Lessons Learned from Death & Near Death Experiences 3

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Published on The Doomstead Diner on June 20, 2017

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LESSONS LEARNED FROM DEATH AND NEAR DEATH EXPERIENCES

Part 3: Type A aortic dissection

By Geoffrey Chia, MBBS, MRCP, FRACP, June 2017

Chest pain is a very common symptom and most of the time is not dangerous – the most common causes are pain from the chest wall (ribs, muscles) or pain from the stomach and gullet due to acid reflux, so-called “heartburn”. Sometimes the exact cause of chest pain cannot be determined, but if we can rule out potentially dangerous causes, then we can strongly reassure the patient. On the other hand, the most lethal causes of chest pain are the unholy trinity of myocardial infarction, pulmonary embolism and a very rare but fatal condition called type A aortic dissection1

 

The trickiest of all to diagnose is aortic dissection, which caused by a tear in the internal lining of the aorta (the main artery emerging from the heart), causing blood to enter and split (but not rupture through) the aortic wall. Blood entering the wall creates a cavity called a “false lumen” which can propagate with each heartbeat and can cause all sorts of mischief. Dissection may not even be thought of or looked for when the patient first presents to hospital, because it is so rare. Theoretically the best diagnostic investigation is a CT scan of the chest with contrast, however even that may not be definitive if images are technically poor, there considerable movement artefact and the vacillating reporting Radiologist is plagued by equivocal uncertainty. Real life is less clear cut and a lot messier than the general public realise. If dissection presents classically with a “tearing interscapular back pain which radiates to the centre of the chest” then most doctors will be alert enough to order the appropriate test(s). However dissection is also a great mimic.

Type A dissection can cause a myocardial infarction by pinching the origin of, say, the right coronary artery. The MI may be correctly diagnosed by ECG, but if the commonly used therapy of thrombolysis is applied, that will kill the patient. If an attempt is made to stent the right coronary artery and the cardiac catheter inadvertently goes into the false lumen, spreading the dissection, that can kill the patient. Even if stenting is successful, post stent care requires the use of blood thinning medications, which can kill the patient. Thus even though the MI may be correctly diagnosed, the failure to diagnose the underlying cause of this particular MI and the adoption of “standard” MI therapy will be catastrophic. 2

Dissection can present as blood leaking into the pericardial sac, causing breathlessness and a drop in blood pressure, "cardiac tamponade". Even though draining the blood which compresses the heart can provide temporary relief, unless the underlying reason for the tamponade is corrected, the patient will die. 2

 

Dissection can also present with a leaky aortic valve, which if severe can cause heart failure. However the murmur of aortic regurgitation is one of the hardest to detect with a stethoscope.

As a junior doctor I had seen one patient who presented with Type A dissection who, while being assessed, abruptly collapsed in hospital from cardiac tamponade and died. In the final year of my cardiology training, I encountered another patient with type A aortic dissection who we thankfully were able to save. He was admitted with severe chest pain (no back pain) and the ECG was normal. Auscultation revealed an early diastolic murmur typical of aortic valve regurgitation. These findings prompted me to check the blood pressures in both his arms (we usually just check the BP in one arm only in most patients). The arm BPs were substantially different. The only condition which can cause chest pain, aortic regurgitation and unequal arm BPs is type A aortic dissection. The next test was a bedside transthoracic echocardiogram (ultrasound of the heart using a probe on the chest wall), which showed a dilated proximal aorta with a double line suggestive of a split in the wall of that artery and of course, aortic valve regurgitation. Thankfully the arterial split had not extended downward to spill blood into the pericardial sac. Transthoracic echoes may not provide the clearest images. The TTE is not considered a gold standard test for the diagnosis of dissection and it was still necessary for us, the medical team, to perform a definitive test before this patient would be accepted by the surgical team for operation3. Time was short, death could occur at any time and arranging a CT scan often took more than an hour. Those were the days before bureaucratic interference demanded that every transoesophageal echo should be done in an operating or endoscopic theatre and sedation could only be given by an anaesthetist4, in my view absurd constraints leading to endless delays. So I grabbed the transoesophageal probe, administered i/v midazolam to the patient and performed the transoesophageal echo at bedside in CCU and obtained crystal clear images showing the presence of dissection with characteristic false lumen and intimal flap in the ascending aorta. Prior to open heart operations we usually perform a coronary angiogram to look for any incidental coronary artery narrowings which may require bypass grafting at the time of surgery. However in aortic dissection, as mentioned earlier, a cardiac catheter may inadvertently enter the false lumen, spread the dissection and kill the patient, hence cardiac catheterisation for coronary angiography must be avoided here. This patient presented in the days before non-invasive CT coronary angiography, which requires super high speed image acquisition technology.

