Foyle’s War’s Teeth

Perhaps it was by design, or perhaps not, but the attention to period detail in the crime series Foyle’s War is remarkable and rare in a seemingly simple way: it gets teeth right.

Foyle’s War is a police drama featuring Detective Superintendent Christopher Foyle (Michael Kitchens). Many of the crimes he investigates in Hastings, Sussex during WWII are related to the conditions on the homefront including profiteering and sabotage, but jealousy and madness also provoke ordinary people to behave wickedly. The show premiered in 2002 and ended in 2015 after 28 90-minute episodes. The last episodes following the war find Foyle in London, working for MI5.

Foyle is a quiet, highly principled man. He is compassionate, but he does not suffer fools. He’s a widower with one son, Andrew, serving in the RAF. From the first episode onwards he is accompanied by Samantha Stewart (Sam) as his driver, and in the first five seasons he works with Sgt. Milner, a policeman who lost part of a leg in the war.

There are perhaps a half dozen other characters who appear in more than one episode, but for the most part, the cast is fluid.

Its creator, Anthony Horowitz, has attributed Foyle’s War appeal to the tone of the show. It defies the sentimental nostalgia for the war years, and Horowitz based many of the situations Foyle investigates on historical events. The New York Times acknowledges that Foyle’s War is typically “celebrated for the ‘historical accuracy’ (those are the words always used) achieved by its creator and writer, Anthony Horowitz. . . . The better word is probably scrupulousness — the special texture of the show owes to the faith we feel in Mr. Horowitz’s depiction of the clamped-down, suspicious yet doughty atmosphere of 1940s Britain, and to the trouble and expense to which the production has gone to recreate those times.”

In contrast, consider the criticism of Downton Abbey, which historian A. N. Wilson called a “sanitized fantasy.” Downton may get the place settings right, but “the servants in the program are far too clean,” according to historian Jennifer Newby: “The reality would have been a lot more grubby, I don’t think people realize that the servants stank.”

All I think you need to do to understand why Downton is fantastical and Foyle’s War is not, is to look at the teeth.

Foyle’s teeth

Christopher Foyle (Michael Kitchen) has acceptable, ordinary teeth. There are no obvious flaws, other than a little yellowing. Foyle smiles easily – he has a very expressive face – but his smiles are usually closed.

Samantha (Sam) Stewart (Honeysuckle Weeks). Sam’s mouth seems to change from the start of the series to its final episodes. In the opening episodes, Sam’s teeth seem to be a bit small for her mouth and there appear to be spaces between her teeth.

In the last series, her teeth seem capped and bonded.

Foyle's War
Sam Stewart (driver)

Sgt. Milner has good teeth, as does Foyle’s son, Andrew. The actors who portray them, Anthony Howell and Julian Mark Ovenden, were stage actors. I expect it would have been hard to find experienced actors to play young men in their twenties who have not had good dentistry.

What’s interesting is that the characters who have obvious problems with their teeth represent all social classes. A fisherman, a police commissioner, doctors, army brass, industrialists – all are at risk. Not everyone has bad teeth: a daughter of a wealthy family in Series 1, episode 1, has perfect teeth, as does a burn victim.

Let’s see some examples:

Foyles War
Fisherman in “White Feather”
Foyle's War
Hilda Pierce, MI5. Yellowed teeth.
Not bad teeth — but not perfect, either
Foyle's War
A doctor’s teeth
"The Funk Hole"
Overlapping teeth
Police Commissioner’s mouth
Series 5, epsiode 2
The brass in “Casualties of War”
Serie 4, episode 2. Guard in “Bad Blood”
The Hide; season 7. episode 3
A nanny missing a tooth
An industrialist’s functional but not dazzling teeth

Some do have good teeth:


I don’t know if in the between-the-wars period imperfect teeth could be fixed to look like what is considered normal today, but the family of Downton Abbey would have had the resources for cosmetic dentistry if needed and available. So it isn’t too surprising that Lady Mary, Mrs. Crawley, and the rest of the Granthams have 21st century American teeth.

But it would be very surprising if the servants of the house also have perfect smiles. And they do. This is a huge oversight for a series that claims to be true to its historical period.

Even scullery maid Daisy has a dazzling smile.
Downton Abbey
Housekeeper Mrs. Hughes’ perfect smile
Downton Abbey
Tenant farmer’s and cook’s healthy mouths. 
Lady's maid Anna's perfect smile
Maid Anna’s teeth are every bit as good as Lady Mary’s.

Let’s face it: imperfect teeth are taboo. There can be no glamour when there’s a crooked tooth.

But there can be no pretense of historical accuracy when the scullery maid has a smile that rivals an aristocrat’s.


