A Student Ate 5-Day-Old Pasta For Lunch. This Is How His Liver Shutdown. AJ is a 20 year old man, presenting to the
emergency room with abdominal pain, nausea, and diffuse bleeding. Paramedics were scrambling because he kept
vomiting in the ambulance until he fell unconscious. AJ was a struggling college student. Like most other people born in his time, he
was looking forward to crushing student loan debt that would wipe away his entire adult life. The most affordable food for him was cheap
pasta, cooked with premade sauce. AJ would make all his food for the week on
Sunday. He’d refrigerate it into containers. This way, he could ration it by day, but sometimes,
he’d accidentally leave his food out overnight, and then eat it following morning. His friends loved to joke that one day, AJ
would die of food poisoning. Except this time, it wasn’t really a joke. Earlier in the week, AJ accidentally left
his pasta out for 2 days. He typically would have thrown that away,
but his roommate didn’t know. He thought it may have just been out for a
few hours so he put it back into the fridge. As AJ reheated the now 5 day old pasta that
was left out for 2 days, he thought it smelled kind of strange. But, he used a different brand of sauce this
time, so he didn’t think much of it. Immediately after finishing the entire plate
of pasta, AJ’s stomach started to hurt. He was bloating. He could feel gas build up in his stomach
and the flatulence was so embarrassing, he had to go outside to air out his pants. A stinging pierced through his cheeks and
he could feel his eyes push out of his skull as he suddenly vomited in a way like never
before. That pasta must have been no good, he thought. It’s probably just a little food poisoning,
he thought. Back in his dorm room now, AJ in a world of
hurt, joked to his roommate Bradley that more than just pasta had exited his body from both
ends. Hoping that he’d feel better, he went to
bed, but before that, he made sure to drink an entire bottle of stomach medicine in hopes
that it would do something for the nausea, vomiting and diarrhea. But it wasn’t enough. 3 am. AJ, laying in a pool of cold sweat, runs to
the bathroom to huddle over the sink for a couple more hours. As his roommate goes into the bathroom, he
sees AJ passed out on the floor, his skin and the whites of his eyes a sickly greenish
yellow. AJ gets up and weakly stumbles around before
falling down again. Bradley calls for 911 and AJ is brought to
the emergency room where we are now. Given this history of present illness, it’s
clear that AJ is suffering from some kind of food poisoning that is causing liver failure. But to the medical team, that's not immediately
obvious. AJ is an otherwise healthy 20 year old man,
who wasn’t taking any medicines. Given that he’s coming from a college dorm,
and he was vomiting and became unconscious, then that sounds like it could be an alcohol
poisoning case. The yellowing of his skin and eyes is called
jaundice and it comes from a chemical called bilirubin something that makes poop brown
and is produced from breaking down red blood cells in the liver. And if bilirubin is floating around in the
blood making the skin yellow, then it means the liver is probably damaged, which brings
us back to the suspicion of alcohol poisoning as that can damage the liver. Similarly, another cause of liver damage and
unconsciousness in a healthy, college-aged person could be a drug overdose, of which
even the roommate may not be aware. Except, a blood test finds no evidence of
alcohol or drug use. Instead, it’s found that AJ has hypoglycemia. Hypo meaning low. Glyce from Ancient Greek (γλυκυς) glykys
meaning sweet referring to sugar. and Emia meaning presence in blood. Low Sugar Presence in Blood. AJ ate his last meal of spoiled pasta about
16 hours ago. Blood sugar levels spike after eating, and
level off 4 hours after, wherein the human body continuously works to maintain normoglycemia,
but for AJ, that mechanism isn’t functioning, meaning something that’s supposed to be releasing
that sugar, isn’t releasing it. Hypoglycemia by itself, is a relatively nonspecific
problem. It means you could have several different problems that could be causing it. But given that the liver is the most immediate
source of stored sugar, then this developing developing hypoglycemia could give us a biochemical basis
for explaining his fulminant liver failure. You see, the liver is a highly metabolic organ. You can’t live for very long without one. Everything that enters your mouth, ends up
