Tag Archives: Death

HOW NOT TO EMBALM A POPE

Pope Francis recently passed away. He lay in state at the Vatican, in an open casket, for three days while over a quarter million people filed by and respected his body. Francis remained remarkedly well preserved unlike Pope Pius XII who died in 1958 and became the poster boy of morbid mortuary fails and the most grotesque example of how not to embalm a pope.

When I saw newsfeed afterlife photos of Pope Francis, eyes closed, dressed in red vestments, wearing a bishop’s miter, and lightly clutching a rosary in his bare hands, I was struck by how life-like he appeared. Having considerable experience around dead bodies and knowing the decomposition process, the first thing in my mind was, “Wow, they did a great job of embalming. I wonder what process they used?”

It was minimal invasive thanatopraxia, not the never-tried-before embalming method employed on Pius XII that resulted in the most undignified incident in papal history which horrified the faithful clergy and nauseated the public mourners.

We’ll look at what went ghastly wrong with incorpsing Pope Pius XII but first let’s review the history of human body preservation and the science of decomposition.

The Ancients and the Afterlife

The practice of embalming goes back more than 6,000 years. The Egyptians get most of the credit, and rightfully so. They mastered a method that mummified bodies so well we’re still unwrapping their secrets today. Of interest, read the Dyingwords article titled The Lost Art of Making Mummies.

Back then, embalming wasn’t just a medical procedure—it was a spiritual rite. The Egyptians believed in an afterlife that required a well-preserved vessel for the soul. So, they developed a meticulous process involving evisceration (organ removal), desiccation (drying), and resin-based sealing.

Here’s what that looked like:

  • The brain? Removed through the nostrils using a hooked instrument.
  • The intestines, stomach, liver, and lungs? Taken out through an abdominal incision and often placed in canopic jars.
  • The heart? Sometimes left in, sometimes not. That depended upon the dynasty and theology of the day.
  • The body? Packed with natron salt for 40 days to dehydrate the tissues before being wrapped in linen soaked in oils and resins.

The results? Bodies that could last for many millennia. Not pretty, but persistent.

Other cultures had their own versions. The Chinchorro of South America were embalming their dead a thousand years before the Egyptians. Greeks and Romans experimented with honey, spices, and lead-lined coffins. The Chinese used mercury. Everyone wanted to cheat time, but none did it with quite the same ritualistic precision as the Pharaohs’ embalmers.

From Sacred to Sanitary — The Middle Ages to the Renaissance

Once Christianity took hold in Europe, embalming practices changed. The early Church frowned on mutilating the body, which was seen as a sacred temple. Instead, burial became the norm, often with little more than prayers and herbs.

But during the Middle Ages, embalming resurfaced—this time for more pragmatic reasons than spiritual ones. Kings, nobles, and church leaders often died far from home, and the only way to get them back without stinking up the countryside was to pack the body with preservatives. That usually meant alcohol, myrrh, or wax, wrapped tightly to delay decay.

Then came the Renaissance. Along with new art and new ideas came new interest in human anatomy. Surgeons, scientists, and physicians began dissecting cadavers, and they needed a way to keep bodies from decomposing before their scalpels could learn anything.

This is when we saw the rise of arterial injection techniques, particularly in Italy. Instead of just treating the surface or packing the cavities, early anatomists began experimenting with injecting preservative fluids into the blood vessels—a precursor to modern embalming.

Modern Embalming Is Born — Thanks to War and a Cold Body Count

The real shift toward modern embalming came with the American Civil War (1861–1865). Thousands of soldiers were dying far from home, and grieving families wanted their boys brought back in a condition fit for burial. Enter Dr. Thomas Holmes, often called the “Father of Modern Embalming in America.”

Holmes developed a formula based on arsenic and alcohol, which allowed him to embalm bodies quickly and effectively. He reportedly embalmed over 4,000 Union soldiers during the war. Word got out. Embalming became a recognized profession, and traveling embalmers followed the carnage across battlefields.

After the war, funeral homes emerged as legitimate businesses, and embalming became standard practice. The U.S. in particular embraced it more than any other country. By the early 20th century, embalming was no longer a battlefield necessity—it was a cultural expectation.

The Rise of Formaldehyde and the Funeral Industry

In the early 1900s, formaldehyde replaced arsenic as the go-to embalming chemical. Arsenic, after all, had a nasty side effect—it poisoned the ground and anyone who tried to exhume the body. Formaldehyde was seen as safer (relatively), more stable, and more effective at halting decomposition.

The technique was refined:

  1. Arterial injection of embalming fluid through the carotid artery.
  2. Drainage through the jugular vein.
  3. Cavity embalming with a trocar (a hollow needle) to remove and replace internal fluids with preservatives.
  4. Surface treatments and reconstruction, particularly for trauma or decomposition cases.

By mid-century, embalming was as routine in North America as brushing teeth. A new profession emerged—the embalmer as technician, equal parts chemist, artist, and psychologist.

But embalming wasn’t just about science. It became part of the “death care” industry, an entire system designed to sanitize and soften death’s realities for the viewing public.

Present Day — From Science to Aesthetics

Modern embalming is as much about presentation as preservation. The goal is often to create a “memory picture”—a final, peaceful image for loved ones. This is where cosmetic restoration comes in.

Today’s embalming fluids are far more sophisticated:

  • Formaldehyde-based solutions are still used, but often mixed with glutaraldehyde, alcohols, humectants (moisturizers), and dyes.
  • Specialized chemicals are used depending on the body’s condition—edema, jaundice, emaciation, or post-autopsy cases each require different formulations.

Prep rooms are sterile and methodical:

  • Embalmers wear PPE.
  • The process is documented.
  • Ventilation systems remove harmful vapors.
  • Green burial movements have also influenced the use of lower-toxicity chemicals.