The Audacity of Getty Images Exploiting Carol Highsmith, America’s Photographer

I first wrote about Carol Highsmith eight years ago, asking “Is Carol M. Highsmith the Most Generous Artist of Our Time?” The answer was yes then and remains so today. Others agree with this valuation, including C. Ford Peatross, director of Architecture, Design and Engineering, Prints and Photographs, Library of Congress, who in 2007 remarked: “The donation of her photographs [The Highsmith (Carol M.) Archive] is one of the greatest acts of generosity in the history of the Library.”

Highsmith has provided the Library of Congress with 31,828 images (as of today, 8/18/16)– and has stipulated that they be placed in the public domain. The Library expects that number will likely approach 100,000.

I was astounded to find an outstanding contemporary photographer’s work could be freely used. No licensing fees are required to use her images, but there should be a credit line, at the least identifying her as the Creator of the work, and preferably using this Credit Line: Library of Congress, Prints & Photographs Division, photograph by Carol M. Highsmith [reproduction number, e.g., LC-USZ62-123456].

After I posted the first time about Highsmith, I learned she was seeking sponsors for an ambitious project, photographing every state so that a record may be had of what America looked like in the first decades of the 21st century.  I’ve been following her progress since she started with Alabama, with sponsorship from philanthropist George F. Landegger.

You can imagine how appalled I was to read about the gross exploitation of Highsmith’s generosity by Getty Images.

In December 2015 Highsmith received notification from Alamay Ltd.’s License Compliance Services (LCS), (on behalf of Getty Images) demanding $120 because she was in breach of Getty’s licensing terms for the content of an image she had used on her website and accusing her of copyright infringement.

The image in question: one of Highsmith’s own and one she placed in the Library of Congress with the stipulation that it be placed in the public domain.

Apparently, Getty Images had been downloading her thousands of images, placing them on its site, and demanding licensing fees, as if Getty owned the images. In other words, they were doing exactly the opposite of Highsmith’s intention, which is to allow free use of her images. Using her images is not the same as owning her images.

Getty had 18,755 of Highsmith’s photos on its site.

The way this all came to light was because Getty “scrapes” the net, looking for uses of its images and checking license fees have been paid.

Eventually the scraper hit Highsmith’s website, and the scheme was exposed. Perhaps if Getty had been careful to credit Highsmith as the photographer, they would have realized sending Highsmith a threatening letter wasn’t a good idea.

Highsmith has filed a $1 billion dollar suit.

Writing for, IP specialist Attorney Bryan Sullivan summarizes the suit:

“against Getty Images targeting the ‘gross misuse’ of 18,755 of Highsmith’s photographs. According to the suit, ‘The defendants [Getty Images] have apparently misappropriated Ms. Highsmith’s generous gift to the American people…. [They] are not only unlawfully charging licensing fees but are falsely and fraudulently holding themselves out as the exclusive copyright owner.’ Highsmith claims that Getty was unlawfully telling users that they would have to buy a copyright license from Getty to use the images. ‘Likewise, nowhere on its website does Getty identify Ms. Highsmith as the copyright owner of the work.’”

Sullivan expects Getty will settle out of court.

A prediction: when she wins, Highsmith’s life will change in one way. She won’t have to seek sponsorships to make it possible for her to work night and day, and this means she’ll have more time to document America.

You can follow Highsmith’s travels on Facebook (Carol M. Highsmith’s America).

Here are four of Highsmith’s photos: “Porter Sculpture Park, Montrose, South Dakota,” “Alpine lakes and forest, Denali National Park, Alaska,” “Monument Valley View, Arizona,” and “July 4th fireworks, Washington, D.C.”Porter Sculpture Park

Alpine lakes and forest, in Denali National Park, Alaska04002rWashington, D.C. July 4th Fireworks

Credits: Library of Congress, Prints & Photographs Division, photographs by Carol M. Highsmith [ LC-DIG-highsm-04547, LC-DIG-highsm-04272, LC-DIG-highsm-04002, LC-DIG-highsm-04460]

ESLD: Holding Steady

This week marks the first anniversary of what I for many months felt was a final descent. In the course of three weeks I had a massive esophageal bleed at my mother’s deathbed, had a transjugular intrahepatic portosystemic shunt (TIPS) installed, and was hospitalized with hepatic encephalopathy.

It took until April 21 for me to stop thinking about dying and to begin to think about living. The evening of the 20th I took a half-dose (by mistake) of a new sleep drug, and I had a paradoxical reaction: I could not sleep at all. I was awake for about 36 hours, and if you have ever experienced that, you know that around about hour 32, things can start to get quite interesting. It was Earth Day, and for three hours in the late afternoon I did nothing but watch the changing colors of the green leaves at the day turned to dusk.