in the liver, as it breaks down chemicals and red blood cells, secretes bile for digestion,
makes blood clotting factors that stop you from bleeding, and processes proteins, among
other functions, and it maintains blood sugar levels, bringing us back to metabolism. Sugar, or glucose is the cell’s primary
source of energy, and the liver, to perform all these functions, commands a high demand
of cellular energy. Given that glucose is no longer being released
from the liver into the blood stream, then it indicates that there is likely a metabolic
problem developing inside AJ’s liver. And because fatty acids are oxidized into
glucose, which then results in ATP production, then it means there is likely fatty deposits
growing inside, stopping all essential liver functions. We can assume here that AJ’s food poisoning
from rotten pasta is likely from some kind of bacterial, maybe fungal source, but something’s
wrong. Typically food poisoning just causes stomach
inflammation, nausea, vomiting and diarrhea. It doesn’t typically cause acute liver failure,
and even worse, we can’t find out which bacteria is causing the problem because culturing
it would take days. Days that AJ doesn’t have, because his liver
is quickly shutting down. His response to broad spectrum
antibiotics is limited. Additional blood tests find multiple liver
enzymes, floating around in his blood at a level 500 times the upper limit of normal,
meaning parts of his liver have started to die and are circulating now all throughout
his body. His kidneys are starting to fail because analysis
of his urine finds blood in it. In liver failure, especially with the presence
of bacteria, the body signals to the immune system that something’s wrong. White blood cells and inflammatory markers
rush to the site, and vasodilate the splanchnic arteries. From Ancient Greek splankhnikos meaning entrails. Because about 30% of systemic blood is in
the splanchnic circulation, this volume expansion decreases the effective blood volume. The heart detects this and secretes hormones
to tell the body to hold on to water and sodium, and to constrict all other blood vessels,
including the ones going into the kidneys, preventing blood flow in and causing acute renal
injury in conjunction to fulminant hepatic failure. If there is no available liver for transplantation
within the next day, AJ has minimal odds of survival. The idea of liver failure arising from toxic
compounds ingested orally was not understood until recent times. In 1778, the ackee tree was transported to
Jamaica from Western Africa by the British. In 1875, unripened ackee fruit was consumed
by people, followed by a record of vomiting, hypoglycemia, hyperammonemia, elevated liver
enzymes in blood, and fat buildup in the liver. This was named Jamaican Vomiting Sickness. It was found 100 years later in 1976 that
hypoglycin A is the chemical that inhibits liver mitochondrial activity, leading to fatty acid
build up, hypoglycemia, hyperammonemia, resulting in liver failure. A famous description of aspirin overdose in
children in the 1960s was published and named Reye’s syndrome. It was noted that children who received aspirin
for fever reduction from the flu had a syndrome of hypoglycemia, hyperammonemia, elevated
liver enzymes and metabolic acidosis, symptoms that looked very similar to those who suffered
from Jamaican Vomiting Sickness. We know today that excess aspirin uncouples
the electron transport chain in mitochondria during ATP synthesis, leading to fat buildup
and liver failure. Today, any aspirin prescribed for a child
is considered a mistake and at medication dispensing will almost always be substituted
for a different drug. For AJ, no liver was available in time for
transplant and autopsy opened the opportunity for further investigation. Liver histologies revealed diffuse microvesicular
steatosis, that is small vesicles of fat that had accumulated inside his liver. The cellular necrosis, that is, dead cells
suggested that mitochondrial toxins were at play meaning that bacteria may not have been
the only problem with his spoiled pasta. Post-mortem laboratory experiments and bacterial
cultures were developed. Samples of AJ’s vomit were collected while
he was admitted, in addition to bile and the pasta he ate. The bacteria Bacillus Cereus was identified
as the causative agent. It’s well known as a foodborne pathogen
that causes gastritis. By itself, the food poisoning that results
from it is usually self-limiting, meaning one can recover from it through intrinsic bodily function. But for AJ, a second agent was found. Additional lab methods were used to detect,