But here’s the truth: no modern embalming is permanent. Today’s best results will preserve a body for 1 to 2 weeks in viewable condition. In extreme cases—with refrigeration, sealing, and advanced fluids—a month or more is possible. But eventually nature, or entropy, always wins.

The Best Modern Results — What Actually Works

If you’re wondering what produces the best results today, here’s the truth from someone who’s worked with too many dead to count:

  • Combination of arterial and cavity embalming is essential.
  • Formaldehyde-based fluids, when balanced with humectants and surfactants, remain the gold standard.
  • Rapid intervention after death—the sooner the body is embalmed, the better the result.
  • Refrigeration slows decomposition and supports the embalmer’s efforts.
  • Cosmetic artistry—restorative work, airbrushes, facial reconstruction—is often the difference between an acceptable viewing and a traumatic one.

It’s not just chemistry—it’s craftsmanship.

Final Thoughts from the Cold Side of the Table

Embalming isn’t a morbid curiosity. It’s a window into how we handle death, both literally and philosophically. From the sands of Giza to the stainless of modern morgues, embalming has always been a human response to the ultimate truth—that we’re here for a short while, and then we’re gone.

We embalm not just to preserve the body, but to hold on to meaning.

So, whether you see it as sacred, sanitary, or strictly scientific, embalming is part of the long story of what it means to live… and what it means to say goodbye.

The Science of Human Body Decomposition — When Nature Takes the Wheel

If embalming is our attempt to delay death’s effects, decomposition is nature’s way of reminding us who’s really in charge.

I’ve seen more bodies in more stages of decomposition than most folks care to imagine. And no two look—or smell—quite the same. But under all the grime, there’s a cold, clear science to what happens when the human machine shuts down and the decomp clock starts ticking.

Whether embalmed, buried, burned, or left to the elements, every body biologically breaks down. Understanding decomposition isn’t just a matter of curiosity—it’s crucial in criminal investigations, disaster recovery, and even public health. So, let’s walk through it, step by step, from the moment the heart stops to the final handful of dust.

The Moment of Death — The Clock Starts Ticking

Death, biologically speaking, is the point at which circulation and respiration stop, halting oxygen delivery to cells. Without oxygen, the body immediately begins to unravel. Two major processes take over:

  1. Autolysis – self-digestion by enzymes already present in the body.
  2. Putrefaction – microbial activity, mainly from bacteria in the gut and respiratory tract.

These aren’t horror movie concepts. They’re predictable, measurable, and driven by temperature, environment, and the body’s own internal makeup. Here are the five decomposition stages.

Stage One: Fresh (0–3 Days Postmortem)

This is the “quiet” phase. From the outside, the body may look peaceful. But inside, the breakdown has already begun.

  • Algor mortis – body temperature drops about 1.5°F per hour until it matches ambient surroundings.
  • Livor mortis – blood settles in the dependent parts of the body, creating purplish staining.
  • Rigor mortis – muscles stiffen due to a lack of adenosine triphosphate (ATP) and calcium ion accumulation. This starts 2–6 hours after death and fades after 24–48 hours.
  • Internally, cells burst. Digestive enzymes start dissolving organ linings. The gut bacteria—primarily Clostridium and E. coli—begin a feeding frenzy.

There’s no smell yet. But it’s coming.

Stage Two: Bloat (3–7 Days Postmortem)

This is where decomposition makes itself known. Gas accumulation, driven by bacterial metabolism, swells the body like a balloon.

  • Hydrogen sulfide, methane, cadaverine, and putrescine are released—these are the famous “death gases” responsible for the foul odor. You’ll never forget that rotting flesh smell.
  • The face distorts. Tongue protrudes. The abdomen balloons.
  • Skin may blister, slough, or split. Marbling of the skin (a green-black web-like pattern) forms due to hemolysis of red blood cells and gas tracking along vessels.
  • The body may leak fluids from the nose, mouth, orifices, and ruptured skin.

Under pressure, a body may rupture or even partially explode—especially in sealed environments or warm temperatures. Yes, this really happens. I’ve seen it, and it happened to Pius XII.

Stage Three: Active Decay (7–20 Days Postmortem)

Now the body is collapsing in on itself.

  • Tissues liquefy. Organs turn to mush. The skin turns green-black or slips off in sheets.
  • Maggots (from blowflies and flesh flies) are often present unless the environment is sealed or too cold.
  • The volume of insect activity and gas discharge peaks.
  • Skeleton begins to show through as soft tissue breaks down.

The odor is at its worst here. It’s a cocktail of ammonia, sulfur, and organic acids—one that clings to your nose hairs and your long-term memory.

Stage Four: Advanced Decay (20–50 Days Postmortem)

Most of the soft tissue is gone.

  • Insect activity slows as the body becomes less nutritious.
  • Fluids are mostly gone. What’s left is dried tissue, skin, cartilage, and partially skeletonized remains.
  • Soil beneath or surrounding the body may show cadaver decomposition islands—patches rich in nitrogen and fatty acids, often visible to forensic searchers.

Stage Five: Dry/Skeletal (50+ Days Postmortem)

Now we’re down to bone and maybe some desiccated tendons or ligaments. This is the final state, though the timeline can vary wildly depending on conditions.

  • In dry, cold, or arid environments, skeletonization can take years.
  • In hot, humid, or insect-rich environments, it can occur in weeks.

Bones themselves can persist for centuries, but they don’t escape the laws of nature. Eventually, they weather, flake, and return to the earth—especially in acidic soil.