And the next day I felt like my brain‘s reset button had been engaged.

I hit a plateau, I guess. It’s like I had been falling, falling, falling into the abyss but then the fall was interrupted, as if I had landed on an anomaly in the walls of this abyss, some unanticipated protuberance.

This doesn’t mean I can get all together out of the abyss; eventually the protuberance will erode, and the fall resume, but it isn’t happening now.

Now I have some distance from the events of the past year, perhaps I can describe some of those psycho-social aspects of my situation.

For much of last year I felt like all my psychic defenses had been breached. I was attracted by its title to Dion Fortune’s classic Psychic Self-Defense in which she describes the effects of psychic attacks by evil magicians or spirits and means of banishing them or protecting one’s self from further harm. I felt as if I had been attacked by malevolent forces – not bad magic mind you – but a free-floating malevolence.

I think magical thinking is an aspect of illness. I’m even a bit hesitant about saying things are going pretty well for fear that the saying so will make them go wrong.

I remember a particularly bad night when my daughter was hours late getting home (she had gone to the movies; phone off, etc.). I envisioned all the worst as having happened, and that here I was thinking things were pretty bad, and the Universe was going to say, “hey, you think things had been bad before but you have no idea just how bad bad can be” – a little like when you hear some particularly stupid parent tell a child who is crying to quit or else “I’ll give you something to cry about” and is then amazed that the child cries harder still.

Then there is last-time-it is. Is this my last Thanksgiving, my last birthday, my last Christmas? It doesn’t make it seem more precious: it ruins it.

Then there is the any of us could die at any time problem. While this is absolutely true, we don’t really believe it. It is a tralse — some truth, more falsity. Sometimes I feel like responding to that observation with a counter-offering: “in that case, why don’t we switch livers?” But these is no reason to offend folks who are trying to be kind.

I neglected my social life. It was easy to do so. I think I was like the spectre at the feast for much of the year, looking as exhausted and as beat as I felt. Maybe I imagined that people were pulling away from me. Maybe they were. It is an awkward situation.

It didn’t help matters when David Bowie died and the initial reports were that liver cancer was the cause (later clarified as pancreatic that had spread to the liver). Not all people who have liver cancer are cirrhotics, and not all cirrohtics get liver cancer. But cirrhosis is a definite risk factor.

I had decided long ago that if I developed liver cancer, I was not going to fight it (in fact, I think there is little that can be done when someone with ESLD gets liver cancer). I am supposed to go every six months to see if I have developed cancer, but I decided, why bother?

I will tell you why: in March we went on a vacation, and after nine months of doing nothing, I wasn’t prepared for walking a lot. After about a half hour, I would hurt worse and worse as a pain developed on my side and radiated to my back. Of course I decided well damn, I must have cancer.

So I went in for the ultrasound and blood test to see if maybe I was wrong. And I was. But I did have a severe vitamin D deficiency.

Throughout much of the night of my 36 hours of wakefulness I watched Bowie on youtube. He lived until he died. Made an album, wrote a play.

Maybe that contributed to my change of attitude, my finding the plateau. Or maybe it takes 9 months to transition from one existence to another.

I just know that when I finally did sleep, when I awoke, I decided that today I was not going to think about My Death.

And now that has become a habit.

This Thing Called End-Stage Liver Disease

This is another post about primary biliary cholangitis (cirrhosis) [PBC]. In my last post, I used the term End-Stage Liver Disease [ESLD]. It’s a very vague and barely useful designation. 

The good news is that my portal hypertension — once the subject of so many gruesome posts — has been effectively controlled by the Transjugular Intrahepatic Portosystemic Shunt [TIPS] I had installed in July 2015. I haven’t had a bleed since, and an exploratory endoscopy in the fall showed I now have a nice, smooth, pinkish esophagus instead of one with red streaks of varicose veins.

But I haven’t felt better. When I look back on what I could do in 2014 or 2013 and compare it with how I’ve felt the past nine months, I know I am at best holding steady.

So at my last hepatologist appointment, I asked the doctor straight out: Do I have ESLD? He looked taken aback, like this was an acronym that doctors use among themselves not with patients. But he said, yes. And so I said, how much longer do I have? Months? Years? And he said he expected years.

When the bleeds happened, they were potentially life-threatening emergencies. Still, I’d get patched up and leave the hospital the next day. Once they started coming much more often, anemia became a big issue until I got Injectafor iron infusions. I avoided remote locations and long airflights, but as nasty as they were, I now look back on the Bleed years (8/10 to 7/15) as the good old days.

