#hyperammonemia

[unhonestlymirror]

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Okay, I have to say something.

One of the main problems of current medicine is not the amount of antivaxxers, but the division of society on pro-vaccines and anti-vaccines. And people like this scientist on the video are only expanding the abyss further and futher - in long run, causing more and more people losing faith in vaccinations and in medicine in general. Why, you ask me?

Because the problem of post-vaccinations' complications didn't disappear anywhere - moreover, it only became bigger.

For the last two decades, people went absolutely nuts, vaccinating everything regardless of time periods between shots, the age, the sex, the overall ability of a pathogen to mutate, etc. It was our absolute failure as of the worldwide medical community - and the best proof is the Covid vaccine and its effect.

But enough about Covid. Let's take another example - the MMR vaccine: live-attenuated, three doses, mostly applied to children at 12-15 months. My friend had one at 12 moths, too - however, back then, ~20 years ago, her parents noticed strange movements of her, after the first doze. She arched her back and did not respond to external stimuli. Her parents didn't attach much importance to it. After the second doze (she was already 4 year-old), she developed severe seizures. She was diagnosed with convulsive syndrome, and she had to take Convulsofin (Valproic acid) for 3 years. If you didn't know, Valproic acid is extremely hepatotoxic and can cause acute pancreatitis, thrombocytopenia, hyperammonemia, coma and death. It was also pretty expensive back then. My friend was prescribed of such medication because anything weaker just didn't improve her condition at all - and her neurologist assumed it would be easier for a child than for an adult to adapt and overcome such a dangerous drug. Luckily, she had survived, but she remained disabled for the rest of her life, even though her parents paid crazy amount of money on rehabilitation. Even nowadays, when we occasionally meet, she sometimes flinches and then complains of a headache. Obviously, her quality of life is pretty impaired and has lots of restrictions.

20 years ago, despite there were MANY of such cases, there were no public researches, publications, algorithms "what to do if" - in Ukraine, I mean. It looked as if there was an order from above to keep silent about everything that was happening. Nowadays, the World Health Organisation writes "febriles may occur but they are typically short-term and do not lead to long-term neurological issues" - I want to show them my friend and ask whether they can pay off her medications and rehabilitation costs for all these years. Because there are no long-term issues! There is no war in Ba Sing Se. Maybe it was just her parents' whim - to waste so much money!

The problem of modern medical system is that no one cares what will happen to you, to your child, after vaccination.

You are not listened to, you are labelled immediately as "antivaxxer" - and if you decide to vaccinate, and it gives you severe complications, and you manage to NOT die because of them, all the doctors around are like:

"Welp, it's your problem now. Who cares if you have to pay for rehabilitation from your own pocket - at least you are an acceptable member of society now!"

Is it really that surprising that between "possibly getting ill" and "assurely getting ill after vaccination", a parent usually chooses the first option for their child? Especially if they know that the risk for complications runs in the family? They do not vaccinate you with some random bacteria but with weak versions of the pathogen - the live-attenuated vaccines are the most heavy to deal with. The overload of immunity does exist and can happen after vaccination - and denying the problem because it is being spoken by the person you don't like is a very immature, very unprofessional behaviour, especially from a doctor/scientist.

There is no compensation for developing complications, there is no genetic screening for a vaccine's safety, there is no emergency help algorithm, there are no rehabilitation programs, hell, there is no education about post-vaccine complications treatment and prevention even. There are no safety guarantees. There is probably no improving of vaccines either.

And then they wonder why people vote for drug-addicted fashists like Trump and Elon Musk.

People are not lab mices. People should have a choice whether to apply medication or not. Just because complications are rare doesn't mean they must be ignored. People should not be ostracised for not wanting to vaccinate. There are people like my friend for whom ANY vaccination is strictly contraindicated for the high risk of complications' reccurance - to vaccinate them is the same as to execute them - but no one listens to them, although its our job as doctors, as scientists - not be indifferent. Indifferent doctors are called flayers, slaughterers, human experimentation perpetrators, sometimes even war criminals.

The guy on the video is indifferent. So is Elon Musk, however, he just simply broadcasts the thoughts and feelings of millions of people around the world, whose loved ones had to suffer from such medical indifference and ostracism. Because those farmaceutical oligarchs are interested in incitement of conflict and hatred between the two sides, in selling as much stuff as possible - regardless whether it's useful and safe - those guys are no different from Elon Musk at all, except for being more two-faced.

In conclusion:

We must not spread hatred. If a person doesn't want to vaccinate, listen to their arguments - maybe they have a good reason for that. Don't be blind, be kind.

We must develop safety guarantees and/or compensation for people who get complications after vaccination. Low risk doesn't mean your loved one won't be a victim of it.

We must educate people about what to do if you develop severe reaction on a vaccination. Ignorance breeds mistrust and ruins the belief in doctors. If the parents of my friend were educated, they wouldn't have ignored the first signs, they wouldn't have done the second shot - and my friend wouldn't have become a disabled for life.

We must not force people to vaccinate unless it's a 100% death-rate disease. We are not Auschwitz.

We must not spend so much time on Internet. We must not divide the society for likes, kudos, reblogs, views, whatever.

[owlservice]

I can't help feeling a little mocked by this.

PaTiEnTs wItH nEoNaTaL hYpErAmMoNeMiA hAd a hIgHeR rAtIo oF pAaK pLaSmA aMmOnIa lEvEl ≥500 μmol/L (P=0.003) aNd wErE MoRe liKeLy tO rEcEiVe pReCiSiOn mEdIcInE (P=0.027)

[delveinsight12]

Urea Cycle Disorders Market Growth Anticipated by 2032 | Major Players: Aeglea BioTherapeutics, Immedica Pharma, Ultragenyx Pharmaceutical, Arcturus Therapeutics, expected to boost the market

In the market landscape of Urea Cycle Disorders, an impressive surge is expected during the study period spanning 2019 to 2032, according to the latest report titled  “Urea Cycle Disorders Market Insights, Epidemiology and Market Forecast 2032” from DelveInsight. 

The Urea Cycle Disorders market report sheds light on Urea Cycle Disorders current treatment practices, upcoming drugs in the Urea Cycle Disorders pipeline, market shares of individual therapies, and the anticipated trajectory of the Urea Cycle Disorders market size from 2019 to 2032 across the 7MM (the United States, the EU-4 comprising Italy, Spain, France, and Germany, the United Kingdom, and Japan).

Driving Forces Behind the Urea Cycle Disorders Market Growth

The market size shall grow during the forecast period, i.e., 2023–2032 owing to the increasing prevalence of Urea Cycle Disorders. The market size is expected to increase during the study period.

Discover the Anticipated Evolution and Growth of the Market @ Urea Cycle Disorders Therapeutics Market Forecast

Therapeutic Advancements and Emerging Treatments:

Urea Cycle Disorders Clinical Trial Progression: The market is set to experience significant growth, driven by the progression of emerging therapies expected for launch between 2023 and 2032. Pioneering companies, including Aeglea BioTherapeutics, Immedica Pharma, Ultragenyx Pharmaceutical, Arcturus Therapeutics, and others, are actively engaged in developing novel drugs for potential market entry.

Urea Cycle Disorders Innovative Therapies: Ongoing research and development activities are fostering the introduction of innovative therapies designed to address the signs and symptoms of Urea Cycle Disorders. Therapies such as LOARGYS (pegzilarginase), DTX301, LUNAR-OTC (ARCT-810), and others are driving the Urea Cycle Disorders market.

