Recurrent Idiopathic Acute Pancreatitis

After trying unsuccessfully over a period of time to join a specific forum on this subject in order to post this, I'm posting it here instead, under the aegis of midlife health issues. The purpose is to share the information and understanding that I have gained through five years of intermittent pancreatitis attacks. There are a lot of experiential hypotheses on the internet, and in one respect, this post simply adds to that collection. In another respect, however, I might have a unique perspective: on one hand I am a scientist with 25 years of education (through PhD) and experience (in academics and industry), and am therefore inclined toward the scientific method; on the other hand, after seven attacks, the condition is still classified as "recurrent idiopathic acute pancreatitis", i.e. inexplicable isolated episodes -- so I am left to draw on the experience of others in an attempt to identify conceivable, albeit unproven, potential solutions.

It is important to distinguish the quality of advice from different sources. As per the experience of others, as well as my own, mileage varies with different medical sources. When doctors make authoritative statements, their statements of fact are at best based on the state of knowledge of medicine, which the more enlightened among them freely admit is not complete. Of course these statements of fact are further mitigated by the thoroughness and currency of any given doctor's awareness of medicine's state of knowledge. Medical systems vary, but in mine, the top gastroenterologist who I see gives me much more thoroughly informed advice than the ER docs who I see on admission, or anywhere else. He openly acknowledges that medicine just doesn't know enough yet.

So where proper medicine falls short, we turn to the anecdotal evidence of other affected people on various and sundry internet forums. I wouldn't have visited them myself if I wasn't going to value the advice found there, but it's important to realise that the "experiments" that we perform on ourselves regarding diet, stress reduction, etc, employ a sample size of one, and are almost totally uncontrolled--meaning we try different things, and come to individual tentative conclusions, but in the end the evidence is only circumstantial. There are many, many, potential factors at work, and we can never know whether or which of the changes we've implemented necessarily made a difference.
I offer the following on the possibility that I may be able to sift through the collective experience of fellow sufferers more constructively than what normally comes up in a search, and that it might help somebody out there in the aether.

Background
The back story is that I had my seventh hit of acute pancreatitis in almost five years last October (2012). Clinically, the severity has been randomly mild or moderate, but irrespective of the classification, up to the sixth hit, I spent about four-six days in hospital each time, with no real complications. Statistically, the most likely cause of pancreatitis is gall stones, gall sludge, or even microlithiasis (tiny crystals). Every ultrasound (endoscopic and otherwise), MRI and CT scan, and every blood test that I've had between episodes has come back completely clear with respect to the pancreas and gall-bladder. The only evidence that anything was sub-optimum was a bit of fatty liver. I've turned down many offers to remove my gall bladder, which were made on the basis of statistics, but it wasn't until the most fervent surgeon saw a totally clear endoscopic ultrasound that I was referred to the specialist who I now see.

The second mostly likely cause of pancreatitis is alcohol (more on this below). My first episode happened in 2008, a few days after a conference dinner, where the red flowed freely. Through my reading at the time, it appeared that one needed to be a proper alcoholic for a number of years, which I wasn't, in order for alcoholic pancreatitis to make sense. But in the absence of any better explanation, that attack got chalked up to alcohol, although many doctors I saw at the time didn't believe it. I didn't believe it either, but being an experimental scientist, I had to do the experiment: I didn't touch a drop of alcohol for the next 18 months, but indeed, that didn't stop the 2nd attack at the 12 month mark. After those 18 dry months, I've had the occasional drink, and occasionally more than the one. The intervals between episodes, in order, have been 12 months, 8 months, 10 months, 16 months, 7 months, and 3 months, and there is no correlation between the intensity of the social event and the timing of the attack. However, as alcohol is the only clinically proven lifestyle factor that I have control over, I've stopped drinking all alcohol again as of the last attack, and have begun re-purposing my home brew equipment. I've also stopped thinking in terms of there being such a black-and-white trigger for the attacks -- alcohol, perhaps stress, or otherwise -- and I have instead begun thinking in terms of minimising potential risk factors.

The first six stays in hospital were inconvenient, left me a bit weak afterward, but were otherwise easily forgotten until the next attack came along. My renewed interest in sorting this out once and for all, however, stems from the last attack being a little worse, as I wound up with pleural effusion (fluid between tissue layers in the lung), and a leaking of fluid into the third space (fluid build-up in the body cavity). I wasn't really completely right again until a few weeks later, and I'd really like not to go through that again.

Now, my comments on some of the advice that seems to appear with some frequency across the internet ...