I also haven’t had another bout of hepatic  encephalopathy [HE], one of the scariest ordeals of this whole PBC ghastliness. 

But there is a very low grade (comparatively) of HE, and especially when I am even more fatigued than usual, I can tell that I’m having trouble with short-term memory and learning new things. For example, my husband and I went to Washington DC last month, and I simply could not grasp the subway system. It’s hard to remember what day of the week it is; then again, there is little to distinguish them.

So what is ESLD? It’s odd. You will find a lot of sites with information on End-Stage Liver Disease, but there’s little mention of when Beginning becomes Middle goes to End. I’m not sure there is a Beginning or Middle variety. End-Stage Liver Disease [ELD]  itself is most commonly mentioned in discussing MELD scores; the M refers to Model, and a MELD score is a complicated and flawed scoring system for transplant urgency. The higher the score — and 40 or so seems to be the cap, the worse off you are. I’m at 12.

More often, I’ve found articles using a different terminology. The NY Times offers this simple comparison.

  • Compensated cirrhosis means that the body still functions fairly well despite scarring of the liver. Many people with compensated cirrhosis experience few or no symptoms.

  • Decompensated cirrhosis means that the severe scarring of the liver has damaged and disrupted essential body functions. Patients with decompensated cirrhosis develop many serious and life-threatening symptoms and complications.

But then there’s another approach using four levels.  

Here’s one that does it in three: inflammation, scarring, failure. I wonder if, since the liver is the only major organ that up to a point can regenerate new cells, it would be possible to get out of inflammation back to normal.

But cirrhotic cells are scarred and ruined; they aren’t going to come back to life. And my PBC continues to destroy the bile ducts, and this blockage continues to damage liver cells.



How PBC Became PBC

I haven’t updated since October of last year. I get comments now and then, asking how things are going. To catch you up if you are new here, I have  been writing about my battles with  Primary Biliary Cirrhosis. While I haven’t had any more esophageal bleeds or episodes of hepatic encephalopathy, this condition continues its destruction.

Although my bilirubin and albumin are worse than they were this time last year, it’s the psycho-social effects that have been devastating this winter. I intend to write more, but shorter, posts on those aspects of End Stage Liver Disease.

But first up is that I no longer have Primary Biliary Cirrhosis, according to the international health community.

I have instead Primary Biliary Cholangitis.

Cholangitis isn’t an altogether accurate a term to take the place of cirrhosis for this illness. I suppose cholangitis  was assumed a good enough switch since in both cholangitis  and primary biliary cirrhosis, the bile ducts are compromised.

But there are some very significant differences. Simple cholangitis is usually caused by a bacterial infection; primary biliary cirrhosis (cholangitis) is an auto-immune condition. The prognosis for simple  cholangitis is good if caught in time. There are a variety of treatments.

Primary Biliary Cirrhosis or Primary Biliary Cholangitis has one drug that may slow the progression of bile duct destruction. It will lead to cirrhosis and end-stage liver disease. How long this will take varies, but it will happen. The only fix is a transplant, and, since this is an auto-immune illness, it isn’t unusual for it to recur. The name made sense: primary (firstly), biliary (bile ducts destoyed), cirrhosis (inevitable effect in the long-run).

But at least the same letters apply, so PBC can become PBC.

Why change to a less accurate name?

Ignorance and prejudice. Although there are many conditions that can cause cirrhosis, the biggie is excessive alcohol use (of course, there are daily drinkers who do not reach end-stage liver disease) and hepatitis (and one of these can be caused by using dirty needles).

And so cirrhosis is a huge trigger word: this person’s lifestyle has caused her condition. For many, the social stigma is as bad as the condition itself, and the medical community decided these people have enough to deal with. They are not even close to fixing the disease, but lessening the instant self-righteousness of the unafflicted is within their range.

Say “I have primary biliary cirrhosis.” Most people hear something like “I gobblledly gook blab blab cirrhosis.” Next, they likely speculate on what vice is the cause of the problem.

It’s a rare enough illness that I have had to explain it to first responders and ER nurses.

You can feel what isn’t said: the emergency personnel have scraped up enough people killed by drunk drivers to have no sympathy for heavy drinkers.

Believe me, there are no heavy drinkers among those with PBC whose livers are failing. If the liver can no longer handle red meat, it isn’t going to be up to processing alcohol.

Maybe we once drank cheerfully and heartily. Maybe we were teetotalers. Neither would have made any difference.

At least the next time I’m hauled in my biggest problem with listing my medical history will be remembering how to spell cholangitis, and not dealing with all the baggage cirrhosis drags around.