Urea Cycle Disorders Treatment Market

The treatment of disorders related to the urea cycle is a lifelong process aimed at managing symptoms and doesn't cure the disorder. Strategies include monitoring ammonia levels using blood tests (serum and plasma levels) at regular intervals and using the results to optimize treatment methods. In the current market scenario, recommended therapies to possibly slow the progression of the disease include sodium benzoate, sodium phenylacetate, Glycerol phenylbutyrate, sodium phenylbutyrate, and antiemetic agents. 

These drugs lower blood ammonia concentrations by conjugation reactions involving acylation of amino acids. For neonates with hyperammonemia, the immediate treatment goal is a rapid lowering of ammonia and reducing dietary protein intake. Hemodialysis is very effective at reducing plasma ammonia and should immediately be initiated if elevated hyperammonemia is observed. Ammonia scavenger medications such as AMMONUL IV are also useful. AMMONUL IV acts by removing glycine and glutamate from plasma thereby their reducing contribution to ammonia formation.

Urea Cycle Disorders Treatment Market

The dynamics of the Urea Cycle Disorders market are expected to change owing to a robust pipeline products. Some of the key players involved in the development of novel drugs are Aeglea BioTherapeutics, Immedica Pharma, Ultragenyx Pharmaceutical, Arcturus Therapeutics, and others.

LOARGYS (pegzilarginase) is an engineered human arginase I enzyme designed to degrade the amino acid arginine. Pegzilarginase is being developed to treat two extremes of arginine metabolism, including arginine excess in patients with Arginase 1 Deficiency, as well as some cancers which have been shown to have a metabolic dependency on arginine. The company has completed a Phase III clinical study which demonstrated reduction in blood arginine levels in patients with ARG1-D. The therapy was well tolerated among the patients. Recently, in October 2023, Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency has adopted a positive opinion recommending marketing authorization of LOARGYS (pegzilarginase) for the treatment of arginase 1 deficiency (ARG1-D) in patients two years and older. 

DTX301 is an investigational gene therapy being developed for the treatment of individuals with ornithine transcarbamylase (OTC) deficiency which is the most common urea cycle disorder. DTX301 is designed by Ultragenyx Pharmaceutical to deliver OTC gene expression in a durable fashion, with the goal of preventing or reducing the occurrence of complications associated with OTC deficiency. It has been granted Orphan Drug Designation in the United States, EU and United Kingdom and Fast Track Designation in the United States. Long term Phase I/II data demonstrated an acceptable safety profile and durable metabolic control and sustained responses. The company is conducting a Phase III (NCT05345171) trial to evaluate the efficacy of DTX301 on the improvement of ornithine transcarbamylase (OTC) function by maintaining safe plasma ammonia levels with removal of dietary protein restriction and alternative pathway medication.

LUNAR-OTC (ARCT-810) is messenger RNA (mRNA) coding for Ornithine Transcarbamylase (OTC) formulated in a lipid nanoparticle (LNP). Arcturus Therapeutics is developing mRNA medicines that enable OTC patients to make healthy functional OTC enzyme in the liver cells. The early phase studies demonstrated efficacy of the therapy in restoration of the urea cycle function to normal levels and increased survival. Currently, ARCT-810 is being investigated in Phase II (NCT05526066) clinical development to evaluate the safety, tolerability and pharmacokinetics of ARCT-810 in adolescent and adult participants with ornithine transcarbamylase deficiency.

Leading Urea Cycle Disorders Companies and Emerging Drugs: Pioneering companies such as Aeglea BioTherapeutics, Immedica Pharma, Ultragenyx Pharmaceutical, Arcturus Therapeutics, among others, are actively developing novel drugs for potential entry into the Urea Cycle Disorders market.

Urea Cycle Disorders Therapeutic Landscape: Key therapies identified for Urea Cycle Disorders treatment include LOARGYS (pegzilarginase), DTX301, LUNAR-OTC (ARCT-810), and more.

Urea Cycle Disorders Overview:

Urea cycle disorders (UCDs) are a group of rare genetic disorders that affect the body's ability to eliminate ammonia, a waste product formed during the breakdown of proteins. Normally, ammonia is converted into urea in the liver through a series of biochemical reactions known as the urea cycle. Urea is then excreted from the body through urine.

In individuals with urea cycle disorders, one of the enzymes involved in the urea cycle is deficient or dysfunctional, leading to the accumulation of ammonia in the blood. This elevated ammonia, known as hyperammonemia, can be toxic to the brain and nervous system, causing neurological damage and potentially life-threatening complications.

There are several types of urea cycle disorders, each caused by mutations in specific genes that encode enzymes critical to the urea cycle. These disorders include:

Ornithine Transcarbamylase (OTC) Deficiency: This is the most common urea cycle disorder, caused by a deficiency in the OTC enzyme. It is an X-linked disorder, primarily affecting males. Symptoms can range from mild to severe and may appear shortly after birth or later in life.

Carbamoyl Phosphate Synthetase (CPS) Deficiency: CPS deficiency is a rare autosomal recessive disorder caused by mutations in the CPS1 gene, leading to reduced or absent activity of the CPS enzyme. Symptoms can be severe and appear soon after birth.

Argininosuccinic Acid Synthetase (AS) Deficiency: AS deficiency results from mutations in the ASS1 gene, leading to decreased production of the AS enzyme. Symptoms can range from mild to severe and may present at different ages, from infancy to adulthood.

Arginase Deficiency: This disorder is caused by mutations in the ARG1 gene, resulting in a deficiency of the arginase enzyme. Symptoms often appear in early childhood and can vary in severity.

Symptoms of urea cycle disorders can include vomiting, lethargy, irritability, seizures, developmental delay, coma, and even death if not promptly treated. Diagnosis involves blood tests to measure ammonia levels and specific metabolites related to the urea cycle, as well as genetic testing to identify the specific enzyme deficiency.

Treatment aims to reduce ammonia levels and prevent its accumulation. This often involves dietary restrictions, medications like ammonia-scavenging drugs, and in severe cases, dialysis to remove excess ammonia from the blood. Long-term management by metabolic specialists and genetic counselors is essential for individuals with urea cycle disorders. Early detection and intervention are critical to minimize the risk of neurological damage and improve outcomes for affected individuals.

Key Facts Urea Cycle Disorders Market Report:

Key players such as Aeglea BioTherapeutics, Immedica Pharma, Ultragenyx Pharmaceutical, Arcturus Therapeutics, and others are investigating its candidates for Urea Cycle Disorders.

Urea Cycle Disorders pipeline includes the major therapies such as LOARGYS (pegzilarginase), DTX301, LUNAR-OTC (ARCT-810), and others. 

In December 2022, the US FDA approved OLPRUVA (sodium phenylbutyrate) to treat certain patients living with urea cycle disorders (UCDs). Acer Therapeutics presented data from a survey designed to quantify preferences of healthcare providers for Urea Cycle Disorders (UCDs) at the 44th Annual Meeting of the Society for Inherited Metabolic Disorders (SIMD) on March 18th to 21st.

Urea Cycle Disorders Epidemiology Segmentation:

According to NORD, OTC deficiency affects males more often than females and most males are symptomatic in nature. In males, symptoms typically begin during the first few days of life.

According to reports published by the Centers for Disease Control and Prevention (2022), the anticipated incidence of UCD is 1 in 8,500 births. The research findings suggest that many of the cases of UCD persist undiagnosed. In some of the cases, the newborn with UCD dies without a conclusive diagnosis.

According to the American Association for Clinical Chemistry (2019), the incidence of Urea Cycle Disorders, or UCDs, in the US is estimated to be around 1 in 8,200 births. The mortality rate is 24% in neonatal cases, and 11% in later onset cases.