Call the Ambulance
Firstly, at least with respect to acute pancreatitis, DO NOT hesitate to go to the Emergency Room. I absolutely understand the desire to manage it at home -- the people in the public hospital system here in my country are great, but the system is an utter shambles. I get no decent sleep with the noise levels at night, I keep better records in my head than can be gleaned from my file in the 60 seconds that every new doctor can spare to review it, and I've started including bathroom cleaner in the bag that I pack for hospital. I've gone to ER both very early, and too late -- I live about an hour from the hospital, but work next door to it. A few times I've tried denying the pancreatitis attack, or thinking I could manage it at home, and put off going in. But then I've also by now picked up on the early signs that an attack is coming, and walked over to ER from work about 2-3 hours before any sign of pain. My firm belief is that I have a lot easier time of it, and a shorter stay by a day or two, if I go in early. Specifically, it's about getting onto the drip as soon as possible.

For me, by about three hours before the pain hits, I get a very dry mouth, I get quickly out of breath in a short walk, and I have a mild awkward feeling about halfway between my navel and sternum, and in the middle left-to-right. Unfortunately, the challenges in presenting to a recalcitrant public health triage system in an apparently well state of being are complex: on one hand, because heavy-duty pain killers are imperative for the pain involved, the system is accustomed to dealing with people walking in off the street falsely claiming pancreatitis as a ticket to get the drugs. This is compounded by the fact that people presenting with bona fide pancreatitis absolutely can not remain stoic about it. It bloody hurts. So those two factors work against somebody trying to present early to ER. I get a bit more respect in ER these days, I think owing to my history (I've never been wrong), and--this is sad--because I can identify myself with a nearby university research facility. It actually works in my favour, I think, if all I ask for initially is a blood test, and not the drugs. Usually the results are back from pathology at just about the time that I need to medicate. The motivation for getting in early is that getting on the drip as early as possible will help to make the whole experience pass faster. That's my anecdotal evidence, and I understand that there are mice that have been bred such that they can specifically induce pancreatitis with diet, and there is a very significant difference in outcome for mice who have had fluids injected vs not before being "given" pancreatitis. We're not mice, of course, but it supports the hypothesis.

As an aside, I've thought in the past that maybe I could avoid a suspected attack if I could drink enough water soon enough before hand, to gain the same effect as (and preclude) early IV fluids. I've more recently been advised that I can't, and probably shouldn't even try. What's worse, if I wait too long, I start feeling like I'm dying of thirst, and that I must drink some water. This should be kept to a minimum, like sucking on ice instead. When an attack is coming on, the gut slows down (called "ileus"), and anything one takes will just sit there in the stomach, and make matters worse (e.g. vomiting).

Blood Tests
That brings me to the blood tests on admission. Everybody focuses on the lipase, and maybe amylase. These results simply confirm (or not) the diagnosis of pancreatitis. The relative level of lipase above the acceptable range is not an indicator of the severity. Different labs have different testing procedures, and therefore the "normal" and "high" ranges will differ from one pathology lab to the next. So even though it isn't much use to quote actual lipase activity ranges, from the same pathology lab I've had initial lipase levels of 4000 (probably U/L) in what turned into my worst experience yet, and on another occasion the lipase levels were 60000, and that was a relatively simple visit to hospital. 60000 is probably high on any scale, and sounds impressive, but ultimately it just means "Yes, it's pancreatitis [prepare the morphine]."

The actual early predictive indicator of severity is un-ionised calcium levels. This is usually run routinely by the blood analyser, but isn't reported unless it's specifically requested, and it SHOULD be specifically requested. This should be done in the first blood test when presenting to ER, and again at six and twelve hours. I will offer a range on this, as it's possible that this test has less lab-to-lab variation than enzyme activity assays: above 2.1 mg/dL, the pancreatitis is (clinically) mild, 1.9-2.1 it's moderate, and below 1.9, I'm told, you should clear your schedule for three weeks and they should book you a bed in ICU straight away. Calcium levels will drop naturally as a consequence of fasting, so calcium tests later into the hospital stay aren't so useful.

What IS useful later in the stay, again, is not lipase levels, but CRP (C-reactive protein), which is a marker for inflammation. This should especially be done from about day 3. If CRP levels are dropping, one can be sure discharge is nigh, and they will start testing you first with clear fluids, then with at least one "real" meal (such as it is in hospital). The conversation with proud ER doctors over what tests should be done and when can be challenging, to say the least.