Protein, Ammonia, Cirrhosis, and Hepatic Encephalopathy: What I Learned

My last post, “Hepatic Encephalopathy: On Knowing I Didn’t Know What I Knew I Know,” ended with me trying to cope with an episode of confusion, temporary loss of lifelong memories and inability to form new ones a week following the installation of a Transjugular Intrahepatic Portosystemic Shunt (TIPS) to deal with the portal hypertension resulting from cirrhosis, a consequence of Primary Biliary Cirrhosis (or Cholangitis) (Regular readers will be used to the growing “This is the house that Jack built” nature of my introductory sentences.).

I believe I have regained all I had lost of my memory. The treatment was (and continues to be as a preventive) an extreme laxative called Lactulose that “works by drawing ammonia from the blood into the colon where it is removed from the body.” It is a sickeningly sweet liquid that makes my intestines feel as if they’ve been invaded by frolicsome ferrets, but this transient discomfort is trivial compared to the frightful alternative of hepatic encephalopathy.

After the TIPS was installed, I was told to avoid fried food and red meat and I complied (by the way, pork is not “the other white meat” when it comes to ammonia: it is a red meat). However, because of the events of the two weeks preceding my encephalopathy (days at the nursing home, my mother’s death, 300 mile each way trip to UAB, two endoscopies with conscious sedation, general anesthesia with the TIPS, etc.) I had become very irregular, backed up as it were.  I was not getting food processed and through my digestive system efficiently, and certainly not quickly (now the Lactulose helps with that).

My understanding of why I should avoid red meat and eat small amounts of protein over the course of the day rather than in two or three sessions was slow in coming.

After release from the hospital, my family and I started a hunt for low-ammonia foods. No luck — just try to find the low ammonia diet. There are horrifying stories about “pink slime” and the use of ammonia to control e coli in food processing plants (remember that? The “pink slime” Wikipedia entry hasn’t been updated since 2013, which doesn’t mean the stuff isn’t still around.). Red meats and rind cheeses were listed as items to avoid if you suffer from cirrhosis, but there wasn’t a clear indication of why. Finally, I contacted a food scientist I knew who provided the key.

I was not going to find low ammonia foods. Ammonia is a by-product of the breakdown of proteins, whether they be animal or plant-based. The thing is, red meats and rind cheeses (and to a lesser extent, chicken and fish) are more protein-intensive than vegetable-based proteins, so more ammonia is produced during their digestion.

For most people this isn’t a problem. The liver takes care of the problem, as it handles other toxins consumed.

But a cirrhotic liver isn’t up to the task. Think of all the drug labels and commercials that tell you to consult with your doctor before using if you have an impaired liver.

Red meat should contain a similar warning.

From the 1950s (at least) into the first years of this century, cirrhotics who had experienced hepatic encephalopathy [HE] were told to eat little protein, period, and malnourishment was common among cirrhotics. As their bodies consumed their own muscle and fat for protein, ammonia was released, and thus HE was not avoided by not eating meat.

Now the advice is for cirrhotics to consume more protein than than non-cirrhotics, and I have been told that while it is most important to get enough protein — to eat chicken and fish if I need to — non-animal sources of protein are less of a challenge to my liver. I am still looking for studies on whether vegetarian or vegan diets are superior for preventing HE in contrast to those that include some animal protein. If it were possible to eliminate the need for Lactolose or rifiximin (an antibiotic used to prevent HE), I would go vegan.

It was easier to give up red meat than I would have imagined. Back when severe anemia was one of my major issues,  I was a staunch defender of meat-eating, arguing that for some of us, a vegetarian diet was not an option, that we couldn’t otherwise get the iron needed to raise our hemoglobin from the 8’s to the 12’s without transfusions or infusions. And I still think that universal vegetarianism isn’t practical, unless you want to require all who live in regions inhospitable to agriculture to eat processed foods shipped in from other climes (are there any Sami, Inuits, or Eskimo thriving on locally-produced vegetarian foods?).

Now I eat far less chicken and fish; they don’t dominate the plate but are supplements to the grains and vegetables, and I eat them only a few times a week. I eat a lot of beans and rice, oatmeal, grains. No fast food — and I don’t miss that at all.

There’s a relief to being forced to do what I’ve known for a long time I should do but have been too lazy to bother doing.

So far, I’ve had no more problems with HE. There are other theories about what causes hepatic encephalopathy, but the prevailing one is that when the liver can’t handle the ammonia that is a by-product of protein digestion, the ammonia crosses the blood-brain barrier, and the brain becomes a sink for this noxious toxin.