For in-depth insights, access the full report @ Urea Cycle Disorders Market Outlook 2032

[molsons112000]

So vitamin C can be used to remove chlorine from water and wastewater before it is dumped into rivers or lakes. See this piece below on using vitamin C to reduce chlorine levels.

Approximately 2.5 parts of ascorbic acid are required for neutralizing 1 part chlorine. Since ascorbic acid is weakly acidic, the pH of the treated water may decrease slightly in low alkaline waters. Sodium ascorbate will also neutralize chlorine. It is pH neutral and will not change the pH of the treated water.

https://www.fs.usda.gov › html

Using Vitamin C to Neutralize Chlorine in Water Systems

National Institutes of Health (NIH) (.gov)

https://www.ncbi.nlm.nih.gov › pmc

Protective effect of probiotics and ascorbic acid on bile duct ligation ...

by C Patel · 2022 · Cited by 2 — The probiotic and ascorbic acid combination significantly decreased the elevated blood ammonia levels in BDL-induced rats.



ResearchGate

https://www.researchgate.net › 229...

Effect of dietary vitamin C and ammonia concentration on the ...

Dietary vitamin C supplementation led to higher oxygen consumption and lower ammonia excretion. Na+/K+ ATPase activity increased with increased ambient ammonia ...



Wiley Online Library

https://onlinelibrary.wiley.com › doi

Effect of dietary vitamin C and ammonia concentration on the ...

by WN Wang · 2005 · Cited by 19 — This study examined the effects of dietary vitamin C and ammonia concentration on the cellular defense

Also, reducing ammonia in the blood increases brain performance. See how green tea can reduce or lower ammonia levels in the blood and increase in brain performance and athletic performance.

As you will see below ammonia Impairs the function of synapses in the brain...

Yes, reducing ammonia in the blood can help brain function. Ammonia is a waste product that the body produces naturally, and high levels of it can be toxic to the central nervous system (CNS). This can lead to a range of neuropsychiatric and neurological symptoms, including impaired memory, confusion, delirium, and even coma. 



NCBI

The Cerebral Effect of Ammonia in Brain Aging: Blood ... - NCBI

Jun 24, 2021 — High levels of ammonia, a natural by-product produced in the body, have been r...



NCBI

Blood Ammonia as a Possible Etiological Agent for Alzheimer's ...

May 4, 2018 — In this context, recent findings of some Lactobacillus strains reducing blood a...



MedlinePlus

Loss of brain function - liver disease - MedlinePlus

Aug 7, 2023 — Mild confusion. Forgetfulness. Personality or mood changes. Poor concentration ...



Cleveland Clinic

Hyperammonemia: What It Is, Causes, Symptoms & Treatment

Aug 24, 2022 — Having high levels of ammonia in your blood is toxic to your central nervous s...



VCU Health

New study shows liver patients see benefits after going meatless ...

May 2, 2024 — “We now need more research to learn if consuming meals without meat goes beyond...



National Institutes of Health (NIH) (.gov)

Identifying the direct effects of ammonia on the brain - PubMed

Elevated concentrations of ammonia in the brain as a result of hyperammonemia leads to cer...

Ammonia is normally processed by the liver and eliminated through urine, but issues with the liver or the urea cycle can cause it to build up in the blood. This condition is called hyperammonemia and can be life-threatening, requiring immediate medical treatment. 

Some research suggests that reducing blood ammonia levels may help with neurological diseases and neuronal functions. For example, certain strains of Lactobacillus bacteria have been shown to reduce blood ammonia levels, which may be relevant to the Mediterranean diet's potential to prevent Alzheimer's disease. Other drugs that target ammonia for treatment include sodium benzoate, glycerol phenylbutyrate, ornithine phenylacetate, AST-120, and polyethylene glycol. 

This is for informational purposes only. For medical advice or diagnosis, consult a professional. Generative AI is experimental.

National Institutes of Health (NIH) (.gov)

www.ncbi.nlm.nih.gov

The Cerebral Effect of Ammonia in Brain Aging: Blood–Brain ...

by D Jo · 2021 · Cited by 19 — Ammonia encourages impaired synaptic function in the aged brain, leading to memory loss. High levels of ammonium contribute to energy metabolism ...

https://www.fs.usda.gov/t-d/pubs/html/05231301/05231301.html

Results

Changes in blood ammonia concentration during and after exercise, and the relationship between blood ammonia concentration and total running time

Blood ammonia concentration gradually increased over time as running continued, and then gradually decreased after the end of running (Fig. 1A). The rate of increase of blood ammonia concentration was significantly negatively correlated with total running time, which was measured as an index of exercise endurance capacity (Fig. 1B; r = −0.57, P < 0.05).

https://healthfully.com/naturally-ammonia-levels-down-body-5845643...

How to Naturally Bring Ammonia Levels Down in the Body

WEBJul 27, 2017 · Green tea includes catechins that help prevent cancer cells and flushes your body free …

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Ammonia Build Up

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EatingWell

https://www.eatingwell.com/is-green-tea-good-for-you-8363574

What Happens to Your Body When You Drink Green Tea Every Day

WEBOct 18, 2023 · Several studies have found that green tea helps lower blood pressure. Scientists at the …

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[omkarpatel]

Ornithine Transcarbamylase (OTC) Deficiency Treatment

Ornithine transcarbamylase (OTC) deficiency is an inherited genetic disorder that affects the body's ability to break down ammonia during protein metabolism. If not treated properly, OTC deficiency can cause serious medical issues and even death. Today, there are several effective treatment options available that can help people with OTC deficiency live healthier lives. Let’s take a closer look at OTC deficiency and its treatment: What is OTC deficiency? OTC deficiency occurs due to mutations in the OTC gene which provides instructions for making the ornithine transcarbamylase (OTC) enzyme. This enzyme helps convert ammonia, which is a byproduct of protein breakdown, into urea that can then be safely excreted from the body through urine. With OTC deficiency, the body is unable to effectively remove ammonia due to malfunctioning or non-existent OTC enzyme. This causes excess levels of ammonia, also known as hyperammonemia, in the blood. If left untreated, hyperammonemia can damage the brain and cause complications like intellectual disabilities, coma and even death. Symptoms of OTC deficiency vary from mild to severe depending on the levels of ammonia in the blood. Babies usually present symptoms within the first week of life which may include vomiting, lack of energy, seizures and breathing problems. In some cases, individuals may experience milder symptoms like headaches, nausea and confusion that only emerge during periods of stress or fasting later in life. Treatment Options While there is no cure for OTC deficiency, early detection and lifelong treatment can help manage the condition effectively. The main goals of treatment are to: - Reduce ammonia production by restricting dietary protein intake - Enable removal of ammonia through alternative pathways - Prevent catabolism that breaks down protein - Supplement essential amino acids that are restricted - Treat episodes of hyperammonemia promptly Some of the major treatment options for OTC deficiency include: Low-protein diet: Restricting protein intake is the primary treatment approach as it reduces the production of excess ammonia during protein metabolism. Foods are assigned point values based on their protein content and individuals follow a careful diet plan tailored to their needs and age. Carglumic acid: This drug helps activate an alternative pathway to remove ammonia from the body. It works by stimulating the N-acetylglutamate synthase enzyme which is necessary for urea cycle function. Sodium phenylbutyrate: This medication helps elimnate excess amino acids and allows nitrogen to be excreted in forms other than ammonia. It is often taken with carglumic acid for added benefit. Protein substitutions: Essential amino acids like lysine, threonine and tryptophan that are otherwise restricted for their protein content are supplemented. This prevents deficiency while maintaining a low protein intake. Drugs for hyperammonemia: Episodes of extremely high ammonia levels are treated promptly with medications like sodium benzoate or sodium phenylacetate to enhance ammonia removal along with other supportive measures. Liver transplantation: For patients who do not respond well to dietary and drug therapies, liver transplantation may be considered as it provides a new organ capable of efficient urea cycle function. However, it carries risks and lifelong immune suppression. Proper treatment protocol and diligence Adhering strictly to the prescribed treatment protocol is very important for effectively managing OTC deficiency over a lifetime. Some key points regarding protocol and diligence include:

[uncloseted]

Is it bad to have a reverse sleep cycle where you stay up all night and sleep through the day?