Factors That Influence Decomposition

Decomposition is not a fixed timeline. It’s shaped by many factors:

  • Temperature – heat speeds it up; cold slows it down.
  • Moisture – promotes bacterial and insect activity.
  • Oxygen – essential for some microbes; absence can slow decay.
  • Burial depth – deeper bodies decompose slower.
  • Container – sealed caskets trap gases; open-air exposure accelerates breakdown.
  • Body fat – fatty tissue decomposes faster and can promote adipocere formation (a soap-like substance often called grave wax).
  • Injuries or trauma – open wounds speed microbial and insect access.

Postmortem Chemistry: What’s That Smell?

That unforgettable odor of death? It comes from a chemical symphony:

  • Putrescine and cadaverine – produced by amino acid breakdown.
  • Hydrogen sulfide – rotten egg smell and the odor added to natural gas.
  • Methanethiol – stinks like rotting cabbage.
  • Dimethyl disulfide and trisulfide – pungent sulfur smells.
  • Butyric acid – rancid butter or animal vomit.

All are volatile organic compounds (VOCs), and all are part of the forensic signature that trained dogs, insects, and even analytical devices can detect.

Final Thoughts on Final Decay

There’s something brutally honest about decomposition. It strips away pretense, makeup, and all our biological illusions. It’s not pretty. It’s not poetic. But it’s real. And it’s one of the few universal truths you can bet your bones on.

From a coroner’s point of view, decomposition isn’t just a horror show. It’s a clock, and every stage offers clues: time since death, cause of death, even location and movement of the body. It’s nature’s forensic diary—and if you know how to read it, it speaks volumes.

In the end, decomposition is the great equalizer. It doesn’t care if you were a pope or a pauper, a saint or a sinner. You’ll break down just the same.

Unless, of course, an embalmer gets to you first.

How Not to Embalm a Pope — The Case of Pius XII

You’d think the Vatican—of all institutions—would have mastered the art of saying goodbye. After all, they’ve been burying popes for centuries. But in 1958, when Pope Pius XII died, his body’s final chapter became the most infamous embalming apocalypse in modern history.

It wasn’t just a bad job. It was a botched-beyond-belief spectacle that left mourners gagging, clergy horrified, and even hardened coroners shaking their heads. The embalming of Pius XII was so catastrophically mishandled, it didn’t just mar his memory—it changed the way popes have been prepared for viewing ever since.

The Death of a Pope

Pope Pius XII died on October 9, 1958, at Castel Gandolfo, the papal summer residence outside Rome. He was 82 years old and had ruled the Church through the Second World War and into the height of the Cold War.

According to Catholic tradition, the body of a deceased pope is to be displayed publicly for several days so the faithful can file past and pay their respects. This requires excellent preservation—not just for the dignity of the Church, but for the viewing masses who line up for hours in the Roman heat.

So, what went wrong?

The “Secret” Embalming Method

Instead of entrusting the body to an experienced mortician or medical professional, the task was assigned to Riccardo Galeazzi-Lisi, the pope’s personal physician. Galeazzi-Lisi, whose ego reportedly rivaled his credentials, decided to use a method that was unorthodox, untested, and ultimately disastrous.

He called it a “natural embalming technique.” In reality, it was frightening—an amateurish blend of foundationless folklore and stunningly stupid science.

Here’s what this guy did:

  • He refused to use formaldehyde or traditional embalming chemicals.
  • Instead, he wrapped the pope’s body in plastic sheeting. Basically, he put the pope in a plastic bag.
  • Inside the bag, he inserted sacks of herbs and spices, supposedly mimicking ancient Roman and Egyptian preservation techniques.
  • To prevent putrefaction, he reportedly coated the body with oils and resins, then placed the pope-in-a-bag in a room cooled only by open windows—not refrigeration.

He claimed this “natural mummification” would slow decomposition while maintaining the pope’s appearance. It didn’t.

The Results: A Decomposition Disaster

Within 24 hours, the signs of failure were obvious. The bound body rapidly generated runaway heat and began to bloat. By the time Pius XII was moved to St. Peter’s Basilica for public viewing, the damage was irreversible.

Here’s what witnesses saw and smelled:

  • The pope’s skin turned greenish-black.
  • His facial features swelled grotesquely from trapped gases.
  • The stench was so overpowering that Swiss Guards reportedly fainted.
  • Fluids leaked from the orifices.
  • His nose and his fingers detached.
  • His edematous (bloated, distended, engorged) abdomen ruptured from extreme internal gas pressure, emitting a giant and long-lasting juicy wet-fart sound, causing one priest present to later say “he actually exploded.”

There are credible accounts that the onlooking public recoiled in horror. Vatican officials tried to cut the viewing short and limit media access, but the damage—both physical and reputational—was done. Pius XII’s once-solemn lying-in-state turned into a macabre cautionary tale.

The Fallout: Scandal and Reform

The scandal reached international press. Photographs were suppressed. Riccardo Galeazzi-Lisi was quickly discredited and banned for life from practicing medicine by the Italian Medical Council. He was also dismissed in disgrace from the Vatican.

But the greater consequence was institutional. The Catholic Church quietly but firmly re-evaluated its postmortem protocols for papal embalming. The old approach—personal physicians using eccentric methods—was scrapped in favor of professional, discreet, and clinically proven techniques.

From that point forward:

  • Certified embalmers and anatomical experts were brought in.
  • Formaldehyde-based arterial embalming became standard.
  • Refrigeration and climate control were mandated for extended viewings.
  • Papal funeral procedures were tightened and codified.

In effect, the failure of Pius XII’s embalming modernized the Vatican’s death care procedures.

The Legacy of a Botched Job

Pius XII was known for his solemn intellect and his deep concern for order, tradition, and dignity. Ironically, his final public appearance became a chaotic debacle that overshadowed the sacred rite it was meant to uphold.