Still, it is amazing to me that cirrhosis has been recognized as a disease for hundreds of years and yet so many questions remain about its treatment and effects, but I suspect that may be because it is largely linked to alcoholism, and the stigma of cirrhosis as a lifestyle and avoidable disease.

Hepatic Encephalopathy: On Knowing I Didn’t Know What I Knew I Know

This post assumes you’ve read the two preceding ones: “My 13th — and Perhaps Final — Portal Hypertension Bleed” and “In Which a Transjugular Intrahepatic Portosystemic Shunt (TIPS) Is Installed in My Liver.” This post is my subjective, and given the subject, patchy account of a few dreadful days. I will share what I later learned about hepatic encephalopathy in a future post.

For well over half a century, I’ve known the answer to the question: What is your birthday?

Even when I was missing my four front teeth and saying “December twenty-six” was a twister, I could answer that question: It’s the day after Christmas.

On July 23, 2015, one week after my TIPS procedure, I couldn’t find the answer. I knew I knew it, and that knowing—that is, knowing this was happening—that I had lost a nearly lifelong memory—was horrifying.

I was suffering from hepatic encephalopathy.

My liver could not handle the ammonia it normally filtered, the ammonia had crossed the blood-brain barrier, and I was unable to make new memories or access information long stored and always before easily within reach.

I left the hospital Sunday, July 19, 2015. The installation of my Transjugular Intrahepatic Portosystemic Shunt (TIPS) was deemed a success. My portal hypertension, which was 15 (dangerously high) when the radiologists began the procedure, had dropped to a normal range of 2-4. At first my liver function numbers were all over the place, but that was to be expected. My ammonia levels were high, but had steadily dropped. My digestive system seemed to have woken up from the general anesthesia. I complained of constipation, but I did have a bm.

I know that Monday I slept all day, and I expect I did on Tuesday and Wednesday as well. I had had a rough two weeks.

The first weirdness was  pre-dawn Thursday. I could not get warm. I like a cold room when I sleep, and keep a lot of covers handy year-round. But I could not warm up.

At some point Thursday morning my husband noticed I wasn’t making sense when he asked if I wanted anything to eat or drink. I was somnolent, very hard to rouse. I have no memory of this.

He told me he called my primary care physician and gastroenterologist. It was only a few days later that I remembered anything at all about having been at the GI’s. Leaving the house, I walked right past a huge display of flowers that had arrived that morning from my brother: I had no memory of them when my husband mentioned them later.

I have a vague memory of either getting into or out of the car at the doctor’s, of looking up and seeing my daughter had joined us in the consulting room, and of sitting in the room (I guess that I wasn’t lying down because they didn’t want me to sleep). I’m told that the physician’s assistant offered to send us along with a prescription for Lactolose, a strong laxative which I’ll discuss in the next post, but since my husband and daughter wouldn’t have known what to do if I didn’t respond to this drug or what to expect or danger signs, they—I believe quite rightly—chose to take me down the street to the ER.

I have no memory of getting there or of the usual procedures (and I’ve been in the ER enough to know), like signing in, waiting in the first waiting room area, going to the triage nurse, and having vitals taken. I do remember being in the second waiting area, and I guess all the action had woken me up enough so that I realized what was happening.

Hepatic encephalopathy is the complication of a TIPs I feared the most because it involves your ability to think and remember. At its worst, it can lead to coma, sometimes reversible, sometimes not.

To the other people in the waiting room, I must have looked fine – no ice packs, bandages, vomit bag, etc. But each moment that passed I believed I was closer to losing my mind. At some point I must have asked for a DNR (Do Not Resuscitate) bracelet because much later I noticed I was wearing a purple bracelet I’d never seen before.

At some point—an hour? two?—I was taken back into the examining area.

After a while, I said to my husband, aren’t they going to do anything? They haven’t even started an IV. They always start IVs. He said, look at your hand.

I looked down, and saw I had an IV. I in fact had what I’ll call a double-barreled I on the back of my hand—a painful place for a stick—and I am one of those people with small veins that roll, etc.

Was I too somnolent to feel an IV going in? Did I feel it but was unable to remember having felt it? Was I, in other words, unable to form new memories?

Then came the questions.

  • What is your phone number? I hadn’t a clue.
  • What is your birthday? I know this, I do, I know this. I couldn’t find it.
  • What month is it? 12?
  • Try again. 6?

How strange. I have this very vivid memory of not knowing these answers.

(Later it occurred to me that the oddness of my response – 12, 6 – rather than the names of the months was because I was still searching for my birthday (12/26) and could not make the leap to the new question. My phone number I simply had to relearn, and it took til Sunday morning before I got it right routinely.)