My understanding is that having an inverted sleep cycle is less healthy than having a normal one, even if you’re getting the same amount of sleep. An inverted sleep cycle is associated with an increase in the risk of developing chronic diseases such as obesity, diabetes and cardiovascular disease. People with reverse sleep cycles may also be more socially isolated, since the world is largely designed for people who are awake during the day. If you regularly find yourself with an inverted sleep schedule (not on purpose), you may want to talk to your doctor about it. I don’t think it’s super common but having too much ammonia in your blood (hyperammonemia) can cause sleep cycle inversion.

[drcpanda12]

In medical science, a coma is a state of profound unconsciousness in which a person is unresponsive to external stimuli and cannot be awakened. It is a severe neurological condition that can be caused by various factors, such as traumatic brain injury, stroke, lack of oxygen to the brain, metabolic disorders, infections, or drug overdose. During a coma, the person is unable to consciously perceive their surroundings, speak, or move purposefully. However, basic life-support functions such as breathing and circulation are usually preserved. The level and depth of coma can vary, with some individuals showing minimal brain activity and others displaying some limited responses. Comas can last for a short period or extend for an indefinite duration, depending on the underlying cause and the individual's response to treatment. Medical professionals assess coma patients using standardized scales, such as the Glasgow Coma Scale, to evaluate their level of consciousness and neurological function. Medical professionals monitor and assess comatose patients closely using various diagnostic tests, such as brain imaging, electroencephalography (EEG), and neurological examinations, to determine the cause and potential prognosis. Treatment aims to address the underlying condition, provide supportive care, and promote recovery if possible. However, the outcome of a coma can vary widely, from full recovery to long-term disabilities or even death. Treatment of coma focuses on addressing the underlying cause, providing supportive care, and preventing complications such as infections, pressure sores, or blood clots. In some cases, medications or surgery may be necessary to reduce swelling or treat the underlying condition. Rehabilitation is often required for individuals who emerge from a coma to regain lost physical and cognitive functions. Causes of Coma Drug Poisoning: Responsible for 40% of comatose conditions. Some drugs, when used under particular conditions, can harm or decrease synaptic functioning in the ascending reticular activating system (ARAS), preventing the system from effectively arousing the brain. Drug side effects such as irregular heart rate and blood pressure, as well as excessive breathing and perspiration, may also indirectly damage ARAS function and lead to coma. Because that drug poisoning is the cause of a high proportion of comas, hospitals screen all comatose patients by watching pupil size and eye movement via the vestibular-ocular reflex. Cardiac Arrest: Lack of oxygen, which usually results from cardiac arrest, is the second most prevalent cause of coma, accounting for around 25% of cases. The Central Nervous System (CNS) relies heavily on oxygen to power its neurons. Hypoxia, or a lack of oxygen in the brain, causes sodium and calcium from outside the neurons to drop and intracellular calcium to rise, compromising neuron communication. In the brain, a lack of oxygen induces ATP fatigue, cellular breakdown due to cytoskeleton damage, and nitric oxide generation. Stroke-Related Coma A stroke-related coma accounts for 20% of all comatose states. Blood flow to a portion of the brain is limited or blocked during a stroke. Blood flow may be restricted as a result of an ischemic stroke, a brain hemorrhage, or a tumor. A lack of circulation to brain cells prevents oxygen from reaching the neurons, causing them to become disturbed and die. When brain cells die, brain tissue deteriorates, potentially impairing function. Other Biological Conditions: Trauma, severe blood loss, starvation, hypothermia, hyperthermia, hyperammonemia, aberrant glucose levels, and a variety of other biological conditions account for the remaining 15% of comatose patients. Additionally, studies reveal that 1 in every 8 patients with severe brain damage goes into a coma. A coma scale is a mechanism for determining the degree of coma. Glasgow Coma Scale The Glasgow Coma Scale is a neurological

scale that tries to provide a reliable, objective manner of monitoring a person's conscious state for both initial and ongoing assessment. The criteria of the scale are applied to a patient, and the resulting points give a patient score ranging from 3(Three) indicating profound unconsciousness to 14 (Fourteen). GCS was originally designed to determine the degree of consciousness following a head injury, but it is now used by first responders, EMS, and clinicians to assess all acute medical and trauma patients. It is also used in hospitals for chronic patient monitoring, such as critical care.  Longest Period of Time in Coma  The longest recorded coma in medical history lasted for 37 years. The patient, Terry Wallis, was involved in a car accident in 1984 at the age of 19 and remained in a coma until 2003. During that time, he was unresponsive and completely dependent on medical care. In 2003, Terry unexpectedly regained consciousness and started to communicate with his family. Although he was still severely disabled and had limited cognitive abilities, his recovery was considered remarkable given the length of time he spent in a coma. It's important to note that Terry Wallis's case is exceptional and not representative of typical comas. Coma duration varies widely among individuals, and most comas are of much shorter duration. Medical professionals continue to research and study comes to better understand their causes and potential treatments. Elaine Esposito : According to Guinness World Records, he held the record for the longest duration of time in a coma, having lost consciousness in 1941 and died in that state more than 37 years later. Edwarda O'Bara and Aruna Shanbaug later broke Esposito's record for the longest comas. She was rushed to a hospital at the age of six with a burst appendix and underwent an appendectomy on August 6, 1941. She never regained consciousness after being sedated. She fell into convulsions as the procedure was drawing to a conclusion, her fever soared to 107.6 °F (42.0 °C), and physicians thought she would not survive the night. The origin of the issue was contested, with some claiming Elaine had encephalitis and others claiming her brain did not receive enough oxygen during the procedure. Her parents spent the first 10 months of her coma in a Chicago hospital until they could no longer afford her treatment, at which time they moved her home so her mother Lucy could care for her 24 hours a day, seven days a week. Throughout her extended coma, she had periods of both deep slumber and open-eyed unconsciousness, and she gained only a few pounds, reaching 85 pounds (39 kg). Elaine has overcome a variety of different health issues throughout the years, including more stomach surgery, pneumonia, measles, and a collapsed lung. The family subsequently relocated to Tarpon Springs, Florida, and she was also flown to Lourdes, France, to pray for a miracle.  Elaine died at the age of 43 years and 357 days, having been in a coma for 37 years and 111 days. Edwarda O'Bara : After catching pneumonia in December 1969, he spent 42 years in a diabetic coma beginning in January 1970. At the age of 16, O'Bara suffered pneumonia on December 20, 1969. Her condition deteriorated over the course of two weeks, and she was admitted to the hospital. According to her relatives, O'Bara "woke up shivering and in considerable pain because the oral type of insulin she had been taking wasn't reaching her bloodstream" around 3 a.m. on January 3, 1970. Her relatives hurried her to the hospital, where she succumbed to a diabetic coma. Edward begged her mother, Kaye O'Bara, not to leave her side before she slipped into a coma. She was fed by a tube, and Kaye repositioned her every two hours to prevent bedsores. Kaye also read to her, played music for her, and conversed with her. Joseph, her father, also quit his work to care for her. Kaye passed away in 2008, at the age of 81