The patient was accepted for surgery on the basis of the TOE result. His operation was successful with replacement of the aortic root and re-suspension of the aortic valve without need for valve replacement. He recovered well.

So far, this case report offers no unique learning points. The various features of this patient's presentation can be found in any medical textbook. However I did learn one fascinating aspect about aortic dissection from this particular patient. When I checked his arm BPs, I found that his right arm BP was consistently higher than his left arm BP which completely went against my preconceived notion as to how a type A dissection should present. Surely anatomy dictated that any dissection commencing from the proximal aorta (especially if it starts just above the aortic valve) would “pinch off” the origin of the right brachiocephalic trunk before it involved the left subclavian artery? Surely this would result in the right arm BP always being lower than the left, if unequal BPs were to manifest at all? How on earth could such a proximally originating dissection cause the right arm BP to be higher than the left? I delved deeper into the literature about aortic dissection and found the explanation. I found a paper which described post mortem findings of aortic dissection patients. It seems that dissections do not progress in a simple longitudinal line along the aorta but tend to spiral around the arterial wall in a random fashion. Hence it is equally likely that the dissection may miss the origin of the right brachiocephalic trunk and pinch off the left subclavian origin, as it is to do the opposite. This personal discovery was like a light bulb going off in my head, an “AHA!' moment which I now share with the two of you who have had the persistence to read this far.

Lesson learned: Reality ALWAYS makes sense. If your findings do not conform with your understanding of your diagnosis, either your findings are wrong, your understanding is wrong or your diagnosis is wrong. In this case, my understanding was wrong. My preconceived notion about the manner in which aortic dissection propagates had been wrong. This experience corrected that misconception. Reality ALWAYS makes sense.

My conclusion yet again: information derived from repeatedly validated scientific research, scrutinised and published in peer reviewed scientific journals, informs us about objective reality. We ignore, dismiss or remain ignorant of such scientific knowledge at our peril.

Every day it pains me to know that even though we have abundant, consistent, repeatedly validated scientific information about the devastation of our ecosphere and why it is happening, unfortunately our nations are run by anti-knowledge, anti-science psychopaths hell bent on accelerating Armageddon for the sake of their short term greed and their lust for power. Shame on them, shame on the power brokers who manoeuvred them into position and shame on the stupid sheeple who voted them into office.

G. Chia, June 2017

FOOTNOTES:

  1. Type A dissection involves the upstream or proximal part of the aorta and may or may not extend past the origin of the left subclavian artery. Type B dissection affects the aorta downstream of the left subclavian origin only and can potentially cause a whole multitude of major problems which may even be fatal in the longer term, but is nowhere near as acutely dangerous as Type A dissection.

  2. I cannot repeat enough that you must determine the underlying cause of a problem in order to manage it properly and failure to do so can be catastrophic