The rest of Thursday is vague to me. I don’t know if I had anything to eat that day. I can’t tell you if it was day or night when I got into a room. This might not seem unusual, except that here going from the ER to the in-patient hospital requires an ambulance ride across a street. But I remember being able to get from the gurney to my bed without help.

Then it was Friday. I remember very little of it until the evening. Then it was time to start trying to figure out what had happened.

My 13th — and Perhaps Final — Portal Hypertension Bleed

At the end of my previous post, My Mother’s Last Three Days, I announced that I had had my thirteenth portal hypertension bleed at my mother’s death bed.*

It had happened. A bleed. A big one. I was taken to the hospital by ambulance.

I think that I have never been nearer to a complete breakdown than I was that night in the ER. Why a bleed now? Even if she had had enough opiates to cloud her memory, my last memory of my mother will be this: not being there for her.

The usual thing, the IV’s, the history, the whole admissions rigmarole proceeded. I told the GI on call that night if I wasn’t going to be scoped in the morning when there may still be a chance of finding the source of the bleed, that I wouldn’t consent at all to an upper endoscopy. The gastroenterologists here have repeatedly delayed up to twenty hours between the start of a bleed and their looking for its source, and then are surprised when they find none. A bleed can stop on its own, and the IV medications, as I have explained before, aid this.

I was taken for the endoscopy at 8:30 or so in the morning.

When I was returned to the room, my husband was there. He had his news, and I had mine. His presence was enough to tell me what his was: my mother was dead.

Mine? The GI who did the endoscopy said that what she had seen was something she could not fix, and neither could her colleagues. I needed to get to a teaching hospital as soon as possible.

I had a stray blood vessel resting over two large varices. Normally, if I understood her correctly, this vessel could have been cauterized, but as it was positioned, there was a risk of burning through the vessel and into my varices, causing a massive bleed.

Things had gone for bad to worse. I was too distressed to be surprised, quite frankly.

So we got in contact with my hepatologist at the University of Alabama in Birmingham about six hours away, and an appointment was set so that he could have a look for himself first thing Monday morning.

Here are the pictures from the July 9 endoscopy clearly showing the problem in my esophagus. I think the doctor said the purple things were large varices that couldn’t be banded because of the blood vessel that couldn’t be cauterized because of its position.

In my next post, I’ll explain how things got worse — again.

*(To catch you up if you are new here, I have Primary Biliary Cirrhosis (or Primary Biliary Cholangitis), and since August 2010, I have had some minor and a some awful episodes of vomiting blood —  hematemesis — because of bursts varices in my esophagus. There have been lots of co-diagnoses along the way, from ordinary ulcer upper GI bleeds, to Cameron’s Erosions, to Dieulafoy’s Lesions, but as will become evident, whatever you want to call the spouting body, the source was likely always the same: the portal pressure in my portal vein in my liver measured 15 on July 16, 2015,  dangerously high. It is now 2 to 4. More on that later.)

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My Mother’s Last Three Days

Easily the most read and commented upon post on this blog is one that I wrote after my father’s death, How to Know When Death is Imminent, Signs Someone is Dying.

My mother died six weeks ago on July 9, 2015. I called my father’s death “hard work.” It was the first for which I had kept vigil, and now I know his was an easy one, at least for me. He suffered from Parkinson’s, dementia, and Alzheimer’s and had been in and out of consciousness for days prior to his death. He couldn’t talk, so I did not know if he was in pai or scared. He rallied to smile once, although I could tell from his eyes he was aware that people were with him.

My mother only lost consciousness at the very end, helped along, I think, by generous doses of morphine.

She had been totally bedridden for 18 months, and full assist (had to be fed) for the last six or so.

But she never became demented.

My mother was disabled by rheumatoid arthritis, and weakened and finally defeated by kidney failure. The last year of her life she was assaulted by edema. Using diuretics compromised her kidney function. Not using diuretics meant her arms especially would look like half-full water balloons, and every time she would be touched, she was in pain. Even the seam allowances on the insides of her sleeves tormented her. This is what we could see. Edema also puts a strain on the heart.

Through careful monitoring, the doctor was adding the diuretics as needed, then pulling back when the kidney function numbers started looking alarming; then repeat and repeat.

My mom had a decent quality of life, primarily because of the graciousness and professionalism of the staff of Pisgah Manor Nursing Home, who I will never be able to praise highly enough. My mom loved her meals, and she raved about the food. I’d leave Pigsah Manor hungry when I’d come to feed her. Let’s stop and consider that: Have you ever heard any visitors say they left a nursing home hungry? And my mom loved to bird watch. We had several feeders going outside her window, and I have never spent so much time bird-watching. This spring and summer brought so many goldfinches.