. In conclusion, prolonged comas are rare and extraordinary medical conditions that challenge our understanding of the human brain and consciousness. The recorded cases of individuals who have spent extended periods in comas, such as Terry Wallis, Elaine Esposito, Edwarda O'Bara, and Sarah Scantlin, serve as remarkable examples of the resilience and unpredictability of the human body. While the experience of individuals during a coma remains largely unknown, these cases highlight the potential for unexpected recoveries and the enduring dedication of caregivers. The medical community continues to explore the underlying causes and potential treatments for comas, seeking to improve our understanding and provide better care for affected individuals. Though each coma case is unique, the stories of these individuals inspire hope and further our commitment to advancing medical research and support systems for those affected by coma. With ongoing research, continued advancements in medical technology, and dedicated healthcare professionals, we aim to improve outcomes and enhance the quality of life for individuals who experience prolonged comas. Ultimately, the study of comas and their associated challenges fuels our collective pursuit of knowledge and pushes the boundaries of medical science, bringing us closer to unlocking the mysteries of consciousness and improving the lives of those affected by these profound states of unconsciousness.

[knewtoday]

In medical science, a coma is a state of profound unconsciousness in which a person is unresponsive to external stimuli and cannot be awakened. It is a severe neurological condition that can be caused by various factors, such as traumatic brain injury, stroke, lack of oxygen to the brain, metabolic disorders, infections, or drug overdose. During a coma, the person is unable to consciously perceive their surroundings, speak, or move purposefully. However, basic life-support functions such as breathing and circulation are usually preserved. The level and depth of coma can vary, with some individuals showing minimal brain activity and others displaying some limited responses. Comas can last for a short period or extend for an indefinite duration, depending on the underlying cause and the individual's response to treatment. Medical professionals assess coma patients using standardized scales, such as the Glasgow Coma Scale, to evaluate their level of consciousness and neurological function. Medical professionals monitor and assess comatose patients closely using various diagnostic tests, such as brain imaging, electroencephalography (EEG), and neurological examinations, to determine the cause and potential prognosis. Treatment aims to address the underlying condition, provide supportive care, and promote recovery if possible. However, the outcome of a coma can vary widely, from full recovery to long-term disabilities or even death. Treatment of coma focuses on addressing the underlying cause, providing supportive care, and preventing complications such as infections, pressure sores, or blood clots. In some cases, medications or surgery may be necessary to reduce swelling or treat the underlying condition. Rehabilitation is often required for individuals who emerge from a coma to regain lost physical and cognitive functions. Causes of Coma Drug Poisoning: Responsible for 40% of comatose conditions. Some drugs, when used under particular conditions, can harm or decrease synaptic functioning in the ascending reticular activating system (ARAS), preventing the system from effectively arousing the brain. Drug side effects such as irregular heart rate and blood pressure, as well as excessive breathing and perspiration, may also indirectly damage ARAS function and lead to coma. Because that drug poisoning is the cause of a high proportion of comas, hospitals screen all comatose patients by watching pupil size and eye movement via the vestibular-ocular reflex. Cardiac Arrest: Lack of oxygen, which usually results from cardiac arrest, is the second most prevalent cause of coma, accounting for around 25% of cases. The Central Nervous System (CNS) relies heavily on oxygen to power its neurons. Hypoxia, or a lack of oxygen in the brain, causes sodium and calcium from outside the neurons to drop and intracellular calcium to rise, compromising neuron communication. In the brain, a lack of oxygen induces ATP fatigue, cellular breakdown due to cytoskeleton damage, and nitric oxide generation. Stroke-Related Coma A stroke-related coma accounts for 20% of all comatose states. Blood flow to a portion of the brain is limited or blocked during a stroke. Blood flow may be restricted as a result of an ischemic stroke, a brain hemorrhage, or a tumor. A lack of circulation to brain cells prevents oxygen from reaching the neurons, causing them to become disturbed and die. When brain cells die, brain tissue deteriorates, potentially impairing function. Other Biological Conditions: Trauma, severe blood loss, starvation, hypothermia, hyperthermia, hyperammonemia, aberrant glucose levels, and a variety of other biological conditions account for the remaining 15% of comatose patients. Additionally, studies reveal that 1 in every 8 patients with severe brain damage goes into a coma. A coma scale is a mechanism for determining the degree of coma. Glasgow Coma Scale The Glasgow Coma Scale is a neurological

scale that tries to provide a reliable, objective manner of monitoring a person's conscious state for both initial and ongoing assessment. The criteria of the scale are applied to a patient, and the resulting points give a patient score ranging from 3(Three) indicating profound unconsciousness to 14 (Fourteen). GCS was originally designed to determine the degree of consciousness following a head injury, but it is now used by first responders, EMS, and clinicians to assess all acute medical and trauma patients. It is also used in hospitals for chronic patient monitoring, such as critical care.  Longest Period of Time in Coma  The longest recorded coma in medical history lasted for 37 years. The patient, Terry Wallis, was involved in a car accident in 1984 at the age of 19 and remained in a coma until 2003. During that time, he was unresponsive and completely dependent on medical care. In 2003, Terry unexpectedly regained consciousness and started to communicate with his family. Although he was still severely disabled and had limited cognitive abilities, his recovery was considered remarkable given the length of time he spent in a coma. It's important to note that Terry Wallis's case is exceptional and not representative of typical comas. Coma duration varies widely among individuals, and most comas are of much shorter duration. Medical professionals continue to research and study comes to better understand their causes and potential treatments. Elaine Esposito : According to Guinness World Records, he held the record for the longest duration of time in a coma, having lost consciousness in 1941 and died in that state more than 37 years later. Edwarda O'Bara and Aruna Shanbaug later broke Esposito's record for the longest comas. She was rushed to a hospital at the age of six with a burst appendix and underwent an appendectomy on August 6, 1941. She never regained consciousness after being sedated. She fell into convulsions as the procedure was drawing to a conclusion, her fever soared to 107.6 °F (42.0 °C), and physicians thought she would not survive the night. The origin of the issue was contested, with some claiming Elaine had encephalitis and others claiming her brain did not receive enough oxygen during the procedure. Her parents spent the first 10 months of her coma in a Chicago hospital until they could no longer afford her treatment, at which time they moved her home so her mother Lucy could care for her 24 hours a day, seven days a week. Throughout her extended coma, she had periods of both deep slumber and open-eyed unconsciousness, and she gained only a few pounds, reaching 85 pounds (39 kg). Elaine has overcome a variety of different health issues throughout the years, including more stomach surgery, pneumonia, measles, and a collapsed lung. The family subsequently relocated to Tarpon Springs, Florida, and she was also flown to Lourdes, France, to pray for a miracle.  Elaine died at the age of 43 years and 357 days, having been in a coma for 37 years and 111 days. Edwarda O'Bara : After catching pneumonia in December 1969, he spent 42 years in a diabetic coma beginning in January 1970. At the age of 16, O'Bara suffered pneumonia on December 20, 1969. Her condition deteriorated over the course of two weeks, and she was admitted to the hospital. According to her relatives, O'Bara "woke up shivering and in considerable pain because the oral type of insulin she had been taking wasn't reaching her bloodstream" around 3 a.m. on January 3, 1970. Her relatives hurried her to the hospital, where she succumbed to a diabetic coma. Edward begged her mother, Kaye O'Bara, not to leave her side before she slipped into a coma. She was fed by a tube, and Kaye repositioned her every two hours to prevent bedsores. Kaye also read to her, played music for her, and conversed with her. Joseph, her father, also quit his work to care for her. Kaye passed away in 2008, at the age of 81

