patient remained stable so I proceeded with the LM stenting. Standard JL catheter, wired with a BMW. IVUS was performed which confirmed tight proximal LAD and distal LM has a circumference of 4.7mm2. No concentric calcium. Means things are favourable for simple balloon followed by stenting now. Since there are sizeable gaps of more than 5mm between the LAD and distal LM lesion, which IVUS proved the area to have less than 50% plaque burden, I have the option of spot stenting the prox LAD and distal left main with two stents with or without overlap. I looked around, David was not around yet, I should keep going in view of time. Next I predilated with 2.5mm balloon, everything went smooth. David just arrived, I felt more relaxed to have a senior and experienced colleague like David around, not that I could not do this alone, its more of getting assurance that I am doing right! David agreed with my strategy.
I choose a 3.5mm x 13 Genous stent for prox LAD lesion, dilated up to 16atm. Then I took a 4.0 x 13mm Genous stent for the distal LM lesion, cross over to LAD but not overlapped with the first stent. Brief inflation over nominal (12atm) performed, there was a momentary chest pain complained though patient remained stable. Angiography and IVUS showed slightly underexpanded stent at the distal LM tight lesion. I therefore went on with a non-compliant balloon postdilation with a 4.0x10mm balloon. Repeat IVUS looked good with areas >9mm2. Final angiography was excellent.
We planned to keep patient on the ticagrelor for at least 15 days, following this he may undergo the surgery. Should an emergency arise, ticagrelor may be witheld and surgery can be undertaken within 3 days.
Praise be to God everything went well. This is a second case of LM stenting pre-op non-cardiac surgey that I had performed successfully with Genous, to allow patient to undergo surgery in a timely manner. According to OCT study, 15 days post implant is enough to give a 70% coverage, which according to renown pathologist Renu Vermani, regarded as minimum coverage required to safely avoid stent thrombosis.
I looked at the time, it was just 15minutes past one. I chatted with David regarding stenting strategy in patients undergoing non-cardiac surgery, and brief update of current DES. Then we spoke about FREEDOM, a latest head to head comparison of PCI with DES vs CABG in Diabetic patients with multivessel diseases. The result, as expected favoured CABG for all cause mortality and reinfarction. There was a trend toward less cardiac death in CABG group though statistically non-significant. The PCI group patients tend to have less stroke, as expected. Another ‘defeat’ for interventionalist? What now after OAT, COURAGE and hence FREEDOM, PCI is getting nowhere better than CABG, or even optimal medical therapy in stable CAD? Interventionalists may still have FAME and FAME 2 to defend themselves, but whichever arguments being put forward, in the overall sense, it is still true that PCI in stable CAD does not confer any prognostic advantage. As for angina relief, it may not be as great, as suggested by COURAGE itself where angina relief were only relevant in the first 3 years.