But in the strange way history works, his botched embalming wasn’t entirely in vain. It forced the Church to confront the realities of death—not in theology, but in biology.

Since then, no pope has decomposed in public. And when Pope John Paul II, Pope Benedict XVI, and even Pope Francis lay in state for days, their bodies appeared serene, preserved, and untroubled by the putrified rot that defamed Pius XII.

After Pius XII, the Vatican accepted what every coroner knows. Death and decomposition are natural and unforgiving. And if you want to embalm a pope, there’s no substitute for doing it right.

THE TRAGIC DEATHS OF GENE HACKMAN AND BETSY ARAKAWA

On February 26, 2025, the decomposing bodies of legendary Hollywood actor Gene Hackman and his wife Betsy Arakawa were found inside their cloistered estate at Santa Fe, New Mexico. The medical investigator ruled both died of natural causes approximately five days apart—Arakawa passing on February 12, and Hackman being deceased on February 17. There was no evidence of foul play or accident, but there is a sad and compelling story behind the tragic deaths of Gene Hackman and Betsy Arakawa.

The bodies were discovered by maintenance workers who became suspicious as neither Arakawa nor Hackman had been seen in some time. They peered through a window and saw a body on the floor. Police immediately attended as did death scene examiners from the New Mexico Office of the Medical Investigator.

Autopsy and investigation information was released to the public on March 7. “It is unprecedented for the Office of the Medical Investigator to make public statements about sudden death investigations so soon in the process. However, the circumstances surrounding these two deaths require accurate dissemination of important information,” the New Mexico Chief Medical Investigator Dr. Heather Jarrell said at a press conference.

This was a prudent move given the high-profile nature of the Hackman-Arakawa case. In the nine days between the body discoveries and the conference, the media—especially social media—was alive with rumours and false assumptions. It’s to be expected with someone as well known as Gene Hackman and the strange circumstances of this death case.

Although the autopsy reports and scene imagery were quickly sealed by a judge acting on a petition from the Hackman-Arakawa estates, the medical investigator did offer a clear account of the death causes and the circumstances leading up to their tragic demise. Here’s what’s publicly known.

Betsy Arakawa, age 64, was last seen alive between 3:30 and 5:00 pm on February 11. She was filmed on surveillance cameras at Sprouts Farmers Market, CVS Pharmacy, and a pet food store in downtown Santa Fe. Her car entered the couple’s gated community at 5:15 pm using the remote control assigned to her. Cell phone records and inquiries established she’d called a private medical clinic on the morning of February 12 and made an afternoon appointment with a doctor. She never showed up.

Arakawa’s body was positioned on the floor of one of their home’s bathrooms. An open vial and scattered pills were near her, but the medical examiner determined they were a routine prescription for a thyroid condition and had nothing to do with her death. It seemed she’d suddenly collapsed, became unconscious, and shortly died.

Her autopsy showed a serious lung condition, and she suffered from an escalating case of hantavirus infection. Without question, this proved fatal and Hantavirus Pulmonary Syndrome (HPS) clearly was the cause of her death. Hantavirus primarily infects rodents and is highly transferable to humans. The death scene property outbuildings showed evidence of deer mouse infestation which results in airborne particles from droppings or discharges being human-inhaled. HPS can manifest in the body for weeks before sharply increasing in respiratory difficulties and then sudden death.

Hantavirus Pulmonary Syndrome is rare, but the State of New Mexico Health Department recorded 136 infections over the last 50 years. Nearly half of the cases were fatal. HPS is treatable if caught in the early stages, but the autopsy conclusions found Betsy Arakawa was in an advanced, chronic condition. Likely, the rapidly escalating symptoms is why she made the doctor appointment and why she expired so quickly.

Gene Hackman was already aged and frail. He was 95 when he died, and his autopsy showed he was in an advanced stage of dementia—confirmed in the brain dissection and MRIs as Alzheimer’s Disease. Hackman also suffered from significant atherosclerotic cardiovascular disease (plaque-clogged heart arteries) as well as renal disease (failing kidneys).

The medical investigator ruled Gene Hackman’s cause of death was due to complications from heart failure, dementia, and his kidneys shutting down. This is also known as Multiple Organ Dysfunction Syndrome (MODS) and is a common end-of-life condition for the very elderly. Basically, the body progressively quits.

There was strong evidence for Hackman’s death date of February 17. That was the day his pacemaker stopped which is proof of death. Although there’s no doubt about where, when, and how Hackman died, the disturbing and unanswered question is what he knew—what he was aware of—while his wife—his sole caregiver and life support system—lay deceased and decomposing on the bathroom floor. This is truly tragic. Just awful to think of that helpless and alone old man.

Additionally tragic is that one of the couple’s dogs also died during the time Hackman and Arakawa went undiscovered. The animal was recovering from a veterinary procedure and was kept caged. The poor pet probably succumbed to dehydration.

In the time after the body discoveries on February 26 and the official information release on March 7, a lot of media speculation went on about the states of the Arakawa and Hackman corpses, specifically around the reports/rumors of mummification. This has been clearly addressed by forensic pathologist Dr. Judy Melinek in her article on MedPageToday.

Long-term followers of DyingWords.net may remember Judy when she guest posted on this site corresponding to the release of her first book Working Stiff: Two Years, 262 Bodies, and the Making of a Medical Examiner which documented her World Trade Center bombing experience.

Here’s Dr. Melinek’s piece titled Gene Hackman’s Death: How the Mystery Unfolded — Determining time of death can help inform the cause of death.