. In conclusion, prolonged comas are rare and extraordinary medical conditions that challenge our understanding of the human brain and consciousness. The recorded cases of individuals who have spent extended periods in comas, such as Terry Wallis, Elaine Esposito, Edwarda O'Bara, and Sarah Scantlin, serve as remarkable examples of the resilience and unpredictability of the human body. While the experience of individuals during a coma remains largely unknown, these cases highlight the potential for unexpected recoveries and the enduring dedication of caregivers. The medical community continues to explore the underlying causes and potential treatments for comas, seeking to improve our understanding and provide better care for affected individuals. Though each coma case is unique, the stories of these individuals inspire hope and further our commitment to advancing medical research and support systems for those affected by coma. With ongoing research, continued advancements in medical technology, and dedicated healthcare professionals, we aim to improve outcomes and enhance the quality of life for individuals who experience prolonged comas. Ultimately, the study of comas and their associated challenges fuels our collective pursuit of knowledge and pushes the boundaries of medical science, bringing us closer to unlocking the mysteries of consciousness and improving the lives of those affected by these profound states of unconsciousness.

[giazillashow]

Tonight on Blunt Force- #8channel #8chan #4chan connection to recent #massshooting Nana's #medicalmalpractice #malpractice #story 8 pm pst ipmnation.com/live1 #seniorszn #ureacycledisorder #genetics #cps1 #hyperammonemia #protein #disorder #hospital #haf #infections #medicalnegligencemx #ageism #nursingschool #nursinghomes #mcad #anaphylaxis #allergies #medallergies #mederrors https://www.instagram.com/p/B0zde6cg6aO/?igshid=at195xk70690

[factmrresearch1]

CARGLUMIC ACID MARKET ANALYSIS

[siglerprescriptiondrugcards]

Topiramate

Brand Name: Topamax, Trokendi XR

Generic Available in immediate release form

Common Dosage Forms:

Sprinkle Capsules, immediate release: 15 mg, 25 mg

Tablets, immediate release: 25 mg, 50 mg, 100 mg, 200 mg

Capsules, extended release (Trokendi XR): 25 mg, 50 mg, 100 mg, 200 mg

FDA Indications/Dosages:

As adjunctive and monotherapy for adults and pediatric patients ages 2-16 years with partial onset seizures, or primary generalized tonic-clonic seizures, and in patients 2 years of age and older with seizures associated with Lennox-Gastaut syndrome (all dosage forms): Adults: The recommended total daily dose as adjunctive therapy is 200-400 mg. Start with 25-50 mg/day followed by titration to an effective dose in increments of 25-50 mg/week.

Pediatric Patients (2-16 years): The recommended total daily dose as adjunctive therapy is 5-9 mg/kg/day. Start with 25 mg (or 1-3 mg/kg) per evening followed by titration to an effective dose in increments of 1-3 mg/kg/week. Sprinkle capsules may be swallowed whole or by carefully opening the capsule and sprinkling the contents onto a small amount (one teaspoon) of soft food. This mixture should be swallowed immediately and not chewed.

For the initial monotherapy treatment of partial onset or primary generalized tonic-clonic seizures in patients over the age of 10 years (IR only): 400 mg/day in two divided doses. This dose should be reached by titrating over a 6-week period in 50-100 mg/day increments.

For the prophylaxis of migraine headache in adults (IR only): 100 mg/day in two divided doses. This dose should be reached by titrating over a 4-week period in 25 mg/day increments.

Dosage in renal impairment (Crc ≤70 mL/min/1.73 m^2): One-half the usual dose is recommended.

Monitor: Serum bicarbonate

Pharmacology/Pharmacokinetics: Although the exact mechanism of action of topiramate is unknown, it may exert its antiepileptic activity by one or a combination of three known properties: (1) action potentials elicited repetitively by a sustained depolarization of the neurons are blocked by topiramate in time-dependent manner, suggestive of a state-dependent sodium channel blocking action, (2) topiramate increases the frequency of GABA-A receptor activation, enhances the ability of GABA to induce a flux of chloride ions into neurons, and (3) topiramate antagonizes the ability of kainite to activate the kainite/AMPA subtype of excitatory amino acid (glutamate) receptor. Peak plasma levels are reached in about 2 hours and steady state plasma levels are reached in 4 days. Most of the absorbed drug is excreted unchanged in the urine.

Drug Interactions: Additive CNS depression may occur if used with alcohol or other CNS depressants. Topiramate may increase the metabolism of estrogens. Topiramate may increase metformin blood levels. Topiramate is a weak carbonic anhydrase inhibitor, avoid use with other drugs in this class. Phenytoin and carbamazepine may decrease topiramate blood levels. Hydrochlorothiazide may raise the blood levels of topiramate. Use with valproic acid may cause hyperammonemia.

Contraindications/Precautions: May cause hyperchloremia, non-anion gap, metabolic acidosis (decreased serum bicarbonate). Periodic measurement of serum bicarbonate is recommended. Acute myopia associated with secondary angle closure glaucoma has been reported in patients taking topiramate. Decreased visual acuity and/or ocular pain are symptoms of this condition and warrant prompt withdrawal of therapy. Typically, topiramate should be withdrawn gradually to minimize the potential of increased seizure activity. Because of its carbonic anhydrase inhibition, kidney stones may develop during therapy. Pregnancy Category D.

Adverse Effects: The most frequent dose-related adverse effects are fatigue, nervousness, difficulty with concentration, confusion, depression, anorexia, and weight decreases. The most frequent adverse effects not dose-related include somnolence, dizziness, ataxia, speech difficulties, psychomotor slowing, abnormal vision, difficulty with memory, paresthesia, and diplopia.

Patient Consultation:

May be taken without regard to meals.

May cause drowsiness. Use caution while operating machinery or when mental alertness is required.

Avoid alcohol while taking this medication.

Store in a cool, dry place away from sunlight and children.

If a dose is missed, take it as soon as possible. If it is closer to the time of your next dose than the dose you missed, skip the missed dose and return to your dosing schedule. Do not double doses.

Contact a physician if the above side effects are severe or persistent.

Contact a physician immediately upon experiencing blurred vision or periorbital pain.

Keep well hydrated during therapy to decrease the risk of kidney stone formation.

Sprinkle Capsules may be swallowed whole or by carefully opening the capsule and sprinkling the contents onto a small amount (one teaspoon) of soft food. This mixture should be swallowed immediately and not chewed.

[reportsandmarkets]

New study: Hyperammonemia Global Clinical Trials Review, H2, 2017

New study: Hyperammonemia Global Clinical Trials Review, H2, 2017

Hyperammonemia Global Clinical Trials Review, H2, 2017 Summary Hyperammonemia Global Clinical Trials Review, H2, 2017″ provides an overview of Hyperammonemia clinical trials scenario. This report provides top line data relating to the clinical trials on Hyperammonemia. Report includes an overview of trial numbers and their average enrollment in top countries conducted across the globe. Browse…

[letssonalim-blog]

ReportsWeb.com published “Hyperammonemia Market” from its database. The report covers the market landscape and its growth prospects over the coming years. The report also includes a discussion of the key vendors operating in this market.  