  3. This brings to mind the case of an old mentor physician teacher of mine, Dr T, who himself experienced back pain radiating to his chest and presented at a hospital in another country. The senior cardiologist in that hospital diagnosed aortic dissection after doing certain tests and sent him to theatre but when the surgeon opened him up, no dissection was found. It was a misdiagnosis. As you can imagine, when Dr T woke up from the anaesthesia and learned of this error, he was absolutely outraged. The classical presentation of type A dissection is with back pain radiating to the chest. However most patients with such symptoms do NOT have dissection. Typically, pain from stomach acid refluxing into the oesophagus tends to be felt in the chest, hence the term "heartburn". However the oesophagus is a posterior thoracic structure and acid reflux when the patient is lying down may also be felt as back pain. When they sit up, the pain may shift to the chest. Another condition which may be felt as back and chest pain is degenerative disease of the thoracic spine. Such "arthritis" of the spine will of course be mainly experienced as back pain, however if there are bony spurs which are pinching certain thoracic intercostal nerve roots (which receive sensory fibres from the chest wall) then the patient can also experience "referred pain" in the chest. On the other hand, not all patients with type A dissection present with pain. I know of one patient who had no pain but presented with a fainting spell because of sudden tamponade. Sometimes tests do not provide clearcut answers because there may be technical difficulties for all sorts of reasons and images may be fuzzy. In such a case judicious interpretation of ALL the information at hand, combined with further information gathering, is absolutely vital, rather than stubbornly sticking with a flawed diagnostic preconception. I liken missing a true diagnosis and making a false diagnosis as similar to type 1 and type 2 statistical errors. Type 1 error rejects (or fails to accept) a true paradigm and type 2 error accepts (or fails to reject) a false paradigm. http://www.statisticshowto.com/type-i-and-type-ii-errors-definition-examples/ Both errors are bad and we must try as hard as possible to detect true paradigms and reject false paradigms in order to deal effectivly with reality. In a wider context, an example of rejecting a true paradigm is global warming denialism. An example of accepting a false paradigm is the idea that our global troubles are purely economic and if we just tweak our economic policies, all will be well. The correct and true paradigm is that our troubles are related to reaching the Limits to Growth, that we are past the point of fixing everything and only a small fraction of the population will survive the impending population cull, depending largely on how they plan in advance, but also depending on future dumb luck.

  4. The only time I ever had difficulties performing a transoesophageal echo was when I was administratively forced to include an Anaesthetist in the proceedings. This was supposedly a routine outpatient TOE which I performed in an endoscopy suite. The anaesthetist gave the patient i/v propofol at a dose he deemed sufficient for sedation but when he advised me to go ahead and insert the probe, the patient struggled terribly. Despite more propofol, the whole procedure was a shambles with poor, jerky images and a constantly wriggling patient who choked so badly that after it was completed and he was observed in the recovery room, his oxygen saturation dropped and he spiked a fever. I ordered a chest Xray which showed he had aspirated fluid down his right bronchus causing a patch in the middle lobe of his right lung which was certain to cause severe pneumonia if we did nothing. Accordingly I had to admit him to hospital for 24 hours of intravenous antibiotics and observation, followed by a full course of oral antibiotics on discharge. Prior to this mess I had been performing TOEs with the help of a capable nursing team without an anaesthetist. I administered tiny doses of midazolam and sometimes fentanyl. There was no risk of the excessive sedation causing respiratory problems because of a stringent protocol: the patient was established on continuous oxygen by intranasal prongs, there was continuous monitoring of the patient's oxygen saturation level, we kept on standby a “bag and mask” for immediate active ventilation if oxygen saturation was to drop and I always ensured the specific intravenous antidotes for both midazolam and fentanyl were at hand for immediate administration should the need arise, which would reverse any respiratory depression should it occur and fully wake the patient within seconds. As it turned out, I never needed to give those antidotes because of my parsimonious use of those sedatives which did not completely knock out the patients and merely induced "twilight" sedation, relaxation and amnesia for the procedure.

 

One Response to Lessons Learned from Death & Near Death Experiences 3

  • Rebecca Zegstroo says:

    I'm one who read it to the end. I like to learn all I can about the human body and medical procedures.

    Your extension of the medical reasoning into the greater reality of resources is fascinating. I too had a recent Aha moment. I've been listening to an audio version of "American Theocracy" by Kevin Phillips, published in 2006. The actionsof US military and government have not made sense to me. They could not possibly be so ignorant of petroleum production peaks as they seem. According to Mr Phillips they certainly are not. They've been aware for at least 20 years now. But the response was to seize Iraq and control of its supposedly vast and relatively untapped oil reserves. The oil companies calculated 50 more years of profits. After that, well, it's not their problem. As for climate change, denial seems to still rule the minds of TPTB. 

    So the political and military objectives are all oil all the time. 

    The Iraqi oil fields have been known for a long time. Didn't Hubbert take them into account in his calculations? I think we're still doomed in the near term.

    And I still hate Versed. It's weird to not remember – but then again, whatever works. A bit of amnesia is better than pneumonia.

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