Diet
As for diet, of course a good diet benefits anyone, and the consequences of a bad diet are perhaps less forgiving to sufferers of pancreatitis. But as far as specific triggers, alcohol is probably the only proven significant risk factor (see below). Nevertheless, I've gone vegetarian, I avoid fried and commercially baked food as much as possible, reduced portion sizes, and started exercising more. I log everything that I swallow -- food, drink, supplements, and medication, and exercise (I use manual entry into  myfitnesspal, although the data tragic in me is curious about syncing this with Fitbit [Amazon] -- does anybody have any experience with this?). I'm finding that, psychologically, this makes me more accountable for--and therefore more conscious of--everything I consume and do. Again, I don't expect to identify any specific triggers, but I'm always willing to give myself the chance to be wrong, and we don't get anywhere without information. While I've lost about 12.5% of my initial weight over the last 3.5 months, and the latest liver tests came back better than they have been in years, statistically I have to go pancreatitis-free for 13-18 months before I can start believing in any correlation.

In my last episode, I left hospital within about 12 hours of admission to ER, after proving I could eat -- two sandwiches, yoghurt, and juice. I had a coffee roll on the way home, too, no worries. I thought I had gotten off lightly. I slept about 12 hours, then woke up the next day at about 5 AM with plans to go to work, and had a small bowl of Cheerios with 2% milk--BANG. Instant pain. But do I believe Cheerios or milk is inherently a problem? No. Coffee is also on a lot of sufferer's no-go lists. In contrast, I've gotten permission to buy coffee from the hospital cafeteria during my recovery phases, and did not suffer at all. Thank goodness for this -- I'm a home-roaster, so it's more a way of life than a beverage for me.

I recently asked my aforementioned expert about the feedback between a meal and stimulation of the pancreas, with regard to some of the anecdotal evidence, as well as less-informed medical opinion I've received. Does the body know it's been fed a high fat meal, for example, and stimulates the pancreas to deliver an extra shot of lipase? The answer was "no". He said that if he were to wave a chocolate bar in front of me, my gall bladder would squeeze out the digestive juices it was storing, and the pancreas would start pumping enzyme, because my body would believe that I was about to eat it. So if diet IS really so specific with regard to stimulating the pancreas, we should probably also avoid even the sight of food! This seems somewhat contrary to the standard practice of starving the pancreatitis patient in hospital for the first few days, which is explained as "giving the pancreas a rest". But note that this is denying all food to the patient, not the exclusion of just high-fat or any other sort of specific food, and so would seem to apply only to those first few days in the acute phase. And there would be no benefit in feeding anyway, given the compound ileus (slowing) induced in the gut by both the pancreatitis itself and the opiate-based pain killers (morphine, endone, tramadol, …). This being the case, to some extent the return of hunger itself is a sign that the pancreas has settled down.

That said, if gall stones, or even "sludge" or biliary microlithiasis (tiny crystals) are to blame, diet may in fact directly help. But then so will plucking out the gall bladder.

Alcohol
The basic pathology in pancreatitis is that the pancreatic digestive enzymes become active too soon -- the majority of the enzymes are meant to become active only upon contact with the lining of the small intestine. A small fraction of the enzyme (trypsin) that in turn activates the digestive enzymes is active already in the pancreas, but there are other proteins that are meant to bind to and inhibit it. The cascade of enzymatic activity is in delicate balance, and many things can throw it off such that the digestive enzymes become active too soon -- genetic mutation, periodic quirks in the immune system, some medication, and other conceivable problems that requires more research (ATTN: research funding councils that are cutting budgets!). As for alcohol, I've read that it thickens the pancreatic secretions, and even aside of this, anything other than a protein's natural conditions can cause it to misbehave. A bit of alcohol in the "solution" too frequently (everything's relative) could be enough to help throw the cascade out of balance.

Stress
Finally, I'm very intrigued by suggestions that stress plays a significant roll in pancreatitis. I've certainly had more than one person's share over the last few years. I do believe this is a much bigger factor in our lives than what we realise, irrespective of the disposition of one's pancreas, and so on some level avoiding stress probably has similar effects on well-being as what healthy eating has, and, again, pancreatitis sufferers are perhaps more vulnerable to this, obviously at least in part due to the condition itself. I read with great interest in an otherwise unrelated book called "Outliers" by Malcolm Gladwell [Amazon, Book Depository] about a population of Italians who had essentially transported itself from a town in Italy to (if I remember correctly) Pennsylvania, and who had a very abnormally low rate of heart disease. Absolutely everything about this population on a physical level was insignificant--they maintained a traditional diet, and had similar genetics to a similarly founded nearby town with normal rates of heart disease. Those studying them were completely stumped. In the end, the difference was in their pace of life; the fact that they stopped at each other's gates for a chat when walking past, and weren't in a hurry about anything. I doubt medicine will be able to quantify this sort of thing any time soon, but it is probably one of the few things that we can address to help ourselves.

I would of course be interested in anybody's experience that supports or refutes anything I've said above. Good luck everybody!

© 2013 J Gaümann