[drcpanda12]

New Post has been published on https://www.knewtoday.net/unveiling-the-longest-recorded-coma-in-history-extraordinary-cases-of-prolonged-unconsciousness/

Unveiling the Longest Recorded Coma in History: Extraordinary Cases of Prolonged Unconsciousness

In medical science, a coma is a state of profound unconsciousness in which a person is unresponsive to external stimuli and cannot be awakened. It is a severe neurological condition that can be caused by various factors, such as traumatic brain injury, stroke, lack of oxygen to the brain, metabolic disorders, infections, or drug overdose.

During a coma, the person is unable to consciously perceive their surroundings, speak, or move purposefully. However, basic life-support functions such as breathing and circulation are usually preserved. The level and depth of coma can vary, with some individuals showing minimal brain activity and others displaying some limited responses.

Comas can last for a short period or extend for an indefinite duration, depending on the underlying cause and the individual’s response to treatment. Medical professionals assess coma patients using standardized scales, such as the Glasgow Coma Scale, to evaluate their level of consciousness and neurological function.

Medical professionals monitor and assess comatose patients closely using various diagnostic tests, such as brain imaging, electroencephalography (EEG), and neurological examinations, to determine the cause and potential prognosis. Treatment aims to address the underlying condition, provide supportive care, and promote recovery if possible. However, the outcome of a coma can vary widely, from full recovery to long-term disabilities or even death.

Treatment of coma focuses on addressing the underlying cause, providing supportive care, and preventing complications such as infections, pressure sores, or blood clots. In some cases, medications or surgery may be necessary to reduce swelling or treat the underlying condition. Rehabilitation is often required for individuals who emerge from a coma to regain lost physical and cognitive functions.

Causes of Coma

Drug Poisoning:

Responsible for 40% of comatose conditions. Some drugs, when used under particular conditions, can harm or decrease synaptic functioning in the ascending reticular activating system (ARAS), preventing the system from effectively arousing the brain.

Drug side effects such as irregular heart rate and blood pressure, as well as excessive breathing and perspiration, may also indirectly damage ARAS function and lead to coma. Because that drug poisoning is the cause of a high proportion of comas, hospitals screen all comatose patients by watching pupil size and eye movement via the vestibular-ocular reflex.

Cardiac Arrest:

Lack of oxygen, which usually results from cardiac arrest, is the second most prevalent cause of coma, accounting for around 25% of cases.

The Central Nervous System (CNS) relies heavily on oxygen to power its neurons. Hypoxia, or a lack of oxygen in the brain, causes sodium and calcium from outside the neurons to drop and intracellular calcium to rise, compromising neuron communication.

In the brain, a lack of oxygen induces ATP fatigue, cellular breakdown due to cytoskeleton damage, and nitric oxide generation.

Stroke-Related Coma

A stroke-related coma accounts for 20% of all comatose states. Blood flow to a portion of the brain is limited or blocked during a stroke.

Blood flow may be restricted as a result of an ischemic stroke, a brain hemorrhage, or a tumor. A lack of circulation to brain cells prevents oxygen from reaching the neurons, causing them to become disturbed and die. When brain cells die, brain tissue deteriorates, potentially impairing function.

Other Biological Conditions:

Trauma, severe blood loss, starvation, hypothermia, hyperthermia, hyperammonemia, aberrant glucose levels, and a variety of other biological conditions account for the remaining 15% of comatose patients. Additionally, studies reveal that 1 in every 8 patients with severe brain damage goes into a coma.

A coma scale is a mechanism for determining the degree of coma.

Glasgow Coma Scale

The Glasgow Coma Scale is a neurological scale that tries to provide a reliable, objective manner of monitoring a person’s conscious state for both initial and ongoing assessment. The criteria of the scale are applied to a patient, and the resulting points give a patient score ranging from 3(Three) indicating profound unconsciousness to 14 (Fourteen). GCS was originally designed to determine the degree of consciousness following a head injury, but it is now used by first responders, EMS, and clinicians to assess all acute medical and trauma patients. It is also used in hospitals for chronic patient monitoring, such as critical care.

 Longest Period of Time in Coma 

The longest recorded coma in medical history lasted for 37 years. The patient, Terry Wallis, was involved in a car accident in 1984 at the age of 19 and remained in a coma until 2003. During that time, he was unresponsive and completely dependent on medical care.

In 2003, Terry unexpectedly regained consciousness and started to communicate with his family. Although he was still severely disabled and had limited cognitive abilities, his recovery was considered remarkable given the length of time he spent in a coma.

It’s important to note that Terry Wallis’s case is exceptional and not representative of typical comas. Coma duration varies widely among individuals, and most comas are of much shorter duration. Medical professionals continue to research and study comes to better understand their causes and potential treatments.

Elaine Esposito :

According to Guinness World Records, he held the record for the longest duration of time in a coma, having lost consciousness in 1941 and died in that state more than 37 years later. Edwarda O’Bara and Aruna Shanbaug later broke Esposito’s record for the longest comas.

She was rushed to a hospital at the age of six with a burst appendix and underwent an appendectomy on August 6, 1941. She never regained consciousness after being sedated. She fell into convulsions as the procedure was drawing to a conclusion, her fever soared to 107.6 °F (42.0 °C), and physicians thought she would not survive the night. The origin of the issue was contested, with some claiming Elaine had encephalitis and others claiming her brain did not receive enough oxygen during the procedure.

Her parents spent the first 10 months of her coma in a Chicago hospital until they could no longer afford her treatment, at which time they moved her home so her mother Lucy could care for her 24 hours a day, seven days a week.

Throughout her extended coma, she had periods of both deep slumber and open-eyed unconsciousness, and she gained only a few pounds, reaching 85 pounds (39 kg). Elaine has overcome a variety of different health issues throughout the years, including more stomach surgery, pneumonia, measles, and a collapsed lung. The family subsequently relocated to Tarpon Springs, Florida, and she was also flown to Lourdes, France, to pray for a miracle.

 Elaine died at the age of 43 years and 357 days, having been in a coma for 37 years and 111 days.

Edwarda O’Bara :

After catching pneumonia in December 1969, he spent 42 years in a diabetic coma beginning in January 1970.

At the age of 16, O’Bara suffered pneumonia on December 20, 1969. Her condition deteriorated over the course of two weeks, and she was admitted to the hospital. According to her relatives, O’Bara “woke up shivering and in considerable pain because the oral type of insulin she had been taking wasn’t reaching her bloodstream” around 3 a.m. on January 3, 1970.

Her relatives hurried her to the hospital, where she succumbed to a diabetic coma. Edward begged her mother, Kaye O’Bara, not to leave her side before she slipped into a coma. She was fed by a tube, and Kaye repositioned her every two hours to prevent bedsores. Kaye also read to her, played music for her, and conversed with her. Joseph, her father, also quit his work to care for her. Kaye passed away in 2008, at the age of 81.

In conclusion, prolonged comas are rare and extraordinary medical conditions that challenge our understanding of the human brain and consciousness. The recorded cases of individuals who have spent extended periods in comas, such as Terry Wallis, Elaine Esposito, Edwarda O’Bara, and Sarah Scantlin, serve as remarkable examples of the resilience and unpredictability of the human body.

While the experience of individuals during a coma remains largely unknown, these cases highlight the potential for unexpected recoveries and the enduring dedication of caregivers. The medical community continues to explore the underlying causes and potential treatments for comas, seeking to improve our understanding and provide better care for affected individuals.

Though each coma case is unique, the stories of these individuals inspire hope and further our commitment to advancing medical research and support systems for those affected by coma. With ongoing research, continued advancements in medical technology, and dedicated healthcare professionals, we aim to improve outcomes and enhance the quality of life for individuals who experience prolonged comas.