When actor Gene Hackman and his wife, pianist Betsy Arakawa, were found dead and decomposed in their Santa Fe, New Mexico home on February 26, much of the media fixated on a phrase in the police report describing “mummification” of their hands and feet. People who hear that phrase tend to immediately think of embalmed cadavers from ancient Egypt, as seen in bad movies.

The medical term, however, describes a natural process of postmortem change. Mummification of the extremities occurs as a process of desiccation: the skin dries out, turns brown, wrinkles up. We usually find it in a warm, dry environment, and though it can happen over the course of weeks, it might also set in as quickly as a matter of days.

Given that these two decedents were found indoors in arid Santa Fe, and that there was a space heater in the bathroom near Arakawa’s body, the finding of mummification is not surprising. Subsequent interrogation of Hackman’s pacemaker indicated that the last cardiac activity was on February 17 — 9 days before the bodies were found — and that workers had last been to the residence approximately 2 weeks prior. Meanwhile, Arakawa was last seen on the gated community CCTV and was communicating via e-mail on February 11.

It’s these circumstantial bits of information from the scene that are often the most helpful clues in narrowing down the time of death in the early phases of a death investigation. Let’s dive deeper into the role of a forensic pathologist and other key players in a mysterious case like Hackman and Arakawa’s.

Narrowing Down Time of Death

Time of death estimation is a complex process that depends on multiple factors both intrinsic to the body and found in the immediate environment around it. These variables can include the body’s weight and clothing, the ambient temperature, whether the death occurred indoors in a controlled environment or outdoors where temperatures fluctuate, the health status of the individual just prior to death, and the presence or absence of animals (including insects) that can feed on the body.

Experienced forensic pathologists carry around a mental library of cases that inform us over the course of a career of what a decomposing human body will look like after 24 hours, 48 hours, weeks, and months — and in all different ambient conditions. Death scene investigators can also take a measurement of the core body temperature at the scene that we can compare to published data to help narrow down a tighter death interval using nomograms opens in a new tab or window.

Post-mortem interval estimation isn’t perfectly empirical, but its reliability increases with each bit of information gleaned about a case, the forensic expertise of the person doing the assessment, and the thoroughness of the police investigation. It’s often our role early on to help the police focus their investigation on a reasonable time frame by providing a ballpark estimate of when the person died, and to help them dismiss incompatible testimony or unlikely suspects.

The Cause of Death

What about the cause of death? You have to be concerned about an environmental toxin like carbon monoxide or natural gas when two people and a pet are dead in the same enclosed residence. So, hazardous-materials crews would need to assess such a scene prior to arrival of medical first responders, who might otherwise be putting their own lives at risk. Environmental testing was performed at the residence of Hackman and Arakawa, and additional carbon monoxide testing was also performed on the human remains. All these tests were negative.

The deaths remained a mystery until Friday, March 7, when the medical examiner held a news conference to report that Arakawa had died from hantavirus, a rare pathogen that can be transmitted from rodent droppings, and that Hackman, who had been suffering from Alzheimer’s and cardiovascular disease and had relied on his wife’s care, likely died of heart disease opens in a new tab or window in the same house a week later. It’s not clear if Hackman knew his wife was dead.

This is a heartbreaking conclusion. It came after extraordinarily intensive and quick work by New Mexico’s state Office of the Medical Investigator (OMI) and underscores their dedication and professionalism. The New Mexico OMI has extensive experience with infectious diseases and is one of the select death-investigation facilities in the U.S. with a BSL-3 biosafety level morgue where they can handle infectious agents that spread through airborne transmission.

I suspect that there might have been signs at autopsy that pointed to a lung infection, and that hantavirus was then detected by identifying its genetic signature through polymerase chain reaction (PCR) testing of a nasopharyngeal or lung tissue swab. The Hackman-Arakawa property was in a remote area of Santa Fe, and there was evidence of rodent activity there. The couple had three dogs, and sometimes pets can come in contact with wild rodents and bring them into the house. The necropsy on the dead dog is still pending and may answer more questions about the source of viral exposure.

The Risk of Isolation

I know a lot of gut-wrenching death stories, and the worst ones always involve either the feeling that death may have been preventable, or that the decedent suffered. Everyone who’s been following this shocking and complex public mystery should be grateful to the New Mexico OMI for giving us — and the Hackman-Arakawa family — a speedy and decisive resolution.

If you have people in your lives who are the sole caregivers to a medically fragile patient, please reach out frequently to give them as much help and support as you can. Balancing their need for privacy with your own concerns for their wellbeing is never simple, but maybe these public deaths will open conversations with them about a less isolated environment for their end-of-life care.

Judy Melinek, MD, is an American forensic pathologist currently working as a contract forensic pathologist in Wellington, New Zealand. She is the co-author with her husband, writer T.J. Mitchell, of the memoir Working Stiff: Two Years, 262 Bodies, and the Making of a Medical Examiner, and the forensic-detective novels First Cut and Aftershock. You can follow her on BlueSky @drjudymelinek and Facebook/DrJudyMelinekMD.

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Tragic is an appropriate word to describe the Hackman/Arakawa death case. Here was once an A-List, Oscar-winning movie star and now a very wealthy man living a recluse life with his also-accomplished wife of 30 years. They have no contact with the outside for two weeks, and no one in the family or friend sphere thinks to check on them. An old, frail, and demented man and his increasingly ill younger wife die alone, days apart, and rot on the floor of their multi million-dollar mansion.

The magazine Architectural Digest once ran a feature on the Hackman/Arakawa Santa Fe home. Here’s some pictures of it. It makes one think.