extract, isolate and purify the toxin from Bacillus Cereus cultures, revealing the protein
known as cereulide, which points us to the final answer of AJ’s case. Certain strains of Bacillus Cereus produce
cereulide in its microenvironment. This protein is an ionophore, meaning it has
an affinity for 1 specific electronically charged ion, namely, potassium. For the bacteria, excess potassium is beneficial
in its survival locally, but in humans this is highly toxic. Cereulide easily diffuses through cell membranes. Inside, they embed onto the surface (inner membrane) of the
mitochondria. Human intracellular fluid is potassium rich,
meaning it gives this toxin sufficient resources to perform its ionophoresis, incessantly pumping
potassium into the mitochondria. This eventually overloads the ability of mitochondria
to perform oxidation required to produce ATP and energy, therefore preventing the use of
glucose and fats. The gradual swelling of the mitochondria causes
it to burst, killing the cell, and on a macroscopic scale, allows fat to pool into the liver,
and causing the entire organ to fail, leading to regional inflammation, splanchnic vasodilation,
leading to the heart to release hormones for the body to hold on to water, and to constrict
the blood vessels of the kidneys, causing kidney failure, and releasing ammonia and
glutamate, that leads to swelling of the brain, ending in death. All because AJ unknowingly ate pasta that
was left out unrefrigerated for 2 days. The final link in this case comes not from
the pasta. but that stomach
medicine AJ drank after initially vomiting Bismuth subsalicylate is a salicylate,
or more colloquially known as aspirin. Aspirin overdoses, just like in Reye's Syndrome also result in liver
failure because aspirin uncouples the electron transport chain in mitochondria, preventing
conversion of glucose into ATP, causing backing up of glucose and pooling of fats in tissue. So adding this medicine overdose to cereulide
poisoning resulted in a dual blockade of ATP synthesis, and leading to acute liver failure. It’s important to note that this is NOT
a typical food poisoning case. Many people eat pasta, or any other kind of noodle that is left over for
a day or two and are fine. But tragic cases such as this one have been
reported in literature, and the fulminant hepatic failure is sudden, with patient expiration
happening within hours after presenting to the emergency room. Some particularly tragic published cases are
from families who go out on a picnic with their children, only to have multiple small
kids under 10 years old suffer from sudden liver failure due to spoiled pasta. And the end of those stories, are the same as in AJ's case. Be careful of food left out for more than
a few hours. If food smells funny, it’s always better
to be safe than sorry, and for cases like cereulide poisoning, sometimes there isn’t
much time left after initially eating the spoiled food, just like for AJ. This case was presented at a grand rounds
in Illinois. It’s based off some famous toxicology cases
that all unfortunately had the same ending, this one modified to teach residents and fellows
about acute cirrhosis from microvesicular steatosis hepatorenal syndrome, and the pathogenesis
of cerebral edema in this particular cereulide poisoning setting. Thank you so much to all my toxicology colleagues
in helping me structure this video to be palatable for a general audience, and thank you for
watching. Take care of yourself. And be well.
In case anyone comes in here who has some kind of medical education, could they have saved this guy if they knew what was wrong with him?
That amount of aspirin would send anyone into liver failure. What kind of idiot drinks an entire bottle of medication?
Ah yes, my monthly dose of anxiety, thanks OP
this is r/MealPrepSunday's worst nightmare
Wow. This is indeed a real case, but some of the details have been changed. He never made it to the ER.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3232990/
TLDR: Food poisoning with multiple types of bacteria coupled with an overdose of asprin (which was in a medicine he took).
This guy has once again scared the shit out of me. Had a couple spoonfuls of sugar to keep the hypoglycemia away during this vid.
Heftig
Food safety should always be taken seriously but let's be real, this guy got super unlucky and also compounded the problem with irresponsible behavior.
No reason to freak out and assume you're going to die from food.