Ultimately, the study of comas and their associated challenges fuels our collective pursuit of knowledge and pushes the boundaries of medical science, bringing us closer to unlocking the mysteries of consciousness and improving the lives of those affected by these profound states of unconsciousness.

[juniperpublishersanesthesia]

Idiopathic Hyperammonemia after Orthotopic Lung Transplantation-Juniper Publishers

Introduction

Idiopathic hyperammonemia is characterized by increased serum ammonia levels (>200umol/L) and is sometimes associated with normal to slightly elevated liver function tests [1]. These patients often present with encephalopathy, cerebral edema, seizures, and coma. Idiopathic hyperammonemia has been reported after high dose chemotherapy, and organ transplants including Orthotopic lung transplant [2]. Hyperammonemia is a rare, severe, and often fatal complication. There are few cases reported in the literature since 1997, including one retrospective analysis of 807 lung transplants; only 8 patients were diagnosed with hyperammonemia [3]. The exact mechanism of idiopathic hyperammonemiais not fully understood with congenital or acquired defects in ammonia metabolism, as well as bacterial infection having been described [3].

Ammonia is primarily cleared by the liver’s urea cycle. The urea cycle converts ammonia to urea through a series of intermediate reactions. Hyperammonemia can be the result of any number of inborn errors (congenital or acquired) of urea cycle metabolism. Another hepatic mechanism for ammonia clearance is through glutamate synthetase, which converts glutamate and ammonia to glutamine. In the kidneys, glutamine is broken down back into glutamate and ammonia, which is then excreted. If hepatic or renal elimination of ammonia is interrupted, then hyperammonemia can occur leading to severe consequences. We present a case below of a female patient who developed hyperammonemia after Orthotopic lung transplant.

Case Presentation

66 year old Caucasian female with past medical history significant for COPD (on 3 litres/minute home O2 at rest and 4litres/minute O2 with activity), emphysema, extensive smoking history, morbid obesity with body mass index 34, obstructive sleep apnea using continuous positive airway pressure therapy, hypertension, hyperlipidaemia, and osteoporosis, presented to the hospital for single left lung transplant via anterolateral thoracotomy. The patient tolerated the procedure well and was transferred to the intensive care unit without any issues. Her post-operative course was initially complicated by acute hypoxic ventilator dependent respiratory failure.

She developed increasing supplemental oxygen requirements and had several bronchoscopies with endotracheal tube changes to help clear thick secretions. Vancomycin and meropenem were prescribed to treat pneumonia. On postoperative day 3, the patient developed atrial fibrillation with a rapid ventricular response, which was treated with cardio version and digoxin. By postoperative day 4, the patient’s mental status became altered and continued to decline. A CT of the head showed no acute intracranial abnormalities. At this time, her blood ammonia levels were noted to be elevated at more than 30 milligrams per deciliter (mg/dL) and lactulose was started. Her ammonia levels continued to rise and rifaximin was added to her treatment. The patient subsequently became hemodynamically unstable and was unable to be weaned off the ventilator. She required vasopressor support and was placed on veno-venous ECMO.

Ammonia levels on postoperative day 8, now approximately 60mg/dL, had not responded to lactulose or rifaximin and she was placed on continuous veno-venous hemodialysis (CVVHD) and prescribed arginine HCl. The patient had been on total parenteral nutrition and this was discontinued. An electroencephalogram was done to rule out seizures. The patient transiently responded to therapy, regaining consciousness and responding to commands. On postoperative day 12, she became agitated and required sedation as she was still ventilated. Ammonia levels had risen to 234 mg/ dL, and sodium benzoate and sodium phenyl acetate infusions initiated. The patient’s ammonia levels began to gradually decline, but her respiratory status also declined. Anti-HLA antibodies were found and she was placed on plasmapheresis, high-dose steroids and IVIG. Ultimately, hemolysis due to plasmapheresis added to her complications. Despite efforts to correct her DIC, the patient was rapidly deteriorating and the family decided to withdraw care after multiple family meetings. The patient’s ammonia level at time of death was 99 mg/dL. The family declined an autopsy.

Discussion

The exact mechanism of idiopathic hyperammonemia is unknown, but logically, increased blood ammonia levels would be due to increased production or decreased metabolism of ammonia. Both types of mechanisms have been reported in the literature. Tuchman, et al. [4] looked at peri- and postmortem liver samples from two patients with hyperammonemia after lung transplant. They found decreased levels of glutamine synthase (12% and 28% of normal) [4]. Bezinover, et al. [5] discovered an apparently acquired defect in the urea cycle in a renal transplant patient who developed postoperative hyperammonemia. The patient had increase orotic acid levels in his urine [5]. Bacterial infections have been identified as causing increased blood ammonia levels in patients. Specifically, Mycoplasma hominis splits arginine as an energy source, releasing large amounts of ammonia as a waste product. This bacterium has been identified as an infectious agent in a lung transplant patient who developed hyperammonemia [6].

Urea plasma infection has also been identified as the cause of hyperammonemia [7]. Once a post-transplant patient develops symptoms of lethargy and altered mental status, acute pathology should be ruled out with CT head and EEG, and ammonia levels checked early. If a patient is found to have symptomatic hyperammonemia, the excess ammonia needs to be removed as quickly and safely as possible. Most reported cases have been treated with multipronged approach. Ammonia has been shown to be effectively cleared with renal replacement therapy. One case series reported by the department of medicine at Washington University shows that prompt initiation of high flux intermittent hemodialysis in conjunction with other methods of lowering ammonia, can lead to better outcomes [3]. Increasing dialysis flux can also maximize small molecule solute clearance (ammonia is a low-molecular weight molecule).

The rapid removal of ammonia by hemodialysis does not cause disequilibrium syndrome since ammonia a gas and is not osmotically active. However, with high efficiency dialysis in these cases, nephrology should be on board to maintain electrolyte abnormalities. In addition to renal replacement therapy, ammonia can also be decreased by limiting nitrogen intake, bowel decontamination and by supplementing the endogenous nitrogen removing mechanisms. Endogenous ammonia production from protein catabolism can be limited by discontinuing TPN and enteral nutrition. Bowel decontamination with lactulose and rifaximin can also reduce the intestinal ammonia production. Arginine supplementation via intravenous infusion can help expedite ammonia uptake into the urea cycle, and therefore expedite ammonia excretion from the body (arginine is the immediate precursor to ornithine, an essential amino acids in the urea cycle) (Figure 1).

Sodium Benzoate binds to glycine, leading to the formation of hippurate, which diverts ammonia away from the defective urea cycle and results in fecal excretion. Sodium phenyl acetate binds serum glutamine to form phenyl acetyl glutamine which is then excreted in the urine [8]. Despite the fact that we began CVVHD on our patient when her ammonia was 61 mg/dL and aggressively treated her with bowel decontamination, stopping exogenous proteins, starting an arginine hydrochloride infusion and ammunol (sodium benzoate and sodium phenyl acetate) infusion – her ammonia levels continued to rise, peaking at 234 mg/dL. Although her ammonia levels were trending down, her course was further complicated by acute rejection of her left lung transplant and disseminated intravascular coagulation.

Conclusion

Idiopathic hyperammonemia after Orthotopic lung transplant is a rare, but often fatal complication of unknown etiology. Currently, treatment of hyperammonemia is largely supportive with methods derived from case reports. More case reports and retrospective/prospective studies need to be conducted so that a standardized hyperammonemia protocol can be formulated.

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