WHAT REALLY KILLED ROBIN WILLIAMS

On August 11, 2014, entertainment genius Robin Williams took his own life inside his Paradise Cay, California home near San Francisco. The coroner initially ruled that Williams, age 63, died by suicide—asphyxia by hanging antecedent to, or caused by, clinical depression. However, when the final autopsy results were in, an entirely different picture played out. Robin Williams was in the advanced stage of a somewhat common, but almost always undiagnosed, brain disease called Lewy Body Dementia or LBD.

As Williams’ window, Susan Schneider Williams who now represents the Lewy Body Dementia Association, stated, “The disease was a terrorist in my husband’s head. Any way you look at it, the presence of Lewy bodies in his brain took his life. Depression was only a symptom. Unfortunately, we as a culture don’t have the vocabulary to discuss brain disease in the way we do about depression. Depression is only a side effect of LBD—it’s rooted in neurology. His brain was literally falling apart, and not one thing could be done about it.”

Lewy Body is a strange term. We’ll examine where that name came from, what exactly LBD is, what causes it, and how this always-fatal disease can be managed in its three progressive stages: early, mid, and late. But first, let’s have a brief look at this remarkable man’s achievements. Perhaps “remarkable” isn’t a powerful enough word for Robin Williams.

Robin McLaurin Williams was born on July 21, 1951, into an average American family. But from an early age, there was nothing average about him. He showed a God-given gift for improvision comedy and acting. By the early 1970s, Williams was in high demand as a San Francisco-based stand-up comedian, and he went on to be one of the funniest funnies of all time.

Few can forget many of Robin Williams’ outstanding character roles. He got his television start in Mork & Mindy and went on to film. Popeye. Hook. Good Will Hunting. Dead Poets Society. Good Morning Vietnam. The World According to Garp. World’s Greatest Dad. Night at the Museum. The Birdcage. Moscow on the Hudson. Jumanji. And, of course, Mrs. Doubtfire.

Williams also did voice-overs in Aladdin, Robots, and Happy Feet. He won numerous awards—six Golden Globes, five Grammys, two Primetime Emmys, two Screen Actors Guilds, and an Oscar for Best Supporting Actor. As well, Williams won the Cecille B. DeMille award in 2005.

Robin Williams had his struggles through life, though. He was addicted to cocaine and alcohol which set him into fitful mood swings. He was in and out of rehab for years. However, by 2010 he was stable and substance free, except for therapeutic prescriptions issues to combat what was thought to be clinical depression.

It was not. Robin Williams had an undiagnosed brain disorder. A disease that was only discovered after his death and was verified by brain sectioning at his autopsy. What was suspected to be Alzheimer’s or Parkinson’s in the last year of his life turned out to be Lewy’s Body Dementia—a condition under the general dementia umbrella and an extremely deadly disease.

You’re likely wondering what this weird name is and what it entails. Rather than me paraphrasing the information, let’s go to the best source available. No, not Wikipedia or ChatGPT.  It’s the website of the Lewy Body Dementia Association, and here’s what it says:

Lewy body dementia (LBD) is the 2nd most common type of progressive dementia after Alzheimer’s disease. The name comes from a discovery by Dr. Friedrich Lewy in the early 1900s of abnormal bodies or deposits of alpha-synuclein proteins in areas of the brain that can only be verified through an autopsy. These bodies alter the production of dopamine and acetylcholine that are vital neural transmitters.

LBD is not a rare disease. It affects more than a million people in the United States alone. Because LBD symptoms may closely resemble other, more commonly known disorders like Alzheimer’s and Parkinson’s disease, it is widely under-diagnosed.

LBD is an umbrella term for two related diagnoses:

  • A person with dementia with Lewy bodies will develop dementia and other LBD symptoms, one of which may be changes in movement, like a tremor (parkinsonism).
  • With the other form of LBD, people will present first with changes in movement, leading to a Parkinson’s disease diagnosis; over time many will develop dementia years later. This is diagnosed as Parkinson’s disease dementia.

As time passes, people with both diagnoses will develop very similar cognitive, physical, sleep, and behavioral symptoms. The earliest symptoms of dementia with Lewy bodies and Parkinson’s disease dementia are different, but both are due to the same underlying biological changes in the brain.

LBD is a multi-system disease and usually requires a comprehensive treatment approach with a collaborative team of physicians and other health care professionals like occupational, physical, or speech therapists. Early diagnosis and treatment may extend your quality of life and independence. Many people with LBD enjoy significant lifestyle improvement with a comprehensive treatment approach, and some may even experience little change from year to year.

For a more in-depth explanation of Lewy Body Dementia disease, here’s a trip to the medical research department at Johns Hopkins University:

Lewy Body Disease (LBD) is a complex and often misunderstood neurodegenerative disorder that affects millions of individuals worldwide. Characterized by the accumulation of abnormal protein deposits called Lewy bodies in the brain, LBD poses significant challenges to both patients and caregivers. In this article, we delve into the neurological aspects of LBD, exploring its development, detection, effects on the human body, and its associated symptoms.

Development of Lewy Body Disease

Lewy Body Disease primarily affects older adults, typically manifesting after the age of 50. While the exact cause of LBD remains unknown, researchers believe that a combination of genetic, environmental, and lifestyle factors may contribute to its development. Genetic mutations, particularly in genes associated with the production and clearance of alpha-synuclein protein, have been implicated in some cases of familial LBD. However, most cases of LBD occur sporadically without a clear genetic link.

Neurological Pathology

At the core of LBD pathology is the abnormal accumulation of alpha-synuclein protein, forming Lewy bodies within neurons. These protein aggregates disrupt normal cellular function and communication within the brain, leading to widespread neurodegeneration. Areas of the brain particularly affected by Lewy bodies include the substantia nigra, which plays a crucial role in movement control, and the cerebral cortex, responsible for cognitive functions.