Then at the end of June, I had a call that my mom was hallucinating horrifying scenarios, like her blankets were on fire and George W. Bush’s dog was bleeding out on her bed (really). The nursing home suspected a urinary tract infection, and the specimen confirmed this; within a few days she seemed much better, but for the first time wasn’t eating every morsel on her plate. I heard a strange sound from her lungs, like a cat mewling.

Monday, July 6, I went out to the home; they were about to call me anyway. My mother had a gurgling sound in her lungs now, but no other cold, flu, or virus symptoms. She obviously did not feel well; she had no appetite and would only drink with persuasion.

When her morning CNA left, she reported that my mom had produced no urine. I knew we were likely in trouble then; I had learned that when my dad died.

That night, I made calls to those I needed to. There was a contingent who thought I should have her transferred to the hospital. They were certain that once there, she’d get some medication that would fix her up just fine. I decided, since she was fully cognizant, to ask her what she wanted to do.

Tuesday a catheter was inserted. After her bladder was drained, it was obvious she was simply not making urine. I told my mother she was very sick, and asked if she wanted to go to the hospital. She declared she would fight this problem at the nursing home among people who cared for her.

The next two days, my mom was frightened and in pain. She said over and over and over again: “I can’t breathe.” And over and over I would tell her that yes she could breathe, if she could not, she couldn’t talk. She had supplementary oxygen; we would tell her to breathe through her nose calmly and slowly and out through her mouth. It didn’t work.

“I can’t breathe.”

She sounded like — and likely felt like — she was drowning. Edema had spread to her lungs.

Still no urine: we were coming to the end. The nurses did not hide this from me. Always there is the caveat that no one knows for sure, people will surprise you and so on, but there was no reason to believe this would be one of those times.

I was encouraged to go home and rest. Wednesday morning when I walked in I immediately noticed two changes. My mom was ashen, especially on her upper lip area, chin, and the region of the face around her mouth.

I am not trying to be poetic when I use “ashen.” It is used for a reason. The color is much the same as ash.

I’m also not trying to be poetic when I say that the light had gone out of her eyes. This is hard to explain, but there was a haziness or dimness. Perhaps only someone who knew my mother before would have seen the difference. She was, however, still fully conscious, and still panicking and saying “I can’t breathe” and “Help me.”

I asked her again about going to the hospital, and she refused. I told her she was very, very sick.

She asked if she might die. I said yes. When? No one knew.

She seemed genuinely surprised by this. Here she was, 6 weeks shy of 86, completely bedridden and disabled, was refusing food and water, not urinating and didn’t think she could breathe — and yet she was surprised.

I asked if she wanted me to make any calls so she could talk. No. The TV had been off for a few days now, and we were down to her caregivers, me, and her.

She said she was scared. I said what of. She looked at me like I was a total fool, and said, “Dying, of course.” She agreed when I offered to call a chaplain.

The rallying that was so dramatic with my father took a different form with my mom. My mom was exceptionally determined. She had strong opinions, and this blog is named after a phrase of her that could strike fear in those on her list (I’m going to have a little talk with him. . .”) while spectators would get the popcorn popping and wait for the fireworks. She was also pretty good at denial.

When my daughter and her boyfriend came by, she brightened up; she loved visits from my daughter. But after ten minutes, my mom told the two to get along with their evening and go out and enjoy themselves, that she had no intention of dying that night and that she would see them tomorrow. And the next day. And the next.

She tried the same with me, and I went outside to make some calls. Coming back in, I encountered the Perfect Daughter, there five days out of seven, who told me my mom bragged that she had “sent them all away.”

That was the last liveliness I saw from her. The night went on. There was no more conversation, just  “I can’t breathe” and “Help me,” and me watching the clock for when she could have more morphine. The intervals were less, the dosages greater.

My mother died around 9 am Thursday morning. I was not there. She was still conscious when my husband arrived to take over, and she was worried about me.

I was in the hospital waiting for an upper endoscopy.

Midnight I had gone to get the meds nurse; she had delivered the shot, and I was feeling a bit woozy, but blamed it on tiredness and stress and leaned my head against my mom’s railing. The next thing I knew, I was looking down on myself, and I was covered in blood, the chair was covered in blood, and there was a pool at my feet.

My mother was crying out,  “I can’t breathe. . . Help me.”

I had to tell her I could not, that I needed her to press the call button. She couldn’t. So I staggered into the hallway and yelled for help.

That was the last I saw of my mother, and the last she saw of me.

I had had my thirteenth portal hypertension upper GI bleed at her deathbed.