Detection and Diagnosis

Diagnosing LBD can be challenging due to its overlapping symptoms with other neurodegenerative disorders such as Parkinson’s disease and Alzheimer’s disease. A comprehensive medical history, neurological examination, and a battery of neuropsychological tests are often employed to assess cognitive function, motor abilities, and psychiatric symptoms.

Brain imaging techniques, such as MRI and PET scans, may reveal characteristic patterns of brain atrophy and dysfunction associated with LBD. Additionally, a definitive diagnosis of LBD can only be made post-mortem through the examination of brain tissue for the presence of Lewy bodies.

Effects on the Human Body

Lewy Body Disease has profound effects on both motor and non-motor functions, significantly impacting quality of life. Motor symptoms include bradykinesia (slowed movements), rigidity, tremors, and gait disturbances resembling those seen in Parkinson’s disease. Non-motor symptoms encompass cognitive impairment, hallucinations, fluctuations in attention and alertness, sleep disturbances, autonomic dysfunction (such as orthostatic hypotension and urinary incontinence), and psychiatric manifestations like depression and anxiety.

Treatment and Management

While there is no cure for Lewy Body Disease, various treatment strategies aim to alleviate symptoms and improve patients’ quality of life. Medications targeting dopamine levels in the brain, such as levodopa, may help alleviate motor symptoms. Cholinesterase inhibitors, commonly used in Alzheimer’s disease, may improve cognitive function and psychiatric symptoms in some LBD patients. Multidisciplinary approaches involving physical therapy, occupational therapy, speech therapy, and psychological support are essential for managing the diverse array of symptoms associated with LBD.

Takeaway

Lewy Body Disease presents a complex clinical picture characterized by the interplay of motor, cognitive, and psychiatric symptoms. Understanding its neurological underpinnings is crucial for early detection, accurate diagnosis, and effective management of the disease. Ongoing research efforts aimed at unraveling the molecular mechanisms underlying LBD pathogenesis hold promise for the development of targeted therapies that can ultimately improve outcomes for individuals living with this challenging condition.

I’ll jump back to the Lewy Body Dementia Association for the diagnostic symptoms of the disease.

Motor Symptoms

  • Bradykinesia (slowed movements)
  • Rigidity (stiffness)
  • Tremors (usually less prominent than in Parkinson’s disease)
  • Gait disturbances (shuffling gait, balance problems)

Cognitive Symptoms

  • Fluctuating attention and alertness
  • Memory loss
  • Executive dysfunction (problems with planning, organizing, and problem-solving)
  • Visuospatial difficulties (problems with spatial awareness and perception)

Psychiatric Symptoms

  • Hallucinations (visual hallucinations are particularly common)
  • Delusions (often related to the hallucinations)
  • Depression
  • Anxiety
  • Apathy
  • Irritability or aggression
  • Sleep disturbances (REM sleep behavior disorder, vivid dreams, acting out dreams)

Autonomic Dysfunction

  • Orthostatic hypotension (drop in blood pressure upon standing)
  • Urinary incontinence or urgency
  • Constipation
  • Erectile dysfunction (in men)

Other Symptoms

  • REM sleep behavior disorder (acting out dreams physically)
  • Sensitivity to neuroleptic medications (may worsen symptoms)
  • Changes in sense of smell
  • Difficulty swallowing (dysphagia)

Note that not all individuals with LBD will experience all of these symptoms, and the severity and combination of symptoms can vary widely from person to person. Additionally, symptoms may fluctuate over time, with periods of relative stability interspersed with episodes of worsening symptoms. Early recognition and management of these symptoms are crucial for improving the quality of life for individuals living with LBD.

Detecting and verifying Lewy Body Disease (LBD) involves a comprehensive approach that combines clinical evaluation, neurological assessments, and diagnostic tests. Here’s a breakdown of the steps involved in the detection and verification process.

Clinical Evaluation

  • A thorough medical history is obtained from the patient and their caregivers, focusing on the onset and progression of symptoms.
  • A neurological examination is conducted to assess motor function, cognitive abilities, and psychiatric symptoms. This may include assessing gait, muscle tone, reflexes, coordination, memory, attention, and mood.
  • Careful observation of symptom patterns, including fluctuations in cognition and alertness, visual hallucinations, and motor symptoms resembling Parkinson’s disease.

Diagnostic Criteria

  • LBD is diagnosed based on established clinical criteria, such as the consensus criteria proposed by the DLB Consortium or the McKeith criteria.
  • These criteria outline the characteristic features and diagnostic markers of LBD, including cognitive fluctuations, visual hallucinations, Parkinsonism, and rapid eye movement (REM) sleep behavior disorder.
  • Criteria may also specify supportive features, such as neuroimaging findings and autonomic dysfunction, which further support the diagnosis of LBD.

Neuropsychological Assessment

  • Neuropsychological tests are administered to evaluate cognitive function, including memory, attention, executive function, and visuospatial abilities.
  • These tests help quantify cognitive impairment and track changes over time.

Neuroimaging Studies

  • Magnetic resonance imaging (MRI) and positron emission tomography (PET) scans may be performed to assess brain structure and function.
  • MRI may reveal patterns of cortical atrophy and changes in brain volume associated with LBD.
  • PET imaging with radiotracers targeting dopamine transporters or amyloid plaques can provide additional evidence supporting the diagnosis and differentiate LBD from other neurodegenerative disorders like Alzheimer’s disease.

Cerebrospinal Fluid Analysis

  • Lumbar puncture may be performed to analyze cerebrospinal fluid (CSF) biomarkers associated with LBD, such as levels of alpha-synuclein protein and markers of neuroinflammation.
  • While not routinely performed, CSF analysis can provide supplementary information to support the diagnosis of LBD in some cases.

Genetic Testing

  • Genetic testing may be considered in cases of familial LBD or when there is a strong family history of neurodegenerative diseases.
  • However, genetic testing is not typically performed as part of routine diagnostic evaluation for sporadic LBD.

Multidisciplinary Evaluation

  • A multidisciplinary team approach involving neurologists, neuropsychologists, geriatricians, psychiatrists, and other healthcare professionals is often utilized to ensure a comprehensive assessment and accurate diagnosis of LBD.
  • Verification of LBD relies on the integration of clinical findings, diagnostic tests, and adherence to established diagnostic criteria.
  • Given the complexity and variability of LBD presentation, accurate diagnosis and ongoing monitoring are essential for effective management and supportive care.

Treatment Options

  • LBD is a multi-system disease and typically requires a comprehensive treatment approach, meaning a team of physicians from different specialties, who collaborate to provide optimum treatment of each symptom without worsening other LBD symptoms.  ​
  • A comprehensive treatment plan may involve medications, physical, occupational, speech or other types of therapy, and counseling.

Medications

  • There are many treatments that can help with the symptoms; all medications prescribed for LBD are approved by the Food and Drug Administration to treat symptoms in other diseases, like Alzheimer’s disease and Parkinson’s disease.
  • These medications can offer symptomatic benefits for cognitive, movement, sleep, mood and behavioral changes in LBD.
  • There are not yet any medications that slow or stop the progression of LBD.

Cognitive Symptoms

  • Medications called cholinesterase inhibitors are considered the standard treatment for cognitive symptoms in LBD.
  • These medications were developed to treat Alzheimer’s disease. However, some researchers believe that people with LBD may be even more responsive to these types of medications than those with Alzheimer’s.
  • These drugs sometimes help control behavior problems and hallucinations as well.
  • Another medication that may be helpful is memantine (Namenda).

Movement Symptoms

  • Movement symptoms may be treated with a Parkinson’s medication called carbidopa/levodopa (Sinemet), but if the symptoms are mild, it may be best to not treat them in order to avoid potential medication side effects.

Visual Hallucinations

  • If the hallucinations are not disruptive, they may not need to be treated. However, if they are frightening or create challenging behavioral changes, a physician may recommend treatment.
  • Cholinesterase inhibitors are sometimes effective in treating hallucinations and other psychiatric symptoms of LBD. In addition, newer ‘atypical’ antipsychotic medications may be tried.
  • Most LBD experts prefer quetiapine or clozapine when treatment is necessary for safety or quality of life concerns.
  • Caution is required to find the lowest effective dose in this situation.
  • A newer medication, pimavanserin, was approved to treat psychosis in Parkinson’s disease; results from another clinical trial of this medication in people with dementia and psychosis are pending.
  • While older ‘traditional’ antipsychotic medications such as thorazine and haloperidol are commonly prescribed for Alzheimer’s patients with disruptive behavior, these medications may cause severe side effects in those with LBD.
  • For this reason, older traditional antipsychotic medications like haloperidol should be avoided.

WARNING: Up to 50% of LBD patients treated with any antipsychotic medication may have a severe reaction, such as worsening confusion, heavy sedation, and increased or possibly irreversible parkinsonism. If severe fever or muscle rigidity occurs, contact your doctor immediately; you may have a potentially life-threatening condition that is treated by stopping the medication.

REM Sleep Behavior Disorder (RBD)

  • RBD can be quite responsive to treatment, so your physician may recommend a medication like melatonin and/or clonazepam.

Medication Side Effects

  • Speak with your doctor about possible side effects.
  • The following drugs may cause sedation, motor impairment, or confusion:
  • Benzodiazepines, tranquilizers like diazepam and lorazepam
  • Anticholinergics (antispasmodics), such as oxybutynin and glycopyrrolate
  • Older antidepressants
  • Certain over-the-counter medications, including diphenhydramine and dimenhydrinate.
  • Some medications, like anticholinergics, amantadine, and dopamine agonists, which help relieve parkinsonian symptoms, might increase confusion, delusions, or hallucinations.

Surgery and Anesthesia

  • Be sure to meet with your anesthesiologist in advance of any surgery to discuss medication sensitivities and risks unique to LBD.
  • People with LBD often respond to certain anesthetics and surgery with acute states of confusion or delirium and may have a sudden significant drop in functional abilities, which may or may not be permanent.
  • Possible alternatives to general anesthesia include a spinal or regional block. These methods are less likely to result in postoperative confusion.
  • If you are told to stop taking all medications prior to surgery, consult with your doctor to develop a plan for careful withdrawal.

Other Types of Treatments

  • Lifestyle interventions include eating a healthy diet, exercising, and remaining socially active.
  • Physical therapy includes cardiovascular, strengthening and flexibility exercises, as well as gait training.
  • Speech therapy may improve low voice volume, poor enunciation, muscular strength, and swallowing difficulties.
  • Occupational therapy helps maintain skills and promotes functional ability and independence.
  • Music and aromatherapy may reduce anxiety and improve mood.
  • Individual and family psychotherapy may be useful for learning strategies to manage emotional and behavioral symptoms and to help make plans that address individual and family concerns about the future.
  • Support groups may be helpful for caregivers and persons with LBD to identify practical solutions to day-to-day frustrations and to obtain emotional support from others.

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This might be a lot of cut & pasted material—some maybe repetitive—however I think it’s important to be aware of Lewy Body Dementia.

So far, LBD is incurable but somewhat manageable if detected early-on. Our population is aging. Today’s demographics represent an ever-increasing older population, and the numbers are that many of our folks and friends around us, including ourselves, will develop some form of a degenerative brain disorder like LBD which is what really killed Robin Williams.